1. Regulation of breathing

2. BREATHING IN DIFFERENT FUNCTIONAL STATES AND LIVING CONDITIONS.

3. PHYSIOLOGY OF THERMOREGULATION.

REGULATION OF RESPIRATION

Respiration is regulated by two mechanisms:Nervous or neural mechanismChemical mechanismNervous Mechanism: It involves respiratory centers, afferent and efferent nerves.

Respiratory centers:

The centres in the medulla oblongata and pons that collects sensory information about the level of oxygen and carbon dioxide in the blood and determines the signals to be sent to the respiratory muscles.Stimulation of these respiratory muscles provide respiratory movements which leads to alveolar ventilation.Respiratory centers are situated in the reticular formation of the brainstem and depending upon the situation in brainstem, the respiratory centers are classified into two groups: Medullary centers Pontine centers

There are two centers in each group: Medullary Centers:

Inspiratory center

Expiratory center

Pontine Centers: Pneumotaxic centerApneustic center

Inspiratory center:

Inspiratory center is situated in upper part of medulla oblongataThis center is also called dorsal group of respiratory neuronsIt is formed by nucleus of tractus solitariusFunction: it is concerned with inspiration.

Expiratory center:

It is situated in medulla oblongata anterior and lateral to the inspiratory centerIt is also called ventral group of respiratory neuronsIt is formed by neurons of nucleus ambiguous and nucleus retro ambiguous Function: this center is inactive during quiet breathing and inspiratory center is the active center, but during forced breathing or when the inspiratory center is inhibited it becomes active.

Pneumotaxic center:

It is situated in upper Pons.It is formed by nucleus parabrachialis.Function: it controls medullary respiratory centers, particularly the inspiratory center through apneustic center. It always controls the activity of inspiratory center so that duration of inspiration is controlled.Apnuestic center:It is situated in lower Pons.Function: this center increases depth of inspiration by acting directly on the inspiratory center.

Nervous connections of respiratory centers:

Afferent pathway:

Respiratory center receive afferent impulses from different parts of the body according to movements of thoracic cage and lungs.From peripheral chemoreceptor and baroreceptor impulses are carried by glossopharyngeal and vagus nerves to respiratory center.

Efferent pathway:

Nerve fiber from respiratory center leaves the brain and descend in anterior part of lateral column of spinal cord. These nerve fibers terminate in the motor neurons in the anterior horn cells of the cervical and thoracic segments of spinal cord. From motor neurons two sets of nerve fiber arise which supplies particular muscle:

Phrenic nerve fibers: supplies diaphragm The intercostal nerve fibers: supplies intercostal muscles.

Factors affecting respiratory centers:

Impulses from higher centers: impulses from higher center can stimulate or inhibit respiratory centers directly.

Impulses from Thermoreceptors:

Thermoreceptors give response to change in the body temperature.They are cutaneous receptors namely cold and warmthWhen this receptors get stimulated they send signals to cerebral cortexCerebral cortex in turn stimulates respiratory centres and causes hyperventilation.

Impulses from pain receptors: Pain receptors give response to pain stimulus.Like other receptors this receptors also send impulses to the cerebral cortex.Cerebral cortex in turn stimulates the respiratory centers ad causes hyperventilation.

Cough reflex: This is a protective reflex caused by irritation of parts of the respiratory tract beyond nose like larynx, trachea and bronchi.Irritation of any of this part causes stimulation of vagus nerve and cough occurs.Cough begins with deep inspiration followed by forceful expiration with closed glottis.So the intrapleural pressure rises above 100 mm Hg.Then, glottis is suddenly opened with explosive outflow of air at a higher velocity. So the irritants may be expelled out of the respiratory tract.

Sneezing reflex:

It is also a protective reflex which occurs due to the irritation of nasal mucus membrane.During irritation of nasal mucus membrane, the olfactory receptors and trigeminal nerve endings present in the nasal mucosa are stimulated leading to sneezing.Sneezing starts with deep inspiration, followed by forceful expiratory effort with opened glottis and the irritants are expelled out of the respiratory tract.

Deglutition reflex:

During swallowing of the food, the respiration is arrested for a while.Temporary arrest of the respiration is called apnea and apnea which occurs during swallowing called swallowing apnea or deglutition apnea.This prevents entry of the food particles into the respiratory tract.

Chemical Mechanism:

Respiratory Chemoreceptors

If respiratory chemoreceptors were not functional, hypoxia would result; no matter what happens, the subject would breathe at a normal, resting rate

1) Central Chemoreceptors are located on both sides of the medulla where cranial nerves IX (glossopharyngeal nerves) and X (vagal nerves) leave the brain. These chemoreceptors are primarily sensitive to pCO₂ and the pH of blood. As pH falls (gets more acidic) and pCO₂ levels rise, these chemoreceptors provide stimulatory inputs to the inspiratory center; this increases ventilation in an attempt to reduce H⁺ and CO₂ in the blood. The chemoreceptors are actually located in the interstitial space, outside of the blood-brain barrier. As H⁺ions cannot diffuse through the blood-brain barrier, the ability of decreased pH to stimulate respiration is due to H⁺ ions combining with bicarbonate ions to form carbonic acid, which diffuses through the blood-brain barrier, some of which dissociates to release H⁺ions in the interstitium.

In fact, the presence of carbon dioxide and H+ are so critical to maintaining normal respiration, that if someone hyperventilates long enough, they will reduce carbon dioxide so much that they may faint.  This is primarily because of the important role of carbon dioxide in maintaining peripheral blood pressure. Carbon dioxide strongly stimulates constriction of arterioles.  When carbon dioxide levels drop with hyperventilation, blood vessels relax, peripheral blood pressure falls, and less blood and oxygen are delivered to the brain. If the level of oxygen in the brain falls low enough, you pass out.  A little bit different than passing out if you hold your breath too long, in which case you just deplete oxygen in the blood.  In both cases, consciousness is lost because of lack of available oxygen for the brain.

2) Remember that the dura mater, arachnoid and pia mater surround the entire CNS, not just the spinal cord The Bone-Dura-Arachnoid-CSF space has a pH of 7.32. This is just slightly more acidic than the pH of arterial (7.40) and venous (7.38) blood. When the pCO₂ is increased in the bloodstream, CO₂ diffuses easily into the CSF space.  Chemoreceptors on the surface of the medulla sense this increase in CO₂ in the CSF and this may be indirectly due to the resultant decrease in pH.  These chemoreceptors increase respiratory rate to remove CO₂ from the blood and eventually from the CSF by increasing ventilation.

The chemical mechanism of the respiration is operated through the chemoreceptors. Chemoreceptors:They are the receptors which give response to change in the chemical constituents of blood like..HypoxiaHypercapneaIncreased hydrogen ions concentration (decreased blood pH)

Chemoreceptors are classified into two groups:

Central chemoreceptors

Peripheral chemoreceptors

Central chemoreceptors The chemoreceptors present in the brain are called central chemoreceptors.

Situation: They are situated in deeper part of medulla oblongata, close to the dorsal group of neurons.This area is known as chemosensitivearea and neurons are called as chemoreceptors.They are in close contact with blood and CSF.

Action: They are very sensitive to increase in hydrogen ion concentration. Hydrogen ion cannot cross the blood brain barrier and blood cerebrospinal fluid barrier. On the other hand if carbon dioxide increases in the blood as it is a gas it can cross both the barrier easily and after entering the brain it combines with water to form carbonic acid.As carbonic acid is unstable, it immediately dissociates into hydrogen and bicarbonate ions. The hydrogen ion now stimulates the central cemoreceptors which stimulates dorsal group of respiratory center (inspiratory group) and increase rate and force of breathing.

Peripheral chemoreceptors:

Situation: The receptors are present in peripheral portions of the body that’s why called as peripheral chemoreceptors.

Action: They are very sensitive to reduction in partial pressure of oxygen. Whenever, the partial pressure of oxygen decreases these chemoreceptors become activated and send impulses to inspiratory center and stimulate them. Thereby increases rate and force of respiration and rectifies the lack of oxygen.

NEURAL CONTROL OF BREATHING

respiratory center - The series of paired and functionally related autonomic nuclei located bilaterally in the reticular formation of the brain stem; this control center consists of the medullary rhythmicity area (containing the dorsal respiratory group (DRG) (formerly the inspiratory area) and the ventral respiratory group (VRG) = (formerly the expiratory area) and the pontine respiratory center (formerly the pneumotaxic and the apneustic areas); these collections of neurons cooperate to regulate the rate and depth of breathing as an involuntary unconscious activity in response to the physiological needs of the body for O₂ and CO₂ exchange and for blood acid-base balance.

medullary rhythmicity area - A collection of neurons in the reticular formation within the medulla oblongata involved in establishing or modifying the pattern for breathing; within this area are two key components:  (1) the ventral respiratory group (VRG) (formerly the inspiratory area) which autorhythmically stimulates spontaneous ventilation, resting or tidal breathing (eupnea), and (2) the dorsal respiratory group (DRG) (formerly the expiratory area) which responds to situations beyond those of the resting or tidal breathing (eupnea) to alter the pattern for ventilation in response to the physiological needs of the body for O₂ and CO₂ exchange and for blood acid-base balance.

dorsal respiratory group (DRG) (formerly the inspiratory area) - The collection of motor neurons forming nuclei within the dorsal portion of the medullary rhythmicity area of the reticular formation within the medulla oblongata which are involved in altering the pattern for ventilation in response to the physiological needs of the body for O₂ and CO₂ exchange and for blood acid-base balance; these neurons stimulate neurons in the ventral respiratory group (VRG) to achieve those effects; they are responsive to sensory information from chemoreceptors and mechanoreceptors.

ventral respiratory group (VRG)  (formerly the expiratory area) - The collection of autorhythmic motor neurons forming nuclei within the ventral portion of the medullary rhythmicity area of the reticular formation within the medulla oblongata; this group contains both inspiratory and expiratory neurons; the inspiratory neurons stimulate the diaphragm and external intercostals for approximately 2 seconds to cause inspirations and then the antagonistic expiratory neurons fire for approximately 3 seconds to permit passive or stimulate active expirations; thereby inspiratory and expiratory neurons cooperate in a negative feedback control relationship, setting the basic rhythm of respiration (spontaneous ventilation, resting or tidal breathing (eupnea)); VRG neurons may be influenced by the dorsal respiratory group (DRG) for ventilations in situations other than eupnea.

pontine respiratory center (formerly pneumotaxic and apneustic areas) - A collection of neurons in the reticular formation within the pons which limit inspiratory duration by sending inhibitory signals to the medullary rhythmicity area reducing duration of inspiratory impulses causing shorter cycles which increases ventilation rate; these pontine respiratory neurons receive input from higher brain centers and peripheral receptors, and their output fine tunes the breathing rhythm during activities such as speaking, sleeping, or exercising.

cortical influences - The action of higher, "conscious" centers in the cerebral cortex which permit voluntary control of ventilation by interacting with and over-riding the autonomic centers in the medullary rhythmicity area; examples include the control of ventilation during speech and singing, as well as deliberate forceful inspirations, expirations, or attempts at breath holding; pain and certain emotional states may also influence the rate and depth of ventilation in this fashion.

Control Systems. Spontaneous respiration is produced by rhythmic discharge of the motor neurons that innervate the respiratory muscles. This discharge is totally dependent on nerve impulses from the brain; breathing stops if the spinal cord is transected above the origin of the premix nerves.

The pattern of motor stimuli during breathing can be divided into inspiratory and expiratory phases. Inspiration shows a sudden, ramped increase in motor discharge to the inspiratory muscles (including pharyngeal dilator muscles). Before the end of inspiration, there is a decline in motor discharge. Exhalation is usually silent, except at high minute ventilation rates.

The mechanism of generation of the ventilatory pattern is not completely understood, but involves the integration of neural signals by respiratory control centers in the medulla and pons. The nuclei known to be involved are divided into regions known as the following:

· medulla (reticular formation)

o ventral respiratory group (nucleus retroambigualis, nucleus ambigus, nucleus parambigualis and the pre-Bötzinger complex). The ventral respiratory group controls voluntary forced exhalation and acts to increase the force of inspiration.

o dorsal respiratory group (nucleus tractus solitarius). The dorsal respiratory group controls mostly inspiratory movements and their timing.

· pons

o pneumotaxic center.

§ Coordinates transition between inhalation and exhalation

§ Sends inhibitory impulses to the inspiratory area

§ The pneumotaxic center is involved in fine tuning of respiration rate.

o apneustic center

§ Coordinates transition between inhalation and exhalation

§ Sends stimulatory impulses to the inspiratory area – activates and prolongs inhalate (long deep breaths)

§ overridden by pneumotaxic control from the apneustic area to end inspiration

There is further integration in the anterior horn cells of the spinal cord.

Control of ventilatory pattern

Ventilation is normally controlled by the autonomic nervous system, with only limited voluntary override. An exception to this is Ondine's curse, where autonomic control is lost.

Two separate neural mechanisms regulate respiration.

One is responsible for voluntary control and the other for automatic control. The voluntary system is located in the cerebral cortex and sends impulses to the respiratory motor neurons via the corticospinal tracts. The automatic system is located in the pons and medulla, and the motor outflow from this system to the respiratory motor neurons is located in the lateral and ventral portions of the spinal cord.

The motor neurons to the expiratory muscles are inhibited when those supplying the inspiratory muscles are active, and vice versa. These reciprocal innervations are not due to spinal reflexes and in this regard differ from the reciprocal innervations of the limb flexors and extensors. Instead, impulses in descending pathways that excite agonists also inhibit antagonists, probably by exciting inhibitory interneurons.

Medullary Centers.Rhythmic discharge of neurons in the medulla oblongata produces automatic respiration. Respiratory neurons are of 2 types: those that discharge during inspiration (I neurons) and those that discharge during expiration (E neurons). Many of these discharge at increasing frequencies during inspiration, in the case of I neurons, or during expiration, in the case of E neurons. Some discharge at decreasing frequencies, and some discharge at the same high rate during inspiration or expiration. I neurons are actively inhibited during expiration, E neurons during inspiration.

The area in the medulla that is concerned with respiration has classically been called the respiratory center, but there are actually 2 groups of respiratory neurons ). The dorsal group of neurons near the nucleus of the tracts solitaries is the source of rhythmic drive to the centra lateral premix motor neurons. These neurons also project to and drive the ventral group. This group has 2 divisions. The cranial division is made up of neurons in the nucleus ambiguous that innervate the ipsilateral accessory muscles of respiration, principally via the vagus nerves. The caudal division is made up of neurons in the nucleus retroambigualis that provide the inspiratory and expiratory drive to the motor neurons supplying the intercostal muscles. The paths from these neurons to expiratory motor neurons are crossed, but those to inspiratory motor neurons are both crossed and uncrossed.

Pontine & Vagal Influences. The rhythmic discharge of the neurons in the respiratory center is spontaneous, but it is modified by centers in the pons and by afferents in the vagus nerves from receptors in the lungs. The interactions of these components can be analyzed by evaluating the results of the experiments summarized diagrammatically in Fig .

Complete transaction of the brain stem below the medulla stops all respiration. When all of the cranial nerves (including the vagi) are cut and the brain stem is transected above the pons regular breathing continues. However, when an additional transaction is made in the inferior portion of the pons , the inspiratory neurons discharge continuously and there is a sustained contraction of the inspiratory muscles. This arrest of respiration in inspiration is called apneusis. The area in the pons that prevents apneusis is called the pneumotaxic center and is located in the nucleus parabrachialis. The area in the caudal pons responsible for apneusis is called the apneustic center.

Figure. Respiratory neurons in the brain stem. Dorsal view of brain stem; cerebellum removed. The effects of transecting the brain stem at various levels are also shown. The spirometer tracing at the right indicate the depth and rate of breathing, and the letters identify the level transaction. DRG, dorsal group of respiratory neurons; VRG, ventral group of respiratory neurons; NPBL, nucleus parabrachialis (pneumotaxic center); APC, apneustic center; 4^th vent, fourth ventricle; IC, inferior colliculus, CP, middle cerebellar pedumcle. (Modified reproduced, with permission, from Mitchell R A, Berger A: State of the art. Review of neural regulation of raspiration/ am. Rev Respir. Dis. 1975;111-206.)

When the brain stem is transected in the inferior portion of the pons and the vagus nerves are left intact, regular respiration continues. In an apneustic animal, stimulation of the proximal stump of one of the cut vagi produces, after a moderate latent period, a relatively prolonged inhibition of inspiratory neuron discharge. There are stretch receptors in the lung parenchyma that relay to the medulla via afferents in the vagi, and rapid inflation of the lung inhibits inspiratory discharge (Hering-Breuer reflex). Thus, stretching of the lungs during inspiration reflexly inhibits inspiratory drive, reinforcing the action of the pneumotaxic center in producing intermittency of inspiratory neuron discharge. This is why the depth of inspiration is increased after vagotomy in otherwise intact experimental animals, although breathing continues as long as the pneumotaxic center is intact.

When all pontine tissue is separated from the medulla , respiration continues whether or not the vagi are intact. This respiration is somewhat irregular and gasping, but it is rhythmic. Its occurrence demonstrates that the respiratory center neurons are capable of spontaneous rhythmic discharge.

The precise physiologic role of the pontine respiratory areas is uncertain, but they apparently make the rhythmic discharge of the medullary neurons smooth and regular. It appears that there are topically discharging neurons in the apneustic center which drive inspiratory neurons in the medulla, and these neurons are intermittently inhibited by impulses in afferents from the pneumotaxic center and vagal afferents.

REGULATION OF RESPIRATORY CENTER ACTIVITY

Ventilatory rate (minute volume) is tightly controlled and determined primarily by blood levels of carbon dioxide as determined by metabolic rate. Blood levels of oxygen become important in hypoxia. These levels are sensed by chemoreceptors in the medulla oblongata for pH, and the carotid and aortic bodies for oxygen and carbon dioxide. Afferent neurons from the carotid bodies and aortic bodies are via the glossopharyngeal nerve (CN IX) and the vagus nerve (CN X), respectively.

Levels of CO₂ rise in the blood when the metabolic use of O₂ is increased beyond the capacity of the lungs to expel CO₂. CO₂ is stored largely in the blood as bicarbonate (HCO₃^-) ions, by conversion first to carbonic acid (H₂CO₃), by the enzyme carbonic anhydrase, and then by disassociation of this acid to H⁺ and HCO₃^-. Build-up of CO₂ therefore causes an equivalent build-up of the disassociated hydrogen ion, which, by definition, decreases the pH of the blood.

During moderate exercise, ventilation increases in proportion to metabolic production of carbon dioxide. During strenuous exercise, ventilation increases more than needed to compensate for carbon dioxide production. Increased glycolysis facilitates release of protons from ATP and metabolites lower pH and thus increase breathing.

Mechanical stimulation of the lungs can trigger certain reflexes as discovered in animal studies. In humans, these seem to be more important in neonates and ventilated patients, but of little relevance in health. The tone of respiratory muscle is believed to be modulated by muscle spindles via a reflex arc involving the spinal cord.

Drugs can greatly influence the control of respiration. Opioids and anaesthetic drugs tend to depress ventilation, especially with regards to carbon dioxide response. Stimulants such as amphetamines can cause hyperventilation.

Pregnancy tends to increase ventilation (lowering plasma carbon dioxide tension below normal values). This is due to increased progesterone levels and results in enhanced gas exchange in the placenta.

Ventilation is temporarily modified by voluntary acts and complex reflexes such as sneezing, straining, burping, coughing and vomiting.

Receptors play important roles in the regulation of respiration; central and peripheral chemoreceptors, and mechanoreceptors.

· Central chemoreceptors of the central nervous system, located on the ventrolateral medullary surface, are sensitive to the pH of their environment.^[1][2]

· Peripheral chemoreceptors act most importantly to detect variation of the oxygen in the arterial blood, in addition to detecting arterial carbon dioxide and pH.

· Mechanoreceptors are located in the airways and parenchyma, and are responsible for a variety of reflex responses. These include:

o The Hering-Breuer reflex that terminates inspiration to prevent over inflation of the lungs, and the reflex responses of coughing, airway constriction, and hyperventilation.

o The upper airway receptors are responsible for reflex responses such as, sneezing, coughing, closure of glottis, and hiccups.

o The spinal cord reflex responses include the activation of additional respiratory muscles as compensation, gasping response, hypoventilation, and an increase in breathing frequency and volume.

o The nasopulmonary and nasothoracic reflexes regulate the mechanism of breathing through deepening the inhale. Triggered by the flow of the air, the pressure of the air in the nose, and the quality of the air, impulses from the nasal mucosa are transmitted by the trigeminal nerve to the breathing centres in the brainstem, and the generated response is transmitted to the bronchi, the intercostal muscles and the diaphragm.

In addition to involuntary control of respiration by the respiratory center, respiration can be affected by conditions such as emotional state, via input from the limbic system, or temperature, via the hypothalamus. Voluntary control of respiration is provided via the cerebral cortex, although chemoreceptor reflex is capable of overriding conscious control.

A rise in the P.CO₂ or H⁺ concentration of arterial blood or a drop in its P.O₂ increases the level of respiratory neuron activity, and changes in the opposite direction have a slight inhibitory effect. The effects of variations in blood chemistry on ventilation are mediated via respiratory chemoreceptors - receptor cells in the medulla and the carotid and aortic bodies sensitive to changes in the chemistry of the blood which initiate impulses that stimulate the respiratory center.

Superimposed on this basic chemical control of respiration, other afferents provide nonchemical controls for the fine adjustments that affect breathing in particular situations held constant, the effects of excess in the blood are combated, and the P.O₂; is raised when it falls to a potentially dangerous level. .

The respiratory minute volume is proportionate to the metabolic rate, but the link between metabolism and ventilation is CO₂, not O₂. The receptors in the carotid and aortic bodies are stimulated by a rise in the P CO₂ or H⁺ concentration of arterial blood or a decline in its PO₂. After denervation of the carotid chemoreceptors, the response to a drop in PO₂; is abolished; the predominant effect of hypoxia after denervation of the carotid bodies is a direct depression of the respiratory center.

Table. Stimuli affecting the respiratory center

Chemical control
CO2	Via CSF H^+concentration
O2	Via carotid and aortic bodies
H^+
Nonchemical control
Afferents from proprioceptors
Afferents from pharynx, trachea, and bronchi for sneezing, coughing, and swolowing
Vagal afferents from inflation and deflation receptors
Afferents from baroreceptors: arterial, ventricular, pulmonary

The response to changes in arterial blood H⁺ concentration in the pH 7.3-7.5 range is also abolished, although larger changes exert some effect. The response to changes in arterial P.CO₂ is affected only slightly; it is reduced no more than 30-35%.

Carotid & Aortic Bodies.There is a carotid body near the carotid bifurcation on each side, and there are usually 2 or more aortic bodies near the arch of the aorta. Each carotid and aortic body (glomus) contains islands of 2 types of cells, type I and type II cells, surrounded by fenestrated sinusoidal capillaries.

NONCHEMICAL INFLUENCES ON RESPIRATION

Afferents from "Higher Centers".

There are afferents from the neocortex to the motor neurons innervating the respiratory muscles, and even though breathing is not usually a conscious event, both inspiration and expiration are under voluntary control. Pain and emotional stimuli affect respiration, so there must also be afferents from the limbic system and hypothalamus.

Since voluntary and automatic control of respiration is separate, automatic control is sometimes disrupted without loss of voluntary control. The clinical condition that results has been called Ondine's curse. In German legend, Ondine was a water nymph who had an unfaithful mortal lover. The king of the water nymphs punished the lover by casting a curse upon him that took away all his automatic functions. In this state, he could stay alive only by staying awake and remembering to breathe. He eventually fell asleep from sheer exhaustion and his respiration stopped. Patients with this intriguing condition generally have disease processes that compress the medulla or bulbar poliomyelitis. The condition has also been inadvertently produced in patients who have been subjected to bilateral anterolateral cervical cordotomy for pain. This cuts the pathways that bring about automatic respiration while leaving the voluntary efferent pathways in the corticospinal and rubrospinal tracts intact.

Afferents from Proprioceptors. Carefully controlled experiments have shown that active and passive movements of joints stimulate respiration, presumably because impulses in afferent pathways from proprioceptors in muscles, tendons, and joints stimulate the inspiratory neuron. This effect probably helps increase ventilation during exercise.

Responses to Irritation of the Air Passages. Sneezing and coughing are reflex responses to irritation of receptors in the mucosa of the large respiratory passages. Irritation of the walls of the trachea or large bronchi produces coughing, which begins with a deep inspiration followed by forced expiration against a closed glottis. This increases intrapleural pressure to 100 mm Hg or more. The glottis is then suddenly opened, producing an explosive outflow of air at velocities up to 965 km (600 miles) per hour. Sneezing is a similar expiratory effort with a continuously open glottis. These reflexes help expel irritants and keep the airways clear.

Other Pulmonary Receptors. The vagally mediated inhibition of inspiration produced by inflation of the lung has been mentioned above. The response is due to stimulation of stretch receptors located in the smooth muscle of the airways. Pulmonary deflation receptors that trigger inflation have also been described, and the expiratory and inspiratory reflex responses to pulmonary inflation and deflation, respectively, have been known as the Hering-Breuer reflexes. However, the deflation receptors respond better to pulmonary congestion and embolization, producing shallow, rapid breathing, and they have come to be called J receptors instead, because of their juxtacapillary location. There are also lung irritant receptors located between the epithelial cells in the bronchi and bronchioles. When stimulated, they initiate hyperventilation and bronchoconstriction, but their function in normal breathing is not known.

Effect of Peripheral Stretch Receptors (proprioceptors) on Respiration

When we exercise, we may experience an increase in depth and rate of respiration to meet the increased oxygen requirement. But the increase in respiration often precedes the actual increased oxygen requirement There are probably at least 2 components to this increase in respiration that precedes the increased oxygen requirement. The first component is "anticipation of exercise" and may involve activation of the sympathetic nervous system. The second component involves activation of stretch receptors (proprioceptors) in skeletal muscle and joints (tendon organs). Increased activity of stretch receptors is detected by the medulla, and results in increased rate and depth of respiration. The effect is very rapid, and shows an "added value" to stretching before exercise (ie. in addition to heating up muscles and connective tissues and reducing stretch-related injuries).

Impulses from ‘J’ receptors of lungs:

‘J’ receptors are juxtacapillary receptors which are present in wall of the alveoli and have close contact with the pulmonary capillaries.These receptors get stimulated during conditions like pulmonary edema, pulmonary congestion, pneumonia as well as due to exposure of exogenous and endogenous chemicals like histamine, serotonin.Stimulation of ‘J’ receptor produces a reflex response called apnea.

Impulses from irritant receptors of lungs:

Irritant receptors are situated on the wall of bronchi and bronchioles of lungs.They got stimulated by harmful chemicals like ammonia and sulfur dioxide. Stimulation of irritant receptors produces reflex hyperventilation along with bronchospasm which prevents entry of harmful chemicals into the alveoli.

Impulses from Proprioceptors: Proprioceptors are the receptors which give response to the change in the position of different parts of the body.This receptors are situated in joints, muscles and tendons. They get stimulated during exercise and sends impulses to the cerebral cortex.Cerebral cortex in turn by activating medullary respiratory centres causes hyperventilation.

Respiratory Components of Other Visceral Reflexes.

The respiratory adjustments during vomiting, swallowing and gagging; inhibition of respiration and closure of the glottis during these activities not only prevent the aspiration of food or vomitus into the trachea but, in the case of vomiting, fix the chest so that contraction of the abdominal muscles increases the intra-abdominal pressure. Similar glottis closure and inhibition of respiration occur during voluntary and involuntary straining.

Hiccup is a spasmodic contraction of the diaphragm that produces an inspiration during which the glottis suddenly closes. The glottis closure is responsible for the characteristic sensation and sound. Yawning is a peculiar "infectious" respiratory act the physiologic basis and significance of which are uncertain. However, under ventilated alveoli have a tendency to collapse, and it has been suggested that the deep inspiration and stretching open them alveoli and prevent the development of atelectasis. Yawning also increases venous return to the heart.

Respiratory Effects of Baroreceptor Stimulation. Afferent fibers from the baroreceptors in the carotid sinuses, aortic arch, atria, and ventricles relay to the respiratory center as well as the vasomotor and cardioinhibitory centers in the medulla. Impulses in them inhibit respiration, but the inhibitory effect is slight and of little physiologic importance. The hyperventilation in shock is due to chemoreceptor stimulation caused by acidosis and hypoxia secondary to local stagnation of blood flow and is not baroreceptor mediated. The activity of the inspiratory neurons affects the blood pressure and heart rate and activity in the vasomotor center and the cardiac centers in the medulla may have minor effects on respiration.

Airway receptors. that may have some relevance to the effect of anesthetics include laryngeal and pulmonary irritant receptors and pulmonary stretch receptors. These receptors play an important role in the regulation of breathing patterns, laryngeal and pulmonary defense mechanisms, and bronchomotor tone. Irritant receptors are situated between airway epithelial cells and may mediate rapid reflex responses such as coughing, laryngospasm, bronchoconstriction, and mucus secretion following the induction of general anesthesia, abrupt increases in the inspired concentration of volatile anesthetics, and sudden mechanical deformation of the laryngotracheobronchial system.

Slow-adapting pulmonary stretch receptors, located within small airway smooth muscle (high concentration near the carina), respond to stretching or changes in lung volume. Increases in lung volume increase afferent nerve traffic via the vagus nerve to the respiratory control center, thereby inhibiting further inspiration (the Hering-Breuer reflex). This limitation of inspiration elicited by pulmonary stretch receptors may determine the relationship between tidal volume and respiratory frequency, but unlike in animals, the Hering-Breuer reflex cannot be demonstrated in the awake resting human during normal tidal volume breathing. The alteration in ventilatory pattern by anesthetics has been attributed to sensitization of pulmonary stretch receptors, leading to lower tidal volumes and tachypnea. The presence of volatile anesthetics increased vagal afferent discharge at varying lung volumes in decerebrate cats (i.e., sensitization of pulmonary stretch receptors), but little evidence exists of such a mechanism in humans. There is evidence in the cat that halothane-induced tachypnea is primarily a suprapontine effect, but the mechanism of production of tachypnea with decreased tidal volume in anesthetized humans remains unclear.

The direct effects of halothane, isoflurane, and enflurane on pulmonary and laryngeal irritant receptors and on tracheobronchial slow-adapting stretch receptors have been investigated in spontaneously breathing and vagotomized, paralyzed dogs. All three volatile anesthetics increase the activity of laryngeal irritant receptors and inhibit pulmonary irritant receptors. In addition, the volatile anesthetics elevate the excitation threshold and increase the sensitivity of low-threshold stretch receptors. The inspiratory activity was augmented while the end-expiratory activity was greatly attenuated. The clinical implications of these findings have yet to be determined, but these anesthetic-induced changes may in part relate to effects on reducing bronchomotor tone.

It has been suggested that general anesthesia may result in posterior tongue displacement, producing upper airway obstruction; however, several recent studies do not confirm this. Anteroposterior displacement of upper airway structures occurs with changes in head position that are in the same direction as that of the mandible. In addition, general anesthesia and paralysis may widen the dimensions of the larynx, but the nasopharyngeal airway decreases in size. Volatile anesthetics produce a greater depression of the upper airway electromyogram or nerve activity as compared to that of the diaphragm in intact anesthetized, spontaneously breathing cats and in paralyzed, ventilated, vagotomized cats. The extent to which this depression of upper airway motoneuron activity is a result of an anesthetic-induced inhibition of the reticular activating system is unknown.

The epithelium of the trachea, bronchi, and bronchioles is supplied with sensory nerve endings that are stimulated by irritants that enter the respiratory airways. These cause coughing and sneezing. They possibly also cause bronchial constriction in such diseases as asthma and emphysema.

Function of Lung "J" Receptors. A few sensory nerve endings occur in the alveolar walls in Juxtaposition to the pulmonary capillaries, from whence comes the name "J" receptors. They are stimulated when irritant chemicals are injected into the pulmonary blood, and they are also excited when the pulmonary capillaries become engorged with blood or when pulmonary edema occurs in such conditions as congestive heart failure. Though the functional role of the J receptors is not known, their excitation perhaps does give the person a feeling of dyspnea.

Limitation of Inspiration by Lung Inflation Signals - the Hering-Breuer Inflation Reflex

This is a reflex triggered to prevent over-inflation of the lungs. Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations.

Once activated, they send action potentials through large myelinated fibers of the paired vagus nerves to the inspiratory area in the medulla and apneustic area of the pons. In response, the inspiratory area is inhibited directly and the apneustic area is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur.

The Hering–Breuer inflation reflex ought not be confused with the deflation reflex discovered by the same individuals, Hering and Breuer. The majority of this page discusses the inflation reflex; the deflation reflex is considered separately at the end.

The Hering–Breuer inflation reflex, named for Josef Breuer and Ewald Hering, is a reflex triggered to prevent over-inflation of the lungs. Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations.

Once activated, they send action potentials through large myelinated fibers^[4] of the paired vagus nerves to the inspiratory area in the medulla and apneustic center of the pons. In response, the inspiratory area is inhibited directly and the apneustic center is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur.

The Hering–Breuer inflation reflex ought not be confused with the deflation reflex discovered by the same individuals, Hering and Breuer. The majority of this page discusses the inflation reflex; the deflation reflex is considered separately at the end.

Located in the walls of the bronchi and bronchioles throughout the lungs are stretch receptors that transmit signals through the vagi into the dorsal respiratory group of neurons when the lungs become overstretched. These signals affect inspiration in much the same way as signals from the pneumotaxic center; that is, they limit the duration of inspiration .

Therefore, when the lungs become overly inflated, the stretch receptors activate an appropriate feedback response that "switches off" the inspiratory ramp and thus limits further inspiration. This is called the Hering-Breuer inflation reflex. This reflex also increases the rate of respiration because of the reduced period of inspiration, the same as is true for signals from the pneumotoxic center.

Figure 3. Effect of vagal stimulation (between arrows) on discharge rate in phrenic nerve fibers in an “isolated inspiratory center preparation.” The cat had been prepared by cutting both vagi and transecting the medulla at the caudal border of the pons, this cutting off the pneumotaxic center. In A, the continuous discharge of the inspiratory neurons is shown. In B and C, stimulation of the proximal stump of one vagus produces, after a considerable latent period, inhibition of inspiratory discharge. The animal exhales when the inspiratory discharge stops, as is shown by the record of respiratory excursions (upper line in B and C; inspiration upward).

However, in human beings, the Hering-Breuer reflex probably is not activated until the tidal volume increases to greater than approximately 1.5 liters. Therefore, this reflex appears to be mainly a protective mechanism for preventing excess lung inflation rather than an important in- gradient in the normal control of ventilation.

EFFECTS OF EXERCISE

We breathe oxygen into the body from the atmosphere. While this oxygen does not itself contain useable energy, it is the key that unlocks the energy stored in previously-ingested food. As the energy demands of the contracting muscles change during exercise, so must their energy and oxygen provision. But oxygen comprises only 21% of the atmospheric air; one therefore needs to inhale a volume of air each minute which is at least five times the volume of oxygen which is being absorbed out of the lungs by the body.

Lung ventilation — the volume breathed in and out per minute — however, is not five times that of the rate of oxygen utilization for metabolism, rather, it is twenty-five times. This is because most of the oxygen is breathed back into the atmosphere during expiration: only 20% or so of the inspired oxygen is actually taken up by the blood coursing through the lungs en route to the cells.

The air taken into the lungs does not all reach the gas-exchange regions (the alveoli). Airways that conduct air to the alveoli do not themselves take part in this exchange: only the volume of air that gets beyond this dead space into the alveoli contributes to the gas exchange. Consequently the alveolar ventilation is less than the total ventilation — and this is the volume which provides the oxygen to be taken up into the body.

The alveolar oxygen concentration, and its equivalent oxygen pressure, is determined by the balance between the supply of oxygen to the alveoli and the demand for its uptake into the blood: the alveolar ventilation per minute and the oxygen consumption per minute. The alveolar oxygen pressure in turn establishes the oxygen pressure in the arterial blood, which is normally maintained at, or close to, a constant level during exercise, the same level as when at rest, despite the body's oxygen consumption increasing more than 10-fold. This can only be achieved if the alveolar ventilation increases proportionally. Normally it does so, increasing so that it maintains a ratio of about twenty times the oxygen uptake rate, for moderate exercise, with the ratio for total ventilation being about twenty five.

While this characterizes the ventilation needed to maintain the level of oxygen in the arterial oxygen, it may or may not be appropriate for the other vital breathing requirement during exercise — the defence of blood and tissue acidity.

The exercise-induced challenge to the body's acidity levels has two different origins. Firstly, foodstuffs that serve as energy sources for exercise (carbohydrates and fats) are composed entirely of hydrogen, carbon, and oxygen atoms. During the progressive metabolic fragmentation of food molecules, hydrogen atoms are stripped away, to link with oxygen, yielding energy.

For example, for glucose:

C₆H ₁₂O₆ + 6O₂ → 6H₂O + 6CO₂

This leaves the carbon and oxygen to be vented into the atmosphere as carbon dioxide. As the body's carbon dioxide production from this source is normally approximately equal to its oxygen consumption during exercise, the same level of ventilation can serve both purposes: intake and exhaust. However, if ventilation does not increase sufficiently during exercise, the oxygen level will fall in the blood and tissues, and the carbon dioxide level will rise. Such an increase in carbon dioxide would increase blood and tissue acidity.

The body's acidity is determined by the concentration of hydrogen ions [H⁺] — the positively-charged protons which form the nuclei of the smallest of all atoms. An increase in carbon dioxide in body fluids increases the concentration of [H⁺]. For [H⁺] to be stabilized in the arterial blood leaving the lungs, the carbon dioxide level needs to be regulated by exhaling the carbon dioxide at a rate equivalent to its production rate

Normally, for moderate exercise, ventilation does indeed increase in proportion to the increased metabolic rate, thereby maintaining arterial blood levels of both oxygen and carbon dioxide (and hence [H⁺]) at, or close to, resting levels. This control is mediated through an interaction of neural and blood-borne mechanisms. The neural mechanisms which lead to muscle contraction also simultaneously signal the breathing control centres of the brain; these receive neural information from the contracting muscles as well. If the resulting drive to breathe is not appropriate, then an ‘error’ in the arterial oxygen, carbon dioxide, and [H⁺] levels is sensed by chemoreceptors which ‘sample’ the blood in the carotid arteries perfusing the brain. This provides the ‘fine tuning’ of the control system.The second challenge to arterial [H⁺] stability occurs only at higher work rates, where the energy demands cannot be met entirely through aerobic (i.e. oxygen-linked) metabolism. At these work rates the aerobic transfer of energy is supplemented by degradation of carbohydrates to lactic acid — present in the form of a lactate ion [L^-] and [H⁺]. This component is anaerobic metabolism (it utilizes no oxygen). The fitter the subject, the higher the work rate at which it begins to contribute (see figure). The resulting increase in [H⁺] has a number of deleterious effects on exercise tolerance: impaired muscle contraction; perception of limb fatigue; and ‘shortness of breath’.

As exercise continues at this high intensity, the body's acidity level can only be maintained (or its increase constrained) if the carbon dioxide-related component of the acidity is reduced. The body therefore ‘compensates’ by increasing ventilation proportionally more relative to carbon dioxide production. This reduces alveolar and arterial carbon dioxide levels (see figure) as a result of the increased carbon dioxide ‘washout’. Clearly, the greater the amount of carbon dioxide ‘washed out’ under these conditions, the less will be the increase in acidity for any given level of lactic acid production.

The additional drive to breathe which is linked to the increased lactic acid levels is thought to result predominantly from the effects of the [H⁺] (and other mediators such as potassium ions released from the active muscles) stimulating the carotid chemoreceptors. Neither hydrogen ions nor potassium ions readily cross the blood-brain barrier, so they do not stimulate the other chemoreceptors on the surface of the brain stem (which in other circumstances also influence ventilation).The increase in ventilation during exercise could, theoretically, be accomplished by an infinite variety of depths (tidal volumes) and number (breathing frequency) of breaths per minute. Very deep and slow breathing requires extra effort because the thorax, and the lungs in particular, become very stiff at high volumes. Rapid shallow breathing, on the other hand, mostly ventilates the dead space. The spontaneously-chosen pattern is typically the one which most effectively combines low breathing effort with a high fraction of the breaths reaching the alveoli. Consequently, most people initially increase ventilation predominantly by increasing tidal volume up to a certain optimal maximum; higher ventilatory demands are then achieved predominantly by increasing breathing frequency. In many sporting events, however (e.g. swimming, rowing, and even running), athletes must, or choose to, link the duration of each breath to the cadence of their limb motions.

Profiles of response of ventilation and arterial lactate and carbon dioxide levels to exercise that progressively increases to the limit of the subject's tolerance. The dashed line represents a subject of normal fitness, the solid line represents an athlete capable of achieving higher levels of oxygen consumption. The solid circle and the open circle represents the levels at which the subjects begin to increase their lactic acid production. Maximum possible ventilation shows the highest level that can be achieved by these subjects

Physical training or increased fitness does little to improve the lung as a mechanical pump or gas exchanger, unlike the beneficial effects of exercise on skeletal muscles and the heart. Luckily, however, the limits of operation of the lungs normally far exceed the demands placed upon them. For example, at maximum levels of exercise, not only is full blood oxygenation maintained in normal subjects, but also ventilation has not reached a maximum: it can be increased further by volitional effort (see figure). Elite athletes may be different in this regard. The unusually high metabolic rates they can achieve require unusually high levels of ventilation and of blood flow through the lungs. Those athletes who have not been graced by their genetic make-up to have large lungs with large airways (allowing high levels of airflow), and large capillary volumes (allowing the high cardiac output of rapidly-flowing blood to be exposed to the gas-exchange surface at the alveoli long enough for oxygenation to be completed), can show a component of ‘pulmonary limitation’ to exercise. This is manifest, only at a very high work rates, by airflow rate reaching a limiting maximum, and by a reduction in arterial oxygenation — but only in those without the appropriate genetically-superior lung structure.

Normal individuals also experience ‘shortness of breath’ (dyspnoea) during exercise. This is quite modest at low work rates — except when the carotid chemoreceptors are sensitized, such as during sojourns at high altitude. At high work rates the dyspnoea is usually more marked and sustained. There is a narrow range of work rates — high but usually sustainable for long periods — for which dyspnoea develops but which then subsides as the exercise continues. This relief of dyspnoea has been termed second wind. This proves difficult to reproduce in the laboratory; consequently its mechanisms are poorly understood. Reduction in the lactic acid-related drive to breathe, as aerobic mechanisms catch up with the high-energy demands, is likely to be contributory.

Many cardiovascular and respiratory mechanisms must operate in an integrated fashion if the O₂ needs of the active tissues are to be met and the extra CO₂ and heat removed from the body during exercise. An increase in ventilation provides extra O₂, eliminates some of the heat, and excretes extra CO₂; circulatory changes increase muscle blood flow while maintaining an adequate circulation in the rest of the body, and there is an increase in the extraction of O₂ from the blood in muscle.

Changes in Ventilation

During exercise, the amount of O₂ entering the blood in the lungs is increased because the amount of O₂ added to each unit of blood and the pulmonary blood flow per minute are increased. The PO₂ of blood flowing into the pulmonary capillaries falls from 40mm Hg to 25 mm Hg or less, so that the alveolar capillary PO₂ gradient is increased and more O₂ enters the blood. Blood flow per minute is increased from 5.5 l/min to as much as 20-35 l/min .

Figure 1.Relation between work load, blood lactic acid, and O₂ uptake. I-VI, increasing work loads produced by increasing the speed and grade of treadmill on which the subjects worked.

The total amount of O₂ entering the blood therefore increases from 250 ml/min at rest to values as high as 4000 ml/min. The amount of CO₂ removed from each unit of blood is increased, and CO₂ excretion increases from 200 ml/min to as much as 8000 ml/min. The increase in O₂ uptakes is proportionate to work load up to a maximum. Above this maximum, O₂ consumption levels off and the blood lactic acid level rises precipitously.

The lactic acid comes from muscles in which aerobic resynthesis of energy stores cannot keep pace with their utilization and an oxygen debt is being incurred.

There is an abrupt increase in ventilation with the onset of exercise, followed by a further, more gradual increase .

With moderate exercise, the increase is due mostly to an increase in the depth of respiration; this is accompanied by an increase in the respiratory rate when the exercise is more strenuous.

Figure 2. Change in ventilation during exercise.

There is an abrupt decrease in ventilation when exercise ceases, followed by a more gradual decline to preexercise values. The abrupt increase at the start of exercise is presumably due to psychic stimuli and afferent impulses from proprioceptors in muscles, tendons, and joints. The more gradual increase is presumably humeral even though arterial pH, P.CO₂ and P.O₂ remain constant during moderate exercise. The increase in ventilation is proportionate to the increase in O₂ consumption, but the mechanisms responsible for the stimulation of respiration are still the subject of much debate. The increase in body temperature may play a role. In addition, it may be that the sensitivity of the respiratory center to CO₂ is increased or that the respiratory fluctuations in arterial P.CO₂ increase so that, even though the mean arterial P.CO₂ does not rise, it is C02 that is responsible for the increase in ventilation. O₂ also seems to play some role despite the lack of a decrease in arterial P.O₂ since, during the performance of a given amount of work, the increase in ventilation while breathing 100% O₂ is 10-20% less than the increase while breathing air .

Thus, it currently appears that a number of different factors combine to produce the increase in ventilation seen during moderate exercise.

When exercise becomes more severe, buffering of the increased amounts of lactic acid that are produced liberates more CO₂, and this further increases ventilation.

Figure 3. Effect of 100% O₂ on ventilation during work at various levels on the bicycle ergometer.

With increased production of acid, the increases in ventilation and CO₂ production remain proportionate, so alveolar and arterial CO₂ change relatively little (isocapnic buffering). The additional increase in ventilation produced by the acidosis is dependent on the carotid bodies and does not occur if they are removed.

The respiratory rate after exercise does not reach basal levels until the O₂ debt is repaid. This may take as long as 90 minutes. The stimulus to ventilation after exercise is not the arterial PCO₂, which is normal or low, or the arterial PO₂, which is normal or high, but the elevated arterial H⁺ concentration due to the lactic acidemia. The magnitude of the O₂ debt is the amount by which O₂ consumption exceeds basal consumption from the end of exertion until the O₂ consumption has returned to preexercise basal levels. Because of the extra CO₂ produced by the buffering of lactic acid during strenuous exercise, the R rises, reaching 1.5-2.0. After exertion, while, the O₂ debt is being repaid, the R falls to 0.5 or less.

Effect of Lactic Acid on Ventilation

Something that is quite obvious in lab is the sudden increase in the ventilation during the exercise tolerance test. In a plot of Ve vs. watts, there is a sudden increase in ventilation at the lactate threshold. What sensor is important for this sudden increase in ventilation?

The RQ also changes at the lactate threshold. At rest, the RQ is usually between approximately 0.8 to 0.9. However, two factors can cause it to rise well above 1.0. The first is hyperventilation, since this increases the rate of exhalation of CO2 without changing the oxygen consumption. The second factor is the addition of lactic acid to the blood. The acid reacts with bicarbonate in the blood, releasing CO2.

Changes in the Tissues

During exercise, the contracting muscles use more O₂ and the tissue PO₂; falls nearly to zero. More O₂ diffuses from the blood, the blood PO₂; of the blood in the muscles drops and more O₂ is removed from hemoglobin. Because the capillary bed is dilated and many previously closed capillaries are open, the mean distance from the blood to the tissue cells is greatly decreased; this facilitates the movement of O₂ from blood to cells.

The oxygen hemoglobin dissociation curve is steep in the PO₂; range below 60 mm Hg, and a relatively large amount of O₂ is supplied for each drop of 1 mm Hg in P.O₂ (Fig 46-2). Additional O₂ is supplied because, as a result of the accumulation of CO₂ and the rise in temperature in active tissues - and perhaps because of a rise in red blood cell 2,3-DPG - the dissociation curve shifts to the right. The net effect is a 3-fold increase in O₂ extractions from each unit of blood. Since this increase is accompanied by a 30-fold or greater increase in blood flow, it permits the metabolic rate of muscle to rise as much as 100-fold during exercise.

Hypoxia.

Hypoxia is O₂ deficiencies at the tissue level. It is a more correct term than anoxia, there rarely being no O₂ at all left in the tissues.

Traditionally, hypoxia has been divided into 4 types. Numerous other classifications are currently in use, but the 4-type system still has considerable utility if the definitions of the terms are kept clearly in mind. The 4 categories are as follows: (1) hypoxic hypoxia (anoxic anoxia), in which the PO₂ of the arterial blood is reduced; (2) anemic hypoxia, in which the arterial P.O₂ is normal but the amount of hemoglobin available to carry O₂ is reduced; (3) stagnant or ischemic hypoxia, in which the blood flow to a tissue is so low that adequate O₂ is not delivered to it despite a normal PO₂; and hemoglobin concentration; and (4) histotoxic hypoxia, in which the amount of O₂ delivered to a tissue is adequate but, because of the action of a toxic agent, the tissue cells cannot make use of the O₂ supplied to them.

Effects of Hypoxia

The effects of stagnant hypoxia depend upon the tissue affected. In hypoxic hypoxia and the other generalized forms of hypoxia, the brain is affected first. A sudden drop in the inspired P.O₂ to less than 20 mm Hg, which occurs, for example, when cabin pressure is suddenly lost in a plane flying above 16,000 m, causes loss of consciousness in 10 to 20 seconds and death in 4-5 minutes. Less severe hypoxia causes a variety of mental aberrations not unlike those produced
by alcohol: impaired judgment, drowsiness, dulled pain sensibility, excitement, disorientation, loss of time sense, and headache. Other symptoms include anorexia, nausea, vomiting, tachycardia, and, when the hypoxia is severe, hypertension. The rate of ventilation is increased in proportion to the severity of the hypoxia of the carotid chemoreceptor cells.

Breathing Low Partial Presssures of Oxygen: High Altitude

High altitude is a circumstance in which a healthy person must deal with a lowered PaO2. At 14,000 feet, for example, the PO2 in moist tracheal air is only 82 mm Hg, compared to 149 mm Hg at sea level.

For most people acclimated to sea level, a fast ascent to roughly 10,000 feet begins producing symptoms of acute mountain sickness, although some people will experience symptoms at the 7,000 to 9,000 feet. Headache is the most common symptom with lassitude and nausea common as well. The level of physical fitness does not seem to to be important.

The cause of acute mountain sickness is not known. There is evidence that the brain swells somewhat with elevation, and some investigators feel this might be the important factor. One reason for the swelling might be that hypoxia leads to vasodilation of blood vessels, cerebral and otherwise. Various factors mediate this. Another suggestion is that the vasodilation leads to a mild form of edema. But whatever the sequence, the swelling could explain the headache and perhaps other problems.

Another interesting factor at higher elevations is respiratory alkalosis. Why does this occur? (Remember that the peripheral chemoreceptor kicks in if the PaO2 falls below 60 mm Hg.)

In some cases acute mountain sickness progresses to serious cerebral edema or pulmonary edema These are both dangerous conditions which require immediate return to lower elevations.

Breathing High Partial Pressures of Oxygen

It's instructive to observe what happens when a normal, healthy person begins breathing oxygen at a higher partial pressure than normal. This occurs, for example, in scuba diving, because the diver must breathe air at the same pressure as that of the surrounding water. Since the water pressure increases by one atmosphere for each 33 feet, a scuba diver often is breathing quite high partial presssures of oxygen.

First think about oxygen transport. About how much would the amount of oxygen in systemic arterial blood increase if the partial pressure of oxgygen in the alveoli were, for example, twice normal?

Next think about the peripheral chemoreceptor. As described above, the peripheral chemoreceptor does not have much effect on ventilation when the PaO2 is above about 60 mm Hg.

Now, what about CO2? Suppose the metabolism of the diver is about the same as at the surface. If so, then CO2 would be produced at about the same rate, and thus the diver would need to breathe at the same rate in order to blow off the CO2. In other words, normal ventilation would keep the PaCO2 at the normal level. And, of course, it is the PaCO2 that is primarily controlling breathing.

Respiratory Stimulation

Dyspnea is by definition difficult or labored breathing in which the subject is conscious of shortness of breath; hyperpnea is the general term for an increase in the rate or depth of breathing regardless of the patient's subjective sensations. Tachypnea is rapid, shallow breathing. In general, a normal individual is not conscious of respiration until ventilation is doubled, and breathing is not uncomfortable (ie, the dyspnea point is not reached) until ventilation is tripled or quadrupled. Whether or not a given level of ventilation is uncomfortable also depends upon the respiratory reserve. This factor is taken into account in the dyspneic index.

Effects of Decreased Barometric Pressure

The composition of air stays the same, but the total barometric pressure falls with increasing altitude. Therefore, the PO₂ also falls. At 3000 m (approximately 10,000 ft) above sea level, the alveolar PO₂ is about 60 mm Hg and there is enough hypoxic stimulation of the chemoreceptor to definitely increase ventilation. As one ascends higher, the alveolar PO₂ falls less rapidly and the alveolar PCO₂ declines somewhat because of the hyperventilation. The resulting fall in arterial PCO₂ produces respiratory alkalosis.

Hypoxic Symptoms Breathing Air/

There are a number of compensatory mechanisms that operate over a period of time to increase altitude tolerance (acclimatization), but in unacclimatized subjects, mental symptoms such as irritability appeared about 3700 m. At 5500 m, the hypoxic symptoms are severe; and at altitudes above 6100 m (20,000 ft), consciousness is usually lost.

Hypoxic Symptoms Breathing Oxygen. The total atmospheric pressure becomes the limiting factor in altitude tolerance when breathing 100% O₂. The partial pressure of water vapor in the alveolar air is constant at 47 mm Hg, and that of CO₂ is normally 40 mm Hg, so that the lowest barometric pressure at which a normal alveolar PO₂ of 100 mm Hg is possible is 187 mm Hg, the pressure at about 10,400 m (34,000 ft). At greater altitudes, the increased ventilation due to the decline in alveolar PO₂ lowers the alveolar PCO₂ somewhat, but the maximal alveolar PO₂; that can be attained when breathing 100% O₂ at the ambient barometric pressure of 100 mm Hg at 13,700 m is about 40 mm Hg. At about 14,000 m, consciousness is lost in spite of the administration of 100% O₂.

However, an artificial atmosphere can be created around an individual; in a pressurized suit or cabin supplied with O₂ and a system to remove CO₂, it is possible to ascend to any altitude and to live in the vacuum of interplanetary space.

At 19,200 m, the barometric pressure is 47 mm Hg, and at or below this pressure the body fluids boil at body temperature. The point is largely academic, however, because any individual exposed to such a low pressure would be dead of hypoxia before the bubbles of steam could cause death.

Delayed Effects of High Altitude.

Many individuals, when they first arrive at a high altitude, develop transient "mountain sickness". This syndrome develops 8-24 hours after arrival at altitude and lasts 4-8 days. It is characterized by headache irritability, insomnia, breathlessness, nausea and vomiting. Its cause is unknown, but the symptoms are reduced or prevented if alkalosis is reduced by procedures such as treatment with acetazolamide.

High altitude pulmonary edema and cerebral edema are serious forms of mountain sickness. Pulmonary edema is prone to occur in individuals who ascend quickly to altitudes above 2500 m and engage in heavy physical activity during the first 3 days after arrival. It is also seen in individuals acclimatized to high altitudes who spend 2 weeks or more at sea level and then rescind. It occurs in the absence of cardiovascular or pulmonary disease. It is associated with marked pulmonary hypertension, but left atrial pressures are normal. The protein content of the edema fluid is high, but the mechanism responsible for its production is unknown. It responds to rest and 0₂ treatments and generally does not develop in individuals who ascend to high altitudes gradually and avoid physical exertion for the first few days of high altitude exposure.

Acclimatization.

Acclimatization to altitude is due to the operation of a variety of compensatory mechanisms. The respiratory alkalosis produced by the hyperventilation shifts the oxygen hemoglobin dissociation curve to the left, but there is a concomitant increase in red blood cell 2,3-DPG, which tends to decrease the O₂ affinity of hemoglobin. The decrease in O₂ affinities makes more O₂ available to the tissues. However, it should be noted that the value of the increase in P₅₀ is lost at very high altitudes, because when the arterial PO₂ is markedly reduced, the decreased O₂ affinity also interferes with O₂ uptake by hemoglobin in the lungs.

The initial ventilatory response to increased altitude is relatively small, because the alkalosis tends to counteract the stimulating effect of hypoxia. However, there is a steady increase in ventilation over the next 4 days because the active transport of H⁺ into CSF, or possibly a developing lactic acidosis in the brain, causes a fall in CSF pH that increases the response to hypoxia. After 4 days, the ventilatory response begins to decline slowly, but it takes years of residence at higher altitudes for it to decline to the initial level. Associated with this decline is a gradual desensitization to the stimulatory effects of hypoxia.

Erythropoietin secretion increases promptly on ascent to high altitude and then falls somewhat over the following 4 days as the ventilatory response increases and the arterial PO₂ rises. The increase in circulating red blood cells triggered by the erythropoietin begins in 2-3 days and is sustained as long as the individual remains at high altitude.

There are also compensatory changes in the tissues. The mitochondria, which are the site of oxidative reactions, increase in number, and there is an increase in myoglobin that facilitates the movement of O₂ in the tissues. There is also an increase in the tissue content of cytochrome oxidase.

The effectiveness of the acclimatization processes is indicated by the fact that in the Andes and Himalayas there are permanent human habitations at elevations above 5500 m (18,000 ft). The natives who live in these villages are markedly polycythemic and have low alveolar PO₂ values, but in most other ways they are remarkably normal.

1. Mechanism of the first breath of child consists of:

irritation of central chemoreceptors by increasing CO₂ tension

irritation of peripheral chemoreceptors by increasing CO₂ tension

irritation of central chemoreceptor by lack of oxygen (hypoxia)

Gering-Brayer’s reflex irritation of inspiratory neurons by afferent influences from thermo receptors of skin

2. What is the breathing frequency of newborn child?

14-16/min. a) 12-14/min. b) 18-20/min. c) 10-12/min. d) 25-30/min

1. Indicate three mechanisms of height acclimatization that are advantageous from the physiological point of view.

2. After previous hyperventilation time of being under water increases for 1-2 min. Why?

3. Two persons were examined. After a slight physical load it was determined that first one has breathing frequency (BF) of 16/min, volume of dead space of 150 ml, breath volume of 600 ml. The second one has BF of 24/min, volume of dead space of 150 ml, breath volume of 400 ml. What can you say about level of training of these people?

Hyperventilation, polycytaemia, increasing of quantity of capillaries in tissues, changes of intracellular activity of oxygenates enzymes.

During hyperventilation, as a result of decreasing of pCO₂ and increasing of pO₂ in alveolar air, some time is needed to reach the basic level of pCO₂ and pO₂ in alveolar air, when the person will stop breathing delay.

The first person has more effective breath because his active inhale (AI) is bigger while their respiratory minute volumes are equal. That’s why the first one is trained better.

Analysis of spirogram of persons of different age groups.

You have to determine BF, lung volume and capacity of lungs according to spirogram, given by the teacher. Put results into the table.

Indices	Children	Adults
Breathing frequency
Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Respiratory minute volume
Vital capacity

Influence of physical loads on human breathing

After five minutes of adaptation, on the device ПА 5-01, determine tidal volume, breathing frequency, respiratory minute volume. Then after 20 squats with the hands ahead of your trunk repeat the experiment in tree minutes. Put the results into the table.

Breathing indices	Before physical exercises	After physical exercises
Breathing frequency
Tidal volume
Respiratory minute volume

TEMPERATURE REGULATION

The human body has the remarkable capacity for regulating its core temperature somewhere between 98°F and 100°F when the ambient temperature is between approximately 68°F and 130°F according to Guyton. This presumes a nude body and dry air.

The external heat transfer mechanisms are radiation, conduction and convection and evaporation of perspiration. The process is far more than the passive operation of these heat transfer mechanisms, however. The body takes a very active role in temperature regulation.

The temperature of the body is regulated by neural feedback mechanisms which operate primarily through the hypothalmus. The hypothalmus contains not only the control mechanisms, but also the key temperature sensors. Under control of these mechanisms, sweating begins almost precisely at a skin temperature of 37°C and increases rapidly as the skin temperature rises above this value. The heat production of the body under these conditions remains almost constant as the skin temperature rises. If the skin temperature drops below 37°C a variety of responses are initiated to conserve the heat in the body and to increase heat production. These include

· Vasoconstriction to decrease the flow of heat to the skin.

· Cessation of sweating.

· Shivering to increase heat production in the muscles.

· Secretion of norepinephrine, epinephrine, and thyroxine to increase heat production

· In lower animals, the erection of the hairs and fur to increase insulation.

Age Factors Very young and very old people are limited in their ability to regulate body temperature when exposed to environmental extremes. A newborn infant’s body temperature decreases if the infant is exposed to a cool environment for a long period. Elderly people also are not able to produce enough heat to maintain body temperature in a cool environment. With regard to overheating in these age groups, heat loss mechanisms are not fully developed in the newborn. The elderly do not lose as much heat from their skin as do younger people. Both groups should be protected from extreme temperatures.

Normal Body Temperature The normal temperature range obtained by either a mercury or an electronic thermometer may extend from 36.2°C to 37.6°C (97°F to 100°F). Body temperature varies with the time of day. Usually, it is lowest in the early morning because the muscles have been relaxed and no food has been taken in for several hours. Temperature tends to be higher in the late afternoon and evening because of physical activity and consumption of food. Normal temperature also varies in different parts of the body. Skin temperature obtained in the axilla (armpit) is lower than mouth temperature, and mouth temperature is a degree or so lower than rectal temperature. It is believed that, if it were possible to place a thermometer inside the liver, it would register a degree or more higher than rectal temperature. The temperature within a muscle might be even higher during activity. Although the Fahrenheit scale is used in the United States, in most parts of the world, temperature is measured with the Celsius thermometer. On this scale, the ice point is at 0° and the normal boiling point of water is at 100°, the interval between these two points being divided into 100 equal units. The Celsius scale is also called the centigrade scale (think of 100 cents in a dollar).

Fever

Fever is a condition in which the body temperature is higher than normal. An individual with a fever is described as febrile. Usually, the presence of fever is due to an infection, but there can be many other causes, such as malignancies, brain injuries, toxic reactions, reactions to vaccines, and diseases involving the central nervous system (CNS). Sometimes, emotional upsets can bring on a fever. Whatever the cause, the effect is to reset the body’s thermostat in the hypothalamus. Curiously enough, fever usually is preceded by a chill—that is, a violent attack of shivering and a sensation of cold that blankets and heating pads seem unable to relieve. As a result of these reactions, heat is generated and stored, and when the chill subsides, the body temperature is elevated. The old adage that a fever should be starved is completely wrong. During a fever, there is an increase in metabolism that is usually proportional to the degree of fever. The body uses available sugars and fats, and there is an increase in the use of protein. During the first week or so of a fever, there is definite evidence of protein destruction, so a high-calorie diet with plenty of protein is recommended. When a fever ends, sometimes the drop in temperature to normal occurs very rapidly. This sudden fall in temperature is called the crisis, and it is usually accompanied by symptoms indicating rapid heat loss: profuse perspiration, muscular relaxation, and dilation of blood vessels in the skin. A gradual drop in temperature, in contrast, is known as lysis. A drug that reduces fever is described as antipyretic. The mechanism of fever production is not completely understood, but we might think of the hypothalamus as a thermostat that is set higher during fever than normally. This change in the heat-regulating mechanism often follows the injection of a foreign protein or the entrance into the bloodstream of bacteria or their toxins. Substances that produce fever are called pyrogens. Up to a point, fever may be beneficial because it steps up phagocytosis (the process by which white blood cells destroy bacteria and other foreign material), inhibits the growth of certain organisms, and increases cellular metabolism, which may help recovery from disease.

In the body, heat is produced by muscular exercise, assimilation of food, and all the vital processes that contribute to the basal metabolic rate. It is lost from the body by radiation, conduction, and vaporization of water in the respiratory passages and on the skin. Small amounts of heat are also removed in the urine and feces. The balance between heat production and heat loss determines the body temperature. Because the speed of chemical reactions varies with the temperature and because the enzyme systems of the body have narrow temperature ranges in which their function is optimal, normal body function depends upon a relatively constant body temperature.

Invertebrates generally cannot adjust their body temperatures and so are at the mercy of the environment. In vertebrates, mechanisms for maintaining body temperature by adjusting heat production and heat loss have evolved. In reptiles, amphibia, and fish, the adjusting mechanisms are relatively rudimentary, and these species are called "cold-blooded" (poikilothermic) because their body temperature fluctuates over a considerable range. In birds and mammals, the ''warm-blooded'' (homeothermic) animals, a group of reflex responses that are primarily integrated in the hypothalamus operate to maintain body temperature within a narrow range in spite of wide fluctuations in environmental temperature. The hibernating mammals are a partial exception. While awake, they are homeothermic, but during hibernation, their body temperature falls.

Normal Body Temperature

In homeothermic animals, the actual temperature at which the body is maintained varies from species to species and, to a lesser degree, from individual to individual. In humans, the traditional normal value for the oral temperature is 37 °C (98.6 °F), but in one large series of normal young adults, the morning oral temperature averaged 36.7 °C, with a standard deviation of 0.2 °C.

Heat Production

A variety of basic chemical reactions contribute to body heat production at all times. Ingestion of food increases heat production because of the specific dynamic action of the food, but the major source of heat is the contraction of skeletal muscle. Heat production can be varied by endocrine mechanisms in the absence of food intake or muscular exertion. Epinephrine and norepinephrine produce a rapid but short-lived increase in heat production; thyroid hormones produce a slowly developing but prolonged increase, Furthermore, sympathetic discharge is decreased during fasting and increased by feeding.

Heat Loss

Radiation is the transfer of heat from one object to another with which it is not in contact.

Conduction is heat exchange between objects at different temperatures that are in contact with one another. The amount of heat transferred by conduction is proportionate to the temperature difference between the 2 objects (thermal gradient).

Convection, the movement of the molecules O₂ a gas or a liquid at one temperature to another location that is at a different temperature, aids conduction. When an individual is in a cold environment, heat is lost by conduction to the surrounding air and by radiation to cool objects in the vicinity. In a hot environment, heat is transferred to the individual by these processes and adds to the heat load.

Thus, in a sense, radiation and conduction work against the maintenance of body temperature. On a cold but sunny day, the heat of the sun reflected off bright objects exerts an appreciable warming effect. It is the heat reflected from the snow, for example, that makes it possible to ski in fairly light clothes even though the air temperature is below freezing.

Since conduction occurs from the surface of one object to the surface of another, the temperature of the skin determines to a large extent the degree to which body heat is lost or gained. The amount of heat reaching the skin from the deep tissues can be varied by changing the blood flow to the skin. When the cutaneous vessels are dilated, warm blood wells up into the skin, whereas in the maximally vasoconstricted state, heat is held centrally in the body. The rate at which heat is transferred from the deep tissues to the skin is called the tissue conductance. Birds have a layer of feathers next to the skin, and most mammals have a significant layer of hair or fur. Heat is conducted from the skin to the air trapped in this layer and from the trapped air to the exterior. When the thickness of the trapped layer is increased by fluffing the feathers or erection of the hairs (horripilation), heat transfer across the layer is reduced and heat losses (or, in a hot environment, heat gains) are decreased. "Goose pimples " are the result of horripilation in humans; they are the visible manifestation of cold-induced contraction of the piloerector muscles attached to the rather meager hair supply. Humans usually supplement this layer of hair with a layer of clothes. Heat is conducted from the skin to the layer of air trapped by the clothes, from the inside of the clothes to the outside, and from the outside of the clothes to the exterior. The magnitude of the heat transfer across the clothing, a function of its texture and thickness, is the most important determinant of how warm or cool the clothes feel, but other factors, especially the size of the trapped layer of warm air, are important also. Dark clothes absorb radiated heat, and light-colored clothes reflect it back to the exterior.

The other major process transferring heat from the body in humans and those animals that sweat is vaporization of water on the skin and mucous membranes of the mouth and respiratory passages.

Vaporization of 1 g of water removes about 0.6 kcal of heat. A certain amount of water is vaporized at all times. This insensible water loss amounts to 50 mL/h in humans. When sweat secretion is increased, the degree to which the sweat vaporizes depends upon the humidity of the environment. It is common knowledge that one feels hotter on a humid day. This is due in part to the decreased vaporization of sweat, but even under conditions in which vaporization of sweat is complete, an individual in a humid environment feels warmer than an individual in a dry environment. The reason for this difference is not known, but it seems related to the fact that in the humid environment sweat spreads over a greater area of skin before it evaporates.

Endothermic evaporation cools body

a. Sweat glands secrete sweat continuously

b. Body temperature increase

Blood vessels dilate

Sweat glands stimulated

During muscular exertion in a hot environment, sweat secretion reaches values as high as 1600 mL/h, and in a dry atmosphere, most of this sweat is vaporized. Heat loss by vaporization of water therefore varies from 30 to over 900 kcal/h.

Some mammals lose heat by panting. This rapid, shallow breathing greatly increases the amount of water vaporized in the mouth and respiratory passages and therefore the amount of heat lost. Because the breathing is shallow, it produces relatively little change in the composition of alveolar air.

The relative contribution of each of the processes that transfer heat away from the body varies with the environmental temperature. At 21 °C, vaporization is a minor component in humans at rest. As the environmental temperature approaches body temperature, radiation losses decline and vaporization losses increase.

Temperature-Regulating Mechanisms

The reflex and semireflex thermoregulatory includes autonomic, somatic, endocrine, and behavioral changes. One group of responses increases heat loss and decreases heat production; the other decreases heat loss and increases heal production. In general, exposure to heat stimulates the former group of responses and inhibits the latter, whereas exposure to cold does the opposite.

Curling up "in a ball" is a common reaction to cold in animals and has a counterpart in the position some people assume on climbing into a cold bed. Curling up decreases the body surface exposed to the environment. Shivering is an involuntary response of the skeletal muscles, but cold also causes a semiconscious general increase in motor activity. Examples include foot stamping and dancing up and down on a cold day. Increased catecholamine secretion is an important endocrine response to cold; adrenal medullectomized rats die faster than normal controls when exposed to cold. TSH secretion is increased by cold and decreased by heat in laboratory animals, but the change in TSH secretion produced by cold in adult humans is small and of questionable significance. It is common knowledge that activity is decreased in hot weather – the "it's too hot to move" reaction.

Then no regulatory adjustments involve local responses and more general reflex responses. When cutaneous blood vessels are cooled, they become more sensitive to catecholamines and the arterioles and venules constrict. This local effect of cold directs blood away from the skin and into the venae comitantes, the deep veins that run alongside the arteries. Heat is transferred from the arterial to the venous blood and carried back into the body without reaching the skin (counter current exchange).

The reflex responses activated by cold are controlled from the posterior hypothalamus. Those activated by warmth are primarily controlled from the anterior hypothalamus, although some thermoregulation against heat still occurs after decerebration at the level of the rostral midbrain. Stimulation of the anterior hypothalamus causes cutaneous vasodilatation and sweating, and lesions in this region cause hyperthermia, with rectal temperatures sometimes reaching 43 °C (109.4 °F). Posterior hypothalamic stimulation causes shivering, and the body temperature of animals with posterior hypothalamic lesions falls toward that of the environment.

There is some evidence that in primates and humans serotonin is a synaptic mediator in the centers controlling the mechanisms activated by cold, and norepinephrine plays a similar role in those activated by heat. However, there are marked species variations in the temperature responses to these amines. Peptides may also be involved, but the details of the central synaptic connections concerned with thermoregulation are still unknown.

The Role of the Hypothalamus Many areas of the body take part in heat regulation, but the most important center is the hypothalamus, the area of the brain located just above the pituitary gland. Some of the cells in the hypothalamus control heat production in body tissues, whereas another group of cells controls heat loss. Regulation is based on the temperature of the blood circulating through the brain and also on input from temperature receptors in the skin. If these two factors indicate that too much heat is being lost, impulses are sent quickly from the hypothalamus to the autonomic (involuntary) nervous system, which in turn causes constriction of the skin blood vessels to reduce heat loss. Other impulses are sent to the muscles to cause shivering, a rhythmic contraction of many muscles, which results in increased heat production. Furthermore, the output of epinephrine may be increased if necessary. Epinephrine increases cell metabolism for a short period, and this in turn increases heat production.

If there is danger of overheating, the hypothalamus stimulates the sweat glands to increase their activity. Impulses from the hypothalamus also cause blood vessels in the skin to dilate, so that increased blood flow to the skin will result in greater heat loss. The hypothalamus may also promote muscle relaxation to minimize heat production. Muscles are especially important in temperature regulation because variations in the activity of these large tissue masses can readily increase or decrease heat generation. Because muscles form roughly one-third of the body, either an involuntary or an intentional increase in their activity can form enough heat to offset a considerable decrease in the temperature of the environment.

Measuring of temperature in different areas of man’s skin

Move the switcher of electro thermometer on panel from position B (switched off) to position K (control) before investigation.

Then to 30-40 seconds regularly press detector to skin of: palm, forehead, neck, forearm. Note the temperature on upper score. Give results in look of table:

nn	Place of measuring	Temperature
1	palm
2	forehead
3	neck
4	forearm

The role of blood’s circulation in supporting of body’s temperature

Observing person hold the hand on the table with relaxed muscles. Put cuff of sphygmomanometer or arm and measure starting temperature of one of the finger of this hand. Then make in cuff pressure 140 mm. And support it during 5 minutes with registration of temperature every minute. Then let out air from cuff and note the time of restoring of temperature. Give results of work graphically.

Write about role of blood circulation in supporting of body’s temperature.

The meaning of vaporization in providing of heat’s emission

Put quadrate drape 4x4 cm on forearm’s surface, damp it and leave it to 1-2 min. during it measure the temperature of shin near drape by electro thermometer. Then take drape and at once carry the detector on this place.

Register the temperature.

Write about the meaning of vaporization in thermoregulation in conclusion.

The acquainting with educational card “Thermographical method of observing”. Write the main principles of it in record.

References:

1. Review of Medical Physiology // W.F.Ganong. – 24th edition, 2012.

2. Textbook of Medical Physiology // A.C.Guyton, J.E.Hall. – Eleventh edition, 2005.

3. Anatomy and Physiology by Barnes and Noble, volume 1.