S3 Cardiac Arrhythmia Drugs Flashcards

1
Q

what are arrhythmias

A

heart condition with disturbances in :
Pacemaker impulse formation (SAN)
Contraction impulse formation (bundle of his)
this results in insufficient contraction to maintain CO
resting potential is created by the distribution of ions across the membrane such as Na, Ca, K and maintained by ion channels and exchangers

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2
Q

Describe the mechanisms of drugs that act on the fast cardiac AP (ventricles)

A

Drugs blocking the Na channels slow conduction in phase 0 (red), AP same duration
Beta blockers decrease phase 4 depolarization
drugs blocking K+ channels increase AP duration
drugs blocking Ca channels affect plateau phase and decrease phase 4 depol

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3
Q

Describe the mechanisms of drugs that act on the slow cardiac AP ( SAN and AVN)

A

Ca channel blockers reduce slope

Beta blockers reduce initial sloping phase and affect automaticity

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4
Q

how can arrhythmias form ?

A

abnormal impulse generation -
ectopic focus - AP arises from sites other than the SAN
Delayed or early after depolarisation
abnormal conduction -
conduction block of impulse from atria to ventricles
reentry - movement around a blocked area
wolf parkinson white (WPW) syndrome ( movement of impulses down AVN then back up pathway
area of infarct can lead to tachycardia

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5
Q

describe the action of drugs to treat arrhythmias

A

in the case of abnormal generation, we want to decrease the phase 4 slope (funny current) so its harder to generate a rhythm E.g Ca channel blocker or bisopralol or we can raise the threshold
in the case of abnormal conduction, we want to decrease conduction velocity (VG Na channels) and increase refractory period to prolong AP so cell cannot be re-excited

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6
Q

what are the different classes of drugs used to treat arrhythmias

A

CLASS - Action - Drugs
1a - moderate phase 0 (Na blockers)- quinidine, procainamide, disopyramide
1b - no change in phase 0 - lidocaine, mexiletine
1c- marked phase 0 - flecainide, propafenone
2 - beta-adrenergic blockers - propranolol, bisoprolol, metoprolol, esmolol
3- prolong repolarization (K blocker) - Amiodarone, Sotalol
4- Ca channel blockers - verapamil, diltiazem

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7
Q

describe class 1a drugs

A

absorption and elimination ; oral or IV
effects on heart : decrease conduction (decrease phase 0 (Na+) of the ap)
increase refractory period (increase APD (K+) and increase Na inactivation)
decrease automaticity (decrease slope of phase 4, fast potentials)
increase threshold (Na+)
quinidine is anticholinergic (atropine like action) to speed AV conduction
ECG ; increase QRS and QT
uses : quinidine : maintain sinus rhytms in atrial fibrillation
procainamide : treatment of ventricular arrhytmias
side effects : hypotension, dizziness, proarrythmia

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8
Q

describe class 1b drugs

A
effects on heart ;
increase threshold
decrease phase 0 conduction in fast beating or ischaemic tissue 
ECG ; increased QRD
Uses : ventricular tachycardia
side effects ; dizziness
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9
Q

describe class 1c drugs

A

effects on heart
decrease phase 0 conduction
decrease automaticity (increase threshold)
increase APD and refractory period
ECG; increase PR and QRS
Uses; used for supraventricular arrhythmias and ventricular contractions
wpw syndrome
side effects - proarrhythmia and sudden death with chronic use

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10
Q

describe class 2 drugs

A

effects on heart
increase APD ( action potential duration)
decreased phase 4 depol
ECG ; increased PR and decrease HR
uses ; treating sinus, CD tachycardia, protect ventricles from high atrial rates
side effects; bronchospasm, hypotension

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11
Q

describe class 3 drug amiodarone

A

amiodarone :
effects on heart ; increase refractory drug and APD
increase threshold
ecg ; increased pr and qrs
uses ; arrythmia , wpw
side effects; pulmonary fibrosis and hepatic injury
may need to reduce the dose of digoxin and monitor warfarin more closely

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12
Q

describe class 3 drug sotalol

A

effects on heart ; increased APD, slow phase 4
ecg ; increase QT, slow HR
uses ; ventricular tachycardia
side effects ; proarrhythmia , fatigue

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13
Q

describe class 4 drugs

A
effects on heart 
slow av conduction
increased refractory period
ecg ; increased PR
uses ; control ventricles during supraventricular tachycardia 
side effects ; asystole or reduced CO
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14
Q

what is the mechanism for adenosine ?

A

natural nucleoside that binds A1 receptors and activates K+ currents in AV and SA node, decreases APD
effects on heart ; slow AV conduction
uses ; convert hypotension

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15
Q

what is the mechanism for Vernakalant ?

A

blocks atrial specific K+ channels
effects on heart ; slow atrial conduction
Uses ; Convert AF to sinus rhythm

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16
Q

what is the mechanism for Ivabradine ?

A

blocks funny current
slows sinus node
reduce sinus tachycardia

17
Q

what is the mechanism for digoxin (cardiac glycosides)

A

effects on heart ; enhances vagal activity, slows AV conduction
uses ; to reduce ventricular rates in AF

18
Q

what is the mechanism for Atropine ?

A

mechanism ; selective muscarinic antagonist
effects on heart ; block vagal activity to speed AV conduction
uses treat vagal bradycardia

19
Q

which drugs can be used in AF

A

bisoprolol, verapamil, diltiazem, sotalol, felcainide with bisoprolol, amiodarone

20
Q

should flecainide be used alone in atrial flutter

A

no give AV nodal blocking drugs to reduce ventricular rates in flutter

21
Q

best drug for treatment WPW

A

flecainide, amiodarone

22
Q

which drugs could be used in re-entrant SVT ?

A

adenosine and verapamil ( block AVN conduction, acute), bisoprolol ( block AVN chronic)

23
Q

which drugs for ectopic beats

A

bisoprolol

24
Q

which drugs to treat sinus tachycardia

A

ivabradine ( blocks SAN conduction)

25
Q

where is cholesterol made and what is it used for ?

A

some obtained from diet but most synthesised in liver. Essential component of membranes (modulates fluidity). Precursor of steroid hormones

26
Q

what is the pro - atherogenic effects of Ox- LDL

A

inhibits macrophage motility. induces T cell activation, enhances platelet aggregation

27
Q

what are some examples of lipid lowering drugs ?

A

statins - simvastatin
fibrates - fenofibrate
Nicotinic acid/niacin
cholesterol lipase inhibitors - ezetimibe

28
Q

describe the mechanism of statins ?

A

inhibit cholestrol synthesis in hepatocytes ( by inhibiting HMG - CoA reductase)
increase clearance of LDL, decrease the production of VLDL
Adverse drug reactions ADRS - increase transaminase levels , myopathy (of muscles)
used to prevent CVD

29
Q

describe the mechanism of fibric acid derivatives

A

ampipathic carboxylic acids
PPARa agonist - increases production of lipoprotein lipase which reduces tryglyceride production
uses ; adjunctive to therapy diet
contraindication ; renal disease

30
Q

describe the mechanism of nicotinic acid

A

reduces VLDL and increases HDL at high doses
Lipid lowering effect by inhibition of lipoprotein synthesis
adverse effects ; ithching, headache, activation of peptic ulcer
contraindications liver disease

31
Q

describe the mechanism of ezetimibe

A

selectively inhibits intestinal cholesterol absorption
decreased intestinal delivery of cholesterol to the liver
increased expression of hepatic LDL receptors
ezetimibe circulates enterohepatically
ADRS : headache, abdominal pain

32
Q

describe combination therapy for cholesterol

A

shall improve triglyceride, LDL, HDL levels

but is associated with increased risk for myopathy and rhabdomyolysis

33
Q

describe what PCSK9 inhibitors

A

LDL receptor becomes internalised and inhibited by PCSK9 this draws more cholesterol but of circulation
offer atorvastatin 20 mg for the primary prevention of CVD
start statin treatment in people with CVD with atorvastatin80 mg
aim for > 40% reduction in non-HDL cholesterol, if this is not achieved may need to adapt lifestyle and diet