approach to heart failure medicos notes-com
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Approach to Heart Failure
Heart Failure
Heart Failure, is a clinical syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate commensurate with the requirements of metabolizing tissues
General Etiologies Of Cardiac Failure
1. CORONARY VASCULAR -> ACUTE MI2. VALVULAR -> AORTIC , MITRAL VALVE
DISEASE3. MYOCARDIAL -> ISCHEMIC CARDIOMYOPATHY 4. HYPERTENSION -> HYPERTENSIVE CRISIS5. RHYTHM DISTURBANCES -> TACHYCARDIA , INDUCED HF6. PERICARDIAL -> TAMPONADE , CONSTRICTION
Underlying cardiac diseaseConditions that Conditions thatdepress ventricular function restrict filling
CAD RESTRICTIVE C.M.PATHYHTN PERICARDIAL DISEASEDCMValvular heart diseaseCongenital heart disease
Precipitating causes
1. Increased salt intake2. Non compliance with anti CHF medications3. Acute myocardial infarction 4. Aggravation of Hypertension 5. Acute arrhythmias 6. Infections and or fever
1. Pulmonary Embolism 2. Anemia 3. Thyrotoxicosis4. Pregnancy 5. Rheumatic, Viral, and Other Forms of Myocarditis 6. Infective Endocarditis 7. Physical, Environmental, and Emotional Excesses
Pathogenesis
1. Myocardial cell loss myocyte hypertrophy and elongation.
2. An increase in ventricular volume (the Starling effect) helps maintain cardiac output (CO), but at the cost of increasing ventricular filling pressures.
3. The increase in diastolic stretch and pressure produces further damage stretch-induced myocyte death (apoptosis)
CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
REMODELLING
INC.FORCE RATE
PRELOAD AFTERLOAD
DEC. RENAL BLD FLOW
RAA. ACTIVATION
CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
DEC. RENAL BLD FLOW
INC.FORCE RATE
PRELOAD AFTERLOAD
RAA. ACTIVATION
CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
DEC. RENAL BLD FLOW
Forms of Cardiac Failure
1. Systolic and diastolic failure2. Low output and high output failure3. Acute and chronic heart failure4. Backward and forward failure5. Left and right heart failure
Approach to the patient
1. RESPIRATORY AND OTHER SYMPTOMS 2. Due to inadequate perfusion of peripheral tissues
1. Fatigue 2. Dyspnoea
3. Due to elevated intracardiac filling pressures1. Orthopnoea2. PND3. Peripheral edema
Symptoms of heart failure1. Respiratory Distress2. Breathlessness- cardinal manifestation of left ventricular
failure3. May present with progressively increasing severity as
1. exertional dyspnea2. orthopnea3. paroxysmal nocturnal dyspnea4. dyspnea at rest5. acute pulmonary edema.
Symptoms.• URINARY SYMPTOMS.1. Nocturia may occur early in the course of heart failure. 2. Oliguria is a sign of late cardiac failure.• CEREBRAL SYMPTOMS.1. Confusion, impairment of memory, anxiety, headache,
insomnia, bad dreams or nightmares, and, rarely, psychosis with disorientation, delirium, and hallucinations.
Symptoms of predominant right-sided Heart Failure
1. Breathlessness is not very prominent because pulmonary congestion is usually absent.
2. Congestive hepatomegaly - dull ache or heaviness in epigastrium.
3. Other gastrointestinal symptoms, including anorexia, nausea, bloating, a sense of fullness after meals, and constipation due to congestion of the liver and gastrointestinal tract.
4. In severe, preterminal heart failure, inadequate bowel perfusion can cause abdominal pain, distention, and bloody stools.
Physical examination
1. JVP2. S3 3. Pulmonary congestion (rales, dullness over
pleural effusion)4. Peripheral edema5. Hepatomegaly6. Ascites
Laboratory Investigations
1. CBC, ESR2. Urine routine3. LFT4. RFT5. CXR6. ECHO7. Measurement of BNP
BRAIN NATRIURETIC PEPTIDE (BNP)
• Pre pro-BNP is formed in the ventricles with myocyte stretch
• Broken down to N-terminal-pro-BNP (NT-pro-BNP) and BNP.
• Highly accurate for identifying or excluding HF with high sensitivity and specificity
• BNP - valuable in differentiating cardiac from pulmonary causes of dyspnea
Framingham Criteria for Diagnosis of Congestive Heart Failure
One major +two minor for diagnosis
1. Paroxysmal nocturnal dyspnea2. Neck vein distention3. Rales4. Cardiomegaly5. Acute pulmonary edema6. S3 gallop7. Increased venous pressure (>16 cmH2O)8. Positive hepatojugular reflux9. Weight loss ≥4.5 kg over 5 days' treatment
Major Criteria
1. Extremity edema2. Night cough3. Dyspnea on exertion4. Hepatomegaly5. Pleural effusion6. Vital capacity reduced by one-third from normal7. Tachycardia (≥120 bpm)
Minor Criteria
NYHA GRADING
• Class 1 : no symptoms• Class 2 : symptoms with ordinary activity• Class 3 : less than ordinary activity• Class 4 : even at rest
Staging of systolic HF
1. STAGE A- ASYMPTOMATIC/ MILD HF NYHA CLASS 1 / 2
2. STAGE B- MILD /MODERATE HF ,NYHA CLASS 2 / 33. STAGE C- ADVANCED HF , CLASS 3 / 44. STAGE D- REFRACTORY HF ,CLASS 3 / 45. SUSTAINED DECOMPENSATION, FREQUENT
HOSPITALISATION
Conditions That MIMIC CHF1. Pulmonary disease
1. Chronic bronchitis2. Emphysema 3. Asthma
2. Other causes of peripheral edema1. Liver disease2. Varicose veins3. Cyclic edema4. Renal dysfunction
General measures1. Prevent HF2. Daily measurement of weight 3. Immunization with influenza and pneumococcal
vaccines 4. Education of the patient and family 5. Avoid Excessive alcohol, temperature extremes,
and tiring trips6. Meals - small in quantity, frequent7. Reduce sodium intake
Activity
1. Releive anxiety.2. Physical and emotional rest 3. Anticoagulants, leg exercises, and elastic
stockings.4. Absolute bed rest is rarely required5. Regular isotonic exercise 6. Weight reduction in obese
• Administration of oxygen • Sleep apnoea - nocturnal continuous positive
airway pressure• Dialysis or ultrafiltration in patients with
severe HF and renal dysfunction • Other mechanical methods - theraputic
thoracocentesis or paracentesis . • CORRECTION OF PRECIPITATING FACTORS
Measures for symptom relief
CONTROL OF EXCESSIVE FLUIDDietDiuretics
Thiazide diuretics Loop diuretics Metalazone Potassium sparing diuretics
Role of diuretics
1. Rapid relief of symptoms2. Controls fluid retention3. Appropriate use of diuretics is the key
element in the success of other drugs
DIURETICS• THIAZIDE DIURETICS -useful alone or in combination with
other diuretics • In chronic mild HF• K+ depletion and metabolic alkalosis• Suited only if GFR >50%of normal • METALAZONE• Site of action and potency similar to the thiazides • Effective in the presence of moderate renal failure• Both metolazone and thiazides potentiate intravenous
loop diuretics
FUROSEMIDE, BUMETANIDE, AND TORSEMIDE
• Useful in all forms of HF, particularly in refractory HF and pulmonary edema.
• Effective in patients with hypoalbuminemia, hyponatremia, hypochloremia, and with reductions in glomerular filtration rate
• The action may be potentiated by I.V. administration and by the addition of other diuretics
POTASSIUM-SPARING DIURETICS
• Spironolactone acts by competitive inhibition of aldosterone
• Amiloride and triamterene act directly on the distal tubule/collecting duct.
• Most effective with loop and/or thiazide diuretics.
• Lower dose of spironolactone (25 mg/d), prolong life in patients with advanced HF
Prevention of deterioration of cardiac function or drugs increasing survival
1. Angiotensin converting enzyme (ACE inhibitors)
2. Angiotensin receptor blockers3. Aldosterone blockers4. Beta adrenoceptor blockers
Angiotensin-Converting Enzyme (ACE) Inhibitors
1. Prevention and treatment of HF at almost all stages
2. Slows remodeling . 3. Cardiac output rises4. Pulmonary wedge pressure falls,5. Afterload is reduced with no or only mild
reduction of arterial pressure.6. Signs and symptoms of HF are relieved
1. Enhance exercise performance2. Reduce long-term mortality .3. Major effect of ACE inhibitors is on inhibition
of local (tissue) renin-angiotensin systems.4. ACE inhibitor should be maintained
indefinitely.
ACE Inhibitor in cardiac failure
Name Starting dose Target Enalapril 1.25-2.5 BD 10 BD Captopril 6.25-12.5 TID 25-50 TIdLisinopril 2.5-5 0D 20-35 OD Ramipril 1.25 -2.5 BD 5 BD
ARB
1. Equally effective2. ACE inhibitor intolerance
BETA BLOCKERS
Drug Start Target Carvedilol 3.125 bd 25bdBisoprolol 1.25 od 10 odMetoprolol 12.5 -25 od 200bd• As ADD on therapy with diuretics and ACEI• Improves ejection fraction,exercise tolerance lowers
rate ,dec.myo O2 demand,,reduces arrythmias reverse LVH,prevents sudden deaths
Use of Beta blockers
1. Optimise volume status2. Start at lowest possible dose3. Increase dose gradually4. Monitor vital signs ,wt , clinical profile
Enhancement of Cardiac contractility
1. Digitalis,digoxin oubain2. Sympatho mimetic amines3. Phosphodiesterase inhibitors
When should Digoxin be used
DIGOXIN
1. Positive inotropic response 2. Inhibit Na+, K+-ATPase3. Effective in systolic HF complicated by atrial flutter
and fibrillation and a rapid ventricular rate4. Does not improve survival in patients with systolic
HF and sinus rhythm, it reduces symptoms of HF 5. No value in diastolic HF.
Sympathomimetic Amines
1. Dopamine and dobutamine ,dopexamine2. Act on β-adrenergic receptors3. Improve myocardial contractility 4. In severe, acute HF5. Constant intravenous infusion6. Can be given for several days 7. Used in refractory HF as a “bridge” to cardiac
transplantation.8. “Downregulation” of adrenergic receptors
Phosphodiesterase Inhibitors
1. Amrinone,milrinone,enoximone,piroximone,fenoximone
2. Inhibit phosphodiesterase III 3. Positive inotropic and vasodilator actions 4. Administered intravenously5. Reverse the major hemodynamic
abnormalities associated with HF
Vasodilators
1. Useful in severe, acute HF with significant systemic vasoconstriction despite ACE inhibitor therapy.
2. Rapid onset and brief duration of action 3. Sodium nitroprusside 4. Intravenous nitroglycerin 20micg/min max
400micg/min 5. Nesiritide iv bolus 2micg/kg+0.01micg/kg/min6. Combination of hydralazine and isosorbide dinitrate
- for chronic oral administration
Nesiritide, a recombinant analog of BNP
1. The newest therapeutic option for ADHF.2. Increase natriuresis, diuresis, and cardiac index 3. Reduce pulmonary capillary wedge pressure, pulmonary
artery pressure, pulmonary vascular resistance, and systemic blood pressure in a dose-dependent manner.
4. Reversal of the deleterious neurohormonal response associated,with HF
5. Reduces levels of endothelin 1, aldosterone,and norepinephrine.
• Nesiritide is more effective than nitroglycerin in producing rapid and significant reduction of LV filling pressures
• Does not require ICU admission or invasive monitoring .
• Lower incidence of tachycardia and proarrhythmic effects.
• Lessen the need for supportive therapies such as diuretics
Survival benefit of different drugs
• Those which reduce MORTALITY• Those which Increase MORTALITY• Those without any proved influence on
MORTALITY
Reduce mortality
1. Beta Blockers2. A.C.E. Inhibitors3. Angiotensin Receptor Blockers4. Spironolactone5. Amiodarone
Drugs increasing Mortality
1. Inotropes&Inotropic dilators2. Antiarrythmics except
1. betablockers&Amiodarone3. Calcium Channelblockers4. High dose Digoxin
DiureticsDigoxin(low dose)Nitrate
Those without any proved influence on MORTALITY
Fluid retention +
Assess volume status
Beta blockers
ACE 1Diuretic titrate to euvolemic
No fluid retention
LVEF <40 %
VENTRICULAR RESYNCHRONIZATION
1. Intraventricular conduction is depressed in about one-fourth of patients with chronic HF
2. “Resynchronization” with a device that has three pacing leads (right atrium, right ventricle, and cardiac vein, which provides left ventricular stimulation) improve performance in patients with HF
3. Increase ejection fraction
MANAGEMENT OF ARRHYTHMIAS
1. Premature ventricular contractions and episodes of asymptomatic ventricular tachycardia are common in advanced HF
2. VT/VF is responsible for about one-half of all deaths
3. Correction of electrolyte and acid-base disturbances
Amiodarone
1. Amiodarone, a class III antiarrhythmicis the drug of choice for patients with HF and atrial fibrillation.
2. Implantable automatic defibrillator prevent sudden deaths
Anticoagulants
1. Increased risk of pulmonary emboli secondary to venous thrombosis and of systemic emboli secondary to intracardiac thrombi
2. Patients with HF and atrial fibrillation, previous venous thrombosis, and pulmonary or systemic emboli are at high risk
3. Heparin followed by warfarin
Management of Diastolic HF
1. HTN regression of LVH important ……ARB,ACE2. Myocardial ischemia…….. Bblockers ,CCB,nitrates3. Chronic AF……. restore sinus rythmn,rate control4. Beta blocker…… slow rate ,reduce O2 demand,lower
BP,regress LVH5. CCB has lusiotropic effect (relaxation enhancing effect)6. ACE inh. Effect uncertain ……ARB use regress LVH7. Exercise conditioning….. improves diastolic function
,dynamic isotonic exercise ideal
8. Better Prognosis9. Bad prognosis-Older age ,males ,lower
ej.fraction,ass,CAD,DM,impaired renal function
Management Of ADHF
• Administration of oxygen • Morphine sulfate• Mechanical ventilation is indicated • A sitting position improves pulmonary function.• Placing the patient on strict bed rest and reducing
pain and anxiety decrease cardiac workload.
1. Intravenous inotropes and vasodilators - The combination of an intravenously administered vasodilator such as nitroglycerin, niseritide, or of a phosphodiesterase inhibitor together with a sympathomimetic amine
2. Hemodynamic monitoring cvc,swan ganz catheter,O2 saturation
3. Extracorporeal ultrafiltration and hemofiltration-Acute hemodialysis and ultrafiltration may be effective, especially in the patient with significant renal dysfunction and diuretic resistance ,removes i.v fluid
1. Mechanical circulatory supports 2. Devices
1. Counter pulsation device(Intra aortic baloon pump and non invasive counter pulsation)
2. Cardiopulmonary assist devices3. Left ventricular assist devices
• In hospitalized patients with refractory HF, therapy to be guided by hemodynamic measurements by a balloon flotation (Swan-Ganz) catheter
• The goal is to achieve pulmonary capillary wedge pressure of 15 to 18 mmHg
• Right atrial pressure of 5 to 8 mmHg• Cardiac index >2.2 L/min per m2• Systemic vascular resistance of 800 to 1200 dyne ·
s/cm5.
SURGICAL THERAPY
• CARDIAC TRANSPLANTATION best predictor peak O2 consumption with maximal exercise (VO2max)NI >20ml/kg/min,<10ml/kg/min ……transplantation ideal
• Novel surgeries– Ventricular remodelling surgeries– Dynamic cardiomyoplasty– Mitral valve repair
NEWER Rx MODALITIES FOR ADHF
1. BALOON COUNTER PULSATION – INTRAAORTIC BALOON PUMP
2. VAD – PULSATILE LOW FLOW VAD3. PACING – BIVENTRICULAR PACING , AV
SEQUENTIAL PACING
B N P analogue Nesiritide
Endopeptidase inhibitor(ACE+neutral peptidases) Omapatrilat
NEWER DRUGS
Pimobendan,Levosibendan• LEVOSIBENDAN is a novel agent with inotropic
properties developed specifically for the management of ADHF.
• It acts by sensitizing troponin C to calcium
Calcium Sensitiser
Endothelin receptor antagonist
BOSENTAN
TEZOZENTAN Effective in acute coronary syndromes, acute
renal failure and acute HF.• Indirectly improve contractility while
decreasing pulmonary capillary wedge pressure.
• VASOPRESSIN ANTAGONISTS (V2 RA) Tolvaptan, Lixiraptan ,Coniraptan
– CAN BE USED AS ADJUVANT to DIURETIC IN ADVANCED HF• ENOXIMONE –TYPE 3 PDEI
– PA Pr. MONITORING REQUIRED– LV FILLING PRESSURE > 15 mm Hg– IDEAL INOTROPE FOR PATIENT ON
ß BLOCKERS
PROGNOSIS
1. Depends primarily on the nature of the underlying heart disease
2. Presence or absence of a precipitating factor3. Prognosis can be estimated by observing the
response to treatment.4. When patients can be rendered free of congestion,
survival may be 80% at two years.
1. High BUN (>43 mg/dL) is the best single predictor of inhospital mortality
2. Severely depressed ejection fraction<15%3. Inability to walk on level at normal
pace>3min4. Low SBP (<115 mm Hg) 5. High serum creatinine (SCr) levels (>2.75
mg/dL).6. Elevations in circulating levels of B-type
natriuretic peptide (BNP)7. Cardiac necrosis marker troponin I
When all available therapeutic measures have been exhausted, comfort care, with continued infusions of inotropic agents, diuretics, and the administration of anxiolytics and analgesics should be considered.
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