Respiratory Physiology

Presented by:Dr. Pravin Prasad

Medical officer, EDGrande International Hospital

Academic Session I

Supervisor:Dr. Ajay Singh ThapaHead of Department, EDGrande International Hospital

Discussion Topics•Lung Mechanics: 13 slides•Alveolar-Blood Gas Exchange: 5 slides•Transport of O2 and CO2: 4 slides•Regulation of Respiration: 4 slides•Hypoxemia and its types: 8 slides

Respiratory PhysiologyLung Mechanics

Volumes and Capacities of Lung

4 volumes:Tidal volumeInspiratory reserve volumeExpiratory Reserve VolumeResidual Volume

4 capacities:Functional residual capacityVital capacityTotal Lung Capacity

InspiratoryReserveVolume

Lung mechanics

Ventilation• Total Ventilation

▫Total volume of air moved in or out of the lungs per minute

• Alveolar ventilation▫Represents room air delivered to the respiratory

zone per minute• Why the gap??

▫Anatomic Dead space is the space in the respiratory system prior to the respiratory zone

*Physiological Dead Space= Anatomic dead space + Alveolar dead space

Lung Mechanics•Muscles of Respiration

▫Inspiration: diaphragm▫Expiration: primarily passive process;

abdominal muscles•Forces acting on Lung System

▫Intra-pleural pressure, Intra-alveolar pressure

▫Lung Recoil (tissue collagen/elastins, surface tension: Laplace law)

Mechanics Under Resting ConditionDuring

Inspiration

Before During End OfIntra pleural

Pressure (cm H2O)-5 More negative

less than -5-8

Lung Recoil Force (cm H2O)

5 More positiveMore than 5

8

Alveolar Pressure 0 slightly negative (-1)

0

Before Inspiration

End Inspiration

Expiration??•Passive process•Relaxation of inspiratory muscles returns

intra-pleural pressure to -5 cm H2O•Followed by lung deflation, driven by lung

recoil till it becomes equal to intra-pleural pressure

•Smaller alveoli containing larger amount of gases: intra-alveolar pressure increases

•Air flows outside and the intra-alveolar pressure becomes zero.

Intra-pleural and Intra-alveolar pressures during respiration

Intra-pleural and Intra-alveolar pressures: Applied Part

•Pneumo-thorax•Positive Pressure Ventilation

▫Assisted Control Mode Ventilation▫Positive End Expiration Pressure

Lung Recoil•Tissue Elastins/ Collagens•Surface Tension: Laplace Law

•Role of Surfactant??▫Decrease surface tension▫Bias the surface tension▫Reduce the chance of pulmonary edema

Surfactant: Applied Aspects

•Respiratory Distress Syndrome

•Atelectasis

•Pulmonary Edema

Lung Compliance•Is the unit change in lung volume for unit

change in pressure.•Has 2 components:

▫steeper part (higher compliance)▫flatter part (lower compliance)

Forced Vital Capacity, Forced Expiratory Volume in 1st second, and their applied aspects

Pulmonary Function Tests: ComparisonObstructive

patternRestrictive

PatternTotal Lung Capacity Forced Expiratory Volume in 1st second (FEV1)

Forced Vital Capacity (FVC) FEV1/FVC Or NormalPeak Flow Functional Residual Capacity (FRC) Residual Volume

Respiratory PhysiologyAlveolar-Blood Gas Exchange

Alveolar Blood Gas Exchange•Partial Pressure of a gas in ambient air:

▫Pgas= Fgas x Patm

•Partial Pressure of a gas in inspired air:▫PIgas = Fgas (Patm-PH2O)

•Partial Pressure of a gas in alveoli:▫PAgas = Fgas(Patm – PH2O)-PAother gases

Alveolar Blood Gas Exchange

Factors Affecting Alveolar CO2 Concentration•CO2

▫PACO2 ▫Increases with increasing CO2 production

(increased metabolism)▫Inverse relation with alveolar ventilation

Hyperventilation: doubled ventilation, PACO2

decreases by half Hypoventilation: halved ventilation, PACO2

doubled

metabolic CO2 productionalveolar ventilation

Factors Affecting Alveolar O2 Concentration

• PAO2 = FO2 (Patm –PH2O)-(PACO2/RR)

▫RR: respiratory ratio = CO2 produced ml/minO2 consumed ml/min

ALVEOLAR-BLOOD GAS TRANSFER:FICK LAW OF DIFFUSION•Vgas = A/T x D x (P1-P2)•Factors affecting rate of diffusion:

▫Structural factors: a. Surface area for exchange: in emphysema,

in exerciseb. Thickness of membranes between alveolar gas

and capillary blood.▫ Factors specific to each gas present:

a. Diffusion constant: solubility clinically significant

b. Gradient across the membrane

Respiratory PhysiologyTransport of O2 and CO2

Transport of Gases: Introduction

•Down hill flow▫O2: From the alveoli to the tissues, ▫CO2: From the tissues to the alveoli

•Transportation made feasible by:▫Combined with the gas- carrying protein: O2

with hemoglobin (Hb)(99%), increase transportation by 70 fold

▫Series of reversible chemical reactions that convert gases into other compounds: CO2, increase transportation by 17 fold

TRANSPORT OF OXYGEN• Transported as:

▫ Dissolved form▫ Combined with Hb

• 1 gm Hb combines with 1.34 mL of O2

• Normal Hb concentration: 15 mg /dL• Total O2 carried with

Hb: 1.34 x 15=20 mL O2/100 mL of blood

Shifts of Oxygen-Dissociation Curve

• Bohr Effect:• Decreased affinity of

Hb for O2 with acidic pH

Transport of Carbon DioxidePlasma RBC

In Dissolved form(0.3mL%)

•As dissolved solution (0.1mL%)•As carbonic acid ((0.2mL%)

•As Carbonic Acid (0.1mL%)

As carbamino compounds(0.7mL%)

•As carbamino-proteins (0.1mL%)

•As carbamino-haemoglobin (0.6mL%)

As bicarbonates(3mL%)

•As NaHCO3 (2.1mL%)• By phosphate buffer• By protein reduction

•As KHCO3 (0.9mL%)

Transport of Carbon dioxide•Haldane Effect:

▫Increased capacity of deoxygenated Hb to bind and carry CO2 resulting in facilitated CO2 binding at tissue level transport in venous blood release in alveoli

•Chloride Shift

Respiratory Acidosis and Alkalosis•Respiratory acidosis:

▫pH decreases▫Increased arterial PCO2 ▫Compensation: excretion of H+ ion and

retention of HCO3- ions by kidneys

•Respiratory alkalosis:▫pH increases▫Decreased arterial PCO2

▫Compensation: retention of H+ ion and excretion of HCO3

- ions by kidneys

Metabolic Acidosis and Alkalosis•Metabolic Acidosis:

▫Decrease in pH▫Strong acids added to blood, H+ ions fixed

by generation of H2CO3, dissociates in to H2O and CO2, CO2 removed by lungs: rapid process

▫No change in PCO2

▫Compensation: increased ventilation to remove PCO2, returning pH to normal

•Metabolic Alkalosis: ??

Respiratory PhysiologyRegulation of Respiration

Control Systems•Neural Control:

▫Medullary Control: Pre-Botzinger complex (pre-BOTC)

Rhythmic discharges passed through phrenic nerves NK1 receptors and μ-opioid receptors on these

neurons: substance P stimulates and opioids inhibit respiration

Dorsal and Ventral groups of respiratory neurons Efferents to pre-BOTC

▫Pontine Control: Puenmotaxic center (Nucleus parabrachialis,

NPBL) Inspiratory areas and Expiratory areas Afferents from lungs and airways: via vagus nerve. Efferents: Medulla

Neural Centers for Respiratory control

Receptors• Central Chemo-receptors

▫ Stimulated by CSF [H+] and CO2▫ Adaptation occurs▫ Insensitive to PO2 and arterial H+

• Peripheral Chemo-receptors▫ Carotid bodies:

near carotid sinus, afferents to CN IX▫ Aortic bodies:

Aortic arch, afferents to CN X▫ Contains:

H+/CO2 receptors: less sensitive, but maintains the normal drive.

Po2 receptors: responds to PO2 (dissolved O2) and not to total oxygen content(bound to Hb).

Do not contribute to normal drive. Activated if PaO2 <50-60 mmHg

▫ Do not adapt.

Peripheral Chemoreceptors

Respiratory PhysiologyHypoxemia

Hypoxia•Hypoxic Hypoxia (Hypoxemia): reduced

arterial PO2•Anaemic Hypoxia: normal arterial PO2,

decreased carriers (Hb)•Ischaemic/stagnant Hypoxia: normal

arterial Po2 and Hb, decreased blood flow to tissues

•Histotoxic Hypoxia: normal arterial Po2 and Hb, normal flow to the tissues, tissues can’t utilize the delivered O2

Hypoxemia: Four Prime Causes•Ventilation-Perfusion (VA/Q) mismatch•Hypoventilation•Diffusion impairment•Pulmonary shunt

Ventilation-Perfusion Mismatch•Regional Differences in Ventilation

▫Due to effects of gravity over intra-plueral fluid column.

•Regional differences in Perfusion▫Gravity▫Pulmonary artery diameter

Regional Differences in Ventilation

A t the Apex At the BaseAt rest Lower Pressure (More

negative)Alveoli relatively distended

Higher Pressure (Less negative)Alveoli relatively small

During Inspiration

Alveoli receives less air (poor ventilation)

Alveoli receives more air (better ventilation)

Regional Differences in Perfusion

At Apex At BasePulmonary arterial

pressure (mainly due to gravity)

Decreases Increases

Vessels diameter (relative hypoxia) And

Resistance

Relatively constrictedHigh resistance

Relatively dilatedLow resistance

Blood Flow Low High

Ventilation-Perfusion Relationships

At Apex At BaseVentilation Low HighPerfusion Low HighRelatively VA/Q ratio

Over ventilated Under ventilated

HypoventilationIn normal condition:• Alveolar PCO2(PACO2): 40 mmHg

and Alveolar PO2 (PAO2): 100 mmHg

• Equilibrium between alveolar and pulmonary capillary partial pressures

• Due to VA/Q mismatch, systemic PO2 (PaO2): 95mmHg

• A-a gradient: 5-10 mmHgDuring Hypoventilation(for example):• Alveolar PCO2(PACO2): 80 mmHg

and Alveolar PO2 (PAO2): 60 mmHg• Equilibrium between alveolar and

pulmonary capillary partial pressures

• Due to VA/Q mismatch, systemic PO2 (PaO2): 55mmHg

• A-a gradient: 5-10 mmHg (i.e. NORMAL)

Diffusion Impairment• Structural Problem in the

lungs− Decreased surface area (A)− Increased thickness of lung

membrane (T) For Diffusion Impairment:• Alveolar PO2 (PAO2): 100 mmHg• Mismatch between alveolar and

pulmonary capillary partial pressures i.e. PO2 < PAO2

• Due to VA/Q and alveolar-capillary mismatch, systemic PO2 (PaO2): 95mmHg

• A-a gradient: increases• Solution: Increase gradient to

facilitate diffusion.

Pulmonary shunt

Respiratory PhysiologyRecommendations

Respiratory PhysiologyThank you!!