25 Myocardial Infarction and its sequelae Flashcards

1
Q

What are the 16 LV segments and which coronary artery supplies every segment and how are the 16 LV segments scored?

A

The 16 segment model divides the LV into thirds (basal, mid and apical) and divides the basal and mid into sixths (anterior, anterolateral, inferolateral, inferior, inferoseptal and anteroseptal) and the apex into quarters (anterior, lateral, inferior and septal).

Normal wall motion during systole is defined as endocardial excursion >5mm and wall thickening >50%.

X = unable to asses, 1 = normokinetic, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic, 5 = aneurysmal.

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2
Q

What is myocardial ischemia and what is myocardial infarction?

A

Myocardial ischemia is secondary to atherosclerotic plaque development in one or more coronary arteries which decreases blood flow to the myocardium. If the artery is >70% obstructed, the patient is likely to develop chest pain.

Myocardial infarction is secondary to atherosclerotic plaque rupture. This causes the development of a thrombus which obstructs blood flow to the myocardium. If this causes myocardial necrosis, cardiac biomarkers increase.

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3
Q

How are myocardial ischemia/infarction assessed?

A

Normally, in ischemia, the myocardium is normokinetic at rest and hypokinetic or akinetic with stress.

Normally, post-MI, areas of myocardial necrosis are akinetic or hypokinetic at rest and stress. However, areas f myocardial stunning or hibernation may show a small increase in LV function with stress.

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4
Q

What are the 8 possible MI complications?

A

VSD, papillary muscle rupture, cardiac tamponade, cardiogenic shock, myocardial scarring, LV aneurysm, mural thrombus and Dressler’s syndrome.

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5
Q

Post-MI, how is a VSD caused and how is it assessed?

A

Post-MI, IVS necrosis and rupture causes a VSD. VSDs are simple (direct) or complex (indirect).

Anterior MIs may cause apical VSDs and inferior MIs may cause basal inferoseptal VSDs.

TTE shows flow from left to right across the IVS and therefore RV volume overload and acute right sided HF.

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6
Q

Post-MI, how is papillary muscle rupture caused and how is it assessed?

A

Post-MI, papillary muscle dysfunction or rupture causes acute severe MR.

An inferior MI causing posteromedial papillary muscle rupture is more common because the papillary muscle is supplied by one coronary artery.

TTE shows MV leaflet prolapse or flail and severe MR.

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7
Q

Post-MI, how is a cardiac tamponade caused and how is it assessed?

A

Post-MI, ventricular free wall rupture causes blood to build up in the pericardium. This causes a pericardial effusion and cardiac tamponade.

TTE shows flow between the heart and the pericardium, a possible thrombus, a pericardial effusion localised to the akinetic LV segment, RA collapse, IVC dilatation with decreased inspiratory collapse and increased MV/TV respiratory variation.

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8
Q

Post-MI, how is cardiogenic shock caused and how is it assessed?

A

Post-MI, cardiogenic shock is characterised by decreased CO hypotension, and other complications.

TTE shows global LV hypokinesis other complications (e.g. VSD).

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9
Q

Post-MI, how is myocardial scarring caused and how is it assessed?

A

Post-MI, the necrotic myocardial tissue is replaced with fibrous scar tissue.

TTE shows echogenic, thin and akinetic LV segments.

Use stress echo to assess myocardial viability.

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10
Q

Post-MI, how is an LV aneurysm caused and how is it assessed?

A

Post-MI, the necrotic myocardial tissue is replaced with fibrous scar tissue. The LV walls are thin and weak so bulge into the LV during systole.

TTE shows thin and scarred akinetic or dyskinetic segments which bulge into the LV.

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11
Q

Post-MI, how is a mural thrombus caused and how is it assessed?

A

Post-MI, LV akinesis and LV aneurysms cause blood stasis which increases the risk of thrombus formation, particularly at the LV apex.

TTE shows an echogenic mass attached to the LV wall, particularly at the LV apex.

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12
Q

Post-MI, how is Dressler’s syndrome caused and how is it assessed?

A

Dressler’s syndrome (post-MI syndrome) is a form of pericarditis (pericardial inflammation). It is due to an autoimmune response to the necrotic myocardial tissue. It occurs in the weeks following an MI.

TTE shows a pericardial effusion and/or a thickened pericardium.

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13
Q

What is takotsubo cardiomyopathy?

A

A rare stress cardiomyopathy which causes ballooning of the LV apex which normally recovers within 2 months. Patients present with chest pain and/or HF and ST elevation in the absence of CAD.

Takotsubo’s cardiomyopathy causes temporary LV dysfunction but an MI can cause permanent LV dysfunction.

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14
Q

How are aneurysms and pseudo aneurysms differentiated?

A

True aneurysms have a wide neck (>50% of the diameter of the aneurysm) and are lined with the myocardium.

Pseudoaneurysms have a narrow neck (<50% of the diameter of the aneurysm) and break the myocardium so are lined with the pericardium.

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