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Class ccf

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Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.
1
Impaired cardiac pumping such that heart is
unable to pump adequate amount of blood to
meet metabolic needs
Not a disease ...
Pulmonary edema
Agitation
Pale or cyanotic
Cold, clammy skin
Severe dyspnea
Tachypnea
Pink, frothy sputum
Fatigue
Dyspnea
...

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Class ccf

  1. 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
  2. 2. Impaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needs Not a disease but a “syndrome” associated with long-standing HTN and CAD
  3. 3. Pulmonary edema Agitation Pale or cyanotic Cold, clammy skin Severe dyspnea Tachypnea Pink, frothy sputum Fatigue Dyspnea Paroxysmal nocturnal dyspnea (PND) Tachycardia Edema – (lung, liver, abdomen, legs) Nocturia
  4. 4. Coronary Artery Disease -CAD Age Smoking HTN Obesity Heart valve disease Diabetes mellitus Cardiomyopathy-dialated, Hypertropic, restrictive
  5. 5. Chronic Acute CAD Hypertensive HD Rheumatic Heart Dis Congenital Heart Dis Cor pulmonale Cardiomyopathy Anemia Bacterial endocarditis Valvular disorders Acute MI Dysrhythmias Pulmonary emboli Thyrotixicosis Hypertensive crisis Rupture of papillary muscle VSD Myocarditis
  6. 6. Cardiac Output Preload Afterload Contractility Heart Rate StrokeVolume= X
  7. 7. Pathologic remodeling Low ejection fraction Death Symptoms: Dyspnea Fatigue Edema Chronic heart failure •Neurohormonal stimulation •Myocardial toxicity Sudden Death Pump failure Coronary artery disease Hypertension Cardiomyopathy Valvular disease Myocardial injury Diabetes
  8. 8. Renin + Angiotensinogen Angiotensin I Angiotensin II Peripheral Vasoconstriction  Afterload  Cardiac Output Heart Failure  Cardiac Workload  Preload  Plasma Volume Salt & Water Retention Edema Aldosterone Secretion ACE Kaliuresis Beta Stimulation • CO • Na+ Fibrosis
  9. 9. Vasoconstric on: ↑’s the resistance against which heart has to pump (i.e., ↑’s a erload), and may therefore ↓ CO Na and water reten on: ↑’s fluid volume, which ↑’s preload. If too much “stretch” (d/t too much fluid) → ↓ strength of contrac on and ↓’s CO Excessive tachycardia → ↓’d diastolic filling me → ↓’d ventricular filling → ↓’d SV and CO
  10. 10. ACC/AHA HF Stage NYHA Functional Class A At high risk for heart failure but without structural heart disease or symptoms of heart failure (eg, patients with hypertension or coronary artery disease) B Structural heart disease but without symptoms of heart failure C Structural heart disease with prior or current symptoms of heart failure D Refractory heart failure requiring specialized interventions I Asymptomatic II Symptomatic with moderate exertion IV Symptomatic at rest III Symptomatic with minimal exertion None
  11. 11. Relief from congestion Ionotropic drugs-DIGOXIN, DOBUTAMINE, DOPAMINE AMRINONE, MIRINONE Diuretics- FUROSEMIDE, THIAZIDES RAS inhibitors-ACE INHIBITORS/ ARBs- ENALAPRIL, VALSARTAN Vasodialators- HYDRALAZINE, NITRATE, NITROPRUSSIDE Beta blockers-METARPOLOL, BISOPROLOL, CARVEDILOL NEBIVOLOL Reversal of progression ACE inhibitors, ARBs, Beta blockers, spironolactone, eplerenone
  12. 12. D ig ita lis p u rp u re a (F o x g lo v e ) W . W ith e rin g (1 7 8 5 ) F ra n c e , U K N a tiv e lle (1 8 6 9 ) •D ig ito x in
  13. 13. Inhibits NaK/ATPase pump Contractility increases as intracellular Ca, Na increases and loss of intracellular K+ • Positive inotropic effect- increases force of contraction without increasing of oxygen consumption • Positive bathmotropic effect-Modifying degree of excitability • Negative chronotropic effect-rate of heart is decreased • Negative dromotropic effect-conduction speed of AV node • CGs are effective in CHF, occurring with normal or accelerated heart rhythm, especially in cases of atrial fibrillation
  14. 14. ARs: bradycardia, AV block, Extra-systoles arrhythmias, accumulation and intoxication. Digoxin toxicity- renal insufficiency, ischemia, hypokalemia calcium channel blockers, beta blockers, cyclosporine and furosemide Normal levels- 0.5-2ng/ml Treatment of toxicity-charcoal. Correct potassium, calcium IV, DIGIBIND antibodies
  15. 15. Preparations of Digitalis (foxglove) Digitoxin (t1/2 168 h) Digoxin (t1/2 40 h): p.o. or i.v. Semisynthetic derivatives of Digoxin – Acetyldigoxin (Lanatilin): p.o. – Methyldigoxin (Lanitop): p.o. Preparations of Strophanthus gratus – Strophanthin G (Ouabain) – i.v.
  16. 16. ATP 3’,5’-AMP AC PDE III Amrinone Enoximone Milrinone (–) cAMP Amrinone, Enoximone, Milrinone These agents are indicated in severe congestive AHF, resistant to other drugs; usually for short i.v. treatment. They have positive inotropic effect, but they increase oxygen consumption. ARs: ventricular and SV arrhythmias, angina, hypotension, headache, hypokalemia.
  17. 17. In AHF with cardiogenic shock Dobutamine (β1-agonist) and Dopamine are administered by i.v. infusion. In high doses dopamine may increase peripheral vascular resistance, while dobutamine does not influence it. Dopamine in low doses activates D2-receptors in renal and mesenterial vessels and in coronaries. It causes arterial vasodilation, activates D5-receptors in myocardium and increases myocardial contractility. Used in low doses (2 to 5 mcg/kg/min i.v.) dopamine does not increase blood pressure. In high doses (> 5 mcg/kg/min i.v.) its α- and β-effects dominate.
  18. 18. They increase salt and water loss, reduce blood volume and lower excessive venous filling pressure, reduce circulating blood volume and preload. The congestive features of oedema, in the lungs and periphery, are alleviated, cardiac output is also increased. Diuretics are administered together with ACE inhibitors and other drugs.
  19. 19. RENAL TUBULAR INTERSTITIUM LUMEN Na+ K+ Cl- TPC Na+ H+ Na+ K+ PARACELLULAR DIFFUSION Na+ K+ Mg++ Ca++ Cl- +8 mV
  20. 20. RENAL TUBULAR INTERSTITIUM LUMEN Na+ K+ Cl- TPC Na+ H+ Na+ K+ PARACELLULAR DIFFUSION Na+ K+ Mg++ Ca++ Cl- +8 mV THICK ASCENDING LOOP LOOP DIURETICS
  21. 21.  Early DCT  Late DCT Na+ Cl- LUMEN K+ Na+ Cl- THIAZIDES
  22. 22. Spironolactone is a weak diuretic. In cases of severe heart failure low doses of Spironolactone are added to the therapy while regularly checking creatinine and electrolyte levels. It blocks aldosterone receptors in the distal renal tubules and reduces increased aldosterone levels in CHF.
  23. 23. In low doses (25 mg/24 h) Spironolactone potentiates the effects of ACE inhibitors. It also saves K+ and Mg2+ and has antiarrhythmic activity. Spironolactone prevents myocardial fibrosis, caused by aldosterone, and in this way increases myocardial contractility. Similar to spironolactone is another aldosterone antagonist – Eplerenone.
  24. 24. ACE inhibitors reduce pre- and afterload. They are administered in lower doses alone or together with diuretics, cardiac glycoside, antiischemic agents in all stages of CHF, due to systolic dysfunction. In preparations with t1/2 ≥ 24 h (Perindopril, Ramipril) the risk of lowering blood pressure after the first dose is avoided.
  25. 25. Vasoconstriction Art+venous Na+ & water retention (Adrenal cortex) Kidney Increased Blood Vol. Rise in BP Increased veonous return, EDV
  26. 26. Competitive antagonist and inverse agonist of AT1 receptor Complete inhibition of AT1 – alternative remains with ACEs Result in indirect activation of AT2 – vasodilatation (additional benefit) Does not interfere with other receptors except TXA2 Blocks all the actions of A-II - vasoconstriction, sympathetic stimulation, aldosterone release and renal actions of salt and water reabsorption No inhibition of ACE
  27. 27. Organic nitrates dilate capacity vessels, reduce preload and myocardium oxygen needs. They connect with thiol groups (-SH) and release nitric oxide (NO). NO combines with new thiol groups in vascular endothelium to form nitrosothiol (R-SNO). Nitrosothiols activates guanylate cyclase which raises the concentration of cyclic GMP. This reduces the bioavailability of intracellular calcium and produces vasodilation Glyceryl trinitrate is prescribed sublingually at 18–20 min intervals in acute left-ventricular heart failure
  28. 28. Trimetazidine has prolonged concentration plateau lasting up to 11 h. It increases ATP synthesis and decreases acidosis in ischemic tissues. It supplies energy for Na+/K+ transmembrane pump, but can cause parkinsonism.
  29. 29. Carvedilol is a blocker of β- and α-receptors. It also has antioxidant, vasodilating and cardioprotective effects. It decreases cardiac output, peripheral vascular resistance and afterload. Carvedilol lowers mortality with 25–67%, but it is contraindicated in CHF, occuring with cor pulmonale. The treatment begins with low doses (3.125 mg/12 h).
  30. 30. Cardioselective beta-blockers Bisoprolol and Metoprolol decrease with 31% mortality in patients with CHF, if used in combination with diuretics, ACE inhibitors and Digoxin.
  31. 31. Levocarnitine is a N-containing amino acid in muscle, which has antioxidant activity. It is indicated in cardiomyopathy and muscle dystrophy caused by carnitine deficiency. Preparations containing Coenzyme Q10 (a part of the mitochondrial redox system), stimulate ATP synthesis and improve myocardial contractility in CHF.
  32. 32. Levosimendan increases sensitivity of troponin in the heart to calcium. This results in increased myocardial contractility. It is infused i.v. for short treatment of severe heart failure.
  33. 33. ACE inhibitor (angiotensin- converting enzyme) ARB (angiotensin receptor blockers) Beta-blocker Digoxin Diuretic Aldosterone blockade Type What it does Expands blood vessels which lowers blood pressure, neurohormonal blockade Similar to ACE inhibitor—lowers blood pressure Reduces the action of stress hormones and slows the heart rate Slows the heart rate and improves the heart’s pumping function (EF) Filters sodium and excess fluid from the blood to reduce the heart’s workload Blocks neurohormal activation and controls volume
  34. 34. EBM Therapies Relative Risk Reduction Mortality 2 year ACE-I 23% 27% Β-Blockers 35% 12% Aldosterone Antagonists 30% 19% ICD 31% 8.5%

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