APEX Respiratory Physiology with PLQ, Quiz, & RE

Anatomic Deadspace begins in the mouth and ends

small airways

terminal bronchioles

respiratory bronchioles

alveolar ducts

terminal bronchioles

what is ventilation

is the process of exchanging gas between the atmosphere and the lungs

2 functions:

O2 is delivered to HGB to support aerobic metabolism

CO2 is the primary end products of aerobic metabolism and is eliminated from the blood

What are the muscles of inspiration

Primary: Diaphragm (tidal breathing and increases the superior-inferior dimension of the chest)

External intercostals (tidal breathing, increase the anterior-posterior diameter)

Sternocleidomastoid (accessory)

Scalene muscles (Anterior, middle & posterior scalene) (accessory)

What is inspiration

Contraction of inspiratory muscles reduces thoracic pressure and increases thoracic volume

Example of Boyle's law

The diaphragm and external intercostals contract during inspiration (tidal breathing)

The diaphragm increases the superior-inferior dimension of the chest

The external intercostals increase the anterior-posterior diameters

What are the muscles of expiration

Internal intercostals

Rectus abdominis

External oblique

Internal Oblique

Transverse Abdominis

What is exhalation

Exhalation is usually passive and is driven by the recoil of the chest wall

Active exhalation is carried out by the abdominal muscles (Think TIREs- transverse abdominis, internal oblique, rectus abdominis, external oblique)

Internal intercostals play a secondary role in active exhalation

Exhalation is active when minute ventilation increases or in pts with lung disease such as COPD

A forced exhalation is required to cough and clear the airway of secretions; VC of at least 15ml/kg is required for effective cough

Divisions of airway

Airway is a conduit to transfer gas between the atmosphere and the blood and follows the pressure gradient

divided into 3 zones

Conducting (1-4), transitional (17), respiratory (20-23)

What is the conducting zone & function

function: bulk gas movement

DOES NOT participate in gas exchange= anatomic deadspace

the conducting zone begins at the nares and mouth ends with the terminal bronchioles

the terminal bronchioles are the last structures perfused by the bronchial ciiculation

What is the transitional zone

Function: bulk gas movement

The region that contains the respiratory bronchioles

these structures serve as dual function of air conduit and gas exchange

What is the respiratory zone

function: gas exchange

this is where gas exchange takes place

the respiratory zone beings at the alveolar ducts and extends to alveolar sacs

The respiratory bronchioles mark the beginning of this zone (controversial per Apex)

Gas exchange occurs the falt type 1 pneumocytes by diffusion

Airway patency

Airways must remain patent for air movement & gas exchange to occur.

Since bronchioles and alveolar ducts don't contain cartilage= compressible

To prevent collapse the pressure inside the airway must be greater than the pressure outside the airway

• alveolar pressure is the pressure in the airway

• intrapleural pressure is the pressure outside the airway

• Transpulmonary pressure is the difference between the 2.

• TPP= Alveolar Pressure- Intrapleural pressure

• if positive= airway open

• If negative= airway collapses

What happens during tidal breathing

TPP is always positive= airway open

Intrapleural pressure is always negative= keeps lungs inflated

Alveolar pressure becomes slightly negatice during inspiration and slightly positive during expiration

There is no airflow in end-inspiration aka FRC

aside from pathological processes (pneumothorax) the ONLY time that intrapleural pressure becomes positive is during forced expiration

Math of Tidal Breathing

What is the primary determinate of CO2 elimination

Minute ventilation

Tidal volume

alveolar ventilation

RR

alveolar ventilation

What happens in tidal breathing with gas exchange

Vt is the gas that is inhaled and exhaled during a breath.

normal= 6-8ml/kg

When you take a breath, part of the Vt is delivered to the respiratory zone (gas exchange), the remainder of the Vt sits in the conducting airways (deadspace)

dead space (Vd)= 2ml/kg

When you exhale the conducting zone is the first to be removed

this is followed by the exhalation of respiratory zone gas

any condition that increases Vd makes it more difficult to eliminate expiratory gases from the lungs

Increased Vd widens the Paco2- EtCo2 gradient causes CO2 retention

What is the ventilation rate

Ventilation rate is the air removed into and out of the lungs in a given period of time.

What is Minute ventilation

aka Ve

the amount of air in single breath (Vt) multiplied by the number of breaths per minute

MV= Vt X RR

Normal = 5L/min

What is alveolar ventilation

aka Va

only measures the fraction of Ve that is avaliable for gas exchange

it removes deadspace gas from the minute ventilation

Alveolar ventilation= (Vt- Vd) X RR

Alveolar ventilation= CO2 production / PaCo2

Va is directly proportional to CO production and inverse to PaCO2

Normal 3.5L/min

Which conditions will MOST likely increase the PaCo2 to EtCo2 gradient? 3

PPV

LMA

hTN

ETT

neck flexion

atropine

PPV

hTN

Atropine

Overview of definitions of deadspace

What is the Vd to Vt ratio

this is the fraction of Vt that contributes to deadspace.

factors that alter Vd or V/Q will affect Vd/Vt ratio

Vd/Vt in a normal 70kg pt= 0.33 (150/450)

Mechanical ventilation increases alveolar pressure and increases ventilation relative to perfusion

mechanical ventilation increases Vd/Vt to 50%

****the most common cause of increases Vd/Vt under GA is reduction in CO. ETCo2 acutely decreases, think hTN before considering other causes

What airway device reduces deadspace

ETT decreases Vd (bypasses most of the conducting zone)

LMA reduces Vd by bypassing anatomic deadspace like the ETT

Neck flexion decreases Vd

What increases deadspace

facemask

neck extension (opens the hypopharynx and increases deadspace

atropine increases Vd because it is a bronchodilator and increases volume of the conducting airway

In deadspace increases what happens to minute ventialtion

must increase RR, Vt, or both to maintain a constant PaCo2.

Where does deadspace begin in the circle ssytem

at the y piece

anything proximal to the y piece does not influcen the deadspace nor does increasing the length of the circuit.

only exception is an incompetent valve (incompetent valve makes the entire limb apparatus deadspace)

How to use the Bohr Equation

To calculate the physiologic deadspace

compares the partial pressure of the CO2 in the blood vs. the partial pressure of the Co2 in the exhaled

The greater the difference the greater the amount of deadspace

many clinicals use the difference between PaCO2 and EtCo2 as a gross estimation of deadspace but this does not determine the cause of deadspace but only that the amount has changed

A pt in the sitting position. When compared to the apex of the lung, which of the following are higher in the base? (select 2)

BF

PP of alveolar gas

V/Q ratio

PP of alveolar CO2

Blood flow

PP of CO2

What is alveolar compliance (V)

this is a change in alveolar volume for a given change in pressure

not all alveoli are ventilated equally. gravitational forces are largely responsible for this d/t the effect on TTP

At end expiration the apex of the lungs is largest (higher TPP) and the alveoli at the base is the smallest (TPP is lowest)

The alveoli that has a greater degree of volumetric change (compliance) is going to be better ventilated and have better gas exchange.

** understand that the alveolar compliance represents a normal lung. At lung volume below FRC (low lung volume)= compliance is less.

Alveoli in the Apex compliance

has the poorest ventilation because they have the least compliance

the slope of the curve is less steeps and has smaller volumetric change throughout the respiratory cycle

Alveoli in the Bases Compliance

have the greatest ventilation, because have the greatest compliance

The slope of the curve is steeper in this region and larger volumetric changes through the respiratory changes

Alveolar Perfusion (Q)

gravity and hydrostatic pressure affects the distribution of BF through the lungs

when standing upright= less BF to apex and more to bases (V/Q higher in apex and less in bases)

Basic Consequences of V/Q and position changes

Understand the picture.

Popular question: if the V/Q is greater in the non-dependent lung region why is ventilation greater in the dependent region?

alveoli with the greatest ventilation undergo the greatest volumetric change through respiratory cycle.

in the wake pt these alveoli are on the steepest slope of the curve= better compliance=better ventilation

Different Surgical positions and V/Q

Identify the statement that represent of MOST accurate understanding of V/Q mismatch (select 2)

Bronchioles constrict to minimize zone 1

The A-a gradient is small

Blood passing through under-ventilated alveoli tend to retain CO2

HPV minimizes deadspace

Bronchioles constrict to minimize zone 1

Blood passing through under-ventilated alveoli tend to retain CO2

V/Q mismatch theory

normal V/Q= 0.8

V/Q=1 is perfect match

V/Q mismatch in practice

Assume the image is of a pt in the sitting position

V/Q are perfectly matched at intersection

Apex V>Q

Base V

How does this apply to clinical

V/Q mismatch (atelectasis) is the most common cause of hypoxia in the PACU

FRC is smaller d/t GA and surgery= less radial traction to hold the airway open= atelectasis and right to left shunt, V/Q mismatch, and hypoxemia

Treatment= humidified O2 and maneuvers to open the airway (coughing, mobility, Incentive spirometry)

What happens to under ventilated alveoli

blood passing through under ventilated alveoli retain CO2 and is unable to take in enough O2

What happens to overventilated Alveoli

BF gives off excess amount of CO2 (CO2 diffuses 20 times faster than O2)

even though blood can get rid of alot of CO2 it cannot proportionally take up O2 in the same way. (Ex: oxyHGB curve, cannot exceed 100mmHg)

What happens in the whole lung

a lung with V/Q mismatch eliminates CO2 from overventilated alveoli to compensate for the under-ventilated alveoli. PACO2 and PaCO2 gradient is small with V/Q mismatch but CO2 retention= failure of compensatory mechanism

V/Q mismatch cannot absorb more O2 from overventilated alveoli to compensate for the underventiated alveoli. PAO2-PaO2 gradient is large in V/Q mismatch

Compensation of V/Q mismatch

body responds by attempting to match ventilation to perfusion

to combat deadspace (zone 1) the bronchioles constrict to minimize ventilation of poorly perfused alveoli

to combat shunt (zone 3) HV reduces PBF to poorly ventilated alveoli

variables described by the law of la place include the following except

tension

pressure

radius

density

density

Law of la place

the relationship of pressure, radius, and wall tension

Surfactant (brief overview we have seen this a million times)

according to la place can determine the tendency of alveoli to collapse

Directley proportional to surface tension (more tension=more collapse)

inverse to alveolar radius (small radius= collapse)

produced by type 2 pneumocytes

each alveoli contain the same amount of surfactant

large alveoli= smaller concentration

small alveoli= larger concentration

as radius changes so does the concentration of surfactant

type 2 pneumocytes begin producing surfactant by 22-26 weeks and peak at 35-36 weeks. (preemie= no surfactant= give betamethasone)

Select the correct statement regarding the west zones of the lungs (select 3)

in zone 3 alveolar pressure exceeds venous pressure

in zone 1 alveolar pressure in higher than arterial pressure

in zone 2 venous pressure is higher than alveolar pressure

in zone 2 ventilation is greater than perfusion

in zone 1 there is no pulmonary BF

In zone 3 PBF is proportional to arterial to venous pressure gradient

in zone 1 alveolar pressure in higher than arterial pressure

in zone 1 there is no pulmonary BF

In zone 3 PBF is proportional to arterial to venous pressure gradient

West zones

Zone 1

Deadspace

PA>Pa>Pv

V/Q= infinity

zone does not occur in normal lungs

increased by hTN, PE, or excessive airway pressure

To combat zone 1= bronchioles of under perfused alveoli constrict to reduce deadspace

Zone 2

Pa>PA>Pv

V/Q= 1

blood flow is directly proportional to the difference between Pa-PA. greater the difference= greater the blood flow

because pulmonary capillary pressure and alveolar pressure changes throughout the respiratory cycle, it is possible for zone 2 to transiently change to zone 1 or 3

zone 3

Shunt= Pa>Pv>PA

Blood flow is a function of pulmonary AV pressure difference (Pa-Pv)

V/Q=0

most zone 3 units are shunt like and are better perfused then ventilated

to combat this zone HPV constricts pulmonary BF to under ventilated units

since pressure in the capillary is always higher than the alveolus, the vessel is always open, and BF is moving

The tip of the PA catheter should be placed in zone 3

NOT ALL SHUNTS OCCUR IN THE LUNGS: anatomic shunts (venous blood emptying directly in the left side of the hear, blood bypasses lungs= no saturation of oxygen)

Ex: thebesian veins, bronchiolar veins (drain into bronchial circulation), pleural veins (drain bronchial circulation_

Zone 4

Pulmonary Edema

Pa>Pist>Pv>PA

the pressure in the interstitial space exceeds pressure of pulmonary capillaries and alveolus

pulmonary edema is a classic example of zone 4

rate of fluid accumulation exceeds the rate of removal by the lymphatic system

Result of 2 things

1. fluid is pushes across the capillary membrane by increase in capillary hydrostatic pressure (fluid overload, MS, severe pulmonary constriction)

2. fluid is pulled across the capillary membrane by profound reduction in pleural pressure (laryngospasm, NPPE)

Other Points about West zone

gravity is believed to be the most significant influence in distribution of perfusion

this hypothesis states the apex has less BF than the bases

BF follows more of a central to peripheral distribution

zone 3 at the lower core and zone 2 and zone 1 radiate out from that point to the periperhy

If a patient is breathing RA at sea level. The ABG reveals PaO2 of 60 mmHg and a PaCO2 of 70mmHg. Claculate patients alveolar oxygen concentration.

alveolar oxygen= fiO2 x (Pb- PH2O) - (PaCO2/RQ)

0.21 x (760-47) - (70/0.8)= 62.23 ~ 62

alveolar gas equation

this is used to estimate the partial pressure of O2 in the alveoli

must understand: hypoventilation can cause hypoxia and hypercarbia, supplemental O2 can easily reverse hypoxemia but not hypercarbia, hypercarbia can go undetected in pt that is breathing supplemental O2

FiO2= fraction of inspried oxygen

Pb= barometrc pressure

PH2O= humidity of inhaled gas (assume 47)

RQ= respiratory quotient (assume 0.8)

FiO2 in the alveolar gas equation

FiO2 is always higher than the partial pressure of O2 in the alveolus

This is because:

inspired O2 becomes 100% humidified as it moves to the alveoli, water takes up space and dilutes O2 concentration

inspired air (lots of O2 and no CO2) mixes the expired air and dilutes concentration of O2 going toward the alveoli

Hypoventilation increases PaCO2 and increased PaCO2 competes for space with O2 inside the alveoli and dilutes the O2 concentration

in this situation supplemental O2 can increase PAO2 and PaO2, this masks the cause and not treat it

R/Q

>1= lipogenesis= overfeeding

0.7= lipolysis= starvation

R/Q= CO2 production/ O2 consumption= 200/250= 0.8

Causes of increased A-a gradient include (select 2)

hypoventilation

V/Q mismatch

hypoxic mixture

diffusion limitation

V/Q mismatch

diffusion limitation

5 causes of hypoxemia

hypoxic mixture, hypoventilation, diffusion limitation, V/Q mismatch, and shunt

If A-a gradient is normal what is the cause

hypoxic mixture and hypoventilation

A-a gradient is increased, what is the cause

diffusion limitation

V/Q mismatch

shunt

When does hypoxemia occur

PaO2<80mmHg

hypoxia is insufficient O2 to tissues

Fixed by supplemental oxygen

V/Q mistmatch and diffusion impairment

NOT SHUNT

Examples of reducied fio2 causing hypoxemia

hypoexmia mixture

oxygen pipeline failure

high altitide

examples of hyperventialtion causing hypoxemia

Opioid OD

Residual anesthetic agent or NMB

Neuromuscular disease

obesity hypoventilion

V/Q mismatch examples causing hypoxia

Most common cause of hypoxemia*

COPD

OLV

Impaired HPV

embolism (air, gas, amniotic fluid)

Examples of diffusion impairement causing hypoxemia

pulmonary fibrosis

emphysema

interstitial lung disease

Examples of shunts causing hypoxemia

atelectasis

PNA
bronchial intubation

intracardiac shunt

A-a gradient calculation

PAO2 (from alveolar gas equation)- PaO2 (from ABG)

what is determined by the A-a difference

if there is a large difference the this implies the degree of shunt, V/Q mismatch, or diffusion limitation

Factors that ncrease A-a gradients

aging (increased CC compared to FRC)

vasodilators (decreased HPV)

Right to left shunt (atelectasis, bronchial intubation, intracardiac defect)

diffusion limitation (increased thickening of the alveolar capillary= decreased O2 diffusion)

Estimate the shunt

shunt increases 1% for every 20 mmHg of A-A gradient

Lung volume graph

Lung volume chart

lung capacities chart

Key facts about the volumes and capacities

Vt= 6-8ml/kg

VC= 65-75ml/kg

FRC-35ml/kg

All of these are calculated from ideal body weight

lung volumes are 25% smaller in females

volumes change with position (larger when sitting and smaller when supine)

Obstructive disease= air trapping (increases RV, CC, TLC)

spirometry can measure everything except RV, therefore it cannot calculate FRC or TLC

CV and CC are dynamic measures and assess small airway closure (also cannot be measured with spirometry)

What conditions reduce FRC (select 2)

Advanced age

pulmonary edema

COPD

Obesity

pulmonary edema

obesity

How to measure FRC

FRC is the reservoir of O2 that prevents desaturation with apnea

FRC= inward elastic recoil of the lungs is balanced by outward elastic recoil of the chest wall (equilibrium)

diaphragmatic tone and position affect FRC

Normal= 35ml/kg

Measured indirectly by: nitrogen washout, helium wash in, body pelthysmography

NOT SPIROMETRY (cannot measure RV)

How long does FRC last during apnea

Time to desat= FRC/VO2 (oxygen consumption)

ensure the pt is preoxygenated

Conditions that alter FRC

these conditions reduce outward expansion or reduce lung compliance, FRC reduced= increased zone 3, alveolar recruitment act to restore FRC by reducing zone 2

CC is the sum of cv and:

RV

ERV

FRC

Vt

RV

what is closing volume

as a person exhales there is a point where pleural pressure exceeds airway pressure= small airway closure (d/t lack of cartilage)

since pleural pressure is higher in the dependent portion= these airways close first

CV is the point of dynamic compression of the airway begins (volume above RV where small airways collapse during expiration)

Factors that increase clsoing volume

(CLOSE-P)

COPD

LV failure

obesity

surgery

extremes of age

pregnancy

what is CC

CC is the absolute volume of gas contained in the lungs when the small airways begin to close

CC= CV+RV

What affects CC

important relationship of FRC and CC, will determine airway collapse in tidal breathing

normal= FRC>CC, airways dont collapse

CC>FRC= airway closure during tidal breathing= intrapulmonary shunting and hypoxemia

anything that decreases FRC to CC or increases CC to FRC will convert a normal V/Q to low V/Q units or shunt untis

PEEP can reverse this by increasing FRC

How does age affect CC

normal= CC just above RV

as we age pleural pressure progressively gets higher and the smaller airways will close sooner (this explains reduction in PaO2 with aging)

Aging=

increased FRC, CC, RV

and decreases VC

How does anesthesia affect CC

30= FRC= CC with GA

44= CC=FRC with supine

66= CC=FRC when standing

how to measure CC and CV

spirometry cannot measure

need nitrogen washout or xenon.

gas is inhales at RV and teh measurement is taken as the pt exhales from TLC

calculate patient’s arterial oxygen content from data set

Hgb 9

HR 100

SV 70

SaO2 90%

PaO2 60

11.034

CaO2= 1.34 x hgb x SaO2) + PaO2 × 0.003)

(1.34 × 9 × 0.9) + (60 × 0.003)

Oxygen content

how much O2 is present in 1 dL (100ml) of blood

O2 transported 2 ways

HGB (97%)

dissolved in plasma

O2 bound to HGB equation

1.34 X HGB X SaO2

men: 15 hgb 45 hct

female: 13 hgb 39%

Dissolved O2 equation

(PaO2 X 0.003)

dissolved O2 is measured by PaO2 (estimated gas exchange not a measure of O2 content in the blood)

dissolved according to HENRY's law (proportional to partial pressure of gas above to solution, solubility co-efficent 0.003, O2 is 20 times less soluble than CO2)

How to calculate O2 delivery

CaO2= O2 contained in the blood

DO2= delivery of the blood to tissues

CO is the driving mechanism of DO2

DO2- CaO2 X CO X 10

calculate VO2 aka O2 consumption

using FICK's principle to calculate

VO2 is the differnce of O2 that leaves the lungs and the amount of O2 that returns to the lungs

VO2= CO X (CaO2-CvO2) X 10

VO2= 3.5ml/kg

VO2= 250ml for 70 kg

P50 is reduced by select 3

HGB f

hyperthermia

hypocarbia

increased DPG

acidosis

carboxyhgb

HGBf

Hypocarbia

carbocyhgb

OxyHGB Curve

the curve tells us the tendency if HGB to bind to HGB

P50=26.5mmhg

max loading= 100mmHg (if increased FiO2 will increase dissolved fraction but not any bound to HGB past 100mmHg)

Tissues that have higher metabolic rate consume more O2 and produce more CO2, hydrogen, and heat

What causes left shift (higher affinity) in oxyhgb curve

(occurs in lungs)

Decreased temp

Decreased 2,3- DPG

Decreased CO2

Decreased H+

Increased pH

Increased Hgb MET (Methemoglobin)

Increased Hgb CO (carboxyhemoglobin)

Increased HgbF (fetal hgb)

What causes right shift (lower affinity) in oxyhgb curve

(Occurs near metabolically active tissue

Increased temperature

Increased 2,3 DPG

Increased CO2

Increased H+

Decreased pH

what is the Bohr effect

CO2 and hydrogen ions cause change in the HGB molecule, facilitates release of O2

increased partial pressure of CO2 and decreased pH= hgb will release O2

What is DPG and why is it important

produced by RBC glycolysis (rapoport-luebering path)

slightly shift to right at all times

hypoxia= increased DPG production

important compensation mechanism in anemia

in banked blood= less DPG= shift to the left and reduces O2 at tissue level

HGB f doesnt respond to DPG (explains why that shifts left and P50=19)

Identify the statement that best describes aerobic metabolism

NADH is the final electron acceptor during electron transport

1 molecule of glucose converts to 38 molecules of ATP

pyruvic acid is converted to lactate

electron transport occurs in the cytoplasm

1 molecule of glucose converts to 38 molecules of ATP