• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/60

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

60 Cards in this Set

  • Front
  • Back

3 Main Cell Type in a Alveoli

1. Type I pneumocyte: simple squamous cell, flat for thin layer for gas exchange
2. Type II pneumocyte: more round shaped, secrete alveolar fluid ( lines the lumen and contains surfactant)
3. macrophage: remove any dust and debris to prevent damage

Layers of Wall (respiratory membrane)

* 1. inner layer: alveolar fluid, contains surfactant
* 2. alveolar epithelium cells
* 3. basement membrane of alveolar epithelium
* 4. interstitial space
* 5. basement membrane of capillary endothelium
* 6. capillary endothelium
* all layers are very thin, ideal for gas exchange

CARDIAC NOTCH:

indentation ON LUNGS to accommodate the heart

hilum

region where we have pulmonary veins and arteries

horizontal fissure:

separates middle lobe and superior lobe on the right lung

oblique fissure:

separates the superior and inferior lobes on both lungs

parietal pleura

closely adheres to the cavity

visceral pleura:

closely adheres to the lung tissue

pleura fluid:

reduces friction but also holds the parietal and visceral pleura together

Atmospheric pressure

1 atm or 760mm Hg

Boyle’s law:

pressure is inverse proportional to volume

* as we decrease the volume, pressure increase
* need change volume in thoracic cavity, inside the lungs and inside the alveoli

Alveolar Pressures during INSPIRATION

* at the end of expiration: we stop breathing for a second, atmospheric pressure is equal to the alveolar pressure
* during inspiration: diaphragm contracts moving downwards and expansion of thoracic cavity….increasing the volume inside the lungs and alveoli = decrease in pressure. Pressure in the atmosphere > pressure in the alveoli = air moving from high pressure to low pressure

Alveolar Pressure during Expiration

* End of Inspiration: air filled the alveoli so much that the P of atmosphere = P of the alveoli, no air movement
* Expiration: Diaphragm relaxes moving upwards and fall of the thoracic cavity (snap back of elastic tissue) = decreasing the volume inside the lungs (lungs elastic tissue snaps back) and alveoli decreases and the pressure inside increase, air drawn out into the atmosphere

Inhalation muscles

1. Diaphragm: involved in resting breathing


2. External intercostals: when they contract they pull on the ribs bellow them, moving upwards (involved in resting breathing)


3. Pectoralis minor*


4. Scalenes*
5. Sternocleidomastoid*

Forced Expiration muscles

1. contract abdominal muscles; push on the organs and the organs push up on the diaphragm and reduce the thoracic cavity size
2. internal costal: pull down on the ribs and reduce the size of thoracic cage
3. transverse: work with internal costal to reduce to the rib components making it smaller

Quiet Inspiration

* diaphragm contract and external intercostals contract, pressure is reduced, 500ml of air inhaled
* Diaphragm moves 1 cm & ribs lifted by muscles (pressure difference of 1-3 mm Hg)
* Intrathoracic pressure falls and 500ml inhaled
* External intercostals increase the anteroposterior and lateral chest cavity

Quite Expiration

* muscles relax
* alveolar fluid creates a surface tension that wants bring the alveoli back to its resting position ‘
* Passive process with no muscle action
* Elastic recoil & surface tension in alveoli pulls inward
* Alveolar pressure increases & air is pushed out

Forced Breathing (exercising)

* uses more muscles
* Forced inspiration: sternocleidomastoid brings ribs up, scalene and elevate first two ribs, pectoralsis minor elevate 3rd-5th ribs
* force expiration: muscle relax, and recruit the abdominal and internal intercostals and transverse thoracic

Role of the pleura during breathing

* to get a negative pressure: as the lung tissue starts to recoil the visceral pleura starts to pull away from the parietal… because the pleura is creating a suction. When they try to pull away it increases the volume and decreases the pressure.
* this negative pressure helps stop the lungs from collapsing,
* as diaphragm contracts the thoracic cage gets bigger and pulls the parietal pleura with it and pulls visceral pleura with it. The volume inside the alveoli gets larger and the pressure drops
* The suction effect of the pleural fluid allows parietal pleura to pull visceral pleura with it.

• As the chest wall expands during inhalation, the parietal pleura lining the cavity moves with the cavity


• Visceral pleura and lungs move with the thoracic cavity


• Intra-alveolar pressure drops lower than atmospheric pressure, and inhalation occurs

Dynamics of Normal Breathing

* without breathing,we have negative pressure
* 1. as we inspire the pressure gets even less because there is more space created between visceral and parietal
* 2. the alveoli increase in volume, the pressure decrease
* 3. as the pressure decreases we get a change in volume and filling of air
* 4. muscles relax and decrease the volume and increases the pressure in the pleura cavity
* 5. Alveoli size starts to decrease
* 6. Lungs loose air
1. Surface tension of alveolar fluid:
* if the fluid is made of mostly water it will attracted to other water molecules and create surface tension. If strong enough it could collapse the alveoli. Surface tension allows for recoil
* surfactant is a lipoprotein that gets in the way of the water molecules being attracted t each other, reduces surface tension and stops walls from collapsing

2. Compliance of the Lungs

• Compliance refers to how much effort is required to stretch the lungs and chest wall


• Compliance related to two factors: a) Elasticity


b) Surface tension


• Due to elastic fibres and surfactant the lungs are usually highly compliant

3. Airway resistance

• Airflow = pressure difference between the alveoli and the atmosphere /resistance


• Bronchioles – reduced resistance during inhalation and increased resistance during exhalation


• SNS (NE) – relaxation of smooth muscle in the airways causing dilation = reduced resistance


• PNS (ACh) – contraction of smooth muscle = increased resistance

Tidal volume:

amount of air inspired or expired with each breath. At rest: 500 mL

Inspiratory reserve volume:

amount that can be inspired forcefully after inspiration of the tidal volume (3000 mL at rest)

Expiratory reserve volume:

amount that can be forcefully expired after expiration of the tidal volume (100 mL at rest)

Residual volume:

volume still remaining in respiratory passages and lungs after most forceful expiration (1200 mL)

Inspiratory capacity:

tidal volume plus inspiratory reserve volume (3500 ml)

Functional residual capacity

expiratory reserve volume plus residual volume (2300 ml)

Vital capacity:

sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume (4600 ml)

Total lung capacity:

sum of inspiratory and expiratory reserve volumes plus tidal volume and residual volume. (5800 ml)

Minute ventilation:

total air moved into and out of respiratory system each minute; tidal volume X respiratory rate

Respiratory rate (respiratory frequency):

number of breaths taken per minute

Anatomic lead space:

formed by nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles

Alveolar ventilation(VA)

volume of air available for gas exchange/minute

Diffusion of gases through the respiratory membrane depends upon four factors:

Diffusion of gases through the respiratory membrane depends upon four factors:


1. Membrane thickness
2. Diffusion coefficient of gas


• measure of how easily a gas diffuses through a liquid or tissue. (how soluble is the gas and how large is the molecule?)


• CO2 is 20 times more diffusible than O2


3. Surface area: doesn't really change unless you have a disease like lung cancer
4. Partial pressure differences

* Gas moves from area of higher partial pressure to area of lower partial pressure
* want high pressure inside than lower outside the alveoli and than lower outside in blood (etc)

Dalton’s Law

• Each gas in a mixture of gases exerts its own pressure (as if all other gases were not present)


• Total pressure is sum of all partial pressures


PA (2 atm) + PB (1 atm) = P total (3 atm)


– atmospheric pressure (P atm =760 mm Hg) P atm=PO2 +PCO2 +PN2 +PH2O

Gas Exchange

* pressure of individual gases in air at sea level:





PO2 = 20.84% x 760 = .209 x 760 = 158.4 mmHg (driving pressure that pushes oxygen into our body)




PCO2 =0.04%x760=.0004x760=0.3mmHg (CO2 out of our body,lower because our body makes C02 so is need to be pushed out)




PN2 = 78.62% x 760 = .786 x 760 = 597.5 mmHg




PH2O =0.5% x760 =.005x760 =3.8mmHg

Henry’s Law

• Concentration of a gas in a liquid is determined by its partial pressure and its solubility coefficient


[dissolved gas] = Pgas x solubility coefficient


• CO2 is ~ 24 times more soluble than O2


• N2 has very low solubility unlike CO2


• dive deep & increased pressure forces more N2 to dissolve in the blood


- decompression sickness

Oxygen and Carbon Dioxide Transport in the Blood

Oxygen

* Moves from alveoli into blood (external respiration)
* Oxygen moves from tissue capillaries into the tissues (internal respiration)
* Moves from tissues into tissue capillaries
* Moves from pulmonary capillaries into the alveoli
* Dissolved (1.5%)
* RBC- bound to Hgb (98.5%)
* Dissolved (7%)
* RBC- bound to Hgb (23%)


Partial Pressure changes in the body

Inspired air


PO2 = 160 mmHg


Alveolar air


PO2 = 104 mmHg Why the decrease?


Addition of H2O and loss of O2 to blood


Pulmonary veins


PO2 = 95 mmHg
Why the decrease? Mixing with deoxygenated


blood from bronchial veins

Oxygen Transport

• The heme groups on Hgb can carry up to 4 oxygen molecules

* hemoglobin saturation changes
* when 4 oxygen are bound, the Hgb is 100% saturated
* 2,3-bisphosphoglycerate (BPG) can also affect the saturation of Hgb
* pressure in the lungs is almost 100% saturated
* P02 tissue = 40 >> 23% release to tissue because it doesn't need much
* curve is based on when hemoglobin is full, it has a high infinity for 02, low infinity when its not full

Effect of pH, temp, C02 and Oxygen Release

* can change hemoglobin shape by shifting
* right shift: reduced affinity for 02 caused by decreased pH & temp and increase c02 (happen if you're exercising, means getting greater drop off of 02 at tissues)
* left shift: increase affinity for 02, caused by increased pH and temp, and decreased c02

pH

* As acidity increases, O2 affinity for Hgb decreases
* Bohr effect
* H+ binds to hemoglobin & alters it
* O2 left behind in needy tissues

CO2

• CO2 converts to carbonic acid & becomes H+ and bicarbonate ions & lowers pH.


CO2 + H2O —CA —> H2CO3 H+ + HCO3-

Temperature and Oxygen Affinity for Hgb

• Metabolism=heat as by-product
• As temperature increases, more O2 is released
• Hypothermia – metabolism slows, less O2 released

Effect of BPG

• 2,3-bisphosphoglycerate(BPG): released by RBCs as they break down glucose for energy


• Binds to hemoglobin and increases release of oxygen

C02 Transport

3 forms of transport:
1. Dissolved CO2 – 7% dissolved in blood plasma


2. Carbaminohemoglobin (23%): Hgb + CO2 ↔ Hgb-CO2


Hemoglobin that has released oxygen binds more readily to carbon dioxide than hemoglobin that has oxygen bound to it (Haldane effect)


3. Bicarbonate ions (70%):


CA addition


CO2 +H2O↔H2CO3 ↔H+ +HCO3-

C02 Transport Tissue Level

* at tissue level we have increased C02 levels
* move toward into plasma
* taken up in RBC, carbonhydronase reaction for bicarbonate
* bicarbonate taken out of membrane (chloride shift) and puts chloride inside to balance negative charge (by anti porters)
* H+ binds on to hemoglobin, affinity for 02 drop (Bohr effect)
* Hyadiade effect

Lung Level

* high C02 outside >> move towards alveoli
* pulls equation to make more C02
* hydrogen atoms leave Hgb >> higher affinity for oxygen so C02 moves off the hemoglobin
* can be used for pH buffer (equation)

Respiratory Structures in the Brainstem

* control centres mostly in medulla
* columns of nuclei
* dorsal connected via phrenic nerve >.> diaphragm (inspiration)
* ventral connected via intercostal nerves to costal muscles ( inspiration and expiration)
* pontine may have some role in switching from inspiration and expiration

Starting Inspiration

• Medullary respiratory centre neurons spontaneously establish basic rhythm


• Input received from receptors that monitor blood gases, temperature, muscle/joint movement.

* Send section potentials to respiratory muscles

Increasing Inspiration

* Increased motor neuron activation - increases breathing depth
* Lasts about 2 sec

Stopping inspiration

• Neurons receive input from pontine group & stretch receptors in lungs.


• Inhibitory neurons activated - relaxation of respiratory muscles


• Relaxation of muscles causes expiration - lasts about 3 sec

* Herin-Bruer:
* stretch receptors, detects lungs and sends to medulla and inhibits further inspiration in bronchi and bronchioles
* chemoreceptors
* central receptors: in medulla, detect changes in decreased ph and increased C02 in the CSF, indicates if the body is producing too much c02: sends signal for increased expiration
* receptors in carotid artery (glossopharyngeal) and aortic (vagus nerve): sends signals about decreased 02 or ph changes
* proprioceptors:
* message about muscles and joints. If moving more 02 is need, increases ventilator rates
* receptors touch, temp and pain:
* increase ventilation rates

Heart sounds

lubb: AV valves close (ventricle systole)


dubb: semilunar valves closing (ventricle diastole)

Heamtocrit

% of red blood cells in your body