Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

69 Cards in this Set

  • Front
  • Back
How do we characterize cardiac dysrhythmias?
They are characterized by abnormalities of impulse generation and/or conduction.
Characterizing by impulse generation...
1. The site of impulse generation
- is automaticity occurring at some site other than the SA node?

2. The rate of impulse generation
- if automoticity is coming from the SA node, does it fire too fast or too slow for normal cardiac fxn
Characterizing by impulse conduction...
1. Does the abnormal conduction follow an anatomically defined re-entry pathway?
- Wolff-Parkinson-White (WPW)
- "classical" atrial flutter
- AV nodal re-entry tachycardia = paroxysmal supraventricular tachycardia (PVST) = paroxysmal atrial tachycardia (PAT)

2. Does the abnormal conduction occur b/c the signal can travel through two different pathways?
Questions before you decide to treat w/ drugs.
1. Is the dysrhythmia a physical sign of extracardiac pathology which needs to be corrected?
- atrial fib seen in pts w/ hyperthyroidism

2. Are there predisposing factors which contribute to the genesis of the dysrhythmia?
- hypoK and hypoMg make heart more likely to display abnormal rhythm
- cardiac ischemia
- drugs

3. Abnormalities of the EKG do not always require pharm treatment and may increase mortality

4. Do you really know the nature of the dysrhythmia?
What about non-pharm treatment indications?
1. Re-entry dysrhythmias w/ anatomically defined pathways can be cured by ablation (physical destruction) of the re-entry pathway w/ a catheter

2. Dual-chamber, rate-adaptive pacemakers are implanted to maintain cardiac rhythm in patients with:
- sinus node dysfxn (sick sinus syndrome, brady/tachycardia syndrome, or carotid sinus hypersensitivity
- AV block (symptomatic or nonsymptomatic Mobitz type II)

3. An automatic implantable cardioverter-defibrillator (AICD or ICD) is used for:
- primary prevention cardiac arrest in pts w/ nonsustained ventricular tachy and decreased LV fxn from CAD
- secondary prevention in pts who have survived cardiac arrest
Strategies in treating cardiac dysrhythmias?

2. Block Na channels to decrease phase 4 automaticity or increase threshold potential

3. Block K channels to prolong repol in atria or ventricles; slowing rate of repol increases the ERP and thus prevents early and late-after-depols

3. Control ventricular rate in atrial tachy by decreasing the number of impulses that pass through AV node (decrease conduction velocity and increase ERP of AV node)

5. Block conduction in re-entrant pathways to restore normal rhythm
Vaughn-Williams Class I antiarrhythmic drugs?

1A = quinidine

1B = lidocaine
Vaughn-Williams Class II antiarrhythmic drugs?

Vaughn-Williams Class III antiarrhythmic drugs?
INCREASE EFFECTIVE REFRACTORY PERIOD (partially block the K current)

Vaughn-Williams combined Class II and III antiarrhythmic drugs?
Vaughn-Williams class IV antiarrhythmic drugs?
Other drugs for the treatment of dysrhythmic disorders
Which drugs have been shown to decrease death during long-term treatment?
Quinidine pharmacological action?
- blocks Na channels
- blocks K channels
- blocks a-adrenoceptors
- blocks muscarinic receptors
Quinidine cardiac effects?
- suppresses phase 4 automaticity in fast fibers
- increases threshold potential for depol
- decreases conduction velocity = QRS widens

- prolongs ADP w/ increased length of the ERP in all cardiac tissue, including the AV node = P-R interval increased
- decreases number of impulses passing through the AV node b/c the ERP of the AV node is increased
- Delayed repol of the ventricles = Q-Tc interval is increased

- tachycardia, but initial tachy is eventually attenuated by direct effect to suppress automaticity
- increased AV conduction, but w/ time AV conduction slows due to direct suppressant effect of quinidine
Other CV effects of quinidine?
- blockade of a-adrenoceptors dilates arterioles and venules

- baroreflexly-mediated tachycardia
Therapeutic uses of quinidine?
- control ventricular rate in patients w/ atrial fib or flutter

- suppress PVCs
Adverse cardio effects of quinidine?
- prolongation of Q-T interval precipitates torsade de pointes in 5% of patients (may occur at therapeutic plasma conc)

- large dose can cause ventric tachy

- muscarinic receptor blockade can cause ventricular tachy in pts w/ atrial fib or flutter

- direct effect can cause AV block

- exerts a direct negative ionotropic effect, but usually does not impair CO in patients w/ HF b/c it decreases afterload via blockade of a-adrenoceptors in arterioles

- blockade of a-adrenoceptors causes hypotension and syncope
Other adverse effects of quinidine?
- diarrhea in 30-50% of patients; K loss from chronic diarrhea increases likelihood of torsade de pointes

- cinchonism = headache and tinnitus

- numerous drug-drug interactions; blocks CYP2D6 and also clearance of digoxin
Procainamide MOA?
Blocks Na and K channels, so its cardiac effects are essentially the same as those caused by quinidine

Has much less anticholinergic effect
Therapeutic use procainamide?
-- given i.v. for acute control of ventricular rate in patients w/ atrial fibrillation or flutter (slows AV conduction to decrease ventricular rate)

-- suppress PVCs

-- seldom used for prolonged outpatient therapy due to toxicity
Procainamide pharmacokinetics?
-- metabolized by active metabolite N-acetylprocainamide (NAPA) by acetylation in the liver

-- NAPA blocks K channels (class III activity) and contributes to prolongation of QT interval

-- acetylation follows a bimodal distribution w/ slow acetylators at the greatest rist for drug toxicity
Procainamide adverse effects?
1. hypotension w/ rapid i.v injection

2. torsade de pointes

3. a syndrome resembling SLE which is characterized by arthralgia, arthritis, pericarditis and positive ANA
-- occurs in 23-50% of pts during long-term therapy
**malvar rash (buzz word)
Lidocaine MOA

- blocks Na channels
- Decreases the ERP and APD of fast fibers
Lidocaine cardiac effects?
1. suppresses automaticity (spontaneous phase 4 depol) in partially depolarized tissue (ischemia, digoxin toxicity) w/ little effect on conduction in normally polarized tissue
-- suppresses PVCs!!
-- main use

2. abolishes ventricular re-entry dysrhythmias by causing 2-way blockade of conduction in the area that allows retrograde transmission b/c they inhibit a one-way block

3. increases threshold potential to further suppress automaticity

4. NO EFFECT on AV conduction

5. Essentially no effect on the EKG

6. "stuns" the heart and makes it less likely to respond to other drugs
Therapeutic uses of lidocaine?
-- given by i.v. b/c of extensive first-pass metabolism

1. used selectively to suppress PVCs in pts immediately after MI b/c prophylactic use post-MI increases mortality

2. digoxin induced PVCs

3. ventriculary tachycardia in pts w/ healed MIs

**amiodarone is replacing lidocaine in the ACLS algorithms for ventricular dysrhythmias
Lidocaine adverse effects?
NEURO - usually after rapid i.v. injection

1. CNS depression - slurred speech, nausea, tremor, paresthesias

2. Seizures - treat w/ diazepam
atenolol, esmolol, propanolol MOA?
blockade of cardiac beta-adrenoceptors

-- atenolol and esmolol are cardioselective
-- propranolol is non-selective
B-blocker cardiac effects?
1. suppress catecholamine-induced automaticity
2. reduces conducion velocity and increases the ERP of the AV node

1. increases the ERP in fast fibers when the ERO has been shortened by stimulation of beta-adrenoceptors
2. decrese rate of discharge of SA node
3. P-R interval is increased
B-blocker therapeutic uses?
1. reduces post-MI sudden death by 25-40% by preventing fatal ventricular dysrhythmias, probably ventricular tachy (V Tach)
2. prevents PVCs triggered by physical or emotional stress
3. suppresses the tachycardia caused by hyperthyroidism
4. controls (reduces) ventric rate in pts w/ atrial tachys (fib or flutter)
5. suppresses AV nodal re-entry tachycardia (AVNRT)
6. b/c the blockers don't affect repol, they are the DOC for trtmt of V Tach in pts w. congenitally prolonged Q-T syndrome

B/C of it's short half-life ---- Esmolol is used to control ventricular rate in pts w/ A fib, A flutter, or sinus tachy during cardiac cath
Adverse cardio effects of B-blockers?
1. negative ionotropic effec
d,l-sotalol MOA?
**combined Class II (b-block) and Class III (delays repol)

1. L-isomer causes non-selective, competitive blockade of B-adrenoceptors in both slow (SA and AV nodes) and fast fibers

2. Blockade of K channel delays repolarization
-- outward K rectifier current (IKr) is responsible for termination of the plateau portion of the cardiac AP in fast fibers of the atria and ventricles (NB: K out causes repol or hyperpol)
-- Both the D- and L-isomers inhibit the rapid component of this outward K repol current
-- This effect delays repol and thus increases both the APD and ERP in the atria and ventricles
Cardiac effect of L-sotalol caused by blockade of B-receptors?
1. decreased HR

2. Fewer depol pass through AV node b/c conduction velocity is decreased and the ERP is increased

3. Increases the APD everywhere in the heart, so the ERP is increased everywhere in the heart

4. Decreases catecholamine-induced automaticity everywhere

****See chart on pg 200
Additional cardiac effects due to blockade of outward repolarizing K current by both D- and L-sotalol?
1. An additional increase in the APD and ERP in fast fibers over and above that caused by B-adrenoceptor blockade

2. An additional increase in the ERP of the AV node

3. Delayed ventricular repol increases the Q-T interval
Therapeutic uses for d,l-sotalol?
1. Cardioversion of atrial fib/flutter to sinus rhythm

2. Control (reduce) ventricular rate in pts w/ persistent A fib

3. Chronic therapy is used to prevent life-threatening V.tach and V.fib. Sotalol is used before amiodarone b/c sotalol causes less long-term toxicity. (DOC!)
Adverse cardiac effects of sotalol?
1. Class III action can precipitate torsade de pointes, especially when serum K is low

2. Decreased ventric contractility in heart failure assoc w/ systolic dysfxn via B-adrenoceptor blockade

3. AV block via B-adrenoceptor block
Amiodarone MOA?
***Class III agent which increases ADP and ERP

1. blocks inward Na and outward K channels

2. Non-competitive a- and B-adrenoceptor blockade
Amiodarone cardiac effects?
1. Extremely effective in suppressing automaticity via blockade of Na channels!

2. Blockade of K channels delays repol and thus prolongs the APD and ERP in the atria and ventricles

3. Prolongs the ERP in the AV node; reduces transmission of depol through the AV node

4. Prolongs the P-R, QRS, and Q-T intervals

5. Reduces the rate of firing of the SA node
Therapeutic uses of amiodarone?
1. cardioconversion of A.flutter/fib to sinus rhythm

2. Control (reduce) ventricular rate in patients w. persistent A.fib/flutter

3. Can be given i.v. to terminate life-threatening V.tach and V.fib

4. Chronic therapy used to prevent life-threatening V.tach adnd V.fib

5. NOT the first-line drug for recurrent V.tach and V.fib (sotalol is the DOC)
Special points on the treatment of V.tach and V.fib...
1. Amiodarone is probably more effective than sotalol in preventing reoccurance but is more toxic

2. An automatic implantable cardioconverter-defibrillator (AICD or ICD) is superior to medical tx w/ either of the above drugs, especially when the pt is symptomatic or has a low EF

3. Pts are usually managed w/ "hybrid" therapy consisting of ICD + sotalol. Trtmt w/ sotalol decreases the number of shocks that the patient experiences from the ICD and does not affect the E required to defib

4. Amiodarone is not used w/ an ICD b/c it increases the E req'd for defib by as much as 50%. Increase in E req'd reduces the safety margin btwn defib E and the max E output
Amiodarone pharmacokinetics?
-- Very large Vd (44 +/- 22L/kg) due to avid binding issues throughout the body -- PURPLE MAN

-- half-life of 53 +/- 24days
Adverse cardio effects of amiodarone?
1. severe bradycardia and/or AV block

2. Despite prolongation of the Q-T interval it SELDOM CAUSES torsade de pointes

3. Minimal effect to suppress myocardial contractility in HF
Other amiodarone adverse effects?
1. pneumonitis which may progress to pulmonary fibrosis (5-15%)

2. corneal microdeposits which cause halos in peripheral vision

3. photodermatitis (25%)

4. Some develop slate grey, blue, or purple skin from cutaneous deposits

5. Peripheral neuropathy w/ weakness in proximal muscles

6. Is 37% iodide by weight, and prolonged therapy can result in hypothyroidism (prevents conversion of T4 to T3) or hyperthyroidism (provides iodide for T4 synth)

7. Reducing daily dose, in attempt to decrease adverse S/Es, also decreases efficacy
-- trtmt A.fib is treated w/ 100-200mg/d to reduce toxicity
-- V.tach/fib still requires 400mg dose to be effective
Amiodarone drug-drug interactions?
decreases hepatic and renal clearance of many other drugs
dofetilide MOA?
***pure Class III - given p.o.

1. structurally related to sotalol, but has no B-blocking ability

2. delays repolarization
-- blocks outward repol K current
-- delayed repol increases the APD and ERP in fast fibers ONLY
dofetilide cardiac effects?
1. produces dose-related increase in the Q-T interval

2. No effect of AV conduction

3. No effect on the P-R interval or the width of the QRS
Therapeutic uses of dofetilide?
1. cardioconversion of A.fib and A.flutter of short duration

2. more effective than amiodarone or sotalol, but also more likely to cause torsade b/c prolonged Q-T

3. No negative effect on mortality after MI or in pts w/ CHF
Adverse effects of dofetilide?
1. Torsade de pointes
2. No effect on BP or cardiac contractility

**beneficial AND toxic effect derived from the same pharm effect --> blocking K channels
verapamil, diltiazem MOA?
** Class IV = calcium channel antagonists (CCAs)

-- Blockade of calcium channels in slow fibers, especially the AV node (slow AV conduction to control ventricular rate)
Cardiac effects of CCAs?
1. Decreased HR

2. Decreased conduction velocity in the AV node = increased P-R interval

3. Decreased ERP in the AV node

4. Decreased contractility (dp/dt)
Therapeutic uses CCAs?
1. to control (reduce) ventricular rate in pts w/ A.fib or flutter

2. Converts AV nodal re-entry tachy (AVNRT) to sinus rhythm by blocking the re-entry pathway in the AV node.
-- HR in AVNRT is 140-220bpm w/ narrow QRS complexes
-- B-blockers also effective in AVNRT trtmt
Adverse effects CCAs?
1. hypotension

2. sinus bradycardia

3. heart block
Digoxin MOA?
**also known as digitalis

1. acts centrally to increase efferent vagal nerve activity

2. acts centrally to decrease sympathetic outflow at serum concentrations w/in the therapeutic window (1-2ng/ml)

3. increases dp/dt via partial inhibition Na-K ATPase
Cardiac effects of digoxin?
1. decreased HR
2. decreased conduction velocity in the AV node
3. increased ERP in the AV node

1. increased SV via increased dp/dt
Therapeutic uses of digoxin?
1. control (reduce) ventricular rate in pts w. atrial tachy (fib/flutter) in presence of heart failure caused by systolic dysfxn
-- b/c NO negative effect on CO

2. Increase dp/dt in pts w/ HF from systolic dysfxn
Adverse effects digoxin?
**at serum conc above therapeutic window

1. Inhib Na-K ATPase and increased intracellular Ca can elicit automaticity in fast fibers resulting in PACs and PVCs

2. Sympathetic activity increased

3. ADP and ERP are decreased in persence of excessive intracellular Ca leading to delayed afterdepol triggered by increased symp activity

4. sinus bradycardia

5. AV block (decreased vagal tone + direct depressant effect)
Adenosine MOA?
1. increases K conductance to hyperpol the AV node

2. inhibits ability of sympth stim to increase Ca conductance in the AV node

3. half-life in circulation is about 10 seconds, so actions are short-lived
Cardiac effects adenosine?
1. decreased conduction velocity and increased ERP in the AV node

2. AV conduction momentarily ceases! Yes, the heart stops!
Therapeutic uses of adenosine?
1. diagnosis of AV nodal re-entry tachycardia (PSVT)

2. conversion of AVNRT to normal sinus rhythm (90+% effective)

3. produce coronary vasodilaiton during technetium scan in pts who cannot exercise
If tachycardia DOES NOT go away w/ adenosine...
Then the tachy is VENTRICULAR and not supraventricular
Explain the therapeutic use of adenosine for PVST diag?
block AV node so circular path will go away --> cardioconvert to sinus rhythm --> then give verapamil + B blocker to prevent________________
adverse effects adenosine?
1. transient asystole

2. short-lived, intense burning sensation in the chest

3. flushing

4. dyspnea
Which is the most common dysrhythmia and what is a cause?
Atrial fib

- ischemic heart disease (CAD)
- systolic heart failure
- valvular heart disease

- increased age

All of the above predispose to sustained A.fib
Lack of atrial coordination leads to?
- blood stasis and formation of thrombi in arterial appendages
Patients w/ A.fib are at high risk for?
- ischemic stroke

**must be treated daily w/ warfarin and/or antiplatelet drug (aspirin, ticlopidine)
Two schools of thought on best way to prevent ischemic strokes in pts w/ A.fib?
- conversion AF to sinus rhythm (drugs or DC shock) and continued maintenance of sinus rhythm reduces stroke incidence and need for warfarin therapy

- don't worry about persistant A.fib as long as drugs are used to control (decrease) ventricular rate and warfarin is given daily
Results of AFFIRM study?
1. overall mortality and incidence of disabling stroke, ischemic encephalopathy, cardiac arrest, and bleeding was the same in both groups

2. When compared to rate group, rhythm control group spent more time in hospital, exhibited more adverse drug effects, and experienced more episodes of torsade and bradycardic arrest

** use of drugs to convert AF to sinus rhythm and maintain sinus rhythm does not decrease incidence of stroke; rather, it increases the risk of potentially-fatal ventricular dysrhythmias and adverse drug effects
Thus if chronic A.fib, control _______ by...?

- verapamil
- B-blocker

Has HF
- digoxin (inc vagal tone)
- B-blocker
Cardiac dysrhythmias graph
See below