Effects of sodium-nitroprusside and urapidil on gas exchange and ventilation-perfusion relationships in patients with congestive heart failure

Adnot, S; Radermacher, P; Andrivet, P; Jl, Dubois-Randé; Dupeyrat, A; Lemaire, F

doi:10.1183/09031936.93.04010069

Cited by 18 publications

(1 citation statement)

References 27 publications

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“…In summary, it is clear that in patients with OOPD, as well as PPH, a lowered (vasodilators) or augmented (almitrine) active pulmonary vascular tone is almost invariably paralleled by a deterioration or enhancement of V AIQ matching, respectively. Whether or not this statement will be altered by the use of new drugs, such as urapidil or nitric oxide [15,19,20], which may have a highly selective effect on the pulmonary vasculature, is still a matter of current research.…”

Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Effect of pulmonary hypertension on gas exchange

Agustí

Rodríguez-Roisin²

1993

Eur Respir J

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This paper reviews the effects of pulmonary artery hypertension on gas exchange by exploring three different issues, namely: 1) how does gas exchange behave in diseases characterized by increased vascular tone (primary pulmonary hypertension (PPH), chronic obstructive pulmonary disease (COPD) and interstitial pulmonary fibrosis (IPF)) or decreased vascular tone ("hepatopulmonary syndrome"); 2) how does exercise, as a non-pharmacological tool of increasing pulmonary blood flow, modify gas exchange in these diseases; and 3) how do several drugs that lower (vasodilators) or increase (almitrine) the active component of pulmonary hypertension interact with gas exchange. Available data show that: 1) in PPH a high pulmonary vascular tone enhances gas exchange and when it is lowered, either by oxygen or vasodilators, ventilation perfusion (VA/Q) distributions deteriorate; 2) in COPD a lowered (vasodilators) or augmented (almitrine) active vascular tone is almost invariably paralleled by a deterioration or enhancement of ventilation-perfusion matching, respectively; 3) in IPF an adequate active response of the pulmonary vasculature is essential to maintain gas exchange, both at rest and during exercise; and 4) in patients with liver cirrhosis a low pulmonary vascular tone induces an abnormal VA/Q distribution. In summary, these data show that any situation and/or therapeutic intervention that lowers the active vascular tone deteriorates VA/Q relationships and vice versa. The final effect of pulmonary vascular tone on arterial oxygen tension (PaO2) is less predictable. The reason for this uncertainty is that the actual PaO2 value depends on the interplay of the intra- and extrapulmonary factors that control gas exchange in humans, and not only on the degree of VA/Q mismatching.

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Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Effect of pulmonary hypertension on gas exchange

Agustí

Rodríguez-Roisin²

1993

Eur Respir J

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Gas Exchange Consequences of Left Heart Failure

Robertson

2011

Comprehensive Physiology

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This review explores the pathophysiology of gas exchange abnormalities arising consequent to either acute or chronic elevation of pulmonary venous pressures. The initial experimental studies of acute pulmonary edema outlined the sequence of events from lymphatic congestion with edema fluid to frank alveolar flooding and its resultant hypoxemia. Clinical studies of acute heart failure (HF) suggested that hypoxemia was associated only with the final stage of alveolar flooding. However, in patients with chronic heart failure and normal oxygenation, hypoxemia could be produced by the administration of potent pulmonary vasodilators, suggesting that hypoxic pulmonary vasoconstriction is an important reflex for these patients. Patients with chronic left HF commonly manifest a reduced diffusing capacity, an abnormality that appears to be a consequence of chronic elevation of left atrial pressure. That reduction in diffusing capacity does not appear to be primarily attributable to increases in lung water but is improved by any sustained treatment that improves overall cardiac function. Patients with heart failure may also manifest an abnormally elevated VE/VCO2 during exercise, and that exercise ventilation abnormality arises as a consequence of both alveolar hyperventilation and elevated physiologic dead space. That elevated exercise VE/VCO2 in an HF patient has proven to be a powerful predictor of an adverse outcome and hence it has received sustained attention in the HF literature. At least three of the classes of drugs used to treat HF will normalize the exercise VE/VCO2, suggesting that the excessive ventilation response may be linked to elevated sympathetic activity.

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The effects of levosimendan and glibenclamide on circulatory and metabolic variables in a canine model of acute hypoxia

et al. 2011

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PurposeTo study the effects of pretreatment with levosimendan (LEVO, a Ca2+-sensitizer and KATP+ channel opener) and/or the KATP+ channel antagonist glibenclamide (GLIB) on systemic hemodynamics, metabolism, and regional gastromucosal oxygenation during hypoxic hypoxemia.MethodsChronically instrumented, healthy dogs (24–32 kg, n = 6 per group, randomized cross-over design) were repeatedly sedated, mechanically ventilated (FiO2 ~0.3) and subjected to the following interventions: no pretreatment, LEVO pretreatment, GLIB pretreatment, or combined LEVO + GLIB pretreatment, each followed by hypoxic hypoxemia (FiO2 ~0.1). We measured cardiac output (CO, ultrasonic flow probes), oxygen consumption (VO2, indirect calorimetry), and gastromucosal microvascular hemoglobin oxygenation (μHbO2, spectrophotometry). Statistics: data are presented as mean ± SEM and compared by one-way ANOVA (direct drug effects within group) and two-way ANOVA (between all hypoxic conditions) both with Bonferroni corrections; p < 0.05.ResultsIn LEVO-pretreated hypoxemia, CO was significantly higher compared to unpretreated hypoxemia. The increased CO was neither associated with an increased VO2 nor with markers of aggravated anaerobiosis (pH, BE, lactate). In addition, LEVO pretreatment did not further compromise gastromucosal μHbO2 in hypoxemia. After combined LEVO + GLIB pretreatment, systemic effects of GLIB were apparent, however, CO was significantly higher than during unpretreated and GLIB-pretreated hypoxemia, but equal to LEVO-pretreated hypoxemia, indicating that GLIB did not prevent the increased CO in LEVO-pretreated hypoxia.ConclusionsLEVO pretreatment resulted in improved systemic circulation (CO) during hypoxemia without fueling systemic VO2, without aggravating systemic anaerobiosis markers, and without further compromising microvascular gastromucosal oxygenation. Thus, LEVO pretreatment may be an option to support the systemic circulation during hypoxia.

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Effects of sodium-nitroprusside and urapidil on gas exchange and ventilation-perfusion relationships in patients with congestive heart failure

Cited by 18 publications

References 27 publications

Effect of pulmonary hypertension on gas exchange

Effect of pulmonary hypertension on gas exchange

Gas Exchange Consequences of Left Heart Failure

The effects of levosimendan and glibenclamide on circulatory and metabolic variables in a canine model of acute hypoxia

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