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Unit VIII Cardiovascular

Terms

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leading cause of death in U.S.
Cardiovascular disease
Arteriosclerosis
chronic disease of the arterial system where there is abnormal thickening and hardening of the vessel walls

most common type of arteriosclerosis
atherosclerosis
Atherosclerosis
local accumulation of lipids and fibrinous tissue within the intima of the artery; progressive process; narrows vessel
three artery layers
intima, media, adventitia
potential causes of initial changes in wall of artery durring development of atherosclerosis
smoking, hypertension, diabetes, increased LDL, decreased HDL, infection, periodontal disease
Treatment to prevent thrombus formation in the presence of someone with atherosclerosis
take one asprin every day
Non-modifiable risk factors of atherosclerosis
age, gender, family history, race/ethnic group
modifiable risk factors of atherosclerosis
-elevated serum lipid levels: LDL, VLDL, triglycerides, chylomicrons
-low HDL
-High blood pressure
-Cigarette smoking
-Diabetes mellitus/impaired glucose tolerance
-inflammation, infection
-sedentary lifestlye
-obesity(BMI >30, W/H >8)
-Diet (high fat, sodium, and cholesteral; low fiber)
-Stress (anger/hostility/aggression, personality type)








What does HDL do?
carries lipids away from arteries and to liver where they can be metabolized
What is LDL?
Low density lipid- contain more cholesteral than any other lipid protiens
What is VLDL
Very low density lipid- contain both cholesterol and triglycerides
What are triglycerides?
fatty acids
What is the normal (preferred)cholesteral levels
140-190
What is the normal (preferred) triglycerides range?
40-190
What is the preferred HDL levels?
want it to be greater than 40, (as high as possible)
What is the normal (preferred) LDL range?
below 130
*if history of heart disease- below 100
What is the value of high blood pressure (hypertension)?
*systolic- greater than 160
results of Study -associated with increased risk for atherosclerosis
increased risk if level of LDL >100, cholesterol >200, Triglycerides >150, and HDL
effects of athersclerosis (3)
1. Arterial occlusion: decreased blood flow, ischemia, infarction
2. Aneurysm formation: Pressure on surrounding structures, occlusion of vessel, rupture
3. combination of 1 and 2

Signs and symptoms of atherosclerosis
vary with tissue/organ affected
Atherosclerosis
signs and symptoms
Brain

Dizziness, flashing lights, confusion, headache, death
Atherosclerosis
signs and symptoms
Heart:

Angina(chest pain), infarction, (MI, heart attack), decreased function, death
Atherosclerosis
Signs and Symptoms
Extremities:

Pale, cool, cyanotic; decreased pulses, slow capillary filling, tingling, numbness, claudication; loss of hair growth; necrosis
Interventions/ Treatment for Atherosclerosis
*Primary
Primary prevention: prevent atherosclerosis by decreasing/managing risk factors; identify those at risk; educate about risk and lifestyle changes to alter risk:

Interventions/treatment for atherosclerosis
Lifestlye changes:
-diet(low fat & cholesteral, decease sodium, lose weight)
-exercise
-Stress management
-Control BP
-Control diabetes
-Stop smoking
-Medications may be used to manage BP and diabetes





Hypertension
consistent elevation of systemic arterial BP; sustained systolic BP of 140mm Hg or greater or a diastolic of 90 mm Hg or greater
Diagnosis of Hypertension
based on two or more properly measured(cuff size, arm placement,noise level, activity), seated blood pressure readings taken at two or more office visits.
Incidence of Hypertension
65% of Americans over 60 have hypertension
29% of Americans have prehypertension
1/3 are not adequately controlled

Prevalence of Hypertension
higher in blacks than whites, men at higher risk than women until age 55, after age 55 women at increased risk
Hypertension contributes to deaths from:
heart attack, heart failure, "brain attack", renal damage
Blood Pressure regulated by:
Autonomic nervous system (vasocontriction/dilation)
Endocrine system:catecholemines (epinephrine/norepinephrine)
Cardiovascular: Heart, blood vessels, baroreceptors
Renal: Renin-angiotensin mechanism (renin-angiotensinI-angiotensinII-vasoconstriction) and aldosterone-> increase Na+ and H2O


Types of Hypertension (8)
1. Primary (essential, idiopathic)
2. Secondary
3. Isolated Systolic Hypertension(ISH)
4. Refractory
5. Pregnancy-induced (PIH)
6. "White Coat" HPTN
7. Malignant
8. Hypertensive crisis






Primary (essential, idopathic)
most common (92-95% of hypertension);no known cause, although risk factors have been identified (comb. of genetics and environmental factors)
Secondary
5-8% of cases; associated with an underlying disorder, such as renal disease, endocrine->(increase aldosteronism), vascular (coarctation of aorta), pregnancy-related, drug-related, trauma, oral contraceptives, antihistamines
Isolated Systolic Hypertension (ISH)
>140mm Hg systolic, normal diastolic(
Refractory
resists treatment
"White Coat" HPTN
walking into DR. office and blood pressure goes up but any other time it is normal.
Malignant
rapidly progressive; Diasolic increase to 140 can cause cerebral edema
Hypertensive crisis
sudden rapid onset, very high, can be life threatening;
Risk factors: factors that may promote HPTN
Non-modifiable:
Family History, gender, age, ethnicity
Modifiable:
high dietary intake of calories, sodium, fat
low dietary intake of calcium, potassium, magnesium
high alcohol consumption
obesity,
occupation,
diabetes/glucose intolerance
stress profile
socioeconomic status
smoking
physical activity










Pathophysiology of Primary
unknown cause
interaction of risk factors- increased blood volume, inappropriate autoregulation, too much vasoconstriction, sympathetic overstimulation, water and sodium retention, increased renin, inhibited Na-K transport across cell walls
Pathophysiology of Secondary
cause identidied as renal, endocrine, CV; treat by correcting cause-(caused by a systemic disease)
Pathophysiology of ISH (isolated systolic hypertension)
aortic valve insuffiecency, ventricular septal deficit, elevated thyriod, arteriosclerosis of aorta; treat by correcting cause
Complecated Hypertension
sustained primary hypertension that had pathologic effects-> edema
Hypertension Main treatment
TREAT BP EVEN IF CANNOT IDENTIFY OR TREAT CAUSE!
Effects of hypertension
certain organs affected most-are called target organs; damage to structure and function of their blood vessels leads to ischemia, edema
Hypertension
effect on CV system
-Ischemia heat disease: hypertrophy of heart because it doesnt have to work hard to pump blood against resistance due to high PVR; hypertrophy-> increase demand for blood by heart muscle; heart arteries damaged by hypertension->cannot increase blood supply->ischemia causes angina->can lead to MI, also Heart failure
-Blood vessel damage: can result in aneurysm, dissection of blood vessel wall (layer seperate), rupture artery
-Peripheal Vascular disease: decreased circulation to extremities, claudication (pain in legs due to ischemia)

Hypertension
Effects on Cerebrovascular system:
transient ischemia of brain (TIA), thrombosis in cerebral circulation, aneurysm, hemmorhage, CVA. Accounts for 1/3 of hypertensive deaths
Hypertension
effect on eyes:
retinal damage, vascular sclerosis of vessels, hemorrhage, exudation
Signs and Symptoms of HPTN (13)
-may be none-"Silent Killer"
-headache-tends to be occipital, may be worse in AM
-Lightheaded
-TIA
-Vertigo
-Flushed face
-Spontaneous epistaxis (nosebleed)
-personality changes, "nervous"
-vision changes, blurring, retinal changes
-dyspnea, orthopnea-difficult breathing in certain positions
-leg edema (heart failure)
-chest pain (myocardial ischemia)
-nocturia













Diagnosis of HPTN based on:
-based on history, physical exam, diagnostic tests,such as accurate serial BP readings
Diagnostic test for HPTN
Urinalysis
Biochemical blood profile
Renal tests-IVP, serum, creantine(give that kidney effected), BUN
Chest x-ray (cardiac enlargement, pulmonary vessels
Electrocardiogram (ECG)-effect on heart







Treatment goals for HPTN are:
1. control so BP is in normal range
2. Prevent morbidity
3. prevent morality

Treatment starts with:
-Lifestyle changes to modify risk factors, than add meds if response inadequate.
-depending on severity of HPTN, may start meds immediately.
Life style changes Treatment for HPTN
-weight loss
-moderate alcohol intake
-regular physical activity
-DASH diet
-decrease sodium intake



Meds used for HPTN
-diuretics (thiazle, loop, K+ sparing, ect.)-tp decrease blood volume
-beta blockers (adrenergics) to slow heart, decrease CO
-vasodilators to decrease PVR
-comb. of more than 1 class of drug=best contol w/ minimal side effects






HPTN-Step care with meds:
1. diuretic or beta blocker-help decrease vasodilation
2. adrenergic inhibitor with diuretic
3. add ACE inhibitor or vasodilator-inhibit angiotensin
4. add other med. calcium channel blockers


Stage: Sys: Dias:
Normal
PreHPTN
1
2







Stage: Sys: Dias: Normal _100
Nursing Role with HPTN
-eduacate
-Bring pressure down
-treat symptoms
-help plan for long term self management
-assist in planning stategies
-identify needs for materials
-follow up





Endocarditis
Infection of the lining of the heart; infective endocarditis
Incidence of Endocarditis
incidence decreasing (due to antibiotics and better diagnostic tests) but still a serious condition/complication
Endocarditis Risk factors(15)
-Can occur in normal heart; more likely with previously damaged valves (rheumatic heart disease, syphilis, mitral valve prolapse, congenital abnormality)
Others: congenital heart problems, cardiac surgery, atificial valves, previous infective endocarditis, male gender, IV drug use, long-term vascular catheters, older person, invasive procedures (surgery, diagnostic tests, oral cavity work)
Endocarditis causative organisms:
Most common: Staphylococcus aureus, and Streptococcus viridans
Other organsims: enterococci, viruses, fungi, rickettsia, parasites, MRSA
Endocarditis Signs and Symptoms due to:
*vary with degree of valvar dysfunction
Sx and Sx due to:
1. infection
2. inflammation
3. microemboli
4. immune complex deposits




Endocarditis
Diagnostic tests (8)
-history and physical
-blood culure: (+), identifies organism
-Erythrocyte Sedimentation Rate (ESR):RBC settling faster than normal=sign of inflammation
-Organ scans: may show emboli(collects at site of infammation then travels elsewhere) in brain, kidney, spleen
-ECG: shows heart damage-altered conduction in heart wall, MI due to emboli, CHF because valve damage interferes with blood flow
-CBC: anemia,luekocytosis (increased WBC)
-Cardiac catheterization: coronary artery condition
-Echocardiogram: heart wall motion, valve action and damage








Endocarditis Treatment
-Prevention BEST:education about risk factors, prophylactic antibiotics(when at risk for getting bacteria in blood)
-Antibiotic therapy based on organism; us. IV antibiotics 1st, then oral; comb. may be used; may need to take antibiotics for 4-6 weeks; monitor w/ blood cultures to see if bacteria eradicated; Dr. follow-up important
-Support and Comfort: antipyetics, rest
-Repair valve damage: risky
-Nursing: patient education re: taking antibiotics, prevention



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