Physiology of shortness of breath Flashcards
what is O2 needed for in our cells?
To produce energy and function
What is needed to supply O2 and continuously remove CO2?
-Enough O2 in the atmosphere
-A controller which controls the rate and depth of breathing
-A ventilatory pump which moves O2 and CO2 in and out of lungs
-A gas exchanges which exchanges O2 and CO2 between the lungs and blood
-A cardiovascular system which moves the blood carrying the O2 and CO2 between the lungs and tissues
-Sufficient blood haemoglobin which carries the O2
role of respiratory controller?
-determines the rate and depth of breathing via efferent signals sent to respiratory muscles from the respiratory centres
role of medulla (respiratory centre)?
Medulla generates the respiratory rhythm
Ventral respiratory group= expiration
Dorsal respiratory group= inspiration
role of pons?
Gives inputs to medulla and modifies respiration (smooths and coordinates it)
what sends stimuli and can influence the respiratory centres (pons and medulla)?
-Central chemoreceptors
-Peripheral chemoreceptors
-Higher brain centres e.g. cerebral cortex, limbic system, hypothalamus
-Stretch receptors in the walls of bronchi and bronchioles – the inflation Hering-Breur reflex – guard against hyperinflation
-Juxtapulmonary (J) receptors - stimulated by pulmonary capillary congestion and pulmonary oedema; also pulmonary emboli rapid shallow breathing
-Joint receptors – stimulated by joint movement
-Baroreceptors: increased ventilatory rate in response to decreased blood pressure
what factors stimulate the respiratory centres, leading to increased awareness of breathing discomfort AKA shortness of brath?
-Hypoxia
-Hypercapnia
-Acidosis
-Central arousal e.g. anxiety
-Increased body temperature
-Pain
-Joint movements during exercise
-Drugs e.g. amphetamines
where are peripheral chemoceptors found?
aortic arch and carotid bodies
role of peripheral chemoceptors?
sense tension of oxygen and CO2 and [H+] in the blood as it leaves the heart (in the arteries)
teachmephysiology: detect pO2 changes
where are central chemoceptors found?
near the surface of the medulla of the brainstem
role of central chemoceptors?
Respond to the [H+] found in CSF (from CO2 that crosses the barrier)
-BBB splits the CSF from the blood
-H+ and HCO3 are impermeable to CSF
-CO2 can freely cross the BBB and react
what is reponsible for the most important stimulant in respiration in people?
central chemoceptors
explain how hypercapnia is detected from hypoventilation?
-Hypoventilation can lead to a build up of CO2 in the body, leading to H+ (generated from CO2)
-Blood becomes very acidic
-Central chemoceptors detect hypercapnia and increase ventilation, returning pCO2 back to normal
what conditions may cause hypercapnia?
-COPD
-Obesity
role of peripheral chemoreceptors?
-Sense tension of oxygen and CO2 and [H+] in the blood
-Hypoxic drive stimulated when pO2 <8kPa
-Important for chronic CO2 retention (e.g. COPD) and high altitudes
what is the H+ drive in peripheral chemoreceptors?
- The effect is via the peripheral chemoreceptors
- H+ doesn’t readily cross the blood brain barrier (CO2 does)
-The peripheral chemoreceptors play a major role in adjusting for acidosis caused by the addition of non-carbonic acid H+ to the blood (e.g. lactic acid during exercise, and DKA)
-Their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body (CO2 can generate H+, so its increased elimination can help reduce the load of H+ in the body) - This is important in acid base balance
what parts of the body act as the ‘ventilatory pump’?
-Respiratory muscles
-Peripheral nerves (transmit signals from the respiratory controller to the respiratory muscles)
-The chest wall
-The pleura (provides transmural pressure gradient to allow the lungs to expand)
-The airways (connects the lung alveoli to the atmosphere)
role of a ventilatory pump?
moves O2 and CO2 out of the lungs
Body parts acting as ventilatory pump:
-Respiratory muscles
-Peripheral nerves (transmit signals from the respiratory controller to the respiratory muscles)
-The chest wall
-The pleura (provides transmural pressure gradient to allow the lungs to expand)
-The airways (connects the lung alveoli to the atmosphere)
what disease might stop the respiratory muscles from working?
Neuromuscular weakness e.g. motor neurones
Body parts acting as ventilatory pump:
-Respiratory muscles
-Peripheral nerves (transmit signals from the respiratory controller to the respiratory muscles)
-The chest wall
-The pleura (provides transmural pressure gradient to allow the lungs to expand)
-The airways (connects the lung alveoli to the atmosphere)
what disease might stop the chest wall from complying?
Kyphoscoliosis
Body parts acting as ventilatory pump:
-Respiratory muscles
-Peripheral nerves (transmit signals from the respiratory controller to the respiratory muscles)
-The chest wall
-The pleura (provides transmural pressure gradient to allow the lungs to expand)
-The airways (connects the lung alveoli to the atmosphere)
what disease might stop the pleura from functioning properly?
Pneumothorax - will cause a loss of the transmural gradient across the lungs
Body parts acting as ventilatory pump:
-Respiratory muscles
-Peripheral nerves (transmit signals from the respiratory controller to the respiratory muscles)
-The chest wall
-The pleura (provides transmural pressure gradient to allow the lungs to expand)
-The airways (connects the lung alveoli to the atmosphere)
what disease might cause a problem with the airways?
Diseases that increase airways resistance
e.g. asthma + COPD
is inspiration an active or passive process?
inspiration is an active process dependant on muscles
what muscles are involved in active inspiration?
-diaphragm and external intercostal muscles
role of diaphragm in active inspiration?
diaphragm contracts and increases the volume of the thorax vertically (diaphragm flattens as it contracts)
role of external intercostal muscles in inspiration?
external intercostal muscles contract, pulling the ribs up and the sternum up and out
-Bucket handle
what law explains how air gets into the lungs during active inspiration?
Boyle’s law
-diaphragm contracts and increases the volume of the thorax vertically (diaphragm flattens as it contracts)
-external intercostal muscles contract, pulling the ribs up and the sternum up and out
-this increases lung volume
-This causes pressure in the lungs to decrease
-Higher pressure in external environment than lungs
-Air moves into lungs down pressure gradient
what nerve innervates the diaphragm?
C3, C4, C5 - keeps the diaphragm alive
Phrenic
explain transmural pressure
Air moves down pressure gradient
-when inspiration happens the lungs expan, decreasing the intra alveolar pressure
-this causes air to move into lungs
-intrapleural pressure is even less than intra alveolar
-this causes a transmural gradient, keeping the lungs from collapsing
explain why lungs collapse in pneumothorax
-Pressure should be the same in the atmosphere and interalveolar
- Pressure lower in intrapleural sac
-This creates a transmural pressure gradient, keeping the lungs open
-In a pneumothorax, air gets into the pleural cavity, increasing the intrapleural pressure, breaking the transmural pressure gradient
what is the primary determinant to airway resistance?
the radius of the airways (bigger the airway, easier it is for air to get in and out)
is expiration or inspiration harder?
expiration
what occurs to intra alveolarpressure in inspiration vs expiration?
inspiration- airways are pulled open by expanding thorax and intra alveolar pressure falls
expiration- chest recoils as diaphragm relaxes and so intra alveolar pressure rises
explain dynamic airway compression in a normal person
Pressure applied to alveolus helps push air out of the lung
-During active inspiration there is an increase in airway resistance, causing an increase in airway pressure upstream, which helps open the airways by increasing the driving pressure between the alveolus and the airways
explain dynamic airway compression in someone with obstructive disease
If there is an obstruction (e.g. asthma or COPD), the driving pressure between the alveolus and airway is lost over the obstructed segment
This causes a fall in airway pressure along the airway downstream, resulting in airway compression by the rising pleural pressure during active expiration
Diseased airway are also more likely to collapse!!
(The problem becomes worse if the patient also has decreased elastic recoil of the lungs e.g. emphysema)
what is lung complicance
-the amount of effort needed to stretch or distend the lungs
Less compliant lungs= more work to inflate
(lungs must inflate for inspiration)
what disease may decrease lung compliance?
-pulmonary fibrosis
-pulmonary oedema
what are the gas exchangers in the lungs?
Exchanges CO2 and O2 between the lungs and the blood
Consists of:
· The aveoli- thin walled inflatable sacs, walls consist of a single layer of flattened type I alveolar cells
· Pulmonary capillaries- encircle each alveolus
· The interstitial space between these
Alveolar treee- large surface area- good for gas exchange
will O2 or CO2 be compromised first in diseased states affecting perfusion of lungs and why?
CO2 is 20x more soluble than O2 BUT
O2 has a much greater partial pressure gradient than O2 and O2 diffuses faster than CO2
-this does mean that if there is a disease affecting the lungs ability to adequately ventilate with oxygen then oxygen exchange will be affected before CO2 exchange
what may cause a decrease in alveolar surface area causing SOB?
-emphysema
-lung collapse
what may increase the thickness of the alveolar causing SOB?
-pulmonary oedema (HF)
-pulmonary fibrosis
-pneumonia
what may decrease the perfusion across the alveolar causing SOB?
-pulmonary embolism
what is the cardiac output?
volume of blood pumped by each ventricle per minute
CO= SV x HR
effect of exercise on CO?
exercise increases CO by about 5 folds
what is the stroke volume?
Stroke volume= volume of blood pumped out by each ventricle per heart beat
SV= end diastolic volume- end systolic volume
what determines changes in SV?
changes in SV are brought about by changes in the diastolic lengthening of myocardial fibres (preload)
-diastolic length is determined by end diastolic volume
-venous return determines end diastolic volume
what Curve is used to explain the relationship between end diastolic volume and stroke volume?
Frank- starling curve
what can occur if venous return is too high?
Heart failure + pulmonary oedema
