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12- Lead Process for Interpreting a 12-lead • • • • • Look at your patient Determine rhythm: NSR, Afib, etc. Determine wall specific ST, T wave changes Identify R wave progression as normal or not Determine axis of “depolarization”: normal vs right axis deviation vs left axis deviations. • Look for bundle branch blocks – RT vs LT – Fascicular • Look for hypertrophies – Atrial – Ventricular • Other stuff – pericarditis – Etc. Cardiac Anatomy Superior vena cava Pulmonary veins Sinoatrial (SA)A node Atrial muscle Atrioventricular (AV) node Left atrium Mitral valve Internodal conducting tissue Tricuspid valve Ventricluar muscle Inferior vena cava Purkinje fibers Descending aorta The Normal EKG 0.12-0.2 s approx. 0.44 s approx. 0.44 s 0.12-0.2 s QT PR SA node Atria AV node R Atrial muscle depolarization T P Q Purkinje Ventricle S Ventricular muscle depolarization Ventricular muscle repolarization Limitations • Sometimes 1 lead can provide clear, accurate interpretation • Sometimes, more than one lead is needed for accurate interpretation • In the case of an MI, multiple leads are definitely needed • Sometimes, 12-leads do not provide adequate information for definitive diagnosis 12-Lead vs. Strip • More leads to look at several parts of the heart • Format: 3 row by 4 column = 12 views • 12-lead provides only a 2.5 second view of each lead – Adequate to identify ischemia, injury or infarction pattern – Catches at least one representative complex – Cannot be used to successful assess rate and rhythm • So a continuous strip is added at the bottom of the print out Time & Voltage • Duration • Amplitude • Configuration Time: Horizontal • Time is usually expressed in SECONDS for typical rhythm interpretation. • IE: Narrow QRS complex < 0.12 sec • However, the 12-lead expresses time in milliseconds • The smaller the unit of measurement, the more accurate the measurement • Remember your metric system conversions .12 sec = 120 ms, moving the decimal 3 spaces Voltage: Vertical • Same measurement expression as used for typical interpretation • 1 small box = 1 millimeter (mm) • 1 large box = 5 mm Voltage: Vertical • Standard calibration: – 1 millivolt (mV) = 10 mm deflection = 10 small boxes = 2 large boxes • If calibration is increased or decreased, so is the deflected wave Lead Placement Lead placement (usually) • White RA-right arm • BlackLA-left arm • Green RL-right leg • RedLL-left leg • BrownC-chest Bipolar Limb Leads • Lead 1 Left Arm View • Lead 2 Left Leg View • Lead 3 Right Leg View Unipolar Limb Leads • aVR Right Shoulder • aVL Left Shoulder • aVF Foot View Frontal Planar View Lead Placement: Chest leads (brown) • • • • • • V1 - 4th Ics, Rsb V2 - 4th Ics, Lsb V3 - Between V2-4 V4 - 5th Ics, MCL V5 - Between V4-6 V6 - 5th Ics, MAL Lead Placement Horizontal View View Obtained From Each Lead is Determined by: 1. Left ventricular dominance • Indirect measurement • Measures net of positive and negative currents • So it is a measurement of the “tug of war” between the right and left ventricle • Which one will win? View Obtained From Each Lead is Determined by: Left ventricular dominance continued: • The QRS complex is a result of the LV electrical activity that is left over after canceling out all of the electrical activity of the RV • Only about 20% of LV electrical activity is measured View Obtained From Each Lead is Determined by: 2. Position of the positive electrode • Position determines which portion of the LV is viewed. • Certain leads view the same portion but at a different angles or from a different perspective because each lead has a different position for its negative electrode Vectors • Each electrode reads AVERAGE current • Each electrode reads Unique perspective • Summation Vector = sum of all vectors • Magnitude of Vector = Relative Mass Hexaxial Reference • • • • • • Lead I = 0 Lead II = +60 Lead III = + 120 aVR = -150 aVL = -30 aVF = + 90 Memorize Lead View I, aVL, V5, V6 Lateral II, III, aVF Inferior V1, V2 Septal V3, V4 Anterior QRS COMPLEX • Represents time required for depolarization of the ventricles • Measured from the beginning of the QRS complex to the point where the last wave of the complex begins to flatten • J-point: the junction between the QRS complex and the ST segment QRS COMPLEX • Normal: – Predominately positive in lead II – .10-.12 seconds or less in duration (note error in book, it says 10 seconds) – How many milliseconds is this? – 2-15 mm in amplitude depending on the lead – Composed of 3 deflections which may or may not always be present • Q wave: negative • R wave: positive • S wave: negative QRS COMPLEX • The width is reflective of the amount time required for an electrical impulse to travel through the ventricles and depolarize the myocardium • If the impulse in not able to follow the natural path of conduction, it is diverted, and thus takes longer to produce depolarization. – QRS > 0.10 to 0.12 sec – How many milliseconds is this? QRS COMPLEX • Variations of the QRS complex: – – – – Q and R wave with no S wave R wave with no Q nor S wave QS complex: entire complex is negative More than one R or S wave: the second R or S is term R prime (R’) and S prime (S’) • To be labeled separately, the wave must cross the baseline. If it does not, it is called a notch Components of the QRS Complex QRS COMPLEX • Capital letters indicate a wave 5 mm in amplitude or more • Lower case letters indicate a wave less than 5 mm in amplitude Sequence of Depolarization • 1-atria depolarize • 2-septum depolarizes • 3-Summation vector Ventricular Depolarizaton • 4-Summation vector Ventricular Repolarization Depolarization Waveforms • Wave of Depolarization TOWARD electrode ---------Positive Deflection-------- Depolarization Waveforms • Wave of depolarization ACROSS the electrode ----------Biphasic or Isoelectric----------- Depolarization Waveforms • Wave of depolarization AWAY from electrode ---------NEGATIVE deflection---------- R Wave Progression • The morphology of the QRS complex changes when progressing from V1 view to V6 view • Initially, it is mostly negative with a very small positive r wave (rS complex) • It begins to progress more positively at the transition zone (V3-V4) Poor R wave progression ST SEGMENT • Represents the end of ventricular depolarization and the beginning of its repolarization • Begins with the end of the QRS complex and ends with the onset of the T wave • Remember that the J-point represents the end of the QRS complex J point ST segment Elevation: ST segment deviation is measured 0.04 seconds after the J-point from the baseline ST SEGMENT • Normal: – Isoelectric • Abnormal: – Elevation or depression by 1 mm in amplitude above or below the isoelectric line (measured 2 small boxes or 0.08 sec after the J-point) • Elevation: MI, vasospasm (Prinzmetal’s angina), percarditis, ventricular aneurysm, or normal in some young males due to early ventricular repolarization • Depression: Ischemia, ventricular hypertrophy, LBBB or RBBB, hypokalemia, and certain drugs (digoxin) Process of Infarction Process of Infarction • A process that results in myocardial tissue death • It is important to understand this process as a continuum. • Early recognition of this process may decrease morbidity • “Myocardially infarcting” Process of Infarction • Infarction occurs when sufficient blood flow to a portion of the myocardium is lacking. – Coronary artery occlusion by clot – Severe vasospasm – Extreme narrowing or occlusion of artery due to atherosclerosis Process of Infarction • Most common cause is blood clot formation that occludes coronary blood flow • Myocardial cells will immediately experience ischemia injury • If clot does not dissolve, persistent ischemia will lead to infarction. Process of Infarction • Ischemia – Temporary oxygen deficiency at cellular level – Usually due to an increase in oxygen demand of myocardial tissue supplied by a narrowed artery – The narrow artery inhibits adequate blood flow to support metabolic needs – Demand is higher than supply – Pain usually subsides when O2 demand is at the level of supply provided by the narrowed artery Nonhomogeneous Epicardial Strain Measurements of Anterior LV During Acute Myocardial Ischemia Process of Infarction • Injury – Supply is less than demand but not necessarily due to increased O2 demands – Usually a result of diminishing blood flow – Myocardial cells are still alive but will die if hypoxia persists – Injury may be significant enough to produce pumping dysfunction and electrical instability Process of Infarction • Infarction: – IschemiaInjuryInfarction – If occlusion is not resolved all cells that are injured will infarct – Irreversible ECG Changes • Learn the clues that indicate – – – – – – Ischemia Injury Infarction Location Extent Duration ECG Changes • Infarction recognition – Determined by change in shape of which wave forms? • QRS, ST, T wave – Each change occurs in relation to certain events during the infarction – Changes often occur in a predictable pattern • Seen in the leads looking at the infarcting site ECG Changes • 1st change: – Usually the development of a Tall T wave – T wave may also become more symmetric • Remember the normal shape of the T wave – T wave may become pointed – Hyperacute phase of the infarction: 1st few minutes Case 1 • A 54-year-old African American female who works out regularly, with no history of hypertension, diabetes mellitus, high cholesterol, smoking or significant family history of CAD presented with one episode of chest pain. • The discomfort was of post-prandial onset and felt like tightness and was of intermittent nature. • She did not have any accompanying nausea or diaphoresis. • Patient states that it felt like upper GI discomfort but she was pain free on arrival to the emergency department. • Her heart rate was 71/min and blood pressure on arrival was 131/70mmHg. She was breathing at the rate of 18/min and appeared in no distress. • Physical examination revealed a normal JVP, normal S1 and S2 and no S3 or S4. • Lungs were clear to auscultation. • Her electrocardiogram showed sinus rhythm, possible left atrial abnormality and tall T wave in lead V2. ECG Changes • 2nd change: – Signs of myocardial injury – ST segment elevation is the primary predictor – May occur within the first hour or first few hours – Acute phase of infarction – May also see inversion of T wave Case 1 • Her admission cardiac markers were slightly elevated: CPK 159U/L, CK MB 2 ng/ml, and Troponin I 0.3ng/ml. • Patient experienced repeat episodes of post prandial chest discomfort over the next 24hrs with some evidence of ST-T changes in the precordial leads while CPK continued to trend down. ST Segment Elevation • Important to remember: – ST segment elevation is a result of changes that affect ventricular repolarization or depolarization – ST segment elevation is not caused by ONLY myocardial infarction – Therefore diagnosing ST elevation as an AMI all of the time would lead to misdiagnosis ST Elevation • Common causes: – – – – – – – – – Increased ICP Electrolyte imbalance Meds Hypothermia LBBB Ventricular rhythms LVH Pericarditis Early repolarizations ECG Changes • 3rd change: – Evidence of tissue death – Pathologic Q wave • More than 40 ms wide • Or new Q wave – Usually seen within the first few hours to first several hours – Still in acute phase Case 1 • Exercise stress test with myocardial perfusion imaging revealed a partially reversible defect of the anteroseptal/anteroapical wall. • She underwent cardiac catheterization, 48hrs after admission. • Cardiac catheterization revealed an 80-90% long stenosis of the proximal LAD. Case 1 • The lesion was wired without difficulty and predilated with a 2.5x25mm PTCA balloon and then a 3mmX30mm OTW stent was deployed. • Post stent deployment angiographic image is shown. ECG Changes • Lastly – T wave regains its normal contour – ST segment returns to baseline (isoelectric line) – If Q wave developed, it will remain as evidence that an infarction occurred – Once baseline is achieved, time of infarct cannot be determined. ECG Changes • Indicative changes: – ST elevation – Provides the strongest evidence for early recognition of “myocardially infarcting” process • Complimentary changes: – T wave inversion • Not specific to MI • May occur with ischemia alone • Definitive changes – Pathologic Q wave formation – May not occur for a few hours ECG Changes • Indicative changes only occur in leads looking at the wall of the heart that is experiencing the ischemiainjuryinfarction • Contiguous leads: – Leads looking at the same wall of the heart – If ST elevation occurs in at least two contiguous leads, suspect MI ECG Changes • When ST segment elevation is observed in two or more leads that are NOT contiguous, MI is NOT suspected • Infarct recognition = Infarct localization • It is necessary to memorize which leads look at which portion of the myocardium Artery Recognition • Once you have localized the infarction, you can identify the artery that is occluded. • This helps to prepare for future clinical situations – Right coronary artery occlusion calls for different treatment than left coronary occlusion Artery Recognition A heart model illustrating the coronary artery tree. • The RT and LT coronary arteries branch off of the proximal aorta – They have different origins – From the origin, the branching distribution differs significantly from right to left. A three-dimensional coronary artery image obtained using MRI. LAD: left anterior descending coronary artery LCX: left circumflex coronary artery RCA: right coronary artery RV: right ventricle Artery Recognition • After leaving the aorta, the LCA quickly divides into two main branches that continue to branch into a network of vasculature – LAD – Circumflex • Supplies the septal, anterior, lateral, and posterior walls Angiogram of the left coronary artery in the anterior-posterior projection. There is a large filling defect consistent with thrombus (large arrow) involving the left main coronary artery, proximal left anterior descending artery, and proximal left circumflex artery. The distal left anterior descending artery is occluded by thrombus (small arrow). Artery Recognition • RCA – Proximal branches supply the RV – Extends to inferior and posterior wall of LV Artery Recognition • It is most important to determine whether the occlusion is in the right or the left. • Differentiating between LAD and circumflex is not feasible because of the large variation of their distribution among individuals • Differentiating between RT and LT produces two very different clinical categories • Unless you see changes in II, III, and AVF, assume LCA occlusion Extent of Infarction • How many leads are showing indicative changes? – The more leads the larger the infarction – The myocardially infarcting process is occurring at a greater extent Extent of Infarction • • • • • Four LCA locations: Aportion of anterior wall: V3 and V4 Bseptum: V1 and V2 Ccircumflex lateral: I, AVL, V5 V6 Dproximal, large portion of LV: most or all of the left leads will be affected – I, AVL, V1-V6 Extent of Infarction • Three RCA locations: Remember that the ECG does not show a significant amount of the tissue supplied by the RCA • Adistal, inferior: II, III, AVF • Blarger amount of tissue, larger infarction: no leads look at the posterior wall, so you will only see indicative changes in II, III, AVF • Cproximal, produces infarction in both ventricles with changes usually only seen in II, III, and AVF RV Infarction • RVIs complicate inferior wall infarctions – 40-45% of inferior wall infarctions involve RVI • Indicates biventricular involvementhuge infarction • Getting a right-sided ECG allows one to “see” the RV • RV involvement will be seen in V4R, V5R, & V6R Acute inferior (diaphragmatic ) MI with coexisting right ventricular infarction. Note STsegment elevation in leads V4R (and V1). The ECG was taken 4 h after the onset of chest pain. RV Infarction • V4R is most specific and sensitive – So if no time to do all right-sided leads, just switch V4 to its equivalent place on the right • Whenever there are ST changes in II, II, and AVF, obtain V4R • Clinical signs of RVI: understand cardiopulmonary blood flow – Hypotensiondecrease in blood volume going into the lungs and LV – Jugular venous distension (JVD)blood backing up from RV – Absence of pulmonary edema (crackles)decreased pumping function of RV Posterior Wall Infarctions • The standard 12-lead does not look at the Posterior wall • What gives suspicion of posterior MI? • We must look at leads looking opposite to the site of interest to identify reciprocal changes • V1, V2, & V3 look at the posterior wall backwards showing the following in the presence of posterior myocardially infarcting process – ST depression – Large (tall) R wave Causes of ST Depression • Reciprocal changes • Digitalis effect • Ischemia – Stress, indicating ischemic heart dz – Zone of ischemia surrounding injured and infarcting tissue – Distant ischemia due to increase WL on tissue taking up the slack for injured/infarcting tissue Exceptions • • • • • • • • Indicative changes may occur in a different order Q waves may never occur Q waves may disappear after the infarct Persistent ST elevation after infarction ECG may appear normal Variance in vascular anatomy Patient positioning Apical infarcts and inferolateral infarcts are difficult to localize What do you think? What do you think? What do you think? What do you think? What do you think? What do you think? What do you think? Intraventricular blocks Significance of BBB • New onset may be very indicative of an acute MI • If it occurs with an MI, mortality rate significantly increases • There is also an increased probability of cardiogenic shock • Why? Significance of BBB • A new BBB is indicative of an extensive MI resulting in a large amount of functional tissue loss – May result in severe hypotension • Unless an ECG is available for comparison, always assume that a BBB is new • Septal and anteroseptal infarctions are most likely to cause BBB Significance of BBB • New BBB also clues in to the possibility of risk for AV block – BBB is an infranodal block that can progress to a complete blockreduced cardiac ratecompromised cardiac output – Standby pacing is indicated when BBB complicates an AMI Review of Conduction System • • • • • • Sinus Node AV Node Bundle of His Right Bundle Branch Left Bundle Branch Left Common Branch Main Stem – Left Anterior fascicle – Left Posterior Fascicle • Purkinje Fibers Primary & Alternate Blood Supply Conduction System Primary Blood Supply Alternate Blood Supply AV Node AV Nodal Artery None Bundle of His Proximal Distal Right Bundle Branch Proximal Distal Left Bundle Branch Main Stem Left Anterior Fascicle Left Posterior Fascicle AV Nodal Artery LAD None AV Nodal Artery LAD LAD AV Nodal Artery None LAD LAD LAD & PDA AV Nodal Artery None None Cause of BB Blocks • Ischemic Heart Disease • Idiopathic Degeneration of the conduction system • Cardiomyopathy • Severe Left Ventricular Hypertrophy • AMI – specific for involvement of each component of the conduction system Miscellaneous Causes • • • • • • • Acute HF, Pulmonary Embolism Aortic valve disease cardiac tumors syphilitic, rheumatic and congenital heart disease Potassium Overdose Trauma including: – cardiac catheterization – Angiograpghy – Surgery Treatment • Specific treatment is usually not indicated for a BBB if it is present alone and not the result of an acute myocardial infarction • TCP may be indicated if: – new RBBB or LBBB or alternating block occurs as the result of an AMI – BBB is complicated by a Fascicular Block in the setting of am AMI – BBB progresses to a Complete Heart Block Identification of BBB • Forget about the notch! – Unreliable • Wide QRS (>120 ms) complex with atrial activity is reliable with a couple exceptions – This is because it is a supraventricular rhythm that is conducted aberrantly • Always measure the width don’t guess Identification of BBB • When measuring for BBB, select the widest QRS complex with a discernible beginning and end • Criteria for BBB can be found in any lead – QRS>120 ms – P wave must be present • When differentiating between RBBB and LBBB, lead criteria is important • Lead V1 is best for differentiation RBBB • Impulse travels through the AV node to the LBB but not the RBB • LBB impulses depolarize the septum in a RT-toLT fashiontoward V1producing initial small R wave • When the LV is completely depolarized it moves away from V1 downward deflection • The RV is finally depolarizes toward V1 2nd R wave of greater amplitude • RSR’ in V1, in the presence of QRS>120 ms preceded by a p wave indicates a RBBB Characteristics of RBBB • QRS - .12 seconds or greater • QRS axis - Normal or deviated to the Right – if LAD is present, then LAF block is also present • QRS Pattern – Q waves - present and normal – R waves - Classic Rabbit Ears in V1 - V2 • Triphasic Pattern • ST segment - depression usually noted • T waves - inversion may be noted Classic Appearance of RBBB MCL1 RBBB Pattern 3 1 1 3 2 2 Left Bundle Branch Block • Common Acute Causes – Anteroseptal AMI – Acute HF – Pericarditis and/or myocarditis • Always indicates a diseased heart LBBB • Impulse travels from the AV node through the RBB but not the LBBB • The septum is depolarized by the RBB (the septum is part of the LV) thus initial net depolarization is away from V1 • The depolarization continues to move away from V1 at the rest of the LV is depolarizedQRS complex continues as a negative deflection • LBBB is indicated if there is a QS pattern in V1 and the QRS of >120 ms is preceded by a P wave Characteristics of LBBB • QRS - .12 seconds or greater • QRS Axis - usually normal but can be LAD • QRS Pattern – Q waves – absent – R waves - usually small in V1 and V2 – S waves - Deep Wide in V1 and V2 • ST Segment - elevation noted in V1 - V3 • T waves - elevation noted in V1 - V3 Common Appearance MCL1 LBBB Pattern MCL1 1 An Easier Way • Not all BBB will present so nicely • Focus on the terminal force (final portion of the QRS) • With a BBB, the ventricles are not depolarized simultaneously but sequentially • The last ventricle to be depolarized is the one with the block. – Its depolarization will make up the later portion of the QRS Bundle Branch Block RBBB Right Ventricle MCL1 Left Ventricle Normal Right Ventricle Left Ventricle LBBB RT vs. LT Exceptions • Presence of P waves: – Junctional rhythms typically do not produce P waves but are supraventricular rhythms that may be seen with a BBB – WPW are wide and are stimulated by supraventricular activity (incidence is 0.1%) – Hyperkalemia can produce wide QRS complexes Exceptions • Differentiating between LBBB and RBBB – Nonspecific intraventricular conduction delay (NSIVCD) – Do not display the typical V1 morphologies – May not be due to complete BBB but may be incomplete BBB Quick Axis Determination • Normal Axis – Lead I & Lead II upright • Left Axis Deviation – Lead I upright - Lead II negative deflection • Right Axis Deviation – Lead I negative deflection – Lead II upright • Extreme Right – Both I & II negative deflection Left Anterior Hemiblock • QRS complex usually less than .10 seconds • QRS Axis – typically deviated to the Left • Must rule out other causes of LAD – Left ventricular Hypertrophy – Inferior myocardial infarction – Emphysema – Usually insignificant unless associated with a RBBB Left Posterior Hemiblock • Normal duration of QRS • Typically deviated to the Right Axis – must rule out other causes of RAD • • • • Right Ventricular Hypertrophy Pulmonary Embolism Anterolateral infarction Emphysema • Most commonly Associated with RBBB – can progress to CHB easily LBBB What do you think? Left Anterior Fascicular Block (aka Left Anterior Hemiblock)--much more common than LPFB • QRS complex usually less than .10 seconds • QRS Axis – typically deviated to the Left • Must rule out other causes of LAD – Left ventricular Hypertrophy – Inferior myocardial infarction – Emphysema – Usually insignificant unless associated with a RBBB • Marked LAD (QRS often > -45 degrees) without other apparent cause • QRS may be slightly widened but rarely > 0.12 sec • qR in I and aVL • rS in II, III, and aVF • Suspect in any patient with RBBB + LAD What do you think? What do you think? Left Posterior Fascicular Block (aka Left Posterior Hemiblock)--much less common than LAFB • • • • • • • Normal duration of QRS Typically deviated to the Right Axis – must rule out other causes of RAD • Right Ventricular Hypertrophy • Pulmonary Embolism • Anterolateral infarction Most commonly Associated with RBBB – can progress to CHB easily QRS more rightward than previously but often within normal range, – i.e. frank RAD is often absent and the diagnosis can often be made only by comparing before & after ECG's. – Note that some authorities require more stringent criteria for LPFB, e.g. marked RAD (> 120') w/o other known cause of RAD QRS may be slightly widened to 0.12 sec rS in I and aVL qR in II, III, and aVF What do you think? Divisional (fascicular) block - left anterior fascicular block (LAFB) and left posterior fascicular block (LAPB) • • LAFB : severe left axis deviation ( -45 - -90 degree) LAPB : severe right axis deviation (+90 - +120 degree) What do you think? What do you think? What do you think? What do you think? : Alternating bundle branch block alternating right and left bundle branch block What do you think? Other Stuff Wolf-Parkinson’s White Syndrome What do you think? Early Repolarization Early Repolarization What do you think? Normal Variant: Early Repolarization-KH Frank G.Yanowitz, M.D. Early repolarization, a misnomer, describes a pattern of localized or diffuse ST segment elevation. This is especially seen in leads with prominent R waves. In this example leads I, II, V5 and V6 illustrate the early repolarization pattern. ST segments usually have a "concave upwards" pattern and take off after a small S-wave is inscribed. Pericarditis • • • • • • • • Diffuse inflammation of the pericardium and adjoining epicardial surface of the heart ST elevation here is not due to injured myocardium Common post-MI and post cardiac surgery ST segment elevation may be found in any lead – The is because it is related to diffuse inflammation rather than localized inflammation – Not grouped in contiguous leads Notching of the J point may occur – This is indicative of noninfarct causes of ST elevation May produce PR segment depression We often compare the isoelectric line to the PR interval – If we are doing this, the ST segment may appear elevated – Use both the TP and PR to establish the isoelectric line to minimize this problem Clinical presentation – CP • Sharp, “knife-like” • Not heavy, pressure • Affected by movement, respiration, and position • May radiate to the base of the neck or between shoulder blades What do you think? Syndrome: 1. "Current of Injury" pattern: thought to be due to pressure and superficial inflammation of the pericardium 2. PR segment changes: PR segment depression (82% of patients) Differentiation from MI: ST segment elevation is typically less pronounced (equal to or less than0.05mV) and the ventricular surface area is greater (more leads involved) What do you think? A ST/T ratio in V6 of 0.25 will allow good separation of the two entities. ST segment elevation is typically less pronounced (equal to or less than 0.05mV) and the ventricular surface area is greater (more leads involved) ST/T ratio • Measure the height of the elevated ST segment - from the level of PR segment to the J point where the ST segment starts. • Measure the height of the T wave - from the level of the PR segment to the top of the T wave. • Calculate the ratio of the height of the ST segment: height of the T wave (ST/T ratio):– ST/T ratio < 0.25 = BER – ST/T ratio > 0.25 = Pericarditis Differentiating early repolarization from pericarditis by ECG The ratio of the ST-segment elevation to the T-wave amplitude in lead V6 is useful in differentiating early repolarization (left) from pericarditis (right). The four stages of electrocardiographic changes in acute pericarditis Ventricular Enlargement Left Ventricular Hypertrophy--all criteria less valid in pts < 35yo; also less valid in the presence of Bundle Branch Blocks which may exaggerate QRS voltages Most specific criteria: R in aVL > 11mm (or > 16mm with LAD) R in I + S in III > 25mm R in aVL + S in V3 > 28mm in men or > 20mm in women (Circ. 3:565, 1987) Less specific criteria: R in II or III > 25mm R in V6 > 27mm R in V5 or V6 + S in V1 or V2 > 35mm (Am. Heart J. 37:161, 1949; Circ. 81:815, 1990) V6 > V5 Loss of R in V1 and V2 R in I > 15mm (or > 18mm with LAD) Right Ventricular Hypertrophy R > S in V1; sometimes RSR' in V1 Deep S wave in V4-6 What do you think? What do you think? What do you think? What do you think? What do you think? Atrial Enlargement Left Atrial Abnormality (e.g. hypertrophy or dilatation) suggested by: p > 2.5mm wide in any lead ("p mitrale") M-shaped p in any lead (humps at least 1mm apart) Negative deflection of terminal portion of p in V1 (at least 1mm x 1mm)--this is the most specific criterion Right Atrial Abnormality (e.g. hypertrophy or dilatation) suggested by: p > 2.5mm tall in II, III, or aVF ("p pulmonale") Biphasic P in V1 with initial portion greater in amplitude What do you think? What do you think? What do you think? • • • • • • • • • • • • • hyperkalemia. narrow and peak T waves (tenting) AV conduction disturbance (PR prolongation or disappeared P wave) and wide QRS cardiac arrest with a slow sinusoidal wave ('sine-wave pattern') asystole renal failure hyperkalemia hypocalcemia "tent on the desert' hypokalemia prominent U wave, prolonged ventricular repolarization (QT interval) hypercalcemia prolonged QT interval hypocalcemia shortened QT interval Digitalis effect • digitalis ECG 'PR prolongation, scooping (sagging)' of ST-T complex, short QT interval • digitalis intoxication What do you think? What do you think? What do you think?