Arrhythmias,

sudden cardiac death

Prof. Beata Mladosievicova, MD, PhD.

Arrhythmiasresult from abnormalities of

impulse formation

and/or

impulse propagation

Types of arrhythmias

Irregular - sinus arrhythmia- atrial fibrillation

Premature systoles -extrasystoles

atrialjunctionalventricular

Escape systoles - atrialjunctionalventricular

Rapid rhythmstachycardia

-atrial-AV junctional-ventricular

flutter-atrial-ventricular

fibrillation -atrial- ventricular

Blocks SA blockAV block 1.- 3. degreebundle branch block

Symptoms of arrhythmias

tachyarrhythmias - palpitations, chest pain, dyspnoe, syncope

bradyarrhythmias – fatigue, presyncope, syncope

conduction system

Arrhythmias

myocardium

distinguish - reversible causes of arrhythmiasin absence of heart disease

(drugs, alcohol, coffein, ANS dysbalance, electrolytes, acidosis, alcalosis,hormones)

- organic causes of arrhythmias in presence of heart diseaseaffecting CCS and/ or myocardium

CAD

CMP Heart failure Hypertrophy Dilation Inflammatory process Atrophy Fibrosis Edema Hemorrhage Congenital Surgery Radiotherapy Cytostatics

CCS and myocardium may be involved by:

arrhythmogenic mechanism

vulnerable parameter (duration AP, conduction, excitability)

therapy (modification of ion current, receptor, CCS, myocardium)

abnormal automaticity (atrial tachycardia)

reentry mechanism(VT, VFi, AVNTR, AVRT, fascicular VT, AFi, AFL)

triggered activity depends on previous impulse

- during repolarisation (EAD)

- after repolarisation (DAD)

Arrhythmogenic mechanisms of tachyarrhythmias

Reentry

depends on refractory period and speed of conduction

concept of dual pathways

one pathway is characterised by faster conduction and longer refractory period than another

unidirectional block in one pathway

Dysrhythmias- supraventricular

extrasystole, tachycardia,

fibrillation and flutter.

39.

SVT

Sinus tachycardia

– Anemia

– Anxiety

– Drug intoxication/coffeine

– Hyperthyroidism

– Hypovolemia

– Infection

– Pain

– Hypoxia

– Myocardial infraction

– Heart failure

– Pulmonary embolus...

AV nodal reentry tachycardia

elektrophysiological dissociation – two pathways:

α pathway – slow, short RP

β pathway - fast, long RP

Atrial premature complex is conducted through αand it is blocked in β

reentry – if conduction through α is slowenough to allow to β recover excitability -

tachycardia results

Retrograde P in II,III, aVF or burried P

Decreased speed of conduction

inhibition of Na channels

closure of connexins in gap junctions

during ischaemia and hypoxia/anoxiaat the microscopic level

anatomical - fixed pathway functional - dispersion of excitability

and/or refractory period

macroreentry - AVNRT, WPW symicroreentry - AS at border zone of

scar after IM

Types of reentry

Accessory pathways – bypass tracts

Wolf-Parkinson-White sy

antegrade conductionwide QRStachycardia

WPW syndrome

• resulting from the presence of an

abnormal (accessory) pathway that

bypasses the AV node (Kent bundles)

between the atria and ventricles

• Wolff–Parkinson–White (WPW) pattern

on the ECG is defined by a short PR

interval and a Δ-wave reflecting early

conduction (pre-excitation):

ECG manifestation of accessorypathways

AP in 0.3%, AP small bounds of tissue

antegrade – with preexcitation

retrograde - without preexcitation

sometimes simultaneuosly

initiated by APC or VPC

Kent, Mahaim bypass tract

WPW syndrome

RISK of ventricular fibrillation

AFi – risk of fast conduction through bypass tract

antegrade AP - ERP less than 250 ms

higher risk !!!

Atrial fibrillation

Increased incidence with age

(above 75r. app. 15%)

In pts with AFi 6-fold increased risk of stroke

Every 5. pt will develop stroke

Reentry circuits esp.in dilated atria

Initiation - extrasystole

Perpetuation - longer duration, more complicatedrecovery of sinus rhythm

Atrial fibrillation

Model pathogenesis of AFi

Decreased conductionElectrolyte abnormalities

Fibrosis

Inflammation

Decreased refractery periodIncreased tonus of symp.

Thyreotoxicosis

Other factorsAlcohol

HTN

Coronary artery disease

Cardiomyopathies

Heart failure

Valvular defects (mitral stenosis)

Drugs

Pulmonary embolus

Classification AFiParoxyzmal

less than 48 hours

Persistentneeds intervention,longer than 48 hoursmaximally 7 days

Permanentintervention without effect

Clinical findings in pts with AFi

Asymptomatic

Embolic complications (brain, heart,mesenterial)

Cardiac decompensation

SymptomsStenocardial painPalpitations

Dyspnoe

Fatigue

Syncope

Dysrhythmias- ventricular

extrasystole, tachycardia,

fibrillation and flutter.

39.

Ventricular tachycardias

bellow His bundle

sustained VT (more than 30 s)

nonsustained VT (less than 30 s)

several wide ventricular complexes

100-250 beats per min

mono/polymorphic

paroxysmal/persistent

QRS duration more than 120 ms

Ventricular tachycardia

– Dilated cardiomyopathy

– Cardiac ischemia

– Hypoxia

– Drug toxicity

– Long QT syndrome (antipsychotics,

ATB)

– Electrolyte abnormalities

Extrasystole

A substrate Modifying factors

VT in context of chronic cardiac damage

Ventricular fibrillation -

etiology

– Acute MI (most common)

– Chronic ischemic heart disease

– Hypoxia

– Acidosis

– Anaphylaxis

– Hypokalemia

– Massive hemorrhage

Ventricular fibrillation

VT- VFi – SCD!!!

Consequences of tachyarrhythmias

LV dysfunction

reduction of blood flow in coronary aa.

embolic complications

damage of CNS

sudden cardiac death

Sudden cardiac death (definition, etiology, pathogenesis, arhythmogenicand non-arhythmogenic SCD).

SCD – natural (not by accidents, murder,suicide)

unexpected death that occurs within 1 hour aftersymptoms begin

Many sudden deaths – oftentimes within seconds and

minutes !!!

SCD – frequently in people with known or suspected

heart disease

- rare in people with no known cardiac

abnormalities

Sudden cardiac death is caused by decrease

in blood flow to the brain

Almost always – SCD is caused by a cardiac

arrhythmia

(ventricular tachycardia, v. fibrillation, extreme

bradycardia and heart block)

which rapidly impair the heart´s ability to pump

blood.

Vast majority will result in SCD unless CPR is

provided !!!

CHF is a more gradual process

Who is at risk of SCD ???

those who have survived a previous cardiac

arrest (25% risk of death per a year)

post – MI pts ( with arrhythmias or with advancedcongestive heart failure)

those with hypertrophic heart disease (high BP, genetic factors)

those with valvular heart disease (aortic stenosis)

inborn genetic disorders

medications (antihistamine allergy m., antipsychotic, ATB –Ery, antidepressants, antiarrhythmics)

ETIOLOGY

• Asystole (confirm in two leads)

• Ventricular fibrillation (VF)

• Pulseless ventricular tachycardia (VT)

• Consider possible reversible causes (6 Hs

and 4 Ts):

– Hypoxia, hypovolemia, hyper- and hypokalemia,

(H+), hypothermia, hypoglycemia

– Cardiac tamponade, thrombosis (pulmonary

embolism, myocardial infarction), toxins

(medications and overdoses – anabolic steroids,

cocain), trauma

OTHER CAUSES OF SUDDEN

DEATH

• Aortic rupture

• Abnormal coronary arteries

Circumstances of SCD

• death during or after exertion

• during sedentary activity

Conduction System

Life-vest wearable defibrillator