physiology, pathology and treatment of heart failure

PHYSIOLOGY, PATHOLOGYAND TREATMENT OF

HEART FAILURE

DON’T FAILMY HEART

OBJECTIVES To understand how a normal heart develops heart

failure, learning the physiologic compensatory mechanisms that play roles in preventing and/or delaying progression to a failing heart.

To learn the different symptoms and signs that signal heart failure and understanding how these develop in the course of the disease; and

To acquire knowledge on how to approach treatment of heart failure addressing the different pathologic insults that lead to the development and progression of the failing heart.

DEFINITIONHeart Failure is a clinical syndrome that

occurs in patient who, because of an INHERITED or ACQUIRED abnormality of cardiac STRUCTURE AND/OR FUNCTION, develop a constellation of clinical SYMPTOMS (dyspnea and fatigue) and SIGNS (edema and rales) that lead to FREQUENT HOSPITALIZATIONS, a POOR QUALITY OF LIFE, and a SHORTENED LIFE EXPECTANCY.

Prevalence in the adult population in developed countries is 2%.

Prevalence rises with age and affects 6-10% of people over the age of 65.

Categorized into 2 groups:HF with a depressed EF (systolic failure)HF with preserved EF (diastolic failure)

BURDEN OF THE DISEASE

TAKE – OFF CASEZA75 years oldFemaleWidowRoman CatholicFrom TondoKnown hypertensive for 50 yearsKnown Diabetic for 15 years

HISTORY OF PRESENT ILLNESS

9 days PTA– Started to complain DOB on excertion

described as drowning.– Difficulty climbing 1 flight of stairs– 2-3 pillow orthopnea– Intermittent chest heaviness radiating to

the upper back.– Decreased urine output from almost 5

glasses/day to 2 cups/day.– Bipedal edema non-pitting noted– Facial edema noted– Decreased appetite

Day of Admission– Bipedal edema, pitting persisted– Facial edema also persisted– 2-3 pillow orthopnea still noted– Intermittent chest heaviness radiating to

the upper back– Decreased urine output still approx. 1-2

cups per day.– Bloatedness which resulted to decreased

appetite– Prompted consult to a DM physician in this

institution– Noticed by the physician to have abdominal

enlargement– Patient was then advised for admission

PAST MEDICAL HISTORY

1958 - HTN (UBP= 120-130/90; Highest BP= 160) Combizar 100mg/25mg/tab, 1 tab OD Atenolol 100mg/tab, 1 tab OD Clopidogrel 75mg/tab, 1 tab OD

1997 – DM type II HUM 70/30 = 28 ‘u’ AM; 14 ‘u’ PM

1990 – S/p TAB for myoma Uteri

1995 – S/P cholecystectomy for cholecystitis 2004 – Mass excision on popliteal area 2006 – Bronchitis Hyperurecemia – allopurinol 100mg/tab, 1 tab OD Dyslipidemia – Simvastatin 40mg/tab, 1 tab qHS

FAMILY HISTORY

(+) HTN – mother (+) Kidney disease – sister (+) Stroke – sister (+) TB – mother (+) DM – mother

PHYSICAL EXAM ON ADMISSION VS: Anicteric sclerae, pink palpebral

conjunctivae, (+) Prominent neck veins, (-) CLADS, (-) TPC

ECE, (+) bibasal crackles, (-) wheezing

AP, distinct S1 and S2, NRRR, (-) murmur

Globular, (+) fluid wave, (-) caput medusae, (-) Bruits

FEP, (+) bipedal edema, pitting

LABORATORIES DONE

CBChemoglobin 125hematocrit 36WBC 10.3 Neutrophils

65

Lymphocytes

30

Eosinophils 4 Basophils 1 Monocytes 0

Normochromic, normocytic

Blood chemistry

Na 131 mmol/L (N: 135-155)

K 3.2 mmol/L (N: 3.5-5.3)

Albumin Mass C 43g/L (N: 38-50)

SGPT 57 Iu/L (N: 6-37)

BUN 10.9 mmol/L (N:3.2-6.8)

Creatinine 160 mmol/L (N:44-106)

ECC 25 at 61kg

UrinalysisCOLOR YELLOWTURBIDITY CLEARREACTION ACIDICSPECIFIC GRAVITY 1.030PROTEIN TRACESUGAR NEGATIVERBC 0-2/HPFWBC 0-2/HPFCASTS 10-15/LPFBACTERIA NONEEPITHELIAL CELLS FEWMUCUS NONECRYSTALS NONEYEASTS NONE

ECGNSRFreq. PVCs in singlesLeft atrial abnormality

HBa1c: 7.5%CBG: 52

Chest X-ray – mild bilateral pulmonary congestion

– biventricular cardiomegaly

– atherosclerotic aorta2D Echom

THE NORMAL HEART

PATHOGENESIS

UNDERLYING CAUSEIschemic Heart Disease

CardiomyopathiesCongenital, Valvular Hypertensive Heart Disease

PRECIPITATING CAUSE Infection Arrhytmia Physical, Dietary, Fluid, Environment Myocardial Infarction Pulmonary Embolism Anemia Thyrotoxicosis and Pregnancy Aggravation of Hypertension Rheumatic, Viral and other forms of

Myocarditis Infective Endocarditis

HEART FAILUREa. Systolic

Dysfunction – Depressed EF

b. Diastolic Dysfunction – EF Preserved

HEMODYNAMIC DERANGEMENT IN HFReduction in Cardiac Reserve

Increased ventricular diastolic pressure

SYSTOLIC DYSFUNCTION

Main Pathology: Decreased Cardiac Output

4 MAJOR DETERMINANTS OF THE SYSTOLIC FUNCTION OF THE HEART AND THE CARDIAC OUTPUTContractile State of the Myocardium

PreloadAfterloadHeart Rate

REPRESENTATIVE CAUSES

DIASTOLIC DYSFUNCTIONMain Pathology: Impaired Ventricular Filling

REPRESENTATIVE CAUSES

Afterload

Contractility

Preload

Myocardial Fiber Shortening

LV Size

Stroke VolumeHeart Rate

Cardiac Output TPR

Arterial Pressure

COMPENSATORY MECHANISMS TO A DECREASED CARDIAC OUTPUTIncreased Sympathetic Activity

Increased Heart Rate Increased Myocardial

Contractility Increased Venous Tone

COMPENSATORY MECHANISMS TO A

DECREASED CARDIAC OUTPUT

Activation of the RAA System

COMPENSATORY MECHANISMS TO A

DECREASED CARDIAC OUTPUT

Secretion of AVP

STAGE DESCRIPTION EXAMPLES

A Patients at high risk for developing heart failure because of the presence of conditions that are strongly associated with the development of heart failure. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown symptoms or signs of heart failure.

Systemic hypertension; coronary artery disease; diabetes mellitus; history of cardiotoxic drug therapy or alcohol abuse; personal history of rheumatic fever; family history of cardiomyopathy.

STAGE DESCRIPTION EXAMPLES

B Patients who have developed structural heart disease that is strongly associated with the development of heart failure but who have never shown symptoms or signs of heart failure.

Left ventricular hypertrophy or fibrosis; left ventricular dilation or hypocontractility; asymptomatic valvular heart disease; previous myocardial infarction.

STAGEDESCRIPTION EXAMPLES

C Patients who have current or prior symptoms of heart failure associated with underlying structural heart disease.

Dyspnea or fatigue due to left ventricular systolic dysfunction; asymptomatic patients who are undergoing treatment for prior symptoms of heart failure.

STAGE DESCRIPTION EXAMPLES

D Patients with advanced structural heart disease and marked symptoms of heart failure at rest despite maximal medical therapy and who require specialized interventions.

Patients who are frequently hospitalized for heart failure and cannot be safely discharged from the hospital; patients in the hospital awaiting heart transplantation; patients at home receiving continuous intravenous support for symptom release or being supported with a mechanical circulatory assist device; patients in a hospice setting for the management of heart failure.

CLINICAL MANIFESTATIONS

CARDINAL SYMPTOMS:• Fatigue• Shortness of breath

• Ortopnea• PND• Cheyne-stokes respiration• Acute pulmonary edema• Others: GI symptoms, nausea, anorexia, early

satiety, RUQ pain, cerebral symptoms, nocturia

PHYSICAL EXAMINATIONGeneral Appearance:• Sitting upright• Labored breathing/shortness of

breath• Normal or high SBP (early)• Low SBP (advanced)• Diminished pulse pressure• Peripheral vasoconstriction

PHYSICAL EXAMINATIONJugular veins• Normal to high

• Pulmonary ExamCrackles (rales or crepitations)Wheezing (pulmonary edema)

PHYSICAL EXAMINATION Cardiac exam• Displaced PMI• Third heart sound (S3)• Murmurs on mitral and tricuspid

regurgitation (advanced)• Abdomen and Extremities

HepatomegalyAscitesPeripheral edema

PHYSICAL EXAMINATION

Cardiac Cachexia•Marked weight loss

DIAGNOSIS

Straightforward when presented with classic signs and symptoms.

Routine Lab Testing• CBC, serum electrolytes, BUN,

Serum creatinine, hepatic enzymes, urinalysis

• FBS, lipid profile, TSH

ECG• Cardiac rhythm• LV hypertrophy• Prior MI• QRS width

• ASSESSMENT OF LV FUNCTION2d echo / doppler

BiomarkersExercise Testing

ALGORITHM FOR CHF TREATMENTDIAGNOSIS OF HF CONFIRMED

ASSESS FOR FLUID RETENTION

FLUID RETENTIONNO FLUID

RETENTION

DIURETICACE

INHIBITORS

BETA BLOCKERS

ARBALDOSTERONE ANTAGONIST

HYDRALAZINE/ISOSORBIDE

DIGOXIN

NYHA I-IV

PERSISTENT

SYMPTOMS

TREATMENTCorrection of Reversible CausesLifestyle ModificationActivityDietCompliance to Medications (anti –

hypertensive, Euglycemic agents, anti – hyperlipidemic drugs, thyroid medications, etc.)

PHARMACOLOGIC TREATMENT

DiureticsACE – IARBΒ – BlockersAnticoagulation and anti – platelet therapy

Anti – arrhythmiasVasodilatorsInotropesVasoconstrictorsVasopressin antagonists

DEVICE THERAPYCardiac Resynchronization

Implantable Defibrillators