espiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy Flashcards

1
Q

what should be measured to aid appropotite therapy for acute respiratory distress and acute ph acid base balance

A

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

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2
Q

determination of blood Ph

A

by using a glass electrode

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3
Q

determination of blood co2

A

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

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4
Q

maximum expiratory flow

A

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

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5
Q

what is the outcome of increased pressure to the outside of the bronchioles

A

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

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6
Q

lungs volume become smaller causes max expiratory airflow to decrease

A

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.

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7
Q

constricted lungs have both

A

reduced total lung capacity and reduced residual volume

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8
Q

what happens in constricted lungs and partial airway obstruction

A

the lungs cannot be expanded to their normal max volume, so the max expiratory flow rate does not reach its normal max extent so

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9
Q

constricted lung diseases include

A

tuberculosis , silicosis

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10
Q

constricted chest cage disease

A

scoliosis, kyphosis and fibrotic pleurisy

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11
Q

severe airway obstructuion diesease

A

asthma emphysema

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12
Q

Another useful clinical pulmonary test, and one that is

also simple, is to record

A

on a spirometer the forced expiratory vital capacity (FVC)

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13
Q

how FVC is measured and what does it explains

A

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.

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14
Q

list down pulmonary abnormaloties

A
emphysema 
tuberculosis
pneumonia 
asthma 
atelectasis
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15
Q

chronic empysema is causes by what pathophysiological changes

A
  1. 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
  2. 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
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16
Q

effect of pulomnary emphysema

A
  1. increase work load on breathing due to compressive force outside the alveoli and bronchioles
  2. decreases diffusion capacity due to destroyed alveolar walls and decreases exchnage of o2 and co2
  3. abnormal ventilation-prefusion ration causes physiological shunt and dead space
  4. causes pulomary hypertension due to decreases amount of pulmonary vessels in the destroyed alveoli which can cause right sided heart failure
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17
Q

what is pneumonia

A

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

18
Q

pneumonia affects what normal function of lung

A

it decreases the total available surface of respiratory membrane
it also decreases the ventilation- perfusion ration causing hyopoxemia and hypercapnia

19
Q

atelectasis

A

the collapse of lungs due to airway obstruction or due to lack of surfactant

20
Q

airway obstruction causes lung to collapse

A
  1. small bronchioles become obstructure
  2. 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
21
Q

Lack of “Surfactant” as a Cause of Lung Collapse

A

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

22
Q

usual cause of asthma

A

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.

23
Q

the allergic person forms?

A

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

24
Q

what happens when an hypersensitive person inhales pollen or an allergen

A

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

25
Q

person suffering from asthma has difficulty expiring which causes

A

dyspnea

26
Q

what is tuberculosis

A

In tuberculosis, the tubercle bacilli cause a peculiar tissue
reaction in the lungs, including (1) invasion of the infected
tissue by macrophages and (2) “walling off” of the lesion
by fibrous tissue to form the so-called tubercle. This
walling-off process helps to limit further transmission of
the tubercle bacilli in the lungs and therefore is part of
the protective process against extension of the infection.
However, in about 3 percent of all people in whom tuberculosis develops, if the disease is not treated, the wallingoff process fails and tubercle bacilli spread throughout the
lungs, often causing extreme destruction of lung tissue
with formation of large abscess cavities.

27
Q

Thus, tuberculosis in its late stages is characterized
by many areas of fibrosis throughout the lungs, as
well as reduced total amount of functional lung tissue.
These effects cause

A

(1) increased “work” on the part of
the respiratory muscles to cause pulmonary ventilation
and reduced vital capacity and breathing capacity;
(2) reduced total respiratory membrane surface area
and increased thickness of the respiratory membrane,
causing progressively diminished pulmonary diffusing
capacity; and (3) abnormal ventilation-perfusion ratio in
the lungs, further reducing overall pulmonary diffusion
of O2 and CO2.

28
Q

Inadequate oxygenation of the blood in the lungs

because of extrinsic reasons

A

Deficiency of O2 in the atmosphere

b. Hypoventilation (neuromuscular disorders)

29
Q

Pulmonary disease causing hypoxia

A

a. Hypoventilation caused by increased airway
resistance or decreased pulmonary compliance
b. Abnormal alveolar ventilation-perfusion ratio
(including either increased physiological dead
space or increased physiological shunt)
c. Diminished respiratory membrane diffusion

30
Q
  1. Inadequate O2 transport to the tissues by the blood
A

a. Anemia or abnormal hemoglobin
b. General circulatory deficiency
c. Localized circulatory deficiency (peripheral,
cerebral, coronary vessels)
d. Tissue edema

31
Q
  1. Inadequate tissue capability of using o2
A

a. Poisoning of cellular oxidation enzymes
b. Diminished cellular metabolic capacity for using
oxygen because of toxicity, vitamin deficiency, or
other factors

32
Q

The

classic cause of inability of the tissues to use O2 is

A

O2 is cyanide
poisoning, in which the action of the enzyme cytochrome
oxidase is blocked by the cyanide to such an extent that
the tissues simply cannot use O2, even when plenty is
available

33
Q

Also, deficiencies of some of the

A

tissue cellular

oxidative enzymes or of other elements in the tissue oxidative system can lead to this type of hypoxia.

34
Q

beriberi

A

in which several
important steps in tissue utilization of oxygen and the
formation of CO2 are compromised because of vitamin B
deficiency

35
Q

effects of hypoxia on body

A

coma

and depressed muscle activity

36
Q

cyanosis

A

The term cyanosis means blueness of the skin, and its
cause is excessive amounts of deoxygenated hemoglobin
in the skin blood vessels, especially in the capillaries. This deoxygenated hemoglobin has an intense dark blue–
purple color that is transmitted through the skin.
In general, definite cyanosis appears whenever the
arterial blood contains more than 5 grams of deoxygenated hemoglobin in each 100 milliliters of blood.

37
Q

who is more likely to suffer from cyanosis and who is not

A

person with anemia is least likely and person with polycythemia vera is most likely

38
Q

hypercapnia occurs in people

A

suffering with circulatory deficiency or hypoventilation

39
Q

dysapnea

A

Dyspnea means mental anguish associated with inability
to ventilate enough to satisfy the demand for air. A
common synonym is air hunger.

40
Q

3 factors that causes dyspanea

A

the abnormility in the gasses in the body fluids such as hypercapnia and hypoxia
or due to amound of work load on the respiratory muscle in order to ventilate
or state of mind