A 55-year-old man with chronic hypertension presents with dyspnea on exertion. Echocardiography shows left ventricular hypertrophy (LVH) with preserved ejection fraction. Regarding the factors affecting his cardiac output, all of the following will increase cardiac output EXCEPT:

Explanation

## Cardiac Output in LVH with Preserved Ejection Fraction **Key Point:** In this patient with LVH and diastolic dysfunction, the question asks which intervention will **NOT** increase cardiac output (CO = HR × SV). Option D (atropine-induced tachycardia) is the EXCEPT answer because increasing HR from 60→100 bpm is the **least effective** intervention and may actually reduce or fail to increase CO in diastolic dysfunction. ### Pathophysiology of LVH with Preserved EF - Chronic hypertension → increased afterload → compensatory concentric LVH - Diastolic dysfunction (impaired relaxation and reduced compliance) develops - Systolic function preserved (EF normal) at rest - **Critical limitation:** Stiff, non-compliant ventricle is highly preload-dependent; diastolic filling is already impaired ### Analysis of Each Intervention | Intervention | Effect on CO | Mechanism | |--------------|--------------|-----------| | **Dobutamine** (↑ contractility) | **↑ CO** | β1-agonist increases force of contraction and SV; also has mild lusitropic effect improving diastolic relaxation | | **Nitroprusside** (↓ afterload/SVR) | **↑ CO** | Reduces wall tension and afterload → improves SV per Frank-Starling; net CO increases in most clinical scenarios | | **Leg elevation + fluids** (↑ preload) | **↑ CO** | Increases ventricular filling → Frank-Starling mechanism; LVH hearts are preload-sensitive | | **Atropine** (↑ HR 60→100) | **Minimal/No ↑ CO** | Tachycardia shortens diastolic filling time → ↓ SV; in diastolic dysfunction, this is particularly detrimental as the stiff ventricle needs adequate time to fill | **High-Yield (Guyton & Hall / Harrison's):** In **diastolic dysfunction** (as in LVH with preserved EF): - Increased HR reduces diastolic filling time disproportionately - The stiff, non-compliant LV cannot compensate by increasing filling pressure rapidly - Net result: HR × SV may not increase meaningfully, or CO may even decrease - **Contrast:** In normal hearts, modest HR increase (60→100) reliably increases CO because diastolic filling reserve is intact > **Clinical Pearl:** The SME note correctly highlights that in some patients with preserved diastolic reserve, a modest HR increase *might* slightly increase CO. However, among all four options, atropine-induced tachycardia is the **least likely** to increase CO and most likely to be detrimental — making it the best "EXCEPT" answer. The other three interventions (inotrope, afterload reduction, preload augmentation) reliably increase CO in this setting. **Why not Option B (nitroprusside)?** While nitroprusside reduces preload (venodilation) in addition to afterload, the dominant effect in a patient with elevated SVR (hypertension) is afterload reduction → increased SV → net increase in CO. Excessive preload reduction could theoretically reduce CO, but this is not the primary expected effect at therapeutic doses in a hypertensive patient. **Mnemonic — CO optimization in LVH (SAID):** - **S**ympathomimetics (inotropes) — ↑ CO ✓ - **A**fterload reduction — ↑ CO ✓ - **I**ncrease preload (fluids, leg elevation) — ↑ CO ✓ - **D**on't increase HR (avoid tachycardia) — ✗ EXCEPT answer