exam 3- presntations and videos Flashcards
heart
what is it
how much moves
Hollow, cones shaped organ, necessary for life
Moves more then 1800 gallons of blood/day
pericardium
atria/ventricals
encases the heart and anchors it to surrounding structures-fits snuggly to prevent overflowing
Atria -top
Ventricles –bottom of heart
heart beat
systole
diastole
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
stroke volume
how often
Stroke Volume: Difference between the end diastolic volume and the end systolic volume -
70—80 tomes a minute
cardiac output
what is
what indicator of
what happens if not pumping correctly
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
ischemia
necrosis
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
preload
frank starling mechaniism
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
compliance
afterload
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
s/s of low potassium level
leg cramps
heart fluttering
Diagnostic Tests cardiac
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
pt assessment cardiac
History—
Personal and family history
Diet history
Socioeconomic factors
Current health problems -perceived or actual
Functional history
risk factors for cardiac
Smoking
Obesity
Physical inactivity
age related changes cardiac
e/c
valves-cause
co/bp/contr
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
Patient Physical Assessment
cardiac
what looking at
General appearance
Skin color/temperature
Extremities
Capillary refill
Edema
Blood pressure//Heart Rate
normal hr
school age
adult
athlete
Pediatric/School Aged 70-110
Adult 60-100
Athletes may have lower heart rate
heart failure
what kind of problem
results in what
cardiac output
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
impaired myocardial function
most at risk for hf
causes of heart failure
coronary heart disease/MI-most risk
cardiomyopathy
rhematic fever
ineffective endocarditis
increase cardiac output
causes of heart failure
hypertension
2.Valve disorder
- anemia
- Congenital heart defects
acute noncardaic conditions
causes of heart failure
Volume overload
2.hyperthyroidim
- fever/infection
- Pulmonary emboli
Incidence, prevalence & Risk factors
incidence
prevelance
risk factors
life exp
risk for
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
systolic vs diabolic failure
manifestations
S-Weakness, fatigue, and decreased exercise tolerance.
D-Shortness of breath, tachypnea, and respiratory crackles
left sided heart failure
culprit
coronary heart disease and hypertension
when Left ventricle function fails
what falls
backwards effect
backs where
Cardiac output falls
Backward effects pressure in left ventricle/atrium increase which….
Backs up into the pulmonary system inc congestion and pressure
lef sided hf manifestations
fatigue/activity intolerance/dizziness
dyspnea,
SOB ,
cough,
orthopnea(SOB when laying flat),
congested lung sounds
Right sided
culprit
–restrict blood flow to lungs
Culprit acute chronic repository issues
when Right ventricle is impaired
cant do what->
increased what
cant pump blood accumulate in systemic venous system
Increased venous pressure
Classic Manifestations:-
right sided hf
abdominal organs congested
, JVD
, peripheral edema
acute vs chronic
acute-abrupt onset resulting in decreased cardiac function/output
chronic-progressive deterioration leading to cardiomyopathies, vascular disease, chd
Diagnosis of Heart Failure
History & Physical
How will your patient present to you??
peripheral edema,
too tight shoes,
tired,
not sleeping good,
sleeping in chair,
stopping halfway,
cant catch breath,
tired, lethargic
diagnostic test for hf
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
ACE inhibitors & ARBS
what kinds
assessment
cough
monitor
take/slow
HF drugs
“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
Beta Blockers
assessments
HF drugs
“OLOL” Medications
Assessment pulse and bp prior
Diuretics-what di
what drugs
assessment
watch
obtain/drink/avoid/sudden/ eat
HF drugs
– 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
Positive Inotropic Agents
what does
what drug
assesmetn
report, monitor, no, eat
HF drugs
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
Respiratory Status, Positioning & Edema
Heart failure
assess
position
elevate
asses pulse ox-might need oxygen therapy
fowlers position- adequeute ventilation and help breath easier
elevate extremities, might have teds on
Nutrition & Activity
heart failure
sodium restriction-possibly fluid
gentle progressive exercise
surgery heart failure
valve replacement
heart transplant or circulatory resistance(balloon pump)
Heart Failure Health Promotion
decreased cardiac output
excess fluid volume
activity intlerance
knowledge defect
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
teaching HF\
diet
meds
weight
monitor
low sodium diet
meds
daily weight
monitor I and o
Pulmonary Edema
what is it
what caused by
What is it? accumulation of fluid in intestinal tissue and avloli in lungs-MEDICAL EMERGENCY
Caused by cardiac and non cardiac issues
patho pulmonary edema
contractibility
ventricle unable
resulting in
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
manifestations of pulmonary edema
resp
cardio
nuero
respiratory
tachypenia,dyspnea, orthopena
cardio
tachycardia,hypotension, cool clammy skin
nuero
restless, anxiety, confusion
Pulmonary Edema Treatment
Medications/Treatment
morphine-anxiety and improve breathing relaxes lungs
oxygen,
cpap
brathing treatments, diuretics and vasodilators
Pulmonary Edema Treatment
emergency
Be prepared: in emergency , need resp equipment,– fatigue, impaired gas exchange, acid base imbalances can lead to cardiac arrest
Pulmonary Edema Treatment
focusing on
diagnostic tests
Focusing on: restoring effective gas exchange, reducing pressure and fluid in pulmonary vasular system
Diagnostic Tests: ABG, chest x ray,
pulmonary edema
improve gas echange
cardiac ouput
fear
IGE-assess rest status, high fowlers, administer oxygen, CDB
co-vs, heart sounds, iv, I and o
fear- emountinal support
what is blood pressure
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
hypertension
excess pressure in the arterial portion of the systemic circulation
Systolic
averafe
felt
rises
less then 120 average
felt as peripheral pulse
pressure rises as the heart contracts during systole, ejecting its blood
diastolic
relax
minumin
average
cardiac relaxation and filling
maintain a minimum pressure to maintain blood flow
average is less then 90
Hypertension
diagnosed
normal
elevated
hypertension stage 1
hypertension stage 2
hypertensive crisis
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
modifiable risk factors hypertension
High sodium intake Low electrolytes
Obesity
Alcohol consumption
Insulin resistance
non modifiable risk factors hypertension
Genetic factors
Family history
Age
Race
manifestations of hypertension
Asymptomatic in early stages
Headache
Nocturia
Confusion
Nausea/vomiting
Visual disturbances
Sustained BP affects the:
cardiovascular
rate of atherosclerosis increases,
inc risk of cardiac coronary heart disease and stroke
Sustained BP affects the:
nueroligal
cerebral infarct(stroke)
microaneurysms
hypertensive encephalopathy- high bp, altered loc, increased cranial pressure, papiledema, seizures
Sustained BP affects the:
renal
nephrosclerosis of small nephrons in kidneys
renal insufficiency
Lifestyle Modification
hypertension
diet
physical activity
alc/tobacco
stress
meds
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
Alpha-Adrenergic Blockers
meds
first dose
assess
can cause
antihypertensive
Doxazosin Prazosin
First dose is bedtime,-fainting
assess bp/apical,
dizziness, orthostatic hypotension,nasal congestion
Angiotensin-Converting Enzyme (ACE) Inhibitors
meds
nursing considerations
cough
assess
when take
report
positional
antihypertensive
“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
Angiotensin II Receptor Blockers (ARBs)
meds
assess
when take
report
positional
antihypertensive
“artan” drugs
assess bp,
1 hr before meals,
report edema,
slow positional changes
Calcium Channel Blockers
meds
assess
toxicity
keep
watch
antihypertensive
“pine” drugs, diltiazem
assess bp, apical pulse,constipation
toxicity-nausea, weakness, bradycardia
keep nitrate available
watch liver, renal function
Beta Blockers
meds
assess
report
antihypertensive
“olol” drugs
assess bp, apical,
report bradycardia, decreased co, hypotension, bronchospasm
Centrally Acting Sympatholytic
meds
take/
pathces/
causes/
relieves
take/
dont/
do not
changes
antihypertensive
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
Vasodilators
meds
what does
changes
antihypertensive
Hydralazine
//vasodilation, decreased bp, slow positional changes,
Diuretics
meds
nrursing considerations
antihypertensive
Furosemide
Hydrochlorothiazide
Spironolactone
Risk of hypokalemia-muscle cramps, leg pain,//take bp and I and o
SP-potassium sparing, avoid salt substitutes
hyperlipidemia
Hyperlipidemia = High Cholesterol
High Density Lipoproteins (HDL):
what does
optimal
help clear cholesterol from arteries, transporting to liver for excretion
Optimal > 60mg/dL
triglycerides
desired
amount of fat in blood
desired is less then 150
Low Density Lipoproteins (LDL):
what does
optimal
high levels
primary carrier of cholesterol
Optimal <100 mg/dL
high levels= promote atherosclerosis, deposits cholesterol on artery wall
Atherosclerosis
what does/cause
deposits of fats and fibron that obtsuct and harden the arteireis,
impair blood flow to peripgeral tissues–PVD
desired HDL,LDL,trig
Desired: high HDL, Low LDL, Low Triglycerides
Treatment of Hyperlipidemia
modifacations
overall goal
medication goal
Lifestyle Modifications
Overall goal to lower total cholesterol, triglycerides & LDL, raise HDL
Medication: Goal lower ldl
Treatment of Hyperlipidemia
chlosteroal lowering agents w/ nursing consideration
meds that inhibit platelet aggregation
Statins: atorvastatin, pravastatin, simvastatin
Nursing Considerations monitor cholesterol level, liver enzymes, cpk levels
Medications to inhibit platelet aggregation aspirin, and clopidogrel
Peripheral Vascular Disease
primary syomtome
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
how else will PVD present
pains
p___
pilses
temp
color
smin
ulcer
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 dependentdark red color
Skin thin, shiny and hariless
Breakdown & Ulceration on toes or side of legs
Peripheral Vascular Disease diagnosis
History and physical –when pain
Diagnostic Tests :
Segmental pressure measurements -
Doppler Ultrasound
Oximetry
Angiography
PVD treatments
smoking
walking
foot care
suport hose
rest
revasulrazaition
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
Medication goals pvd
Inhibit platelet aggregation
vasodilation
decrease blood viscosity
PVD assessment-cms
sudden changes
compare
assess
position changes
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
pain/skin intergirty PVD
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
pvd
promote activity tolerance
what to discuss
PAT- assist with cares, gradual increase in activity, positional changes
smoking cessation, sings of bleeding, skin surveleince, diet and exercise
Raynauds Disease
what is it
what limits
Episodes of intense vasospasm in the small arteries of fingers & toes
limits artieal blood flow
raynauds manifestations
Intermittent pain with skin color changes; Blue-White-Red disease
occurs on digits
raynauds treatment
Avoid Cold/dress warm & Avoid Smoking
Stress management
Vasodilators
Dietary habits, increasing activity, maintain BMI
Acute Arterial Occlusion
-stages-
occlusion
results
resulting
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
thrombus
embolism
Thrombus- blood clot that adheres to vessel wall
Embolism-obstruction of vessels by debris
Manifestations-
Acute Arterial Occlusion
Tissue Ischemia—
Painful, pale and cool,
distal pulses are absent, paresthesia,
cyanosis
and mottling
dec cap refill
Diagnosis,
Acute Arterial Occlusion
Arteriography- used to confirm, locate occlusion, and determine extent
Medications
Acute Arterial Occlusion
med
goal
dischsarge
: 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
Surgery
Acute Arterial Occlusion
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
arterial arteries
Peripheral- atherroclerosis, vascular disease
Pain
Pulses
color
temp
edema
skin changes
ulcerations-where
gangerene
compressions
treatment
assessment
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
venous thrombosis
low pressure
Disorder of Venous Circulation
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,
Deep Vein Thrombosis:
common causes
hospitalization,
surgery
and immobilization
superficial venous thrombosis manifestations
Localized pain and tenderness at site
Redness and warmth along course of affected vein
Swelling & redness
can be from where iv catheters are placed
Deep vein thrombosis manifestations
At times asymptomatic
Dull, aching in extremity with walking
Tenderness, warmth
Cyanosis of affected extremity
Edema of affected extremity
how diagnose and how treat dvt
diagnosed with ultrasound
treated with anticoagulants
Pulmonary Embolism
clot that break loose and enters right side of heart and occludes blood flor to lungs
how to diagnose venous disorders
Leg pain swelling, check peripheral pulse
Duplex Venous Ultrasound vsiuation of vein, velocity of blood flow
treatment venous disorders
med
labs
dosage
normal/therpatuc
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
treatment bridge
med
level
anticipate
pulmonary embolism
Oral (Coumadin)
check INR-therpatic levels are 2-3
Anticipate oral & IV therapy
Coumadin Education & Teaching
Lab follow up
Dietary Teaching: Avoid vitamin K rich foods (Dark Leafy Vegetables)
surgery for
venous disorders
Venous Thrombectomy,
Vena Cava Filter
Priorities in Care-venous disorders
pain
ineffective tissue perfusion
impaired mobility
risk for ineffective tissue perfusion
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
Chronic Venous Insufficiency
what is
what caused by
Inadequate venous return over a prolonged period of time –
caused by varicose veins, dvt, or trauma
manifestations
Chronic Venous Insufficiency
mild leg edema
itching
discomfort with standing
reddish brown color
normal pulses
Stasis ulcers around ankle
Thin and shiny cyanotic looking surrounding skin
Treatment-Chronic Venous Insufficiency
goal
compression
elev
walking
cross
keep
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
venous disorders- DVT
Pain
Pulses
color
temp
edema
skin changes
ulcerations-where
gangerene
compressions
treatment
assessment
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
varicose veins
caused by
impairs
Irregular veins with incompetent valves
Caused by: long standing
The constant pressure, impairs the ability of venous valves to close
varicose veins manifestations
severe aching leg pain,
leg fatigue,
leg heaviness,
itching,
feelings of heat in the legs.
treatments varicose veins
compression therapy
regular daily walking, prolonged sitting discouraged
surgery
Lymphedema
primary
secondary
Primary – rare; associated with genetic disorders
Secondary – acquired
Due to damage, obstruction or removal of lymphatic vessels
lymphedema
manifestations
soft, spongey skin,
subq tissue becomes rough and fibric
Lymphedema
treatments
Gentle exercise
Compression
Antibiotics
limb elevation of affected side above heart
limb restriction (labs/blood/iv)
Dietary restriction- Sodium
Lymphedema
promote tissue integrity
montior fluid volume
pit-assess skin, compression sotckins, elevate extremities,skin clean, dry
monitor fluid volume-i and o, restrictd sodium,
