Lecture 14 - arrhythmias and drugs that act on the cvs Flashcards
what are the causes of arrhythmias ?
outline the different causes and explain them
you may want to check lecture 14 cvs for answers
Tachycardia
• Ectopic pacemaker activity
– damaged area of myocardium becomes depolarised and spontaneously active
– latent pacemaker region activated due to ischaemia dominates over SA node
• Afterdepolarisations
delayed AD (excess ca2+) or Early AD (prolonged AP)
– abnormal depolarisations following the
action potential (triggered activity)
these can causes Ventricular tachycardias
• Atrial flutter / atrial fibrillation
• Re-entry loop
– conduction delay
– accessory pathway
common cause of Atrial Fib
also get AV nodal Re entry
ventricular pre exictation - pathway to Ventricles that is not the Av node causes a re entry loop such as in wolf Parkinson white syndrome
what are the causes of bradycardic arrhythmias ?
outline the different causes and explain them
you may want to check lecture 14 cvs for answers
Bradycardia
• Sinus bradycardia
– Sick sinus syndrome (Intrinsic SA node dysfunction)
– Extrinsic factors such as drugs (beta blockers, some Ca2+ channel blockers)
• Conduction block
– Problems at AV node or bundle of His
– Slow conduction at AV node due to extrinsic factors ((beta blockers, some Ca2+ channel blockers)
outline the types of drugs that affect rate and rhythm of the heart, and hence are used in arrhythmia treatment
Drugs that block potassium channels
drugs that block calcium channels
drugs that block voltage sensitive sodium channels
antagonists of B adrenoceptors
also is adenonsine
outline how drugs that block voltage sensitive sodium channels work
give an example, and use case
- Typical example is the local anaesthetic lidocaine
- Use-dependent block. Only blocks voltage gated Na+ channels in open or inactive state – therefore preferentially blocks damaged depolarised tissue
Little effect in normal cardiac tissue because it dissociates rapidly
• Blocks during depolarisation but dissociates in time for next AP
Lidocaine
• Sometimes used following MI
• Damaged areas of myocardium may be depolarised and fire automatically
• More Na+ channels are open in depolarised tissue
– lidocaine blocks these Na+ channels (use-dependent)
– prevents automatic firing of depolarised ventricular tissue
outline how drugs that are b adrenoreceptor antagonists work
give an example, and use case
• Examples: propranolol, atenolol (Beta blockers)
• Block sympathetic action (noradrenaline)
– act at β1 -adrenoreceptors in the heart
• Decrease slope of pacemaker potential in SA and
slows conduction at AV node
Beta blocker decreases slope of pacemaker potential and rising phase of AP
• Can prevent supraventricular tachycardia
– β-blockers slow conduction in AV node
– Slows ventricular rate in patients with AF
• Used following myocardial infarction
– MI often causes increased sympathetic activity
– Arrhythmias may be partly due to increased sympathetic activity
– β-blockers prevent ventricular arrhythmias
• Also reduces O2 demand
– Reduces myocardial ischaemia
– Beneficial following MI
outline how drugs that block K+ channels work
give an example, and use case
do not need detail for this one
Drugs that block K+ channels (class III)
• Prolong the action potential
– mainly by blocking K+ channels
• This lengthens the absolute refractory period
Drugs that block K+ channels
• Prolong the action potential
• Not generally used because they can be also be pro-arrhythmic
• One exception – amiodarone - as tis crap at its main job, but has other affects
- Used to treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop due to an extra conduction pathway)
- Effective for supressing ventricular arrhythmias post MI
outline how drugs that block ca2+ channels work
give an example, and use case
- Examples: verapamil, diltiazem (non-dihydropyridine types)
- Decreases slope of action potential at SA node
- Decreases AV nodal conduction
- Decreases force of contraction (negative inotropy)
- Also some coronary and peripheral vasodilation
anti arrythmia
• Dihydropyridine Ca2+ channel blockers are NOT effective for this - see later flash cards
outline how adenosine works
give an example, and use case
Acts on A1 receptors at AV node but has a very short
half-life
• Enhances K+ conductance
– hyperpolarises cells of conducting tissue
• Anti-arrhythmic
– doesn’t belong in any of the classes mentioned
outline how ACE inhibitors work for treating hear issues
give a use case
ACE-inhibitors (ACEi)
• Inhibits the action of angiotensin converting
enzyme
• Important in the treatment of hypertension AND
heart failure
• Prevents conversion of angiotensin I to angiotensin II
– Angiotensin II acts on the kidneys to increase
Na+ and water reabsorption
– Angiotensin II is also a vasoconstrictor
- Very valuable in treatment of heart failure (Chronic failure of the heart to provide sufficient output to meet the body’s requirements – can lead to both peripheral and pulmonary oedema)
- ACEi → decrease vasomotor tone (lower blood pressure)
- Reduce afterload of the heart
- ALSO Decrease fluid retention (lower blood volume)
- Reduce preload of the heart
- BOTH effects reduce work load of the heart
outline how angiotensin II receptor blockers work for treating heart issues
give a use case
In patients who can’t tolerate ACEi can use AT1
receptor blocker
• Used in treatment of heart failure and hypertension
outline how duiretics work for treating heart issues
give a use case
• Used in treatment of heart failure and hypertension
• Loop diuretics useful in congestive heart failure
– Example furosemide
– Reduces pulmonary and peripheral oedema
reduce fluid volume is the idea
outline how Ca 2+ blockers (Dihydropiridines) work for treating heart issues
give a use case
• Dihydropyridine Ca2+ channel blockers are not effective in preventing arrhythmias, but act on vascular smooth muscle
• Examples: Amlopidine, nicardipine
– Decrease peripheral resistance
– Decrease arterial BP
– Reduce workload of the heart by reducing afterload
• Ca2+ channel blockers useful in hypertension, angina, coronary artery
spasm, SVTs
what are the uses of positive inotropes ?
• Positive inotropes increase contractility and thus cardiac output
• Cardiac glycosides
– Example: digoxin
work by blocking Na/K atpase, so intracell NA rises, and NCX is less effective and hence intracell Ca also rasies - greater intropy - contractile force
• Cardiac glycosides may be used in heart
failure when there is an arrhythmia such as
AF
flog a dead horse - not good really as making dying heart contract harder
• β-adrenergic agonists
– Example: dobutamine
Selective β1 – adrenoceptor agonist
– Stimulates β1 receptors present at SA node AV node and on ventricular myocytes
– uses
• cardiogenic shock
how do we treat heart failure ?
reduce workload
ACEinhibotors and ARB’s with Diuretics
can also use heart failure
what do nitrates treat ?
how do they work ?
used to treat angina (chest pain)
Angina occurs when O2 supply to the heart does not meet its need
• Ischaemia of heart tissue
– Chest pain • Usually pain with exertion
NO is a powerful vasodilator PARTICULARLY
EFFECTIVE ON VEINS
action on venous system -venodilation lowers preload
– reduces work load of the heart
– heart fills less therefore force of contraction reduced (Starling’s Law)
– this lowers O2 demand
organic nitrates do no really dilate arterioles ( they do dilate some collateral arteries though - minor)
