espiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy Flashcards
what should be measured to aid appropotite therapy for acute respiratory distress and acute ph acid base balance
Among the most fundamental of all tests of pulmonary
performance are determinations of the blood partial pressure of oxygen (PO2), carbon dioxide (CO2), and pH
determination of blood Ph
by using a glass electrode
determination of blood co2
A glass electrode pH
meter can also be used to determine blood CO2. When a weak solution of sodium bicarbonate is exposed to CO2
gas, the CO2 dissolves in the solution until an equilibrium
state is established. In this equilibrium state, the pH of
the solution is a function of the CO2 and bicarbonate
ion concentrations in accordance
maximum expiratory flow
When a person expires with great force, the expiratory airflow reaches a maximum flow beyond which the
flow cannot be increased any more, even with greatly
increased additional force
what is the outcome of increased pressure to the outside of the bronchioles
increases pressure to the outside of the bronchioles and chest cavity causes the air to flow from the alveoli into the bronchioles but at the same time it causes the bronchioles to collapse, so more expiratory force will increase the alveolar pressure but it will cause more bronchioles to collapse thus a resistance in expiratory flow
lungs volume become smaller causes max expiratory airflow to decrease
The
main reason for this phenomenon is that in the enlarged
lung the bronchi and bronchioles are held open partially
by way of elastic pull on their outsides by lung structural
elements; however, as the lung becomes smaller, these
structures are relaxed so that the bronchi and bronchioles
are collapsed more easily by external chest pressure, thus
progressively reducing the maximum expiratory flow rate
as well.
constricted lungs have both
reduced total lung capacity and reduced residual volume
what happens in constricted lungs and partial airway obstruction
the lungs cannot be expanded to their normal max volume, so the max expiratory flow rate does not reach its normal max extent so
constricted lung diseases include
tuberculosis , silicosis
constricted chest cage disease
scoliosis, kyphosis and fibrotic pleurisy
severe airway obstructuion diesease
asthma emphysema
Another useful clinical pulmonary test, and one that is
also simple, is to record
on a spirometer the forced expiratory vital capacity (FVC)
how FVC is measured and what does it explains
for a person with normal lungs and in
Figure for a person with partial airway obstruction. In performing the FVC maneuver, the person first
inspires maximally to the TLC and then exhales into the
spirometer with maximum expiratory effort as rapidly
and as completely as possible. The total distance of the
down slope of the lung volume record represents the
FVC, as shown in the figure.
Now, study the difference between the two records
for (1) normal lungs and (2) partial airway obstruction.
The total volume changes of the FVCs are not greatly
different, indicating only a moderate difference in basic
lung volumes in the two persons. There is, however, a
major difference in the amounts of air that these persons
can expire each second, especially during the first second.
Therefore, it is customary to compare the recorded forced expiratory volume during the first second (FEV1)
with the normal. In the normal person (see Figure
43-3A), the percentage of the FVC that is expired in the
first second divided by the total FVC (FEV1/FVC%) is
80 percent. However, note in Figure 43-3B that, with
airway obstruction, this value decreased to only 47
percent. In persons with serious airway obstruction, as
often occurs with acute asthma, this value can decrease
to less than 20 percent.
list down pulmonary abnormaloties
emphysema tuberculosis pneumonia asthma atelectasis
chronic empysema is causes by what pathophysiological changes
- chronic infection: inhaling of smoke irrate the bronchi and cause infection which paralyses the cilia present respirtory epi due to nicotine and also releases excess muscus which makes it hard to remove mucus from the air passage way
and also inhibits alveolar macrophages.
2.the infection causes inflammatory edema in bronchiole walls and cause chronic oobstruction - due to the obstruction there is less air expired and the antrapment of air in alevoli causes the alveoli to stretch this with the infection causes the alveolar walls to damage
effect of pulomnary emphysema
- increase work load on breathing due to compressive force outside the alveoli and bronchioles
- decreases diffusion capacity due to destroyed alveolar walls and decreases exchnage of o2 and co2
- abnormal ventilation-prefusion ration causes physiological shunt and dead space
- causes pulomary hypertension due to decreases amount of pulmonary vessels in the destroyed alveoli which can cause right sided heart failure
what is pneumonia
it is the inflammation of lungs due to a bacteria pneumoniaccoci or a virus which causes the pulmonary membrane to becomes inflamed and poruous so fluid and wbc and other cells leak into the alveoli and accumulate
sometimes the whole lung lobe becomes consolidated
pneumonia affects what normal function of lung
it decreases the total available surface of respiratory membrane
it also decreases the ventilation- perfusion ration causing hyopoxemia and hypercapnia
atelectasis
the collapse of lungs due to airway obstruction or due to lack of surfactant
airway obstruction causes lung to collapse
- small bronchioles become obstructure
- large bronchioles become obstructed or blocked due to a tumor
if the alveolar wall is pliable it collapses when the air in the pulmonary capillaries is absorbed by the alveoli
if it is rigid or fibrotic it stays open increase the negative pressure inside the alveoli which causes fluid to diffuse from the capillaries into the alveoli causing edema
Lack of “Surfactant” as a Cause of Lung Collapse
surfactant decreases the surface tension and prevents the collapse of lungs
people suffering with hyaline membrane disease does not produce sufficient surfactant and their lungs collapse causing edema
usual cause of asthma
contractile hypersensitivity of the bronchioles in response to foreign substances in
the air. In about 70 percent of patients younger than age
30 years, the asthma is caused by allergic hypersensitivity,
especially sensitivity to plant pollens. In older people, the
cause is almost always hypersensitivity to non-allergenic
types of irritants in the air, such as irritants in smog.
the allergic person forms?
The typical allergic person tends to form abnormally
large amounts of IgE antibodies, and these antibodies
cause allergic reactions when they react with the specific
antigens that have caused them to develop in the first
place . In persons with asthma,
these antibodies are mainly attached to mast cells that
are present in the lung interstitium in close association
with the bronchioles and small bronch
what happens when an hypersensitive person inhales pollen or an allergen
When an asthmatic person breathes in pollen to which he or she is
sensitive (i.e., to which he or she has developed IgE antibodies), the pollen reacts with the mast cell–attached
antibodies and causes the mast cells to release several
different substances. Among them are (a) histamine, (b)
slow-reacting substance of anaphylaxis (which is a mixture
of leukotrienes), (c) eosinophilic chemotactic factor, and
(d) bradykinin. The combined effects of all these factors,
especially the slow-reacting substance of anaphylaxis, are
to produce (1) localized edema in the walls of the small
bronchioles, as well as secretion of thick mucus into the
bronchiolar lumens, and (2) spasm of the bronchiolar
smooth muscle. Therefore, the airway resistance increases
greatly
