Physiology Exam 3 - pulmonary physiology 2

What are the four primary lung volumes?

Tidal Volume (TV), Inspiratory Reserve Volume (IRV), Expiratory Reserve Volume (ERV), Residual Volume (RV)

what are the typical tv, irv, erv, and rv for a healthy 70 kg male

500, 3000, 1000, 1200

what is the physiological meaning at FRC

the lungs are not empty, alveoli remain partially inflated, gas exchange continues between breaths, this is very important because it prevents large fluctuations in blood oxygen levels between breaths

what does the frc act as

oxygen reservoir

what is the clinical importance of the frc

during apnea, and anesthesia, oxygen stored in the frc helps maintain oxygenation for a short period

what are the conditions that have a decreased frc (4)

obesity, pregnancy, acute respiratory distress syndrome, and general anesthesia (these patients desaturate faster during apnea

what are the typical ic, vc, frc, and tlc for a healthy 70 kg male

3500,4500, 2200, 5700

what is the pulmonary function test

spirometry

What is tidal volume (TV)?

Air moved in a normal breath (~500 mL)

What is inspiratory reserve volume (IRV)?

Additional air inhaled after normal inspiration

What is expiratory reserve volume (ERV)?

Additional air exhaled after normal expiration

What is residual volume (RV)?

Air remaining after maximal expiration

Which lung volumes cannot be measured by spirometry?

RV, FRC, TLC

What is vital capacity (VC)? equation

IRV + TV + ERV

What is inspiratory capacity (IC)? equation

TV + IRV

What is functional residual capacity (FRC)? equation

ERV + RV

What is total lung capacity (TLC)? equation

IRV + TV + ERV + RV

What is normal tidal volume?

~500 mL

What is normal IRV?

~3000 mL

What is normal ERV?

~1000–1100 mL

What is normal RV?

~1200 mL

What is normal TLC?

~5700 mL

What is normal VC?

~4500 mL

What is FRC physiologically?

Point where lung recoil = chest wall recoil

Why is FRC important in maintaining in critical care?

prevention of alveolar collapse and improves oxygenation in acute respiratory distress syndrome

What prevents oxygen fluctuations between breaths?

FRC

What is the oxygen reservoir of the lungs?

FRC

What does FRC do during apnea?

Maintains oxygen temporarily

What happens to FRC in emphysema?

Increases

What happens to FRC in COPD?

Increases

What happens to FRC in fibrosis?

Decreases

What happens to FRC in atelectasis?

Decreases

Why does emphysema increase FRC?

Loss of elastic recoil —> lungs stay ore expanded

Why does fibrosis decrease FRC?

Increased lung stiffness —> lungs recoil inward more strongly

What is PEEP used for?

used during mechanical ventilation to help increase frc. prevents alveolar collapse and improves oxygenation in ARDS

what does PEEP stand for

positive end expiratory pressure

A 65 yeard old man with a 40 pack year smoking history presents with progressive dyspnea. PFT shows increases total lung capacity and increased functional residual capacity. CT imaging reveals destruction of alveolar walls.

which of the following best explains the increased functional residual capacity in this patient? and why

a. increased airway mucus secretion

b. loss of lung elastic recoil

c. increased surfactant production

d. increased chest wall stiffness

e. increased pulmonary capillary pressure

b. loss of lung elastic recoil, patient likely has emphysema, a form of chronic obstructive pulmonary disease

what happens in emphysema

alveolar walls are destroyed, elastic fibers are lost, lung elastc recoil decreases, because the lungs no longer recoil inward effectively, the equilibrium point between ling recoil and chest wall recoil occurs at a higher lung volume, which increases frc and leads to lung hyperinflation

What is minute ventilation? equation

RR × tidal volume

Normal minute ventilation?

~6 L/min (6000ml/min)

what is the physiological dead space equation

anatomical dead space + Alveolar dead space

what is anatomical dead space

airway structures (trachea)

what is alveolar dead space

gas got in but no chance to get out

What is alveolar ventilation (VA)? equation

RR × (TV – dead space)

Normal VA?

~4.2 L/min

What is dead space?

Air not participating in gas exchange

What are the types of dead space?

Anatomical and alveolar

What is physiological dead space?

Anatomical + alveolar

What happens when dead space increases?

VA decreases

What happens when tidal volume increases? in terams of VA

VA increases

a patient has a dead space of 150 ml, function residual capacity of of 3 L, tidal volume of 650 ml, expiratory reserve volume of 1.5 L, a total lung capacity of 8 L, respiratory rate of 15 breaths/ min. What is the alveolar ventilation
a. 5 l/min
b. 7.5 l/min

c. 6 L/min

d. 9 L/min

b. 7.5 L/min

What is the key VA equation?

VA = VCO2 / PACO2

What is PACO2 proportional to?

VCO2 / VA

What happens to CO2 in hypoventilation?

Increases in blood

what should you assume PACO2 is equal to

PaCO2

What happens to CO2 in hyperventilation?

Decreases

What acid-base disorder in hypoventilation?

Respiratory acidosis

What acid-base disorder in hyperventilation?

Respiratory alkalosis

What is normal PACO2?

40 mmHg

What is normal VCO2?

200 mL/min

a patients normal TV is 500 ml with a dead space of 100 ml. the metabolism of Co2 is 200 ml/min. the respiratory rate is 10. the patient is then placed on a ventilator for surgery and the TV is 1000 ml with similar metabolism. the machine has an addition dead space of 100 ml with a rate of 10 bpm.

1, what is the VA before and after ventilation

2. what is the PACO2 for this patient after ventilation

1. 4 L/min → 8 L/min

2. 25 mm Hg

Where is breathing rhythm generated?

Medulla

What neurons generate rhythm?

Central rhythm generator

What does DRG control?

normal breathing and inspiration

What does VRG control?

Inspiration but mostly expiration

When is VRG most active?

Forced breathing

What does pneumotaxic center do?

Inhibits inspiration

Effect of pneumotaxic center?

Faster breathing rate by limiting inspiration

What nerve controls diaphragm?

Phrenic nerve

Where are central chemoreceptors?

Medulla

What do central chemoreceptors respond to?

changes in Co2 and H+ (mainly H+)

Which controls ventilation more strongly?

Central chemoreceptors

what do central chemoreceptors do

stimulate respiratory center and appear to play a larger control in respiration that peripheral in the short term

what does increases PCO2 in a cerebral capillary do

increased ventilation through central chemoreceptors

how does H+ stimulate central chemoreceptors

through CO2 getting turned into in through the carbonic anhydrase reaction

Where are peripheral chemoreceptors?

Carotid + aortic bodies

what are the cells called in the peripheral chemoreceptors

glomus cells

Primary stimulus peripheral chemoreceptors? with number

PaO2 < 60 mmHg

Other stimuli peripheral receptors?

↑CO2, ↓pH

What cells detect O2?

Glomus cells

What neurotransmitters do glomus cells release?

ACh, ATP, dopamine

What is the mechanism of a glomus cells

low PO2 inhibits K channels, cell depolarizes, voltage gated Ca channel opens, Ca enters, exocytosis of neurotransmitters, signal to medullary centers to increase ventilations (carotid sinus nerve)

which chemoreceptors are responsible for increased alveolar ventilation and why

peripheral cells, glomus cells are sensitive to O2

What reflexes occur with irritants?

Bronchoconstriction (vagal efferent nerves (M3 receptors on airway, ACh)), Cough, Tachypnea

What nerve mediates bronchoconstriction?

Vagus nerve

What receptor mediates bronchoconstriction?

M3 receptor

What is Hering-Breuer reflex?

Lung stretch inhibits inspiration

What happens in lung overinflation?

stimulates stretch receptors (Vagal afferent nerves), inhibits inspiration at the dorsal inhibitory group)

What is V/Q?

Ratio of ventilation to perfusion

Normal V/Q?

~0.8–1

Example high V/Q?

Pulmonary embolism

Example low V/Q?

Asthma

What is V/Q = infinity?

Dead space

What happens in high V/Q?

Perfusion decreases

What happens in low V/Q?

Ventilation decreases

Compensation in high V/Q?

Bronchoconstriction

Compensation in low V/Q?

Vasoconstriction