cardio

Question 1

Anterior STEMI EKG?

Answer 1

I, aVL, Ant leads (v3-v4)

Question 2

Which carries poorest prognosis? Anterior MI or inferior MI?

Answer 2

Anterior STEMI + NSTEMI

Comparing anterior vs inferior MI, patients with anterior MI had higher incidences of:

In-hospital mortality (11.9 vs 2.8%)
Total mortality (27 vs 11%)
Heart failure (41 vs 15%)
Significant ventricular ectopic activity (70 vs 59%)
Lower ejection fraction on admission (38 vs 55%)

Question 3

Anterolateral MI EKG

Answer 3

I, aVL, Anterior leads (v3, v4), Lateral leads (v5, v6)

Question 4

anterior STEMI occludes which artery?

Answer 4

LAD

Question 5

Precordial leads

Answer 5

Septal leads = V1-2
Anterior leads = V3-4
Lateral leads = V5-6

Question 6

Infarct patterns on EKG

Answer 6

Septal = V1-2
Anterior = V2-5
Anteroseptal = V1-4
Anterolateral = V3-6, I + aVL
Extensive anterior / anterolateral = V1-6, I + aVL

Question 7

Unstable tachycardia

Answer 7

Immediate electrical cardio version

Question 8

Hypertrophic cardiomyopathy? types?

Answer 8

2nd most common cardiomyopathy

Most common hereditary heart disease

Autosomal dominant

Obstructive (HOCM) 70%: HCM with left ventricular outflow tract obstruction (LVOTO) that is dynamic

Non-obstructive HCM 30% : Hypertrophic cardiomyopathy without obstruction of the left ventricular outflow tract (LVOT)

one of the most frequent causes of sudden cardiac death in young patients, especially young athletes

Question 9

sequelae of HCM to SCD

Answer 9

hypertrophy of the left ventricle with asymmetrical septal involvement → diastolic dysfunction (impaired left ventricular relaxation and filling) → reduced systolic output volume → reduced peripheral and myocardial perfusion → cardiac arrhythmia and/or heart failure → increased risk of sudden cardiac death

Question 10

Features of HCM

Answer 10

1. Inc LV wall thickness with septal predominance (no LV dilation)
2. Myofibrillar disarray, interstitial fibrosis, and myocyte hypertrophy
3. Concentric hypertrophy: cardiac remodeling → parallel duplication of sarcomeres → left ventricular wall thickening

Question 11

Concentric hypertrophy other causes

Answer 11

Chronic hypertension
Aortic stenosis
Storage disorders (Fabry disease, amyloidosis)
hereditary syndromes ( Friedreich ataxia, Noonan syndrome)

Mechanism:
Chronic hypertension → increased afterload → increased myocardial wall tension → changes in myocardial gene expression → sarcomeres laid down in parallel → increased left ventricular thickness → decreased left ventricular size → diastolic dysfunction

Question 12

Mechanism of action of statin

Answer 12

Competitive inhibition of enzyme HMG-CoA reductase leads to upregulation of hepatocytes LDL receptors.

Question 13

Adverse effects of statin

Answer 13

Hepatic: ↑ LFTs
Muscular: Statins decrease the synthesis of coenzyme Q10 and impair energy production within the muscle.
Myalgia: continue treatment as long as creatinine phosphokinase (CK) remain normal
Statin-associated myopathy
Muscle pain and weakness, especially when used alongside fibrates or niacin
Myositis: ↑ CK
May progress to rhabdomyolysis; AKI (↑ BUN and ↑ creatinine)
Management: discontinue statin therapy for 2–4 weeks; start treatment with a low-dose statin (e.g., pravastatin or fluvastatin) once symptoms have resolved

Question 14

Handgrip increases which murmurs

Answer 14

Aortic Regurgitation
Mitral regurgitation
ASD
VSD

Question 15

Handgrip , valsalva and standing from squatting decrease the intensity of murmur of?

Answer 15

Aortic stenosis

Question 16

Auscultation in Aortic stenosis

Answer 16

Auscultation
Harsh crescendo-decrescendo (diamond-shaped), late systolic ejection murmur radiates b/l to the carotids
Soft S2
S4 is best heard at the apex.
Early systolic ejection click

Question 17

Indications of statin

Answer 17

High intensity statins:
Clinical ASCVD (CAD, stroke, peripheral arterial disease) , LDL cholesterol levels > 190mg/dl

Low to moderate intensity
Primary Prevention of ASCVD

Question 18

Interactions of statin

Answer 18

CYP3A4 INHIBITORS

Question 19

Mechanism of action of adenosine

Answer 19

activates Gi protein → inhibition of adenylate cyclase → ↓ cAMP → deactivation of L-type Ca2+ channels and activation of K+ channels → ↓ Ca2+ and ↑ K+ efflux → hyperpolarization → transient AV node block (short-acting, ∼ 15 seconds) → acute termination of supraventricular tachycardia

Question 20

Adverse effects of adenosine

Answer 20

Flushing
Hypotension
Chest pain
Sense of impending doom
AV block
Asystole

Question 21

Contraindications to adenosine

Answer 21

Pre-excitation syndromes: antidromic AVRT, WPW
AV block
Asthma

Question 22

HOCM pathomechanism

Answer 22

LVOT obstruction

Question 23

MI and their territories

Answer 23

extensive Anterior MI - Proximal LAD
Septal MI - LAD
Anterior MI - Distal LAD
Ant.Lateral MI - LCX
Lateral MI - Proximal LCX
Inferior MI
(Right ventricle MI) - RCA (more common)
- distal LCX (less common)
Posterior MI - Post Dec. Artery ( from RCA or LCX)