Cardiovascular responses to metabolic acidosis

1965 ◽  
Vol 208 (2) ◽  
pp. 237-242 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Heart Rate ◽  
Metabolic Acidosis ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Precise Control ◽  
Arterial Ph

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po2, and Pco2 were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.

INFLUENCE OF ACIDEMIA ON LEFT VENTRICULAR FUNCTION IN THE NEWBORN LAMB

PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Newborn Lamb ◽  
Precise Control ◽  
Significant Impairment ◽  
Ph Range

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

Inotropic responses of the left ventricle to changes in heart rate in anesthetized rabbits

1987 ◽  
Vol 65 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Leonard B. Bell ◽  
D. Fred Peterson
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Marked Change ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Resting Heart Rate ◽  
Ventricular Contractility ◽  
Inotropic Responses ◽  
Rate Infusion ◽  
Catecholamine Concentration

Factors known to influence left ventricular contractility include preload, afterload, circulating catecholamine concentration, efferent sympathethic discharge, and heart rate. Heart rate influences have been primarily determined in the dog, whereas the influence of heart rate in smaller mammals has not been determined. Eight pentobarbital-anesthetized rabbits were instrumented to measure electrocardiogram, heart rate, left ventricular pressure, end-diastolic pressure, dP/dt, and mean and pulsatile aortic pressures. Systematic bradycardia was induced by stimulating the peripheral end of the sectioned right vagus nerve. Between 293 and 235 beats/min, there was no change in (dP/dt)max as heart rate was decreased. Below this range there was a direct relationship between (dP/dt)max and heart rate. Preload remained unchanged down to 132 beats/min. There was a small but significant decrease in afterload (0.09 mmHg∙beat−1∙min−1; 1 mmHg = 133.32 Pa) throughout the decrease in heart rate. Infusion of propranolol (2.0 mg/kg) produced no marked change in the heart rate – (dP/dt)max relationship, although both resting heart rate and (dP/dt)max were reduced. This study demonstrates that (dP/dt)max is not influenced by changes in heart rate above 235 beats/min in the pentobarbital-anesthetized rabbit. These results differ from findings in other animals, and demonstrate that species and heart rate ranges must be considered when drawing conclusions regarding (dP/dt)max as a reliable index of contractility.

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

1963 ◽  
Vol 205 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Andrew G. Wallace ◽  
N. Sheldon Skinner ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Complex Function ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Pressure Development ◽  
Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

scholarly journals Simulation of Exercise-Induced Syncope in a Heart Model with Severe Aortic Valve Stenosis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Matjaž Sever ◽  
Samo Ribarič ◽  
Marjan Kordaš
Keyword(s):  
Heart Rate ◽  
Aortic Valve ◽  
Vascular Resistance ◽  
Aortic Valve Stenosis ◽  
Case Reports ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Lumped Parameter ◽  
Pulmonary Arterial ◽  
Exercise Induced

Severe aortic valve stenosis (AVS) can cause an exercise-induced reflex syncope (RS). The precise mechanism of this syncope is not known. The changes in hemodynamics are variable, including arrhythmias and myocardial ischemia, and one of the few consistent changes is a sudden fall in systemic and pulmonary arterial pressures (suggesting a reduced vascular resistance) followed by a decline in heart rate. The contribution of the cardioinhibitory and vasodepressor components of the RS to hemodynamics was evaluated by a computer model. This lumped-parameter computer simulation was based on equivalent electronic circuits (EECs) that reflect the hemodynamic conditions of a heart with severe AVS and a concomitantly decreased contractility as a long-term detrimental consequence of compensatory left ventricular hypertrophy. In addition, the EECs model simulated the resetting of the sympathetic nervous tone in the heart and systemic circuit during exercise and exercise-induced syncope, the fluctuating intra-thoracic pressure during respiration, and the passive relaxation of ventricle during diastole. The results of this simulation were consistent with the published case reports of exertional syncope in patients with AVS. The value of the EEC model is its ability to quantify the effect of a selective and gradable change in heart rate, ventricular contractility, or systemic vascular resistance on the hemodynamics during an exertional syncope in patients with severe AVS.

Effects of enhanced ventricular filling on cardiac pump performance in exercising dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1886-1890 ◽  
Author(s):  
L. D. Horwitz ◽  
J. Lindenfeld
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Increase Stroke Volume ◽  
Normal Increase ◽  
Ventricular Filling

The extent to which the normal increase in stroke volume during exercise can be augmented by increasing preload by dextran infusion was studied in seven dogs. Each dog ran 3 min on a level treadmill at mild (3–4 mph), moderate (6–8 mph), and severe (9–13 mph) loads during the control study and immediately after 10% dextran 14 ml/kg iv. During severe exercise dextran-augmented stroke volume (+5.4 ml or 19% vs. exercise without dextran, P less than 0.01) and left ventricular end-diastolic diameter and pressure did not change heart rate, aortic pressure, or maximum derivative of left ventricular pressure but decreased systemic vascular resistance by 16%. Similar increases in stroke volume and preload after dextran occurred during mild and moderate exercise when arterial pressure and heart rate were unchanged or increased and systemic vascular resistance was decreased. Thus altering preload above those levels normally encountered during exercise is a potential mechanism to increase stroke volume and cardiac output.

Stroke Volume Dynamics During Progressive Exercise in Healthy Adolescents

2013 ◽  
Vol 25 (2) ◽  
pp. 173-185 ◽  
Author(s):  
Thomas Rowland ◽  
Viswanath Unnithan
Keyword(s):  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Original Research ◽  
Ventricular Contractility ◽  
Cardiac Responses ◽  
Progressive Exercise

Understanding cardiac responses to exercise in healthy subjects is important in the evaluation of youth with heart disease. This review article incorporates previously published original research from the authors’ laboratory to examine changes in stroke volume during progressive exercise which are consistent with a model in which circulatory responses are controlled by alterations in the systemic vascular resistance. Stroke volume dynamics and cardiovascular responses to a progressive upright cycle test were examined in three groups of healthy, untrained adolescent subjects. These indicated a) a progressive decease in systemic vascular resistance, b) little change in stroke volume after an initial rise related to orthostatic changes in ventricular refilling, c) evidence of a constant or slightly declining left ventricular end diastolic filling pressure, d) and increases in markers of ventricular contractility. These observations are consistent with peripheral (vascular resistance) rather than central (cardiac) control of circulation with exercise. Changes in stroke volume during exercise need to be interpreted in respect to alterations in heart rate and myocardial functional capacity.

Intrinsic effects of heart rate on left ventricular performance

1963 ◽  
Vol 205 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Jere H. Mitchell ◽  
Andrew G. Wallace ◽  
N. Sheldon Skinner
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Pressure Rise ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Wide Range

The effects of heart rate on left-ventricular performance were studied in an areflexic dog right-heart bypass preparation which allowed independent control of aortic pressure, cardiac output, and heart rate. When the heart rate was increased while stroke volume and mean aortic pressure were maintained constant the left-ventricular mean rate of pressure rise during isovolumic systole, the maximal rate of pressure rise during isovolumic systole, and the mean rate of ejection were all increased without any change in left-ventricular end-diastolic pressure. Further, it was shown that the left ventricle performed the same amount of stroke work over a wide range of heart rates without an increase in end-diastolic pressure in spite of the markedly shortened time available for performing this work. This was accomplished because of the increase in stroke power. These observations demonstrate that the performance of the left ventricle becomes intrinsically "faster" as the heart rate is increased. When the transient phenomena that occur when the heart rate is increased are considered, the fact that the same stroke work is produced over a wide range of heart rates without an increase in end-diastolic pressure indicates that the left ventricle has also become "stronger" than it would have been if the adaptive change had not occurred.

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