Respiratory System Flashcards
Functions of the respiratory system
-Gas exchange
-Acid-base balance
-Thermoregulation
-Immune function
-Vocalization
-Enhances venous return
What is the order of structures that air passes through to get to the alveoli?
1) pharynx
2) larynx
3) trachea
4) bronchi
5) bronchioles
6) alveoli
What type of muscle are bronchioles?
Smooth muscle
How do bronchioles control air flow?
Through constriction or dilation
Where is the site of gas exchange?
Alveoli
Characteristics of alveoli
-Thin walled (simple squamous)
-Large surface area for diffusion (75 m square)
-Contain fine elastic fibres
-Pores of Kohn connect to adjacent alveoli
Why are the pores of kohn important?
-They help equalize air pressure so that alveoli do not burst
Type 1 vs Type 2 Alveolar cells. What is a third cell?
Type 1: make up the walls
Type 2: secretes surfactant
Alveolar macrophages: immune response
Define ventilation
The gas exchange between the atmosphere and alveoli in the lungs
Define external respiration
the gas exchange between alveoli and blood
Define internal respiration
gas exchange between blood and tissues
What is inspiration/expiration dependent upon?
Pressure gradients.
Bigger gradient = more air moving
What are the different pressures?
Atmospheric: air, typically 760 mmHg at sea level
Intra-alveolar: in alveoli
Intra-pleural: in pleural space, typically 756 mmHg
Transpulmonary: difference between intrapulmonary and intrapleural, typically 760 mmHg
What is Boyle’s law?
The pressure exerted by a gas varies inversely with the volume of a gas
If volume increases, then pressure decreases.
If pressure changes, gases will flow to equalize pressure.
Muscles of quiet inspiration
Diaphragm and external intercostals (move upwards)
Volume during quiet inspiration
Thoracic volume increases (vertically) and lungs stretch
Pressure during quiet inspiration
Intrapulmonary pressure decreases
-Air flows into the lungs down its pressure gradient until pressure is the same as atmospheric
Muscles of forced inspiration
-Diaphragm and external intercostals
-Recruit scalenus and sternocleidomastoid
Volume during forced inspiration
-Greater increase in thoracic volume (vertically)
Pressure during forced inspiration
Larger decrease in thoracic pressure
-Larger pressure gradient
-More air flows in
Muscles during quiet expiration
-Inspiratory muscles relax (there is no contraction)
Volume during quiet expiration
-Thoracic cavity volume decreases and lungs recoil
Pressure during quiet expiration
-Increase in alveolar pressure
-Air flows out of the lungs until pressure gradients are equal
Muscles during forced expiration
-Relaxation of inspiratory muscles still occurring
-Recruit abdominals and internal intercostals (push up on diaphragm and make space smaller)
Volume during forced expiration
-Larger decrease in thoracic volume
Pressure during forced expiration
-Larger increase in thoracic pressure
-Larger gradient
-More air out
Which receptors control ventilation?
-Chemoreceptors
-Monitor blood gases
-Sensitive to increases in CO2 and H, small reaction to decreases in oxygen
Where do chemoreceptors input to?
-Reticular formation of the medulla and pons
Which respiratory centre establishes rhythmic breathing patterns?
Pre-Botzinger complex
What does the medullary resp centre control?
Dorsal resp group:
-mostly inspiratory neurons
Ventral resp group:
-inspiratory neurons
-expiratory neurons
Receives input from chemoreceptors
Apneustic centre
-Prevents inspiratory neurons from being switched off
-Provides extra boost to inspiratory drive
Pneumotaxic centre
-Sends impulses to DRG that helps “switch off” inspiratory neurons
-Dominates over apneustic centre
Where are peripheral chemoreceptors located?
-Carotid bodies are located in the carotid sinus
-Aortic bodies are located in the aortic arch
How does CO2 affect hydrogen and vice versa?
-They combine to make carbonic acid (affects pH of body)
-If CO2 increases, then so does hydrogen (lactic acid)
What does the central chemoreceptors directly monitor?
-Located in medulla and monitors CSF
-Monitors increases in hydrogen via CO2 because of blood brain barriers
Central vs peripheral: what portion of the CO2 response do they monitor each?
Central: 70%
Peripheral: 30%
What does increased metabolism do?
Leads to higher CO2 (and consequently higher H) and lower oxygen
If oxygen levels drop below ______ mmHg, it becomes the major factor in control of breathing.
60
What is the only thing that will make oxygen levels drop significantly?
High altitude
What does hyperventilation cause?
-Increased depth and rate of breathing
-High removal of CO2
-Causes CO2 levels to decline (hypocapnia)
-Lose trigger for inspiration but doesn’t increase oxygen significantly
-May cause cerebral vasoconstriction and cerebral ischemia (headaches)
What role does the hypothalamus and limbic system play?
-Modifies rate and depth of respiration with hormones
-Breath may hold in anger or in pain
-Body temperature increases to increase respiratory rate
-Cortical controls bypass medullary controls
Hering-Breuer reflex
-Stretch receptors triggered to prevent overinflation of the lungs
-Signals the end of inhalation and allows expiration to occur
Pulmonary irritant reflex
-Receptors in the bronchioles respond to irritants
-Reflex constriction of air passages
-Receptors in the larger airways mediate the cough and sneeze reflexes
What are nonrespiratory air movements?
-Cough, sneeze, crying, laughing, hiccups, yawns
-Reflexes
What changes does exercise make on respiration?
-Increased CO2 production and O2 consumption
-Larger gradients for gas exchange
-Faster and greater diffusion
Physical factors influencing pulmonary ventilation
-Airway resistance
-Alveolar surface tension
-Lung compliance
-Elastic recoil
What is the biggest determinant in airway resistance?
Radius of bronchioles
What is the equation for airflow?
F = pressure gradient between atmosphere and alveoli / resistance
Asthma
-Severe constriction or obstruction of bronchioles
-Prevents ventilation with mucous
What does epinephrine do for airways?
-Dilates bronchioles and reduces air resistance
Eg; Epi pens
Surface tension
-Attracts liquid molecules to one another at a gas-liquid interface
-Resists any force that tends to increase the surface area of the liquid
Surfactant
-Detergent like lipid and protein complex produced by Type 2 alveolar cells
-Decreases surface tension of alveolar fluid and discourages alveolar collapse
Why are premature infants at risk of respiratory distress?
-They do not have surfactant yet
Lung compliance
-Expandability of the lungs
-Relates to effort required to distend the lungs
-Connective tissue makes it more compliant, along with alveolar surface surfactant
What diminishes lung compliance?
-Nonelastic scar tissue (fibrosis)
-Reduced production of surfactant
-Decreased flexibility of the thoracic cage (paralysis of resp muscles)
Elastic recoil
-How fast the lungs rebound after being stretched, returning to their pre-inspiratory volume
-Depends on connective tissue in the lungs (elastin and collagen) and surface tension (increases)
Tidal volume
-Volume of air entering or leaving lungs during a single breath
-500 ml
Inspiratory reserve volume
-Extra air that can be maximally inspired over and above the typically tidal volume
-3000 ml
Inspiratory capacity
-Maximum volume of air that can be inspired at the end of a normal quiet expiration
-3500 ml
IRV + TV
Expiratory reserve volume
-Extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume
-1000 ml
Residual volume
-Minimum volume of air remaining in the lungs even after a maximal expiration
-1200 ml
Functional residual capacity
-Volume of air left in lungs at the end of normal passive expiration
-2200 ml
ERV + RV
Vital capacity
-Maximum volume of air that can be moved out during a single breath following a maximal inspiration
-4500 ml
IRV + TV + ERV
Total lung capacity
-Maximum volume of air that the lungs can hold
-5700 ml
VC + RV
Forced expiratory volume in one second
-Volume of air that can be expired during the first second of expiration in a VC determination
Dead space
-Inspired air that doesn’t contribute to gas exchange
-Anatomical (150ml) or alveolar
Minute ventilation
Total amount of gas flow into or out of the respiratory tract in one minute
Obstructive disease
-High compliance
-Low recoil
-Difficult to breath out
-Emphysema, asthma, chronic bronchitis
Emphysema
-Caused by smoking
-Breakdown of collagen and elastin in septal walls
-Loss of lung recoil
-Tar and mucous production
-Decreased SA and greater diffusion distance
Chronic bronchitis
-Response to chronic irritants (smoking or pollutants)
-Inflamed airways
-High production of mucous which decreases airway diameter
-Triggers cough reflex and bronchoconstriction
Restrictive disease
-Low compliance
-High recoil
-Harder to breath in and hard to hold air in long enough for gas exchange
-More collagen
-Fibrosis, asbestos exposure, mesothelioma
Which method does gas exchange occur by?
Simple diffusion
Gas will move from ________ partial pressure to _________ lower partial pressure
Higher to lower
What is Dalton’s law?
-The partial pressure of each gas is directly proportional to its percentage in the mixture.
(Fraction of gas in atmosphere x the atmospheric pressure)
What is the fraction of oxygen, nitrogen and CO2 in the air?
Oxygen: 21%
Nitrogen: 79%
CO2: <1%
Which pressure DOES change to change partial pressures?
Barometric or atmospheric pressure changes
Why do alveoli contain more CO2 and water vapour than atmospheric air?
-Gas exchange in the lungs
-Humidification of air
-Mixing of alveolar gas that occurs with each breath
Partial pressures of oxygen and carbon dioxide in atmospheric air (mmHg)
P O2 : 160
P CO2 : 0.03
Partial pressures of oxygen and carbon dioxide in alveoli (mmHg)
P O2 : 104
P CO2 : 40
Partial pressures of oxygen and carbon dioxide in arterial blood (mmHg)
P O2 : 100
P CO2 : 40
Partial pressures of oxygen and carbon dioxide in venous blood (mmHg)
P O2 : 40
P CO2 : 46
External respiration (influences)
-Exchange of O2 and CO2 across the respiratory membrane
Influenced by:
-partial pressure gradients and gas solubilities
-ventilation-perfusion coupling
-structural characteristics of the respiratory membrane
What does diffusion depend on?
-Concentration gradient
-Diffusion distance
-Solubility
-Surface area in alveoli
Fick’s law of diffusion
What does fick’s law of diffusion govern?
Rate of gas transfer across the alveoli
When does the respiratory membrane thicken?
-If lungs become waterlogged (edema)
What happens to gas exchange when the respiratory membrane thickens?
-Surface area decreases
-Gas exchange decreases
Even though the partial pressure gradient for CO2 in the lungs is less steep than for O2, why does it still diffuse in equal amounts with oxygen?
-CO2 is 20x more soluble in plasma than oxygen, so it readily flows down it’s concentration gradient
-O2 required hemoglobin to diffuse, since it doesn’t want to be soluble
Internal respiration
Capillary gas exchange in body tissues
Partial pressures and diffusion gradients in internal respiration are ________ compared to external respiration.
Reversed
-PO2 in tissue is always lower than in systemic arterial blood
-PO2 in venous blood is 40 mmHg and PCO2 is 46 mmHg
How does oxygen affect the diameter of arterioles in the alveoli?
High oxygen causes vasodilation
Low oxygen causes vasoconstriction
So that they match
How does carbon dioxide affect the broncioles?
High CO2 causes bronchiole dilation
Low CO2 causes bronchoconstriction
% of oxygen transport in blood
-1.5% is dissolved in plasma
-98.5% is loosely bound to each Fe of hemoglobin (Hb) in RBCs)
-4 O2 per Hb
Percentage of CO2 in its different carrier methods in the blood
-10% is physically dissolved
-30% is bound to hemoglobin
-60% travels as bicarbonate, which is formed from carbonic acid
How much of its oxygen does Hb unload at the level of the tissue?
25-30%
Rate of loading and unloading of O2 is regulated by:
-PO2
-Temperature (lower increases affinity)
-Blood pH (higher increases affinity)
-PCO2 (lower increases affinity)
-Concentration of DPG
Hypoxia
Inadequate oxygen delivery to tissues
How does carbon monoxide poisoning work?
-CO has 200x the affinity for Hb
-Binds Hb and doesn’t let it go
-Blocks sites from oxygen
Transport and exchange of CO2 in systemic capillaries
-Bicarbonate quickly diffuses from RBCs into the plasma
-The chloride shift occurs where Cl moves in from the plasma to balance the outrush of HCO3 from the RBCs
Transport and exchange of CO2 in pulmonary capillaries
-HCO3 moves into the RBCs and binds with hydrogen to form carbonic acid
-Carbonic acid is split by carbonic anhydrase into CO2 and water
-CO2 diffuses into the alveoli
Respiratory acidosis
-If ventilation is hindered (emphysema), CO2 may build up
-Hydrogen will also build up
-This will drop the pH
-The kidney will work to correct hydrogen levels
Respiratory alkalosis
-Fast breathing will cause excessive loss of CO2 and loss of hydrogen
-This will cause the body to be alkalotic
Metabolic acidosis
-High acid (low pH) due to exercise or a kidney problem
-Triggers faster breathing to help reduce CO2
Metabolic alkalosis
-Low H
-Breathing will slow down to try and build H and CO2 levels
