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The Big Heart Disease Lie

Natural Cardiovascular Disease Treatment System

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Color Plates follow p. 270.

Color Plate 1 Fig. 1A,B, Chapter 7: Two-dimensional echocardiography images with Doppler color flow mapping from a normal subject in the apical four-chamber view taken in diastole (A) and systole (B). See complete caption and discussion on p. 212.

Color Plate 2 Fig. 2, Chapter 7: Two-dimensional echocardiographic images and Doppler color flow mapping from a patient with mitral regurgitation taken in the parasternal long axis. See complete caption and discussion on p. 213.

Color Plate 3 Fig. 7B, Chapter 7: Doppler color flow image showing turbulent flow across the left ventricular outflow, in apical four-chamber view. See complete caption on p. 223 and discussion on p. 222.

Color Plate 4 Fig. 12A,D, Chapter 7: Two-dimensional echocardiographic images in the parasternal view from a patient with hypertrophic obstructive cardiomyopathy with severe subaortic obstruction. The diastolic frame (A) shows the open mitral valve allowing the inflow from the left atrium (LA) into the left ventricle (LV). In (D), turbulent outflow as well as some mitral regurgitation. See complete caption and discussion on p. 226.

Color Plate 5 Fig. 3, Chapter 11: Osler-Weber-Rendu syndrome. See complete caption on p. 367 and discussion on p. 365.

Color Plate 6 Fig. 6, Chapter 11: Eruptive xanthoma. Skin lesions over back and chest resemble acne. See complete caption on p. 370 and discussion on p. 369.

Color Plate 7 Fig. 7, Chapter 11: Mitral facies and malar flush in 35-yr-old woman with mitral stenosis and mitral regurgitation. See complete caption and discussion on p. 373.

Color Plate 8 Fig. 12A, Chapter 11: Janeway lesions in infective endocarditis in a 50-yr-old drug addict. See complete caption on p. 378 and discussion on p. 377.

Color Plate 9 Fig. 13A, Chapter 11: Mixed connective tissue diseases: patient with mask facies with puckering of skin around lips and malar depigmentation. See complete caption and discussion on p. 379.

Color Plate 10 Fig. 17, Chapter 11: Amiodarone skin toxicity. See complete caption and discussion on p. 383.

Approach to the Physical Examination of the Cardiac Patient


Reasons for Which Cardiac Assessment Is Sought Cardiac Symptoms and Their Appraisal Generation of Working List of Possible Diagnoses Focused Physical Examination:

Clinical Exercise Focused Cardiac Physical Examination: Practical Points

Performance of a proper cardiac physical examination and the interpretation of the findings require a good understanding of both the physiology of the cardiovascular system and the pathophysiology involved in the abnormal states caused by various cardiac lesions and disorders. The development of good bedside skills requires not only dedication on the part of the student of cardiology, but also that the instruction methods be sound and based on both science and logic. The clinician instructor and the student clinician then come to appreciate that the whole process involves the integration of the science with the art of the physical examination.

While each aspect of the cardiac physical examination is dealt with in a detailed manner in this volume, this chapter is devoted to the general approach to the physical examination of the cardiac patient. In this chapter the following points are discussed:

1. The various reasons for which a cardiac assessment might be sought.

2. The appraisal of the various cardiac symptoms and their proper interpretation in order that an intelligent list of the various possible etiological causes of the problem can be generated.

3. The generation of the possible etiological causes of the symptoms of the patient.

4. The physical examination that is focused to derive pertinent information helpful in the differential diagnosis and thereby enables one to plan the subsequent investigation and management.

5. The material is illustrated by two different patient histories. In the first case the discussion of the physical findings is somewhat general, and in the second case it is more specific. We believe that both clinical cases can be treated as material for self-testing by the interested student or the trainee, both before and after studying the remainder of the book.


The patient for cardiovascular assessment generally presents for one of the following reasons:

1. For confirmation and assessment of a suspected cardiac lesion or disease

2. Because of the presence of abnormal cardiac findings on physical examination (such as a heart murmur) and/or one of the laboratory tests (such as an abnormal electrocardiogram [ECG] chest x-ray or echocardiogram)

3. Because of the presence of cardiac symptoms (such as dyspnea, chest pain, syncope)

In the patient with a suspected cardiac lesion or disease, one needs to have a clear mental picture of associated symptoms and signs and risk factors, if any. The examiner then should analyze the patient's history, symptoms, and signs from this perspective. For instance, if the patient is sent with a diagnosis of atrial septal defect, the mental picture of this lesion should be one of a precordial pulsation dominated by the right ventricle, inconspicuous left ventricle, and fixed splitting of the second heart sound. If that patient were to have a large-area hyperdynamic left ventricular apical impulse, then either the diagnosis is incorrect or the lesion is complicated by an additional condition such as mitral regurgitation, which may be significant.

If the patient was referred because of an abnormal finding on physical examination, such as a heart murmur, the examiner, in addition to confirming the finding, also needs to establish the cause and the severity of the lesion. In patients with abnormal laboratory test results, the abnormality must be identified and confirmed. One needs to have clear knowledge of the associated lesions and causes for proper evaluation of such instances. For instance, patient referred for cardiomegaly on the chest x-ray should have the x-ray reviewed to rule out apparent cardiomegaly from causes such as scoliosis or poor technique. Physical examination and, in some cases, a two-dimensional echocardiogram may be essential to determine the actual chamber dimensions and wall thickness. Sometimes a markedly hypertrophied ventricle with reduced internal dimensions can cause an increased cardiothoracic ratio on the chest radiograph.

In patients with abnormal electrocardiograms, the identification of the abnormality often can give directions to diagnosis. For instance, the presence of left ventricular hypertrophy and strain pattern should indicate the presence of left ventricular outflow obstruction, hypertrophic cardiomyopathy, or hypertensive heart disease. If the ECG were to show an infarct, one needs to consider also conditions other than ischemic heart disease that can cause infarct patterns on the ECG, such as hypertrophic cardiomyopathy or pre-excitation, as seen in Wolff-Parkinson-White syndrome.

Most patients seen for cardiac assessments are referred primarily on account of their predominant cardiac symptoms. A clear evaluation of the symptoms and their severity could lend itself to an analytical approach to diagnosis.


Symptoms can be grouped to identify underlying pathology as follows:

1. Definite orthopnea and/or nocturnal dyspnea should point to the presence of high left atrial pressure and therefore help in generating a list of possible causes to look for in the examination.

2. Triad of dyspnea, chest pain, and exertional presyncope or syncope should indicate fixed cardiac output lesions (where cardiac output fails to increase adequately during exercise) such as due to outflow tract obstruction (e.g., aortic stenosis).

3. Low-output symptoms of fatigue, lassitude, and light-headedness could be caused by severe inflow obstructive lesions, severe cardiomyopathy of ischemic or nonischemic etiology, constrictive pericarditis, cardiac tamponade, or severe pulmonary hypertension.

4. Syncope and presyncope in addition to outflow obstructive lesions may also be caused by significant bradyarrhythmia or tachyarrhythmias, hypotension of sudden onset brought on by postural change, vagal reaction, or be of neurogenic origin.

Symptoms and signs of peripheral edema and ascites may be caused by congestive heart failure, but may also result from other causes such as severe tricuspid regurgitation and constrictive pericarditis. They may also result from other noncardiac causes related to low serum albumin of hepatic, gastrointestinal, or renal causes as well as venous obstruction. Only when the pitting edema is of cardiac origin would significant elevation in the jugular venous pressure be expected.

In the assessment of patients with symptoms described as dizziness, one needs to distinguish as far as possible between presyncopal feeling (weakness or a drained feeling as though one is about to faint) and vertiginous sensation, which often is not cardiac in origin and is related to the peripheral or central vestibular system. Vertiginous feeling should be considered if a sensation of spinning or imbalance is experienced with or without nausea.

Chest pain, which is often a common reason for cardiac referral, needs to be properly assessed with regard to character, location, duration, frequency, provoking and relieving factors, as well as the associated presence or absence of coronary risk factors (history of smoking, gender, age, diabetes, hyperlipidemia, hypertension, obesity, family history). Careful analysis should allow the chest pain to be defined as one of the three following categories:

1. Typical angina: central chest discomfort often described as tightness, heaviness, squeezing or burning sensation, or sensation of oppression or weight on the chest with or without typical radiation to the arms, shoulders, back, neck, and/or jaw with or without accompanying dyspnea related often to activity and relieved usually within a few minutes of rest or after nitroglycerin

2. Atypical angina: the chest discomfort has some features characteristic of angina and yet other features not so typical; e.g., left anterior or central chest tightness related to physical exertion but requiring a long period of rest for relief such as having to lie down for extended period of time

3. Noncardiac chest pain such as that related to musculoskeletal, pleuritic, and esophageal, etc.

Exertional angina, although commonly associated with ischemic (coronary) heart disease, could also be caused by conditions that increase the myocardial oxygen demands such as aortic stenosis, aortic regurgitation, and severe uncontrolled hypertension. Systemic factors, which could aggravate the problem, would also need to be considered, such as anemia and hyperthyroidism. Classical anginal discomfort occurring unprovoked at rest but nevertheless responding to nitroglycerin should elicit consideration of coronary vasospasm (Prinzmetal's or variant angina) as well as possible unstable coronary syndrome. Prolonged (>20 min in duration) and/or severe central chest discomfort or tightness with or without radiation should raise suspicion of acute coronary syndromes and their mimickers. Among the latter conditions, acute pericarditis and dissection ofthe aorta deserve special mention. The discomfort of acute pericarditis is aggravated in the supine position, and relief of the intensity of discomfort is often experienced with the patient sitting upright and leaning forward. The discomfort caused by dissection of the aorta may be described as a sudden tearing sensation or crushing feeling, often with wide radiation, particularly to the back, sometimes to the neck and arms, and occasionally to the abdomen. It may also be intermittent. Sometimes patients with acute myocardial infarction, particularly that of the inferior wall, might have discomfort primarily in the epigastrium accompanied by symptoms of nausea or vomiting. Acute infarct could of course occur without any discomfort and sometimes with minimal symptoms, such as some numbness in the arm or hand. It often requires a high index of suspicion given appropriate clinical markers to identify all of them accurately.

Angina occasionally may present as exertional belching. Occasionally exertional dyspnea and even nocturnal dyspnea, in addition to being symptoms indicative of elevated left atrial pressure, may represent anginal equivalent symptoms with discomfort being totally absent. If the angina is atypical, one should not only consider coronary artery disease, but also other conditions such as mitral valve prolapse syndrome, hypertrophic cardiomyopathy, unrecognized uncontrolled systemic hypertension, pulmonary hypertension, and hyperthyroidism.

Assessment also requires one to define the degree of severity of the cardiac symptomatic disability. This requires one to classify the severity of the cardiac symptoms such as dyspnea or angina using one of the accepted classification systems like that of the New York Heart Association classification of dyspnea or heart failure symptoms into Classes I, II, III, and IV.

Class I is defined as symptoms on severe exertion, while Class IV implies symptoms at rest. Class III implies symptoms on light or less than ordinary exertion, and Class II implies symptoms on a moderate level of exertion or ordinary exertion. The ordinary exertion that the patient could normally do without symptoms would depend on the age of the patient as well as his or her mental attitude or wishes. For instance, in two patients of similar age, one might be satisfied with walking comfortably while the other might insist on playing tennis, considering this to be a normal activity. The Canadian Cardiovascular Society classification has a Class 0, which simply means asymptomatic. It is often used for defining the severity of anginal symptoms.


In the evaluation of the cardiac patient, an analytical approach to a full and complete cardiac history should point to a working list of possible diagnoses. One can enumerate possibilities, which could produce all or most of the predominant symptoms of the patient. The enumeration should draw from broad categories of both congenital and acquired cardiac disorders. The categories can be similar to those shown in Tables 1 and 2.

In addition, one should consider possible precipitating factors, which could be causative in the presence of pre-existing cardiac disorders, which are otherwise asymptomatic. Such precipitating factors may include extracardiac factors such as:

• Infection, such as pneumonia

• Hyperthyroidism

• Pulmonary thromboembolism

• Hypoxemia secondary to pulmonary and ventilatory disorders such as sleep apnea

Table 1

Categories of Congenital Heart Defects

Acyanotic forms without a shunt Outflow obstruction Inflow obstruction Regurgitant lesions

- Pulmonary stenosis, aortic stenosis, coarctation of aorta

- Mitral stenosis

- Mitral - Congenitally corrected transposition, anomalous origin of the left coronary artery from the pulmonary artery

- Tricuspid - Ebstein's anomaly

- Aortic - Bicuspid aortic valve

Acyanotic forms with left-to-right shunts Atrial level Ventricular level Aortic level Other communications

Atrial septal defect primum/secundum Ventricular septal defect

Persistent ductus arteriosus, aorto-pulmonary window Coronary A-V fistulae, ruptured sinus of Valsalva aneurysm

Cyanotic forms Eisenmenger syndrome

Tetralogy/tetralogy-type lesions Common-mixing chamber defects


Conduction system disorders

- Reversed shunt with pulmonary hypertension due to pulmonary vascular disease

- Decreased pulmonary flow

- Common atrium, single ventricle, truncus arteriosus

- Total anomalous pulmonary venous drainage

- Congenital A-V block, accessory pathways

Table 2

Categories of Acquired Cardiac Disorders

1. Valvular disease

• Stenotic lesions

• Regurgitant lesions

2. Infective endocarditis

3. Ischemic heart disease

4. Hypertensive heart disease

5. Myocardial diseases

• Cardiomyopthies

• Hypertrophic, restrictive and dilated

• Myocarditis

6. Pericardial diseases

• Acute pericarditis

• Pericardial effusion with or without cardiac compression (tamponade)

• Chronic constrictive pericarditis

7. Cardiac tumors (atrial myxoma)

8. Conduction system disorders

• Tachyarrhythmia

• Bradyarrhythmia

9. Pulmonary hypertension

• Salt and fluid overload secondary to renal insufficiency

• Iatrogenic causes (e.g., use of nonsteroidal anti-inflammatory drugs or Cox-2 inhibitors).

The next step involves a careful examination and definition of the arterial pulses, the jugular pulsations, the precordial pulsations, as well as the peripheral and systemic signs. All of these need to be evaluated in relation to the possibilities listed from the history. When this is done properly, a clear and definitive diagnosis can often be established or arrived at even before auscultation is performed. Auscultation, which is often the last step in the physical examination of the cardiac patient, may sometimes become the confirmatory step in this process. Only mild lesions are diagnosed on the basis of auscultation alone (e.g., mitral valve prolapse, hypertrophic obstructive cardiomyopathy).


This approach can be illustrated by discussing two different patients, each presenting with specific cardiac symptoms. One could use the following sections as both pre- and posttests, namely before and after studying the remaining chapters in the book.

Patient A: A 70-Year-Old Woman, Previously Healthy, Presenting with Sudden-Onset Dyspnea, Orthopnea With Radiological Signs of Pulmonary Edema.

The symptom complex with radiological evidence of pulmonary congestion obviously indicates a pathological process associated with high left atrial pressure if high altitude and acute pulmonary injury are not involved. The latter two can be easily solved by the relevant history surrounding the onset. One can then develop a list of all possible lesions, both congenital and acquired, that can cause this problem. Then evidence in the history both in favor and against each listed condition should be considered.


The only congenital lesion that could possibly be considered is bicuspid aortic valve with stenosis and/or regurgitation. But the age of the patient is somewhat against this.

Acquired Valvular Lesions

Mitral Stenosis or Obstruction. A patient with mitral stenosis may present with acute pulmonary edema due to the sudden onset of atrial fibrillation. Rapid ventricular rate, such as that accompanying uncontrolled atrial fibrillation, might be the precipitating cause of acute pulmonary edema in a patient with significant mitral stenosis which the patient otherwise is able to tolerate. The rapid heart rate, by shortening the diastolic filling time, impedes emptying ofthe left atrium in mitral stenosis, thereby raising the left atrial pressure acutely. But this type of presentation in rheumatic mitral disease is more likely to be seen in the fourth and the fifth decades. Mitral obstruction due to atrial myxoma, however, could occur in this patient's age group and therefore cannot be excluded. Occasionally a patient with a prosthetic mitral valve with a previous history of mitral valve replacement could present with pulmonary edema because of an acute thrombus on the prosthetic valve obstructing inflow and preventing proper prosthetic valve function.

Chronic Mitral Regurgitation. Chronic mitral regurgitation does not usually present with pulmonary edema unless its severity is suddenly markedly increased. This can happen with rupture of chordae tendineae (spontaneous or due to infective endocarditis) or may be due to other problems, which also affect the mitral valve function (such as ischemic papillary muscle dysfunction with or without avulsion of chordae or severe uncontrolled hypertension).

Acute Severe Mitral Regurgitation. This often is likely to present with acute pulmonary edema and may be caused by spontaneous rupture of chordae tendineae, for instance in a patient with previously unrecognized myxomatous degeneration of the mitral leaflets, sometimes resulting from avulsion of chordae secondary to papillary muscle infarction in a patient with acute coronary syndrome and rarely due to papillary muscle rupture with acute myocardial infarction. None of these could be excluded or considered low on the list based primarily on the history.

Aortic Stenosis. While this lesion on an acquired basis (calcific or degenerative) is more common in men, it can nevertheless present with acute left ventricular failure and usually some preceding history of the presence of a heart murmur and the classical triad of symptoms, namely dyspnea, angina, and exertional presyncope or syncope. Absence of any of these does not, however, exclude this condition from consideration.

Chronic Aortic Regurgitation. This can arise from valvular lesions (bicuspid valve, rheumatic involvement, trauma, endocarditis, etc.) or aortic root dilatation (Marfan's syndrome, syphylitic aortitis, spondylitis, etc.). The compensated state may last for a long time, and when the left ventricular failure sets in, it can be quite dramatic and associated with pulmonary edema. Therefore this needs to be seriously considered.

Acute Severe Aortic Regurgitation. Acute severe aortic regurgitation (often caused by endocarditis on a native valve or a prosthetic aortic valve with virulent pathogens such as staphylococci) obviously can present with acute pulmonary edema. Sometimes the symptom complex and some of the physical signs may be mimicked by ruptured sinus of Valsalva aneurysm, which also needs to be considered.

Ischemic Heart Disease

Acute myocardial infarction is by far the most common cause of sudden de novo acute pulmonary edema and therefore needs to be on the top of the list of all the causes of acute pulmonary edema. While the presence of chest discomfort or pain at onset and/ or the presence of coexisting coronary risk factors raise the suspicion to high levels, neither the absence of chest discomfort nor the absence of significant coronary risk factors excludes it from consideration. The diagnosis would require either electrocar-diographic and/or enzymatic determination of cardiac markers such as an elevated troponin level or creatine kinase MB fraction.

Hypertensive Heart Disease

Acute uncontrolled or poorly controlled hypertension can present with acute pulmonary edema. It can be seen, for instance, in younger females with complicating glomerulonephritis or pregnancy. However, these conditions need not be present. The systolic left ventricular function could be normal and yet, because of significant diastolic dysfunction, the left ventricular diastolic filling pressures could be severely elevated, causing the symptoms. This is not uncommon in the elderly female. Occasionally chronic renal failure might coexist in these patients, aggravating the fluid and volume overload. The renal failure could itself be caused by hypertensive nephrosclerosis and/or diabetic nephropathy. Thus, this is an important entity to consider.


Acute dyspnea and pulmonary edema could occur in patients with hypertrophic obstructive cardiomyopathy with significant resting aortic outflow tract gradient. Similar symptomatology could occasionally occur in patients with dilated cardiomyopathy (of various etiologies including idiopathic, viral, alcoholic, and others). They are therefore not excluded on the basis of the history alone. Restrictive cardiomyopathy with etiologies like those caused by infiltrative processes such as amyloid or myxedema is not likely to present with such dramatic onset.

Conduction System Disorders

These by themselves will not be implicated for this presentation, but conduction system involvement by electrocardiographic findings as part of the underlying cardiac disease may be detected; for instance, the presence of left bundle branch block on the ECG may be noted in a patient with idiopathic dilated or restrictive cardiomyopathy or in calcific aortic stenosis (Lev's disease).

Pericardial Diseases

Pericardial diseases of acute or chronic origin are not expected to cause acute symptoms of high left atrial pressure. While acute dyspnea may be caused by pericardial effusion that is causing significant cardiac compression, it is unlikely to produce radiological signs of pulmonary edema. Unilateral left-sided constriction from chronic con-strictive pericarditis is extremely rare and unlikely to present acutely.

Cardiac Tumors

Primary cardiac tumors such as a myxoma, because of its location and mobility resulting from its attachment by a stalk to the underlying endocardial wall, could cause obstructive symptoms. If the myxoma is left atrial in location, it can cause acute symptoms of high left atrial pressure caused by mitral obstruction.

Pulmonary Hypertension

All lesions listed above that cause significant elevations in the left atrial pressure and symptoms thereof will more than likely raise the pulmonary arterial pressures and cause pulmonary hypertension. However, in this instance the symptoms primarily stem from the high left atrial pressure. In chronic pulmonary hypertension, the right ventricle gets the brunt of the problem and will raise the systemic venous pressures with or without secondary tricuspid regurgitation and will eventually lead to diminished right ventricular output. The former will cause systemic venous congestion and peripheral edema; the latter would only diminish the left ventricular output and cause low cardiac output symptoms but not pulmonary congestion. Therefore, this pathophysiological process is not under consideration here.

In view of the acute onset of symptoms, presumably unprovoked, some of the likely precipitating and/or aggravating factors also need to be considered in the evaluation process because these may be operative when there is pre-existing left ventricular dysfunction, which is otherwise tolerated and asymptomatic.

Precipitating or Aggravating Factors Rapid Ventricular Rate

Rapid heart rate resulting from uncontrolled atrial fibrillation or similar supraventricular tachyarrhythmia, such as uncontrolled atrial flutter, atrial tachycardia, and occasionally even ventricular tachycardia, could precipitate onset of acute pulmonary edema in patients with pre-existing left ventricular dysfunction of varied etiologies (ischemic heart disease with prior myocardial infarction, uncontrolled hypertensive heart disease, hypertrophic or dilated cardiomyopathies), all of which might have been otherwise asymptomatic.

Acute Infection Such as Pneumonia

This needs to be considered in the elderly since both systolic and/or diastolic left ventricular dysfunction of varied and/or multiple etiologies (ischemic, hypertensive, and non-ischemic cardiomyopathies) are common in the elderly, particularly in the very old (in the eighties and above). In these individuals, systemic infection and particularly pulmonary infection might throw them into left ventricular failure because of additional hypoxemia, which can further depress cardiac function unable to meet increased demands in cardiac output.

Acute Pulmonary Embolism

This should not be expected to cause left ventricular dysfunction directly and therefore will not present as acute left ventricular failure when the left ventricular function is normal. However, when the underlying left ventricular function is already previously compromised by other pre-existing cardiac disease, it can aggravate the same leading to pulmonary edema. The mechanisms involve hypoxia, tachycardia, or atrial tachyarrhyth-mia, which it may produce, and increased reflex vasoconstriction (mediated by cat-echolamines, serotonin, etc.), which can raise the afterload.

It is of utmost importance that the patient in acute pulmonary edema be treated for the same with appropriate measures, which should include oxygenation, intravenous diuretics, morphine, as well as ventilatory support when considered essential. It is even appropriate to look at the electrocardiogram quickly for signs of an acute myocardial infarction given the fact that it is often the leading cause of acute pulmonary edema. The discussion here is not meant to be about management of the patient, but rather how one goes about considering the various possible etiologies, because it is important for the complete management of the patient.

We have listed the various possible lesions/disorders that can present with acute pulmonary edema and also indicated the precipitating factors . The physical examination of the cardiovascular system carried out in a systematic manner would bring in either positive or negative findings in relation to each of the diagnosis listed. One makes a mental note of each, as one proceeds with the examination.

First, the arterial pulse is assessed with regard to rate and rhythm. The assessment of heart rate and rhythm would help in identifying the presence of atrial fibrillation. Sometimes the irregularity in the rhythm might be picked up better by auscultation, and one may quickly use this method early on if the rhythm is thought to be irregular but not totally certain by palpation alone. Then the rate of rise of the arterial pulse, particularly the carotid pulse, will help to indicate or rule out significant outflow tract obstruction. Sometimes in the elderly, the rate of rise may be modified by reflected waves secondary to the stiff arterial system. The amplitude of the arterial pulse and its rate of rise together will help distinguish significant mitral regurgitation from aortic regurgitation. The arterial pulse of severe mitral regurgitation will have either normal or fast upstroke with normal or lower than normal amplitude or volume. Severe aortic regurgitation, however, will have a fast rate of rise with increased amplitude. Of course, when the aortic regurgitation, is severe exaggerated peripheral signs will become obvious which can all be looked for including measurement of blood pressure differences between the arms and the leg (Hill's sign). One must remember that severe aortic regurgitation might be simulated by conditions that have exaggerated early run-off as in ruptured sinus of Valsalva aneurysm. This also will give rise to similar peripheral arterial findings. If the arterial pulse is brisk in its upstroke with decreased volume, then hypertrophic cardiomyopathy with obstruction needs to be considered. Sometimes one might feel a bisferiens pulse, which might bring into consideration mixed aortic regurgitation and aortic stenosis as well as hypertrophic cardiomyopathy with obstruction. Besides the character of the arterial pulse, blood pressure measurement would give important information regarding the stroke volume as reflected in the pulse pressure whether increased, decreased, or normal as well as help with regard to the presence or absence of hypertension.

The jugular venous pressure and the venous pulse contour might not directly influence the diagnosis, but it can throw light on the presence or otherwise of secondary pulmonary hypertension and indicate the status of the right ventricular function.

The assessment of precordial pulsations is of crucial importance. When the apical impulse is palpable and considered as left ventricular, as revealed by the presence of medial retraction, then its location, its area, and its character (single, double, or triple, whether it is normal, sustained, or hyperdynamic) will all give important clues to the assessment of the problem and the function of the left ventricle. In addition, assessment for the presence of a right ventricular impulse by subxiphoid palpation, as well as assessment for systolic sternal movement (retraction or outward movement), are also important.

A displaced large-area hyperdynamic left ventricular apical impulse will suggest severe mitral and/or aortic regurgitation. Although severe mitral regurgitation may have a somewhat wider than normal area of medial retraction, the detection of a marked systolic sternal retraction would clearly point to the presence of severe isolated aortic regurgitation. Sustained left ventricular impulse with an atrial kick and a brisk rising arterial pulse would point to hypertrophic obstructive cardiomyopathy, as the presence of a delayed carotid upstroke would indicate significant aortic stenosis, whereas the same in the presence of a normally rising pulse would make one consider moderate left ventricular dysfunction (with possible underlying hypertensive heart disease, ischemic heart disease, or cardiomyopathy of nonischemic etiology). Sustained left ventricular impulse without an atrial kick, on the other hand, would make one strongly suspect the presence of severe left ventricular dysfunction and decreased ejection fraction due to either ischemic or nonischemic cardiomyopthy. If the apical impulse is normal but the first heart sound is loud and palpable, one might consider mitral obstruction (e.g., from mitral stenosis or a left atrial tumor), and this suspicion may be increased if signs of pulmonary hypertension were detected by both jugular venous pressure and jugular pulse contour abnormalities together with a sustained right ventricular impulse detected on subxiphoid palpation. None of these can be ruled out if the apical impulse is not palpable or characterizable.

After this, a careful and complete auscultation is also carried out, first paying attention to the heart sounds (both the normal and the abnormal) and later to the detection and characterization of murmurs if any. By the time one is ready to auscultate, however, if proper thinking were to accompany the physical examination and this type of analytical approach is applied to each of the things being assessed, then the examiner might have actually coned down on the possibilities (for instance, whether one is dealing with acute severe mitral regurgitation, severe aortic regurgitation, or its mimickers, hypertrophic cardiomyopathy, dilated cardiomyopthy, etc.). Then the auscultation may even be tuned and focused to further confirm or rule out suspected lesions.

Patient B: A-35-Year-Old Man, Chronic Smoker, Previously Well, Presents With History of Two Recent Episodes of Lightheadedness (Presyncopal Feeling) While Climbing Two Flights of Stairs


1. Develop a list of possible conditions that might cause these symptoms in this patient.

2. Discuss the physical findings noted on the cardiac examination and synthesize further to narrow down the possibilities to arrive at the proper diagnosis.

Presyncopal symptoms on exertion would point to transient abrupt fall in cardiac output. The first comment that one can make regarding this particular patient is that the exertion that caused the presyncopal symptom in this relatively young man who has been "previously well" appears to be quite minimal. Therefore, the symptoms may or may not be related to the exertion. Therefore, while generating possible conditions that could have caused the symptoms, one cannot totally limit these to lesions associated with exertional syncope (namely, fixed-output lesions such as result from severe outflow obstruction) alone. Abrupt onset of any tachyarrhythmia supraventricular or ventricular if it were rapid (rate >160) and sufficiently long in duration (at least >30 s) could cause a fall in cardiac output and therefore cause symptoms. Similarly, any significant bradycardia (pauses >4.0 s or rates <35) can be associated with a fall in cardiac output, which may be symptomatic.

The ability to generate such a list requires some background knowledge of various disorders and their typical presenting features. But one can certainly think of them in general categories and add individual disorders appropriate to the level ofthe experience and knowledge of the physician. This likely would vary whether the individual is a beginner or student or is a cardiac fellow.

Congenital Etiologies

• Obstructive outflow lesions: significant aortic/pulmonary stenosis

• Inflow obstruction: unlikely

• Severe pulmonary hypertension secondary to Eisenmenger's syndrome: with reversed intracardiac shunt from pulmonary vascular disease

• Disorders associated with significant tendency for tachyarrhythmias: Ebstein's anomaly of the tricuspid valve; arrhythmogenic right ventricle; conduction system disorders with tendency for tachyarrhythmias

• With tendency for bradyarrhythmias: congenital atrioventricular (A-V) block

Acquired Etiologies

• Left ventricular outflow obstruction: valvular aortic stenosis (unlikely at this age unless congenital in origin); hypertrophic obstructive cardiomyopathy

• Inflow obstruction such as due to atrial myxoma (mitral stenosis unlikely)

• Regurgitant valvular lesions: by themselves these are not expected to cause such symptoms. Occasionally, however ventricular tachyarrhythmias may be seen in patients with advanced mitral regurgitation. Rarely severe ventricular tachyarrhthmias might also occur in patients with mitral valve prolapse syndrome with redundant myxomatous degeneration of the valves.

• Ischemic heart disease: ischemia with ventricular arrhythmia (patient relatively young but cannot be excluded); coronary vasospasm with ventricular tachyarrhythmia or bradycardia or A-V block, depending on the coronary artery involved

• Cardiomyopathies: ventricular tchyarrhythmias, in the presence of underlying nonobstructive or obstructive hypertrophic cardiomyopathy, dilated cardiomyopathy, or bradyarrhythmias in the presence of restrictive cardiomyopathy

• Pericardial diseases: unlikely to be associated with the symptoms of presyncope unless there is severe pericardial effusion, then invariably other symptoms such as lassitude, fatigue, and dyspnea would be present.

• Conduction system disorders: with tendency for tachyarrhythmia; pre-excitation syndromes (Wolff-Parkinson-White syndrome, Lown-Ganong-Levine syndrome); long QT syndrome; re-entrant tachycardia in the absence of pre-excitation; paroxysmal atrial tachycardia

• Severe pulmonary hypertension: secondary to severe pulmonary disease, ventilatory disorders such as sleep apnea and others

• Primary pulmonary hypertension: more common in females

• Acute pulmonary embolism: can cause drop in cardiac output suddenly and may also induce arrhythmias; not very typical but cannot be excluded


• Vasovagal reaction: usually occurs secondary to anxiety, acute pain somatic or visceral, and distension of viscus organ and rarely secondary to ischemia.

• Usually associated with sweating, nausea, and/or vomiting.

Cardiac Examination Findings in Patient b

• Patient slightly tachypneic, 5' 7", weighing 185 lb; BP 125/80, heart rate 95/min, respirations 25/min

• Arterial pulse: normal volume or amplitude pulse with normal upstroke in the carotids. All pulses palpable and symmetrical

• Jugular venous pulse:jugular venous pressure 8 cm above the sternal angle at 458. The contour showed X = y; the venous pressure tended to rise on inspiration.

• Precordial pulsations: apical impulse normal with medial retraction; right ventricular impulse palpable on deep inspiration by subxiphoid palpation.

• Auscultation: S2 palpable at the II LICS. S2 splitting appeared to be somewhat wide but appeared to vary normally on inspiration. S3 and S4 were both heard at the lower left sternal area and over the xiphoid area and appeared to increase slightly on inspiration. No significant murmurs. Chest was clear.

Interpretations of the Physical Findings of Patient b

1. Mild dyspnea and increased respiratory rate should raise suspicion about possible hypoxemia.

2. The arterial pulse upstroke being normal rules out significant left-sided obstruction. It also is not suggestive of hypertrophic cardiomyopathy, where the arterial pulse upstroke is often brisk. The normal pulse volume or amplitude and the normal pressure indicate adequate stroke volume and tend to rule out any significant cardiac compression.

3. The elevated jugular venous pressure indicates rise in the diastolic pressures in the right ventricle. The abnormal contour of X descent = y descent can occur both with and without significant pulmonary hypertension. The preservation of X indicates preserved right ventricular systolic function. The prominent y descent would indicate increased v wave pressure head in the right atrium, which is usually caused by raised right ventricular diastolic pressures (the pre-a wave pressure). This contour in the absence of pulmonary hypertension can occur in pericardial effusion with some cardiac compression. The preserved y descent, however, excludes cardiac tamponade because early diastolic emptying of the right atrium must be free and unrestricted. The same X = y contour in the presence of pulmonary hypertension, however, would indicate significant pulmonary hypertension severe enough to alter the diastolic function of the right ventricle.

4. The palpable S2 in the second left interspace and right ventricular impulse subxiphoid together would indicate the presence of pulmonary hypertension. This will be the evidence to conclude that the jugular venous pulse contour abnormalities arise from significant degree of pulmonary hypertension.

5. The apical impulse with medial retraction suggests a left ventricular impulse. It has been described as normal, indicating presumably normal and perhaps no more than mild left ventricular dysfunction. Therefore, the left ventricular dysfunction is not the cause of the pulmonary hypertension.

6. The widely split S2 moving physiologically may indicate some right ventricular dysfunction resulting from pulmonary hypertension because pulmonary hypertension per se, by increasing the pulmonary impedance, would cause P2 to occur earlier and a narrower split S2. Another possibility is an electrical delay, such as a co-existing right bundle branch block.

7. The presence of S3 and S4 heard over the lower left sternal border and xiphoid area, both of which are described as slightly increasing on inspiration, suggest right-sided events compatible with right ventricular diastolic dysfunction and acute decompensation of the right ventricle.


1. So far the predominant right-sided signs all point to the presence of significant pulmonary hypertension with right ventricular diastolic dysfunction. Because the patient is described as previously well and the history is rather of sudden and recent onset, acute cause of pulmonary hypertension, such as acute pulmonary embolism, must be considered to be present unless proven otherwise.

2. Such a conclusion is also suggested by the presence of mild tachycardia and mild tac-hypnea.

3. Such an analysis should lead to immediate application of appropriate measures of management, including treatment and diagnostic investigations.


1. Proper evaluation of the cardiac symptoms and their severity would ultimately require defining the appropriate causal cardiac disorder. Therefore, it helps to group symptoms to identify underlying pathology.

2. Definite orthopnea and/or nocturnal dyspnea should point to the presence of high left atrial pressure. Triad of dyspnea, chest pain, and exertional presyncope or syncope should indicate fixed cardiac output lesions. Fatigue, lassitude, and light-headedness may be due to low output. Significant brady or tachyarrhythmias or hypotension of sudden onset may also cause syncope and presyncope in addition to outflow obstructive lesions. Peripheral edema and ascites represent congestive symptoms resulting from high right atrial pressure.

3. Proper evaluation of cardiac symptoms includes generation of a working list of possible etiologies drawn from a broad range of cardiac disorders and lesions.

4. While a complete and thorough cardiac examination is performed, each finding, both normal and abnormal, should be analyzed with regard to its significance in relation to the etiological causes under consideration for the particular patient problem. This automatically becomes a sound tool or method for arriving at proper conclusions with regard to both diagnosis and management.

Arterial Pulse


Physiology of the Arterial Pulse ASSESSMENT OF THE ARTERIAL PULSE Practical Points in the Clinical Assessment of the Arterial Pulse References


Although the arterial pulse, which is considered a fundamental clinical sign of life, has been the subject of study by many physiologists as well as clinicians in the past (1-28), it received less attention by clinicians for many years after the discovery of the sphygmomanometer (29). There has been a renewed interest in this field in recent years since new techniques such as applanation tonometry are now being applied for its study (3033). The physiology of the arterial pulse is, however, quite complicated, and the subject is often given only cursory description even in the most popular textbooks in cardiology. Also, the retained terminology and nomenclature do not help to clarify the issues (21,34). The most detailed review of the complicated physiology of both the normal and the abnormal arterial pulse can be found in some of the excellent papers of O'Rourke and his co-workers (21,35-38). The subject has, however, remained somewhat elusive even to the most interested clinicians. Therefore, in this chapter an attempt will be made to simplify some of the concepts for the sake of better understanding.

The purpose of the arterial system is to deliver oxygenated blood to the tissues but, more importantly, to convert intermittent cardiac output into a continuous capillary flow. This is primarily achieved by its structural organization (6). The central vessels, namely the aorta up to the iliac bifurcation and its main branches—the carotid and the innominate arteries—are very elastic and act in part as a reservoir in addition to being conduits. The vessels at the level ofthe radial and femoral arteries are more muscular, whereas the iliac, subclavian, and axillary vessels are intermediate or transitional in structure. When an artery is put into stretch, the readily extensible fibers of the vessel wall govern its behavior. The more elastic the vessel, the greater is the volume accommodated for a small rise in pressure.

It is well known that the recording obtained with a pulse transducer placed externally over the carotid artery has a contour and shape very similar to a pressure curve obtained through a catheter placed internally in the carotid artery and recorded with a strain gauge manometer system (Fig. 1). While the former records displacement of the vessel transmitted to the skin through overlying soft tissues, the latter is a true recording of the internal pressure changes. The displacement in the externally recorded tracing is due to

Carotid Tracing
Fig. 1. (A) Simultaneous recordings of electrocardiogram (ECG), phonocardiogram, and the carotid pulse. (B) Intra-aortic pressure recording in the same patient. Note the similarity of the carotid pulse tracing and the aortic pressure recording.

changes in the wall tension of the vessel similar to the recording of an apical impulse reflecting the change in left ventricular wall tension. The wall tension is governed by the principles of Laplace relationship. The tension is directly proportional to the pressure and the radius and inversely related to the thickness of the vessel wall. Since ejection of the major portion ofthe stroke volume takes place in the early and mid-systole, the cause of major change in tension in early and mid-systole is a result of changes in both volume and pressure. During the later part of systole and during diastole, however, the predominant effect must be primarily due to changes in pressure, although volume may also play a part. The dominance of the pressure pulse effect on the tension of the vessel wall for the greater part of the cardiac cycle is the main reason for the similarity of the externally recorded carotid pulse tracing and the internally recorded pressure curve.

The contraction of the left ventricle imparts its contractile energy on the blood mass it contains, developing and raising the pressure to overcome the diastolic pressure in the aorta in order to open the aortic valve and eject the blood into the aorta. As the ventricle ejects the blood mass into the aorta with each systole, it creates a pulsatile pressure as well as a pulsatile flow. By appropriate recording techniques applied in and/or over an artery, one can show the pulsatile nature of the pressure wave, the pulsatile nature of the flow wave, as well as the dimensional changes in the artery as the pressure wave travels (36).

What is actually felt when an artery is palpated by the finger is not only the force exerted by the amplitude of the pressure wave, but also the change in the diameter. For instance, the pressure pulse of both arteriosclerosis and hypertension in the elderly and that caused by significant aortic regurgitation will look similar when recorded. It will show a rapid rise in systole and a steep fall in diastole with an increased pulse pressure (the difference between the systolic and the diastolic pressure). However, the arterial pulse in these two different situations will feel different to the palpating fingers. The difference is essentially in the diameter change. The pulse of aortic regurgitation is associated with a significant change in diameter, whereas this is usually not the case in arteriosclerosis. The diameter change due to the high volume of the pulse in aortic regurgitation can be further exaggerated by elevating the arm, which helps to reduce the diastolic pressure in the brachial and the radial artery.

Since pressure and radius are two important factors that affect wall tension, as shown by Laplace relationship, it is probably reasonable to consider both of them together. What is actually felt when the arterial pulse is palpated can therefore be restated as the effect caused by a change in the wall tension of the artery.

Laplace's law is expressed as follows:

for a thin-walled cylindrical shell. If the wall has a thickness, then the circumferential wall stress is given by Lame's equation, as follows:

Tension « P (pressure) x r (radius) / 2h (wall thickness)

Amplitude of the pulse will depend not only on the amplitude of the pressure wave, but also on the change in dimensions between diastole and systole (or simply the amount of change in wall tension).

The Volume Effect

According to Laplace's law, the volume has a direct effect on the wall tension in that it relates to the radius. The actual volume ofblood received by each segment ofthe artery and its effect on the change in wall tension of that segment depends also on the vessel involved. The proximal elastic vessels (aorta and its main branches) receive almost all of the stroke volume of the left ventricle. The elastic nature of these vessels allows greater displacement and change in their radius. However, as one goes more peripherally, total cross-sectional area increases. Therefore, each vessel receives only a fraction ofthe stroke volume. In addition, the vessels are more muscular and less distensible. For similar rise in pressure, the change in vessel diameter is less. The corollary of this is that to achieve similar diameter change in the peripheral vessels, the pressure developed must be higher.

Phonocardiogram Carotid
Fig. 2. Simultaneous recordings of ECG, carotid pulse tracing, and phonocardiogram. The carotid pulse shows the percussion wave (P), the tidal wave (T), and the dicrotic wave (D), which follows the dicrotic notch (DN).

Pressure in the Vessel

The pressure pulse generated by the contraction of the left ventricle is transmitted to the most peripheral artery almost immediately, and yet the blood that leaves the left ventricle takes several cardiac cycles to reach the same distance. Thus, it must be emphasized that pressure pulse wave transmission is different and not to be confused with actual blood flow transmission in the artery. The analogy that can be given is the transmission of the jolt produced by an engine of the train to a series of coaches while shunting the coaches on the track as opposed to the actual movement of the respective coaches produced by the push given by the engine. This is the classic analogy given by Bramwell (6).

The mechanics offlow dictate that it is the pressure gradient, not the pressure, that causes the flow in the arteries. There is very little drop in the mean pressure in the large arteries. Almost all of the resistance to flow is found in the precapillary arterioles. This is where most of the drop in mean pressure also occurs in the arterial system (11,12,35). The shape of the pressure pulse changes as it propagates through to the periphery. Although the mean pressure decreases slightly, the pulse pressure (systolic pressure minus the diastolic pressure) increases distally so that the peak pressure actually increases as the wave propagates (11,37). The higher peak systolic pressure achieved in the less distensible and more muscular peripheral vessels helps to accommodate the volume received by the distal vessels.


Experimental studies have clearly shown that pressure pulse wave generated artificially by a pump connected to a system of fluid-filled closed tubes or branching tubes with changing calibre gets reflected. The reflective sites appear to be branching points (11,12). This implies that the incident pressure pulse (not flow) produced by the contracting left ventricle gets reflected back. It is reflection ofthe pressure pulse that gives the pulse wave its characteristic contour (Fig. 2). The pressure and the velocity waveforms vary markedly at different sites in the arteries. The peak velocity generally occurs before the peak in pressure at all sites (17). As one moves to the periphery, the pulsatile pressure fluctuations increase while the oscillations of flow diminish as a result of damping. The peripheral pressure fluctuations often become amplified to the extent of exceeding the central aortic systolic pressure. This is further evidence that the pressure waves get reflected peripherally (17,37).

Table 1

Determinants of Arterial Pressure Pulse and Contour

Components Determining factors

Table 1

Determinants of Arterial Pressure Pulse and Contour

Components Determining factors


Incident pressure wave


Compliance of aorta


Stroke volume


Velocity of ejection


Left ventricular pump

' Preload

' Afterload

' Contractility

' Pattern of ejection

' Impedance to ejection


Pulse wave velocity


Mean arterial pressure


Arterial stiffness/compliance


Vasomotor tone


Intensity of reflection


Peripheral resistance (arteriolar tone)

• Increased



• Decreased




Effects of wave reflection


Distance from reflecting sites


Pulse wave velocity


Timing of arrival in cardiac cycle


Duration of ejection

• Diastolic wave


Compliant arteries


Slow transmission


Shortened duration of ejection

• Late systolic wave


Stiff arteries


Rapid transmission


Long duration of ejection

Since the pressure pulse normally travels very fast (m/s), the recorded arterial pressure wave at any site in the arterial system is usually the result of the combination of the incident pressure wave produced by the contracting left ventricle and the reflected wave from the periphery (37,38).

Pulse Wave Contour

When one records the arterial pulse wave with a transducer, one may be able to identify three distinct components in its contour:

• The percussion wave, which is the initial systolic portion of the pressure pulse

• The tidal wave, which is the later systolic portion of the pressure pulse

• The dicrotic wave, which is the wave following the dicrotic notch (roughly corresponding to the timing of the second heart sound) and therefore diastolic.

Factors That Affect the Magnitude ofthe Initial Systolic Wave

Although this portion of the arterial pulse may also be influenced and modified by reflected waves from the periphery, the rate of rise and the amplitude of the incident pressure wave ofthe arterial pulse is still dependent on the ejection ofblood into the aorta by the contracting left ventricle. Thus, the characteristics of the proximal arterial system and the effect of the left ventricular pump become pertinent (Table 1; Fig. 3).

Hypertension Show Diagrammatic
Fig. 3. Diagrammatic representation of factors involved in the arterial pressure pulse wave contour, including the incident pressure wave, pulse wave velocity, transmission, and reflection (see text).

Characteristics of the Proximal Arterial System

Ejection of blood into the aorta by the contracting left ventricle during systole leads to a rise in aortic pressure from the diastolic level at the time of the aortic valve opening to the peak in systole. The rise in aortic pressure from its diastolic to the systolic peak is determined by the compliance of the aorta as well as the stroke volume. The aorta is very compliant because of its greater content of elastin compared to the smooth muscle and the collagen in its walls. Because the walls of the aorta are compliant, it expands to accom modate the blood volume. The increase in pressure for any given stroke volume will be determined by the compliance of the aorta. Increasing age leads to changes in the structural components of the walls of the aorta and reduced compliance (39). When the aorta is rigid and stiff, the pressure will rise steeply to an increased peak systolic pressure, giving rise to an increased pulse pressure.

In some elderly patients the decreased compliance of the proximal vessels could be severe enough to hide the slowly rising percussion wave of the aortic stenosis due to marked increase in pressure despite small increase in volume (36). In addition, the pressure rise will be steeper and faster if the stroke volume is delivered to the aorta with a faster rate of ejection, as would be expected with increased contractility.

The Left Ventricular Pump

The left ventricular output is dependent on the filling pressures (preload), the intrinsic myocardial function, and the afterload against which it pumps (determined by the vascular properties of the arterial system, which affect its compliance, the peripheral resistance, and the peak systolic pressure). When the ventricle begins to contract at the end of diastole, the intraventricular pressure rises as more and more myocardial fibers begin to shorten. When the left ventricular pressure exceeds the left atrial pressure, closing the mitral valve, the isovolumic phase of contraction begins. During this phase the rate of pressure development is rapid. The rate of change of pressure (dP/dt) during this phase usually is reflective of the contractile state of the left ventricle. It is increased when the left ventricle is hypercontractile and is usually depressed when the ventricular function is diminished. When the left ventricular pressure exceeds the aortic diastolic pressure, the aortic valve opens and the ejection phase of systole begins. Recordings of pressures in the left ventricle and the aorta obtained by special microtip sensors show that the left ventricular pressure exceeds that of the aorta in the early part of systole (40-42). This pressure gradient is termed the impulse gradient because it is generated by the ventricular contraction. The aortic flow velocity reaches a peak very soon after the onset of systole. During the latter half of systole, the rate of myocardial fiber shortening slows and the left ventricular pressure begins to fall. When the left ventricular pressure falls below that in the aorta, th

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