last authored: December 2010, Sean Doran
last reviewed: December 2010, David LaPierre
Diagnosis and patient assessment almost invariably begins with a detailed history, particularly important in the assessment and management of patients with suspected cardiovascular disease (hereafter referred to as CV disease). The purpose of this section is to broadly discuss important features that must be elicited from any cardiovascular history and the type of CV disease suggested by certain features.
It is important to explore cardiac risk factors and to inquire about specific symptoms and/or complaints that suggest the existence of CV disease. The various family, social, personal and medical histories of each patient help to identify those at risk for CV disease who potentially require immediate therapeutic intervention(s) to alleviate and/or prevent disastrous consequences from unidentified and untreated disease. Furthermore, specific historical details regarding any symptoms that a patient may be experiencing contribute to painting a patient picture that suggests CV disease. These historical factors - cardiac risk factors and symptoms - serve as prognostic markers for:
Classic symptoms to elicit on history include chest pain or discomfort, dyspnea, palpitations, pre-syncope or syncope, and edema. Although these symptoms are commonly associated with CV disease, these symptoms are often present in individuals with non-CV disease and thus contribute to the diagnostic challenge the clinician faces when patients present with such symptoms. Further elucidation of symptomatic details is critical.
The clinician should be constantly mindful of the potential life-threatening causes of many of the "classic symptoms", and it is critical that every medical student, resident and clinician be well versed on life-threatening causes of symptoms that might be attributed to CV disease.
Chest pain (CP) can be a particularly ominous presenting complaint. The differential diagnosis of life-threatening causes of CP include (but are not limited to) acute myocardial infarction, unstable angina, pulmonary embolism, aortic dissection and esophageal rupture. Other non-cardiac diagnoses are often made.
When obtaining a history from a patient presenting with CP, it is important to inquire about several features of the pain:
The answers to the aforementioned questions provide clues as to the particular diagnosis.
Myocardial infarction (MI) is often described as a tightening/squeezing/pressure/weight on the chest that may radiate to the shoulder blades, arm and/or neck. The pain of acute MI is often described similarly to that of angina. However, MI usually produces more severe and more prolonged symptoms. Pain that is very specific in location and/or reproducible with palpation is suggestive of a non-cardiac cause. The "Levine sign" (patient placing clenched fist over sternum while describing pain) is often described in the literature as being suggestive of acute MI. Dyspnea, diaphoresis, lightheadedness, palpitations, nausea and/or vomiting should increase the clinician's suspicion of MI.
Angina pain is often substernal or located over the left chest. Radiation to the neck, jaw, shoulder and or left arm is common. The pain of angina is often brought on by heightened physiological states (exertional, emotional, etc.) and relieved with rest after a few minutes. Administration of a sublingual dose of nitroglycerin may also lead to alleviation of anginal pain. Dyspnea, diaphoresis, lightheadedness, palpitations, nausea and/or vomiting may also be present.
Acute pericarditis is generally sharper than anginal pain and usually located left of the sternum. Radiation to the neck or left shoulder is common. However, the pain usually lasts for hours (rather than minutes) and is associated with other features: (i) worse with inspiration; (ii) alleviation of the pain with the patient in a seated position and leaning forward; and (iii) presence of a pericardial friction rub.
Acute aortic dissection is usually described as a severe, sharp, "tearing" pain that radiates to the back (although significantly subtler presentations are not uncommon). Other findings that are suggestive of acute aortic dissection include asymmetric pulses and an aortic insufficiency murmur.
Pulmonary embolism (PE) is a rather common diagnosis in Emergency Departments and is usually described as a sharp, pleuritic pain of sudden onset. Shortness of breath is also very common. Non-specific findings that are suggestive of PE include tachycardia and an S1Q3T3 pattern on EKG.
Dyspnea, or shortness of breath, is the sensation of an uncomfortable awareness of one's breathing and is a common symptom of CV disease. Dyspnea that is cardiac in origin is usually related to
Dsypnea often occurs with exertion but may be present at rest. It is important to ask patients how many pillows they sleep on at night (or if they sleep with the head of the bed elevated) as patients with congestive heart failure (CHF) usually suffer from paroxysmal nocturnal dyspnea (PND) whereby excess fluid is redistributed to the lungs upon assuming the supine position. Sleeping with the upper body elevated (as one would with multiple pillows) takes advantage of gravitational forces in order to help prevent fluid from returning to the lungs, termed orthopnea.
Dyspnea that is sudden in onset should raise the suspicion of pulmonary embolism (PE). Finally, dyspnea can also be present in patients suffering from angina or acute coronary syndrome, with or without associated chest pain.
Palpitations refers to a patients' subjective feeling of the heart pounding in the chest, skipping a beat and/or racing. A patient describing palpitations should prompt an investigation of an arrhythmia. A broad differential diagnosis is generated based on this rather common patient complaint:
Premature atrial contractions and premature ventricular contractions are often described as "skipped" beats.
Patients commonly present with a complaint of syncope. In exploring this presentation, the clinician must consider neurologic, physiologic (i.e. vaso-vagal response) and cardiac causes. A description of a transient loss of consciousness followed by witnessed tonic-clonic movements, loss of bladder control and/or an injury to the tongue or buccal mucosa certainly suggests a neurological cause and is more appropriately classified as a seizure. It is helpful to note that the most common causes of syncope are vasovagal and idiopathic. However, the benign etiology of the common causes of syncope should not permit the physician to lax in their diagnostic approach. It is essential to rule out potentially life-threatening causes of syncope - many of which are cardiac in origin.
The underlying pathophysiology of cardiac syncope is insufficient cerebral blood flow. Cardiac causes of syncope can be generalized as
Common specific diagnoses include: valvular heart disease (aortic or mitral stenosis); hypertrophic obstructive cardiomyopahty; tachyarrhythmias or bradyarrhythmias; and rarely carotid artery disease (rare because carotid artery disease would have to be bilateral for syncope to occur).
Edema is a very non-specific symptom that can occur with disease of several organ systems (renal, hepatic, venous, etc). However, cardiac causes of edema cannot be ignored. Edema due to cardiac disease is secondary to increased venous pressure. The increased venous pressure results in an altered balance between hydrostatic and oncotic pressures of the venous system which forces fluid (extravasation) into the extravascular space. The location of edema in the body provides a very important clue to the location of cardiac pathology: (i) elevated left-sided heart pressures leads to pulmonary edema; (ii) elevated right-sided heart pressures lead to pulmonary edema.
Peripheral edema usually presents as pitting of the skin after pressure is applied to an edematous area. Edema commonly occurs in the lower extremities of ambulatory patients and in the sacral area of patients who are supine for prolonged periods of time (i.e. bedridden, ICU patients, etc.). Usually, the edema will be worsened with prolonged periods of standing (therefore worsening as the day progresses in ambulatory patients) and relieved (but delayed relief) with rest/elevation of lower extremities.
Pulmonary edema is usually best identified via a few key features: (i) patient complaint of dyspnea; (ii) patient history suggestive of an increased risk of pulmonary edema; (iii) presence of bi-basilar fine crackles on auscultation of the lungs; and (iv) often confirmed (not very reliable) with fluffy infiltrates on chest X-Ray.
Cyanosis can occur in patients with heart disease. It generally reflects a reduction in the arterial oxygen saturation to a level of approximately 85% or less. Two distinct types are of note: (i) central cyanosis - evident on the lips and/or tongue and usually reflects right-to-left shunting of blood secondary to an atrial or ventricular defect; and (ii) peripheral cyanosis - usually secondary to systemic vasoconstriction in the setting of poor cardiac output. It is important to note that for each of the aforementioned categories, there are multiple causes that are non-cardiac in origin.
Crucial to every cardiovascular history is an assessment of risk factors for cardiac disease. There are different risk factors associated with specific conditions but among the most common risk factors that are routinely assessed fall into two broad categories - modifiable risk factors and non-modifiable risk factors. These categories pertain primarily to the presence of coronary artery disease.
Modifiable risk factors for coronary artery disease include: |
Non-modifiable risk factors for coronary artery disease:
|
The assessment of a patient with potential CV disease begins (after ensuring the patient is stable) with the patients medical history, social and family medical history. The clinician should inquire about symptoms suggestive of CV disease as well as modifiable and non-modifiable risk factors. As information is gathered, the clinician will form a 'picture' of the patients likely diagnosis and can then initiate the appropriate treatment and management strategies.
Andreoli et al. Cecil Essentials of Medicine 7th Ed. Saunders Elsevier. Philadelphia 2007.
Marx et al. Rosen's Emergency Medicine: Concepts and Clinical Practice 7th Ed. Mosby Elsevier. Philadelphia 2010.
Porter et al. The Merck Manual of Patient Symptoms: A Concise, Practical Guide to Etiology, Evaluation, and Treatment. Merck & Co., Inc. New Jersey 2008.
Tintanalli, JE Emergency Medicine (A Comprehensive Study Guide). McGraw-Hill Companies, Inc. USA 2004.
authors: Sean Doran, Caleb Zelenietz, 2010
reviewers: David LaPierre, Dec 2010