Effects of moderate and severe hypocapnia on intracerebral perfusion and brain tissue oxygenation in piglets.

BACKGROUND: Hypocapnia is a common alteration during anesthesia in neonates. AIM: To investigate the effects of hypocapnia and hypocapnia combined with hypotension (HCT) on cerebral perfusion and tissue oxygenation in anesthetized piglets. METHOD: Thirty anesthetized piglets were randomly allocated to groups: moderate hypocapnia (mHC), severe hypocapnia (sHC), and HCT. Cerebral monitoring comprised a tissue oxygen partial pressure and a laser Doppler probe inserted into the brain tissue as well as a near-infrared spectroscopy (NIRS) sensor placed on the skin, measuring regional oxygen saturation. Hypocapnia was induced by hyperventilation (target PaCO2 mHC: 3.7-4; sHC: 3.1-3.3 kPa) and hypotension by blood withdrawal and nitroprusside infusion (mean blood pressure: 35-38 mm Hg). Data were analyzed at baseline, during (Tr20, Tr40, Tr60) and after (Post20, Post40, Post60) treatment. RESULTS: Compared to baseline, tissue oxygen partial pressure decreased significantly and equally during all treatments (mean [SD] at baseline: mHC 35.7 [32.45]; sHC: 28.1 [20.24]; HCT 25.4 [10.3] and at Tr60: mHC: 29.9 [27.36]; sHC: 22.2 [18.37]; HCT: 18.4 [9.5] mm Hg). Decreased laser Doppler flow was detected with all treatments at Tr20 (mHC: 0.9 [0.18]; sHC: 0.88 [0.15]; HCT: 0.97 [0.13] proportion from baseline). Independently of group, regional oxygen saturation varied only after reverting and not during treatment. Blood lactate, pH, HCO3- , and PaO2 increased during treatment with no differences between groups. CONCLUSION: This animal model revealed reduced cerebral blood flow and brain tissue oxygenation during hypocapnia without detectable changes in regional oxygen saturation as measured by NIRS. Changes occurred as early as during moderate hypocapnia.

A case of a chlorine inhalation injury in an Ebola treatment unit.

We present a 26-year-old male British military nurse, deployed to Sierra Leone to treat patients with Ebola virus disease at the military-run Kerry Town Ebola Treatment Unit. Following exposure to chlorine gas during routine maintenance procedures, the patient had an episode of respiratory distress and briefly lost consciousness after exiting the facility. Diagnoses of reactive airways disease, secondary to the chlorine exposure and a hypocapnic syncopal episode were made. The patient was resuscitated with minimal intervention and complete recovery occurred in less than 1 week. This case highlights the issues of using high-strength chlorine solution to disinfect the red zone. Although this patient had a good outcome, this was fortunate. Ensuring Ebola treatment centres are optimally designed and that appropriate management systems are formulated with extraction scenarios rehearsed are important to mitigate the chlorine-associated risk.

Hypocapnia-dependent facilitation of augmented breaths: observations in awake vs. anesthetized rats.

We investigated whether commonly used injectable laboratory anesthetics alter the regulation of augmented breaths (ABs) in different respiratory backgrounds. Male rats were studied on three separate experimental days, receiving one of three injections in randomized order: ethyl carbamate ('urethane'; 1.2mgkg(-1)), ketamine/xylazine (ket/xyl; 80/10mgkg(-1)), or normal saline. Following each of the three interventions, breathing was monitored during 15min exposures to normoxia (room air), hypoxia (10% O(2)) and hypoxia+CO(2) (10% O(2), 5% CO(2)). Urethane anesthesia completely eliminated ABs from the breathing rhythm in room air conditions (p<0.001), and decreased the hypocapnia-dependent component of this response (p<0.001). ket/xyl left the normal incidence of ABs in room air breathing intact but significantly suppressed the hypoxia-induced facilitation of ABs (p=0.0015). These results provide the first clear evidence that laboratory anesthesia can profoundly alter the regulation of ABs including the hypocapnia-dependent component of their facilitation.

Pulmonary embolism caused by polymethylmethacrylate during percutaneous vertebroplasty in orthopaedic surgery.

Vertebroplasty consists of percutaneous injection of acrylic cement--polymethylmethacrylate (PMMA)--into a partially collapsed vertebral body in order to obtain pain relief and augment mechanical stability of the vertebral body. Although vertebroplasty is an efficient treatment it is not free of complications. Our present case report describes a woman with pulmonary polymethylmethacrylate embolism during percutaneous vertebroplasty who presented with hypotension, arrhythmia and hypocapnia.

Aminophylline therapy during endotoxemia in anesthetized spontaneously breathing rats.

Phosphodiesterase inhibitors, such as pentoxifylline and aminophylline, may reduce inflammatory cytokine-induced endothelial permeability. We tested the hypothesis that aminophylline treatment may ameliorate the pulmonary and extrapulmonary effects of endotoxemia in a rat model. In anesthetized rats, a tracheotomy was performed along with catheterization of a femoral vein and artery. Anesthesia, fluid balance, and normothermia were maintained throughout the 6-h experiment. A stable hemodynamic and gas-exchange baseline was established at which time the rats were randomly divided into three groups. Group I received aminophylline (1mg/kg) over 30 min followed by 0.5mg/kg/h. Group II received a single dose of endotoxin (4 mg/kg) while Group III received both aminophylline and endotoxin as described for Groups I and II, respectively. Gas-exchange profiles, mean arterial blood pressure, and heart rate were determined every 2h. At hour 6, the rats were euthanized and lung, kidney, and heart tissue were removed for determination of water content. As our control group, we utilized data from our previously published study involving an identical surgical procedure with normal saline. Endotoxemia produced characteristic respiratory and hemodynamic signs of sepsis including hypotension, hyperventilation, tachycardia, and renal and pulmonary edema. Aminophylline treatment failed to prevent these endotoxemia-induced respiratory and hemodynamic manifestations of sepsis, but significantly improved the acid-base imbalance that developed during surgical procedures in saline-treated control rats. Further studies are warranted to determine potentially beneficial doses of aminophylline and resulting theophylline serum concentrations under such septic conditions.

The influence of increasing concentrations of nitrous oxide on cerebral blood flow velocity in hypocapnic patients with brain tumours.

An increase of more than 50% in cerebral blood flow velocity in the middle cerebral artery was recently reported in hypocapnic volunteers, while inhaling 50% nitrous oxide. We measured cerebral blood flow velocity in the middle cerebral artery in 10 anaesthetized hypocapnic (ETCO2 = 25 mmHg) patients with brain tumours while administering increasing concentrations of nitrous oxide. At an end-tidal concentration of 50% and 70% nitrous oxide in oxygen, neither mean arterial pressure (base-line: 84 +/- 8 mmHg vs. (50% nitrous oxide): 82 +/- 9 mmHg and (70% nitrous oxide): 80 +/- 8 mmHg) nor cerebral blood flow velocity in the middle cerebral artery (base-line: 32 +/- 7 cm s-1 vs. (50% nitrous oxide): 34 +/- 8 cm s-1 and (70% nitrous oxide): 34 +/- 9 cm s-1) changed significantly. The data from our clinical investigation indicate that administration of increasing concentrations of nitrous oxide to already anaesthetized and hypocapnic patients does not change cerebral blood flow velocity in the middle cerebral artery.

Parasympathetic component of 5-hydroxytryptamine-induced pulmonary dysfunctions in healthy calves.

OBJECTIVE: To determine whether a cholinergic mechanism interferes with the pulmonary response to 5-hydroxytryptamine (5-HT) in the bovine species. DESIGN: The protocols differed with regard to the type of pretreatment calves were given 10 minutes before administration of 5-HT (0.05 mg/kg of body weight/min, over 2 minutes). Pretreatment consisted of saline, atropine, or hexamethonium solution given IV. ANIMALS: 6 healthy unsedated Friesian calves. PROCEDURE: Pulmonary function values were obtained before during, and after 5-HT infusions. RESULTS: After saline pretreatment, response to 5-HT consisted of immediate and brief apnea, bradycardia, and hypotension, followed by sustained tachypnea, tachycardia, pulmonary hypertension, and hypocapnic hypoxemia. Lung dynamic compliance (CLdyn) decreased to 19% of its baseline value, and total pulmonary resistance (RL) increased to 235%. Hexamethonium pretreatment resulted in a similar pattern of response except for the immediate and brief 5-HT-induced triad of apnea, bradycardia, and hypotension, which was suppressed. After atropine pretreatment, immediate and brief 5-HT-induced apnea-bradycardia-hypotension triad and sustained hypoxemia were abolished. In contrast, sustained tachypnea, tachycardia, pulmonary hypertension, and hypocapnia were maintained. Changes of CLdyn (59%) and RL (138%) were significantly attenuated. CONCLUSIONS: The initial and short-lasting response to 5-HT (ie. the apnea-bradycardia-hypotension triad) is mediated through a reflex central cholinergic pathway. The 5-HT-induced changes in CLdyn and RL are consistent with development of diffuse bronchoconstriction. Attenuation of these changes by atropine suggests that this bronchoconstrictor response to 5-HT is partly mediated through a cholinergic postganglionic pathway.

Effect of recurrent episodic hypocapnic, eucapnic, and hypercapnic hypoxia on systemic blood pressure.

We have described a rat model that responds to chronic (8 h/day, 35 days) repetitive nonapneic episodic (cycled every 30 s) hypocapnic hypoxia with sustained increase in systemic blood pressure. Because the usual blood gas change of apnea is mildly increased CO2, we hypothesized that episodic hypoxia ranging from eucapnea to hypercapnia might cause a greater chronic increase in blood pressure than hypocapnic hypoxia in this model. Five groups of male Sprague-Dawley rats were studied: unhandled group received no treatment, sham group received compressed air in their chambers, hypocapnic hypoxic group received episodic hypoxia for 35 days, eucapnic hypoxic group received the same level of hypoxia but with 7-10% inspired fraction of CO2, and hybercarbic hypoxic group received hypoxia with 11-14% inspired fraction of CO2. Mean arterial blood pressure was measured in unrestrained conscious animals at baseline and after 35 days under their respective study conditions. Neither episodic eucapnic nor hypercarbic hypoxia had any additional effect on the changes in chronic diurnal blood pressure compared with hypocapnic hypoxia. These results suggest that the sympathetic nervous system or other neurohumoral systems contributing to chronic diurnal blood pressure elevation may be maximally stimulated by hypoxia or there may be some protective mechanism limiting the blood pressure response to asphyxia in this rat model.