Rhythm Clinical Associations ECG Characteristics Clinical Significance Treatment Strip

Sinus Bradycardia
-Conduction path same as
NSR
-SA node fires at <60 bpm
-Symptomatic- HR <60
resulting in symptoms (chest
pain, syncope
Sinus Tachycardia
-Conduction path same as
NSR
-D/c rate from sinus node
increases b/c vagal inhibition
or sympathetic stimulation
-Sinus rate is 101-200 bpm
Premature Atrial
Contraction
-Originates at site other than
SA
-Starts L/R atrium travels
across atrium by abnormal
path creating distorted P
wave
-At AV it may be stopped,
delayed (long PR interval) or
go normally
Supraventricular
Tachycardia
-Originates in ectopic focus
above bundle of His
-Occurs d/t reexcitation of
atria when theres a one-way
block
-Abrupt onset and
termination followed by brief
asystole
-Some degree AV block
possible
Atrial Flutter
-Atrial tachydysrhythmia
-ID by recurring, regular,
sawtooth shaped flutter
waves
-Originate from single
ectopic focus in R atrium (or
L but uncommon)
-Normal in some aerobic
athletes and some pts during
sleep
-Carotid sinus massage,
Vasalva maneuver,
Hypothermia, Increased
intraocular pressure, Vegal
stimulation
-Drugs (b-blockers, CCB)
-Exercise, fever, pain,
hypotension, hypovolemia,
anemia, hypoxia,
hypoglycemia, MI, HF,
hyperthyroidism, anxiety,
fear
-Drugs: epinephrine,
norepinephrine, atropine,
caffeine, theophylline,
Procardia, hydralazine
-Normal Heart: emotional
stress, physical fatigue,
caffeine, tobacco, alcohol
-Electrolyte imbalance,
hyperthyroidism, COPD,
-Heart disease: CAD, valvular
disease
-Normal Heart: overexertion,
emotional stress, deep
inspiration, stimulants
(caffeine and tobacco)
-Rheumatic heart disease,
digitalis toxicity, CAD, cor
pulmonale
-Rarely occurs in healthy
heart
-Diseased states: CAD, HTN,
mitral valve disorders, PE,
chronic lung disease, cor
pulmonale, cardiomyopathy,
hyperthyroidism
-Drugs: digoxin, quinidine,
epinephrine
-HR: <60 bpm -Depends on how pt
-Rhythm: regular hemodynamically tolerates
-P wave: normal, before -S/sx of symptomatic
each QRS Bradycardia: pale, cool skin;
-PR Int: normal hypotension; weakness;
-QRS: normal angina; dizziness or syncope;
shape/duration confusion or disorientation;
shortness of breath
-HR: 101-200 bpm -Depends on pt tolerance of
-Rhythm: regular HR
-P wave: normal, before -Sx: dizziness, dyspnea,
each QRS hypotension due to decreased
-PR Int: normal cardiac output
-QRS: normal - myocardial o2 consumption
shape/duration associated with HR
-Angina or infarction size
may accompany in pt w CAD
or acute MI
-HR: varies with -Not significant if isolated PAC
underlying rate and in healthy heart
frequency of PAC -Pt report palpitations skip a
-Rhythm: irregular beat
-P wave: different shape -Heart disease: freq PAC-
(notched, downward, enhanced automaticity of
hidden in T wave) atria, or reentry (may warn of
-PR Int: longer or more serious dysrhythmias-
shorter but WNL supraventricular tachycardia)
-QRS: usually normal, if
>0.12 abnormal
conduction via vents
-HR: 150-220 bpm -Depends on associated
-Rhythm: symptoms
regular/slightly irregular -Prolonged episode and HR
-P wave: hidden in T >180 may precipitate
wave or irregular shape decreased CO d/t reduced
-PR Int: shortened or stroke volume
normal -Sx often include hypotension,
-QRS: usually normal dyspnea, angina
-HR: Atrial: 200-350 -High ventricular rates and loss
bpm; of atrial kick (sinus P wave)
Vent: varies r/t decrease CO and cause serious
conduction ratio consequences such as HF, esp
-Rhythm: Regular (A if heart disease hx
and V) - Stroke risk d/t risk thrombus
-P wave: None (F formation in atria from stasis
waves- more F waves of blood
than QRS complexes) -Warfarin given to prevent
-PR Int: Variable/not stroke
-Atropine (anticholinergic) if
symptomatic
-Possible pace maker
-D/t drugs: d/c, reduce dose,
hold
-Treat the underlying cause
-Pain: effective pain
management
-Hypovolemia: treat
hypovolemia
-If stable: vagal maneuvers, IV
beta blockers given to reduce
HR and myocardial o2 demand
-Depends on sx
-Withdrawal of caffeine or
sympathomimetic drugs
-B-blockers may decrease PACs
-Vegal stimulation: Vasalva
maneuver and coughing
-Drug tx: IV adenosine (1st),
IV b-blocker, CCB, amiodarone
-If pt remains unstable,
cardioversion is used
-Radiofrequency catheter
ablation (burn foci generating
ectopic rhythm)
-Primary goal: slow ventricular
response by increasing AV
block
-Cardioversion if an emergency
-Antidysrhythmia drugs:
Amiodarone, propafenone,
ibutilide, flecanide
-Radiofreq catheter ablation
 Rhythm
Atrial Fibrillation
-Total disorganization of
atrial electrical activity due
to multiple ectopic foci
resulting in loss of effective
atrial contraction
-Paroxysmal or persistent
(>7 Days)
-Sometimes, atrial flutter
and atrial fibrillation may
coexist
1 AV Block
-Every impulse conducted to
ventricles but AV conduction
is long
-After through AV, ventricles
respond normally
2 AV Block Type 1
(Wenckebach/Mobitz
I)
-Gradual lengthening of PR
interval d/t prolonged AV
conduction time until an
atrial impulse is
nonconducted and a QRS is
blocked
-Most common in AV but can
occur in His-purkinje system
-Once beat is blocked, cycle
repeats w progressive
lengthening of PR interval
until another QRS drops
2 AV Block Type 2
(Mobitz II)
-P wave nonconducted w/o
progressive PR lengthening
-Usually occurs when block
in one of the bundle
branches is present
-More serious type of block
-Certain # of impulses are
not conducted into the
ventricles
-Occur in ratios 2:1, 3:1, etc
(2 P waves for 1 QRS
complex)
-May occur with varying
ratios
Clinical Associations
-Primarily in pts w/
underlying heart disease
(CAD, rheumatic heart dx,
cardiomyopathy, HTN, HF,
pericarditis)
-Often develops acutely w/
thyrotoxicosis, ETOH intox,
caffeine use, electrolyte
imbalances, stress, cardiac
surgery
-MI, CAD, rheumatic fever,
hyperthyroidism, vagal
stimulation
-Drugs: digoxin, B-blockers,
CCB, flecainide
-Digoxin
-Beta-blockers
-CAD
-Other dx that slow AV
conduction
-Rheumatic heart disease
-CAD
-Anterior MI
-Drug toxicity
ECG Characteristics Clinical Significance Treatment Strip
measurable
-QRS: usually Normal
-HR: Atrial: up to 600 -Results in CO d/t ineffective -Goal: vent response (<100),
bpm; Vent: varies 60-100 atrial contractions and/or rapid prevent cerebral embolism,
controlled, >100 Rapid, ventricular response convert to NSR if possible
<60 slow vent response -Thrombi form in atria d/t blood -Drugs (rate control): CCB, B-
-Rhythm: Irregular stasis blockers, digoxin, dronedarone
-P wave: Replaced by -Thrombi may embolize and -Antidysrhythmia drugs:
fibrillatory waves cause stroke (A Fib responsible Amiodarone, ibutilide
-PR Int: Not measurable for 20% all) -Cardioversion or Ablation
-QRS: normal
shape/duration
-HR: Normal -usually not serious but can be -No treatment
-Rhythm: Regular precursor of higher degrees of -Modifications to potentially
-P wave: Normal AV block causative meds may be
-PR Int: Prolonged -asx considered
(>0.20 seconds) -Monitor pts for new changes
-QRS: normal in rhythm (more serious AV
shape/duration block)
-HR: Atrial: normal; -Usually d/t myocardial -If sx: atropine to HR or
vent: possibly slower d/t ischemia or infarction temporary pacemaker
blocked QRS leading to -Generally transient and well (especially if hx MI)
bradycardia tolerated -If asx: rhythm observed with
-Rhythm: Pattern of -In some pts may be warning transcutaneous pacemaker on
grouped beats sign of a more serious standby
-P wave: Normal shape conduction disturbance such -Bradycardia more likely to
-PR Int: Gradual as complete heart block become symptomatic when
lengthening hypotension, HF or shock is
-QRS: normal present
shape/duration
-HR: Atrial: Normal -Often progresses to 3 block -Temporary pacemaker may be
Vent: depends on -Associated with poor necessary if pt becomes
intrinsic prognosis symptomatic prior to insertion
conduction/degree of -HR frequently results in CO of permanent pacemaker (e.g.,
block with hypotension and hypotension, angina)
-Rhythm: Atrial: Regular myocardial ischemia
Vent: may be irregular -Indication for therapy with
-P wave: Normal shape permanent pacemaker
-PR Int: Normal or
prolonged, constant on
conducted beats
-QRS: Usually >0.12 sec
d/t bundle branch block
 Rhythm
3 AV Block
-Complete Heart Block
-No impulses from atria
conducted
-Atria stimulated and
contract independently of
ventricles
-Vent rhythm is escape
rhythm, ectopic pacemaker
may be above or below the
bundle of His
Premature Vent
Contraction
-Contractions from ectopic
focus within ventricles
-Premature wide/distorted
QRS
-Diff foci: diff shape
(multifocal)
-Same foci: same shape
(unifocal)
-Couplet, trigeminy,
bigeminy
-VTach if 3+ consecutive
PVCs
-Can initiate VTach or VFib
Ventricular
Tachycardia (VT)
-Run of 3 PVCs
-Ventricles take control as
pacer
-Different forms r/t QRS conf
-Monomorphic: QRSs equal
-Polymorphic: QRS gradually
change size/shape/direction
-Torsades de pointes:
polymorphic VT r/t prolonged
QT interval of underlying
rhythm
-Sustained (>30 sec)
-Nonsustained (<30 sec)
-Life threatening d/t CO
and possible development of
VFib
Ventricular
Fibrillation (VF)
-Irregular waveforms varying
shapes and amplitudes
-Firing of multiple ectopic
foci in ventricle (quivering)
Clinical Associations ECG Characteristics Clinical Significance Treatment Strip
Severe Systemic dx -HR: Atrial: sinus 60-100 -CO ischemia, HF, and Symptomatic pts
heart dx -Amyloidosis bpm shock -Transcutaneous pacemaker
-CAD -Scleroderma Vent: r/t block site (AV -Syncope d/t severe used until temporary
-MI 60-40, etc) bradycardia or periods of transvenous pacemaker can be
- Drugs -Rhythm: Regular asystole inserted
Myocarditis -Digoxin (unrelated) -Drugs: Atropine, Epinephrine,
- -Beta-blockers -P wave: Normal shape Isoproterenol, Dopamine are
Cardiomyopa -CCB -PR Int: Variable temporary to HR and BP
thy -QRS: Normal or -If d/t CCB tox, tx w calcium
Widened chloride
**No time relationship
b/t P wave and QRS
complex**
Stimulants -Hypoxia -HR: Varies r/t intrinsic -Usually benign in pt w/ normal -Relates to cause PVCs
-Caffeine -Fever rate, # PVCs heart -Assess hemodynamics r/t
-ETOH -Exercise -Rhythm: Irregular d/t -If hx heart dx: may CO and need for drug tx
-Nicotine -Emotion pre beats precipitate angina and HF -Drug tx: Beta-blockers,
- stress -P wave: Usually lost in (depends on frequency) Procainamide, Amiodarone,
Aminophylli Disease States QRS of PVC -Monitor apical pulse b/c PVCs Xylocaine
ne -MI -PR Int: Not measurable usually arent strong enough to -PVCs in CAD or acute MI
- -Mitral -QRS: Wide, Distorted, illicit peripheral pulses possibly indicate vent irritability so
Epinephrin prolapse >0.12 sec leading to pulse deficit monitor pt response
e -HF -T wave: Large,
- -CAD Opposite direction to
Isoproteren direction of QRS
ol
-Digoxin
-Electrolyte
Imb
-MI -HR: Vent: 150-250 bpm -VT stable (pt has pulse) or can -Precipitating cause must be ID *Polymorphic VT (cont)
-CAD -Rhythm: Regular or be and treated -Prolonged QT interval: IV Magnesium,
-Electrolyte imbalance Irregular -VT unstable (pt has no pulse) *Monomorphic VT Isoproterenol, Dilantin, Lidocaine OR
-Cardiomyopathy -P wave: Usually buried -Sustained VT causes severe -Stable w/ L vent function: IV antitachycardia pacing; D/c drugs that prolong
-Mitral valve prolapse in QRS CO d/t vent diastolic filling Procainamide, Stalol, QT interval; Cardioversion needed if not
-Long QT syndrome *Possible AV dissociation times and loss of atrial Amiodarone or Lidocaine responsive
-Drug toxicity with P wave independent contraction -Unstable, poor L vent *Pulseless VT: CPR and rapid defibrillation
-CNS disorders of QRS complex -Results in hypotension, function: IV Amiodarone or followed by vasopressors and antidysrhythmics
-Pts w no hx CV dx -PR Int: Not measurable pulmonary edema, cerebral Lidocaine then cardioversion if defib unsucessful
-QRS: blood flow and *Polymorphic VT
*Distorted in appearance cardiopulmonary arrest -Normal baseline QT interval:
*Duration >0.12 sec -Must treat quickly even if Beta-blockers, Lidovaine,
*ST-T opposite direction occurs briefly and stops Amiodarone, Procainamide, or
as QRS -May reoccur if no prophylaxis Sotalol, Cardiovert if no
*R-R interval regular or -VFib may also develop change
irregular
-Acute MI -HR: Not measurable -Results in an unresponsive, -CPR
-Myocardial Ischemia -Rhythm: Irregular and pulseless, apneic state -ACLS protocols with
-HF Chaotic -Tx rapidly or pt will die defibrillation and definitive
-Cardiomyopathy -P wave: Not visible drug therapy
-During pacing/caths -PR Int: Not measurable
-Accidental shock -QRS: Not measurable
-Hyperkalemia
 Rhythm Clinical Associations ECG Characteristics Clinical Significance Treatment Strip
-No vent contraction.. NO CO -Hypoxemia
-Acidosis
-Drug toxicity
Asystole Result of: -HR: None -Usually cannot be -CPR
-Absence of ventricular -Advanced cardiac disease -Rhythm: None resuscitated -ACLS initiation with definitive
electrical activity (no -Severe conduction -P wave: None, drug therapy, including: Epi
depolarization occurs) disturbance Occasionally seen and Atropine, intubation and
-Pt unresponsive, pulseless, -End stage HF -PR Int: None possible transcutaneous
apneic -QRS: None temporary pacemaker
-VF may look like Asystole,
so rhythm assessed in >1
lead