Rhythm Clinical Associations ECG Characteristics Clinical Significance Treatment Strip

Sinus Bradycardia -Normal in some aerobic athletes -HR: <60 bpm -Depends on how pt hemodynamically -Atropine (anticholinergic) if
-Conduction path same as NSR and some pts during sleep -Rhythm: regular tolerates symptomatic
-SA node fires at <60 bpm -Carotid sinus massage, Vasalva -P wave: normal, before each -S/sx of symptomatic Bradycardia: -Possible pace maker
-Symptomatic- HR <60 resulting in maneuver, Hypothermia, Increased QRS pale, cool skin; hypotension; -D/t drugs: d/c, reduce dose, hold
symptoms (chest pain, syncope intraocular pressure, Vegal -PR Int: normal weakness; angina; dizziness or
stimulation -QRS: normal shape/duration syncope; confusion or disorientation;
-Drugs (b-blockers, CCB) shortness of breath
Sinus Tachycardia -Exercise, fever, pain, hypotension, -HR: 101-200 bpm -Depends on pt tolerance of ↑ HR -Treat the underlying cause
-Conduction path same as NSR hypovolemia, anemia, hypoxia, -Rhythm: regular -Sx: dizziness, dyspnea, hypotension -Pain: effective pain management
-D/c rate from sinus node increases hypoglycemia, MI, HF, -P wave: normal, before each due to decreased cardiac output -Hypovolemia: treat hypovolemia
b/c vagal inhibition or sympathetic hyperthyroidism, anxiety, fear QRS -↑ myocardial o2 consumption -If stable: vagal maneuvers, IV beta
stimulation -Drugs: epinephrine, -PR Int: normal associated with ↑HR blockers given to reduce HR and
-Sinus rate is 101-200 bpm norepinephrine, atropine, caffeine, -QRS: normal shape/duration -Angina or ↑infarction size may myocardial o2 demand
theophylline, Procardia, hydralazine accompany in pt w CAD or acute MI
Premature Atrial Contraction -Normal Heart: emotional stress, -HR: varies with underlying -Not significant if isolated PAC in -Depends on sx
physical fatigue, caffeine, tobacco, rate and frequency of PAC healthy heart -Withdrawal of caffeine or

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-Originates at site other than SA
-Starts L/R atrium travels across alcohol -Rhythm: irregular -Pt report “palpitations” “skip a beat” sympathomimetic drugs

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atrium by abnormal path creating -Electrolyte imbalance, -P wave: different shape -Heart disease: freq PAC- enhanced -B-blockers may decrease PACs
distorted P wave hyperthyroidism, COPD, (notched, downward, hidden automaticity of atria, or reentry (may
-At AV it may be stopped, delayed -Heart disease: CAD, valvular in T wave) warn of more serious dysrhythmias-

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(long PR interval) or go normally disease -PR Int: longer or shorter but supraventricular tachycardia)

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WNL
-QRS: usually normal, if >0.12
abnormal conduction via vents

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Supraventricular -Normal Heart: overexertion, -HR: 150-220 bpm -Depends on associated symptoms -Vegal stimulation: Vasalva maneuver
Tachycardia emotional stress, deep inspiration, -Rhythm: regular/slightly -Prolonged episode and HR >180 may and coughing
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stimulants (caffeine and tobacco) irregular precipitate decreased CO d/t reduced -Drug tx: IV adenosine (1 ),

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-Originates in ectopic focus above
-Rheumatic heart disease, digitalis -P wave: hidden in T wave or stroke volume IV b-blocker, CCB, amiodarone
bundle of His
toxicity, CAD, cor pulmonale irregular shape -Sx often include hypotension, -If pt remains unstable, cardioversion

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-Occurs d/t reexcitation of atria
-PR Int: shortened or normal dyspnea, angina is used
when there’s a one-way block
-QRS: usually normal -Radiofrequency catheter ablation
-Abrupt onset and termination

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(burn foci generating ectopic rhythm)
followed by brief asystole
-Some degree AV block possible
Atrial Flutter -Rarely occurs in healthy heart -HR: Atrial: 200-350 bpm; -High ventricular rates and loss of -Primary goal: slow ventricular
-Atrial tachydysrhythmia
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-Diseased states: CAD, HTN, mitral Vent: varies r/t conduction atrial “kick” (sinus P wave) decrease response by increasing AV block
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-ID by recurring, regular, sawtooth valve disorders, PE, chronic lung ratio CO and cause serious consequences -Cardioversion if an emergency
shaped flutter waves disease, cor pulmonale, -Rhythm: Regular (A and V) such as HF, esp if heart disease hx -Antidysrhythmia drugs: Amiodarone,
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-Originate from single ectopic focus cardiomyopathy, hyperthyroidism -P wave: None (F waves- more -↑ Stroke risk d/t risk thrombus propafenone, ibutilide, flecanide
in R atrium (or L but uncommon) -Drugs: digoxin, quinidine, F waves than QRS complexes) formation in atria from stasis of blood -Radiofreq catheter ablation
epinephrine -PR Int: Variable/not -Warfarin given to prevent stroke
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measurable
-QRS: usually Normal
Atrial Fibrillation -Primarily in pts w/ underlying heart -HR: Atrial: up to 600 bpm; -Results in ↓CO d/t ineffective atrial -Goal: ↓vent response (<100),
-Total disorganization of atrial disease (CAD, rheumatic heart dx, Vent: varies 60-100 controlled, contractions and/or rapid ventricular prevent cerebral embolism, convert to
cardiomyopathy, HTN, HF, >100 Rapid, <60 slow vent response NSR if possible
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electrical activity due to multiple

ectopic foci resulting in loss of pericarditis) response -Thrombi form in atria d/t blood stasis -Drugs (rate control): CCB, B-blockers,
effective atrial contraction -Often develops acutely w/ -Rhythm: Irregular -Thrombi may embolize and cause digoxin, dronedarone
thyrotoxicosis, ETOH intox, caffeine -P wave: Replaced by stroke (A Fib responsible for 20% all) -Antidysrhythmia drugs: Amiodarone,
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-Paroxysmal or persistent (>7 Days)

-Sometimes, atrial flutter and atrial use, electrolyte imbalances, stress, fibrillatory waves ibutilide
fibrillation may coexist cardiac surgery -PR Int: Not measurable -Cardioversion or Ablation
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-QRS: normal shape/duration

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 Rhythm Clinical Associations ECG Characteristics Clinical Significance Treatment Strip
1⁰ AV Block -MI, CAD, rheumatic fever, -HR: Normal -usually not serious but can be -No treatment
hyperthyroidism, vagal stimulation -Rhythm: Regular precursor of higher degrees of AV -Modifications to potentially causative
-Every impulse conducted to -Drugs: digoxin, B-blockers, CCB, -P wave: Normal block meds may be considered
ventricles but AV conduction is long flecainide -PR Int: Prolonged (>0.20 -asx -Monitor pts for new changes in
-After through AV, ventricles seconds) rhythm (more serious AV block)
respond normally -QRS: normal shape/duration

2⁰ AV Block Type 1 -Digoxin -HR: Atrial: normal; vent: -Usually d/t myocardial ischemia or -If sx: atropine to ↑HR or temporary
(Wenckebach/Mobitz I) -Beta-blockers possibly slower d/t blocked infarction pacemaker (especially if hx MI)
-CAD QRS leading to bradycardia -Generally transient and well tolerated -If asx: rhythm observed with
-Gradual lengthening of PR interval
-Other dx that slow AV conduction -Rhythm: Pattern of grouped -In some pts may be warning sign of a transcutaneous pacemaker on standby
d/t prolonged AV conduction time
beats more serious conduction disturbance -Bradycardia more likely to become
until an atrial impulse is
-P wave: Normal shape such as complete heart block symptomatic when hypotension, HF or
nonconducted and a QRS is blocked
-PR Int: Gradual lengthening shock is present
-Most common in AV but can occur
-QRS: normal shape/duration
in His-purkinje system

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-Once beat is blocked, cycle repeats

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w progressive lengthening of PR
interval until another QRS drops
2⁰ AV Block Type 2 -Rheumatic heart disease -HR: Atrial: Normal -Often progresses to 3⁰ block -Temporary pacemaker may be

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(Mobitz II) -CAD Vent: depends on intrinsic -Associated with poor prognosis necessary if pt becomes symptomatic
-Anterior MI conduction/degree of block -↓HR frequently results in ↓CO with prior to insertion of permanent

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-P wave nonconducted w/o
-Drug toxicity -Rhythm: Atrial: Regular hypotension and myocardial ischemia pacemaker (e.g., hypotension, angina)
progressive PR lengthening
Vent: may be irregular -Indication for therapy with
-Usually occurs when block in one

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-P wave: Normal shape permanent pacemaker
of the bundle branches is present
-PR Int: Normal or prolonged,
-More serious type of block
constant on conducted beats
-Certain # of impulses are not

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-QRS: Usually >0.12 sec d/t
conducted into the ventricles
bundle branch block
-Occur in ratios 2:1, 3:1, etc (2 P

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waves for 1 QRS complex)
-May occur with varying ratios

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3⁰ AV Block Severe heart Systemic dx -HR: Atrial: sinus 60-100 bpm -↓CO→ ischemia, HF, and shock Symptomatic pts
-Complete Heart Block dx -Amyloidosis Vent: r/t block site (AV 60-40, -Syncope d/t severe bradycardia or -Transcutaneous pacemaker used until
-No impulses from atria conducted -CAD -Scleroderma etc) periods of asystole temporary transvenous pacemaker
-Atria stimulated and contract -MI

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independently of ventricles -Myocarditis Drugs -P wave: Normal shape -Drugs: Atropine, Epinephrine,
-Vent rhythm is escape rhythm, - -Digoxin -PR Int: Variable Isoproterenol, Dopamine are
Cardiomyopathy -Beta-blockers -QRS: Normal or Widened temporary to ↑HR and BP
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ectopic pacemaker may be above or
below the bundle of His -CCB **No time relationship b/t P -If d/t CCB tox, tx w calcium chloride
wave and QRS complex**
Premature Vent Contraction Stimulants -Hypoxia -HR: Varies r/t intrinsic rate, # -Usually benign in pt w/ normal heart -Relates to cause PVCs
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-Contractions from ectopic focus -Caffeine -Fever PVCs -If hx heart dx: may ↓CO and -Assess hemodynamics r/t need for
within ventricles -ETOH -Exercise -Rhythm: Irregular d/t pre precipitate angina and HF (depends on drug tx
-Premature wide/distorted QRS -Nicotine -Emotion stress beats frequency) -Drug tx: Beta-blockers, Procainamide,
-Diff foci: diff shape (multifocal) - Disease States -P wave: Usually lost in QRS of -Monitor apical pulse b/c PVCs usually Amiodarone, Xylocaine
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-Same foci: same shape (unifocal) Aminophylline -MI PVC aren’t strong enough to illicit -PVCs in CAD or acute MI indicate vent
-Couplet, trigeminy, bigeminy -Epinephrine -Mitral prolapse -PR Int: Not measurable peripheral pulses possibly leading to irritability so monitor pt response
-VTach if 3+ consecutive PVCs -Isoproterenol -HF -QRS: Wide, Distorted, >0.12 pulse deficit
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-Can initiate VTach or VFib -Digoxin -CAD sec

-Electrolyte -T wave: Large, Opposite
Imb direction to direction of QRS
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 Rhythm Clinical Associations ECG Characteristics Clinical Significance Treatment Strip
Ventricular Tachycardia (VT) -MI -HR: Vent: 150-250 bpm -VT stable (pt has pulse) or can be -Precipitating cause must be ID and *Polymorphic VT (cont)
-Run of ≥3 PVCs -CAD -Rhythm: Regular or Irregular -VT unstable (pt has no pulse) treated -Prolonged QT interval: IV Magnesium, Isoproterenol,
-Ventricles take control as pacer -Electrolyte imbalance -P wave: Usually buried in QRS -Sustained VT causes severe ↓CO d/t *Monomorphic VT Dilantin, Lidocaine OR antitachycardia pacing; D/c drugs
-Different forms r/t QRS conf -Cardiomyopathy *Possible AV dissociation with ↓vent diastolic filling times and loss of -Stable w/ L vent function: IV that prolong QT interval; Cardioversion needed if not
-Monomorphic: QRSs equal -Mitral valve prolapse P wave independent of QRS atrial contraction Procainamide, Stalol, Amiodarone or responsive
-Polymorphic: QRS gradually change -Long QT syndrome complex -Results in hypotension, pulmonary Lidocaine *Pulseless VT: CPR and rapid defibrillation followed by
size/shape/direction -Drug toxicity -PR Int: Not measurable edema, ↓cerebral blood flow and -Unstable, poor L vent function: IV vasopressors and antidysrhythmics if defib unsucessful
-Torsades de pointes: polymorphic -CNS disorders -QRS: cardiopulmonary arrest Amiodarone or Lidocaine then
VT r/t prolonged QT interval of -Pts w no hx CV dx *Distorted in appearance -Must treat quickly even if occurs cardioversion
underlying rhythm *Duration >0.12 sec briefly and stops *Polymorphic VT
-Sustained (>30 sec) *ST-T opposite direction as -May reoccur if no prophylaxis -Normal baseline QT interval: Beta-
-Nonsustained (<30 sec) QRS -VFib may also develop blockers, Lidovaine, Amiodarone,
-Life threatening d/t ↓CO and *R-R interval regular or Procainamide, or Sotalol, Cardiovert if
possible development of VFib irregular no change

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Ventricular Fibrillation (VF) -Acute MI -HR: Not measurable -Results in an unresponsive, pulseless, -CPR

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-Irregular waveforms varying shapes -Myocardial Ischemia -Rhythm: Irregular and Chaotic apneic state -ACLS protocols with defibrillation and
and amplitudes -HF -P wave: Not visible -Tx rapidly or pt will die definitive drug therapy
-Firing of multiple ectopic foci in -Cardiomyopathy -PR Int: Not measurable

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ventricle (quivering) -During pacing/caths -QRS: Not measurable

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-No vent contraction.. NO CO -Accidental shock
-Hyperkalemia
-Hypoxemia

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-Acidosis
-Drug toxicity
Asystole Result of: -HR: None -Usually cannot be resuscitated -CPR

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-Absence of ventricular electrical -Advanced cardiac disease -Rhythm: None -ACLS initiation with definitive drug
-Severe conduction disturbance -P wave: None, Occasionally therapy, including: Epi and Atropine,

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activity (no depolarization occurs)
-Pt unresponsive, pulseless, apneic -End stage HF seen intubation and possible
-VF may look like Asystole, so -PR Int: None transcutaneous temporary pacemaker

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rhythm assessed in >1 lead -QRS: None

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