A 38-year-old woman comes to the emergency department due to progressive shortness of breath over the past 2 weeks. The patient states that she can hardly move without gasping for breath. She delivered a healthy baby 8 months ago, and her pregnancy was uncomplicated. For the last 6 months, the patient has experienced palpitations, poor sleep, and unintentional weight loss. She has no known chronic medical conditions. The patient is a lifetime nonsmoker, does not consume alcohol, and does not use illicit drugs or supplements. Her mother has rheumatoid arthritis. Blood pressure is 145/75 mm Hg and pulse is 110/min and regular. Oxygen saturation is 93% on room air. The neck appears full. The skin is warm and moist. Crackles are heard at the bilateral lung bases. The apical impulse is strong, and a 2/6 midsystolic murmur is heard in the second left intercostal space. There is 1+ symmetric peripheral edema. ECG shows sinus tachycardia. Further investigations are likely to demonstrate which of the following?
Cardiovascular effects of hyperthyroidism | |
Increased rate |
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Increased contractility |
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| Peripheral vasodilation |
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Additional effects |
|
This patient's presentation with progressive shortness of breath, peripheral edema, and basilar lung crackles with mild hypoxemia is consistent with decompensated heart failure. Her recent palpitations, poor sleep, and unintentional weight loss suggest hyperthyroidism, a common cause of high-output heart failure.
The primary disturbance in high-output heart failure is decreased systemic vascular resistance (SVR), which, in hyperthyroidism, results from peripheral vasodilation due to increased tissue metabolic demand and direct thyroid hormone vasodilatory effects. This causes decreased diastolic blood pressure; in response, there is a reflexive increase in myocardial contractility and heart rate (thyroid hormone also has a direct sympathetic-like effect on the myocardium). The increased contractility increases stroke volume (eg, wide pulse pressure, increased systolic blood pressure) and cardiac output, with resultant hyperdynamic circulation (which explains this patient's prominent apical point of maximal impulse [PMI] and 2/6 pulmonic flow murmur).
Because the increased cardiac output flows against low SVR, blood returns to the heart quickly and easily, increasing venous return. Despite a sustained elevation in cardiac output, the left ventricle is eventually unable to keep up with the increased venous return, and decompensated heart failure (eg, pulmonary edema, peripheral edema) develops.
(Choice B) A large pericardial effusion can cause subacute cardiac tamponade. Patients can have progressive dyspnea, but hypotension and clear lungs are also expected.
(Choices C and D) Left ventricular apical akinesis occurs with Takotsubo (stress) cardiomyopathy, which can cause heart failure. Mobile heart valve lesions are seen with infective endocarditis, and associated valvular dysfunction (eg, mitral or aortic regurgitation) can lead to heart failure. These types of heart failure are low output (ie, the primary disturbance involves the left ventricle); therefore, a prominent PMI, flow murmur, and wide pulse pressure are not expected.
(Choice E) Right-to-left intracardiac shunting can eventually develop with ventricular septal or atrial septal defect, resulting in Eisenmenger syndrome. Affected patients have pulmonary hypertension and right-sided heart failure; cyanosis and marked hypoxemia (eg, saturation <88%) are expected in the absence of pulmonary edema, unlike in this patient.
Educational objective:
High-output heart failure is caused by decreased systemic vascular resistance that leads to an increase in stroke volume, cardiac output, and venous return and is recognized by a wide pulse pressure and prominent point of maximal impulse. Hyperthyroidism is a common cause of high-output heart failure.