Student Respiratory

8/8/2019 Student Respiratory

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THE RESPIRATORY SYSTEM

I. Definitions

A. Respiration - O2/CO 2 exchange between the body and the environment.

1. Pulmonary ventilation

2. Diffusion of O2 and CO2

3. Transport of gases to and from tissue

B. Breathing - The movement of gas in and out of the lungs.

C. Lungs - air/blood flow for O2 and CO2 exchange. Maintaining correct CO2partial pressure (PCO 2) is more important than PO2 because of pH.

D. Perfusion (Q) - cardiac output

EF. Partial pressure- How gases are measured.

II. Structural Basis of Breathing

A. Airways - structural/functional characteristics

Trachea cartilaginous support Have smooth muscle.

9 Can constrict airways

Bronchi esp. term. bronchioles

9 Have cilia; secrete mucus

Bronchioles conducting zone

9

Terminal

bronchioles

9

Respiratory

bronchioles

9 Diameter depends on

Alveolar ducts "terminal respiratory lung volume

9 unit"; primary areas of

Alveoli gas exchange


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Alveoli have thin walls and a large

surface area.

B.Pulmonary capillaries - cover 70-80% of alveolar walls. Capillary volume can

increase through recruitment and distension.


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C. Definitions

1. Inspiration - active phase of

breathing. Diaphragm and

external intercostal muscles.

2. Expiration - usually a passive

process. Abdominal muscles andinternal intercostal muscles can

participate.

D. Lung expansion and contraction -

1. Transpulmonary pressure - pressure difference between thoracic cavity and

alveoli.

2. Compliance - how easily lung expands.

Determined by:

a. elasticity of tissue

b. surface tension

Lung compliance measures the force that is needed toexpand the lungs, or the ease of expansion. A lung with ahigh compliance is easy to expand, whereas a lung with alow compliance is stiff and hard to expand. The opposing orcompressive forces are the lung elasticity and surfacetension.

Emphysema - loss of elastic fibers, so itincreases compliance and decreases

elastance.

Fibrosis decreases compliance, so lung is

harder to expand and collapses further when

exhaling.

Asthma - Increase in airway resistance due to

constriction of smooth muscles.

3. Surface tension - attraction of water molecules for each other at the

interface with air. This collapses alveoli.

4. Surfactant - Mixture of phospholipids, apoproteins and Ca2+ secreted by

type II alveolar cells. Decreases surface tension.

Neonatal respiratory distress syndrome


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III. Alveolar Ventilation -

A. Typical volumes and capacities:

VT = tidal volume = vol. of air in each breath.


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C. Relationship between


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E. Alveolar Gas Equation - predicts PAO2 based on PACO2.

PAO2. PO2 (air) - PACO2/R (R = Respiratory exchange ratio= CO2production/O 2 consumpt ion) Ideally, R = 0.8

R is related to metabolic rate, energy sources, activity, etc.

Use PACO2 to estimate PAO2:

During exercise, R can decrease to 0.53. PAO2 and PACO2 dont change because

of the ventilation/perfusion ratio (


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IV. Ventilation/Perfusion Ratios (


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Smoking leads to:

1) small bronchioles become obstructed, causing excessive physiological

shunt

2) alveolar walls become damaged causing excessive physiological dead

space. (wasted ventilation)

3) incr. compliance of lungs4) increases in allergies and asthma

Matching Q and


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V. Neural/Central regulation of


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B. Spinal integration - mechanoreceptors in muscles stimulate spinal motor

neurons to inhibit their activity

C. Chemoreceptors - responsive to [H+] and [CO2].

i CO 2 + H2O W H2CO 3W H+ + HCO3- (bicarbonate) i

carbonic anhydrase

1. Central chemoreceptors - along surface of medulla; sensitive to[H+].

2. Peripheral chemoreceptors - carotid bodies; sense PCO2 and PO2

D.


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Change in Va in responseto a change in PCO2

Change in PCO2 inresponse to a change in Va

Likewise, reduced PaO 268


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VI O2 and CO2 Transportation

A. O 2 Transportation - Reversible binding

of O 2 to Hb:

O2-Hemoglobin Equilibrium Curve:

1. O2 is picked up in the lungs and

released in tissues

2. Hb buffers blood PO2 from major

changes.

B. Factors affecting HbO2 equilibrium curve

1. [H+], PCO 2 - Bohr effect.

2. Incr. temp. or 2,3-diphosphoglycerate3. CO - decreases O2 binding capacity

C. CO2 Transport

In the blood, CO2 is transported as:6 HCO3

- (ionic form; 90% of CO2 in blood)

6 protein bound (carbamino-CO2; HbCO2)

6 40 ml/L dissolved in plasma as a gas

CO 2 + H2O W H2CO 3W H+ + HCO3

-

8

Carbonic anhydrase


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In red blood cells this goes very rapidly. End products are eliminated by:

1. H + combining with Hb 6 HHb

2. HCO3- diffuses into plasma in exchange for Cl-.

3. HCO3- attaching to Hb 6 HbHCO3

D. Modulation of CO2 binding to Hb - Haldane effect

PO2 decreasesCO2 binding to Hb. This nearly doubles the CO2 exchange in

the lungs.

= tissue conditions

= alveolar capillaries CO2-

bound

= change going from Hb

tissue to alveoli

E. [H+] Regulation - maintain pH 7 .4, range 7.2-7.6; damaging beyond 6.7

and 7.8.

pH - log[HCO3-]

PCO 2


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1. pH - PCO 2 - HCO3- relationship Bicarbonate is potent buffer;

8acids cause HCO3- to be converted to CO2 and H2O:

carbonic anhydrase

H+

+ HCO3-

6 H2CO 3W CO 2 + H2O

and CO2 is eliminated in lungs. Hb acts as an additional buffer

if8CO 268H+

if8HCO3-69H+

2. pH - bicarbonate diagram

At a given PCO 2, as you increase

pH, [HCO3-] goes up. If you

increase PCO 2, the curve shifts to

the left. The Buffer slope line

represents the buffering

capacity of the blood, especially available Hb.

During exercise, you get an8in acids.

i. Hb buffers some H+, so buffer slope line drops.

ii. HCO3- buffers some, so get 9[HCO3-].iii. 8PCO 2 causes 8 ventilation; with over compensation you get 9PCO 2.

3. Physiologic factors controlling pH

a. respiratory control mechanisms:

b. renal mechanisms (discussed in upcoming lectures on Renal system)


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Nicotine in urine of smokers' babiesBy LEE BOWMAN, Scripps Howard News Service

May 14, 2006

Scientists have found cancer-causing chemicals from tobacco smoke in the urine of nearly half the babies ofsmoking parents they tested in a new study.

The study found "substantial uptake" of nicotine and the chemical NNAL in 67 of 144 infants, or 47 percent, and the

levels were directly related to how much their parents smoked around them in the home or car. NNAL is a byproductof a toxin in tobacco that's known to cause lung cancer.

"The take-home message is: Don't smoke around your kids," said Stephen Hecht, a cancer-prevention researcher atthe University of Minnesota Cancer Center who led the study, published Friday in the journal Cancer Epidemiology,Biomarkers and Prevention.

Hecht and his team collected urine samples from the infants, 3-12 months, and interviewed parents about smokinghabits. Eighty-two percent of the babies' mothers were daily smokers and 72 percent had other family members,including fathers, who smoked.

Parents or other family members of babies who had detectable levels of NNAL smoked an average of 76 cigarettesa week in the home or car with the infants present. Children with undetectable levels of the chemical had familymembers who smoked an average of 27 cigarettes near the babies each week. Nearly all the babies had detectablelevels of nicotine, as well as cotinine, the byproduct that's left as the body metabolizes nicotine.

However, Hecht said that the difference likely reflects the limits of the equipment used by the researchers. "Withmore sensitive analytical equipment, the NNAL from urine of babies in lower-frequency smoking households wouldmost likely be detectable."

The infants' NNAL levels were higher than those seen in studies of adults exposed to secondhand smoke in thehome.

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