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Cardiac patient History

Updated: Thursday, Mar 19,2009, 5:04:39 PM
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Cardiac patient History

Major cardiac diseases have relatively few symptoms, including pain; dyspnea; weakness and fatigue; palpitations; light-headedness, presyncope, and syncope; and other symptoms that may be due to the cardiac disease or may accompany it. Subtle variations in these symptoms require close attention.

A thorough history is fundamental to the diagnosis of cardiovascular disease and cannot be replaced by routine or random noninvasive and invasive testing, which is expensive and inefficient. A thorough family history should be taken because many cardiac disorders (eg, coronary artery disease [CAD], systemic hypertension, bicuspid aortic valve, hypertrophic cardiomyopathy, mitral valve prolapse) have a heritable basis.

Myocardial ischemic pain is usually described as pressing, squeezing, or weightlike. The pain is usually greatest in the central precordium and may be demonstrated by the patient placing a clenched fist over the center of the sternum. The pain frequently radiates in the distribution of the lower cervical nerves and may therefore be felt in the neck, lower jaw, or either shoulder or arm (most commonly the left shoulder and left arm). If the arm and hand are involved, pain is usually on the ulnar side. Myocardial ischemic pain often induces an autonomic response (eg, nausea or vomiting, sweating). A sense of impending doom may be present. Myocardial ischemic pain due to coronary arteriosclerosis is usually exertion-related, at least initially. However, the pain of acute MI may occur suddenly when the patient is at rest. Pain due to dynamic coronary narrowing from arterial spasm, although ischemic, tends to occur at rest or nocturnally. Myocardial ischemic pain usually lasts only minutes.

Cardiac pain can be arbitrarily categorized as ischemic, pericardial, or atypical. Although cardiac pain is sometimes characteristic of an underlying cardiac disorder, there is often significant overlap with other disorders in terms of character, quality, location, pattern of radiation, severity, and duration. Cardiac pain is transmitted to the cerebral cortex along autonomic nerve fibers and has a variable referral area that can extend from the ear to the umbilicus. Extracardiac chest pain of cardiovascular origin includes pain arising from the great vessels and pain due to pulmonary embolism.
Atypical chest pain tends to be stabbing or burning and is often quite variable in position and intensity from one episode to another. It tends to be unrelated to physical exertion and unresponsive to nitroglycerin. Its duration may be evanescent (measured in seconds) or persistent over many hours or days. Some persons with atypical chest pain have physical signs or echocardiographic evidence of mitral valve prolapse. Whether the pain is related to the mitral valve prolapse or whether it is an epiphenomenon is controversial because it is common in the absence of evident prolapse. Vague atypical chest discomfort is also common in those with isolated atrial tachycardia in the absence of significant underlying heart disease. Although atypical chest pain may be debilitating, there is no objective evidence that it indicates serious heart disease, except when due to disease of the great vessels or to pulmonary embolism.
Pain from dissection of the aorta (or rarely the pulmonary artery) is usually very severe and of a tearing or rending character. Pain usually begins with the start of dissection, followed by a quiescent period of hours or days, then recurs with extension of the dissection. It is central in the chest, radiates through to the back or neck, and is unaffected by position unless dissection into the pericardium with hemopericardium has produced an acute pericarditis. If the ostia of the coronary arteries are involved, myocardial ischemic pain may be superimposed on the pain of dissection.
Pulmonary embolism pain may be pleuritic when infarction of the lung results in pleuritis or may be anginal when right ventricular ischemia occurs secondary to sudden onset of pulmonary hypertension. If pulmonary embolism is suspected, the history should address unilateral swelling or pain in the legs, recent surgery, or illness requiring prolonged bed rest. If pericarditis is suspected, the history should address exposure to infectious agents, connective tissue and immune diseases, and previous diagnosis of neoplasia.

Dyspnea is the perception of uncomfortable, distressful, or labored breathing. Cardiac dyspnea results from edema in bronchiolar walls and stiffening of the lung due to parenchymal or alveolar edema, which interfere with airflow. Dyspnea also results when cardiac output is inadequate for the body's metabolic demands and can occur without pulmonary edema.
Cardiac dyspnea is always worsened by exertion and partly or completely relieved by rest. Dyspnea due to elevated pulmonary venous pressure and pulmonary edema is increased in the recumbent position and decreased by sitting or standing (orthopnea). If orthopnea causes awakening during the night and is relieved by sitting, it is called paroxysmal nocturnal dyspnea. Dyspnea in the presence of bronchiolar edema is associated with wheezing due to airflow obstruction; frothy and sometimes blood-tinged sputum is expectorated. A common manifestation of bronchiolar edema and stiff lungs due to heart failure is a dry cough, which must be differentiated from that occurring in 5% of patients treated with ACE inhibitors.
Dyspnea due exclusively to inadequate cardiac output is not affected by posture but varies with physical exertion and may be associated with weakness and fatigue. In many cardiac disorders, dyspnea due to a fixed cardiac output and that due to pulmonary congestion occur simultaneously (eg, in mitral stenosis). The onset of dyspnea in heart disease usually signifies an ominous prognosis. Dyspnea due to CAD may coexist with that due to another cardiac disease. Orthopnea and paroxysmal nocturnal dyspnea are unusual in pulmonary disease, except in a very advanced phase when the increased efficiency of breathing in t
Weakness and fatigue result from inadequate cardiac output for the body's metabolic needs, initially on exertion and eventually at rest. They occur in disorders that limit cardiac output and are not relieved by rest and sleep. It is common for patients with congenital heart disease to deny weakness and fatigue because they consider a limited state to be normal and only recognize the symptoms retrospectively, after surgical correction.

Palpitations are the perception of heart action by the patient. Careful inquiry into the rate and the rhythm of palpitations helps differentiate pathologic from physiologic palpitations. Palpitations due to an arrhythmia may be accompanied by weakness, dyspnea, or light-headedness. Atrial or ventricular extrasystoles are often described as skipped beats, whereas atrial fibrillation is identified as an irregularity. Supraventricular or ventricular tachycardia is most often perceived as being rapid and regular and of sudden onset and termination. Onset of atrial tachyarrhythmia is often followed by the need to urinate because of increased production of atrial natriuretic factor.
Cardiac activity is controlled by the autonomic nervous system and is thus commonly sensed only by persons with abnormally heightened awareness of their body functions, eg, in anxiety states. It may also be sensed in healthy persons during exercise when stroke volume or heart rate increases. Palpitations can occur in disorders such as aortic regurgitation or thyrotoxicosis; the most common cause is abnormal cardiac rhythm. Palpitations accompanied by myocardial ischemia-type chest pain may be indicative of CAD, in which decreased diastolic coronary flow and ischemia result from the tachycardia.
Serious heart disease or arrhythmias that significantly limit cardiac output may cause light-headedness, presyncope, or syncope (a sudden brief loss of consciousness, with loss of postural tone). When associated with palpitations, any of these symptoms indicates an abrupt drop in cardiac output and denotes a serious arrhythmia or underlying organic heart disease. Exertional syncope occurs in aortic stenosis or hypertrophic cardiomyopathy, both of which limit increased cardiac output on exertion. Ventricular tachycardia or fibrillation or severe bradycardias or asystole may cause these symptoms in the form of a Stokes-Adams attack. Onset of syncope denotes a poor prognosis in patients with CAD, myocarditis, cardiomyopathy, and known ventricular arrhythmias. Intracardiac tumors or ball-valve thrombi can intermittently obstruct blood flow within the heart, producing presyncope or syncope. Postural hypotension and vasovagal syncope are the major benign causes of syncope. Syncope must be differentiated from epileptic seizures, although seizures due to brain hypoxia can occur in a syncopal episode.
A history of infections (eg, streptococcal with or without rheumatic fever, viral, syphilitic, protozoan) may raise suspicion of a cardiac disorder resulting from active or temporally remote infectious agents. Endocarditis should be considered in any patient with an unexplained fever and a heart murmur. A cardiac cause should be sought for peripheral or cerebral emboli or in any stroke, which can be caused by emboli arising from a recent MI, valvular disease (particularly mitral stenosis with atrial fibrillation), or cardiomyopathy. A history of cerebrovascular or peripheral vascular disease increases the likelihood of associated CAD. Central cyanosis makes a congenital cardiac disorder highly likely.

1.   Physical Examination of the Heart
2.   Shock Symptoms and Signs
Shock Etiology and Classification
Shock Pathophysiology
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