The prognostic value of pulmonary artery compliance in cardiogenic shock

Figures

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  Fig. 1.. Correlations between pulmonary artery compliance, wedge pressure, age, and catecholamines. Influence of pulmonary artery wedge pressure (PAWP, a), age (b), norepinephrine (c), and dobutamine (d) treatment on pulmonary artery compliance (CPA) in patients with cardiogenic shock. Regression lines (in red) and r2 determination coefficients are shown for each correlation.

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  Fig. 2.. Pulmonary artery compliance and time constant in survivors and nonsurvivors of cardiogenic shock. (a) Mortality (in percent of patients) according to quartiles of pulmonary artery compliance at 24 h (in mL/mm Hg: 1st Q = 0.7–1.7; 2nd Q = 1.7–2.6; 3rd Q = 2.6–3.6; 4th Q = 3.6–6.5). (b) Time to death in nonsurvivors, according to the quartile of CPA (Whiskers represent medians with Q1, Q3, and min/max values). A nonsignificant trend was noted for a shorter time to death with lower CPA quartiles (the 4th quartile of CPA was not included in the analysis, as there was only one death in this quartile). (c–e) Pulmonary vascular resistance (PVR) vs. compliance (CPA) diagrams in survivors (c) and nonsurvivors (d). Fused diagram (e) shows the leftward shift of the curve in nonsurvivors. Curves display the power function fitting of the PVR–CPA relationships. CPA units are mL/mm Hg; PVR units are mmHg s/mL. (f) Time-constant (RC-time) of the pulmonary circulation in survivors and nonsurvivors (dots: individual values; horizontal bars: mean values). Statistics: (a,b) Chi-square test. (f) Wilcoxon’s rank test.

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  Fig. 3.. Variation of pulmonary artery compliance between admission and 24 h. (a) Individual values of CPA in the 64 patients who had the PAC inserted directly upon admission (49 survivors, red squares, and 15 nonsurvivors, black dots), at 0 h (baseline) and 24 h. The dotted lines connect the mean values at 0 h and 24 h in survivors (red) and nonsurvivors (black). Statistical differences between survivors and nonsurvivors at 0 h and 24 h are indicated (Wilcoxon’s rank test). (b) Individual trends of CPA between 0 h (baseline) and 24 h in 49 survivors (left) and 15 nonsurvivors (right) with the PAC inserted directly on admission.

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  Fig. 4.. Hemodynamic variables according to the severity of right ventricle systolic dysfunction. (a) Severity of RV dysfunction in survivors and nonsurvivors (0: no dysfunction; 1: moderate dysfunction; 2: severe dysfunction). Values of PAWP (b), CVP (c), PVR (d), and CPA (e) according to RV dysfunction (dots: individual values; horizontal bars: mean values). Statistics: (a) Contingency analysis, chi-square test. (b–e) Wilcoxon’s rank test.

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  Fig. 5.. Proposed role of reduced pulmonary artery compliance in cardiogenic shock. A triggering factor such as cardiac ischemia leads to severe left ventricle (LV) systolic dysfunction (orange arrow), with subsequent low cardiac output (CO) and cardiogenic shock. The triggering factor may also affect the right ventricle (RV) (orange dotted arrow). LV dysfunction is associated with increased LV filling pressure, which is passively transmitted to the upstream pulmonary circulation, in turn increasing the stiffness of the pulmonary artery (PA), reducing PA compliance and shortening the PA time constant (black arrows). As a result, RV pulsatile afterload is increased, leading to RV–PA uncoupling and RV systolic dysfunction, which promotes further reduction of CO and amplifies acute circulatory failure (red arrows). RV–PA uncoupling may be exacerbated by the depressed RV systolic function due to reduced systolic interaction linked to LV systolic dysfunction.