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Med Surg Exam 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What kind of conditions cause HF

A

conditions that directly damage the heart

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2
Q

What disorders directly damage the heart

A

HTN, CAD (MI), inflammatory heart conditions, congenital defects, cardiomyopathy, postpartum, substance abuse, hypertrophic

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3
Q

What kind of conditions are secondary causes for HF

A

any condition that increase the workload of the heart

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4
Q

what conditions increase the workload of the heart

A

sepsis, thyrotoxins, dysrhythmias (a fib or Vtach), obstructive sleep apnea, pulmonary embolism, hypervolemia

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5
Q

how does cardiac cachexia progress

A

early saiety which causes NV which causes anorexia which causes cardiac cachexia

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6
Q

what are some diagnostic tests you could do to get more info on HF

A

Echocardiogram, 12 lead ECG, chest xray, 6 min walk test, cardiopulmonary stress test, heart cath, endomyocardial biopsy

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7
Q

what does echocardiogram test show you

A

gives info on ejection fraction, shows heart chambers to differentiate between systolic and diastolic HF

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8
Q

what are some ss you would expect to find in someone with HF

A

fatigue, dyspnea, orthopnea, tachycardia, noctura, early satiety,

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9
Q

what does FACES stand for when describing HF ss

A

fatigue, activity limitation, chest congestion/cough, edema, shortness of breath

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10
Q

what are some objective data you will collect when evaluating someone for HF

A

of pillows used, paroxysmal noctural dyspnea, insomnia, chest pain, RUQ pain, abdominal discomfort (from congested liver), behavioral changes, vision changes

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11
Q

what are some subjective data you will collect when evaluating someone for HF

A

skin color, temp changes, edema, RR, lung sounds, frothy blood tinged sputum, HR, abdominal distention, LOC changes, I/O

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12
Q

do you want a positive or negative I/O

A

negative so you know fluid is coming off

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13
Q

what happens to BNP and NT-ProBNP levels with worsening HF

A

increase

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14
Q

what are some ss of pleural effusion

A

dyspnea, cough, chest pain

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15
Q

what kind of dysrhythmias could be caused by HF

A

Afib Vtach

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16
Q

how could HF cause LV thrombus

A

from decrease ejection fraction — risk for stroke

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17
Q

how could HF cause hepatomegaly

A

RV failure = congested liver = decrease liver function= liver cells die = fibrosis and cirrhosis

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18
Q

how could HF cause Renal failure

A

decrease perfusion can lead to insufficiency or failure

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19
Q

what are the goals for treating HF

A

treat the underlying cause, maxamize CO, decrease symptoms, improve ventricular function, preserve target organs

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20
Q

how does ultrafiltration work

A

advanced treatment that works as a form of dialysis for fluid volume overload and resistance to diuretics

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21
Q

if you couldn’t use ultrafiltration what is another advanced treatment option

A

circulatory assistance devices

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22
Q

how do cardiomems work

A

device to help monitor pulmonary pressure remotely (aka at home) via implanting the device in the distal pulmonary artery then at home the patient can lay on a special pillow that will send the info straight to the doctor

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23
Q

how does left ventricular device work

A

assist the failing LV by continuous flow - the heart is pumped via a driveline that exits the abdominal wall and is attached to a system controller with patient specific settings

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24
Q

what must a patient still get for a left ventricular device

A

electrical conduction like ICD/PM

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25
Q

what are the patient risks for a left ventricular device

A

infection, stroke, bleeding (warfarin),

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26
Q

what is the intervention of choice for HF

A

Bi-pap + diuretic + nitro

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27
Q

how does cardiac resynchronizing work

A

an extra lead is placed in the LV and RV to aide in contractions to increase LV function and CO

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28
Q

why would someone need cardiac resynchronizing

A

because of remodeling causing dysrhythmias in LV and RV which can cause wide bundle branch block

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29
Q

how does a extracorporeal membrane oxygenation (ECMO) work

A

providing prolonged cardiac and respiratory support to a person whose heart and lungs are unstable to give adequate amount gas exchange or perfusion to sustain life

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30
Q

what are the risks for the patient receiving ECMO treatment

A

bleeding, stroke, infection, pressure, ulcer

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31
Q

how long can a patient be on ECMO

A

only temporary support

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32
Q

what kind of nutrition teaching would you give for someone with HF

A

smaller meals, low sodium (2g daily), fluid restriction (1.5-2L a day),

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33
Q

What should someone consider when evaluating weight of a person with HF

A

daily weight (gain of 3lbs over 2 days or 3-5 over a week should be reported to doc)

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34
Q

whos treatment of choice is heart transplant

A

refractory end stage HF, inoperable CAD, cardiomyopathy,

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35
Q

what are some immunosuppresants someone with a heart transplant would take

A

predisone, cyclosporine/tacrolimus, myophenolate mofetil

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36
Q

how often is a endomyocradial biopsy taken after transplant

A

from RV weekly for first month, then monthly for next 6 months then yearly

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37
Q

why is endomyocradial biopsy taken after transplant

A

to detect rejection

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38
Q

what kind of evaluation is done from someone trying to get a new heart

A

physical, diagnostic, and psychological

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39
Q

when could acute rejection of a heart transplant happen

A

within a year

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40
Q

why is malignancy a complication of heart transplant

A

because of the immunosuppresants

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41
Q

how can you determine cardiogenic shock via BP

A

systolic BP less then 90 for 30 min or more with tachycardia

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42
Q

what are the ss of cardiogenic shock

A

poor tissue perfusion (oliguria, cyanosis, cool extremities, altered mental status)

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43
Q

what would lactate levels look like in cardiogenic shock

A

Increased levels - tell tissue death

44
Q

what would pulmonary capillary wedge pressure levels look like in cardiogenic shock

A

greater then 15

45
Q

what would cardiac index levels look like in cardiogenic shock

A

less then 2.2 = wet and cold

46
Q

what kind of drugs would be used in patients with inadequate tissue perfusion and adequate intravascular volume

A

inotropic and or vasopressors to maintain MAP at 60-65, to decrease plasma volume and peripheral edema

47
Q

what is the focuses of treatment for cardiogenic shock

A

fluid resuscitation (brings BP and volume up), restoration of coronary blood flow, correction of electrolytes and acid base balance (low K and Magnesium and acidosis), place central line (to monitor central venous pressure), arterial line (continuous BP monitoring)

48
Q

who would you not want to give fluid resuscitation to

A

someone with pulmonary edema

49
Q

how does renin-angiotensin- aldosterone compensate for heart overload

A

the decrease on CO cause a decrease blood flow to the kidneys (decrease volume) so the RAAS system holds fluid and salt which causes vasoconstriction which will increase BP

50
Q

how does ventricular remodeling compensate for heart overload

A

hypertrophy and dilation of ventricles

51
Q

what can ventricular remodeling negatively cause

A

Dysrhythmias and sudden cardiac death

52
Q

what beta blockers are used to help in heart overload

A

metoprolol and carvedlol

53
Q

what 2 meds are more effective in treating heart overload in African Americans

A

hydralazine and isosorbine

54
Q

what diuretics are used for heart overload

A

lasix, bumex,

55
Q

when taking lasix and bumex what should you monitor for

A

hyperkalemia

56
Q

what are the outcomes you want for taking bumex and lasix for heart overload

A

decrease edema, water/sodium secretion

57
Q

what are the ss of digoxin toxicity

A

N/V/D, lethargic, visual halo, decrease HR

58
Q

how does the SNS compensate for heart overload

A

releases catecholamine (norepinephrine and epinephrine) to increase HR and increase myocardial contractility, and peripheral constriction to increase BP

59
Q

what meds inhibit RAAS system

A

ACE, ARBs, aldosterone antagonist or entrestochew (in place of ACE or ARB)

60
Q

what should you monitor in someone taking an ACE

A

hypotension, cough, hyperkalemia, angioedema, and renal insufficiency

61
Q

what does ACEs end in

A

pril

62
Q

what should you monitor for in someone taking an ARB

A

hypotension, hyperkalemia, and renal insufficiency

63
Q

what do ARBs end in

A

sartan

64
Q

who shouldn’t take entrestochew

A

if history of angioedema

65
Q

what should you monitor for when someone is taking aldosterone antagonist

A

hyperkalemia

66
Q

what are some positive inotropic agents

A

digoxin or malirione

67
Q

when should you not give digoxin

A

narrow therapeutic window so hold if HR less then 60 and never redose

68
Q

when is malirione used

A

as a last resort because it requires continuous infusion via PICC

69
Q

what happens to ejection fraction for systolic heart failure

A

reduced ejection fraction less then 40% can be as low as 5-10%

70
Q

what is normal ejection fraction of the heart

A

55-60%

71
Q

what could be some causes of systolic heart failure

A

impaired contractile fraction (MI), increased afterload (HTN), cardiomyopathy, mechanical abnormalities (valve issues)

72
Q

what happens to the heart for diastolic heart failure

A

ejection fraction is good but the ventricles arent filling up enough

73
Q

how could you diagnosis diastolic HF

A

looks like the muscle is too thick

74
Q

what type of med could you give to improve diastolic HF

A

decrease HR to allow the ventricles to fill more

75
Q

what could cause diastolic hf

A

LV hypertrophy from HTN, older age, DM, Obesity

76
Q

what is the most common cause of left sided heart failure

A

HTN and CAD = LV dysfunction

77
Q

what are some ss of left sided HF

A

paroxysmal noctural dyspnea, increased pulmonary wedge pressure, restlessness, increased HR, cyanosis, pulmonary congestion (cough, crackles, blood-tinged sputum)confusion, external dyspnea

78
Q

what implantation is recommended in LV dysfunction

A

cardioverted defib because they are more at risk for sudden cardiac death

79
Q

what happens in the heart for left sided HF

A

blood backs up into the LA and pulmonary veins which increase pulmonary pressure causes leaks = pulmonary congestion

80
Q

what causes right sided HF

A

most common is left sided HF, other causes could be RV infarction, pulmonary embolism, pulmonary hypertension

81
Q

what are the ss of right sided HF

A

fatigue, increase peripheral venous pressure, ascites, enlarged liver/spleen, distended jugular vein, weight gain, dependent edema

82
Q

what happens in the heart in right sided HF

A

fluid backs up in venous system by fluid moving into tissue and organs

83
Q

what does dry - warm mean for acute decompensated HF

A

dry lungs, good perfusion

84
Q

what does dry- cold mean for acute decompensated HF

A

dry lungs, poor perfusion

85
Q

what does wet - warm mean for acute decompensated HF

A

wet lungs, good perfusion

86
Q

what does wet-cold mean for acute decompensated HF

A

wet lungs, poor perfusion

87
Q

what is the early progression of acute decompensated HF

A

increased pulmonary venous pressure (increased HR, decreased PaO2)

88
Q

when do you need to intervene for someone PaO2 levels

A

lower then 60 with bi-pap

89
Q

what is the later progression of acute decompensated HF

A

Interstitial edema (tachypnea)

90
Q

what is the final progression of acute decompensated HF

A

Alveolar edema (respiratory academia = decreased PaO2 and increased Co2) leads to cariogenic shock

91
Q

what is normal PaO2

A

60-80

92
Q

why are diuretics used in acute decompensated HF

A

to decrease volume overload (preload)

93
Q

why are vasodilators used in acute decompensated HF

A

to decrease afterload and improve coronary artery circulation

94
Q

when titrating nitroglycerin (vasodilator) what do you need to do

A

monitor every 5-10min for decreased BP

95
Q

why is morphine used for acute decompensated HF

A

to decrease preload and afterload, relieve dyspnea/anxiety

96
Q

why are positive inotropes used for acute decompensated HF

A

increase myocardial contractility

97
Q

what meds should you stop if they have acute decompensated HF

A

beta blockers

98
Q

what are some positive inotropes

A

milrione, digitails, and b-agonists (beta blockers)

99
Q

what are some ss of acute decompensated HF

A

sudden onset of HF ss, most common is pulmonary edema from pulmonary and systemic congestion due to increase left and right sided filling pressure

100
Q

what is normal Co2

A

35-45

101
Q

what should you monitor for acute decompensated HF

A

Continuous VS,O2, UOP, hemodynamic monitoring (BP), pulmonary artery cath to evaluate CO and pulmonary artery wedge pressure

102
Q

how is therapy titrated for acute decompensated HF

A

to maximize CO and pulmonary artery wedge pressure, so using supplemental O2, Bipap (mech vent if unstable), and high fowlers

103
Q

what is normal pulmonary artery wedge pressure

A

8-12

104
Q

what is the pulmonary artery wedge pressure in someone with acute decompensated HF

A

over 15 can be as high as 30

105
Q

what are some ss of pulmonary edema

A

anxious, pale, cyanotic, cool, clammy skin, dyspnea, orthopnea, increased RR (over 30), cough with frothy sputum, crackles, wheezes, increased HR, decreased BP

Med Surg Exam 2 (8 decks)

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