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Med Surge 1 > Exam #3 > Flashcards

Exam #3 Flashcards

1
Q

structures and fxns of cardo system

A
  • 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
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2
Q

cardiac valves

A
  • 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
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3
Q

auscultation areas

A 
aortic
pulmonic
erb's point
tricuspid
mitral
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4
Q

blood flow through the heart

A
  1. right atrium receives venous blood from the inferior and superior vena cava –> blood passes through tricuspid valve into the right ventricle
  2. with contraction, the right ventricle pumps blood through pulmonic valve into pulmonary artery and to the lungs
  3. oxygenated blood flows from the lungs to the left artium by way of the pulmonary veins
  4. oxygenated blood flows through mitral valve and into left ventricle
  5. heart contracts, blood is ejected through the aoritc valve into the aorta and enters systemic circulation
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5
Q

coronary arteries and veins

A
  • 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
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6
Q

heart’s mechanical system

A
  • 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
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7
Q

cardiac output

A
  • 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

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8
Q

preload

A
  • 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
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9
Q

afterload

A
  • 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
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10
Q

systemic vascular resistence

A
  • opposition encountered by left ventricle
  • increased with vasoconstricotrs, low volume
  • decreased with vasofilators, morphine, nitrates, high co2
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11
Q

pulmonary vascular resistance

A
  • opposition encountered by right ventricle
  • increased with pulmonary hypertension, hypoxia
  • decreased with meds (calcium channel blockers, aminophyline, isoproterenol, oxygen)
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12
Q

contractility

A
  • 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
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13
Q

preload problems

A
  • JVD

- lung sounds

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14
Q

afterload problems

A
  • BP
  • skin temp
  • pulse pressure
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15
Q

contractility problems

A
  • junction fraction
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16
Q

factors affecting heart rate

A
  • autonomic nervous system (ANS)
  • SNS: adrenaline, speeds up everything, vasoconstriction
  • PNS: vagus nerve, slows everything down, vasodilation
  • baroreceptors (perssure) and chemoreceptors (co2 and o2)
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17
Q

blood pressure

A
  • systolic blood pressure: 60 is needed to perfuse organs

- MAP = (syst BP + 2x dia BP)/3

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18
Q

gerontologic considerations

A
  • 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
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19
Q

AFIB

A
  • controlled: vent rate 100 HR
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20
Q

risk factors for heart issues

A
  • all are modifiable
  • increased serum lipids
  • hypertension
  • smoking
  • sedentary lifestyle
  • obestiy
  • stress
  • DM
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21
Q

subjective heart assessment

A
  • 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)
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22
Q

stroke volume

A
  • 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

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23
Q

preload

A
  • 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
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24
Q

afterload

A
  • 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
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25
Q

contractiity

A
  • 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
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26
Q

factors affecting stroke volume

A
  • CO = HR X SV
  • preload
  • afterload
  • contractility
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27
Q

preload problems

A
  • JVD

- lung sounds

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28
Q

afterload problems

A
  • BP
  • skin temp
  • pulse pressure
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29
Q

contractility problems

A
  • ejection fraction
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30
Q

factors affecting Heart Rate

A
  • 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)
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31
Q

Blood Pressure

A
  • systolic: 60 needed to perfuse organs
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32
Q

gerontologic considerations

A
  • 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
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33
Q

Afib

A
  • controlled: vent rate 100 HR
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34
Q

cardio risk factors

A
  • increased serium lipids
  • HTN
  • smoking
  • sedentary lifestyle
  • obesity
  • stress
  • DM
  • all modifiable
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35
Q

cardio assessment

A
  • 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
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36
Q

arterial wound vs venous wound

A
  • arterial: smaller, deeper, dryer

- venous: large, shallow, wet, edema/weeping

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37
Q

PMI

A

point of maximal impulse

- if it is found below 5th intercostal space then means enlarged heart

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38
Q

s1

A

closure of tricuspid and mitral valves

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39
Q

s2

A

closure of aortic and pulmonic valves

- s2 splitting heard during expiration not good

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40
Q

s3

A

ventricular gallop

- kentucky

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41
Q

s4

A

atrial contraction (before s1)

  • CAD or cadiomyopathy
  • tennessee
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42
Q

cardiac lab markers

A
  • 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
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43
Q

risk predictors

A
  • c-reactive protein: marker for inflammation; risk factor for CAD
  • homocysteine: elevated levels increased risk for CAD, PVD, and stroke
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44
Q

serum lipids/lipoproteins

A
  • serum lipids/lipoproteins
  • triglycerides (60 is low risk)
  • LDL (
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45
Q

chest x ray

A
  • shows:
  • contours of heart
  • displacement, enlargement
  • fluid
  • pulmonary congestion
  • size of heart
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46
Q

electrocardiogram

A
  • ECG
  • records cardiac electrical activity
  • event monitor or loop recorder
    exercise or stress test
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47
Q

echocardiogram

A
  • ultrasound of heart
  • with/without contrast
  • shows: structures of heart, work of the heart, size, pericardial sac, ejection fraction
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48
Q

nuclear cardiology (MUGA)

A
  • IV injection of radioactive isotope, pay still for 20 minutes with arms up, may have repeat scans
  • structural info and injection fraction
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49
Q

MRI

A
  • noninvasive, but must lie still
  • cant do if they have a pacemaker
  • ejection fraction, MI recovery
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50
Q

CT

A
  • 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
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51
Q

cardiac catheterization

A
  • 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
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52
Q

regulation of BP

A

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
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53
Q

hypertension

A
  • systoldic > 140, diastolic > 90

- diastolic will increased to age 55 then go down, systolic stays the same

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54
Q

prehypertension

A
  • systolic 120-139, diastolic 80-89
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55
Q

isolated systolic HTN

A
  • systolic > 140 with diastolic
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56
Q

psuedohypertension

A
  • false HTN with severe atherosclerosis

- arteries so hard they can’t collapse when BP cuff is on arm

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57
Q

causes of HTN

A
  • 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
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58
Q

pathophysiology of HTN

A
  • heredity
  • water/sodium retention
  • altered RAAS mechanism
  • stress
  • SNS hyperactivity
  • insulin resistence
  • endothelium dysfunction
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59
Q

risk factors for HTN

A
  • age >50
  • alcohol > 1oz/day
  • smoking
  • DM
  • high serum lipids
  • high sodium
  • men 55
  • obesity
  • AA
  • sedentary lifestyle
  • socioeconomic status
  • stress
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60
Q

S/S HTN

A
  • silent killer - S/s often appear after organ disease occurs
  • fatigue
  • activity intolerance
  • dizziness
  • palpitations
  • angina
  • dyspnea
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61
Q

complications with HTN

A
  • 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
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62
Q

diagnostic studies for HTN

A
  • UA, BUN, creatinine (urinalysis)
  • electrolytes
  • blood glucose
  • lipid profile
  • uric acid
  • ECG
  • echocardiogram
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63
Q

treatment for HTN

A
  • goal: BP
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64
Q

lifestyle modificaitions for HTN

A
  • weight reduction
  • DASH eating plan
  • sodium reduciton
  • limit alcohol
  • regular physical activity
  • avoidance of tobacco use
  • stress management
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65
Q

dietary changes for HTN

A
  • 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:
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66
Q

drug therapy for HTN

A
  • diuretics
  • beta blockers
  • ACE inhibitors
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67
Q

diuretics

A
  • 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
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68
Q

beta blockers

A
  • 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
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69
Q

ACE inhibitors

A
  • 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
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70
Q

Angiotensin II receptor blockers ARB

A
  • 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
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71
Q

calcium channel blockers

A
  • 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
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72
Q

alpha adrenergic blockers

A
  • 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
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73
Q

vasodilators

A
  • 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
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74
Q

drug therapy side effects for HTN

A
  • orthostatic hypotension: HR >50 and BP >100 to give meds
  • sexual dysfunction
  • potassium: ACE and ARB can make it high
  • dry mouth
  • nocturia
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75
Q

HTN nursing interventions

A
  • health promotion, lifestyle modifications
  • ambulatory/home care
  • home BP monitoring
  • patient compliance
  • need to be seen monthly until BP is stable
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76
Q

proper BP measurement

A
  • 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
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77
Q

HTN gerontologic considerations

A
  • 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
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78
Q

hypertensive crisis

A
  • 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
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79
Q

hypertensive crisis treatment

A
  • 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
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80
Q

heart failure

A
  • 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
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81
Q

risk factors for heart failure

A
  • CAD, age, HTN
  • diabetes
  • smoking
  • obesity
  • high cholesterol
  • AA
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82
Q

heart failure patho

A
  • 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
83
Q

compensatory mechanisms for heart failure

A
  • 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
84
Q

counterregulatory mechanisms

A
  • 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
85
Q

types of heart failure

A
  • 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
86
Q

s/s of acute HF

A
  • 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
87
Q

s/s chronic HF

A

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
88
Q

s/s right heart failure

A
  • murmors
  • heaves
  • JVD
  • edema
  • weight gain
  • ascites
  • hepatomegaly
  • fatigue
  • nausea
  • anorexia
89
Q

s/s left heart failure

A
  • s3, s4
  • heaves
  • PMI displaced
  • hypoxia
  • crackles
  • dyspnea
  • restlessness
  • confusion
  • fatigue
  • PND, orthopnea
  • cough
  • frothy, pink tinged sputum
90
Q

comlications from heart failure

A
  • 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
91
Q

diagnostic studies for heart failure

A
  • 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
92
Q

ADHF treatment

A
  • 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
93
Q

ADHF treatment drugs

A
  • 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
94
Q

chronic heart failure treatment

A
  • 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
95
Q

chronic heart failure drug treatments

A
  • diuretics - thiazide is first choice
  • ACE inhibitors or ARBs
  • aldosterone antagonists - spirinolactone
  • BiDIl; only for AA
  • use cautiously: best blockers and digoxin
96
Q

nutrtion for heart failure

A
  • always do an assessment, 3 day diary

- sodium restriction

97
Q

heart failure nursing diagnosis

A
  • 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
98
Q

heart failure nursing internventions

A
  • 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
99
Q

when to call Dr for HF

A

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
100
Q

cardiac transplant

A
  • 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
101
Q

valves of the heart

A
  • Atrioventricular valves
  • mitral
  • tricuspid
  • two semilunar valves
  • aortic
  • pulmonic
102
Q

valvular heart diease

A
  • types of valvular heart diease depend on: valve affected, type of functional alterations (stenosis, regurgitation)
103
Q

Stenosis

A
  • stiff valve
  • constricting/narrowing
  • valve orifice is smaller
  • forward blood flow is impeded
  • pressure differences reflect the degree of stenosis
104
Q

regurgitation

A
  • incompetence/insufficiency
  • incomplete closure of valve leaflets
  • reults in backward flow of blood
  • floppy valve
105
Q

mitral valve stenosis

A
  • 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
106
Q

mitral valve stenosis clinical manifestations

A
  • 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
107
Q

mitral valve regurgitation

A
  • 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
108
Q

patho of mitral regurgiation

A
  • incomplete valve closure
  • backward flow of blood
  • acure MR: pulmonary edema, cardiac schock
  • chronic MR: left atrial enlargement, ventricular hypertrophy –> decrease in CO
109
Q

clinical manifestations of mitral regurgitation

A
  • 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
110
Q

mitral valve prolapse patho

A
  • leaflets prolapse back into left atrium during systole
  • unknown cause but genetic link
  • prolapse = buckle = most common cause of valvular heart disease
111
Q

mitral valve prolapse clinical manifestations

A
  • 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
112
Q

patient education for mitral valve prolapse

A
  • antibiotic prophylaxis if MR present
  • take drugs as prescribed
  • healthy diet, avoid caffeine
  • avoid OTC stimulents
  • exercise
113
Q

aortic valve stenosis

A
  • 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
114
Q

aortic valve stenosis patho

A
  • 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
115
Q

aortic valve stenosis clinical manifestations

A
  • angina
  • syncope
  • exertional dyspnea
  • auscultory findings: normal to soft s1, diminished or absent s2, systolic murmur, prominent s4
  • triad of symptoms: angina, syncope, dyspnea
116
Q

aortic valve regurgitation

A
  • acute AR: IE, trauama, aotic dissection
  • life threatening emergency
  • chronic AR: rheumatic heart diease, congenital bicuspid aoritc valve, syphilis, chronic rheumatic conditions
117
Q

aortic valve regurgitation patho

A
  • 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
118
Q

aortic valve regurgitation, acute clinical manifestations

A
  • severe dyspnea
  • chest pain
  • hypotension
  • cardiogenic shock
  • life threatening emergency
119
Q

aortic valve regurgitation, chronic clinical manifestations

A
  • 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
120
Q

tircuspid valve stenosis

A
  • 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
121
Q

pulmonic valve stenosis

A
  • almost always congenital
  • causes right ventricular hypertension and hypertophy
  • clinical manifestations: fatigue, loud murmur
122
Q

valvular heart disease, diagnostic studies

A
  • 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
123
Q

valvular heart disease, conservative management

A
  • 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
124
Q

valvuloplasty

A
  • 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
125
Q

percutaneous tansluminal balloon valvuloplasty

A
  • for older adults who are poor surgery candidates
126
Q

surgical treatment for HF

A
  • 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
127
Q

biologic (tissue) valves

A
  • 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
128
Q

mechanical valves

A
  • more durable, last longer
  • increased risk of thromboembolism
  • requires long-term anticoagulation thearpy
  • complications: bleeding (if on anticoags), valve leakage, endocarditis
129
Q

nursing assessment subjective, HF

A
  • 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
130
Q

nursing assessment objective, HF

A
  • fever
  • diaphoresis, flushing, cyanosis, clubbing, wheezes, hoarseness
  • S3 & S4
  • dysrhythmias
  • increased or decreased in pulse pressure, hypotension
  • thready peripheral pulses
  • hepatomegaly, ascites
  • weight gain
131
Q

HF nursing diagnosis

A
  • decreased cardiac output
  • excess fluid volume
  • activity intolerance (need rest, don’t overexert)
  • deficient knowledge
132
Q

planning for HF

A
  • patient goals: normal cardiac fxn, improved activity intolerance, understanding of the diease process and health maintenance measures
133
Q

health promotion for HF

A
  • 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
134
Q

nursing implementation HF

A
  • individualize rest and exercise
  • avoid strenuous activity
  • discourage tobacco use
  • ongoing cardiac assessments to monitor drug effectiveness
  • monitor INR
135
Q

infective endocarditis

A
  • 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
136
Q

INfective endocarditis etiology and patho

A
  • 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
137
Q

bacterial endocarditis clinical manifestations

A
  • 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
138
Q

endocarditis clincal manifestations

A
  • 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)
139
Q

diagnostic studies for endocarditis

A

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

140
Q

collaborate care for endocarditis

A

prophylactic antibiotic treatment for patients having:

  • certain dental procedures
  • respiratory tract incisions
  • tonsillectomy and adenoidectomy
  • gi wound infection
  • UTI
141
Q

endocarditis assessment

A
  • 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
142
Q

endocarditis nursing implementation

A
  • 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
143
Q

pericarditis

A
  • 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
144
Q

S/S pericarditis

A
  • 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
145
Q

pericarditis diagnostic studies

A
  • ECG: ST elevations different from MI
  • Echo: look for complications
  • high WBC, CRP, ESR = inflammation
  • may send pericardial fluid or tissue for analysis
146
Q

pericarditis complications

A
  • 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
147
Q

pericarditis treatment

A
  • antibitoics, if bacterial
  • NSAIDS for pain and inflamm
  • corticosteroids if not responding to NSAIDs
  • postion upright leaning forward
  • pericardiocentesis (needle inserted to remove fluid)
148
Q

chronic constrictive pericarditis

A
  • 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
149
Q

chronic constrictive pericarditis, diagnosis and treatment

A
  • 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
150
Q

rheumatic fever

A
  • 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
151
Q

RF S/S

A
  • 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
152
Q

RF Complications

A
  • chornic rheumatic carditis
  • reoccurance
  • DX: no single diagnostic test, use criteria
  • TX: antiinflammatories, bedrest
153
Q

RF nursing care

A
  • 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
154
Q

cardiomyopathy

A
  • 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
155
Q

dilated cardiomyopathy

A
  • 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
156
Q

S/S dilated cardiomyopathy

A
  • acute or slowly develops
  • fatigue
  • dyspnea
  • PND
  • orthopnea
  • heart faiure symptoms
  • risk of emboli
  • complications: heart failure, SCD, cardiomegaly
157
Q

diagnosis and tx of dilated cardiomyopathy

A

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

158
Q

hypertophic cardiomyopathy

A
  • 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
159
Q

hypertophic cardiomyopathy patho

A
  • 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
160
Q

hypertophic cardiomyopathy S/S and DX

A
  • 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
161
Q

restrictive cardiomyopathy

A
  • 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
162
Q

pt edu for cardiomyopathies

A
  • low sodium diet
  • matintain reasonable weight
  • avoid stimulants
  • balance activity and rest
  • ask for exercise guidelines
  • stress reduction
  • report s/s of heart failure
163
Q

common causes of vale problems

A
  • IE

- RF

164
Q

common complications of valve problems

A
  • heart failure
  • IE
  • emboli
  • valve problems
  • RF
  • infection
165
Q

IIE treatment

A
  • IV antibiotics for 4-6 weeks

* prophylactic antibiotics before dental procedures

166
Q

RF treatment

A
  • no antibiotics, NSAIDS, rest

* prophylactic antibiotics before dental procedures

167
Q

peripheral artery disease of lower extremeties

A
  • 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
168
Q

peripheral artery disease of lower extremeties, clinical manifestations

A
  • 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
169
Q

peripheral artery disease of lower extremeties, complications

A
  • 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
170
Q

ankle-brachial infect (ABI)

A
  • 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
171
Q

peripheral artery disease risk factor modification

A
  • decrease stress, caffeine, nicotine
  • control HTN
  • aggressive treatment of hyperlipidemia
  • BP maintained
172
Q

peripheral artery diease drug therapy

A
  • 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
173
Q

drugs prescribed for intermittent claudication

A
  • cilostaol (pletal): inhibits platelet aggregation, increases vasodilation
  • pentoxifylline (trental): increases erythrocyte flexibility, decreases blood viscosity
174
Q

PAD nursing care

A
  • 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
175
Q

leg with critical limb ischemia

A
  • 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
176
Q

interventional radiology procedures for PAD

A

indications:

1) intermittent claudication symptoms become incapacitating
2) pain at rest
3) ulceration or gangrene severe enough to threaten viability of the limb

177
Q

interventional radiology procedures for PAD, percutaneous transluminal angioplasty (PTA)

A
  • 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
178
Q

interventional radiology procedures for PAD, atherectomy

A
  • removal of the obstucting plaque

- performed using a cutting disc, laser

179
Q

interventional radiology procedures for PAD, cryoplasty

A
  • combines percutaneous transluminal angioplasty and cold therapy
  • liquid nitrous oxide
180
Q

surgical therapy for PAD

A
  • 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
181
Q

aortic aneurysm

A
  • out pouching or dilation of aortic wall
  • occur in men more often than women
  • incidence increases with age
  • most serious PAD disorder
182
Q

etiology and pathology of aortic aneurysm

A
  • 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
183
Q

risk factors for aneurysm

A
  • 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
184
Q

S/S aneurysm

A
  • 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
185
Q

DX and TX of aneurysm

A
  • 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
186
Q

nursing care with repair for aneurysm

A
  • 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
187
Q

Aortic Dissection

A
  • 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
188
Q

acute arterial ischemic problems

A
  • 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
189
Q

thromboangitis obliterans (Buerger’s disease)

A
  • 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
190
Q

Raynaud’s phenomenon

A
  • 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
191
Q

venous disorders

A
  • 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
192
Q

superficial vein thrombosis

A
  • 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
193
Q

Deep Vein Thrombosis

A
  • 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
194
Q

DVT drug thearpy

A
  • 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
195
Q

vitamin k antagonists

A
  • 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
196
Q

heparin

A
  • 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
197
Q

direct thrombin inhibitors

A
  • 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
198
Q

novel oral anticoagulants

A
  • dabigatran, rivaroxaban, apixaban, edoxaban
  • no antidote
  • clinically equivalent to warfrin
  • costly
  • for use in Afib to prevent stroke or after DVT occurence
199
Q

surgical management of DVTs

A
  • thrombectomy: not used uless it is a huge occlusion; removal of clot
  • inferior vena cava filter: for recurrent DVT or PE prevention
200
Q

DVT nursing care

A
  • 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
201
Q

varicose veins

A
  • 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
202
Q

chronic venous insufficiency and leg ulcers

A
  • 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
203
Q

arterial disease

A
  • 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
204
Q

venous disease

A
  • 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

Med Surge 1 (7 decks)

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