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
Failure of the CNS
decreased cerebral perfusion detected as increased Pco2 and increased H+: increased central chemoreceptor activation, increased CV control center stimulation
prolonged inadequate cerebral perfusion –> ischemia: decreased neural activity, decreased sympathetic output, decreased vascular and cardiac responses to hemorrhage
trachea midline means what?
pneumothorax is not present; usually that would cause a shift of the trachea on x-ray
pulsus paradoxus means
not getting enough blood during diastole
things that can cause obstructive shock
tension pneumo
foreign object
giant pulmonary embolus/ saddle, etc.
hepatomegaly in shock/ CHF?
from edema
Frank Starling Curve: Systolic Failure
at a given EDV or pressure: decreased SV (decreased CO/ CI) vs. normal
increased EDV remaining after systole in impaired heart results in insignificant increase in SV despite increased LVEDP
What change to the curve is expected in a failing heart with cardiogenic shock?
decreased SV, CO, MAP, tissue perfusion, and inotropy
Cardiorespiratory Effects of LV Heart Failure
increased LV pressure –> increased LA pressure–> increased pulmonary vv pressure–> increased pulmonary capillary hydrostatic pressure
promotes increased filtration –> pulmonary edema (rales!)
MOAN therapy
morphine
oxygen
aspirin
nitrates
what should left atrial filling pressure be?
15- 18 or so
MOst common infections leading to sepsis
lung infection
UTIs
gut infections
skin infections
abdominal associated with the highest mortality rate
gram positives: staph and strep
gram negs: e coli, pseudomonas, and klebsiella
What drives the drop in oxygen availability during sepsis and leading, ultimately, to death?
insult–> trigger (PAMPs, DAMPs)–> complement/ coagulation system, vascular and tissue responses, blood and lymphatid responses (granulocytes,macrophages, monocytes, lymphocytes)
–> confusion, respiratory distress, shock, oliguria/ anuria, liver failure, loss of barrier function in the gut and ileus, capillary lead edema, DIC
what type of shock is septic?
distributive
how do we treat septic shock?
fluids and then pressors
