Week 5 Pharma


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Week 5 Pharma

  1. 1. THE CARDIOVASCULAR SYSTEM Nhelia B. Perez RN, MSN Northeastern College Santiago City
  2. 2. INTRODUCTION <ul><li>The Heart </li></ul><ul><li>The Cardiac Cycle </li></ul><ul><li>Conduction System of the heart </li></ul>
  3. 5. THE CARDIOVASCULAR SYSTEM <ul><li>Circulation </li></ul><ul><li>1. Pulmonary and systemic circulation </li></ul><ul><li>2. arteries, capillaries and veins </li></ul><ul><li>3. coronary circulation </li></ul>
  4. 6. Main Forces that determine the heart’s use of oxygen or oxygen consumption <ul><li>Heart rate </li></ul><ul><li>Preload </li></ul><ul><li>Afterload </li></ul><ul><li>Stretch on the ventricles </li></ul>
  5. 7. <ul><li>Systemic arterial pressure </li></ul><ul><li>Venous pressure </li></ul>
  7. 9. Three elements which determines the pressure in the Cardiovascular System <ul><li>Heart Rate </li></ul><ul><li>Stroke Volume </li></ul><ul><li>Total Peripheral Resistance </li></ul>
  8. 10. <ul><li>Baroreceptors </li></ul><ul><li>Renin-Angiotensin System </li></ul><ul><li>Hypertension </li></ul><ul><li>Hypotension </li></ul>
  9. 12. Anti hypertensive agents <ul><li>STEPPED-CARE APPROACH TO TREATING HYPERTENSION </li></ul><ul><li>1. Lifestyle modifications </li></ul><ul><li>2. drug therapy </li></ul><ul><li>3. combination effect </li></ul><ul><li>4. steps 1,2 and 3 plus more anti hypertensive agents. </li></ul>
  10. 13. DIURETICS <ul><li>Drugs that increase the excretion of sodium and water from the kidney </li></ul>
  11. 14. Sympathetic Nervous System Blockers <ul><li>Beta-blockers block vasoconstriction, decrease heart rate, decrease heart rate, decrease cardiac muscle contraction and tend to increase blood flow to the kidneys leading to a decrease in the release of renin. </li></ul>
  12. 15. <ul><li>Alpha and beta-blockers are useful in conjunction with other agents and tend to be somewhat more powerful, blocking all of the receptors in the symphatetic system. </li></ul>
  13. 16. <ul><li>Alpha-adrenergic blockers inhibit the postsynaptic alpha-adrenergic receptors, decreasing symphatetic tone in the vasculature and causing vasodilation which leads to a lowering of BP. </li></ul>
  14. 17. <ul><li>Alpha-blockers are used to treat hypertension because of their ability to block the postsynaptic alpha-receptor sites. </li></ul>
  15. 18. <ul><li>Alpha Agonists stimulate the alpha receptors in the central nervous system and inhibit the cardio-vascular centers, leading to a decrease in symphatetic outflow from the CNS and a resultant drop in blood pressure. </li></ul>
  16. 19. Angiotensin – Converting Enzyme Inhibitors <ul><li>Blocks the conversion of angiotensin I to angiotensin II in the lungs. This prevents release of aldosterone. </li></ul><ul><li>Captopril, Moexipril </li></ul>
  17. 20. Calcium Channel blockers <ul><li>Calcium channel blockers are a class of drugs and natural substances which disrupt the conduction of calcium channels . </li></ul><ul><li>The main clinical usage of calcium channel blockers is to decrease blood pressure . It is for this action that they are used in individuals with hypertension . </li></ul>
  18. 21. <ul><li>Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy . </li></ul><ul><li>Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart </li></ul><ul><li>Amlodipine, Diltiazem, Felodipine, Nicardepine, Nifedepine, Verapamil </li></ul>
  19. 22. Vasodilators <ul><li>These medicines work by relaxing the smooth muscle of blood vessels, which opens up (dilates) the blood vessels. This allows blood to flow more easily, thereby lowering blood pressure. </li></ul><ul><li>Hydralazine </li></ul>
  20. 23. Antihypotensive Agents <ul><li>Sympathetic Adrenergic Agonists works by acting on the sympathetic adrenergic receptors to cause the effects of sympathetic stress response. </li></ul>
  22. 25. <ul><li>CONGESTIVE HEART FAILURE- “dropsy” heart fails to pump blood around the body. </li></ul><ul><li>CAUSES: </li></ul><ul><li>- CAD- 95% cause of CHF, insufficiency of blood to meet O2 demand of the myocardium (Ms becomes hypoxic & ↓ capacity to contract) </li></ul><ul><li>– CARDIOMYOPATHY- viral infection, alcoholism, steroid abuse, collagen d/o </li></ul><ul><li>– HPN- leads to enlarged cardiac Ms (puts cardiac Ms in constant ↑ oxygen demand) </li></ul><ul><li>– VALVULAR HEART DSE.- overload of the ventricles due to inadequate closing of the valves (leakages of blood / backflow) </li></ul>
  23. 26. TREATMENT: <ul><li>1. VASODILATORS (ACE inhibitors & NITRATES)- ↓workload of the heart </li></ul><ul><li>2. DIURETICS- ↓ blood volume, venous return & BP </li></ul><ul><li>3. BETA ADRENERGIC AGONIST- stimulate beta receptors in SNS (↑ Ca flow in heart cells, myocardial contraction) </li></ul><ul><li>4. CARDIOTONIC (“INOTROPIC” / “PRESSORS”)- ↑ heart contraction </li></ul><ul><li>4.1CARDIAC GLYCOSIDES (lanoxin)- most often used in CHF rapid action onset & can be safely be excreted unchanged in the urine (antidote=digoxin immune fab) </li></ul><ul><li>Action: ↑ intracellular Ca, allows Ca to enter myocardial cells during depolarization. ↑myocardial contraction (inotropic effect) ↑CO & renal perfusion( ↑urine output, ↓ blood vol.↓renin release & renin angiotensin system) ↓ HR (- chronotropic effect) ↓conduction velocity in AV node </li></ul>
  24. 27. ARRYTHMIA / DYSRYTHMIA <ul><li>abnormality / disturbance in normal & rate & rhythm of the heart </li></ul><ul><li>Bradycardia </li></ul><ul><li>Tachycardia </li></ul><ul><li>(PAC / PVC, Atrial flutter / Atrial fibrilation, Vtach / Vfib, AV heart blocks 1-3, bundle blocks) </li></ul><ul><li>CAUSES: changes in automaticity & conductivity) </li></ul><ul><li>Electrolyte disturbance alters action potential </li></ul><ul><li>Oxygen deprivation (hypoxia / anoxia) </li></ul><ul><li>Structural damage in the conduction pathways </li></ul><ul><li>through the heart </li></ul><ul><li>Alteration in bld. Acidity / alkalinity (waste products </li></ul><ul><li>accumulation) </li></ul>
  25. 28. <ul><li>All antiarrhythmic drugs directly or indirectly alter membrane ion conductances, which in turn alters the physical characteristics of cardiac action potentials . </li></ul>
  26. 29. Classes of Drugs Used to Treat Arrhythmias <ul><li>Class I agents </li></ul><ul><li>The class I antiarrhythmic agents interfere with the sodium channel . Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials . </li></ul><ul><li>Class 1 agents are called Membrane Stabilizing agents. The 'stabilizing' is the word used to describe the decrease of excitogenicity of the plasma membrane which is brought about by these agents. (Also noteworthy is that a few class 2 agents like propranolol also have a membrane stabilizing effect .) </li></ul><ul><li>Class I agents are divided into three groups (1a, 1b and 1c) based upon their effect on the length of the action potential. </li></ul><ul><li>1A lengthens the action potential (right shift) </li></ul><ul><li>1B shortens the action potential (left shift) </li></ul><ul><li>1C does not significantly affect the action potential (no shift) </li></ul>
  27. 30. <ul><li>Class II agents </li></ul><ul><li>Class II agents are conventional beta blockers . They act by blocking the effects of catecholamines at the β1-adrenergic receptors , thereby decreasing sympathetic activity on the heart. These agents are particularly useful in the treatment of supraventricular tachycardias . They decrease conduction through the AV node . </li></ul><ul><li>Class II agents include atenolol , esmolol , propranolol , and metoprolol . </li></ul>
  28. 31. <ul><li>Class III agents </li></ul><ul><li>Class III agents predominantly block the potassium channels , thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less likely to interact with tissue that has become refractory). </li></ul>
  29. 32. <ul><li>Class IV agents </li></ul><ul><li>Class IV agents are slow calcium channel blockers . They decrease conduction through the AV node , and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility. </li></ul><ul><li>Class IV agents include verapamil and diltiazem . </li></ul>
  30. 33. ANTIANGINAL DRUGS <ul><li>An antianginal is any drug used in the treatment of angina pectoris , a symptom of ischaemic heart disease . </li></ul>
  31. 34. <ul><li>Nitrates </li></ul><ul><li>Nitrates cause vasodilation of the venous capacitance vessels by simulating the endothelium-derived relaxing factor (EDRF). Used to relieve both exertional and vasospastic angina by allowing venous pooling, reducing the pressure in the ventricles and so reducing wall tension and oxygen requirements in heart. Short-acting nitrates are used to abort angina attacks that have occurred, while longer-acting nitrates are used in the prophylactic management of the condition. </li></ul><ul><li>Agents include nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate . </li></ul>
  32. 35. <ul><li>Beta blockers </li></ul><ul><li>Beta blockers are used in the prophylaxis of exertional angina by reducing the work the heart is allowed to perform below the level that would provoke an angina attack. </li></ul><ul><li>They cannot be used in vasospastic angina and can precipitate heart failure . </li></ul><ul><li>Agents include either cardioselectives such as acebutolol or metoprolol , or non-cardioselectives such as oxprenolol or sotalol . </li></ul>
  33. 36. <ul><li>Calcium channel blockers </li></ul><ul><li>Calcium ion (Ca++) antagonists ( Calcium channel blockers ) are used in the treatment of both exertional and vasospastic angina. In vitro, they dilate the coronary and peripheral arteries and have negative inotropic and chronotropic effects - decreasing afterload , improving myocardial efficiency, reducing heart rate and improving coronary blood flow. In vivo , the vasodilation and hypotension trigger the baroreceptor reflex. Therefore the net effect is the interplay of direct and reflex actions. </li></ul><ul><li>Class I antiarrhythmic agents have the most potent negative inotropic effect and may cause heart failure. </li></ul><ul><li>Class II agents do not depress conduction or contractility. </li></ul><ul><li>Class III agent has negligible inotropic effect and causes almost no reflex tachycardia . </li></ul><ul><li>Examples include Class I agents ( e.g. , verapamil ), Class II agents ( e.g. , amlodipine , nifedipine ), or the Class III agent diltiazem . </li></ul>
  34. 37. LIPID LOWERING AGENTS <ul><li>Hypolipidemic agents , or antihyperlipidemic agents , are a diverse group of pharmaceuticals that are used in the treatment of hyperlipidemias . They are called lipid-lowering drugs (LLD) or agents. </li></ul>
  35. 38. Classes of hypolipidemic drugs <ul><li>There are several classes of hypolipidemic drugs. They may differ in both their impact on the cholesterol profile and adverse effects. For example, some may lower the &quot;bad cholesterol&quot; low density lipoprotein (LDL) more so than others, while others may preferentially increase high density lipoprotein (HDL), &quot;the good cholesterol&quot;. Clinically, the choice of an agent will depend on the patient's cholesterol profile , cardiovascular risk , and the liver and kidney functions of the patient, evaluated against the balancing of risks and benefits of the medications. In the United States, this is guided by the evidence-based guideline from the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATPIII). </li></ul>
  36. 39. <ul><li>bile acid sequestrants (resins) are particularly effective for lowering LDL-C by sequestering the cholesterol-containing bile acids released into the intestine and preventing their reabsorption from the intestine. It decreases LDL by 15-30% and raises HDL by 3-5%. It has little effect on triglycerides but can cause a slight increase. Bile acid sequestrants may cause gastrointestinal problems, and may also reduce the absorption of other drugs and vitamins from the gut. </li></ul>
  37. 40. <ul><li>MHG – CoA Reductase Inhibitors </li></ul><ul><li>Blocks the involvement of the enzyme HMG-CoA reductase in the synthesis of cellular cholesterol. </li></ul><ul><li>When blocked, the serum cholesterol and LDL levels decrease, because more LDLs are absorbed by the cells for processing into cholesterol. </li></ul>
  38. 41. <ul><li>Cholesterol Absorption Inhibitors </li></ul><ul><li>Localizes in the brush border of the small intestine and inhibits the absorption of cholesterol from the small intestine thus less cholesterol is delivered to the liver dropping the serum cholesterol level. </li></ul>
  39. 42. DRUGS AFFECTING BLOOD COAGULATION <ul><li>An anticoagulant is a substance that prevents coagulation ; that is, it stops blood from clotting. A group of pharmaceuticals called anticoagulants can be used in vivo as a medication for thrombotic disorders. </li></ul><ul><li>Heparin, Warfarin, Antithrombin, </li></ul>
  40. 43. <ul><li>Coumarines (Vitamin K antagonists) </li></ul><ul><li>The oral anticoagulants are a class of pharmaceuticals that act by antagonizing the effects of vitamin K . Examples include warfarin . It is important to note that it takes at least 48 to 72 hours for the anticoagulant effect to develop fully. In cases when any immediate effect is required, heparin must be given concomitantly. Generally, these anticoagulants are used to treat patients with deep-vein thrombosis (DVT), pulmonary embolism (PE), atrial fibrillation (AF), and mechanical prosthetic heart valves . </li></ul><ul><li>[ edit ] Adverse effects </li></ul><ul><li>Patients aged 80 years or more may be especially susceptible to bleeding complications with a rate of 13 bleeds per 100 person-years. [1] </li></ul><ul><li>These oral anticoagulants are used widely as poisons for mammalian pests, especially rodents . </li></ul>
  41. 44. <ul><li>An antiplatelet drug is a member of a class of pharmaceuticals that decreases platelet aggregation and inhibits thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect. </li></ul><ul><li>They are widely used in primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease. </li></ul>
  42. 45. <ul><li>Aspirin irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane - powerful vasoconstrictor which lowers cyclic AMP and initiates the platelet release reaction). </li></ul><ul><li>Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2 </li></ul><ul><li>Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex </li></ul><ul><li>Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes: </li></ul><ul><ul><li>Murine-human chimeric antibodies (e.g. abciximab) </li></ul></ul><ul><ul><li>Synthetic peptides (e.g. eptifibatide) </li></ul></ul><ul><ul><li>Synthetic non-peptides (e.g. tirofiban) </li></ul></ul><ul><li>Epoprostenol is a prostacyclin which is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension. </li></ul>