Nightingale Pharm: 22, 23, 24

Front 1

Types of Hyperlipidemia

Back 1

* hypercholesterolemia
* dyslipidemia

Front 2

Hypercholesterolemia

Back 2

elevated blood cholesterol

Front 3

Dyslipidemia

Back 3

abnormal levels of lipoproteins

Front 4

Lipoproteins

Back 4

*carriers of lipid molecules
*consist of cholesterol, triglycerides, and phospholipids with protein carrier
*protein carrier is known as apoprotein

Front 5

3 types of lipoproteins

Back 5

*high-density lipoproteins (HDL)
*low-density lipoproteins (LDL)
*very low-density lipoproteins (VLDL)

Front 6

LDL

Back 6

*trasports cholesterol from liver to tissues and organs
~used to build plasma membranes and synthesize other steroids
*carries highest amount of cholesterol
*known as bad cholesterol
~contributes to plaque deposits and coronary artery disease

Front 7

VLDL

Back 7

Primary carrier of triglycerides in blood

Front 8

HDL

Back 8

*manufactured in liver and small intestine
*reverse cholesterol transport
-assists in transport of cholesterol away from body tissues and back to liver
*known as good cholesterol
-transports cholesterol to the liver for destruction and removal from the body

Front 9

Lifestyle changes (cholesterol)

Back 9

*monitor blood-lipid level
*maintain weight; exercise
*reduce dietary saturated fats and cholesterol
*increase soluble fiber in diet
*reduce or eliminate tobacco use
*use of plant sterols and stanols

Front 10

HMG-CoA Reductase Inhibitors/Statins--Prototype drug:

Back 10

atorvastatin (Lipitor)

Front 11

HMG-CoA Reductase Inhibitors/Statins--mechanism of action:

Back 11

inhibits HMG-CoA reductase

Front 12

HMG-CoA Reductase Inhibitors/Statins--primary use:

Back 12

reduces serum-lipid levels

Front 13

HMG-CoA Reductase Inhibitors/Statins--Adverse effects:

Back 13

headache, fatigue, muscle or joint pain, and heartburn, rarely rhabdomyolsis--be very cautious with concurrent administration of other lipid lower agents such as Ketoconazole (Nizoral)

Front 14

Bile-Acid Resins--prototype drug:

Back 14

cholestyramine (Questran)

Front 15

Bile-Acid Resins--mechanism of action:

Back 15

bind with bile acids increasing cholesterol excretion in stool

Front 16

Bile-Acid Resins--primary use:

Back 16

to lower serum-lipid levels

Front 17

Bile-Acid Resins--adverse effects:

Back 17

GI tract-such as bloating and constipation
-can bind other drugs, increasing potential for drug interactions
-other drugs must be administered more than two hours before, or four hours after, because it can bind to other drugs and interfere with their absorption

Front 18

Nicotinic Acid--Prototype drug:

Back 18

niacin

Front 19

Nicotinic Acid--Mechanism of action:

Back 19

to decrease VLDL levels

Front 20

Nicotinic Acid--Primary use:

Back 20

to reduce triglycerides; increase HDL levels

Front 21

Nicotinic Acid--Adverse effects:

Back 21

flushing, hot flashes, nausea, excess gas, diarrhea; more serious effects like hepatotoxicity and gout possible

Front 22

Fibric-Acid Agents--Prototype drug:

Back 22

gemfibrozil (Lopid)

Front 23

Fibric-Acid Agents--Mechanism of action:

Back 23

unknown

Front 24

Fibric-Acid Agents--Primary use:

Back 24

treating severe hypertriglyceridemia

Front 25

Fibric-Acid Agents--Adverse effects:

Back 25

GI distress, watch for bleeding with clients on anticoagulants

Front 26

Fibric-Acid Agents--Patient education:

Back 26

Take with food to decrease GI upset and increase compliance

Front 27

Fibric-Acid Agents

Back 27

Pregnancy Category B

Front 28

HMG-CoA Reductase Inhibitors/Statins==*Prototype drug: atorvastatin (Lipitor)

Back 28

Pregnancy Category X

Front 29

HMG-CoA Reductase Inhibitors/Statins==*Prototype drug: atorvastatin (Lipitor)

Back 29

Administer with food to decrease GI discomfort, at any time of the day

Front 30

Bile-Acid Resins==*prototype drug: cholestyramine (Questran)

Back 30

Pregnancy category C
mix with liquid and drink immediately to avoid obstruction of GI tract. Give other drugs 2 hours before or 4 hours after

Front 31

Cholesterol Absorption Inhibitor Prototype drug:

Back 31

ezetimibe (Zetia)

Front 32

Cholesterol Absorption Inhibitor--Mechanism of action:

Back 32

inhibits absorption of cholesterol

Front 33

Cholesterol Absorption Inhibitor--Primary use:

Back 33

modest reduction in LDL

Front 34

Cholesterol Absorption Inhibitor--Adverse effects:

Back 34

No serious side effects

Front 35

Statins

Back 35

Interfere with the synthesis of cholesterol
First drugs of choice to reduce blood-lipid levels- inhibit the making of cholesterol by inhibiting HMG-CoA reductase which is necessary for the biosynthesis of cholesterol
Examples: Lescol, Mevacor, Crestor, Zocar

Front 36

Bile Acid–Binding Resins

Back 36

Bind with bile acids to increase excretion of cholesterol in stool-keep cholesterol from being absorbed
Used in combination with statins
Examples: Welchol, Colestid

Front 37

Nicotinic Acid (Niacin)

Back 37

B-complex vitamin
Decreases VLDL and LDL levels

Front 38

Fibric-Acid Agents

Back 38

Drugs of choice for treating severe hypertriglyceridemia
Examples: Atromid-S, Tricor

Front 39

Cholesterol-Absorption Inhibitor

Back 39

New class of drug
Inhibits the absorption of cholesterol
Example: ezetimibe (Zetia)

Front 40

Role of Nurse

Back 40

Monitor client’s condition
Provide education on prescribed medications
Assess client’s triglyceride, total cholesterol, LDL, and HDL levels

Front 41

Statins

Back 41

Monitor liver-function tests and urine output
Contents of muscle cells spill into the systemic circulation causing potentially fatal, acute renal failure.
Urine output of less than 30 ml/hour is considered renal failure
Do not use with pregnancy or breast-feeding
Watch for signs of GI upset
Assess for complaints of muscle pain, tenderness, and weakness as this could indicate a type of myopathy know as rhabdomyolysis- comments such as calf pain or difficulty walking

Front 42

Bile-Acid Resins

Back 42

Monitor for significant GI effects
Assess bowel sounds because they can cause obstruction of the intestines.

Obtain careful history for past GI disorders

Front 43

Nicotinic Acid (Niacin)

Back 43

Monitor client’s liver function
Monitor uric-acid levels, if predisposed to gout
Monitor blood-sugar levels, if diabetic

Taking an aspirin tablet thirty minutes prior to niacin administration can reduce uncomfortable flushing because aspirin decreases the prostaglandin release that may cause a flushing effect

Front 44

Fibric-Acid Agents

Back 44

Assess for complaints of GI distress before starting drug.
Use with warfarin may potentiate anticoagulant effects
Monitor prothrombin time/international normalized ration (PT/INR)

Front 45

Drugs for Lipid Disorders

Back 45

Assessment
*Obtain blood samples
*Assess laboratory tests: triglyceride, total cholesterol, LDL, HDL levels
*Collect client’s height and weight
*Obtain nursing history: lifestyle, current drugs, dietary habits
*Assess client’s and family’s knowledge
Evaluation:
-Ideal outcome criteria
*Lowered serum-lipid levels
*No organ damage, no injury
*Client verbalizes importance of prescribed medications

Front 46

Cardiovascular Disease (CVD)

Back 46

Includes conditions of heart and blood vessels
Hypertension is most common form of CVD
Most frequent causes of death in U.S

Front 47

Hypertension: Classified into Three Categories

Back 47

~~Consistent elevation of systemic arterial blood pressure
*“Normal” B/P at one age; abnormal as we age
~~Three categories
*Prehypertension
*Stage 1
*Stage 2
*Be sure to review what the B/P ranges are for each category

Front 48

Three Factors Responsible for Blood Pressure

Back 48

Cardiac output
Peripheral resistance
Blood volume

Front 49

Blood Volume

Back 49

*Total amount of blood in vascular system
*Increased blood volume increases blood pressure
*Medications that affect blood volume may lower or raise B/P
~~diuretics

Front 50

Central and Autonomic Nervous Systems

Back 50

*Regulate blood pressure
~~Vasomotor center
~~Baroreceptors
The aorta and internal carotid artery have baroreceptors that sense changes in pressure in blood vessels and chemoreceptors that detect oxygen, carbon dioxide, and pH levels
~~Chemoreceptors
recognizes levels of oxygen, carbon dioxide, and pH levels. (p. 298)

Front 51

Emotions Affect Blood Pressure

Back 51

Stress and anger increase
Depression and lethargy decrease

Front 52

Hormones

Back 52

*Affect blood pressure
*Natural hormones affect blood pressure daily
~~~Epinephrine and norepinephrine injections raise B/P
~~~Antidiuretic hormone (ADH) raises B/P by raising blood volume
*Renin-angiotensin-aldosterone system

Front 53

Target Organs Affected by Untreated Hypertension

Back 53

Heart
Brain
Kidneys
Retina

Front 54

Disease Progression Related to Organs Affected

Back 54

*Heart failure
~~Hypertension causes resistance in blood vessels, or afterload; causing the heart to work harder, and weakens
~~The most common cause of increased afterload is an increase in peripheral resistance due to hypertension.
~~Afterload refers to peripheral resistance, not to the amount of blood entering the left ventricle.
~~The ability of the heart to stretch before entering is known as preload
*TIA and/or cerebral vascular accident
*Renal failure
*Visual impairment and blindness

Front 55

Nonpharmacologic Methods to Control Hypertension

Back 55

*Limit alcohol usage
*Restrict sodium consumption
*Reduce saturated fat and cholesterol; increase fresh fruit and vegetable intake
*Increase aerobic physical activity
*Discontinue tobacco use
*Reduce stress
*Maintain optimum weight – what is a normal BMI?

Front 56

Phamacologic Management of Hypertension

Back 56

*Individualized to patient’s risk factors, medical conditions, degree of blood pressure elevation
*Clinician experience plays role in choice of therapy

Front 57

Primary Antihypertensive Agents

Back 57

*Primary Antihypertensive Agents
~~Diuretics
~~Angiotensin-converting enzyme (ACE) inhibitors
~~Angiotensin II receptor blockers
~~Beta-adrenergic antagonists
~~Calcium channel blockers
~~Prescribing two antihypertensives results in additive or synergistic blood pressure reduction

Front 58

Secondary Antihypertensive Agents

Back 58

Alpha1-adrenergic antagonist
Alpha2-adrenergic agonists
Direct-acting vasodilators
Peripheral adrenergic antagonists

Front 59

Assessment of Client’s Lifestyle

Back 59

Dietary habits
Exercise or activity regimen
Use of medication

Front 60

Factors That Can Help Control Blood Pressure

Back 60

Losing weight
Limiting foods high in fat and sodium
Limiting use of tobacco and alcohol
Beginning an exercise program

Front 61

Role of Nurse

Back 61

Obtain complete health history
Obtain vital signs
Physical examination
Obtain blood and urine specimens for analysis

Front 62

Key Assessment and Monitoring Points for Nonpotassium-Sparing Diuretics

Back 62

*Orthostatic hypotension
*Laboratory electrolyte values, especially potassium level, and daily weights
*Intake and output assessment of edema and signs of fluid overload

Front 63

Key Assessment and Monitoring Points for Nonpotassium-Sparing Diuretics (continued)

Back 63

Client’s ability to safely ambulate
Photosensitivity
Possible need to increase potassium in diet or with supplements
Hypokalemia caused may increase digoxin (Lanoxin) toxicity.
What is the normal K+ range?

Front 64

Key Assessment and Monitoring Points for Potassium-Sparing Diuretics

Back 64

Use of salt substitutes and potassium-rich foods
Use in pregnant and lactating women
History of gout and kidney stones
Uric-acid levels
Gynecomastia and hirsutism for spironolactone (Aldactone)

Front 65

Key Assessment and Monitoring Points for Thiazide-like Diuretics

Back 65

Laboratory values (CBC, electrolytes, chemistry panel)
Blood-glucose and uric-acid levels
Possible need to increase potassium in diet or with supplements
Pregnancy and lactation, systemic lupus erythematosus, and use of digoxin

Front 66

Key Assessment and Monitoring Points for Loop Diuretics

Back 66

Severe potassium loss
Hypokalemia
Hypotension
Hearing loss (these drugs are ototoxic)
Glucose and uric-acid levels

Front 67

Key Assessment and Monitoring Points for CCBs (continued)

Back 67

Obtain ECG, heart rate, and B/P prior to therapy
During therapy, monitor heart rate and B/P regularly
Some calcium channel blockers can reduce myocardial contractility and can worsen heart failure.
Crackles in the lungs can indicate pulmonary edema which could indicate heart failure
*Auscultate breath sounds for crackles – priority assessment*
Health history specific for heart dysrhythmias and pregnancy
Signs of CHF and reflex tachycardia

Front 68

Key Assessment and Monitoring Points for CCBs (continued)

Back 68

IV administration, special concern
Dizziness, headache, flushing are minor side effects
Avoid drinking grapefruit juice

Front 69

Key Assessment and Monitoring Points for Renin-Angiotensins

Back 69

Baseline vital signs
Hypotension
Angioedema
Neutropenia or agranulocytosis

Front 70

Key Assessment and Monitoring Points for Renin-Angiotensins (continued)

Back 70

Hypokalemia
Dizziness, light-headedness, headache
Tickling, nonproductive cough
Pregnancy-risk category D

Front 71

Key Assessment and Monitoring Points for Adrenergic Antagonists

Back 71

Baseline vital signs, B/P response
Hold medication for pulse below 60 and B/P below 90/60 mm/Hg
ECG, heart rate and rhythm
Watch for heart block and rebound hypertension

Front 72

Key Assessment and Monitoring Points for Adrenergic Antagonists (continued)

Back 72

Routine blood-glucose monitoring for diabetics
Alpha1, alpha2, and beta-blocker specific effects
Pregnancy-risk categories B and C
Use with caution in clients with asthma
With increased doses, beta-adrenergic blockers can slow the heart rate and cause bronchoconstriction

Front 73

Key Assessment and Monitoring Points for Direct Vasodilators

Back 73

In emergency: monitor V/S, ECG, and pulse oximetry continuously
Can produce reflex tachycardia, a compensatory response to the sudden decrease in blood pressure caused by the drug.
Can produce hypotension and tachycardia,
Contraindicated for
Hypersensitivity, coronary artery disease
Rheumatic mitral-valve disease, cerebrovascular disease
Renal insufficiency, systemic lupus erythematosus

Front 74

Key Assessment and Monitoring Points for Direct Vasodilators (continued)

Back 74

Priapism
IV diazoxide: monitor sodium and water output
Minoxidil (Loniten): monitor for orthohypotension

Front 75

Key Assessment and Monitoring Points for Direct Vasodilators (continued)

Back 75

Nitroprusside IV
Can be used for hypertensive emergencies during labor and delivery
Can lower blood pressure instantaneously
Half-life of only 2 minute
Overtreatment can result in hypotension and severe restriction of blood flow to cerebral, coronary, or renal vascular capillaries

Front 76

Diuretics--Prototype drug:

Back 76

hydrochlorothiazide (Microzide).

Front 77

Diuretics--Mechanism of action:

Back 77

to increase amount of urine produced and excreted, decrease blood pressure by decreasing total blood volume.

Front 78

Diuretics--Primary use:

Back 78

for mild to moderate hypertension

Front 79

Diuretics--Adverse effects:

Back 79

electrolyte imbalances, especially loss of potassium
What are normal potassium levels?

Front 80

Calcium Channel Blockers--Prototype drug:

Back 80

nifedipine (Procardia)

Front 81

Calcium Channel Blockers-Mechanism of action:

Back 81

block calcium ion channels; cause vasodilation, decreasing B/P

Front 82

Calcium Channel Blockers-Primary use:

Back 82

for hypertension and angina

Front 83

Calcium Channel Blockers--Adverse effects:

Back 83

include dizziness, headache, flushing

Some calcium channel blockers can reduce myocardial contractility and can worsen heart failure. Crackles in the lungs can indicate pulmonary edema which could indicate heart failure

Front 84

Drugs Affecting Renin-Angiotensin System==Angiotensin-converting enzyme (ACE) inhibitors--Prototype drug:

Back 84

enalapril (Vasotec)

Front 85

Drugs Affecting Renin-Angiotensin System==Angiotensin-converting enzyme (ACE) inhibitors--Mechanism of action:

Back 85

block effects of angiotensin II, lowering peripheral resistance and decreasing blood volume

Front 86

Drugs Affecting Renin-Angiotensin System==Angiotensin-converting enzyme (ACE) inhibitors--Primary use:

Back 86

for hypertension

Front 87

Drugs Affecting Renin-Angiotensin System==Angiotensin-converting enzyme (ACE) inhibitors--Adverse effects:

Back 87

persistent cough and hypotension, hyperkalemia

Front 88

Drugs Affecting Renin-Angiotensin System==Angiotensin-converting enzyme (ACE) inhibitors--Nursing assessment:

Back 88

monitor b/p (first dose effect of hypotension - first-dose phenomenon), this can result in syncope

Front 89

Drugs Affecting Renin-Angiotensin System==Angiotensin-receptor blockers (ARBs)--Prototype drug:

Back 89

losartan potassium (Cozaar)

Front 90

Drugs Affecting Renin-Angiotensin System==Angiotensin-receptor blockers (ARBs)--Mechanism of action:

Back 90

to block angiotensin receptors in arterial smooth muscle and adrenal glands

Front 91

Drugs Affecting Renin-Angiotensin System==Angiotensin-receptor blockers (ARBs)--Primary use:

Back 91

for hypertension

Front 92

Drugs Affecting Renin-Angiotensin System==Angiotensin-receptor blockers (ARBs)--Adverse effect:

Back 92

hypotension

Front 93

Beta-Adrenergic Blockers--Prototype Drugs:

Back 93

metoprolol (Lopressor, Tropol); atenolol (Tenormin); propranolol (Inderal); Timolol (Timoptic)

Front 94

Beta-Adrenergic Blockers--Mechanism of action:

Back 94

decrease heart rate and contractility; blockade beta1-receptors in juxtaglomerular apparatus

Front 95

Beta-Adrenergic Blockers--Primary use:

Back 95

hypertension
Other uses: ease angina pectoris symptoms; treat dysryhthmias, treat heart failure, migraines

Front 96

Beta-Adrenergic Blockers--Adverse effects:

Back 96

fatigue, decreased libido, erectile dysfunction

Front 97

Alpha1-Adrenergic Antagonists--Prototype drug:

Back 97

doxazosin (Cardura)

Front 98

Alpha1-Adrenergic Antagonists--Mechanism of action:

Back 98

selective for blocking alpha1-receptors in vascular smooth muscle, which results in dilation of arteries and veins

Front 99

Alpha1-Adrenergic Antagonists--Primary use:

Back 99

hypertension

Front 100

Alpha1-Adrenergic Antagonists--Adverse effects:

Back 100

orthostatic hypotension, dizziness, nausea, nervousness, fatigue

Front 101

Alpha2-Adrenergic Agonists--Drugs:

Back 101

Clonidine (Catapres); methyldopa (Aldomet)

Front 102

Alpha2-Adrenergic Agonists--Mechanism of action:

Back 102

decrease outflow of sympathetic nerve impulses from CNS to heart and arterioles

Front 103

Alpha2-Adrenergic Agonists--Primary use:

Back 103

hypertension

Front 104

Alpha2-Adrenergic Agonists--Adverse effects:

Back 104

sedation, dizziness, abnormalities in sexual function

Front 105

Direct Vasodilators--Prototype drug:

Back 105

hydralazine (Apresoline)

Front 106

Direct Vasodilators--Mechanism of action:

Back 106

to cause vasodilation by direct relaxation of arterial smooth muscle

Front 107

Direct Vasodilators--Primary use:

Back 107

for severe hypertension and hypertension crisis

Front 108

Direct Vasodilators--Adverse effects:

Back 108

reflex tachycardia, hypotension, sodium and fluid retention

Front 109

Drugs for Hypertension

Back 109

Assessment
Take client’s B/P in each arm for baseline
Assess client’s height and weight
Obtain blood and urine samples as ordered by physician
Obtain nursing history, including lifestyle, current medications, dietary habits
Assess client’s and family’s knowledge of hypertension and medication regimen

Front 110

Drugs for Hypertension (continued)

Back 110

Planning
Goals
Exhibit a reduction in systolic/diastolic blood pressure
Client is able to explain hypertension and needed medications
Client is able to verbalize ability to follow prescribed therapy

What treatment regimen would you expect for a patient with secondary hypertension?

Hint refer to page 297

Front 111

Drugs for Heart Failure

Back 111

Treat symptoms
Slow heart rate
Increase contractility
Reduce heart workload

Be sure to review the types of heart failure and symptoms – think patient teaching.

Front 112

Nurse’s Role—ACE Inhibitors

Back 112

Monitor CBC
Assess for hypotension
Monitor for impaired kidney function, hyperkalemia, autoimmune disease

Front 113

Client Teaching--Nurse’s Role—ACE Inhibitors

Back 113

Therapeutic response time: weeks or months
Sodium and potassium restrictions
Don’t use with other medications, OTCs, herbals, vitamins

Front 114

Nurse’s Role—Diuretics

Back 114

Assess renal function
Monitor electrolyte levels
Monitor vital signs, intake/output
Monitor blood glucose and blood-urea nitrogen (BUN)

Front 115

Client Teaching--Nurse’s Role—Diuretics

Back 115

Monitor sodium intake
Report weight loss
Report fatigue and muscle cramps
Change position slowly

Front 116

Beta-Adrenergic Blockers (Antagonists)

Back 116

Monitor for worsening symptoms
Monitor liver function/hepatic toxicity
Be aware of contraindications

Front 117

Client Teaching--Beta-Adrenergic Blockers (Antagonists)

Back 117

Monitor blood pressure/pulse
Report pulse below 50
Report signs/symptoms of worsening heart failure
Do not stop taking abruptly

Front 118

Cardiac Glycosides

Back 118

Evaluate for ventricular dysrhythmias
Assess renal function
Monitor for drug interactions
Know restriction on use with antidiarrheals/antacids

Front 119

Client Teaching--Cardiac Glycosides

Back 119

Monitor therapeutic levels with laboratory tests
Know signs/symptoms of toxicity
Monitor pulse rate
Report weight gain
Eat foods high in potassium

Front 120

Phosphodiesterase Inhibitors

Back 120

Assess potassium levels
Monitor for hypotension
Assess for renal impairment
Assess for dysrhythmias

Front 121

IV Phosphodiesterase Inhibitors

Back 121

Monitor for ventricular dysrhythmias

Front 122

Client Teaching--Phosphodiesterase Inhibitors

Back 122

Report irregular or rapid heart rate
Report fever of 101 degrees or higher or increase in chest pain
If given IV, report fever of 101 degrees or higher or pain/swelling at infusion site

Front 123

ACE Inhibitors--Prototype drug:

Back 123

lisinopril (Prinivil, Zestril)

Front 124

ACE Inhibitors--Mechanism of action:

Back 124

to enhance excretion of sodium and water. This is by lowering the secretion of aldosterone from the adrenal cortex. Aldosterone normally increases the reabsorption of sodium and water

Front 125

ACE Inhibitors
Primary use:

Back 125

to decrease blood pressure and reduce blood volume; dilate veins

Front 126

ACE Inhibitors--Adverse effects:

Back 126

first-dose hypotension, cough, hyperkalemia, renal failure

Severe hypotension, known as first-dose phenomenon; can occur after the initial administration of enalapril (Vasotec)

Front 127

Diuretics (CH. 23)--Prototype drug:

Back 127

furosemide (Lasix)

Front 128

Diuretics (CH. 23)--Mechanism of action:

Back 128

to increase urine flow, reducing blood volume and cardiac workload

Front 129

Diuretics (CH. 23)--Primary use:

Back 129

to reduce edema and pulmonary congestion

Front 130

Diuretics (CH. 23)--Adverse effects:

Back 130

dehydration, electrolyte imbalance, hypotension, ototoxicity

Front 131

Cardiac Glycosides--Prototype drug:

Back 131

digoxin (Lanoxin)

Front 132

Cardiac Glycosides--Mechanism of action:

Back 132

to cause more forceful heartbeat, slower heart rate

Front 133

Cardiac Glycosides--Primary use:

Back 133

to increase contractility or strength of myocardial contraction

Front 134

Cardiac Glycosides--Patient education:

Back 134

Report a weight gain of 2 or more pounds per day, this could indicate worsening of heart failure

Front 135

Cardiac Glycosides--Adverse effects:

Back 135

neutropenia, dysrhythmias, digitalis toxicity – what are the signs and sx ?
If used in conjunction with lasix what lab values is imperative to monitor and why?

Front 136

Beta-Adrenergic Blockers (Ch 23)--Prototype drug:

Back 136

Metoprolol (Lopressor, Troprol XL)

Front 137

Beta-Adrenergic Blockers (Ch 23)--Mechanism of action:

Back 137

block cardiac action of sympathetic nervous system to slow heart rate and B/P, reducing workload of heart

Front 138

Beta-Adrenergic Blockers (Ch 23)--Primary use:

Back 138

to reduce symptoms of heart failure and slow progression of disease

Front 139

Beta-Adrenergic Blockers (Ch 23)--Adverse effects:

Back 139

fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block
may enhance the hypoglycemic effects of insulin and oral hypoglycemic agents, so the client might require less insulin

Front 140

Vasodilators--Drugs:

Back 140

hydralazine (Apresoline); (isosorbide dinitrate (Isordil)

Front 141

Vasodilators--Mechanism of action:

Back 141

to relax blood vessels

Front 142

Vasodilators--Primary use:

Back 142

to lower blood pressure
Used for clients who cannot take ACE inhibitors

Front 143

Vasodilators--Patient education:

Back 143

if taken SL the pt should avoid talking or drinking while it is dissolving

Front 144

Vasodilators--Adverse reactions:

Back 144

reflex tachycardia, orthostatic hypotension

Front 145

Phosphodiesterase Inhibitors--Prototype drug:

Back 145

milrinone (Primacor)

Front 146

Phosphodiesterase Inhibitors--Mechanism of action:

Back 146

to block enzyme phosphodiesterase in cardiac and smooth muscle

Front 147

Phosphodiesterase Inhibitors--Primary use:

Back 147

as short-term therapy for heart failure

Front 148

Phosphodiesterase Inhibitors--Adverse effects:

Back 148

hypokalemia, hypotension, ventricular dysrhythmias (most serious adverse effect)
The client’s ECG is usually monitored continuously during the infusion of milrinone (Primacor). Vital signs should be assessed continuously

Front 149

ACE Inhibitors

Back 149

Reduce afterload
Drug of choice for heart failure
Enhance excretion of sodium and water
Lowers peripheral resistance and reduces blood volume
Increases cardiac output
Examples:
Lisinopril (Prinivil, Zestril)
Captopril (Capoten)
Enalapril (Vasotec)

Front 150

Diuretics

Back 150

Increase urine flow
Reduce blood volume and cardiac workload
Examples:
Bumetanide (Bumex) and furosemide (Lasix)—loop diuretics
hydrochlorothiazide (Microzide)—thiazide diuretic
Spironolactone (Aldactone)—potassium-sparing diuretic

Reduce edema and pulmonary congestion
Prescribed in combination with other drugs

Front 151

Beta-Adrenergic Blockers

Back 151

Slow heart rate and reduce blood pressure
Inotropic effect
Reduce workload of heart
Examples:
Carvedilol (Coreg)
Metoprolol extended release (Toprol-XL)

Front 152

Vasodilators

Back 152

Minor role in heart-failure treatment
Lower blood pressure
Relax blood vessels
Examples:
Hydralazine with isosorbide dinitrate (BiDil)
Nesiritide (Natrecor)

Front 153

Cardiac glycosides

Back 153

Increase force of heartbeat, slow heart rate
Improve cardiac output
Second-line treatment for HF
Anorexia and nausea are common adverse effects
Examples:
Digoxin (Digitek, Lanoxin, Lanoxicaps)

Front 154

Phosphodiesterase Inhibitors

Back 154

Block enzyme phosphodiesterase
Increase calcium for myocardial contraction
Cause positive inotropic response and vasodilation
Increase contractility and decrease afterload
Short-term therapy only
Examples:
Inamrinone (Inocor)
Milrinone (Primacor)

Front 155

Drug Therapy for Heart Failure--Assessment:

Back 155

Complete health history, vital signs, urinary output
Cardiac output
Reason for medication
Client’s knowledge

Front 156

Drug Therapy for Heart Failure--Nursing Diagnoses:

Back 156

Ineffective tissue perfusion
Decreased cardiac output
Excess fluid volume
Deficient knowledge

Front 157

Drug Therapy for Heart Failure--Planning:

Back 157

Client Goals and Expected Outcomes
Decreased symptoms
Improved organ function
Understanding of drug therapy
Reporting drug side effects

Front 158

Drug Therapy for Heart Failure--Implementation

Back 158

Monitor ECG
Observe for side effects
Obtain daily weight
Monitor serum-drug levels
Observe for signs of toxicity
Monitor electrolyte levels

Front 159

Drug Therapy for Heart Failure--Evaluation of effectiveness of drug therapy

Back 159

Goals met
Expected outcomes met

Front 160

HDL range

Back 160

40-60 mg/dL

Front 161

LDL range

Back 161

Optimal=Less than 100 mg/dL
borderline high=130-159 mg/dL
Very High=greater than 190 mg/dL

Front 162

Total Cholesterol range

Back 162

~Adults~
Desirable=less than 200 mg/dL
Borderline=200-239 mg/dL
High=greater than 240 mg/dL

Front 163

Digoxin level

Back 163

0.5 and 2 ng per mL.

Front 164

Potassium range

Back 164

3.6-5.4 mEq/liter

Front 165

Magnesium range

Back 165

more than 1.7 mEq

Front 166

Sodium range

Back 166

136-143 mEq/liter

Front 167

calcium range

Back 167

8.5-10.5 mg/dL

Front 168

Chloride range

Back 168

98-108 mmol/liter

Front 169

Carbon dioxide range

Back 169

22-31 mmol/liter

Front 170

BUN range

Back 170

8-22 mg/dL

Front 171

Creatinine range

Back 171

0.6-1.3 mg/dL

Front 172

blood glucose range

Back 172

67-125 mg/dL

Front 173

albumin range

Back 173

3.4-5 g/dL

Front 174

AST (Aspartate aminotransferase) range

Back 174

5-38 IU/liter

Front 175

ALT (Alanine aminotransferase) range

Back 175

7-50 IU/liter

Front 176

Triglycerides range

Back 176

Normal: less than 150
Borderline high: 150-199
High risk: 200-499
Very high risk: less than 500

Front 177

INR range

Back 177

2.0-3.0

Front 178

aPTT range

Back 178

21 – 35 seconds

Front 179

HCT (hematocrit) range

Back 179

34-54

Front 180

HGB (hemoglobin) range

Back 180

11-18

Front 181

RBC

Back 181

3.8-5.6

Front 182

PT range

Back 182

10 – 14 seconds

Front 183

troponin I range

Back 183

0 – 0.1 ng/ml (onset: 4-6 hrs, peak:
12-24 hrs, return to normal: 4-7 days)

Front 184

troponin T range

Back 184

0 – 0.2 ng/ml (onset: 3-4 hrs, peak:
10-24 hrs, return to normal: 10-14 days)

Front 185

myoglobin (Male) range

Back 185

10 – 95 ng/ml (onset: 1-3 hrs, peak:
6-10 hrs, return to normal: 12-24 hrs)

Front 186

myoglobin (Female) range

Back 186

10 – 65 ng/ml (onset: 1-3 hrs, peak:
6-10 hrs, return to normal: 12-24 hrs)

Front 187

Effects of Hypertension

Back 187

systolic >140
diastolic >90
cardiovascular disease risk starts at 115/75 mmHg and doubles with each additional increment of 20/10
artery damage/narrowing: kidney failure, stroke, peripheral artery disease, eye damage aneurysms, chest pain, heart attack, heart failure, CAD,

Front 188

What should be monitored in Milrinone?

Back 188

cardiac monitor should be on at all times!!

Front 189

Side effects of ace inhibitors

Back 189

headache, dizziness, orthostatic hypotension, cough
SEVERE HYPOTENSION (FIRST DOSE PHENOMENON), SYNCOPE, ANGIOEDEMA, BLOOD DYSCRASIAS

Front 190

Medications that increase myocardial contractility

Back 190

Digoxin (Digitek, Lanoxin, Lanoxicaps), Milinone (Primacor)

Front 191

How beta-blockers affect blood glucose

Back 191

a patient with DM taking a Beta-blocker may hide some of the warning signs of low blood sugar because the heart rate might not increase like it normally would with low BS.

Front 192

safety factors for combination of amiodarone and digoxin

Back 192

monitor serum levels and decrease digoxin dose by 50% because amiodarone can increase effect of digoxin

Front 193

Treatment of paroxysmal supraventricular tachycardia

Back 193

*Calcium channel blockers such as verapamil, diltiazem, adenosine
*Beta-blockers such as metoprolol or esmolol.