Overview of Heart Failure

7/27/2019 Overview of Heart Failure

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Fikar Arsyad H.

Faculty of Medicine

Eleventh March University


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Heart blood pumping

Heart failure failure of blood pumping

Failure of ejection systolic heart failure

Failure of filling diastolic heart failure

Failure to meet body requirements


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Failure of ejection

infarct, hypertension, enlargement of

ventricle, myocarditis, toxin (ethanol, cocaine,

amphetamine), amyloidosis, muscular dystrophy

Failure of filling increased stiffness (elder people, chronic

hypertension, amyloidosis)

Failure to meet body requirements

Anemia, hyperthyroidism


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A 19 year study of 13000 adults in the United States (the NationalHealth and Nutrition Examination Survey (NHANES I) found thefollowing causes ranked by Population Attributable Risk score:

Ischaemic Heart Disease 62%

Cigarette Smoking 16%

Hypertension (high blood pressure)10%

Obesity 8% Diabetes 3%

Valvular heart disease 2% (much higher in older populations)

An Italian registry of over 6200 patients with heart failureshowed the following underlying causes:

Ischaemic Heart Disease 40%

Dilated Cardiomyopathy 32%

Valvular Heart Disease 12%

Hypertension 11%

Other 5%


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Based on cardiac output heart failure can beclassified in low-output failure (most of theconditions) or high-output failure (beriberi,pregnancy, anemia, sepsis).

Based on the ventricle affected, heart failurecan be classified in LV failure, RV failure, orbiventricular failure.

Based on the LVEF, heart failure can be classifiedin patients with LV systolic dysfunction (LVEF40%). Based on the onset of symptoms, heart failure

can be acute or chronic.


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Shortness of breath with activity, or after lying down for awhile

Cough

Swelling of feet and ankles

Swelling of the abdomen

Weight gain Irregular or rapid pulse

Sensation of feeling the heart beat (palpitations)

Difficulty sleeping

Fatigue, weakness, faintness

Loss of appetite, indigestion

Decreased alertness or concentration Decreased urine production

Nausea and vomiting

Need to urinate at night


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A physical examination may reveal the

following:

Fluid around the lungs (pleural effusion)

Irregular heartbeat

Leg swelling (edema)

Neck veins that stick out (are distended)

Swelling of the liver

Lung crackles or abnormal heart sounds.


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Major criteria:

Paroxysmal nocturnal dyspnea

Neck vein distention

Rales

Radiographic cardiomegaly (increasing heart size on chest radiography)

Acute pulmonary edema

S3 gallop

Increased central venous pressure (>16 cm H2O at right atrium) Hepatojugular reflux

Weight loss >4.5 kg in 5 days in response to treatment

Minor criteria:

Bilateral ankle edema

Nocturnal cough

Dyspnea on ordinary exertion

Hepatomegaly

Pleural effusion

Decrease in vital capacity by one third from maximum recorded

Tachycardia (heart rate>120 beats/min.)


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Heart failure

Low Perfusion

Activation ofNeuroendocrine

system

Nor/Epinephrine,RAAS, ET-1,Vasopressin

Vasoconstriction,Fluid restriction,

Increasedcontractility

Increased Perfusion

BUT:

Increased wallstress

Cell death/

apoptosisCell renewal

Heart remodelling

- Concentric- Eccentric

Inefficiency ofheart function

- Concentric

- Eccentric

Decreased heartfunction

Heart failure >>


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A classification of patients with heart disease based on therelation between symptoms and the amount of effortrequired to provoke them has been developed by the NYHA.

Class I: No limitations. Ordinary physical activity does notcause undue fatigue, dyspnea, or palpitations.

Class II: Slight limitation of physical activity. Such patientsare comfortable at rest. Ordinary physical activity, such asbending over or walking results in fatigue, palpitations,dyspnea, or angina.

Class III: Marked limitation of physical activity. Althoughpatients are comfortable at rest, less-than-ordinaryactivity leads to fatigue, dyspnea, palpitations, or angina.

Class IV: Symptomatic at rest. Symptoms of CHF arepresent at rest; discomfort increases with any physicalactivity.


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The 2001 ACC/AHA heart failure guidelines introduced astaging classification for heart failure complementary toNYHA classification to reflect the progression of disease.

Stage A Patients at risk of developing heart failure,without evidence of structural heart disease (diabetes

mellitus, hypertension, coronary artery disease, obesity,metabolic syndrome, family history of cardiomyopathy, useof cardiotoxins)

Stage B - Patients with asymptomatic LV dysfunction (post-MI LV dysfunction, valvular cardiomyopathy, dilatedcardiomyopathy); includes NYHA Class I patients

Stage C Symptomatic LV dysfunction; includes NYHA Class

II and III patients Stage D End-stage refractory heart failure; includes NYHA

Class IV patients


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Chest x-ray

ECG

Echocardiogram

Treadmill testHeart catheterization

Nuclear heart scans

MRI of the heart


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Complete blood count

Electrolyte

Renal Function test

Liver function tests Blood chemistry

Pulse oxymetry

ABG

BNP (?)


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Natriuretic peptide: One of the peptidesthat causes natriuresis, the excretion of anexcessively large amount of sodium in theurine. The natriuretic peptides are producedby the heart and vasculature

A-type natriuretic peptide is secreted largelyby the atrial myocardium in response todilatation.

B-type natriuretic peptide is manufactured

mainly by the ventricular myocardium.C-type natriuretic peptide is produced by

endothelial cells that line the blood vessels.


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The release of BNP appears to be in direct proportionto ventricular volume and pressure overload. BNP isan independent predictor of high LV end-diastolicpressure and is more useful than ANP ornorepinephrine levels for assessing mortality risk inpatients with heart failure.

BNP levels correlate with both the severity ofsymptoms and the prognosis in congestive heartfailure. BNP levels correlate closely with the NYHAclassification of heart failure

BNP levels are higher in older patients, women, andpatients with renal dysfunction or sepsis.

BNP levels may be disproportionately lower inpatients who are obese or have hypothyroidism oradvanced end-stage heart failure (the latter due toincreased fibrosis).


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Reference Range

BNP

(pg/mL)

ProBNP

(pg/mL)

Healthy

males

< 100 60

Healthy

females

< 100 12 150

http://www.biomerieux-

diagnostics.com/servlet/srt/bio/clinical-

diagnostics/dynPage?open=CNL_HCP_CRD_HF&doc=CNL_

HCP_CRD_HF_G_CHP_TXT_1&pubparams.sform=2&lang=

en#


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BNP levels of more than 100 pg/mL have betterthan a 95% specificity and greater than a 98%sensitivity when comparing patients withoutheart failure to all patients with heart failure.

Measurement of BNP and N-terminal proBNP (NT-

proBNP) can be useful in the evaluation ofpatients presenting to urgent care setting inwhom the clinical diagnosis of heart failure isuncertain (Class IIa recommendation).

In a pilot study, BNP levels correlated highly withclinical outcomes.

In addition, the last measured BNP level was thesingle most reliable variable in predicting short-term outcomes in patients with heart failure.


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Two Clinical Studies Report Cost Effectiveness

Massachusetts General Hospital Single Center ClinicalStudy

This was the first single-center, blinded study of 599 patientspublished in the American Journal of Cardiology, September 2006.Results of the study showed that using Roches proBNP test in theemergency room resulted in better patient care, shortened hospitalstays and a total cost savings of $474 per patient.

St. Michaels Hospital in Toronto, Canada First Multi-centerStudy

This was the first multi-center randomized-controlled trial with aNT-proBNP guided strategy in the management of patientspresenting with shortness of breath in the emergency department.The trial was conducted in seven hospitals.

It was found that adding this test to physician judgmentsignificantly reduced the duration of the emergency department

visit from an average of 6.3 hours to an average of 5.6 hours. Inaddition, it reduced the number of patients hospitalized within 60days from 51 to 33.


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From Framingham Heart Study (based on Kannel, D'Agostino, Silbershatz, Belanger,Wilson, Levy. 'Profile for Estimating Risk of Heart Failure' - Arch Intern. Med. 1999)


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This population includes patients who have riskfactors for developing heart failure (eg,hypertension, diabetes mellitus, obesity,metabolic syndrome, sleep apnea, patients withfamily history of dilated cardiomyopathy or using

cardiotoxins). These patients should be treatedwith aggressive risk factor modification,education, and ACEI/ARB if diabetes mellitus orvascular disease is present. Patients who have afamily history of dilated cardiomyopathy shouldbe screened with a comprehensive history and

physical examination together withechocardiography and transthoracicechocardiography every 2-5 years.


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Careful diuretic therapy is recommended to avoid hypotension.

ACEI/ARBs are used as indicated for patients with evidence of

atherosclerotic disease, post-myocardial infarction, diabetes melitis, and

hypertension. Some evidence shows LV reverse remodeling using losartan

and valsartan with improvement in diastolic function and regression of

LVH.

Beta-blockers are indicated for patients with prior myocardial infarction,

hypertension, and atrial fibrillation for control of ventricular rate. In the

ADHERE registry, the subset of patients with HFNEF not treated with

beta-blocker had a higher mortality potentially due to the higher

incidence of coronary artery disease in this population.

Calcium channel blockers may improve exercise tolerance via the

vasodilatory properties and nondihydropyridine calcium channel blockers

are also used for ventricular rate control in patients with atrial

fibrillation. Amlodipine has antianginal properties and is also indicated in

hypertension.

Restoration of sinus rhythm should be considered if the patient remains

symptomatic despite above efforts.

Use of digitalis or inotropes in patients with HFNEF is not indicated.


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Medical therapy of heart failure focuses on 3main goals: (1) preload reduction, (2) reductionof systemic vascular resistance (afterloadreduction), and (3) inhibition of both the RAASsystems and vasoconstrictor neurohumoral

factors produced by the sympathetic nervoussystem in patients with heart failure. The first 2goals provide symptomatic relief. While reducingsymptoms, inhibition of the RAAS andneurohumoral factors also results in significantreductions in morbidity and mortality rates.

Therapeutic measures assisting with symptomrelief include diuretics, digoxin, inotropes,oxygen, and morphine.


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Implantable cardioverter-defibrillators (ICDs) are aClass I, level of Evidence A recommendation forsecondary prevention of s udden card iac deathinpatients with current or prior heart failure symptomsand LV dysfunction who survived cardiac arrest, haveevidence ofventricular fibrillation or hemodynamicallyunstable ventricular tachycardia (MADIT I).

ICD therapy is a Class I, level of Evidence Arecommendation forpr imary prevent ion o f suddendeathin patients with nonischemic dilatedcardiomyopathy or ischemic heart disease at least 40dayspost-myocardial infarction who have an LVEF35% or less, have NYHA Class II or III heart failure,are on optimal heart failure therapy, and have a lifeexpectancy of more than 1 year. (SCD-Heft, MADIT II)


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Levy et al found that, in moderately symptomatic heartfailure patients with an ejection fraction of 35% or less,primary prevention with an ICD provides no benefit insome cases but substantial benefit in others, and thatICD benefit can be predicted. Analysis of data from theplacebo arm of the Sudden Cardiac Death in Heart

Failure Trial (SCD-HeFT) showed that patients couldbe classified into 5 groups on the basis of predicted 4-year mortality.

In the treatment arm, ICD implantation decreasedrelative risk of sudden cardiac death by 88% inpatients with the lowest baseline mortality risk versus24% in the highest-risk group (P=0.009 for

interaction). ICD treatment decreased relative risk oftotal mortality by 54% in the lowest-risk group butprovided no benefit (2%) in the highest-risk group(P=0.014 for interaction).29


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Patients with heart failure and low LVEF often haveelectrical conduction abnormalities, left bundle brunchblock (LBBB) being common. Prognosis of patientswith reduced LVEF and LBBB is worse than in patientswithout LBBB. LBBB leads to delayed activation ofmyocardium and therefore mechanical dyssynchrony,

which clinically translates in inefficient LV contractionwith increased LV end diastolic pressure, increasedmitral regurgitation, and pulmonary wedge pressure,decreased cardiac output which leads to decreasedexercise tolerance and progression of heart failuresymptoms. Using RV and LV pacing can restore themechanical synchrony (cardiac resynchronization) and

can lead to LV reverse remodeling with decrease incardiac pressures, mitral regurgitation and improvedLVEF and exercise tolerance.


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Cardiac resynchronization therapy (CRT) is indicatedfor patients with LVEF 35% or less, sinus rhythm, andNYHA Class III and IV symptoms who are on optimalmedical therapy and have evidence of cardiacdesynchrony as evident by QRS duration more than120 msecwith or without an ICD (Class I, level of

Evidence A) (COMPANION, CARE-HF).27

CRT with or without an ICD, maybe reasonable forpatients with chronic atrial fibrillation, LVEF 35% orless, NYHA Class III and IV, QRS duration more than120 msec on optimal medical therapy (Class IIa, levelof Evidence B).

CRT with or without an ICD is reasonable for patient

who have frequent RV pacing, LVEF 35% or less,NYHA Class III and IV, and are on optimal heart failuretherapy (Class IIa, level of Evidence C -- DAVID trial).


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Ultrafiltration (UNLOAD trial) is now a class IIarecommendation for patients with refractory heartfailure not responsive to medical therapy.

Aquapheresis -- also called ultrafiltration -- is atechnique for removing excess fluid from the

body. It involves the placement of an catheter in thebloodstream that continuously runs the patient's bloodthrough a filter. Excess fluid is remove from the bloodthrough this filter, and the blood is then returned to thepatient. Up to half a liter an hourof extra fluid can beprecisely removed from the body in this way. (Thistechnique is different than dialysis, which also involvesthe removal of excess toxins from the body -- usingthe process of diffusion -- when the kidneys havefailed.)


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In the UNLOAD trial, two hundred patients with heart failure wererandomized to receive either intravenous diuretics

or aquapheresis/ultrafiltration. After 48 hours, patientsreceivingaquapheresis had the following results:

38 % greater weight loss over standard care

28 % greater net fluid loss over standard care

Equal improvement in dyspnea score (breathing)

Ninety days after hospital discharge, patientsreceiving aquapheresis showed: 43% reduction in patients requiring re-hospitalizations for heart

failure over standard care

50% reduction in the total number of re-hospitalizations for heartfailure over standard care

52% reduction in emergency department or clinic visits overstandard care

63% total reduction in days re-hospitalized for heart failure overstandard care

SOURCE: http://content.onlinejacc.org/cgi/content/abstract/49/6/675


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Coronary revascularization

Valvular surgery

Assisted circulation

Cardiac transplantation


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Patients admitted with heart failure or pulmonaryedema should maintain a low-salt diet in order tominimize fluid overload.

Dietary sodium restriction to 2-3 g/d is

recommended. Fluid restriction to 2 L/d is recommended for

patients with evidence of hyponatremia (Na


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Patients with decompensated heart failure should be placedon complete bed rest until their decompensation is resolved.This is necessary to maximally reduce myocardial oxygendemand and to avoid exacerbation of the abnormalhemodynamics and symptoms of heart failure.

Once the patient with heart failure has been stabilized,activity should be gradually and progressively increased.Emphasize the importance of cardiac rehabilitation to allpatients with heart failure who require improved cardiacfitness. Encourage patients to exercise daily for at least 20-30 minutes in a low-intensity, endurance-enhancingactivity such as walking, biking, or swimming. Regularexercise improves the quality of life for these patients and

improves efficiency of oxygen utilization at the tissue level,thus reducing the workload of the heart in the role of oxygendelivery to end organs and muscles.


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Overview of Heart Failure

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