Shock Overview & Stages of Shock Flashcards
What is shock?
A condition that results from some type of cause that leads to decreased tissue perfusion, which causes cell hypoxia
If the cell hypoxia is severe enough, it’ll cause organ dysfunction (MODS) & eventually lead to death
Cause of shock depends on what type of shock is presenting
___ shock
Occurs d/t an allergic reaction
Anaphylactic
___ shock
Occurs d/t a severe infection
Septic
___ shock
Occurs d/t a weak heart
Cardiogenic
___ shock
Occurs d/t severe fluid loss
Hypovolemic
___ shock
Occurs d/t severe damage to the neuro system (e.g., spinal injury)
Neurogenic
Distributive shock includes which 3 types of shock?
septic
anaphylactic
neurogenic
Stages of Shock
- Initial
- Compensatory
- Progressive
- Refractory
Initial Stage
✰ CO is low enough to cause the cells to experience ___
Cells switch from aerobic to anaerobic metabolism; the latter will create lactic acid, which’ll accumulate in the blood & lead to lactic acidosis
hypoxia
- Decreased tissue perfusion → LOW CO (HR x SV)
- Normally, body can deal w/lactic acid via the liver, but liver is not functioning @ an optimal lvl b/c of the low amt of O2 its cells are receiving
- In better circumstances when tissue perfusion is adequate, liver takes lactic acid & converts it to pyruvic acid & then to glucose via gluconeogenesis
! Therefore, lactic acid will start to accumulate in the blood (esp as pt adv to other stages of shock)
- Accumulation of lactic acid causes the blood’s pH lvl to drop (acidosis) & further damages cells
Normal serum lactate lvl < ____ mmol/L
1
Abnormal indicating lactic acidosis > ____ mmol/L
4
Compensatory Stage
✰ Body systems are coming to the rescue; will try to compensate by using hormonal, neural, & biochemical processes in the body
- Will try to fight results of anaerobic metabolism; also, will try to increase CO & BP via stimulation of the SNS & RAS, which’ll increase tissue perfusion
- If the cause of shock is corrected during this stage, it’s REVERSIBLE & pt can make a full recovery; if not, next stage
- Body will succeed @ 1st w/increasing CO & BP via rescue team
- Will result in an increase in tissue perfusion, BUT body is limited on how long it can maintain rescue effort
How does the body provide compensation?
- As BP drops, body will sense this (! brain & heart)
1 of the structures to sense this drop in BP is the ____, spec the receptors in the carotid sinus & aortic arch
Will stimulate the SNS to release catecholamines: ___ & ___
baroreceptors
epinephrine; norepinephrine
- Catecholamines will cause vasoconstriction
- This’ll result in an increase in BP & HR; when this occurs, there’s an increased perfusion to the vital organs
- Less blood will go to the non-vital organs (GI, renal, skin, lungs) while more will go to the vital organs (heart & brain)
- B/c there was a drop in BP (arterial pressure) there will be a decrease in capillary hydrostatic pressure (the force of pressure the blood creates around the capillary wall)
- If the BP & CO are low, the force of pressure the blood creates around the capillary wall is definitely low
- This’ll signal the body to try to increase venous blood flow return by shifting fluid from the interstitial compartment to the intravascular compartment
How are other systems affected & how do they play a role in the compensatory stage?
Kidneys
- B/c blood flow is dec to the kidneys they activate the renin-angiotensin system
- Renin stimulates angiotensinogen which creates angiotensin I
- Angiotensin I turns into angiotensin II (a very mighty vasoconstrictor)
- This substance will cause vasoconstriction in both arterial & venous system
- Constriction in venous system will lead to more blood return to the heart, & constriction in arterial system will incr BP
- Together, all will lead to an incr in tissue perfusion & the cells will receive more O2
Presence of angiotensin II will also trigger the release of ____
aldosterone
Aldosterone
- Makes the kidneys keep sodium & water → incr blood volume
- Also, b/c kidneys are incr sodium, it’ll create urine to contain a high amt of sodium, which leads to high osmolality
- High osmolality signals to posterior pituitary gland that body is trying to keep water for some reason, so it releases ADH
- ADH → prevents water from leaving the kidneys; further incr blood volume
- By incr blood volume, CO will be incr along w/tissue perfusion
GI
- Perfusion is dec so this system slows down
- Pt is @ risk for paralysis of intestines in a cond called paralytic ileus
Skin
- Perfusion is dec so blood flow is low, which leads the skin to be cold & clammy
! Is not the case during this stage in septic shock → pt’s skin will be hot & flushed d/t vasodilation presenting
Lungs
- Perfusion is dec so parts of the lung may not be perfused
! Ventilation & perfusion mismatch & O2 lvls become low in blood
- Will lead pt to hyperventilate
Progressive Stage
✰ Rescue effort from prev stage has failed, & body can’t compensate anymore; pt is progressing to MODS
- Is no more compensation in this stage; CO is low, tissue perfusion is low, & cells are NOT receiving O2, which leads to cell hypoxic injury
- Cells will start to swell & CAPILLARY PERMEABILITY is incr
Brain
- Cells to the brain aren’t being perfused; MAP is <60 mmHg
- This means cerebral perfusion pressure (CPP) is inadequate to maintain perfusion to brain’s cells
- Will start to see major mental status changes
- Pt will be very slow in their speech, restless, anxious, agitated, & not respond to stimulation
Lungs
- ARDS will develop
- This occurs d/t incr capillary permeability in the alveoli sacs (where gas exchange occurs); sacs will collapse d/t fluid surrounding them & lung will lose elasticity
! Will need intubation & mech vent to breathe
- Fluid in the lungs (crackles), incr RR, dec O2 lvl, & resp failure
Heart
- Heart cells start to die incl those that play a role in the electrical conduction system of the heart & that help heart contract/pump
! Cardiac dysrhythmias occur along w/death to myocardial tissue
GI
- Gut cells start to die; e.g., cells that protect the lining from its own acid quit working
! Ulcers can develop which can turn into massive GI bleeding (bad b/c clotting abilities are affected d/t liver hypoxia)
Liver
- Dec liver perfusion causes cells to die
- Will be a build-up of toxic waste products (e.g., bilirubin, ammonia)
! Risk for infection & bleeding
?
Occurs when small clots form in the vessels, further compromising blood flow to organs
Depletes body’s platelets & clotting stores & leads to massive, uncontrollable bleeding
DIC (disseminated intravascular coagulation)
____ Stage
- Unmanageable; cannot be reversed; all organs shut down and fail; death inevitable
Refractory
