Manual of Cardiac Diagnosis Kanu Chatterjee
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HistoryCHAPTER 1

Kanu Chatterjee
The history and physical examination are essential, not only for the diagnosis of cardiovascular disorders but also to assess its severity to establish a plan of its management and to assess the prognosis. Appropriate history and physical examination are also essential to decide what tests are necessary for a patient as presently a plethora of tests is available for the diagnosis and management of the same cardiac disorder. For example, for the diagnosis of the etiology of chest pain due to coronary artery disease, one can perform many noninvasive, semiinvasive and invasive tests to establish or exclude the presence of obstructive coronary artery disease. It should also be appreciated that “history and physical examination” are cost-effective. Many tests that are frequently performed today are unnecessary and are much more expensive. During examination of the patient, the physician can gain the confidence of the patient and of the family and can establish a good rapport that is necessary for the appropriate management of the problem of the patient. During examination, the physician has the opportunity to demonstrate sincerity, which facilitates to gain trust of the patient and the family.
In today's electronic age, the patients and their relatives are often more familiar than the physicians about the recent developments in the diagnostic techniques and therapies. It is thus preferable (but sometimes impossible) to have this knowledge before examining the patient. In today's health care environment, there are severe constraints on time available for taking appropriate history and to do adequate physical examination.1 Frequently, the physicians have to order the “tests” because of time constraints even before examining the patient. Furthermore, there is a growing concern about malpractice suits and the medical and paramedical personnels are frequently forced to perform the investigations, which are otherwise would not have been necessary.
 
THE HISTORY
 
General Approach
During taking history, it is desirable to allow the patient to present the symptoms without interruption. Frequent interruptions give2 the impression that the physician is in hurry and impatient and disinterested. While taking history, the physician can observe the manner in which the patient describes the symptoms and the patient's emotional state and mood.
After the patient describes the symptoms, it is appropriate to discuss with the patient and the family to ascertain the chronology of symptoms and their severity. The patient may present with many symptoms. It is pertinent to inquire about each symptom. The major symptoms associated with cardiovascular disorders are chest pain or discomfort, dyspnea, palpitations, dizziness, and syncope.
 
Analysis of Symptoms
 
Chest Pain or Discomfort
Chest pain is one of the very common presenting symptoms that patients present to the cardiologists for their expert views for the diagnosis of its etiology and management. The chest pain or discomfort can be caused by various cardiac and noncardiac causes that are summarized in Tables 1 to 4.
“Cardiac pain” may be due to myocardial ischemia or it can be nonischemic in origin. The cardiac pain resulting from myocardial ischemia is called “Angina pectoris”. The precise mechanism of cardiac pain due to myocardial ischemia has not been elucidated. It has been postulated that small nonmedullated sympathetic nerve fibers, which are present in the epicardium along the coronary arteries, serve as the afferent pathways for angina pectoris.
TABLE 1   Cardiac chest pain
  • Coronary artery disease
  • Acute coronary syndromes
  • Stable angina
  • Ischemic cardiomyopathy
  • Noncoronary artery disease
  • Aortic dissection
  • Acute pulmonary embolism
TABLE 2   Noncardiac chest pain (pulmonary)
  • Pleuritis
  • Pneumonia
  • Tracheobronchitis
  • Pneumothorax
  • Mediastinitis
  • Tumor
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TABLE 3   Cardiac causes of chest discomfort
  • Aortic stenosis
  • Aortic regurgitations
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
  • Pulmonary hypertension
TABLE 4   Noncardiac chest pain
Musculoskeletal
  • Costochondritis
  • Intercostal muscle cramps
  • Cervical disk disease
Other causes
  • Herpes zoster
  • Emotional
  • Chest wall tumor
  • Disorders of breast
The afferent impulses enter the spinal cord in C8 to T4 segments and are transmitted to the sympathetic ganglia of the same segments. The impulses then travel by spinothalamic tract to the thalamus. The pain perception requires activation of the specific cortical centers.
Angina pectoris is a symptom of both of chronic coronary artery disease and of acute coronary syndromes. For the diagnosis of angina pectoris, it is imperative to inquire about the character, location, site of radiation, duration, and precipitating and relieving factors of the chest discomfort.
The character of the discomfort is usually not severe pain. More frequently, it is described as “heaviness”, “pressure”, “tightness”, “squeezing” or “band across the chest”. Sometimes the patients have difficulty describing precisely the character of the chest discomfort. The character of angina pectoris is usually “dull and deep” and not “sharp and superficial”. The “elephant sitting on the chest” is a typical textbook description, and frequently a knowledgeable patient uses this phrase to describe the character of the chest discomfort. However, such description is rather infrequently associated with coronary artery disease.
The location of the chest discomfort can be retrosternal, epigastric or left pectoral. It is infrequently located in the left axilla. Occasionally, the initial location of angina can be left arm and hands, interscapular or left infrascapular area. When the character of pain is stabbing and pleuritic, and it is positional or reproducible with palpation, it is unlikely to be angina and the4 likelihood ratio is 0.2:0.3.2 When chest pain is much localized and can be indicated by one or two finger tips, it is unlikely to be angina pectoris.
The radiation of angina pain may be to one or both shoulders, one or both arms and hands, one or both sides of the neck, lower jaw and interscapular area. The radiation can also occur to armpits, epigastrium, and subcostal areas. The radiation is usually from the center to the periphery (centripetal) and rarely from the periphery to center (centrifugal). The radiation to one or both shoulders is associated with the likelihood ratios of 2.3:4.7.2
Patient's gestures during describing the chest discomfort have been thought to be useful in the diagnosis of its etiology. The prevalences, specificities, and positive predictive values of the Levine sign, the palm sign, the arm sign and the pointing sign (Figs 1A to D) have been assessed in a prospective observational study.3 The prevalence of the Levine, palm, arm and pointing signs was 11%, 35%, 16% and 4%, respectively. The specificities of Levine sign and arm sign were 78% and 86%, respectively, but the positive predictive values were only 50% and 55%, respectively. The pointing sign had a specificity of 98% for nonischemic chest discomfort.
The intensity of angina increases slowly and reaches its peak in minutes, not instantaneously. Similarly, it is relieved gradually, not abruptly. Analysis of the duration of chest discomfort is also helpful to decide whether it is ischemic or nonischemic pain.
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FIGURES 1A TO D: Illustrations of (A) the Levine aign, (B) the palm sign, (C) the arm sign, (D) the pointing sign[Source: Marcus GM, et al. Am J Med. 2007;120:83-9 (Ref 3)]
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FIGURE 2: Description of effort angina by Sir William Heberden in 1768 (Ref 4)
When the duration is extremely short, only 1–2 seconds, it cannot be angina pectoris. Similarly, if the chest pain lasts continuously without remission for several hours and without evidence for myocardial necrosis, it is unlikely to be angina.
The precipitating and relieving factors of the chest discomfort should be analyzed to determine its etiology. The classic angina (Heberden's angina) is precipitated by exercise or by emotional stress and is relieved when the exercise is discontinued. It tends to occur often after meals. The original description of classic angina pectoris by William Heberden is shown in Figure 2.4
The effort angina is also relieved by sublingual nitroglycerin. The time for relief after using nitroglycerin sublingually is not instantaneous. It takes a few seconds (usually 30 seconds or longer). It should be appreciated that chest pain due to esophageal spasm is also relieved by nitroglycerin.
Exposure to cold weather precipitates angina more easily in patients with classic angina. Similarly, carrying heavy objects and heavy meals are also frequent precipitating factors. The character, location and radiation of chest discomfort are similar in the different clinical subsets of angina. However, some distinctive features can be recognized in various subsets.
In patients with vasospastic angina, angina occurs at rest and usually not during exercise. The duration is variable. It tends to have cyclic phenomenon, and in the individual patient, it tends to occur more or less at the same time.
In patients with acute coronary syndromes, the duration is usually longer. In patients with ST segment elevation myocardial infarction (STEMI), the relief of chest pain may not occur until reperfusion therapy is established.
The atypical presentations frequently called “anginal equivalents” are dyspnea, indigestion and belching, and dizziness and syncope without chest pain. The atypical presentations are more common in diabetics, women, and the elderly. A few clinical features of angina are summarized in6 Tables 5 and 6. The chest pain due to acute pericarditis, acute pulmonary embolism, or acute aortic dissection may be similar to that of acute coronary syndromes.
The pericardial pain is usually superficial and sharp and may have a pleuritic quality. It can radiate to both shoulders and infraspinatus areas. Generally, pericardial pain is worse in supine position and less severe in sitting and leaning forward position. Occasionally pericardial pain waxes and wanes with cardiac systole and diastole.
The location of pain of acute pulmonary embolism can be retrosternal and may not have a pleuritic quality. It is frequently associated with tachypnea.
The chest pain resulting from acute aortic dissection is usually severe. The location can be anterior chest. Radiation to the back is common. The downward radiation along the spine is very suggestive of aortic dissection. The onset of pain is frequently instantaneous and the maximal severity may occur at the onset. The character of the pain is “shearing or tearing”. A few clinical features of pain of acute pericarditis, pulmonary embolism, and acute aortic dissection are summarized in Table 7.
The severity of angina is assessed by the Canadian Cardiovascular Society (CCS) functional classification5 (Table 8) or Specific Activity Scale6 (Table 9).
TABLE 5   Clinical features of stable angina
Location
• Usually retrosternal, can be epigastric, interscapular
Localization
• Usually diffuse, difficult to localize
• When is very localized (point sign)—unlikely to be angina
Quality
• Pressure, heaviness, squeezing, indigestion
Radiation
• One or both arms, upper back, neck, epigastrium, shoulder
• Lower jaw (upper jaw, head, lower back, lower abdomen or lower extremities radiation is not feature of angina)
Duration
• Usually 1–10 minutes (not a few seconds or hours)
Precipitating factors
• Physical activity, emotional stress, sexual intercourse
Aggravating factors
• Cold weather, heavy meals
Relieving factors
• Cessation of activity, nitroglycerin (if relief is instantaneous, it is unlikely to be angina)
Associated symptoms
• Usually none, occasionally dyspnea
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TABLE 6   Clinical features of chest pain in acute coronary syndromes
Location
• Same as stable angina
Quality
• Same as stable angina
Duration
• Usually longer than stable angina
Relieving factors
• Usually unrelieved by rest or nitroglycerin
Associated symptoms
• Dyspnea, sweating, weakness, nausea, vomiting presyncope, or syncope
TABLE 7   Clinical features of chest pain due to acute pericarditis, acute pulmonary embolism, and acute aortic dissection
Acute pericarditis
Location
• Anterior chest, superficial
Character
• Sharp, can be pleuritic
Radiation
• Supraspinatus areas, shoulders, back
Relieving factors
• Worse in supine position, less severe in sitting and leaning for-ward position, relieved by analgesics, nonsteroidals and steroids
Acute pulmonary embolism
Location
• Usually retrosternal
Quality
• Deep, may be similar to acute coronary syndromes
Associated symptoms
• Tachypnea and dyspnea
Acute aortic dissection
Location
• Chest, back
Quality
• Shearing, tearing
Onset
• Instantaneous
Radiation
• Downwards along the spine
The CCS functional classification is most frequently used to assess the severity of angina and has been proven to be useful to assess its prognosis.7 The Specific Activity Scale, which is a more quantitative assessment of the severity of angina, is not used in the clinical trials.
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TABLE 8   Canadian Cardiovascular Society (CCS) functional classification
Class I
• Ordinary physical activity, such as walking and climbing stairs, does not cause angina
• Angina with strenuous or rapid or prolonged exertion at work or recreation
Class II
• Slight limitation of ordinary activity. Walking or climbing stairs rap-idly, walking uphill, walking or stair climbing after meals, in cold, in wind or when under emotional stress, or only during the few hours after awakening
• Walking more than two blocks on the level, and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions
Class III
• Marked limitation of ordinary physical activity
• Walking 1–2 blocks on the level and climbing more than one flight in normal conditions
Class IV
• Inability to carry out any physical activity without discomfort—anginal syndrome may be present at rest
TABLE 9   Specific activity scale
Class I
• Patients can perform to completion any activity requiring ≤7 metabolic equivalents [e.g. can carry 24 lbs up eight steps; carry objects that weigh 80 lbs, do outdoor work (shovel snow, spade soil); do recreational activities (skiing, basketball, squash, handball, jog/walk 5 mph)]
Class II
• Patients can perform to completion any activity requiring ≤5 metabolic equivalents (e.g. have sexual intercourse without stopping, garden, rake, weed, roller skate, dance fox trot, walk 4 mph on level ground), but cannot and do not perform to completion activities requiring ≥7 metabolic equivalents
Class III
• Patients can perform to completion any activity requiring ≥2 metabolic equivalents (e.g. shower without stopping, strip and make bed, clean windows, walk 2.5 mph, bowl, play golf, dress without stopping), but cannot and do not perform to completion any activities requiring ≥5 metabolic equivalents
Class IV
• Patients cannot or do not perform to completion activities requiring ≥2 metabolic equivalents. Cannot carry out activities listed above (Specific Activity Scale Class III)
In patients with suspected or documented coronary artery disease, inquiries should be made about the risk factors. The modifiable and nonmodifiable risk factors for atherosclerotic coronary artery diseases are summarized in Table 10.
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TABLE 10   Cardiac and pulmonary causes of dyspnea: Differential diagnosis of dyspnea
Cardiac
Pulmonary
CHF
COPD
CAD
Asthma
Cardiomyopathy
Restrictive lung diseases
Valvular dysfunction
Hereditary lung diseases
LVH
Pneumothorax
Pericardial diseases
Arrhythmias
Congenital HD
(Abbreviations: CHF: Congestive heart disease; HD: Heart disease; CAD: Coronary heart disease; LVH: Left ventricular hypertrophy
Smoking, hypertension, diabetes, obesity, metabolic syndrome, hyperlipidemia, and physical inactivity are risk factors for coronary artery disease. History of peripheral vascular and cerebrovascular disease and stroke is also associated with a higher risk of coronary artery disease. These risk factors are modifiable.
Older age, male gender, and family history of atherosclerotic cardiovascular disease are also risk factors for coronary artery disease, but these risk factors are not modifiable.
 
Dyspnea
Dyspnea is an uncomfortable sensation of breathing. It is also defined as “labored” breathing. The precise mechanism of dyspnea has not been established. It has been suggested that activation of the mechanoreceptors in the lungs, pulmonary artery and heart and activation of the chemoreceptors are involved in inducing dyspnea. Dyspnea can occur during exertion (exertional), during recumbency (orthopnea), or even with standing (platypnea).
There are both cardiac and noncardiac (Table 10) causes of dyspnea. Pulmonary disease, such as chronic obstructive lung disease, is one of the common noncardiac causes of dyspnea. Many patients have both cardiac and pulmonary disease. It is not uncommon in clinical practice to encounter patients who have coronary artery disease and chronic obstructive pulmonary disease. In such patients, to determine the cause of dyspnea, appropriate history and physical examination are essential. To distinguish between cardiac and noncardiac dyspnea, the measurements of serum B-type Natriuretic Peptide (BNP) or N-Terminal ProBNP (NTBNP) is helpful. In noncardiac dyspnea, the natriuretic peptide levels are normal, and in patients with heart failure, they are substantially elevated.
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Exertional dyspnea can be caused by both cardiac and noncardiac causes. Exertional dyspnea is an important symptom of chronic heart failure. However, it is also a symptom of chronic pulmonary diseases and of metabolic disorders, such as obesity and hyperthyroidism. Dyspnea is also a common symptom of anxiety disorders. Cardiac dyspnea gets worse with physical activity. Dyspnea of functional origin frequently improves after exercise.
Orthopnea is defined when patients develop dyspnea lying flat and feel better when the upper part of the torso is elevated. Although orthopnea is a symptom of heart failure, it also occurs in patients with pulmonary disease, such as emphysema and chronic obstructive pulmonary disease.
Paroxysmal nocturnal dyspnea is virtually diagnostic of cardiac cause. After being in the recumbent position for about 15 minutes to 2 hours, the patient develops shortness of breath and has to sit or stand up to get relief. The hemodynamic mechanism is that after assuming the recumbent position, there is an increase in the intravascular and intracardiac volumes, which is associated with an increase in pulmonary venous pressure and transient hemodynamic pulmonary edema. The sitting and/or upright position is associated with a reduction of intravascular and intracardiac volumes due to decreased venous return and reduction of pulmonary venous pressure and relief of dyspnea. Left ventricular systolic and diastolic heart failure and aortic and mitral valve diseases are the common causes of paroxysmal nocturnal dyspnea.
Sleep-disordered breathing, which may be associated with dyspnea, can occur in cardiac patients. Cheyne–Stokes respiration is a specific type of periodic breathing that is characterized by alternating periods of apnea and hyperpnea. During hyperpneic phases, there is a progressive decrease in PCO2 with increased pH which inhibits the respiratory drive; during apneic phase, CO2 accumulates with an increase in respiratory acidosis, and the respiratory center is stimulated and breathing is initiated. It appears that chemoreceptors-mediated stimulation of the respiratory centers is blunted in patients with Cheyne–Stokes respiration. Patients feel shortness of breath during the hyperpneic phase. Central, obstructive, and mixed types of sleep apnea are observed in patients with heart failure. The hemodynamic causes of sleep-disordered breathing in heart failure have not been clearly elucidated. Initially, the Cheyne–Stokes respiration was thought to be due to low cardiac output;8 however, there does not appear to be a good correlation between any hemodynamic changes of systolic heart failure and Cheyne–Stokes respiration. History of sleep-disordered breathing should be inquired, as it is associated with worsening heart failure, pulmonary hypertension, and increased risks of arrhythmias, and sudden cardiac death.
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Wheezing due to constriction of the bronchial smooth muscles associated with dyspnea does not always imply pulmonary diseases. It may be caused by hemodynamic pulmonary edema in patients with systolic and diastolic heart failure and valvular heart diseases (cardiac asthma).
There are many cardiac conditions, which can be associated with episodic severe dyspnea. In between the episodes of dyspnea, these patients are relatively asymptomatic and may have good exercise tolerance. In patients with episodic dyspnea, intermittent severe mitral regurgitation due to papillary muscle dysfunction should be considered in the differential diagnosis. Intermittent mitral valve obstruction due to left atrial myxoma or ball valve thrombus is a rare cause of this syndrome. In patients with left atrial myxoma, dyspnea may be positional and may be associated with syncope. Another cause of episodic severe dyspnea is “stiff heart syndrome”.9 These patients usually have normal left ventricular ejection fraction and have history of hypertension and coronary artery disease (diastolic heart failure). Fluid retention, either from the increased salt intake or from the lack of use of the diuretics, precedes the onset of dyspnea.
Atrial or ventricular tachyarrhythmias usually do not produce episodic severe dyspnea in absence of valvular or myocardial disease. However, it can occur in patients with left ventricular dysfunction and in patients with mild-to-moderate mitral stenosis.
In patients with massive or submassive pulmonary embolism, tachypnea and dyspnea are common presenting symptoms. There may be associated chest pain and wheezing. Patients with pulmonary embolism prefer the supine position as opposed to patients with hemodynamic pulmonary edema who prefer the upright position. Arterial desaturation may be present in both conditions. A plain chest X-ray may be useful to establish the diagnosis. In patients with pulmonary embolism, the chest X-ray is clear and does not demonstrate radiologic evidences of pulmonary venous hypertension. In patients with hemodynamic pulmonary edema, prominent upper lobe vessels, perihilar haziness, and Kerley lines and frank pulmonary edema may be present (Fig. 3).
A careful cardiovascular examination may also reveal the etiology of dyspnea. For example, evidence of valvular and myocardial heart diseases suggests cardiac cause of dyspnea (Table 11). The presence of S3 gallop usually indicates increased left ventricular diastolic pressures except in young people and patients with chronic primary mitral regurgitation. In patients with heart failure, presence of S3 is also associated with the increased levels of B-type natriuretic peptides. The presence of characteristic physical findings of significant valvular heart disease also suggests cardiac dyspnea.
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FIGURE 3: A plain chest X-ray of a patient with acute severe mitral regurgitation showing florid hemodynamic pulmonary edema
TABLE 11   Diagnosis of causes of cardiac dyspnea
Dyspnea
Cardiac or noncardiac dyspnea
Physical examination:
  • Signs of heart failure—diagnostic of cardiac cause, e.g. S3, elevated JVP, positive HJR
Presence of cardiac pathology:
  • Very suggestive of cardiac cause
Chest X-ray:
  • Very helpful when findings of pulmonary venous congestion or pulmonary hypertension are present
ECG:
  • Normal electrocardiogram
  • A negative predictive value has over 90%
(Abbreviations: JVP: Jugular venous pressure; HJR: Hepatojugular refulx
The absence of these signs, however, does not exclude cardiac dyspnea.
 
Palpitation
Palpitation is perceived as an uncomfortable sensation in the chest associated with heartbeats. The most frequent cause of palpitation is premature atrial or ventricular contractions. The premature beat itself is not felt; the normal beat following the compensatory pause is felt as a strong beat. The patients usually describe this uncomfortable sensation as “a thump”, “skipped beat”, “the heart is coming out of chest”, “heart stops” and “heart stops beating”.
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The frequent premature beats may also be associated with other symptoms, such as dizziness, sinking feeling, shortness of breath and chest pain. The chest pain can be troublesome and anxiety provoking. The mechanism of chest pain remains unclear; it is possible that the beat following the compensatory pause is associated with activation of myocardial afferent stretch receptors causing chest pain. The same mechanism can be hypothesized for dyspnea associated with premature beats.
During taking history about palpitation, it is desirable to inquire about the duration, whether it is regular or irregular, fast or slow, and the mode of onset and termination. It is sometimes easier for the patient to recognize the type of arrhythmia if the physician taps with the fingers to describe the type of arrhythmia. If it is fast and irregular, the likely diagnosis is atrial fibrillation; although rarely, it can be due to multifocal atrial tachycardia. A fast irregular palpitation can be due to atrial flutter or very frequent premature beats.
An abrupt onset and abrupt termination of fast regular or irregular tachycardia is a common feature of supraventricular tachycardia, although it may also occur in ventricular tachycardia. The associated symptoms of supraventricular tachycardia, besides palpitation, are dyspnea, chest pain, presyncope or even syncope. Some patients also experience polyuria during prolonged episodes of supraventricular tachycardia. The mechanism of polyuria is probably due to stimulation of release of atrial natriuretic peptide and suppression of vasopressins. The vasodilatory effects of atrial natriuretic peptides may also contribute to hypotension and presyncope.
 
Syncope
Syncope is defined as transient loss of consciousness. Patients with presyncope complain of dizziness and near fainting, although they do not loose consciousness completely. The mechanism of cardiac syncope is reduced cerebral perfusion resulting from decreased cardiac output and hypotension.
A large number of cardiac and noncardiac conditions can cause syncope. Dysrhythmias, abnormalities of function of the autonomic nervous system, anatomic conditions, such as left or right ventricular outflow obstruction, vascular disorders, such as severe pulmonary arterial hypertension, acute coronary syndromes, aortic dissection, and acute massive or submassive pulmonary embolism can be associated with syncope.
Acute coronary syndromes, aortic dissection, or pulmonary embolism do not cause recurrent syncope. However, when syncope is the presenting symptom in these patients, the prognosis is poor.
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A careful history is helpful for the diagnosis of the cause of syncope. Inquiry should be made about the circumstances in which syncope occurred, whether it was accompanied or preceded by palpitation, whether it occurs during exertion or it can also occur at rest, and whether it occurs only during upright position, or it is unrelated to body position.
Stokes–Adams–Morgagni syndrome occurs due to ventricular asystole (cardiac standstill) in patients with advanced atrioventricular block. The syncope is unrelated to body position or exertion. The onset is sudden and recovery is also abrupt. During asystole the skin is pale and white and with the return of circulation, the skin appears red and flushed. There are no premonitory symptoms and after recovery of consciousness, the patients are not confused and are immediately aware of the surroundings. Stokes–Adams–Morgagni syndrome may be familial, suggesting a genetic abnormality may be present.
Vasovagal or neurocardiogenic syncope occurs during upright position and frequently after remaining in a standing position for a few minutes. The onset is not abrupt and premonitory symptoms, such as nausea, abdominal discomfort and urge for bowel movement, may precede syncope. The recovery of consciousness is gradual and patients may appear confused after recovery of consciousness.
Syncope resulting from supraventricular tachyarrhythmias is usually not of abrupt onset. Supraventricular tachycardia more frequently causes presyncope rather than frank syncope. It is associated with fast palpitations and usually occurs during upright position. Some patients with brady–tachy syndrome give history of syncope after the fast palpitations stop and the mechanism appears to be due to prolonged sinus node recovery time. Paroxysmal orthostatic tachycardia syndrome (POTS) syncope usually occurs in patients during exercise and is caused by inappropriate sinus tachycardia.
There are other types of syncope, which are due to stimulation of the parasympathetic nervous system that is associated with cardioinhibitory and vasodepressor response. The history of syncope precipitated by sudden movement of the head, rubbing or shaving the neck, or wearing a tight collar suggests carotid sinus syncope. The history of syncope while swallowing or drinking cold water (glossopharyngeal syncope) is due to stimulation of the ninth cranial nerves, and it may also be associated with neuralgic pain.10
Micturition syncope occurs during or immediately after voiding and is caused by reflex stimulation of the parasympathetic nervous system.11 The posttussive syncope, also known as cough syncope, occurs during or immediately after paroxysms of violent cough.12 The mechanisms of cough syncope remain unclear. A decrease in cardiac output due to decreased venous15 return resulting from increased intrathoracic pressure during paroxysms of prolonged cough is a potential mechanism.
In patients with orthostatic hypotension, syncope occurs in the upright position and the onset is gradual. Inquiries should be made about the use of antihypertensive drugs and sublingual nitroglycerin preceding syncope. Orthostatic hypotension may also occur in patients with diabetes, amyloidosis, and other disorders of autonomic function, and there may be history of impotence, sphincter disturbances, and anhidrosis.
A history of presyncope, blurring of vision with or without arm claudication during exercise of the upper extremities is very suggestive of “subclavian steal” syndrome.13
Syncope due to anatomic causes (aortic stenosis, hypertrophic obstructive cardiomyopathy, pulmonary hypertension) usually occurs during exercise. The mechanism appears to be the inability to increase cardiac output during exercise and disproportionate decrease in metabolically mediated peripheral vascular resistance.
The convulsive disorders, such as epilepsy, can also cause syncope. It can occur in any position. There is usually a history of prodromal aura preceding the seizure. Urinary and bowel incontinence and biting of tongue and other involuntary injuries support the diagnosis of epilepsy.
 
Edema
Patients with edema present with the symptom of “swelling”, usually of the lower extremities. Both cardiac and noncardiac conditions may be associated with edema. Inquiries should be made regarding the initial location and progression of edema. Right heart failure with systemic venous hypertension causes dependant edema, such as in the ankles, feet, and legs. In patients with worsening right heart failure, edema can extend to the thighs, genitalia, and abdomen. In patients who are bedridden, edema can be predominantly in the back.
Chronic venous insufficiency may also be associated with lower extremity edema, and a bluish discoloration of the skin may be present. In patients with idiopathic lower extremity edema, symptoms and signs of systemic venous hypertension are absent.
Generalized edema is uncommon in heart failure, and usually suggests permeability edema, such as in patients with hypoalbuminemia.
The history of edema localized in the upper extremity should raise the suspicion of upper extremity venous obstruction, such as subclavian, innominate, and superior vena cava thrombosis. These patients may also complain of facial edema with bluish discoloration.
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Nonpitting lymphedema of the upper extremity is occasionally observed in patients who had a mastectomy and axillary lymph node removal for breast malignancy.
 
Cough
The paroxysms of cough may be the presenting symptoms of cardiac and noncardiac patients. Patients with left heart failure may complain of nocturnal cough with or without dyspnea. Paroxysms of nonproductive cough are bothersome complications of angiotensin-converting enzyme inhibitor therapy.
Cough with or without expectoration is also a frequent presenting symptom of pulmonary diseases.
Hoarseness with or without cough is a rare complication of mitral stenosis (Ortner's syndrome). A markedly enlarged left atrium and pulmonary artery compress the left recurrent laryngeal nerve causing hoarseness.14 Hoarseness also occurs in patients with aortic aneurysm, if it compresses the left recurrent laryngeal nerve.
 
Hemoptysis
Hemoptysis is an uncommon presenting symptom of cardiac patients. Patients with hemodynamic pulmonary edema may present with history of frothy pink, blood-tinged sputum. These patients also have dyspnea.
Rarely, in patients with mitral stenosis and severe pulmonary hypertension, profuse hemoptysis (pulmonary apoplexy) can occur due to rupture of the bronchopulmonary venous anastomotic vessels. If profuse hemoptysis occurs in a patient instrumented with a balloon flotation catheter, pulmonary artery rupture should be suspected.
Recurrent hemoptysis may be a presenting symptom in patients with precapillary pulmonary arterial hypertension and Eisenmenger's syndrome. The thrombosis in situ of pulmonary vessels appears to be the mechanism.
Hemoptysis associated with pleuritic chest pain should raise the suspicion of pulmonary embolism.
Patients on anticoagulation therapy may present with hemoptysis. It should be appreciated, however, that frank hemoptysis is an uncommon presenting symptom of cardiac patients and primary bronchopulmonary disease, such as malignancy, should always be suspected.
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