End Of Hyperventilation Research Articles

Clinical Reasoning: Hyperventilation-Induced Alternating Hemiplegia With Concomitant Hemispheric EEG Slowing in a 7-Year-Old Girl With Headache.

A 7-year-old right-handed girl presented to the pediatric neurology outpatient clinic after 5 episodes of headache over the previous 3 months. Her family history was positive for migraine in the mother and maternal grandmother and for febrile seizures in the older sister. The neurologic examination and cognitive profile were normal. Five seconds after the end of hyperventilation, video-EEG showed high-amplitude delta waves predominantly over the left hemisphere with concomitant acute aphasia and right-sided weakness. After the event, which self-resolved over 8 minutes, the girl showed intact recall. A second instance of hyperventilation evoked the appearance of pseudo-rhythmic slow activity localized to the right hemisphere, associated with left-sided weakness, 20 seconds after the end of the test. This event spontaneously resolved in 3 minutes and was followed by headache.An exaggerated physiologic response to hyperventilation, the possible epileptic nature of the events, and a migraine variant were all considered in the differential. Nonetheless, the EEG slowing is shorter in duration and generalized in physiologic and paraphysiological conditions. A clear ictal morphology and evolution of the EEG activity were lacking in this case, and migraine attacks induced by hyperpnea have not been reported to date. Instead, EEG alterations similar to that observed in our patient are described in association with vascular abnormalities. We report the clinical presentation and diagnostic workup of a rare cerebrovascular disorder, highlighting the key features in the differential. Our case emphasizes the clinical value of the EEG rebuild-up phenomenon, which can help the clinician in achieving a prompt diagnosis.

Dynamic and static factors predicting vasomotor reactivity in forced hypocapnia (1070.8)

Objectives: In mechanically ventilated patients intensive hyperventilation can be detrimental. Using transfer function (TF) estimates we were interested in which Parameter could be used for monitoring autoregulation in this condition.Methods: 18 healthy persons (9 women; mean age 32 +‐9 years) underwent simultaneously recordings of blood flow velocity (BFV) by means of transcranial Doppler sonography, blood pressure and endtidal pCO2 (ETpCO2) during 4‐5 minute periods of normoventilation and voluntary hyperventilation. Breath holding (BH) as long as possible started immediately at the end of hyperventilation. TF and Coherence were calculated using Welsh's periodogram method. Mean values were calculated for phase and gain in the very low frequency (vlf) range (0.02‐0.07 Hz), low frequency (lf) range (0.07‐0.15 Hz) and high frequency (hf) range (0.15‐0.40 Hz). VMR was indicated by: 1. VMR% = [BFVnormov‐(BFVbh‐BFVhyperv)/BFVnormov]* 100; 2. BHI= VMR% divided by time of BH.Results: Mean BP was 83±10 mm HG in normoventilation (ETpCO2 0.53 ±0.05 Vol%), 84±11 in hyperventilation (ETpCO2 0.36±0.05) and 82±14 at BH release (ETpCO 0.56 ±0.06); BFV was 59±19 cm/sec, 47±17 and 78±28 cm/sec respectively. Stepwise regression analysis indicated: 1. VMR% was significantly related to ETpCO2 (r=0.50, p<0.01), lf gain (r=0.40, p<0.01) and hf gain (r=0.63, p<0.001) each under hypocapnia; 2. BHI was significantly related to lf phase (r=‐0.58; p=0.01) and lf gain (r=0.63; p<0.001) under hypocapnia and to hf gain (r=0.49; p<0.01) under normocapnia.Conclusion: VMR% and BHI remained related to blood pressure derived gain function. The negative correlation between phase and BHI may give a first hint why extreme hypocapnia can be detrimental to patients under mechanical ventilation

The impact of aging on cerebral vasomotor reactivity to carbon dioxide (1069.5)

The objective of this study was to determine the age‐related differences in cerebral vasomotor reactivity (CVMR) to carbon dioxide. Methods: 92 healthy adults aged 23‐77 underwent measurements of cerebral blood flow velocity (CBFV) using transcranial Doppler, mean arterial pressure, and end‐tidal CO2 (EtCO2) during baseline, hyperventilation (HVT), and modified rebreathing (RB). CVMR was determined by the maximal gain between changes in normalized CBFV (CBFV%) and EtCO2 using a 3rd order polynomial model and its derivative. Results: Lower CBFV and EtCO2 were related to increasing age at baseline. HVT decreased EtCO2 by 21±4 mmHg while RB increased by 19±3 mmHg. Increasing age was related to smaller hypocapnic but larger hypercapnic changes in CBFV% at the end of HVT and RB, respectively. The maximal gain between CBFV% and EtCO2 did not differ by age. Advanced age was associated with greater differences in EtCO2 between the baseline and the level at which the maximum gain in CBFV% occurred. Conclusions: These findings suggest that age‐related reductions in baseline CBFV and EtCO2 may lead to a decrease in hypocapnic but an increase in hypercapnic CBFV response. The larger differences in EtCO2 between baseline and the maximal gain of CBFV% with aging may lead to blunted response of CBF to given changes in arterial CO2 at levels close to baseline.Grant Funding Source: Supported by National Institute on Aging

Cerebrovenous Blood Temperature-Influence of Cerebral Perfusion Pressure Changes and Hyperventilation

The objective of the first part of this study was to use an animal model to investigate the relationship between temperature in the cerebrovenous compartment and cerebral perfusion pressure. In the second part of the study, the objective was to examine the influence of hyperventilation and hypothermia on jugular bulb temperature and body temperature in patients undergoing elective neurosurgery. Intracranial pressure was increased artificially by inflating an infratentorial supracerebellar placed balloon catheter in nine pigs under general anesthesia. Temperature was monitored by thermocouples inserted in the sagittal sinus, white matter of the left lobe and abdominal aorta during the ensuing decrease in cerebral profusion pressure (CPP). Cerebrovenous blood temperature (jugular bulb) and body temperature (urinary bladder) were simultaneously monitored in 24 patients undergoing craniotomy. Moderate hyperventilation was performed in all patients. Cerebrovenous blood and core body temperature were recorded and differences between these two temperatures calculated at the beginning and the end of hyperventilation. At the beginning of the intracranial pressure (ICP), increase mean temperatures of cerebrovenous blood and cerebral tissue (left lobe) were lower than core body temperature. During CPP reduction the difference between core body temperature and cerebrovenous blood temperature increased significantly from 0.86+/-0.44 degrees C prior to ICP rise to 1.19+/-0.58 degrees C at maximum ICP. Before hyperventilation, cerebrovenous blood temperature was higher in 19 patients (+/- difference: 0.34 degrees C +/- 0.27) and equal or lower in five patients (difference: -0.08 degrees C +/- 0.11), than core body temperature. At the end of hyperventilation, the difference between cerebrovenous blood temperature and core body temperature increased (+0.42 degrees C +/- 0.24) in those 19 patients who had started with a higher cerebrovenous blood temperature and decreased (-0.10 degrees C +/- 0. 18) in the other five patients. Both studies demonstrated that the temperature of cerebrovenous blood is influenced by maneuvers which are supposed to decrease cerebral blood flow.

Effects of voluntary hyperventilation on cortical sensory responses. Electroencephalographic and magnetoencephalographic studies.

It is well established that voluntary hyperventilation (HV) slows down electroencephalographic (EEG) rhythms. Little information is available, however, on the effects of HV on cortical responses elicited by sensory stimulation. In the present study, we recorded auditory evoked potentials (AEPs) and magnetic fields (AEFs), and somatosensory evoked magnetic fields (SEFs) from healthy subjects before, during, and after a 3- to 5-min period of voluntary HV. The effectiveness of HV was verified by measuring the end-tidal CO2 levels. Long-latency (100-200 ms) AEPs and long-latency AEFs originating at the supratemporal auditory cortex, as well as long-latency SEFs from the primary somatosensory cortex (SI) and from the opercular somatosensory cortex (OC), were all reduced during HV. The short-latency SEFs from SI were clearly less modified, there being, however, a slight reduction of the earliest cortical excitatory response, the N20m deflection. A middle-latency SEF deflection from SI at about 60 ms (P60 m) was slightly increased. For AEFs and SEFs, the center-of-gravity locations of the activated neuronal populations were not changed during HV. All amplitude changes returned to baseline levels within 10 min after the end of HV. The AEPs were not altered when the subjects breathed 5% CO2 in air in a hyperventilation-like manner, which prevented the development of hypocapnia. We conclude that moderate HV suppresses long-latency evoked responses from the primary projection cortices, while the early responses are less reduced. The reduction of long-latency responses is probably mediated by hypocapnia rather than by other nonspecific effects of HV. It is suggested that increased neuronal excitability caused by HV-induced hypocapnia leads to spontaneous and/or asynchronous firing of cortical neurones, which in turn reduces stimulus-locked synaptic events.

Hyperventilation activation on EEG recording in children with epilepsy

In 20 patients with epilepsy, electroencephalography (EEG) slowing was quantitatively characterized during standardized hyperventilation activation (respiratory rate: 30/min, threefold elevation of total expiratory volume, duration: 4 min) and changes in cerebral blood flow and velocity in the right common carotid artery were monitored with the Doppler ultrasonic method. Thirteen age-matched normal children served as controls. The results were as follows: (1) EEG slowing in the epilepsy group was greater compared with controls. (2) There was a significant decrease in mean frequency (decrease in ci power and increase in δ power) during hyperventilation in the epilepsy group, but no significant change in the controls. (3) The decrease in cerebral blood flow (CBF) was greater in the epilepsy group at the beginning of hyperventilation, possibly related to the greater EEG slowing. (4) The percentage of CBF at the end of hyperventilation was similar in the epilepsy and control groups. The difference in EEG response to hyperventilation between the 2 groups may be due to differences in the decrease in CBF volume and the sensitivity of the change in CBF.

Effects of hyperventilation on the inspiratory to end-tidal oxygen difference

We assessed the inspiratory to end-tidal oxygen difference (PIO2-PE'O2) during voluntary hyperventilation in 10 healthy male volunteers. The oxygen difference was measured with a fast-response paramagnetic differential oxygen sensor. As simultaneous changes in metabolism and cardiac output also influence (PIO2-PE'O2), oxygen uptake was measured with indirect calorimetry and non-invasive transthoracic electrical bioimpedance was used for measurement of cardiac output. After a rest period, subjects were instructed to double their minute ventilation volume (VE) and after 5 min triple their resting VE for another 5 min. (PIO2-PE'O2) decreased from a zero value of 6.4 kPa to 3.9 kPa at 5 min (P < 0.01) and 2.9 kPa at 10 min (P < 0.01). At 15 min (i.e. 5 min after the end of hyperventilation) there was an increase in (PIO2-PE'O2) to 8.3 kPa (P < 0.05). Regression analysis between (PIO2-PE'O2) (kPa) and VE (litre m-2 min-1) gave the formula: (PIO2-PE'O2) = 1/(0.059 + 0.034 VE), r = -0.92, n = 158. Oxygen uptake and cardiac output did not change significantly during hyperventilation, but decreased in the post-hyperventilation period. An oxygen difference of more than 8 kPa was associated with significant arterial desaturation.

Hyperventilation as a model for acute ischaemic hypoxia of the brain: Effects on cortical auditory evoked potentials

Controlled hyperventilation (HV) may be used as an experimental procedure to produce transient ischaemic hypoxia of the brain. The effect of HV on the cortical auditory evoked potential (AEP) components N1 and P2 was studied in ten healthy adult subjects. AEP were recorded before HV, during 3 min of controlled HV, and 1 min and 5 min after the end of HV. The P2 amplitude was significantly reduced by HV and regained its initial value 1 min after the end of HV. The P2 amplitude decrease probably reflects an impairment of synaptic function produced by cerebral hypoxia. Thus, the investigation of cortical AEP components may provide a useful parameter in the study of anti-ischaemic or anti-hypoxic therapies.

BREATH BY BREATH MEASUREMENT OF RESPIRATORY MUSCLE GAS EXCHANGE IN CONTINUOUS MAXIMAL VENTILATION

Respiratory muscle gas exchange as well as respiratory muscle strength has been considered to be an index of respiratory muscle performance. Oxygen consumption was measured continuously in the setting of hyperventilatory exercise.MGC 2001 and our CO2 rebreathing device for maintaining Paco2 were able to measure breath-by-breath gas exchange in sustained maximal voluntary ventilation.The time course of respiratory oxygen consumption rate yielded new knowledge, i.e. that oxygen consumption increased at the end of hyperventilation without increasing minute volume in the sitting position. On the other hand, no such phenomenon was observed in the supine position. We concluded that the supine position was most appropriates for testing respiratory muscle gas exchange.The subjects were challenged with a preparative infusion of aminophylline or placebo while in the supine position. Hyperventilation study was also performed in 11 healthy non-athletes.The results were as follows : Neither oxygen consumption nor minute volume difference significantly between the aminophylline-treated and placebo groups. However, in terms of the duration of hyperventilation (P<0.05) and the serum level of blood lactate (P<0.05) there were significant differences between the aminophylline-treated group and the control group.We concluded that aminophylline increases the endurance capacity of respiratory muscle without elevating the oxygen consumption, probably as a result of increased anaerobic metabolism.

Hyperventilation and ergonovine tests in prinzmetal's variant angina pectoris in men

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 ± 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with ≥1 daily attack, while in those with < 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina

In 10 cases of Prinzmetal's angina in which episodes of myocardial ischemia were easily and reproducibly induced by hyperventilation, this test was performed 111 times, 41 times under control conditions and 70 times during treatment with one or more of the following drugs: phentolamine, isosorbide dinitrate, propranolol, verapamil, nifedipine and amiodarone. Seventeen of 18 negative tests performed under the influence of a long-acting drug coincided with total remission of the patient's anginal episodes when this drug was administered on a short- or long-term basis. No patient died or sustained infarction during a follow-up period of 10.9 months. A negative test was thus a good indication that the clinical response to the corresponding drug would be favorable. The electrocardiographic changes and chest pain provoked by hyperventilation occurred not when alkalosis was greatest (hydrogen ion [pH] change from 7.42 to 7.58, p < 0.001), but when pH was approaching normal or control values. The onset of electrocardiographic changes occurred an average of 175 seconds after the end of hyperventilation and, in two cases, the time lag was as much as 480 and 705 seconds, respectively. This raises several questions regarding the true mechanism triggering coronary spasm under such conditions. The hyperventilation test appears to be a useful and safe procedure for selecting the best possible drug for long-term treatment of Prinzmetal's angina as well as for comparing the relative efficacy of different drugs.

Electroencephalographic Findings in Children With Moyamoya Disease

The EEG findings in 25 children with moyamoya disease were studied. Characteristic findings such as posterior slow, centrotemporal slow (CT slow), "rebuildup" after the end of hyperventilation, and sleep spindle depression were observed. Posterior slow activity was mainly observed in the EEGs examined within a short period (mean, 10 months) after onset, CI slow activity after a longer period (mean,, 28 months), and a diffuse low-voltage pattern after these periods (mean, 56 months). Buildup after the end of hyperventilation, which we refer to as "rebuildup," was discovered in more than half of the cases.