Breathlessness and control of breathing Flashcards
VT?
Tidal volume
TTOR?
duration of a single respiratory cycle
VE?
Minute ventilation
Frequency = ?
1/TTOT
60/TTOT ?
converts to respiratory frequency per minute
What are the separate controllers in the brain?
Automatic bulbopontine controller (Brainstem)
Behavioural Suprapontine control (widely distributed)
Involuntary centre is in the?
Involuntary or “metabolic” centre, in the medulla (bulbo–pontine brain)
Voluntary centre is in the?
Voluntary or “behavioural” centre, in motor area of cerebral cortex
Metabolic will always override the ?
Metabolic will always override the behavioural
Other parts of cortex, not under voluntary control, influence the metabolic centre, such as ?
What influences the metabolic centre?
Other parts of cortex, not under voluntary control, influence the metabolic centre, such as emotional responses.
Sleep via reticular formation influences the metabolic centre
Metabolic centre responds to ?
Metabolic centre responds to metabolic demands for and production of CO2 (V´CO2) and determines, in part, the “set point” for CO2, generally monitored as PaCO2.
Behavioural centre controls acts such as ?
What 3 things influence metabolic centre?
Behavioural centre controls acts such as breath holding, singing
Metabolic will always override the behavioural
The limbic system (survival responses [suffocation, hunger, thirst]), and frontal cortex (emotions) and sensory inputs (pain, startle) may influence the metabolic centre.
Where is the peripheral chemoreceptor?
The well perfused carotid body “tastes” arterial blood
It lies at the junction of the internal and external carotid arteries in the neck
It is a rapid response system for detecting changes in arterial PCO2 and PO2
Group pacemake activity comes from?
“group pacemaker” activity coming from about 10 groups of neurons in the medulla near nuclei of IX and X cranial nerves
One group, the pre–Botzinger complex, in ventro–cranial medulla, near 4th ventricle, seems essential for generating the respiratory rhythm, and has been called the “gasping centre”.
Coordination of pre–Botzinger complex with the other “controllers” may be needed to convert “gasping” into an orderly and responsive respiratory rhythm.
Cellular mechanisms and neurotransmitters are a complex and specialised subject
Discrete groups of neurons in the medulla discharge at different phases of the respiratory cycle and have different functions
Early inspiratory initiates ?
Inspiratory augmenting may also ?
Late inspiratory may signal ?
Expiratory decrementing may “brake” ?Expiratory augmenting may activate ?
Late expiratory may signal ?
Discrete groups of neurons in the medulla discharge at different phases of the respiratory cycle and have different functions
Early inspiratory initiates inspiratory flow via respiratory muscles
Inspiratory augmenting may also dilate pharynx, larynx and airways.
Late inspiratory may signal the end of inspiration, and “brake” the start of expiration.
Expiratory decrementing may “brake” passive expiration by adducting larynx and pharynx.
Expiratory augmenting may activate expiratory muscles when ventilation increases on exercise.
Late expiratory may signal the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration.
Reflex control
Vth nerve:
IXth nerve:
Xth nerve:
Vth nerve: afferents from nose and face (irritant)
IXth nerve: from pharynx and larynx (irritant)
Xth nerve: from bronchi and bronchioles (irritant and stretch)
irritant receptors leading to cough, sneezing etc are “defensive”
Hering–Breuer reflex is?
Hering–Breuer reflex from pulmonary stretch receptors senses lengthening and shortening and terminates inspiration and expiration, but weak in humans (ventilatory responses in denervated lungs post–transplantation are normal).
Thoracic spinal cord: from ?
Thoracic spinal cord: from chest wall and respiratory muscles (spindles ~ “stretch”)
What are the 2 parts of the metabolic controller?
Metabolic controller has two parts:
A) central part in medulla responding to H+ ion of ECF
B) peripheral part at carotid bifurcation, the H+ receptors
of the carotid body
CO2 is very diffusible, and H+ changes mirror PCO2 changes, very rapidly for the hyperperfused carotid body, but more slowly in the ECF bathing the medulla. Thus, fast and slow responses exist.
PaO2 is not as tightly controlled as PaCO2 and H+
SaO2 rather than PaO2 appears to be defended.
What happens in a fall in ventilation ?
PaO2 is not as tightly controlled as PaCO2 and H+
SaO2 rather than PaO2 appears to be defended.
Usually, a fall in ventilation causes a fall in PaO2 and a rise in PaCO2, and the fall in PaO2 increases sensitivity of carotid body to PaCO2 and H+ , so ventilation and PaO2 increases, and PaCO2 falls by negative feedback
Compensatory mechanisms for too much acid or alkali are ?
the lung (fast responder) and kidney (slow responder). If the lung is the problem, the response will be slow (hours, days) The causes of acidosis (acidaemia is what is measured) and alkalosis are twofold a) metabolic, b) respiratory
What determines [H+] ?
[H+] = constant x PaCO2/HCO3–
Strong ion difference: [Na+ + H+] – Cl-
What is acidosis: excess production of H+
causes: ?
compensatory mechanisms:?
Acidosis: excess production of H+
causes: diabetic ketoacidosis, salicylate overdose, renal tubular defects
compensatory mechanisms:
Ventilatory stimulation lowers PaCO2 and H+
Renal excretion of weak (lactate and keto) acids
Renal retention of chloride to reduce strong ion difference
What is alkalosis: excess production of H+
causes: ?
compensatory mechanisms:?
Alkalosis: loss of H+ leads to excess HCO3–
causes: vomiting, diuretics, dehydration
compensatory mechanisms
Hypoventilation raises PaCO2 and H+
Renal retention of weak (lactate and keto) acids
Renal excretion of chloride to increase strong ion difference
Respiratory acidosis The lung fails to excrete the CO2 produced by metabolic processes Acute: What happens if the lung cannot cope? Chronic:
The lung fails to excrete the CO2 produced by metabolic processes
Acute: hypoventilation causes PaO2 ↓, PaCO2 and H+ ↑ which stimulates metabolic centre (and carotid body) to increase minute ventilation and restore blood gas and H+ levels.
What happens if the lung cannot cope?
Chronic: ventilatory compensation may be inadequate for PaCO2 homeostasis but a) renal excretion of weak acids (lactate and keto), b) renal retention of chloride to reduce strong ion difference, returns H+ to normal, even though PaCO2 remains high and PaO2 low.
Hypoventilation conditions
both acute and chronic examples
acute: metabolic centre poisoning (drugs and anaesthetics)
chronic: vascular/neoplastic disease of metabolic centre
cogential central hypoventilation syndrome
obesity hypoventilation syndrome (OHS)
chronic mountain sickness
Hypoventilation conditions
peripheral and chronic obstructive pulmonary disease
peripheral
- acute: muscle relaxant drugs, myasthenia gravis
- chronic: neuromuscular with respiratory muscle weakness
chronic obstructive pulmonary disease
-mixture of central (won’t breathe) and peripheral (cannot breathe)
respiratory alkalosis
mechanism: ventilation in excess of metabolic needs
causes: chronic hypoxaemia
excess H+
pulmonary vascular disease
chronic anxiety
what is breathlessness
breathless with excitement/ anticipation
suspended breathing with an emotional cause
out of breath
normal experience when exercise exceeds a threshold of comfort
dyspnea
medical term for breathlessness but with the connotation of discomfort or difficulty
at rest that usually implies difficulty with inspiration or expiration
on exercise it means excessive breathing for the task +- difficulty
what are the 3 types of breathlessness?
tightness
air hunger
increased work and effort
what is tightness
difficulty in inspiring due to airway narrowing, a feeling that the chest is not expanding normally
what is air hunger
sensation of a powerful urge to breath, eg a breath hold during exercise
mismatch between VEdemanded / VEachieved
a) demand: a copy of signal sent by metabolic controller to spinal motorneurones
b) afferents from lung, chest wall and chemoreceptors (carotid body)- output
what is increases work and effort
breathing at a high minute ventilation, or at a normal minute ventilation but at a high lung volume or against an inspiratory or expiratory resistance
scales for measuring breathlessness during an exercise test
borg CR- 10 scale
visual analogue scale
breath holding time (BHT)
tests strength of behavioural versus metabolic controller
break point: prolonged by increases lung volume, lowering PaCo2 or by taking an isoxic/isocapnic breath near the break point
breakpoint is an expression of air hunger
Vt/Ti is?
mean inspiratory flow
- indicator of how fast the diaphragm is contracting
how hard the muscles are being driven
2 equations for VE?
VE = Vt * 60/Ttot
VE= Vt/Ti * Ti/Ttot
determinants of a tidal breath in disease?
-chronic and emphysema
see graph
how does the metabolic centre work?
Metabolic centre: has an H+ controller, detecting ECF H+ and carotid bodies H+ as H+ in equilibrium with CO2 - leading to certain impulse frequency to respiratory spinal motor neurones and then to phrenic nerve to drive diaphragm
Upper airway muscles: dilated on inspiration and narrowed on expiration to ensure smooth air flow - controlled by metabolic controller
Feedback: lung has stretch receptors, respiratory muscles have muscle spindle and blood receptors have chemoreceptors that all signal back to the metabolic concentration to lead to alteration of timing to control breathing
