ECG

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P wave

• Amplitude <2.5mm in limb lead ; <1.5mm in precordial lead

• Width < 0.12s

Abnormality of p wave

• P mitrale/ bifid p wave• P pulmonale/ peak p wave• P inversion• Multifocal atrial rhythm

PR interval

• N 0.12 – 0.2 s

Abnormality • PR prolong = AV block

• Steps in determining type of AV block1. Prolonged PR is fixed = first degree2. see if got p wave not followed by QRS = second degree heart block3. see if got prolonged PR interval = Mobitz type 1(WENCKEBACH)4. see got QRS conduct on its own rate, independent of p wave

• First degree• Second degree• Third degree

Q wave

- Normal left to right interventricular depolarisation- Small septal Q normally seen in left sided leads (1, avL v5 v6)- Not seen in v1 to v3

- Pathological q wave- >1mm (1box) wide, >2mm (2 box) deep, >25% deep of QRS, seen in v1 to 3

- DD- MI****- Cardiomypathies- hcom- Rotation- Lead placement

Loss of abnormal Q wave in v5 v6 normally due to LBBB

QRS

• Normal 0.06-0.10s• >0.12 s suggest bundle branch block

• Look at width (0.06-0.10s)• Look at voltage/height – Low voltage (limb lead <5mm 一个大格 ) ,

(praecordial lead <10mm 两个大格 )– High voltage [(s1 + v5/v6) > 35mm]

• Narrow complex (<0.10s) *supraventricular origin)– SA (present of P wave)– Atrial (abN P- atrial flutter/ atrial fibrillation)– AV (no P or abN p with PR interval <0.12) normal

PR 0.12-0.2

• Broad complex ORS (>0.10 abN, >0.12 bundle branch block)– Bundle branch block– Hyperkalaemia– Tricyclic antidepressant– Hypothermia– Wolf- parkinson white syndrome

• Low voltage QRS [ (limb lead <5mm) (praecordial lead <10mm) ]

• Mechanism– “damping” effect of increased air/ fluid or fat between lead and

heart– Loss of viable myocardium– Infiltration of myxoedematous involvement of the heartCauses– pleural effusion, pericardial effusion, emphysema,

pneumothorax, constricitve pericarditis, obesity– Previous massive MI, end stage dilated cardiomyopathies– hypothyroidism

ST segment

Represents the interval between ventricular depolarisation and repolarisation

ELEVATIONDD - Acute MI (STEMI)- Coronary vasospasm (Printzmetal’s angina)- Pericarditis- Others : benign early repolarisation, LBBB, LVH

STEMI- Septal (v1 v2)- Ant (v3 v4)- Lat (I avL v5 v6)- Inf (II III avF)

**prinzmetal angina – syndrome consist of angina caused by vasospasm (contraction of smooth muscle wall causing narrowing of coronary arteries)

Site of infarct according to lead- Inferior (avF II III)- Anteroseptal (v1 to v4)- Anterolateral (I avL v5 v6, v4)- Posterior (tall R & ST depression in v1 v2)

DEPRESSIONDD- Myocardial ischaemia (NSTEMI)- Reciprocal change in STEMI- Posterior MI- Others : digoxin, hypoK+, supraventricular tachycardia, RBBB, RVH,

LBBB, LVH, ventricular paced rhythm

Morphology- downsloping, upsloping or horizontal- Downsloping and horizontal more or equal to 0.5mm for more than

or equal to 2 consecutive leads indicates Myocardial ischaemia

T wave- Ventricular repolarisation- Normally inverted in lead v1, avR, occasionally v2- Abnormal if inverted in I, II, v4, v5, v6- Abnormalities

- Inverted- Hyperacute- Flatten- Biphasic- Camel hump

Tall T wavetall, narrow, symmetrically peaked T wavehyperkalaemia

- Hyperacute T wave-Broad asymmetrically peak or hyperactive

-seen in the early stages (hours) of STEMI, precede the appearance of ST elevation and Q wave. -Also seen in printzmetal angina.

Irregularly irregular radial pulse

• DD– Atrial fibrillation– Multifocal ventricular ectopics– Atrial flutter with varying block

AV block

• First degree• Second degree• Third degree

• First degree– Prolonged PR

• Second degree – P not followed by QRS– Mobitz I (Wenckebach)– progressively prolonged

PR and

-Mobitz II – PR constant• Third degree- complete heart block– QRS conducted at its own rate and is independent

of p wave

Sinus bradycardia

• Athlete• Myxoedema• hypothermia

Sinus tachycardia

• Exercise• Pain• Fear• Thyrotoxicosis• haemorrhage

Atrial tachyarrythmia

• Including– Atrial fibrillation– Atrial flutter– Atrial ectopic beats

• Smiliarities• Arise from atrial myocardium• Share common etiology

• Etiology***********(a)Cardiac – IHD- ischaemic heart ds (coronary artery & MI)– RHD- rheumatic heart ds– valvular heart ds eg mitral stenosis/ regurg– hypertension

(b)Non cardiac– thyrotoxisosis– pulmonary-disease (pneumonia, COPD) & vascular ds (pulm

embolism)– e- imbalance (hypoK+)– alcohol misused

Mneumonics: I HAVE A FIB- IHD/idiopathic(lone AF), HPT, Valvular heart ds, Embolism(pulmonary), ASD, Failure (CHF), infection (pneumonia)

a) Atrial fibrillation• History taking

– Signs & sx– Etiology (Risk factor)– Complications

• Sign and sx– Palpitation– Dyspnoea– Chest pain

• Complications– Stroke (systemic thromboembolism- blood pools in the atrium as the atrial is

not contracting efficiently, thus cause risk of blood clots in the strium)– Left ventricular failure (esp in fast atrial fib where the atrial cannot filled with

blood properly and pump efficiently to the ventricle, causing raised left atrial pressure and LVF)• exertional dyspnoea/orthopnoea[pillow!!!)/ Paroxysmal nocturnal dyspnoea• peripheraal or central cyanosis dt red C.O.

– Exacerbation of angina

• Mechanisms– Automatic foci that depolarize rapidly– Located predominantly in pulmonary vein– That supply the left atrium. Atrium respond electrically

but the mechanical action is not coordinated– Only portion of the impulse is transmitted to the ventricle

• Clinical classification– Paroxysmal (stop spontaneously within 7 days)– Persistent (require cardioversion to stop)– Permanent

Ix1. ECG

– No p wave– Irreg baseline– Irreg and rapid QRS rhythm, vary btwn __to __bpm

2. (hyperthyroidism) TFT- low TSH, free T4 high3. (Valvular heart ds) Echocardiography- valvular defects, left atrial thrombus, left atrial size4. (Paroxysmal AF) Holter monitoring5. (Pulmonary ds-embolism&infection) CXR6. (hypoK+) BUSE

• Mx– Identify the underlying cause– Treat arrhythmia by

• Cardioversion- electrical or pharmalogical• Digoxin-control ventricular rate if cardioversion fails

– Anticoagulation- prevent thromboembolism, aim INR 2.0-3.0INR– http://www.myvmc.com/investigations/blood-clotting-internation

al-normalised-ratio-inr/

Anticoagulant- CHADS2 (if more than 2 must use anticoagulant, if 1 assess by

CHADS2 VASc)- congestive heart failure, hypertension ,age above 75, diabetes mellitus, stroke/TIA (stroke/TIA scores 2)

- CHADS2 VASc - vascular heart disease, age 65-74, sex: female (previous age above 75 and stroke score 2) (if more than 2 use anticoagulant, if 1 consider anticoag or aspirin)

Atrial flutter

• Regular atrial rhythm with rate of 250-300 bpm

• ECG shows regular saw tooth appearance between QRS complex

Left bundle branch block

• Normally Q wave form due to interventricular depolarization thru septum from left to right, produce Q wave in lateral leads. in LBBB septal depo is reversed from right to left, RV is depo first, to LV via the septum. This cause prolonged QRS (>0.12s) And lost of Q wave

– Direction of depo from R to L cause tall R in lateral leads (I, v5 v6) and deep S in R precordial leads (v1 v2 v3)

– Usually lead to L axis dev

Hypothyroidism • Triads of – Bradycardia (<60bpm)– Low voltage QRS (<5mm for limb lead, <10mm for

praecordium)– Widespread T inversion

• Machanism• Myoedematous infiltration of heart• Reduced thyroxin reduce inotropy(contraction of hear

muscle) and chronotropy(heart rate)• Reduced sympathetic stimulation