Sepsis cool vs warm skin

[Daitong]

Quick 2 questions regarding shock-

1. Why is that in distributive (sepsis, anaphylaxis, neuro/CNS) shock skin is warm/dry due to vasodilation, but with hypovolemic/cardiogenic/obstructive, the skin is cold+clammy? Doesn't vasodilation also occur?



2. Also I read that:


"Peripheral vascular resistance is increased in cardiogenic shock. This is due to the release of catecholamines, ADH, and angiotensin II in response to the decreased cardiac output."


...but isn't periph vas resistance lowered due to extensive vasodilation? Or did the text mean 'in response to cardiogenic shock, this is what happens'?

Thanks in advance, and HAPPY NEW YEAR!

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[DrPicard]

The body's response to shock is catecholamines + ADH + RAA, like you pointed out. In septic shock, toxins override the vasoconstricting effects of these substances to produce vasodilation, and hence warm and dry skin. Thats how sepsis produces shock in fact; toxins --> vasodilation --> lowered TPR.

In neurogenic and anaphylactic shock, again, the vasoconstricting efforts are the body are impeded for obvious reasons.

In hypovolemic, cardiogenic shock etc, vasoconstriction does occur, hence cold + clammy skin.

Later in the course of septic shock the skin can get cold due to a decrease in cardiac function (again due to toxins I believe).

My understanding is that its the vasodilation in septic/neuro/anaphylactic shock thats causing the shock in the first place; having normal or increased TPR in such a condition would mean theres no shock to begin with (or the body is compensating adequately, but the presence of shock means the compensation has failed)

Point 2 is indeed talking about cardiogenic shock.

 

[DrPicard]

Happy new year too

 

[Daitong]

The body's response to shock is catecholamines + ADH + RAA, like you pointed out. In septic shock, toxins override the vasoconstricting effects of these substances to produce vasodilation, and hence warm and dry skin. Thats how sepsis produces shock in fact; toxins --> vasodilation --> lowered TPR.

In neurogenic and anaphylactic shock, again, the vasoconstricting efforts are the body are impeded for obvious reasons.

In hypovolemic, cardiogenic shock etc, vasoconstriction does occur, hence cold + clammy skin.

Later in the course of septic shock the skin can get cold due to a decrease in cardiac function (again due to toxins I believe).

My understanding is that its the vasodilation in septic/neuro/anaphylactic shock thats causing the shock in the first place; having normal or increased TPR in such a condition would mean theres no shock to begin with (or the body is compensating adequately, but the presence of shock means the compensation has failed)

Point 2 is indeed talking about cardiogenic shock.

You are brilliant man-

This is really dumb of me, but I'm guessing that in neurogenic shock the vasoconstrictive efforts fail because there would be no *neurologic* sympathetic alpha-1 activation, but why are the vasoconstricting efforts by the body failing against the histamine activation of vasodilation?

@DrPicard

 

[DrPicard]

Shock, by definition, is a state where the compensating mechanisms of the body have failed to adequately overcome the insult to it. This must mean that in anaphylactic shock the vasoconstricting effects of catecholamines are indeed being outdone by the vasodilating effects of histamine and other anaphylatoxins. If it weren't so, there would be no shock, only a state where the body is responding adequately, at least in cardiovascular terms, to histamine and co.

In neurogenic shock the alpha adrenergic mediated basal tone of blood vessels is lost, resulting in decreased TPR, ie even under normal circumstances your vessels are constricted to some degree.

 

[Entadus]

It's a pharmacology question. Know that mast cell degranulation (histamine release) will activate H1 receptors in the endothelium (increased vascular permeability) and smooth muscle (vasodilatation) will act through Gq protein (PLC pathway).

From there, it's probably best to think about the endothelium's physiologic role in producing vasodilation in the smooth muscle of the vasculature: Nitric Oxide, Prostacyclin, etc. and recall the vasodilator pathway (cGMP production)

At the end of the story, the tissues (skin) will be flushed if the vessels are dilated and leaky... hence the warmth (lots of warm blood/fluid). Organs may not be perfused (hence the anaphylactic shock).

 

[DrSophia]

how does vasoconstriction cause clammy skin? I want to know the
physiopathology :/

 

[Ven0m]

how does vasoconstriction cause clammy skin? I want to know the
physiopathology :/

If clammy refers to sweaty/wet that's because sympathetics also stimulate sweat glands i'm guessing