Cardiac electrical activity,Arrhythmias

Cardiac conduction system

Automaticity - property of cardiac cells to generate spontaneous action potentials. Spontaneous activity is the result of diastolic depolarization caused by an inward current during phase 4 of the action potential, which progressively brings the membrane potential to threshold.

Effects of ANS

Components of atrioventricularconduction

His-PurkinjeSystem

AV Node

Einthoven leads: bipolar: I, II, IIIGoldberger leads: unipolar augmented: aVR, aVL, aVF

When a wave of depolarization moves towards the positive electrode of a lead -a positive deflection

http://www.bem.fi/book/15/15x/1508x.htm

ECG measurements

Vertical

• 10 mm = 1 mV

Horizontal

• 25mm/s: 1 mm = 0.04s

Electrical axis – frontal plane

QRS axis deviationLeft axis deviation: ≥ -30° (i.e., lead II is mostly negative)

• Left ventrucular hypertrophy

• Left Anterior Fascicular Block (LAFB): rScomplex in leads II, III, aVF)

• Some cases of inferior MI

• Some cases of LBBB

• Right Axis Deviation (RAD):

Right axis deviation ≥ +90° (i.e., lead I is mostly negative)

• Many causes of right heart overload and pulmonary hypertension

• Left Posterior Fascicular Block (LPFB): rS complex in lead I

• High lateral wall MI with Qr or QS complex in leads I and aVL

• Some cases of RBBB

• Children, teenagers, and some young adults

Horizontal plane

shift of the septum to the left- right ventricular heart disease- dilated cardiomyopathy

Horizontal plane- clockwise or counterclockwise rotation

Basic ECG analysis

• Measurements HR, PR, QRS, QT, axis

• Rhythm analysis sinus rhythm or not (e.g. Afi);, additional e.g. PVC or PAC, rhythm from atria, AV junction, ventricles;, regularity (e.g. SRA)

• Conduction analysis SA block, AV block, IV block

• Waveform description P waves wide, tall, atypical QRS complexes – wide, voltage;, ST segment –elevation/ depression; T waves inverted, voltage; U waves?

• ECG interpretation (LV hypertrophy, anterior MI, rhythm abnormalities, ST- T abnormalities...)

V6

V5

V4

Normal SR, normal PR int, normal QRS duration , left axisdeviation, (rS in II,III, aVF)

P pulmonale (ie, a P-wave amplitude > 2.5 mm) - predictor of right atrial enlargement(in patients with COPD, the amplitude of the P wave is in fact dynamic, and it tendsto be more prominent during acute exacerbation

Heart rate – calculating - several methods

1) Method 300, 150, 100, 75, 60, 50- Find R wave located on bold line- Then find the next consecutive R wave- The closest bold line represents HR

2) Number of R in 6s interval (30 big boxes)x 10

HR ?

HR?

II

Normal sinus rhythm

Normal sinus rhythm

• HR: 60 - 100 BPM

• Regular

• P waves: Upright, one preceding each QRS complex

• QRS complexes: Narrow, 0.06 - 0.12 sec

• PR Interval: 0.12 - 0.20 sec

Sinus tachycardia

• Anemia• Anxiety• Drug intoxication/coffeine• Hyperthyroidism• Hypovolemia• Infection• Pain• Hypoxia• Myocardial infarction• Heart failure• Pulmonary embolism etc.

AV junctional rhythm• QRS complex normal morphology

• P waves burried

• Initiation of activation between atria and ventricles

• Retrograde activation of atria – negative P wave before, insideor after QRS

Cardiac arrhythmia/dysrhythmia

a variation from the normal

heart rate and/or rhythm

Cardiac arrhythmia

Disordersof impulse formation

Disorders of impulspropagation

SA

other?

CCS

Myocardium

Localised abn Dif. abn.

Pacemaker Hierarchy

SA

Node

(+Atria)

AV Junction

(=AVN/His Bundle)

Ventricles

(= Distal Purkinje System)

Intrinsic Rate of Firing

60-100 min−1

40-60 min−1

30-40 min−1

Rhythm disorders

Irregular arrhythmias - sinus arrhythmia

- atrial fib

Extrasystoles – prematurecomplexes

Escape systoles

Rapid arrhythmias:

tachycardia 150-250 bpmflutter 250-350 bpmfibrillation 230-600 bpm

Bradyarrhythmias:BradycardiaSA blockAV block

Irregular - sinus arrhytmia

• Sinus rhythm

• Difference RR int more than 0.16 s

• Respiratory: increased HR in inspirium, slowing in expirium

Irregular - atrial fibrillation

Extrasystoles

Ectopic foci – abnormalpacemaker sites outsideof the SA node

Bigeminy

Trigeminy

Ventricular flutter

A 45 year old lady with palpitations and history of chronic renal failure

Ventricular tachycardia

Bradyarrhythmias

Sinus bradycardia

1. Physiological slowing of impulse formation in SA node

2. Parasympathetic activity3. Pathological SA dysfunction

Carotid sinus hypersensitivitymediated by the vagus nerve

• Bradycardia

• Hypotension

• Particularly in cancer pts (masses, neurosurgery)

• Increase in blood pressure may lead result in reflex bradycardia

Seizure activity

• may induce an abnormal stimulation of vagus nerve

• Ictal bradycardia

Symptoms of bradycardia

• Dizzines

• Fatigue

• Changes of mental status

• Syncope

• Heart failure

Sinus node dysfunction(Sick Sinus Syndrome)• Abnormalities of SA structure or increased vagal tone

• Manifestation:

- sinus bradycardia

- sinus arrest

- tachycardia-bradycardia (Afi, Afl interspersed with sinus arrest or bradycardia)

Sick sinus syndrome (SSS)

• inability to increase heart rate during physical activity or adrenergicstimulation

SA damage

• Gradual degenerative process (in the elderly)

• Drugs (e.g. cytostatics)

• Metabolic abnormalities

• Tumours

• Radiation

• Amyloidosis

• ATS of coronary a. within SA node

Sinoatrial Block

• First Degree: Prolonged SA conduction time (non-

detectable on EKG; no missing P waves)

• Second Degree: Intermittent non-conduction

(intermittent absence of P waves)

• Third Degree: Persistent non-conduction (complete

absence of P waves; escape rhythms only)

Sinus Arrest → Asystole

Sinus rhythm

Sinus brady.

→ Sinus arrest

→ V. escape

rhythm

Failure of V.

escape rhythm

→ Asystole

P P P

P P P P

P

SA Exit Block

P P P P

4:3 pattern

Missing

P wave

•PP intervals shorten prior to block

•Note unaffected, fixed PR intervals

PP:

Treatment of SA dysfunction in symptomaticpts• Reverse underlying cause

• Atropine

• Ephedrine

• Teophyllin

• Temporary pacing

• Pacemaker

Left bundle branch

Left anterior fascicle

Septal fascicle

Left posterior

fascicle

Right bundle branch

Conduction system

(AV node)

His bundle

AV Block - definitions

• First Degree: Prolonged conduction time

• Second Degree: Intermittent non-conduction

• Third Degree: Persistent non-conduction

AV block first degree

First Degree AV Block(PR > .20 sec [1 big box])

II

P P P

.36

II

Block

P P P PP

• 4:3 conduction ratio

Prolonging PR

Second Degree AV Block - Type I(Wenkebach or Mobitz I block)

IIP P P P P P

2:1 Second Degree AV block

Fixed PR interval

Third Degree AV Block(Complete Heart Block)

P P P P P P

Atrial and ventricular activity are unrelated

II

•1st and 2nd degree AV block may occur

in settings of increased vagal tone (e.g.,

sleep, Valsalva maneuver, well-trained

athletes)

•BUT… persistent 3rd degree AV block is

always pathological

Causes of pathological AV Block• Ischemia

• Cardiomyopathy

• Degenerative changes

• Infiltration (e.g., primary cardiac tumor, mts)

• Drugs that depress AV conduction• digoxin, beta blockers, calcium channel blockers,

antiarrhythmic drugs that depress the inward sodium current

• Myocardial infection,

• Trauma (e.g., surgery; therapeutic ablation)

• Congenital abnormalities

Normal activation of the heart

Right Bundle Branch Block (RBBB)

Late

right ventricular

activation

RV is activated

via the left bundle

Right bundle branchblock

With QRS widening

( .12 sec with “complete”

RBBB)

rSR’

pattern

A 55 year old man with 4 hours of "crushing" chest pain.

Left Bundle Branch Block (LBBB)

LV is activated

via the right bundle

QRS pattern inducedby LBBB

Broad

monophasic

R wave

Entire QRS dominated by

marked leftward delay

and is wide ( .12 sec)

Broad

S wave