Lung Anatomy

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Anatomy: Ventilation and Perfusion
Physiology: Gas Exchange - Oxygen
Physiology: Gas Exchange - Carbon Dioxide
Physiology: Respiratory Control
Physiology: Lung Compliance
Physiology: Respiratory Bellows and Respiration Muscle Activity
Anatomy: Images
References
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II. Anatomy: Ventilation and Perfusion

Images
Human adult lung is composed of more than 20 generations of branching airways that lead to 300 million alveoli
Cellular Respiration (Glycolysis)
1. Balance of oxygen utilization (and carbon dioxide production) is driven by cellular energy needs
2. Cellular ADP, when in excess, drives an increase in Glycolysis to generate ATP
3. ATP, when in excess, provides negative feedback to suppress Glycolysis
Ventilation (V)
1. When filled with a normal Tidal Volume breath, the Bronchi and alveoli contain ~450 ml of inspired air
2. Bronchi and Bronchioles do not participate in gas exchange, are considered Anatomic Dead Space (~150 ml)
3. Alveoli are the functional units of gas exchange and contain a total of ~300 ml of inspired air in an adult
  1. Total Lung Gas Exchange surface area is 145 m^2 (roughly the size of a tennis court)
    1. Based on alveolar diameter range 75-300 µm
4. Each minute, an average male adult breathing at a rate of 16/min
  1. Total ventilation (Ve or expired ventilation): 7200 ml/min
  2. Alveolar ventilation (Va): 4800 ml
Perfusion (Q)
1. Pulmonary artery gives rise to branches that parallel the Bronchi to the capillaries surrounding each alveolus
2. Entire Stroke Volume from the right heart passes through lung circulation with each beat
3. Cardiac Output adult male: ~4800 ml/min
  1. Cardiac Output then roughly has the same volume as alveolar ventilation (V/Q ratio)
4. Unlike the lung, perfusion has no dead space
  1. All blood must circulate from artery to alveolar capillary to vein to reach left atrium
  2. Contrast to ventilation in which inspired air and expired air share the same pathway
Ventilation and Perfusion in General
1. Ventilation is typically greater in the upper lung fields
  1. Ventilation to lung units that receive less perfusion is wasted
2. Perfusion is typically greater in the dependent lung (lung base if upright) due to gravity
3. Lung perfusion prioritizes well ventilated lung regions
  1. Localized lung hypoxia Vasoconstricts pulmonary vessels, resulting in decreased perfusion
    1. Contrast with non-lung tissue localized Hypoxia which triggers vasodilation (increased perfusion)
  2. Pulmonary Vasoconstriction prevents wasted perfusion to under-ventilated lung regions
    1. Pulmonary Hypertension results in a chronically and diffusely hypoxic lung
Ventilation-Perfusion Matching in the Normal Lung
1. Each alveolus receives roughly an equal amount of ventilation and perfusion (V/Q=1)
2. Since blood is heavier than air, gravity has a minor effect on lung perfusion
3. Due to gravity, perfusion to lungs is greater to dependent regions (lung base when patient upright)
  1. Lung base (when upright) has V/Q<1
  2. Lung apex (when upright) has V/Q >1
Ventilation-Perfusion Mismatch in the Abnormal Lung
1. Abnormal lungs may have dramatically mismatched ventilation to perfusion
2. Under ventilated alveoli (V/Q<1) waste perfusion with blood returning to the left heart under-saturated with oxygen
3. Over-ventilated alveoli (V/Q>1) waste ventilation as blood becomes saturated with oxygen at a fixed maximum
  1. Physiologic Dead Space is the total excess ventilation to over-ventilated alveoli (V/Q>1)

III. Physiology: Gas Exchange - Oxygen

See Oxygen Saturation Curve (Oxyhemoglobin Dissociation Curve)
See PaO2 (Arterial Oxygen Partial Pressure)
Background
1. Oxygen is an atmospheric gas required by all cells to burn fuel (esp. Glucose) aerobically
2. Oxygen diffuses into pulmonary capillaries from inspired air within lung alveoli
3. Most oxygen (97%) is transported in circulation bound to Hemoglobin
  1. Each molecule of Hemoglobin binds four O2 molecules (one for each iron molecule)
  2. Each gram of Hemoglobin carries 1.39 ml Oxygen
  3. At Hemoglobin 15 g/dl, blood carries 20.8 ml Hgb-bound oxygen when fully saturated (PaO2 100 mmHg)
4. Oxygen is poorly soluble in plasma
  1. Oxygen dissolved in plasma at only 0.003 ml/100 ml blood/1 mmHg PaO2
  2. When PaO2 100 mmHg, only 0.3 ml oxygen is dissolved in each 100 ml blood
5. Oxygen is transported to tissues, where it is required to sustain core cellular functions
Tissue oxygenation improves with Supplemental Oxygen, increased Hemoglobin And Cardiac Output
1. Supplemental Oxygen improves Hypoxia in decreased gas exchange (e.g. V/Q mismatch, high altitude)
2. Severe Anemia responds poorly to Supplemental Oxygen until oxygen carrying improves (e.g. transfusion)
Minute Ventilation (Respiratory Rate and Tidal Volume) does not significantly affect oxygenation
1. However, decreased dead space and Atelectasis (e.g. PEEP) does improve oxygenation
2. Lung regions with normal gas exchange cannot compensate for lung regions with poor gas exchange
  1. Normal lung regions cannot hyperoxygenate blood once it is fully oxygen saturated
Oyxgen is only a minor mediator of respiration under normal conditions
1. However, in severe Hypoxia (pO2 30-60 mmHg) oxygen becomes an important respiratory trigger
Normal oxygen pressures drop from atmospheric levels to intracellular levels
1. Atmospheric oxygen: 150-160 mmHg
  1. PiO2 = (760 mmHg - 47 mmHg) * 0.21 = 150 mmHg
  2. Where Atmospheric Pressure at sea level = 760 mmHg
  3. Where Fully saturated Water Vapor Pressure = 47 mmHg
  4. Where FiO2 (fraction of inspired air that is Oxygen) = 0.21
    1. Most of remaining inspired air is Nitrogen (0.78)
  5. Inspired Oxygen Pressure decreases with increased altitude and decreased barometric pressure
    1. See Inspired Oxygen Pressure at High Altitude
2. Alveolar capillary oxygen (PAO2): 105 mmHg
  1. Alveolar oxygen pressure is reduced from that in inspired air due to PCO2 within the alveolus
  2. PAO2 = PiO2 - PaCO2/0.8
  3. where PAO2 is the alveolar oxygen Partial Pressure or tension
  4. where PiO2 is the inspired oxygen Partial Pressure (calculated above)
  5. where PaCO2 is the arterial CO2 Partial Pressure (near identical surrogate for alveolar CO2)
  6. where 0.8 is the Respiratory Quotient (RQ)
    1. RQ is the CO2 generated per 1 ml of oxygen utilized in cellular respiration
    2. RQ is 0.7 ml (fat fuel) to 1.0 ml (Carbohydrate fuel)
3. Arterial oxygen (PaO2): 95 mmHg
  1. Arterial Oxygen Pressure (PaO2) is typically <10 mmHg below Alveolar Oxygen Pressure (PAO2)
  2. Known as Alveolar-Arterial Oxygen Tension Difference (A-a Gradient)
  3. A-a Gradient increases with age (ultimately to 20 mmHg at 80 years old)
4. Peripheral interstitial oxygen: 40 mmHg
5. Peripheral intracellular oxygen: 25 mmHg
  1. Peripheral cells need only PO2 of 2 mmHg for adequate functioning
  2. See Cellular Respiration described above
6. Venous oxygen: 40 mmHg
Low arterial oxygen (PaO2)
1. Hypoventilation (e.g. Bellows Failure)
  1. Increased CO2 (PACO2 and PaCO2) accounts for decreased Partial Pressure of oxygen (PAO2 and PaO2)
  2. Normal Alveolar-Arterial Oxygen Tension Difference (A-a Gradient)
2. Low inspired oxygen (FIO2)
  1. Low Oxygen Partial Pressure or tension within inspired air and alveoli
  2. Examples include low Fraction of Inspired Oxygen at High Altitude
  3. Normal Alveolar-Arterial Oxygen Tension Difference (A-a Gradient)
3. Venous admixture (Low V/Q, most common)
  1. Decreased ventilation to segments of lung impaired by acute or chronic lung disorders
  2. Examples include Asthma and COPD
  3. Lower V/Q ratios are correlated with lower PaO2 (approaching venous oxygen levels)
  4. Decreased Alveolar-Arterial Oxygen Tension Difference (A-a Gradient)
  5. Hypoxia (low PaO2) improves with Supplemental Oxygen
4. Right to Left Shunt (V/Q=0)
  1. As with right to left intracardiac shunts, venous blood passing through unventilated lung is not oxygenated
  2. Examples include lobar Pneumonia or Pulmonary Edema
  3. Decreased Alveolar-Arterial Oxygen Tension Difference (A-a Gradient)
  4. Hypoxia (low PaO2) does NOT significantly improve with Supplemental Oxygen
5. Decreased Alveolar-Capillary Diffusion (not a significant factor at rest)
  1. Decreased diffusion across alveoli does not cause significant Hypoxia at rest
  2. RBCs transiting alveolar capillaries have a full second in contact with alveoli to allow for delayed diffusion
  3. However, with increased Heart Rate (e.g. exertion), impaired diffusion may result in Hypoxia
6. Low Mixed Venous Oxygen Tension (PvO2)
  1. Low PvO2 is not significant in normal lungs, but compounds Hypoxemia when lung disorders are present
  2. Significant V/Q mismatch or shunt starting with low PvO2 will exit the lung with lower PaO2
  3. Examples include shock states
  4. Improves with increasing Cardiac Output (e.g. Intravenous Fluids or Blood Transfusion in Hypovolemic Shock)

IV. Physiology: Gas Exchange - Carbon Dioxide

See PaCO2
See Capnography
Carbon Dioxide forms as a volatile waste product during cellular respiration (Glycolysis)
1. Normal CO2 production at rest: 200 ml/min
  1. Assumes Minute Ventilation (MV) 6 L/min (Alveolar Ventilation 4 L/min)
  2. Each MV liter costs 1 ml of oxygen, and generates 0.7 to 1.0 ml CO2 (depending on RQ)
    1. Respiratory Quotient (RQ) varies from 0.7 ml (fat fuel) to 1.0 ml (Carbohydrate fuel)
    2. Normal lungs at rest only generate 6 ml/min CO2
    3. Most CO2 production is from non-respiratory cellular function
2. Heavy Exercise: 4000 ml/min
  1. Increased Minute Ventilation (6 to 100 L) with Exercise prevents hypercarbia (see below)
Carbon Dioxide (CO2) diffuses into Red Blood Cells within capillaries
1. Carbon dioxide may also dissolve in plasma, but represents <5% of CO2 in blood
2. Most plasma CO2 enters Red Blood Cell
  1. CO2 is rapidly converted to other forms in RBC (bicarbonate, Carbaminohemoglobin)
  2. CO2 tension within Red Blood Cell therefore remains low
  3. Gradient from plasma into Red Blood Cell is maintained
3. Most carbon dioxide (70-85%) is converted (hydrated) to biocarbonate in the Red Blood Cell
  1. Facilitated by enzyme carbonic anhydrase found in Red Blood Cells (not in plasma)
  2. Carbonic anhydrase speeds rate of reaction by 10,000 fold
4. Carbaminohemoglobin (CO2 bound to Hemoglobin) accounts for 10-25% of CO2 carried in blood
  1. Carbamino Proteins bind CO2 at the nitrogen binding site and release H+
    1. Protein-NH3 + CO2 => Protein-NH2-COO + H+
  2. Oxygen saturated Hemoglobin binds CO2 less than when desaturated (Haldane Effect)
    1. In peripheral tissue, Hemoglobin releases oxygen, and better binds CO2
    2. In lung, oxygen saturates Hemoglobin, and releases CO2 for excretion
Hydration of Carbon Dioxide within Red Blood Cells, forming bicarbonate
1. Red Blood Cell (RBC) carbonic anhydrase catalyzes conversion of CO2 to carbonic acid (H2CO3)
  1. H2O + CO2 <=> H2CO3
2. Carbonic Acid (H2CO3) dissociates into Bicarbonate (HCO3-) and Hydrogen (H+)
  1. H2CO3 <=> HCO3- + H+
Bicarbonate exits Red Blood Cell and is transported via venous circulation to lungs for expiration
1. Hydrogen Ion remaining in the Red Blood Cell binds Hemoglobin (buffers Hydrogen Ion)
  1. Hydrogen binding alters Hemoglobin molecule making it less oxygen avid (Bohr Effect)
  2. Hydrogen binding favors RBC Hemoglobin unloading of oxygen in peripheral tissue
  3. In the lungs, the process reverses
    1. CO2 is excreted and Hemoglobin is less hydrogen bound
    2. Hemoglobin molecule assumes unbound configuration and becomes more oxygen avid
2. Chloride (Cl-) enters Red Blood Cells to offset the loss of bicarbonates negative charge
  1. Results in a "chloride shift" into RBCs within venous blood compared with arterial blood
Lung expiration
1. CO2, in all its forms (bicarbonate, carbaminohemoglobin and CO2), is excreted via expiration
2. Minute Ventilation (Respiratory Rate x Tidal Volume) controls pCO2
3. CO2 diffuses easily across alveolar membranes (20 fold faster than oxygen)
  1. At end expiration, alveolar PCO2 is roughly equivalent to arterial PCO2
4. Lung excretes more than 15,000 mEq of volatile acid as CO2 per day
  1. Within minutes of apnea onset, Respiratory Acidosis may be lethal
  2. Contrast with the 100 mEq of acid that is renally excreted per day
    1. Unlike in hypercarbic Respiratory Failure, Hemodialysis may be performed every 2-3 days
Carbon Dioxide (and H+, pH) is the primary mediator of respiration under normal conditions
1. See Respiratory Control below
2. Changes in PaCO2 is met by rapid compensatory change in alveolar ventilation
  1. PaCO2 = k x VCO2/Va
  2. where PaCO2 is arterial Partial Pressure of CO2
  3. where correction factor (k) = 0.863
  4. where VCO2 is CO2 production (in ml/min STPD)
  5. where Va is alveolar ventilation (in l/min BTPS)
    1. Va = Ve x (1- Vd/Vt)
    2. where Ve = Total Ventilation
    3. where Vd/Vt = Fraction of Physiologic Dead Space
3. Doubling alveolar ventilation results in half the PaCO2
  1. Increasing Respiratory Rate from 12 to 24, decreases PaCO2 from 40 to 20 mmHg
  2. Further increases in ventilation result in diminishing PaCO2 changes (PaCO2 does not drop <10-20 mmHg)
  3. However, at very low Ventilatory rates, small increases in ventilation result in large decreases in PaCO2
4. Cutting by half the alveolar ventilation results in double the PaCO2
  1. Decreasing Respiratory Rate from 12 to 6, increases PaCO2 from 40 to 80 mmHg
Normal carbon dioxide pressures change little throughout circulation
1. Atmospheric pCO2: 0.3 mmHg
2. Alveolar and Arterial pCO2: 40 mmHg (48 ml per 100 ml blood)
  1. Curvilinear relationship between CO2 content to CO2 pressure (or tension)
    1. Large changes in pressure or tension result in small changes in CO2 content
    2. Allows for significant compensation for CO2 pressure changes
  2. Hyperventilation pCO2: 10 mmHg (30 ml per 100 ml blood)
  3. Apnea pCO2: 80 mmHg (70 ml per 100 ml blood)
3. Interstitial, Intracellular and Venous pCO2: 45 mmHg (54 ml per 100 ml blood)
Increased arterial carbon dioxide (PaCO2)
1. The 3 causes of high PaCO2 relate to the formula PaCO2= k x VCO2/Va (see above)
  1. where Alveolar Ventilation (Va) = Ve x (1- Vd/Vt)
2. Total ventilation (Ve) decreased
  1. Apnea
  2. Airway obstruction
  3. Bellows Failure
3. Fraction of Physiologic Dead Space (Vd/Vt) increased
  1. Wasted ventilation (high Physiologic Dead Space) must be compensated by increasing total ventilation (Ve)
  2. Increased total ventilation (Ve) may come at a high cost of respiratory workload with inadequate results
    1. Air trapping (e.g. COPD, Asthma)
    2. Decreased Lung Compliance
    3. Diaphragm flattening (inefficient contraction)
4. CO2 Production (VCO2) increased
  1. Increased respiratory workload may increase CO2 production significantly
  2. Normal respiration may generate 1 ml CO2 per 1 liter minute respiration
  3. Severe COPD or Asthma may generate 10-20 ml CO2 per 1 liter minute respiration
    1. Total ventilation (Ve) increased to 20 liters/min may cost 400 ml/min CO2 from respiration alone
    2. Normal, resting CO2 production is only 200 ml/min for the entire body
    3. Excreting high CO2 loads (high acid load) is unsustainable with high dead space and work of breathing

V. Physiology: Respiratory Control

See Acute Respiratory Failure
Ventilatory response to Respiratory Control assumes ability to perform respiratory effort
1. See respiratory Muscle activity below
2. Bellows Failure (Hypoxemia and hypercarbia) in Acute Respiratory Failure results from inspiratory effort failure
Neurologic Mediators: Respiratory Center (Brainstem)
1. Medulla Oblongata
  1. Dorsal Respiratory Group (DRG, solitary nucleus)
    1. Initiates inspiration
    2. Sensory input from CN 9, CN 10 and pons respiratory centers
    3. Outputs to ventral respiratory group
  2. Ventral Respiratory Group (VRG)
    1. Composed of four Neuron groups including Nucleus Ambiguous
    2. Active in inspiration and expiration during forceful breathing
    3. Negative feedback loops to Apneustic Center (pons)
2. Pons
  1. Pneumotaxic Center (parabrachial nucleii)
    1. Controls Breathing Rate and pattern by limiting inspiration, Tidal Volume and Respiratory Rate
    2. Acts in a cyclical manner, to inhibit phrenic Nerve Impulses during expiration ("switch-off")
  2. Apneustic Center
    1. Stimulates inspiration centers in the Medulla dorsal respiratory group
Neurologic Mediators: Non-Chemoreceptor Afferent Nerves
1. Afferent signals are passed to Brainstem from Vagus Nerve and spinal nerves
  1. Respiratory Rate increases in response to non-Chemoreceptor afferent triggers
  2. Contrast with the increased Tidal Volume response to increased pCO2
2. Vagus Nerve afferent nerves (airway, lung parenchyma, pulmonary vasculature)
  1. Irritant receptors (e.g. noxious gas, Airway Foreign Body)
  2. Alveolar J Receptors (e.g. congestion in CHF, cell proliferation in intersitial lung disease)
  3. Stretch Receptors (pleura, lung)
3. Spinal afferent nerves (chest wall, respiratory Muscles)
  1. Respiratory spindle Muscle fibers signal amount of Muscle shortening (esp. intercostal Muscles)
  2. Decreased Muscle shortening may reflect increased respiratory workload
Neurologic Mediators: Phrenic Nerve
1. Stimulated by Brainstem respiratory centers
2. Originates in C3, C4, and C5 spinal nerves, exiting the ventral roots and initially following the internal Jugular Veins
3. Innervates the diaphragmatic Muscles, which on contraction, result in inspiration
4. Also receives sensory input from the Pericardium, mediastinal pleura, diaphragmatic peritoneum
  1. Responsible for referred pain to Shoulder and neck from Gall Bladder and heart
Chemical Mediators of Increased Respiratory Effort
1. Increased Carbon Dioxide (pCO2) and Acidosis (increased H+, decreased pH) stimulate increased respiration
  1. Cerebrospinal fluid pH is immediately influenced by PaCO2 changes
  2. Central Chemoreceptors on ventrolateral Medulla detect change in pH
    1. Peripheral Chemoreceptors (carotid bodies) are also Blood pH sensitive, but weaker (25%)
  3. Even small changes in PaCO2 increase has a near immediate response with increased ventilation
    1. Even a PaCO2 increase of 1 mmHg, results in an increase in Minute Ventilation of 2-5 Liters
      1. Increased Tidal Volume accounts for most of the increased Minute Ventilation
    2. Directly stimulate Brainstem respiratory centers (primary affect)
    3. Affect aortic and carotid bodies which stimulate Brainstem respiratory centers (CN 9, CN 10)
    4. Increased respiratory effort due to increased CO2 typically does not cause a Sensation of Dyspnea
  4. When Hypoxia is absent, increased CO2 is the primary stimulator of increased respiration
    1. Corrects hypercapnia as well as acidosis
  5. Concurrent Hypoxia and hypercarbia enhances respiratory response to both O2 and CO2
    1. Respiratory response to hypercapnia is greater with Hypoxemia
    2. Respiratory response to Hypoxemia is greater with hypercarbia (even when PaO2 65-70 mmHg)
      1. The reverse is also true, as excessive Supplemental Oxygen may blunt CO2 response
2. Decreased Oxygen (pO2)
  1. Affect aortic (CN 10) and carotid bodies (CN 9) which stimulate Brainstem respiratory centers
  2. Oxygen (pO2) is a weak trigger for respiration compared with pCO2 under normal conditions
    1. Response to pO2 is primitive in contrast to the finely calibrated response to pCO2
  3. Conditions in which low pO2 (Hypoxia) becomes an important trigger for respiration
    1. Significant Hypoxia (pO2 <50-55 mmHg)
    2. High altitude before acclimitization (lower oxygen concentration in inspired air)
    3. Hypoxemic Respiratory Failure (or physiologic right to left shunting, e.g. ARDS)
Other Mediators of Respiratory Effort
1. Exercise
  1. Direct stimulation from motor cortex, while simultaneously stimulating muscular activity
2. Hering-Breuer Inflation Reflex
  1. Bronchial stretch receptors limit hyperinflation while increasing Respiratory Rate
3. Atmospheric Pressure
  1. Diving (higher atmospheric pressure)
    1. See Decompression Sickness (Nitrogen Toxicity)
    2. Diving concentrates gases into a smaller space at higher atmospheric pressure
    3. More nitrogen gas is dissolved in blood at higher atmospheric pressure
    4. Alveolar pressures increase to meet atmospheric pressure
      1. On returning to surface, atmospheric pressure normalizes
      2. Inhaled gases will expand, requiring diver to release gases on rising
      3. Nitrogen gas comes out of solution and forms bubbles within blood (may embolize)
  2. High Altitude (lower atmospheric pressure)
    1. See High Altitude Sickness
    2. Acclimitization occurs over weeks to months with neovascularization and increased RBC production
    3. At altitude, atmospheric pressure falls (523 mmHg at 10,000 feet, 349 mmHg at 20,000 feet)
      1. Alveolar pressure is limited to atmospheric pressure
      2. Water vapor (47 mmHg), CO2 (16-28 mmHg) and Nitrogen account for most alveolar pressure
      3. Remaining alveolar pressure for oxygen (pO2) is far less at altitude

VI. Physiology: Lung Compliance

Lung Compliance is the increase in Lung Volume per change in alveolar pressure
1. Lung Compliance is high when small changes in alveolar pressure result in large changes in Lung Volume
2. Causes
  1. Lung Compliance is decreased by pulmonary fibrosis, Pulmonary Edema or airway obstruction
  2. Chest wall deformity (e.g. Scoliosis) also decreases Lung Compliance
Lung Elastance is the increase in alveolar pressure per change in Lung Volume (reciprocal of Lung Compliance)
1. Lung elasticity is the tendency of lung to spring back into its resting state volume
2. Lung elastance is high when small changes in alveolar volume result in large changes in alveolar pressure
3. Causes
  1. Conditions that decrease Lung Compliance (e.g. pulmonary fibrosis, Scoliosis), increase lung elastance
  2. Increased alveolar surface tension resists expansion and is a key contributor to increased lung elastance
    1. Alveolar collapse (Atelectasis) occurs when alveolar surface tension is high
    2. Alveolar surfactant normally reduces alveolar surface tension and lung elasticity
    3. Alveolar surfactant is lacking in Respiratory Distress Syndrome in the Newborn and ARDS
4. Manifestations
  1. Increased elasticity results in decreased Tidal Volume
  2. Compensation is with increased Respiratory Rate (Tachypnea)

VII. Physiology: Respiratory Bellows and Respiration Muscle Activity

Background
1. Respiratory Bellows (pump) allows for active expansion of Lung Volume by creating negative intrathoracic pressure
2. Lung expansion decreases alveolar Gas Pressures, drawing in atmospheric gas from pharynx to alveoli
3. Lung's power supply resides primarily in the diaphragm, and secondarily in the chest and neck accessory Muscles
4. Resting position of the lungs is a balance between tendency for lung recoil inward and chest wall recoil outward
  1. Early inspiration is aided by the chest wall tendency for outward recoil
  2. Respiratory workload increases on full inspiration to counter the lungs inner recoil and chest wall stiffness
5. Respiratory Bellows have significant reserve capacity
  1. Resting Minute Ventilation of 6 L/min in a typical adult male
  2. Minute Ventilation may increase to >100 L/min as needed (e.g. Exercise)
Inspiration
1. Diaphragm (core Muscle of inspiration)
  1. Moves downward on contraction, increasing negative pressure within the chest
2. Accessory Muscles of inspiration
  1. Background
    1. Accessory Muscles draw the ribs upward and forward
    2. Changes the chest shape (in cross section) from eliptical to circular
  2. Pectoralis major
  3. Pectoralis minor
  4. Serratus Anterior
  5. Sternocleidomastoid Muscle
  6. Scalene Muscles
  7. Levatores Costarum Muscles
  8. Serratus posterior superior Muscle
Expiration
1. Passive relaxation of the chest assumes expired position (core expiratory function)
  1. Lungs passively recoil inward
    1. Chest wall will also relax and collapse inward to resting position after a full inspiration
  2. Lung Volumes decrease and alveolar Gas Pressure increases
    1. Gas flows from higher alveolar pressures to the lower pressures in pharynx
2. Accessory Muscles of expiration
  1. Background
    1. Internal intercostal Muscles pull ribs down (past their resting downward inclination)
    2. Abdominal Muscles (e.g. rectus abdominis) pushes diaphragm upward towards chest
  2. Triggers for accessory expiratory Muscle use
    1. Coughing
    2. Forced expiration toward Residual Volume
      1. Exercise
      2. Obstructive Lung Disease (Asthma, COPD) with incomplete expiration
  3. External intercostal Muscle
  4. Internal intercostal Muscle
  5. Transversus thoracis Muscle
  6. External oblique Muscle
  7. Internal oblique Muscle
  8. Transversus abdominis Muscle

VIII. Anatomy: Images

Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)

IX. References

Davies (1986) Acute Respiratory Failure, Cyberlog
Goldberg (2014) Clinical Physiology, Medmaster, Miami, p. 51-9
Guyton and Hall (2006) Medical Physiology, Elsevier Saunders, Philadelphia, p. 471-82, 514-23

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