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ICU and critical care Flashcards

1
Q

How is the level of care (hence what bed they get given) a patient needs determined?

A

Given a level from 0-3

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2
Q

Who are level 0 pts. and what care do they require? What is level 0 care?

A

Ward based care IV infusion and b.d ops

normal ward

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3
Q

Who are level 1 pts. and what care do they require? What is level 1 care?

A

Pts. at risk of their conditions deteriorating

additional clinical input (eg. continuous O2, chest drains)
4 hourly jobs
4 hourly GCS

Require higher levels of care (need critical care team advice and support)

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4
Q

Who are level 2 pts. and what care do they require? What is level 2 care?

A

Its needed pre-operative optimisation or extended post-operative care (eg. major elective surgery or emergency operations in high-risk individuals)

pts requiring single organ support:
Basic resp support: eg. O2>50%, CPAP or BIPAP
Basic cardio support: CVP monitoring or one vasoactive drug infusion
Advanced cardio support: multiple vasoactive drug use, cardiac output monitoring
Renal support: renal replacement therapy
Neurological support: ICP monitoring
Dermatological support: major burns

Pt may be suitable for HDU - pts requiring more detailed observations/intervention, single organ system failure, (post-operative care)
hourly obs (for early detection of potential deterioration)
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5
Q

Who are level 3 pts. and what care do they require? What is level 3 care?

A

Pts requiring advanced resp. support alone

OR

support of at least 2 other organ systems. - one or more organ failures

ICU

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6
Q

If pt. has NEWS on 1-4, how often do they need obs?

A

minimum of 4 hourly

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7
Q

If pt. has NEWS of 0, how often do they need obs?

A

minimum of 12 hourly

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8
Q

If pt. has NEWS of 5 -7
OR
3 in one parameter, how often do they need obs?

A

Minimum of 2 hourly (for at least 6 hours)

also: need URGENT review by medical/surgical team, strict hourly fluid balance

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9
Q

If pt. has NEWS of 7 or more, how often do they need observations?

A

minimum of hourly (for at least 6 hours)

registrar must be informed AND critical care outreach team, transfer to level 2 or 3 facility

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10
Q

With a critically unwell pt., what kinds of things can you ask nurses to do?

A

Observations (as regularly as NEWS requires)
Fluid balance chart
?catheter
Oxygen therapy

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11
Q

What is SIRS and what are the criteria?

A

Systemic inflammatory response syndrome

2 or more signs of inflammation:
T >38 or <36
HR >90
WCC>12 or <4
RR>20
Altered conscious level
BM >7.7 (if not diabetic)

If patient is neutropenic then just 1 of the above

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12
Q

What are the red flags of sepsis?

A 
SBO <90mmHg despite fluid chart
Lactate >2 mol/L
Heart rate >130/min
RR > 25/min
O2 sats <91%
Response to voice/pain OR unresponsive
purpuric rash
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13
Q

What pts. can to be sent to ICU?

A

Pts. requiring level 3 care
(one or more organ failures or need for mechanical ventilation)

Pts poor clinical condition must be potentially reversible

Pt who’s long-term health and co-morbidity mean that they are likely to survive AND BENEFIT from critical care

explicit or reasonably assume pt. consent

Some admissions are pre-planed following major surgery

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14
Q

What is the aim of intensive care?

A

Early recognition of deterioration

Ability to keep pts. alive longer (by organ support) so underlying cause can be treated

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15
Q

What are 3 exceptions to single organ failure that move pts. from level 2 to level 3?

A

Resp. failure on ventilation

Kidney failure (on particular treatment)

Sleep apnoea on inotropes

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16
Q

What happens on ICU?

A

Close physiological control (constant monitoring)

Specific therapy (relevant to disease)

Infusion of vasoactive drugs (vasopressors, inotropes)

Mechanical organ support (renal replacement therapy, mechanical ventilation, extracorporeal oxygenation)

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17
Q

Define shock

A

Shock is a state of circulatory failure characterised by tissue perfusion that is inadequate to meet the needs of the body

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18
Q

What are two main common causes of obstructive shock?

A 
PE embolus (saddle embolus)
Tension pneumothorax
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19
Q

What are some causes of cardiogenic shock

A 
Cardiac failure 
MI (causing arrhythmias)
pulmonary oedema (obstruction to blood flow)
complete heart block
valvular defects
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20
Q

What are some causes of neurogenic shock?

A

spinal cord transection (if see pt. with bradycardia following trauma, worry about this)

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21
Q

Why do you get low blood pressure in septic shock?

A

Vasodilation due to release of cytokines

Toxins from infection also cause vasodilation

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22
Q

What’s the difference between pt. with cariogenic and septic shock?

A

Hyperfebrile in septic shock

pt with cariogenic shock will have cold peripheries and be sweaty/clammy

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23
Q

What can cause cariogenic shock and low-grade pyrexia?

A

PE/DVT

Endocarditis

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24
Q

Which receptors does adrenaline work on ( in high doses) in anaphylaxis? How does this help?

A

alpha receptors - cause vasoconstriction

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25
Q

What’s the difference between inotropes and vasopressors?

A

vasopressors act on alpha receptors (increase after load) - cause vasoconstriction

inotropes act on beta receptors - increase contractility of heart (and often HR)

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26
Q

What are common causes of distributive shock?

A 
Sepsis (commonest)
Anaphylaxis
Toxic shock syndrome
Neurogenic shock
Liver failure
Adrenal insufficiency
Drugs and toxic exposure
SIRS secondary to pancreatitis, burns or trauma
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27
Q

Why is RR increased in shock?

A

compensating for high level of lactate in blood

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28
Q

If you can’t get peripheral oxygen sats, what might this tell you about a pt. with shock?

A

They are peripherally shut down

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29
Q

What lactate level is a SERIOUS concern?

A

anything 4 or more

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30
Q

What should you do if you’ve given a pt. 30ml?kg of fluid and their HR/BP don’t improve?

A

Call critical care outreach

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31
Q

What is the volume limit of fluid you should give in resuscitation? (before asking for help)

A

30 ml/Kg

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32
Q

What type of fluid is Hartman’s?

A

Balanced crystalloid

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33
Q

How can you assess whether someone is responsive to fluids? (other than monitoring obs)

A

Lower leg raise

HR down
BP up
= responsive to fluids

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34
Q

What are THE KEY FEATURES of type 1 respiratory failure

A 
Low O2 (pO2<8 ON AIR)
CO2 normal (or low) (pCO2 <6.0)

Hypoxaemic

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35
Q

What are THE KEY FEATURES of type 2 respiratory failure?

A 
Low O2 (pO2<8 ON AIR)
CO2 normal (or high) (pCO2 >6.0)

Hypercapnic

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36
Q

What are the indications of respiratory failure?

A

require supplementary O2 with/without ventilation

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37
Q

What are the indications of cardiovascular failure?

A

low BP

On vasosuppressors or inotropes

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38
Q

What are the indicators of renal failure?

A

reduced or no urine output, raised serum creatinine

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39
Q

What are the indications of liver failure?

A 
Jaundice
Prolonged clotting (bruising)
Encephalopathy
low blood sugary
high lactate
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40
Q

What are the indications of nervous system failure?

A

reduced conscious level

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41
Q

What is included in a clotting screen

A

PT
APTT
Fibrinogen

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42
Q

Below what reading of fibrinogen would you be concerned about DIC in a septic pt?

A

1.5

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43
Q

Describe multiple organ dysfunction syndrome

A

shock causes hypoperfusion

lack of oxygen at cellular level then leads to cellular dysfunction/death

cellular dysfunction/death causes release of inflammatory cytokines and microvascular injury

this cascade then causes further cellular dysfunction and whole organ system failure ensues

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44
Q

how would you manage multi organ failure syndrome

A

oxygenation, ventilation
fluid, inotropes, vasopressors
feeding

treat underlying cause

replacement of organ support

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45
Q

As well as stabling the patient and treating underlying cause, what else might you want to do for a pt. with multiple organ failure

A 
Feeding
Sedate and invasive ventilation
Gastric protection
DVT prevention
Measures to limit nosocomial infection
analgesia
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46
Q

What type of respiratory failure is CPAP useful for? Why?

A

type 1

stops alveolar collapse (keeps alveoli open - good in ‘wet lungs’ eg. oedema (due to LVF), pneumonia (in some cases))

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47
Q

What type of respiratory failure is BIPAP used for?

A

type 2
increase minute volume (by giving them increased tidal volume)
eg. COPD

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48
Q

What is ECMO? What is the benefit of this over ventilation? What type of patient could this be useful for?

A

oxygens the blood - leaves body, goes through machine, goes through membrane oxygenation and back in to body

gives the lungs a rest (compared to ventilation, which is usually an aggressive experience for the lungs)

Would give to previously young and fit pt. who has developed a resp. problem (eg. pneumonia)

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49
Q

What are some cardio specific organ support interventions?

A

vasoactive agents

intra-aortic balloon pump (lots of complications, going out of function)

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50
Q

What are some renal specific organ support interventions?

A

renal replacement therapy

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51
Q

When might you consider pt. for renal replacement therapy (on ICU)

A

uraemia
hyperkalemia
pulmonary oedema (fluid overload)
metabolic acidosis

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52
Q

How would you (temporarily) manage pt. with hyperkalemia (K>6.5/7)

A 
calcium gluconate (can also use calcium chloride)
10 mls

Insulin

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53
Q

What is the definition of respiratory failure (in terms of oxygen levels) and how is it classified?

A

Resp. failure = lack of oxygen (PaO2 <8kPa)

Classified in to type 1 and 2

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54
Q

What are some causes of type 1 resp. failure?

A

ventilation/perfusion mismatch
upper airway obstruction
low oxygen in inspired air

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55
Q

How would you manage type 1 respiratory failure?

A

A-E approach

treat underlying cause
TREAT HYPOXIA: GIVE OXYGEN (generally de-escalation pattern)

If still hypoxic: CPAP
delivers oxygen at pressure

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56
Q

How does CPAP work?

A

Delivers oxygen with positive pressure of between 4-25 cm H2O

Improves FRC (functional residual capacity)

Improves V/Q mismatch 
 - decreases atelectasis
- decreased leakage of fluid into lungs
- splints airways open
(blood going to parts of lung (perfusion), but not being oxygenated - opens up airways and allows these perfused areas to take part in gas exchange)

Decreases work of breathing

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57
Q

When might you use CPAP in type 1 resp failure?

A

When face-mask or high-flow oxygen has failed

pulmonary oedema
fluid overload
atelectasis
chest infection

pt with PaO2 less than 8KPa despite maximal O2 therapy
(consider escalating to HDU/ICU)

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58
Q

When might you not use CPAP in a pt. with type 1 resp failure? why not?

A

Pneumothorax

Make it worse!

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59
Q

What are some of the problems with CPAP?

A

Can expand pneumothoraces

Can cause hypotension (increased intrathoracic pressure, causing decreased venous return and therefore decreased pre-load to the heart - may need to give IV fluids… if not contraindicated y pulmonary oedema)

Difficult to apply if there are facial injuries or if pt. wants to eat

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60
Q

What can cause type 2 respiratory failure? (hypoxia with hypercapnia)

A

Hypoventilation (eg. drug overdose, weakness/muscle fatigue)

Increased dead space in lung (eg. COPD) (these pts. may also have increased airway resistance - patient looks like they are breathing heavily, but amount of air entering alveoli is limited. Alveoli may also be damaged and ineffective at gas exchange, air may get to alveoli, but nothing happens there)

Worsening lung mechanics: increasing bronchial constriction, narrowing and oedema

disordered central ventilatory drive

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61
Q

How would you treat type 2 respiratory failure?

A 
treat hypoxia (but be careful not to make hypercapnia)
BIPAP - patient needs extra support for ventilatory pump

(in emergency: treat hypoxia, but be mindful of hypoventilation - see COPD management protocol on resp. ward. worst case scenario: intubate patient and ventilate them)

62
Q

What is BIPAP?

A

Biphasic positive airway pressure

like CPAP, but with additional pressure to support inspiration (this pressure decreases again on expiration, to prevent patient having to breath against this increased pressure)

Increases minute volume by increasing tidal volume

63
Q

What is EPAP?

A

expiratory positive airway pressure, analogous to CPAP

64
Q

What is IPAP?

A

inspiratory positive airway pressure, the (extra) pressure given to support inspiration.

Augments tidal volume.

65
Q

When is BiPAP indicated?

A

Hypercapnoeic COPD exacerbation (not improved by oxygen therapy) - prevent need for ET tubing

MSK conditions with resp. failure (as long as airway is patent and SECURE)

Obesity hypoventilation syndrome

66
Q

What are some problems with BiPAP?

A

mask intolerance
facial injury

PATIENT CO-OPERATION IS CRUCIAL

67
Q

65 yr M
SOB and chest pain
ECG shows LBBB

ABG on 15L non-rebreathe mask:
pH 7.354
PO2 10 kPa
PCO2 3.12 kPa
Bicarb 24.2

what is the diagnosis?
What type of resp. failure is this?
How should this be managed?

A
  1. cariogenic pulmonary oedema
  2. type 1
  3. Oxygen, CPAP, medical treatment
68
Q

72 yr smoker
worsening SOB
Cough with yellow sputum

ABG on air:
pH 7.35 
pCO2 7.8 kPa
pO   5.1 kPA
HCO3 32mmol/l
on 35% venturi:
pH  7.30
PCO2  10.2kPa
Po2   8.9kPa
HCO3 34mmol/l

what is the diagnosis?
What type of resp. failure is this?
How should this be managed?

A
  1. exacerbations of COPD
  2. type 2
  3. controlled oxygen
    BiPAP
    Medical management
69
Q

What are the indications of invasive ventilation?

A

Respiratory failure that is refractory to other treatment

Respiratory failure with low conscious level

Tiring on other treatment
Airway compromise

Also used in other conditions (sepsis, trauma, head injury, post arrest etc)

70
Q

What are some problems with IPPV?

A

Requires endotracheal tube

Sedation (to almost anaesthetic levels)

  • Hypotension
  • Gastroparesis
  • Immobility
  • Vascular access
  • Risks of pneumonia

Limited to specialist areas (ICU)

71
Q

What is the difference between withholding and withdrawing treatments?

A

Witholding: not starting or increasing interventions

withdrawing: actively stopping a life-sustaining intervention (passive-euthanasia)*
* this is legal if intervention deemed futile

72
Q

What is double effect?

A

treatment used for one indications has a deleterious effect in another aspect.

eg. opiates for treatment of pain, may also shorten life by causing resp. depression

73
Q

What is the criteria for withdrawal of treatment?

A

Futility - sufficiently low efficacy that doctors believe it should not be provided. Three typesL physiological, benefit-centred, cost-based.

Best interests eg. treatment v. futile or burdensome for pt.

Competent pts. refusing treatment (pts. who lack capacity - use MCA 2005, act in pt’s best interests)

74
Q

What drugs are still given in withdrawal of treatment?

A

treatments are reduced down to those that treat symptoms

75
Q

What is the definition of death?

A

Irreversible loss of the capacity for consciousness combined with the irreversible loss of the capacity to breathe

(capacities within the brainstem)

76
Q

How does death of the brainstem USUALLY occur? How is this different in primary brain damage?

A

Most deaths: brainstem damage occurs secondary to ischaemia caused by cardiac arrest

Primary brain damage: brainstem death occurs in the presence of a beating heart. No other cause of unconsciousness is present
- must to 6 extensive brainstem tests and apnoea test

77
Q

What is the critical care outreach team?

A

Senior nursing staff with extensive critical care experience

nurse led service with dedicated ICU consultant available for outreach team

78
Q

What things can the critical care outreach team do/think about?

A

A-E assessment
Hx and clerking notes
NEWS recording
Fluid balance
Look at blood results, radiological reports,
Level of care required and ceilings of care

79
Q

What do you need to think about in a patient with a NEWS of 5 or more?

A

SIRS or Sepsis

80
Q

What is sepsis?

A

SIRS and clinical evidence of infection

81
Q

What is the equation for oxygen delivery?

A

cardiac output x oxygen content

82
Q

What KEY three things impact cardiac function?

A

preload
after load
contractility

83
Q

What are two common causes of hypovolaemic shock?

A

bleeding

dehydration

84
Q

What are 4 main causes of cardiogenic shock?

A 
Pump failure (many causes)
Rhythm abnormalities
valvular defects
obstruction to flow
85
Q

What are 6 main causes of distributive shock?

A 
Sepsis
Anaphylaxis
neurogenic shock
adrenal insufficiency
drugs and toxic exposure
86
Q

What are the different classifications of shock?

A

Hypovolemic
Cardiogenic
Distributive (incl. anaphylaxis, septic shock and neurogenic)
Obstructive

87
Q

How might hypovlemic and cariogenic shock present differently to distributive shock (thinking specifically about patient temp and appearance)?

A

Hypovol and cardio: cool, pale patient

distributive: warm, vasodilator patient

88
Q

What are clinical signs of shock (and what are the attempted compensation mechanisms of the body)?

A

NOT ALL SIGNS HAVE TO BE PRESENT AND NOT ALL SIGNS ALONE MEAN SHOCK

Inadequate perfusion:

General -
SBP < 90 (or fall from baseline of 30)
Lactate > 3
BE < -4
Increased cap refill

Brain -
Lethargy
Somnolence

Kidney - low urine output (oliguria/anuria)

Compensation: tachycardia
tachypnoea

89
Q

Why are lactate and urine output so important when working out if/how badly, someone is n shock?

A

Lactate produced by tissues with inadequate oxygen supply (anaerobic resp bi-product)

Urine output = directly measurable indicator of organ function. Falling urine output indicates, renal perfusion is inadequate, therefore likely to be case in general organs

90
Q

How do you optimise perfusion in a patient who is shocked?

A

Secure airway

Ensure adequate oxygen saturations: adequate ventilation/breathing

Fluid resuscitations (250ml< within 10 mins) - even in pulmonary oedema

Ensure adequate haemoglobin conc. to carry oxygen

91
Q

What monitoring would you do for someone in shock?

A

Regular and repeated assessment of perfusion:

HR and RR
Urine output
ABG and lactate
Conscious level

92
Q

What care/treatment can be done in ICU for shock that is different from a normal ward?

A

More invasive monitoring (arterial line, CVP)

more accurate fluid resuscitation

use of vasoactive medications (restore perfusion to vital organs)

Specific organ support eg. dialysis.

93
Q

where would you send someone with shock due to intra-ado bleeding?

A

surgical team for theatre

94
Q

What does a central venous catheter measure? What else can it be used for?

A

Central venous pressure (like measuring JVP)

Indicator of fluid status (circulating volume) - Trend is more useful than one off reading

Can also be used to give drugs that need to go to central vein, e.g.. noradrenaline

95
Q

What do vasopressors do?

A

Cause vasoconstriction of peripheral vasculature (alpha receptors) - can improve coronary blood flow

96
Q

What do inotropes do?

A

Increase contractility of heart (and often HR too) (beta receptors)

97
Q

What are the two main classes of vasoactive drugs?

A

inotropes

vasopressors

98
Q

What treatment would you give to a hypovolaemic patient out of the following:

Fluid
inotrope
vasopressor

A

Fluid

If this doesn’t work, more fluid

99
Q

What treatment would you give to a patient in cariogenic shock out of the following:

Fluid
inotrope
vasopressor

A

inotrope (dobutamine)

100
Q

What treatment would you give to a patient in distributive shock out of the following:

Fluid
inotrope
vasopressor

A

vasopressor (noradrenaline)

101
Q

What are the physiological goals when treating shock?

A

normalise lactate

restore urine output to >= 0.5 ml/kg/hr
MAP >= 65 (or more if usually hypertensive)

Central venous O2 sats >70%

CVP 8-12

102
Q

What is a downside re. aggressive fluid resuscitation in shock?

A

Increases tissue leak
increases intrcapillary distance
worsens tissue oxygenation

103
Q

What is a potential negative effect of each of the vasoactive classes?

A

vasopressors: tissue ischaemia (due to vasospasm)

inotropes: stress the heart, increase myocardial oxygen consumption - increasing risk of ischaemia
arrhythmia

104
Q

What does withholding treatment mean? How does this compare to withdrawing treatments? Is there a legal or ethical distinction between these two concepts?

A

Witholding: not starting or increasing interventions

Withdrawing: actively stopping life-sustaining intervention (passive euthanasia)
LEGAL IF DEEMED FUTILE

THERE IS NO LEGAL OR ETHICAL DISTINCTION BETWEEN THE TWO

105
Q

How is euthanasia different from witholding/withdrawing life-sustaining treatment?

A

Active shortening of dying process.

UNLAWFUL IN UK

106
Q

What are some criteria for withdrawal of treatment?

A

Futility:
sufficiently low efficacy that doctors believe it should not be provided
(incorporates value judgements)

107
Q

Who does the decision re. whether a treatment is futile lie with? What legal framework outlines this?

A

the doctor - not the patient.

mental capacity act

108
Q

What are the three main types of futility?

A

Physiological
benefit-centred
cost-based

109
Q

How should decisions about futility be made?

A

In patient’s best interests - consult widely to find out patient’s past and present wishes, feelings, beliefs and values

NOT THE VALUES OF THE RELATIVES

110
Q

Which patients can refuse/withdraw treatment?

A

Patients with capacity

BUT CANNOT REQUEST TO BE ASSISTED WITH COMMITTING SUICIDE

111
Q

Can a patient demand treatment?

A

No - doctor makes decision based on best interests

112
Q

If patients’ don’t have capacity to make a decision, how does this get made?

A

(someone may have legal right)

Doctor

Overall balanced on:
recent views expressed by pt
circumstances the would have considered if capable
previously expressed views or beliefs
clinician and peer reviews
113
Q

What drugs would you give someone when withdrawing care? What other things do you need to consider?

A

Infusions or boluses of:
analgesics
anxiolytics
antisialogues

Family wishes
Timing - family, organ donation etc.

consider whether to extubatne or not

114
Q

What is death?

A

Irreversible loss of consciousness + irreversible loss of capacity to breath (these capacities live in brainstem)

115
Q

What are different types of death?

A

Most: brainstem damage secondary to ischaemia caused by cardiac arrest

Sometimes: brainstem death in presence of being heart (primary brain damage). No other cause of unconsciousness present.

116
Q

How do you diagnose death?

A

Loss of cardiac and resp. function for 5 mins

Limited brainstem function:
pupils unreactive
no corneal reflex
no response to supraorbital pressure

117
Q

What is ventilation/perfusion mis-match?

A

alveolus is perfused (receiving blood), but not oxygenated (alveolus is malfunctioning eg. filled with fluid or infection).

This blood remains unoxygenated and then mixes with oxygenated blood from other alveoli. If sufficient alveoli are affected, proportion of blood entering left hear without being oxygenated can be enough to dilute oxygenated blood - causes blood to by ‘hypoxic’

118
Q

What are some causes of Type 1 (HYPOXIC) respiratory failure?

A

V/Q mismatch
Upper airway obstruction
Oxygen oxygen in inspired air

119
Q

Why does hypnocapnoea occur in COPD?

A

muscle fatigue + worsening lung mechanics

increasing bronchial constriction, narrowing and oedema

disordered central ventilatory drive

High PCO2 and low PO2

120
Q

What is one of the key requirements of invasive ventilatory support? How is this achieved?

A

Requires definitive airway to prevent aspiration of gastric contents

ET tubes
tracheostomy tubes

121
Q

Where do the tip of the ET tube, and the cuff (respectively) sit anatomically?

A

ET tube tip: just above carina

cuff: just below vocal cords

122
Q

Why can’t a patient with ET tube speak?

A

No airflow across vocal cords

123
Q

What are the early complications of an ET tube?

A

trauma to airway - incl, mouth, teeth and trachea

aspiration of stomach contents

tube malposition

airway obstruction

hypoxia from prolonged attempts

124
Q

What are some late complications of an ET tube?

A

infection

mucosal damage to mouth or trachea (from cuff pressure)

injury to vocal cords

tracheal stenosis

125
Q

When might you consider using a tracheostomy tube?

A

Patients needing a prolonged airway or ventilatory support

126
Q

How might a tracheostomy be better for a patient than an ET tube?

A

might be better tolerated than an ET tube - may permit withdrawal f sedation

May aid weaning from mechanical ventilation

avoid some of the complications of long-term ET tubes

127
Q

Where is the incision for a tracheostomy made?

A

anterior neck

between tracheal cartilaginous rings

cuff then inflated to form a seal against the tracheal wall - providing definitive airway

128
Q

Other than the tracheostomy set, what else is usually needed to perform the procedure competently?

A

Bronchoscope

129
Q

What are the early complications of tracheostomies?

A

Haemorrhage

pneumothorax

tube misplacement

surgical emphysema

blockage with secretions

stromal infection

mucosal ulceration
and perforation

tracheo-oesophageal fistulas

130
Q

What are some late complications of tracheostomies?

A

Late haemorrhage (erosion into innominate artery)

tracheal granulomata

tracheal stenosis

scarring, persistent sinus

tracheal necrosis

131
Q

Why is oxygen that is delivered to patients in ICU, warmed and humidified?

A

improve patient comfort

reduce complications eg. mucus plugging

132
Q

What is one of the risks of long term oxygen therapy? (>60% for >48 hours)

A

pulmonary injury

133
Q

What is non-invasive respiratory support?

A

CPAP and BIPAP

Both types of Non-invasive ventilation (NIV)

134
Q

what do chronotropes do?

A

increase the heart rate

135
Q 
Why is dobutamine the odd one out of:
dobutamine
adrenaline
noradrenaline
phenylephrine
A

All of the others increase systemic vascular resistance

This increases BP (and therefore vital organ perfusion)

Dobutamine doesn’t do this

136
Q

What are common causes of AKI in critical care patients?

A

shock
sepsis
(reduced perfusion)

137
Q

What is a urine output that indicates AKI?

A

<0.5ml/kg/hr
OR
acute deterioration of eGFR - rising creatinine and urea

138
Q

How is urine output measured in ICU?

A

catheterisation

139
Q

What are some complications of Aki that need to be avoided?

A

hyperkalaemia
acidosis
fluid overload
uraemia

140
Q

How are patients with deteriorating kidney function treated?

A 
Intermittent haemodialysis (like in ESRD) OR
continuous renal replacement therapy

(continous is often better for patient - less large fluid changes)

VENO-VENOUS HAEMOFILTRATION
- large double lumen catheter in central vein

141
Q

What are common reasons for sedation in ICU?

A

aid tolerance of ET tube
Reduce pain and anxiety

status epilepticus treatment

142
Q

What combination of drugs are usually given for sedation in ICU?

A 
Opioid (commonly alfentanil or remifentanil)
Sedative agent (commonly propofol)
143
Q

What are the 3 main types of distributive shock?

A

Septic
anaphylactic
neurogenic

144
Q

What is the pathophysiology of distributive shock?

A

lack of normal responsiveness of blood vessels to vasoconstrictive agents and direct vasodilation

145
Q

What is the pathophysiology of neurogenic (distributive shock)?

A

Neurogenic shock is caused by the loss of vascular (arterial and venous) tone. Leads to decreased vascular resistance. This is caused by damage to CNS (sympathetic nervous system).

Blood doesn’t get to organs as easily/quickly = decreased tissue perfusion

Blood flow back to the heart is reduced - reduces stroke volume = reduces cardiac output (worsens BP and tissue perfusion)

Due to sympathetic nervous system damage, HR drops

146
Q

What is the pathophysiology of anaphylactic (distributive) shock?

A

In anaphylactic shock low blood pressure is related to decreased systemic vascular resistance (SVR) triggered primarily by a massive release of histamine by mast cells

147
Q

What is the pathophysiology of septic (distributive) shock?

A

endothelial cells lining the blood vessels become less responsive to vasocontrictive agents, become leaky.

Causes over expression of nitrous oxide

Changes in clotting cascade

DIC due to thrombin release

148
Q

Causes of neurogenic shock?

A

Trauma

epidural goes wrong

149
Q

What are the symptoms of neurogenic shock?

A

Low BP (due to decreased systemic vascular resistance)

Hypoxia (or symptoms of end-organ damage due to reduced tissue perfusion) - altered mental status, decreased urine output etc.

REDUCED HR - ONLY SHOCK THAT HAS BRADYCARDIA (except for cariogenic shock secondary to bradyarrythmia)

warm skin (due to vasodilation)

150
Q

How would you treat neurogenic shock?

A

Vasopressors (call anaesthetist)
Treat underlying cause
IV fluids
Atropine (blocks parasympathetic nervous system - increase heart rate to increase cardiac output)

151
Q

What are some causes of neurogenic shock?

A

Spinal cord trauma

Most commonly stabbed in the spine

acc (6 decks)

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