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Pharmacology > Cardiovascular Phamacology > Flashcards

Cardiovascular Phamacology Flashcards

1
Q

Antihypertensive Drugs

Hypertension

A
  • Sustained, reproducible increase in blood pressure
  • 15-20% of adult Americans are believed to be hypertensive
  • If left untreated, the sustained increase in blood pressure can lead to cardiovascular problems (stroke, HF), renal disease, and blindness
  • ‘Silent killer’ – asymptomatic
  • Morbidity and mortality is due to the end organ damage
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2
Q

Antihypertensive Drugs

Normal Control of BP

A
  • Short-term = baroreceptor reflex
  • Long-term management = kidneys
  • BP is a product of cardiac output and the total resistance in the peripheral vasculature
  • BP = (CO) x (TPR)
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3
Q

Antihypertensive drugs

Pathogenesis of Hypertension

A

Two major categories

•Primary, or essential, hypertension
–No know cause
–Genetic and environmental factors
–General increase in sympathetic activity

•Secondary
–Renal artery stenosis
–Pheochromocytoma
–Aortic coarctation
–Adrenal tumor

Pharmacological Therapy used primarily for essential hypertension

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4
Q

Baroreflexes

A

1)MAP= set point
2)Reflexes defend set point
1)Arterial Baroreflexes
2)Pressure/Natriuresis
3)Change in MAP opposed by reflex response to maintain set pressure.
4)Hypertension- pressure resets to higher level-defended by reflex systems.
●

CRITICAL POINT!

**Multiple therapies often needed to block reflex compensation.

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5
Q

Treatment Strategy of Hypertension

A

•Goal- normalize pressure- decrease CO and/or TPR
•Strategy- alter volume, cardiac and/or VSM function
•Diagnosis = 3-6 independent measurements
•Determination of primary vs. secondary HTN
•If secondary
–Treat underline pathology
•If primary
–Initiate lifestyle changes
–Pharmacological treatment

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6
Q

Pharmacological Treatment

A
  • Diuretics
  • Alpha-1 antagonists
  • Alpha-2 agonists
  • Beta adrenergic antagonists
  • Anti-angiotensin II receptor blockers
  • Ca2+ channel blockers
  • Vasodilators
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7
Q

Diuretics

A

Often the first type of drugs to treat hypertension

Site of action
–Renal nephron

MOA
–Increase renal excretion of water and sodium => decrease the volume of fluid within the vascular system

Effect on cardiovascular system
–Acute decrease in CO
–Chronic decrease in TPR, normal CO

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8
Q

Classification of Diuretics

A

•Thiazide diuretics
–chlorothiazide (Diuril®), hydrochlorothiazide (Hydrodiuril®)
–Act primarily on the early portion of the distal tubule of the nephron => inhibit Na+ reabsorption

•Loop diuretics
–bumetanide (Bumex®), furosemide (Lasix®), metolazone (Zaroxolyn®)
–Act primarily on the ascending limb of the loop of Henle => inhibit Na+ reabsorption

•Potassium-sparing diuretics
–amiloride (Midamor); spironolactone (Aldactone); triamterene (Dyrenium)
–Prevent K+ secretion into the distal tubule (prevent hypokalemia)

•Osmotic diuretics
–mannitol (Osmitrol); urea (Ureaphil)
–Act in renal proximal tubule => prevent H2O reabsorption
–Extract H2O from systemic body compartments => expanded extracellular fluid volume and increases renal blood flow

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9
Q

Adverse Effects of Diuretics

A

•Fluid depletion
–May cause reflex ↑ in CO and PVR because of activation of baroreflex => excessive demand on the myocardium in certain CHF pts

•Electrolyte imbalances
–Sodium depletion (hyponatremia)
–Potassium depletion (hypokalemia)

  • Orthostatic hypotension
  • GI disturbances
  • Weakness/fatigue
  • Confusion
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10
Q

Therapeutic Considerations for Diuretics

A

•Thiazides (most common diuretics for HTN)
–Generally start with lower potency diuretics
–Generally used to treat mild to moderate HTN
–Use with lower dietary Na+ intake, and K+ supplement or high K+ food

  • K+ Sparing (combination with other agent)
  • Loop diuretics (severe HTN, or with CHF)
  • Osmotic (HTN emergencies)

•Maximum antihypertensive effect reached before maximum diuresis- 2nd agent indicated

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11
Q

Alpha-1 Adrenergic Antagonist

A

doxazosin (Cardura®), prazosin (Minipress®), terazosin (Hytrin®)

•Site of action
–Peripheral arterioles
–Smooth muscle

•MOA
–Competitive antagonist at a-1 receptors on vascular smooth muscle

•Effects on cardiovascular system
–Vasodilation, reduces peripheral resistance

  • Blocking a-receptors on vascular smooth muscle allows muscle relaxation, dilation of vessel, and reduced resistance
  • S/E: reflex tachycardia, orthostatic hypotension
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12
Q

Therapeutic Considerations for alpha 1 adrenergic antagonist

A
  • No reflex tachycardia; small 1st dose
  • Does not impair exercise tolerance
  • Useful with diabetes, asthma, and/or hypercholesterolemia
  • Use in mild to moderate hypertension
  • Often used with diuretic, b antagonist
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13
Q

Central Sympatholytics (a-2 Agonists)

A

clonidine (Catapres), methyldopa (Aldomet)

•Site of action
–CNS medullary cardiovascular centers
–clonidine; direct a-2 agonist
–methyldopa: “false neurotrans.”

•MOA
–CNS a-2 adrenergic stimulation
–Peripheral sympathoinhibition
–Decreased norepinephrine release

•Effect on cardiovascular system
–Decreased NE–>vasodilation–> Decreased TPR

  • Stimulation of a-2 receptors in the medulla decreases peripheral sympathetic activity, reduces tone, vasodilation and decreases TPR
  • S/Es: dry mouth, sedation, impotence
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14
Q

ß Adrenergic Antagonists

A

labetalol (Normodyne); propranolol (Inderal); metoprolol (Lopressor); atenolol (Tenormin); nadolol (Corgard)

•Site of action
–Heart

•MOA
–Competitive antagonist at b- adrenergic receptors

•Effect on cardiovascular system
–Cardiac– ß HR, ¯ SVÞ ß CO
–Renal– ß Renin Þ ß Angiotensin II Þ ß TPR

  • S/Es: impotence; bradycardia; fatigue; exercise intolerance
  • Contraindications: asthma; diabetes; bradycardia; hypersensitivity
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15
Q

Therapeutic Considerations for Beta Adrenergic Antagonists

A

•Selectivity
–nadolol (Corgard) non selective, but 20 hr 1/2 life
–metoprol (Lopresor) b-1 selective, 3-4 hr 1/2 life

  • Risky in pulmonary disease even selective b-1
  • Available as mixed a/b blocker available-labetalol (Trandate, Normodyne)
  • Use post myocardial infarction- protective
  • Use with diuretic- prevent reflex tachycardia
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16
Q

Anti-Angiotensin II Drugs

A

Angiotensin Converting Enzyme (ACE) Inhibitors
•enalopril (Vasotec);
•quinapril (Accupril);
•fosinopril (Monopril);
•lisinopril (Zestril, Prinivil);
•benazepril (Lotensin);
•captopril (Capoten)

Angiotensin Receptor Blockers (ARBs)

  • losartan (Cozaar);
  • candesartan (Atacand);
  • valsartan (Diovan)
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17
Q

Anti-Angiotensin II Drugs Effects

A

•Effect on cardiovascular system
–↓ volume => ↓CO
–↓ HR => ↓SV => ↓SNS => ↓CO
–↓ Angiotensin II => ↓SNS => ↓CO

  • S/Es: hyperkalemia, angiogenic edema (ACE inhib); cough (ACE inhib); rash; itching
  • Contraindications: pregnancy; hypersensitivity; bilateral renal stenosis
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18
Q

Therapeutic Considerations for Anti-Angiotensin II

A
  • Use with diabetes or renal insufficiency
  • Adjunctive therapy in heart failure
  • Often used with diuretic
  • Enalapril, iv for hypertensive emergency
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19
Q

Calcium Channel Blockers

A

•verapamil (Calan); nifedipine (Procardia); diltiazem (Cardizem); amlodipine (Norvasc)

•Site of action
–Vascular smooth muscle

•MOA
–Blocks Ca++ channel decreases/prevents contraction

•Effect on cardiovascular system
–Vascular relaxation
–Decreased TPR

  • S/Es: nifedipine –Increase SymNS activity; headache; dizziness; peripheral edema
  • Contraindications: Congestive heart failure; pregnancy and lactation; Post-myocardial infarction
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20
Q

Therapeutic Consideration for Calcium Channel Blockers

A
  • Verapamil- mainly cardiac; interactions w/ cardiac glycosides
  • Nifedipine- mainly arterioles
  • Diltiazem-both cardiac and arterioles at high doses, AV node block may occur;
  • Nifedipine may increase heart rate (reflex)
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21
Q

Vasodilators

A

hydralazine (Apresoline); minoxidil (Loniten); nitroprusside (Nipride); diazoxide (Hyperstat I.V.); fenoldopam (Corlopam)

•Site of action
–vascular smooth muscle

•MOA
–Systemic vascular vasodilation

  • hydralazine- alters intracellular calcium, increases nitric oxide in arterioles
  • minoxidil- opens K+ channels on arteriolar membranes, stabilizes membrane
  • nitroprusside- induces nitric oxide from endothelial cells (arterioles and veins)
  • diazoxide- opens K+ channels, stabilizes membrane (arterioles)

•fenoldopam- activates dopamine(D1) receptors on VSM (arterioles)
–Low doses dopamine stimulates primarily dopamine receptors- Vasodilation
–Higher doses- stimulates B1 receptors- positive inotropic effect
–Increases CO
–Also releases NE from vascular nerve terminals– vasoconstriction

22
Q

Vasodilators Effects, S/E, Therapeutic Considerations

A

•Effects on cardiovascular system
–vasodilation, decrease TPR

•S/E: reflex tachycardia, Increase SymNS activity (hydralazine, minoxidil,diazoxide), lupus (hydralazine), hypertrichosis (minoxidil), cyanide toxicity (nitroprusside)

•Therapeutic Considerations
–nitroprusside- iv only
–hydralazine- safe for pregnancy
–diazoxide- emergency use for severe hypertension

23
Q

Concerns in Rehab Patients Vasodilators

A
  • Side effects such as hypotension and orthostatic hypotension => caution with change posture or activities that may lower BP
  • Avoid or caution with activities that produce vasodilation esp. if vasodilating agents are used
  • Exercise may cause vasodilation in skeletal musculature which may potentiate the effect of vasodilation induced by alpha blockers, CCBs, or direct acting vasodilators
  • Stress the importance of compliance
  • Suggest nonpharmacologic methods of lowering blood pressure (stress management, relaxation techniques, exercise programs)
24
Q

Hyperlipidemia

A

•Hyperlipidemia, hyperlipoproteinemia, or dyslipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood

  • Lipids are insoluble in aqueous solution
  • Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism

•Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol, one of the most clinically relevant lipid substances, on artherosclerosis Additionally, some forms may predispose to acute pancreatitis

25
Q

Atherosclerosis

A
  • When excess cholesterol deposits on cells and on the inside walls of blood vessels it forms an atherosclerotic plaque
  • The first step of atherosclerosis is injury to the endothelium which results in atherosclerotic lesion formation
  • When the plaque ruptures, blood clots form which lead to decreased blood flow, resulting in cardiovascular events
26
Q

Complications of Hyperlipidemia

A

•Macrovascular complications
–Unstable angina (chest pain)
–Myocardial infarction (heart attack)
–Ischemic cerebrovascular disease (stroke)
–Coronary artery disease (heart disease)

•Microvascular complications
–Retinopathy (vision loss)
–Nephropathy (kidney disease)
–Neuropathy (loss of sensation in the feet and legs)

27
Q

Risk Factors for Hyperlipidemia

A
  • High fat intake
  • Obesity
  • Type 2 diabetes mellitus
  • Advanced age
  • Hypothyroidism
  • Obstructive liver disease
  • Genetics
  • Drug induced: glucocorticoids, thiazide diuretics, beta blockers, protease inhibitors, sirolimus, cyclosporine, progestins, alcohol
28
Q

Diagnosis Hyperlipidemia

A

•The fasting lipid profile (TC, LDL-C, HDL-C, TG) is analyzed

•The following individuals should be screened at least once every 5 years
–All adults 20 years and older should be screened at least once every 5 years
–Individuals with family history of premature cardiovascular disease should be screened more frequently

  • History and physical examination
  • An individual with a combination of lipid profile with history and physical exam will be treated accroding to the ATP III guideline
29
Q

Lipoprotein Level Classification

A

•LDL-C
–< 100mg/dL Optimal
–100-129mg/dL Near or above optimal
–130-159mg/dL Borderline high
–160-189mg/dL High
–> or = 190mg/dL Very high

•Total-C
–<200mg/dL Desirable
–200-239mg/dL Borderline high
–> or = 240mg/dL High

•TG-C
–<150mg/dL Optimal
–150-199mg/dL Borderline high
–200-499mg/dL High
–> or = 500mg/dL Very high

•HDL cholesterol
–<40mg/dL Low
–>60 or =60mg/dL High

30
Q

Treatment Goals Hyperlipidemia

A
  • Reduce total cholesterol and LDL (bad) cholesterol
  • Prevent the formation of atherosclerotic plaques and stop the progression of established plaques
  • Prevent heart disease
  • Prevent morbidity and mortality
31
Q

Non-Pharmacological Treatment Hyperlipidemia

A

•Lipid lowering therapy should be started with lifestyle modification for at least 12 weeks
–Increase physical activity
–Weight reduction
–Diet modification

32
Q

Pharmacological Treatment Hyperlipidemia

A

•If non-pharmacological treatment is not successful, a lipid-lowering drug should be started, especially in high risk populations

•1st step
–Initiate LDL-lowering drug therapy
–Start with statins, bile acid sequestrants, or nicotinic acid
–Evaluate after 6 wks

•2nd step
–If goal is not reached, intensive lipid-lowering treatment should be started
–Increase dose of statins
–Bile acid sequestrants, or nicotinic acid should be added
–Evaluate after 6 wks

•3rd step
–If goal is not reached, intensive lipid-lowering should be continued or individual should be referred to a lipid specialist
–If goal was reached, other lipid risk factors should be treated

•4th step
–Monitor response and compliance

33
Q

Pharmacological Treatment Hyperlipidemia Drug Names

A
  • Statins (HMG CoA Reductase Inhibitors)
  • Atorvastatin (Lipitor®)
  • Simvastatin (Zocor®)
  • Lovastatin (Mevacor®)
  • Pravastatin (Pravachol®)
  • Fluvastatin (Lescol®)
  • Rosuvastatin (Crestor®)
34
Q

Hyperlipidemia

Effectiveness of Statins

A
  • Reduce LDL cholesterol by 18-55%
  • Decrease TG by 7-30%
  • Raise HDL cholesterol by 5-15%
  • Statins are the most effective in lowering LDL cholesterol
  • Statins are the most effective in patient who has low HDL and high LDL
35
Q

Hyperlipidemia

Statins MOA, S/E

A

•MOA
–Statins inhibit HMG-CoA reductase (enzyme involved in cholesterol synthesis) thus decreasing mevalonic acid production and stimulating LDL breakdown

•S/Es: muscle aches, muscle break down leading to renal failure (rhabdomyolisis – caution when taken with fibric acids/niacin, increased liver enzymes, fatigue, HA, mild GI disturbances, rash

36
Q

Hyperlipidemia

Bile Acid Sequestrants

A

•Cholestyramine (Questran®), Colesevelam (Welchol®), Colestipol (Colestid®)

•MOA
–Bind to bile acids in the intestine, thus inhibits uptake of intestinal bile salts into the blood and increases the fecal loss of bile salt-bound LDL

•S/Es: stomach upset, constipation accompanied by heartburn, nausea, and bloating

•Effectiveness
–Reduces LDL cholesterol by 15-30%
–Increases HDL cholesterol by 3-5%
–Increases TG

37
Q

hyperlipidemia

Nicotinic Acid

A

•Niacin, Niacor, and Slo-niacin

•MOA
–Nicotinic acid decreases the clearance of ApoA1 to increase HDL; it inhibits the synthesis of VLDL

•Effectiveness
–Decreases LDL cholesterol by 5-25%
–Increases HDL cholesterol by 15-35%
–Decreases TG by 20-50%
–Most potent drug that increases HDL cholesterol

•S/Es: flushing, hyperglycemia, gout, liver toxicity, GI distress, muscle weakness

38
Q

Hyperlipidemia

Fibric Acids

A

•Gemfibrozil (Lopid®), Fenofibrate (Tricor®)

•MOA
–Up-regulates fatty acid transport protein and fatty acid oxidation; thus it reduces the formation of VLDL, increases formation of HDL, and enhances the breakdown of TG

•Effectiveness
–Reduces LDL cholesterol by 20-50% with normal TG
–Increases LDL cholesterol with high TG
–Reduces TG by 20-50%
–Increases HDL cholesterol by 10-20%
–Fibric acids are very effective in lowering TG and preventing pancreatitis
–Reduce VLDL but might increase LDL and total cholesterol

•S/Es: dyspepsia, gallstones, muscle ache, rash, weakness, tiredness, elevations in muscle enzymes

39
Q

Hyperlipidemia

Ezetimibe (Zetia®)

A

•MOA
–Inhibits absorption of cholesterol in the small intestine => decreases the delivery of cholesterol to the liver and increases the clearance of cholesterol from the blood

•Effectiveness
–Reduces LDL by 15-20%

•S/Es: chest pain, dizziness, diarrhea, abdominal pain

40
Q

Hyperlipidemia

Alternative Therapies

A

•Garlic- 6 out of 10 studies found garlic to be effective TC¯24.8mg/dl, LDL ¯15.3mg/dl & TG¯38mg/dl

Can not be recommended due to low methodological quality of studies.

•Omega 3 Fatty Acids- 10 studies found TC ¯11.6%, LDL¯32.5%, TG¯11.6%.
Not recommended to replace lipid lowering medications. Methodology of studies was weak

41
Q

Considerations in Rehabilitation Hyperlipidemia

A
  • Encourage compliance with pharmacologic and nonpharmacologic methods to lower plasma lipids
  • Help design and implement exercise programs that enable patients to lose weight and increase plasma levels of HDL => maximizing effects of drug therapy
42
Q

Angina Pectoris

A
  • Pain in the chest region resulting from myocardial ischemia => metabolic, electrophysiologic, and contractile changes in the heart (accumulation of lactic acid)
  • Sensation of intense compression and tightness in the retrosternal region, with pain radiating to the jaw or left arm
  • Precipitated by physical exertion but may occur at rest or sleep
43
Q

Antianginal Drugs

A

•Goal: restore or maintain the balance between myocardial oxygen supply and myocardial oxygen demand

•Two drug groups
–Decreases myocardial oxygen demand

•Organic Nitrates

•Beta blockers
–Increases myocardial oxygen supply

•CCBs: Calcium Channel Blockers

44
Q

Antianginal

Organic Nitrates

A

nitroglycerin (Nitrostat, Nitro-Bid, etc); isosorbide dinitrate (Imdur)

•MOA
–Dilate vascular smooth muscle
–Prodrugs (drug precursors) that get converted to nitrous oxide within vascular smooth muscle
–Decrease the amount of blood returning to the heart (preload) => decreased cardiac afterload => decrease in amount of work the heart needs to perform => decrease in myocardial oxygen demand

45
Q

Antianginal

Organic Nitrates Specfic Drugs and S/E

A

•Nitroglycerin
–Oral, buccal (ER), sublingual, ointment, patch
–Administered for both the prevention and the treatment of anginal attacks

•Isosorbide dinatrate
–Administered for both the prevention and the treatment of anginal attacks
–Anitanginal and hemodynamic effects last longer with isosorbide

•S/Es: HA, dizziness, and orthostatic hypotension, nausea

46
Q

Anti-anginal

Beta-adrenergic Blockers

A

•Antagonize beta-1 receptors on the myocardium => decrease HR and the force of myocardial contraction => decrease in the work by the heart => decrease myocardial oxygen demand

•Therapeutic consideration
–Nonselective beta blockers may induce bronchoconstriction in patients with asthma or similar respiratory problems => give these patients more cardioselective beta antagonists like atenolol or metoprolol

47
Q

anti-anginal

Calcium Channel Blockers MOA

A

•MOA
–Block the entry of calcium into vascular smooth muscle => relaxation and vasodilation => increase supply of oxygen to the myocardium
–Small degree of systemic vasodilation => decreased in myocardial oxygen demand => decreased in cardiac preload and afterload (similar to organic nitrates)
–Limit the entry of calcium into cardiac striated cells => decreasing myocardial contractility and oxygen demand
–Can also affect myocardial excitability by altering the conduction of electrical activity throughout the myocardium (more important for treatment of arrhythmias)

48
Q

Anti-anginal

Specific Agents

A

•Nondihydropyridines
–Diltiazem (Cardizem) – less S/Es than other CCBs

•Vasodilates the coronary arteries and peripheral vasculature

•Produces some depression of electrical conduction in the sinoatrial and artrioventricular nodes => slight bradycardia
–Verapamil (Calan, Isoptin)

  • Vasodilates coronary arteries
  • Moderately effective compared to other agents in treatment of angina

•Dihydropyridines
–Selective for vascular smooth muscle as compared to cardiac striated muscle
–Vasodilate the coronary arteries and peripheral vasculature without exerting any major effects on cardiac excitability or contractility

  • Nifedipine (Procardia)
  • Amlodipine (Norvasc)
49
Q

Treatment of Specific Types of Angina Pectoris

A
50
Q

Anti-Anginal

Special Concerns in Rehabilitation

A
  • Must be aware of patients who are taking medications for angina pectoris for prophylaxis or during the attack
  • Activities in rehab increase myocardial oxygen demand => anginal attacks may occur during the therapy session (make sure that patients bring nitroglycerin to therapy)
  • Be aware of the cardiac limitations in patients with angina and use caution in not overtaxing the heart
  • Some patients may experience an increase in exercise tolerance because they are not limited by symptoms of angina
  • Beta blockers and certain CCBs can blunt the ability of the heart to respond to an acute exercise bout by slowing down heart rate and decreasing myocardial contractility during exercise => adjust exercise workloads accordingly since the heart will not be able to handle some workloads
  • Nitrates and CCBs produce peripheral vasodilation => hypotension. Conditions that produce peripheral vasodilation, such as heat or exercise, may produce additive effect on the drug-induced hypotension => dizziness and syncope
51
Q
A

Pharmacology (12 decks)

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