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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