Pulmonary Pulse Pressure Research Articles

Pulmonary Arterial Wall Distensibility Assessed by Intravascular Ultrasound in Children With Congenital Heart Disease: An Indicator for Pulmonary Vascular Disease?

Both pulmonary hypertension and pulmonary overflow are associated with functional and structural changes of the pulmonary arterial wall. Current techniques to evaluate the pulmonary vasculature neglect the pulsatile nature of pulmonary flow. To determine whether the dynamic properties of the pulmonary arterial wall are altered in patients with abnormal pulmonary hemodynamics due to congenital heart defects, and whether these changes are associated with the progression of pulmonary vascular disease (PVD). In 43 children with PVD due to congenital heart defects and 12 control subjects, pulmonary arterial pulsatility (the relative increase in vessel area during the cardiac cycle) and distensibility (the inverse of the stress/strain elastic modulus) were determined with intravascular ultrasound. Results were correlated with clinical and hemodynamic parameters. Pulsatility correlated with pulmonary pulse pressure (p < 0.001), pulmonary-to-systemic vascular resistance ratio (PVR/SVR) [p = 0.001], and hemoglobin concentration (p = 0.01). However, when corrected for these variables, pulsatility did not differ between patients and control subjects. In contrast, arterial wall distensibility decreased with the severity of PVD and correlated independently with pulmonary-to-systemic arterial pressure ratio (p < 0.001) and PVR/SVR (p = 0.03), and with hemoglobin concentration (p < 0.01). Adjusted for hemodynamic variables, distensibility was still decreased in patients with PVD compared to control subjects. These results demonstrate that pulmonary arterial wall distensibility is progressively decreased in PVD; moreover, this decreased distensibility is, in part, related to increased distending pressure as a result of pulmonary hypertension but also, in part, to stiffening of the arterial wall during the disease process. Arterial wall distensibility may be of additional value in the evaluation of pulmonary vasculature and ventricular workload.

Bidirectional cavopulmonary shunt with right ventricular outflow patency: The impact of pulsatility on pulmonary endothelial function

Objective: Although in vitro studies have suggested the importance of flow pulsatility in endothelial function, few reports have focused on pulmonary endothelial function under decreased pulsatile flow after a bidirectional cavopulmonary shunt with or without an additional pulmonary flow source. The purpose of the present study was to assess the pulmonary endothelial function after bidirectional cavopulmonary shunt. Methods and results: Pulmonary vasodilating response was evaluated in 10 patients 0.4 to 7.0 years (median 1.6 years) after bidirectional cavopulmonary shunt who were provided an additional flow source by retaining the pulmonary outflow tract and in 8 control subjects. Average pulmonary flow velocity was measured with a Doppler flow wire placed in the segmental lower lobe pulmonary artery during incremental infusion of acetylcholine (10–8, 10–7, 10–6, and 10–5 mol/L) and then of nitroglycerin (0.5 and 1.0 μg · kg–1 · min–1) after recovery. In the control subjects, a dose-dependent increase in flow velocity was observed in response to acetylcholine (maximum increase was 155% ± 17% of baseline) and to nitroglycerin (maximum increase was 151% ± 20% of baseline). In contrast, patients showed a significantly impaired response to acetylcholine (maximum increase was 124% ± 17% of baseline; P <.01 vs control), whereas the response to nitroglycerin was preserved (138% ± 12% of baseline; P =.09 vs control). In addition, the maximum response to acetylcholine correlated significantly with the pulmonary pulse pressure (r = 0.89, P <.01) and with the pulmonary flow pulsatility (r = 0.88, P <.01). Conclusions: These results clearly suggest that patients after bidirectional cavopulmonary shunt show pulmonary endothelial functional attenuation and, of more importance, that decreased pulsatility of cavopulmonary flow is mainly responsible for this endothelial abnormality. (J Thorac Cardiovasc Surg 2001;121:1161-8)

Effects of calcium and its antagonists on hemodynamics and respiration

Acute tests on cats under Nembutal anesthesia show that intravenous injection of Ca2+ causes pathological respiration of the apneustic type and slight rises in pulmonary and arterial pressures. The calcium channel blockers verapamil and nifedipine decrease the amplitude of respiratory movements, increase the respiration rate and pulmonary pulse pressure, and lower systemic pressure. The introduction of verapamil or nifedipine into the fourth ventricle of the brain does not alter respiration or hemodynamics, whereas the introduction of Ca2+ leads to irreversible respiratory standstill. Hemodynamic parameters decrease 2–3 min after the respiratory standstill.

Mechanism of paradoxic pulse in bronchial asthma.

To elucidate the mechanism of paradoxic pulse in severe bronchial asthma, we performed hemodynamic studies and measured esophageal pressure in nine patients who had status asthmaticus and clinical paradoxic pulse. Two-dimensional echocardiography allowed simultaneous assessment of cyclic changes in right- and left-heart size throughout the respiratory cycle. Esophageal pressure varied from a markedly negative level during inspiration (-24.4 +/- 6.5 cm H2O) to a positive level during expiration (7.6 +/- 6.0 cm H2O). Competition between right- and left-heart chambers for pericardial space during inspiration was suggested by the reduced left ventricular cross-sectional area at end-systole (-24%, p less than 0.01) and end-diastole (-32%, p less than 0.01), the leftward septal shift, and the increased right ventricular internal diameter at end-systole (42%, p less than 0.01) and end-diastole (40%, p less than 0.001). Competition for filling, however, could not entirely account for the paradoxic pulse, for systemic and pulmonary pulse pressures were almost (within one cardiac cycle) in phase: both were minimal at inspiration and maximal at expiration. The increase in impedance to right ventricular ejection is another major factor reducing left ventricular preload at inspiration. This reduction in preload was shown to be the predominant mechanism for the decrease in left ventricular stroke output at inspiration.