What is the pathophysiological mechanism by which fever causes tachycardia?

From the Guidelines

Fever causes tachycardia primarily through the body's thermoregulatory response and increased metabolic demand, leading to an increase in cardiac output and heart rate. This relationship is supported by the understanding that physiological sinus tachycardia, which can be caused by fever, is expected to resolve with correction of the underlying cause 1. The pathophysiological mechanism involves several key factors:

• Increased metabolic rate: With each degree Celsius elevation in body temperature, the metabolic rate increases by approximately 10-13%, requiring increased oxygen delivery to tissues.
• Thermoregulatory response: The body attempts to dissipate heat through peripheral vasodilation, which can lead to relative hypovolemia and a compensatory increase in heart rate to maintain blood pressure.
• Sympathetic nervous system activation: Fever triggers the release of inflammatory cytokines and activates the sympathetic nervous system, leading to increased catecholamine production (epinephrine and norepinephrine), which directly stimulates beta-adrenergic receptors in the heart, increasing both heart rate and contractility.
• Clinical significance: The relationship between fever and heart rate is important in clinical assessment, as a disproportionate tachycardia relative to fever may indicate additional pathology such as sepsis, dehydration, or other cardiovascular compromise, as noted in guidelines for managing adult patients with supraventricular tachycardia 1.

From the Research

Pathophysiological Mechanism of Fever-Induced Tachycardia

The relationship between fever and tachycardia can be understood through the body's thermoregulatory mechanisms and the effects of pyrogens on the hypothalamus. Key points include:

• Fever results from the resetting of the hypothalamus due to prostaglandins produced by pyrogens 2.
• The increase in metabolic demands during fever stresses patients, particularly those with marginal cardiac and cerebral vascular supply, potentially leading to tachycardia 2.
• The hypothalamic-pituitary-adrenal (HPA) axis and sympathetically mediated tachycardia are activated in response to stress, which can also contribute to fever 3.
• The dorsomedial hypothalamus (DMH) plays a crucial role in generating effects seen in emotional stress, including tachycardia and fever, through its projections to sympathetic premotor neurons in the medullary raphe pallidus (RP) 3.

Clinical Observations and Antipyretic Use

Clinical studies have observed the association between fever and tachycardia, as well as the effects of antipyretic administration:

• Fever is associated with tachycardia, with an approximate increase of 10 beats/minute per °Celsius rise in temperature, particularly pronounced in infants 4.
• Antipyretic administration can reduce both fever and heart rate, with an average pulse rate reduction of 21.1 beats/minute/°Celsius decrement in fever 4.
• The use of antipyretics such as paracetamol, nimesulide, and ibuprofen can lower body temperature by inhibiting prostaglandin synthesis, with paracetamol considered the safest option 2, 5.
• The mechanism of action of antipyretic drugs involves inhibiting the enzyme cyclooxygenase and reducing prostaglandin E(2) levels within the hypothalamus, thereby relieving fever 6.