Sepsis and shock Flashcards

(44 cards)

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
Hypovolaemic shock common causes? What happens? How does the pt appear?
- 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
How does distributive shock present
Peripheral vasodilation Eg Sepsis, anaphylactic and neurogenic shock.
27
Key features of neurogenic shock
hypotension, bradycardia, warm peripheries, venous pooling and sometimes priapism
28
Egs of obstructive shock
PE, Aortic stenosis, pericardial effusion and tension pneumothorax.
29
Why does respiratory rate go up in shock
Tissue hypoxia -> metabolic acidosis -> increase RR as compensatory method
30
What are the 4 stages of shock ?
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
In the initial stage of shock why do you get a metabolic acidoiss
- Hypoperfusion -> hypoxia ->anaerobic metabolism -> lactic acid and metabolic acidosis
32
In the compensatory stage of shock what happens?
- 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
Oxygen Delivery =
Oxygen Delivery = CO x Oxygen content (Hb x SpO2 x c)
34
Causes of low oxygen delivery ? Basic management of 3 types
- Low CO - > fluid challenge first line - Anaemia -> blood - Hypoxia -> 02
35
Why do you have to be cautioys with noradrenaline when the patient has low perfusion pressures
- Vasopressor but not not ionotrope. | - > Increases SVR -> creates 'normal' BP but increases afterload and reduces CO which reduces DO2
36
How can you reduce oxygen consumption of septic patient
- May require intubation and ventilation -> reduces WOB and therefore oxygen demand - Sedation of agitated
37
Effect of sympatetic stimulation on B2 reptors
Stimulation of ß2 receptors present in some vascular beds eg lungs vasodilatation
38
Parasympathetic effects on circulation
none significant
39
4 main categories of shock
distributative hypovolaemic cardiogenic obstructive
40
4 causes of cardiogenic shock pathophysiology
filling defect - diastolic HF contractility defect arrhythmias - decreased preload / contractility / HR Structual - valve disease -> backflow / restricted flow
41
2 causes of contractility defects causing cardiogenic shock
MI | Cardiomyopathy
42
What causes filling defect in heart
increased growth of muslce -> smaller space increased stiffness -> less compliant -> less filling All ends in decreased preload
43
Name a cardiac support device for cardiogenic shock
Intra aortic baloon pump ECMO Impala
44
Becks triad seen in? what is it?
cardiac tamponade - obstructive shock Hypotension muffled heart sounds raised JVP