Approaching the ECG: Read Right In A Minute February 3, 2011 BGSMC Cardiology Study Group Nick Sparicino, DO Mohamad Lazkani, MD Tomas Rivera-Bonilla, MD

History of the ECG/EKG During the late 1800’s and early 1900’s, Dutch physiologist Willem Einthoven developed the early electrocardiogram He won the Nobel prize. Hubert Mann first uses the electrocardiogram to describe electrographic changes associated with a heart attack in 1920 Electrocardiograms must be viewed in the context of demographics, health history, and other clinical test correlates. They are especially useful when compared across time to see how electrical activity of the heart has changed (perhaps as the result of some pathology). Why PQRST and not ABCDE? The choice of P is a mathematical convention dating from Descartes by using letters from the second half of the alphabet. N has other meanings in mathematics and O is used for the origin of the Cartesian coordinates. P is simply the next letter. (For more on Descartes see Henson JR. Descartes and the ECG lettering series. J Hist Med Allied Sci. April 1971;181�186)

Electrocardiography A recording of the electrical activity of the heart over time Gold standard for diagnosis of cardiac arrhythmias Helps detect electrolyte disturbances (hyper- & hypokalemia), arrhythmias, myocardial ischemia and infarction, pericarditis, chamber hypertrophy, drug toxicity (i.e. digoxin and drugs which prolong the QT interval) Allows for detection of conduction abnormalities Screening tool for ischemic heart disease during stress tests Helpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia)

Electrocardiogram (ECG/EKG) Is a recording of electrical activity of heart conducted through ions in body to surface Is a representation of the cardiac cycle and sections are electrical impulses/ represent three distinct waves

ECG Rules Wave of depolarization traveling towards a positive electrode causes an upward deflection on the ECG. Wave of depolarization traveling away from a positive electrode causes a downward deflection on the ECG. Rules of ECG Wave of depolarization traveling towards a positive electrode causes an upward deflection on the ECG Wvae of depolarization traveling away from a positive electrode causes a downward deflection on the ECG

Vectors: directions and amplitude Vector 1 – depolarization of atrium(corresponds to P wave) Vector 2 – Ventricular Septum (1st deflection of QRS) Vector 3 – Bulk of ventricular muscle Vector 4 – Repolarization of ventricular muscle

Approach to the ECG Systematic Approach RRIAM: Read Right In A Minute Look at the ECG in a methodical fashion, starting with the rhythm strip at the bottom, keeping in mind that it correlates with the 3 second strips above it. Also note, in a normal EKG, the entire strip is 12 seconds (has 4 total, 3 second strips) RRIAM- Read right in a minute Systematic Approach rhythm, rate, intervals, axis, morphology RRIAM: Read Right In A Minute

RHYTHM Locate the P wave Establish the relationship between P waves and QRS complex If no P wave analyze the QRS morphology Search for other clues Interpret the rhythm in the clinical setting P wave tells you if its sinus or not. Look at each lead as the p waves may not be obvious in some leads. Becareful as p waves may be burried in QRS complex as seen with junctional rhythm or AV nodal reentrant tachycardia. P waves can also be burried in the ST segment as seen with AV reentrant tachycardia or ventricular tachycardia. Are the p waves associated in a 1:1 fasion? If not, are there more or less p waves in QRS complexes, and what are the atrial/ventricular rates? More p waves than QRS then some form of AV block is present. Less p waves than QRS then the rhythm is an accelerated ventricular or junctional rhythm. Analyze QRS morphology ( Narrow <0.12s – impulses above that travels down AV node/Purkinje. if it is wide >0.12s and bizarre, then it is either supraventricular with aberrant conduction or of ventricular origin) Will discuss more on morphology later. Other clues: Regular, Irregular (regularly irregular or irregularly irregular) – Regularly irregular: some form of pattern to the irregular complex (ie: 3rd complex comes sooner than the preceding 2) 2)Irregularly irregular: no pattern Often, clinical history including drugs being taken can help with the diagnosis. In example, a regular wide complex rhythm in an elderly patient first occurring post MI is most likely ventricular tachycardia.

RATE Determining rate: Regular rhythm: Big box: 300, 150, 100, 75, 60, 50 Irregular rhythm: # cycles in a 6 second strip x10 # cycles in a 12 second strip x5 remember to use halves if half a cycle is present in the strip 10mm = 1mV 1mm = 0.1mV ECG paper normally records at a constant speed of 25 mm/sec. Thus each horizontal unit (1-mm box) represents 0.04 sec (25 mm/sec x 0.04 sec = 1 mm)

RATE: Intrinsic rates of pacing cells (transmits the impulses through the inter-atrial septum) SA node 60-100 BPM Atrial cells 55-60 BPM AV node 45-50 BPM His bundle 40-45 BPM Bundle branch 40-45 BPM Purjkinje cells 35-40 BPM Myocardial cells 30-35 BPM

ATRIAL COMPONENTS P wave – atrial depolarization Duration 0.08 to 0.12 sec PR interval - impulse initiation, atrial depol, atrial repol, AV/His/BB/Purkinje stimulation 0.12 to 0.20 seconds (>0.20 seconds = PR prolongation; Heart Block discussed later) Segment (straight line between waves) Interval (wave plus segment) P wave will be discuss in morphology for R vs L sided pathology Tp wave - atrial repolarization Can be seen if no QRS, ie: AV dissociation or nonconducted beats PR segment - transmission through AV node,his bundle branches and purkinje (after p wave, interval is before p wave) Anything > 0.8mm is depressed (pericarditis, atrial infarct)

VENTRICULAR COMPONENTS QRS complex - ventricular depolarization 0.06 to 0.12 seconds Q wave Significance “pathological/MI” >0.03s or >1/3 height of R wave Intrinsicoid deflection - beginning of QRS to top of R wave before negative deflection Represents amount of time impulse travels from purkinje in endocardium to epicardium (increases with thick myocardium, ie LVH or intraventricular conduction delay, ie LBBB) Right precordial leads 0.035 seconds Left precordial leads 0.045 seconds

VENTRICULAR COMPONENTS QT Interval - all the events of ventricular systole Beginning of QRS to end of T wave Duration varies with heart rate, age, sex but should be less than half the RR interval Correction formulas exist to balance HR, a major variable (as HR decreases, QT interval increases) Fridericia Correction (QTf): QTf = QT interval / cubed root of the RR interval (in sec) Bazett’s formula (QTc):  QTc = QT interval / square root of the RR interval (in sec) Increase in HR by 10 = QT -0.02s Ex: HR of 60, QT = QTc Thus QT normally at 0.42s, however if HR at 70, then QTc is 0.40s, HR at 80, then QTc is 0.38s -u waves read by machine This syndrome is associated with an increased risk of a characteristic life-threatening cardiac arrhythmia, known as torsades de pointes (TdP). The primary symptoms in patients with LQTS include palpitations, syncope, seizures, and sudden cardiac death (SCD). -Long QT syndrome can be congenital or acquired. Some common causes include hypokalemia, hypomagnesemia, hypocalcemia, starvation, anorexia, hypothyroidism, antiarrhythmic drugs (quinidine, procainamide, etc) , SSRI, methadone, haldol, etc.

VENTRICULAR COMPONENTS ST segment - electrically neutral period between ventricular depol and repol (time myocardium is maintaining contraction in order to push the blood out of the ventricles) T wave - ventricular repolarization Should be asymmetrical with a slow upstroke and a fast downstroke

AXIS - Quadrant Graphing Method Use the quadrant graphing method. In this method, the hexaxial lead system is divided by leads I and aVF into four equal quadrants. Arrows are drawn on leads I and aVF in the direction of the predominant QRS complex deflection. For example, the QRS complex in lead I is predominantly negative, so an arrow will be drawn toward the negative pole of lead I. Lead aVF is also predominantly negative, so an arrow will be drawn away from its positive pole. This would place the mean electrical axis in the upper right quadrant, indicating a right axis shift. The mean electrical axis can be further estimated by examining the relative size of the QRS complexes in leads I and aVF. The mean electrical axis will be closer to the larger of the two. Since lead aVF is more negative than lead I, the mean electrical axis will be closer to 90 degrees than to 180 degrees. INFARCT LEAD ARTERY Septal wall infarct: V1, V2 [ proximal LAD] Anterior wall infarct: V3, V4 [LAD] Apical wall infarct: V5, V6 [distal LAD, LCx, or RCA] Inferior wall infarct: II, III, avF [RCA, LCx] Lateral wall infarct: I, avL [LCx] RV infarct: V1, V2, V4-R [Proximal RCA] Posterior wall infarct: ST dep V1-V2 [RCA or LCx] I (+) aVF (+) =normal I (+) aVF (-) =LAD I (-) aVF (+) =RAD I (-) aVF (-) =extreme LAD or RAD

AXIS - Isoelectric Method 1 2 Find an isoelectric lead. Identify a lead in which the positive and negative deflections of the QRS complex are equal. The lead that is perpendicular to the isoelectric lead is the lead that will identify the mean electrical axis. If the QRS complex is predominantly positive in the perpendicular lead, then the mean electrical axis is directed toward the positive pole. If the QRS complex is negative, then the mean electrical axis is directed away from the positive pole. LAD: S > R in lead II (beyond -30) RAD: S > R in lead I (beyond +90) Find isoelectric lead Find perpendicular lead If QRS positive, vector towards lead, if negative, away

MORPHOLOGY Hypertrophy (atrial & ventricular) Bundle branch blocks and hemiblocks Segment depressions & elevations PR segment, ST segment U waves T wave morphologies Delta wave Osborne wave ST – T changes

Hypertrophy Criteria Left atrial enlargement Terminal negative P wave deflection in V1 > 0.04s and the amplitude of “same” P wave in V1 > 0.10mV P-mitrale in lead II (notched P wave) Duration b/w peaks of P wave notches >0.04s Max p wave duration >0.11s Ratio of P wave duration to PR duration > 1:1.6 Right atrial enlargement P wave amplitude >2.5 mm in II and/or >1.5 mm in V1 (these criteria are not very specific or sensitive) Better criteria can be derived from the QRS complex; these QRS changes are due to both the high incidence of RVH when RAE is present, and the RV displacement by an enlarged right atrium. QR, Qr, qR, or qRs morphology in lead V1 (in absence of coronary heart disease)   QRS voltage in V1 is <5 mm and V2/V1 voltage ratio is >6 Biatrial enlargement Features of both RAE and LAE in same ECG P wave in lead II >2.5 mm tall and >0.12s in duration  Initial positive component of P wave in V1 >1.5 mm tall and prominent P-terminal force

Hypertrophy Criteria

Hypertrophy Criteria Other LVH Criteria Sokolow-Lyon Criteria S wave in V1 + R in V5 or V6 >= 3.5mV Or R wave in V5 or V6 >2.60mV Cornell Voltage Criteria Female: R in aVL + S in V3 >2.0 mV Male: R in aVL + S in V3 > 2.8 mV Hypertrophic Cardiomyopathy LVH (tall R in V2-V5) Deep narrow Q in aVL and V6 LAE (increased negative terminal p wave in V1) Other Criteria (quick glance) I = R >14mm aVR = S >15 mm aVL = R > 12 mm aVF = R >21 mm V5 = R > 26 mm V6 = R >20 mm

Hypertrophy Criteria Right ventricular hypertrophy RVH Criteria Right ventricular hypertrophy  Any one or more of the following (if QRS duration <0.12 sec):  Right axis deviation (>90 degrees) in presence of disease capable of causing RVH   R in aVR > 5 mm, or   R in aVR > Q in aVR Any one of the following in lead V1:  R/S ratio > 1 and negative T wave   qR pattern   R > 6 mm, or S < 2mm, or rSR' with R' >10 mm Other chest lead criteria:  R in V1 + S in V5 (or V6) 10 mm  R/S ratio in V5 or V6 < 1  R in V5 or V6 < 5 mm  S in V5 or V6 > 7 mm ST segment depression and T wave inversion in right precordial leads is usually seen in severe RVH such as in pulmonary stenosis and pulmonary hypertension.

Hypertrophy Criteria Biventricular Criteria 1. High voltage, biphasic RS complex in midprecordial leads (also common in LV septal defect) 2. LVH criteria in precordial leads with RAD in limb leads 3. Low amplitude S in lead V1 combined with deep S wave in lead V2 4. LVH criteria in left precordial leads combined with prominent R waves in right precordial leads 5. LAE as sole criteria for LVH combined with any criteria suggestive of RVH Left or right strain pattern Criteria ST-T wave changes associated with abnormal repolarisation secondary to increased ventricular tension have classically referred to as "strain" pattern. Left ventricular hypertrophy is often associated with ST depression and deep T wave inversion. These changes occur in the left precordial leads, V5 and V6. In the limb leads the ST-T changes occur opposite the main QRS forces. Therefore, if the axis is vertical, the ST-T changes are seen in II, III and aVF. If the axis is horizontal the ST-T changes are seen in I and aVL. Right ventricular hypertrophy can be associated with ST depression and T wave inversion in the right precordial leads, V1 - V3. Leads II, II and aVF may also show similar ST - T wave changes.

Put it all together Try to come up with a common theme to the differential diagnosis based on the list of abnormalities you’ve created Do not overlook anything Practice, Practice, Practice (look at many ECGs, especially normal ones in the beginning, developing good habits using RRIAM and calculate intervals committing normal values to memory)