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MRCS B - Critical Care (Kanani and Lammy) > ITU > Flashcards

ITU Flashcards

1
Q

Causes of post op confusion?

A

Pain and infection
Hypoglycaemia
Electrolyte disturbances - namely sodium
Respiratory = hypoxia and hypercapnoea
Renal / liver failure = accumulation of toxic metabolites

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2
Q

Investigations of post op confusion?

A

bedside = ABG, bloods, BM, ECG

Radiology

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3
Q

Purpose of sedation in critical care?

A

Anxiolysis
Analgesia
Amnesia
Sedation

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4
Q

How do we. determine level of sedation?

A

Ramsay scoring:
Level 1 = awake, anxious and agitated
2 = Awake, co=operational, orientated and tranquil
3 = Awake, responds to commands only
4 = asleep, risk response to glabellar tap or loud auditory stimulus
5 = Asleep, sluggish response
6 = asleep, no response

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5
Q

Sedative drug classes?

A

Benzos
Opiates
Butyrophenones e.g. Haloperidol = neurotransmitting blocker
Anaesthetic agents e.g. Propofol or ketamine

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6
Q

Major SE of propofol?

A

Can cause hypotension on induction via decreasing SVR and myocardial depression

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7
Q

Sodium thiopentone?

A

Use = RSI
Analgesic effect = none
SE’s = marked myocardial depression and toxic metabolites

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8
Q

Ketamine?

A

Good analgesic and little myocardial depression

SE’s = dissociative nightmares

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9
Q

Etomidate?

A

No analgesic effect
Favourable cardiac profile
SE’s = prolonged use causes adrenal suppression

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10
Q

What can be donated?

A

Organs = kidney, liver, heart, lung, pancreas and small bowel

Tissues = cornea, skin, bone, tendon, heart valves and cartilage

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11
Q

Criteria to donate pre-donation?

A
  1. Diagnosis of brainstem death and circulatory death
  2. Donor maintained on a ventilator in absence of sepsis
  3. No hx of malignancy (except primary brain tumour)
  4. HIV and HBV -ve
  5. High risk groups excluded e.g. IVDU

Often some specific restrictions e.g. heart donor no MI

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12
Q

Why is managing fluid balance particularly important in organ donors with brainstem death?

A

If brainstem death can get cranial diabetes insipidus = severe water loss and subsequent hypernatraemia

If severe can use vasopressin to manage

Occurs in 65% of brainstem death

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13
Q

Physiological changes in brainstem death?

A
  1. Hypotension: due to loss of sympathetic peripheral vascular tone - 81%
    (initially HTN due to immediate increase in sympathetic tone
    Mx = IVF and inotropes
  2. Coagulopathy: e.g. DIC
  3. Hypothermia: Occurs following loss of thermo-regulation via hypothalamus. This is exacerbated by reduced metabolic activity and loss of vascular tone.
    Mx = blankets and warmed IVF
  4. Endocrine: Loss of thyroid function can result in further arrhythmias
    Mx = T3
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14
Q

When is it appropriate to perform an examination

A
  1. Coma - patient must be in a deep coma entirely reliant on ventilator due to absence of spontaneous ventilation
  2. Brain damage = must be irreversible and compatible with diagnosis of brainstem death

Must exclude following reversible causes?
Hypothermia
Metabolic = Hypoglycaemia, Na
Endocrine = hypothyroid, uraemic, encephalopathic
Drugs and ETOH

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15
Q

Criteria for brainstem death?

A
  1. No respiratory drive:
    Preoxygenated got 10 minutes
    PCO2 increases, normally respiratory stimulates at >6.5kPa
  2. Non brainstem function:
    - Absent pupillary light CN2/3
    - Absent corneal reflex CN5/7
    - Absent CNN motor function CN5/7
    - Absent gag CN9
    - Absent vestibulo-occular test following cold caloric test CN8/3
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16
Q

Who can assess for BSD?

A

Must be relevant specialty

x1 consultant and x1 registered GMC for > 5 years

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17
Q

When can confirmation be difficult?

A

COPD
Ocular injury
Brainstem encephalitis

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18
Q

How can we. support circulation in ITU?

A

Need to if cardiac index <2.2 or in septic shock.

Cann give:
Inotropes 
Chronotropes 
Vasoconstrictors or dilators 
Mechanical e.g. intra-arterial balloon pump with counter pulsation
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19
Q

Commonly used drugs?

A

adrenergic e.g. adrenaline or noradrenaline
- increase SVR, HR, SV and CO. With aim of increasing BP

Dopaminergic agents e.g. dopamine or dobutamine

  • HR and SV –> increased CO, to increase BP
  • dose dependent effects however

NON-CATECHOLAMINES

  1. Phosphodiesterase inhibitors e.g. Milrinone
    - increased contractility + SV but reduced SVR via vasodilation
  2. Calcium channel agonists e.g. Levosimendan
    - produce a transient inotropic effect
    - increase sensitivity of myocardial troponin to intracellular calcium
  3. ADH agonist = natural analogue of vasopressin and increase SVR via vasoconstriction
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20
Q

Effect of adrenergic receptors in heart and vessels?

A

a1:

  • Increased vasoconstriction of arterioles = increased afterload and increased peripheral vascular resistance
  • Increased venoconstriction = increased venous return = increased preload

a2 = platelet aggregation

B1 = Increased HR, contractility and automacity/conduction velocity

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21
Q

Effects of different inotropes on adrenergic receptors?

A 
1. Dopamine = dose dependent...
Low does (1-4) = mainly DA1 = increased splanchnic / renal blood flow @ low dose 
Medium dose also B2
High dose also A1
  1. Dopexamine = B2 and DA1 (0.5-0.6)
    - inodilator
    - Used in management of heart failure post cardiac surgery
    - Increases hepatosplanchnic blood flow, and can ameliorate gut ischaemia in SIRS
  2. Dobutamine = B1 and B2 (2.5 - 10)
    - indicator, good in low output / high SVR states e.g. cardiogenic shock
    - not beneficial if low BP e.g. sepsis
  3. Salbutamol (0.1 - 1.0)
    Severe asthma
  4. Adrenaline = alpha 1 and B1 (0.01-0.2)
    - 1st line inotrope
    - High B-adrenoreceptor = increased cardiac output
    - Can vasodilate at low doses, constrict at higher doses
  5. Nor-adrenaline = alpha1 (0.01 - 0.2)
    - Inoconstrictor
    - Very useful in high output / low SVR states e.g. Sepsis
    - Inotropic effect via A1 and B1 myocardial receptors
    - Can cause reflex bradycardia + peripheral / splanchnic ischaemia
  6. Isoprenaline - B1 and B2 (0.01 - 0.2)
    - Reserved for treatment of emergency bradyrhythmias
    - risk of tachyrhythmias
  7. Phenylephrine = alpha 1 = pure vasoconstriction (0.2- 1.0)
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22
Q

Mechanism of PDE3

A

act by inhibiting hydrolysis and degradation of intracellular CAMP.
This causes increase in intracellular calcium = increased cardiac contractility and stroke volume

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23
Q

Effect of PDE3 on cardiac function?

A

Reduces afterload:

  • via reduction of SVR and pulmonary vascular resistance
  • useful in cardiogenic shock when high SVR

Inotropic:
- Increase in HR, but decreased myocardial oxygen requirement as lower filling pressures

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24
Q

Dopamine effects on circulation?

A

Low dose = 1-4 = DA1 only:
- renal and spleen vasodilation = increased renal perfusion and diuresis

Medium dose 4-10 = B1 too = increased contractility

High dose >10 = A1 too = Vasoconstrictor = increased afterload and SVR.

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25
Q

Indications for noradrenaline ?

A

Potent vasoconstrictor

useful in septic shock, but can lead to reduced peripheral perfusion and increased afterload

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26
Q

Affects of noradrenaline on circulation?

A

low doses = B1 = increased CO and reduced SVR

Higher doses = alpha 1 = increased CO and increased SVR

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27
Q

Dobutamine effects?

A

Strong B1 = cardiac output up and SVR down

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28
Q

General problems with inotropes?

A

Tachyarrhythmias
Bradycardia if noradrenaline
HTNN with adrenaline
Hypotension if dobutamine / PDE3

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29
Q

What if cardiac index still <2.2 despite maximal cardiac output?

A

Intra-aortic balloon pump = mechanical assistance
Reduces afterload and increases coronary flow

Sits in descending aorta
Expands during diastole, increasing coronary perfusion pressure
Deflates just prior to systole = reduced afterload

Remember thrombogenic = anticoagulant needed

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30
Q

Indications for ET tube?

A

Operative:
ET = standard when using IPPV and muscle relaxants
Endobronchial = dual lumen allows single lung ventilation cardiothoracic/oesophageal surgery

Non-operative:
airway protection e.g. from gastric aspiration in severe head injury
CPR

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31
Q

How long for ET tube?

A

2 weeks, after this tracheostomy

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32
Q

Basic intubation steps?

A
  1. Pre-oxygenated 100% 3-5 mins
  2. Position = neck extended
  3. Anaesthesia = local or general
    • muscle relaxant if GA
  5. Intubate = laryngoscopy, intubate, inflate cuff, connect tube
  6. Auscultate
  7. Secure
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33
Q

Magill vs Macintosh laryngoscope?

Which one on paediatrics

A 
Magill = straight blade
Macintosh = curved blade

Magill in pads as epiglottis is floppy and U shaped = straight blade passes behind and fixes it in position

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34
Q

Sizes of laryngeal tube?

A

8mm for male, 7mm for female

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35
Q

RSI?

A

Emergency induction e.g. AAA

Important requirements are suction, skilled assistant and cricoid pressure

Cricoid pressure is not released until cuff inflated

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36
Q

When is nasotracheal intubation used?

A

Head and neck procedures

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37
Q

Complications of ET intubation?

A

Trauma - teethe pharynx, larynx

Spinal injury

Acute HTN due to autonomic reflex of laryngoscopy

Spasm = laryngospasm / bronchospasm

Misplacement or disconnection

38
Q

Pre-requisite to successful extubation?

A
  1. Original disease resolved
  2. Adequate lung function, haemodynamically stable
  3. Adequate GCS
  4. Satisfactory nutrition
  5. General e.g. no sepsis
39
Q

What do we mean by adequate lung function for extubation?

A 
RR <35
Pa02 > 11kPA w/ Fi01 < 0.5
Minute volume <10l/min 
Vital capacity >10ml/kg
Tidal volume >5ml / kg
Max inspiratory force > 20cmH20
40
Q

Why optimise nutrition?

A

Increased muscle strength of respiratory muscles

reduced CO2 production as not dependent on glucose

41
Q

Strategies to wean ventilation?

A

T piece = just oxygen delivery

T-piece and CPAP = CPAP enhanced with PEEP, allows T-piece to be used longer

Intermittent mandatory ventilation = certain tidal volume, at specific rate. Between these the patient breathes

Pressure support = patient initiates breath spontaneously then supported via positive pressure

42
Q

Levels of ITU care?

A 
0 = ward
1 = ward patient with critical care input
2 = HDU, more detailed obs / interventions. Often single failing organ or post op. 
3 = ITU, >2 organs failing
43
Q

Some criteria for entering ITU?

A

Respiratory - advanced support e.g. mechanical ventilation to intubation

System support = 2 or more organs

Reversibility

44
Q

Indications for mechanical ventilation?

A 
RR >35
Pa02 <8 kPA w/ Fi01 >0.6 
Vital capacity <10ml/kg
Tidal volume <5ml / kg
PaC02 >8
ICP > 20mmHg
45
Q

What can we adjust on a normal ventilator?

A 
Respiratory rate 
Tidal volume 5-7 ml/kg
FiO2 0.21 - 1.0 
Inspiratory : Expiratory ratio 
Pressure limit 
PEEP and CPAP
46
Q

What do we adjust on ventilator to improve oxygenation?

A

FiO2, PEEP and I:E ratio can all be increased

47
Q

What can we adjust on the ventilator to increase ventilation ?

A

Increase RR, tidal volume and peak pressure

48
Q

Outline some basic ventilator modes?

A

Pressure control = set inspiratory pressure, when reached get expiration

Assisted mode, ventilator simply augments each inspiratory effort

49
Q

What is PEEP and physiological changes?

A

Delivery of additional pressure at end of expiration to ensure no atelectasis

Increases compliance and functional residual capacity

Reaction of physiological shunting which increase V/Q ratio

50
Q

SE’s of IPPV?

A

Respiratory = barotrauma

CVS = Intrathoracic pressure less -ve, so reduced venous return to heart
Lung expansion distorts alveolar capillaries = increased pulmonary vascular resistance

Renal = reduction in renal perfusion = reduced UO

Paralytic ileus ? mechanism

51
Q

Define cardiac index.

A

Cardiac output divided by body surface area

52
Q

What is a pulmonary artery catheter and its purpose?

A

Multilumen, balloon tipped, flow directional catheter

Passed via right heart and into pulmonary artery

Gives picture of left heart function, better than CVP alone

53
Q

How does CVP give measure of left heart function?

A

When inflated inn branch of pulmonary artery, there is essentially a continuous column of blood beyond that extends to left atrium

PACWP is an indirect measure of LA pressure

54
Q

Indicators for a pulmonary artery catheter?

A

Drugs = inotrope use

Surgical e.g. post cardiac surgery

Assessing cause of shock based on mixed venous oxygen saturations

55
Q

What does a pulmonary artery catheter directly measure?

A

MAP and MpulmAP
HR, CO, EF
PACWP
Mixed venous oxygen sats

56
Q

Derived variables of a pulmonary artery catheter ?

A

CI, SV, SVR, PulmVR

57
Q

How do we calculate systemic vascular resistance?

A

[(MAP-CVP)/ CO] x 80

58
Q

How do we calculate pulmonary vascular resistance?

A

(MPAP-PCWP)/ CO. x 80

59
Q

Complications of pulmonary artery catheter?

A

Cardiac = arrhythmias, valve injury to tricuspid or pulmonary

Pulmonary artery rupture = shock and haemoptysis

Pulmonary infarction if balloon wedged too long

Sepsis

60
Q

How does PAC measure cardiac output?

A

One of two methods, either via indicator dilution or thermodilution

Indicator = dye injected and samples taken peripherally. Cardiac output is amount injected divided by area under the curve

Thermodilution is the same except cold fluid injected

61
Q

RRT types?

A

Haemodialysis, haemofiltration, peritoneal

62
Q

Indication for RRT?

A 
potassium > 6.5
pH <7.1
Refractory fluid overload 
Uraemia complications 
Drug OD
63
Q

Haemodialysis vs haemofiltration?

A

HaemoD:

  • Blood interfaces dialysis solution across selectively permeable membrane
  • permit molecules <5kDa
  • Works via diffusion so better with smaller molecules

HaemoF:

  • Continuous convection of molecules across a permeable membrane
  • Fluid removed from patient replaced with physiological solution
  • Better at clearing large volumes of fluid.
  • Works via convection so all molecules equally
64
Q

HD vs. HF pros and cons?

A

HF better BP control and less hyperlipidaemia
- Can only reduce, not normalise solutes

HD = cheaper and easier.
- Toxicity of high weight molecules yet to be proven

65
Q

When is intermittent HD used?

A

CKD, not the critically ill

Need - vascular access, extracorporeal circuit and dialysis machine

66
Q

SE’s of HD?

A

Disequilibrium syndrome - sudden change in osmolality e.g. when taking out urea, can lead to cerebral oedema

Hypotension

Immune reactions e.g. complement activation and. neutrophils can aggregate in lung

Sepsis

67
Q

Types of continuous RRT?

A

Continuous AV HF = flow driven by fistula pressure

ven-ven HF = Relies on roller pumps for flow, which means does not depend on unstable arterial pressure inc critically unwell patient

AV or VV HD = useful for slow ultrafiltration

AV or VV haemodiafiltration = combo breaker
Best rate of urea clearance

68
Q

How does PD work?

A

Relies on peritoneum and. capillary network as a selectively permeable membrane
Dialysate introduced to peritoneum, then removed several hours later

Often useful in paeds if difficult access

69
Q

Classic side effect of PD?

A

SBP = turbid effluent, with WCC > 50

75% G+Ve e.g. Stap epidermis or aureus

Mx = broad spectrum Abx e.g. Cef and gent

70
Q

What is an endotoxin?

A

lipopolysaccharide derived from cell walls of G-ve bacteria

3 parts = Lipid A, core polysaccharide and oligopolysaccharide

71
Q

Difference between bacteraemia, sepsis and severe sepsis?

A

bacteraemia is viable bacteria in blood stream
Sepsis is SIRS with infective source
Severe sepsis is sepsis with organ dysfunction

72
Q

Define septic shock?

A

Sepsis associated with hypotension and hypo perfusion despite adequate IVF

73
Q

septic vs cardiogenic shock?

A

Septic is decreased SVR and increased CO

Cardiogenic is increased SVR in response to reduced CO

74
Q

What is SIRS?

A

Systemic inflammatory response as a result of critical illness, resulting in two of the following:

Temp >38 or <36
HR >90
RR > 20 OR PaCO2 <4.3
WCC >12 or <4

75
Q

Pathophysiology of SIRS?

A

Progressive increase in inflammatory response, 3 phases…

1 = Local acute inflammation, with chemotaxis of neutrophil polymorphs and macrophages
increased cytokines and proteases

2 = Mediators are now systemically distributed
Normally IL-10 will ensure this systemic response is limited

3 = overwhelming cytokine storm = SIRS criteria symptoms
Catabolic state with reduced oxygen delivery despite increased demand

76
Q

Mediators in SIRS?

A

IL-1 = induces pyrexia and leucocyte activation

IL-6 = Acute phase response

IL-8 = neutrophil chemotaxis

Plt activating factor = induces leucocyte activation and increased cap permeability

TNF-alpha = Pyrogen that stimulates leucocyte

77
Q

What is the two hit hypothesis?

A

Those recovering from SIRS can have a can have a rapid systemic response to something seemingly trivial e.g. UTI

78
Q

What is MODS?

A

altered and potentially reversible organ dysfunction in acutely unwell patient such that cannot maintain homeostasis

Primary = organ failure directly attributable to initial insult

Secondary = indirect e.g. sepsis causing AKI

79
Q

Organs that can be involved in MODs?

A

CVS = vasodilation and capillary permeability = reduced SVR
Initially hyperdynamic with increased CO

Resp = acute lung injury –> ARDS

Renal = AKI due to ATN

GI = ileus and translocation of bacteria across gut

80
Q

Why may the gut fail in MODS?

A

Mucosa sensitive to ischaemia and loses function
Mal-distribution of blood flow
Alteration in gut flora

81
Q

Mx of sepsis?

A

ABC

Renal = Ensure UO > 0.5ml/kg/hour
often via cardiac output

Nutrition = enteral feeds

Surgical = drain collection

82
Q

Primary vs secondary transfer?

A

primary = from scene to hospital care

Secondary = between hospitals

83
Q

Dangers of air ambulance transfer

A

Hypoxia = reduced atmospheric pressure, although not usually an issue as get oxygen

Gaseous expansion = can cause rapid tension of simple pneumothorax
May need B/L chest drains pre-transfer

84
Q

Tracheostomy indications?

A
  1. To maintain a patent airway if congenital defects
  2. Acquired pathology e.g. laryngeal trauma / tumour
  3. Emergency settings e.g. foreign body, laryngeal oedema, burns
  4. to allow long term PPV if intubated > 2 weeks
  5. Facilitate suction
  6. Decrease work of breathing and anatomic dead space e.g. severe COPD
85
Q

Types of tracheostomy?

A

Surgical = open procedure

  • divide and ligate thyroid isthmus
  • Dissect midline 2nd to 4th tracheal ring

Non-surgical:

  1. Percutaneous = small skin crease incision between cricoid and sternal notch
    Guide wire then 14-G cannula and dilators
  2. Translaryngeal - guide wire via mouth, that pierces trachea. Cuffed tube passed through mouth
  3. Mini - 4mm diameter uncuffed tube via median cricothyroid ligament under LA
    - permits regular suction and. high flow jet ventilation in emergency setting
86
Q

Tracheostomy incision problems?

A

Too high = subglottic stenosis

Too low = Tracheoinominate fistula

87
Q

How do tracheostomy’s differ in kids?

A
  1. avoid low placement to avoid L brachiocephalic
  2. Avoid cuffed tubes = mucosal ulceration and tracheal stenosis
  3. if <12 avoid percutaneous as can cause oesophageal injury
88
Q

Type of tracheostomy tubes?

A

Metal or plastic
Cuffed or unncuffed
Fenestrated or not:
- fenestrated allows speech

89
Q

Complications of tracheostomy?

A

Short term:

  • bleeding from stump of thyroid isthmus or anterior jugular vessels
  • Injure surrounding structures e.g. oesophageal perf, recurrent laryngeal nerves, subcut emphysema
  • Displacement
  • Blockage

Medium = infection and fistula

Long term = ulceration and tracheal stenosis

90
Q

Tracheostomy ?

A

Secure
Prophylactic ABx
Humidified oxygen

Regular cleaning

MRCS B - Critical Care (Kanani and Lammy) (6 decks)

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