Cardiology + SBM 7 Flashcards
Q: What are the treatment options for high non-HDL and LDL cholesterol levels, especially for statin-intolerant patients or those needing additional LDL lowering?
A: Statins are the primary drugs for treating high non-HDL and LDL cholesterol. For patients who are statin-intolerant or need additional LDL lowering, other options include ezetimibe and proprotein convertase subtilisin/kexin type 9 monoclonal antibodies (PCSK9 MAbs), both of which are effective at lowering LDL and have shown cardiovascular benefits. Newer drugs, like bempedoic acid and inclisiran, may also be used, though they do not yet have cardiovascular outcomes data.
Q: What is the risk of liver damage with cholesterol-lowering drugs, and how should liver function be monitored?
A: Many cholesterol-lowering drugs, including niacin, fibrates, and potentially statins and ezetimibe, can cause liver damage. These drugs should not be used if AST or ALT levels are greater than 3 times the upper limit of normal. Liver function tests (LFTs) should still be monitored during treatment.
Q: How do statins work to lower cholesterol levels?
A: Statins inhibit the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which prevents the conversion of HMG-CoA to mevalonate. This is the rate-limiting step in cholesterol synthesis, ultimately lowering cholesterol levels.
When to use high vs mod intensity statin
Secondary Clinical ASCVD = high intensity
Primary = LDL >/= 190 = high
DM 40-75
LDL 70-188 = high multiple risks
- Mod w/o risks
- 70-189 = ASCVD >/= 20% high, 7.5-19.9 = moderate
High intensity statin
- Atorvastatin (lipitor) 40-80mg
- Rosuvastatin (crestor) 20-40mg
Mod intensity statin
- Atorvastatin 10-20
- Rosuvastatin 5-10
- Simvastatin (zocor) 20-40
- Pravastatin 40-80
- Lovastatin 40
- Fluvastatin 40bid/80xl
- Pitavastatin 2-4
Statin dosing equivulant
Q: What is the most important adverse effect of statins, and how does it present?
A: The most important adverse effect of statins is muscle damage. This typically presents as muscle soreness, tiredness, or weakness that is symmetrical in large muscle groups, such as the legs, back, or arms. Symptoms usually occur within six weeks of starting treatment but can develop at any time.
Q: What are the different ways muscle damage from statins can present?
A: Muscle damage from statins can present as:
Myalgias: muscle soreness and tenderness
Myopathy: muscle weakness, possibly with CPK elevations
Myositis: muscle inflammation
Rhabdomyolysis: muscle symptoms with very high CPK (>10,000 IU/L) and muscle protein in the urine (myoglobinuria), which can lead to acute renal failure.
What to do if myalgias occur while on statin?
IF MYALGIAS OCCUR
Hold statin, check CPK, investigate other possible causes.
After 2-4 weeks: re-challenge with same statin at same or↓ dose.
Most patients who did not toleratea statin will tolerate it when
re-challenged, or will tolerate a different statin.
If myalgias return, discontinue statin. Once muscle symptoms
resolve, use a low dose of a different statin; gradually ↑ dose.
Q: What are the significant drug interactions with statins, and how do they affect treatment?
A: Statin drug interactions, particularly those mediated by CYP enzymes (mainly CYP3A4), increase the risk of adverse effects like muscle damage. Atorvastatin, lovastatin, and simvastatin are CYP3A4 substrates, while rosuvastatin and pravastatin have fewer interactions. Fibrates (especially gemfibrozil) and niacin can increase the risk of myopathies and rhabdomyolysis. Statins should not be used with gemfibrozil. Amlodipine can increase the concentration of atorvastatin, lovastatin, and simvastatin, so the maximum daily dose for these statins should be 20 mg/day.
Q: What are the options for non-statin add-on treatments when LDL remains above goal despite statin use?
A: If LDL remains high despite statin use, the statin dose should be maximized before adding other medications. Ezetimibe and PCSK9 monoclonal antibodies (PCSK9 MAbs) are recommended as initial add-ons due to their cardiovascular benefits. Ezetimibe may be preferred if less than 25% LDL lowering is needed due to cost and oral administration. PCSK9 MAbs are more expensive and injectable, used when greater LDL lowering is required. Other options include bempedoic acid and inclisiran, which lower LDL but lack cardiovascular outcome data, so they should be used after ezetimibe and PCSK9 MAbs. Fish oils and fibrates are used for high triglycerides, with icosapent ethyl recommended for ASCVD reduction in select patients. Bile acid sequestrants are rarely used, except when statins cannot be tolerated.
List of the diff HTN meds and where they work
BP … normal, elevated , stage 1 vs stage 2
Normal: SBP < 120 mmHg and DBP <80 mmHg
Elevated: SBP 120 - 129 mmHg and DBP < 80 mmHg
Hypertension:
Stage 1: SBP 130 – 139 mmHg or DBP 80 - 89 mmHg (start 1 drug)
Stage 2: SBP ≥ 140 mmHg or DBP ≥ 90 mmHg (start 2 drugs)
Thiazide - lsit of drugs, MOA, important things to note
Thiazide - inhibit Na reabsorption in distal convoluted tubule
- Increase excretion of Na, Cl, water, potassium
- Not effective when CrCl <30
- Take early in the day (not HS)
- Chlorthalidone
- HCTZ
- Chlorothiazide (IV is avalible in this one!)
- Indapamide, metolazone
- C/I: hypersensitivity reaction to sulfonamide drugs
- AE: decrease potassium, magnesium, sodium
- Increase: calcium, uric acid, LDL, TG, BG
- Photosensitivity, impotence
- DDI: NSAIDs (decrease effectiveness), decrease lithium clearance (toxic risk)
DHP CCBs (e.g., Amlodipine, Nicardipine, Nifedipine): indication, MOA, warning, C/I, AEs
- Indications: Hypertension (HTN), chronic stable angina, Prinzmetal angina, Raynaud’s disease
- MOA: Inhibit calcium from entering vascular smooth muscle, leading to peripheral arterial vasodilation
- Common Drugs: Amlodipine (Norvasc), Nicardipine IV (Cardene IV), Nifedipine ER (Adalat CC, Procardia XL - preferred in pregnancy)
- Warnings: Hypotension, reflex tachycardia
- Contraindications: Allergy to soy/eggs (for Clevidipine)
- Adverse Effects: Peripheral edema, headache (HA), flushing, palpitations, reflex tachycardia, gingival hyperplasia, hypertriglyceridemia (Clevidipine)
- Monitoring: Peripheral edema
-
Important Notes:
- IR Nifedipine: Not recommended for chronic HTN or acute BP decrease; can cause profound hypotension.
- Clevidipine may cause infections, reflex tachycardia, and hypertriglyceridemia.
- Can be used in Raynaud’s disease to prevent peripheral vasoconstriction.
Non-DHP CCBs (e.g., Diltiazem, Verapamil) - Indication, MOA, AEs, DDI
- Indications: Control heart rate in arrhythmias (e.g., atrial fibrillation), hypertension
- MOA: More selective for the heart; decrease blood pressure and heart rate due to negative inotropic and chronotropic effects
- Common Drugs: Diltiazem (Cardizem, Tiazac), Verapamil (Calan SR)
- Warnings: Heart failure (can worsen symptoms), bradycardia
- Adverse Effects: Edema, constipation (especially with Verapamil), gingival hyperplasia
-
Drug Interactions:
- Caution with beta-blockers, digoxin, clonidine, amiodarone
- Major 3A4 substrates (e.g., grapefruit juice)
- Diltiazem and Verapamil inhibit P-glycoprotein (Pgp) and 3A4
- Lower doses of simvastatin and lovastatin when using with Diltiazem/Verapamil
RAAS Inhibitors (ACEIs & ARBs)
Indications:
ACEIs & ARBs decrease chronic kidney disease (CKD) progression (by reducing albuminuria)
Protect the heart in heart failure (HF)
Mechanism of Action:
ACEIs block Angiotensin I → II conversion, decrease vasoconstriction, aldosterone secretion, and bradykinin degradation (leading to cough).
ARBs block Angiotensin II binding to its receptor, preventing vasoconstriction.
Warnings:
Angioedema (potentially fatal) - avoid in patients with a history of angioedema.
ACEIs: Can cause cough, hyperkalemia, hypotension, renal impairment, and worsen bilateral renal artery stenosis.
ARBs: Fewer incidents of cough and angioedema.
Contraindications:
- History of angioedema
- Within 36 hours of using Entresto (sacubitril/valsartan)
- Pregnancy (BBW: can cause injury or death to fetus)
- ACE inhibitors and ARBs can ↓ lithium renal clearance and ↑ the risk of lithium toxicity.
Potassium sparing diuretics
- Spironolactone (Aldactone)
- Triamterene + HCTZ (dyazide, maxzide)
- Amiloride
- Eplerenone (Inspra)
- BBW: hyperkalemia (K>5.5)
- Contra: hyperkalemia, severe renal impairment, addison’s disease
- AE: hyperkalemia, increase SCr, dizzy
- Monitor: BP, renal function, fluids, s/sx of HF
- DDI: increase hyperkalemia risk, decrease lithium clearance (toxic risk)
Beta-Blockers for Hypertension
-
Indications: Beta-blockers are not first-line for treating hypertension unless the patient has a comorbidity (e.g., post-MI, stable ischemic heart disease, heart failure).
- Preferred in heart failure: Bisoprolol, carvedilol, or metoprolol succinate.
-
Mechanism of Action: Beta-blockers reduce blood pressure by blocking beta-1 and/or beta-2 adrenergic receptors, which decreases heart rate (HR) and myocardial contractility.
- Carvedilol & Labetalol: Beta-blockers with alpha-1 blocking properties, which reduce peripheral vasoconstriction.
- Intrinsic Sympathomimetic Activity (ISA): Beta-blockers like acebutolol, penbutolol, and pindolol partially stimulate beta receptors while blocking catecholamine effects. These do not reduce HR as effectively and are not recommended post-MI.
-
Special Considerations:
- Bronchospastic disease (e.g., asthma, COPD): Prefer beta-1 selective agents to avoid bronchoconstriction.
Stable ischemic heart disease - TX
Drug tx
- Antiplatelet and antianginal
- Antiplatelet
- ASA, plavix
- Antianginal
- Decrease oxygen demand, increase oxygen supply
- BB, CCB, or longer acting nitrates
- Nitroglycerin SL = immediate relief
- High Dose statin
- Control BP (ACEI/ARB) (with CAD and DM)
- A - antiplatelet, antianginal
- B - BP and BB
- C - start statins and stop cigarettes
- D - diet and DM
- E - exercise and education
Antiplatelets - talk about ASA and Plavix MOA
Aspirin & Clopidogrel Mechanism of Action
- Aspirin: Irreversibly inhibits COX-1 and COX-2 enzymes, reducing prostaglandin (PG) and thromboxane A2 (TXA2) production. TXA2 promotes vasoconstriction and platelet aggregation.
- Clopidogrel: A prodrug that irreversibly inhibits P2Y12 ADP-mediated platelet activation and aggregation.
Clopidogrel Boxed Warning, Contraindications, and Warnings
- Boxed Warning: Clopidogrel is a prodrug; its effectiveness depends on conversion by CYP2C19. Poor metabolizers (identified by genetic testing) may have higher cardiovascular risk. Consider alternative treatments for poor metabolizers.
- Contraindications: Active serious bleeding (e.g., GI bleed, intracranial hemorrhage).
-
Warnings:
- Bleeding risk (discontinue 5 days before surgery).
- Do not use with omeprazole or esomeprazole (see Drug Interactions).
- Premature discontinuation increases thrombosis risk.
- Risk of thrombotic thrombocytopenic purpura (TTP).
DAPT - duration for each procedure
- bare metal stent (at least 1mo)
- Drug-eluting stent (at least 6 mo)
- post -CABG (12mo)
ANTIANGINAL TREATMENT for Ischemic heart disease
BB
- 1st line SIHD, decrease HR, contractility, LV wall tension
- HR - 55-60BPM (metoprolol, carvedilol
.
CCB
- Decrease preload, produce vasodilation of veins > arteries
.
Ranolazine (ranexa)
- Warn: increase QT
- Not acute tx
- Not effective for HR or BP
.
Nitroglycerin (nitrostat) 3 doses q5min (0.4mg)
- DO NOT USE with PDE-5 inhibitors - sildenafil, vardenafil, tadalafil, and avanafil
- PRN, immediate relief
- Store in original glass container
- Long acting (oint, patch, pills)
- 10-12hr nitrate free interval to decrease tolerance
- Patch: 12-14hr on, 10-12hr off (chest)
- Oint: bid, 6h apart, 10-12hr free
- Mononitrate: bid 7hr apart (dinitrate same)
- Dinatrate - combo with hydralazine pref in HFrEF
- Long-Acting Nitrates (e.g., ointment, patch, pills):
These formulations are used for chronic angina management and help prevent angina attacks.
Patch: Typically worn for 12-14 hours, then removed for 10-12 hours to allow a nitrate-free interval. This break helps prevent the development of tolerance.
Ointment: Applied twice daily (bid) with a 6-hour gap between doses. A 10-12 hour nitrate-free interval is required to reduce tolerance.
Mononitrate: Typically dosed twice daily (bid) with a 7-hour interval between doses. Dinitrate is dosed similarly.
Important: These long-acting forms need the nitrate-free interval to be effective, as continuous use can lead to tachyphylaxis (tolerance), reducing their effectiveness over time.
ACUTE CORONARY SYNDROMES / “Heart Attack” STEMI/ NSTEMI - Risk, S/S, Dx,
Risks
- Men >45y, women >55yr (or early hysterectomy), smoking, HTN, DM, FH of coronary
event, CAD, chronic stable aging, excessive alcohol, dsylipidemia, lack of exercise
.
S/Sx
- Chest pain (pressure/squeezing) lasting 10+ minutes, severe dyspnea, diaphoresis
- Pain radiate to arms, back, neck, jaw, epigastric region
- Med emergency SL NTG q5min x3 doses
- Not better after 5min after 1st dose = 911
.
Dx
- ST elevation, (STEMI)
- Increase in troponin
.
UA (unstable angina)
- Sx - chest pain
- Cardiac enzymes (-)
- ECG changes none
- Blockage- partial
.
NSTEMI
- Sx - chest pain
- Cardiac enzymes (+)
- ECG changes none
- Blockage - partial
.
STEMI
- Sx - chest pain
- Cardiac enzymes (+)
- ECG changes - ST elevation
- Blockage - complete occlusion
Inital STEMI Tx - PCI/ timing
STEMI Treatment
- Goal: Open blocked arteries quickly with PCI or fibrinolysis.
- PCI is preferred if performed within 90 minutes of hospital arrival (door-to-balloon time) or 120 minutes from first medical contact.
- If PCI cannot be done within 120 minutes, fibrinolytic therapy should be administered within 30 minutes of hospital arrival (door-to-needle time).
DRUG TREATMENT OPTIONS FOR ACS
Morphine - pain, oxygen greater than 90%, Nitrate: dilate, increase blood flow, decrease preload/chest pain
Gp11b/11a - abciximab(ReoPro), eptifibatide(integrillin), tirofiban
- Block platelet glycoprotein iib/iira receptor
- bleeding/thrombocytopenia
Anticoag - LMWH, UFH, bivalirudin (last 2 for STEMI)
P2Y12 - clopidogrel, prasgruel, ticagrelor
- Prasugrel (effrent) (original container): Stop 7d surgery, contra: serious bleed, history of TIA or stroke, warn: purpura
- Ticagrelor (brillinta): 90mg bid x 1yr then 60mg bid, bbw: max asa dose 100mg, stop 5d before surgery, dyspnea
BB - increase longterm survival, B1 selective start within 24h
ACEI - within 24h, indefinite if LVEH <40%
Avoid NSAIDs (except ASA)
Avoid IR nifedipine
Cangrelor (inj) - after PCI transition to orals above (P2Y12)
Secondary prevention after ACS
- ASA 81 indefinite
- Clopidogrel for 12mo
- NTG (SL/spray) indefinite
- BB (3yr, indefinite with HF or HTN)
- ACEI indefinite EF less than 40, htn, ckd, or DM
- Aldosterone antagonist
- Indefinite if EF less than 40 or on target dose of ACEI or BB
- Statin: High intensity indefinitely
HF Stages and Classes
ACC/AHA = staged A-D
A. Nothing at risk
B. Structural HF no s/sx
C. Structural HF with s/sx
D. Advanced HF
.
NYHA functional class I-IV
1. No limits in activities
2. Slight limitations in physical activites, Ordinary activity = HF s/sx
3. bathing/dressing/ at rest = HF s/s
4. No activity w/o HF (even at rest)
Equation for CO (Cardiac Output)
CO = HR x SV (stroke volume)
Medications that can worsen HF
- Dpp4 (alogliptin, saxagliptin), immunosupp, TNF inhibs, interferons, Non DHP CCB,
antiarrhthmias class I (quinidine, flecanide, dronedarone), thiazolidinediones ( pioglitazone), itraconazole, oncology drugs (doxo) , NSAID
GUIDELINE-DIRECTED HFrEF TREATMENT: List of medications
- ACEi, ARB, ARNI
- BB and loop diuretic
- Aldosterone antagonist (spiro)
- SGLT2i
HF
Entresto (sacubitril/valsartan) -NYHA class II-IV
- Nepilysin inhib (enzyme responsible for degradation of vasodilatory peptides)
- Decrease HF hospitalization and CV death, 1st line HFrEF
- BBW: injury/death to fetus, D/c pregnancy
- Contra: no use within 36h of ACEI (ARB is fine), no use with history of angioedema
- Bilateral renal artery stenosis = avoid use
- Cough, potassium and SCr increase
- Monitor: BP, K, SCr, s/sx of HF
ACEI/ARB - MOA/ important notes
decrease cardiac remodel, ACE inhibitors block the conversion of angiotensin I to Ang II, resulting in ↓ vasoconstriction and ↓ aldosterone secretion. ARBs block Ang II from binding to the angiotensin II type-1 (AT1) receptor.
- For all HF patients
- Titrate to target doses (high doses)
- Lit. toxicity!
B Blockers - which agents to use…dosing
Only bisoprolol, carvedilol (IR and ER) and metoprolol succinate ER are recommended in the guidelines. (B,C,M)
.
- Decrease morbidity and mortality, rec for all HF pts
- Bisoprolol, carvedilol, metoprolol succinate (IV:PO 1:2.5)
.
Meto Succ. -Start 12.5-25 mg daily (target 200mg QD)
Carvedilol: Start 3.125 mg BID
Target dose:
≤ 85 kg: 25 mg BID, greater than 85 kg: 50 mg BID
Loop diuretics…notes and dosing equivalent
- Thick ascending loop of henle
- Increase excretion of Na, K, Cl, Mg, Ca, water
- s/sx control don’t improve survival
- Furosemide (lasix) (room temp)
- Bumetanide (bumex)
- Torsemide
- Ethacrynic acid
- Warn: sulfa allergy (except ethacrynic),
- Decrease: K, Mg, Na, Cl, Ca (except thiazide increases)
- Increase: bicarb, UA, BG, TG, TC
- Ototox, ortho hypotension, photosensitiviy
- Monitor: SCr, fluids, BP, electrolytes, audiology
- Avoid NSAIDs, decrease lithium excretion
.
Oral equivalent dosing: furosemide 40 mg = torsemide 20 mg = bumetanide 1 mg = ethacrynic acid 50 mg
.
Furosemide IV:PO ratio 1:2 (furosemide 20 mg IV = furosemide 40 mg PO)
Bumetanide and ethacrynic acid IV:PO ratio 1:1
Aldosterone antags
distal convuluted tube and collecting ducts
- Spiro (non selective): blocks androgen = endocrine AEs - target dose is 25 QD or BID
- Epleronone (selective (no endocrine effects)
- Decrease morbidity and mortality, add to ACEI/ARB/ARNI and BB
- Decrease Na and water retention
- Do not initiate for HF if K > 5 mEq/L
- Do not use triple combination of ACE inhibitor + ARB/ARNI
+ ARA due to a higher risk of hyperkalemia and renal insufficiency.
SGLT2 Inhibitors in Heart Failure
- Indication: Approved for heart failure treatment, even in patients without diabetes, due to reduced mortality and hospitalizations.
- Recommended regimen: First-line treatment with ARNI (or ACE inhibitor/ARB), beta-blocker (BB), and aldosterone receptor antagonist (ARA). - SGLT2I is one of the big 4s!
- Dapagliflozin (farxiga), empagliflozin (jardiance) both 10mg QD
Other TX and add ons for HF
Hydralizine/nitrates (DILE)
- Nitrates - increases NO = vasodilation, decrease preload
- Hydralazine - Arterial vasodilator, decrease afterload
.
Ivabradine (corlanor) - decrease HR, hospitalization (no effect on mortality)
- Sinus rhythm with resting HR >/= 70 BPM (needs)
- Need all other meds at max/target
- HR target 50-60
-AEs: Bradycardia, increase QT, ventricular arrhythmias, htn, afib
.
Digoxin (lanoxin)(digitek, digox) (pgp 3a4 sub)
- Inhibit Na-K-atpase pump, increase CO, decrease HR (inotrop and chronotrope_
- Doesn’t increase survival, decrease HF and hsopitalization
- Can add to other to increase s/sx, exercise, and QOL
- Lower dose if renal insufficient, smaller, older, female
- 0.125 - 0.25mg qd, CrCl <50 decrease dose or freq
- Decrease dose 20-25% when PO to IV
- HF: 0.5-0.9 level
- Tox: s/sx, N/v, loss of appetite, bradycardia
- Sev: vision, green yellow halos, blurry/double
- Antidote: digifab
- Caution with BB, clonidine, non DHP CCB, amiodarone (decrease dose by half)
- Decrease potassium, Mg, increase Ca
.
Vericiguat (verquvo) - soluble guanylate cyclase stimulator, increase cGMP = smooth muscle relax
Arrhyth. - drugs that can cause
Antiarrhythmics - Class la, Ic and III
.
Anti-infectives
antimalarials (e.g., hydroxychloroquine)
Azole antifungals (all except isavuconazonium)
Macrolides
Quinolones
.
Antidepressants
SSRIs (highest risk with citalopram and escitalopram)
Tricyclic antidepressants
Mirtazapine, trazodone, venlafaxine
.
Antiemetics
5-HT3 receptor antagonists
Droperidol, metoclopramide, promethazine
.
Antipsychotics
First generation (e.g., haloperidol, chlorpromazine, thioridazine)
Second generation (highest risk with ziprasidone)
.
Oncology medications
Androgen deprivation therapy (e.g., leuprolide)
Tyrosine kinase inhibitors (e.g., nilotinib)
Oxaliplatin
Cilostazol, donepezil, fingolimod, hydroxyzine, loperamide,
methadone, ranolazine, solifenacin, tacrolimus
Arrthy. CLASSIFYING DRUGS WITH
VAUGHAN WILLIAMS
CLASS I (Na channel)
la: Disopyramide, Quinidine, Procainamide
Ib: Lidocaine, Mexiletine
Ic: Flecainide, Propafenone
.
CLASS II
Beta-blockers
.
CLASS III (K channel)
Dronedarone, Dofetilide, Sotalol, Ibutilide, Amiodarone
.
CLASS IV (nondihydropyridine (non-DHP))
Verapamil, Diltiazem
AF: RATE VS. RHYTHM CONTROL
& STROKE PROPHYLAXIS
Amiodarone (Class III)
- t ½ = 40-60d
- BBW: pulm tox, hepatotox, lifethreatening arrhythmia, proarrythmic - hospital for loading dose
- AE: hypotension, bradycardia, corneal micro depositis, photosensitiviy
- Drug of choice in HF
- Incompatible with heparin, flush line; need filter!
- Decrease digoxin 50%, warfarin 30-50%, 20mg simvastatin/day, 40/d
lovastatin
Stroke - Patho
- Blood flow to brain interrupted
- Acute ischemic stroke (most common at 88%) = thrombus = non-cardioembolic
- Cardioembolic - embolus forms in heart and travels to brain (afib)
- ICH, SAH (other 12%) - bleed in brain (hemmorhagic)
- TIAs not serious = will recover on thier own but need to address cuz can develop to other stroke
STROKE
Alteplase - tissue plasminogen activator (tPA), binds to fibrin conversts plasminogen to plasmin
- If no bleeding only
- Admin wihtin 3hr s/sx onset (select pts 4.5h)
- BP LESS THAN 185/110 (have to lower before!)
- 0.9mg/kg (max dose 90mg), rule out intracranial bleed before
- Contra: activer internal bleed, history of recent stroke (3mo), severe BP increase, INR
>1.7, use of LMWH (24h), DOAcs (48hr) - AE: major bleed
- Monitor: Hgb, Hct, s/sx bleed, neuro assessments and BP
- Dose and contraindication different than ACS
OTher TX for Stroke
- ASA 162-325mg within 24/48h…ASA, dipyridamole or clopidogrel within 24-48h
- HTN management, glucose management, DVT prevention ISCHEMIC stroke secondary prevention
- Control BP less than 130/80, thiazide, ACEI, ARBs
- High intensity statin
- Control DM
- Afib - anticoagulant
- Lifestyle changes: Quit smoking, restrict sodium, diet, physical activity, BMI 18.5-24.9, waists, limit alcohol
Note on CCB - More so amlodipine and nifedipine (DHP CCB)
These can lead to peripheral edema! So not the best for HF patients with volume overload
drugs for thyroid storm: methimazole
Note the usual dose for this is 20-60mg QD…depending on inital/ mantaince dose..it also depends on thyroid free T4 levels
Net fluid loss for HF patient
Depends, but typically -1.5-2L loss per day if hypervolumic
SGTL2i eGFR cut offs for indication of HF (note indication for dm is higher)
Empag - >20
Dapa ->25
What does procalcitonin level indicates?
inflammatory marker -The higher your procalcitonin levels, the higher your risk for infection/ sepsis and septic shock. Even in the absence of a clear infection, patients with heart failure may have slightly elevated PCT levels due to the inflammatory state associated with the condition.
For HF patients what levels should each electrolytes be maintained as : K, phos, mg
K+ : >4
Phos: >3 (lab ordered as PO4 (phosphours))
Mg2+: >2
Replenishing Mg2+…what are the cavets
Mg GLUCONATE - sucks…low elemental Mg…won’t really do anything..
Mg SULFATE is for IV
Mg Oxide is for oral
Cavets for Non DHP CCB: Diltizem/ verapamil
Not first line for HTN…typically used for rate control for arrthy. Can be used for HTN if other stuff don’t work - again…not first line
When looking for QTc / EKG. . .
Make sure to check medications that prolong QTc.. You need to look for EKG..can look for it in cardiac specility notes or in MUSE (MRN: nine numbers in all..if not nine then add 0s at the begining). Look at QTc (make sure its in NORMAL SINUS RHYTHEM - if it’s not the QTc can be misleading / incorrect). if in normal sinus rhythem and QTc is elevated (NORMAL : between 350–450 milliseconds for men and 360–460 milliseconds for women) then also look at QRS.. (120 is upper normal limits..if QRS is above 120 then subtract that # - 120..then use that difference to subtract from QTc then that is your true QTc!….
If no new EKG (EKG is like a week old/ isnt current), then look at electrolytes…are everything good? Look at K, phos, mg! make sure none are LOW! (that’s the real problem = arrthy)
squamous epithelial cells are in your urine = meaning
If squamous epithelial cells are in your urine, it may mean your sample was contaminated/ not CLEAN CATCH
Max fluid rate (any fluids) or HF patient
125 mL / hr
Cavets wiht Glucomander
Does not take in the “carbs” from protein shakes or carbs from dextrose…only MEALS
The ONLY agent the is GDMT for HFpEF
SGLT2i
.
Everything else is symp control or used for other things. They only really need SGLT2i
Elevated Scr …. things to be looking out for the HF patients
- Overdiuresis / drying them out too fast
- Medications…we want to hold off on any meds that can harm kidney - vanco/ zosyn/ gent/ etc/ ACEi/ ARBs / SGLT2i / etc
Methadone for SUD vs Pain
SUD: QD dosing + HIGHER doses (+30mg) - Consult CAMINOS for managment - also need to so AdHoc note for this to !
Pain: Muiltiple times a day dosing + lower doses
Stuff to check for when working up cards patients
- Notes (the heck are they here for)
- Labs / electrolytes
- Med list optimized
- In/Out
- Diuresis IV…if euvolmic can switch to PO
- Orthostatic (may happen if we are diuresising too quick) - look at supine sys/diastolic —> to standing sys/diastolic (-20 changes? bad)
chlorothiazide, chlorthalidone, and metolazone, three common thiazide or thiazide-like diuretics… Compare/Contrast
clopidogrel (plavix) - loading dose per UNMH protocol
300 mg LD then 75 mg MD (wait for 12hrs in between LD and MD)
When you see calcium gluconate being ordered make sure to look at Ca+ level and …
correct for Ca+ for low albumin (less than 4) is need. iCa is more accurate but when looking at Ca+ need to correct that one if albumin is low
TAVI (Transcatheter Aortic Valve Implantation) or TAVR (Transcatheter Aortic Valve Replacement) - Anticoag?
nah.
- Aspirin is usually given post-TAVI/TAVR as standard therapy.
- Anticoagulation is not routinely necessary unless there’s a separate indication (like atrial fibrillation).
- In some cases, dual antiplatelet therapy (aspirin + clopidogrel) may be used temporarily.
Drug Stent for STEMI - DAPT for how many months
12 months
For patients with STEMI/ NSTEMI they will leave hospital with ______
Nitrate (nitroglycerin 0.4mg (400mcg))
When doing iron replenish.. Cavets
Iron surcose is typically reserved for nephology (like HD) patient… if normal patient needs it we can do Ferrous gluconate, Ferrous fumarate
Enox ppx vs heparin ppx
Typicallly we want to use enox when we can…however, heparin comes into play because it has a quick on/off making it benefical for patients who may be going to a procedure/ OR. Heparin is also prefered for patients with VERY POOR KIDNEYS / on HD
Treatment methods for HyperK+
Digoxin - Loading dose vs maintance dose
Loading doses are unnecessary when digoxin is used to treat chronic heart failure. For atrial fibrillation, a loading dose of 0.5 (500mcg) to 0.75 mg (750mcg), followed by a maintenance dose, is warranted when the rate is not controlled with β-blockers.
Digoxin - Goal for HF VS. Afib
For patients with heart failure, the recommended target serum digoxin concentration is generally lower, typically between 0.5 to 0.9 ng/mL. This range is associated with improved outcomes, including reduced hospitalizations and a better safety profile, as higher levels have been linked to increased mortality.[1-4]
In contrast, for patients with atrial fibrillation, the target serum digoxin concentration can be slightly higher, often ranging from 0.8 to 2.0 ng/mL. This higher range is aimed at achieving effective ventricular rate control in AF.[5-6]
Q1: Why is there concern about starting amiodarone in a patient on therapeutic anticoagulation before a TEE and cardioversion?
A1: The concern is that starting amiodarone before performing the TEE and cardioversion could potentially dislodge a clot that might be present in the heart. Since the TEE is being done to assess for clots before cardioversion, it is generally recommended to hold off on starting amiodarone until after the procedure to avoid any risk.
Q2: Is the TEE and cardioversion typically done together?
A2: Yes, typically the TEE (transesophageal echocardiogram) and cardioversion are performed together. If the TEE clears the patient of clots, they can proceed with cardioversion while the patient is sedated, all in one session.
Q3: Why might amiodarone be started before cardioversion and TEE?
A3: Amiodarone may be started before cardioversion with the goal of helping the patient maintain normal sinus rhythm (NSR) more easily after the cardioversion is successful. This is often done in patients who have been in atrial fibrillation for a while, and the goal is to optimize the chances of maintaining NSR post-procedure.
Q4: How long should a patient be on anticoagulation before undergoing cardioversion?
A4: Ideally, patients should be on therapeutic anticoagulation for at least 3-4 weeks before cardioversion to reduce the risk of thromboembolic events. In this case, the patient has been on therapeutic anticoagulation for 7 days, which should be sufficient for consideration of cardioversion.
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A patient should be on anticoagulation therapy for at least 3 weeks before undergoing cardioversion if the atrial fibrillation (AF) has lasted for 48 hours or longer or if the duration is unknown.
Q5: If a patient has been in atrial fibrillation (AF) for a while, is it safe to start amiodarone before cardioversion?
A5: Yes, it is generally safe to start amiodarone prior to cardioversion as long as the patient is anticoagulated and has no concerns about anticoagulation compliance. The goal of amiodarone is to help the patient maintain NSR after cardioversion.
Q6: Why might rate control medications like metoprolol or digoxin be held the morning of a TEE?
A6: Rate control medications such as metoprolol and digoxin may be held before a TEE and cardioversion because they can potentially cause bradycardia or hypotension if the patient is successfully cardioverted back to normal sinus rhythm (NSR). This could “bottom out” the patient’s heart rate, especially if they were sedated or had rate control agents on board.
Do you discontinue other rate control medication like beta blocker or digoxin prior to cardioversion?
…Depends. Some providers will D/C other rate controlling med prior to cardioversion because we do not want the patient’s HR to drop!
Gram negative bacterimea…when can you d/c treatment?
D/C after 6 weeks from negative blood culture - depends on what ID wants
Restarting medications after HD?
Most can be restarted/ given now if it’s not too close to the next dose—diuretics? can prolly be held cuz they got fluid removed already! We also try not to give diuretics at night so they don’t have to get up and pee
Do we treat ALL pulmonary emolism? PE?
No–we don’t have to treat subsegmental PEs- depends on your risk of bleeding and recurrence, as well as your preferences. …but Saddle or Segmental? WE HAVE TO!
Subaortic stenosis (subAS) is a condition characterized by an obstruction below the aortic valve, which can lead to left ventricular outflow tract obstruction (LVOTO). This condition can be dynamic and influenced by changes in preload and afterload…MEDS TO AVOID?
- Nitroglycerin and other nitrates: These reduce preload and afterload, potentially worsening LVOTO.[1-3]
- Diuretics: High doses can reduce preload excessively, exacerbating the obstruction.[4]
- Vasodilators: Agents like hydralazine and ACE inhibitors can reduce afterload, potentially worsening the gradient across the obstruction.
Prasugrel and ticagrelor are both antiplatelet agents used in the management of acute coronary syndromes (ACS), but they have specific caveats and contraindications.
Prasugrel:
* Contraindications: Prasugrel should not be used in patients with a history of transient ischemic attack (TIA) or stroke due to an increased risk of bleeding. It is also contraindicated in patients who are over 75 years old or weigh less than 60 kg, as these populations have shown no net benefit and an increased risk of bleeding. ALSO CANNOT USE IN PATIENT WHO HAVE NOT UNDER GONE PCI. NO PCI NO PRASUGREL
* Side Effects: The primary concern with prasugrel is the increased risk of major bleeding, particularly in the aforementioned populations.
.
Ticagrelor:
* Contraindications: Ticagrelor is contraindicated in patients with a history of intracranial hemorrhage, active pathological bleeding, or severe hepatic impairment. Unlike prasugrel, ticagrelor can be used in patients who have not undergone PCI.
* Side Effects: Ticagrelor is known to cause dyspnea (shortness of breath) and, less commonly, bradyarrhythmias. The dyspnea is thought to be due to ticagrelor’s effect on adenosine metabolism.
Medications for chest pain
Ranolazine, nitrate, BB, CCB, ASA (higher dose)
Caveats of cardioversion and AC
Need to be anticoagulated for 3 weeks before and 4 weeks after cardioversion (unless the afib happened within 48hrs prior to cardioversion then no need to be on 3 weeks of AC - but still need 4 weeks of AC after) …if need to do cardioversion and no 3 weeks of AC? need to do TEE (the invasive one) to see if no clot in heart then can do cardioversion
If patient is NPO you should not use SGLT2i…why
no glucose in take = DKA
Situations where warfarin is the prefered agent
- APS
- Mechanical valve
- Afib with mitral valve stenosis (higher clot risk)
- CTEPH (Chronic Thromboembolic Pulmonary Hypertension)
Cardiology patients with valve replacement will need dental work up..why?
Risk of endocarditis!
Load the maintance dose….how far to seperate them?
Good rule of thumb…when it’s pass the peak level!
For procedures where you have to place in a device…do you hold AC?
No for DOAC, but yes for parenteral
Nonbshockable rhythem
Asystole and PEA - would have to use Epi and CPR (epinephrine 1 mg IV/IO every 3-5 minutes )
The diagnostic criteria for heart failure (HF) are outlined by the American College of Cardiology, American Heart Association, and Heart Failure Society of America in their 2022 guidelines. The diagnosis of HF requires the presence of clinical symptoms and signs of HF, along with objective evidence of cardiac dysfunction.
Key diagnostic criteria include:
- Clinical Symptoms and Signs: These may include dyspnea, fatigue, fluid retention (e.g., peripheral edema, pulmonary congestion), and exercise intolerance.
- Objective Evidence of Cardiac Dysfunction:
* Reduced Ejection Fraction (HFrEF): Left ventricular ejection fraction (LVEF) ≤ 40%.[1-2]
* Mildly Reduced Ejection Fraction (HFmrEF): LVEF 41-49% with evidence of increased left ventricular (LV) filling pressures, such as elevated natriuretic peptide levels or abnormal diastolic parameters on echocardiography.[1-2]
* Preserved Ejection Fraction (HFpEF): LVEF ≥ 50% with evidence of increased LV filling pressures, such as elevated natriuretic peptide levels, echocardiographic diastolic dysfunction, or invasive hemodynamic measurements.[1-2] - Supporting Evidence:
* Elevated levels of natriuretic peptides (BNP or NT-proBNP).
* Echocardiographic findings such as increased left atrial volume index (LAVI) or LV mass index (LVMI).
* Invasive hemodynamic measurements showing elevated filling pressures
Why you should not use beta blocker in cardiogenic shock
If a patient was in cardiogenic shock + was on pressers in the ICU = want to be off pressors for at least 48 hours before beta blocker
BB + NDP CCB (diltizem or verapamil)
Should not combine both becasue they haev similar effects
Nitrate free period (so patient does not build tolerance to it)
need 12 hours of free nitrate period ….so need to give TID in 12 hrs then the other 12 hrs wil be free (so can give 9am, 12pm, 9pm)
TDC - what is that
Tunneled Dialysis Catheter - if it gets removed = no dialysis
If NPO at midnight? then what to do with basal/ glargine dosing?
decrease by 20%
