BME 365S Exam 1

BME 365S Physio II Exam 1

4 functions of the respiratory system

1) Gas exchange

2) regulation of pH: done by retaining or excreting CO₂

3) Protect against inhaled pathogens/irritating substances: respiratory epithelium

4) Vocalization: air moving across vocal cords creates vibrations

External vs internal respiration

External resp is breathing: inspiration & expiration

—>Pulmonary circulation has 500 mL of blood (50% total amt)

Internal resp is exchange of gases between blood & cells

3 functions of the upper resp system (airways)

1) Warm air to body temp

2) Add water vapor —> 100% humidity

—>Prevent exchange epithelium from drying out

3) Filter foreign material: bacteria, viruses, inorganic particles

Explain the airway epithelium (mucus/saline). What cells?

Goblet cells secrete mucus w/ immunoglobulins (Ig aka antibodies)

Underlying cilia push mucus toward pharynx where it’s swallowed

Fluid layer beneath mucus to prevent cilia-mucus sticking

Model of saline secretion

1) NKCC symporter brings Cl- from ECF → inside epithelial cell

2) Apical anion channels allow Cl- epithelial cell → lumen (airway)

3) Na+ goes from ECF→ lumen via paracellular pathway (due to electrochem gradient)

4) NaCl mvmt from ECF→ lumen makes cxn gradient, so water follows into the lumen

Air flow equation (Poiseuille’s law)

Airflow Q = ΔP/R

Poiseuille: R is func of Lμ/r⁴ where L is length of tube

3 types of alveolar cells (and function)

Type I alveolar epithelium: rapid gas exhange, 95% of alveolar surface, thin squamous cell

Type II alveolar epithelium: produce surfactant to dec surface tension & help expansion of lungs

Alveolar macrophage (dust cell); ingest foreign material

What’s between alveoli cells?

Blood vessels fill 80-90% of the space, also connective tissues w/ elastin & collagen fibers to give elastic properties

NO muscle — it would block gas exchange

Explain pleural sac & pleural fluid. Interpleural pressure?

Double MB around lung w/ fluid in between. Creates moist slippery surface so lungs can move within thorax, holds lungs tight against thoracic wall

Interpleural pressure is sub-atmospheric, -3 mmHg.

Ideal gas law & boyle’s law & dalton’s law

Ideal: PV=nRT

Since n & T are constant for humans we get Boyle’s law: P₁V₁ = P₂V₂

Dalton’s law: P_total = P_a + P_b + P_c

P_gas = P_atm* % of the gas in the atmosphere

What happens in inspiration?

Active process: Diaphragm contracts, external intercostals & scalene contract

Scalenes lift sternum & upper ribs

Thoracic cavity expands (inc volume, dec pressure to 759 mmHg)

Air flows inwards into low pressure space

What happens in expiration? Quiet breathing?

Passive process: diaphragm relaxes

Forced: internal intercostals & abdominal muscs contract

Dec volume, pressure increases (to 761 mmHg), air pushed out (return to 760 mmHg)

In quiet breathing, diaphragm causes 60-75% volume change, rib cage mvmt causes remaining 25-40%

Quiet breathing: P_O2 & P_CO2 barely change bc amt O2 entering alveoli = amt O2 entering blood. Also amt fresh air entering lungs is only 10% total lung volume

Ventilation diseases (3)

Neuromuscular diseases that affect motor control of ventilation:

1) Myasthenia Gravis: ACh receps of motor end plates of skeletal musc destroyed

2) Polio: virus that damages MNs @ spinal cord, paralyzes skeletal muscs

Pneomothorax: sealed pleural cavity is opened to atmosphere, lung collapses

→Treated w/ tube thoracostomy (insertion of chest tube)

Resp volumes & capacities

Tidal Volume (TV): normal breathing

Inspiratory reserve volume (IRV): max additional inspiration

Expiratory reserve volume (ERV): max additional expiration

Vital Capacity (VC): TV + IRV + ERV

Can’t be measured w/ spirometer:

Residual volume (RV): air left after complete expiration

Total lung capacity (TLC): VC + RV

Total pulmonary ventilation vs alveolar ventilation?

Total pulmonary ventilation (aka respiratory minute volume): ventilation rate (breaths/min) * tidal volume (mL/breath)

Alveolar ventilation: amt fresh air reaching alveoli per minute: ventilation rate * (tidal vol - dead space vol)

Anatomical dead space: air remaining in airways

Compliance v elastance

Compliance: expansibility, how easily it stretches

Compliance = ΔV/ΔP, aka slope of P-V curve

Elastance: elastic recoil, ability to return to original shape

ex: Emphysema: alveoli enlarge & lose elasticity →difficulty exhaling bc less recoil

Obstructive vs Restrictive lung diseases.

Restrictive: dec in lung compliance→resp musc must work harder to stretch stiff lung

→Caused by scar tissue or inadequate surfactant

Obstructive: dec air flow bc inc airway resistance from physical obstructions: mucus, asthma, bronchoconstriction

How does bronchoconstriction & dilation happen?

Bronchoconstriction

By histamine: allergic rxn or tissue damage → release histamine → bronchoconstriction

By nervous system: inhaling irritants → parasym neurons signal → bronchoconstriction (defense mechanism)

Bronchodilation

By CO₂: during expiration, CO₂ inc, relaxed bronchiolar smooth musc → bronchodilation

By nervous system: epinephrine activates B2 adrenergic receptor → symp nervous system activates → relaxation of bronchial smooth musc → bronchodilation

Role of surfactants. Pathophysiology?

Dec surface tension of alveoli → dec R of lung to stretch so easier to expand → inc lung compliance

Surfactant more concentrated in smaller alveoli

Newborn Respiratory Distress Syndrome: babies born prematurely w/out adequate surfactant, thus expend huge amt energy to breathe. Must treat via aerosol administration of artificial surfactant

Controlling bronchioles & alveolar blood flow. Cause of low alveolar P_O2

Arteriole diameter regulated by O2 content of surrounding interstitial fluid: if ventilation decreases, P_O2 dec so blood near alveoli doesn’t get oxygenated. Thus, constriction around under-ventilated alveoli so that blood flows to better ventilated alveoli

→Cause of low alveolar P_O2: high altitude so air has low O2; inadequate ventilation from inc airway resistance or dec lung compliance or CNS depression from drugs/alcohol

Bronchiolar diameter mediated by CO2 contents

Capillaries & bronchioles are collapsible as function of blood pressure

Diffusion rate across membrane

Fick’s Law: rate of diffusion = (surface area * cxn gradient) / (MB resistance * MB thickness)

Oxygen transport?

Only dissolved O2 can be utilized by body:

98% of oxygen transported in RBCs via hemoglobin (Hb)

2% dissolved in plasma (increases w/ temp)

270 million Hb per RBC

Mass balance: Arterial O2 transport - venous O2 transport = cellular oxygen consumption

O2-Hb Binding saturation curve. How to shift curve? Fetal Hb?

Binding affinity inversely related to acidity & cxn CO2: inc CO2 or lower pH (inc H+) → dec affinity of Hb to O2, SHIFT RIGHT

Inc temp (ex: exercise): shift right so Hb releases more O2. Lactic acid from exercising → lower pH → additional O2 released

Fetal Hb: stronger affinity to O2 (SHIFT LEFT). 2 gamma protein chains allow binding O2 even in the low O2 enviro of placenta

At alveoli P_O2 = 100 mmHg, in resting cells Hb is 75% saturated

In exercising muscle P_O2=20mmHg, Hb is 35% saturated

Carbon dioxide transport?

CO2 20x more soluble in fluids than oxygen: 7% dissolved in blood, 93% diffused into RBCs where 70% converted to bicarbonate ion & 23% binds Hb

High P_CO2 depresses CNS function → confusion, coma, death

Control of ventilation in brain? Respiratory neurons?

Resp neurons in medulla oblongata control inspiration & expiration

→Dorsal Respiratory Group (DRG): insp neurons, control musc of thorax & diaphragm

→Ventral Respiratory group (VRG): neurons control musc for active expiration & forced inspiration

Neurons in pons modulate ventilation

→ Pontine respiratory groups (PRG): provide tonic input to medullary network

Ventilation modulated by CO2, O2, H+

Chemoreceptors in ventilation. Location & function?

Nucleus Tractus Solitarius (NTS, medulla): receive sensory info from central & peripheral chemoreceps

→Central chemoreceps: in medulla, monitor cerebrospinal fluid (CSF) composition & respond changes in CO2

→Peripheral chemoreceps: in aortic wall & carotid artery, sense changes in O2, pH, P_CO2

What are some protective reflexes? What does regulation of respiratory rate depend on?

Reflexes: in response to inhaled particles or noxious gases: bronchoconstriction, coughing, sneezing

Regulation of resp rate: depends on conscious & unconscious thought, emotional state, anticipation

Pathologies causing hypoxia? (4)

Emphysema: destruction of alveoli → less SA for gas exchange

Fibrotic lung disease: thickened alveolar MB & dec lung compliance → slows gas exchange & dec alveolar ventilation

Pulmonary edema: fluid in interstitial space → inc diffusion distance, higher P_CO2 bc higher CO2 solubility in water.

Asthma: inc airway resistance → dec alveolar ventilation