Tachycardia

TSRA Content:

Author: Joav Birjiniuk, MD

Tachycardia is a common finding in the postoperative patient, whether undergoing cardiac or non-cardiac surgery. While tachycardia may be the natural result of emergence from anesthesia in the immediate post-operative period, its persistence or initiation after a period of normalcy may be cause for concern.

As with all abnormalities in vital signs in the postoperative patient, tachycardia is best treated by addressing the underlying etiology. In and of itself, tachycardia does not necessarily require treatment (i.e. with beta blockade, calcium blockade, or other anti-arrhythmics) unless it is prolonged or causing compromise in cardiac function. However, prompt diagnosis of the cause of this abnormal vital sign with appropriate treatment may save the patient from undue stress and other, inappropriate medical treatment.

In the assessment of a patient with tachycardia, diagnosis begins with history and physical examination, as well as understanding the patient’s underlying physiology, operation, and vital sign trends. Broadly, tachycardia in these patients can be considered a result of reactive sympathetic activity, physiologic compensation to meet metabolic demands, or as a result of organic disease.

Sympathetic reaction is the result of some insult to the body leading to activation of autonomic fibers. In the postoperative setting, this may be due to untreated pain, sepsis or infectious insult, myocardial infarction, underlying pump dysfunction, parasympatholysis (eg post-hiatal surgery or vagotomy), or drug-related interactions. It is paramount in these settings to determine and treat the underlying cause, as this tachycardia is very often secondary to other issues.

One may recall that oxygen delivery, a gross measure of tissue perfusion, may be computed using the following:

As cardiac output is directly related to heart rate, defects in oxygen delivery are often compensated for rather quickly by increases in this vital sign. Thus, it is clear to see that tachycardia may often be a compensatory response to improve oxygen delivery. Understanding the etiology based on the missing component in the oxygen delivery equation can aid in adequately treating the source. Decreases in stroke volume may be the result of inadequate preload, depressed myocardial function, or obstructing lesion limiting output. Blood loss, hypoxia, and pulmonary or intracardiac shunt may substantially limit oxygen carrying capacity, also leading to compensatory tachycardia to maintain oxygen delivery.

Tachycardia may also be the result of organic disease. In such cases, underlying disorders may be uncovered by postoperative physiology. Patients with thyroid dysfunction may be placed in a stress leading to derangement of gland function and subsequent refractory tachycardia. Additionally, some arrhythmias, particularly those involving accessory pathways, may be accentuated by postoperative stresses. However, it is important to note that other physiologic insults may trigger entry into dysrhythmia, which should be investigated in each case and treated accordingly.

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