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Pharmacology > Week 6 power points > Flashcards

Week 6 power points Flashcards

1
Q

Four Factors That Affect Cardiac Performance

A

Preload
Afterload
Heart Rate
Contractility

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2
Q

Cardiac Output

A

Volume of blood flowing through either the systemic or the pulmonary circuit per minute = L/min

HR x SV = CO

Normal = 5L/min

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3
Q

Coronary Artery Disease (CAD)

A
  • Progressive growth of atheromatous plaques, in the coronary arteries
  • Injure the endothelial lining of the artery, causing an inflammatory reaction.
  • Triggers development of larger plaques containing foam cells, platelets, fribrin, fats, that collect on the vessel lining.
  • Limits blood flow.
  • These plaques can rupture.
  • Increased incidence among people with high serum lipid levels
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4
Q

Unmodifiable Risk Factors for CAD

A

Genetic predisposition
Age
Gender

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5
Q

Modifiable Risk Factors for CAD

A 
Gout
Cigarette smoking
Sedentary lifestyle
High stress levels
Hypertension
Obesity
Diabetes 
Untreated bacterial infections
Treatment with tetracycline
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6
Q

CAD Treatment

A 
Decrease dietary fats
Losing weight
Eliminating smoking
Increase exercise
Decrease stress
Treat hypertension
Treat diabetes
Treat gout
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7
Q

Lipoproteins Produced in the Liver

A

1) Low-density lipoproteins (LDL): Enter circulation as tightly packed cholesterol, triglycerides, and lipids.
Carried by proteins that enter circulation; broken down for energy or stored for future use as energy.
VLDL are turned into LDL

2) High-density lipoproteins (HDL): Enter circulation as loosely packed lipids.
Used for energy; pick up remnants of fats and cholesterol left in the periphery by LDL breakdown

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8
Q

Causes of Hyperlipidemia

A
  • Excessive dietary intake of fats
  • Genetic alterations in fat metabolism leading to a variety of elevated fats in the blood
  • Hypercholesterolemia, hypertriglyceridemia, and alterations in LDL and HDL concentrations
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9
Q

Action of antihyperlipidemic agents

A
  • Lower serum levels of cholesterol and lipids

- Prevention of CAD

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10
Q

Drugs Used to Treat Hyperlipidemia

A
  • HMG-CoA inhibitors
  • Bile acid resins or sequestrants
  • Fibric Acid Agents
  • Niacin
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11
Q

HMG-CoA Reductase Inhibitors “Statins” Indications

Example: Atorvastatin (Lipitor)

A
  • Adjuncts with diet and exercise for the treatment of increased cholesterol and LDL levels that are unresponsive to dietary restrictions alone
  • Slow progression of CAD
  • Prevent first MI
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12
Q

HMG-CoA Reductase Inhibitors “Statins” Actions

A
  • Inhibit HMG-CoA, decrease serum cholesterol levels, LDLs, and triglycerides, and increase HDL levels
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13
Q

HMG-CoA Reductase Inhibitors “Statins” assessment and teaching

A
  • Undergo first-pass metabolism by the liver
  • Assess Liver function and caution in persons with active liver disease or history of alcoholism
  • Assess for pregnancy and lactation
  • Take at night
  • Can cause GI symptoms
  • Monitor for muscle pain or tremors
  • Rhabdomyolysis
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14
Q

HMG-CoA Reductase Inhibitors “Statins” Interactions

A
  • Macrolides (Erythromycin), “Azoles”, Fibric Acid Agents (Gemfibrozil), Immunosuppresants (cyclosporine), and niacin
  • Digoxin and warfarin
  • Grapefruit juice
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15
Q

HMG-CoA Reductase: Lovastatin (Mevacor)

A

Older, Higher risk of rhabdomyolysis

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16
Q

HMG-CoA Reductase: Simvastatin (Zocor)

A
  • Less liver toxicity
  • Prevents MIs
  • 10-17 yo. OK
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17
Q

HMG-CoA Reductase: Pravastatin (Pravachol)

A
  • Effective at deceasing CAD, MI

- Children 8 and up

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18
Q

A patient is taking a HMG-CoA reductase inhibitor. Which of the following tests should be performed at the start of therapy and periodically after?

Liver function
Electrolyte levels
Complete blood count
ECG

A

Liver function

-Due to the fact that increased liver can occur in those receiving long term HMG-CoA therapy

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19
Q

Bile Acid Resins indications

A

Example: Cholestyramine (Questran)

-Reduce elevated serum cholesterol in patients with primary hypercholesterolemia
allow excretion in feces instead of reabsorption, and cause serum cholesterol levels to fall

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20
Q

Bile Acid Resins assessment and teaching

A
  • Not absorbed systemically, Excreted in the feces
  • Assess for pregnancy or lactation
  • Can cause bloating and constipation
  • Mix powder with water
  • Colesevelam (Welchol)- taken as a tab and less frequently than the prototype
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21
Q

Bile Acid Resins Pharmacokinetics

A

Not absorbed systemically b/c excreted in the feces.

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22
Q

Bile Acid Resins contraindications

A
  • Allergy
  • Complete biliary obstruction: which would prevent bile from being secreted into the intestine
  • Abnormal intestinal function: could be aggravated by the presence of these drugs
  • Pregnancy and lactation: potential decrease in the absorption of fat and fat-soluable vitamins could have a detrimental effect on the fetus or neonate
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23
Q

Bile Acid Resins interactions

A
  • Can be used concurrently with Statins
  • Malabsorption of fat-soluble vitamins
  • Thiazide diuretics, digoxin, warfarin, thyroid hormones, and corticosteroids- and lots others….
  • Do not take with other medications (1 hour after or 4 hours before) these drugs have delayed absorption when taken with BAS
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24
Q

Bile Acid Resins adverse effects

A
  • Headache, fatigue, and drowsiness
  • Direct GI irritation: nausea and constipation
  • Could lead to fecal impaction and aggravation of hemorrhoids
  • Increased bleeding times
  • decreased absorption of
  • Vitamin K and subsequent decreased production of clotting factors
  • Vitamin A and E deficiencies
  • decreased absorption of fat-soluble vitamins, causes rash and muscle pain
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25
Q

Fibric Acid Agents

A
  • Example: Gemfibrozil (Lopid)
  • Inhibits peripheral breakdown of lipids
  • Reduces production of triglycerides and LDL and Increases HDL
  • Can cause GI and muscle discomfort
  • Monitor for Gallstones
  • DO NOT combine with Statins
  • Gemfibrozil (Lopid)
    • Type of fibrate: decrease in lipoprotein and triglyceride synthesis and secretion.
    • Do not combine with statins = increased risk of rhabdo.
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26
Q

Niacin (vitamin B3)

A
  • Vitamin B3, inhibits release of free fatty acids from adipose tissue
  • Much higher doses than typically Vitamin replacement
  • Should be done under the supervision of a physician
  • Increases rate of triglyceride removal from plasma
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27
Q

Niacin (Vitamin B3) side effects

A
  • Severe cutaneous flushing and hot flashes
  • Nausea & abdominal pain
  • Increase in uric acid
  • increased uric acid (gout)
  • Nicotinic acid: Increases rate of triglyceride removal from plasma and generally reduces LDL and triglyceride levels and increases HDL levels.
  • Initial effect within 5-7 days with maximum effect in 3-5 weeks
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28
Q

Lipid lowering agent: Ezetimibe (Zetia) indication

A
  • When combined with a statin it is called Vytorin
  • Purpose
    • Decease serum cholesterol levels.
    • May be used with diet/exercise, Statins, or Bile Acid Resins
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29
Q

Lipid lowering agent: Ezetimibe (Zetia) assessment and teaching

A
  • Monitor for pregnancy

- Most common side effects are GI, however CNS changes can also occur

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30
Q

Cardiovascular Disease (CVD)

A
  • Includes conditions of heart and blood vessels
  • Hypertension is most common form of CVD
  • Most frequent causes of death in U.S
  • Prehypertension (120-139/80-89) affects approximately 22% of the adult population
  • High blood pressure affect 1 in 4 Americans
  • Diabetics are 2-3 times more likely to have hypertension than nondiabetics
  • African Americans have the highest rate (33%)
  • Among people with HTN, more than 32% do not realize they have the disease –”silent killer”
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31
Q

Elements Determining Blood Pressure

A
  • Heart rate
  • Stroke volume: Amount of blood that is pumped out of the ventricle with each heartbeat
  • Total peripheral resistance: Resistance of the muscular arteries to the blood being pumped through them
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32
Q

Physiological Regulation of Blood Pressure

A

1) Central and autonomic nervous systems
- Vasomotor center
- Baroreceptors
- Chemoreceptors

2) Emotions affect blood pressure
- Stress and anger increase
- Depression and lethargy decrease

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33
Q

Endocrine System

A
  • Regulates blood pressure
  • Natural hormones affect blood pressure daily
    • Epinephrine and norepinephrine injections raise B/P
    • Antidiuretic hormone raises B/P by raising blood volume
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34
Q

Bloop pressure lifestyle and genetic factors

A

1) Lifestyle
- Exercise or activity regimen
- Use of medication
- Dietary habits

2) Genetic
- Race
- Gender
- Family history of hypertension

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35
Q
  • Estimated that 20% of the people in the US have hypertension and many are unaware.
  • 90% have essential hypertension: hypertension with no known cause. [Secondary HTN = pheochromocytoma, tumor in the adrenal gland]
A

.

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36
Q

Risks for Coronary Artery Disease Related to Hypertension

A
  • Thickening of the heart muscle
  • Increased pressure generated by the muscle on contraction
  • Increased workload on the heart
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37
Q

Stepped Care Approach to Treating Hypertension

A

-Because an underlying cause of hypertension is usually unknown, treatment is aimed at altering the body’s ability to regulate BP.

Step 1: lifestyle modifications are instituted (weight reduction, smoking cessation, reduce alcohol and salt in the diet, also increase exercise)

Step 2: drug therapy is added if the measures in step 1 are insufficient. May start with a diuretic, Beta blocker, ACE inhibitor or ARB, or CA++ channel blocker.

Step 3: drug dose or class may be changed or another drug added if the patient’s response is inadequate

Step 4: includes all of the above measures with the addition of more antihypertensive agents until blood pressure is controlled

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38
Q

Types of Drugs Used to Control Blood Pressure

A

1) Diuretic
2) Beta-blocker
3) ACE inhibitor
4) Calcium channel blocker

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39
Q

Diuretics

A
  • Drugs that increase the excretion of sodium and water from the kidney.
  • Often 1st HTN treatment agents

1) Thiazide Diuretics: Chlorothiazide, Hydrochlorothiazide
2) Loop Diuretics: Furosemide, Bumetanide(Bumex)
3) Carbonic anhydrase inhibitors: Acetazolamide(Diamox)
4) Potassium-Sparing Diuretics: spironolactone, triamterene

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40
Q 
Diuretics
Mechanism of action
Primary use
Adverse effects
Example drugs
A
  • Mechanism of action: increase amount of urine produced and excreted
  • Primary use: for mild to moderate hypertension
  • Adverse effects: electrolyte imbalances, especially loss of potassium

Example drugs: hydrochlorothiazide (HydroDiuril), furosemide (Lasix)

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41
Q

Calcium Channel Blocker indication

A
  • Example: Nifedipine (Procardia, Adalat)
  • Treatment of essential hypertension in the extended release form
  • Because of all of actions Ca++ Channel Blockers it is used for HTN, Antiarrhythmic and antianginal
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42
Q

Calcium Channel Blocker action

A

Inhibits movement of calcium ions across the membranes of cardiac and arterial muscle cells, depressing the impulse and leading to slowed conduction, decreased myocardial contractility, and dilation of arterioles

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43
Q

Ca++ channel blockers prevent the movement of calcium into the cardiac and smooth muscle cells when the cells are stimulated. This block interferes with?

A

the muscle cell’s ability to contract => loss of smooth muscle tone, vasodilation, and decreased in peripheral resistance. This decreases BP, cardiac workload, and myocardial oxygen consumption.

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44
Q

Calcium Channel Blocker Assessment and teaching

A

-Monitor for heart block or sick sinus syndrome
-Not used in pregnancy or lactation
-Monitor vitals
-Can cause nausea
-Monitor for peripheral edema
-Avoid Grapefruit juice- increases absorption
-Drug-to-drug interaction
Cyclosporine

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45
Q

most Ca++ channel blockers end in?

A

DIPINE (exceptions: Diltiazem and Verapamil)

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46
Q

Calcium channel blockers: Amlodipine (Norvasc)

A
  • Not sustained release
  • Oral used alone or in combo w/other agents to treat HTN
  • Also used for angina
  • does not have to be an extended release form. -
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47
Q

Calcium channel blockers: Felodipine (Plendil):

A

used for HTN in adults, NOT used for angina

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48
Q

Calcium channel blockers: Nifedipine (Procardia XL)

A

sustained release for the treatment of HTN

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49
Q

Calcium channel blockers: Verapamil (Calan SR)

A

Verapamil (Calan SR)
Sustained release used for HTN
Affects both cardiac and periphery

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50
Q

ACE Inhibitors Indications

A

Treatment of hypertension, CHF, diabetic nephropathy, and left ventricular dysfunction following an MI

Example: Enalapril (Vasotec)

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51
Q

ACE Inhibitors action

A

Block ACE from converting angiotensin I to angiotensin II, leading to a decrease in blood pressure, a decrease in aldosterone production, and a small increase in serum potassium levels along with sodium and fluid loss
- Action: Increase in K+, Na+ and fluid LOSS!!!!

Example: Enalapril (Vasotec)

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52
Q

ACE Inhibitors Assessment and Teaching

A
  • Can cause GI irritation
  • Monitor Closely for Angioedema
  • Can cause a dry, annoying, cough
  • Caution in patients with CHF
  • Take first dose at bedtime
  • Monitor potassium level as hyperkalemia can occur
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53
Q

ACE Inhibitors drug-drug interaction

A

Allopurinol

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54
Q

ACE Inhibitors contraindications

A

known to cross the placenta and have serious fetal abnormalities. Several ACE inhibitors have been detected in breast milk.

Caution in CHF :

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55
Q

Benazepril (Lotensin) Adverse effects

A

HTN

**Cough

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56
Q

Enalapril (Vasotec) Adverse effects

A

HTN, CHF
Parenteral Use when oral is not feasible and rapid onset is desired
Enalaprilat (Vasotec IV)

57
Q

Lisinopril (Prinivil, Zestril) adverse effects

A

HTN, CHF

Stable patients 24 hours after MI to improve the likelihood of survival

58
Q

Quinapril (Accupril) Adverse effects

A

HTN, CHF

Less Side Effects

59
Q

Angiotensin II Receptor Blockers indications

A

Hypertension, CHF, slow progression of renal disease in patients with hypertension, and type 2 diabetes.
- ARBs used when patient cannot tolerate the side effects/adverse effects of ACE inhibitors.

60
Q

Angiotensin II Receptor Blockers action

A

Selectively bind with angiotensin II receptor sites in vascular smooth muscle and in the adrenal gland to block vasoconstriction and the release of aldosterone

  • ARBs: Angiotension II Receptor blockers: Angiotenstion I => Angiotension II, but these drugs occupy the receptors on the vascular smooth muscle that when activated by Angiotension II cause vasoconstriction. With these blocked => vasodilation. Aldosterone release is also blocked.
    Example: Losartan (Cozaar)
61
Q

Angiotensin II Receptor Blockers action assessment and teaching

A
  • Monitor for Headache, dizziness, syncope, and weakness
  • Can cause GI complaints, Skin rash and dry skin
  • Not for pregnancy or lactation
  • Caution in situations of hypovolemia
  • NO chronic cough
62
Q

Angiotensin II Receptor Blockers action drug-to-drug inteaction

A

Phenobarbital

63
Q

Angiotensin II Receptor Blockers action metabolism, contraindications and cautions

A

Metabolism: metabolized by cytochrome P450 in the liver.

Contraindications
Known to cross the placenta (fetal abnormalities and death when given in 2nd or 3rd trimester). Unknown if it crosses into the breast milk: so do not use when lactating.

Cautions
Hypovolemia: ARBs block the body’s compensatory mechanism for low BP.

64
Q

Notice the “____” at the end

of the ARBs

A

“sartan”

65
Q 
Adrenergic Antagonists 
Mechanism of action
Primary use
Adverse effects
Example drug
A
  • Mechanism of action: to block affects of the sympathetic nervous system leading to vasodilation
  • Primary use: hypertension
  • Adverse effects: orthostatic hypotension, dizziness, nausea, bradycardia, dry mouth
  • Example drug: doxazosin (Cardura)
66
Q

Vasodilators
Indications:
Actions:

A

Indications: Used when other treatments fail; most reserved for severe hypertension/emergencies

Actions: Relax vascular smooth muscle, decrease peripheral vascular resistance, & reduce BP

Do not block reflex tachycardia when the BP drops

Most are given while in a hospital setting
IV route
Complex care and acute areas
- When other treatment are not working, sometimes necessary to use a direct vasodilator.

67
Q

Vasodilators
Cautions
Adverse effects:
Drug-to-drug interactions

A

Cautions
Peripheral vascular disease, CAD, CHF, and tachycardia

Adverse effects: Related to fall in BP
HA, dizziness, tachycardia, anxiety
N/V, abdominal pain
Cyanide toxicity: Nitroprusside

Drug-to-drug interactions
Based on individual drugs

  • Cautions: all of these can be exacerbated by a fall in BP
  • Adverse effects: r/t drop in BP: dizziness, anxiety, HA, tachycardia, CHF, CP, edmea
    GI: N/V
    Cyanide toxicity: Nitroprusside is metabolized to prussic acid = cyanide.
    Cyanide toxicity: dyspnea, HA, vomiting, dizziness, ataxia, LOC, imperceptible pulse, absent reflexes, dilated pupils, distant heart sounds
68
Q

Vasodilators indication, action, example

A

Indication
maintains increased renal blood flow
IVP on M/S for hypertensive crisis

Action
Act directly on vascular smooth muscle to cause muscle relaxation, leading to vasodilation and drop in blood pressure

Example: Hydralazine (Apresoline)

  • When other methods of HTN treatment fail, direct acting vasodilators are used. These are usually reserved for hypertensive emergencies.

Action: direct relaxation of vascular smooth muscle = > vasodilation => lowers BP. Does not prevent reflex Tachycardia.

69
Q

Vasodilators assessment and teaching

A
  • Monitor for reflex tachycardia
  • Usually taken with a Bets-Blocker to protect the heart
  • Monitor sodium and fluid levels/UO
  • Assess for Lupus
  • Use caution in cerebral insufficiency
  • Priapism may occur as well as impotence
70
Q

Vasodilator: Nitroprusside (Nitropress)

A
  • Used with severe Hypertension
  • Toxic levels will cause Cyanide Poisoning/Toxicity
  • Administer with D5W only
  • Solution is brown
  • Comes with a brown bag over it in some facilities
  • Cautions: all of these can be exacerbated by a fall in BP
  • Adverse effects: r/t drop in BP: dizziness, anxiety, HA, tachycardia, CHF, CP, edema,
    GI: N/V
    Cyanide toxicity: Nitroprusside is metabolized to prussic acid = cyanide.
    Cyanide toxicity: dyspnea, HA, vomiting, dizziness, ataxia, LOC, imperceptible pulse, absent reflexes, dilated pupils, distant heart sounds)
71
Q

Heart failure

A

-Inadequate perfusion of tissues with blood-borne nutrients
1) Left Heart Failure
Systolic heart failure: inadequate systolic contraction
Diastolic heart failure: abnormal diastolic relaxation

2) Right Heart Failure
Most common cause is L sided heart failure
Can be caused by Lung Disease (cor pulmonale)
COPD, CF

  • Bottom line with CHF
    Ventricle not pumping strong enough leading to vascular congestion (fluid)
72
Q

Underlying Problems in CHF Involving Muscle Function

A

-The muscle could be damaged
Atherosclerosis or cardiomyopathy

  • The muscle could be forced to work too hard to maintain an efficient output
  • Hypertension or valvular disease

-The structure of the heart could be abnormal
Congenital cardiac defects

73
Q

Causes of Congestive Heart Failure (CHF)

A

Coronary artery disease (CAD)
Cardiomyopathy
Hypertension
Valvular heart disease

74
Q

Congestive Heart Failure (CHF)
primary treatment
treat symptoms

A

Primary treatment: Helping the heart muscle to contract more efficiently to restore system balance

Treat symptoms:
Slow heart rate
Increase contractility
Reduce heart workload

75
Q

Drugs for Heart Failure

A

1) Diuretics: Decreases blood volume, which decreases venous return and blood pressure
2) Beta-adrenergic Blockers
3) ACE Inhibitors
4) Cardiac Glycoside (Digoxin)
5) Vasodilators
6) Phosphodiesterase Inhibitors

76
Q

Diuretics

A
  • Increase urine flow
  • Reduce blood volume and cardiac workload
  • Reduce edema and pulmonary congestion
  • Prescribed in combination with other drugs
77
Q

Loop-Diuretics assessment and teaching

A

-Loop-Diuretic used in HF to decrease overall fluid volume and excretion from Kidneys

Assessment and Teaching:
Monitor BP, UO, BUN and Creatinine
Assess Potassium frequently
Take earlier in the day
Weigh daily

Example: lasix (Furosemide)

  • Theydothis by interfering with the transport of salt and water across certain cells in thekidneys. (These cells are in a structure called theloopof Henle - hence the nameloop diuretic
78
Q

Nurses role-diuretics

A

1) Assess renal function
2) Monitor electrolyte levels
3) Monitor vital signs, intake/output
4) Monitor blood glucose and blood-urea nitrogen (BUN)
5) Monitor potassium levels closely, diuresis can cause hypokalemia
6) Monitor sodium intake<4000 ng daily
7) Report weight loss of more than 2lb/week
8) Report muscle cramping and fatigue
9) Change positions slowly to avoid dizziness

79
Q 
ACE Inhibitors
primary use
mechanism of action
adverse effects
examples
A

Primary use: to lower blood pressure and peripheral resistance, reduces afterload and is the drug of choice for heart failure

Mechanism of action: to enhance excretion of sodium and water, lowers peripheral resistance and reduces blood volume, Increases cardiac output

Adverse effects: first-dose hypotension, cough, hyperkalemia, renal failure

Examples:
Lisinopril (Prinivil, Zestril)
Captopril (Capoten)
Enalapril (Vasotec)

80
Q

Nurse’s Role—ACE Inhibitors

A
  • Monitor CBC
  • Assess for hypotension
  • Monitor for impaired kidney function, hyperkalemia, autoimmune disease
  • Therapeutic response time may take weeks or months
  • Follow prescribed sodium and potassium restrictions to prevent side effects of hyperkalemia and hyponatremia
  • Do not take other medications, OTC drugs, herbals or vitamins without notifying MD
81
Q

Beta-Adrenergic Blockers

A
  • Slow heart rate and reduce blood pressure
  • Inotropic effect
  • Reduce workload of heart
  • Inotropicdrugs affect the force of cardiac contraction.
  • Chronotropicdrugs affect the heart rate.
82
Q 
Beta-Adrenergic Blockers
Mechanism of action
Primary use
Adverse effects
Contraindications
Example drugs
A

Mechanism of action: reduces sympathetic stimulation of the heart thus reducing workload of heart

Primary use: to reduce symptoms of heart failure and slow progression of disease

Adverse effects: slowing of the heart and hypotension

Contraindications: asthma, cardiogenic shock, sinus bradycardia, heart block

Example drugs: Metoprolol (Lopressor), Carvedilol (Coreg)

83
Q

Vasodilators

A
  • Minor role in heart-failure treatment
  • Lower blood pressure
  • Relax blood vessels

Examples:
Hydralazine (Apresoline)
Isosorbide dinitrate (Isordil)

84
Q 
Vasodilators
Mechanism of action 
Primary use
Adverse reactions
Example drug
A

Mechanism of action: to relax blood vessels

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

Adverse reactions: reflex tachycardia, orthostatic hypotension

Example drug: isosorbide dinitrate (Isordil)

85
Q

Cardiac glycosides

A
  • Increases force of heartbeat and myocardial contraction
  • Slows heart rate, decreased conduction through the AV node
  • Increases cardiac output
  • Second-line treatment for HF

-Indications
Treatment of CHF and atrial fibrillation

-Examples:
Digitoxin (Crystodigin)
Digoxin (Lanoxin)

  • Cardiotonic Drugs: Cardiac Glycosides
    Affect intracellular calcium levels in the heart muscle, leading to increased contractility.
    This increase in contraction strength leads to increased cardiac output, which causes increased renal blood flow, decreases renin release, breaking the effects of the RAS, and increases urine output, leading to decreased blood volume.
86
Q 
Cardiac Glycosides
Mechanism of action
Primary use
Adverse effects
Example drug
A

Mechanism of action: to cause more forceful heartbeat, slower heart rate

Primary use: to increase contractility or strength of myocardial contraction

Adverse effects: neutropenia, dysrhythmias, digitalis toxicity

Example drug: digoxin (Lanoxin)

87
Q

Cardiac Glycosides assessment and teaching

A

-Assess heart rhythm for Ventricular tachycardia or fibrillation, heart block, and sick sinus syndrome
-Use caution in Acute MI or Renal insufficiency
-Monitor for hypokalemia- causes more toxicity
-Serum Digoxin levels 0.5 to 2.0 ng/ml
-Take pulse before administering
Do not administer if less than 60 BPM
-Can cause HA, dizziness, Hypotension, and change in heart rhythm
-Assess concurrent drugs…lots of interactions…specifically Viagra and Potassium-loosing diuretics

-Peds/Geriatric
Increased risk for dig toxicity
Smaller body mass and immature or malfunctioning kidneys

88
Q

Digoxin Toxicity

A

-Digoxin toxicity can be fatal

-Know signs/symptoms of toxicity and immediately report
N/V, anorexia, and visual disturbances (halos, yellow-green tinge or blurring)

-Therapy involves IV infusion of digoxin immune fab (Digibind)

89
Q

Digoxin Antidote

A
  • Digoxin Immune Fab (Digibind, Digifab)
  • Bind to molecules of Digoxin = unavailable
  • Excreted in kidneys
90
Q

Phosphodiesterase Inhibitors

A
  • Block enzyme phosphodiesterase
  • Increase calcium for myocardial contraction
  • Cause positive inotropic response and vasodilation
  • Increase contractility and decrease afterload
  • Short-term therapy only
91
Q

Phosphodiesterase Inhibitors

  • Mechanism of action
  • Primary use
  • Adverse effects
  • Example drug
A

Mechanism of action: to block enzyme phosphodiesterase in cardiac and smooth muscle

Primary use: as short-term therapy for heart failure

Adverse effects: hypokalemia, hypotension, ventricular dysrhythmias

Example drug: milrinone (Primacor)

92
Q

Coronary Artery Disease

A

One of the leading causes of death in United States

Narrowing or occlusion of a coronary artery

Narrowing causes myocardial ischemia

93
Q

Atherosclerosis

A
  • Most common etiology of coronary heart disease (CAD)
  • CAD is one of the leading causes of death in the US
  • Myocardium receives blood supply from 2 coronary arteries during diastole
  • In CAD the vessels become narrowed
  • Caused by presence of plaque due to atherosclerosis
94
Q

CAD

A
  • Supply vs. demand
    • Increased workload = O2 demand
    • Damaged vessels unable to meet demands
  • Angina pectoris
    • “Suffocation of the chest” due to lack of O2
  • Myocardial Infarction
    • Cells in the myocardium become necrotic and die
  • Workload – exercise or other stresses where o2 demands increase
    Demand for o2 (blood) exceeds supply
95
Q

Angina Pectoris

A
  • Acute chest pain due to insufficient O2 to myocardium
  • Accompanies physical exertion or emotional excitement
  • Causes increased myocardial oxygen demand
96
Q

Signs and symptoms for Angina pectoris

A
  • Steady, intense pain in anterior chest
  • Pain radiating to left shoulder, left arm, spine, jaw
  • Fear of impending death
  • Pallor, dyspnea, diaphoresis
  • Tachycardia, elevated blood pressure
  • Pain diminishes with physical rest and stress reduction
97
Q

Types of angina

A

1) Stable angina
- No damage to heart muscle; basic reflexes surrounding the pain restore blood flow

2) Unstable angina
- Episodes of ischemia occur even when at rest

3) Prinzmetal’s angina
- Caused by spasm of the blood vessels, not just by vessel narrowing

  • Stable: When you stop what ever is causing the chest pain, then the pain goes away. NO damage to the heart muscle
  • Unstable: episodes of chest pain even at rest, still not damage to heart muscle, but is considered preinfarction angina.
98
Q

Actions of Antianginal Drugs

A
  • Improve blood delivery to the heart muscle by dilating blood vessels
    • Increase the supply of oxygen
  • Improve blood delivery to the heart muscle by decreasing the work of the heart
    • Decrease the demand for oxygen
  • In early cases on angina, avoidance of exertion or stressful situations may be sufficient to prevent anginal pain.

Antianginal drugs are used to help restore the supply and demand ratio in oxygen delivery to the myocardium when rest is not enough.

These drugs work to improve blood delivery to the heart muscle in one of two ways:

99
Q

Types of Antianginal drugs

A

1) Nitrates
2) Beta-adrenergic blockers
3) Calcium channel blockers

100
Q

Organic Nitrates

  • Indication
  • Mechanism of action
  • Primary use
  • Adverse effects
  • Example
A

Indication:
Prevent and treat attacks of angina pectoris

Mechanism of action:
Potent vasodilator

Primary use:
For lowering myocardial oxygen demand

Adverse effects:
Hypotension, dizziness, blurred vision, dry mouth, headache

Example: Nitroglycerin (Nitro-Bid, Nitrostat, others)

101
Q

Routes for Nitroglycerin

A
  • IV – glass bottles
  • Sublingual/transmucosal– carried with patients, do not swallow or crush; moist mucous membranes, store in a cool dry place in a glass container
  • Translingual spray
  • Oral, SR tablet – Take with water; do not crush
  • Topical ointment – keep away from other meds and products
  • Transdermal – Changed daily, remove old patch & cleanse that area of the skin, apply to areas without hair
  • Patient education on correct route/application.
  • Topical and transdermal preps are associated with many patient errors – not removing old patch.
  • Ointments can be mistaken for hand creams.
  • Take with meals if GI upset noted
102
Q

Organic Nitrates Assessment and teaching

A
  • Do not use in cases with Head trauma and cerebral hemorrhage
  • Assess BP and Vitals before and after- Causes hypotension
  • Causes HA, dizziness, and weakness
  • Do not use concurrently with Antimigraine medications or during a migraine
  • Medication should be given every 5 minutes in an acute attack up to 3 times…any more will not be effective
  • Nurses should wear gloves when handling
  • Medication is light sensitive and should be kept in original bottle
  • Medication should “Pop and Fizz” on the tongue or it may no longer be active
  • Tolerance can develop, discontinue medication at night
  • Rotate location of transdermal patches
103
Q

Organic Nitrates contraindications and cautions

A

1) Contraindications
- Allergy
- Severe anemia: decreased cardiac output could be detrimental
- Head trauma/cerebral hemorrhage: relaxation of cerebral vessels could cause intracranial bleeding
- Pregnancy/lactation: potential adverse side effects on the neonate and ineffective blood flow to the fetus.

2) Cautions
- Hepatic/renal: alter metabolism/excretion of the drugs
- Hypo: make all of these worse

104
Q

Isosorbide mononitrate (ISMO, Imdur)

A
  • Slower onset
  • Last up to 4 hours
  • Taken before CP causing situations
  • NOT for acute attacks
105
Q

A patient comes into the emergency department (ED) complaining of chest pains that began over an hour ago, while he was mowing the lawn. Nitroglycerin was given sublingual as prescribed. Which of the following adverse reactions would be the most likely to occur?

Hypotension
Dizziness
GI Distress
Headache

A

D the most common adverse reaction with nitrates is a headache due to dilation of the blood vessels in the brain

106
Q

Beta-Adrenergic Blockers

  • Mechanism of action
  • Primary use
  • Adverse effects
  • Example drug
A

Prophylaxis for chronic angina

Mechanism of action: to reduce the cardiac workload

Primary use: for prophylaxis of chronic angina

Adverse effects: hypotension, dizziness, fatigue during exercise

Example drug: atenolol (Tenormin)
metoprolol (Lopressor, Toprol XL)
labetalol (Normodyne)

Notice the endings “olol”

107
Q

Calcium Channel Blockers

  • Mechanism of action
  • Primary use
  • Adverse effects
  • Example drugs
A

Reduce cardiac workload and dilate coronary arteries, bring more oxygen to myocardium

Mechanism of action: to reduce cardiac workload

Primary use: for lowering blood pressure

Adverse effects: hypotension, bradycardia, heart failure, constipation

Example Drugs: Norvasc, Vascor, diltiazem (Cardizem)

108
Q

Angina vs. Myocardial Infarction

A
  • Identify and differentiate the two conditions
  • Pharmacological treatment differs considerably between conditions
  • Myocardial infarction carries a high mortality rate
109
Q

Drugs Used in Treatment of Myocardial Infarction

A

-Thrombolytics

  • Antiplatelet and anticoagulant drugs
    • Aspirin, ReoPro
    • Heparin
  • Nitrates
  • Beta-adrenergic blockers
  • Angiotension-converting enzyme (ACE) inhibitors
  • Pain management
    • Morphine
110
Q

Thrombolytics

A
  • Dissolve clots
  • Restore circulation to myocardium
  • Needs to be given within 6 hours of onset of symptoms
  • Drug: Reteplase
  • Major complication: bleeding
  • Contraindications: active bleeding, history of CVA, or recent surgical procedures
111
Q

Clotting process

A
  • Blood-vessel injury causes vessel spasm (constriction)
  • Platelets are attracted to and adhere to injured area
  • Aggregation of platelets forms plug
    • Formation of insoluble fibrin strand and coagulation (coagulation cascade)
    • Normal clotting occurs in six minutes
112
Q

Coagulation Cascade

A
  • Intrinsic or extrinsic pathways lead to formation of fibrin clot.
  • Injured cells release prothrombin activator.
  • Prothrombin activator changes prothrombin to thrombin.
  • Thrombin changes fibrinogen to fibrin.
  • Fibrin forms insoluble web over injured area to stop blood flow.
113
Q

Hemostasis

A

Complex process involving multiple steps
Involves large number of enzymes and clotting factors
Final product is a fibrin clot that stops blood loss

114
Q

Diseases of Hemostasis

A

1) Thromboembolic disorders
- Caused by thrombi, emboli
- Occurs in MIs and types of CVAs

2) Thrombocytopenia – deficiency of platelets

3) Bleeding Disorders
- Hemophilia
- Von Willebrand’s disease – most common genetic bleeding disoder

115
Q

Fibrinolysis

A
  • Clot removal
  • Initiated by release of tissue plasminogen activator (tPA)
  • TPA converts plasminogen to plasmin
  • Plasmin digests fibrin strands – thus, circulation is restored
  • Regulated so unwanted clots are removed and fibrin is left in wounds
116
Q

Action of Coagulation Modifiers

A

1) Inhibiting specific clotting factors
2) Dissolving fibrin
3) Inhibiting platelet function

117
Q

Lab Tests That Measure Coagulation

A
  • Used for diagnosing and treating coagulation disorders
    1) Whole-blood clotting time
    2) Prothrombin time (PT)
    3) International normalized ratio (INR)
    4) Thrombin time
    5) Activated partial thromboplastin time (aPTT)
    6) Liver-function tests
    7) Bleeding time
    8) Platelet count
118
Q

Parenteral Anticoagulants

A 
-Indication
Treatment of thromboembolic disorders
A-fib
MI
PE
CVA

Example: Heparin

119
Q

Anticoagulants

  • Mechanism of action
  • Primary use
  • Adverse effects
  • Example
A

Mechanism of action: to inhibit specific clotting factors to prevent formation or enlargement of clots

Primary use: to prevent thrombi from forming or enlarging, prevent formation of clots in veins, treat thromboembolic disorders

Adverse effects: abnormal bleeding

Example drugs: heparin (parenteral) and warfarin (oral),
Xarelto

120
Q

Parenteral Anticoagulants Assessment and teaching

A
  • Monitor for conditions that are compromised by increased bleeding tendencies
  • Can be used in pregnancy only in emergencies
  • Assess lab values of aPTT at least once daily while on therapy
  • Have Protamine Sulfate on standby as an antidote
  • Monitor for increase in bleeding…hidden or obvious
  • Can cause Priapism
121
Q

Parenteral Anticoagulants drug to drug interactions

A

Oral anticoagulants, salicylates, penicillins, and cephalosporins
nitroglycerine

122
Q

Parenteral Anticoagulants contraindications

A
  • Any condition that could be compromised by increased bleeding tendencies
  • Hemorrhagic disorders, recent trauma, spinal puncture, GI ulcers, recent surgery, OR ANYONE THAT MAY HAVE AN INVASIVE PROCEDURE.
  • Pregnancy: fetal injury and death have occurred
  • Lactation: heparin has been approved if an anticoagulant is needed during lactation
123
Q

Low-Molecular-Weight Heparin

A
  • Inhibit thrombus and clot formation by blocking factors Xa and Iia
  • Do not greatly affect thrombin, clotting, or prothrombin times; therefore, they cause fewer systemic adverse effects
  • Block angiogenesis, the process that allows cancer cells to develop new blood vessels
  • Are indicated for specific uses in the prevention of clots and emboli formation after certain surgeries or bed rest
124
Q

Low-Molecular-Weight Heparin Example

A

Example: Enoxaparin (Lovenox)
Prevention of DVT
Surgery/immobility
Prevention of ischemic complications with MI

Dalteparin (Fragmin)
Prevention of DVT
Orthopedic surgery

125
Q

Low-Molecular-Weight Heparin assessment and teaching

A
  • Give medication only subcutaneous
  • Teach injections as needed
  • Dose will be based on weight or purpose
  • Do not eject the nitrogen bubble in the prepackaged syringe
  • Monitor for bleeding and bruising
126
Q

Oral Anticoagulants

Example: Warfarin (Coumadin)

A
  • Maintains a state of anticoagulation when the patient is susceptible to potentially dangerous clot formation
  • Interferes with Vitamin K dependent clotting factors
  • Indication: who is at risk for clot formation: A-fib, heart valves, valve damage, prevention of venous thrombosis and embolus after MI and PE

Vitamin K: liver makes clotting factors. It makes prothrombin by using Vitamin K. Eventually these factors are depleted and the clotting time is prolonged.

Not drug of choice for acute situations, convenient and useful for prolonged effects

No in pregnancy

Many interactions

127
Q

Oral Anticoagulants assessment and teaching

Drug drug interactions

A
  • PO only
  • Onset of action is 3 days, continue parenteral drug for a few days while full anticoagulation effects are reached
  • Monitor and teach about Vitamin K rich foods to avoid- Vitamin K is antidote
  • Monitor PT and INR for serum levels
  • Do not use in pregnancy

-Drug-Drug Interactions
Lots of them…monitor drug regimen

128
Q

Antiplatelet Drugs

  • Action
  • Indications
  • Example
A
  • Aspirin, ADP receptor blockers
  • Glycoprotein IIb/IIIa receptor antagonists
  • Agents for intermittent claudication
  • Action
    • Inhibit platelet adhesion and aggregation by blocking receptors sites on the platelet membrane
  • Indications
    • Reduce risk of recurrent TIAs or strokes; reduces death or nonfatal MI; MI prophylaxis; anti-inflammatory, analgesic, and antipyretic effects
  • Example: Clopidogrel (Plavix)
129
Q

Antiplatelet Drugs assessment and teaching

A
  • Monitor for Pregnancy & Lactation
  • Monitor for Bleeding
  • Assess bowel function
  • Do not use in recent head injury or major trauma
130
Q

Antiplatelet Agents

A
  • Monitor for bleeding
    • Risk increases if given with anticoagulants
  • Prolonged pressure needed to control bleeding at puncture sites
  • Monitor for gastrointestinal upset with aspirin and Ticlid
  • May increase menstrual bleeding
131
Q

Antiplatelet

  • Aspirin
  • Eptifibatide (Integrilin)
  • Ticlopidine (Ticlid)
  • Eptifibatide (Integrilin): IV drug used when someone is having ACS, and to prevent ischemic episodes in pts. having PTCAs
A

Aspirin
Monitor for GI distress and bleeding

Eptifibatide (Integrilin)
IV
ACS & PTCAs to prevent ischemia during the procedure

Ticlopidine (Ticlid)
Open lines

  • Eptifibatide (Integrilin): IV drug used when someone is having ACS, and to prevent ischemic episodes in pts. having PTCAs
132
Q

Thrombolytics

  • Mechanism of action
  • Primary uses
  • Example drugs
A

-Mechanism of action: to convert plasminogen to plasmin, which digests fibrin and dissolves clot

  • Primary uses:
  • To dissolve existing clots
  • To treat acute myocardial infarction, deep vein thrombosis
  • To treat cerebrovascular accident, pulmonary embolism, arterial thrombosis
  • To clear IV catheters

Example drug: alteplase (Activase)

133
Q

Thrombolytic Agents

  • Action
  • Indications
A

Action
Activate plasminogen to plasmin, which in turn breaks down fibrin threads in a clot to dissolve a formed clot

Indications
Acute MI, pulmonary emboli, and ischemic stroke
Within 6 hours of incident
Open clotted IV catheters

134
Q

Thrombolytic Agents assessment and teaching

A
  • Monitor for Bleeding
  • During IV therapy, continuously monitor ECG
  • Assess vital signs periodically
  • Can cause a hypersensitivity reaction: rash, flushing, bronchospasm, and anaphylactic reaction
  • Assess for changes in cognition indicating intracranial hemorrhage
135
Q

Thrombolytic Agents drug-drug interactions

A

Risk for hemorrhage with concurrent use of Anticoagulants or Antiplatelets

136
Q

Thrombolytic Agents adverse effects

A
  • Bleeding: most common adverse effect

- Cardiac arrhythmias: with cardiac reperfusion

137
Q

Thrombolytic agents
Reteplase (Retavase)
Tenecteplase (TNKase)

A

-Reteplase (Retavase)
Used after an MI

  • Tenecteplase (TNKase)
  • More rapid onset with longer duration
  • Fewer side effects
138
Q

Hemostatic Agent

  • Example
  • Purpose
  • Assessment and teaching
A

-Example: Aminocaproic Acid (Amicar)

-Purpose
Used to decrease bleeding times and increase clotting post surgery

  • Assessment and teaching
  • Monitor for blood clots and DVTs
  • Monitor peripheral circulation
  • Monitor Injection sites
  • Can lead to muscle wasting and weakness
  • Monitor kidney function

Pharmacology (28 decks)

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