Exam 2 Flashcards
(141 cards)
0
Q
Fatty streak
A
This is a stage of development of atherosclerosis. It is characterized by lipid filled smooth muscle cells
1
Q
CAD
A
Type of blood vessels disorder that is included in the general category of atherosclerosis
Begins as soft deposits of fat that harden with age
Atherosclerosis is the major cause of cad
2
Q
Fibrous plaque
A
The second stage of atherosclerosis process. It is the beginning of progressive changes in the endothelium of arterial wall
3
Q
Complicated lesion
A
The third stage In atherosclerosis and the most dangerous.
4
Q
Risk factors for cad
A
Modifiable- elevated serum lipids, elevated BP, tobacco, inactivity, diabetes, metabolic syndrome,!psychological state
Non modifiable- age, gender, ethnicity
5
Q
Simvastatin
A
Increase risk for rhabdomyolosis
6
Q
Niacin
A
Instruct patient that flushing may occur and patient may take aspirin to control the flushing; increases HDL and lowers LDL
7
Q
Angina
A
Chest pain and the clinical manifestation that MI has occurred
8
Q
Silent ischemia
A
Refers to ischemia that occurs in the absence do any subjective symptoms. Patients with diabetes have an increased incidence
9
Q
Nocturnal angina
A
Occurs only at night but not necessarily when the person is I’m recumbent position or asleep
10
Q
Angina decubitus
A
Occurs only while person is laying done and usually relieved by standing
11
Q
Prinzmetals angina
A
Often occurs at rest, usually In response to spasm or a major coronary artery
12
Q
Acute coronary syndrome (ACS)
A
Occurs when ischemia is prolonged And not reversible and encompasses the spectrum on unstable angina, NSTEMI, STEMI
13
Q
MI
A
Occurs because of sustained ischemia, causing irreversible myocardial cell death
Manifestations: chest pain not improved by rest, position change or nitrate; heaviness, tightness, burning
Ashy, clammy and cool to touch; BP and HR increased; fever; nausea and vomiting
14
Q
Complications of MI
A
Dysrhythmias, heart failure, cardiogenic shock, papillary muscle dysfunction ventricular aneurysm, pericarditis, dresser syndrome
15
Q
Goals for ACS
A
1) relief of pain
2) preservation of myocardium
3) immediate and appropriate treatment
4) effective coping
5) participation in rehab
6) reduce risk factors
16
Q
It patient experiences angina….
A
1) position patient upright
2) asses VS
3) obtain 12-lead ECG
4) prompt pain relief with nitrate then opioid
5) auscultation heart and breath sounds
17
Q
Heart failure
A
Inadequate pumping and/or filling of the heart
Causes the heart to be unable to provide sufficient blood to meet the oxygen needs of tissues
HtN and CAD are primarily the risk factors
18
Q
Systolic failure
A
Inability of the heart to pump blood effectively. It is caused b impaired contractile function, increased after load, cardiomyopathy, and mechs hick abnormalities
The left ventricle loses it’s ability to generate enough pressure to eject flood forward through sorta
19
Q
Diastolic failure
A
Inability of ventricles to relax and fill during diastole. Referred to as HF with normal EF; decreased stroke volume and CO
20
Q
Compensatory mechanisms of HF
A
SNS activation, neurohormonal response, dilation, hypertrophy
21
Q
Left sided heart failure
A
Prevents normal forward blood flow and causes blood to back up to left strum and pulmonary veins. This manifests as pulmonary edema
22
Q
Right sided HF
A
Right ventricle fails to context effectively. Back up of blood into the right atrium
The primary causes of right sided heart failure is left sided heart failure
23
Q
Chronic HF manifestations
A
Fatigue, dyspnea, paroxysmal nocturnal dyspnea, tachycardia, edema, nocturnal, skin changes, behavioral changes, chest pain, weight changes
24
Complications of HF
Plural effusion, dysrhythmias, left ventricular thrombus, hepatomegaly, renal failure
25
Diuretics
Decrease fluid volume; decrease preload; decrease pulmonary genius pressure; relieve symptoms of heart failure
26
RAAS inhibitors
Dilate venues and arteriolar; improve renal blood flow; decrease fluid volume; relieve symptoms of HF; promote reverse remodeling; decrease morbidity
27
Vasodilators
Reduce cardiac after load, leading or increased C; dilate arteriolar of kidneys; decrease blood pressure; decrease preload; relieve symptoms of HF
28
Beta blockers
Promote reverse remodeling; decrease after load; inhibit sns; decrease morbidity and mortality
29
Positive into tropes
Increase contractility; increase CO; increase HR; produce mild vasodilation; increase SV and CO; promote vasodilation
30
Morphine
Decreases anxiety; decreases preload and after load
31
Leading cause of PAD
Atherosclerosis
32
With atherosclerosis the vessels have a gradual increase in plaque formation throughout entire vessel and vascular system
True
33
AAA
Patient can have angina from decreasing blood flow to coronary arteries and hoarseness in voice from pressure on laryngeal nerve, pressure of esophagus can cause dysphasia, edema in face, bruit may be heard over aneurysm
34
What will you do to decrease the likelihood of the aneurysm rupturing or dissecting?
Early detection and prom treatment: stopping tobacco use, decreasing BP, optimizing lipid profile, annual monitoring of aneurysm size, beta blockers, statins and antibiotics
35
For PAD of lower extremities, what is causing the symptoms?
The extent of the blockage and the amount of collateral circulation; ischemic pain resulted from the build up of lactic acid from anaerobic metabolism
36
Teaching points for patients with Raynaud's
Wear loose warm clothing, immerse hands in warm ester, stop tobacco use and caffeine intake
37
What is atherosclerosis
Formation of focal deposits of cholesterol and lipids known as plaque, primarily within the intimal walls of arteries, that obstruct circulation
38
Risk factors for CAD
Non-modifiable: increasing at, gender, ethnicity, genetics, family history of heart disease
Modifiable: serum lipid levels, BP, diabetes, tobacco use, physical inactivity, obesity
39
Serum lipid levels
Total cholesterol: 40; female >50
40
What are the cardiac biomarkers that appear after an MI?
Myoglobin: released after muscle trauma, not specific to cardiac muscle
Troponin: elevates quickly, 2 hours after MI
CKMB: peaks two days after cardiac event
41
PAD
Involved thickening of the artery walls, which results in a progressive narrowing of the arteries of the upper and lower extremities. Risk increases with she and in those with diabetes and is related to other cardiovascular diseases
42
Risk factors of PAD
Tobacco use, diabetes, hyperlipidemia, elevated C-reactive protein, uncontrolled HtN, family history, increasing age, obesity, sedentary lifestyle, stress
43
Aneurysm
A permanent localized outpouring or dilation of the vessel wall. Occur more in men then women and incidence with increasing age
44
How to treat angina?
Calcium channel blocker or nitrates
45
Antiplatelet meds
Aspirin, plavix, petal, persantine
46
Beta blockers
Slows heart, less demand, not for asthma, caution with diabetics
47
Calcium Chanel blockers
Vasodilators, decreases rate, negative inotrope
48
Ace inhibitors
Cause cause ARB
49
What is the most common cause of aneurysm?
Age, male gender, HtN, cad, family history, high cholesterol, lower extremities pad, history of stroke, tobacco use and obesity
Three major risk factors: male, older age and tobacco use
50
Classic symptoms or lower extremity PAD
Intermittent claudication which is ischemic muscle pain that is caused by exercise and revolves within 10 minutes of rest. Numbness or tingling of toes. Skim becomes shiny, thin, taunt and hair loss occurs. Pulses are diminished. Pallor I'm the foot and reactive hyperemia when leg is In dependent position
51
HF
An abnormal clinical syndrome involving impaired cardiac pumping and/or filling of the heart
52
Primary risk factors for HF
HTN and CAD
53
Mechanism that cause CHF
Preload, after load, myocardial contractility, heart rate
54
Systolic HF
Results from inability of heart to pump blood effectively
Caused by impaired contractile function, increases after load, cardiomyopathy, and mechanical abnormalities
The left ventricle loses ability to generate enough pressure to eject blood through aorta
Hallmark: decrease in LV ejection fracture
EF: less than 45%
55
Diastolic HF
Inability of ventricles to relax and fill during diastole
Often referred to as HF with normal EF
Decrease stroke volume and CO
Characterized by high filling pressure because of still ventricles
56
Compensatory mechanisms of HF
1) SNS activation: first one triggered but least effective; increases release of catecholamines resulting in increased Hr, increased contractility and peripheral vasoconstriction
2) neurohormonal response: as CO falls, blood flow to kidneys decrease; kidneys release renin, converting angiotensinogen to angiotensin 1 --> angiotensin 2 --> cause the release of aldosterone, increased vasoconstriction increasing BP
3) dilation: enlargement of heart chambers; muscle fibers stretch; initially leads to increased CO and maintence of BP but overtime causes fibers to over stretch and decrease CO
4) hyper trophy: increase I'm muscle mass and cardiac wall thickness; initially increases CO but overtime does not work
57
S/S of left HF
Weakness, fatigue, pulmonary edema, crackles, s3/s4 he's rat sounds, pleural effusion, changes in mental status, confusion
Most common; results from LV dysfunction; prevents normal flow of blood and causes back up into left atrium and pulm veins
58
S/S of right HF
Fatigue, murmurs, RV heaves, jugular distinction, peripheral edema, weight gain, hepatomegaly
Results from Arab failure to contract, causes backup of blood into RA and venous circulation
Primary cause is left sided HF
59
HF is characterized by....
Ventricular dysfunction, reduced exercise tolerance, diminished quality of life, shortened life expectancy
60
Complications of HF
Plural effusion, dysrhythmias, left ventricular thrombus, hepatomegaly, renal failure
61
Preload
Volume of blood I'm ventricles at the end of diastole before the next contraction, determines amount of stretch placed on myocardial fibers
62
After load
Peripheral resistance against which the left ventricle must pump, affected by the size of ventricle, wall tension, and arterial blood pressure
63
Infective endocarditis (IE)
Infection of the endocardium layer of the heart
64
Most common cause of an infective endocarditis
Staphylococcus aureus and streptococcus viridans
Criteria is 2/3:
1) positive blood cultures
2) new or changed murmur
3) intracardiac mass or vegetation on echo
65
What happens when vegetation breaks loose in a patient?
Results in an emboli
Left sided: various organs and extremities
Right: P
66
Treatment for IE
Antibiotic administration : monitor antibiotic serum levels, subsequent blood cultures, monitor renal function, long term IV antibiotics
Subacute bacterial endocarditis:
67
Pericarditis
Inflammation of pericardial sac
Idiopathic, acute signs and symptoms, dressler syndrome 4-6 weeks later
Sharp pain wore with deep inspiration, supine. Pain radiates to trapezium muscle, pericardial friction rub
68
Pericardial effusion
Build up of fluid I'm the spherical dim
| Cough, dyspnea, tachyons, hiccups, hoarseness, heart sounds are distant and muffled, BP is usually maintained
69
Cardiac tamponade
Develops as pericardial effusion increases in volume resulting in compression of heart
The speed of fluid accumulation affects the severity of manifestations
Chest pain, confusion, anxious, restless, decreased CO, distended neck veins
70
PAD
Thickening of artery walls which resulted in progressive narrowing of the arteries of upper and low extremities
Leading cause is atherosclerosis
71
Nursing diagnosis/management for PAD
Ineffective tissue perfusion, impaired skin integrity, activity intolerance, infective self health management
Goals: adequate tissue perfusion, relief of pain, increased exercise tolerance, intact and healthy skim
72
Intermittent claudication
Classic symptom of lower extremity PAD, which is an ischemic muscle pain that is caused by exercise, resolved within 10 minutes or less with rest and is reproducible
73
Acute arterial occlusion
Symptoms: pain, pallo, paralysis, pulselessness, paras thesis, poililothermia
Pharm treatment: statins, aspirin or plavix, ACE
Causes: embolism, thrombus, trauma
Avoid knee flexed position, avoid lots of dependent leg positioning, may have compressions
74
Thrombophlebitis
Venous disorder
| Elevate, anticoagulants, warm and moist heat
75
Care of ulcers
Arterial: dry sterile dressing, hyperbaric the rosy, reverse trendelenburg
Venous: compressions leg elevation, moist dressings, antibiotics
76
Amputations
The goal is to preserve extremity length and function while removing all infected, pathological or ischemic tissues
77
Goals for an amputee
1) adequate relief from underlying health issue 2) pain control 3) reach maximum rehabilitation potential with prosthesis 4) cope with body image changes 5) make satisfying life adjustments
78
Aortic dissection
Is not an aneurysm. Rather, it resulted from the creation of a false lumen between the intima and the media of arterial wall.
A tear develops in the inner layer of the aorta and blood surges through causing the inner and middle layer to separate.
Report abrupt onset of excruciating chest and/or back pain radiating to the neck or shoulders.
If aortic arch is involved then the patient may exhibit neurologic deficits
79
Phlebitis
Inflammation of the walks of small cannula tee veins of the hand or arm. Clinical signs and symptoms include pain, tenderness, warmth, erythema, sweeping and palpable cord
80
Venous thrombosis
Involves formation of a thrombus in association with inflammation of the vein.
81
Virchow's triad
1) venous status 2) damage of the endothelium and 3) hypercoagulability of the blood
82
Arterial ulcers
Tips of toes, foot, or lateral malleolus; rounded, smooth, minimal drainage; black tissue or pale pinkish granulation
Cap refill is greater than 3 seconds
83
Venous ulcers
Nest medial malleolus; irregularly shaped and moderate to large amount of drainage; tissue is yellow or dark res
84
Vasotec (enalapril)
Ace inhibitor/antihypertensive
Manage hypertension
Blocks conversion of angiotensin 1 to angiotensin 2
SE: fatigue, asthenosphere, diarrhea, nausea, dizziness, cough, rash
85
Amlodioline
Calcium channel blocker
| Blocks calcium channels in vascular smooth muscle and myocardial cells which causes dilation
86
Leading cause of PAD
Atherosclerosis
87
With atherosclerosis the vessels have a gradual increase in plaque formation throughout entire vessel and vascular system
True
88
AAA
Patient can have angina from decreasing blood flow to coronary arteries and hoarseness in voice from pressure on laryngeal nerve, pressure of esophagus can cause dysphasia, edema in face, bruit may be heard over aneurysm
89
What will you do to decrease the likelihood of the aneurysm rupturing or dissecting?
Early detection and prom treatment: stopping tobacco use, decreasing BP, optimizing lipid profile, annual monitoring of aneurysm size, beta blockers, statins and antibiotics
90
For PAD of lower extremities, what is causing the symptoms?
The extent of the blockage and the amount of collateral circulation; ischemic pain resulted from the build up of lactic acid from anaerobic metabolism
91
Teaching points for patients with Raynaud's
Wear loose warm clothing, immerse hands in warm ester, stop tobacco use and caffeine intake
92
What is atherosclerosis
Formation of focal deposits of cholesterol and lipids known as plaque, primarily within the intimal walls of arteries, that obstruct circulation
93
Risk factors for CAD
Non-modifiable: increasing at, gender, ethnicity, genetics, family history of heart disease
Modifiable: serum lipid levels, BP, diabetes, tobacco use, physical inactivity, obesity
94
Serum lipid levels
Total cholesterol: 40; female >50
95
What are the cardiac biomarkers that appear after an MI?
Myoglobin: released after muscle trauma, not specific to cardiac muscle
Troponin: elevates quickly, 2 hours after MI
CKMB: peaks two days after cardiac event
96
PAD
Involved thickening of the artery walls, which results in a progressive narrowing of the arteries of the upper and lower extremities. Risk increases with she and in those with diabetes and is related to other cardiovascular diseases
97
Risk factors of PAD
Tobacco use, diabetes, hyperlipidemia, elevated C-reactive protein, uncontrolled HtN, family history, increasing age, obesity, sedentary lifestyle, stress
98
Aneurysm
A permanent localized outpouring or dilation of the vessel wall. Occur more in men then women and incidence with increasing age
99
How to treat angina?
Calcium channel blocker or nitrates
100
Antiplatelet meds
Aspirin, plavix, petal, persantine
101
Beta blockers
Slows heart, less demand, not for asthma, caution with diabetics
102
Calcium Chanel blockers
Vasodilators, decreases rate, negative inotrope
103
Ace inhibitors
Cause cause ARB
104
What is the most common cause of aneurysm?
Age, male gender, HtN, cad, family history, high cholesterol, lower extremities pad, history of stroke, tobacco use and obesity
Three major risk factors: male, older age and tobacco use
105
Classic symptoms or lower extremity PAD
Intermittent claudication which is ischemic muscle pain that is caused by exercise and revolves within 10 minutes of rest. Numbness or tingling of toes. Skim becomes shiny, thin, taunt and hair loss occurs. Pulses are diminished. Pallor I'm the foot and reactive hyperemia when leg is In dependent position
106
HF
An abnormal clinical syndrome involving impaired cardiac pumping and/or filling of the heart
107
Primary risk factors for HF
HTN and CAD
108
Mechanism that cause CHF
Preload, after load, myocardial contractility, heart rate
109
Systolic HF
Results from inability of heart to pump blood effectively
Caused by impaired contractile function, increases after load, cardiomyopathy, and mechanical abnormalities
The left ventricle loses ability to generate enough pressure to eject blood through aorta
Hallmark: decrease in LV ejection fracture
EF: less than 45%
110
Diastolic HF
Inability of ventricles to relax and fill during diastole
Often referred to as HF with normal EF
Decrease stroke volume and CO
Characterized by high filling pressure because of still ventricles
111
Compensatory mechanisms of HF
1) SNS activation: first one triggered but least effective; increases release of catecholamines resulting in increased Hr, increased contractility and peripheral vasoconstriction
2) neurohormonal response: as CO falls, blood flow to kidneys decrease; kidneys release renin, converting angiotensinogen to angiotensin 1 --> angiotensin 2 --> cause the release of aldosterone, increased vasoconstriction increasing BP
3) dilation: enlargement of heart chambers; muscle fibers stretch; initially leads to increased CO and maintence of BP but overtime causes fibers to over stretch and decrease CO
4) hyper trophy: increase I'm muscle mass and cardiac wall thickness; initially increases CO but overtime does not work
112
S/S of left HF
Weakness, fatigue, pulmonary edema, crackles, s3/s4 he's rat sounds, pleural effusion, changes in mental status, confusion
Most common; results from LV dysfunction; prevents normal flow of blood and causes back up into left atrium and pulm veins
113
S/S of right HF
Fatigue, murmurs, RV heaves, jugular distinction, peripheral edema, weight gain, hepatomegaly
Results from Arab failure to contract, causes backup of blood into RA and venous circulation
Primary cause is left sided HF
114
HF is characterized by....
Ventricular dysfunction, reduced exercise tolerance, diminished quality of life, shortened life expectancy
115
Complications of HF
Plural effusion, dysrhythmias, left ventricular thrombus, hepatomegaly, renal failure
116
Preload
Volume of blood I'm ventricles at the end of diastole before the next contraction, determines amount of stretch placed on myocardial fibers
117
After load
Peripheral resistance against which the left ventricle must pump, affected by the size of ventricle, wall tension, and arterial blood pressure
118
Infective endocarditis (IE)
Infection of the endocardium layer of the heart
119
Most common cause of an infective endocarditis
Staphylococcus aureus and streptococcus viridans
Criteria is 2/3:
1) positive blood cultures
2) new or changed murmur
3) intracardiac mass or vegetation on echo
120
What happens when vegetation breaks loose in a patient?
Results in an emboli
Left sided: various organs and extremities
Right: P
121
Treatment for IE
Antibiotic administration : monitor antibiotic serum levels, subsequent blood cultures, monitor renal function, long term IV antibiotics
Subacute bacterial endocarditis:
122
Pericarditis
Inflammation of pericardial sac
Idiopathic, acute signs and symptoms, dressler syndrome 4-6 weeks later
Sharp pain wore with deep inspiration, supine. Pain radiates to trapezium muscle, pericardial friction rub
123
Pericardial effusion
Build up of fluid I'm the spherical dim
| Cough, dyspnea, tachyons, hiccups, hoarseness, heart sounds are distant and muffled, BP is usually maintained
124
Cardiac tamponade
Develops as pericardial effusion increases in volume resulting in compression of heart
The speed of fluid accumulation affects the severity of manifestations
Chest pain, confusion, anxious, restless, decreased CO, distended neck veins
125
PAD
Thickening of artery walls which resulted in progressive narrowing of the arteries of upper and low extremities
Leading cause is atherosclerosis
126
Nursing diagnosis/management for PAD
Ineffective tissue perfusion, impaired skin integrity, activity intolerance, infective self health management
Goals: adequate tissue perfusion, relief of pain, increased exercise tolerance, intact and healthy skim
127
Intermittent claudication
Classic symptom of lower extremity PAD, which is an ischemic muscle pain that is caused by exercise, resolved within 10 minutes or less with rest and is reproducible
128
Acute arterial occlusion
Symptoms: pain, pallo, paralysis, pulselessness, paras thesis, poililothermia
Pharm treatment: statins, aspirin or plavix, ACE
Causes: embolism, thrombus, trauma
Avoid knee flexed position, avoid lots of dependent leg positioning, may have compressions
129
Thrombophlebitis
Venous disorder
| Elevate, anticoagulants, warm and moist heat
130
Care of ulcers
Arterial: dry sterile dressing, hyperbaric the rosy, reverse trendelenburg
Venous: compressions leg elevation, moist dressings, antibiotics
131
Amputations
The goal is to preserve extremity length and function while removing all infected, pathological or ischemic tissues
132
Goals for an amputee
1) adequate relief from underlying health issue 2) pain control 3) reach maximum rehabilitation potential with prosthesis 4) cope with body image changes 5) make satisfying life adjustments
133
Aortic dissection
Is not an aneurysm. Rather, it resulted from the creation of a false lumen between the intima and the media of arterial wall.
A tear develops in the inner layer of the aorta and blood surges through causing the inner and middle layer to separate.
Report abrupt onset of excruciating chest and/or back pain radiating to the neck or shoulders.
If aortic arch is involved then the patient may exhibit neurologic deficits
134
Phlebitis
Inflammation of the walks of small cannula tee veins of the hand or arm. Clinical signs and symptoms include pain, tenderness, warmth, erythema, sweeping and palpable cord
135
Venous thrombosis
Involves formation of a thrombus in association with inflammation of the vein.
136
Virchow's triad
1) venous status 2) damage of the endothelium and 3) hypercoagulability of the blood
137
Arterial ulcers
Tips of toes, foot, or lateral malleolus; rounded, smooth, minimal drainage; black tissue or pale pinkish granulation
Cap refill is greater than 3 seconds
138
Venous ulcers
Nest medial malleolus; irregularly shaped and moderate to large amount of drainage; tissue is yellow or dark res
139
Vasotec (enalapril)
Ace inhibitor/antihypertensive
Manage hypertension
Blocks conversion of angiotensin 1 to angiotensin 2
SE: fatigue, asthenosphere, diarrhea, nausea, dizziness, cough, rash
140
Amlodioline
Calcium channel blocker
| Blocks calcium channels in vascular smooth muscle and myocardial cells which causes dilation
