Acute respiratory acidosis decreases left ventricular contractility but increases cardiac output in dogs.
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To understand the cardiovascular response to respiratory acidosis, we measured hemodynamics, left ventricular pressure, and left ventricular volume (three ultrasonic crystal pairs) during eucapnia and respiratory acidosis in 10 fentanyl-anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope (Emax) and intercept (V0) of the left ventricular end-systolic pressure-volume relation determined by combining end-systolic points from a vena caval occlusion and from brief aortic cross-clamping. Respiratory acidosis (pH 7.09, Pco2 92 mm Hg) reduced contractility by a decrease in Emax (11.4 to 9.2 mm Hg/ml, p less than 0.01) with no change in V0. Despite this, cardiac output increased (1.7 to 2.1 l/min, p less than 0.01), and heart rate increased (96 to 121 beats/min, p less than 0.05), with no change in blood pressure. Systemic vascular resistance fell by 26% (p less than 0.01). During eucapnia, propranolol reduced Emax (11.4 to 4.6 mm Hg/ml, p less than 0.01) with no change in V0. After propranolol treatment, respiratory acidosis further reduced Emax (4.6 to 3.6 mm Hg/ml, p less than 0.05) and increased end-systolic volume more than before propranolol (p less than 0.001). Now cardiac output did not increase even though heart rate increased (81 to 106 beats/min, p less than 0.001) and systemic vascular resistance fell by 20% (p less than 0.01). We conclude that the effect of respiratory acidosis on the circulation is to increase venous return (equals cardiac output) in the face of decreased left ventricular contractility. The beta-adrenergic response to respiratory acidosis substantially ameliorated the increase in end-systolic volume and supported the increase in venous return but did not alter the associated tachycardia or vasodilation. Respiratory acidosis, like propranolol treatment, decreases contractility by decreasing Emax. (+info)
Acute renal response to rapid onset respiratory acidosis.
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Extracorporeal carbon dioxyde removal for additional pulmonary resection after pneumonectomy.
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Additional pulmonary surgery in a previously pneumonectomized patient requires apnea during surgical manipulation of the surviving lung. We report on a novel approach to manage the intraoperative apnea period, combining apneic oxygenation and minimally invasive, low flow extracorporeal CO2 removal. A 69-year-old man previously submitted to left pneumonectomy was scheduled for wedge resection of a single right upper lobe lesion. During the intraoperative apnea period, oxygenation was maintained through apneic oxygenation with continuous positive airway pressure (CPAP) of 5 cmH2O and inspiratory oxygen fraction (FiO2) of 1 and respiratory acidosis was prevented through extracorporeal CO2 removal, performed with the Decap(R) system (Hemodec, Salerno, Italy), a veno notvenous pump-driven extracorporeal circuit including a neonatal membrane lung. The extracorporeal circuit was connected to the right femoral vein, accessed via a 14 Fr double lumen catheter. The blood flow through the circuit was 350 mL/min and the sweep flow of oxygen through the membrane lung was 8 L/min. The intraoperative apnea period lasted 13 minutes. Our approach allowed maintaining normocapnia (PaCO2 38,5 and 40 mmHg before and at the end of the apnea period, respectively), preserving oxygenation (P/F ratio 378, 191, 198 and 200 after 3, 6, 9 and 12 min of apnea, respectively). Our report suggests that the minimally invasive CO2 removal associated with apneic oxygenation is an useful technique for managing anesthesiological situations requiring moderate apnea periods. (+info)
Effects of hypercapnia and hypercapnic acidosis on attenuation of ventilator-associated lung injury.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with impaired gas exchange, severe inflammation and alveolar damage including cell death. Patients with ALI or ARDS typically experience respiratory failure and thus require mechanical ventilation for support, which itself can aggravate lung injury. Recent developments in this field have revealed several therapeutic strategies that improve gas exchange, increase survival and minimize the deleterious effects of mechanical ventilation. Among those strategies is the reduction in tidal volume and allowing hypercapnia to develop during ventilation, or actively inducing hypercapnia. Here, we provide an overview of hypercapnia and the hypercapnic acidosis that typically follows, as well as the therapeutic effects of hypercapnia and acidosis in clinical studies and experimental models of ALI. Specifically, we review the effects of hypercapnia and acidosis on the attenuation of pulmonary inflammation, reduction of apoptosis in alveolar epithelial cells, improvement in sepsis-induced ALI and the therapeutic effects on other organ systems, as well as the potentially harmful effects of these strategies. The clinical implications of hypercapnia and hypercapnic acidosis are still not entirely clear. However, future research should focus on the intracellular signaling pathways that mediate ALI development, potentially focusing on the role of reactive biological species in ALI pathogenesis. Future research can also elucidate how such pathways may be targeted by hypercapnia and hypercapnic acidosis to attenuate lung injury. (+info)
Effects of seasonal vitamin D deficiency and respiratory acidosis on bone metabolism markers in submarine crewmembers during prolonged patrols.
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The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise.
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