Myocardial Infarction

Question 1

Primary vascular supply of myocardium

Answer 1

Coronary artery (arises from the aorta and runs along epicardial muscle before penetrating myocardium)
Blood flow occurs during ventricular systole

Question 2

Secondary vascularisation

Answer 2

LHS main trunk > L anterior descending supplies apex/anterior LV wall/anterior 66% of ventricular septum
LHS main trunk > L circumflex which supplies lateral wall of LV
RHS coronary > supplies RV/posterior basal wall of LV/posterior 33% of ventricular septum

Question 3

Ischemic HD

Answer 3

Group of syndromes arising from myocardial ischemia
Reduced supply due to reduced blood flow/increased demand (shock/hypertrophy)
Leads to stenosis/angina/MI/HF/SCD

Question 4

Etiology of MI

Answer 4

Acute plaque change (fissure/ulceration)
Inflammation
Coronary embolism/thrombus (large- st segment elevation MI and vice versa)
Vasoconstriction
Fixed coronary obstruction can be acute/chronic (leads to IHD)

Question 5

Pathophysiology of MI

Answer 5

Coronary ath - narrowing/obstruction
Thrombus formation
Alteration in myocardial blood flow

Question 6

Macroscopic changes

Answer 6

0-12 hours no change/light mottling
12-24 hours dark mottling
3-7 days peripherally red with yellow core
2-8 weeks grey white scar

Question 7

Microscopic changes

Answer 7

4-12 hours coag necrosis/Hm/edema
12-24 hours nuclear pyknosis/N and E infiltrate
1-3 days coag necrosis/N infiltrate
2 months dense collagenous scar

Question 8

Cellular changes

Answer 8

Infarct extension (new myocardial necrosis) 
Infarct expansion (thinning of infarct zone)
Ventricular thinning and dilation

Question 9

Considerations

Answer 9

MI takes hours to complete
Heart is sensitive to ischemia changes >20 mins leads to necrosis
Necrosis is sequential subendocardium-heart wall
Tissue salvaged if flow restored within 6 hours

Question 10

Transmural MI

Answer 10

Involved full thickness of heart wall
Caused by focal damage/thrombus on ath plaque
Small MI leads to dyskinesia
Large MI leads to akinesia&raquo_space; reduced pump/sys/Dias functions

Question 11

Subendocardial MI

Answer 11

Involves inner 1/3 to 1/2 of ventricular wall

Caused by circumferential damage- hypotension/shock/reduced blood volume/lysed thrombi

Question 12

MI location and outcomes

Answer 12

Anterior septal wall- hemodynamic compromise/altered IV conduction/congestive HF/pulm edema/shock
L/P/I walls of LV and RV wall- hemodynamic disturbances/arrhythmia as blood supply AV/SA nodes is compromised

Question 13

Effects of MI

Answer 13

Contractile dysfunction
Arrhythmia
Pericarditis
Cardiac rupture and SCD

Question 14

MI complications

Answer 14

Infarct extension
Ventricular aneurysm
Mural thrombi
Myocardial rupture

Question 15

Ischemic heart disease

Answer 15

Subendocardial damage
Myocyte vacuolisation
Membrane and Mit disturbances

Question 16

IHD microscopic changes

Answer 16

0-12 hours no change
3 days N infiltrate and coag necrosis
1-2 weeks GT
3 weeks-2 months fine scar>dense scar

Question 17

IHD staining

Answer 17

Triphenyl tetrazolium chloride stains brown with LDH

Unstained-infarction/stained-viable tissue/white-scar

Question 18

Chronic IHD

Answer 18

Observed in transplant/MI/CABG
Compromised ventricular function
Leads to myocyte hypertrophy and vacuolisation

Question 19

MI treatment

Answer 19

Restoration of blood flow and clot lysis
Thrombolytic drugs
CABG/per cutaneous transluminal coronary angioplasty

Question 20

Sudden cardiac death

Answer 20

Unexpected death in one hour due to cardiac causes
With out without prior symptoms
Affects young athletes with IHD/p-HTN/long QT syndrome/defective sodium or potassium channels
Mortality ass. To ventricular fibrillation/arrhythmia
Enlarged heart/myocyte Ht and Vac