Chapter15

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Chapter 15 : 

Chapter 15 Acute Myocardial Infarction (AMI)

AMI: Introduction : 

AMI: Introduction This topic is broad and covers many areas of the heart: Anterior wall Inferior wall Posterior wall Right ventricle Apex It also covers combinations of AMIs that occur: Inferolateral Anterolateral Inferoposterior

Oxygen Deprivation : 

Oxygen Deprivation When a myocardial cell is oxygen-deprived, its function begins to alter. Initiates anaerobic metabolism (production of energy without oxygen). This creates acidosis, and is ineffective. Cell begins to suffer injury, and will die if normal circulation and oxygenation are not restored. Note: Ischemia and injury are reversible. Infarct (cell death) is irreversible.

Ischemia and Injury : 

Ischemia and Injury Ischemia and/or injury develop because demands of the heart are transiently overcome or not met by blood supply to that area. * Either an increase in demand or a decrease in supply can cause ischemia and/or injury to develop.

Cardiac Circulation (1 of 3) : 

Cardiac Circulation (1 of 3) To understand shapes of infarcts and presentation on ECG, look at how blood circulates  throughout myocardium. Think of cardiac circulation as basic tree structure: Lastly, terminal twigs and leaves Large branches divide to form medium branches, etc. Main branches divide to form large branches Main trunk gives rise to main branches

Cardiac Circulation (2 of 3) : 

Cardiac Circulation (2 of 3) Main coronary arteries travel along epicardium and penetrate into myocardium at various points.       Wedges of ischemic and injured areas are thinner along endocardium.

Cardiac Circulation (3 of 3) : 

Cardiac Circulation (3 of 3)  Arteries approach endocardium and divide into smaller branches until they form capillary beds of myocardium.  Single big branch supplies blood to wedge-shaped section of tissue, growing fatter as it moves away from artery’s point of origin.  Cells die along the pattern of distribution of branch, perfusing that section of myocardium.  Infarcted area will be wedge shaped with fatter side along endocardium.

Three Protective Mechanisms of the Heart : 

Three Protective Mechanisms of the Heart Overlap of areas of perfusion supplied by different arteries along endocardium, called collateral circulation, allows some areas of endocardium to be supplied by two different branch systems. Oxygen from ventricles can diffuse into cells of nearby tissue. There may be some vessels, thebesian veins, arising directly from ventricles.

Overlapping Perfusion : 

Overlapping Perfusion

Ischemia : 

Ischemia Area of ischemia is more negative than surrounding normal tissue Causes ST depression; T wave is flipped Causes repolarization to occur along abnormal pathway

Injury : 

Injury Zone of injury does not repolarize completely Remains more positive than surrounding tissue, leading to ST elevation T remains flipped (abnormal repolarization paths along injured/ischemic areas of myocardium)

Infarction : 

Infarction Dead tissue Does NOT generate any action potentials; electrically neutral Acts like electrical “window” in wall of myocardium An electrode can look through and see opposite wall. Unopposed, positive vector produces Q wave.

Q Wave Infarct (1 of 2) : 

Q Wave Infarct (1 of 2) Two main electrocardiographic classifications of infarcts: Q wave and non-Q wave

Q Wave Infarct (2 of 2) : 

Q Wave Infarct (2 of 2)

Non-Q Wave Infarct (1 of 3) : 

Non-Q Wave Infarct (1 of 3) Infarct small enough to not produce visible Q wave, but big enough to cause area of ST depression or T wave abnormalities This is a Q wave infarct. You cannot use presence of Q wave to identify a transmural or nontransmural infarct.

Non-Q Wave Infarct (2 of 3) : 

Non-Q Wave Infarct (2 of 3) Q wave infarcts are associated with higher incidences of acute mortality, increased tissue damage, and development of congestive heart failure. Non-Q wave infarcts have higher long-term mortality if aggressive treatment strategies are not undertaken. ** Every infarct = high chance (about 40%) of arrhythmia leading to sudden cardiac death.** Aggressive treatment could prevent infarct zone from extending into subsequent events.

Non-Q Wave Infarct (3 of 3) : 

Non-Q Wave Infarct (3 of 3)

ECG Progression in Infarct : 

ECG Progression in Infarct ECG pattern in AMI = continuum that extends from normal to full infarct. First: T wave flips in early ischemia. Then: ST elevation either flat or tombstoning (flipped T wave may disappear). Finally: We see Q waves.

Reciprocal Changes (1 of 3) : 

Reciprocal Changes (1 of 3) Refers to “mirror image” that occurs when two electrodes view same AMI from opposite angles Electrode A: Looks through window of neutral infarct zone, registers unopposed vector heading away from it; Q wave results. Next, registers other vectors. More positive zone of injury causes ST elevation.  T wave is flipped due to repolarization abnormalities. Electrode B:  Originally sees unopposed vector coming at it, giving rise to high R wave.  Then registers zones of injury/ischemia as ST depression and upright T wave.

Reciprocal Changes (2 of 3) : 

Reciprocal Changes (2 of 3)

Reciprocal Changes (3 of 3) : 

Reciprocal Changes (3 of 3)

Infarct Regions on ECG : 

Infarct Regions on ECG

Infarct Regions in Combination (1 of 3) : 

Infarct Regions in Combination (1 of 3) Real-life infarcts are caused by blocked arteries that usually involve more than one region of heart and ECG. Amount of tissue infarcted depends on size and location of artery blocked and area it perfuses. Vectors representing LVH, RVH, conduction abnormalities, etc. can alter appearance of ECG in acute AMI. ** There can always be differences caused by factors such as underlying pathology, dominant arterial systems, and presence of collateral blood flow. **

Infarct Regions in Combination (2 of 3) : 

Infarct Regions in Combination (2 of 3) Larger artery usually affects more than one region. Infarct can be small, but zone of injury or amount of myocardium at risk could be much greater. Acute infarcts tend to involve more than one region: Inferoposterior Anteroseptal with lateral extension Posterolateral Especially true of infarcts involving inferior and anterior walls. Result from obstruction of RCA or LAD artery.

Infarct Regions in Combination (3 of 3) : 

Infarct Regions in Combination (3 of 3) Old or age indeterminate infarcts, represented by Q waves, are frequently found to affect isolated inferior or anterior walls. Some acute infarcts do involve only one region: High laterals True posteriors Isolated RV infarcts

Main Arteries and Areas They Perfuse : 

Main Arteries and Areas They Perfuse

Anterior Wall AMI : 

Anterior Wall AMI Rarely presents by itself. Commonly occurs with infarcts of septum, lateral wall, or both. Leads that represent anterior wall = V3 and V4

Types of Anterior Wall AMI : 

Types of Anterior Wall AMI When both anterior wall and septum are affected (anteroseptal AMI), infarct changes appear in leads V1 to V4. When infarct occurs in anterior and lateral walls (anterolateral AMI), changes show in V3 to V6, possibly I and aVL. When anterior wall, septum, AND lateral wall are involved (anteroseptal AMI with lateral extension), V2 to V5 are affected, and usually V1, V6, I, and aVL.

Anterior Wall AMI Regions on ECG : 

Anterior Wall AMI Regions on ECG

Anteroseptal MI : 

Anteroseptal MI A common pattern, frequently associated with hemodynamic compromise and cardiogenic shock

Anteroseptal AMI With Lateral Extension : 

Anteroseptal AMI With Lateral Extension Occurs when there is extension of infarct pattern to leads V5 to V6, I, and aVL. Common presentation for AMI, represents infarct encompassing large percentage of myocardial tissue. Reciprocal changes commonly seen in leads II, III, and aVF.

Anteroseptal AMI With Lateral Extension Regions on ECG : 

Anteroseptal AMI With Lateral Extension Regions on ECG

ECG 15-5 : 

ECG 15-5

ECG 15-7 : 

ECG 15-7

ECG 15-13 : 

ECG 15-13

Lateral Wall AMI (1 of 2) : 

Lateral Wall AMI (1 of 2) Can occur by themselves by showing changes in leads I, aVL, V5, and V6, or can occur in combination with other infarct patterns. Most notable combination: inferolateral, anterolaterals, anteroseptal with lateral extensions. Can also occur in combination with RV and posterior infarcts. High lateral AMIs do show reciprocal changes in inferior leads.

Lateral Wall AMI (2 of 2) : 

Lateral Wall AMI (2 of 2)

Lateral Wall AMI Regions on ECG : 

Lateral Wall AMI Regions on ECG

Inferior Wall AMI : 

Inferior Wall AMI Produce changes in leads II, III, aVF. Commonly associated with additional involvement of lateral wall, posterior wall, and right ventricle. Inferolateral AMIs present with changes in II, III, aVF, and V5 to V6 (may include I and aVL).

Inferolateral AMI Regions on ECG : 

Inferolateral AMI Regions on ECG

Inferolateral AMI : 

Inferolateral AMI Presents with changes in leads II, III, aVF, V5, V6, I, aVL Changes in I and aVL will occur if high lateral wall is involved ST changes can occur in V2 to V4 (depending on how far anteriorly it extends)

Inferolateral AMI Regions on ECG : 

Inferolateral AMI Regions on ECG

ECG 15-17 : 

ECG 15-17

Apical AMI : 

Apical AMI Apical infarct occurs when a large right coronary dominant system infarcts. Causes direct changes in leads I, II, III, aVF, aVL, and V2 to V6.

Apical AMI Regions on ECG : 

Apical AMI Regions on ECG

Additional ECG Leads (1 of 2) : 

Additional ECG Leads (1 of 2) There are some extra precordial leads used when evaluating AMIs. They help diagnose posterior and right ventricular infarcts, which occur frequently in combination with inferior infarcts. Posterior leads V7 to V10 are helpful in diagnosing posterior wall AMIs. Right-sided leads aid in diagnosis of right ventricular infarction. Direct changes occurring in right ventricle are clearly seen in V4R, V5R, and V6R.

Additional ECG Leads (2 of 2) : 

Additional ECG Leads (2 of 2)

Placing Additional Right-Sided Leads (1 of 2) : 

Placing Additional Right-Sided Leads (1 of 2) Placed in a mirror image to V4 to V6 Known as V4R, V5R, V6R Attach patient to ECG normally, then move V4 to mirror image on right to obtain V4R. Repeat process for V5 and V6 to obtain V5R and V6R. Right-sided leads show ST elevation in a right-side infarct. Key point: ANY time you see an inferior infarct, you should obtain right-sided leads.

Placing Additional Right-Sided Leads (2 of 2) : 

Placing Additional Right-Sided Leads (2 of 2)

Placing Additional Posterior Leads(1 of 2) : 

Placing Additional Posterior Leads(1 of 2) Posterior leads are used in diagnosis of posterior AMI. They show direct changes consistent with AMI: ST elevation Flipped T waves Q waves Obtain in any patient with ST depression in V1 to V3 not associated with RBBB. Obtain by moving V4, V5, and V6 to spots for V7, V8, V9.

Placing Additional Posterior Leads(2 of 2) : 

Placing Additional Posterior Leads(2 of 2)

Right Ventricular AMI (1 of 2) : 

Right Ventricular AMI (1 of 2) RV is not working in RVI. Blood gets back almost exclusively by venous return. Atria pump with just enough pressure to push blood into ventricles and assist with blood return slightly. If you increase venous capacitance, you decrease venous return. Nitrates, beta blockers, diuretics, and morphine—all decrease venous return. No return = no blood pressure

Right Ventricular AMI (2 of 2) : 

Right Ventricular AMI (2 of 2)

Criteria for Right Ventricular Infarction : 

Criteria for Right Ventricular Infarction Concentrate on diagnostic criteria Remember: Presence of all criteria is not needed on one ECG to make definitive diagnosis IWMI ST segment elevation greater in lead III than II ST elevation in V1 (possibly extending to V5 to V6) ST depression in V2 (unless elevation extends, as in #3) ST depression in V2 can’t be more than 1/2 ST elevation in aVF More than 1 mm of ST elevation in right-sided leads (V4R to V6R)

Inferior Wall MI : 

Inferior Wall MI Most RVIs (97%) occur in conjunction with IWMIs. Usually caused by obstruction in right coronary artery. Can arise from blocked left circumflex artery, but this is rare (3%). Make it a habit to check for RVI when you see IWMI.

ST Segment Elevation Greater in III Than II : 

ST Segment Elevation Greater in III Than II Infarct allows vector from interventricular septum to pass unopposed. Vector is directed anteriorly, inferiorly, and to right. Lead III lies directly in its path, causing ST segment to be higher in this lead.

ST Elevation in V1 : 

ST Elevation in V1  ST segment elevated in lead V1 because of unopposed vector and direction of injury current.  Normally this will elevate V1 and depress V2 as it passes by.  Vector can cause ST segment elevation that extends through V5 or V6, but it’s uncommon. Remember: If you see ST segment elevation in II, III, and aVF as well as V1, the most probable explanation is RVI.

ST Depression in V2 : 

ST Depression in V2 Direction of vector will produce ST elevation in V1 and depression in V2 . This is because vector path points more towards V1 either away or slightly away from V2.

ST Depression in V2 Cannot Be More Than Half the ST Elevation in aVF : 

ST Depression in V2 Cannot Be More Than Half the ST Elevation in aVF Amount of ST depression in V2 is critical:  If less than ½ height of ST elevation in aVF, it is a simple inferior-RV infarct.  If more than ½ height of ST elevation in aVF, it’s consistent with inferior-RV-posterior AMI (means tremendous amount of myocardium at risk and infarcting, a critical point).

More Than 1 mm ST Elevation in Right-Sided Leads (V4R to V6R) : 

More Than 1 mm ST Elevation in Right-Sided Leads (V4R to V6R) This is most specific sign of RVI. In presence of IWMI, if there is 1 mm or more of ST elevation in V4R, you have made the diagnosis. Sometimes you will find elevation in V6R, so make it a habit to obtain all three right-sided leads.

Right Ventricular AMI: Summary : 

Right Ventricular AMI: Summary

Right Ventricular AMI Regions on ECG: Summary : 

Right Ventricular AMI Regions on ECG: Summary

ECG 15-26 : 

ECG 15-26

Posterior Wall AMI : 

Posterior Wall AMI There are no direct leads that visualize posterior wall on a regular 12-lead ECG. To diagnose: Understand concept of reciprocal leads. See reciprocal changes in V1 and V2. Almost mirror image of direct changes of AMI on complex. You will see: Tall and fat R wave ST depression Upright T wave in leads V1 and V2

Diagnosing Posterior Wall AMI : 

Diagnosing Posterior Wall AMI Possible diagnostic dilemma when you see ST depression in V1 to V2: To make correct diagnosis: Look at rest of complex and get some posterior leads. Normal R:S ratio, thin R wave, flipped T with ST depression = most likely anterior ischemia or non-Q wave AMI Taller R wave, fatter than usual (≥0.03 sec) and upright T wave, or associated IWMI = likely PWMI. (Posterior leads usually positive, but distance of electrodes from heart means ST elevation may not be impressive.)

Posterior Wall AMI on the ECG : 

Posterior Wall AMI on the ECG

Carousel Ponies on ECG: BAD NEWS : 

Carousel Ponies on ECG: BAD NEWS ST depression makes a saddle; T wave is back of saddle. Upright T wave is critical criteria for correct diagnosis. If you can picture someone sitting on complex, holding on to R wave as the pole, there’s a good chance it’s a posterior AMI. RVH with strain: ST depression and tall R wave, should also have asymmetric, flipped T wave rather than an upright, symmetric one.

Carousel Ponies on ECG : 

Carousel Ponies on ECG

Posterior Wall MI: Summary (1 of 2) : 

Posterior Wall MI: Summary (1 of 2) Remember: You’re looking for reciprocal changes in regular 12-lead ECG. If AMI is occurring acutely, you will see ST depression. If you do see it, order additional posterior leads of V7 to V9. Age-indeterminate PWMIs present as isolated R'S ratio >1 in V1 or V2. Most PWMIs are associated with IWMIs and RVIs.

Posterior Wall MI: Summary (2 of 2) : 

Posterior Wall MI: Summary (2 of 2)

Posterior Wall MI Regions on ECG: Summary : 

Posterior Wall MI Regions on ECG: Summary

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