Cardiac Output Derived From Left Ventricular Pressure During Conductance Catheter Evaluations: An Extended Modelflow Method

2007 ◽  
Vol 21 (4) ◽  
pp. 227-235
Author(s):  
Sergio Valsecchi ◽  
Giovanni B. Perego ◽  
Jan J. Schreuder ◽  
Federica Censi ◽  
Jos R. C. Jansen
Keyword(s):  
Cardiac Output ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter

Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 2010-2017 ◽  
Author(s):  
J.J. Schreuder ◽  
F.H. van der Veen ◽  
E.T. van der Velde ◽  
F. Delahaye ◽  
O. Alfieri ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter ◽  
Volume Relation

Left Heart Bypass in the Pig with a Centrifugal Pump Using Cannulae Prepared for Percutaneous Placement

1998 ◽  
Vol 21 (5) ◽  
pp. 285-290 ◽  
Author(s):  
B.H. Walpoth ◽  
V. Mehan ◽  
R. Rogulenko ◽  
B. Aeschbacher ◽  
G. Vucic ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Centrifugal Pump ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Left Heart ◽  
Mean Flow ◽  
Left Heart Bypass ◽  
Heart Bypass

A rapid and efficient circulatory support system may save a patient in cardiogenic shock. Left heart bypass with percutaneous and trans-septal placement of the aspiration cannula simplifies the circuit and eliminates the need for an oxygenator. In this pre-clinical study we assessed left heart bypass support with a centrifugal pump using new cannulae prepared for percutaneous placement (14 F arterial catheter and 16 F left atrial aspiration line) in 5 anaesthetized pigs. Animals were supported for two hours at a mean flow of 3.2 l/min (4,033 rpm), a mean haematocrit of 29% and low heparinisation (ACT double baseline). Hemodynamic measurements and blood samples were taken at baseline (A), 10 minutes (B), one hour (C) and 2 hours (D) on support. Results show maintenance of hemodynamic parameters throughout the 2 hour support period. Only systolic arterial and left ventricular pressure decreased by 12% and 20% respectively from baseline to the end of the support period with a 13% increase in cardiac output. When the pump was turned on (0–3 l/min) there was usually a decrease in heart rate, systolic pressure and left ventricular pressure, with unchanged cardiac output (non failing model). Potassium increased from 3.9 to 4.2 mmol/l (ns), and plasma hemoglobin from 6.0 to 18.2 mg/dl (p<0.05). Thrombocytes decreased from 187 to 155 109/1 (ns). In conclusion, this preclinical study demonstrated the feasibility of an efficient left heart bypass of short duration with a centrifugal pump using cannulae prepared for percutaneous placement. Left heart bypass was well tolerated hemodynamically and no significant laboratory change occurred within the two hours of support. This opens several possibilities for the short term support of patients in cardiogenic shock and eventually also for patients submitted to minimally invasive cardiac surgery.

Effect of lactic acidosis on canine hemodynamics and left ventricular function

1990 ◽  
Vol 258 (4) ◽  
pp. H1193-H1199 ◽  
Author(s):  
K. Teplinsky ◽  
M. O'Toole ◽  
M. Olman ◽  
K. R. Walley ◽  
L. D. Wood
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
Stroke Volume ◽  
Venous Return ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Lactic Acidemia

Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. We reasoned that examination of left ventricular pressure-volume relationships at end systole and end diastole would determine which of these potential mechanisms accounted for reduced cardiac output during progressive lactic acidosis in anesthetized, mechanically ventilated dogs. Left ventricular (LV) volume was estimated from two pairs of epicardial ultrasonic crystals placed in the anterior-posterior and longitudinal planes, and LV pressure was obtained rom a catheter-tipped transducer. During progressive acidemia induced by a continuous intravenous infusion of 0.5 N lactic acid, cardiac output, stroke volume, and mean systemic arterial pressure fell significantly while mean pulmonary artery pressure and right atrial pressure increased significantly. These variables did not change with time in control (no-acid infusion) dogs. Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.

scholarly journals Pharmacodynamics and Pharmacokinetics of Injectable Pimobendan and Its Metabolite, O-Desmethyl-Pimobendan, in Healthy Dogs

2021 ◽  
Vol 8 ◽  
Author(s):  
Poonavit Pichayapaiboon ◽  
Lalida Tantisuwat ◽  
Pakit Boonpala ◽  
Nakkawee Saengklub ◽  
Tussapon Boonyarattanasoonthorn ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Maximum Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial

Objectives: This study was designed to thoroughly evaluate the effects of bolus pimobendan at a dose of 0.15 mg/kg on cardiac functions, hemodynamics, and electrocardiographic parameters together with the pharmacokinetic profile of pimobendan and its active metabolite, o-desmethyl-pimobendan (ODMP), in anesthetized dogs.Methods: Nine beagle dogs were anesthetized and instrumented to obtain left ventricular pressures, aortic pressures, cardiac outputs, right atrial pressures, pulmonary arterial pressures, pulmonary capillary wedge pressures, electrocardiograms. After baseline data were collected, dogs were given a single bolus of pimobendan, and the pharmacodynamic parameters were obtained at 10, 20, 30, 60, and 120 min. Meanwhile, the venous blood was collected at baseline and 2, 5, 10, 20, 30, 60, 120, 180, 360, and 1,440 min after administration for the determination of pharmacokinetic parameters.Results: Compared with baseline measurements, the left ventricular inotropic indices significantly increased in response to intravenous pimobendan, as inferred from the maximum rate of rise in the left ventricular pressure and the contractility index. Conversely, the left ventricular lusitropic parameters significantly decreased, as inferred from the maximum rate of fall in the left ventricular pressure and the left ventricular relaxation time constant. Significant increases were also noted in cardiac output and systolic blood pressure. Decreases were observed in the systemic vascular resistance, pulmonary vascular resistance, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. The heart rate increased, but the PQ interval decreased. There was no arrhythmia during the observed period (2 h). The mean maximum plasma concentration (in μg/L) for ODMP was 30.0 ± 8.8. Pimobendan exerted large volume of distribution ~9 L/kg.Conclusions: Intravenous pimobendan at the recommended dose for dogs increased cardiac contraction and cardiac output, accelerated cardiac relaxation but decreased both vascular resistances. These mechanisms support the use of injectable pimobendan in acute heart failure.

Vasopressin contributes to the cardiovascular response to dynamic exercise

1993 ◽  
Vol 264 (5) ◽  
pp. H1701-H1707 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Ventricular Pressure ◽  
Receptor Inhibition ◽  
Exercise Induced ◽  
Developed Pressure

Vasopressin is a powerful vasoconstrictor that is released into the systemic circulation during exercise. We tested the hypothesis that this peptide contributes to the cardiovascular response during treadmill exercise in the pig. Seventeen miniswine were instrumented with epicardial electrocardiogram leads, left atrial and aortic catheters, and a left ventricular pressure transducer for measurement of heart rate (HR), regional blood flow, arterial blood pressure (MAP), and myocardial contractility [first derivative of left ventricular pressure (dP/dt) at 40 mmHg developed pressure] at rest and during exercise. At a work intensity of 80% of each animal's maximal HR reserve, exercise-induced increases in MAP, HR, dP/dt at 40 mmHg developed pressure, and cardiac output were measured. On a separate day, the workload performed by each animal was replicated in the presence of selective vasopressin V1-receptor inhibition using the specific V1 antagonist, [d(CH2)5Tyr(Me)]arginine vasopressin (10-14 micrograms/kg iv). During exercise, MAP was lower (96 +/- 3 vs. 104 +/- 2 mmHg) and cardiac output was higher (13.5 +/- 0.6 vs. 12.6 +/- 1.0 l/min) in the presence of V1-receptor blockade than during unblocked conditions, respectively. Furthermore, we observed an attenuation of exercise-induced decreases in blood flow to the colon. Increases in vascular resistance in the stomach, small intestine, colon, and pancreas also were diminished by V1-receptor inhibition. However, HR and myocardial contractile responses to exercise were not affected. These results suggest that vasopressin contributes to increases in MAP and to the redistribution of cardiac output during dynamic exercise in the miniswine.

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