Cardiology part 1

CardiologyCardiology

Part 1: Part 1: Cardiovascular Cardiovascular

Anatomy & Anatomy & Physiology, ECG Physiology, ECG Monitoring, and Monitoring, and

Dysrhythmia AnalysisDysrhythmia Analysis

SectionsSections

Cardiovascular Anatomy Cardiac Physiology Electrocardiographic Monitoring Dysrhythmias


Cardiovascular Cardiovascular AnatomyAnatomy Anatomy

of the Heart Location

and Size of the Heart

Anatomy of the Heart Location

and Size of the Heart

Cardiovascular Cardiovascular AnatomyAnatomy Tissue Layers

Endocardium Myocardium Pericardium

• Visceral Pericardium

• Parietal Pericardium

• Pericardial Fluid

Tissue Layers Endocardium Myocardium Pericardium

• Visceral Pericardium

• Parietal Pericardium

• Pericardial Fluid

Cardiovascular Cardiovascular AnatomyAnatomy Valves

Atrioventricular Valves• Tricuspid Valve

• Mitral Valve

Semilunar Valves• Aortic Valve

• Pulmonic Valve

Chordae Tendonae

Valves Atrioventricular

Valves• Tricuspid Valve

• Mitral Valve

Semilunar Valves• Aortic Valve

• Pulmonic Valve

Chordae Tendonae

Cardiovascular Cardiovascular AnatomyAnatomy Blood Flow

From the Body• Right

Atrium

To the Lungs• Right

Ventricle

From the Lungs• Left Atrium

To the Body• Left

Ventricle

Blood Flow From the

Body• Right

Atrium

To the Lungs• Right

Ventricle

From the Lungs• Left Atrium

To the Body• Left

Ventricle

Cardiovascular Cardiovascular AnatomyAnatomy Coronary Circulation

Collateral Circulation

Coronary Circulation Collateral Circulation

Cardiovascular Cardiovascular AnatomyAnatomy Anatomy of the

Peripheral Circulation General Structure

Poiseuille’s Law

Arterial System Arteries,

arterioles, and capillaries

Venous System Capillaries,

venules, and veins

Anatomy of the Peripheral Circulation General Structure

Poiseuille’s Law

Arterial System Arteries,

arterioles, and capillaries

Venous System Capillaries,

venules, and veins

Cardiac PhysiologyCardiac Physiology

The Cardiac Cycle Diastole Systole

Ejection Fraction

Stroke Volume• Preload

• Cardiac Contractility

• Afterload

Cardiac Output

The Cardiac Cycle Diastole Systole

Ejection Fraction

Stroke Volume• Preload

• Cardiac Contractility

• Afterload

Cardiac Output

Cardiac PhysiologyCardiac Physiology Nervous

Control of the Heart Sympathetic Parasympathetic Autonomic

Control of the Heart Chronotropy Inotropy Dromotropy

Role of Electrolytes

Nervous Control of the Heart Sympathetic Parasympathetic Autonomic

Control of the Heart Chronotropy Inotropy Dromotropy

Role of Electrolytes

Cardiac PhysiologyCardiac Physiology

Electrophysiology Cardiac Muscle

Atrial Ventricular Excitatory and

Conductive Fibers• Intercalated discs

• Syncytium

Atrioventricular Bundle

Depolarization

Electrophysiology Cardiac Muscle

Atrial Ventricular Excitatory and

Conductive Fibers• Intercalated discs

• Syncytium

Atrioventricular Bundle

Depolarization

Cardiac PhysiologyCardiac Physiology Cardiac

Depolarization Resting Potential Action Potential Repolarization

Cardiac Depolarization Resting Potential Action Potential Repolarization

Cardiac PhysiologyCardiac Physiology Cardiac Conductive System

Properties• Excitability

• Conductivity

• Automaticity

• Contractility

Cardiac Conductive System Properties

• Excitability

• Conductivity

• Automaticity

• Contractility

Cardiac PhysiologyCardiac Physiology Cardiac

Conductive System Components

• Sinoatrial Node• Internodal Atrial

Pathways• Atrioventricular

Node• Atrioventricular

Junction• Bundle of His• Left and Right

Bundle Branches• Purkinje Fibers

Cardiac Conductive System Components

• Sinoatrial Node• Internodal Atrial

Pathways• Atrioventricular

Node• Atrioventricular

Junction• Bundle of His• Left and Right

Bundle Branches• Purkinje Fibers

Electrocardiographic Electrocardiographic MonitoringMonitoring

The Electrocardiogram Positive and Negative Impulses The Isoelectric Line Artifact

Muscle tremors Shivering Patient movement Loose electrodes 60 Hertz interference Machine malfunction

The Electrocardiogram Positive and Negative Impulses The Isoelectric Line Artifact

Muscle tremors Shivering Patient movement Loose electrodes 60 Hertz interference Machine malfunction

The The ElectrocardiogramElectrocardiogram ECG Leads Bipolar (Limb)

Einthoven’s Triangle Leads I, II, III

Augmented (Unipolar) aVR, aVL, aVF

Precordial V1 – V6

ECG Leads Bipolar (Limb)

Einthoven’s Triangle Leads I, II, III

Augmented (Unipolar) aVR, aVL, aVF

Precordial V1 – V6

The The ElectrocardiogramElectrocardiogram 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.

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 The ElectrocardiogramElectrocardiogram ECG Paper Speed Amplitude and

Deflection Calibration

ECG Paper Speed Amplitude and

Deflection Calibration

The The ElectrocardiogramElectrocardiogram Relationship of the ECG to Electrical Events in the Heart ECG Components

P Wave QRS Complex T Wave U Wave

Relationship of the ECG to Electrical Events in the Heart ECG Components

P Wave QRS Complex T Wave U Wave

The The ElectrocardiogramElectrocardiogram

The The ElectrocardiogramElectrocardiogram 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

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 The ElectrocardiogramElectrocardiogram Refractory Periods

Absolute Relative

Refractory Periods Absolute Relative

The The ElectrocardiogramElectrocardiogram S–T Segment Changes Associated with Myocardial Infarctions

Ischemia Injury Necrosis

S–T Segment Changes Associated with Myocardial Infarctions

Ischemia Injury Necrosis

The The ElectrocardiogramElectrocardiogram Lead Systems and Heart Surfaces Lead Systems and Heart Surfaces

The The ElectrocardiogramElectrocardiogram 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.

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 The ElectrocardiogramElectrocardiogram Five-Step Procedure

Analyze the rate. Analyze the rhythm. Analyze the P-waves. Analyze the P–R interval. Analyze the QRS complex.

Five-Step Procedure Analyze the rate. Analyze the rhythm. Analyze the P-waves. Analyze the P–R interval. Analyze the QRS complex.

The The ElectrocardiogramElectrocardiogram Analyzing Rate

Six-Second Method Heart Rate Calculator Rulers R–R Interval Triplicate Method

Analyzing Rhythm Regular Occasionally Irregular Regularly Irregular Irregularly Irregular

Analyzing Rate Six-Second Method Heart Rate Calculator Rulers R–R Interval Triplicate Method

Analyzing Rhythm Regular Occasionally Irregular Regularly Irregular Irregularly Irregular

The The ElectrocardiogramElectrocardiogram 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?

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?

DysrhythmiasDysrhythmias 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

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 Causes of DysrhythmiasDysrhythmias Myocardial

Ischemia, Necrosis, or Infarction

Autonomic Nervous System Imbalance

Distention of the Chambers of the Heart

Blood Gas Abnormalities

Electrolyte Imbalances

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

Trauma to the Myocardium

Drug Effects and Drug Toxicity

Electrocution Hypothermia CNS Damage Idiopathic

Events Normal

Occurrences

DysrhythmiasDysrhythmias

Dysrhythmia Arrhythmia Mechanism of Impulse Formation

Ectopic Foci Ectopic Beats

Reentry

Dysrhythmia Arrhythmia Mechanism of Impulse Formation

Ectopic Foci Ectopic Beats

Reentry

DysrhythmiasDysrhythmias

Classification of Dysrhythmias Nature of Origin Magnitude Severity Site of Origin

Classification of Dysrhythmias Nature of Origin Magnitude Severity Site of Origin

DysrhythmiasDysrhythmias 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

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

Sinus Bradycardia Sinus Tachycardia Sinus Dysrhythmia Sinus Arrest

Sinus Bradycardia Sinus Tachycardia Sinus Dysrhythmia Sinus Arrest

Dysrhythmias Dysrhythmias Originating in the SA Originating in the SA

NodeNode


NodeNode

NormalQRS

NormalPRI

Upright & normalP Waves

SA nodePacemaker Site

RegularRhythm

Less than 60Rate

Sinus Bradycardia

Rules of Interpretation

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.

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.


NodeNode

Sinus Bradycardia Treatment

Sinus Bradycardia Treatment


NodeNode


NodeNode

NormalQRS

NormalPRI



RegularRhythm

Greater than 100Rate

Sinus Tachycardia


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.

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.


NodeNode


NodeNode

NormalQRS

NormalPRI



IrregularRhythm

60–100Rate

Sinus Dysrhythmia


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.

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.


NodeNode


NodeNode

NormalQRS

NormalPRI



IrregularRhythm

Normal to slowRate

Sinus Arrest


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.

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.


NodeNode

Atrial Tachycardia Multifocal Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular

Tachycardia Atrial Flutter Atrial Fibrillation

Atrial Tachycardia Multifocal Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular

Tachycardia Atrial Flutter Atrial Fibrillation

Dysrhythmias Dysrhythmias Originating in the Originating in the

AtriaAtria


AtriaAtria

NormalQRS

Varies depending on source of impulse

PRI

Variable or absentP Waves

Varies among the SA node, atrial tissue,

and AV Junction

Pacemaker Site

Slightly irregularRhythm

Usually normalRate

Atrial Tachycardia


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.

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.


AtriaAtria


AtriaAtria

VariableQRS

Varies depending on source of impulse

PRI

Organized, nonsinus P waves; at least 3 formsP Waves

Ectopic sites in atriaPacemaker Site

IrregularRhythm

More than 100Rate

Multifocal Atrial Tachycardia


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.

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.


AtriaAtria


AtriaAtria

Usually normalQRS

Varies dependent on foci of impulse

PRI

Occurs earlier than expected

P Waves

Ectopic sites in atriaPacemaker Site

Usually regular except for the PAC

Rhythm

Depends on underlying rhythm

Rate

Premature Atrial Contractions


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.

Premature Atrial Contractions Etiology

Single electrical impulse originating outside the SA node. May result from use of caffeine, tobacco, or alcohol,


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.


AtriaAtria


AtriaAtria

Usually normalQRS

Usually normalPRI

Often buried in preceding T wave

P Waves

Atrial (outside SA Node)Pacemaker Site

RegularRhythm

150–250Rate

Paroxysmal Supraventricular Tachycardia


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.

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.


AtriaAtria

Paroxysmal Supraventricular Tachycardia Treatment

Vagal Maneuvers Pharmacological Therapy

• Adenosine

• Verapamil

Electrical Therapy• Consider if patient symptomatic with HR > 150.

• Synchronized cardioversion starting at 100J.

Paroxysmal Supraventricular Tachycardia Treatment


• Adenosine

• Verapamil

Electrical Therapy• Consider if patient symptomatic with HR > 150.



AtriaAtria

TachycarTachycardia dia

AlgorithAlgorithmm


AtriaAtria

Usually normalQRS

Usually normalPRI

F waves are presentP Waves

Atrial (outside SA node)Pacemaker Site

Usually regularRhythm

Atrial rate 250–350Ventricular rate variesRate

Atrial Flutter


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.

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.


AtriaAtria

Atrial Flutter Treatment

Electrical Therapy• Consider if ventricular rate > 150 and symptomatic.


Pharmacological Therapy• Diltiazem.

• Verapamil, digoxin, beta-blockers, procainamide, and quinidine.





• Verapamil, digoxin, beta-blockers, procainamide, and quinidine.


AtriaAtria


AtriaAtria

NormalQRS

NonePRI

None discernibleP Waves

Atrial (outside SA Node)Pacemaker Site

Irregularly irregularRhythm

Atrial rate 350–50Ventricular rate variesRate

Atrial Fibrillation


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.

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.


AtriaAtria





• Verapamil, digoxin, beta blockers, procainamide, and quinidine.

• Anticoagulant (heparin or warfarin).





• Verapamil, digoxin, beta blockers, procainamide, and quinidine.

• Anticoagulant (heparin or warfarin).


AtriaAtria

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

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 Dysrhythmias Originating Within the AV Junction Within the AV Junction

(AV Blocks)(AV Blocks)



Usually < 0.12 seconds

QRS

> 0.20 SecondsPRI

NormalP Waves

SA node or atrialPacemaker Site



Rate

First-Degree AV Block


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.

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.





Usually < 0.12 secondsQRS

Increases until QRS is dropped, then repeatsPRI

Normal, some P waves not followed by QRSP Waves

SA node or arialPacemaker Site

Atrial, regular; ventricular, irregular

Rhythm

Atrial, normal; ventricular, normal to

slowRate

Type I Second-Degree AV Block


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.

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.





Normal or > 0.12 secondsQRS

Constant for conducted beats, may be > 0.21 secondsPRI

Normal, some P waves not followed by QRSP Waves

SA node or atrialPacemaker Site

May be regular or irregular

Rhythm

Atrial, normal; ventricular, slow

Rate

Type II Second-Degree AV Block


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.

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.





0.12 seconds or greaterQRS

No relationship to QRSPRI

Normal,with no correlation to QRS

P Waves

SA node and AV junction or ventricle

Pacemaker Site

Both atrial and ventricular are regularRhythm

Atrial, normal; ventricular, 40–60

Rate

Third-Degree AV Block


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.

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 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 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 Dysrhythmias Sustained or Sustained or

Originating in the Originating in the AV JunctionAV Junction


Originating in the AV Originating in the AV JunctionJunction

Usually normalQRS

Normal if P occurs before QRS

PRI

Inverted, may occur after QRS

P Waves

Ectopic focus in the AV junction

Pacemaker Site


Rhythm


Rate

Rules of InterpretationPremature Junctional Contractions

Premature Junctional Contractions Etiology

Single electrical impulse originating in the AV node. May occur with use of caffeine, tobacco, alcohol,


Clinical Significance Limited, frequent PJCs may precursor other junctional

dysrhythmias. Treatment

None usually required.

Premature Junctional Contractions Etiology

Single electrical impulse originating in the AV node. May occur with use of caffeine, tobacco, alcohol,


Clinical Significance Limited, frequent PJCs may precursor other junctional

dysrhythmias. Treatment

None usually required.





Usually normalQRS


PRI


P Waves

AV junctionPacemaker Site

Irregular in single occurrence, regular in

escape rhythmRhythm

40–60Rate

Junctional Escape Complexes and Rhythms


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.

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.





NormalQRS


PRI


P Waves


RegularRhythm

60–100Rate

Accelerated Junctional Rhythm


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.

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.





NormalQRS


PRI


P Waves


RegularRhythm

100–180Rate

Paroxysmal Junctional Tachycardia


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.

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.



Paroxysmal Junctional Tachycardia Treatment


• Adenosine• Verapamil

Electrical Therapy• Use if rate is > 150 and patient is hemodynamically

unstable.• Synchronized cardioversion starting at 100J.

Paroxysmal Junctional Tachycardia Treatment


• Adenosine• Verapamil

Electrical Therapy• Use if rate is > 150 and patient is hemodynamically

unstable.• Synchronized cardioversion starting at 100J.



Dysrhythmias Ventricular Escape Complexes and Rhythms Accelerated Idioventricular Rhythm Premature Ventricular Contractions Ventricular Tachycardia Related Dysrhythmia Ventricular Fibrillation Asystole Artificial Pacemaker Rhythm

Dysrhythmias Ventricular Escape Complexes and Rhythms Accelerated Idioventricular Rhythm Premature Ventricular Contractions Ventricular Tachycardia Related Dysrhythmia Ventricular Fibrillation Asystole Artificial Pacemaker Rhythm


VentriclesVentricles



>0.12 seconds, bizarreQRS

NonePRI

NoneP Waves

VentriclePacemaker Site

Escape complex, irregular;escape rhythm, RegularRhythm

15–40Rate

Ventricular Escape Complexesand Rhythms


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.

Ventricular Escape Complexes and Rhythms Etiology

Safety mechanism to prevent cardiac standstill. Results from failure of other foci or high-degree AV block.


levels.

Treatment For perfusing rhythms, administer atropine and/or TCP. For nonperfusing rhythms, follow pulseless electrical

activity (PEA) protocols.



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.

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.






NonePRI

NoneP Waves


Interrupts regular underlying rhythm

Rhythm

Underlying rhythmRate

Premature Ventricular Contractions


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.

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.



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 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

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.

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.






NonePRI

If present, not associated with QRS

P Waves



100–250Rate

Ventricular Tachycardia


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


levels. May deteriorate into ventricular fibrillation.

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


levels. May deteriorate into ventricular fibrillation.



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.

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.



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.

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.



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.

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.





NoneQRS

NonePRI

Usually absentP Waves

Numerous ventricular foci

Pacemaker Site

No organized rhythmRhythm

No organized rhythmRate

Ventricular Fibrillation


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.

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.



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).

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).





AbsentQRS

AbsentPRI

AbsentP Waves

No Electrical ActivityPacemaker Site

No Electrical ActivityRhythm

No Electrical ActivityRate

Asystole


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 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, atropine, and possibly sodium bicarbonate.

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.






If present, variesPRI

None produced by ventricular pacemakers;

pacemaker spikeP Waves

Depends upon electrode placement

Pacemaker Site

May be regular or irregular

Rhythm

Varies with

pacemakerRate

Artificial Pacemaker Rhythm


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.

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.



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

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 Pulseless Electrical ActivityActivity

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.

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 Pulseless Electrical ActivityActivity Treatment

Prompt recognition and early treatment. Epinephrine 1 mg every 3–5 minutes. Treat underlying cause of PEA.

Treatment Prompt recognition and early treatment. Epinephrine 1 mg every 3–5 minutes. Treat underlying cause of PEA.

PulselePulseless ss

ElectricElectrical al

ActivityActivity

Categories of Conductive Disorders Atrioventricular Blocks Disturbances of Ventricular Conduction Preexcitation Syndromes

Categories of Conductive Disorders Atrioventricular Blocks Disturbances of Ventricular Conduction Preexcitation Syndromes

Dysrhythmias Resulting Dysrhythmias Resulting from Disorders of from Disorders of

ConductionConduction

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

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



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.

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.



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

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

ECG Changes Due to ECG Changes Due to Electrolyte Abnormalities Electrolyte Abnormalities

and Hypothermiaand Hypothermia

CardiologyCardiology



Cardiology part 1

Documents

Transcript of Cardiology part 1