CVS 6 Arrthymias And CVS Drugs Flashcards
What is the primary mechanism by which GTN spray alleviates myocardial ischaemia in a patient with stable angina?
Dilation of systemic veins
Causes of tachycardia
- ectopic pacemaker activity - damaged area of myocardium takes over from SAN
- afterdepolarisations - abnormal depolarisations following the AP
- atrial flutter/atrial fibrillation
-
re-entry loop - conduction delay
- accessory pathway
Causes of bradycardia
- sinus bradycardia - SAN does depolarise quick enough - Sick sinus syndrome
- Drugs e.g. B blockers, Ca2+ channel blockers
- conduction block - issue at AVN or bundle of His
Types of tachycardias
Ventricular
Supraventricular - above ventricles
Does hypokalaemia or hyperkalaemia cause early after depolarisations?
Hypokalaemia - delays repolarisation»_space; can cause early after depolarisations
When are early after depolarisations more likely to occur?
When AP is prolonged
(Longer QT interval)
When are delayed after depolarisations more likely to occur?
If intracellular Ca2+ conc is high
What happens in incomplete conduction damage?
Excitation can take longer route to spread the wrong way through damaged area
This sets up a circus of excitation
What happens in AV nodal re-entry?
Fast and slow pathways in the AVN create a re-entry loop
Ventricles stimulated too soon
What happens in ventriuclar pre-excitation?
Example of where this is seen
An accessory pathway between atria and ventricles
creates a re-entry loop
e.g. Wolff-Parkinson-White syndrome
What causes atrial fibrillation?
Multiple small re-entry loops in the atria
What are the 4 classes of anti-arrhythmic drugs?
- drugs that block voltage gated Na+ channel
- antagonists of B-adrenoreceptors (B blockers)
- drugs that block K+ channels
- drugs that block Ca2+ channels
Mechanism of lidocaine
- Blocks voltage gated Na+ channel when open or inactive state
- Blocks VGNC in damaged myocardium spontaneously depolarising after AP»_space; prevents initiation of another AP
- dissociates quickly
What can lidocaine be used for?
Ventricular tachycardia
Example of drugs which blocks voltage gated Na+ channels
lidocaine
Suffix of Beta blockers
-olol
How do beta blockers work?
Effect on SAN + AVN
- Block sympathetic action - B1 adrenoreceptors in heart
- which decreases heart rate due to:
- Decreases slope of pacemaker potential in SAN
- Slows Conduction at AVN by reducing voltage gated Ca2+ channel activity in upstroke of AP
When can B blockers be used?
Prevent supraventriclar tachycardia
Atrial fibrillation
Following myocardial infarction
To reduce O2 demand - reduces myocardial ischamia
Heart failure
How are beta blockers useful after a myocardial infarction?
- MI often increases sympathetic activity - B blockers block sympathetic activity
- increased sympathetic activity can cause arrhythmias
- prevent ventricular arrhythmias
How fast does lidocaine dissociate and what is the importance of this?
<0.5ms
- Bound long enough to prevent inappropriate depolarisations + dissociates in time for next AP
- This means myocardium can depolarise normally + heart beats efficiently
Mechanism of drugs that block K+ channels
- prolong AP
- this lengthens the absolute refractory period
- in theory would prevent another AP occurring too soon but can be pro-arrhythmic - prolonged QT interval
Why are drugs that block K+ channels not generally used?
Can be pro-arrhythmic
Mechanism of amiodarone
Blocks K+ channels
Has other actions so can cause side effects
Examples of drugs that block Ca2+ channels
Verapamil
Diltiazem
Mechanism of drugs that block Ca2+ channels
On myocardium:
- Decreases slope of AP at SAN
- Decreases AVN conduction
- Decreases force of contraction
On smooth muscle:
- dilation of blood vessels»_space; reduces TPR
3 groups of Ca2+ channel blockers and what they act on
- benzothiazapines - act on heart to give negative inotropic + chronotropic effects
- phenylalkamines - act on heart to give negative inotropic + chronotropic effects + dilate vessels to reduce TPR
- dihydropyridine - mainly act on vasculature to reduce TPR
What type of drug are dihydropyridines and why aren’t they use to treat arrhythmias?
Ca2+ channel blockers
Act mainly on peripheral vasculature not the heart
Mechanism of adenosine
Act on a1 receptors at AVN
Enhances K+ conduction - hyperpolarises cells»_space; ‘resets the SAN’
Uses of adeonsine
Terminating re-entrant supra-ventricular tachycardia
What do patients need to be warned of when given adeonsine?
It will feel like their heart has stopped
Suffix of ACE inhibitors
-pril
Mechanism of ACE inhibitors
- Inhibitors action of angiotensin converting enzyme
- prevents conversion of AngI > AngII - reduces effect of RAAS system
- vasodilation > reduces afterload
- reduced ADH and aldosterone release > reduces preload
Side effect of ACE inhibitors
Explain why
Dry cough
- inhibits ACE
- prevents breakdown of bradykinin»_space; build up causes a dry cough
Suffix of angiotensin II receptor blockers
-sartan
Mechanism of angiotensin II receptor blockers
- Blocks Ang receptor 1 which prevents AngII from binding
- reduces effect of RAAS system:
- vasodilation - reduces afterload
- reduces ADH + aldosterone release - reduces preload
Similarity+ difference between ACE inhibitors and angiotensin II receptor blockers
Have the same effect - both reduce effect of RAAS system
Ang II receptors don’t prevent bradykinin breakdown - only ACEi have dry cough, not ARBs
How are ACE inhibitors and ARBs useful in heart failure?
- decreased BP»_space; reduces afterload
- decreases fluid retention (blood volume)»_space; reduces preload
Both of these decrease the work load on the heart
What diuretic is used to treat congestive heart failure? Example
What does it do?
Loop diuretic e.g. furosemide
Reduces pulmonary and peripheral oedema
What types of Ca2+ channel blockers are better at treating arrhythmias?
Benzothiazapines e.g. diltiazem
Phenylalkamines e.g. verapamil
Examples of dihydropyridine Ca2+ channel blockers
amlopidine
nicardipine
Uses of Ca2+ channel blockers
Hypertension
Angina
Coronary artery spasm
Supraventricular tachycardia
What do positive inotropes do?
Increase contractility - heart beats harder»_space; increases CO
Primary mode of action of cardiac glycosides
Block Na+/K+ ATPase»_space; rise in intracellular [Na+]
This causes an increases in intracellular [Ca2+]»_space; increases force of contraction (positive inotropic)
Difference in use of propanolol and bisoprolol
propanolol - non selective B1/B2 antagonist
- B1 - slow HR + reduces force of contraction
- B2 - bronchoconstriction
bisprolol - selective B1 antagonist
- less risk of bronchoconstriction
What drugs are used to treat angina?
Nitrates»_space; NO
- glyceryl trinitrate spray - sprayed under tongue
What does NO do?
Vasodilator - particularly effective on veins
Mechanism of nitric oxide
- NO activates guanylate cyclase
- Increases cGMP
- Lowers intracellular [Ca2+]
- Relaxation of vascular SM
How does nitric oxide help alleviate symptoms of angina?
- venodilation - lowers preload > reduces work load + contraction > lowers O2 demand
- action on coronary arteries improves O2 delivery to ischaemic myocardium
What heart conditions have an increased risk of thrombus formation?
Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves
Examples of anticoagulants
IV heparin - inhibits thrombin
Oral warafin - antagonises action of vit K
Oral dabigatran - thrombin inhibitor
Examples of anti platelet drugs
aspirin
clopidogrel
Selectivity of beta blockers
A-N: cardio-selective B1 blocker
O-Z: non-selective B1+B2 blocker
If suffix is close to olol but not exact: beta + alpha blocker
