Key result
Severe emphysema linked to ~25% lower baseline cardiac index and reduced LV dimensions versus controls.
Why the study?
The prevailing view is that mainly the right side of the heart is involved in COPD, but left ventricular function and dimensions in severe emphysema patients were not well characterized.
Does severe emphysema impair left ventricular dimensions and systolic function compared to non-emphysematous controls?
Case-Control (n=20)
Does severe emphysema impair left ventricular dimensions and systolic function compared to non-emphysematous controls?
p-value: p=<0.001
In patients with severe emphysema, the left ventricle is hypovolemic and operates on a steeper portion of the function curve, but intrinsic systolic function is not significantly impaired.
Severe emphysema impairs LV filling with preserved systolic function; small observational data leave optimal perioperative preload strategies open.
BACKGROUND: Concomitant heart dysfunction during the course of chronic obstructive pulmonary disease is well recognized. The prevailing view is that mainly the right side of the heart is involved. We evaluated left ventricular (LV) function and dimensions in patients with severe emphysema. METHODS: Patients with severe emphysema undergoing lung volume reduction surgery were studied after anesthesia induction (n = 10). Non-emphysematous patients scheduled for lobectomy served as controls (n = 10). LV dimensions were measured with patients in the supine position by transesophageal two-dimensional echocardiography and systemic hemodynamics by a pulmonary artery thermodilution catheter, before and during central blood volume expansion by passive leg elevation. RESULTS: Baseline cardiac index (-25%), stroke volume index (SVI, -32%) stroke work index (-34%) and LV end-diastolic area index (EDAI, -33%) were significantly (P < 0.001) lower in the emphysema group. Passive leg elevation increased SVI and LV area ejection fraction more in the emphysema group than in controls (P < 0.05). The DeltaSVI/Delta pulmonary capillary wedge pressure and the DeltaSVI/DeltaEDAI relationships were significantly (P < 0.05) higher in the emphysema group compared to controls (2.2 +/- 0.71 vs 0.6 +/- 0.2 mL/mm Hg x m2 and 5.8 +/- 0.89 vs 2.8 +/- 0.8 mL/cm2 x m2, respectively). Preload-recruitable stroke work (Deltastroke work index/DeltaEDAI), a load-independent index of systolic LV function, did not differ between the two groups. CONCLUSION: The LV in patients with severe emphysema is hypovolemic, and operates on a steeper portion of the LV function curve, while indices of systolic function are not significantly impaired compared to non-emphysematous controls.
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Jörgensen et al. (2007) conducted a case-control in Severe emphysema (n=20). Severe emphysema vs. Non-emphysematous controls was evaluated on Baseline cardiac index, stroke volume index, stroke work index, and LV end-diastolic area index (p=<0.001). Patients with severe emphysema had significantly lower baseline cardiac index (-25%), stroke volume index (-32%), stroke work index (-34%), and LV end-diastolic area index (-33%) vs controls (P<0.001).
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