Dyslipidemia
First-line, cornerstone therapy for ASCVD risk reduction.
What are statins?
First-line class particularly effective as initial therapy in many patients, including Black adults without CKD/proteinuria.
What are thiazide diuretics (chlorthalidone, HCTZ) - Thiazide diuretics are first line for black patients.
This ARNI is indicated for stable HFrEF to reduce hospitalizations and mortality.
What is sacubitril/valsartan (Entresto)?
This drug is the go-to for acute SVT termination in a stable patient.
What is adenosine?
The oral anticoagulant whose effect is reduced by high vitamin K intake.
What is warfarin?
This drug inhibits intestinal cholesterol absorption and is often used as an add-on to statins.
What is ezetimibe?
ARBs are contraindicated in this population.
What is pregnancy?
These diabetes drugs reduce HF hospitalizations (and improve outcomes in HFrEF).
What are SGLT2 inhibitors (empagliflozin/dapagliflozin)?
Class I antiarrhythmics primarily block this ion channel.
What are sodium channels?
Class II: beta-blockers (rate control) - best for rate control.
Class III: K+ blockers rhythm control, Amio = powerful but toxic.
Class IV: CCBs (verapamil, diltiazem) - rate control (esp. AF, SVT).
These agents are not indicated to prevent AF-related embolism, but are used for acute MI, PE, and ischemic stroke (selected cases).
What are fibrinolytics (thrombolytics)?
A rare but dangerous adverse effect associated with statins.
What is rhabdomyolysis?
This agent is a first-line treatment for orthostatic hypotension—not for chronic HTN.
What is midodrine?
In cardiogenic shock/acute HF, inotropes generally have these effects on HR and BP.
What is increase both HR and BP?
A beta-blocker used post-MI/AF/HF that can slow AV conduction enough to cause this adverse event.
What is heart block?
Patients with mechanical heart valves should be anticoagulated with this agent rather than a DOAC.
What is warfarin?
Patients with LDL ≥190 mg/dL are likely to need high-intensity therapy because this inherited condition is suspected.
What is familial hypercholesterolemia?
A thiazide-type diuretic can cause these electrolyte/lab changes (name two).
What are hypokalemia, hyponatremia, and hyperuricemia (gout)?
For rapid relief of volume overload in decompensated HF, start this diuretic class.
What are loop diuretics (e.g., furosemide)?
Amiodarone is avoided long-term in patients with disease in these two organs due to toxicity risks.
What are the lungs and liver?
Reversal pairing: dabigatran is reversed by this agent; Xa inhibitors by this one.
What are idarucizumab (Praxbind) and andexanet alfa (Andexxa)?
PCSK9 inhibitors are reserved for these two situations due to cost.
What are familial hypercholesterolemia and refractory very-high-risk ASCVD?
For hypertensive emergencies, normalizing BP to “normal” over 2–3 days is not the target; instead, this is.
What is reducing MAP by ~25% in minutes–hours?
Beta-blocker therapy improves survival in HFrEF but can cause this conduction adverse effect.
What is heart block/bradycardia?
Classic triad for digoxin toxicity includes visual changes, GI upset, and this rhythm effect.
What is bradyarrhythmia/AV block?
Compared with warfarin, a key advantage of DOACs regarding lab checks.
What is no routine INR monitoring (check renal/liver function instead)?
In diabetes (age 40–75, LDL 70–189, no ASCVD), guidelines recommend this therapy for primary prevention.
What is statin therapy based on risk?
Nnon-dihydropyridine calcium channel blocker, (Non-DHP CCBs) (verapamil, diltiazem) can worsen this cardiac condition.
What is heart failure?
because their negative inotropic (weakening of heart muscle contraction) and negative chronotropic (slowing of heart rate) effects can worsen the condition and reduce cardiac output
Mineralocorticoid receptor antagonists (e.g., spironolactone) carry this key electrolyte risk requiring close monitoring.
What is hyperkalemia?
Digoxin’s primary cardiac actions include slowing SA/AV nodal conduction and this effect on myocytes.
What is increased contractility via Na⁺/K⁺-ATPase inhibition leading to ↑ intracellular Ca²⁺?
Following valve surgery with subtherapeutic INR, two priority NP actions to reduce thromboembolism risk.
What are adjust warfarin dose and reinforce vitamin K dietary consistency?