HEART FAILURE BY DR. ARWA MAHMOOD FUZI

HEART FAILURE WORLD WIDE  HF is a major cause of morbidity & mortality in developed and developing countries,  HF is a disease of elderly with a median age of around 75 years. In octogenarians, the prevalence of HF increase sharply to >10%.  Patients with HF have a worse quality of life than those with other chronic diseases including COPD, kidney failure & arthritis.  Up to 40% of patients with HF die within one year of diagnosis.  HF is expensive disease, consuming 2-3% of the overall health care budget.

DEFINITION: A COMPLEX CLINICAL SYNDROME THAT CAN RESULT FROM ANY CARDIAC DISORDER THAT IMPAIRS THE ABILITY OF THE VENTRICLES TO EJECT BLOOD, SO THE HEART CANNOT MAINTAIN ADEQUATE CARDIAC OUTPUT, OR CAN DO SO ON EXPENSE OF ELEVATED FILLING PRESSURES RESULTING IN SIGNS &SYMPTOMS OF PULMONARY CONGESTION, SYSTEMIC FLUID RETENTION, OR INADEQUATE CARDIAC PERFUSION.

PATHOPHYSIOLOGY OF H.F. CARD. OUT PUT = STROKE VOLUME BY H.R. STROKE VOLUME : 1- PRELOAD 2-THE AFTERLOAD 3-MYOCARDIAL CONTRACTILITY. STARLING LAW VENTRICULAR PERFORMANCE IS RELATED TO THE DEGREE OF MYOCARDIAL STRECHING, SO INCREASE PRELOAD WILL INHANCE FUNCTION, HOWEVER OVERSTRECHING WILL CAUSE MARKED DETERURATION

COMPENSATORY MECHANISIME IN H. F. 1-ACTIVATION OF SYMPATHATIC N. SYSTEM. 2-ACTIVATION OF RENIN-ANGIOTENSIN – ALDOSTERON SYSTEM. 3-RELEASE OF A.D.H. 4-RELEASE OF N.U. PEPTIDE. 5-INCREASE PEREPH.O2 EXTRACTION. 6-LOCAL CHANGES IN THE HEART: a-CHAMER ENLARGMENT b-CARDIAC HYPERTROPHY c-INCREASE H. R.

COMPENSATED H. F. IMPAIRED CARDIAC FUNCTION, BUT ADAPTIVE CHANGE HAVE PREVENTED THE DEVELOPMENT OF OVERT HEART FAILUR

CAUSES OF HEART FAILURE 1.DECREASE VENT.CONTRACTILITY(MYOCARDITIS,CMP, MI ) 2.VENT. OUTFLOW OBSTRUCTION (HYPERTENSION,AS,PULM.HYPERT.,PS.) 3.VENT. INFLOW OBSTRUCTION (MS,TS.) 4.VENT. VOLUME OVERLOAD (MR,AR,ASD,VSD&INC.MET.DEMAND) 5.ARRHYTHMIA (AF,TACHYCARDIA MYOPATHY, COMPL. H.BLOCK) 6.DIASTOLIC DYSFUNCTION (CONSTR.PERICARDITIS,RESTRICTIVE CMP,LVH,LV FIBROSIS. CARDIAC TAMPONADE).

PRECIPITATING FACTORS FOR H.F. 1-MYOCARDIAL INFARCTION OR ISCHEMIA. 2-INTERCURRENT ILLNESS. 3-ARRTHYMIAS. 4-REDUCTION OF THERAPY. 5-DRUGS ( B.BLOCKERS, NSAID, STEROIDES.) 6-PULM. EMBOLISM. 7-INC. METABOLIC DEMAND. 8-I.V.F. OVERLOAD.

TYPES OF HEART FAILURE 1.ACUTE(DECOMPENSATED)HF & CHRONIC (COMPENSATED) H.F. 2.LEFT SIDED, RT SIDED & BIVENT. F. 3.FORWORED H.F(INADEQUIT C.O) & BACKWORED H.F(MARKED VENOUS CONGESTION). 4.DIASTOLIC H.F(ABNOR VENT. RELAXAT) &SYSTOLIC(ABNOR VENT CONTRACTION) 5.HIGH OUTPUT F (AV SHUNT, BERI BERI, ANEMIA, THYROTOXICOSIS) &LOW OUTPUT H. F.

CLINICAL FEATURES OF H.F.  LOW C.O.P &HYPOPERFUSION TO THE TISS.  FLUID &WATER RETENTION WITH PULM. CONGESTION L.V.F.  SYSTEMIC VENOUS CONGETION IN RT. V.F.

SYMPTOMES OF H.F 1.DYSPNIA.ORTHOPNIA & PND.(LEFT SIDE H.F) 2.FATIGUE &RED. EXERCISE CAPACITY. (L&R SIDE) 3.ANOREXIA, NAUSIA, ABD. PAIN &FULLNESS.WT LOSS (L&R) 4.ANKLE SWELLING (R SIDE F). 5.CEREBRAL SYMPTOMES. 6.NUCTURIA.

PHYSICAL FINDINGS PULSE (TACKYCARDIA, PULS.ALTERNANCE ) BP (HYPOTENTION, DEC.PULSE PRESS.) DISTENTION OF JVP.(R SIDE F) S3 &S4. PULM. CREPITATION.(L SIDE F)

CARDIAC OEDEMA.(R SIDE F) PL. EFFUSION. ASCITES.(RSIDE F) CONGESTIVE HEPATOMEGALY.(R SIDE F) JOUNDICE.(R SIDE F) CARDIAC CACHEXIA. COLD,PALE EXTR.(ACUTE H F) PRE RENAL AZOTEMIA &DEC.UOP.

COMPLICATIONS OF H.F. 1.UREAMIA 2.HYPOKALEMIA, HYPERKALEMIA &HYPONATREMIA. 3.IMPAIRED LIVER F. T. 4.THROMBOEMBOLISM (DVT &SYST. EMBOLISATION) 5.ARRHYTHMIAS.(V ECTOPICS, VT) 6.SUDDEN DEATH.(50% OF PT)

INVESTIGATIONS AIMES:  CONFIRM THE DIAGNOSES.  DEFINE TYPE.  EXCLUDE TREATABLE CAUSES.

 LAB. TEST: 1.BLOOD GAS ANALYSIS 2.INC. LIVER ENZYMES 3.INC.WBC COUNT 4.INC.B.UREA &S.CREATNIN 5.BNP  ECG (MI,LVH,RVH,ARRYTHMIAS)  CXR (CARDIOMEGALY,PULM.EDEMA)

 ECHOCARDIOGRAPHY 1.DETERMINE PRIM. ABN. 2.LV. EF 3.ASSES DIMENTION,THICKNESS&REGI ONAL MOTION 4.EVALUATION OF PERICARDIAL,VALV.&VASC.STR.  RADIONUCLIDE VENTRICULOGRAPHY  MRI