Heart Drugs Flashcards
Name three examples of ACE inhibitors
Ramipril
Lisinopril
Captopril
Perindopril
What is the MoA of ACEIs?
Inhibits angiotensin converting enzyme to reduce the production of angiotensin II.
This causes reduced vasoconstriction, reduced aldosterone secretion and reduced ADH release
State two conditions in which ACEIs are used
Hypertension
Heart failure
State three side effects of ACEIs
Dizziness
Dry cough
Hyperkalaemia
Renal failure
Name two ARBs
Candesartan
Losartan
Valsartan
What is the MoA of ARBs?
Blocks the AT1 (and AT2 but this is less important) receptors.
This causes vasodilation, reduced aldosterone secretion and reduced ADH release.
ACE is still working so bradykinin is still being broken down, therefore pts dont get a dry cough side effect.
State three side effects of ARBs
Hyperkalaemia
Renal failure
Dizziness
State two conditions in which ARBs are used
Hypertension
Heart faillure
Name two dihydropyridine CCBs
Amlodipine
Lercandidipine
Nifedipine
Name a phenylalkamine CCB
Verapamil
Name a benzothiazapine CCB
Diltiazem
State two conditions in which verapamil and diltiazem are used
Hypertension
Arrhythmias - supraV tachycardia, AV nodal re-entry
Angina
What is the MoA of verapamil and diltiazem?
Blocks L-type Ca2+ channels on myocytes - negative inotropy.
Slows SAN firing, and slows the conduction of the AVN - negative chronotropy.
Blocks L-type Ca2+ channels on vascular smooth muscle cells - reduced TPR.
State two side-effects of verapamil
Constipation
Bradycardia (therefore don’t use with beta-blockers)
Flushing
State two side-effects of diltiazem
Constipation
Skin reactions
Flushing
State two conditions in which dihydropyridine CCBs are used
Hypertension
Angina
What is the MoA of dihydropyridine CCBs?
Blocks L-type Ca2+ channels on vascular smooth muscle cells - reduced TPR
State two side-effects of dihydropyridine CCBs
Constipation
Peripheral oedema
Flushing
Headache
Name an alpha-adrenoceptor blocker
Doxazosin
What is the mechanism of action of alpha-adrenoceptor blockers?
Antagonises noradrenaline at post-synaptic alpha-1 receptors on smooth muscle cells of the vasculature.
Causes vasodilation.
Also reduces plasma LDL and TG levels, while increasing HDL levels.
State two conditions in which alpha-adrenoceptor blockers are used
Hypertension
BPH
State two side-effects of alpha-adrenoceptor blockers
Postural hypotension Headache Oedema (especially with dihydropyridine CCBs) Palpitations Cystitis
Name two beta-blockers
Bisoprolol Carvedilol Nebivolol Metoprolol Labetolol (used in pregnancy)
Name two conditions in which beta-blockers are used
- Hypertension
- Angina
- Heart faliure
- Arrhythmias: SVTs, and converts AV nodal re-entry and WPW, protects ventricles from high rates of contraction
- Anxiety
What is the MoA of beta-blockers?
Decreased slope of the pacemaker potential at the SAN, and slowed conduction at the AVN - negative chronotropy
State two side-effects of beta-blockers
Bradycardia (caution in diabetics - mask hypoglycaemic tachycardia)
Lethargy and impaired concentration
Erectile dysfunction
Bronchoconstriction (caution in asthmatics)
What is the MoA of digoxin (cardiac glycoside)?
Increased vagal activity => slower heart rate.
Blocks the Na/K pump to increases intracellular Na+, which reduces the action of the NCX channel therefore more Ca2+ stays in the sarcoplasm to be released on contraction - increased inotropy.
State two condtions in which digoxin is used
Heart failure
Arrhythmias - slows ventricular rates in SVT
What is the MoA of ivabradine in heart failure and sinus tachycardia?
Slows the funny current to slow the heart rate
What is the MoA of hydralazine and nitrate combination in heart failure?
Balanced ateriodilation and venodilation to reduce the pre-load and after-load on the heart
Name a class IA antiarrhythmic
Procainamide
Quinidine
What effects do class IA antiarrhythmics have on the ventricular action potential?
Prolongs the AP by:
- Reducing Na+ conduction, therefore slowing the upstroke
- Prolonging the refractory period
State a use of class IA antiarrhythmics
Acute IV treatment of supraV and V tachycardias
State a side effect of class IA antiarrhythmics
Torsades de Pointes (prolonged QT)
Lupus-like effects
GI effects
Hypotension
Name a class IB antiarrhythmic
Lidocaine
Mexiletine
What is the MoA of class IB antiarrhythmics?
Fast binding offset kinetics
State a condition when class IB antiarrhythmics can be used
V tachycardia
State a side effect of class IB antiarrhythmics
Dizziness
GI effects
Drowsiness
Name a class IC antiarrhythmic
Flecainide
Propafenone
What is the MoA of class IC antiarrhythmics
Slow binding offset kinetics leads to a longer AP duration by:
- Slow upstroke
- Increased refractory period
State two conditions in which class IC antiarrhythmics can be used
- SupraV arrhythmias - atrial flutter and fib
- Premature ventricular contractions
- WPWS
State two side effects of class IC antiarrhythmics
- Sudden death (with chronic use)
- Proarrhythmic
- Increased response of the ventricles to atrial flutter leading to raised HR (therefore can prescribe with bisoprolol)
- Dizziness
- Diplopia and blurred vision
Name two class III antiarrhythmics
Amiodarone Sotalol (class II and III effects)
What is the MoA of class III antiarrhythmics?
Block K+ channels to prolong the AP by:
- Increasing the AP duration (longer plateau)
- Increasing absolute refractory period
Also slows AV conduction
Amiodarone can be used for most arrhythmias. However state two side effects of this drug
All increase with time:
- Pulmonary fibrosis
- Hepatic injury
- Increased LDL cholesterol
- Thyroid disease
- Optic neuritis
Half life of 3mths
What is the class II effect of sotalol?
Increases the time between APs to slow the HR
State a side effect of sotalol
Insomnia
Proarrhythmic
Fatigue
Name the two class IV antarrhythmics
Verapamil
Diltiazem
(Rate-limiting CCBs)
What is the MoA of adenosine?
Give as a rapid IV bolus bc the half-life is only seconds
Binds to Adenosine 1 receptors and activates K+ currents at the SA and AV nodes.
Causes hyperpolarisation
Adadenosine
State a use of adenosine
Convert re-entrant supraV tachycardias e.g. WPW, AVRT (not AF)
Slow the heart rate when doing an ECG to see SVTs more clearly
Diagnose coronary artery disease
When is atropine used?
Symptomatic vagal bradycardia as atropine is a muscarinic antagonist
Matropine
What is the aim of treatment for SVTs?
Rate control:
- Bisoprolol *
- Verapamil *
- Diltiazem *
- Digoxin
Rhythm control:
- Sotalol
- Flecanide with bisoprolol *
- Amiodarone
- Commonly used
Which drugs are commonly used in WPW?
Flecainide and amiodarone
Which drugs are commonly used in VT?
Metoprolol/ bisoprolol
Mexiletine
Amiodarone
How do anti-arrhythmics compare to one another in terms of safety and tolerability?
Safe:
- Bisoprolol
- Verapamil and diltiazem
Increased risk:
- Sotalol
- Flecainide
- Mexiletine
High risk (but most effective): - Amiodarone
