SCIT 1408 Applied Human Anatomy and Physiology II - Respiratory System Chapter 22 B

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

Respiratory VolumesTV tidal vol

IRV Inspiratory

reserve volume

ERV Expiratory reserve volume

RV Residual volume

Amt air in or out @ rest; 500 ml

Amt air forcibly inhaled after TV; 2100-3200 ml

Amt air forcibly exhaled after TV; 1000-1200 ml

Amt air still in lungs after forceful expiration; 1200 ml


Respiratory Capacity

IC Inspiratory capacity

FRC Functional residual capacity

VC Vital capacity

Max. amt that can be inspired after TV expiration; TV + IRV

Max amt that can be expired after max. inspiration; total exchangeable air; TV+IRV+ERV; 4800 mls in young males

Amt air remaining in lungs after TV expiration; RV + ERV


Dead Space Anatomical dead space – volume of air in the

conducting respiratory passages (150 ml) Alveolar dead space – alveoli that cease to act in

gas exchange due to collapse or obstruction Total dead space – sum of alveolar and

anatomical dead spaces; not available for gas exchange


Pulmonary Function Tests Spirometry – evaluates respiratory function; DX between

Obstructive & Restrictive Disease Obstructive - increased airway resistance;

Example: Chronic bronchitis > TLC, FRC, RV

Restrictive - reduction in total lung capacity; Asbestosis, TB < VC, TLC, FRC, RV

FVC – amt air expelled after taking deep breath & forceful exhalation; reduced FEV in obstructive diseases


Pulmonary Function Tests Obstructive disease

Increases: TLC FRC RV

Decreases: FEV

Restrictive disease Decreases:

VC TLC FRC RV


Alveolar Ventilation

Alveolar ventilation rate (AVR) – measures the flow of fresh gases into and out of the alveoli during a particular time

Slow, deep breathing increases AVR and rapid, shallow breathing decreases AVR

AVR = frequency X (TV – dead space)

(ml/min) (breaths/min) (ml/breath)


Nonrespiratory Air Movements Most result from reflex action Examples include: coughing, sneezing, crying,

laughing, hiccupping, and yawning


Basic Properties of Gases: Dalton’s Law of Partial Pressures Total pressure exerted by a mixture of gases is the

sum of the pressures exerted independently by each gas in the mixture

The partial pressure of each gas is directly proportional to its percentage in the mixture


When a mixture of gases is in contact with a liquid, each gas will dissolve in the liquid in proportion to its partial pressure and its solubility

Carbon dioxide: > soluble Oxygen: < (1/20th) soluble Nitrogen is practically insoluble in plasma

Basic Properties of Gases: Henry’s Law


Composition of Alveolar Gas The atmosphere = > oxygen & nitrogen Alveoli = > carbon dioxide & water vapor These differences from:

Gas exchanges in the lungs – oxygen diffuses from the alveoli and carbon dioxide diffuses into the alveoli

Humidification of air by conducting passages The mixing of alveolar gas that occurs with each

breath


External Respiration: Pulmonary Gas Exchange Factors influencing the movement of oxygen and

carbon dioxide across the respiratory membrane

1. Partial pressure gradients and gas solubilities

2. Matching of alveolar ventilation and pulmonary blood perfusion

3. Structural characteristics of the respiratory membrane


Partial Pressure Gradients and Gas Solubilities The partial pressure oxygen (PO2) of venous blood

is 40 mm Hg; the partial pressure in the alveoli is 104 mm Hg

This steep gradient allows oxygen partial pressures to rapidly reach equilibrium (in 0.25 seconds), and thus blood can move three times as quickly (0.75 seconds) through the pulmonary capillary and still be adequately oxygenated


Partial Pressure Gradients and Gas Solubilities Although carbon dioxide has a lower partial

pressure gradient: It is 20 times more soluble in plasma than oxygen It diffuses in equal amounts with oxygen

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22.17

External resp:

O2 in/CO2 out

Air: alveoli: blood

O2 out/CO2 in

Tissues: blood

Oxygen/carbon dioxide exchanges follow gas partial pressure gradients

These gradients refer to plasma gas content, not gases bound to Hgb

Internal resp:O2 out/CO2 inTissues: blood


Oxygenation of Blood

Figure 22.18

Rapid oxygenation of blood in pulmonary capillaries- 0.25 sec


Ventilation-Perfusion Coupling Ventilation – amt gas reaching alveoli Perfusion – blood flow to alveoli Ventilation and perfusion must be tightly regulated

for efficient gas exchange


Ventilation-Perfusion Coupling Autoregulation in pulmonary arterioles: (opposite from all

other arterioles in the circulation) If PO2 is low, arterioles constrict If PO2 is high, arterioles dilate

PCO2 in alveoli cause changes in the diameters of the bronchioles

In passageways where alveolar PCO2 is high, bronchioles dilate

In passageways where alveolar PCO2 PCO2 is low, bronchioles constrict


Ventilation-Perfusion Coupling

Figure 22.19

Reduced alveolar ventilation;excessive perfusion

Reduced alveolar ventilation;reduced perfusion

Pulmonary arteriolesserving these alveoliconstrict

Enhanced alveolar ventilation;inadequate perfusion

Enhanced alveolar ventilation;enhanced perfusion

Pulmonary arteriolesserving these alveolidilate

PO2

PCO2

in alveoli

PO2

PCO2

in alveoli


Surface Area and Thickness of the Respiratory Membrane Respiratory membranes

0.5 - 1 m thick; allows efficient gas exchange >>> surface area Wet lungs, edema = thickened membranes, < gas

exchange Emphysema,walls of adjacent alveoli break

through, decrease surface area, < gas exchange


Internal Respiration The factors promoting gas exchange between

systemic capillaries and tissue cells are the same as those acting in the lungs The partial pressures and diffusion gradients are

reversed

PO2 in tissue is always lower than in systemic arterial blood

PO2 of venous blood draining tissues is 40 mm Hg and PCO2 is 45 mm Hg

PLAY InterActive Physiology ®: Respiratory System: Gas Exchange, page 3–17


Oxygen Transport Molecular oxygen is carried in the blood:

98.5 % Bound to hemoglobin (Hb) in RBCs Rest is dissolved in plasma


Each Hb molecule binds 4 oxygen atoms Oxyhemoglobin (HbO2) Hemoglobin that has released oxygen is called

reduced or deoxyhemoglobin (HHb)

Oxygen Transport: Role of Hemoglobin

HHb + O2

Lungs

Tissues

HbO2 + H+

Fast & reversible rxn

Oxygen unloading Oxygen loading


Hemoglobin (Hb) Saturated hemoglobin – four O2 bound (1 to each

heme) Partially saturated hemoglobin – 1, 2, or 3 O2 bound After the first O2 binds or unbinds, others bind or

unbind more quickly; (affinity increases with degree of saturation)

The rate that hemoglobin binds and releases oxygen is regulated by:

PO2, temperature, blood pH, PCO2, and the concentration of BPG (biphosphoglycerate)


Influence of PO2 on Hemoglobin Saturation Oxygen-hemoglobin dissociation curve =

Hemoglobin saturation plotted against PO2

98% saturated arterial blood contains 20 ml oxygen per 100 ml blood (20 vol %)

As arterial blood flows through capillaries, 5 ml oxygen are released

The saturation of hemoglobin in arterial blood explains why breathing deeply increases the PO2 but has little effect on oxygen saturation in hemoglobin


Hemoglobin Saturation Curve Hemoglobin is almost completely saturated at a PO2

of 70 mm Hg

Further increases in PO2 produce only small increases in oxygen binding

Further, even when PO2 is below normal levels, oxygen loading and delivery to tissues is ok & unloading is stimulated by < PO2


Only 20–25% of bound oxygen is unloaded during one systemic circulation

If oxygen levels in tissues drop: More oxygen dissociates from hemoglobin and is

used by cells Respiratory rate or cardiac output need not increase

Hemoglobin Saturation Curve


Hemoglobin Saturation Curve

Figure 22.20


Other Factors Influencing Hb Saturation

Temperature, H+, PCO2, and BPG Modify the structure of hemoglobin and alter its

affinity for oxygen > in above:

< hb’s affinity for oxygen > oxygen unloading

< act in the opposite manner These parameters are all high in systemic

capillaries where oxygen unloading is the goal


Other Factors Influencing Hemoglobin Saturation

Figure 22.21

In tissues, exercise > temp > unloading

In tissues, > C02, > unloading


Factors That Increase Release of Oxygen by Hemoglobin As cells metabolize glucose, carbon dioxide is

released into the blood causing: Increases in PCO2 and H+ concentration in capillary

blood Declining pH (acidosis), which weakens the

hemoglobin-oxygen bond (Bohr effect) Metabolizing cells have heat as a byproduct and

the rise in temperature increases BPG synthesis All these factors ensure oxygen unloading in the

vicinity of working tissue cells


Carbon Dioxide Transport Carbon dioxide: in blood in 3 forms

7-10% dissolved in plasma 20% bound to hemoglobin as carbaminohemoglobin

70% (HCO3–) Bicarbonate ion in plasma


CO2 + H2O H2CO3 H+ + HCO3–

Carbon dioxide Water Carbonic

acidHydrogen

ionBicarbonate

ion

Transport and Exchange of Carbon Dioxide Carbon dioxide diffuses into RBCs and combines

with water to form carbonic acid (H2CO3), which quickly dissociates into hydrogen ions and bicarbonate ions

In RBCs, carbonic anhydrase reversibly catalyzes the conversion of carbon dioxide and water to carbonic acid


Transport and Exchange of Carbon Dioxide

Figure 22.22a


Transport and Exchange of Carbon Dioxide

Figure 22.22b


Haldane Effect < PO2, & < hb saturation = > CO2 can be carried in

the blood In tissues, as > CO2 enters the blood:

> oxygen dissociates from hemoglobin (Bohr effect)

> CO2 combines with hemoglobin, > HCO3–

This situation is reversed in pulmonary circulation


Haldane Effect

Figure 22.23


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 acid dissociates, releasing H+


Influence of Carbon Dioxide on Blood pH Changes in respiratory rate can also:

Alter blood pH Provide a fast-acting system to adjust pH when it is

disturbed by metabolic factors

PLAY InterActive Physiology ®: Gas Transport, pages 11–15


Respiratory Control Centers


Depth and Rate of Breathing Inspiratory depth- how much respiratory center

stimulates respiratory muscles Rate of respiration- how long inspiratory center is

active Respiratory centers in the pons and medulla are

sensitive to both excitatory and inhibitory stimuli


Depth and Rate of Breathing- chemical regulation

Most important = arterial blood levels of: CO2 O2 H+

Levels detected by: Central chemoreceptors – medulla Peripheral chemoreceptors- aortic arch & carotids


Neural & Chemical Influences on Brain Stem Respiratory Centers

Figure 22.25

1.

2.

3.5.

4.

6.

7.


Depth and Rate of Breathing: PCO2

> levels detected by chemoreceptors in medulla > blood CO2 diffuses into cerebrospinal fluid

CSF cannot buffer the H+ & < pH; brain protection needed

PCO2 levels rise (hypercapnia):

increased depth and rate of breathing; return to homeostasis

CO2 + H2O H2CO3 H+ + HCO3–

Carbon dioxide Water Carbonic

acidHydrogen

ionBicarbonate

ion



hyperventilation



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

Apnea (breathing cessation) may occur until PCO2 levels rise


Peripheral chemoreceptors monitor arterial O2

< PO2 (to 60 mm Hg) before O2 is stimulus for increased ventilation

If CO2 not removed (emphysema, chronic bronchitis), chemoreceptors adapt, become unresponsive to < PCO2

Then, PO2 levels become the principal respiratory stimulus (hypoxic drive)

Depth and Rate of Breathing: PO2


Peripheral Chemoreceptors

Figure 22.27


Depth and Rate of Breathing: Arterial pH < pH or 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 even if O2 & CO2 levels are ok


Respiratory Adjustments: Exercise From intensity and duration of exercise Vigorous exercise:

> Ventilation - 20 fold Breathing- deeper and more vigorous Respiratory rate may by unchanged Above is called 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: High Altitude Move quickly above 8000 ft

acute mountain sickness – headache, shortness of breath, nausea, and dizziness

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

level Chemoreceptors become more responsive to PCO2

Substantial decline in PO2 stimulates peripheral chemoreceptors


Chronic Obstructive Pulmonary Disease (COPD) Chronic bronchitis and obstructive emphysema Pts have a history of:

Smoking Dyspnea, where labored breathing occurs and gets

progressively worse Coughing, frequent pulmonary infections

Respiratory failure, hypoxemia, carbon dioxide retention, and respiratory acidosis


Pathogenesis of COPD

Figure 22.28

genetic


Asthma 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


Tuberculosis Infectious disease caused by the bacterium

Mycobacterium tuberculosis Symptoms include fever, night sweats, weight loss,

a racking cough, and splitting headache Treatment requires a 12-month course of

antibiotics High in homeless population; low compliance

due to length of treatment


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


Mucosae of the bronchi and lung alveoli are present by the 8th week

By the 28th week, a baby born prematurely can breathe on its own; < surfactant before this

During fetal life, the lungs are filled with fluid and blood bypasses the lungs

Gas exchange takes place via the placenta

Developmental Aspects


Respiratory System Development

Figure 22.29


At birth, respiratory centers are activated, alveoli inflate, and lungs begin to function

Respiratory rate is highest in newborns and slows until adulthood

Lungs continue to mature and more alveoli are formed until young adulthood; teen smoking leads to < alveoli; irreversible deficit

Respiratory efficiency decreases in old age

Developmental Aspects

SCIT 1408 Applied Human Anatomy and Physiology II - Respiratory System Chapter 22 B

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