Physiology Control Of Respiration

Front 1

What is inspiration initatied by?

Back 1

burst of action potentials in the spinal motor nerves to inspiratory muscles like the diaphragm.

Front 2

when does expiration occur

Back 2

When the action potentials cease, the inspiratory muscles relax, and expiration occurs as the elastic lungs recoil.
and the INTERCOSTAL MUSCLES CONTRACT!
( the inspiratory muscles, the external and diaphragm relax)

Front 3

what controls the alternative firing of neurons in respiration?

Back 3

medulla oblongata

Front 4

2 main components of the respiratory center, and where it is located

Back 4

medulla respiratory center
dorsal
vetnral

Front 5

dorsal respiratory group

Back 5

neurons of the dorsal respiratory group (DRG) fire action potentials primarily during inspiration—DRG neurons have input to the spinal motor neurons that activate respiratory muscles involved in inspiration.

Front 6

ventral respiratory group

Back 6

he upper area, known as the pre-Bötzinger complex, contains spontaneously firing neurons that may act as the basic pacemaker for the respiratory rhythm.

lower part- The lower part of the VRG contains nerves that fire both during inspiration and expiration.The lower part of the VRG contains nerves that fire both during inspiration and expiration.
The inspiratory neurons of the VRG receive input from the inspiratory neurons of the DRG as well as the rhythm generator and, in turn, have input to the inspiratory motor neurons.
contains expiratory neurons most important when large increases in ventilation are required, for e.g. during strenuous exercise.

These neurons are required for activation and contraction of expiratory muscles.

Front 7

How does VRG regulate contraction of inspiratory and expiratory muscles?

Back 7

Inspiratory and expiratory neurons in the medulla show reciprocal inhibition., are not activated at the samet imd

Front 8

Pontine respiratory group (PRG)

Back 8

in Pons fine-tunes the transition between inspiration and expiration.
modulated by cortext and sensory input

Front 9

peripheral chemoreceptors

Back 9

arterial close to the locations of the baroreceptors involved in reflex control of blood pressure and sense changes in the PO2, pH, and PCO2 of the plasma. They include carotid and aortic bodies.-- will increase ventilation.

caroid-are strategically located to monitor O2 supply to the brain and are the predominant peripheral chemoreceptor involved in respiratory control.
aoritic

Front 10

carotid bodie

Back 10

peripher chromosome
are strategically located to monitor O2 supply to the brain and are the predominant peripheral chemoreceptor involved in respiratory control.

Front 11

Central chemoreceptors

Back 11

located in the medulla
rovide excitatory synaptic input to the medullary inspiratory neurons, and are stimulated by an increase in the H+ concentration of the brain’s ECF. Such changes result mainly from changes in blood
PCO2.

Front 12

glomus cells

Back 12

n the carotid and aortic bodies are activated by a decrease in PO2 or pH or an increase in PCO2.

peripheral- increase in ventilation
from a k+ depolarization andAction potentials in sensory neurons lead to brain stem respiratory networks.

Front 13

is oxygen an important facotr in ventilation?

Back 13

Oxygen is not usually an important factor in regulating ventilation because arterial PO2 must fall to less than 60 mm Hg before ventilation is stimulated.

hronic obstructive pulmonary disease (COPD).

Front 14

central chemoreceptors

Back 14

ventral surfave of the medulla-- and set respiratory pace

respond to pH changes in the CSF— they are not directly responsive to CO2 ..... however, incrased CO2, increase H+ and decreases ph

Front 15

how to central chemoreceptors set respiratory pace

Back 15

Central chemoreceptors set the respiratory pace by providing continuous input into the control network.

1Arterial PCO2 increases.
2. CO2 crosses the blood-brain-barrier.
3 CO2 in the CSF is converted to carbonic acid.
4 Carbonic acid readily dissociates into bicarbonate and H+.
Central chemoreceptors are activated by H+.

Receptors signal the control network to increase rate and depth of ventilation.
CO2 is removed from blood.

Front 16

when does ventilation go up

Back 16

diaphram and inspriatory intercostal contractions increase from firing of inspirtary medullary neurons.

Front 17

intra- alveoli pressure

Back 17

(1) the quantity of air in alveoli and (2) the volume of alveoli

inspiratory-- lungs expand lowers Palv. When Palv < Patm, air is drawn into the lungs.

Front 18

when does air stop flowing in

Back 18

When Palv = Patm, air stops flowing inward.

Front 19

what happens to pALV when lung volume decreases? ?

Back 19

Palv increases, causing air to flow out. As air flows out, the quantity of air in the alveoli decreases, which lowers the pressure toward zero.

Front 20

how does air move in and out of lungs

Back 20

pressure gradient duh

Front 21

Transpulmonary pressure

Back 21

is the distending pressure across the
lung wall.

Transpulmonary pressure = Palv – Pip
Ÿ An increase in transpulmonary pressure creates a larger distending pressure across lungs
- Lungs (alveoli) expand, increasing volume

during inspiration ,ranspulmonary pressure leads to a larger distending pressure across the lungs, so the lungs (alveoli) expand with the chest wall and Palv < Patm, so air flows into the alveoli by bulk flow.

Front 22

intrapleural pressure

Back 22

ntraplural pressure (Pip) is the pressure inside the pleural sac.
• Always negative under normal conditions • Always less than Palv
ŸVaries with phase of respiration
- At rest, -4 mm Hg

decreases during inhaationw hen diaphram contracts, and chest expands

Front 23

when is intra-alveolar pressure negative

Back 23

Given relative to atmospheric pressure Ÿ Varies with phase of respiration
- During inspiration = negative (less than atmospheric)
- During expiration = positive (more than atmospheric)
Ÿ Difference between Palv and Patm drives ventilation

Front 24

Intra-alveolar pressure (Palv)

Back 24

is the pressure of air in alveoli

egative Palv is due to elasticity in lungs and chest wall:
• Opposing pulls on intrapleural space.
• Surface tension of intrapleural fluid hold wall
and lungs together

Front 25

type I alveolar cells.

Back 25

air-facing surface of a single alveolar wall is lined by a continuous layer, one cell thick, of flat epithelial cells termed

Front 26

respiratory zone

Back 26

lower reap tract zone contains ontains the sites of gas exchange within the lungs., much thinner walls than conductig zone

Front 27

conducting zone

Back 27

upper resp tract
functions in conducting air from the larynx to the lungs;
larynx, a tube held open by cartilage in its walls, that contains the vocal cords.

Front 28

where does each broonchi begin and divided

Back 28

left bronchi devides into 2 lobes of secondary bronchi and the right divides into 3 lobes of secondary bronchi

Front 29

where do Alveoli begin and what do they do

Back 29

major sites of gas exchange between themselves and the blood, first begin to appear attached to the walls of the respiratory bronchioles. Their numbers increase in the alveolar ducts, and the airways terminate in clusters called alveolar sacs

Front 30

how does inspriation begin

Back 30

is initiated by neural stimulation of the inspiratory muscles— ACh is released at the NMJ.

Front 31

how does the diaphram and external costal msucles move in inspiration?

Back 31

Contraction of the diaphragm causes it to flatten and move downward.,

Contraction of the diaphragm causes it to flatten and move downward. Contraction of the obliquely oriented external intercostals causes the ribs to pivot upward and outward, expanding the chest wall.

Front 32

2 factors invludencing pulmonory ventialtion

Back 32

1.lung compliance and2. airway resistance

want a larger lung compliences because that decrease transpumonory pressure

Front 33

2 factors influicning lung compliance

Back 33

elasticity and surface tension

more surface tension= work is required, less compliant- surfactant increases surface tneion

more elsastic, - forces oppose lung expansion, less compliant

Front 34

air resistance

Back 34

2nd factor contributing to breahting
but doesn't have much to do with the size of tubes because they have more cross area than the trachea
more subject to relfect control from autonomic

Front 35

titdal volume

Back 35

volume that air moves in and out of hte lungs in a single unforced breath 500

Front 36

inspriatory reserve volume

Back 36

max amount of air isnpirted 3000

Front 37

residual volume

Back 37

amount of air sitll in lungs after max expiraiton 1200 ml

Front 38

expiratory resreve volume

Back 38

max amount that can be expired 1000

Front 39

minute ventilation

Back 39

tital volume* respiratory rate

greater than alveolar ventilation because of dead space-- the upper arways with 150 ml

Front 40

MAP

Back 40

map= systolic- (1/3) (systolic- end diastolic)
Map is ver much determined by the arteriorles, because they are regulated by flow. differences in flow between organs edpend upon their relative resitance of their respective arteries.

complicance doees not play significant role in mean artieral pressure

Front 41

Flow

Back 41

pressure/resistance

Front 42

what does the o2 saturation curve show us

Back 42

as blood passes through the lungs under normal conditions, Hb picks up nearly the maximal amount of O2 that it can carry.

Front 43

how much 02 is bound in arterial vs venous

Back 43

100 arterial
40 vneous

Front 44

how much 02 does one leter of blood have

Back 44

As the solubility of O2 in water is low, only 3 ml dissolves in 1 Liter of blood at the normal arterial PO2 of 100 mm Hg,

98 boudn to hemo
23 % of c02 bound to hemoclobin

Front 45

hyper ventilation

Back 45

Hyperventilation results in a drop in [H+] and thus a more alkaline state. This shifts the Hb O2 saturation curve to the left. Under these circumstances, we’d predict an increase in alveolar loading of O2, but also less unloading of O2 to tissues in systemic circulation.

yperventilation at high altitude does not increase the amount of O2 unloaded in the tissues, and therefore is not by itself a homeostatic response.