Shock Flashcards
Define shock
A syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement
State the three things that normal tissue perfusion relies on
3 P’s
•Cardiac Function (pump)
•Capacity of vascular bed (pipes)
•Circulating blood volume (plasma)
What four clinical markers are used to assess perfusion
- Blood pressure
- Consciousness (Brain perfusion)
- Urine output (Renal perfusion)
- Lactate (General tissue perfusion)
What determines blood pressure
Cardiac output and systemic vascular resistance
(MAP = CO x SVR)
What 3 key measurements determine oxygen delivery (perfusion)
Cardiac output
Hb concentration
O2 saturations
(DO2 = CO x [(1.34 x Hb x SaO2) + (PaO2 x 0.003)])
Name the 5 main types/causes of shock
- hypovolaemic (plasma)
- cardiogenic (pump)
- distributive (most common) (pipes)
- obstructive (pump)
- endocrine (pump & pipes)
What is hypovolaemia, what commonly causes it and what is the pathophysiology of hypovolaemic shock
Loss of plasma or blood volume
- Acute haemorrhage e.g. trauma, surgery, GI haemorrhage
- Severe dehydration e.g. diarrhoea, vomiting
- Burns
Decrease in blood volume → decreased venous return → decreased EDV → decreased SV (Frank-Starling) → decreased CO and BP → inadequate tissue perfusion
What is cardiogenic shock, what commonly causes it and what is the pathophysiology
‘Pump failure’ causes reduced CO
- Ischaemia induced myocardial dysfunction (most common)
- cardiomyopathies,
- valvular problems,
- dysrhythmias
Decreased cardiac contractility (e.g. due to acute MI) → decreased stroke volume → decreased CO and BP → inadequate tissue perfusion
What is distributive (vasoplegic) shock, what commonly causes it and what is the pathophysiology
Disruption of normal vascular autoregulation, and profound vasodilation, resulting in poor perfusion (despite increased CO)
- septic shock
- anaphylactic shock
- neurogenic shock (SC injuries)
- acute liver failure
Loss of sympathetic tone to blood vessels and heart → massive venous and arterial dilation and heart rate slows → decreased venous return and SVR → decreased CO and BP → inadequate tissue perfusion
What is obstructive shock, what commonly causes it and what is the pathophysiology
Mechanical obstruction to normal cardiac output in an otherwise normal heart
- Direct obstruction to cardiac output - PE, air/fat/amniotic fluid embolism
- Restriction of cardiac filling - tamponade, tension pneumothorax
Increased intrathoracic pressure → decreased venous return → decreased EDV → decreased SV (Frank-Starling) → decreased CO and BP → inadequate tissue perfusion
What causes endocrine shock?
- Severe uncorrected hypothyroidism, Addisonian crisis
(both cause reduced CO and vasodilation) - Paradoxically can also be caused by thyrotoxicosis
Describe the baroreceptors response to hypovolaemic shock
- Stretch sensitive receptors in the carotid sinus (CN IX) and aortic arch (CN X)
- Decreased BP → decreased stretch → decreased afferent input to medullary CV centres
- Inhibition of parasympathetic (CN X) and enhanced sympathetic output
Hypovolaemic shock stimulates the sympathetic system through the baroreceptor reflex. How does this affect the heart
Increased chronotropic & inotrophy
Hypovolaemic shock stimulates the sympathetic system through the baroreceptor reflex. What hormones are released as a result? What effect do they have on the vasculature?
Adrenal catecholamines (epinephrine & norepinephrine)
They are vasoconstrictors
This redirects fluid from peripheral & secondary organs
This also increases venous return → increased CO
During hypovolaemic shock, the redirection of fluid as a result of norepinephrine & epinephrine results in what substance accumulating? What effect does this have?
Lactate → lactic acidosis
This drives chemoreceptors that enhance the catecholamine response
As a result of hypovolaemic shock, there is a reduced capillary hydrostatic pressure. What is the relevance of this?
This results in an inward net filtration →
Interstitial fluid is absorbed →
Increased plasma volume
As as result of hypovalaemic shock, intra renal baroreceptors are stimulated. What effect does this have?
Intrarenal baroreceptor stimulation →
Renin release from JGA & RAAS increased→
Ang II causes vasoconstriction &
Ang II also increases aldosterone & vasopressin release →
This increases Na & water reabsorption in kidneys →
What is the effect of hypovolaemic shock on the lungs?
Pulmonary congestion
How does the inflammatory response to shock negatively impact the patient
- Increased vascular permeability (loss of fluid)
- endothelial mediators like NO released (vasodilation)
- lysosomal enzyme release (myocardial depression & coronary vasoconstriction)
- Imbalance between antioxidants & oxidants (oxidative stress)
- overactive complement cascade, cytokine relsease & leukocytes
- secondary immune suppression, leading predisposition to secondary infection
Shock can lead to AV shunting? Is this a good thing?
AV shunting basically ignores/ by-passes the capillary beds.
This leads to tissue hypoxia
Shock can lead to the inappropriate activation of the coagulation system, what complication can this lead to?
Disseminated intravascular coagulation (DIC) ⇒
Can cause organ damage & uncontrollable bleeding
Inflammation due to shock can cause greatly elevated NO. Is this good? Why or why not?
No…
- failure of smooth muscle constriction ⇒
- vasodilation ⇒
- decreased venous return ⇒
- decreased CO & BP
Shock can lead to myocardial dysfunction despite coronary blood flow (usually) being preserved. What is the most likely cause of myocardial dysfunction? (3)
- Circulating cytokines & lysosomal enzymes
- Beta receptor downregulation
- Decreased cardiomyofilament calcium sensitivity
Summarise the hormones that are produced in response to shock
Pituitary - ACTH, ADH, opioids
Adrenal - Cortsiol, aldosterone
Pancreas - Glucagon
Shock clinical presentation
- Common clinical feature - hypotension
- Hypovolaemic- bleeding, pale, cold, prolonged cap refill
- Cardiogenic - signs of myocardial failure
- Obstructive - raised JVP, pulsus paradoxus, signs of cause
- Distributive (septic) - pyrexia, vasodilation, rapid cap refill
- Distributive (anaphylaxis) - vasodilation, erythema, bronchospasm, oedema
Shock investigations (perfusion & CO assessment)
Assess perfusion
- Blood pressure
- Consciousness (brain perfusion)
- Urine output (renal perfusion)
- Lactate (general tissue perfusion)
Assess CO
- Pulse contour analysis (most commonly used)
- Thermodilution with PA catheter (gold standard but rarely used)
Shock management phases
Salvage
- What? -providing life saving measures
- GOAL - adequate BP
Optimise
- What? -ensuring adequate oxygen availability
- GOAL - improved CO, SvO2, lactate
Stabilise
- WHAT? -providing organ support to minimise complications
- GOAL - functioning brain, kidney, heart etc
De-escalate
- WHAT? -weaning off of vasoactive agents
- GOAL - appropriate fluid balance
Shock fluid management
(Crystalloid) Fluid challenge
- rapid fluid administration (~300-500ml over 10-20mins)
- rapid enough to get response
- but not too rapid as to provoke stress response
- assess response before administering more
Shock pharmacological management
- Epinephrine (alpha & beta agonist)
- Norepinephrine (primarily alpha agonist)
- Vasopressin (ADH)
- Dopamine (precursor of above 3)
- Dobutamine/dopexamine (dopamine analogues)
Summary of general shock management
- ABCDE
- Fluid management
- Pharmacological management (if fluids fail)
- Mechanical support management (if drugs fail)
Hypovolaemic shock management
- Assessment of bleeding - volume & speed
- Establish source - may require imaging if stable
- Temporisation - direct pressure, tourniquets
- Damage limitation resuscitation - until definitive control
- Damage limitation surgery
Obstructive & Distributive shock definitive management
- Distributive (septic) - antibiotics
- Distributive (anaphylaxis) - epinephrine
- Obstructive - e.g. tension pneumothorax decompression & drain
Neurogenic shock pharmacological management
Vasopressin & dopamine
After resuscitation, patients often have extra fluid, how is this removed?
Either spontaneous or diuretic or dialysis
Why are shock patients more vulnerable to pulmonary congestion/oedema
Myocardial dysfunction
Fluid resuscitation side effects
- Oedema (intra vascular fluid will leave into extravascular)
- E.g. subcutaneous oedema, ‘wet lung’/ARDS etc
