HEART ANATOMY

ELECTROPHYSIOLOGY
Φ Electrical impulses are produced by the cyclic
exchange of ions across the myocardial cell
membrane.
Φ Ionic exchange results in a process of depolarization
and repolarization of cells. This is called the action
potential.
Φ This in turn results in muscle contraction or
relaxation.
Φ The electrocardiogram ( ECG ) is a record of the
heart’s electrical activity.
 CHARACTERISTICS OF CARDIAC CELLS

A. Automaticity- the ability to initiate an

electrical impulse
B. Excitability- the ability to respond to the
electrical impulse
C. Conductivity- the ability of a cell to transmit
the impulse to other cells
D. Contractility- the ability of a cell to contract
in response to electrical stimulus
HEART FUNCTION
THE NORMAL ELECTRICAL CONDUCTION
SYSTEM
 CARDIAC CONDUCTION CYCLE
A. P wave
B. PR interval
C. The Q wave
D. QRS complex
E. ST segment
F. T wave
G. QT interval
 OVERVIEW OF CARDIOVASCULAR
ARRHYTHMIAS
A. DESCRIPTION
- can occur with any disturbance in the origin,
rate, or conduction of the electrical impulses of
the heart
- these disturbances generally fall into two
broad categories:
a. Problems with the generation of the impulses
b. Problems with conduction of the impulses
 OVERVIEW OF CARDIOVASCULAR
ARRYTHMIAS
B. CAUSES OF ARRYTHMIAS
1. Altered automaticity- an increase or decrease in
the pacemaker firing rate that can result in an
arrhythmia
2. Accelerated firing rate- can cause premature
beats or tachycardia, while a decreased firing
rate can result in bradycardia or escape rhythms
3. Reentry- occurs when myocardial tissue is
stimulated more than once by the same impulse
NORMAL SINUS RHYTHM
Ω Normal impulses initiated by the SA node
Ω Clinical significance
-Signifies a functioning SA node conduction system
-Signifies a normal functioning electrical system
SINUS BRADYCARDIA
- Impulses initiated by the SA node but at a slower rate
-Clinical significance
-> may be normal in certain individuals, eg, athletes
-> monitor patient for signs and symptoms of hypotension, lethargy, or
complaints of syncope
- Treatment : atropine 0.5 mg IV push, up to a total of 3.0 mg. Pacing is also
another treatment option.
SINUS TACHYCARDIA

-Impulses arising out of the sinus node but at an accelerated rate

-Clinical significance
-> Tachycardia is usually a secondary response to sympathetic
stimulation
-> may be caused by fever, caffeine, stress, pain, decreased cardiac
output
- Treatment: monitoring the patient and treating the underlying cause
SINUS ARRHYTHMIA

→ The frequency of depolarization of the SA node is

affected by the vagus nerve, and inspiration and expiration
cause its rate of discharge to increase and decrease
respectively.
SINOATRIAL BLOCK
→ The SA node depolarizes normally but the depolarization
wave fails to penetrate the atrium
SINUS ARREST
→ Loss of SA node activity
→ Can be differentiated from SA block because from time to time the
expected P wave does not appear until after two ( or three ) normal
intervals, and then not at the expected time
PREMATURE ATRIAL CONTRACTION (PAC)
∏ Impulses initiated by atrial tissue that occur before the next anticipated
sinus beat.
∏ Clinical significance:
Caused by some irritation to the atrial tissue
 may be caused by emotional stress, tobacco, alcohol, caffeine, or in some
disease states, eg, heart failure
 originate from foci in the atrium other than the SA node
PAROXYSMAL ATRIAL TACHYCARDIA (PAT)
∑ Impulses arising out of atrial tissue at a rapid rate, which suppress normal sinus
impulses.
∑ Clinical significance
Usually of abrupt onset and termination
Originates in the right atrium above the bundle of His
Causes vary from rheumatic heaert disease and pulmonary edema to stress,
overexertion, and other stimulants.
∑ Treatment
> Valsalva maneuver, digitalis, calcium channel blockers, beta blockers, and if sustained,
electrical cardioversion
ATRIAL FLUTTER
∂ Impulses arising out of the atrium, resulting in variable conduction to the ventricles
∂ Clinical significance
The AV node does not conduct every impulse, so there may be two or more flutter waves
to every ventricular response.
Cardiac output may be decreased
The patient also is at risk for thrombus formation in the atrium secondary to decreased
emptying of the atrium.
∂ Treatment:
Attempts to convert the patient to sinus rhythm are done to control the ventricular
response
Include digoxin, calcium channel blockers, and/or electrical cardioversion
ATRIAL FIBRILLATION

∆ Irregularly irregular rhythm occuring secondary to atrial

irritability
∆ Clinical significance ( same as atrial flutter )
∆ Treatment ( same as atrial flutter )
 INHERENT JUNCTIONAL RATE
 Impulses arising out of the AV node
 The inherent rate of the AV node is 40-60 BPM
 Proximal AV impulses- inverted P wave before the QRS
 Mid-AV impulses- will have no identifiable P wave
 Distal AV impulses- P waves occurring after the QRS
 Clinical significance
- May occur in healthy individuals. However, it may by caused by
excessive slowing of the SA node, in which the AV node takes
over as the primary pacemaker.
 Treatment: atropine and/or pacing are the treatments of choice
if the patient becomes symptomatic.
Proximal AV impulses
Mid-AV impulses
PREMATURE JUNCTIONAL CONTRACTION (PJC)
Ψ Impulses arising out of the AV node before the next anticipated sinus
beat
Ψ Clinical significance:
Caused by irritation to the AV node tissue, but may occur in healthy
persons
Occur post-MI (inferior wall), digitalis toxicity, and post-cardiac surgery
Ψ Treatment: if any is indicated, deals with alleviating underlying causes
( ie, digitalis toxicity )
JUNCTIONAL TACHYCARDIA
αImpulses arising out of the AV node at a rate faster than the
inherent nodal rate
αClinical significance
Usually seen in patients post-AMI or those with digitalis toxicity
Occurs whenever the SA node has failed
 INHERENT VENTRICULAR RATE
 Rhythm arising out of the ventricles
 The inherent rate of the ventricles is 20-40
BPM.
 Clinical significance- this is a lethal rhythm and
usually precedes asystole
 Treatment: involves pacing, atropine,
dopamine, or inotropic/chronotropic support.
 PREMATURE VENTRICULAR
CONTRACTIONS (PVCs)
 Impulses arising out of the ventricles which occur before the
next anticipated sinus beat
 Clinical significance: PVCs may occur during any rhythm and
originate from an irritable focus within the ventricle. PVCs
may be warning signs of an impending lethal rhythm if:
- there are >5-6/min and originate from one primary focus
(unifocal or uniformed)
- they originate from multiple foci (multifocal or multiformed )
- R on T phenomena occurs ( the R wave of the PVC falls on
the T wave of the previous beat, causing venticular
tachycardia)
 PVCs continued...
• Patterns of PVCs include: • Treatment
> Bigeminy: every other - Depends on the
beat is a PVC underlying cause
 Trigeminy: every third - Some causes are hypoxia,
beat is a PVC hypokalemia,
 Quadrigeminy: every hypomagnesemia, digoxin
fourth beat is a PVC toxicity, and ischemia
 Couplet- two consecutive - Lidocaine is the treatment
PVCs of choice if pharmacologic
means are necessary to
 Salvos- three
alleviate PVCs.
consecutive PVCs
PVCs
VENTRICULAR TACHYCARDIA
A rapid rhythm arising out of the ventricles
Clinical significance
-VT may be self-limiting or sustained.
-Can be caused by hypoxia, ischemia, catheters, pacer wires, drug
toxicity, or electrolyte imbalances
-Most patients are symptomatic with cerebral unresponsiveness, but
some patients are able to maintain enough perfusion to remain awake.
Polymorphic VT
VENTRICULAR FIBRILLATION
πChaotic electrical activity arising from multiple foci in the ventricles
πClinical significance
-Results in a complete loss of cardiac output and death occurs within
3-4 minutes unless quick, immediate action is taken
--This rhythm is usually preceded by VT.
 ATRIOVENTRICULAR (AV) BLOCKS
• DEFINITION
-refers to an interruption in the conduction of
an electrical impulse somewhere along the
conduction system of the heart
 FIRST DEGREE AV BLOCK
• Impulses originate out of the SA node, but there is a delay in
conduction through the AV node, resulting in a prolonged PR
interval
• Clinical Significance
>usually insignificant and less dangerous than other types of block
>possible causes include drug
therapy(quinidine,propanolol,procainamide),
rheumatic fever, hypothyroidism, and inferior wall ischemia or
infarction
* Treatment: treat the underlying cause and monitor patient for any
progression in heart block
FIRST DEGREE AV BLOCK
 SECOND DEGREE AV BLOCK TYPE 1
(WENCKEBACH)
• DEFINITION
- Progressive prolongation in conduction of sinus impulses through
the AV node resulting in occasional non-conducted beats
- PR interval lengthens with each beat until a P wave appears
without a QRS complex, then cycle begins again.
- Clinical Significance
a. Causes include post-MI, dysrhythmia, and CAD with ischemia
b. Signs and symptoms, if any, are secondary to a slow ventricular
response rate
* Treatment focuses on the underlying rate, rather than the block.
Treatment is therefore administration of atropine or pacing.
SECOND DEGREE TYPE 1
SECOND DEGREE AV BLOCK TYPE 2
• DEFINITION- delay in conduction through the AV node
resulting in constant prolongation of the PR interval
with non-conducted beats
• Clinical Significance
- Only a certain number of impulses are conducted from
the SA node to the ventricles
- The resulting rhythm will show two or more P waves
for every QRS.
- The block may be intermittent or constant, thus the
rhythm may be regular or irregular.
SECOND DEGREE AV BLOCK TYPE 2
- More serious and frequently progresses to
complete or third-degree heart block
- Possible causes include CAD, acute anterior wall
MI, acute myocarditis, and digoxin toxicity.
- Signs and symptoms include hypotension and
bradycardia
- Treatment depends on the signs and symptoms
exhibited. Pacemakers are the treatment of
choice.
SECOND DEGREE AV BLOCK TYPE 2
 THIRD-DEGREE AV BLOCK
• DEFINITION- this block is characterized by the
atria and ventricles beating independently of
each other
• Clinical Significance
- Third-degree heart blocks with slow ventricular
rates impair cardiac output and pose danger to
the patient.
- If the ventricular pacemaker fails, cardiac arrest
can occur.
 THIRD-DEGREE AV BLOCK
- Possible causes include digoxin toxicity, hypoxia,post-
cardiac surgery complications, congenital abnormalities,
and infections such as rheumatic fever.
- Signs and symptoms depend on ventricular response and
the patient’s ability to adapt to a slower ventricular rate.
- Symptoms include fatigue, hypotension, and congestive
heart failure.
- If block is congenital the patient may be asymptomatic
- Treatment is the same as for bradycardia. The patient
usually requires pacemaker insertion.
THIRD-DEGREE AV BLOCK
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END.... THANK YOU