Cardiac output in pregnancy increases by approximately 40–50% by the end of the first trimester. The primary mechanism driving this early increase is:

• A Increased heart rate from sympathetic activation by elevated progesterone
• B Increased stroke volume from plasma volume expansion and reduced peripheral resistance ✓
• C Direct inotropic effect of hCG on the myocardium
• D Decreased blood viscosity from haemodilution increasing CO

Explanation

Progesterone and relaxin cause systemic vasodilation, reducing total peripheral resistance. This activates the renin-angiotensin-aldosterone system, expanding plasma volume by 40–50% (more than red cell mass, causing physiological haemodilution). Increased venous return augments preload, and by Starling's law, stroke volume increases. Heart rate also rises modestly (~15–20 bpm). The initial driver is vasodilation → RAAS activation → plasma volume expansion → increased SV. This is the 'underfill' theory of pregnancy haemodynamics.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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