Human Anatomy & Physiology, Sixth Edition

22The Respiratory System

Breathing Patterns

Eupnea = normal quiet breathing

Apnea = temporary cessation of breathing

Dyspnea =difficult or labored breathing

Modified Respiratory Movements

Coughing

deep inspiration, closure of rima glottidis & strong expiration blasts air out to clear respiratory passages

Hiccuping

spasmodic contraction of diaphragm & quick closure of rima glottidis produce sharp inspiratory sound

Tidal volume = amount air moved during quiet breathing

MVR= minute ventilation is amount of air moved in a minute

Reserve volumes ---- amount you can breathe either in or out above that amount of tidal volume

Residual volume = 1200 mL permanently trapped air in system

Vital capacity & total lung capacity are sums of the other volumes

Lung Volumes and Capacities

Dalton’s Law

Each gas in a mixture of gases exerts its own pressure

as if all other gases were not present

partial pressures denoted as p

Total pressure is sum of all partial pressures

atmospheric pressure (760 mm Hg) = pO2 + pCO2 + pN2 + pH2O

to determine partial pressure of O2-- multiply 760 by % of air that is O2 (21%) = 160 mm Hg

Henry’s Law

Quantity of a gas that will dissolve in a liquid depends upon the amount of gas present and its solubility coefficient

explains why you can breathe compressed air while scuba diving despite 79% Nitrogen

N2 has very low solubility unlike CO2 (soda cans)

dive deep & increased pressure forces more N2 to dissolve in the blood (nitrogen narcosis)

decompression sickness if come back to surface too fast or stay deep too long

Breathing O2 under pressure dissolves more O2 in blood

Hyperbaric Oxygenation

Clinical application of Henry’s law

Use of pressure to dissolve more O2 in the blood

treatment for patients with anaerobic bacterial infections (tetanus and gangrene)

anaerobic bacteria die in the presence of O2

Hyperbaric chamber pressure raised to 3 to 4 atmospheres so that tissues absorb more O2

Used to treat heart disorders, carbon monoxide poisoning, cerebral edema, bone infections, gas embolisms & crush injuries

External Respiration

Gases diffuse from areas of high partial pressure to areas of low partial pressure

Exchange of gas between air & blood

Deoxygenated blood becomes saturated

Compare gas movements in pulmonary capillaries to tissue capillaries

Internal Respiration

Exchange of gases between blood & tissues

Conversion of oxygenated blood into deoxygenated

Observe diffusion of O2 inward

at rest 25% of available O2 enters cells

during exercise more O2 is absorbed

Observe diffusion of CO2 outward

Oxygen Transport in the Blood

Oxyhemoglobin contains 98.5% chemically combined oxygen and hemoglobin

inside red blood cells

Does not dissolve easily in water

only 1.5% transported dissolved in blood

Only the dissolved O2 can diffuse into tissues

Factors affecting dissociation of O2 from hemoglobin are important

Oxygen dissociation curve shows levels of saturation and oxygen partial pressures

Acidity & Oxygen Affinity for Hb

As acidity increases, O2 affinity for Hb decreases

Bohr effect

H+ binds to hemoglobin & alters it

O2 left behind in needy tissues

pCO2 & Oxygen Release

As pCO2 rises with exercise, O2 is released more easily

CO2 converts to carbonic acid & becomes H+ and bicarbonate ions & lowers pH.

Temperature & Oxygen Release

As temperature increases, more O2 is released

Metabolic activity & heat

More BPG, more O2 released

RBC activity

hormones like thyroxine & growth hormone

Carbon Monoxide Poisoning

CO from car exhaust & tobacco smoke

Binds to Hb heme group more successfully than O2

CO poisoning

Treat by administering pure O2

Carbon Dioxide Transport

100 ml of blood carries 55 ml of CO2

Is carried by the blood in 3 ways

dissolved in plasma

combined with the globin part of Hb molecule forming carbaminohemoglobin

as part of bicarbonate ion

CO2 + H2O combine to form carbonic acid that dissociates into H+ and bicarbonate ion

Summary of Gas Exchange & Transport

The dorsal respiratory group (DRG), or inspiratory center:

Is located near the root of nerve IX

Appears to be the pacesetting respiratory center

Excites the inspiratory muscles and sets eupnea (12-15 breaths/minute)

Becomes dormant during expiration

The ventral respiratory group (VRG) is involved in forced inspiration and expiration

Control of Respiration: Medullary Respiratory Centers

Figure 22.24

Control of Respiration: Medullary Respiratory Centers

Pons centers:

Influence and modify activity of the medullary centers

Smooth out inspiration and expiration transitions and vice versa

The pontine respiratory group (PRG) – continuously inhibits the inspiration center

Control of Respiration: Pons Respiratory Centers

A result of reciprocal inhibition of the interconnected neuronal networks in the medulla

Other theories include

Inspiratory neurons are pacemakers and have intrinsic automaticity and rhythmicity

Stretch receptors in the lungs establish respiratory rhythm

Respiratory Rhythm

Inspiratory depth is determined by how actively the respiratory center stimulates the respiratory muscles

Rate of respiration is determined by how long the inspiratory center is active

Respiratory centers in the pons and medulla are sensitive to both excitatory and inhibitory stimuli

Depth and Rate of Breathing

Medullary Respiratory Centers

Figure 22.25

Pulmonary irritant reflexes – irritants promote reflexive constriction of air passages

Inflation reflex (Hering-Breuer) – stretch receptors in the lungs are stimulated by lung inflation

Upon inflation, inhibitory signals are sent to the medullary inspiration center to end inhalation and allow expiration

Depth and Rate of Breathing: Reflexes

Hypothalamic controls act through the limbic system to modify rate and depth of respiration

Example: breath holding that occurs in anger

A rise in body temperature acts to increase respiratory rate

Cortical controls are direct signals from the cerebral motor cortex that bypass medullary controls

Examples: voluntary breath holding, taking a deep breath

Depth and Rate of Breathing: Higher Brain Centers

Changing PCO2 levels are monitored by chemoreceptors of the brain stem

Carbon dioxide in the blood diffuses into the cerebrospinal fluid where it is hydrated

Resulting carbonic acid dissociates, releasing hydrogen ions

PCO2 levels rise (hypercapnia) resulting in increased depth and rate of breathing

Depth and Rate of Breathing: PCO2

Depth and Rate of Breathing: PCO2

Figure 22.26

Hyperventilation – increased depth and rate of breathing that:

Quickly flushes carbon dioxide from the blood

Occurs in response to hypercapnia

Though a rise CO2 acts as the original stimulus, control of breathing at rest is regulated by the hydrogen ion concentration in the brain

Depth and Rate of Breathing: PCO2

Hypoventilation – slow and shallow breathing due to abnormally low PCO2 levels

Apnea (breathing cessation) may occur until PCO2 levels rise

Depth and Rate of Breathing: PCO2

Arterial oxygen levels are monitored by the aortic and carotid bodies

Substantial drops in arterial PO2 (to 60 mm Hg) are needed before oxygen levels become a major stimulus for increased ventilation

If carbon dioxide is not removed (e.g., as in emphysema and chronic bronchitis), chemoreceptors become unresponsive to PCO2 chemical stimuli

In such cases, PO2 levels become the principal respiratory stimulus (hypoxic drive)

Depth and Rate of Breathing: PCO2

Changes in arterial pH can modify respiratory rate even if carbon dioxide and oxygen levels are normal

Increased ventilation in response to falling pH is mediated by peripheral chemoreceptors

Depth and Rate of Breathing: Arterial pH

Peripheral Chemoreceptors

Figure 22.27

Acidosis may reflect:

Carbon dioxide retention

Accumulation of lactic acid

Excess fatty acids in patients with diabetes mellitus

Respiratory system controls will attempt to raise the pH by increasing respiratory rate and depth

Depth and Rate of Breathing: Arterial pH

Respiratory adjustments are geared to both the intensity and duration of exercise

During vigorous exercise:

Ventilation can increase 20 fold

Breathing becomes deeper and more vigorous, but respiratory rate may not be significantly changed (hyperpnea)

Exercise-enhanced breathing is not prompted by an increase in PCO2 or a decrease in PO2 or pH

These levels remain surprisingly constant during exercise

Respiratory Adjustments: Exercise

As exercise begins:

Ventilation increases abruptly, rises slowly, and reaches a steady state

When exercise stops:

Ventilation declines suddenly, then gradually decreases to normal

Respiratory Adjustments: Exercise

Neural factors bring about the above changes, including:

Psychic stimuli

Cortical motor activation

Excitatory impulses from proprioceptors in muscles

Respiratory Adjustments: Exercise

The body responds to quick movement to high altitude (above 8000 ft) with symptoms of acute mountain sickness – headache, shortness of breath, nausea, and dizziness

Respiratory Adjustments: High Altitude

Acclimatization – respiratory and hematopoietic adjustments to altitude include:

Increased ventilation – 2-3 L/min higher than at sea level

Chemoreceptors become more responsive to PCO2

Substantial decline in PO2 stimulates peripheral chemoreceptors

Respiratory Adjustments: High Altitude

Exemplified by chronic bronchitis and obstructive emphysema

Patients have a history of:

Smoking

Dyspnea, where labored breathing occurs and gets progressively worse

Coughing and frequent pulmonary infections

COPD victims develop respiratory failure accompanied by hypoxemia, carbon dioxide retention, and respiratory acidosis

Chronic Obstructive Pulmonary Disease (COPD)

Pathogenesis of COPD

Figure 22.28

Characterized by dyspnea, wheezing, and chest tightness

Active inflammation of the airways precedes bronchospasms

Airway inflammation is an immune response caused by release of IL-4 and IL-5, which stimulate IgE and recruit inflammatory cells

Airways thickened with inflammatory exudates magnify the effect of bronchospasms

Asthma

Infectious disease caused by the bacterium Mycobacterium tuberculosis

Symptoms include fever, night sweats, weight loss, a racking cough, and splitting headache

Treatment entails a 12-month course of antibiotics

Tuberculosis

Accounts for 1/3 of all cancer deaths in the U.S.

90% of all patients with lung cancer were smokers

The three most common types are:

Squamous cell carcinoma (20-40% of cases) arises in bronchial epithelium

Adenocarcinoma (25-35% of cases) originates in peripheral lung area

Small cell carcinoma (20-25% of cases) contains lymphocyte-like cells that originate in the primary bronchi and subsequently metastasize

Lung Cancer