HEART FAILURE CASE. AS, a 64-year-old woman; emergency department

Transcription

1 HEART FAILURE CASE Patient and Setting: Chief Complaint: AS, a 64-year-old woman; emergency department Over the past couple of weeks, I sometimes wake up short of breath. Last night, I woke up 3 times. I cough a lot and am just so tired. I can t even walk to the mailbox without feeling extremely exhausted. My legs are starting to swell, and I ve gained 14 pounds in the last couple of weeks. History of Present Illness: AS complains of dyspnea and fatigue over the last several months. She gave up exercising about 2 months ago because of a recent diagnosis of osteoarthritis (OA) and the fact that she just gets too tired walking. Over the past 2 weeks, she c/o 3-pillow orthopnea and PND. She c/o cough without sputum and feels fatigued most of the day and cannot perform her usual activities of daily living (ADL). She also noted BLE edema over the past several weeks. Self reported weight gain of 6 7 kg over last 2 months. She denies chest pain. Medical History: HTN and CAD diagnosed at age 54; T2DM diagnosed at age 62; OA diagnosed at age 64 Surgical History: Noncontributory Family/Social History: Mother: HTN; father: died at age 65 S/P MI. Tobacco: quit 10 years; 40 pack-year history. Occasional ETOH use. AS, a retired hotel housekeeper, lives with her husband, a retired mechanic. She has 3 grown children (1 son, 2 daughters) and 3 grandchildren. Medications: Allergies: HCTZ 25 mg PO daily Sotalol 120 mg PO BID Simvastatin 40 mg PO at bedtime Celecoxib 200mg BID Enalapril (angioedema) Physical Examination: GEN: Well-developed, obese white female with noticeable SOB VS: BP 110/78, HR 55, RR 20, T 98.5 F, Wt 70 kg, Ht 5 4 HEENT: PERRL, EOMI, denies headache, denies change in vision NECK: + JVD to 12 cm, no bruits COR: nl S1 and S2, RRR, S3 gallop, point of maximal impulse (PMI) was displaced downward and laterally CHEST: Decreased breath sounds, crackles in bilateral lower lobes 1

2 ABD: Soft, ND, + hepatojuglar reflex, + bowel sounds GU: Deferred RECT: Heme-negative brown stool EXT: 2+ edema to knees bilaterally, slightly cool to touch NEURO: A & O 4 Results of Pertinent Laboratory Tests, Serum Drug Concentrations, and Diagnostic Tests: Na 134 (134) K 4.3 (4.3) Cl 100 (100) CO 2 26 (26) Alb 43 (4.3) BUN 11.4 (32) SCr (1.7) Glucose 8.1 (145) A1c 7.6 % Mg 0.85 (1.7) Ca 2.3 (9.0) PO (3.3) WBC ( ) AST 1 (60) ALT 1.5 (90) Alk Phos 1.67 (100) T Bili 15.4 (0.9) Hgb 140 (14) Hct 0.34 (34) Plts ( ) BNP 1263 pg/ml Fasting: Total cholesterol 4.65 mmol/l (180 mg/dl) LDL 2.3 mmol/l (90 mg/dl) HDL 1.55 mmol/l (60 mg/dl) Triglycerides 1.46 mmol/l (130 mg/dl) Urinalysis: Negative ECG: Sinus bradycardia, ventricular rate 53, QT/QTc 470/453 CXR: Positive cardiomegaly ECHO: LV end diastolic dimension = 6.1 cm, LV end systolic dimension = 5.0 cm, LA dimension = 4.0 cm, inferior hypokinesis, anterior hypokinesis, ejection fraction of 38%, mild mitral regurgitation 2

3 PROBLEM LIST Identify principal problems from the scenario in priority order (see Answers for correct list of problems). SOAP NOTE To be completed by student (see Answers for correct SOAP Note) 1. The most probable cause for AS s dyspnea is: A) Pneumonia B) Heart failure C) Recently added celecoxib D) Pulmonary embolus 2. Which of the following characteristics is NOT a sign or symptom of heart failure that relates to failure of the right ventricle? A) 2-pillow orthopnea B) Dyspnea at rest C) PND D) JVD 3. Which of the following laboratory and physical findings are consistent with systolic heart failure? A) SCr (1.7) with cardiomegaly on CXR B) EF = 50% with enlarged LV end diastolic dimension C) BNP = 563 pg/ml with PND D) BNP = 80 pg/ml with elevated hepatic enzymes 4. AS s presentation is consistent with which of the following stages of heart failure? A) Stage A B) Stage B C) Stage C D) Stage D 5. List at least 3 common etiologies contributing to heart failure in AS. 6. In patients with HF, which of the following side effects often occurs during the initiation and/or dose escalations of beta-blockers? A) Third-degree AV block B) Fluid retention and worsening heart failure C) Tachycardia D) Hypertension 7. Contraindications to the use of ACEIs in AS include which of the following? 3

4 A) History of renal insufficiency B) Asymptomatic bradycardia at 60 bpm C) Interactions with celecoxib D) Angioedema 8. The decision is made to discontinue sotalol. In addition to this intervention, which of the following is an appropriate pharmacotherapeutic change in AS to improve the treatment of her heart failure? A) Do not add another beta-blocker at this time B) Begin carvedilol at mg twice daily C) Begin metoprolol XL at 200 mg daily D) Begin atenolol at heart failure dosing recommendations 9. Which of the following statements regarding heart failure (HF) with preserved EF is correct? A) Patients with HF with preserved EF are more likely to have bilateral edema than DOE on presentation compared with patients with systolic dysfunction. B) Patients with HF with preserved LV function rarely exhibit concomitant systolic dysfunction of the heart. C) Less than 10% of all patients with HF have HF with preserved systolic function. D) Typical causes of diastolic dysfunction include HTN, aortic stenosis, hypertrophic cardiomyopathies, and CAD. 10. Describe the staging system of heart failure as endorsed by the ACC/AHA, and compare that staging system with the NYHA Classification. 11. The cardiologist recommends starting valsartan in AS. Is this an appropriate medication for AS? Explain your answer. 12. Give at least 2 reasons why sotalol would not be an appropriate beta-blocker in AS? 13. Explain the potential problems associated with the use of NSAIDs in patients with heart failure. 14. Summarize the therapeutic, pathophysiologic, and disease management concepts for heart failure using a key points format. 4

5 Model Answer Problem List 1. New-onset heart failure 2. Bradycardia secondary to probable sotalol accumulation/toxicity 3. Renal insufficiency 4. HTN 5. T2DM 6. CAD 7. Allergy to enalapril (angioedema) SOAP Note S: Over the past couple of weeks, I sometimes wake up short of breath. Last night, I woke up 3 times. I cough a lot and am just so tired. I can t even walk to the mailbox without feeling extremely exhausted. And my legs are starting to swell. And, I ve gained 14 pounds in the last couple of weeks. O: BP 110/78, HR 55, BMI 26.5, estimated creatinine clearance ~29 ml/min, 70 kg BW (IBW 55 kg), noticeable SOB, + JVD, decreased breath sounds, S3 gallop, PMI was displaced downward and laterally, 2+ edema to knees, slight elevation AST/ALT, Hct 34%, BNP 1263, sinus bradycardia, ventricular rate 53, QT/QTc 470/453 on ECG, EF 38% with inferior hypokinesis and anterior hypokinesis on ECHO 5

6 A: Problem 1: New-onset heart failure Problem 2: Bradycardia (HR 55, QT/QTc prolonged) with fatigue secondary to chronic kidney disease and probable sotalol accumulation Problem 3: Chronic kidney disease (stage 4 based on estimated creatinine clearance) Problem 4: HTN: on HCTZ and beta-blocker (to be discontinued secondary to toxicity), and no renal protection agent for T2DM Problem 5: T2DM: not controlled with diet and exercise, A1c = 7.6%, no agent for renal protection Problem 6: CAD: on simvastatin, not at LDL goal of <70 Problem 7: Allergy to ACE inhibition with history of angioedema P: Problem 1: New-onset heart failure Admit AS to the hospital for work-up of new-onset heart failure. O 2 BNC; titrate O 2 saturation to >92%. Cardiac enzymes 3. Diuretic administration: Administer 20 mg IV furosemide as a single dose and monitor for symptomatic responsiveness. Can give secondary dose if AS does not respond to 20 mg IV. Start furosemide 40 mg PO daily. Monitor electrolytes for hypokalemia and hypomagnesemia. Initiate angiotensin receptor blocker (ARB) after discussing angioedema with patient, as described later. Daily weights. 6

7 Strict I/Os. Fluid restriction <2 L/d. Na restriction <2g/d. Assess if patient has scale at home for daily weight monitoring. Assess immunization status (may need influenza vaccination depending upon time of the year). Problem 2: Bradycardia (HR 55, QT/QTc prolonged) with fatigue secondary to chronic kidney disease and probable sotalol accumulation Discontinue sotalol: would begin to taper the beta-blocker in normal renal elimination, but considering AS s kidney function and signs of toxicity (bradycardia ± fatigue, BP effects), a taper will occur naturally secondary to decreased renal clearance. Monitor vital signs every 4 hours. 12-lead ECG monitoring every 12 hours until sotalol washout or resolution of QT prolongation. Assess magnesium level and consider replacement if hypomagnesemic (risk of torsades). Problem 3: Chronic kidney disease Monitor BUN/SCr. Monitor I/Os. Monitor electrolytes. 7

8 Assess if current level of kidney function is patient s baseline kidney function (determine from prior labs if available). Work up for secondary complications of CKD (e.g., anemia, secondary HPT) and consult a nephrologist based on guidelines for stage 3 4 CKD. Problem 4: HTN on HCTZ and beta-blocker (to be discontinued secondary to toxicity), and no renal protection agent for T2DM Discontinue HCTZ. Discontinue sotalol (as previously stated). Initiate furosemide 40 mg PO daily. Monitor for electrolyte abnormalities such as hypokalemia, symptomatic hypotension/dizziness, and volume depletion. BP is not currently below goal of 130/80. Monitor BP and HR every 4 hours. Initiate ARB, as described in Problem 5. Consider addition of carvedilol at mg BID once euvolemic and after sotalol washout if BP remains elevated. Problem 5: T2DM: not controlled with diet and exercise, A1c = 7.5, and no agent for renal protection A1c is currently above 7, demonstrating that glucose is not within desired range for last 3 months. Initiate sliding-scale insulin. 8

9 Monitor blood glucose 3 4 times a day. If blood glucose remains elevated, consider starting oral hypoglycemic (not metformin or a thiazolidinedione due to contraindications). Evaluate for microalbuminuria. Initiate an ARB such as valsartan 40 mg PO BID. Monitor BUN, SCr, and K. Consider ASA 81 mg EC PO daily for cardioprotective effects. Consult for diabetes education. Consider referral to diabetes clinic after discharge. Problem 6: CAD: on simvastatin, not at LDL goal of <70 Consider increase in lipid-lowering therapy. Consult dietician to discuss meal planning. Problem 7: Allergy to ACE inhibition with history of angioedema Add an ARB for HF, HTN, and DM. Counsel on risk of secondary angioedema. Possible Epi-Pen. Answers to Case Questions 1. B. Heart failure 9

10 2. D. JVD 3. C. BNP = 563 pg/ml with PND 4. C. Stage C 5. Hypertension, coronary artery disease, and diabetes 6. B. Fluid retention and worsening heart failure 7. D. Angioedema 8. B. Begin carvedilol at mg twice daily 9. D. Typical causes of diastolic dysfunction include HTN, aortic stenosis, hypertrophic cardiomyopathies, and CAD. 10. The progression of HF was recently incorporated in the ACC/AHA Staging System for HF. HF is now classified as stage A, B, C, or D depending on risk factors, structural heart disease, and symptoms. Drug therapy is recommended for each stage of disease based on strength of evidence. This classification allows early interventions to be instituted before the patient develops the syndrome to reduce morbidity and mortality from the disease. 10

11 NYHA augments the ACC/AHA Staging System. NYHA Classification is based on functional capacity (i.e., how well the patient can function without symptoms based upon exertion). As opposed to the ACC/AHA Staging System, in the NYHA Classification, drug therapy can influence the classification by improving the functional capacity of the patient (e.g., furosemide can improve NYHA Classification). 11. Yes, an angiotensin receptor blocker (ARB) may be used in a patient with ACE inhibitor (ACEI) intolerance secondary to angioedema and does offer mortality benefit in patients who cannot tolerate ACEIs. The mortality benefit (studied in ELITE-II, Val- HEFT, and CHARM) must be weighed against the risk of secondary angioedema from the ARB. Case reports confirm that angioedema following ARB administration can occur with all ARBs. Randomized trial data addressing this issue come from the CHARM-Alternative trial, which reported that 39 participants (4%) enrolled had previous angioedema/anaphylaxis from ACE inhibition. In that study, three patients taking candesartan and none taking placebo reported angioedema. Thus, the risk of recurrent angioedema with candesartan (and likely other ARBs) is probably acceptable (<10%) given the benefit in these individuals who cannot take an ACEI. However, careful monitoring and instructions need to be given to the patient regarding secondary angioedema. A prescription for an Epi-Pen may be appropriate. 12. AS is receiving sotalol without indication (i.e., arrhythmia). Sotalol is not approved for the treatment of heart failure and is not an appropriate beta-blocker in patients with systolic HF (increased mortality with d-isomer in SWORD trial). Beta blockade in HF 11

12 with systolic dysfunction should be limited to either carvedilol, metoprolol XL, or bisoprolol because these are the only beta-blockers FDA approved for HF as supported by clinical trial data. Beta blockade in HF should be titrated carefully, and low doses should be used upon initiation. Beta blockade at high doses may decrease myocardial contractility and slow the heart rate, and because of the high dose of sotalol used, beta blockage may have contributed to the exacerbation of heart failure in AS (120 mg BID). Additionally, it is renally eliminated, and AS may be experiencing toxic effects from beta-blocker accumulation (fatigue, HR = 55, prolongation of QT interval) because of her dosing regimen. Dosing recommendations for sotalol in renal insufficiency should be strictly followed because of the risk of torsades. 13. Use of NSAIDs is not recommended in patients with chronic heart failure. In patients with HF, renal function may depend on the compensatory activity of prostaglandins to increase renal blood flood by dilating the afferent arteriole. Inhibition of prostaglandin synthesis by NSAIDs may alter this autoregulatory process and may also result in fluid retention. In HF patients, the use of NSAIDs may be implicated in cases of unexplained azotemia. NSAIDs may also interfere with the therapeutic properties of ACEIs and loop diuretics, the beneficial effects of which require the presence of local renal vasodilatory prostaglandins. A particularly important interaction is that of ACEI and NSAIDS, which work on opposing efferent and afferent arterioles, respectively. The combination can result in decreased GFR, increased fluid retention, and severe renal effects. Although COX-2 inhibitors have not yet been carefully studied in HF patients, the 12

13 above concerns could apply as well because these agents have similar prostaglandinblocking properties. 14. Key Points Heart failure is a progressive complex clinical syndrome associated with significant morbidity and mortality that often presents nonspecifically with dyspnea, fatigue, and fluid retention. The primary mechanisms that underlie the clinical syndrome of heart failure can be from systolic (contracting) dysfunction (i.e., <40%), diastolic (filling) dysfunction (i.e., >40%), or, most commonly, a combination of both. BNP provides a useful screening tool for systolic dysfunction. CAD and HTN are the primary causes of HF, and risk modification of these predisposing conditions is important to slow the progression of heart failure and is the basis for the ACC/AHA Staging System for heart failure. Drug therapy is recommended based on the stage in which the patient presents, with preventative medications (ACE inhibitors and beta-blockers) being started in stages A and B. ACE inhibitors, ARBs, beta-blockers, and aldosterone antagonists block the neurohormonal toxicity, contributing to the overall pathophysiology of the disease. All of these agents are associated with varying degrees of mortality reduction. 13

14 Digoxin and furosemide are medications used for morbidity reduction and symptomatic control of the disease, but these agents are not associated with mortality reduction. Medications that need to be avoided in patients with HF include NSAIDs, COX-2 inhibitors, nondihydropyridine calcium channel blockers, herbals and OTC decongestants, and Vaughn Williams class I antiarrhythmics. Important nonpharmacologic management includes sodium restriction, weight management, alcohol avoidance, and regular exercise training. 14