DISTURBANCES OF RATE AND RYTHEM OF THE HEART

DR. DEEPAK AGRAWAL
Dept. Of Paediatrics
Indira Gandhi Medical College & Hospital
Nagpur(M.S.)

INTRODUCTION

Parts of the heart beat in orderly sequence i.e. contraction of atria followed by contraction of ventricle. The heartbeat originates in a specialised cardiac conducting system and spread via this system in the all parts of myocardium.

Normally SA node discharges more rapidly therefore called as cardiac pacemaker.

In infants and children, life threatening cardiac rhythm disturbances are more frequently the result rather than the cause of acute cardiovascular emergencies.

Primary cardiac arrest is uncommon in this age group. Typically cardiac arrest in the end result of hypoxemia and acidosis resulting from respiratory insufficiency or shock. Therefore in pediatric age group attention must be directed towards establishment of patent air way, effective ventilation adequate oxygenation and circulatory ostabalisatias.

2] ANATOMIC CONSIDERATION OF CONDUCTING SYSTEM.

SA node (node and flakes)

Situated at the juction of SSSVC with right atrium, lat. To the opening os SVC

3 mm wide

15 mm long

1 mm thick

Internodal pathways

3 pathways

ant. Tract:- tract of Bachman

Middle tract:- tract of wenckebach

Post tract:- tract of throat

AV node (node of Aschoff)

Situated in right post portion of interatrial septum

Only pathway for conduction from atria to ventricle.

Bundle of His

Continuation of Av node

Gives off 16 bundle branch at the top of interventricular septum and continues as right branch. 16 bundle branch gives out and post fasicle.

Branches and fascicles run subendocardially, and comes in contact with purkinje system whose fibers spread to all parts of the ventricular myocardium.

3] PROPERTIES OF CARDIAC MUSCLE

ELECTRICAL

Resting membrane potial of cardiac muscle is - 90 MV

Depolarisation of cardiac muscle last for 2 ms and repolarisation for 200 ms

Following as phases of cardiac muscle action potential

Phase 0 Phase of rapid depolarisation, due to opening of voltage gated sodium channels.

Phase 1 Phase of initial rapid repolarisation due to closure ofvoltage gated sodium channels.

Phase 2. Phase of plateau due to blower but prolonged opening of voltage gated calcium channels.

Phase 3. Phase of final repolarisation due to closure of Ca12 channels and K7

Efflux

Phase 4 Phase of resting potential.

Mechanical Properties

Contractile response of cardiac muscle begins just after the start of depolarisation and lasts about 1.5 times as long as action potential. During phase 0 to 2 and half of phase 3 cardiac muscle cannot be excited again by any stimulus called obsolute refractory period. During rest of phases remains in relative refractory period.

4] PACEMAKER POTENTIAL

Rythmically discharging cells have a membrane potential that, after each impulse declines to the firing level called pacemaker Potential with stimulates next impulse.

Action potentials in Sa and Av nodes are largely due to Ca12 with little contribution by Na+ influx, therefore there is no sharp rapid depolarisation spine before the platcan.

When the cholinergi, vagal fibers to nodal tissue are stimulated membrane becomes hyperpolarised and slope of prepotential is ed therefore ing heart rate.

Stimulation of sympoathetic cardiac nerves makes membrane potential fall more rapidly and rate of spontaneous discharge increases.

5] Spread oc Cardiac Excitation

Depolarisation initiated in the SA node spreads radially through atria then converges on AV node.

Atrial depolarisation complete with 0.1 sec.

Because conduction in AV node is slow there is delay of 0.15 called AV nodal delay shortened by sympathetic stimulation

Lenghtened by vagal stimulas.

From top of the interventricular septum, depolarisation reaches to all part of ventricle with 0.08 --0.1 seconds.

Depolarisation of ventricular muscle starts from 16 of the septum spreads to right of septum 1st .

Then spreads to apex, returns along the ventricular walls to the AV groove, proceeding from endocardial to the epicardial surface.

Last parts of the heart to be depolarised are posterobasal of 16 ventricle, pulmonary conus and uppermost portion of septum.

6] The Electro Cardiogram

Surface electrocardiogram is graphic representation of the sequence ofmyocardial depolarisation repolarisation

P Wave Atrial depolarisation

PQ segment delay in AV node

QRs complex ventricular depolarisation

I wave b ventricular repolarisation

Heart rate in children.

Age Awake Rate Mean

New born to 3 month of 5 -205 140

3 month to 2 years 100 - 140 130

2 years to 10 years 60 - 140 80

> 10 years 60 - 100 75

Average QRs Duration

Infants 0.05 sec

1-3 years 0.06 sec

child > 3 years 0.07 sec.

Limit of N PR interval

< 3 years of age - 0.08 secs.

3-16 years - 0.10 secs.

7] Monitoring the Ecg

ECG should be continuosly monitored in children who have evidence of respiratory and cardiovascular instability

ECG. Provides no information about the effectiveness of myocardial activity or quanlity of tissue perfusion.

As a result, therapy must always be based on clinical evaluation of the patient correlated with information derived from ECG.

Monitoring Systemb

Consists of a display screen and heart tachnometer that determines the heart rate from the R.R. interval.

The ECG impulse is conducted from the patient to the cardiac monitor through three coloured coded cabler attached to the patient by adhesive pads.

Pads typically placed on shoulders on lat. Chest surface and ground electrode is placed on the abd. or thigh.

8] Pathophysiologic Basis ob Cardiac Carrythymias

Clinical features of Recentry

Narrow lrange in tachycardia

Abruph anset and termination

Specific pharmacologic response

Successful termination with DC shock

B) Bradyeardia and block

Abnormally slow rate of result from depression of depolarisation in pacemaker cells and for block of electrical activity.

When Sa node automaticity is impaired one of the several latent pacemaker sites in atrium or AV conductions system assumes responsibility of generating cardiac rythm.

Escape rate depends on level lof new pacemake.. More distal the pacekame slower will be the heart rate.

Latent pacemaker lack in rich autonomic influence found at SA node and may exhibit a blunted chromotropic response to exertion and stress.

Evaluation and Management of Cardiac Arrythmia

1) Premature beat

common on pediatric age group

Arial eclopy predominhatging in infants and young childrens.

ventricular ectopy predominalising in adolescence

Isolated premature bealo are usually benigh, but may serve as markers of serious underling pathology in susceptible individuals.

1.  
2. Atrial premature beats
3. Appears of ECG as early P wave with axis and morphology differing from normal P wave usually followed by normal QRs compea.

   If patient is asymptomatic, occassional atrial premature beats are most always benig.

   In child with past H/O dizziness or sustained palpitation, APB, have potential for SVT.

   In asymplomatic patient stie evaluation is expanded if the beats are frequent or seems to arise from multiple foci.

   Hyperthroidism, structural heart disease and cardiomyopathy are possible causes.

4. Junctional premature beats
5. Rare
6. ECG reveals an early normal QRs but no preeceding P wave
7.  
8. Ventricular premature beats
9.  
10. ECG:- 1) early beat, 2) bizzare QRs complex, 3) No preoeding P wave

Modified lowns classification for ventriculer ectomy

0.  
1. No cetopy
2.  
3. Occsonal VPB ( 30 1 hr) isolated 10 W grade
4.  
5. Frequent VPB (> 301 hours) mod
6.  
7. Multiform VPB

4. a) complets Repetitive severe

2. 1.  
   2. VT or Vf

5.  
6. early VPB

Ventricular premature beats altrnating with normal beat called bigemy

VPB floowing every 2 normal beats called trigeniny

Usually patient is unaware of single VPBS, but some may be aware of skipped beal " or a sludder tickle over precordium this is because of increased strokes volume of normal beat following VPB.

2] Tachycardia

Classification

1. 1.  
   2. Tachy cardia causes

0. 1.  
   2. Narrow CRs complex
   3.  
   4. Sinus Tachycardia
   5.  
   6. Ectopic atrial tachycardia
   7.  
   8. Multiiocat atrial tachycardia
   9.  
   10. Juetional ecotopic tachycardia
   11.  
   12. Atrial fuctter
   13.  
   14. Atrial fibrillation
   15.  
   16. Osthodronic WPW syndra

1. 1.  
   2. Tachycardia with wide QRs complex

1. 1.  
   2. ventricular ltachycardia
   3.  
   4. SVT with BBB
   5.  
   6. Antidronie WPW

• •  
  • Decision tree for tachycardia with poor perfusion

A) Sinus tachycardia

2.  
3. Ectopic atrial tachycardia

3. Multifocal Atrial Tachycardia
4. Rare disorder in children

   Multiple foce oflenhanced atrial automaticity

   ECG: Variable P wave morphodology with highly variable PP internal

   Causes: a) Stransisent idopathii disorder in infam b) Postoperative

   Treatment: Medications which enhance AV block

5. Junctional ectopic tachycardia

2. 1. definite familial
   2. post operative tendency

ECG: It is the only narron complex SVT characterised by AV dissociation and ventricular rate greater than atrial rate.

Tlt: Drug therapy proves to be little effective

Pacing – fixed rate atrial pacing greater than tachycardia rate

Use of induced hypothermia i.e. 34⁰C

3. Atriall flutter

1. 1. if DC not performed digoxin should be given Inhibit ventricular response.

2. 1. Atrial fibrillation

C/F Palpitation can be the complaint if age is above 5 years

Syncope can be due to rapid ventricular response

ECG

Atrial nerves are totally irregular and vary in size and shape from beat to beat

Tlt: Tuitial therapy should be directed towards lowering the ventricular rate, usually with digoxin.

Ekectuve DC cardioversion is employed formost patients with sustained Atrial fibrillation such patient should be anticoagulated for at least 1 weekprior to cardio in order to prevent clot for in poorly contracting atrial tissue.

Recentry AV tachycardia

Most common mechanism of supraventricular tachycardia

Two pathways are envolved at least one of which is AV node, connecting atria and ventricle in continous cicus type circuit

e.g. WPW syndrome

earliest understood e.g. recentry Av tachycardia accesory bundle in bundle of kent

two types 1) arthodromic conduction to ventricle is by AV node

most commonly type of WPW

ECG: Narrow QRs retrograd wave morphology dedltawaves

Antidromic conduction to ventricle is by accessory pathway

ECG: widened QRs retrograd P wave morphology

Other accessory fibers are james and mahaim

Management:

Digoxin and verapamil have potential for aulleraty the rate of artial conduction in accessory connection they are contra indication

Dc condioversion for hacmodynamaically unstable patient

Supine position and vahsalva manerver for children

Tutranenous adenosine.

Surgical or cathetor ablation of accessory connection.

H) Vendtricular Tachycardia

Tachycardia that originate from myocyte or purinje cells below the bifurcation of the common bundle of this.

Recentry mechanism account for majority of these disorders

Rare in children, but carries more serious prognosis that SVT

Deaemodynamie disadvantage arises from

1. 1. fast ventricular rate
   2. VT typically occurs in abnormal myocardium withsuboptimal function.

1. 1. QRs complex appear wide and bizzare with a P wave that is either dissociated or arises from passive retrograde conduction.
   2. Reliable sign of ventricular arrythmia is presence of ventricular fusion complex. This is QRs complex produced in part by normally conduct to impulse from above and in part by ectopic ventricular impulse.

Brandycardia

Sinus brandycardia

Rate is slower than normal for patients age and complexes are completely normal

For newborn rate < 80/min

For children rate <70/min

May be significant

Rare in healthy children but occur is trained athletes.

Causes: ICT

Hypothyroidism

Hypothrmia

Profound hypoxia

Hyperkalemia

Digitalis

Betaadrenergic blocker

2) Sick sinus syndrome

Classically results from direct injury to SA node following surgery of cong. Heart disease.

Operation for transposition of great vessels like mustard, senning procedure results in max. incidence of SSS.

ECG shows slow and irregular sinus rates with variety of escape rhythm

UE Pacemaker therapy

Object in conduction i.e. block

Envolves eigher AV node or toroximal bundle of lthis

1^st Degree AvV block

every atrial beat is conducted although conduction velocity is very slow

DN ECG there is prolonged lPC interval

Causes

Congenital Cardiac malfor

Antiarythmic onedication

Myocardial inflamation

Hypothroidism

Surgical Trauma

Requires no therapy is well tolerated condition

IInd Degree Av block

This referes to intermittant failure of conduction for single atrial impulse

Two types (onobiz)

Type I (wenckehach)

Type II

Mobiz type I (wenckebach)

Gradual but progressive increase in P-R interval culminations in single non conducted impulse

Usually due to conduction disorder at the level of AV node

Causes are similar to type 1 block

Well tolerated condition rarly requires tlt.

In some with symtoms

Intraneous atropine provides temporary improvement, but pacemaker is safest long term therapy

Mobiz type II

There is no premonitory conduction delay with abrupt non conduction atrial impulse

Usually occurs with disease of bundle of this

Causes are usually traumatic or inflamatory injury below the level of AV node.

Sudden progression to compolete heart block may occur in this type

Mellesiatiney higher level of conceren than does mobiz type 1.

It is rare in children when occur implantation of pacemaker has been advised.

IIIrd degree (complete) heart block

Electrical communication between the atrial and ventricles is completely interrupted

Atria continues to beat at their own rate. While ventricle start beating at slower rate with impulse generating either from AV or bundle of this

Complete dissociation of P andQRs waves

May be congenital

Aquired

Congenital complete heart block

Causes

Often 1^st diagnosed in utero when slow fetal pulse is detected on routine obstretical evaluation.

If block is seen in absence of anatomical defect, 60% mothers will have clinical a serologic evidence of connective tissue disorder.

Associated with fetal hydrops or death

In most cases fetus adapts to slow heart rate

Short term progress of these patient is generally good, the long term progrosis is guarded.

Risk factors for poor outcome.

1. Ventricular rate < 55/min for neonates
2. Prolonged gT interval
3. Wide QRs
4. Ventricular ectopy
5. Advanced cardioongaly tlt pacemaker implantation to all symptesmative patient

Acquired complete AV block

Most common etiology of this in pediatric age group is direct injuryto conduction tissues during cardiac surgery orcatheterisation

1/3^rd cases of traumatic block are transient, requiring only temporary pacing.

If improvement is not observed within 6 – 10 days, recovery becomes unlikely. Permanent pacingis tlt of chercl.

Clinical Manifestation:

Older Children:- commonly and asymptomative attacks of syneapure may occur

Older infant:- night terror tiredness with frequent naps. Errilability

Pleripheral pulse is prominent

Cannon waves.

Pharmacologic Therapy for arrythmia

Drugs are classified according to their effect on action potentia of cardiac cell

Proposed by Williams

Class I Local anaesthetic agents

Sodium channel blocks reduces upstroke velocity of phase in atrial, ventricular and parkinje cells.

Classified into 3 types depemding upto their effect on upstroke conduction velocity and repolarisation

Class I A es phase O upstroke prolonges conduction velosity

Stones repolarisation

On ELG prolongs QRs and QT intoinve

e.g. Quinidine

procainamide

Disopyramide

Primary used for tlt of atrial flutter, filrillatio neutricular fibriuation

Quinidine most used

IA drug

Dose 15-60 mg (ka) day divided in 4 doses

Class I B es Glope of phase O

Es duration of action potential

e.g. lidocaine, mexiletine phenytain

used for suplpression of most forms of ventricular arrythmia

well suited for long a-T syndrome

e.g Uudocaine due to rapid hepatic metabolism only IV use

Loading dose 1 mg tlkq 1 dose

Every 10 min upto 3 dos

Maintain anoe 20-50 mg 1 k /min

Class IC e.g. fleainide

Marked depression of phase O

No influence on repolarisation and duration of action potential they are potent inhibitors of abnormal automaticity and recentry in atrial, ventricular muscles.

But due to relatively high pro arrythomic potential, use should be reserved for life threatening arythmia not responding to other tlt modalities.

Class Beta blockers e.g. propranolo Alcnolol mechanism of action.

1. competative inhibition of catecholaimine binding at cardiac receptors
2. prolongs duration of the action portential and effective reracler period.

Class III e.g. Amiodarone sotalol Bretylium

Prolongs action potential platau with out affecting phase O

Bretylium: unique

Antiarythmic with automanic effect conc. At sympathetic nerve ends causing acute release of Noradrenative followed by block ofnoradrenative release.

Most imp. Clinical application is for the treatment of ventricular fibrillation in cardiac arrest.

Initial 5 ma 1 kg slowly over 15 min. the drip of 20-50 mg/h/min

Class IV Calcium channel blocker acts predominantly on slow calcium current cells of SA and AV node. So decrease phase and automaticity.

Action on fast response potential is negligible

e.g. Verapaniul, most common clinical use is in supracentricular tachycardia nerapamic is unsafe in infants because of brachycardia and hypoten dose 1-10 mg/kg/day 8 hourly

Miscellaeneous drugs

1. diagnoxin as an antriarrythm agent, it is used for its action on AV node
2. useful in sypraventricular tachycardia to lower down the ventricular rate
3. doses Orally

IV digitalisation and maintenance – 80% of above

Intoxication

1. sinus brandycardia
2. disturbances in AV condn.
3. Nausea

Management of ltoxicity

Withold drug

Correct hypo kalemi, hypercaleum

Use of diagoxic specific tab.

1. Adenosine promising drug in abrupt terminaton of supravenity cells tachycardia

When administered by so lrapid bolus, impairs AV conduction

Promptly removed by RBCD and dothetial cells. Resulting in half life of lets thant 10 seconds

Dose 0.03 – 0.25 mg/kg

By rapid IV bolus

PACEMAKER THERAPY FOR ORRYTHMIA

Previously cardiac pacemakers were implanted for sole purpose ofrelleiving brandycardia. Butnow pacekaker, are capable of treating both body cardia and trachycardia including automative defrillation for malignan rhythm disorder

Size of pacemaker has been drastically reduced

Life ofbatteries has been prolonged

[A] Permanent pacing leads an important techniiques

fore between pacemaker lead and cardiac tissue is most crucial component of pacemaker system.

Lead must be positioned in atrium and lor, ventricle, such that there is proper sensation function.

Epicardial leads

Endocardial leads

[B] Generators and pacing modes

Recently all generators are of demand type i.e. they operate according to subtle variation on this basic demand theme.

Shorthand notion of 3-5 letters has been developed to describe various pacing modes.

1^st letter indicates chamber paced

2^nd letter indicates chamber sensed

3^rd letter describes units respose to sensed event

last 2 letters are for the specialised pacing options like rate modulations and autitacly cancha function.

Surgical and transcathelor therapy for arrythmia

Any arrythmia that involves a discret focus or abnormal pathway is amenable to these thchniques.

e.g. WPW syndrome

ectopic atrial tachycardia

mahaim fibers

successful arrythmia surgery hinges upon accurate mapping of abnormal focus or pathway which can be done with the help of surface ECG and preperative electrophysiologic study.

Direct surgical dissection or local freezing with a cryoprobe are surgical techniques being used commonly.

Translatheror

Method to destroy arrythmia fall with the tip of specialised cathetors at the time of intracardiac electrophysiologic study

Energy forms used are OC shock, radicfrequency energy laser.