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SB252
What is ventilation?
ventilation is breathing: exchanging air from outside the body with the interior of lungs particularly in the alveoli (respiratory space of lungs)
Physiology actions drive ventilation?
Muscle contraction and relaxation, particularly of the diaphragm/ drives ventilation by creating pressure difference in thorax
Pressure differences are transmitted due to vacuum seal of pleural membranes to each other
What determines bulk flow of air in the respiratory system? What basic chemical gas law mathematically models this, and what specific compartment pressures are involve?
Difference in air pressure
- modeled by Boyle’s law P1V1 = P2V2
Muscle action changes thoracic volume changes thoracic pressure transmitted by the pleural seal which changes pressure on the lung wall which changes lung volume which creates a change in lung internal pressure (all in regard to atmospheric pressure)
Mechanisms of inspiration and expiration
(forced) inspiration
(forced) expiration

Inspiration
contraction of diaphragm (lowers) and external intercostals (raises) results in greater thoracic/lung volume
Expiration
relaxation of diaphragm (raises) and contraction of internal intercostals (lowers) results in lesser thoracic/lung volume, movement of air out of lungs
Forced inspiration
engages inspiratory reserve volume - more muscle action and use of scalenes, sternocleidomastoid
forced expiration
Engages expiratory reserve volume - more muscle action and use of abdominals
Mathematical equation relating bulk flow to elements of respiratory function
F = DP/R where DP is atmospheric - intrapleural pressure (+ value inhalation, - value exhalation) resistance is determined by the radius of bronchi/bronchioles
What is wrong with the lungs during atelectasis (collapsed lung) in pneumothorax? (importance of pleurae in lung function)
Damage to lung tissue and/or chest wall has broken vacuum seal of pleural such that no pressure gradient exists. Air in the thorax means no DP means no breathing
chemical nature and role of lung surfactant
biological detergent. it disrupts surface tension in the alveoli which would otherwise exert enough force to collapse most of them. evens out effect of tension on different sizes so they can stay open under ordinary intrapulmonary pressure.
IRDS
Babies haven’t produce sufficient surfactant and have trouble inflating alveoli (low compliance)
Fibrosis
damage and scarring of the lung tissue stiffen the wall, reducing compliance and restricting the amount of air that can enter the lungs (low compliance)
Asthma
bronchioconstriction limits airflow to a significant even dangerous degree (high resistance)
Pneumonia
fluid accumulates in the alveoli preventing air from entering the respiratory spaces (inability to ventilate)
anatomical dead space
amount of air in the upper and conducting lower airways in each breath about 150 of 500mL tidal volume is dead space
alveolar dead space
negligible in healthy tissue. alveoli that get air but not effective blood flow. temporary occlusion of blood vessels due to the filtration of clots V/Q balancing eliminates airflow to alveoli preventing alveolar dead space
How does respiration differ from ventilation?
Respiration is gas exchange between the air and blood or blood and tissues. Dissolution and diffusion is required.
Dalton’s law
Extent of dissolution (amount of CO2 and O2 in blood) is measured as partial pressure which is relationship to atm pressure by this law
Henry’s law
Gas dissolved in liquid (atmospheric partial pressures)
Thee major factors determining external respiration at the lungs and how they combine for efficient gas exchange
Pressure gradients, gas solubilities, thickness (permeability) and surface area of membrane, V/Q coupling
What is V/Q ventilation/perfusion coupling?
local tissue actions balance the amount of air and blood in alveoli/capillaries. an inverse relationship.
Why is V/Q important for effective lung function
When local blood O2 is low (ventilation not adequate) arterioles constrict, limiting perfusion
When local blood CO2 is low (blood flow not adequate) bronchioles constrict, limiting ventilation
What is internal respiration and where does it occur?
Tissue exchange of O2 and CO2 with the bloodstream at the systemic capillaries (NOT cellular respiration, but the driving force)
What two ways is oxygen carried in the blood stream?
1.5% - dissolved in blood plasma 100mmgh in arterial blood
98.5% - bound to hemoglobin / complex multi-subunit protein that carries up to 4O2 per molecule, hemoglobin is almost fully saturated (98%) at 100 mmHg pressure carrying almost 65 time more O2 than the plasma
How much oxygen does hemoglobin release in resting tissue? In metabolically active tissue?
25% O2 unloaded at lest 80% unloaded under metabolism demand
What factors in hemoglobin function combine to release more oxygen in active tissue?
decreased O2 concentration, increased CO2 concentration (decreased pH), increased temperature, and perhaps increased BPG (2,3-Biphosphogylcerate which regulates O2 release/makes it possible to transport CO2)
Bohr effect
O2 binding to Hemoglobin due to the decreased of PH from increased CO2 concentration
Three ways carbon dioxide is carried in the bloodstream?
10% dissolved in plasma, 70% converted to HCO3 through CO2 and H2O, 20% bound to hemoglobin as carbamate (bound to amino groups)
What additional mechanism is at work when CO2 carried in the bloodstream?
CO2 partial pressure does not vary in the plasma anywhere near as much as O2 / bicarbonate buffer system both provides a sink for CO2 and also serves as the main buffer of blood
Haldane effect
The amount of O2 inversely affects the amount of carbaminohemoglobin that can form
Hypoxia
lack of oxygen (in the tissues of the blood)
overarching term for anemic, ischemic, histotoxic, hypoxemic, CO poisoning
Anemic
not enough RBC or Hb (iron deficiency) (silent problem)
Ischemic
Blockage in blood flow (heart attack)
Histotoxic
Cyanide etc blood can’t use oxygen even though its available (silent problem)
Hypoxemic
lack of oxygen in the blood due to respiratory distress
CO poisoning
competitive inhibitor of O2 binding to Hb
Hypercapnia
excessive CO2 in the blood
Reflex mechanisms in neural regulation of breathing that ordinarily prevent hypoxia and hypercapnia
Chemoreceptor reflexes
highly sensitive to CO2 and alter ventilation depth and rate to compensate
O2 sensors
less sensitive / only react to major changes in plasma O2 and serve as a backup to the CO2 sensors (must drop to 60%) for hypoxemia to become a major respiratory drive
Three neural centers in the medulla and pons that regulate breathing
activate an inhibit but also contain pacemaker cells that set the basal respiratory rhythm
VRG, DRG, PRG
VRG
Ventral respiratory group of the medulla
generate contractile stimuli to inspiratory and expiratory muscles in an oscillating/mutually inhibiting pattern
DRG
Dorsal respiratory group of the medulla
integrates chemoreceptor and stretch receptor reflex input from the blood vessels, lungs, and brainstems
modulates VRG activities
PRG
Pontine respiratory group
smooths out transitions between inspiration and expiration / voluntary respiratory such as deep breathing and vocalization
pre-Botzinger complex
first respiratory pacemaker to be discovered (in the VRG)
What other structures in the brain are involved in control of breathing? The diaphragm and intercostal muscles are skeletal muscles
Hypothalmus - integrates emotional and instinctive unconscious respiratory responses ex gasping
Cerebral cortex - classical motor neuron tracts which bypass the medullary respiratory centers to innervate the alpha motor neurons directly (control over ventilation)
Hypo and hyper ventilation and chemical effects in the blood
hypoventilation - accumulation of CO2 due to less ventilation than necessary to compensate for metabolic activity. results in respiratory acidosis
hyperventilation - loss of too much CO2 from blood due to excessive ventilation. O2 levels will not fall but will fail to be delivered to tissues because Bohr effect needed to UNLOAD hemoglobin
Respiratory acidosis
low pH of the blood due to respiratory insufficient / severe will also result in low O2 levels (hypoxemic hypoxia)
Hering-Breuer Reflex
Stretch reflexes also override medullary control to prevent overinflation of the lungs