Pharmacologic and mechanical support of the circulation
The main sources of arrhythmias and rate changes are sympathetic overstimulation, electrolyte disturbances, and cellular damage. Cellular damage, reversible or not, may result from the added actions on the basic disease of ischemia, edema, and hypoxia induced by causes such as direct manipulation of the heart, ischemic injury during cross-clamping of the aorta, and electrolyte disturbances.
The alert anesthesiologist can prevent, correct, or at least minimize the consequences of these rate and rhythm changes by proper anesthetic management and specific drug therapy. The most common situations in which the anesthesiologist can intervene in the general setting of heart surgery are discussed.
In principle, bradycardia is safe, especially for the coronary patient. The rate is mainly under the influence of the sympathetic tone and the pharmacologic effects of drugs such as beta-blockers, fentanyl, halothane, and digoxin.
Before treating bradycardia, its general impact on circulation must be assessed for signs of danger, premature ventricular contractions, signs of reduced cardiac output, atrioventricular block, and imminence of complete block.
In managing bradycardia, treatment is not necessary in all cases, but it is important not to exacerbate it. Treatment consists of atropine, isoproterenol (Isuprel), and the use of pacemakers. As a word of caution, beta-blockers may prevent expected increase in rate in presence of hypovolemia.
Before treating tachycardia, remember that it may be a defense mechanism and can be a normal response to hypovolemia, hypoxemia, and tamponade. These above conditions must be ruled out before a reduction in the rate is attempted. Also, . . .