o bjectives to understand how a normal heart develops heart failure, learning the physiologic...
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PHYSIOLOGY, PATHOLOGYAND TREATMENT OF
HEART FAILURE
DON’T FAILMY HEART
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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.
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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.
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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
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TAKE – OFF CASEZA75 years oldFemaleWidowRoman CatholicFrom TondoKnown hypertensive for 50 yearsKnown Diabetic for 15 years
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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
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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
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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
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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
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FAMILY HISTORY
(+) HTN – mother (+) Kidney disease – sister (+) Stroke – sister (+) TB – mother (+) DM – mother
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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
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LABORATORIES DONE
CBChemoglobin 125hematocrit 36WBC 10.3 Neutrophils
65
Lymphocytes
30
Eosinophils 4 Basophils 1 Monocytes 0
Normochromic, normocytic
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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
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UrinalysisCOLOR YELLOWTURBIDITY CLEARREACTION ACIDICSPECIFIC GRAVITY 1.030PROTEIN TRACESUGAR NEGATIVERBC 0-2/HPFWBC 0-2/HPFCASTS 10-15/LPFBACTERIA NONEEPITHELIAL CELLS FEWMUCUS NONECRYSTALS NONEYEASTS NONE
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ECGNSRFreq. PVCs in singlesLeft atrial abnormality
HBa1c: 7.5%CBG: 52
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Chest X-ray – mild bilateral pulmonary congestion
– biventricular cardiomegaly
– atherosclerotic aorta2D Echom
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THE NORMAL HEART
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PATHOGENESIS
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UNDERLYING CAUSEIschemic Heart Disease
CardiomyopathiesCongenital, Valvular Hypertensive Heart Disease
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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
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HEART FAILUREa. Systolic
Dysfunction – Depressed EF
b. Diastolic Dysfunction – EF Preserved
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HEMODYNAMIC DERANGEMENT IN HFReduction in Cardiac Reserve
Increased ventricular diastolic pressure
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SYSTOLIC DYSFUNCTION
Main Pathology: Decreased Cardiac Output
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4 MAJOR DETERMINANTS OF THE SYSTOLIC FUNCTION OF THE HEART AND THE CARDIAC OUTPUTContractile State of the Myocardium
PreloadAfterloadHeart Rate
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REPRESENTATIVE CAUSES
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DIASTOLIC DYSFUNCTIONMain Pathology: Impaired Ventricular Filling
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REPRESENTATIVE CAUSES
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Afterload
Contractility
Preload
Myocardial Fiber Shortening
LV Size
Stroke VolumeHeart Rate
Cardiac Output TPR
Arterial Pressure
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COMPENSATORY MECHANISMS TO A DECREASED CARDIAC OUTPUTIncreased Sympathetic Activity
Increased Heart Rate Increased Myocardial
Contractility Increased Venous Tone
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COMPENSATORY MECHANISMS TO A
DECREASED CARDIAC OUTPUT
Activation of the RAA System
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COMPENSATORY MECHANISMS TO A
DECREASED CARDIAC OUTPUT
Secretion of AVP
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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.
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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.
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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.
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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.
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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
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PHYSICAL EXAMINATIONGeneral Appearance:• Sitting upright• Labored breathing/shortness of
breath• Normal or high SBP (early)• Low SBP (advanced)• Diminished pulse pressure• Peripheral vasoconstriction
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PHYSICAL EXAMINATIONJugular veins• Normal to high
• Pulmonary ExamCrackles (rales or crepitations)Wheezing (pulmonary edema)
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PHYSICAL EXAMINATION Cardiac exam• Displaced PMI• Third heart sound (S3)• Murmurs on mitral and tricuspid
regurgitation (advanced)• Abdomen and Extremities
HepatomegalyAscitesPeripheral edema
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PHYSICAL EXAMINATION
Cardiac Cachexia•Marked weight loss
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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
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ECG• Cardiac rhythm• LV hypertrophy• Prior MI• QRS width
• ASSESSMENT OF LV FUNCTION2d echo / doppler
BiomarkersExercise Testing
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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
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TREATMENTCorrection of Reversible CausesLifestyle ModificationActivityDietCompliance to Medications (anti –
hypertensive, Euglycemic agents, anti – hyperlipidemic drugs, thyroid medications, etc.)
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PHARMACOLOGIC TREATMENT
DiureticsACE – IARBΒ – BlockersAnticoagulation and anti – platelet therapy
Anti – arrhythmiasVasodilatorsInotropesVasoconstrictorsVasopressin antagonists
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DEVICE THERAPYCardiac Resynchronization
Implantable Defibrillators