ICM Flashcards
(135 cards)
1
Q
Define ICU acquired weakness
A
Clinically detectable weakness in a critically ill patient with no other plausible cause
2
Q
List the classes of ICU acquired weakness
A
- Critical illness polyneuropathy
- Critical illness myopathy (histologically classified to cachectic, thick filament and necrotising myopathies)
- Critical illness neuromyopathy
3
Q
List the risk factors for the development of ICU acquired weakness
A
- Female
- Increasing age
- Sepsis
- Multi-organ failure
- Drug induced encephalopathy
- Increased duration of acute illness
- Increased duration of mechanical ventilation
- Requirement for parenteral nutrition
- Hypoalbuminaemia
- Hyperglycaemia
- High dose steroids
- Neuromuscular blocking agents
- Vasopressors
4
Q
List the clinical features of ICU acquired weakness
A
- Weakness develops after ICU admission
- Generalised symmetrical weakness
- Sparing of facial muscles, cranial nerves and extra-ocular munscles
- Preserved autonomic function
- Difficulties weaning from ventilatory support
- Reduced reflexes
- Normal conscious level
- MRC power score <48/60 (6 muscle groups: shoulder abductors, elbow flexors, wrist extensors, hip flexors, knee extensors, foot dorsiflexors)
5
Q
List investigations that aid the diagnosis of ICU acquired weakness
A
- Creatine kinase
- Nerve conduction studies
- EMG
- Muscle biopsy
6
Q
What proportion of patients diagnosed with ICU acquired weakness will die during their hospital admission?
A
45%
7
Q
What proportion of patients with ICU acquired weakness who survive hospital admission will achieve complete recovery?
A
68%
8
Q
Indications for neuromuscular block in critically ill patients
A
- Tracheal intubation
- ARDS
- COVID-19
- Proning
- Abdominal compartment syndrome
- Transfers
9
Q
Why is lean body weight used for roc?
A
Hydrophillic, so remains in central compartment
10
Q
Give the diagnostic criteria for DKA
A
pH <7.3 and/or bicarb <15mmol/L
Ketones >3mmol/l or ketonuria ++
Capillary glucose > 11mmol/L or known diabetic
11
Q
Give the two components of initial insulin management of a known diabetic adult patient admitted with DKA
A
- Start fixed rate insulin infusion at 0/1units/kg/hr
- Continue patient’s regular long acting insulin
12
Q
State the immediate fluid management of an adult patient admitted with DKA with systolic blood pressure <90mmHg
A
500mls 0.9% NaCl over 10-15mins
13
Q
State the equation for calculation of anion gap
A
(Na+K)-(Cl+Bicarb)
14
Q
List the biochemical findings of severe DKA in an adult that may warrant HDU referral
A
- pH < 7.1
- Ketones > 6mmol/L
- Bicarb < 5mmol/L
- K < 3.5mmol/l on admission
- Anion gap > 16
15
Q
List clinical findings of severe DKA that may warrant a referral to HDU
A
- GCS < 12
- Systolic < 90mmHg
- HR >100 or < 60bpm
- SpO2 < 92%
16
Q
Give the patient groups or comorbidities that may indicate need for HDU referral of a patient with DKA
A
- Young adults 18-25 yrs old
- Elderly
- Pregnancy
- Significant comorbidity e.g. heart failure or renal failure
17
Q
Give the complications of DKA management
A
- Hypo/hyperkalaemia with or without cardiac arrhythmia
- Hypoglycaemia
- Cerebral oedema
- AKI
- VTE
18
Q
List the respiratory symptoms of pulmonary embolism
A
- Pleuritic chest pain
- Breathlessness
- Haemoptysis
19
Q
List the signs of pulmonary embolism
A
- Type 1 respiratory failure/low SpO2/cyanosis
- Pleural rub
- Tachypnoea/increased work of breathing
20
Q
List the neurological features of pulmonary embolism
A
- Syncope/presyncope
- Anxiety/apprehension
21
Q
Give the ECG changes that may be associated with pulmonary embolism
A
- Tachycardia
- Atrial fibrillation
- Right ventricular strain - S1Q3T3, TWI V1-V4, QR pattern V1
- Pulseless electrical activity
22
Q
List the clinical presentations which indicate diagnosis of “high risk” pulmonary embolism
A
- Cardiac arrest
- Obstructive shock (persistent hypotension in association with end-organ hypoperfusion)
23
Q
Give the tests which may be used to confirm the diagnosis in a patient suspected of having high-risk PE
A
- CTPA
- V/Q scan
- ECHO (listed second in the textbook but does not confirm diagnosis)
24
Q
List the contraindications for pharmacological thrombolytic treatment for patients with high risk pulmonary thromboembolism
A
- History of haemorrhagic stroke or stroke of unknown cause
- Ischaemic stroke within 6 months prior
- CNS neoplasm
- Major traum, surgery or head injury in 3 weeks prior
- Bleeding diathesis
- Active bleeding
25
Give two interventional or surgical management options for treatment of high risk PE
* Percutaneous catheter directed therapy
* Surgical embolectomy
26
Give risks to a patient with high risk PE if intubation is required as part of management
* Hypotension, negative inotropic effects of induction agents pre-existing haemodynamic compromise
* Impaired venous return and so reduced right heart output due to positive pressure ventilation
27
State the mechanism of action for therapeutic effect of TCA
Inhibits reuptake of serotonin and noradrenaline into presynaptic terminals, so raises their concentration for postsynaptic receptor activation
28
List three additional receptor actions of TCAs and their clinical effect
* Sodium channel antagonism - cardiac depression
* Alpha adrenergic antagonism - hypotension
* Anticholinergic - pupil dilation, tachycardia, hypotension, ileus, irritability, confusion, seizures, coma, urinary retention, pyrexia
29
What therapeutic interventions an be considered in the management of TCA within 1 hour of ingestion
* Activated charcoal
* Gastric lavage (airway must be protected by pt or you)
30
List indications for intubation for patients after TCA overdose
* Reduction in GCS that compromises airway protection
* Hypoventilation contributing to acidosis
* Refractory seizures
31
Treatments that can be used in the management of hypotension and arrhythmia in presence of TCA overdose
* Fluid resuscitation
* 8.4% sodium bicarbonate
* Alpha agonist e.g. adrenaline infusion
* Magnesium sulphate (for dysrhythmia)
* IV glucagon
32
Apart from tachycardia, give ECG changes seen in TCA overdose
* QRS prolongation
* QTc prolongation
* Nodal or ventricular arrythmia
* R/S ratio > 0.7 in aVR
33
Give one drug that should be avoided for management of seizures in TCA overdose and what you would use instead
Avoid phenytoin (can lead to phenytoin toxicity with ventricular arrythmias)
Use benzodiazepine
34
List perioperative risk factors for the development of acute kidney injury
* Hypovolaemia (dehydration, bleeding)
* Hypotension (heart failure, dehydration)
* Locally impaired renal circulation (ACEI, NSAIDS, abdominal compartment syndrome)
* Systemic inflammation (sepsis)
* Nephrotoxins (aminoglycosides, rhabdomyolysis)
* Renal obstruction (renal calculi, misplaced stent)
35
List patient risk factors for development of AKI perioperatively
* Increasing age
* Male
* CKD
* Chronic liver disease
* CCF
* Hypertension
* Diabetes
36
List the indications for renal replacement in ICU
* Fluid overload not controlled with medical management
* Hyperkalaemia due to AKI not controlled with medical management
* Metabolic acidosis
* Symptomatic uraemia (encephalopathy, pericarditis) due to AKI
* Overdose with dialysable drug or toxin
* Management of pre-existing CKD in a patient requiring ICU admission
37
List the types of RRT available on intensive care
* Intermittent haemodialysis
* Contineous renal replacement therapy e.g. CVVHF, CVVHD, CVVHDF
* Peritoneal dialysis (in patients already using this form)
38
Give possible complications associated with the use of heparin for systemic anticoagulation for maintenance of the RRT circuit
* Heparin-induced thrombocytopenia
* Increased risk of haemorrhage
* Heparin resistance (Reduced antithrombin III production in critically ill patients)
39
Give complications associated with the use of citrate for regional anticoagulation for maintenance RRT circuit
* Alkalosis (citrate converts to bicarbonate)
* Acidosis (accumulation of citrate)
* Hypocalcaemia (citrate binds to calcium)
* Hypomagnesemia (citrate-calcium complex binding and removal in effluent)
40
What are the clinical features of propofol infusion syndrome?
* Metabolic acidosis
* ECG changes
* Rhabdomyolysis
* AKI
* Hyperkalaemia
* Lipidaemia
* Cardiac failure
* Pyrexia
* Elevated liver enzymes/hepatomegaly
* Elevated lactate
41
List risk factors for the development of propofol infusion syndrome
* Low carbohydrate supply
* Higher cumulative propofol dose
* Traumatic brain injury
* Increased severity of critical illness
* High levels catecholamines
* High levels glucocorticoids
* Young age
* Genetic mitochondrial defects
42
List laboratory findings in propofol infusion syndrome
* Raised CK
* Raised lactate
* High potassium
* High creatinine
* High transaminases
* High triglycerides
43
How do you minmise the risk of development of propofol infusion syndrome
* Multimodal sedation
* Adequate carbohydrate supply
* Monitor markers
* Avoid in patients with mitochondrial disorders
44
How do you manage propofol infusion syndrome
* Stop propofol infusion and start alternate sedating agent
* Administer dextrose infusion
* Manage hyperkalaemia
* Fluid resuscitation for hypotension and raised lactate
* Ventilatory management to compensate for metabolic acidosis
45
Define ICU-acquired weakness
New episode of clinically detected symmetrical, peripheral weakness in a critically ill patient without any other plausible aetiology
46
What are the three types of ICU-acquired weakness?
* Critical illness polyneuropathy
* Critical illness myopathy
* Critical illness neuromyopathy
47
What are the risk factors for the development of ICU-acquired weakness?
* Multiorgan failure
* Prolonged immobility
* Hyperglycaemia
* Severe SIRS
* Glucocorticoids
* Electrolyte imbalance
* High lactate
* Parenteral nutrition
* Inappropriate vasoactive drug use
* Abnormal calcium concentration
48
What patient characteristics are associated with increased risk of ICU-acquired weakness
* Female
* Increasing age
49
List the features that contribute to the clinical diagnosis of ICU-acquired weakness
* Low muscle strength as assessed by MRC power grading
* Development of weakness occurs after onset of critical illness
* Generalised, symmetrical, flaccid weakness
* Peripheral weakness, spares cranial nerves
* No autonomic involvement
* Other causes excluded
50
What neurophysiological tests can be used to determine the type of ICU-acquired weakness
* Nerve conduction studies
* Electromyographic studues
* Electrophysiological studies comparing nerve stimulated and muscle stimulated action potentials
51
List two aspects of ICU care that may reduced development of ICU-acquired weakness
* Early physiotherapy and mobilisation
* Reduction in ventilator dependent days to facilitate weaning
* Optimisation of nutrition
* Close management of blood glucose
* Early cessation of neuromuscular blockade during ventilation
52
What are the differences between dialysis and filtration?
53
Define the term ventilator associated pneumonia
Nosocomial lung infection occuring more than 48 hours after starting invasive ventilation
54
List clinical and investigational fiindings that may indicate presence of VAP
Clinical
* Purulent secretions
* Increasing ventilatory requirements
* Pyrexia
Investigational
* Raised WCC
* Infiltrates on CXR
* Positive sputum cultures
55
What factors increase the risk of VAP development
* Prolonged ventilation
* Immunosuppression
* Positive pressure ventilation
* Pre-existing lung disease
* Nasal intubation
* Nasogastric tube
* Severe burns
* Supine positioning
* Low GCS/excessive sedation
* Enteral feeding
* Perioperative
56
What elements of endotracheal tube design help to reduce the risk of VAP development
* Subglottic suction port
* Tapered cuff of thin polyurethane to avoid channelling
* Antimicrobial coating to discourage biofilm
57
Which aspects of ventilator cicuit management may help to reduce the risk of VAP development
* Avoidance of routine ventilator circuit changes
* Minimise circuit disconnections e.g. closed circuit suctioning
* Hand hygeine during necessary interruptions to circuit
58
What are the elements of a ventilator care bundle?
* Patient positioned 30-45degrees head up to avoid passive reflux
* Cuff pressure checking 20-30cmH20
* Daily sedation hold
* Gastric ukcer prophylaxis
* Oral hygeine with chlorhexidine and tooth brushing
* Subglottic aspiration
59
What is a care bundle?
Group of evidence based interventions that relate to a particular aspect of patient care
60
List common causes of acute pancreatitis in the UK
Gallstones
Alcohol
Idiopathic
Post-surgical/post ERCP
Obstructive neoplasm e.g. head of pancreas
Sclerosing cholangitis
CMV
Idiopathic
61
Give the subtypes of acute pancreatitis
Interstitial oedematous pancreatitis
Necrotising pancreatitis
62
Give the diagnostic criteria for acute pancreatitis
Acute persistent severe epigastric pain
Raised serum lipase or amylase
Characteristic radiological findings e.g. fluid around pancreas on CT
63
How is acute pancreatitis classified by severity?
Mild: no organ failure, no complications
Moderate: organ failure that resolves within 48hrs and/or complications
Severe: organ failure beyond 48 hours
64
List local complications of acute pancreatitis
* Peripancreatic fluid collection
* Necrotic collection
* Walled-off necrosis
* Pancreatic pseudocyst
* Portal vein thrombosis
* Pancreatic fistulae
* Abdominal compartment syndrome
* Paralytic ileus
65
Give targets for fluid resuscitation in the initial phase of acute pancreatitis
* Normalisation of lactate
* Urine output > 0.5ml/kg/hr
| Fluid resuscitation: most important aspect of medical management
66
List two approaches to reduce the risk of pulmonary complications of acute pancreatitis
* Avoid excessive intravenous fluids
* Early effective analgesia
67
List the long term sequelae of acute pancreatitis
* Chronic pancreatitis
* Exocrine insufficiency
* Endocrine insufficiency
* Pseudocyst formation
* Gastric outlet obstruction
68
When should enteral nutrition be commenced for a patient with acute pancreatitis admitted to ICU?
Within 48-72hrs
69
Why is enteral nutrition preferred to parenteral nutrition in a patient with acute pancreatitis admitted to ICU?
* Maintains gut integrity
* Reduced infection risk
* Reduced morbidity/mortality
70
What are the essential preconditions that must be met prior to testing an adult for neurological death
1. Evidence of irreversible structural brain damage of known aetiology
2. Patient must have GCS 3 and be on mechanical ventilation with apnoea
3. Haemodynamic instability, medications, hypothermia, abnormal glucose and electrolyte imbalance must be ruled out as causes of the condition
4. 2 clinicians with adequate experience are available to perform brainstem death testing
71
State the values that should be seen on ABG in a previously well patient prior to commencing apnoea testing
* pCO2 ≥ 6kPa
* pH < 7.4 or H+> 40nmol/L
72
State the value that should be seen on arterial blood gas analysis at the end of apnoea testing (alongside allowing a period of 5 minutes to elapse) that would indicate completion of the test
pCO2 rise >0.5kPa
73
-State how and which nerves are tested in the following:
* Pupillary response
* Vestibuloocular reflex testing
* Response to pain
Pupillary response: direct and consensual response to light
* sensory: optic
* motor: occulomotor
Vestibulo-ocular reflex: visualise tympanic membrane, head flexed 30deg, slow injection 50mls ice-cold water over 1 minute checking for eye movement
* sensory: vestibulocochlear
* motor: occulomotor, trochlear, abducens
Response to pain: supraorbital pressure
* sensory: trigeminal
* motor: facial
74
What is the method for vestibulo-ocular reflex testing
* Ensure visualisation of tympanic membranes
* Flex head at 30 degrees
* Check for eye movement during or after slow injection of 50ml or more ice-cold water over one minute into each ear
75
List biochemical changes of diabetes insipidus
* Increased serum osmolality, reduced urine osmolality
* Hypernatraemia
* Hypokalaemia
76
Give the drugs initiated after confirmation of neurological death with their indications
Methylprednisolone - to attenuate systemic inflammation of neurological death and reduce extravascular lung water index
Vasopressin - if vasopressor required, facilitates cessation of noradrenaline and treats diabetes insipidus
Insulin infusion to maintain blood glucose 4-10mmol/L
Dobutamine for inotropic support and organ perfusion
Desmopressin for diabetes insipidus
Thyroxine for hypothyroidism after hypothalamic ischaemia
LMWH to minimise risk of VTE
77
How can you optimise donor lung condition for the purposes of transplantation
* Lung recruitment manouevres after apnoeic testing
* Lung protective ventilation (VT 4-8ml/kg, PEEP 5-10cmH2O
* Chest physio, suctioning
* Head up positioning
* Bronchoscopy and bronchial lavage
78
Give lung related causes of ARDS
* Pneumonia
* Drowning
* PE
* Aspiration
* Inhalational injury
* Pulmonary contusion
79
Give non-lung related causes of ARDS
* Pancreatitis
* Blood transfusion
* Systemic sepsis
* Trauma
* Burns
80
What is the clinical criteria for diagnosis of ARDS
* Onset within one week of clinical insult
* Bilateral opacities on radiology
* Respiratory failure not fully explained by cardiac failure or fluid overload
* Hypoxaemia with PaO2/FiO2≤300mmHg with PEEP 5cmH2O or more
81
What three clinical indices are used to quantify oxygenation in ARDS and what is the equation used to link them?
* Mean airway pressure
* FiO2
* Arterial PaO2
* Oxygenation index = mean airway pressure x FiO2 x 100/PaO2
82
State the appropriate tidal volume in ml/kg for ventilation of a patient with ARDS
<6ml/kg
83
List ventilatory measures that can be taken to improve oxygenation or prevent further deterioration in a patient with ARDS requiring invasive ventilation
* Prone positioning
* Paralysis to facilitate ventilation
* Open lung ventilation strategy (e.g. peak airway pressure < 30cmH2O, PEEP 15cmH2O)
* Recruitment maneouvres
* Protocolised weaning from ventilator
* Ventilator care bundles
84
List non-ventilatory measures that can be taken to improve oxygenation or prevent further deterioration in ARDS
* Conservative fluid management
* ECMO
* Low dose corticosteroid treatment
85
How does pancreatitis cause ARDS?
Production of inflammatory mediators which disrupt the alveocapillary membrane
86
List clinical features of delerium
* Inattention
* Agitation
* Disturbance in cognition
* Acute onset
* Fluctuating in nature
* Occurs as a physiological consequence of another medical condition or drug effect
87
Which tools can be used to diagnose delerium in the ICU setting
* Confusion Assessment Method-ICU
* Intensive Care Delerium Screening Checklist
88
Pre-existing risk factors that may predispose a patient to the development of delerium
* Advanced age
* Previous cognitive impairment e.g. dementia
* Reduced mobility
* Sensory impairments
* Cardiac disease
* Hypertension
* Increased ASA grade
* Alcohol use
89
Intraoperative interventions that reduce the risk of post-operative delerium
* Avoid overly deep anaesthesia (use of pEEG)
* Regional anaesthetic, avoid long acting systemic opiates
* Avoid benzodiazepines and gabapentinoids
* Use dexmetomidine
90
List environmental issues that should be optiised to reduce the risk of developing delerium
* Early mobilisation
* Orientation to time using clocks and windows
* Orientation to place reminding patient where they are
* Correct sensory disturbances e.g. give glasses and hearing aid
* Maintain normal sleep-wake cycle, avoid waking overnight for observations and medications
* Optimise nutrition
91
Physiological or metabolic derangements that can be triggers for delerium
* Electrolyte disturbance
* Derranged blood glucose
* Hypercapnoea
* Hypoxia
* Hypotension
* Pain
* Infection
92
When is pharmacological management indicated for delerium
If patient at risk of harm to self or others
93
Give the signs of life threatening asthma
* Silent chest
* Cyanosis
* Poor respiratory effort
* Hypotension
* Exhaustion
* Depressed consciousness
94
What investigation findings would you see in life-threatening asthma
* Peak flow < 33% predicted
* PO2 < 8kPa or sats <92%
* PCO2 in normal range or raised
95
List drugs used in the management of life-threatening acute asthma
* Nebulised (2.5-5mg) and intravenous (250mcg) salbutamol
* Oral prednsiolone (40mg) or intravenous hydrocortisone (200mg)
* Nebulised ipratropium bromide (500mcg)
* Intravenous magnesium sulphate (2g)
* Nebulised or intravenous adrenaline (10-100mcg)
* Intravenous aminophylline (5mg/kg)
96
Give reasons for hypotension after induction of anaesthesia for a patient with life threatening asthma
* Induction medications attenuate heightened sympathetic drive generated by asthma attack
* Tension pneumothorax
* Significant increase in intrathoracic pressure during PPV with reduction in venous return
* Hypovolaemia due to reduced oral intake and evaporative losses
97
How does life-threatening asthma adversely affect respiratory mechanics?
* Airway narrowing so increased resistance to airflow
* Gas trapping due to hyperventilation
* Increased lung volumes flatten the diaphragm so less efficient ventilation
98
Give the pathophysiological changes in the lungs from asthma
* Mucosal oedema
* Infiltration of inflammatory cells
* Smooth muscle bronchial constriction and hypertrophy
* Excess mucous production
99
Give factors that may cause an asthmatic patient to develop bronchospasm during GA
* Airway manipulation
* Histamine release from medications e.g NMBD, antibiotics, opiates
* Aspiration
* Inadequate depth of anaesthesia
* Use of desflurane
* Pre-operative non compliance with medication
* Anaphylactic/anaphylacticoid reactions
99
List aspects of a suitable ventilatory strategy for life-threatening acute asthma
* Prolonged expiratory time e.g. I:E ratio 1:4
* Low respiratory rate 12-14 bpm
* Minimise PEEP
* Tidal volume 6mg/kg
* Accept low-normal oxygen saturations and low-normal pH with high-normal pCO2
100
Define status epilepticus
* Seizure activity lasting more than 5 minutes or recurrent seizures with failure to regain full consciousness lasting more than 5 minutes
101
Give options for immediate management of convulsive status epilepticus for a patient who does not have an individualised emergency management plan
* 10mg buccal midazolam
* 10mg rectal diazepam
* 4mg IV lorazepam
102
Give three posible underlying causes of convulsive status epilepticus which would require additional pharmacological management in the acute phase
* Eclampsia
* Alcohol withdrawal
* Hypoglycaemia
103
Give three drugs used as second line management in convulsive status epilepticus that is unresponsive to first line agents
* Levetiracetam (40mg/kg, max 3g)
* Phenytoin (20mg/kg max 2g)
* Sodium valproate
104
Give pharmacological approaches used as third line management for status epilepticus
* Phenobarbital 20mg/kg
* GA e.g. propofol 1-2mg/kg induction then infusion titrated to effect e.g. 100-300mg/hr
105
Give neurological complications of convulsive status epilepticus
* Cerebral hypoxia
* Cerebral oedema
* Cerebral haemorrhage
* Excitotoxic CNS injury
106
Give the mechanism of action of phenytoin
Blocks voltage gated sodium channels to reduce AP propagation
107
Give two causes of hypotension from IV phenytoin
* Arrhythmia or bradycardia due to effect on cardiac sodium channels
* Propylene glycol solvent has a negative inotropic effect
108
List the features of phenytoin toxicity
* Nystagmus
* Diplopia
* Slurred speech
* Ataxia
* Confusion
* Hyperglycaemia
109
How does APRV differ to conventional ventilatory modes
| Airway pressure release ventilation
* Prolonged periods of high airway pressure maintained to facilitate recruitment of lung units and maximise oxygenation
* Short periods of low pressure to facilitate carbon dioxide clearance without allowing time for derecruitment, minimising lung injury associated with repetitive opening and closing of lung units
110
Give the appropriate initial settings for commencing APRV
Phigh
Thigh
Plow
Tlow
Phigh: patient's current plateau pressure, ideally < 30cmH2O
Thigh: 3-8s
Plow: 0cmH20
Tlow: 0.3-0.8s (expiratory flow should be terminated before it falls to 75% of peak expiratory flow to prevent derecruitment)
111
What are the benefits of spontaneous ventilation in APRV
* Preferential opening of dependent lung units
* Promotion of venous return, improved haemodynamics
* Prevents respiratory muscle atrophy
* Reduced need for sedation
* Reduced need for paralysis, possible reduced risk of ICU acquired weakness
112
List mechanisms by which haemodynamic compromise may occur with APRV
* High intrathoracic pressures, decreased right sided venous return, reduced left sided filling, reduction in cardiac output
* High mean airway pressure, increased pulmonary vascular resistance
113
List cardiovascular advantages associated with APRV
* Improved oxygenation, improved oxygen delivery to myocardium
* High intrathoracic pressure, reduced cardiac transmural pressure and maximised ejection fraction
114
State the optimum duration of prone positioning in a ventilated patient with ARDS
16 or more hours per 24 hour period
115
Give two absolute contraindications to proning
* Spinal instability
* Open chest post cardiac surgery
* < 24hrs post cardiac surgery
* Veno-arterial ECMO
116
Give relative contraindications to proning
* Polytrauma
* Facial fractures
* Raised intraoccular pressure
* Tracheostomy within preceeding 24hr
117
Which safety issues should you consider before proning
* Use of LocSSip or checklist
* Adequate personell
* Equipment for reintubation
* Resuscitation drugs available in case of haemodynamic instability
* Pre-oxygenation with 100% oxygen
* Secure tube with ties
* Lines dressed
* Adequate sedation and paralysis
* Eyes lubricated and taped
* NG feed stopped, tube aspirated
118
Describe how proning imrpoves oxygenation in patients with ARDS
* Increased size of functional residual capacity
* Reduced amount of lung compressed by mediastinum
* Improved V/Q matching because lung ventilation and perfusion is more homogenous in prone position
* Recruitment of collapsed dorsal lung units
* Improved drainage of secretions from dorsal lung airways to central airways, improving ventilation to diseased lung
119
Give the referral criteria for ECMO
* Reversible severe respiratory failure e.g. PaO2 < 10kPa for 6 or more hours
* Severe hypercapnic acidosis pH ≤ 7.2
* Lung injury score ≥ 3
* Unsuccessful trial of prone position and optimal ventilation
120
Apart from proning, give ventilatory strategies for ARDS
* Open lung ventilation (pPeak < 30, PEEP 15)
* Protective lung ventilation (VT 6ml/kg)
* Recruitment manoeuvres
* Neuromuscular blocking agents
* Ventilator care bundles
* Protocolised weaning from ventilator
121
Give three care bundles that are used in ICU
* CVC care
* Sepsis
* Trachestomy
* Head injury
* Organ donor
122
Give three causative organisms for VAP in UK
Early:
* Strep pneumoniae
* Haem influenzae
* Staph aureus
Late
* Pseudomonas
* Acinetobacter
* Enterobacter
* MRSA
* VRE
| Late: VAP ME
123
What are the pathogenic factors in the development of VAP
* Biofilm on ETT
* Microaspirations
124
Benefits of care bundles in ICU
* Direct benefit to patient
* Shorter ICU stay
* Reduced financial cost
* Improved resource utilization
125
Features of clinical pulmonary infection score
* Pyrexia
* Leucocytosis
* Tracheal secretions
* Sputum culture positive for pathogen
* Radiographical evidence
* P/F ratio less than or equal to 240 mmHg or ARDS
126
Define sepsis
Life threatening response to infection which results in end organ dysfunction
127
Why does organ dysfunction occur in sepsis?
* Direct damage from toxins, free radicals and inflammatory response
* Vasodilatation and caipllary leaking result in intravascular hypovolaemia
* Capillary blood flow in end organs is reduced leading to mitochondrial dysfunction and tissue hypoxia
128
How are pharmacokinetics affected by sepsis?
* Ileus and opiates delay gastric emptying so delay absorption
* Mucosal oedema and NG suctioning reduce absorption
* Increased Vd for hydrophillic drugs due to tissue oedema, reduced plasma proteins for protein bound drugs, acidic environment so less activity of basic drugs
* Impaired hepatic metabolism due to impaired blood flow or CYP350 dysfunction
* Reduced renal perfusion can reduce elimination of renally excreted drugs
129
Describe how the phamacokinetics of a propofol infusion are affected by sepsis
* Reduced plasma binding so increased proportion of unbound drugs and enhanced cardiovascular effect
* Slower redistribution to peripheral compartments (adipose and muscle) due to centralisation of blood flow
* Reduced cardiac output so delayed response to changes in infusion rate
130
Give the mechanisms by which there is a reduced response to vasopressors over time in patients with sepsis
* Tachyphylaxis due to downregulation of catecholamine receptors
* Continued vasodilation due to nitric oxide, prostaglandin, free radicals
* ATP sensitive potassium channels activated by prolonged acidaemia leads to hyperpolarisation of cardiac tissue and vasodilation
131
Give contraindications to organ donation
* HIV/Hep B/C
* Untreated systemic sepsis
* Malignancy
* Previous transplant patient on immunosuppression
* Patient refusal
132
Give the haemodynamic response following brainstem herniation through foramen magnum
* Loss of spinal cord sympathetic activity so reduced vasomotor tone
* Vasodilation leads to reduced cardiac output
* Reduced aortic diastolic pressure due to reduced preload and afterload
* Reduced myocardial perfusion due to reduced aortic diastolic pressure
133
Indications for tracheostomy
* Upper airway obstruction
* Pulmonary toiletting
* Long term ventilation e.g. neuromuscular disease
* To facilitate slower ventilatory wean
* Airway protection
134
Contraindications to percutaneous trachestomy on ICU
* Coagulopathy
* Respiratory failure with significant ventilator dependence
* Infection local to site
* Difficult anatomy e.g. short neck, aberrant vessels, thyroid pathology
| CRID
