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Chapter 35: Structure and Function of the Pulmonary System

Tara Morgan

The primary function of the pulmonary system is the exchange of gases between

the environmental air and the blood.

•

○ Ventilation, the movement of air into and out of the lungs

Diffusion, the movement of gases between air spaces in the lungs and the

bloodstream

○

Perfusion, the movement of blood into and out of the capillary beds of the

lungs to body organs and tissues

○

• There are three steps in this process:

The first two functions (ventilation and diffusion) are carried out by the

pulmonary system and the third (perfusion) by the cardiovascular system.

•

Normally the pulmonary system functions efficiently under a variety of conditions

and with little energy expenditure.

•

Structures of the Pulmonary System

The pulmonary system includes two lungs and the upper and lower airways, and

the blood vessels that serve them; the chest wall, or thoracic cage; and the

diaphragm.

•

○ 3 in the right lung (upper, middle, lower)

○ 2 in the left lung (upper, lower)

• The lungs are divided into lobes:
• Each lobe is further divided into segments and lobules.

The mediastinum is the space between the lungs and contains the heart, great

vessels, and esophagus.

•

• A set of conducting airways, or bronchi, delivers air to each section of the lung.

The diaphragm is a dome-shaped muscle that separates the thoracic and

abdominal cavities and is involved in ventilation.

•

•

FIGURE 35.1 Structural Plan of the Respiratory System. The inset shows alveolar

sacs where the interchange of oxygen and carbon dioxide takes place through the

walls of the grapelike alveoli. Capillaries surround the alveoli.

•

The lungs are protected from a variety of exogenous contaminants by a series of

mechanical and cellular defenses.

•

These defense mechanisms are so effective that in the healthy individual,

contamination of the lung tissue itself, particularly by infectious agents, is rare.

•

STRUCTURE

OR

SUBSTANCE

MECHANISM OF DEFENSE

Upper

respiratory tract

mucosa

Maintains constant temperature and humidification of gas entering

the lungs; traps and removes foreign particles, some bacteria, and

noxious gases from inspired air

Nasal hairs and

turbinates

Trap and remove foreign particles, some bacteria, and noxious

gases from inspired air

Week 2:

Respiratory Disorders and Alterations in Acid/Base Balance,

Fluid and Electrolytes

turbinates gases from inspired air

Branching

airways

Disrupt laminar flow and enhance deposition of particles and

pathogens on ciliated mucosa

Mucous blanket Protects trachea and bronchi from injury; traps most foreign

particles and bacteria that reach the lower airways

Innate immune

proteins

Lysozyme, lactoferrin, defensins, collectins (surfactant protein A

[SP-A] and surfactant protein D [SP-D]), and immunoglobulin A

(IgA); recognize and promote killing of pathogens

Cilia Propel mucous blanket and entrapped particles toward the

oropharynx, where they can be swallowed or expectorated

Alveolar

macrophages

Ingest and remove bacteria and other foreign material from alveoli

by phagocytosis (see Chapter 7)

Surfactant Enhances phagocytosis of pathogens and allergens in alveoli;

down-regulates inflammatory responses

Irritant receptors

in nares

(nostrils)

Stimulation by chemical or mechanical irritants triggers sneeze

reflex, which results in rapid removal of irritants from nasal

passages

Irritant receptors

in trachea and

large airways

Stimulation by chemical or mechanical irritants triggers cough

reflex, which results in removal of irritants from the trachea and

large airways

Conducting Airways

The conducting airways provide a passage for the movement of air into and out of the

gas-exchange structures of the lung.

•

Lined with ciliated mucosa with a rich vascular supply that warms and humidifies

inspired air and removes foreign particles from it as it passes into the lungs.

•

• The nasopharynx, oropharynx, and related structures are called the upper airway.

The mouth and oropharynx provide for ventilation when the nose is obstructed or

when increased flow is required, for example, during exercise. Filtering and

humidifying are not as efficient with mouth breathing.

•

FIGURE 35.2 Structures of the Upper Airway.

The larynx connects the upper and lower airways and consists of the endolarynx and

its surrounding triangular-shaped bony and cartilaginous structures.

•

The slit-shaped space between the true cords forms the

• glottis.

The endolarynx is formed by two pairs of folds: the false vocal cords (supraglottis)

and the true vocal cords.

•

• The vestibule is the space above the false vocal cords.
  • Epiglottis

The laryngeal box is formed by three large cartilages

• Epiglottis

• Thyroid

▪ Arytenoid

▪ Corniculate

▪ Cuneiform

○ And three smaller cartilages-connected by ligaments

• Cricoid

The supporting cartilages prevent collapse of the larynx during inspiration and

swallowing.

•

The internal laryngeal muscles control vocal cord length and tension, and the external

laryngeal muscles move the larynx as a whole.

•

The internal muscles contract during swallowing to prevent aspiration into the trachea

and contribute to voice pitch.

•

The trachea , which is supported by U-shaped cartilage, connects the larynx to the

bronchi , the conducting airways of the lungs.

•

This area is very sensitive and when stimulated can cause coughing and airway

narrowing.

•

• The trachea divides into the two main airways, or bronchi, at the carina

Aspirated fluids or foreign particles thus tend to enter the right lung rather than

the left.

•

The left mainstem bronchus branches from the trachea at about a 45 - degree angle.

The right mainstem bronchus is slightly larger and more vertical than the left

(branches at about a 20- to 30-degree angle from the trachea).

•

The right and left main bronchi enter the lungs at the hila, or “roots” of the lungs,

along with the pulmonary blood and lymphatic vessels.

•

From the hila the main bronchi branch into lobar bronchi and then to segmental and

subsegmental bronchi, and finally end at the sixteenth division in the smallest of the

conducting airways, the terminal bronchioles

•

FIGURE 35.3 Conducting Airways and Respiratory Unit. A, Structures of respiratory

airways. B, Changes in bronchial wall with progressive branching. C, Electron

micrograph of alveoli: long white arrow identifies type II alveolar cells (pneumocytes -

secretes surfactant); short white arrowhead identifies pores of Kohn; red arrow

identifies alveolar capillary. D, Plastic cast of pulmonary capillaries at high

magnification.

• Epithelial lining
• Smooth muscle layer
• Connective tissue layer
• The bronchial walls have 3 layers:

In the large bronchi (up to approximately the tenth division), the connective tissue

layer contains cartilage.

•

The epithelial lining of the bronchi contains single - celled exocrine glands—the mucus-

secreting goblet cells —and ciliated cells.

•

High columnar pseudostratified epithelium lines the larger airways and becomes

progressively thinner, changing to columnar cuboidal epithelium in the bronchioles

and squamous epithelium in the alveoli

•

The submucosal glands of the bronchial lining produce a mucous blanket that

protects the bronchial epithelium.

•

The ciliated epithelial cells rhythmically beat this mucous blanket toward the trachea

and pharynx, where it can be swallowed or expectorated by coughing.

•

and pharynx, where it can be swallowed or expectorated by coughing.

Toward the terminal bronchioles, ciliated cells and goblet cells become more sparse,

and smooth muscle and connective tissue layers thin

•

Gas-Exchange Airways

These thin-walled structures participate in gas exchange, and the clusters of

alveoli are sometimes called the acinus

•

The conducting airways terminate in the respiratory (terminal) bronchioles, alveolar

ducts, and alveoli

•

The walls of the respiratory bronchioles are very thin, consisting of an epithelial

layer devoid of cilia and goblet cells, very little smooth muscle fiber, and a very

thin and elastic connective tissue layer.

•

These bronchioles end in alveolar ducts , which lead to alveolar sacs made up

of numerous alveoli.

•

The bronchioles from the sixteenth through the twenty-third divisions contain

increasing numbers of alveoli and are called respiratory bronchioles.

•

The alveoli

are the primary gas-exchange units of the lung, where oxygen enters the

blood and CO2 is removed

•

Tiny passages called pores of Kohn permit some air to pass through the septa from

alveolus to alveolus, promoting collateral ventilation and even distribution of air

among the alveoli. The lungs contain approximately 50 million alveoli at birth and

about 480 million by adulthood.

•

FIGURE 35.4 Alveoli. Bronchioles subdivide to form tiny tubes called alveolar ducts that end in

clusters of alveoli called alveolar sacs.

• Essential for adequate gas exchange
• Preventing entry of foreign agents
• Regulates ion and water transport
• Maintains mechanical stability of the alveoli
• Lung epithelial cells provide a protective interface with the environment

The alveolar septa consist of an epithelial layer and a thin, elastic basement

membrane but no muscle layer

•

• Type I alveolar cells provide structure

Type II alveolar cells secrete surfactant , a lipoprotein that coats the inner

surface of the alveolus and facilitates its expansion during inspiration, which

lowers alveolar surface tension at end-expiration, thereby preventing lung

collapse (atelectasis).

•

• Two major types of epithelial cells (pneumocytes) appear in the alveolus.

Contribute to control of lung inflammation by decreasing release of

proinflammatory mediators

•

• Prevents oxidative injury
• Regulates the role of fibroblasts in airway remodeling.

Bacteriostatic and function as opsonins in presenting pathogens to alveolar

macrophages.

•

• Surfactant

Macrophages are the most numerous immune cells present in the lung environment

and provide innate immune defense of the airway from the bronchi to the alveoli.

•

In the alveoli, alveolar macrophages provide protection by clearing surfactant from the

lung and ingesting foreign material and pathogens that reach the alveolus, preparing

these substances for removal through the lymphatics - Phagocytosis

•

Surfactant and alveolar macrophages work together with the normal pulmonary

microbiota to prevent lower lung infection.

•

Pulmonary and Bronchial Circulation

• provides an extensive surface area for gas exchange
• delivers nutrients to lung tissues
• acts as a blood reservoir for the left ventricle

serves as a filtering system that removes clots, air, and other debris from the

circulation

•

• The pulmonary circulation;

circulation

• arteries
• capillaries
• veins
• The pulmonary vasculature is composed of three compartments connected in series:

FIGURE 35.5 The Pulmonary Circulation. The right and left pulmonary veins and

arteries and the branching capillaries are illustrated. Note the pulmonary artery

carries venous blood, and the pulmonary vein carries arterial blood.

Although the entire cardiac output from the right ventricle goes into the lungs, the

pulmonary circulation has a lower pressure and resistance than the systemic

circulation.

Pulmonary arteries are exposed to about one-fifth the pressure of the systemic

circulation and have a much thinner muscle layer.

• Mean pulmonary artery pressure is 18 mmHg; mean aortic pressure is 90 mmHg.

About one-third of the pulmonary vessels are filled with blood (perfused) at any given

time.

More vessels become perfused when right ventricular cardiac output increases.

Therefore, increased delivery of blood to the lungs does not normally increase mean

pulmonary artery pressure.

During exercise, pulmonary arterial pressure will normally increase, but not to more

than 30 mmHg and is age and sex dependent.

The pulmonary artery

divides and enters the lung at the hilus, branching with each

main bronchus, and with the bronchi at every division.

The arterioles divide at the terminal bronchiole to form a network of pulmonary

capillaries around the acinus.

Capillary walls consist of an endothelial layer and a thin basement membrane, which

often fuses with the basement membrane of the alveolar septum

• • alveolar epithelium
  • the alveolar basement membrane
  • an interstitial space
  • the capillary basement membrane
  • and the capillary endothelium

The shared alveolar and capillary walls compose the alveolocapillary membrane , a

very thin membrane made up of the;

• Gas exchange occurs across the alveolocapillary membrane.

These extremely thin alveolar walls are easily damaged and can leak plasma and

blood into the alveolar space.

•

With normal perfusion, approximately 100 mL of blood in the pulmonary capillary bed

is spread very thinly over about 70 to 100 m2 of alveolar surface area.

•

FIGURE 35.6 Cross Section Through an Alveolus Showing Histology of the Alveolar -

Capillary Membrane (Respiratory Membrane). The dense network of capillaries forms

an almost continuous sheet of blood in the alveolar walls, providing a very efficient

arrangement for gas exchange.

• Each pulmonary vein drains several pulmonary capillaries.
  • They are similar to veins in the systemic circulation, but they have no valves.

Unlike the pulmonary arteries, which follow the branching bronchi, pulmonary veins

are dispersed randomly throughout the lungs and then leave the lung at the hila and

enter the left atrium.

•

The bronchial circulation is part of the systemic circulation and receives 1% of the

cardiac output.

•

• trachea
• bronchi and its branches
• esophagus
• visceral pleura
• the vasa vasorum of the thoracic aorta
• and the pulmonary arteries
• and to the nerves
• pulmonary veins

and lymph nodes in the thorax.

• The bronchial arteries supply blood to the:

Not all of the capillaries drain into their own venous system. Some empty into the

pulmonary vein and contribute to the normal venous admixture of oxygenated and

deoxygenated blood or right-to-left shunt

•

The bronchial circulation does not participate in gas exchange.

• • The deep lymphatic capillaries begin at the level of the terminal bronchioles.

Fluid and alveolar macrophages migrate from the alveoli to the terminal

bronchioles, where they enter the lymphatic system.

•

The superficial lymphatic capillaries drain the membrane that surrounds the

lungs.

•

Both deep and superficial lymphatic vessels leave the lung at the hilum through

a series of mediastinal lymph nodes.

•

The lymphatic system plays an important role in keeping the lung free of fluid

and providing immune defense.

•

Lung vasculature also includes deep and superficial pulmonary lymphatic

capillaries.

•

Control of the Pulmonary Circulation

The caliber of pulmonary artery lumina decreases as smooth muscle in the arterial

walls contracts.

•

• Contraction increases pulmonary artery pressure.
• Caliber increases as these muscles relax, decreasing blood pressure.

Contraction (vasoconstriction) and relaxation (vasodilation) primarily occur in

response to local humoral conditions, even though the pulmonary circulation is

innervated by the autonomic nervous system (ANS), as is the systemic circulation.

•

The most important cause of pulmonary artery constriction is a low alveolar partial

pressure of oxygen (PAO2).

•

If only one segment of the lung is involved, the arterioles to that segment

constrict, shunting blood to other, well-ventilated portions of the lung. This reflex

improves the lung's efficiency by better matching ventilation and perfusion.

•

If all segments of the lung are affected, vasoconstriction occurs throughout the

pulmonary vasculature, and pulmonary hypertension (elevated pulmonary artery

pressure) can result.

•

Vasoconstriction caused by alveolar and pulmonary venous hypoxia, often termed

hypoxic pulmonary vasoconstriction , results from an increase in intracellular

calcium levels in vascular smooth muscle cells in response to low oxygen

concentration and the presence of charged oxygen molecules called oxygen free

radicals.

•

Chronic alveolar hypoxia can result in inflammation and structural remodeling in

pulmonary arterioles, causing permanent pulmonary artery hypertension that

eventually leads to right heart failure.

•

An elevated PaCO2 value without a drop in pH does not cause pulmonary artery

constriction.

•

• histamine
• prostaglandins
• endothelin
• serotonin

Other biochemical factors that affect the caliber of vessels in pulmonary circulation

are:

•

• serotonin
• nitric oxide
• and bradykinin

Chest Wall and Pleura

• The chest wall (skin, ribs, intercostal muscles) protects the lungs from injury.

The intercostal muscles of the chest wall, in conjunction with the diaphragm , perform

the muscular work of breathing.

•

The t horacic cavity

is contained by the chest wall and encases the lungs

• • It then folds over itself and attaches firmly to the chest wall.
• A serous membrane called the pleura adheres firmly to the lungs.

The membrane covering the lungs is the visceral pleura; that lining the thoracic

cavity is the parietal pleura.

•

Normally only a thin layer of fluid secreted by the pleura (pleural fluid) fills the

pleural space. About 18 mL of fluid is in the pleural space with a pH of about 7.6,

a few cells, about 1 g/dL protein, and glucose and electrolyte concentrations that

approximate those of the plasma.

•

This lubricates the pleural surfaces, allowing the two layers to slide over each

other without separating. Pressure in the pleural space is usually negative or

subatmospheric (−4 to −10 mmHg).

•

• The area between the two pleurae is called the pleural space, or pleural cavity.

FIGURE 35.7 Thoracic (Chest) Cavity and Related Structures. The thoracic cavity is

divided into three subdivisions (left and right pleural divisions and mediastinum) by a

partition formed by a serous membrane called the pleura.

____________________________________________________________________

Chapter 35

Functions of the pulmonary system

Keisha Svitak

Functions of the Pulmonary System:

**1. Ventilate the alveoli

2. Diffuse gases into and out of the blood
3. Perfuse the lungs to send O2 rich blood throughout body**

Ventilation ≠ Respiration

Ventilation- mechanical movement of gas or air into and out of lungs

Respiration- the exchange of O2 and CO2 during cellular metabolism

Ventilatory rate- breaths/min

Tidal volume- volume of air per breath (L/breath)

ventilatory rate/tidal volume = L/min of effective ventilation

Minute volume (Minute ventilation) - volume of air inspired & expired per minute

calculated by

pH- concentration of hydrogen ions (H+)

Observation of ventilatory rate (breaths/min), pattern, effect -- No

By arterial blood gas analysis measurement of PaCO2 --YES

How does the healthcare professional accurately determine adequacy of

ventilation?

CO2 elimination is necessary to maintain normal levels (important role in

regulation of acid-base balance)

CO2 in arterial blood diffuses across blood-brain barrier until PaCO2 is

equal on both sides (blood & CSF)

Regulates ventilation through effect on H+ content in CSF

↑ PaCO2 leads to ↓ pH ( ↑H+)

PaCO2- partial pressure of arterial CO2, normal PaCO2 = 40mm Hg

PaO2- partial pressure of arterial O2, normal PaO2 = 60mm Hg (measured by

arterial blood gas)

↓PaO2 & pH (well below normal) leads to ↑ ventilation

- As PaO2 ↑, O2 moves from plasma into RBC (erythrocytes) and binds to

hemoglobin molecules and continues to bind until hemoglobin molecules are

all binded to oxygen. Oxygen continues to diffuse across alveolocapillary

membrane until PaO2 and PAO2 equilibriate which ceases O2 diffusion.

- PaO2 values <60 reflects steep part of oxyhemoglobin dissociation curve (Fig

35.16) due to decreased hemoglobin affinity for oxygen

- PaO2 values >60 reflects flatter curve on oxyhemoglobin dissociation curve

- PaO2 values >60 reflects flatter curve on oxyhemoglobin dissociation curve

due to maximum saturation of hemoglobin with oxygen in lungs

PAO2- partial pressure of alveolar O2, normal PAO2 = 104mmHg at sea level

with relaxed breathing

Therefore a pressure gradient of about 60mmHg facilitates diffusion of oxygen

from the alveolus into the capillary (Fig 35.15)

- Different values for PAO2 can be calculated if there are changes in the inspired

oxygen content or the PaCO2, which are common occurrences in clinical

settings.

_

Chemoreceptors- monitor pH, PaCO2, & PaO2 levels

CSF = 1-2mmHg PaCO

a. Sensitive to very small changes in pH of

i. Depth & rate of ventilation which leads to

PaCO2 of arterial blood gas < PaCO2 CSF from CO2 diffusing out

CSF leads to

ii.

iii. Return to normal pH level

b. Central chemoreceptors respond to PaCO2 leads to pH ( H+) by:

Which results in prolonged PaCO2 bicarbonate retention

from renal compensation

2. Bicarbonate diffuses in CSF to normalize pH

Except not under long-term conditions such as COPD as receptors

become insensitive to small changes in PaCO2 from hypoventilation

i.

Peripheral Chemoreceptors take over when central chemoreceptors

reset by chronic hypoventilation

ii.

Central chemoreceptors often able to maintain a normal PaCO2 level under

many conditions including strenuous activity

c.

Central Chemoreceptors- monitor arterial blood indirectly by sensing pH

changes in CSF

A.

As PaO2 & pH peripheral chemoreceptors in carotid bodies respond

by ventilation

i.

ii. Additive effect ventilation if PaCO2 in addition to PaO2 & pH

a. Primarily sensitive to O2 levels in arterial blood (PaO2)

b. Somewhat sensitive to PaCO

Peripheral Chemoreceptors-kick in primarily when central chemoreceptors

reset by chronic hypoventilation

B.

Lung is innervated by ANS and has 3 types of lung sensory receptors:

Cough reflex from noxious aerosols (vapors), gases, and particulate

matter (inhaled dust)

a.

Also stimulated by inflammatory mediators (histamine, serotonin,

prostaglandins), by drugs

b.

Located primarily in epithelium of proximal larger airways (nearly absent in

distal airway)

c.

Irritant receptors- cause bronchoconstriction & ventilatory rate

This reflex assists with ventilation and may protect against excess lung

inflation

a.

This reflex active in newborns & only in adults with high tidal volumes

(exercise, mechanical ventilation)

b.

Located in smooth muscles of airways & sensitive to increases in size or

volume of the lungs

c.

Stretch receptors- cause ventilatory rate & volume leads to Hering-Breuer

expiratory reflex

Located near capillaries in the alveolar septa and in other airway locations

as nociceptors

a.

b. Sensitive to increased pulmonary capillary pressure

Pulmonary C-fiber receptors- cause rapid, shallow breathing; laryngeal

constriction on expiration and mucous secretion; hypotension; and

bradycardia; may be associated with dyspnea

ANS- control diameter of airway lumen by stimulating bronchial smooth muscle

to contract (parasympathetic receptors) and relax (sympathetic receptors).

Figure 35.

Neurochemical Control of Ventilation (Fig 35.9)-

occurs in neurons located in brainstem:

1. Ventral Respiratory Group (VRG)-

inspiratory nerve cells (located in medulla) that

transmit impulses out to diaphragm & intercostal

muscles

2. Dorsal Respiratory Group (DRG)- receives

impulses from various receptors & various stimuli

which alter breathing patterns to restore normal

blood gases

a. Receives impulses from:

i. PNS receptors in carotid & aortic bodies

ii. Receptors in the lung

iii. Various stimuli (mechanical, neural,

chemical)

___

Alterations in any of following mechanics of breathing will increase the work of

breathing to achieve adequate ventilation & oxygenation of the blood:

i. primary muscle of ventilation

Flattens with contraction, volume thoracic cavity & negative

pressure draws gas in lungs

ii.

a. Diaphragm

i. Anterior portion of ribs is elevated with contraction

ii. volume of thoracic cavity by AP diameter

b. External intercostal muscles (muscles between the ribs)

4. Major muscles of inspiration (Fig 35.10)

Also enlarge the thorax (but not as efficiently as diaphragm) by its AP

diameter

a.

b. Include the sternocleidomastoid muscle & scalene muscles

Utilized when minute volume is very high (strenuous exercise or from

disease affecting elastic recoil such as emphysema) or disease blocks the

conducting airways

c.

**5. Accessory Muscles of Inspiration (Fig 35.10):

6. Major muscles of expiration (none as exhalation requires no muscular effort)**

Intraabdominal pressure with contraction, pushing diaphragm up &

volume of thorax

i.

a. Includes the abdominal muscles

i. Pulls down the anterior ribs, AP diameter of thorax

b. Includes the intercostal muscles

Utilized when minute volume is high, when coughing, when airway

obstructed

c.

7. Accessory muscles of expiration (Fig 35.10):

As alveolus becomes smaller, more pressure is required to inflate it,

making it harder to breathe, especially if water lines the alveoli

i.

1. As alveolus becomes smaller, the surface tension

Alveoli larger & less numerous in apexes (upper portions) of

the lungs

a.

2. As alveolus becomes larger, the surface tension

If surfactant production is disrupted/suboptimal, the surface

tension causing alveolar collapse, lung expansion, work of

breathing, and severe gas-exchange abnormalities

Alveolar surface tension can be decreased by surfactant (a lipoprotein

produced by alveoli, allows alveolar ventilation and keeps alveoli free

of fluid)

ii.

Alveolar surface tension- tendency liquid molecules to adhere together

when exposed to air

a.

Elastin fibers in the alveolar walls and in surrounding small airways &

pulmonary capillaries

i.

ii. Surface tension at alveolar air-liquid interface

b. Elasticity lungs (recoils by collapse inward around hila) caused by:

Opposing forces of recoil in lungs and chest wall create small

negative intrapleural pressure

i.

During inspiration: diaphragm & intercostal muscles contract, air

flows into lungs with most tidal volume distributed to bases of

lung (where compliance is greater), and chest wall expands

During expiration: the muscles relax and elastic inward recoil of

lungs causes thorax to decrease in volume until balance between

chest wall & lung recoil forces

Balance between recoil in lungs and chest occurs at rest at end of

expiration (Fig 35.11)

ii.

Elasticity of chest wall (recoils by expanding outward laterally) is

supported by configuration of its bones and musculature

c.

Measured by volume change (tidal volume)/pressure change (airway

or pleural pressure)

i.

Compliance- reciprocal of elasticity, measure of lung and chest wall

distensibility (stretch)

d.

8. Elastic properties of the lungs & chest wall

or pleural pressure)

1. Occurs with normal aging and disorders such as emphysema

compliance indicates lungs or chest wall is abnormally easy to

inflate and has lost some elastic recoil

ii.

1. Occurs with ARDS, pneumonia, pulmonary edema, & fibrosis

Work of breathing may be increased considerably when lung

(pulmonary edema) & chest wall compliance (spinal deformity

or obesity) leading to increased O2 consumption & inability to

maintain adequate ventilation

compliance indicates lungs or chest wall is abnormally stiff or

difficult to inflate

iii.

Normally very low airway resistance (especially in conducting airways

of lungs due to large cross-sectional area)

i.

1/2 to 2/3 resistance occurring primarily in the nose, followed by

oropharynx & larynx

ii.

Airway resistance- determined by length, radius, diameter, & cross-

sectional area of the airways

a.

b. Bronchodilation- airway resistance

Bronchoconstriction- airway resistance from irritants, inflammatory

mediators

c.

i. Edema of the bronchial mucosa

Airway obstructions such as mucus plugging (asthma or bronchitis),

tumors, or foreign bodies

ii.

Other means of airway resistance

d.

9. Resistance to airflow through the conducting airways

___

Gas transport involves delivery of O2 to the cells of the body (#1) and removal

of CO2 (#2) (gas exchange is compromised if respiratory or cardiovascular

disorder impairs any step in this process)

Ventilation of the lungs, diffusion of oxygen from alveoli into capillary blood,

perfusion of systemic capillaries with oxygenated blood, & diffusion of oxygen

from systematic capillaries into cells

Diffusion of CO2 from the cells into the systematic capillaries, perfusion of the

pulmonary capillary bed by venous blood, diffusion of CO2 into alveoli, removal

of CO2 from the lung by ventilation

Blood remains in pulmonary capillary bed for about 3/4 second, but only 1/

second required for oxygen concentration to equalize across the

alveolocapillary membrane. This allows for ample time for oxygen to diffuse

into the blood even during increased cardiac output, which speeds blood flow.

Barometric pressure (PB) (atmospheric pressure)- pressure exerted by gas

molecules in air at specific altitudes

A. Sea level (barometric pressure is 760mm Hg)

a. Calculated by % gas x barometric pressure

i. Greater in smaller area due to more collisions of gas molecules

ii. with heat as heat speed of gas molecules which collisions

b. Measurement of gas pressure

That is why pulmonary function laboratories specify temp & humidity

of a gas at time of all pressure & volume measurements.

Partial pressure of water vapor exerts pressure 47mm Hg at 98.6F

regardless of barometric pressure. However, before determining partial

pressures of other gases in the mixture, water vapor must be subtracted

from barometric pressure [ie. (760-47) x % gas].

c.

B. Partial pressure-portion of total pressure exerted by any individual gas

Amount of oxygen in alveoli (PAO2) estimated by using alveolar gas

equation:

i.

Partial pressure of oxygen molecules (PO2) is much greater in alveolar gas

than in capillary blood which promotes rapid diffusion from alveolus into the

capillary

a.

equation:

PAO2 = PiO2 (inspired partial pressure of O2) - PaCO2/0.8 (the respiratory

quotient)

ii.

PiO2 = Barometric pressure (760) - vapor pressure (47mmHg) x FiO

[fraction (%) of inspired air (0.21)]

iii.

b. Figure 35.15 shows partial pressure of respiratory gases in normal respiration

- Ventilation & perfusion are greatest in the lower lobes as most tidal volume

occurs in alveoli lung bases and because greater pressure causes greater

perfusion.

Ventilation-Perfusion Ratio or V/Q: ratio of ventilation to perfusion

A. Ventilation exceeds perfusion in apexes

B. Perfusion exceeds ventilation in bases

Normal V/Q ratio is 0.8 (which is amount perfusion exceeds ventilation under

normal condition)

C.

Ventilation & perfusion

1. Standing or sitting: Pulmonary blood flow greatest to bases of lungs

Right Side-lying: Pulmonary blood flow greatest on lateral side right lung

& medial side left lung

Left Side-lying: Pulmonary blood flow greatest on lateral side left lung &

medial side right lung

4. Supine: Pulmonary blood flow greatest on posterior side of both lungs

depend on body position with areas of lungs most gravity dependent become

the best ventilated and perfused (Fig 35.13)

D.

Blood flow through pulmonary capillary bed increases in regular

increments from apex to base

Distribution of perfusion also affected by alveolar pressure (gas pressure in

alveoli) in lungs (Fig 35.14).

E.

i. No blood flow occurs due to capillary bed collapsing

ii. Located at apex of lung

1. Zone I: Alveolar pressure (PA) > arterial (Pa) & venous pressures (Pv)

Blood flow occurs, but alveolar pressure compresses the venules (venous

ends of capillaries)

i.

ii. Located above level of left atrium

2. Zone II: arterial pressure (Pa) > Alveolar pressure (PA) > venous pressure (Pv)

Blood flow fluctuates, depending on difference between arterial & venous

pressures

i.

ii. Located at base of lung

3. Zone III: Both arterial (Pa) & venous pressures (Pv) > Alveolar pressure (PA)

Oxygen Transport

- Approximately 1000ml (1L) of O2 is transported to the cells of the body each

minute by:

3% oxygen dissolves in plasma (0.003ml/dL per mmHg) (as diffuses across

alveolocapillary membrane) where it exerts pressure of oxygen in arterial blood

(PaO2).

5. 97% oxygen binds to hemoglobin molecules (max 1.34ml/g)

SaO2- % of available hemoglobin that is bound to oxygen (measured using

oximeter)

Figure 35.

Figure 35.

Figure 35.

oximeter)

Total arterial oxygen content- hemoglobin (Hb) available to bind to oxygen,

SaO2, & PaO

Total venous oxygen content- normal venous oxygen content is 15-16ml/dL, the

partial pressure of mixed venous blood (PvO2) & venous oxygen saturation

(SvO2) are used in place of SaO2 & PaO2 above

Often seen as compensatory mechanism in pulmonary diseases that

impair gas exchange

Those with cardiovascular disease compensatory mechanism to

accelerate cardiac output is ineffective, therefore requires compensatory

mechanism of increasing Hb more important

in hemoglobin concentration may O2 content

in hemoglobin concentration below normal value of 15mL/DL of blood O

content

Oxyhemoglobin Association and Dissociation (Fig 35.16)

Oxyhemoglobin (HbO2)- forms when hemoglobin molecules bind with oxygen

in the lungs

Hemoglobin saturation with oxygen-where oxygen binds to hemoglobin

Hemoglobin desaturation- where oxygen is released from hemoglobin (now

able to carry more CO2 than hemoglobin saturated with O2)

Oxyhemoglobin dissociation curve- graph plots hemoglobin saturation &

desaturation results in S-shaped curve

which promotes association in the lungs & inhibits dissociation in the

tissues

**2. Lower partial pressure is necessary to maintain 50% O2 saturation

3. Caused by alkalosis (high pH) & hypocapnia (decreased PaCO2)
4. Caused by hypothermia & decreased 2,3-DPG levels**

*In Lungs caused by CO2 diffusing from blood into alveoli which reduces

CO2 level

A. Left shift- indicates hemoglobin's increased affinity for oxygen

Increase in ease in which oxyhemoglobin dissociates & oxygen moves

into cells

**2. Larger partial pressure is necessary to maintain 50% O2 saturation

3. Caused by acidosis (low pH) & hypercapnia (increased PaCO2)**

Caused by hyperthermia & increased levels of 2,3-DPG (substance in

erythrocytes)

*In tissues caused by increased levels of CO2 & H+ produced by metabolic

activity

B. Right shift- indicates hemoglobin's decreased affinity for oxygen

*Bohr effect-The shift in oxyhemoglobin dissociation curve caused by changes

in CO2 & H+ concentration in the blood

Carbon Dioxide Transport:

- CO2 is 20x more soluble than O2 and diffuses quickly from tissue cells into

blood & enhanced when O2 diffuses out of blood and into cells

- Approximately 200mL of CO2 is produced by the tissues per minute at rest as

byproduct of cellular metabolism transported in blood by:

Dissolved in plasma as CO2 diffuses out of cells into the blood (5% arterial,

10% venous)

- CO2 combines with H20 with the help of the enzyme carbonic anhydrase,

which forms carbonic acid that quickly dissociates into H+ and

bicarbonate (HCO3-)

Transported as bicarbonate (HCO3-) out of RBC into the plasma (60% arterial,

90% venous)

- Drop in SaO2 at tissue level increases ability of Hb to carry CO2 back to

lung by attaching to reduced hemoglobin (desaturated hemoglobin)

Combined with blood proteins (hemoglobin in particular) to form carbamino

compounds (Fig 3.13)

Haldane effect (effect of O2 on CO2 transport)- In tissue capillaries, O

dissociation from hemoglobin facilitates the pickup of CO2 & binding of O2 to

hemoglobin in the lungs facilitates the release of CO2 from the blood.

- Diffusion of CO2 in the lung is so efficient that diffusion defects that cause

hypoxemia (low O2 content in blood) do not cause hypercapnia (excessive CO

in blood).

___________________________________________________________

Chapter 36

- Clinical manifestations of pulmonary alterations-Carlo Enrico Yap

I. Signs and Symptoms of Pulmonary Disease

A. Dyspnea

• Subjective breathing discomfort

-

Most common symptom of cardiac and respiratory dse

• Evolves across 3 constructs: sensory (intensity), affective (distress), and impact on

daily activities

• Severity of the experiences DOES NOT DIRECTLY correlate severity of disease

-

Mechanism:

stimulation of mechanoreceptors and chemoreceptors that interact

with the respiratory centers and motor cortex

• Signs : flaring of nostrils, use of accessory muscles, retractions (common in children

OR adults who are thin)

-

Dyspnea on exertion:

dyspnea that presents during exercise

• Paroxysmal Nocturnal Dyspnea (PND): pulmonary or cardiac dse = waking at

night gasping

for air and must sit up or stand to relieve the dyspnea

B. Cough

• A protective reflex to clear airway with explosive expiration, occurs when irritants

stimulate the receptors in the airway → vagus nerve stimulation

• Fewer irritant receptors in the distal bronchi = secretions can accumulate w/o

stimulating cough reflex

• Opiates and serotonergic agents can modulate cough reflex

o Ex: Upper resp tract infections, acute bronchitis, PNA, CHF, PE, or aspiration

-

Acute cough:

resolves in 2-3 weeks OR resolves w/ treatment of underlying dse

o Non-smokers chronic cough = post nasal drainage, nonasthmatic eosinophilic

bronchitis, asthma, GERD, heightened cough reflex sensitivity

o Smokers chronic cough = chronic bronchitis

o A inhibitors → chronic cou resolved when d

• Chronic cough: >3 weeks , up to 7-8 weeks, seen in some cases of viral infection

C. Abnormal Sputum

• Provides info about disease progression and effectiveness of therapy

o Not to be confused with hemoptysis: vomiting blood → dark, acidic pH + food

Infarction

o Indicates: damage to bronchi d/t infection/inflammation, cancer, pulmonary

• Hemoptysis: bloody sputum → bright red, alkaline pH, + frothy sputum

D. Abnormal Breathing Patterns

• Eupnea = normal breathing, 8-15/min; tidal volume = 400 to 800 mL
• Pathophysiologic changes →

change in rate, depth, regularity, and effort of breathing

o Caused by metabolic acidosis i.e. strenuous exercise

• Kussmaul breathing (hyperpnea) = slight increase in rate, very large tidal volume,

and no expiratory pause

o Obstruction of LARGE airways→ slowed rate but increased effort, long

inspiration and expiration, stridor (high-pitched during inspiration), and wheezing

(whistling sounds on expiration).

o Obstruction of SMALL airways→ rapid ventilation, small tidal volume,

increased effort, prolonged expiration

• Labored breathing: increased work of breathing ←obstruction of airway
• Restricted breathing: stiffened lungs or chest wall, decreased compliance i.e.

Pulmonary fibrosis→ small tidal volume, rapid rate

o i.e. shock and severe cerebral hypoxia

- Gasping : irregular and quick inspiration with expiratory pause

o Apnea Æ high-volume ventilations Æ Apnea

o Results from conditions that lead to slow blood flow to the brain stem Æ

slowed impulses that send info to brain stem

-

Cheyne-Stokes respirations:

alternating periods of deep and shallow.

E. Hypo/Hyperventilation

- Hypoventilation: inadequate alveolar ventilation →increased PaCO2 (hypercapnia)

o Can cause somnolence or disorientation; secondary hypoxemia (high CO

displaces O2 in the alveolus).

→

increased pH in the blood →

respiratory acidosis

o Common is severe anxiety and acute head injury

- Hyperventilation:

lungs expel CO2 at a higher rate → decreased PaCO

(hypocapnia)→respiratory alkalosis

F. Cyanosis: bluish discoloration of the skin and mucus membranes

• Increased desaturated Hgb (appears bluish in the blood).
• Peripheral cyanosis = poor circulation → peripheral vasoconstriction e.g.

Raynaud's dse, cold environments, severe stress

o Caused by pulmonary dses and cardiac right-to-left shunts

• Central cyanosis = decreased oxygen in arteries (low PaO2, seen in oral mucus

membranes and lips

• NO CYANOSIS DOES NOT MEAN NORMAL OXYGENATION e.g. severe anemia

and carbon monoxide poisoning

G. Clubbing: bulbous enlargement of the end of a digit

• Painless
• Develops gradually
• Seen in dses that cause chronic hypoxemia e.g. bronchiectasis, cystic fibrosis,

lung abcess,CHF

H. Pain : usually originates in the pleurae, airways, or chest wall.

• Pleural pain is most common: sharp or stabbing during inspiration d/t

infection/inflammation of parietal pleura i.e. pleuritis, pleurisy, PE

• *pleural friction rub can be auscultated over the painful area

• *pleural friction rub can be auscultated over the painful area
• Central chest pain = tracheal or bronchial infection/inflammation
• Pulmonary HTN can cause pain during exercise and can be mistaken for cardiac

pain (angina pectoris)

• Pain in the chest wall = rib fracture? Excessive coughing, costochondritis; can be

reproduced by pressing on the sternum or ribs

II. Conditions Caused by Pulmonary Disease or Injury

A. Hypercapnia: hypoventilation→ increased PaCO2 → cerebral vasodilation →

increased ICP → coma, somnolence

o Drugs Æ central depression

o Dses of the medullar e.g. CNS infections, trauma

o Abnormalities in spinal conduction pathways

o Neuromuscular disease e.g myasthenia gravis

o Abnormalities of the thoracic cage

o Obstruction of large airways, tumors, sleep apnea

• Causes:
  • Hypoxia: low oxygenation of cells in tissues

o problems in O2 delivery in the alveoli

o problems in diffusion and perfusion

• Causes:

B. Hypoxemia:

low PaO

CAUSES OF HYPOXEMIA

MECHANISM COMMON CLINICAL CAUSES

Decrease in inspired

oxygen (decreased FiO2)

High altitude

Low oxygen content of gas mixture

Enclosed breathing spaces (suffocation)

Hypoventilation of the

alveoli

Lack of neurologic stimulation of the respiratory center

(oversedation, drug overdose, neurologic damage)

Defects in chest wall mechanics (neuromuscular

disease, trauma, chest deformity, air trapping)

Large airway obstruction (laryngospasm, foreign body

aspiration, neoplasm)

Increased work of breathing (emphysema, severe

asthma)

Ventilation-perfusion

mismatch

Asthma

Chronic bronchitis

Pneumonia

Acute respiratory distress syndrome

Atelectasis

Pulmonary embolism

Alveolocapillary diffusion

abnormality

Edema

Fibrosis

Emphysema

Decreased pulmonary

capillary perfusion

Intracardiac defects

Intrapulmonary arteriovenous malformations

C. Acute Respiratory Failure: aka respiratory lung failure

• Inadequate gas exchange where PaO2 is </= 50mmHg or PaCo2 is >/=50 with a

pH </= 7.

• Hypercapnic RF : inadequate alveolar ventilation
• Hypoxemic RF: inadequate exchange of oxygen between the alveoli and capillaries
• Results from either direct or indirect lung injury
• Complication of major surgery or post-op complication (atelectasis, PNA, Pulmonary

edema, or PE).

• Smokers are at higher risk

____________________________________________________________________

Chapter 36:Disorders of the Chest Wall and Pleura

Samantha Garey

Pleural Abnormalities

Clinical manifestations: sudden pleural pain, tachypnea, and dyspnea. Absent or

decreased breath sounds. Tension pneumo: hypoxemia, tracheal deviation away

from affected lung, and hypotension.

Diagnosis: Chest XR, ultrasound, CT scan

Treatment: Aspiration, usually with insertion of chest tube that is attached to a

water seal drainage system with suction

Pneumothorax: the presence of air or gas in the pleural space cause by a rupture in the

visceral pleura (which surround the lungs) or the parietal pleura and chest wall.

➢

• Spontaneous rupture of blebs (blister-like formations) on the visceral

pleura. Ruptured blebs damage visceral pleura creating a conduit for air to

travel from the lower airways into the pleural space (bronchopleural

fistulae)

• Risk factors: smoking, family history of folliculin gene, Birt-Hogg-Dube

syndrome

4. Primary (spontaneous) pneumothorax:
   • Caused by chest trauma such as rib fractures, stab or bullet wounds,

surgical procedure that tears pleura

5. Secondary (Traumatic) pneumothorax:

Primary and secondary can present as either open or tension:

Open pneumothorax: air pressure in the pleural space equals barometric pressure because

air that is drawn into the pleural space during inspiration is forced back out during expiration.

air that is drawn into the pleural space during inspiration is forced back out during expiration.

Tension pneumothorax: the site of pleural rupture act as a one-way valve, permitting air to

enter on inspiration but preventing its escape by closing on expiration. As more air enters the

pleural space, air pressure begins to exceed barometric pressure pushing against the recoiled

lung causing compression atelectasis, displacing the heart, great vessels, and trachea.

•

____

Tension Pneumothorax. Air in the pleural space causes the lung to collapse around the hilum and may shift the trachea and mediastinal contents

(heart and great vessels) toward the other lung.

• Pleural Effusion: The presence of fluid in the pleural space.

TYPE OF

EFFUSION

SOURCE OF ACCUMALATION PRIMARY OR ASSOCIATED DISORDER

Transudate

(Hydrothor

ax)

Watery fluid that diffuses out of capillaries

beneath the pleurae (i.e., capillaries in lung or

chest wall)

Cardiovascular disease-causing hypertension:

liver or kidney disease that disrupts plasma

protein production, causing hypoproteinemia

(decreased oncotic pressure in the blood

vessels)

Exudate

Fluid rich proteins (leukocytes, plasma

proteins of all kinds) that migrate out of

capillaries

Infection, inflammation, or malignancy of the

pleurae that stimulates mast cells to release

biochemical mediators that increase capillary

permeability

Empyema

(pus)

Detritus of infection (microorganisms,

leukocytes, cellular debris) dumped into the

pleural space by blocked lymphatic vessels

Pulmonary infections, such as pneumonia; lung

abscesses; infected wounds

Microorganisms- staphylococcus aureus, E. coli,

anaerobic bacteria, and Klebsiella pneumoniae

Hemothor

ax (blood)

Hemorrhage into the pleural space Traumatic injury, surgery, rupture, or

malignancy that damage blood vessels

Chylothora

x (chyle)

Chyle (milky fluid containing lymph and fat

droplets) that is dumped by lymph vessels

into the pleural space instead of passing from

the gastrointestinal tract to the thoracic duct

Traumatic injury, infection, or disorder that

disrupts lymphatic transport

• Small collections of fluids may not affect lung function and remain undetected.
• Most will be removed by the lymphatic system

Larger effusions can cause dyspnea, compression atelectasis and impaired ventilation causing

hypoxemia.

•

Physical exam: decreased breath sounds, pleural friction rub upon auscultation, dullness to

percussion on the affected side.

•

➢ Infected Empyema effusion: cyanosis, fever, tachycardia, cough, pleural pain

Diagnosis & treatment: Chest imaging and thoracentesis (needle aspiration), sputum culture,

chest tube placement, surgical interventions, antibiotics.

______________________________________________________________

Chapter 36: Pulmonary disorders- Brenda Milner

Restrictive lung disorders are characterized by a decrease in compliance of

lung tissue. This causes more effort to expand the lungs during inspiration.

People with lung restriction have dyspnea, increased resp rate and decreased

tidal volume.

Restrictive lung diseases can cause V/Q mismatch and affect the

alveolocapillary membrane, this can reduce diffusion of O2 from alveoli into the

blood and cause hypoxemia.

Common restrictive disorders:

3 types:

1) Compression atelectasis- external pressure on lung tissue (tumor or

fluid)

2) Absorption atelectasis- gradual absorption of air from obstructed or

hypoventilated alveoli or inhaling concentrated O2.

3) Surfactant impairment- decreased production of surfactant

Aspiration – fluid or solids get passed into the lungs.

Bronchiectasis- persistent abnormal dilation of bronchi.

BOOP is a complication in which the alveoli and bronchioles are filled with

plugs of connective tissue.

BOS is an inflammatory fibrotic process that is a complication of lung

transplant.

Bronchiolitis- most common in children. Inflammation of small airways or

bronchioles.

Idiopathic pulmonary fibrosis- more common in men after age 60. Most

common idiopathic lung disorder, survival rate 2-5 years. Chronic

inflammation at multiple lung sites. Alveolar collapse and fibroproliferative

response cause increased thickening of the alveolocapillary membrane

causing decreased diffusion of O2 and hypoxemia.

Pulmonary Fibrosis- large amount of fibrous or connective tissue in the lungs

(scar tissue).

Environmental lung disorders:

Exposure to toxic gases- Common toxic gases are ammonia, hydrogen

chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide. Inhaled

particles can cause damage to airway epithelium, cilia, and alveoli. Oxygen

toxicity occurs with high concentrations of supplemental oxygen.

Pneumoconiosis- inhalation of inorganic dust particles. The dust of silica,

asbestos and coal are most common cause.

Hypersensitivity pneumonitis- inhalation of organic particles or fumes. Is an

allergic inflammatory disease.

Systemic disorders

Granulomatosis disorders: Sarcoidosis, Wegener granulomatosis,

lymphomatoid granulomatosis, eosinophilic granuloma.

Connective tissue diseases: RA, lupus, scleroderma, polymyositis, Sjogren

syndrome, cystic fibrosis, Goodpasture syndrome.

Pulmonary edema- excess water in the lung. Most common cause left-sided

heart disease. Pulmonary edema begins to develop at the pulmonary capillary

wedge pressure or left atrial pressure of 20mmHg.

Factors for pulmonary edema left-sided heart disease, causing increased

pulmonary venous pressure; injury to pulmonary capillary endothelium (ARDS)

and inhalation of toxic gases; lymphatic obstruction.

Postobstructive pulmonary edema is a rare life-threatening complication that

can occur after relief of upper airway obstruction.

High-altitude pulmonary edema occur at altitudes usually more than 8000- 10000

feet.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)- acute lung

inflammation and diffuse alveolocapillary injury.

ARDS most severe. Acute onset of bilateral infiltrates on xray not explained by

cardiac failure. A low ratio of partial pressure of arterial oxygen to the fraction

of inhaled oxygen. Most common factors genetic, sepsis, trauma.

Exudative (inflammatory)- 72 hours release of inflammatory cytokines.

Lungs become less compliant and work of breathing increases, ventilation

of alveoli decreases, and hypercapnia develops.

Proliferative- within 1-3 weeks after injury resolution of pulmonary edema

and proliferation of fibroblasts, myofibroblasts and type II pneumocytes

with surfactant recover.

Fibrotic- 2 - 3 weeks after injury remodeling and fibrosis occur.

ARDS 3 phases:

Clinical manifestation of ARDS:

Evaluation and treatment:

History of lung injury, examination (Fine inspiratory crackles), ABG’s and chest x - ray.

Treatment include early detection, supportive care, prevention of complications.

Obstructive Pulmonary Disease- airway obstruction that is worse with expiration.

Infiltration of the lung by inflammatory cells with the release of large number of

cytokines that cause airway damage and mucus production. Most common are

asthma and COPD.

Asthma- chronic inflammation of the bronchial mucosa that cause bronchial

hyperresponsiveness, constriction of the airway, and variable airflow obstruction that

is reversible. Can develop at any age. Asthma phenotypes are observable

characteristics that include eosinophilic asthma (allergic) vs. neutrophilic asthma,

exercise-induced asthma, aspirin-sensitive asthma, age-at-onset asthma, or steroid

nonresponsive asthma. Endotypes are subgroups that describe the underlying

pathophysiology to the phenotypes.

Early asthmatic response- acute bronchoconstriction that reaches a maximum in the

first 30 minutes and resolves within 1-3 hours. Antigen exposure to the bronchial

mucosa activates dendritic cells to present the antigen to T helper cells, which

differentiate into Th2 cells releasing cytokines. These activate inflammatory cells and

cytokines causing vasoconstriction, increased capillary permeability, mucosal edema,

bronchial smooth muscle constriction and increased mucus secretion.

Late asthmatic response- 4 - 8 hours after early response. Bronchospasm, edema and

mucus secretion with obstruction to airflow. Impaired expiration causes air trapping,

hyperinflation distal to obstructions and increased work breathing. With progressive

obstruction of expiratory airflow, air trapping is severe and lungs and thorax become

hyperexpanded, respiratory muscles are mechanically disadvantaged leading to

decrease in tidal volume with increasing CO2 retention and respiratory acidosis,

which signals respiratory failure.

which signals respiratory failure.

Management of asthma include avoiding allergens or irritants, control symptoms,

preventing exacerbation.

COPD- a common, preventable disease characterized by airflow limitation that is not

fully reversible and is progressive.

2 primary phenotypes:

Chronic bronchitis- hypersecretion of mucus and chronic cough for 3-12 months for

at least 2 years. Inspired irritants promote bronchial inflammation, causing bronchial

edema.

Emphysema- permanent enlargement of gas exchange airways accompanied by

destruction of alveolar walls. Can be centriacinar: septal destruction occurs in the

respiratory bronchiolar walls and alveolar ducts in the center of the pulmonary lobule

(upper lobes) occurs in smokers, paraseptal; similar to centricinar but occurs adjacent

to the pleura and septa of the pulmonary lobule, panacinar; involves the alveolar and

respiratory bronchiolar walls, resulting in global air space expansion with damage

randomly distributed and involving the lower lobes.

COPD 3

rd

leading cause of death in the US.

Risk factors for COPD smoking, occupational dusts and chemicals, indoor air

pollution, and outdoor air pollution

Respiratory Tract Infections-

cold, sore throat, laryngitis (upper airway)

Acute bronchitis- inflammation of large airways or bronchi 90% caused by viruses

Pneumonia- infection of the lower respiratory tract caused by bacteria, viruses, fungi,

protozoa or parasites. 8

th

leading cause of death in US.

Community-acquired (CAP)- m ost common reason for hospitalization.

Healthcare-associated (HCAP)-

occurring in people with recent hospital stays,

nursing homes or other healthcare facility.

Ventilator-associated (VAP)- intubated patients

Pneumococcal Pneumonia- acute lung infection 4 inflammatory phases:

consolidation, red hepatization, gray hepatization, and resolution.

Viral Pneumonia- lung infection caused by the flu. Seasonal, usually mild

TB- lung infection caused by M. tuberculosis. The pathogen can survive in

macrophages, resist lysosomal killing, multiply in the cell and transmit into a stage of

dormancy making it resistant to host defense and medication treatment. Leading

cause of death from a curable disease throughout the world. Highly contagious,

transmitted person to person by inhalation of airborne droplets.

Pulmonary vascular disease

PE- thrombus blocks a portion of the pulmonary vascular, a tissue fragment, or an air

bubble. Depending on location and size can cause hypoxic vasoconstriction,

pulmonary edema, pulmonary hypertension, or death. Usually come from a DVT in

the lower leg.

Pulmonary artery hypertension- caused by elevated left ventricular pressure,

increased blood flow through the pulmonary system, obstruction of vascular bed,

active constriction caused by hypoxemia or acidosis. Mean pulmonary pressure

greater than 25mmHg at rest.

Cor Pulmonale- caused by pulmonary hypertension which causes right ventricular

enlargement. If pulmonary hypertension is not treated will cause right ventricular

failure.

Malignancies of the respiratory tract

Laryngeal cancer- Squamous cell carcinoma of the vocal cords. Occurs most often

in men. Causes hoarseness.

Lung cancer-

Most frequent cancer deaths in the US. Most common cause from

smoking.

Cancer cell types include non–small cell lung cancer (squamous cell carcinoma,

adenocarcinoma, large cell undifferentiated carcinoma) and neuroendocrine tumors

(small cell carcinoma and bronchial carcinoid tumors). Other tumors include small cell

(oat cell) carcinoma, bronchial adenoma, adenocystic tumors (cylindromas),

mucoepidermoid carcinomas (bronchial tumors), and mesothelioma. Each type arises

in a characteristic site or type of tissue, causes distinctive clinical manifestations, and

differs in likelihood of metastasis and prognosis.

____________________________________________________________________

Chapter 37

- Structure and function- Mittal Patel

____________________________________________________________________

Week 2: Chapter 37 Children Upper Respiratory Disorders-Britt Ware-Ojo

Upper Airway Obstruction (UAO)

Stridor is a harsh, vibratory sound of the variable pitch caused by turbulent flow

through the partially obstructed airway.

o

• A common sign of UAO in children is stridor

Infections

is 2 or more episodes of croup without respiratory tract infection (RTI) ▪

▪ Starts and resolves quickly mostly in older children

▪ Recurrent Croup (spasmodic croup):

▪ Occurs in children 6 months to 5 yrs old, peak incidence is about at 2yrs old

▪ Acute laryngotracheitis (croup):

▪ Subglottic edema from infection

The mucous membrane of the larynx is tight on the cartilage, whereas

those of the subglottic space are loose which causes mucosal and

submucosal edema.

▪

The cricoid cartilage is structurally the narrowest point of the airway,

making edema is this area critical.

▪

With edema it causes increased work of breathing which generates more

negative intrathoracic pressure which can cause collapse of the upper

airway.

▪

▪ Pathophysiology of croup

Rhinorrhea (runny nose) ▪

▪ Sore throat

▪ Low grade fever

▪ Harsh (seal-like) cough

Hoarse voice ▪

• Most cases are mild and will resolves in several days
• Severe cases require urgent treatment

▪ Inspiratory stridor

▪ Clinical Manifestations:

• Croup

A barking cough and viral symptoms require no treatment ▪

▪ Having stridor, retractions, or agitation is a sign it’s a sicker child.

• Stridor
• Retractions
• Air entry
• Cyanosis

▪ The Westley Croup Score is a tool that scores:

• Evaluation & Treatment:

• Cyanosis
• Dyspnea

LOC

▪ Croup is mild, moderate, or severe

• Dexamethasone oral

Nebulized epinephrine stimulates a- and b- adrenergic receptors

which decrease airway secretions and mucosal edema

o

• Budesonide nebulized
• Oxygen
• In rare cases intubation is required

▪ Glucocorticoids are oral or injected which improves symptoms in 6 hours

Caused by Haemophilus influenzas type B (Hib) ▪

There is an immunization for Hib, so cases are rare but 25% of epiglottis is still

caused by Hib. Due to no immunizations.

▪

▪ Infants less than 1 year old are at greater risk.

Non infectious causes include trauma from foreign body inhalation and chemical

burns.

▪

• Acute Epiglottis:

Epiglottis is from the posterior tongue base and covers the laryngeal inlet during

swallowing. It has a rich blood and lymphatic circulation.

o

Bacteria of the mucous and inflammation can cause edema, obstructing the

upper airway

o

• Pathophysiology:

▪ Usually occurs in children 2-6 years old

High Fever ▪

▪ Irritability

▪ Sore throat

▪ Hot potato voice

Inspiratory stridor ▪

▪ Respiratory distress

Children will usually be leaning toward (tripod position), drooling and difficult

swallowing

▪

Examination of the throat can cause laryngospasm and cause respiratory

collapse. Death can occur shortly after.

▪

PNA, cervical lymph nodes inflammation, otitis, and rarely meningitis or septic

arthritis may occur.

▪

• Clinical Manifestations

▪ Don’t exam the throat

▪ Intubation sometimes

▪ Culture of the throat, antibiotics

Corticosteroids ▪

If caused by Hib, rifampin should be administered to the household once daily

for 4 days.

▪

• Evaluation & Treatment:

Occurs sometimes due to group A beta-hemolytic Streptococci (GABHS) and

methicillin-resistant Staphylococcus aureus (MRSA)

▪

▪ It’s swelling of the tonsils and pharynx and may cover the mucosa.

▪ Can also occur from infectious mononucleosis (mono)

Treatment includes antibiotics and corticosteroids ▪

• Is usually unilateral and most often complication of acute tonsillitis.
• Causative agent is GABHS

o Fever

Sore throat o

o Difficulty swallowing

o Trismus

o Pooling of saliva

o Muffled voice

• Symptoms are:
• Peritonsillar bulging and cervical adenopathy are visible.
• The abscess must be drained and antibiotics are given
• If the abscess ruptures death can occur

▪ Peritonsillar abscess

▪ Recurrent tonsillitis may require adenotonsillectomy.

• Tonsillar Infections (tonsillitis)

▪ Most common, life threatening upper airway infection for children

▪ MRSA, Hib, GABHS, or Moraxella catarrhalis

▪ Fungus can be the cause in immunocompromised children

• Sinusitis, otitis, PNA, or pharyngitis

▪ Recurring infection

Caused by ▪

Airway edema and copious purulent secretions lead to airway obstruction ▪

Obstruction can be worse due to mucosal sloughing and tracheal

pseudomembrane.

▪

PNA, cardiac arrest, acute respiratory distress syndrome (ARDS), multiple

organ dysfunction.

▪

▪ Death can occur due to:

Tachypnea ▪

▪ Fever

▪ Stridor

▪ Hoarse voice

Cough ▪

▪ Increased secretions from mouth and nose

▪ Clinical presentation

▪ Antibiotics

Inbutation ▪

▪ Treatment

• Bacterial Tracheitis (pseudomembranous croup)

▪ Aerobic, anaerobic, or polymicrobial infection

▪ GABHS, MRSA

o Caused by

Occurs around 4 years old from other nasopharyngeal infection or penetrating

local injury.

o

Retropharyngeal Abscesses:

local injury.

o

▪ Fever

Neck pain ▪

▪ Drooling

▪ Stridor

▪ Dysphagia

Respiratory distress ▪

o Symptoms include:

Antibiotics ▪

▪ Incision and drain (I&D)

o Treatment:

Aspiration of Foreign Bodies

• Occurs mostly in children ages 1-4 years old
• More than 100,000 cases and 100 deaths happen yearly
• Objects may lodge in the larynx, trachea, or bronchi.

o Nuts,

o Seeds

o Hard candy

o Small pieces of hot dog

Toys o

o Coins

o Beans

o Batteries and magnets

• Objects are:

o Coughing, choking, wheezing, or gagging.

• Aspiration event symptoms:

Cough, stridor, hoarseness, inability to speak, decreased breath sounds,

respiratory distress, agitation or panic.

o

• Objects in the larynx cause:
• Objects in the intrathoracic airways cause wheezing.
• Symptoms are determined by the size of the foreign object

o Sweeping the oral airway or the abdominal thrust

o Bronchoscopic removal

Antibiotics if the a small object is lodged for a long period of time and the child

has atelectasis, PNA, lung abscess, or blood-tinged sputum.

o

• Treatment

Angioedema

Is localized edema involving the deep subcutaneous layers of the skin or mucous

membranes

• Angioedema usually starts in eyes and lips first then goes to the airway

o By allergy to peanuts, cow’s milk, chicken eggs

• Angioedema is caused by a mast cell mediated allergic phenomena

Increased levels of bradykinin mediate this adverse effect by causing vasodilation,

increased vascular permeability, and histamine release.

• Using angiotensin-converting enzyme inhibitors for B/P causes angioedema.

o Epi, antihistamines, and corticosteroids

• Treatment

o This is a rare but serious medical problem

o 50% of the cases happen in childhood, ages 8-19.

Angioedema occurs to the limbs, genitalia, abdominal and pelvic area as well as

the face

o

o Labs diagnose C-1 INH

o Treatment

An inherited deficiency of the plasma protein C-1 inhibitor (C-1 INH) causes

hereditary angioneurotic edema (HAE).

Congenital Malformations

• Larynomalacia
• Tracheomalacia
• Vocal Cord Paralysis
• Subglottic Stenosis

o Choanal atresia

o Laryngeal atresia

Tracheal stenosis o

• Other Congential Malformations

Obstructive Sleep Apnea Syndrome (OSAS):

Is partial or intermittent complete UAO during sleeping with disruption of normal

ventilation and sleep patterns.

• OSAS is common in children. About 60% of obese children have OSAS.
• Vulnerable populations are Blacks, Hispanics and preterm infants.

o Second hand smoke

Snoring o

o Genetics

o Socioeconomic status

Possible influences:

o OSAS involves the CNS, cardiovascular, metabolic, and immune systems

Airway narrowing and increased upper airway collapsibility are common causes

of OSAS

o

Obstruction during sleep causes increase respiratory effort, oxygen

desaturation, hypercapnia and arousal.

o

▪ Adenotonsillar hypertrophy,

▪ GERD

▪ Obesity

Craniofacial anomalies ▪

o Airway narrowing can be caused by

o Infants have a greater risk for OSAS because of their anatomy.

o Cerebral palsy and Down syndrome reduced motor tone of the upper airway.

• Pathophysiology: