Pulmonary Part 2 Flashcards
1
Q
location of breath sounds
A
Tracheobronchial: medial
Bronchovesicular: medio-lateral
Vesicular: lateral
2
Q
abnormal breathing - dyspnea
A
labored respiration
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
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
5
Q
abnormal breath sounds - pleural friction rub
A
sounds like a creaking rocking chair or door
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
7
Q
abnormal breath sounds - stertorous
A
snoring sound associated with secretions in trachea
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
9
Q
average values for Va and Q (CO)
A
Va: 4 L/min
Q: 5 L/min
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
11
Q
ventilation- perfusion scan (V-Q scan)
A
provides info on matching, useful to detect pulm. Emboli.
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
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
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
15
Q
physiological pulmonary shunt
A
normally some part of the lung are under ventilated compared to the level of perfusion
16
Q
pathological pulmonary shunt
A
result of lung disease or obstruction
17
Q
dead space
A
- occurs when regions of the lung are ventilated,
but not perfused - ex: pulmonary embolism in the R middle lobe
18
Q
physiological dead space
A
matching is not 100% so some regions are normally under-perfused for the level of ventilation
19
Q
pathological dead space
A
result of vascular or respiratory disease
20
Q
acid base balance
A
- Think of acids as H+ ion donors
- Think of bases as H+ ion acceptors
21
Q
what is body’s primary base
A
HCO3-
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
23
Q
does arterial or venous blood provide more info in CP system?
A
arterial blood
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
25
the adequacy of ventilation is assessed by what?
PaCO2
26
PaCO2 45-49 mmHg
hypoventilation
27
PaCO2 >50 mmHg
ventilatory failure
28
PaCO2 < 35 mmHg
hyperventilation
29
after looking at PaCO2, what should you do?
- look at the pH to determine if there is compensation
– rapid changes in pH, poorly tolerated
– gradual changes in pH, better tolerated
30
what causes increased RR and work of breathing in respiratory failure
he body cannot get rid of CO2 so it is converted to H2CO3 which dissociates into H+ ions, decreasing pH
31
other buffers besides HCO3:
– Serum proteins
– Hb (accounts for 85% of the non-bicarb buffering)
– H2PO4 buffer
32
when pH is < 7.35
Metabolic Acidosis: low HCO3
Respiratory Acidosis: high PaCO2
33
when pH is > 7.45
Metabolic alkalosis: high HCO3
Respiratory Alkalosis: low PaCO2
34
compensation of metabolic/respiratory acidosis/alkalosis:
the kidney will begin to retain HCO3 (increasing the pH of the body to compensate for the acidosis)
35
compensation by the kidney:
* 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
step by step assessment of ventilation
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
What is the PaCO2: tells you if it’s respiratory or not (then must be metabolic)?
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
3 Determine adequacy of ventilation by PaCO2:
< 35: hyperventilation, 35-45: adequate vent., >45:
hypoventilation
39
see example if ya need it
40
to determine if there is a metabolic or respiratory compensation:
* 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
3 ways oxygen is transported
– 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
what is the most important determinant of oxygen carriage?
hematocrit
43
does giving oxygen to a heathy person change oxygen delivery?
no
Very little O2 is carried in solution and most
Hb is 100% saturated
44
check out oxygen-Hb dissociation curve if ya want
45
pneumonia
* 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
entry of bacterial pneumonia
inhalation vs aspiration
47
lobar bacterial pneumonia
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
bronchopneumonia bacterial pneumonia
patchy lung consolidation
– begins as extension of pre-existing bronchitis
– more frequent at age extremes (old age and infancy)
49
Covid 19 pathophysiology
* 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
ris factors for COVID-19 mortality
* 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
course of covid post-infection
- once infected, COVID-19 patients who do not shed the virus develop acute viremia
52
acute viremia
– 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
acute lung injury
– 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
ARDs:
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
pulmonary insult leads to ARDs:
* Pulmonary edema
* Thickening of inter-alveolar-capillary space
* Acute hypoxia
* Stiff lung (reduced compliance)
* Increased work of breathing
* Fibrosis
56
acute presentation of ARDs
* 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
atypical symptoms of ARDs
– 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
vascular effects of COVID-19
- 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
severe COVID-19 is associated with:
coagulopathy and disseminated intravascular coagulation (DIC) --> Pulmonary emboli contribute to respiratory failure
60
pleuritis
- 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
pleuritis symptoms
back pain, CP (pleuritic CP) and SOB
62
treatment for pleuritis
treat underlying condition (pneumonia, RA, etc....)
and/or glucocorticoids (to decrease inflammation)
63
pulmonary function tests
– decreased lung volumes & compliance, similar to other restrictive lung diseases
– decreased FEV1, but normal FEV1/FVC
64
x-rays of pleuritis
– Meniscus sign
– If there is bacterial pneumonia: consolidation or patchy/lacey
65
arterial blood gases
– hypoxemia, but normal or ↑ PaCO2
66
breath sounds for pleuritis
Diminished breath sounds, rales, rhonchi (stridor), pleural rub, egophony, whispered pectoriloquy, (+) percussion
67
pneumonia - pulmonary function tests
similar to other restrictive lung diseases (decreased FEV1, decreased FEV1/FVC)
68
pneumonia - X-rays
symmetric, bilateral diffuse “fluffy” infiltrates,
similar to atelectasis
69
pneumonia - arterial blood gases
hypoxia, PaCO2-nl
70
pneumonia - breaths sounds
crackles, wheezes, rhonchi or diminished BS secondary to consolidation
71
pneumonia treatment
-- O2, ventilation (w/ peep), electrolytes
– PT: may benefit from ROM & bed mob
72
pulmonary embolism
* Blood clot in the pulmonary capillary leading to infarction of lung parenchyma
– Most common acute pulmonary complication of
hospitalized pts. (most clinically silent)
73
3rd cause of death in US
pulmonary embolism
74
pulmonary embolism - x-ray
may show wedge shaped infiltrate, but often normal until necrosis occurs
75
pulmonary embolism - arterial blood gases
PaO2 is decreased, PaCO2 may decrease & pH increase secondary to hyperventilation
76
symptoms of acute onset of PE
– dyspnea & SOB (90%, may be only symptoms)
– rapid, shallow breathing & hypoxia/cyanosis
– apprehension, cough, syncope
– pleuritic CP and hemoptysis (usually later)
77
pneumothorax
* Entry of air into the pleural space
– loss of negative intrathoracic P, causing collapse
of the lung (down to RV)
78
open pneumothorax
traumatic
– air communicates with atmosphere
79
tension pneumothorax
-- air enters, but can’t exit
– life threatening: as air enters, it is
trapped, increasing the interpleural P, further collapsing lung
80
signs and symptoms of pneumothorax
– rapid, shallow breathing, hypoxia/cyanosis
– sever SOB, dyspnea & respiratory distress
– pleural pain and shock
– intercostal retractions
81
arterial blood gases with pneumothorax
hypoxemia, hypercapnia, acidosis
