1. ECG
Michael Watts

2. Physiology

3. LEAD POSITIONS ANYONE?

4. The trace ECG paper made up of 1mm and 5mm squares
Trace speed =25mm/s so one 5mm =0.20s and one 1mm = 0.04s
P waves = <0.11s and 3mm (0.3mV) high
PR interval = normally 3-5 small squares
QRS = normally <3 small squares

5. Step by step interpretation
Rate (large squares / 100 or 10 second trace x 6)
Rhythm (QRS intervals)
Axis deviation (L is Leaving, R is Returning)
Check P waves
Check PR interval (Heart block) (Delta waves?)
Is there a P wave before every QRS complex?
Is there a QRS wave after every P wave?
Check QRS complex (Broad?)
Any ST changes
What are the T waves like?

6. Axis deviation

8. Sinus Bradycardia
Diagnosis =HR <50bpm with Normal waves & complexes
May be due to high parasympathetic (vasovagal) tone, athletes or sleep. Also caused by opiates, B blockers and many more
Tx = IV atropine (muscarinic receptor antagonist)

10. Sinus Tachycardia
Diagnosis = HR >100bpm with regular rhythm and normal waves & complexes
Increased cardiac output (heart failure, shock, exercise, stress) and many MANY more
Tx = underlying cause. If not then B blocker or verapamil

12. Extrasystoles (ectopic beats)
P wave / QRS complex appears prematurely
Supraventricular ones are common and often insignificant = no treatment
Ventricular look abnormally broad and premature and may be followed by an inverted T wave. Common after acute MI. May cause weak pulse due to poor diastolic filling = no Tx in healthy but may need treating in heart failure etc.

14. Supraventricular Tachycardia
Multifocal (multiple ectopics)
Diagnosis= P waves of varying shape, P wave frequency of bpm, varying PR interval, Irregular rhythm
Fairly uncommon but seen with cor pulmonale, PE, MI and hypoxia. Seen in last stages of life of elderly.
Tx = underlying heart disease

16. Atrial Fibrillation 350-600 atrial bpm
Diagnosis = Fibrillatory line w/ absent P waves, QRS’ irregularly irregular, normal QRS’ but rate 200bpm
No effective systolic contraction = thrombus risk
Reduced diastolic filling = dyspnoea and oedema
Cause assoc. w/ myocardial damage (Ischaemic heart disease, rheumatic mitral valve, HTN, MI, thyrotoxicosis) SHITAP
Tx = acute AF = digoxin or verapamil/B blocker/ DC cardioversion
Chronic AF = digoxin and warfarin (CHA2DS2VASc)

17. Types of AF
Paroxysmal – occurs occasionally then stops. Heart returns to normal rhythm
Persistant – does not stop by itself. Cardioversion necessary for normal rhythm
Permanent – cant be corrected (cardioversion unsuccessful)

19. Atrial Flutter Short circuit within the Atria rate of 250-350bpm
Diagnosis = Flutter waves (saw-tooth), QRS’ regular or irregular, normal size QRS
Assoc. w/ varying degrees of heart failure. Dyspnoea even with slight exercise. Causes similar to AF
Acute flutter can be treated with IV digoxin or IV verapamil. If severe (shock, MI, heart failure) DC cardioversion should be attempted.

21. Ventricular Tachycardia
Diagnosis = Widened QRS of abnormal shape, inverted T waves, QRS > 100bpm, P waves normally not visible
Very serious
Can lead to acute heart failure w/ shock and pulm. Oedema. Most frequently occurs 2-3 days post-MI. Can be due to drug overdose.
Tx as serious incase of VF! In acute VT w/ no haemodynamic change give IV bolus of lignocaine. If haemodynamic upset but concious DC cardioversion. If unconcious = DC defibrillation.

23. Ventricular Fibrillation
Diagnosis = Irregular Rough base line, Wide, abnormal questionable QRS’, frequency bpm
Heart ceases to pump after 10 seconds = cardiac arrest. Death follows within minutes if left untreated.
Caused by coronary artery disease, most commonly first few hours post MI. Can be caused by electrical accident, serious electrolyte imbalance, drowning, choking, hypothermia
Immediate DC shock (CPR until available). IV lignocaine given before next shock

25. First degree Heart Block
Failed impulse conduction from atria to ventricles
Degree depends on severity of damaged myocardium
Diagnosis = PR interval >0.21s w/ normal P wave and QRS. All P waves followed by QRS
Seen in athletes, old people, b blocker treatment, hyperkalaemia, myocarditis

27. Second Degree Heart block – Mobitz type 1 (Wenckebach)
Diagnosis = Normal P waves and QRS complex, gradual increase in PR interval until QRS is dropped
Seen in digoxin overdose and inferior wall infarction

29. Second degree Heart block – Mobitz type 2
Diagnosis = Normal P waves and QRS complexes, constant PR interval, some P waves not followed by QRS
Can occur irregularly or every second, third or fourth beat which is called 2:1, 3:1 or 4:1 heart block
Haemodynamic upset is common. If occurs acutely think MI, if chronic think degeneration of the conductive system. Conversion to complete heart block common.
Tx = IV atropine in acute cases. Pacemakers otherwise required

31. Third degree Heart block
No AV conduction. Nodal escape rhythm gives a rate of 30-40bpm (comes from ventricles) if does not develop it can be fatal
Diagnosis = Normal P waves with regular rhythm, QRS’ with regular rhythm but unrelated to P waves, Slow QRS rate, Wide complexes
Anteroseptal infarctions can cause irreversible damage, can be congenital or in elderly
Tx = IV atropine, permanent pacemaker should be used if persists

33. Myocardial Infarction
Multiple ECG’s are important to see changes!
Minutes – Hours = ST elevation
Hours – Days = pathological Q wave
Days – weeks = T wave inversion

35. Bundle Branch Block
WILLIAM MARROW

36. Antiarrythmic Drugs SOME BADMAN PLAY CHESS Class Example Mechanism
Clinical Use Ia
Disopyramide
Na+ (intermediate dissociation)
VT, VF and Paroxysmal AF Ib
Lidocaine
Na+ (fast dissociation)
VT and VF post MI Ic
Flecanide
Na+ (slow dissociation)
Paroxysmal AF and tachycardias II
Propanolol
Beta Blocker
AF/VF post MI
III
Amiodarone
K+ channel blocker
WPW, SVT and VT (1st line) ?VF IV
Verapamil
CA2+ channel blocker
SVT V
Adenosine
Slows AV node conduction
SOME BADMAN PLAY CHESS

37. Any questions?