INTRODUCTION
History taking is a scientific art of data collection. Appropriate history taking is not only the art of data collection; it is a technique of establishing contact at a personal level and touching the emotions and problems (beyond medical) of the patient. It is one of the greatest means of establishing interpersonal relationship. Therefore, elicitation of the history should be done by the cardiologist himself. Patient's behavior and body language should be noted while elaborating the history.
This also helps in selecting appropriate investigational techniques and collating the data collected from them. Investigations supplement but do not supplant appropriate clinical examination (which includes eliciting the history and conducting a physical examination). The history is the richest source of information regarding the patient's illness.1 Proper history taking establishes a bond between the patient and the physician.2 In our country, history taking has some special problems. This is due to difference in culture, religion, language, literacy status, etc. from region to region, state to state, and even district to district. The doctor has to have special patience when eliciting history from a patient who has linguistic barrier, low intelligence, premonition and fixed ideas about a disease, etc.
Documenting the history in a patient suffering from cardiovascular disease is basically the same as in case of Internal Medicine with some special emphasis on same cardinal symptoms of cardiac patients. This also requires differentiating the features that may arise from any other system (e.g., dyspnea of cardiac and respiratory system).
FUNCTIONAL CLASS
One important aspect of cardiac history taking is placing the patient in a particular functional class (keeping in mind the limitations and fallacies) (Table 1). This helps in present assessment and future follow up about the progress (natural course and effect of treatment). There are several methodologies, a few of which will be discussed in short.
Canadian Cardiovascular Society Functional Classification of Angina Pectoris5
This classification is based on the functional class in relation to angina only (Table 2).
Specific Activity Scale6
Specific activity scale denotes the activity in relation to usual daily life (Table 3).
Class I Activities
- Carry at least 24 pounds up to eight steps: 10 METS
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TABLE 1 New York Heart Association Functional Classifications3,4 Functional capacityObjective assessmentClass IPatie nts with cardiac disease but without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue. Palpitation dyspnea, or angina painNo objective evidence of cardiovascular diseaseClass IIPatients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or angina painObjective evidence of minimal cardiovascular diseaseClass IIIPatients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or angina painObjective evidence of moderately severe cardiovascular diseaseClass IVPatients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or the angina syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increasedObjective evidence of severe cardiovascular diseaseTABLE 2 Functional Class at Angina5 Class IOrdinary physical activity does not cause angina, such as walking and climbing stairs. Angina with strenuous or rapid or prolonged exertion at work or recreationClass IISlight limitation of ordinary activity. Walking or climbing stairs rapidly, walking Uphill, walking or stair climbing after meals, or in cold, or in wind, or 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 stairs at a normal pace and in normal conditionClass IIIMarked limitation of ordinary physical activity. Walking one or two blocks on the level and climbing one flight of stairs in normal condition and at normal paceClass IVInability to carry on any physical activity without discomfort; anginal syndrome may be at restTABLE 3 Specific Activity Scales6 Class IPatient can perform to complete and activity requiring >7 metabolic equivalent (MET)Class IIPatient can perform to complete any activity requiring >5 METS but cannot perform to complete activity requiring >7 METSClass IIIPatient can perform to complete any activity requiring >2 METS but cannot perform to complete activity requiring >5 METSClass IVPatient cannot perform to complete any activity requiring >2 METS - Do outdoor work (shovel snow, spade soil): 7 METS
- Do recreational activities like skiing, basketball, touch football, squash handball, etc.: 7–10 METS
- Jog or walk 5 miles an hour: 9 METS.
Class II Activities
- Carry anything up a flight of eight steps without stopping: 5.0–5.5 METS
- Have sexual intercourse without stopping: 5–5.5 METS
- Garden rake weed: 5–6 METS
- Walk at a 4-mile per hour rate on level ground: 5–6 METS.
Class III Activities
- Walk down a flight of steps without stopping: 4.5–5.2 METS
- Shower without stopping: 3.6–4.2 METS
- Strip and make bed: 3.9–5 METS.
The Canadian Cardiovascular Society Severity of Atrial Fibrillation Scale7
The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation (SAF) Scale is similar to the CCS Angina Functional Class. The CCS-SAF score is calculated using three steps:5
- Symptoms (S): To assess the symptoms
- Association (A): To decide the association of symptoms with atrial fibrillation
Six-minute Walking Test9
This is a reliable, inexpensive, and simple objective test to assess functional capacity in patients with moderate to severe heart failure (HF). Various test protocols, like 2-minute, 6-minute, and 12-minute walking tests have been used. The 6-minute test was first standardized by Lipkin and associates.
- The test is carried out in a level enclosed corridor 20 m long
- Each patient is instructed to cover as much ground as possible in 6 minutes
- Patient is told to walk continuously, if possible but that they could slow down or stop, if necessary
- The aim is that at the end of the test, the patients believe that they could not have walked any further in the 6 minutes
- The test may be repeated twice on the same day with at least 3–4 hours between tests.
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This test may be less discriminating than the maximal or submaximal exercise test, but its simplicity and inexpensiveness are unique. It can be used as serial monitoring of patients with heart failure to assess the treatment.
Technique of History Taking
The patient should be allowed to talk freely about his problems regarding the illness and then appropriate questions are to be asked, so that relevant information is obtained regarding present and past history, personal and occupational history, nutritional history, and history about other systems. History should be obtained about the possible etiological factors and response to treatment. A detailed general medical history has to be collected. There may be effects of cyclic vomiting syndrome (CVS) illness upon other systems and effects of other systemic illness(es) into the CVS; history taking should be in a dialogue fashion, rather than putting some questionnaire, so that assessment about the patient's mental status is done and the confidence of the patient is won.
Cardinal symptoms of CVS disease include dyspnea, chest pain or discomfort, syncope, palpitation, swelling of feet, cough and hemoptysis, and easy fatigability, etc.
DYSPNEA
This is defined as difficulty in breathing- also described as “shortness of breath,” breathlessness, etc.
- Abnormally uncomfortable awareness about one's own breathing
- Varies in nature and degree—may vary from dyspnea on significant exertion to dyspnea at rest to dyspnea on lying down compelling one to sit up and pant (orthopnea)
- Cardinal symptom of cardiac and respiratory system
- At times it becomes difficult to differentiate between “normal” breathlessness on exertion to pathological dyspnea. Associated features of cardiac and/or respiratory disorder often help to decide
- Borg and Noble have developed a scale which is helpful in quantitating the severity of dyspnea
Disorders that cause dyspnea due to different mechanisms include the following:
- Pulmonary
- Airflow limitation [chronic obstructive airways disease (COAD)/bronchial asthma]
- Restrictive pulmonary circulation (pulmonary embolism, pulmonary venous, and/or arterial hypertension)
- Cardiac
- Coronary valvular
- Myocardial (heart failure)
- Anemia
- Metabolic (uremia) obesity
- Anxiety and/or depression malingering
- Deconditioning (inactivity, prolonged bed rest, etc.)
Sudden development of dyspnea includes many causes; important are the following:
- Pulmonary embolism
- Pneumothorax
- Acute pulmonary edema pneumonia
- Bronchial asthma (episodic), airway obstruction, etc.
Assessment of Dyspnea
- Mode of onset
- Duration
- Progress
- Severity
- Functional status
- Special character
- Relieving factor
- Associated symptoms
Severity Assessment
Severity of symptom is scaled by the guideline of American Thoracic Society (Table 5).
Formal Measurement of Dyspnea
Modified Borg scale is a reliable assessment tool for dyspnea. Patients have to find that the language in this scale adequately expressed their dyspnea (Table 6).
Ventilatory capacity is measured prior to exercise, ventilation is measured during exercise, and these are related to the intensity of dyspnea rated using Visual Analog Scale (VAS), which consists of a line, usually 100 mm in length, placed either horizontally or vertically upon a page, with anchors to indicate extremes of a sensation.7
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The anchors on the scale have not been standardized, but phrases such as “not breathless at all” to “extremely breathless” and “no shortness of breath” to “shortness of breath as bad as can be” are frequently used. Scoring is accomplished by measuring the distance from the bottom of the scale (or left side if oriented horizontally) to the level indicated by the subject. The reliability and validity of the VAS as a measure o dyspnea has been reported (Fig. 1).10
- Inspiratory dyspnea suggests upper airway obstruction, whereas expiratory dyspnea suggests obstruction of the lower airways
- Exertional dyspnea is often organic in nature (cardiac or respiratory), whereas dyspnea only at rest is due to functional causes (absence of signs). However, one should remember dyspnea developing at rest and aggravating with exertion, particularly, when sudden, may indicate pneumothorax, pulmonary embolism, pulmonary edema, bronchial asthma, and other serious causes
- A history of relief of dyspnea by bronchodilators and corticosteroids (inhaled or oral) suggests bronchospasm, whereas that relieved by rest, diuretic, and/or digitalis suggests heart failure.
Differentiation Between Cardiac and Pulmonary Dyspnea
- In many patients with dyspnea, there is obvious clinical disease either in the heart or lungs and differentiation is easy; but in some this may be difficult
- Dyspnea due to COAD tends to develop more gradually than in case of heart disease (exceptions—patients with COAD with episodes of infections bronchitis, pneumonia or pneumothorax, exacerbation of asthma, etc.)
- Like patients with HF, patients with COAD may be awaken at night with dyspnea but this is often associated with sputum production (different from pinkish frothy sputum of pulmonary edema) and the patient is relieved on coughing out the expectorate. In COAD cough precedes dyspnea, whereas in HF, dyspnea precedes cough
- When both causes are present (e.g., bronchial asthma patients developing HF), differentiation becomes difficult and management of both problems becomes important
- Aggravating and relieving factors have already been discussed
- Anemia, infection, arrhythmia, thyrotoxicosis, etc. aggravate HF and dyspnea. In lung disease also these factors are important, but less dramatic except in case of pneumonia.
Patients of pulmonary embolism usually develop sudden breathlessness, with anxiety, apprehension, palpitation, pleuritic chest pain, and/or hemoptysis. A feeling of fainting spell may be present. Acute coronary syndrome may be associated with dyspnea; similarly dyspnea on exertion may be an angina equivalent. Aggravating and relieving factors become important in such cases.
Dyspnea occurring in a particular posture and getting relieved by adopting another may be a feature of left atrial myxoma and ball-valve thrombus in LA.
Dyspnea relieved by squatting is a feature of Tetralogy of Fallot (TOF) and Tetralogy physiology.
Gradually progressive exertional dyspnea with insidious onset is the characteristic of mitral stenosis. This is associated with fatigue and decreased exercise tolerance. With severe/critical MS, dyspnea may occur with ordinary activity (NYHA Class III). Paroxysmal nocturnal dyspnea (PND) is characteristic. Dyspnea may be associated with cough, wheezing, and occasional recurrent hemoptysis. Chest infection is common and embolic phenomena may happen. Frank pulmonary edema may happen, which may be precipitated by exercise, emotion, respiratory infection, fever, pregnancy, and AF or other atrial arrhythmias with rapid ventricular rate.
The patient's relatives should be enquired about any signs of sleep-related) disordered breathing, like loud snoring and/or periods of apnea.
Orthopnea
It is defined as dyspnea during recumbency. In the horizontal position, there is redistribution of blood volume from the lower extremities and splanchnic beds to the lungs. In normal individuals, this has little effect, but in patients in whom the left ventricle, because of disease, cannot pump the additional volume out, there is a significant reduction in vital capacity and pulmonary compliance with resultant shortness of breath.
Besides, in heart failure, there may be reabsorption of edema fluid from previously dependent parts of the body, overloading the congested pulmonary circulation. Pulmonary congestion decreases when the patient assumes a more erect position, and this is accompanied by an improvement in symptoms.
Paroxysmal Nocturnal Dyspnea
In a typical episode, patient is suddenly awakened 2–3 hours after going to sleep, gasping for air. He quickly sits up and puts his feet over the side of the bed, coughing, wheezing, and sweating. He gets relief only after sitting for 10–15 minutes.
Pathophysiology is similar to that for orthopnea. The failing left ventricle or stenotic mitral valve is suddenly unable to match the output of a more normally functioning right ventricle, this results in pulmonary congestion. Other mechanisms include decreased responsiveness of the respiratory center in the brain, decreased adrenergic activity in the myocardium during sleep and nocturnal arrhythmia.
Commonest diseases are mitral stenosis, other valvular heart diseases, ischemic heart disease, and dilated cardiomyopathy.
Noncardiac causes of nocturnal dyspnea are nocturnal asthma, COPD, pulmonary embolism, obstructive sleep apnea, anxiety, and hyperventilation. A patient symptomatic with PND is classified as NYHA Class 3.
Trepopnea
May occur with asymptomatic lung disease when the patient lies with the more affected lung down because of gravitational redistribution of blood flow. Left atrial myxoma, by obstructing mitral inflow in lateral decubitus can cause trepopnea.
Platypnea
Upright posture causes increased wasted ventilation ratio and dyspnea in COPD. Platypnea in association with orthodeoxia (arterial deoxygenation in the upright position) has been reported, occasionally in cyanotic 9congenital heart disease. Probable explanation is slight decrease in systemic blood pressure in the upright position, resulting in increased right-to-left shunting.
CHEST DISCOMFORT AND/OR PAINS
This is one of the commonest cardiac complaints. However, it could be cardiac or noncardiac and thoracic or extrathoracic. Causes also vary in the OPD and emergency set up. Associated features often help to differentiate the cause cardiac pain could be ischemic or nonischemic. History has to be noting multiple points and is the mainstay in formulating an idea and planning subsequent physical examination and conducting investigations. Location, radiation, and character of the pain, aggravating and relieving factor, duration, reproducibility, and gesture (e.g., Levine sign) are all important factors.
A reading through all the causes that may present as chest pain or upper abdominal discomfort or pain is essential before making an attempt to differentiate such a symptom.
Angina Pectoris
This is due to increased myocardial oxygen requirement or decreased supply, i.e., demand and supply mismatched. Nature may be variably described as chocking, pressing, squeezing, burning, bursting, strangling, constricting, oppressing, band-like “gaseousness,” “indigestion,” etc. It is located retrosternally with or without radiation to inner side of left, right, or both areas, to either side of the chest, epigastrium, throat, jaw, and teeth. Pain only in the area(s) of reference, rather than retrosternal, may be a presentation. Duration is 5–15 minutes precipitated by exertion or emotion and relieved by rest and/or nitrate. There is no area of pointed pain or tenderness (association of multiple causes should be remembered, however). The degree of exertion that precipitates the angina (angina threshold) varies from day-to-day or from morning to evening. When the threshold is quite variable, does not follow a pattern and is prominent at rest, this may be due to coronary artery spasm (variant or Printzmetal angina).
The typical episode of angina pectoris usually begins gradually and achieves the peak intensity over a period of minutes, then gradually subsides with reducing the degree of exertion or stopping. For a stable angina pectoris, it is unusual to reach the maximum intensity, within seconds, and the patient prefers to decelerate or stop. Chest discomfort that occurs while walking in the cold, uphill and upstairs is suggestive of angina pectoris.
Pleuritic pain, pain localized to the tip of a single finger, pain reproduced by movement, presence of tenderness, etc. go against angina pectoris. Very brief pain and that persisting for a long time are also against typical angina pectoris.
Pain relieved by nitrates suggests angina; however, pain of esophageal origin may also be relieved by nitrates. This happens within minutes usually in case of angina. However, nonischemic pain or very severe ischemic pain may require 9–10 minutes or beyond to get relieved. This may happen with acute coronary syndrome as well. The event of walk-it-off, first-effort, or warm-up angina requires a varying degree exertion in different times of the day (usually more severe or less-threshold pain/discomfort in the morning). Decubitus angina is a severe form of angina, occurring with the patient on lying down.
Unstable angina has any one or more of the following characteristics: (i) it is described as pain rather than discomfort and is more severe, long lasting (more than 20 minutes) and occurring more frequently or with less exertion and even at rest, (ii) occurs in a crescendo pattern often awakening the patient from sleep, (iii) less readily relieved.
Pain of acute myocardial infarction (AMI) is longer lasting (often more than half an hour), described as a severe pain screwing or squeezing in nature, often located or radiating into the areas as described in case of angina. Patient becomes restless, not getting relief in any position, not relieved by nitrate, associated with profuse cold sweating, hypotension or shock, dyspnea, nausea, and/or vomiting. Atypical presentations occur more frequently in NSTEMI, diabetic, elderly, patient with H/o stroke and ladies. At times this is ignored as upper gastrointestinal disturbance, “gaseousness” or flatulence, acidity, etc. Epigastric pain may occur in AMI. An attack of AMI may be from painless, silent MI to unbearable pain leading to tossing on bed and rubbing the chest in search of relief in vain. Severity of infarct presentation may be from asymptomatic, silent, to sudden death. Pain of AMI may be resultant of that 10of unstable angina. This may happen spontaneously or precipitated by exertion or emotion. Many types of presentation may be there; therefore a high degree of suspicion is required.
Pain of acute pericarditis is often preceded by a history of viral upper respiratory infection. The pain is sharper than anginal chest discomfort more left sided than central, better localized, and frequently referred to the neck. This pain lasts for hours and not much affected by exertion but aggravated by deeper breathing, changing posture in bed, twisting, or swallowing. The pain aggravates on lying down and lessens on sitting up and leaning forward. Tuberculosis still remains a common cause of pericarditis in our country. Chronic Constrictive pericarditis or pericardial effusion may be a resultant of acute pericarditis.
Psychogenic chest pain may be a manifestation of hysteria or underlying anxiety. Cardiac neurosis is also known as Da Costa's Syndrome or neuro-circulatory asthenia. The pain is atypical and localized, and characterized by multiple short lasting stabbing pains or persistent localized pain associated with local tenderness on the apex or somewhere nearby. The characteristic aggravation by exertion and relief by rest is absent. This may be associated with palpitation, dyspnea, “sighing,” and tingling and numbness of the limbs and general weakness. Anxiety and panic may be manifest or masked. Analgesics, tranquillizers, antidepressants, and other atypical nonspecific agents may help in relieving the pain, tenderness, and associated symptoms.
Chest wall pains due to myositis or fibromyalgia, costoconditis, Tietze syndrome, herpes zoster, etc. have their characteristic local features.
Chest pain in a very good example of when to use the mnemonic SOCRATES.11
- Site
- Onset
- Character (you may have to provide the patient a few options to describe the nature)
- Radiation
- Alleviating factors
- Timing
- Exacerbating factors
- Severity scale (1–10) (associated symptoms).
But with all these analysis, one thing has to be remembered and that is multiple causes may be associated with ischemic heart disease, causing chest pain.
PALPITATION
Palpitation can be defined as uncomfortable awareness of one's own heartbeat. Patient describes the feeling as skipped or missed beat and a pounding sensation in chest. Most common causes of palpitation are arrhythmia and anxiety. Though, occasionally, it may indicate life-threatening arrhythmia, most often it is a benign symptom.
Etiology
- Cardiac cause: 45% (arrhythmia: 40%; other cardiac causes: 50% cases)
- Anxiety or panic disorder: 30% cases
- Medications: 5% cases
- Other noncardiac causes: 5% cases
- No specific causes: 15% cases.
Cardiac Arrhythmias
Bradycardia and tachycardia, premature ventricular and atrial contractions, sick sinus syndrome, and advanced atrioventricular block, or ventricular tachycardia can cause palpitation. Arrhythmia often, does not cause palpitation. Episodes of ventricular tachycardia and supraventricular tachycardia may not only be perceived as palpitations but also can be asymptomatic or lead to syncope.
Anxiety or Panic Disorder
It is characterized by recurrent unexpected panic attack, more common in relatively younger women who somatize more frequently. However, one should not overdiagnose anxiety and should do a total evaluation, as arrhythmia can coexist with anxiety. Anxiety causes catecholamine surge and may induce VT.
Nonarrhythmic Cardiac Cause
Regurgitant lesions, like aortic and mitral regurgitation and lesions, which cause volume-overload, like atrial 11septal defect (ASD) and ventricular septal defect (VSD) are important causes of palpitation.
Extracardiac Cause
Fever, anemia, hypoglycemia, pheochromocytoma, and hyperthyroidism are some common noncardiac causes of palpitation.
Drugs
Beta-agonist, theophylline, ephedrine, cocaine, alcohol, smoking, and caffeine cause palpitation.
Approach
Patient should be asked to describe the symptom in every detail. Its duration, onset and termination, slow or rapid, regular or irregular, activity and posture, associated giddiness, syncope, angina, or dyspnea should be evaluated. Examiner himself can demonstrate or the patient may be asked to tap out the rhythm.
Symptoms
- Flip-flopping in chest: Suggestive of atrial or ventricular ectopic
- Fluttering in chest: Suggestive of atrial or ventricular tachyarrhythmia
- Vibrating neck: Suggestive of tachyarrhythmia, where atria are contracting against closed AV valves, producing large cannon waves. Patient feels rapid regular vibrating or pounding sensation in neck and a bulging can be seen, called frog sign. Most common cause is AV nodal re-entrant tachycardia.
Circumstances
Palpitation and Syncope
Palpitation turns in an ominous symptom when palpitation is associated with dizziness, presyncope, or syncope. Ventricular tachycardia is a strong probability. Supraventricular tachycardia can occasionally cause syncope, immediately after the onset. Rapid heart rate with low cardiac output and acute vasodilatation are the mechanism of syncope.
Palpitation and Dyspnea
Usually indicate arrhythmia associated with ventricular dysfunction, aortic stenosis, hypertrophic cardiomyopathy (HCM), mitral stenosis, and ischemic heart disease.
Palpitation and Posture
Atrioventricular nodal reentry tachycardia (AVNRT) may be initiated by standing posture from bending over and may be terminated after lying down. Patient with regurgitant lesions feels the pounding sensation more in lying or left lateral decubitus.
Palpitation and Catecholamine Excess
Exercised induced disproportionate rapid palpitation may be due to catecholamine induced idiopathic ventricular tachycardia, atrial fibrillation, or supraventricular arrhythmia. Postexercise palpitation may occur due to vagal induced atrial fibrillation. Mild exertion or emotional stress can cause palpitation in young female patient due to hypersensitivity of beta-adrenergic stimulation. It is called inappropriate sinus tachycardia.
Fatigue
Fatigue is the manifestation of low cardiac output, rather than high ventricular filling pressure in heart failure. Fatigue does not always indicate symptom of heart failure and may be a nonspecific symptom. Feeling of fatigue, even at rest indicates anxiety state, rather than low output, which is manifested as fatigue on exertion.
Fatigue results from inadequate tissue oxygen delivery due to reduced cardiac output. Its exact mechanism in heart failure is due to skeletal muscle myopathy, due to the effect of endothelial dysfunction and systemic inflammatory responses. This myopathy sets in ergoreflex, a muscle reflex stimulated by work done.
Aggressive diuresis in heart failure leading to potassium depletion can cause significant fatigue.12
Edema and Weight Gain
Edema is a late sign of heart failure. It is usually preceded by dyspnea. At the same time, it is early to go with decongestant medications. Distribution of edema fluid is determined by local factor. In an ambulant patient, due to hydrostatic pressure, edema occurs in legs in daytime and diminishes at night. Fluid shifts from legs to sacral region in a patient, who is confined to bed. As tissue pressure around the eyes of children is low, fluid is accumulated in them as periodical edema.
There may be a weight gain of around 10 pounds before appearance of edema. Acute change in weight is a good marker of fluid balance, a gain indicating congestion and loss indicating response to decongestant medications.
Congestion is not always associated with edema or weight gain. Pulmonary congestion may occur in MS or acute hypertensive heart failure, in euvolemic patient.
Hemoptysis and Cough
Hemoptysis: Assessment (Box 3)
One should decide whether it's a brisk bleeding or slow bleeding. Brisk bleeding means coughing out large volume of liquid blood. Brisk bleeding usually indicates arterial bleeding associated with focal ulceration of the bronchus, which may occur in bronchiectasis, bronchogenic carcinoma or aortic aneurysm rupturing into tracheobronchial tree. Slow bleeding means coughing out of small quantities of dark or clotted blood. Slow bleeding indicates bleeding from low-pressure vessel or old bleeding. Common source is bronchial venous system, secondary to mitral stenosis. Blood, intimately mixed with pus, indicates deep-seated pulmonary infection.
However, blood-streaked sputum may be due to cardiac cause. Source is the pulmonary capillaries, which yield to high intravascular pressure. This is the initial stage of pulmonary edema, interstitial pulmonary congestion. Frank pulmonary edema leads to pink frothy sputum.
Mitral Stenosis
It is the commonest cardiac cause of hemoptysis. It is an early feature of mitral stenosis and occurs in 10–35% cases. Varicose bronchial veins are formed by flow from pulmonary veins to azygos and hemiazygos veins. Flow through those veins depends upon the gradient between left atrium, pulmonary veins and right atrium, azygos veins. Rupture of those endobronchial vessels leading to hemoptysis is one of the mechanisms. “Winter bronchitis” and pulmonary infarction are the other possible mechanisms.
Eisenmenger Syndrome
Overall incidence is 33%. Incidence is uncommon before 20 years of age and almost 100% over 40 years. Neither the high pulmonary arterial pressure, nor the initial high pulmonary flow is responsible for hemoptysis. This is evidenced from the fact that incidence of hemoptysis in idiopathic hypertension is just 4% and in uncomplicated ASD is around 3%. A combination of PAH and cyanosis is probably the causative factor.
Cough: Assessment
A dry, nonproductive cough, more on recumbent posture, may be a manifestation of heart failure. A single bout of cough may be a presentation of ventricular premature beat. Cardiac drugs causing chronic cough are ACEI, ARB, β-blockers, and aspirin.
Cough due to pulmonary edema or PND is associated with frothy, pink, blood-tinged sputum. Cough due to chronic bronchitis is associated with white, mucoid sputum and cough due to pneumonia is associated with thick, yellow sputum.13
SYNCOPE12
Syncope is a temporary loss of consciousness usually related to insufficient blood flow to the brain, completely reversed in a short time. This occurs due to transient cerebral ischemia due to hypotension and low perfusion pressure (Table 7).
It can be benign or a symptom of an underlying serious medical condition and warning against SCD.
Higher-risk Syncope
Cardiac syncope is a higher risk in: people older than 60 years; male sex; presence of known heart disease (structural, HOCM, arrhythmic, long or short QT, Brugada's syndrome, etc.); brief palpitations or sudden loss of consciousness; fainting during exertion; fainting while supine; an abnormal cardiac exam (obstructe or dilated heart, etc.); or family history of inheritable conditions. Other existing conditions and medications (e.g., antiarrhythmic drugs with proarrhythmic effects, etc.) used are particularly important in older patients.
History and physical examination are the most specific and sensitive ways to evaluate syncope. The diagnosis is achieved with a thorough history and physical examination in about 50–85% of patients. No single laboratory test has greater diagnostic attribute.
A detailed account of the event must be obtained from the patient and onlooker(s) if any. The circumstances during the episode have to be analyzed: the precipitating factors, what the patient was doing prior to the event and the patient's position when it occurred, etc.
Precipitating factors may include sight of blood, fatigue, sleep or food deprivation, warm ambient environment, dehydration, alcohol consumption, pain, and strong emotions such as fear or apprehension, etc.
Activity prior to syncope may give a clue as to the etiology of symptoms. Syncope may occur at rest; with change of posture; on exertion; after exertion; or with specific situations such as shaving (carotid sinus hypersensivity), coughing (cough syncope), voiding (micturition syncope), or prolonged standing (pooling of blood in lower parts of body). Syncope occurring within 2 minutes of standing suggests orthostatic hypotension (BP has to be measured in supine and standing position).
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Ask whether the patient was standing, sitting, or lying when the syncope occurred. Syncope while seated or lying is more likely to be cardiac.
The following questions have to be answered:
- Was loss of consciousness complete? (Incomplete in presyncope.)
- Was loss of consciousness with rapid onset (occurs suddenly in cardiac arrhythmias) and short duration?
- Was recovery spontaneous, complete, and without sequelae? (Postictal phase occurs in seizure.)
- Was postural tone lost? (In epilepsy usually tone is increased.) (In hysteric episodes, patient resists movement initiated by accompanying personnel.)
If the answers to these questions are positive, the episode has a high likelihood of being syncope. The clinician should attempt to gather all information with respect to symptoms preceding the syncope.
Prior faintness, dizziness, or light-headedness occurs in 70% of patients experiencing true syncope. Other symptoms, such as vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias, may also occur in the presyncopal period.
Symptoms of nausea or diaphoresis prior to the event may suggest syncope rather than seizure when the episode was not witnessed, whereas an aura may suggest seizure (Table 8).
Patients with true syncope do not remember actually falling to the ground. Presyncope involves the same symptoms and pathophysiology but terminates prior to loss of consciousness and can occasionally include loss of postural tone. The duration of symptoms preceding a syncopal episode has been reported to be an average of 2.5 minutes in vasovagal syncope and an average of only 3 seconds in arrhythmia-related cardiac syncope.
Clinicians should specifically inquire as to symptoms like, exertional onset, chest pain, dyspnea, low back pain, palpitations, headache, focal neurologic deficits, diplopia, ataxia, or dysarthria, etc., prior to the syncopal event.
Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma, incontinence, or myalgias.
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A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, seizure, conversion reaction, etc.
Witnesses may help in estimating the duration of unconsciousness and also in assessing whether the patient experienced postevent confusion.
Post-event confusion is the most powerful tool for discriminating between syncope and seizure. A postictal phase suggests that a seizure has occurred. Postevent confusion has been described with syncope, but the confusion should not last more than 30 seconds. Seizure like activity can occur with syncope if the patient is forcibly held in an upright posture.
A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:
- Agents that affect cardiac output (e.g., β-blockers, digitalis, antiarrhythmics, etc.)
- Agents that prolong the QT interval (e.g., tricyclic antidepressants, phenothiazines, quinidine, amiodarone, etc.)
- Agents that alter sensorium (including alcohol, cocaine, analgesics with sedative properties, etc.)
- Agents that alter serum electrolytes (especially diuretics).
Inquiry must be made into any personal or familial past medical history of cardiac disease. Patients with h/o MI, arrhythmia, structural cardiac defects, cardiomyopathies, or congestive heart failure (CHF) have a uniformly worse prognosis than other patient groups.
Details of syncope evaluation are beyond the scope of this chapter.
RHEUMATIC FEVER
It occurs a few weeks after streptococcal sore throat. It affects mainly the school-age children and adolescents. The symptoms vary. The patient can have few symptoms or several, and symptoms can change during the course of the disease. The onset of rheumatic fever usually occurs about 2–4 weeks after a strep throat infection. Rheumatic fever signs and symptoms, which result from inflammation in the heart, joints, skin, or central nervous system, can include the following:
- Fever
- Painful and tender joints—most often in the knees, ankles, elbows, and wrists (large joints)
- Pain in one joint that migrates to another joint (migratory arthritis, flitting from joint to joint)
- Red, hot, or swollen joints (arthritis) or simple arthralgia
- Small, painless bumps (nodules) beneath the skin
- Chest pain
- Heart murmur
- Fatigue
- Flat or slightly raised, painless rash with a ragged edge (erythema marginatum) (rare in our country)
- Jerky, uncontrollable body movements (Sydenham chorea, or St. Vitus’ dance)—most often in the hands, feet, and face
- Outbursts of unusual behavior, such as crying or inappropriate laughing, that accompanies Sydenham chorea.
About half of the patients suffering from rheumatic valvular heart disease do not give history of classical rheumatic fever. In India, the symptoms of rheumatic fever vary widely. A close differential diagnosis is poststreptococcal reactive arthritis and other different arthritidis.
AORTOARTERITIS
The signs and symptoms of aortoarteritis often occur in two stages.
Early Stage
In the first stage, the patient is likely to feel unwell with fatigue, unintended weight loss, general aches and pains, mild fever, etc. Everyone does not have these early signs and symptoms. It is possible for inflammation to damage the arteries for years before the patient realizes something is wrong.
Late Stage
During the late stage, ischemic symptoms appear and these depend upon the territory involved. Weakness or pain in the limbs especially during and after use, lightheadedness, dizziness or fainting, headaches, memory problems, cognitive problems, shortness of breath, visual changes, systemic and rarely pulmonary arterial hypertension, difference in blood pressure in different limbs, decreased or absent pulse distributed in a patchy manner, rarely angina and pulmonary arterial narrowing, etc. are the features of this disease.
A very brief account of the symptoms of congenital heart disease would include the following.
A TRIAD: CARDINAL SYMPTOMS IN LEFT-TO-RIGHT SHUNT
Tachypnea and dyspnea, feeding difficulty and failure to thrive, the triad is the hallmark of CHF, which is obvious in some specific congenital heart diseases. Important issue is, how does it occur in large left-to-right (L-R) shunt. As discussed, pulmonary structural changes rather than pulmonary congestion is responsible for the respiratory distress in L-R shunt in infancy. However, CHF does contribute in its own ways.16
Mechanism
A large L-R shunt, particularly at posttricuspid level has the following effects:
- Left ventricular volume overload: Left ventricle gets dilated and hypertrophied, which lead to increased end-diastolic pressure. Eventually, ventricle may fail, which raises the left ventricular end-diastolic pressure (LVEDP) further
- Pulmonary overcirculation: Excessive flow driven by systemic pressure through the pulmonary capillary bed increases the capillary pressure and alters the pressure relationship with the pulmonary interstitial space.
These two factors lead to interstitial edema, decreased lung compliance, and tachypnea or dyspnea. Occasionally, there may be frank pulmonary edema.
An infant with ASD is less symptomatic. This is because of two factors. Increased left atrial pressure as a reflection of increased LVEDP is vented through the septal defect. Secondly, L-R shunt here is not driven by systemic pressure.
Tachypnea and Dyspnea
Tachypnea is a rapid, shallow breathing without apparent distress. In a quiet child, rate is usually above 60/min from birth to 6 weeks and above 40/min from 6 weeks to 2 years. It is a reflex-response mediated by J-receptors in the interstitial space, stimulated by interstitial edema. Even pulmonary venous pressure of only 8–10 mmHg in the infant can lead to interstitial congestion. In contrast in the adult patient in whom a pressure of about 25–30 mmHg is necessary to cause interstitial edema.
Breathing becomes more difficult along with tachypnea with further increase in pulmonary congestion. This difficult breathing, i.e., dyspnea is manifested by grunting (forced expiration against a partially closed glottis), intercostal, subcostal and suprasternal retraction and flaring of alae nasi.
Feeding Difficulty
The nursing mother can diagnose heart failure in her baby! Mother's description of the feeding pattern is very important. The tachypneic or dyspneic baby sweats and tries shortly during sucking. Feed is interrupted frequently. The exhausted kid falls asleep but to wake up again, being hungry and irritable. He may become lethargic. A normal infant can suck 4–8 oz in 20 minutes or less. The kid with CHF cannot finish if even after 40 minutes.
Failure to Thrive
Labored breathing increases the workload of the respiratory muscle. An infant with labored breathing costs around 30%, whereas normal breathing demands less than 5% of the total oxygen consumption. Besides, congenital heart disease is associated with reduced number of striated muscle and adipose tissue. A tachypneic infant takes less feed and often vomits out. There may be genetic cause of retarded growth. All the above factors lead to failure to thrive.
Pulmonary Problems in Left-to-right Shunt
Children with large L-R shunt develop respiratory difficulties, which are better explained by pulmonary factors rather than CHF.
Large pulmonary flow leads to dilated hypertensive pulmonary arteries, enlarged atrium and overall, dilated heart. Those structures compress the bronchi and lung parenchyma. Pulmonary problems, caused by this compression, are chronic and recurrent atelectasis, pneumonia, bronchiectasis and infantile lobar emphysema.
Left pulmonary artery arches over left main stem bronchus, courses posteriorly around the left upper lobe bronchus.
When dilated, right pulmonary artery can compress, most commonly the right middle lobe bronchus.
Dilated left atrium, lying just below the tracheal bifurcation can cause bronchial compression.
Complete obstruction of the bronchus results in atelectasis or pneumonia, whereas partial obstruction results in infantile lobar emphysema.
Those pulmonary complications due to L-R shunt commonly occurs between 2 and 9 months of age. In the first 2–3 months, smaller-sized pulmonary arteries and higher neonatal pulmonary vascular resistance (PVR) can limit the degree of L-R shunt. Over next 17few months, PVR comes down. It increases shunt and pulmonary vascular sizes. Infant becomes progressively symptomatic. Gradually, the airways become large in size and cartilaginous. They are now stiff enough to prevent the compressive effect of the cardiac structures. This is the most important cause of spontaneous improvement in respiratory symptoms. Decrease in defect's size, development of infundibular obstruction and pulmonary hypertension may also attenuate symptoms.
Infants are sometimes wheezy and their chest radiograph shows hyperinflated lungs. This lower airway obstruction correlates with degree of L-R shunt and pulmonary hypertension. Morphological studies showed smooth muscle hypertrophy of the bronchioles, which at the same time were compressed by hypertrophied arterioles. Thus, morphological changes of the airways are more important factors of the pulmonary symptoms, rather than pulmonary venous congestion or interstitial edema.
A Few Features of Congenital Cyanotic Heart
Disease: Paroxysmal Hypoxic Spell
Hypoxic spell is an ominous symptom, classically found in Fallot's tetralogy. But it may be presenting symptom in other diseases of Fallot's physiology, as well as pulmonary atresia with VSD. It may happen even in absence of cyanosis.
Commonest Age
Four months to twelve months of age. May occur in early infancy, but is rare beyond 2 years of age.
A Typical Spell
It occurs usually in the morning, after a good sleep. It may be precipitated by a feed, crying, or bowel movement. The infant breathes quickly. He looks visibly distressed. Cyanosis as well as pallor deepens. Hyperpnea increases: develops limpness, syncope-convulsion-cerebrovascular accident and, even death.
Not all the spells lead to syncope. Many often, it is not described by parent as spell. Rather, it is described as colic, seizure disorder, or a behavioral variation of an irritated spoiled-infant. It is more common in presence of anemia and hypovolemia. Recurrent spell may affect intelligence quotient, learning, and other neurological development.
Mechanism
- Precipitating events lead to fall in systemic vascular resistance; right ventricular infundibular spasm, owing to endogenous catecholamines may be an additional factor
- All those cause increased right-to-left shunt with deepening hypoxia and acidosis
- Immature respiratory center, after sleep, overreacts on those stimuli of hypoxemia, acidosis, and hyperpnea deepens. Those stimuli decrease system vascular resistance with further increasing right-to-left shut. Thus, a vicious cycle is set
- Paroxysmal atrial tachycardia may be another mechanism.
Associated Finding
Tachycardia, a falling blood pressure, and disappearance of the ejection systolic murmur across the right ventricular outflow tract (RVOT) are the other physical findings.
Squatting
Typically, a cyanotic child with right-to-left shunt may squat to rest after exertion like walking. Exertion increases right-to-left shunt and hypoxemia, which is relieved by squatting.
Squatting brings a two-staged effect. Immediately after squatting, there is increased venous return, which can lower down oxygen saturation. Eventually, squatting causes increased systemic vascular resistance and compression of the femoral arteries, which in turn, reduces right-to-left shunt and venous return, respectively. As pulmonary flow is increased, hypoxemia improves and he patient gets relieved.
After exertion, patient choose this posture effortlessly from intuition. There are some other postures, squatting equivalent, namely, knee-chest position, sitting with legs drawn underneath, standing with crossed-legs which can help the patient for relief.18
Patients with TOF use to squat for relief of dyspnea. However, patients with other cyanotic heart disease, occasionally can squat.
Hyperviscosity Syndrome
Hypoxia leads to compensatory increase in red cell mass, known as polycythemia to maintain the tissue oxygenation. It is better to name it as erythocytosis, as it is a monoclonal response. With gradual rise of RBC-mass, it becomes a maladaptive situation, which include increased viscosity, both pulmonary and systemic vascular resistance. Most importantly, increased viscosity leads to reduce tissue oxygenation and hyperviscosity syndrome (Box 4).
CONCLUSION
This chapter has briefly covered the areas in history taking in cardiovascular disease and has just showed a few paths. Detailed history taking is out of scope of this chapter. Further reading is necessary and larger textbooks have to be consulted. Detailed knowledge of the individual diseases is essential. Gathering experience is mandatory. An open mind and astute senses are essential. The mportance of history in assessing a patient can never be overemphasized.
REFERENCES
- Sapira JD. The history. In: The Art and Science of Bedside diagnosis. Baltimore: Urban Schwartzenberg, 1990, pp. 9–45.
- Braunwald E. The history. In: Heart Disease – A textbook of Cardiovascular Medicine, Ed. Braunwald E. Philadelphia: W.B. Saunders, 4th ed; 1992, pp. 1–12 (Vol. 1).
- The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and blood vessels. Boston: Little Brown, 1964.
- The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little Brown & Co; 1994:253.
- Canadian Cardiovascular Society grading of angina pectoris. Available from: https://www.ccs.ca/images/Guidelines/Guidelines_POS_Library/Ang_Gui_1976.pdf. [Assessed 31 Oct 2017].
- Goldman L, Hashimoto EF, Cook EF, et al. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale. Circulation. 1981;64:1227.
- Dorian P, Cvitkovic SS, Kerr CR, et al. A novel, simple scale for assessing the symptom severity of atrial fibrillation at the bedside: The CCS SAF Scale. Can J Cardiol. 2006;22:383–6.
- Alonso J, Permanyer-Miraldaf G, Cascantf P, et al. Measuring functional status of chronic coronary patients. Reliability, validity and responsiveness to clinical change of the reduced version of the Duke Activity Status Index (DASI), Eur Heart J. 1997;18:414.
- Lipkin DP, Scriven AJ, Crake T. Six minute walking test for assessing exercise capacity in chronic heart failure. Br Med J. 1986;292:653.
- Chest pain history. Avaialble from: http://www.oxfordmedicaleducation.com/history/chest-pain/.
- Available in the site of American Heart Association. http://www.heart.org/HEARTORG/Conditions/Arrhythmia/SymptomsDiagnosisMonitoringofArrhythmia/Syncope-Fainting_UCM_430006_Article.jsp#.WaHDgzVLeUk.