Respiratory System Flashcards
Vt, IRV, ERV and RV definitions
Lung volumes:
Tidal volume (Vt): volumes that moves during a respiratory cycle (single inspiration OR expiration)
Inspiratory reserve volume (IRV): additional volume inspired above tidal volume
Expiratory reserve volume (ERV): forcefully exhaled after the end of a normal expiration
Residual volume (RV): volume of air in the respiratory system after maximal exhalation (cannot be directly measured)
Mechanism of inspiration vs. expiration
Alveolar pressure < atmospheric
Diaphragm contracts and drops towards the abdomen.
External intercostal and scalene muscles contract and pull ribs upwards and out.
Thoracic volume increases, causing alveolar pressure to decrease.
Air flows inwards.
Alveolar pressure > atmospheric
Diaphragm relaxes and rises towards the abdomen.
External intercostal and scalene muscles relax and pull ribs downwards and inwards.
Thoracic volume decreases, causing alveolar pressure to increase.
Air flows outwards
bronchodilation/constriction autonomic control
Low O2 effect on bronchioles, pulmonary arteries and systemic arteries
Airway obstruction
Bronchoconstriction: under parasympathetic neuron control (muscarinic receptors), increases resistance to decrease air intake
Bronchodilation: under sympathetic neuron control, decreases resistance
β2 receptors on smooth muscles relax in response to epinephrine to increase air intake
When PO2 is low or CO2 high, bronchioles dilate while pulmonary arteries constrict, and systemic dilate - all to increase gas exchange and delivery
Airway obstruction affects upper airways to increase resistance
Total pulmonary ventilation vs alveolar ventilation
Total pulmonary ventilation: volume of air moved in and out of lungs per minute.
TPV = Ventilation rate x Tidal volume (Vt)
- Does not account for the significant portion of inspired air that never reaches exchange surfaces (alveoli) and that stay in anatomic dead spaces (conducting airways)
Alveolar ventilation: volume of fresh air that reaches the alveoli per minute
AV = Ventilation rate x (Vt - dead space)
- More accurate indicator of efficiency of breathing.
Hypo/hyperventilation changes in PO2/PCO2
What happens when there is low PO2 alone?
Hypoventilation: when alveolar ventilation decreases, alveolar PO2 is decreased and PCO2 is increased
Hyperventilation: when alveolar ventilation increases, alveolar PO2 is increased and PCO2 is decreased
Low PO2 = arterioles surrounding alveolus constrict, diverting blood flow to better ventilated alveoli
Pathologies causing hypoxia
Emphysema: destroys alveoli resulting in loss of alveolar surface area = less diffusion and also reduced elastance
Fibrotic Lung Disease: thickened alveolar membrane resulting in less permeable barrier = less diffusion
Pulmonary Edema: fluid in interstitial space increases diffusion distance = less diffusion.
Asthma: bronchoconstriction increases airway resistance, decreasing alveolar ventilation.
Hb oxygen binding - how it gets around the limits of partial pressure
Oxygen binding to Hb obeys law of mass action
↑ PO2: shifts reaction to right (Hb + O2 -> HbO2)
↓ PO2: shifts reaction to left (Hb + O2 <- HbO2)
Allows arterial blood to contain oxygen past the equilibrium between alveolar and arterial PO2 .
Factors which shift the HbO2 saturation curve to the left (higher affinity for O2)
Fetal Hb
Higher pH
Lower temperature
Lower PCO2
Low 2,3-BPG (chronic hypoxia ↑ 2,3-BPG)
↑ Hb affinity means right shift of O2 + Hb ⇋ HbO2
Describe CO2 transport
Hb + CO2 → HbCO2 (carbaminohemoglobin)
or
H2O + CO2 → HCO3- + H+
H+ + Hb → HbH
HCO3- antiport with Cl- to enter plasma (and reverse when at lungs for CO2 exhalation)
Regulatory nervous tissues
Ventral respiratory group (VRG)
Pre-Bötzinger complex = pacemaker
contain neurons to keep airways open
Higher activity muscles for expiration/inspiration
Nucleus tractus solitarius (NTS): contains DRG, which controls inspiration muscles
Dorsal respiratory group (DRG) —> phrenic (diaphragm control) nerves and intercostal nerves during quiet respiration
- DRG —> sensory info to pons (PRG) for tonic on/off control of inspiration
- Pontine respiratory group (PRG)
NTS receives signals from chemo and mechanoreceptors
Peripheral vs CNS chemoreceptors for changes in O2/CO2/pH
Peripheral chemoreceptors: located in carotid bodies (in carotid arteries)
Sense changes in PO2 , pH and PCO2
- Glomus cells: activated by ↓PO2 ↑pH and ↑ PCO2, initiate increase in ventilation by reflex. (O2 must fall below 60 mmHg)
Central chemoreceptors: located in medulla in CNS
Respond to changes in PCO2
- ↑ PCO2 causes CO2 to cross into brain ECF (BBB), convert to HCO3- and H+, causing a pH change in the CSF.
H+ detection by chemoreceptors initiates response to increase ventilation.
