Cardiac Output In Dogs Research Articles

Experimental evaluation of a pressure recording analytical method (PRAM), a pulse contour analysis method, for monitoring cardiac output in dogs

Introduction: The PRAM has been evaluated in dogs under steady-state hemodynamic conditions, and this study evaluated PRAM under dynamic circulatory conditions, created by infusion of sympathomimetic drugs.

Evaluation of Right Ventricular Function and Dyssynchrony in a Dog Model of Acute Pulmonary Embolism: Diagnostic Utility and Reversibility.

BackgroundThe diagnosis of acute pulmonary thromboembolism is challenging in dogs. Little has been reported on changes in echocardiographic indices in dogs with acute pulmonary thromboembolism. The objective of this study was to validate the relationship between echocardiographic indices and right heart catheterization variables in dogs with acute pulmonary embolism and to identify a useful echocardiographic index for diagnosing acute pulmonary embolism.Materials and MethodsSix healthy laboratory beagles were included in the study. Echocardiography and right heart catheterization were performed in a dog model of acute pulmonary embolism produced by microsphere injection. Echocardiographic indices, including the right ventricular (RV) Tei index, RV longitudinal strain, and the dyssynchrony index using speckle tracking echocardiography, transmitral flow, and eccentricity index, were measured.ResultsThe mean pulmonary arterial pressure increased (22.2 ± 1.2 mmHg) and the blood pressure decreased after microsphere injection. Although the mean pulmonary arterial pressure remained elevated, the blood pressure recovered 2 days after the microsphere injection. Most echocardiographic indices of RV function were significantly impaired following microsphere injection and recovered after 2 days. In contrast, the RV Tei index was significantly impaired after microsphere injection and the impairment persisted after 2 days. Multivariable analysis revealed that the RV Tei index was an independent echocardiographic predictor of pulmonary vascular resistance (β = 0.88, P < 0.001), and transmitral early diastolic wave was an independent predictor of the cardiac index (β = −0.86, P = 0.001).ConclusionsThe RV Tei index is a useful echocardiographic index for diagnosing acute pulmonary embolism. Ventricular interdependence may be an important factor causing low cardiac output in dogs with acute pulmonary embolism.

Comparison of cardiac output measurements using transpulmonary thermodilution and conventional thermodilution techniques in anaesthetized dogs with fluid overload

ObjectiveTo evaluate the agreement between cardiac output (CO) values obtained using a transpulmonary thermodilution technique (TPTDCO) and conventional thermodilution technique (TDCO) in anaesthetized dogs with fluid overload. Study designProspective experimental study. AnimalsSix healthy Beagle dogs aged 7–8 years. MethodsDogs were anaesthetized with sevoflurane in oxygen, and catheters were inserted for TPTDCO and TDCO measurement. After instrumentation, baseline CO was measured using each technique at a central venous pressure (CVP) of 3–7 mmHg. Dogs were subsequently administered lactated Ringer’s solution and 6% hydroxyethyl starch to induce fluid overload. CO measurements were obtained using each technique at CVP values of 8–12 mmHg, 13–17 mmHg, 18–22 mmHg and 23–27 mmHg. Agreements between CO measurements obtained with the respective techniques were analysed using Dunnett’s test, Pearson’s correlation coefficient and Bland–Altman analysis. ResultsThirty pairs of CO values were obtained, ranging from 1.45 L minute−1 to 4.69 L minute−1 for TPTDCO and from 1.30 L minute−1 to 4.61 L minute−1 for TDCO. TPTDCO and TDCO values correlated strongly (r2 = 0.915, p< 0.001). The bias and mean relative bias between TPTDCO and TDCO were 0.26 ± 0.30 L minute−1 (limits of agreement - 0.29 to 0.81 L minute−1) and 9.7%, respectively. Conclusions and clinical relevanceTPTDCO and TDCO measurements obtained in anaesthetized dogs during fluid overload exhibited good agreement. Accordingly, transpulmonary thermodilution provides an accurate measurement of CO in dogs with fluid overload.

Activation of Baroreflex Instantly Reduces Left Atrial Pressure and Increases Cardiac Output in Dogs with Pacing Induced Heart Failure

Activation of Baroreflex Instantly Reduces Left Atrial Pressure and Increases Cardiac Output in Dogs with Pacing Induced Heart Failure

PNU-282987 Improves the Hemodynamic Parameters by Alleviating Vasopermeability and Tissue Edema in Dogs Subjected to a Lethal Burns Shock

Excessive inflammation and high vasopermeability can lead to blood volume loss and tissue edema, which can affect the resuscitation and prognosis for serious burn patients. In this experiment, we investigated the effect of PNU-282987, an α7 nicotine cholinergic receptor agonist on the hemodynamic parameters and survival rate by inhibiting vasopermeability and tissue edema during the fluid resuscitation for lethal burn shock. Forty Beagle dogs with intubation of the carotid artery and jugular vein 24 hours before the injury were subjected to 50% TBSA full-thickness burns, and were randomly divided into following four groups: no resuscitation group (group NR), venous fluid resuscitation group (group R), PNU-282987 treatment group (group P), and fluid resuscitation group plus PNU-282987 group (group RP), with 10 dogs in each group. Hemodynamic variables and biochemical parameters were determined with animals in a conscious and cooperative state. The plasma volume and the vasopermeability were determined by indocyanine green and fluorescein isothiocyanate-dextran, respectively. The level of tumor necrosis factor-α and interleukin-1β in plasma, and the water content of different organs were also determined. The mean arterial pressure, cardiac output, and plasma volume of all dogs decreased significantly, and the lung extravascular water index and pulmonary vascular permeability index increased remarkably after burn. The hemodynamic parameters deteriorated continually in group N dogs, and then anuria, hyperlactacidemia, and multiple organ dysfunctions developed. The mean arterial pressure and cardiac output of dogs in group R and group RP returned to preinjury levels at 48 hours postburn. The lung extravascular water index and pulmonary vascular permeability in group R were higher than those before preinjury. The dogs in group RP were found to have a significant increase in plasma volume and urine output, and a remarkable decrease in the levels of tumor necrosis factor-α, interleukin-1α, lactic acid, and organ functions compared with those of group R (P <.05). The survival rate of RP group (100%; 10/10) was significantly higher than that of group N (0; 0/10), group P (20%; 2/10), and group R (60%; 6/10). PNU-282987 combined with intravenous fluid resuscitation significantly improved hemodynamics and the survival rate in the early period after this lethal burn shock. The mechanism may be attributable to the lowering of the level of proinflammatory mediators, amelioration of vasopermeability-induced visceral edema, less of blood volume loss, and protection of vital organs through activation of cholinergic anti-inflammatory pathway.

Evaluation of a commercial ultrasonographic hemodynamic recording system for the measurement of cardiac output in dogs

To evaluate the accuracy of a commercial ultrasonographic cardiac output (CO) monitoring system (UCOMS) in anesthetized Beagles as assessed by comparison with thermodilution CO (TDCO). 8 healthy anesthetized Beagles. Simultaneous UCOMS and TDCO measurements of CO were obtained during 4 hemodynamic states: baseline anesthesia (0.5% to 1.5% isoflurane), a higher depth of anesthesia (2% to 3.5% isoflurane) to yield a >or= 15% reduction in systolic arterial blood pressure, IV infusion of colloidal solution to a mean right atrial pressure of >or= 15 mm Hg, and IV infusion of dobutamine at 5 microg/kg/min. Measurements were obtained at 2 probe positions: the subxiphoid region and the right thoracic inlet. Correlation and agreement of results between methods were determined via linear regression analysis and Bland-Altman plots. A significant positive correlation was detected between UCOMS andTDCO measurements obtained at the subxiphoid (R = 0.86) and thoracic inlet (R = 0.83) positions. Bland-Altman plots revealed minimal bias between methods (bias +/- SD, -0.03 +/- 0.73 L/min and -0.20 +/- 0.80 L/min for subxiphoid and thoracic inlet measurements, respectively). However, the percentage error associated with UCOMS measurements made at the 2 positions was > 45%. When compared with the results of TDCO, CO measured with the UCOMS exceeded commonly accepted limits of error in healthy dogs. The UCOMS was, however, able to track changes in CO across hemodynamic states. Additional research is needed to assess the usefulness of the UCOMS for monitoring CO in critically ill dogs.

Cardiovascular Responses to the Induction of Mild Hypothermia in the Presence of Epidural Anesthesia

The combining of epidural anesthesia with general anesthesia impairs central and peripheral thermoregulatory control and therefore is often accompanied by unintended intraoperative hypothermia. However, little is known about the cardiovascular response to hypothermia during combined epidural and general anesthesia. The authors assessed the effects of hypothermia during such combined anesthesia. The authors randomly assigned 30 mongrel dogs anesthetized with isoflurane (1.0%) to three groups of 10: control, receiving general anesthesia alone; thoracic injection, additionally receiving thoracic epidural anesthesia; and lumbar injection, additionally receiving thoracolumbar epidural anesthesia. Core temperature was lowered from 38.5 degrees C to approximately 34 degrees C (mild hypothermia) using a femoral arteriovenous shunt in an external cool water bath. During hypothermia, the authors measured heart rate, cardiac output, and plasma catecholamine concentrations in each group. Ejection fraction was also measured using echocardiography. Compared with measurements during baseline conditions (general anesthesia alone with no epidural injection and no hypothermia) in the control, thoracic, and lumbar injection groups, the injections followed by hypothermia produced 17, 32, and 41% decreases in heart rate; 22, 32, and 47% reductions in cardiac output; 66, 85, and 92% decreases in the epinephrine concentrations; and 27, 44, and 85% decreases in the norepinephrine concentrations. In contrast, ejection fraction did not change in any group. Mild hypothermia during combined epidural anesthesia and general anesthesia markedly reduced cardiac output in dogs, mainly by decreasing heart rate.

Cardiac Output during Total Hip Replacement in Dogs

SummaryTrans-oesophageal pulsed-wave Doppler echocardiography was evaluated as a noninvasive method of determining cardiac output during total hip replacement in 10 dogs. Cardiac output was estimated by determining the crosssectional area of the aorta via caudal transverse echocardiography and the outflow velocity of the ascending aorta via cranial transverse Doppler echocardiography. Thermodilution was used as the reference method. In addition, cardiopulmonary changes, at the time of femoral prosthesis insertion, were determined. Comparison of 160 measurements yielded a correlation coefficient of 0.48. Linear regression analysis revealed the equation, cardiac outputDoppler echocardiography = 0.45 cardiac outputthermodilution + 3.3. In comparison to thermodilution, trans-oesophageal pulsedwave Doppler echocardiography overestimated cardiac output at flow rates less than 61/min and underestimated the cardiac output at flow rates greater than 61/min. There was a significant decrease in the partial pressure of carbon dioxide at end-expiration (PETCO2), the systolic arterial blood pressure (mmHg) and the invasive stroke volume (ml/beat/m2) and a significant increase in the pulmonary vascular resistance (dynes/sec/cm5) immediately after insertion of the femoral prosthesis.The purpose of this study was to evaluate the trans-oesophageal pulsed-wave Doppler echocardiography as a noninvasive method of determining cardiac output in dogs during total hip replacement. Thermodilution was used as the reference method. The correlation coefficient was r = 0.48. In conclusion, this study confirms that the trans-oesophageal Doppler echocardiography is not suitable for measuring the absolute CO-value. This ultrasound technique only allows an approximate estimation of the CO-trend.

Hemodynamic effects of pyruvate infusion in dogs

Purpose: Although pyruvate supplementation enhances endurance in humans and increases cardiac output in dogs, its effects on cardiac and peripheral vascular function are not known. Thus, we assessed the cardiovascular effects of pyruvate infusion. Materials and Methods: Aortic, left ventricular (LV), and pulmonary (Ppa) pressures and LV stroke volume (Sv lv; derived from aortic flow probe) were measured after thoracotomy in eight anesthetized dogs. LV area or volume changes were measured using either an epicardial echocardiography (n = 6) or a conductance catheter (n = 2). LV end-systolic elastance (Ees lv) and preload recruitable stroke force (PRSF lv) relations, as estimates of contractility, were generated by transient inferior vena cave occlusion. Simultaneous stroke volume to arterial pressure relations during the occlusions were used to measure arterial elastance (Ea), and steady-state systemic and pulmonary vascular resistances were used as measures of arterial tone. Graded doses of pyruvate (8, 16, and 32 mg/kg/min), dobutamine (positive control) and propranolol (negative control) and placebo (volume control) were sequentially given. Results: Dobutamine increased Ees lv PRSF lv, whereas propranolol had the opposite effect on Ees lv and PRSF lv. Pyruvate at 32 mg/kg/min increased heart rate, Ppa, and SV lv and decreased LV end-diastolic area, and systemic vascular resistance without changing arterial pressure, Ees lv PRSF lv. or Ea. Conclusions: We conclude that pyruvate infusion in normal dogs induces venodilation but does not alter either cardiac contractility or arterial tone.

Monitoring urine oxygen tension during acute change in cardiac output in dogs.

To evaluate whether renal blood flow (RBF) can be monitored during acute change in cardiac index, ureter urine oxygen tension (PuO2) and bladder urine oxygen tension (PbO2) were measured in six mongrel dogs. PuO2, cardiac index, and RBF increased after dobutamine infusion and decreased after propranolol infusion. PuO2 had an excellent correlation with RBF (r = 0.94) and a fair correlation with cardiac index (r = 0.50) and mean blood pressure (r = 0.56); RBF had a fair correlation with mean blood pressure (r = 0.52, P < 0.05) but was not related to cardiac index. With multiple-regression analysis, PuO2 was found to be the significant factor related to RBF. PbO2 had a good correlation with PuO2 (r = 0.94) at control levels. Furthermore, when two dogs were added to evaluate relationships among PbO2, PuO2, and RBF, PbO2 had an excellent correlation with PuO2 (r = 0.92) and RBF (r = 0.91). These data indicate that PuO2 is a more sensitive predictor of RBF than cardiac index and mean blood pressure and that PbO2 can be a noninvasive indicator reflecting RBF during acute circulatory change in dogs.

全脊髄麻酔を用いた表面冷却低体温時の臓器血流分布に関する研究

全脊髄麻酔を用いた表面冷却低体温時の臓器血流分布に関する研究

Does atrial appendectomy aggravate secretory function of atrial natriuretic polypeptide?

The present study was designed to clarify how atrial appendectomy affects hemodynamics and secretory function of atrial natriuretic polypeptide in the failing heart. Eleven mongrel dogs were prepared for the experimental model of high-output heart failure by creation of arteriovenous fistulas between femoral arteries and veins. Two months after the first operation, effects of bilateral atrial appendectomies on basal and pacing-induced secretions of atrial natriuretic polypeptide were investigated in five dogs with simultaneous measurement of various hemodynamic indices. In the remaining six dogs, used as a control group, pacing-induced secretion of atrial natriuretic polypeptide was examined in the same way as in the appendectomy group. After excision of the atrial appendages, neither systolic blood pressure nor either atrial pressure changed, but plasma atrial natriuretic polypeptide level was decreased (292 +/- 54 to 188 +/- 47 pg/ml, p less than 0.01) and cardiac output fell (3.7 +/- 0.9 to 3.0 +/- 0.8 L/min, p less than 0.01). During pacing-induced tachycardia, the peak level of plasma atrial natriuretic polypeptide was lower in the appendectomy group than in the control groups (593 +/- 213 versus 1170 +/- 324 pg/ml, p less than 0.05), despite similar left atrial pressures in the two groups. The excised appendages contained approximately 30% of the total amount of atrial natriuretic polypeptide. These results demonstrate that atrial appendectomy decreases secretory function of atrial natriuretic polypeptide and reduces cardiac output in dogs with experimental high-output heart failure.

The Effects of Methoxamine and Epinephrine on Survival and Regional Distribution of Cardiac Output in Dogs with Prolonged Ventricular Fibrillation

This study compares the effects of methoxamine, a pure alpha 1-agonist, and epinephrine on cerebral and myocardial blood flow, central hemodynamics, and survival in a randomized placebo-controlled fashion during prolonged ventricular fibrillation (VF) in a canine model. Twenty-four anesthetized and ventilated adult mongrel dogs were instrumented for regional blood flow determinations using radio-labeled microspheres. The dogs were randomized to receive either 20 mg of methoxamine as a single intravenous bolus or repeated boluses of 0.02 mg/kg of epinephrine, 0.2 mg/kg of epinephrine, or normal saline solution placebo beginning at three minutes following induction of VF and initiation of closed chest cardiac massage (CCCM). Organ blood flow measurements were determined during normal sinus rhythm and after five and 20 minutes of VF. All six dogs receiving methoxamine were successfully resuscitated in contrast to only one in each of the epinephrine-treated groups and none of the dogs receiving placebo (p less than .01). Although epinephrine was associated with significantly higher blood pressures than placebo during cardiopulmonary resuscitation (CPR), blood pressures achieved with methoxamine were significantly higher than those observed in the other three treatment groups (p less than .001). Cerebral blood flow was significantly higher with both methoxamine and high-dose epinephrine (p less than .05). Mean left and right ventricular myocardial flows were highest with methoxamine but this did not achieve statistical significance. In contrast, organ flows measured in the animals receiving the lowest dose of epinephrine were not significantly higher than those associated with placebo. Cardiac output after 20 minutes of CPR was significantly lower with high-dose epinephrine than with methoxamine or placebo (p less than .05). Our results suggest that methoxamine significantly improves regional cerebral blood flow and survival during CPR and although high-dose epinephrine is associated with comparable improvements in regional cerebral blood flow, this treatment is associated with deterioration in central hemodynamics during prolonged VF and does not enhance survival.

Acute respiratory acidosis decreases left ventricular contractility but increases cardiac output in dogs.

To understand the cardiovascular response to respiratory acidosis, we measured hemodynamics, left ventricular pressure, and left ventricular volume (three ultrasonic crystal pairs) during eucapnia and respiratory acidosis in 10 fentanyl-anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope (Emax) and intercept (V0) of the left ventricular end-systolic pressure-volume relation determined by combining end-systolic points from a vena caval occlusion and from brief aortic cross-clamping. Respiratory acidosis (pH 7.09, Pco2 92 mm Hg) reduced contractility by a decrease in Emax (11.4 to 9.2 mm Hg/ml, p less than 0.01) with no change in V0. Despite this, cardiac output increased (1.7 to 2.1 l/min, p less than 0.01), and heart rate increased (96 to 121 beats/min, p less than 0.05), with no change in blood pressure. Systemic vascular resistance fell by 26% (p less than 0.01). During eucapnia, propranolol reduced Emax (11.4 to 4.6 mm Hg/ml, p less than 0.01) with no change in V0. After propranolol treatment, respiratory acidosis further reduced Emax (4.6 to 3.6 mm Hg/ml, p less than 0.05) and increased end-systolic volume more than before propranolol (p less than 0.001). Now cardiac output did not increase even though heart rate increased (81 to 106 beats/min, p less than 0.001) and systemic vascular resistance fell by 20% (p less than 0.01). We conclude that the effect of respiratory acidosis on the circulation is to increase venous return (equals cardiac output) in the face of decreased left ventricular contractility. The beta-adrenergic response to respiratory acidosis substantially ameliorated the increase in end-systolic volume and supported the increase in venous return but did not alter the associated tachycardia or vasodilation. Respiratory acidosis, like propranolol treatment, decreases contractility by decreasing Emax.

Effect of negative-pressure ventilation on lung water in permeability pulmonary edema

We have previously shown (Am. Rev. Respir. Dis. 136: 886-891, 1987) improved cardiac output in dogs with pulmonary edema ventilated with external continuous negative chest pressure ventilation (CNPV) using negative end-expiratory pressure (NEEP), compared with continuous positive-pressure ventilation (CPPV) using equivalent positive end-expiratory pressure (PEEP). The present study examined the effect on lung water of CNPV compared with CPPV to determine whether the increased venous return created by NEEP worsened pulmonary edema in dogs with acute lung injury. Oleic acid (0.06 ml/kg) was administered to 27 anesthetized dogs. Supine animals were then divided into three groups and ventilated for 6 h. The first group (n = 10) was treated with intermittent positive-pressure ventilation (IPPV) alone; the second (n = 9) received CNPV with 10 cmH2O NEEP; the third (n = 8) received CPPV with 10 cmH2O PEEP. CNPV and CPPV produced similar improvements in oxygenation over IPPV. However, cardiac output was significantly depressed by CPPV, but not by CNPV, when compared with IPPV. Although there were no differences in extravascular lung water (Qwl/dQl) between CNPV and CPPV, both significantly increased Qwl/dQl compared with IPPV (7.81 +/- 0.21 and 7.87 +/- 0.31 vs. 6.71 +/- 0.25, respectively, P less than 0.01 in both instances). CNPV and CPPV, but not IPPV, enhanced lung water accumulation in the perihilar areas where interstitial pressures may be most negative at higher lung volumes.

Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac assistance with electrically stimulated skeletal muscle

This study examined the ability of a skeletal muscle-powered assist ventricle (SMV) to augment cardiac output in ten dogs with pharmacologically induced heart failure under acute conditions. An SMV was surgically constructed in each dog by wrapping the untrained rectus abdominis muscle around a compressible pouch that was inserted into a left ventricular apex-to-aortic vascular conduit. The multiple motor nerves to the rectus muscle were then stimulated during ventricular diastole at a rate which equalled a ratio of 1:2, 1:3, or 1:4 with the natural ventricular beat. There was an increased cardiac output during SMV assistance compared with preassistance values in all ten dogs at each stimulation ratio with a mean increase of 46 +/- 4 per cent with a ratio of 1:2, 25 +/- 4 per cent with a ratio of 1:3, and 31 +/- 7 per cent with a ratio of 1:4 (p less than 0.01 for all values). The diastolic blood pressure and mean blood pressure were both increased (p less than 0.01 and p less than 0.05, respectively) during SMV stimulation at ratios of 1:2 and 1:3, but not 1:4. We have shown that untrained rectus abdominis muscle, when used as the power supply for a SMV in an apico-aortic conduit, can temporarily augment cardiac output in dogs with pharmacologically induced heart failure.

Transtracheal Doppler

An endotracheal tube with a 5 mm diameter ultrasonic transducer incorporated into its distal end was inserted into the tracheas of six anesthetized dogs. The device provides for ultrasound measurement of aortic diameter and blood velocity in the ascending aorta to obtain cardiac outputs. Because measurements are made proximal to the origins of the aortic arch vessels, total cardiac output is obtained. Procedures for measurement of aortic diameter, aortic blood velocity, and cardiac output are discussed. The resulting data were used to empirically determine the angle of incidence of the ultrasound beam that gave the best least squares fit over a range of thermodilution cardiac outputs. For an angle of incidence of 62.3 degrees, the relationship between cardiac output determined by thermal dilution and by transtracheal Doppler was transtracheal Doppler cardiac output = -.69 + 1.19 thermal dilution cardiac output. R2 = .82. The results from this preliminary assessment of the feasibility of measuring cardiac output in dogs using transtracheal Doppler suggest that additional studies should be pursued. Additional issues that require investigation include confirmation of constancy of human anatomy and demonstration of lack of tracheal trauma from the Doppler equipped endotracheal tube.

P-362 - Effects of midodrine and its active metabolite, ST-1059, on cardiac output in dogs

P-362 - Effects of midodrine and its active metabolite, ST-1059, on cardiac output in dogs

Effect of cardiac output on extravascular lung water measurements made with the thermoconductivity method.

The authors tested the effects of injectate temperature and of changing cardiac output on the measurement of lung water by the thermoconductivity technique (ETVL). Cardiac output in dogs was increased and decreased with isoproterenol and halothane, respectively. Post mortem extravascular lung water (pulmonary extravascular tissue weight [PETW] was determined using a weighing technique. Cardiac output varied between 0.7 and 8.8 l/min and did not influence the ETVL measurement. The authors conclude ETVL measured by the thermoconductivity technique is not influenced by large changes in cardiac output.