The Respiratory System

The Respiratory SystemFunctions:

– To provide the body with means of taking in(O2) for the production of ATP and eliminating (CO2) a byproduct of aerobic respiration.

– To help maintain the body’s pH, by regulating the blood CO2 levels in the body.

– Work in conjunction with the cardiovascular system to move these gases from the lungs to the cells and from the cells to the lungs.

Organs of Respiratory System

Conducting Zone

• Conducting zone – Provides rigid

conduits for air to reach the sites of gas exchange

– Respiratory structures include (nose, nasal cavity, pharynx, trachea, primary, secondary and tertiary bronchi)

– No Gas exchange

Respiratory Zone• Respiratory zone:

– begins as terminal bronchioles → respiratory bronchioles → alveolar ducts, → alveolar sacs composed of alveoli

– This is where gas exchange occurs!

Nose• Functions

– Nasal choanae creates turbulent air flow that allows air to contact mucus membranes and superficial nasal sinuses.

• The result is cleaner, warmer more humidified inhaled air.

– detects odors via the olfactory cranial nerve which also enhances our sense of taste.

– Resonating chamber that amplifies the voice

Pharynx

Larynx

• Larynx (“voice box”)– contains vocal cords allowing speech production

• Glottis – vocal cords • Epiglottis

– flap of tissue that guards glottis, directs food and drink to esophagus

Trachea• Flexible and mobile tube extending from the larynx to the

carina (split into primary bronchi)• Composed of three layers

– Mucosa – made up of pseudostratified ciliated epithelium that contain goblet cells that secrete mucus to trap dirt.

• Mucociliary escalator: cilia beats in an upward fashion toward the pharynx where debris can be swallowed.

– Submucosa – connective tissue deep to the mucosa– Adventitia – outermost layer made of C-shaped rings of

hyaline cartilage which prevent the airway from collapsing.

Trachea

Respiratory Zone

• Approximately 300 million alveoli:– Account for most

of the lungs’ volume

– Provide tremendous surface area for gas exchange

– Equivalent to 2 tennis courts in surface area.

Respiratory Membrane

Respiratory MembraneAir-blood barrier is composed of alveolar and capillary

walls.– Alveolar walls: contain 2 main types of cells1. Type I epithelial cells (simple squamous epithelium)

that permit gas exchange by simple diffusion2. Type II cells (cuboidal epithelium ) secrete

surfactant which enables the lungs to expand.3. White blood cells are found in the lumen of the

alveoli.1. Function to protect against infections from inhaled

pathogens

4 Processes of Respiration 1. Pulmonary ventilation – air moving into and out of the

lungs along their pressure gradients. • Inspiration – air(O2)flows into the lungs

• Expiration – air (CO2) exit the lungs

2. External respiration – gas exchange between the lungs (alveolus) and the blood (pulmonary capillaries)

3. Transport – transport of oxygen and carbon dioxide between the lungs and tissues via the circulatory system.

4. Internal respiration – gas exchange between systemic blood vessels (capillaries) and the tissues (cells)

• Gases must diffuse into interstitial fluid prior to any exchange between the tissue and the cell.

Pulmonary Ventilation• Taking of air into and out of the lungs.• A mechanical process that depends on

respiratory muscles changing the size of the thoracic cavity – Because this cavity is connected to the lungs

via the parietal membranes it may also influence the lung (alveolar )volume.

• A increase in alveolar volume will move air into the lungs down it concentration gradient.

• A decrease in alveolus volume will move air out of the lungs.

Boyle’s Law• The changes in thoracic volume is necessary to

move air in and out of the lungs. The movement of air in dependant of:– Boyle’s law – Pressure and Volume are

inversely proportional.• P ×V= Constant• If pressure increases volume decreases• If pressure decreases volume increases

and vise versa • This mechanism is dependent on a double-

layered membrane system called (Pleurae)

Pleurae

Parietal pleurae

Visceral pleurae

Intrapleural space

Pleurae• Parietal pleura

– Covers the thoracic wall and superior face of the diaphragm

– Continues around heart and between lungsVisceral pleura– Covers the external lung surface

• Intrapleural Space – Space between the parietal and visceral pleurae.– There is a small amount of fluid (pleural fluid) within

the space that hold the 2 pleurae together• This will reduce friction between the lungs and the thoracic

cavity.– Similar to a small amount of water between 2 plains of

glass.• Slides easily but difficult to separate.

Pulmonary Pressures• Intrapulmonary pressure and intrapleural pressure

fluctuate with the phases of respiration.– Intrapulmonary pressure aka. alveolar is the pressure

with in the alveolus– Intrapleural pressure is the pressure within the pleural

space• created by many hydrogen bonds between the water

molecules of the pleural fluid.• Intrapleural pressure must always less than

intrapulmonary pressure and atmospheric pressure

Pulmonary Pressures

Intrapulmonary pressure

Atmospheric pressure

intrapleural pressure

Lung Collapse

• Caused by equalization of the intrapleural pressure with the intrapulmonary pressure

• Transpulmonary pressure keeps the airways open– Transpulmonary pressure – difference

between the intrapulmonary and intrapleural pressures (Ppul – Pip)

Muscles of Respiration

Inspiration

Expiration

Figure 22.13.2

Respiratory muscles• The muscles collectively work to change the

volume of the thorax during ventilation.• Inspiration

– Diaphragm via the phrenic nerve flattens out increasing thoracic volume depth

– External intercostals via intercostal nerves pull the ribs up and out.

• This collectively increase the size (volume) of the thorax and the lungs via its attachment to the pleura.

• Expiration – Normal expiration is a passive process that involves the

relaxation of the inspiratory muscles. – Forced expiration is an active process involving the

internal intercostals and abdominals contracting forcing the ribs down decreasing the size (volume) of the thorax.

• coughing

• What is the mechanism of action for the Heimlich Maneuver?

Lung Compliance• The lungs ability to expand despite the lungs

tendency to collapse.• Determined by two main factors:

– Distensibility of the lung tissue and surrounding thoracic cage

– Reducing surface tension of the alveoli: as the lungs expand it stretches the type II cell to produce more surfactant.

• Surfactant is a detergent-like complex, reduces surface tension by breaking H-bonds allowing the lungs to expand.

Factors That Diminish Lung Compliance

• Scar tissue or fibrosis that reduces the natural resilience of the lungs preventing them to expand during inhalation.

• Blockage of the smaller respiratory passages with mucus or fluid

• Reduced production of surfactant• Decreased flexibility of the thoracic cage or its

decreased ability to expand• Examples include:

– Deformities of thorax– Ossification of the costal cartilage– Paralysis of intercostal muscles

Deformities of Thorax

• Barrel Chest Pectus Excavatum

• The amount of gas flowing into and out of the alveoli is directly proportional to Pressure– The greater the pressure gradient between

the atmosphere and the alveoli the more air will enter the lungs

• Atmospheric pressure (Patm)– Pressure exerted by the air surrounding the

body • Altitude and (Patm) are inversely proportional.

– It is much easier to breath at sea level than it is a 10,000 ft above. Why?

Environmental Influences of Ventilation:

Airway Resistance

• Gas flow is inversely proportional to resistance– The resistance increases as vessel diameter

decreases. • This will lead to less gas reaching the alveoli for exchange.• As airway resistance rises, breathing movements become

more strenuous

– Severely constricted or obstructed bronchioles: • Can occur during acute asthma attacks which

stops ventilation .– Epinephrine released via the sympathetic nervous

system or medically induced dilates bronchioles and reduces air resistance.

Dalton’s Law of Partial Pressures

• The air that we breath is made up of 4 main gases– N2, O2, H2O and CO2 – There is a different % of each of the above gases

in the atmospheric air.– Each gas therefore makes up a different

proportion of the total mixture.• The sum of the partial pressures of each individual

gas is equal to the total pressure of the air.• The partial pressure of the various gases are

important in establishing the gradients which drives the gases throughout the system.

Partial Pressure Gradients

Partial Pressures Gradients During Internal Respiration

• PCO2 (45mmHg) in peripheral tissues is higher than in the arteries returning from the lungs(40mmHG) because CO2 is a end product of cellular respiration.

• The PO2(40mmHg)is lower in the tissues than the arterial blood (95mmHg) because O2 is being continuously being used by the cells.

• O2 and CO2 will diffuse along their concentration gradients – O2 from blood to tissues

– CO2 from tissue to blood

Partial Pressure Gradients During External Respiration

• Following (internal respiration)O2 unloading to the tissues and CO2 uptake into the blood the (PO2) in venous blood decreases to 40 mmHg and the PCO2

increases to 45mmHg

• Following ventilation the PO2 in the alveoli is104 mmHg and PCO2 decreases to 40mmHg

• O2 and CO2 will diffuse along its pressure gradient from high to low– PO2 =lungs → blood– CO2 = blood → lungs– Diffusion will occur until equilibrium is met. – Blood PO2 and PCO2 will = the alveolus partial pressures.

• Molecular oxygen is carried in the blood: – Bound to hemoglobin (Hb) within red blood cells (99%)

• The hemoglobin-oxygen combination is called oxyhemoglobin (HbO2)

– Dissolved in plasma (1%)

• Carbon dioxide is transported in the blood in three forms– Dissolved in plasma – 7 to 10% – Chemically bound to hemoglobin – 20% is carried in

RBCs as carbaminohemoglobin– Bicarbonate ion in plasma – 70% is transported as

bicarbonate (HCO3–)

Gas Transport: Role of Hemoglobin

Internal Respiration

At the tissues:• Carbon dioxide diffuses into RBCs • The high concentration of CO2 causes the above equation to shift to the right.

– combines with water to form carbonic acid (H2CO3)• (H2CO3), which quickly dissociates into hydrogen ions and bicarbonate ions• Hydrogen ions attach to one of 4 heme molecules in the RBC dislodging on of

the O2 (Bohr effect)– Oxygen travels down its concentration gradient to the tissues

• Bicarbonate levels quickly build up and will quickly diffuses from RBCs into the blood plasma

• The chloride shift – to counterbalance the out rush of negative bicarbonate ions from the RBCs, chloride ions (Cl–) move from the plasma into the erythrocytes

Internal RespirationCO2 + H2O H2CO3 H+ + HCO3

–

Carbon dioxide Water Carbonic

acidHydrogen

ionBicarbonate

ion

External Respiration

• When the blood gets to the lungs these processes are reversed.– The above reaction will shift to the left.

• Bicarbonate ions move into the RBCs and bind with hydrogen ions to form carbonic acid

• Carbonic acid is then split by carbonic anhydrase to release carbon dioxide and water– CO2 levels quickly rise in the cell

• CO2 diffuses from the blood into the alveoli along its concentration gradient.

External RespirationCO2 + H2O H2CO3 H+ + HCO3

–

Carbon dioxide Water Carbonic

acidHydrogen

ionBicarbonate

ion

Oxygen-Hemoglobin Dissociation Curve

• The higher the PO2 in the blood the greater the percent O2 saturation.

• The percent O2 saturation plotted against blood PO2 – this tells us the amount of

oxygen that is bound to hemoglobin at a particular PO2 in the blood

– We monitor O2 saturation levels with patients with pulmonary issues

• Below 90% is termed hypoxemia

• Increases in Temperature, H+, PCO2, and BPG increase O2 unloading from the hemoglobin.– This will result in a shift to the right on the curve

• When the cells are more metabolically active there is a greater need for O2.

• Temperature increases in metabolically activity, the tissues because heat is a byproduct of cellular respiration.

• Active cells will also produce more CO2 and H20 which ultimately will lead to greater amounts of H+

– Both these byproducts ensure that O2 will be unloaded from the RBC and delivered to the tissues.

• Decreases in Temperature, H+, PCO2, and BPG will act in the opposite manner– This will result in a shift to the left on the curve

Other Factors Influencing Hemoglobin Saturation

Factors Influencing Hemoglobin Saturation

Medullary Respiratory Centers

• Ventral Respiratory Group: Sets the underline breathing rate .It activates the – Diaphragm stimulated via

the Phrenic Nerve – External Intercostals

stimulated via the Costal Nerves

• Dorsal Respiratory Group (DRG): receives input from multiple areas.– It modulates the breathing

rate of the VRG so it can adapt to various situations.

Pons (Secondary Centers) • Apneustic Center

• Stimulation of this center causes strong inspirations or aids in prolong inspiration.

• stimulations the inspiratory center • Pneumotaxic Center

• inhibits the VRG to end inspiration – provides for a smooth transition between inspiration and

expiration • Stimulation of this center inhibits the Apneustic center • Contributes to expiration

• Cortical control: we can actively effect our respiratory rate such as• holding breath under water

• The Limbic system and hypothalamus also stimulate the respiratory centers. • Emotional effect on respiration

• Inflation reflex (Hering-Breuer) – stretch receptors in the lungs are stimulated by lung inflation – Upon inflation, inhibitory signals are sent to

the medullary inspiration center to end inhalation and allow expiration

• Pulmonary irritant reflexes – irritants promote reflexive constriction of air passages

Depth and Rate of Breathing: Reflexes

• Changing PCO2 levels are monitored by Central chemoreceptors of the brain stem – Carbon dioxide in the blood diffuses into the

cerebrospinal fluid CO2 + H2O H2CO3 HCO3

- + H+

• PCO2 levels rise (hypercapnia) resulting in increase in H+ ion level concentration in the medulla.

• This stimulations of( DRG) increased depth and rate of breathing– CO2 (expired) + H2O H2CO3 HCO3

- + H+

• This will allow the body to blow off more CO2 thus reducing CO2 levels reestablishing homeostasis.

Central Chemoreceptors

Depth and Rate of Breathing: PCO2

Peripheral Chemoreceptors

• Arch of the Aorta – main vessel originating from the heart

• Carotid sinus– main artery in the neck

• Elevated arterial P CO2 and H+ ion concentration or decrease in PO2 will stimulate DRG to increase respiratory rate.– CO2 levels are the main driving force behind

respiratory rate.

• Hypoventilation – When PCO2 levels are abnormally low the body will slow its respiratory rate. – Holding your breath or breathing slow and shallow will

cause CO2 levels to start to raise in your blood

• As the CO2 levels start to rise again this will trigger chemoreceptors to stimulate DRG to increase ventilation causing thus exhaling more CO2 levels in the blood CO2

– Apnea (breathing cessation) may occur until PCO2 levels rise

Depth and Rate of Breathing: PCO2

• Hyperventilation – increased depth and rate of breathing that:– Quickly flushes CO2 from the blood

• CO2 (expired) + H2O H2CO3 HCO3- + H+

– Occurs in response to hypercapnia( high CO2 in blood)

• Though a rise CO2 acts as the original stimulus, control of breathing at rest is regulated by the hydrogen ion concentration in the brain

• Why do you give someone a bag to breath into if they are hyperventilating?

Depth and Rate of Breathing: PCO2

Respiratory Acidosis• pH of CSF (most powerful respiratory stimulus)• Respiratory acidosis (pH < 7.35) caused by decline in pulmonary

ventilation ( not blowing CO2 off)• PCO

2(Normal 35-45)=>45 Acidic

– hypercapnia: PCO2 > 45 mmHg

• CO2 easily crosses blood-brain barrier• in CSF the CO2 reacts with water and releases H+

CO2 + H2O H2CO3 HCO3- + H+

• central chemoreceptors strongly stimulate inspiratory center (DRG) stimulates phrenic and intercostal nerve which targets inspiratory muscles increasing respiratory rate.

– “blowing off ” CO2 pushes reaction to the left CO2 (expired) + H2O H2CO3 HCO3

- + H+

• so hyperventilation reduces H+ (reduces acid)

Respiratory Alkalosis• Respiratory alkalosis (pH > 7.35)

– hypocapnia: PCO2 < 35 mmHg

• CO2 (expired) + H2O H2CO3 HCO3- + H+

– Hypoventilation ( CO2), pushes reaction to the right CO2 + H2O H2CO3 HCO3

- + H+

H+ (increases acid), lowers pH to normal• pH imbalances can have metabolic causes

– uncontrolled diabetes mellitus• fat oxidation causes ketoacidosis, may be

compensated for by Kussmaul respiration(deep rapid breathing)

Hypoxia• Causes: Reduced levels of oxygen particularly in the blood.

– hypoxemic hypoxia - usually due to inadequate pulmonary gas exchange

• high altitudes, drowning, aspiration, respiratory arrest, degenerative lung diseases, CO poisoning

– ischemic hypoxia - inadequate circulation• DM, Atherosclerosis

– anemic hypoxia – anemia• Diet and internal bleed

– histotoxic hypoxia - metabolic poison • cyanide poisoning

• Signs: cyanosis - blueness of skin, finger nail clubbing• All types of hypoxia can lead to tissue necrosis ( death)

Signs of Cyanosis

Chronic Obstructive Pulmonary Disease

• Asthma– Chemical irritants cause the release of

release of histamine which activates the PNS. This leads to intense bronchoconstriction (blocks air flow)

– Treatment is Epinephrine. Why?• Other COPD’s usually associated with smoking

– chronic bronchitis – emphysema

• Chronic Bronchitis typically occurs in the larger airways.

• Patients have a history of:– Smoking– Dyspnea: labored breathing occurs and gets

progressively worse– Coughing and sputum production leading to

frequent pulmonary infections.• COPD patients may develop respiratory failure

accompanied by hypoxemia, carbon dioxide retention resulting in respiratory acidosis

Chronic Bronchitis

Chronic Obstructive Pulmonary Disease

• Emphysema– An inflammatory response destroys the

alveolar walls ( respiratory membrane) reducing the surface area for gas exchange

– Lungs become more fibrotic and less elastic– Air passages collapse with exhalation

trapping CO2 in lungs.

Effects of COPD

pulmonary compliance and vital capacity• Hypoxemia, hypercapnia, respiratory

acidosis– hypoxemia stimulates erythropoietin release

and leads to polycythemia • cor pulmonale

– hypertrophy and potential failure of right heart due to obstruction of pulmonary circulation

Smoking and Lung Cancer

• Lung cancer accounts for more deaths than any other form of cancer– most important cause is

smoking (15 carcinogens)

– If you smoke the equivalent of 50 pack years your chance of getting lung cancer is 100%

• 50% of smokers die from smoke related illness.