Presented by:

Lorena E. Abiera RN,MAN

CARDIAC
DYSRHYTHMIAS
 HEART
• conduction system for
generating rhythmic electrical
impulses and for moving these
impulses rapidly throughout the
heart to cause coordinated
contraction of the myocardium
 HEART
• Electro physiologic properties of the heart
❖Excitability- to respond and generate action potential
❖Automaticity –to initiate spontaneously an impulse
❖Pacemaker ,Ectopic Pacemaker
❖Contractility- force of contraction of the heart muscle
❖Refractoriness – interval in repolarization period if
uncontrolled leads to dysthymias
❖Conductivity – to transmit action potential
THE ELECTRICAL CONDUCTION SYSTEM

• SA Node

• AV Node

• Bundle of HIS

• Purkinje Fibers
Source: https://www.youtube.com/watch?v=TnFoJ7Hhi-M
THE ELECTRICAL CONDUCTION SYSTEM

❖SA node: Fastest rate of automaticity

➢“Primary” pacemaker of the heart.
➢Rate: 60 to 100 bpm

❖AV node: Has a delay which allows for atrial

contraction and a more filling of the ventricles.
➢Rate: 40-60 bpm
THE ELECTRICAL CONDUCTION SYSTEM
❖Bundle of His: Has the ability to self-initiate
electrical activity
➢Rate: 40-60 bpm
❖Purkinje Fibers: Network of fibers that carry an
electrical impulses directly to ventricular muscle
cells.
➢Rate: 20- 40 bpm
SOURCE: HTTPS://WWW.YOUTUBE.COM/WATCH?V=FTHXJUFWURW
THE ELECTRICAL CONDUCTION SYSTEM
 Event/Interval/Segment Corresponds to: Normal range

P wave (rounded ,upright) Atrial depolarization 0.06-0.12 seconds

PR interval* AV nodal delay 0.12-0.20 seconds

QRS interval* Ventricular depolarization 0.04-0.12 sec.

Time between Ventricular

ST
depolarization and 0.12 sec
Segment(flat/isoelectric)
repolarization

T wave (upright) Ventricular repolarization 0.16 sec

Total duration of ventricular

0.34 up to 0.43 sec (must be
QT interval* depolarization and
corrected for heart rate)
repolarization (all myocytes)

Time between beats - is used 0.6 to 1 sec

R-R interval (heart rate)*
to calculate heart rate (heart rate: 60 - 100 bpm)
5 BOXES = 1 SECOND
1 LARGE BOX = 1 MINUTE
300 LARGE BOXES /MIN (60SEC/MIN DIVIDED BY 0.20SEC /LARGE BOX
1500 SMALL BOXES/MIN (60SEC/MIN DIVIDED BY 0.04SEC/SMALL BOX)

REGULAR HR = A. R IN 6 SEC.STRIP X 10
B. __300____
# OF BIG SQUARES BETWEEN ONE R-R INTERVAL

C. ___1500___
# OF SMALL BOXES BETWEEN ONE R-R INTERVAL
• DETERMINING THE RATE

• 10-times method
• 1,500 method
• Sequence method
• Number of small blocks Heart rate
• 5 (1 large block) 300
• 10 (2 large blocks) 150
• 15 (3 large block) 100
• 20 (4 large block) 75
• 25 (5 large block) 60
• 30 (6 large block) 50
• 35 (7 large block) 43
• 40 (8 large block) 37
•
CAN YOU IDENTIFY THE RATE?
ELECTROCARDIOGRAM (ECG)

•Defines the graphic

representation of
the electrical activity
of the heart
ELECTROCARDIOGRAM (ECG)

•The printed record of

the electrical activity of
the heart is called a
rhythm strip or an
ECG strip.
 INFORMATION OBTAINABLE
FROM ECG
• Heart rate
• Rhythm (its regularity)

• Disturbance in Automaticity
• Abnormal conduction pathways
ECG LEADS

• On the limbs
• Bipolar limb leads ; l , ll, lll,
• Augmented leads : AVR, AVL, AVF

• On the chest
• Unipolar precordial leads : V1,
V2,V3,V4,V5,V6
ECG LEADS PLACEMENT
V1, AVR – right side of the heart
V2,V3,V4 - transition between right and left sides of the heart
V5,V6, l, AVL- left side of the heart
ll, lll, AVF -inferior heart
ECG LEADS
PLACEMENT
Einthoven's Triangle!
TYPES
❖
OF
Rate:
RHYTHMS
➢ Bradycardia = rate of <60 bpm
➢Normal = rate of 60-100 bpm
➢Tachycardia = rate of >100 100-160 bpm
❖Where its coming from:
➢Sinus; SA node
➢Atrial ; SA node fails, impulse comes from the atria ( internodal or
the AV node)
➢Ventricular; SA node or AV junction fails,ventricles will shoulder
responsibility of pacing the heart
SINUS RHYTHMS
•Normal Sinus Rhythm (NSR)
• Sinus Bradycardia
• Sinus Tachycardia
NORMAL SINUS RHYTHM
• Regular rhythm- both atrial and ventricular
• Regular P-P interval and R-R interval
• 60-100 beats/min
• One upright P wave preceding to QRS complex
• P-R interval is 0.12-0.20sec., consistent
• QRS complex 0.04-0.10sec.(<.12sec.), consistent
• Q-T interval < 0.40 sec
NORMAL SINUS RHYTHM
DYSRHYTHMIA
• Also called as arrhythmias
• it is abnormal electrical conduction or
automaticity that initiate changes the heart
rate and rhythm of contraction
SINUS TACHYCARDIA
• HR > 100 beats/min (100-180 beats/min)
• Begins in sinus nodes with regular atrial and ventricular
rhythm
• P waves and QRS complex are normal
❖Response to increase sympathetic stimulation or decrease
vagal stimulation
SINUS TACHYCARDIA
SINUS TACHYCARDIA
• Causes: • Symptoms:
• Anxiety,fever,shock • Occasional palpitation
• Stress • ↑HR
• MI; Heart failure • Hypotension
• Fluid volume loss • Angina pectoris
• Medication (atropine,Levophed)
• Caffeine, nicotine
• Exercise
• Hyperthyroidism
 SINUS TACHYCARDIA
• Management:
• Alleviating the cause and reducing the demands on heart
• IV adenosine and B-adrenergic blockers (metoprolol) may be
used to reduced HR and decrease myocardial oxygen demand.
• Drug alert for Adenosine: Monitor patient’s ECG
continuosly.Brief period of asytole may be
observed.Observe for flushing,dizziness, chestpain or
palpitations
SINUS BRADYCARDIA
• SA node fires at less than 60beats/min
(absolute bradycardia)
• Begins in sinus nodes with regular atrial and
ventricular rhythm
• P wave and QRS complex are normal
SINUS BRADYCARDIA
 SINUS BRADYCARDIA
• Causes: Aso.Disease:
• Increase vagal (parasympathetic • Hypothyroidism
system) carotid sinus massage
• Increased ICP
• Valsalva manuever
• Obstructed jaundice
• trained athletes
• MI
• Hypothermia
• Increased IOP
• Administration of
parasympathomimetic drugs (Duviod)
SINUS BRADYCARDIA
• SYMPTOMS • Management:
• HR fall to 40beats/min
• Fatigue • medication-atropine
• Hypotension • Dopamine
• Light headedness • Epinephrine
• Dizziness • Temporary transvenous
pacemaker
• Shortness of breath
• Exercise
• Decrease LOC
• Pale ,cool skin
 ATRIAL
RHYTHMS
• SA node fails to generate an impulse, the atrial tissue or areas in
the internodal pathways may initiate an impulse.
• These are called atrial dysrhythmias
• Generally, not considered life threatening or lethal, careful and
deliberate patient assessment must be continuous.
TYPES OF ATRIAL RHYTHMS
• Premature Atrial Contraction(PAC)

• Atrial Flutter

• Atrial Fibrillation

• Supraventricular Tachycardia
VENTRICULAR RHYTHMS
• SA node or the AV junctional tissue fails to initiate an electrical impulse,
the ventricles will shoulder the responsibility of pacing the heart.

• This group of rhythms are called ventricular dysrhythmias are

considered lethal

• An electrical impulse can be instigated from any pacemaker cell in the

ventricles, including the bundle branches or the fibers of the Purkinje
fibers.
TYPES OF VENTRICULAR
RHYTHMS
•Premature Ventricular Complexes
•Ventricular Tachycardia
• Torsades de Pointes
• Ventricular Fibrillation
• Asystole
JUNCTIONAL DYSRHYTHMIAS
• Dysrhythmias that originate in the area of AV node
because SA node has failed to fire
• AV node becomes pacemaker
• P wave is occurring just before or after the QRS or
is hidden in the QRS complex
SOURCE: HTTPS://WWW.YOUTUBE.COM/WATCH?V=K7TBHRUIPMO
TYPES OF HEART BLOCKS
• First Degree AV Block
• Second-Degree AV Block
• (Mobitz Type I) or Wenckebach
• (Mobitz Type II)
• Third Degree AV Block (Complete)
• CAUSES: CAD, digitalis toxicity, congenital
anomalies, rheumatic fever, viral infection, MI
FIRST DEGREE AV BLOCK
• Delay in passage of impulse from atria to ventricles→ prolong P-R
interval→ > .2o sec. but constant
• Regular rhythm (P wave is followed by QRS )
• Associated with: Structural abnormalities:
• right atrial enlargement and atrial septal defect
• No manifestation and management
• Stop the digitalis drugs if that is the cause
• Routine evaluation(ECG)→ progress
FIRST DEGREE AV BLOCK
 SECOND-DEGREE AV BLOCK
(MOBITZ TYPE I) OR WENCKEBACH

• Abnormal long refractory period at the AV node

• Delay cause PR interval progressively lengthen
• Typically “group” of QRS complex (by 2’s, 3’s)
• Record the number of P wave compared to the number of
QRS complex, R-R interval becomes shorter
• Develop vertigo, weakness, other symptoms of ↓CO
• No intervention- ventricular rate maintain adequate perfusion
SECOND-DEGREE AV BLOCK
(MOBITZ TYPE I) OR WENCKEBACH
SECOND -DEGREE AV BLOCK
(MOBITZ TYPE II)
• Normal P wave followed by normal QRS at regular interval
until P wave is not conducted , resulting in a sudden
dropped QRS
• P-R interval remain constant without prolongation
• Unstable rhythm cause by infranodal conduction disturbance
SECOND -DEGREE AV BLOCK
(MOBITZ TYPE II)
 SECOND -DEGREE AV BLOCK
(MOBITZ TYPE II)

• Symptoms: progress the Mobitz type I manifestation

• Requires close ECG monitoring for possible progression to
complete heart block
• Management:
• Administration of atropine or Isoproterenol →
speed the rate of impulse conduction
• Insertion of temporary or permanent pacemaker
• Withholding cardiac depressant drugs( digitalis,
beta-blockers.and calcium channel blockers
Management:
THIRD -DEGREE AV BLOCK
• Complete dissociation of impulse between atria and ventricles →
AV dissociation
• The atria is regularly pace by SA node but it is completely block in
the ventricle
• Ventricles are regularly paced by ventricular ectopic pacemaker
• Atria is equal or faster than ventricular rate
• Ventricular rate 40-60 beats/min
THIRD -DEGREE AV BLOCK
THIRD -DEGREE AV BLOCK
• Symptoms: • Treatment
• Sign of cardiac output and • Atropine
circulatory impairment • Transcutaneous pacing
• Hypotension • Catecholamine infusion
• Angina pectoris (dopa/epi)
• Heart failure • Transvenous pacemaker
• Dyspnea • If asystole develops→ CPR until
• dizziness transvenous pacemaker is inserted
Transcutaneous pacing
A Pilot Study to Examine the Effect of Passive Straight Leg Raise Performed
During Cardiopulmonary Resuscitation on Cerebral Perfusion Measured by
Noninvasive Cerebral Oximetry
Lorensini, Scott Prakash, Shivesh McNeill, David ,Spencer, Neil ,Bihari,
Shailesh April 2023

OBJECTIVES:
Passive leg raise (PLR) during cardiopulmonary resuscitation (CPR) is
simple and noninvasive maneuver, which can potentially improve patient-
related outcomes. Initial CPR guidelines have previously advocated
“elevation of the lower extremities to augment artificial circulation during
CPR.”
Study among 10 subjects with in-hospital cardiac arrest for whom CPR was
undertaken. Passive leg raise (PLR) was randomly used “first” in five of
subjects whereas it was used “second” in the remaining five subjects. In
subjects in whom PLR was performed during first two cycles (Group I), NIRS
values were initially significantly greater. The performance of PLR during CPR
in Group II attenuated the decline in NIRS readings during CPR.

CONCLUSIONS:
PLR during CPR is feasible and leads to augmentation of cerebral blood flow.
Furthermore, the expected decline in cerebral blood flow over time during CPR
may be attenuated by this maneuver. The clinical significance of these findings
will require further investigations.

Source:https://journals.lww.com/ccejournal/Fulltext/2023/04000/A_Pilot_Study
_to_Examine_the_Effect_of_Passive.3.aspx
 REFERENCES
• 1.Hinkle,J.L.& Cheever,K.H.(2018).Brunner & Suddarth’s Textbook of Medical
Surgical Nursing,14th Ed.Wolters Kluwer .LWW.com
• 2.Borromeo,A.R.et.al (2014).Lewi’s Medical-Surgical Nursing .Assessment
and Management of Clinical Problems.Philippine Ed.8th Ed. Mosby Elsevier
(Singapore)Pte Ltd
• https://journals.lww.com/ccejournal/Fulltext/2023/04000/A_Pilot_Study_to_Ex
amine_the_Effect_of_Passive.3.aspx
• 9.Google search engine for images
• 10.Youtube.com
THANK YOU…