Cardiovascular and respiratory effects of thiopental administration in hypovolemic dogs

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.     

Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs.

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.     

The Cardiopulmonary Effects of Oxymorphone in Hypovolemic Dogs

Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.
Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.
Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.     

Effects of a peripheral alpha2 adrenergic-receptor antagonist on the hemodynamic changes induced by medetomidine administration in conscious dogs

OBJECTIVE: To evaluate the effects of administration of a peripheral alpha(2)-adrenergic receptor antagonist (L-659,066), with and without concurrent administration of glycopyrrolate, on cardiopulmonary effects of medetomidine administration in dogs. ANIMALS: 6 healthy adult dogs. PROCEDURES: Dogs received saline (0.9% NaCl) solution (saline group), L-659,066 (group L), or L-659,066 with glycopyrrolate (group LG). These pretreatments were followed 10 minutes later by administration of medetomidine in a randomized crossover study. Hemodynamic measurements and arterial and mixed-venous blood samples for blood gas analysis were obtained prior to pretreatment, 5 minutes after pretreatment, and after medetomidine administration at intervals up to 60 minutes. RESULTS: After pretreatment in the L and LG groups, heart rate, cardiac index, and partial pressure of oxygen in mixed-venous blood (PvO2) values were higher than those in the saline group. After medetomidine administration, heart rate, cardiac index, and PvO2 were higher and systemic vascular resistance, mean arterial blood pressure, and central venous pressure were lower in the L and LG groups than in the saline group. When the L and LG groups were compared, heart rate was greater at 5 minutes after medetomidine administration, mean arterial blood pressure was greater at 5 and 15 minutes after medetomidine administration, and central venous pressure was lower during the 60-minute period after medetomidine administration in the LG group. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of L-659,066 prior to administration of medetomidine reduced medetomidine-induced cardiovascular changes in healthy dogs. No advantage was detected with concurrent administration of L-659,066 and glycopyrrolate.     

Comparison of the cardiopulmonary effects of etomidate and thiamylal in dogs.

The cardiopulmonary effects of etomidate, a nonbarbiturate, short-acting, IV anesthetic, were compared and contrasted with those of thiamylal sodium in chronically instrumented conscious dogs. Etomidate, when administered IV at dosages of 1.5 and 3.0 mg/kg of body weight, produced anesthesia lasting from 8 +/- 5 and 21 +/- 9 minutes, respectively. Heart rate, aortic blood pressure, left ventricular peak pressure, left ventricular end diastolic pressure, left ventricular contractile force, and myocardial oxygen consumption were unchanged after administration of either dose of etomidate; however, the dosage of 1.5 mg/kg produced significant (P less than 0.05) increases in respiratory rate and decreases in tidal volume. The minute volume remained unchanged from base-line values. Significant (P less than 0.05) decreases in tidal volume, arterial pH, and partial pressure of oxygen were produced, and minute volume remained unchanged when 3.0 mg of etomidate/kg of body weight was administered. Thiamylal sodium (8.0 mg/kg of body weight; given IV) produced anesthesia lasting for 14 +/- 5 minutes. Significant increases (P less than 0.05) in heart rate, arterial blood pressure, left ventricular peak pressure, and myocardial oxygen consumption were observed after IV administration. Left ventricular contractility was significantly (P less than 0.05) decreased. Respiratory rate was not significantly (P less than 0.05) affected by thiamylal although tidal volume and minute volume were decreased. These respiratory alterations resulted in significant (P less than 0.05) increases in the arterial partial pressure of carbon dioxide and decreases in pH and the partial pressure of oxygen. On the basis of cardiopulmonary function, etomidate offered rapid, safe, short duration anesthesia superior to that of thiamylal sodium.     

The cardiovascular sparing effect of fentanyl and atropine, administered to enflurane anesthetized dogs.

Cardiovascular effects of high dose opioid together with low dose inhalant were compared with inhalant alone to determine whether opioid/inhalant techniques were less depressant on the cardiovascular system. The effects of positive pressure ventilation and increasing heart rate to a more physiological level were also studied. Cardiovascular measurements recorded during administration of enflurane at 1.3 minimum alveolar concentration (MAC; 2.89 +/- 0.02%) to spontaneously breathing dogs (time 1) and during controlled ventilation [arterial carbon dioxide tension at 40 +/- 3 mmHg (time 2)] were similar. At time 2, mixed venous oxygen tension and arterial and mixed venous carbon dioxide tensions were significantly decreased, while arterial and mixed venous pH were significantly increased compared to measurements at time 1. After administration of fentanyl to achieve plasma fentanyl concentration of 71.7 +/- 14.4 ng/mL and reduction of enflurane concentration to yield 1.3 MAC multiple (0.99 +/- 0.01%), heart rate significantly decreased, while mean arterial pressure, central venous pressure, stroke index, and systemic vascular resistance index increased compared to measurements taken at times 1 and 2. Pulmonary arterial occlusion pressure was significantly increased compared to measurements taken at time 2. After administration of atropine until heart rate was 93 +/- 5 beats/min (plasma fentanyl concentration 64.5 +/- 13.5 ng/mL) heart rate, mean arterial pressure, cardiac index, oxygen delivery index, and venous admixture increased significantly compared to values obtained at all other times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary Effects of Using Carbon Dioxide for Laparoscopic Surgery in Dogs

Cardiopulmonary effects of laparoscopic surgery were investigated in five crossbred dogs (21 ± 1.9 kg). Premedicated dogs were anesthetized with thiopental and maintained with halothane at 1.5 times minimum alveolar concentration in oxygen. Controlled ventilation maintained partial pressure of end-tidal co₂ at 40 ± 2 mm Hg. Vecuronium was used for skeletal muscle relaxation. After instrumentation and stabilization, baseline measurements were made of cardiac output (thermodilution technique), mean systemic, mean pulmonary arterial and pulmonary wedge pressures, heart rate, saphenous vein and central venous pressures, and minute ventilation. Baseline arterial and mixed venous blood samples were drawn for analysis of pH, Pao₂, Paco₂, Pvo₂, Pvco₂, and bicarbonate concentrations. Systemic and pulmonary vascular resistances, oxygen delivery and consumption, shunt fraction, and dead space ventilation were calculated using standard formulas. Abdominal insufflation using co₂ to a pressure of 15 mm Hg for 180 minutes resulted in significant ( P <.05) increases in heart rate (15 to 180 minutes), minute ventilation (75 to 135 minutes), and saphenous vein pressure (15 to 180 minutes), and decreases in pH (60 to 180 minutes) and Pao₂ (60 to 180 minutes). For 30 minutes after desufflation, there was a significant decrease in Pao₂, and increases in cardiac output, o₂ delivery, and heart rate, compared with baseline. There was a significant increase in shunt fraction and decrease in pH at 15 minutes after desufflation only. The changes were within physiologically acceptable limits in these healthy, ventilated dogs.     

Cardiovascular effects of desflurane following acute hemorrhage in dogs

Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end‐tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO₂), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO₂, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO₂ increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO₂ increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage.     

Cardiovascular effects of hydralazine HCl administration in horses

Six standing awake adult horses were instrumented for measurement of mean arterial, central venous, and pulmonary arterial blood pressures (mm of Hg), thermodilution cardiac output (ml/kg/min), and pulmonary arterial blood temperature (C). Total peripheral resistance was calculated from these values. Base-line data were accumulated, and a single dose of hydralazine HCl (0.5 mg/kg) was administered IV. Horses were monitored for 420 minutes after hydralazine administration. Mean arterial and central venous blood pressures did not change from the base-line values. Cardiac output and heart rate were increased above base-line values for 260 minutes. Total peripheral resistance was decreased for 240 minutes. Pulmonary arterial blood temperature was decreased for 60 minutes after drug administration. Mean pulmonary arterial pressure relative to the base-line mean was intermittently decreased during the study. Intravenously administered hydralazine HCl appears to be an effective vasodilator, with moderate duration of action in horses.     

Effects of detomidine in young water buffalo

Following preliminary studies with detomidine hydrochloride in 10 young buffaloes (Bubalus bubalis), the effects of an intramuscular injection of 40 /ixg.kg-¹ were studied in 6 healthy buffaloes of VA to 2 years of age, weighing between 85 and 140 kg. Arterial blood pressure, central venous pressure, heart rate, electrocardiogram, electroencephalogram, respiratory rate, arterial pH, arterial and venous blood gases and rectal temperature were monitored before, and for an hour after, intramuscular injection of detomidine. Marked ataxia and sternal recumbency occurred within 10 minutes of injection, and an apparent complete recovery occurred in about 90 minutes. The electroencephalograms never demonstrated the high-voltage-low-frequency wave forms normally associated with sedation, but the animals appeared well sedated.
After injection there was marked decrease in heart rate which then tended to increase but it remained significantly (P < 0.05) below pre-injection values at 60 minutes. The mean arterial pressure increased initially, especially when electrocardiogram showed AV block, but after 15 minutes it had declined to below pre-injection values. These changes in the arterial blood pressure were, however, not statistically significant. Central venous pressure tended to increase during sedation but except at 30 minutes this increase was not statistically significant.
Rectal temperature, arterial pH, arterial carbon dioxide tension, standard bicarbonate and cranial vena caval oxygen tension did not show any significant variation. Respiratory rate and arterial oxygen tension decreased significantly.     

Effects of gastric distention-volvulus on coronary blood flow and myocardial oxygen consumption in the dog

Gastric distention-volvulus (GDV; at 50 mm of Hg gastric inflation pressure) was experimentally induced in 8 dogs anesthetized using pentobarbital. Hemodynamic indices including heart rate, mean arterial pressure, cardiac output, and coronary blood flow (4 dogs) were measured during a 20-minute period of GDV and for 10 minutes after decompression. Arterial and coronary venous oxygen tensions were also measured for calculation of myocardial oxygen extraction (7 dogs) and myocardial oxygen consumption (4 dogs). Dogs were monitored for 72 hours postoperatively for the occurrence of arrhythmias, then were euthanatized for gross and histologic examination of the heart. Experimental GDV resulted in significant (P less than 0.05) decreases in cardiac output (89%), mean arterial pressure (45%), and coronary blood flow (50%) compared with control values. Myocardial oxygen extraction increased (30%) and overall myocardial oxygen consumption decreased (50%), compared with control values. Evidence of subendocardial necrosis was seen in 6 dogs, 4 of which had developed ventricular arrhythmias 8 to 24 hours postoperatively.     

Acute hemodynamic effects of hydralazine in dogs with chronic mitral regurgitation

The hemodynamic response to hydralazine administration was evaluated in 6 conscious small dogs with chronic mitral regurgitation. All dogs underwent invasive and noninvasive hemodynamic monitoring before and after hydralazine administration. Cardiac output and pulmonary capillary wedge pressure were measured with a Swan-Ganz thermodilution catheter. Systemic arterial blood pressure (AP) was measured directly by inserting a needle into the femoral artery. Standard M-mode echocardiograms and thoracic radiographs were obtained. Other hemodynamic variables were calculated. Base-line hemodynamic variables were altered severely in all dogs. Hydralazine decreased mean arterial blood pressure from 104 +/- 18 (mean +/- SD) to 78 +/- 12 mm of Hg (P less than 0.005), total systemic resistance index from 2,946 +/- 625 to 1,261 +/- 420 dynes-s-cm-5m2 (P less than 0.005), and pulmonary capillary wedge pressure from 40 +/- 5 to 26 +/- 3 mm of Hg, (P less than 0.005). Cardiac index increased from 2.92 +/- 0.72 to 5.36 +/- 1.67 L/min/m2 of body surface area (P less than 0.005). Mixed venous oxygen tension (PvO2) increased from 28.4 +/- 4.3 to 41.2 +/- 5.2 mm of Hg (P less than 0.001). Pulmonary edema resolved, as determined on thoracic radiographs. Mixed venous oxygen tension correlated well with the cardiac index (r = 0.92; P less than 0.001). It was concluded that hydralazine administration caused a small decrease in end diastolic diameter (4.8 +/- 0.9 to 4.5 +/- 0.8 cm, P less than 0.05) and end systolic diameter (2.6 +/- 0.8 to 2.3 +/- 0.7 cm, P less than 0.05). Fractional shortening and heart rate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Xylazine and xylazine-ketamine in dogs

The cardiopulmonary consequences of IV administered xylazine (1.0 mg/kg) followed by ketamine (10 mg/kg) were evaluated in 12 dogs. Xylazine caused significant decreases in heart rate, cardiac output, left ventricular work, breathing rate, minute ventilation, physiologic dead space, oxygen transport, mixed venous partial pressure of oxygen, and oxygen concentration. It caused significant increases in systemic blood pressure, central venous pressure, systemic vascular resistance, tidal volume, and oxygen utilization ratio. The subsequent administration of ketamine was associated with significant increases in heart rate (transient increase), cardiac output, the alveolar-arterial PO2 gradient and venous admixture (transient increase), and arterial PCO2 (transient increase). It caused significant decreases in stroke volume (transient decrease), left ventricular stroke work (transient decrease), effective alveolar ventilation, arterial PO2 and oxygen content (transient decrease).     

The effects of intrathoracic pressure during continuous two-lung ventilation for thoracoscopy on the cardiorespiratory parameters in sevoflurane anaesthetized dogs

The cardiopulmonary effects of different levels of carbon dioxide insufflation (3, 5 and 2 mm Hg) under two-lung ventilation were studied in six sevoflurane (1.5 minimum alveolar concentration; MAC) anaesthetized dogs during left-sided thoracoscopy. An arterial catheter, Swan-Ganz catheter and multianaesthetic gas analyser were used to monitor the cardiopulmonary parameters during the experiment. Baseline data were obtained before intrathoracic pressure elevation and the measurements were repeated at intervals after left lung collapse induced by insufflation with carbon dioxide gas. The intrapleural pressure levels used were 3, 5 and 2 mm Hg. Arterial blood pressures, cardiac index, stroke index, left and right ventricular stroke work index, arterial haemoglobin saturation, arterial oxygen tension and systemic vascular resistance decreased significantly during hemithorax insufflation, whereas heart rate, right atrial pressure, mean, systolic and diastolic pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance and arterial carbon dioxide tension significantly increased during intrapleural pressure elevation. Although carbon dioxide insufflation into the left hemithorax with an intrapleural pressure of 2-5 mm Hg compromises cardiac functioning in 1.5 MAC sevoflurane anaesthetized dogs, it can be an efficacious adjunct for thoracoscopic procedures. Intrathoracic view was satisfactory with an intrapleural pressure of 2 mm Hg. Therefore, the intrathoracic pressure rise during thoracoscopy with two-lung ventilation should be kept as low as possible. Additional insufflation periods should be avoided, since a more rapid and more severe cardiopulmonary depression can occur.     

Acid-base values of standardbred horses recovering from strenuous exercise.

Blood gases, lactic acid concentrations, and pH were measured in arterial and mixed venous blood in moderately conditioned Standardbred horses after a standardized exercise load of 1.6 km in 2 minutes, 40 seconds. Samples were obtained at rest, immediately after exercise, and at 3, 6, 15, 30, and 60 minutes after exercise. Arterial oxygen tension and mixed venous oxygen tension increased after exercise, reaching peak values at 6 minutes. Arterial oxygen tension returned to the resting (preexercise) value by 15 minutes, and mixed venous oxygen tension by 30 minutes. Arterial carbon dioxide tension decreased immediately after exercise, reaching its lowest value at 6 minutes, and returned to resting value by 30 minutes. Mixed venous carbon dioxide tension reached its highest value immediately after exercise, then decreased to less than the resting value, reaching its lowest value by 15 minutes, and returned to normal by 60 minutes. Lactic acid concentration increased immediately after exercise, reaching its highest value at 6 minutes, and returned toward normal by 60 minutes. Arterial pH decreased immediately after exercise, reaching its lowest value at 6 minutes, and returned to normal by 60 minutes. Mixed venous pH reached its lowest value immediately after exercise, then began to increase, and returned to normal by 60 minutes. The decrease in mixed venous pH was more pronounced than that in arterial blood since, in addition to the increase in lartic acid, there was a considerable increase in mixed venous carbon dioxide tension.     

Effects of atracurium on intraocular pressure, eye position, and blood pressure in eucapnic and hypocapnic isoflurane-anesthetized dogs

OBJECTIVE: To determine effects of atracurium on intraocular pressure (IOP), eye position, and arterial blood pressure in eucapnic and hypocapnic dogs anesthetized with isoflurane. ANIMALS: 16 dogs. PROCEDURE: Ventilation during anesthesia was controlled to maintain Paco2 at 38 to 44 mm Hg in group- I dogs (n = 8) and 26 to 32 mm Hg in group-II dogs (8). Baseline measurements for IOP, systolic, diastolic, and mean arterial blood pressure, central venous pressure (CVP), and heart rate (HR) were recorded. Responses to peroneal nerve stimulation were monitored by use of a force-displacement transducer. Atracurium (0.2 mg/kg) was administered i.v. and measurements were repeated at 1, 2, 3, and 5 minutes and at 5-minute intervals thereafter for 60 minutes. RESULTS: Atracurium did not affect IOP, HR, or CVP Group II had higher CVP than group I, but IOP was not different. There was no immediate effect of atracurium on arterial blood pressure. Arterial blood pressure increased gradually over time in both groups. Thirty seconds after administration of atracurium, the eye rotated from a ventromedial position to a central position and remained centrally positioned until 100% recovery of a train-of-four twitch response. The time to 100% recovery was 53.1 +/- 5.3 minutes for group I and 46.3 +/- 9.2 minutes for group II. CONCLUSIONS AND CLINICAL RELEVANCE: Atracurium did not affect IOP or arterial blood pressure in isoflurane-anesthetized dogs. Hyperventilation did not affect IOP or the duration of effect of atracurium.     

Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs.

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.     

Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse.

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.     

Cardiopulmonary effects of intramuscular xylazine-ketamine in calves.

The cardiopulmonary effects of an intramuscular xylazine (0.088 mg/kg)-ketamine (4.4 mg/kg) drug combination were evaluated in calves. Heart rate, central venous and mean pulmonary artery blood pressures, and cardiac output did not change after drug administration. Mean arterial blood pressure decreased significantly (P less than 0.05) 15 minutes after drug administration. Respiratory frequency increased significantly (P less than 0.05) whereas arterial partial pressure of oxygen (PaO2) decreased significantly (P less than 0.05) after drug administration. The duration of lateral recumbency was 55.7 +/- 10.4 minutes. Immediate or long-term adverse effects were not observed.     

Cardiopulmonary effects of a halothane/oxygen combination in healthy cats.

The effects of a halothane/oxygen combination on the cardiopulmonary function of 11 healthy cats were studied. Test parameters included cardiac output, measured via thermo-dilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and blood gas analysis. Values for systemic vascular resistance, cardiac index and stroke volume were calculated from these data. Cardiac output, cardiac index, heart rate, stroke volume, arterial blood pressure (systolic, diastolic and mean) and arterial blood pH were significantly decreased (p less than 0.001). Respiratory rate was also significantly decreased (p less than 0.007) with arterial CO2 tension being significantly increased (p less than 0.001). Statistically significant changes, where seen, persisted for the duration of the anesthetic period. Arterial O2 tension and systemic vascular resistance remained unchanged. All parameters returned to near pretest values within 30 minutes following cessation of halothane anesthesia.