Shock Flashcards
what is shock
A syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement that results in a state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation, or a combination of these processes
how do you calculate mean arterial pressure
cardiac output x systemic vascular resistance
how can you measure perfusion
BP
lactate, urine output
what are the causes of shock
hypovolaemic (haemorrhage, dehydration, burns= volume depletion= reduced SVR= vasoconstriction= reduced pre load and CO)
cardiogenic (MI, cardiomyopathy, valvular problems, dysrthmias = pump failure= reduced CO)
distributive (septic, anaphlylaxis, acute liver failure, spinal cord injuries = disruption of normal vascular autoregulation + profound vasodilation flushed, hot = poorly perfused despite increase CO)
obstructive (CO obstructed- PE, air embolism. Cardiac filling obstructed= tamponade, tension pneumothorax)
endocrine (severe hypo/hyperthyroidism, addisonian crisis = reduced CO and vasodilation)
what is the most common type of shock
distributive (septic)
- in reality usually a mixed picture
what is the most important pathway in BP autoregualtion
sympatho-adrenal response
(baroreceptors and chemoreceptors increased sympathetic nervous activity)
adrenal medulla increases aldosterone and renin to activate RAAS system)
what is the neuroendocrine response to shock
release of pituitary hormones: ACTH, ADH, endogenous opioids
release of cortisol: fluid retension, antagonises insulin to release glucose
release of glucagon
what is reperfusion injury
when local vasoconstriction, thrombosis, regional variations in perfusion, release of free radicals and direct cellular trauma cause activation on inflammatory mediators
this results in worsening cellular ischaemia, vasoconstriction and oedema which make shock worse
what are the components of the inflammatory response in shock
Activation of complement cascade – attraction and activation of leucocytes
Cytokine release – Interleukins, TNF-alpha
Platelet activating factor – Increased vascular permeability, platelet aggregation
Lysosomal enzymes – Mycardial depression, coronary vasoconstriction.
Adhesion molecules – damage to vessel walls, further leucocyte attraction
Endothelium derived mediators – Nitric oxide
Imbalance between antioxidents and oxidents
what haemodynamic changes happen in shock
vasodilation/ constriction maldistribution of blood flow microcirculatory abnormalities- AV shunting, poor functioning capillary beds, increased capillary permeability inappropriate coagulation activation DIC reperfusion injuries
what happens to vascular reactivity in shock
vascular smooth muscle fails to constrict (nitric oxide plays big role)
what causes myocardial dysfunction in shock
circulatory cytokines with direct myocardial effect
beta receptor down regulation
decreased cardiomyofilament calcium sensitivity
what are the different clinical features for the types of shock
ALL usually hypetensive
cardiogenic- signs of myocardial failure: pale, clammy, cold
obstructive: myocardial failure + raised JVP, pulsus paradoxus, signs of cause
Distributive:
- septic shock (distributive): pyrexia, vasodilation, rapid cap refill
- anaphylaxis: profound vasodilation, erythema, bronchospasm, oedema
what are the classes of hypovolaemia
(on approx blood loss) class 1 <15% class 2 (mild) 15-30% class 3 (mod) 31-40% class 4 (severe) >40%
what are the signs of class 1 hypovolaemia
normal obs
base deficit 0 to -2
monitor need to blood products
what are the signs of class 2 hypovolaemia
Hr normal or increased
pulse pressure decreased
base deficit -2 to -6
possible need for blood products
what are the signs of class 3 hypovolaemia
HR increased BP normal/ decreased PP decreased RR normal/ increased urine decreased GCS decreased base deficit -6 to -10 need blood products
what are the signs of class 4 hypovolaemia
HR increase/ v increasd BP decreased PP decreased RR increased urine output V decreased GCS decreased vase deficit -10 or less massive transfusion protocol needed
what is pulse pressure
the difference between diastolic and systolic BP
what is urine output a measure of
renal perfusion
what is GCS an indicator of
cerebral perfusion
how can you measure BP
cuff
invasive- arterial line
what is central venous pressure used to measure
response to fluid
useful to follow trends not so much for one off valvue
what pulmonary pressures can be meausred
pulmonary artery pressure
pulmonary capillary wedge pressure
(not done in practise usually)
how is cardiac output monitored
gold standard- thermodilution with a PA catheter
pulse contour analysis
doppler ultrasonography
when do you start fluid resus
ASAP- when investigating cause
what are the steps of shock management (hypovolaemic)
obtain minimal acceptable BP (70-80)
oxygen (optimise CO, SVO2, lactate)
provide organ support
wean from vasoactive agents, achieve a negative fluid balance
what is the goal MAP for most
65-70
what are the biggesr influences on oxygen delivery
Hb- correct anaemia
SpO2- oxygen
CO- optimise
why do you have to be careful wit rapid fluid replacement in shock
as shocked patients more at risk of pulmonary oedema due to microvascular dysfunction
what is a fluid challenge
300-500mls in 15-20mins
MUST asses response
avoid other procedures that will stress the patient in this time
can be repeated but if patient unresponsive should stop
what are the pros and cons of each type of fluid
crystalloids (saline, hartmanns) P- convenient, safe, cheap. C- rapidly lost from circulation into extravascular space, large volumes required
colloids - P-cheap, reduced volumes required. C- can cause anaphlyaxis
blood P- O2 carrying capacity, will stay in circulation. C- scarce resource, multiple risks
what drugs can be given in hypovolaemic shock
(only when fluids not working, only by experienced specialist)
adrenaline (alpha/beta adrenergic, increases HR, contractility, vasodilation)
noradrenaline (alpha agonist, vasoconstriction)
vasopressin (ADH)
dopamine (precursor to the above)
dobutamine/ dopexamine
what mechanical methods can be used to treat shock
in cardiogenic: balloon pumps, L-VADs, RVADs
if severe- VA-ECMO
what is the management for hypovolaemic shock
Assessment of bleeding – estimation of volume loss, and speed of ongoing loss.
Establish source – may require imaging if stable
Temporisation – Direct pressure, tourniquet’s
Damage limitation resuscitation – until definitive control
Damage limitation surgery
what are possible side effects of resus
extra vascular overload- sub cutaneous oedema, wet lungs/ ARDS, bowel oedema
what is de-escalation
removing extra fluid from patient once shock resolved- spontaenous, diuretic, dialysis
