11/9 Exercise Testing - Scardella Flashcards
interdependency of physiologic mechanisms for gas transport and energy production
CV response to exercise
CO increases in proportion to severity of exercise : 5L/min at rest → max 25-30L/min
- SV initially increases (until 45% of VO2max)
- beyond that, all CO incr is due to incr in HR
blood flow to specific tissues is regulated in proportion to metabolic activity
comparing untrained-trained-elite athletes, diff lies in how much of the response is due to increase in HR vs increase in SV
- elite and trained will have a high and medium SV response respectively
how to estimate SV during exercise training
CO = SV x HR
CO = VO2/(A-v)O2
assuming that early exercise makes O2 extraction maximal,
SV x HR = VO2
and SV = VO2/HR
respiratory response to exercise
3 features
why only modest incr in PA pressure? location/overal effect
at conclusion of exercise?
light to moderate exercise:
- ventilation incr linearly with O2 consumption
- high CO2 production
- significant incr in pulmo blood flow but only modest incr in PA pressure
- why? recruitment and dilation of large numbers of pulmo capillaries
- pulmo blood increases most in upper lung zones → reduction in dead space ventilation
- effect: deadspace/total decreases from 30-40 (rest) to 15-20 (exercise)
at conclusion of exercise, minut ventilation is still below max voluntary ventilation (both normal and trained)
- minute vent lower in trained than in normal for any given level of oxygen consumption
- minute vent much lower in pt with COPD
- minute vent at exercise conclusion reaches MVV in COPD
acid base response to exercise
initial phase of exercise:
- ventilation increases linearly with O2 consumption, CO2 production, HR, CO
- no significant change in pH or ABG
when lactate production exceeds LA utilization…
- blood LA incr
- lactate buffered by HCO3 → incr in CO2 production → rise in ventilation above metabolic reqs
“anaerobic threshold”
initially, believed to be point during exercise where aerobic mechs failed to meet energy demands
- result: SWITCH to anaerobic glycolysis (ehhh) → rise in blood LA
- LA buffered by bicarb → incr in CO2 production
now, ventilation incr no longer linear with metabolic rate because ventilation now also driven by CO2 levels
concept: eventually, LA would overwhelm bicarb buffering system, stimulate chemoreceptors, and result in increase in minute ventilation
anaerobic threshold is the point at which CO2 production outstrips O2 production
why does blood lactate increase?
fact: we do not “switch” over from aerobic to anaerobic mech
- studies show that intracellular PO2 doesnt sdrop to levels that would result in muscle hypoxia, that LA is produced even at start of exercise
- plus, liver and non-exercising muscle can metabolize LA
therefore: LA accumulates when rate of production exceeds rate of metabolism
* LA production higher in non-conditioned pts or pts with cardiac disease (bc of worse O2 delivery to tissues)
respiratory and metabolic responses to exercise
- minute ven during exercise INITIALLY driven by metabolic rate
- when excess H+ ions from LA combine with bicarb, CO2 is produced, driving an incr in ventilation
- as bicarb buffering system overwhelmed, pH falls further and exercise ends
* exercise in normals is limited by accumulated lactate stimulating incr vent
exercise pathophysiology
hallmark feature
reasons?
due to reduced max O2 consumption (VO2max)
why? look at specifics too
- inability to increase SV
- inability to increase vent
- inability to increase PO2
dx of pulmonary hypertension on exercise testing
cardiac findings (recall: RV CO = LV CO)
- low anaerobic threshold (low CO)
- low oxygen pulse (low SV)
- elevated HR (since SV is low, only way to try to boost CO)
pulmonary findings
- LACK of fall in VD/VT (physiologic dead space, which is supposed to fall during exercise)
- fall in PaO2 (high CO but limited pulmo vasc bed → not enough time to RBC to pick up oxygen)
main ideas
main ideas x2
obstructive lung disease limitation
cardiac disease limitation
