Transcript ECG - PeerMedics

ECG
Michael Watts
www.peermedics.com
Physiology
LEAD POSITIONS ANYONE?
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
Step by step interpretation
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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?
Axis deviation
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)
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
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.
Supraventricular Tachycardia
 Multifocal (multiple ectopics)
 Diagnosis= P waves of varying shape, P wave frequency
of 120-150bpm, 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
Atrial Fibrillation
 350-600 atrial bpm
 Diagnosis = Fibrillatory line w/ absent P waves, QRS’
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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)
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)
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.
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.
Ventricular Fibrillation
 Diagnosis = Irregular Rough base line, Wide,
abnormal questionable QRS’, frequency 250-600bpm
 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
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
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
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
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
Myocardial Infarction
 Multiple ECG’s are important to see changes!
 Minutes – Hours = ST elevation
 Hours – Days = pathological Q wave
 Days – weeks = T wave inversion
Bundle Branch Block
WILLIAM MARROW
Antiarrythmic Drugs
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
SVT
SOME BADMAN PLAY CHESS
Any questions?