Applied respiratory physiology: part 1

by;

Dr Mohd Ridhwan bin Mohd Noor

Intensivist

HSNZ 2013

Pre master basic science

Ouchh!

Knowledge decay after specialist graduation

Content

1. Functional anatomy

2. Deadspace/ lung volumes/ shunts

3. Ventilation/perfusion abnormalities

4. Control of respiration

5. Non respiratory functions of lungs

Functional anatomy

• Nose, mouth & pharynx humidify & filter the air gases

• Larynx is 18 mm in diameter & 11 cm in length

• Trachea divides to main stem bronchus at carina (T4)

• Bronchi divides 23 times (generations) & the first 16 are

termed conducting zone & forms anatomical deadspace

• Generation 17-23 where gas exchange occurs with 300

million alveoli & about 2-3 litres in volume

• Consists of 3 type of cells;

1. Type 1

• Provide thin layer of cytoplasm & cover 80% of gas

exchange zone

2. Type 2

• Formation of surfactant & other enzymes

3. Type 3

• Maintain lungs defense system – alveolar

macrophages

Weibels classification of airways

Clinical points

• ETT should be 1-2 cm above carina or at T3

• Right main bronchus divides from trachea at less acute

angle, therefore prone to endobronchial intubation

• ® upper lobe bronchus arises few cm from carina,

therefore for one lung ventilation (L) double lumen

ETT is favored to avoid risk of ® upper lobe collapse

with ® double lumen tube

Dead space

• Def; lung volume that does not participate in gas

exchange (wasted ventilation) or ventilation without

perfusion

• Types:

1. Anatomical deadspace

2. Physiological deadspace

3. Alveolar deadspace

4. Apparatus deadspace

Anatomical deadspace

• Volume of conducting airways (150 mls in

adults)

• Mostly atmospheric gas & it’s exhaled gas

before CO2 flowing to the alveoli & expired

• Influenced by age, position, height,

hypoventilation, atropine, hypothermia

Fowler’s methods (anatomical deadspace)

• Subject breathing to

pneumatachograph &

rapid nitrogen analyser

• Subject breaths 100%

of O2 & N2

concentration plotted

against time & volume

Alveolar deadspace

• Part of inspired gas that enter the alveoli BUT

does not participate in gas exchange

• Represents ventilated but underperfused alveoli

• Can be measured by comparing PAO2 & PaCO2

• Negligible in healthy adult & PACO2 almost

equal PaCO2

Causes ETCO2 < PaCO2

1. Low cardiac output or hypotension

2. High inspiratory pressure esp high PEEP

3. Pulmonary embolus

4. Posture changes – leading to changes in

regional perfusion

Physiological deadspace

• Alveoli + anatomical deadspace

• Part of tidal volume not participate in gas exchange

• Calculated using Bohr equation;

Vd = PaCO2 – PECO2

Vt PaCO2

• Normally ~ 30% of tidal volume

• Clinical: increase in physio deadspace cause alveolar ventilation

reduced unless compensatory increase in minute volume e.g. COPD

Lung volumes

Spirometry Tacing in adult male

Lung volumes

The volume (per kg)

• Residual volume 15-20 mls

• Expiratory reserve volume

15 mls

• Tidal volume 6-8 mls

• Inspiratory reserve volume

45 mls

The capacities (per kg)

• Total lung capacity 75-80

mls

• Vital capacity 60-70 mls

• Inspiratory capacity 50 mls

• Funtional residual capacity

30 mls

Which volumes & capacities can’t be measured by spirometry?

1. Residual volume

2. Any capacities which contain residual

volumes

– FRC

– Total Lung Capacity (TLC)

Functional residual capacity (FRC)

• Def: volume of gas which remains at the end

of normal expiration (FRC = RV + ERV)

• It is a balance point between tendency of

the chest wall to move outward & tendency

of the lungs to collapse

Forces exerted on the thorax

The tendency of the chest wall and diaphragm to separate from the lungs is the reason why intrapleural pressure is negative

Functions of FRC

1. Oxygen store

2. Buffer to maintain a steady arterial pO2

3. Prevent atelectasis

4. Minimise work of breathing (by keeping the lungs on

the steep part of the compliance curve)

5. Minimise pulmonary vascular resistance

6. Minimise V/Q mismatch

1. FRC as oxygen store

• At room air PAO2 of 100 mmHg & FRC of 2200 mls,

the lungs contain 290 mls of O2.

• Pre-oxygenation with 100%, it can increase up to

1800 mls of O2 in the lungs

2. Buffer for arterial PO2

• Continuous presence of gas containing in

the lungs converts the intermittent tidal

delivery into continuous availability of O2

for gas exchange.

• Prevent large swings in PaO2 during

ventilatory cycle

3. Prevent atelectasis

• FRC maintain partial state of partial inflation

in the lungs & prevent atelectasis

• At a balance point between the tendency of

the chest wall to move outward & the

tendency of the lung to collapse

4. Minimize work of breathing

– At FRC, the lung work at the steep part of

compliance curve

5. Minimise pulmonary vascular resistance

– PVR varies with lung volume, high at both high

and small lung volume

– PVR lowest at FRC

PVR & lung volume

6. Minimize V/Q mismatch

– FRC prevent lung closure at tidal ventilation &

minimize ventilation abnormality

Measurement of FRC

1. Gas dilution methods (nitrogen washout/helium

washin)

– Subject rebreathing from closed circuit that contain

initial volume (V1) & concentration of helium (He1)

– After period of rebreathing final helium (He2)

measured

V1 x (He1) = (V1 + FRC) x (He2)

Factors affecting FRC

Increase

• Height

• Changing from supine to

erect position

• Decreased lung elastic

recoil (e.g. emphysema)

• PEEP

Decrease

• Obesity

• Muscle paralysis

• Changing from erect to supine

• Pregnancy

• Anaesthesia

• Pulmonary ds causing

increased elastic recoil of the

lungs

2. Body plethysmography

Closing capacity

• Lung volume at which airways start to close in

expiration ( CC = CV + RV)

• Factors increasing CC;

– Increasing age

– Smoking/asthma/emphysema/bronchitis

– Prolonged recumbency

– Increase left atrial pressure

Closing volume measurement

Single breath Nitrogen washout

Relationship between FRC and closing capacity

66 yrs

44 yrs

Ventilation-perfusion abnormalities

Describe West’ zones of the lung

• Describe relationships of pulmonary arterial, venous

& alveolar pressure in zones from apex to the base

• Changes occur due to gravity that cause distension

of vessels at the upright lung base & compression at

the apex

• PAP decrease by 1 cmH2O per cm vertical distance

of the lung

• At the base PAP 10 cmH2O (16 26) & PVP

fr 11-21 cmH2O

• At the apex PAP 15 cmH2O (16 1) &

venous pressure fr. 11 to -4 cmH20

# need to put head down position to avoid air embolism

during CVC insertion#

West’s zones

• Zone 1: alveolar

pressure exceed

arterial pressure.

Creating no flow in

apex and deadspace

# Contribute to deadspace. Rarely occur in healthy subject but in hypotension, hemorrhage or use of PEEP will increase zone 1.#

West’s zones

• Zone 2; Pa exceeds PA

but PA still above PV on

expiration. The flow or

perfusion depends on

difference ( Pa – PA) &

called waterfall effect

West’s zones• Zone 3; Pv more than PA in

inspiration & expiration.

Flow depend on (Pa –Pv).

• Pulmonary blood flow is

constant in this region &

provide optimal condition

for gas exchange

#Swan-Ganz should float here posteriorly in supine position#

West’s zone

• Zone 4: the lung has

positive interstitial

pressure (PE, mitral

stenosis, pulmonary

edema)

• Flow depends on

difference between Pa and

Pi

What the 7 differences between apex and base of lungs?

• Alveoli at the top of the lungs;

– Larger at end-expiration

– Have lower ventilation

– Have lower perfusion

– Have higher V/Q ratio (3.3 vs 0.63)

– Higher pO2 (132 at apex, 89 at base)

– Lower pCO2 (28 at apex, 42 at base)

– Higher pH (7.51 vs 7.39)

Shunts

• True shunts is perfusion without ventilation (V/Q =

0)

• Refers to blood that enter arterial system without

passing ventilated areas of the lungs

• Effects;

– Reduce PaO2

– Increase A-a gradient

Venous admixture

• Amount of mixed venous blood has to be

added to pulmonary end capillary blood to

see drop in arterial PaO2

• Sometimes used interchangeably with shunts

2 main sources of blood contribute to venous

admixture

1. True shunts – 2 sources

– Bronchial vein

– Thebesian vein

2. Blood from alveoli with V/Q less than 1 e.g.

atelectasis, consolidated area, edema

Recollection

V/Q = 1

V/Q < 1V/Q > 1

Shunts vs Venous admixture

Shunt equation

Total flow = Qt

Shunted flow = Qs

Flow thro lungs = Qt - Qs

Shunt O2 content =

CvO2

Total O2 delivery = O2 delivery from ventilated lungs + O2 delivery from shunt

O2 flux/delivery = cardiac output x O2 content

Qt x Ca = (Qt – Qs) x CcO2 + (Qs x CvO2)

Qs = (CcO2 – CaO2)

Qt (CcO2 – CvO2

Total O2 delivery = O2 delivery from ventilated lungs + O2 delivery from shunt

Finally what we get…..

V/Q = ∞

V/Q = 0

What methods used to measure V/Q inequalities?

1. A-a oxygen gradient (normal 5-15 mmHg)

– Need alveolar gas equation PAO2= FiO2 x (760-47) –

(PaCO2/R) R = 0.8

– Increased in V/Q mismatch, shunting, diffusion

abnormalities

Measurement V/Q abnormalities (2)……

2. Shunt equation

– For low V/Q unit

3. Bohr equation

– For high V/Q unit

4. PaCO2 – ETCO2 difference

– ETCO2 normally 2-5 mmHg lower than PaCO2

– Increase in high alveolar deadspace (PE, low cardiac

output, venous air embolism)

Pulmonary blood flow & resistance

• Mixed venous blood frm RV main PA branches

of PA with bronchi/bronchioles central acinar

arterioles pulm capillaries small peripheral

acinar pulm veins pulm vein with

bronci/bronchioles 4 main pulm vein LA

Difference between pulmonary and systemic circuit

• Pulmonary is low pressure conduit (mean PAP 15 mmHg) (25/8)

• More pulsatile than systemic circuit

• Vessel much thinner

• Not all vessel are open at resting CO, increase flow recruitment & distension

Factors affecting pulmonary vessels

Pulmonary vascular resistance

1. Lung volume

– Both low and high lung volume with increase

PVR

2. Hypoxic pulmonary vasoconstriction

3. Metabolic substance

PVR = 80 x (MPAP –PCWP)/CO

Hypoxic pulmonary vasoconstriction

• Reflex vasoconstrictive effect of low alveolar PO2

• When alveoli are not ventilated HPV will

effectively shunt the blood away frm this alveoli to

a better ventilated unit

• Will reduce V/Q in equalities in the lungs &

improving oxygenation esp. in condition like LVF,

pulmonary edema

HPV…so what?

• Particular interest for anesthetist;

1. Effect of volatile agent on HPV

2. Role of HPV during one lung anaesthesia

Etiology of hypoxemia…..anyone?

1. Low inspired FiO2

2. Hypoventilation

3. Deadspace

4. Shunts

5. Increase diffusion capacity

Control of respiration

• Control of breathing is about supply and

demand

• Resp. system as supplier of oxygen &

provide the blood (road system) to the cells

(consumer) to perform aerobic metabolism

2 levels of control

Local control

• Location: alveoli, capillaries &

bronchioles

• Role; ensure gas & blood go to

appropriate part of lungs for

efficient gas exchange

• When: changes in CO2 and O2

• Mechanism: local adjustment to

blood flow (perfusion) & oxygen

delivery (alveolar ventilation) to

alveolar

Central control

• Location: RC located in medulla

oblongata & pons and modified by

sensory neuron (peripheral & CSF)

and higher centre

• Role: adjust the depth & rate of

ventilation

• When: during normal breathing &

during larger demand

• Mechanism: involuntary reflex via

sensory feedback and voluntary

control via RC

Local control of lung perfusion

Local control of alveolar ventilation

Local control tries to reduce V/Q imbalance………..

• Common value for V/Q ratio is 0.8• Local control aims at maintaining optimal V/Q

ratio

Central controlInvoluntary control

• Direct the depth & rate of

breathing via output from

respiratory centre

• Modified by influence from

receptors from the lungs and

CSF to ensure appropriate

levels of ventilation

Voluntary control

• Influenced indirectly from

cerebral cortex & affect the

output of respiratory centres

in the medulla oblongata

• Influential factors include

emotion, anticipation of

exertion & activities requiring

alteration to normal breathing.

Respiratory centers and breathing

• DRG is part of NTS which obtain info from

mechano & chemoreceptors, and project to

neuron of phrenic nerve which supply

diaphragm.

– Involves inspiratory process & timing

• VRG resides in nucleus ambiguus &

concerned with amplitude of respiration

Respiratory control reflexes

1. Sensors

– Peripheral & central chemoreceptors

– Muscle proprioceptors

– Lung, upper airway & pharyngeal receptors

2. Contoller

– Cortex (voluntary control)

– Brainstem (automatic control)

– Spinal cord (integration)

3. Effectors

– Muscle of respiration (via spinal respiratory

motor efferents

– Lungs, pharynxs, laryngx (via cranial nerve

respiratory motor efferent)

Hering-Breuer reflex

• Inflation & deflation reflexes occur during

forced breathing.

• With the cooperation of two reflexes, the

volume and stretch of the lungs is controlled

to avoid over expansion or over deflation

Respiratory functions

1. Non gas exchange functions

2. Gas exchange

Non gas exchange functions

1. Blood reservoir functions

– Contain ~ 450 mls of blood

– Increase PAP will increase pulmonary blood volume in

2 mechanisms

• Recruitment (more vessel open up)

• Distension (open vessel got bigger)

– “Central blood volume” defined as volume in the lungs

(450 mls) and heart (350 mls) = 800 mls

Intra-thoracic blood volume

2. Elimination of volatile substance

– Alcohol, acetones, volatile anesthetics

3. Blood filter – thrombi, microaggregates etc.

4. Metabolic activity

– Activation of AT 1 to AT 2 (maintaining sodium balance)

– Inactivation of noradrenaline, bradykinin, serotonin & prostatglandin

5. Immunological – IgA secretion into bronchial mucus

6. Miscellaneous

– Protein syntesis (collagen, elastin)

– Surfactant (DPPC) synthesis

– CHO metabolism (mucin & proteoglycan synthesis)