Successfully reported this slideshow.

1 drugs acting on cardiovascular system

1,940 views

Published on

Published in: Health & Medicine, Technology
  • Be the first to comment

1 drugs acting on cardiovascular system

  1. 1. Drugs acting on Cardiovascular system
  2. 2. The drugs acting on cardiovascular system are divided into four groups:     Cardiotonic drugs Anti-hypertensive drugs Anti-arrhythmic drugs Anti-anginal drugs
  3. 3. Cardiotonic drugs  Drugs which increase the force of contraction of the heart, are called cardiotonic drugs.  Classification: 1. Cardiac glycosides 3. Anticholinergic drugs – Digoxin – Digitoxin 2. Sympathetic drug -Adrenaline -Dopamine -Isoprenaline -Atropine -Scopolamine 4. Xanthines -Theophylline -Theobromine
  4. 4. Cardiac glycosides • Cardiac glycosides are those glycosides which have specific action to the failing heart. • Increase the force of contraction of failing heart and lower the heart rate and thereby maintain an effective circulation. • Classification of cardiac glycosides: Natural A). Plant source – From leaves of foxgloves: • Digitalis purpurea: Digoxin, Digitoxin • Digitalis lanata: Digoxin, Lanatoside-C
  5. 5. – From the seeds of foxgloves: • Strophanthus kombe: Cymarin, Cymarol • Strophanthus gratus: Ouabain squill B) Animal source: Toad venom: Bufotoxin Synthetic: -Digitoxigenin -Digoxigenin -Gitoxigenin
  6. 6. Digitalis • Digitalis is a powerful inhibitor of Na+/K+ ATPase. As a result they increase the efficiency of failing heart increasing Na+ concentration within cell membrane;which enhances Ca++ availability to the contractile apparatus and increase the contractility.
  7. 7. Mechanism of action: • It alters ion transport system by inhibiting membrane bound enzyme Na+/K+ ATPase, which is associated with Na+ pump. So – It decreases active transport of Na+ out of the cell increasing intracellular Na+ concentration; this in turn decreases Ca++ transport out of cell. – Release of stored Ca++ from the sarcoplasmic reticulum increases. – Permeability of Ca++ increases. The net effect is increased intracellular Ca++ ions which increases the force of contraction of the cardiac muscles.
  8. 8. • Pharmacological actions:  Cardiac effects: On normal heart – Direct positive inotropic action – Decrease heart rate so decrease cardiac output – Increase systolic and mean systemic arterial pressure due to direct arteriolar contraction – Decrease central venous pressure On failing heart – Direct action: Positive inotropic action – Indirect action: decrease sinus rate, so decrease heart rate
  9. 9. • Extra-cardiac effects: 1. Kidneys: – Diuresis(due to increase renal perfusion) – oedema(due to aldosterone antagonism) 2. Eye: Xanthopsia (appearance of yellow-green tings cause visual disturbance 3. CNS: paraesthesia, toxic psychosis 4. Blood vessels: vasoconstriction, venodilation 5. GIT: anorexia, nausea, vomiting 6. Gynaecomastia (due to prolonged use)
  10. 10. Indications of Digitalis: 1. Congestive heart failure due to ischemia, hypertensive or valvular heart disease. 2. Atrial fibrillation 3. Atrial flutter 4. Paroxysmal supraventricular tachycardia 5. Left ventricular failure
  11. 11. Contraindications – Digitalis toxicity – CVS • Recent myocardial infarction • Heart block • Arrhythmia – renal impairment – Hepatic failure – Electrolyte imbalance specially hypokalaemia and hypocalcaemia
  12. 12. • Digitalisation: Subjection of a patient to the action of digitalis is called digitalisation. • Cautions: – Therapeutic index of digitalis is low ( therapeutic dose is very near to toxic dose) – The dose of digitalis should be individualized. – Danger signs of digitalis toxicity after initial dose are: nausea, vomiting, sinus bradycardia (HR<60beats per min)
  13. 13. • Digitalisation is done by three ways: 1. Emergency digitalisation 2. Rapid digitalisation 3. Slow digitalisation  Total digitalisation dose (TDD): It is the initial loading dose of digoxin. -Oral route: 0.75-1.25mg -i/v route: 0.5-1mg
  14. 14. • Maintenance dose: Oral route: 0.125-0.5mg i/v route: 0.25mg
  15. 15. Anti-hypertensive drugs • Hypertension: Persistent rise of blood pressure above the upper limit of normal level according to the age and sex of the individual is called HYPERTENSION (HTN) • Normal limits of blood pressure: – Systolic: 100-140 mm Hg(120±20) – Diastolic: 60-90 mm Hg (75±15)
  16. 16.  Causes of hypertension: • Primary hypertension (90-95%): – also called as essential hypertension – Unknown etiology or idiopathic • Secondary hypertension(5-10%): – Renal disease – Endocrine diseases (Conn’s disease, acromegaly, Phaeochromocytoma) – Cushing's disease – Vascular causes (renal artery stenosis, coarctation of aorta) – Drugs (sympathomimetics, NSAIDs, contraceptive pills, steroids
  17. 17. • Risk factors: – – – – Age Hereditary Anxiety Obesity and lack of exercise – Alcohol consumption – Salt intake • Special patient groups – – – – – – – Race Elderly Diabetes Renal disease Stroke Pregnancy Hormone replacement therapy – Oral contraceptives
  18. 18. Management of hypertension Non-pharmacologic approaches:  Weight reduction in obese patients: reduces about 2.5/1.5 mm Hg per kg wt. lost  Restriction to salt intake: not more than 6 g NaCl  Dietary considerations: legumes, fresh fruits and vegetables, whole grains  Regular exercise  Restricted alcohol intake  Smoking cessation to reduce cardiovascular risk
  19. 19.  Pharmacologic approach:  Classification: A. Diuretics: – – – – – B. Carbonic anhydrase inhibitors : acetazolamide Loop diuretics: Furosemide, ethacrynic acid , mercurials Thiazide diuretics: Hydrochlorthiazide Potassium sparing: amiloride , triamterene, spironolactone Osmotic diuretics : mannitol Sympatholytics: – – – – Centrally acting: Methyl-dopa, Clonidine Beta-blockers: Atenolol, Propranolol, Metoprolol Alpha-blockers: Prazosin, Phentolamine Adrenergic neuron blockers: Guanethidine, Reserpine
  20. 20. C. Direct vasodilators: • Arteriolar dilators • • • • • Diazoxide Hydralazine Minoxidil Prazosin Vasodilators (non-selective) • • Nitroprusside Prazosin
  21. 21. D. Calcium Channel blockers: – Nifedipine – Verapamil – Diltiazem E. Angitensin converting enzyme (ACE) inhibitors: – – – – Captopril Enalapril Lisinopril Ramipril
  22. 22. α-Methyl dopa • It is useful in treatment of mild to moderately severe hypertension. • It reduces the BP chiefly by reducing peripheral vascular resistance. • It inhibits noradrenaline synthesis: DOPA Dopamine DOPA decarboxylase α-methyl dopa methyldopamine α methylnoradrenaline • Remains inside the vesicles and released in the same way as noradrenaline.
  23. 23. Mechanism of Action • α-Methyl dopa forms false neurotransmitter α-Methyl noradrenaline which combines with α-adrenoceptors present in the surface of the lower brain stem, inhibiting the neurons of nucleus of tractus solitarius of vagus which in turn decrease central and peripheral sympathetic activities resulting in decreased BP. • It also inhibits the decarboxylation of DOPA and 5-HT, thus decreased sympathetic tone. • It also directly reduces renin activity which is responsible for conversion of angiotensin-I to angiotensin-II thereby reducing BP.
  24. 24. • Pharmacokinetics: – – – – – Well absorbed from the GIT Half-life: 1.5 hrs Antihypertensive effects; 4-6 hrs Effective twice daily Dose: 1-2 g in divided doses • Indications: – – – – Moderate to severe hypertension Hypertensive crisis Pheochromocytoma Malignant carcinoid
  25. 25. • Adverse effects: – – – – – – – – – – Mental symptoms (sedation, lassitude, vertigo) Electrolyte imbalance Thrombocytopenia Headache Psychic depression Lactation Dryness of mouth Oedema Postural hypotension Allergic reaction
  26. 26. Unique side effects: • Flushing of skin • Failure of ejaculation • Depression • Hemolytic anemia • Granulocytopenia • Hepatic disturbance
  27. 27. Clonidine • It is centrally acting sympatholytic agent (α2 adrenoceptor agonist) and acts by decreasing central sympathetic activity. • Mechanism of action: It combines with α2 – receptors of lower brainstem which in turn inhibits release of noradrenaline from the neurons. It decreases sympathetic activity which results in decreased cardiac output due to decrease heart rate and relaxation of capacitance vessels. Thus BP is decreased.
  28. 28. Pharmacological actions of Clonidine: 1. CNS: suppress sympathetic outflow 2. CVS: decrease heart rate; decrease CO 3. Blood vessels: reduction in resistance and relaxation of capacitance vessels Indications: 1. Hypertension 2. Prophylaxis of migraine 3. Diagnosis of pheochromocytoma
  29. 29. • Adverse effects: – Sedation – Dry mouth – Drowsiness – Rebound hypertension
  30. 30. • Pharmacokinetics of Clonidine: – – – – Bioavailability: 75% Half-life : 8-12 hours Excretion: half of the drug excreted unchanged Dose: 0.2 and 1.2 mg/day • Sudden withdrawal effects: It can result in life threatening crisis. Patient exhibit nervousness, tachycardia, headache and sweating if one or two dose is omitted. Note: sudden withdrawal of the drug must be avoided. If required should be done gradually.
  31. 31. Calcium channel blockers • Calcium is the chief ion required for – Cardiac contraction – Smooth muscle contraction – Propagation of cardiac impulse • Classification of Ca++ channel blockers 1. Dihydropyridine family: – – – – – Nifedipine Nicardipine Nisoldipine Amlodipine isradipine
  32. 32. 2. Miscellaneous: – Verapamil – Deltiazem – Bepridil • General pharmacokinetics for Ca++ channel blockers – – – – Orally administered Highly protein bound Hepatic first pass metabolism Renal excretion
  33. 33. • Mechanism of action: Calcium channel blockers bind with voltage dependent Ca++ channel (L-type) in depolarised membrane. The resultant effect is relaxation of the smooth muscles and negative ionotropic and chronotropic action in the heart.
  34. 34. • Pharmacological action of Calcium channel blockers 1. CVS: 1. 2. 3. 4. • Dilates main coronary vessels: improves myocardial perfusion Negative chronotropic effect: cardiac slowing and AV block Negative ionotropic effect: decrease force of contraction Vasodilation: decrease total peripheral resistance Smooth muscles Smooth muscles: 1. 2. 3. Vascular smooth muscle: generalized relaxation Coronary vasodilation: antianginal action Visceral smooth muscle: relaxation of biliary tract; uterus and bladder.
  35. 35. • Indications: 1. 2. 3. 4. Angina pectoris (variant) Hypertension Cardiac arrhythmias Prevention of ischemic neurological damage due to subarachnoid damage 5. Raynaud’s disease 6. Migraine 7. Premature labour
  36. 36. • Contraindication: – Heart failure – Bradycardia – Second or third degree AV block – Sick sinus syndrome – Wolf Parkinson-White syndrome
  37. 37. • Adverse effects: • Due to vasodilation: – Postural hypotension, reflex tachycardia – Bradycardia, palpitation – Headache, flushing, dizziness, ankle edema • Gastrointestinal – Constipation – Nausea, vomiting – Gum hypertrophy
  38. 38. ACE-Inhibitors • Angiotensin converting enzyme (ACE) inhibitors are : – – – – Captopril Enalapril Lisinopril Ramipril • ACE inhibitors act by inhibiting the conversion of angiotensin I to angiotensin II; which is a powerful vasoconstrictor. It acts preferably on angiotensin sensitive vascular bed of kidney, brain and brain.
  39. 39. Mechanism of Action • It inhibits the conversion of angiotensin I to angiotensin II, thus vasoconstrcitive action of angiotensin II is inhibited. • Also ACE causes inactivation of bradykinin (vasodilator peptides) but in presence of ACE inhibitors bradykinin is active and causes vasodilation which in turn decrease TPR and finally BP.
  40. 40. Pharmacological actions 1. Vasodilation (reduction of TPR) 2. Reduce preload and afterload 3. Reduction in the secretion of aldosterone so decreased salt and water retention. 4. Increase in renal blood flow.
  41. 41. Indications • Hypertension • • • • Renovascular hypertension due to excess renin Malignant hypertension Hypertensive crisis of scleroderma End stage renal disease • Refractory heart failure • Ischemic heart disease
  42. 42. Adverse effects • • • • • • • • • • First dose hypotension Dry cough Angioneurotic oedema Hyperkalaemia Loss of appetite Stomatitis Abdominal pain Neutropenia Proteinuria Blood disorders
  43. 43. Contraindications • • • • Systolic blood pressure < mm Hg Bilateral renal artery stenosis Second and third trimester of pregnancy Renal failure
  44. 44. Angiotension receptor blockers • These are the agents that act on the angiotensin type I (AT1) receptor. • Drugs: – Losartan – Valsartan – Candesartan – Eprosartan – Irbesartan – Telmisartan
  45. 45. • Unique features of ARBs from ACE-inhibitors: – These agents are unique from ACE –inhibitors in that they don’t have effect on bradykinin. – They cause more complete inhibition of angiotensin action because besides ACE other enzymes are present which can angiotensin II.
  46. 46. Losartan: Mechanism of action: It causes antagonism in the angiotensin receptor thus causing a complete blockade of angiotensin II activity. Pharmacokinetics: – Orally administered – Extensively metabolized; metabolites retain activity – Plasma half-life: 2 hrs – Dose: 50 mg/d; can range from 25-100 mg/d
  47. 47. • Indications: – Hypertension • Adverse effects: similar to ACE-inhibitors except that no angioedema and cough is present; both of which are mediated via bradykinin. • Contraindications: – pregnancy
  48. 48. • Saralasin is an analog and competitive inhibitor of angiotensin II at its receptors. • It also blocks the pressor and aldosterone releasing effect of infused angiotensin II and reduce blood pressure in high renin activity state such as renal artery stenosis. • It has been withdrawn from market due to its unpredictable pharmacological outcomes.
  49. 49. Vasodilators • Drugs: 1. Oral vasodilators: • • Hydralazine Minoxidil 2. Parenteral vasodilators: • • • Nitroprusside Diazoxide Fenoldopam • Mechanism of action : This class of compounds cause the dilation of arteries or both arteries and veins; thus reducing overall peripheral resistance and in turn decreases the blood pressure.
  50. 50. • Hydralazine: – It is a hydrazine derivative and is known to dilate arterioles only but not veins. – It causes tachyphylaxis to hypertensive effects developed rapidly. – It can be used in combination. • Pharmacokinetics: – – – – – Orally administered Extensive 1st pass metabolism Low bioavailability Half-life 2-4hrs Dose: 40-200mg/day.
  51. 51. • Adverse effects: – Headache – Nausea – Anorexia – Palpitations – Seating – Flushing – Systemic lupus erythrematosus (SLE)
  52. 52. • Minoxidil – Orally active; half life-4hrs; 5-10mg/d in two doses – Vasodilation results due to opening of K+ ions which brings the membrane to hyperpolarized state, producing relaxation. – It also dilates arterioles but not veins. – Headache, sweating and hypertrichosis, tachycardia and angina and edema are side effects
  53. 53. • Fenoldopam: • It is indicated for severe hypertension and postoperative hypertension. • Acts as Dopamine (D1 receptors) agonist resulting dilation of peripheral ateries. • Given parenterally (i.v. infusion); extensively metabolized and very short half-life of 5 mins. • Very small dose of 0.025-0.05µg/kg/min.
  54. 54. Individualised care approach Calcium channel blockers : Suited for : 1) Elderly 2) Isolated systolic hypertension 3) Asthma/COPD patients 4) Raynauds disease/ migraine 5) Pregnant hypertensive Avoid in : 1) CHF 2) Conduction defects 3) Patients receiving beta blockers 4) IHD/ post MI 5) Left ventricular hypertrophy 6) Males with enlarged prostate 7) GERD
  55. 55. ACE Inhibitors • Suited for : 1) High renin cases or those on low salt 2) Physically active 3) Diabetics/ with nephropathy 4) Co existing angina / post MI cases 5) Coexisting Left ventricular failure / left ventricular hypertrophy 6) Gout/PVD?Dyslipidemic patients • Avoided in : 1) Bilateral renal artery stenosis 2) Pregnancy 3) Hyperkalemia 4) Pre existing dry cough
  56. 56. Beta adrenergic blockers • Suited for : 1) Angina or post MI cases 2) Coexisting anxiety or techycardia 3) Non obese high renin hypertensive 4) Pregnancy • Avoided in : 1) CHF 2) Bradycardia , conduction defects 3) Asthma / PVD 4) Diabetic or borderline glucose tolerance 5) Abnormal lipid profile 6) Patient to remain physically active
  57. 57. Diuretics : • Suited for : 1) Elderly patients 2) Low renin hypertensive 3) Isolated systolic hyeprtension 4) Obese with volume overload 5) Renal disease with salt retention 6) Low cost therapy • 1) 2) 3) 4) 5) Avoided in : Young active hypertensive Diabetes Gout Abnormal lipid profile Pregnancy induce hypertension
  58. 58. Combination therapy 1) Drugs increasing renin activity ( diuretics . Vasodilators , CCBs, ACE inhibtors ) with drugs having low renin activity ( beta blockers , clonidine , methyl dopa ) 2) Drugs causing fluid retention( adrenergic blockers except beta blockers ) with diuretics 3) Drugs causing tachycardia ( hydralazine , DHPs) with non selective beta blockers 4) ACE inhibitors / AT1 blockers with diuretics 5) CCB with diuretics 6) Beta blocker + prazosin
  59. 59. • Combinations to be avoided : 1) Adrenergic blocker with clonidine 2) Hydralazine with prazosin 3) Verapamil/diltiazem with beta blocker 4) Methyl dopa + clonidine
  60. 60. Hypertension in pregnancy Suitable drugs 1) Methyl dopa 2) Hydralazine 3) Dihydropyridine CCBs 4) Cardioselective adrenergic blockers ( atenolol, pindolol, acebutolol) 5) Prazosin 6) Clonidine Drugs to be avoided 1) Diuretics 2) ACE inhibitors 3) Reserpine 4) Non selective beta blockers 5) Sod nitroprusside
  61. 61. ABCD method of drug sequencing Younger and non black • Step 1 : A Older and black • Step 1: C or D • Step 2: A+ c or D • Step 3 : A+C+ D • Step 4 : Add alpha blocker or spironolactone or Beta blocker
  62. 62. Diabetes • First line therapy : Type 1 : monotherapy :ACE inhibitors / AT1 blockers Combination : + beta blockers / CCBs / thiazides/ alpha blockers Type 2 : ACE inhibitors / AT1 blockers / CCBs
  63. 63. Renal disease • ACE inhibitors • Thiazide diuretics not used in severe renal impairment, instead loop diuretics are used
  64. 64. Anti-anginal drugs • Angina pectoris – It is a clinical syndrome characterized by pre-cardiac pain or discomfort due to myocardial ischemia, which is precipitated by exercise and relief by rest or sublingual nitro-glycerine. – It occurs when coronary blood flow is insufficient to meet the metabolic requirement of the heart muscle. – Myocardial oxygen demand mainly depends on • Preload, • After load and • Heart rate
  65. 65. • atherosclerotic angina, classic angina(angina of effort) • vasospastic or variant angina(Prinzmetal's angina) • Unstable angina
  66. 66. Determinants of Myocardial Oxygen Consumption. • • • • • • Wall stress Intraventricular pressure Ventricular radius (volume) Wall thickness Heart rate Contractility
  67. 67. Regulation of smooth muscle contraction and relaxation 1) Increasing cGMP: dephosphorylation of myosin light chains, nitric oxide 2) Decreasing intracellular Ca2+: 3) Stabilizing or preventing depolarization of the vascular smooth muscle cell membrane: increase the permeability of K+ channels, 4) Increasing cAMP in vascular smooth muscle cells: cAMP increases the rate of inactivation of myosin light chain kinase
  68. 68. • Drugs: Organic nitrites and nitrates: – Nitrites: sodium nitrite, amy-nitrite, octyl-nitrite – Nitrates: glyceryl trinitrate, isosorbide dinitrate and isosorbide mononitrate Calcium channel blockers: – Nifedipine – Verapamil – deltiazem
  69. 69. Beta-adrenoceptor blockers – Atenolol – Propranolol – Oxaprenolol Xanthines: – Theophylline – Aminophylline Miscellaneous – Dipyradimol
  70. 70. Drugs or Drug Groups under Investigation for Use in Angina. • • • • • • • • • Metabolic modulators:eg, ranolazine Direct bradycardic agents, eg, ivabradine Potassium channel activators, eg, nicorandil Rho-kinase inhibitors, eg, fasudil Sulfonylureas:eg, glibenclamide Thiazolidinediones/glitazones Nitric oxide donors: eg, L-arginine Capsaicin Amiloride
  71. 71. Organic nitrates • • • • • • • Pharmacokinetics of organic nitrates: Glyceryl trinitrate is a short-acting Undergoes 1st pass metabolism if given orally Given sublingually usually 500mg tab/day Onset of action within 15-30 mins Duration:20-30mins Used mainly in acute attack.
  72. 72. • Isosorbide di-and mono-nitrates are long acting • Orally given • Systemic availability more than GTN • Used in prophylaxis.
  73. 73. Mechanism of action: Organic nitrates act by relaxing smooth muscles of blood vessels. It occurs in following steps: 1. Denitration of org. nitrates ( org nitrates into inorganic) 2. Inorganic nitrates converted to NO (like EDRF) 3. Activation of guanylyl cyclase i.e. raised cGMP 4. Reduces intracellular Calcium concentration 5. Relaxation of vascular smooth muscles
  74. 74. • Pharmaclogical actions: • CVS: – Reduces preload (due to venodilation) – Reduces afterload (due to generalized vasodilation) – Dilates coronary arteries and increase blood flow to ischemic areas • Others: – Relaxation of bronchial smooth muscle – Relaxation of GIT smooth muscle i.e. decreased motility – Relaxation of smooth muscle of biliary tract, urethra and uterus.
  75. 75. • Indications: – Angina pectoris – Congestive heart failure – Myocardial infarction • Adverse effects: – – – – – Flushing of face Throbbing headache Postural hypotension Syncope Nitrate tolerance
  76. 76. • Contraindication: – Organic nitrate intolerence – Angina due to severe anemia – High intra-cranial pressure – Glaucoma – Migraine
  77. 77. • Nitrate tolerance: • During long term use , the nitrate effects is gradually lowered and finally resulting in partial or complete loss of its benefit. • Mechanism is reduced production of cGMP in vascular smooth muscles. • Nitrate free period of 1-2 hours every 24 hrs helps prevent development of tachyphylaxis.
  78. 78. Anti-arrhythmic drugs • Cardiac arrhythmias: The disorder in rate and rhythm of cardiac contraction due to myocardial damage is known as cardiac arrhythmias. • Cardiac arrhythmias consist of cardiac depolarizations that deviate form the normal in one or more aspects; – Abnormality at site of origin of impulse – Its rate and regularity – Its conduction
  79. 79. • Vaughan Williams classification Class-I: Na+ channel blocker Group A:  Quinidine  Procainamide  Disopyramide Pharmacological actions: – Membrane stabilizing action – Prolongs refractory period – Prolongs action potential
  80. 80. Group B:  Lidocaine  Mexiletine  Tocainide  Phenytoin Membrane stabilizing action Shortens refractory period Shortens action potential
  81. 81. Group C:  Flecainide  Encanide Membrane stabilizing action No effect on action potential
  82. 82. Class-II drugs: β-blockers (counteracts catecholamines)  Propranolol  Atenolol  Metoprolol  Sotalol Abolish SA firing Decrease contractility Increase AV refractoriness
  83. 83. Class-III drugs: Repolarization prolonging  Amidarone  Bretylium Prolongs refractory period Prolongs action potential Prevents re-entry rhythm
  84. 84. Class-IV drugs: Calcium channel blockers  Verapamil  Deltiazem Inhibits slow Calcium channels Depress contractility of AV node.
  85. 85. Quinidine • It is a class-I anti-arrhythmic drug. It is an optical isomer of quinine (anti-malarial drug). Pharmacokinetics: – Orally active; i.v. in emergency; i.m. painful – 80% bound to plasma proteins – Half-life: 4-6 hrs – Metabolized by liver (75%) – Excretion: unchanged fraction by kidney
  86. 86. Pharmacological actions of quinidine: – Cardiac tissue: • • • • • Reduce automaticity Reduce excitability Reduce conductivity Prolong refractory period Reflex tachycardia – Other action: • Anti-malarial • Anti-pyretic • Decrease B.P (vasodilation)
  87. 87. • Adverse effects: – – – – – – – – – – Heart block Sinus arrest Myocardial depression Q-T prolongation Ventricular fibrillation Nausea Vomiting Diarrhoea Rash Oedema
  88. 88. • Indications: • As anti-arrhythmic used in, – – – – – Atrial fibrillation and flutter Ventricular fibrillation and flutter Paroxysmal supra-ventricular tachycardia Premature supra-ventricular tachycardia Atrial, nodal and ventricular premature beats • Also as anti-malarial • Anti-pyretic • During digitalis therapy
  89. 89. • Cinchonism: – Headache, vertigo – Blurred vision – Tinnitus • Contraindications: – – – – – Quinidine intolerance Digitalis intoxication Heart failure Hypotension hypokalemia
  90. 90. • Propranolol as anti-arrhythmic drug: – It blocks β-receptors in heart, thereby exerts • • • • Negative inotropic effect Negative chronotropic effect Depress atrioventricular conduction Depresses automaticity – It has: • Anti-arrhythmic effect • Anti-hypertensive effect • Anti-anginal-effect in CVS.
  91. 91. Lidgnocaine • It is a local-anesthetic agent. • Can terminate arrhythmia if quinidine fails • Parenteral administration: i.v./i.m Indications: – As local anesthetic – As anti-arrhythmic
  92. 92. • Mechanism of anti-arrhythmic effect of lignocaine: – It has membrane stabilizing effect by blocking both activated and inactivated sodium channels; which in turn supresses SA node and also ectopic beats. – Shortens refractory period and action potential; make uniform rhythm
  93. 93. • Adverse effects: – Bradycardia – Hypotension – Dizziness – Blurred vision – Sleepiness – Confusion – Convulsion

×