Human The Anatomy Respiratory & Physiology...

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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Human Anatomy & PhysiologySEVENTH EDITION

Elaine N. MariebKatja Hoehn

PowerPoint® Lecture Slidesprepared by Vince Austin,Bluegrass Technicaland Community College

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R22TheRespiratorySystem

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Carbon Dioxide Transport

Carbon dioxide is transported in the blood in threeforms

Dissolved in plasma – 7 to 10%

Chemically bound to hemoglobin – 20% is carriedin RBCs as carbaminohemoglobin

Bicarbonate ion in plasma – 70% is transported asbicarbonate (HCO3

–)

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Bicarbonateion

HCO3–

Hydrogenion

H+↔+ H2O

Water

↔

Carbonicacid

Carbondioxide

+H2CO3CO2

Transport and Exchange of Carbon Dioxide

Carbon dioxide diffuses into RBCs and combineswith water to form carbonic acid (H2CO3), whichquickly dissociates into hydrogen ions andbicarbonate ions

In RBCs, carbonic anhydrase reversibly catalyzesthe conversion of carbon dioxide and water tocarbonic acid



Figure 22.22a

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At the tissues:

Bicarbonate quickly diffuses from RBCs into theplasma

The chloride shift – to counterbalance the outrushof negative bicarbonate ions from the RBCs,chloride ions (Cl–) move from the plasma into theerythrocytes



At the lungs, these processes are reversed

Bicarbonate ions move into the RBCs and bindwith hydrogen ions to form carbonic acid

Carbonic acid is then split by carbonic anhydraseto release carbon dioxide and water

Carbon dioxide then diffuses from the blood intothe alveoli

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Figure 22.22b


Haldane Effect

The amount of carbon dioxide transported ismarkedly affected by the PO2

Haldane effect – the lower the PO2 and hemoglobinsaturation with oxygen, the more carbon dioxidecan be carried in the blood

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Haldane Effect

At the tissues, as more carbon dioxide enters theblood:

More oxygen dissociates from hemoglobin (Bohreffect)

More carbon dioxide combines with hemoglobin,and more bicarbonate ions are formed

This situation is reversed in pulmonary circulation


Haldane Effect

Figure 22.23

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Influence of Carbon Dioxide on Blood pH The carbonic acid–bicarbonate buffer system resists blood

pH changes

If hydrogen ion concentrations in blood begin to rise,excess H+ is removed by combining with HCO3

–

If hydrogen ion concentrations begin to drop, carbonic aciddissociates, releasing H+

Changes in respiratory rate can also: Alter blood pH

Provide a fast-acting system to adjust pH when it isdisturbed by metabolic factors


Control of Respiration:Medullary Respiratory Centers Inspiration is mostly done by movement of the diaphragm

Diaphragm is controlled by the phrenic nerve

Basic respiratory cycle is controlled by the PaceMakwerNeurons (PN)in the medulla oblongata

The PN communicates with the dorsal respiratory group(DRG), or inspiratory center:

Is located near the root of nerve IX

Excites the inspiratory muscles (via phrenic nerve andintercostal nerves) and sets eupnea (12-15 breaths/minute)

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Control of Respiration:Medullary Respiratory Centers The dorsal respiratory group (DRG), also sends signals to

the ventral respiratory group (VRG) :

Appears to be the involved in expiration

Sends signals to the solitary nuclei in medulla

They in turn send inhibitory signals to the DRG. This thusturns off the stimulation of the phrenic nerve and starts theexhalation process.


Control of Respiration:Medullary Respiratory Centers

PN

DRGDRG

DRG Phrenic Nerves

stimulationinhibition

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Pons Respiratory Centers

Pons centers:

Influence and modify activity ofthe medullary centers

Smooth out inspiration andexpiration transitions and viceversa

The pontine respiratory group(PRG)

Pneumotaxic center

Apneustic center


Pons Respiratory CentersPneumotaxic center (PC)

Provides inhibition to the DRG,resulting in shorter periods ofinspiration

Apneustic Center

Provides stimulation of the DRGand could result in deeperinspiration or even breath-holdingat end of inspiration

Main function of PC is to providesmooth transition betweeninspiration and expiration. It tends toinhibit the apneustic center as well.

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Regulation of Respiration

Mammals contain twogroups of chemoreceptors that influencerespiration

Central chemoreceptorsin medulla

Peripheralchemoreceptors (aorticand carotid bodies)


Depth and Rate of Breathing: PCO2

Changing PCO2 levels are monitored by chemoreceptors ofthe brain stem

Carbon dioxide in the blood diffuses into the cerebrospinalfluid where it reacts with water to form hydrogen ions andbicarbonate ions

Since the CFS does not have proteins, it cannot buffer thehydrogen ions and CSF pH drops rapidly

The rising H+ levels, due to an increase in PCO2 levels,prods the central chemoreceptors into activity and resultsin increased depth and rate of breathing

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Depth and Rate of Breathing: PCO2

Hyperventilation – increased depth and rate ofbreathing that:

Quickly flushes carbon dioxide from the blood

Occurs in response to hypercapnia

Hypoventilation – slow and shallow breathing dueto abnormally low PCO2 levels

Apnea (breathing cessation) may occur until PCO2levels rise


Arterial oxygen levels are monitored by the aorticand carotid bodies

Substantial drops in arterial PO2 (to 60 mm Hg) areneeded before oxygen levels become a majorstimulus for increased ventilation

If carbon dioxide is not removed (e.g., as inemphysema and chronic bronchitis),chemoreceptors become unresponsive to PCO2chemical stimuli

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

Depth and Rate of Breathing: PO2

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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22.26


Depth and Rate of Breathing: Reflexes

Pulmonary irritant reflexes – irritants promotereflexive constriction of air passages

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

Upon inflation, inhibitory signals are sent to themedullary inspiration center to end inhalation andallow expiration

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Depth and Rate of Breathing: Higher BrainCenters 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 increaserespiratory rate

Cortical controls are direct signals from thecerebral motor cortex that bypass medullarycontrols

Examples: voluntary breath holding, taking a deepbreath


Depth and Rate of Breathing: Arterial pH 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 mediatedby peripheral chemoreceptors

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 byincreasing respiratory rate and depth

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Medullary Respiratory Centers

Figure 22.25


Chronic Obstructive Pulmonary Disease(COPD) Exemplified by chronic bronchitis and obstructive

emphysema

Patients have a history of: Smoking

Dyspnea, where labored breathing occurs and getsprogressively worse

Coughing and frequent pulmonary infections

COPD victims develop respiratory failureaccompanied by hypoxemia, carbon dioxideretention, and respiratory acidosis

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Pathogenesis of COPD

Figure 22.28


Asthma

Characterized by dyspnea, wheezing, and chesttightness

Active inflammation of the airways precedesbronchospasms

Airway inflammation is an immune responsecaused by release of IL-4 and IL-5, whichstimulate IgE and recruit inflammatory cells

Airways thickened with inflammatory exudatesmagnify the effect of bronchospasms

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Tuberculosis

Infectious disease caused by the bacteriumMycobacterium tuberculosis

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

Treatment entails a 12-month course of antibiotics


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 inperipheral lung area

Small cell carcinoma (20-25% of cases) containslymphocyte-like cells that originate in the primarybronchi and subsequently metastasize

Lung Cancer

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