High altitudes,anxiety, and panic attacks: is there a relationship?

People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to altitude and anxiety are apparent in all three leading models of panic, namely, hyperventilation (hypoxia leads to hypocapnia), suffocation false alarms (hypoxia counteracted to some extent by hypocapnia), and cognitive misinterpretations (symptoms from hypoxia and hypocapnia interpreted as dangerous). Furthermore, exposure to high altitudes produces respiratory disturbances during sleep in normals similar to those in panic disorder at low altitudes. In spite of these connections and their clinical importance, evidence for precipitation of panic attacks or more gradual increases in anxiety during altitude exposure is meager. We suggest some improvements that could be made in the design of future studies, possible tests of some of the theoretical causal links, and possible treatment applications, such as systematic exposure of panic patients to high altitude.     

Influence of a twofold voluntary hyperventilation on visually evoked cortical potentials and human pupillogram

We studied the direct and aftereffects of twofold hyperventilation (HV) on pattern reversing VEPs and pupillograms (PGs) of 19 healthy volunteers. The VEP-N₈₀ and P₁₀₀ latencies increased during HV. Both peak times were maintained for a longer period, up to 20 minutes after HV-2 ended. In addition, the PG-latency time during HV and the PG-construction time during and after HV were increased. The results indicated a temporary delay of neural afferent transmission in the visual system during and after HV. A similar delay of the nervous transmission appeared in the efferent part of the system regulating the pupillary movements after HV ended. The observed changes of the VEP and PG parameters most probably resulted from the hypocapnia cased by HV and its effect on the brain vessels, although other explanations for the changes of the VEP- and PG-parameters may have been possible.     

RENAL REGULATION OF PHOSPHATE EXCRETION IN ENDOTOXAEMIC RATS

1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)-treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia. 2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n= 8) or saline vehicle (n = 9). Thirty-minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx- (n= 7) and saline-treated (n = 8) rats. 3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3′,5′-cyclic mono-phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late-phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH-mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline, and constant dopamine excretion were observed in endo-toxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle. 4. To test whether renal tubular sensitivity to parathyroid hormone related-protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx- (n = 7) and saline-treated rats (n= 7) was examined. Parathyroid hormone related-protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx- than in saline-treated rats. 5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH-mediated phosphaturia after PTH infusion.     

A comparative study of two near infrared spectrophotometers for the assessment of cerebral haemodynamics

Conventional near infrared spectroscopy (NIRS), introduced by Jobsis in 1977, can be considered as a reliable trend monitor for cerebral oxygenation. Quantisation, however, is complex and cumbersome. Recently a relatively simple system for cerebral oximetry (INVOS 3100, Somanetics Corporation, USA) was developed, measuring the regional oxygen saturation (rSo₂) in the capillary bed of the cerebrum, presented as a numerical figure for easy interpretation. In this study a comparison was made between a conventional NIRS instrument and the new INVOS instrument, in order to obtain information about sensitivity and usefulness of the INVOS system. Changes in cerebral haemodynamics were induced by a moderate decrease of the arterial oxygen saturation (S_ao₂) and by varying the arterial carbon dioxide level (PaCO₂). This will result in a higher (hypercapnia) or lower (hypocapnia) cerebral blood flow and subsequent change of both NIRS signals and INVOS signal. Healthy volunteers were used for this study. It was found that the steady state value for rSo₂ was 70 ± 6% (mean ± SD). During the lowering of arterial saturation a poor correlation was found between rSo₂ and S_a0₂ (r=0. 47). Increased cerebral blood flow induced by hypercapnia was detected by both conventional NIRS and the INVOS. Decreased cerebral blood flow induced by hypocapnia could only be detected by conventional NIRS. It was concluded that due to the variation in displayed rSo₂ and the high amount of averaging in the algorithm the INVOS instrument does not yet provide more information than conventional NIRS.     

Interregional differences in brain intracellular pH and water compartmentation during acute normoxic and hypoxic hypocapnia in the anesthetized dog

Interregional differences in intracellular pH (pH_i) in brain tissue, and its regulation following 1 and 5 h of respiratory alkalosis (with and without hypoxemia) were determined in N₂O anesthetized dogs. Two techniques for pH_i estimation were used (Tco₂ and¹⁴C-DMO) and included corrections for measured extracellular fluid (³⁵SO₄²⁻) space (ECS). Cortical pH_i by the two techniques agreed closely in control and in 3 of the 4 experimental conditions, suggesting: (a) our estimation of extracellular fluid (ECF) [HCO₃⁻] from measured CSF [HCO₃⁻] was a valid ssumption; and (b) our method had sufficient resolution to determine the magnitude of brain pH_i regulation during respiratory acid-base disturbances.When moderate normoxic respiratory alkalosis (PaCO₂ ≈ 25 mm Hg) was imposed for 5 h, pH_i (in most brain regions) was well regulated and always exceeded the incomplete regulation noted in bulk CSF. When moderate hypoxemia (PaO₂ ≈ 45 mm Hg) accompanied hypocapnia, pH_i was more closely regulated during the early phase (1 h) of respiratory alkalosis.Increased levels of metabolic acids (especially lactic acid) were critical to brain pH_i regulation during the initial hour of respiratory alkalosis and accounted for much of the independent effect of hypoxemia on pH_i regulation. However, these metabolic acids remained unchanged as pH_i was more completely regulated between 1 and 5 h of continued hypocapnia or hypoxic hypocapnia. This time-dependent tregulation of pH_i may involve some regulatory role for changed transmembrane fluxes of H⁺ and/or HCO₃⁻.Significant interregional differences were observed in both pH_i and in ECS; with tendencies toward more alkaline pH_i and lower ECS in brain stem and white matter. With respiratory alkalosis ECS fell and intracellular fluid increased in both cortex and caudate nucleus, possibly reflecting an osmotic effect of increased metabolic acid levels or reduction in cell membrane ion pumping.     

Seizure duration in unilateral electroconvulsive therapy

ABSTRACT– Seizure duration in unilateral electroconvulsive therapy (ECT) was recorded by means of EEG in an intraindividual comparison under different alveolar O₂- and CO₂-concentrations. Hypocapnia induced by hyperventilation to an alveolar CO₂-concentration of 2 % (2 kPa) resulted in a highly significant increase in seizure duration compared to a normal CO₂ of 5 %, when the alveolar O₂-concentration was constant at 92 %. Oxygen ventilation to an alveolar O₂-concentration of 92 % gave no significant increase in seizure duration compared to 15 %, obtained by ventilation with air, when the CO₂-concentration was kept constant at 5 %. Seizure duration seems to augment progressively with decreasing alveolar CO₂-concentration.     

Brain energy metabolism and blood flow during sevoflurane and halo thane anesthesia: effects of hypocapnia and blood pressure fluctuations

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood How (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (³¹P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco₂ of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco₂ of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50%) of the control value when Paco₂ was ≤2.7 kPa with 2 MAC of sevoflurane and ≤4.0 kPa with 2 MAC of halothane. Abnormal brian energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnie) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco₂ of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.