What is Sepsis?  Vascular Injuries

When we talk about septic shock, we think of patients who are hypotensive in spite of heroic attempts of the cardiovascular system to compensate: the patients are hot and hypotensive, unlike those in cardiogenic shock, who are cold and hypotensive. Many healthcare providers misunderstand septic shock as merely a vasodilated state. It is much more complicated than that. There are three major cardiovascular upsets:

1. Vasodilatation – due to loss of normal sympathetic tone, caused by the combination of local vasodilator metabolites, which cause activation of ATP-sensitive potassium channels – leading to hyperpolarization of smooth muscle cells (8;9;9) , and the production of inducible nitric oxide synthetase, which produces excessive amounts of nitric oxide. This vasodilatation leads to relative hypovolemia. Vascular tone is characteristically resistant to catecholamine therapy, but very sensitive to vasopressin.
2. Reduced stroke volume, due to the presence of a circulating myocardial depressant factor. There is reversible biventricular failure, a decreased ejection fraction, myocardial edema and ischemia. Although you may have noted that cardiac output usually increases in sepsis, this is invariably due to an increase in the heart rate. The heart as a pump is malfunctioning (10).
3. Microcirculatory failure (11): this is the major area of cardiovascular injury. The small blood vessels vasodilate, and there is widespread capillary leak, maldistribution of flow, arterio-venous shunting and oxygen utilization defects (12). These abnormalities are incompletely understood. In addition, there is initial activation of the coagulation system, and deposition of intravascular clot, causing ischemia.

It is not important that you remember or understand all of these abnormalities. Rather it is important that you realize that the hemodynamic upsets associated with sepsis are complex and multifaceted. Many undereducated practitioners use insensitive calculations such as SVR (systemic vascular resistance) as endpoints to therapy (mistakenly thinking that vasodilatation is the major problem in sepsis: it is not). Sepsis is a microcirculatory disorder, the problem starts there and finishes there, and that is where future therapies (starting with activated protein C) lie.

References

CLICK HERE FOR REFERENCES

THIS TUTORIAL BY PATRICK NELIGAN MD, UNIVERSITY OF PENNSYLVANIA

Please note: these tutorials are for personal study purposes only.  They are not currently peer reviewed, and no responsibility will be taken for mistakes or inaccuracies. Reproduction of information is forbidden. All material is copyrighted by the GasWorks Group.