Arrythmias Flashcards
How do you diagnose a broad complex tacchycardia with an ECG?
How do u confirm a dx of VT by ECG?
Should be assumed to be a VT until proven otherwise.
- AV dissociation: independent P wave activity.
- QRS duration > 160ms. VT from intraventricular septum quite narrow:130-150ms.
- Superior axis: RBBB (-45 to -135 degrees)
- Inferior axis- LBBB
- Onset of R wave to deep S wave.
- Comcordance in ALL leads: all QRS complexes are +ve or -ve.
If in doubt. Its safer to treat an SVT as a VT than treat a VT as an SVT.
What is the role of IV adenosine in arrythmias?
- Short acting IV drug,
Blocks the specialised conducting tissue of the AV node, lesser effects on sinus node and atrial MI.
Transient AV block- stops SVTs.not involve vagus.
A1 receptro ! - ‼️ main: cause transient AV nodal block. So any tachy dependent on AV node conduction will terminate when AV block occurs.
- Tachy that are not dependent on AV conduction will continue (AF, flutter) .
- Rare: may stop and re-initiate after secs.
- High doses may induce AF in 5-10% g
What are the effects of adenosine in specific tachys?
Sinus tachy: transient slowing of sinus rate, transient AV block with ongoing P waves. As adenosine wears off, sinus tachy may increase.
Atrial tachy: 60% “”. 10% of autonomic atrial tachys are adenosine sensitive and will terminate. No effect on remaing ones.
AF: transient AV block.
Atrial Flutter: “. Flutter waves clearly visible till AV conduction back.
Av nodal tachy + AV re-entrant tachy: terminates and sinus rhythm returns.
AF +. Accessory pathway: can result in VFib.
VT: no effect ussually, some idiopathic ones however may terminate.
What is sinus tachycardia?
Its a physiological response usually in respones to exercise or emotional stress.
Rate: 100-160bpm. Not constant; variation.
Almost alays an identifyable cause.
Rare: inappropriate sinus T: mean resting rate>100bpm.
Causes: pain, anxiety, sepsis, hypoxia, (asthma, PE, pulm oedema) anaemia, inotrope infusions
Thyrotoxicosis.
ECG dx: rapid rates, P hard to identify. (+ve in lead II)
P wave normal shape and axis,
Tx the cause.
AF- what happens?
- Commonest clinical arrythmia- 1% of population. More common that Atrial flutter and atrial tachy.
- Sx: from rapid , irregular ventricular rate + loss of atrial contribution to ventricular filling and cardiac output.
- Pts can be asx, have palpitations, chest pain, dyspnoea, syncope, presyncope, frank Pulmonary oedema.
- May be 🔹 paroxysmal( will spontaeneously revert to sinus rhytm)
🔹 persistent - requires pharmacological and cardioversion tx to return back to sinus rhytm.
🔸 permanent- sinus rhythm cannot be restored 😕
Thromboembolic risk !! When you bring him back.
Thrombus in Left atrium: results from loss of atrial contractility + ⬆️ stasis + pooling of blood in LA appendage. Restoration of sinus rhythm will restore atrial contractility function and may result in any atrial thrombus present.
Risk should be the same whether pharmacological or electrical cardioversion performed.
🔹 fibrillatory waves: uneven baseline fibrillation caused by initiation of chaotic impulses from multiple ectopic sites in the atria. Depolarisation cannot spread in organised manner as atria quiver insteaf of conduct.
What are the principal causes of AF and how do you diagnose it on an ECG?
FAST AND FURIOUS.
Rate: 400bpm.
Idiopathic, HTN, mitral valve disease, cardiomyopathy ( ishaemic, dilated, hypertrophic), acute infx, thyrotoxicosis, post- surgery. Coffee Alcohol, cigarttes, fatigue, stress Drugs: aminophyline, digoxin, Catecholamine release during exercise.
ECG dx: irrefular ventricular rhythm. No discrete atrail activity, although V1 often has a rapid, coarse fibrillatory baseline.
Rhytm: irregularly irregular,
Rate: atrial- cant. Vs- 130bpm..
Pwave: replaced by fine fibrillatory waves.
QRS0.08.
Av node blocks erratic atrial impulses to protect the ventricles.
Ventricles only respond to the impulses that manage to oass through AV node.
How do you treat AF?
- Restoration of sinus rhytm
- ventricular rate control
🔹Duration >48hrs- ⬆️ thromboembolic risk assc w/ cardioversion. And restoration to sinus rhytm.
↪️ them cardioversion only if: Pt on long term anti-coagulation, or has had transoesophageal ECHO to exclude LA thrombus or haemodynamically stable.
Risks of cardioversion must outweight the the thromboembolic risk.
48hrs.
What does an ECG lead show in AF?
🔹 Irregular QRS complexes.
🔸No obvious discrete P waves although not unsusual to see V1 activity w/ sharp bumps every 4-6 squares.
Whats atrial Flutter?
Supraventricular tachycardia characterised by atrial rate of >250-400 bpm. Generallt around 300bpm.
Originating in single atrial focus, this rhythm results from circuit reentry and possibility increased automaticity.
Commonly assc w/ 2nd degree heart block- in that case, the AV node fails to allow conduction of impulses to the Vs. As a rsult-> ventricular rate is slower.
Rarely occurs in healthy person. If it does: intrinsic cardiac disease indication.
- Macro reentrqnt atrial tachy with an electrical wavefront rotating around the tricuspid valve.
- Can be paroxysmal, persistant or permanent.
- Typical atrial flutter circuit is restricted to the RA and the rest of the heart is passivelt activated.
- Regular rate280-320bpm. Vs activated in 2:1 form.
- Sx occur from rapid ventricular rate and loss of atrial contribution to ventricular filling and cardiac output. - chest pain, palpitations, dyspnoea, presyncope, syncope , frank pulm oedema.
What are some causes of Atrial Flutter?
Why would we have misleading pulses?
Conditions enlarging atrial tissue or elevating atrial pressure- severe mitral valve dysfx, 🔸Hyperthyroidism 🔹Pericardial disease 🔹Cardiac surgery 🌙COPD 🔹Acute MI 🔹Systemic arterial hypoxia
Cariomyopathy (ischaemic, dilated, hypertrophic)
Acute infx
Post op.
Misleading pulses: cz we count ventricular contractions and not atrial ones. If ventricular rate normal, pt might be asx.
If fast: signs and sx of reduced cardiac output and caridac decompression.
How do u diagnose atrial flutter on an ECG?
Saw tooth baseline with flutter waves at 300bpm. 1 flutter evry 1 bif square. Mainly negative deflections in lead II, III, aVF.
Ventricular rate usually regular at 150bpm. 2:1 ratio. (Rapid rate reduces V filling)
Rhytm: atrial: regular, V- irregular.
PR interval: unmesearable
Regular QRS: 0.08 (2 small sq) should be 3-5.
Twave + QT interval : unidentifyable.
During 2:1 AV conduction alternate flutter may be hiding behing QRS complexes. V1 good one for atrial activity.
-ve in II, III, aVF.
How will you treat atrial flutter?
- Restoration of sinus rhythm
- Ventricular rate control.
Tailored to haemodynamic compromise and thromboembolic risk.
What happens when the pt ha s atrial flutter and swvere haemodynamic compromise?
Ventricular rate >150bpm or 1:1 conduction, HTN, hypoperfusion, pulm oedema, cardiac ischaemia.
Oxygen
Heparin (5-10000 iu Iv) then SC LMWH
Synchronised DC shock under sedation/GA.
What is the treatment of choice in Atrial flutter?
Cardioversion: delivers an electrical stimulus during depolarisation, making part of the Myocardium refractory to ectopic impulses and terminates the circiut reentry moevements.
Drugs: digoxin + CCB will decrease AV conduction time.
Quinidine may be given to convert flutter to fibrilation (easier to treat)
❌‼️ alert: bradycardias, digoxin supresses SA node.
What is atrial tachycardia?
Supraventricular tachy- rate of 150-200bpm.rapid rate , decrasing ti,e for ventricular filling, ⬆️ myocardial O2 consumption, and decreases o2 supply.
shortens diastole,- loss of atrial kick-> ⬇️ Cardiac output, coronary hypoperfusion, ischamic myocardial changes.
Ectopic or focal AT.
Discrete focus firing automatically at a rate freater than the SA node.
Common sources of tachycardia: pulmonary veins in LA and crista terminalis in RA.
Ventricles activated in 1:1 fashion, unless Atria too fast >200bpm or AV nodal blocking drugs used.
Sx- from tapid ventricular rate- chest pain, palpitations, dyspnoea, presyncope.
Angina, HF, ischaemic mi changes and even an MI can occur ❗️
