Cardiac Dysrhythmias
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Transcript Cardiac Dysrhythmias
Cardiac
Dysrhythmias
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
automaticity
Describe and define the major cardiac waves in an EKG
Define normal sinus rhythm
Differentiate between rate, conduction, atrial, and ventricular
arrhythmias
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
body
Automaticity
Impulse Generation
Under Usual circumstances
Impulse generated from pacemaker cells in SA
node
Impulse then travels to AV node
Impulse then travels to Bundle of His
Impulse then travels to Right and Left Bundle
Branches
Impulse travels to Perkinje Cells that innervate
ventricles
Components of an EKG
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
electrodes
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
(left)
Smoke (black) over Fire (red),
Snow (white) on the Trees
(green)
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,
V6)
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
down)
PR interval 0.12-0.2
Determine atrial rate
Compare atrial rate to
ventricular rate
The QRS Complex
Represents normal
depolarization of the
ventricles
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
depolarization
BBB
Ventricular pre-excitation
Cardiac pacemaker
The T Wave
Represents Ventricular
repolarization
Occurs during end of ventricular
systole
Typically in same direction as QRS
complex
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
LVH
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
impulse
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
wave
Ectopic P Wave
Electrical impulse for ectopic P wave originated
outside SA node or in AV junction
Occur in
PAC’s
Atrial tacchycardia
SVT
PAC’s
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
ventricles
Irregular QRS
present in
Bundle Branch Block
Ventricular
preexcitation
Cardiac pacemaker
QT Interval
Represents time it takes for
ventricles to depolarize and
repolarize
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
ventricles
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
Arrhythmias
Rate Arrhythmias
Tachycardia
Bradycardia
Atrial Arrhythmias
Afib/Aflutter
WPW
SVT
Conduction Arrhythmias
Bundle Branch Blocks
AV Conduction Block (1st, 2nd, 3rd Degree)
Life Threatening Arrhythmias
V Fib
Complete Heart Block
Asystole
Living Arrhythmias
https://www.youtube.com/watch?v=TJR2AfxVHs
M
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
disease
Palpitations, nervousness, anxiety
Perfusion
Syncope
Workload of heart
Nursing Assessment
Atrial Tachycardia
A Flutter
Causes
Cardiomyopathy
Atrial dilation
Valve Disease
Thyrotoxicities
Hypoxia
CHF
ETOH Abuse
A Flutter
Risks; Incomplete emptying of ventricles
Thrombi formation
Loss of atrial kick
Syncope, hypotension
CHF
Treatments
Beta Blockers
CCB
Digoxin
Warfarin
Cardioversion if uncontrolled
Ablation
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 =
uncontrolled
Irregularly irregular rate
P waves absent, F waves absent
Atrial Fib
Causes and treatments similar to A Flutter
SVT
Rapid rhythm (>100) that generated outside the
ventricles
AKA Paroxysmal Atrial Tach (PAT)
Symptoms
Palpitations
Lightheadedness
Dizziness
Maybe symptomless, self limiting
Treatments
Beta Blockers, CCB,antiarrhythmics
SVT
WPW
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
Pacemaker
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
Pacemaker
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)
Hyperkalemia
First Degree AV Block
Second Degree Type I AV
Block
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
again
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
Block
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
bradycardia
Medications
Atropine
Vasopressors
CCB
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
CHF
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
Couplet
Run PVC
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
CAD
ACS
Cardiomyopathy
LVH
Dig Toxicity
QT interval Prolongation
Electrolyte disturbances
Liquid protein diets
Clinical Significance of V
Tach
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
PULSELESS V TACH IS TREATED THE SAME AS V FIB!
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
EMERGENCY
Cardiac output CEASES
Nursing Considerations
V FIB
Asystole
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
Treatments
Cardioversion and Defibrillation
Medical Management
Atropine
Vasopressors
Calcium Channel Blockers
Beta Blockers
Nursing Considerations
Oxygen, Pain management
Atropine
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
Atropine
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
Vasopressors
Cause vasoconstriction on arterioles and venous
circulation
Improves blood pressure
Increases HR and Strength of Contraction
Epinephrine
Vasopressin (DOC in asystole)
Dopamine
Norepinephrine
Dobutamine
Isopreterenol
Antidysrhythmics
Adenosine; depress AV node and Sinus node
activity
SVT, Tachycardia
Will not terminate Afib/flutter but will slow rate
Amiodarone; Affects NA, K, and Ca channels
SVT
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
SVT
To control rate in Afib Aflutter
Time for a Game
EKG Jeopardy!
jeopardylabs.com/play/ekgjeopardy#.VOLPYmdso-w.gmail
Fifteen Question EKG Rhythm Strip Analysis
http://www.12leadecg.com/arrhythmias/index.cf
m
Wave Matching
1. Ventricular
Depolarization
2. Irregular Ventricular Beat
3. Atrial Depolarization
4. 0.12-0.20
5. Ventricular Repolarization
6. Backup pacemaker Rate
40-60
10. Sets Normal Heart Rate
A. AV Node
B. T wave
C. PAC
D. SA Node
E. PVC
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,
ischemia…)
Treatments also very similar (BB, CCB,
antiarrhythmic)
References
http://lifeinthefastlane.com/ecg-library/
http://ekg.academy/learnekg.aspx?seq=11&courseid=315
http://my.clevelandclinic.org/services/heart/pati
ent-education