Week 4: Cardiovascular And Cerebrovascular Disorders Flashcards
(180 cards)
1
Q
Cardiovascular Changes with Aging: Heart
A
- Slight increase in the size of the heart (especially the left ventricle) is not uncommon (cardiomyopathy).
- Heart wall thickens and heart fills more slowly.
2
Q
Cardiovascular Changes with Aging: Valves
A
Thicker and stiffer due to lipid deposits, collagen degeneration and fibrosis.
3
Q
Cardiovascular Changes with Aging: Conductivity of the Heart
A
- SA node cells decrease in number as myocardial fat, collagen and elastin fibers increase.
- Results in slightly slower HR.
4
Q
Cardiovascular Changes with Aging: Contractility of the Heart
A
Prolonged most likely due to slower release of calcium into the contractile portion of heart during systole.
5
Q
Cardiovascular Changes with Aging: Blood Vessels
A
- Diminished elasticity d/t changes in collagen and elastin.
- Thickened vessel walls
- Pooling of blood increases venous pressure diminishing effectiveness of peripheral valves.
- Baroreceptors become less sensitive -> orthostatic hypotension
- Aorta becomes thicker, stiffer and less flexible
6
Q
Thickened blood vessel walls are a result of
A
- Reorganization of cellular and extracellular matrix.
- Leads to slightly slower rate of exchange of nutrients and waste.
7
Q
Baroreceptors
A
Monitors and makes changes to help maintain BP
8
Q
Thicker, stiffer and less flexible aorta can result in
A
Higher BP and makes heart work harder which may lead to thinking of heart muscle (hypertrophy).
9
Q
What are the effects of changes to the heart in older adults?
A
An older heart may not be able to pump blood as well when a patient makes it work harder.
10
Q
Things that make the heart work harder include
A
Certain medications (NSAIDs) Emotional stress Physical exertion Illness Infections Injuries
11
Q
Atherosclerosis
A
Beings as soft deposits of fat that harden with age.
Referred to as “hardening of the arteries”
12
Q
Although atherosclerosis can occur in any artery in the body, the fatty deposits prefer
A
The coronary arteries.
13
Q
What is a major cause of CAD?
A
Atherosclerosis; endothelial injury and inflammation play a major role in development.
14
Q
C-reactive protein
A
- Nonspecific marker of inflammation.
- Increased in many patients with CAD.
15
Q
Chronic exposure to C-reactive protein is linked with
A
Unstable plaques and oxidation of LDL cholesterol -> further contributing to atherosclerosis
16
Q
Collateral Circulation
A
Arterial anastomoses or connections that exist within coronary circulation.
17
Q
What are two factors that contribute to the growth and extent of collateral circulation?
A
- Inherited predisposition to develop new blood vessels (angiogenesis)
- Presence of chronic ischemia
18
Q
Increases collateral circulation develops when
A
When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic.
19
Q
When occlusion of the coronary arteries occurs slowly over a long period,
A
There is a greater chance of collateral circulation developing and the heart muscle may still receive adequate amount of blood and oxygen.
20
Q
Collateral circulation development with rapid-onset CAD or coronary spasm
A
- With rapid-onset CAD or coronary spasm, time is inadequate for collateral circulation development.
- Consequently, a reduced blood flow results in more severe ischemia or infarction.
21
Q
What are non-modifiable risk factors for CAD?
A
- Age
- Gender
- Ethnicity
- Family History
- Genetic Inheritance
22
Q
Non-modifiable risk factors for CAD: Age/Gender
A
- After age 75, the incidence of serious heart events in men and women equalizes, although CAD causes more deaths in women than men.
- On average, women with CAD are older than men who have CAD and are more likely to have co-morbidities (i.e. hypertension, diabetes).
23
Q
Non-modifiable risk factors for CAD: Ethnicity
A
African Americans have an earlier onset and more severe CAD than there CAD counterparts
24
Q
Non-modifiable risk factors for CAD: Family history
A
Family history is a risk factor for CAD and MI. Often, patients with angina or MI can name a parent or sibling who has died of CAD.
25
What are major modifiable risk factors for CAD?
1. HTN
2. Elevate serum lipids
3. Tobacco use/second-hand smoke
4. Physical inactivity
5. Obesity
26
Major modifiable risk factors for CAD: HTN
- Hypertension increases the risk of death from CAD 10-fold in all persons.
- The stress of an elevated BP increases the rate of atherosclerosis. This relates to the shearing stress that causes endothelial injury.
27
What is the goal BP in people older than 60 years of age?
less than 150/90 mmHg is recommended to prevent stroke, CAD and heart failure.
28
What is a high cholesterol level?
>200 mg/dL
29
What is an elevated triglyceride level?
>150 mg/dL
30
What is an abnormal range for high-density lipoproteins?
<50
31
What is an elevated low-density lipoprotein?
>130
32
What are contributing modifiable risk factors for CAD?
- Diabetes
- Metabolic syndrome
- Substance abuse
- Stress
33
What drugs are used to treat CAD?
```
Lipid lowering agents:
-Statins
-Ezatimibe (Zetia)
-Niacin
Antiplatelets:
-ASA
-Clopidogrel (Plavix)
```
34
Statins: MOA
Inhabit cholesterol synthesis, decreases LDL and increases HDL
35
What should you monitor in patients taking statins?
Monitor for liver damage and myopathy. Therefore monitor liver enzymes and recheck with increased dosages.
36
Serious adverse effects of statins
Liver damage and myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle)
37
Ezatimibe (Zetia): MOA
Inhibits the absorption of dietary and biliary cholesterol across the intestinal wall.
38
Ezatimibe (Zetia) serves as
An adjunct to dietary changes, especially in patients with primary hypercholesterolemia.
39
Niacin: MOA
- Lowers LDL and triglyceride by inhibiting synthesis
| - Increases HDL
40
Niacin: Side Effects
- Flushing*
- Pruritus
- GI side effects
- Orthostatic Hypotension
41
Aspirin use in older adults with CAD
- Unless contraindicated, low-dose aspirin is recommended.
- Considered in healthy women 60 years or older if BP is controlled and the benefit for MI prevention outweighs the risk of GI bleed or hemorrhagic stroke.
42
For high-risk women with CAD that are intolerant to aspirin, what can be used as a substitute?
Clopidogrel (Plavix)
43
What are necessary modifications to guidelines for physical activity in older adults?
- Longer warm-up
- Longer periods of low-level activity
- Longer rest periods
- Avoid extremes of temperature → heat intolerance results from a decreased ability to sweat
- 30 minutes most days minimum
44
Angina
When O2 demand of heart is greater than the O2 supply -> myocardial ischemia.
45
Myocardial ischemia occurs when
- Arteries are blocked 70% or more.
| - 50% or more for left main coronary artery.
46
Chronic Stable Angina
Intermittent chest pain that occurs over a long period with same pattern of onset, duration and intensity of symptoms.
47
Chronic Stable Angina is provoked by
Physical exertion, stress, or emotional upset.
48
When patient’s are asked to describe chronic stable angina, they may
- Deny pain but describe a pressure, heaviness or discomfort in chest.
- Discomfort is often described as squeezing, heavy, tight or suffocating sensation.
49
How long does pain for chronic stable angina last for?
Lasts for only a few minutes and commonly subsides when the precipitating factor is resolved (resting, calming down, using sublingual NTG)
50
Goal of Chronic Stable Angina
↓ O2 demand and/or ↑ O2 supply
51
Short-acting nitrates: Nitroglycerin
- Dilate peripheral and coronary blood vessels
- Given via sublingual or oral spray.
- Can be used prophylactically
52
Frequency of taking Nitroglycerin
- One dose every 5 minutes with no more than 3 doses in 15 minutes
- If chest pain continues after 3rd dose call for emergency help or go to ER.
53
Nitroglycerin: Patient teaching
- Warn the patient that a headache, dizziness, or flushing may occur.
- Caution the patient to change positions slowly after NTG use because orthostatic hypotension may occur.
54
Long-acting nitrates
To reduce angina incidence
55
Main side effects of long-acting nitrates
Headache*
| Orthostatic hypotension
56
Long-Acting nitrates: Methods of administration
- Oral [Isosorbide dinitrate (Isordil) or isosorbide mononitrate (Imdur)]
- Nitroglycerin (NTG) ointment [Nitropaste 2%]
- Transdermal controlled-release NTG
57
What are other medications that can be used to treat chronic stable angina?
- Beta-blockers
- CCB
- ACE inhibitors
- ARBs
58
Chronic Stable Angina Treatment: Beta-blockers
- Relief of angina symptoms.
| - Patients who have LV dysfunction, elevated BP, or have had an MI should start and continue β-blockers indefinitely.
59
Calcium channel blockers to treat chronic stable angina
Used if beta-blockers are contraindicated or poorly tolerated.
60
Angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARBs) to treat chronic stable angina
- Result in vasodilation and reduced blood volume.
| - Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI.
61
Congestive Heart Failure
- An abnormal condition involving impaired cardiac pumping/filling.
- Heart is unable to produce an adequate cardiac output (CO) to meet the oxygen needs of the tissues.
62
CHF if characterized by:
- Ventricular dysfunction
- Reduced exercise tolerance
- Diminished quality of life
- Shortened life expectancy
63
Primary Risk Factors for CHF
- HTN
| - CAD
64
Co-morbidities that contribute to development of CHF
Diabetes
Vascular disease
Advanced age
65
Primary causes of CHF
Conditions that directly damage the heart (CAD including MI, HTN, Rheumatic heart disease)
66
Precipitating causes of CHF
Conditions that increase workload of ventricles (Anemia, Infection, Nutritional deficiencies).
67
Systolic HF
Inability of the heart to pump blood effectively
68
Causes of Systolic HF
- Impaired contractile function (i.e. MI)
- Increased afterload (i.e. Hypertension)
- Cardiomyopathy
- Mechanical abnormalities (i.e. Valve disease)
69
Ejection Fraction
The amount of blood ejected from the left ventricle.
70
Hallmark finding of systolic failure is
A decrease in left ventricular ejection fraction.
| Less than 45%, can be as low as 10%.
71
Normal Ejection Fraction
55%-60%
72
Diastolic HF
Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO.
73
How is diastolic heart failure diagnosed?
Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and normal EF.
74
What causes diastolic heart failure?
- Left ventricular hypertrophy from chronic hypertension
- Aortic stenosis
- Cardiomyopathy
75
What are the compensatory mechanisms are activated to maintain adequate cardiac output in patients with HF?
1. Sympathetic Nervous System
2. Dilation
3. Hypertrophy
76
Compensatory Mechanisms: Sympathetic Nervous System
First and least effective mechanism.
- Release of catecholamines
- Increased HR
- Increased myocardial contractility
- Peripheral vasoconstriction
77
Compensatory Mechanisms: Dilation
- Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated.
- Initially an adaptive mechanism.
78
Consequences of Compensatory Mechanisms: Dilation
Eventually this mechanism becomes inadequate and CO decreases.
79
Consequences of Compensatory Mechanisms: Hypertrophy
- Increase in the muscle mass and cardiac wall thickness in response to overwork → strains the heart.
- Can lead to dysrhythmias.
80
Left-sided CHF
- Most common form
- Blood backs up into left atrium and pulmonary veins.
- Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema → excess fluid in the lungs.
81
Left-sided CHF results from inability of LV to:
- Empty adequately during systole
| - Fill adequately during diastole
82
Left-sided CHF is further classified as:
Systolic
Diastolic
Mixed systolic and diastolic
83
Right-sided CHF
Back up of blood into the right atrium and venous systemic circulation.
84
Signs and symptoms of right-sided CHF
- Jugular venous distention
- Hepatomegaly, splenomegaly
- Vascular congestion of GI tract (Ascites)
- Peripheral edema
85
Acute Decompensated HF
An increase in the pulmonary venous pressure is caused by the failure of the LV.
86
ADHF Clinical Manifestations:
Pulmonary Edema:
- Anxious, pale, cyanotic
- Clammy and cold skin
- Dyspnea and orthopnea
- RR is greater than 30 breaths/minute
- Lungs: crackles, wheezing, and coughing
- Frothy blood tinged sputum
- HR : rapid
- BP: elevated or decreased
87
Goals of nursing care for patients with CHF
- Decrease patient symptoms.
- Improve LV function.
- Reverse ventricular remodeling.
- Improve quality of life.
- Decrease morbidity and mortality.
88
What drugs are used to treat CHF?
- Diuretics
- Vasodilators
- Morphine
- Positive Inotropes
89
Nutritional Therapy for CHF
- Fluid restriction not generally required
- Daily weights are important: same time, same clothing each day
- Sodium usually restricted to 2,000 mg daily.
90
What weight gain characteristics should be reported to HCP?
Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week
91
Planning: Overall goals for patients with CHF
- Decrease in symptoms (i.e. shortness of breath, fatigue)
- Decrease in peripheral edema
- Increase in exercise tolerance
- Compliance with the medical regimen
- No complications related to CHF
92
Patient and Caregiver Education for CH
- Medications, diet, and exercise regimens
- Home BP monitoring
- Signs of hypokalemia and hyperkalemia if taking diuretics that deplete or spare potassium
- Instruct patient in energy-conserving and energy-efficient behaviors
93
What should be evaluated in patients with CHF?
1. Respiratory status
2. Fluid balance
3. Activity tolerance
4. Anxiety control
5. Knowledge of disease process
94
Atrial Fibrillation
- Most common.
- Total disorganization of atrial electrical activity due to multiple ectopic foci, resulting in loss of effective atrial contraction.
95
Atrial Fibrillation promotes
Thrombus/embolus formation, increasing the risk stroke
96
Treatment for atrial fibrillation include
- HR rate control
- Cardioversion
- Anti-dysrhythmics
- Systemic anticoagulation
97
A-fib: usually occurs with underlying heart disease such as
- Rheumatic heart disease
- CAD
- Cardiomyopathy
- CHF
- Pericarditis
98
Clinical Significance of A-fib
- Can result in decrease in CO due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response.
- Thrombi may form in the atria as a result of blood stasis
- Embolus May develop and travel to brain causing a stroke.
99
Goals of Treatment: A-fib
- Decrease ventricular rate
| - Prevent embolic stroke
100
A-fib: drugs for rate control include
Digoxin
B-blockers
CCB
101
A-fib: Long term anticoagulation medication includes
Coumadin
102
Treatment used for conversion from a-fib to normal sinus rhythm include
- Anti-dysrhythmic drugs: Amiodarone
| - Cardioversion
103
If patient has been in a-fib for >48 hours, what is the recommended therapy?
anticoagulation therapy with warfarin (Coumadin) is recommended for 3 to 4 weeks before cardioversion and for 4 to 6 weeks after successful cardioversion.
104
Atrial flutter usually occurs with
- CAD
- Hypertension
- Mitral valve disorders
- Pulmonary embolus
- Chronic lung disease
- Cardiomyopathy
- Hyperthyroidism
105
Clinical significance of atrial flutter
- High ventricular rates (>100) and loss of the atrial “kick” can decrease CO and precipitate HF.
- Risk for stroke due to risk of thrombus formation in the atria.
106
Atrial flutter treatment: primary goal
Slow ventricular response by increasing AV block
107
Treatment for atrial flutter
1. Drugs to slow HR: Beta-blockers, CCB
2. Anti-Dysrhythmia drugs: amiodarone (to convert a-flutter to sinus rhythm or to maintain sinus rhythm)
3. Radiofrequency catheter ablation
108
Treatment to convert atrial flutter to normal sinus rhythm
Electrical cardioversion may be used to convert the atrial flutter to sinus rhythm emergently and electively.
109
Peripheral Artery Disease
- Involves progressive narrowing and degeneration of arteries of upper and lower extremities.
- Atherosclerosis leading cause in majority cases
110
Patients with PAD are more likely to have
Coronary artery disease and/or cerebral artery disease.
111
Risk factors for peripheral artery disease include
- Tobacco use
- Chronic kidney disease
- Diabetes mellitus
- Hypertension
- Hyperlipidemia
112
Clinical Manifestations of Peripheral Artery Disease
- Claudication
- Paresthesia
- Thin,shiny, taut skin
- Loss of hair on the lower legs
- Diminished or absent pedal, popliteal, or femoral pulses
- Pallor of foot with leg elevation
- Reactive hyperemia of foot with dependent position
- Pain at rest
113
PAD Clinical Manifestations: Claudication
- Ischemic muscle pain that is caused by a constant level of exercise
- Resolves within 10 minutes or less with rest
- Reproducible
114
PAD Clinical Manifestations: Paresthesia
- Numbness or tingling in the toes or feet
- Produces loss of pressure and deep pain sensations
- Injuries often go unnoticed by patient
115
PAD Clinical Manifestations: Pain at rest
- As PAD progresses
- Occurs in feet or toes
- Aggravated by limb elevation
- Occurs from insufficient blood flow
- Occurs more often at night
116
Critical Limb Ischemia: Characterized by
- Chronic ischemic rest pain lasting more than 2 weeks.
| - Arterial leg ulcers or gangrene.
117
Who has an increased risk for critical limb ischemia/PAD?
Those who have PAD and also have diabetes, CHF, and history of stroke are at increased risk.
118
Complications of Critical Limb Ischemia/PAD
- Atrophy of skin and underlying muscles
- Delayed healing
- Wound infection
- Tissue necrosis
- Arterial ulcers
119
Most serious complications of critical limb ischemia/PAD are
- Non-healing arterial ulcers and gangrene.
| - May result in amputation if adequate blood flow is not restored or if severe infection occurs.
120
Diagnostic studies used for critical limb ischemia/PAD
- Arterial Doppler ultrasound with ankle-brachial index (ABI)
- Angiography and magnetic resonance angiography
- Duplex imaging: Bidirectional, color Doppler
121
Risk Factor Modifications for Critical Limb Ischemia/PAD
- Tobacco cessation
- Glycosylated hemoglobin <7.0% for diabetics
- Aggressive treatment of hyperlipidemia
- BP control
122
Drug Therapy for Critical Limb Ischemia/PAD
- ACE inhibitors: Ramipril (Altace)
| - Antiplatelet agents: Aspirin, Clopidogrel
123
PAD/Critical Limb Ischemia Drug Therapy: Ramipril (Altace)
```
↓ Cardiovascular morbidity
↓ Mortality
↑ Peripheral blood flow
↑ ABI
↑ Walking distance
```
124
What drugs are prescribed for treatment of intermittent claudication associated with PAD?
- Cilostazol (Pletal)
| - Pentoxifylline (Trental)
125
Claudication Treatment: Cilostazol
- Inhibits platelet aggregation.
| - ↑ Vasodilation
126
Claudication Treatment: Pentoxifylline (Trental)
- Improves deformability of RBCs and WBCs
| - Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity
127
Exercise Therapy for PAD/Critical Limb Ischemia
- Improves oxygen extraction in legs and skeletal metabolism.
- Walking is most effective for individuals with claudication: 30-45 minutes daily, 3 times/week.
128
Nutrition Therapy for PAD
- BMI <25 kg/m2
- Waist circumference <40 inches for men and <35 inches for women
- Recommend reduced calories and salt for obese or overweight persons
129
Leg with critical limb ischemia: conservative treatment includes
- Protect from trauma
- Decrease ischemic pain
- Prevent/control infection
- Improve arterial perfusion
130
Indications for interventional radiology procedures in patients with PAD
- Intermittent claudication symptoms become incapacitating
- Pain at rest
- Ulceration or gangrene severe enough to threaten viability of the limb
131
Percutaneous Transluminal Angioplasty
- Involves insertion of a catheter through femoral artery
- Catheter contains a cylindrical balloon
- Balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining
- Stent is placed
132
Surgical Therapy for PAD
- Peripheral artery bypass surgery with autogenous vein or synthetic graft to bypass blood around the lesion
- PTA with stenting may also be used in combination with bypass surgery
133
Nursing Assessment for PAD: Past Health History
- Diabetes mellitus
- Smoking
- Hypertension
- Hyperlipidemia
- Obesity
134
Overall goals for patient with PAD
- Adequate tissue perfusion
- Relief of pain
- Increased exercise tolerance
- Intact, healthy skin on extremities
- Increased knowledge of disease and treatment plan
135
Ambulatory care for patients with PAD
- Management of risk factors
- Long-term antiplatelet therapy
- Importance of supervised exercise training after revascularization
- Importance of meticulous foot care: daily inspection of feet, comfortable shoes with rounded toes and soft insoles, shoes lightly laced.
136
Evaluation of PAD
- Adequate peripheral tissue perfusion
- Increased activity tolerance
- Effective pain management
- Knowledge of disease and treatment plan
137
What are the two types of strokes?
1. Ischemia (inadequate blood flow) to the part of the brain
| 2. Hemorrhage into the brain that results in death of brain cells
138
Non-modifiable risk factors for strokes
Age
Gender
Race
Genetics
139
Modifiable Risk Factors for Strokes
- Hypertension
- Heart disease
- Diabetes
- OSA
- ETOH abuse
- Poor diet
- Drug abuse
- Smoking
- Obesity
- Physical inactivity
140
Mini-strokes
Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction of the brain.
141
Symptoms of mini-strokes
Symptoms last <1 hour; low oxygen, precursor to ischemic stroke.
142
Types of Ischemic Stroke
Thrombotic and embolic
143
Types of Hemorrhagic stroke
Intracerebral and subarachnoid
144
Ischemic Stroke: Thrombotic Stroke
- Result of thrombosis or narrowing of the blood vessel - blood clot formation.
- Most common cause of stroke.
145
Ischemic Stroke: Embolic Stroke
- Embolus lodges in and occludes a cerebral artery.
- Results in infarction and edema of the area supplied by the involved vessel.
- Second most common cause.
146
Ischemic stroke results from
-inadequate blood flow to the brain from partial or complete occlusion of an artery
147
Characteristics of Ischemic Stroke
- Occurs rapidly
- Patient remains conscious
- May have a headache
- PMH: a-fib, MI, rheumatic heart disease (not sure what this means)
148
Hemorrhagic strokes results from
Bleeding into the brain tissue itself or into the subarachnoid space or ventricles.
149
Hemorrhagic Stroke: Intracerebral Hemorrhage
- Bleeding within the brain caused by rupture of a vessel.
- Prognosis is poor.
- Commonly occurs during periods of activity.
150
What is the most important cause of intracerebral hemorrhage?
Hypertension.
151
A hemorrhage in what location of the brain is the most serious?
Hemorrhage in the pons is most serious (respiration; hemiplegia, coma, hyperthermia, and death.
152
Hemorrhagic Stroke: Subarachnoid Hemorrhage
Occurs when there is an intracranial bleeding into the CSF fluid filled space between the arachnoid and pia mater.
153
Majority of aneurasym are in the
Circle of Willis
154
Subarachnoid Hemorrhage Characteristics
- History of illicit drug use.
- Sudden “worst headache” (ruptured aneurysm).
- About 40% with ruptured aneurysm die during the first episode.
155
Strokes can affect what motor functions?
```
Mobility
Respiratory function
Swallowing and speech
Gag reflex
Self-care abilities
```
156
A stroke affecting the middle cerebral artery leads to
leads to a greater weakness in the upper extremity than the lower extremity.
157
Effects of stroke on communication
- Aphasia
- Receptive aphasia (loss of comprehension)
- Expressive aphasia ( inability to produce language)
- Global aphasia (total inability to communicate)
158
How can a stroke effect affect?
Frustration
| Depression
159
How can a stroke in the left brain affect intellectual function?
Memory problems related to language, more cautious
160
How can a stroke in the right brain affect intellectual function?
Tends to be more impulsive and to move quickly
161
How can a stroke affect elimination?
- Initially the patient may experience: frequency, urgency, incontinence.
- CONSTIPATION is associated with weak abdominal muscles, dehydration, and diminished response to the defecation reflex.
162
Diagnostic Tests used for Stroke
- Non contrast head CT or MRI- size and location
- Cardiac imaging
- Transcranial Doppler ultrasonography
163
Preventative Therapy for Strokes include
- Healthy Diet: salt and sodium intake
- Weight Control
- Regular Exercise
- No Smoking
- Limitation on Alcohol Consumption
- Routine Health Assessment
- Close Management: DM, HTN, Obesity, High Serum Lipids, Cardiac Dysfunction
164
Preventative Drug Therapy for Strokes
TIA: Aspirin 81mg daily or Clopidogrel (Plavix)
| A-fib: Warfarin (Coumadin) or Riviroxaban (Xarelto)
165
Surgical Therapy for TIA
Carotid Endarterectomy: common treatment for embolic and ischemic stroke; may be done to prevent stroke.
166
Diagnosis of CVA
Non contrast MRI or CT scan
167
Treatment for CVA
- Fibronolytic therapy should not be delayed
- tPA must be administered within 3 to 4 1/2 hours of the onset of clinical signs of ischemic stroke
- Preparation: multiple IV’s, foley catheter, NG tube
- Monitor VS and neurologic status
- BP control
168
Goals of stroke prevention include
- Health promotion for the well individual
- Education and management of modifiable risk factors to prevent a stroke
- Patients with known risk factors require close management: Diabetes, Hypertension, Obesity, High serum lipids, Cardiac dysfunction
169
How can you prevent a stroke?
- Smoking should be discontinued
- Limited alcohol intake
- Healthy diet
- Weight control
- Regular exercise
- Routine health examinations
170
Primary Assessment for CVA: focus on
Cardiac and respiratory status first:
1. Description: onset and duration
2. History of similar symptoms previously experienced
3. Current medications
4. History of risk factors: HTN
5. Family history of stroke or cardiovascular diseases
171
Nursing Care for CVA: Respiratory
- Swallowing, risk for aspiration pneumonia is high d/t dysphagia
- Regular oral care is important
- Suctioning
172
Nursing Care for CVA: Neurologic
Increasing ICP
173
Nursing Care for CVA: Cardiovascular
- Risk for venous thromboembolism on weak side
- Sequential compression device of bilateral lower extremities to improve blood flow
- Enoxaparin (Lovenox) anticoagulant to prevent clot formation.
174
Nursing Care for CVA: Musculoskeletal
Avoid subluxation of the shoulder, foot drop.
175
Nursing Care for CVA: Integumentary
Skin care and skin hygiene
176
Nursing Care for CVA: GI
- Loss of gag reflux
| - Constipation: fiber and stool softeners
177
Nursing Care for CVA: Urinary
-Incontinence, short term catheter recommended
178
Nursing Care for CVA: Nutrition
-Swallowing evaluation, thin liquids needs to be thickened.
179
Hemianopsia in CVA
Decreased vision or blindness in 1/2 visual field.
| Arrange food tray to accommodate for field of vision.
180
Diplopia
Double vision
