L10 - Respiratory Physiology 2 Flashcards
how does gas exchange go when in a steady state?
- volume of O2 added into the blood in the lungs is the same as volume of O2 removed by the tissues
- volume of CO2 removed from the blood into the lungs is the same as volume of CO2 added into the blood by tissues
- O2 consumption of CO2 production match ventilation, but do not have to match each other
- Respiratory quotient (RQ) ratio of CO2 produced and O2 consumed. Normal RQ = 0.8 (8CO2 produced for 10 O2 consumed)
explain the partial pressures involved with gas exchange
- the pressure of a mixture of gasses = the sum total of the pressures of each individual gas
Dalton’s law:
- in a gas mixture (air(, each gas exerts its own individual pressure, called partial pressure (P)
- gas diffusion occurs from high to low partial pressures
- between liquid - liquid phases and gas - gas phases but also liquid - gas phases
what are alveolar PO2 and PCO2 affected by?
- changes in PO2 of inspired air (high altitude)
- changes in alveolar ventilation (breathing pattern, PO2 and PCO2)
- changes in O2 consumption (PO2) and CO2 production (PCO2) by tissue
Hypoventiliation: alveolar ventilation cannot keep with CO2 production (PCO2 high, PO2 low)
Hyperventialation: alveolar ventilation is too great for CO2 production (PCO2 low, PO2 high)
describe the ventilation-perfusion match of gas exchange (explain graph on slide as well with response to decreased airflow to region or lung)
Match between alveolar airflow and capillary blood flow in each alveolus (both O2 uptake and CO2 elimination)
Mismatch:
- alveoli with low airflow will decrease pulmonary capillary blood flow
- alveoli with low capillary blood flow will decrease aleveolar airflow
- homeostatic mechanism is based on minimising ventilation-perfusion mismatch
how is O2 transported in the blood? and explain cooperatively and binding slope
- haemoglobin has 4 O2 binding sites to Fe2+
- HbO2 does not contribute to PO2 only dissolved O2
HbO2 is crucial for increasing total oxygen quantity in the blood
Cooperativity: binding of one O2 molecule to Hb increases he affinity of the remaining sites on Hb - non-linear
Plateau (70-100mmHg): is a safety factor - moderate drop in lung function maintains substantial Hb-O2 saturation
Steep slope (20-60mmHg): unloading O2 in tissues
describe transport of CO2 and H+ in the blood (plus carbonic anhydride reaction)
CO2:
- 10% dissolved in plasma
- 25-30% bound to carbaminohemoglobin
- 60-65% converted to bicarbonate (HCO3-)
H+:
- binds to Hb to form HbH (tissues/venous blood)
- is released in lungs to react with HCO3- (forming CO2)
Hyperventilation: low PCO2 can cause low H+ (respiratory alkalosis)
Hypoventilation: High PCO2 can cause high H+ (respiratory acidosis)
describe hyperventilation in dental practice (what should be done)
Anxious patient - uncontrollable hyperventilation
Large amount of CO2 being exhaled (CO2 offloaded) (without increase in CO2 production due to metabolic increase). alveolar ventilation is too great for CO2 production
Arterial PO2 high - arterial PCO2 low - mild alkalosis (low H+)
- More CO2 will solve the issue (NOT O2)
describe the neural control of respiration (and look at diagram on slide)
Pons: pneumotaxic centre - apneustic centre
Medulla oblongata: Dorsal respiratory group (DRG) - Ventral respiratory group (VRG)
Action potentials of spinal motor neurons trigger inspiratory muscles (diaphragm and intercostal muscle) - ispiration
Action potentials cease and inspiratory muscles realx
Expiration is due to elastic recoil of the lungs (at rest) (additional neurons can trigger expiratory muscles like during excerisie)
describe the control of respiration in terms of PO2 and H+ (look at the flow chart thing as how that signalling plays a role)
Central and peripheral chemoreceptors!
Central chemoreceptors in medulla (DRG/VRG) sensitive to H+ driven by PCO2
- ventilation much more sensitive to changes in PCO2
Peripheral chemoreceptors: carton bodies and aortic bodies sensitive to PO2 (and H+)
- ventilation increases only when PO2 below 60 mmHg
Central chemoreceptors control about 70% of firing, and peripheral control about 30% of firing
what is hypoxia and what are the four versions of it (need to look at image on slides to for numbers to make sense)
Hypoxia - deficiency of O2 at the tissue levels
- hypoxic hypoxia - low arterial PO2 - high altitude (1. change due to inspired air) or lung disease (2. change alveolar ventilation)
- stagnant hypoxia (ischaemia) - tissue perfusion is low (3. O2 delivery problem, heart failure, cariogenic shock)
- histotoxic hypoxia - O2 content, PO2 and O2 delivery normal, but tissue has inability to use O2 (4. poisoning)
- anemic hypoxia - low arterial O2 content (5.) but normal arterial PO2 (low concentrations of Hb in blood, carbon monoxide poisoning)
describe anemia in dental practice
Anemia: low concentrations of Hb in blood (normal arterial PO2 - low arterial O2 content)
Some oral manifestationsL
a. pallor of oral mucosa, especially soft palate and floor of the mouh
b. depapillated and atrophic tongue
c. glossodynia and mucosal ulcers
d. gingival hypertrophy and bleeding
Causes:
- iron deficiency, but also Vitamin B12, folate and copper deficiency
- intestinal disorder - impaired nutrient absorption in intestine (Crohn’s disease and celiac disease)
Dental considerations:
- refer endemic patients to primary care physicians
- avoid elective surgical procedures - increased risk of poor wound healing and haemorrhage
- avoid medications linked to haemolysis
describe the lungs protective reflexes (for sneeze)
While inflating or deflating the lungs - afferent input from stretch receptors to medulla - efferent output back to lungs
receptors also detect irritation - trigger sneeze or cough
Sneeze:
- powerful expiration due to irritation of nasal mucosa stimulating mechanoreceptors
- several inspirations are superimposed followed by powerful expiration
- the high expiratory airflow velocity is to remove the irritant
- don’t hold in a sneeze - purpose is to remove irritant
describe the lungs protective reflexes (or cough)
- mechanoreceptors in the larynx ae stimulated by irritants
- a long slow inspiration occurs followed by a rapid powerful expiration, initially agains a closed glottis
- the high expiratory airflow velocity achieved helps to remove the irritant
Dentist to patient:
- irritants enter the oropharynx - cause cough
- sedation or general anaesthesia might blunt protective respiratory reflexes (dental issues might even be the cause of cough)
Patient to dentist:
- dentist are highest risk of exposure to aerosols/viruses because of being positioned at the patients head
describe anaphylaxis
anaphylaxis is severe, potentially life treating mostly sudden allergic reaction
- the immune system releases a flood of chemicals that can cause you to go into shock. blood pressure drops suddenly and the airways narrow, blocking breathing (increased airway resistance)
Common triggers:
- foods, medications (antibiotics, aspirin), local anaesthetics, mouthwashes, latex
Anaphylaxis required immediate injection of epinephrine/adrenaline
- increase blood pressure (vasoconstriction) and
- opens up the airways (bronchodilation)
