The impulse from the SA node travels to the atrioventricular (AV) node through the internodal pathways.

Rationale

A heart attack, or myocardial infarction, occurs when blood flow through a coronary artery is obstructed, leading to ischemia and damage to the heart muscle. This affects the myocardium supplied by the blocked artery, most often the left ventricle, which is critical for systemic circulation. Physiologically, ischemia triggers chest discomfort or pressure, often radiating to the arm, jaw, or back, due to nerve stimulation and inflammatory responses. Additional symptoms include shortness of breath from reduced cardiac output, fatigue from impaired perfusion, nausea from vagal stimulation, and lightheadedness from hypotension or arrhythmias, reflecting the heart’s decreased ability to meet the body’s metabolic demands.

A. Increases vasodilation: The renin-angiotensin-aldosterone system (RAAS) primarily promotes vasoconstriction via angiotensin II to maintain perfusion pressure. It does not cause vasodilation; therefore, this is not a compensatory mechanism in heart failure.

B. Increased blood pressure: Activation of RAAS leads to angiotensin II–mediated vasoconstriction and aldosterone-mediated sodium retention, both of which increase systemic vascular resistance and blood pressure. This helps maintain perfusion to vital organs despite reduced cardiac output.

C. Increases heart rate: RAAS indirectly increases heart rate by promoting sympathetic nervous system activation. Elevated angiotensin II levels stimulate catecholamine release, contributing to tachycardia as a compensatory mechanism to maintain cardiac output.

D. Increases water retention: Aldosterone released by the adrenal cortex in response to RAAS activation enhances sodium and water reabsorption in the kidneys. This increases intravascular volume, which can help raise preload and temporarily improve stroke volume, though excessive retention may worsen edema.

E. Increases respirations: RAAS does not directly influence respiratory rate. Increased respirations in heart failure typically result from pulmonary congestion or hypoxia, not from RAAS activation.