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At least 1,747 records · Page 97Linked to original sources
PubMed1983

Pentazocine overdose.

A patient who ingested 1.5 g pentazocine developed status epilepticus, coma, respiratory depression, acidosis, profound hypotension, and ventricular arrhythmias. Although this patient survived after institution of general supportive measures, she did not respond to usual doses of naloxone. We describe the clinical symptoms and course of recovery of a patient with pentazocine overdose. Our case suggests that pentazocine overdose may require higher doses of naloxone (5 to 20 mg) than are customarily used for narcotic overdoses.

Acidosis↗
PubMed1997

Increased artificial deadspace ventilation is a safe and reliable method for deliberate hypercapnia.

OBJECTIVES: To develop a simple method in an animal model to achieve deliberate hypercapnia, which can be used easily and safely to regulate the pulmonary vascular resistance without changing mean airway pressure and compromising oxygenation. DESIGN: Prospective study, with each animal used as its own control. SUBJECTS: Minipigs, weighing 11 to 14 kg (n = 7). INTERVENTIONS: A quadrilumen thermodilution pulmonary artery catheter was placed in minipigs via the internal jugular vein. Systemic blood pressure was measured with use of a femoral arterial catheter. The animals' lungs were ventilated with an FIO2 of 1.0, and a stable state of eucapnia was achieved and maintained for 30 mins. The artificial deadspace was increased every 30 mins, by connecting 45-mL (3- to 4-mL/kg) corrugated tube segments until a total deadspace volume of 180 mL was added. MEASUREMENTS AND MAIN RESULTS: Hemodynamic performance was evaluated at baseline and after 45 mL (3 to 4 mL/kg), 90 mL (6 to 8 mL/kg), 135 mL (9 to 11 mL/kg), and 180 mL (12 to 15 mL/kg) of added deadspace. Data were indexed to the animal's weight (in kg). Increased artificial deadspace produced a significant (p < .05) increase in PaCO2. These increases in PaCO2 were associated with significant (p < .05) increases of 23%, 32%, 45%, and 46% in the mean pulmonary vascular resistance values, and 6%, 16%, 23%, and 23% in the mean pulmonary arterial pressure, respectively. The systemic pH was decreased from a mean baseline value of 7.45 to 7.39, 7.28, 7.20, and 7.11, respectively. There were no significant changes in PaO2, oxygen consumption, systemic vascular resistance, and cardiac output throughout the experiments. CONCLUSIONS: A gradual increase in artificial deadspace ventilation produces a state of deliberate hypercapnia. In our animal model, a moderate increase in artificial deadspace significantly increased the pulmonary vascular resistance but was not associated with detrimental respiratory acidemia. Larger volumes of added artificial deadspace had no detrimental effect on cardiac output, oxygen content, oxygen consumption, and systemic vascular resistance, but were associated with significant respiratory acidemia and therefore should be avoided.

Acidosis, Respiratory↗
PubMed2000

Effects of inspired gas content during respiratory arrest and cardiopulmonary resuscitation.

Mouth-to-mouth and bag-valve-mask ventilation have been an indispensable part of cardiopulmonary resuscitation (CPR). However, only recently have the effects of different tidal volumes on arterial oxygenation been reported for mouth-to-mouth and bag-valve-mask ventilation. Currently recommended tidal volumes (10-15 mL/kg) are associated with an increased risk of gastric inflation because they produce high peak inspiratory pressures. An animal model of ventilation with an unprotected airway showed that a smaller tidal volume (6 mL/kg) is as effective as a larger tidal volume (12 mL/kg) in maintaining Sao2 at >96%. However, a smaller tidal volume with exhaled gas ventilation produced a mean Sao2 of 48%, which is ineffective. Ventilation gas mixtures have been studied in models of cardiac arrest and CPR. One study showed that ventilation with air during 6 mins of CPR resulted in a return of spontaneous circulation in 10 of 12 animals compared with only 5 of 12 animals ventilated with exhaled gas (p<.04). Arterial and mixed-venous Po2 were significantly higher, and Pco2 was significantly lower in the air ventilation group. Investigations of the cardiovascular effects of mouth-to-mouth ventilation during CPR suggest that there are adverse effects during low blood flow states. However, mouth-to-mouth ventilation during respiratory arrest is lifesaving and should continue to be taught and emphasized in basic life support courses.

Acidosis, Respiratory↗
PubMed1986

Ammonium chloride induced acidosis and aldosterone secretion in the goat.

Responses to 30-min intraduodenal infusion of NH4Cl (total amount 75 mmol) were studied in conscious goats. The infusion caused an immediate, transient rise in plasma aldosterone concentration (PA) from a mean of 78 to 221 pmo l-1. As expected, the NH4Cl administration also induced metabolic acidosis, initially subjected to partial respiratory compensation. The acidosis did not become fully developed until 1 h after cessation of the infusion, when PA had almost returned to its initial level. Renal compensation of the acidosis was shown by acidification of the urine and reduced Na excretion being most pronounced 1-2 h post-infusion. During the infusion blood haemoglobin concentration and the haematocrit increased by 25 and 13%, respectively, without simultaneous increase in plasma protein concentration and with persisting ear vasodilatation, indicating a mobilization of stored erythrocytes in the absence of a general increase in sympathetic tone. The results suggest that the reduction of blood pH is not the cause of the increase in PA occurring in association with NH4Cl-induced metabolic acidosis, but leave open the possibility that this increase may be due to some centrally mediated or direct adrenal influence of NH+4. As regards the apparent NH4Cl-induced mobilization of stored erythrocytes, it is suggested that such a response may play a role in the defence against acidosis by increasing the buffering capacity of the circulating blood.

Acid-Base Equilibrium↗