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Difficulty: MediumHematology and Oncology

A 32-year-old G1P0 woman at 30 weeks gestation comes to the emergency department due to progressively worsening shortness of breath and orthopnea over the past two weeks. She says she has to prop herself up on three pillows at night to breathe comfortably. Medical history is significant for Hodgkin lymphoma diagnosed 5 years ago, which was successfully treated with six cycles of a chemotherapy regimen containing doxorubicin. She also has a history of mild asthma for which she uses an albuterol inhaler as needed. Her temperature is 37.0°C (98.6°F), blood pressure is 112/70 mm Hg, pulse is 108/min, and respirations are 24/min. Pulse oximetry is 94% on room air. Physical examination shows prominent jugular venous distention. Cardiac auscultation reveals a regular rate and rhythm with an apical S3 gallop. Lung auscultation reveals fine bibasilar crackles without wheezing. There is 2+ bilateral pitting edema in the lower extremities. Laboratory studies show:

ParameterResult
Hemoglobin11.2 g/dL
Leukocyte count9,200/mm³
Thyroid-stimulating hormone (TSH)2.1 µU/mL (normal: 0.4–4.0 µU/mL)
Arterial blood gas (room air):
pH7.48
pCO₂28 mm Hg
HCO₃⁻20 mEq/L

Which of the following is the most likely underlying mechanism for this patient's current presentation?

  1. Oxidative damage to cardiomyocytes leading to left ventricular dilationAnswer
  2. B
    Physiologic volume expansion and diaphragmatic elevation typical of late gestation
  3. C
    Airway smooth muscle constriction and bronchial mucosal inflammation
  4. D
    Autoimmune destruction of thyroid gland follicles leading to hormone deficiency
  5. E
    Primary metabolic acidosis with appropriate respiratory compensation

Answer

The correct answer is oxidative damage to cardiomyocytes leading to left ventricular dilation.
The correct answer identifies the pathophysiology of anthracycline-induced cardiotoxicity. The patient is presenting with classic signs of acute decompensated heart failure, including orthopnea, an S3 gallop, elevated jugular venous pressure, and pulmonary crackles. Her history of receiving doxorubicin (an anthracycline) puts her at high risk for dose-dependent cardiotoxicity. Anthracyclines generate reactive oxygen species that cause oxidative damage to cardiomyocytes, leading to myocyte necrosis and replacement fibrosis, which manifests as a dilated cardiomyopathy. The profound physiological volume expansion and increased cardiac output required during pregnancy act as significant stressors that frequently unmask previously asymptomatic, compensated ventricular dysfunction in cancer survivors.

Step-by-Step Solution

1
Analyze the patient's acute clinical presentation and physical exam findings.
The presence of orthopnea, jugular venous distention, an S3 gallop, bibasilar crackles, and peripheral edema strongly indicates acute decompensated heart failure (fluid overload).
Identifying the active clinical syndrome is the necessary first step to determine the underlying etiology.
2
Connect the heart failure diagnosis to the patient's past medical history.
The patient received doxorubicin for Hodgkin lymphoma 5 years ago. Doxorubicin is a known anthracycline.
Anthracyclines are notorious for causing irreversible, dose-dependent cardiotoxicity presenting as dilated cardiomyopathy.
3
Explain the trigger for her acute decompensation at this specific time.
The normal physiologic plasma volume expansion that peaks in the late second and early third trimester of pregnancy has increased her cardiac preload.
Increased cardiac demand during pregnancy frequently acts as a stressor that unmasks underlying, previously asymptomatic anthracycline-induced ventricular dysfunction.

Key Concept

Anthracycline-induced cardiotoxicity (dilated cardiomyopathy) unmasked by the physiological volume expansion of pregnancy.
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Topics

Hematology and Oncology

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