Mid-Term Exam - Part 2, Pathophysiology

Question 1

a) Hypoxemia
b) Hypoxia
c) Anoxia

Answer 1

a) low PaO2
b) low O2 in the tissues resulting from inadequate O2 delivery to meet tissue oxidative requirements.
c) absence of O2, the extreme of hypoxia

Question 2

Causes of Hypoxemia

Answer 2

Respiratory: reduced inspired oxygen tension, alveolar hypoventilation, impairment of diffusion, ventilation-perfusion mismatching.
Other systems: blood volume loss, anemia, carbon monoxide poisoning (240x more binding capacity to Hgb), hypothermia

Question 3

Signs / Sx of Hypoxemia

Answer 3

cyanosis
acute cerebral hypoxia (impaired judgement, confusion, coma, death)
chronic cerebral hypoxia (fatigue, apathy, reduced attention, drowsiness)
cardiac arrythmia
pulmonary artery vasoconstriction

Question 4

a) hypercapnia

b) hypocapnia

Answer 4

a) increase in PaCO2 (hypoventilation > 45mmHg
b) low PaCO2 (hyperventilation <35mmHg)

normal = 35-45mmHg

Question 5

Signs / Sx of Hypercapnia

Answer 5

increased HR and BP
dizziness
Headache (HA)
confusion or loss of consciousness
muscle twitching and tremor
irritability
CO2 Narcosis: a condition of confusion, tremors, convulsions, and possible coma that may occur if blood levels of carbon dioxide increase to 70 mm Hg or higher.

Question 6

Signs / Sx of Hypocapnia (Hyperventilation Syndrome)

Answer 6

lightheadedness
fatigue
irritability
inability to concentrate
tingling
impaired consciousness

Question 7

Restrictive Lung Dysfunction

Answer 7

an abnormal reduction in pulmonary ventilation. lung expansion is diminished. the volume of gas moving in/out of the lungs is decreased.
flow rates are often maintained, while volumes are less

Question 8

Obstructive Lung Dysfunction

Answer 8

diseases of the respiratory tract which produce an obstruction to airflow, and can ultimately affect the mechanical function and gas exchanging capability. flow rates impaired. tissue damage, airway destruction.

i.e. chronic bronchitis, emphysema, asthma, bronchiectasis

though a disease may present with more obstructive or restrictive pattern, there are components of both patterns in most diseases.

Question 9

Restrictive Lung Dysfunction: Clinical Manifestations: Signs

Answer 9

Tachypnea
Hypoxemia ( < 80mmHg), V/Q mismatching
Decreased breath sounds (dry inspiratory rales (velcro crackles)
Decreased lung volumes
Decreased diffusing capacity
Cor pulmonale ( alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system)

Question 10

Restrictive Lung Dysfunction: Clinical Manifestations: Symptoms

Answer 10

Dyspnea (shortness of breath (SOB))
Dry, non-productive cough
Emaciation (SOB when eating, high fat diet)

Question 11

Restrictive Lung Dysfunction: pathogenesis

Answer 11

1) chest wall or lung compliance reduced = increased transpulmonary gradient needed just to expand the lungs
2) eventually causes all lung volumes and capacities to be reduced.
3) work of breathing is increased (increased airway resistance, increased flow rates, decreased lung/chest wall compliance)

Question 12

Identifying RLD by Spirometry

Answer 12

Total Lung Capacity (IRV + TV + ERV + RV) and Vital Capacity (ERV + TV + IRV) are the two most common measures used to identify RLD.
Decreases in TLC and FRC (ERV + RV) are a direct result of a decrease in lung compliance.

RLD: more pressure, less volume

Question 13

RLD Compensatory Strategies

Answer 13

to overcome the decrease in pulmonary compliance, the RR is usually increased.
Accessory muscles of inspiration are recruited to assist in chest wall expansion when at rest of at lower activity level.
with RLD the % of VO2 required to support the work of breathing can be 25% or more (normally 5%).

Question 14

Treatment RLD; permanent or progressive

Answer 14

i.e. pulmonary fibrosis
supportive measures:
antibiotic therapy
measures to promote adequate ventilation
supplemental oxygen
prevention of accumulation of pulmonary secretions
nutritional support
flexibility/posture
more prone to infection, secretion accumulation

Question 15

Treatment RLD; acute and reversible, or chronic and reversible

Answer 15

i.e. guillian-barre syndrome, myasthenia gravis

aimed at specific corrective interventions as well as supportive measures.

Question 16

OLD: pathogenesis

Answer 16

1) altered expiratory flow rate
2) increased residual volume
3) increased airflow resistance
4) loss of elastic recoil
5) increased work of breathing

Question 17

OLD: clinical manifestations: Signs

Answer 17

hypoxemia
increased production of mucous/impaired mucous clearance
inflammation of the mucosal lining of the bronchi and bronchioles
mucosal thickening
spasm of the bronchial smooth muscle
pulmonary hypertension
polycythemia (blood more viscous, clots spO2 is low)
Cor Pulmonale
hyperinflation of lungs - deep breathing makes them feel worse

Question 18

OLD: clinical manifestations: Symptoms

Answer 18

chronic cough
expectoration of mucus
wheezing
dyspnea on exertion (DOE)

Question 19

OLD: Work of Breathing

Answer 19

respiratory muscles must work harder to overcome the increased airway resistance
diaphragm excursion may be limited due to hyperinflation of the lungs (flatter shape, inability to contract strongly)
alveolar ventilation is reduced
alveolar-capillary membrane surface area may be reduced
force air out of the lungs = a lot of abdominal contraction

Question 20

OLD: Classification of location of airway obstruction (3)

Answer 20

a) bronchi or airways with cartilage in their walls (>2mm diameter)
b) bronchioles or airways without cartilage in their walls (<2mm diameter)
c) lung parenchyma (alveolar units); portion of lung involved in gas exchange

Question 21

OLD: Alteration in Airflow

Answer 21

narrowing of the bronchial lumen: increased resistance to airflow
loss of normal elastic recoil of lung tissue = tendency for the airways to collapse hyperinflation

Question 22

Emphysema

Answer 22

an alveolar or parenchyma disease. an abnormal and permanent enlargement or air spaces distal to the terminal nonrespiratory bronchioles, accompanied by destructive changes of the alveolar walls. loss of elastic recoil, excessive collapse of the airways on exhalation and chronic airflow obstruction.

Question 23

Pulmonary Fibrosis: description

Answer 23

RLD: an inflammatory process involving all the components of the alveolar wall that progresses to gross distortion of the lung architecture. first inflammatory, then scar and become fibrotic.

Question 24

Bronchiectasis

Answer 24

a permanent abnormal dilation and distortion of one or more bronchi that is caused by destruction of the elastic and muscular components of the bronchial walls.

Etiology: cystic fibrosis, bronchial obstruction, etc

Question 25

Asthma

Answer 25

a disease of airways characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli. hypersensitivity.
airways are dynamic (alter diameter): airway reactivity is increased
Extrinsic asthma: allergens (begins in childhood)
Intrinsic Asthma: begins after 35, more severe

Question 26

SCI

Answer 26

damage to or interruption of the neurological pathways contained within the spinal cord
paradoxical breathing
over time pulmonary compliance decreased, shallow breathing, atelectasis of lung
hypoxemia
Treatment: strength and endurance respiratory muscles, chest wall stretching, assisted cough, postural drainage, suctioning

Question 27

Brain Injury

Answer 27

postural support, musculoskeletal

Question 28

Chronic Liver Conditions

Answer 28

enlarged liver = fluid in abdomen = do not allow lungs to fully extend = impaired function of diaphragm

Question 29

Ankylosing Spondylitis

Answer 29

chronic inflammatory disease of the spine characterized by immobility of the sacroiliac and vertebral joints and ossification of the paravertebral ligaments (stiff spine).
markedly decreased chest wall compliance
VC and IC decreased
RV and FRC increased
CXR may show areas of fibrosis (hemoptysis)
DOE

Question 30

Pulmonary Fibrosis: clinical manifestation

Answer 30

PFTs:
decreased TLC, VC, FRC and RV
normal or slightly decreased flow rates
diffusing capacity decreased
as disease progresses, RR increases, TV decreases
PaO2 decreased
PaCO2 WNL
breath sounds: bibasilar end-inspiratory dry rales and possibly decreased breath sounds

Question 31

Pulmonary Fibrosis: symptoms

Answer 31

dyspnea
repetitive no productive cough
weight loss
anorexia
sleep disturbances

Question 32

Pulmonary Fibrosis: treatment

Answer 32

corticosteroids to combat inflammation

supportive measures: supplemental O2, ventilatory, nutritional support, energy conservation, chest wall flexibility

Question 33

Pulmonary Fibrosis: CV findings

Answer 33

as the pulmonary capillary bed is destroyed, pulmonary hypertension develops. this can lead to cor pulmonale due to the strain on the right ventricle.
jugular venous distension, edema in extremities, liver tenderness, HA (can drain blood)

Question 34

Pneumonia

Answer 34

an inflammatory process of the lung parenchyma. this inflammation usually begins with an infection of the lower respiratory tract.
community acquired
hospital acquired
postural drainage: vibration, percussion

Question 35

SCI: autonomic dysreflexia

Answer 35

vasoconstriction below the level of the injury which causes hypertension. the cns above the level f the lesion tries to compensate by causing vasodilatin and bradycardia

Question 36

Asthma: Treatment

Answer 36

relieve bronchospasm
drugs: sympathomimetis; theophylline; antichoinergics; cromolyn; corticosteriods
mobilize secretions
maintain alveolar ventilation
PFTs: FEV1 and FEV1/FVC are reduced during an attack
Intermittent wheezing: prolonged exhale

Question 37

Types of Bronchietasis (3)

Answer 37

1) Cylindric: tubular bronchi
2) Varicose: dilated and irregular in form and shape
3) Saccular: bronchi are very dilated and ballooning in shape