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Eliciting a good history is invaluable in diagnosing, and managing heart disease. There is overlap between symptoms arising from cardiovascular disease and those originating from other pathology. The following symptoms occur with heart disease:
-chest pain
-dyspnoea
-palpitations
-syncope
-fatigue
-peripheral oedema
The severity of anginal pain, dyspnoea, palpitations or fatigue may be classified according to the New York Heart Association grading of 'cardiac status'.
Chest pain
This is the symptom most commonly associated with heart disease.
The pain of angina pectoris and myocardial infarction is due to myocardial hypoxia. Classically, it is felt as crushing, gripping or heavy pain behind the sternum in the centre of the chest, radiating to the neck, shoulder or jaw, or more rarely to the teeth, back or abdomen. It may be associated with pain, paraesthesia or heaviness in one (commonly the left) or both arms. Typically, the pain of angina pectoris is provoked by exercise and promptly relieved by rest or short-acting nitrates. Angina occurring on lying flat is termed decubitus angina. The level of exertion required to provoke pain - for example, after walking on the flat for 200 yards - should be elicited.
Angina that is becoming more frequent or unpredictable, or occurs at rest is classified as unstable, a component of the 'acute coronary syndrome'. Even quite significant ischaemia/infarction may not be associated with chest pain but rather with dyspnoea, nausea and sweating. This is 'silent' ischaemia due to loss of pain-sensing fibres within the heart, and is more common in the diabetic and elderly. Ischaemia may also present with atypical (e.g. dyspeptic) pain.
Central chest pain radiating to the back may be due to cardiac ischaemia but a dissecting or enlarging thoracic aortic aneurysm also produces a similar pain and sometimes ECG changes.
Pericarditis pain is also felt at the centre of the chest. However, its character is similar to pleuritic pain, i.e. sharp, exacerbated by movement, respiration and coughing. Unlike pleuritic pain, however, some relief may be afforded by sitting forwards.
Left submammary stabbing pain, so-called 'precordial catch', is usually associated with anxiety (called effort syndrome or Da Costa's syndrome), although cardiac conditions such as mitral valve prolapse may produce a similar sensation. Oesophageal disease may also produce central (retrosternal) chest pain, which can be difficult to differentiate from cardiac pain.
Dyspnoea
Dyspnoea is an abnormal awareness of breathlessness. Pain, particularly within the chest and abdomen, may also lead to dyspnoea. However, the main causes are cardiac and pulmonary pathologies; in the cardiovascular system, this is most commonly due to left ventricular failure (LVF).
Left ventricular failure causes dyspnoea due to oedema of the pulmonary interstitium and alveoli. This makes the lungs stiff (less compliant), thus increasing the respiratory effort required to ventilate the lungs. Tachypnoea (increased respiratory rate) is usually also present owing to stimulation of pulmonary stretch receptors.
It is clinically valuable to grade dyspnoea in a similar manner to chest pain (see above), by the level of exertion required to provoke its onset and by the patient's cardiac status as this is an indication of severity. As LVF worsens, other forms of breathlessness such as orthopnoea and paroxysmal nocturnal dyspnoea occur.
Orthopnoea refers to breathlessness on lying flat. Blood is redistributed from the legs into the torso leading to an increase in central and pulmonary blood volume, worsening pulmonary oedema. Furthermore, whilst recumbent, the abdominal contents push up against the diaphragm, restricting its movement (splinting). Orthopnoea is usually overcome by the patient using an increasing number of pillows to sleep. The number of pillows required indicates the severity.
Paroxysmal nocturnal dyspnoea (PND) occurs when a patient is woken from sleep fighting for breath, a dramatic and frightening experience. The patient sits up, stands or opens the window for fresh air. PND is in essence a variation of orthopnoea, in that it is due to the same mechanisms. However, as sensory awareness is reduced whilst asleep, the pulmonary oedema can become quite severe before the patient is awoken.
Some symptoms of LVF may mimic respiratory pathology leading to diagnostic difficulty. Most notoriously, oedema of the bronchial endothelium can cause a 'cardiac wheeze' leading to the misdiagnosis of airways disease. Pulmonary oedema may also produce a cough, productive of a frothy blood-tinged sputum. Conversely, PND-like episodes with coughing may occur in asthma, but conventionally the term PND is reserved for cardiac problems.
In severe heart failure, alternate episodes of hyperventilation and apnoea may occur (Cheyne-Stokes respiration). If hypopnoea occurs rather than apnoea, the phenomenon is termed 'periodic breathing', but the two variations are known together as central sleep apnoea syndrome (CSAS). This occurs due to malfunctioning of the respiratory centre in the brain, caused by poor cardiac output with concurrent cerebrovascular disease.
The symptoms of CSAS, such as daytime somnolence and fatigue, are similar to those of obstructive sleep apnoea syndrome and there is considerable overlap with the symptoms of heart failure. CSAS is believed to lead to myocardial hypertrophy and fibrosis, deterioration in cardiac function and complex arrhythmias including non-sustained ventricular tachycardia, hypertension and stroke. Studies conducted on patients with heart failure show that patients with CSAS have a worse prognosis compared to similar patients without CSAS.
Palpitations
Palpitations represent an increased awareness of the normal heartbeat or the sensation of slow, rapid or irregular heart rhythms.
The normal heartbeat may be sensed because of anxiety, excitement, exercise or recumbency on the left side. Therefore, a careful history may help to rule out a pathological cause for palpitations. The most common arrhythmias felt as palpitations are premature ectopic beats and paroxysmal tachycardias. A useful trick is to ask patients to tap out the rate and rhythm of their palpitations, as the different arrhythmias have different characteristics.
Premature beats are felt by the patient as a pause followed by a forceful beat. This is because premature beats are usually followed by a pause before the next normal beat, as the heart resets itself. The next beat is more forceful as the heart has had a longer diastolic period and therefore filled with more blood before this beat. These premature beats may occur in clusters and may lead to great anxiety although they are usually benign.
Paroxysmal tachycardias start abruptly and may be felt as a sudden racing heartbeat. They may terminate as suddenly, but often tend to slow down first, therefore leading to the sensation of the palpitations fading away. Paroxysmal atrial fibrillation is irregular in rhythm whereas other supraventricular or ventricular tachycardias are regular. Paroxysmal tachycardias, especially when prolonged, may lead to other symptoms such as syncope, presyncope, dyspnoea or chest pain. Supraventricular arrhythmias, especially atrial fibrillation and AV nodal re-entry, may also produce polyuria after the palpitations owing to the release of atrial natriuretic peptide (ANP), which leads to sodium and water loss from the kidneys.
Some patients experience tachycardia on standing, associated with a mild drop in blood pressure and symptoms of dizziness or near syncope. This is due to a form of autonomic dysfunction termed the postural orthostatic tachycardia syndrome (POTS) and is due to sinus tachycardia.
Bradycardias may be appreciated as slow, regular, heavy or forceful beats. Most often, however, they are simply not sensed. All palpitations may be graded by the NYHA cardiac status.
Syncope
Transient loss of consciousness due to inadequate cerebral blood flow is termed syncope, and may be due to a variety of causes.
Vascular
Neurocardiogenic (vasovagal)
Postural hypotension
Postprandial hypotension
Micturition syncope
Carotid sinus syncope
Obstructive
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Pulmonary stenosis
Tetralogy of Fallot
Pulmonary hypertension/embolism
Atrial myxoma/thrombus
Defective prosthetic valve
Arrhythmias
Rapid tachycardias
Profound bradycardias (Stokes-Adams)
Significant pauses (in rhythm)
Artificial pacemaker failure
Vascular
The most common cause of syncope is the vasovagal attack, also known as neurocardiogenic or situational syncope, or more commonly as a simple faint. It may be triggered by prolonged orthostatic (standing upright) stress or strong emotion. The mechanism begins with peripheral vasodilatation and venous pooling of blood leading to a reduction in the amount of blood returned to the heart. The near-empty heart responds by contracting vigorously, which in turn stimulates mechanoreceptors (stretch receptors) in the inferoposterior wall of the left ventricle. These in turn trigger reflexes via the central nervous system, which act to reduce ventricular stretch (i.e. further vasodilatation and sometimes profound bradycardia), but this causes a drop in blood pressure and therefore syncope. These episodes are usually associated with a prodrome of dizziness, nausea, sweating, tinnitus, yawning and a sinking feeling. Recovery occurs within a few seconds, especially if the patient lies down.
A drop in systolic blood pressure of 20 mmHg or more on standing from a sitting or lying position is termed postural (orthostatic) hypotension. This occurs as blood pools in the legs because of gravity. Usually, reflex vasoconstriction prevents a drop in pressure but if this is absent or the patient is fluid-depleted, postural hypotension can occur. This condition is more prevalent in the elderly because of age-related autonomic dysfunction, but also may be related to vasodilating or diuretic drugs.
Postprandial hypotension is commonly defined as a drop in systolic blood pressure of 20 mmHg or more within 2 hours of the start of a meal. It is also said to occur if the systolic blood pressure drops from above 100 mmHg to under 90 mmHg in the same time period. It is thought to occur very commonly, even more so than postural hypotension, especially in the elderly and hypertensive populations. The mechanism has not been firmly established but it is believed to commence with pooling of blood in the splanchnic vessels. In normal subjects, this elicits a homeostatic response via activation of baroreceptors and the sympathetic system, peripheral vasoconstriction and an increase in cardiac output. Abnormalities in these mechanisms are believed to cause postprandial hypotension.
Micturition syncope refers to loss of consciousness whilst micturating. Some cases occur due to orthostatic hypotension. Bladder evacuation may produce parasympathetic overactivity, resulting in bradycardia and vasodilatation.
Carotid sinus syncope occurs when there is an exaggerated vagal response to carotid sinus stimulation, again leading to bradycardia and vasodilatation. It may be so severe as to provoke syncope by wearing a tight collar, looking upwards or turning the head.
Obstructive.
Obstructive cardiac causes all lead to syncope due to restriction of blood flow from the heart into the rest of the circulation, or between the different chambers of the heart.
Arrhythmias.
Stokes-Adams attacks have been defined as sudden loss of consciousness unrelated to posture. It is usually due to intermittent high-grade atrioventricular block, profound bradycardia or ventricular standstill. Without warning, the patient falls to the ground, pale and deeply unconscious. The pulse is usually very slow or absent. After a few seconds the patient flushes brightly and recovers consciousness as the pulse quickens. Often there are no sequelae, but patients may injure themselves during falls.
Occasionally a generalized convulsion may occur if the period of cerebral hypoxia is prolonged, leading to a misdiagnosis of epilepsy.
Fatigue
Fatigue may be a symptom of inadequate systemic perfusion in heart failure. However, other factors may be responsible:
poor sleep due to paroxysmal nocturnal dyspnoea, orthopnoea, decubitus angina, nocturia (due to diuretic therapy) or nightmares (due to amiodarone therapy)
direct side-effect of medication, particularly beta-blockers
electrolyte imbalance due to diuretic therapy
as a systemic manifestation of infection such as endocarditis.
Peripheral oedema
Heart failure results in salt and water retention due to renal underperfusion and consequent activation of the renin-angiotensin-aldosterone system.This leads to dependent pitting oedema.
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