lecture 13 Flashcards
(10 cards)
definitions (rise in breathing)
hyperpnea
- an increase in ventilation that is proportional to metabolic demands
- blood gases remain “normal” (i.e. PO2 and PCO2)
hyperventilation
- an increase in ventilation that exceeds metabolic demands
- blood gases deviate from “normal”
why does exercise impact breathing?
air to mitochondria, then mitochondria to air
exercise —> increase muscle work —> increase metabolism (ATP) energy —> increase VO2 (oxygen); increase VCO2 (carbon dioxide) —> increase Va (alveolar ventilation specifically); increase Ve (ventilation)
why do we breathe during exercise?
- exercise imposes 2 great challenges that must be met:
1. CO2 produced must be cleared
- prevent arterial PCO2 and H+ from rising
2. O2 extracted by the muscles from blood must be replenished
- prevent arterial PO2 from falling - these requirements are met only if alveolar ventilation (Va) increases in proportion to metabolic rate (VCO2 and VO2)
replenish oxygen —> PaO2 = Va/VO2
prevent CO2 retention —>PaCO2 = VCO2/Va
which of PaO2 should be regulated most tightly?
large changes in PaO2 at the lungs don’t effect O2 saturation drastically, but even small changes in PaCO2 can greatly impact pH (the body does not tolerate well even minor changes in the acdity of its tissues)
[H+] = 24 (PaCO2/HCO3)
- if arterial CO2 rises, increase H+ and reduce pH if you hold your breath
- if arterial CO2 not regulated, increase H+ concentrate
- H+ + HCO3 <—> H2O + CO2
Va = VCO2/PaCO2
- Va and VCO2 must match
80mmHg of PO2 is hypoxic still almost at 100 OHb stat %
how does breathing change as a function of exercise intensity?
Ve = Vt x BF
Va = VCO2/PaCO2
Ve graph
- Va = Ve - Vd
- Vd = doesn’t participate in exchange
- Va, perfectly matched to PaO2
Vd/Vt graph
- porportion of Va, Vd reduced to less than 20%
PaCO2 pH decrease causes hyperventilation
mechanisms controlling exercise hyperpnea
- neural feed-forward
- supra medullary inputs
- sleep, emotion, locomotion, learning experiences - neural feedback
- mechano/metaboceptor afferents (dorsal columns) - humoral feedback
- medullary ISF [H+] chemoreceptors
- hydrogen in concentration changes
- carotid chemos [PaO2, PaCO2, H+a, K+a]
- by coratid artery, hydrogen ion pH changes
neural and humoral factors
- electrically-induced hindlimb contractions on Dog 1 (neural dog) while perfusing the hindlimbs of Dog 1 with blood from Dog 2 (humoral dog)
- Ve rose, and maintained an elevated state - dog 2 received venous blood from the hindlimbs of dog 1
- both dogs increased breathing independent of central command or feedforward mechanisms
- no feedforward mechanism
- Ve = 2L change then maintained at elevated level
feedforward factors
cat with all sensory afferent signal remove
“stimulated” exercise
increase in phrenic activity = increase in respiratory drive
cat began to breathe during exercise independent of any feedback
- that feedforward is the only thing needed to breathe during exercise
- got a breathing response
blocking neural input from muscle in humand
fentanyl injection in lumbar selectively blocks all afferent signals arising from skeletal muscle
proportion of Ve attributed to skeletal muscle afferents
- 325W
proportion of Ve attributed to “central command” or humoral factors?
matching of Ve to VCO2
biggest mystery to solve
Va = VCO2/PaCO2
