The absolute refractory period is caused by the closing of the excitatory Na+ channels.

The duration of the

absolute refractory period is fixed while that of the relative refractory period is not.

The absolute refractory period is the interval from the beginning of the action potential until the fiber is
able to conduct another action potential. The relative refractory period follows and is the time
period in which, although the cell has not fully recovered, a small, weak action potential can be generated
as the result of a strong input stimulus. The absolute refractory period is the time period during which the
rapid influx of Na+ rapidly decreases the negativity of the cardiac cell. As Vm (membrane potential)
approaches zero the electrostatic force pulling Na+ into the cell is neutralized. The concentration gradient
of Na+ however continues to push Na+ into the cell and the cell begins to hyperpolarize as Vm begins to
become positive. This closing of the Na+ channels signals the beginning of the absolute refractory period.
Once these channels close, they cannot reopen for a set period of time. When Vm becomes positive by
about 20mV, Na+ continues to to enter the cell because the concentration gradient overpowers the
electrostatic forces. The influx is slow however, and many of the inactivation gates have already closed.
At about 30mV, Na+ influx ceases. The channels remain closed until the first half of repolarization, and
thus the cell is absolutely refractory during this entire period. No action potential can be generated by the
cell during this time, and the cell will not respond to further excitation. This mechanism prevents
sustained, tetanic contraction of cardiac muscle. Tetanus would preclude the normal intermittent pumping
action of the heart and interrupt the pattern of electrical conduction throughout the cardiac muscle. The
result would be fibrulation. The relative refractory period immediately follows the absolute refractory
period, and is due to the efflux of K+ ions. During the second half of repolarization, the excitatory Na+
channels are mostly ready to open, and a small weak action potential can be generated. However, it is
better to wait until the channels are fully ready before continuing with the next excitation. Full excitability
is not regained until the cardiac fiber has been fully repolarized. In order for an action potential to be
generated during the relative refractory period the stimulus must be greater than that which would normally
elicit a response. Unlike the absolute refractory period, the duration of the relative refractory period can
change. As heart rate increases, and systole decreases, the action potential becomes narrower due to a
decrease in relative refractory period. At rest, the heart rate slows, and the action potential becomes wider
as the relative refractory period increases. This allows greater oxygen supply to reach needy areas during
exercise and other stress conditions. These refractory periods are important because during this time the
gradient concentrations of important ions (Na+, K+) are restored. This allows further excitation of the
cardiac fiber. The results of the refractory periods can be seen in the plateau of the cardiac fiber action
potential.

Pulmonary Physiology
 Respiratory system has two important sections: conducting and respiratory zones. Conducting
zones where air travels and respiratory zones where respiration happens!
 Generation 1-16- conducting. 17-23= respiratory zone.
 Conducting zone: cilia permit the movement of air faster into the respiratory zone, cilia is where
no alveolus! Fresh air pass through this part, usually 150 ml of air. It is called the anatomical dead
space.
 Anatomical dead space- quantity of volume passing through to alveolus. Why is there this dead
space? Means no gas exchange!
 As fresh air moving with aid of cilia, reach respiratory zone, we reach certain alveolus and have
gas exchange. Each one of alveolus surrounded by alveolar vessels also known as pulmonary
capillaries. Simple diffusion oxygen pass alveolus to circulation, whereas the co2 passes from
circulation to alveolus.
 The volume inside respiratory zone, depends, 2-3 L.
 Inspiration- diaphragm contracting, it descends, increasing volume of lungs. When breathing
normally- tidal volume!
 Another patient having disease- chest radiography- breathe forcefully- patient inspiring-
contraction! Normal breathing diaphragm descend 1 cm, but forcefully inspiration- diaphragm
descend 10 cm, that’s when pic taken!
  The ribs go up, increase cross-sectional area during inspiration. Each alveoli surrounded by gas-
blood barrier…surface area of 50-100 m.
 Lungs have pleura- FRC, open glottis relax respiratory muscles- 2-3 cm of pressure
 Elasticity and resistance, resistance in lungs are reduced! When in exercise, blood reaches lungs
the resistance reduced to enhance the cardiac output!
 The control of respiration- CNS- dorsal inspiration in medulla activated! Sympathetic signals.
Expiration- ventral exp., expel air to outside.
 Lungs in respiratory zones, contain surfactant, type 2 alveoli cells, if we don’t have surfactant- air
is gonna dry- produce collapse of alveoli.
 Alveolar pressure greater than arteriole pressure- collapse! Pneumothorax!
 Moment inspiring, nose cilia clean from bad particles. Those cilia prevent these harmful
substances from passing.
 Sinuses- produce mucous. Maintain dust particles, we speak because of the sinuses. Frontal
sinuses protect from head trauma.
 Trachea is sensitive to presence of bacteria.
 Alveolar marcophages- they are present in lungs! Get rid of bacteria via lysosomes, kill the
bacteria! Life span- 1 to 5 weeks, once protecting us, move to lymphatic circulation and die.
 Problem with them- decrease production in unhealthy patients, and have respiratory problems!
 Reflexes- brain is activated and involuntarily breath higher, inspiration greater, diaphragm
descend, pressure in lungs rise, intercostal muscles pull diaphragm drastically, uvula is descend
 Cough reflex! Particle in trachea, receptors send info to brain, brain cough center is activated,
involuntariy forceful respiration.
 Broncho constriction- patient with asthma, histamine less! Patient not gonna live. Leukotrienes
have patient great! For broncho constriction. Blocking the production of leukotrienes protect
them!
 A place with contamination- broncho constriction present as a defense mechanism.
 A-alveoli, a- arteriole
 Dalton’s- barometric pressure= nitrogen+ oxygen+ water vapor pressure+ co2
 Nitrogen and oxygen is what we breathe!
 Barometric pressure at sea level 760 mmHg, subatmospheric- 0 atm.
 Cusco, high elevation- hyperventilation and more RBCS production.
 Doubles of ventilation= 80 mmhg, and lower 20 mmhg hypoventilation. Normal is 100 mmHg

Ventillation:
 Spirometer- device, insert tube in mouth, subject expires prolonged and
forcefully in order to check different volumes and capacity.
 Patient expires, the bell goes up and pen goes down! The first important
volume- tidal volume- 500 ml, normal breathing!
 Inspire forcefully- oscillation goes up. Expiration- goes down.
 TL+IRV = inspiratory reserve capacity
 TL+ERV+IRV= vital capacity
 Expiration after the normal tidal volume- functional residual capacity.
 FRC= ERV+RV
 Residual volume- maximum expiration, but we expire all we can and the
remaining air after forceful expiration is called residual volume.
 FRC= is part of residual volume, erv
  Residual volume cant be measured by spirometer.
 Pletysmograph can measure RV, FRC
 TLC= VC+FRC+RV
 Tlc frc, rv CANT BE measured by spirometer, but pletysmograph!
 Our tidal volume 500 ml
 Restrictive disease- patient cant have normal entrance of air, smaller chest-
fibrosis, ribs fractures, so lungs cant expand! Fibrotic tissues- cant expand.
Rib fractures- it hurts to expand.
 Obstructive disease- hyperinflation. TLC greater than normal lung, because of
RV increases abnormally. Increase compliance, inspiratory efforts increase!
 Example- emphysema, constant smoker, destroying alveoli, can breathe but
cant breathe completely.
 Obstruction of single alveolar capillary pressure, oxygen partial pressure will
be 80 instead 100, tissues have hypoxia
 The role of surfactant- decrease the surface tension, which is caused by
intramolecular attractions in the surface of alveoli, causes the tendency to
collapse…alveolus is like a bubble, inside it is covered by thin layer of water,
inside is filled by air…water molecules have attraction, intramolecular
attraction….the attraction of water molecules makes circle smaller,
surfactant reduces surface tension so lungs can expand easily.
 Lung when overstretched when high volume, and becomes rigid, so
compliance increases.
 Giving difference between pressure and volume when inspiring and expiring,
its related to surface tension.
 Compliance is change of volume over change in pressure.
 Water filled lung is more compliant….we don’t have air water interface! So no
surface tension…
 Tidal volume avg- 500 ml
 Intrapleural space pressure- negative 5
 Intrapleural pressure in apex and base is not the same! Because of gravity.
The chest wants to expand but lungs want to collapse. The greater the force
in opposite direction- intrapleural pressure….the greater recoil tendency of
lung the more negative the intrapleural pressure
 Alveoli in apex larger than base, more compliant in base alveoli, less
distended, -2.5.
 The base of lung is better ventilated.

Problems Notes
In order for proper gas exchange to happen, ventilation and blood flow need to
match. If perfusion exceeds ventilation, the amount of oxygen diffusing into the
capillary blood and the amount of carbon dioxide diffusing out of capillary blood are
reduced. Lower than normal Po2 and higher than normal CO2, the lower Po2 will
cause vascular resistance to rise!
A rise or fall in the oxygen saturation of hemoglobin is caused by a decrease in the
arterial O2 tension, from a low V/Q ratio, hypoventilation or anatomical right to left
shunt.
The physiological dead space includes the anatomical dead space (the conducting
airways) and the areas of the lung that are ventilated by not perfused or poorly
perfused, the areas of the lung with a high V/Q ratio.
During inspiration respiratory muscles pull the chest wall out and the diaphragm
down and IP becomes more negative.