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nurs pathophysiology > rrd 8 > Flashcards

rrd 8 Flashcards

disorders of pulmonary system

1
Q

purpose of ABGs

A

to check for efficacy/disruption of gas exchanges and acid/base balance

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2
Q

ABGs measure

A
  • pH
  • gas levels (PO2, SO2, PCO2, HCO3) in blood
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3
Q

pH

A
  • indicates level of acidity of blood
  • decreased: acidic
  • increased: less acidic (basic)
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4
Q

pH norm range, acidosis, alkalosis

A
  • norm: 7.35 to 7.45
  • acidosis: < 7.35
  • alkalosis: > 7.45
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5
Q

PO2

A

partial pressure of oxygen in arterial blood (O2 gas dissolved in plasma)

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6
Q

norm PO2 range, hypoxemia

A
  • norm: 80 - 100 mmHG
  • hypoxemia: < 80 mmHg
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7
Q

SO2

A
  • oxygen saturation, indicates O2 that is carried by hemoglobin
  • how great a percent of each Hgb molecule in the arterial circulation is saturated with O2
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8
Q

cycle of oxygenation

A
  1. lungs: O2 conc high, Hgb bind w/ O2 for transport to tissues
  2. if all 4 O2-binding sites on hemoglobin loaded up w/ O2, Hgb saturated
  3. shows as o2 saturation percent
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9
Q

PCO2

A

partial pressure of CO2 gas in the blood (acid)

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10
Q

PCO2 norm

A

35 - 45 mmHg

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11
Q

when the ____ in a set of ABGs is out of the normal range, it is due to some sort of respiratory problem as long as ____ is normal.

A

PCO2, HCO3

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12
Q

HCO3

A

level of bicarbonate in the blood (basic guy)

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13
Q

HCO3 norm

A

22 - 28 mEg/L

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14
Q

when the ____ in a set of ABGs is out of the normal range, it is due to some sort of metabolic problem as long as ___ is normal.

A

HCO3, PCO2

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15
Q

steps to analyzing and interpreting ABGs

A
  1. analyze pH and decide: acidosis or alkalosis
  2. analyze pCO2: out of norm, acidosis/alkalosis is RESP origin
  3. analyze HCO3: out of norm, acidosis/alkalosis is METABOLIC origin
  4. analyze pO2 and O2 sat: low, hypoxemic
  5. figure out underlying etiology causing problem and what kind of compensatory changes the body needs to make
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16
Q

ROME

A
  • Respiratory Opposite (PCO2 up, pH down)
  • Metabolic Equal (HCO3 up, pH up)
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17
Q

respiratory acidosis

A
  • state of low pH by inhibition of norm breathing pattern
  • ex: diminished effectiveness of breathing or decreased RR (hypovent)
  • retention + accumulation of CO2 -> more acid in blood
  • hypercapnia (high PCO2)
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18
Q

classic patient with resp acidosis

A
  • unconscious and RR decreased from norm to 8 breaths a min -> not breathing out enuf CO2 -> retains CO2 -> blood CO2 high, pH low
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19
Q

body’s compensation for resp acidosis

A
  • lungs are sick
  • compensation by kidneys
  • to buffer CO2 accumulation: kidneys increase HCO3 production or decrease its excretion
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20
Q

respiratory alkalosis

A
  • state of high pH caused by increase in norm breathing pattern (hyperventilation)
  • increased rate of breathing -> blow off more CO2 -> less CO2 in blood -> not enough acid
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21
Q

classic patient with respiratory alkalosis

A
  • states that cause hypervent: anxiety, panic attack, acute asthma, emphysema exacerbations
  • RR increases from norm to 28 breaths/min -> breath out too much CO2 -> blood CO2 low, pH high
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22
Q

normal resp rate

A

12- 20 breaths a min

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23
Q

body’s compensation for resp alkalosis

A
  • sick lungs, compensation by kidneys
  • increase CO2 in blood by kidneys decreasing amt of HCO3 made or increase excretion
  • can also hang on to acidic substances like H+
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24
Q

metabolic acidosis

A
  • low pH caused by accumulation of acids due to metabolic problems like renal failure + diabetic ketoacidosis
  • acid gang accumulation overwhelms alkali guy, HCO3 low
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25
Q

classic patient with metabolic acidosis

A
  • patient with DKA has accumulated byproducts of sustained gluconeogenesis - acidic ketones
  • acid gang -> blood acid high, pH low
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26
Q

body’s compensation for metabolic acidosis

A
  • metabolic side sick, lungs compensate
  • lungs decrease acid in blood by increasing RR -> blow of CO2
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27
Q

Kussmaul respirations

A
  • pattern of rapid + deep breathing to blow off accumulated acid
  • compensation for metabolic acidosis
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28
Q

metabolic alkalosis

A
  • high pH caused by metabolically-induced loss of acid gang and/or accumulation of alkali guy
  • HCO3 high
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29
Q

classic patient with metabolic alkalosis

A
  1. patient w/ extreme vomiting
  2. loss of HCL
  3. blood acid low, pH high
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30
Q

body’s compensation for metabolic alkalosis

A
  • metabolic side sick, lungs compensate
  • lungs increase acid in blood by decreasing RR -> retain CO2
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31
Q

a person in _____ due to dangerously low RR will be artificially helped to ____ faster

A

respiratory acidosis, breathe

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32
Q

a person in _____ will have buffering help by the administration of HCO3 in IV

A

metabolic acidosis

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33
Q

two phases in breathing cycle

A

inhalation and exhalation

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34
Q

inhalation process

A
  1. diaphragm drops, intercoastal muscles pull outward
  2. thorax gets bigger
  3. creates (-) pressure
  4. air sucked into bronchi and alveoli
    5.1. O2 passes across alveolocapillary membrane into blood
    5.2. CO2 passes across alveolocapillary membrane from blood into alveoli
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35
Q

components of inhalation

A
  • ventilation (V)
  • perfusion (Q)
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36
Q

ventilation

A

portion of inhalation in which air passes into bronchi and alveoli (lung tissue)

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37
Q

perfusion

A

portion of inhalation in which the lung blood vessels bring CO2 to the alveoli and take away O2 to pass on to the rest of the body

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38
Q

exhalation

A

diaphragm and intercostal muscles elastically return to resting state and CO2 is expelled from the body

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39
Q

lungs are healthy, compliant, and elastic, norm breathing occurs. what does norm breathing look like?

A

easy, low- energy, mostly passive process w/ respirations that are within 12-20, fairly reg in rhythm and of norm depth

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40
Q

a patient with three-pillow orthopnea would say?

A

“I have to have 3 pillows to prop me up when I lie down or else I get SOB”

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41
Q

commonality of all pulmonary disease processes is that they _____ the work of breathing in various ways

A

increase

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42
Q

general S/S that indicate increased work of breathing

A
  • dyspnea
  • observable breathing patterns that are out of the norm
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43
Q

dyspnea

A
  • subjective sensation of not being able to get enough air
  • “I’m short of breath”
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44
Q

example of different presentations of dyspnea

A
  • DOE
  • orthopnea
  • PND
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45
Q

DOE

A

dyspnea on exertion

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46
Q

orthopnea

A
  • dyspnea upon lying down
  • usually related to LHF
  • blood return to heart increase when person lies down + compromised LV can’t pump it forward -> back-up to lungs
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47
Q

PND

A
  • paroxysmal nocturnal dyspnea
  • suddenly awakening at night feeling SOB -> same reason as orthopnea
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48
Q

rate-related breathing patterns that are out of norm

A
  • hypoventilation (bradypnea)
  • hyperventilation (tachypnea)
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49
Q

hypoventilation

A

RR < 12 breaths/min

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50
Q

hyperventilation

A

RR > 20 breaths/min

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51
Q

etiological factors of hyperventilation

A
  • air hunger: need for more oxygen by those w/ pulmonary problem
  • psychological etiology (fright, anxiety)
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52
Q

etiological factors of hypoventilation

A
  • neuromuscular and/or CNS problems
  • EX: increased pressure on resp centers from intracranial bleeding
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53
Q

abnormal depth-related breathing patterns

A
  • hypopnea
  • hyperpnea
  • apnea
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54
Q

hypopnea

A

shallow breathing

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55
Q

hyperpnea

A

increased depth (tidal volume) of respirations

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56
Q

apnea

A

no respirations at all

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57
Q

abnormal use of muscles to breathe causing abnormal breathing patterns

A
  • inappropriate use of accessory muscles
  • nasal flaring
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58
Q

inappropriate use of accessory muscles

A
  • use of certain muscles like diaphragm + intercoastal muscles are norm during inhalation
  • seeing them + others used during exhalation is abnormal; indicates person is trying to hard to breath
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59
Q

nasal flaring

A

esp seen in children having difficulty breathing

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60
Q

____ and ____ is often seen in pulmonary diseases

A

cough, sputum

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61
Q

coughing is a ____ reflex; can be ___ (____) or _____ (______).

A
  • protective
  • acute (bronchitis)
  • chronic (COPD, gastroesophageal reflux disease or GERD)
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62
Q

hemoptysis

A

coughing up of blood

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63
Q

hemoptysis is usually bright ___ or ____ because if there is ___ in alveoli from ____ or ____ processes, there is likely to be some _____ in the ___.

A
  • pink or red
  • fluid
  • inflammatory, congestive
  • RBCs
  • fluid
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64
Q

hemoptysis also makes the cough _____ because mixed with ___ in alveoli

A

frothy, air

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65
Q

hemoptysis can result from

A
  • local infection/inflammation that damages bronchi or part of lung tissue (bronchitis, pneumonia, TB, cancer)
  • more generalized problem throughout lung tissue (pulmonary edema)
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66
Q

purulent sputum

A

green, yellow, or brown and may be foul-smelling; usually means infectious process

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67
Q

resp distress used to refer to?

A

certain combos in S/S and indicate malfxn in some facet of breathing

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68
Q

example of resp distress

A
  • patient complain of dyspnea
  • RR: 32 and SO2: 91%
  • use intercostal muscles during expiration
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69
Q

respiratory failure

A
  • patient can no longer breathe adequately on his own
  • SO2 + PO2 low, PCO2 high
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70
Q

restrictive lung diseases refers to dis processes related to difficulty with?

A

inhalation

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71
Q

since problems with inhalation usually means _____ O2 getting in, one sign often found with restrictive lung diseases is ___.

A

decreased, hypoxemia

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72
Q

restrictive lung disease manifestations and how is it measured numerically

A
  • increased work of breathing
  • low SO2 and/or low PO2
  • pH + PCO2 only sometimes affected
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73
Q

another finding in restrictive diseases is?

A

V/Q mismatch

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73
Q

V in V/Q means

A
  • ventilation
  • norm amt of air breathed in/out per min is 4 L
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74
Q

Q in V/Q

A
  • perfusion
  • norm amt of blood in lungs available for gas exchange per min is 5 L
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75
Q

norm V/Q ratio is?

A

0.8 (4 L / 5 L)

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76
Q

V/Q mismatch means

A

V/Q ratio is out of the norm - either lower or higher than normal

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77
Q

can’t actually see mismatch when assessing patients, but it usually exists to some degree in?

A

most restrictive pulm diseases + contribute to S/S

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78
Q

sometimes V/Q is measured to have clear diagnosis - measured by nuclear imaging test called ____.

A

V/Q scan

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79
Q

low V/Q disorders

A
  • person is having difficulty w/ ventilation
  • not getting usual # of L of air from atmosphere to blood -> less ventilation than norm
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80
Q

example of low V/Q disorders

A
  • pneumonia
  • alveoli filled w/ secretions and portions collapse
  • less air can pass into alveoli -> low vent
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81
Q

if patient only gets 3 L of air to alveoli, but perfusion remains the same, what is their V/Q?

A

3/5 = 0.6

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82
Q

high V/Q disorders

A
  • person is having difficulty w/ perfusion
  • during inhalation, not getting usual # of L of blood to alveoli for gas exchange
  • less perfusion than norm
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83
Q

example of high V/Q disorders

A

pulmonary embolus blocks one or more branches of the pulm arterial vasculature

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84
Q

if a patient van only get 4 L of blood to alveoli and ventilation is the same, what is their V/Q?

A

4/4 = 1

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85
Q

low V/Q disorders

A
  • chest wall restriction
  • airway restriction
  • pleural restriction
  • lung tissue restriction
86
Q

chest wall restriction

A
  • deformity (kyphosis)
  • obesity
  • neuromuscular weakness from diseases that affect junction btw neurons + muscle cells
87
Q

examples of diseases that causes chest wall restriction from neuromuscular weakness

A
  • polio
  • myasthenia gravis
88
Q

airway restriction

A
  • foreign body, tumors of trachea + bronchi
  • inflammation of upper airways - croup
89
Q

most diseases that cause inflammation in larynx and bronchi are caused by?

A
  1. virus
  2. inflammation
  3. airways narrowed
  4. stridor heard upon inspiration (high pitched, raspy sound caused by turbulent flow in airways)
90
Q

croup

A
  • laryngotracheobronchitis: inflammation of larynx and bronchi
  • usually occurs in infants and children younger than 1 year
91
Q

S/S croup

A
  • fever
  • increased RR
  • barking cough
  • stridor
92
Q

tx croup

A

cool mist, sometimes steroids

93
Q

types of pleural restriction

A
  • pleural effusion
  • pneumothorax
94
Q

pleural effusion

A

extra fluid in pleural space

95
Q

normally, the space between the visceral + parietal pleura has?

A

very little fluid - just enough for lubrication

96
Q

the amount of fluid in the pleural space ____ when something causes irritation/inflammation. examples for this situation

A
  • increases
  • cancer cells in lung
  • heavy coughing from bronchitis, pneumonia, etc.
97
Q

S/S pleural effusion

A
  • chills and fever if related to infection
  • pleuritic pain (pleurisy) = pain upon deep breaths, cough, or movement in local area of chest
  • respirations shallow - restricted by pain + fluid build-up
98
Q

pneumothorax

A

presence of air in the space btw lung and chest wall (aka in pleural space)

99
Q

pneumothorax results in __________ of lungs; ie, thorax pressure because the same as __________ as air comes in pathologically.

A
  • disruption of normal negative pressure
  • the atmosphere
100
Q

lungs affected by pneumothorax begins to _____ as air accumulates in the ____.

A

collapse, thorax

101
Q

two problems with pneumothorax

A
  • lack of usual (-) pressure to guide norm breathing process
  • collapse of varying amts of lung tissue
  • ^ = chest pain and SOB
102
Q

types of pneumothorax

A
  • traumatic
  • spontaneous
  • tension
103
Q

traumatic pneumothorax can be a result from:

A
  • penetrating (something enters the pleura from outside the chest)
  • nonpenetrating (fractured/broken rib from blunt trauma punctures pleura)
104
Q

spontaneous pneumothorax can sometimes happen:

A
  • in healthy ppl who are tall, thin, smokers
  • when a patient has underlying disease, such as when a weakened, emphysema alveoli ruptures
105
Q

tension pneumothorax can occur when

A
  • injury to the chest
  • respiratory structures permits air to enter but not leave pleural space
106
Q

tension pneumothorax has rapid ____ in pressure of “_____” air that can affect the _____ lung (_______) + reduce the ______.

A
  • increase
  • trapped
  • uninjured, opposite side of the original injury
  • cardiac output
107
Q

tension pneumothorax results in

A

a life-threatening condition that requires urgent treatment

108
Q

tx pneumothorax varies with

A
  • the cause
  • extent of disorder
  • symptoms of the patient (asses oxygen level and breathing effort)
109
Q

basic treatment for pneumothorax is done to

A

reestablish negative pressure

110
Q

to reestablish negative pressure in a patient w/ pneumothorax, what is done?

A
  • insert chest tube btw two pleura
  • end of tube covered by few centimeters of water (water seal drainage system)
111
Q

water seal drainage system for pneumothorax

A
  • water acts a one-way valve
    1. air breathed in thru mouth + bronchi
    2. air goes into chest tube w/ every breath
    3. water won’t let air back in
    4. (-) pressure reestablished
    5. person can breath norm
    6. after few days: lungs seals off og hole that caused problem
    7. chest tube removed
112
Q

individuals who ____ are most likely to get pneumonia. why?

A
  • smoke
  • irritants (tobacco smoke) paralyze the cilia -> secretions accumulate
  • secretions contain bacteria -> pneumonia
113
Q

types of lung tissue restriction

A
  • pneumonia
  • pulmonary edema
  • lung cancer
114
Q

pneumonia

A

acute infection of lower respiratory tract caused by bacteria, viruses, fungi, or parasites

115
Q

pneumonia is the _____ leading cause of death in the US, esp takes its toll on ____.

A

6th, elderly

116
Q

risk factors of pneumonia

A
  • either end of age-spectrum
  • immunocompromised
  • underlying lung diseases (COPD, lupus, etc.)
  • alcoholism & other mechs of altered consciousness
  • smoking
  • endotracheal intubation
  • malnutrition
  • immobilization
117
Q

types of pneumonia

A
  • community-acquired (CAP)
  • hospital-acquired (nosocomial)
  • aspiration pneumonia
  • each usually involves diff organisms + level of seriousness + need diff treatment
118
Q

community-acquired pneumonia (CAP)

A
  • organisms most commonly gram (+) and less virulent
  • walking pneumonia: don’t have to be hospitalized
119
Q

exceptions for people with CAP

A

immunocompromised and debilitated individuals in community can get virulent CAP bc susceptible to opportunistic infections

120
Q

nosocomial pneumonia

A
  • most commonly caused by virulent gram (-) microbes like pseudomonas
  • patients need very strong antibiotics
121
Q

aspiration

A

to inhale something that shouldn’t be going into the lungs (ex: nasal drip, food, liquid, foreign body) w/ resultant inflammation to lung tissue

122
Q

aspiration pneumonia can be?

A

CAP or nosocomial

123
Q

if someone aspirated enough material to completely close airway, can cause?

A

death

124
Q

aspiration pneumonia usually happens in _____ or other individuals whose ______ are depressed or absent.

A
  • debilitated
  • gag, swallowing, and/or cough reflexes
125
Q

example of elderly person who got aspiration pneumonia

A
  1. elderly, weak patient cant swallow very well (dysphagia)
  2. food particles/fluid go into lungs instead stomach
    3, creates breeding ground for microbes in lungs
  3. aspiration pneumonia
126
Q

example of alcoholic get aspiration pneumonia

A
  1. alcoholic passes out
  2. if supine: sometimes stomach contents will be regurgitated and go down trachea into lungs
  3. cough reflex suppressed by alc and deep unconsciousness
  4. breeding ground for microbes in lungs
  5. aspiration pneumonia
127
Q

other examples of aspiration pneumonia include

A
  • brain injured
  • post-seizure
  • post-CPR
128
Q

who will not get aspiration penumonia?

A
  • an alert and otherwise healthy person
  • cough, swallow, gag reflexes are unimpaired
129
Q

atelectasis can happen in other situations, such as not breathing deeply. what is the steps to get pneumonia?

A
  1. air doesn’t get to lower alveoli, collapse
  2. collapsed alveoli breeding ground for bacteria
  3. pnemonia
130
Q

example of atelectasis and pneumonia

A
  1. post-abdominal surgery: person doesn’t breathe deeply enough due to pain
  2. atelectasis
  3. pneumonia
131
Q

patho of pneumonia

A
  1. microorganisms settle into alveoli + attacked by alveolar macrophages
  2. attack ineffective or body overwhelmed by #s of organisms
  3. full-scale activation of body’s defense mechanisms take place
  4. inflammatory/infectious debris accumulate in alveoli + surrounding tissue (infiltrates)
  5. infiltrates cause collapse of portions of lung tissue (atelectasis)
  6. infiltrates + atelectasis = consolidation
132
Q

atelectasis

A

-grps of alveoli cave in due to blockage in the bronchioles (ex: collections of mucus from inflamm changes)
- air can’t get into alveoli so they collapse

133
Q

consolidation

A
  • areas of lung that become stiff + diminished fxn
  • either local area such as single lobe (lobar pneumonia) or may be more diffuse (bronchopneumonia)
134
Q

S/S pneumonia

A
  • fever, chills, malaise, pleural pain, cough, dyspnea
  • upon auscultation: crackles (from inflamm fluid in alveoli) or locally diminished breath sounds (consolidated tissue has no air going thru it, so no sound)
  • abnormal chest x-ray
135
Q

dx pneumonia

A
  • chest x-ray
  • gram stain and cultures of sputum
136
Q

tx pneumonia

A
  • antibiotics
  • hydration
  • pulmonary toilet (cough, turn, deep breath, suction)
137
Q

pulmonary edema

A

excess water in alveoli

138
Q

pulmonary edema is usually thought of as

A

cardiogenic vs noncardiogenic

139
Q

noncardiogenic etiology for pulmonary edema

A
  1. injury to capillary endothelium (from inhalation of noxious/harmful substances like smoke from a fire)
  2. increased capillary permeability
  3. movement of fluid and plasma proteins from capillary to alveoli
  4. edema in the alveoli will cause damage to the alveolar cells that produce surfactant
  5. loss of surfactant
  6. atelectasis
  7. grps of alveoli that collapse and no longer available for gas exchange
140
Q

S/S pulmonary edema

A
  • cough
  • dyspnea
  • inspiratory crackles
  • pink frothy sputum
  • hypoxemia
141
Q

cardiogenic etiology for pulmonary edema

A

pulmonary edema due to LHF

141
Q

two types of atelectasis

A
  • blockage from mucous as seen in pneumonia
  • lack of surfactant as a result of damage to alveolar cells from edema
142
Q

_______ of alveoli/atelectasis results in ______ of the patient.

A
  • collapse
  • poor oxygenation
143
Q

lung cancer (bronchogenic carcinoma)

A

arise from epithelium of respiratory tract (lung is also site of metastasis for many other types of cancer)

144
Q

most common cause of lung cancer is?

A
  • cigarette smoking
  • 1 in 10 smokers will develop lung cancer
145
Q

patho of lung cancer in smokers

A
  1. carcinogens in tobacco smoke (has > 40)
  2. cause multiple genic abnormalities in bronchial cells
  3. carcinoma in stiu
  4. invasive carcinoma
146
Q

examples of genetic abnormalities seen in bronchial cells caused by carcinogens in tobacco smoke

A
  • deletions of chromosomes
  • activation of oncogenes
  • inactivation of tumor suppressor genes
147
Q

to establish diagnosis of bronchogenic cancer, a ____ is done. what is the procedure process?

A
  • bronchoscopy
  • a sample of sus area is taken and sent for biopsy -> usually classified as small cell lung cancer (SCLC) or non-small cell (NSCLC)
148
Q

S/S lung cancer

A
  • pleural effusion
  • cough
  • hemoptysis
  • chest wall pain
  • SOB
  • anorexia
  • weight loss
149
Q

problems that result in high V/Q

A
  • structural problems in vessels
  • pulmonary embolus
150
Q

types of structural problems of vessels

A
  • strictures in pulmonary vessels
  • malformations
  • birth defects
151
Q

most common perfusion problem is ______, which is?

A
  • pulmonary embolus
  • occlusion of portion of pulm vessels by an embolus, which can be a blood clot, some type of tissue frag or air bubble
152
Q

pulmonary embolus is an increased risk in patients with?

A
  • Virchow’s triad: endothelial injury, hypercoagulability, venous stasis
  • virchow’s -> CVT -> dislodge and travels to lung
153
Q

when ____ lodges in portion of pulm artery or its branches, it prohibits ____ blood from getting to the ____ in the alveoli to be ____ -> blood pulm veins that returns to the heart + beyond is less _____ and person will start to feel ____.

A
  • embolus
  • deoxygenated
  • air
  • oxygenated
  • saturated with O2
  • SOB and chest pain
154
Q

the seriousness of pulmonary embolus depends on?

A

how large and how proximal the blockage is

155
Q

embolus enters pulm artery -> smaller arterioles -> gets stuck. how does patient get SOB and chest pain?

A

embolus blocks deoxygenated venous blood from getting to alveoli to get oxygenated

156
Q

embolus enters pulm artery -> smaller arterioles -> gets stuck. how does patient get hemoptysis?

A
  1. embolus irritates arterial intima
  2. inflammation
  3. leakage of blood into lung tissue
157
Q

embolus enters pulm artery -> smaller arterioles -> gets stuck. how does patient get shock?

A
  1. if large enuf portion of lung tissue inflamed
  2. massive release of inflammatory mediators
  3. systemic vasodilation
158
Q

obstructive lung disease is due to?

A

difficulty with exhalation

159
Q

the obstruction of airways results in more ____ needed to ____ air

A

force, expire

160
Q

norm: exhalation is a ____ process that works bc of the natural ___ recoil of lungs. in people w/ obstructive disease, air gets ____ and must be _____.

A
  • no-energy, autonomic, passive
  • elastic
  • trapped
  • forced
161
Q

patients must use _______ muscles to force out air if they have ____ diseases. use of ______ muscles is often manifested as ______. _____ muscles ____ upon expiration to help get air out of lungs.

A
  • accessory
  • obstructive
  • accessory
  • retractions
  • supraclavicular, substernal, intercostal
  • sucking in
162
Q

some patients also have ______ as a compensatory mechanism (the length of time to exhale beings to get ____) with obstructive pulm diseases.

A
  • prolonged expiratory phase
  • longer
163
Q

one test that is used to measure how well patients can force out air is?

A

peak flow (PF) test

164
Q

peak flow test

A
  • measured by a PF meter - patient blows into it like blowing out a candle
  • measures how many mL can be blown out in first second of exhalation
  • the less the PF, the worse the obstructive pulm disease
165
Q

most common obstructive pulm diseases

A
  • asthma, bronchitis, emphysema
  • cystic fibrosis
166
Q

since many patients have both bronchitis and emphysema, these two are lumped together and are often called? what about asthma?

A
  • chronic obstructive pulmonary disease - COPD
  • if asthma is bad + chronic enough, it is also lumped with COPD
167
Q

asthma

A

chronic inflammatory disorder of the airways due to bronchial hyperresponsiveness to stimuli (ex: allergens in env)

168
Q

T/F asthma begins at any age

A

TRUE
- about half of all cases develop in childhood, 1/3 in adulthood (usually under age 40)

169
Q

basic patho of asthma

A
  1. inhaled irritants
  2. inflammatory mediators (histamine, leukotriene, prostaglandins)
    3.1. vasodilation + increased capillary permeability, inflation by neutrophils + eosinophils
    3.2. bronchial smooth muscle directly react to all mediators
    4.1. swelling of bronchial lining
    4.2. spasm + constriction of bronchial musculature
170
Q

with asthma, patients can _____, inhalation is an active process that can _______, but exhalation through ______ is more ____.

A
  • usually inhale ok
  • get air past swollen bronchi
  • swollen and constricted airways
  • difficult
171
Q

asthma: hear ____ sound caused by expiration of air through ____ passageways (if bronchial swelling + constriction gets very bad, can also hear ____ during _____).

A
  • wheezing
  • narrow
  • wheezing
  • inhalation
172
Q

S/S asthma

A
  • pattern of remission/exacerbation
173
Q

S/S asthma during exacerbation

A
  • wheezing upon exhalation (+inhalation if bad)
  • accessory muscle use (intercostal + supraclavicular retractions while exhale)
  • prolonged expirations
  • SO2 drop -> compensation for hypoxemia by hypervent
  • ABGS = resp alkalosis
  • baseline PF lower + worsen
174
Q

tx asthma

A
  • monitor daily status w/ baseline PF readings = good indicator of impending exacerbations
  • meds: bronchodilators, anti-inflamm drugs
175
Q

examples of bronchodilators and anti-inflammatory drugs for asthma

A
  • ventolin via aerosol nebulization
  • inhalers
  • oral/IV steroids (decrease swell, stabilize capillary membranes)
176
Q

some hyperventilation during an asthma attack is?

A

desirable - patient is employing adequate compensatory response

177
Q

while hyperventilation during an asthma attack is desirable, treatment is still needed because?

A

can decompensate - tire out, be unable to maintain higher rate, become hypoxemic, retain CO2, go into resp acidosis

178
Q

COPD

A

collective term for emphysema and/or chronic bronchitis

179
Q

in most cases, the cause of both types of COPD is?

A

smoking

180
Q

S/S in both types of COPD is

A
  • prolonged expirations
  • certain degree of accessory muscle use
  • chronically low PF
  • S/S worse than usual during exacerbation
181
Q

tx COPD for both types

A
  • smoking cessation
  • give O2 appropriately
  • bronchodilators
  • sometimes steroids
182
Q

emphysema cause

A

smoking

183
Q

patho of emphysema

A
  • inspired irritants (usually from smoking) -> inability to expel them due to altered cilia
  • destruction of areas of alveolocapillary membrane -> O2 diffusion compromised and hypoxemia develops (air hunger)
184
Q

emphy(1). airway ______ and abnormally _____ activity of proteolytic enzymes like ______

A
  • inflammation
  • increased
  • elastase: enzyme that breaks down the proteins that make lungs flexible + elastic
185
Q

emphy(2). destruction of patches of the _____ and some walls between _____.

A
  • alveolocapillary membrane
  • alveoli clusters
186
Q

emphy(3). results in _____ that have no elastic recoil

A

large, stiff, hyperinflated alveoli

187
Q

emphy(4). due to ______, these areas act as air traps (large, over-inflated areas sometimes called -___)

A
  • loss of elastic recoil
  • blebs
188
Q

emphy(5). once air is ____ and ___, it becomes harder to exhale it

A

inhaled, trapped

189
Q

in emphysema, to tap into areas where the alveolocapillary membrane has not been _____ and get more _____, it helps to ___ RR.

A
  • destroyed
  • O2 diffusion
  • increase
190
Q

the emphysemic typically lives in a state of compensatory ______ to try to get more air

A

chronic hyperventilation

191
Q

S/S for emphysema is known as?

A

pink puffer

192
Q

S/S emphysema

A
  • tachypnea: RR of 26-30 breaths/min
  • patients stay pink (well-oxygenated) as long as they keep puffing (hypervent)
  • hard work = thin and no appetite (no energy to eat)
  • increased anteroposterior (AP) diameter of chest
  • certain techniques to help exhale + get more air
  • maybe wheezing - lung sounds usually diminished bc no air flow
  • ABGs: resp alkalosis
193
Q

in emphysema: the patient foes from norm AP-to-lateral diameter ratio of ____ to an ___ diameter both ways.

A
  • 1 to 2
  • equal (2 to 2)
194
Q

why is there an increased AP diameter of the chest with emphysema? what does it look like?

A
  • compensatory change to accommodate years of air trapping and lungs getting bigger
  • rounder thorax = barrel chest
195
Q

what techniques patients with emphysema unconsciously use to help exhale and get more air?

A
  • tripod position: maximize chest expansion
  • pursed lip breathing: increase pressure in chest to get air out + prolong expiratory time
196
Q

some hyperventilation in an emphysema is ______. means the patient is employing ____. most emphysemics live their lives in compensatory state of?

A
  • desirable
  • adequate compensatory response
  • tachypnea
197
Q

during exacerbation periods, people with emphysemas need treatment because?

A
  • decompensate: tire out, be unable to maintain higher rate, become hypoxemic, retain CO2 (hypercapnia), go into resp acidosis, in danger of resp failure
198
Q

chronic bronchitis

A

hypersecretion of mucus and chronic productive cough for at least 3 mons of the year for at least 2 consecutive years

199
Q

patho for chronic bronchitis

A
  1. inspired irritants usually from smoking
  2. inability to expel them due to altered cilia
  3. irritation to bronchial walls
  4. inflammation and infiltration of neutrophils + macrophages into bronchial wall
  5. bronchial edema + thick mucus from increase in # of mucus glands
  6. obstruction
  7. air trapping
  8. difficulty in expelling air
200
Q

acute bronchitis is different to chronic bronchitis in that?

A

acute bronchitis short-lived viral/bacterial infection that causes inflamm of bronchi + S/S of cough, fever, malaise (LIKE BAD COLD)

201
Q

S/S of chronic bronchitis is known as?

A

blue bloaters

202
Q

etiology of blue in chronic bronchitis

A
  • mucus plugs in bronchi + overall bronchial narrowing
  • hypoxemia (doesn’t help to puff)
  • clubbing of fingers
203
Q

mucus plugs in bronchi and overall bronchial narrowing in chronic bronchitis, which results in?

A
  • decreased areas of ventilation
  • decreased surface area where oxygen can diffuse from alveoli to capillaries
204
Q

hyperventilating is not seen in a pt with chronic bronchitis because?

A

extra inhaled O2 cannot get thru the mucus plugs = cyanosis develops

205
Q

what is clubbing of fingers and what is it associated with?

A
  • bulbous, bluish enlargement of distal segment of digit
  • associated w/ diseases w/ chronic oxygenation problems (long-term lung cancer, cystic fibrous, congenital heart disease)
206
Q

etiology of bloater

A
  • hyperventilation won’t do any good
  • cor pulmonale - RHF due to lung disease
207
Q

the body knows with chronic bronchitis, it will ____ to increase the RR in an effort to fight for breath.

A

not help very much

208
Q

with chronic bronchitis, they usually don’t have weight loss. instead, they try to ____ energy by ____. therefore, what do the patients’ weight look like?

A
  • conserve
  • not moving much
  • bit overweight “bloated”
209
Q

cor pulmonale in chronic bronchitis

A
  • patho of disease makes it difficult for RV to get blood into stiff, mucous-filled lungs
  • RV strained and RHF results -> peripheral edema (bloat)
210
Q

ABGs of chronic bronchitis

A
  • chronically retain CO2 (hypercapnia) bc inability to exchange gases (mucus prevents good diffusion of O2 in and CO2 out to alveoli)
  • pt has baseline of resp acidosis
211
Q

which disease has normal resp alkalosis?

A
  • asthma exacerbation
  • daily emphysema
212
Q

which disease has normal resp acidosis?

A

chronic bronchitis

nurs pathophysiology (13 decks)

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