Why do certain cardiac conditions, such as heart failure, cause orthopnea?

Orthopnea in Cardiac Conditions: Pathophysiological Mechanisms

Orthopnea in cardiac conditions primarily occurs because supine positioning causes mobilization of fluid from dependent venous reservoirs in the abdomen and lower extremities to the thoracic compartment, increasing venous return by 250-500cc, which elevates already high right and left-sided filling pressures, resulting in interstitial pulmonary edema, reduced pulmonary compliance, increased airway resistance, and dyspnea. 1

Hemodynamic Mechanisms

Fluid Redistribution

• When a patient with heart failure lies flat, gravity facilitates the redistribution of approximately 250-500cc of fluid from the lower extremities and abdomen into the central circulation 1
• This increased venous return overwhelms the already compromised heart's ability to manage the additional volume
• Pulmonary venous and capillary pressures rise further, elevating already high filling pressures

Pulmonary Congestion Cascade

1. Increased venous return → elevated right and left-sided filling pressures
2. Elevated pulmonary capillary wedge pressure (PCWP) → interstitial pulmonary edema
3. Pulmonary edema → reduced pulmonary compliance and increased airway resistance
4. These changes → increased work of breathing and dyspnea

Respiratory Consequences

Mechanical Changes

• Reduced lung compliance (C,L) when supine (0.08 ± 0.02 L/cm H₂O sitting vs. 0.07 ± 0.01 supine) 2
• Increased airway resistance (R,L) in supine position (4.7 ± 1.2 cm H₂O/L × s sitting vs. 7.9 ± 2.5 supine) 2
• Increased diaphragmatic effort as measured by pressure time product (PTPdi/min) (181 ± 54 cm H₂O × s/min sitting vs. 243 ± 97 supine) 2

Expiratory Flow Limitation

• Expiratory flow limitation (FL) is common in acute left heart failure patients 3
• FL is induced or aggravated by the supine position in many patients
• This coincides with orthopnea in most cases, suggesting a causal relationship
• Control subjects without heart failure do not exhibit FL in either position

Bronchial Circulation Contribution

• The bronchial circulation may become engorged in heart failure 4
• This engorgement leads to thickened bronchial mucosal and submucosal tissues
• Reduced airway compliance results in airway obstruction and restriction
• These structural changes contribute to "cardiac asthma" and orthopnea

Clinical Significance

Diagnostic Value

• Orthopnea correlates with high PCWP with a sensitivity approaching 90% 1
• Persistent orthopnea is associated with higher rates of hospitalization during 6-month follow-up 1, 5
• Patients with persistent orthopnea show no improvement in left ventricular ejection fraction (LVEF), while those who become orthopnea-free show significant LVEF improvement (11% ± 13% vs. -1% ± 6%) 5

Assessment Technique

• Test for orthopnea by asking the patient to lie supine for a defined period (e.g., 2 minutes) while monitoring respiratory rate and breathlessness 1
• At discharge, patients should ideally be able to lie flat or with no more than one pillow without developing breathlessness 1

Common Pitfalls and Caveats

• Orthopnea is not specific to cardiac conditions and may have non-cardiac origins 1
• The severity of orthopnea may reflect both the rapidity of rise in PCWP and its absolute value 1
• In cyanotic heart disease, dyspnea within 30 seconds of exercise is due to hypoxemic and acidotic blood reaching central receptors, not pulmonary congestion 1
• High-output heart failure states (anemia, AV fistulae, hyperthyroidism) can also present with orthopnea despite different underlying mechanisms 6

Understanding these mechanisms helps clinicians appreciate why orthopnea is such a valuable clinical sign in heart failure assessment and management, with both diagnostic and prognostic implications.