Review
Hypertension *** Hypertension is defined as BP ≥140/90 mmHg (per JNC8).
Non-Black population treatment *** Start with thiazide diuretic, ACE inhibitor, ARB, or CCB.
Black population treatment *** Start with thiazide diuretic or CCB.
DM or CKD treatment *** Include ACE inhibitor or ARB for kidney protection.
Age ≥60 years treatment *** Treat if BP ≥150/90 mmHg.
Age <60 years treatment *** Treat if BP ≥140/90 mmHg.
Contractility *** Force of cardiac muscle contraction.
Preload *** Volume in ventricles at end-diastole (central venous volume).
Afterload *** Resistance heart must pump against (arterial pressure).
Aortic Stenosis (AS) *** Calcification narrows aortic valve → outflow obstruction.
Aortic Regurgitation (AR) *** Incompetent aortic valve due to root dilation or endocarditis.
Mitral Stenosis (MS) *** Often post-rheumatic fever, calcification of mitral valve.
,Mitral Regurgitation (MR) *** Commonly due to MI, CHF-induced LV dilation, papillary rupture, or
endocarditis.
Direct Oral Anticoagulants (DOACs) *** Do NOT require INR monitoring.
Factor Xa inhibitors *** Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa).
Direct thrombin inhibitor *** Dabigatran (Pradaxa).
Warfarin (Coumadin) *** Onset: Delayed — requires bridging with LMWH or heparin.
Bridging with Warfarin *** Bridging is required until INR reaches ≥2.0 for at least 24 hours.
Dopamine *** Dose-dependent: low = renal perfusion, high = pressor.
Dobutamine *** Inotrope (↑ contractility).
Norepinephrine (Levophed) *** Vasoconstrictor + mild inotrope.
Epinephrine *** Mixed alpha & beta agonist.
Nitroglycerin *** Venodilator; ↓ Preload; avoid if hypotensive.
Nitroprusside *** Potent arterial/venous vasodilator; risk of cyanide toxicity with prolonged use.
,Statins *** HMG-CoA reductase inhibitors used as first-line therapy for lipid management.
High-intensity statins *** Atorvastatin 40-80 mg daily and Rosuvastatin 20-40 mg daily.
Indications for high-intensity statins *** Clinical ASCVD (e.g., MI, stroke), LDL ≥190 mg/dL, Diabetes age
40-75 with ≥7.5% 10-year ASCVD risk.
Ezetimibe *** A secondary therapy for mild LDL-lowering, often required before insurance approval of
PCSK9 inhibitors.
PCSK9 inhibitors *** Injectable monoclonal antibodies reserved for very high-risk patients or statin-
intolerant.
ASCVD *** Atherosclerotic Cardiovascular Disease, includes MI, stroke, angina, revascularization, and
peripheral artery disease.
10-year risk categories *** Low risk: <5%, Moderate risk: 5%-7.4%, High risk: ≥7.5%, Very high risk: ≥20%
or known ASCVD.
Aortic Stenosis (AS) *** Caused by calcification of the valve leading to outflow obstruction, with a classic
triad of angina, syncope, dyspnea.
Aortic Regurgitation (AR) *** Occurs when the valve fails to close, leading to wide pulse pressure and
bounding pulses.
Mitral Stenosis (MS) *** Often caused by post-rheumatic fever, symptoms include dyspnea, orthopnea,
and atrial fibrillation.
, Mitral Regurgitation (MR) *** Caused by papillary muscle rupture, dilated LV, or endocarditis,
characterized by a holosystolic murmur.
HFrEF *** Heart failure with reduced ejection fraction, defined as EF <40% and associated with systolic
dysfunction.
HFpEF *** Heart failure with preserved ejection fraction, defined as EF ≥50% and associated with
diastolic dysfunction.
First-line medications for HFrEF *** Include beta-blockers (Carvedilol, metoprolol succinate, bisoprolol),
ACE inhibitors or ARBs, loop diuretics, and spironolactone.
Shock categories *** Include hypovolemic, cardiogenic, distributive, and obstructive types.
Hypovolemic shock *** Caused by hemorrhage or dehydration, treated with fluids and blood products.
Cardiogenic shock *** Caused by MI or CHF, treated with inotropes (dobutamine) and vasopressors.
Distributive shock *** Caused by sepsis or anaphylaxis, treated with vasopressors (norepinephrine) and
fluids.
Obstructive shock *** Caused by PE, tamponade, or tension pneumothorax, treated by relieving the
obstruction.
Norepinephrine (Levophed) *** First-line treatment in septic shock.
Dobutamine *** Used for low-output states in cardiogenic shock to improve contractility.