Respiratory Physiologyclinsoft.org/drmayrovitz/PHYSIOLOGY/RESPIRATION/COM...2 x P ATM = 0.21 x 760 =...

Respiratory Physiology

Dr HN Mayrovitz

Harvey N. MayrovitzRoom 1313

e-mail: mayrovit@nova.eduWebsite: drmayrovitz.com

1. 9/13 11-12

2. 9/16 1-2

3. 9/16 2-3

4. 9/17 10-11

5. 9/17 11-12

6. 9/20 10-11

7. 9/20 11-12

8. 10/2 8-9

• The objectives have been better defined for a more detailedand easier interpretation. These will appear before each lectureand supersede any prior listing.

• My exam questions will be based on the objectives as reflected bymaterial presented in lecture via slides and discussion

• I provide a “handout” with additional words that might be usefulfor some. It covers more topics than will be presented.

• If we fail to complete the material for a given lecture the planis to finish on the next lecture

• After-lecture questions if “short” usually can be handled via emailOtherwise we should plan on scheduling one-on-one time byappointment via email contact for mutual availability

Preliminaries

Dr. HN Mayrovitz

Lecture 19/13/19

Respiratory Design andStructure-Function

Dr HN Mayrovitz

Eastman Kodak 1937

Heart Shadow

Lung Shadow

OBJECTIVES

To describe and explain the following elements of respiratory physiology

• Physical aspects of oxygen and carbon dioxide dissolution in blood

• Concepts of dead space and its calculation

• Concepts total and alveolar ventilation and their calculation

• Factors affecting lung fluid exchange and its calculation

• Pulmonary blood flow and factors and processes that affect it

• Basic aspects of respiratory control processes

Trachea

Thorax

Lung and

the Alveoli

Simple BreathingModel

Dr HN Mayrovitz

Trachea

Thorax

Lung and

the Alveoli

AirAir ~ 21% O2

755 mmHg

760 mmHg

At end ofExpiration

Dr HN Mayrovitz

PO2 = 100 mmHg

Dissolved O2

[O2] = 0.3ml/dl

[O2]d = KO2 x PO2

K = solubility= 0.003 mlO2/

ml/mmHg If CO = 6 L/min

O2 delivered= 60x 0.3= 18 ml O2/min

Only 18ml/300ml~ 6% of needed

Gas Basics: O2 Dissolved in Blood

1/18 Dr HN Mayrovitz

PO2 = 100 mmHg

@100% Saturation

(34 g/Hb/100 ml rbc) x Hct34 x 0.44 = 15 gHb/100 ml blood

Hb O2 binding capacity ~ 1.34 mlO2/gHb

15 x 1.34 = 20.1 mlO2/dl

Normally 97% sat

0.97 x 20.1 = 19.5 mlO2/dl

+ 0.3 ml dissolved

~ 20 mlO2/dl

Gas Basics: O2 Bound to Hemoglobin in RBC

O2 Bound to Hemoglobin

in RBC

Gas Basics: Carbon Dioxide

PCO2 = 40 mmHg

Dissolved CO2

[CO2] = 2.4ml/dl

[CO2]d = KCO2 x PO2 = 2.4 ml/dl

K = solubility= 0.06 mlCO2/

100ml/mmHg CO2

As BicarbonateHCO3 →90%

CO2 in Blood48 ml/dl

2.4/48 →5%

Carbon Dioxide@ PCO2

of 40 mmHg

NoseMouth

Trachea

Bronchi

Bronchioles

T.Bronchioles

ConductingZone

No GasExchange

Dead Space

Ventilation

Perfusion

Diffusion

Respiratory ZoneGas

Exchange

Transition Zone

Alveoli

Respiratory Bronchiolesand Alveolar Ducts

0.5 mm thick

Airways and Alveoli Schematically Summarized

Dr HN Mayrovitz4/18

MixedVenousBloodFrom RV

Upper Airways(Conducting zone)

(Anatomical Dead Space(ADS)

TotalVentilation

Respiratory zone

Alveolar Ventilation

Blood Perfusion

Respiratory Processes: Ventilation-Perfusion-Diffusion

Gas Diffusion

ArterializedBlood to LA

[O2] = 0.21 → FIO2

[CO2] = 0%[N2] = 0.79

PATM=760 mmHg

PO2 = FIO2 x PATM = 0.21 x 760 = 159.6 → 160 mmHg

QT = Volume/breath x Respiratory RateQT = Tidal volume x RR = TV x RR

QA = (TV – ADS) x RR

PO2 = (PATM – 47)FIO2 149.7 → 150 mmHg

PO2 = 40 mmHgPCO2 = 46 mmHgSO2 = 75%

PO2 = 100 mmHgPCO2 = 40 mmHgSO2 = 97.4%

Gas fractionsat sea level

Dr HN Mayrovitz

Capillary Blood Flow(Perfusion)

Alveolar Gas VolumeEntering and Leaving

Per Breath = VA

Arterialized BloodExiting Lung to LA

MixedVenousBlood

from RV

PCO2 = 40

Dr HN Mayrovitz6/18

• Collect one TV of expired air• Measure CO2 fraction (FECO2)

(1) CO2 volume = FECO2 x TV

CO2 source is volume from alveoliduring that tidal volume

CO2 from alveoli is(2) FACO2 x VA

Alveolar Dead SpaceVentilation but No Perfusion

Dead Space: Physiological = Anatomical + Alveolar

(3) FECO2 x TV = FACO2 x VA

VDCO2 = TV(PACO2 - PECO2 ) / PACO2

Physiological Dead Space

Interpret If: PACO2 = PECO2

Interpret If: PECO2 = 0

Alveolus

Type II Cell

Fluid withSurfactant

Type ICell

Capillary

MacrophageO2

Alveolar Cells and Capillaries

Dr HN Mayrovitz7/18

Capillary

Alveolar Inward Forces

SurfaceTensionForces

ElasticRecoilForces

Dr HN Mayrovitz8/18

AlveolarEpithelium

InterstitialSpaceCapillary

Endothelium

Gas Exchange Interface

Alveolus

Dr HN Mayrovitz9/18

Visceral

Pleura

Intrapleural

Pulmonary

Capillary

Systemic

Capillary

Parietal

Pleura

Intrapleural Space (simplified)

Dr HN Mayrovitz10/18

P = 10

P = 25

Lymphaticdrainage

pulmonary

capillary

visceral pleura

PulmonaryInterstitium

ProteinLeak

P = -2

P = 17

Pulmonary Fluid Balance

Pressures in mmHg

DPeff = TMP –s DP = [10 –(-2)] – 0.5 (25-17) = 8

systemic

capillary

P = -5

P = 7P = 10

P = 25P = 25

P = 25

Small enough volume to maintain cohesive force

Just large enough volume to provide lubrication

Parietal pleura

intrapleural

Lymphaticdrainage

Route forAlveolarFlooding

InterstitialEdema

PleuralEffusion

Filtration

Pressure

Lymphatic drainage

pulmonary

capillary

visceral pleura

PulmonaryInterstitium

ProteinLeak

P = -2

P = 17

Pressures in mmHg

Pulmonary Fluid Balance DPeff = TMP –s DP = [10 –(-2)] – 0.5 (25-17) = 8

Cervical

ganglion

Vagus n.

Pulmonary

plexus

Medulla

Phrenic n.

Intercostal n.

Sympathetic Chain

Respiratory Muscles

Airways

Vessel

Control

+Vagus =AW constrict

Neural: Muscles

Diaphragm

Dr HN Mayrovitz

Forced inspirationor expiration

Cervical

ganglion

Vagus n.

Pulmonary

plexus

Medulla

Phrenic n.

Intercostal n.

Sympathetic Chain

Respiratory Muscles

Airways

Vessel

Control

+Vagus =AW constrict

Neural: Muscles and Airways

Diaphragm

Systemic

Pulmonary

RVPressure

FlowPulse

LV PressurePulse

FlowPulse

(14)→(12)→→→9

120/80DP=91

Pressures (mmHg)Mean Values ( )

•Low Pressure•High Flow ~ CO•Low Resistance~ 10-12 %

Blood Volume

Pulmonary Pressure and Flow Features

Ventilation Control

RespiratoryMuscles

Brain Stem• Pons • Medulla

Lung and

Thorax

Rhythmic Impulses

Inspiration/Expiration

Tidal Volume (TV)Respiratory Rate (RR)

VENTILATION

Central

Chemoreceptors

Peripheral

Mechanoreceptors

Stretch

HigherBrain

CenterspH & CO2

CO2 & pH

Lung volume changes

NormalEupneicBreathing

Inspiration Expiration Inspiration

RightSide Brachio-

cephalic

CommonCarotids

AorticBodies

XExternalCarotid

CarotidBody

Hering n.

MedullaryRespiratory

Center

Aortic n.

Peripheral Chemoreceptor Locations

(glosssopharyngeal)

TidalVolume

TV = 500 ml QT = Total (minute) Ventilation

QT = RR x TV = 6000 ml/min

RR = Respiratory Rate = 12/min

AlveolarGas Volume

AnatomicDead SpaceADS=150 ml(~1 ml/lb)

PO2 = 40SO2 = 75%PCO2= 46

MixedVenousBlood

from RVPO2 = 100SO2 = 97%PCO2= 40

QA=Alveolar Ventilation

QA = (TV - ADS) RR

QA = (350 X 12)

= 4200 ml/min

PO2 = 102 PCO2 = 40

PO2 = 160 → Partial Pressure (mmHg)

PCO2 = 0.3 760 x 0.21 = 159.6

Main Respiratory Function: Review

End Lecture 1

Dr HN Mayrovitz

Lecture 29/16/19

Lung Volumes and Pressures

Dr HN Mayrovitz

OBJECTIVES

• Lung volumes and capacities and how to calculate capacity from volumes

• The methods used to measure lung volumes and capacities

• Calculation of lung volumes from helium dilution

• Calculation of lung volumes from whole body plethysmography

• Respiratory pressures and how these are determined and used

Pulley

RotatingDrum

Volume Measurements - Spirometer

Doublewalleddrum

Inspiration

Up with Inspiration

Dr HN Mayrovitz1/16

FRC3.0

VC4.2 TV

IRV2.5IC

TLC6.0

EndInspiration

EndExpiration

TidalVolume

Maximum Inspiratory Level

ERV1.2

Residual VolumeRV1.8

Lung Volumes and Capacities

Maximum Expiratory Level

“Equilibrium”at FRC

Dr HN Mayrovitz2/16

KNOW ABREVIATIONSTV = Tidal VolumeIRV = Inspiratory reserve volumeERV = Expiratory Reserve VolumeRV = Residual volumeIC = Inspiratory CapacityFRC = Functional Residual CapacityVC = Vital CapacityTLC = Total Lung Capacity

Spirogram up is inspiration

10% He

FRC & RV via Helium Dilution→ Start

Assume

3000 ml total

Start breathing gas at FRC

Before starting test

He concentration in spirometer = 10%

Dr HN Mayrovitz3/16

At Equilibrium → End

He Concentration

Measured

He concentration

In lung = 5%

He concentration in lung & spirometer = 5%

Dr HN Mayrovitz4/16

Calculations

Initial He volume = Final He volume

He in lungs + He in spiro = He in combined (lung + spiro)

Start End

0 + 0.10x3000 = 0.05 (FRC + 3000)

RV = FRC - ERV

Measured

by SSCalculated

VL & FL are Volume & Fractional Lung concentration

Vsp & Fsp are Volume & concentration in Spirometer

FRC = 3000

VL x FL_start + Vsp x Fsp_start = (VL + Vsp) FL_end

FL_end = Fsp_end

Dr HN Mayrovitz5/16

FRC by Body Plethysmography

Airway

Pressure

Shutter

closes

at end of

expiration

Eupneic

Breathing

Lung volume

at end of

Expiration = FRC

Air Tight Chamber

Dr HN Mayrovitz6/16

p’=palv

At end of expiration

p=palv=patm

V is unknown

Inspiration

•Thorax enlarges

•Gas decompresses

•Volume increases

V’ = V + DV

•Pressure decreases

p’ < p

Box Pressure

increases

DPbox=kDV

Boyles Law: p V = p’ ( V + DV )

p p’

DPbox/K

Shutter

closed

V = FRC

Air Tight Chamber

Inspire with shutter closed

FRC by Body Plethysmography

Dr HN Mayrovitz7/16

He dilution (and N2 washout) methodsmeasure COMMUNICATING GAS VOLUME

Lung gas that can mix with the breathing mixture

Body plethysmographic methodmeasures TOTAL gas volume

Gas that is or is not in communication with alveoli

Method Comparisons

Both methods require good patient compliance

Dr HN Mayrovitz8/16

Pressures

Elastic SurfaceTension

At any specific volumePALV = PREC

Volume

Alveolar and Recoil Pressures

Dr HN Mayrovitz9/16

PALV = PREC + PE

To maintain the same sizePALV must change by PE

PALV – PE = PREC

If PE is intrapleuralPressure PPL then

PALV = PREC + PPL

Enter Intrapleural Pressure

Chest WallRib Cage

1. RespiratoryMusclesExpand

2. IntrathoracicPressure (PTH)decreases

3. Pleural spacetries to enlargecausing PPL to decrease

4. PALV = PREC + PPL

decreases

5. Air is drawn in Q = PATM - PALV

Inspiration → Air Flow

PATM = 0

Diaphragm

Intrapleural

Parietal

Pleura

(chest

wall)Alveolus

Intrapleural space (fluid)

Alveolar

(PALV)

Pressure Summary

Recoil

Lung Recoil

(PREC)

PALVPALV = PREC + PPL

Visceral

Pleura

recoil

Intrathoracic (PTH)

PALV = PREC + PTH

Airway (PAW)

PATM = 0

Trans-Airway

Pressure

(PAW - PPL)

PTL is the pressure that serves to expand alveoli

If PBS =0

PTW = PPL

Total Respiratory

System Pressure

PRS = PTL + PTW

Trans-Lung Pressure

PTL= (PALV - PPL) = PREC

= (PALV - PTH)

Transmural Pressures: Total Respiratory

Trans-Wall

Pressure

(PPL- PBS) PRECwall

Dr HN Mayrovitz

PPL = -5 (assumed)

PATM = 0

Pressure: NO AIRFLOW: End Expiration

Recoil balances PPL

PALV=(PREC+ PPL) = 0

= 5 + (- 5)

Volume Fixed

1. Under no flowconditions (Static)PALV must = PATM = 0

PTL= PALV – PPL = 0 – (-5) = +5

2. Volumeis determinedby PTL alongwith lungcompliance

Dr HN Mayrovitz

PATM = 0

PALV=(PREC+ PPL) = 0

= 8 + (- 8)

Volume Fixed

3. To sustain thenow larger volumePPL is more neg and is again balancedby the recoil pressure, PREC

Volume

PTL= PALV – PPL = 0 – (-8) = +8

Pressure: NO AIRFLOW: End Inspiration

Dr HN Mayrovitz

0 1 2 3 4Seconds

Intrapleural-5

Inspiration Expiration

Q (l/sec) has same form as PALV

Dynamic Pressure and Flow Changes

Air Flow depends onthe difference between alveolar pressure andatmospheric pressure

Q ~ PATM - PALV

Air flow is zero twice during cycleIf Q=0 PALV = PATM

Change in lung volume

Alveolar

Dr HN Mayrovitz

End Lecture 2

Dr HN Mayrovitz

Lecture 39/16/19

Compliance and Resistance

Dr HN Mayrovitz

C = DV/dP

R = DP/Q

OBJECTIVES

• Respiratory compliances (lung, thoracic and total) and their determination

• The physical factors that affect these compliances

• The overall respiratory system pressure-volume relation and its interpretation

• The concepts of elastic and inelastic energy and their graphical interpretation

• The Valsalva maneuver and its respiratory and cardiovascular effects

• Airflow and airway resistance within the pulmonary tree

• Calculation of resistance and flow in collapsible airways

• Vascular resistance changes due to changes in lung volume and gravity

Transmural Pressure (dP)

Larger dP for thesame DV thus

less compliance

Slope of P-V curveis DV/dP which isCompliance

Compliance

dP = Pin - Pout

Dr HN Mayrovitz1/18

0 +10 +20 cmH2O Translung (Transpulmonary) Pressure

LungVolume(% TLC)

open closed alveoli against surface tension

Lung Pressure-Volume Relations

DynamicStatic

Dr HN Mayrovitz2/18

0 10 20 Translung Pressure (cm H2O)

Lung ComplianceC = DV/DP

= 0.5L / 2.5 cmH2O= 0.2 L / cmH2O

Expand

Lung ComplianceReduced Compliance• Scarring• Fibrosis• Edema• Reduced surfactant

• Surface Tension = T causes inward pressure P = 2T/r• T is reduced by presence of lung surfactant (LS)

Effects of Lung Surfactant1. Increases Compliance2. Reduces tendency for closure (atelectasis)3. Reduces tendency for alveolar capture4. Reduces tendency for fluid transudation

Alveoluspictured

as a Soap

Bubble rP

Dr HN Mayrovitz3/18

0 -2.5 -5.0 -7.5 cmH2O PPL

0 +2.5 +5.0 +7.5 cmH2O PTL

Elastic vs. Inelastic Work

Work to overcomepure elasticity

WE ~ ½ DV x DP~ 250 x 2.5

Work to overcome

AirwayResistance

Work toovercome

tissueviscosity

Elastic ~ 2/3 Inelastic ~ 1/3

1/5ml DV

Dynamic LoopArea ~ Energy Loss

Dr HN Mayrovitz4/18

Lung and Chest Wall Forces

•Lung Elastic Forces:tend to close the lung at any lung volume

At FRC: Forces are equal but oppositely directed

Inspiration: Lung force Chest force

At ~70% TLC: Chest force = 0 (at 0 stress position)

•Chest Wall Elastic Forces:tend to expand lung for most lung volumes

> ~60-70% TLC: Lung & Chest forces tend to close lung

Lung + Thorax Interactions DetermineRespiratory System P-V and Compliance

Dr HN Mayrovitz5/18

Lung and Thorax as Springs

LungsAlone

ThoraxAlone

Lungs+Thoraxheld

togetherby pleuralsurfaces Air

Pneumothorax

FRC~50%

LungRecoil

ChestRecoil

IntrapleuralPressure

0 mlA B C D

Dr HN Mayrovitz6/18

-10 -5 0 5 10 15 20 25 30

Recoil Pressure (cm H2O)+ is direction to reduce volume

Volume%TLC

Chest Expands

Lung ExpandsPRECL Increases

Respiratory System PRS = PTL + PTW = PALV

Respiratory System P-V relations

Chest Outward Recoil

ChestInwardRecoil

Lung Recoil is + at all lung volumes

ChestNo Recoil

PRS = 0 @ FRC

PRS = PTL All recoil Is due to lung

PTLPTW

Dr HN Mayrovitz

1/CRS = 1/CL + 1/CW

CL ~ CW = 0.2 l/cm H2O

CRS = 0.1 l/cm H2O

0 10 20 30 40 50

Surface Tension (dynes/cm)

Normal

Extract

Respiratory Distress Syndrome

Deflation: Low surfactant

• Normal decrease in surface tension not present

• Greater force at any alveolar volume acts to close alveoli

Newborn succumbed

to RDSLung

extract

Inflation: Once closed:

• Big work/breath neededto re-inflate lungs

• Increased muscular workfatigues diaphragm

Dr HN Mayrovitz8/18

-100 -80 -60 -40 -20 0 +20 +40 +60 +80 +100

Valsalva maneuverForced EXPIRATION

against closed glottis

Expiratory Effort

Muller maneuver

Inspiration against

closed glottis

Inspiratory Effort

Forced Expiration at

different lung volumes

Forced Inspirations at

Max PALV

Higher Negative Pressures

At lower volumes

Total Respiratory Pressure (PRS) = Alveolar Pressure

Muller and Valsalva ManeuversLarge Pressures Associated with Active/Forced

Inspiration/Expiration

Dr HN Mayrovitz

-100 -80 -60 -40 -20 0 +20 +40 +60 +80 +100

Valsalva maneuverForced EXPIRATION

against closed glottis

Expiratory Effort

Muller maneuver

Inspiration against

closed glottis

Inspiratory Effort

Forced Expiration at

Forced Inspirations at

Max PALV

Higher Negative Pressures

At lower volumes

Total Respiratory Pressure (PRS) = Alveolar Pressure

•Straining at stool

•Childbirth

•Weight lifting

Large (+) Pressures•Lung rupture danger•Aortic → +BP→-HR•Vena Cava → - VR

Large (-) pressures cause large blood vessel transmural pressureHemorrhage danger

Muller and Valsalva Maneuvers – Potential Dangers

Phase I: (Onset of strain)a) +PTH & +PAB → +BP (A & V & chambers)b) Baroreceptor mediated – HRc) MBP begins to fall

Phase II: (continued strain & pressure recovery)a) SVC compression → - Venous return → - SVb) Further decrease in MBP (systolic & PP)c) Decreased BP → +SYMP → +TPR & +HRd) BP recovery (above baseline)

Phase III: (Release)a) Normalized PTH

b) Transient precipitous -BP with reflex +HR

Phase IV: Recoverya) Venous return back to normal → + SV → +COb) +CO combined with prior +SYMP → BP overshootc) Baroreceptor reflex rapid -HR

Phase: I II III IV

0 10 25 sec

Valsalva

Valsalva Maneuver – CV Effects (basic)

“Typical” Featureswith Valsalva initiatedfrom a normal inspiration

Valsalva – Clinical Correlation

63 year male → Normal

56 year male → Autonomic Neuropathy

Valsalva

Time (sec)

Airway Flow Features and Resistance

DP = K2Q2

Turbulent

DP = K1 Q + K2Q2

Bronchial Tree

DP= K1Q

Laminar

Intra-alveolar

With inspiration PPL

decreases causingvessel widening

PTM = PA - PPL

Extra-AlveolarBlood vessels

Expanded alveolicompress capillaries

Alveolus

©Dr. HN Mayrovitz 2011

Extra-alveolar Intra-alveolar

Lung Volume Affects Vascular ResistanceOpposite effects of intra and extra alveolar vessels

Total Vascular Resistance

Extra-Alveolar

Alveolar

Total R = Alveolar R + Extra-Alveolar R

RV FRC TLC

Minimum at About FRC

Gravity Affects Vascular Resistance

12 mmHg16 cmH2O16 cm

P=16-16=0 cmH2O

P = 16+16 = 32 cmH2O

PulmonaryArteriole

Blood Flow Distribution

Base Apex

Simplified main concept

At Base: - TMP Greater- Vascular Resistance Less- Blood Flow is Greater

Pa>PA>Pv

PA>Pa>PvI

Pa>Pv>PA

Alveoli Dead space (ventilated but not perfused)

Uneven Blood Flow: The Zone Model

± 2.5

Blood Flow

Q=(Pa-PA) / Rx

IIIQ=(Pa-Pv) /RT

~Uniform with depth

Pa Increaseswith depth

R decreaseswith depth

if Pa abnormally low

0 maxDr HN Mayrovitz17/18

Pu PdP1 P2Q

Increase P1 – P2 but hold P1 – Pe constant

1. Fix P1 - Pe & lower P2 (~cvp decrease with + CO)

2. Fix P2 & raise P1 & Pe equally (~ forced expiration)

Same result: Q increases as P1 - P2

increases until PTM becomes critical

and buckling starts. Now Q depends

on P1 – Pe not on P1 – P2.

Closed chamber

with external pressure

Collapsible tube in chamber. Connected

to upstream and downstream reservoirsRigid

If Pi < Pe at any point then Q ~ (P1- Pe)/Rx

Air Flow in Collapsible Airways

Flow Limiter“Check Valve”

EPP: Pi = Pe

P1 → PALV Pi→ PAW Pe→ PPL

PALV - PPL

Equal Pressure Point

Remember me?

End Lecture 3

Dr HN Mayrovitz

Lecture 4 9/17/19Obstructive and Interpreting Pulmonary

Function Tests

Restrictive Disease

Dr HN Mayrovitz

OBJECTIVES

To describe, explain and interpret the following aspects of respiratory physiology

• Dynamic compression and the concept of Equal Pressure Point (EPP)

• Features of obstructive and restrictive lung disease

• Concept of Flow-Volume and Volume-Time graphics

• Pulmonary function tests and their utilization

• Breathing pattern changes associated with obstructive and restrictive disease

• Neural pathways associated with control of airway smooth muscle

A. Small intrapulmonary airways are distensible and compressible. Held open by combination of: (1) Airway transmural pressure (P) and (2) TRACTION by attachments to surrounding tissue.

B. During a forced expiration, PPL becomes + causing pressure surrounding someairways to become greater than pressure inside.

C. This collapsible condition causes airflow to be determined mainly by PREC alone which itself decreases with lung volume.

D. As volume falls so does PREC ultimately causing airway closure. Net result: Nofurther volume can be expelled. This occurs in normal lungs at low volumes. In obstructive lung conditions the volume at which closure occurs is larger.

Dynamic Compression-Airway Closure: Basic Concept

Airway

Traction15

Alveolus

Airway

Q Q = PREC

A B C D

PRECPREC

Dr HN Mayrovitz

Q = PALV - PATM

Q = PALV - PPL

Q = PREC

PALV = PREC + PPL

Collapsible Airway

Dynamic Compression Summary and ExampleNormally

PAW = PALV - QR

1. PPL becomes +

2. Pressure surroundingairways is ~PPL

3. PALV = PPL + PREC

Dr HN Mayrovitz2/16

PAW = PALV - QRx

Forced Expiration Events

1. PPL becomes +

2. Pressure surroundingairways is ~PPL

3. PALV = PPL + PREC

Dr HN Mayrovitz3/16

Lung Volume (liters)

TLC RV

LargeAir

SmallAir

WaysAir

EPP moving toward alveolus

Equal Pressure Point (EPP)Enters Small Airways

Airflow now depends on PRECOIL that is decreasing with

decreasing volume

Forced Expiration: Role of EPP

Dr HN Mayrovitz4/16

Lung Volume (liters)

TLC RV

Start by inspiring to TLC then force air out with sustained effort

PPL exceeds PAW

Q ~ PREC / R

As V further

reduces, PREC

falls more &

R increases.

Ceases

maxQ=PEFR Max

Effort

Least Effort

Less Effort

Forced Expiration Flow-Volume Summary

Dr HN Mayrovitz5/16

Obstructive and Restrictive Lung Diseases

Basic Concepts

Obstructive = Abnormal Increase in R

Restrictive = Abnormal Decrease in C→ More difficult to expand→ Greater recoil force

Could have combinations – mixed disease

Dr HN Mayrovitz6/16

Obstructive Diseases: Increased Airway Resistance

• Asthma:

Bronchoconstriction – Mucus - Inflammation

• Chronic Bronchitis:

Mucus and inflammatory processes

• Emphysema

Airway lumen reduction due to wall thickening & mucus

Collagen deposition (fibrosis)

Hyperplasia of mucous-secreting glands

Hyperplasia of mucous-containing airway epithelial cells

Airway lumen reduction due to loss of tethering support*

*Elastic tissue lost-traction force less

So … Airways narrowed & reduced in number

**In emphysema: Alveolar tissue loss - Air space increaseLungs more compliantExpiration more difficult - low recoil Dr HN Mayrovitz

Restrictive Diseases: Restricts Lung Expansion

Pleural → Scarring or Effusion or fibrosis etc

Alveolar → Edema or Hemorrhage

Interstitial → Interstitial Lung Disease or Fibrosis

Neuromuscular → ALS or Myopathy

Thoracic/Extra-thoracic →Obesity or Ascites

“PAINT”

SITE → CAUSES

•Interstitial Fibrosis+ alveolar fibrous tissueLung becomes stiffer (-) complianceInspiration more difficult

• Allergic AlveolitisAlvoli Wall Thickens (-) compliance

• Pleural EffusionIntrapleural Fluid buildup: (-) compliance

Pleural fibrosis & + rigidity: (-) compliance

Dr HN Mayrovitz8/16

0 10 20 30Translung Pressure (cm H2O)

Volume

“normal”

Emphysema -

Normal

Fibrosis

High C and Low Recoil

Low C High Recoil

NormalFRC

•Vascular Engorgement•Lung edema•Atelectasis•Low surfactant

DecreasedCompliance

Compliance Abnormalities

Alveolar tissue loss

Dr HN Mayrovitz9/16

0 -2.5 -5.0 -7.5 Intraplerual2500

Normal

RestrictiveDisease

ObstructiveDisease

Lung Disease Increases Dynamic Work

0 +2.5 +5.0 +7.5 TranslungcmH2O

0TLCE TLCA RVETLCN RVN RVRTLCR

Normal

RestrictiveEmphysema(obstructive)

- Elastic-AW traction+ AWRAW close athigher VL

Larger RV

Forced Expiratory Flow-Volume

Asthma

N=NormalE=EmphysemaA=AsthmaR=Restrictive

RAW RAWPREC

Decreasing Lung Volumes Dr HN Mayrovitz

Forced Expiration

Forced Inspiration

Lung Chest

PIFR DETERMINANTSFRC

Complete Flow-Volume Loop

Time (sec)

Volume

(liters)

Forced

Capacity

(FVC)FEV1

Forced Expiratory Volume-Time Test

FEV1 = Forced Expiratory Volume after 1 sec

FEV1 FVC

Forced Vital

Capacity

FEV1/FVC = 0.8NORMAL

Seconds

Factors and Reference Ranges for “Normal”• Gender →Male > Female• Age → Younger > Older• Height → Taller > Shorter• Race → Caucasian>Hispanic>African A.

Lung Volume

TLC RV

LargeAir

SmallAir

Indicator of smallairway obstruction

Forced Expiratory Volume-Time Test

SmallAirways

IncreasingObstructiveDisease

Normal

Respiratory Rate (breaths/min)

) Normal

Restrictive

Obstructive

Disease Related Adaptations

Obstructive“slow & deep”

Restrictive“rapid & shallow”

ASMM3-receptors

b2-Receptors

Parasympathetic

ganglion in AW wall

cnssympathetic

ganglion

Adrenal

Medulla

a-receptors

NEAirway

arteriole

Sympathetic

• Bronchoconstriction

• Mucus secretion• Bronchodilation

b-agonist

Anticholinergic drugs

Airways - Neural Mechanism (In Brief)

b2-receptors

End Lecture 4

Dr HN Mayrovitz

Lecture 59/17/19

Gas Pressures and Lung Ventilation

OBJECTIVES

• Respiratory gas values by location

• Ventilation and alveolar gas movements

• Alveolar ventilation equation application and calculation

• Alveolar gas equation and application

• Causes of uneven lung ventilation including gravity and time constants

Gas Pressures

Dr HN Mayrovitz

Dry Moist Alveolar Arterial Venous

Air Tracheal Gas Blood Blood

PO2 159.6 147.2 104 100 40PCO2 0.0 0.3 40 40 46PH2O 0.0 47 47 47 47

PN2 600.4 563.5 569 573 573

P total 760 760 760 760 706

Respiratory Gas Partial Pressures

e.g. Dry Air = 0.21 x 760 torr = 159.6 Torr

Dr HN Mayrovitz1/16

PO2 159.6 149.7 104 100 40PCO2 0.0 0.0 40 40 46PH2O 0.0 47 47 47 47

PN2 600.4 563.3 569 573 573

P total 760 760 760 760 706

e.g. Dry Air = 0.21 x 760 torr = 159.6 torre.g. Trachea = 0.21 x (760 - 47) = 149.7 torr

Humidification @ 37o C

Dr HN Mayrovitz2/16

PO2 160 150 104 100 40PCO2 0.0 0.0 40 40 46PH2O 0.0 47 47 47 47

PN2 600 563 569 573 573

P total 760 760 760 760 706

e.g. Dry Air = 0.21 x 760 torr = 159.6 torre.g. Trachea = 0.21 x (760 - 47) = 149.7 torr

Humidification @ 37o C

ROUND-OFFS

TO BE REMEMBERED

Dr HN Mayrovitz3/16

PO2 160 150 104 100 40PCO2 0.0 0.0 40 40 46PH2O 0.0 47 47 47 47

PN2 600 563 569 573 573

P total 760 760 760 760 706

Dr HN Mayrovitz4/16

PO2 160 150 104 100 40PCO2 0.0 0.3 40 40 46PH2O 0.0 47 47 47 47

PN2 600 563 569 573 573

P total 760 760 760 760 706

exiting

the lung

Dr HN Mayrovitz5/16

Dry Moist Alveolar Arterial MixedAir Tracheal Gas Blood Venous

Air BloodPO2 160 150 104 100 40PCO2 0.0 0.0 40 40 46PH2O 0.0 47 47 47PN2 600 563 569 573 P total 760 760 760 760

Mixed Venous Blood = Pulmonary Artery BloodPO2 and PCO2 in dry air and trachea are “round-offs”

Dr HN Mayrovitz6/16

Ventilation

TidalVolume500 ml QT = Total (minute) Ventilation

QT = RR x TV = 6000 ml/min

RR = Respiratory Rate = 12/min

AlveolarGas Volume

AnatomicDead SpaceADS=150 ml(~1 ml/lb)

PO2 = 40SO2 = 75%PCO2= 46

SystemicVenousBlood

from RV

PO2 = 100SO2 = 97%PCO2= 40

QA=Alveolar Ventilation

QA= (TV - ADS) RR

QA= (350 X 12)

= 4200 ml/min

PO2 = 102 PCO2 = 40

PO2 = 160 → Partial Pressure (mmHg)

PCO2 = 0.3 760 x 0.21 = 159.6

Ventilation Related Processes: REVIEW

Dr HN Mayrovitz7/16

Alveolar Gas Movements

VO2VCO2

QA x FACO2

Metabolic CO2

Production

AlveolarCO2 Removed

O2 Consumed

QA x FAO2

AlveolarO2 Removed

QA x FIO2

ALVEOLARO2 Input per

Minute

BloodFrom

Pulmonary To LA

Steady State Balance for CO2 and O2

Dr HN Mayrovitz8/16

PACO2 ~ Alveolar Ventilation

CO2 Production

• Hypoventilation if ratio high: PACO2 rises

• Hyperventilation if ratio is low: PACO2 falls

Alveolar Ventilation Equation: Basic Concept

K = 0.863 with VCO2 in ml/min and QA in L/minute.

Dr HN Mayrovitz9/16

Alveolar Ventilation (L/min)

PACO2 =KVCO2

PACO2=0.863 x 200 ml/min

4.2 l/min

Hyper ventilation

• Normally

Arterial PCO2

very close to

Alveolar PCO2

• PaCO2 ~ PACO2

Arterial Alveolar

• So when we talk

about alveolar

CO2 tension it

almost always

applies to arterial

Curve is for fixed CO2 production

Alveolar Ventilation Equation

“Blowing-off” CO2

Dr HN Mayrovitz

~41 Torr

Alveolar Gas Equation

PAO2 depends on:

Basic Concept

• Composition of inspired air (FIO2)

• Atmospheric pressure (PATM)

• Respiratory Quotient (R = CO2/O2)

• PACO2

PAO2 = (PATM - 47) x FIO2 - PACO2 [FIO2 + (1-FIO2)/ R]

R = respiratory exchange ratio= CO2 produced/O2 consumed

PAO2 = (760-47) x .21 - 40 [.21 + (1-.21)/.8]

PAO2 = (713) x .21 - 40 [1.2]

PAO2 ~ = 150 - 40 [1.2] = 102 torr

PAO2 ~ 150 - 1.2 PACO2 for room air at sea level

Alveolar Gas Equation

Uneven Alveolar Ventilation

Gravity Main Effects

• Alveoli at base have less volumebut greater compliance

• Result is a better ventilation ofbase alveoli during normal TV

PTL = PALV - PPL

Gravity Effects

Does not

depend

gravity

PPLdoes!

So ….

PTLvaries

height

1. Lung tissue behavesas a low density fluidr= 0.28 g/cm2

2. Intrapleural fluid heightrepresents a “column”

Higher intrapleural pressure (PPL)

•Less Transmural Pressure•Less Alveolar Volume• Less PREC → Greater C

Dr HN Mayrovitz

Uneven Ventilation – Variable Time Constants

Time Constant Effects

• Time Constant = R x C = t

• Time to fill/empty ~ t

• Variability in t causes uneven

alveolar ventilation within lung

Fills Slower

80% at 2 sec

(Normal)

Take inspiration time = 2 seconds

Uneven Ventilation due to

variability in Time Constants

B&L 27.3

Seconds

C Fills Faster but

only half as much

Effects of Uneven Time Constants

A source of non-gravity related uneven ventilation

End Lecture 5

Dr HN Mayrovitz

Lecture 69/20/19

Gas Diffusion and Transport

Dr HN Mayrovitz

OBJECTIVES

• Blood oxygen content equation application and calculation

• Oxygen delivered – carbon dioxide removed circuit with calculations

• Lung diffusion capacity and factors affecting its value

• Oxygen loading and unloading dynamics

• Carbon dioxide loading and unloading dynamics

• Oxygen deficiency terms and sources

0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 95 100 105

PO2 (mmHg)

Blood Oxygen Content EquationSO

PO2 (mmHg)

23, 400

PO2 [ PO22 + 150]

1SAT =

Severinghaus Equation

venous

Arterial blood20 ml O2/dl

D = 5 mlO2/dl

pH = 7.40T = 37oC

Dr HN Mayrovitz

[O2] = 1.34 [Hb] (%Sat/100) + 0.003PO2

ml/dl wb

g/dl whole blood (wb)(34 g/dl rbc x Hct)34 x 0.44 = 15 gHb/dl wb

Amountdissolved

[O2] = 1.34 x 15 x 0.974 = 19.6 mlO2/dl + 0.27

SYSTEMIC

300 ml O2/dl/min

“Average” O2 needed

240 ml CO2/dl/min

“Average”CO2 generated

Air in – and –Air out →O2 delivered and CO2 removed

For every ml of O2 used 0.8 ml CO2 produced

5 mlO2/dl bloodmust be supplied

4 mlCO2/dl bloodmust be removed

CO = 6 L/min = 60 (dl units/min)

Dr HN Mayrovitz

Respiratory QuotientCO2 produced/O2 consumed

Lipid → 0.70Protein → 0.80Carbohydrate → 1.0Average →0.80

Each dl unitmust get5 mlO2

PAO2PaO2

AlveolusCapillary

f = D (A/d) DP

1. Area (A)2. Thickness (d)3. Pressure Difference (DP)4. Diffusion coefficient (D)

Lung“Membrane”

Main Factors

Here “a” refers to blood exitingpulmonary capillaries.

Basic Diffusion Processes

Dr HN Mayrovitz 3/11

Lung Diffusing Capacity

DL takes into account all factors that effect whole lung diffusion

DL = ml O2/min from alveoli to blood

(alveolar) PAO2 - PaO2 (capillary)

Alveolar Gas

Capillary PaO2

fO2DL is a form of “conductance”

i.e. flow/DP

PA O2 - PaO2

Dr HN Mayrovitz4/11

Factors Decreasing DL

Diffusion Distance

•Alveolar Wall Thickening

•Alveoli-Capillary separation by:

edema, exudate or fibrous tissue

Surface Area

•Fewer functioning capillaries

•Fewer functioning alveoli

•Disrupt normal alveolar architecture

Red Blood Cells and Diffusion Resistance

•Decreased rbc membrane permeability

•Decreased Hb O2 affinity

•Decreased total amount of Hb available

Dr HN Mayrovitz5/11

Gas dynamics

Loading up with O2 in Lung

Alveoli

Lung Capillaries

Airways

PCO2 RBC “carrier that is carried”

0 20 40 60 80 100

(%)ml O2

100 mlblood

20Arterial Blood

Venous15

Loading O2 in Lung

Blood PO2 (mmHg)

PCO2 = a [O2]

40 80 100 100 100 100 PCO2

100 mmHg

Equilibrates at ~ 1/3 capillary length

a = 1/KO2

Unloading O2 to Tissues

40 40 40 40 80 100 PCO2

Equilibrates at ~ 1/3 capillary length

Tissue Fluid PTO2

Cell using O2

PCELLO2

40 40 40 40 40 40

0 20 40 60 80 100

(%)ml O2

100 mlblood

20Arterial Blood

Venous15

Loading O2 in Lung

Blood PO2 (mmHg)

Picking Up CO2 from Tissues

46 46 46 44 42 40 PCCO2HbHb

Tissue Fluid PTCO2

Cell producing CO2

PCELLCO2

CO2 + H20 → H2CO3

Carbonic Acid 5%

Carbamino Compounds 5%

HCO3- 90%

Bicarbonate dissolved

[CO2]ml/100 ml

PCO2 (mmHg)

PCCO2END of

Lung Capillary

SO2 = 97%

SO2 = 75%

PCCO2START of

Lung Capillary

Systemic Capillary

To Lung

From Lung

0 0.15 0.30 0.45 0.60 0.75

Time RBC in Capillary (sec)or Distance Traversed (mm)

Enters Leaves

Normal Diffusion

ModerateImpairment

SevereImpairment

PAO2=102

Exercise - capillary transit time reduced

PvO2 = 40 PaO2 =?

Capillary Blood Oxygenation

~1 mm/sec

CO2 vs. O2 Curves

0 10 20 30 40 50 60 70 80

O2 or CO2 Pressure (Torr)

BloodO2 or CO2

Content(ml/100 ml)

O2Near-Flat

If REDUCED VENTILATIONAlveolar PCO2 risesBlood PCO2 directlyfollows

If REDUCED VENTILATIONAlveolar PO2 falls but

PO2 change is “buffered”

Oxygen Deficiency Terms and Sources

ANOXIA = No O2

HYPOXIA = Inadequate O2 Available for Tissue NeedsHYPOXEMIA = Hypoxic Hypoxia = Low PaO2

HEMATOLOGICAL HYPOXIALow Hb to bind/carry O2 but normal PO2 → Anemia, Carbon Monoxide Poisoning

ISCHEMIC HYPOXIA (Hypoperfusion Hypoxia or Stagnant Hypoxia)Low tissue O2 due to low systemic blood flow to the area (blood PO2 is normal)

HISTOXIC HYPOXIANormal O2 supplied (Normal PaO2 and blood flow) but O2 can’t be utilized bytissue → Cyanide Poisoning (Blocks oxidative phosphorylation)

Ventilation/Perfusion 15/20

Low FIO2 → Low O2 in inspired air → Fire

Low PATM → Altitude

Low QA → +Air way resistance, CNS depression, neural or muscular deficits

Low V/Q → increased number of low ventilation or high blood perfusion areas

Low DL → Edema, Fibrosis

R-L Shunt → Anatomical → Blood bypasses alveoli

End Lecture 6

Lecture 7 9/20/19Ventilation –Perfusion Matching

Dr HN Mayrovitz

OBJECTIVES

• Ventilation-perfusion (V/Q) matching concept

• Evaluate sources and effects of altered (V/Q) on blood gasses

• Hypoxic pulmonary vasoconstriction (HPV)

• Pulmonary shunting types and effects on blood gasses

• A – a gradient: Concept and application

Ventilation-Perfusion Matching

Basic ConceptIt is neither ventilation nor perfusionalone that determines arterial bloodgases. It is the ratio of ventilationto perfusion that is the determinant!

Ventilation/Perfusion = V/Q ratio

Dr HN Mayrovitz1/15

A. Ventilation-Perfusion Concept

PO2 = 40

SO2 = 75%

PCO2= 46

Systemic

Venous

from RVPO2 = 100

SO2 = 97%

PCO2= 40

QA = Alveolar Ventilation

= 4200 ml/min

250 ml O2/min

5000 ml/min

Assume that an alveolar ventilation of 4200 ml/min

will deliver 250 ml O2/min to capillary blood.

Each 100 ml blood unit picks up 5 ml of O2

If blood flow is 5000 ml/min then each of the (50) 100 ml of blood must pick up 5 ml of O2. This results in a proper

“arterialization” of blood exiting the lung.

5000 ml =50 ‘100 ml blood’ units

250mlO2/50units = 5 mlO2/unit

V/Q 4200/5000

Ventilation/Perfusion Dr HN Mayrovitz

PO2 = 40

SO2 = 75%

PCO2= 46

Systemic

Venous

from RV

= 4200 ml/min

250 ml O2/min

10,000 ml/min

Now suppose ventilation stays constant but blood flow increases to 10,000 ml/min.

Each 100 ml blood unit picks up 2.5 ml of O2

100 “100 ml blood” units

250mlO2/100units

= 2.5 mlO2/unit

Now, 100 “100 ml units” pass each minute. Soooo….. each will pick up only 2.5 ml of O2 since QA is constant. Since this is 1/2 as much as needed to properly saturate the blood, Sooo …….. PaO2 will fall!

B. Ventilation-Perfusion Concept

V/Q 4200/10000

Dr HN Mayrovitz

PO2 = 40

SO2 = 75%

PCO2= 46

Systemic

Venous

from RVPO2 = 100

SO2 = 97%

PCO2= 40

= 2100 ml/min

125 ml O2/min

2500 ml/min

Now suppose ventilation and perfusion become 1/2 of

what they originally were. Now each 100 ml of blood

again picks up 5.0 ml of O2. Thus Ventilation is again

optimally matched to perfusion to properly cause the

needed blood O2 saturation.

Each 100 ml blood unit picks up 5.0 ml of O2

C. Ventilation-Perfusion Concept

25 “100 ml blood” units

125mlO2/25units

= 5.0 mlO2/unit

V/Q 4200/5000

Dr HN Mayrovitz

Number of lung units with low V/Q

Another View of Mismatching

Dr HN Mayrovitz5/15

PaCO2 PaO2

(V/Q)0.4 0.84 1.2 1.6

Hypoxemia

Hypocapnia

Respiratory

Alkalosis

Respiratory

Acidosis

Effects of Changes in V/Q

IncreaseDecrease

Hyperoxemia

Hypercapnia

Dr HN Mayrovitz6/15

TopBottom

Regional V/Q Variations

PCO2 42T

PCO2 28T

PO2 90T

PO2 130T

Matched

>match

V/Q<match

Position Vertically in Lung

Dr HN Mayrovitz7/15

PaCO2 PaO2

(V/Q)0.4 0.84 1.2 1.6

Hypoxemia

Hypocapnia

Respiratory

Alkalosis

Respiratory

Acidosis

Hyperoxemia

Hypercapnia

Good Arterialized

MixedVenousBlood

(PulmonaryArtery Flow)

Perfectly Matched

Clinical Correlation: Ventilation matched to Perfusion

PaCO2 PaO2

(V/Q)0.4 0.84 1.2 1.6

Hypoxemia

Hypocapnia

Respiratory

Alkalosis

Respiratory

Acidosis

Hyperoxemia

Hypercapnia

MixedVenousBlood

PulmonaryEmbolism

LOWPaO2

Clinical Correlation: Pulmonary Embolism

Low V/Q

V/Q V/Q

MixedVenousBlood

High V/Q

Clinical Correlation: Hyperventilation

PaCO2 PaO2

(V/Q)0.4 0.84 1.2 1.6

Hypoxemia

Hypocapnia

Respiratory

Alkalosis

Respiratory

Acidosis

IncreaseDecrease

Hyperoxemia

Hypercapnia

LOWPaCO2

BloodFlow(% )

Alveolar PO20 50 100 150 200 250 300 350

Hypoxic Pulmonary Vasoconstriction (HPV)

Effect of reducing ALVEOLAR PO2 on Local Blood Flow

~70 mmHg

Flow reduction Produces Better V/Q match

Poorly

oxygenated

Vasconstriction

shunts blood to

better oxygenated

alveoli

100 60

Shunts

Anatomical Shunts: systemic venous blood• Bronchial veins• Thebesian veins• Pleural veins

Intrapulmonary Shunts: • Mixed venous blood has

zero alveolar gas exchange (e.g. airway obstruction)

• Low V/Q → low O2 mixes with all oxygenated blood

Blood fromLow V/Q units

Blood fromAlveolar DS

INTRAPULMONARY SHUNTS

Bronchial V.Anatomical

PHYSIOLOGICAL SHUNT Anatomical Shunt + Intrapulmonary Shunt

Mixing of low oxygenated blood with arterial blood

Normal: Minimal Shunting

PO2=40PCO2=46

PO2=104PCO2=40

PO2=100PCO2=40

PulmonaryArtery

AnatomicDead Space

PIO2=150PCO2=0Alveoli

Normal

A – a Gradient

Rule of thumb: Normal gradient should be ≤ (Age/4) + 4

60 year old might have a gradient of (60/4) + 4 = 19 TorrDr HN Mayrovitz12/15

• 100% O2 will not abolish hypoxemia• Shunted blood never exposed to O2

• Non-shunted blood already near max saturation

Anatomical shunt: Features

PO2=40PCO2=46

PO2=104PCO2=40

PO2=60PCO2=39

PulmonaryArtery

AnatomicDead Space

PIO2=150PCO2=0Alveoli

Normal

PO2=40PCO2=46

PulmonaryVeinO2

“diluted”

ShuntRight-to-Left

Ventilation Deficit• e.g. mucous obstruction - airway edema - bronchospasm• foreign body - tumor - etc

100% O2 WILL improve situation

Low V’

Intrapulmonary Shunt

Low V/Q

Low PO2

High PCO2

A-a Gradient Question to Ponder

PAO2=102 PaO2=94

Right Heart Left Heart

Thebesian Veins

Bronchial V. Aorta

Dr HN Mayrovitz

Bill is 24 years old. A) What is his A-a gradient and B) is it within the normal range for his age?

End Lecture 7

Dr HN Mayrovitz

Lecture 8 10/2/19Respiratory System

Controls and Reflexes

Dr HN Mayrovitz

OBJECTIVES

• Overall respiratory control defining feed back variables and mechanisms

• Medullary and Pontine respiratory groups and their actions

• Normal vs. abnormal breathing patterns

• Respiratory mechanical receptors: types and actions

• Herring-Breuer reflexes

• Peripheral (PCR) and Central (CCR) Chemoreceptors: types and actions

• Ventilation changes due to O2 changes, CO2 changes and high altitude

Impulses to

Respiratory

Muscles

Ventilation control

Via changes in

RR and TV

Peripheral and Central

Chemo and Mechanical

Receptor Feedback

Other Inputs

Basic Respiratory Control Overview

Inspire Exp Inspire

Central Pattern Generator

Brain stem

Respiratory

Center

Respiratory

Center

Spinal Respiratory

Motorneurons

Respiratory Muscles

Ventilation: TV/RR

Blood Gases

Skeletal

Muscle

Receptors

Receptors: lung & airways

chest wall & diaphragm

Peripheral Chemoreceptors

Central ChemoreceptorsCSF [H+]

Emotions

(Forebrain)LimbicReticular

Formation

Sensory (pain, startle, etc)

Airway

Muscles

pharynx

larynx

flare nostrils

open mouth

Airway

Smooth

Muscle

Brain stem

Respiratory

Center

Phrenic (diaphragm)

Spinal n. (intercostals, abd)

Neocortex

(Voluntary)

+CO2, -pH

-O2, +CO2, -pH

Impulses

Inspiration Expiration Inspiration

Impulses to Respiratory Muscles From MedullaryCentral Pattern Generator (CPG) Cause Inspiration

Impulses

per sec

Volume

Spinal Cord

1st cervical

4th Ventricle

Ventral

Respiratory

ApneusticCenter

Respiratory Cell Groups

phrenic

Receptorfeedback

Dorsal

Respiratory

Pontine Respiratory Group(Pneumotaxic Center)

4/21Dr HN Mayrovitz

Internal intercostalabdominal muscles

Diaphragmand external intercostals

INDiaphragm

and external intercostals& accessory

UpperAirwaysLarynxpharynxtongue

VRG DRG

Medullary Respiratory Center

Pre-Botzingercomplexpossible

pacemakerregion

IN = InspiratoryE = Expiratory

Pneumotaxic Center

• In upper pons

• Some neurons active during

inspiration & some in expiration

• Important role in switching

off/limiting inspiration

• If damaged leads to apneusis:

prolonged inspiratory spasms

with short intervals of expiration

• Also fine-tunes breathing based

on receptor feedback

Pontine Respiratory Group (PRG)

Pneumotaxic Center (PRG)

Apneustic Center

Inspiratory

Center

Expiratory

Center

Maintenance of signal

Prolongs inspiration

Inhibits apneustic output

Switches off Inspiration

To inspiratory m.

Impulses/s

Receptor

Feedback

Via IX & X

Basic rhythm is generated in medulla

(Central Pattern Generator)

CPG → Cause is unknown

Respiratory Center Actions: Summary

Medulla

Brain stem

Respiratory

Center

NTS = Nucleus Tractus Solatarius

Normal

Apneustic

Pneumotaxic Center (PRG)

Apneustic Center

Inspiratory

Center

Expiratory

Center

Maintenance of signal

Prolongs inspiration

Inhibits apneustic output

Switches off Inspiration

To inspiratory m.

Impulses/s

Receptor

Feedback

Via IX & X

Inhibitionlost

Cheynes-Stokes

Over-correction

Abnormal Breathing Patterns

Tidal VolumeCrescendo

C-Fiber

Endings

Slowly

Adapting

Receptors

Rapidly

Adapting

Receptors

Pharyngial

Epipharyngeal

Laryngial

Respiratory MechanoreceptorsReceptors Located in

• Upper respiratory

• Tracheo-bronchial tree

• Lung parenchyma

Broadly three types

• Slowly Adapting (SAR)

Among ASM cells

• Rapidly Adapting (RAR)

Among airway epithelial cells

• C-fiber endings (J-receptors)

near blood vessels/capillaries

Vagal Afferents

• Connect to respiratory cntr

• Initiate many reflexes

Bronchoconstriction:

• Prevents deeper penetration into airway

• Produces higher velocity airstream during sneeze or cough

Sneeze: Stimulation of nose or nasopharynx receptors

Afferent pathways via trigeminal and olfactory nerves

Cough: Stimulation of tracheobronchial receptors

Afferent pathways via vagus nerves

Mechanical/Chemical Irritant Reflexes (RAR)

Receptors in nasal mucosa, upper airways, tracheobronchial tree

and possibly alveoli trigger bronchoconstriction and sneeze or cough

Cough/Sneeze Process:

•Deep inspiration is followed by forced expiration with closed glottis

•Intrapleural pressure rises precipitously ~ 100 mmHg

•Glottis opens and high velocity exhalation air stream results

Sneeze: Through nose Cough: Through mouth10/21 Dr HN Mayrovitz

Hering-Breuer INFLATION Reflex

Inspiratory m.

Impulses to inspiratory muscles

are decreased

•Reduces inspiration duration

•Reduces TV •Prevents overdistention

SAR among ASM cells

H-B Inflation Reflex Operative in •Adults if TV > 800 ml• Infants

Too much lung Inflation

Inhibitory impulses to DRG via Vagus

Hyperpnea•Tachypnea +RR•Hyperpnea +TV & +RR

• Pneumothorax → RAR• Trigger for sighs• Maintain Infant FRC

low chest wall force

Less stretch receptor activitycauses a reflex that promotes either/bothincreased TV and RR

Impulses to inspiratory muscles

are increased

Hering-Breuer DEFLATION Reflex

12/21Dr HN Mayrovitz

chemoreceptor

CSFSkull

Capillary

Central Chemoreceptors (CCR)

Blood-BrainBarrier

VentilationControl

• CCR in brain parenchyma bathed in brain extracellular fluid/CSF

• If blood gases and pH near normal CCR are main control of ventilation

• CCR are sensitive to arterial hypercapnia (and associated fall in pH)

• CCR actually sense pH (H+) around receptor neurons bathed in CSF

• pH changes may occur due to:

1) increased cerebral blood CO2 diffusing across the blood brain

barrier resulting in a rapid (60 sec) decrease in the pH of CSF

2) decreased pH of brain or CSF not due to changes in PaCO2 (delayed)

• CCR do not respond to hypoxia

• CCR and PCR both affect ventilation response to increased CO2 levels

Dependence of Ventilation

on pH of CSF

pH of CSF

7.15 7.20 7.25 7.30 7.35

Normal

REVIEW: Central Chemoreceptors (CCR)

chemoreceptor

CSFSkull

Capillary

Blood-BrainBarrier

VentilationControl

Peripheral Chemoreceptors (PCR)

• Located bilaterally in carotid and aortic bodies

• Respond to Hypoxia, Hypercapnia and Acidosis

• Afferent pathways for:

Carotid body → Hering’s nerve

Aortic body → vagus nerve

• Large afferent impulse traffic at normal blood gases

• Increased afferent activity caused by

(1) decreased arterial PaO2

(2) increased PaCO2

(3) decreased arterial pH

• Feedback to respiratory center → increased V’

• Response to hypoxemia depends on PaCO2 & pH

More PaCO2 or lower pH → greater DV’ for same DPaO2

NTS IN

Sympathetic N. Arteriole

FenestratedCapillaries

GlomusCell

MedullaOblongata

Respiration•RATE•TIDAL VOLUME

Afferent Response to changes in PaO2

Note large rate of increase

below about 60-70 torr

PaO2 of blood perfusing

carotid body is varied

PaCO2 and pH normal

0 50 100 200

cPaO2 (mmHg)

Ventilation Response to changes

in PaO2depends on level of PaCO2

20 40 60 80 100 120

PaO2 (mmHg)

PaCO2 = 40 mmHg

PaCO2 = 50 mmHg

Slope of lines define the

sensitivity of the response

to changes in PaO2

Normal

PaCO2 Effect on Response to Changes in PaO2

20 40 60 80 100 120

PaO2 (mmHg)

PaCO2 = 40 mmHg

PaCO2 = 50 mmHg

to changes in PaO2

+V’ due to

+ PaCO2

Normal

PaCO2 Effect on Response to Changes in PaO2

20 40 60 80 100 120

PaO2 (mmHg)

PaCO2 = 40 mmHg

PaCO2 = 50 mmHg

to changes in PaO2

• Ventilation response to hypoxia depends on level of PaCO2

• +PaCO2 and -pH cause more DVent (DV’) for same D in PaO2

dV’/dPaO2

+V’ due to

+ PaCO2

Normal

PaCO2 Affects Response to Changes in PaO2

Ventilation Response to CO2

Carotid Body Perfusion-High CO2

Ventilation

increase

TV & RATE

INCREASE

Hyperpnea19/21 Dr HN Mayrovitz

REVIEW: Ventilation Responses to CO2

• Breath rate & depth regulated to maintain PaCO2 close to 40 mmHg• Ventilation increases nearly linearly with PaCO2 AT FIXED PaO2

• Change in ventilation for equal changes in PaCO2 depends on PaO2

Lower PaO2 → greater change in ventilation (k is greater)So HYPOXEMIA increases sensitivity of the CO2 ventilatory response

sensitivity = dV’/dPaCO2 = k = f (PaO2)• At any PaCO2 level → a pH decrease causes greater impulse response

30 35 40 45 50 55

PaCO2 (mmHg)

pH=7.25

pH=7.45

Carotid Body AfferentVentilation Response to changes in PaCO2

30 35 40 45 50 55

PaCO2 (mmHg)

PaO2=40

PaO2=60

PaO2=100

Actions of

both CCR

and PCR

V = k PaCO2

k=f(PaO2)

High Altitude: Respiratory Adaptation

Decreased Atmospheric Pressure ~ Hypoxemia

Peripheral Chemoreceptors drive increased ventilation• Increases PaO2 but Decreases PaCO2

• Decreased CO2 effects Central Chemoreceptors (+pH) • Initially counter to hypoxia induced hyperpnea• CSF and arterial pH tend to normalize over days • Renal excretion of HCO3-

• Early acute Mountain Sickness possiblePolycythemia - Increases O2 carrying capacity

P50 Shift to Right - Better O2 unloading

Increased Capillary Density

End Lecture 8

Dr HN Mayrovitz

Respiratory Physiologyclinsoft.org/drmayrovitz/PHYSIOLOGY/RESPIRATION/COM...2 x P ATM = 0.21 x 760 =...

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