Docstoc

RESPIRATORY PHYSIOLOGY – PART 1

Document Sample
RESPIRATORY PHYSIOLOGY – PART 1 Powered By Docstoc
					RESPIRATORY PHYSIOLOGY – PART 1
Fiona Collingwood
Consultant facilitator – Dr Julia Coldrey
MODULES
 BI – Anatomy of the respiratory system

 BII – control of ventilation

 BVIII – Pulmonary circulation
CONTROL OF VENTILATION
 The respiratory centre
 Central chemoreceptors
 Peripheral chemoreceptors
 Other receptors/ inputs
THE RESPIRATORY CENTRE
 Composed of groups of neurons in the medulla
 oblongata
   Dorsal (inspiratory) group
   Ventral (expiratory) group


 And the pons
   Pneumotaxic centre
DORSAL NEURONS OF THE RESPIRATORY
CENTRE
 Located in the nucleus tractus solitarus
 termination of vagus and glossopharyngeal nerves - transmit
 signals from peripheral chemoreceptors, baroreceptors and other
 lung receptors.

 Provides a basal rhythm for inspiration - like pacemaker rhythm.

 The signal transmitted to the diaphragm – inspiratory ramp, for
 about 2 secs.
 Then ceases abruptly for 3 secs, which turns off excitation of the
 diaphragm and allows for elastic recoil and expiration.
    gradual increasing contraction of the diaphragm and thus lung volumes
    The rate of increase in the ramp signal controls the rapidity of lung
    expansion
    The limiting point at which the ramp ceases (or duration of action
    potential) controls duration of inspiration and thus also expiration.
VENTRAL NEURONS OF THE RESPIRATORY
CENTRE

 Located in the nucleus ambiguus and nucleus
 retroambigualis
 The neurons are almost completely inactive during
 quiet respiration. Therefore expiration is passive,
 caused by elastic recoil of the lungs and thoracic
 cage.
 When there is increased pulmonary drive,
 respiratory signals transmit from the dorsal group to
 the ventral group to increase both inspiration and
 expiration.
 Provide expiratory signals to abdominal muscles.
PNEUMOTAXIC CENTRE
 Located dorsally in the nucleus parabrachialis in the
 upper pons
 Transmits signals to the dorsal (inspiratory) area.
 It controls the switch off point of the inspiratory
 ramp, controlling the filling phase of the lung cycle.
 The stronger the pneumotaxic signal, the shorter
 the ramp time, and thus faster the respiratory rate.
 The role of the pneumotaxic centre is therefore to
 limit inspiratory time and thus control respiratory
 rate as well as volume.
CENTRAL CHEMORECEPTORS
 Chemosensitive area - in the medulla, separate to the dorsal and ventral
 groups.
 Highly sensitive to changes in CSF H+ concentration – inputs to the
 respiratory centre to alter ventilation
 Carbon dioxide indirectly stimulates the chemosensitive area by C02
 reacting with H20 to produce carbonic acid, which then dissociates into
 bicarbonate and H+ ions; the H+ directly activates the respiratory area.
 C02 can readily cross the BBB thus any plasma increases will cause a
 significant effect.
 Plasma H+ cannot readily cross the BBB, therefore causing only modest
 effect on respiration.
 Chronic C02 elevation – response to a high C02 is reduced.
    Renal compensatory increase in HCO3- , which crosses the BBB and binds
    with H+ ions adjacent to the respiratory centers that are produced by the high
    C02 levels.

 Therefore PC02 levels have a potent acute but only weak chronic effect
 on respiratory control.
PERIPHERAL CHEMORECEPTORS
 Carotid bodies
   afferent nerves pass through the glossopharyngeal nerves to
   the dorsal area

 Aortic bodies
   afferent nerves pass through the vagus nerve to the dorsal
   area.

 The bodies have their own high volume arterial blood
 supply.

 Once P02 falls below normal, and particularly below
 60mmHg then the carotid bodies are strongly
 stimulated. It is particularly sensitive to changes
 between 30 - 60mmHg.
EFFECTS OF P02 ON VENTILATION
EFFECTS OF PC02 ON VENTILATION




 C02 and H+ also stimulate peripheral chemoreceptors -
 the effect is much weaker than the central effect.
 However the peripheral receptors are activated much
 more rapidly than the central receptors and therefore
 may cause a quicker response to increased C02 and
 acidosis
EFFECTS OF P02, PC02 AND PH ON
VENTILATION
OTHER FACTORS THAT CONTROL VENTILATION
 Hering – Breuer reflex
   Stretch receptors in the walls of the bronchi and
   bronchioles transmit signals through the vagus nerves
   into the dorsal respiratory group of neurons, when the
   lungs become overstretched.
   Active a feedback loop that switches off the inspiratory
   ramp.
   Reflex is not activated until tidal volume is 2-3 times
   normal (>1L per breath) - likely a protective
   mechanism rather than an integral control of
   ventilation.
 Cortical and limbic system inputs, temperature,
 baroreceptors (hypotension)
 Voluntary control.
SITUATIONS AFFECTING VENTILATION
 Exercise
 Pregnancy
 Anaesthetic agents
 Altitude
EXERCISE
 Increase in respiration and minute volume, despite
 little actual change in pH, P02 or PC02.
 Initial drop in PC02 due to increased ventilation.
 Anticipatory
 It is believed that both cortical centres and joint and
 muscle receptors send signals to the respiratory
 centre to increase ventilation in response to
 movement.
PREGNANCY


 Minute ventilation increases,
  up to 50% increase at term
 Increase in TV and respiratory rate
 Progesterone stimulates respiratory centre
 Left shift in ventilation/C02 response curve
    PC02 26 – 32mmHg by 1st trimester
    Restored to normal rapidly post delivery
 During labour minute ventilation further increases due
 to pain. Contractions increase 02 consumption
 After contractions hypocapnic (transient)
 hypoventilatory period that can lead to desaturation
ANAESTHETIC AGENTS
 Volatiles, barbituates and opioids
 Depress ventilatory responses
 Ventilation/C02 curve flattened
    As PCO2 increases, the minute ventilation response is
    suppressed
 Increased apnoeic threshold – increased PC02 at which
 ventilation resumes after hyperventilation
 Volatiles particularly suppress ventilatory response to
 hypoxia (P02/ventilation curve flattened)

 The effects of anaesthetic agents persist into the early
 post-operative period, therefore prolonged risk of
 hypoxia or hypoventilation.
ALTITUDE

 Barometric pressure reduces exponentially as
 altitude increases
 Decreased ambient P02
 Decreased arterial and alveolar P02
 Stimulation of peripheral chemoreceptors and
 increased minute ventilation
 At 6000m MV increased by 160%
 Consequent respiratory alkalosis and hypocapnia
 MV continues to increase with time at altitude
   Due to renal compensation for alkalosis
   Local CSF compensation
   Respiratory centre resets at lower PC02
THE PULMONARY CIRCULATION
 Physiological differences between pulmonary and
 systemic circulation
 Factors that affect pulmonary vascular resistance
 The pulmonary circulation of the fetus and newborn
PHYSIOLOGICAL DIFFERENCES BETWEEN
PULMONARY AND SYSTEMIC CIRCULATION

 Low pressure system
   Minimises transudation into interstitial spaces
   Reduced RV workload
 Highly distensible vessels
   PA is much shorter and more thin walled than the aorta
   Pulmonary arterioles contain little smooth muscle, but
   can produce vasoconstriction
   Venules are devoid of smooth muscle
   Capillaries are arranged around alveoli, increased SA
   for gas exchange
   Capillary flow governed by PA and venous pressure,
   and alveolar pressure
   PA and PV diameter increased by lung expansion
THE PULMONARY CIRCULATION
 PA systolic pressure – 25mmHg
 PA diastolic pressure – 10mmHg
 LA pressure – 5mmHg
 Pulmonary capillary pressure – 8mmHg
FACTORS THAT ALTER PULMONARY VASCULAR
RESISTANCE

 α andβreceptors present
 Vagal nerve supply – acetylcholine acts at
 muscarinic receptors to cause vasodilation
 Sympathetic ganglia cause vasodilation and can
 increase pulmonary blood flow by 30%
 Humoral factors – angiotensin II, bradykinin,
 endothelin, histamine, adenosine
FACTORS THAT ALTER PULMONARY VASCULAR
RESISTANCE

 Nitric oxide is main determinant responsible for local
 control of pulmonary blood flow
 Continuously synthesised by the pulmonary artery
 endothelium in the presence of a normal alveolar P02.
   If alveolar P02 falls below 70mmHg, endothelial NO synthesis
   is reduced causing local vasoconstriction.
 Systemic hypoxia leads to generalised vasoconstriction
 Low PC02 stimulates local vasoconstriction
 H+ stimulates local vasconstriction

   Allows for ventilation perfusion matching
   Diversion of blood flow to better ventilated areas
PULMONARY VASCULAR RESISTANCE




 PVR =
PULMONARY CIRCULATION OF THE FETUS AND
NEWBORN
PULMONARY CIRCULATION OF THE FETUS AND
NEWBORN

 Lungs receive only 10% RV output
 Lungs are collapsed
 PVR is high (due to lung collapse, low 02 tension,
 high C02 tension)

 At birth
 Closure of ductus arteriosus and foramen ovale –
 increased pulmonary blood flow
 Lung expansion, increased 02 tension, reduced
 C02 tension
 Reduced PVR and PAP
EXAM QUESTIONS

Control of ventilation
  Physiol-06A10 List the physiological factors which increase
  respiratory rate. Include a brief explanation of the mechanism
  by which each achieves this increase. 62%

Pulmonary circulation
  Physiol-05B9 Describe the gravity dependent processes
  which affect pulmonary blood flow. What changes take place
  when the pressure increases in the pulmonary vessels? 82%
  Physiol-04A9 Briefly outline the differences between the
  pulmonary circulation and the systemic circulation 26%
  Physiol-02A4 Outline the physiological factors that influence
  pulmonary vascular resistance 57%

				
DOCUMENT INFO