Bradyarrhythmias

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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58 Bradyarrhythmias

Epidemiology

Bradycardia is a frequent finding in clinical practice, and its significance is dependent on the underlying cause and clinical effects. The baseline heart rate in an individual patient is determined predominantly by the balance between the parasympathetic and sympathetic nervous systems, and a “normal” heart rate has been defined arbitrarily as 60 to 100 beats/min at rest. The heart rate will vary depending on age, physical condition, and time of observation. Normal ranges for a healthy asymptomatic individual will vary from 46 to 93 beats/min in men and 51 to 95 beats/min in women during the day to rates as low as 40 beats/min at night.1 The heart rate should fluctuate with respiration, the Valsalva maneuver, and other vagal influences confirming normal autonomic control of the sinus node. Bradycardia is a frequent finding in trained athletes, in whom heart rates lower than 40 beats/min are often observed at rest.2 Bradycardias of clinical significance increase in frequency with age and in the setting of illnesses or medications affecting the heart and its conduction system.

Metabolic Ischemia and infarction — Other

From Ford M. Clinical toxicology. Philadelphia: Saunders; 2001. pp. 23-5.

Intrinsic Causes

Certain conditions result in failure of elements of the conduction system because of aging, ischemia or infarction, surgical trauma, or infiltration (Table 58.2). The latter cause encompasses a large group of conditions that include infectious and rheumatologic diseases.35 The associated rhythms are typically those that indicate failure of one element of the conduction system rather than failure to generate a rhythm:

Table 58.2 Intrinsic Causes of Bradyarrhythmias

Ischemia and infarction

Infection Malignancy Rheumatologic Other

MI, Myocardial infarction.

Presenting Signs and Symptoms

Cardiac output is dependent on the patient’s stroke volume and heart rate. Bradycardias are symptomatic only to the extent that they affect cardiac output, which is a product of the heart rate and stroke volume. In the setting of a normal stroke volume, heart rates as low as 20 to 30 beats/min can sustain a reasonable cardiac output. A heart rate of 40 beats/min may be physiologically normal for some individuals, whereas a rate of 60 beats/min may be inadequate for patients with conditions that compromise stroke volume, such as cardiomyopathies, bleeding, or sepsis.

Symptoms of low cardiac output are due to hypoperfusion of vital organs and muscle tissue. Mild reductions in cardiac output usually cause exertional fatigue and dyspnea. Greater reductions in cardiac output can produce signs and symptoms of cerebral ischemia, congestive heart failure, mesenteric ischemia, and renal insufficiency. Complete heart block with slow escape rhythms or bradycardia in the setting of profound reductions in stroke volume can manifest as syncope, pulmonary edema, and cardiogenic shock.

Alternatively, a profound bradycardia that does not result in hemodynamic compromise does not need to be treated but should be considered an important diagnostic clue. The classic example is a patient with intracranial hemorrhage and Cushing reflex, which will be manifested as hypertension and often profound bradycardia. In this case the bradycardia is a sign of elevated intracranial pressure, and treatment should focus on reducing it.

Differential Diagnosis and Medical Decision Making

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