Only $2.99/month

Terms in this set (48)


1. Decreases surface tension
2. The number of surfactant molecule is inversely proportional with the area of the surface; surface tension doesn't depend on the surface area.
3. The concentration of surfactant is less during inspiration than during expiration
4. Keep the alveoli of different radius in equilibrium; small alveoli - more concentrated surfactant -> less surface tension -> compensate higher pressure in smaller alveoli

*its major component is a phospholipid.



1.In fact during expiration, the alveoli becomes smaller and the surfactant molecules becomes
closer forming micelles. The micelles are degraded or taken into Type II alveolar cells and macrophages and leave the surface of the alveoli. Hence, there's less surfactant present on the alveolar wall
and this fact help the recoiling of lungs
and the collapsing of the alveoli. This
fact explain why during inspiration the
pressure needed to expand lungs is much higher (because the concentration of surfactant is smaller).

2.Furthermore the surfactant also has a stabilizing effect on alveoli of different sizes. Because of Laplace's law, if two bubbles have the same surface tension, the small bubble will have higher pressure.
So smaller alveoli would be unstable and collapse into large alveoli. As an alveolus gets smaller, the molecules of surfactant on its inside surface are more concentrated thus reducing surface tension. The reduction in surface tension helps to maintain the pressure in smaller alveoli equal to the pressure present into larger one.

3.if there is no surfactant, it can cause respiratory distress syndrome of the newborn. they needs lots of effort to breath due to high surface tension.
Minute ventilation (mL/min)= Tidal volume (mL/Breath) x Respiratory rate (Breaths/min) = 6L/min

The total pulmonary ventilation is greater than the alveolar ventilation because of the dead space(150ml). Exchanges of gases with the blood occur only in the alveoli.

The volume of fresh air = tidal volume - dead space = 500 - 150 = 350

The dead space ventilation is approximately of 1.2 L/min [Death space volume x Ventilation rate]
The alveolar ventilation is approximately 4.8 L/min [Alveolar volume (Tidal volume-Dead space volume) xVentilation rate]

-> Alveolar ventilation , rather than minute ventilation, is the more important factor in the effectiveness of gas exchange.

The anatomical dead space is not the only type of dead space. Some fresh inspired air is not used for gas exchange with the blood even if it reaches the alveoli.It is called alveolar dead space. The sum of the anatomical and alveolar dead space is known as physiological dead space.

Ventilation/perfusion ratio = Alveolar Ventilation /Cardiac Output = normal value 0.8

It is approximately 3 at the apex, and 0.3 at the
base(less air than blood).

In fact, when breathing, we expand the bases of the
lungs more than the apices. The alveoli at the base
(which are smaller) expand more and so there will
be a higher degree of ventilation at the level of the
basal alveoli.

-> The base of each lung has a higher ventilation and a higher degree of perfusion, and so a lower value of Ventilation- Perfusion Ratio
As we can see from the graph(9p) the total amount of oxygen carried by hemoglobin depends on:
• Partial pressure of O2
• Concentration of Hemoglobin
• Affinitiy of Hb for O2
This curve applies to blood at 37° C and a normal arterial H+ concentration.

1)partial pressure of O2

- sigmoid : show the cooperative behavior among the different subunits of hemoglobin

- has a steep slope between 10 and 60 mmHg PO2 : good for unloading oxygen, for a small decrease in PO2, a large quantity of Oxygen can be delivered to the tissues.

From 60 mmHg to 100mmHg - plateau like region -The plateau provides an important safety factor so that even a significant limiation of lung function still allows almost normal oxygen saturation of hemoglobin. (60mmHg - 100% saturation)

The oxygen bound to hemoglobin does not contribute directly to the PO2 of the blood.
about 25% of oxygen is dissociated at tissue. The only dissolved O2 has a critcal role in determining pO2!

The plasma and erythrocytes entering the lungs have a PO2 of 40 mmHg, and the hemoglobin saturation is 75 %. The alveolar PO2 is 105 mmHg, facilitating oxygen diffusion from alveoli to plasma.

Most of the oxygen diffusing into the blood from the alveoli does not remain dissolved but combines with
hemoglobin. This maintain the PO2 of the blood at a lower level than the PO2 of alveoli, facilitating the diffusion.

Movement of inspired air into the alveoli is by bulk flow, all movements across membranes are by diffusion.

2) affinity of HB
*2-3 BPG, temperature, PH, pCO2 -> allosteric moduation; binding of a ligand to protein changes the behavior of hemoglobin; change the shapes of hemoglobin -> cause the curve to shift to the right

*fatal/maternal HB

3) concentration of HB
respiratory muscles are the effectors of ventilation. It is important to remember that respiratory muscles are skeletal striated.

voluntary muscle controlled by alpha motorneurons.
Inspiration is initiated by a burst of action potentials in the spinal motor nerves.

The control of ventilation affects:
• The frequency of respiration
• The volume of each breath (depth of breath)

1) Voluntary control: This type of control is mediated by our will and arises from the cortex. The cortex sends fibers along the corticospinal tract.

2) Emotional control: This type of control is mediated by the limbic lobe.

3) Autonomic control: arises from pacemaker cells located in the medulla oblongata.

Pacemaker cells then synapse on lower motorneurons:
◦ Cervical spinal cord levels affecting the diaphragm via phrenic nerves
◦ Thoracic spinal cord levels affecting the diaphragm via intercostal nerves.

4) metabolic control : mediated by a complex reflex; to maintain homeostasis.
- receptors, afferent pathways, integrative centers, efferent pathways and finally the effectors, the muscle of respiration. The integrative centers of this complex reflex arc are the respiratory centers located in the medulla oblongata and in the pons.

- peripheral chemo receptors; carotid body, aortic body, located outside of wall, thorugh small arteries, control respiration
!!!! baroreceptors - in the wall, mechanoreceptor, control cardiovascular

The peripheral chemoreceptors, located high in the
neck at the bifurcation of the common carotid arteries and in the thorax on the arch of the aorta.
There they provide excitatory synaptic input to the medullary inspiratory neurons. The carotid body input is the predominant peripheral chemoreceptor involved in the control of respiration.

- central chemoreceptor
neurons sensitive to H+ in CSF (depends on CO2 in blood). The central chemoreceptors are located in the medulla and, like the peripheral chemoreceptors, provide excitatory synaptic input to the medullary inspiratory neurons. They are stimulated by an increase in the H+ concentration of the brain's extracellular fluid. As we will see later, such changes result mainly from changes in blood PCO2.

Inputs from both the peripheral and central chemoreceptors stimulate the medullary inspiratory neurons to increase ventilation. The end result is a return of arterial and brain extracellular fluid PCO2 and H+ concentration toward normal. Of the two sets of receptors involved in this reflex response to elevated PCO2 , the central chemoreceptors are the more important, accounting for about 70% of the increased ventilation.

5) Drug control : that can act on medullary inspiratory neurons. these centers are very sensitive to drugs effects

6) Pulmonary stretch receptors(mechanoreceptors) control


When the pulmonary stretch receptors are activated by an increase in respiratory volumes, inspiratory centers in the medulla are inhibited; this phenomenon is known as Herin-Breuer reflex
1. peripheral
- aortic body : in the outer layter of arch of aorta, innervated by vagus nerve, to monitor the PO₂, PCO₂ and pH, also contains baroreceptors
- carotid body : in the outer layer of common carotid artery, the PO₂, (PCO₂) and pH of blood that flows toward the brain, innervated by glossharingeal nerve

These receptors are not directly in contact with the blood flowing into the vessels, but they are located outside or embedded in the walls of the arteries.

2. The structure of aortic body and carotid body
they are formed by two types of cells
- type 1 cells are receptor cells that send catecholamines to first order sensory neuron (nerve ending of glosspharingel nerve or vagus nerve in aortic body)
- Type II cells are similar to glial cells and are considered supporting cell

they are excitatory on medullary inspiratory neurons which respond to decrease in O2 and
increase in H+ (and CO2) -> increase in ventilation
The signaling pathway mediated through a change in K+ channel(O2 sensitive) permeability which generate a depolarization -> let Ca2+ to enter the type I cell -> Ca 2+ ions act as a second messenger and induce the release of neurotransmitters on
nerve endings, causing the sensory neurons to fire.

2. central
on ventral surface of medulla : central
chemoreceptors located on the ventral surface of the medulla oblongata. These chemoreceptors are mainly sensitive to H+ concentration in the CSF. The Carbon Dioxide that reaches the CSF is transformed into Bicarbonate and H+ ions.

In general small changes in [H+] are not sensed by central chemoreceptors. For this reason only considerable changes in the pH or H+ concentration are able to induce a response. The response produced by the central chemosensitive areas are generally strong but slow.

There is no response of chemoreceptors in the cases of anemia (low levels of Hb) or in presence of CO (Carbon Monoxide poisoning).
1. pO2 mainly by peripheral chemoreceptor

when arterial PO₂ is lower than 60 mmHg, a marked reflex increase in ventilation.This reflex is mediated by the peripheral chemoreceptors.
The low arterial PO₂ increases the rate at which the
receptors discharge, resulting in an increased in ventilation.

There is no response in anemia and presence of Carbon Monoxide.
Anemia is a decrease in the amount of hemoglobin present in the blood without a decrease in arterial PO ₂, because the concentration of dissolved
oxygen in the arterial blood is normal.
The same analysis can be made in
presence of Carbon Monoxide, which reduces the amount of oxygen combined with hemoglobin.

2. pCO2 -

- Even a small increase in arterial PCO₂
causes a marked reflex that produce a considerable increase in ventilation
- the central chemoreceptors are stimulated more and accounts for the 70 % of the response.
- PO2 level is linked to pCO2. A decreased PO₂ in the alveoli result in a more sensitive response to PCO₂.
- The stimulus is mostly dependent on H+ and so on the increase of PCO₂.
- Ventilation is more sensitive to pCO2 than pO2.

3. H+ control regardless of pCO2
There are many normal and pathological conditions in which a change in arterial H+ concentration is due to some cause other than a primary change in PCO₂ - which conditions are called metabolic acidosis/alkalosis

detected by peripheral receptor and increase/decrease ventilation
e.g) exercise - higher ventilation
vomiting - loss of H+ - lower ventilation

For example, the addition of lactic acid to the blood, as in strenuous exercise, causes hyperventilation almost entirely by stimulation of the peripheral chemoreceptors. This is because H+
penetrates the blood-brain barrier very slowly. In contrast, as described earlier, carbon dioxide penetrates the blood-brain
barrier easily and changes brain H 1 concentration load up - O2 consumption up - ventilation up
*Over the maximal work load, the work load
can increase with no increase in oxygen
consumption, because of lactate.
Lactate is comes from anaerobic metabolism and
is responsible for the oxygen debt.

2. ventilation and moderate exercise [6.3 note 10p graph]

at start of exercise, a sudden increase of ventilation by proprioceptor and phychological factors -> and then ventilation gradually increases (this mechanism is unclear, cannot explain because there is no changes of pCO2, pO2 and pH2 during moderate exercise. During moderate exercise, the alveolar ventilation increases in exact proportion to the increased carbon dioxide production, so alveolar and therefore arterial PCO2 do not change)

Several hypothesis could explain this increase in ventilation such as:
• Proprioceptors and stretch receptors in muscles of respiration and lungs
• Increase in body temperature
• Inputs from motor pathways to
respiratory neurons or reflexes
• Increase in plasma potassium coming
from muscles
• Increase in plasma epinephrine.
• Reflexes conditioned

3.After strenuous exercise, there is an increased rate of oxygen intake(excess post-exercise oxygen consumption) to repay oxygen debt.
- increased H+ keeps ventilation higher till all the
oxygen debt is repaid

Some factors that contribute to EPOC include the replenishment of Phosphocreatine and ATP, the conversion of lactate to pyruvate, and the re-synthesis of glycogen.

4. The maximum rate at which O2 is transported to the mitochondria(O2 uptake limit in exercising muscle) is not depends on saturation of Hb(it's always 100%) or O2 uptake in lungs; it depends on

1) 3 fold increase in O2 extraction from a unit of blood
◦ Muscles use more O2 and consume more CO2, causing a change in partial pressure
◦ More gases diffuse from and to the blood.
◦ more O2 is removed from Hb
◦ Dilation of capillaries and vasodilation.

2) 30 fold increase in blood flow
3) 100 fold increase in metabolic rate in muscle
during strenuous exercise