Cardiac output assessment using oxygen consumption estimated from the left ventricular pressure-volume area

2010 ◽  
Author(s):  
J A Negroni ◽  
E C Lascano ◽  
A M Bertolotti ◽  
Carmen B Gómez ◽  
Carlos A Rodríguez Correa ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure

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.

Nicotine increases heart adenosine release, oxygen consumption, and contractility

1985 ◽  
Vol 249 (3) ◽  
pp. H463-H469 ◽  
Author(s):  
R. A. Fenton ◽  
J. G. Dobson
Keyword(s):  
Oxygen Consumption ◽  
Cardiac Contractility ◽  
Left Ventricular Pressure ◽  
Physiological Saline ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adenosine Release ◽  
Adenosine Uptake ◽  
Pressure Development ◽  
Transient Elevation

The effect of nicotine on adenosine release, oxygen consumption, and contractility was investigated in perfused rat hearts. Continuous infusion of nicotine into the perfusing physiological saline (PS) elicited a propranolol (10(-6) M) sensitive transient elevation of developed left ventricular pressure (LVP) and maximum rates of left ventricular pressure development and relaxation (+/- dP/dtmax) within 20 s, which subsequently declined to maintained elevated plateau levels by 1 min. The continuous infusions of nicotine to achieve PS concentrations of 5 X 10(-4), 1 X 10(-4), or 5 X 10(-5) M, respectively resulted in significant increases in the mean plateau levels of LVP (33.4, 10.1, or 6.3%), +dP/dtmax (26.3, 10.8, or 6.9%) and-dP/dtmax (35.0, 11.9, or 9.0%) at 1 min. The inclusion of propranolol (10(-6) M) with or without atropine (10(-6) M) did not alter these maintained plateau responses to nicotine. During the plateau phase of the contractile response oxygen consumption of the hearts was significantly elevated by 36, 19, or 11%, and mean levels for adenosine in the coronary effluent rose by 261, 76, or 74% in response to 5 X 10(-4), 1 X 10(-4), or 5 X 10(-5) M nicotine, respectively. Nicotine did not influence [14C]adenosine uptake by the hearts. These results suggest that nicotine is capable of 1) augmenting cardiac contractility and oxygen consumption independent of beta-adrenergic or muscarinic influence, and 2) elevating the appearance of adenosine in the coronary circulation presumably by enhancing myocardial production of the nucleoside.

Sign in / Sign up

Export Citation Format

Share Document