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Respiratory > Pulmonary Ventilation > Flashcards

Pulmonary Ventilation Flashcards

1
Q

Inspiration

A

▪️active
▪️initiates by respiratory control centre in medulla
▪️activation of medulla causes contraction of
diaphragm and external intercostal muscles leading to expansion of thoracic cavity and decrease in pleural space pressure

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2
Q

Expiration

A

▪️passive
▪️due to elastic recoil of the lungs
▪️however durning exercise (greater amount needed to be removed) internal intercostal muscles and anterior abdominal muscles contract and accelerate expiration by raising pleural pressure

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3
Q

Types of pressure

A 
▪️atmospheric pressure 
-pressure outside the body 
▪️intrapulmonary/intra-alveolar pressure
-pressure in the lungs 
▪️intrapleural pressure 
-pressure in pleural cavity (thin layer of lubricant)
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4
Q

Pressure changes when breathing

A

▪️inhalation
-intrapulmonary pressure < atmospheric pressure
-air flows in
▪️exhalation
-intrapulmonary pressure > atmospheric pressure
-air flows out
▪️transpulmonary pressure
- intrapulmonary - intrapleural pressure
-allows lungs to expand as thoracic wall expands

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5
Q

Boyle’s law

A

▪️pressure of a gas in inversely proportional to its volume

  • an increase in lung vol in inspiration decreases IPp pressure below AP-air in
  • a decrease in lung vol in expiration increases IPp above AP-air out
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6
Q

Muscles in breathing

A

▪️diaphragm
-contracts in inspiration, flattens increasing vol in thoracic cavity
-relaxes in expiration, raise decreasing vol in thoracic cavity
▪️EIM
-raise rib cage during normal or quite inspiration
▪️IIM
-lower rib cage during forced expiration
▪️scalene, pectoralis minor, sternocleidomastoid
-forced inspiration
▪️abdominal muscles
-forced expiration

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7
Q

Central control of breathing

A

▪️medullary respiratory centre-dorsal and ventral medullary neurones
▪️apneustic centre
▪️pneumotaxic centre

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8
Q

Dorsal medullary neurones

A

▪️inspiration

  • spontaneous intrinsic periodic firing of these neurones are responsible for basic rhythm of breathing
  • when the neurones are active, their AP travel through the reticulospinal tract in the spinal cord and phrenic and intercostal nerve to stimulate respiratory muscles
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9
Q

Ventral medullary neurones

A

▪️expiration

  • silent during quite breathing (passive) but activated during forced expiration when rate and depth of breathing is increased (exercise)
  • during heavy breathing DRG activates VRG, VRG inhibits DRG and stimulates muscle of expiration
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10
Q

Apneustic centre

A

▪️lower pons
-damage to area causes an abnormal rhythm and increase apnoea (missing breaths)
▪️nerve impulses stimulate the inspiratory centres and without it breaths become shallower and irregular

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11
Q

Pneumotaxic centre

A

▪️upper pons
-inhibitory effect on both DRG and apneustic centre
-inhibits DRG to terminate inspiration
-regulates volume and secondary rate of respiration
-fine tuning rhythm
▪️hypo-activation causes prolonged deep inspiration and limited expirations (inspiration centre active longer than normal)
▪️hyper-activation results in shallow inspirations

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12
Q

Respiratory cycle

A

▪️activation of DRG stimulates muscle of inspiration and also the pneumotaxic centre
▪️pneumotaxic centre inhibits both apneustic and DRG centres
▪️initiation of expiration
▪️spontaneous activity of neurones in DRG starts another cycle

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13
Q

Mechanoreceptors in breathing

A

▪️responds to forces eg stretching
▪️walls of bronchi and bronchiole
▪️prevent over inflation of lungs
▪️Hering-Breuer reflex:
-inflation of lungs activate the receptors which inhibits neurone in DRG via vagus nerve
-when expiration happens, receptors gradually deactivate therefore activating DRG again
-important for infants and in exercise in adults

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14
Q

Peripheral chemoreceptors in breathing

A

▪️O2 sensitive receptors are located at the bifurcation of carotid artery in neck and in the aortic arch
▪️encapsulated in connective tissue
▪️connected to medulla by glossopharyngeal nerve (carotid) and vagus nerve (aorta)

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15
Q

Central chemoreceptors in breathing

A

▪️bilaterally in medulla and is exposed to CSF and local blood flow
▪️respond to changes in H+ conc
▪️when blood PCO2 is increased, CO2 diffuses into CSF from blood vessels and reacts with water to form H+ and HCO3-
▪️increase in H+ stimulates receptors resulting in hyperventilation which which reduced PCO2 in blood therefore CSF
▪️cerebral vasodialation enhances diffusion of CO2 into CSF-lower buffering capacity due to less protein
-changes in pH compared to PCO2 is always bigger than the change in blood

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16
Q

CO2 as a regulator of breathing

A

▪️major regulator
▪️more important than O2
▪️small change in PCO2 (hypercapnia) in blood causes large increases in rate and depth of respiration
▪️hypocapnia-lower than normal PCO2 causes periods when you don’t breathe
▪️PO2 changes are quite minor- hypoxia occurs after 50% decrease in PO2

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17
Q

Higher centres of the brain in breathing

A

▪️can be controlled consciously from cerebral cortex
▪️primary motor cortex is the neural centre for voluntary respiratory control
▪️ascending respiratory pathway
-PMC senses signals to spinal cord which sends signals to muscle to contract
-required when talking, coughing and vomiting
▪️other parts of the brain (limbic and hypothalamus) can also alter breathing pattern eg strong emotions

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18
Q

Ventilation/perfusion ratio

A

▪️relationship between a month of ventilation in alveoli and amount of perfusion through capillaries
▪️determines quality of gas exchange across alveolar-capillary membrane therefore the amount of O2 entering and CO2 leaving
▪️normal lung V/Q is 1 (V=Q)
-never exists due to gravity on blood blow, structure of lungs and shunting of blood

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19
Q

Shunting in blood

A

▪️perfusion of poorly ventilated alveoli eg with fluid/mucous
▪️oxygenated blood mixes with poorly oxygenated blood to have decreases oxygenated blood.
-pneumonia or acute asthma

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20
Q

Physiological dead space in alveoli

A

▪️ventilation of poorly perfused alveoli
▪️ oxygenated blood from a few alveoli
-cardiovascular shock, COPD, pulmonary embolism

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21
Q

Hypoxic pulmonary vasoconstriction

A

▪️HPV combats shunt
▪️decreased tissue PO2 around under-ventilated alveoli constricts their arteriole diverting blood to better ventilated alveoli
▪️in diseased lungs where there are a lot of under-ventilated alveoli can lead to pulmonary hypertension
▪️contributed to altitude sickness

22
Q

Mechanism for HPV

A

▪️inhibition of hypoxia sensitive voltage gates potassium channels in pulmonary artery smooth muscle leading to depolarisation
▪️this activates voltage dependent Ca channels which increases intracellular Ca leading to vasoconstriction in smooth muscle

23
Q

Tidal volume

A

▪️amount of air in a single normal inspiration or expiration
-500ml

24
Q

Functional residual capacity

A

▪️volume of air that remains in the lungs at the end of normal respiration
-2400ml

25
Q

Vital capacity

A

▪️volume is air that can be exhaled after maximal inspiration
-4800ml

26
Q

Residual volume

A

▪️amount of air remaining in the lungs after maximal expiration
-1200ml

27
Q

Total lung capacity

A

▪️maximum volume of air in the lungs after maximal inspiration
-6000ml

28
Q

Airflow resistance

A 
▪️resistance of the respiratory tract to airflow during inhalation and expiration 
▪️influenced by 
-diameter of airways 
-laminar(smooth) or turbulent airflow 
▪️not constant- asthma attack
29
Q

Spirometry

A 
▪️most common pulmonary function test 
-done at bedside 
▪️measures:
-effort
-volume 
-speed/flow of air 
▪️take a deep breath in and exhale into sensor as hard and fast as possible for as long as possible (6secs), finish by fast inspiration
30
Q

Flow volume loop

A

▪️y=flow (L/s) x=volume (L)
-expiratory phase
▪️1st few seconds, large peak- due to the air in the trachea and primary bronchi-where most of air is
▪️gradual decline- due to air in bronchioles and alveoli, takes longer time to empty
-inspiratory phase
▪️bowl shaped in the negatives-removing the air from the sensor
-has to be an uninterrupted breath out, with the most amount of effort otherwise it won’t work

31
Q

Time volume curve

A

▪️y=volume(L) x=time(secs)
▪️sharp increase in first second, rounds off to a stop by 6 seconds
-FVC- total vol of air coming out of lungs after full inspiration
-FEV1-forced expiratory volume volume in 1sec after full inspiration
-FEV1/FVC ratio: normal 0.7-0.8
▪️used to see if patient is fit for procedure

32
Q

Interpret spirometry results

A

▪️FEV1/FVC ratio: 0.7-0.8
▪️FEV1 % predicted: >or=80% -FEV1 of individual divided by FEV1 of healthy population with similar age, height and gender
▪️FVC % predicted >or=80% -FVC of individual divided by FVC of healthy population with similar age, height and gender

33
Q

Spirometry possible outcomes

A

▪️normal 0.7-0.8
▪️obstruction-obstructive disease <0.7
▪️restriction-restrictive disease >0.8
▪️mix obstructive and restrictive disease- normal values

34
Q

Obstructive disease spirometry

A

▪️FEV1/FVC <0.7
-regales of FEV1Z and FVC% predicted
-asthma or COPD or cystic fibrosis
▪️time volume curve-under the normal curve, no high peak at the start, gradual increase, lower FVC and lower FEV1=lower ratio
▪️flow volume loop- E: same peak at first few seconds, decreases very rapidly and levels of near the bottom. I: same as normal

35
Q

Restrictive disease spirometry

A

▪️FEV1/FVC >0.8
- < 80% predicted for FEV1 and FVC
-obesity, pregnancy, neuromuscular disorders
▪️time volume curve- under normal curve, smaller peak at the start but levels of quickly, lower FVC and FEV1, FEV1 and FVC are almost the same, ratio is around 1
▪️flow volume loop- E: similar to normal but decreases just under normal, but does not reach max volume. I: meets E line before max volume

36
Q

Mixed obstructive and restrictive diseases spirometry

A

▪️FEV1/FVC normal

  • <80% predicted for both
  • clinical history
  • COPD or pulmonary thrombosis
37
Q

Limitations of spirometry

A

▪️depends on patient cooperation and effort
▪️FVC can be underestimated
▪️repeated 3 times to ensure reproducibility- 5% variation
▪️stable asthmatics have a normal spirometry reading

38
Q

Respiratory muscle strength

A

▪️maximal inspiratory pressure (MIP or PImax)
-reflects strength of inspiratory muscles
▪️maximal expiratory pressure (MEP or PEmax)
-reflects strength of expiratory muscles
▪️use a mechanical pressure gauge with an mouthpiece

39
Q

Maximal inspiratory pressure (MIP) measurement

A

▪️patients seals lips around the mouthpiece
▪️exhale slowly and completely
▪️suck out the air hard

40
Q

Maximal expiratory pressure (MEP) measurement

A

▪️seal lips around mouthpieces
▪️inhale completely
▪️blow out as hard as possible

41
Q

Diffusion capacity

A

▪️measures ability of lungs to extract O2 from inhaled air in capillaries
▪️depends on
-SA (directly proportional) and membrane thickness (inversely proportional)
-Hb level- strong affinity for O2 and CO, decrease in O2 affinity is also decrease in CO affinity

42
Q

Diffusion capacity measurement

A

▪️blow out all air to leave residual volume
▪️quickly inhale gas mixture( 0.3%CO 10% helium) for 10secs
-helium is freely distributed throughout alveolar space but does not cross into capillaries unlike CO
▪️exhale
-the exhaled gas is analysed for the difference in CO and helium conc between inspired and expired gas
-cannot smoke 4-6hours before, contains CO

43
Q

Transfer coefficient (KCO)

A

▪️KCO is DC corrected for alveolar volume
-KCO=DC/VA
▪️VA is lung volume after inhalation of CO/helium gas mixture
-if part of lung is removed, DC will be lower as there is less SA, but KCO will be the same as the rest of the lung works normal

44
Q

Alveolar-arteriole gradient (A-a gradient)

A

▪️difference between A conc of O2 and a conc of O2
▪️diagnosing source of hypoxemia
▪️A O2 is always higher than a O2
-due to shunting and gravity

45
Q

VO2 max and exercise

A

▪️VO2 max- amount of oxygen that an individual can utilise during peak exercise (L/min of O2)
▪️limited by
-max ability of CVS to deliver O2to muscles
-ability of muscle to extract O2 from blood
▪️person on a treadmill or exercise bike, intensity increased gradually whilst measuring ventilation, O2 and CO2 conc
▪️VO2 max is reached when O2 consumption remains at a steady rate despite increase work load

46
Q

Blood gas analysis

A

▪️pH
-normal, high (alkalosis), low (acidosis)
▪️PCO2
-normal, high (respiratory), low (metabolic)
▪️HCO3-
-normal, high (compensated), low (uncompensated)
-fully or partially compensated

47
Q

15 yo which chronic cough:

▪️pH 7.40 (7.35-7.45)
▪️PCO2 55 (35-45mmHg)
▪️HCO3- 35 (22-26mEQ/L)

A

▪️pH normal, PCO2 high, HCO3- high

  • fully compensated respiratory acidosis
48
Q

12 yo up a mountain:

▪️pH 7.50 (7.35-7.45)
▪️PCO2 20 (35-45mmHg)
▪️HCO3- 23 (22-26mEQ/L)

A

▪️pH high, PCO2 low, HCO3- normal

  • uncompensated respiratory alkalosis
49
Q

3 yo with temperature for 2days:

▪️pH 7.30 (7.35-7.45)
▪️PCO2 55 (35-45mmHg)
▪️HCO3- 29 (22-26mEQ/L)

A

▪️pH low, PCO2 high, HCO3- high

  • partially compensated respiratory acidosis
50
Q

6 yo with thirst and weight loss :

▪️pH 7.22 (7.35-7.45)
▪️PCO2 25 (35-45mmHg)
▪️HCO3- 13 (22-26mEQ/L)

A

▪️pH low, PCO2 low, HCO3- low

  • partially compensated metabolic acidosis
51
Q

1 mo with projectile vomit:

▪️pH 7.52 (7.35-7.45)
▪️PCO2 40 (35-45mmHg)
▪️HCO3- 36 (22-26mEQ/L)

A

▪️pH high, PCO2 normal, HCO3- high

  • uncompensated metabolic alkalosis
52
Q

How does the body respond to altitude

A 
▪️respiratory 
-hyperventilation 
-pulmonary hypertension 
▪️renal 
-erythropoietin to increase RBC
▪️haemoglobin 
-anaerobic respiration 
-Hb dissociation curve shifts to right, better unloading of O2 in tissues

Respiratory (9 decks)

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