Dysrhythmia Basic A Test Answers

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Sinus Rhythm
Sinus Rhythm
60-100bpm Present P-wave PRI 0.12-0.20 seconds QRS 0.12> seconds
Sinus Bradycardia
Sinus Bradycardia
40-60bpm Present P-wave PRI 0.12-0.20 seconds QRS 0.12> seconds
Sinus Tachycardia
Sinus Tachycardia
100-160bpm Present P-wave PRI 0.12-0.20 seconds QRS 0.12> seconds
Sinus arrhythmia
Sinus arrhythmia
Irregular Normal or slow Present P-Wave PRI 0.12-0.20 seconds QRS 0.12> seconds
Sinus Arrest/Exit block
Sinus Arrest/Exit block
Regular rhythm w/ pause P-wave not seen until next complex
Atrial Fibrillation (A-Fib)
Atrial Fibrillation (A-Fib)
Grossly irregular 400< ventricular varies Wavy P-wave PRI not measureable QRS 0.12> seconds
Atrial Flutter
Atrial Flutter
Regular or Irregular 250-400 (depending on conduction) “Saw-tooth” P-waves PRI not measureable QRS 0.12> seconds
Paced Atrial
Paced Atrial
“Spike” before P-wave
1° AVB
1° AVB
Rate determined by rhythm 1 P-wave to each QRS PRI prolonged >0.20 seconds QRS 0.10>
2° AVB Type I (Wenkebach)
2° AVB Type I (Wenkebach)
“Long, Long, Longer, Dropped… then you have a Wenkebach” Persistent P-waves until not included PRI progressively lengthen QRS 0.10>
2° AVB Type II (Mobitz)
2° AVB Type II (Mobitz)
Irregular ventricular P-wave before each QRS until no QRS PRI normal until no QRS QRS 0.10>
2° AVB 2:1
2° AVB 2:1
Every other beat has a lone P-wave
3° AV Block (Complete Heart Block)
3° AV Block (Complete Heart Block)
P-save has no relation to QRS PRI varies greatly QRS normal-wide
Bundle Branch Block (BBB)
Bundle Branch Block (BBB)
Rate determined by rhythm Normal P-wave PRI 0.12-0.20 QRS wide 0.12<
Bigeminy
Bigeminy
every other beat is premature
Trigeminy
Trigeminy
pattern in which every third complex is a premature beat
Premature Atrial Contraction (PAC)
Premature Atrial Contraction (PAC)
Irregular Rate determined by rhythm P-wave is premature and abnormally sized PRI 0.12-0.20 seconds QRS <0.12 seconds
Premature Junctional Contraction (PJC)
Premature Junctional Contraction (PJC)
Irregular Rate determined by rhythm P-wave is premature and abnormally sized PRI can be prolonged QRS narrow
Junctional Rhythm (Junctional Escape Rhythm)
Junctional Rhythm (Junctional Escape Rhythm)
40-60bpm Absent P-wave PRI not measureable QRS 0.12> seconds
Junctional Tachycardia
Junctional Tachycardia
>100bpm Inverted/Absent P-wave PRI not measureable QRS <0.12
Accelerated Junctional
Accelerated Junctional
60-100bpm Inverted/Absent P-wave PRI not measureable QRS 0.12> seconds
Wandering Atrial Pacemaker
Wandering Atrial Pacemaker
Occasional “spike” for P-wave
Premature Ventricular Complex (PVC)
Premature Ventricular Complex (PVC)
Usually regular Rate determined by rhythm Absent P-wave PRI not measureable QRS premature and wide
Idioventricular Rhythm
Idioventricular Rhythm
Regular 20-40bpm Absent P-wave PRI N/A QRS wide >0.10
Accelerated Idioventricular Rhythm
Accelerated Idioventricular Rhythm
Regular 40-100bpm Absent P-wave PRI N/A QRS >0.12 wide & bizarre
Supraventricular Tachycardia (SVT)
Supraventricular Tachycardia (SVT)
Regular >150bpm Not discernible P-wave PRI can’t measure QRS narrow
Ventricular tachycardia (V-tach)
Ventricular tachycardia (V-tach)
Regular 140-250bpm No P-wave PRI N/A QRS wide
Ventricular fibrillation (V-fib)
Ventricular fibrillation (V-fib)
No rhythm No P-wave PRI N/A QRS absent
Paced Ventricular
Paced Ventricular
“Spike” after P-wave to fire ventricular contraction
Torsades de pointes (polymorphic VT)
Torsades de pointes (polymorphic VT)
Regular of irregular >200bpm No P-waves PRI N/A QRS twisting “Ribbon”
Ventricular Standstill (Asystole)
Ventricular Standstill (Asystole)
Regular Atrial beats Only atrial depolarization exists P to P intervals No PRI No QRS
SA node BPM
60-100 bpm
AV node BPM
55-60 BPM
Bundle of His BPM
40-45 BPM
normal PR interval
0.12-0.20 seconds
normal QRS
0.08-0.10
premature atrial contraction
premature atrial contraction
PACs – distinguishing features
PAC is premature and abnormal in size, shape and direction; commonly found in preceding T wave distorting T wave contour
Sinus Rhythm
Sinus Rhythm
Normal Conduction Path
Sinus Bradycardia
Sinus Bradycardia
Conduction same as NSR; SA node fires < 60bpm
sinus rhythm – clinical associations
normal intrinsic rhythm, sinus node dominant PM of the heart
Sinus bradycardia – clinical associations
common after AMI; reperfusion arrhythmia, vagal stimulation, OSA, hyperkalemia, Inc ICP, drugs (dig/BB/CCB)
Sinus Tachycardia
Sinus Tachycardia
What rhythm is this?
Sinus Arrhythmia
Sinus Arrhythmia
What rhythm is this?
Premature Atrial Contraction
Premature Atrial Contraction
What rhythm is this?
Paroxysmal Atrial Tachycardia / SVT
Paroxysmal Atrial Tachycardia / SVT
What rhythm is this?
Atrial Flutter
Atrial Flutter
What rhythm is this?
Atrial Fibrillation
Atrial Fibrillation
What rhythm is this?
Wandering Atrial Pacemaker
Wandering Atrial Pacemaker
What rhythm is this?
Premature Juncture Contraction
Premature Juncture Contraction
What rhythm is this?
Junctional Rhythm
Junctional Rhythm
What rhythm is this?
Accelerated Junctional Rhythm
Accelerated Junctional Rhythm
What rhythm is this?
Junctional Tachycardia
Junctional Tachycardia
What rhythm is this?
1st degree AV block
1st degree AV block
What rhythm is this?
2nd degree AV block - Mobitz 1
2nd degree AV block – Mobitz 1
What rhythm is this?
2nd degree AV block - Mobitz 2
2nd degree AV block – Mobitz 2
What rhythm is this?
3rd degree AV block
3rd degree AV block
What rhythm is this?
Premature Ventricular Contraction
Premature Ventricular Contraction
What rhythm is this?
Idioventricular Rhythm
Idioventricular Rhythm
Which rhythm is this?
Accelerate Idioventricular Rhythm
Accelerate Idioventricular Rhythm
What rhythm is this?
Ventricular Tachycardia
Ventricular Tachycardia
What rhythm is this?
Ventricular Fibrillation
Ventricular Fibrillation
What rhythm is this?
Asystole
Asystole
What rhythm is this?
Sinus Rhythm ECG Characteristics
Rate: 60-100; regular rhythm: Normal P wave 1:1 w/ QRS; PR interval 0.12-20sec; QRS < 0.10 seconds
Sinus Rhythm – Clinical Associations
Normal intrinsic rhythm, sinus node dominant PM of the heart
sinus arrhythmia – clinical significance
atria and ventricles depolarize in synchrony, optimizing cardiac output
treatment for symptomatic bradycardia
atropine 0.5mg IVP; TCP, TV pacing, PPM implantation
ECG characteristics of symptomatic bradycardia
rate < 60; regular rhythm, Pwave, PR/QRS intervals
clinical associations of symptomatic bradycardia
common after AMI; reperfusion arrhythmia, vagal stimulation, OSA< hyperkalemia, increasing ICP, drugs (dig/BB/CCB)
clinical significance of symptomatic bradycardia
normal response under certain conditions (sleep/sedation); persistent SB may decrease CO d/t low SV
ECG characteristics of Sinus tach
Rate > 100; regular rhythm; normal conductance
clinical associations w/ sinus tachycardia
anxiety, hypoxia, hypovolemia, hypotension, heart failure, fever, pain, drugs, stress, exercise
clinical significance w/ sinus tachycardia
normal response to increased metabolic demand. begins/ends gradually; persistent ST may decrease CO d/t low SV
sinus tachycardia tx
tx underlying cause w/ AV nodal blockers (BB, CCB, digoxin)
sinus arrhythmia tx
does not require tx unless associated w/ sx bradycardia
premature atrial contraction tx
frequent ones may initiate more serious arrhythymias like afib; check electrolytes
clinical associations w/ sinus arrhythmia
normal phenomenon, often seen in youth, sometimes in adults
clinical association w/ PACs
emotional stress, hypoxia, electrolyte imbalances, CHF, ingestions
clinical association w/ paroxysmal atrial tachycardia / SVT
normal heart: overexertion, emotional stress, stimulants (caffeine and tobacco)
clinical association w/ atrial flutter
CAD, HTN, mitral valve disorders, PE, chronic lung dz; cor pulmonale, cardiomyopathy, hyperthyroidism
clinical association w/ AFIB
CAD, rheumatic heart dz, cardiomyopathy, HTN, HF, pericarditis; can develop acutely w/ thyrotoxicosis, ETOH intox, caffeine use, e- imbalances, stress, cardiac surgery
clinical associations w/ wandering atrial pacemaker
usually caused by increased vagal tone; can be d/t digoxin toxicity
clinical associations w/ premature junctional contraction
caffeine, ETOH, tobacco, e- imbalance, IWMI, digoxin toxicity –> increased automaticity of the AV junction
clinical associations w/ junctional rhythm;
digoxin toxicity, IWMI, occurs when SR rate < AV jxn
clinical associations w/ accelerated junctional rhythm
IWMI, digoxin toxicity, SR rate < AV jxn
clinical associations for junctional tachycardia
IWMI and digoxin toxicity; SR < AV jxn
clinical associations for 1st degree AVB
MI, CAD, rheumatic fever, hyperthyroidism, vagal stimulation, drugs (BB, CCB, fleicanide)
clinical associations for 2nd degree AVB – mobitz 1
digoxin, beta-blockers, CAD, other dx that slow AV conduction
clinical associations for 2nd degree AVB – mobitz 2
rheumatic heart dz, CAD, AWMI, drug toxicity
clinical associations for 3rd degree AVB
severe heart dz (CAD, MI, myocarditis, CM,) systemic dx (amyloidosis, scleroderma), drugs (digoxin, BB, CCB)
clinical associations w/ PVC
stimulants (caffeine, ETOH, nicotine); drugs (aminophylline, epinephrine, isoproterenol, digoxin); e- imbalances, hypoxia, fever, exercise, emotion stress, disease states, MI, mitral prolapse, HF, CAD
clinical association w/ idioventricular rhythm
intermittent short runs are usually d/t increased vagal effect on the SA node; continuous IVR occurs in advanced heart dz and is gen associated w/ poor prognosis;
clinical association w/ AIVR
common after acute IWMI, common reperfusing rhythm following thrombolysis or angioplasty
clinical association w/ VTACH
MI, CAD, e- imbalance, CM, MVP, long QT syndrome, drug tox, CNS disorders, Pts w/ no hx of CV dx
clinical association in VFIB
acute MI, MI, HF, CM, during pacing/caths; accidental shock: hyperkalemia, hypoxemia, acidosis, drug toxicity
clinical associations with asystole
hypoxia, acidosis, hyper/hypokalemia, hypovolemia, tamponade, toxins, tension PHTX, PE, ACS
clinical significance of asystole
usually cannot be resuscitated
treatment for asystole
CPR; ACLS initiation w/ definitive drug therapy including EPI/atropine, intubation and possible transQ temporary pacemaker
treatment for VFIB
CPR, ACLS protocols w/ defibrillation and definitive drug therapy
clinical significance of VFIB
results in a unresponsive, pulseless, apneic state; tx rapidly or pt will die
tx for VTACH (monomorphic VT w/ LV fxn)
IV procainamide, stalol, amiodarone or lidocaine
tx for VTACH (monomorphic, unstable w/ poor LV fxn)
IV amiodarone, or lidocaine then cardioversion
tx for polymorphic VT
beta-blockers, lidocaine, amiodarone, procainamide, sotalol, cardiovert if no change
tx for AIVR
none, usually spontaneous and resolves spontaneoulsy
treatment for idioventricular rhythm
bradycardia ACLS algorithm
clinical significance of VTACH
can cause severe decreased CO and hypotension, pulmonary edema, decreased cerebral bloodflow and CP arrest; must treat quickly
clinical significance of IVR
normal rhythm of the ventricles; may deteriorate into an agonal rhythms
tx for PVCs
beta-blockers, procainamide, amiodarone, lidocaine, can indicate ventricular irritability
tx for 3rd degree AVB
transQ pacing until transvenous PM insertion; atropine, epinephrine, isoproterenol, dopamine to increase HR and BP; calcium chloride to reverse Ca tox

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