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ICM Flashcards

1
Q

Define ICU acquired weakness

A

Clinically detectable weakness in a critically ill patient with no other plausible cause

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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
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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
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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)
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5
Q

List investigations that aid the diagnosis of ICU acquired weakness

A
  • Creatine kinase
  • Nerve conduction studies
  • EMG
  • Muscle biopsy
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6
Q

What proportion of patients diagnosed with ICU acquired weakness will die during their hospital admission?

A

45%

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7
Q

What proportion of patients with ICU acquired weakness who survive hospital admission will achieve complete recovery?

A

68%

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8
Q

Indications for neuromuscular block in critically ill patients

A
  • Tracheal intubation
  • ARDS
  • COVID-19
  • Proning
  • Abdominal compartment syndrome
  • Transfers
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9
Q

Why is lean body weight used for roc?

A

Hydrophillic, so remains in central compartment

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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

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11
Q

Give the two components of initial insulin management of a known diabetic adult patient admitted with DKA

A
  1. Start fixed rate insulin infusion at 0/1units/kg/hr
  2. Continue patient’s regular long acting insulin
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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

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13
Q

State the equation for calculation of anion gap

A

(Na+K)-(Cl+Bicarb)

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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
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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%
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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
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17
Q

Give the complications of DKA management

A
  • Hypo/hyperkalaemia with or without cardiac arrhythmia
  • Hypoglycaemia
  • Cerebral oedema
  • AKI
  • VTE
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18
Q

List the respiratory symptoms of pulmonary embolism

A
  • Pleuritic chest pain
  • Breathlessness
  • Haemoptysis
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19
Q

List the signs of pulmonary embolism

A
  • Type 1 respiratory failure/low SpO2/cyanosis
  • Pleural rub
  • Tachypnoea/increased work of breathing
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20
Q

List the neurological features of pulmonary embolism

A
  • Syncope/presyncope
  • Anxiety/apprehension
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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
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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)
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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)
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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
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25
Q

Give two interventional or surgical management options for treatment of high risk PE

A
  • Percutaneous catheter directed therapy
  • Surgical embolectomy
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26
Q

Give risks to a patient with high risk PE if intubation is required as part of management

A
  • 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
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27
Q

State the mechanism of action for therapeutic effect of TCA

A

Inhibits reuptake of serotonin and noradrenaline into presynaptic terminals, so raises their concentration for postsynaptic receptor activation

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28
Q

List three additional receptor actions of TCAs and their clinical effect

A
  • Sodium channel antagonism - cardiac depression
  • Alpha adrenergic antagonism - hypotension
  • Anticholinergic - pupil dilation, tachycardia, hypotension, ileus, irritability, confusion, seizures, coma, urinary retention, pyrexia
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29
Q

What therapeutic interventions an be considered in the management of TCA within 1 hour of ingestion

A
  • Activated charcoal
  • Gastric lavage (airway must be protected by pt or you)
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30
Q

List indications for intubation for patients after TCA overdose

A
  • Reduction in GCS that compromises airway protection
  • Hypoventilation contributing to acidosis
  • Refractory seizures
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31
Q

Treatments that can be used in the management of hypotension and arrhythmia in presence of TCA overdose

A
  • Fluid resuscitation
  • 8.4% sodium bicarbonate
  • Alpha agonist e.g. adrenaline infusion
  • Magnesium sulphate (for dysrhythmia)
  • IV glucagon
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32
Q

Apart from tachycardia, give ECG changes seen in TCA overdose

A
  • QRS prolongation
  • QTc prolongation
  • Nodal or ventricular arrythmia
  • R/S ratio > 0.7 in aVR
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33
Q

Give one drug that should be avoided for management of seizures in TCA overdose and what you would use instead

A

Avoid phenytoin (can lead to phenytoin toxicity with ventricular arrythmias)

Use benzodiazepine

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34
Q

List perioperative risk factors for the development of acute kidney injury

A
  • 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)
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35
Q

List patient risk factors for development of AKI perioperatively

A
  • Increasing age
  • Male
  • CKD
  • Chronic liver disease
  • CCF
  • Hypertension
  • Diabetes
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36
Q

List the indications for renal replacement in ICU

A
  • 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
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37
Q

List the types of RRT available on intensive care

A
  • Intermittent haemodialysis
  • Contineous renal replacement therapy e.g. CVVHF, CVVHD, CVVHDF
  • Peritoneal dialysis (in patients already using this form)
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38
Q

Give possible complications associated with the use of heparin for systemic anticoagulation for maintenance of the RRT circuit

A
  • Heparin-induced thrombocytopenia
  • Increased risk of haemorrhage
  • Heparin resistance (Reduced antithrombin III production in critically ill patients)
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39
Q

Give complications associated with the use of citrate for regional anticoagulation for maintenance RRT circuit

A
  • Alkalosis (citrate converts to bicarbonate)
  • Acidosis (accumulation of citrate)
  • Hypocalcaemia (citrate binds to calcium)
  • Hypomagnesemia (citrate-calcium complex binding and removal in effluent)
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40
Q

What are the clinical features of propofol infusion syndrome?

A
  • Metabolic acidosis
  • ECG changes
  • Rhabdomyolysis
  • AKI
  • Hyperkalaemia
  • Lipidaemia
  • Cardiac failure
  • Pyrexia
  • Elevated liver enzymes/hepatomegaly
  • Elevated lactate
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41
Q

List risk factors for the development of propofol infusion syndrome

A
  • 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
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42
Q

List laboratory findings in propofol infusion syndrome

A
  • Raised CK
  • Raised lactate
  • High potassium
  • High creatinine
  • High transaminases
  • High triglycerides
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43
Q

How do you minmise the risk of development of propofol infusion syndrome

A
  • Multimodal sedation
  • Adequate carbohydrate supply
  • Monitor markers
  • Avoid in patients with mitochondrial disorders
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44
Q

How do you manage propofol infusion syndrome

A
  • 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
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45
Q

Define ICU-acquired weakness

A

New episode of clinically detected symmetrical, peripheral weakness in a critically ill patient without any other plausible aetiology

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46
Q

What are the three types of ICU-acquired weakness?

A
  • Critical illness polyneuropathy
  • Critical illness myopathy
  • Critical illness neuromyopathy
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47
Q

What are the risk factors for the development of ICU-acquired weakness?

A
  • Multiorgan failure
  • Prolonged immobility
  • Hyperglycaemia
  • Severe SIRS
  • Glucocorticoids
  • Electrolyte imbalance
  • High lactate
  • Parenteral nutrition
  • Inappropriate vasoactive drug use
  • Abnormal calcium concentration
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48
Q

What patient characteristics are associated with increased risk of ICU-acquired weakness

A
  • Female
  • Increasing age
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49
Q

List the features that contribute to the clinical diagnosis of ICU-acquired weakness

A
  • 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
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50
Q

What neurophysiological tests can be used to determine the type of ICU-acquired weakness

A
  • Nerve conduction studies
  • Electromyographic studues
  • Electrophysiological studies comparing nerve stimulated and muscle stimulated action potentials
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51
Q

List two aspects of ICU care that may reduced development of ICU-acquired weakness

A
  • 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
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52
Q

What are the differences between dialysis and filtration?

A
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53
Q

Define the term ventilator associated pneumonia

A

Nosocomial lung infection occuring more than 48 hours after starting invasive ventilation

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54
Q

List clinical and investigational fiindings that may indicate presence of VAP

A

Clinical
* Purulent secretions
* Increasing ventilatory requirements
* Pyrexia

Investigational
* Raised WCC
* Infiltrates on CXR
* Positive sputum cultures

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55
Q

What factors increase the risk of VAP development

A
  • 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
Q

What elements of endotracheal tube design help to reduce the risk of VAP development

A
  • Subglottic suction port
  • Tapered cuff of thin polyurethane to avoid channelling
  • Antimicrobial coating to discourage biofilm
57
Q

Which aspects of ventilator cicuit management may help to reduce the risk of VAP development

A
  • Avoidance of routine ventilator circuit changes
  • Minimise circuit disconnections e.g. closed circuit suctioning
  • Hand hygeine during necessary interruptions to circuit
58
Q

What are the elements of a ventilator care bundle?

A
  • 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
Q

What is a care bundle?

A

Group of evidence based interventions that relate to a particular aspect of patient care

60
Q

List common causes of acute pancreatitis in the UK

A

Gallstones
Alcohol
Idiopathic

Post-surgical/post ERCP
Obstructive neoplasm e.g. head of pancreas
Sclerosing cholangitis
CMV
Idiopathic

61
Q

Give the subtypes of acute pancreatitis

A

Interstitial oedematous pancreatitis
Necrotising pancreatitis

62
Q

Give the diagnostic criteria for acute pancreatitis

A

Acute persistent severe epigastric pain
Raised serum lipase or amylase
Characteristic radiological findings e.g. fluid around pancreas on CT

63
Q

How is acute pancreatitis classified by severity?

A

Mild: no organ failure, no complications
Moderate: organ failure that resolves within 48hrs and/or complications
Severe: organ failure beyond 48 hours

64
Q

List local complications of acute pancreatitis

A
  • Peripancreatic fluid collection
  • Necrotic collection
  • Walled-off necrosis
  • Pancreatic pseudocyst
  • Portal vein thrombosis
  • Pancreatic fistulae
  • Abdominal compartment syndrome
  • Paralytic ileus
65
Q

Give targets for fluid resuscitation in the initial phase of acute pancreatitis

A
  • Normalisation of lactate
  • Urine output > 0.5ml/kg/hr

Fluid resuscitation: most important aspect of medical management

66
Q

List two approaches to reduce the risk of pulmonary complications of acute pancreatitis

A
  • Avoid excessive intravenous fluids
  • Early effective analgesia
67
Q

List the long term sequelae of acute pancreatitis

A
  • Chronic pancreatitis
  • Exocrine insufficiency
  • Endocrine insufficiency
  • Pseudocyst formation
  • Gastric outlet obstruction
68
Q

When should enteral nutrition be commenced for a patient with acute pancreatitis admitted to ICU?

A

Within 48-72hrs

69
Q

Why is enteral nutrition preferred to parenteral nutrition in a patient with acute pancreatitis admitted to ICU?

A
  • Maintains gut integrity
  • Reduced infection risk
  • Reduced morbidity/mortality
70
Q

What are the essential preconditions that must be met prior to testing an adult for neurological death

A
  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
Q

State the values that should be seen on ABG in a previously well patient prior to commencing apnoea testing

A
  • pCO2 ≥ 6kPa
  • pH < 7.4 or H+> 40nmol/L
72
Q

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

A

pCO2 rise >0.5kPa

73
Q

-State how and which nerves are tested in the following:
* Pupillary response
* Vestibuloocular reflex testing
* Response to pain

A

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
Q

What is the method for vestibulo-ocular reflex testing

A
  • 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
Q

List biochemical changes of diabetes insipidus

A
  • Increased serum osmolality, reduced urine osmolality
  • Hypernatraemia
  • Hypokalaemia
76
Q

Give the drugs initiated after confirmation of neurological death with their indications

A

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
Q

How can you optimise donor lung condition for the purposes of transplantation

A
  • 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
Q

Give lung related causes of ARDS

A
  • Pneumonia
  • Drowning
  • PE
  • Aspiration
  • Inhalational injury
  • Pulmonary contusion
79
Q

Give non-lung related causes of ARDS

A
  • Pancreatitis
  • Blood transfusion
  • Systemic sepsis
  • Trauma
  • Burns
80
Q

What is the clinical criteria for diagnosis of ARDS

A
  • 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
Q

What three clinical indices are used to quantify oxygenation in ARDS and what is the equation used to link them?

A
  • Mean airway pressure
  • FiO2
  • Arterial PaO2
  • Oxygenation index = mean airway pressure x FiO2 x 100/PaO2
82
Q

State the appropriate tidal volume in ml/kg for ventilation of a patient with ARDS

83
Q

List ventilatory measures that can be taken to improve oxygenation or prevent further deterioration in a patient with ARDS requiring invasive ventilation

A
  • 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
Q

List non-ventilatory measures that can be taken to improve oxygenation or prevent further deterioration in ARDS

A
  • Conservative fluid management
  • ECMO
  • Low dose corticosteroid treatment
85
Q

How does pancreatitis cause ARDS?

A

Production of inflammatory mediators which disrupt the alveocapillary membrane

86
Q

List clinical features of delerium

A
  • Inattention
  • Agitation
  • Disturbance in cognition
  • Acute onset
  • Fluctuating in nature
  • Occurs as a physiological consequence of another medical condition or drug effect
87
Q

Which tools can be used to diagnose delerium in the ICU setting

A
  • Confusion Assessment Method-ICU
  • Intensive Care Delerium Screening Checklist
88
Q

Pre-existing risk factors that may predispose a patient to the development of delerium

A
  • Advanced age
  • Previous cognitive impairment e.g. dementia
  • Reduced mobility
  • Sensory impairments
  • Cardiac disease
  • Hypertension
  • Increased ASA grade
  • Alcohol use
89
Q

Intraoperative interventions that reduce the risk of post-operative delerium

A
  • Avoid overly deep anaesthesia (use of pEEG)
  • Regional anaesthetic, avoid long acting systemic opiates
  • Avoid benzodiazepines and gabapentinoids
  • Use dexmetomidine
90
Q

List environmental issues that should be optiised to reduce the risk of developing delerium

A
  • 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
Q

Physiological or metabolic derangements that can be triggers for delerium

A
  • Electrolyte disturbance
  • Derranged blood glucose
  • Hypercapnoea
  • Hypoxia
  • Hypotension
  • Pain
  • Infection
92
Q

When is pharmacological management indicated for delerium

A

If patient at risk of harm to self or others

93
Q

Give the signs of life threatening asthma

A
  • Silent chest
  • Cyanosis
  • Poor respiratory effort
  • Hypotension
  • Exhaustion
  • Depressed consciousness
94
Q

What investigation findings would you see in life-threatening asthma

A
  • Peak flow < 33% predicted
  • PO2 < 8kPa or sats <92%
  • PCO2 in normal range or raised
95
Q

List drugs used in the management of life-threatening acute asthma

A
  • 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
Q

Give reasons for hypotension after induction of anaesthesia for a patient with life threatening asthma

A
  • 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
Q

How does life-threatening asthma adversely affect respiratory mechanics?

A
  • Airway narrowing so increased resistance to airflow
  • Gas trapping due to hyperventilation
  • Increased lung volumes flatten the diaphragm so less efficient ventilation
98
Q

Give the pathophysiological changes in the lungs from asthma

A
  • Mucosal oedema
  • Infiltration of inflammatory cells
  • Smooth muscle bronchial constriction and hypertrophy
  • Excess mucous production
99
Q

Give factors that may cause an asthmatic patient to develop bronchospasm during GA

A
  • 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
Q

List aspects of a suitable ventilatory strategy for life-threatening acute asthma

A
  • 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
Q

Define status epilepticus

A
  • Seizure activity lasting more than 5 minutes or recurrent seizures with failure to regain full consciousness lasting more than 5 minutes
101
Q

Give options for immediate management of convulsive status epilepticus for a patient who does not have an individualised emergency management plan

A
  • 10mg buccal midazolam
  • 10mg rectal diazepam
  • 4mg IV lorazepam
102
Q

Give three posible underlying causes of convulsive status epilepticus which would require additional pharmacological management in the acute phase

A
  • Eclampsia
  • Alcohol withdrawal
  • Hypoglycaemia
103
Q

Give three drugs used as second line management in convulsive status epilepticus that is unresponsive to first line agents

A
  • Levetiracetam (40mg/kg, max 3g)
  • Phenytoin (20mg/kg max 2g)
  • Sodium valproate
104
Q

Give pharmacological approaches used as third line management for status epilepticus

A
  • Phenobarbital 20mg/kg
  • GA e.g. propofol 1-2mg/kg induction then infusion titrated to effect e.g. 100-300mg/hr
105
Q

Give neurological complications of convulsive status epilepticus

A
  • Cerebral hypoxia
  • Cerebral oedema
  • Cerebral haemorrhage
  • Excitotoxic CNS injury
106
Q

Give the mechanism of action of phenytoin

A

Blocks voltage gated sodium channels to reduce AP propagation

107
Q

Give two causes of hypotension from IV phenytoin

A
  • Arrhythmia or bradycardia due to effect on cardiac sodium channels
  • Propylene glycol solvent has a negative inotropic effect
108
Q

List the features of phenytoin toxicity

A
  • Nystagmus
  • Diplopia
  • Slurred speech
  • Ataxia
  • Confusion
  • Hyperglycaemia
109
Q

How does APRV differ to conventional ventilatory modes

Airway pressure release ventilation

A
  • 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
Q

Give the appropriate initial settings for commencing APRV

Phigh
Thigh
Plow
Tlow

A

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
Q

What are the benefits of spontaneous ventilation in APRV

A
  • 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
Q

List mechanisms by which haemodynamic compromise may occur with APRV

A
  • 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
Q

List cardiovascular advantages associated with APRV

A
  • Improved oxygenation, improved oxygen delivery to myocardium
  • High intrathoracic pressure, reduced cardiac transmural pressure and maximised ejection fraction
114
Q

State the optimum duration of prone positioning in a ventilated patient with ARDS

A

16 or more hours per 24 hour period

115
Q

Give two absolute contraindications to proning

A
  • Spinal instability
  • Open chest post cardiac surgery
  • < 24hrs post cardiac surgery
  • Veno-arterial ECMO
116
Q

Give relative contraindications to proning

A
  • Polytrauma
  • Facial fractures
  • Raised intraoccular pressure
  • Tracheostomy within preceeding 24hr
117
Q

Which safety issues should you consider before proning

A
  • 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
Q

Describe how proning imrpoves oxygenation in patients with ARDS

A
  • 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
Q

Give the referral criteria for ECMO

A
  • 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
Q

Apart from proning, give ventilatory strategies for ARDS

A
  • 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
Q

Give three care bundles that are used in ICU

A
  • CVC care
  • Sepsis
  • Trachestomy
  • Head injury
  • Organ donor
122
Q

Give three causative organisms for VAP in UK

A

Early:
* Strep pneumoniae
* Haem influenzae
* Staph aureus

Late
* Pseudomonas
* Acinetobacter
* Enterobacter
* MRSA
* VRE

Late: VAP ME

123
Q

What are the pathogenic factors in the development of VAP

A
  • Biofilm on ETT
  • Microaspirations
124
Q

Benefits of care bundles in ICU

A
  • Direct benefit to patient
  • Shorter ICU stay
  • Reduced financial cost
  • Improved resource utilization
125
Q

Features of clinical pulmonary infection score

A
  • Pyrexia
  • Leucocytosis
  • Tracheal secretions
  • Sputum culture positive for pathogen
  • Radiographical evidence
  • P/F ratio less than or equal to 240 mmHg or ARDS
126
Q

Define sepsis

A

Life threatening response to infection which results in end organ dysfunction

127
Q

Why does organ dysfunction occur in sepsis?

A
  • 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
Q

How are pharmacokinetics affected by sepsis?

A
  • 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
Q

Describe how the phamacokinetics of a propofol infusion are affected by sepsis

A
  • 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
Q

Give the mechanisms by which there is a reduced response to vasopressors over time in patients with sepsis

A
  • 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
Q

Give contraindications to organ donation

A
  • HIV/Hep B/C
  • Untreated systemic sepsis
  • Malignancy
  • Previous transplant patient on immunosuppression
  • Patient refusal
132
Q

Give the haemodynamic response following brainstem herniation through foramen magnum

A
  • 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
Q

Indications for tracheostomy

A
  • Upper airway obstruction
  • Pulmonary toiletting
  • Long term ventilation e.g. neuromuscular disease
  • To facilitate slower ventilatory wean
  • Airway protection
134
Q

Contraindications to percutaneous trachestomy on ICU

A
  • Coagulopathy
  • Respiratory failure with significant ventilator dependence
  • Infection local to site
  • Difficult anatomy e.g. short neck, aberrant vessels, thyroid pathology

CRID

FRCA CRQs (9 decks)

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