The hemodynamic effects of prolonged respiratory alkalosis in anesthetized newborn piglets (original) (raw)
Related papers
The effect of respiratory alkalosis on oxygen consumption in anesthetized patients
Journal of Clinical Anesthesia, 1992
Study Objective: To investigate whether hyperventilation sign$cantly altered oxygen consumption in anesthetized and paralyzed patients undergoing surgery. Design: Open crossover trial with 1 hour of hyperventilation preceded and followed by I hour of normoventilation. Setting: University medical center. Patients: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis. Interventions: After baseline normoventilationfor I hour (Period l), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO,) of 20 to 25 mmHg for I hour {Period 2). Patients then experienced another hour of normoventilation (Period 3). Measurements and Main Results: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO, (P&O&, oxygen consumption (VO,), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, PH was significantly higher and FE&O2 and PaCO, signaficantly lower compared with the periods of normoventilation. VO, was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods. Conclusions: In anesthetized paralyzed patients, there is an increase in whole-body VO, with hypocapnic alkalosis.
The Journal of Pediatrics, 1984
Twenty-three newborn infants with severe bilateral pulmonary disease and persistent pulmonary hypertension received mechanical ventilation to pH >7.55 and Paco2 <25 torr. Response, as defined by attainment of a Paoe >100 torr, occurred in 87% of patients. Analysis of sequential arterial pH determinations revealed a linear increase in the number of infants responding as arterial pH increased. However, individual patients varied greatly in the optimal pH necessary to correct hypoxemia (range pH 7.50 to 7.75). Sixteen patients who had received mechanical hyperventilation were observed for 11.1 +-2.3 months. Virtually all had normal growth and development on follow-up physical and neurologic examinations, often despite profound or prolonged alkalosis and hypocarbia. In l I infants at a corrected gestational age of I year, Bayley Scales of Infant Development revealed normal mental developmental indices (mean 106.2 +_ 15.4) and normal, but significantly lower, psychomotor developmental indices (93.2 + 11.7) (P < 0.005). Although response and short-term outcome of neonatal hyperventilation appear favorable, this technique should be reserved for critically ill infants, because its long-term effects on the central nervous system are unknown. (J PEDIATR 105:457, 1984) ELEVATED PULMONARY VASCULAR RESISTANCE, causing systemic hypoxemia from right-to-left shunting at the level of the ductus arteriosus or foramen ovale, occurs in newborn infants with a variety of underlying pulmonary diseases? -9 Therapy for this syndrome of PPH has been directed at decreasing the ratio of pulmonary to systemic vascular resistance, thereby decreasing the amount of right-to-left shunting. Recently, several groups have demonstrated that hypocarbic alkalosis induced by mechanical ventilation is an effective mode of therapy for decreasing pulmonary artery resistance in affected newborn infants~ thereby improving systemic oxygenation. 5-8 Hypocarbia, however, has also been shown in laboratory animals and in From the
Injurious Effects of Hypocapnic Alkalosis in the Isolated Lung
American Journal of Respiratory and Critical Care Medicine, 2000
Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated bufferperfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (F I CO 2 ϭ 0.06) or groups with hypocapnia (F I CO 2 ϭ 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusioninduced acute lung injury. Surgical Dissection After premedication with intramuscular ketamine (85 mg kg Ϫ 1), anesthesia was induced with pentobarbital sodium (15-25 mg kg Ϫ 1) given intravenously, and heparin (1,000 IU) was administered. The surgical preparation used in this study was similar to that previously reported
Plasma potassium response to acute respiratory alkalosis
Kidney International, 1995
Plasma potassium response to acute respiratory alkalosis. Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes, acute respiratory alkalosis was induced by voluntary hyperventilation for 20 (18 and 36 liter/mm) and 35 minutes (18 liter/mm). The plasma potassium response to acute respiratory alkalosis was compared to time control, isocapnic and isobicarbonatemic (hypocapnic) hyperventilation as well as beta-and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic hyperventilation (standard acute respiratory alkalosis) at 18 or 36 liter/mm (PCO2-16 and-22.5 mm Hg, respectively) resulted in significant increases in plasma potassium (ca + 0.3 mmollliter) and catecholamine concentrations. During recovery (post-hyperventilation), a ventilation-rate-dependent hypokalemic overshoot was observed. Aipha-adrenoreceptor blockade obliterated, and beta-adrenoreceptor blockade enhanced the hyperkalemic response. The hyperkalemic response was prevented under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinically significant increase in plasma potassium. The hyperkalemic response is mediated by enhanced alphaadrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate. Acute respiratory alkalosis is the frequent acid-base disorder that results from hyperventilation. Hyperventilation is a common and important clinical event which occurs in response to pain (myocardial infarction), anxiety (stage fright, panic attacks), drugs (cocaine), hypoxemia (asthma attacks, pulmonary thromboembolism) and infection (sepsis). The importance of recognizing the electrolyte disturbances (that is, altered potassium homeostasis) produced by acute respiratory alkalosis has been emphasized owing to the potential for electrolyte-induced complications such as cardiac arrhythmias. The clinical importance attributed to alterations in potassium homeostasis during acute hyperventilation is underscored by the practice of administering potassium salts to treat hyperventilation-induced electrocardiographic abnormalities [1, 2]. Although, according to standard textbooks, it seems widely accepted that acute respiratory alkalosis results in hypokalemia in humans [3], a critical review of the literature reveals conflicting
Pediatric Pulmonology, 1999
Inhaled nitric oxide (NO) is currently used as an adjuvant therapy for a variety of pulmonary hypertensive disorders. In both animal and human studies, inhaled NO induces selective, dose-dependent pulmonary vasodilation. However, its potential interactions with other simultaneously used pulmonary vasodilator therapies have not been studied. Therefore, the objective of this study was to determine the potential dose-response interactions of inhaled NO, oxygen, and alkalosis therapies. Fourteen newborn lambs (age 1-6 days) were instrumented to measure vascular pressures and left pulmonary artery blood flow. After recovery, the lambs were sedated and mechanically ventilated. During steady-state pulmonary hypertension induced by U46619 (a thromboxane A 2 mimic), the lambs were exposed to the following conditions: Protocol A, inhaled NO (0, 5, 40, and 80 ppm) and inspired oxygen concentrations (FiO 2) of 0.21, 0.50, and 1.00; and Protocol B, inhaled NO (0, 5, 40, and 80 ppm) and arterial pH levels of 7.30, 7.40, 7.50, and 7.60. Each condition (in randomly chosen order) was maintained for 10 min, and all variables were allowed to return to baseline between conditions. Inhaled NO, oxygen, and alkalosis produced dose-dependent decreases in mean pulmonary arterial pressures (P < 0.05). Systemic arterial pressure remained unchanged. At 5 ppm of inhaled NO, alkalosis and oxygen induced further dose-dependent decreases in mean pulmonary arterial pressures (P<0.05). At inhaled NO doses >5 ppm, alkalosis induced further doseindependent decreases in mean pulmonary arterial pressure, while oxygen did not. We conclude that in this animal model, oxygen, alkalosis, and inhaled NO induced selective, dose-dependent pulmonary vasodilation. However, when combined, a systemic arterial pH >7.40 augmented inhaled NO-induced pulmonary vasodilation, while an FiO 2 >0.5 did not. Therefore, weaning high FiO 2 during inhaled NO therapy should be considered, since it may not diminish the pulmonary vasodilating effects. Further studies are warranted to guide the clinical weaning strategies of these pulmonary vasodilator therapies.
American journal of physiology. Lung cellular and molecular physiology, 2003
We previously found that nitric oxide synthase (NOS) inhibition fully blocked alkalosis-induced relaxation of piglet pulmonary artery and vein rings. In contrast, NOS inhibition alone had no effect on alkalosis-induced pulmonary vasodilation in isolated piglet lungs. This study sought to identify factors contributing to the discordance between isolated and in situ pulmonary vessels. The roles of pressor stimulus (hypoxia vs. the thromboxane mimetic U-46619), perfusate composition (blood vs. physiological salt solution), and flow were assessed. Effects of NOS inhibition on alkalosis-induced dilation were also directly compared in 150-350-microm-diameter cannulated arteries and 150-900-microm-diameter, angiographically visualized, in situ arteries. Finally, effects of NOS inhibition on alkalosis-induced vasodilation were measured in intact piglets. NOS inhibition with N(omega)-nitro-L-arginine fully abolished alkalosis-induced vasodilation in all cannulated arteries but failed to alte...
Respiratory Alkalosis: A Quick Reference
Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by the body. There is a decrease in PaCO 2 , increase in pH, and compensatory decreases in blood HCO 3 À concentration. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO 3 À , followed by longer lasting decreases in renal reabsorption of HCO 3 À. Chronic respiratory acidosis can be well compensated, and the arterial pH can be normal or near normal.