Shock pathophysiology
|
Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Shock pathophysiology On the Web |
|
American Roentgen Ray Society Images of Shock pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
In general, blood pressure (BP) can be factored as a product of cardiac output (CO) x peripheral resistance (PR, also known as systemic vascular resistance). Cardiac output itself is determined by stroke volume (SV) x heart rate (HR):
CO = HR x SV
BP = CO x PR
Therefore a loss of blood pressure can be due to a fall in cardiac output as will be seen in cardiac disease, outflow obstruction or hemorrhagic shock. Blood pressure may also fall as peripheral resistance falls due to massive vasodilatation as may be seen in sepsis.
Preload and Afterload
- Preload
- This is a concept rather than a true value. It cannot be measured as such, but various measurable physiological parameters can act as surrogates, e.g. CVP or pulmonary artery wedge pressure. It can be thought of as the filling pressure of heart chambers. So long as the heart is not overwhelmed, the greater the initial filling of a heart chamber, the greater the force of contraction.
- Afterload
- This can be thought of as the amount of force required for the heart to eject blood. It is influenced by preload, systemic vascular resistance and external pressure (e.g. in positive pressure ventilation).
Homeostatic Mechanisms
A fall in blood pressure usually results in
- Baroreceptor generated reflex rise in heart rate and sympathetic drive
- Adrenaline release from the adrenal medulla
- Sympathetic nervous system drive leads to noradrenaline release
- Activation of renin-angiotensin-aldosterone system
- Stress response with cortisol release from adrenal cortex
- Individual usually falls to a supine position which is preferable
- Release of ACTH and vasopressin