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NRSG 110: Med Surg 2 > [Exam 1] Chapter 27: Management of Patients with Coronary Vascular Disorders (Page 750-773) > Flashcards

[Exam 1] Chapter 27: Management of Patients with Coronary Vascular Disorders (Page 750-773) Flashcards

1
Q

What is Coronary Atherosclerosis (CAD)?

A

An abnormal accumulation of lipid, or fatty substances and fibrous tissue in the lining of arterial blood vessel walls.

They block and narrow the coronary vessels in a way that reduces blood flow to the myocardium

Involves a repetitious inflammatory response to injury

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2
Q

Coronary Atherosclerosis: Pathophysiology: Inflammatory response involved begins with

A

injury to the vascular endothelium and progresses over many years

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3
Q

Coronary Atherosclerosis: Pathophysiology: Injury may be initiated by

A

smoking, hypertension, hyperlipidemia and other factors

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4
Q

Coronary Atherosclerosis: Pathophysiology: Presence of inflammation attracts

A

inflammatory cells such as monocytes (macrophages). They ingest lipids, becoming foam cells that transport the lipids into the arterial wall. This forms fatty streams.

They also release biochemical substances that further damage the endothelium by contributing to oxidation of LDL. LDL is toxic to the endothelial cells and fuels progression.

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5
Q

Coronary Atherosclerosis: Pathophysiology: Following transport of lipid into the arterial wall

A

smooth muscle cells proliferate and form a fibrous cap over a core filled with lipid. These are called atheromas and protrude into the lumen or vessel and narrow and obstruct the blood flow.

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6
Q

Coronary Atherosclerosis: Pathophysiology: If severe, blood flow may become obstructed and leads to

A

an acute coronary syndrome (ACS) which may result in an acute myocardial infarction (MI). When MI occurs, portion of the heart muscle no longer receives blood flow and become snecrotic

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7
Q

Coronary Atherosclerosis: Pathophysiology: What is an Aneurysm

A

When the buildup starts to bulge out and protude on other tissues. The fear is that this may rupture allowing someone to hemmorhage.. l

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8
Q

Coronary Atherosclerosis: Complications: Symptoms caused by

A

myocardial ischemia

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9
Q

Coronary Atherosclerosis: Complications: Symptoms and complications are related to

A

the location and degreee of vessel obstruction

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10
Q

Coronary Atherosclerosis: Complications: Angina pectoris is the most

A

common manifestation

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11
Q

Coronary Atherosclerosis: Complications: Other symptoms

A

Epigastria distress, pain that radiates to jaw or left arm, SOB, atypicial symptoms in women

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12
Q

Coronary Atherosclerosis: Complications: Life threatening complications inclde

A

MYocardial Infarction

Heart Failure

Sudden cardiac death

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13
Q

What is Ischemia?

A

When there is an impediment to blood flow is usually progressive, causing an inadequate blood supply that deprives the muscle cells of oxygen needed for their survivial.

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14
Q

What is Angina Pectoris?

A

Chest pain that is brought about by myocardial ischemia. Usually causeed by significant coronary athersclerosis

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15
Q

Coronary Atherosclerosis: Risk Factors:

A

Cholesterol Abnormalities - Elevated LDL (Are sticky and cause CAD)

Tobacco Use (Chemicals in blood cause inflammation)

Hypertension, increased pressure on arterial walls causes inflammation)

Diabetes

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16
Q

Coronary Atherosclerosis: What is CRP?

A

Inflammatory marker for cardiovascular risk. Live produces CRP in response to a stimulus such as tissue injury and hand levels of this protein may occur in people with diabetes who are lkely to have an acute coronary event

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17
Q

Coronary Atherosclerosis: Prevention: What four elements of fat embolism are known to affect the development of heart diseas?

A

Total Cholesterol

LDL

HDL

TRiglycerides

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18
Q

Coronary Atherosclerosis: Prevention: What is the clinical practice guideline on the treatment of blood cholesterol to reduce cardiovascular risk in adults?

A

Those 20 years and older should have a fasting lipid profile performed once every 5 years or more if profile abnnormal.

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19
Q

LDL should be less than

A

100 mg/dL

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20
Q

Total cholesterol should be less than

A

200 mg/dL

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21
Q

HDL should be

A

40 mg/dL or higher

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22
Q

Triglycerides should be lessthan

A

150 mg/dL

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23
Q

Coronary Atherosclerosis: Prevention: Cholesterol prevention includes

A

Keep LDL low, Triglyercides and lipids low

Keep HDL high

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24
Q

Coronary Atherosclerosis: Prevention: Dietary Measures include a diet that

A

is low in saturated fat and low trans fat while high in soluble fiber

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25
Q

Coronary Atherosclerosis: Prevention: Exercise

A

Should exercise 30 minutes 3-4 times a week.

Should also try to weight lifting workout two times a week as well

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26
Q

Coronary Atherosclerosis: Prevention: Medications they can use include

A

Antihypertensives,
lipid and cholesterol lowering ,
ASA to prevent platelet aggregation,
ACE and ARBS to high risk patients

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27
Q

Coronary Atherosclerosis: Prevention: Tobacco Use and Nicotinic Acid

A

This triggers the release of catecholamines which raise the heart rate and blood pressure. Can cause the coronary arteries to constrict

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28
Q

Coronary Atherosclerosis: Prevention: Tobacco and smoking

A

Can increase oxidation of LDL, daming the vascular endothelium

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29
Q

Coronary Atherosclerosis: Prevention: Tobacco and Inhalation

A

Increases the blood carbon monoxide level and decreases the supply of oxygen to the myocardium

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30
Q

Coronary Atherosclerosis: Prevention: Controlling Diabetes is known to accelerate the development of heart disease. What does it affect?

A

Hypgerglycemia fosters dyslipidemia, increased platelet aggregation and altered red blood cells function which can lead to thromus formation and impair endothelial cell-dependent vasodilatin

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31
Q

Angina Pectoris: What is this?

A

Clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest.

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32
Q

Angina Pectoris: Simple definition cause of this?

A

Insufficent blood flow resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress

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33
Q

Angina Pectoris: Is usually caused by

A

Atheroscletotic disease

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34
Q

Angina Pectoris: Associated with a

A

significant obstruction of at least one major coronary artery

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35
Q

Angina Pectoris: What does physical exertion or emotional stress do?

A

Increases myocardial oxygen demand, and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand

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36
Q

Angina Pectoris: This is the medical term for

A

chest pain

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37
Q

Several factors are associated with typical anginal pain such as

A

Physical exertion

Exposure to cold

Eating a heavy meal

Stress

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38
Q

What is a Stable Angina?

A

Predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin

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39
Q

Stable Angina- Arteries cannot do what

A

cannot increase blood supply to heart during activity or stress, stops with rest, no damage

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40
Q

What is Unstable Angina?

A

Symptoms increase in frequency and severity, may not be relieved with rest or nitroglycerin

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41
Q

Unstable Angina - can occur at

A

rest, shows worsening CAD, rest does not relieve pain, increasing frequency of pain, risk for damage

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42
Q

What is intractable or refactory angina?

A

Severe incapacitating chest pain

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43
Q

What is Variant Angina?

A

Pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm

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44
Q

Variant Angina cause dby

A

arterial spasms and usually comes at same time of day and last same amount of time, rest does not stop pain and no damage

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45
Q

What iis Silent Ischemia

A

Objective evidence of ischemia (such as electrocardiographic changes with a stress test) but patient reports no pain

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46
Q

Silent Ischemia detailed

A

myocardial damage is occuring but patient does not feel pain

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47
Q

Angina Pectoris: Pain is typically poorly localized and may radiate to the

A

neck, jaw, shoulders, or the inner aspects of the upper arms usually the left ar,

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48
Q

Angina Pectoris: Patient often feels

A

tightness or a heavy choking or strangling sensation that has a viselike, insistent quality.

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49
Q

Angina Pectoris: Unstable angina is characterized by

A

attacks that increase in frequency and severity and are not relieved by rest and administering Nitroglycerin. REquire medical intervention

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50
Q

Angina Pectoris: Pain of typical angina subsides with

A

rest or nitroglycerin

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51
Q

Angina Pectoris: Diagnosis begins with

A

patients history related to the clinical manifestation so fischemia

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52
Q

Angina Pectoris: What tests are performed?

A

12 Lead ECG shows changes

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53
Q

Angina Pectoris: What lab tests are performed

A

these generally include cardiac biomarker testing to rule out ACS. MAy undergo exercise or pharmacologic stress test.

54
Q

Angina Pectoris: Medical management objectives include

A

decrease the oxygen demand of the myocardium and to increase the oxygen supply.

55
Q

Angina Pectoris: Standard treatment include

A

Nitrates. Nitroglycerin is a potent vasodilator that improves blood flow . This in turn lowers the blood pressure and decreases afterload.

56
Q

Angina Pectoris: How may Nitroglycerin be given?

A

Sublingual tablet or spray, Oral capsule, topical agent and intravenous IV administration

57
Q

Angina Pectoris: Nitroglycerin is usually not given if

A

systolic pressure is less than 90 mm Hg.

58
Q

Angina Pectoris: What do Beta-Adrenergic Blocking Agents do?

A

Metoprolol (Lopressor) reduce myocardial oxygen consumption by blocking beta-adrengeric sympathetic sitmulation to the heart. Results in reduced heart rate and reeduced contractility.

59
Q

Angina Pectoris: Diagnosis

A

risk for decreased cardiac tissue perfusion

Anxiety RT cardiac symptoms and possible death

Deficient knowledge about the underlying disease and methods for avoiding complications

Noncompliance, ineffective management of therapeutic regimen related to failure to accept changes

60
Q

Angina Pectoris: Collaborative Problems

A

MI

Dysrhythmias and Cardiac Arrest

Heart Failure

Cardiogenic Shock

61
Q

Angina Pectoris: Goals

A

Immediate and appropriate treatment of angina

Prevention of angina

REduction of anxiety

Awareness of the disease process

Understanding of prescribed care

Absence of complications

62
Q

Angina Pectoris: Treating Angina: Treatment seeks to decrease

A

myocardial oxygen demand and increase oxygen supply - stay calm

63
Q

Angina Pectoris: Treating Angina: Patient is to stop all

A

activity and sit or rest in bed to reduce oxygen requirement . Assess if angina is teh same as normal

64
Q

Angina Pectoris: Treating Angina: If in hospital, this is usually obtained

A

12-lead ECG and assessed for ST- segment and T-wave changes

65
Q

Angina Pectoris: Treating Angina: Assess the patient while performing other

A

necessary interventions

Assessment includes VS, observation for respiratory distress and assessment of pain.

66
Q

Angina Pectoris: Treating Angina: ADminister medications as ordered, usually

A

Nitroglycerin sublingually. If unchanged, nitroglycerin administration is repeated up to three doses.

67
Q

Angina Pectoris: Treating Angina: Administer oxygen at a rate of

A

2L/min by nasal canula.

68
Q

Angina Pectoris: Treating Angina: If nothing worked, the patient is furthehr

A

evaluated for acute MI and may be transferred to a higher-acuity nursing unit

69
Q

Angina Pectoris: Reduce Anxiety: This is done by

A

providing information about the illness, its treatment, and methods of preventing its progression are important nursing interventions

70
Q

Angina Pectoris: Nitroglycerin, what is this?

A

A vasodilator that allows for maximum blood supply with the least resistance to reach the heart

71
Q

Angina Pectoris: How long is Nitroglycerin good for?

A

Good for six months and msut be kept in original bottle

72
Q

Angina Pectoris: What does Nitroglycerin cause?

A

HA, dizzyness, and orthostatic hypotension

73
Q

Angina Pectoris: Can take nitroglycerin before

A

activity known to cause chest pain but be aware of hypotension

74
Q

Angina Pectoris: Beta-Adrenergic Blocking Agents: work to

A

reduce myocardial oxygen consumption by blocking beta-adrengeric sympathetic stimulation to the heart

Are vasodilators

75
Q

Angina Pectoris: Beta-Adrenergic Blocking Agents: THe result is

A

reduction in heart rate, slowed conduction of impulses through the conduction system , decreased blood pressure and decrease contractility.

76
Q

Angina Pectoris: Beta-Adrenergic Blocking Agents: Beta blockers balance

A

the myocardial oxygen demands and oxygen available

77
Q

Angina Pectoris: Beta-Adrenergic Blocking Agents: CArdiac side effects include

A

hypotension, bradycardia, and acute heart vailure

78
Q

Angina Pectoris: Calcium Channel Blocking Agents: This is a way to reduce

A

demand

79
Q

Angina Pectoris: Calcium Channel Blocking Agents: What does it do?

A

Reduces heart workload by decreasing HR and myocardial contraction therefore decreasing demand

Also increase myocardial myocardial oxygen supply by dilating the smooth muscle wall of the coronary arterioles

80
Q

Angina Pectoris: Antiplatelet and anticoagulant medications do what?

A

Clot prevention due to turbulent blood flow

81
Q

Angina Pectoris: How does Aspirin help?

A

Clot prevention due to inflammatory process

Prevent platelet aggregation and reduces the incidence of MI and death in patients with CAD

82
Q

Angina Pectoris: How does Heparin help?

A

Unfractioned IV heparin prevents the formation of new blood clots. Reduces the occurence of MI

83
Q

Angina Pectoris: Patient teaching

A

Follow up with doctor

Maintain normal bp

Rest after activity

Avoid OTC meds

DASH Diet

84
Q

What is an Acute Coronary Syndrome (ACS)?

A

Emergent sitation characterized by an acute onset of myocardial ischemia that results in myocardial death if definity interventions do not occur promptly.

85
Q

Although the terms coronary occlusion, heart attack, and MI are used synonymously, the preferred term is

A

MI

86
Q

In unstable angina, there is reduced blood flow in a coronary artery often due to

A

reupture of an atherosclerotic plaque

87
Q

In an MI, plaque repture and subsequent thrombus formation result in

A

complete occlusion of the artery leading to ischemia and necrosis of the myocardium supplied bby that artery

88
Q

Myocardial Infraction: AS the cells are deprived of oxygen

A

ischemia develops, cellular injury occurs, and lack of oxygen results in infarction or the death of cells

89
Q

Myocardial Infraction: 12 lead ECG identifies type and location of the MI but Q wave and patient history determine the

A

timing

90
Q

Myocardial Infraction: Clinical Manifestations is chaest pain that occurs

A

suddenly and continues despite rest and medication is the presenting symptom in most patients with ACS

91
Q

Myocardial Infraction: Clinical Manifestations: Patients may present with

A

a combination of symptoms including chest pain, shortness of breath, indigestion, nausea, and anxiety

Cool, pale skin, increase HR , RR

92
Q

Myocardial Infraction: Signs and Symptoms for women include

A

indigestion, nausea, palpitations, numbness, weakness

93
Q

Myocardial Infraction: 12 lead ECG provides informaiton that assists in ruling out or diagnosing

A

an acute MI

94
Q

Myocardial Infraction: ECG and ST Segment

A

We would be expecting an elevated ST segment here, showing us that the tissue is dying

95
Q

Myocardial Infraction: Appearance of abnormal Q waves shows

A

MI. Devleops within 1-3 days because there is no depolarization.

96
Q

Myocardial Infraction: Echocardiogram useful because

A

it can detect hypokinetic and akinetic wall motion and can determine the ejection fraction

97
Q

Myocardial Infraction: What three lab tests can be performed with cardio biomarkers?

A

Troponin

Creatine Kinase and Its Isoenzymes

Myoglobin

98
Q

Myocardial Infraction: What is Troponin?

A

Is a protein found in myocardial cells realsed when damaged and stayed elevated in blood for up to 3 weeks. It is used to detect mycardial damage.

99
Q

Myocardial Infraction: Troponins I and T are specific for

A

cardiac muscle

100
Q

Myocardial Infraction: Troponin: Can be detected within

A

a few hours during acute MI

101
Q

Myocardial Infraction: What is Creatine Kinase ?

A

CK-MB (Heart Muscle) is a specific isoenzyme to cardiac tissue and is released during damage it peaks at 24 hours during an acute MI and is used as an indicator of an acute MI

102
Q

Myocardial Infraction: Troponin: What is Myoglobin?

A

It is a heme protien that helps transport oxygen found in skeletal and cardiac muscle so not specific for MI but negative results can help rule out an MI

103
Q

Myocardial Infraction: MEdicla Management goal

A

Minimize myocardial damage, preserve myocardial function and prevent complications

104
Q

Myocardial Infraction: Initial Management: Pt with suspected MI should immediately receive

A

supplemental oxygen, aspirin, nitroglycerin, and morphine

Beta blocker may also be used if dysrhythmias occur.

105
Q

Myocardial Infraction: Diagnoses

A

Acute pain related to increase myocardial oxygen demand

Risk for decreased cardiac tissue perfsuin

RF imbalance fluid volume

Risk for ineffective peripheral tissue perfusion

106
Q

Myocardial Infraction: Collaborative Problems

A

Acute pulmonary Edema

Heart Failure

Cardiogenic Shock

Dysyrhythmias and Cardiac Arrest

Pericardial Effusion and Cardiac Tamponade

107
Q

Myocardial Infraction: Nursing MAnagement

A

Relief of Pain or Ischemic Signs

Prevention of myocardial damage

Maintenance of effective respiratory function, adquat tissue perfusion

Reduction of anxiety

Adherence to self care program

Early recognition of complications

108
Q

Myocardial Infraction: Nursing Interventions: Oxygen should be given along with medication therapy to

A

assist with relief of symptoms. Admiistration of oxygen raises the circulating level of oxygen to reduce pain

109
Q

Myocardial Infraction: Nursing Interventions: Vital signs are assessed

A

frequently as long as the patient is experiencing pain and other signs or symptoms of acute ischemia

110
Q

Myocardial Infraction: Nursing Interventions: Physical rest in bed with the head of the bed elevated or in a supportive chair helps decrease

A

chest discomfort and dyspnea

111
Q

Myocardial Infraction: Nursing Interventions: Relief of pain helps decrease

A

workload of the heart

112
Q

Myocardial Infraction: Nursing Interventions: You should monitor

A

I/O and tissue perfusion

113
Q

Myocardial Infraction: Nursing Interventions: Frequent position changes happen to

A

prevvent respiratory complications

114
Q

Myocardial Infraction: Nursing Interventions: Report changes in

A

patients condition and evaluate interventions

115
Q

Myocardial Infraction: Nursing Interventions: MONA Acronym

A

This includes what you could do for an MI

Give morphine (reduce oxygen demand and take care of pain), oxygen, ntiro for vasodilation, and aspirin to prevent clots

116
Q

Myocardial Infraction: Nursing Interventions: BEtablockers (slow heart rate to decrease demand), ACE, Heparin (decrese clots) given within

A

24 hours

117
Q

Myocardial Infraction: Nursing Interventions: For discharge, make sure that they know

A

how to monitor for MI

Cardiac Rehab

Slow progressive rgulated exercise

DASH diet

Weight Loss

BP, Blood Sugar, Cholesterol

118
Q

Why are invasive coronary atery procedures done?

A

To reperfuse ischemic myocardial tissue when patients are refactory to more conservative management methods

119
Q

Percutaneous Transluminal Coronary Angioplasty: What is done here?

A

Balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia.

120
Q

Percutaneous Transluminal Coronary Angioplasty: Purpose of this?

A

To improve blood flow within a coronary artery by compressing the atheroma. Done with cardiologist believes that PTCA can improve blood flow

121
Q

Percutaneous Transluminal Coronary Angioplasty: Carried out in the

A

cardiac catheterization laboratory

122
Q

Percutaneous Transluminal Coronary Angioplasty: How is the procedure done?

A

Hollow catheters called sheaths are isnerted via the femoral artery up through the aorta and into the coronary artery with the blockage

123
Q

Percutaneous Transluminal Coronary Angioplasty: Once at the blockage,

A

balloon is inflated to compress the plaque against the and open artery for blood flow . Balloon is then decompressed and removed

124
Q

Percutaneous Transluminal Coronary Angioplasty: Stend can be placed to

A

keep the artery open

125
Q

Percutaneous Transluminal Coronary Angioplasty: Pt may complain of

A

chest pain during procedure

126
Q

Percutaneous Transluminal Coronary Angioplasty: nursing care is same as cardiac cath but

A

pt will stay 24 hours

127
Q

Percutaneous Transluminal Coronary Angioplasty: Angiography is performed using

A

injected radiopaque contraast agents to identify location and extend of blockage. Physician determines teh catheter position by examining markers on teh balloon that can be seen with fluroscopy

128
Q

Percutaneous Transluminal Coronary Angioplasty: ECG may display

A

ST segment changes.

129
Q

Percutaneous Transluminal Coronary Angioplasty: Coronary artery stend may be placed because

A

the area that has been treated may close off partialy or completely. This could lead to vasoconstriction, clotting, and scar tissue formation

130
Q

Percutaneous Transluminal Coronary Angioplasty: Coronary artery stent can stay because

A

the skin will grow around it and allow it to be apart of it.

NRSG 110: Med Surg 2 (29 decks)

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