What is the physiology of orthopnea (shortness of breath when laying flat)?

Physiology of Orthopnea (Shortness of Breath When Lying Flat)

Orthopnea occurs primarily due to increased venous return in the supine position, which mobilizes 250-500 cc of fluid from dependent areas to the thoracic compartment, elevating pulmonary venous and capillary pressures, resulting in interstitial pulmonary edema, reduced pulmonary compliance, and increased airway resistance. 1

Pathophysiological Mechanisms

• Supine positioning causes mobilization of fluid from dependent venous reservoirs in the abdomen and lower extremities, increasing venous return to the thoracic compartment 1
• This fluid shift elevates pulmonary venous and capillary pressures, further raising already high right and left-sided filling pressures 1
• The increased pressures may result in interstitial pulmonary edema, reduced pulmonary compliance, increased airway resistance, and subsequent dyspnea 1
• Orthopnea correlates with high pulmonary capillary wedge pressure (PCWP) with a sensitivity approaching 90% 1

Respiratory Mechanics in Orthopnea

• Expiratory flow limitation (EFL) is a common finding in patients with heart failure when lying supine, but is typically absent when sitting 2, 3
• In the supine position, patients with heart failure experience:
  • Decreased lung compliance (stiffer lungs) 4
  • Increased airway resistance 4, 3
  • Increased diaphragmatic pressure-time product (PTPdi/min), indicating higher respiratory muscle workload 4
• The increased respiratory effort strongly correlates with the severity of orthopnea 4

Cardiac Contributions

• Heart failure is the most common cause of orthopnea 1, 5
• Persistent orthopnea is associated with higher rates of hospitalization in heart failure patients 1
• In heart failure patients, orthopnea severity may reflect both the absolute value of PCWP and the rapidity of its rise 1
• The best predictors of orthopnea in heart failure patients include systolic pulmonary artery pressure, supine maximal inspiratory pressure, and the percentage change in inspiratory capacity from seated to supine position 3

Clinical Assessment

• Orthopnea can be objectively tested by asking the patient to lie supine for a defined period (e.g., 2 minutes) while monitoring respiratory rate and breathlessness 1
• Orthopnea is considered present when there is a positive difference in dyspnea scores between measurements made with the patient in the supine versus seated positions 2
• At hospital discharge, patients with heart failure should ideally be able to lie flat or with no more than one pillow without developing breathlessness 1

Special Considerations

• While orthopnea typically worsens in the supine position, some conditions like platypnea-orthodeoxia syndrome present with the opposite pattern - dyspnea and hypoxemia that worsen in the upright position and improve when lying flat 6, 7
• Central sleep apnea in heart failure often presents with Cheyne-Stokes respiration pattern and may be accompanied by orthopnea and paroxysmal nocturnal dyspnea 8
• In non-cardiac conditions like stroke, the supine position may be beneficial for cerebral perfusion in patients who can maintain oxygenation while lying flat, but those at risk for airway obstruction should have the head of the bed elevated 15° to 30° 1

Treatment Implications

• Short-term treatment with vasodilators and diuretics can control orthopnea and remove supine expiratory flow limitation in most patients with acute left heart failure 2
• Non-invasive mechanical ventilation in the supine position can significantly reduce the diaphragmatic workload and improve orthopnea in heart failure patients 4
• Addressing the underlying cause (typically heart failure) is essential for long-term management of orthopnea 1

Understanding the physiological mechanisms of orthopnea is crucial for appropriate clinical assessment and management of patients with this common symptom.