Pharm Cardio Flashcards
Class 1a
Drugs
Quinidine
Procainamide
Disopyramide.
Class 1a
Drugs:
Quinidine
Procainamide
Disopyramide.
–>MOA
Inhibit Na+ channels= slower depolarization
Inhibit K+ channels =slower rate of repolarization
on atrial & ventricular myocytes cells of the purkinje fibers.
How is moa class 1a different
to class 1b&1c
Work also on Inhibit K+ channels =slower rate of repolarization = lengthen the QT (and QRS )
which mean more likely to cause torsade de point
SE of 1a antiarrhythmics
longer QRS complex and a longer Q-T segment = torsade de pointes
Hypotension
Avoid in HF
Procainamide use & side effect
Type 1a
Rx WWP
SE: SLE
(think caines)
Action of 1B antiarrhythmics
Not as potent in blocking Na+ channel activity
Potency and selectiveness for ischemic tissue, c
Examples 1B antiarrhythmics
(Na channels)
Mexiletine
Lidocaine.
Action of 1C antiarrhythmics
Inhibit the Na+ channels in atrial and ventricular myocytes and purkinje fiber cells.
strongest potency
= dramatic decrease in the slope of phase 0.
Examples 1C antiarrhythmics
Flecainide
Propafenone.
SE 1C antiarrhythmics
- longer QRS complexes
- Avoid in ischemia = sudden death
propafenone is that it causes a bitter or metallic taste
SE: Quinidine
1A ANTIARRYTHMIC
Cinchonism (headache, tinnitus, thrombocytopaenia)
Where are pacemaker cells found
SA node
AV NODE
Bundle of HIS
Na channels on cardiac myocyte control what on ECG
the QRS
hence Na blocker=type 1 antiarrhythmics= prolong qrs
K channels on cardiac myocyte control what on ECG
QT
1a drug long qt = torsade de point
What channels do beta blockers work on and how do they alter myocyte and pacemaker AP
How is this reflected in the ECG
B- blocker decrease Decrease amount of Ca2+ Entering
Pacemaker cells = phase 4 take longer to get to threshold (decrease Rate of contraction)
–> Prolonged PR interval
Decrease amount of Ca2+ Entering Myocyte = affecting phase 2 = decreased force of contraction (recue O2 demand)
Beta blcker effect on DM
decrease hypoglycemia awareness
Beta blker contra indications (3)
pheochromocytoma
Cocaine toxicity
CBB use
What receptor do b-blocker block
B1 adrenergic receptors - g proteins receptors
What phase do K blker work on
Give examples of drugs
phase 3 of myocyte AP (prolonged repolarization)
Slower rate of K leaving the cell
amiodarone
sotalol
Explain ECG changes with K blkers
Potassium blkers – phase 3 of myocyte contraction (repolarization)
Slower rate of K leaving the cell = slower repolarization = Longer QT = slower HR
What type of antiarrhythmic is Amiodarone
What else does it block (4)
Amiodarone
1. blk K channels,
2. Blk Na channel,
3. Beta adrenergic receptors
4. Ca2+(L type)
Half life of amiodarone
20-100 days
SE: amiodarone
Hrt (3)
Lungs (1)
Endocrine (1)
Liver/GI (2)
Neuro (2)
Eyes (1)
Skin (2)
HRT: bradycardia, heart block, and HF.
Endo: thyroid dysfunction,hypo/hyperthyroidism;
Lung pulmonary fibrosis
GI& Liver:Liver dysfunction,constipation
Neurological
-tremor, paresthesia
Eyes corneal deposits; Skinblue-gray skin discoloration; & photosensitivity.
On the flip side, amiodarone can still cause
MOA Sotalol
K blocker
Non selective Beta blker
What phase do C2+ L channel in myocyte contract effect
Phase 2
Adenosine MOA
increases K efflux & inhibits Ca2+ influx to hyperpolarize the cell and slow down t = HR
Describe the 4 phases Myocyte depolarization
phase 4-resting phase - mainly Ca2+ leak = membrane slowly depolarizes
Phase 0-Depolarisation
Threshold potential met. Na channels open = Na in the cell = +ve membrane potential
Phase 1- initial repolarization
- Na channels close;
- K channels open up, = K out of cell = Membrane potential falls
Phase 2 /plateau phase
- Ca2+ channels open, CA2+ into cell- counterbalances the k ions out,
Phase 3, or repolarization
- CA2+ channels close,
- K channels remain open, = return to resting potential
Describe depolarization of cardiac pacemaker cell
3 phases
Phase 4-pacemaker potential
- Opening funny current (If) = Na in
- T-type C2+ channels open up, = further depolarizing the pacemaker cell.
Phase 0 - depolarization phase
- SLOW influx of Ca2+ ions through the L-type C2+ channels
- T-type C2+ channels close.
Phase 3 repolarization phase
- L-type C2+ channels close
- K channels open up, = +ve current.
How do beta blker
act on
Pacemaker cell &
Non- pace maker cells
Block B adrenergic receptors- ATP & adenylyl cyclase don’t make cAMP= Less Ca2+ enter the cell
Pacemaker Cell – Decreased Ca2+ affects phase 4 = decrease HR SAN= Longer PR interval
Non pacemaker cell- Less Ca2+ effects phase 2 = decrease contraction & cardiac O2 demand
Anti arrhythmic effect of CCB
blk L- type Ca2+ channel
Non Dihydropyridine- anti arrhythmic target:
- Pacemaker cells - Decrease Ca entry into the cells = prolong effective refractory period = decrease SN firing rate and AV = Prolonged PR
- In myocytes decrease Ca2+ = decrease contraction
Slower action than b-blker
Diff btwn verapamil an diltiazem ?
diltiazem affects smooth mscl; Used HTN & svt
verapamil - is cardiac specific; Angina & SVT
SE of Calcium channel Blockers
Constipation
flushing
Hyperprolactinemia
Heart blk
SA node depression
MAO of Digoxin
Stim of vagal nerve
MAO of nitrates (4)
Nitrates are Converted into NO to simulate cGMP
= vasodilation of veins > Arteries
= Decrease in afterload & preload
= reduced cardiac O2 demand.
Also vasodilate hrt vessel = increase o2 delivery
Contraindications to Nitrates
R sided HF
Erectile dysfunction meds
what should be prescribed with nitrates to reduce SE
Beta blkers
MOA Statins
- inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
- Reduced Cholesterol= increase hepatic LDL receptors = increase uptake of LDL from body (Mild uptake of triglycerides )
- Increases HDL
SE statins
myalgias - Coenzyme Q decrease in e-transport chain
rhabdomyolysis.
hepatotoxic.
teratogenic.
Indications for statins (4)
Indications
* anyone with a 10-year cardiovascular risk >= 10%
- Pts w. CVD (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
- DM2 Pts with assessed w/ QRISK2
- DM1 Pts w/ dx> 10 years ago OR are aged over 40 OR have established nephropathy
MOA Ezetimibe
is a cholesterol absorption inhibitor
MOA Fibrates
Example
Agonist of PPAR-alpha therefore increases lipoprotein lipase expression
used to reduce triglyceride levels
bezafibrate and fenofibrate.
