Shock Flashcards

1
Q

what does the normal perfusion of tissue rely on

A

Cardiac function
Capacity of vascular bed
Circulating blood volume

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2
Q

how is perfusion measured

A

no easy way to measure

blood pressure is a surrogate

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3
Q

how do you calculated mean arterial pressure (MAP)

A

cardiac output x systemic vascular resistance

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4
Q

what are the causes of shock

A

Hypovolaemia - not enough blood in the system

Cardiogenic - pump not working

Distributive - circuit gets bigger (eg mass vasodilation)

Obstructive (somethings blocking normal CO)

Endocrine

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5
Q

what is hypovolaemic shock (and causes)

A

Tissue under perfusion due to loss of blood/plasma from the circuit

caused by :

  • acute haemorrhage
  • severe dehydration
  • burns
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6
Q

what is the physiology behind hypovolaemic shock

A

volume depletion

causes reduced systemic vascular resistance

causes reduced preload leading to reduced cardiac output

overall causing a major drop in MAP

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7
Q

what is cardiogenic shock

A

‘pump failure’ - heart can no longer pump blood around the body causing big drop in CO therefore big drop in MAP

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8
Q

Causes of cariogenic shock

A

Ischaemia due to myocardial dysfunction

Cardiomyopathies

Vascular problems

Dysrhthmias

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9
Q

if an MI causes cardiogenic shock what does it suggest

A

> 40% of the left ventricle is involved

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10
Q

what is obstructive shock

A

mechanical obstruction to cardiac output in a normal heart

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11
Q

causes of obstructive shock

A

direct obstruction to cardiac output

  • PE
  • Air-embolism

Restriction of cardiac filling:

  • tamponade
  • tension pneumothorax
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12
Q

what is distributive shock

A

‘hot’ shick

due to disruption of normal vascular auto-regulation causing profound vasodilation

poor perfusion despite increased cardiac output

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13
Q

causes of distributive shock

A

sepsis
anaphylaxis
acute liver failure
spinal cord injuries

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14
Q

causes of endocrine shock

A

severe uncorrected hypothyroidism

addisonian crisis

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15
Q

what is endocrine shock

A

reduced CO and vasodilation with endocrine cause

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16
Q

what is the most common type of shock

A

Distributive (septic)

17
Q

what is the sympatho-adrenal response

A

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)

18
Q

what is the neuroendocrine response

A

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

19
Q

what is the pathophysiology behind shock

A

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

20
Q

what causes the inflammatory response in shock

A

Part of the pathological process (sepsis)

a consequence of persisting hypo perfusion

can lead to secondary immunosuppression leading to infection

21
Q

what is the inflammatory response

A

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

22
Q

haemodynamic changes in shock

A

vascular abnormalities (vasodilation or vasoconstriction)

maldistribution of blood flow

circulatory abnormalities (AV shunting, increased permeability etc)

inappropriate activation of coagulation

reperforation injuries

23
Q

what does nitric oxide do

A

regulates blood flow, coagulation, neural activity and immune function

activated by inflammatory pathway to prevent vasoconstriction

24
Q

what is myocardial dysfunction

A

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
25
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 ```
26
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
27
how do you monitor cardiac output
thermodilution with a PA catheter (gold standard) pulse contour analysis doppler ultrasound
28
management of shock
Prompt diagnosis and treatment critical ABC approach establish wide bore IV access and resuscitate will investigating identify and treat underlying cause
29
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
30
what are the biggest components to oxygen delivery
Hb SpO2 CO correct anaemic and insure SpO2 is normal
31
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
32
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
33
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
34
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
35
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)
36
what are the side effects of resuscitation
Extravascular fluid overload sub-cutaneous oedema obvious bowel oedema, acute respiratory distress, lung oedema
37
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)
38
what does de-escalation (de-resuscitation) involve
removing extra fluid once shock has resolved diuretics, dialysis, spontaneous