ECG

Definition

Transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes

How it works? The ECG works mostly by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle "depolarizes" during each heart beat.

Cardiac conduction system

How to do ECG? Place the patient in a supine or semi-Fowler's position. If the patient cannot tolerate being flat, you can do the ECG in a more upright position. Instruct the patient to place their arms down by their side and to relax their shoulders. Make sure the patient's legs are uncrossed. Remove any electrical devices, such as cell phones, away from the patient as they may interfere with the machine. If you're getting artifact in the limb leads, try having the patient sit on top of their hands. Causes of artifact: patient movement, loose/defective electrodes/apparatus, improper grounding. ECG below show artifacts.

Placement of electrodes Electrodes- usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Ten electrodes are used for a 12-lead ECG.

	The limb electrodes RA - On the right arm, avoiding thick muscle LA - In the same location that RA was placed, but on the left arm this time. RL - On the right leg, lateral calf muscle LL- In the same location that RL was placed, but on the left leg this time.
	The 6 chest electrodes V1 - Fourth intercostal space, right sternal border. V2 - Fourth intercostal space, left sternal border. V3 - Midway between V2 and V4. V4 - Fifth intercostal space, left midclavicular line. V5 - Level with V4, left anterior axillary line. V6 - Level with V4, left mid axillary line.

Leads

Leads- the tracing of the voltage difference between two of the electrodes and is what is actually produced by the ECG recorder.

Limb leads	Limb leads refer to lead I, II and III. Lead I - voltage between LA &; RA Lead II - voltage between LL &; RA Lead III - voltage between LL &; LA These three are the only bipolar leads (have one +ve & one -ve pole) Einthoven's triangle = triangle formed by the limb leads.
Augmented limb leads	aVR, aVL, aVF (also derived from RA, LA, LL, they measure the electric potential at one point with respect to a null point)
Precordial leads	V1, V2, V3, V4, V5 and V6 (Because of their close proximity to the heart, they do not require augmentation)

These leads help to determine heart’s electrical axis. The limb leads and the augmented limb leads form the frontal plane. The precordial leads form the horizontal plane.

Leads	Anatomical representation of the heart
V1, V2, V3, V4	Anterior
I, aVL, V5, V6	left lateral
II, III, aVF	inferior
aVR, V1	Right atrium

ECG Graph paper Standard calibration speed= 25mm/s Amplitude = 0.1mV/mm 12 Lead ECG- short segment of the recording of each of the 12-leads.

Waves and Intervals

ECG Interpretation

We go systematically:

rate, rhythm, cardiac axis, QRS complexes, hypertrophies, bundle branch block, ST segment, QT interval, T wave, other waves.

Rate	Rate= 300/(the number of large square between R-R interval), or Rate= 1500/(number of small square between R-R interval), example below Heart Rate = 300/3 = 1500/15 = 100 bpm If the rhythm is not regular, count the number of electrical beats in a six-second strip and multiply that number by 10.(Note the ECG strip has 3 second marks) Example below: Heart rate = 8 x 10 = 80 bpm Or count the number of beats on any one row over the ten-second strip (the whole lenght) and multiply by 6. Example:   Findings: Interpretation bpm Causes Normal 60-99 - Bradycardia <60 hypothermia, increased vagal tone (due to vagal stimulation or e.g. drugs), atheletes (fit people) hypothyroidism, beta blockade, marked intracranial hypertension, obstructive jaundice, and even in uraemia, structural SA node disease, or ischaemia. Tachycardia >100 Any cause of adrenergic stimulation (including pain); thyrotoxicosis; hypovolaemia; vagolytic drugs (e.g. atropine) anaemia, pregnancy; vasodilator drugs, including many hypotensive agents; FEVER, myocarditis
Rhythm	Look at p waves and their relationship to QRS complexes. Lead II is commonly used Regular or irregular? If in doubt, use a paper strip to map out consecutive beats and see whether the rate is the same further along the ECG. Measure ventricular rhythm by measuring the R-R interval and atrial rhythm by measuring P-P interval. * rhythms can come from SA node (sinus), AV or internodal node (atrial) or ventricular Rhythm findings: Interpretation Findings Normal sinus rhythm (NSR) ECG rhythm characterized by a usual rate of anywhere between 60-99 bpm, every P wave must be followed by a QRS and every QRS is preceded by P wave The P wave is upright in leads I and II   Sinus bradycardia rate < 60bpm, otherwise, as normal as sinus rhythm   Sinus tachycardia rate >100bpm, otherwise, as normal as sinus rhythm.   Sinus pause or arrest In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing function. If failure is brief and recovery is prompt, the result is only a missed beat (sinus pause). If recovery is delayed and no other focus assumes pacing function, cardiac arrest follows.   Escape rhythm An escape beat is a heart beat arising from an ectopic focus in failed sinus node or heart block. The ectopic impulse appears only after the next anticipated sinus beat fails to materialize- usually a single escape beat. If prolong failure/block: rhythm of escape beats is produced to assume full pacing function. (cardiac protection mechanism). Examples Atrial escape: a cardiac dysrhythmia occurring when sustained suppression of sinus impulse formation causes other atrial foci to act as cardiac pacemakers. Rate= 60-80bpm, p wave of atrial escape has abnormal axis and different from the p wave in the sinus beat. However QRS complexes look exactly the same. Junctional escape: depolarization initiated in the atrioventricular junction when one or more impulses from the sinus node are ineffective or nonexistent. Rate: 40-60 bpm, Rhythm: Irregular in single junctional escape complex; regular in junctional escape rhythm, P waves: Depends on the site of the ectopic focus. They will be inverted, and may appear before or after the QRS complex, or they may be absent, hidden by the QRS. QRS is usually normal Ventricular escape: the depolarization wave spreads slowly via abnormal pathway in the ventricular myocardium and not via the His bundle and bundle branches. Premature beats A premature beat also arises from an ectopic pacemaker: The non-sinus impulse is early, initiating a heart beat before the next anticipated sinus beat, competing with the sinus node. Examples Atrial premature beat  (APB): arises from an irritable focus in one of the atria. APB produces different looking P wave, because depolarization vector is abnormal. QRS complex has normal duration and same morphology . Junctional Premature Beat: rises from an irritable focus at the AV junction. The P wave associated with atrial depolarization in this instance is usually buried inside the QRS complex and not visible. If p is visible, it is -ve in lead II and +ve in lead aVR and it it may occur before or after QRS. Premature Ventricular Complexes (PVCs) is a relatively common event where the heartbeat is initiated by the heart ventricles(arrow) rather than by the sinoatrial node,Rate depends on underlying rhythm and number of PVCs. Occasionally irregular rhythm, no p-wave associated with PVCs. May produce bizarre looking T wave. Atrial Fibrillation (A-fib) A-fib is the most common cardiac arrhythmia involving atria. Rate= ~150bpm, irregularly irregular, baseline irregularity, no visible p waves, QRS occur irregularly with its length usually < 0.12s Atrial Flutter Rate=~300bpm, similar to A-fib, but have flutter waves, ECG baseline adapts ‘saw-toothed’ appearance’. Occurs with atrioventricular block (fixed degree), eg: 3 flutters to 1 QRS complex: Supraventricular Tachycardia (SVT) SVT is any tachycardic rhythm originating above the ventricular tissue.Atrial and ventricular rate= 150-250bpm Regular rhythm, p is usually not discernable. Types: Sinoatrial node reentrant tachycardia (SANRT) Ectopic (unifocal) atrial tachycardia (EAT) Multifocal atrial tachycardia (MAT) A-fib or A flutter with rapid ventricular response. Without rapid ventricular response both usually not classified as SVT AV nodal reentrant tachycardia (AVNRT) Permanent (or persistent) junctional reciprocating tachycardia (PJRT) AV reentrant tachycardia (AVRT) Ventricular tachycardia (V-tach or VT) fast heart rhythm, that originates in one of the ventricles- potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death. Rate=100-250bpm, Torsades de Pointes literally meaning twisting of points, is a distinctive form of polymorphic ventricular tachycardia characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. Rate cannot be determined. Ventricular fibrillation (V-fib or VF) A severely abnormal heart rhythm (arrhythmia) that can be life-threatening. Emergency- requires Basic Life Support Rate cannot be discerned, rhythm unorganized Asystole a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow. Rate, rhythm, p and QRS are absent Pulseless Electrical Activity (PEA) Not an actual rhythm. The absence of a palpable pulse and myocardial muscle activity with the presence of organized muscle activity (excluding VT and VF) on cardiac monitor. Pt is clinically dead. Artificial Pacemaker Rate depends on pacemaker, p wave maybe absent or present  Ventricular paced rhythm shows wide ventricular pacemaker spikes Heart/AV blocks findings: First degree AV block P wave precedes QRS complex but P-R intervals prolong (>5 small squares) and remain constain from beat to beat. Second degree heart block 1. Mobitz Type I or Wenckenbach Runs in cycle, first P-R interval is often normal. WIth successive beat, P-R interval lengthens until there will be a P wave with no following QRS complex. 2. Mobitz Type 2 P-R interval is constant, duration is normal/prolonged. Periodacally, no conduction between atria and ventricles- producing a p wave with no associated QRS complex. (blocked p wave). Third degree AV block (complete heart block) No relationship between P waves and QRS complexes An accessory pacemaker in the lower chambers will typically activate the ventricles- escape rhythm. Atrial rate= 60-100bpm. Ventricular rate based on site of escape pacemaker. Atrial and ventricular rhythm both are regular.
Cardiac/ QRS axis	Electrical impulse that travels towards the electrode produces an upright (positive) deflection (of the QRS complex) relative to the isoelectric baseline. One that travels away produces negative deflection. And one that travels at a right angle to the lead, produces a biphasic wave. To determine cardiac axis look at QRS complexes of lead I, II, III. Axis Lead I Lead II Lead III Normal Positive Positive Positive/Negative Right axis deviation Negative Positive Positive Left axis deviation Positif Negative Negative Remember, positive(upgoing) QRS complex means the impulse travels towards the lead. Negative means moving away. Cardiac Axis Causes Left axis deviation Normal variation in pregnancy, obesity; Ascites, abdominal distention, tumour; left anterior hemiblock, left ventricular hypertrophy, Q Wolff-Parkinson-White syndrome, Inferior MI Right axis deviation normal finding in children and tall thin adults, chronic lung disease(COPD), left posterior hemiblock, Wolff-Parkinson-White syndrome, anterolateral MI. North West emphysema, hyperkalaemia. lead transposition, artificial cardiac pacing, ventricular tachycardia
QRS complexes	Non-pathological Q waves are often present in leads I, III, aVL, V5 and V6 R(V6) < R(V5) The depth of the S wave usually > 30mm Pathological Q wave > 2mm deep and >1mm wide or 25% amplitude of subsequent R wave
P wave / Atrial hypertrophy	Look at lead II and V1 Normal 3 small square wide, and 2.5 small square high. Always positive in lead I and II in NSR Always negative in lead aVR in NSR Commonly biphasic in lead V1 P pulmonale Tall peaked P wave. Generally due to enlarged right atrium- commonly associated with congenital heart disease, tricuspid valve disease, pulmonary hypertension and diffuse lung disease. Biphasic P wave Its terminal negative deflection more than 40 ms wide and more than 1 mm deep is an ECG sign of left atrial enlargment. P mitrale Wide P wave, often bifid, may be due to mitral stenosis or left atrial enlargement.
Ventricular Hypertrophy	Left ventricular hypertrophy (LVH) Sokolow &; Lyon Criteria: S (V1) + R(V5 or V6) > 35mm Cornell Criteria: S (V3) + R (aVL) > 28 mm (men) or > 20 mm (women) Others: R (aVL) > 13mm Example: Refer to the following ECG strip S (V1) + R(V5) = 15 + 25 = 40mm R(aVL) =14 cm S(V3) + R (aVL)= 15 + 14 =29mm Right Ventricular Hypertrophy Right axis deviation (QRS axis >100o) V1(R>S), V6 (S>R) Right ventricular strain T wave inversion
Bundle Branch Block	Look at QRS complexs in V1 and V6 Left Bundle Branch Block (LBBB) indirect activation causes left ventricle contracts later than the right ventricle. Right bundle branch block (RBBB) indirect activation causes right ventricle contracts later than the left ventricle QS or rS complex in V1 - W-shaped RsR' wave in V6- M-shaped Terminal R wave  (rSR’) in V1 - M-shaped Slurred S wave in V6 - W-shaped Mnemonic: WILLIAM Mnemonic: MARROW
ST segment	Normal ST segment flat (isoelectric) ± Same level with subsequent PR segment ‡Elevation or depression of ST segment by 1 mm or more, measured at J point is abnormal. J point is the point between QRS and ST segmen Diagnosing MI Criteria: ST elevation in > 2 chest leads > 2mm elevation ST elevation in  > 2 limb leads > 1mm elevation Q wave > 0.04s (1 small square) Be careful of LBBB The diagnosis of acute myocardial infarction should be made circumspectively in the presence of pre-existing LBBB. On the other hand, the appearance of new LBBB should be regarded as sign of acute MI until proven otherwise. Localizing MI Look at ST changes, Q wave in all leads. Grouping the leads into anatomical location, we have this: Ischaemic change can be attributed to different coronary arteries supplying the area. Location of MI Lead with ST changes Affected coronary artery Anterior V1, V2, V3, V4 LAD Septum V1, V2 LAD left lateral I, aVL, V5, V6 Left circumflex inferior II, III, aVF RCA Right atrium aVR, V1 RCA *Posterior Posterior chest leads RCA *Right ventricle Right sided leads RCA *To help identify MI, right sided and posterior leads can be applied Posterior leads: V7: posterior axillary line, lead V8: midscapular, V9: paraspinal Right sided leads (V4R-V6R) There are 2 types of MI: STEMI &; NSTEMI. Described below: STEMI ECG changes in ST-elevation MI(STEMI) / transmural MI: Pronounced T Wave initially Generally visible in total occlusion (STEMI) Not visible in Non-STEMI ST elevation (convex type) Depressed R Wave, and Pronounced T Wave. Pathological Q waves may appear within hours or may take greater than 24 hr.- indicating full-thickness MI. Q wave is pathological if it is wider than 40 ms or deeper than a third of the height of the entire QRS complex Exaggeration of T Wave continues for 24h. T Wave inverts as the ST elevation begins to resolve. Persistent ST elevation is rare except in the presence of a ventricular aneurysym. ECG returns to normal T wave, but retains pronounced  Q wave. NSTEMI ECG changes in Non ST-elevation MI / subendocardial MI: ST Depression (A) T wave inversion with or without ST depression (B) Q wave and ST elevation will never happen *A ST depression is more suggestive of myocardial ischaemia than infarction Myocardial ischaemia 1mm ST-segment depression Symmetrical, tall T wave Long QT- interval Pericarditis ST elevation with concave shape, mostly seen in all leads Digoxin Down sloping ST segment depression also known as the "reverse tick" or "reverse check" sign in supratherapeutic digoxin level.
Q-T interval	Normal QT QT interval decreases when heart rate increases. A general guide to the upper limit of QT interval. For HR = 70 bpm, QT<0.40 sec. For every 10 bpm increase above 70 subtract 0.02s. For every 10 bpm decrease below 70 add 0.02 s As a general guide the QT interval should be 0.35- 0.45 s,(&lt;2 large square) and should not be more than half of the interval between adjacent R waves (R-R interval) To calculate the heartrate-corrected QT interval QTc. Bazett's formula is used: If abnormally prolonged or shortened, there is a risk of developing ventricular arrhythmias.
T wave	Normal T wave assymmetrical, the first half having more gradual slope than the second half >1/8 and < 2/3 of the amplitude of corresponding R wave Amplitude rarely exceeds 10mm Abnormal T waves are symmetrical, tall, peaked, biphasic, or inverted.

Others ECG signs

Hyperkalemia	Narrow and tall peaked T wave (A) is an early sign PR interval becomes longer P wave loses its amplitude and may disappear QRS complex widens (B) When hyperkalemia is very severe, the widened QRS complexes merge with their corresponding T waves and the resultant ECG looks like a series of sine waves (C). If untreated, the heart arrests in asystole
Hypokalemia	T wave becomes flattened together with appearance of a prominent U wave. The ST segment may become depressed and the T wave inverted. these additional changes are not related to the degree of hypokalemia.
Hypercalcemia/ hypocalcemia	Usually, signs are not obvious Hypercalcemia is associated with short QT interval (A) and hypocalcemia with long QT interval (B). Interval shortening or lengthening is mainly in the ST segment.
Pulmonary embolism	SIQIIITIII = deep S wave in lead I, pathological Q wave in lead III, and inverted T wave in lead III. The ECG is often abnormal in PE, but findings are not sensitive, not specific Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG. Only tachycardia and incomplete RBBB differentiated PE from no PE.