Exam #3 Flashcards
structures and fxns of cardo system
- heart
- 4 chambers
- composed of three layers: endocardium, myocardium, epicardium
- pericardium: fibrous sac that heart sits in and holds 15 ml of fluid
- left ventricular wall is 2-3 times thicker than right
cardiac valves
- mitral: left vent & left atria
- tricuspid: right vent & right atria
- pulmonic (semilunar): right heart, keeps blood from going into pulmonary artery when heart is pumping
- aortic (semilunar): left heart, keeps blood from flowing into aorta from left vent
auscultation areas
aortic pulmonic erb's point tricuspid mitral
blood flow through the heart
- right atrium receives venous blood from the inferior and superior vena cava –> blood passes through tricuspid valve into the right ventricle
- with contraction, the right ventricle pumps blood through pulmonic valve into pulmonary artery and to the lungs
- oxygenated blood flows from the lungs to the left artium by way of the pulmonary veins
- oxygenated blood flows through mitral valve and into left ventricle
- heart contracts, blood is ejected through the aoritc valve into the aorta and enters systemic circulation
coronary arteries and veins
- coronary circulation: heart’s own blood flow; flows to heart muscles during diastole
- left coronary artery blockage = widow maker
- right coronary artery = provides blood supple to nodes so a blockage here = issues with electrical system of heart and can cause arhythmias
- coronary sinus: most blood from coronary circulation drains into this and emotied into right atrium
heart’s mechanical system
- systole: contraction of myocardium = ejection of blood from ventricles (depolarization) = s1
- diastole: relaxation of myocardium = s2
- s1 = start of systole, “lub”, closure of tricuspid and mitral valves, radial or apical pulse = point of maximal impusle
s2 = strat of diastole, “dub”, closure of aortic and pulmonic valves
cardiac output
- CO: amount of blood pupmed by each ventricle in one minute
- normal = 4-8L/min
- cardiac index: CO/BSA = more precise measure of efficiency of the pumping action of the heart
- normal = 2.8-4.2L/min/m2
- CO is increased with fluid overload and decreased with fluid deficit
** CO = HR X SV
preload
- stretch or filling pressure
- volume in ventricle at the end of diastole
- diuresis (MI, aortic stenosis) if preload is high
- give fluids if preload is low (hypovolemia, vasodilation)
- PAWP = left ventricle preload
- CVP = right vetricle preload
afterload
- squeeze
- peripheral resistance against which the left ventricle must pump SVR and PVR
- heart’s pushing strength to get blood to body
- the more afterload = the less cardiac output
- increased with: HTN, hardened arteries, CAD, pulm HTN, hypoxia, catecholemines
- decreased with: vasodilators, acidosis, oxygen
systemic vascular resistence
- opposition encountered by left ventricle
- increased with vasoconstricotrs, low volume
- decreased with vasofilators, morphine, nitrates, high co2
pulmonary vascular resistance
- opposition encountered by right ventricle
- increased with pulmonary hypertension, hypoxia
- decreased with meds (calcium channel blockers, aminophyline, isoproterenol, oxygen)
contractility
- strength of contraction
- when increased, stroke volume and oxygen demand and increased
- increased with: positive inotropes meds (epi, norepi, isoproteronol, dopamine, dobutamine, digitalis)
- decreased with: negative inonotropes, heart failure, alcohol, calcium channel blockers, beta blockers, acidosis
preload problems
- JVD
- lung sounds
afterload problems
- BP
- skin temp
- pulse pressure
contractility problems
- junction fraction
factors affecting heart rate
- autonomic nervous system (ANS)
- SNS: adrenaline, speeds up everything, vasoconstriction
- PNS: vagus nerve, slows everything down, vasodilation
- baroreceptors (perssure) and chemoreceptors (co2 and o2)
blood pressure
- systolic blood pressure: 60 is needed to perfuse organs
- MAP = (syst BP + 2x dia BP)/3
gerontologic considerations
- risk for CVD increases with age
- CVD leading cause of death in adults >85
- cardivascular changes result of aging, disease, environmental factors, and lifetime behaviors (smoking, drinking)
- heart rate changes: no change in resting supine HR; decreased HR response to stress; HR takes longer to increase for activity and longer to decrease with rest; give a while to relax before taking BP
- BP changes: HTN is not expected with age, increased SBP; decreased or no change in DBP; increased pulse pressure, orthostatic hypotension
- postrandial hypotension = decrease in BP of at least 20 mm hg that occurs within 75 minutes after eating (don’t give BP meds near meal time)
- heart sound changes: murmur from reguritation/narrowing of mitral and aortic valves
- ECG changes: decreased pacemaker cells; sinus and atrial dysrhythmias, heart block, abnormal resting ECG in 50% of elderly
- medication response changes: less sensitive to beta blockers, increased sensitivity to vasopressin (ADH)
- physical changes: dependent edema due to incompetent venous valves
AFIB
- controlled: vent rate 100 HR
risk factors for heart issues
- all are modifiable
- increased serum lipids
- hypertension
- smoking
- sedentary lifestyle
- obestiy
- stress
- DM
subjective heart assessment
- allergies to iodine (contrast procedures)
- familiar disorders
- constipation (vagus nerve stimulation can cause fainting)
- exercise intolerance
- PND (paroxysmal nocturnal dyspnea), orthopnea, sleep apnea
- sexual problems (vagus nerve)
stroke volume
- SV: volume of blood (in ml) ejected with each heartbeat
- normal = 50-100ml
- determined by preload, afterload, and contractility
- SV Index: adjusted for BSA
- normal = 25-45ml
- increased with volume overload, inotropy, hyperthermia, meds (digitalis, dopamine, dobutamine)
- decreased with impaired cardiac contractility, valve dysfunction, CHF, bet blockers, MI
- factors affecting stroke volume: preload, afterload, contractility
** CO = HR X SV
preload
- stretch or filling pressure
- volume in ventricle at the end of diastole (totally filled ventricle)
- increased with: fluid overload, MI, and aortic stenosis
- decreased with: hypovolemia, and vasodilation
afterload
- squeeze
- peripheral resistence against which the left ventricle must pump
- the more afterload = less cardiac output
- increased with: HTN, hardened arteries, CAD
- decreased with: vasodilators, acidosis, oxygen
- Systemic Vascular Resistence SVR: opposition encountered by left ventricle; increased with vasoconstrictors, low volume; decreased with vasodilaros, morphine, nitrates, high co2
- pulmonary vascular resistance PVR: opposition encountered by right ventricle; increased with pulmonary hypertension, hypoxia; decreased with meds
contractiity
- strength of contraction
- when increased, stroke volume and oxygen demand are increased
- increaesd with meds (epi, norepi, isoproteronol, dopamine)
- decreased with: heart failure, alcohol, calcium channel blockers, beta blockers, acidosis
factors affecting stroke volume
- CO = HR X SV
- preload
- afterload
- contractility
preload problems
- JVD
- lung sounds
afterload problems
- BP
- skin temp
- pulse pressure
contractility problems
- ejection fraction
factors affecting Heart Rate
- autonomic nervous system
- sympathetic nervous system: adrenaline, speeds everything up, vasoconstriction
- parasympathetic nervous system: vagus nerve, slows everything down, vasodilation
- baroreceptors (pressure sensors) and chemoreceptors (sense co2 and 02)
Blood Pressure
- systolic: 60 needed to perfuse organs
gerontologic considerations
- risk for CVD increases with age
- CVD leading cause of death in adults >85
- cardio changes result of: aging, disease, enviro, lifetime behaviours (drinking, smoking)
- heart rate changes: no change in resting supine HR, decreased HR response to stress
- takes longer for HR to increase with activity and decreae with rest
- BP changes: HTN is not an expected result of aging
- increased systolic with decrease/no change in diastolic
- orthostatic hypotension
- postprandial hypotension = decrease in BP of at least 20 mmhg that occurs within 75 minutes ofter eating (don’t take BP right after a meal)
- heart sound changes: murmur from regurgitation/narrowing of mitral and aortic valves
- ECG changes: (decreased pacemaker cells)
- sinus and atrial dysrhythmias (Afib)
- abnormal resting ECG in 50%
- medication response changes: less sensitive to beta blockers, increased sensitivity to vasopressin (ADH)
- physical changes: dependent edema due to incompetent venous valves
Afib
- controlled: vent rate 100 HR
cardio risk factors
- increased serium lipids
- HTN
- smoking
- sedentary lifestyle
- obesity
- stress
- DM
- all modifiable
cardio assessment
- allergies to iodine (contrast)
- familial disorders: heart disease before age 55
- constipation: vagust nerve stimulation
- exercise intolerance
- dependent rubor: A redness or purple color of a leg when it is in the dependent or lowered position. If the leg blanches on elevation it may be a sign of lower leg ischemia
- JVD
- venous stasis ulcers
arterial wound vs venous wound
- arterial: smaller, deeper, dryer
- venous: large, shallow, wet, edema/weeping
PMI
point of maximal impulse
- if it is found below 5th intercostal space then means enlarged heart
s1
closure of tricuspid and mitral valves
s2
closure of aortic and pulmonic valves
- s2 splitting heard during expiration not good
s3
ventricular gallop
- kentucky
s4
atrial contraction (before s1)
- CAD or cadiomyopathy
- tennessee
cardiac lab markers
- troponin: protein released after an MI, highly specific to cardiac tissue - greater than 2.3 = positive for MI
- CK-MB: iozyme released after cardiac tissue injury, levels increased 4-6 hours after MI, >4-6% = positive for MI
- Myoglobin: protein sensitive for MI, rises 30-60 minutes after MI, range is about 24
- BNP (b-type naturetic peptide): determines whether dyspnea is from a cardiac or respiratory cause, >100 = heart failure
risk predictors
- c-reactive protein: marker for inflammation; risk factor for CAD
- homocysteine: elevated levels increased risk for CAD, PVD, and stroke
serum lipids/lipoproteins
- serum lipids/lipoproteins
- triglycerides (60 is low risk)
- LDL (
chest x ray
- shows:
- contours of heart
- displacement, enlargement
- fluid
- pulmonary congestion
- size of heart
electrocardiogram
- ECG
- records cardiac electrical activity
- event monitor or loop recorder
exercise or stress test
echocardiogram
- ultrasound of heart
- with/without contrast
- shows: structures of heart, work of the heart, size, pericardial sac, ejection fraction
nuclear cardiology (MUGA)
- IV injection of radioactive isotope, pay still for 20 minutes with arms up, may have repeat scans
- structural info and injection fraction
MRI
- noninvasive, but must lie still
- cant do if they have a pacemaker
- ejection fraction, MI recovery
CT
- visualizes heart anatom, circulation, and big vessels
- can be performed instead of cardiac cath
- calcium can be seen in atherosclerotic plaques
- heart anatomy, circulation, vessels, calcium deposits, atherosclerotic plaque
cardiac catheterization
- invasive outpatient procedure
- angiography involves injection of dye, shows coronary lesions
- intracoronary ultrasound done with angiography, shows vessel walls and plaque
- obtains info about 02 levels, pressure readings in heart chambers, structures and motions of the heart,
- insertion of catheter into vein
- determines source of dysrhythmias
- pre-op: pt needs to be NPO for 6 hours before, requires sedation, cough or deep breath when dye is injected
- post op: neurovascular checks q 15 minutes x 1 hr, compression device over injection site, close monitoring of VS and ECG
- complications: bleeding, hematoma, allergic reaction, infection, clot, aortic dissection, dysrhythmias, MI, stroke, puncture ventricles or lung
regulation of BP
BP = CO X systemic vascular resistence
- sympathetic nervous system: increases HR, vasoconstriction, release od RENIN from kidneys
- baroreceptors: send inhibitory impulses to the sympathetic vasomotor center in the brainstem
- renal system: control sodium excretion and ECF volume, increase venous return and SV, RAAS system
- endocrine system: epinephrine increases HR and contractility, increased blood sodium osmolarity stimulating release of ADH
hypertension
- systoldic > 140, diastolic > 90
- diastolic will increased to age 55 then go down, systolic stays the same
prehypertension
- systolic 120-139, diastolic 80-89
isolated systolic HTN
- systolic > 140 with diastolic
psuedohypertension
- false HTN with severe atherosclerosis
- arteries so hard they can’t collapse when BP cuff is on arm
causes of HTN
- primary: 95% of people with HTN, no identifiable cause
- secondary: 5% of those with HTN, caused by something specific that can be identified and treated
- suspect if >50, suddenly develop high BP
pathophysiology of HTN
- heredity
- water/sodium retention
- altered RAAS mechanism
- stress
- SNS hyperactivity
- insulin resistence
- endothelium dysfunction
risk factors for HTN
- age >50
- alcohol > 1oz/day
- smoking
- DM
- high serum lipids
- high sodium
- men 55
- obesity
- AA
- sedentary lifestyle
- socioeconomic status
- stress
S/S HTN
- silent killer - S/s often appear after organ disease occurs
- fatigue
- activity intolerance
- dizziness
- palpitations
- angina
- dyspnea
complications with HTN
- hypertensive heart disease: CAD, left ventricular hypertrophy, heart failure
- cerebrovascular disease: atherosclerosis, #1 cause of stroke, HTN, encephalopathy
- peripheral vascular disease: PVD, aortic aneurysm, aortic dissection
- nephrosclerosis: end-stage renal disease, renal dysfunction
- retinal damage: blurred vision, retinal hemorrhage, blindness
diagnostic studies for HTN
- UA, BUN, creatinine (urinalysis)
- electrolytes
- blood glucose
- lipid profile
- uric acid
- ECG
- echocardiogram
treatment for HTN
- goal: BP
lifestyle modificaitions for HTN
- weight reduction
- DASH eating plan
- sodium reduciton
- limit alcohol
- regular physical activity
- avoidance of tobacco use
- stress management
dietary changes for HTN
- DASH eating plan:
- emphasizes fruits, veggies, fat-free or low fat milk, whole grains, pultry, beans, seeds, nuts
- decreased red meat, satl sweets, added sugars, sugarded beverages
- no restriction on caffein or protein
- sodium restriction:
drug therapy for HTN
- diuretics
- beta blockers
- ACE inhibitors
diuretics
- lasix, hydrochlorothiazide, sprionalactone (K+ sparring)
- used for HTN, fluid overlaod
- decreased preload by decreasing fluid buildup
- side effects: low potassium, low magnesium, dehydration
- if K+ is low, digoxin toxicity is a higher risk
- take in the morning
beta blockers
- atenolol, betaxolol, esmolol
- used for HTN, angina, dysrhythmias, post-MI – not recommended for heart failure or asthmatics
- blocks the effects of epi, decreases HR, lowers BP lowers cardiac output, vasodilates, decreases contractility
- side effects: fatigue, impotence, wheezing, SOB
ACE inhibitors
- benazepril, captopril, enalapril, lisinopril
- used for: HTN, heart failure, diabetes (protects kidneys), can prevent heart attack and stroke
- lowers levels of antiotensin II, lowers BP, vasodilates (Decreased afterload)
- side effects: dry cough, low BP, high K+, angioedema (swelling of lips and face)
- dont take with ASA or NSAIDs
Angiotensin II receptor blockers ARB
- candesartan, eprosartan, losartan
- used for: HTN, heart failure, give if unable to tolderate ACE
- blocks angiotensin II from having any effect, lowers BP, vasodilates
- side effects: high K+, decreased kidney fxn
calcium channel blockers
- diltiazem, verapamil, amlodipine, clevidipine
- used for: angina, HTN, dysrhythmias, do not use after MI or with heart failure
- interrupts the movement of calcium into the cells of the heart, vasodilates (Decreased afterload), decreases contractility (pumping strength)
- side effects: bradycardia, low BP, headache, dizziness, nausea
- DO NOT give with grapefruit juice
alpha adrenergic blockers
- clonidine, hytrin, cardura
- used for: HTN, BPH
- vasodilates, lowers BP. lowers cardiac output
- side effects: dry mouth, sedation, fatigue, impotence, low BP
- dont take with alcohol or sedatives, may need to take at bedtime
vasodilators
- nitrates
- used for: angina, HTN, MI, heart failure
- vasodilates (decreases afterload), decreases preload
- side effects: headaches, low BP, dizziness
- must monitor BP (above 100 to give), repeat every 5 mins for 3 times
- dont take if take erectile dysfunction meds
drug therapy side effects for HTN
- orthostatic hypotension: HR >50 and BP >100 to give meds
- sexual dysfunction
- potassium: ACE and ARB can make it high
- dry mouth
- nocturia
HTN nursing interventions
- health promotion, lifestyle modifications
- ambulatory/home care
- home BP monitoring
- patient compliance
- need to be seen monthly until BP is stable
proper BP measurement
- proper cuff size
- arm at level of the heart
- measure in both arms and use arm with higher reading
- do not smoke, exercise, drink caffeine 30 minutes before
- sit quietly after resting 5 minutes with arm supported at heart level
- both feet flat on floor
- take first thing in AM and at night
- take two readings, wait 1 minute between
- single value is not as important as a series of values
HTN gerontologic considerations
- higher incidence of ISH (isolated systolic) and white coat HTN
- be careful of auscultory gap
- more sentitive to slight BP changes
- resistant to ACE inhibitors and ARBs
- orthostatic hypo
- postprandial hypotension is common
hypertensive crisis
- can develop over hours or days
- rate of rise, not actual BP, is most important
- MAP is more important than BP
- most common cause is failure to take BP meds
- another cause is cocaine/crack use
- S/S: severe headache, n/v, seizures, confusion, coma, pailledema, tremors, decreased urine output
hypertensive crisis treatment
- goal is to slowly lower BP (decrease MAP by 25% in 1 hour)
- IV sodium nitropursside along with oral BP meds
- check BP q 2-3 minutes
- monitor ECG for dysrhythmias
- hourly urine output
- bedrest
- frequent neuro checks
heart failure
- R. heart failure: peripheral edema, JVD
- L. heart failure: pulmonary edema
- abnormal cardiac fxn involving imparied cardiac pumping and/or filling
- associated with HTN, CAD, MI
- primarily affects older adults
- high morbidity and mortality
risk factors for heart failure
- CAD, age, HTN
- diabetes
- smoking
- obesity
- high cholesterol
- AA
heart failure patho
- systolic: problem with pumping
- caused by MI, HTN, cardiomyopathy, valve disease
- S/S: left ventricular hypertrophy, decreased EF
- Diastolic: problem with filling
- caused by sfiff ventricles, left ventricular hypertophy from HTN, aortic stenosis, hypertophic cardiomyopathy, majority have no identifiable heart disease
- s/s: pulm congestion, pulm HTN, ventricular hypertophy, normal EF
compensatory mechanisms for heart failure
- SNS activation
- release of epi/norepi (short term)
- neurohormonal responses
- RAAS cascade, ADH release, endothelin release, inflamm response
- ventricular dilation
- way to cope with increased volume
- ventricular hypertrophy
- increase in muscle mass and wall thickness
counterregulatory mechanisms
- production of ANP (reduces water and sodium), BNP (decreases BP), and NO (nitric oxide, vasodilation, decreases afterload)
- causes vasodilation and diuresis
- locks effects of the RAAS
- inhibit the development of hypertrophy
types of heart failure
- usually biventricular but one may precede the other
- left: most common
- caused by left ventricular dysfunction
- blood backs up into the pulmonary veins
- pulmonary congestion and edema
- right
- caused by eft sided heart failure or cor pulmonale (right vent dilates as reults of pulmonary disease)
- blood backs up into the venous circulation
- JVD, hepatomegaly, spelnomegaly, peripheral edema
- pitting edema, JVD, enlarged liver and spleen
s/s of acute HF
- ADHF (acute decompensated HF)
- pulmonary edema: anxious, pale, cyanotic, cold and clammy skin, severe dyspnea, tachypnea, orthopnea, frothy blood-tinged sputum, increased HR, crackles, wheezes, rhonci
s/s chronic HF
FACES
- fatigue
- activity
- cough - dry, nonproductive, may be 1st clinical symptom
- edema
- SOB, orthopnea
- Paroxysmal nocturnal dyspnea
- tachycardia
- nocturia
- weight gain - sudden gain of 3lbs/day
s/s right heart failure
- murmors
- heaves
- JVD
- edema
- weight gain
- ascites
- hepatomegaly
- fatigue
- nausea
- anorexia
s/s left heart failure
- s3, s4
- heaves
- PMI displaced
- hypoxia
- crackles
- dyspnea
- restlessness
- confusion
- fatigue
- PND, orthopnea
- cough
- frothy, pink tinged sputum
comlications from heart failure
- pleural effusion: increasd pressure in pleaural capillaries
- dysrhythmias: Afib (most common dysrhythmias in elderly), clots are major concern with pooling blood when heart isn’t pumping correctly, coumadin
- left ventricular thrombus
- hepatomegaly: enlarged liver, congested with edema
- renal failure: decreased perfusion to kidneys
diagnostic studies for heart failure
- goal is to determine cause
- Ejection fraction distinguishes between systolic and diastolic HF
- BNP: differentiates between dyspnea from resp or heart failure
- chronic HF; exercise stress testing
- acute HF: LV function measurement, endomyocardial biopsy
ADHF treatment
- high fowlers position with feet horizontal or dangling
- oxygen
- ECG, oxygen sat monitoring
- VS, urine output hourly
- hemodynramic monitoring
- ultrafiltration for colume overload
- circulatory assist devices
- treat depression
ADHF treatment drugs
- morphone: decreases pre and afterload, decreases anxiety, helps with dyspnea
- diuretics: durosemide/lasix, decreases preload
- vasodilators: IV nitro, sodium nitropursside
- positive inotropes: only if nothing else works, digitalis, dopamine, dobutamine, epinephrine, norepinephrine
chronic heart failure treatment
- oxygen
- physical emotional rest
- cardiac rehab
- biventricular pacing or cardiac resynchronixation thearpy (CRT)
- may also have implanted cardioverter defribilator ICD
- telehealth monitoring
- circulatory assist devices
chronic heart failure drug treatments
- diuretics - thiazide is first choice
- ACE inhibitors or ARBs
- aldosterone antagonists - spirinolactone
- BiDIl; only for AA
- use cautiously: best blockers and digoxin
nutrtion for heart failure
- always do an assessment, 3 day diary
- sodium restriction
heart failure nursing diagnosis
- excess fluid volume realted to increased venous pressure and decreased renal perfusion
- imparied gas exchange r/t increased preload and alveolar capillary membrane changes
- activity intolerance r/t fatigue from cardiac insufficiency and pulmonary congestion
- deficient knowledge
heart failure nursing internventions
- health promotion: flu and pneumonia vaccine, educate about diet/meds/exer
- acute: conserve energy, decrease anxiety, salt and fluid restriction
- home care: take meds even if feeling well, treat anxiety and depression, know s/s of worsening HF, know what to call doctor for
when to call Dr for HF
FACES
- fatigue, weakness, dizziness, fainting
- activities needing to be limited
- chest congestion/cough
- edema, swelling of ankles, feet, abdomen, weight gain or 3lbs/day or 3-5 in week
- shortness of breath, diff breathing when lying flat or with exertion, waking up breathless at night
cardiac transplant
- indications: end stage heart failure , severe/decompensated/inoperable valvular heart disease, recurrent life threatning dysrhythmias, any other with mortality risk 50% or more within 2 years
- surgery: donor’s heart is harvested, then implnated, required cardiopulmonary bypass
- post op: many complications including SCD, acute rejection, infection, lymphoma, accelerated CAD
- requires frequent endomyocardial biopsies
valves of the heart
- Atrioventricular valves
- mitral
- tricuspid
- two semilunar valves
- aortic
- pulmonic
valvular heart diease
- types of valvular heart diease depend on: valve affected, type of functional alterations (stenosis, regurgitation)
Stenosis
- stiff valve
- constricting/narrowing
- valve orifice is smaller
- forward blood flow is impeded
- pressure differences reflect the degree of stenosis
regurgitation
- incompetence/insufficiency
- incomplete closure of valve leaflets
- reults in backward flow of blood
- floppy valve
mitral valve stenosis
- majority of adult cases result from rheumatic heart diease
- scarring of valve leaflets and chordae tendinae
- less common causes: congentital mitral stenosis, rheumatoid arthritis, systemic lupus erythematosus
- results in decreased blood flow from left atrium to left ventricle
- increased left atrial pressure and volume
- increased pressure in pulmonary vasculature
- risk for Afib
- fish mouth valves
- blood trickles through and causes increased pressure in atria
mitral valve stenosis clinical manifestations
- exertional dyspnea
- loud s1
- diastolic murmor: rumbling at apex, low pitched
- fatigue
- palpitations
- hoarseness (laryngeal nerve), hemoptysis (frothy bloody sputum)
- ches pain (from decreased CO), seizures (from embolism, stagnant blood in atria increases risk for clot formation), stroke
mitral valve regurgitation
- valve function depents on intact: mitral leaflets, mitral annulus, chordae tendineae, papillary muscles
- a defect in any of these structures can result in regurgitation
- damage is caused by: MI, chronic rheumatic heart diease, mitral valve proplapse, ischemic papillary muscle dysfunction, infective endocarditis
patho of mitral regurgiation
- incomplete valve closure
- backward flow of blood
- acure MR: pulmonary edema, cardiac schock
- chronic MR: left atrial enlargement, ventricular hypertrophy –> decrease in CO
clinical manifestations of mitral regurgitation
- acute: thready peripheral pulses and cool, clammy extremities (decreased perfusion)
- chronic: asymptomatic for years until development of some degree of left ventricular failure –> weakness, fatigue, palpitations, progressive dyspnea, peripheral edema, S3, murmur
mitral valve prolapse patho
- leaflets prolapse back into left atrium during systole
- unknown cause but genetic link
- prolapse = buckle = most common cause of valvular heart disease
mitral valve prolapse clinical manifestations
- confirmed with ECG
- most pts are asymptomatic for life, only 10% with symptoms
- murmur d/t regurgitation, louder during systole
- severe MR uncommon
- dysrhythmias, palpitations, light headedness, dizziness, chest pain unresponsive to nitrates
- infective endocarditis
- treat symptoms with beta blockers
- valvular surgery for MR
patient education for mitral valve prolapse
- antibiotic prophylaxis if MR present
- take drugs as prescribed
- healthy diet, avoid caffeine
- avoid OTC stimulents
- exercise
aortic valve stenosis
- congenital stenosis usually discovered in childhood, adolescence or young adulthood
- can also be degenerative or caused by rheumatic fever
- poor prognosis if symptomatic and not corrected
- use nitroglycerin cautiously: reduced preload and BP, can worsen chest pain
aortic valve stenosis patho
- obstruction of flow from left vent to aorta during systole
- left vent hypertrophy and increased myocardial oxygen consumption
- leads to decreased CO, pulmonary hypertension, and HF
- heart increases in size and requires more O2 to work
aortic valve stenosis clinical manifestations
- angina
- syncope
- exertional dyspnea
- auscultory findings: normal to soft s1, diminished or absent s2, systolic murmur, prominent s4
- triad of symptoms: angina, syncope, dyspnea
aortic valve regurgitation
- acute AR: IE, trauama, aotic dissection
- life threatening emergency
- chronic AR: rheumatic heart diease, congenital bicuspid aoritc valve, syphilis, chronic rheumatic conditions
aortic valve regurgitation patho
- backward blood flow from ascending aorta into left ventricle
- with chronic AR, left vent dilation and hypertrophy
- decreased myocardial contractility
- pulmonary hypertension and right ventricular failure
aortic valve regurgitation, acute clinical manifestations
- severe dyspnea
- chest pain
- hypotension
- cardiogenic shock
- life threatening emergency
aortic valve regurgitation, chronic clinical manifestations
- may be asymptomatic for years
- exertional dyspnea, orthopnea, paroxysmal dyspnea
- angina
- water hammer pulse if severe (strong quick beat that collapses immediately)
- soft or absent s1
- s3 or s4
- murmur
tircuspid valve stenosis
- occurs in patients with Rheumatic Fever and IV drug abuse
- right atrial enlargement and increased systemic venous pressure
- clinical manifestations: peripheral edema, ascites, hepatomegaly, murmur
pulmonic valve stenosis
- almost always congenital
- causes right ventricular hypertension and hypertophy
- clinical manifestations: fatigue, loud murmur
valvular heart disease, diagnostic studies
- patient’s history/physical exam
- CT scan of chest (w/ contrast is the gold standard)
- echocardiogram - valve structure, size, anatomy
- chest x-ray - heart size, alterered pulmonary circulation, valve calcification
- ECG
- Cardiac catheterization - pressure changes in heart chambers, measures sixe of valve openings
valvular heart disease, conservative management
- prophylatic antibiotic therapy to prevent recurrent RF and IE
- dependent on valve involved and disease severity
- prevent exacerbations of HF, pulmonary edema, thromboembolism, recurrent endocarditis
- drugs to treat/control HF: vasodilators (nitrates, ACE inhibitors), positive inotropes (digoxin), diuretics, B-adrenergic blockers
- sodium restriction - prevents H20 retention
- anticoagulation therapy - increased risk of clot formation when vlaves dont work, stagnant blood
valvuloplasty
- opens diseased valves
- percutaneous transluminal balloon valvuloplasty
- split open fused commissures
- for mitral, tricuspid and pulmonic stenosis
- balloon-tipped catheter inserted via femoarl artery
- inflated to separate valve leaflets
percutaneous tansluminal balloon valvuloplasty
- for older adults who are poor surgery candidates
surgical treatment for HF
- palliative not curative
- valve repair (valvulotomy, valvuloplasty, annuloplasty - last about 6 months): less risky, sometimes requires bypass, sometimes uses replacement rings
- valve replacement: used esp for combined aortic stenosis/regurgitation, can have mechanical or biologic valves
biologic (tissue) valves
- made from bovine, porcine, and human cadaver tissue with some man-made materials
- less durable, cause early calcification, tissue breakfown, leaflet stiffening
- do not require anticoagulation therapy
mechanical valves
- more durable, last longer
- increased risk of thromboembolism
- requires long-term anticoagulation thearpy
- complications: bleeding (if on anticoags), valve leakage, endocarditis
nursing assessment subjective, HF
- past medical history
- IV drug abuser
- palpitations, weakness, activity intolerance, dizziness, fainting
- Dyspnea on exertion, cough, hemoptysis, orthopnea, paroxysmal nocturnal duspnea
- angina, atypical chest pain
nursing assessment objective, HF
- fever
- diaphoresis, flushing, cyanosis, clubbing, wheezes, hoarseness
- S3 & S4
- dysrhythmias
- increased or decreased in pulse pressure, hypotension
- thready peripheral pulses
- hepatomegaly, ascites
- weight gain
HF nursing diagnosis
- decreased cardiac output
- excess fluid volume
- activity intolerance (need rest, don’t overexert)
- deficient knowledge
planning for HF
- patient goals: normal cardiac fxn, improved activity intolerance, understanding of the diease process and health maintenance measures
health promotion for HF
- diagnosing and treating streptococcal infection (RF comes from strep throat)
- prophylatic antibiotics for patients with history
- encourage compliance
- teach patient when to seek medical treatment
nursing implementation HF
- individualize rest and exercise
- avoid strenuous activity
- discourage tobacco use
- ongoing cardiac assessments to monitor drug effectiveness
- monitor INR
infective endocarditis
- infection of the inner layer of the heart, including the cardiac valves
- improved prognosis with antibioitc therapy
- subacute form: preexisting valve disease, longer clinical course
- acute form: healthy valves, rapidly progressive
- caused by: bacteria (stepto, staphylo), virus, fungi
INfective endocarditis etiology and patho
- occurs when blood turbulence within heart allows causative organisms to infect previously damaged valves or other endothelial cells
- vegetation: firbrin, leukocytes, platelets and microbes can cause emboli, adheres to valves aor endocardium, parts can break off and enter circulation
- risk factors: age, 50% of older people with aortic stenosis. IVDA, prosthetic valves, use of intravascular devices (MRSA), renal dialysis
bacterial endocarditis clinical manifestations
- nonspecific
- low grade fever occurs in 90% of people
- chills
- weakness
- fatigue
- anorexia
- subacute form: arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, clubbing of fingers
- vascular manifestations: splinter hemorrhages in nail beds, petaechiae, osler nodes on fingers and toes, janeways lesions on palms or soles, roth spots
endocarditis clincal manifestations
- murmur in most patients
- heart failure
- secondary to embolism: spleen (sharp pain), kidneys (flank pain, renal failure), limbs (ischemia, gangreen), brain (LOC, neuro issues), lungs (pulmonary embolism, dyspnes)
diagnostic studies for endocarditis
2 or more items must be found to be endocarditis:
1 positive blood culture
2 heart murmur
3 mass on echo or vegetation
- lab tests: blood cultures, CBC with differential, ESR, CRP
- echocardiography: valves and heart structures
- chest xray: enlarded heart
- ECG: heart blocks
- cardiac caths: valve function
collaborate care for endocarditis
prophylactic antibiotic treatment for patients having:
- certain dental procedures
- respiratory tract incisions
- tonsillectomy and adenoidectomy
- gi wound infection
- UTI
endocarditis assessment
- subjective
- IVDA, alcohol abuse, weight changes, chills, hematuria, exercise intolerance, wekaness, fatigue, cough, DOE, night sweats, pain, headache
- objective
- fever, osler’s nodes, splinter hemorrhage, janeway lesions, petechiae, purpura, peripheral edema, clubbing, tachypnea, crackles
endocarditis nursing implementation
- antibitoic thearpy for 4-6 weeks
- assess home setting
- assess iv lines
- adequate rest
- compression stockings
- ROM exercises
- depp breath and cough every 2 hours
- monitor body temp
pericarditis
- inflammation of the pericardial sac
- heart looks “Shaggy”, pericardium holds 15ml of fluid
- commonly idipathic or viral
- also occurs after infection, MI, trauma
- 2 syndromes after MI: 48-72 hours post MI = acute pericarditis; 4-6 weeks pot MI is dressler syndrome
- inflammatory response
S/S pericarditis
- pericardial friction rub
- may have fever
- progressive, severe chest pain, worse laying down and on inspiration, relieved by sitting and leaning forward, may refer to shoulder and neck
- if they hold their breath and you still hear a rub it is a heart issue
pericarditis diagnostic studies
- ECG: ST elevations different from MI
- Echo: look for complications
- high WBC, CRP, ESR = inflammation
- may send pericardial fluid or tissue for analysis
pericarditis complications
- pericardial effusion: build up of fluid in pericardium
- can compress nearby structures, cause cough, dyspnea, tachypnea, hiccups, hoarseness
- S/S include distant, muffled heart sounds with normal BP
- Cardiac tamponade: pericardial effusion worsesn and compresses the heart, heart can’t expand and push
- S/S include chest pain, confusion, restlessness, muffled heart sounds, narrowed pulse pressure, tachypnea, tachycardia, marked JVD, pulsus paradoxus (greater than 10mmhg
pericarditis treatment
- antibitoics, if bacterial
- NSAIDS for pain and inflamm
- corticosteroids if not responding to NSAIDs
- postion upright leaning forward
- pericardiocentesis (needle inserted to remove fluid)
chronic constrictive pericarditis
- caused by scarring and loss of elasticity of pericardial sac after acute pericarditis
- S/S include JVD, dyspnea, peripheral edema, fatiuge, no pulsus paradozus
- heart sounds: pericardial knock
chronic constrictive pericarditis, diagnosis and treatment
- ECG changes are non-specific
- CXR: enlarded heart
- confirmed by color m-mode echo: wall thickening without pericardial effusion
- TX: pericardial window or pericardiectomy, may take time to show improvement
rheumatic fever
- inflammatory disease that occurs after group a strep infection, can affect heart, joints, skin and brain
- biggest complication is rheymatic heart disease
- can cause vegetations in the valves leading to valve regurgitation and schoff’s bodies leading to pericarditis
RF S/S
- major criteria to confirm disease:
- carditis (murmur, heart enlargement, pericarditis)
- polyarthritis
- sydenham’s chorea, can’t control movements
- erythema marginatum lesions (flat, not itchy, on trunk and inner arm/theigh)
- SQ nodules, hard, painless, on bony surfaces
- minor criteria:
- fever
- polyarthraliga
- increased WBCs, CRP, ESR - inflamamtion
- evidence of group a strep infection: tachy, murmur, friction rub
RF Complications
- chornic rheumatic carditis
- reoccurance
- DX: no single diagnostic test, use criteria
- TX: antiinflammatories, bedrest
RF nursing care
- RF is preventable with early detection and tx of strep a pharyngitis
- bedrest
- prevent recurrence of RF with montly IM penicillin sometimes for up to 10 years
- tonsil removal is not helpful
cardiomyopathy
- disease that affect structural/functional ability of the heart muscle
- primary: idiopathic, only affects heart muscle
- secondary: cause is known and secondary to another disease process
- 3 types
1) dilated
2) hypertophic
3) restrictive - leading cause for heart transplant
dilated cardiomyopathy
- enlarged heart chambers with thin walls
- cause: most common type, some genetic link, often follows infectious myocarditis, can be caused by alcohol abuse, pregnancy
- patho: diffuse inflammation, rapid degeneration of myocardium, no ventricular hypertrophy but will have dilation
S/S dilated cardiomyopathy
- acute or slowly develops
- fatigue
- dyspnea
- PND
- orthopnea
- heart faiure symptoms
- risk of emboli
- complications: heart failure, SCD, cardiomegaly
diagnosis and tx of dilated cardiomyopathy
DX: cardiac cath, echo, endomyocardial biopsy for infectious organisms
TX: doesnt respond well to therapy, treat like heart failure, may need VAD and ultimately heart transplant
CARE: usually very ill pts with poor prognosis, caregivers must know CPR, goal is to keep them at optimal fxn and out of hospital
hypertophic cardiomyopathy
- 50% is genetic
- assymmetric left ventricular hypertophy without ventricular dilation
- usually diagnosed in young adulthood in active, athletic people
- most common cause of Sudden cardiac death in young people
- most commonly genetic or idiopathic caused
hypertophic cardiomyopathy patho
- enlarged heart muscle with smaller chambers
- massive ventricular hypertrophy
- rapid/forceful contraction of left vent
- impaired relaxation
- obstruction to aortic outflow
- causes decreased CO, especially with exertion
hypertophic cardiomyopathy S/S and DX
- S/S: may be asymptomatic or cause dyspnea, fatigue, syncope, angina
- DX: apical impulse is exaggerated and displaced laterally, s4, systolic murmur, ECG changes, ventricular dysrhythmias
- TX: beta blockers, digoxin, AV pacing
- CARE: avoid strenuous activity and dehydration, vasodilators can make it worse
restrictive cardiomyopathy
- stiff heart muscle that doesnt push blood well
- cause/patho: systolic fxn is unaffected, unknown cause, ventricles are resistent to increasing pressure from filling
- S/S: fatigue, exercise intolerance, dyspnea
- DX: CXR, echo, ecg changes
- TX: no specific treatment, restrict exercise, may consider heart transplant
pt edu for cardiomyopathies
- low sodium diet
- matintain reasonable weight
- avoid stimulants
- balance activity and rest
- ask for exercise guidelines
- stress reduction
- report s/s of heart failure
common causes of vale problems
- IE
- RF
common complications of valve problems
- heart failure
- IE
- emboli
- valve problems
- RF
- infection
IIE treatment
- IV antibiotics for 4-6 weeks
* prophylactic antibiotics before dental procedures
RF treatment
- no antibiotics, NSAIDS, rest
* prophylactic antibiotics before dental procedures
peripheral artery disease of lower extremeties
- involves progressive narrowing and degeneration of arteries of upper and lower extremities
- atheroscleosis is the leading cause in majority of cases
- typically appears at ages 60s - 80s
- largely undiagnoses
- risk factors: cig smoking, hyperlipidemia, hypertension, DM
peripheral artery disease of lower extremeties, clinical manifestations
- syptoms appear when vessels are 60-75% occluded
- classic symptom of PAD = intermittent claudication: ischemic muscle pain that is caused by a constant level of exercise; resolves within 10 minutes or less with rest; reproducible
- paresthesia: numbness or tingling in toes or feet, produces loss of pressure and deep pain sensations, injuries often go unnoticed by patient
- thin, shiny, and taut skin
- loss of hair on lower legs
- diminished or absent pedal, popliteal, or femoral pulses
- pallor of foot with leg elevation
- dependent rubor: redness of foot with dependent position
- pain at rest: occurs in the foot or toes, aggravated by limb elevation, occurs from insufficient blood flow, occurs more often at night
peripheral artery disease of lower extremeties, complications
- atrophy of the skin and underlying muscles
- delayed healing
- wound infection: gangrene, tissue necrosis
- arterial ulcers: may result in amputation
- DX studies: dopper ultrasound, duplex imaging, segmental BPs (drop of greater than 30 mmhg), ankle brachial index, angiography
ankle-brachial infect (ABI)
- done using a hand held doppler
- calculated by dividing the ankle systolic BPs by the higher of the left and right brachial systolic BP
- normal is 0.91-1.30 and indicates adequate BP in the extremities
- an ABI between 0.71 and 0.90 indicates mild PAD
- ## between 0.41 and 0.70 indicates moderate PAD
peripheral artery disease risk factor modification
- decrease stress, caffeine, nicotine
- control HTN
- aggressive treatment of hyperlipidemia
- BP maintained
peripheral artery diease drug therapy
- tx is necessary regardless of symptoms
- ACE inhibitors: ramipril (Altace), decrease cardiovascular morbidity, decrease mortality, increase peripheral blood flow, increase ankle brachial index, increase walking distance
drugs prescribed for intermittent claudication
- cilostaol (pletal): inhibits platelet aggregation, increases vasodilation
- pentoxifylline (trental): increases erythrocyte flexibility, decreases blood viscosity
PAD nursing care
- exercise: walk until pain, rest, then walk further
- limit elevatin of legs (stops blood flow)
- dont cross legs
- no restrictive clothing (TEDs)
- can apply warmth but NOT cold (vasoconstriction is bad)
- may be on low dose of aspirin and/or plavix
leg with critical limb ischemia
- revascularization via bypass surgery
- protect fro trauma
- decrease ischemic pain
- prevent control infection
- improve arterial perfusion
- other: spinal cord stimulation to decrease pain, angiogenesis to stimulate blood vessel growth
interventional radiology procedures for PAD
indications:
1) intermittent claudication symptoms become incapacitating
2) pain at rest
3) ulceration or gangrene severe enough to threaten viability of the limb
interventional radiology procedures for PAD, percutaneous transluminal angioplasty (PTA)
- involves the insertion of a catheter through the femoral artery
- catheter contains a cylindrical balloon
- balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining
- stent is placed
interventional radiology procedures for PAD, atherectomy
- removal of the obstucting plaque
- performed using a cutting disc, laser
interventional radiology procedures for PAD, cryoplasty
- combines percutaneous transluminal angioplasty and cold therapy
- liquid nitrous oxide
surgical therapy for PAD
- peripheral artery bypass surgery with autogenous vein or synthetic graft to bypass blood around the lesion
- PTA with stenting may also be used in combination with bypass surgery
aortic aneurysm
- out pouching or dilation of aortic wall
- occur in men more often than women
- incidence increases with age
- most serious PAD disorder
etiology and pathology of aortic aneurysm
- may have aneursym in more than one location, most occur in the renal artery
- aorta larger than 3cm in diameter is considered aneurysmal
- growth rate unpredictable, the larger the aneurysm the greater the risk of rupture
- dilated aortic wall becomes lined with thrombi that can embolize –> leads to acute ischemic symptoms in distal branches
- true aneurysm: involves all 3 layers of artery
- false aneurysm: not aneurysm but leaking hole in arterial wall
- causes: degenerative, congenital, mechanical (trauma), inflammatory, infectious, most common = atherosclerosis
risk factors for aneurysm
- age
- male
- high BP
- coronary artery diease
- family history
- high cholesterol
- lower extremeity PAD
- carotid artery disease
- previous stroke
- smoking
- obesity
- white and native americans have high risk than AA
S/S aneurysm
- signs and sypmtoms depend on location
- oftentimes asymptomatic
- found on routine exam or when evaluated for another problem
- may have pulsating mass or bruit
- back or abdominal pain
- complication: rupture causing massive hemorrhage and hypovolemic shock
DX and TX of aneurysm
- dx: CT is best, Xray, ecg to r/o MI, ultrasound, nangiography
- tx: control BP, modify risk factors, monitor size, goal is to prevent rupture and extension, be conservative is
nursing care with repair for aneurysm
- ICU for 1-2 days post op
- Circulatory
- Movement
- Sensation
- Temperature
- lost of pain post op
- watch for dysrhytmias, increased 02 demans
- GI paralytic ileus is common, NG tube
Aortic Dissection
- not a type of aneurysm
- happens after intimal tear or with degredation of teh aortic wall medial layer, worsens with high BP
- risk factors: age, aortitis, trauma, HTN, connective tissue disorders, cocaine use, atherosclerosis, males, pregnancy, margans
- S/S: sudden, severe excruciating chest/back pain radiating to shoulders/neck
- high mortality event
- complications: cardiac tamponade, ruptured aorta, ischemia to spinal cord, kidneys, abdomen
- DX: CT and TEE are standard of care, CXR, MRI
- TX: decrease BP with IV esmolol, endovascular repair or may need surgical repair
- nursing care: frequent, close monitoring of BP, teach about recurrence
acute arterial ischemic problems
- suden interuption in the arterial blood supply
- causes: embolism, thrombosis, trauma; usually lodge in arterial branches or areas of narrowing
- S/S: 6ps (pain, pallor, paralysis, pulselessness, paresthesia, poiklothermia (coolness))
- tx: immediately call HCP, may do IV herparin infusions, may need removal of embolus/thrombus
thromboangitis obliterans (Buerger’s disease)
- nonatherosclerotic, recurrent vaso-occlusive disorder of small arteries/veins in the extremities
- usually occurs in young men with long hx of smoking use but no other CV risk factors, significant periodontisi
- S/S: intermittent claudication, ischemic ulcerations, sensitivity to cold
- dx: by exclusion
- TX: stop tobacco use, avoid trauma, cold to extremities, may need finger or toe amputation
Raynaud’s phenomenon
- episodic vasospasm of fingers and toes
- usually in young women (15-40)
- S/S: digits become white, then blue, then red; throbbing pain, tingling, swelling; attacks c/b cold, stress, tobacco, caffeine
- tx: try to prevent episodes (wear gloves, no tobacco, no caffeine)
- calcium channel blockers may help
venous disorders
- virchow’s triad - primary cause of venous thromboembolism
1) venous stasis: obestiy, pregnancy, afib, long trips, prolonged surgeries, immobility
2) endothelial damage: chemo, diabetes, sepsis, trauma
3) hypercoagulability: blood disorders, corticosteroids, estrogen, tobacco usage
superficial vein thrombosis
- S/S: firm, cordlike vein that is re, warm, tender; may or may not have edema
- usually caused by vein trauma from IV cannulation, varicose veins
- DX: physical exam
- TX: immediate removal of IV catheter, elevate extremity, warm/moist heat, oral NSAIDs, no systemic anticoagulants
Deep Vein Thrombosis
- S/S unilateral edema, pain, paresthesia, warm, red, temp >100.4, tenderness
- complications: PE, chronic venous insufficiency, phlegmasia cerulea dolens (extremity swollen and blue)
- tx: prevention with early walking, change position q 2 hrs, compression stockings, SCDs, may need preventitive anticoagulation
- if confirmed DVT, no SCDs, iv heparin and oral warfrin for 5 days, may need thrombolytcs or surgery
DVT drug thearpy
- goal is to prevent clot formation or further clot development and embolization
- antigoagulants do not dissolve clots (body lyses clot)
- vitamin k antagonists - warfrin
- direct thrombin inhibitors: synthetics
- factor xa inhibitors - not for used with renal problems or artifical valves
- ASA alone is not recommended
vitamin k antagonists
- reduce blood clotting by inhibiting vitamin k
- warfarin - oral
- used for longer tem anticoagulation
- takes 3-4 days to start working so need to overlap with heparin for 5 days
- monitor levels with INR
- dont give with ASA, NSAIDs, dilantin
- levels affected by green, leafy veggies
- vitamin k is antidote
heparin
- heparin is SQ (prevention) or IV (VTE tx), LMWH is SQ
- closely monitor aptt levels
- cx: bleeding, Heparin induced thrombocytemia
- LMWH: fewer complications and does not typically require monitoring and dose adjustment
- protamine sulfate is antidote
direct thrombin inhibitors
- hirudin derivatives or synthetic, IV or SC
- refludan, angiomax, acova, arixtra
- can be used for pts with HIT
- monitor aptt or activated clotting time
- no antidote
novel oral anticoagulants
- dabigatran, rivaroxaban, apixaban, edoxaban
- no antidote
- clinically equivalent to warfrin
- costly
- for use in Afib to prevent stroke or after DVT occurence
surgical management of DVTs
- thrombectomy: not used uless it is a huge occlusion; removal of clot
- inferior vena cava filter: for recurrent DVT or PE prevention
DVT nursing care
- bed rest with limb elevation for acute DVT
- no massage or SCDs for acute DVT
- assess for PE (SOB, chest pain)
- teach about prevention and risk factors: smoking, no oral BC, prevent dehydration, no pillows behind knees, no crossing legs, ambulate, ROM, get moving, compression stockings, SCDs
_ TEDs = veins, no teds for arteries - clot = teds
- prevent clot = teds and SCDs
varicose veins
- cause/patho: congenital vein weakness, previous VTE, can also have them in the esophagus, spermatic cords, anorectal areas lots of risk factors
- S/S: heavy, achy feeling after prolonged standing, swelling, leg cramps, looks ugly
- cx: superficial vein thrombosis
- dx: by appearance, duplex ultrasound
- tx: not for cosmetic reasons, sclerotherapty (injected chemical into vein), laser therapy, vein ligation/removal
chronic venous insufficiency and leg ulcers
- cause/patho: occurs rom vein valve incompetence, common in elderly, not life threatening
- S/S: lethargy, brown skin, prolonged edema, stasis dematitis, itching, painful ulcers, no claudication
- cx: cellulitis, slow wound healing
- tx: compression therapy, moist dressings, good diet, weight loss, tight blood glucose control, no antibiotics unless signs of infection
- care: TED hose day and evening, legs elevated 4-5 x day
arterial disease
- pain: sharp, intermittent claudication, relieved by rest
- pulses: decreased absent
- edema: none
- skin: cool, shiny, scaly, hairless, pale when elevated and red when dependent
- tx: compression thearpy, moist fressings, good diet, weight loss, tight blood glucose control, no antibiotics unless signs of infection
venous disease
- pain: aching, deep, heaviness, fatigue, relieved by activity or elevation
- pulses: present
- edema: present
- skin: warm, thickened, tough, dark/bronze, rubor, stasis ulcers
- tx: elevate, TED hose/compression