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NURS 2500 > Class 24: Heart Failure > Flashcards

Class 24: Heart Failure Flashcards

1
Q

describe the differences in pressure in the pulmonary arteries, left ventricle, systemic bp, and CVP (around the right atrium)
what does this mean

A
  • pulmonary & CVP = very low
  • LV and systemic = higher

= does not take much increase in pressure to cause edema in the pulmonary artery & CVP

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2
Q

what is SBP and DBP

A
  • systolic blood pressure

- diastolic blood pressure

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3
Q

what is pulse pressure

A

systolic pressure - diastolic

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4
Q

what is MAP

A
  • average blood pressure in arteries during one cardiac cycle
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5
Q

what is the formula for MAP

A

SBP +DBP + DBP /3

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6
Q

what is CVP

A
  • central venous pressure = pressure around R atrium
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7
Q

what is CVP reflected by

A
  • JVP
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8
Q

what is LVEDV/P

A
  • left ventricle end diastolic volume or pressure from the volume
    = preload
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9
Q

what is SVR

A

-systemic vascular resistance = afterload

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10
Q

what is PVR

A
  • pulmonary vascular resistance
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11
Q

what is SV

A
  • stroke volume

- vol of blood pumped out per contraction

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12
Q

what is EF

A
  • ejection fraction
  • what percent of blood in the ventricle is pumped with contraction
  • tells us how good the heart is pumping
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13
Q

how is EF determined

A

SV / EDV

%

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14
Q

what is CO

A

how much blood pumped per minute

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15
Q

what is CI

A
  • cardiac index
  • CO adjusted for body size
  • relates the estimation of CO related to someones size
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16
Q

what does the heart need to be effecient

A
  • volume & pressure
  • mechanical structures
  • electrical conduction
  • fuel (O2 and nutrients)
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17
Q

where does fluid in the RV get backed into

A
  • body & JV
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18
Q

where does fluid in the LV get backed into

A
  • lungs = pulmonary edema
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19
Q

what is normal EF? what is significantly low?

A
  • normal = 50-60

- low = less than 30%

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20
Q

what are important mechanical structures of the heart

A
  • heart muscle

- valves

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21
Q

what dont you want to occur in heart muscle

A
  • hypertrophy

- dilation

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22
Q

what dont you want to occur with the heart valves

A
  • no regurgitation (leaky = blackflow)

- no stenosis

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23
Q

what is aortic stenosis

A
  • aortic valve gets smaller = hard to get blood through = increased afterload
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24
Q

what is the formula for CO

A

= HR x SV

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25
Q

what is the formula for BP

A

= CO x SVR

= HR x SV x SVR

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26
Q

how does theSNS & kidneys compensate for low bp, CO, and perfusion

A
  • increased HR
  • increased contracility
  • fill up more = increased preload (thru RAAS)
  • carry more stuff: increased Hgb, RR, O2
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27
Q

what occurs if compensation becomes chronic (aka during HF)? what does this lead to?

A
  • remodelling

- changes in shape of heart = further HF & decompensation

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28
Q

what results from the heart pumping faster

A
  • increased workload
    = exhaust
  • consider reserve
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29
Q

what is cardiac reserve

A
  • range between normal pumping & maximum pumping for exertion, SNS, etc.
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30
Q

describe cardiac reserve in an athlete

A
  • high cardiac reserve
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31
Q

describe cardiac reserve in a HF pt

A
  • EF < 30% = low cardiac reserve

- can’t ask too much extra of the heart

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32
Q

what remodelling occurs with the heart squeezing harder

A
  • increased workload = hypertrophy = thickening
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33
Q

what remodelling occurs from the heart filling up more

A

= stretch = dilation = bigger & thinner

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34
Q

how does the RAAS respond to the low bp

A
  • triggers vasoconstriction & keep more fluid

= increased afterload

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35
Q

what remodeling of the heart occurs after “carrying more stuff”? what does this lead to?

A

= polycythemia = increased viscosity & risk of clots

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36
Q

what causes dilation of the heart

A
  • chronically increased volume, preload, pressure, and stretch
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37
Q

what changes occur in the myocytes with dilation

A
  • elongation

- think of it like worn out yoga pants that wont snap back

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38
Q

what causes hypertrophy of the heart

A
  • from the ventricle constantly pushing against high afterload
  • think of how muscles get from working out = stiff & inflexible
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39
Q

what is cor pulmonale

A
  • abnormal enlargment of the RS of the heart
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40
Q

what causes cor pulmonale

A
  • r/t to hypertrophy

- result of disease of the lungs or pulmonary blood vessels

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41
Q

what is the difference between hypertrophy and hyperplasia

A
  • hypertrophy = increased size

- hyperplasia = increased number

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42
Q

how do the myocytes become less effective (decompensate) in dilation and hypertrophy?

A
  • less stretch when filling
  • less contraction in systole
  • increased O2 use
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43
Q

recap the process of cardiac compensation if prolonged

A

cardiac compensation –> prolonged –> cardiac remodeling & decompensation –> HF

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44
Q

define cardiac dilation: describe the cells, walls, cavity

A
  • long cells, baggy walls
  • decreased starling response
  • large heart size with slightly thicker walls
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45
Q

define hypertrophy: describe the cells, walls, and cavity

A
  • thick cells
  • thick walls
  • smaller cavity
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46
Q

what is cardiomegaly

A
  • big heart
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47
Q

what is cardiomyopathy

A
  • disease of all heart muscle
  • global
    = weak heart
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48
Q

how does HF affect CO

A
  • decreases CO
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49
Q

what causes acute HF

A
  • immediate loss or decrease in CO
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50
Q

how can an MI cause acute HF

A

= stunned heart & loss of tissue

= decreased contractility

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51
Q

how can arrhythmias cause acute HF

A
  • can cause decreased CO

ex. brady, tachy, vfib

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52
Q

how can HTN crisis cause acute HF

A
  • massive increase in bp = increase in afterload heart cannot pump against
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53
Q

how can a PE cause acute HF

A

= decreased return to LV

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54
Q

what is the function of papillary muscles in the heart

A
  • papillary muscle supports heart valves

- prevents them from opening against resistance & preventing back flow

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55
Q

how can rupture of the papillary muscle cause acute HF

A

= immediate backflow = decreased forward flow = decreased CO

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56
Q

what is myocarditis

A
  • global inflammation of the heart
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57
Q

how can myocarditis cause acute HF

A
  • inflamed heart = decreased function & contraction = decreased CO
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58
Q

how can chemotherapy cause acute HF

A
  • will destroy heart tissue along w cancer tissue = decreased function
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59
Q

how can pregnancy cause acute HF

A
  • often towards end of pregnancy
    = increased strain, demand, etc. & heart cannot cope w it
  • also get electrolyte imbalances
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60
Q

what is the purpose of the thyroid gland

A
  • “engine of metabolism”

- secretes thyroid hormone which regulates metabolism

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61
Q

what is thyrotoxicosis

A
  • hyperthyroidism

= overactivity of the thyroid gland

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62
Q

how can thyrotoxicosis cause acute HF

A
  • too much thyroid hormone = high metabolism = energy & O2 consuming = increased demand of heart
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63
Q

what is chronic HF

A
  • slow development
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64
Q

how can chronic hypertension cause chronic HF

A
  • heart has to work against constant increased afterload
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65
Q

how can DM cause chronic HF

A

= increased BP, atherosclerosis

= changes in microvasculature of heat = stiff muscle

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66
Q

what is the number one cause of chronic CF

A
  • ischemic heart disease
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67
Q

how can pulmonary diseases cause chronic CF

A
  • make heart work harder
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68
Q

how can valve disease lead to chronic HF

A
  • chronic regurgitation

- aortic stenosis

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69
Q

what is endocarditis

A
  • infection on the valves
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70
Q

how can endocarditis lead to chronic HF

A

= valve does not close properly due to vegetation

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71
Q

how can chronic anemia lead to chronic CF

A
  • anemia = poor O2 capacity
    = have to increase workload of heart to move blood around
  • also heart is also suffering from low O2 due to anemia
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72
Q

what can cause cardiomyopathy

A
  • ischemia
  • ETOH (alcohol) = toxin to heart
  • viral infection –> can permanently injure
  • chemo
  • idiopathic
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73
Q

what are 3 descriptors from cardiomyopathy

A
  • dilated
  • hypertrophic
  • restrictive
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74
Q

what are 4 different ways to look at HF

A
  • acute v chronic
  • reduced EF v preserved EF
  • systolic v diastolic
  • RS v LS
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75
Q

what is meant by chronic HF being progressve

A
  • always worsening

- we can slow down but cannot stop

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76
Q

what occurs in the heart with systolic dysfunction

A
  • heart fails to generate enough force to pump blood
    = decreased contractility & SV
    = back up of fluid
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77
Q

what occurs in the heart w diastolic dysfunction

A
  • reduced ability of ventricles to fill

= increased end diastolic pressure = congestion

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78
Q

what can cause diastolic dysfunction

A
  • failure of myocardium to relax

- increased stiffness of ventricle

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79
Q

do systolic & diastolic dysfunction occur separately?

A
  • often occur together
  • a heart that does not fill cannot pump adeqaute blood
  • heart does not pump properly becomes overfilled
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80
Q

what is the formula for EF

A

SV / EDV (preload of LV)

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81
Q

how is EF measured?

A

use:

  • echo
  • mri
  • angiogram
  • muga
  • mibi
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82
Q

what does 60% EF mean

A
  • normal
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83
Q

what does 40-59% EF mean

A
  • mild dysfunction
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84
Q

what does 20-39% EF mean

A
  • moderate dysfunction
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85
Q

what does <20% EF mean

A
  • severe dysfunction
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86
Q

how is systolic dysfunction in LS HF assessed

A
  • using EF
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87
Q

is diastolic or systolic dysfunction associated w HF with reduced EF? what is the EF ?

A
  • systolic dysfunction

- < 50%

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88
Q

describe HFrEF

A
  • inability to move blood forward effectively

- unable to overcome SVR (LV) or PVR (RV)

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89
Q

what might cause HRrEF

A
  • loss of muscle cells
  • decrease in contractility
  • structural changes
  • high afterload
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90
Q

what does HFeEF eventually lead to

A
  • not meeting needs of tissue

= decreased CO

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91
Q

does diastolic or systolic dysfunction occur with HFpEF

A
  • diastolic
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92
Q

what is the EF in HFpEF

A
  • symptoms w >50%
93
Q

describe what occurs during HFpEF

A
  • stiff ventricle = diminished relaxation in early diastole & diminished compliance (stretch) in late diastole
  • shifts pressure-volume curve
94
Q

explain how HFpEF causes decreased CO

A
  • EF is still normal
  • but, it is of a smaller volume
    ex. 50% of 100 mL = 50 mL –> not bad
    ex. 50% of 50 mL = 25 mL forward = bad
95
Q

what occurs in people w HFpEf during high demand

A
  • when get extra demands, heart cannot stretch to accommodate = tip into HF quickly, get fluid back up etc.
    = activity intolerance
96
Q

what is biventricular HF

A
  • when both sides of the heart are affected

- typically one sided HF leads to the other

97
Q

what can cause RS HF

A
  • LV failure
  • loss of muscle mass
  • cor pulmonale
  • congenital defects
98
Q

how can LV failure cause RS HF

A
  • LSHF = pulmonary edema = increased afterload on RV
99
Q

what can cause loss of muscle mass leading to RSHF

A
  • right ventricular or inferior MI
100
Q

describe how cor pulmonale can cause RSHF

A
  • impaired ventilation = pulmonary vasoconstriction = increased afterload –> failure
    = RSHF secondary to pulmonary disease
101
Q

what congenital defects can lead to RSHF

A
  • pulmonary obstructions or shunts increase the workload on the RV –> fail
102
Q

how does RSHF effect CO? what does this lead to?

A
  • RV ventricle weakens and cannot empty = decreased CO

= SNS stim to increase HR, vasoconstriction, etc. = increased workload

103
Q

how does RSHF effect the kidneys? what does this lead to?

A
  • kidney misinterprets low CO as low volume = triggers RAAS & aldo secretion
    = keep H2O = increased workload
104
Q

how does RSHF effect the JVP and the brain

A
  • fluid backs up:
    = increased JVP = distension
    = cerebral edema
105
Q

how does RSHF effect the body system

A
  • get back up of blood into the systemic circulation
106
Q

where do we see edema in RSHF

A
  • legs
  • liver
  • brain
  • pulmonary edema
  • periphery
  • abdomen
  • organs congested
  • JV distension
107
Q

what are symptoms of RSHF

A

congest BODY:

  • edema (abdominal distension, pedal)
  • weight gain
  • fatigue
  • decreased appetite
  • catabolize muscle mass = tiny in frame, hands, etc.
108
Q

how come decreased appetite is associated with RSHF

A
  • get distended/edematous bowel

= bowel does not digest = no appetite

109
Q

what type of spacing is fluid in the abdomen (ascites)

A
  • 3rd spacing = difficult to remove
110
Q

what can cause LVHF

A
  • volume overload
  • pressure overload
  • loss of muscle mass
  • loss of contractility
  • restricted filling
111
Q

what is the most common problem with LSHF

A

pulmonary edema

112
Q

how does LSHF effect CO? what does this lead to?

A

= decreased CO, BP, perfusion

= SNS stimulation = increased hr, contractility, vasoconstriction = more work

113
Q

how does LSHF affect the kidneys

A
  • kidneys misinterpret decreased CO as low volume = triggers RAAS & aldo secretion = overloads heart
114
Q

how does LSHF effect the lungs

A
  • get backup of blood into pulmonary vein = get increased pressure in pulmonary capillaries = pulmonary congestion/edema
115
Q

how does LSHF affect the RV

A
  • increased P in lungs = increased afterload for RV
116
Q

what effect does pulmonary edema have

A
  • decreased O2 sats
  • increased WOB/SOB
  • increased RR
  • decreased A/E
  • fine crackles
  • cyanosis
  • dry cough (to try and get rid of fluid) that progresses to pink frothy sputum
  • orthopnea
  • paroxysmal nocturnal dyspnea
  • possible angina
  • accessory muscle use
117
Q

how does edema cause pulmonary manifestations

A
  • get high hydrostatic pressure = pushes fluid out

- fluid in alveoli = decreased gas exchange = hypoxia

118
Q

what causes orthopnea

A
  • when lay down the fluid spread out to effect whole lung instead of just base
119
Q

what are the symptoms of LSHF

A
  • pulmonary manifestations
  • flutter in chest
  • angina if also IHD
  • nocturia
  • fatigue/activity intolerance
  • confusion
  • pale, cold, sweaty, cyanotic skin
  • 3rd heat sound
120
Q

why is nocturia associated with LSHF

A
  • renal perfusion is reduced especially during the day = decrease in urine produced
  • when person is recumbent, renal perfusion improves = urine production
121
Q

why does confusion occur with LSHF

A
  • reduced perfusion into cerebrum
122
Q

why do we get pale, cold, sweaty, cyanotic skin with LSHF

A
  • get compensatory vasoconstriction to get more blood flow to important organs = cold
  • sweating bc body heat cannot be dissipated thru constricted vascular beds
  • mild cyanosis from hypoxia
123
Q

why do we get a 3rd heart soud with LSHF

A
  • common with fluid overload
124
Q

what causes paroxysmal nocturnal dyspnea

A
  • when lay down = increased venous return = after few hours = SOB
  • sitting up = decreased SOB = recover quick
125
Q

what are symptoms of HF (R and L) on the nervous system

A
  • difficulty concentrating
  • confusion
  • dizziness
  • pre-syncope, syncope
  • lightheaded
  • fatigue
126
Q

what are symptoms of HF (R and L) on CVS

A
  • drop in bp
  • orthostatic hypotension
  • faint pulse
  • increased HR
  • palpitations
  • lifts, heaves, thrills
  • arrhythmia - flutter in chest
  • angina (due to decreased O2 sat &
  • complicated if anemia or polycythemia
  • activity intolerance
127
Q

what are symptoms of HF (R and L) psychosocially

A
  • anxiety
  • depression
  • feeling of profound sadness
128
Q

what are symptoms of HF (R and L) on resp. system

A
  • dyspnea/SOB
  • increased RR
  • decreased O2 sats
  • crackles
  • cyanosis
  • PND
  • orthopnea
  • pulmonary edema
  • pleural effusion
  • cough (dry –> pink, frothy)
129
Q

what changes in ABGs are seen w HF

A
  • decreased PaO2

- slight increase in PaCO2

130
Q

what changes in fluid retention are seen w HF (R and L)

A
  • fluid retention due to RAAS, increased Na, decreased albu,in
  • increased weight
  • increased JVP
  • edema
  • nocturia
131
Q

what GI symptoms are seen w HF (R and L)

A
  • ascites
  • nausea
  • anorexia
  • GI bloating
132
Q

what changes in the kidney do we see w HF

A
  • renal insufficiency / injury due to low CO
133
Q

how come a thrombus may form during HF

A
  • weak contractions and low EF = blood stasis = form thrombus
  • thrombus can become an emboli
134
Q

where does an emboli in the RV go? LV?

A
  • RV = lungs

- LV = brain

135
Q

how do we prevent thrombus formation in HF patients

A
  • many pts with EF < 25% on anticoagulants
136
Q

what is HF functional classification

A
  • similar to angina classes but sees how much activity can be done without SOB, fatigue, or palpitations
137
Q

what are the HF stages

A
  • 4 stages –> A to D

- one way

138
Q

what is stage A of HF

A
  • high risk
  • no structura changes
  • no symptoms
139
Q

what is stage B of HF

A
  • structural changes

- no symptoms

140
Q

what is stage C of Hf

A
  • structural changes

- past or present symptoms

141
Q

what is stage D of HF

A
  • structural changes
  • refractory symptoms
  • specialized interventions
142
Q

how do the stages & classes of HF line up

A
  • stage A + B correlate with class 1 = asymptomatic
  • stage C = class 2 & 3 where there are symptoms with moderate or minimal exertion
  • stage D = class 4 where symptoms at rest
143
Q

what does increased Na possibly indicate?

A
  • increased Na = increased water retention

- RAAS? diet?

144
Q

what do we want to look for when considering diagnostics for HF

A
  • look for anything reversible

- IHD? stressor (ex. uncontrolled HTN)? fluid?

145
Q

why should we just K+ levels

A
  • could be altered by drugs –> ACE-I, ARB, BB, diuretics

- arrhythmia concern

146
Q

why should we assess BUN/Cr

A
  • tells us about renal function r/t meds, perfusion
147
Q

what should we assess Mg

A
  • arrythmias
148
Q

why should we assess Hgb/Hct

A
  • anemia? = decreased O2 carrying capacity

- polycythemia = increased viscosity = increased overload

149
Q

why shoudl we asses WBC levels

A
  • infection?

ex. myocarditis? endocarditis?

150
Q

why should we assess myoglobin, CK-MB, troponin?

A
  • indicate an MI
151
Q

why should we assess thyroid

A
  • to rule out thyrotoxicosis
152
Q

why should we asses LFTs

A
  • liver function test

- see if congested, how it is functioning

153
Q

why should we assess BNP

A
  • B-type natriuretic peptide
  • biomarker for HF
  • released from ventricle with chronic HF stress
  • released by stretched vent
  • causes diuresis
154
Q

what is the acronym for MI treatment? what does it stand for>

A

Morphine
Oxygen
Nitroglycerin
Aspirin

155
Q

what is the acronym for HF treatment

A

A prils
B ols
C pines
D iuretics

156
Q

what does A stand for for HF treatment

A
  • ACE Inhibitors = prils
  • aldo
  • ARBs (sartans)
  • decrease vol
157
Q

what does B stand for, for HF treatment

A 
Beta blockers "ols"
Brady = decreased HR 
Blood pressure = decreased
Bronchi constriction (B2)
158
Q

what does C mean for HF treatment

A

Calcium Channel Blockers (pines)

- decrease hardness

159
Q

what does D mean for HF treatment

A

diuretics

  • lasix/furosemide K+ wasting
  • thiazide
  • spironolactone = K+ sparing
160
Q

what do we first want to give as treatment for HF

A
  • ACE inhibitor & BB
161
Q

what should we give if they are intolerant to ACEI or BB

A
  • ARB (angiotensin receptor blockers)
162
Q

what are devices used to treat HF

A
  • ICD
  • CRT
  • VAD
  • transplant
163
Q

what is an ICD? what do we use it for?

A
  • implanted cardioverter defibrillator

- for pts with EF < 30%

164
Q

what is a CRT? what do we use it for?

A
  • cardiac resynchronization therapy

- for low EF and wide QRS

165
Q

what is a VAD

A
  • ventricular assist device
166
Q

what interventions should be used for all patients experiencing symptoms of Hf

A
  • education
  • reduce risk factors
  • lifestyle modifiation
  • salt & fluid control
  • diuretic therapy
167
Q

what should we do if after the pt has been on ACEI and BB, but symptoms are not improving?

A
  • add ARB, digoxin, or nitrates
168
Q

what are 6 classes of drugs used for HF

A
  • diuretics
  • RAASi
  • BB
  • ivabradine
  • inotropic agents
  • vasodilators
169
Q

what are different types of RAASi

A
  • ACE-I
  • ARB
  • ARNI
  • aldosterone antagonists (MRA)
  • direct renin inhibitors
170
Q

what is the first line for volume overload

A
  • diuretics
171
Q

what do diuretics do

A
  • reduce afterload, edema, and cardiac dilation
172
Q

what is a caution w diuretics

A
  • not to overeduce CO & BP
173
Q

what is the goal of using diuretics for HF

A
  • symptoms reduction
174
Q

what are 3 types of diuretics? do they save or get rid of K

A
  • furosemide = reduced K
  • hydrochlorothiazide = reduce K
  • spironolactone = K sparing
175
Q

what should you not give spironolactone with

A
  • ACE-I or ARN
176
Q

what is the suffix for ACE-I

A

____pril

177
Q

what is the first line for HF

A
  • ACE-I &BB
178
Q

what is the MOA of ACE-I

A
  • prevents conversion of angiotensin 1 to angio 2
179
Q

how do ACE-I affect Kinins? what does this cause?

A
  • causes increased kinin = causes inflammation

= reduced remodelling but also chronic cough

180
Q

what do ACE-Is do

A
  • decrease aldo

- & atrial & venous dilation

181
Q

what are the S/E of ACE-I

A
  • hypotension
  • hyperkalemia
  • cough
  • angioedema
  • renal impairment (check BUN/Cr)
182
Q

how should we start a dose of ACE-I

A
  • start low & titrate up
183
Q

what are examples of ACE-I

A
  • captopril
  • enalopril
  • ramipril
  • lisinoril
184
Q

what is the suffix for ARBs

A

___sartan

185
Q

describe the use of ARBs

A
  • very similar to ACE-I
  • no increased kinin = less reduced remodelling
  • used if intolerant of ACE-I
186
Q

what is ARNI

A

angiotensin receptor neprilysin inhiibitor

187
Q

describe use of ARNI

A
  • new, very effective drug
  • can replace ACE-I and ARB
  • for class 2-4 HF
188
Q

what does ARNI do

A
  • increases natriuretic peptides (ANP, BNP)

- decreases RAAS

189
Q

what is a type of ARNI

A

sacubitril/valsartan (enestro)

190
Q

what does MRA stand for

A

mineralcorticoid receptor antagonist

191
Q

what is MRA often added to

A
  • add to ACE-I or ARB for residual aldo
192
Q

what does MRA do

A
  • reduces symptoms
  • prolongs life
  • blocks receptors (not production)
193
Q

what are side effects of MRAs

A
  • risk of harmful effects on heart
  • increased K
  • renal impairment risk
194
Q

what are two types of MRAs

A
  • spironolactone

- eplerenone

195
Q

what is a side effect w spironolactone

A
  • painful breast development in men
196
Q

what are direct renins use for

A
  • HTN, no HF

- seems ideal but not proven in trials

197
Q

what is an example of direct renin inhibitors

A
  • aliskiren
198
Q

what do BB block

A
  • decreases SNS, decreased arrythmia
199
Q

what kind of dose should we start w for BB? why?

A
  • low

- watch for bradycardia

200
Q

describe the use/action of BB

A
  • originally thought as harmful due to decreased contractility
  • beneficial with slow congtrol
  • slows progression
  • increases HF
  • prolongs life
201
Q

what is the suffic for BB

A

_____olol

202
Q

what is Ivabradine

A
  • new drug

- for stable, symptomatic HF with low EF, NSR

203
Q

what might ivabradine replace

A
  • BB if contraindicated
204
Q

what does ivabradine do

A
  • slows HR in nodal cells
205
Q

what are 3 types of inotropic agents

A
  • digitalis (digoxin)
  • dopamine
  • milrinone
206
Q

why isnt digoxin used too often?

A
  • high toxicity, narrow therapeutic range
207
Q

what do inotropic agents do

A

change the force of heart’s contractions

208
Q

what does dopamine do

A
  • sympathomimetic =increased SNS
209
Q

what does milrinone do?

A
  • IV & short term use

- for severe HF

210
Q

what are 2 types of vasodilators

A
  • nitroglycerine

- isosorbide with hydralizine

211
Q

what does nitro do

A
  • potent vasodilator

- reduced preload

212
Q

what are 2 concerns w nitroglycerin

A
  • decreased bp

- tachycardia

213
Q

what does isosorbide with hydralizine do

A
  • reduced afterload & improve renal function
214
Q

what is the goal of HF management for stage 1

A
  • delay/prevent onset of stage B
215
Q

how do we delay onset of stage B

A
  • ACE-I or ARB for HTN. DM, and atherosclerosis
  • reduce smoking & alcohol use
  • exercise
216
Q

what is the goal of management for someone in stage B of HF

A
  • prevent S&S
  • prevent injury
  • slow progression/remodelling
217
Q

how will we prevent S&S, injury, and remodelling in stage B

A
  • add BB to ACE-I or ARB
218
Q

what type of structural changes are seen in stage B of HF

A
  • LV hypertrophy/fibrosis
  • LV dilation
  • hypocontractility
  • valvular heart disease
  • previous MI
219
Q

what type of symptoms are seen in stage C of Hf

A
  • dyspnea
  • fatigue
  • edema
  • increased JVP
220
Q

what is the goal of treatment for stage C of HF

A
  • relieve congestive symptoms
  • improve functional capacity & QOL
  • slow remodelling
  • prolong life
221
Q

what meds might be given for stage C of HF

A
  • diuretic
  • ACE-I or ARB
  • BB
222
Q

what do you want to avoid in stage C of HF?

A
  • nsaids
  • CCB
  • most antiarrhythmics
223
Q

what do you want to avoid nsaids in stage C of HF

A
  • promote Na retention

- increases toxicity of diuretics/ACE-I

224
Q

what do you want to avoid CCB during stage C

A
  • bc they suppress contractility
225
Q

what is the goal of management for stage D of Hf

A
  • symptoms management
226
Q

what is done for stage D of HF

A
  • monitor weight
  • maximize medical therapy
  • periodic IV meds
  • prn diuretics
227
Q

what might BB and ACE-I cause during stage D of HF

A
  • bradycardia
  • hypotension
  • renal failure
228
Q

what is initiated during stage D of HF

A
  • end of life palliative care
229
Q

what can acute care of HF include

A
  • bedrest
  • O2
  • cardiac monitoring
  • angina? nitro or morphine
  • IV diuretic
  • anticoagulants to avoid clots

NURS 2500 (5 decks)

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