control o
TRANSCRIPT
![Page 1: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/1.jpg)
Dr . Nahid Sherbini
Consultant IM &Pulmonary
KFH ,Medina ,Saudi Arabia
![Page 2: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/2.jpg)
Breathing is controlled by the central
neuronal network to meet the metabolic
demands of the body
– Neural
– Chemical
![Page 3: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/3.jpg)
Keep arterial levels of O2 & CO2 constant.
Match perfusion by pulmonary blood
flow with ventilation of the lungs with
overall metabolic demand.
![Page 4: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/4.jpg)
Control of Breathing
Central neurons determine minute
ventilation (VE) by regulating tidal
volume (VT) and breathing
frequency (f).
VE = VT x f
![Page 5: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/5.jpg)
Definition:
A collection of functionally similar neurons
that help to regulate the respiratory
movement.
![Page 6: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/6.jpg)
Higher respiratory center: cortex,
hypothalamus & limbic system.
Medulla & Pons :
Basic respiratory center: produce and
control the respiration.
Spinal cord: motor neurons.
![Page 7: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/7.jpg)
Affect rate and depth of ventilation
Influenced by:• higher brain centers
• peripheral mechanoreceptors
• peripheral & central chemoreceptors
![Page 8: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/8.jpg)
![Page 9: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/9.jpg)
Voluntary breathing center
Cerebral cortex.
Automatic (involuntary) breathing center
– Medulla
– Pons
![Page 10: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/10.jpg)
CAN BYPASS LOWER CENTERS.
SPEECH,SINGING,COUGHING, BREATH
HOLDING .
![Page 11: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/11.jpg)
Voluntarily – speaking, blowing, whistling, pushing, defecation.
Voluntary control is bilateral – cannot contract half of diaphragm or larynx.
Descend via pyramidal tracts.
Destroy voluntary control without losing involuntary control can be.. i.e. stroke
![Page 12: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/12.jpg)
To larynx and bronchi
To respiratory muscles
Nucleus parabrachialis medialis (part of PRG)
Dorsal respiratory group
– nucleus of the solitary tract
Pons
Medulla
Ventral respiratory group
- Nucleus ambiguus
- Nucleus retroambigualis
PRG = pontine respiratory group
![Page 13: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/13.jpg)
Rhythmicity center:
• Controls automatic
breathing.
• Interacting neurons
that fire either during
inspiration
(I neurons) or
expiration
(E neurons).
![Page 14: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/14.jpg)
I neurons located primarily in dorsal respiratory group (DRG):• Regulate activity of phrenic nerve.
E neurons located in ventral respiratory group (VRG):• Passive process.
Activity of E neurons inhibit I neurons.• Rhythmicity of I and E neurons may be due to
pacemaker neurons
![Page 15: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/15.jpg)
Inspiratory Muscles
Expiratory Muscles
Inspiratory Neurons
Expiratory Neurons
• This implies that each group exhibits “self-inhibition” – they can switch themselves off.
• Stops breathing getting stuck in inspiration or expiration.
![Page 16: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/16.jpg)
Apneustic center (lower pons) – to
promote Inspiration.
Pneumotaxic center (upper pons)
– inhibits apneustic center & inhibits
inspiration
-helps control the rate and pattern of
breathing.
![Page 17: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/17.jpg)
Pons
Medulla
Cuts off
Produces apneustic effect – long, powerful inspirations
Stops breathing since no automated output to respiratory system – cause of death
![Page 18: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/18.jpg)
DRG
VRG
pons
medulla
Neural Control
of Breathing –
Respiratory
neurons
![Page 19: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/19.jpg)
Neural Control
of Breathing –
The efferent
pathway
Phrenic n.
muscle supply
autonomic
![Page 20: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/20.jpg)
DECENDING BULBOSPINAL FIBRES
ARE IN THE VENTRAL AND LATERAL
COLUMNS.
RESP NEURONS ARE IN VENTRAL Horn
EXP NEURONS -VENTROMEDIAL
INSP NEURONS- LATERAL
![Page 21: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/21.jpg)
ASCENDING SPINORETICULAR FIBRES
CARRY PROPRIOCEPTIVE INPUTS TO
STIMULATE RESP CENTRE.
BILAT CERVICAL CORDOTOMY
LEADS TO RESPIRATORY
DYSFUNCTION (SLEEP APNEA).
![Page 22: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/22.jpg)
Diaphragm controlled directly by motor neurons – “C3,4 & 5 keeps the diaphragm alive”.
Motor neurons take turns to stimulate different groups of muscle fibres active to minimise fatigue.
Due to poor supply of muscle spindles , control comes from DRG &VRG.
And this explains why rare to feel fatigue in diaphragm.
![Page 23: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/23.jpg)
Larynx movements are synchronized with breathing.
Superior and recurrent laryngeal nerves are branches of vagus nerve.
Expiration – vocal cords together.Inspiration – vocal cords apart.
Automatic rhythm that we can override consciously.
Opera singers try and maximise control of breathing using these muscles.
![Page 24: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/24.jpg)
Control of breathing affected profoundly by vagus nerves (Cranial Nerve X).
Two of these run down either side of neck and torso, near trachea.
Regulate receptors which are most involved in respiration:• Slowly-adapting pulmonary stretch receptors (PSR’s)
• Rapidly-adapting (irritant) receptors (RAR’s)
• C-fibre receptors (J receptors)
![Page 25: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/25.jpg)
Paintel et al (1970) :
Propose J receptors function TO LIMIT
EXERCISE WHEN INTERSTITIAL
PRESSURE INCREASES(J REFLEX)
MECHANISM:
INHIBITION OF RESP MOTOR
NEURONS.
![Page 26: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/26.jpg)
• + when pulmonary caps are
engorged or pulmonary edema.
create a feeling of dyspnea
![Page 27: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/27.jpg)
UNMYELINATED NERVE ENDINGS .
RESPONSIBLE FOR BRONCHOSPASM IN ASTHMA.
INCREASED TRACHEOBRONCHIAL SECRETIONS.
MEDIATORS:HISTAMINE, PROSTAGLANDINS ,
BRADYKININ.
![Page 28: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/28.jpg)
Herring-Breuer Inflation reflex• stretch receptors located in wall of airways• + when stretched at tidal volumes > 1500 ml• inhibits the DRG
Inflation
Apnoea
Phrenic nerve activity
Lung volume
Safety threshold that
triggers reflex
![Page 29: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/29.jpg)
Airway Receptors:
Slowly adapting (stretch - ends
inspiration)
Rapidly adapting (irritants -
cough)
Bronchial c-fiber (vascular
congestion - bronchoconstriction)
Parenchymal c-fiber (irritants -
bronchoconstriction)
Xth n.
Reflex Control of
Breathing –
Neural receptors
afferents
![Page 30: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/30.jpg)
EXPT ANIMAL STUDIES
Rapid shallow breathing pattern in
response to bronchospasm is mediated
through vagal afferents.
![Page 31: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/31.jpg)
MECHANORECEPTORS - SENSE
CHANGES IN LENGTH ,TENSION AND
MOVEMENT.
ASCENDING TRACTS IN ANTERIOR
COLUMN OF SPINAL CORD TO RESP
CENTRE IN MEDULLA.
![Page 32: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/32.jpg)
SENSE CHANGES IN MSL LENGTH.
INTERCOSTALS > DIAPHRAGM .
REFLEX CONTRACTION OF MUSCLE IN RESPONSE TO STRETCH.
INCREASE VENTILATION IN EARLY STAGES OF EXERCISE.
![Page 33: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/33.jpg)
SENSE DEGREE OF CHEST WALL
MOVT.
INFLUENCE THE LEVEL & TIMING OF
RESP ACTIVITY.
![Page 34: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/34.jpg)
Neural control Beta receptors causing dilatation
Parasympathetic-muscarinic receptors causing constriction
NANC nerves (non-adrenergic, non-cholinergic)○ Inhibitory release VIP and NO bronchodilitation
○ Stimulatory bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”.
![Page 35: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/35.jpg)
Local factors• histamine binds to H1 receptors-constriction
• histamine binds to H2 receptors-dilation
• slow reactive substance of anaphylaxsis-
constriction-allergic response to pollen
• Prostaglandins E series- dilation
• Prostaglandins F series- constriction
![Page 36: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/36.jpg)
![Page 37: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/37.jpg)
Monitor changes in
blood PC02, P02, and
pH.
Central:
• Medulla.
Peripheral:
• Carotid and aortic
bodies.
Control breathing
indirectly.
![Page 38: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/38.jpg)
![Page 39: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/39.jpg)
RESPONSE TO HYPERCAPNIA
• 20-50% CAROTID BODIES
• 50-80% CENTRAL CHEMORECEPTORS
![Page 40: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/40.jpg)
CO2, H+
Control of
Breathing by
Central
chemoreceptors
Central
chemoreceptors
major regulators of
breathing
CO2, H+
Central
chemoreceptors
Resp
neurons
VE
![Page 41: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/41.jpg)
Carotid
body
O2
Chemical
Control of
Breathing –
Peripheral
chemoreceptorsIXth n.
CO2
pH
~10% contribution
to breathing
![Page 42: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/42.jpg)
CO2 tension in blood (mm Hg)
35 40 45
VE
5
50
(L/min)quiet breathing
hypercapnia
CO2 drives ventilation
![Page 43: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/43.jpg)
CO2 tension in blood (mm Hg)
35 40 45
VE
5
50
(L/min)
Hypoxia is a weak ventilatory
stimulus
blood pO2 =
100 mmHg
blood pO2 =
50 mmHg
![Page 44: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/44.jpg)
Are not stimulated directly by changes in
arterial PC02.
H20 + C02 H2C03 H+
Stimulated by rise in [H+] of arterial blood.• Increased [H+] stimulates peripheral
chemoreceptors.
![Page 45: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/45.jpg)
NO CHANGE CAROTID BODY ACTIVITY TILL PaO2 < 75mmHg.
VENTILATION MARKEDLY INCREASED When
PaO2<50mmHg
![Page 46: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/46.jpg)
RAPID PHASE- RAPID INCREASE IN VE
WITHIN SECONDS DUE TO
ACIDIFICATION OF CSF.
SLOWER PHASE- DUE TO BUILDUP OF
H+ IONS IN MEDULLARY
INTERSTITIUM.
CHRONIC HYPERCAPNIA- WEAKER
EFFECT DUE TO RENAL RETENTION
OF HCO3 WHICH REDUCES THE H+.
![Page 47: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/47.jpg)
VENTILATORY RESPONSE TO ALV O2
CO2 POTENTIATES
VENTILATORY
RESPONSE TO
HYPOXEMIA .
BOTH HYPOXEMIC
AND HYPERCAPNIC
RESPONSES
DECREASE WITH
AGEING AND
EXERCISE
TRAINING.
![Page 48: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/48.jpg)
Normal level of HCO3- = 25 mEq/L
Metabolic acidosis (low HCO3-) will
stimulate ventilation (regardless of CO2
levels).
Metabolic alkalosis (high HCO3-) will
depress ventilation (regardless of CO2
levels) .
![Page 49: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/49.jpg)
EFFECT OF PaCO2 & pH ON
VENTILATION
![Page 50: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/50.jpg)
![Page 51: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/51.jpg)
SENSATION OF DYSPNEA WHEN
INCREASED RESP EFFORT DUE TO
“LENGTH- TENSION
INAPPROPRTATENESS”
REMOVAL OF FLUID RESTORES THE
END EXP MSL FIBRE LENGTH
RESTORES THE LENTH TENSION
RELATIONSHIP RELIEF.
![Page 52: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/52.jpg)
SV & CO decreasedCoronary blood flow decreasedRepolarization of heart impairedOxyhemoglobin affinity increasedCerebral blood flow decreasedSkeletal muscle spasm & tetanySerum potassium decreased
• (common thread in most of above is hypocapnic alkalosis)
![Page 53: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/53.jpg)
Effect of brain edema• depression or inactivation of respiratory centers
Effect of Anesthesia/Narcotics• respiratory depression
sodium pentobarbital
morphine
![Page 54: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/54.jpg)
BILATERAL CAROTID BODY
RESECTION
CAROTID ENDARTERECTOMY
REDUCES VE.
30% DECREASE IN RESPONSE TO
HYPERCAPNIA.
![Page 55: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/55.jpg)
59Y FEMALE COPD,CVA ( OLD)CAROTID ENDARTERECTOMY 1YR
ELECTIVE CE (R) DONEPREOP ABG ON R/A- 7.43/50/48/31DAY 3 EXTUBATED O2 3L/MINDAY5: SOMNOLENT AND CONFUSEDABG- 7.28/62/69/31BiPAP INITIATED IMPROVEDABG-7.38/72/54/36
![Page 56: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/56.jpg)
COPD WITH HYPERCAPNIA &
WORSENING RESP ACIDOSIS FULL
OXYGEN THERAPY• LOSS OF HYPOXIC DRIVE
• WORSENING V/Q MISMATCH
PHYSIOLOGIC DEAD SPACE
• CO2 CARRYING CAPACITY AS
OXYGENATION OF Hb IMPROVES
( HALDANE EFFECT)
![Page 57: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/57.jpg)
PERIODIC BREATHING PATTERN WITH
CENTRAL APNEAS.
Causes
1. BILATERAL SUPRAMEDULLARY
LESION
2. CARDIAC FAILURE
3. HIGH ALTITUDE
4. SLEEP
![Page 58: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/58.jpg)
Response to hypoxia and
hypercapnia.
Response to
MECHANORECEPTORS
Pa O2 AND PaCO2 BY 4-8 mmHg
![Page 59: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/59.jpg)
HYPOTONIA OF UPPER AIRWAY-
OBSTR SLEEP APNEA.
HYPOTONIA OF SKELETAL& RESP
MUSCLES- (Ventilation DEPENDS ON
DIAPHRAGM)
![Page 60: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/60.jpg)
PHASE I - IMMED VE WITHIN
SECONDS,NEURAL IMPULSES MSL
SPINDLES, JOINT PROPRIOCEPTORS .
PHASE II- WITHIN 20-30 SEC VENOUS
BLD FROM MSL,SLOW VE(
VENTILATION LAGS BEHIND CO2).
![Page 61: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/61.jpg)
PHASE III - PULM GAS EXCHANGE
MATCHES THE METAB RATE TO
MAINTAIN STABLE O2, CO2, PH.
PHASE IV - BEGINS AT ANAOERBIC
THRESHOLD, O2 CONSUMTION> O2
DELIVERY AND LACTIC ACID
ACCUMULATES.
![Page 62: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/62.jpg)
VENTILATORY RESPONSE TO EXERCISE
![Page 63: Control o](https://reader033.vdocuments.net/reader033/viewer/2022042817/55a72a0f1a28ab885e8b47dc/html5/thumbnails/63.jpg)