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cardiology > 6) OX Supraventricular tachyarrhythmias. > Flashcards

6) OX Supraventricular tachyarrhythmias. Flashcards

1
Q

paroxysmal supraventricular tacycardia is an arrhythmia arising from ?

A

defect in atrioventricular conduction , heart beats sporadically faster

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2
Q

what re he different from of PSVT?

A

atrioventricular nodal reentrant tachycardia- 2/3rds (AVNRT)

atrioventricular reentrant tachycardia

atrial tachycardia

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3
Q

which syndrome has a classic example of AVRT ?

A

wolff parkinson white syndrome - bundle of kent (accessory pathway) between the atria and the ventricles

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4
Q

describe the physiology of atrioventricular re-enterant tachycardia - AVRT?

A

there is the normal av conduction pathway

and the accessory pathway

signal ges from SAN node to AV node - in the AV node the conduction slows down to supply the ventricles

however in the accessory pathway it does not slow down - stimulating the ventricles faster

the accessory pathway can be in the refectory period where the signal from the san node only goes to the van node through the ventricles and then to through the accessory pathway to stimulate the the AVN node again = causing the reentry circuit

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5
Q

what do we see in the ECG for AVRT ?

A

======

orthodromic AVRT - most common
premature atrial beat encounters refectory acesory pathway but normal av node conduction

narrow QRS complex
normal antegrade conduction through avNODE -
but retrograde conduction through accessory pathway

retrograde p wave following QRS complex - in the st segment or in the t wave
p wave is retrograde in lead 2 ,3 and avf

rp interval is short

==========
ANTIDROMIC AVRT -
shortened P-R interval

due antegrade conduction through the accessory pathway -

delta wave in QRS - slurred upstroke in QRS due to
pre excited ventricles ventricles = WIDE QRS complex
however delta waves cannot be found in a patient going through tachycardia

= commonly found in WPW = BUT DELTA WAVE CANNOT BE OBSERVED IN state TACHYCARDIA

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6
Q

what is the physiology of AVNRT?

A

no acessory pathway

where in the AVN node has two pathways - slow and fast

slow - shorter refectory period
fast - longer refectory period

signal comes down and goes through both pathway
after it has gone through the fast pathway
the fast pathway will go through refactory period
by the time the slow pathway signals make it to the common pathway -p it is going to be terminated - because it is in refactory period by the conduction of the fast pathway
slow pathway now enters its own refactory perikod
and recovers
the fast pathway will recover
however if there is a premature beat - where the fast pathway is recovering from refac tory period
and slow pathway has finished it refactory pathway - so the impulse comes down the slow pathway
the fast track has now finishned its refactory period and sends the signal from the slow pathway 0 and sends signal retrogradely
and innervate the slow pathway again
= casing reneterant loop

100-250 beats per minute

supraven tachycardia = with narrow qrs complex

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7
Q

what causes atrial tachycardia ?

A

chronic hypertension, congestive heart failure,

digoxin poisoning which typically presents with concomitant AV block.

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8
Q

what are the other categories for supraventricular tachycardia ?

A

Atrial fibrillation

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9
Q

what do we see in the ECG of AVNRT typical (slow fast) and uncommon (fast slow)

A

tachycardia of 140-280

typical - impulse travels along the slow pathway towards the ventricles and returns via the fast pathway

QRS most cases there is no P wave it is hidden in the QRS complex - retrograde impulse

sometimes we can see the p waves in LEAD 2, 3 and AvF as a pseudo s wave

the same p wave is positive in lead V1 =pseudo r wave

Narrow QRS complexes
=<0.12s

===========

uncommon - only occurs in 10 percent

retrgroade p wave after qrs
giving QRS-P-T complexes

Narrow QRS complexes

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10
Q

how can we treat hemodynamicaly unstable patient with supraventricular tachycardia ?

A

Cardioversion is a synchronized administration of shock during the R waves or QRS complex

Regular narrow-complex tachycardia: 50–100 J biphasic waveform
Irregular narrow-complex tachycardia: 120–200 J biphasic waveform (preferred) OR 200 J monophasic [9]
Regular wide-complex tachycardia: 100 J biphasic waveform

(120–360J subsequently) x 2

=====
check electrolytes

======

Amiodarone 300mg IV over
≥20min; consider repeat shock;
then 900mg/24h IVI via central line

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11
Q

how can we treat hemodynamically stable patient with supraventricular tachycardia ?

A

acute :
vagal maneuver - carotid sinus massage - at the level of bifurcation - UNILATERALLY FOR 5-10 SECONDAS THE MOST
- decrease the heart rate

valsalva manuever

diving reflex - immersion of head in ice cold water

medical is manoeuvres have failed
AVNRT and orthodromic AVRT :
first line IV adenosine (Avn block)
second line - iv verapamil (av block) and iv diltiazem
IV metoprolol (av block)

antidromic AVRT -
Antidromic AVRT is often indistinguishable based on ECG appearance alone from preexcited atrial flutter and fib . Blocking the AV node in these cases could allow for unrestricted conduction of atrial impulses (that originate independently of the AV node) through the accessory pathway to the ventricles

procainamide
AV nodal blocking contraindicated!!!

Established diagnosis of AVRT: AV nodal blocking agents are safe.

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12
Q

what is the long term managment of PSVT ?

A

well tolerated infrequent episodes - vagal manuevers

first line
percutaneous catheter radio frequency ablation then of slow pathway
and acesory pathway

======
AVNRT

second line - medical
beta blockers propranolol
verapamil , diltiazem (non DHP ca blockers)

======

AVRT

Preexcitation pattern is visible.
Known heart disease: sotalol OR dofetilide
No known heart disease: flecainide OR propafenone

Preexcitation pattern is not visible.
CCBs: verapamil OR diltiazem
Beta blockers: propranolol OR metoprolol

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13
Q

what are the clinical features of paroxysmal supraventricular tachycardia ?

A

palpitations
dizziness
chest pain
dyspnea
syncope

urinary urgency - increase release of ANP

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14
Q

what is atrial fib ?

A

electrical signals fire from multiple locations in the atria (typically from root of pulmonary veins),
resulting in an irregular ventricular response.

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15
Q

cardiac and non cardiac risk factors of atrial fib ?

A

cardiac
valvular rheumatic heart disease - mitral (ACUTE AFB)
coronary heart disease - atrial ischemia

atrial myxoma (acute afib)

Pre-excitation tachycardia. e.g., Wolff-Parkinson-White

non cardiac
lungs - COPD , pneumonia , pulmonary embolism (ACUTE AFIB)!!!!

anemia - acute afib !!!!!

catecholamine release or increased sympathetic activity- sepsis(acute afib ), stress , post surgery ,
pheochromocytoma, cocaine , amphetamines

drugs - adenosine , digoxin

ethanol - acute afib!!!!!

hypothermia
smoking , DM
hyperthyroidism - acute afib
electrolyte imbalance

ACUTE AFIB - pirates
Pulmonary causes (OSA, PE, COPD, pneumonia)
Ischemia/Infarction/CAD
Rheumatic heart disease and Mitral Regurgitation (abnormal heart valve)
Alcohol / Anemia (high output failure)
Thyrotoxicosis / Toxins, especially stimulant medications, caffeine, tobacco or alcohol
Electrolytes/Endocarditis
Sepsis (infection) / Sick sinus syndrome.

OSA = Obstructive sleep apnea

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16
Q

what are the clinical features of atrial fib ?

A

usually asymptomatic
dizziness, syncope
shortness of breath
palpitations

signs
tachycardia
irregularly irregular pulse

mitral stenosis murmur

==========
long-standing Afib

Acute left heart failure → pulmonary edema

Thromboembolic events: stroke/TIA, renal infarct, splenic infarct , intestinal ischemia , acute limb ischemia

Life-threatening ventricular tachycardia

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17
Q

what are the complications of atrial fib ?

A

Afib - atria contracts rapidly but ineffectively - stagnation of blood and clot formation in the atria- increases the risk of stroke and other thromboembolic complications.
brain , kidney and spleen most likely

acute left heart failure - pulmonary edema

life threatening ventricular tachycardia

18
Q

how do you diagnose AFIB

A

ECG showing indiscernible P waves
irregularly irregular RR intervals
minute oscillation in the BASELINE(f waves)
varying morphology not identical to each other

and a narrow QRS complex less than 0.12s

tachycardia

with irregular QRS intervals- irregular RR

===========
Echocardiography is used in patients with Afib - rule out structural heart disease and detect presence of atrial thrombi

transthoracic echo
Indications: all patients with new-onset Afib to assess cardiac function and rule out underlying structural cardiac disease

transesophageal echo
indications
New-onset atrial fibrillation or atrial flutter for > 48 hours or for an unknown duration
No previous anticoagulant use or subtherapeutic anticoagulation for the past 3 weeks
CHF exacerbation or hemodynamic instability
Symptomatic Afib (e.g., palpitations, chest pain, dyspnea, syncope, fatigue, lightheadedness

  • better visualisation of atria and LEFT ATRIAL APPENDAGE - BEST HOSTSPOT FOR THROMBOGENSIS - this is identify thrombi before attempting cardioversion
19
Q

classification of AFIB

A

hemodynamically stable or unstable

heart rate
afib with ventricular rate more than 100bpm (tachycardia)
Afib with a ventricular rate < 60 bpm (bradycardia)

onset and duration
New-onset Afib- less than 48 hours in duration

Paroxysmal Afib - resolves within 7 days of onset either following treatment or spontaneously

Persistent Afib -Continuous Afib for > 7 days

Long-standing persistent Afib - Continuous Afib for > 1 year

Permanent Afib

mitral valve involvement - ALWAYS CHECK

Valvular Afib - patients with mitral valve stenosis, artificial heart valves

20
Q

what further tests are required in afib ?

A

TSH T4
serum electrolytes
troponin
d - dimer - for dvt or pulmonary embolism
BNP for heart failure
CBC - anemia
ethanol , dioxin - urine toxicology

21
Q

what is the treatment for AFIB ?

A

A-E

===========

treatable condition such as hyperthyroidism electrolyte imbalance etc

controlling heart rate or rhythm
1) unstable - IMMEDIATE electrical cardioversion !

120–150J for
AF), then 120–360J
up to three times

Consider either pharmacological (e.g.
Inpatient regimens using intravenous or oral antiarrhythmics:
Dofetilide
Ibutilide
Flecainide
flecainide,
amiodarone

2)stable - rate or rhythm control
people with atrial fibrillation presenting acutely without life‑threatening haemodynamic instability, offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain.

==========

No thrombus identified: 3 weeks of preceding anticoagulation is not required.
Thrombus identified: Patients should ideally receive ≥ 3 weeks of anticoagulation and a repeat TEE

In people with atrial fibrillation in whom the duration of the arrhythmia is greater than 48 hours or uncertain and considered for long‑term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks. During this period offer rate control as appropriate

provide anticoagulant

===============

AF is commonly triggered by other factors (see PIRATES above)

22
Q

what is rate control and who are indicated for it in afib ?

A

normalising the ventricular heart rate and this is indicated in elderly patients

23
Q

rate control is contraindicated in afib treatment management when ?

A

afib due to preexcitation syndrome such as WFW syndrome

24
Q

for rate control in afib what is the first line of treatment ?

A

1) betal blockers - metoprolol , propranolol atelol
/ non DHP calcium channel blocker - diltiazem and verapamil

(Not used if hypotension)

2) digoxin

3) dronedarone , amiodarone

25
Q

what is the second line of therapy on rate control in afib ?

A

AV nodal ablation and implantation of a permanent ventricular pacemaker

26
Q

for afib what is rhythm control and who is it indicated for ??

A

terminate the atrial fib and restoring sinus rhythm to prevent atrial remodelling

indicated for - failure in rate control with still symptomatic
and in younger patients

Paroxysmal atrial fib

27
Q

what are the contraindications for rhythm control in afib ?

A

long standing persisting afib

28
Q

what is the first line management of rhythm control in afib ?

A

1st choice - electrical cardioversion
Gradually increasing strengths of direct current shock (synchronized with the R wave) are administered under procedural sedation until sinus rhythm is restored

2nd choice - pharmacological cardioversion with antiarrythmic drugs such as flecainide and amiodarone first choice
propafenone
ibutilidie

IV or oral

29
Q

what is the second line of management in rhythm control for afib patients ?

A

percuitaneous catheter based radio frequency ablation of atrial tissue around the pulmonary vein opening

With ablation use amiodarone

30
Q

what score do we use to asses for long term anticoagulation for afib ?

A

CHA(2) DS(2) - VASc score

all 1pt except the one with two

C- CHF or left sided heart failure
H - hypertension
A2 - age above 75 - 2 pts
D - diabetes
S2 - stroke or TIA (transient ischemic attack / thromboembolism) - 2pts
V - vascular - prior MI , peripheral artery disease , aortic plaque
A - age 65-74
Sc - female sex

31
Q

according to the CHA(2)DS(2) -VASc score what will be the indication for treatment ?

A

2 or more male
3 or more female

Valvular Afib
Patients with nonvalvular Afib with either:
Severe hepatic dysfunction [45]
Advanced chronic kidney diseas
= warfarin

First-line in the long-term management of nonvalvular Afib
Direct thrombin inhibitor (e.g., dabigatran )
Factor Xa inhibitor
Rivaroxaban

32
Q

what are the clinical features of atrial flutter ?

A

mos patients are asymptomatic

  • sometimes palpitation , dizziness , syncope fatigue

signs of underlying disease - mitral stenosis murmur

tachycardia with REGULAR pulse

33
Q

what is the diagnosis of atrial flutter ?

A

sawtooth p waves - flutter waves - called f waves which are identical
regular and narrow qrs complex (regular , irregular)

34
Q

what is the treatment for atrial flutter ?

A

similar to afib

Rate control: more difficult to achieve in atrial flutter than in Afib
Rhythm control
Better results and lower recurrence compared to Afib
Catheter ablation may be the most effective rhythm control strategy.

Pharmacological cardioversion also more effective in aflutter

Inpatient regimens using intravenous or oral :
antiarrhythmics:
Dofetilide
Ibutilide
Flecainide
Propafenone

same parameters for anticoagulation in Afib

35
Q

what are the complications of atrial flutter ?

A

degenerates into atrial fib

36
Q

multifocal atrial tacycardia ?

A

A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.
Most commonly seen in patients with severe COPD or congestive heart failure.
It is typically a transitional rhythm between frequent premature atrial complexes (PACs) and atrial flutter / fibrillation.

37
Q

ecg features of MAT ?

A

Heart rate > 100 bpm (usually 100-150 bpm; may be as high as 250 bpm).
Irregularly irregular rhythm with varying PP, PR and RR intervals.
At least 3 distinct P-wave morphologies in the same lead.
Isoelectric baseline between P-waves (i.e. no flutter waves).
Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent PACs).
Some P waves may be nonconducted; others may be aberrantly conducted to the ventricles.

38
Q

treatment of multifocal atrial tacycardia ?

A

Most commonly occurs in COPD. Correct hypoxia and
hypercapnia. Consider verapamil if rate remains >110bpm.

39
Q

What patients should not use flecainide

A

Heart failure/ ichemic HD - studies mortality goes up

40
Q

When someone is on flecainide they should also be on what drug?

A

A small dose of beta blocker - to avoid complication with flecainide

41
Q

Amiodarone side effects

A

Thyroid problems - hypo and hyper
Pulmonary fibrosis - usually amiodarone should only be used for 6-12
Severe hepatitis and liver failure
Qt interval - not
Amiodarone affects the INR
Skin - skin more affected by sun lights - tan more easily and burn more easily - patients on amiodarone should use sun block

Takes two weeks for a therapeutic range to reach and takes months for amiodarone to come out of the body

42
Q

When would you refer for someone for ablation

A

Prove patients feel better in sinus rhythm than in afib ( give them a DC cardio version to compare symptoms - when they are in sinus rhythm for some weeks and then after that weeks they notice symptoms being worst )

If they qualify for flecainide then do that but if that fails

forced to use amiodarone only ( because it should not be used for long term - not for more than 6-12 months)

cardiology (32 decks)

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