Shock Flashcards
What is shock
insuff tissue perfusion causing impaired cellular metabolism
What shock relates to low blood flow
Cardiogenic
Hypovolemic
What shock relates to the distribution of blood
Septic
Anaphylactic
Neurogenic
Can edema be a cause of hypovolemia
yes with massive edema
What are the causes of cardiogenic shock
things that cause heart failure
So if cardiogenic shock is caused from HF then what would be a diagnositic test to assess for HF
using a swans gans cath in the pulmonary artery
How much fluid needs to be lost for hypovolemic shock to kick in
more than 30%
What are some causes of relative hypovolemia
Sepsis, burns, bowel obstruction
What happens in neurogenic shock
SNS is turned off so no more vasoconstriciton, increased HR, RR, etc.
What are some causes of neurogenic shock
spinal injury
spinal anesthesia
opioids
benzodiazepines
If the SNS is turned off in neurogenic shock then what takes over
the parasympathetic
So then if the parasymp has taken over in neurogenic shock then what manifestations would we likely see
bradycardia
hypotension
What is a big difference with the heart rate between hypovolemic/cardiogenic and neurogenic shock
the first two will increase HR while neuro decreases it
What happens in anaphylactic shock
massive vasodilation from histamine release so permeability increases
What is a distinctive mani of anaphylactic shock
angioedema
What happens in septic shock
vasodilation from infection
What is indicative symptoms of septic shock
warm flushed skin
What is obstructive shock
Occurs when blood flow is restricted by decreased cardiac output
so everything works you just have something cause a restriction
What are some causes of obstructive shock
Tamponade. Pneumothorax, abdominal compartment syndrome
RV thrombi, PE
What indicative symptom might be seen in obstructive shock
JVD and pulsus paradoxus
What do we see in the initial stage of shock
not much
little lactic acid build up from anaerobic meta from lack of perfusion
What happens in the compesatory stage of shock
start seeing the body compensate like SNS kicking in, ADH prod, RAAS
Start seeing BP drop from less CO
With ↓ CO baroreceptors stimulate SNS vasoconstriction (epinephrine & norepinephrine) and blood to vital organs is maintained but is cut off to non-vital (kidneys, GI, skin, lungs, etc.)
With ↓ flow to kidneys RAAS system is initiated vasoconstriction of veins and arteries ↑ return to the heart and ↑ BP
At the same time the adrenal cortex is stimulated ADH increased reabsorption of water and sodium at kidneys increases circulating volume and ↑BP and ↑CO.
↓ blood to GI ↓ GI motility (potential paralytic ileus)
↓ blood to skin cool & clammy (septic patient will be warm)
↓ blood to lungs means there will be decreased chance for oxygenation at the same time that the heart has begun to work harder (↑ oxygen demand) compensatory ↑rate and ↑ depth of respirations remember VQ mismatch from the respiratory lecture
Coronary arteries dilate, heart speeds up, increases output and all is well. If we can correct the insult at this point there will probably be a full recovery . . . . . And if not . . . . The progressive stage
What are some manifestations during the compensatory stage
the signs of compensation
What happens as you enter the progreessive stage
metabolic acidosis after the compensatory mechs have failed
What are other manifestations of the progressive stage
organs start to fail
systemic interstitial edema
anasarca
What happens in the refractory stage
interventions are a lot less responsive
What are the interventions for shock
oxygenate
give fluids
give a blanket (from cold fluids entering the vessels)
blood transfusions
vasoconstrictors like epi
vasodilators for cardiogenic shock
parenteral feeding for first 24 hrs if shock was stabalized
What ratio do we give fluids when replacing it during hypovolemic shock
3:1
What is one of the last things to go in the nervous system
pain response
