Angina, Cardiac Arrest and Arrhythmias Flashcards
Give 2 examples of calcium channel blockers and 2 indications for their use:
- amlodipine, nifedipine, diltiazem, verapamil
- hypertension rx - to reduce risk of stoke, MI and death
- stable angina - symptom control
- Supraventricular arrhythmia rx - control heart rate (diltiazem, verapamil)
MOA of CCBs
- decrease Ca2+ ion entry into vascular and cardiac cells, reducing intracellular calcium concentration
- this causes…
- effect on inotropy and conduction?
- overall these together reduce ___ so reduces ..
- causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure
- in heart, CCBs reduce myocardial contractility
- they supress cardiac conduction (esp across AVN) –> slowing ventricular rate
- together, reduces afterload so reduces myocardial O2 demand - preventing angina
CCBS can be
- dihydropyridines: relatively selective for the vasculature e.g. ____ and ___
- non-dihyropyridines: more selective for the heart, most cardioselective CCB is ___
- dihydropyridines: e.g. amlodipine and nifedipine
- non-dihyropyridines: cardioselective = verapamil
-Amlodipine and nifedipine (CCBs): name 2 SEs caused by vasodilation and compensatory tachycardia
- ankle swelling
- flushing
- headache
- palpitations
Verapamil (CCB) commonly causes ______ less often can cause: ….. (due to effects on heart)
Therefore in who should Verapamil be used with caution, give 2 e.gs?
- constipation
- bradycardia, heart block, heart failure
- Caution: pts with poor LV function (precipitates/worsens HF) and
- people with AV nodal conduction delay (can provoke complete heart block)
-Amlodipine and nifedipine (CCBs): name 2 CIs
(one relates to the vasodilation causing a reflex in contractility and tachycardia, which increases the __ ___)
(other relates to risk of provoking collapse in pts with this pathology)
CI: UNSTABLE ANGINA (increases O2 demand)
SEVERE AORTIC STENOSIS
-Non-dihydropyrididine CCBs e.g. verapail, diltiazem, should not be prescribed with _____ except under specialist supervision as both drug classes are negatively ionotropic and chronotropic so together can cause: HF, bradycardia and asystole
-B-BLOCKERS
Rough dosages for CCBs
- amlodipine for HT e.g. ___ mg orally daily
- diltiazem for angina e.g. ___mg orally 12-hrly
- verapamil for SV arrhythmias e.g. ___mg orally 8-hrly
- amlodipine 5-10mg for HT
- diltiazem 90mg for angina
- verapamil 40-120mg for SV arrhythmias
Amiodarone is indicated in the treatment of several _______ such as:
(only when other therapeutic options-drugs/electrical cardioversion are ineffective)
-tachyarrhythmias e.g. AF. atrial flutter, SVT, VT, refractory VF
Amiodarone MOA:
-effect on myocardial cells is: blockade of..
-so therapeutically in the following can…
AF:
SVT AVNRT:
VT/VF:
- blockades Na+, Ca2+ and K+ channels and alpha & beta adrenergic receptors
- this reduces spontaneous depolarisation, slows conduction velocity and increases refractiveness inc. in the AVN
- so it can reduce ventricular rate in AF/atrial flutter
- can increase chance of conversion and maintenance of sinus rhythm
- in SVT AVNRT can break the circuit and restore sinus rhythm
- can treat and prevent VT and improves chance of successful defibrillation in refractory VF
3 Amiodarone SEs
NB: amIODarone
- pneumonitis
- bradycardia, AV block
- hepatitis
- photosensitivity and grey discolouration of skin
- due to IODine content can –> thyroid abnormalities
(NB: half life is very long, months to clear)
Avoid amiodarone if possible in what 2 pt groups (based on MOA/SEs)
- severe hypotension
- heart block
- active thyroid disease
Amiodarone interacts with very many drugs
Name 2 that in can increase the plasma concentration of which increases risk of bradycardia, AV block and heart failure…
- digoxin
- diltiazem (CCB)
- verapamil (CCB)
- so half the dose of these drugs if amiodarone is started
In ALS algorithm, immediately after the 3rd shock in cardiac arrest with VF or pulseless VT, Amiodarone is given followed by 20ml 0.9% sodium chloride or 5% glucose as a flush. What is the dose of Amiodarone given?
-300mg IV (bolus dose in pre-filled syringe)
Why in a setting outside cardiac arrest if continuous/repeated IV infusions of amiodarone are anticipated should it be given in a central line? What is the risk of peripheral IV administration?
-Can cause significant phlebitis peripherally
2 indications for Digoxin prescription:
- AF and atrial flutter to reduce the ventricular rate (but a B-blocker or non-dihydropyridine CCB is often more effective)
- in severe HF: for pts already taking an ACEi, B-blocker, and an Aldosterone antagonist/ARB
Digoxin MOA
-effect on HR and contractility? How is is useful in AF and how does it help in HF - different aspects
- negatively chronotropic
- positively ionotropic
- increases vagal parasympathetic tone , reduces conduction at AVN, reducing ventricular rate in AF/AFlutter
- in HF: inhibits Na+/K+ ATPase so Na+ accumulates in cell, as cell extrusion of Ca2+ requires low intracellular Na+ concs, elevated Na+ conc causes calcium to accumulate in cell so increases contractile force.
3 adverse effects of Digoxin therapy:
- bradycardia
- GI disturbance
- rash
- diziness
- visual disturbances (blurred or yellow vision)
- pro-arrhythmic in digoxin toxicity (!)
2 Contraindications for use of Digoxin and 2 cautions for its use:
-CI: 2ND DEGREE HEART BLOCK
-CI: INTERMITTENT COMPLETE HEART BLOCK
-CI: PTS W/AT RISK OF VENTRICULAR ARRYTHMIAS
Caution: reduce dose in renal failure (is eliminated renally)
Caution: hypoK+, hypoMg2+ and hyperCa2+ increase the risk of digoxin toxicity
By what mechanism do some diuretics increase the risk of digoxin toxicity? Name 1 other drug that increases plasma conc of digoxin so increases risk of toxicity?
- loop and thiazides can cause hypokalaemia, as result when K+ is low, competition with K+ to bind to Na/K+ ATPase is low so effects of Digoxin are enhanced
- Amiodarone, CCBs, Spironolactone and Quinine can increase plasma conc of Digoxin
What ECG change may be seen with therapeutic levels of Digoxin therapy?
-ST-segment depression, reverse tick sign on ECG
expected effect, doesn’t signify toxicity
-Atropine, hyoscine butylbromide (buscopan) and glycopyrronium are all medications belonging to the class “______ “
give 1 cardio and 1 GI indication for their use.
Anti-muscarinics
- bradycardia
- IBS (anti-spasmodic)
- in care of dying patients to reduce copious respiratory secretions
Anti-muscarinics antagonise the rest and digest effects therefore name 3 SEs associated with their use?
- tachycardia, dry mouth, constipation
- reduce detrusor activity so –> urinary retention in BPH pts
- blurred vision
- drowsiness and confusion
Pts susceptible to ___-__ ___ should not have anti-muscarinics as they can precipitate a rise in ___. And avoid in pts at risk of ____
- acute-angle glaucoma
- rise in ICP
- arrhythmias
Atropine dose for bradycardia. give incremental doses by __, can start from ___micrograms and give up to ___mg
- IV in incremental doses
e. g. 500micrograms every 1-2mins until an acceptable HR is reached, up to maximum of 3mg.
Lidocaine is indicated for what? (2)
- local anaesthetic e.g. in urinary catheterisation and minor procedures
- VT and VF rx refractory to electrical cardioversion but amiodarone is preferred
Lidocaine MOA
- enters cell
- accepts a …. –> —
- from inside cell it enters then blocks ….
- this prevents …
- in heart …
- enters cell
- accepts a proton to become + charged
- from inside cell it enters then blocks VGNa+Channels on surface membrane
- this prevents initiation and propagation of APs in nerves and muscle
- in heart reduced duration of APs slows conduction velocity and increases refractory period
SEs of Lidocaine administration
- stinging
- rarely systemic effects: drowsiness, restlessness, tremor, fits
- OD can cause hypotension/arrhythmias
-as lidocaine depends heavily on hepatic blood flow for its elimination, lower doses should be used in states of reduced ____ ____
-cardiac output
What is the first line drug in the treatment of supraventricular tachycarida (SVT)?
-Adenosine
What is the ECG appearance of SVT (NB: adenosine is the 1st line treatment)
-regular narrow complex tachycardia
Adenosine binds to adenosine receptors on cell surfaces in the heart, it activates these GPCRs leading to what effects
(treats SVT)
- overall = increases AV node refractoriness
- reduces frequency of spontaneous depolarisations
- increases resistance to depolarisation
- so transiently slows the sinus rate and conduction velocity
What is the approximate half life of adenosine in plasma ?
-10seconds
adenosine can break the re-entry circuit of a SVT taking place in the AVN by increasing the refractoriness, this allows SAN to resume control of heart rate = “cardioversion”. Why can it not induce cardioversion in atrial flutter, and why is it still given in atrial flutter then?
- in atrial flutter the circuit does not involve the AVN so it won’t induce cardioversion
- but it blocks conduction to the ventricles so allows closer inspection of the atrial rhythm on ECG by slowing the HR so may help reveal the diagnosis
As adenosine interferes with SAN and AVN functions adenosine can induce what v adverse effects during it’s brief action? What do pts report?
- induce bradycardia and even asystole
- pts feel sinking in chest, with breathlessness and sense of impending doom
3 CI to adenosine use relate to pts that wouldn’t tolerate it’s bradycardic effects, suggest 2:
- CI: HYPOTENSION
- CI: CORONARY ISCHAEMIA
- CI: DECOMPENSATED HEART FAILURE
Adenosine should be avoided in pts with asthma/COPD due to the risk of it inducing what?
-Bronchospasm
Dipyridamole (an antiplatelet agent) has what effect on cellular uptake of adenosine, (____ the half-life) therefore what should you do if co-prescribed?
- dipyradamole blocks adenosine cellular uptake
- so prolongs half life/potentiates effect
- so halve the dose of adenosine
the initial dose of adenosine is usually 6mg, by what route is it given?
IV
