Transcript
Page 1: The Respiratory System. ANATOMY OF THE RESPIRATORY SYSTEM

The Respiratory System

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ANATOMY OF THE RESPIRATORY SYSTEM

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The Respiratory Tract:

The Lungs

Alveoli

TABLE OF CONTENT

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1) Respiratory Tract:Nose through bronchi 2) The lungs.

THE RESPIRATORY SYSTEM CONSISTS OF:

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The respiratory tract

further divided into the upper and lower respiratory tract

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The upper respiratory tract from the nose through the pharynx

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The lower respiratory tract (The Bronchial Tree)

from the larynx to tertiary bronchi

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The Bronchial Tree

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Alveoli

The Bronchial Tree Extends to Bronchioles and Alveoli

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Bronchioles and Alveoli

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Cartilage Plates

No Cartilage but Smooth Muscles

Bronchioles

Cartilage Ring

asthmaattack

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Cross Section Longitudinal Section

Ciliary Lining of the Lower Respiratory Tract

Cilia

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Electron Micrograph of Cilia

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The cilia beat upward and drive the debris-laden mucus to the pharynx, where it is swallowed.

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THE LUNGS

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The Lungs overlap with the respiratory tract.

Secondary Bronchi

Tertiary Bronchi

Bronchioles

Alveoli

Bronchioles

Alveoli

Primary Bronchi

Inside Lungs

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THE LUNGS

- consist of the left and the right lungs

- The left lung is divided into two lobes; the right into three.

- receives the

bronchus, blood

and lymphatic

vessels, and nerves

through its hilum.

- The bronchi

extend into alveoli

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ALVEOLI

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~700 SF surface area

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Alveoli consists of :

1) type I alveolar cells (95%), thin

2) type II alveolar cells (5%), secrete surfactant.

3) macrophages (dust cells), defense

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- Each alveolus is surrounded with a basket of capillaries.

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surrounded with capillaries

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The respiratory membrane:

1) the wall of the alveolus

2) the endothelial wall of the capillary

3) their fused basement membranes

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Alveoli contain elastic fibers which helps expiration.

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Low blood pressure keeps alveoli dry.

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Gas exchange occurs only in alveoli.

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Dead Space

- starts from nose to terminal bronchiole

- where there is no gas exchange

- ~ 150 mlterminal bronchiole

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The Respiratory Tract:

The Lungs

Alveoli

ANATOMY OF THE RESPIRATORY SYSTEM

SUMMARY

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ventilation

gas exchange

transport by blood

gas exchange

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MECHANICS OF VENTILATION

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Driving Force for Air Flow

Resistance to Airflow

Measurements of Ventilation

Alveolar Ventilation

TABLE OF CONTENTS

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Terms:

inspiration or inhalation: breathing in

expiration or exhalation: breathing out

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Driving Force for Air Flow

Airflow driven by the pressure difference between atmosphere (barometric pressure) and inside the lungs (intrapulmonary pressure).

760 mmHg

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atmospheric pressure = 760 mmHg

Before inspiration

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atmospheric pressure = 760 mmHg

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atmospheric pressure = 760 mmHg

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atmospheric pressure = 760 mmHg

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Mechanism for the Change in Intrapulmonary pressure

Boyle’s Law:

Volume x Pressure = Constant

gas

P V

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Volume Pressure Volume Pressure

Inspiration: Expiration:

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Volume Pressure Volume Pressure

Inspiration: Expiration:

Can the lungs expand/shrink by

themselves?

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1) The Diaphragm

2) External Intercostal Muscles

3) Internal Intercostal Muscles

4) The Abdominal Muscles

- the principal muscle of inspiration

- pulls the diaphragm down, increasing all three dimensions of the thoracic cage.

Major Respiratory Muscles

1) The Diaphragm

2) External Intercostal Muscles

- Inspiration muscles

- increases the anteroposterior and transverse dimensions of the chest.

1) The Diaphragm

2) External Intercostal Muscles

3) The Abdominal Muscles

- Expiration muscles

- pulls the diaphragm up, reducing the vertical dimension of the thoracic cage.

1) The Diaphragm

2) External Intercostal Muscles

3) The Abdominal Muscles

4) Internal Intercostal Muscles

- Extra Expiration muscles

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Coupling Between Lungs and Thoracic Cage

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Visceral pleura covers the surface of each lung; parietal pleura lines the chest cavity.

- The lungs and thoracic cage are coupled by the pleurae.

pleural cavity

- The two pleurae form the pleural cavity.

- The pleural fluid serves to reduce friction during chest expansion.

- Intrapleural pressure: The pressure in the pleural cavity is negative.

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Parietal pleura visceral pleura

Potential pleural cavity(negative intrapleural pressure)

lung

The thoracic cage is larger than the natural size of the lungs.

Generation of the negative intrapleural pressure

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Parietal pleura visceral pleura

Potential pleural cavity(negative intrapleural pressure)

air

air

pneumathorax

lung

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Conclusion

Lungs Thoracic Cagepleurae- pressure

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Inspiration

Contraction of1) diaphragm

2) external intercostal muscles

The lungs are carried along.

Lung volume

pressure

Air flows in.

active

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passive

Resting Expiration

Relaxation of1) diaphragm

2) external intercostal muscles

The lungs shrink.

Lung volume

pressure

Air flows out.

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Forced Expiration

Relaxation of1) diaphragm 2) external

intercostal musclesand

Contraction ofabdominal, internal intercostal and other accessory respiratory

muscles.

Lung volume

pressure

Air flows out.

active

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Driving Force for Air Flow

Atmosphere-lung pressure gradient

Major respiratory muscles

Coupling between lungs and thoracic cage

SUMMARY

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Resistance to Airflow

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TABLE OF CONTENTS Resistance

1) Alveolar Surface Tension

2) Elastic Resistance

3) Airway Resistance

Compliance

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1) Alveolar Surface Tension

- generated by a thin film of liquid over the surface of alveolar epithelium,

- tends to cause a collapse of the alveoli,

- Resists against inspiration.

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Alveoli

Alveolar surface tension is a resistance against inspiration.

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- Surface tension is reduced by surfactant. ( type II alveolar epithelial cells)

Pre-term infants don't have enough surfactant.

type II surfactant

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Resistance 1) Alveolar Surface Tension

2) Elastic Resistance

3) Airway Resistance- Against inspiration due to elastic fibers in the lungs and chest wall,

- Increases in pulmonary fibrosis.

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Resistance 1) Alveolar Surface Tension

2) Elastic Resistance

3) Airway Resistance- Due to friction, affected by airway caliber.

- Against inspiration and expiration!

- Increases during asthma attack (smooth muscle contraction in bronchiole.

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Resistance 1) Alveolar Surface Tension

2) Elastic Resistance

3) Airway Resistance

Compliance

- The reciprocal of resistance,

- An indicator of ease with which the lungs expand.

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Measurements of Ventilation using Spirometer

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Dead Space

inspiration expiration

Alveolar ventilation rate =(tidal volume – dead space) x resp freq (/min)

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Restrictive disorders - (pulmonary fibrosis)

- compliance & vital capacity.

Changes in Spirometric Measures

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- No change in respiratory volumes

- FEV1.

one-second forced expiratory volume

Obstructive disorders

Changes in Spirometric Measures

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MECHANICS OF VENTILATION

SUMMARY

Driving Force for Air Flow

Resistance to Airflow

Measurements of Ventilation

Alveolar Ventilation

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NEURAL CONTROL OF VENTILATION

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Rhythm?

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1) inspiratory center

- stimulates inspiration muscles.

2) expiratory center

- inhibits the inspiratory center,

- stimulates expiration muscles.

Center in the medulla oblongata

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The pons fine-tunes ventilation.

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Afferent Connections to the Respiratory Centers

the limbic system

Hypothalamus

Chemoreceptors the lungs

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Chemoreceptor-initiated Reflexes

Peripheral chemoreceptors

- aortic and carotid bodies,

- monitor O2, CO2 and pH of the blood.

Central chemoreceptors

- close to the surface of the medulla oblongata,

- monitor the pH of the cerebrospinal fluid.

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O2, CO2, or pH

stimulate chemoreceptors

reflex

frequency and depth of respiration

CHEMORECEPTOR-MEDIATED REFLEX

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Voluntary Control

- the motor cortex,

- bypass the brainstem

respiratory centers,

- limited voluntary control.

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GAS EXCHANGE in the LUNGS

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ventilation

gas exchange

transport by blood

gas exchange

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- The gas exchange between

alveolar air and the blood is via

diffusion of O2 and CO2.

- Diffusion of a gas is driven

by O2 and CO2 partial

pressure gradient.

PO2 = 40 mmHgPCO2 = 46 mmHg

PO2 = 104 mmHgPCO2 = 40 mmHg

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The partial pressure of a gas refers to the share of the total pressure generated by a mixture of gases.

O2 CO2

N2

H2O

Total = 760 mmHg

5.3%40 mmHg

13.6%104 mmHg

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PO2 = 40 mmHgPCO2 = 46 mmHg

PO2 = 104 mmHgPCO2 = 40 mmHg

Oxygen and carbon dioxide cross the respiratory membrane and the air-water interface easily.

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Overview of Gas Exchange in the Lungs

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Factors That Affect the Efficiency of Alveolar Gas Exchange

1. partial pressure

2. solubility

3. respiratory membrane thickness/area

4. ventilation-perfusion coupling

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O2

CO2

N2

O2 CO2

N2

H2O

Total = 760 mmHgTotal = 760 mmHg

Air

a) High altitudeb) Hyperbaric chamberc) Obstructive disease

PO2104 mmHgPCO2 40 mmHg

1) Partial pressure

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CO2 has a higher solubility than O2.

CO2 O2

Pressure Gradient 6 mmHg 64 mmHg

PO2104 mmHgPCO2 40 mmHg

2) Solubility

PO2 40 mmHgPCO2 46 mmHg

1) Partial pressure

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2) Solubility

1) Partial pressure

3) Respiratory membrane thickness/area

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4) Ventilation-perfusion Coupling

- average V-P ratio = 0.8

- autoregulated by:

2) Solubility

1) Partial pressure

3) Respiratory membrane thickness/area

PO2 and PCO2

causes:1) vasoconstriction of

pulmonary arterioles2) dilation of bronchioles

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summary

1) Driving force for gas exchange

2) Factors that affect the efficiency of alveolar gas exchange

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Gas transport by the blood

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TABLE OF CONTENT

1) Carbon Dioxide Transport

2) Oxygen Transport

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7% dissolved in the blood as a gas,

23% as carbamino-hemoglobin,

70% as carbonic acid in the plasma.

Carbon Dioxide Transport

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Oxygen Transport

- About 98.5% of O2 in the blood are carried by hemoglobin.

- The rest is physically dissolved in plasma.

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Blood Oxygen Content

- average 20 ml/dL

- determined by:

1) saturation of hemoglobin

2) content of hemoglobin

HypoventilationCO poisoning

anemia

Hypoxemia

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Carbon monoxide competes with oxygen for hemebinding with a much higher affinity.

Problem: deoxygenate hemoglobin

Treatment: hyperbaric oxygen chamber

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GAS EXCHANGE in the TISSUES

1. Carbon Dioxide Loading 2. Oxygen Unloading

How to dissociate?

O2

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O2

PO2 dissociation

PCO2 dissociation

pH dissociation

DPG dissociation

(2,3-diphosphoglycerate)

Temperature dissociation

Dissociation of O2 from hemoglobin (HB) is affected by:

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O2High PO2, low PCO2

association with HG

favor the loading of O2

In Lungs

100% saturated

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High PCO2, low PO2,

low pH, DPG

dissociation of O2

from HG

favor the unloading

O2

In tissues

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High PCO2, low PO2,

low pH, DPG

dissociation of O2

from HG

favor the unloading

O2

In tissues

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Utilization Coefficient

- The amount of oxygen uptake by tissue versus the arterial blood oxygen content

blood

20 ml O2/dL

cellcell

cell cell cell

Utilization Coefficient = 4.4 ml / 20 ml = 22%

15.6 ml O2/dL

4.4 ml O2/dL

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Function of Oxygen ?

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with oxygenwithout oxygen

glucose

2 ATP 38 ATP

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Can human beings produce oxygen?

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Oxygen Toxicity

- Excessive oxygen generates hydrogen peroxide and free radicals, which destroy enzymes and damage nervous tissue.

- Oxidative toxicity with aging.

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Hypercapnia

- PCO2 < 37 mmHg - caused by hyperventilation

Hypocapnia

- PCO2 > 43 mmHg - caused by hypoventilation (respiratory diseases)

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Summary of the Respiratory System

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ventilation

gas exchange

transport by blood

gas exchange

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Oxyhemoglobin Dissociation Curve

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Oxygen Dissociation & Temperature

Active tissue - more O2 released

PO2 (mmHg)

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Oxygen Dissociation & pH

Bohr effect: release of O2 in response to low pH

Active tissue - more O2 released