Artificial Hyperventilation Research Articles

Artificial hyperventilation normalizes haemodynamics and arterial oxygen content in hypoxic rats.

Although humans are capable of enduring critically low levels of oxygen, many hypoxaemic patients die despite aggressive therapies. Mimicking the physiological hyperventilation necessary to survive extreme hypoxic conditions could minimize the derangements caused by acute hypoxic-hypoxia. The objective of this study was to measure the haemodynamic-biochemical response to artificially induced hyperventilation in hypoxic rats. Twenty-four deeply anaesthetized and mechanically ventilated rats were allocated to 3 groups: control (n = 5, FiO2 = 1); hypoxic spontaneously hyperventilating (n = 10, FiO2 = 0.08); and hypoxic artificially induced hyperventilation (n = 9, targeting PaCO2 = 10 mm Hg, FiO2 = 0.08). We compared the spontaneously and artificially hyperventilating groups. P-values < 0.01 were considered statistically significant. Mean arterial pressure (MAP) and serum chemistry were measured for 180 minutes. The control group remained stable throughout the experiment. The hypoxic groups developed profound hypotension after the decrease in FiO2. However, the artificially induced hyperventilated rats recovered their MAP to levels higher than the spontaneously hyperventilating group (117.1 ± 17.2 vs. 68.1 ± 16.0, P = 0.0048). In regard to the biochemical derangements, even though the serum lactate and PaO2 were not different among the hypoxic groups, the artificially hyperventilated group achieved significantly higher SaO2 (94.3 ± 3.6 vs. 58.6 ± 9.6, P = 0.005), pH (7.87 ± 0.04 vs. 7.50 ± 0.13, P = 0.005), and CaO2 (17.7 ± 2.6 vs. 10.2 ± 1.3, P = 0.005) at 180 minutes. Artificially induced hyperventilation led to the correction of arterial oxygen content, severe serum chemistry, and haemodynamic derangements. These findings may represent anovel rescue manoeuvre and serve as abridge to apermanent form of support, but should be further studied before being translated to the clinical setting.

The effectiveness of hyperbaric oxygen therapy on mortality in adults with craniotrauma: a systematic review protocol

Review question/objective What is the effectiveness of hyperbaric oxygen therapy on the mortality of patients with craniotrauma? Inclusion criteria Types of participa nts Adults, who are over 18 years, with craniotrauma of various severity, including mild, moderate, severe, or duration, including acute and chronic. Patients with isolated craniotrauma or with craniotrauma in the context of polytrauma will also be included. Children, who are under 18 years, and adults who have atraumatic brain injury will be excluded. Types of intervention This review will consider studies that investigated the effect of hyperbaric oxygen therapy for 30 to 120 minutes at 1.5 atmosphere absolute to 3 atmosphere absolute. Studies in which hyperbaric oxygen therapy was administered up to 40 sessions per patient will also be considered. According to the critical status of patients, the application of hyperbaric oxygen therapy at different times at acute and chronic craniotrauma will also be considered: 1) Within the first 24 hours 2) After 24 hours 3) After 48 hours 4) After “stabilization” of patients (one week) 5) Chronic status. The effect of hyperbaric oxygen therapy will be compared against standard intensive care regimens, including neurointensive care monitoring, head elevation to 30°, sedation, paralysis, barbiturate-induced coma, cerebrospinal fluid drainage, artificial ventilation-appropriate oxygenation, osmotherapy, therapeutic hypothermia, hyperventilation, and decompressive craniotomy. Types of outcomes This review will consider studies that included the following outcome measures: overall mortality,long-term effect on cognitive-behavioral functions measured by any standardized scales any time after hyperbaric oxygen therapy; and oxygen supply improvement for brain tissues as measured by oxygen tension in brain tissue (P br O 2; local), cerebral venous oxygen saturation monitoring (SjO 2 ; global), cerebral perfusion pressure, intracranial pressure values before hyperbaric oxygen therapy and after hyperbaric oxygen therapy.

Early and long-term results for correction of total anomalous pulmonary venous drainage (TAPVD) in neonates and infants

To present our 17-year experience of surgical repair of total anomalous pulmonary venous drainage (TAPVD) in 71 consecutive neonates and infants, with particular emphasis on the role of preoperative pulmonary venous obstruction (PVO), the management of postoperative pulmonary hypertensive crises and the long-term results. From July 1977 to May 1994, 36 newborns and 35 infants, aged between 1 and 300 days, had repair TAPVD in our Department. Fifty-four patients had decompensated heart failure, whereas three were moribund. The anomalous drainage was supracardiac in 32 (45%), cardiac in 17 (24%), infracardiac in 17 (24%) and mixed in 5 infants (7%). Major associated cardiac anomalies coexisted in nine cases. Forty-five (63%) exhibited signs of PVO. The repair was performed under moderate hypothermia in 15 and deep hypothermic arrest in 56 patients. In case of postoperative pulmonary hypertensive crises, artificial hyperventilation with high oxygen concentration, sedation and relaxation, inotropic support and afterload reduction with phentolamine were applied selectively. The actual follow-up is based on functional symptomatology and cardiac echo-doppler studies. Six children (8.5%) died early: four perioperatively, two on the 2nd and 10th postoperative day, respectively. Poor preoperative condition, operation before 1987 and preoperative PVO were the main incremental risk factors for death. No death occurred among the last 38 cases. There were complications in 45 patients, in particular pulmonary hypertensive crises in 27. Two patients died late, after 80 and 118 days, respectively, of progressive intrapulmonary vein fibrosis: the second despite reoperation. The risk of late death approaches zero after 6 months. Among the 63 survivors, 56 (86%) are asymptomatic and without medication, 3 months-17 years after operation. Five have mild symptoms with ordinary physical activity. Two are lost to follow-up. Early repair of TAPVD with aggressive management of pulmonary hypertensive crises carries low operative mortality nowadays. Preoperative PVO as a risk factor has been neutralized since 1987. Long-term results are gratifying: no late death after 6 months, no reoperation and functional good results. Progressive pulmonary vein fibrosis remains an unpredictable rare cause of death within the 1st year after surgery.

Provoked flux motion of cochlear blood flow measured with laser Doppler flowmetry in guinea pig.

Although progress has been made in the study of cochlear blood flow (CBF) regulation since laser Doppler flowmetry (LDF) was introduced, cochlear vasomotion has not been investigated. Therefore, the primary objective of this study was to determine if oscillatory fluctuations of CBF could be provoked. Guinea pigs were anesthetized with diazepam (5 mg/kg) and fentanyl (0.32 mg/kg). Blood pressure (BP) was recorded from a carotid artery cannula. The cochlea and pons cerebellum were ventrally exposed; the bilateral CBF and brain blood flow (BBF) or skin blood flow (SBF) were monitored by LDF. After administration of phentolamine (0.25-0.75 mg/kg, i.v.), ipsilateral CBF in 7 of 16 animals showed a 2-5 min episode of oscillation. During artificial hyperventilation, continuous oscillation of CBF was recorded (the flux motion frequency was 3.5 +/- 0.5 cycles per min and its amplitude 25.8 +/- 5.6% from baseline). The time-dependent flux change (the waveform) was the same throughout a single cochlea but different between cochleae of the same animal. Compared to BBF, CBF vasomotion frequency was lower, and amplitude larger. SBF exhibited no such motion. Flux motion could be eliminated by inhalation of pure oxygen or 5% CO2 in oxygen or by the smooth muscle relaxants, papaverine and hydralazine. Phentolamine-induced vasomotion may be due to a hypotensive perfusion pressure, and hyperventilation-enhanced vasomotion may be caused by changing blood gas concentrations and by hormonal or neuronal activity. Oxygen and CO2 inhalation slightly increased BP and this change in perfusion pressure was probably associated with weakened vasomotion.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of indomethacin on intracranial pressure, cerebral blood flow and cerebral metabolism in patients with severe head injury and intracranial hypertension

In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP greater than 20 mmHg) by artificial hyperventilation (PaCO2 level 3.5-4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2 h. After 7 h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.

Quantitative EEG changes under various conditions of hyperventilation in the sensorimotor cortex of the anaesthetized cat

The effects on the EEG rhythms recorded from the sensorimotor cortex (post-sigmoid gyrus) of anaesthetized cats were studied under 4 conditions of artificial mechanical hyperventilation (HV) before and after cervical bilateral vagotomy. In animals with intact vagus nerves, using visual examination, EEG changes were only observed within the 2nd min during HV produced by increased stroke volume (ΔV) with associated hypocapnia. Quantitative EEG (qEEG) showed that, for the same increase in minute ventilation and the same degree of hypocapnia, ΔV induced a greater and earlier relative decrease (2nd min) in the power density of delta, theta and alpha bands, than increased pump frequency (ΔF). The ΔF tests produced a fall only in the theta band and within the 3rd min. With constant p aCO 2, transient modifications occurred only with ΔV and were limited to the first 30 sec. In bivagotomized cats, moderate EEG responses to ΔV plus associated hypocapnia persisted partly in the alpha band. Finally, no changes appeared with ΔV or ΔF when the vagus nerves were cut and p aCO 2 was maintained constant. The present data suggest strongly that, in anaesthetized cats, peripheral vagal afferents from the respiratory system play a major role in the EEG changes caused by artificial hyperventilation.

Hyperventilation-Induced Reduction in Cerebral Blood Flow: Assessment by Positron Emission Tomography

The use of positron emission tomography (PET) has been well documented as a relatively noninvasive method of measuring cerebral blood flow (CBF), both globally and regionally. The utility of readily detecting alterations in CBF is apparent, particularly when applied to the evaluation of therapeutic interventions thought to influence CBF. We report the effects of hypocapnia, an experimental condition of known cerebral vasoconstriction, in ten normal volunteers. Subjects had brain blood flow evaluated utilizing H215O as the positron emitter before and after approximately five minutes of hyperventilation. Baseline CBF was measured as a mean +/- SD of 61.2 +/- 16.3 mL/min/100 g of tissue. Mean baseline arterial blood gas values were PaO2 107.4 +/- 14 mm Hg, PaCO2 37.7 +/- 0.89 mm Hg, and pH 7.39 (calculated from mean [H+]). Post hyperventilation, global CBF was measured as 31.1 +/- 10.8 mL/min/100 g. Mean arterial blood gas values were PaO2 141.7 +/- 21 mm Hg, PaCO2 19.7 +/- 5 mm Hg, and pH 7.63 (calculated from mean [H+]). CBF decreased by a mean of 49.5 +/- 11 percent. Data analysis using the Student's t-test showed a significant change over baseline in PaCO2 (p less than 0.001) and CBF (p less than 0.001), in the hyperventilated state. Correlations were noted between the decrease in CBF and change in PaCO2 (r = 0.81) as well as between hyperventilation PaCO2 and the change in CBF (r = 0.97). We conclude that, as measured by PET, CBF decreases significantly during a state of artificial hyperventilation to a degree consistent with results seen using other methods. PET appears to be a valuable tool in the assessment of interventions that could influence CBF.

Die Bedeutung von EMG-Artefakten im isoelektrischen EEG

Five potential organ donors showed muscle artefacts during isoelectrical EEG recording. The electromyographic examination revealed MUAP activity occurring as doublets, triplets and quadruplets. All patients had normal blood chemistry except reduced CO2 and increased O2 partial pressures. We assume that the recorded "tetaniform" muscle activity is due to hyperexcitability of the nerve membrane caused by artificial hyperventilation.

High-dose thiopental pharmacokinetics in brain-injured children and neonates.

High-dose thiopental was administered in 8 children with uncontrollable seizures or hypoxic encephalopathy (group A) and 7 full-term neonates with neonatal asphyxia (group B). All of them were submitted to artificial hyperventilation to maintain pCO2 near 3.5 kPa. Rectal temperature was kept at about 35 degrees C. Thiopental was infused with a rate of 2-4 mg X h-1 X kg-1, with treatment lasting 32-192 h for group A (mean 103 h), and 36-48 h for group B (mean 38.5 h). Plasma concentration-time data were analysed pharmacokinetically. Thiopental elimination half-life was 14.5 h (group A) and 20.9 h (group B). The clearance of thiopental was 0.27 liters X h-1 X kg-1 (group A) and 0.32 liters X h-1 X kg-1 (group B). The volume of distribution at steady-state was 5.41 liters X kg-1 (group A) and 8.26 liters X kg-1 (group B). These results show that high-dose thiopental pharmacokinetics is not very different for full-term newborns, children and adults. Elimination half-life and volume of distribution are changed when compared to single-dose studies, while clearance is only slightly modified. The time for disappearance of thiopental from blood is also very long (2 to 5 days). These pharmacokinetic characteristics would be worthy of consideration in cases where there may be prolonged use of thiopental, considering the risk of accumulation and toxicity.

Pressor effect of CO 2 in the rat: different thresholds of the central cardiovascular and respiratory responses to CO 2

Rats were anesthetized with urethane and the vagi, aortic and carotid sinus nerves were sectioned bilaterally. Hypocapnia was induced by artificial hyperventilation with 100% O 2. Administration of 5% CO 2 in O 2, without alteration of the respiratory rate or tidal volume, induced significant increases in mean systemic arterial pressure (mSAP) in rats with intact central nervous system (CNS) and after midcollicular section (36 ± 4 and 34 ± 2 mm Hg, respectively; mean ± S.E.). Smaller but significant increases in mSAP (17 ± 3 mm Hg) were induced by inhalation of 5% CO 2 after section of the spinal cord at the C 4 level. Ganglionic blockade with hexamethonium completely abolished the pressor response to CO 2. In hypocapnic (p aCO 2 15.5 ± 0.7 mm Hg) apneic rats with intact CNS, after denervation of the peripheral chemoreceptors, inhalation of 1.5% CO 2 in O 2 increased p aCO 2 to 22.3 ± 1.2 mm Hg and mSAP by 16 ± 1 mm Hg, but the animals remained apneic for up to 45 min of continuous CO 2 administration. Higher F ICO 2s induced further immediate increases in mSAP and, after delays of up to 6–7 min, also a resumption of central rhythmic respiratory activity (monitored by the intercostal muscles or phrenic nerve electrogram). The p aCO 2 threshold for this respiratory response was 25 ± 1 mm Hg. When rhythmic respiratory activity resumed, a further slight increase in mSAP and the appearance of respiratory modulated oscillations of the SAP were observed in most animals. When, after a period of CO 2 inhalation, 100% O 2 was again administered to the animals mSAP fell immediately, reaching the control level within 20–30 s, while the respiratory activity, if present, disappeared only after 1.5–2 min. From these experiments we conclude that in the hypocapnic rat, after denervation of the peripheral chemoreceptors: (1) CO 2 induces a neurogenic hypertensive response even in the absence of rhythmic respiratory activity; (2) the central chemosensitive sites appear to be located in the ponto-medullary region and in the spinal cord; and (3) the central mechanisms responsible for the pressor response have a lower CO 2 threshold and a much shorter latency than those responsible for the initiation of the rhythmic respiratory activity.

Severe Acute Encephalitis–Improved Outcome after Barbiturate Treatment?

Six cases of severe encephalitis due to measles, varicellae, mononucleosis, influenza, rubella and pertussis were treated with high doses of barbiturates in combination with steroids and artificial hyperventilation. Four of the patients also received antiviral therapy. They all survived without neurological sequelae. The use of barbiturates in high doses may be of importance for an improved outcome in patients with severe encephalitis.

Chemical pulmonary burn injury and chemical intoxication.

Two large groups of patients with chemical pulmonary burns who sustained their injuries in the same environment were presented. Data from the blaze smoke analysis of two imitative experiments which were performed under the same conditions as were present when these patients sustained their burns showed a high concentration of carbon monoxide of 35700-571400 ppm and multivariable components of chemicals. The environmental conditions, the clinical course, laboratory findings and blaze analysis clearly demonstrated the close relationship between chemical pulmonary burn injury and chemical intoxication which increased the difficulty in treatment. Ideally, the initial treatment at the site of the fire is the application of 100 per cent oxygen in high flow by mask, and temporary artificial hyperventilation after hospitalization will give a satisfactory result if the fire victim suffers severe carbon monoxide poisoning. In order to treat chemical intoxication in the patient with chemical pulmonary burns successfully, we have adopted a regimen of 'over-loading fluid resuscitation', together with diuretics and positive end expiratory pressure (PEEP) under the monitoring of central venous pressure.

Effect of Artificial Hyperventilation on Potassium Metabolism and pH in Anesthetized Patients

Effect of Artificial Hyperventilation on Potassium Metabolism and pH in Anesthetized Patients

The role of branchial ventilation in hemolymph acid-base changes in the shore crabCarcinus maenas during hypoxia

1. When exposed to hypoxia in the ambient medium, the crabCarcinus maenas increased and sustained high levels of branchial ventilation for up to 70 h (Fig. 1). 2. The role of hyperventilation in establishing changes in hemolymph acid-base status during hypoxia was investigated. Hemolymph pH and\(P_{CO_2 } \) changes in hypoxic crabs (Figs. 2 and 4) were compared with crabs whose branchial chambers were artificially hyperventilated in normoxia by siphoning water through a mask attached to the carapace (Fig. 3). 3. Hyperventilation alone does not account for the observed alkalosis during hypoxia. It is suggested that changes in both CO2 production and ventilation may be responsible for altering hemolymph acid-base status. 4. Artificial hyperventilation in normoxic crabs resulted in a respiratory alkalosis which is fully compensated after 16 hours by a metabolic acidosis (Fig. 3). 5. Reduction of the hemolymph bicarbonate pool during hypoxia did not interfere with the ability of crabs acclimated to low salinity to regulate hemolymph chloride ion concentration (Fig. 5).

Changes in the requirements for blood transfusion in brain surgery.

The amount of blood used in transfusions during certain neurosurgical operations was less in 1978-79 than in 1971-72 and in 1965-66. The operations investigated were for gliomas and meningiomas of the brain, pituitary adenomas, acoustic neurinomas, arteriovenous malformations, and arterial aneurysms. The major change in anaesthetic techniques between 1965-66 and 1971-72 was the introduction of hypocapnia by controlled artificial hyperventilation. We suggest that this was the main factor responsible for the reduction in the need for blood transfusions. The avoidance of halothane, the use of induced hypotension, and microsurgical technique may have been responsible for the smaller drop between 1971-72 and 1978-79. Good neurosurgical anaesthesia demands anaesthetic expertise, reliable apparatus, and instant laboratory service, but may also reduce costs by reducing the need for blood transfusions.

Hypercapnia and hyperkalaemia

Studies in patients undergoing peritoneal laparoscopy, in which carbon dioxide was used as insufflating gas, showed that artificial hyperventilation was an effective means of preventing serious hypercapnia. The hypercapnia caused a rapid hyperkalaemia and there was a linear relationship between the two. Reversal of the hypercapnia caused the serum potassium to fall towards normal but the speed of this fall did not match the speed of reduction in Paco2. It is suggested that the changes in serum potassium following changes in Paco2 may have some clinical relevance in potassium-depicted patients.

Why do patients with respiratory muscle paralysis require artificial hyperventilation?

The primary reason for the need of hyperventilation in patients with respiratory paralysis is the insufficiency of the inhibitory Hering-Breuer reflex. The artificial distension of the lungs with normal tidal volume cannot inhibit the respiratory centre in contrast to the normal state.

Patterns of bulbar respiratory neurons during and after artificial hyperventilation

Single bulbar respiratory unit activity was recorded in urethane-anesthetized rabbits. During artificial ventilation, reflex contractions of the diaphragm were elicited by the forced deflations of the respirator. Out of 44 neurons, four I, one E and two EI units exhibited a shift of their discharge relative to the contractile phase of the diaphragm, compared to normal respiration. During hypocapnic apnea, some 1, IE and E neurons became silent. Other cells belonging to all phase types, however, continued to fire tonically at a rate less than the peak rate in normal bursts. When rhythmic respiration resumed after termination of the apneic pause, five (I, IE and E) units exhibited a transient phase shift of their burst discharge compared to normal respiration. The results of simultaneous recordings of two neurons belonging to different phase types are compatible with the assumption that inspiratory units are periodically inhibited by inspiratory-expiratory cells.

Effect of intermittent positive pressure ventilation on cardiac systolic time intervals.

The measurement of systolic time intervals (STI) has been widely used as a non-invasive method of assessing the inotropic state of the heart, and normal values are available for healthy individuals breathing spontaneously. The present study was performed in order to evaluate how intermittent positive pressure ventilation (IPPV) affects STI. Ten subjects were investigated before and during halothane anaesthesia for routine surgery. Oesophageal pressure, respiratory minute volume and frequency, arterial blood-gas tensions, cardiac output and heart rate were also measured simultaneously. As expected, the institution of IPPV was associated with a reduction in cardiac output and an increase in oesophageal pressure. Paco2 was reduced. These changes were associated with a considerable lengthening of electro-mechanical systole. This was due to a lengthened pre-ejection period (PEP), whereas the left ventricular ejection time (LVET) was slightly shortened. These changes were even more marked during artifical hyperventilation. The changes in STI are attributed mainly to the reduction of venous return to the heart, subsidiary factors being intrathoracic pressure, myocardial inotropy and vascular resistance.

Baroreceptor and chemoreceptor influences on heart rate during the respiratory cycle in the dog.

1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with pentobarbitone or chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0-2-0-5 ml. warmed, CO2-equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline, or of freshly drawn arterial blood, into the external carotid artery after first clamping the common carotid artery. 2. Brief baroreceptor stimuli had no noticeable effect on breathing. Brief chemoreceptor stimuli had no effect on breathing in some dogs, but in many produced a reflex increase in the depth of inspiration when delivered during inspiration. In these same dogs, brief chemoreceptor stimuli delivered in expiration either prolonged the expiratory pause or evoked an active expiratory effort. 3. Prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered during inspiration. If the carotid sinus nerve or the vagus nerves were cut the responses were abolished. 4. Brief chemoreceptor or baroreceptor stimuli remained effective in evoking prompt decreases in heart rate during periods of apnoea in the end-inspiratory position (Hering-Breuer inflation reflex). In periods of apnoea after prolonged artificial hyperventilation the stimuli were sometimes ineffective at first, but were always effective late in the period of apnoea, again producing prompt cardiac slowing. 5. After denervation of the lungs, brief baroreceptor and chemoreceptor stimuli continued to evoke prompt falls in heart rate when given during expiration. When delivered during inspiration the same stimuli were either ineffective, or less effective.