SAINT LOUIS UNIVERSITY

SCHOOL OF MEDICINE
DEPARTMENT OF PHYSIOLOGY

Physiology and Pathophysiology

2:00 – 5:00 PM Monday R505

MODULE 6
(1st Semester)
RESPIRATORY PHYSIOLOGY

Submitted by:
GROUP NO. 5-A
Heraña, Ma. Vanessa
Laguisma, Heranee
Laranang, Nicole
Leones, Casmin
Lo, Cindy
Lopez, Dave
Manuzon, Sedlex

Submitted to:
Dr. Lizalyn Marie Revilla
Dr. Margot Schlaaff-Yasay
Laboratory Coordinators

Date Performed: November 18, 2019

Date Submitted: November 23, 2019
1. Diagram the pulmonary volumes and capacities and label the following: RV, IRV, TLC, TV, ERV, FRC, VC and IC.

2. Draw the flow volume loop of the following:

3. What happens to FRC, ERV, IRV, and VC when a person lies supine from a standing position? Why?

● Various lung volumes and capacities will change when changing from standing to sitting to supine
(lying down) position. Inspiratory and expiratory volumes will be greater when sitting than lying.
This is explained by gravity pulling the abdominal contents away from the diaphragm when
standing, therefore increasing the volume of the thoracic cavity.
● In a supine position the patient’s TV, IRV and ERV will decrease as the abdominal organs rest
against the diaphragm limiting its movements. Thus, the vital capacity will decrease.

II. RESPIRATORY CALCULATIONS: LUNG VOLUMES, DEAD SPACE AND ALVEOLAR VENTILATION

1. Using the information provided in figure 1-1, what are the values for the tidal volume, inspiratory capacity, expiratory reserve
volume, functional residual capacity, vital capacity, and total lung capacity?

Tidal volume = 500 mL

Inspiratory capacity = Tidal Volume + Inspiratory reserve volume

● Inspiratory capacity = 500 mL + 3100 mL = 3600 mL

Expiratory reserve volume = Functional reserve volume - Residual Volume

● Expiratory reserve volume = 2400 mL - 1200 mL = 1200 mL

Functional residual capacity = Reserve volume + Expiratory reserve volume

● Functional residual capacity = 1200 mL + 1200 mL = 2400 mL

Vital capacity = Inspiratory reserve volume + Tidal volume + Expiratory reserve volume

● Vital capacity = 3100 mL + 500 mL + 1200 mL = 4800 mL

Total lung capacity = Vital capacity + Residual volume

● Total lung capacity = 4800 mL + 1200 mL = 6000 mL

2. What is the name of the volume remaining in the lungs after maximal expiration that is not measurable by spirometry? What other
lung volumes or capacities are not measurable by spirometry?

Residual volume (RV) is the volume that remains in the lungs after maximal expiration and cannot be measured by spirometry . The other lung
volumes that are not measurable by spirometry are Functional residual capacity (FRC) and total lung capacity (TLC) because they already contain
residual volume.

3. Define and differentiate anatomic dead space, alveolar dead space and physiologic dead space?

Alveolar dead space

 ● sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries.
● is negligible in healthy individuals but can increase dramatically in some lung diseases due to ventilation perfusion mismatch.

Anatomical dead space

● is the volume of the conducting airways (150-250mL). It is the portion of the airways which conducts gas to alveoli.
● No gas exchange is possible in the spaces.

In healthy lungs where the alveolar dead space is small, anatomical dead space is constant regardless of circulation.

Physiological dead space

● is the part of the tidal volume which does
not participate in gas exchange

III. MEASUREMENT OF PEAK EXPIRATORY FLOW RATE

1. What is peak expiratory flow rate?

Peak expiratory flow rate or PEFR is highest flow rate during the expiratory maneuver. This is among the three main pulmonary function tests in
creating a flow-volume loop; the other two includes the FVC and expiratory flow rates.

2. Discuss the advantage of PEFR monitoring and mention clinical conditions where it is useful.

Measuring PEFR, or the maximum speed of expiration, is important for monitoring a patient’s lungs. An example of where this is useful is
monitoring the progress of asthma, meaning its severity. It is also relatively simple to measure PEFR as a peak flow meter (PFM) can be operated
even by children. Thus, a patient can participate in monitoring the progress of their disease by providing data to their physician. This is useful for
adjusting medications according to the patient’s well-being. This is not limited to asthma and monitoring PEFR can also be useful for chronic
obstructive pulmonary disease (COPD).

IV. EXAMINATION OF CHEST AND LUNGS

1. What happens to the vibration, percussion note and breath sounds if there were:

Vibration Percussion note Breath sounds

Air in the pleural cavity Decreased Hyper resonant Absent

Fluid in the pleural cavity Decreased Dull Absent/Decreased

Solidification of lung segment Increased Dull Bronchial breath sounds

2. When do you hear the following adventitious sounds?

a. Wheeze: Can be heard when there is an obstruction in the airways that narrows the passage. Wheezing can be heard upon exhalation.
Diseases that cause wheezing including pertussis (commonly known as whooping cough), COPD, and tumors in the trachea.
b. Crackles: Can be heard more often on inspiration rather than on expiration. Crackles are commonly described as a snapping sound on
auscultation. Can be indicative of fluid in the alveoli of the lungs or inflammation and/or infection of bronchi or bronchioles.

3. What is egophony?

Egophony is the increased resonance of higher frequencies of the voice that can be heard on auscultation of the lungs. Often compared with the
bleating sounds of a goat. The sound is due to high frequencies having enhanced transmission through fluid while lower frequencies are filtered
out. Commonly seen amongst patients with pleurisy with effusion.

CASE 1

1. What is the expected spirometry results for Bronchial Asthma? Based on the patient’s spirometry results, what parameters
denote presence of obstructive airway disease? Explain.

Spirometry results for Bronchial Asthma:

● Low FEV1
● Low FEV1/FVC ratio
 Optimally, the initial spirometry should also include measurements before and after inhalation of a short-acting bronchodilator in all
patients in whom the diagnosis of asthma is considered. Spirometry measures the forced vital capacity (FVC), the maximal amount of air expired
from the point of maximal inhalation, and the forced expiratory volume in one second (FEV1). A reduced ratio of FEV1 to FVC, when compared
with predicted values, demonstrates the presence of airway obstruction. Reversibility is demonstrated by an increase of 12% and 200 mL after the
administration of a short-acting bronchodilator.

During episodes of acute asthma, pulmonary function tests reveal an obstructive pattern. This includes a decrease in the rate of maximal
expiratory air flow (a decrease in FEV1 and the FEV1/FVC ratio) due to the increased resistance, and a reduction in forced vital capacity (FVC)
correlating with the level of hyperinflation of the lungs. Because these patients breathe at such high lung volumes (near the top of the pressure-
volume curve, where lung compliance greatly decreases), they must exert significant effort to create an extremely negative pleural pressure, and
consequently fatigue easily. Overinflation also reduces the curvature of the diaphragm, making it less efficient in generating further negative
pleural pressure.

2. What lung volumes and capacities are affected in bronchial asthma? Compare these changes to normal PFT.

The following lung volumes and capacities are affected in Bronchial Asthma:
● Residual volume: increased
● Functional residual capacity: increased
● Expiratory reserve volume: reduced
● Vital capacity: reduced
● Tidal volume: becomes deeper

3. Define“work of breathing”.What are the factors that affect work of breathing? List and explain all the clinical manifestations
of Nene that shows affectation of the work of breathing.

Work of breathing is the work done by respiratory muscles during breathing to overcome the resistance in thorax and respiratory
tract.
During the work of breathing, the energy is utilized to overcome three types of resistance:
a. Airway Resistance
Airway resistance is the resistance offered to the passage of air through respiratory tract. Resistance increases during bronchiolar constriction,
which in creases the work done by the muscles during breathing. Work done to overcome the airway resistance is called airway resistance work.

b. Elastic Resistance of Lungs and Thorax

Energy is required to expand lungs and thorax against the elastic force. Work done to overcome this elastic resistance is called compliance work.

c. Non-elastic Viscous Resistance

Energy is also required to overcome the viscosity of lung tissues and tissues of thoracic cage. Work done to overcome this viscous resistance is
called tissue resistance work.
4. Interpret initial ABG results. Explain the reason behind the noted abnormality. What abnormality should be the foremost
consideration in making corrections?

pH (7.35-7.45*) 7.48 Alkalosis

pCO2 (38-42*) 35 Respiratory

HCO3 (22-26*) 22 Uncompensated

*values given are based on used references

The patient experiences alkalosis due to elevated pH (7.48 against the normal range of 7.35 - 7.45). The alkalosis is respiratory in nature since
there is decreased carbon dioxide pressure in the arterial blood, taking into consideration that carbon dioxide is accounted for blood acidity. The
pCO2 is less than 38 making it respiratory in nature. The type of respiratory alkalosis is uncompensated because the bicarbonate levels is still
within normal. In order to consider it as partially or fully compensated, the bicarbonate (which accounts for the basicity of the blood) should have
been increased or is greater than the normal which is greater than 26.

Final Diagnosis: Uncompensated Respiratory Alkalosis

CASE 2

1. What is the most likely predisposing factor to Noynoy’s condition? Explain how this leads to his present illness.

The most likely predisposing factor for Noynoy’s condition is smoking. Smoking damages the air sacs, airways, and the lining of the lungs. This
allows less air to flow in and out of the airways due to the:

● Stiffening of the air sacs

● Deterioration of the walls between air sacs
● Thickening and inflammation of the airway walls
● Increased production of mucus in the airways causing obstruction

Cigarette smoke contains harmful toxins that can lead to severe lung irritation, triggering the onset of COPD.

2. Interpret the spirometry results of Noynoy. What are the criteria for diagnosing his disease? Differentiate this from a spirometry of a
bronchial asthma patient like Nene.
The spirometry results in pre-bronchodilation show a low FEV1/FVC ratio, abnormal FEV1, and an abnormal FVC. Post-bronchodilation results
are still abnormal, with less than 12% increase in FEV1.

The criteria for diagnosing COPD is a one second/forced vital capacity ratio of less than 70% of the predicted value.

The post-bronchodilation results help separate asthma from COPD. If FEV1 increases by 12% or 200ml after taking albuterol, it means that the
airway blockage is reversible. Reversibility is a sign of asthma.

3. Draw the MEF of a COPD patient alongside a normal MEF. Which of the lug volumes and capacities change in COPD patients?

● FEV1 and FVC are reduced

○ FEV1 is reduced more than FVC is: thus, FEV1/FVC is decreased.
● Increased Total lung capacity (TLC)
● Increased residual volume (RV) and function residual capacity (FRC)
● Increase in RV/TLC ratio
○ RV increase to a greater extent than TLC
● Vital capacity is decreased

4. Explain the physiologic basis for the following clinical manifestations of Noynoy:

a. Chronic cough, progressive dyspnea and wheezing

● Airflow limitation and hyperinflation
○ Intrinsic airway factors relate to bronchial wall inflammation and include mucosal inflammation/edema,
bronchial wall remodeling/fibrosis, and increased mucosal secretions.
○ Extrinsic factors involve the loss of elastic tissue support for small airways and the dynamic expiratory
compression of these airways.
○ Other factors such as respiratory muscle dysfunction can further limit airflow in some patients.
○ Hyperinflation can also occur, leading increase in functional residual capacity (FRC) and residual volume (RV).
● As a consequence, there is an augmentation of the inspiratory work of breathing, which is an important factor in producing
dyspnea. As the expiratory time is essential for lung emptying, factors that decrease this time, such as an increasing
respiratory rate during exercise, result in a progressive increase in FRC. This phenomenon is called dynamic hyperinflation
and is largely responsible for exercise limitation in COPD.
●
b. Pursed lip breathing
● Ventilatory muscle dysfunction
○ A major factor is a consequence of hyperinflation, which limits force generation and endurance, and places the
inspiratory muscles at a mechanical disadvantage.
○ Other factors include nutritional alterations, a sustained inflammatory response that affects the contractile
apparatus, tissue hypoxia, and loss of muscle mass.
●
c. Neck vein engorgement and bipedal edema
● Cardiovascular disturbances
○ Lung inflammation may directly affect atherogenesis by driving systemic inflammation.
○ Pulmonary hypertension is a late complication of COPD and independently worsens its prognosis.
○ A major factor is chronic hypoxia, which can result in pulmonary vasoconstriction. Right ventricular dysfunction and
failure (cor pulmonale) may eventually develop and add to the morbidity and mortality of this disease. This phenomenon
will lead to the increase volume in venous system resulting to neck vein engorgement and bipedal edema.

5. Interpret the ABGs of Noynoy. Explain the decrease in pO2 and the increase in pCO2. What could have caused his deterioration?
Why was there a change in Noynoy’s sensorium? How will the abnormality in the blood gas alter the delivery of O2 to the tissue?
 ADMISSION AFTER 2 HOURS AFTER 12 HOURS

pH 7.32 7.28 7.10

pCO2 48 mmHg 54 mmHg 68 mmHg

HCO3 26 28 30

pO2 56 mmHg 92 mmHg 81 mmHg

FiO2 21 % 40 % 40 %

RESPIRATORY ACIDOSIS

● An increase in pCOs is an indication that it is “respiratory” instead of “metabolic”

● Destruction of bronchial walls or accumulation of sputum, there is insufficient oxygenation process, increasing the CO2 accumulation
and decreasing the O2 supply. Increase CO2 results to hypercapnia and hypoxemia, resulting to decrease delivery of O2 to the tissues.

Mechanisms of hypoventilation in COPD:

● Decreased responsiveness to hypoxia and hypercapnia

● Increased ventilation-perfusion mismatch leading to increased dead space ventilation
● Decreased diaphragmatic function due to fatigue and hyperinflation

CASE 3

1. What are the factors that predisposed to Nini’s condition? Explain the mechanism behind its occurrence.
● Nini was predisposed to asbestos exposure from working in the shipyard. mesothelioma is the most common form of
cancer associated with asbestos exposure. When inhaled, asbestos stays in the lungs for a long time. When asbestos fibers
are breathed in, they may get trapped in the lungs and remain there for a long time. Over time, these fibers can accumulate
and cause scarring and inflammation, which can affect breathing and lead to serious health problems.

2. Why is the dyspnea worse during exertion? What factors are affected that caused the increase in the work of breathing.
● Dyspnea usually worsens during exertion due to the increased demand for oxygen. The patient already has impaired
function of the lungs due to the mesothelioma, there will not be adequate intake or replacement of oxygen. Mesothelioma
affects the lung pleura, therefore upon breathing there is pain felt in the area around the tumors which then leads to
dyspnea.

3. Interpret the ABG results. Explain the difference in the findings pre and post exercise. How does her ABG result differ from
that of Noynoy?
● Nini’s ABG result shows that she has a partially compensated respiratory alkalosis due to the following ABG results:
○ pH of 7.46 (alkalosis; partially compensated)
○ pCO2 of 32 mmHg (low)
 ○ HCO3- of 18 (low)
■ Thus, it is respiratory.
● Calculating for pO2/fiO2 ratio will measure hypoxemia. The patient’s pO2/fiO2 ratio is approximately 362 which indicates
that the ABG result after a 6-minute walk will worsen than pre-exercise levels. This is because of impaired gas exchange in
the patient’s lungs due to fibrosis in the interstitium. On the other hand, Nonoy has partially compensated respiratory
acidosis which is different from Nini’s.

4. What is the expected PFT result for Nini? Draw the MEF of a patient with pulmonary fibrosis compared to normal and
COPD patient. What other lung function tests may be used to confirm the diagnosis? Explain the mechanism behind the
examination.
● Nini suffers from interstitial pulmonary fibrosis, therefore she has restrictive type of ventilatory defect. The expected PFT
result would be a normal FEV1/FVC ratio due to a lower value due to low FEV1 (<80%) and a low FVC (<80%).

Figure 1. MEF of patient with pulmonary fibrosis. Figure 2. MEF of patient with COPD

Other lung function tests that may be used to confirm pulmonary fibrosis are the following:
● Spirometry – it measures the rate of air flow and estimates the lung size. The patient will be asked to breathe multiple times, with
regular and maximal effort, through a tube that is connected to a computer for reading measurements.
● Lung volume test – most accurate way to measure how much air your lungs can hold. The procedure is similar to spirometry,
except that you will be in a small room with clear walls.
● Lung diffusion capacity – this is a type of assessment to determine how well oxygen gets into the blood from the air you breathe.
Blood may be needed to be drawn in order to measure the hemoglobin level.
● Pulse oximetry – estimates the oxygen level in your blood by placing a probe on the patient’s finger or another skin surface such as
the ear.
● Fractional exhaled nitric oxide tests – measure how much nitric oxide is in the air that one exhale. In this test, the patient is
requires to breathe out into a tube that is connected to the portable device. A steady but not intense breathing is also required.