Related Experiment Videos
Characteristics of ventricular function in severe hemorrhagic shock
Insights
Severe hemorrhagic shock (HS) impairs left ventricular (LV) diastolic function, leading to decreased compliance. While systolic function (Emax) initially appears preserved, it declines in non-survivors, indicating diastolic dysfunction is key in HS outcomes.
Area of Science:
- Cardiovascular Physiology
- Hemorrhagic Shock Research
- Cardiac Mechanics
Background:
- Left ventricular (LV) function is altered in severe hemorrhagic shock (HS), but the underlying mechanisms remain unclear.
- Distinguishing between systolic and diastolic dysfunction is crucial for understanding HS-induced cardiac alterations.
- Emax, a rate and load-independent index of contractility, offers a novel method to assess systolic performance.
Purpose of the Study:
- To investigate the mechanisms of left ventricular (LV) dysfunction following severe hemorrhagic shock (HS).
- To differentiate between systolic and diastolic functional changes using Emax and LV diastolic pressure-strain relationship.
- To assess the impact of HS and reinfusion on cardiac contractility and compliance.
Main Methods:
- Measurements of Emax and LV diastolic pressure-strain relationship in 15 instrumented dogs.
- Induction of HS (mean aortic pressure 40 mm Hg) for 2 hours, followed by reinfusion.
- Utilized sonomicrometric and micromanometric techniques for data acquisition.
Main Results:
- Immediately post-reinfusion, Emax was unchanged, but LV compliance significantly decreased in all dogs.
- Survivors showed progressive recovery of LV compliance over 4 days, with stable Emax.
- Non-survivors exhibited progressive loss of LV compliance and a significant decrease in Emax prior to death.
Conclusions:
- Cardiac contractility (Emax) may be initially preserved or improved after HS, but diastolic dysfunction (decreased compliance) is a consistent early finding.
- Recovery of diastolic function is observed in survivors, while progressive diastolic and systolic dysfunction characterize non-survivors.
- Diastolic dysfunction plays a critical role in the cardiac response to and outcome from severe hemorrhagic shock.
Abstract:
Although left ventricular (LV) function appears altered by severe hemorrhagic shock (HS), the mechanisms of this dysfunction have been difficult to characterize. Depression in the LV function curve could be caused by altered diastolic or systolic function. It has been difficult to assess the systolic function, but the use of the rate and load independent index of contractility, Emax (the slope of the end-systolic pressure-dimension relationship), offers a new approach to the quantification of systolic mechanical performance. Emax and the LV diastolic pressure-strain relationship were measured in 15 chronically instrumented dogs by sonomicrometric and micromanometric techniques. Gradual LV unloading was obtained from transient vena caval occlusion. After control study, each dog underwent 2 hours of HS (mean aortic pressure 40 mm Hg), followed by reinfusion of all shed blood. Upon reinfusion, Emax was not decreased; however, all dogs had a significant decrease in LV compliance. During the next 4 days, the LV compliance of the eight survivors progressively returned toward control, while Emax remained stable. All seven nonsurvivors demonstrated progressive loss of LV compliance, and Emax was significant decreased prior to death. Cardiac contractility appeared improved immediately after shock, but a consistent decrease in compliance was observed. Reversal of abnormal diastolic function was demonstrated in all survivors and progressive depression in all nonsurvivors. Depression in systolic function was observed only in nonsurvivors immediately prior to death.