Width of the QRS complex :

- Wide = > VT, SVT with aberrant conduction

- Narrrow => SVT
Bradyarrythmia
Heart rate < 60 bpm

1. Sinoatrial node
a. Sinus Bradycardia
 Slowing of heart rhythm
Caused by intrinsic SA node disease (aging caused decreased SA automaticity,
ischemic heart disease, cardiomyopathy) / extrinsic factor affect the node
(medication : beta blocker, calcium channel blocker, hypothyroidism)
 Physiologic at sleep / rest / trained athlete
Pathologic when causing fall in caridac output with fatigue, light headedness,
confusion, syncope

b. Sick sinus syndrome

 Inappropriate bradycardia
Caused by intrinsic SA node dysfunction (fibrosis)
 Diziness, confusion, syncope. May present with SVT (AF) -> Bradycardia-
tachycardia syndrome
Treatment : Antiarrythmia with prior pacemaker placement

2. Atrioventricular node
a. Junctional escape Rhythm - serves as protective mechanism to maintain heartbeat &
cardiac output when the sinus node / normal AV conduction fails
 Conduction block of impulse from SA node, escape rythms emerge from latent
pacemakers
 Normal, narrow QRS complex, appear at rate of 40-60 bpm
Not preceded by normal P waves because impulse origianates below the atria
b. AV Block (AV node, bundle of His, left & right bundle branches)
 First degree AV block
- Caused by impairment in AV node (reversible causes such as heightened vagal
tone, transient AV nodal ischemia, drugs, or structural defect such as
myocardial infarction / chronic degenerative disease
- Prolongation of normal delay b/w atrial & ventricular depolarization (PR
interval > 0.2 sec), P wave : QRS complex = 1 : 1
- Asymptomatic ocndition and doesn’t require treatment

 Second degree AV block

- Caused by intermittent failure of AV conduction
- P waves not followed by a QRS complex
- In type 1 block (Wenckebach block)
 AV delay gradually increases with each beat until impulse is completely
blocked, so there is no QRS after the P wave for a single beat
 Caused by conduction impairment in AV node
 Usually benign and temporary, but in symptomatic cases need
administration of IV atropine / isoproterenol and permanent pacemaker
- In type 2 block
 Sudden intermittent loss of AV conduction w/o preceding gradual
lengthening of PR interval, and the block may persist for two or more
beats
 Caused by conduction block distal to the AV node (His system)
 Dangerous (arise from extensive myocardial infarction involving
  Third degree AV blok / Complete heart block (AV dissocation)
- The block electrically disconnects atria & ventricle aused by complete failure of
conduction between atria & ventricle (acute myocardial infarction & chronic
degeneration of conduction pathway) so the atria depolarize by stimulation of
SA node, but distal escape rhythm drives the ventricle independently
- No relationship b/w P wave and QRS complexes
- Symptoms can be light headedness / syncope, and the patient is treateed using
pacemaker implantation

3. Ventricle
a. Ventricular escape rhythm - serves as protective mechanism to maintain heartbeat &
cardiac output when the sinus node / normal AV conduction fails
 Conduction emerges from a distal point in the conduction system
 Abnormal QRS complex, at rate of 30-40 bpm . Morphology of QRS depends on
the site of origin of the escape rhythm
Tacchyarrhytmia
Supraventricular Tacchyarythmia : Tacchyarrythmia originates in atria / AV node

1. Regular Rhythm (Constant P-P interval)

a. Sinus tachycardia
 SA nodes discharge rate 100 – 180 bpm
Caused by increased sympathetic and/or decreased vagal tone
 Normal P wave & QRS complexes
 Response to carotid sinus massage : Atrial rate may slow
 In physiologic condition : Exercise
In pathologic condition : Fever, hypoxemia, anemia, hyperthyroidism
Treatment is according to underlying causes

b. Paroxysmal Supraventricular Tachycardias

Manifestation : Sudden onset & termination, atrial rates between 140 – 250 bpm,
normal QRS complexes
Caused by reentry involving the AV node, atrium or an accessory pathway between
atrium & ventricle. AV node consists of several atrial extensions, they constitute
potential pathway : slow (shorter refractory period) and fast (longer refractory period).
Normally, only the fast pathway impuls makes its way forward to the ventricles

 AVNRT (AV Nodal Reentrant Tachycardia) – most common PSVT

- Hidden / clearly visible retrogade P wave
- Fast pathway is unexcitable because it is still in its refractory period. Impuls
travels down to slow pathway, and arrives when it has been repolarized. Then
the impulse is porpagate to venricles and to atria , up the fast pathway,
completing the reentrant loop
Retrograde atrial depolarization occurs simultanoeusly with ventricular
depolarization
- Treatment : Adenosine (impairs AV nodal conduction), calcium channel
antagonists,beta blocker, vagal maneuvers, catheter ablation
  ARVT (Atrioventricular Reentrant Tachycardia)
- Impulse conduct in anterograde or retrograde conduction
- Reentrant loop is constituted by an accessory pathway (abnormal band of
myocyte that spans the AV groove and connects atrial to ventricular tissue
separately from the normal conduction system)

- Ventricular Preexcitation Syndrome

Atrial impulses can pass in anterograde direction through both AV node and
accessory pathway.
Orthodromic AVRT (Impuls travels anterogradely down the AV node to
ventricles and retrogradely up the accessory tract to atria)
Antidromic AVRT (Impuls travel anterogradely down accessory pathway and
retrogradely up to AV node)
PR interval is shortened, @RS has a widened slurred upstorke due to fusion of
two excitation waves, retrofrade P waves seen after each QRS complex

c. Focal atrial tachycardia

 Automaticity of an atrial ectopic site / reentry, atrial rate 130-250
Caused by digitalis toxicity, increased sympathetic tone
 An abnormal p wave (depolarization from an abnormal location of the atrium)
before each QRS complex
 Respones to carotdi sinus massage : AV block may increase, doesn’t usually revert
 Treatment : beta blocker, calcium channel blocker, antiarrythmic drug, catheter
ablation
 d. Atrial flutter
 Atrial rate 180 – 350 bpm with slower ventricular rate. Many of the fast impulses
reach AV node at its refractory period & do not conduct to the ventricle
Caused by reentry over a large anatomically fixed circuit (ex. Tissue along the
tricupsid valve annulus or areas of atrial scarring from disease/surgery)
 Saw toothed / sinusoidal p wave
 Response to carotid sinus massage : AV block may increase
 Symptoms depend on accompanying ventricular rate (<100 bpm is asymptomatic)
Treatment : Electrical cardioversion (for recent onset), pacemaker (following
cardiac surgery), beta blockers/calcium channel blockers/digoxin (without
immediate need for therapy), antiarrythmia drugs (if sinus rhythm has been
restored), catheter ablation (in chronic cases)

2. Irregular rhythm
a. Multifocal atrial tacchycardia
 Atrial rate is >100 bpm
Caused by abnormal automaticity in several foci within the atria / trigerred
acitivity, in severe pulmonary disease and hypoxemia setting
 Multiple P wave morphologies, with an isoelectric baseline between p waves
 Mortality rate is high, treatment is aimed at the causative disorder ; calcium
channel blocker

b. Atrial fibrillation
 Atrial rate 350-600 bpm, ventricular rate 140-160 bpm
Many of the atrial impulses encounter tissue at the AV node, allowing only some
of them to be conducted to the ventricles
 Caused by reentrant circuits within the atria, exacerbated by atrium enlargement ,
heart failure, hypertension, coronary artery disease, pulmonary disease,
thyrotoxicosis, alcohol consumption
 Distinct p waves are not discernible
 Asymptomatic if the ventricular rate is <100 bpm
Loss of normal atrial contraction
--> reduced left ventricular filling -> hypotension & pulmonary congestion
--> blood stasis in atria -> thrombus formation
Treatment : Ventricular rate control (beta blockers, calcium channel antagonists
ex. diltiazem, verapamil), reduced risk of thrombus formation (cardioversion),
restore sinus rhythm (catheter ablation to interrupt potential reentry circuits
followed by pacemaker placement)

c. Atrial premature beats

 Caused by automaticity / reentry in atrial focus outside SA node, exacerbated by
sympathetic stimulation
 Abnormal shape, earlier than expected p wave
- Blocked APB : not followed by QRS complex
- APB with abberant conduction : may abnormally wide QRS complex
 Response to carotid sinus massage : May abruptly terminate
 Can be presence in healthy & disease heart
Can be induced by caffeine, alcohol, emotonal stress
Only need treatment if APV is symptomatic (beta blocker)
Ventricular Tacchyarrytmia – Tacchyarrythmia originates in ventricle, more dangerous than
supraventricular disorders

1. Ventricular Premature Beats (VPBs)

 Ectopic ventricular focus fires an action potential, than the impulse travels through the
ventricles via slow cell to cell connections
 Widened QRS comple, not related to preceding p wave
 Bigeminy - every other/alternate beat is a VPB
Trigeminy - two normal beats precede every VPB
Quadrigeminy - three normal beats precede every VPB
Couplet - two consecutive VPBs
Triplet – three consecutive VPBs
 APBs & VPBs are common among healthy people (asymptomatic)
Precipitans of VPBs include medications (beta adrenergic receptor agonists), caffeine,
electrolite abnormalities & hypoxia
Can be dangerous in patients with heart disease history, and increased risk of sudden death
 Can be treated using beta blockers or implantable cardioverter defibrillator (for life
threatening ventricular arrythmia)

2. Ventricular Tachycardia (VT)

 A series of three or more consecutive VPBs
 Common in patient with structural heart disease, MI, heart failure, ventricular hypertrophy,
primary electrical diseases, valvular heart disease & congenital cardiac abnormalities
 There are 2 types :
a. Sustained VT : Persists > 30 sec, produce severe symptoms, requires termination by
cardioversion / antiarrythmic drug
b. Non sustained VT : Shorter, self-terminating episodes
 QRS complexes of VT are wide, with rate of 100-200 bpm
a. Monomorphic VT : Every QRS complex appears the same & the rate is regular, caused by
myocardial infarction / idiopathic
b. Polymorphic VT : QRS complexes continually change in shape & rate from beat to beat,
caused by myocardial infarct or torsade de pointes or abnormalities of cardiac ion
channels / calcium handling.
Sustained polymorphic VT usually degenerates to VF
  Symptoms vary depending on the rate, duration and underlying condition of the heart
 Sustained VT can cause low cardiac output -> syncope, pulmonary edema or progress to
cardiac arrest. If at slow rate, only cause palpitations

Torsades de pointes

- A form of polymorphic VT, caused by trigerred activity, prolonged QT interval (from electrolyte
disturbances, persistent bradyvardia, drugs
- Varying amplitudes of the QRS
- Usually causes syncope & self limited, but can be degenerated into VF.
Treatment : Correcting the underlying trigger, magnesium IV andministration (prevent
recurrent), beta adrenergic stimulating agents (isoproterenol) and artifical pacemaker

3. Ventricular Fibrillation (VF)

 A life threatening arrythmia, results in rapid stimulation of ventricles with no coordinated
contractions -> cessation of cardiac output and death
 Occurs in patients with severe underlying heart disease
 Initiated by an episode of VT, which degenerates by the breakup of excitation waves into
multiple smaller wavelets of reentry that wander through the myocardium
 Chaotic irregular appearane w/o discrete QRS waveforms
 Treatment : Electrical defibrilation. After has been converted to a safe rhythm, ybderlying
precipitans (MI, electrolyte imbalances, hypoxemia, acidosis) should be corrected. IV
antiarrythmic drugs to prevent recurrences.