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Summary Critical care and ICU notes
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- The University Of Edinburgh (ED)
Notes for critical care and ICU modules. Covers content for medical school finals
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Critical Care TeachingMonitoring
Capnography – 4 phases as seen on graph
1. Inspiratory baseline (no exhaled CO2)
2. Expiratory upstroke
3. Expiratory plateau
4. Expiratory downstroke
No hat – patient may also be in cardiac arrest.
Exhaled CO2 is a marker of cardiac output (no
cardiac output = not able to exhale CO2)
Invasive BP monitoring – arterial line
- Plastic catheter in artery (normally
radial)
- Beat by beat BP and waveform
- Waveform shows systolic and diastolic
BP, MAP
- MAP ~ 65mmHg is normally good for
perfusion
Arterial lines can be flushed – only with
0.9% NaCl, but never inject anything into an
arterial line.
Ventilation
Modes of ventilation – how is the breath delivered: pre-set pressure or pre-set volume?
Pressure dependent on ‘elasticity of lungs’ – very elastic lungs with a set pressure will deliver a
greater volume than for inelastic lungs
- Set frequency (controlled mode) – ventilator does all the work
- In response to patient’s respiratory efforts (spontaneous mode)
- Combination (spontaneous-assisted/assist-controlled)
Volume control ventilation aka – continuous mandatory ventilation : user selects volume of gas to be
delivered with each breath and the rate at which this is delivered
Must have safety mechanism – pressure limitation if pressure becomes too high during the breath
Pressure control ventilation – delivers gas at a set pressure for a certain period of time and set
frequency
Important in patients who have rapidly changing lung compliance e.g. bronchospasm in acute asthma.
Must keep an eye on the size of the breath
Synchronous intermittent mandatory ventilation – mixed mode of ventilation which offers the patient
pressure supported breaths when they are generating spontaneous breaths
PEEP – positive end expiratory pressure, pressure applied to the lungs at the end of expiration to
ensure that the alveoli don’t collapse. This ‘recruits’ the closed alveoli in the sick lung and improves
oxygenation
Ventilatory aims
- Tidal volume < 6ml/kg of ideal body weight
- Peak airway pressure of < 30cm H2O
,Gas exchange rules
To improve oxygenation
- Increase FIO2
- Increase PEEP
To reduce CO2 (improve ventilation)
- Increase RR
- Increase tidal volume (not above safe limits)
Drugs in critical care
1. Propofol
a. Glycine agonist – lipid emulsion
b. Causes vasodilation and bradycardia, BP and CO, respiratory depression
c. If too much is given can develop propofol infusion syndrome – metabolic acidosis and
cardiac abnormalities (generally not used in children)
2. Alfentanil
a. Causes vasodilation, reduced gut motility, respiratory depression
3. Clonidine – alpha agonist with degree of sedation + anxiolysis
4. Midazolam – GABA agonist benzodiazepine
a. Slower onset/offset than propofol
Indications for sedation
- A – facilitate intubation and tolerance of ETT
- B – To facilitate invasive ventilation
- C – reduction of oxygen consumption
- D – comfort and analgesia, manage raised ICP, behavioural control
Assessing sedation
- GCS
- AVPU
- Sedation scores (RASS – Richmond agitation and sedation score)
o Negative scores indicate sedation
o 0 = awake, co-operative patient
o Positive scores indicate agitated patient
Adverse effects of sedation
- Prolonged mechanical ventilation (and ventilator-associated pneumonia)
- Longer ICU stay
- Difficulty in neurological assessment
- Increased risk of delirium
Cardiovascular support
Vasopressors – increased vascular tone, peripheral vasoconstriction - systemic vascular resistance
- Noradrenaline, mainly acts on peripheral circulation with alpha activity. Very little beta-action
therefore does not improve heart contractility
Inotropes
Positive – increased myocardial contractility
Negative – decreased myocardial contractility
Adrenaline can work as vasopressor and inotrope. At low doses mainly vasopressor (alpha activity) but
also has beta effects at higher doses
, AKI and RRT
- Increase in serum creatinine by > 26.5 micromol/L
- Increase in serum creatinine by x1.5 baseline
- Urine vol. < 0.5ml/kg/hr for > 6 hrs
Risk factors
- Critical illness
- Age
- CKD, PVD, IHD, HTN, DM, Chronic liver disease
- Nephrotoxic medication
Causes
Pre-renal:
- Hypovolaemia – GI losses, 3rd spacing, urinary, bleeding
- Hypervolaemia (reduced effective circulating volume) – cirrhosis, HF, nephrotic syndrome, IAH
- Vasculature – renal artery stenosis
- Hypotension – shock, drug-induced hypotension
Renal:
- Glomerulonephritis
- Tubular: ATN, nephrotoxins, rhabdomyolysis
- Interstitial: Drugs, infection, systemic disease e.g. sarcoid, SLE
Post-renal:
- Stones, tumours, retroperitoneal fibrosis, stricture
- BPH, neurogenic bladder, prostate cancer
- AAA, pelvic malignancy
Indications for urgent RRT
- Severe metabolic acidosis
- Hyperkalaemia (life-threatening or non-responsive to medical therapies)
- Symptomatic uraemia – especially encephalopathy or uraemic pericarditis
- Fluid overload e.g. pulmonary oedema
- Toxins – BLAST
o Barbiturates, lithium, toxic alcohols, salicylates, theophyllines
Methods
Continuous haemofiltration – gentle method of removing solutes and doesn’t tend to affect fluid balances as
much. Not as efficient – only removes LMW molecules
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