CONTROL OF BREATHING

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CONTROL OF BREATHING DR ARNAB MAJI MD PGT RESPIRATORY MEDICINE NRSMCH

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The control of breathing results from a complex interaction involving the respiratory centers , which feed signals to a central control mechanism that, in turn, provides output to the effector muscles .

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SENSORS PERIPHERAL CHEMORECEPTORS, LUNG AND OTHER RECEPTORS CENTRAL CHEMORECEPTER PONS MEDULLA AND OTHER PARTS OF BRAIN EFFECTORS RESPIRATORY MUSCLES Input Output

Concept map: 

Concept map ? cortex

RESPIRATORY CENTRES: 

RESPIRATORY CENTRES The afferent input into the central system is provided primarily by four groups of neural receptors : 1. Peripheral arterial chemoreceptors 2. Central (brainstem) chemoreceptors 3. Intrapulmonary receptors 4. Chest wall and muscle mechanoceptors

PERIPHERAL ARTERIAL CHEMORECEPTORS: 

PERIPHERAL ARTERIAL CHEMORECEPTORS Consists of aortic bodies and carotid bodies The physiologic significance of the aortic bodies in humans is difficult to determine but likely to be small the carotid bodies appear to have preeminent importance

LOCATION OF AORTIC AND CAROTID BODIES : 

LOCATION OF AORTIC AND CAROTID BODIES The carotid bodies are located at the junction of the internal and external carotid arteries , and are small, measuring 1.5, 2.0, 3.7 mm each with a weight of 10.6 to 12.6 mg

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receive their blood supply from branches of the external carotid artery, and their sensory supply from the carotid sinus branch of the glossopharyngeal nerve consist of two different cell types, glomus cells (type I) and sheath cells (type II) . Both cells are innervated primarily by the carotid sinus nerve, which contains both parasympathetic and sympathetic neurons with both afferent (sensory) and efferent (motor) components . The afferent neurons terminate on glomus cells

TYPE 1/ GLOMUS CELL CONTAINS: 

TYPE 1/ GLOMUS CELL CONTAINS RER RIBOSOME GOLGI APPARATUS DENSE CORE VESICLES DOPAMINE NOREPINEPHRINE EPINEPHRINE 5HT, SUB P, VIP, Ach Both NO AND CO INHIBIT CAROTID BODY HYPOXIA INHIBITS NO SYNTHASE INCREASE CAROTID BODY DISCHARGE Metaloprotoporphyrins inhibit HO-2 thereby decreases CO level

How hypoxia stimulates type 1 cells: 

How hypoxia stimulates type 1 cells 1 st hypothesis Hypoxia acts on the cell membrane Decreases conductance in oxygen sensitive potassium channels That leads to cell depolarisation That inturn leads to calcium influx and release of neurotransmitters 2 nd hypothesis METABOLIC HYPOTHESIS Hypoxia interferes with respiratory energy production That in turn triggers chemoreceptor discharge Cytochrome A 3 is the biochemical substance responsible here

CAROTID BODY AFFERENT SIGNALS RELAYED IN THE GLOSSOPHARYNGEAL NERVE EFFERENT INNERVATION : 

CAROTID BODY AFFERENT SIGNALS RELAYED IN THE GLOSSOPHARYNGEAL NERVE EFFERENT INNERVATION VIA SYMPATHETIC NERVES STIMULATION LEADS TO AN INCREASED CAROTID BODY DISCHARGE DUE TO LOCAL CHANGES IN BLOOD FLOW WITHIN THE ORGAN VIA GLOSSOPHARYNGEAL NERVES STIMULATION LEADS TO INHIBITION OF CHEMORECEPTOR DISCHARGE DUE TO RELEASE OF NO

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The carotid body has a uniquely high arterial blood supply (2L/min/100 g) that allows for its oxygen needs to be met by the dissolved oxygen in the blood , unlike other tissues that depend primarily on oxygen initially bound to hemoglobin In addition, Pao2 is the specific signal sensed by the glomus cell Therefore, the carotid body is insensitive to conditions that lower arterial oxygen content such as anemia and carbon monoxide poisoning This accounts for the clinical observation that carbon monoxide intoxication, regardless of severity, does not include signs and symptoms of respiratory stimulation such as dyspnea or hypoventilation

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The carotid body responds to both Pao2 and hydrogen ion concentration . The intensity of the response of the glomus cells varies according to the severity of the arterial hypoxemia or acidosis in a nonlinear manner . The greatest increase is seen in response to hypoxemia, especially when Pao2 falls to 70 mm Hg, at which point the firing frequency is reached and, subsequently, minute ventilation (V˙ e) increase in an accelerated fashion.

At a constant PC02 a hyperbolic relationship exists between carotid body discharge and PO2, whereas at a constant P02 the relationship b/w activity and PCO2 is linear: 

At a constant PC02 a hyperbolic relationship exists between carotid body discharge and PO2, whereas at a constant P02 the relationship b/w activity and PCO2 is linear

CAROTID BODY RESPONSE: 

CAROTID BODY RESPONSE

In humans, bilateral carotid body resection or carotid endarterectomy: 

In humans, bilateral carotid body resection or carotid endarterectomy Reduces resting V˙ e Raising resting Paco2 by 2 to 4 mm Hg, Essentially eliminates the ventilatory response to hypoxia both at rest and during exercise

Central control of respiration: 

Central control of respiration

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Central chemoreceptor CCR is a pH receptor CCR is serotinergic (green & yellow). Located in medulla arteries near lumen. Chemical control of breathing

CENTRAL CHEMORECEPTOR: 

CENTRAL CHEMORECEPTOR The central chemoreceptors are located at or near the ventral surface of the medulla , deeper sites near the nucleus tractus solitarius , and rostrally close to the locus ceruleus . Stimulation of these receptors increases both the rate of rise and the intensity of the inspiratory “ramp” signal, thereby increasing the frequency of the respiratory rhythm Physiologically, these central chemoreceptors respond primarily to alterations of [H+] in the cerebrospinal fluid (CSF) and medullary interstitial fluid.

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Central chemoreceptor is stimulated by H + Chemical control of breathing

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Elevated arterial CO2 rapidly penetrates the blood-brain barrier because CO2 is highly membrane permeable, is converted to carbonic acid (H2CO3), and rapidly dissociates into hydrogen ions and HCO32. This causes [H+] in the CSF and interstitium to rise in parallel with Paco2 . This increased [H+] stimulates respiration by a direct action on the central chemo-receptors. Conversely, a decreased Paco2 or [H+] inhibits ventilation. The ventilatory response to an increased Paco2 is divided into an initial rapid phase (within seconds) due to the relatively rapid acidification of the CSF, and a slower phase (within minutes) due to hydrogen ion build-up in the more highly buffered medullary interstitium . In addition, when compared with the highly membrane-permeable CO2, hydrogen ions in the arterial blood penetrate the blood-brain barrier relatively slowly (minutes to hours)

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acute change in Pco2 has a greater effect on alveolar ventilation than a chronic change ( chronically elevated Paco2 is associated with renal compensation with the retention of HCO3. This HCO3 gradually diffuses through the blood-brain barrier and into the CSF, where it binds to the excess hydrogen ions produced by the elevated Paco2 and negates their effect on ventilatory drive) Change of pH has a slower change

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Ventilation Time, days  PCO 2 CSF and blood pH =  HCO3-  PCO2 PCR & CCR stimulated Only PCR stimulated Acute vs. chronic hypercapnia

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In patients with chronic hypercapnia , low oxygen may be the primary stimulus driving ventilation.

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Acute hypoxia is a weaker stimulus to breathing than chronic hypercapnia . there is a brief increase in ventilation immediately after exposure to low PO2 . This hyperventilation is beneficial by lowering alveolar PCO2 (raises alveolar PO2) but causes respiratory alkalosis which, within minutes, inhibits the peripheral and central CO2/pH receptors leading to the decrease in ventilation . After a few days of exposure to low PO2, the pH is compensated and the pH inhibition of ventilation ceases. Then, the ventilation increases to a steady state value . This higher level of ventilation can persist for life if you reside at high altitude

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Property Central chemoreceptors Peripheral chemoreceptors Signal responded to [H+] PCO 2 [H+] Low PO 2 Response time Slow, hours to days Rapid, seconds Contribution to total ventilatory response 80% 20% (for CO 2 ) Comparison between central & peripheral response to CO 2

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Stimuli for ventilation Voluntary control

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Vagal Afferent Receptors airway smooth muscle Hering-Breuer reflex = Infl. Defl. No movement airway epithelium Irritant  gasp cough , bronchocon. Interstitial vol. (edema), embolism,rapid shallow breathing Nasal, pharyngeal, laryngeal Laryngeal Chemoreflex to fluids = apnea - SIDS? Blood vessel walls Bronchial circ.-congestion

PULMONARY RECEPTORS: 

PULMONARY RECEPTORS Pulmonary receptors are present in the airways and lung parenchyma They are all innervated by the vagus nerve , with myelinated fibers supplying the airway receptors and un- myelinated C fibers supplying the lung parenchyma. The airway receptors are subdivided into- 1. SARs- PULMONARY STRECH RECEPTOR 2. RARs- IRRITANT/ COUGH RECEPTOR

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SARS- situated in airways responsible for Hering-breuer inflation reflex Activation of these receptors also causes the tracheobronchial smooth muscle to relax, thus dilating the airways . The Hering -Breuer reflex is the prolongation of expiratory time and the decrease in respiratory rate in response to lung inflation.

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The SARs are thought to participate in ventilatory control by prolonging inspiration in conditions that reduce lung inflation, such as airway obstruction or decreased chest wall compliance . Conversely, in conditions that prolong expiration, lung deflation is slow and the increased SAR activity increases the force of contraction of the expiratory muscles and also prolongs expiratory time. This prevents an increase in end expiratory volume, thus decreasing the resting length of the inspiratory muscles and allowing them to function along the most advantageous portion of their length-tension curve

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The RARs lie between the airway epithelial cells and are irritant receptors, responding to noxious stimuli such as dust, cigarette smoke, and histamine . They are concentrated in the carina and primary bronchi, and are also believed to be cough receptors.

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These RARs are innervated by myelinated fibers and have a more rapid rate of adaptation than SARs. During normal breathing, their discharge is independent of the phases of inspiration and expiration, and therefore these receptors do not seem to be an important influence on breathing at rest These receptors may be important in the sensations of chest tightness, dyspnea , bronchoconstriction , and the rapid and shallow breathing that occurs in asthma.

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The pulmonary parenchymal receptors/ juxta -capillary receptors are innervated by the unmyelinated C fibers of the vagus nerve. In animals, these receptors respond both to hyperinflation of the lungs and to chemicals present in the pulmonary circulation. The reflex response is apnea followed by rapid breathing, bradycardia and hypotension. may be involved in the sensation of dyspnea in conditions causing interstitial congestion ( eg , heart failure) or embolism.

CHEST WALL & MUSCLE MECHANOCEPTORS: 

CHEST WALL & MUSCLE MECHANOCEPTORS The primary mechanoreceptors in the chest are the muscle spindle endings and tendon organs of the respiratory muscles and the joint proprioceptor . Afferent information from these receptors is carried in the anterior columns of the spinal reticular pathway and terminates in the region of the respiratory centers in the medulla

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Muscle receptor afferents are involved in the level and timing of respiratory activity. These receptors may also play a role in the increase in ventilation occurring during the early stages of exercise These mechanoreceptors may also be important in the sensation of dyspnea when respiratory effort is increased by the mechanism of length-tension inappropriateness

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Large pleural effusion Stretch on the chest wall muscle Inspiratory muscle activation and contraction Degree of tension in the muscle sensed by tendon organs Impulse received at cerebral cortex dyspnea Removal of the pleural fluid in this case had the effect of reducing end-expiratory muscle fiber length and restoring the relationship of muscle contraction and muscle tension to normal, thereby immediately reducing dyspnea

CENTRAL RESPIRATORY CONTROLLER: 

CENTRAL RESPIRATORY CONTROLLER 2 subsets- pneumotaxic Brainstem gr (involuntary) apneustic medullary centres Cerebral cortex gr (voluntary)

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4 th Ventricle DRG (NTS) VRG Pneumotaxic Center Respiratory Motor Paths Vagus & Glossopharyngeal ? Apneustic ctr. Pons Medulla Brainstem Respiratory Center “ramp” signal 3 groups of neurons control respiration Chemo, baro, Lung receptors Basic rhythm Controls “off switch of insp. ramp signal = freq. control extra drive SNS stim. Dyspnea of CHF, HT, anemia exercise

PNEUMOTAXIC CENTRE: 

PNEUMOTAXIC CENTRE The pneumotaxic center consists of the nucleus parabrachialis and the Kolliker -Fuse nucleus in the pons This center is important in influencing the timing of the inspiratory cut-off by providing a tonic input to the respiratory pattern generators located in the inspiratory center Thus, this center may modulate the respiratory response to stimuli such as hypercapnia , hypoxia, and lung inflation, and is of importance in regulating the duration of inspiration.

APNEUSTIC CENTRE: 

APNEUSTIC CENTRE The apneustic center is found in the lower pons and seems to function as the source of impulses that terminate inspiration , an “ inspiratory cut-off switch”. Inactivation of this center results in apneustic breathing, which is rhythmic respiration with a marked increase in inspiratory time and a short expiration phase

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DRG located in the nucleus of tractus solitarius in the medulla integrating impulses from visceral afferents from the upper airways, intraarterial chemoreceptors , and lung parenchyma through the fifth, ninth and 10th cranial nerves respectively may also be the site of projection of proprioceptive afferents from the respiratory muscles and chest wall processing center for respiratory reflexes and is the site of origin of the normal rhythmic respiratory drive consisting of repetitive bursts of inspiratory action potentials VRG consists of both inspiratory and expiratory neurons and is located within the nucleus ambiguus rostrally and nucleus retroambiguus caudally innervates respiratory effector muscles through the phrenic , intercostal , and abdominal respiratory motorneurons Its output increases with the need for forceful expiration such as in exercise or in any condition of increased airway resistance to breathing ( eg , COPD or asthma).

The Respiratory Related Neurons [RRN] in the Medulla The Dorsal & Ventral Respiratory Groups contain Neurons that Fire in Phase with the Respiratory Cycle: 

The Respiratory Related Neurons [RRN] in the Medulla The Dorsal & Ventral Respiratory Groups contain Neurons that Fire in Phase with the Respiratory Cycle

CEREBRAL CORTEX: 

CEREBRAL CORTEX plays a role in ventilatory control and can also influence or bypass the central respiratory control mechanism in order to accomplish behavior -related respiratory activity such as cough, speech, singing, voluntary breath holding, and other such activities

EFFECTOR SYSTEM: 

EFFECTOR SYSTEM The effector system consists of those pathways and muscles that are involved in the actual performance of inspiration and expiration 2 connector pathways- 1. descending pathway 2. ascending pathway

DESCENDING PATHWAY: 

DESCENDING PATHWAY The descending pathways connect the DRG and VRG to the ventrolateral columns of the spinal cord, the phrenic nerves, and the intercostal and abdominal muscles of respiration. These pathways are used for the inhibition of the expiratory muscles during inspiration and inhibition of inspiratory muscles during expiration to prevent opposing muscles from contracting at the same time

ASCENDING PATHWAY: 

ASCENDING PATHWAY The ascending pathway connect the respiratory muscles to the higher brainstem levels Impairment of the ascending spinal pathways ( eg , following bilateral percutaneous cervical cordotomy or anterior spinal operations) may lead to respiratory dysfunction in the form of apnea during sleep that is reversed by arousal

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Inspiration at rest is active and expiration is a passive event in patients with normal lungs. During exercise or in patients with airway obstruction, both inspiration and expiration become active, with expiratory contraction of the abdominal wall and internal intercostal muscles

RESPIRATORY MUSCLE: 

RESPIRATORY MUSCLE We breath by co- ordinated action of thoracic and upper airway muscle. Principle among these is diaphragm Diaphragm generates negative pressure in the chest, inflating the lung contraction-shortening → descent of the diaphragm ≈ 1-2 cm during quiet breath→ contraction of the abdominal content→ resist further descent→ elevation of lower ribs→↑vertical + transverse dimension of thorax Expiration is quiet breathing occurs passively by relaxation of the inspiratory muscles except during its first portion where the diaphragm, by briefly continuing its activity, brakes the release of air from the lungs. In deep or rapid breathing the abdominal and other expiratory muscles augment the expulsion of air.

Muscles of respiration: 

Muscles of respiration

RESPONSE TO INCREASED PCO2 : 

RESPONSE TO INCREASED PCO2 ventilation increases in a directly proportional manner to increasing CO 2 production The slope of the ventilatory response to increases in PaCO 2 is greater in the presence of a lower PaO 2 Abnormalities of the response of the central control system’s to CO2 may occur ( eg , central alveolar hypoventilation when lesions of the CNS are present ). If no lesions are detected, the condition is called primary alveolar hypoventilation

RESPONSE TO DECRESED PAO2 : 

RESPONSE TO DECRESED PAO2 The response to a falling PaO 2 demonstrates an exponential type of curve rather than the linear relationship of increasing ventilation in response to increasing PaCO 2 There is little increase in V˙ e until the PaO 2 falls to 60 mm Hg . At this point, any further decrease in Pao2 causes a marked increase in V˙e However, if CO 2 is added to the inspired gas during testing to cause hypercapnia , then the resultant ventilatory response is markedly increased

VENTILATORY RESPONSE TO pH: 

VENTILATORY RESPONSE TO pH Ventilation is stimulated by a primary metabolic acidosis/ acidemia and inhibited by alkalosis/ alkalemia This response is mediated primarily through the peripheral chemoreceptors At any level of Pao2, the carotid body responds to an increase in hydrogen ions by increasing the firing rate of the glomus cells and vice versa

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In the clinical setting, hyperventilation in response to metabolic acidosis is easy to overlook. BUT WHY? This is because the primary mechanism of compensation involves an increase in Vt , which is more difficult to detect clinically than an increase in respiratory rate. In metabolic alkalosis, respiratory compensation for the increased serum HCO3 2 occurs with a decrease in minute alveolar ventilation. This elevates Paco2 to cause a respiratory acidosis, and tends to normalize pH.

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CONTROL OF BREATHING IN COMMON DISEASED STATES

IN ASTHMA: 

IN ASTHMA Symptomatic asthmatics normally breathe at a normal or increased frequency. Their ventilatory drive (as measured by mouth occlusion pressure ) increases during exacerbations, probably in response to the resistive load imposed by increased airflow resistance. This compensation is usually excellent , as most asthmatics hyperventilate during an episode of wheezing with dyspnea .

CONTD….............................................: 

CONTD…............................................. The clinical importance of increased respiratory drive in severe asthma is well known to physicians, as the majority of asthmatics have a low Paco2 on presentation for emergency care A normal or increased Paco2 signifies severe airway obstruction, patient fatigue, and incipient ventilatory failure

CONTD……………………………………….: 

CONTD………………………………………. A final issue of potentially life-saving clinical importance is that asthmatic patients with histories of acute asthma and respiratory failure (near-fatal asthma) may have an inherently blunted perception of the resistance to their breathing imposed by worsening bronchospasm . Thus, they are unable to sense when they are reaching the point of critical airflow obstruction

IN COPD: 

IN COPD The main issue in COPD is HYPERCAPNIA. The causes of hypercapnia in COPD are multiple and complex , and include 1. the degree of airflow obstruction 2. inspiratory muscle function 3. the native ventilatory response to CO2 4. the coexistence of nocturnal hypoventilation The most important determinant of arterial CO2 retention in these patients is the magnitude of airflow obstruction

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Another possible explanation for chronic hypercapnia is inspiratory muscle dysfunction or weakness in association with an increase in lung resistance This combination of inspiratory muscle weakness and increased lung resistance is associated with hypercapnia and may be a protective strategy to avoid overloading the inspiratory muscles, thereby causing fatigue and ultimately irreversible respiratory failure. One interindividual factor that may contribute to this variable hypercapnia in COPD patients is the native ventilatory response to Paco2

IN NEURO-MASCULAR DISEASES: 

IN NEURO-MASCULAR DISEASES These patients typically have generalized muscle weakness of a proportionately severe degree, including pharyngeal airway dysfunction. Therefore, the impending respiratory failure is a conspicuous, rather than an unexpected, feature of their illness Disproportionate respiratory muscle dysfunction with respiratory failure can occur, especially in patients with associated kyphoscoliosis

DRUGS AFFECTING RESPIRATORY CONTROL: 

DRUGS AFFECTING RESPIRATORY CONTROL From a clinical standpoint, the most important classes of drugs that influence ventilatory control are Inhalational anesthetics , Narcotics, Minor tranquilizers

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Inhalational anesthetics such as halothane, ether, and nitrous oxide cause respiratory depression in normal subjects by decreasing resting V˙e and the response to increasing Paco2 or hypoxemia .

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Narcotics such as morphine, meperidine , fentanyl , and methadone typically cause mild arterial hypercapnia in clinically recommended doses With oral administration, this effect is usually mild compared with their sedative properties, unless another substance such as ethanol is present concurrently. Although oral benzodiazepines do not usually cause an increase in Paco2 in COPD patients, very cautious use is recommended during exacerbations, as hypoventilation may occur

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Alcohol alone tends to depress the ventilatory response to CO2 and will shift the response curve to the right

Respiratory stimulants: 

Respiratory stimulants Doxapram all increase Aminophylline ventilation and Progesterone decrease PCO 2 Methylprogesterone can be used to stimulate ventilatory drive in patients with obesityhypoventilation syndrome Drugs such as the opioid antagonist naloxone and the benzodiazepine antagonist flumazenil may be used to counter the respiratory depressive effects of these drugs

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INTEGRATED RESPONSES OF THE CONTROL SYSTEM

RESPONSE TO EXERCISE: 

RESPONSE TO EXERCISE

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PHASE 1- initial rapid increase at the onset, neurally mediated ( This response is thought to be neurally mediated by impulses originating from the muscle spindles in the exercising muscles, tendons, and proprioceptors in the joints. There may also be stimuli that originate from a region of the brain rostral to the pons and medulla (possibly the hypothalamus and motor cortex) and operate independently of the other stimuli) PHASE 2- slower and exponential increase, within 30 sec of initiation ( an interval that approximates the circulation time for venous blood from the exercising muscles to reach the respiratory centers ) PHASE 3- the steady state, within 4 mins of initiation Then the recovery phase that occurs with the cessation of the activity

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In severe exercise further increase occurs d/t accumulation of lactic acid when oxygen consumption exceeds the anaerobic threshold and lactic acid accumulates in the blood.

ABG DURING PHASES OF EXERCISE: 

ABG DURING PHASES OF EXERCISE PHASE 1 - no detectable change in PaO 2 and PaCO 2. PHASE 2 - PaO 2 decreases and PaCO 2 increases. Started within 30 secs from initiation of exercise. PHASE 3 - stable PaO 2 , PaCO 2 and Ph, started within 4 min of initiation ( pulmonary gas exchange matches metabolic rate) PHASE 4 - arterial hypocapnia d/t lactic acidosis

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Termination of exercise is associated with an abrupt decrease in ventilation followed by an exponential decay to resting levels. This abrupt decrease is usually of a lesser magnitude than the abrupt increase seen at the onset of exercise. It may be secondary to the removal of neural stimuli from the higher neural centers and exercising limbs , while the slow decay may be related to the removal of the remaining stimuli (hypoxia, hypercapnia , and short-term potentiation ) present during steady-state exercise

RESPONSE TO ALTITUDE: 

RESPONSE TO ALTITUDE ALTITUDE INCREASE BAROMETRIC PRESSURE DECREASES THE ABSOLUTE PRESSURE OF OXYGEN AND NITROGEN DECREASES This mild hypoxemia result in an increase in alveolar ventilation and a lower arterial Paco2 (respiratory alkalosis).

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THERE IS ALSO AN INCREASE IN CO2 SENSITIVITY ACCLIMATIZATION

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Slow return of ventilation when acclimatised individual return to sea level These slow processes occur mainly via changes in the peripheral chemoreceptor activity rather than central effect of hypoxia

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Acute mountain sickness may develop following rapid ascent to moderate altitude as a result of hypoxemia that causes cerebral vasodilatation with increased perfusion pressure, leading to the development of cerebral edema Symptoms include headache, nausea and vomiting, lethargy, and sleep disturbances Hypoxemia-induced hyperventilation and pulmonary hypertension are probably important in the common complaint of dyspnea at altitude. Prevention- 1. slow ascent 2. 2 days prophylaxis of acetazolamide

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High-altitude pulmonary edema is a form of noncardiogenic pulmonary edema secondary to hypoxia of high altitudes that may develop in normal subjects without preexisting cardiac or pulmonary disease.

RESPONSE TO SLEEP: 

RESPONSE TO SLEEP Periods of apnea during REM and lighter forms of NREM sleep Ventilatory response to hypoxia and hypercapnia is reduced Increased upper airway resistance Decreased compliance of lung Response to mechanoceptors stimulation is also altered Airway obstruction during sleep usually terminates with arousal

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ABNORMALITIES IN RESPIRATORY RHYTHM

CHEYNE-STOKES RESPIRATION: 

CHEYNE-STOKES RESPIRATION A TYPE OF PERIODIC BREATHING CYCLIC RISE AND FALL IN VENTILATION WITH RECURRENT PERIODS OF APNEA OR NEAR APNEA MECHANISMS: 1. INCREASED SENSITIVITY TO PCO 2 d/t DISRUPTION OF NEURAL PATHWAYS. 2. PROLONGATION OF “LUNG-TO-BRAIN” CIRCULATION TIME- the respiratory control oscillates because the negative feed-back loop from lungs to brain is abnormally long

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Causes- Congestive heart failure Uremia Brain damage

KUSSMAUL RESPIRATION: 

KUSSMAUL RESPIRATION Known as acidotic breathing or air hunger Seen in diabetic ketoacidosis Accummulation of acidic ketone bodies in the blood Prolonged respiratory stimulation Producing rapid and deep respiration

KUSSMAUL BREATHING: 

KUSSMAUL BREATHING

BIOT’S RESPIRATION: 

BIOT’S RESPIRATION Biot's respiration , sometimes also called ataxic respiration , is an abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea . indicates a poor prognosis

BIOT’S RESPIRATION: 

BIOT’S RESPIRATION CAUSES- Damage to medulla oblungata d/t stroke or trauma Tentorial or uncal herniation Opioid use

APNEUSTIC BREATHING: 

APNEUSTIC BREATHING Apneustic respiration ( a.k.a. apneusis ) is an abnormal pattern of breathing characterized by deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release

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CAUSES Damage to pons and upper medulla ketamin

Ondine’s curse/ CCHS: 

Ondine’s curse/ CCHS Ondine was a water nymph in German mythology. She was very beautiful and (like all nymphs) immortal. However, should she fall in love with a mortal man and bear his child - she will lose her "gift" of everlasting life. Ondine fell in love with a dashing knight - Sir Lawrence - and they were married. When they exchanged vows, Lawrence said, "My every waking breath shall be my pledge of love and faithfulness to you." A year after their marriage Ondine gave birth to Lawrence’s child. From that moment on she began to age. As Ondine’s physical attractiveness diminished, Lawrence lost interest in his wife. One afternoon Ondine was walking near the stables when she heard the familiar snoring of her husband. When she entered the stable, however, she saw Lawrence lying in the arms of another woman. Ondine pointed her finger at him, which he felt as a kick, waking up with a start. Ondine uttered a curse: "You swore faithfulness to me with every waking breath, and I accepted your oath. So be it. As long as you are awake, you shall have your breath, but should you ever fall asleep, then that breath will be taken from you and you will die !"

How can I explain it?........by afferents from higher centres like limbic system and hypothalamus: 

How can I explain it?........by afferents from higher centres like limbic system and hypothalamus The pathways of voluntary control pass from the neo-cortex to the motor neurons innervating the respiratory muscles bypassing the medullary neurons. Since voluntary and autonomic control of resp are separate, autonomic control is sometimes disrupted without loss of voluntary control. The clinical condition where it can occur? ......... BULBAR POLIOMYELITIS R X - MECHANICAL VENTILATION or DIAPHRAGM SPACING

THANK YOU: 

THANK YOU