Critical care Flashcards
(194 cards)
1
Q
What is the Acute Physiology and Chronic Health Evaluation (APACHE) II score calculated from
A
Degree of disturbance from normal of 12 acute physiological variables
Age of patient
Chronic health status
2
Q
What does the APACHE II score correlate with
A
Mortality
3
Q
Critical care resuscitation drill - how should patients be treated in order of priority
A
Airway (with cervical spine control in a trauma patient)
Breathing
Circulation
Disability (simplified neurological assessment with AVPU)
Exposure
DEFG (don’t ever forget glucose)
4
Q
Critical care systematic drill - how should each organ-system be assessed in a logical order
A
Respiratory
Cardiovascular
Gastrointestinal
Renal
Neurological
Haematology
Metabolic
Skin
Microbiology
Family/social
5
Q
What are the four steps in seeing a critically-ill patient
A
Measure
Institute treatment
Reassess
Stabilize or increase intensity of treatment
6
Q
What should you do if shock persists despite fluid therapy?
A
Vasoactive agents:
Inotropes (adrenaline, dobutamine, dopexamine) - increase cardiac contractility and cardiac output
Vasopressors (noradrenaline) - increase blood pressure by vasoconstriction in excessive vasodilatation
7
Q
Name two drugs that are not safe to give peripherally
A
Noradrenaline
Concentrated potassium
8
Q
How can temporary pacing be achieved
A
External pads
Inserting a trans-venous internal pacing wire
9
Q
What may be used to support the failing left ventricle following a myocardial infarction or after cardiac surgery
A
Intra-aortic balloon pump
10
Q
How is cardiac output monitoring achieved
A
Oesophageal Doppler and pulse contour analysis with the LiDCo and PICCO
11
Q
List three indications for mechanical ventilation
A
Hypoxaemic or hypercapnic respiratory failure
Septic shock and cardiogenic shock
Severe head injury
12
Q
What is bi-level positive airway pressure used particularly for
A
Type 2 respiratory failure secondary to an exacerbation of COPD
13
Q
Describe the actions of bi-level positive airway pressure machine
A
When the patient triggers a breath, the machine cycles from low pressure to high pressure.
Causes gas to flow into the lungs, providing an extra boost of inflation.
Useful to reduce elevated carbon dioxide
14
Q
Patients in liver failure lose the ability to perform what functions
A
Synthetic function - production of albumin and coagulation proteins
Detoxification of ammonia
Blood sugar control
Metabolism of lactate
15
Q
What is ventilation divided into
A
Intermittent positive pressure ventilation
Non-invasive positive pressure ventilation
* Continuous positive airway pressure
* Bi-level positive airway pressure
16
Q
List the hepatic support using the systemic approach
A
Respiratory - toxins build up and high ammonia level lead to encephalopathy with reduced conscious level. May require intubation and ventilation to protect the airway.
Cardiovascular - Massive fluid shifts, bleeding and vasodilatation lead to intravascular volume loss and reduced cardiac output. Albumin may be required if severe ascites or paracentesis.
Gastrointestinal - Lactulose is given to reduce reabsorption of toxins and bile by encouraging rapid bowel transit time.
Renal - Hepato-renal syndrome.
Neurological - Hepatic encephalopathy
Metabolic - Blood glucose
Haematology - Abnormal coagulation. Fresh frozen plasma and cryoprecipitate
Social - Prophylaxis for alcohol withdrawal
17
Q
In what scenarios would IPPV be suitable?
A
Severe respiratory failure
Management of secretions
Severe head injury
18
Q
In what scenarios would CPAP be suitable
A
Hypoxia
Left ventricular failure
Alveolar recruitment
19
Q
List the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) Classification of intervention
A
Immediate - Immediate life, limb or organ saving intervention. Decision to operate is within minutes. Resuscitation is likely to be ongoing
Urgent - Intervention for acute onset or clinical deterioration of potentially life threatening conditions, for those conditions that may threaten the survival of limb or organ, for fixation of many fractures and relief of pain. Decision to operate is usually within hours
Expedited - Patient requiring early treatment where the conditions is not an immediate threat to life, limb, or organ survival
Elective - Intervention planned or booked in advanced of routine admission to hospital timing to suit patient hospital and staff
20
Q
List the 30-day mortality versus degree of operative urgency
A
Immediate - 13%
Urgent - 4%
High risk - <1%
21
Q
List the Royal College of Surgeons surgical procedure risk categories
A
High risk (cardiac risk >5%)
* Open aortic
* Major vascular
* Peripheral vascular
* Urgent body cavity
Intermediate risk (cardiac risk 1-5%)
* Elective abdominal
* Carotid
* Endovascular aneurysm
* Head and neck
* Major neurosurgery
* Arthroplasty
* Elective pulmonary
* Major urology
Low risk (cardiac risk <1%)
* Breast
* Dental
* Thyroid
* Ophthalmic
* Gynaecological
* Reconstructive
* Minor orthopaedic
* Minor urology
22
Q
List the complications that can occur after cardiac surgery and due to cardiopulmonary bypass
A
Hypovolaemia
Myocardial oedema
Cardiac tamponade
Cardiac arrest
23
Q
List the possible complications after open abdominal aortic aneurysm repair
A
coagulopathy
arrhythmias
major adverse cardiac events
AKI, acidosis
24
Q
List the indications for emergency laparotomy ICU admission
A
Prolonged surgery >5 hours
Patient needs cardiovascular system support: vasopressors, respiratory support
Persistent acidosis
Significant comorbidities
Faecal soiling of the peritoneum
25
List the American Society of Anaesthesiologists physical status classification
Grade 1
A healthy non-smoking patient with no systemic disease
Grade 2
Mild to moderate systemic disease, including obesity, smoking, social alcohol use, well controlled diabetes, mild lung disease
Grade 3
Severe systemic disease imposing functional limitation on the patient. Examples: morbid obesity, end stage renal disease, poorly controlled hypertension, history of MI or CVA more than 3 months previously
Grade 4
Severe systemic disease which is a constant threat to life. Examples: recent MI or CVA, unstable angina, severe valve disease
Grade 5
Moribund patient who is not expected to survive without the operation. Examples: ruptured abdominal aortic aneurysm. Intracranial bleed with mass effect
Grade 6
A brainstem-dead patient whose organs are being removed for donor purposes
26
List the comorbidities associated with significant perioperative 30-day mortalities
Cirrhosis
Congestive cardiac failure
Arrhythmia
Cerebrovascular accident
Insulin dependent diabetes
Ischaemic heart disease
Cancer
Respiratory disease
27
List the factors increasing the risk of postoperative pulmonary complications
COPD
Current smoker
Advancing age
Comorbidities
OSA
Pulmonary hypertension
Surgery over 2 hours duration
Abdominal and thoracic surgery
28
What are patients with anaemia more likely to require after an operation?
Non-invasive or mechanical ventilation
Vasopressors / inotropic support
Red cell transfusion
29
What are the peri-operative complications associated with poorly controlled diabetes
hypo- and hyperglycaemia
increased infections both systemic and surgical site
30
Describe the postoperative global oxygen consumption changes
Typically rising to 5 mlO2/kg/min after urgent body cavity surgery.
Represents a 150% increase in oxygen requirement compared with baseline resting oxygen consumption of 3 mlO2/kg/min
31
What does VO2 equal to
Cardiac output multiplied by arterial-mixed venous oxygen difference.
32
What is anaerobic threshold
The VO2 at the point at which muscle cells will begin generating ATP anaerobically.
At the AT, the slope of increasing VCO2 curve exceeds that of the VO2 curve, and the respiratory exchange ratio will increase above 1
33
Describe the changes in oxygen consumption after a major intra-cavity surgery
Increase in oxygen consumption from 110 ml/min/m2 at rest to 170 ml/min/m2 postoperatively.
Requirement to increase VO2 by 50%.
34
What is an AT required to safely undertake significant surgery
at least 11 ml/kg/min
35
What does peak VO2 correlates best with
postoperative cardiopulmonary complication rate after oesophagectomy
36
When is non-invasive monitoring of blood pressure appropriate
Relatively stable patients where temporary/slight drops in perfusion pressure are relatively inconsequential
Patients not requiring inotropes
37
When is non-invasive monitoring of blood pressure not appropriate
Arrhythmias
Inappropriate cuff size
Shivering and movement
External pressure on cuff
Very low blood pressure
38
List the complications for non-invasive monitoring of blood pressure
Tissue damage or ischaemia:
* Skin irritation
* Bruising
* Nerve damage
Venous pooling and congestion
May be uncomfortable for the awake patient
39
List the indications for invasive blood pressure monitoring
haemodynamic instability
regular blood gas analysis: ventilated, septic, acid base disturbance, renal failure and pulmonary disease
vasoactive drugs
undergoing/recovering from major surgery (cardiac, vascular, neuro)
40
List the complications for invasive blood pressure monitoring
Bleeding
Infection
Haematoma
Air embolism
Thrombosis
Distal limb ischaemia/infarction
Inadvertent intra-arterial drug injection
Damage to local structure, eg. nerves
41
List the indications for inserting a central line
Monitoring of central venous pressure
Administration of medications: noradrenaline, dopamine, high-concentration potassium, amiodarone, magnesium
Lack of peripheral access
Total parenteral nutrition (more safely PICC)
42
List the indications for CVP measurement
Confirmation of IV placement of line
To assist in fluid management
Cardiac failure
43
List the complications for
Carotid puncture
Pneumothorax
Vascular rupture
Bleeding
Haematoma
Infection (late)
44
Give the equation quantifying oxygen delivery
oxygen delivery (ml/min) = cardiac output * blood oxygen content
45
Give the equation quantifying systemic vascular resistance
Systemic vascular resistance = (Mean arterial pressure - Central venous pressure) / Cardiac output
46
What can cardiac output be used to assess?
Fluid responsiveness
Cardiac function
Peripheral circulation
47
What type of patients typically undergo cardiac output monitoring?
On high-dose vasopressors and inotropes
Evidence of inadequate oxygen delivery: rising lactate, oliguria, poor peripheral perfusion
Poor cardiac function
High-risk surgical patients during perioperative management
48
List the methods to measure cardiac output
Non-invasive:
* Echocardiography
* Transthoracic/transoesphageal Doppler
* Impedance cardiography
Invasive:
* Pulse contour analysis: PICCO (Pulse index Continuous Cardiac Output) / LiDCO
* Pulmonary artery catheter
49
In what patients may capnography show sloping plateau
Obstructive airways disease
(different alveoli are emptying at different rates)
50
Give the normal mean ICP of a supine patient
8-10 mmHg
51
What ICP would compromise microcirculation and require medical review.
15-20 mmHg
52
What happens when ICP is at 20-25 mmHg
Impede venous drainage and risk cerebral oedema and potentially coning.
Urgent medical treatment / neurosurgical review is required.
53
Perfusion cannot be maintained at which ICP
Within 50 mmHg of Mean Arterial Pressure
54
Give the normal intra-abdominal pressure
0-5 mmHg
55
What may happen with an intra-abdominal pressure of >15 mmHg?
Management?
Restrict perfusion to the abdominal organs
Can be restored by increasing the systemic blood pressure
56
What may be an intra-abdominal pressure of >25 mmHg be associated with?
Management?
Organ dysfunction:
Oliguria (renal ischemia)
Increased peak airway pressures and reduced tidal volumes result in hypoxemia and hypercarbia (restriction of the diaphragm)
Hypotension and decreased cardiac output - decreased venous return
Bowel ischaemia
Abdominal compartment syndrome requires laparostomy decompression.
57
What does the dichrotic notch on an arterial line trace represent
Closure of the aortic valve
58
List the indications for capnography
Assess adequacy of ventilation
Detect oesophageal intubation
Indicate leaks or disconnection of the breathing system or ventilator
Assist in the diagnosis of circulatory problems
59
List the risk factors for VTE in the critical care setting
Mechanical ventilation and sedation
Immobilisation/paralyisis
Heart failure, stroke, recent MI
Respiratory failure
Obesity (BMI>30)
Severe sepsis
Trauma - SCI, pelvic/lower limb fracture
Previous VTE/known thrombophilia
Recent surgery
Malignant disease and its treatment
Pregnancy, puerperium, oestrogen therapy
Increasing age (>60)
Indwelling central venous catheter
Nephrotic syndrome, IBD, haemolytic disorders, polycythaemia
60
Which malignant diseases have the highest risks of VTE
Pancreas
Stomach
Lung
Prostate
Brain
61
List the contraindications to pharmacological prophylaxis
Hereditary bleeding disorders eg. haemophilia
Platelets <40x10^9/L
Recent intracranial/retinal bleed
Recent surgery to CNS, including brain, spinal cord and retina
Active or recent GI bleeding
Severe liver disease
Heparin/platelet factor 4 antibodies (HIT). Use alternative non-heparin anticoagulants
62
List the measures that can be used to prevent VTE
Anticoagulant drugs
* LMWH
* Unfractionated heparin
* Vitamin K antagonists: warfarin
* Pentasaccharides: fondaparinux
* Direct anti-thrombin / anti-Xa inhibitors
Mechanical methods
* Graduated compression stockings
* Intermittent pneumatic compression
* IVC filters
63
When should surgery fit in around LMWH
Invasive procedures with a high bleeding risk should generally be delayed for 12 hours after an injection
Minimum 2 hours before the next dose after the procedure.
64
How should LMWH dose be titrated if the creatinine clearance is reduced
Between 10-30 ml/min, reduce the dose to half
<10 ml/min, use UFH
65
When is UFH suitable? Give its route.
Suitable for patients where a short half-life is desirable or renal failure
5000 units given subcutaneously 2/3 times a day
66
When is mechanical methods of VTE prophylaxis contraindicated
peripheral vascular disease
skin trauma
sepsis of the leg
gross oedema
67
When could an IVC filter be useful?
Head and pelvic trauma when anticoagulants are contraindicated
68
When are GCS and IPC most useful?
As an adjunct to pharmacological prophylaxis in patients with very high thrombotic risk
As an alternative to anticoagulant drugs, where there is a high bleeding risk
69
List the steps for VTE prophylaxis in critical care
1. Risk assess for VTE and bleeding risk on admission to ICU and at regular intervals as the patient's condition changes
2. Prescribe LMWH or fondaparinux unless contraindicated
3. In renal failure: reduce dose of LMWH or use UFH subcutaneously. IV UFH may be used where short duration of action is required
4. Where bleeding risk is high, use GCS or IPC and switch to pharmacological prophylaxis if bleeding risk is reduced or eliminated
70
Give the pathophysiology in stress ulceration
1. Critical illness
2. Increased catecholamines, decreased cardiac output, pro inflammatory cytokine release
3. Increased vasoconstriction and splanchnic hypoperfusion
4. Reduced HCO3- secretion, reduced mucosal blood flow, decreased GI motility, acid back-diffusion
5. Acute stress ulcer
71
List the risk factors for stress ulceration with clinically significant bleeding
Strong independent risk factors:
Respiratory failure requiring mechanical ventilation for 48 h or more
Coagulopathy
Hypotension
Sepsis
Liver, renal failure
Glucocorticoids
Organ transplant
Anticoagulant therapy
72
List the risk factors for stress-related mucosal diseas
major surgery
major trauma
severe burns (Curling's ulcers)
head trauma or coma (Cushing's ulcers)
multi-organ failure
73
Lists the approaches to prevent stress ulcers
1. Optimise haemodynamics to prevent gut ischaemia
* oxygenation, ventilation, and tissue perfusion (fluid resuscitation + vasoactive drugs)
2. Acid suppression therapy
* Histamine2 receptor blocker: Ranitidine
* PPI: omeprazole
* Antacids
3. Enteral nutrition
4. Mucosal protection treatment: sucralfate
74
Give two complications of ranitidine use
ventilator associated pneumonia
tolerance with prolonged use
75
Give two complications of sulcralfate use
decrease the absorption of other concomitantly administered oral drugs
unsuitable in gastric ileus
76
Give the management in clinically significant stress ulcer bleeding
1. Resuscitation: IV access, fluids, blood transfusion (keep Hb≥10 g/dl)
2. In stable patients - endoscopy: sclerotherapy, injection treatment, electrocoagulation, haemostatic clipping
3. Referral to a surgeon - haemodynamically unstable: on-table endoscopy ± emergency laparotomy
After endoscopic treatment: IV omeprazole 80mg bolus followed by 8mg/h for 72h (reduces risk of recurrent bleeding)
77
How does Stress Ulcer Present?
Asymptomatic: ulceration typically in the fundus and body of the stomach
Clinically overt bleeding: 'coffee grounds' NG aspirate, haematemesis, melaena
Clinically significant bleeding: overt bleeding + hypotension / a drop in haemoglobin >2 g/dl
78
List the adverse effects of malnutrition on cardiac muscle, connective tissue, GI system, and skeletal muscle
Cardiac muscle
* Myocardial contractility is depressed in severe cases of malnutrition.
* Free fatty acids (dominant source of energy during starvation) are arrhythmogenic.
Connective tissue
* Wounds heal poorly
* Decreased collagen content of anastomotic scar tissue and overall scar strength.
GI system
* Gut permeability is increased, which may increase the risk of translocation.
Skeletal muscle
* Skeletal muscle bulk and power are reduced, fatiguability is increased.
* Respiratory muscles - vital capacity and maximal voluntary minute ventilation are reduced.
79
Give the effect of nutritional support on protein metabolism in critical care settings
Nutritional support does not change the actual rate of protein catabolism but does reduce net catabolism by stimulating protein synthesis.
80
List the risks of overfeeding in critically-ill patients
Higher levels of feeding increase O2 consumption and CO2 production - may worsen respiratory failure
Severely-ill patients are often insulin-resistant - high levels of feeding can produce relative hyperglycemia
81
List the NICE guidelines for energy requirements
Total energy, including energy from protein: 25-35kcal/kg/day
Protein: 0.8-1.5g (0.13-0.24g nitrogen)/kg/day
Fluid per day: 30-35ml/kg
82
List the benefits of enteral feeding
Cheaper
Safer
Most physiological, maintaining mucosal perfusion and limiting bacterial overgrowth
Reduces risk of stress ulceration
83
List the complications of enteral feeding
NG and NJ tube insertion and post-insertion problems: epistaxis, skin erosion around the naris, misplacement /feeding into the lungs
Increased risk of vomiting/reflux and subsequent aspiration, advise to elevate head of bed to at least 30o
GI intolerance: aspiration, nausea, diarrhoea
Metabolic disturbances
84
Intolerance of enteral feeding is common in critically-ill patients due to what?
Impaired GI motility leading to high gastric residual volumes, 200-250ml
85
List the complications of intolerance of enteral feeding
abdominal distension, diarrhoea, constipation and vomiting
ventilator-associated pneumonia, infection, bacterial translocation
86
List the factors that increase the risk of impaired GI motility
Trauma, burns, sepsis
Opioids
Catecholamines, particularly dopamines
Alpha2 adrenoceptor agonists, anticholinergics, proton-pump inhibitors
Positive fluid balance including gut oedema
Delay in initiating enteral feeding
87
List the most commonly used prokinetic drugs in critical care patients
Erythromycin (motilin agonist) - more effective than metoclopramide
Metoclopramide (dopaminergic D2 receptor antagonist)
88
What can block the actions of erythromycin
Ondansetron
5-HT3 antagonist
Partially blocked by atropine
89
List the complications of parenteral feeding
General central venous catheter-related complications
Thrombophlebitis of smaller veins
Metabolic and biochemical disturbances
90
When is Parenteral Nutrition necessary
Intestinal failure/gut dysmotility (most common indication)
Enteric anastomosis
Ischaemic bowel
Enteric fistula
Imminent bowel resection, endoscopy
Bowel obstruction
High NG losses on admission
Severe exacerbation of inflammatory bowel disease
91
What can high carbohydrate burden versus fat lead to?
Higher CO2 production and levels.
Detrimental in respiratory insufficiency
In these cases, it is better to supply energy as 50% fat and 50% carbohydrate.
92
How to convert grams of nitrogen to grams of protein
1g Nitrogen = Protein (g) x 6.25
93
List the advantages of providing lipids as energy
source of essential fatty acids
concentrated energy source
low osmolality compared to glucose
Critically-ill patients often use fat better than carbohydrate as an energy source.
94
List the situations where there is a high risk of developing refeeding problems
One of more of:
BMI <16kg/m2
Unintentional weight loss >15% within the last 3-6 months
Little/no nutritional intake for >10 days
Low levels of K+, phosphate or Mg2+ prior to feeding
Two or more of:
BMI <18kg/m2
Unintentional weight loss >10% within the last 3-6 months
Little/ no nutritional intake for >5 days
A history of alcohol abuse or drugs including insulin, chemotherapy, antacids or diuretics
95
List the additional factors when initiating nutrition in patients at risk of refeeding syndrome
Nutritional support should be commenced at a maximum of 50% requirements for 2 days
Never initiate nutrients and fluids without electrolytes and micronutrients, vitamins and trace elements
Generous prescribing of K+, Mg2+ and phosphate, and then close monitoring after feeding has been initiated
High-dose thiamine and B-group vitamins to prevent Wernike-Korsakoff
Generous multivitamin and trace element supplementation
96
What increased monitoring would you routinely want to have in place when starting a patient on TPN?
Blood glucose
Fluid balance
Urea and creatinine
Electrolytes
97
How does insulin alter the use of free fatty acids
Insulin increases glucose use.
During a stress response, there is a relative insulin resistance, and free fatty acids are used instead, increasing the risk of cardiac dysrhythmias.
98
Why should prokinetic therapy not be continued for more than 5 days in most cases
Both erythromycin and metoclopramide demonstrate tachyphylaxis.
99
List the typical daily requirements for sodium and potassium
Sodium: 0.8-2 mmol/kg per day
Potassium: 1 mmol/kg per day
100
List the indications for sedation in critical care
Analgesia
Anxiety
Dyspnoea
Mechanical ventilation
To facilitate nursing care
To decrease oxygen consumption
Delirium
101
List the advantages of opioids
CNS
* Potent analgesia
* Mild to moderate anxiolysis
Resp - Best for attenuating dyspnoea and cough reflex
CVS - Little effect on euvolaemic patients
102
List the disadvantages of opioids
CNS
* No amnestic properties
* Hallucinations
Resp
* Dose-dependent, centrally mediated, respiratory depression (decreased respiratory rate and preserved tidal volumes)
* CO2-response curve shifted to the right
* Ventilatory response to hypoxia obliterated
CVS
* Significant hypotension in hypovolaemic patients and elevated sympathetic tone
* Mild hypotension in euvolaemic patients (sympatholysis, vagal-mediated bradycardia, histamine release)
* Synergistic effects with benzodiazepines
GI
* Nausea/Vomiting
* Gastric hypo-motility
103
Give the mechanism of action of benzodiazepines
Bind to the α-subunit of GABA-A receptors
Increases the frequency of Cl- channel opening
Influx of Cl- results in hyperpolarization and neuronal inhibition.
104
List the advantages of benzodiazepines
CNS
* Dose-dependent sedation throughout whole spectrum, including hypnosis
* Potent anterograde amnestics (lorazepam longest duration)
* Potent anxiolytics
* Potent anticonvulsants
CVS - Minimal effects in euvolaemic patients
105
List the disadvantages of benzodiazepines
CNS - Paradoxical state of agitation especially in the elderly
Resp
* Dose-dependent, centrally-mediated respiratory depression, less than, but synergistic with opioids (decrease in tidal volume and an increase in respiratory rate)
* Even low doses abolish the ventilatory response to hypoxia
CVS - Hypotension in the hypovolaemic patient
106
Give the onset / offset properties of midazolam
Rapid onset: 0.5-5 minutes
Short duration of action: 2 hours after bolus dosing.
Accumulates significantly in lipid-rich tissues and after infusions.
Once stopped, the stored drug maintains plasma levels and prolongs clinical effect from many hours to days.
107
List the drug interactions with benzodiazepines
Azole antifungals, erythromycin/clarithromycin, diltiazem, verapamil, rifampicin
- Cause prolonged effects due to cytochrome P450 3A4 inhibition
108
List the drug interactions with morphine
All other opioids and sedative agents (CNS/resp depression, profound sedation, hypotension)
Anticholinergic drugs: antihistamines, phenothiazines, TCAs (severe constipation, paralytic ileus)
109
Name the opioid where hypotension is unusual as it causes minimal histamine release
Fentanyl
Naturally occurring opioids, e.g. morphine and codeine, are more likely to cause a non-allergic release of histamine from mast cells, which can result in venules dilatation, mooth muscles contraction, stimulation of mucous gland secretion
110
How is Remifentanil metabolised
Metabolized by tissue esterases
Therefore rapid offset after termination of infusions
111
List the advantages of propofol
CNS
* Excellent dose-dependent sedation throughout whole spectrum (including hypnosis)
* Potent anxiolytic
* Potent amnestic
* Anticonvulsant
* Reduces cerebral metabolic rate for oxygen (CMRO2)
112
List the disadvantages of propofol
CNS - No analgesic properties
Resp
* Apnoea, especially after loading dose
* Respiratory depression (reduced tidal volumes + increased respiratory rate)
* CO2 response curve shifted to the right
CVS - Significant hypotension (especially in hypovolaemia) due to preload reduction from dilation of venous capacitance vessels and myocardial depression
Metabolic
* Hypertrigyceridaemia (stop infusion if levels >500 mg/dl)
* High caloric load due to lipid content
* Iatronic transmission of bacteria and fungi as the suspension supports growth
* Lactic acidosis and poor outcome in paediatric patients (not licensed)
* Syndrome of dysrhythmias, heart failure, metabolic acidosis, hyperkalaemia and rhabdomyolysis reported in adults on high doses (<80 mcg/kg/min)
113
Give the onset / offset properties of propofol
Rapid onset 1-5 minutes
Rapid offset, 2-8 minutes, following redistribution to peripheral tissues.
After infusion, clinical effect is prolonged due to release from lipid-rich tissues, but it rarely exceeds 60 minutes.
Clinical effect is terminated solely by redistribution (no hepatic/renal).
114
Give the drug interactions of propofol
Suxamethonium can cause a severe bradycardia by an unknown mechanism
115
Give the onset / offset properties of morphine
Relatively slow onset: 5-10 minutes due to low lipid solubility
Dose-dependent duration of action: 4 hours after 5-10 mg bolus.
116
Give the onset / offset properties of fentanyl
Rapid onset 1 minute (high lipid-solubility)
Short duration of action: 0.5-1 hour after bolus dosing (redistribution into tissues)
117
Give the drug interactions of fentanyl
MAOIs - increased risk of serotonin syndrome
Amiodarone, clarithromycin, erythromycin, isoniazid - prolonged effects due to inhibition of hepatic metabolism
All other opioids and sedative agents (CNS/resp depression, profound sedation, hypotension)
Anticholinergic drugs: antihistamines, phenothiazines, TCAs (severe constipation, paralytic ileus)
118
What is the most cardiovascularly stable opioid
Fentanyl
119
Describe the CVS stability of remifentanil
Like fentanyl, remifentanil is a cardiovascularly stable opioid as it does not cause histamine release.
However, in high dose it can cause bradycardia and hypotension.
120
Give the onset / offset properties of remifentanil
Rapid onset, 1 minute
Ultra-short duration of action, <10 minutes, even after long infusions.
121
Give the drug interactions of remifentanyl
MAOIs - increased risk of serotonin syndrome
All other opioids and sedative agents (CNS/resp depression, profound sedation, hypotension)
Anticholinergic drugs: antihistamines, phenothiazines, TCAs (severe constipation, paralytic ileus)
122
Give the onset / offset properties of alefentanil
Onset is rapid, 1 minute, after bolus injection due to its mainly unionized state in blood.
Dose-dependent duration of action is short, 30-60 minutes, due to its small volume of distribution and rapid elimination.
123
Give the onset / offset properties of lorazepam
Slightly slower onset, 5 minutes, than midazolam (lower lipid solubility and smaller volume of distribution)
Long, dose-dependent, duration of action, 6-10 hours, post bolus in healthy volunteers.
Alone, it is unlikely to keep a critically-ill patient comfortable on mechanical ventilation for 6 hours.
124
Give the onset / offset properties of diazepam
Fast onset after an IV bolus, 1-3 minutes, with a short duration of action, 30-60 minutes.
However, rarely given by infusion due to long terminal elimination.
Intermittent bolus dosing is usual. Once the peripheral compartment is saturated, recovery can take several days.
125
What is the first-line drug of choice for control of delirium
Haloperidol
126
List the advantages of haloperidol
CNS - Causes a dissociative mental and psychological indifference to the environment in previously agitated or psychotic patients
GI - Potent anti-emetic
127
List the disadvantages of haloperidol
CNS
* Cataleptic immobility is possible
* Extra-pyramidal symptoms (occasional), but less so with IV than PO
* No effect on seizure activity and can reduce seizure threshold
Resp - Mild respiratory depression when administered with opioids
Metabolic - Rarely causes neuroleptic malignant syndrome
128
Give the CVS stability profile of haloperidol
QTc prolongation - severity associated with increasing doses and IV route
Ventricular arrhythmias
Mild hypotension
129
Give the onset / offset properties of haloperidol
Fast onset, 2-5 minutes, after a 1-10 mg IV bolus.
Half-life is dose-dependent at 2 hours.
130
List the drug interactions with haloperidol
Cisapride (prolonged QT syndrome)
Hepatic enzyme inhibitors - prolong effects
Quinolones, antidepressants, antiarrhythmics - prolong the QT syndrome
All other opioids and sedative agents may increase the risk of CNS or respiratory depression, profound sedation and hypotension
131
Give the mechanisms of action by Alpha-2 agonists
Stimulates pre-synaptic alpha-2 receptors in the lateral reticular nucleus reducing central sympathetic outflow
In the spinal cord augments endogenous opioid release and modulate descending noradrenergic nociceptive pathways.
132
List the advantages of Alpha-2 agonists
CNS
* Produce profound analgesia alone and act synergistically with opioids
* Good anxiolytics and particularly useful when substance withdrawal is the cause
Resp - No significant respiratory depression, therefore safe in spontaneously breathing patients
CVS - Reduces sympathetic tone resulting in a lower resting heart rate
133
List the disadvantages of Alpha-2 agonists
CVS
* Produce an initial rise in arterial blood pressure followed by a prolonged depression
* Increased sensitivity to exogenous catecholamines may occur
* Rebound hypertensive crisis have been reported
GI tract - Dry mouth and reduced gastric motility
134
List two alpha-2 agonists
Clonidine
Dexmedetomidine
(used as an adjunct to wean patients off other sedative agents.)
135
List the drug interactions with Clonidine
MAOIs may cause a hypertensive crisis
Beta-blockers may cause hypertensive crisis due to unopposed alpha-adrenergic stimulation
All other opioids and sedative agents may increase the risk of CNS or respiratory depression, profound sedation and hypotension
136
Give the onset / offset properties of clonidine
Onset and offset are moderately slow.
137
Give the onset / offset properties of dexmedetomidine
Rapid distribution phase, distribution half-life 6 minutes
Terminal elimination half-life: 2 hours.
138
Which anaesthetic sedative is associated with alpha-1 blockade
Haloperidol - causing mild, hypotension, reflex tachycardia and prolonged QT interval.
139
Which anaesthetic sedative has Minimal effects on cognition
Dexmedetomidine - major potential advantage for this agent.
140
Which anaesthetic sedative is associated with rhabdomyolysis
Propofol - as part of the idiosyncratic propofol infusion syndrome.
141
What is respiratory depression in opioid characterised by
low respiratory rate and high tidal volumes
142
List the sedative agents that have active metabolites that contribute to clinical effects
Midazolalm
* 1-α hydroxymidazolam is conjugated with glucoronic acid before excreted in the urine. 5% of midazolam is metabolized to oxazepam.
Haloperidol
Fentanyl (norfentanyl, inactivated by hydroxylation)
143
What do pharmacokinetics consist of
Absorption
Protein binding
Metabolism
Excretion
144
How may pharmacokinetics be altered in ICU patients
GI tract
* Gastric stasis (opioids, underlying conditions, nociception)
* Diarrhoea
IM/SC
* Tissue injury
* Reduced CO
* Vasoconstrictors
145
What does the proportion of free drug available for interaction with receptors depend on
availability of plasma protein binding sites
146
What is morphine metabolised to and excreted in urine
morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G)
M3G is neurotoxic and M6G is sedative
147
How does suxamethonium work
Binds and activates nicotinic acetylcholine receptors causing persistent depolarisation and subsequent paralysis.
148
List the non-depolarising muscle relaxants
Aminosteroids - Rocuronium
Benzylquinoliniums - Atracurium
149
What is Hofmann degradation?
A process independent of renal and hepatic function
Results in loss of the positive charges of Atracurium by molecular fragmentation to laudanosine and a monoquaternary acrylate.
150
Which muscle relaxant is preferred for continuous infusions
Atracurium
(metabolism does not rely on renal/hepatic function, eliminated via Hofmann degradation (45%) and non-specific ester hydrolysis)
151
How do electrolyte and pH disturbances affect muscle relaxant action
Hypokalaemia prolongs non-depolarising agent duration of action + inhibit neostigmine's ability to reverse the block
HyperMg2+ prolongs duration of neuromuscular blockade (Mg2+ inhibits Ca2+ channels in the presynaptic terminal and inhibits post-junctional potentials)
HyperCa2+ decreases the duration of neuromuscular blockade (Ca2+ is responsible for acetylcholine release)
Acidosis (metabolic or respiratory) may augment NMBA effect
152
Which muscle relaxant can be used for rapid sequence induction
Rocuronium (rapid onset + intermediate duration of action)
At a dose of 1.2 mg/kg, intubating conditions are reached at 1 minute
153
How can rocuronium be rapidly reversed
Sugammadex
154
Which muscle relaxant is preferred for continuous infusions
Atracurium (metabolism does not rely on renal/hepatic function)
155
How does Sugammadex work?
It inactivates rocuronium by chelating the molecule and forming a stable complex with a very low rate of dissociation.
The drug does not produce any metabolites and is mostly excreted through urine in the unchanged form within 24 hours.
156
Give the drug interaction of sugammadex
Decrease the effectiveness of the oral contraceptive pill for up to 7 days
157
What is the recommended dose for sugammadex to reverse neuromuscular blockade 3 minutes after administration of a single dose of 1.2 mg/kg of Rocuronium.
16 mg/kg
158
List the Main Indications For the Use of NMBAs
Endotracheal intubation
ARDS
Raised ICP
Raised IAP
Hypothermia
Status asthmaticus
159
Lung-protective ventilation strategies have been shown to prevent ventilator-induced injury in patients with acute respiratory distress syndrome (ARDS) and reduce mortality. How might NMBAs help facilitate lung-protective ventilation strategies?
Prevention of spontaneous respiratory effort
Reduction in oxygen consumption
Eliminating resting muscle tone
160
Define abdominal compartment syndrome
Raised intra-abdominal pressure (IAP) exceeds 20 mmHg + signs of organ dysfunction
161
List the features in abdominal compartment syndrome
Increased ICP, decreased CCP
Increased CVP, falsely elevated Wedge pressure
Rising IAP pushes diaphragm further into chest - increased lung dysfunction
Worsening vena caval compression, further decreased cardiac output
Increased bowel oedema and ischaemia
Decreased perfusion, oliguria, difficulty mobilising fluids
Increased acidosis
162
Why is Atracurium avoided in asthmatics
Associated histamine release which may exacerbate bronchospasm
163
What is the preferred neuromuscular blocker in patients with hepatic insufficiency or renal dysfunction
Atracurium
164
What may happen when using Suxamethonium in patients with renal failure
Life-threatening hyperkalaemia
165
Describe the effects of hypo and hyper K+ on neuromuscular blockers
Hypokalaemia potentiates non-depolarising agents + antagonises depolarising agents.
Hyperkalaemia potentiates depolarising agents + antagonises non-depolarising agents.
166
List the complications of NMBAs in critical care
ICU acquired weakness
Immobility
* VTE
* Corneal abrasions (abolished eyelid and blink reflex)
Anaphylaxis
167
What physiological changes may prolong NMBA duration of action
Hypothermia
Hypokalaemia (non-depolarising agnet)
Hypermagnesaemia
Metabolic acidosis
168
How does hypothermia prolong NMBA duration action
Altered sensitivity of the neuromuscular junction
Reduced acetylcholine mobilisation
Decreased muscle contractility
Reduced renal and hepatic excretion
Inhibited Hofmann degradation
169
How to calculate Total Body Water
0.6 * body mass
170
Give the proportion of extracellular fluid (ECF) and intracellular fluid (ICF) compartments
ECF = 1/3 * TBW (0.2 * body mass)
ICF = 2/3 * TBW (0.4 * body mass)
171
How to calculate the amount of intravascular and interstitial fluid
Intravascular fluid = 1/4 ECF (0.05 * body mass)
Interstitial fluid = 3/4 ECF (0.15 * body mass)
172
What does NICE recommend that maintenance fluids should provide
Water - 25-30 ml/kg/day for adults
Sodium - 1 mmol/kg/day
Potassium - 1 mmol/kg/day
Glucose - 50-100 g/day
173
What is the rationale for using fluid boluses in shock states
Improve organ perfusion by increasing stroke volume (SV) or cardiac output (CO)
174
List the physical signs that can be used to assess organ perfusion
Hypotension
Tachycardia
Cool peripheries
Prolonged capillary refill time
Confusion/depressed conscious level
Oliguria
Tachypnoea
175
List the Cohen and Woods classification of lactate acidosis
Type A - Inadequate tissue oxygen delivery
* Hypotension
* Hypoxia
* Anaemia
* High intensity exercise
Type B - Adequate tissue oxygen delivery but impaired utilisation/clearance
1. Underlying diseases
* Diffuse malignancy
* Liver/renal failure
2. Medication/drug induced
* Andrenaline
* Β-agonists
* Cyanide
* Biguanides
* Anti-retrovirals
3. Inborn errors of metabolism
* Pyruvate carboxylase deficiency
* Pyruvate dehydrogenase inactivity
176
What may be required if fluid is either ineffective or causing harm in a patient with hypotension or hypoperfusion
vasopressors / inotropes
177
Why is balanced crystalloids (Hartmann's / Plasma-Lyte) for resuscitation favoured in the majority of patient
Lower incidence of 'major adverse kidney events'
* death
* new requirement for renal replacement therapy
* persistent renal dysfunction
178
Give the step wise approach in resuscitation fluids
1. Assess baseline organ perfusion/cardiac output. Consider fluid challenge if evidence of impairment.
2. Ideally, predict fluid-responsiveness to avoid a fluid challenge.
3. Give 250-500 ml balanced crystalloid over 5-15 mins and reassess immediately after. Expect around 50% of patients to not respond.
4. Give a further bolus only if positive response in at least one of HR, BP, CRT, cardiac output or conscious level and only if perfusion remains impaired. Stop if adverse effects of fluid start to outweigh the benefit.
179
Fluid loss from where are particularly high in potassium
diarrhoea and colostomy
180
Give fluid replacement approaches for upper GI losses and colonic losses
balanced crystalloid for upper GI losses
balanced crystalloid + potassium-containing fluid (0.18% NaCl/4% glucose/0.15% KCl) for colonic losses
181
How to calculate CaO2 (oxygen content of arterial blood (20 ml/dL blood))
CaO2 = (1.34 x [Hb] x SaO2) + (0.0225 x PaO2)
CaO2 = oxygen content of arterial blood (20 ml/dL blood)
1.34 = volume of O2 bound to 1g of saturated haemoglobin (ml/g)
[Hb] = concentration of haemoglobin (g/dL)
SaO2 = percentage of haemoglobin fully saturated with O2
0.0225 = solubility coefficient of O2 in plasma (ml/dL/kPa)
PaO2 = partial pressure of O2 dissolved in arterial blood (kPa)
182
Under normal circumstances, haemoglobin is nearly fully saturated at which partial pressure
13.4 kPa
183
List the physiological effects of hypoxia to the brain
Acute hypoxia: cerebral vasodilation + increased cerebral blood flow
PaO2<6kPa (~SaO2 80%) = confusion, decreased mental functioning
PaO2<4kPa (~SaO2 56%) = loss of consciousness
184
List the physiological effects of hypoxia to the cardiovascular system
Coronary vasodilatation
Decreased systemic vascular resistance predominantly through splanchnic vasodilatation
Tachycardia and increased cardiac output
185
List the physiological effects of hypoxia to the lungs
Hypoxic pulmonary vasoconstriction
186
List the physiological effects of hypoxia to the renal system
Activation of the renin-angiotensin system
Increased erythropoietin production
187
The British Thoracic Society recommend oxygen delivered by a reservoir mask at which flow rate in all critically-ill patients as a minimum
15L/min
188
What can be adjusted to target peripheral oxygen saturation
Flow rate
FiO2
Preferable to maximize the flow rate first in an attempt to keep the FiO2 ≤0.6; however, an increase in FiO2 may be necessary to achieve adequate oxygenation.
189
List the indications for high-flow oxygen therapy
Respiratory Failure Type 1 - hypoxaemia
Pre-oxygenation during anaesthesia induction
Apnoea ventilation during ENT cases
Post-extubation in ICU
Postoperative respiratory support
190
List the conditions for oxygen toxicity
FiO2 1.0 >12 hours at atmospheric pressure.
FiO2 0.8 >24 hours.
FiO2 0.6 >36 hours.
191
List the clinical features of oxygen toxicity
Retrosternal discomfort, Carina irritation and coughing. Progresses to severe dyspnoea with paroxysmal coughing.
Nausea, facial twitching and numbness, disturbance of smell and taste. Progress to convulsions and coma.
Progressively impaired gas exchange with decreased lung compliance.
192
Optimal gas exchange occurs when ventilation is matched with perfusion. What is the ratio in healthy individuals
0.95
193
What kind of patients are sensitive to oxygen therapy - prone to toxicity
Bleomycin
Mitomycin C
194
