Shock CIS (Tieman) Flashcards
capillary refill should be
2-3 seconds; less indicates hypoperfusion to the skin/ shunting to the organs
clammy skin
sweating; blood going to organs instead of skin
pulmonary pressure
should be about 25/15
Hypovolemic shock: mild, moderate, severe
mild: less than 20% blood volume loss, cool extremities, increased capillary refill time, diaphoresis, collapsed veins, anxiety
moderate 20-40% blood volume loss: add tachycardia, tachypnea, oliguria, postural changes
severe more than 40% blood volume loss: add hemodynamic instability, marked tachycardia, hypotension, mental status deterioration (coma)
Receptors which detect effects of hypotension/hypovolemia
High-pressure baroreceptors
Low-pressure baroreceptors
Renal Juxtaglomerular apparatus
Central and peripheral chemoreceptors
blood loss -> decreased central venous pressure –> decreased stroke volume –> decreased cardiac output –> decreased arterial pressure
What is the autonomic response to hypotension?
increased sympathetic
decreased parasympathetic
–> increased HR, contractility, TPR, circulating epinephrine, renin, and sweat gland activity (sympathetic cholinergic stimulation)
Humoral regulation of vascular tone in response to hypotension/hypovolemia:
ADH/ AVP –> vasoconstriction
ANG II –> vasoconstriction (via RAAS)
How can loss of blood volume be corrected?
- Renal fluid conservation
- Stimulation of thirst water intake
- Net capillary reabsorption (Starling’s forces)
“Transcapillary refill”
Which factors promote renal retention of Na+ and H2O
increased sympathetic activity (renal vasoconstriction–> direct stimulation of Na+ reabsorption by renal tubule cells)
increased Ang II –> aldosterone, ADH/ AVP, THIRST
Aldosterone –> Na+ reabsorption
Anti-diuretic hormone/ arginine vasopressin –> H2O reabsorption
Transcapillary Refill: Correction for volume loss
Net reabsorption of fluid: from interstitial fluid –> capillaries
Reabsorption of interstitial fluid helps replace lost blood volume
Result: initial hemodilution
Hypovolemic shock- negative-feedback (compensatory) mechanisms and positive-feedbakc (decompensatory) mechanisms
Hypovolemic Shock:
- Tachycardia
- Hypotension
- Generalized arteriolar vasoconstriction & venoconstriction
- Oliguria
Outcome of acute blood loss:
Depends on gains of different feedback mechanisms
Balance between positive- and negative-feedback mechanisms
Negative-feedback (compensatory) mechanisms:
- Baroreceptor reflexes
- Chemoreceptor reflexes
- Transcapillary reabsorption of interstitial fluid
- Renal conservation of salt and water
Positive-feedback (decompensatory) mechanisms:
- Cardiac failure
- Acidosis
- CNS depression
Irreversible Hemorrhagic Shock
After temporary improvement: hemorrhagic shock may become irreversible (even with transfusion) due to multiple failures:
Vasoconstrictor response
Capillary refill response
Heart failure
CNS response
Failure of the Vasoconstrictor Response
Prolonged hemorrhagic hypotension:
TPR: initial increase tapers off and return to pre-hemorrhage levels
Possible failures:
1. “Sympathetic escape” Desensitization α1-adrenoceptors Depletion of neurotransmitters 2. Metabolites and vasodilators released by ischemic tissues Counteract vasoconstrictor stimuli Late phases of irreversible shock: May be completely unresponsive to vasoconstrictor drugs 3. Decline in plasma AVP/ADH from early peak response Decline in trigger to release Depletion of AVP/ADH posterior pituitary stores Restoration of ADH to initial peak can significantly increase BP
Failure of Transcapillary Refill Process
Failure of vessels to sustain resistance:
Precapillary vessels tend to fail before post capillary vessels
decreased precapillary constriction–> decreased postcapillary constriction
increased relative ratio Rpost/ Rpre –> increased Pc –> promotes net filtration
Failure of the Heart
Prolonged, severe hypovolemic shock –> cardiogenic shock (inadequate coronary perfusion)
Negative inotropy
Ischemic cardiac tissue
Acidosis
Other ischemic organs may release cardiotoxic factors
