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Cardiopulmonary I > Test 2 (Dr. Karius and Cole Combined Lecture) > Flashcards

Test 2 (Dr. Karius and Cole Combined Lecture) Flashcards

1
Q

Structure and Function of the Respiratory System

A
  • The respiratory system consists of Three portions:
    1) An AIR-CONDUCTIN Portion (Also conditions inspired air)
    2) A Respiratory portion for GAS EXCHANGE between blood and air
    3) A Mechanism of VENTILATION controlled by the INSPIRATORY and EXPIRATORY RATE of the THORACIC Cage
  • Olfaction
  • Phonation
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2
Q

Conductiong versus Respiratory Portions

A

Conducting:
- A series of Tubes. Cavities that carry air to and from site of gas exchange

  • Comprised of Nasal Cavity, Nasopharynx, Larynx, Trachea, Bronchi, Bronchioles, and Terminal Bronchioles
  • In HEAD and NECK

Respiratory:
- Where gas exchange (Oxygen and Carbon Dioxide) occurs

  • Etends from Respiratory Bronchioles to Alveoli
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3
Q

Nasal Cavity and Paranasal Sinuses

A
  • The functions are WARMING and MOISTENING AIR and FILTERING DUST Particles present in INSPIRED AIR
  • Respiratory portion is lined by PSEUDOSTRATIFIED CILIATED EPITHELIUM with GOBLET CELLS supported by a Lamina Propria with SEROMUCOUS GLANDS, and a rich SUPERFICIAL VENOUS PLEXUS
  • Incoming air is WARMED by Blood in the Venous Plexus and moistened by SECRETIONS of the SEROMUCOUS Glands and Goblet Cells
  • Superior, Middle, and Inferior Conchae create turbulence to help warm and moisten air
  • PARANASAL SINUSES are lined by a Thin Psuedostratified Columnar ciliated Epithelium with few Goblet Cells
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4
Q

Respiratory System Wall Structure

A
  • “Respiratory Epithelium” lines most of the Tract. CILIATED PSEUDOSTRATIFIED COLUMNAR EPITHELIUM and GOBLET CELLS
  • LAMINA PROPRIA: Looce CT containing (zero) mucous Glands, Elastic Fibers, Bone/ Cartilage, and Smooth Muscle. COMPOSITION CHANGES THROUGHOUT LENGTH
  • ADVENTITIA: Collagen and Elastic Fibers
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5
Q

Respiratory Epithelium

A
  • CILIATED COLUMNAR Cells predominate
  • Coordinated CILIA movement moves Mucus and/or particulate Matter TOWARDS the PHARYNX
  • GOBLET CELLS contain Large, Light-staining Granules
  • HYDROPHILIC GLYCOPROTEINS called MUCINS, hydrated EXTRACELLULARLY to for MUCUS
  • Cell population tapers off in Terminal Bronchioles
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6
Q

Respiratory Epithelium- Mucus Secretion

A
  • Airway Mucus traps INHALED Particles and transports them OUT of the LUNGS by CILIARY BEATING and COUGHING. Excessive Mucus or deficient clearance are characteristics of ALL COMMON Airway Diseases
  • Airway mucus is produced by Three Cell Types:
    1) Goblet Cells
    2) Clara Cells of the Teminal Bronchioles
    3) Serous cells of the Submucosal Glands
  • Mucus contains:
    1) MUCINS (At least 30 different types)

2) ANTIMICROBIAL MOLECULES (Defensins, Lysozyme, and Immunoglobulin A)
3) Immunomodulatory Molecules (Secretoglobin and Cytokines)

4) Protective Molecules (Trefoil proteins and Heregulin)
- Trefoil proteins have to do with the barrier function of the Respiratory Epithelium

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7
Q

Goblet Cells

A
  • Goblets cells produce MUC5AC
  • Ciliated cells produce MUC1, MUC4, and possibly MUC16
  • Mucus gland cells produce MUC5B and MUC16
  • MUC1, MUC4, and MUC16 are known as TETHERED MUCINS and are found in a Cell Associated form and in a Secreted form
  • MUCIN MOLECULES are designed for OPTIMUM Binding and Trapping of INHALED BACTERIA and particles for clearance from the Lung, this is because the DIVERSE CARBOHYDRATE SIDE CHAINS
  • It has been suggested that Mucins BIND MOST BACTERIA, Viruses, and Inhaled Particles
  • MUC5AC and MUC5B are the MAIN COMPONENT of the Mucin Raft!
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8
Q

Respiratory Epithelium- Mucus Secretion

A
  • Normal airway mucus is 97% WATER and 3% SOLID (Mucins, Non-mucin Proteins, Salts, Lipids, and Cellular Debris)
  • The hydration of the Mucus determines its VISCOSITY and ELASTIC PROPERTIES, two essential Characteristics for NORMAL CLEARANCE of Mucus by CILIARY ACTION and COUGH
  • Airway Mucus consists of TWO LAYERS:
    1) A Periciliary Layer
    2) A Mucus gel layer atop the Periciliary Layer
  • Polymeric MUC5C and MUC5B are continuously synthesized and secreted to REPLENISH the MUCUS GELL LAYER cleared by Ciliary BEATING to ELIMINATE INHALED Particles, Pathogens, and Dissolved Chemicals that might damage the LUNGS
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9
Q

Basal Cells and Neuroendocrine Cells

A
  • Basal Cells and Neuroendocrine Cells (NE Cells of KULCHITSKY) rest ON the BASAL LAMINA but DO NOT Extend to the LUMEN!
  • BRONCHIAL CARINOID TUMORS arise from NE Cells (of Kulchitsky)
  • These cells SECRETE PEPTIDE HORMONES (Serotonin, Somatostatin, Calcitonin, Antidiuretic Hormone [ADH], Adrenocorticotropic Hormone [ACTH], and others)
  • BRONCHIAL CARCINOID TUMORS (Including small Cell Lung Carcinoma) can invade locally and metastasize to Regional Lymph Nodes

***The symptoms of these tumors are from the SECRETIONS that are occurring (Hormone Secretions)

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10
Q

Smoker’s Respiratory Epithelium

A
  • METAPLASIA
  • Change to STRATIFIED SQUAMOUS (Better Protection)
  • DECREASE in CILIATED COLUMNAR Cells (Decreases in Movement of MUCUS)
  • INCREASE in GOBLET CELLS (Protect against Pollutants)
  • Congestion of SMALLER AIRWAYS

SMOKERS MELANOSIS:
- Benign Focal Pigmentations of Oral Mucosa

  • Tends to INCREASE SIGNIFICANTLY with TOBACCO CONSUMPTION (Nicotine)
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11
Q

Trachea

A
  • “Respiratory Epithelium” lines most of the Tract = CILIATED PSEUDOSTRATIFIED COLUMNAR Epithelium with GOBLET CELLS
  • LAMINA PROPRIA: Loose CT containing (zero) mucous glands, Elastic Fibers, Bone/ Cartilage, and Smooth Muscle
  • TRACHEA: 15 to 20 C Shaped Rings of HYALINE CARTILAGE
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12
Q

Trachea Cont

A
  • FIBROELASTIC LIGAMENT: Collagen and Elastic Fibers. Prevents OVERDISTENSION of the LUMEN
  • TRACHEALIS MUSCLE: Smooth Muscle that results in Narrowing during COUGH REFLEX
    • **DECREASES the Radius of the Trachea
  • Smaller diameter of Trachea INCREASES the VELOCITY of EXPIRED AIR
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13
Q

Bronchi

A
  • As Bronchi divide into INTRAPULMONARY BRONCHI, the Tracheal C-shaped RINGS Break Down into CARTILAGE PALTES (Distributed around the Lumen) and Smooth Muscle bundles SHIFT between the Mucosa and the Cartilage Plates
  • Aggregates of LYMPHOID TISSUES are observed in the wall of Intrapulmonary Bronchi (known collectively as BALT, Bronchial-Associated Lymphoid Tissue)

***Smooth Muscle is still present INCASE we want to Change the Diameter of the BRONCHUS!!!

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14
Q

Trachea, Primary, and Secondary Bronchi

A

Trachea:
- Cartilage Rings

Primary Bronchi:
- Cartilage Rings

Secondary Bronchi:
- Cartilage Plates

**As we go through successive divisions, the Bronchi start to LOSE their CARTILAGE

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15
Q

Bronchi

A

SECONDARY BRONCHI:
- Wall structure similar to MAIN BRONCHI EXCEPT, Supporting Cartilage form IRREGULAR PLATES or ISLANDS rather than Rings

TERITARY (Segmental) BRONCHI:
- Smaller diameter than mainstream Bronchi

  • Multiple branchings leading to smaller Bronchi and eventually Bronchioles!!!!
  • **Segmental Bronchi are VERY IMPORTANT when it comes to diseases in the Lungs
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16
Q

Bronchioles

A

EPITHELIUM:

  • Respiratory
  • Gradually REDUCES in THICKNESS
  • The number of Goblet Cells is REDUCED and the Epithelium becomes SIMPLE CILIATED COLUMNAR WITHOUT GOBLET CELLS in the Terminal Bronchioles

GOBLET CELLS:
- Are replaced by CLARA CELLS which PRODUCE a LESS VISCOUS SECRETION

LAMINA PROPRIA:
- Becomes dominated by a SPIRALING LAYER of MUSCULAR MUCOSA in the TERMINAL BRONCHIOLES

  • Cartilage and glands disappear at the level of the Bronchioles; only a THIN LAYER of ADVENTITIA remains in the Terminal Bronchioles
  • With further divisions and Reduction in the DIAMETER of the Bronchioles the CONDUCTING AIRWAYS END with the so called TERMINAL BRONCHIOLES (0.5 mm in Diameter)
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17
Q

Asthma

A
  • Characterized by REVERSIBLE BRONCHOCONSTRICTION of the Smooth Muscle bundles encircling the Bronchiolar Lumen and Mucus Hypersecretion by GOBLET CELLS
  • Can be triggered by ALLERGENS or AUTONOMIC NEURAL FACTORS, leads to a REDUCTION in the Lumen of the Airways
  • WHEEZING, COUGH, and SHORTNESS of BREATH (DYSPNEA) are CLASSIC SYMPTOMS

**Response of the Smooth Muscle to somewhat that has irritated it!!!

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18
Q

Terminal Bronchiole

A

PULMONARY LOBULE:
- A Terminal Bronchiole and the associated Regions of Pulmonary Tissues that it SUPPLIES!!!

***Once we leave the Terminal Bronchiole we start to get into the Respiratory Part!!

***Respiratory Bronchiole: Alveoli start to appear and you can EXCHANGE GAS!!

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19
Q

Club (Clara) Cells

A
  • Club cells are EPITHELIAL CELLS with a DOME-SHAPED APICAL DOMAIN LACKING CILIA
  • They represent 80% of the Epithelial cell population of the Terminal Bronchiole
  • Club Cells SECRETE SURFACTANT that differs from that produced by TYPE II ALVEOLAR CELLS!!!
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20
Q

Club (Clara) Cells Cont

A
  • After AIRWAY INJURY, Club Cells can proliferate and Migrate to replenish ALVEOLAR EPITHELIAL CELLS. This Process is known as ALVEOLAR BRONCHIOLIZATION!!!!!!!!!!!
  • Club cells engulf airborne toxins and break them down via they CYTOCHROME P-450 ENZYMES (Particularly CYP4B1, which is only present in the Club Cells) present in their Smooth Endoplasmic Reticulum
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21
Q

Cystic Fibrosis

A
  • Cystic Fibrosis results in the production of ABNORMALLY THICK MUCUS by glands lining the respiratory and Gastrointestinal tracts
  • Inherited MUTATIONS of CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) results in Defective Cl- TRANSPORT and Increased Na+ ABSORPTION
  • Bacterial infections are associated with the THICK MUCUS plugs consisting of entangled MUC5AC and MUC5B polymers and Dehydrated Mucus
  • Cough, Purulent Secretions, and Dyspnea are typical Symptoms
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22
Q

What happens Physiologically in the Conduction Portion?

A
  • This is the ANATOMIC DEAD SPACE

- It is MOVING THE AIR!!!!!

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23
Q

Control of Bronchiole Diameter (Airway Resistance)

A
  • When air flows through a tube, the AIRWAY RESISTANCE makes the airflow more difficult
  • If AIRWAY resistance is HIGH, Airflow SLOWS DOWN (and takes more muscle effort to produce), while if Airway Resistance is LOW, airflow is FAST and EASY
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24
Q

What controls the Airway Resistance?

A
  • SMOOTH MUSCLE controls the airway resistance!!!
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25
Q

Control of Bronchiole Diameter (Airway Resistance) Equation

A

R = (8nL)/ r^4

R = Resistance

n = Viscosity

L = Length of the Tube

r = Radius of the Tube

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26
Q

Why do we want to change the Airway Resistance?

A

1) I want to send the air in my lungs to the “right” places

2) For right now, that means Alveoli that have a GOOD BLOOD SUPPLY

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27
Q

Describe how the resistance of the always is controlled and the consequences of changes in airway resistance

A
  • Contraction of Smooth Muscle produces changes in radius
  • Since Resistance is INVERSELY PROPORTIONAL to radius to the fourth power, a small Change in Radium —> BIG CHANGE in RESITANCE

***DECREASE Radius —> INCREASE Resistance to Airflow

***INCREASES Radius —> DECREASE Resistance to Airflow

  • We use the changes in Resistance to DIRECT the AIR to the “Right” part of the Lung
    • **The “Right” part of the Lung is the Part with BLOOD!!!
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28
Q

When you Inhale

A

1) Air Travels into:
a) Trachea

b) Bronchi
c) Bronchioles
d) Eventually to ALVEOLI (Gas Exchange)

The Trachea, Bronchi, and Bronchioles AREN’T DESIGNED for GAS EXCHANGE, they do not participate in Gas Exchange!!!!!!!!*

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29
Q

Dead Space

A
  • The conducting airways are DEAD SPACE because no Gas Exchange occurs there
  • In a normal person, ANATOMICAL DEAD SPACE holds about 150 mL of Air

QUICK ESTIMATE: The body weight in lbs = DEAD SPACE in mL (Ex: in a 150 lb person, we expect 150 mL of dead space)

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30
Q

Dead Space Cont

A
  • Occasionally we have ALVEOLI that do NOT participate in GAS EXCHANGE.
  • This ALVEOLAR DEAD SPACE occurs when either there is no Blood Flow to the ALVEOLUS getting air!

**Physiological Dead Space is the SUM of ANATOMIC and ALVEOLAR DEAD SPACE. In young, healthy individuals, Physiologic DEAD SPACE is not much Greater than ANATOMIC Dead Space

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31
Q

Anatomic Dead Space

A
  • Areas of the Respiratory System that do not participate in Gas Exchange by design
  • Ex: Trachea, Bronchi
  • Air must travel through them to get to the Gas Exchange surface in the ALVEOLI
32
Q

Alveolar Dead Space

A
  • Alveoli that do not participate in Gas Exchange (despite the fact that they should be)
  • Results when an Alveoli gets AIR but NO BLOOD
  • We all have some, but shouldn’t have too much
33
Q

Physiologic (Total) Dead Space

A
  • Sum of Anatomic and Alveolar Dead Space
34
Q

Respiratory Portion

A
  • The wall of a Respiratory Bronchiole is DISCONTINUOUS, Interrupted by the SACCULAR OUTPACING of Alveoli.
  • The wall of Terminal Bronchioles is NOT ASSOCIATED with Alveoli
  • Bundles of Smooth Muscle fibers form knobs bulging into the Lumen and the lining epithelium is CUBOIDAL- to -SIMPLE SQUAMOUS.
  • Elastic Fibers are important components of the Bronchioles and Alveolar Walls
35
Q

Gas Exchange in the Tissue

A
  • In the Tissue, OXYGEN and CO2 are TIED TOGETHER.

- This is the ONLY PLACE IN THE BODY where they are connected like that!!!

36
Q

The point of Lungs

A
  • The point of lungs is to bring Ventilation (V) and Perfusion (Q) together in the Alveolus (Alveolar Gas Exchange: Diffusion of Gases)!!!!!
37
Q

Normal Tidal Volume and Alveolar Volume

A

Tidal Volume:
- 500 mL

Alveolar Volume:
- 350 mL

38
Q

Alveolar Ventilation (VA)

A
  • Volume of air reaching the Alveoli
  • If per minute: VA (dot)
  • 4 L/min is AVERAGE VALUE

***Calculated as
Alveolar Ventilation = (Tidal Volume - Dead Space) x Respiratory Rate

39
Q

Perfusion (Q)

A
  • From RIGHT VENTRICLE
  • 5 L Blood/ min
  • How much BLOOD to the LUNGS
  • Cardiac Output (SV x HR)
  • LEFT and RIGHT VENTRICLES should Match!!!
40
Q

Alveolar Gas Exchange: Diffusion of Gases

A

J = [(S.A.) x D x (P1 - P2)] / Distance

J = Diffusion Rate in mL/ min

D: Diffusion coefficient for Each Gas

(P1 - P2) = Pressure gradient across alveolar membrane

S.A. = Surface Area available for diffusion

Distance = Diffusion distance (Thickness of Alveolar Barrier)

**This equation is solved for EACH Gas INDIVIDUALLY!!!!!!

41
Q

How much gas is Exchanged every minute?

  • Translation: What is J?
A

Under normal conditions:
1) 250 mL O2 are Exchanged EVERY MINUTE

2) 200 mL CO2 are Exchanged EVERY MINUTE

**NO THEY ARE NOT EQUAL!!!!

42
Q

Diffusion of Each Gas

A
  • The Diffusion of Each Gas (O2 and CO2) is INDEPENDENT of one another!!!!!!!!
43
Q

Surface Area and Distance in Gas Diffusion are dependent on what?

A
  • The Surface Area and Distance depend DIRECTLY on the STRUCTURE of the ALVEOLUS!!!
44
Q

Alveoli

A
  • Thin walled structures about 0.2 mm in Diameter
  • In a typical section of Lung Tissue, most of the Tissue sample will be composed of Alveoli
  • Alveoli are separated by INTERALVEOLAR SEPTA that consist of TWO SIMPLE SQUAMOUS EPITHELIAL Layers with and INTERSTITIAL (Nonfenestrated Capillaries embedded in an Elastic Connective Tissue) between them
  • The structure of the walls enhance Diffusion and Gas Exchange
45
Q

Alveolar Ducts and Sacs

A
  • The lining of Terminal Bronchiole consists of few Ciliated and Conciliated CUBOIDAL EPITHELIAL CELLS (Clara Cells). And Goblet Cells are NO LONGER PRESENT
  • Respiratory Bronchiole is interrupted at intervals by Saccular Outpocketings, the ALVEOLI
  • Several ALVEOLAR DUCTS result from the division of a Single Bronchiole. The wall of an Alveolar Sac consists of Alveolar Openings. Remnants of the muscle knobs lined by a LOW CUBOIDAL to SQUAMOUS Simple Epithelium can be seen at the Alveolar Openings
  • An ALVEOLAR SAC is continuous with a cluster of Alveoli sharing a wider space called the Alveolar Sac. The Alveolar Duct- Alveolar Sac junction is called the ATRIUM!!!
46
Q

Alveolar Epithelium

A
  • The alveolar Epithelium consists of TWO Cell Types lining the surface of the Capillaries (terminal Branches of the Pulmonary Artery), and the Alveolar Wall
    1) TYPE I Alveolar cells represent about 40% of the ALVEOLAR EPITHELIAL Cell population and cover 90% of the ALVEOLAR SURFACE!!!!!!!
    2) TYPE II Alveolar Cells, about 60% of the Cells, cover only about 10% of the Alveolar Surface and are preferentially located at the angles formed by adjacent ALVEOLAR SEPTA

***TYPE II Alveolar Cells produce SURFACTANT!!!!!

47
Q

Alveolar Macrophages

A
  • Part of the Mononuclear Phagocyte System
  • Found along the Alveolar Surface, within the INTERSTITIAL; often seen detached in Alveolar Lumen of Histological Sections
  • REMOVES DEBRIS that escapes MUCUS and CILIA in the Conducting Portion of the System
  • Many migrate to Bronchi and are transported via Ciliary action to PHARYNX to be swallowed or EXPECTORATED
48
Q

Alveolar Macrophages (Dust Cells)

A
  • Called HEART FAILURE CELLS in CONGESTIVE HEART FAILURE!!!!!!!!
  • Left Ventricle faults to keep pace with Venous return from Lungs
  • Lungs become CONGESTED WITH BLOOD
  • RBCs pass into ALVEOLI and are PHAGOCYTOSED!!!
49
Q

Surface Area available for Diffusion

A
  • The Surface Area corresponds to the NUMBER of Alveoli in the Lungs!!!!

****AS Surface Area INCREASES, Diffusion Rate (J) INCREASES!!!!!!

*****AS Surface Area DECREASES, Diffusion Rate (J) DECREASES!!!!!

Cross Section through the normal Lung:

  • LOTS of Alveoli (millions)
  • If a Single Layer (70 sq meters)
50
Q

Surface Area and “Open” Pulmonary Capillaries

A

The Surface Area also depends on the number of “OPEN” Pulmonary Capillaries
- Number varies with Demand

  • At REST: about 70 mL of blood in Pulmonary Capillaries
  • During EXERCISE: as much as 200 mL of Blood in Capillaries!!!!!!
51
Q

Emphysema

A
  • Emphysema is caused by a PERMANENT ENLARGEMENT of the air space Distal to the Terminal Bronchioles due to the PROGRESSIVE and IRREVERSIBLE Destruction of Elastic Tissue of the Alveolar Walls
  • Elastic Tissue in the INTERALVEOLAR WALL can be DESTROYED by ELASTASE released by Neutrophils present in the ALVEOLAR LUMEN
  • Serum Alpha1-ANTITRYPSIN (Serum Trypsin Inhibitor) NEUTRALIZES ELASTASE!!!!!!!
  • In its absence, NEUTROPHIL ELASTASE is free to BREAK DOWN ELASTASE, which contributes to the ELASTICITY of the LUNGS, resulting in respiratory complication such as EMPHYSEMA or COPD (Chronic Obstructive Pulmonary Disease)

*Lungs cant empty out all the way!!!

***Damaged Eastic Fibers cannot recoil when stretched and, as a result, adjacent Alveoli become Confluent, producing Large Air Spaces, or BLEBS, the structural landmark of EMPHYSEMA

***The Loss of Elastic Tissue also affects TERMINAL and RESPIRATORY BRONCHIOLES

52
Q

The Blood- Air Barrier

A

Blood- Air barrier refers to the structures that O2 and CO2 much cross during Gas Exchange. It contains:

1) CYTOPLASM of Squamous Epithelial Cells (Type I Alveolar Cells or Pneumocytes)
2) Fused BASAL LAMINA of Type I Alveolar Cells and Capillary Endothelial Cells
3) CYTOPLASM of Capillary Endothelial

***There is a lining of Surfactant covering the epithelium and this is done t help facilitate the exchange and help aid the diffusion

53
Q

Distance in correlation with Diffusion Rate

A
  • The Distance is the DIFFUSION DISTANCE (Thickness of Alveolar Barrier)

Includes:

1) Fluid Layer
2) Alveolar Epithelium
3) Interstitial Space
4) Blood Vessel Wall

Average: 0.6 microns

**As Distance INCREASES, Diffusion Rate (J) DECREASES

54
Q

Deposition of Collagen in Interstitial Spaces

A
  • The DEPOSITION of COLLAGEN within the Interstitial Spaces INCREASES the DIFFUSION DISTANCE and DECREASES the DIFFUSION of the gases across the Barrier!!!
55
Q

Acute Respiratory Distress Syndrome (ARDS)

A
  • A form of PULMONARY EDEMS that causes Acute Respiratory Failure, Acute Respiratory Distress Syndrome (ARDS) results from INCREASED PERMEABILITY of the Alveolocapillary Membrane
  • Results from an INCREASE in the HYDROSTATIC PRESSURE in the Alveolar Capillaries (Cardiogenic) or DAMAGE to the Alveolar Epithelial Lining caused by Bacterial Endotoxins or Trauma (Noncardiogenic)
  • FLUID ACCUMULATES in the Lung INTERSTITIAL, Alveolar Spaces, and Small Airways, causing the LUNG TO STIFFEN. This stiffening impairs Ventilation, prohibiting adequate Oxygenation of PULMONARY CAPILLARY BLOOD
  • Severe ARDS can cause INTRACTABLE and FATAL HYPOXEMIA, but patient who recover may have little of no permanent Lung Damage
56
Q

Diffusion Coefficient for Each Gas in Correlation to the Diffusion Rate (J)

A

Diffusion Coefficient for Each Gas Depends on:

1) The SOLUBILITY of the Gas in Water (in your body)
- O2 is LESS SOLUBLE in WATER than CO2

2) The Molecular Weight of the Gas
- CO2 weighs MORE THAN O2

  • **The solubility of CO2 MOER THAN COUNTERS the difference in Molecular Weight so:
    • DCO2 is 20x the DO2!!!!!!!!!!!!!!!!!!!!!
57
Q

Pressure Gradient in Correlation to the Diffusion Rate (J)

A
  • This is the Pressure Gradient ACROSS Alveolar Membrane

Alveolar Space:
- PvO2 = 40 mm Hg

  • PAO2 = 104 mm Hg

(P1 - P2) = (104 - 400 = 60 mm Hg

  • PvCO2 = 45 mm Hg
  • PACO2 = 40 mm Hg

(P1 - P2) = 40 - 45 = -5 mm Hg

O2 has a LARGER GRADIENT!!!!!!!!!!!!!!**

58
Q

Oxygen Diffusion

A
  • A RBC spends about 0.75 seconds in a Pulmonary Capillary (Under Resting Conditions)
  • O2 requires about 0.25 seconds in a Pulmonary Capillary to reach EQUILIBRIUM (PO2 of 100 mm Hg to PO2 of 40 mm Hg)
  • **We have a Large “safety” margin of time before the RBC leaves the Capillary
  • DURING EXERCISE, a RBC spends about 0.25 seconds in a Pulmonary Capillary!!!
  • **Now we have NO “Safety” MARGIN of time before the RBC leaves the Capillary

**Someone with Lung Disease will first notice problems during exertion because of this

59
Q

Quantifying the diffusion of O2

A

Normal Person:
- DLO2: Diffusion Capacity of the Lung for OXYGEN

  • About 21 mL O2/ min/ mm Hg at REST!!!!!!!!
  • mm Hg: AVERAGE GRADIENT along Alveolar Capillary
60
Q

Measuring the DLO2

A
  • Use CARBON MONOXIDE
  • Binds to HB so avidly that it doesn’t dissolve in the Plasma
  • The Paco is 0 mm Hg
  • Have patient INHALE a Single Breath of air will a SMALL PERCENTAGE of CO added!!!!!

Correction Factor:
DLO2 = 1.23 x DLCO!!!!!!!!!!!!!!!!!

61
Q

Quantifying the diffusion of CO2

A
  • A RBC spends about 0.75 seconds in a Pulmonary Capillary (under resting conditions)
  • We have a HUGE “Safety” margin of time before the RBC leaves the Capillary
  • Therefore a person has to have PRETY EXTENSIVE LUNG Disease before that have problems with CO2 retention!!!
  • **EQUILIBRIUM is almost IMMEDIATE!!!
  • PCO2 45 mm Hg initially to 40 mm Hg

*****The DLCO2 at REST has been estimated at about 400 mL CO2/ min/ mm Hg!!!!!!!!

62
Q

Measure Oxygen Diffusion

A
  • Measured using Carbon Monoxide
  • To convert from DLCO to DLO2 multiply by 1.23!!!!!!
  • Calculates to about 21 mL O2/ min/ mm Hg
63
Q

Measure Carbon Dioxide Diffusion

A
  • So FAST/ HIGH that we have a hard time measuring it

- Estimated at 400 mL CO2/ min/ mm Hg

64
Q

Fetal Development

A

1) CANALICULAR STAGE
- Formation of Respiratory Bronchioles and Terminal Sacs (Alveoli)

  • A baby may be viable because of the amount of alveoli bing made
  • Occurs in weeks 17 to 16
  • Vascularization ICNREASES
  • Capillaries found in walls!!!!!

2) TERMINAL SAC STAGE:
- Real formation of the ALVEOLI

  • Type I and Type II Cells

**You don’t make enough A and B SURFACTANT until the Fetus is in weeks 22 and 24

***STEROIDS can elicit more SURFACTANT formation form the Type II Alveolar Cells

65
Q

Phases of Lung Development

A
  • It is not until have sufficient number of ALVEOLI (Canalicular Stage)
  • Need sufficient Capillaries
  • Need sufficient Surfactant
66
Q

Why surfactant matters: Surface Tension

A

AIR/ WATER INTERFACE

  • Air (In Alveolus)
  • Water (The Tissue)

What does water do when exposed to air?
- There is an Air/ Water Interphase where the Air and Water try to remain as SEPARATE as POSSIBLE (One Big Bubble)

  • The minimum number of air molecules are in contact with the minimum number of water molecules
  • The CONFIGURATION is the best way to MINIMIZE the SURFACE TENSION!!!!!!!
67
Q

LaPlace’s Law

A

Pressure = 2T/ r

T: Tension

r: Radius

68
Q

Large Alveolus

A
  • In Large Alveolus, the radius is LARGE

So the PRESSURE is relatively LOW!!!!!

**Alveoli are different sizes

69
Q

Small Alveolus

A
  • In Small Alveolus, the radius is SMALL

So the PRESSURE is relatively HIGH!!!

**Alveoli are different sizes

70
Q

Alveoli

A
  • ***Alveoli are different sizes and share airways
  • Air moves from the Small Alveolus into the Big Alveolus

Therefore: the Pressure in the Big Alveolus got a little smaller because the radius of the Big Alveolus Increased!!!!!!!!

BIG ALVEOLUS GETS BIGGER:

  • This is bad for Surface Area
    1) It reduces the Surface Area available in the Lung tremendously

2) This Alveolus becomes like a balloon that is getting more full so it becomes more difficult to INFLATE!!!!!

***Clearly this doesn’t happen in a normal person because of SURFACTANT, which controls the Surface Tension!!!!!!!!

71
Q

Surfactant

A

1) Surfactant changes the Surface Tension (T)
- It reduces the T in the Smallest Alveoli more than in Larger Alveoli

  • **Surfactant has a BIGGER EFFECT in the Smaller Alveoli than the Large Alveoli!!!
  • In the Small Alveolus, the blobs are much closer together and they move so this is tied to why the surface tension in the small alveoli is affected more. Therefore the small alveoli’s PRESSURE is not HIGH like it should be but its Pressure is the SAME as the Big Alveolus
72
Q

Small Alveolus

A
  • In the Small Alveolus, the radius is Small but SURFACTANT DECREASES the T in proportion to the Radius

Pressure = 2T/ r

***This REDUCES the Pressure in the Small Alveoli

73
Q

Big and Small Alveolus Coexisting

A
  • The Small Alveolus has a Small Pressure and the Big Alveolus has a Small pressure too
  • **There is now NO GRADIENT for Air to Move Down!!!!!
  • SURFACTANT then prevents the Collapse!

**The SURFACTANT allows the Little and Big Alveoli to COEXIST PEACEFULLY!!!!

74
Q

Pressure in the Alveolus

A
  • Pressure in any Alveolus is 2T (Surface tension)/ Radius
    1) Large Radius Alveoli have LOW Internal Pressures
    2) Small Alveoli have HIGH Internal Pressure
    3) Small Alveoli will empty into Big Alveoli given Chance

***SURFACTANT REDUCES the Surface Tension in Small alveoli so the Pressure (Small T/ Small R) is the SAME as in the BIG ALVEOLI!!!!

75
Q

Neonatal Respiratory Distress Syndrome

A
  • Big Alveolus does not have a lot of Capillaries around it anymore, therefore it is HARDER to INFLATE the LUNG and therefore HIGHER and HIGHER Pressures on the Ventilators are needed to INFLATE the Lung and can damage the LUNGS even more!!!!
  • When you see this in a Infant, it si related to the fact that they do not have a SUFFICIENT AMOUNT of SURFACTANT to keep the Alveoli OPEN!!!!!

Cardiopulmonary I (12 decks)

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