Increase In Arterial PCO2 Research Articles

Selected and shared hematological responses to apnea in elite human free divers and northern elephant seals (Mirounga angustirostris).

Despite elite human free divers achieving incredible feats in competitive free diving, there has yet to be a study that compares consummate divers, (i.e. northern elephant seals) to highly conditioned free divers (i.e., elite competitive free-diving humans). Herein, we compare these two diving models and suggest that hematological traits detected in seals reflect species-specific specializations, while hematological traits shared between the two species are fundamental mammalian characteristics. Arterial blood samples were analyzed in elite human free divers (n = 14) during a single, maximal volitional apnea and in juvenile northern elephant seals (n = 3) during rest-associated apnea. Humans and elephant seals had comparable apnea durations (∼6.5 min) and end-apneic arterial Po2 [humans: 40.4 ± 3.0 mmHg (means ± SE); seals: 27.1 ± 5.9 mmHg; P = 0.2]. Despite similar increases in arterial Pco2 (humans: 33 ± 5%; seals: 16.3 ± 5%; P = 0.2), only humans experienced reductions in pH from baseline (humans: 7.45 ± 0.01; seals: 7.39 ± 0.02) to end apnea (humans: 7.37 ± 0.01; seals: 7.38 ± 0.02; P < 0.0001). Hemoglobin P50 was greater in humans compared to elephant seals (29.9 ± 1.5 and 28.7 ± 0.6 mmHg, respectively; P = 0.046). Elephant seals overall had higher carboxyhemoglobin (COHb) levels (5.9 ± 2.6%) compared to humans (0.8 ± 1.2%; P < 0.0001); however, following apnea, COHb was reduced in seals (baseline: 6.1 ± 0.3%; end apnea: 5.6 ± 0.3%) and was slightly elevated in humans (baseline: 0.7 ± 0.1%; end apnea: 0.9 ± 0.1%; P < 0.0002, both comparisons). Our data indicate that during static apnea, seals have reduced hemoglobin P50, greater pH buffering, and increased COHb levels. The differences in hemoglobin P50 are likely due to the differences in the physiological environment between the two species during apnea, whereas enhanced pH buffering and higher COHb may represent traits selected for in elephant seals.NEW & NOTEWORTHY This study uses similar methods and protocols in elite human free divers and northern elephant seals. Using highly conditioned divers (elite free-diving humans) and highly adapted divers (northern elephant seals), we explored which hematological traits are fundamentally mammalian and which may have been selected for. We found differences in P50, which may be due to different physiological environments between species, while elevated pH buffering and carbon monoxide levels might have been selected for in seals.

Measuring Cerebrovascular Reactivity: Sixteen Avoidable Pitfalls.

An increase in arterial PCO2 is the most common stressor used to increase cerebral blood flow for assessing cerebral vascular reactivity (CVR). That CO2 is readily obtained, inexpensive, easy to administer, and safe to inhale belies the difficulties in extracting scientifically and clinically relevant information from the resulting flow responses. Over the past two decades, we have studied more than 2,000 individuals, most with cervical and cerebral vascular pathology using CO2 as the vasoactive agent and blood oxygen-level-dependent magnetic resonance imaging signal as the flow surrogate. The ability to deliver different forms of precise hypercapnic stimuli enabled systematic exploration of the blood flow-related signal changes. We learned the effect on CVR of particular aspects of the stimulus such as the arterial partial pressure of oxygen, the baseline PCO2, and the magnitude, rate, and pattern of its change. Similarly, we learned to interpret aspects of the flow response such as its magnitude, and the speed and direction of change. Finally, we were able to test whether the response falls into a normal range. Here, we present a review of our accumulated insight as 16 “lessons learned.” We hope many of these insights are sufficiently general to apply to a range of types of CO2-based vasoactive stimuli and perfusion metrics used for CVR.

Ventilatory responses of the clown knifefish, Chitala ornata, to arterial hypercapnia remain after gill denervation.

The aim of this study was to corroborate the presence of CO2/H+-sensitive arterial chemoreceptors involved in producing air-breathing responses to aquatic hypercarbia in the facultative air-breathing clown knifefish (Chitala ornata) and to explore their possible location. Progressively increasing levels of CO2 mixed with air were injected into the air-breathing organ (ABO) of one group of intact fish to elevate internal PCO2 and decrease blood pH. Another group of fish in which the gills were totally denervated was exposed to aquatic hypercarbia (pH ~ 6) or arterial hypercapnia in aquatic normocarbia (by injection of acetazolamide to increase arterial PCO2 and decrease blood pH). Air-breathing frequency, gill ventilation frequency, heart rate and arterial PCO2 and pH were recorded during all treatments. The CO2 injections into the ABO induced progressive increases in air-breathing frequency, but did not alter gill ventilation or heart rate. Exposure to both hypercarbia and acetazolamide post-denervation of the gills also produced significant air-breathing responses, but no changes in gill ventilation. While all treatments produced increases in arterial PCO2 and decreases in blood pH, the modest changes in arterial PCO2/pH in the acetazolamide treatment produced the greatest increases in air-breathing frequency. These results strengthen the evidence that internal CO2/H+ sensing is involved in the stimulation of air breathing in clown knifefish and suggest that it involves extra-branchial chemoreceptors possibly situated either centrally or in the air-breathing organ.

Ventilatory responses of the clown knifefish, Chitala ornata, to hypercarbia and hypercapnia.

The aim of the present study was to determine the roles of externally versus internally oriented CO2/H+-sensitive chemoreceptors in promoting cardiorespiratory responses to environmental hypercarbia in the facultative air-breathing fish, Chitala ornata (the clown knifefish). Fish were exposed to environmental acidosis (pH ~ 6.0) or hypercarbia (≈ 30torr PCO2) that produced changes in water pH equal to the pH levels of the acidotic water to distinguish the relative roles of CO2 versus H+. We also injected acetazolamide to elevate arterial levels of PCO2 and [H+] in fish in normocarbic water to distinguish between internal and external stimuli. We measured changes in gill ventilation frequency, air breathing frequency, heart rate and arterial blood pressure in response to each treatment as well as the changes produced in arterial PCO2 and pH. Exposure to normocarbic water of pH 6.0 for 1h did not produce significant changes in any measured variable. Exposure to hypercarbic water dramatically increased air breathing frequency, but had no effect on gill ventilation. Hypercarbia also produced a modest bradycardia and fall in arterial blood pressure. Injection of acetazolamide produced similar effects. Both hypercarbia and acetazolamide led to increases in arterial PCO2 and falls in arterial pH although the changes in arterial PCO2/pH were more modest following acetazolamide injection as were the increases in air breathing frequency. The acetazolamide results suggest that the stimulation of air breathing was due, at least in part, to stimulation of internally oriented CO2/H+ chemoreceptors monitoring blood gas changes.

CO&lt;sub&gt;2&lt;/sub&gt; 환경에서의 넙치(Paralichthys olivaceus) 심기능의 경시적 변화

Cardiorespiratory variables were measured in flounder Paralicthys olivaceus exposed to acidified seawater equilibrated with a gas mixture containing 5% CO2 gas for 72 h at 20°C. It was found that CO2 produced a significant increase in arterial PCO2 (PaCO2) and significant decreases in arterial pH (pHa). CO2 transiently increased heart rate within 30 min of exposure. After cardiac output was elevated by the increase in heart rate within 30 min, was then reduced by the decrease in both stroke volume and heart rate. The heart responses of flounder differ from those of yellowtail to high CO2 environment.

Focal microdialysis of CO2 in the perifornical-hypothalamic area increases ventilation during wakefulness but not NREM sleep

We investigated whether the perifornical-lateral hypothalamic area (PF-LHA), where the orexin neurons reside, is a central chemoreceptor site by microdialysis of artificial cerebrospinal fluid (aCSF) equilibrated with 25% CO2 into PF-LHA in conscious rats. This treatment is known to produce a focal tissue acidification like that associated with a 6–7mm Hg increase in arterial PCO2. Such focal acidification in the PF-LHA significantly increased ventilation up to 15% compared with microdialysis of normal aCSF equilibrated with 5% CO2 only in wakefulness but not in sleep in both the dark (P=0.004) and light (P<0.001) phases of the diurnal cycle. This response was predominantly due to a significant increase in respiratory frequency (11%, P<0.001). There were no significant effects on ventilation in the group with probes misplaced outside the PF-LHA. These results suggest that PF-LHA functions as a central chemoreceptor site in the central nervous system in a vigilant state dependent manner with predominant effects in wakefulness.

Breathe, Breathe in the Air

See related article, pp 106–113 Blood flow to the brain is highly regulated through an array of interacting cells and molecular signals, all impinging on the vasculature. Although many mechanisms influence cerebrovascular resistance and, thus, cerebral blood flow,1 2 of the most powerful regulators are molecular oxygen and carbon dioxide.1,2 The impact of sustained hypoxia (decreases in arterial Po2) and hypercapnia (increases in arterial Pco2) on cerebral blood flow has been studied widely in animal models and in people.2 Both hypoxia and hypercapnia can occur as a result of environmental factors but also occur under some pathophysiological conditions. For example, periodic hypoxia and hypercapnia are both key elements of sleep-disordered breathing, a group of abnormalities that include obstructive sleep apnea.3 Obstructive sleep apnea is an increasingly prevalent condition with a complex pathophysiology that encompasses activation of the sympathetic nervous system and vascular abnormalities, as well as disturbed sleep patterns.3 Obstructive sleep apnea is often associated with hypertension and is known to increase the risk for cerebrovascular disease, stroke, and cognitive decline.4,5 Because intermittent hypoxia is one element of obstructive sleep apnea and is relatively easy to produce experimentally, many investigators have studied effects of this type of hypoxia using animal models. Although intermittent hypoxia does not mimic the entire array of changes that occur, there is evidence that brief repetitive periods of hypoxia contribute to the overall pathophysiology of obstructive sleep apnea.6 Previous studies of the effects of intermittent hypoxia have described diverse vascular effects that include activation of oxidant- and immune-related pathways, endothelial dysfunction, vascular hypertrophy, and the progression of atherosclerosis.3,6 Although obstructive sleep apnea is a risk factor for stroke and cognitive decline,4, …

Comparison of extubation times between protocolized versus automated weaning systems after major surgery

Background. Prolonged mechanical ventilation is associated with adverse clinical outcomes for critically ill patients. Objective. To assess the the extubation times of protocolised versus automated weaning systems in patients after major surgery in intensive care unit. Design. Retrospective analysis.Measurements and results. We analyzed 70 patients with major abdominal or pelvic surgery. Patients that were used Draeger Evita2 Dura for weaning process named as the C (control) group (n=35) and patients that were used Draeger Evita2 XL Smartcare/PS named as the SC group (n=35). A physician evaluate the patient every 5 or 10 minutes in group C. Gender, age, weight, operation time, operation type, the total volume of intravenous infusion, bleeding, total dose of propofol, fentanyl citrate, rocuronium during surgery and extubation time were all recorded. All side effects included reintubation, bleeding, stroke, death, postoperative myocardial infarction were all recorded. The partial oxygen pressure (Pa02) and partial carbondioxide pressure (PaC02) were recorded before and after extubation.Results. Demographic data and operative data were similar between groups (p>0.05). The extubation time was similar between groups (SC group versus C group: 191,14±79,1 min versus 188,29±51,47 min, p=0,534. There was significant decrease in arterial PO2 and increase in arterial PCO2 after extubation in all groups. No side effects were observed. Conclusion. In conclusion, although we found no differences between SmartCare and control groups, the evaluating of the patient increased the workload in the control group. We think that SmartCare decreased the workload. Thus, it can be recommended for weaning process of patients after major surgery in intensive care unit.

μ‐Opioid Receptor‐Sensitive Muscle Afferents Contribute to the Circulatory Response to Exercise in Humans

We investigated the role of somatosensory feedback on hemodynamic and ventilatory responses to exercise. Nine males performed knee-extensor exercise (15/30/45 W, 3-min each) with and without lumbar intrathecal fentanyl (L3–L4) impairing the central projection of spinal μ-opioid receptor-sensitive muscle afferents. Femoral venous and arterial catheterization was combined with Doppler femoral blood flow measures (FBF). Pulmonary/hemodynamic variables were recorded continuously, FBF measures and blood was simultaneously taken during the final min of each workload. To evaluate whether a cephalad migration of fentanyl affected cardioventilatory control centers in the brainstem, we compared resting hypercapnic ventilatory responses (HCVR). Similar HCVR excluded direct medullary effects of fentanyl. Resting measures were similar between conditions. Cardiac output was 19–22% lower during Fentanyl exercise, secondary to significant reductions in heart rate and stroke volume. Throughout Fentanyl exercise, FBF, arterial pressure and vascular conductance were 14–16%, 6–7%, and 8–10% lower (p < 0.05). Venous pressure was similar in both conditions. Ventilation during Fentanyl exercise was 4–7% lower leading to a 1–1.5 mmHg increase in arterial PCO2 (p < 0.05). Our findings demonstrate the essential contribution of muscle afferents to hemodynamic and ventilatory responses to rhythmic human exercise.

Commentaries on Viewpoint: Central chemoreception is a complex system function that involves multiple brain stem sites

to the editor: Amniote vertebrates adjust the acid-base status of the blood through ventilatory alterations of PaCO2 and, to some degree, by renal modulation of bicarbonate concentration. Receptor systems for the ventilatory acid-base regulation has been studied mainly in mammals, in which the

Dysfunction of the canine respiratory muscle pump in ascites

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial PCO2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.

The effects of mechanical ventilation on the gut and abdomen

Mechanical ventilation generates an increase in airway pressure and, therefore, in intrathoracic pressure, which may decrease systemic and intraabdominal organ perfusion. Critically ill patients rarely die of hypoxia and/or hypercarbia but commonly develop a systemic inflammatory response that culminates in multiple-organ dysfunction syndrome and death. In the pathogeneses of this syndrome the gastrointestinal tract and liver have received considerable attention. Mechanical ventilation with high positive end-expiratory pressure has been found to decrease splanchnic perfusion. Hepatic arterial buffer response is preserved and an increased hepatic arterial blood flow will compensate the decrease in portal blood flow. Despite an increased cardiac output with an acute moderate increase in arterial PCO2 during protective ventilation it cannot be expected that splanchnic and gut perfusion is improved. In the absence of a significant rise in intraabdominal pressure without impairment in cardiovascular function, splanchnic and gastrointestinal function remained unchanged during short periods of prone positioning. Spontaneous breathing during ventilator support improves systemic blood flow and gastrointestinal and splanchnic perfusion. In critically ill patients mechanical ventilation should be adjusted to avoid conditions known to be associated with decreased gastrointestinal and splanchnic perfusion.

Inhaled Nitric Oxide Attenuates Hyperoxic Lung Injury in Lambs

Cytochrome P450 (CYP) inhibition with cimetidine reduces hyperoxic lung injury in young lambs. Nitric oxide (NO), also a CYP inhibitor, has been shown to either aggravate or protect against oxidant stress depending on experimental context. The objective of this study was to determine whether NO, like cimetidine, would protect young lambs against hyperoxic lung injury, and whether its effect was associated with CYP inhibition. Three groups of lambs were studied: 1) room air exposure, 2) >95% O2, and 3) >95% O2 plus inhaled NO. After 72 h, hyperoxia alone resulted in a significant increase in arterial P(CO2) and number of polymorphonuclear leukocytes in bronchoalveolar lavage (BAL), and a significant decrease in arterial/alveolar O2 tension (a/A). The addition of inhaled NO significantly decreased the hypercarbia and BAL polymorphonuclear cellular response associated with hyperoxia but had no beneficial effect on a/A ratio. There were no significant differences in F2-isoprostanes or isofurans (markers of lipid peroxidation) measured in BAL or lung tissue among study groups. No intergroup differences were detected in BAL epoxyeicosatrienoic acid levels (index of CYP activity). The results of this study indicate that hypercarbia and inflammation accompanying hyperoxic lung injury in young lambs can be attenuated by inhaled NO. However, this study provides no direct evidence that NO is inhibiting CYP-mediated oxidant lung injury.

Impact of carbon dioxide and helium insufflation on cardiorespiratory function during prolonged pneumoperitoneum in an experimental rat model.

Experimental studies on laparoscopic surgery are often performed in rats. However, the hemodynamic and respiratory responses related to the pneumoperitoneum have not been studied extensively in rats. Therefore, the aim of this study was to investigate in spontaneously breathing rats the effects of CO2 and helium, insufflation pressure, and duration of pneumoperitoneum on blood pressure, arterial pH, pCO2, pO2, HCO3-, base excess, and respiratory rate. Five groups of 9 Brown Norway rats were anesthetized and underwent CO2 insufflation (6 or 12 mmHg), helium insufflation (6 or 12 mmHg), or abdominal wall lifting (gasless control) for 120 min. Blood pressure was monitored by an indwelling carotid artery catheter. Baseline measurements of mean arterial pressure (MAP), respiratory rate, arterial blood pH, pCO2, pO2, HCO3-, and base excess were recorded. Blood gases were analyzed at 5, 30, 60, 90, and 120 min during pneumoperitoneum, and MAP and respiratory rate were recorded at 5 and 15 min and at 15-min intervals thereafter for 2 h. CO2 insufflation (at both 6 and 12 mmHg) caused a significant decrease in blood pH and increase in arterial pCO2. Respiratory compensation was evident since pCO2 returned to preinsufflation levels during CO2 insufflation at 12 mmHg. There was no significant change in blood pH and pCO2 in rats undergoing either helium insufflation or gasless procedures. Neither insufflation pressure nor the type of insufflation gas had a significant effect on MAP over time. The cardiorespiratory changes during prolonged pneumoperitoneum in spontaneously breathing rats are similar to those seen in clinical practice. Therefore, studies conducted in this animal model can provide valuable physiological data relevant to the study of laparoscopic surgery.

Cardiorespiratory responses of white sturgeon to environmental hypercapnia.

Cardioventilatory variables and blood-gas, acid-base status were measured in cannulated white sturgeon (Acipenser transmontanus) maintained at 19 degrees C during normocapnic and hypercapnic (Pw(CO(2)) approximately 20 Torr) water conditions and after the injection of adrenergic analogs. Hypercapnia produced significant increases in arterial PCO(2), ventilatory frequency, and plasma concentration of cortisol and epinephrine, and it produced significant decreases in arterial pH and plasma concentration of glucose but no change in arterial PO(2), hematocrit, and concentration of lactate or norepinephrine. Hypercapnia significantly increased cardiac output (Q) by 22%, mean arterial pressure (MAP) by 8%, and heart rate (HR) by 8%. However, gut blood flow (GBF) remained constant. In normocapnic fish, phenylephrine significantly constricted the splanchnic circulation, whereas isoproterenol significantly increased Q and produced a systemic vasodilation. During hypercapnia, propranolol significantly decreased Q, GBF, MAP, and HR, whereas phentolamine significantly decreased MAP and increased GBF. These changes suggest that cardiovascular function in the white sturgeon is sensitive to both alpha- and beta-adrenergic modulation. We found microspheres to be unreliable in predicting GBF on the basis of our comparisons with simultaneous direct measurements of GBF. Overall, our results demonstrate that environmental hypercapnia (e.g., as is experienced in high-intensity culture situations) elicits stress responses in white sturgeon that significantly elevate steady-state cardiovascular and ventilatory activity levels.

Cigarette smoke and hypoxia induce acute changes in testicular and celebral microcirculation

The acute effects of cigarette smoking and hypoxia on the cerebral and testicular microcirculation were studied in anestethised adult rats. Smoking for 2 min did not influence arterial pO2, pCO2 or pH but it induced an increase in cerebral blood flow by 34% and inhibited vasomotion in the testis for about 1 h. One hour after smoke exposure apnea induced a slight increase in arterial pCO2, a significant decrease in pO2, and an increase in cerebral blood flow (CBF) by 54%. In animals not previously exposed to cigarette smoke apnea increased CBF by 121%, demonstrating that a short-term exposure to tobacco smoke influences the cerebrovascular reactivity for more than one hour. In the testis, apnea resulted in a decreased blood flow by 39% and a complete depression of vasomotion. Breathing 10% O2/90% N2 resulted in moderate hypoxia, a total disappearance of the vasomotion in the testis, a 24% decrease in testicular blood flow, but a 23% increase in CBF.Our results indicate that short- term exposure to tobacco smoke induces marked acute vascular effects in both the brain and the testis. Apnea and moderate hypoxia elicted totally differnt effect in the brain and testis, indicating different vascular control mechanisms.

Dynamics of cardiovascular responses to repeated partial umbilical cord compression in late-gestation sheep fetus.

We characterized the detailed hemodynamics of fetal blood pressure, heart rate, common umbilical blood flow, and femoral blood flow responses to partial compression of the umbilical cord and tested the hypothesis that repeated cord compression modulates fetal cardiovascular responses in 10 chronically instrumented fetal sheep at approximately 130 days of gestation. In five fetuses (group I), partial compression of the umbilical cord was induced 12 times, each for 5 min at 15-min intervals. Each cord compression reduced common umbilical blood flow by 50% and produced modest falls in fetal pH (7.33 +/- 0 to 7.29 +/- 0) and arterial PO2 (21.1 +/- 0.2 to 16.8 +/- 0.2 mmHg) and a mild increase in arterial PCO2 (49.9 +/- 0.5 to 54.9 +/- 0.4 mmHg). Sham experiments were performed in five other fetuses (group II). Second-by-second analysis of group I fetal cardiovascular data revealed a clear biphasic response to partial cord compression. Phase I (1st min of cord compression) was characterized by a rapid bradycardia and a rapid femoral vasoconstriction (primary response); phase II (minutes 2-5 of cord compression) was characterized by a delayed bradycardia and a return of femoral vascular resistance toward baseline (secondary response). Repeated cord compression abolished the primary, but not the secondary, cardiovascular responses. These results demonstrate that fetal cardiovascular responses to stress may be modified by preexposure to repeated intrauterine challenges.

Effects of one-lung ventilation on pulmonary hemodynamics and gas exchange in the newborn.

For major thoracoscopic surgery, one-lung ventilation is mandatory. This is reasonably well tolerated in adults and children. The effects of one-lung ventilation on hemodynamics and gas exchange in newborns, however, are not known yet. Eight neonatal domestic pigs with a median age of 6 days (range: 3-9 days), and a mean body weight of 2.3 kg (1.7-2.8 kg) were intubated and ventilated in pressure-controlled mode (FIO2 = 1). Anesthesia was maintained with i.v. fentanyl/metomidate. After tracheotomy an endotracheal tube was positioned in the trachea, and a second tube in the left mainstem bronchus. One-lung ventilation was maintained for 120 min. Serial measurements were done before, during, and until 90 min. after one-lung ventilation. During one-lung ventilation, pulmonary artery pressure and intrapulmonary shunt increased from 15 +/- 1 to 18 +/- 1 mmHg (p = 0.004), and from 2.6 +/- 0.3 to 3.7 +/- 0.4% (p = 0.02), respectively. Arterial oxygen saturation remained unchanged at 100%. A slight increase in arterial PCO2 could easily be treated by increasing the respiratory rate. In conclusion, one-lung ventilation was not associated with major side effects in regard to hemodynamics and gas exchange in the neonatal pig.

Cardiac function in a rat model of chronic aortic stiffness.

Cardiac function was investigated in conscious normotensive rats in which increased aortic stiffness was produced as a result of vascular calcium overload after treatment with vitamin D3 plus nicotine (VDN rats, n = 16; controls, n = 17). Baseline stroke volume, cardiac output, and cardiac response to a venous volume overload were unchanged after 1 mo of exposure to increased aortic stiffness, as were baseline venous return and total vascular capacitance. The latter was estimated from the change in mean circulatory filling pressure after modification of circulatory volume. Cardiovascular reflexes were modified in VDN rats. Bradycardia evoked by an increase in arterial PCO2 (PaCO2) or hypotensive hemorrhage was more pronounced. The PaCO2-induced bradycardia was accompanied by a fall in cardiac output in VDN rats but not in controls. In VDN rats, the attenuation of sympathetic reflexes may explain the slower recovery of blood pressure after hypotensive hemorrhage. In conclusion, a chronic increase in aortic stiffness does not compromise cardiac performance, but cardiovascular reflexes are impaired in VDN rats. Whether this is because of the increase in aortic stiffness or the effect of VDN treatment on the baroreceptors or other components of the reflex arc remains to be elucidated.

Mechanical ventilation may not be essential for initial cardiopulmonary resuscitation: Chest 1995; 108/3 (821–827)

Background In a rodent model of cardiac arrest and resuscitation in which the inspired gas mixture was enriched with oxygen, resuscitability and survival were unaffected by positive pressure ventilation. In the present study, in a larger animal model, tidal volumes generated during precordial compression and with spontaneous gasping were quantitated. Methods Domestic pigs with an average weight of 34 kg were anesthetized with pentobarbital. Ventricular fibrillation (VF) was induced electrically. Precordial compression was begun after 4 min of untreated VF. Each of 22 animals received one of two interventions in conjunction with precordial compression: positive pressure ventilation with oxygen or oxygen supplied at the port of a tracheal tube at ambient pressure. After 8 min of precordial compression, defibrillation was attempted. Results Only very moderate increases in arterial Pco2 were documented during cardiopulmonary resuscitation in the absence of mechanical ventilation but arterial oxygen tension was consistently in excess of 100 mm Hg. Cardiac resuscitability and 48-h survival were approximately the same in animals maintained on inspired oxygen whether or not they were mechanically ventilated (7/11 or 8/11). In the absence of mechanical ventilation, precordial compression and spontaneous gasping yielded minute volumes that exceeded 5 L. Conclusion Positive pressure mechanical ventilation did not improve resuscitability or postresuscitation outcome in this porcine model of cardiac arrest.