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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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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)
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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
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Paroxysmal atrial tachycardia
- Narrow QRS (above ventricles)
- Terminates on its own; not sustained
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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
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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
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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
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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
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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.)
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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
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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
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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
- Tx: hemodynamically stable (amiodarone), hemodynamically unstable (cardioversion), pulseless (immediate defibrillation)
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Torsades De Pointes
- "Twisting around a point"
- Triggered by prolonged QT (hard to treat)
- Tx: magnesium sulfate, overdrive pacing, cardioversion
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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
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What are the priority actions in treating V fib?
- Defibrillation
- CPR until defibrillation is available then continue CPR and recheck rhythm
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Asystole
- V fib deteriorates into asystole
- Rule out fine v-fib
- Poor prognosis
- Tx: CPR, ACLS, epinephrine, atropine, pacing
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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
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Artifact
- Make sure not to mistake an artifact for v fib/v tach and vice versa
- Proper lead placement
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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
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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
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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
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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
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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
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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"
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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
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Implantable cardioverter-defibrillator
- indicated for cardiac arrest survivors, recurrent arrhythmias, high risk patients
- Include pacemaker functions
- Post-op care similar to pacemaker insertion
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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
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