UNIT 3 Flashcards
1
Q
can work in various ways. depends on the route
-can interfere with microorganism such as germs and destroy abnormal cell
A
Drug
2
Q
pumps blood from the heart to the lungs to get the oxygen
A
Cardiovascular system/circulatory system
3
Q
denses deoxygenated blood through the arteries to the rest of the body
A
Heart
4
Q
Carry oxygen, pour blood back to the heart to start the circulation process over
A
Veins
5
Q
Is critical to healthy organs, muscles, and tissue
A
Circulatory system
6
Q
Oxygenated;___
Unoxygenated
A
Artery ; Vein
7
Q
defined as a persistent systolic pressure of greater than 140 mm Hg and/or a diastolic pressure greater than 90 mm Hg, affects approximately 50 million people in the United States and approximately 1 billion people worldwide, designating it as the most common disease state.
A
Hypertension
8
Q
- Major risk factor for coronary artery disease, cardiovascular disease, and the death resulting from the cardiovascular causes
- Most important factor for stroke and heart failure, renal failure
A
Hypertension
9
Q
Is determine by the product of the cardiac output (dapat 4-8L / min) and systemic vascular resistance
A
blood pressure
10
Q
Is the amount of blood ejected from the left ventricle and is measured in liters per minute (svr)
- is the resistance to blood flow determined by the diameter of blood vessel
-It is calculated by the blood pressure divided by the cardiac output
A
Cardiac output
11
Q
ANTI HYPERTENSIVE AGENT TABLE
Under cardiac output there are:
A
Cardiac factors and circulating volume
12
Q
ANTI HYPERTENSIVE AGENT TABLE Under cardiac factors there are
A
Heart rate and contractibility
13
Q
ANTI HYPERTENSIVE AGENT TABLE Drugs under Cardiac factors
A
Beta blockers, Calcium channel blockers, Centrally acting adrenergics
14
Q
ANTI HYPERTENSIVE AGENT TABLE Under circulating volume there are:
A
Salt and aldosterone
15
Q
ANTI HYPERTENSIVE AGENT TABLE Drugs under circulating volume
A
ACE inhibitors and diuretics
16
Q
ANTI HYPERTENSIVE AGENT TABLE Under systemic vascular resistance there are:
A
Hormones, Peripheral sympathetic receptors, CNS, and Local
17
Q
ANTI HYPERTENSIVE AGENT TABLE Under hormones there are:
A
Vasodilators and vasoconstrictors
18
Q
ANTI HYPERTENSIVE AGENT TABLE Drugs under hormones
A
Vasodilators, prostaglandins, ACE inhibitors, calcium channel blockers, Angiotensin II blockers
19
Q
ANTI HYPERTENSIVE AGENT TABLE Drugs under peripheral sympathetic receptors
A
Alpha Alpha1 blockers and Beta Beta blockers
20
Q
ANTI HYPERTENSIVE AGENT TABLE
CNS; __ Local; ____
A
Centrally acting adrenergic ; Peripherally acting adrenergic
21
Q
CATEGORIES AND SUBCATEGORIES OF ANTIHYPERTENSIVE DRUGS
A
- Adrenergic drugs
- Angiotensin-converting enzyme inhibitors, Angiotensin II Receptor Blockers, Calcium Channel blockers
- Diuretics
-Vasodilators
-Direct Renin Inhibitors
22
Q
Usually are large group of anti-hypertensive drugs
A
Adrenergic drugs
23
Q
Contraindications of Adrenergic drugs
A
drug allergy and may also include acute heart failure, concurrent use of monoamine oxidase inhibitors, severe mental depression, peptic ulcer, and severe liver or kidney disease
24
Q
adverse effects of Adrenergic drugs
A
bradycardia with reflex tachycardia, postural and postexercise hypotension, dry mouth, drowsiness, dizziness, depression, edema, constipation, and sexual dysfunction
25
Interactions of Adrenergic drugs
additive CNS depression when taken with alcohol, benzodiazepines, and opioids.
26
Indications Adrenergic drugs
used primarily for the treatment of hypertension, either alone or in combination with other antihypertensive drugs. Various forms of glaucoma may also respond to treatment with some of these drugs.
27
How many ace inhibitors available for clinical use?
10
28
Mechanism of Action and Drug Effect of Angiotensin-Converting Enzyme (ace) Inhibitors
Kininase is an enzyme that normally breaks down bradykinin, a potent vasodilator in the human body
29
5 examples of ACE inhibitors
benazepril
captoril
enalapril
fosinopril
ramipril
30
Indications of Angiotensin-Converting Enzyme (ace) Inhibitors
They are excellent antihypertensives and adjunctive drugs for the treatment of heart failure
30
Explain the development of ACE inhibitors
The development of ACE inhibitors was because of the discovery of an animal substance found to have beneficial effects to humans. This substance was the venom of the south american viper
31
Contraindications of Angiotensin-Converting Enzyme (ace) Inhibitors
allergy, especially a previous reaction of angioedema (e.g., laryngeal swelling) to an ACE inhibitor. Patients with a baseline potassium level of 5 mEq/L or higher may not be suitable candidates for ACE inhibitor therapy because it promotes HYPERKALEMIA, Lactating women
32
Adverse effect of Angiotensin-Converting Enzyme (ace) Inhibitors
fatigue, dizziness, mood changes, and headaches, cough.
33
The most pronounced symptom of an overdosed ACE inhibitors
Hypotension
34
Interaction of Angiotensin-Converting Enzyme (ace) Inhibitors
Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen, can reduce the antihypertensive effect of ACE inhibitors
35
Mechanism of Action and Drug Effect
Angiotensin II Receptor Blockers
The ARBs block the binding of AII to type 1 AII receptors.
36
Indications
Angiotensin II Receptor Blockers
The therapeutic effects of ARBs are related to their potent vasodilating properties
37
Contraindications.
Angiotensin II Receptor Blockers
drug allergy, pregnancy, and lactation
38
Adverse Effects
Angiotensin II Receptor Blockers
The most common adverse effects of ARBs are upper respiratory infections and headache. Occasionally dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and fatigue can occur.
39
Adverse Effects
The most common adverse effects of ARBs are upper respiratory infections and headache. Occasionally dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and fatigue can occur.
40
may be used to treat angina, dysrhythmias, and hypertension and help to reduce blood of blood vessels. If calcium is not present, then the smooth muscle of the blood vessels cannot contract.
CALCIUM CHANNEL BLOCKERS
41
Mechanism of Action and Drug Effect CALCIUM CHANNEL BLOCKERS
Calcium plays an important role in the excitation-contraction coupling process that occurs in the heart and vascular smooth muscle cells, as well as in skeletal muscle..
42
Contraindications of CALCIUM CHANNEL BLOCKERS
drug allergy, acute MI, secondor third-degree AV block (unless the patient has a pacemaker), and hypotension
43
They act directly on arteriolar and venous smooth muscle to cause relaxation
Vasodilators
44
Indications CALCIUM CHANNEL BLOCKERS
considered first-line drugs for the treatment of such conditions as angina, hypertension, and supraventricular tachycardia. Often effective for the treatment of coronary artery spasms (vasospastic or Prinzmetal angina).
45
Adverse effects CALCIUM CHANNEL BLOCKERS
Hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea, rash, flushing, peripheral edema
46
TOXICITY AND MANAGEMENT WITH VASODILATORS
hypotension- treatment is administration of iv fluid and beta blockers
47
How do ARBs work?
by blocking the binding of angiotensin at the receptors; the end result is a decrease in blood pressure.
48
ACE inhibitors work by blocking a critical enzyme system responsible for the production of AII (angiotensin II; a potent vasoconstrictor)
They (1) prevent vasoconstriction caused by AII, (2) prevent aldosterone secretion and therefore sodium and water resorption, and (3) prevent the breakdown of bradykinin (a potent vasodilator) by AII.
49
A thorough nursing assessment includes
determining whether the patient has any underlying causes of hypertension, such as renal or liver dysfunction, a stressful lifestyle, Cushing’s disease, Addison’s disease, renal artery stenosis, peripheral vascular disease, or pheochromocytoma.
50
REMEMBER
Always assess for the presence of contraindications, cautions, and potential drug interactions before administering any of the antihypertensive drugs. Contraindications include a history of MI or chronic renal disease. Cautious use is recommended in patients with renal insufficiency or glaucoma. Drugs that interact with antihypertensive drugs include other antihypertensive drugs, anesthetics, and diuretics.
51
Hypertension is managed by ____ AND ____ . Patients need to consume a diet low in fat, make any other necessary modifications in their diet (such as possibly decrease the intake of sodium and increase fiber intake), engage in regular supervised exercise, and reduce the amount of stress in their lives.
both pharmacologic and nonpharmacologic measures
52
useful for heart failure
-wherein the heart is not able to effectively pump the blood towards diff. body organ
Cardiotonic agents
53
are drugs used to increase the contractility of the heart. Included below is a pharmacology guide for nurses on the various effects of cardiotonic-inotropic agents.
Cardiotonic agents
54
is a syndrome characterized by dysfunction of cardiac muscles.
-can occur with the number of heart condition that can result to overworking of the heart
Heart failure
55
Insufficient blood supply for the myocardium
-also the most common cause of heart failure (HF)
Coronary Artery Disease (CAD)
56
Enlargement of the heart and nagkaroon ng myocardial fatigue
Cardiomyopathy
57
Reflux, overloading of blood to the ventricles which over stretches the myocardium
Valvular Heart Disease
58
Primarily reflects pulmonary manifestations because the left ventricle cannot push blood towards the peripheral systems.
Left-sided HF
59
Occurs when the right side of the heart has the need to exert more force in order to push blood towards the pulmonary circulation.
- neck veins become distended, liver and spleen are enlarged
Right-sided HF
60
They exert their effects on the cardiac muscles by affecting levels of intracellular calcium. In turn, the contractility of the muscles is increased.
Cardiac Glycosides
61
Therapeutic Action Cardiac Glycosides
Allows more calcium to enter during contraction, therefore increasing the force of contraction – positive inotropic effect.
62
This drug can increase the strength of contractility without increasing the rate of contraction
Cardiac Glycosides
63
Indications Cardiac Glycosides
Primarily indicated for decreasing workload of the heart and relieving HF.
64
For atrial flutter, fibrillation
- widely use for children but the dosage should be calculated
Digoxin
65
notes for digoxin
Walang caution sa lactating women, pero proven na humahalo sya sa gatas kaya ingat pa rin. Mas susceptible sa older people
66
Contraindications Cardiac Glycosides
Allergy to any component of digitalis preparation,Ventricular tachycardia or fibrillation, Heart block (sick sinus syndrome),
Idiopathic hypertrophic subaortic stenosis (IHSS),
Acute myocardial infarction (MIRenal insufficiency, Can cause potential adverse effects to the fetus or neonate.
67
Pharmacokinetics Cardiac Glycosides
Oral: 30-120 min, 2-6 h peak, 6-8 days duration
IV: 5-30min, 1-5 h peak, 4-5 days duration
68
Adverse Effects Cardiac Glycosides
CNS: headache, weakness, drowsiness, vision changes (most commonly reported is seeing yellow halo around objects)
CV: arrhythmias
GI: GI upset, anorexia
69
NURSING ALERT! Signs and symptoms of digitalis toxicity
anorexia, nausea, vomiting, malaise, depression, irregular heart rhythms (e.g. heart block, heart arrhythmias, and ventricular tachycardia)
70
Interactions Cardiac Glycosides
Digoxin immune Fab or DigiFab: antidote; these antibodies bind molecules of digoxin, making them unavailable at site of action. Used when serum digoxin is >10 ng/mL and serum potassium is >5 mEq/L.
Verapamil, amiodarone, quinine, erythromycin, tetracycline, cyclosporine: increased therapeutic and toxic effects of digoxin. Combination of digoxin with any of these drugs would warrant decrease in dose of digoxin to prevent toxicity.
Potassium-losing diuretics: increased risk of cardiac arrhythmias
Thyroid hormones, metoclopramide, penicillamine: decreased therapeutic effects of digoxin. Increasing the dose of digoxin is important.
Cholestyramine, charcoal, colestipol, antacids, bleomycin, cyclophosphamide, methotrexate: decreased absorption of digoxin. In this case, digoxin must be taken 2-4 hours after taking any of these drugs.
St. John’s wort, psyllium: decreased therapeutic effect of digoxin
Ginseng, hawthorn, licorice: increased risk of digoxin toxicity
71
Nursing Considerations Cardiac Glycosides
IMPORTANT! Count apical pulse for one full minute before administering drug to monitor for adverse effects.
Drug is withheld if pulse is less than 60 beats per minute in adults and 90 beats per minute in infants.
Apical pulse is taken after one hour and if it remains low, nurse must document it, withhold the dose, and inform doctor.
72
aid in increasing force of myocardial contractility through their enzyme-blocking effect. This in turn, increases the flow of calcium into the myocardial cells.
Phosphodiesterase inhibitors
73
Therapeutic Action Phosphodiesterase Inhibitors
By blocking the enzyme phosphodiesterase, cyclic adenosine monophosphate (cAMP) increases. cAMP stimulates flow of calcium towards the myocardium and thereby, increases force of cardiac contractility. This leads to three major effects: vasodilation, increase oxygen consumption, arrhythmias
74
Indications Phosphodiesterase Inhibitors
Only indicated for short-term treatment of patients not responding to cardiac glycosides, vasodilators, and diuretics.
75
t OR F
Phosphodiesterase Inhibitors ARE SAFE FOR CHILDREN
F. NOT SAFE
76
Contraindications Phosphodiesterase Inhibitors
Allergy to phosphodiesterase inhibitors and bisulfites.
Severe aortic or pulmonary valvular disease.
Acute MI.
Conditions with fluid volume deficit.
77
Adverse Effects Phosphodiesterase Inhibitors
CV: ventricular arrhythmias, ventricular fibrillation, hypotension, chest pain
GI: nausea, vomiting, GI upset, abdominal pain
Hema: thrombocytopenia
Associated hypersensitivity reactions: vasculitis, pericarditis, pleuritis, and ascites
Burning at intravenous injection site
78
Nursing Considerations Phosphodiesterase Inhibitors
Assess for the mentioned contraindications to this drug (e.g. fluid volume deficit, acute MI, hypersensitivity, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose.
Determine urinary pattern and output to assess gross indication of renal function.
Obtain baseline electrocardiogram (ECG) to identify heart rate and rhythm.
Monitor serum electrolyte, complete blood count, and renal and hepatic function test results to determine whether changes in drug dose is needed or not.
79
Examples of anti-anginal drugs
Nitrates and nitrites
Beta-Adrenergic Blockers
Calcium- channel blockers
80
is the narrowing of blood vessels supplying oxygen and nutrients to the heart, primarily due to the development of fatty tumors (atheromas) in the lumen of blood vessels in a process called atherosclerosis.
Coronary Artery Disease (CAD)
81
This pathologic process attracts platelets and clotting factors to the area, causing a much larger obstruction to the vessels. The vessels also lose their natural ability to be elastic, resulting to inability to dilate and constrict. The heart stimulates the blood vessels to deliver more blood but blood delivery is limited by narrow vessel diameter, resulting to low oxygen supply of the heart.
Coronary Artery Disease (CAD)
82
As a consequence of hypoxia, ____ is felt.
pain (angina)
83
Two types of angina:
classic angina (of exercise), & vasospastic/Prinzmetal’s/variant angina
84
type of angina which occurs due to diminished coronary blood flow to the heart
classic angina (of exercise),
85
type of angina which is caused by reversible vasospasm even at rest. Both types decrease oxygen supply of the heart.
vasospastic/Prinzmetal’s/variant angina
86
Provides FAST ACTION to directly relax smooth muscles and depress muscle tones without affecting the nerve activity
-dilates veins & oxygen
Nitrates and nitrites
87
Therapeutic Action
-The main effect is drop in systemic blood pressure.
-It compensates by increasing blood flow to healthy arteries and veins because affected vessels already lose their elasticity.
88
Indications Nitrates and Nitrites
Children: May be used only for congenital heart defects and cardiac surgery because they can cause potentially dangerous changes in blood pressure.
Adults: Should be educated on drug’s various forms and their proper administration, storage, effectiveness, and manifestations that would warrant prompt medical help.
Older adults: Safety measures should be instituted as they are prone to adverse effects like arrhythmias and hypotension.
89
Contraindications Nitrates and Nitrites
Allergy to nitrates; Severe anemia – decreased cardiac output; Head trauma and cerebral hemorrhage; Pregnancy and lactation – potential harm to fetus; Conditions that can limit CO (e.g. hypovolemia, hypotension, etc.
90
Adverse Effects Nitrates and Nitrites
CNS: throbbing headache, dizziness, weakness
GI: nausea, vomiting, incontinence
CV: hypotension, reflex tachycardia, syncope
EENT: pallor, flushing, sweating\
Large dose leads to methemoglobinemia and cyanosis.
91
Interactions Nitrates and Nitrites
Ergot derivatives: risk for hypertension; decreased antianginal effect\
Heparin: decreased therapeutic effect of nitrates
PDE-5 inhibitors: risk for severe hypotension
92
Nursing Considerations Nitrates and Nitrites
Presence of mentioned contraindications and cautions
Skin color and integrity, especially for transdermal or topical forms of nitrates
Pain and activity level
Neurological status (level of consciousness, affect, reflexes, etc.)
Cardiopulmonary status (BP; take heart rate in full minute)
Electrocardiogram as ordered
Laboratory tests (e.g. CBC, liver and kidney function tests, etc.)
93
The most effective for recurrent variant of angina
Sublingual nitroglycerines
94
for unstable angina
Continuous transfusion or transdermal patch
95
are drugs which block or lyse the effects of sympathetic stimulation. Hence, they are also called as sympatholytics.
Beta-Adrenergic Blockers
96
Therapeutic Action Beta-Adrenergic Blockers
Decrease in blood pressure, contractility or heart rate by blocking beta receptors in the heart. Reduce the oxygen demand of the heart.
97
Indications Beta-Adrenergic Blockers
Nadolol is used for management of chronic angina. It is the drug of choice in angina patients with hypertension.
Propranolol is the prototype drug of this class. It is used for treatment of angina and syncope.
Nebivolol, the newest adrenergic blocking agent does not produce the same adverse effects seen in propranolol.
98
is used for management of chronic angina. It is the drug of choice in angina patients with hypertension.
Nadolol
99
is the prototype drug of this class. It is used for treatment of angina and syncope.
Propranolol
100
, the newest adrenergic blocking agent does not produce the same adverse effects seen in propranolol.
Nebivolol
101
Contraindications Beta-Adrenergic Blockers
Bradycardia, heart block, and cardiogenic shock – blocking effect of drugs exacerbates these conditions
Pregnancy and lactation – potentially harmful effects to the fetus or neonate
Diabetes, chronic obstructive pulmonary disease (COPD), thyrotoxicosis, and peripheral vascular diseases – blocking effect prevents maintaining homeostatic requirements of these diseases
102
Adverse Effects Beta-Adrenergic Blockers
CNS: emotional depression, dizziness, fatigue, sleep disturbances
GI: gastric pain, nausea, vomiting, colitis, diarrhea
CV: heart failure, reduced cardiac output, arrhythmia
Respiratory: dyspnea, cough, bronchospasm
103
Interactions Beta-Adrenergic Blockers
Clonidine: increased rebound hypertension
NSAIDs: decreased antihypertensive effects
Epinephrine: hypertension followed by bradycardia
Ergot alkaloids: peripheral ischemia
Insulin and oral hypoglycemic agents: alteration in blood glucose levels without the patient experiencing manifestations of hypo- or hyperglycemia
104
Nursing Considerations Beta-Adrenergic Blockers
Assess for presence of mentioned contraindications and cautions.
Assess neurological status to determine presence of neurological adverse effects. Focus on level of orientation and sensory function.
Monitor blood pressure and heart rate accurately. Be sure to count the heart rate in one full minute.
Auscultate lungs to determine presence of possible respiratory adverse effects.
Check color and sensation of extremities. Measure capillary refill. This is to evaluate presence of insufficiencies in the peripheral vascular system.
Monitor laboratory test results (e.g. electrolyte levels and renal function tests) to ascertain risk for arrhythmia and discern whether dose adjustment is needed.
105
are drugs which block heart contraction by inhibiting movement of calcium ions, thereby altering arterial and cardiac muscle action potentials.
Calcium-Channel Blockers
106
Therapeutic Action Calcium-Channel Blockers
blocking the contractions, loss of muscle tone and vasodilation occur. Decreasing peripheral resistance. It relieves various spasm in variant angina
107
Indications Calcium-Channel Blockers
Treatment of variant angina, chronic angina and effort-associated angina
108
Contraindications
Allergy to drugs
Heart block and sick sinus syndrome – conduction problems in these disease may be exacerbated by slow conduction effect of drugs
Renal and hepatic dysfunctions – alteration with metabolism and excretion of drugs
Heart failure – worsened by decreased cardiac output effect of the drug
109
Adverse Effects Calcium-Channel Blockers
CNS: dizziness, lightheadedness, fatigue, and headache
GI: nausea, hepatotoxicity effect of the drug
CV: hypotension, bradycardia, peripheral edema
EENT: flushing, rash
110
Interactions Calcium-Channel Blockers
Cyclosporine with diltiazem: increased serum level and toxicity of cyclosporine
Cyclosporine with verapamil: heart block and digoxin toxicity. Verapamil increases level of digoxin.
Digoxin with verapamil: depressed myocardial conduction
General anesthesia with verapamil: serious respiratory distress
111
Nursing Considerations Calcium-Channel Blockers
Assess for presence of mentioned contraindications and cautions.
Inspect skin color and integrity to determine presence of adverse effects on skin.
Assess the patient’s complaint of pain and the activity level prior to and after the onset of pain to aid in identifying possible contributing factors to the pain and its progression.
Monitor cardiopulmonary status closely as the drug can cause severe effects on these two body systems`
112
Antiarrhythmics address arrhythmia by altering cells’ automaticity and conductivity.
Antiarrhythmics
113
is the term applied for disruptions that interfere with generation of impulses and conduction of these impulses to the myocardium.
Arrhythmia
114
T or F
All cells in the heart are capable of undergoing spontaneous contractions (automaticity). Therefore, these cells are capable of generating excitatory impulses.
Disruptions in the conduction of these impulses affect contractility of the heart as well as the volume of blood pumped by the heart each minute (cardiac output).
T
115
Examples of antiarrhythmic
I, II, III, IV,
116
Also called dysrhythmia, involves changes in automaticity and the conductivity of the heart cells
Arrhythmia
117
is the property of the heart cells to transmit spontaneous impulses starting from the sinoatrial (SA) node, activating all parts of the heart muscle almost spontaneously.
-is the basis of cardiac contraction and relaxation, allowing the heart to beat.
Conductivity
118
____ – impulse generation of 60-100 impulses per minute
____ – 40-50 impulses per minute
_____ – 10-20 impulses per minute
SA node ; AV node ; Ventricular muscle cells
119
Different areas of the specialized conductive system include:
SA node
AV node
Ventricular muscle cells –
120
is the property of the heart cells to undergo spontaneous depolarization during relaxation
Automaticity
121
Here are the five phases of action potential:
Phase 0 – depolarization phase; This phase is characterized by open sodium gates and sodium ions rushing towards the cell leading to action potential.
Phase 1 – a very short period wherein concentration of sodium equalizes inside and outside of the cell
Phase 2 – plateau phase; stage in which cell is trying to go back to its resting stage (repolarization).
Phase 3 – rapid repolarization phase
Phase 4 – resting phase; stage in which sodium-potassium pump restores the cell’s resting membrane potential in preparation for the next action potential.
122
Types of arrhythmias
Depending on factors causing them, here are different types of arrhythmias:
Changes in rate: tachycardia, bradycardia
Stimulation from ectopic focus: premature atrial contractions (PACs), premature ventricular contractions (PVCs), atrial flutter and/or fibrillation (AF), ventricular fibrillation
Alterations in conduction through the muscle: heart blocks, bundle branch block
It can be triggered by the following: electrolyte disturbances, decreased oxygen supply to the cells, structural damage of the conduction system, drug effects, acidosis, and lactic acid accumulation.
123
This class blocks sodium channels in the cell membrane during action potential. Subgroup under this class is based on their mechanism in blocking sodium channels.
These class are local anesthetics and membrane-stabilizing agents because of their ability to bind more quickly to sodium channels.
Class I antiarrhythmics
124
Therapeutic Action Class I antiarrhythmics
Class I antiarrhythmics stabilize cell membrane by depressing phase 0 of action potential. They bind to sodium channels and change the duration of action potential of the cells.
Class Ia drugs depress phase 0 and prolong duration of action potential.
Class Ib drugs somewhat depress phase 0 and shorten duration of action potential.
Class Ic drugs markedly depress phase 0 and extremely slows conduction but has little effect on the duration of action potential.
125
Indications Class I antiarrhythmics
Primarily indicated for decreasing workload of the heart and relieving HF
Digoxin is especially indicated for atrial flutter, atrial fibrillation, and paroxysmal atrial tachycardia.
126
Class Ia drugs ____
Class Ia drugs depress phase 0 and prolong duration of action potential.
127
Class Ib ____
Class Ib drugs somewhat depress phase 0 and shorten duration of action potential.
128
Class Ic ____
drugs markedly depress phase 0 and extremely slows conduction but has little effect on the duration of action potential.
129
t OR F antiarrhythmics IS SAFE FOR PREGNANT WOMEN
antiarrhythmics NOT SAFE F IT IS PROHIBITED
130
T OR F antiarrhythmics SUSCEPTIBLE TO ADULTS
T
131
Contraindications Class I antiarrhythmics
Allergy to Class I antiarrhythmics. Prevent severe hypersensitivity reactions.
Bradycardia, heart block. Unless an artificial pacemaker is in place, the conduction-altering effect of drug can lead to total heart block.
HF, hypotension, shock. Exacerbated by effects of drug on action potential.
Electrolyte imbalance. Can alter drug effectiveness
Renal, hepatic dysfunction. Interfere with drug bioavailability and excretion
Pregnancy and lactation. Can cause potential adverse effects to the fetus or neonate.
132
Adverse Effects Class I antiarrhythmics
CNS: dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech, vision changes, tremors
CV: arrhythmias, hypotension, vasodilation, potential for cardiac arrest
Respiratory: respiratory depression
Hema: bone marrow depression
EENT: rash, hypersensitivity reactions, hair loss
133
Interactions
Class I antiarrhythmics
Digoxin, beta-blockers: increased risk for developing arrhythmias
Quinidine with digoxin: quinidine competes with digoxin at renal transport sites so it can increase chances of developing digoxin toxicity
Cimetidine: increased Class Ia toxicity
Anticoagulants: increased risk of bleeding
134
This class interferes with action potential by blocking beta receptors in the heart and kidneys. This, in turn, blocks phase 4 of action potential.
are beta-adrenergic blockers.
Class II antiarrhythmics
135
Therapeutic Action Class II antiarrhythmics
Class II antiarrhythmics engage in competitive inhibition of beta receptors specifically found in the heart and kidneys. For this reason, there is decreased in heart rate, excitability, and cardiac output. Conduction through AV node also slows down. In the kidneys, release of renin is decreased.
These effects decrease blood pressure and the stabilize the highly-excitable heart. As a result, workload of the heart is lessened.
136
Indications Class II antiarrhythmics
This class is specifically indicated for treatment of supraventricular tachycardia and premature ventricular contractions (PVCs).
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.
137
Contraindications Class II antiarrhythmics
Sinus bradycardia (<45 beats per minute), heart block. Exacerbated by the therapeutic effects of the drug.
HF, cardiogenic shock, asthma, respiratory depression. Exacerbated by blocking beta receptors.
Pregnancy and lactation. Can cause potential adverse effects to the fetus or neonate.
Diabetes, thyroid dysfunction. Altered by blockade of beta-receptors
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.
138
Adverse Effects Class II antiarrhythmics
CNS: dizziness, fatigue, dreams, insomnia
CV: arrhythmias, hypotension, bradycardia, AV blocks, alteration in peripheral perfusion
Respiratory: bronchospasm, dyspnea
GI: anorexia, diarrhea, constipation, nausea, vomiting
Other: loss of libido, decreased tolerance to exercise, alterations in blood glucose level
139
Interactions Class II antiarrhythmics
Verapamil: increased adverse drug effects
Insulin: increased hypoglycemia
140
This class prolongs and slows down the outward movement of potassium during phase 3 of action potential. These drugs act directly on the heart muscles to prolong repolarization and refractory period.
All of these drugs are proarrhythmic and have the possibility of inducing arrhythmias.
Class III antiarrhythmics
141
Indications Class III antiarrhythmics
Amiodarone is the drug of choice for ventricular fibrillation and pulseless ventricular tachycardia.
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.
142
Therapeutic Action Class III antiarrhythmics
Class III antiarrhythmics’ ability to prolong refractory period and repolarization increases the threshold for ventricular fibrillation.
These are used to treat life-threatening arrhythmias for which no other drugs have been effective.
This class can also act on peripheral tissues to decrease peripheral resistance..
143
Contraindications
Class III antiarrhythmics
AV Block. Ibutilide and dofetilide exacerbate this health condition.
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.
Shock, hypotension, respiratory depression, prolonged QT interval. Depressed action potentials can worsen these health problems.
144
Adverse Effects Class III antiarrhythmics
CNS: weakness, dizziness
CV: arrhythmias, HF
GI: nausea, vomiting, GI distress
Amiodarone is associated with liver toxicity, ocular abnormalities, and very serious cardiac arrhythmias.
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Interactions Class III antiarrhythmics
Digoxin, quinidine: increased toxic drug effects
Antihistamines, phenothiazines, tricyclic antidepressants: increased risk of proarrhythmias
Dofetilide combined with ketoconazole, verapamil, cimetidine: increased risk for adverse drug effects
Sotalol combined with antacids, NSAIDs, and aspirin: loss of effectiveness of sotalol
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Include two calcium-channel blockers, namely: diltiazem and verapamil.
This class blocks the movement of calcium towards the cell membrane..
Class IV antiarrhythmics
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Therapeutic Action Class IV antiarrhythmics
Class IV antiarrhythmics depress action potential generation and slows down phases 1 and 2 of action potential. This action slows down both conduction and automaticity.
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Indications
Class IV antiarrhythmics
Other uses of diltiazem and verapamil include treatment for hypertension and angina.
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.
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Contraindications Class IV antiarrhythmics
Allergy to calcium-channel blockers. Prevent hypersensitivity reactions.
Heart block (sick sinus syndrome). Unless an artificial pacemaker is in place, heart blocks can be exacerbated by the effects of the drug.
HF, hypotension. Exacerbated by hypotensive effect of the drug.
Pregnancy, lactation. Potential adverse effects to neonate or fetus.
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.
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Adverse Effects Class IV antiarrhythmics
CNS: weakness, dizziness, fatigue, depression, headache
CV: hypotension, shock, edema, HF, arrhythmia
GI: nausea, vomiting, GI distress.
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Interactions Class IV antiarrhythmics
Verapamil with beta-blockers: increased risk of cardiac depression
Digoxin: additive slowing of AV node conduction
Atracurium, pancuronium, vecuronium: increased respiratory depression
Increased risk of cardiac depression if IV preparation of these drugs were given 48 hours within administration of IV beta-adrenergic blockers.
Diltiazem can increase serum level of cyclosporine.
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Nursing Considerations for Antiarrhythmics
These are the important things the nurse should include in conducting assessment, history taking, and examination:
Assess for the mentioned contraindications to this drug (e.g. renal dysfunction, heart blocks, hypersensitivity, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Assess patient’s neurological status to determine potential CNS drug effects.
Assess cardiac status closely (e.g. blood pressure, heart rate and rhythm, heart sounds, ec.) to determine whether change in drug dose is imperative.
Monitor respiratory rate, rhythm, and depth to assess for respiratory depression and detect changes associated with development of HF.
Monitor laboratory test results including complete blood count, renal and liver function tests to determine the need for possible change in dose and identify toxic effects.
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lower serum levels of cholesterol and various lipids. They are also called as lipid-lowering agents; these drugs provide effective treatment for hyperlipidemia (increased lipid level in the blood).
lipid lowering agents/ antihyperlipidemic drug
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Due to various reasons, fatty streaks begin to develop in the endothelium of coronary arteries. Over time, these fatty streaks develop into plaques (atheromas) and injure the lining of blood vessels. The inflammatory reaction begins, and it attracts white blood cells and platelets to the area. These cells collect on the injured vessels and cause the atheroma to grow bigger, further narrowing the diameter of blood vessels, and therefore, limiting the blood flow.
The injury decreases the flexibility of the vessels, rendering it less distensible and less reactive to neurochemical stimuli. Coronary arteries are now unable to balance oxygen demand and blood supply.
If not acted promptly, this can lead to total vessel blockage and vessel rupture. CAD is the leading cause of death worldwide, and its incidence is high in people with hyperlipidemia.
The cause of CAD remains unknown, but certain risk factors were identified, and these include increasing age, male gender, sedentary lifestyle, smoking, obesity, high-fat diet, high-stress levels, menopause, and medical conditions like hypertension, gout, and diabetes.
Coronary Artery Disease (CAD)
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Examples of lipid lowering agents
- Bile Acid Sequestrants
- HMG-CoA Reductase Inhibitors
- Cholesterol Absorption Inhibitors
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These drugs are used to normalize high serum level of cholesterol.
Bile Acid Sequestrants
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Therapeutic Action Bile Acid Sequestrants
Bile acid sequestrants exert their effect in the intestines by binding into bile acids which contain a high level of cholesterol.
The resultant insoluble complex formed by this combination is then excreted through feces.
As this happens, more LDL segments from the circulation will be absorbed by the intrahepatic circulation to make more bile acids.
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Indications Bile Acid Sequestrants
Bile Acid Sequestrants are used as the treatment for primary hypercholesterolemia (high cholesterol and high LDL) as an adjunct to diet and exercise.
Cholestyramine is also used to treat pruritus associated with partial biliary obstruction.
Children: limited because lipids are important for development
Adults: combination with ChMg
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Pharmacokinetics Bile Acid Sequestrants
Not absorbed systemically and is excreted in the feces.
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Contraindications Bile Acid Sequestrants
Allergy to bile acid sequestrants. Prevent severe hypersensitivity reactions.
Complete biliary obstruction. Prevent bile from being secreted into the intestines.
Abnormal intestinal function. Aggravated by the presence of bile acid sequestrants.
Pregnancy and lactation. Potential decrease in absorption of fat and fat-soluble vitamins can be detrimental to fetus or neonate
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Adverse Effects Bile Acid Sequestrants
CNS: headache, anxiety, fatigue, drowsiness
GI: GI upset, constipation, fecal impaction, nausea, aggravated hemorrhoids
Hema: increased bleeding time, decreased production of clotting factors
Musculoskeletal: muscle aches, muscle pains
Other: rash, fat-soluble vitamin deficiencies
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Interactions Bile Acid Sequestrants
Bile acid sequestrants delay the absorption of thiazide diuretics, corticosteroids, digoxin, warfarin, and thyroid hormones. Therefore, if needed, these drugs are taken 1 hour before or 4-6 hours after a meal.
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Nursing Considerations Bile Acid Sequestrants
Assess for the mentioned contraindications to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess neurological status, particularly orientation and alertness to determine any CNS effects.
Assess bowel elimination patterns, including frequency of stool passage and stool characteristics to monitor the development of constipation and possible fecal impaction.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose
Inspect abdomen for distention and auscultate bowel sounds to assess for changes in GI motility.
Monitor results of laboratory tests, particularly serum cholesterol and lipid levels to evaluate the effectiveness of drug therapy.
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This drug group increases the cell absorption of LDL by blocking the enzyme (HMG-CoA reductase) regulating the rate-limiting step in the synthesis of cholesterol. With this alteration in fat metabolism, HDL increases slightly.
-chemically modified from the products of fungi
HMG-CoA Reductase Inhibitors
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Therapeutic Action HMG-CoA Reductase Inhibitors
These are primarily indicated as adjunct medicine with diet and exercise for treatment of high cholesterol and LDL levels in the blood.
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Indications HMG-CoA Reductase Inhibitors
Pravastatin, lovastatin, and simvastatin are indicated for patients with documented CAD to slow progression of the disease.
Together with these three agents, atorvastatin is used as prophylaxis for first myocardial infarction attack for patients with multiple risk factors for CAD.
PREGNANCY CATEGORY X For women who are pregnant, this drug class is contraindicated (pregnancy category X).
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Contraindications HMG-CoA Reductase Inhibitors
Allergy to HMG-CoA reductase inhibitors. Prevent severe hypersensitivity reactions.
Active liver disease. Exacerbated by drug’s therapeutic effect and has potential to lead to severe liver failure.
Pregnancy, lactation. Potential for drug adverse effects to fetus or neonate.
Impaired endocrine function. Problems can arise due to alteration in the formation of steroid hormones.
Renal impairment. Caution is given to patients taking other statins and close monitoring in instituted. Atorvastatin is not affected by renal diseases.
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Interactions HMG-CoA Reductase Inhibitors
Cyclosporine, erythromycin, gemfibrozil, niacin, antifungal drugs: increased risk for rhabdomyolysis
Digoxin, warfarin: increased serum levels and resultant toxicity of HMG-CoA reductase inhibitors
Oral contraceptives: increased serum estrogen
Grapefruit juice: increased serum levels and resultant toxicity
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HMG-CoA Reductase Inhibitors Adverse Effects
CNS: headache, dizziness, insomnia, fatigue, blurred vision, cataract development
CV: increased risk for cardiovascular effects with simvastatin started at 80 mg for new patients
GI: flatulence, nausea, vomiting, cramps, abdominal pain, constipation
Hepatobiliary: increase liver enzymes, acute liver failure with use of atorvastatin and fluvastatin
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Nursing Considerations HMG-CoA Reductase Inhibitors
Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess neurological status with particular focus on consciousness, reflexes, and affect.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose.
Assess bowel patterns to determine possibility of developing constipation and resultant fecal impaction.
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are one of the new class of drugs approved (2003) to lower serum cholesterol levels.
- contreversy, fail to show its effects, further studies need to validate this
Cholesterol Absorption Inhibitors
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Therapeutic Action Cholesterol Absorption Inhibitors
Acting on the brush border of intestines, cholesterol absorption inhibitors block the absorption of dietary cholesterol. Consequently, less cholesterol goes to the liver and it increases the cholesterol clearance to make up for the drop..
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Indications Cholesterol Absorption Inhibitors
Adjunct to diet and exercise as a monotherapy or in combination with HMG-CoA inhibitors or bile acid sequestrants.
Used in combination with statins to treat homozygous familial hypercholesterolemia.
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Contraindications Cholesterol Absorption Inhibitors
Allergy to cholesterol absorption inhibitors. Prevent severe hypersensitivity reactions.
Liver disease, pregnancy, lactation: not used if combined with statins because of the effects of statins to these health conditions. Effect of this class to fetuses and neonates is not known.
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Adverse Effects Cholesterol Absorption Inhibitors
CNS: headache, dizziness, fatigue
Respiratory: upper respiratory tract infection (URI)
GI: mild abdominal pain, diarrhea
Musculoskeletal: muscle aches and pains, back pain
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Interactions Cholesterol Absorption Inhibitors
Cholestyramine, fenofibrate, antacid, gemfibrozil: elevated serum level of cholesterol absorption inhibitors
Cyclosporine: increased toxicity of cholesterol absorption inhibitors
Fibrates: increased risk for development of cholelithiasis
Warfarin: increased serum warfarin levelsy
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Nursing Considerations Cholesterol Absorption Inhibitors
Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.). To prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy. To establish baseline status, determine effectivity of therapy and evaluate potential adverse effects.
Assess neurological status. Give with a particular focus on orientation and reflexes to determine CNS drug effects.
Assess closely patient’s heart rate and blood pressure. To identify cardiovascular changes that may warrant a change in drug dose.
Assess bowel patterns. To determine the possibility of developing constipation and resultant fecal impaction.
Monitor laboratory test results of serum cholesterol, LDL, and liver function. To determine the potential for drug adverse effects and monitor effectiveness of therapy.
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These groups of drugs affect clot formation and resolution by hindering different steps in clotting formation which include altering the formation of platelet plug (antiplatelet drugs), interfering the clotting cascade and thrombin formation (anticoagulant drugs), and stimulating the plasmin system to break down the formed clot (thrombolytic agents).
Drugs Affecting Coagulation
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Examples of Drugs Affecting Coagulation
- Antiplatelet Agents
- Anticoagulants
- Thrombolytic Agents
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Disorders that directly affect coagulation process
Thromboembolic and Hemorrhagic Disorders
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Disorders that directly affect coagulation process are divided into two main categories:
thromboembolic disorders and hemorrhagic disorders
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which involve overproduction of clots
thromboembolic disorders
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which is characterized by ineffective clotting process leading to excessive bleeding.
hemorrhagic disorders
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include medical conditions (e.g. CAD) which involve overproduction of clots which result into decreased blood flow and total vessel occlusion. Manifestations include hypoxia, anoxia, and even necrosis. These disorders are treated by drugs that interfere with normal coagulation process to prevent formation of clots.
Thromboembolic disorders
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Antiplatelet Agents
This drug class exerts its action by decreasing the responsiveness of platelets to stimuli that cause it to clump or aggregate. Through this, formation of platelet plug is decreased.
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Therapeutic Action Antiplatelet Agents
By blocking receptor sites on the platelet membrane, platelet adhesion and aggregation is inhibited.
Also, platelet-platelet interaction as well as interaction of platelets to clotting chemicals are prevented.
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Indications Antiplatelet Agents
Primarily indicated for cardiovascular diseases that have potential for development of vessel occlusion.
Other indications include maintenance of arterial and venous grafts, preventing cerebrovascular occlusion, and including them as adjunct to thrombolytic therapy for treatment of myocardial infarction.
One drug, anagrelide, blocks the production of platelets in the bone marrow.
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Contraindications Antiplatelet Agents
Allergy to antiplatelet agents. Prevent severe hypersensitivity reactions.
Known bleeding disorder. Increased risk of excessive blood loss
Recent surgery. Increased risk of bleeding in unhealed blood vessels
Closed head injuries. Increased risk of bleeding in injured blood vessels of the brain
History of thrombocytopenia. Anagrelide decreased bone marrow production of platelets.
Pregnancy, lactation. Generally inadvisable because of potential adverse effects to fetus or neonate
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Adverse Effects Antiplatelet Agents
Adverse Effects
CNS: headache, dizziness, weakness
GI: GI distress, nausea
Skin: skin rash
Hema: bleeding (oftenly occurs while brushing the teeth)
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Interactions Antiplatelet Agents
Increased risk of bleeding if combined with another drug that affects blood clotting.
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Nursing Considerations Antiplatelet Agents
Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count and clotting studies to determine any potential adverse effects.
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By interfering with clotting cascade and thrombin formation, anticoagulants are able to interfere with the normal clotting process.
Anticoagulants
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Indications Anticoagulants
Among the many indications for this drug class include: stroke and systemic emboli risk reduction, nonvalvular atrial fibrillation, and deep vein thrombosis.
Heparin is used for prevention of blood clots in blood samples, dialysis, and venous tubing. It also does not enter breastmilk so it is the anticoagulant of choice for lactating women.
Antithrombin is a naturally-occurring anticoagulant and is a natural safety feature in the clotting system.
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Therapeutic Action Anticoagulants
Warfarin, an oral agent in this class, reduces Vitamin K-dependent clotting factors. As a result, clotting process is prolonged.
Two new oral agents, dabigatran and rivaroxaban, directly inhibits thrombin (last step in clotting process) and factor Xa, respectively.
Heparin and antithrombin block formation of thrombin from prothrombin.
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Contraindications Anticoagulants
Allergy to anticoagulants. Prevent severe hypersensitivity reactions.
Known bleeding disorder, recent trauma/surgery, presence of indwelling catheters, threatened abortion, GI ulcers. These conditions can be compromised by increased bleeding tendencies.
Pregnancy, lactation. Warfarin is a contraindication.
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Adverse Effects Anticoagulants
Warfarin is associated with alopecia, dermatitis, bone marrow depression, and less frequently with prolonged and painful erections.
Direct drug toxicity is characterized by nausea, GI upset, diarrhea, and hepatic dysfunction
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Interactions Anticoagulants
Anticoagulants, salicylates, penicillin, cephalosporin: increased bleeding if combined with heparin
Nitroglycerin: decreased anticoagulation if combined with heparin
Cimetidine, clofibrate, glucagon, erythromycin: increased bleeding if combined with warfarin
Vitamin K, phenytoin, rifampin, barbiturates: decreased anticoagulation if combined with warfarin
Antifungals, erythromycin, phenytoin, rifampin: alteration in metabolism of dabigatran and rivaroxaban
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Nursing Considerations Anticoagulants
Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count and clotting studies to determine any potential adverse effects.
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agents promote clot resolution, the process of activating the plasmin system to break down the thrombus or clot that has been formed.
Thrombolytic Agents
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Indications Thrombolytic Agents
For treatment of acute MI, pulmonary embolism, and acute ischemic stroke.
Also for clearing of occluded intravenous catheters and central venous access devices.
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Therapeutic Action Thrombolytic Agents
The conversion of plasminogen to plasmin is the body’s natural anticlotting system. Thrombolytic agents’ action to activate this promotes breakdown of fibrin threads and dissolution of formed clots.
It is necessary to prevent vessel occlusion and therefore, to deliver adequate blood flow to body systems.
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Contraindications Thrombolytic Agents
Allergy to thrombolytics. Prevent severe hypersensitivity reactions.
Known bleeding disorder, recent trauma/surgery, acute liver disease, cerebrovascular accident within 2 months, GI ulcers. These conditions can affect normal clotting factors and normal plasminogen production.
Pregnancy, lactation. Potential adverse effects to fetus or neonate.
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Adverse Effects Thrombolytic Agents
CV: cardiac arrhythmias, hypotension
Hema: bleeding (most common)
Hypersensitivity reaction (uncommon) is characterized by rash, flushing, and bronchospasm.
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Interactions Thrombolytic Agents
Anticoagulant, antiplatelet: increased risk of bleeding
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Nursing Considerations Thrombolytic Agents
Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, CVA within 2 months, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count, fecal occult blood test (FOBT), and clotting studies to determine any potential adverse effects.
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Condition slowly arising all across country.
-hemoglobin concentration is lower than normal
-not specific disease state
Anemia
207
results from the inability of bone marrow to produce adequate numbers of red blood cells.
Hypoproliferative anemia
208
Premature destruction of erythrocytes that results the liberation of hemoglobin from the erythrocytes
Hemolytic anemia
209
The formation of new blood cells is one of the primary functions of bones. This process is known as
hematopoiesis, and it includes the production of erythrocytes (red blood cells, or RBCs), as well as leukocytes (white blood cells) and thrombocytes (platelets)
210
is a mineral that is essential for the proper function of all biologic systems in the body. It is stored in many sites throughout the body (liver, spleen, and bone marrow). Deficiency of this mineral is the principal nutritional deficiency resulting in anemia.
IRON
211
Therapeutic Action IRON
is an oxygen carrier in both hemoglobin and myoglobin (oxygen-carrying molecule in muscle tissue) and is critical for tissue respiration. Iron is also a required component of a number of enzyme systems in the body and is necessary for energy transfer in the cytochrome oxidase and xanthine oxidase enzyme systems
212
IRON Indications
Supplemental iron contained in multivitamins plus iron or iron supplements alone are indicated for the prevention or treatment of iron-deficiency anemia.
213
Adverse Effect IRON
Nausea, constipation, epigastric pain, black and tarry stools, vomiting, diarrhea, temporarily discolored tooth enamel, eyes pain on injects
214
Contraindications IRON
Contraindications to the use of iron products include known drug allergy, hemochromatosis (iron overload), hemolytic anemia, and any other anemia not associated with iron deficiency.
215
Interactions IRON
The absorption of iron can be enhanced when it is given with
ascorbic acid and decreased when it is given with antacids and
calcium. Iron preparations can decrease the absorption of certain antibiotics, including tetracyclines and quinolones.
216
is a water-soluble B-complex vitamin. It is also referred to as folate, the name of its anionic form.
FOLIC ACID
217
Therapeutic Action FOLIC ACID
Folic acid is converted in the body to tetrahydrofolic acid, which is used for erythropoiesis and for synthesis of nucleic acids (DNA and ribonucleic acid [RNA]).
218
Adverse Effect FOLIC ACID
Adverse effects associated with folic acid use are rare. Allergic
reaction or yellow discoloration of urine may occur.
219
Indications FOLIC ACID
Folic acid is primarily used to prevent and treat folic acid deficiency. Anemias caused by folic acid deficiency can be treated by exogenous supplementation of folic acid.
220
Contraindications FOLIC ACID
Contraindications to the use of folic acid include known allergy to a specific drug product and any anemia not related to folic acid deficiency (e.g., pernicious anemia). Folic acid is not to be used to treat anemias until the underlying cause and type of anemia have been determined.
221
Interactions FOLIC ACID
No significant drug interactions occur with folic acid.
222
OTHER ANEMIA DRUGS
Cyanocobalamin (vitamin B12)
223
used to treat pernicious anemia and other megaloblastic anemias. It can be given orally or intranasally to treat vitamin B12 deficiency but is usually given by deep intramuscular injection to treat pernicious anemia. Once remission of the anemia is seen, cyanocobalamin can be dosed once a
month.
Cyanocobalamin (vitamin B12)
224
are ineffective without adequate body iron stores.
Erythropoiesis-stimulating agents
225
are very important in the treatment of many disorders and diseases (e.g., malignancies) to achieve RBC and hemoglobin formation that is as adequate as possible and to help prevent nutritional deficits that can affect all body systems, especially the immune system
Iron and folic acid
226
are often used in the treatment of pernicious anemia, malabsorption syndromes, hemolytic anemias, hemorrhage, and renal and liver diseases.
Blood-forming drugs
227
T or F
Instruct patients to take iron products exactly as ordered. Parenteral dosage forms may cause anaphylaxis and orthostatic hypotension.
T
228
The primary treatment for heart failure (HF) is ___________.
Increasing contractility so the heart will be able to pump more blood
