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115 Cards in this Set

  • Front
  • Back
What is the normal pacemaker in the heart? What is the normal number of impulses generated per minute?
Sinoatrial Node = SA node

60-100 impulses/min
Describe the conduction impulse through the heart
1. SA node generates impulse

2. SA node impulse spreads thru atria to enter AV node
-Conduction slows to allow time for Atrial contraction to propel blood into the Ventricles

3. AV node -> Bundle of His -> Bundle Branches -> Purkinje system
What is SA node activity regulated by?
Reciprocal changes in:
1. Sympathetic stimulation thru Beta-adrenergic receptors
-increases HR, Contractility, & Ventricular Pressure
2. Parasympathetic inhibition thru Muscarinic receptors
Describe the K+ ion concentration in the heart

Describe the Na+ concentration

What are the ion gradients maintained by?
K+ is higher inside the cell = promotes outward movement

Na+ is higher extracellularly

Na+/K+ ATPase = Na+ out/K+ in
Describe the electrical charge at REST or during DIASTOLE
Electrical charges are not flowing
1. the cell is negatively charged inside & positively charged outside so that the Sarcolemma is polarized

2. Na+ does not enter, despite the substantial concentration gradient for Na+, b/c sodium channels are closed

3. K+ ions cross (b/c Sarcolemma is highly permeable to K+) leaving unbalanced negative charges that make the cell negative inside with a resting transmembrane potential of -85 mV
Explain the Voltage-gated Ion Channels
1. "gates" control the diffusion of each ion thru specific ion channels on the cell membrane
2. Ion channels change from 'closed' to 'open' state to allow highly selective pathways
3. opening & closing of each channel is controlled by 2 or more gates operated by voltage changes for Na+ & Ca+ which can enter the cell only when both gates are open
4. with ACTIVITY as the myocardial cells contract, ion movements will cause polarity to become reversed
-Sarcolemma becomes depolarized & transmembrane potential is elevated from -85 mV to 0
-channels open allowing Na+ & Ca+ to enter, while K+ leaves the cell
How many phases does the Cardiac Action Potential have?
5 Phases
-Phase 0 = rapid upstroke = voltage-gated Na+ channels open
-Phase 1 = initial repolarization = inactivation of voltage gated Na+ channels; voltage-gated K+ channels begin to open
-Phase 2 = Plateau = Ca++ influx balances K+ efflux; Ca++ triggers Ca++ release from Sarcoplasmic Reticulum & myocyte contraction
-Phase 3 = rapid repolarization = massive K+ efflux due to opening of voltage-gated Slow K+ channels & closure of Ca++ channels
-Phase 4 = Resting Potential = high K+ permeability thru K+ channels
Ionic changes in Pacemaker cells during which phase cause spontaneous depolarization?
Phase 4
What places have latent pacemaker activity?
SA node, AV node, & Purkinje fibers b/c they have Phase 4 slope
What does a steeper Phase 4 slope mean? List the order of steepness
Steeper slope = higher automaticity = higher HR

SA node > AV node > Purkinje cells
This ECG wave forms as depolarization spreads from the SA node thru both atria
P wave
At the AV node conduction slows considerable to produce the interval between these 2 waves on the ECG
P & Q waves = PR interval
Conduction thru His-Purkinje fibers accelerates to produce what?
Small Q wave on reaching the septum & QRS deflection spreading thru the Left Ventricle
Ventricular Repolarization follows until the end of what wave?
T wave = Ventricular repolarization
QRS duration = ?
time required for ventricular activation = ventricular depolarization
QT interval = ?
duration of ventricular action potential = mechanical contraction of the ventricles
What is the most useful noninvasive method available for diagnosing arrhythmia & evaluating effects of Antiarrhythmic drugs?
How are Cardiac Arrhythmias classified?
Supraventricular = SA node, atria, or AV node origination

Ventricular = originating in the ventricles
Cardiac Arrhythmias cause heart rates to become irregular, too fast, or too slow due to abnormalities in?
1. Site of impulse generation
2. impulse rate or regularity
3. impulse conduction
When do Cardiac Arrhythmias frequently occur?
25% of patients treated with Digoxin

50% of anesthetized patients

85% of pts with Acute MI
What is Atrial Flutter?
rates of > 300 bmp often occuring with AV block
What is Atrial Fibrillation?
Atrial beating is asynchronous & P waves are not recognizable

Chaotic & erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes
Ventricular Premature Beats
Discrete identifiable premature QRS complexes found on ECG
Ventricular Tachycardia
A run of atleast 4 consecutive Ventricular Premature Beats
Ventricular Fibrillation = completely erratic rhythm with no identifiable waves
Shown by variations in size & frequeny of ECG deflections, is lethal if it lasts for more than a few minutes
Basic arrhythmogenic mechanisms generally result from disturbances in Automaticity (impulse formation) or disturbances in Impulse Conduction, or combos of both. Automaticity is determined by steepness of the Phase 4 slope...
1) what reduces the steepness?
2) what increases the slope? (3)
1. Vagal stimulation, Beta blockade or CCA's

2. Beta-adrenergic stimulation, Ca++, or Hypokalemia
When will arrhythmias from abnormal automatocity occur?
1. when SA node rates are too fast or too slow

2. AV node & Purkinje cells overcome or usurp the SA node
-latent pacemakers can become 'ectopic' pacemakers by usurpation
Common conduction abnormality in which a cardiac impulse reenters & excites the same pathway repeatedly
Reentry or "circus movement"
What are 3 conditions required for Reentry to occur?
1. conduction has to be blocked by an anatomic or physiologic obstacle creating a circuit around which the reentrant impulse can propagate

2. the block must be unidirectional at some point in the circuit such that conduction is prevented in one direction but allow to proceed in the opposite direction

3. Conduction time around the circuit must exceed the effective Refractory period
Explain Re-entry or Circus Movement
What is the mechanism of Class I Antiarrhythmic drugs?
Block Na+ channels -> elevate threshold for excitation -> inhibit automaticity & conduction velocity -> prolong PR & QRS -> prevent recurrence of reentrant arrhythmias
What drugs are contained within Class IA Antiarrhythmics? What are their actions?
Quinidine, Amiodarone, Procainamide, Disopyramide
"Queen Amy Proclaims Disco PYramid"

Increase Action Potential Duration
Moderate Na+ channel block
What drugs are contained within Class IB Antiarrhythmias?
Lidocaine & Mexiletine

No effect on Action Potential Duration
Mild Na+ channel block
What drugs are contained within Class IC Antiarrhythmics?

minimal effect on Action Potential Duration
marked Na+ channel block
What drugs are contained within Class II Antiarrhythmias?

What is their mechanism of action?
Beta blockers = Propranolol + Timolol + Esmolol + Metoprolol + Atenolol

Decrease Heart Rate & Contractility
What drugs are contained within Class III Antiarrhythmias?

What is their mechanism of action?

Block K+ channels to prolong Action Potential Duration & Effective Refractory Period
What are the Class IV Antiarrhythmics?
CCA's = Verapamil + Diltiazem + Bepridil
What effects does Quinidine possess (Class IA)?
1. Slows upstroke of the action potential by blocking Na+ channel
2. Slows conduction
3. Prolongs QRS duration, PR interval, & QT interval on the ECG
What are the uses of Quinidine (Class IA)?
Maintaining Sinus Rhythm in Atrial Flutter or Fibrillation

**"When I Dine" (QUINIDINE) I don't get Atrial Flutter or Fibrillation**
What are the 2 Antiarrhythmic mechanisms of Quinidine?
1. Mainly by blocking activated Na+ channels -> reduce automaticity especially on ectopic pacemakers

2. Block K+ channels to prolong Action Potential Duration; Longer APD reduces Reentry frequency & Tachycardia
What are the side effects of Quinidine? (5)
1. Blocks Alpha-adrenergic receptors to cause:
-Vasodilation -> marked hypotension -> Reflex tachycardia

2. Blocks Muscarinic receptors
-can overcome its direct myocardial effects to result in faster AV conduction
-in pts with Atrial Fibrillation or Flutter the vagal inhibition can accelerate AV node conduction to increase Ventricular rate & cause Paradoxical Ventricular Tachycardia

3. GI = NVD
-Cinchonism = Headache, dizziness, tinnitus

4. Increases plasma Digoxin & can precipitate Digoxin toxicity

5. Syncope may occur due to Torsade de Pointes
What is Cinchonism? What antiarrhythmic can cause it?
Headache + Dizziness + Tinnitus

What is Torsade de Pointes? How is it manifested on the ECG?
Atypical Ventricular Tachycardia

Wide & narrow QRS complexes
What predisposes to Torsade de Pointes?
changes in Na+ or K+ channels -> changes in Phase 2 of the action potential -> PROLONG QT interval & Action Potential Duration

Occurs when the Potassium Channel gene (HERG) is blocked by Antiarrhythmic drugs (quinidine, Sotalol) or Electrolyte abormalities (hypokalemia, hypomagnesemia, hypocalcemia)
What can Torsades de Pointes progress to?
Ventricular Fibrillation
Procainamide has weaker ______ activity compared to Quinidine

Ganglion-blocking activity may cause Vasodilation & Hypotension but these effects are less pronounced than those of Quinidine
What is the most troublesome adverse effect of Procainamide with long-term therapy?
Lupus-like syndrome
-Renal lupus
What are the other adverse effects of Procainamide? (other than SLE-like syndrome)
10% = Nausea & diarrhea

>5% = Rash, Fever, or Hepatitis

0.2% = Agranulocytosis = drop in Neutrophils, Eosinophils, & Basophils in the blood
Procainamide is better tolerated than Quinidine when given IV, but it is not useful for long-term oral treatment. Why?
Short half-life & adverse effects
-SLE-like syndrome
What is Procainamide clinically used for?
Orally or Parenterally for Atrial & Ventricular Arrhythmias
List the intensity of Antimuscarinic activity in descending order among the Class IA Antiarrhythmics
Disopyramide > Quinidine > Procainamide

= Disopyramide has most intense Antimuscarinic activity
What is Disopyramide approved for the treatment of?
Ventricular Arrhythmias
Why is Disopyramide not a first-line Antiarrhythmic?
Because its negative Inotropic action may induce CHF even without previous history of myocardial dysfunction
What are the adverse effects of Disopyramide?
Anticholinergic effects
1. Urinary retention (usually in males with enlarged prostate)
2. Dry mouth, blurred vision, constipation
3. Worsening of preexisting glaucoma
What is the mechanism of action of Lidocaine (Class IB)?
blocks both activated & inactivated Na+ channels in Purkinje fibers & Ventricular cells to:
1. elevate excitation threshold & reduce automaticity
2. suppress electrical activity of depolarized arrhythmogenic tissues with minimal effects on polarized normal or atrial tissues
Class I Antiarrhythmic that must be given INTRAVENOUSLY b/c only 3% appears in plasma if given orally due to 1st pass hepatic metabolism
What arrhythmias is Lidocaine effective against?

What arrhythmias is Lidocaine ineffective against?
those associated with Depolarization as in Ischemia (post-MI) or Digoxin toxicity arrhythmias

Normally poralized tissues as in Atrial Flutter or Fibrillation
The least Cardiotoxic of currently used Na+ blockers
-exacerbates Ventricular Arrhythmias in <10% of pts = good
-BUT may precipitate SA node standstill or worsen impaired conduction in 1% of pts with MI
What do large doses of Lidocaine cause in patients with preexisting Heart Failure?
Hypotension by depressing myocardial contractility
What are the most common adverse effects of Lidocaine?
-paresthesias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, & convulsions
When do seizures most commonly occur when given LIdocaine?
After rapid IV administration in Elderly patients
What is Lidocaine mainly used for?
Acute termination of Ventricular Arrhythmias & to prevent Ventricular Fibrillation after cardioversion (=restoration of the heartbeat to normal functioning by the application of electrical shock or by the use of medication)

*DOC for Ventricular problems
Lidocaine analog that is resistant to 1st-pass hepatic metabolism and is effective orally
-elimination half-life of 8-20 hrs allows oral administration 2-3 times daily
What are the predominant adverse effects of Mexiletine?
Neurologic = tremor, blurred vision, lethargy, nausea

"mEXILED" to neurologic ADR's
What is Mexiletine useful in the treatment of?

What is it also used to treat?
Ventricular Arrhythmias

Relief of chronic pain especially that due to Diabetic Neuropathy & Nerve Injury

"mEXILEd" to the VA for treatment neuropathy
When have the Class IC Antiarrhythmics (Flecainide, Propafenone, Moricizine) been found to increase mortality?
From cardiac arrest or Arrhythmic sudden death in patients with recent MI = contraindicated Post-MI
1. Class?
2. Mechanism
3. Use
4. Down side
1. Class IC
2. blocks Na+ & K+ channels without antimuscarinic effects
3. For maintaining Sinus Rhythm in Supraventricular Arrhythmias; effective for suppressing Premature Ventricular contractions
4. may exacerbate arrhythmias in pts with preexisting ventricular tachyarrhythmias or MI
1. Class
2. Mechanism
3. Use
4. downside
1. Class IC
2. blocks Na+ channels & structurally similar to Propranolol with weak Beta-blocking activity
3. For maintaining Sinus Rhythm in Supraventricular Arrhythmias; effective for suppressing Premature Ventricular contractions
4. may exacerbate arrhythmias & cause constipation
Class IC Antiarrhythmic that has a metallic taste

"Propane tastes like metal"
Class IC antiarrhythmic that is a phenothiazine derivative used for Ventricular Arrthymias
What is the mechanism of action of Moricizine?

Down side/ADR
Potent Na+ channel blocker that does not prolong Action Potential Duration

May exacerbate Arrhythmias
Nausea & vomiting
What are Propranolol & Metoprolol most frequently used for? (2)
1. treatment of Supraventricular & Ventricular Arrthythmias caused by Sympathetic stimulation tachycardia

2. to prevent Ventricular Fibrillation
Short-acting Class II Antiarrhythmic used primarily for Acute Arrhythmias occuring during surgery
What are the beneficial effects of Beta blockers due to in the treatment of Arrhythmias?
Diminished Sympathetic activation of heart & blood vessles -> reduced cardiac activity & reduced vasoconstriction -> hypotension & bradycardia -> diminished Cardiac Workload -> reduced Myocardial Oxygen demand

Prevents recurrent infarction & sudden death in patients with Acute MI
What are the harmful effects of Beta blockers as Antiarrhythmics?
1. Negative inotropic effect may induce or worsen CHF in pts with Acute MI or Decompensated Heart Failure

2. CNS penetration -> Insomnia & Depression
What is Amiodarone used for clinically? (4)
1. Serious/Life-threatening Ventricular Arrhythmias
2. Preventing Recurrent Ventricular Arrythmias
3. treatment of Supraventricular Arrhythmias like Atrial Fibrillation
4. adjuvant treatment to decrease uncomfortable discharges of implanted Cardioverter-defibrillators
What are the mechanisms of action of Amiodarone? (3)
1. decreases re-entry by blocking the Potassium Rectifier current to prolong AP duration & QT interval
2. Decreases rate of firing of pacemaker cells by blocking inactivaetd Na+ channels
3. Block Alpha & Beta adrenergic receptors & Ca+ channels & thus inhibit AV node conduction to produce BRADYCARDIA
Class III Antiarrythmic that has relatively high efficacy with low incidence of Torsade de Pointes despite prolonged QT
Explain the Elimination half-life of Amiodarone
Rapid component = 3-10 days (50% of drug)

Slow component = lasts for several weeks

**measurable tissue levels occur even after a year
By what CYP is Amiodarone metabolized?

"Amare Stoudemire wears #34
What drugs inhibit CYP3A4 and therefore increase tissue levels of Amiodarone?
Cimetidine (H2 blocker)

Inhibitors: "Inhibitors Stop Cyber-Kids from Eating Grapefruit
-Grapefruit juice
What drugs induce CYP3A4 and therefore decrease tissue levels of Amiodarone?
Inducers: Queen Barb take Phen-Phen & Refuses Greasy Carbs
-St. John's wort
What drugs does Amiodarone elevate the levels of? How?
Digoxin & Warfarin

inhibits other Liver cytochrome metabolizing enzymes

"Amio loves to Dig Wars"
What are the most important ADR's of Amiodarone? (7)
2. Corneal deposits, reduced visual acuity, & optic neuritis leading to blindness
3. Skin deposits resulting in Photodermatitis = grayish-blue skin discoloration in sun-exposed areas = "smirf skin"
4. Neurologic effects
6. Thyroid dysfunction = hypo or hyperthyroidism
7. Constipation, heart block, CHF, Bradycardia

Amare Stoudemire
-Pulmonary is he in such good shape?
-Corneal does he shoot so well?
-Smirf Skin = photodermatitis
-Neuro defects
-Thyroid dysfunction
What is the mechanism of action of Bretylium?

What are its effects most pronounced in?
Lengthens Ventricular (but not atrial) AP duration & Effective Refractory Period

Ischemic cells
What does Bretylium initially cause?
release of Catecholamines which may be inotropic and cause Ventricular Arrhythmias
Antiarrhythmic available only as an IV bolus for emergency use during attempts at resuscitation from Ventricular Fibrillation when Lidocaine & Cardioversion have failed
Bretylium = Class III
What is the major ADR of Bretylium? How can it be prevented?
Postural Hypotension

Concomitant administration of TCA's such as Protriptyline

**Nausea & vomiting may also occur after IV bolus
**"Bret Winblad" has postural hypotension
Class III non-selective Beta-blocker that also prolong Action Potential Duration & has Antiarrhythmic properties
How is Sotalol formulated?
As racemic mixture of d- & l-isomers
-all Beta-adrenergic blocking activity resides in the l-isomer
-AP prolongation is shared by L-isomer & D-isomer
What are the ADR's of Sotalol?
1. Torsades de Pointes = due to prolonged Repolarization
2. excessive Beta-block
How is Sotalol administered?
100% bioavailability orally
12 hours
unchanged in kidneys
What is Sotalol used for clinically?
1. treatment of life-threatening Ventricular Arrhythmias
2. maintaining Sinus Rhythm in Atrial Fibrillation
3. treatment of Supraventricular & Ventricular Arrhythmias in PEDIATRICS
What is the mechanism of action of Dofetilide & Ibutilide?
block the rapid component of the Delayed Rectifier Potassium current to slow cardiac repolarization
What are the clinical uses of Dofetilide & Ibutilide?
Effective for restoring Normal Sinus Rhythm in Atrial Fibrillation or Flutter
What are the common side effects of Dofetilide & Ibutilide?
Prolonged QT & Torsades de Pointes
Which CCA is not used as an Antiarrhythmic? Why?

b/c it is likely to cause Reflex Tachycardia due to pronounced Vasodilation
Which CCA's are used as Antiarrthymics?

What is their mechanism of action?
Verapamil & Diltiazem

Block L-type Ca++ channels in Myocardium = depress SA & AV nodes directly to:
1. decrease contractility
2. reduce SA node automaticity
3. slow AV node conduction
What are the oral CCA's used for?
Supraventricular & Ventricular Arrhythmias
Nucleoside normally formed by dephosphyrlation of ATP then metabolised by Adenosine Deaminase to form Inosine
What 2 receptors does Adenosine act on?
A1 in myocardium -> negative inotropic, chronotropic, & dromotropic

A2 in Endothelium & Vascular Smooth Muscles -> Coronary Vasodilation
What mechanism does Adenosine possess?
Enhances K+ conductance (Hyperpolarizing effect) & inhibits Ca++ influx -> prolonged AV node refractory period and slowed conduction
What is Adenosine the current drug of choice for?
Rapid IV injection for converting Paroxysmal Supraventricular Tachycardia to Sinus Rhythm
-highly efficient & very short acting
What are some ADR's of Adenosine?
Shortness of breast or chest burning
What is Magnesium Chloride or Sulfate used to treat?
1. prevention of Torsades de Pointes

2. Digoxin-induced Arrhythmias
What can Hypokalemia produce?
Ectopic pacemaker activity especially during Digoxin treatment
What do Potassium administration antiarrhythmic effects result from?
Increasing K+ ions -> hyperpolarization -> lowered Phase 4 slope -> decreased Automaticity
What are the 2 types of benefits of Antiarrhythmic therapy which are both difficult to establish?
1. Reduction in Arrhythmic symptoms like palpitations, syncope, or Cardiac arrest

2. reduction in Long-term mortality in asymptomatic pts
What do all Antiarrhythmic drugs have a narrow range of?
Margin of Safety
-ration b/w Therapeutic vs. Toxic doses varies widely from one patient to another;
In general, what strongly influences the Antiarrhythmic drug response?
The heart condition causing the Arrhythmia
-pts with defective impulse conduction are at greater risk for developing AV block during treatment with Quinidine than those whose impulse conduction is normal
Increased mortality from Cardiac Arrest or Sudden death in patients with recent ________ has occured with almost all Antiarrhythmic drugs, and only _________ have been shown to reduce mortality

Antiarrhythmic contraindicated in Prostatism
Disopyramide = causes urinary retention due to marked Anticholinergic activity
Antiarrhythmic contraindicated in Chronic Arthritis
Procainamide = causes lupus-like syndrome
Antiarrhythmic contraindicated in Advanced Lung Disease
Amiodarone = causes Pulmonary Fibrosis