afterload in hypovolemic shock
Started by MudPhud20XX
No.
1) You are hypovolemic, so your venous return is low.
2) Your venous return is low so your cardiac output is low
3) In response, to maintain perfusion pressure your afterload increases.
CNS injury (esp early cervical spinal trauma) causes changes to your sympathetic tone causing distributive shock.
1) You are hypovolemic, so your venous return is low.
2) Your venous return is low so your cardiac output is low
3) In response, to maintain perfusion pressure your afterload increases.
CNS injury (esp early cervical spinal trauma) causes changes to your sympathetic tone causing distributive shock.
1) In hypovolaemia you constrict arterioles to increase total peripheral resistance (alpha-1 agonism; cortisol will increase alpha-1 expression and then your catecholamines will bind). Pressure proximal to the arterioles (i.e., abdominal aorta with branches to vital organs) increases (like constricting a hose where you get a proximal buildup of pressure). In sepsis there's arteriolar dilatation due to inflammatory cytokines, so resistance decreases.
2) CNS injury can lead to parasympathetic outflow (e.g., Cushing ulcers). Neurogenic shock can occur in the setting of injury.
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This is what confuses me about this case: are we supposed to think about what happens after a response or before a response? In hypovolemia, pressure is way way down, until boom, the "response" happens, then arterioles constrict, then pvr increases, causing increased after load. So, which point should we be thinking about on the timeline? Before or after the response ??
To answer OP:
1. Hypovolemic shock ----> Sympth activation ----> Inc HR, Inc TPR as a compensation. The increased TPR causes increased afterload.
2. Distributive shock is any shock with peripheral vasodilation being (atleast one of) the primary problems.. Includes but is not limited to: Septic Shock, Neurogenic Shock and Anaphylactic Shock. Spinal injury ---> decreased sympathetic outflow ---> Vasodilation ---> Neuro Shock
@Phloston
Neurogenic shock is primarily due to interruption of sympathetic outflow and not increased parasympathetic outflow. The logic for Cushing's is correct i.e. Increased parasymp. However, I disagree with this being significant in neurogenic shock.
Also, Hypovolemic shock is an acute condtion.. cortisol mediated Alpha 1 expression would take time ? That wouldn't really plan any role in hypovolemic shock induced vasoconstriction which leads to increasd afterload.. It would happen in a while..hours to days.. but i believe it would take some time to kick in..
So that explains it. We are to assume that and answer the question based on the physiological response. Thanks! This can sometimes get confusing with labs in endocrinology as well.
He asked about head trauma. Parasympathetic change is a known manifestation. And cortisol effects don't take that long. There are usmle questions on cortisol's permissive effects following injection.
