EKG's made EZ

The NCLEX exam doesn't expect you to be a highly trained cardiologist, and the
USMLE on average only asks 2 questions about EKGs, but recognition of important
pathological rhythms is a requirement for all future nurses and physicians. One of the
most important, yet daunting tasks in the nursing and medical fields is to learn to
recognize, both accurately and rapidly, Electrocardiograms (ECGs). Variations from
the normal p, QRS, and T waves can be completely harmless to fatal in minutes, and
it is up to us in the healthcare field to be able to tell the difference, and act
accordingly.
Lets take a look at these variations and see if there is a way to make this a bit easier
to understand. We will divide these variations up into three
groups: Bradyarrhythmias (abnormal rhythms with rate usually below
60),Tachyarrhythmias (abnormal rhythms with rate usually above 100 bpm),
and Dysrhythmias (alterations to the normal sinus rhythm pattern).

Bradyarrhythmias
1.Sinus Bradycardia
HR less than 60 requires treatment with Atropine only if

symptomatic
2.AV

Block
A.1st DegreeKey: PR interval above 0.2 seconds; Delay is in AV node
Usually benign but low HR responds to Atropine

B.2nd Degree type IKey: Progressive prolongation of PR until a P wave

fails to conduct and no QRS follows a P wave; Delay is in AV node
Usually benign condition seen with normal aging not requiring treatment, but if
symptomatic with bradycardia, will respond to Atropine

C.2nd Degree type II

Key: Normal EKG with a sudden drop of a QRS; Block usually in the His-Purkinje
system usually as aresult of ischemia
Can turn into the deadly 3rd degree so temporary transcutaneous pacer may be
needed until an implantable pacemaker can be inserted

D.3rd Degree
AV dissociation often from irreversible damage to the AV node following a MI
Key: P-P length does not equal R-R length
Ventricles do not pump fast enough to maintain CO and requires pacemaker

Tachyarrhythmias
Atrial impulse
A.Sinus TachycardiaHR 100-140, may occur with exercise or anxiety, but
also may be earliest indication of hypovolemia
Usually not symptomatic until above 140 when diastolic filling time is impaired
Count the large boxes from top of a QRS to another: 1 box = 300bpm, 2 box =
150bpm, 3 box = 100bpm, 4 box = 75bpm, 5 box = 60bpm
TX: Eliminate cause (i.e. anemia, stimulant; fluid bolus)

B.SupraVentricular TachycardiaA conduction signal loops and reenters

the atrium causing rapid, atrial driven HR usually above 140bpm
Atrial tachycardia results in narrow QRS complexes
TX: Adenosine given rapid IV push

D.Atrial FlutterOne foci in atrium fires rapidly, leading to sawtooth P

waves and regular QRS with HR between 75-175
Occurs most often in COPD, but may be seen with CAD and Atrial septal defects
(ASD)
TX: Identical to AFib

Atrial

FibrillationMultiple atrial foci cause lack of P waves and

very irregular QRS waves with widely varied HR from 75-175 bpm

Caused by CAD, MI, HT, PE, Pericarditis, Hyperthyroidism

Major risk for thrombotic events (CVA) so treat according to protocol
Treatment Protocol; Determine length/onset of AFib:
Acute: less than 48hrs
Unstable: (Hypotensive, AMS) Immediate cardioversion
Stable:
Tachycardic: Control Rate w/ Beta Blocker (Atenolol) then electrical cardioversion
NSR: Proceed directly to cardioversion (electrical preferred to pharmacologic;
If electrical fails or is unfeasible use Amiodarone to convert)
Acute: greater than 48 hrs or unknown duration
Before cardioversion: If longer than 2 days must use Warfarin to anticoagulate for 3
weeks before and 4 weeks after
Avoid the wait: Can obtain an echo to r/o thrombus and load pt
with Heparin and proceed tocardioversion; Still require the 4 week
Warfarin anticoagulation after
Chronic: Under 60 with no heart disease or risk factors require no treatment; All
others get Warfarin for good

Tachyarrhythmias
Ventricular impulse
A.Ventricular Tachycardia
Ventricular foci initiate rapid HR with wide QRS complexes
Caused by prior MI (most common), active ischemia, hypotension,
cardiomyopathy, Drugs, Electrolyte abnormalitiesMay initially have a pulse, but
can rapidly evolve into a deadly pulseless VTach
TX: VTach with a pulse treated with 150mg Amiodarone
TX: Pulseless VTach treated identical to VFib with Code being called: CPR,
Defibrillation, Epinephrine, Amiodarone, and Lidocaine (Alternate drugs w/ Epi
being only drug you can not max out on)

B.Ventricular Fibrillation
Ventricular foci initiates rapid rhythm which causes heart to fatigue and quiver
Typically evolves from VTach
Ischemic heart disease most common cause
Always pulseless, so initiate a code as above

C.Torsades de PointeA polymorphic VTach with varying direction of QRS

amplitude (points alternate down to up)
Often caused by electrolyte problems and long QT, so give a trial of Mag and
Calcium

D.Asystole
Loss of electrical signal initiation so it doesnt respond to Defibrillation (basically
resets rhythm to asystole)
Epinephrine and Atropine are only hopes

Arrhythmias
Dysrhythmias

A.Premature Ventricular Contraction (PVC)Abnormal Foci

causes random, wide QRScontractions
May not progress to any other rhythm and have no symptoms
Can progress to VTach and VFib, so treat more than 6/min or if symptoms
present with BBs

B.ST Elevation
Usually an ominous sign of actual myocardial infarction
Treat with ACS protocol including ECG and Enzymes
If present in all 12 leads may suggest Pericarditis

C.T wave Inversion

An ominous sign of cardiac ischemia, can precede B
D.Q wave
If deeper than of QRS, suggests a prior infarction, Follows B
E.U wave
Suggestive of hypokalemia
F.ST Depression
Often a sign of ischemia, use MONA, ECG, Enzymes

G.Peaked

T waveSuggestive of hyperkalemia

H.Prolonged QT
QT width is more than the width of QRS-QRS
Often caused by low Mg or Ca, as well as many drugs that effect these
electrolytes
TX: Withdrawal medication that caused and check/treat electrolyte
abnormalities