Arrhythmias Flashcards
What are the ECG changes in first degree heart block?
Prolonged PR in isolation
ECG changes in 2nd degree Mobitz type 1?
progressively prolonged PR intervals with complete drop of QRS, return to sinus/previous pattern
ECG changes in 2nd degree Mobitz type 2?
three consecutive P waves may be followed by a QRS complex, giving the ECG a normal appearance, then the fourth P wave may suddenly not be followed by a QRS complex since it does not conduct through the AV node to the ventricles.The PR interval may be normal or prolonged, however it is constant in length unlike second-degree AV block Mobitz Type I (Wenckebach) in which the PR interval progressively lengthens until a P wave is not conducted.
Are type 1 and type 2 mobitz reversible?
type 1 is however type 2 is not, therefore pacemaker required
When can QRS complex be increased and decreased in amplitutde?
incr- LVH, can be normal
decr- fluid overload
What are deep Q-waves a sign of?
previous MI damage
How should normal R-wave progression appear across ECG leads? What can poor R wave progression be a sign of?
it should increase throughout the leads. ? MI
When is ST elevation significant?
if >1 in limb leads, >2 in chest leads
What are U-waves pathognomonic of?
hypokalaemia
Which drugs increase QT interval?
Antipsychotics, TCAs, antiarrhythmic drugs
You see ST depression in anterior leads V1-V3. What are you worried about?
posterior STEMI
What is the evidence on ECG of right heart strain?
RBBB, r.axis deviation, T-wave inversion
What are findings of PE in ECG?
tachycardia and S1Q3T3 (only occus in 10% of people)
Example of supraventricular tachycardia?
atrial flutter
What is the AV ratio in atrial flutter and what heart rate does this give rise to?
2:1, 150bpm (3:1, 4:1 can happen as well, therefore 300 bpm or 450 bpm!)
Where does the re-entry circuit arise in atrial flutter?
right atrium
List three causes of hyperkalaemia
- Increased intake- potassium supplements, excess in diet
- Excessive endogenous- rhabdomyolysis, extensive burns, tumour lysis syndrome, trauma, haemolysis
- Redistribution (shift from intra to extracellular) e.g. acidosis, insulin deficiency, drugs
- Diminished potassium excretion e.g. AKI, drugs
Which drugs can result in hyperkalaemia?
ACEi, NSAIDs, K+ sparring -> reduce potassium excretion
Beta blockers and digoxin -> alter transmembrane potassium movement
A patient has an anterior STEMI. Which coronary artery is affected?
LAD
Inferior STEMI, which coronary artery?
R coronary A
Lateral STEMI. Which coronary artery?
L circumflex
List three causes of a prolonged QTc?
TIMME Toxins/drugs Inherited: e.g. Romano-Ward, Jervell (c¯ SNHL) Ischaemia Myocarditis Mitral valve prolapse Electrolytes: ↓Mg, ↓K, ↓Ca, ↓ temp
List two drugs that prolong the QTc interval
- Macrolides
antiarrhythmics: amiodarone - TCAs
- Histamine antagonists
List one causes of shortened PR interval?
accessory conduction e.g. WPW
In which leads are T waves inverted normally? In which leads would T wave inversion be absolutely abnormal
aVR and V1
Abnormal in LI LII V4-V6
List two causes of abnormal T wave inversion
Strain ischaemia ventricular hypertrophy BBB digoxin
When are U waves observed?
Hypokalaemia (following T waves)
When are J waves observed?
SAH
hypercalcaemia
hypothermia
positive deflections occurring at the junction between the QRS complex and the ST segment
What are the features of WPW on EGC?
slurred upstroke of QRS= delta wave, usually in V3/V4
Shortened PR intervals
What are two features on ECG of brugada syndrome
RBBB
ST elevation in V1-V3
Name three features on ECG of hyperkalaemia
Tall tented T waves
Widened QRS
Absent P waves
What are two features of PE on ECG?
SI QIII TIII
- deep S wave in I (RAD)
- pathological Q in III
- T inversion in III
Right vent strain
- RAD (S wave in I)
- Dominant R wave and T
wave inversion in V1-V3
Two features of hypokalaemia?
Small T waves
ST depression
Prolonged QT interval
Prominent U waves
List three causes of bradycardia
DIVISIONS Drugs Ischaemia Vagal hypertonia Infection Sick sinus syndrome Infiltration (autoimmune, sarcoid, amyloid) O- hypOthyroidism, hypOkalaemia Neuro (Incr ICP) Septal defect Surgery or catheterisation
State two drugs that can cause bradycardia
Antiarrhythmics (type 1a, amiodarone)
β-blockers
Ca 2+ -channel blockers (verapamil)
Digoxin
List two infections that cause bradycardias
Viral myocarditis
Rheumatic fever
Infective endocarditis
What is the medical treatment for bradycardia?
atropine 0.6-1.2 mg IV, isoprenaline IV
What is the definitive treatment for bradycardias?
pacemaker insertion
When do you not need to treat a bradycardia?
If asymptomatic and rate <40
Differentials for narrow complex tachycardia? (SVT)
Sinus tachy AF Atrial flutter AVNRT AVRT
If tachyarrhythmia is ID as non AF i.e. regular rhythm, how should management proceed of patient?
Continuous ECG trace
Vagal manoeuvres
Adenosine 6mg IV bolus
Then 12mg, then 12mg
If tachyarrhythmia is AF what is the treatment?
Control rate with beta blocker or digoxin
If onset <48 hr then cardioversion with amiodarone or DC shock
Consider anticoagulation with heparin
What is the mechanism of action of adenosine?
temporary block of AVN
Why do you give adenosine for SVT?
unmasks atrial rhythm, cardioverts AVNRT/AVRT to sinus rhythm
If adenosine doesn’t work in treating SVT, what other options do you have?
Digoxin, atenolol, verapamil, amiodarone
What are the contraindications of adenosine?
asthma, 2/3rd degree heart block
List two differentials for broad complex tachycardias
VT
Torsades de pointes
SVT with BBB
Three causes of VT?
Infarction Myocarditis Valve abnormality Iatrogenic: digoxin, antiarrhytmic drug Cardiomyopathy Electrolyte imbalances: hypokalaemia, low Mg, hypoxia, acidosis
