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Pulse wave velocity (PWV) is the most important index of arterial stiffness. It is conventionally estimated by noninvasively measuring central and peripheral blood pressure (BP) and/or velocity (BV) waveforms and then detecting the foot-to-foot time delay between the waveforms wherein wave reflection is presumed absent. We developed techniques for improved estimation of PWV from the same waveforms. The techniques effectively estimate PWV from the entire waveforms, rather than just their feet, by mathematically eliminating the reflected wave via an arterial tube-load model. In this way, the techniques may be more robust to artifact while revealing the true PWV in absence of wave reflection. We applied the techniques to estimate aortic PWV from simultaneously and sequentially measured central and peripheral BP waveforms and simultaneously measured central BV and peripheral BP waveforms from 17 anesthetized animals during diverse interventions that perturbed BP widely. Since BP is the major acute determinant of aortic PWV, especially under anesthesia wherein vasomotor tone changes are minimal, we evaluated the techniques in terms of the ability of their PWV estimates to track the acute BP changes in each subject. Overall, the PWV estimates of the techniques tracked the BP changes better than those of the conventional technique (e.g., diastolic BP root-mean-squared errors of 3.4 versus 5.2 mmHg for the simultaneous BP waveforms and 7.0 versus 12.2 mmHg for the BV and BP waveforms (p

Pulse transit time (PTT) measured as the time delay between invasive proximal and distal blood pressure (BP) or flow waveforms (invasive PTT [I‐PTT]) tightly correlates with BP. PTT estimated as the time delay between noninvasive proximal and distal arterial waveforms could therefore permit cuff‐less BP monitoring. A popular noninvasive PTT estimate for this application is the time delay between ECG and photoplethysmography (PPG) waveforms (pulse arrival time [PAT]). Another estimate is the time delay between proximal and distal PPG waveforms (PPG‐PTT). PAT and PPG‐PTT were assessed as markers of BP over a wide physiologic range using I‐PTT as a reference. Waveforms for determining I‐PTT, PAT, and PPG‐PTT through central arteries were measured from swine during baseline conditions and infusions of various hemodynamic drugs. Diastolic, mean, and systolic BP varied widely in each subject (group average (mean ± SE) standard deviation between 25 ± 2 and 36 ± 2 mmHg). I‐PTT correlated well with all BP levels (group average R 2 values between 0.86 ± 0.03 and 0.91 ± 0.03). PPG‐PTT also correlated well with all BP levels (group average R 2 values between 0.81 ± 0.03 and 0.85 ± 0.02), and its R 2 values were not significantly different from those of I‐PTT. PAT correlated best with systolic BP (group average R 2 value of 0.70 ± 0.04), but its R 2 values for all BP levels were significantly lower than those of I‐PTT (P

We developed a technique to calculate forward and backward arterial waves from proximal and distal pressure waveforms. First, the relationship between the waveforms is represented with an arterial tube model. Then, the model parameters are estimated via least-squares fitting. Finally, the forward and backward waves are calculated using the parameter estimates. Thus, unlike most techniques, the arterial waves are determined without a more difficult flow measurement or an experimental perturbation. We applied the technique to central aortic and femoral artery pressure waveforms from anesthetized dogs during drug infusions, volume changes, and cardiac pacing. The calculated waves predicted an abdominal aortic pressure waveform measurement more accurately (2.4 mmHg error) than the analyzed waveforms (5.3 mmHg average error); reliably predicted relative changes in a femoral artery flow measurement (14.7% error); and changed as expected with selective vasoactive drugs. The ratio of the backward- to forward-wave magnitudes was 0.37 ± 0.05 during baseline. This index increased by ∼50% with phenylephrine and norepinephrine, decreased by ∼60% with dobutamine and nitroglycerin, and changed little otherwise. The time delay between the waves in the central aorta was 175 ± 14 ms during baseline. This delay varied by ±∼25% and was inversely related to mean pressure.

Objective—To determine the effect of semen in urine specimens on urine protein concentration measured by means of dipstick analysis. Sample Population—14 urine samples from 3 adult castrated male dogs and 14 semen samples from 7 adult sexually intact male dogs. Procedures—Serial dilutions of the whole ejaculate or spermatozoa-free seminal fluid in urine were created, and unaltered and diluted urine samples were analyzed by means of a commercially available dipstick; pH and specific gravity of the samples were also measured. Spermatozoa and WBC counts of the semen samples and protein concentration of the seminal fluid were determined. Results—Protein concentrations determined by means of dipstick analysis of urine samples to which whole ejaculate (dilutions of 1:1, 1:2, 1:16, 1:64, and 1:256) or seminal fluid (dilutions of 1:1, 1:2, 1:16, and 1:64) had been added were significantly higher than concentrations in unaltered urine samples. All 13 samples to which whole ejaculate was added at a dilution of 1:2 and 10 of 12 samples to which seminal fluid was added at a dilution of 1:2 were positive for blood on dipstick analysis. There was no significant linear correlation between spermatozoa or WBC count of the semen sample and protein concentration of the spermatozoa-free seminal fluid. Conclusions and Clinical Relevance—Results suggested that regardless of whether spermatozoa were present, semen contamination could result in false-positive results for protein and blood during dipstick analysis of urine samples from sexually intact male dogs.

Objective: To report a case of myocardial perforation by a stick foreign body in a dog. Case Summary: A 3-year-old castrated male Labrador Retriever was examined because of a puncture wound seen after an unsupervised run in the woods. The wound was suspected to penetrate into the thoracic cavity on the basis of physical exam and radiographs. Uniform ventricular premature complexes (VPCs) and junctional beats were noted on electrocardiogram (ECG). Thoracotomy was performed and a 6-cm wooden stick was seen protruding from the right ventricle through the pericardium toward the sternum. The stick was removed while purse string sutures were tied around the resultant myocardial defect. Follow-up echocardiography revealed intact intracardiac structures. VPCs were treated with lidocaine and resolved completely within 24 hours of presentation. New or Unique Information Provided: Thoracic trauma can result in myocardial injury; penetration into the myocardium represents a life-threatening situation for the emergency clinician. Cardiac injury should be included in the differential diagnoses of penetrating thoracic foreign bodies.

Objective—To determine whether autologous jugular veins provide functional grafts with high 30-day patency rates in an experimental model of systemic-to-pulmonary shunting performed with a modified Blalock-Taussig procedure. Animals—15 healthy Beagles. Procedure—A segment of the left jugular vein was implanted between the left subclavian and pulmonary arteries. Echocardiograms were obtained prior to surgery, at day 4 to 7, and at day 30 after surgery. Selective angiograms were performed immediately after surgery and on day 30. Oximetric shunt calculations were made via terminal angiography prior to euthanasia. Gross and histologic evaluations of the grafts were conducted. Results—Grafts were patent in 12 of 15 dogs 30 days after surgery as assessed via auscultation, color Doppler ultrasonography, angiography, and histologic examination. Echocardiographic analysis revealed compensatory eccentric left ventricular hypertrophy. Mean pulmonary-to-systemic flow ratio was 1.5:1. Histologic evidence of endothelialization of the anastomotic sites and vein graft arterialization was detectable at 30 days. Conclusions and Clinical Relevance—Autologous jugular vein grafts were effectively used to create a systemic-to-pulmonary shunt by use of a modified Blalock-Taussig procedure. High patency, ready accessibility, low cost, and theoretical adaptative remodeling during patient growth make autologous jugular vein grafts a valuable alternative to synthetic materials.

Pulse transit time (PTT) is a proven, simple to measure, marker of blood pressure (BP) that could potentially permit continuous, noninvasive, and cuff-less BP monitoring (after an initial calibration). However, pulse arrival time (PAT), which is equal to the sum of PTT and the pre-ejection period, is gaining popularity for BP tracking, because it is even simpler to measure. The aim of this study was to evaluate the hypothesis that PAT is an adequate surrogate for PTT as a marker of BP. PAT and PTT were estimated through the aorta using high-fidelity invasive arterial waveforms obtained from six dogs during wide BP changes induced by multiple interventions. These time delays and their reciprocals were evaluated in terms of their ability to predict diastolic, mean, and systolic BP (DBP, MBP, and SBP) per animal. The root mean squared error (RMSE) between the BP parameter predicted via the time delay and the measured BP parameter was specifically used as the evaluation metric. Taking the reciprocals of the time delays tended to reduce the RMSE values. The DBP, MBP, and SBP RMSE values for 1/PAT were 9.8 ± 5.2, 10.4 ± 5.6, and 11.9 ± 6.1 mmHg, whereas the corresponding values for 1/PTT were 5.3 ± 1.2, 4.8 ± 1.0, and 7.5 ± 2.2 mmHg ( P < 0.05). Thus tracking BP via PAT was not only markedly worse than via PTT but also unable to meet the FDA BP error limits. In contrast to previous studies, our results quantitatively indicate that PAT is not an adequate surrogate for PTT in terms of detecting challenging BP changes.

We developed a new technique to mathematically transform a peripheral artery pressure (PAP) waveform distorted by wave reflections into the physiologically more relevant aortic pressure (AP) waveform. First, a transfer function relating PAP to AP is defined in terms of the unknown parameters of a parallel tube model of pressure and flow in the arterial tree. The parameters are then estimated from the measured PAP waveform along with a one-time measurement of the wave propagation delay time between the aorta and peripheral artery measurement site (which may be accomplished noninvasively) by exploiting preknowledge of aortic flow. Finally, the transfer function with its estimated parameters is applied to the measured waveform so as to derive the AP waveform. Thus, in contrast to the conventional generalized transfer function, the transfer function is able to adapt to the intersubject and temporal variability of the arterial tree. To demonstrate the feasibility of this adaptive transfer function technique, we performed experiments in 6 healthy dogs in which PAP and reference AP waveforms were simultaneously recorded during 12 different hemodynamic interventions. The AP waveforms derived by the technique showed agreement with the measured AP waveforms (overall total waveform, systolic pressure, and pulse pressure root mean square errors of 3.7, 4.3, and 3.4 mmHg, respectively) statistically superior to the unprocessed PAP waveforms (corresponding errors of 8.6, 17.1, and 20.3 mmHg) and the AP waveforms derived by two previously proposed transfer functions developed with a subset of the same canine data (corresponding errors of, on average, 5.0, 6.3, and 6.7 mmHg).

Background: Accurate detection of drug-induced QT interval changes is often confounded by concurrent heart rate changes. Application of heart rate correction formulas has been the traditional approach to account for heart rate–induced QT interval changes, and thereby identify the direct effect of the test article on cardiac repolarization. Despite numerous recent studies identifying the imprecision of these formulas they continue to be applied. Methods: Using a chronic atrioventricular dissociated His-paced canine model, heart rate correction methods were evaluated for their ability to generate a corrected QT interval independent of original heart rate. Additionally, His bundle pacing at a heart rate of 60 beats/min allowed calculation of the magnitude of error introduced by application of heart rate correction formulas. Results: Of the fixed parameter heart rate correction formulas, only Van de Water was able to predict corrected QT values independent of the original heart rate. The magnitude of error discovered by application of heart rate correction formulas varied, but in many cases was very large. Bazett's formula was associated with a mean overcorrection of 67.9 ms; Fridericia's 28.7 ms. Van de Water was the best fixed parameter formula with a mean error of 10.8 ms. As expected, group and individual corrections derived from linear regression of the HR-QT data offered improvement over the traditional formulas. Both were able to predict QTc values independent of the heart rate. However, errors of the magnitude of 10 and 6 ms, respectively, were still introduced. Conclusion: Van de Water and linear regression correction methods were superior to others in this study, but all methods generated QTc errors equal to or much greater than the magnitude of interest for drug safety evaluation.