Cardiopulmonary function in dogs with serious chronic heartworm disease.

Cardiopulmonary function was examined in 18 dogs with serious chronic heartworm disease showing ascites, subcutaneous edema, prostration, weakness, jaundice and so on. After surgical heartworm removal from the pulmonary arteries, 10 dogs recovered (surviving group), and 8 dogs died or were euthanatized because of poor prognosis (nonsurviving group). The number of live heartworms residing in the pulmonary arteries of the surviving group tended to be larger than that in the nonsurviving group. At necropsy, severe pulmonary arterial lesions such as thromboembolism including dead heartworms, proliferative and villous lesions and intimal hyperplasia were noticed in all dogs examined, and tended to be severer in the nonsurviving group. Heartworm-coiling around the tricuspid valve chord was found in 1 dog of the surviving group and 4 dogs of the nonsurviving group. Before heartworm removal, there was no significant difference in the mean pulmonary arterial pressure (MPAP) between the surviving and nonsurviving group. Right atrial pressure (v-wave) was higher, and the cardiac index (CI) was lower in the nonsurviving group. Arterial oxygen tension was lower in the surviving group than in the heartworm-free group, and it was lower in the nonsurviving group than in the surviving group. Carbon dioxide tension was lower in the surviving group than in the heartworm-free group. Bicarbonate concentration (HCO3-) was lower both in the surviving and nonsurviving groups than in the heartworm-free group. One week after heartworm removal, MPAP decreased (P less than 0.05), and CI and HCO3- tended to increase in the surviving group.     

Investigation of Caval Syndrome in Dogs Experimentally Infected With Dirofilaria immitis

Nine of 16 dogs inoculated with 200 infective heartworm larvae developed caval syndrome (CS) of heartworm disease (HWD). There was no difference between dogs that did and did not develop CS with regard to total heartworm burden, burden relative to body weight, or female heartworm burden, indicating that factors other than worm mass are involved in the pathogenesis of CS. Male dogs were twice as frequently affected as females, although this finding was not statistically significant. Dogs afflicted with CS exhibited radiographic, pathologic, and hemodynamic evidence of chronic HWD. In a model of single heartworm exposure, these findings strongly support the theory that CS develops due to retrograde migration of adult worms from the pulmonary arteries and right ventricle to the right atrium and venae cavae. Pulmonary artery pressures were dramatically and significantly greater in dogs with CS (60 +/- 18 torr) as compared to non-CS (30 +/- 4 torr) dogs with equal worm burdens.     

Serum creatine kinase activities in dogs with dirofilariasis.

Total serum creatine kinase (CK) and its isozyme activities were determined in dogs with dirofilariasis. Before heartworm removal, total CK and isozyme activities in dogs of the mild group were not different from those in dogs of the heartworm-free group. BB activity was higher in dogs of the hemoptysis group. Dogs of the ascites group displayed a mild increase in MM activity. In dogs of the caval syndrome (CS) group, total CK and MM activities were highest among the heartworm-free and heartworm-infected dogs, and MM isozyme accounted for most (75%) of total CK activity. MB and BB activities were also higher. However, there were no significant differences in CK activities between the surviving and non-surviving cases. In dogs with pulmonary heartworm disease (mild and ascites groups), MM activity correlated significantly with the number of heartworms (r = 0.45), hematocrit value (Ht, r = -0.40), serum alanine aminotransferase (ALT, r = 0.42) and lactate dehydrogenase (LDH, r = 0.46) activities, mean pulmonary arterial pressure (r = 0.64) and total pulmonary resistance (r = 0.50). In dogs with CS, MM activity did not correlate with any parameter, but BB activity correlated with the number of heartworms at the right atrium (r = 0.61), Ht (r = -0.53), ALT (r = 0.80), LDH (r = 0.73) and serum urea nitrogen (r = 0.47). At 1 week after heartworm removal, BB and MM activity decreased in dogs of the hemoptysis and ascites groups, respectively. In dogs of the CS group, total CK and MM isozyme activities decreased markedly (P less than 0.01) regardless of their prognosis.     

Regional hypoxic pulmonary vasoconstriction in dogs with asymptomatic dirofilariasis

The pulmonary hemodynamic response to unilateral alveolar hypoxia was investigated in pentobarbital-anesthetized dogs with mild heartworm (HW) disease and in dogs free of HW (HWF). Left lung nitrogen ventilation in HWF dogs resulted in a decrease in the fraction of the cardiac output (QT) perfusing the left lung (QL) from 0.37 +/- 0.03 (SEM) to 0.20 +/- 0.02 (P less than 0.01). In contrast, dogs with mild HW disease did not develop a significant decrease in QL/QT which decreased from 0.38 +/- 0.02 to 0.33 +/- 0.02. This attenuated pulmonary vascular response to regional alveolar hypoxia in dogs with HW disease was associated with a normal pulmonary arterial pressure (14.8 +/- 1.5 mm of Hg) that was not different from that seen in HWF dogs (15.8 +/- 1.7 mm of Hg). These results indicate that mild HW disease interferes with the ability of hypoxic pulmonary vasoconstriction to redistribute pulmonary blood flow away from hypoxic regions of the lung.     

Cardiopulmonary values in dogs with artificial model of caval syndrome in heartworm disease.

Cardiopulmonary values were determined in dogs with an artificial model of heartworm caval syndrome, which was produced by insertion of heartworm-like silicone tubes into the tricuspid valve orifice and right atrium. Fifteen to 25 tubes with some knots were inserted in 6 dogs (knot group), and 7 to 11 tubes (small-number group) or 29 to 37 tubes (large-number group) without a knot in 3 dogs, respectively. After tube insertion, angiographic contrast medium infused into the right ventricle regurgitated to the right atrium in all cases, and the regurgitation was the most severe in the large-number group. On electrocardiographic findings, the atrial and/or ventricular premature beat developed. The height of a- and v-wave of right atrial pressure curves elevated in all groups. The elevation in v-wave was obvious in the large-number group. The pulmonary arterial pressure tended to fall or to elevate slightly, and total pulmonary resistance increased in all groups. The right cardiac output decreased significantly in all cases. The right heart hemodynamics of the model might resemble those in spontaneous cases without disturbed pulmonary circulation.     

Effect of changes in ionized calcium concentration in arterial blood and metabolic acidosis on the arterial partial pressure of oxygen in dogs

OBJECTIVE: To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca2+) concentration on PaO2 in dogs. ANIMALS: 33 anesthetized dogs receiving assisted ventilation. PROCEDURE: Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO2, Ca2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. RESULTS: In group II, PaO2 increased from baseline value (96 +/- 2 mm Hg) within 10 minutes (pHa, 7.33 +/- 0.001); at 60 minutes (pHa, 7.21 +/- 0.02), PaO2 was 108 +/- 2 mm Hg. For the same pHa decrease, the PaO2 increase was less in group III. In group I, hypocalcemia caused PaO2 to progressively increase (from 95 +/- 2 mm Hg to 104 +/- 3 mm Hg), which correlated (r = -0.66) significantly with a decrease in systolic blood pressure (from 156 +/- 9 mm Hg to 118 +/- 10 mm Hg). Parathyroidectomy did not alter PaO2 values. CONCLUSIONS AND CLINICAL RELEVANCE: Induction of hypocalcemia and metabolic acidosis each increased PaO2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.     

Balloon Dilation of Congenital Subaortic Stenosis in the Dog

Balloon dilation during cardiac catheterization was evaluated for the treatment of congenital subaortic stenosis (SAS) in nine dogs. Under general anesthesia, bilateral cardiac catheterization was performed through the right jugular vein and carotid artery. Thermodilution cardiac output, and left ventricular and aortic root pressures and angiograms were obtained before and after balloon dilation. Balloons measuring 18–20 mm in diameter and 30–40 mm in length were positioned across the stenosis and three inflations 4–5 minutes apart were performed. There was no significant change in cardiac output, aortic pressure, or degree of aortic regurgitation after balloon dilation. For the entire group balloon dilation resulted in significant decreases in left ventricular systolic pressure (-61.2 ± 37.2 mm Hg [mean change ± SD], range -14 to -123), mean systolic pressure gradient (-39.6 ± 24.4 mm Hg, range –8.4 to -72.2), and peak systolic pressure gradient (-64.3 ± 46.5 mm Hg, range –17 to –143). Calculated left ventricular outflow cross-sectional area increased significantly (+.4 ± .5 cm², range –.06 to + 1.30). Clinical signs improved in the five symptomatic dogs. Individual hemodynamic responses varied widely, but the magnitude of improvement correlated with the severity of obstruction. Three dogs showed a decrease of 60% or greater (≥100 mm Hg), and six dogs showed a decrease of 25–50% (17–71 mm Hg) in peak systolic gradient after balloon dilation. Complications were frequent but most were transient and manageable. These preliminary results suggest that balloon dilation can acutely decrease outflow resistance in dogs with SAS and may be effective therapy for some affected dogs.     

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)     

Effects of atropine, acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog

Gastroesophageal sphincter (GES) pressure was 47.9 +/- 1.2 mm of Hg in nontreated dogs. Treatment with atropine, acepromazine, and xylazine reduced GES pressure to 13.2 +/- 2.03, 18.6 +/- 2.14, and 11.7 +/- 1.19 mm of Hg, respectively. Treatment with meperidine resulted in phasic contractions with minimum and maximum pressures of 27.9 +/- 4.55 and 98.9 +/- 9.16 mm of Hg, respectively. Drugs used in anesthetic procedures can reduce GES pressure in dogs.     

Hemodynamic alterations in dogs with shock induced by intravenous injection of heartworm extract

To elucidate one way of the shock mechanisms, the hemodynamic alterations were examined in 7 dogs with heartworm (HW) extract-induced shock. The first alteration observed after injection of HW extract was a decrease in right ventricular end-diastolic pressure (RVEDP). After that, left ventricular (LV) end-diastolic pressure, LV systolic pressure, and LV dp/dt fell significantly, followed by a decrease in the cardiac output of all dogs to below the detectable level (1.00 l/min). Since RVEDP depends on blood flow into the right ventricle, the decrease in RVEDP means a reduction in venous return. Therefore, this study showed that the first trigger of a decrease in blood pressure in HW extract-induced shock is the reduction in venous return.     

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.     

Postadulticide pulmonary hypertension of canine heartworm disease: successful treatment with oxygen and failure of antihistamines

Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/- 3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic estimation of mean left atrial pressure in a canine model of acute mitral valve insufficiency

High mean left atrial pressure (MLAP) due to canine degenerative mitral valve disease is associated with clinically relevant morbidity and mortality. The ability to noninvasively measure MLAP would assist in the diagnosis and treatment of disease. Doppler echocardiography allows measurement of early transmitral blood flow (E) and the velocity of the mitral valve annulus (Ea). The ratio of early mitral inflow velocity to early mitral annular velocity (E: Ea) correlates well with MLAP in human subjects. We sought to determine the ability of E: Ea to predict MLAP in dogs with experimentally induced mitral regurgitation. Nine anesthetized purpose-bred dogs underwent placement of a Swan-Ganz catheter into the left atrium and recording of MLAP. Simultaneous transthoracic echocardiographic and hemodynamic studies were performed after acute chordae tendineae rupture and during IV infusion with nitroprusside (2.5-5.0 microg x kg(-1) x min(-1)) or hydralazine (1-1.5 mg/kg). Mitral regurgitant fraction, measured by single-plane angiography and thermodilution, ranged from 17% to 81%. MLAP increased from 5.4 +/- 2.5 mm Hg to 17.4 +/- 9.4 mm Hg after creation of mitral valve regurgitation (MR; P = .018). Forty sets of echocardiographic measurements were obtained from 7 dogs, and E, as well as E: Ea, were linearly related to MLAP. The R2 value for the linear regression equation containing E: Ea as the dependent variable (0.83) was greater than that for E (0.73). The 95% confidence intervals were calculated for predicting MLAP = 20 mm Hg from E:Ea, and E:Ea >9.1 or <6.0 indicated a 95% probability that MLAP was >20 mm Hg or <20 mm Hg, respectively. Echocardiography can be used to predict MLAP in isoflurane-anesthetized dogs with experimentally induced acute mitral valve insufficiency.     

Pathophysiologic mechanism of cardiac dysfunction in experimentally induced heartworm caval syndrome in dogs: an echocardiographic study

In dogs with experimentally induced heartworm infection, the onset of caval syndrome (CS) was characterized by a murmur, loudest over the tricuspid valve, and a large worm mass in the right ventricular lumen detectable during diastole by use of M-mode echocardiography. Two-dimensional echocardiography indicated that the worm mass was located in the right atrium and venae cavae and was "flowing" into the right ventricle during rapid diastolic filling. Paradoxical septal motion and vigorous right ventricular cranial wall motion also were observed. Other echocardiographic changes included decreased size of the left atrium and ventricle, aortic root, and ratio of left-to-right ventricular diastolic luminal diameter, compared with values obtained 6 months after experimentally induced heartworm infection. Right ventricular end diastolic diameter increased considerably. Most echocardiographic indices of left ventricular function (fractional shortening, velocity of circumferential fiber shortening, ejection fraction, and preejection period) were not altered appreciably, but estimates of cardiac index and stroke volume were markedly decreased. Electrocardiography revealed ventricular and supraventricular premature complexes in 7 of the 8 dogs studied, evidence of right ventricular enlargement in 6 of the 8 dogs studied, and increased mean heart rate, compared with that measured 6 months after inoculation of infective larvae, before the onset of CS. Cardiac catheterization was performed in 3 days at the onset of CS. Severe pulmonary arterial and right ventricular hypertension and decreased cardiac index (compared with values obtained before inoculation) were observed. Evidence of right ventricular inflow obstruction was not detected. Mean aortic blood pressure decreased with the onset of CS, but right ventricular end diastolic pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic estimation of systemic systolic blood pressure in dogs with mild mitral regurgitation

BACKGROUND: Systemic hypertension is likely underdiagnosed in veterinary medicine because systemic blood pressure is rarely measured. Systemic blood pressure can theoretically be estimated by echocardiography. According to the modified Bernoulli equation (PG = 4v(2)), mitral regurgitation (MR) velocity should approximate systolic left ventricular pressure (sLVP), and therefore systolic systemic blood pressure (sSBP) in the presence of a normal left atrial pressure (LAP) and the absence of aortic stenosis. The aim of this study was to evaluate the use of echocardiography to estimate sSBP by means of the Bernoulli equation. HYPOTHESIS: Systemic blood pressure can be estimated by echocardiography. ANIMAL: Seventeen dogs with mild MR. No dogs had aortic or subaortic stenosis, and all had MR with a clear continuous-wave Doppler signal and a left atrial to aorta ratio of < or = 1.6. METHODS: Five simultaneous, blinded continuous-wave measurements of maximum MR velocity (Vmax) and indirect sSBP measurements (by Park's Doppler) were obtained for each dog. Pressure gradient was calculated from Vmax by means of the Bernoulli equation, averaged, and added to an assumed LAP of 8 mm Hg to calculate sLVP. RESULTS: Calculated sLVP was significantly correlated with indirectly measured sSBP within a range of 121 to 218 mm Hg (P = .0002, r = .78). Mean +/- SD bias was 0.1 +/- 15.3 mm Hg with limits of agreement of -29.9 to 30.1 mm Hg. CONCLUSION: Despite the significant correlation, the wide limits of agreement between the methods hinder the clinical utility of echocardiographic estimation of blood pressure.     

Eructation of gas through the gastroesophageal sphincter before and after truncal vagotomy in dogs

The function of the gastroesophageal sphincter (GES) to eructate gas before and after vagotomy was investigated in conscious, fed dogs. Gastric and GES pressures were measured in 5 dogs, using a perfused 4-lumen catheter with a Dent sleeve. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through 1 channel of the catheter. After base-line studies were completed on each dog, bilateral truncal vagotomy was performed 5 cm cranial to the diaphragm. Mean (+/- SE) GES pressure was 51.5 +/- 1 mm of Hg before vagotomy and 28 +/- 1.7 mm of Hg after vagotomy (P less than 0.001). Mean gastric contraction rates were the same, 4.91 +/- 0.11/min and 4.78 +/- 0.06/min in dogs before and after vagotomy, respectively. During insufflation, gastric pressures increased to 11.8 +/- 0.7 mm of Hg before eructation in dogs before vagotomy and to 18.4 +/- 0.8 mm of Hg in dogs after vagotomy (P less than 0.001). Eructation occurred at intervals of 1.79 +/- 0.09 minutes before vagotomy and 5.71 +/- 0.41 minutes after vagotomy (P less than 0.001). Atropine resulted in an interval of 1.98 +/- 0.18 minutes before vagotomy. Eructation was not seen in 2 dogs after vagotomy and was sometimes not seen in the 3 others. Gastroesophageal sphincter pressure in dogs before vagotomy began to decrease 4.5 +/- 0.2 s before the GES-pressure gradient disappeared, and GES pressure remained there for 5.3 +/- 0.3 s before the gradient began to return.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of a rebound tonometer for measuring intraocular pressure in dogs and horses

OBJECTIVE: To compare intraocular pressure (IOP) measurements obtained with a rebound tonometer in dogs and horses with values obtained by means of applanation tonometry and direct manometry. DESIGN: Prospective study. ANIMALS: 100 dogs and 35 horses with clinically normal eyes, 10 enucleated eyes from 5 dogs, and 6 enucleated eyes from 3 horses. PROCEDURES: In the enucleated eyes, IOP measured by means of direct manometry was sequentially increased from 5 to 80 mm Hg, and IOP was measured with the rebound tonometer. In the dogs and horses, results of rebound tonometry were compared with results of applanation tonometry. RESULTS: For the enucleated dog and horse eyes, there was a strong (r2 = 0.99) linear relationship between pressures obtained by means of direct manometry and those obtained by means of rebound tonometry. Mean +/- SD IOPs obtained with the rebound tonometer were 10.8 +/- 3.1 mm Hg (range, 5 to 17 mm Hg) and 22.1 +/- 5.9 mm Hg (range, 10 to 34 mm Hg) for the dogs and horses, respectively. Mean IOPs obtained with the applanation tonometer were 12.9 +/- 2.7 mm Hg (range, 8 to 18 mm Hg) and 21.0 +/- 5.9 mm Hg (range, 9 to 33 mm Hg), respectively. Values obtained with the rebound tonometer were, on average, 2 mm Hg lower in the dogs and 1 mm Hg higher in the horses, compared with values obtained with the applanation tonometer. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that the rebound tonometer provides accurate estimates of IOP in clinically normal eyes in dogs and horses.     

Effects of mechanical and pharmacologic manipulations on portal pressure, central venous pressure, and heart rate in dogs

Central venous pressure (CVP), portal pressure (PP), and heart rate (HR) were monitored in 6 female, sexually intact, middle-age Beagles during temporary portal vein obstruction, anesthetic recovery, abdominal bandaging, and propranolol administration. Intraoperative baseline PP was 7.3 mm of Hg (+/- 1.7 SD). Portal pressure was significantly increased throughout portal vein occlusion, but returned to baseline values 2 minutes after release of the ligature. Central venous pressure was significantly decreased throughout portal vein occlusion, but did not differ significantly from baseline values 3 minutes after release of the portal vein ligature. Portal pressure increased significantly (8 +/- 3.3 mm of Hg) over baseline values after application of an abdominal bandage; however, CVP did not change significantly. During postoperative monitoring, CVP and PP did not change significantly from respective 18-hour mean postoperative values in resting dogs. At 60 and 75 minutes after surgery, heart rate was significantly increased over the 18-hour mean. Portal pressure and CVP, respectively, were significantly increased over intraoperative baseline values in the first hour and the first 8 hours after surgery. Postoperative CVP and HR were significantly correlated. Individual measurements of PP in dogs that were abdominal pressing during barking or defecation were significantly increased (9 +/- 3 mm of Hg) above measurements taken after cessation of abdominal press. Portal pressure measurements in standing dogs decreased 7.5 +/- 2 mm of Hg, compared with measurements of the same dog in lateral recumbency. Central venous pressure was inaccurate in dogs performing abdominal press. Portal pressure did not decrease significantly from baseline after injection of propranolol (2 mg/kg, IV).(ABSTRACT TRUNCATED AT 250 WORDS)     

Eructation of gas through the gastroesophageal sphincter before and after gastric fundectomy in dogs

The gas eructation function of the gastroesophageal sphincter (GES) was investigated in 6 conscious, fed dogs before and after gastric fundectomy. Using a perfused 4-lumen catheter with a Dent sleeve, gastric and GES pressures were measured. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through one channel of the catheter. After base-line studies were completed on each dog, fundectomy, to remove 30% of the stomach, was performed. Mean (+/- SEM) GES pressure was 45.3 +/- 3.3 mm of Hg before fundectomy and 41.4 +/- 1.9 mm of Hg after fundectomy (P greater than 0.05). Before fundectomy, treatment with metoclopramide or cisapride increased GES pressure to 62.2 +/- 4.1 mm of Hg (P less than 0.001) and 61.1 +/- 5.0 mm of Hg (P less than 0.05), respectively. Gastric contraction rates were the same, 4.92 +/- 0.24/min and 4.80 +/- 0.16/min before and after fundectomy, respectively. During insufflation, gastric pressures before eructation increased to 12.2 +/- 1.3 mm of Hg before fundectomy and to 13.6 +/- 0.9 mm of Hg after fundectomy (P greater than 0.05). Eructation occurred at intervals of 1.44 +/- 0.20 minutes before fundectomy and 1.56 +/- 0.13 minutes after fundectomy (P greater than 0.05). Before fundectomy, administration of metoclopramide or cisapride resulted in eructation intervals of 1.72 +/- 0.21 minutes and 1.39 +/- 0.02 minutes, respectively; these intervals were not significantly different from those measured in dogs not given drugs. After fundectomy, the GES pressure in 5 dogs decreased and remained low during insufflation. After a series of normal eructation intervals, multiple eructations were observed in 4 of these dogs. Fundectomy did not impair ability to eructate gas from the stomach.     

Evaluation of peripheral and central venous pressure in awake dogs and cats

OBJECTIVE: To determine whether peripheral venous pressure (PVP) was correlated with central venous pressure (CVP) when measured by use of different catheter sizes, catheterization sites, and body positions in awake dogs and cats. ANIMALS: 36 dogs and 10 cats. PROCEDURES: Dogs and cats with functional jugular and peripheral venous catheters were enrolled in the study. Peripheral venous catheters (18 to 24 gauge) were placed in a cephalic, lateral saphenous, or medial saphenous vein. Central venous catheters (5.5 to 8.5 F) were placed in the jugular vein and advanced into the cranial vena cava. Catheters were connected to pressure transducers and a blood pressure monitor capable of displaying 2 simultaneous pressure tracings. For each animal, the mean of 5 paired measurements of PVP and CVP was calculated. The relationship between PVP and CVP when measured by use of different catheter sizes, catheterization sites, and body positions was determined. RESULTS: Mean +/- SD PVP was 5.7 +/- 5.8 mm Hg higher than CVP in dogs and 6.0 +/- 6.9 mm Hg higher than CVP in cats. However, results of multiple regression analysis did not indicate a significant correlation between PVP and CVP, regardless of catheter size, catheter position, or body position. The relationship was weak in both dogs and cats. CONCLUSIONS AND CLINICAL RELEVANCE: The PVP was poorly correlated with CVP when different catheter sizes, catheterization sites, and patient positions were evaluated. Peripheral venous pressure should not be used to approximate CVP in awake dogs and cats.