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7118 - clinical therapeutics for core conditions > Critical Care > Flashcards

Critical Care Flashcards

1
Q

What is starling forces

A

the balance of forces defining the rate of fluid movement across the capillary endothelial barrier

The movement of fluid is increased with conditions associated with systemic inflammation such as trauma and sepsis owing to the increased capillary permeability

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2
Q

crystalloids are

A
  • sodium chloride 0.9% balanced solutions (154 mol of each)
  • various strengths of glucose (comes in various strengths, 50% very irritant - central line only) Provides 200kcal

They are iso-osmotic with plasma. distribution is determined by sodium concentration.

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3
Q

colloids are

A
  • blood products (packed red cells, platelets, fresh frozen plasma, albumin (various strengths)
  • gelatin
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4
Q

5 R’s (but not all R’s)

A

1) Resuscitation (hypovolaemia)
2) Maintenance
3) Replacement
4) Redistribution
5) Reassessment

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5
Q

daily requirements

A

water 25-35ml//kg/day

sodium and potassium 1mmol/kg/day

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6
Q

what is shock?

A

life threatening condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function

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7
Q

signs of shock

A 
low BP
tachycardia
poor end organ perfusion such as olig/anuria
confusion/loss of consciousness
weak pulses
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8
Q

Shock can be divided into the following categories

A

1) hypovolaemic - usually due to direct loss of circulating blood volume e.g. trauma
2) cariogenic eg post myocardial infarction
3) distributive(Septic), this includes septic, anaphylactic, endocrine, neurogenic shock. vasodilation, fluid leaks out into tissues
4) obstructive iclusing cardiac tamponate, PU, aortic stenosis

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9
Q

what is sepsis

A

infection

organ dysfunction - SOFA SCORE

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10
Q

what is QSOFA (quick score at bedside) SOFA is more extensive

A

1) RR >22 BPM
2) systolic BP < 100mmHh
3) altered mentation (mentation activity)

2 = 8%
3 = 20%
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11
Q

Cardiac output

A

Range 4-6

Determined by LV function, HR, preload and after load, by altering these factors we can alter cardiac output

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12
Q

Cardiac index

A

Range 2.5-3.5

cardiac output adjusted for body surface area

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13
Q

central venous pressure

A

Range 2-6
right atrium pressure = right ventricular preload
- if low = hypovolaemia, vasodilation
- if raised - inc intravascular volume, RV failure, PE, cor pulonale and others

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14
Q

systemic vascular resistance

A

960-1400
measure of left ventricular after load
low value could be vasodilation due to septic shock

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15
Q

mean arterial pressure

A
  • the average mean arterial pressure across one full cardiac cycle
  • 80-100
  • commonly used measure of BP on ICU
  • this is measured using an arterial catheter
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16
Q

PICCO and LIDCO

A

advanced hamody namic monitoring systems
both invasive measure arterial pule pressures to derive a set of cardiovascular parameters
- measures CO, CI, SVR

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17
Q

SIRS criteria

A

pyrexia, neutrophilic, increased HR ( unhelpful in identifying sepsis as many patients have this)

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18
Q

Persisting hypotension requires….

A

vasopressors such as noradrenaline or vasopressin to maintain a mean arterial pressure >65mmHg and having serum lactate >2 despite adequate fluid resuscitation

This plus sepsis is known as septic shock

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19
Q

fluid initially given in sepsis is

A

500ml hartmans or NaCl (has to be glucose free)

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20
Q

timescale to get IV ABX in a patient with sepsis is

A

60 mins

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21
Q

vasopressors cause

A

a rise in blood pressure and are used to reverse circulatory failure in critically ill patients
- noradrenaline or dopamine

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22
Q

Vasopressin (also known as anti-diuretic hormone) has two primary functions

A
  • increase water retention via tubular reabsorption while causing smooth muscle contraction, particularly in the capillary bed sense diminishing leaky capillaries in patients with sepsis
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23
Q

inotropes are

A

adrenaline and dobumatine
They preferentially stimulate the B1 adrenoeceptors which leads to increased myocardial contractility. However they can also contribute to myocardial schema therefore the minimum dose should be used for the shortest time. adrenaline as vasoconstrictor properties as well as being an inotropic/

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24
Q

drotrecogin alfa

A

recombinant human activated protein

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25
Q

levosimendan

A

positive ion trope with dual mechanism of action

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26
Q

inotropic

A

cardiac contraction force

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27
Q

chronotropic

A

rate of contractions

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28
Q

sepsis

A

can cause AF which can then cause an MI which can then cause cariogenic shock

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29
Q

Albumin

A

4.5% albumin is the same amount as blood
20% albumin will draw fluid from the tissues back into the circulation
gellyfuse is a plasma volume replacer

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30
Q

ideal sedative

A 
anxiolytic
somnolent
analgesic
respiratory depressant
no accumulation properties
no effects of haemodynamic
amnesic properties
suppress gag reflect
amti-tussive(prevent or relief cough)/reduce bronchospasm
inexpensive
minimal/no interactions
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31
Q

Problems if we over sedate

A 
excessively prolonged
respiratory depression
haemodynamic disturbances
immunosuppression
GI stasis
cost
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32
Q

If we undersedate

A 
agitation/stess
pain
removal of tubes/lines by patient
poor ventilation
HTN
tachycadic
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33
Q

What is propofol?

A

IV anaesthetic
1-4mg/kg (practically 0-20ml/hour)

  • advantages
  • fast onset
  • short duration of action (starts and stops quickly) half life about 10-70 minutes
  • good for assessing patient e.g. head injury
  • anti-jussive/bronchospasm

Disadvantages

  • only licensed for 3 days
  • expensive
  • patients build a tolerance
  • high lipid load (1kcal/1ml) ALOT
  • C/I in children
  • causes hypotension - can reduce CO and BP by 30%. May cause hypertension once it restarts.
  • no analgesic affects
  • peanut gallery
  • propofol infusion syndrome
34
Q

Sedatives are

A
  • propofol
  • midazolam
  • clonidine (longer activg, may drop BP)
  • thiopental
  • remifental
  • ketamine
  • morphine
35
Q

midazolam

A

0.03-0.3mg/kg/hour

advantages

  • short acting - half like 2 hours
  • respiratory depression
  • anterograde amnesia (inability to create new memories after event that caused it)

disadvantaged

  • respiratory depression
  • anterograde amnesia
  • accumulation especially in renal impairment
  • hypotension
  • paradoxical agitation (at higher doses)
  • no analgesia effects
36
Q

Analgesics

A

Mainly opiates. Mainly used in combination with a sedative

They all cause:

  • analgesia and sedation
  • resp depression
  • nausea
  • reduced gastric motility
  • histamine release - hypotension/bronchospasm
37
Q

opioid doses

A

morphine 50-70mcg/kg/hr (0-10mg/hr)
fentanyl 5-20mcg/kg/hr
alfentanyl 20-120mcg/kg/hr
remifentanil 0.1-0.75mcg/kg/min

38
Q

Disadvantage of morphine

A

it accumulates in hepatic and renal impairment.

It is metabolised in the liver to (active) morphine-6-glucuronide and (inactive) morphine-3-glucoronide

39
Q

Fentanyl/alfentanil advantages and disadvantages

A

Advantages:

  • Potent synthetic opioid with quick onset of action and short half life.
  • Liver metabolised to inactive compounds (alfentanil is ideal for use in renal impairment)

Disadvantage:

  • less sedating
  • fentanyl has a large volume of distribution therefore it accumulates in prolonged use.
  • potent respiratory depressant
40
Q

Remifentanyl advantages and disadvantages

A

Advantages

  • very potent
  • very short acting
  • predictableelimination
  • can be used in addiction to morphine in painful procedure e.g. dressing changes

disadvantages:

  • VERY potent respiratory depressant - Do not bolus!
  • very expensive
  • unfamiliar
41
Q

Epidurals what do they contain and why are they used?

A

bupivicaine +/- fentanyl

They allow patients to be awake pain free post procedure

Bupivicaine - worked in 10-20 minutes and has a duration of 5-16 hours.

Fentanyl - highly sedative. 100 times more potent than morphine as an analgesic. Half like 30-60 minutes.

42
Q

paracetamol eGFR <30ml/min

A

reduce to 6 hourly rather than 4 hourly

43
Q

ketoralac may be used as long as

A

urine output is ok

44
Q

how do we monitor BP in ITU

A

Arterial catheter - mean arterial pressure

PiCCO

45
Q

Why do we use ionotropes??

A

To correct BP if it cannot be corrected by fluids

46
Q

Ionotropes

A
  • improve BP
  • improve systemic blood flow - cardiac output
  • vasoconstrictors
  • improve cardiac ejection fraction and/or stroke volume
  • Increase HR
  • control arrhythmias
  • volume addition - crystalloid & colloid
47
Q

Vasopressors

A

increase systemic vascular resistance

Vasoconstriction increases SVR.
Vasodilation decreases SVR

48
Q

ionotrope and vasopressors are

A

adrenaline
noradrenaline
dobutamine
vasopressin

They require invasive monitoring to achieve a desired outcome.

49
Q

Ionotropes and vasopressors

A
  • A vasopressors causes vasoconstriction
  • An ionotrope increases the force of contraction
  • both drugs work via the autonomic nervous system
  • Majority are endogenous cetcholamine or semi-synthetic derivatives
50
Q

Autonomic nervous system

A

Does not have voluntary control.

Things like HR, force of contraction, constriction and dilation o blood vessels, contraction and relaxation of smooth muscle in various organs.

51
Q

Acting on the beta 1 receptor causes….

A

Cardiac effect:

  • increase force of contraction
  • increase stroke volume
  • increase conduction
  • increase heart rate

Main response:

  • ionotropic increase in cardiac output
  • minor chronotrope
  • increase in blood glucose
  • constipating

Other effects:
lipolysis
relaxes smooth muscle

52
Q

Acting on the beta 2 receptor causes

A

Cardiac Effects
- increase in heart rate

Main response:

  • chronotropic increase in cardiac output
  • reduction in systemic vascular resistance
  • reduction in bronchospasm

Other effects:

  • arterial vasodilation
  • bronchodilation
53
Q

Alpha 1 + 2

A

Main effects:

  • increase in systemic vascular resistance
  • increase in BP

Other effects
- arterial vasoconstriction

54
Q

D1 - dopaminergic

A

Main outcome:
increase renal blood flow
- increase glomerular filtration rate
- improved clearance of urea and creatinine

Other effects
Renal and mesenteric vasodilation

55
Q

Adrenaline (epinephrine)

A
  • acts on alpha 1 and beta 1 & 2
  • prepares body for fight or flight
  • very short length of action

CVS:

  • A positive ionotrope and chronotrope.
  • Increases HR and force of contraction to produce and increase in cardiac output
  • increase in systolic BP
  • at low doses the diastolic BP may drop due to vasodilation and increase blood flow through skeletal muscle beds (B2)
  • At higher doses the vasoconstrictor effects of alpha 1 stimulation become apparent

Respiratory:
Bronchial smooth muscle relaxation resulting in bronchodilation (b2)

56
Q

Adrenaline (epinephrine) other effects

A
  • reduced insulin secretion
  • mobilises blood glucose from glycogen to increase blood glucose

Side effects
- ventricular arrhythmias & HTN

Indication
Cardiogenic shock with reduced cardiac output

57
Q

Noradrenaline (norepinephrine)

A
  • Acts predominantly on the alpha 1 receptors but also has some activity on the B1 receptors
  • An extremely potent vasopressor (vasoconstrictor)

CVS:

  • increases BP (and SVR) via arterial and venous vasoconstriction
  • cardiac output may increase or decrease depending on clinical circumstances

Indication:
Sepsis/septic shock when peripheral vasodilation may be causing hypotension

58
Q

Dobutamine

A
  • Acts by direct action on cardiac B1 receptors with some action on B1 and A1 receptors

Increases cardiac output and reduces after load

Indication:
Use to provide inotropic support in patients with low CO secondary to 
-MI (cariogenic shock)
-sepsis
-cardiac surgery
-cardiomyopathy
59
Q

Vasopressin

A
  • synthetic copy of naturally occurring peptide hormone
  • vasopressin agonist
    -vasocontrictor
  • used as an adjunct to therapy (usually combined with NA)
    Dose 0.03units/min
60
Q

Receptor activity

A

Adrenaline: Alpha 1, BETA 1, BETA 2
Noradrenaline: ALPHA 1, beta 1
Dobutamine: alpha 1, BETA 1, beta 2

61
Q

What do the drugs do?

A

Adrenaline : +ve ionotrope & chronotrope and some vasoconstriction.

Noradrenaline: Vasoconstriction

Dobutamine: +ve ionotrope and peripheral vasodilator

DX: renal and splanchnic vasodilator. Less ionotropic/chronotropic than DA

Vasopressin: Vasoconstrictor

62
Q

When are they used?

A

A - if CO/CI reduced (cardiogenic shock)

NA - If SVR is reduced (septic shock)

DB - Low CI due to cardia insufficiency (MI, sepsis, cardiomyopathy, cardiac surgery)

DX - similar to DB without the increase HR

V - to increase SVR if NA not working

63
Q

Doses of drugs:

A

In practice the doses are rarely based on weight. The rate of infusion is adjusted according to response.

Dose

A = 0.05mcg/kg/min 4mg/50ml
NA= 0.05mcg/kg/min 4mg/50ml
DB 2.5-50mcg/kg/min 250-500mg/5ml
DX 0.5-6.0mcg/kg/min 50mg/50ml

64
Q

Stress ulcer prophylaxis

A

erosions/ulcerations in the UGI tract due to gastric mucosal ischaemia

Risk factors are:
shock, sepsis, head injury, burns.

ranitidine IV 50mg TDS or omeprazole 40mg Od/BD in high risk

65
Q

Insulin

A

critically ill patients can produce insulin resistance which causes high glucose.

This is usually always the case in sepsis

Aim for BMs <11.9

Hyperglycaemia can cause other complications: apoptosis, coagulation, wound healing, infection, neutrophil function.

66
Q

Steroids

A

Used in patients with high inotropic requirements

Hydrocortisone 200mg IV daily.

This up regulates receptors

S/E’s = immunosuppression, further infection, fungal, increase BM’s

67
Q

how long to we continue pro-kinetics for ?

A

24 hours after patient starts to absorb

68
Q

What are also extremely important to be prescribed

A

laxatives

- bowel perforation and death (immobile/opioids)

69
Q

Reasons for RRT on crit care

A
  • renal failure
  • fluid overload
  • metabolic acidosis
  • electrolyte disturbance (mainly potassium)
  • oliguria/anuria
  • drug toxicity - lithium
  • poisoning - ethylene glycol, paraquat
  • sepsis, hyperthermia
70
Q

Dialysis is hardly every used on its now because

A
  • sudden big shifts in fluids/electrolytes make haemodynamically unstable patients difficult to manage.

Other examples

  • haemofiltration
  • haemodiafiltraion (combo of the two)

-continuous vs intermittent

71
Q

Comparison of dialysis and filtration

A

Dialysis - moves down the conc gradient across a semipermeable membrane whereas filtration uses a pressure gradient which drives the molecules through a highly permeable membrane

A septic critically ill patient would have continuous whereas a chronic stable patient would have intermittent

72
Q

Dual system

A

a system that combines filtration and dialysis is more effective at removing middle size molecules as they are removed by convection and diffusion

73
Q

Anticoagulation

A
  • Heparin
  • Epoprostanol - inhibitor of platelet activation
  • citrate of ionised calcium
74
Q

haemofiltration fluid

A
  • sterile

- contains the main blood electrolytes and buffer

75
Q

What affects the clearance?

These aspects match those of renal extorted drugs e.g. gentamicin or penicillins

A
  • Lower molecular weight
  • only free drug can move across the membrane - protein bound drugs cannot as they usually bind to albumin.
  • the more water soluble a drug the more likely it is to be removed. highly lipid soluble drugs tend to have high volume of distribution which further reduces clearance.
  • VD - drugs with lower volume of distribution are cleared more. For water soluble drugs VD increases in sepsis.
  • If drugs have low renal clearance anyway for example remifentanyl - Then RRT will have little impact
  • membrain interactions
  • pre or post dilution
  • volume of ultra filtrate produced
  • blood/dialysate flow rate
76
Q

Drugs less likely to clear

A
  • large lipophilic substances
  • high protein binding (warfarin, flucloxacillin)
  • large volume of distribution (digoxin, amiodorone)
  • short half life (ionotropes)
77
Q

what sedative is good in renal impairment?

A

alfentanil

78
Q

what sedative do we have to worry about rebound HTN when it stops?

A

propofol

79
Q

Which of the two cause vasoconstriction ?

A

Noradrenaline

Vasopressin

80
Q

Sedative regime and score

A

RASS core

Anaesthetic or benzo plus opioid

7118 - clinical therapeutics for core conditions (31 decks)

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