Mechanics of Breathing Chapter 17 Mechanics of Breathing

About this Chapter Structure and function of the respiratory pumps How gases are exchanged with blood The role of pressures and surfactants in rate of exchange How respiration is regulated

Respiratory System: Overview Lungs: exchange surface 75 m2 Thin walled Moist Ribs & skin protect Diaphragm & ribs pump air

Interesting Facts about the Lungs Each lung contains approximately 150 million alveoli We lose half a liter of fluid a day from breathing Normal breathing rate is between 12-16 breaths per minute, but women and children breathe faster than men Breathing rate may to increase to 60 after exercise The capillaries in the lung would extend approximately 1000 miles if laid end to end Approximately 1500 miles of airways are found in the lungs A typical sneeze travels at a velocity of 100 miles per hour The right lung is larger than the left lung and has three lobes as compared to 2 for the left Every minute we breathe 13 pints of air or 6.15 Liters/min We inhale and exhale approximately 22,000 times/day

Respiratory System: Overview Figure 17-2 b: Anatomy Summary

Respiratory System Structure Conduction zone: pathway for pulmonary ventilation Respiratory zone: membrane for gas exchange  external respiration Clinically, two parts: Upper respiratory tract Lower respiratory tract

Cross Section Through Lung

Smoker’s Lungs Non-smoker 

Lung Tissue slide Respiratory Bronchiole Alveolar Duct Alveoli Alveolar Sac

Functions of the Respiratory System: Overview Exchange O2 Air to blood Blood to cells Exchange CO2 Cells to blood Blood to air Regulate blood pH Vocalizations Protect alveoli Figure 17-1: Overview of external and cellular respiration

The Airways: Conduction of Air from Outside to Alveoli Filter, warm & moisten air Nose, (mouth), trachea, bronchi & bronchioles Huge increase in cross sectional area Figure 17-4: Branching of the airways

Key Gas Laws Reviewed Gas is compressible & flow  with  resistance Air is a mix of gases, each diffuses independently

Key Gas Laws Reviewed Solubility of a gas depends on: Partial pressure of that gas (example: O2 =156 mmHg) Temperature Solubility in a particular solvent Water: solvent for life O2 into water: 0.1 m moles/L (poor) CO2 into water: 3.0 m mole/L (good)

Ventilation: The Pumps Inspiration Expiration Diaphragm Low energy pump Concavity – flattens Thorax: ribs & muscles Pleura: double membrane Vacuum seal Fluid-lubrication

Ventilation: The Pumps Figure 17-11 a: Surfactant reduces surface tension

Respiratory Damage & Diseases Pneumothorax ("collapsed lung") Fibrotic Lung Disease Emphysema Chronic Bronchitis Asthma NRDS

Pink Puffer-Emphysema is Primary Problem A "pink puffer" is a person where emphysema is the primary underlying pathology. As you recall, emphysema results from destruction of the airways distal to the terminal bronchiole--which also includes the gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood.  So, not only is there less surface area for gas exchange, there is also less vascular bed for gas exchange--but less ventilation-perfusion mismatch than blue bloaters.  The body then has to compensate by hyperventilation (the "puffer" part).  Their arterial blood gases (ABGs) actually are relatively normal because of this compensatory hyperventilation.  Eventually, because of the low cardiac output, people afflicted with this disease develop muscle wasting and weight loss.  They actually have less hypoxemia (compared to blue bloaters) and appear to have a "pink" complexion and hence "pink puffer".  Some of the pink appearance may also be due to the work (use of neck and chest muscles) these folks put into just drawing a breath.

Blue Bloater-Chronic Bronchitis is Primary Problem A "blue bloater" is a person where the primary underlying lung pathology is chronic bronchitis. Just a reminder, chronic bronchitis is caused by excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi.  Unlike emphysema, the pulmonary capillary bed is undamaged. Instead, the body responds to the increased obstruction by decreasing ventilation and increasing cardiac output. There is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia.  In addition, they also have increased carbon dioxide retention (hypercapnia).  Because of increasing obstruction, their residual lung volume gradually increases (the "bloating" part).  They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces--the "blue" part. Link to website detailing pathophysiology of emphysema and chronic bronchitis is listed below: http://www.pathophys.org/copd/#Pathogenesis_pathophysiology_and_clinical_features

Respiratory Damage & Diseases Figure 17-11b: Surfactant reduces surface tension

Factors Affecting Ventilation Airway Resistance Diameter Mucous blockage Bronchoconstriction Bronchodilation Alveolar compliance Surfactants Surface tension Alveolar elasticity Figure 17-2e: Anatomy Summary

Lung Volumes: Spirometer Measurements Figure 17-12: The recording spirometer

Spirometry

Efficiency of Breathing: Normal & High Demand Total Pulmonary Ventilation (rate X tidal vol about 6 L/min) Alveolar ventilation (– dead air space – 4.5 L/min) Little variation [O2] & [CO2] Exercise- High Demand  Depth of breathing Use inspiratory reserve

Efficiency of Breathing: Normal & High Demand Figure 17-14: Total pulmonary and alveolar ventilation

Mucociliary Escalator Figure 17-6: Ciliated respiratory epithelium

Gas Exchange in the Alveoli Thin cells: exchange Surfactant cells Elastic fibers Recoil Push air out Thin basement membrane Capillaries cover 90% of surface

Gas Exchange in the Alveoli Figure 17-2 h : Anatomy Summary

Gas Exchange External Respiration The exchange membrane components and organization

Capillaries in Alveolar Wall

Gas Exchange External Respiration arteriole end PO2 = 40 mm Hg PCO2 = 46 mm Hg PO2 = 100 mm Hg PCO2 = 40 mm Hg inspired air O2 pulmonary capillary alveolus CO2 expired air PO2 = 40 mm Hg PCO2 = 46 mm Hg PO2 = 100 mm Hg PCO2 = 40 mm Hg venule end

Gas Exchange Internal Respiration arteriole end PO2 = 100 mm Hg PCO2 = 40 mm Hg PO2 = 40 mm Hg PCO2 = 46 mm Hg O2 systemic cell systemic capillary CO2 PO2 = 100 mm Hg PCO2 = 40 mm Hg PO2 = 40 mm Hg PCO2 = 46 mm Hg venule end

Gas Exchange What happens when alveolar PO2 drops? Solubility rules indicate that If PO2 drops, then the amount dissolved in blood also drops! Creating a hypoxic condition Factors that may cause low arterial PO2 Not enough O2 reaching alveoli Exchange between alveoli and pulmonary capillaries has a problem Not enough O2 transported in blood

Low [O2] in alveoli  vasoconstriction of arteriole Matching Ventilation with Alveolar Blood Flow (Perfusion)---How does the lung match ventilation with perfusion? Mostly local regulation using CO2 to control bronchiolar dilation and O2 to control arteriolar dilation Low [O2] in alveoli  vasoconstriction of arteriole Reduced blood flow at rest (lung apex ) saves energy High blood [CO2]  bronchodilation

Matching Ventilation with Alveolar Blood Flow (Perfusion)

Ventilation & Gas Exchange Relationship Net effect of ventilation is to exchange air within the alveoli to Maintain a partial pressure gradient which is required for gas exchange in the tissues and in the lungs! Blood flow and ventilation rate are optimized to ensure a usable gradient remains despite changing conditions, this is mainly controlled at the local (lung) level by the pulmonary capillaries collapse at low bp, diverting blood to areas of the lung with higher bp (away from the apex, towards the base) Bronchiole diameter is affected by CO2 levels PCO2 in expired air =  in bronchiole diameter (and vice versa) Arteriole diameter in the lungs, controlled by blood gas levels With a  PCO2 and a  PO2, the pulmonary arterioles constrict With a  PCO2 and a  PO2, the pulmonary arterioles dilate weakly

Summary Diaphragm & rib cage are pumps for inspiration Alveolar surface exchanges O2 & CO2 with blood The gasses in air act independently & move down a pressure gradient Airway resistance can limit ventilation efficiency Typically ventilation matches blood perfusion via local regulators of vasodilation & bronchodilation