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Biomedical subjects

S Javaheri

Publications and source records attributed to S Javaheri.

70 records · Page 4Linked to original sources
PubMed1982

Compensatory hypoventilation in metabolic alkalosis.

Although hyperventilation is a well-known compensatory mechanism in metabolic acidosis, compensatory hypoventilation has been inconsistent and controversial in metabolic alkalosis. Six healthy subjects were studied under baseline conditions and during steady-state metabolic acidosis (seven episodes) and alkalosis (14 episodes). Minute ventilation (VE) fell in metabolic alkalosis and rose in metabolic acidosis. These changes in ventilation were entirely due to reduction and elevation of tidal volume (VT) respectively, while respiratory frequency (f) remained unchanged. Alveolar ventilation fell during metabolic alkalosis and resulted in elevation of arterial PCO2 in all subjects. The ventilatory response to arterial PCO2 in all subjects. The ventilatory response to CO2 breathing was also diminished. There was a linear relationship between PaCO2 and plasma [HCO-3] in metabolic acidosis and alkalosis which was defined as PaCO2 (mm Hg = 0.7 [HCO-a] + 20 (+/- SEM), r = 0.95. Although arterial PO2 and plasma [K+] fell during metabolic alkalosis, minute ventilation did not change upon breathing oxygen and there was no correlation between changes in plasma [K+] and plasma H+ regulation.

Acidosis↗
PubMed1981

Severe metabolic alkalosis: a case report.

A 45-year-old man who was admitted with nausea, vomiting, and abdominal pain was found to have severe metabolic alkalosis, with a PaCO2 of 11.4kPa (85.5 mm Hg), PaO2 of 5.8 kPa (43.5 mm Hg), pH of 7.61, and plasma bicarbonate concentration of 82.0 mmol/l. He was treated with oxygen, intravenous physiological saline, and phenytoin and improved within 48 hours. Radiographs showed gastric outlet obstruction secondary to peptic ulcer, which was treated by surgery. Though sever, the rise in carbon dioxide concentration in this patient was probably lifesaving. The PaCO2 was therefore allowed to fall gradually as the alkalosis was treated. The return of both PaCO2 and plasma bicarbonate values to normal in parallel suggests that hypoventilation compensated for the metabolic alkalosis and emphasises the importance of conservative treatment in cases of metabolic alkalosis.

Acid-Base Equilibrium↗
PubMed1981

Pattern of breathing and carbon dioxide retention in chronic obstructive lung disease.

Carbon dioxide (CO2) retention occurs in some but not all patients with obstructive pulmonary disease. In order to assess if the pattern of ventilation modulates CO2 retention, 15 normocapnic (group 1) and 15 hypercapnic (group 2) patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 second (FEV1) less than or equal to 1.0 liter) were studied retrospectively. Utilizing clinical information, anion gap and acid-base nomogram, subjects with superimposed acid-base disturbances were eliminated. Therefore, only patients who exhibited steady state ventilatory patterns were studied. In group 1, mean arterial carbon dioxide tension (PaCO2) was 40 ł 2 torr and mean arterial pH (pHa) was 7.410 ł0.004. In group 2, mean PaCO2 was 52.5 ł1.2 torr and pHa was 7.390 ł0.007. No statistically significant differences between groups were present with respect to age. height, sex, lung volumes and flow rates, diffusing capacity and CO2 production. Minute ventilation was similar in both groups (7.631 liters and 7.81 liters). In group 2, the patients had a significantly higher respiratory rate per minute (22 versus 16.5) and smaller tidal volume (355 versus 463 cc) than the patients in group 1. This pattern of ventilation resulted in a larger dead space ventilation (3.98 liters versus 2.95 liters) and a lower alveolar ventilation (3.82 liters versus 4.61 liters) with consequent CO2 retention. The higher respiratory frequency in the patients in group 2 may be due to vagal stimulation from the lungs since this group had a fivefold greater incidence of chronic bronchitis and a seven-fold greater incidence of cor pulmonale than the patients in group 1.

Carbon Dioxide↗
PubMed1981

Electrolyte composition of cerebrospinal fluid in acute acid-base disorders.

Electrolyte composition of cisternal CSF was measured during 4 hours of respiratory and metabolic acid-base disturbance in anesthetized dogs. Three groups of dogs were studied: (1), isocapnic metabolic alkalosis; (2), acute respiratory acidosis; and (3), combined respiratory acidosis and metabolic alkalosis. Cisternal CSF [K+] remained unchanged despite significant changes in plasma [K+], PCO2 and [HCO3-]; suggesting that mechanisms involved in regulation of CSF [K+] continue to operate normally under such conditions. Cisternal [Na+] and osmolality remained unchanged with almost identical reciprocal equimolar changes in CSF concentration of Cl- and HCO3- during the acid-base disorders studied. The regulatory mechanisms involved in this Cl- -HCO3- exchange may be different in different acid-base disorders, but since CSF [Na+] is kept constant, CSF [HCO3-] in any acid-base disorder equals the difference between CSF [Na+] and CSF [Cl-].

Acid-Base Imbalance↗
PubMed1981

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis.

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

Acidosis↗
PubMed1981

Regional edema formation in isolated perfused dog lungs.

Studies using gravimetric analysis of lungs of frozen animals have suggested that the differences in pulmonary microvascular pressure between non-dependent and dependent lung do not influence the formation of regional pulmonary edema. We wondered if the inability to detect variation in regional extravascular lung water (EVLW) was due to the slow freezing process and, therefore, reassessed the distribution of EVLW in vertically suspended isolated perfused dog lungs with a radioisotopic technique that does not require freezing. Total lung water (TLW), blood or intravascular lung water (IVLW), and EVLW were measured in absolute quantities using a positron camera and the positron-emitting isotopes C15O as a blood label and H2(15)O as a total lung water label. Mean isotopic TLW in 17 lungs that were normal or moderately edematous (wet:dry ratio < 7) was 142 +/- 9 (SE) ml compared to the gravimetric estimate of 148 +/- 7 ml (r = 0.92) and isotopic EVLW was 64 +/- 6 ml compared to the gravimetric estimate of 70 +/- 6 ml (r = 0.8). Analysis of the distribution of regional isotopically measured EVLW in the 17 lungs in various states of spontaneous edema formation revealed a small non-dependent to dependent, gravity-related increase in percent regional EVLW compared to percent regional TLW, which did not vary with the degree of edema in the lung. Serial measurements of absolute regional EVLW in four lungs during spontaneously developing edema also failed to show a disproportionate increase in accumulation of EVLW in any lung zone. Thus, despite the wide variation in microvascular hydrostatic pressure between top and bottom of the vertical isolated lung, edema formation seems to be uniform.

Animals↗
PubMed1979

Role of PCO2 as determinant of CSF [HCO-3] in metabolic acidosis.

To study regulation of CSF [HCO-3] in metabolic acidosis and in particular the role of CSF PCO2 in establishing CSF bicarbonate level, acute metabolic acidosis was induced by the intravenous infusion of HCl in three groups of anesthetized dogs for six hours when PaCO2 was changed at different rates. Plasma [HCO-3] was lowered to 12 +/- 2 meq/L within one hour and maintained at that level thereafter in all groups. (I) Seven dogs were kept isocapnic while metabolic acidosis was induced. The cisternal CSF [HCO-3] fell by only 2.6 meq/L after six hours and was not significantly different from control. (II) In 11 dogs metabolic acidosis was induced while the dogs breathed spontaneously. There was a gradual drop in PaCO2 accompanied by a similar drop in CSF PCO2 of 14.5 torr. CSF [HCO-3] fell significantly by 6.1 meq/L at 6 hours and in parallel with the fall in CSF PCO2. (III) In order to show interdependence of the rate of fall in CSF [HCO-3] with rate of fall in cisternal PCO2 six dogs were mechanically hyperventilated and PaCO2 reduced to 21 torr rapidly and maintained there for six hours. CSF PCO2 followed PaCO. CSF bicarbonate fell rapidly and by 5 meq/L. In groups II and III the fall in cisternal [HCO-3] paralleled the drop in PCO2. Therefore, in metabolic acidosis the rate of the fall in cisternal bicarbonate appears to be a function of the rate of fall in CSF PCO2. It is speculated that the coupling of CSF [HCO-3] reduction in metabolic acidosis to CSF PCO2 fall is primarily for the benefit of CNS H+ homeostasis.

Acidosis↗
PubMed1978

Interaction between PCO2 and plasma [HCO-3] in regulation of CSF [HCO-3] in respiratory alkalosis and metabolic acidosis.

The results of studies presented may be interpreted in light of the dual contribution theory of regulation of CSF acid-base balance, indicating significant interaction between systemic and local CNS mechanisms in H+ homeostasis in the brain and CSF. Both systemic and local mechanisms are at work in H+ homeostasis in the brain and CSF and depending on the specific acid-base disorder or the duration of the imbalance one or the other of the two factors may be the dominant one in maintaining H+ levels in the "normal" range. These factors come into play only when there has been a change in central pH with the primary aim of bringing the CNS [H+] towards normal.

Acidosis↗
PubMedDate not supplied

PH changes on the surface of brain and in cisternal fluid in dogs in cardiac arrest.

We measured brain surface pH and cisternal cerebrospinal fluid (CSF) acid-base variables in Na-pentobarbital anesthetized dogs during KCl induced cardiac arrest. Electrocardiographically, an agonal rhythm occurred within seconds, presumably resulting in rapid fall in cerebral blood flow. The mean arterial blood pressure fell from 125 +/- 22 (mean +/- 1 SD) to 35 +/- 28 mm Hg at 30 seconds and to 19 +/- 3 mm Hg at 60 seconds after KCl injection. The mean brain surface pH (n = 8) dropped abruptly from 7.30 to 6.80 within 3 minutes after induction of cardiac arrest. Changes in cisternal CSF pH, however, occurred slowly with the mean pH falling from 7.33 to 7.27 at 4 minutes and to 6.99 at 10 minutes after induction of cardiac arrest. The fall in cisternal CSF pH was due to a rise in CSF concentration of organic acids as well as a rise in CSF Pco2; the mean cisternal CSF [HCO3-] fell 3.6 mEq/l while the mean cisternal CSF lactate concentration and the mean CSF Pco2 rose, respectively, 2.1 mEq/l and 37.8 mm Hg 10 minutes after induction of cardiac arrest. We conclude that during acute ischemic anoxia gross pH disequilibria develop between brain extracellular fluid and cisternal CSF; analyses of the latter fluid provide unreliable information about brain metabolic status and its acid-base balance even up to ten minutes after induction of cardiac arrest.

Acidosis↗
PubMedDate not supplied

Hypercapnic ventilatory response in unanesthetized normal hamsters.

In order to measure the hypercapnic ventilatory response (HCVR) in experimental animals, it is desirable that the animals be unanesthetized and unrestrained. In the present study, we used a barometric chamber to measure steady state HCVR of hamsters with chronic cannulation of their aortas. In 16 hamsters, the mean (+/- SD) of HCVR, defined as changes in ventilation divided by changes in Paco2 (range 53-73 mmHg), was 10.1 +/- 4.9 ml X min-1 X mmHg-1. The rise in ventilation during CO2 inhalation at low concentrations was due to a rise in mean inspiratory flow and tidal volume. As inhaled Pco2 increased, frequency of breathing increased because expiratory time fell progressively. Inspiratory time rose slightly with small increases in inhaled CO2, but returned to baseline values as the concentration of inhaled Pco2 increased. These changes in ventilation and its components appear to resemble those found in the unanesthetized cat and in man, but are somewhat different from those found in the rat.

Animals↗
PubMedDate not supplied

Changes in brain surface and cisternal fluid pH during Na-pentobarbital induced cardiac arrest in dogs.

This paper describes the changes in the brain surface pH and cisternal cerebrospinal fluid (CSF) acid-base variables during Na-pentobarbital induced cardiac arrest in anesthetized dogs. Brain surface pH, reflecting brain extracellular fluid (ECF) pH was measured by rapidly responding flat surface pH electrodes. Cardiac arrest was induced by intravenous injection of large amounts of Na-pentobarbital (60 to 400 mg/kg). The mean arterial blood pressure fell from 138 +/- 20.8 (mean +/- 1 SD; n = 5) to 33.0 +/- 9.8 mmHg within 30 s after bolus injection of pentobarbital, indicating a rapid fall in cerebral blood flow. Brain surface pH fell abruptly and profoundly; 1 1/2 and 3 min after induction of cardiac arrest, the mean pH had fallen from 7.34 to, respectively, 7.05 and 6.81. Cisternal CSF pH changes were considerably slow with the mean pH falling from 7.35 to 7.00, 10 min after induction of cardiac arrest. This study demonstrates that during stagnant hypoxia there is abrupt and profound cerebral acidosis; more importantly, however, the data indicate that cisternal CSF pH changes lag behind brain ECF pH changes under such circumstances; analysis of cisternal CSF will grossly underestimate the magnitude of severity of brain metabolic derangement up to 10 min after cardiac arrest.

Animals↗