Cardiovascular Flashcards
ACS, CAD, CHF, HTN, Dyslipidemia
What is the etiology of Acute Coronary Syndrome (ACS)?
Atherosclerotic plaque rupture → thrombus formation → myocardial ischemia.
W/U for chest pain (4)
- EKG
- CXR
- Troponins
- D-dimer (r/o PE)
(DDX: ACS, pericarditis, PE, GERD, MSK pain)
7 Risk Factors: ACS
- hypertension
- hyperlipidemia
- diabetes
- smoking
- family history of coronary artery disease
- age
- obesity
How is ACS evaluated?
- ECG: STEMI (ST elevation), NSTEMI (ST depressions/T-wave inversions)
- Troponins: Elevated
What is the treatment for ACS?
(Immediate vs. Definitive)
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)
Risk stratification: ACS
(determines tx: PCI vs. medical management)
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
What are the 5 MC complications of ACS?
- Arrhythmia → V-fib/V-tach → sudden cardiac death
- Rupture → Papillary muscle, septum, free wall (3-7 days)
- Refractory HF→ Cardiogenic shock
- Pericarditis → Early = fibrinous, Late = Dressler
- Dilated aneurysm → Persistent ST elevations + thrombus risk
(mnemonic ARRP-D)
tx: post-MI pericarditis
- NSAIDs
- colchicine
- steroids (if refractory)
(remember: Dresslers syndrome is just auto-AB to the necrotic tissue/pericarditis. Both are pericarditis, but different pathophys. same tx)
What is the mnemonic for Virchow’s Triad?
SHE:
* Stasis
* Hypercoagulability
* Endothelial injury
CAD can progress to heart failure by which 2 main mechanisms?
(HFrEF or HFpEF)
- ACS or MI →HFrEF
- Ischemic cardiomyopathy→fibrosis) →HFpEF
ECG findings of CAD vs. ACS?
- 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)
CAD tx (3 general)
- Rx: statins, aspirin, beta-blockers, ACE inhibitors
- revascularization if severe
- Lifestyle changes to risk factors (smoking cessation, obesity, sedentary life, diet)
CAD gold standard dx test
coronary angiography
(stress test commonly used)
when would you NOT use B-blockers in HF?
acute decompensation
4 clinical findings of aortic regurgitation
- de Musset sign (head bobbing wpulse)
- “water-hammer” pulse
- Quincke pulse (pulsing nail bed)
- CHF sings: ortopnea, pulm edema, dyspnea on exertion
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)
concentric LVH secondary to long-standing hypertension.
(Other potential causes include acute myocardial infarction and restrictive cardiomyopathy)
What makes a Q wave pathologic
deep or wide
Best diagnostic test for AAA?
CT: abdomen, chest pelvis = intimal flap w/false lumen
pulses paradoxis is indicitive of which dx?
(decrease in systolic pressure > 10 mmHg w/inspiration)
cardiac tamponade
(becks triad, dilated IVC, collapsing atria and low voltage ECG also seen)
Beck triad: hypotension, JVD, muffled heart sounds indicates which diagnosis?
(also dilated IVC, collapsable atria and low voltage ECG)
cardiac tamponade
(Sudden collapse + tamponade signs 5-7 days after MI? Free wall rupture.)
Which 3 conditions cause pleuritic chest pain?
- PE
- Pleural effusion
- Pericarditis
- Restrictive Cardiomyopathy is … (HFrEF/HFpEF)
- Dialated Cardiomyopathy is … (HFrEF/HFpEF)
- RCM = HFpEF → S4 gallop
- DCM = HFrEF → S3 gallop
(at first!)
How can you distinguish between the presentation of RCM and DCM?
(initial disease process of restrictive or dilated cardiomyopathy)
- 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
Echo findings: RCM vs. DCM
(initial disease process of restrictive or dilated cardiomyopathy)
- RCM: Biatrial enlargement, normal LV size, stiff myocardium, diastolic dysfunction
- Dilated ventricles, low EF, mitral/tricuspid regurgitation
RCM vs. DCM tx
(cardiomyopathies are like “functional heart failure”)
- 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)
Causes of CHF:
* HFrEF (Reduced EF, <40%)
* HFpEF (Preserved EF, >50%)
- ischemic heart disease, cardiomyopathies→Dilated, weak heart
- chronic HTN, LVH, restrictive cardiomyopathy → stiff, non-compliant heart
Results of Right heart cath (Swan-Ganz) in CHF: Right vs. Left Heart failure
Left HF: elevated PCWP
Right HF: elevated CVP
CHF tx (8)
- ACE/ARBs (improves survival)
- BB (prevents remodeling)
- Spironolactone (reduces mortality)
- SGLT2 inhibitors (reduces mortality)
- Diuretics (sx relief)
- hydralazine + nitrates (AA, reduces mortality)
- Digoxin (sx relief only)
- ICD (EF < 35%,)
Hypertension is diagsnoses as 140/90 mmHg after…
confirmed on 2 separate readings
(HTN emergency ≥180/120 + end-organ damage (e.g., stroke, MI, AKI)
Hypertension general tx (Rx classes)
(if ≥140/90 or 130-139/80-89 + diabetes, CKD, CAD, etc)
- ACE inhibitors/ARBs
- CCBs
- thiazides
(Complications: Stroke, MI, CKD, hypertensive emergency)
Define hypertensive emergency (2)
≥180/120 + end-organ damage (e.g., stroke, MI, AKI)
(tx=
Complications of HTN
- Stroke
- ACS/MI
- CKD
- hypertensive emergency
(Treatment: Lifestyle, ACE inhibitors/ARBs, CCBs, thiazides)
Treatment for a Black patient with HTN & no CKD?
CCB or thiazide
(DO NOT pick an ACE inhibitor, unless they have CKD e.g. proteinuria)
Dyslipidemia tx
(Start screening at age 40 for men, 50 for women)
Statins (1st-line)
ezetimibe/PCSK9 inhibitors (if statin-intolerant)
How do you treat HTN in a patient with HFrEF
ACE/ARB + BB + Aldosterone Blocker
Treatment for HTN post MI?
ACE + BB
ACE/ARB slows … which complication of diabetes
nephropathy
Elevated … (lipid) is a risk factor for pancreatits
triglycerides
When does screening for dyslipidemia start?
USPSTF guideline vs. ACC/AHA
- 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
patient with no symptoms of dyslipidemia, but has risk factors like smoking, HTN, or diabetes. What is the next step in management?
fasting lipid panel
If a patient has known ASCVD, tx with which statin?
high-intensity statin
(Atorvastatin 40-80mg or Rosuvastatin 20-40mg)
If a patient has diabetes, age 40-75, and LDL 80 mg/dL → treatment?
Give a statin, even if LDL isn’t that high!
Alternative if a patient develops muscle aches while being treated with a statin?
Try a different statin or lower the dose (don’t stop it unless CK is elevated).
When is Ezetimibe (cholesterol absorber) used?
add-on if statin is not working
(alternatively, can use PCSK9 inhibitors Alirocumab, Evolocumab)
Wen is PCSK9 inhibitor used?
(Alirocumab, Evolocumab)
familial hypercholesterolemia or statin-intolerant patients
Use … if TGs > 500 to prevent pancreatitis
fibrates
(increases HDL. Remember: bile acid sequestrants can increase TGs)
When is a high-intensity statin used (4)?
- PMH of ASCVD (MI, stroke, PAD, angina, revascularization)
- LDL ≥190 mg/dL (familial hypercholesterolemia)
- Diabetes (age 40-75) + LDL ≥70
- 10-year ASCVD risk ≥7.5% (per calculator)
Give a moderate-intensity statin if … (2)
- Age 40-75 + Diabetes + LDL 70-189 (but no ASCVD history)
- 10-year ASCVD risk 5-7.5% (shared decision-making)
