WorksheetsGroup 6 AIIMS Rajkot
Total questions: 10
Worksheet time: 6mins
A 62-year-old male presents with crushing chest pain. His ECG shows 3mm ST-elevation in leads V2-V4. According to the "Vector Theory" of the injury current, why does the ST segment appear elevated in these leads
The electrical vector points away from the infarcted tissue
The vector points towards the area of transmural (full-thickness) damage.
The "Window Effect" allows the electrode to see the opposite wall
Leaky membranes cause a constant voltage difference that shifts the baseline downward.
Which of the following best describes the progression of atherosclerosis as it leads to an acute Myocardial Infarction (MI)
Foam cells, Fatty streak ,Atheroma, Plaque Rupture, Thrombus
Stenosis, Endothelial injury, Hyperlipidemia ,Rupture.
Fibro-atheroma, Smooth muscle accumulation, Fatty streak, Rupture
Damage, Stenosis, Ischemia, Plaque formation.
A patient’s ECG reveals "Sawtooth" F-waves with a 2:1 conduction block. According to the ECG Diagnosis Master Flowchart, this should be classified as:
A-Fib
SVT
A-Flutter
V-Tach
In the "Evolution of a STEMI," which ECG finding typically represents the "Marker of Necrosis" and appears hours to days after the initial insult?
Hyperacute T waves
ST-segment elevation
Pathological Q waves
T wave inversion
What is the fundamental physiological "Problem" in Ischemic Heart Disease
A primary electrical failure of the SA node
A mismatch between myocardial oxygen demand and the body’s ability to supply it
The accumulation of calcium in the pericardial sac
An increase in the "Injury Vector" magnitude beyond $200\text{ms}$.
Which pharmacological agent is specifically used in the management of IHD to "stabilize plaques" and improve long-term clinical outcomes
Nitrates
High-intensity Statins
Morphine
Unfractionated Heparin (UFH)
According to the "Window Theory," a Pathological Q wave occurs because
he tissue is hyper-excitable, creating a large negative deflection
The electrode looks through electrically silent dead tissue to see activation moving away
The PR interval is fixed at>200ms
There is a "scooped" ST depression caused by Digoxin.
A patient is diagnosed with an NSTEMI (Subendocardial Ischemia). Which statement regarding the damage is correct?
There is 100% complete occlusion of the coronary artery.
The entire thickness of the wall from endocardium to epicardium is necrotic
Only the innermost layer (subendocardium) is starving, while the outer layer remains viable.
The ECG will primarily show ST elevation $>1\text{mm}$.
In the "Immediate Assessment" of a patient with suspected ACS, what is the specific threshold for initiating Oxygen Therapy?
Whenever the patient feels anxious
If SpO2<94% on room air
If SpO2<90% or the patient is in respiratory distress
Only after the first dose of Aspirin is administered.
What is the "Gold Standard" reperfusion therapy for a STEMI, and what is the target "Door-to-Balloon" time?
Thrombolysis; < 12 hours
Primary PCI; < 90 minutes
Beta-blockers; < 60 minutes
Coronary Artery Bypass Graft (CABG); < 24 hours.
