myocardial infarction case analyse

Editorial Team / Admin · Apr 10, 2014

A very good site for information r/t ICU is ICUFAQs.org: http://www.icufaqs.org/

This has some good info at the end (focus on the anterior MI): Myocardial Infarction - ECGpedia

It also gives clues how the VS may change.

Need to check cardiac enzymes ("markers"), are they elevated?

Rise in enyzmes, plus clinical presentation plus ECG changes combine for the diagnosis of acute ST-elevation MI (STEMI).

Read up on anterior STEMI.

The ST depression you see is most likely reciprocal changes in the ECG, r/t the evolving MI.

Gotta go, do your research, will check later.

Esme12, ASN, BSN, RN · Apr 10, 2014

THINK about your cardiac anatomy and what an interruption of the blood flow means to that area of the heart.

[TABLE]

[TR]

[TD]Wall[/TD]

[TD] Artery Lead[/TD]

[TD] Reciprocal Wall[/TD]

[TD] Reciprocal Leads[/TD]

[/TR]

[TR]

[TD] Inferior[/TD]

[TD] RCA II, III, aVF

[/TD]

[TD] Lateral[/TD]

[TD] I, aVL[/TD]

[/TR]

[TR]

[TD] Anterior[/TD]

[TD] LAD V3, V4[/TD]

[TD] Inferior[/TD]

[TD] II, III, aVF[/TD]

[/TR]

[TR]

[TD] Lateral[/TD]

[TD] Cx I, aVL, V5, V6[/TD]

[TD] Inferior[/TD]

[TD] II, III, aVF[/TD]

[/TR]

[/TABLE]

Esme12, ASN, BSN, RN · Apr 10, 2014

Now that you know it is the anterior wall ....which is the left ventricle. How does this affect your patient. Tell us what your research has revealed to you and what you think?

zergling8 · Apr 11, 2014

Now that you know it is the anterior wall ....which is the left ventricle. How does this affect your patient. Tell us what your research has revealed to you and what you think?

I

II: ST elevation

III: ST depression

V1: seems ok

V2: ST elevation

V3: ST elevation

V4: ST elevation

V5

V6: ST elevation

aVL

aVF: seems ok

aVR: seems not P wave??

...........I am not sure if my interpreting is right...........and I dont know what happened with Lead I, V, aVL and aVR....

um..........the function of left ventricle is to fill rapidly with oxygenated blood flowing from the lung veins, contract rapidly and forcibly to force the majority of this blood into the aorta. The V2,3,4 ST elevation on ECG indicates anferior wall infarction, so the left anterior descending artery might be blocked completely?? less blood supply to subendocardial ? transmural..? then the contractility of left ventricle decrease and same with the function of dialation------less oxygenated blood being delivered to the body --- pump failure?? (Patient is pale), it also causes the decrease of gas exchange and pulmonary ventilation----> hypoxia??--- increase RR and decrease O2 sats?

The repolarization phase of the T wave and ST segment is usually the first to be involved during myocardial ischemia and injury. As the involved area becomes ischemic, myocardial repolarization is altered, causeing changes in T wave. Acute severe ischemia reduces the resting membrane potential and shortens the duration of the action potential in the ischemic area. these changes create a voltage difference between the mornal and ischemic areas of the myocardium that leads to a current of inury between these regions

it says that anterior wall infarction causes tachycardia and hypotension but why this patient's HR is normal and BP is slightly high???

and with regard to the ECG, is there any other problems, I cant read Lead I, V, aVL and aVR........and does he also have a lateral infarction????

Thank you

Esme12, ASN, BSN, RN · Apr 11, 2014

If you look at the isoelectric line (in this EKG the "PR" interval) that squiggly little something is the QRS and yes there is ST elevation. AVL is Q'd indication death of the myocardium. There is ST elevation of L1, AVL, V2-6. Lead II MIGHT be ischemic but it needs to be reflected in 2 leads AND at least 2mm in height to be clinically significant and it probably related to strain. http://www.fpnotebook.com/CV/CAD/ElctrcrdgrmInMycrdlInfrctn.htm

Anterior wall MI's are known for tachyarrythmia. The Left ventricle is irritated and can be prone to V Tach/V Fib. With death of the pumping chamber the danger is pump failure and cardiogenic shock. This population the listening of heart tones can be significant for the cardiac system supplies the papillary muscle which supplies blood to the mitral valve. Especially in the presence of the lateral wall changes.

Please read this.....Complications of Acute Myocardial Infarction

The presence of a low B/P is an ominous sign of pump failure and cardiogenic shock. The B/P is elevated here due to the strain of the heart pumping chamber being compromised and is straining (having to work harder) to keep up with demand....as well as anxiety and pain. Look here.....Critical Care Medicine Tutorials: Shock

Esme12, ASN, BSN, RN · Apr 11, 2014

check out ICUFAQ's.org

[h=3]Localizing Infarcts On a 12-Lead EKG - Icufaqs.org[/h]

Esme12, ASN, BSN, RN · Apr 11, 2014

The repolarization phase of the T wave and ST segment is usually the first to be involved during myocardial ischemia and injury. As the involved area becomes ischemic, myocardial repolarization is altered, causing changes in T wave. Acute severe ischemia reduces the resting membrane potential and shortens the duration of the action potential in the ischemic area. these changes create a voltage difference between the normal and ischemic areas of the myocardium that leads to a current of injury between these regions
Thank you

The two main types of acute myocardial infarction

Transmural AMI is associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral, or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply.In addition, on ECG, ST elevation and Q waves are seen.
Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.

Acute Myocardial Infarction

The ECG remains a key test in the diagnosis of acute and chronic coronary syndromes.The findings vary considerably, depending importantly on four major factors: (1) the duration of the ischemic process (acute vs. evolving/chronic), (2) its extent (transmural vs. subendocardial), (3) its topography (anterior vs. inferior-posterior and right ventricular), and (4) the presence of other underlying abnormalities (e.g., LBBB, Wolff-Parkinson-White [WPW], or pacemaker patterns) that can mask or alter the classic patterns.
Repolarization (ST-T Wave) Abnormalities
The earliest and most consistent ECG finding during acute ischemia is deviation of the ST segment as a result of a current-of-injury mechanism. Under normal conditions, the ST segment is usually nearly isoelectric (i.e., flat along the baseline) because healthy myocardial cells attain approximately the same potential during early repolarization, which corresponds to the plateau phase of the ventricular action potential. Ischemia has complex time-dependent effects on the electrical properties of myocardial cells. Severe, acute ischemia can reduce the resting membrane potential, shorten the duration of the action potential in the ischemic area, and also decrease the rate of rise and amplitude of phase 0.These changes cause a voltage gradient between normal and ischemic zones that leads to current flow between these regions. These currents of injury are represented on the surface ECG by deviation of the ST segment.