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 a result 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
to cardioversion; 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 QRS contractions
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