ITU Flashcards
(90 cards)
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
2
Q
Investigations of post op confusion?
A
bedside = ABG, bloods, BM, ECG
Radiology
3
Q
Purpose of sedation in critical care?
A
Anxiolysis
Analgesia
Amnesia
Sedation
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
5
Q
Sedative drug classes?
A
Benzos
Opiates
Butyrophenones e.g. Haloperidol = neurotransmitting blocker
Anaesthetic agents e.g. Propofol or ketamine
6
Q
Major SE of propofol?
A
Can cause hypotension on induction via decreasing SVR and myocardial depression
7
Q
Sodium thiopentone?
A
Use = RSI
Analgesic effect = none
SE’s = marked myocardial depression and toxic metabolites
8
Q
Ketamine?
A
Good analgesic and little myocardial depression
SE’s = dissociative nightmares
9
Q
Etomidate?
A
No analgesic effect
Favourable cardiac profile
SE’s = prolonged use causes adrenal suppression
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
11
Q
Criteria to donate pre-donation?
A
- Diagnosis of brainstem death and circulatory death
- Donor maintained on a ventilator in absence of sepsis
- No hx of malignancy (except primary brain tumour)
- HIV and HBV -ve
- High risk groups excluded e.g. IVDU
Often some specific restrictions e.g. heart donor no MI
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
13
Q
Physiological changes in brainstem death?
A
- Hypotension: due to loss of sympathetic peripheral vascular tone - 81%
(initially HTN due to immediate increase in sympathetic tone
Mx = IVF and inotropes - Coagulopathy: e.g. DIC
- 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 - Endocrine: Loss of thyroid function can result in further arrhythmias
Mx = T3
14
Q
When is it appropriate to perform an examination
A
- Coma - patient must be in a deep coma entirely reliant on ventilator due to absence of spontaneous ventilation
- 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
15
Q
Criteria for brainstem death?
A
- No respiratory drive:
Preoxygenated got 10 minutes
PCO2 increases, normally respiratory stimulates at >6.5kPa - 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
16
Q
Who can assess for BSD?
A
Must be relevant specialty
x1 consultant and x1 registered GMC for > 5 years
17
Q
When can confirmation be difficult?
A
COPD
Ocular injury
Brainstem encephalitis
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
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
- Phosphodiesterase inhibitors e.g. Milrinone
- increased contractility + SV but reduced SVR via vasodilation - Calcium channel agonists e.g. Levosimendan
- produce a transient inotropic effect
- increase sensitivity of myocardial troponin to intracellular calcium - ADH agonist = natural analogue of vasopressin and increase SVR via vasoconstriction
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
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
- 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 - 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 - Salbutamol (0.1 - 1.0)
Severe asthma - 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 - 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 - Isoprenaline - B1 and B2 (0.01 - 0.2)
- Reserved for treatment of emergency bradyrhythmias
- risk of tachyrhythmias - Phenylephrine = alpha 1 = pure vasoconstriction (0.2- 1.0)
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
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
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.
25
Indications for noradrenaline ?
Potent vasoconstrictor
| useful in septic shock, but can lead to reduced peripheral perfusion and increased afterload
26
Affects of noradrenaline on circulation?
low doses = B1 = increased CO and reduced SVR
Higher doses = alpha 1 = increased CO and increased SVR
27
Dobutamine effects?
Strong B1 = cardiac output up and SVR down
28
General problems with inotropes?
Tachyarrhythmias
Bradycardia if noradrenaline
HTNN with adrenaline
Hypotension if dobutamine / PDE3
29
What if cardiac index still <2.2 despite maximal cardiac output?
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
30
Indications for ET tube?
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
31
How long for ET tube?
2 weeks, after this tracheostomy
32
Basic intubation steps?
1. Pre-oxygenated 100% 3-5 mins
2. Position = neck extended
3. Anaesthesia = local or general
4. + muscle relaxant if GA
5. Intubate = laryngoscopy, intubate, inflate cuff, connect tube
6. Auscultate
7. Secure
33
Magill vs Macintosh laryngoscope?
Which one on paediatrics
```
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
34
Sizes of laryngeal tube?
8mm for male, 7mm for female
35
RSI?
Emergency induction e.g. AAA
Important requirements are suction, skilled assistant and cricoid pressure
Cricoid pressure is not released until cuff inflated
36
When is nasotracheal intubation used?
Head and neck procedures
37
Complications of ET intubation?
Trauma - teethe pharynx, larynx
Spinal injury
Acute HTN due to autonomic reflex of laryngoscopy
Spasm = laryngospasm / bronchospasm
Misplacement or disconnection
38
Pre-requisite to successful extubation?
1. Original disease resolved
2. Adequate lung function, haemodynamically stable
3. Adequate GCS
4. Satisfactory nutrition
5. General e.g. no sepsis
39
What do we mean by adequate lung function for extubation?
```
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
Why optimise nutrition?
Increased muscle strength of respiratory muscles
| reduced CO2 production as not dependent on glucose
41
Strategies to wean ventilation?
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
Levels of ITU care?
```
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
Some criteria for entering ITU?
Respiratory - advanced support e.g. mechanical ventilation to intubation
System support = 2 or more organs
Reversibility
44
Indications for mechanical ventilation?
```
RR >35
Pa02 <8 kPA w/ Fi01 >0.6
Vital capacity <10ml/kg
Tidal volume <5ml / kg
PaC02 >8
ICP > 20mmHg
```
45
What can we adjust on a normal ventilator?
```
Respiratory rate
Tidal volume 5-7 ml/kg
FiO2 0.21 - 1.0
Inspiratory : Expiratory ratio
Pressure limit
PEEP and CPAP
```
46
What do we adjust on ventilator to improve oxygenation?
FiO2, PEEP and I:E ratio can all be increased
47
What can we adjust on the ventilator to increase ventilation ?
Increase RR, tidal volume and peak pressure
48
Outline some basic ventilator modes?
Pressure control = set inspiratory pressure, when reached get expiration
Assisted mode, ventilator simply augments each inspiratory effort
49
What is PEEP and physiological changes?
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
SE's of IPPV?
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
Define cardiac index.
Cardiac output divided by body surface area
52
What is a pulmonary artery catheter and its purpose?
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
How does CVP give measure of left heart function?
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
Indicators for a pulmonary artery catheter?
Drugs = inotrope use
Surgical e.g. post cardiac surgery
Assessing cause of shock based on mixed venous oxygen saturations
55
What does a pulmonary artery catheter directly measure?
MAP and MpulmAP
HR, CO, EF
PACWP
Mixed venous oxygen sats
56
Derived variables of a pulmonary artery catheter ?
CI, SV, SVR, PulmVR
57
How do we calculate systemic vascular resistance?
[(MAP-CVP)/ CO] x 80
58
How do we calculate pulmonary vascular resistance?
(MPAP-PCWP)/ CO. x 80
59
Complications of pulmonary artery catheter?
Cardiac = arrhythmias, valve injury to tricuspid or pulmonary
Pulmonary artery rupture = shock and haemoptysis
Pulmonary infarction if balloon wedged too long
Sepsis
60
How does PAC measure cardiac output?
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
RRT types?
Haemodialysis, haemofiltration, peritoneal
62
Indication for RRT?
```
potassium > 6.5
pH <7.1
Refractory fluid overload
Uraemia complications
Drug OD
```
63
Haemodialysis vs haemofiltration?
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
HD vs. HF pros and cons?
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
When is intermittent HD used?
CKD, not the critically ill
Need - vascular access, extracorporeal circuit and dialysis machine
66
SE's of HD?
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
Types of continuous RRT?
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
How does PD work?
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
Classic side effect of PD?
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
What is an endotoxin?
lipopolysaccharide derived from cell walls of G-ve bacteria
| 3 parts = Lipid A, core polysaccharide and oligopolysaccharide
71
Difference between bacteraemia, sepsis and severe sepsis?
bacteraemia is viable bacteria in blood stream
Sepsis is SIRS with infective source
Severe sepsis is sepsis with organ dysfunction
72
Define septic shock?
Sepsis associated with hypotension and hypo perfusion despite adequate IVF
73
septic vs cardiogenic shock?
Septic is decreased SVR and increased CO
Cardiogenic is increased SVR in response to reduced CO
74
What is SIRS?
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
Pathophysiology of SIRS?
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
Mediators in SIRS?
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
What is the two hit hypothesis?
Those recovering from SIRS can have a can have a rapid systemic response to something seemingly trivial e.g. UTI
78
What is MODS?
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
Organs that can be involved in MODs?
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
Why may the gut fail in MODS?
Mucosa sensitive to ischaemia and loses function
Mal-distribution of blood flow
Alteration in gut flora
81
Mx of sepsis?
ABC
Renal = Ensure UO > 0.5ml/kg/hour
often via cardiac output
Nutrition = enteral feeds
Surgical = drain collection
82
Primary vs secondary transfer?
primary = from scene to hospital care
Secondary = between hospitals
83
Dangers of air ambulance transfer
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
Tracheostomy indications?
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
Types of tracheostomy?
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
Tracheostomy incision problems?
Too high = subglottic stenosis
Too low = Tracheoinominate fistula
87
How do tracheostomy's differ in kids?
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
Type of tracheostomy tubes?
Metal or plastic
Cuffed or unncuffed
Fenestrated or not:
- fenestrated allows speech
89
Complications of tracheostomy?
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
Tracheostomy ?
Secure
Prophylactic ABx
Humidified oxygen
Regular cleaning
