HEART FAILURE

Martina Frost, PA-CDesert Cardiology of Tucson

Northwest Medical Center

Heart Failure in the USPrevalence ~ 6 million Expected to rise by 46% by 2030 Leading cause for hospitalization of pts above age 65 (nearly 2% of all admissions) Average stay 6 days w/high readmission rate

50% mortality at 5 yearsCost in US at 30.7 billion/yr > half of that cost is spent on over 1 million

hospitalizationshttps://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_failure.htm

Jan 8, 2019

Heart Failure (HF)A complex clinical syndrome heart incapable of maintaining cardiac output

adequate to accommodate metabolic requirements and venous return

abnormality of ejection (forward failure = systolic dysfunction) and/or ventricular filling (backward failure = diastolic dysfunction) or both

Associated with episodes of decompensation interspersed with periods of relative stabilityAssociated with significant reduction of quality of life

Mortality and HF

Mortality following hospitalization: 10% at 30 days, 20% at 1 year, 42% at 5 years Mortality for cardiogenic shock is ~80%

Prevalence of HF by Gender and Age

Pathophysiology of HF

Pathophysiology of HF

The Heart:“2 Halves with Lungs In Between”

Right Heart

Lungs Left heart

Rest of the Body

Determinants of Cardiac Output

Preload Contractility Afterload

StrokeVolume

CardiacOutput

Heart Rate

Etiology (List not inclusive)Ischemic - CADNon-ischemic Hypertension Diabetes Uncontrolled tachy-arrhythmia (e.g. Afib) Valvular disease Drugs (ETOH, cocaine, meth, cardiotoxic meds) Infection/inflammation (myocarditis, viruses, Lupus/RA) Others – postpartum, Chagas disease, OSA ‘Idiopathic’

RHF LV HF Pulmonary pathology (PAH, PE, COPD)

> 75% due to CAD and HTN

Types of HF

Left sided HF Systolic –> HF with reduced EF (HFrEF) Diastolic –> HF with preserved EF (HFpEF) Acute Chronic Acute on Chronic

Right Heart Failure

Systolic versus Diastolic HF

Systolic heart failure = HFrEF decreased LV pump function -> decreased EF

< 45%forward failure

Diastolic heart failure = HFpEF normal or slightly reduced EF >45% impaired LV relaxation and stiffness

decreased filling and amount of blood pumped per contraction

increased LV diastolic filling pressure backward failure

Left versus Right HF

Both side of heart can failLeft HF Left ventricle pumps blood into systemic circulation damage due to CAD, HTN etc affects left ventricle > 75% of left HF due to CAD and HTN

RHF Right ventricle pumps blood into pulmonary system Damage due to LV HF

Majority of RHF is due to LHF Pulmonary pathology (Pulmonary HTN, Pulmonary

Embolism, COPD)

Types of CardiomyopathyDilated most common Left Ventricular dilatation Multiple causes

Hypertrophic Ventricular muscle mass enlargement can obstruct blood flow if septal hypertrophy

Restrictive least common myocardium becomes "rigid“ (e.g. amyloidosis)

NYHA Functional Classificationfocus on exercise capacity and symptomatic status of disease

Class 1 no limitations of physical activity

Class 2 slight limitation of physical activity

Class 3 marked limitation of physical activity

Class 4 symptoms at rest and unable to do physical

activity without discomfort

ACC/AHA Stages of HFemphasize on development and progression of disease

Stage A: At high risk for HF in the future but no functional or structural heart disorder

Stage B: Structural heart disorder but no symptoms at any stage

Stage C: Previous or current symptoms of HF in the context of an underlying structural heart problem, but managed with medical treatment

Stage D: Advanced disease requiring hospital-based support, a heart transplant or palliative care refractory HF

Left Ventricular FailureSymptoms

Exertional dyspnea

Orthopnea

Paroxysmal Nocturnal Dyspnea (PND)

Cough

Swelling

Fatigue

Exercise intolerance

Physical Signs Basilar rales/crackles

Pleural effusions

Jugular Venous Distension (JVD)

Edema

S3 Gallop

Tachycardia

Abdominal distension

Jugular Venous

Distention

Right Ventricular Failure

Symptoms

Swelling

Abdominal Pain

Anorexia

Nausea

Bloating

Constipation

Physical Signs

Peripheral Edema

Ascites

Jugular Venous Distention

Abdominal-Jugular Reflux

Hepatomegaly

EvaluationEKGEcho Establishes EF and

ventricular shapeLabs CBC, glucose

kidney/liver/thyroid, electrolytes, BNP/ NT pro-BNP, UA

Chest X-rayCoronary angiogram

BNP/NT-proBNPReleased by ventricles in response to ventricular volume and pressure overload Can help distinguish between cardiac and pulmonary

etiology of dyspneaMany factors increase BNP/NT-proBNP CKD, HTN, pulmonary disease, age, sepsis/critical

illness, cirrhosis, hyperthyroidismKnow which assay is used by your facility/lab

“Treat the patient, not the number”

Richard W. Troughton, and A. Mark Richards JIMG 2009;2:216-225

American College of Cardiology Foundation

Cascade of Cardiorenal SyndromePoorly functioning Heart Renal hypoperfusion Activation of RAAS Increased central venous pressure Poorly functioning Kidneys

Electrolyte abnormalitiesAnemiaIncreased cardiac workload Poorly functioning Heart

The Vicious Cycle of Heart Failure Management

Chronic HF

MD’s Office

Emergency Room

Hospitalization

SOB

Weight

PO LasixIV Lasix or Admit

Diurese & Home

Management of HFrEFPharmacology Rx mainstay“Start low, Go slow”Goals of Rx Symptomatic Relief

Reduce PreloadReduce systemic vascular resistance (afterload reduction)

Improve morbidity, mortality, quality of lifeInhibition of RAAS and vasoconstrictor neurohormonalfactors produced by SNS

Prevent stage progression (and thus hospitalizations and death)

Device Therapy CRT/Biventricular Pacing

Management of HFpEF“Conspiracy of Co-morbidities” Age, gender, HTN, DM, CKD, obesity, Afib,

frailty S/S of HF w/elevated BNP, LVH and/or LAE and

diastolic dysfunction BUT EF > 50%Associated with low mortality but high morbidity

No effective Rx to reduce either mortality or morbidity Supportive Rx Diuretics, sodium restriction Treat HTN, CAD, etc Ok to use diltiazem/verapamil for rate control in AF

(contraindicated in HFrEF)

General MeasuresPatient educationDaily weightsFluid and sodium restriction “2 and 2” (2l fluid, 2 g sodium)

Weight reductionSmoking CessationAvoid alcohol and other cardiotoxicsubstances (NSAIDS!)Exercise

Medical Considerations

Treat HTN, hyperlipidemia, diabetes, anemia, arrhythmias, sleep apneaCoronary revascularizationAnticoagulationImmunizationClose outpatient monitoring – HF ClinicEarly and regular follow-up with cardiologist, PCP, nephrologist

DiureticsFor relief of congestive symptoms (pulmonary and peripheral edema) no mortality benefit, symptom relief only never use as only drug for HF

First choice: Loop diuretics Furosemide, bumetanide, torsemide

Thiazide diuretics Chlorthalidone, metolazone Typically used in severe HF in combination with loop

diuretics for synergistic effectPotassium-sparing - spironolactoneMonitor: renal functions and electrolytes, esp K+

Beta BlockersReduce mortality and symptomatic HFFor all patients with reduced EF with or without history of MI or ACS (recent or remote) Stages B to D and all functional classes

Only three BB have shown to be effective in reducing risk of death in HF Carvedilol, sustained-release metoprolol (‘succinate’),

bisoprololBlockade of excessive SNS stimulationMonitor: HR and BPSE: bradycardia, hypotension, fatigue

Reduce mortality and symptomatic HFFor all patients with reduced EF with or without history of MI or ACS (recent or remote) Stages B to D and all functional classes

Only three BB have shown to be effective in reducing risk of death in HF Carvedilol, sustained-release metoprolol (‘succinate’),

bisoprololBlockade of excessive SNS stimulationMonitor: HR and BPSE: bradycardia, hypotension, fatigue

Ace InhibitorsFor all patients with reduced EF with or without history of MI or ACS (recent or remote) Stages B to D and all functional classes

Reduce mortality and disease progression Reduce hospitalizations

RAAS blockadeLisinopril, Ramipril, Captopril, EnalaprilMonitor: K+, BPSE: hyperkalemia, hypotension, cough, angioedema

Angiotensin Receptor Blockers

RAAS blockadeNo benefit in combination of ACEI and ARB (potentially harmful)Alternative for patients intolerant of ACEI due to cough or angioedemaCan be used first lineLosartan, valsartan, candesartanSE: same as ACEI except cough

Valsartan/Sacubitril = EntrestoApproved in 2015 for HFrEF 2016 guideline update gives it Class I

recommendation as alternative to ACEI/ARB Requires 36 hr ‘washout period’ when

switching from ACEI Decreases HF hospitalizations and death 16% additional survival benefit Sacubitril inhibits neprilysin improves renal

blood flow and improves diuresisSE: hypotension, hyperkalemia

Aldosterone AntagonistsShown to reduce heart failure-related morbidity and mortalityImproves survival among patients with moderate to severe or chronic HF (NYHA class III – IV) and HF after myocardial infarctionAdd-on to ACEI/ARB/BBSpironolactone, Eplerenone ‘potassium-sparing diuretics’

Monitor: K+, Cr, BPSE: hyperkalemia, gynecomastia

Hydralazine and Nitrates

Hydralazine Direct vasodilator that decreases afterload

Isosorbide Mononitrate Long-acting nitrate that decreases preload

Combination has similar effects to ACEI/ARB but without RAAS blockade Consider in African Americans with Class

III/IV HF Alternative when ACEI/ARB contraindicated

Device TherapyAdded to optimal medical therapy in persistently symptomatic patients with EF <35%Can improve quality of life, functional class and exercise capacity Biventricular pacemakers Defibrillators

Acute decompensated HFRequires hospitalization – telemetry, ICUOxygen to maintain SPO2 > 94%; may need CPAP or BiPAPInitial Goal: symptom relief/ preload and afterload reduction Diuretics – loop diuretics Vasodilators - nitrates, hydralazine, nipride, nesiritide (human

BNP analogue) Inhibition of neurohormonal activation (RAAS and sympathetic nervous system) ACEI/ARB, beta-blockers, and aldosterone antagonists

Hemodynamic instability may require inotropic agents and/or mechanical circulatory support Dobutamine, milrinone Intra-aortic balloon pump, left ventricular assist devices

DiureticsIV administration preferred Bolus vs continuous infusion

Dose based on response to first dose 2-4 hrs after it was given Increase dose or frequency if inadequate response Sometimes loop diuretic combined w/thiazide diuretic

for synergistic effectMetolazone “kickstarts” lasix; give 30min before lasix

Close monitoring of electrolytes usually 2:1 dosing of Lasix/potassium Keep serum potassium between 4 – 5 mmol/L

Transition to PO when pt reaches near-euvolemicstateStrict I/Os and DAILY weights!

What do patients need to do?Medication compliance (even if NO symptoms)Fluid restriction 2 liters, 2 quarts or 68 fl oz/day

Low sodium diet < 1.5 g/day Salt increase fluid retention ‘No salt shaker at the table’

Avoid alcohol and other cardiotoxicsubstancesSmoking cessation, weight reduction

What do patients need to do?

Daily weights Learn ‘dry’ weight Unexpected rapid weight gain

3 lbs/day or 5 lbs/weekEarliest sign of decompensation before symptoms

Call cardiologist for new or worsening symptoms with or without weight gain

Don’t wait until they are severe enough to need ER

Regular exercise without overdoing itRegular cardiology and PCP F/U

SummaryHeart failure is a chronic progressive disease that is generally not curable, but is treatableMost recent guidelines promote lifestyle modifications and medical management with ACE inhibitors, beta blockers, and diuretics Close follow-up of the heart failure patient is essential, with necessary adjustments in medical managementUnfortunately HF continues to have high mortality and morbidity even with treatment