get with the guidelines… · 2018. 4. 14. · systolic vs diastolic heart failure :dxand treatment...

Systolic vs Diastolic Heart Failure :Dx and TreatmentKristine A. Scordo, PhD, RN, ACNP-BC, FAANP

Heart Failure Update for Primary Care Providers: Recognition and Treatment of Systolic (HFrEF) vs Diastolic Heart Failure (HFpEF):

Kristine Anne Scordo PhD, RN, ACNP-BC, FAANPProfessor and DirectorAdult Gero-Acute Care Nurse Practitioner ProgramWright State UniversityDayton, OhioACNP Schuster Cardiology and Associates, Dayton Ohio [email protected]

Get with the Guidelines…

https://doi.org/10.1016/j.jacc.2017.11.025

GDMT=goal directed medical

therapy


Why worry about heart failure in primary care?

Epidemiology of HF

1in 9 death certificates in the US mentioned heart failure.

Prevalence increased form 5.7 million to 6.5 million in Americans >20yrs of age

5 year survival after MI improved from 54% (2001) to 61% (2000)

Seventy-five percent of HF cases have antecedent hypertension

Hospitalized HF events: 53% had HFrEF and 47% had HFpEF

~$34.4 billion per year in health care costs

Circulation. 2017;135:00–00. DOI: 10.1161/CIR.0000000000000485


All Cause Mortality After Each Subsequent Hospitalization for HF

Time Since Admission

0.0

0.2

Kap

lan-

Mei

er C

un. M

orta

lity

0.8

1.0CHF1st Admission (n = 14,374)2nd Admission (n = 3,358)3rd admission (n = 1,123)4th Admission (n = 417)

1st hospitalization: 30 d mortality = 12%; 1 yr = 34%

0.6

0.4

0.0 0.5 1.0 1.5 2.0

Key is to prevent hospitalizations

But first…..What’s in a name?

Definition of Heart Failure*Classification Ejection

FractionDescription

I. Heart Failure with Reduced Ejection Fraction (HFrEF)

≤40% Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date.

II. Heart Failure with Preserved Ejection Fraction (HFpEF)

≥50% Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified.

a. HFpEF, Borderline 41% to 49% These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF.

b. HFpEF, Improved ~1/3 casesFew clinical trails to guide care

>40% It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients.

*2013 ACCF/AHA Guideline for the Management of Heart Failure


Common Causes of HF• HFrEF

• DCM

• CAD/AMI

• Valvular

• Hypertensive heart disease

• Congenital heart disease

• HFpEF• Old age

• Hypertension with LVH

• Proinflammatory etiology• Diabetes Mellitus, obesity

• Restrictive cardiomyopathy

• Hypertrophic states

Characteristics of Patients with HFpEF vs HFrEF

Characteristic HFpEF HFrEF

Age Frequently elderly All ages, typically 50-70 yr

Sex Frequently female More often male

LVEF Preserved or normal, 50% or higher

Depressed ~40% or lower

LV Cavity size Usually normal, with LVH Usually dilated

CXR Congestion with or without cardiomegaly

Congestion & cardiomegaly

Gallop S4 S3

Symptomatic HF is only the tip of the iceberg


PRIMARY PREVENTION!!!

The Cardiovascular ContinuumRisk Factors and HF: The Link*

ObesityDiabetes

Hypertension

SmokingDyslipidemia

LVH

MI

Systolicdysfunction

Diastolicdysfunction

HF

Normal LVstructure & function

LV remodelingSubclinical LVdysfunction

Overt heart failure


Prevention is the Key

• Treat HTN

• Treat insulin resistance/metabolic syndrome

• Treat lipid disorders

• Smoking cessation

• Regular cardiovascular exercise

• Weight loss• OBESITY INDEPENDENT RISK FACTOR

• ACEI/ARBS/Beta blockers with DM/CVD/HTN

• Periodic surveillance of EF

Treating Hypertension to Prevent HF

• Aggressive blood pressure control:

• Aggressive BP control in patients with prior MI:

Decreasesrisk of new HF

by ~ 80%

Decreasesrisk of new HF

by ~ 50%56% in DM2

Lancet 1991;338:1281-5 (STOP-HypertensionJAMA 1997;278:212-6 (SHEP)UKPDS Group. UKPDS 38. BMJ 1998;317:703-713

HF Risk Factor Treatment Goals

Risk Factor Goal

Hypertension Generally < 130/80 (ACEI/ARB)

Diabetes ADA guidelines

Hyperlipidemia GDMT

Inactivity 20-30 min. aerobic 3-5 x wk.

Obesity Weight reduction < 30 BMI

Alcohol Men ≤ 2 drinks/day, women ≤ 1

Smoking Cessation

Dietary Sodium Maximum 2-3 g/day


Diagnosing HF: Early Recognition is KEY

Differential Diagnosis for HF Symptoms and Signs

• Myocardial ischemia

• Pulmonary disease (pneumonia, asthma, chronic obstructive pulmonary disease, pulmonary embolus, primary pulmonary hypertension)

• Sleep-disordered breathing

• Obesity

• Deconditioning

• Malnutrition

• Anemia

• Hepatic failure

• Chronic kidney disease

• Hypoalbuminemia

• Venous stasis

• Depression

• Anxiety and hyperventilation syndromes

• Hyper or hypo-thyroidism

Diagnostic Tests

Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone.

Serial monitoring, when indicated, should include serum electrolytes and renal function.

I IIa IIb III

I IIa IIb III


Class I for dx and establishing prognosis/disease severity;IIa BNP post discharge prognosis

BNP Level

Maisel, Alan S., et al. “Bedside B-Type natriuretic peptide in the emergency diagnosis of heart failure with reduced or preserved ejection fraction: Results from the Breathing Not Properly Multinational Study.” Journal of the American College of Cardiology (JACC), v. 41 issue 11, 2003, p. 2010-2017.

Causes for Elevated Natriuretic Peptide Levels

Cardiac Noncardiac Heart failure, including RV

syndromes Acute coronary syndrome Heart muscle disease,

including LVH Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Cardioversion

Advancing age Anemia Renal failure Pulmonary causes: obstructive

sleep apnea, severe pneumonia, pulmonary hypertension

Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults,

including cancer chemotherapy and

envenomation


Signs to Evaluate in Patients Suspected of Having HF

Cardiac Abnormality Sign

Elevated cardiac filling pressures and fluid overload

Elevated JVP, S3 gallop, rales, +HJ reflux, ascites, edema

Cardiac enlargement Laterally displaced or prominent apical impulse, murmurs suggesting valvular dysfunction

Reduced cardiac output Narrow pulse pressure, cool extremities, tachycardia with pulsus alternans

Arrhythmia Irregular pulse suggestive of atrial fibrillation or frequent ectopy

In office determination of suspicion of heart failure

Square valve response to Valsalva

• Check BP and hold~ 15mmHg above systolic-perform Valsalva --normal response-hear for a few beats and disappears

• Abnormal hear sounds continuously = increased LA pressure• Patients with severely depressed EF unable to

alter stroke output in response to acutely increased intrathoracic pressure. A square wave pressure response is a likely consequence of a fixed stroke output during the strain maneuver.


Common Symptoms of HF

Congestion

• orthopnea, PND

• NVD

• ascites, edema

• hepatic tenderness

• hepatojugular reflux

• rales

Low Perfusion

• hypotension

• cool extremities

• narrow pulse pressure

• sleepiness, obtundation

• elevated BUN, creatinine

• hyponatremia

Signs/Symptoms…vary

comfortable at rest to dyspneic during conversation/PND/orthopnea

long-standing HF may appear cachectic or cyanotic/ascites/scrotal edema

VS may be normal, tachycardia, hypotension and reduced pulse pressure may be present

increased sympathetic nervous system activity--cold extremities/diaphoresis


Symptoms

• fatigue & exercise intolerance• correlate poorly with degree of cardiac dysfunction

• RUQ pain (RV failure) due to passive congestion of liver

• loss of appetite & nausea (edema of gut or impaired GI perfusion)

• restlessness; depression• weight gain

• short-term changes in fluid status more reliable• over time loss skeletal muscle mass and body fat –

cardiac cachexia

Less specific s/s

Early satiety, nausea and vomiting, abdominal discomfort

Wheezing or cough

Unexplained fatigue

Confusion/delirium

Depression/weakness (especially in the elderly)

• is activity limitation due to• angina, musculoskeletal disorders or

intermittent claudication or by heart failure

• is dyspnea due to HF or pulmonary disease

• unexplained confusion (especially in elderly)

• disorders may co-exist• can perform O2 saturation during graded levels

of exercises


HFpEF (Heart failure preserved ejection fraction)

• Difficult dx

• Not one dx test-clinical syndrome

• 25% have increased LV mass

• Pathophysiology-more inflammatory response—multiple systems involved-not only the heart

Evaluation of a Patient with Heart Failure—or what do I have and why

Assess clinical severity and functional limitation by history, physical examination, and determination of functional class

Assess cardiac structure and function

Determine the etiology of HF

Evaluate for coronary disease and myocardial ischemia

Evaluate the risk of life threatening arrhythmia

Identify any exacerbating factors for HF

Identify co-morbidities which influence therapy

Identify barriers to adherence and compliance


Question…..• sodium intake• ETOH intake• exercise• glucose control• weight loss• smoking cessation• Misc

• edema due to calcium channel blockers?• use of NDAIDs• use of TZDs (Avandia, Actos)• medication adherence• failure to renew prescriptions http://www.helpingpatients.org/• misunderstanding• ??multiple providers ?? discontinuation of therapy

Assessment of Volume Status

• Presence of PND and /or orthopnea

• Elevated JVP

• + hepatojugular reflux (HJ reflux)

• S3 or S4 gallop

• pleural effusion• reflect chronic elevation of filling

pressures

• unilateral pleural effusion usually right sided

Assessment of Volume Status

presence and severity of organ congestion (pulmonary rales & hepatomegaly), magnitude of peripheral edema in legs, abdomen, presacral area or scrotum

most reliable physical sign of volume overload is JVD


CHECK JVP??? NEED 45O

ANGLE?????

What about crackles?

most patients in chronic HF do not have crackles (rales), even with end-state disease

presence of rales generally reflects the rapidity of onset of HF rather than the degree of volume overload

so . . . finding of clear lung fields on PE in patient with chronic HF shouldn’t suggest that fluid retention has been adequately treated


Assessment of Volume Status: Weight measurement

record weight, review home recordings

short-term changes in fluid status are most reliably gauged by measuring short-term changes in body weight

changes in body weight may be less reliable during long periods of follow-up

• patients lose skeletal muscle mass and body fat as the disease advances (cardiac cachexia)

• ~ 50% HF patients have sleep disordered breathing• Poor prognostic indicator• Stimulates neurohormonal vasoconstrictor activity• Increases systemic BP• Associated with higher prevalence of ventricular

arrhythmias• CPAP improves survival rates and s/s of heart failure

Send for sleep study

• witnessed apnea

• not responsive to treatment

• arrhythmias (bradyarrhythmias)

• obese

• diastolic HF

• HTN

Class IIa


How do I classify my patient?

Classification of HF: ACC/AHA stage vs NYHA class (1920’s)

• little relation between cardiac performance and symptoms produced by the disease

• pts with very low EF are frequently asymptomatic, whereas pts with preserved LV systolic function may have severe disability

• contributing factors• peripheral vascular function• skeletal muscle physiology• pulmonary dynamics• neurohormonal and reflex autonomic activity


Treatment

Major Goals

Improve symptoms and quality of life

Slow progression or reverse cardiac and peripheral dysfunction

Reduce mortality

General Treatment Measures

• lose weight

• stop smoking

• avoid alcohol

• control concomitant conditions (HTN, DM)

• influenza and pneumococcal vaccines

• avoid heavy labor or exhaustive sports

• AF-restore to sinus rhythm if possible; control VR

• stress need for follow-up


• salt restriction (2 Grams sodium a day or less)

• avoid excessive fluid intake • fld restriction not advisable unless hyponatremia

present; careful with salt restriction + free water

• sodium excess is the main reason for heart failure exacerbation (gravy, Chinese food, ETOH, canned food, prepared meats)

• reporting weight gain

• risk factor reduction

• exercise

Pixabay.com


PATIENTS CAN OUT EAT, OUT DRINK

ANY SODIUM RESTRICTION

Pharmacologic Therapy


What do you start with?

ACEI/ARB or BetaBlocker

ACEI? ARB? Beta Blocker?

Data from CIBIS (Cardiac Insufficiency Bisoprolol) III trial suggest that either is safe

Starting ACE/ARB often better tolerated with patient is still congested

Beta blockers better tolerated when patient is less congested with adequate resting HR

https://doi.org/10.1016/j.jacc.2017.11.025


Beta Blockers

Beta Blockers

• all pts with stable HF due to LV systolic dysfunction should receive a B-blocker unless contraindicated*

• common misperception that patients with mild symptoms don’t need beta blockers---not true• patients are high risk for morbidity and

mortality and are likely to deteriorate

• don’t use unless diuretic on board in patients with current or recent history of fluid retention

*COLD patient requires steroids—avoidsymptomatic bradycardia or advanced heart block without pacemaker

Beta Blockers—Preserved LVEF

• Beta blocker treatment is recommended in patients with HF and preserved LVEF who have:• Prior MI• Hypertension• Atrial fib. requiring control of ventricular rate

• THE ELDERLY• Beta-blocker and ACE inhibitor therapy is recommended as

standard therapy in all elderly patients with HF due to LV systolic dysfunction.

• In the absence of contraindications, these therapies are also recommended in the very elderly (age > 80 years).


HFpEF

• prevent tachycardia with beta blockers

• need atrial contraction• maintain sinus rhythm

Beta Blockers Used in Clinical Trials

Generic Name Trade Name Initial Daily Dose

Target Dose Mean Dose in Clinical Trials

Bisoprolol Zebeta 1.25 mg qd 10 mg qd 8.6 mg/day

Carvedilol Coreg 3.125 mg bid 25 mg bid 37 mg/day

Carvedilol Coreg CR 10 mg qd 80 mg qd

Metoprolol succinate CR/XL

Toprol XL 12.5-25 mg qd 200 mg qd 159 mg/day


from the trenches. . .

• slowly titrate up – stay at dose for 2-4 weeks• COMET: up-titration at 2-week intervals

• first few days when increasing dose, may need to dose down ACEI

• have patient take higher dose in PM the first day or first few days, then increase to BID

• space out medications—don’t take vasodilators all at once

• daily weights; may retain fluid; increase diuretic dose• discuss with patient what to expect – more likely to

“tough it out” for a few days

Angiotensin Converting Inhibitors (ACEI)


ACE Inhibitors Used in Clinical TrialsGeneric Name Trade Name Initial Daily

DoseTarget Dose Mean Dose in

Clinical Trials

Captopril Capoten 6.25 mg tid 50 mg tid 122.7 mg/day

Enalapril Vasotec 2.5 mg bid 10 mg bid 16.6 mg/day

Fosinopril Monopril 5-10 mg qd 80 mg qd N/A

Lisinopril Zestril, Prinivil 2.5-5 mg qd 20 mg qd 4.5 mg/day, 33.2 mg/day*

Quinapril Accupril 5 mg bid 80 mg qd N/A

Ramipril Altace 1.25-2.5 mg qd 10 mg qd N/A

Trandolapril Mavik 1 mg qd 4 mg qd N/A

*No mortality difference between high and low dose groups, but 12% lower

risk of death or hospitalization in high dose group vs. low dose group.

ACE Inhibitors: Side effects

• cough

• hypotension (orthostatic)

• angioedema (0.1%)

• hyperkalemia

• neutropenia and/or agranulocytosis

Pharmacologic Therapy: Substitutes for ACEI

• In patients who cannot tolerate ACE inhibitors due to cough, ARBs are recommended.

• The combination of hydralazine and an oral nitrate may be considered in such patients not tolerating ARBs.

• Patients intolerant to ACE inhibitors from hyperkalemia or renal insufficiency are likely to experience the same side effects with ARBs. In these cases, the combination of hydralazine and an oral nitrate should be considered.


Angiotensin Receptor Blockers Used in Clinical Trials

Generic Name Trade Name Initial Daily Dose

Target Dose Mean Dose in Clinical Trials

Candesartan Atacand 4-8 mg qd 32 mg qd 24 mg/day

Losartan Cozaar 12.5-25 mg qd 150 mg qd 129 mg/day

Valsartan Diovan 40 mg bid 160 mg bid 254 mg/day

ARNI

Angiotensin II Receptor Blocker Neprilysin Inhibitor

Paradigm of Heart Failure


ARNI

B-R = level B, randomized trial

Approved by FDA July 7, 2015

ENTRESTO is indicated to reduce the risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.

ENTRESTO is usually administered in conjunction with other heart failure therapies, in place of an ACE inhibitor or other ARB

ENTRESTO is contraindicated with concomitant use of aliskiren in patients with diabetes.

.

Key PointsFor ACEI to ARNI need 36 hr washout to avoid angioedema

Change from ARB to ARNI


Buyer Beware

BNP, but not NT-proBNP, is a substrate for neprilysin.

Therefore, ARNI increases BNP levels (12) but not NT-proBNP levels

Diuretics

Diuretics

• should be prescribed for all pts with symptoms of HF who have evidence for or a predisposition to fluid retention

• do not use as monotherapy• dose by daily body weights• underdose

• fluid retention, may diminish response to ACEI and increase risk of treatment with B-blockers

• overdose• volume depletion, increase likelihood of

hypotension with ACEI and risk of renal insufficiency with ACEI


Diuretics

• thiazide• Not as effective if GFR below 30ml/min• cause less acute diuresis• greater decrease in K for same quantity of diuresis

• loop diuretics• start with 20-40 mg furosemide qd• double dose rather than give BID• higher doses give BID (240 mgm qd)

• combination• zaroxolyn (metolazone)

• severe hypokalemia• monitor K q3 days• serum K can be unreliable of K stores; <4.0 give KCl

Loop Diuretics

Agent Initial Daily Dose

Max Total Daily Dose

Elimination: Renal – Met.

Duration of Action

Furosemide 20-40mg qd or bid

600 mg 65%R-35%M 4-6 hrs

Bumetanide 0.5-1.0 mg qd or bid

10 mg 62%R/38%M 6-8 hrs

Torsemide 10-20 mg qd 200 mg 20%R-80%M 12-16 hrs

Ethacrynic acid

25-50 mg qd or bid

200 mg 67%R-33%M 6 hrs

Potassium-Sparing Diuretics

Agent Initial Daily Dose

Max Total Daily Dose

Elimination Duration of Action

Spironolactone 12.5-25 mg qd

50 mg Metabolic 48-72 hrs

Eplerenone 25-50 mg qd

100 mg Renal, Metabolic

Unknown

Amiloride 5 mg qd 20 mg Renal 24 hrs

Triamterene 50-75 mg bid

200 mg Metabolic 7-9 hrs


??single dose of diuretic in AM??

in AM, body’s fld volume is lowest

patients has been in horizontal position for 4-8 hours

gets up and takes ACE, B blocker, Aldactone, ? ARB, ? nitrate

experiences fatigue, hypotension, weakness and wasted, tired feeling

+ during AM diuretic likely to more vigorously accentuate already highly activated RAAS-forces to retain more fld now further enhanced as day proceeds

Remember . . .

patients with HF are magnesium-depleted unless it is replaced

serum Mg level unreliable

clue is hypokalemia; virtually all patients with low serum K are magnesium-depleted

Mg is an obligatory metallo-coenzyme for Na-K-ATPase

K replacement hindered till Mg deficiency corrected

Watch Na++

Why????


OPTIME-CHFPredictive Value of Hyponatremia in Hospitalized Patients

14 DaySurvival

60 DaySurvival

Na+ = 135

3 NA+

mortality 30%

Klein L et al. J Card Fail. 2003;9:S83

Subcutaneous Furosemide

In clinical trials

You may soon see use in out-patient setting

Furoscix

• IV Lasix alkaline pH (8.0-9.3) can’t use SC

• Reformulated

• Uses sc2Wear Furosemide Infusor

• Administered over 5 hours• 30 mg first hour, followed by 12.5 mg/h

for 4 hours


Ivabradine (Corlandor)

• Heart rate independently predicts outcomes in HFrEF

• HR lowering is directly related to improved outcomes

• Some pts on optimal beta blocker therapy continue to have a persistent resting HF >70 BPM

Corlanor (ivabradine)


Corlanor (ivabradine)

Indicated to reduce risk of hospitalization for worsening heart failure in pts with stable, symptomatic chronic HF with LV EF <35% who are in sinus rhythm

With HR >70 BPM

On maximally tolerated doses of beta-blockers or have a contraindication to beta-blocker use

Unlike β blockers, does not modify myocardial contractility and intracardiac conduction.

Corlanor: contraindications

Acute decompensated HF

BP < 90/50 mmHg

Bradycardia/AF

Severe hepatic impairment

Total pacemaker dependence

Concomitant use of strong CYP inhibitors

Corlanor: DosingRecommended dose is 5 mg BID with mealsAssess pt after two weeks and adjust dose to achieve rest

HR 50-60 BPM.Maximum dose is 7.5 mg daily


Digitalis

consider to improve symptoms in patients with reduced LVEF (LVEF <40%) who have signs or symptoms of HF while receiving standard therapy, including ACE inhibitors and beta blockers:

dose 0.125 mg daily in majority of patients

serum digoxin level should be <1.0 ng/mL, generally 0.7-0.9 ng/mL.

control ventricular response to AF in HF

Digoxin Blood LevelsDecreased• Antacids• Kaolin-pectin• Cholestyramine• Bran• Phenytoin• Propafenone• PAS• Neomycin• Cathartics

Increased• Quinidine• Amiodarone• Propafenone• Flecainide• Verapamil• Spironolactone• Triamterene• Indomethacin• Cyclosporine


Aldosterone Receptor Antagonists

Aldosterone receptor antagonists [or mineralocorticoid receptor antagonists (MRA)] are recommended in patients with NYHA class II-IV and who have LVEF of 35% or less, unless contraindicated, to reduce morbidity and mortality.

Patients with NYHA class II should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists.

I IIa IIb III

Aldosterone Antagonists and Renal Function

• Aldosterone antagonists are not recommended when:• Creatinine > 2.5mg/dL (or clearance < 30 mL/min)

• Serum potassium> 5.0 mmol/L

• Therapy includes other potassium-sparing diuretics

• Measure potassium at baseline, then 1 week, 1 month, and every 3 months

• Supplemental potassium is not recommended unless potassium is < 4.0 mmol/L

Aldosterone Antagonist

Effective but underused

NYHA Class II-IV with EF < 40% (class I)

Cr < 2.0 (women) and Cr < 2.5 (men)

Do not initiate if K > 5; hold the course if K < 5.5

Start with spironolactone

Transition to eplererone if gynecomastia with spironolactone


Calcium Channel Blockers

• considered in patients with HF and preserved LVEF and:• Atrial fibrillation requiring control of

ventricular rate and intolerance to beta blockers. Use diltiazem or verapamil

• In pts with angina-amlodipine and felodipine preferred with decreased systolic function

• Use with caution…may worsen heart failure

HFpEF

Treatment


HFpEF: Treatment

• diuretics• avoid positive inotropes (digoxin)• salt restriction and diuretics to relieve edema• venodilators to lower filling pressures (avoid

hypotension)• regression of hypertrophy where appropriate

(ACEI/ARB)• relieve ischemia when appropriate• maintain sinus rhythm at a slow rate• removal of pericardium where appropriate (1/3

increase in diastolic pressure due to external forces, i.e. pericardium)

Aldosterone in HFpEF

HFpEF Conclusions

Emerging HFpEF model: systemic inflammation fibrosis/hypertrophy cardiac remodeling/ skeletal muscle dysfxn

Not all patients with HFpEF have LVH. Some have normal filling pressures at restà right heart cath w/ exercise

Mainstays of therapy for HFpEF are BP control, diuretics, risk factor control

Spironolactone may reduce HF hospitalizations


Tips to Optimize Medical Therapy

Share the Seattle Heart Failure Model with the patient to promote buy-in with medical therapy

Go slow (marathon, not a sprint); increase in small increments every 1-2 weeks

Tolerate asymptomatic hypotension

Diuretic requirements may decrease with positive remodeling

“Treat the patient, not the creatinine”

Repeat TTE 3-6 months after med optimization

My patient was stable but now is short of breath….what is going on?


Exacerbation Triggers

• New onset atrial fibrillation or any SVT*

• Sinus tachycardia*• Stress

• Infection

• Pain

• Cardiac ischemia

• Increased sodium intake

• Mitral regurgitations ??new murmur

Need for Hospitalization

• clinical or EKG evidence of acute ischemia

• pulmonary edema or respiratory distress

• complicating other medical illness (pneumonia, renal failure)

• anasarca

• symptomatic hypotension or syncope

• symptoms refractory to outpatient therapy

Heart Failure Patient Education

• patients with HF and their family members or caregivers should receive individualized education and counseling that emphasizes self-care.

• This education and counseling should be delivered by providers using a team approach.

• Teaching should include skill building and target behaviors.

•


Improving adherence

Follow Up Assessments

Signs and symptoms evaluated during initial visit

Functional capacity and activity level

Changes in body weight

Patient understanding of and compliance with dietary sodium restriction and medical regimen

History of arrhythmia, syncope, pre-syncope, palpitation, or ICD discharge

Adherence and response to therapeutic interventions

Exacerbating factors for HF, including worsening ischemic heart disease, hypertension, and new or worsening valvular disease

One of the Best Devices for Monitoring Heart Failure


“Drugs don’t work in patientswho don’t take them”

C. Everett Koop, M.D.

Jhund et al. Abstract at ESC. 2016.

References-American College of Cardiology Foundation (ACCF) American Heart Association (AHA) Physician Consortium for Performance Improvement (PCPITM) Heart Failure Performance Measurement Set 2012--Allen LA, O’Conner CM; CMAJ 2007: 176 (6): 797-800-Seo,R Kam,L F Hsu Treatment of Heart Failure – Role of Biventricular Pacing for Heart Failure. SingaporeMedJ2003Vol44(3):114-122 The 2010 Heart Failure Society of America Comprehensive Heart Failure Practice GuidelineSarraf Mohammad ; Masoumi Amirali ; Schrier Robert W. Cardiorenal Syndrome in Acute Decompensated Heart Failure CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY Volume: 4 Issue: 12 Pages: 2013-2026

Meyer, Theo, et al. “In the Clinic Heart Failure With Preserved Ejection Fraction (Diastolic Dysfunction).” Annals of Internal Medicine, v. 158 issue 1, 2013, p. ITC1-1.

Maisel, Alan S., et al. “Bedside B-Type natriuretic peptide in the emergency diagnosis of heart failure with reduced or preserved ejection fraction: Results from the Breathing Not Properly Multinational Study.” Journal of the American College of Cardiology (JACC), v. 41 issue 11, 2003, p. 2010-2017.

get with the guidelines… · 2018. 4. 14. · systolic vs diastolic heart failure :dxand treatment...

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