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. References 1. Hoeper MM , Bogaard HJ , Condliffe R , et al . Definitions and diagnosis of pulmonary hypertension . J Am Coll Cardiol . 2013 ; 62 ( 25 ): D42 – D50 . doi: 10.1016/j.jacc.2013.10.032 2. Hoeper MM , Ghofrani HA , Grunig E
enlargement of the pulmonary artery was consistent with a diagnosis of pulmonary hypertension with secondary right-sided heart failure. However, the llama did not have any history of respiratory tract disease, and no signs of respiratory tract disease were
subsequent development of pulmonary hypertension was considered likely. Differential diagnoses included an atrial septal defect, ventricular septal defect, and a patent ductus arteriosus (PDA). Figure 2 Same radiographic images as Figure 1
supported a diagnosis of right-sided congestive heart failure secondary to pulmonary hypertension. Coelomocentesis was performed to improve respiratory function by providing more room for expansion of the air sacs. Clinicians were careful to remove as
discretion of the attending clinician. The LVIDd, LVIDs, and LA:Ao were measured by means of standard echocardiographic techniques. 15,16 Detection of tricuspid regurgitation by use of echocardiography was recorded. Pulmonary hypertension was arbitrarily
pulmonary hypertension was present (as measured via tricuspid valve regurgitation velocity, when present, and defined as a tricuspid valve regurgitation velocity > 3.2 m/s). 7 Additionally, the cardiologists performing the examination were asked to detail
indicative of pulmonary hypertension. Results of a follow-up heartworm antigen test were negative. The cat was discharged with instructions that the owners administer prednisone (1.25 mg/kg, PO, q 24 h) and dalteparin h (100 U/kg [45 U/lb], SC, q 24 h for
Abstract
Objective—To determine whether inhaled nitric oxide (NO) prevents pulmonary hypertension and improves oxygenation after IV administration of a bolus of dexmedetomidine in anesthetized sheep.
Animals—6 healthy adult sheep.
Procedure—In a crossover study, sevoflurane-anesthetized sheep received dexmedetomidine (2 µg/kg, IV) without NO (DEX treatment) or with inhaled NO (DEX-NO treatment). Cardiopulmonary variables, including respiratory mechanics, were measured before and for 120 minutes after bolus injection of dexmedetomidine.
Results—Dexmedetomidine induced a transient decrease in heart rate and cardiac output. A short-lived increase in mean arterial pressure (MAP) and systemic vascular resistance (SVR) was followed by a significant decrease in MAP and SVR for 90 minutes. Mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance increased transiently after dexmedetomidine injection. The PaO2 was significantly decreased 3 minutes after injection and reached a minimum of (mean ± SEM) 13.3 ± 7.8 kPa 10 minutes after injection. The decrease in PaO2 was accompanied by a sudden and prolonged decrease in dynamic compliance and a significant increase in airway resistance, shunt fraction, and alveolar dead space. Peak changes in MPAP did not differ between the 2 treatments. For the DEX-NO treatment, PaO2 was significantly lower and the shunt fraction significantly higher than for the DEX treatment.
Conclusions and Clinical Relevance—Inhalation of NO did not prevent increases in pulmonary arterial pressures induced by IV administration of dexmedetomidine. Preemptive inhalation of NO intensified oxygenation impairment, probably through increases in intrapulmonary shunting. (Am J Vet Res 2005;66:1496–1502)
Abstract
Objective—To identify clinical signs, underlying cardiac conditions, echocardiographic findings, and prognosis for horses with congestive heart failure.
Design—Retrospective study.
Animals—14 horses.
Procedure—Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; treatment; and outcome were determined by reviewing medical records.
Results—All 14 horses were examined because of a heart murmur; tachycardia was identified in all 14. Twelve horses had echocardiographic evidence of enlargement of 1 or more chambers of the heart. Other common clinical findings included jugular distention or pulsation, crackles, cough, tachypnea, and ventral edema. Nine horses had signs consistent with heart failure for > 6 days. Underlying causes for heart failure included congenital defects, traumatic vascular rupture, pericarditis, pulmonary hypertension secondary to heaves, and valvular dysplasia. Seven horses were euthanatized after diagnosis of heart failure; 5 were discharged but were euthanatized or died of complications of heart disease within 1 year after discharge. The remaining 2 horses were discharged but lost to follow-up.
Conclusions and Clinical Relevance—Results suggest that congestive heart failure is rare in horses. A loud heart murmur accompanied by either jugular distention or pulsation, tachycardia, respiratory abnormalities (crackles, cough, tachypnea), and ventral edema were the most common clinical signs. Echocardiography was useful in determining the underlying cause in affected horses. The long-term prognosis for horses with congestive heart failure was grave. (J Am Vet Med Assoc 2002;220:1512–1515)
Abstract
Objective—To characterize structural changes in pulmonary vessels of dogs with dirofilariosis.
Animals—8 dogs with dirofilariosis and 2 unaffected control dogs.
Procedure—Pulmonary artery pressure was measured in affected dogs, and dogs then were euthanatized. Scanning electron microscopy was used to examine vascular corrosion casts of pulmonary vasculature. Tissue sections of pulmonary vasculature were evaluated by use of histologic examination.
Results—Pulmonary artery pressure was higher in dogs with severely affected pulmonary vessels. In tissue sections, dilatation, as well as lesions in the tunica intima and proliferative lesions resulting in constriction or obstruction, were frequently observed in branches of the pulmonary artery. Numerous dilated bronchial arteries were observed around affected pulmonary arteries. Hyperplastic venous sphincters were observed in small pulmonary veins and venules. In corrosion casts, affected pulmonary lobar arteries had dilatation, pruning, abnormal tapering, constriction, and obstruction. In small arteries and arterioles, surface structures representing aneurisms and edema were seen. Bronchial arteries were well developed and extremely dilated, and they formed numerous anastomoses with pulmonary arteries at all levels, from the pulmonary trunk to peripheral vessels. Capillaries in the lungs were dilated with little structural change. Small pulmonary veins and venules had irregular annular constrictions that were caused by hyperplastic smooth muscle cells of venous sphincters.
Conclusions and Clinical Relevance—Scanning electron microscopy of microvascular casts delineated links between the bronchial and pulmonary circulations in dogs with dirofilariosis. Results of scanning electron microscopy provided a structural explanation for the development of pulmonary circulatory disturbances and pulmonary hypertension in dogs affected by dirofilariosis. (Am J Vet Res 2002:63:1538–1544)
