During a Valsalva manoeuvre phase II (forced expiration against resistance), heart rate increases. The mechanism is:

• A Increased intrathoracic pressure compresses the heart directly, releasing catecholamines from adrenal medulla
• B The Bainbridge reflex directly causes tachycardia due to elevated right atrial filling pressure
• C Vagal activation during expiration (respiratory sinus arrhythmia) causes phase II tachycardia
• D Elevated intrathoracic pressure reduces venous return, causing a fall in cardiac output and blood pressure; baroreceptors trigger sympathetic activation and tachycardia ✓

Explanation

In phase II of the Valsalva manoeuvre, sustained high intrathoracic pressure impedes venous return to the right heart, progressively reducing stroke volume and arterial blood pressure. Arterial baroreceptors (carotid sinus and aortic arch) detect the fall in blood pressure and reflexly increase sympathetic efferent activity while withdrawing vagal tone, producing tachycardia and peripheral vasoconstriction. In phase IV (release), the sudden restoration of venous return and stroke volume causes an 'overshoot' hypertension, which then reflexly slows the heart (bradycardia). Phase II tachycardia is therefore a baroreceptor-mediated reflex, not a direct cardiac compression effect.

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

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