Impact of rapid versus gradual changes in arterial partial pressure of carbon dioxide on blood flow and myocardial oxygenation in an experimental anaesthetized model

Abstract

Introduction Hyper- and hypocapnia have known vaso-modulatory effects in the coronary circulation. Oxygenation-sensitive cardiovascular magnetic resonance (OS-CMR) detects changes in tissue oxygenation and can provide a comprehensive assessment of the impact of systemic blood gas changes on the myocardium. The purpose of this study was to compare the physiological responses to rapid blood gas changes induced by hyperventilation followed by apnea in comparison to steady-state levels of hypocapnia and hypercapnia in an experimental animal model. Methods Eighteen anaesthetized female swine were used in this study. A blood flow probe was attached to the left descending coronary artery (LAD) after a left-sided thoracotomy. In ten animals a hemodynamically significant LAD stenosis was induced, while eight animals served as controls. In a 3 Tesla MRI, paCO2 was modulated from a pre-set baseline (paO2=100mmHg/paCO2=40mmHg) to 30mmHg and subsequently 50mmHg by minor changes in ventilation rate. Rapid changes in paCO2 were achieved by 60s of hyperventilating (30/min) from baseline followed by an apnea of up to 90 seconds. OS-CMR images, coronary blood flow (CBF) of the LAD and arterial blood gases were recorded at each state. Results Targeting stable hypocapnia of 30mmHg from baseline did not alter CBF or myocardial oxygenation. Subsequent stable hypercapnia (paCO2=50mmHg) increased CBF significantly in control (5±5%, p=0.007) and stenosed (4±6%, p=0.036) animals, and myocardial oxygenation rose in both post-stenotic territories (4.2±6.2%, p=0.036) and in control subjects (6.2±6.2%, p=0.011). Rapid hyperventilation induced a similar degree of hypocapnia (control: paCO2=25±7mmHg, stenosed: 27±3mmHg) and showed a significant decrease of CBF by -34±23% (p=0.012) in healthy animals, and a significant decrease of -10±6% (p=0.010) in stenosed animals. This had no effect on tissue oxygenation. Apnea resulted in a similar paCO2 (control: paCO2=52±9mmHg, stenosed: 47±7mmHg) compared to steady-state blood gas levels, which increased CBF significantly in controls 346±327% (p=0.008) and stenosed 82±110 (p=0.039) animals markedly. By the end of apnea, a rise in tissue oxygenation of 2.9±2.2% was observed in controls (p=0.008), -2.7±5.1 (0.125) was observed in the stenosed group (Figure). Significant difference in myocardial oxygenation responses observed between control and stenosed subject was exclusively observed with apnea (p=0.011). Discussion Rapid hyperventilation followed by apnea results in more pronounced changes in myocardial blood flow than similar steady state deflections in paCO2. Only apnea after hyperventilation induced deoxygenation in the stenotic myocardium, which is in agreement with the concept of hypercapnia induced intercoronary steal, while steady state deviation did not compromise myocardial oxygenation. Similar breathing maneuvers may be seen in the induction phase of anaesthesia, which could potentially be a harbinger of perioperative ischemic myocardial events.