Symptomatic partial anomalous pulmonary venous connection in a kitten

A 3-month-old intact female American Shorthair cat, with syncope and tachypnea, underwent cardiac examination which identified no heart murmur or gallop. Thoracic radiography disclosed mild generalized enlargement of the cardiac silhouette and a bronchial and interstitial pattern throughout the lungs. Echocardiography identified tubular structures near the left atrium. After agitated saline contrast imaging, persistent left cranial vena cava with unroofed coronary sinus was suspected. Computed tomography angiography showed the right cranial, right caudal and left caudal pulmonary veins draining into the coronary sinus and flowing into the right atrium. The left cranial pulmonary vein drained normally into the left atrium. Partial anomalous pulmonary venous connection (PAPVC) was diagnosed. The kitten was treated with diuretics but died of heart failure 2 months later. Permission for necropsy was not granted. This case represents symptomatic PAPVC in a kitten. Most pulmonary veins were connected abnormally with the coronary sinus. The prognosis was grave because of refractory heart failure.     

Partial anomalous pulmonary venous connection with portosystemic shunt in a cat

A nine-month-old castrated male domestic shorthair presented for evaluation with a three-month history of hematuria. Portosystemic shunts and calculi within the bladder were suspected, and computed tomography angiography was performed. Computed tomography angiography identified an extrahepatic portosystemic shunt and a partial anomalous pulmonary venous connection, with the lobar vein of the right caudal lobe draining into the caudal vena cava. After anesthesia was administered to the cat, tachypnea and wheezing respiratory sounds were observed, and thoracic radiography revealed the right middle lung lobe atelectasis and an unstructured interstitial pattern in the left cranial lobe. Echocardiography showed left and right atrial enlargement and slight interventricular septal flattening in diastole. Based on these findings, cardiogenic pulmonary edema was suspected, and the cat was treated with furosemide. The clinical symptoms were resolved the next day. Closure of the extrahepatic portosystemic shunt was performed on days 47 and 157. Left atrial enlargement and interventricular septal flattening were attenuated after the procedure. At the time of writing this report (seventeen months after diagnosis), the cat exhibited no clinical signs, but subjective right atrial enlargement remained at approximately the same level. This report represents the first case of a partial anomalous pulmonary venous connection and a portosystemic shunt in a cat.     

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.     

Partial anomalous pulmonary venous connection in a dog

A 2-year-old male intact Belgian Malinois was presented for exercise intolerance. A grade III/VI left basilar systolic murmur was detected. Echocardiography revealed moderate right atrial and ventricular dilation and increased pulmonic outflow velocity. Thoracic radiographs showed right heart enlargement and a dilated caudal vena cava. In addition, on the left lateral projection, an enlarged aberrant right cranial pulmonary lobar vein was suspected to be diverging ventrally from the course of the right cranial lobar bronchus and inserting more ventrally than normal in the region of the right atrium. A left-to-right pulmonary vascular shunt was suspected, and the patient underwent further diagnostics under general anesthesia. An agitated saline study was positive, suggestive of a concurrent right to left shunt. A right heart catheterization was performed. Angiography was inconclusive. Oximetry testing revealed an increase in oxygen saturation within the right atrium at the level of the caudal cava supportive of a left-to-right shunt in this region. Computed tomography angiography revealed a large single pulmonary vein that anomalously entered into the caudolateral aspect of the right atrium (left-to-right shunt) and was suspicious for a small arteriovenous malformation between the right caudal pulmonary artery and the right pulmonary vein returning to the left atrium (right to left shunt). The patient was diagnosed with a partial anomalous pulmonary venous connection and a possible arteriovenous malformation.     

Cardiopulmonary changes in conscious dogs with induced progressive pneumothorax

Cardiopulmonary function was measured in 6 conscious dogs with progressive degrees of induced pneumothorax. Minute volume, respiratory rate, central venous pressure, systemic arterial pressure, pulmonary arterial pressure, pulmonary arterial occlusion pressure, heart rate, cardiac output, and arterial and mixed venous blood gases were determined before pneumothorax and at progressive volumes of pneumothorax equivalent to 50, 100, and 150% of the calculated lung volume. Tidal volume, pulmonary vascular resistance, alveolar to arterial O2 tension difference, physiologic dead space fraction, and pulmonary venous admixture also were calculated. Linear increases in respiratory rate, central venous pressure, alveolar to arterial O2 tension difference, and pulmonary venous admixture differed significantly (P less than 0.05). Linear decreases in tidal volume, pHv, pHa, PvO2, and PaO2 were also significantly different. Quadratic increases were significantly different for pulmonary arterial pressure and pulmonary vascular resistance. Trends were not significantly different for other values.     

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.     

Induced pasteurellosis and pulmonary vascular adrenoceptor function in bull calves

Effects of Pasteurella haemolytica inoculation on pulmonary vascular function were studied in 5 conscious standing Jersey bull calves. Instruments were implanted in each calf to measure pulmonary arterial, pulmonary arterial wedge, left atrial, and systemic arterial pressures and cardiac output. Each calf was challenge exposed with 5 sequential 3-minute infusions of isoproterenol (a beta agonist) or phenylephrine (an alpha agonist) for maximal doses of 1.8 micrograms of isoproterenol or 2.3 micrograms of phenylephrine/kg of body weight/min. The calf was allowed 1 hour to recover, was anesthesized, and administered a 20-ml intratracheal infusion of live P haemolytica (10(6) colony-forming units/ml) followed by a 20-ml saline flush. The pulmonary hemodynamic response to isoproterenol and phenylephrine was examined again in each calf 4 days later. Calves developed a pneumonic pasteurellosis involving 26 to 43% of the lungs. There was a significantly (P less than 0.05) reduced resistance in the pulmonary arterial compartment after inoculation. Isoproterenol infusion decreased resistance in the pulmonary arterial, pulmonary venous, and systemic vascular compartments. The decrease in the pulmonary venous compartment in response to isoproterenol was significantly (P = 0.01) smaller after P haemolytica inoculation. After administration of 1.8 micrograms of isoproterenol/kg/min, resistance in the pulmonary venous compartment was 0.90 +/- 0.22 (mean +/- SD) before and 1.25 +/- 0.39 after Pasteurella inoculation. Phenylephrine resulted in an increase in pulmonary arterial, pulmonary venous, and systemic vascular compartments. There was a mild (P = 0.08) decrease in the pulmonary arterial compartment response to phenylephrine. Seemingly, Pasteurella inoculation blunted beta-receptor function in the pulmonary vascular bed, mainly in the veins, contributing to edema.     

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.     

Hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats. ANIMALS: 12 healthy adult domestic shorthair cats. PROCEDURE: Cats were anesthetized by administration of isoflurane in oxygen. After instruments were inserted, end-tidal isoflurane concentration was set at 1.25 times the individual minimum alveolar concentration, and nitrous oxide was administered in a Latin-square design at 0, 30, 50, and 70%. Each concentration was administered for 25 minutes before measurements were obtained to allow for stabilization. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured before and during noxious stimulation for each nitrous oxide concentration. Arterial and mixed-venous bicarbonate concentrations and oxygen saturation, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, arterial and mixed-venous oxygen contents, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. RESULTS: Arterial pressure, central venous pressure, pulmonary arterial pressure, rate-pressure product, systemic and pulmonary vascular resistance indices, arterial PCO2, and PCV increased during administration of 70% nitrous oxide. Arterial and mixed-venous pH, mixed-venous PO2, and alveolar-to-arterial oxygen difference decreased during administration of 70% nitrous oxide. Results before and during noxious stimulation were similar. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of 70% nitrous oxide to isoflurane-anesthetized cats resulted in improved arterial pressure, which was related to a vasoconstrictive effect.     

Chromosomal trisomy in an anormalous bovine fetus

This case report describes an anomalous male fetus of approximately six months gestation with abnormal karyotype containing an extra metacentric chromosome of medium size. The fetus had severe phenotypic abnormalities including anasarca, eye malformations, cardiac hypertrophy, pulmonary hypoplasia, adrenal dysplasia, and an umbilical hernia.     

Unexpected death in an adult dog with anomalous origin of the left coronary artery from the pulmonary trunk

A two-year-old female miniature poodle died unexpectedly while romping with its owner. Anomalous origin of the left coronary artery from the left pulmonic sinus was discovered at necropsy. Histologically, the right ventricle was unremarkable, but multifocal to coalescing necrosis and fibrosis occurred in the myocardium and endocardium of the left ventricle. Medial hypertrophy of small muscular pulmonary arteries was observed in the lung. The cardiac lesions were similar to those of children with anomalous origin of the left coronary artery from the pulmonary trunk. Pulmonary hypertension, which is suggested by the pulmonary arterial medial hypertrophy, could have increased left ventricular myocardial perfusion and delayed the ischemic myocardial damage that resulted in the death of this dog.     

RADIOGRAPHIC FINDINGS IN DOGS WITH SPONTANEOUS PULMONARY THROMBOSIS OR EMBOLISM

Thoracic radiographs of 21 dogs with necropsy-confirmed pulmonary thrombosis or embolism (PTE) were reviewed. Two major lung patterns were seen: (1) regional oligemia, giving the impression of a hyperlucent zone; (2) alveolar pulmonary infiltrate, indicating hemorrhage or infarction. Hemorrhage and infarction could not be differentiated radiographically. Other common findings were attenuation or loss of visualization of a lobar artery or lobar vein and pleural effusion, particularly with infarction and cardiac disease. PTE was often associated with renal disease (glomerulonephritis, amyloidosis), septic processes, pancreatitis, systemic venous or right heart thrombosis, cardiac insufficiency, and hypercorticism.     

Cardiac musculature of the intrapulmonary vein in the musk shrew.

The cardiac musculature of intrapulmonary veins was examined to elucidate its distribution pattern in the musk shrew, the primitive mammalian type, using by both light and electron microscopies. The musculature was distributed extensively from the hilum to the small veins less than 50 microns in diameter, suggesting that the phylogenic origin of this musculature may be traceable to the primitive mammalian types. Ultrastructure of cardiac myocyte in the intrapulmonary venous walls was essentially similar to that of left atrial myocyte. This suggests that the cardiac musculature may contribute to the regulation of pulmonary blood circulation. The abundance of large lipid droplets in both atrial and pulmonary myocytes was also observed and seemed to be the characteristic ultrastructure related to the physiological condition in this animal.     

Hemodynamic response of calves to tiletamine-zolazepam-xylazine anesthesia.

Six healthy Holstein calves were anesthesized with isoflurane in O2 and instrumented for hemodynamic studies. A saphenous artery was catheterized for measurement of blood pressure and withdrawal of blood for determination of the partial pressure of carbon dioxide (PaCO2), oxygen (PaO2), and arterial pH (pHa). Respiration was controlled throughout the study. The ECG and EEG were monitored continuously. A thermodilution catheter was passed via the right jugular vein into the pulmonary artery for determination of cardiac output and measurement of central venous pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. Baseline values (time 0) were recorded following recovery from isoflurane. Tiletamine-zolazepam (4 mg/kg)-xylazine (0.1 mg/kg) were administered IV immediately after recording baseline values. Values were again recorded at 5, 10, 20, 30, 40, 50, and 60 minutes after injection. Changes in left ventricular stroke work index, PaCO2, and pHa were insignificant. Arterial blood pressure and systemic vascular resistance increased above baseline at 5 minutes and then gradually decreased below baseline at 40 minutes, demonstrating a biphasic response. Values for pulmonary capillary wedge pressure, pulmonary arterial pressure, central venous pressure, and PaO2 were increased above baseline from 5 to 60 minutes. Stroke volume, stroke index, and right ventricular stroke work index were increased from 20 or 30 minutes to 60 minutes. Pulmonary vascular resistance increased at 10 minutes, returned to baseline at 20 minutes, and was increased again at 60 minutes. Heart rate, cardiac output, cardiac index, and rate pressure product were decreased at 5 minutes, and with the exception of cardiac output, remained so for 60 minutes. Cardiac output returned to the baseline value at 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arteriovenous shunts resembling patent ductus arteriosus in dogs: 3 cases

Three dogs presented for the evaluation of cardiac murmurs were diagnosed with aberrant arteriovenous shunts. All cases demonstrated the following findings: 1) relatively soft continuous murmur loudest at the left heart base resembling patent ductus arteriosus (PDA); 2) shunt flow signals in the pulmonary artery on echocardiography; and 3) no PDA on selective angiography, but evidence of anomalous shunting vessels from thoracic aorta to pulmonary vasculature. An aberrant arteriovenous shunt should be considered when a continuous murmur of relatively small intensity is heard.     

Treatment of cardiovascular disease in cattle.

Cardiac diseases of cattle may involve valvular structures, myocardium, pericardium, or blood vessels and are manifested by the clinical signs of cardiac dysrhythmias, cardiac murmurs, generalized edema, muffled heart sounds, jugular venous distention, jugular venous pulsations, pulmonary edema, pleural effusion, or ascites. Digoxin, quinidine, and furosemide can be used effectively to control signs of CHF and cardiac arrhythmias. Combination antimicrobial therapy can be successful for cows with infective endocarditis and thrombophlebitis. Pericardial fluid drainage may temporarily improve cattle with traumatic pericarditis or lymphosarcoma so that short-term goals may be reached.     

Cardiac musculature of the cranial and caudal venae cavae and the pulmonary vein in the fowl.

The cardiac musculature of cranial and caudal venae cavae and pulmonary vein was examined to clarify its distribution pattern in the fowl using both light and electron microscopies. The musculature was distributed from the heart to the root of subclavian vein in the cranial vena cava, to the cranial margin of the liver in the caudal vena cava, and to the left and right distal pulmonary veins in the pulmonary vein, respectively. Judging from the morphology and distribution pattern in the venous wall, the cardiac musculature in the fowl is thought to share the same phylogenic origin with that in mammals. The ultrastructure of cardiac myocytes including transitional cells in the cranial vena cava and the pulmonary vein resembled that of atrial myocytes. While, the typical specialized myocytes such as Purkinje fiber were found in the caudal vena cava of the fowl.     

Complete atrioventricular canal defect in a foal: Clinical and pathological features

Atrioventricular (AV) canal defects comprise a rare category of congenital heart disease associated with abnormal development of the endocardial cushions. These anomalies include a broad spectrum of lesions involving the atrial septum primum, the inlet portion of the ventricular septum, and the atrioventricular valves. In severe cases heart failure may result. The present report describes cardiopulmonary findings in a six-week-old, female Thoroughbred foal with persistent tachypnea and tachycardia since birth. Clinical, echocardiographic, cardiac catheterization, and pathologic findings were compatible with complete AV canal defect with bi-directional shunting, congestive heart failure, and pulmonary hypertension. Gross cardiac pathologic findings included a large atrioventricular septal defect, a common atriovalvular orifice, five atrioventricular leaflets, with two free-floating bridging leaflets. Histopathologic lesions in the lung included hypertrophy of the pulmonary arteriolar walls due to thickening of the tunica media. This represents a well documented case of complete endocardial cushion defect with anomalous development of the atrioventricular valves and resultant pulmonary hypertension and heart failure.     

Anesthesia for severe mitral and tricuspid regurgitation.

Anesthesia for mitral or tricuspid regurgitation should be designed to maintain cardiac output by decreasing systemic and pulmonary vascular resistance to aortic and pulmonary outflow, respectively, and by carefully preserving venous return. A moderate increase in heart rate may be helpful with mitral regurgitation; bradycardia should be avoided. Isoflurane, halothane, or opioid anesthesia is preferred.     

The effect of moderate hypovolemia on cardiopulmonary function in dogs

Objective: To collate canine cardiopulmonary measurements from previously published and unpublished studies in instrumented, unsedated, normovolemic and moderately hypovolemic dogs. Design: Collation of data obtained from original investigations in our research laboratory. Setting: Research laboratory, School of Veterinary Medicine. Subjects: Sixty‐eight dogs. Interventions: Subjects were percutaneously instrumented with an arterial catheter and a thermodilution cardiac output catheter. A femoral artery catheter was percutaneously placed for blood removal. Measurements and main results: Body weight, arterial and mixed‐venous pH and blood gases, arterial, pulmonary arterial, pulmonary artery occlusion, and central venous blood pressure, cardiac output, and core body temperature were measured. Body surface area, bicarbonate concentration, standard base excess, cardiac index (CI), stroke volume, systemic and pulmonary vascular resistance, left and right ventricular work and stroke work indices, left and right rate‐pressure product, alveolar PO₂, alveolar–arterial PO₂ gradient, arterial and mixed‐venous and pulmonary capillary oxygen content, oxygen delivery, oxygen consumption, oxygen extraction, venous admixture, arterial and venous blood carbon dioxide content, arterial–venous carbon dioxide gradient, carbon dioxide production were calculated. In 68 dogs, hypovolemia sufficient to decrease mean arterial blood pressure (ABPm) to an average of 62 mmHg, was associated with the following changes: arterial partial pressure of carbon dioxide (PaCO₂) decreased from 40.0 to 32.9 mmHg; arterial base deficit (BDa) increased from ?2.2 to ?6.3 mEq/L; lactate increased from 0.85 to 10.7 mm /L, and arterial pH (pHa) did not change. Arterial partial pressure of oxygen (PaO₂) increased from 100.5 to 108.3 mmHg while mixed‐venous PO₂ (PmvO₂) decreased from 49.1 to 34.1 mmHg. Arterial and mixed‐venous oxygen content (CaO₂ and CmvO₂) decreased from 17.5 to 16.5 and 13.8 to 9.6 mL/dL, respectively. The alveolar–arterial PO₂ gradient (A‐a PO₂) increased from 5.5 to 8.9 mmHg while venous admixture decreased from 2.9% to 1.4%. The ABPm decreased from 100 to 62 mmHg; pulmonary arterial pressure (PAPm) decreased from 13.6 to 6.4 mmHg; and pulmonary arterial occlusion pressure (PAOP) decreased from 4.9 to 0.1 mmHg. CI decreased from 4.31 to 2.02 L/min/m². Systemic and pulmonary vascular resistance (SVRI and PVRI) increased from 1962 to 2753 and 189 to 269 dyn s/cm⁵, respectively. Oxygen delivery (DO₂) decreased from 787 to 340 mL/min/m² while oxygen consumption (VO₂) decreased from 172 to 141 mL/min/m². Oxygen extraction increased from 20.9% to 42.3%. Conclusions: Moderate hypovolemia caused CI and oxygen delivery to decrease to 47% and 42% of baseline. Oxygen extraction, however, doubled and, therefore, oxygen consumption decreased only to 82% of baseline.