SVT Flashcards
definition of supraventricular tachycardia
originate between the SAN and AVN
arrhythmias that originate in the sinoatrial node, atrial myocardium, or atrioventricular node (regular QRS complex)
generally refers to atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular re-entry tachycardia (AVRT) and atrial tachycardia (focal or multifocal), junctional
It does not usually include atrial fibrillation.
aetiology of SVT
idiopathic
wolff-parkinson-white syndrome
younger people in abscence of heart disease
usually paroxysmal - episodes may be regular/infrequent and last for minutes/months
caused by abnormalities of impulse conduction (re-entrant tachy), disorders of impulse initiation = narrow complex tachycardia
RF for SVT
- previous MI
- mitral valve prolapse
- congenital heart disease
- previous cardiac surgery
- rheumatic heart disease
- pericarditis
- pneumonia
- chronic lung disease
- current alcohol intoxication
- digoxin toxicity
- FH of SVT or sudden cardiac death
aetiology of atrioventricular nodal re-entrant tachycardia (AVNRT)
2 functionally and anatomically distinct conducting pathway in the AVN - one fast and one slow conducting
the impulse circles around the AVN in both pathways = tachycardia
in episode of SVT - one acts as antegrade limb of a re-entrant circuit and the oitehr is the retrograde limb
ECG - tachy, narrow QRS, regular, no P
aetiology of Atrioventricular re-entrant tachycardia (AVRT)
an accessory bypass pathway that bridges the normal insulation between the atria and ventricles. The pathway lies outside the atrioventricular node.
eg WPW syndrome
Accessory pathways may be capable of antegrade or retrograde conduction, or both.
orthodromic AVRT - conduction down AVN and up accessory = narrow QRS, P after QRS
antidromic - antegrade = accessory, retrograde = AVN = wide QRS, short PR
aetiology of macro re-entrant atrial tachycardia
circuit involves a large area of the atrium
atrial flutter - reentrant loop circles the RA
aetiology of focal junctional tachycardia
abnormally rapid discharged from the junctional region - ie abnormal pacemaker activity
This type of SVT originates from the atrioventricular node, or bundle of His.
also known as automatic or paroxysmal junctional tachycardia
paroxysmal - congenital, post MI
accelarated - digoxin toxicity, catecholamine use, COPD, high K
ECG - p wave inverted in lead 2 or late or in QRS
aetiology of focal atrial tachycardia
regular atrial activation from atrial areas with centrifugal spread ie ectopic pacemaker activity
Neither the sinus nor the atrioventricular node plays a role in the initiation or continuation of this type of SVT.
idiopathic
chronic conditions - HTN, heartb diseasem cardiomyopathy
acute - MI, infection, alcohol poisening
drugs - digoxin, theophylline, cocaine
worsened by adrenergic activity
triggered activity
microreentry (slow conduction at discrete regions of fibrotic cardiac tissue)
enhanced automaticity - accelaration of normal automatic pacemaker
ECG - regular rhythm, abnormally shaped P
epidemiology fo supraventricular tachycardia
Prevalence of SVT is approximately 2 per 1,000.
Incidence of PSVT (paroxysmal) is about 36 per 100,000 people per year.
women more
sx of SVT
PSVT - minimal symptoms/syncope
Symptoms vary with the ventricular rate and duration of the SVT. Symptoms are more likely in those with underlying heart disease.
palpitations (in PSVT they start and end abruptly)
light-headedness
Patients with AVNRT being more likely to describe ‘shirt flapping’ or ‘neck pounding’ than patients with AVRT, possibly due to right atrial contraction against a closed tricuspid valve
fatigue
chest discomfort
dyspnoea
polyuria
syncope
signs of SVT
may be normal
tachycardia 140-250bpm
resulting HF may = tachypnoea, hypotension, raised JVP, 3rd heart sound, basal lung crepitations
Ix for SVT
- ECG
- Ambulatory 24-hour Holter recording - for pts with frequent but transient tachy
- cardiac enzymes
- electrolyte levels - disturbances might be the underlying cause
- FBC
- TFT
- digoxin levels
- CXR - pul oedema, infections - associated with PSVT
- echo
ECG for SVT
Allows classification of the tachyarrhythmia (particularly its regularity) and may allow a precise diagnosis.
no p waves, or normal or abnormal depending on mechanism of atrial depol
narrow QRS complex
pre-excitation on the resting ECG and a history of paroxysmal palpitations signifies an AVRT
- Pre-excitation (WPW pattern) on ECG is defined as short PR (<0.12 s) and the presence of a delta wave (slurred, broad upstroke of QRS complex) which represents the more rapid conduction in the accessory pathway compared with conduction in the AV node.
Mx of SVT
if pt is compromised - DC cardioversion
identify rhythm and treat accordingly - The most important thing is to decide whether the rhythm is regular or not (irregular is likely AF).
Vagal manoeuvres (carotid sinus massage, Valsalva manoeuvre) transiently increase AV block, and may unmask an underlying atrial rhythm.
If unsuccessful, give adenosine, which causes transient AV block - transiently slows ventricles to show the underlying atrial rhythm; cardioverts a junctional tachycardia to sinus rhythm.
If adenosine fails, use verapamil 2.5–5mg IV over 2min. NB: NOT if on a B-blocker. If no response, a further 5mg IV over 3min (if age <60yrs).
Alternatives: atenolol 2.5mg IV repeated at 5min intervals until 10mg given; or amiodarone.
If unsuccessful, use DC cardioversion.
complications of SVT
haemodynamic collapse - more likely if have underlying heart disease, unable to tolerate increases in HR
DVT
systemic embolism
cardiac tamponade
MI, CHF, syncope, sudden death
Patients with pre-excitation risk sudden cardiac death due to ventricular fibrillation induced by rapidly conducting atrial fibrillation.
SVT that persists for weeks or months may lead to a tachycardia-mediated cardiomyopathy.
