EKG

Atrial depolarization

0.06-0.10 sec

Time taken for impulse to spread thru atria, AV node, bundle of His, bundle branches, and Purkinje fibers

0.12-0.20 sec

Indicates AV block

Ventricle depolarization

< 0.10 sec

• Bundle branch blocks
• Will be > 0.12 sec

• Myocardial infarction
• Q wave is wider than 0.4 sec and measures more than 1/3 of the R wave

Repolarization of ventricles

• Flat on isoelectric line
• Should not be elevated or depressed

• Myocardial injury
• Also, pericarditis and ventricular aneurysm

• Ischemia
• Coronary arteries not receiving enough oxygen for demand

Ventricular repolarization and diastole

• Relative refractory period
• This means the heart is vulnerable to a strong stimuli, which could trigger V tach

Total time needed for ventricular depolariztion and repolarization

• Lengthens relative refractory period
• Prolongs the vulnerability of the heart
• Can trigger a lethal arrhythmia
• Can cause early death
• This is what they think is behind young athletes dying
• Disorder of Na and K channels
• Child or young adult may have a syncopial episode, dizziness, &/or palpitations

• Rate
• Rhythm
• P wave before each QRS
• PR interval
• QRS complex
• ST segment
• T wave
• Any ectopic beats

P-P intervals

R-R intervals

• May lead to a decrease in cardiac output -> decreased perfusion
• May be caused by a synergistic effect of negative chronotropes, calcium channel blocks, beta blockers, Digoxin, and vagal stimulation

• If symptomatic, treat w/ Atropine, pacemaker
• Stool softener to prevent vagal stimulation during valsalva maneuver

• Increases workload on heart
• May be due to volume problems, oxygen deficit, infection, exercise, fever, pain, anxiety, SNS (normal compensatory mechanism)
• Decreases diastole, which is the filling phase for the coronary arteries
• Rate 100-150 (coming from SA node)

• Check if patient is symptomatic
• Treat the cause!
• Beta blocker

• In a healthy heart, nothing
• In CAD, can lead to atrial tachyarrhythmias (a fib/flutter)
• Usually no treatment

• In presence of CAD, decreases cardiac output
• May precipitate HF or MI
• Still regular but very rapid
• Rate is 150-250 (not coming from SA node; coming from one irritabile foci in the atria)

• Assess for symptoms (chest pain, LOC, BP, lightheadedness, dizziness, pulmonary congestion)
• If QRS is narrow (<0.12), treat as atrial: Vagal maneuver (to trigger PNS), adenosine, cardizem
• If QRS is wide (>0.12), treat as ventricular: Amiodarone, magnesium
• If patient becomes unstable, cardioversion

• No discernable or true P waves (saw-tooth pattern)
• Loss of atrial kick
• Can lead to a. fib
• Atrial rate 250-350 BPM

• Goal is to control the rate then the rhythm with: Cardizem, amiodarone, dromedarone (Multaq)
• Anticoagulants (blood pooling and clotting)
• Cardioversion if necessary

• The ventricular rate!
• "A. fib w/ RVR or uncontrolled ventricular rate of ___"
• Controlled if < 100
• Uncontrolled if > 100

• Coming from multiple irritable foci in atria
• Loss of atrial kick
• Decreased cardiac output
• Decreased perfusion

• Same as atrial flutter:
• Treat rate & rhythm (ventricular rate is very important!)
• Vagal maneuver
• Cardizem
• Amiodarone
• Anticoagulants
• Cardioverson

• A delayed PRI
• PRI > 0.20
• All sinus impulses eventually reach the ventricles
• May need pacemaker

• PRI gets longer & longer & then one is eventually blocked
• Lengthening of PRI resulting in a P wave w/ no QRS
• Some impulses reach the ventricles but other's don't 

• Alternates between a P wave followed by a QRS and a P wave without a QRS
• Can be 2:1, 3:1, etc.
• (2 P waves to each QRS complex conducted)
• Episodes of no ventricular depolarization
• Atropine most likely will not help -> need pacemaker

• Atria and ventricles not communicating at all
• P waves are not conducting QRS complexes 
• AV node not letting anything thru to ventricles
• Purkinje fibers are triggering ventricular depolarization (@ 20-40 BPM)
• Pt will show S/S of decreased C.O.
• Usually happens after MI

• If it's unifocal or multifocal
• Bigeminy
• Trigeminy
• Quadreminy
• Etc.

V tach

• In presence of CAD, sign of ventricular myocardial irritability
• Forerunner for lethal arrhythmias
• If > 500 PVCs in 24 hours, rx for beta blocker

• Treatment if pt is symptomatic
• Consider the cause: electrolyte depletion, oxygen depletion, acidosis, ischemia, and hypovolemia

• Pulse deficit
• Not every PVC initiates a contraction in the heart
• This is why we assess our patients!
• HR on monitor won't necessary match the palpated pulse during pxy assessment

• K and Mg depletion
• Oxygen depletion
• Hypovolemia
• Acidosis
• Ischemia

If it's monomorphic or polymorphic (Torsades)

• Decreased C.O. - little or none!
• Precursor to v. fib

• If unstable, cardioversion is necessary
• If stable, Amiodarone, Pronestyl, Sotolol, Lidocaine
• Treat electrolyte imbalances
• * If pulse is not present, treat as V FIB!

• No cardiac output!
• No pulses - call a code blue

• CPR until defibrillator available (pump hard & fast)
• Defibrillate the patient
• Defib possibly followed by Epi, vasopression, amiodarone, magnesium
• Check for pulse after defib to assess if it was successful

• It's a dying heart (ventricles are trying to save it)
• Pulseless electrical activity
• Patient won't last very long

• Pacemaker, emergency drugs
• Treatment often not successful
• HR < 40 BPM