Shock Flashcards
what does the normal perfusion of tissue rely on
Cardiac function
Capacity of vascular bed
Circulating blood volume
how is perfusion measured
no easy way to measure
blood pressure is a surrogate
how do you calculated mean arterial pressure (MAP)
cardiac output x systemic vascular resistance
what are the causes of shock
Hypovolaemia - not enough blood in the system
Cardiogenic - pump not working
Distributive - circuit gets bigger (eg mass vasodilation)
Obstructive (somethings blocking normal CO)
Endocrine
what is hypovolaemic shock (and causes)
Tissue under perfusion due to loss of blood/plasma from the circuit
caused by :
- acute haemorrhage
- severe dehydration
- burns
what is the physiology behind hypovolaemic shock
volume depletion
causes reduced systemic vascular resistance
causes reduced preload leading to reduced cardiac output
overall causing a major drop in MAP
what is cardiogenic shock
‘pump failure’ - heart can no longer pump blood around the body causing big drop in CO therefore big drop in MAP
Causes of cariogenic shock
Ischaemia due to myocardial dysfunction
Cardiomyopathies
Vascular problems
Dysrhthmias
if an MI causes cardiogenic shock what does it suggest
> 40% of the left ventricle is involved
what is obstructive shock
mechanical obstruction to cardiac output in a normal heart
causes of obstructive shock
direct obstruction to cardiac output
- PE
- Air-embolism
Restriction of cardiac filling:
- tamponade
- tension pneumothorax
what is distributive shock
‘hot’ shick
due to disruption of normal vascular auto-regulation causing profound vasodilation
poor perfusion despite increased cardiac output
causes of distributive shock
sepsis
anaphylaxis
acute liver failure
spinal cord injuries
causes of endocrine shock
severe uncorrected hypothyroidism
addisonian crisis
what is endocrine shock
reduced CO and vasodilation with endocrine cause
what is the most common type of shock
Distributive (septic)
what is the sympatho-adrenal response
pathways to preserve normal cardiac output and hence blood pressure
increased sympathetic response
increased noradrenaline
increased adrenaline
causes and increase in HR, contractility, and decreased veno-dilation
this maintains cardiac output
(RAAS maintains BP)
what is the neuroendocrine response
release of pituitary hormones (adrenocorticotrophic hormone, anti-diuretic hormone, endogenous options)
release of cortisol leads to fluid retention
release of glucagon
some shock states blunt the ACTH response
what is the pathophysiology behind shock
poor perfusion
cascade of inflammatory mediators as a consequence of ischaemia
causes a vicious cycle of vasoconstriction and oedema which worsens cellular ischaemia and causes direct cytotoxic damage
what causes the inflammatory response in shock
Part of the pathological process (sepsis)
a consequence of persisting hypo perfusion
can lead to secondary immunosuppression leading to infection
what is the inflammatory response
activation of complement cascade and leukocytes
cytokine release (interleukins, TNF alpha)
lysosomal enzymes released (myocardial depression, coronary vasoconstriction)
adhesion molecules (damage to vessel walls, further leukocyte attraction)
endothelium mediators (nitric oxide)
imbalance between antioxidants and oxidants
haemodynamic changes in shock
vascular abnormalities (vasodilation or vasoconstriction)
maldistribution of blood flow
circulatory abnormalities (AV shunting, increased permeability etc)
inappropriate activation of coagulation
reperforation injuries
what does nitric oxide do
regulates blood flow, coagulation, neural activity and immune function
activated by inflammatory pathway to prevent vasoconstriction
what is myocardial dysfunction
reversible biventricular systolic and diastolic dysfunction
NOT because of reduced coronary blood flow but because of:
- circulating cytokines with myocardial effect
- beta-receptor down regulation
- decreased cardiomyofilament calcium sensitivity
what are they types of hypovolaemia
Class I - <15% blood loss Class II (mild) - 15-30% blood loss Class III (moderate) - 31-40% blood loss Class IV (severe) - >40% blood loss
Clinical signs of hypovolaemic shock
Examination
-pale, cold skin, prolonged cap refill
Urine output
-indicator of renal perfusion
Neuro exam
-disturbed consciousness means decreased cerebral perfusion
biochemical markers
- acidosis
- lactate levels
how do you monitor cardiac output
thermodilution with a PA catheter (gold standard)
pulse contour analysis
doppler ultrasound
management of shock
Prompt diagnosis and treatment critical
ABC approach
establish wide bore IV access and resuscitate will investigating
identify and treat underlying cause
what are the goals of shock management
re-establish sufficient perfusion to allow adequate tissue oxygen delivery
MAP target 65-70 but depends on patient
what are the biggest components to oxygen delivery
Hb
SpO2
CO
correct anaemic and insure SpO2 is normal
how do manage fluids in shock treatment
Increase pre-load
Rapid fluid replacement (minutes)
balance between rapid volume replacement and fluid overload
shock patients are more susceptible to pulmonary oedema
what is a fluid challenge
rapid administration of fluid and assessment of response
not so fast to provoke stress response
usually 300-500ml over 10-20 mins
what types of fluids can be used
Crystalloids
- convenient, safe, cheap
- rapidly lost to extravascular space so need to give a lot
colloids
- cheapish, reduced volume required
- can also cause anaphylaxis and no benefit over crystalloids
blood
- oxygen carrying and will stay in circulation
- scarce resource, multiple risks
If fluids stop working, what can be used instead to bring up blood pressure
Pharmacological treatments
Adrenaline (alpha/beta adrenergic agonist)
Noradrenaline (alpha agonist)
Vasopressin (ADH)
Dopamine (precursor to the above)
Dobutamine/dopexamine
what to do if fluids and pharmacological management fail to increase MAP
mechanical support
cariogenic shock - balloon pumps, ventricular assist devices
VA-ECMO (mechanical circulatory support)
what are the side effects of resuscitation
Extravascular fluid overload
sub-cutaneous oedema obvious
bowel oedema, acute respiratory distress, lung oedema
four stages of shock management
salvage (get a minimal acceptable BP)
optimise (provide adequate oxygen deliver)
Stabilisation (provide organ support)
de-escalation (wean from vasoactive agents, get a -ve fluid balance)
what does de-escalation (de-resuscitation) involve
removing extra fluid once shock has resolved
diuretics, dialysis, spontaneous
