1. Conduction system
    • SA node - pacemaker of the heart; initiates electrical impulses at a rhythmic rate of 60 - 100 bpm
    • AV node - provides electrical link between atrium and ventricle; can fire 40 - 60 bpm
    • Bundle of His - connects AV node with the two bundle branches
    • Perkinje fibers - special network of fibers in the ventricular myocardium that have intrinsic pacemaker ability at 20 - 40 bpm
  2. Properties of cardiac tissue
    • Automaticity: ability to initiate a spontaneous and continuous impulse
    • Contractility: ability to respond mechanically to an impulse
    • Conductivity: ability to transmit an impulse along a membrane in an orderly manner
    • Excitability: ability to be electrically stimulated
  3. Cardiac waves/segments
    • P wave - atrial depolarization
    • PR interval - spread of impulse through AV node, bundle of His; normally 0.12 - 0.20 seconds; shortens with increase HR
    • Prolonged PR interval - conduction problem above ventricle at AV node
    • QRS interval - ventricular depolarization; normally 0.04 - 0.12 seconds
    • Prolonged QRS interval - ventricular conduction block/defect
    • ST segment - represents early part of ventricular repolarization; ST segment depression represents ischemia or hypokalemia; ST segment elevation represents an MI
    • T wave - ventricular repolarization
    • QT interval - ventricular activity
    • Prolonged QT interval - risk for dysrhythmias
    • EKG graph: small boxes - 0.04 seconds, large boxes - 0.20 seconds
  4. Etiology of arrhythmias
    • Accessory pathways (abnormal path precipitates tachy-arrhythmias)
    • Conduction defects (rhythm coming from somewhere other than normal SA node)
    • MI
    • CAD
    • Myocardial hypertrophy
    • Acid-base imbalances
    • Alcohol (can cause atrial fib; acute toxicity)
    • Drug toxicity (street drugs, digoxin)
    • Antiarrhythmics
    • Electrolyte imbalances (potassium, calcium)
    • Hypoxia
    • Thyroid disease (hyperthyroidism)
  5. Evaluating an arrhythmia
    • Evaluate the patient, not just the monitor (hemodynamic response)
    • Assess LOC
    • Assess vitals, pulse ox
    • Assess skin/perfusion
    • Assess for myocardial ischemia
    • Assess respiratory
  6. Rate measurement
    • Six second method: simplest, quickest way to determine HR; # of QRS complexes in 6 seconds, multiplied by 10; gives ventricular rate
    • R-R method 1: 300 divided by # of large squares (example: 300/6 squares = 50 bpm)
    • R-R method 2: 1500 divided by # of small squares
  7. R-R Method 1
    • 1 box = 300 bpm
    • 2 boxes = 150 bpm
    • 3 boxes = 100 bpm
    • 4 boxes = 75 bpm
    • 5 boxes = 60 bpm
    • 6 boxes = 50 bpm
  8. Analyzing a rhythm strip
    • What is rate?
    • Is rhythm regular or irregular?
    • Is there a P wave before each QRS?
    • Is the PR interval within normal limits?
    • Is the QRS narrow or wide?
    • Interpret the rhythm
  9. Normal sinus rhythm
    • Rate: 60 - 100 bpm
    • Rhythm: atrial and ventricular regular
    • P wave: uniform, upright, one preceding each QRS interval
    • PR interval: 0.12 - 0.20 seconds
    • QRS: 0.10 seconds or less (contraction of ventricles)
    • Depolarization of atria; SA node fires
  10. Sinus bradycardia
    • Rate: less than 60 bpm
    • Rhythm: atrial and ventricular regular
    • P waves: normal
    • PR interval: 0.12 - 0.20 seconds
    • ORS: usually 0.10 seconds or less
    • Etiology: athletic training, MI, hypothyroidism, sick sinus syndrome, medications (beta blockers, nondihydroperidines - Verapamil or Diltiazem, digoxin, amiodarone)
    • Tx: None may be indicated; treat underlying cause; atropine (incr HR, block parasympathetic vagus nerve); pacemaker (permanent or temporary)
    • Atropine is tx of choice unless bradycardia is caused by a block
  11. Sinus tachycardia
    • Rate: usually 100 - 140 bpm
    • Rhythm: atrial and ventricular regular
    • P wave: normal
    • PR interval: 0.12 - 0.20 seconds
    • QRS: usually 0.10 seconds or less
    • Etiology: stress, anemia, fever, shock, hyperthyroidism (incr metabolic demand), drugs (beta agonists, street drugs, sudafed), CHF, pain
    • Tx: treat underlying cause, beta blocker (decr HR), calcium channel blocker (Varapamil, Diltiazem), digitalis (decr preload, afterload, and HR)
  12. Sinus arrest (pause)
    • Sinus impulses are not generated
    • May be because of digitalis, quinidine, CAD, rheumatic heart disease, MI, myocarditis
    • If hemodynamic compromise is present, IV atropine, or insertion of permanent pacemaker
  13. Premature atrial contraction (PAC)
    • Atria fire before SA node
    • P wave: premature, differ from sinus P waves; may be flattened, pointed, or absent
    • QRS still follows normal pathway once hits AV node
    • Etiology: CHF, myocardial ischemia, fatigue, COPD, atrial enlargement, digitalis toxicity, hypokalemia, hypomagnesemia, excessive use of caffeine, tobacco, or alcohol; occasionally occurs in healthy individual (isolated PAC)
    • Tx: usually not necessary; treat underlying cause
  14. Supraventricular tachycardia (SVT)
    • Originates above ventricles
    • Rapid atrial contractions
    • ORS narrow (less than 0.10)
    • If v-tach, ORS is wider
    • Etiology: accessory pathways, MI, stimulants, CAD, COPD
    • Tx: carotid massage (stimulates vagus nerve, baroreceptors in carotids), adenosine IV push (resets heart rhythm; push drug fast), beta blocker, calcium channel blocker, ablation (try to find pathway and cauterize)
  15. Paroxysmal supraventricular tachycardia
    • SVT that starts and ends suddenly
    • The onset or cessation of the SVT and identification of the underlying rhythm that precedes it should also be known
  16. Paroxysmal atrial tachycardia
    • Narrow QRS (above ventricles)
    • Terminates on its own; not sustained
  17. Atrial flutter
    • "Normally abnormal"
    • Rate: atrial rate 250 - 350 bpm; ventricular rate is variable
    • Rhythm: atrial regular, ventricular may be regular or irregular
    • No P waves
    • QRS conducted in 2:1, 3:1, 4:1 ratio
    • Loss of atrial kick
    • Risk of atrial fib, embolization, stroke
    • "Saw tooth"
    • Etiology: valve disease, COPD, CAD, medications, hyperthyroidism
    • Tx: rate control with digoxin, ablation; chemical cardioversion with amiodarone, sotalol, rhythmol; DC cardioversion
  18. Atrial fibrillation
    • Most common; clot stuck in chamber causing atria to barely quiver
    • Loss of time in diastole; incr HR
    • Control rate with beta blocker, amiodarone, digoxin, varapamil, diltiazem
    • Atrial rate: 350 - 600 bpm
    • Ventricular rate variable
    • "Irregularly irregular"
    • Narrow QRS
    • Loss of atrial kick (loss of cardiac output because not filling ventricles effectively)
    • Embolization risk (may need Coumadin to prevent stroke)
    • Target INR 2.0 - 3.0, 2.5 - 3.5 when involves a mechanical valve
    • Etiology: valve disease, CAD, cardiomyopathy, COPD, hyperthyroidism, atrial enlargement
    • Tx: rate control, anticoagulation, chemical cardioversion (amiodarone most effective), DC cardioversion, ablation, maze procedure
  19. Warfarin (Coumadin) teaching
    • Observe for bleeding (report to health care provider or ER if severe)
    • PT/INR (need for routine lab monitoring)
    • Missed dose (don't double up unless instructed to)
    • Avoid OTC
    • Multiple drug interactions
    • Vitamin K foods (avoid excessive consumption or fluctuation in intake)
    • Avoid trauma (soft toothbrush, electric razor; no contact sports)
    • Medic-Alert bracelet
    • Direct pressure to stop bleeding
  20. Junctional escape rhythm
    • Rhythms coming out of AV node
    • Rate: 40 - 60 bpm
    • P wave: absent or is inverted; may occur before, during, or after QRS; if visible, P wave is inverted
    • Etiology: MI, sinus node dysfunction, digoxin toxicity
    • Tx: do not suppress, stop digoxin, atropine
  21. Heart blocks
    • 1st degree: prolonged PR interval; no treatment indicated
    • 2nd degree type 1 (Wenckebach): PR interval progressively lengthens until non-conducted
    • 2nd degree type 2: intermittent conduction of P's; MI, digoxin toxicity
    • 3rd degree AV block: no relationship between the atrial and ventricular rhythm (no communication); emergent treatment; no P wave pattern; none of impulses from atria are going through; QRS not prompted by atria
    • 1st degree block will progress to 2nd and 3rd if patient becomes compromised w/ another illness (renal, liver, etc.)
  22. Idioventricular rhythm
    • A slow v-tach
    • Etiology: MI, reperfusion
    • Escape rhythm
    • Do not suppress
    • Intrinsic rate: 20 - 40 bpm
    • Wide QRS
    • When all else fails, the ventricles will try to keep the heart going
  23. Premature ventricular contraction (PVC)
    • Ectopic ventricular contraction (ectopic pacemaker causes PVC; not SA node firing)
    • Blood is not being perfused
    • QRS wide and bizarre
    • No P wave before QRS
    • Unifocal (coming from same place) vs. multifocal (different shapes; more than 1 place is firing when not supposed to)
    • Bigeminy (every other beat is a PVC), trigeminy
    • Couplet (2 PVCs in a row), triplet (3 PVCs in a row), vtach (4 PVCs in a row)
    • Occasionally occur in healthy hearts
    • Etiology: CAD, MI, stimulants, digoxin, hypokalemia
    • No treatment or treat cautiously
  24. Ventricular tachycardia (V-tach)
    • Rapid rate, wide QRS
    • May be pulseless, treat as v fib; treat with amidarone
    • Can deteriorate into v fib
    • If it is unclear whether a regular, wide QRS tachycardia is VT or SVT with an intraventricular conduction defect, treat the rhythm as ventricular tachycardia until proven otherwise
    • Etiology: acute MI, CAD, reperfusion, hypokalemia, prolonged QT, antiarrhythmic
    • Tx: hemodynamically stable (amiodarone), hemodynamically unstable (cardioversion), pulseless (immediate defibrillation)
  25. Torsades De Pointes
    • "Twisting around a point"
    • Triggered by prolonged QT (hard to treat)
    • Tx: magnesium sulfate, overdrive pacing, cardioversion
  26. Ventricular fibrillation
    • No ventricular contractions
    • Coarse large spikes; no complexes
    • No cardiac output
    • Pulseless
    • Brain cells die in 4 - 6 minutes
    • Immediate defibrillation, ACLS
    • Initiate CPR until defibrillator is available
  27. What are the priority actions in treating V fib?
    • Defibrillation
    • CPR until defibrillation is available then continue CPR and recheck rhythm
  28. Asystole
    • V fib deteriorates into asystole
    • Rule out fine v-fib
    • Poor prognosis
    • Tx: CPR, ACLS, epinephrine, atropine, pacing
  29. Etiology of cardiac arrest
    • Hypovolemia
    • Hypoxia
    • Hydrogen ions (acidosis)
    • Hyper or hypokalemia
    • Hypoglycemia
    • Hypothermia
    • Toxins
    • Tamponade
    • Tension pneumothorax
    • Thrombosis or coronary artery or pulmonary artery
    • Trauma
  30. Artifact
    • Make sure not to mistake an artifact for v fib/v tach and vice versa
    • Proper lead placement
  31. Pulseless electrical activity (PEA)
    • Electrical activity does not result in contraction
    • Poor prognosis
    • Etiology: acidosis, potassium imbalances, drug overdose, cardiac tamponade, PE, MI, tension pneumothorax
    • Tx: correct cause, CPR, epinephrine, atropine, ACLS
  32. Pacing
    • Indications: heart blocks, tachyarrhythmias (overdrive pacing, try to regain control of aberrant area), sinus node dysfunction
    • Temporary: transcutaneous, transvenous (thru subclavian vein to vena cava), epicardial (pacer wires inserted into heart)
    • Permanent
  33. Failure to sense or capture
    • Failure to sense: pacer is not reading heart beat
    • Failure to capture: pacer is firing but heart is not responding
    • Pacemaker is programmed to fire only if there is not an intrinsic heart beat
  34. Nursing care for pacemaker insertion
    • Monitor for signs and symptoms of infections
    • Know type of pacer and settings
    • Monitor telemetry for sensing and capture
    • Assess and treat pain
    • Educate patient
  35. Pacemaker patient education
    • Keep site dry until healed
    • Avoid using operative side arm until healed
    • Monitor pulse
    • Avoid MRIs
    • Must be interrogated
    • Can use microwave
    • Carry pacemaker card
  36. Elective cardioversion
    • Informed consent if patient is alert and stable
    • IV sedation
    • Manage airway
    • Synchronization
    • Not as emergent
    • Patient still has BP and pulse
    • Sync switch: reads rhythm and will delay the shock until after T wave (never want to shock during T wave)
    • If person is in v fib or pulseless v tach, just need to shock them (don't care about sync switches, sedation, or informed consent) otherwise they will die
    • "Cardiovert the living, defibrillate the dead"
  37. Cardioversion vs defibrillation
    • Cardioversion: elective procedure, client is awake and freq sedated, sync with QRS, 50 - 200 joules, consent form, EKG monitor, sync switch on
    • Defibrillation: emergency, v fib, v tach, no cardiac output, 360 joules, client unconscious, EKG monitor
  38. Implantable cardioverter-defibrillator
    • indicated for cardiac arrest survivors, recurrent arrhythmias, high risk patients
    • Include pacemaker functions
    • Post-op care similar to pacemaker insertion
  39. Amiodarone
    • Antiarrhythmic
    • Most efficacious, but also most toxic
    • Contains iodine like pigments, sometimes causes bluish tinge to skin ("smurf drug")
    • Half life of around 100 days
    • Can cause serious organ toxicities; monitor for thyroid, liver, lung toxicity (pulmonary fibrosis; damage can be permanent)
    • Should get PFTs every 6 months, liver function and thyroid function tests
Card Set
Med Surg I Arrhythmias