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.
Pericardial pain, which is due to inflammation involving the parietal pericardium, feels like stabbing, burning, or cutting and is made worse by coughing, swallowing, deep breathing, or lying down. It is less variable in character, position, and referral area than myocardial ischemic pain. It is diminished by leaning forward and remaining still. Pericardial pain can last for hours or days. It is not relieved by nitroglycerin.
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 the upright position is manifest.
Merck Manual Diagnosis and Therapy; Section 16, Cardiovascular Disorders; Chapter 197, Approach To The Cardiac Patient.