Heart Failure Study Guide PDF

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Heart Failure Study Guide I.

Heart Failure Pathophysiology a. Ventricular remodeling i. Thickening of the myocardium ii. Caused by overstimulation of beta receptors 1. Causes a lower ejaculation fraction (EF) 2. Less than 40% gets pumped b. Naturetic Peptides i. Cardiac hormones with beneficial physiology effects 1. Produces are during periods of volume overload (myocardial muscle stretching) ii. Types 1. A type (ANP) a. Secreted by atria when stretched 2. B type (BNP) a. Secreted by ventricles b. Focus in HF (NT pro BNP) for diagnosis/prognosis i. Diagnosis: have specific guidelines ii. Prognosis: can monitor overtime to see if levels are getting better 3. C type (CNP) c. Cardiac output i. Preload 1. Volume a. Returning to the right (venous) side b. Increase in blood volume 2. Increase in preload can exacerbate HF a. High sodium diets i. More water retention, more fluid in body ii. Afterload 1. Resistance – SVR a. Stress that the heart has to pump against b. Increase in afterload = increase in cardiac work c. As pressure goes up, takes more strength to pump blood out 2. Ex: a. Vasoconstriction b. HTN c. Atherosclerosis d. Aortic stenosis: narrow aortic valve opening d. Drug induced heart failure i. Inhibition of contractility—do not use *** know this 1. Diltiazem, verapamil

a. Worsen mortality 2. Can use DHPs ii. Proarrhythmic effects—do not use *** nice to know 1. Class 1a and 1c iii. Plasma volume expansion—mostly okay *** nice to know 1. NSAIDs, steroids, estrogens 2. High Na+ antibiotics a. Piperacillin, ticarcillin 3. Thiazides: except rosiglitazone, pioglitazone a. Should not be used in Class III or Class IV HF iv. Anti-cancer agents *** nice to know 1. Trastuzumab 2. Anthracyclines (Doxorubicin) 3. Tyrosine kinase inhibitors e. Classification i. NYHA 1. Gold standard 2. Categorizes patients based on symptoms a. Most stay in Class II/III range b. Patients can move up and down the classes ii. ACC/AHA 1. Developed a system (ABCD) where patients can never move up or down 2. Stage D—advanced HF patients a. Candidates for transplants f. Evidence i. Subjective 1. Dyspnea on exertion (DOE) 2. Shortness of breath 3. Orthopnea—need to sleep upright with pillows a. Inability to lie flat without feeling SOB b. Can judge overall level of HF by how upright they have to sleep 4. Paroxysmal Nocturnal Dyspnea (PND) 5. Fatigue 6. Use “faces” counseling point – endorsed by HFSA a. Fatigue, activities limited, chest congestion, edema or ankle swelling, shortness of breath ii. Objective 1. Weight gain a. Surrogate marker for volume b. Outpatient: weight at home c. Hospitalized: know they have volume overload, look to see a decrease in it 2. Peripheral edema 3. Chest X-ray

4. + NT pro BNP a. BNP levels *** nice to know i. T1/2 = 20 minutes ii. Not standardized iii. Cut off values 1. > 500 pg/mL 2. < 100 pg/mL a. CHF unlikely b. NT pro BNP levels *** know this i. T1/2 = 120 minutes ii. Standardized iii. Cut off values – sensitive 1. Age < 50: Level > 450 pg/mL 2. Age > 50: Level > 900 pg/mL 3. Levels < 300 pg/mL a. CHF unlikely iv. Negative BNP says that the signs and symptoms are not related to HF 5. Tachycardia 6. Hypotension 7. +S3,4 8. Rales, Crackles a. Not evident in all patients b. Says that patients have fluid in lungs 9. + Jugular Venous Distention (JVD) a. Bulging neck veins b. Surrogate marker for volume overload 10. + Hepatojugular reflex (HJR) a. Can induce JVD by pressing on someone’s liver II.

Drug Therapy a. Principles i. Start with standard of care medications (ABCD) 1. Ace Inhibitors (or Aldosterone receptor antagonists) 2. Beta blockers 3. Check the doses 4. Diuretics ii. Medications used in selected patients 1. Digoxin 2. ARBs 3. Isosorbide dinitrate + hydralazine 4. Ivabradine iii. Emerging therapy 1. ARNi- angiotensin/neprilysin inhibitor a. Sacubitril/Valsartan (Entresto) b. ACE Inhibitors—Standard of care

i. Advantages 1. Improve a. NYHA Functional Class b. Symptoms and exercise capacity 2. Reduce the risk of hospitalization 3. Reduce mortality 4. Used in all patients with EF < 40% ii. Contraindications 1. History of angioedema 2. Bilateral renal artery stenosis 3. Pregnancy/planning pregnancy iii. Drugs 1. Dosing a. Target doses i. Doses used in clinical trial that showed mortality benefit ii. Dosing matters in HF b. Captopril (Capoten) i. Initial dose: 6.25 mg PO TID ii. Target dose: 50 mg PO TID iii. Short T1/2 c. Enalapril (Vasotec) i. Initial dose: 2.5 mg PO BID ii. Target dose: 10 mg PO BID d. Lisinopril (Zestril, Prinvil) i. Initial dose: 2.5-5 mg PO QD ii. Target dose: 10-20 mg PO QD 2. Titration a. Start with low doses b. Outpatients i. Double the dose no sooner than in 2 week intervals ii. Want to get to the target dose, but not tomorrow iii. Want patient to get used to the new doses both signs and symptom wise c. Hospitalized patients i. More flexible 1. Get to check vital levels and labs consistently ii. Beware of BP, renal function and electrolytes (mostly K) d. Monitor patients for response and tolerability iv. Monitoring Parameters – use these 3 at a surrogate for tolerability 1. Serum potassium a. Baseline, 1-2 weeks after initiation and dose changes b. Monthly for next 3-4 months 2. Renal function (serum creatinine) a. Baseline, 1-2 weeks after initiation and dose changes

b. Monthly for next 3-4 months 3. Blood pressure v. Counseling Parameters 1. Stress adherence a. Reduces risk of dying, improves symptoms, reduces hospitalization b. HF symptoms will improve within a few weeks of starting therapy c. Patient won’t get mortality benefits if they don’t take the drugs 2. Side effects a. Cough b. Blood pressure related side effects i. Usually resolve over time c. Communicate all side effects to health care team 3. Minimize use of NSAIDs and salt substitutes a. Occasional PRN doses are okay vi. Clinical Pearls 1. Asymptomatic “low” blood pressures do not require dose changes a. No number where patient is really low b. If patient has SBP in the 90s but they don’t feel symptoms, it’s okay i. Use symptoms more than numbers ii. Don’t drop doses to treat a number 2. Lower or d/c other medications that may also effect BP a. Nitrates b. CCBS c. Stopping other medications allow us to start an ACE or titrate a dose 3. Worsening renal function and increasing K a. Small increases in both expected b. Increases in creatinine up to 50% is acceptable c. K increase to 5 – 5.5 mEq/L acceptable i. Timing matters ii. If you see a sharp increase early, this is a bad sign c. Beta- Blockers – Standard of care i. Advantages 1. Improves symptoms 2. Decreases hospitalization for worsening HR 3. Decreases mortality 4. Used in all patients with EF < 40% ii. Contraindications 1. 2nd or 3rd degree AV block without a pacemaker 2. Critical limb ischemia iii. Drugs

1. Dosing a. Carvedilol (Coreg) i. Initial dose: 3.125 mg PO BID ii. Target dose: 25 mg PO BID for patients 85kg b. Metoprolol Succinate (Toprol XL) i. Initial dose: 25mg PO QD ii. Target dose: 250mg PO QD c. Bisoprolol (Zebeta) 2. Titration a. Must be clinically stable i. Failure to follow this can lead to negative outcomes in patients b. Start with low doses c. Titrate slowly i. Fastest titration is doubling doses every 2 weeks ii. Consider tolerability, symptoms iii. Aim for the target dose iv. Monitoring Parameters – originally reduce CO 1. HR 2. BP 3. Fluid (volume) status 4. Signs of congestion due to volume overload v. Counseling Parameters 1. Adherence a. Reduces risk of dying, hospitalization for HR 2. Temporarily may feel worse before feeling better a. Especially true when starting or titrating 3. Symptom improvement may take longer in some patients a. 3-6 months 4. Report signs of fatigue and tiredness a. Can be managed by changing other medications b. Patients initially feel worse vi. Clinical pearly 1. Asymptomatic “low” HR or BP does not require change in dose a. Leave numbers the same 2. Patients who develop mild symptoms after initiation a. Try to adjust diuretic dose for SOB/fluid overload b. Try to adjust other BP meds for hypotension/dizziness c. Can decrease dose by ½ if adjusting doesn’t work 3. If HR < 50BPM can ½ the dose a. Clinical gray area b. Look at other medicine that alters HR i. If can’t get rid of any other drugs, then cut dose 4. Patients who present to the hospital with acute exacerbation

a. If already on, keep the same doses b. If not already on, do not start until stable d. Aldosterone Receptor Antagonists i. Advantages 1. Improve symptoms 2. Reduce hospitalizations 3. Reduce mortality 4. Use in all patients with EF < 40% ii. Contraindications 1. Allergies 2. ADRs iii. Drugs 1. Dosing a. Eplerenone b. Spironolactone 2. Titration a. Start with appropriate dosing b. Patients need adequate renal function i. Creatinine: 1. Men: < 2.4 mg/dL 2. Women: < 2.0 mg/dL ii. CrCl: > 30 mL/min iii. Ideally stable c. Serum Potassium < 5 mEq/L i. No history of hyperkalemia iv. Monitoring Parameters 1. K and SCr a. Upon initiation b. Within 2-3 days after initiation c. 1 week after imitation d. Month for 1st 3 months e. Every 3 months after 2. Repeat above cycle whenever a. Dose changes i. ACEIs, ARBs ii. Eplerenone, Spironolactone v. Clinical Pearls 1. Reduce dose by ½ if a. K > 5.5 mEq/L i. Check continuously b. CrCl < 30 mL/min or SCr < 2.5 mg/mL 2. Discontinue if a. K > 6 mEq/L i. Patients proved they can retain K well, no longer need the antagonists

b. CrCl < 20 mL/min or SCr < 3.5 mg/mL 3. Avoid/minimize other medications that can increase K a. K sparring diuretics i. Triamterene, amiloride ii. K supplements iii. NSAIDs iv. Salt substitutes that have a higher K content e. Loop Diuretics i. Advantages 1. Removes excessive fluid, maintains normal volume a. Euvolemia b. Eventually, all patients need to be on loops c. On them for life 2. Decrease preload 3. Improve symptoms a. Work the fastest 4. No effect on mortality ii. Use 1. Used in all patients who have signs and symptoms of congestion a. Regardless of EF 2. Acutely to treat symptomatic fluid retention 3. Maintenance of euvolemia (“dry weight”) a. Goal weight b. Weight where patients are asymptomatic 4. Thiazide diuretics are not effective enough iii. Drugs 1. Bioavailability ***all considered equally effective a. Bumetanide 80-90% b. Furosemide 60% c. Torsemide 90% i. Preferred for chronic management (outpatient) d. Ethacrynic Acid 100% 2. Dosing – no target dose a. Bumetanide i. Initial dose: 0.5 – 1mg PO QD or BID ii. Max daily dose: 10mg b. Furosemide i. Initial dose: 20-40 mg PO QD or BID ii. Max daily dose:600mg c. Torsemide i. Initial dose: 10-20 mg PO QD or BID ii. Max daily dose: 200mg d. Ethacrynic Acid i. Initial dose: 25-50 PO QD or BID ii. Max daily dose: 200mg

3. Equivalent doses *** used to switch patients from 1 agent to another a. Furosemide: 40 mg b. Torsemide: 20 mg c. Bumetanide: 1 mg 4. Titration a. Outpatient i. Use lowest effective doses ii. Highly individualized 1. Relief of symptoms 2. Maintenance of dry weight and euvolemic b. Inpatient i. Furosemide IV is the mostly commonly IV loop 1. Lasix = lasts six hours ii. If new to diuretics, use initial dose iii. If patient is taking diuretics at home 1. First dose is double the home dose a. Torsemide: give double of home doses as furosemide IV b. Furosemide: give the same dose as home dose i. CAN ALSO DOUBLE DOSE iv. Subsequent doses are based on clinical response 1. If minimal response after 1st dose, try to double it 2. If good urine output, keep the dose the same iv. Monitoring Parameters 1. Daily body weight 2. Symptoms relief 3. Renal function 4. Electrolytes a. K+ and Mg2+ 5. Urine output 6. I/O: fluid intake/ urine output a. Goal for intake/output i. Outpatients — “even” 1. Input = output ii. Hospitalized — negative 1. 1-2 L per day until dry weight is achieved a. Varies 2. Input = 1,000mL, output = 2,000 or 3,000 mL 7. Look diuretic resistance a. Minimal or no response to high dose loops i. I/Os are even or less than goal negative set for patient b. Can try doubling the dose i. Bolus ii. Can repeat bolus multiple times day (T1/2 = 6 hours)

c. Consider furosemide continuous IV infusion i. Dosing range: 5 mg / hour – 40 mg / hour ii. Consider current furosemide requirements iii. May be more effective than bolus d. Add thiazide diuretics for synergy i. Chlorothiazide IV ii. Metolazone iii. Administered 30 minutes prior to loops v. Counseling Parameters 1. Adherence, purpose of taking diuretics 2. Sodium restricted diet 3. When to take doses a. Daily: in the AM i. If working night shift can switch it b. BID: in the morning, early afternoon 4. Check weight daily a. Same time, same way, same location 5. Signs of dehydration a. Dry mouth b. Increased thirst c. Dizziness, hypotension 6. Minimize/avoid NSAIDs vi. Clinical Pearly 1. Asymptomatic “low” BP a. May be able to reduce dose if no signs of congestion 2. Hypo K+ or Mg2+ a. Increase ACE/ARB dose b. Add aldosterone antagonist if not added already 3. Hyperuricemia/gout a. Avoid NSAIDs, consider allopurinol 4. Doses will fluctuate over time 5. Chronic NSAIDs may reduce diuretic effectiveness 6. Torsemide is preferred for outpatients f. Digoxin i. Advantages 1. Reduced hospitalization 2. Reduced symptoms 3. No mortality benefit ii. Use 1. In selected patients a. Frequently hospitalized patients in sinus rhythm despire good medical therapy iii. Dosing 1. Low doses a. 125 mcg PO QD

i. Highest dose to use b. Dose adjustment based on reduced renal function 2. Younger patients, normal renal function, larger body weight patients a. 250 mcg PO QD b. Patients can tolerate the higher doses 3. Therapeutic range a. Textbook: 0.8 – 2.0 ng / mL i. No clinical data to support this!! ii. Comes from surrogate endpoints b. Heart failure: 0.5 – 1 ng / mL i. If they’re above 1, then ½ the dose iv. Monitoring Parameters 1. Serum digoxin concentrations 2. HR 3. EKG 4. BUN / creatinine 5. Signs of toxicity 6. K+, Mg 2+ a. Low levels can enhance digoxin sensitivity v. Drug Interactions 1. Pharmacist can prevent/minimize risk of digoxin toxicity 2. Drugs that can increase digoxin levels a. Amiodarone: decrease digoxin dose by 50% *** b. Quinidine: decrease digoxin dose by 50% *** c. Erythromycin d. Verapamil e. Dronedarone: decrease digoxin dose by 50% *** 3. Drugs that can decrease digoxin a. Antacids b. Cholestyramine c. Metamucil g. ARBs i. Advantages 1. Improves symptoms 2. Reduce HF hospitalization 3. Do reduce mortality, but only in patients not taking ACEI 4. Do not add in patients taking ACEIs a. Kills people ii. Use 1. Not 1st line, not substitute to ACE 2. Not in patients already on ACE and beta blockers 3. Indicated for ACEI intolerance a. Renal impairment b. Hyperkalemia c. Cough

d. Angioedema iii. Drugs 1. Dosing a. Losartan (Cozaar) i. Initial dose: 12.5 mg PO QD ii. Max daily dose: 150mg PO QD b. Valsartan (Diovan) c. Candesartan (Atacand) h. Hydralazine + Isosorbide (BiDil) i. Background 1. Hydralazine a. Arteriolar vasodilator b. Decreased afterload 2. Isosorbide Dinitrate a. Venodilator b. Decreases preload 3. Benefits a. Can reduce mortality in patients not taking ACE inhibitors b. 1st line option for African American patients ii. Use 1. African Americans already on ACE/BBs/ARBs who are persistently symptomatic (class 1a) 2. ACE/ARB intolerant patients a. Renal insufficiency i. If ACE/ARBs will affect renal function b. Hyperkalemia c. Angioedema i. Not worth re-challenging 3. Limitations a. Difficulty tolerating both patients b. Need to use high doses c. Complaints i. TID/QID regimen ii. Difficult to maintain adherence iii. Dosing**** 1. Hydralazine a. Initial: 10mg PO QID b. Target: 75mg PO QID 2. Isosorbide Dinitrate a. Initial: 5mg PO QID b. Target 40mg PO QID 3. BiDil a. Combo formulation b. 37.5mg hydralazine and 20mg isosorbide

c. Initial: 1 tab PO TID d. Target: 2 tabs PO TID iv. Side Effects 1. Hydralazine a. GI Upset b. Headache i. Common c. Flushing d. Tachycardia i. Almost all patients are already on beta-blockers ii. Don’t feel tachycardia as much e. SLE (lupus) 2. Isosorbide Dinitrate a. Headache b. Hypotension c. Orthostasis i. Ivabradine (Corlanor) i. Only for patients with HR > 70 BPM *and* ii. On “max tolerated” dose of beta-blocker or target dose 1. Often times patients do not get to target dose of beta-blocker a. Due to side effects/HR 2. Originally used for arrhythmias a. Inhibits funny current b. Slows AV nodal conduction iii. Dose: 2.5-7.5 mg PO BID j. ARNi: Sacubitril/Valsartan (Estresto) i. Background 1. Fused molecule a. Can’t be separated 2. Combo neprilysin inhibitor and ARBs a. Blocks RAAS and degradation of BNPs b. Defeated ACEIs in clinical trials c. Reduces mortality 3. Hospitals are evaluated for 30 day readmission for heart failure a. If hospitals are higher than the standard (more readmissions), Medicaid funding is taken away b. 30 day readmission is for anything i. If someone comes in for HF and comes in in less than 30 days with a broken bone or something, that still counts ii. Doesn’t have to be related to HF ii. Use 1. When a. Switch stable patients taking target/ max tolerated doses of ACEs and ARBs i. Done in outpatient

ii. Not used often in inpatient setting 1. Don’t want 30 day readmission b. Not upfront replacement for ACE/ARBs i. Don’t know how patients will react if they are started on these ii. Patients are more often switched to these c. Patients that can afford this i. ACE/ARBs are generic ii. Estresto is brand = $$$ 2. How to use a. 50mg (24mg sacubitril/26mg valsartan) BID is recommended in the following patients i. Who have never taken an ACEI or ARB ii. Who are taking low doses of these iii. With a eGFR...