Effects of isoflurane on oxygenation during one‐lung ventilation in pulmonary emphysema patients

F or decades the pulmonary circulation was not considered as important as the systemic ("greater") circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in understanding pulmonary vascular physiology and pathophysiology. This review discusses basic physiology, clinical concepts, and treatment options for pulmonary hypertension and the related right ventricular heart failure focusing on secondary pulmonary hypertension in patients during anesthetic procedures. Physiology of Pulmonary CirculationThe pulmonary vascular bed is a high-flow, lowpressure circulation system. Pulmonary vessels have less resistance in comparison to the systemic circulation under normal conditions because of higher compliance of pulmonary precapillary arterioles with a thinner media and less smooth muscle cells (SMCs) compared with the corresponding systemic arterioles. In addition, the cross-sectional area of the pulmonary vascular bed is large and highly distensible with recruitable vessels available to accommodate increase in flow resulting in low pressure and low resistance.In contrast to the systemic arteries, pulmonary vessels constrict with hypoxia (Euler-Liljestrand reflex) and relax in the presence of hyperoxia. Furthermore, changes in cardiac output (CO), airway pressure, and gravity affect the pulmonary more than the systemic circulation. Increases in CO distend open vessels and recruit previously closed vessels. Therefore, the crosssectional area of pulmonary circulation enlarges and results in a decrease in pulmonary vascular resistance (PVR). An increase in CO has very little effect on pulmonary arterial pressure (PAP) because of the recruitment and distension of pulmonary vessels. An increased PAP or left atrial pressure (LAP) may also distend and recruit pulmonary vessels. Clinically, this means that enhanced CO caused by the administration of inotropic drugs or enlarged blood volume will passively decrease PVR.

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“…In patients with pulmonary emphysema, arterial oxygenation was not affected by small isoflurane concentrations (0.5%-2%) during OLV (134).…”

Section: Volatile Anestheticsmentioning

confidence: 93%

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Fischer¹,

Aken²,

Rkle³

2003

Anesthesia & Analgesia

171

108

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“…In fact, when the same anesthetic was studied in humans, it did not suppress HPV. In a study of 10 patients undergoing thorascopic laser ablation of bullous emphysema, isoflurane was administered at varying concentrations from 2 to 0.5% and there was no significant difference seen in PaO 2 /FiO 2 , PaCO 2 , cardiac output, pulmonary arterial pressure, or PVR [72]. Due to both species, differences and the unique occurrence of chronic lung diseases in humans, the weighting of the literature on anesthetics and HPV should favor human studies (when the goal is altering medical practice).…”

Section: Inhalational Anesthetics Inhibit Hypoxic Pulmonary Vasoconstmentioning

confidence: 98%

An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: implications for managing single-lung anesthesia and atelectasis

Nagendran

Stewart

Hoskinson

et al. 2006

Current Opinion in Anaesthesiology

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“…Intravenous anesthetics, in particular propofol, seem to have even less (if any) of an inhibitory effect on HPV during unilateral ventilation 42–45 . Consequently, it is possible that this patient’s hypoxemia would have been less with intravenous rather than inhalational anesthesia, although the effect of isoflurane on arterial oxygenation in patients with emphysema undergoing unilateral ventilation in the lateral decubitus position appears to be minimal 46 .…”

Section: Case I: Lung Resection In a Patient With Copdmentioning

confidence: 99%

Pulmonary Pathophysiology and Lung Mechanics in Anesthesiology

Melo

Musch

Kaczka

2012

Anesthesiology Clinics

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The induction and maintenance of anesthesia, surgical requirements, and patients’ unique pathophysiology all combine to create a setting in which our accumulated knowledge of respiratory physiology and lung mechanics take on immediate and central importance in patient management. In this review we will take a case-based approach to illustrate how the complex interactions between anesthesia, surgery, and patient disease impact patient care with respect to pulmonary pathophysiology and clinical decision-making. We will examine two disparate scenarios: a patient with chronic obstructive pulmonary disease undergoing a lung resection, and a patient with coronary artery disease undergoing cardiopulmonary bypass. In each example we will illustrate how important concepts in pulmonary physiology and respiratory mechanics impact clinical management decisions.

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Effects of isoflurane on oxygenation during one‐lung ventilation in pulmonary emphysema patients

Abstract: In patients with pulmonary emphysema, arterial oxygenation is not affected by low isoflurane concentration during OLV in the lateral decubitus position.

Cited by 11 publications

References 18 publications

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: implications for managing single-lung anesthesia and atelectasis

Pulmonary Pathophysiology and Lung Mechanics in Anesthesiology

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