Sepsis and shock Flashcards

1
Q

Score system for patinets risk in sepsis

A

qSOFA

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2
Q

Define SIRS

A

2 or more of:

  • Temperature < 36°C or > 38°C
  • Heart rate > 90 beats/min
  • Respiratory rate > 20 or PaCO2 less than 4.5 kPa ormechanically ventilated
  • White Cell Count < 4 or > 11 or > 10%immature forms
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3
Q

Define sepsis

A

SIRS plus documented or suspected infection

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4
Q

Define Septic shock

A

Sepsis with hypotension (Systolic blood pressure <90mmHg or need for vasopressor infusion) despite adequate fluid resuscitation

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5
Q

Name 3 non infective causes of SIRS

A
- Burns
  Trauma
  Pancreatitis
  Cardiopulmonary bypass
- Massive transfusion.
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6
Q

What are Toll like receptors for

A

recognition of molecules Eg lipopolysaccahride on microorganisms

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7
Q

What happens when toll like receptors activated

A

Activate transcription factors eg Nuclear factor kappa beta -> secretion of pro/antiinflammatory mediators

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8
Q

Name 2 inflammatory mediators

A

Interleukins 1,2 and 6

Tumour necrosis factor alpha

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9
Q

What do inflammatory mediators do

A

Activate leukocytes
activate coagulation cascade
endothelial damage
synthesize NO -> vasodilation and poor perfusion

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10
Q

How much fluid in septic shock

A

30ml/kg in first 3 hours

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11
Q

Sepsis in ITU hour 1

A

Measure lactate level*

Obtain blood cultures before administering antibiotics.

Administer broad-spectrum antibiotics.

Begin rapid administration of 30mL/kg crystalloid for hypotension or lactate level ≥ 4 ​mmol/L.

Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP ≥ 65 mm Hg.

  • Remeasure lactate if initial lactate is elevated (> 2 mmol/L)
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12
Q

Additional sepsis considerations

A

Hydrocortisone 200mg IV once daily if adequate fluid resus / vasopressors and still haemodynamic instability

Keep glucose <10mmol

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13
Q

Define shock

A

circulatory insufficiency with inadequate oxygen delivery resulting in hypoperfusion and tissue hypoxia

Essentialy DO2

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14
Q

Vasopressor 1st line in shock
For shock of unknown cause ?

For septic shock?

For cardiogenic shock?

A

For shock of unknown cause use adrenaline.

For septic shock use noradrenaline.

For cardiogenic shock use dobutamine.

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15
Q

Where does the sympathetic autonomic system originate?

A

Sympathetic autonomic nervous system originates from T1-L2

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16
Q

After originating in T1-L2 where does the sympathetic autonomic system go

A
  • connect through synapses to postganglionic neurons.

- These synapses are located in the two sympathetic chains that lie on either side of the vertebral column

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17
Q

Main parasympathetic nerve? Where are key parasympathetic ganglia?
Which key receptor in parasympathetic system

A

Vagus

  • Parasympathetic ganglia are embedded in the heart, mainly on the SA and AV nodes
  • ß2receptors are present on other organs, stimulation causes relaxation e.g. of bronchial and uterine smooth muscle.
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18
Q

Effect of sympathetic systm on heart

A
  • increase chronotropy and ionotrphy

- B1 / B2 receptors

19
Q

What type of parasympathetic receptors in heart?
What effect when stimulated?
How can you block the parasympathetic effect ?

A
  • acetylcholine receptors located on the SA and AV nodes
  • negative chronotropic effect and reduces the speed of conduction through the AV node.
  • Constant vagal tone limiting heart rate
  • Block this tone by administering atropine
20
Q

Sympathetic receptor in smooth muscle ? When might it be reduced? effect ?

What happens when stimulated?

A
  • α1 in smooth muscles
  • If reduced - e.g. high spinal transection or spinal anaesthesia -> decreased tone
  • Increase -> increase in vascular tone and resistance -> increased blood pressure (but a reduction in blood flow)
21
Q

Blood pressure (BP) =

A

Blood pressure (BP) = Cardiac output (CO) X systemic vascular resistance (SVR)

22
Q

CO =

A

CO = Stroke volume (SV) x Heart rate (HR).

23
Q

What is hypoperfusion (Low BP) caused by

A
  • low cardiac output (cardiogenic shock, outflow obstruction, hypovolaemic shock)
  • low SVR (neurogenic or septic shock) or both (septic shock).
24
Q

What is the most common cause of low stroke volume in critically unwell pt

A

low pre-load from either hypovolaemia or relative hypovolaemia is probably the most common cause of a low SV and subsequent low CO and reduced perfusion

25
Q

Hypovolaemic shock common causes?
What happens?
How does the pt appear?

A
  • fluid loss; haemorrhage, salt and water loss, sepsis, burns,
  • decrease the stroke volume and cardiac output - >tachycardia and increased SVR
  • Cold and shut down
26
Q

How does distributive shock present

A

Peripheral vasodilation Eg Sepsis, anaphylactic and neurogenic shock.

27
Q

Key features of neurogenic shock

A

hypotension, bradycardia, warm peripheries, venous pooling and sometimes priapism

28
Q

Egs of obstructive shock

A

PE, Aortic stenosis, pericardial effusion and tension pneumothorax.

29
Q

Why does respiratory rate go up in shock

A

Tissue hypoxia -> metabolic acidosis -> increase RR as compensatory method

30
Q

What are the 4 stages of shock ?

A

1 Initial

2- Compensatory

3 Progressive

  • Once compensatory mechanisms fail / can’t keep up
  • ->worsening metabolic acidosis + fluid loss into extravascular interstitial places

4 Refactory
- Organs fail -> death

31
Q

In the initial stage of shock why do you get a metabolic acidoiss

A
  • Hypoperfusion -> hypoxia ->anaerobic metabolism -> lactic acid and metabolic acidosis
32
Q

In the compensatory stage of shock what happens?

A
  • Hyperventilation - Resp alkalosis to neurtralise acidosis
  • Catecholamine response - if hypotensive nor/adrenaline released -> increase SVR and CO
  • Renin-angiotensin response -
    (Agiotensin II, aldoserone) release -> thirst and vasoconstriction
    Vasopressin (ADH) ->fluid retention
33
Q

Oxygen Delivery =

A

Oxygen Delivery = CO x Oxygen content (Hb x SpO2x c)

34
Q

Causes of low oxygen delivery ? Basic management of 3 types

A
  • Low CO - > fluid challenge first line
  • Anaemia -> blood
  • Hypoxia -> 02
35
Q

Why do you have to be cautioys with noradrenaline when the patient has low perfusion pressures

A
  • Vasopressor but not not ionotrope.

- > Increases SVR -> creates ‘normal’ BP but increases afterload and reduces CO which reduces DO2

36
Q

How can you reduce oxygen consumption of septic patient

A
  • May require intubation and ventilation -> reduces WOB and therefore oxygen demand
  • Sedation of agitated
37
Q

Effect of sympatetic stimulation on B2 reptors

A

Stimulation of ß2 receptors present in some vascular beds eg lungs
vasodilatation

38
Q

Parasympathetic effects on circulation

A

none significant

39
Q

4 main categories of shock

A

distributative
hypovolaemic
cardiogenic
obstructive

40
Q

4 causes of cardiogenic shock pathophysiology

A

filling defect - diastolic HF
contractility defect
arrhythmias - decreased preload / contractility / HR
Structual - valve disease -> backflow / restricted flow

41
Q

2 causes of contractility defects causing cardiogenic shock

A

MI

Cardiomyopathy

42
Q

What causes filling defect in heart

A

increased growth of muslce -> smaller space
increased stiffness -> less compliant -> less filling

All ends in decreased preload

43
Q

Name a cardiac support device for cardiogenic shock

A

Intra aortic baloon pump
ECMO
Impala

44
Q

Becks triad seen in? what is it?

A

cardiac tamponade - obstructive shock

Hypotension
muffled heart sounds
raised JVP