Phys-shock Flashcards
___ is the most common type of shock, and it is typically associated with ___ and leads to ___
- Hypovolemic
- Hemorrhage or severe dehydration
- Decreased effective circulating volume (hypovolemia)
___ shock is associated with PE that reduces pulmonary a. flow resulting in reduced ____. This in turn results in a reduction in ___ and ___
- Obstructive
- LV filling
- CO
- Low BP
___ shock occurs as a result of heart failure. ___ shock is a result of generalized autonomic failure leading to ___ and ___.
- Cardiogenic
- Neurogenic
- Reduced CO
- Peripheral vasodilation
___ shock is associated with his inappropriate peripheral vasodilation (too much) such that CO cannot increase sufficiently to overcome the massive decrease in peripheral vascular resistance.
Causes?
Distributive
- sepsis secondary to infection or GI dysfunction
- anaphylaxis
- neurogenic shock
Features of early hypovolemic shock
6
ATTOCA
- Altered mental status
- Tachypnea
- Tachycardia, weak pulse, orthostatic hypotension
- Oliguria
- Cool, clammy, poor refill time, sweating
- Anemia
Features of late hypovolemic shock
9
TOCCCALMA
- Tachypnea and resp. failure
- Obtunded CNS (dull reflexes)
- Cool, clammy, cyanotic, poor refill time
- Cardiac failure, arrhythmias, hypotension
- Coagulopathy
- Anuria
- Liver failure
- Mucosal bleeding
- Acidosis, hypocalcemia, hypomagnesemia
Initial treatment of shock
- Supplemental O2
- Lay the pt down
- Warm the pt
- Determine cause and address it
- Restore and stabilize the effective circulating blood volume
Response to low ECBV
~10% = no change in arterial pressure or CO ~20% = CO drops, no change in arterial pressure >20% = both drop
Systems that work together to make compensation possible for decreases in ECBV
- Baroreceptors
- Chemoreceptors
- Cerebral ischemia
- Reabsorption of tissue fluid
- Vasoconstrictors
- Renal conservation of Na and H2O
- CNS ischemic response
A decrease in ECBV will elicit a baroreflex that will do what?
- Increase sympathetic output to the heart (increases rate and SV to increase CO) and peripheral circulation (for arteries: shunts blood away from non essential organs. For veins: enhances venous return to restore CO and arterial pressure)
- Decrease parasympathetic activity to the heart (increases rate)
What “non-essential” organs suffer when the baroreflex increases sympathetic output and arteries shunt blood to the heart?
- Skeletal muscle
- Skin
- Kidneys
- GI tract
When MAP falls below the baroreceptor threshold (which is ___), what happens?
60 mmHg
- the low perfusion pressure and low flow leads to hypoxemia and acidosis
- this stimulates the chemoreceptors in the carotid bodies to increase ventilation to increase PO2 and “blow off” CO2 to minimize the acidosis (by decreasing PCO2)
- stimulating respiration also aids venous return and enhances lymphatic flow
When the MAP falls below ___, perfusion of the brain will be impaired resulting in ___. The response that follows is solely targeted at ___
- 40 mmHg
- Cerebral ischemia and hypoxia
- increasing brain blood flow
How does the cerebral ischemic response work?
- Sympathetic and adrenal discharge causing vasoconstriction and increased myocardial contractility (+ inotropic effect)
- Parasympathetic flow to the heart decreased rate and VO2
Peripheral vasoconstriction decreases capillary hydrostatic pressure relative to plasma oncotic pressure which shifts the balance of starling forces, favoring ___
Reabsorption from the interstitial space into the vascular space (-Jv)
If there is an increase in osmotic pressure within the extracellular space what happens?
Water leaves the intracellular space to increase extracellular volume
-net effect can be hemodilution
Circulating endogenous vasoconstrictors
- NE - neural release, some from adrenal medulla
- Epinephrine - from adrenal medulla
- Angiotensin II - symp. reminds release from kidney leads to formation of angiotensin I
- Vasopressin/ADH - from posterior pituitary in response to changes in plasma osmolality
___ controls the reabsorption of water from the distal nephron. Sensitivity for ___ is increased in low volume states due to ___
- ADH/Vasopressin
- ADH release
- Increased levels of angiotensin II
___ activates the renin-angiotensin-aldosterone system (RAAS)
Low volume
Low renal perfusion pressure elicits ___
Increases in solute and water reabsorption
Functions of angiotensin II
- Vasoconstriction
2. Increases reabsorption of NaCl and H2O in the proximal tubule of the kidney
__ stimulates the release of aldosterone from the adrenal cortex, which ___
- Angiotensin II
2. Increases NaCl and H2O reabsorption in the collecting ducts of the nephron
Functions of vasopressin/ADH
- Vasoconstriction
2. Increases reabsorption of H2O from the cortical and medullary collecting ducts in the nephron (antidiuretic)
When does decompensation occur?
If the pt is not stabilized in time, the compensatory mechanisms begin to fail and then decompensation begins
What happens in decompensation?
- Cardiac failure
- Vascular failure
- Metabolic acidosis
- CNS depression
- Inappropriate clotting
- Depression of mononuclear phagocytic system
Decompensation:
Cardiac failure
- Starts as cardiac depression
- Low arterial pressure leads to low coronary perfusion and not enough O2 to the myocardium
- Cardiac function is impaired
- CO falls which further compromises peripheral perfusion
Decompensation:
Vascular failure
- Peripheral vasoconstriction begins to fail
- relative vasodilation causes peripheral resistance to fall
- Due to desensitization of alpha 1 receptors resulting in a sympathetic escape
Decompensation:
Metabolic acidosis
- As CO falls, O2 perfusion drops
- Lactic acid production increases
- pH decrease consumes bicarbonate resulting in metabolic acidosis
- Acidosis further depressed cardiac function (- inotropic effect) and causes peripheral vasodilation)
What is metabolic acidosis ?
Low HCO3
Decompensation:
CNS depression
- Falling arterial pressure leaders to decreased cerebral blood flow and cerebral hypoxia
- Sympathetic outflow increases in response (CNS ischemic response)
- Eventually results in failure of symp. output which then causes pressure to collapse
Decompensation:
Clotting
Hypocoagulauon and fibrinolysis
*during the early stages of shock there is hypercoagulation (which can be treated with heparin)
Decompensation:
Mononuclear phagocytic system
Endotoxins in the gut flora increase and cause widespread vasodilation, which exacerbates the shock
Treatment for shock:
ORDER
- Oxygen asap
- Restore circulating volume using crystalloids, colloids, or blood products
- Drug therapy (inotropic agents: e.g. dopamine, dobutamine)
- Evaluate response
- Remedy underlying cause
What things must you monitor during shock?
Vitals Mental status Urine output Capillary refill Electrolyte status Saturation
What systems are affected in late hypovolemic shock but not early?
Hepatic
GI
Metabolic
