1. How to diagnose STEMI?

Answer:
STEMI must be differentiated with unstable angina pectoris and NSTEMI. Chest
pain always be the most important symptom in patient with acute coronary syndrome.
Pain which is usually described as pressure, squeezing, or a burning sensation across the
precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either
arm. STEMI is when there is a transmural infarction of the myocardium - which just
means that the entire thickness of the myocardium has undergone necrosis - resulting in
ST elevation. Usually due to a complete block of a coronary artery (occlusive thrombus).
Therefor, UA or NSTEMI is when there is a partial dynamic block to coronary arteries
(non-occlusive thrombus). There will be no ST elevation or Q waves on ECG. The main
difference between NSTEMI and unstable angina is that in NSTEMI the severity of
ischemia is sufficient to cause cardiac enzyme elevation. In unstable angina, the cardiac
enzymes remain normal or are only very minimally elevated.
2. How is the pathophysiology of ACS?
Answer:
Substance known as tissue factor is located within the necrotic core of the plaque.
When exposed to the bloodstream, tissue factor activates the clotting cascade and
thrombosis occurs. Tissue factor is exposed when the fibrous cap that covers the plaque
becomes disrupted or ulcerated. This disruption of the fibrous cap is called plaque
rupture or plaque erosion.
Plaque rupture and plaque erosion (ulceration) can result in coronary thrombosis.
STEMI is most often from coronary thrombosis after plaque rupture and less often from
fixed obstruction. Unstable angina has a lower incidence of coronary thrombosis
compared to NSTEMI or STEMI and is more often the result of fixed atherosclerotic
stenosis. Plaque rupture (most common) or erosion resulting in coronary occlusion is the
predominant mechanism in NSTEMI and STEMI.

3. What is KILLIP Classification?

Answer:
Killip classification
Class 1 No rales, no3rd heart sound
Class 2 Rales in<12 lung field or presence of a 3rd heart sound
Class 3 Rales in>12 lung fieldpulmonary edema
Class 4 Cardiogenicshockdeterminedclinically
4. In your presentation your diagnose is inferior STEMI, what is the ECG findings
of inferior STEMI?
Answer:
An inferior wall myocardial infarction (IWMI, inferior MI or inferior STEMI) occurs
when inferior myocardial tissue supplied by the right coronary artery (RCA), is injured
due to thrombosis of that vessel. The ECG findings of an acute inferior myocardial
infarction include:
a.

ST segment elevation in the inferior leads (II, III, and aVF)

b.

Reciprocal ST segment depression in the lateral and/or high lateral leads (I,
aVL, V5 and V6)

5. What is the evolution of electrocardiographic changes in ST-segment elevation

myocardial infarction?
Answer:
1. Hyperacute T waves: The earliest sign of acute myocardial infarction are T waves
become more prominent, symetrical and pointed.
2. ST segments changes
3. Pathological Q waves
4. Resolution of changes in ST segment and T waves
5. Reciprocal ST segment depression

6. Why is streptase used in treating STEMI?

Answer:
ST elevation myocardial infarction (STEMI) most commonly occurs when thrombus
formation results in complete occlusion of a major epicardial coronary vessel. This
requires the use of thrombolytics like Streptokinase to lyse the thrombus. Evidence has
proven that it is very effective and not as risky (Benefits > Risk). Fibrinolytic therapy
must be instituted within 24 hours of symptom onset. After this time frame, fibrinolytic
therapy is contraindicated and likely will not be effective.
Patients with STEMI usually have complete occlusion of an epicardial coronary
vessel caused by an acute thrombotic obstruction. The earlier the patient presents, and the
earlier the artery can be recanalized, the better. The benefits of fibrinolytic therapy are
well established during the initial 12 hours after symptom onset. The new guidelines
mention that you should consider administration of a fibrinolytic agent in symptomatic
patients presenting more than 12 to 24 hours after symptom onset with STEMI affecting a
large area of myocardium or hemodynamic instability if PCI is not available.
Fibrinolytic therapy is a proven treatment for the management of acute MI (AMI). It
is more universally available to patients without contraindications, can be administered
by any properly trained health care provider, and can be given in the prehospital setting.
Its efficacy declines as the duration of ischemia increases. The goal is a door-to-needle
time of less than 30 minutes, and every effort must be made to minimize the time to
therapy. Patients older than 75 years derive significant benefit from fibrinolytic therapy,
even though their risk of bleeding is higher. Fibrinolytic agents are given in conjunction
with antithrombin and antiplatelet agents, which help to maintain vessel patency once the
clot has been dissolve.
The adult dose of streptokinase for AMI is 1.5 million U in 50 mL of 5% dextrose in
water (D5W) given IV over 60 minutes.

7.

How does diabetes mellitus causes myocardial infarction?

Answer:
Abnormalities in endothelial and vascular smooth muscle cell function, as well as a
propensity to thrombosis, contribute to atherosclerosis and its complications. Endothelial
cells, regulate vascular function and structure. In normal endothelial cells, biologically
active substances are synthesized and released to maintain vascular homeostasis, ensuring
adequate blood flow and nutrient delivery while preventing thrombosis and leukocyte
diapedesis. Among the important molecules synthesized by the endothelial cell is nitric
oxide (NO), which is constitutively produced by endothelial NO synthase (eNOS). O
protects the blood vessel from endogenous injury. Many of the metabolic derangements
known to occur in diabetes, including hyperglycemia, excess free fatty acid liberation,
and insulin resistance, mediate abnormalities in endothelial cell function by affecting the
synthesis or degradation of NO.

Type
2 diabetes
mellitus is

characterized by insulin resistance. Insulin stimulates NO production from endothelial

cells by increasing the activity of NOS. The pathophysiology of vascular disease in
diabetes involves abnormalities in endothelial, vascular smooth muscle cell, and platelet
function. The metabolic abnormalities that characterize diabetes, such as hyperglycemia,
increased free fatty acids, and insulin resistance, each provoke molecular mechanisms
that contribute to vascular dysfunction. These include decreased bioavailability of NO,
increased oxidative stress, disturbances of intracellular signal transduction, and activation

of receptors for AGEs. In addition, platelet function is abnormal, and there is increased
production of several prothrombotic factors. These abnormalities contribute to the
cellular events that cause atherosclerosis and subsequently increase the risk of the adverse
cardiovascular events that occur in patients with diabetes and atherosclerosis.
8.

What are the complications of STEMI?

Answer:
Complications of MI include arrhythmic, mechanical, and inflammatory (early

pericarditis and post-MI syndrome) sequelae.

Arrhytmic
Myocard infarction is characterized by generalized autonomic dysfunction that
results in enhanced automaticity of the myocardium and conduction system. Enhanced
efferent sympathetic activity, increased concentrations of circulating catecholamines, and
local release of catecholamines from nerve endings in the heart muscle itself have been
proposed to play roles in the development of peri-infarction arrhythmias. Peri-infarction
arrhythmias can be broadly classified into the following categories:
a.

Supraventricular tachyarrhythmias, including sinus tachycardia, premature atrial

contractions, paroxysmal supraventricular tachycardia, atrial flutter, and atrial
fibrillation

b.

Accelerated junctional rhythms

c.

Bradyarrhythmias, including sinus bradycardia and junctional bradycardia

d.

Atrioventricular (AV) blocks, including first-degree AV block, second-degree AV

block, and third-degree AV block

e.

Intraventricular blocks, including left anterior fascicular block, right bundle branch
block (RBBB), and left bundle branch block (LBBB)

f.

Ventricular arrhythmias, including premature ventricular contractions (PVCs),

accelerated idioventricular rhythm, ventricular tachycardia, and ventricular
fibrillation

g.

Reperfusion arrhythmias

The 3 major mechanical complications of AMI are ventricular free wall rupture
(VFWR), ventricular septal rupture (VSR), and papillary muscle rupture with severe
mitral regurgitation (MR). Associated with large transmural infarctions.
Left ventricular mural thrombus, LVMT is a well-known complication of AMI
and frequently develops after anterior infarcts of the LV wall. contributing to LVMT
formation include LV regional-wall akinesia or dyskinesia with blood stasis, injury to and
inflammation of the endocardial tissue that provides a thrombogenic surface, and a
hypercoagulable state.
Pericarditis is caused by inflammation of pericardial tissue overlying infarcted
myocardium. The clinical presentation may include severe chest pain, usually pleuritic,
and pericardial friction rub.
Post-MI syndrome (Dressler syndrome), post-MI syndrome is considered to be an
autoimmune process. Clinical features include fever, chest pain, and other signs and
symptoms of pericarditis occurring 2-3 weeks after AMI. Management involves
hospitalization and observation for any evidence of cardiac tamponade. Treatment
comprises rest, use of NSAIDs, and/or steroids in patients with recurrent post-MI
syndrome with disabling symptoms.