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First Swine Flu DNA Test: Unveiled and Delivered

2010-03-25T07:28:00.000-07:00

First Swine Flu DNA Test: Unveiled and Delivered

team of genetics experts in Southampton have produced swine flu real-time PCR kit, the world’s first DNA test for influenza A(H1N1). The first shipment of rapid-results tests has been sent to Mexico and various territories to aid the authorities in monitoring the number of suspected cases.

The test kit was developed by PrimerDesign Ltd, a UK-based firm founded by University of Southampton. This company already manufactures genetic detection kits for other viruses. When the Center for Disease Control published the genetic data of the deadly swine flu virus early this month, PrimerDesign’s swine flu DNA project team announced that the development the ultimate diagnosis tool was imminent.

The real-time PCR kit works by rapidly multiplying a sample of DNA taken from a suspected swine flu patient. This test quickly differentiates common strains of the flu virus from H1N1. While the current tests for swine flu are accurate, medical professionals would have to wait for 2 days for the result. The new Swine Flu test kit, on the other hand, detects the presence of the virus within 2 hours. At the rate the swine flu virus is spreading, early detection is unquestionably significant. According to Dr. Jim Wicks of PremierDesign, the new DNA test will contribute to the worldwide effort against Swine flu.

The swine flu real-time test kit is sold primarily for research purposes but could also be used to diagnose the disease in laboratories globally. At present, 29 countries have officially reported 4379 cases of influenza A(H1N1) infection. Updates and other information about swine flu can be found on the World Health Organization’s website.

References:
University of Southampton (2009, May 2). Scientists Race To Deliver DNA Swine Flu Test
University of Southampton (2009, May 10). First Swine Flu DNA Test Produced.

Brain Cyst - Can they be diagnosed with CT scan?

2010-03-25T07:18:00.000-07:00

Brain Cyst - Can they be diagnosed with CT scan?

Dear Dr. Joshua,

I am trying to find out if a brain cyst can be diagnosed and said to be benign if only a cat scan was done. I was told today that I have one and I am very concerned because no treatment or follow up or futher testing was discussed. I can find out how to post a question can you please help me. I am a 53 year old female who has had a horrible painful migraine since last wed January 2nd and it has been accompanied by vomiting. It is the worst migraine I have ever had. I spent friday and saturday in the er and that is where the cat scan was done. I need to know if it is possible to diagnose without seeing me or futher testing. And if it is benign cyst does anything need to be done and is this the cause of this massive migraine.

Dr. Joshua’s Answer:

Certain types of cysts can be reliably diagnosed with CT (Cat scan) alone, for instance, typical arachnoid cysts, which commonly occur in the temporal region. Often they require no treatment or follow up at all, and are usually congenital, in other words, something you’re born with. Sometimes arachnoid cysts build up pressure and cause symptoms, but more often than not they are an incidental finding.

Typically they are found when doing a CT due to headaches, but they rarely explain the headaches.

There are a variety of possible “cysts” that can be seen on CT, and if the finding is unclear, an MRI is usually done. Only your doctor can tell you what exactly it is they saw, and why they chose not to do any further investigations. Please call your doctor and ask him/her to explain the finding and its significance to you.

Good luck-

Dr. Joshua

MSCT RENAL

2008-12-14T01:11:00.000-08:00

Multi–Detector Row CT Urography in the Evaluation of Hematuria1 Sandor A. Joffe, MD, Sabah Servaes, MD, Stephen Okon, MD and Mitchell Horowitz, MD
1 From the Department of Radiology, Beth Israel Medical Center, 1st Ave at 16th St, New York, NY 10003. Presented as an education exhibit at the 2002 RSNA scientific assembly. Received March 28, 2003; revision requested April 15; revision received May 21; accepted May 27. Address correspondence to S.A.J. (e-mail: sjoffe@bethisraelny.org).

Abstract
TopAbstractIntroduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Hematuria can be well evaluated with a comprehensive contrast material–enhanced multi–detector row computed tomography (CT) protocol that combines unenhanced, nephrographic-phase, and excretory-phase imaging. Unenhanced images are obtained from the kidneys to the bladder and allow optimal detection of renal calculi, a common cause of hematuria. Renal parenchymal abnormalities, particularly masses, are best visualized on nephrographic-phase images, which also provide excellent evaluation of the other abdominal organs. Thin-section delayed images obtained from the kidneys to the bladder demonstrate the urinary tract distended with contrast material and are useful in detecting urothelial disease. Intravenous urography, ultrasonography, CT, retrograde ureterography and pyelography, cystoscopy, and ureteroscopy can all be used to evaluate patients with hematuria. In the past, a combination of several of these examinations was necessary to fully evaluate these patients. Now, however, this CT protocol may permit evaluation of hematuria patients with a single comprehensive examination, although more experience and data are needed to determine its efficacy in this setting.
© RSNA, 2003
Index Terms: Computed tomography (CT), multi–detector row, 80.1211 • Genitourinary system, CT, 80.1211 • Urography, technology, 80.1221

Introduction
Top AbstractIntroductionImaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Many imaging modalities have been used in the evaluation of patients with hematuria. Historically, intravenous urography (IVU) has been the primary method of imaging in these patients (1,2). Currently, the examinations that are commonly used to evaluate patients with hematuria include IVU, ultrasonography (US), computed tomography (CT), magnetic resonance (MR) imaging, retrograde ureterography and pyelography, cystoscopy, and ureteroscopy (3).
Hematuria can have a wide range of causes, including calculi, neoplasms, infection, trauma, drug toxicity, coagulopathy, and varices (4). Occasionally, the cause is revealed by a clinical history of prolonged exercise or recent instrumentation.
Evaluation of patients with hematuria frequently requires several imaging modalities. Assessment for urologic malignancy is probably the most important reason for evaluating these patients; therefore, examinations with a high sensitivity for the detection of neoplasms are essential. The ability to detect other possible causes of hematuria is also important.
Unenhanced CT is routinely used to evaluate for calculi and hydronephrosis (5). Renal masses are usually characterized with CT, US, or MR imaging. Urothelial disease has traditionally been evaluated with IVU or retrograde ureterography and pyelography. Excretory-phase CT can now be used to evaluate the ureters (2,6). Although excretory-phase CT is a relatively new technique, preliminary results demonstrate a high sensitivity (95%) in detecting upper tract uroepithelial malignancy (7). Although CT may also demonstrate bladder disease, flat tumors of the bladder are unlikely to be identified with CT, and cystoscopy remains the study of choice in evaluating for bladder malignancy.
With the advent of spiral CT and particularly multi–detector row CT, it is possible to perform a comprehensive evaluation of hematuria patients with a single examination (8–10). CT urography can be performed with a combination of unenhanced, nephrographic-phase, and excretory-phase imaging. The unenhanced images are ideal for detecting calculi. Renal masses are detected and characterized with a combination of unenhanced and nephrographic-phase imaging. The excretory-phase images provide evaluation of the urothelium. Three-dimensional (3D) reformation of the excretory-phase images can produce images that mimic the appearance of intravenous urograms, thus providing images in a format that is familiar to many referring physicians. Alternatively, post-CT conventional radiography can provide similar information (11).
In this article, we review multi–detector row CT technique in patients with hematuria. We also discuss and illustrate a variety of entities that are frequently associated with hematuria, including calculi, renal masses, papillary and caliceal abnormalities, renal pelvic and ureteral disease, bladder disease, and congenital anomalies. In addition, we briefly discuss the role of other imaging modalities in the evaluation of hematuria patients.

Imaging Technique
Top Abstract IntroductionImaging TechniqueCalculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Examinations were performed on a Lightspeed CT scanner (GE Medical Systems, Milwaukee, Wis). All imaging was performed with a 1.5:1 pitch, four detector rows, and a table speed of 15 mm per rotation. Typically, the examinations were performed at 120 kV and 340 mA with a rotation time of 0.8 seconds, although the milliamperage was often adjusted depending on patient size. To facilitate 3D reformatting, orally administered contrast material was not used for this technique. Unenhanced images were obtained from the kidneys through the bladder. One hundred milliliters of iopromide (Ultravist 300; Schering AG, Berlin, Germany) was administered intravenously at a rate of 2 mL/sec, and nephrographic-phase images of the abdominal organs were obtained. Following the injection of contrast material, a 250-mL bag of normal saline solution was administered rapidly by intravenous drip to distend the ureters. Excretory-phase images were obtained 8 minutes after contrast material administration (Table). Overlapping reconstruction of the excretory-phase data was performed and the resulting images sent to a Vitrea workstation (software: Vital Images version 2.6, Plymouth, Minn). At one of our sites, patients were also sent for a single abdominal radiograph (kidney, ureter, bladder) immediately after undergoing CT.

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Multi-Detector Row CT Protocol
The unenhanced images were obtained to evaluate the urinary tract for calculi and to assist in the characterization of renal masses. An alternative technique, which we did not use, consists of obtaining unenhanced images of the kidneys only and nephrographic-phase images of the entire abdomen and pelvis. Occasionally, however, contrast material excretion can be seen on nephrographic-phase images and may obscure ureteral calculi. The additional benefit of dynamic imaging of the pelvis with this technique was thought to be small, and we elected not to use the technique.
Some investigators have included arterial-phase images through the kidneys and bladder to evaluate for vascular abnormalities (12). Arterial-phase images may be particularly helpful in detecting arteriovenous malformations and demonstrating the arterial anatomy in surgical candidates. Other vascular abnormalities such as aberrant renal veins and venous thrombosis can usually be seen on nephrographic-phase images. Others advocate the addition of corticomedullary-phase imaging of the abdomen for better characterization of renal masses and particularly for better evaluation of the liver (13,14). Although these additional imaging techniques may increase the diagnostic yield of the CT examination, the additional benefit is small and, in our opinion, routine use of corticomedullary-phase imaging is not justified because of the potential risks posed by the additional radiation dose (15).
Recently, a new technique has been described that can reduce the examination to two phases (16). With use of a dual contrast material bolus, nephrographic- and excretory-phase imaging can be performed concurrently, thus reducing radiation exposure and the number of images generated.
Three-dimensional reformation was performed with volume rendering (VR) or maximum-intensity-projection (MIP) techniques. Although both techniques demonstrate the urinary tract well, VR was preferred at our institution because it does not obscure superimposed structures such as the pelvic bones and ureters. However, caliceal detail was occasionally better seen on MIP images. The 3D reformation was performed by the radiologist and could usually be completed within 5 minutes.
One concern about this comprehensive CT technique is radiation dose to the patient. Each series of the examination delivers a dose of approximately 10 mGy (1 rad). This dose is significantly higher than the typical dose for IVU. To limit the dose, we decided not to cover the entire abdomen and pelvis on all phases of the examination and to limit the examination to three phases.

Calculi
Top Abstract Introduction Imaging TechniqueCalculiRenal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Renal, ureteral, and bladder calculi are a common cause of hematuria. Twelve percent of people develop kidney stones at some point during their lifetime (17). The best imaging modality for evaluating calculi is unenhanced helical CT, which is commonly performed in patients with renal colic to detect obstructing calculi (18–20). In patients with hematuria, unenhanced CT is also helpful in detecting nonobstructing calculi. Although conventional radiography may help detect urinary calculi, it is not as sensitive as unenhanced CT (5). US is also useful in detecting renal calculi and may demonstrate hydronephrosis due to obstructing ureteral calculi but often does not allow direct visualization of ureteral calculi (21,22). The unenhanced portion of our CT examination provides optimal evaluation of all urinary calculi as well as evaluation for hydronephrosis related to the calculi.

Renal Masses
Top Abstract Introduction Imaging Technique CalculiRenal MassesPapillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Renal masses frequently manifest with hematuria. Characterization of a renal mass as a simple cyst, a complex cyst, or a solid mass is essential. Simple cysts are benign and do not warrant further evaluation. Solid masses, with the exception of angiomyolipomas, are presumed to be malignant and usually require surgery.
Features of complex cysts that must be evaluated include wall thickness, presence and thickness of septa, calcifications, attenuation of the cyst, and foci of enhancement. Cystic renal masses are often characterized according to the Bosniak classification system (23–25). Category I lesions are simple cysts. Category II lesions are slightly more complicated and may contain a few thin septa, thin calcifications, or high-attenuation fluid. Category III lesions are still more complex and may contain foci of wall or septal thickening. Category IV lesions have solid enhancing areas. As a general rule, category I and II lesions are benign, whereas category III and IV lesions are possibly malignant and warrant surgery. In cystic masses that are difficult to differentiate as category II or category III lesions and in cysts with thick calcifications, category IIF may be used, and these lesions warrant close follow-up (26). In addition, small renal masses may be difficult to characterize because of lack of accurate evaluation of enhancement characteristics due to volume averaging or pseudoenhancement (27).
CT, US, and MR imaging are all excellent for differentiating renal cysts from neoplasms. CT characterization of a renal mass depends on a combination of unenhanced and contrast material–enhanced imaging. The best phase for contrast-enhanced imaging is the nephrographic phase, which is performed slightly later than the typical corticomedullary-phase imaging com-monly used for the abdomen (28–30). These imaging sequences permit characterization of masses as simple cysts, complex cysts, or solid neoplasms (Figs 1, 2). Although US is also excellent for differentiating cystic from solid renal masses, it is less sensitive in detecting solid masses that may be isoechoic relative to normal renal parenchyma. MR imaging is also excellent for characterizing renal masses, although it does not clearly demonstrate calcification in these masses. IVU is much less sensitive in detecting renal masses and is not reliable for differentiating cystic from solid renal masses. Because our protocol includes both unenhanced and nephrographic-phase imaging, it provides excellent evaluation of all types of renal masses.

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Figure 1a. Bosniak category II renal cyst in a 47-year-old man. (a) Axial unenhanced CT scan demonstrates a large cyst with an attenuation value of 23 HU at the upper pole of the left kidney. (b) On an axial nephrographic-phase CT scan, the cyst has an attenuation value of 25 HU, indicating no significant enhancement.

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Figure 1b. Bosniak category II renal cyst in a 47-year-old man. (a) Axial unenhanced CT scan demonstrates a large cyst with an attenuation value of 23 HU at the upper pole of the left kidney. (b) On an axial nephrographic-phase CT scan, the cyst has an attenuation value of 25 HU, indicating no significant enhancement.

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Figure 2a. Renal cell carcinoma in a 52-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates a heterogeneous mass with central necrosis at the upper pole of the right kidney (arrows). (b) Coronal excretory-phase MIP image demonstrates the relationship of the mass (arrows) to the collecting system.

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Figure 2b. Renal cell carcinoma in a 52-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates a heterogeneous mass with central necrosis at the upper pole of the right kidney (arrows). (b) Coronal excretory-phase MIP image demonstrates the relationship of the mass (arrows) to the collecting system.

Papillary and Caliceal Abnormalities
Top Abstract Introduction Imaging Technique Calculi Renal MassesPapillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References Papillary necrosis can have a wide range of causes, including diabetes, analgesic abuse, sickle cell disease, pyelonephritis, renal vein thrombosis, and obstructive uropathy. Traditionally, papillary necrosis has been diagnosed primarily with IVU. In papillary necrosis, contrast material in the collecting system fills a necrotic cavity that may be located centrally within or at the periphery of the papilla. Excretory-phase CT may provide similar visualization of the collecting system, allowing the diagnosis of papillary necrosis to be made, although its sensitivity in detecting this pathologic condition has not been determined (Fig 3).

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Figure 3a. Papillary necrosis in a 51-year-old man. (a) Excretory-phase CT scan demonstrates small collections of contrast material in the papillae (arrows). (b, c) Coronal MIP (b) and multiplanar reformatted (c) images demonstrate involvement of multiple papillae bilaterally (arrows).

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Figure 3b. Papillary necrosis in a 51-year-old man. (a) Excretory-phase CT scan demonstrates small collections of contrast material in the papillae (arrows). (b, c) Coronal MIP (b) and multiplanar reformatted (c) images demonstrate involvement of multiple papillae bilaterally (arrows).

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Figure 3c. Papillary necrosis in a 51-year-old man. (a) Excretory-phase CT scan demonstrates small collections of contrast material in the papillae (arrows). (b, c) Coronal MIP (b) and multiplanar reformatted (c) images demonstrate involvement of multiple papillae bilaterally (arrows).
Like papillary necrosis, pelvocaliceal diverticula may manifest as contrast material–filled fluid adjacent to the calices, but these two entities can usually be distinguished on the basis of the location of the fluid collections. Pelvocalicealdiverticula are not located in the papilla but adjacent to the fornices of the calices or, less commonly, adjacent to an infundibulum or the renal pelvis (Fig 4).

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Figure 4a. Caliceal diverticulum with calculi in a 64-year-old man. (a, b) Axial unenhanced (a) and nephrographic-phase (b) CT scans demonstrate calculi (arrowhead) layering in a fluid collection (black arrow in b) at the lower pole of the left kidney. An inferior vena cava filter (white arrow) is incidentally noted. (c, d) Axial excretory-phase CT scans demonstrate contrast material excretion into a portion of the fluid collection (arrow), a finding that represents a caliceal diverticulum. An unenhanced fluid-attenuation mass representing a cyst is seen adjacent to the diverticulum (arrowhead in d). (e) Excretory-phase MIP image demonstrates the caliceal diverticulum (arrow).

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Figure 4b. Caliceal diverticulum with calculi in a 64-year-old man. (a, b) Axial unenhanced (a) and nephrographic-phase (b) CT scans demonstrate calculi (arrowhead) layering in a fluid collection (black arrow in b) at the lower pole of the left kidney. An inferior vena cava filter (white arrow) is incidentally noted. (c, d) Axial excretory-phase CT scans demonstrate contrast material excretion into a portion of the fluid collection (arrow), a finding that represents a caliceal diverticulum. An unenhanced fluid-attenuation mass representing a cyst is seen adjacent to the diverticulum (arrowhead in d). (e) Excretory-phase MIP image demonstrates the caliceal diverticulum (arrow).

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Figure 4c. Caliceal diverticulum with calculi in a 64-year-old man. (a, b) Axial unenhanced (a) and nephrographic-phase (b) CT scans demonstrate calculi (arrowhead) layering in a fluid collection (black arrow in b) at the lower pole of the left kidney. An inferior vena cava filter (white arrow) is incidentally noted. (c, d) Axial excretory-phase CT scans demonstrate contrast material excretion into a portion of the fluid collection (arrow), a finding that represents a caliceal diverticulum. An unenhanced fluid-attenuation mass representing a cyst is seen adjacent to the diverticulum (arrowhead in d). (e) Excretory-phase MIP image demonstrates the caliceal diverticulum (arrow).

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Figure 4d. Caliceal diverticulum with calculi in a 64-year-old man. (a, b) Axial unenhanced (a) and nephrographic-phase (b) CT scans demonstrate calculi (arrowhead) layering in a fluid collection (black arrow in b) at the lower pole of the left kidney. An inferior vena cava filter (white arrow) is incidentally noted. (c, d) Axial excretory-phase CT scans demonstrate contrast material excretion into a portion of the fluid collection (arrow), a finding that represents a caliceal diverticulum. An unenhanced fluid-attenuation mass representing a cyst is seen adjacent to the diverticulum (arrowhead in d). (e) Excretory-phase MIP image demonstrates the caliceal diverticulum (arrow).

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Figure 4e. Caliceal diverticulum with calculi in a 64-year-old man. (a, b) Axial unenhanced (a) and nephrographic-phase (b) CT scans demonstrate calculi (arrowhead) layering in a fluid collection (black arrow in b) at the lower pole of the left kidney. An inferior vena cava filter (white arrow) is incidentally noted. (c, d) Axial excretory-phase CT scans demonstrate contrast material excretion into a portion of the fluid collection (arrow), a finding that represents a caliceal diverticulum. An unenhanced fluid-attenuation mass representing a cyst is seen adjacent to the diverticulum (arrowhead in d). (e) Excretory-phase MIP image demonstrates the caliceal diverticulum (arrow).
Patients with medullary sponge kidney are often asymptomatic but may present with hematuria, infection, or renal colic. These patients have dilatation of the collecting tubules, which typically have a "paintbrush" appearance at IVU. In addition, affected patients frequently have small calculi. Unenhanced CT may demonstrate these small calculi, and the paintbrush appearance can be seen at excretory-phase CT (Fig 5).

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Figure 5a. Medullary sponge kidney and an obstructing calculus in the right distal ureter in a 62-year-old woman. (a) Axial unenhanced CT scan demonstrates right hydronephrosis (arrowheads) with a nonobstructing calculus (arrow). (b) Axial unenhanced CT scan demonstrates a calculus in the distal right ureter (arrow). (c, d) Axial excretory-phase CT scan (c) and post-CT radiograph (d) demonstrate a paintbrush appearance in the papillae of the left kidney (arrows). Right hydronephrosis is again noted (arrowheads in c).

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Figure 5b. Medullary sponge kidney and an obstructing calculus in the right distal ureter in a 62-year-old woman. (a) Axial unenhanced CT scan demonstrates right hydronephrosis (arrowheads) with a nonobstructing calculus (arrow). (b) Axial unenhanced CT scan demonstrates a calculus in the distal right ureter (arrow). (c, d) Axial excretory-phase CT scan (c) and post-CT radiograph (d) demonstrate a paintbrush appearance in the papillae of the left kidney (arrows). Right hydronephrosis is again noted (arrowheads in c).

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Figure 5c. Medullary sponge kidney and an obstructing calculus in the right distal ureter in a 62-year-old woman. (a) Axial unenhanced CT scan demonstrates right hydronephrosis (arrowheads) with a nonobstructing calculus (arrow). (b) Axial unenhanced CT scan demonstrates a calculus in the distal right ureter (arrow). (c, d) Axial excretory-phase CT scan (c) and post-CT radiograph (d) demonstrate a paintbrush appearance in the papillae of the left kidney (arrows). Right hydronephrosis is again noted (arrowheads in c).

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Figure 5d. Medullary sponge kidney and an obstructing calculus in the right distal ureter in a 62-year-old woman. (a) Axial unenhanced CT scan demonstrates right hydronephrosis (arrowheads) with a nonobstructing calculus (arrow). (b) Axial unenhanced CT scan demonstrates a calculus in the distal right ureter (arrow). (c, d) Axial excretory-phase CT scan (c) and post-CT radiograph (d) demonstrate a paintbrush appearance in the papillae of the left kidney (arrows). Right hydronephrosis is again noted (arrowheads in c).
Nephrocalcinosis is characterized by medullary calcifications and is most commonly seen in patients with hyperparathyroidism, renal tubular acidosis, and medullary sponge kidney. These calcifications are best visualized at unenhanced CT, which is more sensitive than radiography in this setting (Fig 6).

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Figure 6a. Nephrocalcinosis in a 33-year-old woman. Axial unenhanced (a) and excretory-phase (b) CT scans demonstrate medullary calcifications bilaterally (arrowheads). Left hydronephrosis is also noted (arrow in b). The calcifications were not visible at abdominal radiography.

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Figure 6b. Nephrocalcinosis in a 33-year-old woman. Axial unenhanced (a) and excretory-phase (b) CT scans demonstrate medullary calcifications bilaterally (arrowheads). Left hydronephrosis is also noted (arrow in b). The calcifications were not visible at abdominal radiography.

Renal Pelvic and Ureteral Disease
Top Abstract Introduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...Conclusions References A filling defect in the renal pelvis or ureter can be due to a neoplasm, calculus, blood clot, mycetoma, or vascular impression (Fig 7). Obstruction at the ureteropelvic junction (UPJ) may occur due to a short segment of nonfunctional smooth muscle and typically manifests with hydronephrosis (Fig 8). Other types of ureteral abnormalities include narrowing due to stricture or extrinsic disease. Complications of ureteroscopy may also occur (Fig 9).

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Figure 7a. Transitional cell carcinoma of the left ureter with associated left hydronephrosis in a 77-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates left hydronephrosis (arrowheads) with associated delayed medullary enhancement (arrows). (b) Axial nephrographic-phase CT scan demonstrates left hydroureter (arrowheads). (c) Axial nephrographic-phase CT scan obtained several centimeters below b demonstrates an enhancing mass in the ureter (arrow). (d) Coronal excretory-phase reformatted image demonstrates left hydronephrosis and hydroureter (arrowheads) with an obstructing soft-tissue mass in the ureter (arrow).

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Figure 7b. Transitional cell carcinoma of the left ureter with associated left hydronephrosis in a 77-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates left hydronephrosis (arrowheads) with associated delayed medullary enhancement (arrows). (b) Axial nephrographic-phase CT scan demonstrates left hydroureter (arrowheads). (c) Axial nephrographic-phase CT scan obtained several centimeters below b demonstrates an enhancing mass in the ureter (arrow). (d) Coronal excretory-phase reformatted image demonstrates left hydronephrosis and hydroureter (arrowheads) with an obstructing soft-tissue mass in the ureter (arrow).

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Figure 7c. Transitional cell carcinoma of the left ureter with associated left hydronephrosis in a 77-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates left hydronephrosis (arrowheads) with associated delayed medullary enhancement (arrows). (b) Axial nephrographic-phase CT scan demonstrates left hydroureter (arrowheads). (c) Axial nephrographic-phase CT scan obtained several centimeters below b demonstrates an enhancing mass in the ureter (arrow). (d) Coronal excretory-phase reformatted image demonstrates left hydronephrosis and hydroureter (arrowheads) with an obstructing soft-tissue mass in the ureter (arrow).

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Figure 7d. Transitional cell carcinoma of the left ureter with associated left hydronephrosis in a 77-year-old woman. (a) Axial nephrographic-phase CT scan demonstrates left hydronephrosis (arrowheads) with associated delayed medullary enhancement (arrows). (b) Axial nephrographic-phase CT scan demonstrates left hydroureter (arrowheads). (c) Axial nephrographic-phase CT scan obtained several centimeters below b demonstrates an enhancing mass in the ureter (arrow). (d) Coronal excretory-phase reformatted image demonstrates left hydronephrosis and hydroureter (arrowheads) with an obstructing soft-tissue mass in the ureter (arrow).

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Figure 8a. UPJ obstruction and nonobstructing calculi in a 35-year-old man. (a, b) Axial unenhanced (a) and excretory-phase (b) CT scans demonstrate right hydronephrosis with thickening of the urothelium in the renal pelvis (arrowheads). Note the calculi layering in the collecting system (arrows in a). (c) Three-dimensional VR image of the collecting systems demonstrates right hydronephrosis due to UPJ obstruction. Note that the left renal collecting system is incompletely distended.

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Figure 8b. UPJ obstruction and nonobstructing calculi in a 35-year-old man. (a, b) Axial unenhanced (a) and excretory-phase (b) CT scans demonstrate right hydronephrosis with thickening of the urothelium in the renal pelvis (arrowheads). Note the calculi layering in the collecting system (arrows in a). (c) Three-dimensional VR image of the collecting systems demonstrates right hydronephrosis due to UPJ obstruction. Note that the left renal collecting system is incompletely distended.

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Figure 8c. UPJ obstruction and nonobstructing calculi in a 35-year-old man. (a, b) Axial unenhanced (a) and excretory-phase (b) CT scans demonstrate right hydronephrosis with thickening of the urothelium in the renal pelvis (arrowheads). Note the calculi layering in the collecting system (arrows in a). (c) Three-dimensional VR image of the collecting systems demonstrates right hydronephrosis due to UPJ obstruction. Note that the left renal collecting system is incompletely distended.

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Figure 9a. Transitional cell carcinoma of the renal pelvis and ureteral perforation that occurred during ureteroscopy in a 47-year-old man. (a-c) Axial unenhanced (a), nephrographic-phase (b), and excretory-phase (c) CT scans demonstrate an enhancing soft-tissue mass in the renal pelvis (arrows) with no invasion of the renal parenchyma. (d, e) Axial CT scan (d) and coronal MIP image (e) demonstrate a large collection of contrast material (arrowheads) adjacent to the ureter (arrow in d) due to perforation of the proximal ureter. The irregular filling defect in e (arrows) represents transitional cell carcinoma.

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Figure 9b. Transitional cell carcinoma of the renal pelvis and ureteral perforation that occurred during ureteroscopy in a 47-year-old man. (a-c) Axial unenhanced (a), nephrographic-phase (b), and excretory-phase (c) CT scans demonstrate an enhancing soft-tissue mass in the renal pelvis (arrows) with no invasion of the renal parenchyma. (d, e) Axial CT scan (d) and coronal MIP image (e) demonstrate a large collection of contrast material (arrowheads) adjacent to the ureter (arrow in d) due to perforation of the proximal ureter. The irregular filling defect in e (arrows) represents transitional cell carcinoma.

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Figure 9c. Transitional cell carcinoma of the renal pelvis and ureteral perforation that occurred during ureteroscopy in a 47-year-old man. (a-c) Axial unenhanced (a), nephrographic-phase (b), and excretory-phase (c) CT scans demonstrate an enhancing soft-tissue mass in the renal pelvis (arrows) with no invasion of the renal parenchyma. (d, e) Axial CT scan (d) and coronal MIP image (e) demonstrate a large collection of contrast material (arrowheads) adjacent to the ureter (arrow in d) due to perforation of the proximal ureter. The irregular filling defect in e (arrows) represents transitional cell carcinoma.

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Figure 9d. Transitional cell carcinoma of the renal pelvis and ureteral perforation that occurred during ureteroscopy in a 47-year-old man. (a-c) Axial unenhanced (a), nephrographic-phase (b), and excretory-phase (c) CT scans demonstrate an enhancing soft-tissue mass in the renal pelvis (arrows) with no invasion of the renal parenchyma. (d, e) Axial CT scan (d) and coronal MIP image (e) demonstrate a large collection of contrast material (arrowheads) adjacent to the ureter (arrow in d) due to perforation of the proximal ureter. The irregular filling defect in e (arrows) represents transitional cell carcinoma.

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Figure 9e. Transitional cell carcinoma of the renal pelvis and ureteral perforation that occurred during ureteroscopy in a 47-year-old man. (a-c) Axial unenhanced (a), nephrographic-phase (b), and excretory-phase (c) CT scans demonstrate an enhancing soft-tissue mass in the renal pelvis (arrows) with no invasion of the renal parenchyma. (d, e) Axial CT scan (d) and coronal MIP image (e) demonstrate a large collection of contrast material (arrowheads) adjacent to the ureter (arrow in d) due to perforation of the proximal ureter. The irregular filling defect in e (arrows) represents transitional cell carcinoma.
Traditionally, ureteral disease has been evaluated with IVU or retrograde ureterography. However, these examinations only demonstrate the lumen of the ureter and do not allow direct visualization of extrinsic abnormalities that involve the ureter. In the case of a vascular impression, in addition to demonstrating the impression on the collecting system, CT may directly demonstrate the vessel that is causing the impression (Fig 10). If a crossing vessel is suspected of causing an extrinsic impression on the ureter or UPJ obstruction, the addition of arterial-phase images should be considered for better visualization.

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Figure 10a. Vascular impression on the left renal pelvis in a 25-year-old woman. (a) Intravenous urogram demonstrates a nonspecific filling defect in the left renal pelvis (arrows). (b) Three-dimensional VR image (posterior projection) demonstrates the filling defect (arrows). (c, d) Sagittal reformatted image (c) and axial excretory-phase CT scan (d) demonstrate an extrinsic impression on the posterior aspect of the renal pelvis (arrows). (e) Axial nephrographic-phase CT scan demonstrates a branch of the left renal vein (arrowheads) that is causing the extrinsic impression on the renal pelvis.

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Figure 10b. Vascular impression on the left renal pelvis in a 25-year-old woman. (a) Intravenous urogram demonstrates a nonspecific filling defect in the left renal pelvis (arrows). (b) Three-dimensional VR image (posterior projection) demonstrates the filling defect (arrows). (c, d) Sagittal reformatted image (c) and axial excretory-phase CT scan (d) demonstrate an extrinsic impression on the posterior aspect of the renal pelvis (arrows). (e) Axial nephrographic-phase CT scan demonstrates a branch of the left renal vein (arrowheads) that is causing the extrinsic impression on the renal pelvis.

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Figure 10c. Vascular impression on the left renal pelvis in a 25-year-old woman. (a) Intravenous urogram demonstrates a nonspecific filling defect in the left renal pelvis (arrows). (b) Three-dimensional VR image (posterior projection) demonstrates the filling defect (arrows). (c, d) Sagittal reformatted image (c) and axial excretory-phase CT scan (d) demonstrate an extrinsic impression on the posterior aspect of the renal pelvis (arrows). (e) Axial nephrographic-phase CT scan demonstrates a branch of the left renal vein (arrowheads) that is causing the extrinsic impression on the renal pelvis.

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Figure 10d. Vascular impression on the left renal pelvis in a 25-year-old woman. (a) Intravenous urogram demonstrates a nonspecific filling defect in the left renal pelvis (arrows). (b) Three-dimensional VR image (posterior projection) demonstrates the filling defect (arrows). (c, d) Sagittal reformatted image (c) and axial excretory-phase CT scan (d) demonstrate an extrinsic impression on the posterior aspect of the renal pelvis (arrows). (e) Axial nephrographic-phase CT scan demonstrates a branch of the left renal vein (arrowheads) that is causing the extrinsic impression on the renal pelvis.

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Figure 10e. Vascular impression on the left renal pelvis in a 25-year-old woman. (a) Intravenous urogram demonstrates a nonspecific filling defect in the left renal pelvis (arrows). (b) Three-dimensional VR image (posterior projection) demonstrates the filling defect (arrows). (c, d) Sagittal reformatted image (c) and axial excretory-phase CT scan (d) demonstrate an extrinsic impression on the posterior aspect of the renal pelvis (arrows). (e) Axial nephrographic-phase CT scan demonstrates a branch of the left renal vein (arrowheads) that is causing the extrinsic impression on the renal pelvis.
Excretory-phase CT allows visualization of both the ureteral lumen and periureteral abnormalities; however, it is a new technique, and only preliminary data are available concerning its sensitivity in detecting small urothelial neoplasms (7). Accurate evaluation of excretory-phase images requires a wide window setting (eg, bone windows). The 3D reformatted images depict the collecting system and ureters in a format that is familiar to most referring clinicians. In our experience, renal pelvic and ureteral disease is best evaluated and almost always appreciated on the axial source images, but in rare instances we have detected ureteral disease on the 3D reformatted images that was not identified at initial review. In one case, for example, we failed to detect mild hydronephrosis on the axial source images but identified it on the 3D reformatted images, even though in retrospect the hydronephrosis was also depicted on the axial source images.
A potential problem with excretory-phase CT is that the ureters are imaged only once during this phase, whereas IVU may be used to obtain either one or multiple images of the ureters depending on the protocol of the institution. Therefore, if segments of the ureters are not filled with contrast material at a given moment, they may not be completely evaluated. Intravenous or oral hydration of patients can be used to distend the ureters with contrast material and has been shown to significantly improve ureteral opacification (31,32). Others have used compression technique to achieve better distention and evaluation of the collecting systems (32,33). Even in cases of incomplete opacification of the ureters, the unopacified portions can often be followed and evaluated on the axial images.

Bladder Disease
Top Abstract Introduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder DiseaseCongenital Anomalies Roles of Other Imaging...Conclusions References Bladder abnormalities are a common cause of hematuria and include neoplasms, usually transitional cell carcinoma, particularly in patients with exposure to aniline dyes, phenacetin, tobacco, and prior radiation therapy (Fig 11). Squamous cell carcinoma and adenocarcinoma are less common bladder neoplasms. Cystitis and diverticula are other types of bladder disease that may also cause hematuria. Bladder diverticula may be congenital, such as Hutch and urachal diverticula, or they may be acquired. Diverticula can predispose to carcinoma, calculi, or infections (Fig 12).

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Figure 11. Transitional cell carcinoma of the bladder in a 79-year-old man. Excretory-phase CT scan demonstrates a papillary mass in the right side of the bladder (arrow). Note the impression on the bladder base caused by the enlarged prostate gland (arrowheads).

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Figure 12. Neurogenic bladder and multiple diverticula in a 25-year-old man. CT scan shows diverticula (arrows).
Many imaging modalities including CT, US, cystography, IVU, and MR imaging can be used to evaluate the bladder. Bladder distention is essential for optimal CT evaluation. Urine, contrast material excreted by the kidneys, and contrast material or air instilled directly into the bladder (CT cystography) all provide adequate contrast to visualize bladder disease at CT. However, flat tumors of the bladder may go undetected. Therefore, cystoscopy remains the standard for evaluation of the bladder for neoplasms and may be a necessary additional study in patients suspected of having bladder carcinoma.

Congenital Anomalies
Top Abstract Introduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder DiseaseCongenital AnomaliesRoles of Other Imaging...Conclusions References Some congenital anomalies of the urinary tract are associated with hematuria, such as polycystic kidney disease. During the work-up of patients with hematuria, anomalies may also be detected incidentally. Congenital renal and ureteral anomalies include anomalies of position, form, number, or function. Most renal anomalies are well demonstrated with CT, US, IVU, and MR imaging (Fig 13). Ureteral anomalies are best demonstrated by filling the ureters with contrast material, with either IVU or excretory-phase CT (Figs 14, 15).

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Figure 13a. Horseshoe kidney and long-standing hydronephrosis of the left kidney in a 33-year-old man. (a, b) Axial nephrographic-phase (a) and excretory-phase (b) CT scans demonstrate hydronephrosis of the left kidney (arrows) with atrophy of the kidney. Note the contrast material layering in the renal collecting system on the excretory-phase image (arrowhead in b) due to the lack of mixing with the urine in the dilated renal pelvis. (c) Excretory-phase VR image demonstrates a horseshoe kidney. Note that the left renal collecting system is not well opacified (arrows) due to the layering of contrast material in the hydronephrotic kidney.

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Figure 13b. Horseshoe kidney and long-standing hydronephrosis of the left kidney in a 33-year-old man. (a, b) Axial nephrographic-phase (a) and excretory-phase (b) CT scans demonstrate hydronephrosis of the left kidney (arrows) with atrophy of the kidney. Note the contrast material layering in the renal collecting system on the excretory-phase image (arrowhead in b) due to the lack of mixing with the urine in the dilated renal pelvis. (c) Excretory-phase VR image demonstrates a horseshoe kidney. Note that the left renal collecting system is not well opacified (arrows) due to the layering of contrast material in the hydronephrotic kidney.

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Figure 13c. Horseshoe kidney and long-standing hydronephrosis of the left kidney in a 33-year-old man. (a, b) Axial nephrographic-phase (a) and excretory-phase (b) CT scans demonstrate hydronephrosis of the left kidney (arrows) with atrophy of the kidney. Note the contrast material layering in the renal collecting system on the excretory-phase image (arrowhead in b) due to the lack of mixing with the urine in the dilated renal pelvis. (c) Excretory-phase VR image demonstrates a horseshoe kidney. Note that the left renal collecting system is not well opacified (arrows) due to the layering of contrast material in the hydronephrotic kidney.

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Figure 14a. Duplication of the left renal collecting system and ureter in a 48-year-old man. (a) Axial excretory-phase CT scan demonstrates two left ureters (arrowheads). (b) Excretory-phase VR image demonstrates duplication of the left renal collecting system (arrows) and ureters (arrowheads).

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Figure 14b. Duplication of the left renal collecting system and ureter in a 48-year-old man. (a) Axial excretory-phase CT scan demonstrates two left ureters (arrowheads). (b) Excretory-phase VR image demonstrates duplication of the left renal collecting system (arrows) and ureters (arrowheads).

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Figure 15a. Ureterocele in a 31-year-old woman. The left kidney had been removed many years earlier due to an unknown "benign cause." (a) Axial excretory-phase CT scan demonstrates right hydronephrosis (arrows). (b) Axial excretory-phase CT scan demonstrates a dilated ureter (arrowhead) terminating in a ureterocele (arrows). (c) Excretory-phase VR image demonstrates hydronephrosis (black arrows), hydroureter (arrowhead), and the ureterocele (white arrow).

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Figure 15b. Ureterocele in a 31-year-old woman. The left kidney had been removed many years earlier due to an unknown "benign cause." (a) Axial excretory-phase CT scan demonstrates right hydronephrosis (arrows). (b) Axial excretory-phase CT scan demonstrates a dilated ureter (arrowhead) terminating in a ureterocele (arrows). (c) Excretory-phase VR image demonstrates hydronephrosis (black arrows), hydroureter (arrowhead), and the ureterocele (white arrow).

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Figure 15c. Ureterocele in a 31-year-old woman. The left kidney had been removed many years earlier due to an unknown "benign cause." (a) Axial excretory-phase CT scan demonstrates right hydronephrosis (arrows). (b) Axial excretory-phase CT scan demonstrates a dilated ureter (arrowhead) terminating in a ureterocele (arrows). (c) Excretory-phase VR image demonstrates hydronephrosis (black arrows), hydroureter (arrowhead), and the ureterocele (white arrow).

Roles of Other Imaging Modalities
Top Abstract Introduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital AnomaliesRoles of Other Imaging...Conclusions References In the evaluation of patients with hematuria, IVU and cystoscopy have been the primary methods of evaluation, along with a cross-sectional examination of the kidneys. Cystoscopy is still an essential part of this evaluation because radiologic examinations are not as sensitive in the detection of small bladder neoplasms, particularly superficial tumors. Although the results of CT urography are still preliminary, IVU will probably play only a small role in this work-up, particularly with the advent of new CT technology (eg, 16-detector CT), which will improve z-axis resolution.
US is less sensitive than CT in the detection of small solid renal masses and calculi and should not be the primary examination in patients with hematuria. However, US may still be helpful in characterizing cystic renal masses that are indeterminate at CT and in patients in whom intravenous contrast material is contraindicated.
MR imaging should be used to study the kidneys and ureters in such patients because it provides excellent evaluation of the renal parenchyma for masses, and MR urography can be used to evaluate the ureters (34). However, MR imaging is not sensitive in detection of urinary calculi, and its spatial resolution is inferior to that of CT.

Conclusions
Top Abstract Introduction Imaging Technique Calculi Renal Masses Papillary and Caliceal...Renal Pelvic and Ureteral...Bladder Disease Congenital Anomalies Roles of Other Imaging...ConclusionsReferences Many different imaging modalities have been used in the evaluation of patients with hematuria, and patients frequently require multiple examinations for work-up. Contrast-enhanced multi–detector row CT urography performed with a combination of unenhanced, nephrographic-phase, and excretory-phase imaging can demonstrate a wide spectrum of disease in these patients with a single study. Unenhanced imaging provides optimal detection of calculi, a common cause of hematuria. In addition, the combination of unenhanced and nephrographic-phase imaging provides outstanding evaluation of renal masses. Findings at excretory-phase imaging mimic IVU findings and allow excellent evaluation of the collecting systems and ureters. Bladder disease, a common cause of hematuria, is often well seen on unenhanced or excretory-phase images, although cystoscopy may still be necessary. Although more experience and data are necessary, this protocol has the potential to provide accurate evaluation of patients with hematuria with a single comprehensive CT examination.

Cardiac

2008-11-24T08:16:00.001-08:00

Heart
From Wikipedia, the free encyclopedia
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This article is about the organ. For other uses, see Heart (disambiguation).

Human heart with coronary arteries.
The heart is a muscular organ in all vertebrates responsible for pumping blood through the blood vessels by repeated, rhythmic contractions, or a similar structure in annelids, mollusks, and arthropods. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart."
The heart of a vertebrate is composed of cardiac muscle, an involuntary muscle tissue which is found only within this organ. The average human heart, beating at 72 beats per minute, will beat approximately 2.5 billion times during a lifetime (about 66 years).
Contents[hide]
1 Early development
2 Structure
3 Functioning
4 First aid
5 History of discoveries
6 Healthy heart
7 Food use
8 See also
9 References
10 External links
//

[edit] Early development
Main article: Heart development
The mammalian heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the inner lining of the heart. The outer lining of the heart, lymphatic and blood vessels develop from endothelium. Myocardium develops into heart muscle.[1]
From splachnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity and begin to fuse together and are completely fused at approximately 21 days.[2]

At 21 days after conception, the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.
The human embryonic heart begins beating around 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM). The embryonic heart rate (EHR) then accelerates linearly for the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.[3] At about 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is Age in days = EHR(0.3)+6
There is no difference in male and female heart rates before birth.[4]

[edit] Structure
The structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.) Cephalopods have two "gill hearts" and one "systemic heart". Fish have a two-chambered heart that pumps the blood to the gills and from there it goes on to the rest of the body. In amphibians and most reptiles, a double circulatory system is used, but the heart is not always completely separated into two pumps. Amphibians have a three-chambered heart.
Birds and mammals show complete separation of the heart into two pumps, for a total of four heart chambers; it is thought that the four-chambered heart of birds evolved independently from that of mammals.
In the human body, the heart is usually situated in the middle of the thorax with the largest part of the heart slightly offset to the left (although sometimes it is on the right, see dextrocardia), underneath the breastbone (see diagrams). The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense fibrous connective tissue; and a double membrane structure containing a serous fluid to reduce friction during heart contractions (the serous pericardium). The mediastinum, a subdivision of the thoracic cavity, is the name of the heart cavity. [5]
The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. It is located posterior to the 5th intercostal space in the left mid-clavicular line. In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about three quarters the size of a clenched fist, but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria (singular: atrium ) and the two lower ventricles.

[edit] Functioning

This section does not cite any references or sources.Please help improve this section by adding citations to reliable sources. Unverifiable material may be challenged and removed. (June 2008)
In animals, the function of the right side of the heart (see right heart) is to collect de-oxygenated blood, in the right atrium, from the body and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through the passive process of diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body. On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.
Starting in the middle atrium, the blood flows through the tricuspid valve to the right ventricle. Here it is pumped out the pulmonary semilunar valve and travels through the pulmonary artery to the lungs. From there, blood flows back through the pulmonary vein to the left atrium. It then travels through the mitral valve to the left ventricle, from where it is pumped through the aortic semilunar valve to the aorta. The aorta forks, and the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries to the smaller arterioles, then finally to the tiny capillaries which feed each cell. The (relatively) deoxygenated blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally back to the right atrium where the process began.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.

[edit] First aid

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Heart
The heart is one of the critical organs of an animal's body, as it pumps oxygenated blood to feed the body's biological functions. The cessation of the heartbeat, referred to as cardiac arrest, is a critical emergency. Without intervention, death can occur within minutes of cardiac arrest since the brain requires a continuous supply of oxygen and cannot survive for long if that supply is cut off.
If a person is encountered in cardiac arrest, cardiopulmonary resuscitation (CPR) should be started and help called. Use of a defibrillator is preferred, if available, to attempt to restore a normal heartbeat; many public areas have portable defibrillators available for such emergencies. Usually, if there is enough time, the person can be rushed to the hospital where he or she will be resuscitated in the Emergency Department.
Electrical innervation of the heart in health is supplied by two closely intertwined mechanisms. The first mechanism is well demonstrated in electrical coil systole (interpreted by the electrocardiogram as QRS) as an individualized myocardial electrical tree initiated by the sinoatrial node. Secondary diastolic electrical control is posited to represent autonomic recoil control from the vagus nerve and cardiac branches and the thoracic ganglia.

[edit] History of discoveries

This section does not cite any references or sources.Please help improve this section by adding citations to reliable sources. Unverifiable material may be challenged and removed. (June 2008)
The valves of the heart were discovered by a physician of the Hippocratean school around the 4th century BC. However their function was not properly understood then. Because blood pools in the veins after death, arteries look empty. Ancient anatomists assumed they were filled with air and that they were for transport of air.
Philosophers distinguished veins from arteries but thought that the pulse was a property of arteries themselves. Erasistratos observed that arteries that were cut during life bleed. He ascribed the fact to the phenomenon that air escaping from an artery is replaced with blood that entered by very small vessels between veins and arteries. Thus he apparently postulated capillaries but with reversed flow of blood.
The 2nd century AD, Greek physician Galenos (Galen) knew that blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Growth and energy were derived from venous blood created in the liver from chyle, while arterial blood gave vitality by containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.
Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right by passing through 'pores' in the inter ventricular septum, air passed from the lungs via the pulmonary artery to the left side of the heart. As the arterial blood was created 'sooty' vapors were created and passed to the lungs also via the pulmonary artery to be exhaled.

[edit] Healthy heart
Obesity, high-blood pressure and high blood cholesterol can increase the risk of developing heart disease. Heart disease is a major cause of death (and the number one cause of death in the United States and England and Wales).[6][7][8][9]

[edit] Food use

This section does not cite any references or sources.Please help improve this section by adding citations to reliable sources. Unverifiable material may be challenged and removed. (June 2008)
The hearts of cattle, sheep, pigs, chickens and certain fowl are consumed in many countries. They are counted among offal, but being a muscle, the taste of heart is like regular meat. It resembles venison in structure and taste.

[edit] See also
Cardiac cycle
Heart disease
Electrocardiogram
Electrical conduction system of the heart

Cardiac

2008-11-24T08:16:00.000-08:00

X ray ( Eng Ver )

2008-11-24T08:00:00.001-08:00

X-ray
From Wikipedia, the free encyclopedia
(Redirected from X Ray)
Jump to: navigation, search
For other uses, see X-ray (disambiguation).

Hand mit Ringen (Hand with Rings): print of Wilhelm Röntgen's first "medical" X-ray, of his wife's hand, taken on 22 December 1895 and presented to Professor Ludwig Zehnder of the Physik Institut, University of Freiburg, on 1 January 1896. The dark oval on the third finger is a shadow produced by her rings.[1][2]
X-radiation (composed of X-rays) is a form of electromagnetic radiation. X-rays have a wavelength in the range of 10 to 0.01 nanometers, corresponding to frequencies in the range 30 petahertz to 30 exahertz (30 × 1015 Hz to 30 × 1018 Hz) and energies in the range 120 eV to 120 keV. They are shorter in wavelength than UV rays. In many languages, X-radiation is called Röntgen radiation after one of its first investigators, Wilhelm Conrad Röntgen.
X-rays are primarily used for diagnostic radiography and crystallography. As a result, the term "X-ray" is metonymically used to refer to a radiographic image produced using this method, in addition to the method itself. X-rays are a form of ionizing radiation and as such can be dangerous.
X-rays span 3 decades in wavelength, frequency and energy. From about 0.12 to 12 keV they are classified as soft x-rays, and from about 12 to 120 keV as hard X-rays, due to their penetrating abilities.
The distinction between x-rays and gamma rays has changed in recent decades. Originally, the electromagnetic radiation emitted by x-ray tubes, called x-rays, generally had a longer wavelength than the electromagnetic radiation emitted by radioactive nuclei, called gamma rays.[3] So older literature distinguished between x- and gamma radiation on the basis of wavelength, with radiation shorter than some arbitrary wavelength, such as 10-11 m, defined as gamma rays.[4] However, as shorter wavelength continuous spectrum 'x-ray' sources such as linear accelerators and longer wavelength 'gamma ray' emitters were discovered, the wavelength bands largely overlapped. So the two types of radiation are now usually defined by their origin: x-rays are emitted by electrons outside the nucleus, while gamma rays are emitted by the nucleus.[3][5][6][7]
Contents[hide]
1 Units of measure and exposure
2 Medical physics
3 Detectors
3.1 Photographic plate
3.2 Photostimulable phosphors (PSPs)
3.3 Geiger counter
3.4 Scintillators
3.5 Image intensification
3.6 Direct semiconductor detectors
3.7 Scintillator plus semiconductor detectors (indirect detection)
3.8 Visibility to the human eye
4 Medical uses
5 Other uses
6 History
6.1 Wilhelm Röntgen
6.2 Johann Hittorf
6.3 Ivan Pulyui
6.4 Nikola Tesla
6.5 Fernando Sanford
6.6 Philipp Lenard
6.7 Thomas Edison
6.8 The 20th century and beyond
7 See also
8 References
9 External links
//

[edit] Units of measure and exposure
The measure of x-rays ionizing ability is called the exposure:
The coulomb per kilogram (C/kg) is the SI unit of ionizing radiation exposure, and measures the amount of radiation required to create 1 coulomb of charge of each polarity in 1 kilogram of matter.
The roentgen (R) is an obsolete older traditional unit of exposure, which represented the amount of radiation required to create 1 esu of charge of each polarity in 1 cubic centimeter of dry air. 1 roentgen = 2.58×10−4 C/kg
However, the effect of ionizing radiation on matter (especially living tissue) is more closely related to the amount of energy deposited rather than the charge. This is called the absorbed dose:
The gray (Gy) which has units of (J/C), is the SI unit of absorbed dose which is the amount of radiation required to deposit 1 joule of energy in 1 kilogram of any kind of matter.
The rad (roentgen absorbed dose) is the (obsolete) corresponding traditional unit, equal to 0.01 J deposited per kg. 100 rad = 1 Gy.
The equivalent dose is the measure of the biological effect of radiation on human tissue. For x-rays it is equal to the absorbed dose.
The sievert (Sv) is the SI unit of equivalent dose, which for x-rays is equal to the gray (Gy).
The rem (roentgen equivalent man) is the traditional unit of equivalent dose. For x-rays it is equal to the rad or 0.01 J of energy deposited per kg. 1 sievert = 100 rem.
Medical x-rays are a major source of manmade radiation exposure, accounting for 58% in the USA in 1987, but since most radiation exposure is natural (82%) it only accounts for 10% of total USA radiation exposure.[8]
Reported dosage due to dental X-rays seems to vary significantly. Depending on the source, a typical dental X-ray of a human results in an exposure of perhaps, 3[9], 40[10], 300[11], or as many as 900[12] mrems (30 to 9,000 μSv).

[edit] Medical physics
X-ray K-series spectral line wavelengths (nm) for some common target materials.[13]
Target
Kβ₁
Kβ₂
Kα₁
Kα₂
Fe
0.17566
0.17442
0.193604
0.193998
Co
Ni
0.15001
0.14886
0.165791
0.166175
Cu
0.139222
0.138109
0.154056
0.154439
Zr
0.070173
0.068993
0.078593
0.079015
Mo
0.063229
0.062099
0.070930
0.071359
W
Re
X-rays are generated by an x-ray tube, a vacuum tube that uses a high voltage to accelerate electrons released by a hot cathode to a high velocity. The high velocity electrons collide with a metal target, the anode, creating the x-rays.[14] In medical x-ray tubes the target is usually tungsten or a more crack-resistant alloy of rhenium (5%) and tungsten (95%), but sometimes molybdenum for more specialized applications, such as when soft X-rays are needed as in mammography. In crystallography, a copper target is most common, with cobalt often being used when fluorescence from iron content in the sample might otherwise present a problem.
The maximum energy of the produced x-ray photon in keV is limited by the energy of the incident electron, which is equal to the voltage on the tube, so an 80 kV tube can't create higher than 80 keV x-rays. When the electrons hit the target, x-rays are created by two different atomic processes:
X-ray fluorescence: If the electron has enough energy it can knock an orbital electron out of the inner shell of a metal atom, and as a result electrons from higher energy levels then fill up the vacancy and X-ray photons are emitted. This process produces a discrete spectrum of x-ray frequencies, called spectral lines. The spectral lines generated depends on the target (anode) element used and thus are called characteristic lines. Usually these are transitions from upper shells into K shell (called K lines), into L shell (called L lines) and so on.
Bremsstrahlung: This is radiation given off by the electrons as they are scattered by the strong electric field near the high-Z (proton number) nuclei. These x-rays have a continuous spectrum. The intensity of the x-rays increases linearly with decreasing frequency, from zero at the energy of the incident electrons, the voltage on the X-ray tube.
So the resulting output of a tube consists of a continuous bremsstrahlung spectrum falling off to zero at the tube voltage, plus several spikes at the characteristic lines. The voltages used in diagnostic x-ray tubes, and thus the highest energies of the x-rays, range from roughly 20 to 150 kV.[15]
In medical diagnostic applications, the low energy (soft) x-rays are unwanted, since they are totally absorbed by the body, increasing the dose. So a thin metal (often aluminum) sheet is placed over the window of the x-ray tube, filtering out the low energy end of the spectrum. This is called hardening the beam. Very hard X-rays overlap with the range of "long"-wavelength (lower energy) gamma rays, however the distinction between the two terms in medicine depends on the source of the radiation, not its wavelength; X-ray photons are generated by energetic electron processes, gamma rays by transitions within atomic nuclei.[citation needed]
Both x-ray production processes are extremely inefficient (~1%) and thus to produce a usable flux of X-rays plenty of energy has to be wasted into heat, which has to be removed from the x-ray tube.
Radiographs obtained using X-rays can be used to identify a wide spectrum of pathologies. Due to their short wavelength, in medical applications, X-rays act more like a particle than a wave. This is in contrast to their application in crystallography, where their wave-like nature is most important.
To take an X-ray of the bones, short X-ray pulses are shot through a body with radiographic film behind. The bones absorb the most photons by the photoelectric process, because they are more electron-dense. The X-rays that do not get absorbed turn the photographic film from white to black, leaving a white shadow of bones on the film.
To generate an image of the cardiovascular system, including the arteries and veins (angiography) an initial image is taken of the anatomical region of interest. A second image is then taken of the same region after iodinated contrast material has been injected into the blood vessels within this area. These two images are then digitally subtracted, leaving an image of only the iodinated contrast outlining the blood vessels. The radiologist or surgeon then compares the image obtained to normal anatomical images to determine if there is any damage or blockage of the vessel.
A specialized source of x-rays which is becoming widely used in research is synchrotron radiation, which is generated by particle accelerators. Its unique features are brightness many orders of magnitude greater than x-ray tubes, wide spectrum, high collimation, and linear polarization.[16]

[edit] Detectors

[edit] Photographic plate
The detection of X-rays is based on various methods. The most commonly known methods are a photographic plate, X-ray film in a cassette, and rare earth screens. Regardless of what is "catching" the image, they are all categorized as "Image Receptors" (IR).
Before computers and before digital imaging, a photographic plate was used to produce radiographic images. The images were produced right on the glass plates. Film replaced these plates and was used in hospitals to produce images. Now computed & digital radiography has started to replace film in medicine, though film technology is still used in industrial radiography processes (e.g. to inspect welded seams). Photographic plates are a thing of history, and their replacement (intensifying screens) is now becoming part of that same history. Silver (necessary to the radiographic & photographic industry) is a non-renewable resource, that has now been replaced by digital (DR) and computed (CR) technology. Where film required wet processing facilities on site, these new technologies do not. Archiving of these new technologies is also space saving for facilities.
Regardless of whether the image receptor technology is plate, film or CR/DR Since photographic plates were sensitive to X-rays, they provide a convenient and easy means of recording the image, but they required a lot of exposure (to the patient). This is where intensifying screens came into the picture. The use of such, allowed for a lower dose to the patient – because the screens took the X-ray information and "intensified" it so that it could be recorded on the film lying next to the intensifying screen.
The part of the patient to be X-rayed is placed between the X-ray source and the image receptor to produce what is a shadow of all the internal structure of that particular part of the body being X-rayed. X-rays are somewhat blocked ("attenuated") by dense tissues such as bone, and pass more easily through soft tissues. Those areas where the X-rays strike the image receptor will produce photographic density (ie. it will turn black when developed). So where the X-rays pass through "soft" parts of the body such as organs, muscle, and skin, the plate or film turns black.
Contrast compounds containing barium or iodine, which are radiopaque, can be ingested in the gastrointestinal tract (barium) or injected in the artery or veins to highlight these vessels. The contrast compounds have high atomic numbered elements in them that (like bone) essentially block the X-rays and hence the once hollow organ or vessel can be more readily seen. In the pursuit of a non-toxic contrast material, many types of high atomic number elements were experimented with. For example, the first time the forefathers used contrast it was chalk, and was used on a cadaver's vessels. Unfortunately, some elements chosen proved to be harmful – for example, many years ago thorium was used as a contrast medium (Thorotrast) – which turned out to be toxic in some cases (causing injury and occasionally death from the effects of thorium poisoning). Contrast material used today has come a long way, and while there is no way to determine who may have a sensitivity to the contrast – the occasions of having an "allergic-type reaction" are very low. (The risk is compared to that associated with penicillin ... that is, just as many people are allergic to penicillin as they are to radiographic contrast material.)

[edit] Photostimulable phosphors (PSPs)
An increasingly common method of is the use of photostimulated luminescence (PSL), pioneered by Fuji in the 1980s. In modern hospitals a photostimulable phosphor plate (PSP plate) is used in place of the photographic plate. After the plate is X-rayed, excited electrons in the phosphor material remain 'trapped' in 'colour centres' in the crystal lattice until stimulated by a laser beam passed over the plate surface. The light given off during laser stimulation is collected by a photomultiplier tube and the resulting signal is converted into a digital image by computer technology, which gives this process its common name, computed radiography (also referred to as digital radiography). The PSP plate can be used over and over again, and existing X-ray equipment requires no modification to use them.

[edit] Geiger counter
Initially, most common detection methods were based on the ionization of gases, as in the Geiger-Müller counter: a sealed volume, usually a cylinder, with a mica, polymer or thin metal window contains a gas, and a wire, and a high voltage is applied between the cylinder (cathode) and the wire (anode). When an X-ray photon enters the cylinder, it ionizes the gas and forms ions and electrons. Electrons accelerate toward the anode, in the process causing further ionization along their trajectory. This process, known as a Townsend avalanche, is detected as a sudden current, called a "count" or "event".
Ultimately, the electrons form a virtual cathode around the anode wire, drastically reducing the electric field in the outer portions of the tube. This halts the collisional ionizations and limits further growth of avalanches. As a result, all "counts" on a Geiger counter are the same size and it can give no indication as to the particle energy of the radiation, unlike the proportional counter. The intensity of the radiation is measurable by the Geiger counter as the counting-rate of the system.
In order to gain energy spectrum information, a diffracting crystal may be used to first separate the different photons. The method is called wavelength dispersive X-ray spectroscopy (WDX or WDS). Position-sensitive detectors are often used in conjunction with dispersive elements. Other detection equipment that is inherently energy-resolving may be used, such as the aforementioned proportional counters. In either case, use of suitable pulse-processing (MCA) equipment allows digital spectra to be created for later analysis.
For many applications, counters are not sealed but are constantly fed with purified gas, thus reducing problems of contamination or gas aging. These are called "flow counters".

[edit] Scintillators
Some materials such as sodium iodide (NaI) can "convert" an X-ray photon to a visible photon; an electronic detector can be built by adding a photomultiplier. These detectors are called "scintillators", filmscreens or "scintillation counters". The main advantage of using these is that an adequate image can be obtained while subjecting the patient to a much lower dose of X-rays.

[edit] Image intensification

X-ray during Cholecystectomy
X-rays are also used in "real-time" procedures such as angiography or contrast studies of the hollow organs (e.g. barium enema of the small or large intestine) using fluoroscopy acquired using an X-ray image intensifier. Angioplasty, medical interventions of the arterial system, rely heavily on X-ray-sensitive contrast to identify potentially treatable lesions.

[edit] Direct semiconductor detectors
Since the 1970s, new semiconductor detectors have been developed (silicon or germanium doped with lithium, Si(Li) or Ge(Li)). X-ray photons are converted to electron-hole pairs in the semiconductor and are collected to detect the X-rays. When the temperature is low enough (the detector is cooled by Peltier effect or even cooler liquid nitrogen), it is possible to directly determine the X-ray energy spectrum; this method is called energy dispersive X-ray spectroscopy (EDX or EDS); it is often used in small X-ray fluorescence spectrometers. These detectors are sometimes called "solid state detectors". Cadmium telluride (CdTe) and its alloy with zinc, cadmium zinc telluride detectors have an increased sensitivity, which allows lower doses of X-rays to be used.
Practical application in medical imaging didn't start taking place until the 1990s. Currently amorphous selenium is used in commercial large area flat panel X-ray detectors for mammography and chest radiography. Current research and development is focused around pixel detectors, such as CERN's energy resolving Medipix detector.
Note: A standard semiconductor diode, such as a 1N4007, will produce a small amount of current when placed in an X-ray beam. A test device once used by Medical Imaging Service personnel was a small project box that contained several diodes of this type in series, which could be connected to an oscilloscope as a quick diagnostic.
Silicon drift detectors (SDDs), produced by conventional semiconductor fabrication, now provide a cost-effective and high resolving power radiation measurement. Unlike conventional X-ray detectors, such as Si(Li)s, they do not need to be cooled with liquid nitrogen.

[edit] Scintillator plus semiconductor detectors (indirect detection)
With the advent of large semiconductor array detectors it has become possible to design detector systems using a scintillator screen to convert from X-rays to visible light which is then converted to electrical signals in an array detector. Indirect Flat Panel Detectors (FPDs) are in widespread use today in medical, dental, veterinary and industrial applications. A common form of these detectors is based on amorphous silicon TFT/photodiode arrays.
The array technology is a variant on the amorphous silicon TFT arrays used in many flat panel displays, like the ones in computer laptops. The array consists of a sheet of glass covered with a thin layer of silicon that is in an amorphous or disordered state. At a microscopic scale, the silicon has been imprinted with millions of transistors arranged in a highly ordered array, like the grid on a sheet of graph paper. Each of these thin film transistors (TFTs) are attached to a light-absorbing photodiode making up an individual pixel (picture element). Photons striking the photodiode are converted into two carriers of electrical charge, called electron-hole pairs. Since the number of charge carriers produced will vary with the intensity of incoming light photons, an electrical pattern is created that can be swiftly converted to a voltage and then a digital signal, which is interpreted by a computer to produce a digital image. Although silicon has outstanding electronic properties, it is not a particularly good absorber of X-ray photons. For this reason, X-rays first impinge upon scintillators made from eg. gadolinium oxysulfide or caesium iodide. The scintillator absorbs the X-rays and converts them into visible light photons that then pass onto the photodiode array.

[edit] Visibility to the human eye
While generally considered invisible to the human eye, in special circumstances X-rays can be visible.[17] Brandes, in an experiment a short time after Röntgen's landmark 1895 paper, reported after dark adaptation and placing his eye close to an X-ray tube, seeing a faint "blue-gray" glow which seemed to originate within the eye itself.[18] Upon hearing this, Röntgen reviewed his record books and found he too had seen the effect. When placing an X-ray tube on the opposite side of a wooden door Röntgen had noted the same blue glow, seeming to emanate from the eye itself, but thought his observations to be spurious because he only saw the effect when he used one type of tube. Later he realized that the tube which had created the effect was the only one powerful enough to make the glow plainly visible and the experiment was thereafter readily repeatable. The knowledge that X-rays are actually faintly visible to the dark-adapted naked eye has largely been forgotten today; this is probably due to the desire not to repeat what would now be seen as a recklessly dangerous and potentially harmful experiment with ionizing radiation. It is not known what exact mechanism in the eye produces the visibility: it could be due to conventional detection (excitation of rhodopsin molecules in the retina), direct excitation of retinal nerve cells, or secondary detection via, for instance, X-ray induction of phosphorescence in the eyeball with conventional retinal detection of the secondarily produced visible light.
Though X-rays are invisible it is possible to see the ionization of the air molecules if the intensity of the X-ray beam is high enough. The beamline from the wiggler at the ID11 at ESRF is one example of such high intensity [19]

[edit] Medical uses

X-Ray Image of the Paranasal Sinuses, Lateral Projection
Since Röntgen's discovery that X-rays can identify bony structures, X-rays have been developed for their use in medical imaging. Radiology is a specialized field of medicine. Radiologists employ radiography and other techniques for diagnostic imaging. This is probably the most common use of X-ray technology.
X-rays are especially useful in the detection of pathology of the skeletal system, but are also useful for detecting some disease processes in soft tissue. Some notable examples are the very common chest X-ray, which can be used to identify lung diseases such as pneumonia, lung cancer or pulmonary edema, and the abdominal X-ray, which can detect ileus (blockage of the intestine), free air (from visceral perforations) and free fluid (in ascites). In some cases, the use of X-rays is debatable, such as gallstones (which are rarely radiopaque) or kidney stones (which are often visible, but not always). Also, traditional plain X-rays pose very little use in the imaging of soft tissues such as the brain or muscle. Imaging alternatives for soft tissues are computed axial tomography (CAT or CT scanning), magnetic resonance imaging (MRI) or ultrasound. Since 2005, X-rays are listed as a carcinogen by the U.S. government.[20]
Radiotherapy, a curative medical intervention, now used almost exclusively for cancer, employs higher energies of radiation.

[edit] Other uses

Each dot, called a reflection, in this diffraction pattern forms from the constructive interference of scattered X-rays passing through a crystal. The data can be used to determine the crystalline structure.
Other notable uses of X-rays include
X-ray crystallography in which the pattern produced by the diffraction of X-rays through the closely spaced lattice of atoms in a crystal is recorded and then analyzed to reveal the nature of that lattice. A related technique, fiber diffraction, was used by Rosalind Franklin to discover the double helical structure of DNA.[21]
X-ray astronomy, which is an observational branch of astronomy, which deals with the study of X-ray emission from celestial objects.
X-ray microscopic analysis, which uses electromagnetic radiation in the soft X-ray band to produce images of very small objects.
X-ray fluorescence, a technique in which X-rays are generated within a specimen and detected. The outgoing energy of the X-ray can be used to identify the composition of the sample.
Industrial radiography uses x-rays for inspection of industrial parts, particularly welds.
Paintings are often X-rayed to reveal the underdrawing and pentimenti or alterations in the course of painting, or by later restorers. Many pigments such as lead white show well in X-ray photographs.
Airport security luggage scanners use x-rays for inspecting the interior of luggage for security threats before loading on aircraft.

[edit] History
X-rays were discovered emanating from Crookes tubes, experimental discharge tubes invented around 1875, by scientists investigating the cathode rays, that is energetic electron beams, that were first created in the tubes. Crookes tubes created electrons by ionization of the residual air in the tube by a high DC voltage of anywhere between a few kilovolts and 100 kV. This voltage accelerated the electrons coming from the cathode to a high enough velocity that they created x-rays when they struck the anode or the glass wall of the tube. Many of the early Crookes tubes undoubtedly radiated x-rays, because early researchers noticed effects that were attributable to them, as detailed below, before Wilhelm Röntgen first systematically studied them in 1895. Among the important early researchers in X-rays were Ivan Pulyui, William Crookes, Johann Wilhelm Hittorf, Eugen Goldstein, Heinrich Hertz, Philipp Lenard, Hermann von Helmholtz, Nikola Tesla, Thomas Edison, Charles Glover Barkla, Max von Laue, and Wilhelm Conrad Röntgen.

[edit] Wilhelm Röntgen
On November 8, 1895, German physics professor Wilhelm Conrad Röntgen, stumbled on x-rays while experimenting with Lenard and Crookes tubes and began studying them. He wrote an initial report "On a new kind of ray: A preliminary communication" and on December 28, 1895 submitted it to the Würzburg's Physical-Medical Society journal.[22] This was the first paper written on X-rays. Röntgen referred to the radiation as "X", to indicate that it was an unknown type of radiation. The name stuck, although (over Röntgen's great objections), many of his colleagues suggested calling them Röntgen rays. They are still referred to as such in many languages, including German. Röntgen received the first Nobel Prize in Physics for his discovery.
There are conflicting accounts of his discovery because Röntgen had his lab notes burned after his death, but this is a likely reconstruction by his biographers.[23] Röntgen was investigating cathode rays with a fluorescent screen painted with barium platinocyanide and a Crookes tube which he had wrapped in black cardboard so the visible light from the tube wouldn't interfere. He noticed a faint green glow from the screen, about 1 meter away. The invisible rays coming from the tube to make the screen glow were passing through the cardboard. He found they could also pass through books and papers on his desk. Röntgen threw himself into investigating these unknown rays systematically. Two months after his initial discovery, he published his paper.
Röntgen discovered its medical use when he saw a picture of his wife's hand on a photographic plate formed due to X-rays. His wife's hand's photograph was the first ever photograph of a human body part using X-rays.

[edit] Johann Hittorf
German physicist Johann Hittorf (1824 – 1914), a coinventor and early researcher of the Crookes tube, found when he placed unexposed photographic plates near the tube, that some of them were flawed by shadows, though he did not investigate this effect.

[edit] Ivan Pulyui
In 1877 Ukranian-born Pulyui, a lecturer in experimental physics at the University of Vienna, constructed various designs of vacuum discharge tube to investigate their properties.[24] He continued his investigations when appointed professor at the Prague Polytechnic and in 1886 he found that that sealed photographic plates became dark when exposed to the emanations from the tubes. Early in 1896, just a few weeks after Röntgen published his first X-ray photograph, Pulyui published high-quality x-ray images in journals in Paris and London.[24] Although Pulyui had studied with Röntgen at the University of Strasbourg in the years 1873-75, his biographer Gaida (1997) asserts that his subsequent research was conducted independently.[24]
The first medical X-ray made in the United States was obtained using a discharge tube of Pulyui's design. In January 1896, on reading of Röntgen's discovery, Frank Austin of Dartmouth College tested all of the discharge tubes in the physics laboratory and found that only the Pulyui tube produced X-rays. This was a result of Pulyui's inclusion of an oblique "target" of mica, used for holding samples of fluorescent material, within the tube. On 3 February 1896 Gilman Frost, professor of medicine at the college, and his brother Edwin Frost, professor of physics, exposed the wrist of Eddie McCarthy, whom Edwin had treated some weeks earlier for a fracture, to the x-rays and collected the resulting image of the broken bone on gelatin photographic plates obtained from Howard Langill, a local photographer also interested in Röntgen's work.[25]

[edit] Nikola Tesla
In April 1887, Nikola Tesla began to investigate X-rays using high voltages and tubes of his own design, as well as Crookes tubes. From his technical publications, it is indicated that he invented and developed a special single-electrode X-ray tube [26] [27], which differed from other X-ray tubes in having no target electrode. The principle behind Tesla's device is called the Bremsstrahlung process, in which a high-energy secondary X-ray emission is produced when charged particles (such as electrons) pass through matter. By 1892, Tesla performed several such experiments, but he did not categorize the emissions as what were later called X-rays. Tesla generalized the phenomenon as radiant energy of "invisible" kinds.[28] [29] Tesla stated the facts of his methods concerning various experiments in his 1897 X-ray lecture [30] before the New York Academy of Sciences. Also in this lecture, Tesla stated the method of construction and safe operation of X-ray equipment. His X-ray experimentation by vacuum high field emissions also led him to alert the scientific community to the biological hazards associated with X-ray exposure.[31]

[edit] Fernando Sanford
X-rays were generated and detected by Fernando Sanford (1854-1948), the foundation Professor of Physics at Stanford University, in 1891. From 1886 to 1888 he had studied in the Hermann Helmholtz laboratory in Berlin, where he became familiar with the cathode rays generated in vacuum tubes when a voltage was applied across separate electrodes, as previously studied by Heinrich Hertz and Philipp Lenard. His letter of January 6, 1893 (describing his discovery as "electric photography") to The Physical Review was duly published and an article entitled Without Lens or Light, Photographs Taken With Plate and Object in Darkness appeared in the San Francisco Examiner.[32]

[edit] Philipp Lenard
Philipp Lenard, a student of Heinrich Hertz, wanted to see whether cathode rays could pass out of the Crookes tube into the air. He built a Crookes tube (later called a 'Lenard tube') with a 'window' in the end made of thin aluminum, facing the cathode so the cathode rays would strike it.[33] He found that something came through, that would expose photographic plates and cause fluorescence. He measured the penetrating power of these rays through various materials. It has been suggested that at least some of these 'Lenard rays' were actually x-rays.[34] Hermann von Helmholtz formulated mathematical equations for X-rays. He postulated a dispersion theory before Röntgen made his discovery and announcement. It was formed on the basis of the electromagnetic theory of light[35]. However, he did not work with actual X-rays.

[edit] Thomas Edison

Diagram of a water cooled X-ray tube. (simplified/outdated)
In 1895, Thomas Edison investigated materials' ability to fluoresce when exposed to X-rays, and found that calcium tungstate was the most effective substance. Around March 1896, the fluoroscope he developed became the standard for medical X-ray examinations. Nevertheless, Edison dropped X-ray research around 1903 after the death of Clarence Madison Dally, one of his glassblowers. Dally had a habit of testing X-ray tubes on his hands, and acquired a cancer in them so tenacious that both arms were amputated in a futile attempt to save his life. "At the 1901 Pan-American Exposition in Buffalo, New York, an assassin shot President William McKinley twice at close range with a .32 caliber revolver." The first bullet was removed but the second remained lodged somewhere in his stomach. McKinley survived for some time and requested that Thomas Edison "rush an X-ray machine to Buffalo to find the stray bullet. It arrived but wasn't used . . . McKinley died of septic shock due to bacterial infection."[36]
[edit] The 20th century and beyond
The many applications of x-rays immediately generated enormous interest. Workshops began making specialized versions of Crookes tubes for generating x-rays, and these first generation cold cathode or Crookes x-ray tubes were used until about 1920.
Crookes tubes were unreliable. They had to contain a small quantity of gas (invariably air) as a current will not flow in such a tube if they are fully evacuated. However as time passed the X-rays caused the glass to absorb the gas, causing the tube to generate 'harder' x-rays until it soon stopped operating. Larger and more frequently used tubes were provided with devices for restoring the air, known as 'softeners'. This often took the form of a small side tube which contained a small piece of mica – a substance that traps comparatively large quantities of air within its structure. A small electrical heater heated the mica and caused it to release a small amount of air restoring the tube's efficiency. However the mica itself had a limited life and the restore process was consequently difficult to control.
In 1904, John Ambrose Fleming invented the thermionic diode valve (vacuum tube). This used a hot cathode which permitted current to flow in a vacuum. This idea was quickly applied x-ray tubes, and heated cathode x-ray tubes, called Coolidge tubes, replaced the troublesome cold cathode tubes by about 1920.
Two years later, physicist Charles Barkla discovered that X-rays could be scattered by gases, and that each element had a characteristic X-ray. He won the 1917 Nobel Prize in Physics for this discovery. Max von Laue, Paul Knipping and Walter Friedrich observed for the first time the diffraction of X-rays by crystals in 1912. This discovery, along with the early works of Paul Peter Ewald, William Henry Bragg and William Lawrence Bragg gave birth to the field of X-ray crystallography. The Coolidge tube was invented the following year by William D. Coolidge which permitted continuous production of X-rays; this type of tube is still in use today.

ROSAT image of X-ray fluorescence of, and occultation of the X-ray background by, the Moon.
The use of X-rays for medical purposes (to develop into the field of radiation therapy) was pioneered by Major John Hall-Edwards in Birmingham, England. In 1908, he had to have his left arm amputated owing to the spread of X-ray dermatitis [1].
The X-ray microscope was invented in the 1950s.
The Chandra X-ray Observatory, launched on July 23, 1999, has been allowing the exploration of the very violent processes in the universe which produce X-rays. Unlike visible light, which is a relatively stable view of the universe, the X-ray universe is unstable, it features stars being torn apart by black holes, galactic collisions, and novas, neutron stars that build up layers of plasma that then explode into space.
An X-ray laser device was proposed as part of the Reagan Administration's Strategic Defense Initiative in the 1980s, but the first and only test of the device (a sort of laser "blaster", or death ray, powered by a thermonuclear explosion) gave inconclusive results. For technical and political reasons, the overall project (including the X-ray laser) was de-funded (though was later revived by the second Bush Administration as National Missile Defense using different technologies).

MDCT

2008-11-06T07:50:00.000-08:00

Accuracy of 64-MDCT in the Diagnosis of Ischemic Heart Disease Konstantin Nikolaou1, Andreas Knez2, Carsten Rist1, Bernd J. Wintersperger1, Alexander Leber2, Thorsten Johnson1, Maximilian F. Reiser1 and Christoph R. Becker1
1 Department of Clinical Radiology, University Hospitals, Ludwig-Maximilians University, Klinikum Grosshadern, Marchioninistr. 15, 81377 Munich, Germany.2 Department of Cardiology, University Hospitals, Grosshadern Ludwig-Maximilians University, Munich, Germany.
OBJECTIVE. The aim of this study was to evaluate the potential clinical value of a new generation of 64-MDCT systems with that of invasive coronary angiography in the diagnosis of coronary artery disease (CAD).
SUBJECTS AND METHODS. Seventy-two consecutive patients with known or suspected CAD underwent both 64-MDCT and quantitative coronary angiography (QCA). A CT system with acquisition of 64 slices per gantry rotation was used with a spatial resolution of 0.4 x 0.4 x 0.4 mm and a gantry rotation time of 330 milliseconds. Sensitivity, specificity, and diagnostic accuracy of 64-MDCT in the detection or exclusion of CAD were evaluated on both a per patient and a per segment basis.
RESULTS. Sixty-eight of 72 coronary CT angiograms (CTAs) (94%) were of diagnostic image quality. QCA showed significant CAD (i.e., one or more stenoses in > 50%) in 57% (39/68) and nonsignificant disease or healthy CTAs in 43% (29/68) of the patients. Sensitivity, specificity, and the negative predictive value (NPV) of 64-MDCT per patient were 97%, 79%, and 96%, respectively. Per segment, 923 of 1,020 coronary artery segments were assessable (90%). For the detection of stenoses of more than 50% and more than 75% per segment, 64-MDCT showed a sensitivity of 82% and 86%, respectively. Per segment, specificity and NPV were as high as 95% and 97%, respectively.
CONCLUSION. In clinical routine, coronary CTA will primarily be used for risk stratification on a per patient basis. In the present study, coronary 64-MDCT showed a high diagnostic accuracy on both per patient and per segment analyses.
Keywords: CT angiography • CT coronary arteriography • MDCT

MSCT

2008-11-06T06:44:00.001-08:00

64-slice CT in the diagnosis of ischemic heart disease
This new article by Nikolaou K et al in the July issue of the AJ R is one more article that shows the significance of this technique. In their results, "Sensitivity, specificity, and the negative predictive value (NPV) of 64-MDCT per patient were 97%, 79%, and 96%, respectively".
As with all similar articles, the negative predictive value was very high. The specificity was low but to maintain a high sensitivity, this is acceptable. The main reason for the low specificity was the overestimation of disease. In fact the logic that they have used and which makes sense practically is that the idea is not to miss a single patient of coronary artery disease (CAD). If that means that a few lesions are overdiagnosed, that is a much better evil than to underdiagnosis potentially significant disease. Also, once one significant lesion is diagnosed in a patient and it is obvious, he/she needs to go for a catheter angiography, the need to be very accurate in the rest of the vessels is less of an issue as well.
This is a 56-years old doctor who had an attack of angina. He came for a cardiac CT and we found a severe distal LAD stenosis (Fig. 1), which was confirmed on angiography (Fig. 2). There was another lesion in the proximal RCA (Fig. 3), which was overdiagnosed as compared to the catheter angiogram (Fig. 3). The proximal PDA lesion was well seen on both studies (Figs. 5, 6).

Coronary

2008-11-06T06:42:00.000-08:00

Coronary artery calcification
Taking off from last Friday's post, where Micheal Budoff has an excellent review of the paper discussed, comes the need to discuss the role of coronary artery calcium measurements.
As Budoff points out, there is enough data now to show that a calcium score of 0 is associated with a very low risk of a possible future cardiac event. This is something that we have seen anecdotally as well. In this setting, the additional yield of looking for soft plaques in a screening population, for picking up coronary artery disease, is very low.
In an individual patient, this may still be justified, especially if the patient has intermediate to high risk. This is why despite a calcium score of 0, we still go ahead and perform an angiogram. When we see soft plaques, there is a further stratification that can be then performed based on the LDL levels and the patient can be advised accordingly. However, from a mass screening perspective, it may be very dificult to justify looking for soft plaques, especially with all the associated issues of radiation and contrast injection.

Dual Source CT Scan

2008-11-06T06:40:00.000-08:00

Siemens Definition - DSCT - dual source CT - first review article
This is the first of two articles published this quarter on DSCT (the Siemens Definition Dual Source CT) in European radiology journals (the second article is discussed here). This article by Flohr et al in the Feb 2006 issue of European Radiology explores the physics behind the dual-source CT. In brief, there are two tubes and gantries at 90degrees to each other rotating at 330ms. The use of this dual-tube technology allows a temporal resolution of 83ms and with two-segment reconstruction, 42ms. Apparently, we do not need to use beta-blockers, since we can scan at pretty much any heart-rate.
With single-source scanners, we reach a temporal resolution of 83ms at heart rates of 66, 81 and 104, whereas with a DSCT scanner, this resolution is reached at any heart rate.
The big advantage of course, seems to be the ability to scan at any heart rate without pre-preparing with beta-blockers. Practically, this means that patients need not have to wait and can be taken into the scanner with just 4 hours of fasting, making a cardiac CT study a routine study.
Below are two images of the RCA (Fig. 1) and LAD (Fig. 2) showing the vessels at 25% and 70% reconstruction, though the heart rate has not been specified. These images have been obtained from the press release area of the Siemens Dual-Source site, where they have been released for press use.

CARDIAC DSCT

2008-11-02T03:43:00.001-08:00

Principles of cardiac dual source CT (DSCT)
Technique
Image acquisition
Data analysis
Dual source CT (DSCT), which combines two arrays of X-ray tube and dectector in one gantry, provides a temporal resolution of 82.5 ms which is not dependant on the heart rate, because each of two arrays travels only 90 degrees to acquire sufficient data. Each detector has 40 detector rows (32 central rows with 0.6 mm collimated slice width and 4 other rows with 1.2 mm collimated slice width). Using the Z-flying focal spot technique, two subsequent 32-slice readings with 0.6 mm collimated slice width are combined to one 64-slice projection with a sampling distance of 0.3 mm at the isocenter. In this way, 64 overlapping 0.6 mm slices per rotation are acquired. The gantry rotation time is 330 msec in cardiac mode (1-5).
No Beta-blockade is administrated prior to the scan. After placing an 18 G-intravenous access antecubitally, four ECG leads are attached to the patients’ chest. The ECG is continuously recorded to the scan. 80 mL of iodinated contrast material (400 mgI/mL), using flow tracking set at 100 HU, plus 50 ml NaCl chaser bolus are injected at 5 mm/sec for all patients by the use of a dual-head power injector.
The scanner settings are as follows: tube voltage 120 kV and tube current 400 mA for both tubes, ECG pulsing window 30-80% of the RR-interval and slices are 0.75-mm thick with a reconstruction interval of 0.5 mm. The pitch is adapted for the lowest expected heart rate during scanning. Scan direction is craniocaudal starting above the coronary ostia and ending at the diaphragm.
Data sets are reconstructed from 30 to 80% of the cardiac cycle in 10% increments, and if necessary at every % of the R-R interval, especially at higher heart rates.
The data set with highest image quality for each coronary artery is evaluated and used for further evaluation using axial and oblique multiplanar reconstructions, curved multiplanar reconstructions, oblique maximum intensity projections, and three-dimensional volume rendering technique reconstructions.

CARDIAC MRI

2008-11-02T03:39:00.001-08:00

Cardiac MRI Provides New 3-D Images of Beating Heart
next article
04.10.2002

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For Karen Pressley, Duke’s new Cardiovascular Magnetic Resonance Center revealed critical details of her heart that could enable her to have an angioplasty.
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Physicians at her home medical center in Fort Walton Beach, Fla. were reluctant to perform a heart procedure on 55-year-old Pressley because conventional techniques could not determine the extent of possible heart muscle death from a recent silent heart attack. So Pressley was referred to Duke University Medical Center, where cardiologists used magnetic resonance imaging (MRI) technology to clearly distinguish dead from damaged, but still living, heart muscle. “My doctors in Florida didn’t want to perform an angioplasty until they could get a better view of my heart,” Pressley said. “The MRI scan they performed at Duke showed that there was very little muscle death. That meant there was a good chance that angioplasty could restore function to my heart. It is a great relief to know that I can have the procedure.” Duke cardiologists estimate that about 30 percent of patients with heart disease -- like Pressley -- find that conventional methods for imaging the heart fall short in providing accurate information on which to guide treatment. The cardiologists believe that cardiac MRI can help this significant number of heart patients. Pressley is among the first patients to have their hearts “scanned” at the new Duke Cardiovascular Magnetic Resonance Center (DCMRC), the only facility in Duke’s service region -- and the first of its kind nationwide -- devoted exclusively to cardiovascular MRI. Unlike similar facilities where MRI machines may be used for many different clinical problems, the Duke scanner is devoted entirely to imaging the heart. The DCMRC is directed by biomedical engineer Robert Judd, Ph.D., and cardiologist Raymond Kim, M.D. They say that MRI provides crisp 3-D views of cardiac anatomy with no interference from adjacent bone or air. Its image quality surpasses that of echocardiography -- a more common imaging technique -- and MRI is able to capture views that echocardiography cannot. Cardiac MRI can show physicians how well the heart muscle is contracting, as well as precisely reveal areas of damaged tissue. The non-invasive, radiation-free technique is especially useful for evaluating such conditions as coronary artery disease, heart failure and congenital heart disease. Already a valuable diagnostic technique, cardiac MRI is still in its infancy, according to Judd. “It wasn’t until a few years ago that engineers developed scanners fast enough to clearly capture a beating heart,” Judd said. “The discipline is still defining itself. We want to advance the field by improving existing cardiovascular imaging techniques and also by creating entirely novel ways to look at the heart and its vessels.” During an MRI examination, a patient is guided through the cavity of a large doughnut-shaped magnet. The magnet causes atomic nuclei in cells to vibrate and give off characteristic “radio” signals, which are then converted by computers into three-dimensional images of the heart and its structures. While MRI technology itself is 20 years old, only in the past few years has technology improved to the point where accurate images of moving tissues can be taken. “For the first time, we can look at the heart in a totally non-invasive way with a precision not available with other techniques,” said Pascal Goldschmidt, M.D., chief of the division of cardiology at Duke. “It’s a like an astronomer being able to use the Hubbell telescope for the first time to look at galaxies never visible before. The detail MRI provides is the big difference -- the exquisite definition of layers of tissue that form the heart and the membranes that surround the heart is unique to MRI.” In addition to using the machine to help cardiologists diagnose heart problems, the DCMRC will also be the site of concentrated research aimed at developing new applications of MRI technology for cardiology. Just as importantly, the researchers say, the center offers to first advanced cardiac MRI training program to teach the next generation of cardiologists in the promising new technology. The center will devote about 40 percent of its resources to research, including basic research to improve the detection of salvageable heart tissue, research to improve imaging technology and clinical trials that use MRI to determine how new therapies affect heart function. For Kim, being able to distinguish damaged from dead heart tissue is one of the main early benefits of MRI technology. “With other techniques, damaged tissue can look dead,” Kim explained. “Being able to distinguish dead tissue from damaged -- but still alive tissue -- is crucial, because with techniques like angioplasty or bypass surgery, we can re-supply the tissue with nourishing blood flow. “MRI can take the guesswork out of diagnosing heart problems -- we can see exactly what disease processes are going on,” Kim continued. “The MRI is not just providing better pictures of the heart -- which it does -- but it also provides new and better forms of information, such as the metabolism of heart muscle cells.” For Pressley, the cardiac MRI was able to provide her physicians with the detailed answer they needed for a specific clinical problem. As more research is conducted at the DCMRC, the Duke investigators believe that cardiac MRI will revolutionize their ability to diagnose heart problems. “For the future, we foresee a ‘one-stop shop’ where any question about the heart and its vessels can be answered definitively using this technology,” Kim said. “Unlike the other imaging technologies, cardiac MRI can be used to answer many different issues we face daily in treating our patients.” The DCMRC currently operates the $2.6 million, four-ton scanner in its outpatient clinic. A second scanner will be installed later this year in the inpatient area of Duke Hospital to better serve patients who are hospitalized.
Richard Merritt Source: EurekAlert! Further information: dcmrc.mc.duke.edu/

Vertigo

2008-10-15T07:17:00.000-07:00

Vertigo (medical)
From Wikipedia, the free encyclopedia
Jump to: navigation, search

This article needs additional citations for verification.Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (January 2008)
Vertigo (medical)Classification and external resources
ICD-9
438.85
eMedicine
neuro/
Vertigo (from the Latin vertere, to turn, and the suffix -igo, a condition, i. e., "a condition of turning about"[1]) is a specific type of dizziness, a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is actually stationary with respect to the surroundings.
There are two types of vertigo: subjective and objective. There is a subjective vertigo when a person has a false sensation of movement. In the case of objective vertigo, the surroundings appear to move past a person's field of vision.
The effects of vertigo may be slight. It can cause nausea and vomiting and, in severe cases, it may give rise to difficulties with standing and walking.
Contents[hide]
1 Causes
2 Neurochemistry
3 Diagnostic testing
4 Treatment
5 References
6 External links
//

[edit] Causes
Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the syndrome]] and Meniere's disease.
Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or viruses.
Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway. These are peripheral or central vertigo. Each category has a distinct set of characteristics and associated findings.
Vertigo can also occur after long flights or boat journeys where the mind gets used to turbulence, resulting in a person's feeling as if he is moving up and down. This usually subsides after a few days.
There is also documented evidence that Genital Warts can cause it.[citation needed]

[edit] Neurochemistry
The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles.
Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA.
Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and the lateral vestibular nucleus, and the vertical VOR.
Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.
The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholine, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.

[edit] Diagnostic testing
Tests of vestibular system (balance) function include electronystagmography (ENG), rotation tests, Caloric reflex test,[2] and Computerized Dynamic Posturography (CDP).
Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER).
Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT or CT).

[edit] Treatment
Treatment is specific for underlying disorder of vertigo:
vestibular rehabilitation
anticholinergics
antihistamines
benzodiazepines
calcium channel antagonists, specifically Verapamil and Nimodipine
GABA modulators, specifically gabapentin and baclofen
neurotransmitter reuptake inhibitors such as SSRI's, SNRI's and tricyclics
benign paroxysmal positional vertigo (BPPV), a special kind of vertigo, is treated with the Epley maneuver (performed by a doctor or physical therapist, or with a BPPV maneuver at home)

[edit] References
^ "Definition of vertigo - Merriam-Webster Online Dictionary". Retrieved on 2007-09-19.
^ "Core Curriculum: Inner Ear Disease - Vertigo". Retrieved on 2007-09-19.

[edit] External links
Vertigo (medical) at the Open Directory Project
Vertigo information
Vertigo Information - Causes, Symptoms, Treatment

Cardiac arrest

2008-10-15T06:57:00.000-07:00

Cardiac arrest
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see Cardiac arrest (disambiguation).
Cardiac arrestClassification and external resources
ICD-10
I 46.
ICD-9
427.5
MeSH
D006323
A cardiac arrest, also known as cardiorespiratory arrest, cardiopulmonary arrest or circulatory arrest, is the abrupt cessation of normal circulation of the blood due to failure of the heart to contract effectively during systole.[1]
A cardiac arrest is different from (but may be caused by) a heart attack or myocardial infarction, where blood flow to the still-beating heart is interrupted.
"Arrested" blood circulation prevents delivery of oxygen to all parts of the body. Cerebral hypoxia, or lack of oxygen supply to the brain, causes victims to lose consciousness and to stop normal breathing, although agonal breathing may still occur. Brain injury is likely if cardiac arrest is untreated for more than 5 minutes,[2] although new treatments such as induced hypothermia have begun to extend this time.[3][4] To improve survival and neurological recovery immediate response is paramount.[5]
Cardiac arrest is a medical emergency that, in certain groups of patients, is potentially reversible if treated early enough (See "Reversible causes" below). When unexpected cardiac arrest leads to death this is called sudden cardiac death (SCD).[1] The primary first-aid treatment for cardiac arrest is cardiopulmonary resuscitation (commonly known as CPR) which provides circulatory support until availability of definitive medical treatment, which will vary dependent on the rhythm the heart is exhibiting, but often requires defibrillation.
Contents[hide]
1 Characteristics and diagnosis
2 Causes of cardiac arrest
2.1 Reversible causes
2.1.1 Hs
2.1.2 Ts
3 Treatment
3.1 Out of hospital arrest
3.2 Hospital treatment
3.3 Therapeutic hypothermia
3.4 Peri-arrest period
4 Prognosis
5 Prevention
6 Implantable cardioverter defibrillators
7 Ethical issues
8 See also
9 References
10 External links
//

[edit] Characteristics and diagnosis
Cardiac arrest is an abrupt cessation of pump function (evidenced by absence of a palpable pulse) of the heart that with prompt intervention could be reversed, but without it will lead to death.[1]
However, due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest, which shares many of the same features) is lack of circulation, however there are a number of ways of determining this.
In many cases, lack of carotid pulse is the gold standard for diagnosing cardiac arrest, but lack of a pulse (particularly in the peripheral pulses) may be a result of other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals[6][7] or lay persons.[8]
Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,[9] have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.[10]
Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resusciation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse [9]. These signs included coughing, gasping, colour, twitching and movement.[11] However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally.[9]
Following initial diagnosis of cardiac arrest, healthcare professionals further categorise the diagnosis based on the ECG/EKG rhythm. There are 4 rhythms which result in a cardiac arrest. Ventricular fibrillation (VF/VFib) and pulseless ventricular tachycardia (VT) are both responsive to a defibrillator and so are colloquially referred to as "shockable" rhythms, whereas asystole and pulseless electrical activity (PEA) are non-shockable. The nature of the presenting hearth rhythm suggests different causes and treatment, and is used to guide the rescuer as to what treatment may be appropriate[10] (see Advanced life support and Advanced cardiac life support, as well as the causes of arrest below).

[edit] Causes of cardiac arrest
Cardiac arrest is synonymous with Clinical death. All disease processes leading to death have a period of (potentially) reversible cardiac arrest: the causes of arrest are, therefore, numerous. However, many of these conditions, rather than causing an arrest themselves, promote one of the "Reversible causes" (see below), which then triggers the arrest (e.g. choking leads to hypoxia which in turn leads to an arrest). In some cases, the underlying mechanism cannot be overcome, leading to an unsuccessful resuscitation.
Among adults, ischemic heart disease is the predominant cause of arrest.[12] At autopsy 30% of victims show signs of recent myocardial infarction[citation needed]. Other cardiac conditions potentially leading to arrest include structural abnormalities, arrhythmias and cardiomyopathies. Non-cardiac causes include infections, overdoses, trauma and cancer, in addition to many others.

[edit] Reversible causes
Cardiopulmonary resuscitation (CPR), including adjunctive measures such as defibrillation, intubation and drug administration, is the standard of care for initial treatment of cardiac arrest. However, most cardiac arrests occur for a reason, and unless that reason can be found and overcome, CPR is often ineffective, or if it does result in a return of spontaneous circulation, this is short lived.[10] As highlighted above, a variety of disease processes can lead to a cardiac arrest, however they usually boil down to one or more of the "Hs and Ts".[13][14][15]

[edit] Hs
Hypovolemia - A lack of circulating body fluids, principally blood volume. This is usually (though not exclusively) caused by some form of bleeding, anaphylaxis, or pregnancy with gravid uterus. Peri-arrest treatment includes giving IV fluids and blood transfusions, and controlling the source of any bleeding - by direct pressure for external bleeding, or emergency surgical techniques such as esophageal banding, gastroesophageal balloon tamponade (for treatment of massive GI bleeding such as in esophageal varices), thoracotomy in cases of penetrating trauma or significant shear forces applied to the chest, or exploratory laparotomy in cases of penetrating trauma, spontaneous rupture of major blood vessels, or rupture of a hollow viscus in the abdomen.
Hypoxia - A lack of oxygen delivery to the heart, brain and other vital organs. Rapid assessment of airway patency and respiratory effort must be performed. If the patient is mechanically ventilated, the presence of breath sounds and the proper placement of the endotracheal tube should be verified. Treatment may include providing oxygen, proper ventilation, and good CPR technique. In cases of carbon monoxide poisoning or cyanide poisoning, hyperbaric oxygen may be employed after the patient is stabilized.
Hydrogen ions (Acidosis) - An abnormal pH in the body as a result of lactic acidosis which occurs in prolonged hypoxia and in severe infection, diabetic ketoacidosis, renal failure causing uremia, or ingestion of toxic agents or overdose of pharmacological agents, such as aspirin and other salicylates, ethanol, ethylene glycol and other alcohols, tricyclic antidepressants, isoniazid, or iron sulfate. This can be treated with proper ventilation, good CPR technique, buffers like sodium bicarbonate, and in select cases may require emergent hemodialysis.
Hyperkalemia or Hypokalemia - Both excess and inadequate potassium can be life-threatening. A common presentation of hyperkalemia is in the patient with end-stage renal disease who has missed a dialysis appointment and presents with weakness, nausea, and broad QRS complexes on the electrocardiogram. (Note however that patients with chronic kidney disease are often more tolerant of high potassium levels as their body often adapts to it.) The electrocardiogram will show tall, peaked T waves (often larger than the R wave) or can degenerate into a sine wave as the QRS complex widens. Immediate initial therapy is the administration of calcium, either as calcium gluconate or calcium chloride. This stabilizes the electrochemical potential of cardiac myocytes, thereby preventing the development of fatal arrhythmias. This is, however, only a temporizing measure. Other temporizing measures may include nebulized albuterol, intravenous insulin (usually given in combination with glucose, and sodium bicarbonate, which all temporarily drive potassium into the interior of cells. Definitive treatment of hyperkalemia requires actual excretion of potassium, either through urine (which can be facilitated by administration of loop diuretics such as furosemide) or in the stool (which is accomplished by giving sodium polystyrene sulfonate enterally, where it will bind potassium in the GI tract.) Severe cases will require emergent hemodialysis. The diagnosis of hypokalemia (not enough potassium) can be suspected when there is a history of diarrhoea or malnutrition. Loop diuretics may also contribute. The electrocardiogram may show flattening of T waves and prominent U waves. Hypokalemia is an important cause of acquired long QT syndrome, and may predispose the patient to torsades de pointes. Digitalis use may increase the risk that hypokalemia will produce life threatening arrhythmias. Hypokalemia is especially dangerous in patients with ischemic heart disease.
Hypothermia - A low core body temperature, defined clinically as a temperature of less than 35 degrees Celsius (95 degrees Fahrenheit). The patient is re-warmed either by using a cardiac bypass or by irrigation of the body cavities (such as thorax, peritoneum, bladder) with warm fluids; or warmed IV fluids. CPR only is given until the core body temperature reached 30 degrees Celsius, as defibrillation is ineffective at lower temperatures. Patients have been known to be successfully resuscitated after periods of hours in hypothermia and cardiac arrest, and this has given rise to the often-quoted medical truism, "You're not dead until you're warm and dead."
Hypoglycemia or Hyperglycemia - Low blood glucose from overdose of oral hypoglycemics such as sulfonylureas, or overdose of insulin. Rare endocrine disorders can also cause unexpected hypoglycemia. Generally, hyperglycemia is itself not fatal, however DKA will cause pH to drop, and nonketotic hyperosmolar coma leads to a severely hypovolemic state. Hypoglycemia is corrected rapidly by intravenous administration of concentrated glucose (typically 25 ml of 50% glucose in adults, but in children 25% glucose is used, and in neonates 10% glucose is used.) However, the patient will often require a continuous intravenous drip until the causative agent is completely metabolized. In DKA, the goal is correction of acidosis. In NKH, the goal is adequate fluid resuscitation.

[edit] Ts
Tablets or Toxins - Tricyclic antidepressants, phenothiazines, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, acetominophen. This may be evidenced by items found on or around the patient, the patient's medical history (i.e. drug abuse, medication) taken from family and friends, checking the medical records to make sure no interacting drugs were prescribed, or sending blood and urine samples to the toxicology lab for report. Treatment may include specific antidotes, fluids for volume expansion, vasopressors, sodium bicarbonate (for tricyclic antidepressants), glucagon or calcium (for calcium channel blockers), benzodiazepines (for cocaine), or cardiopulmonary bypass. Herbal supplements and over-the-counter medications should also be considered.
Cardiac Tamponade - Blood or other fluids building up in the pericardium can put pressure on the heart so that it is not able to beat. This condition can be recognized by the presence of a narrowing pulse pressure, muffled heart sounds, distended neck veins, electrical alternans on the electrocardiogram, or by visualization on echocardiogram. This is treated in an emergency by inserting a needle into the pericardium to drain the fluid (pericardiocentesis), or if the fluid is too thick then a subxiphoid window is performed to cut the pericardium and release the fluid.
Tension pneumothorax - The build-up of air into one of the pleural cavities, which causes a mediastinal shift. When this happens, the great vessels (particularly the superior vena cava) become kinked, which limits blood return to the heart. The condition can be recognized by severe air hunger, hypoxia, jugular venous distension, hyperressonance to percussion on the effected side, and a tracheal shift away from the effected side. The tracheal shift often requires a chest x-ray to appreciate (although treatment should be initiated prior to obtaining a chest x-ray if this condition is suspected. ) This is relieved in by a needle thoracotomy (inserting a needle catheter) into the 2nd intercostal space at the mid-clavicular line, which relieves the pressure in the pleural cavity.
Thrombosis (Myocardial infarction) - If the patient can be successfully resuscitated, there is a chance that the myocardial infarction can be treated, either with thrombolytic therapy or percutaneous coronary intervention.
Thromboembolism (Pulmonary embolism) - hemodynamically significant pulmonary emboli are generally massive and typically fatal. Administration of thrombolytics can be attempted, and some specialized centers may perform thrombolectomy, however, prognosis is generally poor.
Trauma (Hypovolemia) - Reduced blood volume from acute injury or primary damage to the heart or great vessels. Cardiac arrest secondary to trauma, particularly blunt trauma, has a very poor prognosis.

Checking respiration.

Checking carotid pulse.

Insulfation mouth-to-mouth.

[edit] Treatment

[edit] Out of hospital arrest
Most out-of-hospital cardiac arrests occur following a myocardial infarction (heart attack), and present initially with a heart rhythm of ventricular fibrillation. The patient is therefore likely to be responsive to defibrillation, and this has become the focus of pre-hospital interventions. Several organisations promote the idea of a "chain of survival", of which defibrillation is a key step. The links are:
Early recognition - If possible, recognition of illness before the patient develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival - for every minute a patient is in cardiac arrest, their chances of survival drop by roughly 10% [10]
Early CPR - This buys time by keeping vital organs perfused with oxygen whilst waiting for equipment and trained personnel to reverse the arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
Early defibrillation - This is the only effective treatment for ventricular fibrillation, and also has benefit in ventricular tachycardia [10] and should be employed in such cases if the patient has signs of hemodynamic compromise, or if the patient has pulseless ventricular tachycardia. If defibrillation is delayed, then the rhythm is likely to degenerate into asystole, for which outcomes are markedly worse.
Early advanced care - Early Advanced Cardiac Life Support is the final link in the chain of survival.
If one or more links in the chain are missing or delayed, then the chances of survival drop significantly. In particular, bystander CPR is an important indicator of survival: if it has not been carried out, then resuscitation is associated with very poor results. Paramedics in some jurisdictions are authorised to abandon resuscitation altogether if the early stages of the chain have not been carried out in a timely fashion prior to their arrival.
Because of this, considerable effort has been put into educating the public on the need for CPR. In addition, there is increasing use of public access defibrillation. This involves placing automated external defibrillators in public places, and training key staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services, and has been shown to lead to increased chances of survival. In addition, it has been shown that those who suffer arrests in remote locations have worse outcomes following cardiac arrest [16]: these areas often have first responder schemes, whereby members of the community receive training in resuscitation and are given a defibrillator, and called by the emergency medical services in the case of a collapse in their local area.

[edit] Hospital treatment
Treatment within a hospital usually follows advanced life support protocols. In the US, non-traumatic adult resuscitation is described by ACLS (advanced cardiac life support), pediatric resuscitation is described by PALS (pediatric advanced life support), and neonatal resusciation is described by NALS (neonatal advanced life support.) Depending on the diagnosis, various treatments are offered, ranging from defibrillation (for ventricular fibrillation or ventricular tachycardia) to surgery (for cardiac arrest which can be reversed by surgery - see causes of arrest, above) to medication (for asystole and PEA). All will include CPR.
While specific details may vary, all hospitals have protocols as to how resuscitations should be performed in patients, visitors, or employees who have arrested unexpectedly in the hospital. These protocols are often initiated by a Code Blue, which usually denotes impending or acute onset of cardiac arrest or respiratory failure, although in practice, Code Blue is often called in less life-threatening situations that require immediate attention from a physician.
If not already done, a definitive airway will be establish by the placement of an endotracheal tube which is then attached to a mechanical ventilator.
Cardiac arrest is generally divided into two cases: presence of disorganized mechanical cardiac activity, or complete absence of mechanical cardiac activity.
Disorganized mechanical cardiac activity includes ventricular fibrillation and hemodynamically unstable or pulseless ventricular tachycardia. This also includes torsade de pointes. These must all be treated primarily with defibrillation. Advanced cardiac life support algorithms also detail the stepwise administration of epinephrine, vasopressin, the antiarrhythmic agent amiodarone, as well as attempts to correct possible underlying causes.
Complete absence of mechanical cardiac activity includes asystole and pulseless electrical activity. This is treated entirely with pharmacologic agents, specifically epinephrine and atropine. However, resuscitation is rarely successful without effective treatment of the underlying cause.

[edit] Therapeutic hypothermia
Main article: Therapeutic hypothermia
In some cases, doctors may choose to induce hypothermia after return of spontaneous circulation (ROSC). This procedure is called therapeutic hypothermia. The first study conducted in Europe focused on people who were resuscitated 5-15 minutes after collapse. Patients participating in this study experienced spontaneous return of circulation (ROSC) after an average of 105 minutes. Subjects were then cooled over a 24 hour period, with a target temperature of 32-34°C (89.6-93.2°F). 55% of the 137 patients in the hypothermia group experienced favorable outcomes, compared with only 39% in the group that received standard care following resuscitation.[17] Death rates in the hypothermia group were 14% lower, meaning that for every 7 patients treated one life was saved.[17] Notably, complications between the two groups did not differ substantially. This data was supported by another similarly run study that took place simultaneously in Australia. In this study 49% of the patients treated with hypothermia following cardiac arrest experienced good outcomes, compared to only 26% of those who received standard care.[18]

[edit] Peri-arrest period
The period (either before or after) surrounding a cardiac arrest is known as the peri-arrest period. During this period the patient is in a highly unstable condition and must be constantly monitored in order to halt the progression or repeat of a full cardiac arrest. The preventative treatment used during the peri-arrest period depends on the causes of the impending arrest and the likelihood such an event occurring.

[edit] Prognosis
The out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% at discharge and 8-22% on admission), than an in-hospital cardiac arrest (15% at discharge). The principal determining factor is the initially documented rhythm. Patients with VF/VT have 10-15 times more chance of surviving than those suffering from pulseless electrical activity or asystole (as they are sensitive to defibrillation, whereas asystole and PEA are not).[citation needed]
Since mortality in case of OHCA is high, programs were developed to improve survival rate. A study by Bunch et al. showed that, although mortality in case of ventricular fibrillation is high, rapid intervention with a defibrillator increases survival rate to that of patients that did not have a cardiac arrest.[12][19]
Survival is mostly related to the cause of the arrest (see above). In particular, patients who have suffered hypothermia have an increased survival rate, possibly because the cold protects the vital organs from the effects of tissue hypoxia. Survival rates following an arrest induced by toxins is very much dependent on identifying the toxin and administering an appropriate antidote. A patient who has suffered a myocardial infarction due to a blood clot in the left coronary artery has a lower chance of survival as it cuts of the blood supply to most of the left ventricle (the chamber which must pump blood to the whole of the systemic circulation).
Cobbe et al (1996) conducted a study into survival rates from out of hospital cardiac arrest. 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to an acute hospital ward. Of these, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff), however 97.5% suffered a mild to moderate neurological disability, and 2% suffered a major neurological disability. Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.[20]
Ballew (1997) performed a review of 68 earlier studies into prognosis following in-hospital cardiac arrest. They found a survival to discharge rate of 14% (this roughly double the rate for out of hospital arrest found by Cobbe et al (see above)), although there was a wide range (0-28%).[21]

[edit] Prevention
With positive outcomes following cardiac arrest so unlikely, a great deal of effort has been spent in finding effective strategies to prevent cardiac arrest.
As noted above, one of the prime causes of cardiac arrest outside of hospital is ischemic heart disease. Vast resources have been put into trying to reduce cardiovascular risks across much of the developed world. In particular schemes have been put in place to promote a healthy diet and exercise. For people considered to be particularly at risk of heart disease, measures such as blood pressure control, prescription of cholesterol lowering medications, and other medico-therapeutic interventions, have been widely used. A magnesium deficiency, or lower levels of magnesium, can contribute to heart disease and a healthy diet that contains adequte magnesium may help prevent heart disease.[22] Magnesium can be used to enhance long term treatment, so it may be effective in long term prevention.
Patients in hospital are far less likely to have a cardiac arrest caused of primary cardiac origin, and hence present in asystole or PEA, and have bleak outcomes.[citation needed] Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs[10][23]. This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration[10] and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:
Crash teams (also known as code teams) - These are designated staff members who have particular expertise in resuscitation, who are called to the scene of all arrests within the hospital.
Medical emergency teams - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest.
Critical care outreach - As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted - the outreach team offers support to ward staff to prevent this from happening.

[edit] Implantable cardioverter defibrillators
A technologically based intervention to prevent further cardiac arrest episodes is the use of an implantable cardioverter-defibrillator (ICD). This device is implanted in to the patient. They act as an instant defibrillator in the event of arrhythmia. Note that standalone ICDs do not have any pacemaker functions, but they can be combined with a pacemaker, and modern versions also have advanced features such as anti-tachycardic pacing as well as synchronized cardioversion. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada.[24] An accompanying editorial by Simpson explores some of the economic, geographic, social and political reasons for this.[25] Patients who are most likely to benefit from the placement of an ICD are those with severe ischemic cardiomyopathy (with systolic ejection fractions less than 30%) as demonstrated by the MADIT-II trial.[26]

[edit] Ethical issues
Cardiopulmonary resuscitation and advanced cardiac life support are not always in a person's best interest. This is particularly true in the case of terminal illnesses when resuscitation will not alter the outcome of the disease. Properly performed CPR often fractures the rib cage, especially in older patients or those suffering from osteoporosis. Defibrillation, especially repeated several times as called for by ACLS protocols, may also cause electrical burns.
Some people with a terminal illness choose to avoid such measures and die peacefully. People with views on the treatment they wish to receive in the event of a cardiac arrest should discuss these views with both their doctor and with their family. A patient may ask their doctor to place a do not resuscitate (DNR) order in the medical record. Alternatively, in many jurisdictions, a person may formally state their wishes in an advance directive or advance health directive.

[edit] See also
Asystole
Clinical death
Death
Defibrillation
Myocardial infarction
Near-death experience
Ventricular fibrillation

[edit] References
^ a b c Harrison's Principles of Internal Medicine 16th Edition, The McGraw-Hill Companies, ISBN 0-07-140235-7
^ Safar P (1986). "Cerebral resuscitation after cardiac arrest: a review". Circulation 74: IV138–153. Lippincott Williams & Wilkins. Retrieved on 2007-01-05.
^ Holzer M, Behringer W (2005). "Therapeutic hypothermia after cardiac arrest". Current Opinion in Anaestesiology 18: 163–168. Lippincott Williams & Wilkins. Retrieved on 2007-01-03.
^ Safar P et al (1996). "Improved cerebral resuscitation from cardiac arrest in dogs with mild hypothermia plus blood flow promotion". Stroke 27: 105–113. Lippincott Williams & Wilkins. Retrieved on 2007-01-07.
^ Irwin and Rippe's Intensive Care Medicine by Irwin and Rippe, Fifth Edition (2003), Lippincott Williams & Wilkins, ISBN 0-7817-3548-3
^ Flesche CW, Breuer S, Mandel LP, Breivik H, Tarnow J. (1994) The ability of health professionals to check the carotid pulse. Circulation Vol. 90: I–288.
^ F. Javier Ochoa, E. Ramalle-Gomara, J.M. Carpintero et al. (1998) Competence of health professionals to check the carotid pulse. Resuscitation Vol. 37 pp. 173–175
^ Bahr, J., Klingler, H., Panzer, W., Rode, H., Kettler, D. (1997). Skills of lay people in checking the carotid pulse. Resuscitation. Vol. 35(1) pp. 23-26
^ a b c American Heart Association (2005) 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation Vol. 112 pp. 19-34
^ a b c d e f g Resuscitation Council UK (2005). Resuscitation Guidelines 2005 London: Resuscitation Council UK.
^ St John Ambulance, St Andrew's Ambulance Association, British Red Cross (2002) (8th Ed.) First Aid Manual. London: Dorling Kindersley
^ a b Cardiac Resuscitation Mickey S. Eisenberg, M.D., Ph. D., and Terry J. Mengert, M.D. New England Journal of Medicine, Volume 344:1304-1313, April 26, 2001
^ ACLS: Principles and Practice. p. 71-87. Dallas: American Heart Association, 2003. ISBN 0-87493-341-2.
^ ACLS for Experienced Providers. p. 3-5. Dallas: American Heart Association, 2003. ISBN 0-87493-424-9.
^ "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 7.2: Management of Cardiac Arrest." Circulation 2005; 112: IV-58 - IV-66.
^ Lyon, R.M, Cobbe, S.M., Bradley, J.M., Grubb, N.R. (2004)Surviving out of hospital cardiac arrest at home: a postcode lottery? Emergency Medical Journal Vol. 21 pp. 619-624
^ a b Holzer, Michael. “Mild Hypothermia to Improve the Neurologic Outcome After Cardiac Arrest.” New England Journal of Medicine. (2002) Vol. 346, No. 8.
^ Bernard, Stephen et al. "Treatment of Comatose Survivors of Out-of-Hospital Cardiac Arrest with Induced Hypothermia." N England Journal of Medicine. (2002) Vol. 346, No. 8. http://content.nejm.org/cgi/content/abstract/346/8/557
^ Long-Term Outcomes of Out-of-Hospital Cardiac Arrest after Successful Early Defibrillation T. Jared Bunch, M.D., Roger D. White, M.D., Bernard J. Gersh, M.B., Ch. B., Ryan A. Meverden, B.S., David O. Hodge, M.S., Karla V. Ballman, Ph. D., Stephen C. Hammill, M.D., Win-Kuang Shen, M.D., and Douglas L. Packer, M.D., New England Journal of Medicine, Volume 348:2626-2633, June 26, 2003
^ Survival of 1476 patients initially resuscitated from out of hospital cardiac arrest Stuart M Cobbe, Kirsty Dalziel, Ian Ford, Andrew K Marsden, British Medical Journal 1996;312:1633-1637 (29 June)
^ Recent advances: Cardiopulmonary resuscitation Kenneth A Ballew, British Medical Journal 1997;314:1462 (17 May)
^ Rosanoff, Andrea (PhD); Seelig, Mildred S (MD) (2004). "Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals" (PDF). Journal of the American College of Nutrition 23 (5): 501S–505S.
^ Kause J, Smith G, Prytherch D, et al. (2004) A comparison of antecedents to cardiac arrests, deaths and emergency intensive care admissions in Australia and New Zealand, and the United Kingdom--the ACADEMIA study. Resuscitation Vol 62 pp. 275-82
^ Birnie, David H; Sambell, Christie; Johansen, Helen; Williams, Katherine; Lemery, Robert; Green, Martin S; Gollob, Michael H; Lee, Douglas S; Tang, Anthony SL (July 2007). "Use of implantable cardioverter defibrillators in Canadian and IS survivors of out-of-hospital cardiac arrest". Canadian Medical Association Journal 177 (1). Retrieved on 2007-07-29.
^ Simpson, Christopher S (July 2007). "Implantable cardioverter defibrillators work - so why aren't we using them?". Canadian Medical Association Journal 177 (1): 49. doi:10.1503/cmaj.070470. Retrieved on 2007-07-29.
^ Moss, AJ; Cannom, DS; Daubert, JP; Hall, WJ; Higgins, SL; Klein, H; Wilber, D; Zareba, W; Brown, MW (1999). "Multicenter automatic defibrillator implantation Trial II (MADIT II) : Design and clinical protocol". Annals of non-invasive electrocardiology 4 (1): 83–91. doi:10.1111/j.1542-474X.1999.tb00369.x.

[edit] External links
Sudden Cardiac Arrest Association
Sudden Cardiac Arrest Foundation
New Studies Confirm Chest Compressions Alone are Life-saving for Cardiac Arrest
Cardiac Arrest Videos - Inside Cardiac Arrest
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Electrocardiogram

2008-10-15T06:51:00.000-07:00

Electrocardiogram
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"ECG" redirects here. For other uses, see ECG (disambiguation).

12 Lead ECG of a 26 year old male.
An electrocardiogram (ECG or EKG, abbreviated from the German Elektrokardiogramm) is a noninvasive transthoracic graphic produced by an electrocardiograph, which records the electrical activity of the heart over time. Its name is made of different parts: electro, because it is related to electrical activity, cardio, Greek for heart, gram, a Greek root meaning "to write". In the US, the abbreviation "EKG" is often preferred over "ECG", while "ECG" is used universally in the UK and many other countries. It is preferred as "EKG" in the US because doctor's handwriting of "ECG" can often be confused as "EEG" when transcribing orders or with echocardiography which is also abbreviated "ECG".
Sympathetic electrical impulses in the heart originate in the sinoatrial node and travel through the heart muscle where they impart electrical initiation of systole or contraction of the heart.[citation needed] The electrical waves can be measured at selectively placed electrodes (electrical contacts) on the skin. Electrodes on different sides of the heart measure the activity of different parts of the heart muscle. An EKG displays the voltage between pairs of these electrodes, and the muscle activity that they measure, from different directions, also understood as vectors. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle. It is the best way to measure and diagnose abnormal rhythms of the heart,[1] particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by levels of dissolved salts (electrolytes), such as potassium, that are too high or low.[2] In myocardial infarction (MI), the ECG can identify damaged heart muscle. But it can only identify damage to muscle in certain areas, so it can't rule out damage in other areas.[3] The ECG cannot reliably measure the pumping ability of the heart; for which ultrasound-based (echocardiography) or nuclear medicine tests are used.
Contents[hide]
1 History
2 ECG graph paper
3 Filter selection
4 Leads
4.1 Limb
4.2 Augmented limb
4.3 Precordial
4.4 Ground
5 Waves and intervals
5.1 P wave
5.2 QRS complex
5.3 PR/PQ interval
5.4 ST segment
5.5 T wave
5.6 QT interval
5.7 U wave
6 Clinical lead groups
7 Axis
8 Electrocardiogram Heterogeneity
8.1 Background
8.2 Research
8.3 Future Applications
9 See also
10 References
11 Conference References
12 External links
//

[edit] History
Alexander Muirhead attached wires to a feverish patient's wrist to obtain a record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in 1872 at St Bartholomew's Hospital.[4] This activity was directly recorded and visualized using a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[5] The first to systematically approach the heart from an electrical point-of-view was Augustus Waller, working in St Mary's Hospital in Paddington, London.[6] His electrocardiograph machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat was projected onto a photographic plate which was itself fixed to a toy train. This allowed a heartbeat to be recorded in real time. In 1911 he still saw little clinical application for his work.
The breakthrough came when Willem Einthoven, working in Leiden, The Netherlands, used the string galvanometer which he invented in 1901, which was much more sensitive than the capillary electrometer that Waller used.[7]
Einthoven assigned the letters P, Q, R, S and T to the various deflections, and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.[8]
Though the basic principles of that era are still in use today, there have been many advances in electrocardiography over the years. The instrumentation, for example, has evolved from a cumbersome laboratory apparatus to compact electronic systems that often include computerized interpretation of the electrocardiogram.[9]

[edit] ECG graph paper

One second of ECG graph paper
Timed interpretation of an EKG was once incumbent to a stylus and paper speed. Computational analysis now allows considerable study of heart rate variability. A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.

[edit] Filter selection
Modern ECG monitors offer multiple filters for signal processing. The most common settings are monitor mode and diagnostic mode. In monitor mode, the low frequency filter (also called the high-pass filter because signals above the threshold are allowed to pass) is set at either 0.5 Hz or 1 Hz and the high frequency filter (also called the low-pass filter because signals below the threshold are allowed to pass) is set at 40 Hz. This limits artifact for routine cardiac rhythm monitoring. The high-pass filter helps reduce wandering baseline and the low pass filter helps reduce 50 or 60 Hz power line noise (the power line network frequency differs between 50 and 60 Hz in different countries). In diagnostic mode, the high pass filter is set at 0.05 Hz, which allows accurate ST segments to be recorded. The low pass filter is set to 40, 100, or 150 Hz. Consequently, the monitor mode ECG display is more filtered than diagnostic mode, because its bandpass is narrower.[10]

[edit] Leads

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or mean electrical vectors), and complexes displayed on the ECG.
The word lead has two meanings in electrocardiography: it refers to either the wire that connects an electrode to the electrocardiograph, or (more commonly) to a combination of electrodes that form an imaginary line in the body along which the electrical signals are measured. Thus, the term loose lead artifact uses the former meaning, while the term 12 lead ECG uses the latter. In fact, a 12 lead electrocardiograph usually only uses 10 wires/electrodes. The latter definition of lead is the one used here.
An electrocardiogram is obtained by measuring electrical potential between various points of the body using a biomedical instrumentation amplifier. A lead records the electrical signals of the heart from a particular combination of recording electrodes which are placed at specific points on the patient's body.
When a depolarization wavefront (or mean electrical vector) moves toward a positive electrode, it creates a positive deflection on the ECG in the corresponding lead.
When a depolarization wavefront (or mean electrical vector) moves away from a positive electrode, it creates a negative deflection on the ECG in the corresponding lead.
When a depolarization wavefront (or mean electrical vector) moves perpendicular to a positive electrode, it creates an equiphasic (or isoelectric) complex on the ECG. It will be positive as the depolarization wavefront (or mean electrical vector) approaches (A), and then become negative as it passes by (B).
There are two types of leads—unipolar and bipolar. The former have an indifferent electrode at the center of the Einthoven’s triangle (which can be likened to the ‘neutral’ of a wall socket) at zero potential. The direction of these leads is from the “center” of the heart radially outward. These include the precordial (chest) leads and augmented limb leads—VR, VL, & VF. The bipolar type, in contrast, has both electrodes at some potential, with the direction of the corresponding lead being from the electrode at lower potential to the one at higher potential, e.g., in limb lead I, the direction is from left to right. These include the limb leads—I, II, and III.
Note that the colouring scheme for leads varies by country.

[edit] Limb

Lead I

Lead II
Leads I, II and III are the so-called limb leads because at one time, the subjects of electrocardiography had to literally place their arms and legs in buckets of salt water in order to obtain signals for Einthoven's string galvanometer. They form the basis of what is known as Einthoven's triangle.[3] Eventually, electrodes were invented that could be placed directly on the patient's skin. Even though the buckets of salt water are no longer necessary, the electrodes are still placed on the patient's arms and legs to approximate the signals obtained with the buckets of salt water. They remain the first three leads of the modern 12 lead ECG.
Lead I is a dipole with the negative (white) electrode on the right arm and the positive (black) electrode on the left arm.
Lead II is a dipole with the negative (white) electrode on the right arm and the positive (red) electrode on the left leg.
Lead III is a dipole with the negative (black) electrode on the left arm and the positive (red) electrode on the left leg.

[edit] Augmented limb

Proper placement of the limb leads, color coded as recommended by the American Health Association [2]
Leads aVR, aVL, and aVF are augmented limb leads. They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal, which is derived by adding leads I, II, and III together and plugging them into the negative terminal of the EKG machine. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode" or a unipolar lead. This is possible because Einthoven's Law states that I + (-II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I - II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5, and V6.
Lead aVR or "augmented vector right" has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm.
Lead aVL or "augmented vector left" has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm.
Lead aVF or "augmented vector foot" has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.
The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane.

[edit] Precordial
The precordial leads V1, V2, V3, V4, V5, and V6 are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's central terminal is used for the negative electrode, and these leads are considered to be unipolar. The precordial leads view the heart's electrical activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is referred to as the Z axis.
Leads V1, V2, and V3 are referred to as the right precordial leads and V4, V5, and V6 are referred to as the left precordial leads.
The QRS complex should be negative in lead V1 and positive in lead V6. The QRS complex should show a gradual transition from negative to positive between leads V2 and V4. The equiphasic lead is referred to as the transition lead. When the transition occurs earlier than lead V3, it is referred to as an early transition. When it occurs later than lead V3, it is referred to as a late transition. There should also be a gradual increase in the amplitude of the R wave between leads V1 and V4. This is known as R wave progression. Poor R wave progression is a nonspecific finding. It can be caused by conduction abnormalities, myocardial infarction, cardiomyopathy, and other pathological conditions.
Lead V1 is placed in the fourth intercostal space to the right of the sternum.
Lead V2 is placed in the fourth intercostal space to the left of the sternum.
Lead V3 is placed directly between leads V2 and V4.
Lead V4 is placed in the fifth intercostal space in the midclavicular line (even if the apex beat is displaced).
Lead V5 is placed horizontally with V4 in the anterior axillary line
Lead V6 is placed horizontally with V4 and V5 in the midaxillary line.

[edit] Ground
An additional electrode (usually green) is present in modern four-lead and twelve-lead ECGs. This is the ground lead and is placed on the right leg by convention, although in theory it can be placed anywhere on the body. With a three-lead ECG, when one dipole is viewed, the remaining lead becomes the ground lead by default.

[edit] Waves and intervals

Schematic representation of normal ECG
A typical ECG tracing of a normal heartbeat (or cardiac cycle) consists of a P wave, a QRS complex and a T wave. A small U wave is normally visible in 50 to 75% of ECGs. The baseline voltage of the electrocardiogram is known as the isoelectric line. Typically the isoelectric line is measured as the portion of the tracing following the T wave and preceding the next P wave.

[edit] P wave
During normal atrial depolarization, the main electrical vector is directed from the SA node towards the AV node, and spreads from the right atrium to the left atrium. This turns into the P wave on the ECG, which is upright in II, III, and aVF (since the general electrical activity is going toward the positive electrode in those leads), and inverted in aVR (since it is going away from the positive electrode for that lead). A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm.
The relationship between P waves and QRS complexes helps distinguish various cardiac arrhythmias.
The shape and duration of the P waves may indicate atrial enlargement.

[edit] QRS complex

Various QRS complexes with nomenclature.
See also: Electrical conduction system of the heart
The QRS complex is a structure on the ECG that corresponds to the depolarization of the ventricles. Because the ventricles contain more muscle mass than the atria, the QRS complex is larger than the P wave. In addition, because the His/Purkinje system coordinates the depolarization of the ventricles, the QRS complex tends to look "spiked" rather than rounded due to the increase in conduction velocity. A normal QRS complex is 0.06 to 0.10 sec (60 to 100 ms) in duration represented by three small squares or less, but any abnormality of conduction takes longer, and causes widened QRS complexes.
Not every QRS complex contains a Q wave, an R wave, and an S wave. By convention, any combination of these waves can be referred to as a QRS complex. However, correct interpretation of difficult ECGs requires exact labeling of the various waves. Some authors use lowercase and capital letters, depending on the relative size of each wave. For example, an Rs complex would be positively deflected, while a rS complex would be negatively deflected. If both complexes were labeled RS, it would be impossible to appreciate this distinction without viewing the actual ECG.
The duration, amplitude, and morphology of the QRS complex is useful in diagnosing cardiac arrhythmias, conduction abnormalities, ventricular hypertrophy, myocardial infarction, electrolyte derangements, and other disease states.
Q waves can be normal (physiological) or pathological. Normal Q waves, when present, represent depolarization of the interventricular septum. For this reason, they are referred to as septal Q waves, and can be appreciated in the lateral leads I, aVL, V5 and V6.
Q waves greater than 1/3 the height of the R wave, greater than 0.04 sec (40 ms) in duration, or in the right precordial leads are considered to be abnormal, and may represent myocardial infarction.
"Buried" inside the QRS wave is the atrial repolarization wave, which resembles an inverse P wave. It is far smaller in magnitude than the QRS and is therefore obscured by it.

Animation of a normal ECG wave.

[edit] PR/PQ interval
The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It is usually 120 to 200 ms long. On an ECG tracing, this corresponds to 3 to 5 small boxes. In case a Q wave was measured with a ECG the PR interval is also commonly named PQ interval instead.
A PR interval of over 200 ms may indicate a first degree heart block.
A short PR interval may indicate a pre-excitation syndrome via an accessory pathway that leads to early activation of the ventricles, such as seen in Wolff-Parkinson-White syndrome.
A variable PR interval may indicate other types of heart block.
PR segment depression may indicate atrial injury or pericarditis.
Variable morphologies of P waves in a single ECG lead is suggestive of an ectopic pacemaker rhythm such as wandering pacemaker or multifocal atrial tachycardia

[edit] ST segment
Main article: Myocardial infarction
The ST segment connects the QRS complex and the T wave and has a duration of 0.08 to 0.12 sec (80 to 120 ms). It starts at the J point (junction between the QRS complex and ST segment) and ends at the beginning of the T wave. However, since it is usually difficult to determine exactly where the ST segment ends and the T wave begins, the relationship between the RT segment and T wave should be examined together. The typical ST segment duration is usually around 0.08 sec (80 ms). It should be essentially level with the PR and TP segment.
The normal ST segment has a slight upward concavity.
Flat, downsloping, or depressed ST segments may indicate coronary ischemia.
ST segment elevation may indicate myocardial infarction. An elevation of >1mm and longer than 80 milliseconds following the J-point. This measure has a false positive rate of 15-20% (which is slightly higher in women than men) and a false negative rate of 20-30%.[11]

[edit] T wave
The T wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period (or vulnerable period).
In most leads, the T wave is positive. However, a negative T wave is normal in lead aVR. Lead V1 may have a positive, negative, or biphasic T wave. In addition, it is not uncommon to have an isolated negative T wave in lead III, aVL, or aVF.
Inverted (or negative) T waves can be a sign of coronary ischemia, Wellens' syndrome, left ventricular hypertrophy, or CNS disorder.
Tall or "tented" symmetrical T waves may indicate hyperkalemia. Flat T waves may indicate coronary ischemia or hypokalemia.
The earliest electrocardiographic finding of acute myocardial infarction is sometimes the hyperacute T wave, which can be distinguished from hyperkalemia by the broad base and slight asymmetry.
When a conduction abnormality (e.g., bundle branch block, paced rhythm) is present, the T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance.

[edit] QT interval
Main article: QT interval
The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Normal values for the QT interval are between 0.30 and 0.44 (0.45 for women) seconds.[citation needed] The QT interval as well as the corrected QT interval are important in the diagnosis of long QT syndrome and short QT syndrome. The QT interval varies based on the heart rate, and various correction factors have been developed to correct the QT interval for the heart rate. The QT interval represents on an ECG the total time needed for the ventricles to depolarize and repolarize.
The most commonly used method for correcting the QT interval for rate is the one formulated by Bazett and published in 1920.[12] Bazett's formula is , where QTc is the QT interval corrected for rate, and RR is the interval from the onset of one QRS complex to the onset of the next QRS complex, measured in seconds. However, this formula tends to be inaccurate, and over-corrects at high heart rates and under-corrects at low heart rates.
QTc may also be found via the following formula: QTc = QT + 1.75(Ventricular Rate - 60).

[edit] U wave
The U wave is not always seen. It is typically small, and, by definition, follows the T wave. U waves are thought to represent repolarization of the papillary muscles or Purkinje fibers. Prominent U waves are most often seen in hypokalemia, but may be present in hypercalcemia, thyrotoxicosis, or exposure to digitalis, epinephrine, and Class 1A and 3 antiarrhythmics, as well as in congenital long QT syndrome and in the setting of intracranial hemorrhage. An inverted U wave may represent myocardial ischemia or left ventricular volume overload.[13]

[edit] Clinical lead groups

Diagram showing the contiguous leads in the same color
Main article: Myocardial infarction
There are twelve leads in total, each recording the electrical activity of the heart from a different perspective, which also correlate to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at the same anatomical area of the heart are said to be contiguous (see color coded chart).
The inferior leads (leads II, III and aVF) look at electrical activity from the vantage point of the inferior (or diaphragmatic) surface.
The lateral leads (I, aVL, V5 and V6) look at the electrical activity from the vantage point of the lateral wall of left ventricle. The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads. Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads.
The septal leads, V1 and V2 look at electrical activity from the vantage point of the septal wall of the ventricles.
The anterior leads, V3 and V4 look at electrical activity from the vantage point of the anterior surface of the heart.
In addition, any two precordial leads that are next to one another are considered to be contiguous. For example, even though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.
Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

[edit] Axis

Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to estimate the heart's electrical axis in the frontal plane.
The heart's electrical axis refers to the general direction of the heart's depolarization wavefront (or mean electrical vector) in the frontal plane. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although -30o to +90o is considered to be normal.
Left axis deviation (-30o to -90o) may indicate left anterior fascicular block or Q waves from inferior MI.
Right axis deviation (+90o to +180o) may indicate left posterior fascicular block, Q waves from high lateral MI, or a right ventricular strain pattern.
In the setting of right bundle branch block, right or left axis deviation may indicate bifascicular block.

[edit] Electrocardiogram Heterogeneity
Electrocardiogram (ECG) heterogeneity is a measurement of the amount of variance between one ECG waveform and the next. This heterogeneity can be measured by placing multiple ECG electrodes on the chest and by then computing the variance in waveform morphology across the signals obtained from these electrodes. Recent research suggests that ECG heterogeneity often precedes dangerous cardiac arrhythmias

[edit] Background
There are over 350,000 cases of sudden cardiac death (SCD) in the United States each year, and over twenty percent of these cases involve people with no outward signs of serious heart disease. For decades, researchers have been attempting to come up with methods of identifying electrocardiogram (ECG) patterns that reliably precede dangerous arrhythmias. As these methods are found, devices are being created that monitor the heart in order to detect the onset of dangerous rhythms and to correct them before they cause death.

[edit] Research
Research being conducted[14] suggests that a crescendo in ECG heterogeneity, both in the R-wave and the T-wave, often signals the start of ventricular fibrillation. In patients with coronary artery disease, exercise increases T-wave heterogeneity, but this effect is not seen in normal patients. These results, when combined with other pieces of emerging evidence, suggest that R-wave and T-wave heterogeneity both have predictive value.

[edit] Future Applications
In the future, researchers hope to automate the process of heterogeneity detection and to augment the clinical evidence supporting the validity of ECG heterogeneity as a predictor of arrhythmia. Someday soon, implantable devices may be programmed to measure and track heterogeneity. These devices could potentially help ward off arrhythmias by stimulating nerves such as the vagus nerve, by delivering drugs such as beta-blockers, and if necessary, by defibrillating the heart.[15]

[edit] See also
Advanced cardiac life support (ACLS)
Ballistocardiograph
Bundle branch block
Cardiac cycle
Electrical conduction system of the heart
Electrocardiogram technician
Electroencephalography
Electrogastrogram
Electropalatograph
Electroretinography
Heart rate monitor
Holter monitor
Intrinsicoid deflection
Myocardial infarction
Treacherous technician syndrome

[edit] References
^ Braunwald E. (Editor), Heart Disease: A Textbook of Cardiovascular Medicine, Fifth Edition, p. 108, Philadelphia, W.B. Saunders Co., 1997. ISBN 0-7216-5666-8.
^ "The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775
^ "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." Circulation 2005; 112: IV-89 - IV-110.
^ Ronald M. Birse, rev. Patricia E. Knowlden [1] Oxford Dictionary of National Biography 2004 (Subscription required)
^ Burdon Sanderson J (1878). "Experimental results relating to the rhythmical and excitatory motions of the ventricle of the frog heart". Proc Roy Soc Lond 27: 410–14. doi:10.1098/rspl.1878.0068.
^ Waller AD (1887). "A demonstration on man of electromotive changes accompanying the heart's beat". J Physiol (Lond) 8: 229–34.
^ Einthoven W. Un nouveau galvanometre. Arch Neerl Sc Ex Nat 1901; 6:625
^ Cooper J (1986). "Electrocardiography 100 years ago. Origins, pioneers, and contributors". N Engl J Med 315 (7): 461–4. PMID 3526152.
^ Mark, Jonathan B. (1998). Atlas of cardiovascular monitoring. New York: Churchill Livingstone. ISBN 0443088918. .
^ Mark JB "Atlas of Cardiovascular Monitoring." p. 130. New York: Churchill Livingstone, 1998. ISBN 0-443-08891-8.
^ Sabatine MS (2000). Pocket Medicine (Pocket Notebook). Lippincott Williams & Wilkins. ISBN 0-7817-1649-7.
^ Bazett HC (1920). "An analysis of the time-relations of electrocardiograms". Heart 7: 353–70.
^ Conrath C, Opthof T (2005). "The patient U wave". Cardiovasc Res 67 (2): 184–6. doi:10.1016/j.cardiores.2005.05.027. PMID 15979057.
^ In the lab of Richard L. Verrier of Harvard Medical School
^ Verrier, Richard L. “Dynamic Tracking of ECG Heterogeneity to Estimate Risk of Life-threatening Arrhythmias.” CIMIT Forum. September 25, 2007.

[edit] Conference References
Verrier, Richard L. “Dynamic Tracking of ECG Heterogeneity to Estimate Risk of Life-threatening Arrhythmias.” CIMIT Forum. September 25, 2007.

[edit] External links
electrocardiogram ECG
Learn the ECG online 24/7 with educational video, quizzes and crosswords
CIMIT Center for Integration of Medicine and Innovative Technology
ECG Interpretation Video
ECGpedia: Course for interpretation of ECG
The whole ECG - A basic ECG primer
12-lead ECG library
Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
ECG information from Children's Hospital Heart Center, Seattle.
ECG Challenge from the ACC D2B Initiative
National Heart, Lung, and Blood Institute, Diseases and Conditions Index
A history of electrocardiography
Interpretation of electrocardiograms in infants and children.
Information about home made ECGs, including open source ECG software