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Inferior Wall M.I.

Inferior Wall M.I. With Atrial Fibrillation or Atrial Flutter

Sat, 02/23/2019 - 22:17 -- Dawn

The Patient   This ECG was obtained from a 74-year-old man who had a history of COPD. He was complaining of severe chest pain at the time of the ECG.

The ECG     The rhythm is atrial fib or flutter (the R to R intervals are irregular, but seem to repeat about 4 interals).  Flutter waves are seen during some of the longer intervals. The rate is approximately 90 beats per minute.  The ST segments are very noticeably elevated in Leads II, III, and aVF.  There is reciprocal ST depression in Leads I and aVL, and also in all the precordial leads. 

Inferior Wall M.I. With Right Ventricular M.I.

Sat, 10/28/2017 - 18:36 -- Dawn

This ECG was recorded from a 75-year-old man with substernal chest pain and diaphoresis.  It shows a pretty classic picture of acute inferior wall M.I. The second ECG is a repeat tracing with the V4 wire moved to the V4 Right position, and it is positive for right ventricular M.I.  The patient was found to have a 100% occlusion of the right coronary artery, which was opened and stented in the cath lab.

There are several other examples of IWMI with RVMI in our archives, so we will confine this commentary to the ECG signs that make these tracings so typical of right coronary artery occlusion. Once you are familiar with the typical pattern of IWMI / RVMI, it is easy to see, even when the ST elevation is subtle (as this one certainly is NOT).

Signs of IWMI in these ECGs are

·         ST elevation in inferior leads II, III and aVF.

·         Reciprocal ST depression in leads I and aVL. 

Signs of RVMI in these ECGs are:

·         ST elevation in V4 right.

·         ST elevation in V1 without ST elevation in V2.

Inferior Wall M.I. and Right Bundle Branch Block

Wed, 09/06/2017 - 20:45 -- Dawn

These ECGs were taken from a 76 year-old-man who was complaining of chest pressure for 20 minutes.  He had a remote history of coronary artery bypass graft surgery.

This case has several good teaching points, including:

Significant artifact.  The limb leads show artifact which is severe enough to hamper our assessment of the j point location. Every effort should be made to eliminate artifact.  Some measures that might help are:

        *  clean and slightly "rough up" the skin where the electrode will be placed.  A rough wash cloth or gauze pad will work.

        *  shave hair if necessary.

        *  avoid areas of movement if possible.  Precordial electrodes must be placed in specific spots, but limb leads may be placed anywhere on the limb or on the trunk if it is impossible to avoid movement on the limbs.

       *   use fresh electrodes that have been protected from drying out.

Subtle STEMI changes.   This patient has an inferior wall M.I., which was confirmed as a complete occlusion of the right coronary artery in the cath lab.  The ST elevation in Leads II, III, and aVF is subtle, and more difficult to measure because of the artifact.  However, the SHAPE of the ST segments is a giveaway - they are very straight.  A convex-upward shape is normal (see Lead I).  Also, Lead aVL shows typical ST DEPRESSION, as a reciprocal view of the STE in Lead III.  More ST depressions can be seen in Leads V1 through V3, and they end abruptly there.  These localized ST depressions represent a reciprocal view of the posterior (also called lateral) wall, and represent an "extension" of the inferior wall M.I. up the back of the heart.  A V4 Right lead was obtained and shows no measurable ST elevation, but the shape is straight to slightly "frowning", indicating that the right ventricle may soon have STE.  Repeat ECGs should be obtained to watch for more definite ST elevations.

Inferior Wall M.I. With Wide QRS and Complete AV Block

Wed, 06/28/2017 - 14:13 -- Dawn

This ECG is from a 66-year-old woman who called 911 for a complaint of chest pain for the past four hours. She also complained of nausea, vomiting, and diarrhea for that time. She was pale and diaphoretic, and her BP was 77/43 sitting up, improving to 90/54 reclining. She denied “cardiac” history.  Her medications included:  aspirin, an SSRI, cilostazol, amlodipine, umeclidinium and vilanterol inhaler, atorvastatin, levothyroid, and metoprolol. We don’t have a previous ECG.  The EMS crew followed their chest pain protocol and delivered the patient to a facility with an interventional cath lab, but they did not designate a “STEMI Alert” because of the wide QRS.  It is their protocol to use the term “STEMI Alert” only when no M.I. mimics, such as left bundle branch block, are present. 

What does this ECG show?     There is an underlying sinus rhythm at 75 bpm.  There is AV dissociation, with regular, wide QRS complexes at a rate of 44 bpm.   This meets the criteria for complete heart block (third-degree AV block).  The morphology of the QRS complexes meets the criteria for left bundle branch block (wide, upright in Leads I and V6, negative in V1).  At a rate of 44 bpm, two options for this escape rhythm are possible:  1)  junctional escape with LBBB and 2) idioventricular escape rhythm. Because the LBBB criteria are met and the rate is over 40 bpm, we are voting for 1).  Also, in the presence of IWMI, AV node ischemia is very likely, resulting in AV blocks at the level of the AV node.  CHB at the AV node would result in junctional escape rhythm, and CHB below that, in the fascicles of the bundle branches, would result in idioventricular escape. The issue for this patient, and ANY patient, is cardiac output, and we see several reasons for cardiac output to be lower:

·         Wide QRS

Inferior-lateral M.I. With QRS Fragmentation

Sat, 08/13/2016 - 23:33 -- Dawn

SUBTLE ST CHANGES   This ECG was obtained from an 87-year-old man who was experiencing chest pain.  Due to the subtle ST elevation in Leads II, III, aVF, V5, and V6, (inferior- lateral walls) the ECG was transmitted to the hospital by the EMS crew, and the cath lab was activated.  The patient denied previous cardiac history. 

In addition to the subtle ST elevation, there is ST depression in V1 through V4, which represents a reciprocal view of the injury in the inferior-posterior-lateral wall.  Because the anterior wall is superior in its position in the chest, it is opposite the inferior/posterior wall, and can show ST depression when the inferior-posterior area has ST elevation. This ECG was the 6th one done during this EMS call.  Prior to this one, the ST segments were elevated less than 1 mm.  This is a good example of the value of repeat ECGs during an acute event.  

RIGHT VENTRICULAR M.I.?     This ECG was done with V4 placed on the right side, to check for right ventricular M.I., which is a protocol for this EMS agency. When the right coronary artery is the culprit artery (about 80% of IWMIs), RVMI is likely.  In RVMI, we would usually see reciprocal ST depression in Leads I and aVL, but the STE is very subtle here, so the depression would likely be also.  When the culprit artery is the left circumflex artery (<20%), lateral lead ST elevation is more likely, as we see here in V5 and V6. 

WHAT ABOUT RHYTHM?     The rhythm is sinus with PACs.  PACs are considered to be benign in most situations, but in a patient with acute M.I., any dysrhythmia can be concerning. The QT interval, measured as QTc (corrected to a heart rate of 60 bpm), is slightly prolonged at .458 seconds (458 ms).  Over .440 seconds is considered prolonged in men, and over .500 sec. places the patient at increased risk of developing torsades de pointes.  CAD and myocardial ischemia can lead to this modest increase in QTc.

Inferior Wall M.I. With Subtle ST Elevation

Mon, 01/18/2016 - 00:24 -- Dawn

This ECG is a good example of an inferior wall M.I. that was confirmed and treated in the cath lab.

The ST segments are elevated in Leads II, III, and aVF, but the amount of elevation may look subtle to some.   When the amount of elevation seems small, what other signs can help us recognize acute ST-elevation M.I.? 

PATIENT HISTORY AND PRESENTATION   This patient had acute chest pain, and was over the age of 50. We do not know his past medical history. His chest pain was described as substernal and epigastric, radiating to his back.  He had nausea and diaphoresis.  His past medical history is unknown, but it would be significant if he had a history of coronary artery disease, past M.I., smoking, metabolic syndrome, strong family history of heart disease, etc.

ST SEGMENT ELEVATION DISTRIBUTION   In acute STEMI, the elevation will be seen in “related leads”. That is, the leads that are affected will reflect a region of the heart that is supplied by the same artery. Some M.I.s are larger than others, affecting more leads, because some obstructions are more proximal than others in the artery.  This ECG shows STE in the inferior wall leads:  II, III, and aVF.  The culprit artery for this patient was the right coronary artery, which supplies the inferior and posterior wall of the left ventricle, the right ventricle, and the right atrium in the majority of people.

RECIPROCAL ST DEPRESSION   Finding reciprocal ST depression in the leads that are OPPOSITE the affected leads is a very reliable sign to confirm that the STEs are due to an acute M.I.  In fact, often the reciprocal depression is “stronger” or easier to see than the elevation.  It is important to teach your students how the standard leads are oriented to the heart, so they will recognize the 12-Lead ECG as a “map” of the heart.  The reciprocal ST depression in this ECG is seen in Leads aVL and I (subtle), which are across the frontal plane from Lead III.   We also note reciprocal ST depression in the precordial leads, especially notable in Leads V1 through V3.  This can reflect the injured area extending up the back of the heart from the inferior wall (posterior wall).  The R waves in V2 and V3 are a bit higher than normally expected, which could indicate a reciprocal view of pathological Q waves on the posterior wall.  Print the ECG out on paper, turn it upside down, and look at V2 and V3 through the back.  V2 and V3 will look like a “classic” STEMI.  This should be approximately the view you would get from additional posterior leads.

Inferior Wall M.I.

Tue, 11/17/2015 - 14:38 -- Dawn

This ECG shows a common manifestation with inferior wall M.I., BRADYCARDIA.  We see the signs of acute inferior wall M.I. in the inferior leads:  II, III, and aVF all have ST segment elevation.  There almost appear to be pathological Q waves in Leads III and aVF.  There are still VERY tiny r waves, and the downward deflections are not wide, but should full-blown Q waves develop in these leads, they would signify necrosis in the area.  A repeat ECG would certainly be warranted. 

Another sign that there is an inferior wall STEMI is the ST segment depression in Leads I and aVL, which are reciprocal to Lead III.  ST depression can have many meanings, but when it is localized in the leads which are opposite ST elevation, it is reciprocal.  There is also ST depression in Leads V1 and V2.  These leads are reciprocal to the POSTERIOR wall, otherwise known as the upper part of the inferior wall.  If an inferior wall M.I. is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. 

The rhythm is a marked sinus bradycardia, at just under 40 beats per minute.  Sinus bradycardia is very common in inferior wall M.I., because the inferior wall and the sinus node are usually both supplied by the right coronary artery.  AV blocks can also occur because the AV node is also supplied by the RCA in most people. 

It is important to remember that bradycardia does not always need to be treated.  In patients with acute M.I., a well-tolerated bradycardia may actually be beneficial to the injured heart, reducing supply/demand ischemia.  A well-tolerated bradycardia is a rate that does not produce low blood pressure and poor peripheral perfusion.  Some people tolerate rates in the 40’s quite well.  If the patient shows signs of poor perfusion: low BP, decreased mentation, pallor, shortness of breath, the rate should be cautiously increased with medication or electronic pacing.  

 

Acute Inferior-Lateral M.I. In A Patient With A Dominant Circumflex Artery

Fri, 10/30/2015 - 22:59 -- Dawn

This ECG was obtained from a patient who suffered an obstruction of the circumflex coronary artery.  Unfortunately, he was in the approximately 15-18% of the population in whom the circumflex artery is dominant.  That means that it connects with the posterior descending artery, perfusing not only the lateral wall of the left ventricle, but also the posterior and inferior walls.  In this case, the obstruction is in the midportion of the artery, and the high lateral wall is spared.  The large number of leads with ST elevation indicate the large amount of myocardium affected.  Leads II, III, and aVF have ST elevation, as do Leads V3 through V6.  Lead aVL has reciprocal ST depression. The T waves in the affected leads are "hyperacute", or taller than normal.  This is usually an early change in acute M.I., and disappears after the onset of ST elevation.

It is not always easy to determine from the ECG that the circumflex artery is the culprit artery, rather than the right coronary artery, which perfuses the inferior wall in the majority of people.  Some clues are:  Lead III has ST elevation equal to that of Lead II, the low lateral wall (V5 and V6) are affected, and aVL has reciprocal depression but Lead I does not.

This is a very large M.I., due to the dominance of the circumflex artery.  The patient did not survive, in spite of aggressive treatment.

Second-Degree AV Block, Type I

Sat, 06/13/2015 - 22:07 -- Dawn

This ECG is from an 80-year-old woman who had an acute inferior wall M.I. with a second-degree AV block.
 
Some people incorrectly call ALL second-degree AV blocks that are conducting 2:1 "Type II".  This is incorrect, as Mobitz Type I can also conduct with a 2:1 ratio.  The progressive prolongation of the PR interval will not be seen with a 2:1 conduction ratio, because there are not two PR intervals in a row.

This is a good example of a Type I, or Wenckebach, block which is initially conducting 2:1.  At the end of the ECG, two consecutive p waves conduct, showing the "progressively-prolonging PR interval" hallmark of a Type I block. Type I blocks are supraHisian - at the level of the AV node - and generally not life-threatening.  Blocks that are conducting 2:1 present a danger, however, in the effect they have on the rate.  Whatever the underlying rhythm is, the 2:1 block will cut the rate in half!  This patient has an underlying sinus tachycardia at 106, so her block has caused a rate of 53.  In light of her acute M.I., that rate is probably preferable to the sinus tach. This patient’s BP remained stable, and she did not require pacing. 

The ST signs of acute M.I. are rather subtle here. Note the "coving upward" shape in Lead III, and the reciprocal depressions in I, aVL, V1, and V2.  Type I blocks are common in inferior wall M.I., since the AV node and the inferior wall often share a blood supply - the right coronary artery. 

While the print quality of this ECG is not the best, it is a great teaching ECG because it starts out with 2:1 conduction, then at the end of the strip, proves itself to be a Wenckebach block.   

Acute Inferior Wall M.I. With Right Ventricular M.I. and Atrial Fibrillation

Tue, 05/19/2015 - 11:10 -- Dawn

This 31-year-old man presented to the Emergency Dept. complaining of chest pain, shortness of breath, and nausea. His heart rate on admission was 120 - 130 bpm and irregular, and the monitor showed atrial fibrillation. His rate slowed with the administration of diltiazem. His 12-lead ECG shows the classic ST elevation of inferior wall M.I. in Leads II, III, and aVF. This patient also had JVD, bibasilar rales, orthopnea, and exertional dyspnea, signs of CHF. He had no history of acute M.I., CHF, or atrial fibrillation. He offered no history of drug use or medications.

This ECG is very useful for the basic student, in that the ST elevations are readily seen, and the atrial fib is definitely irregularly-irregular. For the more advanced student, the ST depression in V2 indicates posterior wall injury, while the flat ST segment in V1 indicates a possible right ventricular M.I.  While the posterior wall is trying to depress the ST segment, the right ventricle is trying to elevate it, resulting in flattening. Also, Lead III has a greater STE than Lead II, which has been shown to be a reliable indicator of RV infarction.  This should be confirmed with a V4 right, or all chest leads done on the right side. Right ventricular injury has been shown to increase mortality, and it also requires different management of hemodynamics.

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