ICU Flashcards
Level 0, 1, 2 and 3 based patients
Level 0 = ward care, no organ support
Level 1 = ward care, at risk
Level 2 = HDU (single organ support, 1:2 ratio)
Level 3 = ICU (1+ organ support, technical ventilation, 1:1 ratio)
What is an Apache II score
Estimates ICU mortality based on age, health status, bloods etc
What do different levels of NEWS scores mean?
0 = monitor 12 hourly
1-4 = low risk, 4-6 hourly review
>3 / 5-6 = urgent ward based response, review 1 hourly
>7 = emergency response, critical care/airway management involvement
What do different levels of NEWS scores mean?
0 = monitor 12 hourly
1-4 = low risk, 4-6 hourly review
>3 / 5-6 = urgent ward based response, review 1 hourly
>7 = emergency response, critical care/airway management involvement
Indications for sedation
Toleration of distressing procedure Optimising mechanical ventilation Decreasing agitation Decrease in O2 sats Decreased ICP Facilitation of cooling
Sedative agents used on ICU
Propofol
Thiopentone
What is the Bohr affect?
Hb gives up oxygen to tissues more readily at high partial pressures of CO2 (because lowers ph) = right shift of curve = tissues get MORE oxygen more easily
Types of hypoxia
- Hypoxic hypoxia == reduced supply of O2
- Anaemic hypoxia == reduced Hb - reduced arterial PO2
- Stagnant hypoxia == reduced cardiac output - reduced delivery to tissues
- Histotoxic hypoxia == normal delivery to tissues but impaired metabolism
- Cytotoxic hypoxia == caused by chemicals e.g. cyanide - tissues can’t use oxygen
Dead space in context of respiratory failure
Normal ventilation of alveolus, but perfusion fails to supply the ventilated area (e.g. PE)
Shunt in the context of respiratory failure
Normal perfusion, but ventilation fails to supply the perfused area (e.g. obstruction)
Signs of hypercapnia
Headache Peripheral vasodilation Tachycardia Bounding Pulse Tremor/flap Confused/drowsy/coma
Explain type 1 respiratory failure and why it occurs
Hypoxia with normocapnia
Ventilation perfusion (V/Q) mismatch: air flowing in and out does not match the flow of blood to the lung tissue. PO2 starts to fall, PaCO2 starts to rise so RR increases, which blows of CO2 and corrects it, but PaO2 remains low.
Causes of T1RF
Anything causing REDUCED VENTILATION but with NORMAL PERFUSION == pneumonia, oedema, fibrosis, pneumothorax
Reduced perfusion, normal ventilation = PE
Explain T2RF
Hypoxia + hypercapnia
Occurs due to alveolar HYPOventilation
Muscle fatigue and poor lung mechanics cause increased bronchial constriction and narrowing, and a disordered central ventilatory drive gets used to being hypoxic, so does not recognise high CO2.
Causes of T2RF
COPD Life threatening asthma CF Neuromuscular disease Chest wall deformity
Explain ARDS
Bilateral pulmonary infiltrates and severe hypoxaemia
Caused by a lot of things
Late stage causes fibrosis
Explain ARDS
Bilateral pulmonary infiltrates and severe hypoxaemia
Caused by a lot of things
Late stage causes fibrosis
CPAP explanation and indications
Continuous positive air pressure - recruits alveoli and keeps airways expanded so airways do not collapse
Can deliver 100% oxygen
Indications: obstructive sleep apnoea, congestive cardiac failure, acute pulmonary oedema, chest infection
(type 1 rest failure)
Explain BiPAP and indications
Cycles from high to low pressures - increased pressures help with inspiration.
Indications = T2RF, normally secondary to COPD.
Must be ACIDOTIC and PaCO2 >6
Which tests must be carried out before BiPAP is used?
CXR - rule out pneumothorax
ABG - ensure T1RF
Indications for mechanical ventilation
Respiratory failure due to:
- Apnoeas
- Haemodynamic instability/ CV collapse
- Acute ventilatory failure
- Impending ventilatory failure (declining ABGs, respiratory distress)
- Respiratory muscle fatigue (rising PCO2, low tidal volume)
- Obstruction
Adverse effects of ventilation
VAP
Barotrauma (alveolar rupture from excessive pressure –> pneumothorax)
Volutrauma (high pressure caused by large volume ventilation)
Haemodynamic compromise (higher inspiration pressures can cause decreased venous return)
Ventilator malfunction
What are FiO2 and PEEP
FiO2 = oxygenation PEEP = peak end expiratory pressure (positive airway pressure during expiration to maintain alveolar recruitment)
Explain shock
Inadequate tissue perfusion and oxygenation causes ABNORMAL METABOLIC FUNCTION
Intracellular calcium overload = reduced myocardial contractility
H+ excess = decreased myocardial function
Anaerobic respiration = lactic acidosis = further exacerbation of issues
How to calculate oxygen delivery to tissues
10 x cardiac output x concentration of O2 in blood
What are crystalloid and colloid fluids
Crystalloid = sodium etc dissolved in water, short lived effect. Either hypotonic or isotonic.
Colloid = high molecular weight particles e.g. gelatine, albumin. Expand the intravascular volume. Risk of anaphylaxis.
Explain ionotropes and vasopressors + examples
Iontropes = work on beta receptors increase cardiac muscle contractility by increasing calcium availability for myocyte contraction (thus increasing stroke volume). Used when reduced CO.
E.g. Adrenaline, noradrenaline, dobutamine
Vasopressors = work on alpha receptors to increase SVR (thus increasing BP and tissue perfusion). E.g. adrenaline, phenylephrine, vasopressin.
Explain obstructive shock
Shock caused by cardiac output problem but NOT caused by the heart itself e.g. cardiac tamponade, tension pneumothorax
AKI grades
GRADE 1 = creatinine rise of 150-200% OR >26.4 –> UO <0.5ml/kg/h for 6 hours
GRADE 2 = creatinine rise of 200-300% –> UO <0.5ml/kg.h for 12 hours
GRADE 3 = creatinine rise of >300% or >354umol.L –> anuria for 12 hours or <0.3ml/kg/h for >24 hours
Indications for acute dialysis
Acidosis Electrolyte abnormalities (treatment resistant hyperkalaemia) Intoxication Oedema (severe/unresponsive) Uraemia
Difference between renal filtration and dialysis
Filtration = purely high pressure forces filtrate across a membrane
Dialysis = moves filtrate in opposite direction to blood, creates a concentration gradient
Equation for CPP
CPP = MAP - ICP
so raised ICP decreases CPP –> physiological response is increased BP –> further hydrocephalus and herniation
Explain Munro-Kellie doctrine
3 tissues in the brain are in equilibrium (blood, CSF, Brain parenchyma). Increase in one has to be compensated by a decrease in volume of another –> i.e. downward displacement of CSF into spinal canal (can compensate for 100-120ml change in volume).
After this = cushing’s triad –> hypertension, bradycardia, irregular respiration.
Terminal event = cerebral ischaemia.
GCS categories of brain injury
13-15 = minor 9-12 = moderate 3-8 = severe
At what level should mean arterial pressure be maintained above on ICU
> 90 mmHg
Signs of coning (cerebral herniation)
Reduction in GCS
Bradycardia, tachycardia, hypertension
Irregular breathing
Fixed, dilated pupils
Common issues post-ICU
Airway problems
Joint mobility problems - contractures
Cognitive issues - memory, problem solving, organisation
Psychological issues - insomnia, PTSD, nightmares
Weakness of muscles
Legally, how should decisions on patient care for an incapacitous patient be made if no close relatives are able to give insight?
an independent mental capacity advocate (IMCA) should be assigned
How do brainstem death and circulatory death differ in terms of organ donation?
BRAIN STEM DEATH = diagnose death –> optimise –> mobilise team –> organ retrieval
CIRCULATORY DEATH = mobilise team –> stop support, heart must stop within 5 minutes –> diagnose death –> organ retrieval
