Presentation on theme: "12 Lead EKG 101 A Basic Overview of How to Interpret 12 Lead EKGs and Treat a Cardiac Patient Region IV Pre-Hospital Systems Coordination Committee."— Presentation transcript:
112 Lead EKG 101A Basic Overview of How to Interpret 12 Lead EKGs and Treat a Cardiac PatientRegion IV Pre-Hospital Systems Coordination Committee
2Purpose:The purpose of this course is to provide pre-hospital clinicians with the tools necessary to identify the basic A&P of the heart, interpret 12 Lead EKGs, localize and treat AMIs as well as recognize imposters and potential complications.
3Basic Cardiac Anatomy & Physiology Muscular pump about the size of your fistprimary function is to pump oxygenated blood to the rest of the body.Made up of four chambers,right and left atriaright and left ventriclesThe septum is a thin muscular wall that separates the right and left sides of the heart.Each contraction of the heart occurs in response to an electrical impulse that starts in the upper portion of the heart.Blood is moved in a closed circuit through the body by the pumping of the heart.
4Basic Cardiac Anatomy & Physiology The heart contracts and pumps blood out to the body (systole) and relaxes to fill with more blood (diastole).The heart muscle itself is like all other organs in the body and requires oxygen to function.The oxygen-rich blood is circulated to the heart muscle through the coronary arteries.There are two main arteries:Right coronary arteryLeft main coronary arteryboth start at the aortaThese vessels then branch off into smaller and smaller vessels along the surface of the heart.
5In order to perform work, the heart needs oxygen and nutrients. There are two main arteries:Right coronary artery (RCA)Left coronary artery (LCA).The left coronary artery divides into:Left anterior descending (LAD) branchLeft circumflex branch(LCX)The right coronary artery and the branches of the left coronary artery provide numerous smaller branches which penetrate the heart muscle, supplying it with blood.Both coronary arteries originate from the aorta and run along the surface of the heart.In the majority of human hearts, coronary circulation follows a predictable pattern.
6Left Main Coronary Artery Branches quickly into the LAD & LCX. Involves almost 2/3 of the heart muscleRight Coronary Artery (RCA) The RCA supplies blood to the bottom (inferior) portion and part of the back (posterior) portion of the left ventricle. The posterior portion of the septum is also supplied with blood from the RCA.SA Node 55%AV Node 90%AV BlocksLeft Anterior Descending Branch (LAD) The LAD supplies blood to the front (anterior) portion of the left ventricle, apical including most of the anterior portion of the septum separating the ventricles.Bundle Branch Block, AMI, CHFLeft Circumflux Branch (LCX) The LCX supplies blood to the left side (lateral) portion and the back (posterior) portion of the left ventricle.SA Node 45%AV Node 10%Lateral & posterior MI
7Sino-Atrial (SA) Node: natural cardiac pacemaker Sino-Atrial (SA) Node: natural cardiac pacemaker. The heartbeat starts here and spreads throughout the network of conduction fibers in the two atria causing them to contract.Normally, the heartbeat can only reach the ventricles (the two lower chambers), after it has passed through the atrioventricular (AV) node.Atrioventricular (AV) Node: slows down the electrical signal so that the atrial contractions can finish filling the ventricles completely. The AV node also prevents the lower chambers from beating too fast if the atria develops a fast rhythm (tachyarrhythmia).His Bundle, bundle branches, and the Purkinje system : The electrical signal finally passes to the ventricles causing the ventricles to contract
8Anatomy of an EKGThe EKG, or a measure of this electrical activity of the heart, is comprised of 3 primary parts...1. P wave---electrical depolarization of the atria...contraction follows...2. QRS COMPLEX---electrical depolarization of the ventricles...contraction follows...3. T wave---electrical repolarization of the ventricles...and thus, relaxation...
9P wave: Represents positive and negative deflections of atrial contraction and relaxation PR Interval: Distance between the P wave and the R wave. Should be consistentQRS ComplexQ wave: First negative deflectionNormal in I, aVL, V1, V6Significant or pathologic is one box wide and/or 1/3 the height of the R waveR Wave: First positive deflectionS Wave: Next negative deflection
10ST Segment: Essentially isoelectric, slopes gentely upward J point: the point at which the ST Segment takes off from the QRS complexT Wave: Upright always in leads I, II, V2-V6. aVR is always negative. Leads III, aVL, aVF, and V1 can be positive or negativeU Wave: Seen best in V3, same polarity as T wave, sign of hypokalemiaQT Interval: One complete ventricular cycle. None are > ½ the preceding R-R
12Einthoven’s Triangle Lead I - + Lead III Lead II extends from the right to the left armLead IIIextends from the left arm to the left footLead IIextends from the right arm to the left foot
13This is an example a 12-lead EKG. Anatomy of a 12-Lead EKGThis is an example a 12-lead EKG.
14Anatomy of a 12-Lead EKG (cont.) At the bottom of this 12-lead are rhythm strips (highlighted).Any of the 12-leads can be shown as rhythm strips.You can configure the device to show you any of the six limb leads on the rhythm strip (I, II, III, aVR, aVL or aVF).
15Anatomy of a 12 Lead EKG (cont.) The format of the 12-lead EKG is very standard. While there are a few exceptions, the format you see here is typical of what you will see in most 12-lead EKGs done in North America.
16Anatomy of a 12-Lead EKG (cont.) The 12-lead can provide a computer generated interpretation.When you see “ACUTE MI SUSPECTED” the machine is right about 98% of the time.In order to attain specificity, if the computer isn’t absolutely sure that an AMI is present, it will not say anything about it.In other words YOU are the primary interpreter, the computer is your backup.
17Anatomy of a 12-Lead EKG (cont.) The 12-Lead is very good at measuring intervals and durations.It is better at measuring the PR-interval and the QRS width.We express these intervals and durations in seconds12-lead expresses them in milliseconds. It is simple to convert milliseconds to seconds.
18Anatomy of a 12-Lead EKG (cont.) When you use an EKG to determine the cardiac rate and rhythm, certain sampling time is required.12-lead interpretation: Only one beat from each lead is needed to make an interpretation.
19Anatomy of a 12-Lead EKG (cont.) There are six positive electrodes on the chest, yielding six leads.There are four electrodes on the limbs from which the EKG machine makes another six leads.Each lead has one positive electrode.Positive electrode is a camera.view is from the positive electrode toward the negative electrode.The portion of the left ventricle that each leads “sees” is determined by the location of that positive electrode.Different placements of the electrodes will yield different viewpoints.
20Anatomy of a 12-Lead EKG (cont.) Types of LeadsLimb LeadsChest LeadsI aVR V1 V4II aVL V2 V5III aVF V3 V6
21Anatomy of a 12-Lead EKG (cont.) View of Posterior Heart WallLeads V1 & V2Tall RST DepressionUpright T-WaveTall R Wave and ST Depression are hallmarks of Posterior Wall MI
22Anatomy of a 12-Lead EKG (cont.) View of Inferior Heart WallLeads II, III, aVFLooks at inferior heart wallLooks from the left leg up
23Anatomy of a 12-Lead EKG (cont.) View of Lateral Heart WallLeads I and aVLLooks at lateral heart wallLooks from the left arm toward heart*Sometimes known as High Lateral*
24Anatomy of a 12-Lead EKG (cont.) View of Lateral Heart WallLeads V5 & V6Looks at lateral heart wallLooks from the left lateral chest toward heart*Sometimes referred to as Low Lateral or Apical view*
25Anatomy of a 12-Lead EKG (cont.) View of Entire Lateral Heart WallLeads I, aVL, V5, V6- Looks at the lateral wall of the heart from two different perspectivesLateral Wall
26Anatomy of a 12-Lead EKG (cont.) View of Anterior Heart WallLeads V3, V4Looks at anterior heart wallLooks from the left anterior chest
27Anatomy of a 12-Lead EKG (cont.) View of Septal Heart WallLeads V1, V2Looks at septal heart wallLooks along sternal borders
28Anatomy of a 12-Lead EKG (cont.) I LateralII InferiorIII InferioraVRaVL LateralV1 SeptalaVF InferiorV2 SeptalV3 AnteriorV4 AnteriorV5 LateralV6 Lateral
29Anatomy of a 12-Lead EKG - ST Segment The ST segment is normally iso-electric (baseline) neither elevated or depressed.May slope upward toward a relatively tall T waveThe ST segment is probably the single most important element to identify on the ECG when looking for evidence of AMI.
30The Three I’s Ischemia Injury Infarct lack of oxygenation ST depression or T inversionInjuryprolonged ischemiaST elevationInfarctdeath of tissuemay or may not show in Q waveThis information will aid in understanding the ECG subsets in the next section.Define ischemia, injury and infarct.Note that the definitions are correlated with specific ECG criteria.Note that “injury” is also ischemia and does not imply any permanent damage or death to tissue. The term injury simply means ischemia identified by ST segment elevation.
31CARDIAC ISCHEMIA( Myocardial ischemia, Ischemic heart disease, Ischemia, Myocardium ischemia, Silent ischemia )Cardiac ischemia is a situation in which the blood flow within a coronary artery is limited to the point where the oxygen needs of the heart muscle cannot be met (hypoxia).
32CARDIAC ISCHEMIAMinor episodes of cardiac ischemia tend to cause little long-term damage to the heart, but these episodes can sometimes cause serious effects in some patients:They can cause arrhythmias, which can lead to either syncope or cardiac arrest and sudden cardiac death.Severe or lengthy episodes can trigger a result in myocardial infarction.The collective effects of minor episodes of cardiac ischemia can potentially lead to cardiomyopathy.
33Symptoms of Cardiac Ischemia May be painful symptoms of cardiac ischemia,Pain, pressure or discomfort from cardiac ischemia is angina. Angina may feel like a squeezing vise or crushing pressure deep in the chest behind the sternum. May also be felt in the shoulders, arms, back, neck or jaw.
34EKG in Acute IschemiaTracing taken during an episode of anginal pain that occurred while the patient was at rest. Marked ST elevation in leads V2‑5 with some ST depression in aVF.
35EKG after Acute Ischemia This tracing was taken 30 minutes after the initial. The patient was pain‑free and asymptomatic. The ST segments are isoelectric, and the ECG is normal
36Evaluation after Acute Ischemia Subsequent clinical evaluationserial ECGsenzyme determinations,revealed no evidence of acute myocardial infarction. Disappearance of the ST elevation and the absence of clinical and electrocardiographic evidence of infarction on subsequent examinations indicate that initial ECG is representative of severe, acute, and reversible ischemia.
37Well Perfused Myocardium Epicardial Coronary ArteryLateral Wall of LVSeptumLeftVentricularCavityPoint out the epicardial artery and it’s branches reaching toward the endocardium.The endocardium is less well perfused and has higher oxygen demand than epicardial tissue. Illustrate higher demand with glass of water.When the myocardium is well perfused, the ST segments are isoelectric (equal to the T-P segment).Positive ElectrodeInterior Wall of LV
39Ischemia Epicardial Coronary Artery Lateral Wall of LV Septum Left VentricularCavityThe vessel lumen is now narrowed by a clot. If the clot is incomplete or collateral circulation is good, only the hardworking, poorly perfused sub-endocardial tissue will become ischemic.This is represented on the ECG by ST depression or T wave inversion.Positive ElectrodeInterior Wall of LV
40Ischemia Inadequate oxygen to tissue Subendocardial Represented by ST depression or T inversionMay or may not result in infarctDefine ischemia.Inadequate oxygen to tissue.Represented by ST depression or T inversion.May or may not result in infarct (duration of clot and demand).If infarct develops, may or may not display Q wave.The direction of ST deviation is a poor predictor of Q wave development.
41ST depressionNote widespread ST depression and T waves inverted in several leads.
42Injury Prolonged ischemia Transmural Represented by ST elevation Usually results in infarctDefine injury. Ischemia affecting the epicardium represented by ST elevation.Lack of oxygenation to tissueRepresented by ST elevation. Refereed to as the “injury pattern”.Usually results in infarct (presumptive evidence of MI)If infarct develops, may or may not develop Q waveThe direction of ST deviation is a poor predictor of Q wave development.
43ST elevation Ask group to look for ST elevation. The ST elevation implied epicardia ischemia (injury pattern).
44Injury Thrombus Ischemia If the clot is complete or the collateral circulation is poor, the ischemia will be transmural (through to wall). This is seen on the ECG as ST segment elevation.Most often this occurs due to a complete and persistent clot. Spontaneous lysis at this point is rare and the tissue is expected to infarct unless acute reperfusion therapy can be rapidly initiated.ST segment elevation is presumptive evidence of ACUTE MI.
45Infarct Death of tissue Represented by Q wave Not all infarcts develop Q wavesDeath of tissue.Traditionally represented by wide (equal to or greater than 40ms) Q wave.Not all infarcts develop Q waves.The direction of ST deviation (elevation or depression) is a poor predictor of Q wave development.
46Infarction Many infarcts do not develop Q waves Infarcted Area Electrically SilentDeath of myocardial tissue may result in the development of a pathologic Q wave.Q wave development can not be predicted by the direction of ST segment deviation.It does not occur with all infarcts.DepolarizationMany infarcts do not develop Q waves
47Q WavesPathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle.
48Thrombus Infarcted Area Electrically Silent Ischemia Depolarization During the evolution of an infarct, Q waves, ST elevation, and T inversion may occur together.ST elevation is the most important finding to the emergency care provider. It is presumptive evidence of acute myocardial infarction.Depolarization
49Summary A normal ECG does NOT rule out ACS ST segment depression represents ischemiaPossible infarctST segment elevation is evidence of AMIQ wave MI may follow ST elevation or depressionA normal ECG does NOT rule out any Acute Coronary Syndrome.ST segment depression represents ischemia, infarction is possible.ST segment elevation represents epicardial ischemia, and is presumptive evidence of AMI.Since necrosis may occur under all the these situations, a Q wave MI may follow ST elevation, ST depression or even a normal ECG.
50Pathophysiology of the AMI Chronic accumulation of atherosclerotic plaque in coronary vessels around the heartFibrous plaque prone to rupture, lead to thrombytic blockageClots form due to damaged tissue and plateletsBoth release chemicals causing a clot to formForms a substance called fibren that traps cells and platelets eventually blocking and narrowingTissue damage in AMI results from rupture of plaque on vessel walls creating a chain reaction that forms a clot in the coronary artery.
51Process of an AMI Impaired blood flow: Produces varying degrees of myocardial injuryDamage dependent on flow reduction and durationTissue death progress quickly in a wave patternBegins with endocardiumEnds with epicardiumInfarction becomes larger toward the surface of the heart.Ischemia – Shortage of oxygen at cellular levelInjury – Diminishing supply of oxygenInfarct – cardiac cells die of anoxia.
52EKG Changes from Infarction First Detectable Change in EKGTall T-wavesincrease in heightmore symmetricmay occur in the first few minutes*Known as hyper acute phase*
53EKG Changes from Infarction “The Acute Phase” Signs of Myocardial InjuryST Segment ElevationPrimary indication of injuryOccurs in first hour to hoursST Segment Elevation in Leads1mm or greater in limb leads2 mm or greater in chest leadsHallmark indication of AMI*Known as Acute Phase*
54EKG Changes of Infarction “Reciprocal Changes” ST elevation in contiguous leads most often represents acute infarctionST depression in contiguous leads may represent acute ischemiaIn acute infarction, ST elevation in contiguous leads coupled with reciprocal ST depression in non-infarcting leads is added evidence of an AMI.
55Reciprocal ST segment depression Acute ST segment elevation
56EKG Changes from Infarction “T Wave Inversion” Signs of Myocardial InjuryT wave inversionpresence of ischemiaMay precede ST elevationProminent in precordial chest leadsInversion in limb leads is pathologicT wave inversion can be caused by other things than ischemia
57EKG Changes from Infarction “The Indeterminate Phase” Signs of Myocardial InfarctionPathologic Q-waveFirst indication of tissue deathFirst few to several hoursQ-wave ¼ size of QRS suggests infarctRepresent current or past eventsDetermine timing through ST elevation and T-wave inversion
58Natural Progression of EKG in Infarction Over time:T-wave regains normal contourST-segment returns to isometric lineQ-wave remains as evidence of infarctIndicates presence of previous MI*ST segment elevation provides the strongest evidence of early recognition of AMI*
59EKG Changes from Infarction (cont.) All of the changes in the previous slides are: Indicative ChangesST segment elevation is helpful in detecting an MI in its early stagesHyperacute (Tall) T-waves alone are specific enough to diagnose an MIT-wave inversion can occur with simple angina and is therefore not specificPathological Q-wave is the most accurate recognition of an MINot in the first few hoursST segment elevation provides the strongest evidence for early recognition of an MI
60ECG Variants Coronary Spasm: “Printzmetals angina” Injury pattern that resolves w/ rest, NTG,O2 etc.Early Repolarization: elevated “J” point seen best in V3,4. Key to Dx pt’s are usually young & asymptomaticPericarditis: ST elevation usually global associated w/ fever, pleuritic c/p.
61ECG Variants due to Drugs or Electrolytes Imbalances Hypokalemia: lg U waves ( usually taller than T) seen best in precordial leads. <2.7Hyperkalemia:Tall peaked T waves > 6.0PR prolongs, QRS widensP waves disappear > 8.0Hypocalcemia:Prolonged QT intervalHypercalcemia:Shortened QT intervalDigitalis effect:ST depression- downsloping, curved ST segments.“scooping”, “sagging”, flat or inverted T’s in lateral leadsPR prolongedQT shortened
62Bundle Branch Blocks “Turn Signal Rule” This is a simple method for differentiating right bundle branch block from left bundle branch block. V1 will be the only lead you need to view1. Locate the terminal (last) force of the QRS complex2. Determine if it is pointing up or down.3. Compare to the turn signal in your car:Up is for a right turn & RBBBDown is for a left turn and LBBBClinical significance:Bundle branch is a significant complication of infarction. Since the left anterior descending artery is the primary supplier of the bundle branches, BBB is considered a complication of anterior septal infarcts.When BBB is the result of MI, the incidence of pump failure is 65-70% and the in-hospital mortality rate is 40%-60%. The BBB itself is not dangerous, but the high mortality rate is due to the extensive amount of tissue death occurring when an infarct is serious enough to cause a BBB. Another manifestation of BBB is in the form of AV Block. This is why infranodal AV blocks are more serious and have wide QRS complexes.
63Localizing the Area of Infarction Indicative changes are not found in every leadOnly present in leads looking at the infarctIndicative changes in two or more leads looking at the same portion of the heart are anatomically contiguous leadsSuspect AMIST segment elevation in two or more leads that are not contiguousAMI not the suspected cause
64Recognition & Localization Recognizing infarct: Know which part of the heart each lead looks atLocalizing Infarct: Note which lead is displaying evidence and which portions of heart they are looking atLeads Displaying Indicative ChangesII, III, aVFV1 & V2V3 & V4V5, V6, I, and aVLLocation of Infarct SiteInferiorSeptalAnteriorLateral*Simply knowing the changes to look for and which part of the heart each lead looks at*
65Anterior Wall MIAnterior Wall infarct: Occlusion of the Left Anterior Descending Artery (LAD)2mm ST segment elevation in two or more of leads V1-V4Reciprocal changes in leads II, III, aVFLethal due to large myocardium involvementPossible conduction defects:Bundle Branch Block2nd Degree Block Type IICHB
67Inferior Wall MIInferior Wall MI: Occlusion of Right Coronary Artery (RCA)At least 1mm ST segment elevation in leads II, III, aVFReciprocal ST depression in leads I & aVL or precordial leadsConduction defects:Sinus bradycardiaSinus arrest1st degree blockAccelerated Idoventricular rhythmComplications:Bradyarrhythmias – protective mechanism, 90% of blood supply for SA & AV nodes from the RCAHypotension – treated with fluids, consider right side involvement
69Lateral Wall MILateral Wall MI: results from occlusion of the Left Circumflex ArteryAt least 1 mm ST segment elevation in leads I, aVL, V5 & V6 and /or 2 mm ST segment elevation in V5 & V6Reciprocal ST depression in V1Sometimes an extension of an Anterior or Inferior MIConduction defects are rare
71*Associated with dangerous conduction disturbances* Posterior Wall MIPosterior Wall MI: Occlusion of the Right Coronary Artery (RCA) or the Posterior Descending ArteryNo leads that look at the posterior wallLeads look at the infarct site from the opposite side(backwards)ST depression in V1 & V2Tall R waves in V1 and/or V2Most often associated with Inferior MI*Associated with dangerous conduction disturbances*
73Right Ventricular MIRight Ventricular MI: caused by proximal occlusion of the Right Coronary Artery (RCA)Associated with Inferior Wall MICan happen independentlyStandard 12-Lead does not assess right side of heartInfarction is significantIndicates large infarctionIndicates involvement of both ventriclesIf the possibility of RVI exists a set of chest leads can be applied to the right side of the chestV1-6R leads look at right ventricleLead V4R most accurateEvidence of a Right Ventricular MI are present in Lead V4R only for the first four (4) hours of an MI
75Septal Wall MISeptal Wall MI: caused by septal perforation involving the LAD or the Posterior DescendingMost often in the setting of an Anterior MILoss of R-wave in leads V1, V2 or V3May have ST segment elevation in V1 & V2No reciprocal changes
76Overview of Infarcts Location of Infarct Arterial Supply Indicative ChangesReciprocal ChangesAnteriorLADV1-V4II, III, aVFInferiorRCAI, aVLLateralCircumflexI, aVL, V5, V6V1PosteriorPosterior Descending (RCA)NoneV1, V2SeptalSeptal Perforating (LAD)Posterior Descending (RCALoss of R wave in V1, V2, or V3Maybe just some discussion of reciprocal changes? Debate of significance? Not all MI’s have reciprocal changes, that their presence may indicate a bigger infarct, more ischemic area. Sometimes reciprocal changes are more evident (stick out more) than ST elevation and help zero in on infarcted region.
77Overview of InfarctsSuspect infarction when there are indicative changes in at least two anatomically contiguous leadsIndicative changes in many leads suggests larger infarctWith Inferior Wall MI suspect Right Ventricular Wall InfarctSigns of possible Right Ventricular Wall Infarct:HypotensionJVDClear lung soundsCauses of ST segment depression include digitalis, ischemia and reciprocal changesSuspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3
78Complications of Myocardial Infarction Chest Pain: Most common complicationTreatment:Oxygen and ASA (162 to 325)mgNTG initially with Morphine if pain persistsUsually very effectiveRight Ventricular Wall Infarct:Reduces output of right ventricle decreasing left ventricular filling (decreased preload)NTG and Morphine can worsen conditionsDecrease in blood pressure will worsen area of injuryPresence of Inferior Wall Infarction with no EKG or clinical evidence of right side infarct does not merit any extra caution when using NTG and MorphineShould also stress that NTG should be given cautiously to patients with borderline blood pressure when evidence of RV Infarct exists.
79Complications of Myocardial Infarction AV Block Location: indicates electrical impulse from atrium is blocked from depolarizing the ventriclesMost common block is in the AV Node (nodal block)Second most common block is in the Bundle Branches (infranodal)Infarct frequently produces AV Block due to increase in parasympathetic toneLocal ischemia around node can produce the blockLess serious than block caused by tissue injury or deathBlocks in AV node produce narrow QRS complexBundle Branches produce wide complexes
80Complications of Myocardial Infarction Determining the type of QRS presented with is a useful tool in determining the location of the blockNodal BlockInfranodal BlockCoronary SupplyRight Coronary ArteryLeft Coronary ArteryQR WidthNarrowWideStabilityGenerally StableOften UnstableAtropine ResponseUsually improvesOften does not respondSlide may be confusing. Better stated that if the QRS is narrow, then the block lies at the junction of the AV Node. If the QRS is wide, then the block lies below the level of the AV Node
81Complications of Myocardial Infarction Hypotension: A common treatment for hypotension which is secondary to the infarct is to administer fluid boluses and inotropic drugs (dopamine)Hypotension in the setting of an inferior wall infarction is most likely secondary to right ventricular involvement.Although RV Infarcts may require significant boluses to offset loss of preload, continuously monitor the patient for signs and symptoms of developing left sided failure.Hypotension in the setting of an anterior wall infarction may not tolerate fluid boluses and may require a dopamine infusion.Inferior Wall MI’s with RV involvement and hypotension may respond to fluid challenges of up to 2 liters. Boluses should be administered in 250 ml increments while assessing left ventricular function. Anterior Wall MI’s may not tolerate even small amounts of fluid and may require pressor intervention in the setting of hypotension.
82Complications of Myocardial Infarction Left Coronary Artery OcclusionsRight Coronary Artery OcclusionsLeads Showing Indicative ChangesV1-V6, I, aVLII, III, aVF, V4R-V6RLocalizationSeptal, Anterior, Lateral, PosteriorInferior, Posterior, Right VentricularPain ControlNTG & Morphine as appropriateNTG & Morphine used with caution if RVI presentAV BlockInfrequent, usually wide ORS, often unstable, Atropine may be ineffective, use standby pacingFrequent, usually narrow QRS, Generally stable, Atropine often effective, May not require treatmentHypotensioncc fluid bolus, inotropic medicationsVigorous fluid therapy if RVI present, inotropic medications
83Clinical PearlsSuspect infarction when there are indicative changes in at least two anatomically contiguous leadsIndicative changes in a greater number of contiguous leads suggests a more extensive infarctionRV or Posterior infarcts should be considered in setting of Inferior Wall MIRV: ST segment elevation in rV4Posterior: ST depression +/or Tall Rwave in V1 & V2Other clinical signs of RV Infarct may include:Hypotension and JVD in the setting of clear lung soundsOther causes of ST segment depression besides ischemia include digitalis effects and ventricular hypertrophySuspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3