Cardiovascular

Question 1

What is the etiology of Acute Coronary Syndrome (ACS)?

Answer 1

Atherosclerotic plaque rupture → thrombus formation → myocardial ischemia.

Question 2

W/U for chest pain (4)

Answer 2

1. EKG
2. CXR
3. Troponins
4. D-dimer (r/o PE)

(DDX: ACS, pericarditis, PE, GERD, MSK pain)

Question 3

7 Risk Factors: ACS

Answer 3

1. hypertension
2. hyperlipidemia
3. diabetes
4. smoking
5. family history of coronary artery disease
6. age
7. obesity

Question 4

How is ACS evaluated?

Answer 4

1. ECG: STEMI (ST elevation), NSTEMI (ST depressions/T-wave inversions)
2. Troponins: Elevated

Question 5

What is the treatment for ACS?

(Immediate vs. Definitive)

Answer 5

Immediate: MONA (Morphine, Oxygen, Nitroglycerin, Aspirin)
Definitive: STEMI (PCI or fibrinolysis), NSTEMI (DAPT, anticoagulation, beta-blockers, PCI depends on risk stratification).

(DAPT = dual anti-platelet = aspirin + P2Y12 inhibitor i.e. clopidogrel, Anticoagulation = heparin, enoxaprin or bivalirudin)

Question 6

Risk stratification: ACS

(determines tx: PCI vs. medical management)

Answer 6

TIMI score (used in ER, predicts 30 day mortality)
GRACE score (used for long-term risk)

(if both are high = PCI, if STEMI→ straight to PCI)

High TIMI > 3; high Grace > 140

Question 7

What are the 5 MC complications of ACS?

Answer 7

1. Arrhythmia → V-fib/V-tach → sudden cardiac death
2. Rupture → Papillary muscle, septum, free wall (3-7 days)
3. Refractory HF→ Cardiogenic shock
4. Pericarditis → Early = fibrinous, Late = Dressler
5. Dilated aneurysm → Persistent ST elevations + thrombus risk

(mnemonic ARRP-D)

Question 8

tx: post-MI pericarditis

Answer 8

1. NSAIDs (high-dose aspirin)
2. colchicine
3. steroids (if refractory)

(remember: Dresslers syndrome is just auto-AB to the necrotic tissue/pericarditis. Both are pericarditis, but different pathophys. same tx)

Question 9

What is the mnemonic for Virchow’s Triad?

Answer 9

SHE:
* Stasis
* Hypercoagulability
* Endothelial injury

Question 10

CAD can progress to heart failure by which 2 main mechanisms?

(HFrEF or HFpEF)

Answer 10

1. ACS or MI →HFrEF
2. Ischemic cardiomyopathy→fibrosis) →HFpEF

Question 11

ECG findings of CAD vs. ACS?

Answer 11

• CAD: Normal or ST depressions during exertion (stress test)
• ACS: ST elevations (STEMI) or ST depressions/T-wave inversions (NSTEMI/UA)

(CAD is essentially the precursor to ACS, tx by reducing risk factors)

Question 12

CAD tx (3 general)

Answer 12

1. Rx: statins, aspirin, beta-blockers, ACE inhibitors
2. revascularization if severe
3. Lifestyle changes to risk factors (smoking cessation, obesity, sedentary life, diet)

Question 13

CAD gold standard dx test

Answer 13

coronary angiography

(stress test commonly used)

Question 14

when would you NOT use B-blockers in HF?

Answer 14

acute decompensation

Question 15

4 clinical findings of aortic regurgitation

Answer 15

1. de Musset sign (head bobbing wpulse)
2. “water-hammer” pulse
3. Quincke pulse (pulsing nail bed)
4. CHF sings: ortopnea, pulm edema, dyspnea on exertion

Question 16

S4 presents as a low-pitched, extra heart sound heard immediately prior to S1. it is most commonly the result of…

(Usu normal in adults aged > 70 years)

Answer 16

concentric LVH secondary to long-standing hypertension.

(Other potential causes include acute myocardial infarction and restrictive cardiomyopathy)

Question 17

What makes a Q wave pathologic

Answer 17

deep or wide

Question 18

Best diagnostic test for AAA?

Answer 18

CT: abdomen, chest pelvis = intimal flap w/false lumen

Question 19

pulses paradoxis is indicitive of which dx?

(decrease in systolic pressure > 10 mmHg w/inspiration)

Answer 19

cardiac tamponade

(becks triad, dilated IVC, collapsing atria and low voltage ECG also seen)

Question 20

Beck triad: hypotension, JVD, muffled heart sounds indicates which diagnosis?

(also dilated IVC, collapsable atria and low voltage ECG)

Answer 20

cardiac tamponade

(Sudden collapse + tamponade signs 5-7 days after MI? Free wall rupture.)

Question 21

Which 3 conditions cause pleuritic chest pain?

Answer 21

1. PE
2. Pleural effusion
3. Pericarditis

Question 22

• Restrictive Cardiomyopathy is … (HFrEF/HFpEF)
• Dialated Cardiomyopathy is … (HFrEF/HFpEF)

Answer 22

• RCM = HFpEF → S4 gallop
• DCM = HFrEF → S3 gallop

(at first!)

Question 23

How can you distinguish between the presentation of RCM and DCM?

(initial disease process of restrictive or dilated cardiomyopathy)

Answer 23

• RCM: Right-sided heart failure symptoms (JVD, peripheral edema, hepatomegaly, ascites), Kussmal signs (JVP↑ with inspiration)
• DCM: Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), displaced PMI laterally

Question 24

Echo findings: RCM vs. DCM

(initial disease process of restrictive or dilated cardiomyopathy)

Answer 24

• RCM: Biatrial enlargement, normal LV size, stiff myocardium, diastolic dysfunction
• Dilated ventricles, low EF, mitral/tricuspid regurgitation

Question 25

RCM vs. DCM tx (cardiomyopathies are like "functional heart failure")

Answer 25

* **RCM**: Treat underlying cause, diuretics (use cautiously), transplant * **DCM**: Same as HFrEF: ACE inhibitors, beta-blockers, diuretics, ICD if EF <35% (DCM often progresses to left and right-sided heart failure)

Question 26

Causes of **CHF**: * HFrEF (Reduced EF, <40%) * HFpEF (Preserved EF, >50%)

Answer 26

* ischemic heart disease, cardiomyopathies→**Dilated**, weak heart * chronic HTN, LVH, **restrictive** cardiomyopathy → stiff, non-compliant heart

Question 27

Results of Right heart cath (Swan-Ganz) in CHF: Right vs. Left Heart failure

Answer 27

Left HF: elevated PCWP Right HF: elevated CVP

Question 28

CHF tx (8)

Answer 28

1. ACE/ARBs **(improves survival)** 1. BB (prevents remodeling) 1. Spironolactone (reduces mortality) 1. SGLT2 inhibitors (reduces mortality) 1. Diuretics (sx relief) 1. hydralazine + nitrates (AA, reduces mortality) 1. Digoxin (sx relief **only**) 1. ICD (EF < 35%,)

Question 29

Hypertension is diagsnoses as 140/90 mmHg after...

Answer 29

confirmed on 2 separate readings (HTN emergency ≥180/120 + end-organ damage (e.g., stroke, MI, AKI)

Question 30

Hypertension general tx (Rx classes) (if ≥140/90 or 130-139/80-89 + diabetes, CKD, CAD, etc)

Answer 30

1. ACE inhibitors/ARBs 1. CCBs 1. thiazides (Complications: Stroke, MI, CKD, hypertensive emergency)

Question 31

Define hypertensive emergency (2)

Answer 31

≥180/120 + end-organ damage (e.g., stroke, MI, AKI) (tx=

Question 32

Complications of HTN

Answer 32

1. Stroke 1. ACS/MI 1. CKD 1. hypertensive emergency (Treatment: Lifestyle, ACE inhibitors/ARBs, CCBs, thiazides)

Question 33

Treatment for a Black patient with HTN & no CKD?

Answer 33

CCB or thiazide (DO NOT pick an ACE inhibitor, unless they have CKD e.g. proteinuria)

Question 34

Dyslipidemia tx (Start screening at age 40 for men, 50 for women)

Answer 34

Statins (1st-line) ezetimibe/PCSK9 inhibitors (if statin-intolerant)

Question 35

How do you treat HTN in a patient with HFrEF

Answer 35

ACE/ARB + BB + Aldosterone Blocker

Question 36

Treatment for HTN post MI?

Answer 36

ACE + BB

Question 37

ACE/ARB slows ... which complication of diabetes

Answer 37

nephropathy

Question 38

Elevated ... (lipid) is a risk factor for pancreatits

Answer 38

triglycerides

Question 39

When does screening for dyslipidemia start? **USPSTF guideline vs. ACC/AHA**

Answer 39

* **USPSTF**: age 40 for men, 50 for women (earlier if risk factors like DM, HTN, obesity, smoking, familly Hx, premature ASCVD) * **ACC/AHA**: screen all adults ≥20 years old & repeat every 4-6 years

Question 40

patient with no symptoms of dyslipidemia, but has risk factors like smoking, HTN, or diabetes. What is the next step in management?

Answer 40

fasting lipid panel

Question 41

If a patient has known ASCVD, tx with which statin?

Answer 41

high-intensity statin (Atorvastatin 40-80mg or Rosuvastatin 20-40mg)

Question 42

If a patient has diabetes, age 40-75, and LDL 80 mg/dL → treatment?

Answer 42

Give a statin, even if LDL isn’t that high!

Question 43

Alternative if a patient develops muscle aches while being treated with a statin?

Answer 43

Try a different statin or lower the dose (don’t stop it **unless CK is elevated).**

Question 44

When is Ezetimibe (cholesterol absorber) used?

Answer 44

add-on if statin is not working (alternatively, can use PCSK9 inhibitors Alirocumab, Evolocumab)

Question 45

Wen is PCSK9 inhibitor used? (Alirocumab, Evolocumab)

Answer 45

familial hypercholesterolemia or statin-intolerant patients

Question 46

Use ... if TGs > 500 to prevent pancreatitis

Answer 46

fibrates (increases HDL. Remember: bile acid sequestrants can increase TGs)

Question 47

When is a high-intensity statin used (4)?

Answer 47

1. PMH of ASCVD (MI, stroke, PAD, angina, revascularization) 1. LDL ≥190 mg/dL (familial hypercholesterolemia) 1. Diabetes (age 40-75) + LDL ≥70 1. 10-year ASCVD risk ≥7.5% (per calculator)

Question 48

Give a moderate-intensity statin if ... (2)

Answer 48

* Age 40-75 + Diabetes + LDL 70-189 (but no ASCVD history) * 10-year ASCVD risk 5-7.5% (shared decision-making)

Question 49

When is a Holter monitor used for assessment?

Answer 49

detects arrhythmias or sx like syncope (don't order more testing unless sx warrant it)

Question 50

What are the 4 types of AV Block?

Answer 50

🧩 Analogy (to make it stick) Think of it like a bad relationship: * First-Degree = Always late to reply, but still shows up. * Mobitz I = Takes longer and longer to reply… and then ghosts occasionally. * Mobitz II = Seems reliable… until BAM, they vanish mid-convo. * Third-Degree = You’re both texting different people entirely.

Question 51

Increasing PR (a little late) PR longer, longer, drop PR same, same, drop PR dissociated from QRS (name these AV blocks)

Answer 51

First Degree Second Degree Type I; Mobitz I Second Degree Type II; Mobitz II Third Degree