02 - Respiratory Mechanics III&IV

breathing pressure changes in spontaneous breathing vs positive pressure ventilation

• spontaneous breathing

  • inspiration → intra-alveolar pressure decreases and then increases to 0, intrapleural decreases to below -5

  • expiration → intra-alveolar pressure increases then decreases to 0, intrapleural increases to -5

  • parabolic curve in intra-alveolar pressure due to recoil of lungs

  • decreased intrapleural pressure pulls on lungs and lowers intra-alveolar pressure to pull air in

• positive pressure ventilation

  • inspiration → intra-alveolar pressure increase, intrapleural pressure increase

  • expiration → intra-alveolar pressure rapidly decreases, intrapleural pressure rapidly decreases

  • generates force by raising intra-alveolar pressure

positive intrapleural pressure

during normal respiratory cycle, intrapleural pressure fluctuates solely in the negative range

• intrapleural pressure can become positive under special circumstances:

  • inspiration → positive pressure respiration, where outward movement of lungs compresses intrapleural space to raise its pressure

  • expiration → active respiration, where respiratory muscles compress intrapleural space so lungs can return to pre-inspiratory level more quickly and forcefully

assisted control mode ventilation (ACMV)

form of positive pressure respiration or mechanical breathing where inspiratory cycle initiated by patient, or automatically if no signal is detected within a specified time window

positive end expiratory pressure (PEEP)

form of positive pressure respiration or mechanical breathing where lung is kept at a larger volume by not allowing intra-alveolar pressure to return to 0 at the end of expiration

• starts at positive pressure, which distends conducting airway and decreases resistance to keep airway open with low resistance

• lung volume is elevated at end of expiration 

• functional residual capacity is increased, with larger lung volume at end of expiration

positive pressure ventilation (PPV)

aka mechanical breathing

• three forms → assisted control mode ventilation (ACMV), positive end expiratory pressure (PEEP), continuous positive airway pressure (CPAP)

• ideally, trans-alveolar pressure should be low as possible during mechanical respiration to minimize development of ventilator-induced lung injury

  • less than 28-30 cmH₂O

  • if plateau pressure is kept at 28-30 cmH₂O, trans-alveolar pressure can never exceed this level

air trapping in mechanical ventilation

air trapping or auto-PEEP occurs when a new breath begins before the lungs have fully expired the previous one, trapping air in the lungs

• leads to increased pressure and over-inflation of the lungs

• flow never returns to baseline due to increased pressure and resistance 

continuous positive airway pressure (CPAP)

form of positive pressure respiration or mechanical breathing that is not a true support-mode of ventilation

• breathing is spontaneous but via a circuit that is pressurized

• used to maintain airway size and prevent respiratory muscle atrophy

• raises pressure in environment to distend airways and start ventilation at a higher pressure, making it easier to breathe

obstructive sleep apnea

occurs due to critical negative pressure during inspiration

• due to sleep reducing tone of muscles of oropharynx, obesity reducing airway size, alcohol depressing muscle activity, and increased nasopharynx resistance that reduces downstream pressure

• clinical consequences → cognitive and behavioral deficits like excessive daytime sleepiness, mood swings, poor decision making

• major risk factor for cardiovascular diseases like endothelial dysfunction, hypertension, arrhythmias, ventricular hypertrophy

pressure change with forced expiration

transmural pressure is responsible for lung movement and is the difference between intra-alveolar pressure and intrapleural pressure

• pre-inspiration → IAP and atmospheric pressure are equal

• during inspiration → lowered IPP pulls alveolus open to increase alveolus volume and lower IAP, creating a gradient of low pressure in alveolus compared to atmosphere

• end-inspiration → intrapleural pressure remains negative, and air rushes into alveolus to approach atmospheric pressure

• forced expiration → increased IPP due to thoracic muscle contraction compresses on lungs and increases IAP to push air out of lungs, but alveolar elastic recoil opposes dynamic compression from lung collapse

• expiration is effort-dependent at high lung volumes and effort-independent at low lung volumes

regional variation in intrapleural pressure

due to gravity, intrapleural pressure varies with the position of the thorax

• apex → intrapleural volume is higher due to stretch from gravity pulling lung down, where change in volume at apex when taking a breath is less than change in volume at base due to greater distension and being stiffer at apex

• base → intrapleural tension is less due to gravity pulling lung down, creating intrapleural pressure gradient from apex to base

• less IPP at apex, more IPP at base of thoracic cavity

lung compliance on alveolar ventilation

due to gravity, there is more IPP at the base of thoracic cavity than at the apex

• alveoli at apex are more distended at apex than at the base, causing respiratory cycle to start higher on the compliance curve

• change in volume with each breath is greater at the base because they are more compliant

ventilation-perfusion ratio (V/Q)

since blood flow is affected more by gravitational forces than air flow, the V/Q ratio increases as one moves up the lung towards the apex

• gas exchange is greater at the apex of the lung than the base

pneumothorax

perforation of the chest wall or lung that causes air to move into the intrapleural space because IPP is negative

• presence of air in the intrapleural space breaks the liquid seal that attaches the lungs to the best wall, causing that region of the lung to collapse while chest wall expands at the same time

• if volume of air in intrapleural space is small, it will be absorbed into venous blood

• if volume of air in intrapleural space is large, it must be drained using a chest tube

• traumatic or spontaneous

traumatic pneumothorax

• wound to chest moves air from environment to IPS

• rupture of alveolus by barotrauma moves air from intra-alveolar space to IPS

spontaneous pneumothorax

spontaneous rupture of alveolus moves air from intra-alveolar space to IPS

• occurs mostly at apex where more negative IPP is suspected of imposing large stress on alveolar wall

• flaps of ruptured wall usually reseal and limit volume of air that accumulates

• leads to tension pneumothorax → lung collapse due to air accumulation, compromising both gas exchange and cardiac mechanics

lung elasticity

elasticity resists distortion, where elastic tissues return to its original shape after having been deformed

• elasticity = P / V = 1 / compliance

• tells how “stiff” a lung is

• more elastic = more stiff = more work to get a set volume

• work of breathing = P x V

lung compliance

elastance is non-linear

• P-V relationship for normal lung → fall in IPP is required to obtain a change in lung volume

  • at small starting volume, a small change in pressure elicits large volume change

• slope of the curve (V/P) → measure of compliance, where compliance is inverse of elasticity

  • elastic limit is reached at higher volumes, where more stretch makes it harder to stretch even more

• P-V curve is non-linear and becomes flat at high expanding pressures

compliance in diseased lungs

affects work of breathing, functional residual capacity, and expiration

• emphysema → damage to alveoli, causing more compliant and non-elastic lungs

  • obstructive disease

  • very small pressure changes cause large volume changes

• fibrosis → scarring of lung, causing less compliant and more elastic lungs

  • restrictive disease that makes lung stiff

  • large pressure changes cause small volume changes

surfactant

reduces surface tension to increase lung compliance and greatly reduce work of respiration by sitting between water molecules at air-water interface to disrupt cohesive forces of water

• surface tension develops at air-water interface due to water particles interacting with air and pulling in to cause lung collapse

• surfactant normalizes surface tension to prevent lung collapse

• in absence → surface tension of film lining inside of alveolus is at a high constant

  • P = 2 ST / r

  • the smaller the radius, the greater the pressure

  • small alveoli would inflate larger alveoli if connected

• in presence → lung compliance is increased because lung stability is promoted

  • no inter-alveolar pressure gradient

  • pressure of small alveoli and large alveoli are equal

compliance at air-water interface

it takes more work to inflate a lung with air than a lung with saline

• air forms surface tension when in contact with water

• effect of surface tension is less with surfactant

• water-water interaction counteracts itself, so there is no developed surface tension

respiratory distress syndrome (RDS) of newborns

infants with respiratory distress syndrome (RDS) have high surface tension that shows little variation in surface tension with area

• lungs are very elastic and difficult to inflate

• premature birth and maternal diabetes are risk factors

  • gestational age of 34 weeks divides incidence/mortality from disorder-free

• interdependence → alveoli share septa and do not exist as independent units

effects on functional residual capacity (FRC)

functional residual capacity is the volume of air remaining in lungs after passive expiration, achieved when respiratory muscles are relaxed and inward recoil of lungs is balanced by outward elastic recoil of thorax

• elastic properties of lungs and chest wall determines FRC

• elastic lungs (fibrosis) → FRC is decreased and patient appears sunken-chested due to balance happening at less stretch of lungs

• non-elastic lungs (emphysema) → FRC is increased due to narrowed airway, where there is less flow out of lungs that results in air trapping

pulmonary function tests

pulmonary function tests should be compared for age and gender

• vital capacity (VC) or forced vital capacity (FVC) → maximum volume of air that individual can move in single breath as quickly and forcefully as possible

• forced expiratory volume_1sec (FEV_1sec) → volume of air exhaled in first second of FVC maneuver

• normal ratio of FEV_1sec to FVC → value of 80% when IPP becomes positive and airways are compressed and effort-independent

• peak expiratory flow rate (PEF) → maximum flow rate achieved during FVC

• forced expiratory volume_25-75 (FEV_25-75) → volume of air exhaled in mid-portion of FVC, between 25-75% of VC exhaled

flow-time and flow-volume relationship

• flow time curve→ forced vital capacity (FVC), FEV_1sec, FEF_25-75

  • shows flow change over time during each breath

• flow-volume loop → shows peak expiration flow (PEF) and measures forced vital capacity (FVC), developed from total lung capacity (TLC) to residual volume (RV)

  • shape of loop reveals lung problems

  • obstructive lung → lung volume is big because it is stretched at rest

  • restrictive lung → lung volume is lower due to its elasticity, with higher flow rate because lungs don’t collapse

obstructive pulmonary disease

characterized by increase in airway resistance, and is measured as a decrease in expiratory flow rates

• chronic bronchitis → hypertrophied smooth muscle and muscle glands with increased mucus secretions, leading to narrow airways

• asthma → hyperreactive airways and inflammation, leading to narrow airways

• emphysema → loss of tissue elasticity and loss of support for small airways, leading to easily distorted airways

• results in reduced vital capacity → FEV_1sec is 50%, when normal is 80%

flow-volume relationship in obstructive diseases

flow-volume loop may begin and end at abnormally high lung volumes and expiratory flow rate is lower than normal, but inspiratory flow rate remains relatively normal

• pulmonary function tests

  • FVC → decreased or same

  • FEV_1sec → decreased

  • FEV_1sec / FVC → decreased

  • FEF_25-75 → decreased

• lung volumes

  • FRC → increased (due to increased resistance that traps air in lungs from previous cycle)

  • RV → increased or normal

  • TLC → increased or normal

restrictive lung disease

characterized by an increase in elasticity that is measured as a decrease in all lung volumes

• respiratory distress syndrome of the newborn

• fibrotic lung disease

• pulmonary vascular congestion (congestive heart failure)

• pulmonary edema (ARDS, pneumonia)

flow-volume relationship in restrictive diseases

flow-volume loop begins and ends at unusually small lung volumes, where expiratory flow rates in restrictive disease is greater than normal

• pulmonary function tests

  • FVC → decreased

  • FEV_1sec → decreased

  • FEV_1sec / FVC → increased or normal

  • FEF_25-75 → increased or normal

• lung volumes

  • FRC → decreased (due to inability of lung to expand normally)

  • RV → decreased

  • TLC → decreased