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2-health promotion(former alteration) > exam 3- presntations and videos > Flashcards

exam 3- presntations and videos Flashcards

1
Q

heart
what is it

how much moves

A

Hollow, cones shaped organ, necessary for life

Moves more then 1800 gallons of blood/day

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2
Q

pericardium

atria/ventricals

A

encases the heart and anchors it to surrounding structures-fits snuggly to prevent overflowing

Atria -top
Ventricles –bottom of heart

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3
Q

heart beat

systole

diastole

A

One heart beat = contraction and relaxation of heart—aka cardiac cycle

Systole contraction-ventircles are contracting/atria filling-5o ml of blood remaining

Diastole atria are contracting and ventricles are relaxing filling

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4
Q

stroke volume

how often

A

Stroke Volume: Difference between the end diastolic volume and the end systolic volume -

70—80 tomes a minute

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5
Q

cardiac output

what is

what indicator of

what happens if not pumping correctly

A

HR X Stroke Volume

Indicator of: amount of blood pumped into ventricles in one minute—how well heart is functioning as a pump-how well heart is working//

if not pumping correctly, cardiac output and tissue perfusion are decreased

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6
Q

ischemia

necrosis

A

I-depreivation of oxygen, body tissues do not get enough blood/

/N- one step further, tissues will start to die as a Result of not enough oxygen in blood

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7
Q

preload

frank starling mechaniism

A

Preload: new rubber band-stretch and release which will snap back into place and shape-overstretching will become relaxed and lose ability to recoil –overstretching cardiac muscle fibers eventually leads to ineffective contraction

Frank Starling Mechanism: -repeatedly stretch past a certain point it will eventually lose elasticity-cant snap back into oringal shape/size

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8
Q

compliance

afterload

A

Compliance: take a lot of force/work to inflate at first. As it stretches more often it becomes more complaint and expands easily with less force as time goes on

Afterload: force ventricles must overcome to eject blood volume

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9
Q

s/s of low potassium level

A

leg cramps

heart fluttering

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10
Q

Diagnostic Tests cardiac

A

Cardiac Cath - npo,allergies to iodine, assess aspirin, vs

CT Scan-iodine allergy, npc 4 hr

Echocardiogram

Electrocardiogram

Lipids -low fat meal then no food for 8-12 hrs

Dobutamine Stress Test -npo , discontinue beta blockers, ace

Treadmill Stress Test -comfortbael clothes, npo and no smoking

TEE-npo, vs

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11
Q

pt assessment cardiac

A

History—

Personal and family history

Diet history

Socioeconomic factors

Current health problems -perceived or actual

Functional history

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12
Q

risk factors for cardiac

A

Smoking

Obesity

Physical inactivity

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13
Q

age related changes cardiac

e/c
valves-cause
co/bp/contr

A

efficiency and contractiblity decreases-leads to decresaded ardiac output.

Valves become more thicker/ rigid causing increased BP.

Older adults have decreased cardiac output, INC blood pressure, Decreased contractility

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14
Q

Patient Physical Assessment
cardiac

what looking at

A

General appearance

Skin color/temperature

Extremities

Capillary refill

Edema

Blood pressure//Heart Rate

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15
Q

normal hr

school age
adult
athlete

A

Pediatric/School Aged 70-110

Adult  60-100

Athletes may have lower heart rate

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16
Q

heart failure
what kind of problem

results in what
cardiac output

A

Filling & pump/Contracting problem…

results in  metabolic needs of the body are not met due to not enough blood being pumped—

cardiac output falls leading to decreased tissue perfusion and vascular congestion/Congestive heart failure

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17
Q

impaired myocardial function

most at risk for hf

causes of heart failure

A

coronary heart disease/MI-most risk

cardiomyopathy

rhematic fever

ineffective endocarditis

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18
Q

increase cardiac output

causes of heart failure

A

hypertension

2.Valve disorder

  1. anemia
  2. Congenital heart defects
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19
Q

acute noncardaic conditions

causes of heart failure

A

Volume overload

2.hyperthyroidim

  1. fever/infection
  2. Pulmonary emboli
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20
Q

Incidence, prevalence & Risk factors

incidence
prevelance
risk factors
life exp
risk for

A

Incidence and prevalence increase with age

Prevalence & Mortality: African Americans have higher risk

Risk factors: impaired myocardial function- mi, hypertension

Life expectancy: dependent on underlying cause, and how quickly its treatment

Risk for sudden cardiac death increased

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21
Q

systolic vs diabolic failure

manifestations

A

S-Weakness, fatigue, and decreased exercise tolerance.

D-Shortness of breath, tachypnea, and respiratory crackles

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22
Q

left sided heart failure
culprit

A

coronary heart disease and hypertension

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23
Q

when Left ventricle function fails

what falls
backwards effect
backs where

A

Cardiac output falls

Backward effects pressure in left ventricle/atrium increase which….

Backs up into the pulmonary system inc congestion and pressure

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24
Q

lef sided hf manifestations

A

fatigue/activity intolerance/dizziness

dyspnea,

SOB ,

cough,

orthopnea(SOB when laying flat),

congested lung sounds

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25
Q

Right sided

culprit

A

–restrict blood flow to lungs

Culprit acute chronic repository issues

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26
Q

when Right ventricle is impaired

cant do what->
increased what

A

cant pump blood  accumulate in systemic venous system

Increased venous pressure

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27
Q

Classic Manifestations:-
right sided hf

A

abdominal organs congested
, JVD
, peripheral edema

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28
Q

acute vs chronic

A

acute-abrupt onset resulting in decreased cardiac function/output

chronic-progressive deterioration leading to cardiomyopathies, vascular disease, chd

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29
Q

Diagnosis of Heart Failure

History & Physical

How will your patient present to you??

A

peripheral edema,

too tight shoes,

tired,

not sleeping good,

sleeping in chair,

stopping halfway,

cant catch breath,

tired, lethargic

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30
Q

diagnostic test for hf

A

BNP (Brain natriuretic peptide): hormone released by heart when blood volume changes, inc in HF-levels are normally less then 100

Electrolytes-potassium sodium and chloride

BUN & Creatinine-renal function

Blood Gases-resp status

Chest X ray-congestion

EKG-dysrymthias, ischemia , infarction

Echo-blood flow through heart

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31
Q

ACE inhibitors & ARBS

what kinds
assessment
cough
monitor
take/slow

HF drugs

A

“PRIL” Medications & “ARTAN” Medications

Assessment vasodilation, lower systolic pressure

ACE cough dry, persistent cough, constantly clearing throat

monitor-bp,hr, potassium,wbc, renal function

take at same time each day/slow position changes

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32
Q

Beta Blockers

assessments

HF drugs

A

“OLOL” Medications

Assessment pulse and bp prior

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33
Q

Diuretics-what di
what drugs
assessment
watch
obtain/drink/avoid/sudden/ eat

HF drugs

A

– will help reduce preload

Furosemide, metolazone, bumetanide, spironolactone

Assessment increases urine output, input,

Watch electrolyte imbalances; hypokalemia –may be on potassium supplement

obtain weight/vs, drink water, avoid sudden changes, eat high potassium

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34
Q

Positive Inotropic Agents
what does
what drug
assesmetn
report, monitor, no, eat

HF drugs

A

Increases cardiac output and improve contractility

Digoxin

Assessment take apical pulse for 1 minute.

report anorexia,nv,monitor renal failure, no antacids, eat high potassium

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35
Q

Respiratory Status, Positioning & Edema

Heart failure

assess
position
elevate

A

asses pulse ox-might need oxygen therapy

fowlers position- adequeute ventilation and help breath easier

elevate extremities, might have teds on

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36
Q

Nutrition & Activity

heart failure

A

sodium restriction-possibly fluid

gentle progressive exercise

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37
Q

surgery heart failure

A

valve replacement

heart transplant or circulatory resistance(balloon pump)

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38
Q

Heart Failure Health Promotion

decreased cardiac output

excess fluid volume

activity intlerance

knowledge defect

A

Decreased cardiac output support them, resp system, assess vitals, asses pulse ox, oxygen therapy, fowlers position

Excess fluid volume  FV, diuretics, IV transition oral, watch electrolyte imbalance, monitor labs and ECG, avoid foods high in sodium, I and o, restrict fluids

Activity intolerance  help with ADL, encourage to participate as able/tolerated.

Knowledge deficit daily wights, if gain more then2 pounds a day- call doctor, don’t want gaining weight.//

/take BP, take pulse, keep all appointments and follow ups

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39
Q

teaching HF\

diet
meds
weight
monitor

A

low sodium diet

meds

daily weight

monitor I and o

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40
Q

Pulmonary Edema

what is it
what caused by

A

What is it?  accumulation of fluid in intestinal tissue and avloli in lungs-MEDICAL EMERGENCY

Caused by cardiac and non cardiac issues

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41
Q

patho pulmonary edema

contractibility
ventricle unable
resulting in

A

Contatialbility of left ventricle impaired severely

ventricle is unable to eject the blood that enters it

Resulting in sharp rise in end diastolic pressure, pulmonary capillaries are congested and interfere with gas exchange

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42
Q

manifestations of pulmonary edema

resp
cardio
nuero

A

respiratory
tachypenia,dyspnea, orthopena

cardio
tachycardia,hypotension, cool clammy skin

nuero
restless, anxiety, confusion

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43
Q

Pulmonary Edema Treatment
Medications/Treatment

A

morphine-anxiety and improve breathing relaxes lungs

oxygen,

cpap

brathing treatments, diuretics and vasodilators

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44
Q

Pulmonary Edema Treatment

emergency

A

Be prepared: in emergency , need resp equipment,– fatigue, impaired gas exchange, acid base imbalances can lead to cardiac arrest

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45
Q

Pulmonary Edema Treatment

focusing on

diagnostic tests

A

Focusing on: restoring effective gas exchange, reducing pressure and fluid in pulmonary vasular system

Diagnostic Tests: ABG, chest x ray,

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46
Q

pulmonary edema

improve gas echange

cardiac ouput

fear

A

IGE-assess rest status, high fowlers, administer oxygen, CDB

co-vs, heart sounds, iv, I and o

fear- emountinal support

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47
Q

what is blood pressure

A

tension or pressure exerted on blood on aretial walls, certain amounts of pressure are required to keep walls open and capillary perfusion and ixygenation of all tissue

48
Q

hypertension

A

excess pressure in the arterial portion of the systemic circulation

49
Q

Systolic
averafe
felt
rises

A

less then 120 average

felt as peripheral pulse

pressure rises as the heart contracts during systole, ejecting its blood

50
Q

diastolic
relax
minumin
average

A

cardiac relaxation and filling

maintain a minimum pressure to maintain blood flow

average is less then 90

51
Q

Hypertension
diagnosed

normal
elevated
hypertension stage 1
hypertension stage 2
hypertensive crisis

A

Based on the average of three or more readings taken on separate occasions

< 120 <80-normal

elevated-120-129and <80

HTN1-130-139 OR 80-89

HTN 2At least 140 OR At least 90

Crissi>180 AND/OR >120

52
Q

modifiable risk factors hypertension

A

High sodium intake Low electrolytes

Obesity

Alcohol consumption

Insulin resistance

53
Q

non modifiable risk factors hypertension

A

Genetic factors

Family history

Age

Race

54
Q

manifestations of hypertension

A

Asymptomatic in early stages

Headache

Nocturia

Confusion

Nausea/vomiting

Visual disturbances

55
Q

Sustained BP affects the:

cardiovascular

A

rate of atherosclerosis increases,

inc risk of cardiac coronary heart disease and stroke

56
Q

Sustained BP affects the:

nueroligal

A

cerebral infarct(stroke)

microaneurysms

hypertensive encephalopathy- high bp, altered loc, increased cranial pressure, papiledema, seizures

57
Q

Sustained BP affects the:

renal

A

nephrosclerosis of small nephrons in kidneys

renal insufficiency

58
Q

Lifestyle Modification

hypertension

diet
physical activity
alc/tobacco
stress
meds

A

DASH- reduce sodium, fat maintain potassium /caclium level, —grains, veggies, fruit lean meat

Physical Activity-regular exercise -30-45 mins

Alcohol and Tobacco- smoking directly related to heart disease, alcohol in moderation

Stress Reduction Stress increases vasoconstriction increasing BP…solution relaxation techniques/alternative therapies

Medications: ACE, ARBs, Calcium Channel Blockers, Beta Blockers, Vasodilators, diuretics

59
Q

Alpha-Adrenergic Blockers

meds
first dose
assess
can cause

antihypertensive

A

Doxazosin Prazosin

First dose is bedtime,-fainting

assess bp/apical,

dizziness, orthostatic hypotension,nasal congestion

60
Q

Angiotensin-Converting Enzyme (ACE) Inhibitors

meds

nursing considerations

cough
assess
when take
report
positional
antihypertensive

A

“pril” drugs

Prevents constriction and sodium/water retention –Watch BUN, creatinine and potassium levels/

/ace cough
assess bp,
1 hr before meals,
report edema,
slow positional changes

61
Q

Angiotensin II Receptor Blockers (ARBs)

meds

assess
when take
report
positional
antihypertensive

A

“artan” drugs

assess bp,
1 hr before meals,
report edema,
slow positional changes

62
Q

Calcium Channel Blockers

meds

assess
toxicity
keep
watch
antihypertensive

A

“pine” drugs, diltiazem

assess bp, apical pulse,constipation

toxicity-nausea, weakness, bradycardia

keep nitrate available

watch liver, renal function

63
Q

Beta Blockers

meds

assess
report
antihypertensive

A

“olol” drugs

assess bp, apical,

report bradycardia, decreased co, hypotension, bronchospasm

64
Q

Centrally Acting Sympatholytic

meds

take/
pathces/
causes/
relieves
take/
dont/
do not
changes

antihypertensive

A

Clonidine

take at bedtime
patches to dry skin
causes dry mouth
relives dry mouth with water
take with meals,
dont abruptly discontinue,
do not drive dt drowsiness
slow positional changes

65
Q

Vasodilators

meds

what does
changes
antihypertensive

A

Hydralazine
//vasodilation, decreased bp, slow positional changes,

66
Q

Diuretics

meds

nrursing considerations
antihypertensive

A

Furosemide
Hydrochlorothiazide
Spironolactone

Risk of hypokalemia-muscle cramps, leg pain,//take bp and I and o

SP-potassium sparing, avoid salt substitutes

67
Q

hyperlipidemia

A

Hyperlipidemia = High Cholesterol

68
Q

High Density Lipoproteins (HDL):
what does
optimal

A

help clear cholesterol from arteries, transporting to liver for excretion

Optimal > 60mg/dL

69
Q

triglycerides

desired

A

amount of fat in blood

desired is less then 150

70
Q

Low Density Lipoproteins (LDL):

what does

optimal

high levels

A

primary carrier of cholesterol

Optimal <100 mg/dL

high levels= promote atherosclerosis, deposits cholesterol on artery wall

71
Q

Atherosclerosis

what does/cause

A

deposits of fats and fibron that obtsuct and harden the arteireis,

impair blood flow to peripgeral tissues–PVD

72
Q

desired HDL,LDL,trig

A

Desired: high HDL, Low LDL, Low Triglycerides

73
Q

Treatment of Hyperlipidemia

modifacations
overall goal
medication goal

A

Lifestyle Modifications

Overall goal to lower total cholesterol, triglycerides & LDL, raise HDL

Medication: Goal lower ldl

74
Q

Treatment of Hyperlipidemia

chlosteroal lowering agents w/ nursing consideration

meds that inhibit platelet aggregation

A

Statins: atorvastatin, pravastatin, simvastatin

Nursing Considerations monitor cholesterol level, liver enzymes, cpk levels

Medications to inhibit platelet aggregation aspirin, and clopidogrel

75
Q

Peripheral Vascular Disease

primary syomtome

A

Impaired blood supply to tissues:

primary symptom-Intermittent claudication pain with activity/ cramping while walking /aching calves, legs thighs and buttocks accompanied by weakness and is relieved by rest

76
Q

how else will PVD present
pains
p___
pilses
temp
color
smin
ulcer

A

Intermittent claudication –pain with activity dt low blood supply

Rest Pain during inactivity, burning sensation and increased with leg elevation and decreased with dependent(hanging) legs

Paresthesia – numbness /decreased sensation

Pulses diminished or abset
Temperature; cool

Color with elevation pallor Color when dependentdark red color

Skin thin, shiny and hariless

Breakdown & Ulceration on toes or side of legs

77
Q

Peripheral Vascular Disease diagnosis

A

History and physical –when pain

Diagnostic Tests :
Segmental pressure measurements -
Doppler Ultrasound
Oximetry
Angiography

78
Q

PVD treatments
smoking
walking
foot care
suport hose
rest
revasulrazaition

A

Smoking cessation, nicotine cases further vasospasms-reduced blood flow

Walking gentle exercise

Foot care  sores, blisters, prevent ulceration

No support hose elastic will further reduce circulation

Rest with claudication encourage to rest then go back to activity

Revascularization surgery for progressive severe or disabling pvd

79
Q

Medication goals pvd

A

Inhibit platelet aggregation

vasodilation

decrease blood viscosity

80
Q

PVD assessment-cms
sudden changes
compare
assess
position changes

A

Sudden change in CMS??—cold painful pulseless//looking for color, motion and sensation

Compare sides & notify

Assess pulses, pain, color, temperature, cap refill

Position changes promote blood flow

81
Q

pain/skin intergirty PVD

A

Pain
assess pain & warmth vasodilation improves atrial flow and reduces pain

Skin Integrity risk of oxygen and nutrient deprivation to skin

Clean and dry skin

Position changes prevent breakdown –looking for ulcers, blisters, tight fitting shoes,

apply bed cradle and egg crate mattress

82
Q

pvd

promote activity tolerance

what to discuss

A

PAT- assist with cares, gradual increase in activity, positional changes

smoking cessation, sings of bleeding, skin surveleince, diet and exercise

83
Q

Raynauds Disease
what is it
what limits

A

Episodes of intense vasospasm in the small arteries of fingers & toes

limits artieal blood flow

84
Q

raynauds manifestations

A

Intermittent pain with skin color changes; Blue-White-Red disease

occurs on digits

85
Q

raynauds treatment

A

Avoid Cold/dress warm & Avoid Smoking

Stress management

Vasodilators

Dietary habits, increasing activity, maintain BMI

86
Q

Acute Arterial Occlusion
-stages-
occlusion
results
resulting

A

A peripheral artery may be occluded by the development of a thrombus (clot)or emboli

results in impaired blood flow to tissues

resulting in ischemia, then necrosis, then gangrene

87
Q

thrombus

embolism

A

Thrombus- blood clot that adheres to vessel wall

Embolism-obstruction of vessels by debris

88
Q

Manifestations-
Acute Arterial Occlusion

A

Tissue Ischemia—

Painful, pale and cool,

distal pulses are absent, paresthesia,

cyanosis

and mottling

dec cap refill

89
Q

Diagnosis,
Acute Arterial Occlusion

A

Arteriography- used to confirm, locate occlusion, and determine extent

90
Q

Medications
Acute Arterial Occlusion
med
goal
dischsarge

A

: Anticoagulation or iv heparin
Goal:prevent further clot destruction and reoccuratn emboli

Oral Anticoagulants at discharge Follow up labs and education, what can/cant eat

91
Q

Surgery
Acute Arterial Occlusion

A

Embolectomy (within 4-6 hours)
procedure of choice to prevent further occlusion

risk of complications and limb loss if surgery is delayed 12 or more hours

92
Q

arterial arteries
Peripheral- atherroclerosis, vascular disease

Pain
Pulses
color
temp
edema
skin changes
ulcerations-where
gangerene
compressions
treatment
assessment

A

Pain-intermittent claudication, rest-inc with elevation, dec with dependent

Pulses-diminsihed

color-pallor w elevation, when dependent rubor

temp-cool

edema-absent or mild

skin changes-thin shiny hairless, thick toenails

ulcerations-deep, toes feet

gangerene-may occur

compressions-no

treatment-smoking cessation, foot care, regular exercise

assessment-CMS

93
Q

venous thrombosis
low pressure

Disorder of Venous Circulation

A

Venous Thrombosis: blood clot that forms in wall of vein, supperfical and deep, infmallation and obstruction

Low pressure & flow within venous system more common then atrial,

94
Q

Deep Vein Thrombosis:
common causes

A

hospitalization,

surgery

and immobilization

95
Q

superficial venous thrombosis manifestations

A

Localized pain and tenderness at site

Redness and warmth along course of affected vein

Swelling & redness

can be from where iv catheters are placed

96
Q

Deep vein thrombosis manifestations

A

At times asymptomatic

Dull, aching in extremity with walking

Tenderness, warmth

Cyanosis of affected extremity

Edema of affected extremity

97
Q

how diagnose and how treat dvt

A

diagnosed with ultrasound

treated with anticoagulants

98
Q

Pulmonary Embolism

A

clot that break loose and enters right side of heart and occludes blood flor to lungs

99
Q

how to diagnose venous disorders

A

Leg pain swelling, check peripheral pulse

Duplex Venous Ultrasound vsiuation of vein, velocity of blood flow

100
Q

treatment venous disorders
med

labs

dosage
normal/therpatuc

A

Anticoagulation: IV heparin (Prolongs clotting times)

aPTT-closely monitor this lab

Dosage: Goal is to reach therapeutic

Normal (control) aPTT: 30 to 40 seconds
Therapeutic aPTT = twice the control value

101
Q

treatment bridge
med
level
anticipate

pulmonary embolism

A

Oral (Coumadin)

check INR-therpatic levels are 2-3

Anticipate oral & IV therapy

102
Q

Coumadin Education & Teaching

A

Lab follow up

Dietary Teaching: Avoid vitamin K rich foods (Dark Leafy Vegetables)

103
Q

surgery for
venous disorders

A

Venous Thrombectomy,

Vena Cava Filter

104
Q

Priorities in Care-venous disorders

pain
ineffective tissue perfusion
impaired mobility
risk for ineffective tissue perfusion

A

Pain: measure area and cirucmfenrce, maintain bedrest os ordered, give pain meds, reassess pain

Ineffective Tissue Perfusion: asses pulses, skin intergrity, cap refill, elevate extremities, ted stocking -remove at ngiht, mild soap to cleanse area

Impaired mobility: positon changes, rom, minimize atrophy, cough and deep breath

Risk for ineffective tissue perfusion:assess resp status, pe system–sob ancuety, impending doom, vital signs

105
Q

Chronic Venous Insufficiency

what is

what caused by

A

Inadequate venous return over a prolonged period of time –

caused by varicose veins, dvt, or trauma

106
Q

manifestations

Chronic Venous Insufficiency

A

mild leg edema

itching

discomfort with standing

reddish brown color

normal pulses

Stasis ulcers around ankle

Thin and shiny cyanotic looking surrounding skin

107
Q

Treatment-Chronic Venous Insufficiency

goal
compression
elev
walking
cross
keep

A

Goal focus on reducing edema and treating ulcerations

Compression hose- beneficial! –remove once a day and while sleeping

elevation

walking, avoid long periods of standing and sitting

dont cross legs

keep legs soft/dry

108
Q

venous disorders- DVT

Pain
Pulses
color
temp
edema
skin changes
ulcerations-where
gangerene
compressions
treatment
assessment

A

Pain-mild, aching, itching

Pulses-regular

color-cyanosis + brown red

tempnormal

edema-worsens with standing

skin changes-brown, around shiny

ulcerations-ankle

gangerene-no

compressions-yes

treatment-elevation, teds, dont cross,

assessmentCMS

109
Q

varicose veins
caused by
impairs

A

Irregular veins with incompetent valves

Caused by: long standing

The constant pressure, impairs the ability of venous valves to close

110
Q

varicose veins manifestations

A

severe aching leg pain,

leg fatigue,

leg heaviness,

itching,

feelings of heat in the legs.

111
Q

treatments varicose veins

A

compression therapy

regular daily walking, prolonged sitting discouraged

surgery

112
Q

Lymphedema

primary

secondary

A

Primary – rare; associated with genetic disorders

Secondary – acquired
Due to damage, obstruction or removal of lymphatic vessels

113
Q

lymphedema
manifestations

A

soft, spongey skin,

subq tissue becomes rough and fibric

114
Q

Lymphedema

treatments

A

Gentle exercise

Compression

Antibiotics

limb elevation of affected side above heart

limb restriction (labs/blood/iv)

Dietary restriction- Sodium

115
Q

Lymphedema

promote tissue integrity

montior fluid volume

A

pit-assess skin, compression sotckins, elevate extremities,skin clean, dry

monitor fluid volume-i and o, restrictd sodium,

2-health promotion(former alteration) (10 decks)

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