Intrinsic myocardial recovery from the negative inotropic effects of acute hypercapnia

Foëx, P.; Fordham, Richard

doi:10.1093/cvr/6.3.257

Cited by 21 publications

(4 citation statements)

References 12 publications

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“…Acute hypercapnia depresses the contractility of isolated myocardium, 6 although this is compensated rapidly during sustained hypercapnia, as a result of correction of intracellular acidosis. 7 In vivo, decreased contractility is offset by increased sympathetic stimulation, and cardiac output increases. 8 Recent studies of patients with ARDS have found that cardiac output increased in all patients during low volume ventilation with permissive hypercapnia.…”

Section: Discussionmentioning

confidence: 99%

Permissive hypercapnia and gas exchange in lungs with high Qs/Qt: a mathematical model

Joyce

Hickling

1996

British Journal of Anaesthesia

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Low volume ventilation with permissive hypercapnia is becoming widely used in the treatment of acute respiratory distress syndrome. A mathematical model was developed to examine the effects of hypoventilation on pulmonary gas exchange in lungs with a range of shunt fractions. Hypoventilation did not worsen gas exchange, provided the inspired oxygen concentration was high enough to maintain PAO2 at an adequate level. In lungs with a high shunt fraction, some improvement in gas exchange may result, but these effects are small. A rightwards shift of the oxygen-haemoglobin dissociation curve induced by hypercapnia, is likely to be beneficial rather than detrimental in patients with acute respiratory distress syndrome. This analysis was limited to the direct effects of hypoventilation in lungs with constant shunt fractions, and did not encompass a number of possible secondary effects such as changes in cardiac output with PaCO2, changes in shunt fraction associated with a reduction in mean airway pressure and possible direct effects of hypercapnia on the pulmonary vasculature or airways.

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Section: Discussionmentioning

confidence: 99%

Permissive hypercapnia and gas exchange in lungs with high Qs/Qt: a mathematical model

Joyce

Hickling

1996

British Journal of Anaesthesia

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“…18 It is this indirect sympathetic outpouring that largely mediates the effects of hypercapnia on the circulatory system. Numerous investigators have demonstrated the direct myocardial depressant effects of hypercapnia and intracellular acidosis, [19][20][21] which are largely due to the interference with myofilament response to calcium. 22 Hypercapnia results in coronary vasodilation in the normal heart, though this effect is blunted in ischemic left ventricular failure.…”

Section: Cardiovascular Effectsmentioning

confidence: 99%

Acute Respiratory Distress Syndrome: Adjuncts to Lung-Protective Ventilation

Kress

Marini²

2001

Seminars in Respiratory and Critical Care Medicine

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Despite recent advances in understanding, the management of acute respiratory distress syndrome (ARDS) remains a challenging clinical problem. Optimization of gas exchange and preventing the iatrogenic propagation of lung injury are cornerstones of its clinical management. A number of novel approaches and adjuncts to mechanical ventilation have been described over the past decade to help achieve these goals, and some have been widely implemented with varying degrees of success. This chapter will review the rationale and evidence supporting the use of such adjunctive strategies.

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“…1 Hypercapnic acidosis directly reduces contractility in isolated heart muscle preparations, 2 causes peripheral vasodilation, and indirectly increases the release of catecholamines from sympathetic nerve endings and adrenal glands. 3 , 4 We have previously observed that thoracolumbar epidural anesthesia (EA) in dogs abolishes the physiologic increase in circulating catecholamine concentrations and reduces cardiac output (CO) and mean arterial blood pressure (MAP) during marked hypercapnic acidosis.…”

mentioning

confidence: 99%

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits

Mizukoshi

Sato

Yoshida

2001

Can J Anesth/J Can Anesth

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Purpose: We have previously observed that sympathetic blockade by epidural anesthesia (EA) modifies the cardiovascular response to marked hypercapnic acidosis in dogs. Our objective was to determine whether the combination of marked hypercapnic acidosis and EA reduce left ventricular contractility.Methods: We randomly assigned 22 Japanese white rabbits anesthetized with isoflurane (1.0%) to two groups according to the absence (control group, n=11) or presence (EA group, n=11) of thoracolumbar EA. After epidural injection (0.5 mL·kg -1 of 0.9% saline in the control group or 1% mepivacaine in the EA group) and during subsequent hypercapnia (mean arterial CO 2 tension 85 mmHg), we measured left ventricular pressure, left ventricular volume by using conductance catheter and plasma catecholamine concentrations. Left ventricular contractility was assessed by the slope of the linear approximation of the left ventricular end-systolic pressure-volume relationship, [i.e., end-systolic elastance (Ees)].Results: The combination of hypercapnic acidosis and thoracolumbar EA caused a 65% decrease in Ees (P <0.05). Hypercapnic acidosis alone caused a 16% decrease (P <0.05) and thoracolumbar EA alone caused a 49% decrease in Ees (P <0.05). In the EA group, epidural injection caused an 85% decrease in the epinephrine concentration (P <0.05) and a 39% decrease in the norepinephrine concentration (P <0.05), even during hypercapnic acidosis. However, in the control group, hypercapnic acidosis caused no change in the circulating epinephrine concentration but a 74% increase in the circulating norepinephrine concentration (P <0.05).

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Intrinsic myocardial recovery from the negative inotropic effects of acute hypercapnia

Cited by 21 publications

References 12 publications

Permissive hypercapnia and gas exchange in lungs with high Qs/Qt: a mathematical model

Permissive hypercapnia and gas exchange in lungs with high Qs/Qt: a mathematical model

Acute Respiratory Distress Syndrome: Adjuncts to Lung-Protective Ventilation

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits

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