Shock Flashcards
normal tissue perfusion relies on what 3 factors?
cardiac function
capacity of vascular bed
circulating blood volume
how can normal perfusion be measured?
no perfect method
can use BP and MAP
how is MAP measured?
CO X SVR
classifications of shock?
hypovolaemic (blood loss)
cardiogenic (blood not working)
distributive (includes septic, anaphylactic, neurogenic etc)
obstructive
what can cause hypovolaemic shock?
acute haemorrhage
severe dehydration
burns
volume depletion > reduced SVR > vasoconstriction > reduced pre-load > reduced CO)
what causes cardiogenic shock?
pump failure (reduced CO) usually ischaemia induced dysfunction of heart can be cardiomyopathy, valvular problem, dysrhythmias
what causes obstructive shock?
mechanical obstruction to normal cardiac output in an otherwise normal heart
direct obstruction of CO eg PE, air embolism
restriction of cardiac filling eg tamponade, tension pneumothorax etc
what causes distributive shock?
“hot shock”
septic, anaphylactic, acute liver failure, spinal cord injury
causes disruption of normal vascular autoregulation and profound vasodilation
results in poor perfusion despite cardiac output causing regional perfusion differences and alteration of oxygen extraction
endocrine shock?
severe uncorrected hypothyroidism, Addisonian crisis can cause reduced CO and vasodilation
paradoxically thyrotoxicosis can also cause it
most common shock?
distributive (septic, anaphylactic etc)
realistically more mixed in most cases
what is the sympatho-adrenal response?
pathways to preserve normal cardiac output and hence BP
organs have a degree of autoregulation between what MAP?
50-60 <> 150
what is the neuroendocrine response?
release of pituitary hormones (ACTH, ADH and endogenous opiods) to maintain BP
cortisol = fluid retention, antagonises insulin
glucagon released
pathophysiology of shock?
lack of perfusion > cell ischaemia > cascade of inflammatory mediators > cycle of vasoconstriction and oedema causing worsening cell ischaemia and cytotoxic damage
what is reperfusion injury?
cellular hypoxia causes local vasoconstriction, thrombosis, regional variations in perfusion, release of free-radicals and direct cellular trauma
followed by activation of neutrophils, release of pro-inflammatory cytokines
inflammatory response in shock?
can be due to pathological process (sepsis) or consequence of persisting hypoperfusion of tissues
causes harm when disseminated
what follows inflammatory response in shock?
2ndary immune suppression leaving predisposition to 2ndary infection
components of inflammatory response in shock?
complement cascade = attraction and activation of leucocytes
cytokine release = interleukins, TNF alpha
platelet activating factor = increased vascular permeability, platelet aggregation
lysosomal enzymes = myocardial depression, coronary vasoconstriction
adhesion molecules = damage to vessel walls, leucocyte attraction
endothelium derived mediators (NO)
imbalance between antioxidents and oxidents
what haemodynamic changes occur in shock?
vascular abnormalities (vasodilation/constriction)
maldistribution of blood flow
microcirculatory abnormalities (AV shunt, changed flow in capillary beds, failure of capillary recruitment, increased capillary permeability)
inappropriate activation of coagulation system
DIC
reperfusion injuries
how does loss of vascular reactivity occur in shock?
inflammation pathways activate isoform of cNOS (iNOS) in vessel smooth muscle walls which produces lots of NO resulting in failure of vascular smooth muscle constriction (NO = vasodilator)
what causes myocardial dysfunction?
(not due to reduced coronary blood flow)
circulating cytokines have direct myocardial effect
downregulation of beta receptors
decreased cardiomyofilament calcium sensitivity
clinical features of cardiogenic shock?
hypotension + signs of myocardial failure
signs of septic shock?
hypotension + pyrexia, vasodilation, rapid cap refill
signs of hypovolaemic/obstructive? shock?
hypotension + raised JVP
pulsus paradoxus
signs of cause
signs of anaphylactic (distributive) shock?
hypotension + profound vasodilation, erythema, bronchospasm, oedema
classes of hypovolaemia in terms of blood loss?
class 1 = <15% class 2 = 15-30% class 3 = 31-40% class 4 = >40%
changes in class 2?
HR may increase
pulse pressure decreased
-2 to -6 mEg/L base deficit
possible need for blood products
changes in class 3?
increased HR normal/decreased BP decreased PP normal/increased RR reduced urine output reduced GCS -6 to -10 base deficit needs blood products
changes in class 4?
increased/very increased HR decreased BP decreased PP increased RR very reduced urine output reduced GCS -10+ base deficit needs massive transfusion protocol
clinical monitoring in shock?
examination (colour, temp, cap refill)
urine output (indicator of renal perfusion)
neurological (GCS indicates cerebral perfusion)
biochemical (acidosis and lactate levels are measure of general perfusion)
how can BP be measured?
cuff or invasive via arterial line
can be normal pressure due to vasoconstriction but still hypoperfusing tissues
how can central venous pressure be measured?
put a line in and measure via fluid?
what other pressures should be measured?
pulmonary artery pressure
pulmonary capillary wedge pressures (surrogate for LA pressure)
- rarely used in practice due to risk
how is CO monitored in shock?
gold standard = thermodilation with a PA catheter (rarely used outside specialist units)
can use pulse contour analysis or doppler US
how is shock managed?
ABCDE
establish reliable wide bore IV access and resuscitate while investigating
identify and treat cause
4 stages of management of shock?
salvage - obtain minimal BP (70-80), perform lifesaving measures optimization - provide oxygen availability - optimize CO, SvO2 and lactate stabilization - organ support, minimise complications de-escalation - wean from vasoactive agents, achieve negative fluid balance
MAP goal in shock?
65-70
however needs to be assed with clinical picture (e.g if patient is oliguric at 65 then aim for higher, if still haemorrhaging aim for lower)
how is oxygen delivery measured?
CO X (1.39 x Hb x SpO2) + (PaO2 x 0.003) SvO2 can help estimate balance between supply and demand
biggest components of oxygen delivery?
Hb
SpO2
CO
fluid management of shock?
increase pre-load
rapid fluid replacement (mins)
- fluid challenge (300-500ml over 10-20 mins) with a target in mind (stop if non responsive)
- use either crystalloids, colloids or blood
risks of rapid fluid replacement in shock?
balance rapid volume replacement and risk of fluid overload as shock increases risk of pulmonary oedema due to microvascular dysfunction
how to decide which fluids to use?
crystalloids cheap and safe but lost from circulation quickly
colloids cheap but blood volumes required and can cause anaphylaxis
blood has good O2 and stays in circulation but scarce resource with multiple risk
what is used as pharmacological treatment in shock when fluids don’t work?
adrenaline (apha/beta agonist) noradrenaline (most commonly used, alpha agonist) vasopressin (ADH) dopamine (ADH precursor) dobutamine/dopexamine
what is used in shocj when drugs don’t work?
mechanical support
cardiogenic = balloon pumps, L-VADs, R-VADs
severe cases = VA- ECMO
side effects of resuscitation?
positive fluid balance (volume delivered never remains intra-vascular)
extra-vascular overload in an intra-vascularly dry patient causes sub-cutaneous oedema, wet lungs/ARDS, bowel oedema etc
how can excess fluid be removed after shock has resolved (de-escalation)?
spontaneously
diuretic
dialysis
