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CLINICAL OVERVIEW ON CV DRUGS

CLINICAL OVERVIEW ON CV DRUGS. BY RAGAB ABDELSALAM (MD). HEART FAILURE. Digitalis. Digitalis:- increases the strength of the heart's contractions, - reduces heart size, - reduces certain arrhythmias.

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CLINICAL OVERVIEW ON CV DRUGS

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  1. CLINICAL OVERVIEW ON CV DRUGS BY RAGAB ABDELSALAM (MD)

  2. HEART FAILURE

  3. Digitalis. Digitalis:- increases the strength of the heart's contractions, - reduces heart size, - reduces certain arrhythmias. * It is derived from the foxglove plant, it has been used to treat heart disease since the 1700s and is still the only oral inotropic agent in general use

  4. * In general, > digitalis does not reduce mortality rates, > although it improves symptoms; > patients who take digitalis are also hospitalized slightly less often than those not taking the drug.

  5. ** Many experts now believe that patients should first be prescribed drugs proven to prolong life, such as an ACE inhibitor or the beta blocker carvedilol, before digitalis is recommended.

  6. ** Digitalis may be useful for patients with: > systolic dysfunction ( low EF%) > heart failure & atrial fibrillation, ** Digitalis may even be harmful in some patients with HF, particularly when caused by diastolic dysfunction characterized by normal EF..

  7. > Most physicians prescribe digoxin (Lanoxin). > The most serious side effects are arrhythmias, abnormal heart rhythms that can be life-threatening. > Factors which increase the risk of toxicity include advanced age, low blood potassium levels , hypothyroidism, anemia, valvular heart disease, and impaired kidney function

  8. - Digitalis interacts with many other drugs, including,>> quinidine, amiodarone, verapamil, flecainide, amiloride and propafenone. - Early signs of toxicity : >arrhythmia, nausea and vomiting, stomach pain, fatigue, visual disturbances (e.g., yellow vision, seeing halos around lights, which may also flicker or flash), and emotional and mental disturbances.

  9. > Toxic side effects used to be experienced by nearly 25% of patients taking digitalis, but now that a blood test can be used to monitor the level of the drug in the blood, toxicity is down to 2%.

  10. > If side effects exist, but are mild, patients should still consider continuing with digitalis if other benefits are experienced. > It was found that patients who stopped taking digoxin after using it in combination with ACE inhibitors were at risk for worsening HF.

  11. Vasopressors And Inotropes - Useful for resuscitation of seriously ill patients, and for the treatment of hypotension in theatre. - Act directly or indirectly on the SNS, but the effect of each varies according to which sympathetic receptor the drug has greatest affinity for.

  12. -The duration of action also varies. - Direct acting drugs act by stimulating the SNS receptor whereas indirect acting drugs cause the release of noradrenaline from the receptor . - Some drugs have a mixed effect

  13. > A1 Peripheral arteriolar vasoconstriction > B1  Cordiac increased heart rate and force of conctraction

  14. > B2  Bronchial smooth muscle dilation, vasodilation in skeletal muscle, also some cardiac effects > D  Increased renal blood flow .

  15. Adrenaline (Epinephrine) Adrenaline acts on a1, b1 and b2 receptors. It is said to prepare the body for a "fight or flight" response

  16. Ephedrine Ephedrine acts directly on b1 and b2 receptors, and indirectly on a1 receptors by causing noradrenaline release

  17. * Indications: > Low blood pressure due to vasodilation e.g. following spinal or epidural anaesthesia and drug overdoses. Best vasopressor to use in pregnancy as it does not reduce placental blood flow * Dose 3-10 mg boluses iv, repeat until effective. Maximum dose is 60mg. > Duration of action 5-15 minutes, repeated doses less effective (i.e. it demonstrates tachyphylaxis

  18. Methoxamine - Methoxamine acts on a1 receptors - Actions Increases blood pressure. There may be a reflex decrease in HR, and therefore it is good for hypotension with tachycardia. >> Useful during spinal anaesthesia - Side effects May produce bradycardia - Dose 2-4mg boluses IV, repeated as necessary

  19. Phenylephrine - Acts directly on a1 receptors - Action Hypertension and a reflex decrease in heart rat - Dose 2-5mg im or sc, 0.1-0.5mg iv, by infusion 20-50mcg/min

  20. Noradrenaline - Acts mainly on a1 receptors with few effects on b receptors - Actions Increases blood pressure by vasoconstriction. Less likely to cause tachycardia than adrenaline - Indications Septic shock where peripheral vasodilation may be causing hypotension

  21. > Cautions Acts by increasing afterload and therefore not appropriate for use in patients in cardiogenic shock. Blood supply to kidneys and peripheries may be reduced > Dose - 1-30mcg/min > Add 4mg to 250ml 0.9% NaCl or 5% dextrose to give 16mcg/ml. Run at 0-112ml/hr

  22. Dopamine - Acts on D, b1, b2 and a1 receptors, depending on the dose administered - Actions Dose dependent.

  23. Dobutamine - Acts on b1 and b2, with minimal action on a1 receptors - Actions: increases COP and reduces afterload ** Indications : - Cardiogenic shock - Severe HF Dose 2-30mcg/kg/min Add 3mg/kg to 50mls 0.9%NaCl or 5% glucose 1ml/hr = 1mcg/kg/min

  24. Dopexamine > Acts on b2 and D receptors > Actions: -It increases COP and reduces afterload. - Increases blood supply to the kidneys and possibly also the GIT . > Dose 0.5-6mcg/kg/min

  25. Salbutamol - Acts on b2 receptors - Actions Relaxes bronchial smooth muscle i.e. bronchodilation, may increase HR Indications Severe acute asthma ** Dose By infusion 5-20mcg/min. ** Can also be given in bolus form iv in the initial treatment of an attack at a dose of 5mcg/kg over several minutes

  26. Isoprenaline - Acts on b1 and b2 receptors - Main action is increased heart rate. Also increased force of contraction, and bronchodilation * Indications: >CHB, overdose of B- blocker or severe bradycardia unresponsive to atropine. Can be used to treat asthma, >but less suitable than drugs that act only on b2 receptors e.g. salbutamol

  27. Phosphodiesterase inhibitors (e.g. aminophylline, enoximone) ** Prevent breakdown of cAMP this produces effects at b1 and b2 receptors ** Actions increased rate and force of contraction, vasodilation in skeletal muscle. Also bronchodilation ** Indications : > Aminophylline: asthma, cardiac failure > Enoximone: HF in patients failing to respond to dobutamine

  28. * Carvedilol: > As the output of the heart drops in patients with CHF, the body is stressed and releases catecholamines > These adrenergic substances increases HR and stimulates the weak muscle to contract more forcefully. > This is known as a "beta adrenergic effect" and increases the work that the heart has to perform. The sick heart gets sicker as it works harder

  29. >The adrenergicsubstances also cause the arterial walls to constrict or tighten. > This is knownas "alpha adrenergic effect" and helps to raise the blood pressure when the weak heart cannot do so on its own. > However, this increases the resistance putting an additional load on the struggling heart.

  30. ** Carvedilol: > A drug blocks both the alpha and beta blocking effects. >> The HR is slowed, >> the weak heart muscle is protected from the "whipping" or stimulating effects >> the arteries are dilated so as to make it easier for the heart to empty. >>> Improve symptoms, decrease the need for hospitalization and improve survival in patients with CHF..

  31. >> Carvedilol and other agents in its class are always considered in the treatment of CHF unless they are contraindicated or not tolerated. >>They are generally avoided in patients with asthma, extremely slow heart rates and very low blood pressure

  32. Angiotensin converting Enzyme Inhibitors (ACEI)

  33. Adrenomedullin > A potent vasodilator that reduces blood pressure while increasing cardiac output. > It is produced by many tissues, including heart and vascular smooth muscle when stimulated by pro-inflammatory cytokines > It probably acts via nitric oxide and cAMP, but the principal signalling system varies between tissues and species.

  34. Aldosterone > It is produced by the adrenal cortex when stimulated by angiotensin II. > It causes sodium and water retention by the kidney, and a urinary potassium losses. > It is also regulates salt resorption in the colon and sweat glands, and promotes collagen synthesis in cardiac muscle leading to myocardial fibrosis.

  35. ** Spironolactone is a non-specific aldosterone antagonist that has been in use for several years, but it also binds to sex steroid receptors leading to unwanted side effects. >> It is commonly added to other drug regimes

  36. Bradykinin - A vasodilator peptide released from clotting factor XII by a tissue protease called kallikrein. - It plays little role in the regulation of normal blood flow, but becomes more important following injury or infection.

  37. Brain natriuretic peptide - (BNP, nesiritide) has recently been approved for clinical use. - This peptide is released naturally from overstretched ventricular muscle.

  38. Calcium sensitizers > There is dispute about their mode of action, and levosimendan also activates the ATP sensitive potassium channel in vascular smooth muscle plasmalemma, leading to an increase in coronary flow

  39. Chemokines and cytokines -They are produced by macrophages and many other cell types. -They are raised in CHF, and there is increased expression within the failing myocardium. - They are implicated in the pathogenesis of dilated cardiomyopathy

  40. - These peptides act on the hypothalamus to increase body temperature, reduce food intake and result in the mobilisation of energy and protein stores. -They stimulate the liver to secrete C-reactive protein and mannan-binding lectin as part of the acute phase response. -Various anti-cytokine trials have so far yielded disappointing result

  41. Endothelin - It is a potent vasoconstrictor and smooth muscle mitogen secreted by endothelial cells lining the blood vessel walls. -The endothelin system is activated in several disease states including hypertension and heart failure.

  42. * Two classes of endothelin receptor: a) ETAR located mainly on vascular smooth muscle cells >>> signaling causes both vasoconstriction and myoproliferation b) ETBR located mainly on the endothelial cells themselves..>>> signals vasodilation when expressed on endothelial cells but vasoconstriction when expressed on smooth muscle cells

  43. > Selective and non-selective endothelin receptor antagonistsETRAhave been developed. > Pre-clinical studies have shown limited effects on hypertension, but these drugs have an excellent ability to prevent end organ damage

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