Ventricular hypertrophy

Although ventricular hypertrophy may occur in either the left or right or both ventricles of the heart, left ventricular hypertrophy (LVH) is more commonly encountered.
Contents

1 Physiology
2 LVH
3 RVH
4 See also

Physiology
The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or the rest of the body (left ventricle). Increased ventricular mass is an adaptation by the ventricle(s) of the heart to increased stress, such as chronically increased volume load (preload) or increased pressure load (afterload).
It is a physiological response that enables the heart to adapt to increased stress; however, the response can become pathological and ultimately lead to a deterioration in function. For example, hypertrophy is a normal physiological adaptation to exercise that enables the ventricle to enhance its pumping capacity. Aerobic training results in the heart being able to pump a larger volume of blood through an increase in the size of the ventricles. Anaerobic training results in the thickening of the myocardial wall to push blood through arteries compressed by muscular contraction. This type of physiologic hypertrophy is reversible and non-pathological, increasing the heart's ability to circulate blood. Chronic hypertension causes pathological ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
If the precipitating stress is volume overload (as through aerobic exercise, which increases blood return to the heart through the action of the skeletal-muscle pump), the ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e. the sarcomeres lengthen rather than thicken). This results in ventricular dilation while maintaining normal sarcomere lengths - the heart can expand to receive a greater volume of blood. The wall thickness normally increases in proportion to the increase in chamber radius. This type of hypertrophy is termed eccentric hypertrophy.
In the case of chronic pressure overload (as through anaerobic exercise, which increases resistance to blood flow by compressing arteries), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed concentric hypertrophy. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced) which can impair filling and lead to diastolic dysfunction.
LVH
See main article, Left ventricular hypertrophy The most common cause is high blood pressure. Other causes are exercise (athletic hypertrophy) and congenital bases (hypertrophic cardiomyopathy or HCM).
The diagnosis of LVH is usually made by echocardiography. Also, ECG, electrocardiogram is used in the detection of Left ventricular hypertrophy. The walls of the ventricle can be measured and a thickness of greater than 1.5 cm is considered enlarged. Athletic hypertrophy is usually less than this thickness and will return to normal size with cessation of the activity. HOCM may be diagnosed in the absence of other causes of LVH and with the presence of a family history.
RVH
The common causes of right ventricular hypertrophy (RVH) are:
Pulmonary hypertension
Fallot tetralogy
Pulmonary valve stenosis
Ventricular septal defect (VSD)
See also
cardiology
cardiovascular disease
cardiomegaly

Cardiac stress test

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This article or section may be confusing or unclear for some readers.Please improve the article or discuss this issue on the talk page. This article has been tagged since December 2006.

An elderly man takes a spin on a stress test treadmill to check his heart's functioning.
A cardiac stress test is a medical test performed to evaluate the ability for arterial blood flow to the myocardium (heart muscle) to increase during the stress of physical exercise, compared to blood flow while at rest. As an exercise test, results also reflect overall physical fitness. These tests do not assess emotional stress, or other connotations of the term stress.
Stress test abnormalities reflect marked imbalances of relative blood flow to different portions of the left ventricular muscle tissue. This is important, because the left ventricle portion of the heart performs the greatest amount of work involved in pumping blood around the body. Blood flow imbalances within the heart muscle of the other three heart chambers are not detected.
Usually, only high grade stenoses of the larger surface heart arteries can be detected. Severe stenoses, e.g. stenoses greater than 75% lumen narrowing, are one possible result of advanced arterial disease and are the usual basis for both "stable" or reproducible exercise-related angina (chest pain) and for "positive" stress tests. Less severe stenoses are automatically compensated for by dilation of the ventricular arterioles during exercise and do not usually produce enough imbalance of relative blood flow to be detectable by stress test methods.
Severe stenoses, as detected by stress tests, essentially always reflect advanced arterial disease. However, stress tests do not detect atheromata present throughout the heart or other body arteries, nor do they reveal the vulnerable plaques, which are the cause of most heart attacks. Recent (late 1990s) clinical studies have demonstrated that the vulnerable plaques which produce most myocardial infarctions are commonly present within multiple regions of the heart arteries, yet are typically relatively flat, i.e. not protruding into the artery lumen sufficiently to produce enough stenosis (usually less than 50%), to be detected by stress test methods.
Contents
[hide]
1 Test overview
2 Purpose
3 Variations
4 Diagnostic value
5 Risks
6 Further research
7 See also
8 References

//
Test overview
The patient either walks on a treadmill or is given IV medication which simulates exercise while connected to an ECG machine, usually the standard 10 connections used to record a 12-lead ECG. Patient symptoms and blood pressure response are repeatedly checked. Using ECG and blood pressure monitoring alone, the test is variously called a cardiac stress test, exercise stress test, exercise treadmill test, exercise tolerance test, stress test or exercise ECG test.
If radioactive isotopes are also used (commonly, Technetium Tc99m Sestamibi and rarely, Thallium-201), then it is usually called a nuclear stress test. Given the ability to visualize the relative amounts of radioisotope within different regions of the heart muscle, nuclear stress tests are more accurate in detecting regional relatively normal versus decreased blood flow to cardiac cells. However, balanced global reductions may still not be recognized because absolute blood flow is not quantitatively measurable, only regional comparative variations.
Purpose
The American Heart Association recommends EKG treadmill testing as the first choice for patients with medium risks of coronary heart disease based on the risk factors of smoking, family history of coronary stenosis, hypertension, diabetes and high cholesterol.
Perfusion (Cardiolite®) stress testing is appropriate for select patients, especially those with an abnormal resting EKG. More severe stenosis (probably greater than 70% occlusion) can produce abnormalities in both EKG waveforms and cardiac wall motion at rest or under stress echocardiographic testing. Such high grade narrowings are typically the primary culprit responsible for those angina episodes which reproducibly occur at a given level of exercise. However, most heart attacks result from rupture of atheroma lesions associated with only mild narrowing (20% on average by intravascular ultrasound (IVUS) clinical studies), thus stress tests do not work well for detecting the vulnerable plaques which are responsible for most heart attacks. Like all tests, stress testing has problems with both falsely positive and falsely negative results compared with other clinical tests.
Angiogram and/or intracoronary ultrasound (preferably in a hospital capable of Percutaneous Coronary Intervention [PCI] with stenting) can provide even greater information, but at the risk of complications associated with cardiac catheterization.
Variations
Some patients with abnormal resting EKGs, or those who are unable to walk safely, can be "exercised" pharmacologically instead of walking on a treadmill. The patient will typically receive a pharmaceutical such as dypridamole or adenosine (both vasodilators) while a cardiologist or physician's assistant reviews the electrocardiogram (EKG) tracing and checks blood pressure periodically.
A radiotracer (typically Tc99m Sestamibi although Thallium is possible) is injected during the simulated exercise portion. After a suitable waiting period, pictures are taken with a gamma camera. The pictures are then compared with the patient's resting images in order to assess the status of the patient's coronary arteries.
Diagnostic value
The American Heart Association journal, Circulation, describes:Treadmill test: sensitivity of 67%, specificity of 70%Nuclear test: sensitivity of 81%, specificity of 99%
However, these numbers reference detection of advanced artery luminal narrowing as assessed by stress methods compared with angiography as the "gold standard". As a predictor of future heart attack, both methods suffer in that they only detect lumen stenosis, a common symptom of some very advanced atheroma, but not the vulnerable plaques which produce most heart attacks. Because of this, most clinical cardiology experience demonstrates that the actual sensitivity and specificity values for detecting likelihood of future heart attack, as opposed to lumen narrowing, are much lower than stated above.
Whatever the actual numbers, the value of stress tests has increasingly been recognized as limited, especially for people without symptoms. Yet, according to United States data from 2004, for about 65% of men and 47% of women, the first symptom of cardiovascular disease is heart attack or sudden death (death within one hour of symptom onset).
Over the last couple of decades, other methods have been increasingly developed as ways to better detect atherosclerotic disease before it becomes symptomatic. These have included both (a) anatomic detection methods and (b) physiologic measurement methods.
Examples of anatomic methods include: (1) coronary calcium scoring by CT, (2) carotid IMT (intimal medial thickness) measurement by ultrasound, e.g. IntiMaTe, and (3) IVUS.
Examples of physiologic methods include: (1) lipoprotein subclass analysis, (2) HbA1c, (3) hs-CRP, (4) homocysteine, and (5) the metabolic syndrome.
Advantages: The anatomic methods directly measure some aspect of the actual atherosclerotic disease process itself, thus offer potential for earlier detection, including before symptoms start, disease staging and tracking of disease progression. The physiologic methods are often less expensive and safer and changing them for the better may slow disease progression, in some cases with marked improvement.
Disadvantages: The anatomic methods are generally more expensive and several are invasive, such as IVUS. The physiologic methods do not quantify the current state of the disease or directly track progression. For both, clinicians and third party payers have been slow to accept the usefulness of these newer approaches.
Risks
Absolute contraindications to cardiac stress testing include acute myocardial infarction [MI] (heart attack) within 48 hrs, unstable angina not yet stabilized with medical therapy, uncontrolled arrhythmia which may have significant hemodynamic responses (for example ventricular tachycardia), symptomatic severe aortic stenosis, aortic dissection, pulmonary embolism, pericarditis.
Major side effects from cardiac stress testing can include palpitation, chest pain, shortness of breath, headache, nausea, or fatigue. Adenosine and dipyridamole can cause mild drug-induced hypotension. However, hypotension caused by exercise stress testing or dobutamine is almost always abnormal and concerning for severe coronary disease.
Stress tests using radiological agents confer a definite (albeit low) long term risk of cancer, but patients undergoing such examinations often receive little or inaccurate information about these risks. For comparison, the annual background radiation per annum a person receives is approximately 3 mSv. A chest xray is approximately 0.1 mSv. A coronary angiogram (cardiac catheterization) has an effective dose of 3-20 mSv (depending on operator skill, type of intervention, etc). A routine chest helical MDCT is around 5-7 mSv. A cardiac CT (with retrospective EKG gating) is around 8-13 mSv (Morin). A sestamibi scan is approximately 12 mSv. A thallium scan is approximately 25 mSv. A thallium scan corresponds the dose of 250 chest x rays, or an extra cancer risk of about 1 in 16000 exposed patients (A. de González). The lifetime risk of fatal cancer development is 4%/Sv or 0.004%/mSv or about 0.1% for a thallium scan. Therefore, frequent usage of these tests has to balance the benefits against the risks of radiation.
Another major risk of stress testing, whether by exercise or pharmacological agents, is the possibility of inducing an MI, especially in patients with severe multi-vessel coronary artery disease. This risk, however, is substantially lower than the risk (about 1%) of major complications (such as inducing a heart attack, stroke, peripheral artery clot and embolism) from cardiac catheterization.
The choice of pharmacologic stress agent to be used (dobutamine, adenosine, dipyridamole) depends on factors such as concurrent medications and diseases. Dobutamine is usually used when a patient has asthma or severe COPD, takes the medication theophylline or has ingested coffee or chocolate (anything with caffeine), or has 2nd or 3rd degree AV block (a type of heart block). Adenosine or dipyridamole is generally used when a patient has poorly controlled hypertension, glaucoma, or has left bundle branch block (LBBB, another type of heart block). It is well known that patients with LBBB can have false positive septal ischemia if dobutamine is used as a pharmacologic agent in nuclear stress test.
Conclusion Most physicians support the population-wide reduction of risk factors which cause heart attack. These risk factors are contained in the well-known cardiac Framingham Risk Score. Physicians typically take a history; perform a physical and then obtain baseline bloodwork and a resting EKG. Stress testing is the established method of investigating moderate-risk patients for coronary artery disease as well as obtaining prognostic information for the patient.
Further research
Magnetic resonance imaging (MRI) has expanded the choice of modalities available for cardiac stress testing. MRI has superior spatial resolution (on the order of around 1.5 mm for cine imaging and 2.5 mm for perfusion imaging), and temporal resolution (around 40 ms for cine imaging), compared with that of a nuclear or PET stress test (spatial resolution of around 9mm for nuclear and 6mm for PET). The increased spatial resolution allows for more sensitive detection of ischemia, which initially starts at the thin subendocardial layer, due to stenotic epicardial supply vessels. First-pass stress perfusion cardiac MR imaging is performed using a rapid bolus injection of gadolinium based contrast and rapidly obtaining T1 weighted images of the myocardium at every R-R interval after pharmacologic stress induced with adenosine. The stress and resting first-pass perfusion MRI data can then be analyzed using a convolution model (such as the Marquard-Levenberg least-squares algorithm) to determine the quantitative global myocardial perfusion reserve (Michael Jerosch-Herold). Delayed hyper-enhancement imaging can be done after 10-15 minutes of contrast injection to evaluate for regions of infarction or fibrosis which has increased signal due to the slower washout of contrast from these areas (Thomson LE). Stress cardiac MRI perfusion testing thus is sensitive enough to detect subtle ischemia and myocardial infarctions even if they are limited only to the subendocardial level. The major problem again is that they still do not detect the "vulnerable plaques" which is the major cause of most heart attacks.
Stress testing, even if done in time, will detect only some of these people before symptoms, debility or death. Stress testing methods, though more effective than a resting EKG, only detect medium to high grade flow limitations; this assuming the testing is fully and aggressively performed. However, most acute artery flow disrupting events leading to heart attacks are due to rupture of "vulnerable plaques". Most of the "vulnerable plaques" cause less than 40% lumen narrowing, a degree of stenosis too small for most stress testing methods to detect.
Historically, through the mid-1980s, it was believed that detecting these high grade stenoses was the key to recognizing people who would have heart attacks in the future. However, there was also long-standing experience that some people could exercise all the way to maximum predicted heart rate, have no abnormal symptoms and completely normal stress test results, only to die of a massive heart attack within a few days to weeks. From the 1960s to 1990s, despite the success of stress testing identifying many who were at high risk for heart attack, its failure to correctly identify many others was a conundrum, discussed in medical circles but unexplained.
The high grade stenoses which are detected by stress test methods are often, though not always, responsible for recurring symptoms of angina. Cardiac stress tests do detect some individuals who already have with very advanced coronary arterial disease and stenosis, some of whom did not recognize that they had advanced disease. However, stress test results (especially stress perfusion cardiac MRI which can detected subtle diffuse subendocardial decreased perfusion due to microvascular disease) are also sometimes abnormal in some people who do not have high grade narrowings of their coronary arteries as visualized by coronary angiography, which provides more accurate information and partial visualization of the coronary artery lumens. This was long viewed as a false positive result, with some of these individuals diagnosed as having Syndrome X, i.e meaning clear recurring signs of angina, though with smooth open coronary artery lumens on coronary angiography. The actual underlying issues responsible for this apparent conundrum are now better understood, see atheroma and microvascular disease.
In the 1950s, heart attacks were commonly attributed to coronary thrombosis, a clot closure of a coronary artery, based on post mortem examination findings. In the late 1950s to early 1960s, this concept became replaced by the concept of stenosis based on the angiographic view of the lumens of the coronary arteries. In turn the angiographic view led to promotion of cardiac stress testing to detect stenoses, i.e. the severe ones more commonly present in people experiencing recurrent angina with physical exertion.
By the early to mid-1990s, it became more widely recognized that rupture of more rapidly evolving and unstable atheroma, hidden within the walls of the coronary arteries, called "vulnerable plaques", even though they often produce little or no stenosis of the coronary lumen, is the primary event which produces most heart attacks; thus back to the coronary thrombosis view, though with more sophistication of understanding some of the complexities. Two clinical trials published in the late 1990's, focusing on the relation between plaque structure, lumen stenosis and myocardial infarction, in which each individuals coronary anatomy was tracked with both angiography and IVUS found that 75% or greater stenotic areas were responsible for only about 14% of heart attacks. The typical heart attack occurred at an artery location with extensive, eccentric plaque within the wall but a luminal stenosis of only 20%. This finding added further evidence to the importance of the concept of vulnerable plaques. The detection of these vulnerable plaques using high resolution CT, MRI, IVUS, OCT (Optical Coherence Tomography), and molecular imaging is currently hotly researched. For CT, as of 2005, 64-slice multidetector machines are providing the best artery and lumen images, yet still do not clearly reveal which plaques are vulnerable. It is hope that perhaps with better resolution and ability to characterize the content of the plaques that an imaging modality may in the future be able to indicate which plaques is "vulnerable" as it is clear that detecting stenosis itself, however subtle, is not enough.
Unfortunately, cardiac stress tests are only capable of detecting medium to high grade limitations of blood flow to the left ventricular heart muscle which may produce recurring angina, not the atheroma which produce heart attacks. Stress test methods do not evaluate blood flow to non-left-ventricle heart muscle. Thus stress test results are often falsely negative for many people, in terms of predicting who is at high risk for myocardial infarction due to atheroma or ruptured "vulnerable plaques".
It has become clear that stress testing recognizes most people at risk for heart attacks too late, unfortunately only after the disease and symptoms of the disease have developed. By the time, a majority of people would already have at least medium stenosis of coronary vessels with development of atheroma or have already had heart attacks or died. It is hoped that research in higher resolution imaging techniques will allow for earlier detection and characterization of subtle atheroma and to initiate lifestyle changes and optimal medical therapy in "vulnerable patients" before they develop symptoms.
See also
Atherosclerosis
Atheroma
Cardiac arrhythmia
Coronary circulation
Cardiology diagnostic tests and procedures
References
Circulation, Fletcher et al. AHA Exercise Standards for Testing. 201:104:1694.
National Guideline Clearinghouse. Cardiac Stress Test Supplement. ICSI:2003Nov.26p.87.
Michael Jerosch-Herold (2004). "Analysis of myocardial perfusion MRI". Journal of Magnetic Resonance Imaging 19 (6): 758-770..
Thomson LE (2004). "Magnetic resonance imaging for the assessment of myocardial viability". Journal of Magnetic Resonance Imaging 19 (6): 771-788..
A. de González (2004). "Risk of cancer from diagnostic X-rays: estimates for the UK and 14 other countries". The Lancet 363 (9406): 345-351..
Morin (2003). "Radiation Dose in Computed Tomography of the Heart". Circulation 107: 917-922..

Aorta

The aorta (generally pronounced /eɪ.oʊɹ.tə/ or "ay-orta") is the largest artery in the human body, originating from the left ventricle of the heart and bringing oxygenated blood to all parts of the body in the systemic circulation.
Contents

1 The course of the aorta
2 Features
3 Diseases/pathology
4 In popular culture
5 References
6 External links
//
The course of the aorta
The aorta is usually divided into three segments/sections [1] [2] :
Ascending aorta — the section between the heart and the arch of aorta
Arch of aorta — the peak part that looks somewhat like an inverted "U"
Descending aorta — the section from the arch of aorta to the point where it divides into the common iliac arteries
Thoracic aorta — the half of the descending aorta above the diaphragm
Abdominal aorta — the half of the descending aorta below the diaphragm
Features
The aorta is an elastic artery, and as such is quite distensible. When the left ventricle contracts to force blood into the aorta, the aorta expands. This stretching gives the potential energy that will help maintain blood pressure during diastole, as during this time the aorta contracts passively.
Diseases/pathology
Aneurysm of sinus of Valsalva
Aortic aneurysm - myotic, bacterial (e.g. syphilis), senile, genetic, associated with valvular heart disease
Dissecting aortic aneurysm
Aortic coarctation - pre-ductal, post-ductal
Atherosclerosis
Marfan syndrome
Trauma, most often thoracic and distal to the left subclavian artery[3] and frequently quickly fatal[4]
In popular culture
One of the Twin Peaks baddie, Windom Earle's better known lines is "I haven't felt this excited since I punctured Caroline's aorta".
References
^ Tortora, Gerard J: "Principles of Human W. & Karen A. Koos: "Human Anatomy, second edition", page 479. Wm. C. Brown Publishing, 1994 (ISBN 0-697-12252-2)
^ De Graaff, Van: "Human Anatomy, fifth edition", pages 548-549. WCB McGraw-Hill, 1998 (ISBN 0-697-28413-1)
^ Samett EJ. Aorta, Trauma. eMedicine.com. URL: http://www.emedicine.com/radio/topic44.htm. Accessed on: August 9, 2006. ^ "Aortic Trauma in Scotland - A Population Based Study.". Eur J Vasc Endovasc Surg. PMID 16750920

Ventricle (heart)

From Wikipedia, the free encyclopedia
In the heart, a ventricle is a heart chamber which collects blood from an atrium (another heart chamber that is smaller than a ventricle) and pumps it out of the heart.
In a four-chambered heart, such as that in humans, there are two ventricles: the right ventricle pumps blood into the pulmonary circulation for the lungs, and the left ventricle pumps blood into the systemic circulation for the rest of the body. (See Double circulatory system for details.)
Ventricles have thicker walls than the atria, and thus can create the higher blood pressure. Comparing the left and right ventricle, the left ventricle have thicker walls because it needs to pump blood to the whole body.

Pulse

From Wikipedia, the free encyclopedia
For other uses, see Pulse (disambiguation).
In medicine, a person's pulse is the throbbing of their arteries as an effect of the heart beat. It can be felt at the neck, at the wrist and other places.
Pressure waves move through the blood vessels, which are pliable; these waves are not caused by the forward movement of the blood. When the heart contracts, blood is ejected into the aorta and the aorta stretches. At this point the wave of distention (pulse wave) is most pronounced, but relatively slow-moving (3 to 6 m/s). As it travels towards the peripheral blood vessels, it gradually diminishes and becomes faster. In the large arterial branches, its velocity is 7 to 10 m/s; in the small arteries, it is 15 to 35 m/s. The pressure pulse is transmitted 15 or more times more rapidly than the blood flow.
The term pulse is also used, although incorrectly, to denote the frequency of the heart beat, usually measured in beats per minute. In most people, the pulse is an accurate measure of heart rate. Under certain circumstances, including arrhythmias, some of the heart beats are ineffective and the aorta is not stretched enough to create a palpable pressure wave. The pulse is irregular and the heart rate can be (much) higher than the pulse rate. In this case, the heart rate should be determined by auscultation of the heart apex, in which case it is not the pulse. The pulse deficit (difference between heart beats and pulsations at the periphery) should be determined by simultaneous palpation at the radial artery and auscultation at the heart apex.
A normal pulse rate for a healthy adult, while resting, can range from 60 to 100 beats per minute (BPM). During sleep, this can drop to as low as 40 BPM; during strenuous exercise, it can rise as high as 200–220 BPM. Generally, pulse rates are higher in younger persons. A resting heart rate for an infant is as high as or higher than an adult's pulse rate during strenuous exercise.
Besides its rate, the pulse has other qualities which reflect the state of the cardiovascular system, such as its rhythm, fullness and the shape of the pulse wave. Certain diseases cause characteristic changes in these qualities. The absence of a pulse at the temple of the skull can be a sign of giant cell arteritis; absent or decreased pulses in the limbs may indicate peripheral artery occlusive disease.
Pulses are manually palpated with fingers or thumb. When palpating the carotid artery, the femoral artery or the brachial artery, the thumb may be used. However, the thumb has its own pulse which can interfere with detecting the patient's pulse at other points, where two or three fingers should be used. Fingers or thumb must be placed near an artery and pressed gently against a firm structure, usually a bone, in order to feel the pulse.
An alternative way of finding pulse rate is by listening to the heartbeat. This is most commonly done with a stethoscope but can also be done using anything that will transmit sound to the ears, or by pressing the ear directly to the chest.
Attributes of pulse measurement include the rate or frequency of the pulse and its rhythm including its regularity and quality expressed as volume or strength.
Checking the radial pulse.

Common pulse points
radial pulse - located on the thumb side of the wrist (radial artery)
ulnar pulse - located on the little finger side of the wrist (ulnar artery)
carotid pulse - located in the neck (carotid artery). The carotid artery should be palpated gently. Stimulating its baroreceptors with vigorous palpitation can provoke severe bradycardia or even stop the heart in some sensitive persons. Also, a person's two carotid arteries should not be palpated at the same time, to avoid a risk of fainting or brain ischemia.
brachial pulse - located between the biceps and triceps, on the medial side of the elbow cavity; frequently used in place of carotid pulse in infants (brachial artery)
femoral pulse - located in the thigh (femoral artery)
popliteal pulse - located behind the knee in the popliteal fossa, found by holding the bent knee. The patient bends the knee at approximately 120°, and the physician holds it in both hands to find the popliteal artery in the pit behind the knee.
dorsalis pedis pulse - located on top of the foot (dorsalis pedis artery)
tibialis posterior pulse - located in the back of the ankle behind the medial malleolus (posterior tibial artery).
temporal pulse - located on the temple directly in front of the ear (temporal artery)
The ease of palpability of a pulse is dictated by the patient's blood pressure. If his or her systolic blood pressure is below 90 mmHg, the radial pulse will not be palpable. Below 80 mmHg, the brachial pulse will not be palpable. Below 60 mmHg, the carotid pulse will not be palpable. Since systolic blood pressure rarely drops that low, the lack of a carotid pulse usually indicates death. It is not unheard of, however, for patients with certain injuries, illnesses or other medical problems to be conscious and aware with no palpable pulse.

Heart transplantation

Diagram illustrating the placement of a donor heart in an orthotopic procedure. Notice how the back of the patient's left atrium and great vessels are left in place.
Heart transplantation or cardiac transplantation, is a surgical transplant procedure performed on patients with end-stage heart failure or severe coronary artery disease. The most common procedure is to take a working heart from a recently deceased organ donor (allograft) and implant it into the patient. The patient's own heart may either be removed (orthotopic procedure) or, less commonly, left in to support the donor heart (heterotopic procedure). It is also possible to take a heart from another species (xenograft), or implant a man-made artificial one, although the success of these two procedures has been less successful in comparison to the far more commonly performed allografts.
Contents

1 History
2 Indications
3 Contraindications
4 Procedures
4.1 Pre-Operative
4.2 Operative
4.2.1 Orthotopic procedure
4.2.2 Heterotopic procedure
4.3 Post-Operative
5 'Living Organ' transplant
6 Prognosis
7 References
8 External links
//
History
The first heart transplant was performed by Professor Christiaan Barnard at Groote Schuur Hospital in December 1967. The patient was a Louis Washkansky of Cape Town, South Africa, who lived for 18 days after the procedure before dying of pneumonia.The donor was Denise Darvall, who had recently been critically injured in a car accident.
Indications
In order for a patient to be recommended for a heart transplant they will generally have advanced, irreversible heart failure with a severely limited life expectancy. Other possible treatments, including medication, for their condition should have been considered or attempted prior to recommendation. Generally, the following causes of heart failure can be treated with a heart transplant:
Cardiomyopathy
Congenital heart disease
Coronary artery disease
Heart valve disease
Life-threatening arrhythmias.
Contraindications
Some patients are less suitable for a heart transplant, especially if they suffer from other circulatory conditions unrelated to the heart. The following conditions in a patient would increase the chances of complications occurring during the operation:
Kidney, lung, or liver disease
Insulin-dependent diabetes with other organ dysfunction
Life-threatening diseases unrelated to heart failure
Vascular disease of the neck and leg arteries.
Procedures
Pre-Operative
A typical heart transplantation begins with a suitable donor heart being located from a recently deceased or brain dead donor. The transplant patient is contacted by a nurse coordinator, and instructed to attend the hospital in order to be evaluated for the operation and given pre-surgical medication. At the same time, the heart is removed from the donor and inspected by a team of surgeons to see if it is in a suitable condition to be transplanted. Occasionally it will be deemed unsuitable. This can often be a very distressing experience for an already emotionally unstable patient, and they will usually require emotional support before being sent home.
Operative
Once the donor heart has passed its inspection, the patient is taken into the operating theatre and given a general anesthetic. Either an orthotopic or a heterotopic procedure is followed, depending on the condition of the patient and the donor heart.
Orthotopic procedure
The orthotopic procedure begins with the surgeons removing the patient's faulty heart. This involves making a vertical incision through the center of the ribcage in order to expose the chest cavity. The patient is attached to a heart-lung machine, in order for the surgeons to open the pericardium and remove the heart by dissecting the great vessels leading from it. The rear section of the left atrium and the pulmonary vein are the only parts of the patient's original heart left in place. The donor heart is then trimmed, in order for it to fit onto the patients remaining left atrium and vessels. It can then be sutured in place. The newly implanted heart is restarted and the patient's chest cavity is closed.
Heterotopic procedure
In the heterotopic procedure, the patient's own heart is not removed before implanting the donor heart. The new heart is positioned so that the chambers and blood vessels of both hearts can be connected to form what is effectively a 'double heart'. The procedure can give the patients original heart a chance to recover, and if the donor's heart happens to fail (eg. through rejection), it may be removed, allowing the patients original heart to start working again. Heterotropic procedures are only used in cases where the donor heart is not strong enough to function by itself (due to either the patients body being considerably larger than the donor's, the donor having a weak heart, or the patient suffering from pulmonary hypertension).
Post-Operative
The patient is taken into ICU to recover. When they wake up, they will be transferred to a special recovery unit in order to be rehabilitated. How long they remain in hospital post-transplant depends on the patient's general health, how well the new heart is working, and their ability to look after their new heart. Once the patient is released, they will have to return to the hospital for regular check-ups and rehabilitation sessions. They may also require emotional support. The number of visits to the hospital will decrease over time, as the patient adjusts to their transplant. The patient will have to remain on lifetime immunosuppressant medication to avoid the possibility of rejection. Since the vagus nerve is severed during the operation, the new heart will beat at around 100 bpm until nerve regrowth occurs.
'Living Organ' transplant
Doctors made medical history in May 2006, at Papworth Hospital in Cambridgeshire, England, when they successfuly transplanted a 'beating heart' into a patient. Normally a donor's heart is injected with potassium chloride in order to stop it beating, before being removed from the donor's body and packed in ice in order to preserve it. The ice can usually keep the heart fresh for a maximum of four to six hours, depending on its condition to start with. Rather than freezing the heart, this new procedure involves keeping it at body temperature and hooking it up to a special machine called an Organ Care System that allows it to continue beating with warm, oxygenated blood flowing through it. This can maintain the heart in a suitable condition for much longer than the traditional method.
Prognosis
The prognosis for heart transplant patients following the orthotopic procedure has greatly increased over the past 20 years, and as of July 15, 2005, the survival rates were as follows:[citation needed]1 year survival rate: 86.4% (males) and 84.6% (females)3 year survival rate: 78.9% (males) and 76.1% (females)5 year survival rate: 72% (males) and 68.5 (females).
References
http://www.capegateway.gov.za/eng/pubs/public_info/C/99478#
http://news.bbc.co.uk/1/hi/health/5041054.stm
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Congenital heart defect

From Wikipedia, the free encyclopedia
(Redirected from Heart defects)

A congenital heart defect (CHD) is a defect in the structure of the heart
and great vessels of the newborn. Most heart defects either obstruct blood flow in the heart or vessels near it or cause blood to flow through the heart in an abnormal pattern, although other defects affecting heart rhythm (such as long QT syndrome) can also occur. Heart defects are among the most common birth defects, and are the leading cause of birth defect-related deaths.
Contents

1 Overview
2 Epidemiology
3 Aetiology
4 Major categories
4.1 Patent ductus arteriosus
4.2 Hypoplasia
4.3 Obstruction defects
4.4 Septal defects
4.5 Cyanotic defects
4.6 Other defects
5 Signs and Symptoms
6 Treatment
7 Defects
8 References
//

Congenital heart defects can be broadly categorised into two groups, acyanotic heart defects ('pink' babies) and cyanotic heart defects ('blue' babies).
Epidemiology
Slightly less than 1% of all newborn infants have congenital heart disease. Eight defects are more common than all others and make up 80% of all congenital heart diseases, whereas the remaining 20% consist of many independently infrequent conditions or combinations of several defects. Ventricular septal defect (VSD) is generally considered to be the most common type of malformation, accounting for about 1/3 of all congenital heart defects.
The incidence is higher when a parent or a sibling has a heart defect (4-5%), in stillborns (3-4%), abortuses (10-25%), and premature infants (2%).
The number of adults with problems connected to a congenital heart defect is rising and is passing the number of children with congenital heart defects in most western countries. This group is called GUCH patients.
Aetiology
The cause of most congenital heart defects is unknown.
Where a cause is known, it may be of a multifactorial origin and/or a result of genetic predisposition and environmental factors.
Known genetic causes of heart disease includes chromosomal abnormalities such as trisomies 21, 13, and 18, as well as a range of newly recognised genetic point mutations, point deletions and other genetic abnormalities as seen in syndromes such as CATCH 22, familial ASD with heart block, Alagille syndrome, Noonan syndrome, and many more.
Known antenatal environmental factors include maternal infections (Rubella), drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus).
Major categories
Patent ductus arteriosus
Main article: Patent ductus arteriosus
The ductus arteriosus is a temporary pathway in the foetal heart between the pulmonary artery and aorta, which allows blood to bypass the fetus' nonfunctioning lungs until birth. Normally, the ductus closes within a few hours or days of birth; when it does not, the result is patent ductus arteriosus. This defect is common in premature infants but rare in full-term infants.
Hypoplasia
Main article: Hypoplastic left heart syndrome
Hypoplasia can affect the heart, which typically results in the failure of either the right ventricle or the left ventricle to adequately develop, leaving only one side of the heart capable of pumping blood to the body and lungs. Hypoplasia of the heart is rare but is the most serious form of CHD; it is called hypoplastic left heart syndrome when it affects the left side of the heart and hypoplastic right heart syndrome when it affects the right side of the heart. In both conditions, the presence of a patent ductus arteriosus (and, when hypoplasia affects the right side of the heart, a patent foramen ovale) is vital to the infant's ability to survive until emergency heart surgery can be performed, since without these pathways blood cannot circulate to the body (or lungs, depending on which side of the heart is defective). Hypoplasia of the heart is generally a cyanotic heart defectObstruction defects
Obstruction defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common obstruction defects include pulmonary valve stenosis, aortic valve stenosis, and coarctation of the aorta, with other types such as bicuspid aortic valve stenosis and subaortic stenosis being comparatively rare. Any narrowing or blockage can cause heart enlargement or hypertension.
Septal defects
The septum is a wall of tissue which separates the left heart from the right heart. It is comparatively common for defects to exist in the interatrial septum or the interventricular septum, allowing blood to flow from the left side of the heart to the right, reducing the heart's efficiency. Ventricular septal defects are collectively the most common type of CHD, although approximately 30% of adults have a type of atrial septal defect called patent foramen ovale. Septal defects may or may not cause cyanosis depending on the severity of the defect.
Cyanotic defects
Cyanotic heart defects are called such because they result in cyanosis, a bluish-grey discoloration of the skin due to a lack of oxygen in the body. Such defects include persistent truncus arteriosus, total anomalous pulmonary venous connection, tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia.
Other defects
Ebstein's anomaly
Brugada syndrome
Marfan syndrome
DiGeorge Syndrome
Signs and Symptoms
Symptoms and signs are related to the type and severity of the heart defects. Some children have no signs while others may exhibit shortness of breath, cyanosis, chest pain, syncope, sweating, heart murmur, respiratory infections, underdeveloping of limbs and muscles, poor feeding, or poor growth. Most defects cause a whispering sound, or murmur, as blood moves through the heart causing some of these symptoms. All of these symptoms occur at a young age of a child or infant which is typically found during a physical examination.
Treatment
Sometimes CHD improves with no treatment necessary. At other times the defect is so small and does not require any treatment. Most of the time CHD is serious and requires surgery and/or medications. Medications include diuretics which aid the baby in eliminating water, salts, and digoxin, which aids in strengthening the contraction of the heart. This slows the heartbeat and removes some fluid from tissues. Some defects require surgical procedures to repair as much as possible to restore circulation back to normal. In some cases, multiple surgeries are needed to be performed to help balance the circulation. Interventional cardiology now offers patients minimally invasive alternatives to surgery. Device closures can now be treated with a standard transcatheter procedure using a closure device mounted on a balloon catheter. Equally stenosis can be treated using a balloon dilation procedure to dilate the obstruction during cardiac catheterization.[1]
Defects
Aortic stenosis
Atrial septal defect (ASD)
Atrioventricular septal defect (AVSD)
Coarctation of the aorta (CoA)
Dextrocardia
Ebstein's anomaly
Hypoplastic left heart syndrome (HLHS)
levo-Transposition of the great arteries (l-TGA)
Partial anomalous pulmonary venous connection (PAPVC)
Patent ductus arteriosus (PDA)
Pulmonary atresia
Pulmonary stenosis
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection (TAPVC)
dextro-Transposition of the great arteries (d-TGA)
Tricuspid atresia
Truncus arteriosus
Ventricular septal defect (VSD)
This is an incomplete list, which may never be able to satisfy certain standards for completeness. Revisions and sourced additions are welcome.

References
^ W. Hellenbrand (2006). Non-surgical Alternatives in the Treatment of Congenital Heart Defects.