1. HEART FAILURE l.l.

5. l MECHANISMS WHICH INFLUENCES THE HEART MUSCLE SHORTENING AND STROKE VOLUME: 1) PRELOAD: LENGTH OF THE MUSCLE AT THE ONSET OF CONTRACTION. 2) THE INOTROPIC STATE OF THE MUSCLE: THE POSITION OF ITS FORCE - VELOCITY- LENGTH RELATION. 3) AFTERLOAD: THE TENSION THE MUSCLE MUST DEVELOP DURING CONTRACTION HARRISON´S

6. HEART FAILURE l PRELOAD. ( END DIASTOLIC VOLUME) THE FRANK - STARLING MECHANISM: WITHIN A CERTAIN LIMIT THE GREATER THE MYOCARDIAL FIBER STRETCH OR TENSION ( THE GREATER THE VOLUME CONTAINED WITHIN THE CHAMBER), THE GREATER IS THE FORCE OF CONTRACTION THAT EJECTS THAT VOLUME (AND THE GREATER THE CARDIAC OUTPUT). HANSEN PATHOPHYSIOLOGY.

7. HEART FAILURE l MAJOR DETERMINANTS OF PRELOAD: * TOTAL BLOOD VOLUME. * DISTRIBUTION OF BLOOD VOLUME. BODY POSITION INTRATHORACIC PRESSURE INTRAPERICARDIAL PRESSURE VENOUS TONE SKELETAL MUSCLE PUMPING * ATRIAL CONTRACTION. HARRISON´S

8. HEART FAILURE l INOTROPIC STATE. ( MYOCARDIAL CONTRACTILITY): FACTORS THAT DETERMINE THE VENTRICULAR PERFORMANCE ACT BY ALTERING THE CONCENTRATION OF Ca2+ IN THE VICINITY OF THE MYOFILAMENTS, WHICH IN TURN TRIGGER CROSS-BRIDGE CYCLING. HARRISON´S.

9. HEART FAILURE l FACTORS THAT INFLUENCE THE INOTROPIC STATE: * ADRENERGIC NERVE ACTIVITY. NOREPINEPHRINE * CIRCULATING CATECHOLAMINES. RELEASED BY THE ADRENAL MEDULLA * THE FORCE-FREQUENCY RELATION. HEART RATE AND RHYTHM * EXOGENOUSLY ADMINISTERED INOTROPIC AGENTS. SYMPATHOMIMETIC AGENTS, CARDIAC GLYCOSIDES, CALCIUM, AMRINONA, MILRINONA HARRISON´S

10. HEART FAILURE l INOTROPIC STATE: PHYSIOLOGIC DEPRESSANTS: HYPOXIA, ISCHEMIA, ACIDOSIS PHARMACOLOGIC DEPRESSANTS: PROCAINAMIDE, CALCIUM ANTAGONISTS, BETA-BLOCKERS, BARBITURATES, ALCOHOL, GENERAL ANESTHETICS. LOSS OF MYOCYTES. ISCHEMIA, MYOCARDIAL INFARCTION, APOPTOSIS. INTRINSIC MYOCARDIAL DEPRESSION. HARRISON´S

11. HEART FAILURE l VENTRICULAR AFTERLOAD: IS THE TENSION OR STRESS DEVELOPED IN THE VENTRICULAR WALL DURING EJECTION. IS DETERMINED BY: AORTIC PRESSURE VENTRICULAR VOLUME VENTRICULAR CAVITY THICKNESS HARRISON´S

12. HEART FAILURE l HEART FAILURE DEFINITION: IS THE ABNORMALITY OF THE HEART TO PUMP BLOOD ENOUGH TO PROVIDE THE METABOLIC TISSUES REQUIREMENTS AND/OR CAN DO SO FROM AN ABNORMALLY ELEVATED VENTRICULAR DIASTOLIC VOLUME. HARRISON´S

13. HEART FAILURE l ADAPTIVE MECHANISMS: 1) INCREASE IN PRELOAD THROUGH THE FRANK-STARLING MECHANISM. 2) MYOCARDIAL HYPERTROPHY. 3) BLOOD FLOW REDISTRIBUTION TO VITAL ORGANS ( BRAIN, HEART ). 4) NEUROHUMORAL ADJUSTMENTS TO MAINTAIN ARTERIAL PRESSURE ( RAAS, CATECHOLAMINES, NOREPINEPHRINE ). HARRISON´S

14. HEART FAILURE l BIOCHEMICAL ABNORMALITIES: A) EXTERNAL HEART WORK TO ENERGY CONSUMED RATIO IS DEPRESSED. B) ALTERATIONS IN ENERGY METABOLISM : DECREASED CREATINE PHOSPHATE, CREATINE KINASE C) ALTERATIONS IN REGULATORY PROTEINS: LOWER MYOSIN ATPase ACTIVITY; ALTERED TROPONIN T AND/OR MYOSIN LIGHT KINASE 2 EXPRESSION. D) ABNORMALITIES OF EXCITATION-CONTRACTION COUPLING WITH REDUCED DELIVERY OF Ca2+. HARRISON´S

15. HEART FAILURE l ADRENERGIC NERVOUS SYSTEM ROLE: 1) PROGNOSIS VARIES INVERSELY WITH NOREPINEPHRINE BLOOD LEVELS. 2) SUPPORTS VENTRICULAR CONTRACTILITY. 3) INCREASES AFTERLOAD BY RAISING VASCULAR RESISTANCE. 4) MAY CAUSE ARRHYTMIAS AND DIRECT MYOCARDIAL DAMAGE. 5) CAN BE WORSEN BY LARGE-DOSES OF BETA - BLOCKERS AND IMPROVED BY GRADUALLY INCREASING DOSES OF THEM. HARRISON´S

16. HEART FAILURE l EFFECTS OF REDUCED DENSITY OF ADRENERGIC RECEPTORS AND CARDIAC NOREPINEPHRINE. REDUCED ADENYLATE CYCLASE ACTIVITY. REDUCED INTRACELLULAR cAMP. REDUCED PROTEIN KINASE ACTIVATION. REDUCED CA2+ CHANNELS PHOSPHORILATION. REDUCED TRANSARCOLEMMAL CA2+ ENTRY. REDUCED PHOSPHOLAMBAN PHOSPHORILATION. DEPRESSED CA2+ REUPTAKE BY THE SARCOPLASMIC RETICULUM. INCREASED ACTIVITY OF THE GUANINE REGULATORY PROTEINS WHICH COUPLES BETA RECEPTOR TO AC. HARRISON´S

17. HEART FAILURE l PATHOPHYSIOLOGY: THE BASIC PROBLEM IN HEART FAILURE IS THE DEPRESSION OF THE MYOCARDIAL FORCE-VELOCITY RELATIONSHIP AND OF THE LENGTH- ACTIVE TENSION CURVE REFLECTING REDUCTION IN THE CONTRACTILE STATE OF THE MYOCARDIUM.. HARRISON´S

18. HEART FAILURE l PRECIPITATING CAUSES: *ANEMIA l *PHYSICAL, DIETARY, FLUID, ENVIRONMENTAL AND EMOTIONAL EXCESS l *PULMONARY EMBOLISM HARRISON´S

19. HEART FAILURE l FORMS OF HEART FAILURE: A) SYSTOLIC: INABILITY TO CONTRACT NORMALLY AND EXPEL SUFFICIENT BLOOD. B) DIASTOLIC: INABILITY TO RELAX AND FILL NORMALLY. C) HIGH OUTPUT: HEART´S BURDEN LIKE REGURGITANT VALVE LESIONS; MYOCARDIAL IMPAIRMENT IN THYROTOXICOSIS AND BERIBERI; ANOXIA IN ANEMIA. D) LOW OUTPUT: ISCHEMIC HEART DISEASE, HYPERTENSION, DILATED CARDIOMYOPATHY, VALVULAR AND PERICARDIAL DISEASE. HARRISON´S

20. HEART FAILURE l FORMS OF HEART FAILURE D) ACUTE: A SUFFICIENT HEART WHICH DEVELOPS A MYOCARDIAL INFARCTION OR A RUPTURE OF A CARDIAC VALVE. IS USUALLY SYSTOLIC WITH SYSTEMIC HYPOTENSION WITHOUT EDEMA. E) CHRONIC: TYPICALLY OBSERVED IN DILATED CARDIOMYOPATHY OR MULTI- VALVULAR HEART DISEASE THAT DEVELOPS OR PROGRESSES SLOWLY. THE ARTERIAL PRESSURE IS MAINTAINED UNTIL LATE BUT THERE IS OFTEN PRESENCE OF EDEMA. HARRISON´S

21. HEART FAILURE l FORMS OF HEART FAILURE: F) RIGHT- SIDED: THE EXCESS OF FLUID RESULTS IN SYSTEMIC VENOUS DISTENTION, EDEMA, CONGESTIVE HEPATOMEGALY. G) LEFT-SIDED: THE EXCESS FLUID RESULTS IN PULMONARY CONGESTION, DYSPNEA AND ORTHOPNEA. IT CHANGES WHEN THE HEART FAILURE EXISTS FOR MONTHS OR YEARS. DUE TO THE INVOLVEMENT OF BOTH VENTRICLES. HARRISON´S

22. HEART FAILURE l FORMS OF HEART FAILURE: H) BACKWARD: THE VENTRICLE FAILS TO DISCHARGE ITS CONTENTS OR FAILS TO FILL NORMALLY. RESULTING IN RAISED PRESSURE IN THE ATRIUM, VENOUS SYSTEM AND CAPILLARIES BEHIND IT WITH WATER AND SODIUM RETENTION AND INTERSTITIAL TRANSUDATION. I) FORWARD: AN INADEQUATE DISCHARGE OF BLOOD INTO THE ARTERIAL SYSTEM RESULTING IN LOWER RENAL PERFUSION, RENIN-ANGIOTENSIN ALDOSTERONE-SYSTEM ACTIVATION AND SALT AND WATER RETENTION. HARRISON´S

24. HEART FAILURE l CLINICAL MANIFESTATIONS: * DYSPNEA * ORTHOPNEA * PAROXYSMAL (NOCTURNAL) DYSPNEA * CHEYNE-STOKES RESPIRATION * FATIGUE, WEAKNESS AND ABDOMINAL SYMPTOMS * CEREBRAL SYMPTOMS HARRISON´S

25. HEART FAILURE l PHYSICAL FINDINGS: * INTRANQUILITY WHEN LYING FLAT * DIMINISHED PULSE PRESSURE * DIASTOLIC HYPERTENSION * CYANOSIS * HYPOTENSION * TACHYCARDIA * NEED OF SITTING UPRIGHT * DISTENTION OF THE YUGULAR VEINS * POSITIVE ABDOMINOJUGULAR REFLUX HARRISON´S

26. HEART FAILURE l PHYSICAL FINDINGS: * THIRD OR FOURTH HEART SOUNDS * PULSUS ALTERNANS * PULMONARY RALES * CARDIAC EDEMA * HYDROTHORAX AND ASCITES * CONGESTIVE HEPATOMEGALY * JAUNDICE * CARDIAC CACHEXIA * LOW URINE FLOW * ALBUMINURIA

27. HEART FAILURE l PHYSICAL MANIFESTATIONS: * PRERENAL AZOTEMIA * IMPOTENCE * DEPRESSION l ROENTGENOGRAPHIC FINDINGS: * CARDIOMEGALY * PULMONARY VEINS DISTENTION * REDISTRIBUTION TO THE APICES * PLEURAL EFFUSIONS * INTERLOBAR EFFUSIONS HARRISON´S

30. HEART FAILURE l DIFFERENTIAL DIAGNOSIS: 1) PULMONARY DISEASE 2) PULMONARY EMBOLISM 3) EDEMA DUE TO VARICOSE VEINS, CYCLIC EDEMA OR GRAVITATIONAL EFFECTS 4) RENAL DISEASE 5) HEPATIC CIRRHOSIS HARRISON´S

31. HEART FAILURE l TREATMENT: 1) REMOVAL OF THE PRECIPITATING FACTOR 2) CORRECTION OF THE UNDERLYING CAUSE 3) CONTROL OF THE CONGESTIVE STATE A) REDUCTION OF CARDIAC WORK LOAD BY REDUCING PRELOAD AND AFTERLOAD B) CONTROL OF SALT AND WATER RETENTION C) ENHANCEMENT OF MYOCARDIAL CONTRACTILITY HARRISON´S

32. HEART FAILURE l TREATMENT: REDUCTION OF CARDIAC WORK LOAD: * PHYSICAL ACTIVITY REDUCTION * EMOTIONAL REST * WEIGHT REDUCTION * VASODILATOR THERAPY HARRISON´S

33. HEART FAILURE l TREATMENT: CONTROL OF EXCESSIVE FLUID: 1) DIET: REDUCTION OF SODIUM INTAKE REDUCTION OF WATER INTAKE ADEQUATED NUTRITIONAL GUIDE 2) DIURETICS: THIAZIDES METOLAZONE LOOP DIURETICS ALDOSTERONE ANTAGONISTS TRIAMTERENE AND AMILORIDE HARRISON´S

34. HEART FAILURE l TREATMENT: VASODILATOR THERAPY A) ARTERIAL: HYDRALAZINE MINOXIDIL PRAZOCIN B) VENOUS: NITROGLYCERINE ISOSORBIDE DINITRATE C) “BALANCED VASODILATORS”: ACE INHIBITORS SODIUM NITROPRUSSIDE PRAZOCIN HARRISON´S

35. HEART FAILURE l TREATMENT: ENHANCEMENT OF MYOCARDIAL CONTRACTILITY: 1) DIGITALIS 2) SYMPATHOMIMETIC AMINES: NOREPINEPHRINE EPINEPHRINE ISOPROTERENOL (ISOPRENALINE) DOPAMINE DOBUTAMINE 3) AMRINONE AND MILRINONE HARRISON´S

36. HEART FAILURE l TREATMENT: * ANTICOAGULANTS * BETA-ADRENOCEPTOR BLOCKERS * MANAGEMENT OF ARRHYTMIAS * INTRAORTIC BALLOON-PUMP * CARDIAC TRANSPLANTATION HARRISON´S

37. HEART FAILURE l TREATMENT OF ACUTE PULMONARY EDEMA: 1) MORPHINE 2 TO 5 MG I.V. 2) 100% OXYGEN 3) SITTING POSITION WITH DANGLING LEGS 4) LOOP DIURETICS AS FUROSEMIDE OR ETHACRINIC ACID (40 TO 100 mg), OR BUMETANIDE (1 mg) 5) AFTERLOAD REDUCTION WITH SODIUM NITROPRUSSIDE 20 TO 30 MICROG/MIN WHEN SYSTOLIC BLOOD PRESSURE >100 mm Hg HARRISON´S

38. HEART FAILURE l TREATMENT OF ACUTE PULMONARY EDEMA: 6 ) INOTROPIC SUPPORT WITH DOPAMINE OR DOBUTAMINE. DIGOXIN 1 mg I.V. WHEN SYSTOLIC FAILURE IS PRESENT 7) BRONCHOCOSTRICTION TREATMENT WITH AMINOPHYLLINE 240 TO 480 MG I.V 8) ROTATING TOURNIQUETS 9) MECHANICAL VENTILATION HARRISON´S

39. HEART FAILURE l FACTORS ASSOCIATED WITH POOR PROGNOSIS: A) SEVERE HEART FAILURE WITHOUT A PRECIPITATING CAUSE B) POOR RESPONSE TO MEDICATION C) EJECTION FRACTION < 25% D) REDUCED MAXIMAL O2 UPTAKE (< 15mL/kg/MIN) E) INABILITY TO WALK ON THE LEVEL AT A NORMAL PACE FOR MORE THAN 3 min HARRISON´S

40. HEART FAILURE l FACTORS ASSOCIATED WITH POOR PROGNOSIS : F) REDUCED SODIUM CONCENTRATION ( < 133 mEq/L) G) REDUCED POTASSIUM CONCENTRATION (< 3 mEq/L) H) HIGH ATRIAL NATRIURETIC FACTOR I) HIGH NOREPINEPHRINE CONCENTRATION J) FREQUENT VENTRICULAR EXTRASYSTOLES HARRISON´S

41. CT Angiography l The development of Coronary Computed Tomographic Angiography (CCTA) promises to revolutionize how coronary artery disease is diagnosed and treated. CCTA currently provides the only non-invasive technique which allows doctors to look at not only the arteries of the heart, but also the early development of fatty plaque which is often the source of heart attacks.