Exam 4: Pulmonary Disorders Flashcards
1
Q
normal value for blood gas pH
A
pH: 7.35-7.45
2
Q
normal value for PaO2
A
PaO2: 80-100
3
Q
normal value for PaCO2
A
PaCO2: 35-45
4
Q
what is oxygenation
A
Refers to the ability to take in oxygen from the lungs and distribute it to the tissues and organs
5
Q
Blood gas parameters- (to calculate total arterial oxygen content, must know)
A
- PaO2 less than 80 (partial pressure of O2)
- Hemoglobin concentration (amount of hgb available to bind w O2)
- Oxygen saturation SPO2 (% of available hgb that is bound to O2)
6
Q
why is there a large drop in PO2 inspired air compared to PO2 in alveoli?
A
because of the water vapor at body temp is 47
7
Q
How is oxyhemoglobin formed?
A
o Oxygen diffuses across the alveolar capillary membrane, it dissolves in the plasma, where it exerts pressure. As PaO2 increases oxygen in the plasma moves into the RBCs and binds with hemoglobin forming oxyhemoglobin
Binding occurs in the lungs= oxyhgb association/hgb saturation w/ O2
8
Q
why is the CO2 in the tissue level increased?
A
at the tissue level, theres more CO2 because metabolism has occurred.
- the tissue creates CO2 and allows the CO2 in the venous blood to increase
9
Q
describe bronchial vein
A
the venous blood does not go through the pulm system–>makes a little bypass through an internal shunt as a result there’s a small dilution that occurs.
10
Q
what is hemoglobin desaturation
A
o Reverse process, O2 is released from hgb (this occurs in the tissues at cellular level)
11
Q
describe oxyhemoglobin dissociation curve
A
o When hemoglobin saturations and desaturations are plotted on a graph, the result is a S-shaped curve known as, oxyhemoglobin dissociation curve.
For PaO2 <60 mmHg, oxygen is readily unloaded to peripheral tissues and hemoglobin’s affinity for oxygen molecule diminishes reflecting the steep part of the curve.
For PaO2 >60 mmHg, the curve becomes relatively flat, reflecting the maximum saturation of hemoglobin with oxygen in the lungs.
**The oxygen-hemoglobin dissociation curve shows how the hemoglobin saturation with oxygen (SO2,), is related to the partial pressure of oxygen in the blood (PO2)
12
Q
The oxyhemoglobin curve is shifted to the right during
A
o Acidosis
o Hypercapnia
o Hyperthermia
o abnormal hemoglobin
o high levels of 2,3 DPG
Indicates decreased affinity of oxygen or increased ease with which oxyhemoglobin dissociates and oxygen moves into the cells
** decrease pH=curve shifts to right
13
Q
The oxyhemoglobin curve is shifted to the left during
A
o Acute alkalosis
o hypocapnia (in the lungs when CO2 diffuses out of the blood into the lungs, the affinity for oxygen increases)
o hypothermia
o carboxyhemoglobin
o abnormal hemoglobin.
Indicates increased affinity for oxygen, which promotes association in the lungs and inhibits dissociation in the tissues.
- low levels 2,3 DPG
**increase pH=curve shifts to left and holds O2 more
14
Q
what is the Bohr effect?
A
The shift in the oxyhemoglobin dissociation curve caused by changes in CO2 and hydrogen ion concentration in the blood
15
Q
what is failure of ventilation
A
failure to get gas in/out of lungs for exchange
16
Q
describe ventilation
A
Refers to ability to take in oxygen and remove CO2
* mechanical movement of gas or air into and out of the lungs
* known also as “Respiration”
17
Q
what does ventilation depend on?
A
- production and elimination of carbon dioxide
- alveolar minute ventilation
o The amount of air that successfully got into the alveoli and could be removed from the body
o Calculated by-> RR x TV= minute ventilation
18
Q
What can cause low ventilation?
A
- drug use
- low oxygen in the environment (low PIO2)
19
Q
where is the respiratory center located?
A
- in the brainstem controls respiration from transmitting impulses to the respiratory muscles, causing them to relax and contract.
20
Q
When CO2 rises, it can be detected by?
A
o Central chemoreceptors are in the MEDULLA and monitor arterial blood indirectly by sensing the changes in the pH of CSF.
They control rate of breathing!!!
Monitor pH, PCO2, PaO2
They sense pH low by detecting increase CO2 by detecting increase in H
* As CO2 converts to carbonic acid to enter CSF as H
If alveolar ventilation is low (i.e. COPD) PaCO2 in the arteries increases CO2 diffuses into CSF pH decreases chemoreceptors get activated and they increase the depth and rate of ventilation.
* In COPD, chemoreceptors become insensitive and kidneys have to compensate the low pH by retaining bicarb.
o Peripheral chemoreceptors are located in aortic bodies, aortic arch, and carotid bodies at the bifurcation of the carotids, near the baroreceptors.
Primarily sensitive to PaO2 and pH.
They will detect increase in CO2 and H (acidity) and lactic acid, as well as decrease PaO2 and pH
PaO2 (must drop below 60%) and pH drop cause them to be activated and ventilation is increased.
Play into effect when central receptors become insensitive d/t chronic hypoventilation.
21
Q
describe lung innervation and the three types
A
(by the ANS) three type of lung sensory receptors, that send impulses from the lungs to the dorsal respiratory group;
o stretch receptors
sensitive to increase size or volume of the lungs -> decrease RR and volume
o irritant receptors
sensitive to aerosols, gases, dust -> initiates a COUGH REFLEX, bronchospasm, and increased RR
o pulmonary C-receptors “J-receptors”
sensitive to increased pulmonary capillary pressure, -> stimulates rapid shallow breathing, laryngeal constriction on expiration, and mucus secretion, hypotension and bradycardia
22
Q
what is the overall function of lung innervation
A
- cause bronchospasm (constriction of airway) to prevent foreign things from entering
*damage to spinal cord —>causes them to not be able to feel ventilation, they don’t have the perception
23
Q
describe hyperventilation
A
Alveolar ventilation that exceeds metabolic demands
The lungs remove CO2 at a faster rate than it is produced by cellular metabolism, resulting in decreases PaCO2
* PaCO2 <50
* PaCO2 <36mmHg –> hypocapnia –>respiratory alkalosis
24
Q
describe hypoventilation
A
Inadequate ventilation in relation to metabolic demands
It is caused by alterations in pulmonary mechanics or in the neurologic control of breathing
Alveolar minute volume is reduced
Less O2 available in the alveoli for diffusion into the blood
Can be corrected if alveolar ventilation is improved by increases in the rate and depth of breathing
* PaCO2 >50, low PaO2
* PaCO2 >44 mmHg CO2 is retained (hypercapnia) elevated H+ ions in blood resulting in respiratory acidosis.
25
what are some causes of low partial pressure inhaled O2 (PIO2)? (3)
- high altitude
- when o2 is taken out of your environment (e.g. nitrogen leaking into environment)
- fires with smoke (displaces O2)
26
what is VQ mismatch
the area in our lungs that are receiving ventilation are not well match with the areas of our lungs that are being perfused
(e.g. have a local atelectasis, alveoli are collapsing= those alveoli not going to give much o2 and not going to remove much CO2, the blood flow to that area is going to see decrease O2 and increase CO2 and pulm capillary are going to constrict and blood flow is going to be directed to other areas in the lungs that have good gas exchange--->when there is pathology going to have more areas in the lungs that have more VQ mismatch)
27
what are two components of the work of breathing?
* Elastic Forces
o Compliance
* Frictional Forces
o Resistance
28
describe compliance
Ability of alveoli, lungs, thorax to expand under pressure (measure of lungs and chest wall distensibility)
* Determined by alveolar surface tension and the elastic recoil of the lungs/chest wall (elastic and collagen fibers and surface tension)
* THE PRESSURE NEEDED TO KEEP THE LUNGS OPEN!!
o “increase compliance means lungs are easier to expand/inflate, and has lost some elastic recoil”
i.e., Emphysema, aging
o “decrease compliance means that the lungs/chest is abnormally stiff/difficult to inflate”
i.e., Pneumonia, ARDS, pulmonary edema and fibrosis, problems with alveolar
* breath sounds; crackles
* Opposite of Elasticity:
“ability of alveoli, lungs, and thorax to contract/recoil”
“change in alveolar pressure over alveolar volume”
o decreased elasticity (thin rubber band) increased compliance
o increase elasticity (thick rubber band) decrease compliance
29
what is compliance measured by?
* Volume change/ pressure change (C = V/P)
o V, usually TV
o P, airway or pleural pressure
30
examples of problems: compliance
* Small airway obstruction will see increased RR and small tidal volume
o You will see increased work of breathing, prolonged expiration, and wheezing
* Restricted breathing often seen with pulmonary fibrosis.
o There is stiffening of the lungs of chest wall and decreased compliance
o Small tidal volumes and increased RR
31
describe resistance
* Frictional Forces
o Resistance
The resistance of the respiratory tract to airflow during inhalation and exhalation
* Determined by length, radius, diameter of airways, also density and velocity of gas (tissue and viscous resistance and airway resistance)
o Resistance to flow in the airways depends on whether the flow is laminar or turbulent, on the dimensions of the airway, and on the viscosity of the gas.
* THE PRESSURE TO PUSH AIR INTO THE LUNG Normally very low
* Most resistance occurs in nose followed by the larynx/oropharynx
32
what is resistance measured by?
* pressure/rate of flow (R= P/F) Ohm’s law
o P, trans-airway pressure
o F,
33
examples of problems: resistance (2)
* Bronchodilation -> resistance is decreased to airflow (caused by SNS)
* Bronchoconstriction -> resistance is increased (caused by parasympathetic receptors)
o Resistance can also be increased by -> pulmonary edema, mucous, tumors, or foreign bodies, airway problems
Breath sounds; wheezes, stridor
34
describe work of breathing
- Determined by the muscular effort required for ventilation normally low
o The two forces of work that the body needs to do to get air inside lungs
- Will increase when compliance and resistance are disrupted.
- More muscular effort needed when lung and chest wall compliance is decreased/ resistance increased
35
Describe pathophysiological mechanisms that can result in hypoxemia.
Hypoxemia
- Reduced oxygenation of arterial blood (PaO2)
- Results from problems with one more of the major mechanisms of oxygenation
o Oxygen delivery to the alveoli
*Oxygen content of the inspired air (FiO2 or PiO2)
*Ventilation of the alveoli
o Diffusion of oxygen from the alveoli into the blood
*Balance between alveolar ventilation and perfusion (V/Q mismatch)
*Diffusion of O2 across alveolocapillary membrane
o Perfusion of pulmonary capillaries
36
clinical manifestations of hypoxemia (5)
- Cyanosis
- confusion
- tachycardia
- edema
- decreased renal output
37
Describe Normal P(A-a) O2 that can result in hypoxemia.
o Partial pressure of O2 in the alveoli is called, PAO2 (the big A)
o Partial pressure of O2 in the arterial blood is called, PaO2 (small a)
o “ALVEOLAR-arterial gradient measures the difference between oxygen concentration in the alveoli and arterial system—important to help narrow the different diagnosis for hypoxemia”
38
what is Normal P(A-a) O2 dependent on?
Dependent of two factors;
* Amount of O2 in inspired air and is expressed as %, called PiO2
* Amount of alveolar minute ventilation (TV x RR)
39
Oxygen delivery to the alveoli (#)
Normally 12-15mmHg
* Increases as you age
40
Problems that are considered as a “Normal A-a”
1. Low PiO2 (inhaled oxygen concentration)
(caused by low oxygen in the environment)
o i.e., in an airplane (high altitude)
2. Alveolar hypoventilation
* Results in an increase PACO2 and decrease in PAO2
* Examples-
o Lack of neurologic stimulation of the respiratory center
- over sedation, drug overdose, neurologic damage
o Defects in chest wall mechanics
- neuromuscular disease, trauma, chest deformity, air trapping
o Large airway obstruction
- laryngospasm, foreign body aspiration, neoplasm
o Increased work of breathing
- emphysema, severe asthma
These processes are happening outside the body:
* High altitude
* Low oxygen content of gas mixture
* Enclosed breathing spaces (suffocation)
**** If the A-a gradient is normal, then the cause of hypoxia is low oxygen content in the alveoli, either due to low O2 content in the air (low FiO2, as in the high altitude) or more commonly due to hypoventilation like the central nervous system (CNS) depression, OHS, or obstructed airways as in COPD exacerbation.
41
Increased P(A-a) O2 that can result in hypoxemia.
o Problems that are considered as a “Wide A-a”
*V/Q mismatch
* “balance between alveolar ventilation and perfusion”
o V: amount of air getting into alveoli
o Q: amount of blood perfusing the capillaries around the alveoli
* Most common cause of hypoxemia!!
* Refers to an abnormal distribution of ventilation and perfusion
42
examples of Increased P(A-a) O2 : VQ mismatch
o Atelectasis
o Pulmonary embolism
o Acute respiratory distress syndrome
i.e., mucus plug-
* mucus impedes some ventilation
* there is low ventilation in relation to blood flow
o asthma
o chronic bronchitis
o pneumonia
43
describe shunt that can result in hypoxemia.
- a form of mismatch
o Very bad (worse than V/Q)
o “Alveoli are not ventilating enough” (low V/Q)
o INADEQUATE VENTILATION OF WELL-PERFUSED AREAS OF THE LUNGS
o No ventilation but there is blood flow through capillaries
When blood passes through portions of the pulmonary capillary bed that receive no ventilation, right-to-left shunt occurs, resulting in decrease systemic PaO2 and hypoxemia
o The alveoli could be filled with infection, fluid, secretions
As a result- there is no way for air to reach capillary bed for oxygen/CO2 exchange
44
what are some examples of shunt
ARDS/ pulmonary edema (alveoli are filled with fluid)
Asthma (bronchoconstriction)
Atelectasis
45
describe Alveolar Dead Space that can result in hypoxemia.
* “Alveoli are not perfused enough” (high V/Q)
* POOR PERFUSION OF WELL VENTILATED PORTIONS OF THE LUNGS results in “wasted ventilation”
o i.e., embolus- most common cause of high V/Q
impairs blood flow to a segment of a lung
46
describe Diffusion of O2 from alveoli into the blood (diffusion defect) that can result in hypoxemia.
* “Diffusion of oxygen across alveolocapillary membrane abnormality”
o The membrane is thickened or surface area for the diffusion is decreased!
o Alveoli can’t inflate fully
* CO2 diffusion is not altered as it can easily diffuse in and out
* Example-
o Pulmonary Edema
There is excess fluid that can come around alveoli (abnormal thickness/tissue swelling)
o Fibrosis
Formation of fibrous lesions/tissues makes it thick
* Interstitial lung disease (ILD)
Increases the time required for diffusion
o Emphysema
Destruction of alveoli, decreases the alveolocapillary membrane surface area available for diffusion
47
describe perfusion of capillaries that can result in hypoxemia.
* Decreased pulmonary capillary perfusion
o Blood flow bypasses the lungs
organ infarction
lead to increased pressure in pulmonary artery
right sided HF (cor pulmonale)
* Can occur because of-
o Intracardiac effects that cause right to left shunting
o Intrapulmonary arteriovenous malformations
48
describe diffusing capacity
- Helps determine how easy it is for O2 (air you are breathing in) to get to blood stream
- With DLCO test, you give patients small amount of carbon monoxide, which is easier to measure than oxygen. Know the concentration of CO that is inhaled subtract it with exhaled CO.
o If there is a big difference indicates = diffused a lot (carbon monoxide is being diffused a lot into the blood stream)
[Basically, tells you how much crossed the alveolar membrane into pulmonary capillaries and how efficient gas exchange is]
49
DLCO Interpretation: DLCO is decreased (4)
Pulmonary fibrosis
* Thickening outside of alveolar wall makes it difficult for O2 to pass through alveoli capillary membrane leading to less O2 to diffuse
Pulmonary vascular diseases (PE)
* No blood flow because blood clot. There is a decrease ability of O2 to diffuse to bloodstream
Restrictive lung diseases
* d/t Loss of lung volume
* Fibrotic lung disease
Obstructive lung diseases
* Especially emphysema
o Since there is a breakdown of alveolar walls there is loss of surface area between alveolus and pulmonary capillary
* Chronic bronchitis—DLCO will be closer to NORMAL!
* Other obstructive lung diseases with V/Q mismatch
50
DLCO Interpretation: DLCO is increased
Anemia
* Fewer blood cells for O2 to connect with, DLCO is higher due to all blood cells pass through and gobble up the O2
51
what are indications for DLCO (5)
o Monitor progress of parenchymal lung diseases
o Evaluate pulmonary involvement in systemic diseases
Rheumatoid arthritis
Sarcoidosis
SLE
Systemic sclerosis
Mixed connective tissue disease
o Evaluate obstructive lung disease
o Evaluate cardiovascular diseases
o Quantify disability associated with interstitial lung disease
52
what is DLCO affected by? (8)
Hgb
Carboxyhemoglobin (COHb)
Altitude
PAO2
Body position
Pulmonary capillary blood volume
Asthma
Obesity
53
describe COPD (obstructive)
o Characterized by airflow limitation that is not fully reversible and is usually progressive, and associated with an abnormal inflammatory response
o Alveoli are destroyed
o Surface area available for diffusion decreases!!
o EFFECTS-
Decreased alveolar ventilation
Hypercapnia
V/Q mismatching with hypoxemia
* -->leads to polycythemia and cyanosis
54
describe chronic bronchitis
HYPERsecretion of mucus and chronic productive cough
* Cough continues for 3 months of the year, for at least 2 consecutive years
Continual bronchial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium, smooth muscle hypertrophy with fibrosis and narrowing of airways
Thick mucus can’t be cleared, due to impaired ciliary function
* Can lead to obstruction
The airways collapse early on expiration, trapping gas in the distal portions of the lung
Air trapping expands the thorax, putting the respiratory muscles at a mechanical disadvantage
Airway obstruction results in decreased alveolar ventilation and increased PaCO2
55
describe emphysema
Abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis, and breakdown of elastin
* Apoptosis occurs from an inflammatory response (contributes to the loss of alveolar cells and reduced surface area)
Loss of elastic recoil
* Lost elastic tissue, there is NO elasticity to push air out [think of a grocery plastic bag]
* Alveoli are big and floppy— start smushing the airways further decreases ventilation
o Lost all air sacs, have one floppy alveolus and working so hard all the time to get O2 to body
* Air traps in the alveoli and alveoli becomes bigger
o Due to defective expiration from the loss of recoil in bronchioles
Elastin fibers are degraded, significantly more compliance, but NO elastance. So the alveoli contract and empty much more slowlyyyy, therefore you see exhalation issues
56
describe Fibrotic lung disorders (restrictive)
o Characterized by decreased lung compliance
o “Restrict”
Lung becomes stiff and difficult to ventilate, and the diffusing capacity of the alveolocapillary membrane may decrease, causing hypoxemia
Takes more effort to expand the lungs during inspiration
* Elastic fibers are replaced with collaged decrease in compliance
* Unable to expand alveoli as much to fill and have inhalation issues
o Alveolar capillary membranes thicken resulting in decreased oxygen diffusion and hypoxemia
o Excessive amount of fibrous or connective tissue in the lung
Can be caused by formation of scar tissue after active pulmonary disease; ARDS/TB in association with autoimmune disorders or by inhalation of harmful substances
o Results from chronic inflammation, alveolar epithelialization, and myofibroblast proliferation
57
Describe the mechanisms responsible for airway obstruction in COPD.
* COPD: air trapping/ impaired expiration
o Emphysema
Damage wall collapses or airway becomes obstructed
Loss of elasticity
due to lack of elasticity alveoli become saggy and big and start pushing on the airways. Trapped gas in the alveoli further pushes into the airway
o Chronic bronchitis
Loss of elasticity
Increased residual volume and overinflated lungs
airways are obstructed due to mucous and bronchial edema due to chronic irritation
o Preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients
o Risk factors-
Tobacco smoke
Occupational dusts
Chemicals
Indoor air pollution from biomass fuel used for cooking and heating
Outdoor air pollution
Any factor that affects lung growth during gestation and childhood
58
describe air trapping
- Air trapping can occur with diseases like emphysema or COPD.
o There is a narrowing or plug that causes air trapping and hyperinflation on expiration
During inspiration
* the airways are pulled open allowing gas to flow past the obstruction
During expiration
* decreased elastic recoil of the bronchial walls results in collapse of the airways and prevents normal respiratory airflow
o Results in increased WOB and eventually hypoventilation and hypercapnia
o Persistent inflammation in the airways can result in hyperactivity of the bronchi with bronchoconstriction.
May be partially reversible with bronchodilators
59
air trapping is an issue with what kind of disorder?
-This is an issue with OBSTRUCTIVE DISORDERS-
o Elastic recoil that is needed to expel inspired air is lost
o Becomes difficult to get air out
Air gets trapped in the alveoli leads to alveoli becoming hyperinflated
* A normal alveolus has a natural recoil that pushes air back up
o In emphysema for example
the alveoli are not elastic.
They are also surrounded by other alveoli have extra air inside big and floppy alveoli.
These neighboring alveoli can collapse airways
60
what complications can air trapping lead to? (3)
o increased pressure and possibly R sided HF
o decreased surface area for gas exchange
o flat diaphragm d/t breathing in high lung volumes resulting in hyper expansion of the lungs/chest
“barrel chest”
61
what factors affect blood flow through the pulmonary vasculature? Give examples (3)
- Decreased blood flow to alveoli results in increased V/Q ratio known as “dead space”
- Pulmonary embolus
- Pulmonary hypertension
- Anemia
62
how does pulmonary embolus affect blood flow through the pulmonary vasculature?
o Causes obstructed blood vessel
o Prevents transport of blood to the lungs for gas exchange
o DLCO will be lower
63
how does pulmonary hypertension affect blood flow through the pulmonary vasculature?
o Elevated pressure in the pulmonary vasculature
o DLCO will be lower -->less blood
o workload on the right ventricle increases-->resulting in right ventricle hypertrophy ->Cor Pulmonale
64
how does anemia affect blood flow through the pulmonary vasculature?
o Decreases oxygen carrying capacity of the blood
o Body compensates by breathing faster and tachycardia
o DLCO will be higher-> higher affinity for oxygen
65
what is obstructive lung diseases?
characterized by airway obstruction that is worse with expiration. More force (use of accessory muscles) or more time is required to expire a given volume of air, and emptying of lungs is slowed
* These disorders are characterized by infiltration of lung by inflammatory cells with the release of numerous cytokines that contribute to airway damage and mucus production
* Dyspnea, wheezing, increased WOB, mismatch V/Q, decreased FEV1
66
what are examples of obstructive lung diseases?
- asthma
- COPD
- cystic fibrosis
- bronchiectasis
67
describe asthma
o Hyperactive airways – more likely to constrict in response to stimuli
o Reversible bronchoconstriction*** (difference between asthma and COPD)
o Thick mucus, mucosal edema, and smooth muscle spasm cause obstruction of small airways.
68
clinical manifestations of asthma
breathing becomes labored, expiration becomes difficult -> wheezing, hyperinflation
69
risk factors for asthma (3)
- allergens
- obesity
- familial component
70
describe COPD
o 3rd leading cause of death
o Common preventable disease characterized by airflow limitation that is not fully reversible.
o Progressive
71
risk factors for COPD (4)
- smoking
- occupational dusts/chemicals
- air pollution
- genetic component.
72
describe COPD: Emphysema
Destruction of alveoli -> bigger and floppier, resulting in decreased elastic recoil
Bronchioles are more likely to collapse
This results in difficulty getting air out -> hyperinflation and air trapping
* Trapped air will affect right side of heart -> HF
Decreases the surface area available for gas exchange in alveoli
73
describe COPD: Chronic bronchitis
Hypersecretion of mucus and chronic productive cough that continues for at least 3 months/2 consecutive years
* Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall
* Continual bronchial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium
Inflammation and thickening of mucous membranes with accumulation of much and pus leading to obstruction and productive cough
Bronchial edema, smooth muscle cell hypertrophy and narrowing of airways.
Initially affects larger bronchi (unlike asthma)
Bacterial colonization of airways ->frequent infections
74
describe cystic fibrosis
o Autosomal recessive inheritance – caused by gene mutation
o Viscous secretions causing obstruction (due to chloride channel abnormalities)
o Predisposes to infections
75
describe bronchiectasis
o Abnormal dilation of a bronchus
o Congenital or secondary to an infection that could lead to inflammation and destruction of the airway.
o Recurrent infections of cystic fibrosis are a common cause for bronchiectasis
76
describe restrictive lung disorders
characterized by decreased compliance of lung tissue (takes more effort to expand during inspiration, which increases WOB)
* Dyspnea, increased RR, decreased TV, decreased FVC, V/Q mismatch
* All these disorders are characterized by activation of macrophages, polymorphonucleocytes, lymphocytes with release of numerous inflammatory and immune cytokines
77
what are examples of restrictive lung disorders (6)
- pneumonia
- ARDS
- pulmonary fibrosis
- atelectasis
- skeletal restrictions
- aspiration
78
describe pneumonia
o Inflammatory mediators respond to foreign pathogen and start damaging bronchial, mucosal and alveolocapillary membranes.
o Alveoli get filled with infectious debris and exudates
79
describe ARDS
o Acute onset of bilateral infiltrates on chest radiograph (with no cardiac explanation)
o Low ratio of partial pressure of arterial oxygen to the fraction of inhaled oxygen perfusion disorder.
o Results from acute inflammatory response resulting in increased capillary permeability, inflammation -> results in pulmonary edema, V/Q mismatch (shunting), decreased lung compliance, hypoxia.
80
risk factors for ARDS (2)
sepsis, multiple trauma
81
describe pulmonary fibrosis
o Excessive amount of fibrous and connective tissue in lung
o Lung compliance decreases
o Diffusing capacity of the alveolar membrane decreases due to alveolar thickening
82
risk factors for pulmonary fibrosis
o Risk factors:
chronic inflammation, side effect of a pulmonary disease (ARDS)
o Idiopathic pulmonary fibrosis – cause unknown
83
describe atelectasis and the three types
o Is the collapse of lung tissue
o Three types-
Compression- external pressure exerted on lung tissue; tumors/fluid/air in pleural space
Absorption-Gradual absorption of air from obstructed or hypoventilated alveoli OR After surgery (inhalation of concentrated O2 or anesthetic agent)
Surfactant impairment- decrease production or inactivation
o Increases pulmonary shunt, decreases compliance and may lead to perioperative hypoxemia
84
describe skeletal restrictions
o Kyphoscoliosis
o Restrict chest wall – decreased chest wall compliance
o Less of a problem with alveoli ribcage issue
85
describe aspiration
o Normal swallowing mechanism is impaired by a decrease level of consciousness or central nervous system abnormalities
86
what is FEV1
the amount of air blown out in the first second
87
what is FVC (forced vital capacity)?
the amount of air that can be forcefully expired after a maximal inspiration
88
what is FEV1/FVC
the amt of air that can be exhaled in one second, compared to the total amount that can be exhaled
89
Discuss the use of the FEV1/FVC ratio restrictive disease.
o FEV1
Close to normal because they have such elastic lungs
Almost all of their air is out in the first second
* FEV1 decreases less than FVC due to increased elastic recoil of stiff lungs
o FEV1/FVC ratio
Normal or increased
* This is worse
o FVC
There is a large loss of volume so it is very low
o CURVE-
Tall and narrow
90
Discuss the use of the FEV1/FVC ratio obstructive disease.
o FEV 1
Diminished
o FEV1/FVC ratio
Lower than normal
o FVC
Stays normal
o CURVE-
PEF flow not as high, scoop pattern
91
what is intrapulmonary shunt?
Intrapulmonary shunt develops when blood passes through the lungs but fails to take part in gas exchange
92
what is diffusion of oxygen from the alveoli into the blood dependent on?
V: the balance between the amount of air getting into alveoli
Q: the amount of blood perfusing the capillaries around the alveoli
93
what is the common cause of hypoxemia
o An abnormal ventilation-perfusion ratio (V/Q)
94
what is V/Q mismatch refer to?
an abnormal distribution of ventilation and perfusion
95
what can cause hypoxemia? and what does it occur in?
can be caused by inadequate ventilation of well perfused areas of the lung (low V/Q)
o Occurs in atelectasis
o Occurs in asthma as a result of bronchoconstriction
o Occurs in pulmonary edema and pneumonia when alveoli are filled with fluid
o When blood passes through portions of the pulmonary capillary bed that receive no ventilation, right to left shunt occurs, resulting in decreased systemic PaO2 and hypoxemia
- Hypoxemia can also be caused by poor perfusion of well-ventilated portions of the lung (high V/Q) resulting in wasted ventilation
o The most common cause is a pulmonary embolus that impairs blood flow to a segment of the lung
o An area where alveoli are ventilated but not perfused is alveolar dead space
96
Describe how lung volumes identify a restrictive pattern.
o Restrictive pattern= TLC
97
S/S of restrictive pattern (4)
1. Dyspnea
2. Increased respiratory rate
3. Decreased tidal volume
4. PFTs decreased FVC (forced vital capacity)
98
common restrictive lung diseases
- Aspiration
- Atelectasis
- Pulmonary fibrosis
- skeletal restriction
- ARDS
- pneumonia
99
Discuss factors that affect blood flow through the pulmonary vasculature.
o Pulmonary vasculature
i. Controlled by ANS
ii. Can be influenced by local conditions
o In chronic hypoxia
i. Pulmonary vasculature will constrict to improve the V/Q matching caused by membrane depolarization and increases intracellular calcium levels in response to low O2 concentration
1. This reflex will improve the lung’s efficiency to better match ventilation/perfusion
2. Acidemia also causes PA constriction d/t increased PaCO2 levels with drop in pH level
3. Other factors that impact pulmonary vessels
a. Histamine – vasoconstrict
b. Prostaglandins – dilate
c. Endothelin – constrict
d. Serotonin – both but constrict
e. Nitric oxide – dilate
f. Bradykinin – dilate
100
main characteristics of restrictive lung disorders
o Main characteristic: decreased lung compliance it takes more effort to expand the lungs during inspiration, which increases the work of breathing
101
s/s of restrictive lung disorders
Dyspnea
Increased RR
Decreased tidal volume
Decreased FVC
102
common types of restrictive lung disorders
Aspiration
Atelectasis
Bronchiectasis
Bronchiolitis
Pulm fibrosis
Pulm edema
ARDS
103
Clinical manifestations of ARDS
Dyspnea and hypoxemia with poor response to O2
Hyperventilation and respiratory alkalosis
Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
Increased WOB, decreased tidal volume and hypoventilation
Hypercapnia, respiratory acidosis, and worsening hypoxemia
Decreased cardiac output, hypotension and death
104
main characteristics of obstructive lung disorders
airway obstruction that is worse with expiration. More force or more time is required to expire a given volume of air, and emptying of the lungs is slowed
105
clinical presentations of obstructive lung disorders (5)
Infiltration of the lung by inflammatory cells with the release of cytokines that contribute to airway damage and mucous production
Dyspnea
Wheezing
V/Q mismatch
Decreased FEV1
106
common types of obstructive lung disorders
Asthma
COPD
107
Asthma clinical manifestations
Asymptomatic between attacks with normal PFTs
During asthma attack: chest constriction, expiratory wheezing, dyspnea, non productive cough, prolonged expiration, tachycardia and tachypnea
Pulses paradoxus
108
COPD clinical manifestations (3)
Dyspnea on exertion to dyspnea at rest
Lots of sputum
Chronic respiratory infections
109
airway problems (5)
* Hypercarbia
* Increased resistance- resistance to gas flow, bc as gas molecules moves down airways, meets resistance
* Decreased flow rates
* Fev1/VC
* PEFR
* BS: wheezes, stridor
110
alveolar problems (5)
* Hypoxemia
* Decreased compliance
* Decreased lung volume
* Decreased DLCO
* BS: crackles
111
what is DLCO testing?
tell you if you have a diffusion defect
112
DLCO interpretation: emphysema
have multiple alveoli that are clustered together like grapes
- emphysema has destruction of the alveoli wall and when the alveoli walls get destroyed so does the pulmonary capillaries
- this is why the DLCO is very low, you have one big non-elastic alveolus and limited number of pulmonary capillaries
113
DLCO interpretation: Anemia
have normal alveoli capillary membrane but just have fewer transporters inside the hgb within the RBC to absorb O2
114
DLCO interpretation: pulmonary emboli
patient might have tiny micro-emboli in some of the pulm capillaries and that will limit the blood flow to the individual alveoli-->the individual will have normal blood flow in the capillaries across some of the alveoli or they would not be alive
115
DLCO interpretation: fibrosis/pneumonitis
have thickening of the alveolar capillary membrane-> makes it more difficult for O2 with normal breathing or carbon monoxide with this test (PFT) to cross over in the membrane
116
DLCO interpretation: atelectasis
have fewer alveoli-->result=DLCO will be lower
