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NURS 401 > Week 4: Cardiovascular And Cerebrovascular Disorders > Flashcards

Week 4: Cardiovascular And Cerebrovascular Disorders Flashcards

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.
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2
Q

Cardiovascular Changes with Aging: Valves

A

Thicker and stiffer due to lipid deposits, collagen degeneration and fibrosis.

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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.
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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.

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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
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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.

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7
Q

Baroreceptors

A

Monitors and makes changes to help maintain BP

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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).

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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.

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10
Q

Things that make the heart work harder include

A 
Certain medications (NSAIDs)
Emotional stress
Physical exertion
Illness
Infections
Injuries
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11
Q

Atherosclerosis

A

Beings as soft deposits of fat that harden with age.

Referred to as “hardening of the arteries”

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12
Q

Although atherosclerosis can occur in any artery in the body, the fatty deposits prefer

A

The coronary arteries.

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13
Q

What is a major cause of CAD?

A

Atherosclerosis; endothelial injury and inflammation play a major role in development.

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14
Q

C-reactive protein

A
  • Nonspecific marker of inflammation.

- Increased in many patients with CAD.

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15
Q

Chronic exposure to C-reactive protein is linked with

A

Unstable plaques and oxidation of LDL cholesterol -> further contributing to atherosclerosis

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16
Q

Collateral Circulation

A

Arterial anastomoses or connections that exist within coronary circulation.

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17
Q

What are two factors that contribute to the growth and extent of collateral circulation?

A
  1. Inherited predisposition to develop new blood vessels (angiogenesis)
  2. Presence of chronic ischemia
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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.

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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.

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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.
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21
Q

What are non-modifiable risk factors for CAD?

A
  1. Age
  2. Gender
  3. Ethnicity
  4. Family History
  5. Genetic Inheritance
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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).
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23
Q

Non-modifiable risk factors for CAD: Ethnicity

A

African Americans have an earlier onset and more severe CAD than there CAD counterparts

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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.

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25
Q

What are major modifiable risk factors for CAD?

A
  1. HTN
  2. Elevate serum lipids
  3. Tobacco use/second-hand smoke
  4. Physical inactivity
  5. Obesity
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26
Q

Major modifiable risk factors for CAD: HTN

A
  • 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.
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27
Q

What is the goal BP in people older than 60 years of age?

A

less than 150/90 mmHg is recommended to prevent stroke, CAD and heart failure.

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28
Q

What is a high cholesterol level?

A

> 200 mg/dL

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29
Q

What is an elevated triglyceride level?

A

> 150 mg/dL

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30
Q

What is an abnormal range for high-density lipoproteins?

A

<50

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31
Q

What is an elevated low-density lipoprotein?

A

> 130

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32
Q

What are contributing modifiable risk factors for CAD?

A
  • Diabetes
  • Metabolic syndrome
  • Substance abuse
  • Stress
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33
Q

What drugs are used to treat CAD?

A 
Lipid lowering agents:
-Statins
-Ezatimibe (Zetia)
-Niacin
Antiplatelets: 
-ASA
-Clopidogrel (Plavix)
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34
Q

Statins: MOA

A

Inhabit cholesterol synthesis, decreases LDL and increases HDL

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35
Q

What should you monitor in patients taking statins?

A

Monitor for liver damage and myopathy. Therefore monitor liver enzymes and recheck with increased dosages.

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36
Q

Serious adverse effects of statins

A

Liver damage and myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle)

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37
Q

Ezatimibe (Zetia): MOA

A

Inhibits the absorption of dietary and biliary cholesterol across the intestinal wall.

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38
Q

Ezatimibe (Zetia) serves as

A

An adjunct to dietary changes, especially in patients with primary hypercholesterolemia.

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39
Q

Niacin: MOA

A
  • Lowers LDL and triglyceride by inhibiting synthesis

- Increases HDL

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40
Q

Niacin: Side Effects

A
  • Flushing*
  • Pruritus
  • GI side effects
  • Orthostatic Hypotension
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41
Q

Aspirin use in older adults with CAD

A
  • 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.
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42
Q

For high-risk women with CAD that are intolerant to aspirin, what can be used as a substitute?

A

Clopidogrel (Plavix)

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43
Q

What are necessary modifications to guidelines for physical activity in older adults?

A
  • 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
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44
Q

Angina

A

When O2 demand of heart is greater than the O2 supply -> myocardial ischemia.

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45
Q

Myocardial ischemia occurs when

A
  • Arteries are blocked 70% or more.

- 50% or more for left main coronary artery.

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46
Q

Chronic Stable Angina

A

Intermittent chest pain that occurs over a long period with same pattern of onset, duration and intensity of symptoms.

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47
Q

Chronic Stable Angina is provoked by

A

Physical exertion, stress, or emotional upset.

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48
Q

When patient’s are asked to describe chronic stable angina, they may

A
  • Deny pain but describe a pressure, heaviness or discomfort in chest.
  • Discomfort is often described as squeezing, heavy, tight or suffocating sensation.
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49
Q

How long does pain for chronic stable angina last for?

A

Lasts for only a few minutes and commonly subsides when the precipitating factor is resolved (resting, calming down, using sublingual NTG)

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50
Q

Goal of Chronic Stable Angina

A

↓ O2 demand and/or ↑ O2 supply

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51
Q

Short-acting nitrates: Nitroglycerin

A
  • Dilate peripheral and coronary blood vessels
  • Given via sublingual or oral spray.
  • Can be used prophylactically
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52
Q

Frequency of taking Nitroglycerin

A
  • 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.
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53
Q

Nitroglycerin: Patient teaching

A
  • 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.
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54
Q

Long-acting nitrates

A

To reduce angina incidence

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55
Q

Main side effects of long-acting nitrates

A

Headache*

Orthostatic hypotension

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56
Q

Long-Acting nitrates: Methods of administration

A
  • Oral [Isosorbide dinitrate (Isordil) or isosorbide mononitrate (Imdur)]
  • Nitroglycerin (NTG) ointment [Nitropaste 2%]
  • Transdermal controlled-release NTG
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57
Q

What are other medications that can be used to treat chronic stable angina?

A
  • Beta-blockers
  • CCB
  • ACE inhibitors
  • ARBs
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58
Q

Chronic Stable Angina Treatment: Beta-blockers

A
  • Relief of angina symptoms.

- Patients who have LV dysfunction, elevated BP, or have had an MI should start and continue β-blockers indefinitely.

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59
Q

Calcium channel blockers to treat chronic stable angina

A

Used if beta-blockers are contraindicated or poorly tolerated.

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60
Q

Angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARBs) to treat chronic stable angina

A
  • Result in vasodilation and reduced blood volume.

- Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI.

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61
Q

Congestive Heart Failure

A
  • 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.
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62
Q

CHF if characterized by:

A
  • Ventricular dysfunction
  • Reduced exercise tolerance
  • Diminished quality of life
  • Shortened life expectancy
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63
Q

Primary Risk Factors for CHF

A
  • HTN

- CAD

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64
Q

Co-morbidities that contribute to development of CHF

A

Diabetes
Vascular disease
Advanced age

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65
Q

Primary causes of CHF

A

Conditions that directly damage the heart (CAD including MI, HTN, Rheumatic heart disease)

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66
Q

Precipitating causes of CHF

A

Conditions that increase workload of ventricles (Anemia, Infection, Nutritional deficiencies).

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67
Q

Systolic HF

A

Inability of the heart to pump blood effectively

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68
Q

Causes of Systolic HF

A
  • Impaired contractile function (i.e. MI)
  • Increased afterload (i.e. Hypertension)
  • Cardiomyopathy
  • Mechanical abnormalities (i.e. Valve disease)
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69
Q

Ejection Fraction

A

The amount of blood ejected from the left ventricle.

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70
Q

Hallmark finding of systolic failure is

A

A decrease in left ventricular ejection fraction.

Less than 45%, can be as low as 10%.

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71
Q

Normal Ejection Fraction

A

55%-60%

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72
Q

Diastolic HF

A

Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO.

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73
Q

How is diastolic heart failure diagnosed?

A

Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and normal EF.

74
Q

What causes diastolic heart failure?

A
  • Left ventricular hypertrophy from chronic hypertension
  • Aortic stenosis
  • Cardiomyopathy
75
Q

What are the compensatory mechanisms are activated to maintain adequate cardiac output in patients with HF?

A
  1. Sympathetic Nervous System
  2. Dilation
  3. Hypertrophy
76
Q

Compensatory Mechanisms: Sympathetic Nervous System

A

First and least effective mechanism.

  • Release of catecholamines
  • Increased HR
  • Increased myocardial contractility
  • Peripheral vasoconstriction
77
Q

Compensatory Mechanisms: Dilation

A
  • Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated.
  • Initially an adaptive mechanism.
78
Q

Consequences of Compensatory Mechanisms: Dilation

A

Eventually this mechanism becomes inadequate and CO decreases.

79
Q

Consequences of Compensatory Mechanisms: Hypertrophy

A
  • Increase in the muscle mass and cardiac wall thickness in response to overwork → strains the heart.
  • Can lead to dysrhythmias.
80
Q

Left-sided CHF

A
  • 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
Q

Left-sided CHF results from inability of LV to:

A
  • Empty adequately during systole

- Fill adequately during diastole

82
Q

Left-sided CHF is further classified as:

A

Systolic
Diastolic
Mixed systolic and diastolic

83
Q

Right-sided CHF

A

Back up of blood into the right atrium and venous systemic circulation.

84
Q

Signs and symptoms of right-sided CHF

A
  • Jugular venous distention
  • Hepatomegaly, splenomegaly
  • Vascular congestion of GI tract (Ascites)
  • Peripheral edema
85
Q

Acute Decompensated HF

A

An increase in the pulmonary venous pressure is caused by the failure of the LV.

86
Q

ADHF Clinical Manifestations:

A

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
Q

Goals of nursing care for patients with CHF

A
  • Decrease patient symptoms.
  • Improve LV function.
  • Reverse ventricular remodeling.
  • Improve quality of life.
  • Decrease morbidity and mortality.
88
Q

What drugs are used to treat CHF?

A
  • Diuretics
  • Vasodilators
  • Morphine
  • Positive Inotropes
89
Q

Nutritional Therapy for CHF

A
  • Fluid restriction not generally required
  • Daily weights are important: same time, same clothing each day
  • Sodium usually restricted to 2,000 mg daily.
90
Q

What weight gain characteristics should be reported to HCP?

A

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
Q

Planning: Overall goals for patients with CHF

A
  • 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
Q

Patient and Caregiver Education for CH

A
  • 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
Q

What should be evaluated in patients with CHF?

A
  1. Respiratory status
  2. Fluid balance
  3. Activity tolerance
  4. Anxiety control
  5. Knowledge of disease process
94
Q

Atrial Fibrillation

A
  • Most common.
  • Total disorganization of atrial electrical activity due to multiple ectopic foci, resulting in loss of effective atrial contraction.
95
Q

Atrial Fibrillation promotes

A

Thrombus/embolus formation, increasing the risk stroke

96
Q

Treatment for atrial fibrillation include

A
  • HR rate control
  • Cardioversion
  • Anti-dysrhythmics
  • Systemic anticoagulation
97
Q

A-fib: usually occurs with underlying heart disease such as

A
  • Rheumatic heart disease
  • CAD
  • Cardiomyopathy
  • CHF
  • Pericarditis
98
Q

Clinical Significance of A-fib

A
  • 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
Q

Goals of Treatment: A-fib

A
  • Decrease ventricular rate

- Prevent embolic stroke

100
Q

A-fib: drugs for rate control include

A

Digoxin
B-blockers
CCB

101
Q

A-fib: Long term anticoagulation medication includes

102
Q

Treatment used for conversion from a-fib to normal sinus rhythm include

A
  • Anti-dysrhythmic drugs: Amiodarone

- Cardioversion

103
Q

If patient has been in a-fib for >48 hours, what is the recommended therapy?

A

anticoagulation therapy with warfarin (Coumadin) is recommended for 3 to 4 weeks before cardioversion and for 4 to 6 weeks after successful cardioversion.

104
Q

Atrial flutter usually occurs with

A
  • CAD
  • Hypertension
  • Mitral valve disorders
  • Pulmonary embolus
  • Chronic lung disease
  • Cardiomyopathy
  • Hyperthyroidism
105
Q

Clinical significance of atrial flutter

A
  • 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
Q

Atrial flutter treatment: primary goal

A

Slow ventricular response by increasing AV block

107
Q

Treatment for atrial flutter

A
  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
Q

Treatment to convert atrial flutter to normal sinus rhythm

A

Electrical cardioversion may be used to convert the atrial flutter to sinus rhythm emergently and electively.

109
Q

Peripheral Artery Disease

A
  • Involves progressive narrowing and degeneration of arteries of upper and lower extremities.
  • Atherosclerosis leading cause in majority cases
110
Q

Patients with PAD are more likely to have

A

Coronary artery disease and/or cerebral artery disease.

111
Q

Risk factors for peripheral artery disease include

A
  • Tobacco use
  • Chronic kidney disease
  • Diabetes mellitus
  • Hypertension
  • Hyperlipidemia
112
Q

Clinical Manifestations of Peripheral Artery Disease

A
  • 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
Q

PAD Clinical Manifestations: Claudication

A
  • Ischemic muscle pain that is caused by a constant level of exercise
  • Resolves within 10 minutes or less with rest
  • Reproducible
114
Q

PAD Clinical Manifestations: Paresthesia

A
  • Numbness or tingling in the toes or feet
  • Produces loss of pressure and deep pain sensations
  • Injuries often go unnoticed by patient
115
Q

PAD Clinical Manifestations: Pain at rest

A
  • As PAD progresses
  • Occurs in feet or toes
  • Aggravated by limb elevation
  • Occurs from insufficient blood flow
  • Occurs more often at night
116
Q

Critical Limb Ischemia: Characterized by

A
  • Chronic ischemic rest pain lasting more than 2 weeks.

- Arterial leg ulcers or gangrene.

117
Q

Who has an increased risk for critical limb ischemia/PAD?

A

Those who have PAD and also have diabetes, CHF, and history of stroke are at increased risk.

118
Q

Complications of Critical Limb Ischemia/PAD

A
  • Atrophy of skin and underlying muscles
  • Delayed healing
  • Wound infection
  • Tissue necrosis
  • Arterial ulcers
119
Q

Most serious complications of critical limb ischemia/PAD are

A
  • Non-healing arterial ulcers and gangrene.

- May result in amputation if adequate blood flow is not restored or if severe infection occurs.

120
Q

Diagnostic studies used for critical limb ischemia/PAD

A
  • Arterial Doppler ultrasound with ankle-brachial index (ABI)
  • Angiography and magnetic resonance angiography
  • Duplex imaging: Bidirectional, color Doppler
121
Q

Risk Factor Modifications for Critical Limb Ischemia/PAD

A
  • Tobacco cessation
  • Glycosylated hemoglobin <7.0% for diabetics
  • Aggressive treatment of hyperlipidemia
  • BP control
122
Q

Drug Therapy for Critical Limb Ischemia/PAD

A
  • ACE inhibitors: Ramipril (Altace)

- Antiplatelet agents: Aspirin, Clopidogrel

123
Q

PAD/Critical Limb Ischemia Drug Therapy: Ramipril (Altace)

A 
↓ Cardiovascular morbidity 
↓ Mortality 
↑ Peripheral blood flow
↑ ABI 
↑ Walking distance
124
Q

What drugs are prescribed for treatment of intermittent claudication associated with PAD?

A
  • Cilostazol (Pletal)

- Pentoxifylline (Trental)

125
Q

Claudication Treatment: Cilostazol

A
  • Inhibits platelet aggregation.

- ↑ Vasodilation

126
Q

Claudication Treatment: Pentoxifylline (Trental)

A
  • Improves deformability of RBCs and WBCs

- Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity

127
Q

Exercise Therapy for PAD/Critical Limb Ischemia

A
  • Improves oxygen extraction in legs and skeletal metabolism.
  • Walking is most effective for individuals with claudication: 30-45 minutes daily, 3 times/week.
128
Q

Nutrition Therapy for PAD

A
  • 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
Q

Leg with critical limb ischemia: conservative treatment includes

A
  • Protect from trauma
  • Decrease ischemic pain
  • Prevent/control infection
  • Improve arterial perfusion
130
Q

Indications for interventional radiology procedures in patients with PAD

A
  • Intermittent claudication symptoms become incapacitating
  • Pain at rest
  • Ulceration or gangrene severe enough to threaten viability of the limb
131
Q

Percutaneous Transluminal Angioplasty

A
  • 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
Q

Surgical Therapy for PAD

A
  • 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
Q

Nursing Assessment for PAD: Past Health History

A
  • Diabetes mellitus
  • Smoking
  • Hypertension
  • Hyperlipidemia
  • Obesity
134
Q

Overall goals for patient with PAD

A
  • Adequate tissue perfusion
  • Relief of pain
  • Increased exercise tolerance
  • Intact, healthy skin on extremities
  • Increased knowledge of disease and treatment plan
135
Q

Ambulatory care for patients with PAD

A
  • 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
Q

Evaluation of PAD

A
  • Adequate peripheral tissue perfusion
  • Increased activity tolerance
  • Effective pain management
  • Knowledge of disease and treatment plan
137
Q

What are the two types of strokes?

A
  1. Ischemia (inadequate blood flow) to the part of the brain

2. Hemorrhage into the brain that results in death of brain cells

138
Q

Non-modifiable risk factors for strokes

A

Age
Gender
Race
Genetics

139
Q

Modifiable Risk Factors for Strokes

A
  • Hypertension
  • Heart disease
  • Diabetes
  • OSA
  • ETOH abuse
  • Poor diet
  • Drug abuse
  • Smoking
  • Obesity
  • Physical inactivity
140
Q

Mini-strokes

A

Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction of the brain.

141
Q

Symptoms of mini-strokes

A

Symptoms last <1 hour; low oxygen, precursor to ischemic stroke.

142
Q

Types of Ischemic Stroke

A

Thrombotic and embolic

143
Q

Types of Hemorrhagic stroke

A

Intracerebral and subarachnoid

144
Q

Ischemic Stroke: Thrombotic Stroke

A
  • Result of thrombosis or narrowing of the blood vessel - blood clot formation.
  • Most common cause of stroke.
145
Q

Ischemic Stroke: Embolic Stroke

A
  • 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
Q

Ischemic stroke results from

A

-inadequate blood flow to the brain from partial or complete occlusion of an artery

147
Q

Characteristics of Ischemic Stroke

A
  • Occurs rapidly
  • Patient remains conscious
  • May have a headache
  • PMH: a-fib, MI, rheumatic heart disease (not sure what this means)
148
Q

Hemorrhagic strokes results from

A

Bleeding into the brain tissue itself or into the subarachnoid space or ventricles.

149
Q

Hemorrhagic Stroke: Intracerebral Hemorrhage

A
  • Bleeding within the brain caused by rupture of a vessel.
  • Prognosis is poor.
  • Commonly occurs during periods of activity.
150
Q

What is the most important cause of intracerebral hemorrhage?

A

Hypertension.

151
Q

A hemorrhage in what location of the brain is the most serious?

A

Hemorrhage in the pons is most serious (respiration; hemiplegia, coma, hyperthermia, and death.

152
Q

Hemorrhagic Stroke: Subarachnoid Hemorrhage

A

Occurs when there is an intracranial bleeding into the CSF fluid filled space between the arachnoid and pia mater.

153
Q

Majority of aneurasym are in the

A

Circle of Willis

154
Q

Subarachnoid Hemorrhage Characteristics

A
  • History of illicit drug use.
  • Sudden “worst headache” (ruptured aneurysm).
  • About 40% with ruptured aneurysm die during the first episode.
155
Q

Strokes can affect what motor functions?

A 
Mobility
Respiratory function
Swallowing and speech
Gag reflex
Self-care abilities
156
Q

A stroke affecting the middle cerebral artery leads to

A

leads to a greater weakness in the upper extremity than the lower extremity.

157
Q

Effects of stroke on communication

A
  • Aphasia
  • Receptive aphasia (loss of comprehension)
  • Expressive aphasia ( inability to produce language)
  • Global aphasia (total inability to communicate)
158
Q

How can a stroke effect affect?

A

Frustration

Depression

159
Q

How can a stroke in the left brain affect intellectual function?

A

Memory problems related to language, more cautious

160
Q

How can a stroke in the right brain affect intellectual function?

A

Tends to be more impulsive and to move quickly

161
Q

How can a stroke affect elimination?

A
  • Initially the patient may experience: frequency, urgency, incontinence.
  • CONSTIPATION is associated with weak abdominal muscles, dehydration, and diminished response to the defecation reflex.
162
Q

Diagnostic Tests used for Stroke

A
  • Non contrast head CT or MRI- size and location
  • Cardiac imaging
  • Transcranial Doppler ultrasonography
163
Q

Preventative Therapy for Strokes include

A
  • 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
Q

Preventative Drug Therapy for Strokes

A

TIA: Aspirin 81mg daily or Clopidogrel (Plavix)

A-fib: Warfarin (Coumadin) or Riviroxaban (Xarelto)

165
Q

Surgical Therapy for TIA

A

Carotid Endarterectomy: common treatment for embolic and ischemic stroke; may be done to prevent stroke.

166
Q

Diagnosis of CVA

A

Non contrast MRI or CT scan

167
Q

Treatment for CVA

A
  • 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
Q

Goals of stroke prevention include

A
  • 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
Q

How can you prevent a stroke?

A
  • Smoking should be discontinued
  • Limited alcohol intake
  • Healthy diet
  • Weight control
  • Regular exercise
  • Routine health examinations
170
Q

Primary Assessment for CVA: focus on

A

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
Q

Nursing Care for CVA: Respiratory

A
  • Swallowing, risk for aspiration pneumonia is high d/t dysphagia
  • Regular oral care is important
  • Suctioning
172
Q

Nursing Care for CVA: Neurologic

A

Increasing ICP

173
Q

Nursing Care for CVA: Cardiovascular

A
  • 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
Q

Nursing Care for CVA: Musculoskeletal

A

Avoid subluxation of the shoulder, foot drop.

175
Q

Nursing Care for CVA: Integumentary

A

Skin care and skin hygiene

176
Q

Nursing Care for CVA: GI

A
  • Loss of gag reflux

- Constipation: fiber and stool softeners

177
Q

Nursing Care for CVA: Urinary

A

-Incontinence, short term catheter recommended

178
Q

Nursing Care for CVA: Nutrition

A

-Swallowing evaluation, thin liquids needs to be thickened.

179
Q

Hemianopsia in CVA

A

Decreased vision or blindness in 1/2 visual field.

Arrange food tray to accommodate for field of vision.

180
Q

Diplopia

A

Double vision

NURS 401 (26 decks)

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