Influence of CO<sub>2</sub> on cardiovascular response to hypoxia in conscious dogs

Koehler, Raymond C.; McDonald, Brian; Krasney, J. A.

doi:10.1152/ajpheart.1980.239.4.h545

Cited by 38 publications

(67 citation statements)

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“…The fact that this change was no more apparent under normocapnia seems to support this inference. Such influence of CO2 on hypoxic heart rate response has already been reported by KOEHLER et al (1980). They examined the effect of CO2 on the circulatory response to hypoxia, and observed that heart rate response to hypoxia was enhanced under hypocapnia.…”

Section: Resultssupporting

confidence: 62%

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

1986

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The effect of airway anaesthesia by lidocaine inhalation on the hypoxic ventilatory response was examined together with the heart rate response by the isocapnic progressive hypoxia test in human subjects. During the test, end-tidal P~o2 (PETCo2) was maintained at the resting level. However, because resting PETCoz tends to decrease by airway anaesthesia, we conducted the test at the resting PETCo2 determined both before (normocapnic) and after lidocaine (hypocapnic). Ventilatory and heart rate response were evaluated as a linear function of oxygen saturation of the arterial blood (Sao2). In the "hypocapnic" runs, ventilatory responses tended to be depressed, while the slope of heart rate response-PET~o2 relationship increased after lidocaine. However, when PETC02 was restored to the normocapnic level, ventilation apparently increased from the control, and the augmented slope in the heart rate response disappeared. Although the elevated ventilation in normocapnic hypoxia might be due simply to the increased ventilatory response to C02, we suggested that the augmented slope in the heart rate response in hypocapnic hypoxia might be related not only to PET~o2 level itself but also to the direct effect of airway anaesthesia.Key words : airway anaesthesia, hypoxia, control of breathing, control of heart rate.It has been repeatedly confirmed by many investigators that airway anaesthesia induces enhanced ventilatory response to hypercapnia (CROSS et al., 1976; SULLIVAN and YU,1983;WINNING et al., 1985). However, it seems uncertain at present if this is also the case with response to other ventilatory stimuli. Recently, SULLIVAN and DEWEESE (1985) reported the lack of effect of lidocaine inhalation on hypoxic ventilation, and stated that only hypercapnic ventilation is increased after airway

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Section: Resultssupporting

confidence: 62%

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

1986

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“…During hypercapnic hypoxia as expected, V02 also decreased significantly; however, unlike the eucapnic group, cardiac output increased probably due to the highly stimulant effect of C 0 2 on the autonornjc nervous system (10, 17,24). Therefore for the same decrease in,V02, CaOrCVOn decreased significantly owing to the increased Q.…”

Section: Discussionsupporting

confidence: 65%

The Effect of High or Low Oxygen Affinity Red Cells on Tissue Oxygenation and Myocardial Function in Hypoxic Newborn Lambs with or without Hypercapnia

et al. 1983

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SummaryP:," increased so that it is in the range of adult human blood (27 mmHg). In order to compare high and low oxygen affinity blood under conditions of severe respiratory failure, the effects of a high or low PSO were evaluated in two groups of newborn lambs (Pso, 20 mmHg MATERIALS AND METHODS versus 30 mmHg), under conditions of h~poxic hypoxia (Fio2,10%)Twenty-six mixed breed newborn lambs less than 48 h old were and h~~r c a~n i c h~poxia (Fioz, 10% and Fico2, 10%). Data on included in this study. Intramuscular diazepam was used as secardiovascular function, blood gas Parameters, and tissue oxygen-dation (0.2 mg/kg as a loading dose, 0.1 mg/kg repeated at hourly ation were collected under normoxic conditions and during severe intervals). Infiltration of lidocaine 2% provided local anesthesia at h~poxia. During h~poxic h~poxia, a higher arterial oxygen content catheterization site. In an attempt to maintain constant metabolic was noted in the high affinity group throughout the experiment; demands, the animals were curarized with d-tubocurarine (0.2 however, there were no significant differences detected in the mg/kg intravenously), half of this dose being repeated if necessary. remainder of the parameters studied. During hypercapnic hypoxia, They were intubated and mechanically ventilated. Rectal temperthe position of the oxygen dissociation curve did not cause any ature was constantly controlled at 38.5 + 0.2"C. significant differences. When, however, h~perca~nic h~poxia wasPolyethylene catheters were positioned in descending aorta and compared to h~~x i c h~~x i a , there was a significant increase in right atrium. A Swan-ganz balloon catheter 5F was also placed in cardiac output and myocardial contraction during h~~r c a~n i a . the pulmonary artery as described previously ( 13,26). Stat ham P23Dc transducers provided pressure curves which were registered Abbreviations on a Grass model 7 paper recorder, giving heart rate, systolic, diastolic, and mean pressure values of both systemic and pulmoHbOz, hemoglobin oxygen saturation nary circulations. The position of the catheters was determined by LV, left ventricle the morphology of the pressure curve. For the right atrium the LVET, left ventricular ejection time catheter was advanced until the appearance of atrial extrasystoles. PEP, pre-ejection periodAt the end of the experiment the position of all catheters were ODC, oxygen dissociation curve confirmed at autopsy. The lambs were divided in four groups, two PVOz, venous oxygen tension of which had their high affmity red blood cells exchanged for low affinity red blood cells (Fig. 1). This was achieved by a two volume exchange transfusion (160 ml/kg) of fresh heparinized Recent studies in our laboratory have shown that a lower mixed adult sheep blood. The first series of 12 experiments were carried venous oxygen tension (PVon) in presence of high Oz affinity red out to compare the high and low oxygen affinity groups (six cells occurs in normoxemic newborn lambs and that severe anemic animals in each group...

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“…(5) and Koehler et at. (19) have shown that CO2changes coronary vascular resistance in the same direction as it does cerebral vascular resistance. Our data suggest that in the myocardium as in the brain, hypocarbia has an adverse effect on the adaptive responses to hypotension and anemia.…”

Section: Discussionmentioning

confidence: 94%

“…Our data do not indicate whether these differences are due to direct local effects of CO2 or are mediated through changes in vasoactive hormones or through reflexes. The studies of Koehler and Cowards in unanesthetized adult dogs suggest that the effects of CO2on systemic vascular resistance and blood pressure may be a reflex whereas its effect on myocardial flow is a local direct effect of CO2 (19).…”

Section: Discussionmentioning

confidence: 99%

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

et al. 1983

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SummaryNineteen newborn lambs, spontaneously breathing room air, were hemorrhaged of 50% of their measured blood volume over a 30-min period. They were then observed for the following 90 min. No fluid or blood was reinfused during the study. Eight of the 19 lambs survived beyond the study period, the other 11 died at the end of the hemorrhage or during the recovery period. All lambs became hypotensive and bradycardic during the hemorrhage. All became tachycardic after the hemorrhage. Blood pressure of the survivors returned towards baseline levels whereas it continued to fall in the non-survivors. All animals became anemic, acidotic, and hypocarbic but remained normoxemic.Myocardial blood flow fell to approximately 50% of baseline levels in both survivors and non-survivors during, and at the end of the hemorrhage. It returned to near baseline levels in the survivors by 90 min posthemorrhage. Cerebral blood flow remained at baseline levels during the hemorrhage in the survivors but cerebral oxygen delivery decreased. Flow rose 10% above baseline levels 90 min after hemorrhage but oxygen delivery remained low. In the non-survivors, cerebral blood flow fell to 60% of baseline and cerebral oxygen delivery was 50% of baseline by the end of the hemorrhage.A group of five lambs was hemorrhaged and studied in the same fashion as the 19, except that they breathed 4.5% CO 2 beginning 15 min before the hemorrhage, during the hemorrhage and 90 min recovery period. Four of these five survived the study period. They remained normocarbic and became more acidotic than the animals that breathed room air. Blood pressure and heart rate fell during hemorrhage but these decreases were less than in either group of room air breathing animals. During recovery they became tachycardic and blood pressure returned to baseline levels. Myocardial blood flow increased 20% above baseline by the end of hemorrhage and 40% above baseline by 90 min posthemorrhage. Cerebral blood flow increased 40% above baseline during the hemorrhage and remained at that level at the end of hemorrhage and 90 min afterwards. The increase in brain blood flow was sufficient to maintain oxygen delivery to the brain at baseline levels throughout the experiment. SpeculationWe speculate that the normal response for the normocarbic lambs is to increase cerebral and myocardial blood flow in response to anemia and hypotension. Spontaneous hyperventilation with hypocarbia tends to interfere with this response both in the brain and in the myocardium. The effect of hypocarbia is greater in the myocardium. The net result is a decrease in oxygen delivery to these tissues. If the same responses were to occur in the human infant it might be important to maintain normocarbia during resuscitation of infants suffering from hemorrhagic shock. 70

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Influence of CO₂ on cardiovascular response to hypoxia in conscious dogs

Cited by 38 publications

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Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

The Effect of High or Low Oxygen Affinity Red Cells on Tissue Oxygenation and Myocardial Function in Hypoxic Newborn Lambs with or without Hypercapnia

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

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Influence of CO2 on cardiovascular response to hypoxia in conscious dogs

Cited by 38 publications

References 0 publications

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia.

The Effect of High or Low Oxygen Affinity Red Cells on Tissue Oxygenation and Myocardial Function in Hypoxic Newborn Lambs with or without Hypercapnia

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

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Influence of CO₂ on cardiovascular response to hypoxia in conscious dogs