Transcript cardio i - jan 2015

CARDIOLOGY I
MASON COUNTY EMS
ALS/ILS OTEP
Topics
 Review of Cardiovascular
Anatomy
 Cardiac Physiology
 Electrocardiographic Monitoring
 Dysrhythmias
Cardiovascular Anatomy
Blood Flow
 From the Body
• Right Atrium
 To the Lungs
• Right
Ventricle
 From the
Lungs
• Left Atrium
 To the Body
• Left Ventricle
Cardiovascular Anatomy
Coronary Circulation
 Collateral Circulation
Cardiac Physiology
 The Cardiac
Cycle
Diastole
Systole
 Ejection Fraction
 Stroke Volume
• Preload
• Cardiac Contractility
• Afterload
 Cardiac Output
Cardiac Physiology
 Electrophysiology
Cardiac Muscle
 Atrial
 Ventricular
 Excitatory and
Conductive Fibers
• Intercalated discs
• Syncytium
 Atrioventricular Bundle
Depolarization
Cardiac Physiology
Cardiac Depolarization
 Resting Potential
 Action Potential
 Repolarization
Cardiac Physiology
Cardiac Conductive System
 Properties
•
•
•
•
Excitability
Conductivity
Automaticity
Contractility
Cardiac Physiology
Cardiac
Conductive
System
 Components
• Sinoatrial Node
• Internodal Atrial
Pathways
• Atrioventricular
Node
• Atrioventricular
Junction
• Bundle of His
• Left and Right
Bundle Branches
• Purkinje Fibers
Electrocardiographic
Monitoring
 The Electrocardiogram
 Positive and Negative Impulses
 The Isoelectric Line
 Artifact






Muscle tremors
Shivering
Patient movement
Loose electrodes
60 Hertz interference
Machine malfunction
The Electrocardiogram
 ECG Leads
Bipolar (Limb)
 Einthoven’s Triangle
 Leads I, II, III
Augmented (Unipolar)
 aVR, aVL, aVF
Precordial
 V1 – V6
The Electrocardiogram
The Electrocardiogram
 Routine Monitoring
 Information from a single
lead shows:
 Rate & regularity.
 Time to conduct an
impulse.
 A single lead cannot:
 Identify/locate an infarct.
 Identify axis deviation or
chamber enlargement.
 Identify right-to-left
differences in
conduction.
 The quality or presence
of pumping action.
The Electrocardiogram
 ECG Paper
Speed
Amplitude and
Deflection
Calibration
The Electrocardiogram
 Relationship
of the ECG to
Electrical
Events in the
Heart
ECG Components




P Wave
QRS Complex
T Wave
U Wave
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
Time Intervals
 P–R Interval
(PRI) or P–Q
Interval (PQI)
• 0.12–0.20
Seconds
 QRS Interval
• 0.08–0.12
Seconds
 S–T Segment
 Q–T Interval
• 0.33–0.42
Seconds
The Electrocardiogram
Refractory Periods
 Absolute
 Relative
The Electrocardiogram
 S–T Segment Changes
Associated with Myocardial Infarctions
 Ischemia
 Injury
 Necrosis
The Electrocardiogram
 Lead Systems and Heart Surfaces
The Electrocardiogram
 Interpretation of Rhythm Strips
Basic Criteria
 Always be consistent and analytical.
 Memorize the rules for each dysrhythmia.
 Analyze a given rhythm strip according to a specific
format.
 Compare your analysis to the rules for each
dysrhythmia.
 Identify the dysrhythmia by its similarity to
established rules.
The Electrocardiogram
Five-Step Procedure





Analyze the rate.
Analyze the rhythm.
Analyze the P-waves.
Analyze the P–R interval.
Analyze the QRS complex.
The Electrocardiogram
 Analyzing Rate




Six-Second Method
Heart Rate Calculator Rulers
R–R Interval
Triplicate Method
 Analyzing Rhythm




Regular
Occasionally Irregular
Regularly Irregular
Irregularly Irregular
The Electrocardiogram
 Analyzing P Waves





Are P waves present?
Are the P waves regular?
Is there one P wave for each QRS complex?
Are the P waves upright or inverted?
Do all the P waves look alike?
 Analyzing the P–R Interval
 Analyzing the QRS Complex
 Do all the QRS complexes look alike?
 What is the QRS duration?
Dysrhythmias
 Normal Sinus Rhythm
 Rate
 60–100
 Rhythm
 Regular
 P waves
 Normal, upright, only before each QRS complex
 PR Interval
 0.12–0.20 seconds
 QRS Complex
 Normal, duration of <0.12 seconds
Causes of Dysrhythmias
 Myocardial
Ischemia, Necrosis,
or Infarction
 Autonomic Nervous
System Imbalance
 Distention of the
Chambers of the
Heart
 Blood Gas
Abnormalities
 Electrolyte
Imbalances
 Trauma to the
Myocardium
 Drug Effects and
Drug Toxicity
 Electrocution
 Hypothermia
 CNS Damage
 Idiopathic
Events
 Normal
Occurrences
Dysrhythmias
 Dysrhythmia
 Arrhythmia
 Mechanism of Impulse Formation
Ectopic Foci
 Ectopic Beats
Reentry
Dysrhythmias
 Classification of Dysrhythmias
Nature of Origin
Magnitude
Severity
Site of Origin
Dysrhythmias
 Classification by Site of Origin
 Dysrhythmias Originating in the SA Node
 Dysrhythmias Originating in the Atria
 Dysrhythmias Originating Within the AV Junction (AV
Blocks)
 Dysrhythmias Sustained in or Originating in the AV
Junction
 Dysrhythmias Originating in the Ventricles
 Dysrhythmias Resulting from Disorders of Conduction
Dysrhythmias Originating
in the SA Node
 Sinus Bradycardia
 Sinus Tachycardia
 Sinus Dysrhythmia
 Sinus Arrest
Dysrhythmias Originating
in the SA Node
Rules of Interpretation
Sinus Bradycardia
Rate
Rhythm
Pacemaker
Site
P Waves
Less than 60
Regular
SA node
Upright & normal
PRI
Normal
QRS
Normal
Dysrhythmias Originating
in the SA Node
 Sinus Bradycardia
 Etiology
 Increased parasympathetic (vagal) tone, intrinsic disease
of the SA node, drug effects.
 May be a normal finding in healthy, well-conditioned
persons.
 Clinical Significance
 May result in decreased cardiac output, hypotension,
angina, or CNS symptoms.
 In healthy, well-conditioned person, may have no
significance.
 Treatment
 Generally unnecessary unless hypotension or ventricular
irritability is present.
Dysrhythmias Originating
in the SA Node
Rules of Interpretation
Sinus Tachycardia
Rate
Rhythm
Pacemaker
Site
P Waves
Greater than 100
Regular
SA node
Upright & normal
PRI
Normal
QRS
Normal
Dysrhythmias Originating
in the SA Node
 Sinus Tachycardia
 Etiology
 Results from an increased rate of SA node discharge.
 Potential causes include exercise, fever, anxiety,
hypovolemia, anemia, pump failure, increased
sympathetic tone, hypoxia, or hypothyroidism.
 Clinical Significance
 Decreased cardiac output for rates >140.
 Very rapid rates can precipitate ischemia or infarct.
 Treatment
 Treatment is directed at the underlying cause.
Dysrhythmias Originating
in the SA Node
Rules of Interpretation
Sinus Dysrhythmia
Rate
Rhythm
Pacemaker
Site
P Waves
60–100
Irregular
SA node
Upright & normal
PRI
Normal
QRS
Normal
Dysrhythmias Originating
in the SA Node
 Sinus Dysrhythmia
Etiology
 Often a normal finding, sometimes related to the
respiratory cycle.
 May be caused by enhanced vagal tone.
Clinical Significance
 Normal variant.
Treatment
 Typically, none required.
Dysrhythmias Originating
in the SA Node
Rules of Interpretation
Sinus Arrest
Rate
Rhythm
Pacemaker
Site
P Waves
Normal to slow
Irregular
SA node
Upright & normal
PRI
Normal
QRS
Normal
Dysrhythmias Originating
in the SA Node
 Sinus Arrest
 Etiology
 Occurs when the sinus node fails to discharge.
 May result from ischemia of the SA node, digitalis
toxicity, excessive vagal tone, or degenerative fibrotic
disease.
 Clinical Significance
 Frequent or prolonged episodes may decrease cardiac
output and cause syncope.
 Prolonged episodes may result in escape rhythms.
 Treatment
 None if patient is asymptomatic.
 Treat symptomatic bradycardia.
Dysrhythmias Originating
in the Atria
 Atrial Tachycardia
 Multifocal Atrial Tachycardia
 Premature Atrial Contractions
 Paroxysmal Supraventricular
Tachycardia
 Atrial Flutter
 Atrial Fibrillation
Dysrhythmias Originating
in the Atria
Rules of Interpretation
Atrial Tachycardia
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
Usually normal
Slightly irregular
Varies among the SA
node, atrial tissue,
and AV Junction
Variable or absent
Varies depending on
source of impulse
Normal
Dysrhythmias Originating
in the Atria
 Atrial Tachycardia
 Etiology
 Variant of sinus dysrhythmia, which is a natural
phenomenon in the very young or old.
 May also be caused by ischemic heart disease or atrial
dilation.
 Clinical Significance
 None, but may be precursor to other atrial dysrhythmias.
 Treatment
 Typically, none required.
Dysrhythmias Originating
in the Atria
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
Dysrhythmias Originating
in the Atria
 Multifocal Atrial Tachycardia
 Etiology
 Often seen in acutely ill patients.
 May result from pulmonary disease, metabolic disorders,
ischemic heart disease, or recent surgery.
 Clinical Significance
 Presence of multifocal atrial tachycardia often indicates a
serious underlying illness.
 Treatment
 Treat the underlying illness.
Dysrhythmias Originating
in the Atria
Rules of Interpretation
Premature Atrial Contractions
Rate
Depends on
underlying rhythm
Rhythm
Usually regular
except for the PAC
Pacemaker
Site
P Waves
PRI
QRS
Ectopic sites in atria
Occurs earlier than
expected
Varies dependent on
foci of impulse
Usually normal
Dysrhythmias Originating
in the Atria
 Premature Atrial Contractions
 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
 None. Presence of PACs may be a precursor to other
atrial dysrhythmias.
 Treatment
 None if asymptomatic. Treat symptomatic patients by
administering high-flow oxygen and establishing IV
access.
Dysrhythmias Originating
in the Atria
Rules of Interpretation
Paroxysmal Supraventricular
Tachycardia
Rate
150–250
Rhythm
Regular
Pacemaker
Site
P Waves
Atrial (outside SA
Node)
Often buried in
preceding T wave
PRI
Usually normal
QRS
Usually normal
Dysrhythmias Originating
in the Atria
 Paroxysmal Supraventricular
Tachycardia
Etiology
 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.
Dysrhythmias Originating
in the Atria
 Paroxysmal Supraventricular
Tachycardia
Treatment
 Vagal Maneuvers
 Pharmacological Therapy
• Adenosine
• Verapamil
 Electrical Therapy
• Consider if patient symptomatic with HR > 150.
• Synchronized cardioversion starting at 100J.
Dysrhythmias Originating
in the Atria
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
Dysrhythmias Originating
in the Atria
 Atrial Flutter
 Etiology
 Results when the AV node cannot conduct all the
impulses.
 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.
Dysrhythmias Originating
in the Atria
 Atrial Flutter
Treatment
 Electrical Therapy
• Consider if ventricular rate > 150 and symptomatic.
• Synchronized cardioversion starting at 100J.
 Pharmacological Therapy
• Diltiazem.
• Verapamil, digoxin, beta-blockers, procainamide, and
quinidine.
Dysrhythmias Originating
in the Atria
Rules of Interpretation
Atrial Fibrillation
Rate
Atrial rate 350–50
Ventricular rate varies
Rhythm
Irregularly irregular
Pacemaker Site
P Waves
PRI
QRS
Atrial (outside SA
Node)
None discernible
None
Normal
Dysrhythmias Originating
in the Atria
 Atrial Fibrillation
 Etiology
 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.
Dysrhythmias Originating
in the Atria
 Atrial Fibrillation
 Treatment
 Electrical Therapy
• Consider if ventricular rate > 150 and symptomatic.
• Synchronized cardioversion starting at 100J.
 Pharmacological Therapy
• Diltiazem.
• Verapamil, digoxin, beta blockers, procainamide, and
quinidine.
• Anticoagulant (heparin or warfarin).
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
 AV Blocks
 Locations
 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
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
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
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
 First-Degree AV Block
 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
 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.
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
Rules of Interpretation
Type I Second-Degree AV Block
Rate
Rhythm
Pacemaker Site
Atrial, normal;
ventricular, normal to
slow
Atrial, regular;
ventricular, irregular
SA node or arial
P Waves
Normal, some P waves
not followed by QRS
PRI
Increases until QRS is
dropped, then repeats
QRS
Usually < 0.12 seconds
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
 Type I Second-Degree AV Block
 Etiology
 Also called Mobitz I, or Wenckebach.
 Delay increases until an impulse is blocked.
 Indicative of ischemia at the AV junction.
 Clinical Significance
 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.
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
Rules of Interpretation
Type II Second-Degree AV Block
Rate
Rhythm
Pacemaker Site
P Waves
PRI
QRS
Atrial, normal;
ventricular, slow
May be regular or
irregular
SA node or atrial
Normal, some P waves
not followed by QRS
Constant for conducted
beats, may be > 0.21
seconds
Normal or > 0.12
seconds
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
 Type II Second-Degree AV Block
 Etiology
 Also called Mobitz II or infranodal.
 Intermittent block of impulses.
 Usually associated with MI or septal necrosis.
 Clinical Significance
 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.
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
Rules of Interpretation
Third-Degree AV Block
Rate
Rhythm
Pacemaker
Site
P Waves
PRI
QRS
Atrial, normal;
ventricular, 40–60
Both atrial and
ventricular are regular
SA node and AV
junction or ventricle
Normal,with no
correlation to QRS
No relationship to QRS
0.12 seconds or
greater
Dysrhythmias Originating
Within the AV Junction
(AV Blocks)
 Third-Degree AV Block
 Etiology
 Absence of conduction between the atria and the
ventricles.
 Results from AMI, digitalis toxicity, or degeneration of the
conductive system.
 Clinical Significance
 Severely compromised cardiac output.
 Treatment
 Transcutaneous pacing for acutely symptomatic patients.
 Treat symptomatic bradycardia.
 Avoid drugs that may further slow AV conduction.
Dysrhythmias Sustained or
Originating in the
AV Junction
 Dysrhythmias
 Premature Junctional Contractions
 Junctional Escape Complexes and Rhythm
 Accelerated Junctional Rhythm
 Paroxysmal Junctional Tachycardia
 Characterisitics
 Inverted P Waves in Lead II
 PRI of < 0.12 Seconds
 Normal QRS Complex Duration
Dysrhythmias Sustained or
Originating in the AV
Junction
Rules of Interpretation
Premature Junctional Contractions
Rate
Rhythm
Pacemaker Site
P Waves
PRI
QRS
Depends on
underlying rhythm
Depends on
underlying rhythm
Ectopic focus in the
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Usually normal
Dysrhythmias Sustained or
Originating in the AV
Junction
 Premature Junctional Contractions
 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
 Limited, frequent PJCs may precursor other junctional
dysrhythmias.
 Treatment
 None usually required.
Dysrhythmias Sustained or
Originating in the AV
Junction
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
Dysrhythmias Sustained or
Originating in the AV
Junction
 Junctional Escape Complexes and
Rhythms
 Etiology
 Results when the AV node becomes the pacemaker.
 Results from increased vagal tone, pathologically slow
SA discharges, or heart block.
 Clinical Significance
 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 as
indicated.
Dysrhythmias Sustained or
Originating in the AV
Junction
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
Dysrhythmias Sustained or
Originating in the AV
Junction
 Accelerated Junctional Rhythm
 Etiology
 Results from increased automaticity in the AV junction.
 Often occurs due to ischemia of the AV junction.
 Clinical Significance
 Usually well tolerated, but monitor for other
dysrhythmias.
 Treatment
 None generally required in the prehospital setting.
Dysrhythmias Sustained or
Originating in the AV
Junction
Rules of Interpretation
Paroxysmal Junctional Tachycardia
Rate
100–180
Rhythm
Regular
Pacemaker
Site
P Waves
PRI
QRS
AV junction
Inverted, may occur
after QRS
Normal if P occurs
before QRS
Normal
Dysrhythmias Sustained or
Originating in the AV
Junction
 Paroxysmal Junctional Tachycardia
 Etiology
 Rapid AV junction depolarization overrides the SA node.
 Occurs with or without heart disease.
 May be precipitated by stress, overexertion, smoking, or
caffeine ingestion.
 Clinical Significance
 May be well tolerated for brief periods.
 Decreased cardiac output will result from prolonged
episodes, which may precipitate angina, hypotension, or
congestive heart failure.
Dysrhythmias Sustained or
Originating in the AV
Junction
 Paroxysmal Junctional
Tachycardia
Treatment
 Vagal Maneuvers
 Pharmacological Therapy
• Adenosine
• Verapamil
 Electrical Therapy
• Use if rate is > 150 and patient is hemodynamically
unstable.
• Synchronized cardioversion starting at 100J.
Dysrhythmias Originating
in the Ventricles
 Dysrhythmias
 Ventricular Escape Complexes and Rhythms
 Accelerated Idioventricular Rhythm
 Premature Ventricular Contractions
 Ventricular Tachycardia
 Related Dysrhythmia
 Ventricular Fibrillation
 Asystole
 Artificial Pacemaker Rhythm
Dysrhythmias Originating
in the Ventricles
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
Dysrhythmias Originating
in the Ventricles
 Ventricular Escape Complexes and
Rhythms
 Etiology
 Safety mechanism to prevent cardiac standstill.
 Results from failure of other foci or high-degree AV block.
 Clinical Significance
 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.
Dysrhythmias Originating
in the Ventricles
 Accelerated Idioventricular Rhythm
 Etiology
 A subtype of ventricular escape rhythm that frequently
occurs with MI.
 Ventricular escape rhythm with a rate of 60–110.
 Clinical Significance
 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.
Dysrhythmias Originating
in the Ventricles
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
Dysrhythmias Originating
in the Ventricles
 Premature Ventricular Contractions
 Etiology
 Single ectopic impulse resulting from an irritable focus in
either ventricle.
 Causes may include 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.
Dysrhythmias Originating
in the Ventricles
 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.
Dysrhythmias Originating
in the Ventricles
 Premature Ventricular Contractions
 Treatment
 Non-malignant 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.
• If PVCs are not suppressed, 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.
Dysrhythmias Originating
in the Ventricles
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
Dysrhythmias Originating
in the Ventricles
 Ventricular Tachycardia
 Etiology
 3 or more ventricular complexes in succession at a rate of
>100.
 Causes include myocardial ischemia, increased
sympathetic tone, hypoxia, idiopathic causes, acid–base
disturbances, or electrolyte imbalances.
 VT may appear monomorphic or polymorphic
 Clinical Significance
 Decreased cardiac output, possibly to life-threatening
levels.
 May deteriorate into ventricular fibrillation.
Dysrhythmias Originating
in the Ventricles
 Ventricular Tachycardia
 Treatment
 Perfusing patient
• Administer oxygen and establish IV access.
• Consider immediate synchronized cardioversion starting at 100J
for hemodynamically unstable patients.
• Initially administer lidocaine 1.0–1.5 mg/kg IV.
• Administer repeat doses of lidocaine 0.5–0.75 mg/kg to the max
dose of 3.0 mg/kg, or until VT is suppressed.
• Amiodarone 150–300 mg IV.
 Nonperfusing patient
• Follow ventricular fibrillation protocol.
Dysrhythmias Originating
in the Ventricles
 Torsade de Pointes
 Polymorphic VT.
 Caused by the use of
certain antidysrhythmic
drugs.
 Exacerbated by
coadministration of
antihistamines, azole
antifungal agents and
macrolide antibiotics,
erythromycin,
azithromycin, and
clarithramycin.
Dysrhythmias Originating
in the Ventricles
 Torsade de Pointes
 Typically occurs in nonsustained bursts.
 Prolonged Q–T 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.
 Amiodarone 150–300 mg is also effective.
Dysrhythmias Originating
in the Ventricles
Rules of Interpretation
Ventricular Fibrillation
Rate
No organized rhythm
Rhythm
No organized rhythm
Pacemaker Site
Numerous
ventricular foci
P Waves
Usually absent
PRI
None
QRS
None
Dysrhythmias Originating
in the Ventricles
 Ventricular Fibrillation
Etiology
 Wide variety of causes, often resulting from
advanced coronary artery disease.
Clinical Significance
 Lethal dysrhythmia with no cardiac output and no
organized electrical pattern.
Dysrhythmias Originating
in the Ventricles
 Ventricular Fibrillation
Treatment
 Initiate CPR.
 Defibrillate with 200J, repeated with 200–300J and
360J if the rhythm does not convert.
 Control the airway and establish IV access.
 Administer epinephrine 1:10,000 every 3–5 minutes.
 Consider second-line drugs such as lidocaine,
bretylium, amiodarone, procainamide, or
magnesium sulfate.
 Consider 40 IU Vasopressin IV (one time only).
Dysrhythmias Originating
in the Ventricles
Rules of Interpretation
Asystole
Rate
No Electrical Activity
Rhythm
No Electrical Activity
Pacemaker Site
No Electrical Activity
P Waves
Absent
PRI
Absent
QRS
Absent
Dysrhythmias Originating
in the Ventricles
 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.
Dysrhythmias Originating
in the Ventricles
 Asystole
Treatment
 Administer CPR and manage the airway.
 Treat for ventricular fibrillation if there is any doubt
about the underlying rhythm.
 Administer medications
• Epinephrine, atropine, and possibly sodium bicarbonate.
Dysrhythmias Originating
in the Ventricles
Rules of Interpretation
Artificial Pacemaker Rhythm
Rate
Rhythm
Varies with
pacemaker
May be regular or
irregular
Pacemaker
Site
Depends upon
electrode placement
P Waves
None produced by
ventricular pacemakers;
pacemaker spike
PRI
QRS
If present, varies
>0.12 seconds,
bizarre
Dysrhythmias Originating
in the Ventricles
 Artificial Pacemaker Rhythm
Etiology
 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.
Dysrhythmias Originating
in the Ventricles
 Artificial Pacemaker Rhythm
Problems with Pacemakers
 Battery failure
 “Runaway” pacers
 Displaced leads
Management Considerations
 Identify patients with pacemakers.
 Treat the patient.
Use of a Magnet
Pulseless Electrical
Activity
 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.
Pulseless Electrical
Activity
 Treatment
 Prompt recognition and early treatment.
 Epinephrine 1 mg every 3–5 minutes.
 Treat underlying cause of PEA.
Dysrhythmias Resulting from
Disorders of Conduction
 Categories of Conductive
Disorders
Atrioventricular Blocks
Disturbances of Ventricular Conduction
Preexcitation Syndromes
Dysrhythmias Resulting from
Disorders of Conduction
 Disturbances of Ventricular
Conduction
Aberrant Conduction
Bundle Branch Block
Causes
 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
Dysrhythmias Resulting from
Disorders of Conduction
 Pre-excitation
Syndromes
 Excitation by an
impulse that bypasses
the AV node
 Wolff-Parkinson-White
Syndrome (WPW)
• Short PRI and long QRS
duration
• Delta waves
 Treat underlying
rhythm.
ECG Changes Due to Electrolyte
Abnormalities and Hypothermia
 Hyperkalemia
 Tall Ts
 Suspect in patients with
a history of renal failure.
 Hypokalemia
 Prominent U waves
 Hypothermia
 Osborn wave (“J” wave)
 T wave inversion, sinus
bradycardia, atrial
fibrillation or flutter, AV
blocks, PVCs, VF,
asystole
Summary
 Review of Cardiovascular
Anatomy
 Cardiac Physiology
 Electrocardiographic Monitoring
 Dysrhythmias