Transcript V3ch02a2 - SchultzMedic

 Wandering
Atrial Pacemaker
 Multifocal Atrial Tachycardia
 Atrial Tachycardia
 Premature Atrial Contractions
 Paroxysmal Supraventricular Tachycardia
 Atrial Flutter
 Atrial Fibrillation
Rules of Interpretation
Wandering Pacemaker
Rate
Rhythm
Pacemaker
Site
P Waves
Usually normal
Slightly Irregular
Varies
Changes from beat to
beat
PRI
Normal
QRS
Normal
 Wandering

Etiology



Transfer of pacemaker sites from the sinus node to
other latent pacemaker sites in the atria and AV
junction
A variant of sinus dysrhythmia, a normal phenomenon
in the very young or the aged, Ischemic heart disease,
atrial dilation
Clinical significance



Pacemaker
Usually has no detrimental effects
Precursor of other atrial dysrhythmias such as atrial
fibrillation
Treatment

If the patient is symptomatic, consider adenosine or
verapamil
Rules of Interpretation
Multifocal Atrial Tachycardia
Rate
Rhythm
More than 100
Irregular
Pacemaker Site
Ectopic sites in atria
P Waves
Organized, nonsinus P
waves; at least 3 forms
PRI
Varies depending on
source of impulse
QRS
Variable
 Multifocal

Etiology



Often seen in acutely ill patients
May result from pulmonary disease, metabolic
disorders, ischemic heart disease, or recent surgery
Clinical Significance


Atrial Tachycardia
Presence of multifocal atrial tachycardia often
indicates a serious underlying illness
Treatment

Treat the underlying illness
Rules of Interpretation
Premature Atrial Contractions
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
Depends on
underlying rhythm
Usually regular
except for the PAC
Ectopic sites in atria
Occurs earlier than
expected
Varies dependent on
foci of impulse
Usually normal
 Premature

Etiology



Single electrical impulse originating outside the SA node
May result from use of caffeine, tobacco, or alcohol,
sympathomimetic drugs, ischemic heart disease, hypoxia,
or digitalis toxicity, or may be idiopathic
Clinical Significance


Atrial Contractions
None. Presence of PACs may be a precursor to other atrial
dysrhythmias.
Treatment

None if asymptomatic. Treat symptomatic patients by
administering high-flow, high-concentration oxygen and
establishing IV access.
Rules of Interpretation
Paroxysmal Supraventricular
Tachycardia
Rate
Rhythm
Pacemaker
Site
P Waves
150–250
Regular
Atrial (outside SA
Node)
Often buried in
preceding T wave
PRI
Usually normal
QRS
Usually normal
 Paroxysmal

Etiology



Supraventricular Tachycardia
Rapid atrial depolarization overrides the SA node
May be precipitated by stress, overexertion, smoking,
caffeine
Clinical Significance


May be tolerated well by healthy patients for short
periods
Marked reduction in cardiac output can precipitate
angina, hypotension, or congestive heart failure
 Paroxysmal

Supraventricular Tachycardia
Treatment


Vagal Maneuvers
Pharmacological Therapy


Adenosine
Electrical Therapy
Consider if patient symptomatic with HR >150.
 Synchronized cardioversion starting at 50-100 J (or
biphasic equivalent

Rules of Interpretation
Supraventricular Tachycardia
Rate
Rhythm
Pacemaker Site
P Waves
PRI
QRS
150-250 bpm
Regular
In the atria
Difficult to see
Usually normal
Normal
 Supraventricular

Etiology



Refers to tachycardias that originate above the
ventricles
Use of caffeine, nicotine, or alcohol, cocaine
sympathomimetic drugs, ischemic heart disease
Clinical Significance


Tachycardia
Rapid rates can cause a marked reduction in cardiac
output because of inadequate ventricular filling time
Treatment

Manage with tachycardia algorithm
Click here to view the Tachycardia Management diagram.
Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association.
Rules of Interpretation
Atrial Flutter
Rate
Rhythm
Pacemaker
Site
P Waves
Atrial rate 250–350
Ventricular rate varies
Usually regular
Atrial (outside SA
node)
F waves are
present
PRI
Usually normal
QRS
Usually normal
 Atrial

Etiology

Results when the AV node cannot conduct all the
impulses



Flutter
Impulses may be conducted in fixed or variable ratios
Usually associated with organic disease such as
congestive heart failure (rarely seen with MI)
Clinical Significance



Generally well tolerated
Rapid ventricular rates may compromise cardiac
output and result in symptoms
May occur in conjunction with atrial fibrillation
 Atrial

Flutter
Treatment

Electrical Therapy
Consider if ventricular rate >150 and symptomatic
 Synchronized cardioversion starting at 100 J


Pharmacological Therapy
Diltiazem or beta blockers
 Do not use a calcium channel and beta blockers
concomitantly

Rules of Interpretation
Atrial Fibrillation
Rate
Atrial rate 350–750
Ventricular rate varies
Rhythm
Irregularly irregular
Pacemaker Site
P Waves
PRI
QRS
Atrial (outside SA Node)
None discernible
None
Normal
 Atrial

Etiology



Fibrillation
Results from multiple ectopic foci; AV conduction is
random and highly variable
Often associated with underlying heart disease
Clinical Significance



Atria fail to contract effectively, reducing cardiac
output
Well tolerated with normal ventricular rates
High or low ventricular rates can result in cardiac
compromise
 Atrial

Fibrillation
Treatment

Electrical Therapy
Consider if ventricular rate >150 and symptomatic
 Synchronized cardioversion starting at 100 J


Pharmacological Therapy

Diltiazem or beta blockers
 AV
junction serves two important
physiological purposes:


Slows the impulse between the atria and the
ventricles
Backup pacemaker if the SA node or cells
higher in the conductive system fail to fire
 AV

Locations




Blocks
At the AV node
At the Bundle of His
Below the Bundle of His
Classifications




First-Degree AV block
Type I Second-Degree AV
block
Type II Second-Degree AV
block
Third-Degree AV block
Rules of Interpretation
First-Degree AV Block
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
Depends on
underlying rhythm
Usually regular
SA node or atrial
Normal
>0.20 Seconds
Usually <0.12
seconds
 First-Degree

Etiology



Delay in the conjunction of an impulse through the AV
node
May occur in healthy hearts, but often indicative of
ischemia at the AV junction
Clinical Significance


AV Block
Usually not significant, but new onset may precede a
more advanced block
Treatment


Generally, none required other than observation
Avoid drugs that may further slow AV conduction
Rules of Interpretation
Type I Second-Degree AV Block
Rate
Rhythm
Pacemaker Site
P Waves
Atrial, normal;
ventricular, normal to
slow
Atrial, regular;
ventricular, irregular
SA node or atrial
Normal, some P waves
not followed by QRS
PRI
Increases until QRS is
dropped, then repeats
QRS
Usually <0.12 seconds
 Type

Etiology




Also called Mobitz I, or Wenckebach
Delay increases until an impulse is blocked
Indicative of ischemia at the AV junction
Clinical Significance


I Second-Degree AV Block
Frequently dropped beats can result in cardiac
compromise
Treatment



Generally, none required other than observation
Avoid drugs that may further slow AV conduction
Treat symptomatic bradycardia
Rules of Interpretation
Type II Second-Degree AV Block
Rate
Rhythm
Pacemaker Site
Atrial, normal;
ventricular, slow
May be regular or
irregular
SA node or atrial
P Waves
Normal, some P waves
not followed by QRS
PRI
Constant for conducted
beats, may be >0.21 seconds
QRS
Normal or >0.12
seconds
 Type

Etiology




Also called Mobitz II or infranodal
Intermittent block of impulses
Usually associated with MI or septal necrosis
Clinical Significance



II Second-Degree AV Block
May compromise cardiac output and is indicative of MI
Often develops into full AV blocks
Treatment


Avoid drugs that may further slow AV conduction
Treat symptomatic bradycardia


Consider transcutaneous pacing
Atropine
Rules of Interpretation
2:1 AV Block
Rate
Rhythm
Atrial, normal;
ventricular, slow
Regular
Pacemaker Site
SA node or atrial
P Waves
2 P waves for each
QRS
PRI
QRS
Constant for conducted
beats, may be >0.21 seconds
Normal or >0.12
seconds
 2:1

Etiology



Second degree AV block where there are two P waves
for each QRS
Associated with acute myocardial infarction and septal
necrosis
Clinical significance



AV Block
Can compromise cardiac output
Can develop into full AV block
Treatment


Prepare for transcutaneous pacing
Atropine
Rules of Interpretation
Third-Degree AV Block
Rate
Atrial, normal;
ventricular, 40–60
Rhythm
Both atrial and
ventricular are regular
Pacemaker
Site
SA node and AV
junction or ventricle
P Waves
Normal, with no
correlation to QRS
PRI
No relationship to QRS
QRS
0.12 seconds or greater
 Third-Degree
Block)

Etiology



Absence of conduction between the atria and the
ventricles
Results from AMI, digitalis toxicity, or degeneration of
the conductive system
Clinical Significance


AV Block (Complete Heart
Severely compromised cardiac output
Treatment



Transcutaneous pacing for acutely symptomatic
patients
Treat symptomatic bradycardia
Avoid drugs that may further slow AV conduction
 Dysrhythmias




Premature junctional contractions
Junctional escape complexes and rhythm
Junctional bradycardia
Accelerated junctional rhythm
 Characteristics



of all junctional rhythms
Inverted P Waves in Lead II
PRI of <0.12 Seconds
Normal QRS Complex Duration
Rules of Interpretation
Premature Junctional Contractions
Rate
Depends on
underlying rhythm
Rhythm
Depends on
underlying rhythm
Pacemaker Site
Ectopic focus in the
AV junction
P Waves
Inverted, may occur
after QRS
PRI
QRS
Normal if P occurs
before QRS
Usually normal
 Premature

Etiology



Single electrical impulse originating in the AV node
May occur with use of caffeine, tobacco, alcohol,
sympathomimetic drugs, ischemic heart disease, hypoxia,
or digitalis toxicity, or may be idiopathic
Clinical Significance


Junctional Contractions
Limited, frequent PJCs may be precursor to other
junctional dysrhythmias
Treatment

None usually required
Rules of Interpretation
Junctional Escape Complexes
and Rhythms
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
40–60
Irregular in single
occurrence, regular
in escape rhythm
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Usually normal
 Junctional

Etiology



Results when the AV node becomes the pacemaker
Results from increased vagal tone, pathologically slow SA
discharges, or heart block
Clinical Significance


Escape Complexes and Rhythms
Slow rate may decrease cardiac output, precipitating
angina and other problems
Treatment


None if the patient remains asymptomatic
Treat symptomatic episodes with atropine or pacing
Rules of Interpretation
Junctional Bradycardia
Rate
Rhythm
Pacemaker Site
P Waves
PRI
QRS
Less than 40
Irregular in single
occurrence, regular in
escape rhythm
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Usually normal, may
be greater than 0.12
 Junctional

Etiology



Junctional dysrhythmia with a heart rate less than the
intrinsic rate of the AV node
Increased vagal tone, pathological slow SA node
discharge, heart block, intrinsic disease
Clinical Significance


Bradycardia
Decreased cardiac output
Treatment


Prepare for transcutaneous pacing
Consider Atropine
Rules of Interpretation
Accelerated Junctional Rhythm
Rate
60–100
Rhythm
Regular
Pacemaker Site
P Waves
PRI
QRS
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Normal
 Accelerated

Etiology



Results from increased automaticity in the AV junction
Often occurs due to ischemia of the AV junction
Clinical Significance


Junctional Rhythm
Usually well tolerated, but monitor for other
dysrhythmias
Treatment

None generally required in the prehospital setting
Rules of Interpretation
Accelerated Junctional Rhythm
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
60-100
Regular
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Normal
 Accelerated

Etiology



Results from increased automaticity in the AV junction
Ischemia of the AV junction
Clinical Significance


Junctional Rhythm
Patient should be monitored for other dysrhythmias
Treatment

Prehospital treatment generally is unnecessary
 Ventricular
escape
complexes and
rhythms
 Accelerated
idioventricular
rhythm
 Premature
ventricular
contraction
 Ventricular
tachycardia
 Torsades
de
pointes
 Ventricular
fibrillation
 Asystole
 Artificial
pacemaker rhythm
Rules of Interpretation
Ventricular Escape Complexes
and Rhythms
Rate
Rhythm
Pacemaker
Site
15–40
Escape complex, irregular;
escape rhythm, Regular
Ventricle
P Waves
None
PRI
None
QRS
>0.12 seconds, bizarre
 Ventricular
Rhythms

Etiology



Safety mechanism to prevent cardiac standstill
Results from failure of other foci or high-degree AV
block
Clinical Significance


Escape Complexes and
Decreased cardiac output, possibly to life-threatening
levels
Treatment


For perfusing rhythms, administer atropine and/or TCP
For nonperfusing rhythms, follow pulseless electrical
activity (PEA) protocols
Rules of Interpretation
Accelerated Idioventricular
Rhythm
Rate
Rhythm
Pacemaker
Site
60-100
Escape complex,
irregular;
escape rhythm, Regular
Ventricle
P Waves
None
PRI
None
QRS
>0.12 seconds,
bizarre
 Accelerated

Etiology



A subtype of ventricular escape rhythm that frequently
occurs with MI
Ventricular escape rhythm with a rate of 60–110
Clinical Significance


Idioventricular Rhythm
May cause decreased cardiac output if the rate slows
Treatment


Does not usually require treatment unless the patient
becomes hemodynamically unstable
Primary goal is to treat the underlying MI
Rules of Interpretation
Premature Ventricular Contractions
Rate
Underlying rhythm
Rhythm
Interrupts regular
underlying rhythm
Pacemaker Site
Ventricle
P Waves
None
PRI
None
QRS
>0.12 seconds, bizarre
 Premature

Ventricular Contractions
Etiology



Single ectopic impulse resulting from an irritable focus
in either ventricle
Myocardial ischemia, increased sympathetic tone,
hypoxia, idiopathic causes, acid-base disturbances,
electrolyte imbalances, or as a normal variation of the
ECG
May occur in patterns
Bigeminy, trigeminy, or quadrigeminy
 Couplets and triplets

 Premature

Ventricular Contractions
Clinical Significance

Malignant PVCs


More than 6/minute, R on T phenomenon, couplets or runs
of ventricular tachycardia, multifocal PVCs, or PVCs
associated with chest pain
Ventricles do not adequately fill, causing decreased
cardiac output
 Premature

Ventricular Contractions
Treatment


Nonmalignant PVCs do not usually require treatment in
patients without a cardiac history
Cardiac patient with nonmalignant PVCs


Administer oxygen and establish IV access
Malignant PVCs:
Lidocaine 1.0 –1.5 mg/kg IV bolus
 Repeat doses of 0.5-0.75 mg/kg to max dose of 3.0 mg/kg
 If PVCs are suppressed, administer lidocaine drip 2–4
mg/min
 Reduce the dose in patients with decreased output or
decreased hepatic function and patients >70 years old

Rules of Interpretation
Ventricular Tachycardia
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
100–250
Usually regular
Ventricle
If present, not
associated with
QRS
None
>0.12 seconds,
bizarre
 Ventricular

Etiology



3 or more ventricular complexes in succession at a
rate of >100
Causes include myocardial ischemia, increased
sympathetic tone, hypoxia, idiopathic causes, acidbase disturbances, or electrolyte imbalances
VT may appear monomorphic or polymorphic


Tachycardia
Torsade’s De Pointes
Clinical Significance


Decreased cardiac output, possibly to life-threatening
levels
May deteriorate into ventricular fibrillation
Click here to view an animation on dysrhythmia.
Click here to view the Tachycardia Management diagram.
Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association.
 Torsades
de pointes
Polymorphic VT
 Use of certain
antidysrhythmic
drugs
 Exacerbated by
coadministration of
antihistamines, azole
antifungal agents and
macrolide

 Torsades

Typically occurs in nonsustained bursts




de pointes
Prolonged QT interval during “breaks”
QRS rates from 166–300
RR interval highly variable
Treatment



Do not treat as standard VT
Administer magnesium sulfate 1–2 g diluted in 100 ml
D5W over 1–2 minutes
Overdrive pacing
Rules of Interpretation
Ventricular Fibrillation
Rate
Rhythm
No organized
rhythm
No organized
rhythm
Pacemaker
Site
Numerous
ventricular foci
P Waves
Usually absent
PRI
None
QRS
None
 Ventricular

Etiology


Fibrillation
Wide variety of causes, often resulting from advanced
coronary artery disease
Clinical Significance

Lethal dysrhythmia with no cardiac output and no
organized electrical pattern
 Ventricular

Fibrillation
Treatment

Initiate CPR

Defibrillate with 360 J (or biphasic equivalent)

Control the airway and establish IV access

Administer epinephrine 1:10,000 every 3–5 minutes



Consider 40 IU Vasopressin IV (one time only)
Consider second-line drugs

Amiodarone

Lidocaine
Provide continuous compressions
Rules of Interpretation
Asystole
Rate
Rhythm
Pacemaker
Site
No Electrical
Activity
No Electrical
Activity
No Electrical
Activity
P Waves
Absent
PRI
Absent
QRS
Absent
 Asystole

Etiology



Primary event in cardiac arrest, resulting from massive
myocardial infarction, ischemia, and necrosis
Final outcome of ventricular fibrillation
Clinical Significance


Asystole results in cardiac arrest
Poor prognosis for resuscitation
 Asystole

Treatment



Administer CPR and manage the airway
Treat for ventricular fibrillation if there is any doubt
about the underlying rhythm
Administer medications:

Epinephrine and Atropine
Click here to view the Pulseless Arrest diagram.
Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Care,” Circulation 2005, Volume 112, IV-59. © 2005 American Heart Association.
Rules of Interpretation
Artificial Pacemaker
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
Varies with
pacemaker
May be regular or
irregular
Depends upon
electrode placement
None produced by
ventricular pacemakers;
pacemaker spike
If present, varies
>0.12 seconds,
bizarre
 Artificial

Etiology



Pacemaker Rhythm
Single vs. dual chamber pacemakers
Fixed-rate vs. demand pacemakers
Clinical Significance

Used in patients with a chronic high-grade heart block,
sick sinus syndrome, or severe symptomatic
bradycardia
 Artificial

Problems with Pacemakers




Battery failure
“Runaway” pacers
Displaced leads
Management Considerations



Pacemaker Rhythm
Identify patients with pacemakers
Treat the patient
Use of a Magnet
 Characteristics
Electrical impulses are present, but with no
accompanying mechanical contractions of the
heart
 Treat the patient, not the monitor

 Causes

Hypovolemia, cardiac tamponade, tension
pneumothorax, hypoxemia, acidosis, massive
pulmonary embolism, ventricular wall rupture
 Treatment



Prompt recognition and early treatment
Epinephrine 1 mg every 3–5 minutes
Treat underlying cause of PEA
 Categories
of Conductive Disorders
Atrioventricular Blocks
 Disturbances of Ventricular Conduction
 Pre-excitation Syndromes

 Disturbances

Aberrant Conduction


All supraventricular beats are conducted through the
ventricles in a delayed manner
Causes



A single supraventricular beat conducted through the
ventricles in a delayed manner
Bundle Branch Block


of Ventricular Conduction
Ischemia or necrosis of a bundle branch
PAC or PJC that reaches one of the bundle branches in
a refractory period
Differentiation of SVT and Wide-Complex
Tachycardias
 Pre-excitation
Syndromes

Excitation by an impulse
that bypasses the AV
node


Creates Delta wave slur
Wolff-Parkinson-White
(WPW) syndrome


Conduction from the atria to
the ventricles is abnormal
Associated with
tachydysrhythmias
 Wolfe-
ParkinsonWhite
Syndrome
 Hypokalemia



Normal potassium
levels are 3.5–-5.0
mEg/L
Flattened T waves
Prominent U waves
 Hyperkalemia

Tall Ts

Suspect in patients with a
history of renal failure
 Hypocalcemia


Can be caused by the
use of diuretics and
certain endocrine
conditions
Prolongs ST segment
 Hypercalcemia


Can be caused by
adrenal insufficiency,
hyperparathyroidism,
kidney failure, or
malignancies
Shortens ST segment
 Digitalis


use
Sagging or scooping
of the ST segment
Prolonged PR interval
 Hypothermia


Osborn wave (“J”
wave)
T wave inversion,
sinus bradycardia,
atrial fibrillation
or flutter, AV
blocks, PVCs, VF,
asystole
 Cardiovascular
Anatomy
 Cardiovascular Physiology
 Electrocardiographic Monitoring
 Dysrhythmias