Pressor Therapy in Critically III Patients

Vasopressors are agents that increase systemic vascular resistance by increasing vasoconstriction. Therapy with intravenous vasopressors may be required in critically ill patients when efforts to optimize cardiac output and blood pressure with intravascular fluid therapy fail. Increasing systemic vascular resistance can promote a favorable perfusion pressure gradient to vital organs in critically ill patients with severe, unresponsive vasodilation. Improperly administered, vasopressors may impede cardiac output and reduce oxygen transport to vital tissue sites. The understanding of systemic and regional effects of vasopressors is currently evolving. Recent literature of the commonly used agents is reviewed. Individual drugs, drug combinations, and potential new therapies are discussed. (Vet. Emerg. & Crit. Care, 10:19–33, 2000)     

Skeletal muscle blood flow in anaesthetized horses. Part II: effects of anaesthetics and vasoactive agents

OBJECTIVE: This review aims at evaluating studies investigating the effects of anaesthesia on skeletal muscle blood flow and associated cardiovascular function in anaesthetized horses and discusses how the results of these studies contribute to our understanding of the pathogenesis and prevention of post-anaesthetic myopathy. DATABASE USED: Pubmed & personal files. CONCLUSION: There is little published information on the effects of anaesthesia on skeletal muscle blood flow in horses. Available reports predominantly refer to halothane and isoflurane. The effects of vasoactive drugs have mainly been studied in halothane-anaesthetized horses. The results of these studies support the importance of cardiac output in the maintenance of adequate arterial blood pressure, perfusion pressure and muscle blood flow. Adequate perfusion pressure appears to be important for overcoming the detrimental effects of high intra-compartmental pressure in dependent muscles and hydrostatic pressure in nondependent muscles.     

Pathogenesis of sodium selenite and dimethylselenide acute toxicosis in pigs: Cardiovascular changes

In pigs and other food producing animals, relatively little is known about the mode of action of excess selenium. This study reports the cardiovascular effects brought about in anaesthetised Landrace pigs by 2 mg selenium kg-1 bodyweight intravenously as either sodium selenite or dimethylselenide. Sodium selenite dosing was characterised by a dramatic fall in systemic blood pressure with an increase in cardiac output and heart frequency. The only significant change elicited by dimethylselenide was a linear rise of cardiac output. Neither of the tested compounds significantly affected pulmonary arterial pressure. These results suggest that under the experimental conditions in this study, sodium selenite induces a vasculogenic shock without primarily affecting cardiac performance. The lack of detrimental effects on cardiovascular parameters with dimethylselenide indicates the importance of methylation in detoxifying excess selenium.     

Cardiopulmonary resuscitation: current recommendations

Early recognition of CPA is the key to its successful management. For resuscitation to be managed successfully, effective forward blood flow must be established at the onset of the arrest. In our clinical experience, we have found that the Doppler unit allows us to assess the effectiveness of cerebral perfusion better than any other method of blood pressure evaluation. If, by Doppler monitoring results, cerebral perfusion is found to be poor, blood flow may be mechanically improved by instituting high dose epinephrine therapy and interposed abdominal counter-pressure techniques. There is an understandable reluctance on the part of many veterinarians to enter the chest in the course of CPR. Unfortunately, this delay in performing internal compressions is often the reason that open-chest CPR is deemed ineffective by so many practitioners. If external chest CPR is not effective within 1 to 2 min (maximum) of its initiation, an emergency thoracotomy and direct cardiac massage should be performed. We know that perfusion pressure increases three to five times with open versus closed-chest CPR. This improvement in perfusion with direct cardiac massage is due, in part, to the absence of venous pressure elevations created during external chest compression. It follows that better coronary and cerebral blood flow will result in better resuscitation when direct cardiac massage is performed early. The "bottom line" in CPR is successful resuscitation of the patient with resultant good neurologic function. It is hoped that through the use of these techniques and new cytoprotective drugs, the survival rate will rise.     

Vasopressin therapy in dogs with dopamine-resistant hypotension and vasodilatory shock

Objective: To describe the therapeutic use of vasopressin in dogs with dopamine‐resistant hypotension and vasodilatory shock. Series summary: We report the effects of intravenous vasopressin therapy on mean arterial blood pressure and central venous pressure (CVP) in 5 dogs with dopamine‐resistant hypotension from vasodilatory shock. All subjects had documented hypotension and vasodilation, despite adequate intravascular volume and catecholamine therapy. There was an increase in mean arterial pressure following vasopressin administration. No cardiac arrhythmias were noted, nor were there clinically significant changes in CVP. New information provided: Mean arterial blood pressure increased following vasopressin therapy in all of the dogs. Vasopressin may prove useful in the treatment of vasodilatory shock, however further research is warranted.     

Effects of norepinephrine and a combined norepinephrine and dobutamine infusion on systemic hemodynamics and indices of renal function in normotensive neonatal thoroughbred foals

BACKGROUND: Norepinephrine is a potent vasopressor that increases arterial blood pressure but may have adverse effects on renal blood flow. The combination of norepinephrine and dobutamine may lead to improved renal perfusion compared to an infusion of norepinephrine alone. The effects of these drugs in the normotensive neonatal foal have not been reported. HYPOTHESIS: Norepinephrine increases arterial blood pressure. Adding dobutamine to a norepinephrine infusion will change the renal profile during the infusions without changing the arterial blood pressure. ANIMALS: Eight conscious Thoroughbred foals were used in this study. METHODS: Each foal received norepinephrine (0.1 microg/kg/min), combined norepinephrine (0.1 microg/kg/min) and dobutamine (5 microg/kg/min), and a control dose of saline in a masked, placebo-controlled study. Heart rate, arterial blood pressure (direct), and cardiac output (lithium dilution) were measured, and systemic vascular resistance, stroke volume, cardiac index, and stroke volume index were calculated. Urine output, creatinine clearance, and fractional excretion of sodium, potassium, and chloride were measured. RESULTS: Norepinephrine and a combined norepinephrine and dobutamine infusion increased arterial blood pressure and systemic vascular resistance and decreased heart rate and cardiac index as compared to saline. The combination resulted in higher arterial pressure than norepinephrine alone. There was no significant difference in urine output, creatinine clearance, or fractional excretion of electrolytes with either infusion as compared to saline. CONCLUSIONS AND CLINICAL IMPORTANCE: These data suggest that norepinephrine and a combined norepinephrine and dobutamine infusion cause unique hemodynamic effects without affecting indices of renal function, and this effect warrants further investigation.     

Haemodynamic changes during sedation in ponies

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (greater than 90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal. alpha 2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 micrograms/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation. Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the alpha 2-agonistic sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance. The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.     

Effects of norepinephrine and combined norepinephrine and fenoldopam infusion on systemic hemodynamics and indices of renal function in normotensive neonatal foals

Background: Norepinephrine increases arterial blood pressure but may have adverse effects on renal blood flow. Fenoldopam, a dopamine-1 receptor agonist, increases urine output in normotensive foals. The combination of norepinephrine and fenoldopam may lead to improved renal perfusion compared with an infusion of norepinephrine alone. The combined effects of these drugs have not been reported in the horse.
Hypothesis: Norepinephrine will alter the hemodynamic profile of foals without affecting renal function. Addition of fenoldopam will change the renal profile during the infusions without changing the hemodynamic profile.
Animals: Five conscious pony foals.
Methods: Each foal received norepinephrine (0.3 μg/kg/min), combined norepinephrine (0.3 μg/kg/min) and fenoldopam (0.04 μg/kg/min), and a control dose of saline in a masked, placebo-controlled study. Heart rate (HR), arterial blood pressure (direct), and cardiac output (lithium dilution) were measured, and systemic vascular resistance (SVR), stroke volume, cardiac index (CI), and stroke volume index were calculated. Urine output, creatinine clearance, and fractional excretion of electrolytes were measured.
Results: Norepinephrine and a combined norepinephrine and fenoldopam infusion increased arterial blood pressure, SVR, urine output, and creatinine clearance and decreased HR and CI compared with saline. The combination resulted in higher HR and lower arterial blood pressure than norepinephrine alone.
Conclusions and Clinical Importance: Norepinephrine might be useful for hypotensive foals, because in normal foals, this infusion rate increases SVR without negatively affecting renal function (creatinine clearance increased). Fenoldopam does not provide additional benefit to renal function. These findings warrant further investigation.     

Effect of the proteinase inhibitor aprotinin in the management of hemorrhagic shock in the dog.

Aprotinin, a proteinase inhibitor, was evaluated as a pharmacologic aid in dogs subjected to lethal hemorrhagic shock. Survival time, hemodynamic changes, and plasma enzyme analysis were measured as criteria for drug effects. Mixed-breed dogs (n = 14) were divided into 2 groups of 7 each: nontreated dogs in shock (group 1) and aprotinin-treated dogs in shock (group 2). One of 7 dogs in group 1 and 2 of 7 dogs in group 2 survived. Survival time, for the remaining dogs in group 1 (190 min, n = 6) and group 2 (188 min, n = 5) were not significantly different. There was no significant difference in mean arterial pressure, mean pulmonary arterial pressure, cardiac output, or left ventricle systolic pressure associated with aprotinin treatment at any time after hemorrhagic shock. There was no significant difference in plasma lactic acid, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, alpha-amylase, and beta-glucuronidase associated with treatment at any time; however, there were significant (P less than 0.05) increases with time. The gastrointestinal tract was the site of most obvious lesions found at necropsy. Lesions varied considerably in extent and severity without apparent correlation to the treatment regimen. These experiments did not show beneficial effects of aprotinin in dogs subjected to hemorrhagic shock, but neither did they completely rule out some valuable actions that may have been obscured by the type of model used.     

The efficacy of dexamethasone and flunixin meglumine in treating endotoxin-induced changes in calves

Eicosanoids have been implicated in the pathophysiology of endotoxic shock. Drugs which alter eicosanoid production such as corticosteroids and non-steroidal anti-inflammatory drugs (NSAID) are beneficial in treating endotoxic shock. Experiments were conducted to investigate the efficacy of dexamethasone, a corticosteroid, and/or flunixin meglumine, a NSAID, in treating endotoxin-induced changes in calves.Fourteen male calves were assigned to one of four treatment groups: group 1, endotoxin-untreated; group 2, endotoxin-flunixin meglumine treated; group 3, endotoxin-dexamethasone-treated; group 4, endotoxin-flunixin meglumine and dexamethasone-treated. Each calf was given three intravenous and intraperitoneal injections of E. coli endotoxin. Hemodynamic, blood gas, blood chemical and eicosanoid level determinations were obtained.Thirty minutes after endotoxin injection, pulmonary artery pressure (PAP) increased and cardiac output (CO) decreased compared with baseline, corresponding to increased thromboxaneB₂ levels in groups 1 and 3. These groups exhibited a decreased mean arterial pressure (MAP) at three and five hours corresponding to increased 6-keto-prostaglandinF_lalpha. The MAP, PAP and CO of group 4 remained near baseline for the entire six hours, except for a late drop in MAP. Lactic acid levels were significantly increased and arterial bicarbonate levels were reduced by six hours in all groups except for group 4. These results indicate that the combination treatment of flunixin meglumine and dexamethasone prevents many of the metabolic derangements observed during endotoxic shock in calves.     

The relationship of muscle perfusion and metabolism with cardiovascular variables before and after detomidine injection during propofol–ketamine anaesthesia in horses

Objectives To study in horses (1) the relationship between cardiovascular variables and muscle perfusion during propofol–ketamine anaesthesia, (2) the physiological effects of a single intravenous (IV) detomidine injection, (3) the metabolic response of muscle to anaesthesia, and (4) the effects of propofol–ketamine infusion on respiratory function. Study design Prospective experimental study. Animals Seven standardbred trotters, 5–12 years old, 416–581 kg. Methods Anaesthesia was induced with intravenous (IV) guaifenesin and propofol (2 mg kg^?1) and maintained with a continuous IV infusion of propofol (0.15 mg kg^?1 minute^?1) and ketamine (0.05 mg kg^?1 minute^?1) with horses positioned in left lateral recumbency. After 1 hour, detomidine (0.01 mg kg^?1) was administered IV and 40–50 minutes later anaesthesia was discontinued. Cardiovascular and respiratory variables (heart rate, cardiac output, systemic and pulmonary artery blood pressures, respiratory rate, tidal volume, and inspiratory and expiratory O₂ and CO₂) and muscle temperature were measured at pre‐determined times. Peripheral perfusion was measured continuously in the gluteal muscles and skin using laser Doppler flowmetry (LDF). Muscle biopsy samples from the left and right gluteal muscles were analysed for glycogen, creatine phosphate, creatine, adenine nucleotides, inosine monophosphate and lactate. Arterial blood was analysed for PO₂, PCO₂, pH, oxygen saturation and HCO₃. Mixed venous blood was analysed for PO₂, PCO₂, pH, oxygen saturation, HCO₃, cortisol, lactate, uric acid, hypoxanthine, xanthine, creatine kinase, creatinine, aspartate aminotransferase, electrolytes, total protein, haemoglobin, haematocrit and white blood cell count. Results Circulatory function was preserved during propofol–ketamine anaesthesia. Detomidine caused profound hypertension and bradycardia and decreased cardiac output and muscle perfusion. Ten minutes after detomidine injection muscle perfusion had recovered to pre‐injection levels, although heart rate and cardiac output had not. No difference in indices of muscle metabolism was found between dependent and independent muscles. Anaerobic muscle metabolism, indicated by decreased muscle and creatine phosphate levels was evident after anaesthesia. Conclusion Muscle perfusion was closely related to cardiac output but not arterial blood pressure. Total intravenous anaesthesia with propofol–ketamine deserves further study despite its respiratory depression effects, as the combination preserves cardiovascular function. Decreases in high‐energy phosphate stores during recovery show that muscle is vulnerable after anaesthesia. Continued research is required to clarify the course of muscle metabolic events during recovery.     

Cardiovascular and haemodynamic effects of intramuscular doses of xylazine in conscious sheep

OBJECTIVE: To determine if a commonly used analgesic dose of xylazine has detrimental cardiovascular or haemodynamic effects in sheep. DESIGN: A physiological study following intramuscular administration of xylazine. PROCEDURE: Xylazine (50 micrograms/kg) was injected intramuscularly into six healthy Merino ewes. For 60 min heart rate, mean arterial blood pressure and cardiac output were recorded; arterial blood samples for the measurement of blood gas tensions were also collected. RESULTS: There were no significant changes in heart rate, mean arterial blood pressure, cardiac output or arterial carbon dioxide tension. A slight degree of arterial hypoxaemia was noted with a 10% reduction in arterial oxygen tension values at 30 min. CONCLUSION: The minimal changes to cardiovascular and respiratory values in this study verify the safety of previously suggested analgesic dosing regimens for sheep. Previously reported hypoxaemic effects in sheep as a result of intravenous xylazine administration appear to be reduced as a result of intramuscular administration.     

Some effects of acupuncture at Jen Chung (Go-26) on cardiovascular dynamics in dogs.

The cardiovascular effects of two types of acupuncture, needling with twirling and moxibustion by electrocautery, at Jen Chung (Go-26) were studied in dogs with chronically implanted electromagnetic flowmeter probes, during 0.75% halothane anesthesia with a succinylcholine drip to allow controlled ventilation. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, acid-base and blood gases were measured over a two hour period. During and following moxibustion by electrocautery at Jen Chung (Go-26) there was a generally significant increase (5% level) in cardiac output and stroke volume and an initially significant increase in heart rate, mean arterial pressure and pulse pressure. There was a significant decrease in total peripheral resistance following moxibustion by electrocautery and an initially significant decrease in total peripheral resistance following moxibustion by electrocautery and an initially significant decrease in total peripheral resistance following needling with twirling. It was observed in this investigation that moxibustion by electrocautery at Jen Chung (Go-26) produced more significant changes in cardiovascular dynamics in dogs than needling with twirling.     

Pathophysiology of the gastric dilation-torsion complex in the dog*

The gastric dilation-torsion complex in the dog involves a series of related pathophysiological changes which may culminate in death if therapy is not promptly initiated. This complex probably starts with gastric dilation which may or may not lead to gastric torsion. Gastric dilation interferes with blood flow through the caudal vena cava as well as the portal vein. Venous return to the heart is decreased, cardiac output decreases, and arterial hypotension ensues. With the onset of this hypotension, the animal is subjected to impairment of tissue perfusion, cellular catabolism, and decreased renal function. In addition, endotoxic shock and disseminated intravascular coagulation may occur. These two processes will likely lead to death of the animal.     

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.     

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.

OBJECTIVE: To evaluate the cardiovascular effects of the alpha2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats. ANIMALS: 7 clinically normal cats. PROCEDURE: Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 microg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration. RESULTS: Heart rate, cardiac index, stroke index, rate-pressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered alone to clinically normal cats, medetomidine (20 microg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central alpha2-adrenergic effect over peripheral vascular effects.     

Cardiovascular and respiratory effects of inspired oxygen fraction in halothane-anesthetized horses

Anesthesia of equids is associated with pulmonary dysfunction. Cardiovascular and respiratory effects of inhalation anesthetic agents and duration of anesthesia have been studied, using oxygen as the carrier gas. To our knowledge, the effects of inspired oxygen have not been determined. We studied the cardiovascular and respiratory effects of 2 inspired oxygen fractions (0.30 and greater than 0.85) in 5 laterally recumbent, halothane-anesthetized horses. Mean systemic arterial blood pressure, cardiac output, central venous pressure, pulmonary arterial pressure, arterial pH, and arterial base excess were similar in horses of the 2 groups during 4 hours of anesthesia at constant end-tidal halothane concentration. End-tidal partial pressure of CO2, arterial partial pressure of CO2 and O2, and alveolar-to-arterial O2 tension difference were greater in horses exposed to the higher oxygen concentration. On the basis of the data obtained, we suggest that greater hypoventilation and ventilation/perfusion mismatch occur when horses are breathing high-oxygen fraction. Arterial partial pressure of O2 was not different between the 2 groups of horses after they were disconnected from the anesthesia circuit and allowed to breathe room air. Horses recovered from anesthesia without complications.     

Inotropic mechanisms of dopexamine hydrochloride in horses.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 micrograms/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta 1, and beta 2-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta 1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. beta 2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dtmax. These data indicate that baroreflex activity, beta 1- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.     

Hemodynamic effects of ionized calcium in horses anesthetized with halothane or isoflurane

OBJECTIVES: To evaluate the effects of halothane and isoflurane on cardiovascular function and serum total and ionized calcium concentrations in horses, and to determine whether administration of calcium gluconate would attenuate these effects. ANIMALS: 6 clinically normal adult Thoroughbreds. PROCEDURE: Catheters were inserted for measurement of arterial blood pressures, pulmonary arterial blood pressures, right ventricular pressure (for determination of myocardial contractility), right atrial pressure, and cardiac output and for collection of arterial blood samples. Anesthesia was then induced with xylazine hydrochloride and ketamine hydrochloride and maintained with halothane or isoflurane. An i.v. infusion of calcium gluconate was begun 75 minutes after anesthetic induction; dosage of calcium gluconate was 0.1 mg/kg of body weight/min for the first 15 minutes, 0.2 mg/kg/min for the next 15 minutes, and 0.4 mg/kg/min for an additional 15 minutes. Data were collected before, during, and after administration of calcium gluconate. RESULTS: Halothane and isoflurane decreased myocardial contractility, cardiac index, and mean arterial pressure, but halothane caused greater depression than isoflurane. Calcium gluconate attenuated the anesthetic-induced depression in cardiac index, stroke index, and maximal rate of increase in right ventricular pressure when horses were anesthetized with isoflurane. When horses were anesthetized with halothane, a higher dosage of calcium gluconate was required to attenuate the depression in stroke index and maximal rate of increase in right ventricular pressure; cardiac index was not changed with calcium administration. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of calcium gluconate may support myocardial function in horses anesthetized with isoflurane.     

Hypertonic saline/dextran resuscitation of dogs with experimentally induced gastric dilatation-volvulus shock.

We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (GDV) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to GDV for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, iv, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, IV, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h) of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this GDV-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.