Perfusion Flashcards
(280 cards)
1
Q
Perfusion
A
the blood flow through arteries and capillaries delivering nutrients and oxygen to cells
2
Q
Clotting
A
physiological process in which blood is converted from a liquid to a semisolid gel
3
Q
Central Perfusion
A
Force of blood movement generated by cardiac output
4
Q
Central perfusion requires
A
adequate cardiac function, bp, and blood volume
5
Q
Central perfusion equation
A
Cardiac output (CO) = stroke volume x heart rate
6
Q
Tissue or local perfusion
A
Volume of blood that flows to target tissue
7
Q
Tissue or local perfusion requires
A
patent vessels, adequate hydrostatic pressure, and capillary permeability
8
Q
When does impairment of central perfusion occur
A
cardiac output is inadequate
9
Q
Reduced cardiac output results in
A
reduced oxygenated blood reaching the body tissues
10
Q
If impaired central perfusion is not treated
A
if it is severe it leads to shock
if completely untreated leads to ischemia, cell death and cell injury
11
Q
Impairment of tissue perfusion is associated witH
A
Loss of vessel patency
12
Q
Impaired blood flow to affected body tissues leads to
A
Ischemia, cell death if uncorrected
13
Q
Populations at greatest risk for impaired perfusion are
A
Middle aged and older adults
men
African Americans
14
Q
Signs of inadequate central perfusion in infants
A
Poor feeding
Poor weight gain
Failure to thrive
Dusky colour
15
Q
Signs of inadequate Central perfusion in Toddlers and children
A
Squatting and fatigue
Development delay
16
Q
Ischemia
A
Poor blood supply to an organ
17
Q
Ischemic Heart Disease
A
Poor blood supply to the heart muscle
Athersclerosis
Coronary artery disease
18
Q
Myocardial Infarction
A
Necrosis, or death of cardiac tissue
Disabling or fatal
19
Q
Hemostasis
A
General term for any process that stops bleeding
20
Q
What is coagulation
A
Hemostasis that occurs because of the physiological clotting of blood
21
Q
Thrombus
A
Technical term for a blood clot
22
Q
Embolus
A
Thrombus that moves through blood vessels
23
Q
Coagulation system
A
Each activated factor serves as a catalyst that amplifies the next reaction
24
Q
Coagulation system Result is
A
Fibrin, a clot forming substance
25
Fibrinolytic System
The breakdown of clots and serves to balance the clotting process
26
Fibrinolysis
Mechanism by which formed thrombi are lysed to prevent excessive clot formation and blood vessel blockage
27
Fibrin
In the clot binds to a circulating protein known as plasminogen. This binding converts plasminogen to plasmin
28
Plasmin
Is the enzymatic protein that eventually breaks down the fibrin degradation products. This keeps the thrombus localized to prevent it from becoming an embolus
29
Systemic clotting Problem
Problem extends to entire body; is usually the result of a significant haematological event
30
Localized clotting problem
Problem is localized; is usually a problem in a vein or artery, either injury to a vessel or a clot within a vessel
31
Factors affecting Blood Flow
Pressure, Resistance and Neural control of total peripheral resistance
32
Pressure
Force exerted in a liquid per unit area
33
Resistance
Opposition to force
| Diameter and length of the blood vessels contribute to resistance
34
Neuralcontrol of total peripheral resistance
Change in diameter of the vessels
Baroreceptors
Arterial Chemoreceptors
35
Factors affecting blood flow
Velocity
Laminar versus turbulent flow
Vascular compliance
36
Atherosclerosis
Type of blood vessel disorder
| Begins with soft fat deposits that harden with age
37
Terms to describe the disease process of Atherosclerosis
Arteriosclerotic heart disease
Cardiovascular heart disease
Ischemic heart disease
Coronary artery disease
38
Atherosclerosis is the major cause of
Coronary Artery Disease
39
Step 1 of Atherosclerosis
LDL enters intimate through intact endothelium
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Step 2 of Atherosclerosis
Intimal LDL is oxidized into pro inflammatory lipids
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Step 3 of Atherosclerosis
oxidized LDL causes adhesion and entry of monocytes and T Lymphocytes across endothelium
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Step 4 of Atherosclerosis
Monocytes differentiate into macrophages and then consume large amounts of LDL, transforming into foam cells
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Step 5 of Atherosclerosis
Foam cells release growth factors (cytokines) that encourage Atherosclerosis
44
C-reactive protein CRP
Nonspecific marker of inflammation
45
What is increased in many clients with CAD
CRP C-reactive protein
46
Chronic exposure to CRP is associated with?
Unstable Plaques and oxidation of LDL cholesterol
47
Developmental stage: Fatty streak of Coronary Artery Disease
Earliest lesions
Characterized by lipid-filled smooth muscle cells
Potentially reversible
48
Developmental stages: Fibrous plaque of Coronary Artery Disease
Beginning of progressive changes in the arterial wall
49
Developmental stages: Fibrous plaque of Coronary Artery Disease - Lipoproteins Transport Cholesterol and other lipids where?
Arterial intima
50
Developmental stages: Fibrous plaque of Coronary Artery Disease - Fatty streak is covered by ________ forming fibrous plaque that appears_____________
1. collagen
| 2. Grayish or whitish
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Developmental stages: Fibrous plaque of Coronary Artery Disease- Result
Narrowing of vessel lumen
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Developmental Stages: Complicated lesion of coronary heart disease
Continued inflammation can result in plaque instability ulceration, and rupture
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Developmental Stages: Complicated lesion of coronary heart disease- Platelets accumulate and ______ forms.
Thrombus
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Developmental Stages: Complicated lesion of coronary heart disease- result
Increased Narrowing or total occlusion of lumen
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Collateral circulation
Normally, some arterial anastomoses (or connections) exist within the coronary circulation
56
Growth and extent of collateral circulation are attributed to two factors
1. Inherited predisposition to develop new vessels (angiogenesis)
2. Presence of chronic ischemia
57
Nonmodifiable Risk factors of CAD
```
Age
Gender
Ethnicity
Family History
Genetic Predisposition
```
58
Modifiable Risk Factors of CAD
```
Elevated serum lipids
Hypertension
Tobacco Use
Physical Inactivity
Obesity
Diabetes
Metabolic Syndrome
Psychological States
Homocysteine level
```
59
Nontraditional Risk Factors for CAD
```
Markers of inflammation and thrombosis
Troponin I
Hyperhomocysteinemia
Adipokines
Infection
```
60
If an Embolus lodges in a coronary artery it causes a..,.
Myocardial Infarction
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If an embolus obstructs a brain vessel it causes
Stroke (cerebrovascular accident)
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If an embolus travels to the lungs it is a ...
Pulmonary Embolus
63
If an embolus travels to a vein in the leg it is called a...
DVT Deep vein thrombosis
64
Events including an embolus are referred to as
Thromboembolic events
65
Thrombus Formation in Veins
Obstruction of venous flow leading to increased venous pressure
66
Factors of Thrombus formation in veins
Triad of Virchow
- Venous Stasis
- Venous endothelial damage
- Hypercoagulable states
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Triad of Virchow
- Venous Stasis
- Venous endothelial damage
- Hypercoagulable states
68
Varicose Veins
Vein in which blood has pooled
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With Varicose veins the veins are...
Distended, tortuous, and palpable
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Varicose Veins are caused by
Trauma or gradual venous distension
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Risk Factors for Varicose Veins
```
Age
Female Gender
Family History
Obesity
Pregnancy
DVT
Prior Leg Injury
```
72
Chronic Venous Insufficiency
Inadequate venous return over a long period due to varicose veins or valvular incompetence
73
Superior Vena Cava Syndrome
Progressive occlusion of the superior vena cava that leads to venous distension of upper extremities and head
74
Peripheral Artery Diseases
Thromboangitis Obliterans
| Raynaud Phenomenon
75
Tromboangitis Obliterans (Buerger's Disease)
Inflammatory Disease of peripheral arteries
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Tromboangitis Obliterans (Buerger's Disease) is strongly associated with
Smoking
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Tromboangitis Obliterans (Buerger's Disease) is an ________ disease
Autoimmune
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Tromboangitis Obliterans (Buerger's Disease) Characterized by....
The formation of thrombi filled with inflammatory and immune cells
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Tromboangitis Obliterans (Buerger's Disease) Symptoms
Causes pain and tenderness in the affected area, also caused by slow and sluggish blood flow
80
Tromboangitis Obliterans (Buerger's Disease) can lead to
Gangrenous lesions and amputations
81
Raynaud Phenomenon
Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes
82
Primary Raynaud Phenomenon
Vasospastic disorder of unknown origin
83
Secondary Raynaud Phenomenon
```
Secondary to other diseases like:
Collagen Vascular Disease
Smoking
Pulmonary Hypertension
Myxedema
Cold Environment
```
84
Manifestations of Raynaud Phenomenon
Pallor
Cyanosis
Cold
Pain
85
Anticoagulants are also known as
Antithrombotic drugs
86
Anticoagulants have no effect on.....
Blood clots that are already formed
87
Anticoagulants prevent
Intravascular thrombosis by decreasing blood coagulability
88
Anticoagulants are used prophylactilly to prevent
```
Clot formation (Thrombus)
An Embolus (Dislodged Clot)
```
89
General Actions of Anticoagulants
Work on different points of the clotting cascade
Prevent intravascular thrombosis by decreasing blood coagulability
Do not lyse existing clots
90
Anticoagulants Indications
Used to prevent clot formation in certain settings in which clot formation is likely
- Myocardial infarction
- Unstable Angina
- Atrial Fibrillation
- Mechanical Heart Valves
- Conditions where blood flow may be slowed or blood may pool
91
Anticoagulants Contraindications
Drug Allergy
| Acute bleeding process or high risk of occurrence
92
Warfarin is strongly contraindicated in
Pregnancy
93
Low- molecular-weight heparins are contraindicated in
Patients with an indwelling epidural catheter risk of epidural hematoma
94
Anticoagulants Adverse Effects
```
Bleeding- Risk Increases with increased dosages
Heparin induced thrombocytopenia
Nausea
Vomiting
Abdominal Cramps
```
95
Adverse effects of warfarin
```
Bleeding
Lethargy
Muscle pain
Skin Necrosis
Purple Toes syndrome
```
96
Anticoagulants Drug- Drug Interactions
Interactions are profound and complicated
Enzyme Inhibition of metabolism
Displacement of the drug from inactive protein-binding sites
Decrease in Vit K absorption or synthesis by the bacterial flora of the large intestine
Alteration of platelet count or activity
97
Heparin Action
Inhibit clotting factors IIa (thrombin), Xa, and IX. Factors XI and XII are also inhibited but do not play as important a role
98
Low-Molecular- weight heparins
Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Nadroparin Calcium (Fraxiparine)
Tinzaparin Sodium (Innohep)
99
Heparin Sodium
Natural Anticoagulant obtained form the lungs or intestinal mucosa of pigs
100
Amount of heparin given for DVT prophylaxis
5,000 units subcutaneously 2-3 times a day
101
Heparin Induced Thrombocytopenia
Abnormally low levels of platelets
102
Heparin Induced Thrombocytopenia Symptoms
Excessive bruising
Prolonged bleeding from cuts, gums, nose, in still and urine
Enlrged spleen
103
Type I Heparin Induced Thrombocytopenia
Gradual Reduction in platelets
| Heparin Therapy can generally be continued
104
Type II Heparin Induced Thrombocytopenia
Acute fall in the number of platelets (more than 50% reduction from baseline)
Discontinue Heparin Therapy
105
Toxic effects Of heparin Symptoms
```
Hematuria
Melena (blood in the stool)
Petechiea
Ecchymoses
Gum or Mucous Membrane Bleeding
```
106
When toxic effects of heparin occur
Stop drug immediately
107
How to reverse toxic effects of heparin
IV Protamine sulphate 1mg can reverse the effects of 100 units of heparin
108
Do not give subcutaneous doses of heparin within 5 cm of...
```
The umbilicus
Abdominal incisions
Open wounds
Scars
Drainage tubes
Stomas
Areas of bruising or oozing
```
109
Do not ______ or __________ the heparin injection site
1. aspirate subcutaneous injections
| 2. Massage
110
Heparin may cause
Hematoma formation
111
Heparin doses are given...
Subcutaneously
112
Name of Heparin Flush
Heparin Leo
113
The Risk of development of heparin induced thrombocytopenia has caused most hospitals to use
0.9% normal saline as a flush for heparin-lock IV ports
114
Heparin flushes (100 units/mL) are still used for...
Central catheters
115
Warfarin
Inhibits Vit k synthesis by bacteria in the gastrointestinal tract
116
Warfari action
Inhibits Vit K dependent clotting factors II, VII, IX, and X which are normally synthesized in the liver
117
Warfarin needs careful monitoring of the
Prothrombin time (PT)/ international normalized ratio (INR)
118
What is normal INR (without warfarin)
0.8-1.2
119
A therapeutic INR ( with warfarin) ranges from
2-3.5
120
Warfarin may be started while the patient is still on heparin until...
PT/INR levels indcicate adequate anticoagulation
121
Full their[eutic effects of warfarin take
Several days
122
Antidote to warfarin is
Vit K
123
Herbal products that have potential interactions with Warfarin are...
```
Capsicum Pepper
Garlic
Ginger
Ginkgo
St. Johns Wort
Feverfew
```
124
Reversible effects of warfarin by Vit K may take
36-42 hours
125
When Vit K is given, Warfarinresistance will occur for up to
7 days
126
Toxic effects of warfarin include
Severe bleeding
127
Antithrombins Action
Inhibit thrombin (Factor IIa)
128
Natural antithrombins
Human antithrombin III (Thrombate)
129
Synthetic Antithrombins
Lepirudin (Refludan)
Argatroban (Argatroban)
Bivalirudin (Angiomax)
Dabigatron (Pradaxa)
130
Direct acting Xa inhibitors action
Inhibit factor
131
Direct acting Xa inhibitors examples
Fondaparinux (Arixtra)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)
132
Direct Thrombin Inhibitor
Dabigatran
133
Antiplatelet drugs Prevent
Platelet adhesion
134
Examples of anti platelet drugs
```
Aspirin
Clopidogrel bisulfate (Plavix)
Dipyridamole (Aggrenox, Persantine)
Prasugrel (Efficient)
Treprostinil (Remodulin)
Abciximab (ReoPro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Anagrelide hydrochloride (Agrylin)
```
135
Three major types of Antiplatelet drugs
1. Glycoprotein platelet inhibitors
2. Platelet aggregation inhibitors
3. Protease activated receptor 1 antagonists
136
Adverse effects of anti platelet drugs
Risk for inducing bleeding
drug-drug interactions
Monitor for abnormal bleeding
137
Lipids
Triglycerides
Phospholipids
Steroids
138
Triglycerides
Most common form of lipids
Major storage of fat in the body
Important energy source
139
Phospholipids
Used for building plasma membranes
| Found in egg yolks and soybeans
140
Steroids
Most common is cholesterol
Important part of plasma membranes
Building block for Vit D, Bile acids, Cortisol, estrogen, and testosterone
Body only needs small amount of cholesterol
141
VLDL- Very Low Density Lipoproteins
Primary carrier of triglycerides
| VLDL eventually changes to LDL
142
LDL- Low density lipoproteins
LDL transports cholesterol from liver to tissues and organs
| Known as the bad cholesterol as it contributes to plaque deposits
143
HDL- High Density Lipoproteins
Transports cholesterol back to the liver from organs and tissues to be broken down and mixed with bile for excretion
The good cholesterol
144
Normal HDL level for males
1.94mmol/L
145
Normal LDL level for males
<2.59mmol/L
146
Normal Triglycerides levels for males
0.45-1.81mmol/L
147
Normal cholesterol level for males
<5mmol/L
148
Normal HDL levels for females
>1.94mmol/L
149
Normal LDL levels for females
<2.59mmol/L
150
Normal Triglyceride level for females
0.40-1.52mmol/L
151
Normal Cholesterol levels for females
<5mmol/L
152
Pharmacotherapy In Lipid Disorders
Statins (HMG-COA Reductase Inhibitors)
Bile Acid Resins
Nicotinic Acids
Fibric Acid Agents
153
Statins action
Inhibits HMG-COA reductase (enzyme needed to synthesize cholesterol) resulting in less cholesterol biosynthesis
154
Atorvastatin (Lipitor) Uses
Primary Hypercholesterolemia
Elevated triglyceride levels
Prevention of heart attacks in those with mild elevated cholesterol
155
Atorvastatin (Lipitor) Contraindications
Pregnancy category X
| Active liver disease
156
Atorvastatin (Lipitor) precautions
```
Past liver disease
Alcoholism
Infections
Severe metabolic disorders
Electrolyte Imbalance
```
157
Atorvastatin (Lipitor) adverse effects
```
Abdominal Cramps
Constipation
Diarrhea
heart burn
Flatus
Rhabdomyolysis
ALS
Liver dysfunction
Pancreatitis
```
158
Atorvastatin (Lipitor) Interactions
Do not take with grapefruit juice, may increase digoxin
159
Atorvastatin (Lipitor) nursing consideration
```
Asses nutrition
Asses muscle pain and tenderness
monitor bowel patterns
LFTs
Renal tests
Asses eys annually
```
160
If taking Statins while child bearing age pt must
take birth control
161
While on statins do not drink
large quantities of alcohol
162
Take statins with evening meal to prevent
Stomach upset
163
Bile acid Renins Action
Binds with bile acids thusnincreasing the excretion of cholesterol
Prevent resorption of bile acids from small intestine
Bile acids are necessary for absorption of cholesterol
164
Bile Acids Prototype Drug
Cholestyramine (Questran)
165
There are lots of GI side effects with Bile Acid Renins but no...
Systemic effects
166
Nicotinic Acid Action
Acts by decreasing VLDL levels, decreasing triglycerides and increasing HDL levels
Thought to increase activity of lipase which break down minds
Reduces the metabolism or Catabolism of cholesterol and triglycerides
167
Nicotinic acid is a
B complex vitamin
168
Nicotinic acid prototype drug
Niacin (Niacin)
169
Fibric Acid agents Action
Suppress the release of free fatty acids from adipose tissue, inhibits synthesis of triglycerides in the liver and increase secretion of cholesterol in the bile
170
Prototype Fibric Acid Agent
Gemfibrozil (Lopid)
171
Side effects of Fibric Acid
```
Abdominal discomfort
Blurred vision
Diarrhea
Nausea
Headache
```
172
Precautions of Fibric Acid
Increased risk of gallstones
Prolonged thrombin time
Increased liver enzyme levels
173
Fibric Acid Interactions
```
Oral anticoagulants (may need lower doses)
Statins ( increased risk for myostistis, myalgias, rhabdomyolysis)
```
174
Adverse effects of garlic
```
Dermatitis
Vomiting
Diarrhea
Flatulence
Antiplatelet activity
```
175
Garlic can be used as...
Antispasmodic
Antihypertensive
Antiplatelet
Lipid Reducer
176
Garlic drug interactions
warfarin & Diazepam
| May enhance bleeding when taken with NSAIDS
177
Garlic should be ______ after surgery
Discontinued
178
Hypertension
Sustained elevation of systemic arterial BP
179
As BP increases, so does the risk for
Myocardial Infarction, Heart failure, stroke and renal disease
180
Cardiac output
the total blood flow through the systemic or pulmonary circulation per minute
181
Cardiac output can be described as
Stroke volume multiplied by the heart rate for 1 min
182
Systemic vascular resistance
The force opposing the movement of blood within the vessels
183
a1 and a2 adrenergic
Vasoconstriction
184
B1 adrenergic
Increased heart rate and conduction
185
B2 adrenergic
Vasodilation and increased renin secretion
186
Dopaminergic
vasodilation
187
Primary symptoms of Hypertension
Hypertension is asymptomatic until it becomes severe and target organ disease has occurred
188
Secondary Symptoms of Hypertension
```
Ftaigue
Reduced Activity Tolerance
Dizziness
Palpitations
Angina
Dyspnea
```
189
Primary Hypertension
Focus in primary related to prevalence in clinical practice
190
Secondary Hypertension
Many causes; treatment aimed at eliminating the underlying cause
191
Isolated systolic hypertension
Sustained elevation of SBP>= 140mm Hg and a DBP < 90 mm Hg
192
Malignant Hypertension
Rapidly progressive hypertension
Diastolic pressure is usually >140 mmHg
Life threatening organ damage
193
Orthostatic (postural) hypotension
Decrease in both systolic and diastolic BP upon standing
| Lack of normal BP compensation in response to gravitational changes on the circulation
194
Contributing Factors to Primary Hypertension
```
+ SNS activity
+ sodium retaining hormones and vasoconstrictors
+ sodium intake
Diabetes mellitus
> ideal body weight
+ sodium intake
Excessive Alcohol intake
```
195
Primary Hypertension Risk Factors
```
Heavy Alcohol Consumption
Advancing Stage
Cigarette Smoking
Diabetes Mellitus
Elevated Serum Lipids
High Dietary Sodium
Gender
Family History
Obesity
Ethnicity
Sedentary Lifestyle
Socioeconomic Status
Psychosocial Stress
```
196
Primary Hypertension Complications
```
Hypertensive Heart Disease
Coronary Artery Disease
Left Ventricular Hypertrophy
Heart Failure
Cerebro-vascular disease
Peripheral Vascular Disease
Nephrosclerosis
Retinal Damage
```
197
Secondary Hypertension Contributing Factors
Unprovoked Hypokalemia
Abdominal Bruit
Variable pressures with history of tachycardia, sweating, and tremor
Family History of Renal Disease
198
Secondary Hypertension Causes
Contraction or congenital narrowing of the aorta
Renal disease such as renal artery stenosis and parenchymal disease
Endocrine Disorders
Neurological disorders
Sleep Apnea
Medications
Pregnancy- induced hypertension
199
Lifestyle modifications for Hypertension
```
Nutritional Therapy
Weigh Reduction
Modification in alcohol consumption
Physical activity
Avoidance of tobacco products
Stress management
```
200
Pharmacological Therapies of Hypertension
```
Diuretics
Calcium Channel Blockers
ACE Inhibitors
Angiotensinogon II Receptors Blockers
Adrenergic Agents
```
201
Diuretics
First line of treatment for hypertension
| Lowers BP by decreasing blood volume
202
Different. Classes of Diuretics
Loop/ High Ceiling Diuretics
Thiazide and Thiazide like diuretics
Potassium Sparing Diuretics
203
Loop Diuretics Action
Inhibits reabsorption of Na and Cl from loop of Henle and distal renal tubule
204
Therapeutic Effects of Loop Diuretics
Diuresis and subsequent mobilization of excess fluid
| Decrease BP
205
Half Life of Loop Diuretics
30-60 minutes
206
Onset of Loop Diuretics
30-60 min PO
| 5 min IV
207
Peak of Loop Diuretics
1-2 hours PO
| 30 min IV
208
Contraindications of Loop Diuretics
Cross sensitivity with thiazides
209
Caution Loop Diuretics
```
Liver Disease
Electrolyte Depletion
Diabetes
Hypoproteinemia
Severe Renal Impairment
```
210
Side Effects of Loop Diuretics
```
Blurred vision
Dizziness
Headache
Vertigo
Hearing loss
Tinnitus
Hypotension
Hypovolemia
```
211
Loop Diuretics Drug-drug interactions
```
Antihypersensitives
Nitrates
Alcohol
Corticosteroids
Stimulant laxatives
NSAIDS
Lithium
```
212
Thiazide Diuretics Action
Increases excretion of Na and water by inhibiting Na reabsorption from the distal tubule
213
Thiazide Diuretics Prototype
Hydrochlorothiazide
214
Thiazide Diuretics Indication
Antihypertensive
| Thiazide diuretic
215
Thiazide Diuretics Therapeutic Effects
Decrease Bp
| Diuresis for edema
216
Thiazide Diuretics Pharmacokinetics
Rapid PO absorption
217
Thiazide Diuretics Half Life
6-15 hours
218
Thiazide Diuretics Onset
2 hours
219
Thiazide Diuretics Peak
3-6 hours
220
Thiazide Diuretics Duration
6-12 hours
221
Thiazide Diuretics Contraindications
Sulfa allergy
| Anuria
222
Thiazide Diuretics Caution
Renal/ liver impairment
| Pregnancy- jaundice or thrombocytopenia in newborn
223
Thiazide Diuretics Side effects
```
Dizziness
Drowsiness
lethargy
Weakness
Hypotension
Glaucoma
Myopia
Steven Johnson Syndrome
Hypokalemia
Dehydration
Hypomagnesemia
Hyponatremia
Hypovolemia
```
224
Potassium Sparing Diuretics Action
Acts by blocking the normal exchanges of Na+ for K+ in the distal tubules and the body retains K+
225
Potassium Sparing Diuretics prototype
Spironolactone (Aldactone)
226
Potassium Sparing Diuretics Indications
Counteract K loss caused by other diuretics
Used with thiazides to treat edema or hypertension
Primary hyperaldosterone
227
Potassium Sparing Diuretics Therapeutic Effects
Weak diuretic and antihypertensive
| Conservation of K
228
Potassium Sparing Diuretics percentage of protein binding
90%
229
Potassium Sparing Diuretics Half life
78-84 min
230
Potassium Sparing Diuretics peak
2-3 days
231
Potassium Sparing Diuretics Duration
2-3 days
232
Potassium Sparing Diuretics Contraindications
Hyperkalemia
Anuria
Renal Failure
233
Potassium Sparing Diuretics Cautions
Liver dysfunction
Age related renal dysfunction increases risk for hyperkalemia
Diabetes increases risk for hyperkalemia
Concurrent use of K supplements
234
Potassium Sparing Diuretics Side Effects
```
Dizziness
Clumsiness
Headache
Arrhythmias
Steven Johnson Syndrome
Toxic epidermal necrolysis
Breast tenderness
Gynecomastia
Ireggular menstrual cycles
Agranulocytosis
```
235
Potassium Sparing Diuretics Interactions
```
Antihypersenstitives
Alcohol
Nitrates
ACE inhibitors
ARBs
NSAIDS
K supplements
Cyclosporine
Tacrolimus
Digoxin
Litium
```
236
Potassium Sparing Diuretics Interaction with Antihypersensitives, Alcohol and nitrates
Increases risk for hypotension
237
Potassium Sparing Diuretics interaction with ACE Inhibitors, ARBs, NSAIDS, K supplements, Cyclosporine and Tacrolimus
Increases risk for hyperkalemia
238
Potassium Sparing Diuretics interactions with Digoxin
May increase effects of digoxin
239
Potassium Sparing Diuretics interactions with Lithium
May increase risk for lithium toxicity
240
Potassium Sparing Diuretics Nursing Considerations
```
Monitor intake and output, weigh daily
Monitor BP
Access for hypokalemia
Access for hyperkalemia
Access for skin rash- Steven Johnson Syndrome
```
241
Calcium channel Blockers action
Block calcium from entering the cells thus limiting muscular contraction. This decreases vascular resistance.
242
Two groups of calcium channel blockers
1. Selective for blood vessels
| 2. Non- selective for blood vessels and the heart
243
Calcium channel Blockers Prototype
Nifedipine (Adalat)
244
Calcium channel Blockers Nursing Considerations
CCB reduce myocardial contractility & thus increases the risk of heart failure
245
Calcium channel Blockers Contraindications
heart block
246
Calcium channel Blockers monitor
Vasodilation and heart failure
247
ACE stands for
Angiotension converting enzyme
248
ACE inhibitors action
Inhibit angiotensin converting enzyme which assists in converting angiotensin 1 into angiotensin 2
Decreases BP by lowering peripheral resistance & decreasing blood volume
249
ACE inhibitors Prototype
enalapril (Vasotec)
250
ACE inhibitors Nursing considerations
Persistent cough
Postural Hypotension
Angioedema
251
Angiotensin 2 Receptor Blockers (ARBs) Action
Blocks the effects of angiotensin II by blocking the receptors in the arteriolar smooth muscle and in the adrenal gland
Decreases BP by lowering peripheral resistance & decreasing blood volume
252
ARBs are the class of choice in
Diabetes
253
ARBs prototype
Nil
254
ARBs Nursing Considerations
Monitor electrolytes
May also cause cough but not as frequent as with ACE
May cause birth defects
Patients appear more prone to upper respiratory infections
255
ARBs Contraindications
Do not use in pregnancy
| Do not take with potassium sparing diuretics
256
Adrenergic agents
```
Beta blockers (antagonists)
Alpha 1 Blockers (antagonists)
Alpha 2 Blockers Agonists
Alpha1 & Beta Blockers
Adrenergic Neuron Blockers
```
257
Beta Blockers (antagonists) Action
Blocks both Beta1 and beta 2 thus inhibiting the fight or flight response
258
Beta Blockers (antagonists) Prototype
Metoprolol (Lopressor)
259
Beta Blockers (antagonists) Indication
Hypertension
Angina
Prevent MI and decrease mortality in recent MI
Management of stable heart failure, hypertension or cardiomyopathies
260
Beta Blockers (antagonists) Therapeutic effect
Decreases BP, Heart rate, frequency of angina attacks
261
Beta Blockers (antagonists) Contraindications
```
Uncompensated heart failure
Pulmonary edema
Cardiogenic shock
Bradycardia
Heart block or sick sinus rhythm
```
262
Beta Blockers (antagonists) Caution
```
Renal and hepatic impairment
Increased sensitivity in older adults
pulmonary disease
Diabetes
Hyperthyroidism
```
263
Beta Blockers (antagonists) Side effects
```
Fatigue
Weakness
Bradycardia
HF
Pulmonary edema
Respiratory distress
Hypotension
```
264
Beta Blockers (antagonists) Nursing Implications
Monitor BP, ECG, HR, Intake and output, daily weight
| Access for heart failure
265
Alpha1 Blockers (Antagonists) Action
Blocks alpha1, thus causes the relaxation of blood vessels
Decreases BP
Used for enlarged prostate & urinary obstruction
266
Alpha1 Blockers (Antagonists) Prototype
Doxazosin (Cardura)
267
Alpha2-Adrenergic Agonists Action
Acts on the presynaptic adrenergic nerve terminal by tricking the body by converting the drug into a false transmitter and blocking the real norepinephrine.
268
Alpha2-Adrenergic Agonists is the drug of choice for....
Pregnancy
269
Alpha2-Adrenergic Agonists side effect
hypotension
270
Alpha2-Adrenergic Agonists Prototype
Methyldopa (Aldomet)
271
Alpha 1 & beta blockers Action
Acts on all sympathetic organs including the heart also dilates blood vessels and dilates pupils
272
Alpha 1 & beta blockers Drug
Labetalol (Trandate, Normodyne)
273
Beta & Alpha Antagonists Nursing Considerations
Baseline BP and HR reassess regularly
Do not administer if HR <60 bpm
Diabetics needs to monitor Blood glucose regularly
Monitor for fatigue, dizziness, orthostatic hypotension
May cause impotence
274
Hypertensive Crisis
Severe abrupt increase in DBP
Rate of increase in BP is more important than the absolute value
Often occurs in clients with a history of hypertension who have failed to comply with medications or who have been unmedicated
275
Hypertensive emergency =
evidence of acute target organ damage
276
Clinical Manifestations of a Hypertensive Crisis
```
Hypertensive Encephalopathy
Cerebral hemorrhage
Acute renal failure
Myocardial infarction
Acute left ventricular failure with pulmonary edema
Dissecring aortic aneurysm
```
277
Hypertensive Crisis treatments
IV drug therapy: titrated to mean arterial pressure
Monitor cardiac and renal function
Neurological checks
Determine cause
278
Vasodilators Action
acts directly to dilate smooth muscles
279
Vasodilators are used in a ...
Hypertensive Crisis
280
Vasodilators Prototype drug
Hydralazine (app-hydralazine)
