Outpatient Management of Chronic Heart Failure

Transcription

1 Outpatient Management of Chronic Heart Failure Tracy K. Pettinger, PharmD, BCPS Clinical Associate Professor Idaho State University College of Pharmacy

2 Disclosure Statement I have no relevant financial relationships or commercial interests to disclose in conjunction with this presentation.

3 Objectives for Pharmacists, Nurses, and Prescribers Explain the complexity of the pathophysiology of heart failure (HF) including compensatory mechanisms. Describe the role of various pharmacologic agents in the treatment of HF. Determine proper monitoring and education for patients using medications for HF.

4 Objectives for Technicians Name common causes of HF. State differences between HF with reduced vs. preserved ejection fraction. Recognize classes of medications used to treat heart failure.

5 HF with Reduced Ejec/on Frac/on is now used to describe what type of HF? A. Systolic dysfunc/on B. Diastolic dysfunc/on C. Right- sided dysfunc/on D.???, that s why I m here

6 Chronic Heart Failure (CHF) A clinical syndrome resulting from any disorder that Impairs the ability of the ventricle to fill with (diastole) or eject blood (systole) Heart unable to pump blood at a rate sufficient to meet the metabolic demands of the body Previously defined as Congestive Heart Failure Cardiac Output = Heart rate x Stroke Volume CO = HR x SV

7 Terms Ejection Fraction (EF) The percentage of left ventricular blood volume ejected during systole (contraction) Normal EF is 60% to 70% Right-sided & left-sided HF Anatomical

8 Terms Afterload Tension developed in the left ventricular wall as systole occurs Regulated by systemic vascular resistance or the impedance which the left ventricle must pump against Mainly determined by arterial blood pressure Preload Volume in the left ventricle at the end of diastole

9 HFrEF (Systolic Dysfunction) Low EF <40% Unable to eject enough blood to keep up with the metabolic demands of the body Ventricle has difficulty contracting à ventricles become dilated à congested with retained blood Most common cause of systolic heart failure MI (CAD)

10 HFpEF (Diastolic Dysfunction) Associated with an EF >40% Ventricle has diastolic stiffness Reduced compliance Unable to fill adequately Most common cause of diastolic heart failure is hypertension Therapy aimed at heart rate & blood pressure control

11 HFrEF Heart Failure with Reduced Ejection Fraction

12 Pathophysiology Compensatory Mechanisms Intended to be short term responses Maintain circulatory homeostasis after acute reductions in blood pressure or renal perfusion Detrimental long term May occur after an acute or chronic event Neurohormonal Model Sympathetic nervous system (SNS) Renin-Angiotensin-Aldosterone System (RAAS)

13 SNS Causes tachycardia Tries to increase CO by increasing HR Causes increase in oxygen demand Eventually decreases filling time actually decreases SV Increases contractility Tries to increase CO by increasing SV Causes increase in oxygen demand

14 Beta Receptors Overstimulation of β receptors Causes a down regulation and synthesis of Initiates uncoupling of receptors Blunting of the sympathetic response in a failing heart Unable to respond to environmental stressors These changes in receptor dynamics are important when initiating beta blockers and especially in a decompensated state

15 Direct remodeling of cardiac tissue Increased fibrosis of cardiac tissue Angiotensin II receptors on the heart Increases thirst drive Increases ADH release Increases water reabsorption from collecting duct RAAS Increased fibrosis of endothelial & cardiac tissue Adapted from cpharm.vetmed.vt.edu/.../ CARDIOVASCULAR/chf.htm Increased Preload Direct remodeling of cardiac tissue

16 Treatments Treatment of HFrEF focuses on Manipulation of SNS & RAAS Management of concomitant disease states Lifestyle changes / management HF guidelines (2013)

17 Which of the following has NOT been shown to decrease mortality in HFrEF? A. Carvediolol B. Spironolactone C. Lisinopril D. Digoxin

18 Presentation Signs Pulmonary rales Lower leg edema Jugular venous distention Increase BNP Symptoms Dyspnea (on exertion) Orthopnea Paroxysmal nocturnal dyspnea Edema Fatigue Exercise intolerance

19 Current Treatments Live Longer Medications Shown to improve mortality Beta-Blockers ACE-I ARB Aldosterone Antagonists Hydralazine & isosorbide dinitrate Feel Better Medications No benefit on mortality Can help with hospitalizations Diuretics Loop Thiazide (Metolazone) Digoxin

20 Live Longer Medications

21 β Blockers Cornerstone for patients with HFrEF Start as soon as diagnosed Will increase ejection fraction Especially if due to ischemic causes MOA Decreases contractility (acutely) Resets β receptors Decreases cardiac remodeling; allowing the heart to return to normal or near normal functioning **NDP CCB are NOT an alternative

22 Drugs & Dosing β blockers should NOT be started too quickly Start only in stable, euvolemic patients Start low and go slow Titrate every 2-4 weeks if stable Dose usually doubled Stop at max dose

23 ADR: Educate! May worsen symptoms at first Four main ADR that require attention Fluid retention & worsening HF Fatigue Bradycardia Hypotension Quality of Life fatigue Exacerbate depression Decrease libido/ed Constant monitoring Symptoms BP, HR

24 ACE-I Recommended for all pts with HFrEF Improve symptoms and exercise tolerance MOA in HF Decrease preload Na & H 2 0 retention blood volume Decrease afterload ( arteriole pressure) Postulated vasodilation benefits of bradykinin & PG Cardiac remodeling hypertrophy, fibrinogen, & collagen in cardiac myocyte

25 Drugs & Dosing Current data suggests class effect Dosing controversy Current guidelines still recommend target doses until more information is available

26 ACE-I Considerations Assess volume status Prior to starting and increasing ACE-I Hypotension Elevated BUN/SrCr BP & HR Remove other agents that K+ Potassium-sparing diuretics Salt substitutes Potassium supplements Monitoring K+ SrCr BUN BP, HR

27 Use of ARBs in HFrEF Major role Consider as an alternative to ACE-I in pts w/ intolerance May be used when AA is not tolerated Combination therapy with ACE-I Controversial Use as 4th agent in combo w/ ACE-I, β blockers, aldosterone inhibitors. Routine use not recommendedà potential harm

28 Drugs & Dose Possible class effect Monitoring, contraindications, ADR same as ACEI (except cough)

29 Aldosterone Antagonists Starting to be used more often and sooner Recommend in NYHA II-IV EF<35% After optimal doses β blockers, ACE-I, (and diuretics) Of note, class II pts need CV hospitalization or high BMP After acute MI with EF<40% Useful in pts needing additional antihypertensive agents

30 MOA Aldosterone receptor antagonist Decreases preload Diuretic effect in distal tubule; K+ sparing Decreases afterload Possible decrease of sympathetic activation Increase arterial compliance Cardiac remodeling Decrease myocardial and vascular fibrosis Decrease baroreceptor dysfunction

31 Drugs & Dose Spironolactone Studied in NYHA class III & IV Generically available Dose Initiate at 12.5 mg to 25mg daily Target of 25mg daily Anti-androgen effects Eplerenone Studied in NYHA class II CHF after MI Cost ~$4/day Dose Initiate at 25mg daily Target of 50 mg once daily Benefits More selective Better tolerated

32 ADR & Monitoring Potassium Baseline, w/in the 1st week & at 1 week after initiation or dose adjustment Then monthly for the 1 st 3 months Depending on other drugs that affect potassium Then q3-6 mo thereafter Renal function (BUN/SrCr) BP & HR

33 Hydralazine/Nitrates NYHA class III-IV HFrEF In addition to optimal therapy with ACEI/ARB and beta-blockers (and AA) Use as an alternative to ACE-I and ARBs Intolerant of ACE-I or ARB Pts w/ severe renal dysfunction Persistent hyperkalemia on ACE-I or ARB May improve mortality but not to the extent of ACE-I or ARBs May play more of a role in African Americans In addition to ACE-I

34 Feel Better Medications

35 Diuretics Symptomatic relief of volume overload Can improve exercise tolerance Elimination of sodium and water results in a reduction of preload Furosemide is most commonly used; but bumentanide and torsemide have better oral bioavailability

36 Loops Diuretic Dosing Begin at low dose Furosemide 20 to 40mg po q day Titrate to a loss of 1-2 lbs/day acutely, then tailor Self-adjusted diuretics for some pts Once euvolemia is achieved and pt is stable try tapering dose Ceiling dose No more benefit than lower doses w/ higher toxicity

37 Loop Diuretics Important notes on furosemide IV:Oral dose is ~1:2 If dosed twice daily, should keep second dose no later than 4 PM Patients with pulmonary edema or with marked volume overload should be given intravenous furosemide initially

38 Thiazide Diuretics Diuretic resistance: long-term use changes tubule or ion transport dose or add thiazide to loop regimen Metolazone is most common Thiazide diuretics Generally not very effective in pts with a CrCl < 30 ml/min Metolazone (Zaroxolyn ): The thiazide exception Caution when used with loop: can cause marked volume losses à hypotension, hypokalemia

39 ADR & Monitoring Volume status Overdiuresis: may cause acute renal failure / hypotension Underdiuresis: worsening symptoms of volume overload Electrolyte Disturbances Loop vs. thiazide Supplementation of potassium Chem panel 3-5 days after starting regimen & changes in doses Inpatient vs. outpatient Response and compliance to regimen

40 Digoxin Used in HFrEF only Added to pts with persistent symptoms despite treatment with optimal doses of neurohormonal antagonists Positive inotropic effects Negative chronotropic effects

41 Digoxin Dosing The usual oral maintenance dose: to 0.25 mg Levels Titrate to an adequate serum digoxin level ng/ml No need to push higher doses in HF Levels >2.0 are considered toxic Females may not benefit and increased mortality Use may worsen symptoms in diastolic HF

42 HFpEF Heart Failure with Preserved Ejection Fraction

43 What is the primary cause of HFpEF? A. Hyperlipidemia B. Hypertension C. Myocardial Infarc/on D. Diabetes

44 HFpEF Limited literature available Treat underlying etiology Tight control of HTN No specific goal in HF guidelines Follow JNC 8 Rate control Allows enough time for ventricle to fill completely More important in tachycardia rather than normal resting heart rate

45 Other Drugs ACEI / ARBs BP control ARBs or ACE-I? CHARM Preserved ARB may be beneficial Non-significant trend toward improved mortality β Blockers Consider in those post- MI, hypertension, afib Rate control Diuretics Symptomatic relief due to volume overload

46 Other Drugs Spironolactone Decrease ventricular stiffness BP control TOPCAT (2013) Spironolactone 30mg-45mg daily vs. placebo No difference in mortality Significant decrease in hospitalizations Calcium Channel Blockers Non-dihydropyridine Rate control, especially when pt is intolerant of BB Dihydropyridine BP control Watch for swelling and HR increase

47 Questions?

48 Evaluation Starting with Pharmacists, Nurses and Prescribers

49 Which equa/on best describes the targets for compensatory mechanisms used by the body in a HF state? A. Blood Pressure = Cardiac Output x Peripheral Vascular Resistance B. Cardiac Output = Heart Rate x Stroke Volume C. Cardiac Output = Peripheral Vascular Resistance / Heart Rate D. Energy = (Mass x Speed of Light) 2

50 What home- monitoring technique is best to determine the efficacy of a diure/c regimen? A. Blood Pressure B. Daily oxygen levels using a home pulse oximeter C. Thirst drive D. Daily weights

51 This drug is specific for the aldosterone receptor and has good data for use in HFrEF class II. A. Eplerenone B. Spironolactone C. Candesartan D. Isosorbide dinitrate

52 Techs Turn!

53 Heart failure is a syndrome where the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the body. A. True B. False

54 Which of the following best describes HFrEF? A. Low EF, dilated ventricle B. Low EF, thick ventricle C. Normal/high EF, dilated ventricle D. Normal/high EF, thick ventricle

55 Which class of medica/ons is used for HFrEF symptoms only? A. Diure/cs B. ACE- Inhibitors C. Hydralazine & Isosorbide dinitrate D. Beta- blockers