Cardiovascular pharmacology Flashcards
For this lecture, what is important to know
You will likely not be using class 1 and 4 - those will be written by cardio
likely not hammered on boards
What does amiadorone cause?
Thyrotoxicity
What do drugs change?
Action potential
What is the action potential of an SA node
Does not have a flat segment that needs repolariztiation
phase 4 sodium INflux
phase 0 Ca++
phase 3 K+ EFflux (brings back to resting potential)
What happens if you block Ca++
Slows depolarization because less Ca2+ go in
What happens if you block phase 3
Block K+ efflux - meaning that it will take longer to fire again, causing bradycardia
What does an atrium AP look like
What cells have a flat resting potential?
Myocardial cell, meaning that it needs an impulse.
Na+ block takes it longer to meet threshold
What creates the plataue of a myocardial AP
K+ going out and Ca2+ coming in
(want a long squeeze, and then we relax)
blocking these will stretch it out the plateau (know this)
What causes arrythmias?
Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse propagation.
What is the aim of arrythmia therapy
- The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement
- Antiarrhythmic drugs decrease the automaticity of ectopic pacemakers more than that of the SA node.
Lower the ability for abnormal pacemakers to fire on it’s own
What is a problem with arrhythmia therapy
Can cause blocks if you slow too much
and other cells can take over, and become the pacemakers themselves
What is the overview of how antiarrhtmics work?
Phase 4 (works on potassium)
Phase 1 (sodium)
Phase 3 (potaassium going out)
Decrease phase 4 slope
increase threshold
Increase maximum diastolic potential
increase actional potential duration
What are the 4 classes of drugs?
- class I drugs that block fast sodium channels
- those that are beta blockers (class II)
- those that block potassium channels (class III)
- those that are calcium channel blockers (class IV)
What are the class of CCB we use for arrhythmia
non-dihydropyrodine
verapmil
ditalzem
Class I antiarrythmias
Ia: quinidine, procainamide, disopyramide
Ib: lidocaine, mexiletine
Class IA MOA
prolongs ventricular depolarization and repolarization (prolongs the QT)
Class IB MOA
Mild effect
Work better on ischemic tissue (scar-mediated - during a heart attack)
small quick attachment and release - no prolong QT
Class IC MOA
Good block with a fast release
Widens QRS (depolarization)
Does not effect plateau and repolarization - so no prolong QT
Qunidine problems
QT prolongation
Can lead to Torsades
Works on SA and AV nodes - so you can cause other arrythmias
SE of qunidine
N/V/D
CYP3A4
Procainamide
Does not have anticholinergic activity of quinidine
for Wide complex SVT if stable
Widens QT
Lupus drug reaction,
Disopyramide use
for restrictive cardiomyopathy
negative iontropic property - so it relaxes myocardium
not used for weak hearts
Anticholinergic effects
Do we ever use class Ia?
NEVER pretty much
Class IB Lidocaine
typically used for numbing - it is injectable
but it is used for MI with constant V tach
Lidocaine CI
Liver failure
Lidocaine SE
CNS effects of dizziness, paresthesia, disorientation, tremor, agitation, seizures and respiratory arrest
Class IB mexiletine
It is a pill
Typically sent on home in place of lidocaine to control their arrythmias
typically for scar-mediated
often a combo drug
Mexiletine SE
N/V
major neurologic - same as lidocaine
Class IC Flecainide
Slows velocity and widens QRS (not QT)
Indication of Flecainide
afib/flutter
heart is completely fine otherwise - NOT for heart with other effects
SE of flecainide
Neuro
SE of propafenone
Same effect as flecanide, but the SE is metallic taste
Class II
BBs
What is the MC used BB
metoprolol
not a good anti-HTN, because it does not reduce HR that much
What BB do you use IV
esmolol because it is short acting
Indications of BB
ventricular dysrhythmias, as well as supraventricular dysrhythmias
works on SA node and AV node
Low level of efficacy - mainly used to control HR as a whole
SE of BB
bradycardia
exercise intolerance (because they are not able to increase HR)
Dizziness
Fatigue
Sexual dysfunction (often not for young folks)
typically used with others
What does class III lead to
Widen QRS and prolong QT
need to worry about other QT prolonging drugs
What psych med can you not be on for class III?
Lexipro = no
MC class III drug
amiodarone
MOA of amiodarone
Works on ALL cardiac cells, all 4 classes
Primarily a K+ channel blocker
Effect of amiodarone
Used for anything except slow HR
No negative iontropic effect (can use for low EF)
CI of amiodarone
NO cardiac contraindications!
amiodarone halflife
LOTS of SE because it has a super long half-life of 28 days because it breaks down and deposits everywhere
- takes 10 grams of amiadrone to be therapeutic
-need a few weeks to get fully loaded on amiadorone
if you wanna switch drugs, you need to be off for at least a month!
SE of amiodarone for pulm
Pulm toxicity: annual lung exam (PFT or CXR) to make sure there is no interstitial fibrosis. Stop immediately especially if acute
SE of amiodarone for thyroid
MC SE = hypothyroidism (because of iodine)
need to scan TSH levels
Hypothyroidism = still stay on
Hyperthyroidism = change
SE of amiodarone for eyes
Deposits in eyes (only need to stop if it effects visual field or if there is neuropathy/neuritis)
Need annual eye exams
SE of amiadaone for GI
Livertoxicity
need LFTs
SE of amiadaone for neuro
tremors, peripheral neuropathy, insomnia
stop if these appear
SE of amiadaorone for derm
blue/gray
typically men, refuse to wear a hat
sunscreen needs to be on
look like papa smurf
DDI for amiadarone
Potent CYP 3A4 inhibitor
can raise digoxin
Warfarin
Overview of amiadrone
Works very very well, but TONS of SEs over time
good for older patients because they will likely die before the SEs
Not good for patient with bad compliance
Sotalol Class III
BB properties (not a BB though)
effects contractility
Not something you hold and restart
QT prolongation
CI of sotalol
Not for LV dysfunction because it decreases contractility
When to discontinue sotalol
Discontinue if QT interval > 550 ms
Avoid combining with other QT prolonging drugs
SE of sotalol
BB SE
Monitoring of sotalol
Need to monitor for QT prolongation before they leave the hosptial (for like 24-48 hours)
Dofetilide major concern
QT prolongation
other SEs are not
Dofetilide monitoring
6 doses (2 doses a day) for three days
need to monitor EKG for QT prolongation
What can be used for HF
dofetilide and amiodarone
Dofetilide clearance
Renally cleared, so do not use in patients with CrCl < 20 mL/min
Dronedarone
like amiodarone (does not work as well)
not used for Heart failure
not used with liver usages
bradycardia
QT prolongation
does not have pulm or thyroid toxicity seen in amiodarone
Ibutilide (Corvert) only inditaion
Only for afib/flutter cardioversion
can cause tarsades
electrolytes need to be normal
2 CCB used for antiarrythmias
Verapamil and dilatezam
not for LV dysfunction (HF)
Digoxin MOA
AV node block by blocking Ca2+ and has cholinergic properties
Indication of digoxin
slowing the ventricular rate in afib/flutter, as well as terminating reentrant arrhythmias involving the AV node
Major EKG changes of digoxin
Diffuse PR prolongation and ST segment depression not better explained by LBBB, LVH
leave them on their digoxin
Digoxin administeration
IV or oral
gut flora helps stop toxicity, so if there is meds that effect flora, there could be toxicity
How long does it take to clear dig?
36 hour half-life
When do you need to lower dose of digoxin?
Amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, and flecainide decrease digoxin clearance - so you need lower dose
Also renal insufficiency - as it is renally cleared
Digoxin toxicity
Any arrhythmia (which is why it can lead to a paradoxical increased HR)
Orange/yellow vision
GI effects N/V/D
Adenosine MOA
Activates potassium
Blocks AV node to reset SVTs
allows SA node to take over and become the pacemaker
short half life (<10 seconds)
DOES NOTHING FOR THE ATRIA
SE of Adenosine
Chest discomfort, dyspnea, flushing, and headache
Atropine MOA
Speeds everything up
parasympatholytic drug that enhances both sinus nodal automaticity and AV nodal conduction through direct vagolytic action
shortens AV node pause
Use of atropine
SYMPTOMATIC bradycardia
works for a few minutes
they need to be actively DYING
If someone becomes tachycardiac with an MI, what do you do with atropine?
May worsen it
What can Mobitz type II lead to?
third degree AVB
