Sepsis is a life-threatening condition characterized by an overwhelming immune response to infection, leading to widespread inflammation and tissue damage. Septic shock represents the extreme end of the spectrum, where the body's systemic response results in significant cardiovascular dysfunction. A critical feature of septic shock is vasoplegia, a pathological state characterized by profound vasodilation and reduced responsiveness to vasoconstrictive agents. This hemodynamic disturbance can be effectively represented using a pressure-volume (PV) diagram, which provides insights into the changes in cardiac function and vascular resistance. Please refer to this post for understanding the pressure-volume diagram in a normal heart.
Hemodynamic Profile in Severe Sepsis and Septic Shock
In severe sepsis and septic shock, systemic vascular resistance (SVR) and arterial elastance (Ea) are markedly decreased due to the vasodilatory effects of inflammatory mediators. This decrease in SVR leads to a lower end-systolic pressure (Pes), reflecting the reduced afterload on the heart. This is reflected as a leftward shift in the arterial elastance line on the pressure-volume loop of the left ventricle. Despite these changes, end-systolic elastance (Ees), a measure of the heart's contractile strength, remains unaffected.
The reduction in Ea/Ees ratio signifies a decrease in afterload relative to the heart's contractility, leading to an increased ejection fraction (EF). This is because the ratio of Ea/Ees decreases, making it easier for the heart to eject blood, thus improving EF. However, the clinical picture is complicated by significant venodilation, which reduces the end-diastolic volume (EDV) due to a decrease in stressed blood volume (SBV) and systemic venous return. Consequently, the stroke volume (SV) which is the amount of blood pumped by the left ventricle per beat is also reduced, resulting in a compromised cardiac output if the heart rate is not increased as a compensatory mechanism.
Hemodynamic Changes with Intravascular Volume Resuscitation
When intravascular volume is increased through the administration of fluids or blood, several key hemodynamic parameters are positively influenced. The total blood volume and stressed blood volume (SBV) increase, enhancing venous return. This leads to a rise in the end-diastolic volume (EDV), which subsequently increases the stroke volume (SV) and end-systolic pressure (Pes).
The PV diagram in this scenario shifts rightward, indicating an augmented preload. The increased EDV translates into a higher SV due to the Frank-Starling mechanism, which states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the EDV).
Effects of Adding Vasopressor Arginine Vasopressin (AVP)
Arginine vasopressin (AVP) is a potent vasopressor used to counteract the vasodilation in septic shock. The administration of AVP on top of volume resuscitation increases arterial elastance (Ea), thereby raising the Ea/Ees ratio. This leads to a decrease in both the ejection fraction (EF) and stroke volume (SV), as the heart must work against a higher afterload. Consequently, the end-systolic pressure (Pes) increases.
The increase in afterload results in a higher end-systolic volume and coupled with an increase in stressed blood volume (SBV), this leads to an elevated end-diastolic volume (EDV) and end-diastolic pressure.
Conclusion
The hemodynamic profile in severe sepsis and septic shock is markedly altered due to systemic vasodilation, resulting in decreased SVR and arterial elastance (Ea). These changes lead to a reduction in end-systolic pressure (Pes) and an increase in ejection fraction (EF), though the stroke volume (SV) and end-diastolic volume (EDV) are significantly reduced. The administration of fluids or blood can mitigate these effects by increasing total blood volume, venous return, and preload. Meanwhile, vasopressor agents like arginine vasopressin (AVP) increase arterial elastance (Ea), thereby raising afterload and end-systolic pressure (Pes), but at the cost of reduced stroke volume (SV) and ejection fraction (EF). Understanding these hemodynamic shifts through the lens of the pressure-volume diagram provides valuable insights for the effective management of patients with septic shock.
The following table summarizes these hemodynamic changes.
Hemodynamic Parameter | Sepsis with Vasoplegia | Volume Addition | Vasopressin |
Systemic Vascular Resistance (SVR) | Decreased | No change | Increased |
Arterial Elastance (Ea) | Decreased | No change | Increased |
End-Systolic Elastance (Ees) | Unaffected | No change | No change |
End-Systolic Pressure (Pes) | Decreased | Increased | Increased |
Ejection Fraction (EF) | Increased | No change | Decreased |
End-Diastolic Volume (EDV) | Decreased | Increased | Increased |
Stroke Volume (SV) | Decreased | Increased | Decreased |
Stressed Blood Volume (SBV) | Decreased | Increased | Increased |
Venous Return | Decreased | Increased | No change |
By comprehensively grasping the dynamic changes in the PV diagram, clinicians can better tailor interventions to optimize cardiac function and improve patient outcomes in severe sepsis and septic shock. In the next post, we will discuss treatment of septic shock with decreased left ventricular (LV) contractility using volume plus vasopressor, volume plus inoconstrictor, and volume plus inodilator.
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