Pulmonary Adaptations in Obesity and Pregnancy: Comprehensive Review, Exams of Advanced Education

A detailed overview of pulmonary adaptations in specific physiological conditions, focusing on obesity and pregnancy. It explores the effects of increasing bmi on lung function, including changes in frc, ic, and respiratory system compliance. The document also examines the mechanisms of breathlessness during exercise in obese individuals, highlighting the role of neural drive and respiratory mechanics. Additionally, it discusses the impact of bariatric surgery on respiratory function and the respiratory adaptations during pregnancy, including changes in chemoreflex sensitivity and lung volumes. Useful for medical and paramedical students, and healthcare professionals seeking a deeper understanding of respiratory physiology in these conditions. (447 characters)

Typology: Exams

2024/2025

Available from 07/10/2025

Prof-Cornel
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EDKP - 485 FINAL TEST WITH
ACCURATE SOLUTION
explain the pulmonary adaptations of obesity, do the lungs get bigger/smaller? or is it
the lung volumes? - ANSWER - with increasing BMI, FRC gets worse and IC is greater
what happens to all these in obesity:
- lung, chest wall and total respiratry system compliance
- FEV-1
- airway resistance
- EFL
- TLC
- FRC
- IC
- respiratory muscle strength
- insp neural drive
- work and O2 cost of breathing - ANSWER - decrease
- decrease
- increase
- increase
- UNCHANGING
- decreases
- increases
- either unchanging or decreases
- increases
- increases
what happens to neural drive in obesity - ANSWER as BMI increases so does neural
drive for a given ventilation
- heavier you are the more the brain is asking to breathe, needs to go up to support a
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EDKP - 485 FINAL TEST WITH

ACCURATE SOLUTION

explain the pulmonary adaptations of obesity, do the lungs get bigger/smaller? or is it the lung volumes? - ANSWER - with increasing BMI, FRC gets worse and IC is greater what happens to all these in obesity:

  • lung, chest wall and total respiratry system compliance
  • FEV-
  • airway resistance
  • EFL
  • TLC
  • FRC
  • IC
  • respiratory muscle strength
  • insp neural drive
  • work and O2 cost of breathing - ANSWER - decrease
  • decrease
  • increase
  • increase
  • UNCHANGING
  • decreases
  • increases
  • either unchanging or decreases
  • increases
  • increases what happens to neural drive in obesity - ANSWER as BMI increases so does neural drive for a given ventilation
  • heavier you are the more the brain is asking to breathe, needs to go up to support a

certain level of inflation why do obese ppl experience breathlessness - ANSWER when ND is too high -> lungs are constraint -> demand and supply mismatch -> neuromechanical uncoupling when high dyspnea for any given WR or VO2, but normal for any given level of V'E, cause is... - ANSWER high ventilatory demand (i.e., increased Ve/V'CO2, increased inspiratory ND) when high dyspnea for any given WR or VO2, and V'E, cause is... - ANSWER dynamic respiratory mechanical factors explain respiratory mechanics vs drive and the breathlessness-ventilation relationship in obesity:

  • how they feel
  • how much are they breathing during exercise
  • the ND to breathe
  • is the neural drive matched to the level of ventilation
  • how do they feel for a given level of ventilation
  • how do they feel for a given ND what does all this suggest? - ANSWER - so they feel breathless
  • ventilation much higher for a given work rate, they might reach same level but earlier -> lower tolerance
  • greater ND for a given level of ex
  • respond appropriately to what the brain is asking, no neuromechanical uncoupling, matched
  • they feel the same, tells us appropriate level of drive for ventilation
  • feel sslightly worse there is an appropriate level of IND for a given level of ventilation = NO neuromechanical uncoupling If abnormal restrictive constraints on VT expansion was responsible for exertional breathlessness in obesity, then breathlessness-ventilation slopes should be _____________ in OB vs. NOB adults. - ANSWER greater If an exaggerated drive to breath was responsible for exertional breathlessness in

behavior of dynamic operating lung volumes during exercise in OB - ANSWER OB have lower operating lung volumes at any given ventilation (i.e., their IC and IRV are bigger) for any given IRV, the drive to breathe is _______________ in OB. However, bc the respiratory system adapted and the IRV is already ___________ than NW, this prevents _________________ - ANSWER - greater

  • bigger
  • excessive increases in drive to breath in OB what happens in order to accomodate the greater ventilatory requirements of exercise compared to NW, without greater reductions in dynamic IRV - ANSWER - utilize a greater proportion of their IC
  • adopt a rapid breathing pattern Relative preservation of ventilation-EMGdi%max and of breathlessness-ventilation relationships during exercise in OB vs. NOB reflected maintenance of _________________
  • ANSWER a more mechanically advantageous IRV at any given ventilation throughout exercise in OB conclusion: In adults with mild-to-moderate obesity, exertional breathlessness could not be explained by greater _____________________________________, but reflected the ________________________________ needed to support the higher ______________________________________ of exercise in obesity. - ANSWER - restrictive constraints on VT expansion
  • awareness of a higher inspiratory neural drive
  • metabolic and ventilatory demands effects of bariatric surgery on respiratory mechanics and breathlessness during ex, lowers what (3) - ANSWER - O2 consumption
  • ventilation
  • HR all lower for a given PO after bariatric surgery _____________ get worse as they are breathing closer to ___________ - ANSWER - operating lung volumes
  • TLC Relief of breathlessness during exercise following bariatric surgery could not be explained by improved dynamic breathing mechanics, but reflected the ________________________________________________ - ANSWER awareness of reduced metabolic and ventilatory requirements.

effects of pregnancy on central chemoreflex and non-chemoreflex drives to breathe - ANSWER - increased central chemoreflec sensitivity -> stimulation occurs at lower CO levels -> slightly higher wakefulness drive The hyperventilation and attendant hypocapnia/alkalosis of human pregnancy resulted from a complex interaction between alterations in ___________________________________ and other factors that directly affect ventilation, including increased ______________________________, increased ___________________________________, increased _____________ and decreased _____________________ - ANSWER - in arterial (peripheral) and central (brain) acid-base balance

  • wakefulness drives to breathe
  • central (but not peripheral) chemoreflex sensitivity
  • V'CO
  • cerebral blood flow. ventilatory responses in late gestation: more ___________ = more _____________ - ANSWER effort (pressure) -> more work respiratory mechanical/muscular responses to exercise in late gestation: - ANSWER respiratory system is not imposing mechanical limitations -> WOB is proportional so there is mechanical adaptation effects of pregnancy on static lung volumes & capacities - ANSWER - increase in IC
  • decrease in FRC Behavior of Dynamic Operating Lung Volumes during Exercise in Late Gestation: lung volumes ________ -> IC __________ and EELV _________ so dont need to breathe near ___________; they are not short of breath but they _________________ more, not disproportionally breathless ______________________ - ANSWER decrease increases decreases TLC ventilate in relation to neural drive
  1. pregnancy induced increase in exertional breathlessness reflects the _________________________ & ________________________
  2. respiratory mechanical adaptations (recruitment of IC) accomodates the
  1. Monocytes mature & differentiate into macrophages and increase the expression of Toll-like scavenger receptors, which ingest sub-endothelial __________ and become ___________________. - ANSWER - the site of activation
  • sub-endothelial space
  • LDL
  • macrophage 'foam cells'
  1. Macrophages also produce inflammatory cytokines, proteases and growth factors that cause inflammation, cell/tissue damage and further contribute to the development of the atherosclerotic plaque (atheroma).
  2. As macrophage foam cells develop into an atheroma, __________________ migrate from the media to the intima & proliferate (hyperplasia) to form a _______________ over the lipid core of the atheroma through the production of extracellular matrix proteins (e.g., collagen & elastin) = vessel repair/wound healing. - ANSWER - fibrous cap
  • VSMC
  1. Separates ________________________ of the atherosclerotic plaque from ________________________ involved in the coagulation of blood.
  2. Contains inflammatory cells (macrophages, T cells, mast cells) that aid in the ________________________________ process.
  3. Confers ___________________ to an atherosclerotic lesion - ANSWER - the thrombogenic lipid rich core
  • platelets and proteins
  • 'wound healing/vessel repair'
  • structural stability

so what determines the stability of the lesion - ANSWER the thickness of the cap

the only cells capable of synthesizing the fibrous cap - ANSWER VSMC

Progression of an atherosclerotic plaque reflects the interaction between - ANSWER

sub-endothelial inflammation and the local reactive 'vessel repair/wound healing' response of the VSMC's

Positive association between the risk of non-fatal myocardial infarction (MI) or fatal Coronary Heart Disease (CHD) & circulating levels of the inflammatory cytokine, __________________ - ANSWER interleukin 6 (IL-6)

Frequency of asymptomatic atheroma's are: - ANSWER - more common in men than woman

  • increase with age

First mechanisms by which atherosclerosis leads to symptoms, such as angina pectoris, non-fatal or fatal myocardial infarction, etc... - ANSWER If the legion becomes sufficiently large to restrict coronary blood flow & myocardial O2 supply

  • particularly under conditions of increased myocardial O2 demand (e.g., exercise)
  • then myocardial ischemia & stable angina pectoris (chest pain) will occur.

Myocardial Ischemia = myocardial __________________ > myocardial _________________ - ANSWER O2 extraction O2 delivery

its not necessarily the size, but the __________________ that matter, explain - ANSWER - stability of the plaque

  • Although a larger lesion may be more likely to cause stenosis (blockage) of the lumen, larger lesions are more stable and less likely to rupture because of the repeated injury-repair process, which generates a large, stable fibrous cap

Second mechanisms by which atherosclerosis leads to symptoms, such as angina pectoris, non-fatal or fatal myocardial infarction, etc... - ANSWER Rupture/erosion of the fibrous cap exposes the pro-thrombotic lipid rich core of the atheroma to the circulation and leads to platelet accumulation & activation (i.e., clotting).

mechanisms of exercise intolerance in CAD - ANSWER - myocardial ischemia (angina)

  • impaired LV function

impaired LV function can cause what - ANSWER decreased SV/O2 pulse -> decreased CO & peripheral locomotor muscle O2 delivery -> decreased symptom-limited peak VO

in ppl with CAD, VO2 often _________ normally with ΔV'O2/ΔWR slope equal to ___________ during mild-to-moderate intensity exercise. - ANSWER - increases

  • 10 ml O2/min/watt

ischemic threshold - ANSWER where myocardial O2 supply < myocardial O2 demand

what happens to the VO2/WR and VCO2/WR slopes once the myocardium reaches its ischemic threshold - ANSWER VO2/WR abruptly plateaus while the VCO2/WR slope continues to rise

what does the VO2/WR plateau reflect - ANSWER reduced SV (myocardial dyskinesis) & impaired O2 delivery

whats up with the AT in CAD vs health, what does this reflect - ANSWER similar, reflecting normal submaximal O2 delivery & utilization

what happens to VCO2 above AT in CAD, what does that reflect - ANSWER increases more steeply reflecting decreased O2 delivery -> decreased muscle oxygenation -> increased anaerobiosis -> increased rate of accumulation of metabolites -> metabolic acidosis -> increased HCO3- buffering of H+ -> increased VCO2 (non-metabolic) -> increased peak RER

during exercise in CAD vs health, what indicates severe metabolic acidosis and its the consequence of what? - ANSWER - abnormally high RER

  • of impaired peripheral locomotor msucle O2 delivery (secondary to myocardial schema)

compared to health, HR is often ___________, while O2 pulse (an index of ___________) is often ___________ at rest and during exercise in CAD - ANSWER higher lower

what explains the increased HR in CAD - ANSWER compensating for the decrease in SV in attempt to match cardiac output with exercise intensity

Ve/Vo2 and Ve/VCO2 ratios are ________ at rest and during exercise in CAD - ANSWER normal

AT and respiratory compensation for metabolic acidosis during heavy exercise is often ________ in CAD - ANSWER normal

under most circumstances, exercise is NOT _____________ in ppl with CAD - ANSWER ventilatory limited

imapired supply not _________________ in CAD - ANSWER extraction

3 month exercise not enough to make ___________ adaptations to exercise, only ______________ + what were they - ANSWER central, peripheral

  • capillary density, succinate, peak extraction

12 week HIT on flow mediated dilation in CAD - findings - ANSWER - for less work, more of a benefit

  • good improvement on PO
  • tolerate more ex before anaerobic threshold
  • improvments in vascular endothelial cell function
  • drug
  • = to 130-140 mins/week of walking

what has a protective effect in any LDL level - ANSWER exercise, low cardiorespiratory fitness makes you much worse off in any level

Fat loss through dieting or exercise produces ________________ changes in plasma lipoprotein (________) concentrations! - ANSWER comparable and favorable HDL-C

it is important to combine _________________ in the treatment of elevated LDL- C levels in elderly adults at risk for CAD - ANSWER diet and exercise

findings when studying the factors influencing the effects of exercise on lipids and lipoproteins - ANSWER lean ppl may benefit more form the exercise interventions

Exercise endurance training-induced increases in HDL-C levels are inversely related to ______________________. What may have to occur during exercise training in order for blood lipid profiles to improve in a clinically significant way, particularly in people who are overweight or obese at baseline. - ANSWER - baseline BMI and waste circumference

  • Body weight, body fat and body composition changes

Studies have shown a close relationship between ____________________ fat deposition and indices of CVD risk, including low HDL-C/Total cholesterol ratio.

- This type of fat deposition is more characteristic of men, who generally exhibit _____________ adiposity (apple shape), than of women, who generally exhibit ____________ adiposity (pear shape). - ANSWER - intra-abdominal

  • android
  • gynoid

______________________, regardless of how frequently it's performed and/or at which intensity it's performed, appears to be the most important determinant of physical activity-induced improvements in HDL-C levels. - ANSWER duration of exercise (volume)

what type of training was seen to decrease TC, TC/HDL-C, LDL-C, tris and increase HDL-C. However, there were no significant improvements in HDL-C, where the authors suggest that perhaps ______________________ may be more appropriate in improving HDL-C in adults. - ANSWER resistance aerobic exercise

what has a cardioprotective effect - ANSWER HDL

While dietary changes and aerobic exercise training both improve HDL-C, only the ________________ lowers LDL-C to a significant level. - ANSWER combination of both

what most effectively decreases LDL-C and increases HDL-C and why - ANSWER - endurance + strength

  • possibly due to longer session durations.

how is hypertension defined (numbers) - ANSWER 140/90 or higher

primary hypertension - ANSWER unknown etiology

  • can result from genetic, physiological and behavioural factors (increased CO< decreased vascular conductance, RAAS dysfunction)

MAP equation - ANSWER CO/TVK

high energy pressure for blood flow to muscles, organs & tissues - ANSWER MAP

changes in _________________ can show disproportionate changes in MAP - ANSWER conductance or resustance

increased resistance

abnormal endothelium- dependent vasodilation in hypertensive adults is not due to impaired vascular smooth muscle responsiveness to EDRF's but ____ - ANSWER impaired release of vasodilating influences

T or F: Normalization of arterial blood pressure via antihypertensive pharmacotherapy does not improve the already impaired endothelial- dependent vasodilator response to acetylcholine in hypertensive patients. - ANSWER true

Among hypertensive populations (SBP ≥140 mmHg), the SBP-lowering effects of exercise (all types and intensities) was similar to that of _______ - ANSWER commonly used antihypertensive medications

The anti-hypertensive effect of endurance training is mediated (primarily) through a reduction in _______________ [i.e., an increase in total vascular conductance (TVK)], secondary to adaptations of __________ (↓ plasma norepinephrine) and ___________ (↓ plasma renin) activity levels - ANSWER - systematic vascular resistance

  • SNS
  • RAAS

do the benefits of exercise training on SBP depend on age? - ANSWER no

The benefits of exercise training on SBP & DBP are established within the first _________ of training and don't change much thereafter. - ANSWER 10 weeks

T or F: Low-to-moderate intensity exercise training is just as (if not more) effective as higher intensity training for reducing SBP & DBP in hypertensive patients. - ANSWER true

Regular aerobic exercise produces favorable, non-localized (i.e., systemic) adaptations of ___________________ (i.e., endothelial function) that are associated with clinically important reductions in blood pressure in older men and women with primary/essential

hypertension - ANSWER - vasodilatory capacity

explain hypotension and exercise duration - ANSWER post-ex hypo occurs after any duration but is of greater magnitude and longer duration following longer vs shorter bouts

heart failure - ANSWER syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

The inability of the ventricle to fill with or eject blood limits the ability of the heart to _________________________ at a rate corresponding to ________________________ requirements of the metabolizing tissues, particularly during exercise. - ANSWER - deliver oxygenated blood (decrease cardiac output)

  • oxygen uptake (V'O2)

systemic compensatory mechanisms activated to maintain adequate tissue perfusion, are they good? - ANSWER - Frank-Starling mechanism

  • SNS activation
  • RAAS activation
  • ventricular remodeling

beneficial in the short term but detrimental over the long term -> maladaptive adaptations

most common reasons for HF - ANSWER - CAD (ischemia & myocardial infarction)

  • systemic hypertension
  • diabetes

main symptoms of HF similar to those of _______, what are they - ANSWER - COPD

  • dyspnea & impaired exercise tolerance

- SV/CO

so even if __________ is rising ______ is not responding as it should - ANSWER - preload/ventricular contractility

  • SV

compensatory increase in SNS and RAAS activity serve to increase __________________ as well as both __________ and _________ - ANSWER - myocardial contractility

  • preload anf after load

the negative effect of a high resistance (after load) is disproportionally worse than the positive effect of a better preload. even if you have good preload and body is able to take advantage of the F-S mechanism to increase contractility, its not enough to compensate for high resistance - ANSWER

t or f: Stretch or increase in cardiac chamber volume leads to release of natriuretic peptides - ANSWER true

associated with worsening of cardiac function (LVEF < 40%) due to alterations in the size, haste, structure & function of the ventricle - ANSWER ventricular remodelling

______________ occurs initially as an adaptive response that counteracts increased wall stress and forces placed on the chambers of the heart:

  • failing heart enlarges to increase ______________ -> _________ increase via F-S
  • increase in myocardila wall thickness & ventricular mass -> increases _________________ - ANSWER - remodeling
  • ventricular volume
  • SV/CO
  • myocardial contractility

what happens to VO2/WR slope, VCO2/WR slope, RER/WR slope, Ve/WR slope in HF vs.

health - ANSWER - lower

  • higher
  • higher
  • higher

CO in ex in HF - ANSWER much lower at any given WR, cannot match demand

SV in ex in HF - ANSWER lower, plateaus on graph

HR in ex in HF - ANSWER tries to compensate by increasing, but not good enough

C(a-v)DO2 in ex in HF - ANSWER increases (widening), diff from CAD trying to compensate for low CO

incomplete compensation for decreased CO in HF - ANSWER widening of central arteriovenous oxygen difference

MAP in HF - ANSWER maintained

whats being compromised to maintain MAP? - ANSWER CO, relationship b/w inflow and outflow is preserved

LBF in HF in ex, whats responsible for this - ANSWER reduced -> less supply, a lot more resistance in HF (LBF = CO/LVR)

In both health and HF, symptom-limited peak V'O2 correlated positively with (1) ______________________ and (2) _______________________. What does this tell us? - ANSWER - peak exercise cardiac output

  • peak exercise leg blood flow