Hypokalaemia with Respiratory Alkalosis in Anaesthetised Goats (original) (raw)
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Canadian Anaesthetists’ Society Journal, 1981
The purpose of these studies was to determine the reasons for the hypokalaemia observed in rabbits studied in our laboratory. The rabbits consumed standard rabbit chow which is rich in potassium and remained in potassium balance. Hypokalaemia was only observed following anaesthesia. A number of additional investigations were undertaken to clarify the mechanisms involved. The hypokalaemia could not be attributed to technical factors, alkalaemia, hyperinsulinaemia or hyperaldosteronism, but seemed to be a function of anaesthesia. This effect of pentobarbitone anaesthesia was not unique to the rabbit, as similar changes also occurred in the anaesthetized dog.
The effect of respiratory alkalosis on oxygen consumption in anesthetized patients
Journal of Clinical Anesthesia, 1992
Study Objective: To investigate whether hyperventilation sign$cantly altered oxygen consumption in anesthetized and paralyzed patients undergoing surgery. Design: Open crossover trial with 1 hour of hyperventilation preceded and followed by I hour of normoventilation. Setting: University medical center. Patients: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis. Interventions: After baseline normoventilationfor I hour (Period l), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO,) of 20 to 25 mmHg for I hour {Period 2). Patients then experienced another hour of normoventilation (Period 3). Measurements and Main Results: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO, (P&O&, oxygen consumption (VO,), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, PH was significantly higher and FE&O2 and PaCO, signaficantly lower compared with the periods of normoventilation. VO, was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods. Conclusions: In anesthetized paralyzed patients, there is an increase in whole-body VO, with hypocapnic alkalosis.
Comparative Clinical Pathology, 2010
This study was conducted to evaluate the effect of xylazine-ketamine-diazepam anesthesia on heart rate, respiration rate, rectal temperature, rumen motility, peripheral blood pH, PaO2, and PaCO2 in adult female nonpregnant Awassi sheep and adult female nonpregnant Damascus goats. Anesthesia was induced using 0.1 mg/ kg, 5 mg/kg, and 0.25 mg/kg xylazine, ketamine, and diazepam respectively as a single intravenous injection. The heart rate, respiration rate, rectal temperature, rumen motility, peripheral arterial blood pH, PaO2, and PaCO2 were evaluated 15 min before and at 15, 30, and 60 min during anesthesia. In sheep, the heart rate, rumen motility, and PaO2 were decreased significantly (P<0.05) at 15, 30, and 60 min following anesthesia. The respiration rate and rectal temperature and blood pH were decreased significantly (P<0.05) at 30 and 60 min. The peripheral PaCO2 was increased significantly (P<0.05) at 15 and 30 min. In goats, the heart rate and rumen motility were decreased significantly (P<0.05) at 15, 30, and 60 min while the respiration rate was decreased only significantly (P<0.05) at 60 min. Rectal temperature was decreased significantly (P<0.05) at 30 and 60 min. The blood pH was decreased significantly (P<0.05) at 15 and 30 min. PaO2 was only significantly (P<0.05) decreased at 15 min while PaCO2 was increased significantly (P<0.05) at 15 and 30 min.
Plasma potassium response to acute respiratory alkalosis
Kidney International, 1995
Plasma potassium response to acute respiratory alkalosis. Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes, acute respiratory alkalosis was induced by voluntary hyperventilation for 20 (18 and 36 liter/mm) and 35 minutes (18 liter/mm). The plasma potassium response to acute respiratory alkalosis was compared to time control, isocapnic and isobicarbonatemic (hypocapnic) hyperventilation as well as beta-and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic hyperventilation (standard acute respiratory alkalosis) at 18 or 36 liter/mm (PCO2-16 and-22.5 mm Hg, respectively) resulted in significant increases in plasma potassium (ca + 0.3 mmollliter) and catecholamine concentrations. During recovery (post-hyperventilation), a ventilation-rate-dependent hypokalemic overshoot was observed. Aipha-adrenoreceptor blockade obliterated, and beta-adrenoreceptor blockade enhanced the hyperkalemic response. The hyperkalemic response was prevented under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinically significant increase in plasma potassium. The hyperkalemic response is mediated by enhanced alphaadrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate. Acute respiratory alkalosis is the frequent acid-base disorder that results from hyperventilation. Hyperventilation is a common and important clinical event which occurs in response to pain (myocardial infarction), anxiety (stage fright, panic attacks), drugs (cocaine), hypoxemia (asthma attacks, pulmonary thromboembolism) and infection (sepsis). The importance of recognizing the electrolyte disturbances (that is, altered potassium homeostasis) produced by acute respiratory alkalosis has been emphasized owing to the potential for electrolyte-induced complications such as cardiac arrhythmias. The clinical importance attributed to alterations in potassium homeostasis during acute hyperventilation is underscored by the practice of administering potassium salts to treat hyperventilation-induced electrocardiographic abnormalities [1, 2]. Although, according to standard textbooks, it seems widely accepted that acute respiratory alkalosis results in hypokalemia in humans [3], a critical review of the literature reveals conflicting
European Journal of Anaesthesiology, 2001
Background and objective Few and conflicting data are available regarding the changes of plasma potassium concentration during acute respiratory acidosis in human beings. This study compares the acute changes in plasma potassium concentration in acutely hypercapnic patients and in non-hypercapnic patients during general anaesthesia. Methods Thirty-three patients undergoing interventional rigid bronchoscopy were studied. Ventilation of the lungs was randomly conducted using either spontaneous-assisted ventilation or intermittent negative-pressure ventilation. All patients received the same anaesthetic protocol. Arterial blood gases and osmolality, and plasma concentrations of glucose, sodium, potassium and chloride were measured.
Köpeklerde Ksi̇lazi̇n-Ketami̇n Anestezi̇si̇ni̇n Göz İçi̇ Basinci Üzeri̇ne Etki̇si̇
İstanbul Üniversitesi Veteriner Fakültesi Dergisi, 2014
Glaucoma is defined as the increase in the intraocular pressure (IOP) causing visual loss due to the circulation deficits of the aqueous humor. The IOP measurement can be obtained without any problem in calm animals. However, some animals do not allow IOP measurement without sedation or anesthesia. The purpose of this study is to determine the effect of xylazine HCl (as a sedative) and ketamine HCl (as an anesthetic in combination with xylazine HCl) on the IOP in dogs. In this study, 35 dogs of different breed, age and gender that were brought to Istanbul University Veterinary Faculty Education and Research Hospital Surgery Department with different surgical indications were used. As a result xylazine HCl sedation and xylazine HCl + ketamine HCl anesthesia decrease the intraocular pressure significantly and the IOP measurements in glaucoma suspicious dogs must be obtained without xylazine HCl sedation or xylazine HCl + ketamine HCl anesthesia were determined.
Comparison of racemic ketamine and S-ketamine as agents for the induction of anaesthesia in goats
Veterinary Anaesthesia and Analgesia, 2010
Objective To compare racemic ketamine and S-ketamine as induction agents prior to isoflurane anaesthesia. Study design Prospective, blinded, randomized experimental study. Animals Thirty-one healthy adult goats weighing 39-86 kg. Methods Goats were premedicated with xylazine (0.1 mg kg)1) intravenously (IV) given over 5 minutes. Each goat was assigned randomly to one of two treatments for IV anaesthetic induction: group RK (15 goats) racemic ketamine (3 mg kg)1) and group SK (16 goats) S-ketamine (1.5 mg kg)1). Time from end-injection to recumbency was measured and quality of anaesthetic induction and condition for endotracheal intubation were scored. Anaesthesia was maintained with isoflurane in oxygen for 90 minutes. Heart rate, invasive arterial blood pressure, oxygen saturation, temperature, end-tidal carbon dioxide and isoflurane were recorded every 5 minutes. Arterial blood samples were taken for analysis every 30 minutes. Recovery time to recurrence of swallowing reflex, to first head movement and to standing were recorded and recovery quality was scored. Two-way repeated measures ANOVA, Mann-Whitney and a Mantel-Cox tests were used for statistical analysis as relevant with a significance level set at p < 0.05. Results Induction of anaesthesia was smooth and uneventful in all goats. There was no statistical difference between groups in any measured parameter. Side effects following anaesthetic induction included slight head or limb twitching, moving forward and backward, salivation and nystagmus but were minimal. Endotracheal intubation was achieved in all goats at first or second attempt. Recovery was uneventful on all occasions. All goats were quiet and needed only one or two attempts to stand. Conclusions and clinical relevance S-ketamine at half the dose rate of racemic ketamine in goats sedated with xylazine and thereafter anaesthetised with isoflurane induces the same clinically measurable effects.
Hypertonic Saline Treatment of Severe Hyperkalemia in Nonnephrectomized Dogs
Academic Emergency Medicine, 2000
Objectives: To determine whether a hypertonic saline bolus improves cardiac conduction or plasma potassium levels more than normal saline infusion within 15 minutes of treatment for severe hyperkalemia. Previously with this model, 8.4% sodium chloride (NaCl) and 8.4% sodium bicarbonate (NaHCO 3) lowered plasma potassium equally effectively. Methods: This was a crossover study using ten conditioned dogs (14-20 kg) that received, in random order, each of three intravenous (IV) treatments in separate experiments at least one week apart: 1) 2 mmol/kg of 8.4% NaCl over 5 minutes (bolus); 2) 2 mmol/kg of 0.9% NaCl over one hour (infusion); or 3) no treatment (control). Using isoflurane anesthesia and ventilation (pCO 2 = 35-40 torr), 2 mmol/kg/hr of IV potassium chloride (KCl) was infused until conduction delays (both absent p-waves and Ն20% decrease in ventricular rate in Յ5 minutes) were sustained for 15 minutes. The KCl was then decreased to 1 mmol/kg/hr (maintenance) for 2 hours and 45 minutes. Treatment (0 minutes) began after 45 minutes of maintenance KCl. Results: From 0 to 15 minutes, mean heart rate increased 29.6 (95% CI = 12.2 to 46; p < 0.005) beats/min more with bolus than infusion and 23.4 (95% CI = 2.6 to 43.5; p < 0.03) beats/min more with bolus than control. No clinically or statistically significant difference was seen in heart rate changes from 0 to 30 minutes. Decreases in potassium from 0 to 15 minutes were similar with bolus, infusion, and control. Conclusions: In this model, 8.4% NaCl bolus reversed cardiac conduction abnormalities within the first 15 minutes after treatment, more rapidly than did the 0.9% NaCl infusion or control. This reversal occurred despite similar reductions in potassium levels.