HEART FAILURE-UPDATES AND PRACTICAL APPROACHES TO PATIENT CARE

DR DEAN T. GOROSKI, BCPS, CAPT, USPHS

2018 MPA WINTER CE AND SKI MEETING

BIG SKY, MT JANUARY 6, 2018

DISCLOSURE

➢Dr. Goroski has no actual, perceived, probable, suggested,

potential, imaginary, conceptualized, likely, hopeful, aggravated,

insinuated, or otherwise conflict of interest in relation to this

program/presentation.

OBJECTIVES

➢At the completion of this presentation, participants

will be able to :

➢Describe and differentiate the main diagnoses of heart failure

➢Describe the pharmacologic goals of heart failure treatment

and identify opportunities to optimize treatment

➢ Identify lifestyle changes to promote positive patient

outcomes in heart failure management

OBJECTIVES

➢Describe and differentiate the main diagnoses of heart failure

➢Describe the pharmacologic goals of heart failure treatment

and identify opportunities to optimize treatment

➢ Identify lifestyle changes to promote positive patient

outcomes in heart failure management

CHRONIC HEART FAILURE (CHF)

➢HF is a complex clinical syndrome that results from any

structural or functional impairment of ventricular

filling(diastole) or ejection(systole) of blood.

➢The cardinal manifestations of HF are dyspnea and fatigue-

which may limit exercise tolerance, and fluid retention-which

may lead to pulmonary and/or splanchnic congestion and/or

peripheral edema.

Clyde W. Yancy et al. Circulation. 2013;128:e240-e327

HF DEFINITION IN BASIC TERMS

➢Previously defined as Congestive Heart Failure

➢Heart is unable to pump blood a sufficient volume of blood

(cardiac output) to meet metabolic demands of the body

➢Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume

(SV)

MORE DEFINITIONS

➢Afterload--tension developed

in the LV wall as systole

occurs. Mainly determined by

arterial blood pressure

➢Preload--combination of

pressure and volume in the

left ventricle at the end of

diastole (completely filled

ventricle)

AND MORE DEFINITIONS…

➢Ejection Fraction (EF)

➢The percentage of left ventricular blood volume ejected

during systole(contraction)

➢Normal is generally defined as 60-70%

➢Right-sided and Left-sided HF

➢Anatomical definitions only

HFPEF (DIASTOLIC DYSFUNCTION)

➢Associated with an EF >40%

➢Ventricle has diastolic stiffness

➢Reduced compliance

➢Unable to fill adequately

➢Most common cause of HFpEF is

hypertension

➢Therapy aimed at heart rate & blood

pressure control

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 ventricles become dilated congested with retained blood

➢Most common cause of HFrEF➢MI (CAD)

PRESENTATION

SIGNS

➢Pulmonary rales

➢Lower leg edema

➢ Jugular venous distention

➢ Increase BNP

SYMPTOMS

➢Dyspnea (on exertion)

➢Orthopnea

➢Paroxysmal nocturnal dyspnea

➢Edema

➢Fatigue

➢Exercise intolerance

ASSOCIATED COMPLICATIONS IN HF MANAGEMENT

➢Cardiac-AF, heart block, valvular abnormalities, CAD, anti-

clotting therapies

➢Organ systems-renal failure, hepatic failure, respiratory

disease

➢Endocrine-DM, hypo/hyperthyroidism, endocrine tumors

➢Other-obesity, nutrition, tobacco, toxins, emotional,

economic, social, educational, financial, geographic, physical,

transplant considerations, gout, etc…..

CLASSIFICATION SYSTEMS

➢ACC/ AHA -- based on disease

evolution & progression

➢A -- High risk for development but

without of structural heart disease

➢B – Structural heart disease but

without signs or symptoms of HF

➢C – Structural heart disease but

with symptoms now or in past

➢D -- Refractory, end-stage HF

➢NYHA -- functional status

based on symptom severity

➢ I -- No symptoms with

activity

➢ II -- Symptoms with usual

activity

➢ III -- Symptoms with minimal

activity

➢ IV -- Symptoms at rest

GOALS OF HF MANAGEMENT

➢Reduce morbidity/mortality rates

➢ Increase health-related quality of life measures and functional

status

➢Decrease health care associated costs

OBJECTIVES

➢Describe and differentiate the main diagnoses of heart failure

➢Describe the pharmacologic goals of heart failure treatment and

identify opportunities to optimize treatment

➢ Identify lifestyle changes to promote positive patient

outcomes in heart failure management

PATHOPHYSIOLOGY

➢Damage heart is unable to meet demands

➢Compensatory Mechanisms

➢The body’s response to decreased CO

➢ Intended to be short term response, detrimental in long term

➢Maintain circulatory homeostasis after acute reductions in blood

pressure or renal perfusion

➢Neurohormonal Model

➢Sympathetic nervous system (SNS)

➢Renin-Angiotensin-Aldosterone System (RAAS)

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

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

Angiotensin II

receptors on the

heart

Increased fibrosis of

cardiac tissue

Direct remodeling of

cardiac tissue

Increases water

reabsorption

from collecting

duct

Increases

ADH

releaseIncreases

thirst

drive

Increased

Preload

Increased

fibrosis of

endothelial &

cardiac tissue

Direct remodeling of

cardiac tissue

CURRENT TREATMENTS

“LIVE LONGER”

MEDICATIONS

➢Shown to improve mortality

➢Beta-Blockers

➢ACE-I/ARB

➢Aldosterone Antagonists

➢Hydralazine & isosorbide dinitrate

➢*Sacubitril / valsartan

“FEEL BETTER”

MEDICATIONS

➢No benefit on mortality

➢Can help with hospitalizations

➢Diuretics

➢Loop

➢Thiazide (Metolazone)

➢Digoxin

➢*Ivabradine

BETA BLOCKERS

➢Recommended in stage B HFrEF and beyond, even if

asymptomatic

➢ Can increase EF, especially if due to ischemic causes

➢ if compelling need for HR control (reduction of

symptoms)

➢Carvedilol, metoprolol SUCCINATE, bisoprolol only

➢ not a “class effect” for all beta blockers

BETA BLOCKERS

➢ Initiate therapy at low dose and advance, generally by

doubling Q2-4 weeks, to predefined target doses

➢Monitor closely for changes in vitals and symptoms (HF

worsening, fatigue, bradycardia, hypotension)

➢PEARL—metoprolol succ. for hypotensive pts and/or

concomitant respiratory disease

➢PEARL—carvedilol for hypertensive and/or DM

ACE INHIBITORS/ARBS

➢Recommended in all stages and diagnoses of HF, unless

contraindicated (angioedema, bilateral RAS, hyperkalemia)

➢ACEIs generally considered over ARBs, unless

➢ development of kinin related cough (approx 10-20%)

➢ already on ARB therapy

➢Data suggest class effect for ACEI, possible class effect for

ARB

ACE INHIBITORS/ARBS

➢Check renal function and electrolytes in 1-2 weeks after

initiation, periodically thereafter

➢ Initiate therapy at low dose and advance, generally by

doubling, to predefined target doses

➢ If target doses not tolerated, intermediate dosing acceptable

➢PEARL—losartan is the only antihypertensive capable of

reducing uric acid levels (0.5-1.0mg/dl), so………

ALDOSTERONE ANTAGONISTS

➢Recommend in NYHA II-IV or AHA Stage C (stage B?)

➢EF<35%

➢After β blockers, and ACE-I titrated to max dose

➢Of note, class II pts need CV hospitalization or high BNP

➢After acute MI with EF<40%

➢Useful in pts needing additional antihypertensive agents

ALDOSTERONE ANTAGONISTS

➢Spironolactone initial dose 12.5-25mg daily, target 25mg daily

➢Eplerenone initial dose 25mg daily, target 50mg daily

➢More selective, better tolerated

➢Do not start if SCr > 2.5 in men, >2.0 in women, or GFR <

30, or if potassium is greater than 5.0 mEq/L

➢Recheck potassium and renal function 2-3 days after start,

again at 7 days, and again with dose changes (including ACEI

or ARB)

HYDRALAZINE/ISDN

➢Recommended for pts of African descent with symptomatic

HFrEF (NYHA III-IV or AHA Stage C)

➢ADD ON therapy for patients already on optimal

ACEI/ARB and B blocker

➢Recommended in pts of any race with current or prior

symptomatic HFrEF that cannot be given ACEI or ARB

therapy

➢DO NOT substitute hydralazine/ISDN for ACEI or ARB

SACUBITRIL / VALSARTAN (ENTRESTO)

➢Newest Class of Medications for HF treatment

➢Angiotensin Receptor-Neprilysin Inhibitor (ARNI) combination

➢Approved for treatment of HFrEF, currently being studied in HFpEF

➢*2016 and 2017 Update: “In patients with chronic symptomatic HFrEF

NYHA class II or III who tolerate an ACE-I or ARB, replacement with an

ARNI is recommended to further reduce morbidity and mortality.” (Used in

place of ACEI or ARB)

➢Target Dose is 97mg/103mg BID

➢ Initial 24mg/26mg BID in ACEI/ARB naïve

➢49mg/51mg BID previously on ACEI/ARB

ADDITIONAL INFO

➢Precautions/

Contraindications

➢Angioedema

➢Contraindicated

with those with

history

➢Hypotension

➢Drugs that increase

potassium

➢Adverse Effects

➢Hypotension

➢Hyperkalemia

➢Cough

➢Dizziness

➢Renal failure

➢Angioedema

LOOP DIURETICS

➢Furosemide, bumetanide and torsemide

➢Bumetanide and torsemide better availability and BP effects

➢Reduce symptoms and hospitalizations, but not mortality

➢Recognized as a “threshold” medication (think of QD vs BID)

➢Risks-hypotension, fluid depletion, azotemia, hypokalemia,

hypomagnesemia, arrhythmia

LOOP DIURETICS

➢Hypotensive effects predominant during threshold phase, less

afterwards

➢Can be used even with GFR < 15ml/min

➢Can potentiate gout through serum concentration effects

➢Long-term use can potentiate diuretic resistance with need

to increase dose or add thiazide

THIAZIDE-LIKE DIURETIC

➢Metolazone acts distal tubule in addition to mild effects in

proximal tubule

➢VERY potent diuresis in combination with loop

➢Retains benefits even with GFR < 30ml/min

➢CAUTION—C-SO2-NH2

➢PEARL—delayed onset, delayed persistence

THIAZIDE DIURETICS

➢Hydrochlorothiazide and Chlorthalidone

➢Effects in the distal tubule (after loop)

➢Greater blood pressure effects and longer persistence than

loop diuretics

➢Remove more sodium from system than loops

➢Beneficial in hypertensive patients with mild fluid retention

➢Can potentiate gout by blocking uric acid excretion

DIURETIC SUMMARY

➢Factors to consider for diuretic therapy

➢ Blood pressure

➢ Volume status-degree of challenge, fluid overload vs fluid

depletion

➢ Electrolyte balance-chem panel 3-5 days after starting or

changing therapy

➢ Response and compliance to therapy

➢ Gout, allergies, lifestyle, adherence, morbidity/mortality

DIGITALIS

➢May be added to HFrEF patients with persistent symptoms

despite optimized GDMT

➢Digoxin + B blocker = better control of ventricular response,

esp during exercise

➢Goal serum levels of 0.5-0.9ng/ml

➢Multiple drug interaction and toxicity concerns

➢ If (Funny) Channel Inhibitor in SA node

➢Consider in those who have a high HR despite optimal treatment

➢ Reduce the risk of hospitalization in chronic HF with the following

characteristics:

➢ Stable, symptomatic heart failure

➢ LVEF <35%

➢ Sinus rhythm with resting HR >70 bpm

➢On maximum tolerated doses of BB or contraindication to BB

therapy

➢ Initial dosing 5mg BID, target dose 10mg BID

IVABRADINE (CORLANOR)

➢ NNT for all-cause hospital admission is 25 over 2 years

➢ Reduction in deaths due to HR over 2 years: NNT 50

➢ BEAUTIFUL Trial

Swedberg K etal. Lancet 2010;376: 880

➢Adverse Effects

➢Bradycardia

➢Atrial fibrillation (d/c in this instance)

➢Phosphenes (visual brightness)

➢Monitoring

➢BP, HR and rhythm

➢Dizziness/fatigue

➢Cost—approx. $375/month

ADDITIONAL INFO

OBJECTIVES

➢Describe and differentiate the main diagnoses of heart failure

➢Describe the pharmacologic goals of heart failure treatment

and identify opportunities to optimize treatment

➢ Identify lifestyle changes to promote positive patient outcomes in

heart failure management

MEDICATIONS TO AVOID

➢Antiarrythmics (except amiodarone and dofetilide)

➢Calcium channel blockers (except amlodipine)

➢NSAIDS

➢Thiazolidinediones

➢Nutritional supplements (except Omega 3s) and hormonal

supplements unless to replace true deficiency

LIFESTYLE MODIFICATIONS

➢Dietary sodium considerations

➢Self-assessment and management

➢Obesity management

➢Exercise

➢End of life considerations

DIETARY SODIUM RECOMMENDATIONS

➢Stage A and B HF—take salt shaker off the table, avoid adding

extra to cooking

➢Stage C and D HF—excessively low and high sodium intake

associated with worse outcomes, restrict <3gm sodium daily

➢Sodium intake generally > 4gm/day in general population

➢Salt substitutes may contain potassium!!

DAILY SELF-ASSESSMENT AND SELF-MANAGEMENT

➢Monitoring of blood pressure at home

➢ direct comparison of personal and clinic readings

➢Daily weight assessment and planning

➢ morning weight and charting

➢ finding “dry” or goal weight

➢ pre-determined strategies for out-of-range

OBESITY MANAGEMENT ??

➢Obesity considered BMI > 30

➢HF-lowest mortality and hospitalization rates seen in BMI 30

- 35

➢Highest mortality— cardiac cachexia > morbidly obese >

normal > overweight > obese —lowest

➢Consider appropriate weight loss if indicated

EXERCISE

➢Exercise training (or regular physical activity) is

recommended as safe and effective for HF patients able to

participate

➢ Regular walking is considered gold standard

➢Cardiac rehabilitation

➢ can increase HRQOL, functional capacity, exercise

duration and morbidity

END OF LIFE PLANNING

➢My take—medical treatments and guidelines focus on battling

mortality to the end, but fail to address acceptance of

mortality and finding peace in dying with dignity.

➢Have “the talk” with patients and family

➢Plan for advanced directives, DNR/DNI, final resting place,

estate planning, etc.

➢Five Wishes Document (excellent resource!!)

QUESTION 1

HF with Reduced Ejection Fraction (HFrEF)is now used to

describe what type of HF?

A. Systolic Heart Failure

B. Diastolic Heart Failure

C. Right-sided Heart Failure

D. Broken-heart syndrome (Tatsukobu’s)

E. No idea………

QUESTION 1

HF with Reduced Ejection Fraction (HFrEF)is now used to

describe what type of HF?

A. Systolic Heart Failure

B. Diastolic Heart Failure

C. Right-sided Heart Failure

D. Broken-heart syndrome (Tatsukobu’s)

E. No idea………

QUESTION 2

Which of the following medications has NOT been shown to

decrease mortality in HFrEF?

A. Carvedilol

B. Spironolactone

C. Furosemide

D. Lisinopril

QUESTION 2

Which of the following medications has NOT been shown to

decrease mortality in HFrEF?

A. Carvedilol

B. Spironolactone

C. Furosemide

D. Lisinopril

QUESTION 3

What home-monitoring technique is best to determine the

efficacy of a diuretic regimen?

A. Skin pinch technique

B. Seeing how your pants fit

C. Asking a friend if you look “puffy”

D. Daily home weights

QUESTION 3

What home-monitoring technique is best to determine the

efficacy of a diuretic regimen?

A. Skin pinch technique

B. Seeing how your pants fit

C. Asking a friend if you look “puffy”

D. Daily home weights

RECOGNITION OF PEERS

➢Dr. Tracy K. Pettinger, Clinical Associate Professor, Idaho State

University

➢Thank you for allowing me to use content from your

2017 presentation at Northwest Pharmacy Conference!!

➢Dr Timothy Murray, CAPT USPHS, BCPS-AQ Cardiology

➢Thank you for years of mentorship and collaboration on

our patients in the Indian Health Service!!

REFERENCES

➢ 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for

the Management of Heart Failure. Available at:

http://circ.ahajournals.org/content/early/2017/04/26/CIR.0000000000000509

➢ 2016 ACC/AHA/HFSA Focused Update on Pharmacological Therapy for Heart

Failure: An Update of the 2013 ACCF/AHA 2013 Guidelines for the

Management of Heart Failure. Available at

http://circ.ahajournals.org/content/circulationaha/early/2016/05/18/CIR.0000000

000000435.full.pdf

➢ACC/AHA Guidelines for the evaluation and management of heart failure. A

report of the American College of Cardiology Foundation/American Heart

Association Task Force on Practice Guidelines. Am J Cardiol. 2013 May 19.

Available at: http://circ.ahajournals.org/content/128/16/e240

REFERENCES CONTINUED

➢ McMurray JJ, et al. Angiotension-neprilysin inhibitor versus enalapril in

heart failure. N Engl J Med 2014; 371:993-1004.

➢ Swedberg K, et al. Ivabradine and outcomes in chronic heart failure

(SHIFT): a randomised placebo-controlled study. Lancet 2010; 376: 875-

85.

➢ Fox, K et al. Ivabradine for patients with stable coronary artery diesase

and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised,

double-blind, placebo-controlled trial. Lancet 2008; 372: 807-16

➢ Klein L, O’Connor CM, Gattis WA, et al. Pharmacologic therapy for

patients with chronic heart failure and reduced systolic function:

Review of trials and practical considerations. Am J Cardiol 2003; 91:18F-

40F.

QUESTIONS??

CAPT Dean T. Goroski

Pharmacy Supervisor

Crow/N. Cheyenne Hospital

Crow Agency, MT

406-638-3578

dean.goroski@ihs.gov