heart failure

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heart failure

  1. 1. HEARTFAILUREPrepared by:•Sohail khan•Rana Rabnawaz•Momina zaib•Sufia yasmeen
  2. 2. INTRODUCTION• Inability of the heart to pump an adequate amount of blood to the body’s needs• CO is inadequate to provide oxygen needed by peripheral tissues
  3. 3. AFTERLOAD AND PRELAOD • Afterload is the tension or stress developed in the wall of the left ventricle during ejection • Preload is the stretch exerted on the muscle in the resting state. (diastolic phase.)
  4. 4. PATHOPHYSIOLOGICAL CAUSES OFFAILURE Increased work load Improper Contraction of muscles Compensatory mechanisms
  5. 5. PATHOPHYSIOLOGY OF CHF
  6. 6. CAUSES OF HEARTFAILURE• Hypertension• Prolonged Alcohol or Drug Addiction• Previous Heart Attack• Chronic Rapid Heart Beats
  7. 7. SYMPTOMS OF HEART FAILURE• Edema of the bronchial mucosa• Pulmonary edema• Cardiomegaly• Edema in other body parts• Tachycardia• Coughing• Dyspnea• Fatigue
  8. 8. Types of heart failure• SYSTOLIC DYSFUNCTION• DIASTOLIC DYSFUNCTION• HIGH OUTPUT FAILURE• ACUTE HEART FAILURE• CHRONIC HEART FAILURE
  9. 9. SYSTOLIC DYSFUNCTION (FORWARDFAILURE)• Inadequate force is generated to eject blood normally• Reduce cardiac output, ejection fraction (< 45%) Typical of acute heart failure• Responsive to inotropics
  10. 10. DIASTOLIC DYSFUNCTION (BACKWARDFAILURE) • Inadequate relaxation to permit normal filling • Hypertrophy and stiffening of myocardium • Cardiac output may be reduced • Ejection fraction is normal • Do not respond optimally to inotropic agents
  11. 11. HIGH OUTPUT FAILURE • Increase demand of the body with insufficient cardiac output • Hyperthyroidism, beri-beri, anemia, AV shunts • Treatment is correction of underlying cause
  12. 12. ACUTE HEART FAILURE • Sudden development of a large myocardial infarction or rupture of a cardiac valve in a patient who previously was entirely well, usually predominant systolic dysfunction
  13. 13. CHRONIC HEART FAILURE • Typically observed in patients with dilated cardiomyopathy or multivalvular heart diseases that develops or progresses slowly
  14. 14. COMPENSATORY MECHANISMS OFBODY DURING HEART FAILURE• Three types of compensatory mechanisms2. Neuronal Responses3. Neuro-endocrinal system4. Autoregulatory systems
  15. 15. Neuronal Responses• Baroreceptors in the vascular system detect decrease in BP• Enhanced sympathetic outflow to the heart and to peripheral vasculature• Individual feeling status will also increase sympathetic system• Results in release of nor adrenaline and catecholamines which increase heart rate and redistribution of blood to vital organs• Kidney will also help by retention of water and electrolytes•
  16. 16. Neuro-endocrinal system• Reduced blood pressure will Stimulate the renin angiotensin system• Reduced blood supply to kidney lead to secretion of renin• Production of angiotensin II• Retention of water and electrolyte• Less oxygen supply to kidney enhances production of erythropoetin which increases RBC’s production
  17. 17. FLOW CHART OF COMPENSATORYMECHANISMS  CARDIAC OUTPUT Heart rate  SYMPATHETIC  BLOOD ACTIVITY PRESSURERedistributiontowards vitalorgans  RENAL BLOOD FLOW  RENIN ANGIOTENSIN II  ALDOSTERONE  SODIUM RETENTION
  18. 18. Autoregulatory systems• Neuronal structures of heart capable of secreting catecholamines due to anoximia• Self stimulation of heart muscle called as catecholamine heart drive• Do not work during congestive heart failure
  19. 19. ATRIAL NATRIURETIC FACTOR• Atrio-peptide• Natriuretic and vasodilatory effect• Atrial muscle detects tachycardia• Releases atrio-peptide• Suppress aldosterone and vasopressin secretion• Suppress compensatory mechanisms
  20. 20. AUTOREGULATORY MECHANISMS  Atrial pressure  Oxygen supply Tachycardia Self Stimulation of heart muscle Atrio-peptide releases Release of catecholamine Relaxation of blood vessels  Heart rate  Compensatory mechanism
  21. 21. STRATEGIES FOR CHF• Increase cardiac contractility• Decrease preload ( left ventricular pressure)• Decrease after load (systemic vascular resistance)• Normalize heart rate and rhythm
  22. 22. REDUCE WORK LOAD OF HEART 1.Adjustment of heart rate(AV and SA nodal blocking agents) 2. Restrict sodium (low salt diet) 3. Give diuretics (removal of retained salt and water) 4. Give angiotensin-converting enzyme inhibitors (decreases afterload and retained salt and water) 5. Give digitalis (positive inotropic effect on depressed heart) 6. Give vasodilators (decreases preload & afterload)
  23. 23. STRATEGIES TO TREAT CHF Factor Mechanism Therapeutic Strategy1. Preload (work or stress increased blood volume -salt restrictionthe heart faces at the end of and increased venous -diuretic therapydiastole) tone--->atrial filling -venodilator drugs2. After load (resistance pressure sympathetic increased - arteriolar vasodilatorsagainst which the heart stimulation & activation of -decreased angiotensin IImust pump) renin-angiotensin system (ACE inhibitors) ---> vascular resistance ---> increased BP3. Contractility decreased myocardial -inotropic drugs (cardiac contractility ---> decreased glycosides) CO4. Heart Rate decreased contractility and decreased stroke volume --- > increased HR (via activation of b adrenoceptors)
  24. 24. CLASSIFICATION OF DRUGS USE TOTRAET CONGESTIVE HEART FAILURE• Drugs improving force of cardiac contractility(postive ionotropic)• Drugs improving compensatory stresses upon the cardiac performance
  25. 25. Drugs improving force of cardiaccontractility(positive ionotropic) • Cardiac glycosides (digoxin,digitoxin) • Phospho-di-estrase inhibitors (Inamrinone) • Beta I agonists(dobutamine)
  26. 26. Drugs improving compensatory stressesupon the cardiac performance• Diuretics(Thaizides)• Vasodilators(diazoxide,minoxidil)• ACE Inhibitors(captopril,inapril)• Angiotensin II receptor inhibitor(losartan,candisartan)• Beta-blockers (atinolol,propranol)
  27. 27. CARDIAC GLYCOSIDES• Stimulates myocardial contractility(+ inotropic)• Improves ventricular emptying• Increase cardiac output• Augments ejection fraction• Promotes diuresis so lowers blood volume.• Reduce cardiac size• Used in acute congestive HF• Not used with diuretics• Reduces pace maker conduction by stimulating vegal nerve
  28. 28. PHOSPHO-DI-ESTRASE ENZYMEINHIBITORS(INAMRINONE,MILRENONE)• Increase CAMP and CGMP levels that activates IP3• These enzymes inhibitors increase cytosolic ca level• Alter intracellular SR calcium• Increase cardiac contractility(positive ionotropic effect)• Cause vasodilatation• Reduce preload• Used in acute or refractory HF
  29. 29. Beta I agonists• Stimulate cardiac muscles for rapid contractility• Increase cardiac output with decrease ventricular filling pressure• Used in last stages when patients is in ICU in proper monitoring• Used to keep alive the patients at last stages
  30. 30. DIURETICS(THIZIDES)• Increase water secretion from kidney• Decrease blood volume• Redude oedema• Decrease venous return(reduce oxygen demand)• Reduce cardiac size• Decrease ventricular pre load• Improve cardiac efficiency• E.g Spironolactone• Aldosterone receptors inhibitors• Aldosterone cause myocardial and vascular fibrosis and baro- receptors dysfunctioning• Beneficial in patients receiving ACE inhibitors
  31. 31. VESODILATORS• Reduce TPR by dilating vessels• Reduce preload and after load• Beneficial in CHF
  32. 32. ACE INHIBITORS• Inhibits ACE• Reduce TPR• Reduce blood volume• Reduce sodium water retention by inhibiting aldosterone• Reduce after load and some how preload• Reduction in sympathetic outflow• Excellent drug for long term remodeling of heart and blood vessels
  33. 33. Angiotensin II receptorinhibitor(losartan,candisartan)• Block AT1 receptors on blood vessels• Reduce vasoconstriction• Reduce preload and after load• Used in patient with angioedema and cough
  34. 34. BETA- BLOCKER(atinolol,propranalol)• Blocks beta I receptors on heart• Relax cardiac muscle by reducing cardiac work• Save from extra heart muscle exercise• Used in long term therapy
  35. 35. CARDIAC GLYCOSIDES• Also called as cardinolides.• In 1875 William Withering wrote a treatise on Digitalis.• It was considered essential in the treatment of CHF.• It is used in chronic CHF. with chronic atrial fabriliation.• It is still extremely favoured drug.
  36. 36. Images of Cardiac Glycosides Digitalis purpurea Digitalis lanata Strophanthus gratus
  37. 37. ADVANTAGES:• It has two main advantages2. It is an inotropic agent ( increases myocardial contractility)3. It can be administered orally.
  38. 38. DISADVANTAGES:• Its therapeutic index is low.• Its correct dose, correct therapeutic blood level ranges are uncertain.• It has many interactions.
  39. 39. CHEMISTRY:• Molecule consisting of2. A CPP ring3. Sugar4. Lactone• CCP ring + Lactone together is called Aglycon
  40. 40. CHEMICAL STRUCTURES OF CARDIACGLYCOSIDES
  41. 41. BIOLOGICAL ORIGIN:• Digitalis purpurea• Digitalis lanata• Stropenthus gratus• Stropenthus kombe• Most popular Cardiac glycoside is Digoxin and Digitoxin
  42. 42. PHARMACOKINETICS OF CARDIACGLYCOSIDES:• Administration• Absorption• Metabolism• Excretion
  43. 43. ADMINISTRATION• It is administered orally
  44. 44. ABSORPTION• Digoxin is less lipid soluble than Digitoxin• Digitoxin completely absorbed after oral administration• Digoxin can be converted to ineffective agent by bacteria of gut flora• Half life of digoxin is 1.5 days• Half life if digitoxin is 5 days
  45. 45. METABOLISM• Therapeutic window of digoxin is narrow• Metabolized by liver microsomal enzymes• Digitoxin is converted to inactive products• Digitoxin is converted into digoxin after hydroxylation of digitoxin• Digoxin level should be measured in patients receiving this drug
  46. 46. THERAPEUTIC INDICATIONS OFDIGITALIS• In chronic CHF with chronic atrial fibrillation• In chronic CHF with sinus rhythm
  47. 47. CONTRAINDICATIONS• Obstructive cardiac myopathy• Diastolic dysfunction of heart• AV nodal block
  48. 48. ADVERSE EFFECTS• Cardiac dysrhythmias• Delayed AV conduction• Heart block ventricular tachycardia• Ventricular fibrillation• Nausea• Vomiting• Anorexia• Headache• Blurring of vision• Mental confusion
  49. 49. FACTORS FACILLATING TOXICITY• Depletion of serum potassium level• Concomitant use of drugs• Presence of renal failure• Hypothyroidism• Old age
  50. 50. PHARMACODYNAMICS OF DRUGSDEALING WITH CHF• Cardiac glycosides (digoxin,digitoxin)• Phospho-di-estrase inhibitors (Inamrinone)• Beta 1 agonists(dobutamine)• Diuretics(Thaizides)• Vasodilators(diazoxide,minoxidil)• ACE Inhibitors(captopril,inapril)• Angiotensin receptor inhibitor(losartan,candisartan)• Beta-blockers (atinolol,propranol)
  51. 51. DRUG INTERACTIONS• Cholestyramine, cholestipol• Quinidine• Beta blocker, verapamil,edrophonium• Erythromycin,omeprazole• Sypathomimetics• Thiazides
  52. 52. CARDIAC GLYCOSIDES• MODE OF ACTION:• Direct Effect on Myocardial contractility, and electrophysiological properties and also has vagomimetic effect• Force of contraction: • Dose dependent increase in force of contraction in failing heart – positive ionotropic effect • Systole is shortened and prolonged diastole • Contracts more forcefully when subjected to increased resistance • Increase in cardiac output – complete emptying of failed and dilated heart• Tone: • Decrease end diastolic size of failing ventricle • Reduction in oxygen consumption
  53. 53. Contd. ---• Rate and Conduction: 1. Bradycardia 2. Slowing of impulse generation (SAN) 3. Delay of conductivity of AVN• Direct depressant action on SA and AV nodes (extravagal)• Increase in vagal tone: • Is due to improvement in circulation • Also due to direct stimulation in vagal center, sensitization of baroreceptors and sensitization of SA node to Ach
  54. 54. Digitalis – mechanism of action
  55. 55. EFFECTS ON HEART• Increases force of myocardial contraction• Heart size• Ejection fraction• Refractory period in AV node and bundle of hiss• Number and irregularity of ventricular contraction
  56. 56. VAGAL EFFECTS• Vagal effects at early stages when there is minimum therapeutic value• Slowed down the activity of pace maker• Relaxation phase• Ejection fraction
  57. 57. PHOSPHODIESTRASE INHIBITORS• Mechanism of Action• inhibition of type III phosphodiesterase  ↑ intracellular cAMP  ↑ activation of protein kinase A o Ca2+ entry through L type Ca channels• ↑ cardiac output• ↓ peripheral vascular resistance
  58. 58. BETA I AGONISTMechanism of Action:Stimulation of cardiac β1−adrenoceptors: ↑inotropy > ↑ chromotropyperipheral vasodilatation
  59. 59. ACE INHIBITORS• Mechanism of Action:• Afterload reduction• Preload reduction• Reduction of facilitation of sympathetic nervous system• Reduction of cardiac hypertrophy
  60. 60. BETA BLOCKERS• Mechanism of Action: • influences in the heart (tachycardia, arrhythmias, remodeling) • Reduction in damaging sympathetic inhibition of renin release
  61. 61. DIURETICS• Mechanism of Action:• Preload reduction: reduction of excess plasma volume and edema fluid• After load reduction: lowered blood pressure• Reduction of facilitation of sympathetic nervous system
  62. 62. VASODILATORS • MODE OF ACTION: • Reduction in preload through venodilatation or reduction in afterload through arteriolar dilation or both
  63. 63. ANY QUESTION

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