CARDIOVASCULAR DRUGS
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Transcript of CARDIOVASCULAR DRUGS
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CARDIOVASCULAR DRUGS
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Reference:Pharmacology inRehabilitation4th EditionCharles D. Ciccone, PT, PhD
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Diuretics
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Diureticsincrease the formation and excretion of
urine. increase the renal excretion of water and
sodium, thus decreasing the volume of fluid within the vascular system.
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Classification of DiureticsThiazide Diuretics. • act primarily on the early portion of the
distal tubule of the nephron, where they inhibit sodium reabsorption.
• the most frequently used type of diureticLoop Diuretics. • act primarily on the ascending limb of the
loop of Henle (hence the term inhibit the reabsorption of sodium and chloride from the nephron, thereby preventing reabsorption of the water that follows these electrolytes
Potassium-Sparing Diuretics. prevent the secretion of potassium into the
distal tubule. Normally, there is sodium-potassium
exchange - sodium is reabsorbed and potassium is secreted.
Potassium-sparing agents interfere with this exchange so potassium is spared from secretion and sodium
is excreted. potassium sparing drugs have the advantage
of reducing potassium loss and thus preventing hypokalemia.
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Classification of DiureticsPotassium-Sparing Diuretics. • prevent the secretion of potassium into the
distal tubule. • Normally, there is sodium-potassium
exchange - sodium is reabsorbed and potassium is secreted.
• Potassium-sparing agents interfere with this exchange so potassium is spared from secretion and sodium is excreted.
• Potassium sparing drugs have the advantage of reducing potassium loss and thus preventing hypokalemia.
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Adverse Effects of Diuretics• fluid depletion and electrolyte imbalance.• decreased extracellular fluid volume as
well as produce sodium depletion (hyponatremia) and potassium depletion (hypokalemia).
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Sympatholytic Drugs
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Sympatholytic Drugs• an increase in sympathetic - a factor in
essential hypertension. • sympatholytic agents - drugs that
interfere with sympathetic discharge• classified according to where and how
they interrupt sympathetic activity.
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Sympatholytic drugs:
beta-adrenergic blockersalpha-adrenergic blockerspresynaptic adrenergicneurotransmitter depletorscentrally acting drugsganglionic blockers
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Beta Blockers• Beta-adrenergic blockers-a mainstay of
antihypertensive• exert their primary effect on the heart-
decrease heart rate and force of myocardial contraction.
• (-) inotropic effect, (-) chronotropic effect = lowers BP
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Adverse Effects• Nonselective beta blockers (equal affinity for
beta-1 and beta-2 receptors) may• produce bronchoconstriction in patients with
asthma• Cardiovascular side effects include
excessive depression of heart rate and myocardial contractility as well as orthostatic hypotension.
• may impair glucose and lipid metabolism
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Alpha Blockers• block the alpha-1–adrenergic receptor on
vascular smooth muscle = decrease in vascular resistance.
• decreases total peripheral resistance
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Adverse Effects• When peripheral vascular resistance due to
alpha blockers, the baroreceptor reflex often responds by generating a compensatory increase in heart rate (reflex tachycardia)
• To prevent reflex tachycardia, a beta blocker may be administered with the alpha blocker
• to negate the increase in heart rate
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Presynaptic Adrenergic Inhibitorsinhibit the release of norepinephrine from
the presynaptic terminals of peripheral adrenergic neurons
Adverse EffectsOrthostatic hypotension gastrointestinal disturbances such as
nausea, vomiting and diarrhea.
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Centrally Acting Agentsinhibit sympathetic discharge from the
brainstem.
Adverse Effectsdry mouth, dizziness, and sedation.
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Vasodilators
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Vasodilatorsdirectly vasodilate the peripheral vasculature
by decreasing peripheral vascular resistance.
inhibit smooth-muscle Adverse EffectsReflex tachycardia dizziness, postural hypotension, weakness,
nausea, fluid retention, and headache
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Inhibition of the renin-angiotensin system
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Renin-Angiotensin SystemRenin -formed in the renal juxtaglomerular
cells in response to certain types of stimuli:
• salt depletion• β2 stimulation• decrease in renal perfusion that might be
found in hypotension or hypovolemia.
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• renin mediates the formation of angiotensin-I in the liver.
• When angiotensin-I reaches the lungs, it is converted by the angiotensin converting enzyme into angiotensin-II.
• Angiotensin-II causes vasoconstriction, promotes the release of norepinephrine, and stimulates aldosterone production resulting in sodium and water retention.
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Additional effects of angiotensin-II include increased systemic vascular resistance, arterial blood pressure, and intravascular volume.
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Inhibition of the Renin-Angiotensin Systemtwo pharmacologic strategies: • inhibit the enzyme that converts angiotensin I
to angiotensin II = angiotensin converting enzyme (ACE) inhibitors.
• block angiotensin II receptors on various tissues = angiotensin II blockers
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Result: a decrease in norepinephrine levels, prevention of systemic vasoconstriction and decreased blood pressure.
aldosterone production is no longer stimulated by Angiotensin II, which results in decreased intravascular volume.
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Adverse Effectsallergic reaction - skin rash. persistent dry cough
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Calcium channel blockers
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Adverse Effects• may cause excessive vasodilation as
evidenced by swelling in the feet and ankles
• orthostatic hypotension.
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Nitrates
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Organic nitrates • dilate vascular smooth muscle • Nitrates are actually drug precursors
(prodrugs) that become activated• when they are converted to nitric
oxide within vascular smooth muscle
Nitroglycerin- the most well known antianginal drug.
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Drugs Used for Overclotting
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Antithrombotic Drugs• anticoagulants affect the synthesis and
function of clotting factors• antithrombotics primarily inhibit the
function of platelets• prevent the formation of arterial clots, such
as those• that cause coronary artery occlusion or
cerebral infarction.
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Aspirin• suppresses platelet aggregation by
inhibiting the synthesis of prostaglandins and thromboxanes.
• inhibit the cyclooxygenase enzyme that initiates synthesis of prostaglandins and thromboxanes.
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• Certain prostaglandins and thromboxanes, especially thromboxane A2, have a potent ability to induce platelet aggregation.
• By inhibiting the synthesis of these proaggregation substances, aspirin prevents platelet-induced thrombus formation.
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• very low aspirin doses = meaningful antithrombotic effect
• adequate antithrombotic effects with one baby aspirin tablet each day
• During the acute phase of an infarction, aspirin is critical in helping to limit the progression of platelet-induced occlusion, reducing the extent of damage to the myocardium
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Adverse Effects of Antithrombotic Drugs
• aspirin increases risk of bleeding• may cause gastric irritation• high doses of aspirin may be toxic to
the liver and kidneys
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Thrombolytic Drugs• Thrombolytics facilitate the
breakdown and dissolution of clots formed.
• activate conversion of plasminogen (profibrinolysin) to plasmin (fibrinolysin)
• used to dissolve clots that have already formed, thus reopening occluded blood vessels.
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• extremely valuable in treating acute myocardial infarction.
• When administered at infarction onset, these drugs can reestablish
• blood flow through occluded coronary vessels,
preventing or reversing myocardial damage decreasing morbidity /mortality
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• can help reopen occluded coronary vessels when administered within 12 hours after symptom onset.
• Thrombolytics produce best results when administered soon after the symptom onset.
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Streptokinase and Urokinaseboth cause activation of plasmin. Streptokinase indirectly activates
plasmin (fibrinolysin) Urokinase directly converts plasminogen
to plasmin
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Adverse Effects of Thrombolytic DrugsHemorrhage is the major adverse effect
associated withthrombolytic agents.
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Drugs That IncreaseMyocardial Contraction Force
(Positive Inotropic Agents)
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(Positive Inotropic Agents) Digitalis• “digitalis" - term used to represent
these drugs• cardiac glycosides include digoxin,
digitoxin• one of the primary drugs used to treat
congestive heart failure.• digitalis improves cardiac pumping
ability and therefore improves the primary symptoms of congestive heart failure.
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Adverse Side Effectsgastrointestinal distress (nausea,
vomiting, diarrhea) and central nervous system (CNS) disturbances (drowsiness, fatigue, confusion, visual disturbances)
arrhythmias such as premature atrial and ventricular contractions, paroxysmal atrial tachycardia, ventricular tachycardia, and high degrees of atrioventricular block
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Agents Used to Treat Hyperlipidemia
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Hyperlipidemia• one of the primary causes of
cardiovascular disease• causes deposition of fatty plaquelike
lesions on the walls of large and mediumsized arteries (atherosclerosis), which can lead to thrombosis and infarction.
Hyperlipidemia is often caused by poor diet
and lifestyle, as well as genetic conditions
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Agents Used to Treat Hyperlipidemia• are used when plasma lipid levels are
unsuccessfully controlled by nonpharmacologic
• methods such as low-fat diets, weight reduction, regular exercise, and smoking cessation
• endogenous control of lipid metabolism
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Adverse Effect of Antihyperlipidemia Agentsgastrointestinal distress
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