lecture regulation of resp

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    Regulation of respiration

    Controls of Ventilation

    A). Brain1.Respiratory Center

    i). Dorsal Respiratory Groupii). Ventral Respiratory Groupiii) Pneumotaxic Area of the Pons

    2). Hypothalamus:3). Higher Cortical Functions

    B). Chemical Signals1). PCO22) H a Rate of breathing increases3). PO2

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    Respiratory center(RC) is located in the medulla oblongata which is thelowermost part of the brain stem. RC receives controlling signals of neural,chemical and hormonal natures and controls the rate and depth of respiratorymovements of the diaphragm and other respiratory muscles. Injury to this centermay lead to central respiratory failure which necessitates mechanical ventilation

    but usually the prognosis is grave

    The groups of nerve cells in the brain which regulates the respiration rhythmicallyare collectively known as respiratory centres. respiratory centre is composed ofseveral widely dispersed groups of neurons.

    Groups: Respiratory centre is divided four major groups.

    Respiratorycentres

    Location Name of nucleus

    Function

    1. Inspiratorycentre ( Dorsalrespiratorygroup)

    Dorsal portion ofmedullaoblongate

    Nucleus ofTractus solitarius

    It causes inspirationwhile stimulated.

    2. Expiratorycentre ( VentralrespiratoryGroup)

    Antero- lateralpart of medulla,about 5 mmanterior andlateral to dorsalrespiratory group

    Nucleusambiguous andnucleus retroambiguous.

    1. It causes eitherexpiration or inspirationdepending upon whichneuron in the group arestimulated. Butgenerally causes

    expiration

    2. It sends inhibitoryimpulse to theapneustic centre.

    3. Pneumotaxiccentre

    Upper part ofpons

    Nucleusparabrachialis

    1.It controls both rateand pattern ofbreathing

    2. It sends impulses to

    limit inspiration.

    http://en.wikipedia.org/wiki/Medulla_oblongatahttp://en.wikipedia.org/wiki/Brain_stemhttp://en.wikipedia.org/w/index.php?title=Central_respiratory_failure&action=edit&redlink=1http://en.wikipedia.org/wiki/Medulla_oblongatahttp://en.wikipedia.org/wiki/Brain_stemhttp://en.wikipedia.org/w/index.php?title=Central_respiratory_failure&action=edit&redlink=1
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    Apneustic centre In the lower partof the pons.

    1. It dischargesstimulatory impulse tothe inspiratory centrecausing inspiration.

    2. It receives inhibitoryimpulse frompneumotaxic centre andfrom stretch receptor oflung.

    3. It dischargesinhibitory impulse toexpiratory centre.

    (Ref. Guyton & Hall11th P. 515)

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    Apneustic respirationApneustic respiration (apneusis) is an abnormal pattern of breathingcharacterized by deep, gasping inspiration with a pause at full inspirationfollowed by a brief, insufficient release.

    Causes

    It is caused by damage to the pons or uppermedulla caused by strokes ortrauma. Specifically, concurrent removal of input from the vagus nerve and the

    pneumotaxic centercauses this pattern of breathing.

    It can also be temporarily caused by some drugs, such as ketamine.

    Nervous regulation of respiration/Rhythmic breathingInhaling & expiring of air at a regular interval of time is rhythmic breathing.

    http://en.wikipedia.org/wiki/Ponshttp://en.wikipedia.org/wiki/Medulla_oblongatahttp://en.wikipedia.org/wiki/Vagus_nervehttp://en.wikipedia.org/wiki/Pneumotaxic_centerhttp://en.wikipedia.org/wiki/Ketaminehttp://en.wikipedia.org/wiki/Ponshttp://en.wikipedia.org/wiki/Medulla_oblongatahttp://en.wikipedia.org/wiki/Vagus_nervehttp://en.wikipedia.org/wiki/Pneumotaxic_centerhttp://en.wikipedia.org/wiki/Ketamine
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    Process

    Spontaneous inspiratory rampsignal produced b inspiratory center. \

    Passing through phrenic & intcostal nervesafter 2 sec. ramp signal switch-off by pneumotaxic center

    expiration fakes place by passive way.

    Chemical regulation of respirationThe rhythmic discharge is regulated by alteration in arterial PO2, PCO2, & [H

    +] thischemical control is supported by non-chemical influences.

    A number of chemical factors such as1) Elevated bloodPco2 for concentration of C02.2) Elevatedblood H+ (i.e. PH) and

    3) Decreased blood P02 (or concentration of 02) areinvolved in chemical controlof respiration.

    Effects of C02 on alveolar ventilation:-- C02 itself has little direct effect in stimulating the respiratory centre.-- Reflex action:The C02 diffuses through the blood- brain barrier into CSF and combines withwater to form carbonic acid, which dissociates into H+ and HCO3

    - ions. The H+

    then stimulates the central chemoreceptor area.

    As a result the rate and depth of respiration is increased.

    A maximal increase in CO2 can increase alveolar ventilation about 10- fold.

    Effect of H+ (i.e.pH) on alveolar ventilation:Increased blood H concentration (i.e. decreased pH increased alveolar ventilation.The effects of blob H+ concentration on ventilation are thought to be mediated byway of peripheral chemoreceptors in addition to direct effects on the respiratorycentre.Central chemoreceptors are stimulated only slightly by increased, H+

    concentration in the blood because the blood- brain barrier is relatively

    impermeable to H+

    A maximalincrease in H+

    concentration can increase alveolarventilation about 4-fold.

    Effect of decreasedO2 on alveolar ventilation:Peripheral chemoreceptors in the carotid and aortic bodies are stimulated bydecreased 02 in the arterial blood. But, the arterial P02must decrease to below60 mm Hg for stimulation to occur.

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    Exercise on respiration

    Effect of exercise on respiration

    Para meter Effect

    1. O2 Consumption Increase

    2. O2 Production and elimination Increase

    3. Ventilation Increase

    4. Arterial PO2 + PCO2 No overall change

    5. Arterial pH No change in moderate exercise

    Decreases in strenuous exercise

    6. Venous PCO2 Increases

    7. Pulmonary blood flow Increases ( which always equals thecardiac out put)

    8. Ventilation perfusion ratio More evenly distributed in lung

    Regulation of respiration during exercise

    During exercise, the rate of respiration increases. This increases in respiration iscontrolled by both neural and chemical mechanisms.

    1. Nervous factor or direct stimulation of respiratory centre from motorcortex:

    a. During exercise the brain transmitting impulses to, the contracting musclesalso transmit collateral impulses to therespiratory centre.

    b. This stimulation of respiratory centre increases the rate ofrespiration.\

    2. Chemical factors or stimulation caused by chemical substances:

    a. During exercise, the Pco2 increases andO2 decreases due to excessmetabolism in the cells.

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    b. This then stimulates chemosensitive area of brainthroughchemoreceptors which then increase the rate of respiration.

    3. . Indirect stimulation from proprioceptors

    a. During exercise, the movements of the limbs and body excites theproprioceptors

    b. This then transmits impulse to the respiratory centres

    c. This increase rate ofrespiration

    4. Hypoxia: During exercise, hypoxia develops in the muscles that elicitsafferent nerve signal to the respiratory to excite respiration

    How is extra amount of 02 supplied to the tissues during exercise?

    Ans. Extra amount of O2 is supplied to the tissues during exercise by:1. Breathing: Increase in pulmonary ventilation introduces large amounts of

    fresh air into the lung.2. O2 uptake in the lung: Large amount of oxygen are taken up from the

    lungs by the blood. \3. Supply of oxygen to the tissues: A great blood supply to the muscle due to

    increased cardiac out put and redistribution of blood to the systemiccirculation.

    4. Removal of oxygen by the tissues: This is effected as follows-

    a. Dilatation and increase in the number of patent capillaries in themuscles slows the rate of the blood how.

    b. Low oxygen tension allows oxygen to diffuse more rapidly and to agreater extent. \

    c. High CO2 tension and raised temperature increases the extent andrate of dissociation of oxyhaemoglobin,

    Respiratory insufficiency

    It means abnormalities in normal rate & depth of respiration.Cause:

    1.inadequate ventilation.2. Reduce gaseous diffusion through respiratory membrane.3.Abnormal ventilationperfusion ratio.Eupnea: Means normal breathing.

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    Tachypnea: Means rapid breathing than normal. Bradypnea: Means slow breathing than normal.Hypoxia: Means decreased O2 in tissue.Anoxia: Means total lack of O2Hypoxaemia: Means reduced O2in blood.

    Hypercapnia: Means excess CO2 in blood.Hypocapnia: Means depressed CO2 in blood.Dyspnoea: Means difficulty in breathing.Apnoea: Means temporary cessation of breathing.

    HYPOXIA

    Hypoxia is oxygen (O2) deficiency at the tissue level.

    Types with causes:1. Hypoxic hypoxia (anoxic anoxia): PO2 of the arterial blood is reduced.

    When a person exposed to high altitude (e.g. - in the plane flying above16,000 meters), Hypoxic hypox develops. It is due to a sudden drop in theinspired Po2 (

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    b. Ventilation-perfusion imbalance.ii. Shunt Venous to arterial shunt (right to left cardiac shunt).

    iii. Pump failure (ventilatory failure)a. Fatigue

    b. Mechenical defects

    c. Depression of respiratory controller in the brain.

    2.Anaemic hypoxia: It occurs due to-

    a. Lack of hemoglobin

    b. CO poisoningc. Abnormal Hb due to poisoning with nitrates, nitric oxide and other

    metals.

    3. Stagnant or ischaemic hypoxia:It occurs due to-a. Decreased cardiac output due to heart failure.b. Decreased blood flow to the organ.c. Impaired venous return. haemorrhage and shock.

    4. Histotoxic hypoxia: It occurs due to-a. Poisoning with potassium cyanide which interferes tissue oxidation by

    paralysis the enzyme cytocrom oxidase.b. Narcotics also depressed tissue oxidation by interfere with dehydrogenous

    system.

    Acclimatization:Acclimatization means the adjustment of the human body to suit in a new

    climate. (E.g.-High altitude)

    The five principal means by which acclimatization occur are:1. Pulmonary ventilation.2. Red blood cell & Hb (about 20 gm/dl)3. Diffusion capacity of the lungs.4. Vascularity of the tissues.5. Ability of the cells to utilize 02 despite low P02.

    CYANOSISBluish discoloration or skin of mucous membrane due to presence of largeamount of reduced Hbin subcutaneous vessels.

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    Amount of reduced fib showed the at least 5-7gm/dl.Occurs in arterial hypoxia of stagnant hypoxia.

    Causes:o Formation ofaltered Hbo Polycythemia

    oRt of left shunt of heart

    Type:Central Cyanosis- Causedby cardiac failure or pulmonary disorder. eg- Tip ofthe tongue.Peripheral cyanosis- Local vascular stains, shock, cold, temperature eg- Tip ofthe fingers.

    Hypercapnea

    Hypercapnea means excess CO2 in the body fluid

    Cause

    1. Hypoventilation

    2. Obstruction in respiratory

    3. Respiratory diseases such as asthma

    Clinical features:

    1. Depression of CNS : confusion

    2. Respiratory depression

    3. Come & death.

    Effects of hypercapnoea:1. PCO2 more than 60 -75 mm Hg causes severe dyspnoea.2. PCO2 more than 80-100 mm Hg causes a person lathergic some times evensemicomatoes.3. PCO2 more than 100-150 mm Hg causes anaesthesia & death.

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    Cheyne stokes breathing

    It is characterized by slow waxing & waning respiration occurring over againevery 40 60 sec.Mechanism:

    When the respiration becomes much more rapid & deeper than usual,the PCO2in pulmonary blood decreases.This decreased PCO2 inhibit respiration by depressing respiratory center.

    As a result, the pulmonary blood PCO2 increases.Then this blood enters into the respiratory center & stimulate respiration

    again, thus making the person over breath once again & initiating a new cycle ofdepressed respiration.

    Thecycle thus continue on & on, causing Cheyne-stokes breathing.

    Cheyne-Stokes breathing and its effect on arterial O2 saturation. Cheyne-

    Stokes breathing occurs frequently during sleep, especially in subjects at highaltitude, as in this example. In the presence of preexisting hypoxemia secondaryto high altitude or other causes, the periods ofapnea may result in further falls of O2 saturation to dangerous levels.Falling PO2 and rising PCO2 during the apnea intervals ultimatelyinduce a response and breathing returns, reducing thestimuli and leading to a new period of apnea.

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    Ventilation-perfusion ratioAns.D efinition : The ratio of alveolar ventilation and alveolar blood flow is called

    ventilation - perfusion ratio. It isabout 0.8.VA .... Alveolar ventilation (V)This is expressed as Q ..... Cardiac output (Q)

    4.2 L/min5L/min= 0.84

    Explanation:1. When VA & Q is normal for a given alveolus, The VA/Qwill be normal.2. When VA is zero but Q of the alveolus is normal, then VA/Qwill he zero.3.When VA is normal but Q is zero,then VA/Q will be infinity.At a ratio of either zero or infinity, there is no exchange of gases through the

    respiratory membrane of the affected alveoli.

    Physiologic shuntThe total quantitative amount of shunted blood per minute is called physiologicshunt. The greater the amount of physiologic shunt the greater the amount ofblood fails to be oxygenated as it passes through the lungs.

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    Respiratory exchange ratio

    The ratio of carbondioxide outside to oxygenuptake is called the respiratory

    e.\change ratio (R). That is.Rate of carbon dioxide outputR = Rate of oxygen uptake

    The value for R changes under different metabolic conditions. When a person isusing exclusively carbohydrates for body metabolism. R rises to 1.00.Conversely, when the person is using exclusively fats for metabolic energy, the Rlevel falls to as low as 0.7.