Further evidence favoring a cardiac mechanism in irreversible hemorrhagic shock

1962 ◽  
Vol 203 (2) ◽  
pp. 248-252 ◽  
Author(s):  
Jack W. Crowell ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Hemorrhagic Shock ◽  
Blood Volume ◽  
Cardiac Failure ◽  
Left Atrial ◽  
Progressive Failure ◽  
Continuous Recording ◽  
Output Curve ◽  
Early Stages ◽  
The Right

Cardiac output curves of normal dogs and dogs in various stages of hemorrhagic shock were determined with devices for continuous recording of cardiac output and atrial pressures to feed an X-Y recorder. Normal cardiac output curves were recorded during the early stages of shock but, after the animal had developed irreversible shock, a cardiac output curve indicative of cardiac failure was always recorded. As the irreversible shock progressed, successive cardiac output curves indicated progressive failure of the heart. A special feature of these experiments was that by increasing or decreasing the blood volume the cardiac output could be held constant. When the cardiac output was held constant, both the right and left atrial pressures slowly rose to extremely high values as shock progressed, and after a time the heart was unable to maintain normal output at even extremely high atrial pressures. The evidence is entirely consistent with the idea that the irreversible stage in hemorrhagic shock is caused by rapid progressive cardiac failure.

Evidence favoring a cardiac mechanism in irreversible hemorrhagic shock

1961 ◽  
Vol 201 (5) ◽  
pp. 893-896 ◽  
Author(s):  
Jack W. Crowell ◽  
Arthur C. Guyton
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Pulmonary Artery ◽  
Hemorrhagic Shock ◽  
Left Atrial ◽  
Peripheral Resistance ◽  
Arterial System ◽  
Operating Parameters ◽  
The Right ◽  
Oxygen Difference

Shock was induced in 55 dogs by removing blood until the arterial pressure had fallen to 30 mm Hg. The pressure was kept at this level for as long as 10 hr by constantly adding additional blood to the reservoir. The hematocrit was kept constant to prevent large variations in the viscosity. Mean pressures of the right and left atrium, the pulmonary artery, and the systemic arterial system were recorded as well as oxygen consumption and A-V oxygen difference. Total peripheral resistance and cardiac output were calculated. That period of time during which the animal passed from a reversible stage of shock to an irreversible stage of shock was studied. It was found that no significant change occurred in oxygen consumption, cardiac output, or peripheral resistance during this transition phase. However, changes did occur in the operating parameters of the heart. The left atrial pressure began rising with the transition from reversible to irreversible shock and continued rising until death of the animal. It is suggested that irreversible hemorrhagic shock is due to acute cardiac failure.

Extracorporeal life support with an integrated left ventricular vent in children with a low cardiac output

2013 ◽  
Vol 24 (4) ◽  
pp. 654-660 ◽  
Author(s):  
Stany Sandrio ◽  
Wolfgang Springer ◽  
Matthias Karck ◽  
Matthias Gorenflo ◽  
Alexander Weymann ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiac Failure ◽  
Life Support ◽  
Extracorporeal Life Support ◽  
Left Ventricular ◽  
Neurological Dysfunction ◽  
Left Heart ◽  
Low Cardiac Output ◽  
Cardiac Thrombus ◽  
The Right

AbstractBackground: The aim of this study was to evaluate our experience in central extracorporeal life support with an integrated left ventricular vent in children with cardiac failure. Methods: Eight children acquired extracorporeal life support with a left ventricular vent, either after cardiac surgery (n = 4) or during an acute cardiac illness (n = 4). The ascending aorta and right atrium were cannulated. The left ventricular vent was inserted through the right superior pulmonary vein and connected to the venous line on the extracorporeal life support such that active left heart decompression was achieved. Results: No patient died while on support, seven patients were successfully weaned from it and one patient was transitioned to a biventricular assist device. The median length of support was 6 days (range 5–10 days). One patient died while in the hospital, despite successful weaning from extracorporeal life support. No intra-cardiac thrombus or embolic stroke was observed. No patient developed relevant intracranial bleeding resulting in neurological dysfunction during and after extracorporeal life support. Conclusions: In case of a low cardiac output and an insufficient inter-atrial shunt, additional left ventricular decompression via a vent could help avoid left heart distension and might promote myocardial recovery. In pulmonary dysfunction, separate blood gas analyses from the venous cannula and the left ventricular vent help detect possible coronary hypoxia when the left ventricle begins to recover. We recommend the use of central extracorporeal life support with an integrated left ventricular vent in children with intractable cardiac failure.

Progressive changes in cardiovascular function after unilateral heart irradiation

1964 ◽  
Vol 206 (2) ◽  
pp. 289-293 ◽  
Author(s):  
H. L. Stone ◽  
V. S. Bishop ◽  
A. C. Guyton
Keyword(s):  
Left Ventricle ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Pulse Rate ◽  
Left Atrial ◽  
Pressure Pulse ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Before And After ◽  
The Right

Chronic heart failure was produced by giving 20,000 r Co60 irradiation to either the right or left ventricle in nine closed-chest animals. Measurements of right and left atrial pressures, arterial pressure, pulse rate, body weight, and blood volume were made before and after irradiation. The right and left atrial pressures rose progressively until death in three animals irradiated on the right side. In six animals irradiated on the left side, the left atrial pressure rose progressively, but the right atrial pressure either did not rise or rose only during the latter stages of failure. Declining arterial pressure and increasing pulse rate were common to both groups. Increases in blood volume were observed in all animals, but this increase was only significant in the group irradiated on the left side. At autopsy, 70–100% of the right ventricular muscle was damaged in dogs irradiated on the right side, and 40–70% of the left ventricle in dogs irradiated on the left side. Hydrothorax and liver congestion were found in the right-sided group and pulmonary congestion in the left-sided group.

Pulmonary neutrophil kinetics in sheep: effects of altered hemodynamics

1985 ◽  
Vol 59 (6) ◽  
pp. 1796-1801 ◽  
Author(s):  
J. A. Cooper ◽  
R. Bizios ◽  
A. B. Malik
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Left Atrial ◽  
Recovery Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Blood Volume ◽  
Neutrophil Kinetics

We investigated the effect of elevated left atrial pressure and reduced cardiac output on pulmonary neutrophil kinetics in the sheep. Sheep neutrophils were isolated, labeled with 111In-oxine, and reinfused. Erythrocytes were labeled with [99mTc]pertechnetate. A gamma camera measured the lung activities of the labeled neutrophils and erythrocytes. The results indicated that 38.5% of the total injected neutrophils marginated in the lung. Pulmonary hemodynamics were altered by inflating a left atrial balloon three times in each sheep for 15–30 min to achieve 5- to 25-mmHg increments in pulmonary arterial wedge pressure. At least a 30-min recovery period was allowed between inflations. After each left atrial balloon inflation, neutrophil uptake remained unchanged from base line, despite decreased mean cardiac output to 0.67 +/- 0.24 (+/- SD) 1/min and increased pulmonary blood volume. The absence of pulmonary neutrophil uptake was confirmed by arterial-venous measurements. Increased pulmonary blood volume had little effect on lung neutrophil uptake, suggesting that most of the pulmonary neutrophils are marginated. We conclude that the lungs have a large marginated neutrophil pool compared with the circulating pool and that reduced cardiac output and elevated left atrial pressure have no effect on pulmonary neutrophil kinetics in the sheep.

Vasodilating Drugs: Contrasting Haemodynamic Effects

1976 ◽  
Vol 51 (s3) ◽  
pp. 575s-578s ◽  
Author(s):  
R. C. Tarazi ◽  
H. P. Dustan ◽  
E. L. Bravo ◽  
A. P. Niarchos
Keyword(s):  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Blood Volume ◽  
Pulmonary Artery Pressure ◽  
Cardiac Failure ◽  
Haemodynamic Effects ◽  
Artery Pressure

1. We investigated the haemodynamic effects of intravenously administered hydrallazine, diazoxide and nitroprusside and orally administered minoxidil to determine whether vasodilators (such as nitroprusside) which do not increase cardiac output might be better treatment for hypertensive complications associated with, or caused by, myocardial failure than those that do. 2. Hydrallazine and diazoxide caused increases in heart rate, cardiac output, cardiopulmonary blood volume, the ratio of cardiac output to cardiopulmonary volume, and pulmonary artery pressure. Nitroprusside, although decreasing pressure and vascular resistance, caused no significant change in the other functions except for reducing pulmonary artery pressure. Minoxidil, when given orally, had the potential for causing pulmonary hypertension. This seemed explained by increased flow (hyperdynamic type) in some but by congestive cardiac failure in others; the latter condition was probably intensified by the marked fluid retention that the drug can cause. 3. On the basis of these results a classification of vasodilators was constructed which depends on the presence or absence of a venodilating effect. Vasodilators which produce no (or little) venodilatation, increase heart rate, cardiac output, cardiopulmonary blood volume and pulmonary artery pressure. In this class are diazoxide, hydrallazine and minoxidil. Those that cause venodilatation do not stimulate the heart nor do they cause pulmonary hypertension. Nitroprusside and nitroglycerine are drugs of this type. 4. These results suggest that drugs producing both venodilatation and arteriolar dilatation may be more specific therapy for hypertensive complications associated with cardiac failure than those that cause only arteriolar dilatation.

Distribution of fetal cardiac output: importance of pacemaker location

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
Author(s):  
PT Pitlick ◽  
SE Kirkpatrick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Foramen Ovale ◽  
Rate Versus ◽  
Left Ventricular Output ◽  
The Right

Important questions exist about the relative roles of changes in heart rate versus extent of myocardial shortening in regulating fetal cardiac output, because increases in heart rate created by left atrial pacing have been shown to increase right ventricular output and decrease left ventricular output. Since the pacemaker site could importantly influence foramen ovale flow and, hence, each ventricle's output, changes in individual ventricular outputs were examined when both the right and left atria were paced at a rate of 270 beats/min in five acute and in eight chronically instrumented fetal lamb studies. With pacing of either atrium, total cardiac output was unchanged compared to control values. However, the right ventricle contributed more to total cardiac output with left atrial pacing (73% acute, 65% chronic) than with right atrial pacing (51% acute, 57% chronic). Converse changes were observed in left atrial pacing (27% acute, 35% chronic) as compared to right atrial pacing (49% acute, 43% chronic). Thus the disparity that exists normally in the contributions of the right and left ventricles to total cardiac output is accentuated with left atrial pacing and minimized with right atrial pacing. Pressure measurements demonstrated changes in the atrial pressure relations that would be expected to alter flow across the foramen ovale depending on the chamber initially activated. Previous experimental differences can, therefore, be attributed to changes in the magnitude of shunting across the foramen ovale and depend on pacemaker location.

CARDIOVASCULAR RESPONSES IN DOGS TO INTRAVENOUS INFUSIONS OF WHOLE BLOOD, PLASMA, AND PLASMA FOLLOWED BY PACKED ERYTHROCYTES

1955 ◽  
Vol 33 (3) ◽  
pp. 349-360 ◽  
Author(s):  
F. A. Sunahara ◽  
J. D. Hatcher ◽  
L. Beck ◽  
C. W. Gowdey
Keyword(s):  
Cardiac Output ◽  
Blood Plasma ◽  
Blood Volume ◽  
Carrying Capacity ◽  
Whole Blood ◽  
Cardiovascular Responses ◽  
Controlling Factors ◽  
Intravenous Infusions ◽  
Oxygen Carrying Capacity ◽  
The Right

The effects of intravenous infusions of large volumes of blood or of plasma followed by packed erythrocytes were studied in anesthetized normal dogs. During plasma infusion the right auricular pressure (RAP) and cardiac output increased as the hematocrit decreased. Blood infusion caused a rise in RAP but was, in most cases, not accompanied by an increased output. It is concluded that, although the blood volume and RAP may be important in the regulation of cardiac output, they are not under all conditions the controlling factors. The relative oxygen-carrying capacity of the blood appears to be more important in the cardiovascular adjustments to hypervolemia.

CARDIOVASCULAR RESPONSES IN DOGS TO INTRAVENOUS INFUSIONS OF WHOLE BLOOD, PLASMA, AND PLASMA FOLLOWED BY PACKED ERYTHROCYTES

1955 ◽  
Vol 33 (1) ◽  
pp. 349-360
Author(s):  
F. A. Sunahara ◽  
J. D. Hatcher ◽  
L. Beck ◽  
C. W. Gowdey
Keyword(s):  
Cardiac Output ◽  
Blood Plasma ◽  
Blood Volume ◽  
Carrying Capacity ◽  
Whole Blood ◽  
Cardiovascular Responses ◽  
Controlling Factors ◽  
Intravenous Infusions ◽  
Oxygen Carrying Capacity ◽  
The Right

The effects of intravenous infusions of large volumes of blood or of plasma followed by packed erythrocytes were studied in anesthetized normal dogs. During plasma infusion the right auricular pressure (RAP) and cardiac output increased as the hematocrit decreased. Blood infusion caused a rise in RAP but was, in most cases, not accompanied by an increased output. It is concluded that, although the blood volume and RAP may be important in the regulation of cardiac output, they are not under all conditions the controlling factors. The relative oxygen-carrying capacity of the blood appears to be more important in the cardiovascular adjustments to hypervolemia.

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