5. Cardio 3 Flashcards
Common causes of AF using the SMITH mnemonic:
Sepsis
Mitral valve stenosis or regurgitation
Ischaemic heart disease
Thyrotoxicosis
Hypertension
+ Alcohol, caffeine
There are 2 differential diagnoses for an irregularly irregular pulse, and what would suggest one over the other?
Atrial fibrillation OR ventricular ectopics
Ventricular ectopics disappear during exercise / higher heart rate
Which valve pathology is referred to in ‘valvular AF’:
Mitral stenosis or a mechanical heart valve
Discuss immediate cardioversion in AF:
Immediate can be done if <48 hours since onset OR if there is life threatening haemodynamic instability.
Pharmacological:
Amiodarone (if structural disease)
Fleicanide (can be done if structural disease has been ruled out via echo)
Or electrical
When is delayed cardioversion indicated, and what method is recommended?
> 48 hours since onset + stable
Must be anticoagulated for 3 weeks prior to delayed cardioversion
TOE, to exclude Left Atrial appendage, then electrical cardioversion
?Amiodarone before and after
What ablation options are available in AF when drugs for rate or rhythm control hasn’t worked / not tolerated?
Left atrial ablation - scar tissue does not conduct electrical activity
AV node ablation (+ permanent pacemaker, which is inserted before ablation)
NICE suggests that all patients with AF should have rate control first line except: (+ rate control options)
NOT rate control first line if:
Reversible
New onset <48 hours
Heart failure
Symptoms despite being effectively rate controlled
- BB / CCB rate limiting (ccb should NOT be used in HF)
- digoxin, in persistent AF, sedentary. Monitor closely
Digoxin toxicity, including features and precipitators. :
Can occur even within therapeutic range.
Unwell
N&V
Anorexia
Confusion
Yellow / green vision
AV block
Bradycardia
Gynaecomastia
HYPOKALAEMIA precipitates digoxin toxicity, as they normally bind to the same site.
Mx = digibind, correct arrhythmias, monitor K
How often are DOACs taken?
Apixaban & Dabigatran = OD
Edoxaban & Rivaroxaban = BD
Reversal agents:
A,E,R = andexanet alpha. These are Xa antagonists.
D = idracizumab. D is a direct thrombin inhibitor.
What option is available for patients with contraindications to anticoagulation and a high stroke risk?
Left atrial appendage occlusion
CI to anticoagulation, high stroke risk
High stroke risk
What are the 4 types of pacemakers?
Single chamber (RA if SAN abnormal, RV if AVN abnormal)
Dual chamber (RA, RV)
Biventricular (RA,RV, LV) aka CRT. Indicated in severe heart failure
ICD = apply shock if they detect VF/VT
Who gets an ICD?
Risk of VT / VF:
Previous cardiac event
HOCM
Long-QT syndrome
ECG changes you get with a pacemaker:
Sharp vertical lines in all leads:
Atrial; line before each p wave
Ventricular; line before each QRS
SVT vs AF vs flutter:
AF: irregularly irregular, no p waves
Flutter: sawtooth
SVT: regular, QRS immediately followed by t wave
3 main types of SVT:
AVNRT - AV nodal re-entrant tachycardia, re-entry back through the AV node - most common!
AVRT - AV re-entrant tachycardia. Re-entry via accessory pathway e.g. WPW.
Atrial tachycardia - electrical signal comes from somewhere other than the SAN.
Another name for WPW, and what is the definitive management?
Pre-excitation syndrome; may be asx or have many episodes of SVT
Bundle of Kent?
Radiofrequency ablation
What should be avoided in patients with WPW and why?
Avoid antiarrhythmics in patients with WPW presenting with AF or flutter:
They can have a polymorphic wide QRS than can develop into VT and cardiac arrest, and this progression risk is increased by the use of antiarrhythmics that block AV conduction and increase the use of the accessory pathway in WPW.
E.g. BB, CCB, dig, adenosine
How does adenosine work?
Slows cardiac conduction through AV node (+ accessory pathway), ‘resetting’ to sinus rhythm.
Synchronised vs unsynchronised DC cardioversion:
Synchronised - to avoid shocking a patient during a t wave which can result in VF and cardiac arrest.
During cardiac arrest with pulseless VT or VT you don’t need synchronised as there is no organised electrical activity, no ‘t’ waves to shock.
MOA of digoxin + ecg features:
Decreases conduction through the AV node, slowing ventricular rate in fibrillation and flutter.
Increases force of cardiac muscle contraction due to inhibition of the Na/K ATPase pump (positively inotropic).
Also stimulates the vagus nerve.
Downsloping st depression, flattened t waves, short QT interval, AV block, bradycardia
MOA of amiodarone:
Blocks K+ channels, which inhibits repolarisation and hence prolongs the action potential, lengthening the QT interval
Also blocks sodium channels
Indications for pacemakers;
Symptomatic bradycardia e.g. sick sinus syndrome
Mobitz type II block
Third degree / complete heart block
AV node ablation for AF
Severe heart failure (biventricular pacemaker)
Amiodarone thyroid disease, hypo vs toxicosis and management:
AIHypothyroidism; thyroxine formation inhibited due to high levels of iodide / Wolff-Chaikoff effect.
Can continue amiodarone if needed.
AIThyrotoxicosis:
Type 1- excess iodine-induced thyroid hormone synthesis. GOITRE present. Manage with carbimazole.
Type 2 - amiodarone related destructive thyroiditis. No goitre. Treat with corticosteroids.
First line medical treatment of chronic heart failure with ABAL mnemonic:
ACEi
BB
Aldosterone antagonist e.g. spiro / eplerenone
Loop diuretics furosemide
Further include SGLT2i, ARNI, ivabridine , hydralazine and dig
