DYSRHYTHMIAS AND EKG INTERPRETATION 1 | P a g e

RHYTHM

EKG

NORMAL SINUS RHYTHM (NSR)

I N T E R P R E T R H Y T H M , A S S E S S
RATE
RHYTHM
EKG
(BPM)

60 100

Regular
rhythm:
R to R and P
to P interval
constant

T R E A T M E N T
INTERVENTIONS

P wave:
present and
similar
PR interval:
.12 .20 seconds
and consistent

None, normal.

QRS segment:
.04 - .10 seconds
and consistent
SINUS BRADYCARDIA
Causes:
Noncardiac
Athlete
Sleeping

Elderly

Cardiac
SA node disease
Vagal stimulation
Drug Induced
Beta blockers

P wave:
present and
similar

MI
CAD
Less than
60

Antianxiety

Signs and symptoms:

Pale, cool skin
Weakness
Dizziness
Confusion
SOB

Regular

Digitalis

PR interval:
present and
normal
QRS segment:
present and
normal

Hypotension
Angina
Syncope
Disorientation

Assessment
Decreased cardiac output
related to slow heart rate
Blood pressure
Are you dizzy? Light
headed?
Treat only if the patient is
symptomatic
Atropine*
Stimulate patient.

SINUS TACHYCARDIA
Causes
Noncardiac
Anxiety, fright, stress
Pain
Alcohol ingestion
Hypovolemia
Cardiac
MI

Exercise
Fever
P wave:
present and
similar

CHF

Drug Induced
Aminophylline
Caffeine
Dopamine
Nicotine

Amphetamines
Atropine*
Epinephrine

Signs and Symptoms:

Dizziness
Dyspnea
Hypotension
Angina
Increased myocardial oxygenation
Decreased cardiac output

greater than
100

Regular

PR interval:
present and
normal
QRS segment:
present and
normal

Assessment
Decreased cardiac output
related to decreased filling
time
Treatment
Treat the cause*
Pain
Pain management
Hypovolemia
Resolve hypovolemia
Vagal maneuvers*
IV beta blockers*
(Lopressor)

DYSRHYTHMIAS AND EKG INTERPRETATION 2 | P a g e

I N T E R P R E T

R H Y T H M ,

A S S E S S

T R E A T M E N T

ATRIAL DYSRHYTHMIAS
RHYTHM

EKG

Rate

Rhythm

EKG

Treatment

PAC
PREMATURE ATRIAL
CONTRACTIONS (PACS)
Action:
Originates in the atrium
Ectopic foci (irritable cell) in the atria
Not life-threatening
Unifocal versus multifocal

Conducted PAC

P wave:
Different, down
deflection
notched*

Disoriented P wave
AV node stopped (nonconducted PAC)
delayed (lengthened PR
inter.)
Causes
Emotional stress
Fatigue
Caffeine
Tobacco
Alcohol
COPD
Valvular disease
Hypoxia
Electrolyte imbalances
CAD

Variable

Irregular

Nonconducted PAC

Asymptomatic:
No treatment needed
Treat the cause* because
it can cause more lethal
dysrhythmias.

PR Interval
Varies but WNL

Withdraw from drug or

caffeine

QRS
Usually normal*
(NORMAL FOR
ALL ATRIAL
ARRHYTHMIAS)

Oxygen

Termed as NSR
with PACs

Electrolyte replacement
Medications*

Digoxin

Quinidine (IA)

Pronestyl (IA)

Signs and Symptoms

Isolated PACs: Not important
Palpitations
Frequent PACs: SVT warming *
Assessment:
Decreased cardiac output
related to decreased filling
time
ineffective myocardial
contraction

ATRIAL FLUTTER
Action
Recurring, regular sawtooth-shaped
flutter waves

Variable Atrial Flutter

Rapid atrial depolarization

Single Ectopic focus
SA node not repolarizing
Causes
Atrial ischemia
Stretched atria such as in fluid overload
or CHF
Signs and Symptoms
Decreased CO: HF with underlying
disease
Increased risk of stroke:
Thrombus formation in atria

Atrial Flutter

Atrial rate:
200-350 per
minute
Ventricular
rate:
< 150

Atrial
Regular*
Ventricular
Irregular*

Flutter waves:
Saw tooth waves
Two or more
before each QRS
PR Interval:
Not measurable
QRS
Usually normal*
(NORMAL FOR
ALL ATRIAL
ARRHYTHMIAS)

Drugs to control rate

Decrease ventricular
response rate for filling time.
Digoxin*
Esmolol (Brevibloc)*
Diltiazem (Cardizem)*
Drugs to control Rhythm
Medications convert back
from atrial flutter to normal
sinus rhythm.
Ibutilide (Corvert) (III)
Pronestyl (IA)
Amiodarone (III) to
cardiovert chemically
Cardioversion
Atrial Pacing

DYSRHYTHMIAS AND EKG INTERPRETATION 3 | P a g e

I N T E R P R E T

R H Y T H M ,

A S S E S S

T R E A T M E N T

ATRIAL DYSRHYTHMIAS
RHYTHM
ATRIAL FIBRILLATION

EKG

RATE

Irregular
Chaotic

Total disorganization of atrial

electroactivity
Loss of effective atrial contraction
Most common*
Clinical Associations
CAD
Rheumatic heart disease
Alcohol intoxication
Stress
Cardiac surgery
Cardiomyopathy
Hypertensive heart disease
Caffeine use
HF
Pericarditis
Electrolyte Imbalances

RHYTHM

Controlled A. Fib:

Atrial rate:
Too fast to
determine

Faster the
rate, the
more regular
it may
appear. But it
is not regular!

>350 BPM
Ventricular
Rate:
Varies

Uncontrolled A. Fib:

Clinical Significance
Decreased CO: ineffective atrial
contractions

Controlled
Less than
100
Uncontrolled
>100

Thombi in atria emboli brain

(stroke)
Complications
Emboli
Cardiac output decreased 20-25%

*they also
have atrial
flutter. When
they see
flutter they
think it is a P
wave. But it
is not a
frigken P
wave! All P
waves must
look the
same.
Random
flutter wave
not P Wave.

EKG

P wave
Not identifiable
Chaotic
PR interval
Not measurable
QRS
Usually normal*
(NORMAL FOR
ALL ATRIAL
ARRHYTHMIAS,
initiated above
the ventricles. )

Cardiac output
likely to be lower
(20-25%):
normally, atria
will squeeze to
increase and rid
of blood and put
it in ventricle
(atrial kick).

SUPRAVENTRICULAR
TACHYCARDIA
(AKA SVT / PAT / PSVT)

COPD
CHF
Hypoxia

P wave:
Often not
identifiable
Absent

PAT / PSVT
150-200 /
minute

Cor Pulmonale
CAD
Post CABG
Anesthesia

Cardiac anomalies
Sypathomimetic drugs
Signs and Symptoms
Prolonged HR
Decreased CO r/t decreased CV
Hypotension
Dyspnea
Angina

Brevibloc
Ibutilide
Digoxin
Dugs to control Rhythm
Pronestyl (IA)
Amiodarone (III)
Anticoagulation***
Warfarin for a fib longer than
48 hours
TEE to rule out presence of
clot in atria, stasis of blood,
emboli
Long term anticoagulation
Cardioversion
Atrial Pacing
Ablation (unresponsive to
cardioversion)
MAZE: stops A fib by
interrupting electrical signals

Treatment
Vagal stimulation through
Valsava maneuver
Slows heart rate down

An irritable foci above the ventricles

Overrides the SA node
Causes
Common in children and young adults
Fever
Sepsis
Caffeine
Tobacco
Alcohol
Stress

TREATMENT
Drugs to control rate
Diltiazem (CCB) (IV)
Decreases ventricular
response

NSR PAC PAT

Regular or
Slightly
Irregular

PR Interval:
Shortened /
normal
QRS:
Usually normal,
initiated above
the ventricles.

Coughing
Carotid massage:
dont do it!
Can have person stroke. Do
not massage both sides at
the same time.
Cardioversion
AV ablation
Surgical cardiac cath EPS
study
Medications

Digoxin

Pronestyl (IA)

Inderal (II)

IV Adenosine*

DYSRHYTHMIAS AND EKG INTERPRETATION 4 | P a g e

I N T E R P R E T

R H Y T H M ,

A S S E S S

T R E A T M E N T

HEART BLOCKS
RHYTHM

EKG

RATE

RHYTHM

TREATMENT
Usually asymptomatic
No treatment needed.
Monitor and drugs.

FIRST DEGREE HEART BLOCK

Impulse is slowed through the AV node
Clinical Conditions Associated
MI
CAD
Rheumatic Fever
Vagal stimulation
Hyperthyroidism
Drug use of: digoxin, b-blockers, CCB,
flecainimide

EKG

Varies but
normal

Regular

PR Interval:
Greater than .20
seconds,
prolonged*
QRS:
Normal

Prolonged PR interval. Looks like NSR but PR interval is LONGER.

Adjust drug therapy

Atropine: if symptomatic
and bradycardic
Monitored for progression
into more advanced degree of
block

SECOND DEGREE HEART BLOCK

TYPE I MOBITZ I * / WENKEBACH
Gradual lengthening of PR interval
Occurs in the AV node
Clinical Associations

Digoxin Use

Beta blocker use

CAD
Clinical Significance
MI or infarction
Warning signs of *more serious AV
conduction
Disturbance

Normal
Dropped QRS. PR interval progressively becoming prolonging. The
PR interval, longer, longer, longer, then it DROPS a QRS complex.

Atrial
Rhythm:
Normal

Pattern of
grouped beats

Ventricular
Rhythm:
Slow
blocked QRS

PR progressively
lengthens until a
QRS complex is
dropped*

Symptomatic:
Atropine* to increase HR
Temporary pacemaker
Asymptomatic:
Closely observe rhythm

Poor conduction through the AV node.

Discontinue causative
medications

SECOND DEGREE HEART BLOCK

TYPE II AKA MOBITZ II*
Clinical Associations
Rheumatic Heart Disease
CAD
Anterior MI
Drug toxicity

Atrial
Rate:
Normal
Ventricular
Rate
Slow

Clinical Significance
Progressive to type III heart block
Poor prognosis
Conduction through AV node variable.

Same constant PR interval.

Atrial
Rhythm:
Normal
Ventricular
Rhythm:
Irregular
Sudden
dropped
complex*

P wave:
Normal
PR Interval:
Constant
CONSISTENT*
QRS:
Suddenly dropped
complex
Often WIDE

Drugs Used
Atropine*
Epinephrine*
Temporary pacemaker
Permanent pacemaker
needed*
Increases sinus rate
Monitor for progression into
third degree heart block

DYSRHYTHMIAS AND EKG INTERPRETATION 5 | P a g e

I N T E R P R E T

R H Y T H M ,

A S S E S S

T R E A T M E N T

HEART BLOCKS
RHYTHM
THIRD DEGREE HEART BLOCK
AKA COMPLETE HEART BLOCK

EKG

RATE

RHYTHM

AV dissociation
Independent atrial and ventricular
activity
No impulses from atria and ventricles
Clinical Associations
Severe heart disease
Myocarditis
Amyloidosis

CAD
MI
Cardiomyopathy
Sclerosis

Medications: digoxin

B-blockers

P wave:
Normal

Atrial faster
than
ventricular

Atria and
ventricular
independently
regular

CCB

Clinical Significance
Asymptomatic or Life threatening
Decreased CO with subsequent
ischemia, HF, and stroke

EKG

More than 1 P wave for every QRS. Totally miscommunication. P

to P. No dropped beat.

PR Interval:
varies
QRS interval:
Normal or wide
Normal: above
bundle
Widened: Below
of His

TREATMENT

Atropine*
Increases HR and BP
For bradycardia
More effective with Mobitz I,
does not work well with
Mobitz II
Calcium Chloride
For CCB toxicity
Pacemaker:
Temporary, and if no
improvement permanent
Transthoracic pacemaker

Syncope: severe bradycardia / asystole

VENTRICULAR DYSRHYTHMIAS
RHYTHM
PREMATURE VENTRICULAR
CONTRACTIONS (PVCS)

EKG

RATE

RHYTHM

EKG

Unifocal PVC

Ectopic focus or foci in the ventricle,

emitting impulses which are early in the
cycle and override the SA node impulse
Each focus creates an impulse which
looks the same each time
Depends on
underlying
rhythm and
the # of
PVCs

Potentially lethal* and lead to V. tach

1.
2.
3.
4.
5.

Unifocal: same shaped PVCs

Multifocal: PVCs appearing
different
V. trigeminy: every 3rd beat as
PVC
V. Bigeminy: every 2nd beat as
PVC
Couplet: two consecutive PVCs

Causes
cardiac disease
electrolyte imbalance
K and Mg

Multifocal PVCs

Similar to
atrial.
Because
they are
occurring
early, QRS
complex
gets wide.

Runs of PVCs

hypoxemia
stimulants (caffeine)
Signs and Symptoms
Reduced CO: angina and acute MI
Pulse deficit

"

Irregular

TREATMENT
CRITERIA FOR
TREATMENT:
More than 6 per minute
Multiform
Runs of PVCs: indicates
ventricular tachycardia*
R on T

P wave:
No P wave
preceding PVC

CORRECT CAUSE:
Correct hypoxia with oxygen
therapy

PR Interval:
Immeasurable

Check pulse ox

QRS of PVC:
>0.12 seconds
Premature
occurrence of the
QRS wide and
distorted
T wave:
Large and
opposite direction

Correct electrolyte
imbalance with electrolyte
replacement
Especially Mg and K
Before administering
medications, consider the
underlying rhythm/rate
MEDICATIONS:
Lidocaine* if underlying rate
normal or tachycardic (IB) to
erase PVC and what is
causing it. If land on T wave,
can put them into code.
Atropine* if underlying rate
is bradycardic

DYSRHYTHMIAS AND EKG INTERPRETATION 6 | P a g e

RHYTHM
VENTRICULAR TACHYCARDIA

EKG

I N T E R P R E T R H Y T H M , A S S E S S
RATE
RHYTHM
EKG

Three or more PVCs

Foci fire repetitively: ventricle takes
control as pacemaker
1.
2.

Monomorphic: QRS complexes

same
Polymorphic: QRS complexes
change back and forth

Hypokalemia
Hypoxia

T R E A T M E N T
TREATMENT

If conscious and stable:

Lidocaine
bolus and drip (IB)

Torsades De Pointes* TREATMENT MUST BE MAGNESIUM, OR YOU

WILL NOT GET THEM BACK.

Cough CPR
Cardioversion

Torsades de Pointes:
Polymorphic VT associated with
prolonged QT
Life-threatening dysrhythmia*
Causes
MI
Hypomagnesimia

P wave:
Usually not
identifiable
Ventricular Tachycardia

150 200
per minute

Regular

PR Interval:
Not applicable
QRS Complex:
>0.12 seconds

Signs and Symptoms

Stable (with a pulse)
Unstable (Pulseless)

If unconscious and
pulseless
CPR - full code
Defibrillation
Vasopressors Epinephrine
Antidysrhythmics
Aminodarone
Treat cause
electrolytes
drug toxicities
AICD

Sustained:
Less than 30 seconds
Decreased CO leading to:
Hypotension
Pulmonary Edema
Decreased cerebral blood flow
Cardiopulmonary arrest

Torsades de Pointe:
Magnesium first!

VENTRICULAR FIBRILLATION
Asynchronous, chaotic, impulses
emitted from multiple foci in the
ventricle.
Quivering of the heart
No cardiac output
Cardiac arrest
Clinical Associations
Acute MI
Myocardial ischemia
Cardiac pacing Catheterization
Chronic HF
Cardiomyopathy
Coronary Perfusion
Accidental electrical shock
Hyperkalemia
Hypoxemia
Acidosis
Drug toxicity
Clinical significance
Unresponsive
Pulseness
Apneic
Death

Defibrillation
CPR
P wave
Not visible
Defibrillation

Not
measurable

Irregular and
chaotic

PR Interval and
QRS:
Not measurable

Medications
Amiodorone (III)
Lidocaine (IB)
This is the most common
terminal event in sudden
cardiac death syndrome*
AED