CONGESTIVE CARDIAC FAILURE Dr.T.Rajathilagam, M.D., S.R.M. Medical College
HEART FUNCTIONS Your heart is an amazing powerhouse that pumps and circulates 5 or 6 gallons of blood each minute through your entire body.
CARDIAC MUSCLE Excitability- depolarisation Contractility-Contraction & relaxation Automaticity- spontaneous electrical impulses
CARDIAC ACTION POTENTIAL Phase 0 (fast upstroke)- rapid depolarisation, sodium channels Phase 1 (partial repolarisation)- efflux of potassium ions Phase 2 (plateau)- slow entry of calcium ions Phase 3 (repolarisation)- efflux of potassium ions Phase 4 (resting phase)
HEART FAILURE Unable to pump sufficient blood to meet the metabolic demands Impaired ability to adequately fill &/or eject blood CONGESTIVE dyspnoea, edema Compensatory mechanisms- Increased sympathetic activity- heart rate & force of contraction, vasoconstriction Activation of RAS- peripheral resistance, sodium & water retention Myocardial hypertrophy
LV Dysfunction causes Decreased cardiac output Decreased Blood Pressure and Decreased Renal perfusion Stimulates the Release of renin, Which allows conversion of Angiotensin to Angiotensin II. Angiotensin II stimulates Aldosterone secretion which causes retention of Na+ and Water, increasing filling pressure
CHRONIC HEART FAILURE : NEUROHORMONAL STATUS SNS RAAS Vasopressin Endothelin-1 DILATATION CONSTRICTION Natriuretic peptides Nitric oxide Vasodilatory PGs Adrenomedullin
CONGESTIVE CARDIAC FAILURE RISK FACTORS Smoking High BP High Cholestrol Obesity Some of the risk factors for heart disease include smoking, high blood pressure, high cholesterol, diabetes, and obesity.
CONGESTIVE CARDIAC FAILURE RISK FACTORS Lack of Exercise Unhealthy Diet Stress TYPE A Personality
PATHOGENESIS OF HEART FAILURE Ischemia Hemodynamic overload Symptoms LV EF LV Remodeling Pump Failure Genetics Inflammation Arrhythmias Asymptomatic Symptomatic
CLINICAL PRESENTATION OF HEART FAILURE Due to excess fluid accumulation: Dyspnea (most sensitive symptom) Edema Hepatic congestion Ascites Orthopnea, Paroxysmal Nocturnal Dyspnea (PND) Due to reduction in cardiac ouput: Fatigue (especially with exertion) Weakness
CONGESTIVE CARDIAC FAILURE - SYMPTOMS Left-Side Heart Failure: Fatigue and shortness of breath (dyspnea) are the first symptoms. They are caused by fluid in the lungs. Fluid retention. Patients may complain of leg or abdominal swelling. Loss of muscle mass. Over time, patients may lose muscle weight due to low cardiac output. Wheezing or cough. Patients may have asthma-like wheezing or a dry hacking cough that occurs a few hours after lying down, but then stops after the patient sits up.
CONGESTIVE CARDIAC FAILURE - SYMPTOMS Right-Side Heart Failure: Fatigue. As with left-side heart failure, an early symptom of right-side (right-ventricular) failure is extreme tiredness.
CONGESTIVE CARDIAC FAILURE - SYMPTOMS Right-Side Heart Failure: Fluid accumulation. This first occurs in the feet, then the ankles and legs, and finally in the abdomen. The liver may also be enlarged. Weight gain. Although appetites are often depressed, patients with heart failure gain weight because they retain salt and water. Loss of muscle mass.
CONGESTIVE CARDIAC FAILURE - SYMPTOMS Besides chest pain (angina) and shortness of breath, some other common symptoms of heart disease include jaw pain, back pain, and heart palpitations
Low output failure- IHD, hypertension, valvular & congenital heart diseases High output failure- anemia, thyrotoxicosis Edema, dyspnoea, hepatomegaly, urine output, fatigue
Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living
THERAPEUTIC GOALS Symptom relief Slow disease progression Improve survival
CONGESTIVE CARDIAC FAILURE - TREATMENT Dietary Changes Lifestyle Changes Exercises Medications
DRUGS TO RELIEVE SYMPTOMS Inotropes- Digoxin, Dobutamine/Dopamine, Amrinone Diuretics- Furosemide, Thiazides Vasodilators- ACEI, ARBs, directly acting Beta blockers- metoprolol, bisoprolol, carvedilol SLOW DISEASE PROGRESSION & IMPROVE SURVIVAL ACEI/ARBs Beta blockers Aldosterone antagonist- Spironolactone
INOTROPES- CARDIAC GLYCOSIDES Digitalis purpura, D.lanata (Foxglove) Increase myocardial contraction & output No increase in oxygen consumption & heart rate Improves cardiac efficiency Digitoxin, Digoxin, Ouabain
CARDIAC MUSCLE CONTRACTION
MECHANISM OF ACTION
HEART ACTIONS Positive inotropy ( force of contraction) Systole is shortened, diastole prolonged cardiac output HR, peripheral resistance, myocardial oxygen demand Electrophysiology- APD, ERP, slow AV conduction
ACTIONS BLOOD VESSELS Reflex sympathetic overactivity is withdrawn peripheral resistance Improved venous tone KIDNEY Diuresis CNS CTZ stimulation Confusion, disorientation, visual disturbances
PHARMACOKINETICS PARAMETERS DIGITOXIN DIGOXIN Oral absorption Very good (90-100%) PPB 95% 25% T1/2 5-7 days 40 hrs. Good (70-90%) Duration of action 2-3 wks 2-6 days Daily maintenance dose 0.05-0.2 mg 0.125-0.5 mg metabolism liver Renal excretion Used for maintenance Routine treatment & emergency
CARDIAC ADVERSE EFFECTS Arrhthymias- p.bigeminus, VES,VT, partial to complete AV block, VF, AES, AF, AFl STOP DIGOXIN Tachyarrhthymias- KCL 20m.mol/hr i.v. or oral Ventricular arrhthymias- Lignocaine i.v. Supraventricular arrhthymias- Propranolol i.v. or oral AV block- Atropine i.m. DIGOXIN ANTIBODY- Fab fragment (DIGIBIND), nonimmunogenic, effective in toxicity
ADVERSE EFFECTS EXTRACARDIAC GIT Anorexia, nausea, vomiting, abd.pain, diarrhoea CNS Fatigue, headache, confusion, restlessness, disorientation, visual disturbances
CONTRAINDICATIONS Hypokalemia Elderly, renal & hepatic disease children MI Thyrotoxicosis Hypothyroidism VT Myocarditis WPW syndrome
CHF THERAPEUTIC USES Low output failure & systolic dysfunction Positive inotropy ( force of contraction) ventricular ejection, improved tissue perfusion, HR Diuresis, edema & dyspnoea relieved Unable to reverse or retard the pathology No effect on remodelling
CURRENT STATUS Slow oral digitalisation Bradycardia Withdraw after compensation restored Low safety margin No alteration of disease progression
THERAPEUTIC USES ARRHYTHMIAS AF AFl PSVT ERP of AV node Reduces ventricular rate
DIURETICS It is an agent which increases urine volume Natriuretic: It causes an in renal Na+ excretion As it also water excretion they are also known as diuretics
CLASSIFICATION HIGH EFFICACY/ LOOP Furosemide, Bumetanide, Torsemide MEDIUM EFFICACY Thiazides WEAK OR ADJUNCTS CA inhibitors- Acetazolamide Potassium sparing- Spironolactone Osmotic- Mannitol
FUROSEMIDE
THIAZIDES
DIURETICS High ceiling diuretics- Furosemide ECF, venous return, PRELOAD Cardiac efficiency improved Edema, pulmonary congestion i.v- Rapid symptom relief Intermittent therapy- mild CCF excretion of H+ & K+ Arrhythmias, digoxin toxicity Thiazides- adjuvant in chronic cases resistant to loop diuretics
VASODILATORS Acute & chronic CHF Venodilators ( preload) Nitrates Arteriolar dilators ( afterload) CCB, hydralazine, minoxidil Mixed dilators ( pre & afterload) ACE inhibitors- Enalapril, Lisinopril ARBs- Losartan, Telmisartan Prazosin PDE III inhibitors
NITRATES ventricular EDP & volume i.v- acute LVF Nitrate tolerance HYDRALAZINE aortic impedance Tachycardia, fluid retention
ACE INHIBITORS/ARBS
ACE INHIBITORS/ARBS preload, afterload RAP, PAP, systemic vascular resistance, BP, HR stroke volume, cardiac output, renal perfusion Retard disease progression & prolongs survival First line therapy REDUCES MORBIDITY & MORTALITY
DIURETICS, ACE INHIBITORS Reduce the number of sacks on the wagon
BETABLOCKERS Carvedilol, metoprolol, bisoprolol Blocks activation of ANS inhibits renin release Prevents arrhythmias Decreases remodelling, hypertrophy & cell death Adjuvant in Mild to moderate CHF No role in decompensated patients Start from low dose & step up
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ALDOSTERONE ANTAGONIST Spironolactone Aldosterone- expands E.C.F, fibrotic changes in myocardium, hypokalemia & hypomagnesemia Moderate to severe CHF Add-on therapy to ACEI & other drugs Retards disease progression & death Low doses 12.5-25mg/d hyperkalemia, gynaecomastia
PDE III INHIBITORS AMRINONE, MILRINONE PDE III- degrades Camp in heart & smooth muscles Camp in myocardium- Direct vasodilation Positive inotropy- influx of Ca INODILATOR Severe & refractory CHF short term i.v.- 5-10µg/kg/min No oral maintenance therapy Thrombocytopenia, liver damage, arrhythmias
SYMPATHOMIMETICS Dobutamine, Dopamine Βeta & dopaminergic agonists Acute CHF No role in long term therapy
STAGE A MANAGEMENT OF HEART FAILURE Risk factors reduction, treat hypertension, DM, dyslipidemia, ACEIs/ARBs STAGE B- ACEIs/ARBs in all patients, beta blockers in selected patients STAGE C- diuretics, ACEIs, beta blockers Aldosterone antagonist, ARBs, hydralazine, digoxin STAGE D- intervention
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