Arrhythmias

when are tachycardias more symptomatic

when are tachycardias more symptomatic

arrhythmia is fast and sustained

supra vs ventricular tachys

supra - arise from atrium or av jxn

ventricular - arise from ventricles

sinus arrhythmia

hr quickens on inspiration

hr falls on exp

mechanisms generating tachycardia

• accelerated automaticity

• triggered activity

• re-entry (ring cardiac tissue surrounds inexcitable core)

bradycardias may be due to :

failure of impulse formation or failure of impulse conduction (from a → v)

causes of sinus bradycardia

hypothermia, hypothyroidism, cholestatic jaundice, raised intracranial p, b blockers or other antiarrhythmics

infarction, fibrosis, sick sinus syndrome

sick sinus syndrome

caused by idiopathic fibrosis of sinus node, episodes of sinus brady or sinus arrest, w/ paroxysmal atrial tachyarrhythmias

neurally mediated syndromes are due to a reflex result in __________, presenting as ________-

bradycardia and reflux peripheral vasodilation

syncope or dizzy spells (pre-syncope)

carotid sinus syndrome

neurally mediated sinus brady, in elderly, leads to brady

neurocardiogenic (vasovagal) syncope

in young adults or old, from situations affecting ANS → brady, vasodilatory or mixed

POTS

type of neurogenic sinus brady, sudden increase HR + mild reduction bp from standing, due to failure peripheral vasc, usually iatrogenic syncope (from meds)

management sinus bradycardia

remove extrinsic cause, temporary pacing if reversible or pacemaker if chronic degenerative

treatment chronic symptomatic sick sinus syndrome

permanent pacing (DDD), antiarrhythmic drugs

treatment carotid sinus hypersensitivity

pacemaker

treatment vasovagal attacks

avoidance, lying down + applying counter-p

increased salt, compression stockings, b blockers, a agonists or neg inotropoes

treatment malignant neurocardiogenic syncope (w/ injuries + asystole)

dual chamber pacemaker w/ rate drop response feature

block in av node or his bundle vs lower

av/his - av block

low - bbb

first degree av block

prolongation pr interval >0.2 s

second degree av block + types

some p waves don’t conduct

1. Mobitz I - progressive PR prolongation until P wave fails

2. Mobitz II - dropped qrs complex not preceded by progressive PR prolongation, wide QRS

3. 2/3:1 block - every 2/3rd p wave conducts to ventricles

wenckebach av block

from block in av node, usually monitored (unlike Mobitz II where needs pacemaker + from his)

acute MI may produce what block

second degree heart block (temporary pacing indicated)

narrow complex escape rhythm

third degree/complete av block, adequate rate and reliable rhythm

broad-complex escape rhythm

escape rhythm originates below His bundle → slow rhythm + unreliable, Stokes-Adams attacks (blackouts)

causes broad-complex escape rhythm in elderly vs young

elderly - Lev’s disease, degenerative fibrosis + calcification

young - Lenegre’s disease, progressive cardiac conduction disease

_________produces slight widening of qrs, known as incomplete bbb

bundle branch conduction delay (up to .12s)

right bbb ecg

late activation right ventricle, deep S waves in leads 1 + V6, tall late R wave in lead V1

left bbb on ecg

deep s wave in lead V1, tall R wave in leads 1 + V6

hemiblock causes what effect

swing in direction of depolarization

bifascicular block is a combo of any two of

block of right bundle branch, left antero-sup division and left postero-inf division

clinical signs left vs right bbb

right - wide split s2

left - reverse splitting s2

combo of right bbb and left axis deviation is seen in

patients w/ ostium primum atrial septal defects

diffuse conduction tissue disease

complete left bbb is often associated with

left ventricular disease

supraventricular tachys (SVTs) arise from

atrium or av jxn

inappropriate sinus tachycardia

type of SVT, persistent increase resting HR, in young women

av nodal re-entrant tachycardia

type of av junctional tachy (SVT), in young women, attacks triggered by smth

av re-entrant tachy

due to macro re-entry circuit → atrial activation occurs after ventricular, P wave bw qrs and T wave

patients w/ history palpitations and pre-excited ecg have a condition known as

wolff-parkinson-white syndrome

ecg features AVNRT

absent or inverted p wave

ecg features afib

irregularly irregular rr intervals, no organized atrial activity

atrial flutter ecg features

flutter waves @ 300 bpm, 2:1 av conduction

atrial tachy ecg features

organized atrial activity w/ p wave different from sinus rhythm preceding qrs

multifocal atrial tachy

multiple p wave morphologies and irregular RR intervals

accelerated jxnal tachy has a similar ecg to

AVNRT

leading symptom of SVTs (especially AVNRT + AVRT)

rapid regular palpitations - abrupt onset, ends by valsava

AVNRT symptoms

rapid regular palpitations, polyuria, prominent jugular

management AVNRT + AVRT if patients have SVTs and hemodynamic instability

er cardioversion

management AVNRT + AVRT if patients are hemodynamically stable

vagal manoeuvres → if didn’t work, iv adenosine

long-term management AVNRT + AVRT

ca blockers (verapamil, diltiazem), b blockers

catheter ablation

atrial tachyarrhythmias all arise from

atrial myocardium

afib occurs in a paroxysmal form in who

younger

anything resulting in raised atrial p, increased atrial m mass, atrial fibrosis or inflammation of atrium may cause

afib

causes of afib

rheumatic disease, alcohol, thyrotoxicosis, htn, hf

symptoms afib

variable - er w/ rapid palpitations, dyspnea, chest pain

signs afib

irregularly irregular pulse

clinical classification afib

first detected

paroxysmal - stops within 7d

persistent - >7d

longstanding persistent - continuous >1y

permanent - continuous

acute management afib

drugs to control ventricular rate

cardioversion - by dc shock or med (biphasic waveform defib)

long term management afib

rate control - av nodal slowing agents + anticoags

rhythm control (antiarrhytmics + dc cardioversion + anticoags)

recurrent paroxysms of afib may be prevented w

oral meds

treatment patients w/ afib + hf or lvh

amiodarone

treatment patients w/ paroxysmal or early persistent afib

left atrial ablation

when is rate control used in patients with afib

permamnent arrhythmia + symptoms that can be improved by slowing hr

persistent tachyarrhythmias + failed cardioversions + serial antiarrhythmic drugs

rate control for afib

digoxin for elderly, b blockers or verapamil/diltiazem

ablate and pace strategy

AV node ablation and pacemaker implantation in older patients w/ afib + poor rate control despite optimal medicla therapy, + life-long anticoagulation

a high HAS-BLED score identifies patients with a high risk of

bleeding in afib (demonstrates need for anticoagulation)

what anticoags are used in afib

warfain or DOACs

what may be offered in patients with afib when oral anticoags COed

percutaneous left atrial appendage occlusion

atrial flutter

organized atrial rhythm with atrial rate bw 250-350bpm from macro re-entrant right atrial circuit

ecg atrial flutter

sawtooth-like waves (F waves) bw qrs complexes

f waves in clockwise vs counter-clockwise atrial flutter

counter-clockwise : - in inf leads, + in V1+2

management symptomatic acute paroxysm atrial flutter

cardioversion

treatment atrial flutter for >2d

anticoag then cardioversion

drugs for atrial flutter

class Ic (flecainide) or III (dofetilide)

recurrent paroxysms of atrial flutter may be prevented by

class III antiarrhythmics (sotalol)

recurrent paroxysms in atrial flutter treatment

catheter ablation

class III antiarrhytmics (sotalol) → av nodal blocking agents

what may happen after surgery for congenital heart disease

macro re-entrant tachycardia

atrial tachycardia w/ block is often a result of

digitalis poisoning

mechanisms atrial tachycardia

enhanced automaticity, triggered activity or intra-atrial re-entry

treatment atrial tachycardia

cardioversion, antiarrhytmics, av nodal slowing agents, sometimes ablation

what appear as early P waves and treated by b blockers

atrial ectopic beats

ventricular tachy is most likely when there is what criteria

broad qrs, av dissociation, bifid qrs + taller first peak in V1, deep S wave in V6

sustained ventricular tachy manifestations

pre-syncope/dizzy, syncope, hypotension, cardiac arrest

ecg in sustained ventricular tachy

rapid ventricular rhythm + broad abnormal qrs complexes

visible p waves

capture beats (narrow qrs)

management sustained ventricular tachy

if hemodynamic compromise → er dc cardioversion

iv b blockers, class I drugs or amiodarone → cardioversion

ventricular fibrillation

rapid and irregular ventricular activation with no mechanical effect - patient pulseless and unconcscious → cardiac arrest

ecg ventricular fibrillation

shapeless rapid oscillations, no organization

_______ is provoked by a ventricular ectopic beat

ventricular fib

treatment ventricular fibrillation

defib

management - implantable cardioverter-defibs

brugada’s syndrome

idiopathic inheritable (SCN5A gene) ventricular fibrillation in boys

how to diagnose brugadas

ecg changes spontaneously or provoked after administering class I antiarrhytmics (flecainide) - right bbb w/ st elevation in leads V1-3

manifestations brugada syndrome

sudden death during sleep, cardiac arrest, syncope

treatment brugadas

ICD

congenital long qt syndrome - types

associated/not with congenital deafness

causes of long qt syndrome

congenital - AR Jervell-Lange-Nielsen syndrome or AD Romano-Ward syndrome

acquired from electrolyte abnormalities (hypokalemia), drugs, organophosphate poisoning

subtypes congenital long qt syndrome

LQT1 (KCNQ1 gene), LQT2 (KCNH2 gene), LQT3 (SCN5A gene)

qt prolongation and torsades de pointes are usually provoked by

bradycardia

clinical features long qt

syncope + palpitations from torsades de pointes (polymorphic ventricular tachy) - if doesn’t resolve spontaneously → death

torsades de pointes on ecg

rapid irregular sharp complexes that change from upright to inverted, long qt

management acute/acquired long qt syndrome

pacing, mg sulphate, iv isoprenaline

management long-term/congenital long qt syndrome

b blockade, pacemaker, left cardiac symp denervation → ICD

____ is cused by genetic abnormalities making ventricular arrhythmias and sudden death may occur, requiring an ICD

short qt syndrome