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PubMed1993

Hyperventilation in head injury does it do more harm than good?

During the past decade the management of clients with severe head injuries has been influenced by the use of hyperventilation. Increased intracranial pressure (I.C.P.) is the major cause of death following head injury and outcome has been linked to the ability of the practitioner to control intracranial hypertension. Hyperventilation is one method that is frequently employed to control increases in I.C.P. There is no doubt that hyperventilation effectively reduces intracranial pressure, but controversy surrounds the influence that this procedure may inflict upon the cerebral hemodynamic reserve (C.H.R.). The literature indicates that in spite of normal cerebral perfusion pressure, associated with raised I.C.P., that C.H.R. may be compromised. This paper will examine the controversy that surrounds the use of hyperventilation in the client with severe head injury.

Cerebrovascular Circulation↗
PubMed1996

Continuous monitoring of brain tissue PO2: a new tool to minimize the risk of ischemia caused by hyperventilation therapy.

Secondary ischemic events worsen the outcome of patients with severe head injury. Such a secondary ischemic event may be caused by a forced hyperventilation. A consequence of the induced vasoconstriction is the risk of ischemia with an adverse effect on outcome. As a reliable and on-line technique, brain tissue pO2 (p(ti)O2) is used for monitoring regional microcirculation, to detect critical hypoperfusion. On 22 patients with a severe head injury 70 hyperventilation tests were performed from day 0-9 after trauma, calculating TCD-CO2-reactivity (% change of mean flow velocity per mm Hg paCO2 change). Additionally brain p(ti)O2-CO2-reactivity (% change of brain p(ti)O2 per mm Hg paCO2 change) was calculated and introduced. Group A +2 (p(ti)O2 < or = 15 mm Hg, TCD-CO2-reactivity > or = 2.5%, p(ti)O2-CO2-reactivity > 0%) and group B +2 (p(ti)O2 > 15 mm Hg, TCD-CO2-reactivity > or = 2.5%. p(ti)O2-CO2-reactivity > 0%) was formed. P(ti)O2 values in group A+2 decreased to an ischemic level or ischemia aggravated during hyperventilation. In group B+2 no ischemic events occurred. TCD-CO2-reactivity, p(ti)O2-CO2-reactivity and decrease of paCO2 were not significantly different in both groups. 6 out of 22 patients showed, from day 0-9, at least once a risk of (aggravating) ischemia by hyperventilation therapy.

Brain↗
PubMed1977

Activation of partial complex seizures by hyperventilation.

Hyperventilation evoked abnormal EEG discharges or discharges and clinical seizures in 11% our patients with partial complex seizures. Hyperventilation is useful in the diagnosis of this kind of epilepsy, but may need to be pursed more vigorously and for a longer duration than is usual practice. The vigorous use of hyperventilation in selected patients with partial seizures should be employed before the use of other more complicated, expensive, and potentially harmful activating procedures.

Adolescent↗
PubMed2005

Central neurogenic hyperventilation: a case report and discussion of pathophysiology.

BACKGROUND: Central neurogenic hyperventilation is a rare condition with poorly understood pathophysiology. OBJECTIVE: To describe a patient with central neurogenic hyperventilation caused by an infiltrative brainstem lymphoma. CONCLUSION: Based on analysis of this patient and other case reports, we propose that central neurogenic hyperventilation is uniquely the result of infiltrative tumors that stimulate pontine respiratory centers and central chemoreceptors.

Adenocarcinoma↗
PubMed1982

Central neurogenic hyperventilation in an awake patient with brainstem astrocytoma.

A patient had the rare combination of central neurogenic hyperventilation (PaCO2 of 9 torr) and a normal level of consciousness for eight days. Morphine attenuated but never corrected the hyperventilation. Experimental effects of hypocapnia, which decreases both cerebral blood flow and metabolism in humans, are at odds with the normal mentation initially seen in this patient despite her marked and persistent hypocapnia. Death occurred after progressive brainstem dysfunction. Pathological study showed a well-differentiated astrocytoma involving primarily the medulla and pons, with scattered tumor foci throughout the entire neuraxis. Possible mechanisms for central neurogenic hyperventilation are discussed briefly in relation to the pathological findings and the observed response to morphine.

Arteries↗
PubMed2002

Visually evoked gamma responses in the human brain are enhanced during voluntary hyperventilation.

Hypocapnia induced by hyperventilation (HV) has powerful effects on neuronal excitability and synaptic transmission. We have studied the effect of hyperventilation on the phase-locked oscillatory components of the evoked responses in the human brain. We recorded visually evoked magnetoencephalographic responses before, during, and after voluntary hyperventilation to pattern-reversal checkerboard stimuli. Gamma-band (30-45 Hz) responses phase-locked to the stimuli were generated in the occipital visual cortex. A wavelet-based time-frequency analysis revealed that the gamma responses increased during HV whereas their frequency did not change significantly. A recent in vitro study in the rat hippocampus demonstrated that the stability of spontaneous gamma activity increases during hypocapnia as a result of enhanced GABAergic transmission. To test if a similar mechanism could account for our findings, we performed simulations on a network of 100 Hodgkin-Huxley neurons connected by inhibitory synapses. We found that enhanced GABA(A) transmission, paired with enhanced excitability, can explain the increase in evoked gamma activity without changing the frequency.

Adult↗
PubMed1988

Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study.

The pulmonary effects of hyperventilation following infusion of sodium salicylate into the cisterna magna was studied in 16 spontaneously breathing adult sheep. We found a fall in PaO2, a decrease in the static compliance of the respiratory system, abnormal chest roentgenographic films, and grossly abnormal lungs following 3.5 to 13 h of hyperventilation. A control group of 15 sheep (10 sheep similarly injected with sodium salicylate, but then sedated and paralyzed and ventilated at normal tidal volume and respiratory rate on a mechanical ventilator, and 5 sheep infused with saline alone and breathing spontaneously) showed no pulmonary or arterial blood gas abnormalities. We conclude that prolonged hyperventilation under the conditions of this experiment precipitated events that resulted in acute lung injury.

Animals↗
PubMed1991

Nimodipine tested in a human model of cerebral ischaemia. Electroencephalographic and transcranial Doppler ultrasound investigations in normal subjects during standardized hyperventilation.

The anti-ischaemic properties of nimodipine 30 mg and 60 mg t.i.d. for 4 days has been tested in a double-blind, placebo-controlled, cross-over study based on the use of hyperventilation to reduce flow velocity in cerebral arteries. Whether the anti-ischaemic properties were due to a vasodilatator action on cerebral blood vessels or to an anti-ischaemic effect on cerebral neurons was studied. There was a slight cardiovascular effect, without any significant change in the EEG at rest. During standardized hyperventilation, there was no difference in the reduction in the blood flow velocity in the nimodipine and placebo groups (namely 56%, 56% and 59%). Both doses of nimodipine, however, significantly attenuated the hyperventilation-induced increase in slow EEG activity in the 1.5-6.0 Hz range. It is concluded that the anti-ischaemic properties of nimodipine are due to an effect on the central nervous system rather than to an effect on cerebral blood flow.

Adult↗
PubMed1986

The influence of hyperventilation on the measurement of stroke volume using a CO2 rebreathing method.

The influence of different degrees of hyperventilation on stroke volume measured with a CO2 rebreathing method was studied in seven normal subjects and seven patients with aortic regurgitation. Hyperventilation was initially performed with a rebreathing rate of 30 min-1 and a tidal volume corresponding to 60% of the subject's vital capacity. The tidal volume was then randomly decreased or increased by 0.5 and 1.01 and the procedure was repeated with rebreathing rates of 25 and 35 min-1. The possible influence of habituation to repeated measurements was tested in seven of the subjects. No significant differences in response to hyperventilation of stroke volume, cardiac output or heart rate were found between normal subjects and patients. When the tidal volume was increased, there was a significant increase in heart rate and also an increase in cardiac output, which was significant when comparing measurements performed with the lowest and highest tidal volumes. When comparing initial and final measurements, there was a significant decrease in heart rate and a tendency to decrease in cardiac output. Stroke volume was not affected by variations in rebreathing rate from 25 to 35 min-1 or tidal volume changes of +/- 0.51 and was also unaffected by repeated measurements.

Adult↗
PubMed1988

Rebreathing to cope with hyperventilation: experimental tests of the paper bag method.

To explore if and how the common rebreathing (paper bag) approach to hyperventilation works, two experiments were carried out. In the first experiment, 12 normal volunteers, aware of the common physiological rebreathing rationale, were twice asked to overbreath intensely and then either to rebreath or to restart normal ventilation. Alveolar CO2 increased more quickly and physical symptoms disappeared earlier in the rebreathing condition. The second experiment had a similar design; however, this time the subjects were led to believe that, after both hyperventilation provocation tests, they were rebreathing in a semiclosed tube system. On one of the occasions, the tube system was, in fact, open. The CO2 restoration again differed in the two conditions. In this second experiment, the moment of symptom disappearance was not significantly earlier in the rebreathing condition. The combined results of the studies suggest that expectation and suggestion play a role in the effects of rebreathing approaches on hyperventilation.

Adult↗
PubMed1989

On octanoic acid-induced hyperventilation--implications for hepatic encephalopathy and Reye's syndrome.

Medium chain fatty acid sodium octanoate was infused into rabbits as a 0.2 M solution over 4 h resulting in blood and brain octanoate levels of 200-800 mumol/l. The infused animals developed marked hyperventilation leading to a mild respiratory alkalosis. Additionally, octanoate infusion brought about hyperammonemia and hyperlactate acidemia. Another group of rabbits also infused with octanoate but pretreated with indomethacin (10 mg/kg b.wt.) developed neither hyperventilation nor hyperammonemia. Therefore, the conclusion made was that octanoate causes the above mentioned disorders through stimulation of prostaglandin synthesis and especially the PGE2 synthesis. Patients with hepatic encephalopathy and Reye's syndrome have elevated levels of plasma octanoate. The present study suggests that octanoate might be the cause for both the hyperventilation and hyperammonemia observed in patients with hepatic encephalopathy and Reye's syndrome.

Alkalosis, Respiratory↗
PubMed1997

Effect of exercise-induced hyperventilation on airway resistance and cycling endurance.

The purpose of the present study was to investigate the effect of exercise induced hyperventilation and hypocapnia on airway resistance (Raw), and to try to answer the question whether a reduction of Raw is a mechanism contributing to the increase of endurance time associated with a reduction of exercise induced hyperventilation as for example has been observed after respiratory training. Eight healthy volunteers of both sexes participated in the study. Cycling endurance tests (CET) at 223 (SD 47) W, i.e. at 74 (SD 5)% of the subject's peak exercise intensity, breathing endurance tests and body plethysmograph measurements of pre- and postexercise Raw were carried out before and after a 4-week period of respiratory training. In one of the two CET before the respiratory training CO2 was added to the inspired air to keep its end-tidal concentration at 5.4% to avoid hyperventilatory hypocapnia (CO2-test); the other test was the control. The pre-exercise values of specific expiratory Raw were 8.1 (SD 2.8), 6.8 (SD 2.6) and 8.0 (SD 2.1) cm H2O.s and the postexercise values were 8.5 (SD 2.6), 7.4 (SD 1.9) and 8.0 (SD 2.7) cm H2O.s for control CET, CO2-CET and CET after respiratory training, respectively, all differences between these tests being nonsignificant. The respiratory training significantly increased the respiratory endurance time during breathing of 70% of maximal voluntary ventilation from 5.8 (SD 2.9) min to 26.7 (SD 12.5) min. Mean values of the cycling endurance time (tcend) were 22.7 (SD 6.5) min in the control, 19.4 (SD 5.4) min in the CO2-test and 18.4 (SD 6.0) min after respiratory training. Mean values of ventilation (VE) during the last 3 min of CET were 123 (SD 35.8) l.min-1 in the control, 133.5 (SD 35.1) l.min-1 in the CO2-test and 130.9 (SD 29.1) l.min-1 after respiratory training. In fact, six subjects ventilated more and cycled for a shorter time, whereas two subjects ventilated less and cycled for a longer time after the respiratory training than in the control CET. In general, the subjects cycled longer the lower the VE, if all three CET are compared. It is concluded that Raw measured immediately after exercise is independent of exercise-induced hyperventilation and hypocapnia and is probably not involved in limiting tcend, and that tcend at a given exercise intensity is shorter when VE is higher, no matter whether the higher VE occurs before or after respiratory training or after CO2 inhalation.

Adult↗
PubMed2006

Comparison of moderate hyperventilation and mannitol for control of intracranial pressure control in patients with severe traumatic brain injury--a study of cerebral blood flow and metabolism.

OBJECTIVE: To compare the respective effects of established measures used for management of traumatic brain injury (TBI) patients on cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGlc) and lactate (CMRLct). METHODS: Thirty-six patients suffering from severe traumatic brain injury (TBI) were prospectively evaluated. In all patients baseline assessments were compared with that following moderate hyperventilation (reducing PaCO2 from 36 +/- 4 to 32 +/- 4 mmHg) and with that produced by administration of 0.5 gr/kg mannitol 20% intravenously. Intracranial and cerebral perfusion pressure (ICP, CPP), CBF and arterial jugular differences in oxygen, glucose and lactate contents were measured for calculation of CMRO2, CMRGlc and CMRLct. RESULTS: Following hyperventilation, CBF was significantly reduced (P < 0.0001). CBF remained most often above the ischemic range although values less than 30 ml x 100 gr(-1) x min(-1) were found in 27.8% of patients. CBF reduction was associated with concurrent decrease in CMRO2, anaerobic hyperglycolysis and subsequent lactate production. In contrast, mannitol resulted in significant albeit moderate improvement of cerebral perfusion. However, administration of mannitol had no ostensible effect either on oxidative or glucose metabolism and lactate balance remained mostly unaffected. CONCLUSIONS: Moderate hyperventilation may exacerbate pre-existing impairment of cerebral blood flow and metabolism in TBI patients and should be therefore carefully used under appropriate monitoring. Our findings rather support the use of mannitol for ICP control.

Adolescent↗
PubMed1987

Usefulness of ST deviation induced by prolonged hyperventilation as a predictor of cardiac death in angina pectoris.

One hundred ninety patients with chronic angina for an average of 2 years were followed. Forty-seven had at least 1 mm of ST deviation in response to provocation of coronary vasoconstriction by prolonged hyperventilation (group I); 143 had no ST deviation (group II). The angiographic response to this test was studied in 21 patients from group I, and revealed 25 to 100% diameter reduction; in group II 9 patients showed a 5 to 14% diameter reduction. In group I, 15 patients (32%) died (hazard rate = 0.17 deaths/patients X years) vs 18 (13%) in group II (hazard rate = 0.06) (p less than 0.01). Seven patients in group I (15%) and 3 in group 2 (2%) died while waiting for surgery (p less than 0.01). All patients who died had coronary stenoses of at least 70%. A Cox regression analysis, using 24 variables (invasive and noninvasive), showed a positive hyperventilation test (ST deviation at least 1 mm), low ejection fraction and systolic blood pressure of at least 160 mm Hg to be independent predictors of death (p less than 0.05). Considering only deaths in non-operated patients (patients waiting for surgery and patients not planned to undergo operation), a rate-pressure product/100 of 150 or less at exercise stress testing, left ventricular end-diastolic pressure of 15 mm Hg or more and duration of angina less than 1 year were also independent predictors of death. Thus, the hyperventilation test may be useful for identifying angina patients who are at high risk of cardiac death due to dynamic coronary obstructions.

Adult↗
PubMed1987

Oscillatory hyperventilation in severe congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy.

Thirty-one subjects with chronic congestive heart failure (CHF) were separated into 3 groups according to ventilatory patterns during graded exercise: Group 1--oscillators (n = 6); group 2-intermediate oscillators (n = 14); and group 3--nonoscillators (n = 11). Group 1 patients showed cyclic fluctuations in minute ventilation (change of 30 to 40 liters/min) and arterial PO2 (change of 38.0 +/- 4.1 mm Hg) and PCO2 (change of 11 +/- 2.8 mm Hg). The nadir in arterial PO2 occurred at times when wasted ventilatory effort was maximal. The amplitude of ventilatory oscillations in group 1 patients increased in the transition from rest to light exercise and damped with heavy exercise. There was no evidence of alveolar hypoventilation at the nadirs of minute ventilation; arterial PCO2 was always 40 mm Hg or less. Substantial hyperventilation (ventilatory equivalent for CO2 twice normal) occurred with maximal minute ventilation in group 1 patients. Oscillatory hyperventilation correlated with severity of CHF. Maximal oxygen uptake was significantly lower in group 1 (11.7 +/- 1.1 ml/kg/min) than group 3 (17.9 +/- 1.8 ml/kg/min) (p less than 0.05). Oscillatory hyperventilation during exercise may accompany severe CHF and compounds the inadequate delivery of oxygen by the failing heart.

Adult↗
PubMed1990

Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men.

To verify that myocardial ischemia occurring during either the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 +/- 31 at baseline to 168 +/- 55 mm Hg x beats/min/100 at the onset of ST-segment depression; p less than 0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 +/- 24 at baseline to 158 +/- 46 mm Hg x beats/min/100 at the onset of electrocardiographic changes; p less than 0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 +/- 35 at baseline vs 102 +/- 27 mm Hg x beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1984

Absence spells. Hyperventilation syndrome as a previously unrecognized cause.

Absence spells in adults have been recognized in association with disorders of excessive somnolence, transient ischemia of the temporal lobes, and seizure disorders. A 66-year-old man who presented with a history of absence spells for more than 20 years is described. After diagnosis of a hyperventilation syndrome without an associated seizure disorder, educational and behavioral therapy without the use of medication has produced a long, continuing remission of these spells. The hyperventilation syndrome continues to present in many ways, often without recognition by physicians for prolonged periods. The case presented exemplifies this problem and may be the first report of absence spells caused by hyperventilation.

Aged↗
PubMed1988

Panic attacks during relaxation and relaxation-induced anxiety: a hyperventilation interpretation.

This paper explains how a hyperventilation theory of panic disorder accounts for panic attacks during relaxation and relaxation-induced anxiety. The explanation is based on the observation that chronic hyperventilators maintain a steady state of low pCO2 (arterial carbon dioxide tension) and are, therefore, sensitive to relatively small increases in ventilation when metabolism is low and to relatively sudden reductions in metabolism when ventilation is relatively constant. Thus, if minute volume of air breathed remains constant while the metabolic production of CO2 decreases, as in the case of one who sits down or lies down to relax, respiratory hypocapnea may increase in intensity until it produces the familiar sensations which mark the panic attack. Data from relevant studies of panic attacks during relaxation support the hyperventilation interpretation.

Anxiety Disorders↗