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| Respiratory system functions to exchange gases between the external environent and the body |
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| intracellular metabolic processes of the mitochondria |
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| gas exchange across respiratory epithelia of the lungs |
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| Air enters through the nose/mouth then passes through the nasopharynx/oropharynx, the glottis and larynx and then to the tracheobronchial tree |
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| Airways branch into bronchi and bronchioles then respiratory bronchioles and alveolar ducts |
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| Site of gas exchange in the lung |
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- Air moves from areas of higher P to lower P
- V = ∆P/R = (PAlv-Patm)/R
- Alveolar Pressure (PAlv): pressure inside the lung
- Atmospheric Pressure (Patm)
- Intrapleural Pressure (Pip): pressure at the interface of the lung and chest wall |
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- diaphragm and external intercostal muscles
- Diaphragm is the primary muscle for inspriation and is innervated by the phrenic nerve.
- Contraction of the diaphragm causes it to dome downwards
- External intercostal muscles are innervated by the intercostal nerves
- Contraction of the external intercostal muscles raises and enlarges the rib cage |
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| Muscles of inspiration are activated to contract -> Thoracic volume increases -> intrapleural P becomes more negative -> Alveoli enlarge passively -> Increase in alveolar volume causes a decrease in alveolar pressure (below that of PAtm) -> Air flows into lungs |
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- Expiration is passive during normal quiet breathing
- The muscles that contracted during inspiration relax and the elastic recoil of the lungs increases the alveolar pressure above that of atmospheric pressure so air moves out of the lungs
- A forced/active expiration will contact the muscles of the abdominal wall |
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| Tidal Vol. (TV): volume of air entering and leaving the lungs with each normal breath |
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| Inspiratory Reserve Vol. (IRV): additional volume of gas that can be inhaled above TV during a forced maximal inspiration |
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| (ERV): additional volume of gas that can be expelled from the lungs beyond TV during a forced maximal expiration |
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| (RV): volume of gas left after a maximal forced expiration |
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(TLC): total volume of air in the lungs after a maximal inspiration
TLC = RV+ERV+TV+IRV |
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| Functional Residual Capacity |
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Definition
- Functional Residual Capacity (FRC): volume of gas remaining in the lungs at the end of normal tidal expiration
- Allows air to be available for gas exchange constantly since breathing is episodic, but blood flow to the lungs is continuous. It also prevents the lungs from collapsing after each breath.
FRC = ERV+RV |
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- Vital Capacity (VC): volume of air expelled from the lungs after a maximal inspiration and expiration
VC = ERV+TV+IRV |
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Minute Ventilation (VE) : volume of air that was moved in and out of the lungs per minute
VE = TV x RR
TV – tidal volume (mL/breath)
RR – respiratory rate (breaths/min) |
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Dead Space Ventilation (VDS): volume of air not participating in gas exchange per minute
VDS = DSvol x RR |
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Alveolar Ventilation (VA): part of the tidal volume that enters or leaves the gas exchange area of the lung per breath per minute
VA = (TV – DSvol) x RR = VE - VDS |
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Gases will diffuse from areas of higher partial pressure to areas of lower partial pressure
Blood in the pulmonary circulation has a partial pressure gradient for oxygen to move into the blood and carbon dioxide to move out of the blood |
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Carbon dioxide diffuses from the cell to the capillary blood and can react in 3 major ways
~8% will react slowly to form bicarbonate
~65% will enter RBC and react rapidly with water and carbonic anhydrase (CA) to form bicarbonate
~27% will enter the RBC and react with terminal amine groups of blood proteins. Since the most abundant protein in the RBC is hemoglobin most will react to form carbaminohemoglobin |
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Breathing is spontaneously initiated by the CNS (pons and medulla)
Medullary Respiratory Center:
Dorsal Respiratory Group (DRG): contain mostly inspiratory neurons (ie, phrenic nerve)
Ventral Respiratory Group (VRG): contain inspiratory and expiratory neurons, but is generally not active in quiet breathing
Breathing can be modified by a number of mechanisms, including the peripheral and central chemoreceptors |
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Stretch receptors are located in the smooth muscle of large and small airways
Afferent fibers travel through the vagus nerve and project into the brainstem.
When there is an increase in stretch there will be an inhibition of inspiratory neurons, to prevent the overexpansion of the lungs. The opposite will happen if there is a decrease in stretch. (Hering-Breuer Reflex) |
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- Located in the medulla
- Sense increases in PCO2 and decreases in pH by sensing the increase in [H+] in cerebral spinal fluid
CO2+H2O<-->H2CO3<-->H+ +HCO3
- This is a “slow” reaction but when the chemoreceptors are activated it will cause an increase in ventilation rate |
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| Peripheral Chemoreceptors |
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Definition
- Found in the carotid bodies and aortic arch (Note these are not the baroreceptors although they are found in the same area)
- Able to sense decreases in arterial PO2 and to a lesser extent increases in PCO2 and decreases in pH
- Activation of the receptors will cause an increase in ventilation rates |
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Definition
- Decrease in ventilation leading to an increase in arterial PCO2 (hypercapnia)
- Carbon dioxide will start to build up throughout the body
- The increase in PCO2 will cause a decrease in pH (respiratory acidosis)
- This will activate chemoreceptors to increase respiratory rate |
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Definition
- Increase in ventilation by an increase in respiratory rate and/or increasing tidal volume leading to a decrease in PCO2 (hypocapnia)
- Rate of ventilation is higher than what is needed to remove carbon dioxide from blood
- A decrease in PCO2 will decrease the inspiratory drive (Are able to hold breath for a longer period of time)
- Prolonged hyperventilation will lead to respiratory alkalosis (increase in pH) which can cause arterioles in the brain to constrict -> decrease in blood flow to the brain -> dizziness |
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- Hyperpnea : increase in ventilation matching an increase in metabolic activity (ex. Exercise)
- Ventilation rate matches demand for carbon dioxide removal so there is no decrease in arterial PCO2 that was seen in hyperventilation
- Exercise increases demand for oxygen and produces more carbon dioxide
- There is an increase in perfusion of the upper lungs (that are normally closed at rest) to increase gas exchange, because the increase in CO2 during exercise increases pulmonary vascular pressure
- The mechanisms that control the respiratory response to exercise are not understood well |
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