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Cardiac Drugs Flashcards

1
Q

Drugs acting on the Renin-Angiotensin-Aldosterone System

A

-Angiotensin-converting enzyme inhibitors (ACE inhibitors)
-Angiotensin II receptor blockers (ARB)
-Direct Renin Inhibitors
-Aldosterone inhibitors

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2
Q

RAAS System

A

-Plays an important role in regulating blood pressure, blood volume, and fluid & electrolyte balance.
-Mediates certain pathophysiologic changes associated with HTN, heart failure and MI.

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3
Q

Angiotensin

A

-Precursor of Angiotensin II.
-Weak biological activity.

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4
Q

Angiotensin II

A

-Participates in all processes regulated by the RAAS.
-Prominent actions are vasoconstriction and stimulation of aldosterone.
-Raises blood pressure.
-Can act on the heart and cause pathologic changes in their structure and function.

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5
Q

-Vasoconstriction caused by Angiotensin II

A

-Acts directly on vascular smooth muscle to cause constriction.
-Prominent in arterioles and less so on veins.

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6
Q

Aldosterone

A

-Released from the adrenal cortex.
-Acts on distal tubules of the kidney to cause retention of sodium and excretion of potassium and hydrogen.
-Since sodium is retained so is water which increases blood volume.
-Regulates blood volume and blood pressure.

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7
Q

Angiotensin II

A

-Formed by renin and angiotensin-converting enzyme (ACE)
-More potent than angiotensin 1

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8
Q

Renin

A

-catalyzes the formation of angiotensin I from angiotensinogen.
-Produced from the juxtaglomerular cells of the kidney and undergoes controlled release into the bloodstream.

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9
Q

Angiotensin-converting enzyme

A

-Located on blood vessel surfaces and vasculature of the lungs.
-catalyzes the conversion of angiotensin I to angiotensin II.

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10
Q

Renin-angiotensin-aldosterone-system

A

-Helps regulate blood pressure in the presence of hemorrhage, dehydration, or sodium depletion.

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11
Q

Two basic processes of the RAAS raising blood pressure:

A

Acting through angiotensin II
1. Vasoconstriction
2. Renal retention of water and sodium

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12
Q

Angiotensin II acts in two ways in two ways to promote renal retention of water.

A

-Constricts renal blood vessels, angiotensin II reduces renal blood flow and thereby reduces glomerular filtration.
-Angiotensin II stimulates the release of aldosterone from the adrenal cortex. Aldosterone acts on the renal tubules to promote retention of sodium and water and the excretion of potassium.

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13
Q

ACE Inhibitors

A

-Used for treating hypertension, heart failure, diabetic neuropathy, and MI.
-Decrease levels of angiotensin II being produced.
-Increase levels of bradykinin (through inhibition of kinase II)

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14
Q

ACE Inhibitors

A

-Dilate blood vessels (primarily at the arterioles, and to a lesser extent veins)
-reduce blood volume through effects of the kidneys
-prevent or reverse pathologic changes in the heart and blood vessels mediated by angiotensin II and aldosterone.
-Can cause hyperkalemia

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15
Q

ACE inhibitors

A

-Increase bradykinin causes vasodilation.
-Given after an MI
-Drugs end in -pril

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16
Q

ACE inhibitor therapeutic uses

A

-Hypertension
-Heart failure
-Myocardial infarction-stops further deuteriation of vessels
-Diabetic and nondiabetic neuropathy
-Prevention of stroke, MI, and death of patients at high cardiovascular risk.

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17
Q

ACE inhibitors adverse effects

A

-First dose hypotension- risk for fall. Dizziness
-Fetal injury
-Cough caused by accumulation of bradykinin secondary to inhibition of kinase II.
-Angioedema- swelling in face. Stop immediately and do not take again.
-Hyperkalemia- interrupts normal process and holds onto potassium
-Dysgeusia (change in taste) and rash
-Renal failure- contraindicated for people with kidney issues. Bilateral renal artery stenosis.
-Neutropenia- associated with captopril
-Do not give to pregnant women

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18
Q

ACE inhibitors drug interactions

A

-Diuretics- may cause electrolyte issues.
-Antihypertensive agents
-Drugs that raise potassium levels- ACE inhibitors are potassium sparing.
-Lithium- can cause lithium to accumulate to toxic levels
-NSAIDS- may reduce antihypertensive effects

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19
Q

ACE inhibitor administration

A

-Administered orally, except enalapril can be given IV.
-Captopril (capoten) and Moexipril need to be administered with food.

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20
Q

ACE inhibitor drugs

A
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21
Q

Benazepril (Lotensin)

A

-Hypertension

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22
Q

Captopril (Capoten)

A

-Hypertension
-Heart failure
-LVD after MI
-Diabetic neuropathy
-Needs to be given one hour before meals

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23
Q

Enalapril (Vasotec)

A

-Hypertension
-Heart failure
-Asymptomatic LVD
-Can be given IV

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24
Q

Fosinopril

A

-Hypertension
-Heart failure

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25
Lisinopril (Prinivil, Zestril, Qbrelis)
-Hypertension -Heart failure -Acute MI
26
Moexipril
-Hypertension -Needs to be given one hour before meals
27
Perindopril (Aceon)
-Hypertension -Stable CAD
28
Quinapril (Accupril)
-Hypertension -Heart failure
29
Ramipril (Altace)
-Hypertension -Heart failure after MI -Prevention of MI, stroke, and death in people at high risk for cardiovascular disease
30
Trandolapril
-Hypertension -Heart failure after MI -LVD after MI
31
Angiotensin II Receptor Blockers (ARBs)
-Block actions of angiotensin II -Cause dilation of arterioles and veins -Prevent angiotensin II from inducing pathologic changes in cardiac structures -Reduce excretion of potassium -Decrease release of aldosterone -Increase renal excretion of sodium and water -Do not inhibit kinase II -Do not increase levels of bradykinin- does not cause cough like ACE inhibitors.
32
Angiotensin II receptor blockers (ARBs) therapeutic uses
-Hypertension -Heart failure -MI -Diabetic neuropathy -Give if someone is not able to tolerate ACE inhibitors
33
Angiotensin II receptor blockers (ARBs) adverse effects
-Angioedema- swelling in face -Fetal harm -Renal failure- not good for bilateral renal artery stenosis -Do not give to pregnant people
34
Angiotensin II receptor blocker administration
-Given PO -Can be given with or without food
35
Angiotensin II receptor blocking (ARBs) drugs
-End in -sartan
36
Azilsartan (Edarbi)
-Hypertension
37
Candesartan (Atacand)
-Hypertension -Heart failure
38
Irbesartan (Avapro)
-Hypertension -Heart diabetic neuropathy
39
Losartan (Cozaar)
-Hypertension -Stroke prevention -Diabetic neuropathy
40
Olmesartan ( Benicar)
-Hypertension
41
Telmisartan (Micardis)
-Hypertension -Prevention of MI, stroke, and death in people at high risk for cardiovascular disease but who cannot take ACE inhibitors
42
Valsartan (Diovan)
-Hypertension -Heart failure -MI
43
Direct Renin Inhibitors
-act on renin to inhibit the conversion of angiotensinogen into angiotensin I. -Decreasing production of angiotensin I, the entire RAAS system is suppressed.
44
Direct Renin Inhibitor drug Aliskiren (Tekturna)
-Binds tightly with renin and prevents the division of angiotensinogen to angiotensin I.
45
Aliskiren (Tekturna) side effects
-Angioedema -Cough -GI effects- dose dependent diarrhea -Hyperkalemia -Fetal injury
46
Aldosterone Antagonists
-Blocks effects of aldosterone
47
Aldosterone Antagonists Drug Eplerenone (Inspra)
-SELECTIVE blockade of aldosterone receptors -Therapeutic uses: Hypertension and heart failure. -Absorption is not affected by food -Adverse Effects: Hyperkalemia -Drug interactions: inhibitors of CYP3A4, drugs that raise potassium and lithium
48
Aldosterone Antagonists Drug Spironolactone (Aldactone)
-Blocks aldosterone receptors, binds with receptors for other steroid hormones. -Less selective than Eplerenone -Therapeutic uses: HTN, Heart failure -Adverse Effects: Hyperkalemia, Gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of the voice. -Given PO -Do not want to use potassium supplements or salt substitutes.
49
Calcium Channel Blockers
-Prevent calcium ions from entering cells
50
Physiologic Functions of calcium channel blockers
-Vascular smooth muscle: -calcium channels open=contractile process -calcium channels blocked=vasodilation. relaxes smooth muscle. So contraction is not as forceful. -Selectively on peripheral arterioles and arteries and arterioles of the heart. No significant effect on the veins.
51
Calcium effect on the heart
-Calcium increases force of contraction. If calcium channels are blocked contractile force diminish. -Pacemaker activity of the sinoatrial node. When calcium channels are open, spontaneous discharge of the SA node is increased. When channels are blocked, pacemaker activity declines. -Regulates the excitability of AV nodes.
52
2 classifications of calcium channel blockers
-Dihydropyridines- Nifedipine (Procardia) -Non-dihydropyridines-Verapamil and Diltiazem (Cardizem)
53
Sites of action
-Dihydropyridines act primarily on arterioles -Non-dihydropyridines act on arterioles and on the heart.
54
Non-dihydropyridines Verapamil (Calan)
-Blocks calcium channels in blood vessels. Act on vascular smooth muscle and the heart.
55
5 hemodynamic effects of Verapamil:
1. Blockade at peripheral arterioles causes dilation and thereby reduces arterial pressure. 2. Blockade at arteries and arterioles of the heart increases coronary profusion. Increases oxygen profusion. 3. Blockade at SA node reduces heart rate. 4. Blockade at AV node decreases AV nodal conduction. 5. Blockade in the myocardium decreases the force of contraction.
56
Indirect hemodynamic effect
-Baroreceptor reflex. Reflex tachycardia
57
Non-dihydropyridine Verapamil administration
-Given orally or IV. -When given orally, undergoes extensive metabolism on its first pass through the liver.
58
Verapamil therapeutic uses
-Angina pectoris- vasospastic angina and angina of effort. Benefits derive from vasodilation. -Essential hypertension- second line agent. Used after a thiazide diuretic. Lowers blood pressure by dilating arterioles. -Cardiac dysrhythmias- slows down ventricular rate in patients with atrial flutter, a fib, and paroxysmal supraventricular tachycardia. Benefits derive from suppressing impulse conduction through the AV node.
59
Verapamil adverse effects
-Constipation- results from blockade of calcium channels in smooth muscle of the intestines. Can be decreased by increasing dietary fiber and fluids. -Dizziness, facial flushing, headache, edema of ankles and feet secondary to vasodilation. -Gingival hyperplasia -Heart block- Not given to people with diagnosed heart block
60
Verapamil drug interactions
-Digoxin -Beta adrenergic blocking agents-same effects on the heart. Risk of excessive cardio suppression -Grapefruit juice
61
Verapamil toxicity
-Severe hypotension- treated by giving IV norepinephrine, which promotes vasoconstriction. -Bradycardia and AV block -Ventricular tachydysrhythmias
62
Non-dihydropyridines Diltiazem (Cardizem)
-Blocks calcium channels in the heart and blood vessels. -Lowers blood pressure by arteriolar dilation and direct suppressant/reflex cardiac stimulation.
63
Diltiazem (Cardizem) therapeutic use
-Angina Pectoris -Hypertension -Cardiac dysrhythmias- atrial flutter, a fib, paroxysmal tachycardia
64
Diltiazem (Cardizem) adverse effects
-Less constipation -Dizziness, flushing, headache, edema of ankles and feet due to vasodilation -Exacerbates bradycardia, sick sinus syndrome, heart failure, second or third degree heart block.
65
Diltiazem (Cardizem) drug interactions
-Digoxin -Beta adrenergic blocking agents
66
Dihydropyridines
-Act mainly on vascular smooth muscle -Significant blockade of calcium channels in blood vessels -Minimal blockade of calcium channels in the heart. -Drugs end in -pine
67
Dihydropyridines Nifedipine (Procardia)
-Vasodilation by blocking calcium channels -Blocks in vascular smooth muscle -CANNOT be used to treat dysrhythmias -Less likely to exacerbate pre-existing cardiac conditions
68
Nifedipine direct effects
-Limited to blockade of Ca channels in vascular smooth muscle -No direct suppressant effects on: automaticity, AV conduction, or contractile force
69
Nifedipine indirect effects
-Lowered blood pressure activates baroreceptor reflex -Primarily with fast-acting vs. sustained release
70
Vasodilation by blocking calcium channels net effect
-Lowers blood pressure -Increases heart rate -Increases contractile force
71
Nifedipine therapeutic uses
-Angina Pectoris -Hypertension
72
Nifedipine adverse effects
-Flushing -Headache -Peripheral edema -Gingival hyperplasia -Chronic eczematous rash in older patients -Reflex tachycardia- increases cardiac O2 demand -To prevent reflex tachycardia, can be combined with beta blocker.
73
Therapeutic uses of vasodilators
-Essential HTN -HTN crisis -Angina Pectoris -Heart failure -MI -Pheochromocytoma- -Peripheral vascular disease -Pulmonary arterial hypertension -Production of controlled hypotension during surgery
74
Adverse effects of vasodilators
-Postural hypotension -Reflex tachycardia -Expansion of blood volume
75
Hydralazine (Apresoline)
-Selective dilation of arterioles
76
Therapeutic uses of hydralazine
-Essential hypertension -Hypertensive crisis -Heart failure
77
Adverse effects of hydralazine
-Reflex tachycardia -Increased blood volume -Systemic lupus erythematosus-like syndrome -Headache, fatigue, dizziness, weakness- educate patients
78
Drug interactions with hydralazine
-Other antihypertensive agents -Combined with a beta blocker to protect against reflex tachycardia and diuretics to prevent sodium and water retention and expansion of blood volume.
79
Minoxidil (Loniten)
-Selective dilation of arterioles -More intense dilation than hydralazine, but more severe adverse reactions -Used for severe hypertension that is unresponsive to safer drugs
80
Minoxidil (Loniten) adverse effects
-Reflex tachycardia -Sodium and water retention -Hypertrichosis- hair growth -Pericardial effusion
81
Sodium Nitroprusside (Nitropress)
-Fast acting antihypertensive -Causes venous and arteriolar dilation -Used for hypertensive emergencies -Given by IV infusion- patient needs to be on a monitor.
82
Sodium Nitroprusside (Nitropress) adverse effects
-Excessive hypotension -Cyanide poisoning- metabolic breakdown -Thiocyanate toxicity
83
Two categories of HTN
-Primary (essential) hypertension -No identifiable cause -Chronic, progressive disorder -Population: older adults, african americans, mexican americans, postmenopausal women -Treated but not cured -Secondary hypertension -Identifiable primary cause -Possible to treat the cause directly -some individuals can be cured
84
Consequences of hypertension
-Heart disease -Myocardial infarction -heart failure -angina pectoris -Kidney disease -Stroke
85
Lifestyle considerations for hypertension
-Sodium restriction -DASH (dietary approaches to stop HTN) eating plan -Alcohol restriction -Aerobic exercise -Smoking cessation -Maintenance of sodium and potassium intake
86
Cardiac (Digitalis) Glycosides Digoxin (Lanoxin)
-Positive inotropic action on the heart -Increases the force of ventricular contraction -Increases myocardial contractility
87
Digoxin and potassium
-An increase in potassium can impair therapeutic response of digoxin, whereas a decrease in potassium can cause toxicity. -Potassium needs to be within therapeutic range-3.5-5 mEq/L
88
Digoxin (Lanoxin) adverse effects
Cardiac dysrythmias -Predisposing factors: -Hypokalemia secondary to diuretic use. -Elevated Digoxin levels -Heart disease
89
Digoxin (Lanoxin) non cardiac adverse effects
-Nausea -Vomiting -Anorexia -Fatigue -Visual disturbances
90
Therapeutic levels for digoxin
-Narrow therapeutic range- 0.5-0.8 mg/mL -Dige levels need to be drawn to make sure levels are within normal range
91
Management of digoxin induced dysrhythmias
-Withdraw digoxin and potassium wasting diuretics -Monitor serum potassium -Some patients may require and antidysrhythmic drug such as Phenytoin and lidocaine. -For overdose, administer Digifab IV
92
Golden Rule for Digoxin
-If heart rate is <60, notify provider and hold the drug.
93
Digoxin (Lanoxin) drug interactions
-Diuretics -ACE inhibitors and ARBs -Sympathomimetics -Quinidine -Verapamil
94
Digoxin (Lanoxin) administration
-Monitor heart when giving digoxin for the first time. -Given PO and IV -Eliminated by renal excretion -Half-life about 1.5 days- very strong drug
95
Angina
-Sudden pain beneath the sternum, often radiating to left shoulder and arm. -Oxygen supply to the heart is insufficient to meet oxygen demand
96
Three forms of angina pectoris
1. Chronic stable angina (exertional angina) 2. Variant angina (Prinzmetal or vasospastic angina) 3. Unstable angina
97
Organic Nitrates Nitroglycerin
--Acts on vascular smooth muscle and veins. Vasodilator. -Decreases the pain of exertional angina primarily by decreasing oxygen demand.
98
Nitroglycerin adverse effects
-Headache -Orthostatic hypotension -Reflex tachycardia
99
Nitroglycerin drug interactions
-Hypotensive drugs -Phophodiesterase type 5 inhibitors (Viagra)- tanks blood pressure -Beta blockers, calcium channel blockers-verapamil and diltiazem -Cannot take nitro and viagra together
100
Nitroglycerin preparations and routes of administration
-Sublingual tablets -Sustained release oral capsules -Transdermal delivery systems -Translingual spray -Topical ointment -IV infusion -Half-life=5-7 min -Nitro is light sensitive

Pharmacology (5 decks)

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