Drug therapy - Implications for the anaesthetist Flashcards
(32 cards)
What is the severity and mortality of chronic digoxin toxicity
Variable severity
Mortality at 1 week 15 - 30%
What are the main features of digoxin toxicity
GIT distress
Hyperkalaemia
Dysrhythmias (Increased automaticity and AV block
What is the antidote for digoxin toxicity
Digoxin specific Fab fragments (digibind)
What is the mechanism of action of digoxin
Direct and indirect effects resulting in
- Increased inotropy (mild)
- Increased automaticity
- Negative dromotropy (Slowing of AV conduction)
- Increased vagal tone
DIRECT:
Inhibition of Na-K ATPase
–> Increased IC Na+ –> increased IC Ca+ (Na/Ca antiport) –> inotropy and increased automaticity
–> decreased IC K= leads to negative dromotropy (slower repolarization of AV node and longer refractory period)
INDIRECT:
Increased vagal tone (vagomimetic effect)
What is dromotropy
Dromotropy = conductivity in cardiac muscle
What are the ECG features that demonstrate the digoxin EFFECT
ST - downsloping ST depression with the characteristic “Salvador Dali” sagging appearance
Abnormal T-waves - usually biphasic
Shortened QT interval
What are the clinical features of digoxin toxicity
GIT: Nausea, vomiting, anorexia, diarrhoea
Visual: Blurred vision, yellow/green discolouration, haloes
CVS: Palpitations, syncope, dyspnoea
CNS: Confusion, dizziness, delirium, fatigue
What are the principles in understanding ECG in suspected digoxin toxicity
The classic digoxin toxic dysrhythmia combines:
- Supraventricular tachycardia (due to increased automaticity)
- Slow ventricular response (due to decreased AV conduction)
- Frequent PVCs (the most common abnormality), including ventricular bigeminy and trigeminy
- Sinus bradycardia
- Slow Atrial Fibrillation
- Any type of AV block (1st degree, 2nd degree & 3rd degree)
- Regularised AF = AF with complete heart block and a junctional or ventricular escape rhythm
- Ventricular tachycardia, including polymorphic and bidirectional VT
What are the anaesthetic implications of MAOIs
Used in refractory depression (rarely)
Can cause intra-op seizures if ephedrine is used
Must be stopped 2 weeks before –> consult psychiatrist for appropriate substitutes
Avoid indirectly acting inotropes such as ephedrine
Use phenylephrine if required
Which vasopressor can be used in an emergency patient on MAOI
Phenylephrine (NOT ephedrine)
Give 3 examples of MAOIs
Tranylcypromine
Phenelzine
Isocarboxazid
Which drugs potentiate block with ND-NMB agents
Magnesium Rx in Pre-eclampsia
Gentamicin prophylaxis used in sepsis and urology
Furosemide, Cyclosporin, cyclophosphamide in patients undergoing renal transplant
Which drugs can prolong the duration of SUX
Carbamazepine
Echothiopate (eye drops)
Which drugs antagonize NMB
Phenytoin
Carbamazepine
Azathioprine
Implication - may need frequent top ups of NMBs.
What type of surgery is antagonism of NMB most relevant requiring vigilance with regard to NMB top ups
Intracranial aneurysm repair
– Many of these patients are on anti-convulsants
USE peripheral nerve stimulator
List 1 drug interaction which may lead to intra-operative hypertension
Pethidine in patient’s on MAOI
Which intra-operative drugs can cause hypertension and tachyarrhythmia
10% phenylephrine eye drops in ophthalmic surgery (ask surgeon to use 2.5%)
Pethidine + MAOI
Adrenalin in local anaesthetic infiltrations + halothane anaesthesia
Digoxin –> cause tachyarrhythmia
- Increased Ve –> Resp. Alkalosis –> H+/K shift –> hypokalaemia –> Digoxin toxicity (K+ must be maintained at high normal levels for patient’s on digoxin)
Which drugs are reported to cause bradyarrhythmias
Timolol eye drops
Digoxin
Verapamil
What are ganglion blockers. Give three examples and suggest a possible anaesthetic implications of patients using these drugs
A ganglionic blocker (or ganglioplegic) is a type of medication that inhibits transmission between preganglionic and postganglionic neurons in the Autonomic Nervous System.
Methyldopa (MOA: Stimulation of central alpha-adrenergic receptors by a false neurotransmitter (alpha-methylnorepinephrine) that results in a decreased sympathetic outflow to the heart, kidneys, and peripheral vasculature)
Reserpine: (MOA: Reduces blood pressure via depletion of sympathetic biogenic amines (norepinephrine and dopamine)
Guanethidine: (MOA: preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues)
A patient on methyldopa –> if ephedrine is administered, the entire SNS outflow from CNS has been inhibited so the release of endogenous catecholamines induced by ephedrine is likely to be less effective.
–> use a direct acting agent: phenylephrine
When should aspirin be stopped prior to surgery
48 hours
> 48 hours if daily dose is > 300mg
What is the minimum platelet count required prior to surgery
100
When should clopidogrel be stoped prior to surgery and what should be considered here
7 days prior to surgery
Consider risk-benefit of stopping clopidogrel –> discuss with cardiology –> consider averting a neuraxial block
When should Warfarin be stopped prior to surgery
4 days –> INR > 1.4
heparin should be administered to maintain anticoagulation which can be titrated perioperatively
What should be done about a patient on the combined oral contraceptive pill
Swap to progesterone only
OR
Appropriate precautions against VTE peri-operatively
