The document summarizes regulation of respiration, including:
1- The respiratory center is located in the medulla and pons and contains three major neuron groups that control inspiration, expiration, and breathing depth. Peripheral chemoreceptors also detect oxygen levels and signal the respiratory center.
2- Chemical control of respiration, mainly by carbon dioxide and hydrogen ions, directly stimulates the respiratory center. Oxygen does not directly affect the center but is detected by peripheral chemoreceptors.
3- Other factors like exercise, lung inflation, brain edema, anesthesia, and irritant receptors can also influence respiration. Periodic breathing disorders like Cheyne-Stokes and sleep apnea involve irregular breathing patterns during
Regulation of respiration (the guyton and hall physiology)Maryam Fida
Normal respiration is spontaneous and unconscious.
There are 4 groups of neurons on each side in the Pons and medulla oblongata which are involved in regulation of respiration. These include
1. Medullary centers
Dorsal respiratory group of neurons
Ventral respiratory group of neurons
2. Pontine centers
Pneumotaxic centre
Apneustic centre.
It contains “I”neurons which are inspiratory neurons.
It’s located in dorsal portion of medulla oblongata.
It also includes the nucleus of tractus solitarius which is the sensory termination of afferent fibers in 9th ( GLOSSOPHARYNGEAL NERVE) and 10th (VAGUS NERVE) cranial nerves.
They receive impulses from peripheral chemoreceptors, carotid and aortic baroreceptors and also other receptors in the lungs.
In this group inspiratory ramp signals are produced spontaneously.
If we cut the medulla oblongata from other parts of brain and also the afferent nerves which enter the medulla, still inspiratory ramp signals are produced which indicate it’s the inherent property of medulla.
Initially the signal is weak and then it progressively increases and then fades away.
Each ramp signal’s duration is 2 sec and then for 3 seconds there is no ramp signal.
So each cycle lasts for 5 seconds and there are 12 cycles /minute which is the respiratory rate.
Significance of the signal in the form of ramp is that it causes progressive expansion of the lungs. After production, these ramp signals are transmitted to the contra lateral motor neurons supplying the inspiratory muscles.
Rate and duration of inspiratory ramp signals is controlled by impulses from the Pneumotaxic centre and impulses from the lungs via vagi.
Regulation of respiration (the guyton and hall physiology)Maryam Fida
Normal respiration is spontaneous and unconscious.
There are 4 groups of neurons on each side in the Pons and medulla oblongata which are involved in regulation of respiration. These include
1. Medullary centers
Dorsal respiratory group of neurons
Ventral respiratory group of neurons
2. Pontine centers
Pneumotaxic centre
Apneustic centre.
It contains “I”neurons which are inspiratory neurons.
It’s located in dorsal portion of medulla oblongata.
It also includes the nucleus of tractus solitarius which is the sensory termination of afferent fibers in 9th ( GLOSSOPHARYNGEAL NERVE) and 10th (VAGUS NERVE) cranial nerves.
They receive impulses from peripheral chemoreceptors, carotid and aortic baroreceptors and also other receptors in the lungs.
In this group inspiratory ramp signals are produced spontaneously.
If we cut the medulla oblongata from other parts of brain and also the afferent nerves which enter the medulla, still inspiratory ramp signals are produced which indicate it’s the inherent property of medulla.
Initially the signal is weak and then it progressively increases and then fades away.
Each ramp signal’s duration is 2 sec and then for 3 seconds there is no ramp signal.
So each cycle lasts for 5 seconds and there are 12 cycles /minute which is the respiratory rate.
Significance of the signal in the form of ramp is that it causes progressive expansion of the lungs. After production, these ramp signals are transmitted to the contra lateral motor neurons supplying the inspiratory muscles.
Rate and duration of inspiratory ramp signals is controlled by impulses from the Pneumotaxic centre and impulses from the lungs via vagi.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Cvs changes during exercise BY PANDIAN M # MBBS#BDS#BPTH#ALLIED SCIENCESPandian M
INTRODUCTION
TYPES OF EXERCISE - Dynamic exercise, static exercise
AEROBIC AND ANAEROBIC EXERCISES
METABOLISM IN AEROBIC AND ANAEROBIC EXERCISES
SEVERITY OF EXERCISE- Mild exercise, moderate exercise, severe exercise
EFFECTS OF EXERCISE- On blood, on blood volume, on heart rate, on cardiac output, on venous return, on blood flow to skeletal muscles, on blood pressure
Hypoxia :types , causes,and its effects Aqsa Mushtaq
hypoxia :oxygen defecincy at tissue level.in these slides you are going to in touch with its types ,causes effects.share whatever you wanted to say comment us .
these notes are provided by our loving mam MAM SANIA .thanks to teach us mam :)
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Cvs changes during exercise BY PANDIAN M # MBBS#BDS#BPTH#ALLIED SCIENCESPandian M
INTRODUCTION
TYPES OF EXERCISE - Dynamic exercise, static exercise
AEROBIC AND ANAEROBIC EXERCISES
METABOLISM IN AEROBIC AND ANAEROBIC EXERCISES
SEVERITY OF EXERCISE- Mild exercise, moderate exercise, severe exercise
EFFECTS OF EXERCISE- On blood, on blood volume, on heart rate, on cardiac output, on venous return, on blood flow to skeletal muscles, on blood pressure
Hypoxia :types , causes,and its effects Aqsa Mushtaq
hypoxia :oxygen defecincy at tissue level.in these slides you are going to in touch with its types ,causes effects.share whatever you wanted to say comment us .
these notes are provided by our loving mam MAM SANIA .thanks to teach us mam :)
Regulation of Respiration - Animal PhysiologyMuhammad Yousaf
This document contain detailed study about The Regulation of Respiration and it covers all of the aspects of terms and topics related to regulation of respiration.
Like heartbeat, breathing must occur in a continuous, cyclic pattern to sustain life processes.
Inspiratory muscles must rhythmically contract and relax to alternately fill the lungs with air and empty them.
The rhythmic pattern of breathing is established by cyclic neural activity to the respiratory muscles
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This a presentation on regulation of respiration, control of the rate of increase of the the ramp signal, control of the limiting point at which ramp suddenly ceases
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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2. Respiratory center
• Respiratory center is composed of several groups of neurons located bilaterally in
the medulla oblongata and pons of the brain stem.
Its divided into three major collections of neurons:
• 1- dorsal respiratory group located in the dorsal portion on the medulla ,which
mainly causes inspiration.
• 2- a ventral respiratory group located in the ventrolateral part of the medulla
,which mainly causes expiration.
• 3-the pneumotaxic center, located dorsally in in the superior portion of the pons,
which mainly controls the depth of breathing
• The dorsal respiratory group of neurons plays the most fundamental role in the
control of respiration.
3. Dorsal respiratory group of neurons- its control
of inspiration and of respiratory rhythm
• Most of its neurons are located within the nucleus of the tractus solitarius,also
additional neurons in the adjacent reticular substance of the medulla.
• The nucleus of tractus solitarius is the sensory termination of both the vagal and
the glossopharyngeal nerves, which transmit sensory signals into the respiratory
center from the peripheral chemoreceptors,barorecepters and several types of
receptors in the lungs.
• Rhythmical inspiratory discharges from the dorsal respiratory group: it emits
repetitive bursts of inspiratory neuronal action potentials.
4. Dorsal respiratory group of neurons- its control
of inspiration and of respiratory rhythm
• Inspiratory ramp signal: the nervous signal that is transmitted to the inspiratory
muscles mainly from the diaphragm.
• in normal respiration it begins weakly and increases steadily in a ramp manner for
about 2 seconds, then it ceases abruptly for the next 3 seconds, which turns off
the excitation of the diaphragm and allows elastic recoil of the lungs and the chest
wall to cause expiration.
There are two qualities of the inspiratory ramp that are controlled aw follows:
• 1- control the rate of increase of the ramp signal so the ramp increases during
heavy exercise.
• 2- control of the limiting point at which the ramp suddenly ceases (the earlier the
ramp ceases the shorter duration of inspiration also shorten the duration of
expiration so the frequency of respiration increased)
5. A pneumotaxic center limits the duration of
inspiration and increases the respiratory rate
• The primary effect of this center is to control the switch off point of the inspiratory
ramp, thus controlling the duration of the filling phase of the lung cycle (0.5 to 5
seconds)
• Its function primarily to limit inspiration.
• Has a secondary effect of increasing the rate of breathing .
• A strong pneumataxic center can increase the rate of breathing to 30 to 40 breaths
per minute whereas a weak pneumotaxic signal may reduce the rate to only 3 to 5
breaths per minute
6. Ventral respiratory group of neurons –functions
in both inspiration and expiration
• The function of this neural group differs from that of the dorsal respiratory group
in several important ways:
• 1- the neurons of the ventral respiratory group remain almost totally inactive
during normal quiet respiration.
• 2-when the respiratory drive for increased pulmonary ventilation becomes greater
than normal, the ventral respiratory area contributes to the extra respiratory drive
as well.
• 3-these neurons contribute to both inspiration and expiration ,they are important
in providing powerful expiratory signals to the abdominal muscles during heavy
exercise
7. Lung inflation signals limit inspiration-the
Hering-Breuer inflation reflex
• Stretch receptors located in the muscular portions of the walls of the bronchi and
bronchioles through the lungs transmit signals through the vagus into the dorsal
respiratory group of neurons when the lungs become over stretched
• When the lungs become over inflated the stretch receptors activate a feedback
response that switches off the inspiratory ramp and stops further inspiration.
• The Hering-Breuer reflex is a protective mechanism for preventing excess lung
inflation rather than an important ingredient in normal control of ventilation.
8. Chemical control of respiration
• The ultimate goal of respiration is to maintain proper concentration of oxygen,
carbon dioxide and hydrogen ions in the tissues so the respiratory is highly
responsive to changes of these.
• Excess carbon dioxide or hydrogen in blood act directly on the respiratory center
causing increase respiration.
• Oxygen doesn’t have a significant direct effect on the respiratory center, it acts
almost entirely on peripheral chemoreceptors located in the carotid and aortic
bodies and these transmit nervous signals to the respiratory center to control
respiration.
9. Direct chemical control of respiratory center
activity by carbon dioxide and hydrogen ions
• Chemosensitive area of respiratory center: located beneath ventral surface of the
medulla, is highly sensitive to changes in either blood PCO2 or hydrogen ions
concentration .
• Excitation of the chemosensitive neurons by hydrogen ions is likely the primary
stimulus
• Carbon dioxide stimulates the chemosensitive area: have little direct effect on the
chemosensitive areas, it does this by reacting with water of the tissues to form
carbonic acid which dissociates into hydrogen and bicarbonate ions ,and the
hydrogen ions have a potent direct stimulatory effect on respiration.
10. Direct chemical control of respiratory center
activity by carbon dioxide and hydrogen ions
• Why does blood carbon dioxide have a more potent effect in stimulating the
chemosensitive neurons than do blood hydrogen ions?
The blood brain barrier is not very permeable to hydrogen ions, but carbon dioxide
passes through this barriers completely.(after its dissociation it stimulate the
chemosensitive neurons)
• Decreased stimulatory effect of carbon dioxide after the first 1 to 2 days: part of
this decline results from renal adjustment of the hydrogen ions concentration in
the circulating blood back toward normal after the carbon dioxide firstly increases
the hydrogen concentration ,the kidney achieve this by increasing the blood
bicarbonate which binds with hydrogen in blood to reduce their concentration
• so change in blood carbon dioxide concentration had a potent acute effect on
controlling respiratory drive but a weak chronic effect after a few days adaptation
11.
12. Direct chemical control of respiratory center
activity by carbon dioxide and hydrogen ions
• Quantitative effects of blood CO2 and hydrogen ion concentration on alveolar
ventilation: there is tremendous effect that carbon dioxide changes have in
controlling the respiratory center so CO2 is the major controller of respiration.
• Unimportance of oxygen for control of the respiratory center: it has no direct
effect on the respiratory center itself. There is special mechanism for respiratory
control located in the peripheral chemoreceptors outside the brain respiratory
center, this mechanism responds when blood oxygen falls too low, mainly below a
Pco2 of 70 mmHg
13.
14. Peripheral chemoreceptor system for control of
respiratory activity-role of oxygen in respiratory
control
• Peripheral chemoreceptors located outside the brain ,in carotid and aortic bodies,
are specially important for detecting changes in oxygen in blood, also responds to
a lesser degree to changes in CO2 and H ions concentrations.
• The carotid bodies are located bilaterally in the bifurcations of the common carotid
arteries, their afferent nerve fibers through Hering's nerve to the glossopharyngeal
nerve.
• The aortic bodies are located along the arch of the aorta ,their afferent nerve
fibers pass through the vagus also to the dorsal medullary respiratory area.
• Blood flow through these bodies is extreme so the percentage of oxygen removed
from the blood is zero, so the chemoreceptors are exposed at all times to arterial
blood not venous blood.
15.
16. Peripheral chemoreceptor system for control of respiratory
activity-role of oxygen in respiratory control
• Stimulation of the chemoreceptors by decreased arterial oxygen: the impulse rate
is sensitive to changes in arterial Po2 in the range of 60 down to 30 mmHg, a range
in which hemoglobin saturation with oxygen decreases rapidly.
• Basic mechanism of stimulation of the chemoreceptors by oxygen deficiency: the
aortic and carotid bodies have multiple glandular like cells(glomus cells) that
synapse directly or indirectly with the nerve endings.
• Effect of low arterial PO2 to stimulate alveolar ventilation when arterial carbon
dioxide and hydrogen ion concentrations remain normal: there's no effect on
ventilation as long as the arterial PO2 remains greater than 100 mm Hg,but at
pressures lower than that, ventilation doubles when the arterial PO2 falls to 60
mm Hg
17. Peripheral chemoreceptor system for control of respiratory
activity-role of oxygen in respiratory control
• Chronic breathing of low oxygen stimulates respiration even more –the
phenomenon of “acclimatization”: mountain climbers have found that when they
ascend a mountain slowly over a period of days rather than period of hours ,they
breathe much more deeply and therefore can withstand lower atmospheric
oxygen concentrations than when they ascend rapidly.
• The reason for acclimatization is that within 2 to 3 days the respiratory center in
the brain stem loses about four fifths of its sensitivity to changes in Pco2 and
hydrogen ions
18. Regulation of respiration during exercise
• In healthy athlete alveolar ventilation ordinarily increases almost exactly in step
with the increased level of oxygen metabolism .the arterial PO2 ,PCO2 and PH
remain almost exactly normal.
• Its likely that most of the increase in respiration results from neurogenic signals
transmitted directly into the brain stem respiratory center at the same time that
signals go to the body muscles to cause muscle contraction
19.
20.
21.
22. Regulation of respiration during exercise
• Interrelations between chemical factors and nervous :factors in the control of
respiration during exercise: at the onset of exercise ,the alveolar ventilation
increases instantously without an initial increase in arterial Pco2 but it actually
decrease it below normal. After 30 to 40 seconds the amount of carbon dioxide
released into the blood from the active muscles matches the increased rate of
ventilation and the arterial PCO2 returns to normal (40 mm Hg)..
• If PCO2 greater than 40 mmHg it stimulates the ventilaion,and if it is less than that
it has a depressant effect on ventilation.
• Controlling the ventilation during exercise is a learned response from the brain.
23. Other factors that affect respiration
• Voluntary control of respiration: can hypoventilate or hyperventilate.
• Effect of irritant receptors in the airway : the epithelium of the trachea, bronchi
and bronchioles supplied with sensory nerve endings called pulmonary irritant
receptors that cause coughing and sneezing, it may also cause bronchial
constriction in asthma and emphysema.
• Function of lung “ J receptors”: a few sensory nerve endings in the alveolar walls in
juxtaposition to the pulmonary capillaries named “j receptors", they are
stimulated especially when the pulmonary capillaries become engorged with
blood or when pulmonary edema occurs in congestive heart failure ,their
excitation may give the person a feeling of dyspnea.
24. Other factors that affect respiration
• Effect of brain edema: respiratory depression resulting from brain edema can be
relieved temporarily by intravenous injection of hypertonic solutions such as highly
concentrated mannitol solution that osmotically remove some of the fluids of the
brain ,thus relieving intracranial pressure and sometimes re-establishing
respiration within a few minutes.
• Anesthesia: the most prevalent cause of respiratory depression and respiratory
arrest is overdosage with anesthetics or narcotics.
25. Periodic breathing
• An abnormality of respiration called periodic breathing occurs in a number of
disease conditions.
• One type of periodic breathing is cheyne-stokes breathing which is characterized
by slowly waxing and waning respiration occurring about every 40 to 60 seconds.
Basic mechanism of cheyne-stokes breathing:
• When a person over breaths ,thus blowing off too much carbon dioxide from the
pulmonary blood while at the same time increasing blood oxygen so the center
become depressed, then the opposite cycle begins that is CO2 increases and O2
decreases in the alveoli and when the brain responds to these changes the person
breathes hard once again and the cycle repeats.
26.
27. Periodic breathing
Causes for Cheyne-Stokes breathing:
• 1- when along delay occurs for transport of blood from the lungs to the brain (in
severe cardiac failure)
• 2-increased negative feedback gain in the respiratory control areas(in brain
damage).
28. Sleep apnea
• Is the absence of spontaneous breathing. Occasional apneas occur during sleep
but in patients with sleep apnea the frequency and duration are greatly increased
,episodes of apnea lasting for 10 seconds or longer occurring 300 to 500 times
each night.
Obstructive sleep apnea is caused by blockage of the upper airway :
• especially those individuals with narrow passage and relaxation of these muscles
during sleep causes the pharynx to completely close so that the air cant flow to
the lungs.
• those patients have loud snoring and labored breathing occur soon after falling
asleep.
• There is decrease in PO2 and increase in PCO2 which greatly stimulates respiration
• Patients have excessive daytime drowsiness.
29. Sleep apnea
Obstructive sleep apnea is caused by blockage of the upper airway(continued):
• it occurs in older ,obese persons in whom there is increased fat deposition in the
soft tissues of the pharynx .
• It may be associated with nasal obstruction, a very large tongue ,enlarged tonsils ,
or certain shapes of palate that greatly increase resistance to the flow of air to the
lungs during inspiration.
The most common treatment of obstructive sleep apnea:
• 1- surgery to remove excess fat tissue at the back of throat
(uvulopalatopharyngoplasty),to remove enlarged tonsils or adenoids or to create
an opening in the trachea(tracheastomy) to bypass the obstructs airway during
sleep.
• 2- nasal ventilation with continuous positive pressure (CPAP).
30. Sleep apnea
Central sleep apnea occurs when the neural drive to respiratory muscles is transiently
abolished:
• disorders that can cause cessation of the ventilatory drive during sleep include
damage to the central respiratory centers or abnormalities of the respiratory
neuromuscular apparatus.
• they have decreased ventilation when they are awake.
• The cause is unknown ,although the instability of the respiratory drive can result
from strokes or other disorders that make the respiratory centers of brain less
responsive to the stimulatory effect of CO2 & H ions
• Patients are extremely sensitive to even small doses od sedatives or narcotics
• Medications that stimulate the respiratory centers are helpful but ventilation with
CPAP at night is necessary.