What is the likely cardiac output state in a patient with symptoms of heart failure, including shortness of breath, palpitations, and peripheral edema, following a recent pregnancy and delivery?

High Cardiac Output State in Peripartum Thyrotoxic Heart Failure

This patient has high-output heart failure secondary to hyperthyroidism presenting in the postpartum period, and further investigations will demonstrate high cardiac output (option a).

Clinical Presentation Analysis

This 38-year-old woman presents with a classic constellation of findings pointing to thyrotoxicosis-induced high-output heart failure:

• Hyperthyroid symptoms: 6 months of palpitations, poor sleep, unintentional weight loss, warm moist skin, and full neck appearance (likely goiter) 1
• Heart failure signs: Progressive dyspnea, bilateral crackles, peripheral edema, elevated jugular venous pressure ("full neck"), and oxygen desaturation 2, 3
• Hemodynamic findings: Tachycardia (110 bpm), widened pulse pressure (145/75 mmHg), strong apical impulse, and flow murmur 1

Pathophysiology of High-Output Heart Failure

Hyperthyroidism causes peripheral vasodilation and reduced systemic vascular resistance, leading to compensatory increases in cardiac output that eventually overwhelm the heart's capacity. 4 The thyroid hormones directly increase metabolic demands while simultaneously decreasing systemic vascular resistance through peripheral vasodilation, creating a high-output state that can progress to overt heart failure 4.

The clinical presentation differs fundamentally from typical low-output heart failure:

• Warm, moist skin (versus cool, clammy skin in low-output states) 1
• Bounding pulses and widened pulse pressure 1
• Strong/hyperkinetic apical impulse (versus weak in systolic dysfunction) 1

Why Other Options Are Incorrect

Large pericardial effusion (option b) would present with:

• Muffled heart sounds (not present here) 1
• Paradoxical pulse 1
• Electrical alternans on ECG 1
• The strong apical impulse argues strongly against significant pericardial effusion 1

Left ventricular apical akinesis (option c) suggests:

• Takotsubo cardiomyopathy or peripartum cardiomyopathy with regional wall motion abnormalities 1
• However, this patient's warm skin, bounding pulses, and hyperkinetic precordium indicate preserved or increased contractility, not regional dysfunction 1
• Peripartum cardiomyopathy typically presents with low-output failure and displaced apical impulse with reduced contractility 1

Right-to-left intracardiac shunt (option d) would cause:

• Cyanosis disproportionate to pulmonary findings 1
• Differential cyanosis or clubbing 1
• This patient's oxygen saturation of 93% is explained by pulmonary edema, not shunting 2

Diagnostic Approach

The systematic evaluation should prioritize excluding cardiac mimics before diagnosing primary heart failure. 1, 5 In this case:

1. Thyroid function tests are essential given the classic hyperthyroid symptoms occurring postpartum 1
2. Echocardiography will likely show:
   • Preserved or hyperdynamic left ventricular function 4
   • Increased cardiac output 4
   • Normal or mildly dilated chambers 4
3. BNP/NT-proBNP may be elevated despite high output due to volume overload 2, 6

Critical Clinical Pearls

Postpartum thyroiditis occurs in 5-10% of women and can present with hyperthyroidism 1-6 months postpartum, exactly matching this patient's timeline. 1 The combination of recent pregnancy and hyperthyroid symptoms should immediately raise suspicion for this diagnosis 1.

High-output heart failure requires fundamentally different management than low-output failure. 4 Standard heart failure therapies like ACE inhibitors and vasodilating beta-blockers can worsen hemodynamics by further reducing systemic vascular resistance 4. Treatment must focus on:

• Correcting the underlying hyperthyroidism 4
• Cautious diuresis for volume overload 4
• Rate control with non-vasodilating agents if needed 4

The midsystolic murmur at the left upper sternal border represents a flow murmur from increased cardiac output, not structural valve disease. 1 This is a common finding in high-output states and pregnancy-related hemodynamic changes 1.