Can restrictive physiology cause high pulmonary capillary wedge pressures?

Restrictive Physiology and Pulmonary Capillary Wedge Pressure

Yes, restrictive physiology can cause elevated pulmonary capillary wedge pressure (PCWP) due to impaired ventricular filling and increased left ventricular end-diastolic pressure.

Pathophysiology of Restrictive Physiology

Restrictive physiology is characterized by:

• Impaired ventricular filling during diastole
• Increased myocardial stiffness
• Rapid early filling followed by abrupt cessation (dip and plateau pattern)
• Preserved systolic function in many cases

Hemodynamic Consequences

In restrictive physiology, several hemodynamic changes occur that directly affect PCWP:

1. Elevated LV Filling Pressures: Restrictive cardiomyopathy causes increased left ventricular end-diastolic pressure due to decreased ventricular compliance 1

2. Diastolic Dysfunction: Grade 3 diastolic dysfunction (restrictive filling pattern) is characterized by:

   • E/A ratio > 2.5
   • Deceleration time < 150 msec
   • Isovolumic relaxation time < 50 msec
   • Decreased septal and lateral e' velocities (3-4 cm/sec) 1

3. Backward Pressure Transmission: Elevated LV filling pressures are transmitted backward to the left atrium, pulmonary veins, and ultimately to the pulmonary capillary bed, resulting in elevated PCWP 2

Clinical Conditions with Restrictive Physiology

Several conditions can present with restrictive physiology and elevated PCWP:

Primary Restrictive Cardiomyopathies

• Idiopathic restrictive cardiomyopathy
• Cardiac amyloidosis
• Sarcoidosis
• Hemochromatosis
• Genetic causes 3

Hypertrophic Cardiomyopathy (HCM)

• Advanced HCM can develop restrictive physiology
• Characterized by E/e' ratio >14, LA volume index >34 mL/m², and pulmonary vein atrial reversal velocity 1

Heart Transplantation

• Heart transplant patients often show restrictive physiology early after transplantation
• Even "healthy" heart transplant patients can have normal intracardiac pressures at rest but dramatic increases in LV end-diastolic pressure during exercise 1

Constrictive Pericarditis vs. Restrictive Cardiomyopathy

• Both conditions can present with elevated PCWP
• Differentiation is important as constrictive pericarditis is potentially curable with surgery
• In constrictive pericarditis, septal e' is often higher than lateral e' (annulus reversus), unlike restrictive cardiomyopathy 1

Diagnostic Approach

When evaluating elevated PCWP in the context of suspected restrictive physiology:

1. Echocardiography:

   • Look for restrictive filling pattern (E/A ratio >2.5, shortened DT <150 ms)
   • Evaluate e' velocities (typically reduced in restrictive cardiomyopathy)
   • Assess LA volume (usually enlarged >34 mL/m²)
   • Rule out dynamic LVOT obstruction which can also cause elevated PCWP 1

2. Hemodynamic Assessment:

   • Right heart catheterization shows elevated PCWP
   • Dip and plateau pattern ("square root sign") in ventricular pressure tracings
   • Equalization of diastolic pressures in all four chambers in constrictive pericarditis

3. Differential Diagnosis:

   • Distinguish from other causes of elevated PCWP such as:
     • Left ventricular systolic dysfunction
     • Severe mitral regurgitation
     • Left-sided valvular disease
     • Volume overload states

Clinical Implications

Understanding that restrictive physiology causes elevated PCWP has important clinical implications:

• In patients with unexplained pulmonary hypertension, consider restrictive physiology as a potential cause 1
• Elevated PCWP in the setting of preserved ejection fraction should prompt evaluation for restrictive cardiomyopathy or HCM with restrictive physiology 1
• The ratio of pulmonary venous to mitral A velocity can be a useful marker for predicting elevated PCWP in patients with left ventricular dysfunction 4

Management Considerations

Management should target the underlying cause of restrictive physiology:

• For HCM with preserved EF and symptoms: beta-blockers or non-dihydropyridine calcium channel blockers are recommended 1
• Diuretics may be added when dyspnea persists despite beta-blockers or calcium channel blockers 1
• In heart transplant patients with restrictive physiology, careful monitoring is needed as this may be the first sign of acute rejection 1

Conclusion

Restrictive physiology significantly impacts ventricular filling dynamics, leading to elevated left ventricular end-diastolic pressures that are transmitted backward through the pulmonary circulation, resulting in elevated PCWP. Recognition of this relationship is crucial for proper diagnosis and management of patients with unexplained pulmonary hypertension or heart failure symptoms with preserved ejection fraction.