A. vasorum infection causes only a mild increase in PAP following inoculation and anthelmintic therapy. The absence of important PH may in part be explained by the recruitment of AV shunts in the presence of vascular obstructive disease. TDI echocardiographic parameters may be more sensitive to detect mild changes in RV function than conventional parameters.

Background: Boxers are predisposed to subaortic and pulmonic stenosis (SAS, PS). Screening of puppies may be useful in estimating the risk of their developing a defect that potentially compromises life expectancy or exercise tolerance.Hypothesis: Presence of SAS or PS in adult Boxers can be predicted by auscultation and Doppler echocardiography at 9-10 weeks of age.Animals: Eighty-five Boxer puppies examined at 9-10 weeks of age and at 12 months of age. Methods: Prospective, longitudinal observational study. Auscultation by stethoscope and continuous wave-Doppler echocardiography for peak velocities (V max ) in the aorta (Ao) and pulmonary artery (PA).Results: Intensity of heart murmurs in puppies correlated with V max Ao and V max PA in adults. V max Ao and V max PA in puppies correlated with V max Ao and V max PA in adults, respectively. From puppy to adult, V max Ao increased and V max PA remained unchanged. The negative predictive value for absent or only a soft ( II/VI) murmur in puppies being associated with V max Ao and PA 2.4 m/s as an adult was 90% and 3.5 m/s 100%. The negative predictive value of a V max 2.4 m/s as a puppy still being 2.4 m/s as an adult was 94% for Ao and 96% for PA, and of a V max 3.5 m/s, 99% for Ao and 100% for PA.Conclusions and Clinical Importance: Even though V max Ao increases during growth in Boxer puppies, indicating relative narrowing of the aorta, puppies with V max Ao 2.4 m/s do not usually progress to clinically have relevant SAS at 12 months of age.

A 5-month-old, 20 kg, intact female, German Shepherd Dog was presented to the Veterinary Hospital of the University of Zurich for evaluation of severe panting, exercise intolerance, and cyanosis. On clinical examination, the dog was thin but bright, alert, and responsive. A grade 5/6 systolic heart murmur was detected with the point of maximum intensity over the cranial left thorax. The peripheral pulse was weak, mu-cous membranes were pink, and capillary refill time was 2 seconds. Noninvasive blood pressure measurement was normal. Arterial oxygen saturation measured by pulse oximetry (SpO 2) on the tongue was 100% while in lateral recumbency and breathing room air. Based on these findings, congenital ventricular outflow tract obstruction was suspected and thoracic radiographs and echocardi-ography were performed. On radiography, moderate right-sided and mild left-sided cardiomegaly were present. The pulmonary vasculature was smaller than normal, with the exception of an enlarged and tortuous pulmonary artery and vein in the right cranial lung lobe. Moderate widening of the mediastinum was identified on the ventrodorsal projection (Fig 1). The abnormal vasculature in the right cranial lung lobe was considered compatible with an arterio-venous (AV) fistula. Widening of the cranial mediastinum was attributed to the presence of the thymus gland. Two-dimensional echocardiographic a findings included severe right ventricular hypertrophy with flattening of the septum and severe dilatation of the right atrium. Severe valvular pulmonic stenosis with a maximal systolic blood flow velocity (v max) of 5.0 m/s, a perimembranous ventric-ular septal defect with left-to-right shunting (v max 1.8 m/s), and mild subaortic stenosis (v max 2.4 m/s) were diagnosed by color Doppler and spectral Doppler examination, respectively. Considering the normal SpO 2 at rest, the shunting fraction through the AV fistula was judged to be clinically irrelevant. Adequate oxygen delivery at rest but cyanosis with slight effort was thought to be caused by right-to-left shunting through the AV fistula and ventric-ular septal defect associated with exercise-induced changes in pulmonary and systemic arterial pressures, possibly combined with peripheral cyanosis associated with decrease cardiac output caused by severe valvular pulmonic stenosis. During catheterization of the left jugular vein for ballooning of the pulmonic stenosis, the catheter could not be advanced into the right atrium, and entered the great cardiac vein instead. For better orientation, angiography of this aberrant vessel was performed and revealed a persistent left cranial vena cava (PLCVC) and dilated coronary sinus (Fig 2). Uneventful catheterization of the right heart through the right femoral vein followed by successful balloon valvuloplasty led to a reduction in pulmonic v max to 3.7 m/s. After the procedure, the owners reported normal respiratory rate, improved exercise tolerance, and no reccurrence of cyanosis. On a follow-up examination 3 years later, the owner consented t...

This is the first report in which BIS is documented together with standard monitoring techniques during cardiopulmonary arrest and resuscitation in a calf. BIS varied with cardiovascular performance, and may be indicative of cerebral blood flow in this context. Further research may be warranted to define the role of BIS for monitoring cerebral activity during CPR.

A 3-year-old male, castrated, miniature pinscher weighing 9 kg was presented to the University of Zurich Veterinary Teaching Hospital Cardiology Service for evaluation of lethargy, a newly recognized cardiac murmur, and labored breathing. For the previous 3 days, the dog had been progressively reluctant to move and breathing had become labored. Before the current presentation, the dog had always been in excellent health.On admission, the dog was in sternal recumbency, profoundly lethargic, and showed expiratory dyspnea. Diffuse petechiation was visible on the skin and mucous membranes. Heart and pulse rate were 160 beats per minute and irregular, pulse quality was weak, and rectal temperature was 37.1uC (98.8uF). On auscultation, no respiratory or cardiac sounds were heard on the left side and muffled sounds were heard on the right side with a continuous heart murmur, grade 3/6. The jugular veins were distended and abdominal palpation disclosed hepatomegaly and ascites.Laboratory abnormalities on presentation included severe thrombocytopenia (11,000/mL; reference range, 130,000-394,000/mL), hypoproteinemia (43 g/L, reference range: 56-71 g/L), hypoalbuminemia (22 g/L, reference range: 29-37 g/L), hyponatremia (136 mmol/ L; reference range, 152-159 mmol/L), and hyperkalemia (5.4 mmol/L; reference range, 4.3-5.3 mmol/L). A coagulation profile was normal.An ECG indicated sinus tachycardia with single ventricular premature complexes and non-sustained ventricular tachycardia with a left bundle branch block pattern. The QRS complexes during sinus tachycardia were consistent with right ventricular enlargement and the ST segments were depressed in leads I, II, and aVF and increased in lead aVR.Thoracic radiographs revealed marked pleural effusion, moderate right heart enlargement, diminished pulmonary vasculature, engorged caudal vena cava, hepatomegaly, and ascites. Analysis of abdominal and pleural fluids indicated that they were modified transudates.On 2-dimensional and M-mode transthoracic echocardiography, a the right ventricle (RVDd, 2.45 cm) and right atrium (RA, 4 cm) appeared markedly dilated with flattening of the interventricular septum. The left ventricle was hypovolemic (LVDd, 1.4 cm). In the main pulmonary artery, a membranous structure that originated laterally slightly above the pulmonary valve annulus was bulging into the lumen (Fig 1a). An echodense structure suggestive of a thrombus at the site of the pulmonary artery bifurcation completely occluded the left pulmonary artery. Color Doppler echocardiography indicated moderate tricuspid insufficiency (TI), mild pulmonic insufficiency (PI), and continuous turbulent flow from the descending aorta to the main pulmonary artery through a patent ductus arteriosus (PDA). Furthermore, the systolic outflow signal above the pulmonary valve was only a narrow turbulent jet that passed medially to the described membrane. Behind the membrane, there was no systolic flow but only diastolic blood flow in the main pulmonary artery towards the pulmonary valve (Fig 1b). Sp...