Figure 7
From: A Feline HFpEF Model with Pulmonary Hypertension and Compromised Pulmonary Function
Concept of pathobiological and functional abnormalities due to elevated left-sided filling pressures. Slow-progressive pressure overload induces LV hypertrophy and interstitial fibrosis which subsequently causes impaired relaxation (prolongation of τ, decreased dP/dtmin) and impairment in systolic reserve function. LV remodeling and dysfunction results in elevated LV filling pressures (LVEDP), LA enlargement and LA dysfunction. Passive backward transmission of elevated pressures causes an increase in hydrostatic venous pressure and leads to pulmonary arterial hypertension, which promotes endothelial disruption with protein and fluid loss into the interstitium and alveoli (alveolar-capillary stress failure). Interestingly, not only capillaries are affected, but extra-alveolar vessels also show distinct perivascular fluid cuff formation. These cardiopulmonary abnormalities result in decreased respiratory compliance and impaired oxygenation. A-aDO2 = alveolar-arterial oxygen difference, Ao banding = aortic banding, LA = left atrium, LVH = left ventricular hypertrophy, mPAP = mean pulmonary arterial pressure, PaO2 = partial pressure of oxygen in arterial blood. Red boxes = structural changes, dark blue = functional changes, light blue = novel morphological pulmonary finding.
