Drugs used in an emergency Flashcards
What is the definition of hypotension for healthy patients otherwise undergoing an uncomplicated anaesthetic?
85mmHg
Hypotension, Rash and bronchospasm??
Suspect anaphylaxis
How is the definition of hypotension different for patients with significant CVS disease?
Significant hypotension may be present at a higher systolic BP
What is the most common side effects of IV and general anaesthetic agents?
Hypotension
Give an example of a directly acting and an indirectly acting sympathomimmetic
Direct: phenylephrine
Indirect: Ephedrine
Which anticholinergic drug can be used for simple hypotension?
Atropine and glycopyrrolate
When would an anticholinergic considered for the treatment of hypotension?
When it is associated with pronounced bradycardia
Discuss the presentation and preparation of ephidrine
1 ml glass ampoule with 30mg Ephidrine
Preparation: 9ml saline plus 1 ml ephidrine in 10 ml syrinage = 3mg/ml
What is the dose of ephidrine and at what dose do the effects become less pronounced
3-6 mg (1ml) bolus doses are titrated to effect
Effects become less pronounced beyond the total dose of 30mg
What is the mode of action of ephidrine
Ephidrine causes release of NA from SNS nerve terminals, which then stimulates adrenoreceptors non-specifically
TACHYPHYLAXIS is seen as a result of depletion of noradrenalin stores
Ephidrine also has a weak direct effect on adrenoreceptors
What are the effects of ephidrine
Non-specific activation of alpha and beta receptors cause increase CO and increase SVR –> increase in BP
How long do the CVS effects last
a few minutes (Google says 1 hour)
When is ephidrine used?
Modest hypotension with normal or slow heart rate
What is the presentation and preparation of phenylephrine?
10mg/ml –> add to 100 ml of 0.9% NaCl –> 100ug/ml
What is the dose of phenylephrine
50 - 100 ug titrated to effect
What is the mode of action of phenylephrine
Acts directly on alpha receptors –> no effect on beta receptors
What are the effects of phenylephrine?
alpha 1 stimulation –> vasconstriction and increased SVR
What are the side effects of phenylephrine?
Reflex bradycardia due to increased SVR and no beta receptor stimulation
What is phenylephrine used for
Severe hypotension with normal or FAST heart rate
What is the presentation and preparation of mataraminol
10mg/ml. Dilute to 20 ml syringe with NaCl 0.9%. 0.5 mg/ml
What is the dose of metaraminol
0.5 mg bolus doses titrated to effect
What is the mode of action and effects ofmetaraminol
Same as phenylephrine with minimal effects on beta-adrenoreceptors
What is the use of metaraminol
Same as phenylephrine: hypotension and normal or fast heart rate
What are the most common causes of intra-operative bradycardia (rate<50)?
Vagal stimulation
Combination of well beta blocked patient and a general anaesthetic
Severe hypoxia
How does vagal stimulation occur
Stretching or pulling of any part of the airway or gut that is innervated by the vagus nerve.
Stimulation of
1. Inferior surface of the epigottis
2. Pneumoperitoneum (esp. higher pressures)
3. Manipulation of bowel
Apart from vagus stimulation, stimulation of what other nerves may cause bradycardia
Traction on structures innervated by the sacral parasympathetic outflow (GUS)
What is the treatment of intraoperative bradycardia
- Remove the stimulus
- Treat pharmacologically –> allowing the stimulus to be repeated if required.
If bradycardia is recurrent an delaying surgery, pharmacological treatment may be needed.
What is the fundamental similarity and difference between atropine and glycopyrrolate?
Both drugs contain Nitrogen atoms
Glycopyrrolate N atom carries permanent + charge –> unable to cross the BBB
Atropine N atom does not carry a + charge –> crosses BBB
Therefore, glycopyrrolate is free of unwanted central effects of atropine, such as sedation
Compare the presentation of Atropine and Glycopyrrolate
Atropine: 0.5 mg/ml or 0.6 mg/ml
Glycopyrrolate: 0.2 mg/ml
Compare the dose of Atropine and Glycopyrrolate for the treatment of bradycardia
Atropine: 0.5 mg doses every 3 to 5 minutes titrated to effect (max 3mg)
Glycopyrrolate: 0.2 mg doses every 3 to 5 minutes titrated to effect(max 0.6 mg)
Compare the Mechanism of action of Atropine and Glycopyrrolate
Same
Block M receptors in the heart –> increasing heart rate
When does acute bronchospasm most commonly occur
Shortly after induction of anaesthesia
Under which circumstances is bronchospasm more likely
- Asthmatics
- Atopy
- Smokers
- Drugs that release histamine (Morphine/Atracurium)
How is bronchospasm differentiated from anaphylaxis?
Anaphylaxis is usually associated with severe hypotension and cutaneous signs
List 3 non-pharmacological interventions for bronchospasm
- Optimise I:E ration (1:4) - avoid air trapping
- Consider pressure controlled ventilation
- Optimize patient position: minimize pneumoperitoneum
List 5 immediate pharmacological interventions
Oxygen Inhaled anaesthetics Salbutamol Aminophylline Adrenaline
Since isoflurane is an irritant, can it be administered to a patient with bronchospasm?
Isoflurane is an upper airway irritant
Isoflurane relaxes bronchial smooth muscle
It will be beneficial to administer isoflurane to a patient with bronchospasm
Why should FiO2 be increased in bronchospasm
Acute bronchospasm may lead to reduced alveolar ventilation –> Increase FiO2 to ensure sufficient
What is the most effective way to administer salbutamol to a patient in theatre
Intravenously
Describe the presentation, preparation and dose of salbutamol and aminophylline
Salbutamol
- 500ug/ml –> dilute to 500ug/10ml (50ug/ml)
- Theatre dose 250 ug over 20 minutes
- ICU dose: 250 ug over 50 minutes
Aminophylline
- 250mg/10mls (further dilution not required)
- 250 mg over 20 minutes
Compare the mechanism of action of Salbutamol to aminophylline
Salbutamol
Beta 2 agonist (at high doses it acts on beta 1)
Aminophylline
Non-specific phosphodiesterase inhibitor –> increasing cAMP within cells –> smooth muscle relaxation
Compare the side effects of salbutamol with aminophylline
Salbutamol
- Tachycardia
- dysrhythmia
- exacerbate hypokalaemia
Aminophylline
- contra-indicated in patient’s already on theophylline –> if plasma concentrations become toxic: seizures/dysrhythmias
What is the treatment of acute SEVERE bronchospasm –> almost no air movement possible after intubation
0.5ml of 1:10 000 Adrenalin titrated to affect
50ug
Describe how the dose of adrenalin affects the action at the different adrenoreceptors
At low dose (e.g. 50 ug increments in bronchospasm) - adrenalin is mainly active at beta receptors. Potent Beta 2 stimulation is achieved with low dose adrenalin
At high dose (1mg in cardiac arrest) - alpha adrenoreceptor affects predominate to increase coronary perfusion by increasing SVR
What common equipment related issue might mimmic acute SEVERE bronchospasm
Blockages at any point in the breathing circuit
What is the incidence of anaphylaxis due to anaesthetic drugs
1 in 10 000 - 20 000
55 suspected anaphylactic reactions per year in the UK
Which group of drugs are the most commonly involved in causing anaphylaxis?
Neuromuscular blocking Agents –> especially the Benzylisoquinolinium drugs (Atracurium, Cisatracurium, Mivacurium)
What is the triad for the most common features of anyphylaxis
CVS collapse
Bronchospasm
Widespread erythema
Describe the initial management of a patient with anaphylaxis
- Stop suspected agent
- Call for HELP
- Airway, O2 100%, patient flat and elevate legs
- Adrenalin IV: 50ug -100ug increments
Adrenalin IM: 0.5mg - 1 mg repeated as required every 10 minutes
Can undiluted adrenalin be given IV for anaphylaxis
No - it is not possible to give the chosen dose accurately
Describe the secondary management of anaphylaxis
Isotonic balanced salt solution IV administration
Chlorphenamine - 10mg IV
Hydrocortisone - 100mg IV
What does adrenalin 1: 1000 mean
1g in 1000 mls
1000mg in 1000ml
1mg/ml
What does adrenalin 1: 10 000 mean
1g in 10 000 ml
0.1mg/ml
100ug/ml
Describe the mendelian inheritance of malignant hyperthermia
Autosomal dominant
Which agents can trigger malignant hyperthermia
Volatile anaesthetic agents and succinylcholine
In patient’s with genetic predisposition for malignant hyperthermia, does this condition manifest on first exposure to a precipitating agent
Not necessarily manifested on first exposure
What are and what are not common clinical features of malignant hyperthermia?
Common clinical features
- Increasing ETCO2
- Tachycardia
- Increased O2 consumption
Hyperthermia is NOT an early sign
What is the significance of masseter muscle spasm and generalied muscle rigidity after succinylcholine?
These clinical findings indicate a high risk of malignant hyperthermia but RARELY progress to full blown MH and are usually transient
Describe the treatment for malignant hyperthermia
- Call for help
- Remove trigger
- FiO2 100%
- Dantrolene 2mg/kg up to 10mg/kg
- Active cooling
- ICU postop as recurrence occurs
What is the modern mortality for malignant hyperthermia and why has it decreased from 70 - 80 % which it was in the past
5 - 10 %
- Early detection via capnography
- Early use of dantrolene sodium
Describe the morbidity rate of malignant hyperthermia
Overall: 34.8%
Renal dysfunction 97% Coma - 9 % Cardiac dysfunction - 9% Pulmonary oedema - 9% DIC - 9% Hepatic dysfunction - 4.5%
What dose and why is adrenalin given during cardiac arrest
1mg every 3 - 5 minutes
High dose adrenalin –> predominant alpha-adrenergic effect –> increasing cardiac and cerebral perfusion by increasing peripheral SVR
When should amiodarone be given during cardiac arrest?
For refractory: VF/pulseless VT. Expert consensus suggests that if VT/VF persists after 3 shocks: Amiodarone 300mg bolus
One additional bolus of 150mg can be given after 3 - 5 minutes if VF/VT still present
When can lignocaine be given during cardiac arrest and what is the dose?
For refractory VF/VT persistent after 3 shocks when amiodarone is not available and NOT when amiodarone has already been given
Dose: 1,5 mg/kg followed by 0.5mg/kg (max 3mg/kg)
When should MgSO4 be given during cardiac arrest?
What is the dose?
- For refractory VF where hypomagnesaemia is suspected
- potassium-losing diuretics
- alcoholic/malnourished - Torsades de Pointes
- Digitalis toxicity
Dose: 2g in 10ml slow bolus
When should Sodium Bicarbonate be administered in cardiac arrest and what is the dose?
- Severe hyperkalaemia
- Overdose
- TCA
- Aspirin
- Cocaine - Severe Metabolic acidosis present (must be intubated)
Dose: 1ml/kg of 8.5% solution
When is Calcium chloride indicated in cardiac arrest and what is the dose?
- Severe hyperkalaemia
- BB or CCB overdose
- Hypocalcaemia
- Magnesium overdose (Rx pre-eclampsia)
Dose: 10ml of 10% slow IV bolus
Which drugs in cardiac arrest cannot be administered through the same IV line
Calcium containing solutions and sodium bicarbonate –> PRECIPITATION
What is a quaternary Nitrogen and give an example of a drug whose pharmacodynamics are altered by the presence of this
A quaternary nitrogen atom is permanently charged –> Glycopyrrolate has a quaternary N atom which means that it cannot cross the BBB. Therefore the unwanted central effects of the agent are avoid unlike atropine (which does not contain a quaternary nitrogen atom and crosses the BBB)
