Exam 1: perfusion Flashcards

1
Q

term:

end diastolic volume =

A

preload

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2
Q

if we need to INCREASE preload, what do we manipulate? and how?

A

volume - give fluids

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3
Q

if we need to DECREASE preload, what do we manipulate?

A

volume - diuretics

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4
Q

term:

pressure at the end of systole/resistance the heart must overcome to perfuse the body

A

afterload

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5
Q

if we need to INCREASE afterload, what do we do?

A

give vasoconstrictors

(shock)

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6
Q

if we need to DECREASE afterload, what do we do?

A

give vasodilators / antihypertensives

(HTN)

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7
Q

type of valvular heart disease:

Prevents normal blood flow from left atrium to left ventricle b/c of narrowing

A

mitral valve stenosis

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8
Q

with mitral valve stenosis (blood doesn’t flow properly from L atrium to L ventricle), what is happening to the flow of blood…. walk through the patho

A

blood flow increased in left atrium… then backs up into lungs… then causes right ventricle to hypertrophy b/c of increased pulmonary pressure –> R sided HF

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9
Q

with mitral valve stenosis, when would the murmur be heard?

A

diastole (when valve is open)

not open enough so makes an abnormal sound

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10
Q

s+s of mitral valve stenosis (incl. manifestations you’d see further on in disease progression)

A

pulmonary congestion (coughing, dyspnea): r/t increased atrial pressure / L sided HF

R sided HF (JVD, edema, splenomegaly)

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11
Q

type of valvular heart disease:

Fibrotic and calcific changes that prevent the mitral valve from closing during systole; backflow of blood into left atrium

A

mitral valve regurgitation

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12
Q

which valvular heart disease puts a person at highest risk of a fib?

A

mitral valve regurgitation

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13
Q

what changes in the atrium and ventricle occur with mitral valve regurgitation ?

A

BOTH hypertrophy!!

atrium b/c of increased blood flow BACK into atrium
ventricle b/c of the excess blood flow from atrium spilling back into ventricle when valve opens again

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14
Q

with mitral valve regurgitation, when would the murmur be heard?

A

systolic (when mitral valve is supposed to be CLOSED, blood is flowing back which causes abnormal sounds)

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15
Q

s+s of mitral valve regurgitation

A

L sided HF
(Fatigue, weak, anxious, SHOB, etc)….. eventually leads to R sided HF

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16
Q

hallmark assessment finding of mitral valve prolapse

all she wanted us to know

A

“clicking sound” murmur

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17
Q

what is most common cardiac valve dysfunction?

A

aortic stenosis

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18
Q

type of valvular heart disease:

Aortic valve narrows and prohibits normal left ventricular outflow

A

aortic stenosis

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19
Q

with aortic stenosis, what is happening to the flow of blood…. walk through the patho

A

blood cannot flow properly from L ventricle to aorta, so pressure builds in the L ventricle, causing L ventricle hypertrophy… then L sided HF…..then eventually backs up into the lungs….& eventually causes R sided HF

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20
Q

aortic stenosis caused a person to have a fixed _____ ______

A

cardiac output
(cannot meet demands of body)

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21
Q

which valvular disease is most associated with major activity intolerance?

A

aortic stenosis (r/t fixed CO)

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22
Q

with aortic stenosis, when would the murmur be heard?

A

systole (when valve is OPEN)

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23
Q

name some s+s of aortic stenosis (4)

A
  1. activity intolerance
  2. syncope
  3. fatigue
  4. peripheral cyanosis

= all r/t fixed cardiac output

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24
Q

type of valvular heart disease:

Aortic valve leaflets don’t close well during diastole; Blood flows back from aorta to left ventricle

A

aortic regurgutation

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25
Q

with aortic regurgitation, when would the murmur be heard?

A

diastole (when aortic valve should be CLOSED)

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26
Q

aortic regurgitation causes what to happen to the left ventricle?

A

hypertrophy (b/c of increased pressure from backflow of blood)

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27
Q

s+s of aortic regurgitation

A

L sided HF s+s
difficulty breathing
nocturnal dyspnea/angina
…later on, R sided HF s+s

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28
Q

gold standard for valvular heart disorderdx

A

Echocardiogram (US of heart)

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29
Q

general intervention for valvular heart disease (once they’ve developed symptoms of HF)

A

manipulating preload and afterload

ex: diuretics (preload), BBs (afterload), dig (contractility), anticoagulants (a fib)

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30
Q

procedures to address valvular heart disease (2)

A
  1. balloon valvuloplasty (stenotic valves)
  2. TAVR (valve replacement)
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31
Q

with valve replacement surgery, which population would you choose to receive a prosthetic/mechanical valve? what about a biologic valve? whyy?

A

prosthetic/mechanical: young person (will last longer, requires lifetime anticoagulation)

biologic: older person (doesn’t last as long, doesn’t require lifetime anticoagulation)

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32
Q

post open heart surgery for valve replacement, what main things should you monitor for? (2 - broad)

A
  1. cardiac output
  2. HF s+s
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33
Q

what is main infection risk with valve replacement heart surgery?

A

infective endocarditis !! (will be on prophylactic ABX)

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34
Q

what is happening in the heart with infective endocarditis?

A

infective vegetation (bacteria, platelets, fibrin) grown on valve –> DESTROYS VALVE

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35
Q

symptoms for infective endocarditis often occur how long after exposure? what are 2 major s+s?

A

2 weeks
1. fever
2. new onset murmur

36
Q

biggest concern for embolization of vegetation with infective endocarditis

A

PE!!

(vegetation traveling to pulmonary system)

37
Q

what are 2 unique symptoms of PE r/t infective endocarditis?

A
  1. petechiae
  2. splinter hemorrhages
38
Q

diagnostics used for infective endocarditis (2)

A
  1. blood cultures (to determine which ABX to use)
  2. echocardiogram
39
Q

what is main intervention for infective endocarditis?

A

long term IV ABX (4-6 weeks)

40
Q

term:

Subacute or Chronic Disease of the Cardiac Muscle

A

cardiomyopathy

41
Q

which type of cardiomyopathy has a high rate of ventricular dysrhythmias?

A

Hypertrophic Cardiomyopathy
(asymmetric hypertrophy of ventricle)

42
Q

Hypertrophic Cardiomyopathy is most commonly seen with which population?

A

young athletes

43
Q

intervention for hypertrophic cardiomyopathy + what these patients need to avoid

A

implanted cardiac defibrillator

avoid extreme exercise (marathons)

44
Q

term:

Chest pain that occurs when the heart’s demand for O2 exceeds the coronary arteries’ ability to supply O2

A

angina

45
Q

type of angina:

Occurs with activity
Usually associated with a fixed plaque
Usually relieved by nitroglycerin and rest (within 15 minutes)

A

chronic stable

46
Q

type of angina:

occurs at rest
not relieved by nitroglycerin and rest
unpredictable
lasts longer than 15 mins

A

unstable angina

47
Q

chest pain. what do you do as RN?

A

12 lead, O2, pain assessment

48
Q

acute coronary syndromes include what 2 things?

A
  1. Unstable Angina
  2. Acute Myocardial Infarction (non STEMI or STEMI)
49
Q

a STEMI is what % occlusion?

A

100%!!!

50
Q

a nonSTEMI is what % occlusion?

A

80-90%

51
Q

unstable angina

what are the changes in EKG and cardiac enzymes?

A

ST segment changes (depression)

NO CHANGE in cardiac enzymes

52
Q

term:

Heart tissue is deprived of oxygen –> TISSUE IS DAMAGED/DYING

A

acute MI

53
Q

ischemia develops when blood flow is reduced by what %?

A

80-90%

54
Q

term:

No ST elevation on EKG

A

non-STEMI

55
Q

non-STEMI

what are the changes in EKG and cardiac enzymes?

A

ST changes (depression) + T wave changes (inversion)

cardiac enzymes ELEVATED

56
Q

what is happening with a STEMI (re: EKG, occlusion, tissue)?

A

ST elevation
100% occlusion
Tissue is dying

57
Q

an older person that’s compensated for long term CAD has better outcomes rather than younger person b/c of this:

A

collateral circulation

58
Q

tissue remodeling after MI occurs when? / needs revascularization within this time frame

KNOW

A

within 6 hours

59
Q

re: MI, if revascularization doesn’t occur, what happens to the heart? (series of events)

A

scar tissue –> ventricular remodeling –> increased risk of ventricular dysrhythmias :(

60
Q

re: MI, where is the worst place for a blockage to occur??

A

left anterior descending (supplies left ventricle)
= widow maker

61
Q

re: MI diagnostics, which cardiac enzyme is most cardiac specific?

A

troponin (1st on the scene)

62
Q

re: MI, what is the best way to see occlusion?

A

cardiac catheterization

63
Q

what is troponin? when is it released? when does it peak?

A

released in response to damage to the cardiac muscle

within 2-4 hours

peaks 12 hours

64
Q

troponin can remain elevated for how many days?

A

14 !!

65
Q

priority interventions for MI

A

pain management (uses up O2)
O2
ASA (chew 325)

66
Q

why would beta blockers be indicated for MI?

A

slow HR, reduce ventricular remodeling, decrease mortality rate after MI

67
Q

re: MI, tPa should be given within what time frame? and for which type of ACS only?

A

within 6 hours of event

STEMI only

68
Q

re: MI, percutaneous coronary intervention should happen within what time frame?

A

within 2-3 hours of event

69
Q

what would be the assessment findings that indicated perfusion had been restored? (2)

A

EKG changes are RESOLVED ◡̈

no pain ◡̈

70
Q

with patient post-MI, which of the following are NOT ok after fibrinolytic therapy?

  1. excessive bleeding from gums
  2. excessive bleeding from IV site
  3. changes in LOC
  4. ventricular tachycardia that goes away
A
  1. changes in LOC = NOT OKAY!

all the others are okay. excessive bleeding should be assessed, but is not grounds to stop the fibrinolytic infusion. ventricular tachycardia is common reperfusion dysrhythmia and shows therapy is effective.

71
Q

after MI, what medications would you expect the patient to be on?

A
  1. ASA
  2. plavix (1 yr)
  3. beta blocker (indefinitely - prevent ventricular remodeling)
72
Q

term:

invasive method of measuring pressures in heart and vessels; Inserted into the right side of heart

A

pulmonary artery catheter

73
Q

term: cardiac output specific to patient size

A

cardiac index

74
Q

term: direct measurement of arterial blood pressure (inserted into radial artery or femoral artery)

A

arterial line (art line)

75
Q

term: occluded coronary arteries are bypassed with the patient’s venous, arterial or synthetic grafts

A

coronary artery bypass graft (CABG)

76
Q

all MI patients should have referral for what?

A

cardiac rehabilitation

77
Q

term:

dilation of artery; middle layer of artery weakens; outer layers stretch

A

aneurysm

78
Q

what increases chance of aneurysm rupture?

A

HTN

79
Q

biggest risk factor for aneurysm

A

atherosclerosis

80
Q

s+s of abdominal aortic aneurysm (3)

A
  1. abdominal, flank or back pain
  2. pulsation in upper abdomen
  3. bruit listen, no palpation
81
Q

s+s of thoracic aortic aneurysm (4)

A
  1. back pain
  2. SHOB
  3. hoarseness
  4. difficulty Swallowing
82
Q

s+s of AAA rupture (6)

A
  1. sudden back /abd pain
  2. hypotension
  3. diaphoresis
  4. loss of distal pulse
  5. abd distention
  6. flank bruising (retroperitoneal hemorrhage)

= sudden pain + signs of shock

83
Q

general interventions for AAA (2)

A

monitor for size/growth + control HTN

surgery when certain size

84
Q

term:

tear in inner layer of artery; blood fills in aortic wall

A

aortic dissection

85
Q

s+s of aortic dissection (4)

A
  1. ripping, tearing pain 10/10
  2. diaphoresis
  3. hypertension until worsens…. then sudden hypotension!
  4. feeling of doom

= sudden pain + signs of shock

86
Q

interventions for aortic dissection (5)

A
  1. 2 larger bore IVs –>
  2. reduce BP
  3. pain management
  4. foley (UO monitoring)
  5. surgery