Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure

1986 ◽  
Vol 60 (2) ◽  
pp. 604-612 ◽  
Author(s):  
M. R. Pinsky ◽  
G. M. Matuschak ◽  
L. Bernardi ◽  
M. Klain
Keyword(s):  
Stroke Volume ◽  
Cardiac Cycle ◽  
Intrathoracic Pressure ◽  
Canine Model ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Cardiac Performance ◽  
Hemodynamic Effects ◽  
Volume Measurements ◽  
Systemic Venous Return

Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.

Determinants of cardiac augmentation by elevations in intrathoracic pressure

1985 ◽  
Vol 58 (4) ◽  
pp. 1189-1198 ◽  
Author(s):  
M. R. Pinsky ◽  
G. M. Matuschak ◽  
M. Klain
Keyword(s):  
Stroke Volume ◽  
Cardiac Function ◽  
Blood Volume ◽  
Intrathoracic Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Respiratory Frequency ◽  
Stroke Work ◽  
Inspiratory Time ◽  
Ventricular Failure

We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. We found that pertubations in mean ITP induced by ventilator adjustments accounted for all observable steady-state hemodynamic changes independent of respiratory frequency, inspiratory time, or phasic respiratory swings in ITP. Changes in ITP were associated with reciprocal changes in both intrathoracic vascular pressures (P less than 0.01) and blood volume (P less than 0.01). When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.

Hemodynamic effects of synchronous high-frequency jet ventilation in mitral regurgitation

1990 ◽  
Vol 69 (6) ◽  
pp. 2120-2125 ◽  
Author(s):  
K. L. Stein ◽  
D. J. Kramer ◽  
A. Killian ◽  
M. R. Pinsky
Keyword(s):  
Mitral Regurgitation ◽  
High Frequency ◽  
Cardiac Cycle ◽  
Intrathoracic Pressure ◽  
Canine Model ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Jet Ventilation ◽  
Forward Flow ◽  
High Frequency Jet Ventilation

We tested the hypothesis that increases in intrathoracic pressure (ITP), by decreasing the pressure gradient for anterograde left ventricular (LV) ejection, should augment cardiac output in acute mitral regurgitation (MR). In a pentobarbital-anesthetized closed-chest canine model, LV stroke volume (SLLV) was measured by integration from an aortic flow probe signal. MR was induced by a regurgitant ring. ITP was elevated over apnea by means of intermittent positive-pressure ventilation (IPPV), asynchronous (asynch) high-frequency jet ventilation (HFJV), and cardiac cycle-specific (synch) HFJV. IPPV resulted in the greatest increase in ITP. MR caused a fall in SVLV and a rise in LV filling pressure that were not altered by IPPV. Compared with IPPV or apnea, both asynch and synch HFJV increased SVLV and reduced LV filling pressures (P less than 0.05). Systolic synch HFJV induced a greater increase in SVLV (32%) than diastolic synch HFJV (26%) despite similar ventilatory settings. Our data suggest that when LV contractility is normal but MR impairs forward flow, cardiac cycle-specific increases in ITP will augment forward flow.

Effect of synchronous increase in intrathoracic pressure on cardiac performance during acute endotoxemia

1990 ◽  
Vol 69 (4) ◽  
pp. 1502-1508 ◽  
Author(s):  
J. G. Guimond ◽  
M. R. Pinsky ◽  
G. M. Matuschak
Keyword(s):  
Cardiac Cycle ◽  
Intrathoracic Pressure ◽  
Canine Model ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Specific Effects ◽  
Ventricular Filling Pressure ◽  
Induced Changes ◽  
Ventricular Filling

In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min after infusion of 1 mg/kg Escherichia coli endotoxin (serotype 055:B5) and then after 2 mg/kg propranolol at both low (less than 10 mmHg) left ventricular filling pressure (LVFP) and high (greater than 10 mmHg) LVFP. Ventricular function curves, aortic pressure-flow (P-Q) relationships, and venous return (VR) curves were analyzed. We found that endotoxin did not alter VR curves but shifted the aortic P-Q curves to the left with pressure on the x-axis (P less than 0.05). Volume loading increased SV (P less than 0.01) because of a rightward shift of the VR curve. No specific differences occurred with either sync or async HFJV during endotoxin, presumably because of preserved VR and shifted aortic P-Q. The lack of cardiac cycle-specific effects of ITP appears to be due to the selective endotoxin-induced changes in peripheral vasomotor tone that counterbalance any depressed myocardial contractility.

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.

scholarly journals Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure

1997 ◽  
Vol 83 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Oommen P. Mathew
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systolic Blood Pressure ◽  
Cardiac Cycle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Intrathoracic Pressure ◽  
Systemic Arterial Pressure ◽  
Pressure Changes

Mathew, Oommen P. Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure. J. Appl. Physiol. 83(2): 371–375, 1997.—The purpose of the study was to determine the effect of transient changes in intrathoracic pressure on systemic arterial pressure by utilizing hiccups as a tool. Values of systolic and diastolic pressures before, during, and after hiccups were determined in 10 intubated preterm infants. Early-systolic hiccups decreased systolic blood pressure significantly ( P < 0.05) compared with control (39.38 ± 2.72 vs. 46.46 ± 3.41 mmHg) and posthiccups values, whereas no significant change in systolic blood pressure occurred during late-systolic hiccups. Diastolic pressure immediately after the hiccups remained unchanged during both early- and late-systolic hiccups. In contrast, diastolic pressure decreased significantly ( P < 0.05) when hiccups occurred during diastole (both early and late). Systolic pressures of the succeeding cardiac cycle remained unchanged after early-diastolic hiccups, whereas they decreased after late-diastolic hiccups. These results indicate that transient decreases in intrathoracic pressure reduce systemic arterial pressure primarily through an increase in the volume of the thoracic aorta. A reduction in stroke volume appears to contribute to the reduction in systolic pressure.

Negative intrathoracic pressure decreases independently left ventricular filling and emptying

1989 ◽  
Vol 257 (1) ◽  
pp. H120-H131 ◽  
Author(s):  
J. Peters ◽  
C. Fraser ◽  
R. S. Stuart ◽  
W. Baumgartner ◽  
J. L. Robotham
Keyword(s):  
Stroke Volume ◽  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Intrathoracic Pressure ◽  
Esophageal Pressure ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Phrenic Nerve Stimulation

The mechanism for the fall in left ventricular (LV) stroke volume with normal and obstructed inspiration is controversial with changes proposed in LV preload and afterload. During respiration extending over several cardiac cycles, changes in both LV filling and emptying could occur, rendering demonstration of any responsible mechanism difficult. To evaluate the independent effects of negative intrathoracic pressure (NITP) on LV filling and emptying, we have analyzed the effects of NITP confined to either diastole or systole using electrocardiogram (ECG)-triggered phrenic nerve stimulation in six anesthetized closed-chest dogs. Lung volume was either maintained by completely obstructing the airway or allowed to increase during NITP. With diastolic NITP and the airway obstructed during phrenic nerve stimulation, LV filling volume (integrated mitral flow) significantly decreased (-37 +/- 6.1% SE) associated with increases in LV and right atrial filling pressures at end diastole relative to both atmospheric and esophageal pressures. Right atrial pressure relative to either atmospheric or esophageal pressure increased significantly more than left atrial pressure. The ensuing LV stroke volume (integrated ascending aortic flow) decreased significantly (-30.8 +/- 5.9%). With NITP confined to systole and at constant LV preload, LV stroke volume also decreased (-12.9 +/- 2.5%) associated with an increase in LV systolic pressure relative to esophageal pressure. Similar significant changes were observed despite a smaller fall in esophageal pressure when lung volume was allowed to increase during either diastolic or systolic NITP. We conclude that 1) NITP confined to diastole decreases LV filling and the ensuing LV stroke volume, most likely by ventricular interdependence; 2) NITP confined to systole also decreases LV stroke volume, presumptively by imposing an increased afterload on the LV; 3) both diastolic and systolic mechanisms should contribute to a decreased LV stroke volume during normal and obstructed inspiration; and 4) if the effects of intrathoracic pressure changes were to extend over several cardiac cycles, mechanisms exist to account for either increases or decreases in LV volumes.

Buffering of respiratory variations in venous return by right ventricle: a theoretical analysis

1994 ◽  
Vol 267 (6) ◽  
pp. H2163-H2170 ◽  
Author(s):  
W. P. Santamore ◽  
J. N. Amoore
Keyword(s):  
Arterial Pressure ◽  
Stroke Volume ◽  
Right Ventricle ◽  
Venous Return ◽  
Fold Increase ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Venous Flow ◽  
Systemic Venous Return ◽  
Percentage Basis

The role of the right ventricle (RV) in buffering systemic venous return, thereby dampening respiratory-induced variations, left ventricular (LV) stroke volume, and systemic arterial pressure variations was examined using a computer model of the cardiovascular system. Respiration was simulated by cyclical variations in intrathoracic and abdominal pressures (cycle time 5 heartbeats), causing a 43-ml fluctuation in venous return per heartbeat (mean 71 ml) compared with fluctuations of 19 ml in RV stroke volume, 6 ml in pulmonary venous flow, and only 3 ml in LV stroke volume. On a percentage basis, the RV provided 56% of the total buffering of systemic venous return, the lungs another 30%, whereas the LV only 7%. A 10-fold increase in RV diastolic compliance increased the RV stroke volume variations from 26 to 57% of the venous return variations; a 10-fold increase in RV elastance increased them from 24 to 60%, whereas decreasing pulmonary arterial pressure from 28 to 10 mmHg increased them from 28 to 56%. The results also suggest that an underrecognized function of the RV is to buffer systemic venous return and thereby keep LV stroke volume relatively constant.

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