Abnormal ECG - Arrhythmias Flashcards
How are arrhythmias dangerous?
Reduction in cardiac output
What allows all parts of the heart to become latent pacemakers?
Phase 4 depolarisation
Bradyarrhythmia:
< 60 bpm
Tachyarrhythmia:
> 100 bpm
Which types of arrhythmias are easiest to treat?
Supraventricular rather than ventricular
Those of atrial or AVN origin
What is complete (third degree) heart block?
Complete dissociation of beating between the atria and the ventricles
What dictates the speed of the bradyarrhythmia in third degree heart block?
The location of the ectopic pacemaker: slower more distal to the SAN
What causes complete (third degree) heart block?
Atherosclerosis
CHD
Dilated cardiomyopathy
Idiopathic
ECG findings in complete (third degree) heart block?
QRS complex and T waves completely dissociated from the P waves as the ventricles beat independently of the SAN firing
How does re-entry cause arrhythmia?
Because the wave of depolarisation in the heart is no longer homogenous and the rate becomes too rapid
How can you treat a unidirectional bundle branch block?
Deepen the block to prolong the refractory period with a drug
What paradoxically can cause early afterdepolarisations?
Anti-arrhythmics e.g. digoxin (also too much calcium and catecholamines)
What do both early and delayed after-depolarisations cause?
Re-entry
In atrial fibrillation, where is the ectopic pacemaker located?
Atria / pulmonary artery / pulmonary vein
Why does atrial fibrillation cause decreased cardiac output?
Ventricles beat too quickly and are not primed with blood
What drugs can treat atrial fibrillation?
Adenosine and digoxin
How do adenosine and digoxin treat atrial fibrillation?
Slow AVN conduction
How do you describe the rhythm of beating in atrial fibrillation?
Regularly irregular
Describe the ECG of atrial fibrillation
No p waves
F waves of varying amplitudes
Very frequent QRS complexes
Why is the QRS complex in ventricular fibrillation broader than in a normal patient?
Ectopic site in the ventricle wall and muscle conducts slower than the conduction system
Why can ventricular fibrillation occur post-MI
MI scar allows re-entry
Describe the ECG of ventricular fibrillation
Either: Broad QRS which can be regular (monomorphic0 or irregular (polymorphic) and p waves don’t capture
Or: No ventricular beat so disorganised and chaotic activity reflected in the ECG
How does an implanted defibrillator work?
Cardioversion back to sinus rhythm
Class 1 drugs:
Na channel blockers, suppress conduction
Give an example of a class 1 drug:
Flecainide
Class 2 drugs:
Beta receptor blockers, reduce excitability and inhibit AVN conduction (-olol)
Give an example of a class 2 drug:
Bisoprolol
Class 3 drugs:
Drugs which prolong the AP and refractory period
Give an example of a class 3 drug:
Amiodarone
Class 4 drugs:
Ca channel blockers, inhibit AVN conduction
Give an example of a class 4 drug:
Verapamil
Function of adenosine:
Slows AVN conduction
Function of digoxin:
Stimulates the vagus and thus slows AVN conduction
What drugs could be used to slow AVN conduction as a rate control strategy for treatment?
Class 2 (bisoprolol), class 4 (verapamil), adenosine and digoxin
What drugs could be used to block the re-entrant pathway and treat the source of the arrhythmia as a rhythm control strategy for treatment?
Class 1 (flecainide), class 3 (amiodarone)
Name class 2 drugs:
Carvedilol Propranolol Esmolol Timolol Metoprolol Atenolol Bisoprolol Nebivolol
Name class 1 drugs:
1a: Quinidine
Procainamide
Disopyramide
Ajmaline
1b: Lidocaine
Mexiletine
1c: Flecainide
Propafenone
Name class 3 drugs:
Amiodarone Dronedarone Sotalol Bretylium Ibutilide Dofetilide
Name class 4 drugs:
Verapamil
Diltiazem
Nifedipine
The majority of paroxysmal tachycardias are caused by what?
Re-entry
Chronic degenerative cause of bradycardia?
Sick sinus syndrome / sinoatrial disease
What is sick sinus syndrome?
Fibrosis of the SAN (usually idiopathic)
Important prophylaxis in tachy-brady syndrome?
Anti-coagulation
Drugs used for vasovagal attacks:
Beta-blockers, alpha-blockers (e.g. amiodarone) and myocardial negative inotropes (e.g. disopyramide)
First degree AV block =
Prolongation of the PR interval to > 0.22s
Every atrial depolarisation is followed by ventricular depolarisation but with delay
Second degree AV block =
Some p waves conduct and others do not
Progressive PR interval prolongation until a p wave fails to conduct is which type of heart block?
PR interval before the p wave fails is broader than after
Second degree AV block: Mobitz I block
Dropped QRS complex not preceded by a progressive PR interval prolongation. QRS complex is wide > 0.12s
Which type of heart block?
Second degree AV block: Mobitz II block
Every second or third p wave conducts to the ventricles.
Which type of heart block?
Second degree AV block: 2:1 / 3:1 / advanced block
What does a broad complex escape rhythm > 0.12s imply?
That the escape rhythm occurs below the bundle of His more distally in the His-purkinje system
Narrow onset escape rhythm is characterised by which differential?
QRS complex < 0.12s
Narrow onset escape rhythm suggests what?
Escape rhythm lies in the bundle of His more proximal to the AVN
Treatment for narrow onset escape rhythm?
IV atropine for recent and transient onset, pacemaker for for chronic onset AV block
Which drugs can induce complete heart block?
Digoxin, beta-blockers, CCBs (non-dihydropyridine) amiodarone
What is the commonest cause of re-entry in patients with normal hearts?
AVN re-entry (AVNRT)
ECG of AVNRT? (or accelerated junctional tachycardia)
No visible p wave or inverted p wave immediately before or after the QRS complex
ECG of AV reciprocating tachcardia?
P wave visible between QRS complex and t wave
ECG of atrial flutter?
Flutter waves of 300/min usually with a 2:1 AVN conduction rate
ECG of atrial tachycardia?
Organised atrial activity with p wave morphology different to sinus rhythm preceding the QRS
ECG of multifocal atrial tachycardia?
P waves of differing morphologies and irregular RR interval
Why should amiodarone be reserved until last as a rhythm control treatment in a heart with no significant disease?
Adverse extra cardiac effects
When is amiodarone only recommended treatment for rhythm control?
When the patient has heart failure or left ventricular hypertrophy
Where are the ectopic triggers for atrial fibrillation typically found?
Pulmonary veins
Drug causes of long QT syndrome:
Quinidine, disopyramide, sotalol, amiodarone, TCAs (e.g. amitriptyline)
Phenothiazine drugs (e.g. chlorpromazine)
Antipsychotics (e.g. haloperidol, olanzapine)
Macrolides (e.g. erythromycin)
Quinolones (e.g. ciprofloxacin)
Methadone
Cardiac causes of long QT syndrome:
Other causes: diabetes, fasting and liquid protein diets
Bradycardia
Mitral valve prolapse
Acute MI
Treatment for long QT syndrome?
Beta blokade, pacemaker, left cardiac sympathetic denervation
Arrhythmogenic right sided cardiomyopathy ECG and treatment?
ECG: abnormality/inverted t waves in V1-3 and terminal notch in the QRS
Treatment: solatolol, ablation, defibrillator
What is a differential for ST elevation in inferior ECG leads?
Aortic dissection
Adverse complication of beta blockers?
Worsen peripheral vascular disease if this is present
Contraindications for beta blockers?
Uncontrolled heart failure
Asthma
Sick sinus syndrome
Concurrent verapamil use; may precipitate severe bradycardia
Side-effects of beta-blockers?
Bronchospasm Cold peripheries Fatigue Sleep disturbance (nightmares) Erectile dysfunction
Indications for beta blockers?
Angina Post-MI Heart failure Arrhythmias Hypertension Thyrotoxicosis Migraine prophylaxis Anxiety
ECG showing ST wave going down with inverted T wave =
Subendocardial ischaemia
Innermost layer has most resistance due to contraction of the myocardium - this innermost layer is ischaemic so repolarises slower so heart wall depolarises from the outer layer in rather than in-out causing inversion
How does ischaemia cause SOB?
Slower relaxation in diastole so pressure in LA increases as not properly relaxed and blood is entering from lungs so this pressure is backed up to the lungs
What do pathologic Q waves indicate?
Previous MI
Detecting ischaemia?
Look for abnormal signs of repolarisation such as ST segment abnormalities or T wave inversion
Test for left bundle branch block?
Cannot trust ECG, must move on to CTCA as cannot properly assess ST and T wave as depolarisation is already delayed so repolarisation follows in an inverted direction
When do you offer CTCA?
If clinical assessment includes typical or atypical angina
or if assessment indicates non-anginas chest pain but the 12-lead resting ECG has been done and indicates ST-T changes or Q waves
What is CTCA?
Perfusion X-ray imaging that allow you to visualise contrast in the coronary arteries
Anatomical assessment, not a functional assessment
Give stressor e.g. bicycle or vasodilatory/inotropic drug a d image again
Second-line non-invasive functional testing?
MPS with SPECT
(first pass contrast enhanced MRI perfusion or MRI for stress induced wall motion abnormalities
Invasive functional assessment:
> 20% drop in perfusion pressure will be angina causing
If a positive fractional flow reserve is measured from the pressures, this is an indication for re-vascularisation
Anatomical assessment of CAD:
CTCA
Invasive angiography
Functional assessment of CAD:
ECG, exercise ECG Nuclear medicine: SPECT and PET Stress ECHO Stress MRI CT FFR Invasive coronary physiology
What drug is used for functional wall motion testing?
Dobutamine which causes inotropic stimulation
Induces true ischaemia
Which drugs are used to measure perfusion?
Vasodilators: adenosine, regadenoson, dipyridamole
Induction of true ischaemia is exceptional
Side effects of adenosine?
Bronchospasm
AV block I, II and III
Hypotension
Hyperventilation
Side effects of dobutamide?
Sustained or non-sustained VT Paroxysmal AF Transient 2:1 block Severe hypertensive reaction Hypotension Nausea
Mechanism of amiodarone:
Class III anti-arrhythmic, blocks K channels and thus prolongs the AP (also has a class I effect and blocks Na channels) Used in the treatment of atrial, nodal and ventricular tachycardias
S1:
Closure of mitral and tricuspid valves
Soft if long PR or mitral regurgitation
Loud in mitral stenosis
S2:
Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal
S3 (third heart sound):
Caused by diastolic filling of the ventricles
Normal <30 (up to 50 in women maybe)
Heard in dilated cardiomyopathy (aka left ventricular failure), constrictive pericarditis (aka pericardial knock) and mitral regurgitation
S4 (fourth heart sound):
Heard in aortic stenosis, HOCM and hypertension
Caused by atrial contraction against a stiff ventricle
In HOCM a double palpable pulse may be felt as a result of S4
Problems with amiodarone?
Interacts with warfarin, increasing warfarin concentration
May cause statin-induced rhabdomyolysis (raised CK)
Pro-arrhythmic affect of prolonging QT interval
Pulmonary/liver fibrosis, thyroid dysfunction, bradycardia, myopathy, neuropathy
Which coronary artery blockage would present ECG changes in leads V1 to V4? (anteroseptal)
Left anterior descending
Which coronary artery blockage would present ECG changes in leads II, III and aVF? (inferior)
Right coronary
Which coronary artery blockage would present ECG changes in leads V4-6, I and aVL? (anterolateral)
Left anterior descending or left circumflex
Which coronary artery blockage would present ECG changes in leads I, aVL +/- V5-6? (lateral)
Left circumflex
Which coronary artery blockage would present ECG changes in leads V1-2 with tall R waves? (posterior)
Usually left circumflex, also right coronary
S1:
Closure of mitral and tricuspid valves
Soft if prolonged PR or mitral regurgitation
Loud in mitral stenosis
S2:
Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal
S3 (third heart sound):
Caused by diastolic filling of the ventricle
Normal if <30 y/o (women up to 50)
Left ventricular failure e.g. dilated cardiomyopathy
Constrictive pericarditis
Mitral regurgitation
S4 (fourth heart sound):
Atrial contraction against a stiff ventricle
Aortic stenosis, HOCM, hypertension
HOCM may have palpable double apical pulse due to S4
