1. Pharmacology in Nursing Antidysrhythmic Drugs

2. Conditions Causing Dysrhythmias
CAD MI
Cardiac Surgery
Valvular disease
Hypoxia
Electrolyte imbalance
Acid/Base imbalance
Hypovolemia
External forces
Disturbances result of abnormally functioning cardiac cells.

3. Antidysrhythmics Dysrhythmia Antidysrhythmics
Any deviation from the normal rhythm of the heart
Antidysrhythmics
Drugs used for the treatment and prevention of disturbances in cardiac rhythm

4. Cardiac Cell
Inside the resting cardiac cell there exists a net negative charge relative to the outside of the cell
This difference in the electronegative charge results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane
Resting membrane potential (RMP)
This net negative charge is referred to as the resting membrane potential.

5. Resting Membrane Potential (RMP)
An energy-requiring pump is needed to maintain this uneven distribution of ions
Sodium-potassium ATPase pump

6. Uneven distirbution is known as polarization.
Each ion moves primarly through its on specific channel which is a specialized protein molecule that sits across the cell membrane.
Proteins work continuosly to resotre the specific the specific intracellular and extracellular concentrations of each ion.
At RMP the ionic concentration gradient ( distribution) for the different ions is such that K is more jighly concentrated inside ( intracellularly) and Na Ca extracellularly.
NA K ATPase pump energy requiring ionic pump. Energy comes from moecule ATP ( adenosine triphosphate) .

7. Action Potential
A change in the distribution of ions causes cardiac cells to become excited
The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading across the cardiac cells
This electrical impulse leads to contraction of the myocardial muscle
Results in excitation of cardiac muscle fibers, weak electrical current
Action potential occur such as SA node, AV node His-Purkinje fibers.
All of these tissues have property of spontaneous electrical excitability known as automaticity. Excited state creates action potential which in turn creates action potentials which in turn generates electrical impulses that travel through myocardium ultimately to create the heartbeat via contraction of cardiac muscle ffibers.

8. Action Potential (cont’d)
Four phases
The SA node and the Purkinje cells each have separate action potentials
Phase 0: resting cardiac cell membrane suddenly becomes highly permeable to sodium ions which rush in through sodium channels. This discruption known as deppolarization: temporary equalization of positive and negative charges across cell membrane. This release spurts spurts an electrochemical enerfy that drive the resulting electrical impulse through adjecaent cells.
Phase 1: the action potential begins a rapid process of repolarization, Na ions close
Phase 2: Ca ions slow channels, K ions flow from inside to outside to offset elevated positive charge from the Ca and Na ions.
Phase 3: Na and K pump working to reestablish baseline polarized state.
3,4 continue

9. 3 Types of Electrical Current
Resting Membrane Potential: Sodium Potassium Pump activated, membrane is relatively permeable to K+, but much less to Na+ and Ca+
Depolarization: cell membrane suddenly becomes permeable to sodium, sodium enters cell, sharp increase in positivity, potassium migrates outside of cell
Repolarization: re-establishment of resting membrane potential

10. Four Phases to Action Potential
Phase 1: Fast sodium channel closes ; period of repolarization begins
Phase 2: Calcium ion influx occurs through slow channels
Phase 3: Potassium ions flow outward, cell is repolarized to baseline
Phase 4: Resting membrane potential

11. Variation in time periods.
RMP different SA: -50/-60 slow channel
Purkinje:
Less negative closer to zero the slower the upstolr velocity/
Steeper slope faster conduction. Purkinje fast response cells.
Many antidysrhymic drugs affect RMP which influences rate of conduction.
Slow channel blockers: Ca channels drugs affect calcium channel blockers affect calcium ion movement SA/AV node.

12. Action Potential Duration
Absolute or effective refractory period
Relative refractory period
Threshold potential
Automaticity or pacemaker activity
0-4 APD
0-midway phase 3 ERP
During ERP cardiac cell cannot be restimulated to depolarize and generate another action potential.
During RRP remainder of phase 3 to RMP phase 4 cardiac cell can be deplolarized again if it recevies and powerful impulse such as pacemaker ( electtrical ) or drug therapy.
TP spontaneous depolarization automaticity or pacemaker, normal when occurs in the SA node. When occurs elsewhere dysthymia occurs. SA node natural pacemaker: intrinsic rate of depolarition or beats per minuts. AV node: 40-60

13. APFD action potential duration
ERP: Effective refractory period
RRP relative refractory period

14. Electrocardiography ECG or EKG P wave PR interval QRS complex
ST segment
T wave

15. P wave: spontaneous impulse generation in the SA node followed immediatley by depolaraization of the atrial myocardial fibers and their muscular contraction.
QRS complex: depolarazation and contraction of the ventricular fibers
J point start of ST segment which corresponds to the beginning of ventricular repoarization
T wave completion of repolrazation of ventricular fibers
U wave not always present believed to be repolarzation of Purkinje fibers.

16. Common Dysrhythmias Atrial dysrhythmias Supraventricular dysrhythmias
Ectopic foci
Conduction blocks
Ectopic: occur outside the conduction system ( atrial or ventricular cells)
Conduction blocks: dysrhtumias that involve disruption of impulse conduction between atrial and venticle through the AV node and may also originate in the HIS-Purkinje system

17. Supraventricular Dysrhythmias

18. Ventricular Dysrhymias

19. Ventricular Fibrillation

20. Premature Ventricular Contractions

21. Atrial Fibrillation
Most concerning is throwing of clot to brain = stroke
WPW= wolf parkinson white syndrome, ectopic impulses begin near AV node bypass AV node and reach the His purkinje system before the normal AV –geneerated impulses,

22. Atrial Fibrillation with Rapid Ventricular Response

23. Bradycardia & Heart Blocks
Varying levels of disrupted conduction of impuslses from the AV node and HIS purkinje system to the ventricls.
Bradycardia, first degree hear bolck

24. Vaughan Williams Classification
System commonly used to classify antidysrhythmic drugs
Based on the electrophysiologic effect of particular drugs on the action potential

25. Vaughan Williams Classification (cont’d)
Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
Other

26. Vaughan-Williams Classification
Basic Mechanism
Comments I
Sodium-channel blockade
Reduce phase 0 slope and peak of action potential IA
-moderate
Moderate reduction in phase 0 slope; increase APD, increade ERP IB
-weak
Small reduction in phase o slope IC
-strong
Pronounced reduction in phase 0 slope II
Beta-blockade
Block sympathetic activity, reduce rate and conduction
III
Potassium-channel blockade
Delay repolarization, increase action potential IV
Calcium-channel blockade
Block L-type calcium channels, reduce rate and conduction, most effective at SA & AV nodes
Chart page 339 very helpful.

27. Vaughan Williams Classification: Mechanism of Action
Membrane-stabilizing drugs
Sodium channel blockers
Divided into Ia, Ib, and Ic drugs, according to effects (weak to strong)

28. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class Ia: quinidine, procainamide, disopyramide
Block sodium (fast) channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome
Procainamide side effect 30% of patients on long term theraoy lupus erthematosus –like syndrome, GI problems, and more…..contraindicated in pt with complete heart blocl, 2nd or 3rd degree HB.
Quinidine can cause cinchonism such as tinnitus loss of hearing slight blurring of vision may occur.
Disopyramide side effect dry mouth.

29. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class Ib: mexiletine, phenytoin, lidocaine, tocainide
Block sodium channels
Accelerate repolarization
Increase or decrease the APD
Used for ventricular tachyarrhythmias only
Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation
Many characteristics with class Ia but are grouped together because they act preferntially on ischemic myocardial tisse
Lidocaine one of the most effective for ventricular dysthymias, Because of extensive hepatic metabolism doasge reduction by 50% recommended for patients in frank liver failure or cirrhosis. May also be necessary for patients with renal impairmnet due to excretion. Lidocaine reasiede the ventricular fibrillation threshold. Does this by increasind the sensitivity of the cardiac cell membrane to impulses decreases automaticity, many effects by blcoking sodium channels. Lidocaine is the drug of choice for treating acute ventricular dysrhymias associated with MI. Significant side effects: CNS toxicites-confusion.

30. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class Ic: flecainide, propafenone , moricine
Block sodium channels (more pronounced effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter, Wolff-Parkinson-White syndrome, supraventricular tachycardia dysrhythmias
Marked effect on conduction.
Cardiac arrhythmia supression trial ( CAST) conducted by National heart lung and blood institute changed labeling only for documented life threatening ventricular dysthymias.

31. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class II: b-blockers: atenolol, esmolol, metoprolol, propranolol, nadolol, sotalol
Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system
Depress phase 4 depolarization
General myocardial depressants for both supraventricular and ventricular dysrhythmias
Also used as antianginal & antihypertensive drugs
Cardioprotective quality
Reduced HR, delayred AV node conduction reduced myocardial contractility, decreased myocardial automaticity.
Very benficial after MI because catelcholamines released during MI cuases heart to be hyperirritable predisposed to dysrhymias.

32. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class III: amiodarone, sotalol,* ibutilide, bretylium
Increases action potential
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
*Sotalol also exhibits Class II properties

33. Drug to Know: Amiodarone (Cordarone)
Classification: Antiarrhythmics (class III)
Indication: Life-threatening ventricular arrhythmias , part of ACLS protocol
Action: Prolongs action potential, slows sinus rate, prolongs QT interval, suppresses arrhythmias
Side Effects: Dizziness, fatigue, pulmonary fibrosis, CHF, bradycardia, hypotension, hypo or hyperthyroidism, nausea, vomiting, constipation, anorexia, corneal microdeposits, photosensitivity
Clinically one of the most effective. Effective in 40-60% of patients. Very lipophilic+ fat loving can penetrate and concenrate in the adipose tissue also iodine in the chemical structure. Thyroid gland sequesters idodine from the diet can case hypo or hyper thyroidism.
Approximately 75% of pateints treated with drug have side effects.
Mose serious pulmonary fibrosis= 10%.
Long half life=many days

34. Amiodarone Nursing Assessment
Monitor ECG continuously during IV therapy
Monitor for QT prolongation
Assess for signs of pulmonary toxicity
Assess for signs of thyroid dysfunction
Monitor BP for hypotension
Regular ophthalmic exams for oral route
Monitor for neurotoxicity

35. Vaughan Williams Classification: Mechanism of Action and Indications (cont’d)
Class IV: verapamil, diltiazem
Calcium channel blockers
Inhibit slow-channel (calcium-dependent) pathways
Depress phase 4 depolarization
Reduce AV node conduction
Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter
Also used for HTN, most commonly for dysthymias above the vetricle.
Prolonging refractoriness of AV node , block and slow inward flow of calcium ions into the slow Ca channels. Litltle effect on ventricles.
Cardizem commonly used for arial fibrillation or flutter
Cardizem contraindicated acute MI, hypersens and more….

36. 3 Classes of Calcium Channel Blockers
Dihydropyridines
amlodipine (Norvasc)
nicardipine (Cardene)
nimodipine (Nimotop)
Non-dihydropyridines
Verapamil (Calan)
Diltiazem (Cardizem)

37. Vaughan Williams Classification: Other Antidysrhythmics
digoxin, adenosine
Have properties of several classes and are not placed into one particular class

38. Unclassified Antidysrhythmic
adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds
Other adverse effects minimal

39. Adenosine Injection

40. Antidysrhythmics: Adverse Effects
ALL antidysrhythmics can cause dysrhythmias!
Hypersensitivity reactions
Nausea
Vomiting
Diarrhea
Dizziness
Blurred vision
Headache

41. Nursing Implications Obtain a thorough drug and medical history
Measure baseline BP, P, I&O, and cardiac rhythm
Measure serum potassium levels before initiating therapy

42. Nursing Implications (cont’d)
Assess for conditions that may be contraindications for use of specific drugs
Assess for potential drug interactions
Instruct patients regarding dosing schedules and adverse effects to report to physician

43. Nursing Implications (cont’d)
During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, heart and lung sounds
Assess plasma drug levels as indicated
Monitor for toxic effects
Nursing dx: risk for injury.

44. Nursing Implications (cont’d)
Instruct patients to take medications as scheduled and not to skip doses or double up for missed doses
Patients who miss a dose should contact their physician for instructions if a dose is missed
Instruct patients not to crush or chew any oral sustained-release preparations

45. Nursing Implications (cont’d)
For class I drugs, monitor ECG for QT intervals prolonged more than 50%
IV infusions should be administered with an IV pump
Solutions of lidocaine that contain epinephrine should not be given IV—they are to be used ONLY as local anesthetics

46. Nursing Implications (cont’d)
Ensure that the patient knows to notify health care provider of any worsening of dysrhythmia or toxic effects
Shortness of breath
Edema
Dizziness
Syncope
Chest pain
GI distress
Blurred vision

47. Nursing Implications (cont’d)
Patients taking b-blockers, digoxin, and other drugs should be taught how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose of medication

48. Nursing Implications (cont’d)
Monitor for therapeutic response
Decreased BP in hypertensive patients
Decreased edema
Decreased fatigue
Regular pulse rate
Pulse rate without major irregularities
Improved regularity of rhythm
Improved cardiac output

49. Nonpharmacologic Treatment of Cardiac Dysrhythmias
Pacemaker
Catheter Ablation
Direct current cardioversion
Implantation of AICD