Cardiovascular and pulmonary effects of morphine in conscious pigs

1991 ◽  
Vol 261 (5) ◽  
pp. R1286-R1293 ◽  
Author(s):  
J. P. Hannon ◽  
C. A. Bossone
Keyword(s):  
Cardiac Output ◽  
Hemoglobin Concentration ◽  
Hemoglobin Saturation ◽  
Morphine Administration ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Left And Right ◽  
O2 Delivery ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

Cardiovascular and pulmonary effects of morphine (1 mg/kg bolus iv) were investigated in conscious chronically instrumented pigs, a species exhibiting an excitable response. Control animals received an equivalent volume (less than 2 ml) of normal saline. Morphine induced an immediate but small increase in cardiac output and substantial increases in heart rate, mean systemic and pulmonary arterial pressure, left and right ventricular work, hematocrit, and hemoglobin concentration, but did not change stroke volume or systemic vascular resistance. Morphine administration also led to a gradual increase in ventilatory rate and rapid increases in tidal volume, expired and alveolar ventilation, ventilation-perfusion ratio, and shunt fraction. In addition, morphine administration produced substantial decrements in arterial and mixed venous PO2, hemoglobin saturation and mixed venous O2 content; no change in arterial O2 content; and a widening of the arteriovenous O2 difference. Arterial O2 transport was increased slightly. Finally, it produced substantial increments in arterial and mixed venous PCO2 and substantial decrements in arterial and mixed venous pH. It was concluded that arterial O2 delivery did not adequately rise to meet tissue O2 demand, in part because an appropriate increase in cardiac output was attenuated by morphine, and in part because morphine impaired pulmonary gas exchange.

Effect of pentoxiphylline on oxygen transport during hypothermia

1989 ◽  
Vol 66 (1) ◽  
pp. 96-101 ◽  
Author(s):  
M. B. Hershenson ◽  
J. A. Schena ◽  
P. A. Lozano ◽  
M. J. Jacobson ◽  
R. K. Crone
Keyword(s):  
Cardiac Output ◽  
Blood Viscosity ◽  
Critical Level ◽  
Hemoglobin Concentration ◽  
Base Line ◽  
Mechanically Ventilated ◽  
O2 Transport ◽  
O2 Extraction ◽  
O2 Delivery ◽  
Mixed Venous

At least two investigators have demonstrated a reduction in O2 extraction during induced hypothermia (Cain and Bradley, J. Appl. Physiol. 55: 1713–1717, 1983; Schumacker et al., J. Appl. Physiol. 63: 1246–1252, 1987). We hypothesized that administration of pentoxiphylline (PTX), a theobromine that lowers blood viscosity and has vasodilator effects, would increase O2 extraction during hypothermia. To test this hypothesis, we studied O2 transport in anesthetized, paralyzed, mechanically ventilated beagles exposed to hypoxic hypoxia during either 1) normothermia (38 degrees C), 2) hypothermia (30 degrees C), or 3) hypothermia + PTX (30 degrees C and PTX, 20 mg.kg-1.h-1). Measurements included arterial and mixed venous PO2, hemoglobin concentration and saturation, cardiac output, systemic vascular resistance (SVR), blood viscosity, and O2 consumption (VO2). Critical levels of O2 delivery (DO2, the product of arterial O2 content and cardiac output) were determined by a system of linear regression. Hypothermia significantly decreased base line cardiac output (-35%), DO2 (-37%), and VO2 (-45%), while increasing SVR and blood viscosity. Addition of PTX increased cardiac output (35%) and VO2 (14%), and returned SVR and blood viscosity to normothermic levels. Hypothermia alone failed to significantly reduce the critical level of DO2, but addition of PTX did [normothermia, 11.4 +/- 4.2 (SD) ml.kg-1.min-1; hypothermia, 9.3 +/- 3.6; hypothermia + PTX, 6.6 +/- 1.3; P less than 0.05, analysis of variance]. The O2 extraction ratio (VO2/DO2) at the critical level of DO2 was decreased during hypothermia alone (normothermia, 0.60 +/- 0.13; hypothermia, 0.42 +/- 0.16; hypothermia + PTX, 0.62 +/- 0.19; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

Effect of analyzer on determination of mixed venous PCO2 and cardiac output during exercise

1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands
Keyword(s):  
Cardiac Output ◽  
Gas Mixture ◽  
Arterial Pco2 ◽  
Venous Pco2 ◽  
The Face ◽  
High O2 ◽  
Collision Broadening ◽  
Rebreathing Methods ◽  
Mixed Venous

Cardiac output (CO) during exercise can be determined noninvasively by using the indirect Fick CO2-rebreathing technique. CO2 measurements for this technique are usually performed with an infrared analyzer (IA) or mass spectrometer (MS). However, IA CO2 measurements are susceptible to underreading in the face of high O2 concentrations because of collision broadening. We compared an IA (Ametek model CD-3A) with a MS (Marquette model MGA-1100) to see the effect this would have on mixed venous PCO2 (PVCO2) and CO measurements. After calibration with room air and a gas mixture of 5% CO2–12% O2–83% N2, both devices were tested with three different gas mixtures of CO2 in O2. For each gas mixture, IA gave lower CO2 values than did the MS (4.1% CO2: IA, 3.85 +/- 0.01% and MS, 4.13 +/- 0.01%; 9.2% CO2: IA, 8.44 +/- 0.07% and MS, 9.19 +/- 0.01%; 13.8% CO2: IA, 12.57 +/- 0.15% and MS, 13.82 +/- 0.01%). Warming and humidifying the gases did not alter the results. The IA gave lower values than did the MS for eight other medical gases in lower concentrations of O2 (40–50%). Equilibrium and exponential rebreathing procedures were performed. Values determined by the IA were > 10% higher than those determined by the MS for both rebreathing methods. We conclude that all IAs must be checked for collision broadening if they are to be used in environments where the concentration of O2 is > 21%. If collision broadening is present, then either a special high O2-CO2 calibration curve must be constructed, or the IA should not be used for both arterial PCO2 and PVCO2 estimates because it may produce erroneously low PVCO2 values, with resultant overestimation of CO.

Ventilation-perfusion relationships with high cardiac output in lobar atelectasis

1981 ◽  
Vol 50 (2) ◽  
pp. 341-347 ◽  
Author(s):  
P. T. Schumacker ◽  
J. C. Newell ◽  
T. M. Saba ◽  
S. R. Powers
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Shunt Fraction ◽  
Mechanically Ventilated ◽  
Arteriovenous Fistulas ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
Mixed Venous

Pulmonary gas exchange was evaluated in 10 anesthetized mechanically ventilated dogs. Cardiac output (QT) was increased approximately 50% by opening peripheral arteriovenous fistulas. With both lungs ventilated, increasing QT increased mixed venous O2 both pressure (PO2) and pulmonary arterial pressure, but neither shunt fraction nor the distribution of ventilation-perfusion was consistently altered. During left lung atelectasis, increasing QT again increased mixed venous PO2 and pulmonary arterial pressure, but two different responses in shunt-like perfusion were measured. In four dogs, left lung atelectasis caused a shunt fraction of 46 +/- 6% that was not changed by high QT (P greater than 0.05). In six dogs, atelectasis caused a shunt fraction of 24 +/- 3% during normal QT that increased to 42 +/- 2% during high QT (P less than 0.001). Dogs whose shunt fraction during atelectasis was high and unchanged by QT had lower arterial pH (7.24 +/- 0.03) than dogs whose shunt fraction was initially lower and was increased with QT (7.36 +/- 0.02) (P less than 0.01). We conclude that increased QT can worsen shunt flow during lobar atelectasis when hypoxic vasoconstriction has been effective in limiting perfusion to the collapsed region at normal levels of QT.

A modelling study of atrial septostomy for pulmonary arterial hypertension, and its effect on the state of tissue oxygenation and systemic blood flow

2010 ◽  
Vol 20 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Gerhard-Paul Diller ◽  
Astrid E. Lammers ◽  
Sheila G. Haworth ◽  
Konstantinos Dimopoulos ◽  
Graham Derrick ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Tissue Oxygenation ◽  
Arterial Blood ◽  
Atrial Septostomy ◽  
Pulmonary Arterial ◽  
Mixed Venous ◽  
Content Of Oxygen

AbstractAtrial septostomy is performed in patients with severe pulmonary arterial hypertension, and has been shown to improve symptoms, quality of life and survival. Despite recognized clinical benefits, the underlying pathophysiologic mechanisms are poorly understood. We aimed to assess the effects of right-to-left shunting on arterial delivery of oxygen, mixed venous content of oxygen, and systemic cardiac output in patients with pulmonary arterial hypertension and a fixed flow of blood to the lungs. We formulated equations defining the mandatory relationship between physiologic variables and delivery of oxygen in patients with right-to-left shunting. Using calculus and computer modelling, we considered the simultaneous effects of right-to-left shunting on physiologies with different pulmonary flows, total metabolic rates, and capacities for carrying oxygen. Our study indicates that, when the flow of blood to the lungs is fixed, increasing right-to-left shunting improves systemic cardiac output, arterial blood pressure, and arterial delivery of oxygen. In contrast, the mixed venous content of oxygen, which mirrors the average state of tissue oxygenation, remains unchanged. Our model suggests that increasing the volume of right-to-left shunting cannot compensate for right ventricular failure. Atrial septostomy in the setting of pulmonary arterial hypertension, therefore, increases the arterial delivery of oxygen, but the mixed systemic saturation of oxygen, arguably the most important index of tissue oxygenation, stays constant. Our data suggest that the clinically observed beneficial effects of atrial septostomy are the result of improved flow of blood rather than augmented tissue oxygenation, provided that right ventricular function is adequate.

Effect of simulated altitude erythrocythemia in women on hemoglobin flow rate during exercise

1988 ◽  
Vol 64 (4) ◽  
pp. 1644-1649 ◽  
Author(s):  
R. J. Robertson ◽  
R. Gilcher ◽  
K. F. Metz ◽  
C. J. Caspersen ◽  
T. G. Allison ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Flow Rate ◽  
Maximal Exercise ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Peak Exercise ◽  
Simulated Altitude ◽  
Test Conditions ◽  
Placebo Infusion ◽  
Mixed Venous

The effect of simulated altitude erythrocythemia on hemoglobin flow rate and maximal O2 uptake (VO2max) was determined for nine women sea-level residents. Test conditions included normoxia and normobaric hypoxia (16% O2-84% N2). Cycle tests were performed under normoxia (T1-N) and hypoxia (T1-H) at prereinfusion control and under hypoxia 48 h after a placebo infusion (T2-H) and 48 h after autologous infusion of 334 ml of erythrocytes (T3-H). Hematocrit (38.1-44.9%) and hemoglobin concentration (12.7-14.7 g.dl-1) increased from control to postreinfusion. At peak exercise, VO2max decreased from T1-N (2.40 l.min-1) to T1-H (2.15 l.min-1) then increased at T3-H (2.37 l.min-1). Maximal arterial-mixed venous O2 difference decreased from T1-N to T1-H and increased at T3-H. Cardiac output (Q), stroke volume, heart rate, and total peripheral resistance during maximal exercise were unchanged from T1-N through T3-H. Hemoglobin flow rate (Hb flow) at maximum did not change from T1-N to T1-H but increased at T3-H. When compared with submaximal values for T1-N, VO2 was unchanged at T1-H and T3-H; Q increased at T1-H and decreased at T3-H; arterial-mixed venous O2 difference decreased at T1-H and increased at T3-H; Hb flow did not change at T1-N but increased at T3-H. For young women, simulated altitude erythrocythemia increased peak Hb flow and decreased physiological altitude (227.8 m) but did not affect maximum cardiac output (Qmax).

scholarly journals Transition from selexipag to oral treprostinil in a patient with pulmonary arterial hypertension

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401989803 ◽  
Author(s):  
Ifeoma Oriaku ◽  
Amol Patel ◽  
Zeenat Safdar
Keyword(s):  
Cardiac Output ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Maximum Dose ◽  
Mixed Venous Oxygen Saturation ◽  
Maximal Dose ◽  
Venous Oxygen Saturation ◽  
Pulmonary Arterial ◽  
Mixed Venous ◽  
Severe Pulmonary Arterial Hypertension

Prostacyclins are the mainstay treatment for patients with severe pulmonary arterial hypertension. This case highlights the transition from selexipag to oral treprostinil. Our patient improved both subjectively and objectively. Cardiac output and index, as measured by the echocardiogram, improved 12% and 7.7%, respectively. Invasive hemodynamic data revealed greater improvements: cardiac output improved by 25% and cardiac index by 28%. Mixed venous oxygen saturation improved from 65% to 71%. A possible explanation is that selexipag has a maximal dose, whereas there is no recommended maximum dose of oral treprostinil. Another theory is oral treprostinil has higher affinity to the IP receptor, though selexipag has a higher specificity. However, there are no bio-equivalency data, and data comparing pharmacodynamics of both drugs are lacking. Furthermore, no head-to-head trials comparing these agents exist.

An Evaluation of Rebreathing Methods for Measuring Mixed Venous Pco2 During Exercise

1972 ◽  
Vol 42 (3) ◽  
pp. 345-353 ◽  
Author(s):  
S. Godfrey ◽  
Eliana Wolf
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Direct Methods ◽  
Extrapolation Method ◽  
Venous Pco2 ◽  
Technical Factors ◽  
End Tidal ◽  
Male Subjects ◽  
Rebreathing Methods ◽  
Mixed Venous

1. Measurements have been made of mixed venous Pco2 (PV̄co2) by two methods during exercise at 50 and 100 W in five adult male subjects. 2. The equilibration (plateau) method and the extrapolation (Defares) method were performed alternately, five times each, during the steady-state exercise. 3. The coefficient of variation of PV̄,co2 by the extrapolation method was much higher than that of the plateau method. The PV̄,co2 can be estimated to within ± 1 mmHg by the plateau method, and the derived cardiac output to within ± 0·5 1/min in most cases. The cardiac output calculated by this method agrees closely with that found by direct methods in other studies, whereas the extrapolation method usually overestimates the cardiac output in adults. 4. It is suggested that the degree of variation in the extrapolation method is due to technical factors in construction of the line and to the difficulty of deciding what constitutes the end-tidal Pco2.

Estimation of Cardiac Output from the Rate of Change of Alveolar Carbon Dioxide Pressure during Rebreathing

1980 ◽  
Vol 58 (4) ◽  
pp. 263-270 ◽  
Author(s):  
Mary Winsborough ◽  
J. N. Miller ◽  
D. W. Burgess ◽  
G. Laszlo
Keyword(s):  
Cardiac Output ◽  
Co2 Concentration ◽  
Co2 Exchange ◽  
Rate Of Change ◽  
Venous Pco2 ◽  
The Difference ◽  
Dissociation Curves ◽  
Mixed Venous

1. A new CO2-rebreathing method for estimating cardiac output is described, and compared with a method employing N2O performed at the same time. 2. The subject inhales from a reservoir of 30% O2 in N2 and rebreathes into and out of an empty bag for 10s. 3. Oxygenated mixed venous Pco2 is then determined by rebreathing 7–15% CO2 in O2, the mixture being selected to obtain a plateau of CO2 concentration. 4. Pco2 rises exponentially towards the plateau value during the rebreathing of 30% O2. Cardiac output is calculated from the rate of change of the alveolar—mixed venous Pco2 difference by a differential version of the Fick equation employing published CO2 dissociation curves for whole blood in vitro. 5. The slope of the regression of cardiac output on V̇o2 is similar to that obtained in other studies employing direct Fick measurements. The slope is some 15% greater than obtained with N2O but the difference is significant only when Oz consumption is greater than 2 litres/min. 6. The CO2 dissociation slope of blood does not differ during pulmonary gas exchange in vivo from that determined at equilibrium in vitro. 7. The volume of pulmonary blood available for CO2 exchange may rise to about 1 litre in heavy exercise, with a transit time of 1–2 s in the lungs. 8. The method can be employed for estimating pulmonary blood flow during physiological studies in subjects with normal lungs.

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