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Cardio Pulm Eval > Pulmonary Part 2 > Flashcards

Pulmonary Part 2 Flashcards

1
Q

location of breath sounds

A

Tracheobronchial: medial
Bronchovesicular: medio-lateral
Vesicular: lateral

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2
Q

abnormal breathing - dyspnea

A

labored respiration

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3
Q

abnormal breathing - wheezing

A
  • constant pitch sound produced by air moving
    through narrowed (obstructed) passage (bronchi &
    bronchioles)
  • usually heard during expiration
  • COPD/asthma
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4
Q

abnormal breathing - crackles

A

– discontinuous, rattling sound
– Usually during inspiration, but can occur with expiration
– Like crumpling of a cellophane bag, distant fireworks
– Occurs with secretions in air passages, CHF

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5
Q

abnormal breath sounds - pleural friction rub

A

sounds like a creaking rocking chair or door

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6
Q

abnormal breath sounds - stridor

A

– harsh, high-pitched crowing sound
– occurs with upper airway obstruction due to narrowing at glottis
– characteristic of mucous plugging of tracheal or
foreign object

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7
Q

abnormal breath sounds - stertorous

A

snoring sound associated with secretions in trachea

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8
Q

ventilation depends on body position:

A

– upright: better ventilation of base (VA base = 2.5 x apex)
– supine: better ventilation of posterior segments, but worse with CHF secondary to pulmonary edema and fluid re-distribution

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9
Q

average values for Va and Q (CO)

A

Va: 4 L/min
Q: 5 L/min

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10
Q

matching of ventilation to perfusion:

A

– overall: matching is 0.8 (so 80% matching)
– apex: Ventilation > Perfusion
– base: Perfusion > Vent
– but base overall more than 2 x the V/Q ratio then apex

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11
Q

ventilation- perfusion scan (V-Q scan)

A

provides info on matching, useful to detect pulm. Emboli.

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12
Q

Alveolar partial pressure of oxygen

A

– 102 mmHg
– arterial blood PaO2 = 90 mmHg
– the difference is due to physiologic dead space
and R-to-L shunts

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13
Q

In alveoli, the partial pressure of CO2 =

A

40 mmHg or only slightly less
– This is the same for the PaCO2 (40 mmHg)
– secondary to increased CO2 diffuses more easily

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14
Q

pulmonary shunts

A
  • occur when regions of the lung are perfused, but not ventilated
  • Ex: bronchial obstruction by a foreign body or secondary to bronchospasm
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15
Q

physiological pulmonary shunt

A

normally some part of the lung are under ventilated compared to the level of perfusion

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16
Q

pathological pulmonary shunt

A

result of lung disease or obstruction

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17
Q

dead space

A
  • occurs when regions of the lung are ventilated,
    but not perfused
  • ex: pulmonary embolism in the R middle lobe
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18
Q

physiological dead space

A

matching is not 100% so some regions are normally under-perfused for the level of ventilation

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19
Q

pathological dead space

A

result of vascular or respiratory disease

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20
Q

acid base balance

A
  • Think of acids as H+ ion donors
  • Think of bases as H+ ion acceptors
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21
Q

what is body’s primary base

A

HCO3-

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22
Q

2 kinds of acid in the body

A

– volatile acids: carbonic acid
– nonvolatile acids:
* H2SO4, H2PO4, etc….
* keto acids (products of protein breakdown)
* lactic acid

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23
Q

does arterial or venous blood provide more info in CP system?

A

arterial blood

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24
Q

arterial blood gas report:

A
  • pH: 7.35-7.45
    -PaO2: > 80 mmHg
  • PaCO2: 35-45 mmHg
  • SAO2: 95%
  • HCO3-: 22-28 mE
  • BE: 0-2 mE
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25
Q

the adequacy of ventilation is assessed by what?

A

PaCO2

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26
Q

PaCO2 45-49 mmHg

A

hypoventilation

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27
Q

PaCO2 >50 mmHg

A

ventilatory failure

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28
Q

PaCO2 < 35 mmHg

A

hyperventilation

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29
Q

after looking at PaCO2, what should you do?

A
  • look at the pH to determine if there is compensation
    – rapid changes in pH, poorly tolerated
    – gradual changes in pH, better tolerated
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30
Q

what causes increased RR and work of breathing in respiratory failure

A

he body cannot get rid of CO2 so it is converted to H2CO3 which dissociates into H+ ions, decreasing pH

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31
Q

other buffers besides HCO3:

A

– Serum proteins
– Hb (accounts for 85% of the non-bicarb buffering)
– H2PO4 buffer

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32
Q

when pH is < 7.35

A

Metabolic Acidosis: low HCO3
Respiratory Acidosis: high PaCO2

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33
Q

when pH is > 7.45

A

Metabolic alkalosis: high HCO3
Respiratory Alkalosis: low PaCO2

34
Q

compensation of metabolic/respiratory acidosis/alkalosis:

A

the kidney will begin to retain HCO3 (increasing the pH of the body to compensate for the acidosis)

35
Q

compensation by the kidney:

A
  • The kidneys secrete acid and retain bases to
    compensate –> time course is relatively slow: 12-24 hours for any compensation to be seen
  • The lungs, on the other hand, compensate
    almost immediately (minutes)
36
Q

step by step assessment of ventilation

A

1 What is the pH: acidosis vs alkalosis?
2 What is the PaCO2: tells you if it’s respiratory or not (then must be metabolic)?
3 Determine adequacy of ventilation by PaCO2
4 calculate the expected pH given the PaCO2

37
Q

What is the PaCO2: tells you if it’s respiratory or not (then must be metabolic)?

A

Is the normal relationship between pH and PaCO2
preserved? (does pH go down when PaCO2 goes
up?)
if yes, primary respiratory, if no, then probably metabolic

38
Q

3 Determine adequacy of ventilation by PaCO2:

A

< 35: hyperventilation, 35-45: adequate vent., >45:
hypoventilation

39
Q

see example if ya need it

A
40
Q

to determine if there is a metabolic or respiratory compensation:

A
  • calculate the expected pH given the PaCO2
  • absolute difference between PaCO2 and 40:
  • divide this number by 100 to get %
  • take 1/2 of this value and subtract from 7.4 if
    PaCO2 is < than 40. Or, add whole value to 7.4 if
    the PaCO2 > than 40.
  • Acute: when actual pH further from expected
  • Chronic: when actual pH is < than expected
41
Q

3 ways oxygen is transported

A

– Dissolved (undissociated): only 3 ml/100ml blood
– Dissociated as ions: minimal contribution
– Bound to Hb: 147 grams Hb/ml blood so 197ml O2/ 100 ml blood

42
Q

what is the most important determinant of oxygen carriage?

A

hematocrit

43
Q

does giving oxygen to a heathy person change oxygen delivery?

A

no
Very little O2 is carried in solution and most
Hb is 100% saturated

44
Q

check out oxygen-Hb dissociation curve if ya want

A
45
Q

pneumonia

A
  • Inflammatory process of the lung parenchyma
  • Community acquired –> 5th leading cause of death in the US
  • Nosocomial or hospital acquired –> To be considered Nosocomial, pneumonia must be
    diagnosed 72 hrs. or more after admission
  • Bacterial vs Viral Pneumonia Vs fungal
    (histoplasmosis in our region)
46
Q

entry of bacterial pneumonia

A

inhalation vs aspiration

47
Q

lobar bacterial pneumonia

A

consolidation of a single or a few lobes
– elicits a rapid edematous response
– infrequent secondary to responsive to antibiotics
– polymorphonuclear cells (phagocytosis & fibrin)
– high fever, chills, dyspnea, increased RR, cough, pleuritic pain

48
Q

bronchopneumonia bacterial pneumonia

A

patchy lung consolidation
– begins as extension of pre-existing bronchitis
– more frequent at age extremes (old age and infancy)

49
Q

Covid 19 pathophysiology

A
  • Effects on the respiratory system account for
    majority of fatalities & morbidity –> But secondary effects seen in multiple organ systems
  • the S-protein targets ACE-II expressing cells:
    – ACE-II is heavily expressed in the respiratory tree epithelium
    • Nasal passages, throat, trachea, bronchi, etc….
    • Possible involvement of other aspects of Renin-Angiotensin system as well
50
Q

ris factors for COVID-19 mortality

A
  • Long-term care residents: mortality rate ~30%
  • Age 65 years or > have 2- 6 X mortality than < 65
  • Mean # of comorbid conditions for patients who expire = 2.7
  • < 1% of deaths in patients without comorbidities
  • According to the CDC, obesity, heart disease, CA, smoking, and many other comorbidities associated with increased morbidity & mortality from COVID-19
51
Q

course of covid post-infection

A
  • once infected, COVID-19 patients who do not shed the virus develop acute viremia
52
Q

acute viremia

A

– Virus particles can be detected in conducting airways, pneumocytes, alveolar macrophages, and hilar lymph nodes
– The total viral burden can be very high in the most acutely affected patients
– Virus can be detected in plasma and stool
– No virus detectable in other organs such as heart, liver, and kidney

53
Q

acute lung injury

A

– Diffuse alveolar damage
– Alveolar edema, cellular exudates, & desquamation of pneumocytes
– Hyaline membrane formation
– Alveolar collapse & reduced lung compliance*
– Loss of surfactant in alveoli
– Decreased diffusion capacity
– Decreased O2 diffusion into capillaries & transport
– leads to ARDS

54
Q

ARDs:

A

any severe, systemic or pulmonary insult resulting in strong inflammatory or immune
response:
* pancreatitis, pneumonia, acute renal failure, shock, etc….
– Intense inflammatory reaction in distal airway

55
Q

pulmonary insult leads to ARDs:

A
  • Pulmonary edema
  • Thickening of inter-alveolar-capillary space
  • Acute hypoxia
  • Stiff lung (reduced compliance)
  • Increased work of breathing
  • Fibrosis
56
Q

acute presentation of ARDs

A
  • The most common symptoms are cough, fever, and dyspnea
    – Lymphopenia is present 75-90% of patients
    – Majority show shadow or ground glass on radiograph or CT
57
Q

atypical symptoms of ARDs

A

– atypical symptoms include:
* GI symptoms or loss of smell
* Other even less typical presentations are hemoptysis, venous and arterial thrombosis, cardiac, neurological or cutaneous manifestations

58
Q

vascular effects of COVID-19

A
  • critical time point is 7-10 days post-infection
    – At this stage attack of ACE-II receptors in non-respiratory tissues may lead to widespread effects:
    – Activation of the coagulation pathway leads to formation of blood clots
  • Pulmonary emboli
  • Stroke
  • Peripheral, GI and other organ thrombosis
59
Q

severe COVID-19 is associated with:

A

coagulopathy and disseminated intravascular coagulation (DIC) –> Pulmonary emboli contribute to respiratory failure

60
Q

pleuritis

A
  • Inflammatory reaction in pleura secondary to
    underlying disease (pneumonia, RA, SLE, TB)
  • accumulation of fluid in pleural space
  • transudate: thin, watery, low protein
  • exudate: high protein
61
Q

pleuritis symptoms

A

back pain, CP (pleuritic CP) and SOB

62
Q

treatment for pleuritis

A

treat underlying condition (pneumonia, RA, etc….)
and/or glucocorticoids (to decrease inflammation)

63
Q

pulmonary function tests

A

– decreased lung volumes & compliance, similar to other restrictive lung diseases
– decreased FEV1, but normal FEV1/FVC

64
Q

x-rays of pleuritis

A

– Meniscus sign
– If there is bacterial pneumonia: consolidation or patchy/lacey

65
Q

arterial blood gases

A

– hypoxemia, but normal or ↑ PaCO2

66
Q

breath sounds for pleuritis

A

Diminished breath sounds, rales, rhonchi (stridor), pleural rub, egophony, whispered pectoriloquy, (+) percussion

67
Q

pneumonia - pulmonary function tests

A

similar to other restrictive lung diseases (decreased FEV1, decreased FEV1/FVC)

68
Q

pneumonia - X-rays

A

symmetric, bilateral diffuse “fluffy” infiltrates,
similar to atelectasis

69
Q

pneumonia - arterial blood gases

A

hypoxia, PaCO2-nl

70
Q

pneumonia - breaths sounds

A

crackles, wheezes, rhonchi or diminished BS secondary to consolidation

71
Q

pneumonia treatment

A

– O2, ventilation (w/ peep), electrolytes
– PT: may benefit from ROM & bed mob

72
Q

pulmonary embolism

A
  • Blood clot in the pulmonary capillary leading to infarction of lung parenchyma
    – Most common acute pulmonary complication of
    hospitalized pts. (most clinically silent)
73
Q

3rd cause of death in US

A

pulmonary embolism

74
Q

pulmonary embolism - x-ray

A

may show wedge shaped infiltrate, but often normal until necrosis occurs

75
Q

pulmonary embolism - arterial blood gases

A

PaO2 is decreased, PaCO2 may decrease & pH increase secondary to hyperventilation

76
Q

symptoms of acute onset of PE

A

– dyspnea & SOB (90%, may be only symptoms)
– rapid, shallow breathing & hypoxia/cyanosis
– apprehension, cough, syncope
– pleuritic CP and hemoptysis (usually later)

77
Q

pneumothorax

A
  • Entry of air into the pleural space
    – loss of negative intrathoracic P, causing collapse
    of the lung (down to RV)
78
Q

open pneumothorax

A

traumatic
– air communicates with atmosphere

79
Q

tension pneumothorax

A

– air enters, but can’t exit
– life threatening: as air enters, it is
trapped, increasing the interpleural P, further collapsing lung

80
Q

signs and symptoms of pneumothorax

A

– rapid, shallow breathing, hypoxia/cyanosis
– sever SOB, dyspnea & respiratory distress
– pleural pain and shock
– intercostal retractions

81
Q

arterial blood gases with pneumothorax

A

hypoxemia, hypercapnia, acidosis

Cardio Pulm Eval (10 decks)

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