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NURS 1250 > Perfusion > Flashcards

Perfusion Flashcards

1
Q

What causes Angina?

A

Reduced coronary blood flow. Identified by a identifiable event. Relieved by rest

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2
Q

Types of Angina (3)

A

Stable: caused by physical exertion, stress, or exposure to cold. most common.

prinzmetal (variant): caused by coronary vasospasm

Unstable: Caused by transient formation and dissolution of a blood clot.

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3
Q

What does decreased coronary blood flow cause?

A

Vasospasm, fixed stenosis (althersclerosis), thrombosis (blood clot)

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4
Q

What does increase need for O2 cause?

A

Increased heart rate, increased contractility, increased preload/afterload

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5
Q

What are the clinical manifestations of myocardial infarction?

A

sudden, continuous chest pain that lasts 15-20 mins.
pain that radiates to shoulder, neck, arms, jaw
chest pain that gets worse

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6
Q

What is the pathopysiology of myocardial infarction?

A

plaque formation –> plaque rupture –> endothelial cell injury and inflammation –> decreased blood supply and increased O2 demand –> myocardial ischemia –> myocardial cell necrosis

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7
Q

Ischemia Definition

A

Blood flow is restricted or reduced

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8
Q

Myocardial Ischemia Signs & Symptoms

A

BF to portion of cardiac muscle is completely blocked.

angina, hypoxia, tachycardia, extra heart sound (S3)

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9
Q

Acute Coronary Syndrome

A

Unstable angina, NSTEMI, STEMI

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10
Q

Difference between CAD, angina, and heart attack

A

CAD: plaque builds up in an artery
Angina: plaque makes it harder for blood to get through an artery
Heart Attack: plaque cracks and a blood clot blocks the artery

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11
Q

CAD Risk Factors

A

Age, gender, race, ethnicity, family history, DM, hyperlipidemia, HTN, smoking, inactivity, obesity, unmanaged stress

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12
Q

Electrocardiogram

A

Performed and interpreted within 10 min. Most common. Repeat ECG every 10-15 minutes if first time with angina

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13
Q

Tropinin

A

Protein found in muscles of heart.
hs-cTn should be <14 if >14 ICU
Check troponin at 0-2-6 hours

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14
Q

Echocardiogram - Normal EF

A

Checks how heart chambers and valves are pumping blood

Normal EF is 50-70%

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15
Q

Stress Echocardiogram

A

Treadmill test and echocardiogram. Dobutamine test for pt. who cannot excercise

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16
Q

Nuclear scan-myocardium perfusion imaging

A

shows how well blood flows to the heart.
3-part test
lexiscan dilates BV

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17
Q

CAD Treatment Goals

A

Relieve chest pain, reduce extent of myocardial damage, maintain cardiovascular stability, manage risk factors

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18
Q

Statins

A

Lower cholesterol by increasing LDL excretion from circulation

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19
Q

Nitrates

A

Treat angina. Produce coronary artery and peripheral vasodilation. Take 3.

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20
Q

Beta Blockers

A

Manage stable angina. “lol” suffix. Blocks the effect of epinephrine.

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21
Q

Non-Pharmocological Therapy (2)

A
  • Percutaneous Coronary Intervention prev. known as angioplasty w/ stent
  • Coronary Artery Bypass Grafting - use veins or artery to create connection to construct a detour around blocked portion of artery
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22
Q

What is a good diet for somebody with CAD?

A

Low-fat diet rich in antioxidants. Foods containing bioflavinoids. Supplement C, E, B6, B12, Folic Acid

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23
Q

What is HTN a risk factor for?

A

CHD, heart failure, stroke, renal failure

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24
Q

Elevated BP category

A

120-129, <80

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25
Q

Stage 1 HTN

A

130-139 or 80-89

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26
Q

Stage 2 HTN

A

> 140 or >90

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27
Q

hypertensive crisis

A

BP > 180/120

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28
Q

HTN risk factors

A

age, ethnicity, smoking, high salt intake, health problems, inactive lifestyle, alcohol, high stress, obesity

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29
Q

HTN complications

A

Stroke, heart failure, sexual dysfunction, vision loss, heart attack, kidney disease

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30
Q

Primary HTN symptoms

A

Usually asymptomatic

headache, confusion, nausea/vomiting, visual distrubances (most common), nocturia

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31
Q

Treating HTN - Diuretics

A

First drug of choice. Thiazide. Watch K+ levels

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32
Q

Treating HTN: Beta Blockers

A

metoprolol, atenolol. For newly diagnosed pt.

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33
Q

Treating HTN: ACE inhibitors

A

lisinopril, benazepril, Block angiotensin, which causes BV to open

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34
Q

Treating HTN: Angiotensin 2 receptor blockers

A

losartan, valsartan

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35
Q

Treating HTN; Calcium Channel Blockers

A

diltiazem, amlodipine. block CA from entering smooth muscle cells of heart.

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36
Q

Treating HTN: Alpha Blockers

A

not common. doxazosin, prazosin. reudce the arteries resistance

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37
Q

Treating HTN: alpha 2 receptor agents

A

clonidine, methyldopa.

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38
Q

Treating HTN: combined alpha and beta blockers

A

carvedilol, labetalol

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39
Q

vasodilators

A

last effort. hydralazine. for HTN emergency

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40
Q

Drug regime for HTN

A

1 antihypertensive medication given at low dose and slowly increased until optimal BP reached.

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41
Q

What is a good diet for somebody with HTN?

A

Low calorie, low fat, low sodium

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42
Q

What is preload?

A

Stretch of vesicle. Amount of blood in vesicles at end of distole

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43
Q

What is afterload?

A

Relaxation. The resistance left ventricle must overcome to circulate blood.

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44
Q

Left Sided Heart Failure

A

Prevents delivery of oxygenated blood. Main cause of right sided heart failure. There are 2 types: systolic heart failure, diastolic heart failure

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45
Q

Left sided heart failure symptoms

A
  • paroxysmal nocturnal dyspnea (most common)
  • cough,
  • pulmonary congestion: cough, crackles, wheezes, blood tinged sputum, tachapnea
  • restlessness
  • confusion
  • tachycardia
  • exertional dyspnea
  • fatigue
  • cyanosis
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46
Q

Systolic Heart Failure

A
  • pumping problem
  • reduced ejection fraction
  • inability of heart to contract enough to push blood foward
  • stretch and thin chambers 0 heart gets bigger
  • increased afterload
  • impaired contrile ability
  • incompetent valves
  • cardiomyopathy
47
Q

Diastolic Heart Failure

A
  • filling problem
  • preserved ejection fraction - it could remain normal
  • inability of left ventricle to relax, resulting in fluid backing up into lungs
  • increased preload
  • left ventriclular hypertrophy
48
Q

Right Sided Heart Failure

A
  • Oxygen depleted blood
  • heart loses ability to move o2 depleted blood into lungs
  • Caused by left sided heart failure
49
Q

Right sided heart failure symptoms

A
  • edema
  • ascites
  • fatigue
  • enlarged liver and spleen
  • distended jugular vein
  • anorexia and GI distress
  • weight gain
50
Q

heart failure risk factors

A

atherosclerosis, HTN, DM, fautly heart valves/muscles, smoking, alcohol, obesity

51
Q

HF Compensatory Mechanism: Nervous System

A
  • Catecholamines released (help body respond to stress)
  • alpha and beta effects activated - lead to increased HR, increased BP, increased cardiac output
  • baroreceptors stimulated: sense pressure change by response to changes in tension in arterial wall
52
Q

HF Compensatory mechanism: hormones

A

Renin - decreases fluid eliminated as urine
Angiotensin: narrows BV to increase BP
Aldosterone: sends signals to organs to regulate sodium they send to the blood stream

53
Q

HF Compensatory mechanisms: Cardiovascular System

A
  • Ventricular Dilation: initial cardiact response to pump more blood
  • myocardial hypertorphy: stronger, thicker muscles
  • Frank Starling Mechanism: hypertrophy of L ventricle
54
Q

PRO BNP normal value

A

<100. Detects hormone released from the ventricles in response to increased wall tension

55
Q

Ejection Fraction Values

A

Normal: 55-70%
Less blood is ejected: 40-54%
Mild heart failure: 35-39%
Severe Heart Failure: <35%

56
Q

Managing HF: ACE Inhibitors

A

Lisonopril, benzepril

57
Q

Managing HF: beta Blockers

A

Metoprolol, atenolol

58
Q

Managing HF: diuretics

A

Furosemide, HCTZ

59
Q

Managing HF: Vasodilators

A

hydralazine

60
Q

Managing HF: Cardiac Glycoside

A

Digoxin (monitor for toxicity. Arrythmia, visual disturbances, tiredness, loss of appetite, confusion)
Lanoxin

61
Q

Goals of HF Therapy

A

improve cardiac output, reduce pulmonary and systemic congestion, prevent complications, improve quality of life, educate pt. and family

62
Q

Abdominal Aortic Aneurism

A

arterial walls weak, enlarged

63
Q

Types of aneurisms

A
  • Fusiform: bulge on all sides
  • Saccular: 1 side has bulge
  • pseudo: BV injured and leak
64
Q

AAA Etiology

A

altherosclerosis, hypertension, BV disease (CVD, MI, ANGINA), Trauma, Genetic diseases

65
Q

AAA risk factors

A

High BP, High Cholesterol, Smoking, sedentary, family history

66
Q

AAA clinical manifestations

A

Back, leg, abdominal pain
pulsing sensation in abdomen
IF RUPTURED: clammy, sweaty skin. dizziness. fainting, tachycardia, dyspnea, nausea/vomiting

67
Q

When is surgical management recommened for AAA?

A

when it’s 4-5 cm

68
Q

6 P’s of peripheral vascular disease

A 
Pain
Paresthesia
poikilothermia
paralysis
pallor
pulselessness
69
Q

Peripheral Artery Disease

A

Narrow, weak, blocked arteries
Result of build up of fat and cholesterol
Arterioslerosis
Atheroslecrosis

70
Q

PAD Patho

A

athermatous plaque formation in intima of vessel –> calcification of medial layer and loss of elasticity –> inadequate blood supply to tissues leads to tissue hypoxia

71
Q

PAD manifestations

A

Claudation
rest pain
ulceration
gangrene

72
Q

PAD Risk Factors

A 
CAD/PAD
Diabetes
HTN
obesity
smoking
> 50
73
Q

PAD Risk Factor Modifaction

A 
Antiplatelet Therapy
Lipid lowering agents
glycemic control
BP control
smoking cessation
lifestyle modication  heart healthy diet
Excercise
74
Q

CVI (DVT)

A

vein blockage or valve leakage in leg veins, blood flows back and pools in legs

DVT most common

75
Q

DVT patho

A

hemdynamic changes/veno status –> endothelial injury/dysfunction –> hypercoagulability

76
Q

CVI/DVT manifestions

A

edema, vericous veins, skin changes/discoloration, skin ulceration

77
Q

DVT Risk Factors

A 
> 50
obesity
smoking
family history
hormonal fluctuation
poor lyfestyle choices
78
Q

DVT nursing management

A 
avoid long periods of sitting or standing
elevate legs
exercise regularly
lose weight
hygiene
79
Q

Vessel Differation DVT

A

Ateriole: dangle legs, pain sharp and worse at night, intesne pain, intermittent claudation, skin cool to touch, skin thin/dry/scaly/hairless, rubor, poor or absent pulse, edema not common, located toes/feet/shin

Venous: elevation of legs, aching, throbbing, pain worse when sitting/standing/dangling/walking, skin warm to touch, skin thick/tough/leathery, pulse present, edema present, located over ankle

80
Q

Diabetes Patho

A

Food is broken down into glucose, the pancrease produces insulin. Type 1 no insulin is produced due to damage of B cells. Type 2, over production of insulin so body becomes desnsitized.

81
Q

Diabetes Type I etiology

A 
Autoimmune
Juvenile DM
Insuin Dependent
Exposure to virus
Climate (oceanic)
82
Q

Type I Diabetes Manifestations

A

3 P’s : polyuria, polydipsia, polyphagia

83
Q

Diabetes Type II Clinical Manifestations

A

Increased urination, increased thirst, increased hunger, fatigue, blurred vision, frequent infections, erectile dysfunction, pain/tingling in hands and feet

84
Q

Increased BP Risk for Diabetes

A

130/85 or higher

85
Q

High Triglycerides for Diabetes

A

150 mg/Dl or above

86
Q

Large Waistline Risk for Diabetes

A

Men: 40” or more
Women: 35” or more

87
Q

LOW HDL risk for diabetes

A

Men: <40
Women: <50

88
Q

Elevated Fasting BS Risk for Diabetes

A

100 or more

89
Q

C-Peptide Test

A

0.5-2.7 NG/mL. Increased in Type 2 DM, insulinoma, cushings, kidney disese
decreased in Type 1 DM, Addisons disease, liver disease

90
Q

Hemoglobin A1C

A

<5.7 normal

>6.5 diabetes

91
Q

Fasting Blood Sugars

A

70-100 normal
100-125 risk of diabetes
126 or higher diabetes

92
Q

Glucose Tolerance Test

A

200 or above

93
Q

Hypoglycemia Symptoms

A

45-60 mg/DL

sweating, pallor, irritability, hunger, lack of coordination, sleepiness

94
Q

Hypoglycemia Management

A

15 g fast acting carb. Avoid protein it slows absorption of sugar

Wait 15 min. If Blood glucose <70 repeat

95
Q

Hyperglycemia Symptoms

A

180-200

Dry mouth, increased thirst, weakness, headache, blurred vision, frequent urination

96
Q

HHS

A 
Common in Type II Dm
BS >600
Osmality >340
Shallow breaths
ALOC
Dehydration
Develops slowly
97
Q

DKA

A 
Type I Diabetes Common
BS >300
Osmality >340
Kassumauls respiration
Abdominal pain
Nausea/vomiting
Develops quickly
98
Q

Hyperglycemia Etiology (8 I’s)

A 
Infection
Infarction
Infraction (non-compliant)
Ischemic
Illegal
Iatrogenic
Idiopathic
99
Q

DKA/HHS management

A
  • maintain airway
  • decrease blood glucose
  • Blood glucose monitor every 1-2 hours
  • improve dehydration
100
Q

Acute Diabetes Complications

A

DKA, HHS

101
Q

Microvascular Diabetes Complications

A

Retinopathy
Nephropathy
Neuropathy

102
Q

Macrovascular (Chronic) Diabetes Complications

A

Atherosclerosis
Cardiovascular/Peripheral Vascular
Cerebrovascular

103
Q

Retinopathy

A

Microvascular damage and occulsion of retinal capillaries due to changes in retina. Have eyes dilated every year

104
Q

Nephropathy

A

Albumin in urine

Detioration of kidney function to overfiltering of glucose

105
Q

Peripheral Neuropathy

A

numbness/tinling in lower extremities.

106
Q

Managing Diabetes: Biguanides

A

Control hepatic glucose production

Metformin. Do not use in pt. with kidney, liver, or heart failure. Cautious with contrast medium

107
Q

Sulfonylureas

A

stimulate pancreas to make more insulin. Glyburide, glizipizide, glimepiride, take with meals, watch for hypoglycemia

108
Q

Glucose Inhibitors

A

Slows the absorption of starches/CHO. Best used for those with normal FBS, but elevated post prandial blood sugars. Arcabose, miglitol

109
Q

Incretin Mimetics

A

Insulin pen. Do not use with insulin. May combine with oral agents

110
Q

Rapid Acting Insulin

A

Bolus. Lispro (humalog)

111
Q

Short-Acting Insulin

A

Bolus/Prandial. Regular Insulin (humulin R)

112
Q

Intermediate acting insulin

A

NPH (humulin N)

113
Q

Long-Acting Insuin

A

Basal. Lantus

114
Q

Diabetes Dietary Recommendation

A

Non Starchy Veggies, grains and starchy foods, protein, high fiber, non fat dairy

NURS 1250 (6 decks)

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