Respiratory Physiology NOTES

ADVENTIST UNIVERSITY OF THE PHILIPINES – COLLEGE OF MEDICINE (BATCH 2019)

Subject Topic No. Lecturer Transcribe r

Respiratory Physiology Title Dr. Torres Date 1.

Pulmonary Ventilation 2.

Main functions: 1. 2. 3. 4.

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Pulmonary ventilation Diffusion of O2 and CO2 Transport of O2 and CO2 Respiratory regulation  Normal quiet breathing: right diaphragm  Inspiration- Respiratory diaphragm contraction  Expiration- elastic recoil  Heavy breathing: extra force contraction of abdominal muscles  Muscles that raise the rib cage: inspiratory muscles External intercostals ‘bucket handle’ Sternocleidomastoid Serratus anterior Anterior scalenius  EFFUSION  Muscles that depress the rib cage: expiratory muscles, internal intercostals, rectus abdominis  Pressures for movement of air in and out of the lungs 1. Pleural 2. Alveolar Going up increase atmospheric pressure

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Transpulmonary pressure: difference between alveolar and pleural pressure PTB- rupture of alveoli= ATELECTASIS , destruction of surfactant Normal compliance= 200ml/cm of h20 Depends on: 1. elastic forces of the lungs 2. elastic forces by surface tension surface tension elastic force: 2/3 of the lungs **total tska dalwang residual di namemeasure ng spirometer

SURFACTANT 

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Measured by spirometer Total Lung capacity, Force residual capacity and Residual Volume: cannot be measured

DEAD SPACE AIR 1. 2. 3. 

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Anatomic dead space Do not engage in gas exchange (fowler’s) Alveolar dead space Cannot engage in gas exchange=0 Physiologic dead space ADS+AlDS= total dead space air (bohr’s) Upper respiratory passages: a) Trachea b) Bronchi (L more vertical, R more horizontal) c) Bronchioles (Primary, secondary, tertiary) 20-25 generations before reaching the alveoli Bronchioles (great resistance in larger bronchi) AUTONOMIC 1. Symphatetic= bronchodilation (beta 2 receptor, adrenergic) 2. Parasympha= bronchoconstriction Lined by goblet cells and cilia (upward stroke) protective Pseudostratified columnar with motile cilia + goblet cells Cigarette smoking- paralysis of cilia and increase mucus secretion

LUNG COMPLIANCE 

 secreted by type II alveolar cells (pneumocytes II) DPPC- dipalmitoyl phosphatidylcholine (type 2 alveolar cell) Aka lamellar bodies (in histology) Type 1- alveolar macrophages La place: pressure in alveoli inversely related to radius “smaller alveoli the greater the collapse pressure Stabilization of the size of the alveoli:

Interdependence- alveolo, ducts, air spaces- share common septal cells Fibrous tissue- 50,000 units surrounded by fibrous septa Surfactant- reduce the surface tension

PULMONARY VOLUMES AND CAPACITIES

LUNG COMPLIANCE 

January 19, 2016

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Most important diagnostic tool differentiating obstructive from restrictive lung disease. restrictive lung disease- decrease FEV1/FVC obstructive lung disease—FEV-1 reduced more than the FVC; marked decrease in ratio. distensibility of lungs and chest wall:  transmural pressure: alveolar pressure- intrapleural pressure  intrapleural pressure negative: lungs expand/ lung volume increase  intrapleural pressure positive: lungs collapse/ lung volume decrease Page 1 of 3

TOPIC TITLE INCREASED 1. 2.

emphysema old age (decreased elastic tissue)

DECREASED 1. 2. 3. 4. 5.

GAS EXCHANGE  

atelectasis pulmonary hypertension pulmonary fibrosis no surfactant pulmonary embolism

RESPIRATORY LAWS 1. 2.

3.

LA PLACE  P2T/R (surfactant action) POISEULLE’S  R= 8nl/r4  Resistance= 8 x viscosity x length/ diameter (radius to the 4th power) BREATHING CYCLE

PULMONARY CIRCULATION

V/Q Ratio (alveolar ventilation/ pulmonary blood flow)  

LUNGS: important blood reservoir= 450 ml (pulmonary blood volume) Hydrostatic pressure gradients in the lungs:  

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Zone 1: top APEX- no blood flow Commonly attacked by TB Zone 2: middle- intermittent blood flow during systole (arterial pressure greater than the alveolar pressure) Less commonly affected by pathologic diseases Zone 3: bottom (base)- high continuous blood flow (capillary pressure greater than alveolar pressure)

PULMONARY EDEMA    

Accumulation of fluid in the lungs Common in Left sided congestive heart failure and mitral valvular disease Damage to pulmonary capillary membraneinfections or breathing Noxious substances-leakage of plasma proteins

Fluid between parietal and visceral fluid 3 ml Etiologies: *same mechanism in edema 1. Blockage of lymphatic drainage 2. CHF 3. Decreased plasma colloid osmotic pressure (oncotic) 4. Increased capillary permeabilityinfection or infection

Highest (>1.0) APEX- PO2 highest PCO2 lowest (ventilation) Lowest (