File - Kelly Marchant RN

Nuro 438
February 2015
Learning Objectives
At the completion of this presentation, the
nursing student will be able to successfully
 Describe cardiac anatomy and physiology
 Describe the function of the heart, including circulation and
 Describe and define the major cardiac waves in an EKG
 Define normal sinus rhythm
 Differentiate between rate, conduction, atrial, and ventricular
 Recognize life-threatening dysrhythmias
 Identify nursing considerations related to various cardiac dysrhythmias
 Differentiate types of medications to treat arrhythmias
 Identify risks for cardiac arrhythmias
 Identify adverse effects associated with cardiac dysrhythmias
 Analyze EKG Rhythm strips
Cardiac Anatomy
Cardiac Anatomy
 4 Chambers, 2 Atria, 2 Ventricles
 4 Valves
 Acts as a PUMP
 Receives deoxygenated blood from body,
pumps to lungs
 Receives oxygenated blood from lungs, pumps
to body
Cardiac Circulation
Cardiac Function
Heart functions a pump to deliver blood to the
Impulse Generation
 Under Usual circumstances
 Impulse generated from pacemaker cells in SA
 Impulse then travels to AV node
 Impulse then travels to Bundle of His
 Impulse then travels to Right and Left Bundle
 Impulse travels to Perkinje Cells that innervate
Components of an EKG
 Graph
 X Axis = time
 Y Axis = amplitude
 Displays electrical activity of heart
 Electrical impulse precedes contraction
 Depolarization and repolarization are depicted as waves
Atrial Depolarization = P wave
Atrial repolarization occurs during ventricular depolarization
Ventricular depolarization = QRS complex
Ventricular repolarization = T wave
EKG Basics
 Bipolar lead: positive and negative electrode.
Measures electrical potential between the
 AKA ‘Standard Limb Leads’
 Leads I,II,III
 Used to monitor only for dysrhythmias
 Lead II most commonly used
Telemetry Placement
 Red = Brake (right), Green = Gas
 Smoke (black) over Fire (red),
Snow (white) on the Trees
 Stars and Stripes
Lead II
12 Lead EKG
 3 Standard (bipolar) Limb Leads
 3 Augmented (unipolar) Leads (aVR, aVL, aVF)
 Triaxial reference- measures the difference in
electrical potential between one of three extremity
electrodes and the central terminal
 6 Precordial (unipolar) Leads (V1, V2, V3, V4, V5,
aVR, aVL, aVF
The V Leads
Cardiac Waves
The P wave
 Pacemaker is SA node,
rate 60 - 100
 Correlates with atrial
depolarization (begins in
SA node moves R-> L and
 PR interval 0.12-0.2
 Determine atrial rate
 Compare atrial rate to
ventricular rate
The QRS Complex
 Represents normal
depolarization of the
 Normal duration 0.06- 0.12
 Measured from Q wave (first
deviation from isoelectric
line) to S wave (the return to
isoelectric line)
 Abnormal QRS is abnormal
 Ventricular pre-excitation
 Cardiac pacemaker
The T Wave
 Represents Ventricular
 Occurs during end of ventricular
 Typically in same direction as QRS
 Lasts 0.10 – 0.25
U Wave
 Final stage of
repolarization, thought to
be repolarization of
Perkinje Fibers
 Not usually seen
 May indicate
 Hypokalemia
 Cardiomyopathy
 Dig toxicity
EKG Paper
At the 25 mm speed,
Each mark at top is 3 seconds
There are three large boxes between each mark
Each large box is 1 second or 25 mm
Each large box has 5 medium boxes in it
Each medium box is 0.2 seconds or 5 mm
Each medium box is made up of 5 small boxes (or dots)
Each small box (dot) = 0.04 seconds or 1 mm
EKG Paper
Steps to Interpreting
Cardiac Rhythms
 Determine the Heart Rate
 Determine the Regularity
 Identify and analyze P waves or flutter
 Determine PR interval and AV conduction
 Identify and analyze QRS complex
 Determine site of origin of dysrhythmia
 Identify dysrhythmia
 Evaluate significance of dysrhythmia
Determine the Heart Rate
 The Six-second Method
 Most common/least accurate
 Simplest, quickest
 Heart Rate Calculator
 The Rule of 300
 Must be regular
 R-R Interval Method
 Rhythm must be regular
 Distance between peaks of 2 R
waves and /60
Describe the Rate & Rhythm
 Normal = 60-100
 Tacchycardia >100
 Bradycardia <60
 Regular
 Irregular
 Regularly-irregular
Sinus Arrhythmias
 ST = HR >100
 SB = HR ,60
Steps to Interpreting
Cardiac Rhythms
 Determine the Heart Rate
 Determine the Regularity
 Identify and analyze P waves or flutter
 Determine PR interval and AV conduction
 Identify and analyze QRS complex
 Determine site of origin of dysrhythmia
 Identify dysrhythmia
 Evaluate significance of dysrhythmia
Measuring the Waves
PR Interval
 Represents progression of electrical impulse
from the SA node or an ectopic pacemaker
(in atria or AV junction) through entire
conduction system of the heart to the
ventricular myocardium
 Normal duration 0.12 – 0.20
 PR >0.20 represents delayed conduction of
Irregular P Wave
 Remember P wave represents
atrial depolarization
 Irregular P represents altered,
damaged, or abnormal atria
 Increased Right Atrial Pressure or
hypertrophy as seen in COPD and
CHF = tall peaked P wave
 Increased left atrial pressure or
hypertrophy = wide notched P
Ectopic P Wave
 Electrical impulse for ectopic P wave originated
outside SA node or in AV junction
 Occur in
 PAC’s
 Atrial tacchycardia
 Premature Atrial Contraction
 P wave followed by normal QRS
 Generally followed by noncompensatory pause
 P waves vary, PR intervals normal
 AV Ratio 1:1 Conduction
Causes of PAC’s
 Increased sympathetic tone
 Infection
 Emotional Stress
 Stimulants
 Medications; epinephrine
 Hypoxia
 Digitalis toxicity
 ACS or CHF
QRS Complex
 Represents normal
depolarization of the ventricles
 Onset is point where first wave
(Q) deviates from isoelectric line
 End is where last wave (S) returns
to isoelectric line
 Duration 0.06 – 0.12
Irregular QRS
 Represents abnormal
depolarization of
 Irregular QRS
present in
 Bundle Branch Block
 Ventricular
 Cardiac pacemaker
QT Interval
 Represents time it takes for
ventricles to depolarize and
 Prolonged QT associated with
pericarditis, myocarditis, MI,
LVH, hypothermia, CVA,
increased IC trauma or
hemorrhage, medication SE,
electrolyte imbalances (K, Ca),
or liquid protein diets
ST Segment
 Represents early part of
repolarization of right and left
 Duration < 0.20
 Normally ST segment is flat
 Elevation can be evidence of
myocardial ischemia or infarction,
coronary vasospasm, pericarditis,
LBBB, LVH, raised ICP
Steps to Interpreting
Cardiac Rhythms
 Determine the Heart Rate
 Determine the Regularity
 Identify and analyze P waves or flutter
 Determine PR interval and AV conduction
 Identify and analyze QRS complex
 Determine site of origin of dysrhythmia
 Identify dysrhythmia
 Evaluate significance of dysrhythmia
 Rate Arrhythmias
 Tachycardia
 Bradycardia
 Atrial Arrhythmias
 Afib/Aflutter
 Conduction Arrhythmias
 Bundle Branch Blocks
 AV Conduction Block (1st, 2nd, 3rd Degree)
 Life Threatening Arrhythmias
 V Fib
 Complete Heart Block
 Asystole
Living Arrhythmias
Atrial Arrhythmias
 Atrial Tacchycardia
 Atrial fibrilation
 Atrial flutter
 Supra Ventricular Tacchycardia
 Wolf-Parkinson-White
 8 Steps
 ID P or F waves
 Conduction ratio, is every P followed by QRS
Atrial Tachycardia
 Rate is usually 160-240 beats
 Type of SVT, where generation for impulse is
outside SA node
 A Fib and Aflutter are most common forms
 P waves are uniform
 PR intervals are normal
 AV conduction is 1:1
Atrial Tachycardia
 Clinical significance
 Dependent on presence and extent of heart
 Palpitations, nervousness, anxiety
 Perfusion
 Syncope
 Workload of heart
 Nursing Assessment
Atrial Tachycardia
A Flutter
 Causes
 Cardiomyopathy
 Atrial dilation
 Valve Disease
 Thyrotoxicities
 Hypoxia
 ETOH Abuse
A Flutter
 Risks; Incomplete emptying of ventricles
Thrombi formation
Loss of atrial kick
Syncope, hypotension
 Treatments
Beta Blockers
Cardioversion if uncontrolled
Atrial Flutter
 Impulse generated by ectopic pacemaker or
reentry pathway
 F waves have a saw-tooth appearance
 Rate; Atrial 240-360, Ventricular half the atrial rate
 Rate is regular
 Normal P waves absent
 Unable to measure PR intervals
 Expressed as ratio 4: 1 Flutter
Atrial Fibrillation
 Atrial Rate 350-600
 Ventricular rate < 100 = controlled, >100 =
 Irregularly irregular rate
 P waves absent, F waves absent
Atrial Fib
 Causes and treatments similar to A Flutter
 Rapid rhythm (>100) that generated outside the
 AKA Paroxysmal Atrial Tach (PAT)
 Symptoms
 Palpitations
 Lightheadedness
 Dizziness
 Maybe symptomless, self limiting
Beta Blockers, CCB,antiarrhythmics
 Ventricular pre-excitation; early activation of
ventricles by impulse that bypasses the AV node
 Impulse can be generated in accessory pathway
or bypass tract that abnormally
 Most frequent AV bypass tract in WPW is Bundle
of Kent
 Presence of Delta wave
Wandering Atrial
 Dysrhythmia originating in multiple pacemaker
sites that shift between SA node and AV junction
 Rate 60 – 100
 Irregular
 P waves vary in size and shape
 PR intervals are normal to very short
 AV Conduction ratio 1:1
Wandering Atrial
Conduction Arrhythmias
 Conduction Block/ AV Block
 Bundle Branch Block
AV Blocks
 First Degree AV Block
 Second Degree Type I AV Block
 Second Degree Type II AV Block
 Third Degree AV Block
First Degree AV Block
 Delay in conduction of electrical impulse, usually
through the AV node
 Most common Heart Block
 Prolonged PR (> 0.20)
 Rate and Rhythm Regular
 AV Conduction 1:1
 Causes 1* AV Block
Acute Inferior Wall MI
Ischemic Heart Disease
Digitalis Toxicity
Medications (B Blockers, CCB)
First Degree AV Block
Second Degree Type I AV
 AKA Wenckebach
 Usually temporary condition, and asymptomatic
 Prolonging PR form one QRS to the next until one QRS is
not conducted or “dropped” then pattern starts over
 P to P intervals are regular
 R to R intervals are irregular
 More P waves than QRS complexes
 Causes; Acute inerior wall MI, Ischemic heart disease,
Dig Toxicity, BB, CCB, Hyperkalemia
Second Degree AVB, Type I
Second Degree Type II AV
 Dysrhythmia with constant P-R interval with
missing QRS complexes
 Complete block of conduction in one bundle
branch and an intermittent block in the other
bundle branch
 Can present as pattern, ie 2:1 block or 3: 1 block
OR without pattern of QRS/ unstable QRS
 Causes; Damage to Bundle Branches p MI,
 Very high potential to convert to Third Degree
(Complete) Heart Block
 Excessively slows HRMay require pacemaker,
Atropine not effective
Second Degree AVB
Third Degree COMPLETE HB
 Complete absence of conduction of electrical
impulse through AV node, Bundle of His, and BB
 Atria rhythm independent from Ventricular
rhythm; Regular P-P and regular R-R
 LIFETHREATENING Rhythm, will lead to asystole
 Requires Pacing
 Causes; Inferior wall MI, Ischemic Heart Disease,
Medications (Dig, BB, CCB), hyperkalemia
Complete Heart Block
Treatment of CHB
 Cardioversion or Defibrillation
 Transcutaneous pacing for symptomatic
 Medications
 Atropine
 Vasopressors
 BB
 Nursing Assessment
Bundle Branch Block
 Irregular conduction or block of electrical
pathway through bundle branches
 Ventricles do not contract simultaneously
 QRS > 0.12, appears “notched”
Ventricular Arrhythmias
 PVC’s
 Ventricular Tachycardia
Ventricular Fibrillation
Premature Ventricular
Contraction, PVC’S
 Abnormally wide, bizarre QRS complex, not
associated with P wave
 Electrical impulse generated in ventricle, Bundle
Branch, or Perkinje Fibers
 Does not lead to contraction of ventricles,
therefor not “perfused”
 Usually followed by compensatory pause
 Can be observed with or without a pattern
Causes of PVCs
 Increased Catecholamine and increased
sympathetic tone
 Stimulants
 Amphetamine and cocaine
 Myocardial ischemia or infarction
 Hypoxemia
 Acidosis
 Dig Toxicity
 Hypokalemia
 Hypomagnesemia
Significance of PVCs
 Isolated PVC without hx heart disease are usually
insignificant, and require no treatment
 May indicate presence of ventricular abnormality
 Can lead to V tach or V fib
Single PVC
Ventricular Bigeminy
Ventricular Trigeminy
Ventricular Tachycardia
 AKA V Tach
 Dysrhythmia originating in an ectopic
pacemaker in the bundle branches, perkinje
fibers, or ventricular myocardium
 Rate 100 – 250 bpm
 P wave absent
 QRS abnormally wide and bizarre
V Tach
Causes of V Tach
 Significant Cardiac Disease
 Dig Toxicity
 QT interval Prolongation
 Electrolyte disturbances
 Liquid protein diets
Clinical Significance of V
 Determine inset and termination
 More than 3 PVCs is sustained V Tach
 Can be short, nonsustained and asymptomatic
 Increased frequency can lead to Ventricular
Fibrillation which is LIFETHREATENING
Ventricular Fibrillation
 No coordinated ventricular beats are present
 No P wave or QRS complexes noted
 Electrical Chaos in Heart
 Ventricles ‘contract’ at rate of 300 – 500 bpm
 Cardiac output CEASES
 Nursing Considerations
 Total Absence of electrical activity in heart
 Pt is clinically dead
 Absence of P wave and QRS complex
 Flat line
 Remember, if your patient is speaking to you then
they are NOT in a systole
 Cardioversion and Defibrillation
 Medical Management
 Atropine
 Vasopressors
 Calcium Channel Blockers
 Beta Blockers
 Nursing Considerations
 Oxygen, Pain management
 Blocks parasympathetic nervous system influence
on the heart
 Accelerates SA node firing rate
 Increases HR
 Increases conduction velocity
 Administered by IV bolus
 Used in
Symptomatic Bradycardia
Second Degree Type I AVB
Second Degree 2:1 AVB
Third Degree AVB with narrow QRS complexes
 Ineffective in Second Degree Type II AVB
 Advanced AVB with wide QRS complexes
 Third Degree AVB with wide QRS Complexes
 Use with Caution
 Acute MI
 Worsening myocardial ischemia
 Heart Transplant patient
 Cause vasoconstriction on arterioles and venous
 Improves blood pressure
 Increases HR and Strength of Contraction
 Epinephrine
 Vasopressin (DOC in asystole)
 Dopamine
 Norepinephrine
 Dobutamine
 Isopreterenol
 Adenosine; depress AV node and Sinus node
 SVT, Tachycardia
 Will not terminate Afib/flutter but will slow rate
 Amiodarone; Affects NA, K, and Ca channels
 VT Vfib
 Lidocaine; Widely used, ? Effectiveness in VT
 SE; altered consciousness, seizures, bradycardia
 Procainamide; supresses atrial and ventricular
dysrhythmias by slowing conduction
 VT, control of rate in AF/AF, PVST
Calcium Channel Blockers
 Diltiazem and Verapamil
 Slow conduction and increase conduction time
through AV node
 Used in
 Afib and A flutter with rapid ventricular response
 Contraindicated in
 2nd and 3rd Degree AVB
 With Beta Blocker Therapy
 Use with caution on CHF and hypotension
Beta Blockers
 Decrease HR and BP
 Used in
 To control rate in Afib Aflutter
Time for a Game
 EKG Jeopardy!
 Fifteen Question EKG Rhythm Strip Analysis
Wave Matching
1. Ventricular
2. Irregular Ventricular Beat
3. Atrial Depolarization
4. 0.12-0.20
5. Ventricular Repolarization
6. Backup pacemaker Rate
10. Sets Normal Heart Rate
A. AV Node
B. T wave
D. SA Node
7. Early atrial beat
F. P wave
8. Pacemaker site
G. QRS Complex
9. 0.06-0.12
Take Home Points
 EKG is measurement of ELECTRICAL activity
 Look at the patient
 Irregular activity can progress from
asymptomatic to life threatening
 Causes are similar (electrolytes, hypoxia,
 Treatments also very similar (BB, CCB,