Cardiac Troponin I in Doberman Pinschers with Cardiomyopathy

Background: Cardiac troponin I (cTnI) is useful for detection of cardiac myocyte damage, but its efficacy in detecting various stages of dilated cardiomyopathy (DCM) in Doberman Pinschers is unclear. Objectives: To evaluate the diagnostic value of cTnI in various stages of DCM in Dobermans. Animals: Six hundred and fifty‐three cTnI measurements of 336 Doberman Pinschers. Methods: Using a longitudinal study design, staging of the disease was based upon 24‐hour‐ambulatory‐ECG (Holter) and echocardiography. A total of 447 cTnI measurements were performed in 264 healthy Dobermans, and 206 cTnI measurements in 75 Dobermans with cardiomyopathy. Eighty‐eight cTnI samples were from dogs with >100 ventricular premature contractions (VPCs)/24 hour, but without echocardiographic changes (“VPC group”). Additional 19 samples originated from dogs with only echocardiographic changes (“ECHO group”), and 56 samples from dogs with both VPCs and echocardiographic changes (“VPC plus ECHO group”). Twenty samples were from dogs with clinical signs (“clinical group”). The group “incipient” included 23 dogs, that were considered to be normal according to Holter and echocardiography at the time of the exam, but that developed DCM within 1.5 years. Results: cTnI values of dogs in all disease groups, including the “incipient” (0.30 ± 0.20) and “VPC group” (0.36 ± 0.34), were significantly (P= .04, P < .001) higher than the control group (0.07 ± 0.16). A cut‐off value of >0.22 ng/mL had a sensitivity of 79.5% and a specificity of 84.4% to detect all forms of cardiomyopathy. Conclusions and Clinical Importance: cTnI measurement is a valuable diagnostic test that can detect cardiomyopathy in dogs that are otherwise clinically normal.     

Echocardiographic changes in heart size in hypohydrated horses

Background: Hypohydration causes transient echocardiographic changes in pigs, dogs, humans, and cats. These changes mask the diagnosis of some cardiac diseases (valvular regurgitation, dilated cardiomyopathy) and promote the diagnosis of others (hypertropic cardiomyopathy and infiltrative disease), thus inhibiting accurate echocardiographic evaluation. Objectives: To describe the echocardiographic changes associated with hypohydration in normal horses. Animals: Ten adult horses without detectable cardiac disease. Methods: Experimental study. Echocardiographic examinations were performed on horses in the euhydrated and hypohydrated states. Horses were hypohydrated by combined water deprivation and furosemide administration until a 4–7% reduction in bodyweight was achieved. Statistical analyses were performed by paired t‐tests. Results: Hypohydration decreased left ventricular internal diameter in systole (0.8 ± 0.6 cm) and diastole (1.7 ± 0.9 cm), left atrial diameter (1.5 ± 0.4 cm) and left ventricular volume (490 ± 251 mL) (P‐values < .01), and increased septal wall thickness in diastole (0.6 ± 0.3 cm), free wall thickness in diastole (0.5 ± 0.3 cm), mean wall thickness (0.5 ± 0.2 cm) and relative wall thickness (0.2 ± 0.1 cm) (P‐values < .01). Conclusions and Clinical Importance: Hypohydration produces changes in left ventricular and atrial size that could mask or promote the severity of cardiac disease. The thickened, “pseudohypertrophied” appearance of the left ventricle in hypohydrated horses could affect interpretation of echocardiographic variables that are applied to the prediction of athletic performance. Echocardiography may prove a noninvasive method of monitoring volume status and response to fluid therapy in hypovolemic horses.     

T2‐WEIGHTED MAGNETIC RESONANCE IMAGING MEASUREMENTS OF OPTIC NERVE SHEATH DIAMETER IN DOGS WITH AND WITHOUT PRESUMED INTRACRANIAL HYPERTENSION

Intracranial hypertension is a cause of cerebral ischemia and neurologic deficits in dogs. Goals of this retrospective study were to test interobserver agreement for MRI measurements of optic nerve sheath diameter and associations between optic nerve sheath diameter, signalment data, and presumed intracranial hypertension status in a cohort of dogs. A veterinary radiologist interpreted scans of 100 dogs and dogs were assigned to groups based on presence or absence of at least two MRI characteristics of presumed intracranial hypertension. Two observers who were unaware of group status independently measured optic nerve diameter from transverse T2‐weighted sequences. Mean optic nerve sheath diameter for all dogs was 3 mm (1–4 mm). The mean difference between observers was 0.3 mm (limits of agreement, ?0.4 and 1.0 mm). There was no correlation between optic nerve sheath diameter and age for either observer (r = ?0.06 to 0.00) but a moderate positive correlation was observed between optic nerve sheath diameter and body weight for both observers (r = 0.70–0.76). The 22 dogs with presumed intracranial hypertension weighed less than the 78 dogs without (P = 0.02) and were more often female (P = 0.04). Dogs with presumed intracranial hypertension had a larger ratio of optic nerve sheath diameter to body weight for each observer‐side pair (P = 0.01–0.04) than dogs without. Findings indicated that the ratio of MRI optic nerve sheath diameter relative to body weight may be a repeatable predictor of intracranial hypertension in dogs.     

Echocardiographic and tissue Doppler imaging alterations associated with spontaneous canine systemic hypertension

Background: Feline systemic arterial hypertension (SHT) is associated with a wide spectrum of left ventricular (LV) geometric patterns as well as diastolic, and to a lesser extent, systolic myocardial dysfunction. However, little is known about SHT‐related cardiac changes in dogs. Hypothesis: SHT in dogs is responsible for morphological and functional cardiac alterations. Animals: Thirty dogs with spontaneous untreated SHT and 28 age‐ and body weight‐matched healthy dogs as controls. Methods: Prospective observational study. Conventional echocardiography and 2‐dimensional color tissue Doppler imaging were performed in SHT dogs by trained observers and compared with controls. Results: Forty‐seven percent of SHT dogs (14/30) had diffuse concentric hypertrophy. None had left atrial dilatation and 10/30 (33%) had aortic insufficiency (AoI) associated with proximal aortic dilatation. Longitudinal diastolic left ventricular free wall (LVFW) motion was altered in all SHT dogs at the base (early to late diastolic wave ratio, E/A = 0.5 ± 0.1 versus 1.3 ± 0.3 for controls, P < .0001) and the apex (E/A = 1.6 ± 1.7 versus 3.9 ± 3.1, P < .05). Longitudinal motion of the interventricular septum at the base (E/A = 0.7 ± 0.4 versus 1.1 ± 0.1, P < .01) and radial LVFW motion in the subendocardium (E/A = 0.9 ± 0.5 versus 1.6 ± 0.3, P < .01) were also altered in dogs with SHT. Longitudinal LVFW systolic velocities and gradients were also significantly decreased (P < .05) in SHT dogs. Conclusion and Clinical Importance: As in SHT in cats, SHT in dogs is associated with myocardial dysfunction independently of the presence of myocardial hypertrophy. However, unlike feline SHT, it results in a homogeneous LV geometric pattern with a relatively high prevalence of AoI.     

Lithium dilution cardiac output and oxygen delivery in conscious dogs with systemic inflammatory response syndrome

Objective: Compare cardiac index (CI) and oxygen delivery index (DO₂I) in conscious, critically ill dogs to control dogs; evaluate the association of CI and DO₂I with outcome. Design: Prospective non‐randomized clinical study. Setting: Veterinary teaching hospital. Animals: Eighteen client‐owned dogs with systemic inflammatory response syndrome (SIRS) and 8 healthy control dogs. Measurements and Main Results: CI of dogs with SIRS was measured using lithium dilution at times 0, 4, 8, 16, and 24 hours. Data collected included physical exam, arterial blood gas (ABG) and hemoximetry. CI of control dogs was measured 3 times with 1 measurement of ABG. Mean CI ± SE in SIRS patients was 3.32 ± 0.95 L/min/m²; lower than controls at 4.18 ± 0.22 L/min/m² (P<0.001). Mean DO₂I ± SE in SIRS patients was 412.91 ± 156.67 mL O₂/min/m²; lower than controls at 785.24 ± 45.99 mL O₂/min/m² (P<0.001). There was no difference in CI (P=0.49) or DO₂I (P=0.51) for dogs that survived to discharge versus those that did not. There was no difference in mean CI (P=0.97) or DO₂I (P=0.50) of survivors versus non‐survivors for 28‐day survival. Survivors had lower blood glucose (P=0.03) and serum lactate concentrations (P=0.04) than non‐survivors. Conclusions: CI and DO₂I in conscious dogs with SIRS were lower than control dogs, which differs from theories that dogs with SIRS are in a high cardiac output state. CI and DO₂I were not significantly different between survivors and non‐survivors. Similar to previous studies, lactate and glucose concentrations of survivors were lower than non‐survivors.     

A radiographic study of breed‐specific vertebral heart score and vertebral left atrial size in Chihuahuas

Although echocardiography is the gold standard for the diagnosis of cardio‐structural disease, thoracic radiography is a rapid, cost‐effective, and widely accessible method for evaluating cardiac size in dogs. The vertebral heart score (VHS) and the vertebral left atrial size (VLAS) are established as objective measures of cardiomegaly on thoracic radiographs. However, several studies have shown significant variations in the VHS among different breeds. The Chihuahua is predisposed to both congenital and acquired cardiac diseases. The aim of this prospective, single‐center, cross sectional study was thus to evaluate the VHS and the VLAS in healthy adult Chihuahua dogs. A total of 30 Chihuahuas were included. The VHS values in our sample population of Chihuahuas were 10.0 ± 0.6 (95% range, 8.9‐11.0). This was significantly greater than the canine reference value of 9.7 ± 0.5 established by Buchanan and Bücheler (P = .002). The VLAS of Chihuahuas in our study was 1.8 ± 0.2 (95% range, 1.3‐2.1). This was significantly lower than the values previously reported by Malcolm et al (2.07 ± 0.25; P = .0004). The VHS and the VLAS were not influenced by sex, body weight, short or long hair, and body condition score in normal Chihuahuas. Our results indicated that breed‐specific reference values for radiographic VHS and VLAS are needed. In Chihuahuas, the values found in this study can be used as a normal reference in order to help avoid overinterpretation of cardiomegaly in these dogs.     

Comparison of a computed tomographic pulmonary trunk to aorta diameter ratio with echocardiographic indices of pulmonary hypertension in dogs

There are limited criteria for the detection of pulmonary hypertension in dogs undergoing computed tomography (CT) for pulmonary disease. This retrospective analytical exploratory study compared a CT pulmonary trunk to aorta ratio with echocardiographic estimates of pulmonary hypertension. Dogs having both a contrast thoracic CT and echocardiogram were selected and maximal pulmonary trunk and descending aorta diameters were measured by two observers on a single transverse CT image. Computed tomographic diameter ratios were compared with the echocardiographic parameters of tricuspid regurgitation gradient, right ventricular acceleration time‐to‐ejection time ratio, pulmonary insufficiency gradient, and pulmonary artery to aorta diameter. A total of 78 dogs were sampled, with 44 dogs having one or more finding suggestive of pulmonary hypertension. A moderate positive correlation was shown between tricuspid regurgitation gradient and CT pulmonary trunk to aorta ratio (r = 0.61, P‐value < 0.0001). Mean CT pulmonary trunk to aorta ratio of dogs with moderate (P = 0.0132) and severe (P < 0.0003) pulmonary hypertension were significantly higher than normal dogs. There was no significant difference in mean CT pulmonary trunk to aorta ratio between normal and mild pulmonary hypertension dogs (P = 0.4244). The intraclass correlation coefficient (0.72) showed good reproducibility of the ratio. Findings indicated that CT pulmonary trunk to aorta ratio is a reproducible and potentially useful method to predict moderate and severe pulmonary hypertension in dogs, but not mild pulmonary hypertension. In dogs undergoing thoracic CT for pulmonary disease, an increased ratio should prompt follow up echocardiography.     

Echocardiographic Assessment of Hemodynamic Changes Produced by Two Methods of Inducing Fluid Deficit in Dogs

Background: Hydration status is important to the cardiovascular system because of its effects on preload. Decreased preload can alter echocardiographic measurements of systolic and diastolic function, potentially confounding interpretation of results. Hypothesis/Objectives: Mild fluid deficits are associated with measurable echocardiographic changes that are validated by physical and biochemical markers of decreased intravascular volume. Animals: Twenty‐five healthy staff/student‐owned dogs with no evidence of cardiac or renal disease. Methods: Prospective, interventional laboratory study. Dogs were randomly assigned to water deprivation (WD) alone for 8 hours (n = 13) or to furosemide treatment (FTx, 2.5 mg/kg IV) followed by WD for 8 hours (n = 12). Echocardiograms, biochemical sampling, and physical parameters were measured at baseline, and after 4 and 8 hours. Results: Both protocols induced fluid deficit as indicated by significant (P < .00001) decreases in weight at 4 hours (WD, 1.1%; FTx, 3.7%) and 8 hours (WD, 2.7%; FTx, 4.5%). Furosemide significantly decreased left ventricular end‐diastolic volume (54.3 ± 19.3–42.1 ± 17.3 mL, P < .0001), cardiac index (4.2 ± 1.1–2.9 ± 0.9 L/min/M², P < .0001), and mitral valve E wave velocity (0.79 ± 0.2–0.66 ± 0.2 m/s, P= .0004). These changes were accompanied by significant increases in blood urea nitrogen concentration (13.8 ± 2.6–14.8 ± 2.7 mg/dL, P= .04), vasopressin concentration (1.4 ± 1.2–3.3 ± 1.9 pg/mL, P= .045), and PCV (49.8 ± 4.5–53.2 ± 6.5%, P= .006). Effects of water deprivation alone were similar, but less pronounced. Conclusions and Clinical Importance: Mild fluid deficits have measurable hemodynamic effects in dogs. Hydration status should be considered when evaluating cardiac function by echocardiogram.     

Effects of 6% Tetrastarch and Lactated Ringer's Solution on Extravascular Lung Water and Markers of Acute Renal Injury in Hemorrhaged,Isoflurane‐Anesthetized Healthy Dogs

Background

Tetrastarch can cause acute kidney injury (AKI) in humans with sepsis, but less likely to result in tissue edema than lactated Ringer's solution (LRS).

Objectives

Compare effects of volume replacement (VR) with LRS and 6% tetrastarch solution (TS) on extravascular lung water (EVLW) and markers of AKI in hemorrhaged dogs.

Animals

Six healthy English Pointer dogs (19.7–35.3 kg).

Methods

Prospective crossover study. Animals underwent anesthesia without hemorrhage (Control). Two weeks later, dogs hemorrhaged under anesthesia on 2 occasions (8‐week washout intervals) and randomly received VR with LRS or TS at 3 : 1 or 1 : 1 of shed blood, respectively. Anesthesia was maintained until 4 hour after VR for EVLW measurements derived from transpulmonary thermodilution cardiac output. Neutrophil gelatinase‐associated lipocalin (NGAL) and creatinine concentrations in plasma and urine were measured until 72 hour after VR.

Results

The EVLW index (mL/kg) was lower at 1 hour after TS (10.0 ± 1.9) in comparison with controls (11.9 ± 3.4, P = 0.04), and at 4 hour after TS (9.7 ± 1.9) in comparison with LRS (11.8 ± 2.7, P = 0.03). Arterial oxygen partial pressure‐to‐inspired oxygen fraction ratio did not differ among treatments from 0.5 to 4 hour after VR. Urine NGAL/creatinine ratio did not differ among treatments and remained below threshold for AKI (120,000 pg/mg).

Conclusions and Clinical Importance

Although TS causes less EVLW accumulation than LRS, neither fluid produced evidence of lung edema (impaired oxygenation). Both fluids appear not to cause AKI when used for VR after hemorrhage in healthy nonseptic dogs.     

The effect of furosemide on left atrial pressure in dogs with mitral valve regurgitation

Background: The effects of furosemide on left atrial pressure (LAP) in dogs with mitral regurgitation (MR) have not been documented in a quantitative manner and between different routes of administration. Objective: To document LAP and echocardiographic parameters in MR dogs administered furosemide IV or PO, in order to document changes in LAP after furosemide treatment. Animals: Five healthy Beagle dogs (3 males and 2 females; aged 2 years) were used. Methods: Experimental, cross‐over, and interventional study. LAP was measured before the administration of furosemide, and 30 minutes, 1, 1.5, 2, 3, 4, 5, 6, 8, 12, and 24 hours after administration. Furosemide 1, 2, or 4 mg/kg IV, PO or placebo was administered. Results: LAP was significantly decreased with all administrations of furosemide but not after placebo (P < .05, respectively). The max reduction was observed 1 hour (1 mg/kg IV, 15.04 ± 7.02 mmHg), 3 hours (2, 4 mg/kg IV, 13.28 ± 8.01, 9.23 ± 4.92 mmHg), 4 hours (1 mg/kg PO, 14.68 ± 11.51 mmHg), and 5 hours (2, 4 mg/kg PO, 13.19 ± 10.52, 10.70 ± 7.69 mmHg). E wave and E/Ea were significantly decreased corresponding to the reduction of LAP after administration of 2 and 4 mg/kg (P < .05, respectively). Conclusions and Clinical Importance: LAP was decreased in proportion to the dosage of furosemide, which did not significantly differ between IV and PO of the same dosages. E wave and E/Ea might be useful for the treatment evaluation of furosemide.     

Pulmonary blood volume in mitral regurgitation in Cavalier King Charles spaniels

Background: Pulmonary edema and venous congestion are well‐recognized signs of congestive heart failure (CHF) in advanced canine chronic mitral regurgitation (MR). However, little is known about pulmonary blood volume (PBV), blood pulmonary transit time (PTT), and the regulation of these. Objectives: To measure and evaluate the relationships of PBV, forward stroke volume (FSV), and heart rate normalized blood pulmonary transit time (nPTT) in healthy dogs and dogs with MR. Animals: Thirty‐three Cavalier King Charles Spaniels; 11 healthy, 4 in modified New York Heart Association (NYHA) class I, 11 in class II, and 7 in CHF. Methods: Heart rate normalized PTTs were measured by radionuclide angiocardiography. Left ventricular end diastolic and systolic diameter, left atrial/aortic root ratio, and FSV were measured by echocardiography. PBV and pulmonary blood volume index (PBVI) were calculated by established formulas. Results: PBVI was 308 ± 56 (mean ± SD) mL/m² for healthy dogs, 287 ± 51 mL/m² in NYHA class I, 360 ± 66 mL/m² in Class II, and 623 ± 232 mL/m² in CHF (P= .0008). Heart rate normalized PTT, not FSV, was a predictor of PBV (r= 0.92 and 0.02, respectively). Conclusions and Clinical Importance: Increased PBV, not decreased FSV, is the main cause of increased nPTT in MR. Increased nPTT can be used as an indicator of abnormal cardiopulmonary function in dogs with MR.     

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

ObjectiveTo assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia.Study designProspective, randomized, crossover experimental trial.AnimalsA total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation).MethodsDogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg^–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg^–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg^–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg^–1 minute^–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg^–1 minute^–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05).ResultsWhen administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments.Conclusion and clinical relevanceLidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs.     

Heart rate variability in relation to severity of mitral regurgitation in Cavalier King Charles spaniels

Heart rate variability was measured in 81 Cavalier King Charles spaniels to investigate if it could be used to evaluate the severity of mitral regurgitation and to predict decompensation. Heart rate variability was assessed by the natural logarithm of the variance of the R-R intervals for 20 consecutive beats obtained from electrocardiographic recordings. Twenty-two of the dogs were clinically normal and 59 had mitral regurgitation caused by chronic valvular disease. The severity of mitral regurgitation was evaluated by echocardiography and thoracic radiography. Heart rate variability was found to be reduced (P < 0.001) among dogs with severe left atrial and ventricular dilatation and clinical signs of congestion. No significant differences in heart rate variability were found among normal dogs, dogs with only cardiac murmur, and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation. Overall, an association was found between heart rate variability and left atrial to aortic root ratio and left ventricular end diastolic diameters (r = 0.72 and 0.64, respectively, P < 0.001), as well as heart and respiratory rate (r = 0.80 and 0.69, respectively, P < 0.001). Multiregression analysis showed that, in order of importance, heart rate, left atrial diameter and respiratory rate had significant effects on heart rate variability. Among these parameters, heart rate variability and left atrial diameter were found to be most efficient in separating decompensated dogs from compensated. It is concluded that heart rate variability may provide the clinician with valuable information when assessing the severity of mitral regurgitation caused by chronic valvular disease.     

COMPUTED TOMOGRAPHIC MEASUREMENT OF THE MAIN PULMONARY ARTERY TO AORTIC DIAMETER RATIO IN HEALTHY DOGS: A COMPARISON TO ECHOCARDIOGRAPHICALLY DERIVED RATIOS

Indicators of pulmonary hypertension in dogs examined with thoracic computed tomography (CT) are not well established in the veterinary literature. In humans, the main pulmonary artery to aortic diameter ratio (MPA:Ao) measured via CT, has been shown to be more sensitive than echocardiographic variables for predicting presence and severity of pulmonary hypertension, in some cases. In veterinary literature, the MPA:Ao has been determined echocardiographically to have an upper limit of about 1:1. Measurement of this ratio has not been described in dogs using CT. The objectives of this cross‐sectional, prospective study were to compare echocardiographic measurement of MPA:Ao with that obtained via CT, determine if measurement of MPA:Ao via CT is repeatable and reproducible, and determine the effect of respiration and contrast administration on the measurement of MPA:Ao via CT. Ten healthy dogs without pulmonary hypertension were anesthetized to undergo thoracic CT using three protocols and echocardiography. The MPA:Ao was measured three times by three observers for each of the three CT protocols and compared to echocardiographic measurements. The mean MPA:Ao measured among all observers and CT protocols was 1.108 ± 0.152 (SD). The effect of CT scan protocol on MPA:Ao significantly differed among the three methods (P = 0.0014), where expiratory scans had lower MPA:Ao than inspiratory scans. The ratio measured on inspiratory CT scans consistently overestimated MPA:Ao when compared to echocardiography (bias = 0.226). Findings did not support the echocardiographically derived upper limit of MPA:Ao as an upper limit for determination of main pulmonary arterial enlargement on CT.     

The Effect of Angiotensin‐Converting Enzyme Inhibitors of Left Atrial Pressure in Dogs with Mitral Valve Regurgitation

Background: Despite many epidemiological reports concerning the efficacy of angiotensin‐converting enzyme (ACE) inhibitors in dogs with mitral regurgitation (MR), the hemodynamic effects of ACE inhibitor administration have not been fully evaluated. Objectives: To document left atrial pressure (LAP) in dogs with MR administered ACE inhibitors, in order to obtain interesting information about daily LAP changes with administration of ACE inhibitors. Animals: Five healthy Beagle dogs weighing 9.8 to 14.2 kg (2 males and 3 females; aged 2 years). Methods: Experimental, crossover, and interventional study. Chordae tendineae rupture was induced, and a radiotelemetry transmitter catheter was inserted into the left atrium. LAP was recorded for 72 consecutive hours during which each of 3 ACE inhibitors—enalapril (0.5 mg/kg/d), temocapril (0.1 mg/kg/d), and alacepril (3.0 mg/kg/d)—were administered in a crossover study. Results: Averaged diurnal LAP was significantly, but slightly reduced by alacepril (P= .03, 19.03 ± 3.01–18.24 ± 3.07 mmHg). The nightly drops in LAP caused by alacepril and enalapril were significantly higher than the daily drops (P= .03, ?0.98 ± 0.19 to ?0.07 ± 0.25 mmHg, and P= .03, ?0.54 ± 0.21–0.02 ± 0.17 mmHg, respectively), despite the fact that the oral administrations were given in the morning. Systolic blood pressure (122.7 ± 14.4–117.4 ± 13.1 mmHg, P= .04) and systemic vascular resistance (5800 ± 2685–5144 ± 2077 dyne × s/cm⁵, P= .03) were decreased by ACE inhibitors. Conclusions and Clinical Importance: ACE inhibitors decrease LAP minimally, despite reductions in left ventricular afterload. ACE inhibitors should not be used to decrease LAP.     

The cardiovascular effects of dexmedetomidine given by continuous infusion during isoflurane anesthesia in dogs

In a previous study we showed that the MAC of isoflurane was decreased by 18 ± 12% and 59 ± 7% by constant rate infusions of dexmedetomidine at 0.5 and 3 μg kg^–1 hour^–1. The purpose of this study was to document the cardiovascular changes associated with these infusions of dexmedetomidine at 1.3 MAC isoflurane/ dexmedetomidine. Dogs were anesthetized with isoflurane in oxygen given by mask. A cephalic venous catheter, a dorsal pedal arterial catheter and a balloon tipped, Swan–Ganz, pulmonary arterial catheter were placed percutaneously. After instrumentation the dogs were maintained at 1.3 MAC isoflurane for 60 minutes. At this time a set of measurements was made including, heart rate, respiratory rate, core body temperature, pulmonary and systemic arterial blood pressures (SAP, MAP, DAP, CVP, SPAP, MPAP, DPAP and PAOP), cardiac output and arterial and mixed venous blood samples were collected for the measurement of blood gases, pH, hemoglobin concentration, PCV and total protein. Calculated variables included base excess (BE), (HCO₃^?), cardiac index, systemic and pulmonary vascular resistance indices, oxygen delivery, oxygen consumption, oxygen utilization ratio and shunt fraction. After these measurements to dogs were randomly assigned to receive a loading dose of 0.5 or 3 μg kg^–1 of dexmedetomidine given over 6 minutes followed by an infusion of 0.5 (LD) or 3 μg kg^–1 hour^–1 (HD), respectively. The concentration of isoflurane was reduced by the above percentages, respectively, to maintain 1.3 MAC. Full sets of measurements were repeated at 10, 30, 60, 90, 120, 150 and 180 minutes after the start of the loading dose. Measured and calculated variables were compared with baseline using an anova and a post‐hoc Tukey's test. Significance was set at p = 0.05 and results are given as mean ± SD. The initial concentration of isoflurane was 1.73 ± 0.02% and was reduced to 1.41 ± 0.02 and 0.72 ± 0.09% for the LD and HD, respectively. Heart rate decreased with both doses but no other parameter changed significantly with the LD. With the HD there were significant changes in SAP, MAP, DAP, CVP, MPAP, PAOP, CI, SVRI, PCV, DO₂ and shunt fraction. The LD appeared to have minimal effect on the cardiopulmonary values measured, whereas the HD caused typical changes expected with an alpha‐2 agonist.     

The echocardiographic effects of romifidine in dogs with and without prior or concurrent administration of glycopyrrolate

Objective To determine the cardiopulmonary response to romifidine (RO) in the dog with or without prior or concurrent administration of glycopyrrolate. Study Design Randomized, cross‐over experimental study. Animals Six (three male, three female) cross‐bred dogs weighing 23 ± 2.4 kg. Methods Two‐dimensional guided M‐mode echocardiography was performed in conscious dogs simultaneously with measurement of systolic arterial blood pressure (SBP) and heart rate (HR). Dimensions of the left ventricle (LVID), interventricular septum (IVS), and left ventricular free wall (LVFW) were obtained in systole (S) and diastole (D). Amplitude of motion (Amp) of the IVS and LVFW were also measured. From these, measures of wall stress (WS) and fractional shortening (FS) of the left ventricle were derived. Baseline echocardiographic measurements were recorded, following which one of the five treatments was administered. Glycopyrrolate (G) 0.01 mg kg^?1, or saline (S) 0.5 mL, was administered IM as pre‐medication (Gp or Sp), or G was administered concurrently (Gc) with romifidine (RO). Treatments were: T₁, Sp + RO (40 μg kg^?1); T₂, Gp + RO (40 μg kg^?1); T₃, Sp + RO (120 μg kg^?1); T₄, Gp + RO (120 μg kg^?1); and T₅, Sp + Gc +RO (120 μg kg^?1). Romifidine or RO + Gc was administered SC 20 minutes after pre‐medication (time 0), and further measurements were taken 10, 20, 30, 60, and 90 minutes after RO. Results Echocardiographic indices of cardiac systolic function (LVID‐S, FS, Amp‐LVFW) and HR were decreased in RO‐sedated dogs (p < 0.0001) . The magnitude of change in cardiac indices was least with low‐dose RO. At most sampling times, high‐dose RO produced significantly more alteration in cardiac indices. Systolic blood pressure increased in all treatment groups, with the greatest increases in those groups receiving G. Glycopyrrolate significantly increased HR; however, cardiac indices were further reduced. Wall stress significantly increased, with a more dramatic increase in groups receiving G. Conclusions Indices of LV systolic function were reduced in RO‐sedated dogs in a dose‐related manner. Glycopyrrolate further reduced these indices and dramatically increased measurements of wall stress in dogs sedated with RO. Clinical relevance Use of low‐dose RO minimizes cardiac dysfunction; however, it should still be used cautiously in dogs with cardiomyopathy or heart failure. The routine use of G is not recommended to alleviate the bradycardia associated with RO in conscious dogs.     

Effect of experimental endotoxemia on thrombelastography parameters, secondary and tertiary hemostasis in dogs

Background: Thrombelastography (TEG) and indicators of secondary and tertiary hemostasis might be altered in dogs with endotoxemia. Hypothesis: Endotoxemia influences measures of coagulation in dogs. Animals: Ten healthy cross‐bred dogs. Material and Methods: Prospective laboratory study between controls (n = 5) receiving 0.9% saline IV and the study group (n = 5) treated with low‐dose lipopolysaccharide (0.02 mg/kg IV). Physical examination and sampling for measurement of leukocytes, platelets, and coagulation variables were performed at time points 0, 1, 4, and 24 hours. Coagulation variables included kaolin‐activated TEG, 1‐stage prothrombin time (OSPT), activated partial thromboplastin time (aPTT), fibrinogen, factor VIII, antithrombin, protein C, protein S, activated protein C (APC)‐ratio calculated from aPTT with and without presence of APC), and D‐Dimers. Results: Endotoxemia‐induced clinical signs included lethargy (n = 5/5), diarrhea (n = 4/5), emesis (n = 4/5), and abdominal pain (2/5). After 1 hour there was severe leukopenia (2.5 ± 0.7 × 10⁹/L; mean ± SD, P < .0001) and a 2.2‐fold increase in D‐Dimers (0.81 ± 0.64 mg/L, P < .0001). After 4 hours there was hyperthermia (40.3 ± 0.4°C, P < .0001) and increases in OSPT (10.5 ± 2.7 seconds, P < .0001), aPTT (16.7±5.2 seconds, P= 0.002). A significant decrease in fibrinogen (1.5±1.0 g/L, P= 0.001), protein C (31 ± 33%, P <.0001), protein S (63 ± 47%, P < .0001), TEG α (58 ± 19, P= .007), and TEG maximal amplitude (50 ± 19 mm, P= .003) was seen compared with the controls. APC‐ratio rose significantly (2.5 ± 0.2, P < .0001) without exceeding the reference interval (n = 4/5). Conclusion and Clinical Importance: D‐Dimers are the earliest indicator for endotoxemia‐associated coagulation abnormalities followed by decreased protein C concentration. APC‐ratio and TEG were not good screening variables.     

Radiographic vertebral left atrial size: A reference interval study in healthy adult dogs

Thoracic radiography is a useful technique for the evaluation of cardiac dimensions, especially when echocardiography is not possible. The vertebral left atrial size (VLAS) has recently been proposed as a new radiographic method for quantifying left atrial dimensions in dogs. The aims of this retrospective, reference interval, observational study were to describe values for VLAS in a group of healthy adult dogs and to compare intraobserver and interobserver agreement for VLAS versus vertebral heart score (VHS) methods. Thoracic radiographs of 80 healthy adult dogs were evaluated. Normal left atrial size was determined based on an echocardiographic left atrial‐to‐aorta ratio < 1.6. The VLAS and vertebral heart score values were measured from right lateral radiographs. The correlations between VLAS, the vertebral heart score, and the left atrial‐to‐aorta ratio were evaluated. The effects of body weight, sex, and age were also tested using regression analyses. The median value of VLAS were 1.9, with a reference interval of 1.4‐2.2. A positive correlation was found between VLAS and vertebral heart score values (r = 0.53; P < .0001). No effect of body weight, sex, and age on VLAS was detected. Excellent intraobserver and interobserver agreements were found for both VLAS and vertebral heart score methods (intraclass correlation coefficients ≥ 0.91). Findings from this sample of healthy dogs indicated that VLAS is a repeatable radiographic method for quantifying left atrial size. Further studies are warranted to evaluate this measure in clinically affected dogs.