The most common symptoms of heart disease are dyspnea, chest pain, palpitations, syncope or presyncope, and fatigue. None are specific, and interpretation depends on the entire clinical picture and, in many cases, diagnostic testing.
Chest pain and other forms of discomfort are common symptoms
that can occur as a result of pulmonary, pleural, or musculoskeletal
disease, esophageal or other gastrointestinal disorders, or anxiety
states, as well as many cardiovascular diseases. Myocardial ischemia
is a frequent cause of cardiac chest pain and is usually described
as dull, aching, or as a sensation of “pressure,” “tightness,” “squeezing,” or “gas,” rather
than as sharp or spasmodic. Ischemic symptoms frequently
are first noted only with exercise or cardiac stress from cold exposure,
meals, or a combination of factors and often resolve quickly once
the inciting event is over. Progressive symptoms or symptoms at
rest may represent unstable angina due to coronary plaque rupture
and thrombosis. Protracted episodes often represent myocardial infarction, although one-third
of patients with acute myocardial infarction do not have chest pain.
When present, the pain is commonly accompanied by a sense of anxiety
or uneasiness. The location is usually retrosternal or left precordial.
Because there are not the appropriate sensory nerves on the heart,
the central nervous system interpretation of pain location often
results in pressure or “heaviness” being referred
to the throat, lower jaw, shoulders, inner arms, upper abdomen,
or back. Ischemic pain is not related to position or respiration
and is usually not elicited by chest palpation. One clue that the
pain may be ischemic is the presence of other symptoms associated
with the pain, such as shortness of breath, dizziness, a feeling
of impending doom, and vagal symptoms, such as nausea and diaphoresis.
Of importance, depression may mask symptoms, especially in women. When compared to men, women do appear to have a higher frequency of atypical angina (even with significant coronary disease) and, in some cases, evidence for microvascular coronary disease even when epicardial coronary disease is not evident at cardiac catheterization.
Hypertrophy of either ventricle, such as in aortic stenosis or
hypertrophic cardiomyopathy, may result in subendocardial underperfusion
during stress and may also give rise to atypical ischemic pain.
Myocarditis, pulmonary hypertension, and mitral valve prolapse are
also associated with chest pain atypical for angina pectoris. Pericarditis
may produce pain that is greater supine than upright, and may increase
with respiration, or swallowing. Pleuritic chest pain is not ischemic, and
pain on palpation should signal a musculoskeletal etiology. Aortic
dissection classically produces an abrupt onset of tearing pain
of great intensity that often radiates to the back.
Anderson JL et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. Circulation. 2007 Aug 14;116(7):e148–304. Erratum in: Circulation. 2008 Mar 4;117(9):e180.
Ebell MH. Evaluation of chest pain in primary care patients. Am Fam Phys. 2011 Mar 1;83(5):603–5.
Farkouh ME et al. Clinical risk stratification in the emergency department predicts long-term cardiovascular outcomes in a population-based cohort presenting with acute chest pain: primary results of the Olmsted County Chest Pain Study. Medicine (Baltimore). 2009 Sep;88(5):307–13.
Hildreth CJ et al. JAMA patient page. Chest pain. JAMA. 2009 Apr 8;301(14):1498.
Nugent L et al. Gender and microvascular angina. J Thromb Thrombolysis. 2011 Jan;31(1):37–46.
Rutledge T et al. Depression severity and reported treatment
history in the prediction of cardiac risk in women with suspected
myocardial ischemia: the NHLBI-sponsored WISE study. Arch Gen Psychiatry.
Dyspnea due to heart disease is generally precipitated or exacerbated
by exertion and usually results from elevated left atrial (LA) and
pulmonary venous pressures or from hypoxia, though some patients with
purely right heart disease complain of dyspnea as well. The former
are most commonly caused by left ventricular (LV) systolic dysfunction,
LV diastolic dysfunction (due to hypertrophy, fibrosis, or pericardial
disease), or valvular stenosis or regurgitation. Exertional dyspnea
may be an angina equivalent. The acute onset or worsening of LA
hypertension may result in pulmonary edema (see eFigure 10–1); (see eFigure 10–2). Hypoxia may be a consequence
of pulmonary edema, inherent lung disease, or right to left shunting.
Dyspnea should be quantified by asking if commonly performed tasks
can precipitate it, such as climbing stairs, housework, grocery
shopping, mowing the lawn, vacuuming, etc. It is also a common symptom
of primary and secondary pulmonary disease, and the etiologic distinction
may be difficult. The diagnosis of heart failure (HF)
may be aided by measurement of B-type natriuretic peptide (BNP)
or N terminal pro-BNP (pro-BNP), though high levels may also result from
right ventricular (RV) dysfunction and pulmonary embolism. Recent studies on their use in the emergency department suggest the routine use of these peptides may not be justified based on lack of evidence that the measurements improve outcomes. Trends may be useful, though, especially in heart failure and the evaluation of valvular heart disease. Shortness
of breath may also occur in sedentary or obese individuals who have
reduced lung capacity and is also associated with anxiety states,
anemia, and many other illnesses.
Pulmonary edema. (Courtesy of H Goldberg.)
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