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 not only requires dedication on the part of the student of cardiology but also require 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 of the various aspects of the cardiac physical examination is dealt with in a detailed manner in the subsequent chapters, the very first chapter is devoted to the general approach to the physical examination of the cardiac patient.
In this chapter the following points are discussed:
- The various reasons for which a cardiac assessment might be sought.
- The appraisal of the various cardiac symptoms and their proper interpretation in order that an intelligent list of the various possible etiologic causes of the problem can be generated.
- The generation of the possible etiologic causes of the symptoms of the patient.
- 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.
- 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.
REASONS FOR WHICH CARDIAC ASSESSMENT IS SOUGHT
The patient for cardiovascular assessment may present generally as a result of one of the following reasons:
- For confirmation and assessment of a suspected cardiac lesion or disease.
- 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 ECG, chest X-Ray or echocardiogram).
- Because of symptoms pertaining to other systems or regions of the body that, however, might have a cardiac source.
- Because of the presence of cardiac symptoms (such as dyspnea, chest pain and 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 were 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 a clear knowledge of the associated lesions and causes for proper evaluation of such instances. For instance a 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. Sometime a markedly hypertrophied ventricle with reduced internal dimensions may cause an increased cardiothoracic ratio on the chest radiograph.
In patients with abnormal electrocardiograms (ECGs), 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, besides ischemic heart disease, one needs to consider other conditions that can cause infarct patterns on the ECG, such as hypertrophic cardiomyopathy or pre-excitation as seen in Wolff-Parkinson-White syndrome.3
Patients may sometimes present with clinical symptoms and signs pertaining to other systems or regions of the body that may actually have resulted from a cardiac source. These include symptoms consistent with systemic arterial embolism that could vary depending on the territory or region involved. They are often of sudden onset and result in ischemic symptoms related to arterial occlusion that could be either transient and/or of prolonged duration. When the source of the systemic embolism arises from the heart, the most common region that will be affected is the brain. This, of course, will cause stroke and/or transient cerebral ischemic symptoms. The cardiac sources that need to be considered include infective endocarditis with vegetations on the valve, formation of a left ventricular mural thrombus over an area of akinetic myocardium as a result of a recent and large myocardial infarction. The most common cause is often the onset of atrial fibrillation that will predispose to formation of thrombus in the left atrial appendage due to loss of atrial contraction and the resultant tendency for blood to sludge in the left atrium. The atrial fibrillation can occur in patients with pre-existing valvular disease most commonly mitral disease. However, atrial fibrillation unrelated to valvular disease is becoming the most common arrhythmia especially in the elderly patients and often the cause in a substantial portion of patients who present with stroke and/or transient cerebral ischemia.1–3 Rarely the thrombus may in fact be of systemic venous origin such as due to a deep venous thrombosis in the lower extremities and/or the pelvic veins and embolize not only to the lungs but also end up in the arterial system. In order for this to occur, one will have to have a communication between the right and the left side of the heart. Patients who present with such a paradoxical embolism may often have a patent foramen ovale and/or a small atrial septal defect that had been undetected previously. Such communications are usually associated with small left-to-right shunts, since the left atrial pressure is normally higher than the right atrial pressure, and the right ventricle offers less resistance to filling than the left ventricle. However, when sudden venous embolism occurs into the right heart and to the lungs, it can cause elevation of right ventricular and right atrial pressure. This can set the stage for transient reversal of flow across the atrial septum and result in paradoxical embolism. This may have to be considered especially when transient cerebral ischemia or stroke occurs in relatively younger patients with no significant risk factors for stroke or obvious cause such as valvular disease and/or atrial fibrillation. However, one will have to resort to two-dimensional echocardiographic (either transthoracic or transesophageal) study for confirmation, since cardiac physical examination may not necessarily reveal anything abnormal due to very small left-to-right shunt at rest.4
However, most of the patients seen for cardiac assessments are referred primarily on account of their predominant cardiac symptoms. Often a clear evaluation of the symptoms and their severity could lend itself to an analytical approach to diagnosis.4
CARDIAC SYMPTOMS AND THEIR APPRAISAL
Symptoms could be grouped to identify underlying pathology:
- Definite orthopnea and/or nocturnal dyspnea should point to the presence of high left atrial pressure and therefore help in generating possible list of causes to look for in the examination.
- 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).
- Low output symptoms of fatigue, lassitude and light-headedness could be caused by severe inflow obstructive lesions, severe cardiomyopathy of ischemic or non-ischemic etiology, constrictive pericarditis, cardiac tamponade or severe pulmonary hypertension.
- Syncope and presyncope in addition to outflow obstructive lesions may also be caused by significant brady- or tachyarrhythmias, hypotension of sudden onset brought by postural change, vagal reaction or of neurogenic origin.
While symptoms and signs of peripheral edema and ascites may be caused by congestive heart failure, may also be due to other causes such as severe tricuspid regurgitation and constrictive pericarditis. They may also be due to other non-cardiac 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, significant elevation in the jugular venous pressure would be expected.
In the assessment of patients with symptoms described as dizziness, one needs to distinguish as far as possible presyncopal feeling (weakness or a drained feeling as though one is about to faint) from vertiginous sensation that often is not cardiac in origin and often 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 asone of the three following categories:
- 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 nitroglycerine).5
- Atypical angina (meaning that the chest discomfort has some features 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).
- Non-cardiac chest pain such as those related to musculoskeletal, pleuritic, esophageal and others.
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 nitroglycerine should elicit consideration of coronary vasospasm (Prinzmetal's or variant angina) as well as possible unstable coronary syndrome. Prolonged (>20 minutes 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 of the aorta deserve special mention. The discomfort of acute pericarditis gets aggravated in the supine position and relief in the intensity of the discomfort is often experienced with patient sitting upright and leaning forward. The discomfort caused by dissection of aorta may be described as 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 requires often 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 consider not only coronary artery disease but also other conditions such as mitral valve prolapse syndrome, hypertrophic cardiomyopathy, unrecognized uncontrolled systemic hypertension, pulmonary hypertension and hyperthyroidism.
The 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 (NYHA) Classification of dyspnea or heart failure symptoms into classes I, II, III and IV.56
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 moderate level of exertion or ordinary exertion. The ordinary exertion that the patient could normally do without symptoms would also depend both on the age of the patient as well as on the mental attitude or wishes. For instance, even between two patients of similar age, one could be satisfied with walking comfortably while the other might insist on playing tennis, considering this to be a normal activity for him. The Canadian Cardiovascular Society classification has a class 0 that simply means asymptomatic. It often is used for defining severity of anginal symptoms.6
GENERATION OF WORKING LIST OF POSSIBLE DIAGNOSES
- 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 what is shown in Tables 1.1 and 1.2.
Congenital: This is a simplified scheme useful for the purposes of thinking about possible congenital cardiac lesions in the adults. For more complete list, one can refer to a pediatric cardiology textbook.
In addition, one should also 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 some extracardiac factors. These will include:
- Infection such as pneumonia
- Anemia
- Hyperthyroidism
- Pulmonary thromboembolism
- Hypoxemia secondary to pulmonary and ventilatory disorders such as sleep apnea
- Salt and fluid overload secondary to renal insufficiency
- Iatrogenic causes (e.g. use of non-steroidal 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. Each and all of these need to be evaluated in relation to the possibilities listed from the history. When this is done properly, often a clear and definitive diagnosis can be established or arrived at even before auscultation is performed.7
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 only on the basis of auscultation alone (e.g. mitral valve prolapse, hypertrophic obstructive cardiomyopathy and others).
THE APPROACH TO A FOCUSED PHYSICAL EXAMINATION
Clinical Exercise
This approach can be illustrated by discussing two different patients each presenting with specific cardiac symptoms. One could use the following sections that deal with two patients both as pre- and post–tests, namely before and after studying the remaining chapters in the book.8
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Case A. A 70-year-old woman previously healthy presents with sudden onset of dyspnea and orthopnea with radiologic signs of pulmonary edema.
The symptom complex with radiologic evidence of pulmonary congestion obviously indicates a pathologic 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, which can cause this problem. Then evidence in the history both in favor and against each listed condition should be considered.
Congenital
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
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 that the patient otherwise is able to tolerate. The rapid heart rate by shortening the diastolic filling time impedes emptying of the 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. However, mitral obstruction due to atrial myxoma could occur in the age group of this patient and therefore cannot be excluded. Occasionally, patient with prosthetic mitral valve with previous history of mitral valve replacement could present in pulmonary edema because of an acute thrombus formation on the prosthetic valve obstructing inflow and preventing proper prosthetic valve function.
Mitral Regurgitation
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 additional problems, which also affect the mitral valve function (such as due to ischemic papillary muscle dysfunction with or without avulsion of chordae or severe uncontrolled hypertension).
Acute severe mitral regurgitation: This 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 due to avulsion of chordae, due 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, 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, should be looked for. However, absence of any of these does not exclude this condition from consideration.
Aortic Regurgitation
Chronic aortic regurgitation: This can arise from valvular lesions (bicuspid valve, rheumatic involvement, trauma, endocarditis and others) or aortic root 10dilatation (Marfan's syndrome, syphilitic aortitis, spondylitis and others). 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 of course 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 exclude it from consideration. The diagnosis of course would require either electrocardiographic 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 sometimes with acute pulmonary edema. It can be seen, for instance, in younger females when complicating glomerulonephritis or pregnancy. However, these conditions need not be present. The systolic left ventricular function could be normal and yet due to significant diastolic dysfunction, the left ventricular diastolic filling pressures could be severely elevated causing the symptoms. This is particularly 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.
Cardiomyopathies
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 11history 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; however, 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 radiologic signs of pulmonary edema. Unilateral left- sided constriction from chronic constrictive pericarditis is extremely rare and unlikely to present acutely.
Cardiac Tumors
Primary cardiac tumors such as a myxoma because of its location and mobility due to attachment by a stalk to the underlying endocardial wall could cause obstructive symptoms. If the myxoma is left atrial in location, then it can cause acute symptoms of high left atrial pressure due to 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. However, in chronic pulmonary hypertension when significant, 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 pathophysiologic process is not under consideration here.12
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 since these may be really operative when there is pre-existing left ventricular dysfunction that is otherwise tolerated and asymptomatic.
Precipitating or Aggravating Factors
Rapid ventricular rate: Rapid heart rate due to 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 cardio myopathies) 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 failuredue to additional hypoxemia, which can further depress cardiac function.
Acute Pulmonary Embolism: This will 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, then it can aggravate the same leading to pulmonary edema. The mechanisms involve hypoxia, tachycardia or atrial tachyarrhythmia, which it may produce, and increased reflex vasoconstriction (could be mediated by catecholamines, serotonin and others), 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 ECG quickly for signs of an acute myocardial infarction given the fact that it is often the most leading cause of acute pulmonary edema. The discussion here is not meant to be about management of the patient rather as to how one goes about considering the various possible etiologies, since it is important for the complete management of the patient.13
We listed the various possible lesions/disorders above that can present with acute pulmonary edema and also indicated the factors that may be precipitating. 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 does 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 irregularly irregular but not totally certain by palpation alone. Then the rate of rise of the arterial pulse particularly the carotid pulse will help to suspect or rule out significant outflow tract obstruction. Sometimes in the elderly, the rate of rise may be modified due to 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 a fast upstroke with normal or lower than normal amplitude or volume. However, severe aortic regurgitation will have fast rate of rise with increased amplitude. Of course, when the aortic regurgitation is severely exaggerated, peripheral signs will become obvious that 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 runoff 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 of mixed aortic regurgitation and aortic stenosis as well as hypertrophic cardiomyopathy with obstruction. Besides the character of the arterial pulse, the measurement of the blood pressure 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; however, 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 the 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, 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 14the 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) is also important.
A displaced large area hyperdynamic left ventricular apical impulse will suggest severe mitral and/or aortic regurgitation. While severe mitral regurgitation may have somewhat of a 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, the same in the presence of a delayed carotid upstroke would indicate significant aortic stenosis, while 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 non-ischemic etiology). Sustained left ventricular impulse without an atrial kick, on the other hand, would make one suspect strongly the presence of severe left ventricular dysfunction and decreased ejection fraction due to either an ischemic or nonischemic cardiomyopathy. If the apical impulse is normal but the first heart sound is loud and palpable, one might consider mitral obstruction (e.g. due to 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, 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 that are 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 cardiomyopathy and so on). Then the auscultation may even be tuned and focused to further confirm or rule out suspected lesions.
Case B. 35-year-old man, chronic smoker, previously well, presents with history of two recent episodes of light-headedness (presyncopal feeling) while climbing two flights of stairs.
Exercise
- 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”, however, 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 due to 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 seconds) could cause a fall in cardiac output and therefore cause symptoms. Similarly, any significant bradycardia (pauses > 4.0 seconds 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 of the experience and knowledge of the physician. This likely would vary whether the individual is a beginner or student or he/she is a cardiac fellow.
The list of possible etiologies would include the following.
Congenital
- Obstructive outflow lesions: Significant aortic/pulmonary stenosis
- Inflow obstruction: Unlikely but cannot exclude atrial myxoma
- 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 AV block
Acquired
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 they are not expected to cause such symptoms. Occasionally, however, ventricular tachyarrhythmias may 16be seen in patients with advanced mitral regurgitation. Rarely severe ventricular tachyarrhythmias 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 AV block depending on the coronary artery involved.
Cardiomyopathies: Ventricular tachyarrhythmias, in the presence of underlying non-obstructive 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
Others
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
- 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
- Mild tachypnea and increased respiratory rate should raise suspicion about possible hypoxemia.
- 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.
- 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 (thepre a wave pressure). This contour in the absence of pulmonary hypertension can occur in pericardial effusion with some cardiac compression. However, the preserved y descent excludes cardiac tamponade since 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.
- Both the palpable S2 in the second left interspace and right ventricular impulse subxiphoid 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.
- 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.
- The widely split S2 moving physiologically may indicate some right ventricular dysfunction due to pulmonary hypertension, since pulmonary 18hypertension per se by increasing the pulmonary impedance would make the P2 to occur earlier and cause a narrower split SOther possibility is an electrical delay such as a coexisting right bundle branch block.
- The presence of S3 and S4 heard over the lower left sternal border and xiphoid area; both of which being described as slightly increasing on inspiration suggest right-sided events compatible with right ventricular diastolic dysfunction and acute decompensation of the right ventricle.
Synthesis
- So far the predominant right-sided signs all point to the presence of significant pulmonary hypertension with right ventricular diastolic dysfunction. Since the patient is described previously well and the history being 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.
- Such a conclusion is also suggested by the presence of mild tachycardia and mild tachypnea.
- Such an analysis should lead to immediate application of appropriate measures of management including treatment and diagnostic investigations.
PRACTICAL POINTS TO A FOCUSED CARDIAC PHYSICAL EXAMINATION
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