Clinical Methods in Cardiology RS Sharma
Chapter Notes

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History TakingChapter 1

A detailed but not time wasting history is essential and most useful part of diagnosis making. Sometime nonverbal “Body language” gives tremendous information. Mood, distress anxiety can be seen better but may not be said.
The physician's questioning should be unhurried and nonthreatening but nonetheless thorough. Skillful interrogation, appropriate to the urgency of the situation, must be matched by thoughtful listening. Questions should not be suggestive of answer.
The patient must be encouraged to raise questions at appropriate times.
Artful history taking brings the patient and physician close together. For this reason, it is a critical factor not only in establishing the diagnosis but also in determining the outcome of subsequent therapy.
Proper communication is the lifeline of a good history. Communication is a bigger thing than history taking (Fig. 1.1).
The modern tendency for patients with no symptoms to consult physicians for routine “checkup” examinations has increased the likelihood that doctors will cause unnecessary anxiety in their patients even though the intent of such examinations is to discover latent or developing illness. Since symptoms of disease are often exaggerations of normal findings (e.g. dyspnea, fatigue), the borderline between normality and disease is often difficult to define. The problem becomes greater as the patient becomes older because the range of normality widens with advancing years. Some patients deny the existence of symptoms, fearing to be told that they are ill and may die; and some may exaggerate symptoms, if being ill seems to have usefulness as a weapon or problem-solving device. Decreasing activity, failing memory, and wishful thinking may lead people to defer seeking advice until disease is far-advanced. Persons with no complaints are technically not “patients”, and a distinction should be maintained between conditions discovered during routine examinations and the diseases of patients with true symptoms. Experience in dealing with clinical and laboratory information obtained from checkup examinations is relatively small, and physicians tend to forget that under such circumstances they are dealing with a pre-symptomatic phase of disease.
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Fig. 1.1: Proper history taking establishes good communication and is valuable in diagnosis making
The physician should avoid unnecessary and prolonged personal talks or jokes with patients, as this is likely to reduce the “higher image” of doctor in whom patent usually finds solace. A respectful distance should be maintained in author's opinion. Ideally, a room free of noises is preferred.
The difficulty of interpreting a symptom, which may also be a normal physiologic response, is perhaps most strikingly demonstrated in the case of the cardinal symptom of heart disease—dyspnea, or shortness of breath. Shortness of breath on exertion is a normal phenomenon. In most cases, exercise performance is limited by shortness of breath rather than by fatigue, chest pain, leg pain, dizziness, or syncope. Dyspnea on progressively less severe exertion is also a normal accompaniment of the common modern combination of’ a sedentary life, increasing weight, and increasing age. The insidious onset of shortness of breath on exertion—a characteristic of heart disease is thus more difficult to assess than some obviously abnormal symptom like hemoptysis or severe chest pain.
The history is crucial to make a diagnosis. Heart disease commonly occurs without abnormal physical findings; for example, examination is often normal in intermittent arrhythmias between episodes. Examination may confirm a cardiac or peripheral vascular diagnosis, e.g. when examining a patient with a murmur, heart failure or an abdominal aortic aneurysm, but physical signs may be completely absent in serious disease:
  • Patients with severe carotid artery disease may have no neck bruit because flow through the stenosis is too slow
  • Large abdominal aortic aneurysms can be impalpable in the obese
  • Patients with extensive deep vein thrombosis often appear to have normal legs.
Presenting Complaint
Establish the frequency, duration and severity of symptoms, and causative and relieving factors. Urgently attend to breathlessness, recent chest or lower limb pain. Many cardiovascular diseases are slowly progressive and the evolution of symptoms guides the timing of investigations and treatment, e.g heart valve surgery is indicated for significantly limiting symptoms and surgery for carotid artery disease is most effective soon after a cerebral event.
Cardiovascular disease presenting with ‘noncardiac’ symptoms
Central nervous system
Cerebral embolism
Abdominal pain
Liver congestion secondary to heart failure
Mesenteric embolism
Heart failure
Functional Impairment
Assess the impact of symptoms on the patient's functional capacity. For chest discomfort or breathlessness, establish the intensity of exercise required to induce symptoms.
  • Does gentle walking or only strenuous exercise like climbing hills or stairs provoke symptoms?
  • Can patients keep up when walking with their partners or friends of the same age?
  • What is the extent of domestic, e.g. cooking, cleaning, shopping; social, e.g. mobility, hobbies, sport, and occupational disability?
Light-headedness and syncope may impair confidence, raise fear of physical injury, and have significant implications for patients’ safety when driving.3
Calf leg pain on walking (intermittent claudication) from lower limb arterial disease is the most common symptom of peripheral vascular disease:
  • How far can the patient walk before the pain comes on, and is this on the flat or uphill?
Past History
Ask about rheumatic fever or heart murmurs during childhood and conditions associated with heart disease, including:
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Kidney disease
  • Thyrotoxicosis (atrial fibrillation)
  • Alcohol intake (arrhythmias and cardiomyopathy)
  • Marfan's syndrome (aortic regurgitation or aortic dissection).
In suspected infective endocarditis, ask about recent dental work and other potential causes of bacteremia, e.g. skin infections, intravenous drug use, penetrating trauma. Consider possible links between other organ system diseases and cardiovascular illness: for example, patients with renal failure or disseminated cancer and pericardial effusion; heart failure and cytotoxic drugs; radiotherapy and radiation arteritis in the affected area. Patients with chronic respiratory disease may develop right-sided heart failure (cor pulmonale) or atrial fibrillation. Connective tissue diseases such as rheumatoid arthritis are associated with Raynaud's phenomenon and pericarditis.
Drug History
Drugs may cause or aggravate symptoms such as breathlessness, chest pain, edema, palpitation or syncope. Starting thyroxine for hypothyroidism may precipitate or aggravate angina. ‘Recreational’ drugs such as cocaine and amphetamines can cause arrhythmias, chest pain and even myocardial infarction. Ask about over-the-counter purchases such as NSAIDs and alternative medicine and herbal remedies, as these may contain ingredients with cardiovascular actions. Beta-blockers may worsen the symptoms of intermittent claudication and any drug that lowers blood pressure tends to impair the peripheral circulation.
Genetically determined cardiovascular disorder
Single-gene defects
  • Hypertrophic cardiomyopathy
  • Marfan's syndrome
  • Familial hypercholesterolemia
  • Muscular dystrophies
  • Long Q-T syndrome
Polygenic inheritance
  • Ischemic heart disease
  • Hypertension
  • Type 2 diabetes mellitus
  • Hyperlipidemia
  • Abdominal aortic aneurysm
Family History
Many cardiac disorders have a genetic component. Ask about a family history of either premature coronary artery disease in a first-degree relative (< 60 years in a female or < 55 years in a male) or sudden unexplained death at a young age, raising the possibility of a cardiomyopathy or inherited arrhythmia disorder. Patients with peripheral arterial and venous thrombosis may have inherited thrombophilia, Familial hypercholesterolemia is associated with premature cardiac and peripheral arterial disease.
Social History
Smoking is the strongest reversible risk factor for coronary artery disease and peripheral vascular disease. Take a detailed smoking history. Alcohol can induce atrial fibrillation, and alcohol excess is associated with obesity, 4hypertension and dilated cardiomyopathy. Excess alcohol intake with poor nutrition also predisposes to peripheral arterial and venous disease. Intravenous drug use can damage peripheral arteries and veins, most commonly causing an infected false aneurysm of the common femoral artery in the groin: a potential source for infective endocarditis.
Occupational History
Heart disease may impair physical activity and affect employment. This may be a source of anxiety and an indication for treatment. The diagnosis of heart disease has medicolegal consequences in certain occupations, such as commercial drivers and pilots. Workers exposed to occupational vibration using air-powered tools may develop ‘vibration white finger’, which presents with vasospasm (Raynaud's phenomenon) and neurosensory (numbness, tingling) symptoms.
Mechanism of Dyspnea
The unpleasant sensation of the need for increased ventilation is the best description of dyspnea. Two main varieties have been distinguished. With the first variety, the patient feels that extra work on the part of the respiratory muscles is required to achieve adequate ventilation. With the second type, the patient is aware of a feeling of smothering and feels an urgent need to take another breath; the smothering sensation is akin to that associated with breath holding. Dyspnea is a cortical sensation involving consciousness and must be distinguished from hyperpnea, or increased ventilation, which may occur without any discomfort or distress and which may be seen in unconscious patients or tachypnea which is increased rate.
Dyspnea in Heart Disease
The dyspnea of patients with heart disease that most closely resembles the dyspnea of normal exertion. Characteristically, it is directly related to the degree of exertion. The patient complains that some effort that previously did not result in awareness of breathing now causes an unpleasant gasping sensation. The feeling of discomfort is in the chest but is not well localized to any single structure such as the diaphragm or the intercostal muscles.
In contradiction to cardiac dyspnea, shortness of breath at rest is more common in many lung diseases such as asthmatic attacks, bronchitis, pneumonia, pneumothorax, but not in emphysema. Making the distinction between cardiac and pulmonary dyspnea can be extremely difficult. This is not surprising, since the mechanisms may be quite similar in certain circumstances.
  1. Dyspnea Associated with Cardiac Output: When cardiac output is inadequate to meet the metabolic needs of the body, hyperventilation and dyspnea occur. Pulmonary congestion need not be present, although the dyspnea is similar to that occurring in pulmonary congestion and is quantitatively related to exertion.
  2. Dyspnea due to Pulmonary Edema: Dyspnea on exertion is the cardinal symptom of pulmonary congestion. It results from a rise in left ventricular end-diastolic pressure or a raised left atrial pressure with a normal left ventricle in mitral valve disease. In both cases, increased pulmonary venous and pulmonary capillary pressures increase the stiffness of the lungs and the work of breathing by decreasing the compliance of the lungs, mainly by causing interstitial pulmonary edema. In addition to the mechanical changes, there is also a reflex autonomic visceral sensation, probably 5mediated through nonmedullated sensory fibers in the lungs and passing up the vagus nerves to the medulla, which contributes to dyspnea by direct autonomic sensory stimulation. In the early stages of heart disease, dyspnea only occurs with severe exertion, but as pulmonary congestion becomes more severe, permanent changes in the lungs occur. Resting lung compliance is reduced, and increased lymphatic drainage, thickening of interstitial tissues, and other compensatory changes occur. Such changes reduce the chances of acute pulmonary edema and enable the body to tolerate high pulmonary capillary pressures of thickened barriers between the blood in the capillaries and the gas in the alveoli.
  3. Dyspnea in Acute Pulmonary Edema: When pulmonary congestion is acute and severe, dyspnea occurs with minimal exertion, avid pulmonary edema results as fluid is forced into the alveolar spaces by capillary congestion. This congestion may seriously interfere with gas exchange and cause hypoxia and respiratory acidosis with CO2 retention.
  4. Dyspnea Associated with other Forms of Heart Disease: Dyspnea occurs in forms of heart disease other than those involving pulmonary congestion and low cardiac output. In cyanotic congenital heart disease, shunting of venous blood into the systemic circulation lowers arterial oxygen tension and contributes to dyspnea by stimulating the carotid bodies and increasing the ventilation needed for a given work load.
In pulmonary embolism and pulmonary infarction, dyspnea may result from reflex stimulation of medullary centers by impulses from vagal nerve endings in the lungs and pulmonary arteries, Such dyspnea may be in addition to that due to inadequate cardiac output, which has already been described.
Dyspnea Resulting from Chemical Stimuli
Other mechanisms involved in dyspnea include chemical stimuli to ventilation mediated through hypoxia, increase in CO2 (hypercapnia), and metabolic acidosis. The chemoreceptor cells of the carotid and aortic bodies respond primarily to hypoxia and secondarily to increased CO2. The central chemosensitive areas in the medulla stimulate respiration primarily in response to acidosis resulting from CO2 and only secondarily in response to hypoxia. Chemically mediated stimuli to ventilation provide slowly responding and long-lasting control mechanisms and are chiefly involved in controlling depth and rate of breathing rather than causing dyspnea. Hypoxia, as demonstrated by a lowered arterial oxygen tension breathing air at rest or during exercise (PO2 < 70 mm Hg), is not generally found in dyspneic cardiac patients. Hyperventilation with low pH, and a normal or raised PO2 is the usual finding. It is caused in cardiac patients by the release of acid metabolites from inadequately perfused tissues rather than by anxiety. Dyspnea also results from acute changes in the permeability of the pulmonary capillaries, as when pulmonary edema develops in heroin overdose, or on exposure to toxic fumes such as chlorine, phosgene, or other noxious gases.
Attacks of Dyspnea
Episodic dyspnea and dyspnea at rest, which is relieved by sitting up (orthopnea), are important indicators of severe disease. The mechanism of’ orthopnea involves an increase in pulmonary capillary pressure and a decrease in lung volume when lying flat. Lung compliance decreases and respiratory resistance increases to cause an acute increase in the work of breathing. Paroxysmal dyspnea classically occurs at night, often after a strenuous day or an evening out dancing, or after excessive salt or fluid intake. It characteristically wakes the patient up around 2:00 am and is so 6clearly relieved by sitting or standing and made worse by lying fiat that a patient who has once experienced this symptom will often never sleep flat in bed again.
In acute pulmonary congestion in bedridden patients, the least exertion, such as eating, use of a bedpan or commode, washing, or the minor excitement of a visitor, may provoke an episode of dyspnea. The dyspnea of acute pulmonary congestion, if not relieved, will progress to acute pulmonary edema, which can cause circulatory collapse, with restlessness, anxiety, apprehension, sweating, tachycardia, tachypnea, and acute respiratory distress.
Dyspnea Associated With High-Altitude
Pulmonary Edema
Dyspnea due to pulmonary edema may occur in persons acutely exposed to hypoxia at altitudes of 2000 m or more. The breathlessness usually comes on in the evening or during the night of the first day at high altitude. The patient often gives a history of unaccustomed exertion during the day. Even previously, acclimatized persons returning to high altitude after a stay at sea level may be affected. Dyspnea, cough, frothy pink sputum, and circulatory collapse may develop if treatment is not forthcoming, and mountain climbers have died from the condition. Oxygen inhalation, aid returning to lower altitude are effective methods of treatment. The causative mechanism is almost certainly increased permeability of the alveolocapillary membrane of the lungs. The left atrial pressure has been shown to be normal person with the condition, and left heart failure is not the primary cause. The chest X-ray shows dramatic changes that disappear rapidly with treatment.
How to Diagnose with Aid of Dyspnea?
Certain features may occasionally help to show that dyspnea is due to specific forms of heart disease. In left ventricular failure, as opposed to pulmonary congestion, dyspnea is often associated with a heavy oppressive substernal discomfort, which tends to merge into angina of effort. Patients with mitral stenosis often complain of angina like pain, but only when there is severe pulmonary hypertension. The distinction between dyspnea alone and angina plus dyspnea on the one hand, and between angina alone and dyspnea plus angina on the other, is difficult for both the patient and the physician to make. Acute left ventricular distention causes both severe discomfort in the chest and dyspnea resulting from acute pulmonary congestion. Similarly, acute imbalance between myocardial oxygen supply and demand often causes an acute rise in left ventricular end-diastolic pressure. In left ventricular failure, dyspnea appears first, and the discomfort never occurs without the dyspnea. The discomfort may radiate like anginal pain and is described as a sensation of heaviness, rather than pain, as in angina. Aortic valve disease, hypertension and cardiomyopathy are the commonest causes of the discomfort. The basic mechanism is an increase in the work required from the left ventricle, and acute left ventricular distention may be involved.
Dyspnea in Normal Subjects
Dyspnea normally limits exercise performance in almost everyone. A person becomes conditioned to a certain level of discomfort arising from some particular task, such as walking up a familiar hill. The ease with which dyspnea is provoked varies with the amount of ventilation required for that task. This in turn depends on a person's physical condition, weight, age, and lifestyle. In sedentary persons, the ability of the circulation to distribute maximum blood flow to the exercising muscles while decreasing perfusion of relatively nonessential vascular beds (e.g. adipose tissue, skin, and viscera) is impaired. A simple exercise program combined with weight reduction will often improve performance adequately within 4–6 weeks.7
Dyspnea at Rest
Dyspnea at rest commonly accompanies anxiety. The patient complains that normal breathing is not satisfactory, and it is only by taking deep sighing breaths that relief is obtained. This form of dyspnea is not generally provoked by exertion and is associated with symptoms due to hyperventilation. The deep sighing breaths reduce alveolar and arterial CO2 resulting in respiratory alkalosis. This provokes cerebral arterial vasoconstriction. Increased anxiety, headaches, dizziness, faintness, and even loss of consciousness can result. In addition, the ionized calcium level decreases with respiratory alkalosis, which can provoke numbness and tingling in fingers and lips, tetany, carpopedal spasm, and convulsions (hyperventilation syndrome). The cycle of anxiety resulting in hyperventilation and causing cerebral symptoms, which in turn increase anxiety, is extremely common and can be broken by the old-fashioned remedy of having the patient rebreathe expired air from a bag (recycling).
Supraventricular tachyarrhythmias such as atrial fibrillation rarely cause syncope. The most common cause is bradyarrhythmia, due to sick sinus syndrome or to atrioventricular block, i.e. Stokes-Adams attacks. Drugs, including digoxin, β-blockers and rate-limiting calcium channel blockers, e.g. verapamil, may aggravate attacks. Ventricular tachyarrhythmias often cause syncope or presyncope, especially in patients with impaired left ventricular function.
Chest pain is considered to be very important feature of ischemic heart disuse.
Chest pain occurs in many varieties of heart disease and also in noncardiac diseases. Its correct interpretation is occasionally so difficult that it is almost impossible.
Ischemic Cardiac Pain (Angina Pectoris): It is said in a lighter vein that ischemic cardiac pain can occur anywhere from jaw to umbilicus (Fig. 1.2).
The classic ischemic pain of angina pectoris can be either so obvious that no one has the slightest difficulty in recognizing the symptom and arriving at a correct diagnosis, or so atypical that even after complete investigation, significant doubt about the nature of the pain still exists, although the latter is uncommon. The basic mechanism of ischemic pain is an increase in the demand for both coronary blood flow and oxygen delivery, which exceeds the available supply.
  1. Clinical Features: The original subjective description in the late eighteenth century by William Heberden of his own angina has not been surpassed. Angina of effort is described as a pain or tightness in the chest which is substantial heaviness, burning, and sharp (i.e. severe but not stabbing). It may radiate to the throat, anterior neck and lower jaw (never to the upper jaw), arms, and upper back, but not to the lower spine or below the umbilicus, and rarely to the abdomen alone.
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    Fig. 1.2: Location of pain in angina pectoris
    It more often radiates to the left arm than to the right, and more commonly into both arms than to the right alone. It travels down the ulnar and volar surface of the arm to the wrist but only into the ulnar fingers, never down into the thumb or down the outer surface of the upper arm. Pain may occasionally start in the arms and move to the chest (angina inversus). It occurs more readily after a heavy meal: in cold, windy weather; and with excitement, anger, emotion, or tension. It sometimes comes on more readily with exercise involving the arms. A patient attempting to describe the pain often subconsciously clenches the fists.
  2. Effects of Temperature: In cold weather, walking against the wind with the face unprotected is likely to provoke anginal pain, cold showers or baths may precipitate pain, and brisk toweling after a shower or bath may also provoke it. The sensory effects of temperature on the face are mediated through the fifth nerve and cause reflex autonomic changes in blood pressure and heart rate. Cold showers raise blood pressure and heart rate. Excitement, mental activity, and physical tension such as simple clenching of the fist raise arterial pressure and heart rate, and increase the work of the heart. When the coronary circulation is severely diseased, even these minor circulatory changes are sufficient to provoke anginal pain. Anginal pain comes on more readily in the presence of fever, anemia, or arrhythmia, both bradycardia and tachycardia.
  3. Mechanism of Cardiac Pain: The mechanism producing cardiac pain is not clearly understood. Nonmedullated, small sympathetic nerve fibers running with the coronary vessels are thought to provide the afferent pathway. The pain, like other forms of visceral sensation, is referred to the equivalent spinal segments C8 and Tl–5. Relief of angina following nonspecific surgical procedures such as thoracotomy, mammary artery ligation, and pericardial removal is well recognized but is not consistently found. Although it is thought to be a placebo effect, the severing of afferent autonomic nerves may play a role in relieving pain.
  4. lschemia without Pain: Ischemia without pain is often demonstrable on the ECG. In diabetic patients with autonomic nervous system disease, pain may be absent even though ischemia is severe. Chemical substances such as adenosine may provoke pain by stimulating sympathetic nerve endings. Certain compounds such as nicotine provoke visceral sensations that resemble cardiac pain when they are injected into the circulation in normal subjects.
  5. Variant (Prinzmetal's) Angina: A paradoxical form of angina occurs in some patients as a result of coronary arterial spasm. The pain resembles that of classic angina but occurs at rest rather than on effort. Pain is associated with ST segment elevation rather than depression on the ECG. This form of angina either may be noted in patients with normal coronary arteries when angiography is performed or may occur in the presence of significant coronary atherosclerosis.
Pain of Myocardial Infarction
The pain of myocardial infarction is similar in type and distribution to that of angina of effort, but it is more severe, longer lasting, and associated at times with a feeling of impending death (angor animi) and also with circulatory collapse and shock. The patient may be short of breath, but pain is dominant. Sweating is usually evident.
Pain in Acute Thoracic Disease
Pain similar to that of myocardial infarction also occurs with other acute intrathoracic 9disorders. Aortic dissection can cause severe chest pain. This frequently starts in the back or radiates to it. Acute pulmonary embolism also causes acute chest pain and shock, which may be indistinguishable from that clue to myocardial infarction. The cause is thought to be sudden acute right ventricular distention that stimulates ventricular receptors whose sensory representation resembles that of the left ventricle. Spontaneous pneumothorax and acute pleurisy, especially at the onset of lobar pneumonia also cause chest pain and must be distinguished from pericardial disease, which causes a pain similar in distribution to other cardiac pains but more related to posture. Like pleural pain, pericardial pain is often worse with respiration, but relief obtained from sitting up and leaning forward or even from crouching on all fours face down is particularly suggestive of pericardial pain. Such maneuvers presumably alter tension on the pericardial sac. Like pleural pain, pericardial pain is often relieved when effusion develops.
Pain Associated with Anxiety States
The most troublesome pain to explain is the non-cardiac pain of anxiety states and effort syndrome. The pain is stabbing, felt at the apex of the heart in the left inframammary region, and associated with a feeling of anxiety, breathlessness, and inability to take a satisfying deep breath (Da Costa's syndrome). It seems to be related to the sympathetic nervous system responses of fright. The more knowledge the patient has of heart disease, the more difficult it may be to interpret such pain, because the description may be unconsciously molded to emphasize or minimize a possible cardiac illness.
Pain Associated with Herpes Zoster
The pain of herpes zoster classically precedes the rash, and this diagnosis should be borne in mind, especially in older persons. The pain is radicular in nature, gripping, tight, and constricting, and it may be severe. The diagnosis, which may be suspected when hyperesthesia is found in the affected area, becomes obvious when the eruption develops in a few days.
Musculoskeletal Pain
Musculoskeletal pain due to cervical or thoracic spinal bone or joint disease is readily confused with cardiac pain. Dorsal root pain (girdle pain) tends to be gripping and constricting and causes tightness. It is often associated with local tenderness, whereas angina is not. The presence of degenerative changes in spinal radiograms is no positive evidence of a musculoskeletal origin of the pain, any more than ST and T wave changes on the ECG indicate a cardiac origin. Provocation of the pain by movement, jarring, coughing, and sneezing, and relief of pain by means of massage, heat, and manipulation are useful in suggesting a musculoskeletal origin. Tenderness of the anterior rib cage suggests costochondritis (Tietze's syndrome). Pain, which can be easily pointed as localized by finger is usually non-ischemic/non-cardiac.
Abdominal Pain
Abdominal pain sometimes occurs in patients with heart disease, especially in acute, severe right-sided failure. Hepatic distention is usually invoked as the causative mechanism. Abdominal pain also occurs in angina and in myocardial infarction, but the pain is never solely abdominal.
Esophageal spasm and pain associated with hiatal hernia can also be difficult to interpret. The esophagus and the stomach are innervated by the autonomic nervous system and are capable of causing visceral pain having the same area of radiation as the heart. Any disease of the epigastric viscera can cause chest pain, which can be confused with cardiac pain. The pain of gallbladder disease is also difficult to distinguish from cardiac pain, and since gallbladder disease and coronary disease often coexist, accurate diagnosis of the cause of the pain may be extremely difficult.10
Abnormal awareness of one's own heartbeats is called palpitations. Awareness of the beating of the heart varies with the sensitivity of the patient and the severity of any disturbance of the force or rhythm of the heartbeat. The variation in these factors is great. Awareness of each ectopic beat or even of normal sinus rhythm may be extremely troublesome to some patients. Others may have an extremely forceful heartbeat owing to free aortic incompetence, or they may be subject to episodes of ventricular or supraventricular tachycardia with heart rates of over 180 beats/min without noticing anything. One must therefore differentiate between awareness of forceful heart action and an arrhythmia when the patient complains of palpitations. Most patients notice irregular rhythms more than they do regular tachycardia, but the more rapid the heartbeat, the more likely the patient is to notice an abnormality. In some cases, arrhythmia is only noticed during exercise when the heart rate is rapid.
Associated Symptoms
An important question is whether the palpitations are accompanied by any other symptoms such as dizziness, chest pain, or dyspnea. The functional effect of an arrhythmia may sometimes be a clue to its cause, as for example in mitral stenosis, in which dyspnea is usually provoked when the arrhythmia occurs.
Examination and Recording of an ECG During an Attack
It is imperative to examine any patient with palpitations and record an ECG during an episode of palpitation. Until this has been done, it is essential to keep an open mind concerning the diagnosis. Palpitations often begin abruptly and cease gradually, and because the sinus tachycardia resulting from anxiety caused by the arrhythmia subsides only gradually, the patient may not be aware that the arrhythmia itself has stopped. The functional consequences of an episode of palpitations depend on the duration, the rapidity of the heart rate, and the state of the heart before the episode started. A paroxysm of tachycardia at a rate of about 140 beats/min may be well tolerated for a day or two, but any rapid arrhythmia with an acute onset and lasting for more than a week to 10 days is likely to provoke heart failure, even in healthy young persons. In older, sicker patients, especially those with anemia or hypoxia, a shorter time elapses before serious heart failure develops.
Dizziness and syncope are difficult symptoms to interpret if the patient's consciousness has been impaired and recollection of the events surrounding the attack is hazy. Dizziness and syncope both occur more commonly as benign manifestations than as symptoms of serious disease. They are most commonly due to noncardiac causes such as epileptic seizures, transient ischemic attacks due to cerebral or carotid vascular disease, and cerebrovascular accidents and vertigo due to vestibular disease rather than cardiac disease. A description of the episode from witnesses is of great value, but much can be learned from the circumstances surrounding the episode, as related by the patient. Dizziness is a frequent but not a necessary precursor of syncope, and one or both occur in three main types of conditions involving the cardiovascular system. The commonest form of cardiac syncope is simple vasovagal fainting resulting from certain autonomic nervous system effects. The next most common is cardiac syncope due to arrhythmia or cardiac standstill, in which the heartbeat does not maintain adequate blood flow to the brain. The least 11common is syncope on unaccustomed effort, in which the demand for systemic perfusion exceeds the supply during severe stress, and cerebral ischemia ensues. Effort syncope can also occur in severe pulmonary stenosis, in primary pulmonary hypertension, and in severe aortic stenosis.
Fainting Attacks in Tetralogy of Fallot
A specific form of syncope occurs in patients with tetralogy of Fallot in whom infundibular obstruction is present. Spasm of the muscle of the outflow tract of the right ventricle results in an acute decrease in pulmonary blood flow. Right-to-left shunting of blood through the ventricular septal defect into the aorta increases as a result, and acute severe arterial hypoxemia occurs, leading to loss of consciousness. The factors precipitating the infundibular spasm are not known. Beta-blocking agents such as propranolol are the most effective remedies. The condition is most commonly seen in children but can occur in adults.
Carotid Sinus Syncope
Another rare cause of syncope is excessive sensitivity of the carotid sinus baroreceptor mechanism. Extreme bradycardia and peripheral vasodilatation may occur in response to minor mechanical stimulation of the neck, as in sharp turning of the head or pressure on the neck from too tight a collar. The condition is generally seen in older atherosclerotic men.
Cough Syncope
Syncope sometimes follows a bout of coughing. In this case, the repeated large (> 100 mm Hg) increases in intrathoracic pressure reduce systemic venous return enough to lower the systemic arterial pressure to levels of 50 mm Hg or less. Syncope results from inadequate cerebral perfusion. Either continuous or intermittent coughing spasms may cause these effects, which are commonest in middle-aged male smokers.
Cough and Hemoptysis
Hemoptysis may occasionally be the first symptom of heart disease, and since there can be no hemoptysis without cough, cough is technically the presenting svrnptom. Mitral valve stenosis is the commonest condition in which hemoptysis is the presenting manifestation, and pulmonary congestion, frank pulmonary hemorrhage due to a ruptured vessel, and pulmonary infarction account for almost all cases. Cough without hemoptysis also occurs in any condition causing pulmonary congestion, and cough on exercise is sometimes seen in patients with mitral stenosis. Dry and unproductive cough is usually the earliest manifestation of impending pulmonary edema and precedes the profuse, watery, frothy pink sputum seen in the fully developed picture of acute pulmonary edema.
Cough may also occur as a manifestation of pressure on the bronchial tree in patients with cardiovascular disease. Left atrial enlargement may compress the left main bronchus in patients with mitral valve disease, and it may irritate the recurrent laryngeal nerve on the left side as it hooks under the aorta. Enlarging aortic aneurysms involving the aortic arch and tumors involving the heart may also cause cough when they compress mediastinal structures. Cough that occurs when the patient lies flat and is relieved when the patient sits up is particularly suggestive of pressure on the bronchial tree.
Fatigue is the most difficult cardiac symptom to evaluate. Whereas other symptoms of heart disease have associated outward manifestations. Fatigue is entirely subjective. Although it is 12sometimes due to heart disease, fatigue is far more frequently due to noncardiac causes. Fatigue as a cardiac symptom is almost never of diagnostic value except as an indication of low cardiac output. It is rarely the first or the only symptom of significant organic heart disease, although it is a prominent symptom of neurocirculatory asthenia (Da Costa's syndrome). It commonly accompanies severe long-standing heart disease, especially chronic valvular disease with persistent right heart failure and low cardiac output. It is seen in patients with severe coronary artery disease after myocardial infarction, in mitral stenosis with marked increase in pulmonary vascular resistance, and in primary pulmonary hypertension. Dehydration due to excessive diuretic therapy and potassium depletion are two additional contributing factors.
Nocturia and Polyuria
Nocturia is occasionally the earliest symptom of raised left atrial pressure in left ventricular failure or mitral stenosis. The exact mechanism is not known, but transfer of fluid from the legs to the thorax when the patient lies down may play a part. Reflex connections have been demonstrated between left atrial receptors and the central nervous system, and the efferent pathway is known to involve the kidneys. Nocturia implies the passage of an abnormally large amount of urine at night, rather than an increased frequency of micturition at night, as occurs in prostatic disease. In the healthy state, the cardiac output is sufficient to provide adequate renal blood flow during the day, and urine flow at night is therefore conveniently reduced to a minimum. It may be that in early heart failure this mechanism breaks down because of inadequate cardiac output. There is also a connection between cardiac function and urinary output in patients with paroxysmal tachycardia due to any cause. Some patients note an increased urinary volume within 15–30 minutes of the start of tachycardia. The urine is of low specific gravity. The possibility of a reflex mechanism involving left atrial distention remains to be proved.
Exertional dyspnea that is relieved by squatting during recovery from exercise strongly suggests the diagnosis of tetralogy of Fallot. Squatting is seldom seen after puberty. It is a convenient means of increasing systemic venous return by lowering the patient's center of gravity and counteracting any tendency for blood to pool in the veins of the legs and pelvis. The central blood volume and pulmonary blood flow, both are increased by squatting. It has been shown that it is the change in the amount of venous return and not the change in posture which is important, because squatting in water has no hemodynamic effect. Thus, in tetralogy of Fallot, squatting increases the arterial pressure and provides more blood flow to the lungs by decreasing the right-to-left shunt across the ventricular defect. It provides more pulmonary blood flow and a greater left ventricular inflow and also raises the arterial oxygen saturation by reducing the shunting effect. A similar result can be obtained by lying down, but children find it easier to squat after exertion. It is the pooling of blood in the legs in the upright position after stopping exercise that is the primary problem; if this does not occur, as in patients with a large pulmonary blood volume, the benefit from squatting is not seen.
Surprisingly squatting does not help when patient is in water.
Hoarseness as a manifestation of heart disease is seldom, if ever, a presenting symptom. It occurs in cardiac patients with gross left atrial enlargement in mitral valve disease, in giant left atrium, and in aortic dissection. All of these conditions cause pressure on the left recurrent laryngeal nerve and result in hoarseness. Hoarseness is also seen in patients with myxedema, in whom it may be the first clue to diagnosis.13
Since edema due to cardiac disease is a result of right heart failure, it is seldom seen early, because right heart failure is a late development in heart disease. A complaint of edema as a primary symptom implies a noncardiac cause such as venous stasis, thrombophlebitis. nephrotic syndrome, lymphedema, or idiopathic edema. Edema is seldom seen in patients with congestive heart failure under good medical control now that effective diuretic therapy is available. Right heart failure can be surprisingly severe, with hepatic enlargement, ascites, and a raised venous pressure, but no significant pitting edema of the ankles.
Cyanosis is more a sign than a symptom, although patients do occasionally complain of blueness of the extremities, face, and lips. Cyanosis may be peripheral and associated with a low cardiac output, peripheral vasoconstriction, and a feeling of coldness. In this case, the blueness is due to a high concentration of reduced hemoglobin in the blood in the veins of the skin, and arterial saturation is normal. In true central cyanosis, the arterial oxygen saturation is reduced because of right-to-left shunting or lung disease. In this case, the patient's extremities are often warm, or, if they are made warm, the blue color does not disappear.
Loss of Weight (Cardiac Cachexia)
Loss of weight is not a presenting symptom of heart disease, but it does occur in chronically ill cardiac patients, especially when the cardiac output is low. It is probably related to secondary anorexia. The patient characteristically loses weight from the limbs and accentuates fluid in the abdomen. It is difficult to establish the true extent of the cachexia, because the accumulation of fluid tends to maintain total body weight.
The patient's overall disability is conventionally expressed in terms of the New York Heart Association's criteria for functional capacity and therapeutic class.
Functional Capacity (Four Classes)
Class I: No limitation of physical activity.’ Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
Class II: Slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
Class IV: Unable to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency, or of the anginal syndrome, may be present even at rest. If any physical activity is undertaken, discomfort is increased.
While this classification gives a good overall indication of the patient's status, many physicians prefer to subdivide class II into classes lla and lIb. In class lla, the patient can keep up with others walking on the flat but has limitation on more severe exercise such as climbing stairs. In class llb, the patient has slight limitation on all forms of physical activity.
Therapeutic Classification (Five Classes)
Class A: Physical activity need not be restricted.
Class B: Ordinary physical activity need not be restricted, but unusually severe or competitive efforts should be avoided.14
Class C: Ordinary physical activity should be moderately restricted, and more strenuous efforts should be discontinued.
Class D: Ordinary physical activity should be markedly restricted.
Class E: Patient should be at complete rest, confined to bed or chair.
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