Antiarrhythmics Flashcards
Cardiac cell membrane electrical activity is determined by which ions?
sodium
potassium
calcium
(chloride)
What path does a cardiac electrical impulse follow?
SA node
internodal tracts
AV node
Bundle of His
L and R bundle branches
Purkinje fibers
Stellate ganglion blocks knock out what important cardiac feature? What level?
cardiac accelerators
T4
Describe “arrhythmia”
electrical impulses/cardiac depolarization that deviates from the normal pathway in site of origin, rate or regularity, or conduction pathway
Which ion regulates resting potential?
K+
When are cells most permeable to Na+?
at the start of an action potential
(most cells are impermeable to Na+ at rest)
During which period of repolarization is an action potential least likely to fire?
absolute refractory period
Summarize what happens during Phase 0 of a ventricular action potential:
- threshold potential is reached
- gates open, Na+ enters the cell
- permeability to K+ decreases
- fast depolarization
- very brief
Summarize what happens during Phase 1-2 of a ventricular action potential:
- depolarization peaks (+30mV)
- repolarization slowly starts
- Na+ influx stops
- Ca2+ influx starts
- K+ moves OUT
- Cl- moves IN
Summarize what happens during Phase 3 of a ventricular action potential:
- fast repolarization
- K+ moves OUT faster than Na+ and Ca2+ move in
- @ end of phase 3: cardiac cells will respond to a stimulus greater than normal intensity
Summarize what happens during Phase 4 a ventricular action potential:
- resting potential reaches repolarized state (-90mV)
- Na+ constantly leaking out
- diastole occurs
Describe the ion changes during each phase of the ventricular action potential:
Phase 0: Na+ in
Phase 1: Cl- in, K+ out
Phase 2: Ca2+ in
Phase 3: K+ out faster than Na+ and Ca2+ in
Phase 4: Na+ leaking out constantly
Is the concentration of Na+ inside cardiac cells higher or lower than the concentration outside the cells?
lower inside (Na+ wants to move in)
Is the concentration of K+ inside cardiac cells higher or lower than the concentration outside the cells?
higher inside (K+ wants to move out)
Is the concentration of Ca2+ inside cardiac cells higher or lower than the concentration outside the cells?
lower inside (Ca2+ wants to move in)
What is the resting membrane potential of a pacemaker/nodal cell?
-60mV
Which ion is not involved in nodal APs?
chloride
Describe ion movement during Phase 0 of the nodal action potential?
- Ca2+ moves in (L-type channels)
Describe ion movement during Phase 1 of the nodal action potential?
trick question - there is no Phase 1
Describe ion movement during Phase 2 of the nodal action potential?
trick question - there is no phase 2
Describe ion movement during Phase 3 of the nodal action potential?
- K+ moves out
Describe ion movement during Phase 4 of the nodal action potential?
- K+ moves out
- Na+ moves in (funny channels)
- Ca2+ moves in (T-type in late stage)
What are the 2 (general) causes of arrhythmias?
1) abnormal pacemaker activity
2) abnormal impulse propagation
List the 4 major mechanisms for antiarrhythmics:
- sodium channel blockade
- sympathetic autonomic blockade
- calcium channel blockade
- prolongation of effective refractory period
What are two causes of bradycardia?
- intra-op hypoxia
- improper ventilation
What are some causes of sinus tachycardia?
- CHF
- hypovolemia
- hypoxemia
- sepsis
- anxiety
Atrial ectopy is often due to:
poor oxygenation
What drug can lead to PSVT?
digitalis toxicity
What are some anesthesia-based causes of arrhythmias?
- mechanical stimulation (intubation)
- abnormal ventilation leading to hypercapnia, hypoxia
- anesthetic agents
What are the 3 ways heart rate can be manipulated?
- rate of spontaneous phase 4 depolarization
- threshold potential
- resting membrane potential
What effect does sympathetic stimulation have on the nodal action potential?
faster diastolic depolarization
What effect does parasympathetic stimulation have on nodal action potential?
- lower maximum diastolic potential
- slower diastolic depolarization
- longer action potential duration
(slide 20)
What does the mnemonic No Body Kisses Cats mean?
No - Na+ channel blockers - class 1
Body - beta-blockers - class 2
Kisses - K+ blockers - class 3
Cats - Ca2+ blockers - class 4
What phase of the nodal action potential do sodium channel blockers affect?
phase 0
Drugs with higher affinity for Na+ channels produce (more/less) QT prolongation
more
C > A > B
Describe Class 1A antiarrhythmics:
- lengthen the duration of the AP
- interact, bind, and unbind with Na+ channels
- intermediate affinity for Na+ channels
- produce moderate QT prolongation
- used for WPW
Describe Class 1B antiarrhythmics:
- shorten the duration of the nodal AP
- rapidly interact with Na+ channels
- lowest affinity for Na+ channels
- minimal QT prolongation
Describe Class 1C antiarrhythmics:
- little to no effect on nodal AP
- slowly interact with Na+ channels
- highest affinity for Na+ channels
- significant QT prolongation
What effect do Class 2 antiarrhythmics have on the heart?
reduce adrenergic activity
What effect do Class 3 antiarrhythmics have on the heart?
- prolong the effective refractory period by a mechanism other than or in addition to Na+ channel blockade
- K+ channel blockers
What effect do Class 4 antiarrhythmics have on the heart?
- slow conduction
- increase refractory period
- CCBs
What class does Quinidine belong to and what is its MOA?
- class 1
- binds and blocks activated sodium channels
What effect does Quinidine produce?
- depresses pacemaker rate
- depresses conduction and excitability
- lengthens AP duration (prolongs QT)
*proarrhythmic, dirty drug
What class does Procainamide belong to?
Class 1A
What arrhythmias is Quinidine used to treat?
- paroxysmal AFib/flutter
- PVCs
Which patient populations may experience a prolonged effect of Quinidine?
- hepatic dz
- CHF
What is the metabolite of Procainamide and why is it relevant?
N-acetyl procainamide (NAPA)
relevant because both Procainamide and NAPA are eliminated by the kidneys and renal pts need reduced doses
What is the most important difference between Quinidine and Procainamide?
Procainamide has less prominent antimuscarinic action
this makes it more difficult to counteract the increased ventricular rate response
Procainamide has ganglionic blocking properties. What effect does this have on the body?
- reduced peripheral vascular resistance
- hypotension
What is the most problematic side effect of Procainamide?
lupus-like syndrome characterized by arthralgia and arthritis
What is the dose/onset/duration/half-life of Procainamide?
- dose: 100mg q5min, max 1000mg
- onset: immediate
- duration: 2.5 hrs
- half-life: 3-4 hours (frequent dosing)
What class does Lidocaine belong to and what is its MOA?
- Class 1B (less potent)
- exclusively on inactivated Na channels
What is the agent of choice for suppression of intraoperative VT and VF after cardioversion if the pt has good cardiac function?
Lidocaine
Lidocaine toxicity risk increases with which drugs?
(drugs that decrease liver BF)
- propranolol
- cimetidine
If a large dose of Lidocaine is given to a patient with preexisting HF, what side effect can occur?
hypotension d/t depressed contractility
List the most common side effects of Lidocaine:
- parasthesias
- tremor
- nausea
- lightheadedness
- hearing disturbances
- slurred speech
- convulsions
What class does Flecainide belong to and what is its MOA?
- Class 1C
- potent Na+ channel blocker (ventricular arrhythmias)
- potent K+ channel blocker (atrial arrhythmias)
What medication is known as the “pill in the pocket”?
Flecainide
What class does Propafenone belong to?
Class 1C
This drug has some structural similarities to Propranolol but has only weak B-blocking activity:
Propafenone
Through which route is Propafenone given and what are 2 resulting side effects?
- oral route
SE: metallic taste and constipation
What is another name for Class 2 antiarrhythmics? What is their primary effect?
beta blockers
decrease the rate of spontaneous phase 4 depolarization (rate control)
Which class 2 antiarrhythmics is most commonly administered in the OR? What dose?
Esmolol
dose: 10mg (30?) IVP q5-10min
Hypovolemic patients in the OR should not receive this drug class because it can cause hypotension:
beta blockers
List 3 class 2 antiarrhythmics used in anesthesia:
Esmolol
Metoprolol
Propranolol
Carvedilol belongs to which drug class? What does it do?
technically in Class 2
- alpha and beta blocker
- blocks: K+, Ca2+, Na+
- prolongs AP depolarization
What benefit can prolonged use of Carvedilol have on the heart?
upregulation of Na, K, and Ca channels (beneficial for diseased hearts)
What arrhythmia is Digoxin used to treat?
supraventricular arrhythmias
Describe the effects of Digoxin:
- decreased activity of SA node
- prolonged conduction through AV node
- increased contractility
- decreased myocardial O2 consumption
Synchronized cardioversion performed on a patient with Dig toxicity can result in what? Why?
VFib
releases Ca2+ from the sarcoplasmic reticulum and increases r/f arrhythmias
What class does Sotalol belong to? What is its MOA?
- Class 3
- nonselective B-blocker
- prolongs AP duration
What arrhythmias is Sotalol used to treat?
SVT & ventricular arrhythmias
Which Class 3 antiarrhythmic can result in Torsades de Point? Why?
- Sotalol
- toxicity associated with beta blockade and AP prolongation
Ibutilide is a (Class 1/2/3/4) drug used to treat ______.
- Class 3
- acute onset of AFib or AFlutter
Verapamil belongs to which class? What is its MOA?
- Class 4
- blocks activated and inactivated Ca2+ channels
What are some effects of Verapamil?
- peripheral vasodilation (good)
- AV block (treated with Atropine, B-receptor stimulants, or Ca2+)
- constipation
- nervousness
- peripheral edema
Verapamil is extensively metabolized by which system?
liver
Which drug is used to treat reentry SVT?
Verapamil
Diltiazem is a (Class 1/2/3/4) drug used to produce which effect?
- Class 4
- arterial vasodilation
Amiodarone is used to treat which arrhythmias?
supraventricular and ventricular arrhythmias
What is the MOA of Amiodarone?
- very effective Na+ channel blocker (low affinity for activated channels; prefers inactivated)
- blocks K+ channels (lengthens AP duration)
- weak CCB
- noncompetitive inhibitor of B-receptors
List the intended effects of Amiodarone:
- slows sinus rate and AV conduction
- prolongs QT
- prolongs QRS duration
- increases atrial, AV nodal, ventricular refractory periods
- antianginal effects
Describe how Amiodarone produces antianginal effects:
- noncompetitive alpha and beta blocking effects
- Ca+ blocking in coronary arterial smooth muscle
What are the side effects of Amiodarone?
- peripheral vascular dilation
- symptomatic bradycardia in pts with sinus or AV node dz
- concentrated in every tissue & organ
- pulmonary fibrosis/inflammation
- reduced drug clearance
Amiodarone can reduce the clearance of which drugs?
- Flecainide
- Procainamide
- Quinidine
- Theophylline
- Warfarin
What is the MOA of Adenosine?
- enhanced K+ conductance
- inhibition of cAMP-induced Ca2+ influx
How does Adenosine reduce HR?
- marked hyperpolarization and suppression of Ca2+-dependent APs
- inhibition of AV nodal conduction
- increased AV nodal refractory period
What are some side effects of Adenosine?
- flushing
- SOB, CP (bronchospasm?)
- HA
- hypotension
- nausea
- parasthesias
Which arrhythmia is Adenosine used to treat?
ONLY confirmed PSVT
What ion channels does Mg influence?
- Na/K ATPase
- Na+ channels
- certain K+ channels
- Ca2+ channels
IV potassium influences both the inside and outside of the cardiac cell membrane. What effects does it have?
- resting potential depolarizing action
- membrane potential stabilizing action
