6) OX Supraventricular tachyarrhythmias. Flashcards
paroxysmal supraventricular tacycardia is an arrhythmia arising from ?
defect in atrioventricular conduction , heart beats sporadically faster
what re he different from of PSVT?
atrioventricular nodal reentrant tachycardia- 2/3rds (AVNRT)
atrioventricular reentrant tachycardia
atrial tachycardia
which syndrome has a classic example of AVRT ?
wolff parkinson white syndrome - bundle of kent (accessory pathway) between the atria and the ventricles
describe the physiology of atrioventricular re-enterant tachycardia - AVRT?
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
what do we see in the ECG for AVRT ?
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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
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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
what is the physiology of AVNRT?
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
what causes atrial tachycardia ?
chronic hypertension, congestive heart failure,
digoxin poisoning which typically presents with concomitant AV block.
what are the other categories for supraventricular tachycardia ?
Atrial fibrillation
what do we see in the ECG of AVNRT typical (slow fast) and uncommon (fast slow)
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
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uncommon - only occurs in 10 percent
retrgroade p wave after qrs
giving QRS-P-T complexes
Narrow QRS complexes
how can we treat hemodynamicaly unstable patient with supraventricular tachycardia ?
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
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check electrolytes
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Amiodarone 300mg IV over
≥20min; consider repeat shock;
then 900mg/24h IVI via central line
how can we treat hemodynamically stable patient with supraventricular tachycardia ?
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.
what is the long term managment of PSVT ?
well tolerated infrequent episodes - vagal manuevers
first line
percutaneous catheter radio frequency ablation then of slow pathway
and acesory pathway
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AVNRT
second line - medical
beta blockers propranolol
verapamil , diltiazem (non DHP ca blockers)
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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
what are the clinical features of paroxysmal supraventricular tachycardia ?
palpitations
dizziness
chest pain
dyspnea
syncope
urinary urgency - increase release of ANP
what is atrial fib ?
electrical signals fire from multiple locations in the atria (typically from root of pulmonary veins),
resulting in an irregular ventricular response.
cardiac and non cardiac risk factors of atrial fib ?
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
what are the clinical features of atrial fib ?
usually asymptomatic
dizziness, syncope
shortness of breath
palpitations
signs
tachycardia
irregularly irregular pulse
mitral stenosis murmur
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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
what are the complications of atrial fib ?
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
how do you diagnose AFIB
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
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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
classification of AFIB
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
what further tests are required in afib ?
TSH T4
serum electrolytes
troponin
d - dimer - for dvt or pulmonary embolism
BNP for heart failure
CBC - anemia
ethanol , dioxin - urine toxicology
what is the treatment for AFIB ?
A-E
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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.
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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
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AF is commonly triggered by other factors (see PIRATES above)
what is rate control and who are indicated for it in afib ?
normalising the ventricular heart rate and this is indicated in elderly patients
rate control is contraindicated in afib treatment management when ?
afib due to preexcitation syndrome such as WFW syndrome
for rate control in afib what is the first line of treatment ?
1) betal blockers - metoprolol , propranolol atelol
/ non DHP calcium channel blocker - diltiazem and verapamil
(Not used if hypotension)
2) digoxin
3) dronedarone , amiodarone
