week 1 corrections Flashcards

1
Q

how much of the o2 carried by hb is used by the body tissue at rest

A

25%- rbcs in systemic arterial blood are almost 100% saturated whereas its 75% in venous blood so only 25% is taken up by the tissues.

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2
Q

what does an increase in pCO2 do to the binding power of hb

A

shifts the graph to the right, so less o2 is bound to hb. increasing pCO2 decreases affinity of hb for o2

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3
Q

what does a decrease in body temp do to the curve

A

moves to the left, increasing affinity of hb for O2

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4
Q

why is hypothermia so dangerous

A

because a 20degreese hb is still fully sat so holds onto the o2 and doesnt let it go to tissues

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5
Q

what are the peripheral chemoreceptors in the carotid bodies stimulated by

A

increase in blood acidity as they respond to H+ from anywhere but central chemoreceptors only respond to H+ made in repsponse to CO2

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6
Q

when is gas exchange at rest normally completed

A

within a third of the time of contact, there is contact with the alveoli for 75seconds and its completed in 25s

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7
Q

why does hb saturation decrease as blood passes through the tissue

A

tissues have lower po2(40) than plasma (100) and o2 moves down its concentration gradient until it reaches equilibrium

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8
Q

where are ventilation and perfusion the greatest

A

at the base of the lung, they decrease with height. however blood flow decreases faster than vent. so blood flow > vent at base
vent > blood flow at apex
start of w more blood

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9
Q

how does alkalosis affect affinity of hb for o2

A

increases, pushes curve to the left

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10
Q

why does hyperventilation shift o2 dissociation to the left

A

hypervent blows off more co2, reducing pCO2 so the curve shifts to the left. loss of CO2 drives the equation to the left. decreasing H+ conc so increasinf ph

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11
Q

do perfusion/vent problems impact CO2 or O2 more

A

O2 as CO2 is more soluble so can diffuse more readily

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12
Q

is nitrous oxide a safe sedative

A

Nitrous oxide is well tolerated in most individuals. In terms of respiratory function it is safe for most individuals as it does not affect central chemoreceptor activity on which most individuals rely. However it does impair peripheral chemoreceptor function. As such it should be used in caution in patients with chronic lung diseases who may be on “hypoxic drive”. Patients with chronic lung disease have had long term exposure to elevated arterial PCO2 due to impaired gas exchange and overtime the central chemoreceptors become desensitised to CO2. In these circumstances the peripheral chemoreceptors take over setting the rhythm of ventilation

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13
Q

what chemoreceptors respond to hypoxia

A

0nly the peripheral chemoreceptors can detect hypoxia. The central chemoreceptors only respond to hypercapnia

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14
Q

what does surfactant do in the alveoli

A

urfactant decreases surface tension within the alveoli. It reduces the attraction of one water molecules for another, thus reducing surface tension and the tendency of the alveoli to collapse.

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15
Q

what are the two lobes in the left lung separated by

A

the oblique fissure

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16
Q

how does anaemia affect the o2 haemoglobin sat curve

A

the oxyhaemglobin binding curve is unaffected in anaemia. In anaemia the amount of oxygen in solution in the plasma is unaffected (providing the lungs are healthy) and therefore the binding of oxygen to red blood cells is normal. The term anaemia describes a fall in the total oxygen content of the blood but remember 98% of the oxygen in the blood is wrapped up in the haemoglobin in red blood cells, it is not in solution in the plasma. If the lungs are working normally, anaemia therefore comes about due to diminished ability of red blood cells as a whole to carry oxygen for one reason or another

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17
Q

is blood flow affected by gravity

A

blood flow is always affected by gravity hence why sometimes if you stand up too quickly you feel light headed until a reflex kicks in to adjust your blood pressure

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18
Q

how do u calculate the inspiratory capacity

A

resting tidal vol + inspiratory reserve

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19
Q

why are patients with chronic lung disease reliant on peripheral chemoreceptors

A

Some patients with chronic lung disease have had long term exposure to elevated arterial PCO2, due to impaired gas exchange. Overtime the central chemoreceptors, which detect changes in PCO2 and on which healthy individuals rely to set the rhythm of ventilation, become desensitised to CO2. In these circumstances the peripheral chemoreceptors take over setting the rhythm of ventilation. As these chemoreceptors respond to falling oxygen levels, sometimes these individuals are described as being on hypoxic drive. This is clinically important, because giving these people too much supplementary oxygen can therefore dampen their respiratory drive.

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20
Q

what can spirometry measure

A

Spirometry can only measure the volume of air that can be exhaled

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21
Q

how much of their vital capacity can healthy individuals exhale in the first second of forced exhalation

A

80%

22
Q

where does the phrenic nerve take its origin from

A

The phrenic nerve takes it origins from the C4, C4 and C5 spinal nerves

23
Q

what mediates hypercapnia that occurs in high altitudes

A

The lower atmospheric PO2 at altitude means arterial PO2 also falls. This is detected by the peripheral chemoreceptors which stimulate ventilation in an attempt to restore normal PO2. The resulting hyperventilation blows of more CO2 than normal leading to hypocapnia.

24
Q

what is carboxyhaemoglobin

A

The term “carboxyhaemoglobin” describes carbon monoxide binding to haemoglobin – your carboxyhaemoglobin levels should be neglible!

25
Q

what is forced vital capacity

A

FEV1 is the Forced Expired Volume in one second. FVC is the total amount of air that can be forced out of the lungs after a maximum inspiration over any time period. FVC should be the same in volume as Vital Capacity but VC is not necessarily forced, nor the time to exhale measured.

26
Q

does respiratory acidosis often accompany severe lung pathology

A

yes, Most lung pathologies lead to an impairment of gas exchange for one reason or another. This impairment increases CO2 levels in arterial blood. An increase in CO2 leads to an increase in H+ concentration

27
Q

what is the majority of CO2 transported as in the body

A

CO2 is mostly (70%) transported in the form of bicarbonate ions. Only 23% is transported in the form of carbamino compounds

28
Q

what is lung compliance defined as

A

the change in lung volume for any given change in transpulmonary pressure

29
Q

what does a shift in the O2 Hb curve to the right indicate

A

A rightward shift means that for any given value of PO2, less oxygen will be bound to haemoglobin than if that shift had not happened

30
Q

do peripheral chemoreceptors respond to changes in arterial pO2 or arterial O2 content

A

peripheral chemoreceptors respond to changes in levels of oxygen in solution (PO2) and not the amount of oxygen wrapped up in hemoglobin

31
Q

what does alveolar ventilation describe

A

the volume of gas that reaches the alveoli (and hence is available for gas exchange) per minute. Not all the air we breathe in reaches the alveoli as some gets trapped in dead space and cannot participate in gas exchange.

32
Q

is there a difference between the vol of blood flowing through the pulmonary and systemic circulation

A

no, The two systems are in series with each other so the same volume of blood must flow through each for any given period of time.

33
Q

what does a pneumothorax disrupt

A

he relationship between the parietal pleural membrane and the visceral pleural membrane.

34
Q

is expiration at rest a passive process

A

yes, During passive expiration, all that happens is your muscles of inspiration (mainly the diaphragm and external intercostal muscles) stop contracting and gently relax to their resting positions, in doing so decreasing the volume of the thoracic cavity and thus increasing pressure which forces the air out.

35
Q

what happens to the vol of the thoracic cavity during inspiration

A

During inspiration the diaphragm flattens and the external intercostal muscles elevate the ribs. Both these actions increase the volume of the thoracic cavity and in doing so decrease the pressure inside. This causes air to be drawn into the lungs from the higher pressure of the atmosphere.

36
Q

what is pulmonary circulation described as

A

high flow, low pressure system. High flow because the entire volume of blood that travels through the rest of the body (systemic circulation) in one minute travels through the lungs (pulmonary circulation) in one minute too. Low pressure because systolic pressure in the pulmonary circulation is around 25mmHg while it is 120mmHg in the systemic circulation.

37
Q

how does hyperventilation aggravate alkalosis

A

Hyperventilation will blow off extra CO2. As CO2 is related to H+ via the equation shown in the lectures, if you blow off extra CO2, you also reduce H+ formation. With an alkalosis you would want to hypoventilate to retain CO2 and boost H+ concentration offset the alkalosis. Hyperventilation would therefore aggravate, and not compensation for, the alkalosis.

38
Q

what is the problem in anaemia

A

the problem is a decrease in oxygen binding capacity of the red blood cells, providing the lungs are healthy the amount of oxygen in solution in the plasma will be normal so the peripheral chemoreceptors will not be activated.

39
Q

what happens to the activity of the phrenic nerve during inspiration

A

The phrenic nerve innervates the diaphragm, the main muscle of inspiration, so activity would increase during inspiration.

40
Q

what can tell you the proportion of FVC a patient can exhale in one sec

A

A useful clinical measure of lung function is FEV1 divided by FVC

41
Q

how does a pneumothorax affect intrapleural pressure

A

Normally intrapleural pressure is negative (i.e. less than atmospheric pressure). In a pneumothorax, penetration of the thoracic wall allows air (at atmospheric pressure) to enter the pleural cavity and thus equalises the pressure between the cavity and the atmosphere. In doing so intrapleural pressure rises to become the same as atmospheric pressure.

42
Q

why is pulmonary vent vol greater than alveolar vent vol

A

Pulmonary (or minute) ventilation describes the total amount of air breathed in or out per minute (basically tidal volume x respiration rate). Alveolar ventilation accounts for the volume of air that gets stuck in dead space and never reaches the alveoli, so dead space volume must be subtracted from tidal volume before multiplying by respiration rate ((TV-DS) x RR), making alveolar ventilation smaller than pulmonary ventilation

43
Q

how does a pneumothorax affect the chest wall

A

The loss of relationship between the parietal and visceral pleural membranes means the lungs are no longer effectively attached to the chest wall. The equilibrium between elastic lung recoil and elastic chest wall expansion is then also lost so the lungs recoil and the chest wall expands.

44
Q

what does vital capacity describe

A

Vital Capacity describes the largest volume of air that can be voluntarily exhaled after a maximum inhalation.
Inspiratory capacity + Expiratory Reserve Volume
Inspiratory Reserve Volume + Tidal Volume + Expiratory Reserve Volume

45
Q

what shift is seen kin the curve for foetal haemoglobin

A

The shift is to the left. Foetal haemoglobin has a higher affinity for oxygen than adult haemoglobin, so at any given value of PO2 foetal haemoglobin has a higher oxygen saturation than adult haemoglobin. This allows the foetus to extract oxygen effectively from maternal blood.

46
Q

how does a pneumothroax affect functional residual capacity

A

FRC (volume of air left in the lungs after a forced expiration) will decrease in pneumothorax as the affected lung has recoiled and thus has a smaller volume than before.

47
Q

do central chemoreceptors respond to changes in [H+]

A

yes, they respond to changes in H+ concentration in the cerebrospinal fluid (CSF). These H+ are wholly derived from CO2 present in the CSF, which in turn is in equilibrium with CO2 in the plasma so indirectly the central chemoreceptors are responding to increases in CO2 in the plasma. H+ from other metabolic sources cannot cross the blood brain barrier and so do not stimulate the central chemoreceptors

48
Q

what does an increase in DPG do to the curve

A

shifts it to the right.2, 3- diphosphoglycerate is produced by red blood cells under stress as may occur during hypoxic conditions (this could be due to e.g. poor ventilation or heart disease). In this case the rise in 2,3-DPG allows more oxygen to be released from the haemoglobin in the periphery by reducing the affinity of haemoglobin for oxygen, and in doing so shifts the curve to the right.

49
Q

where is compliance greatest

A

at the base of the lung so a greater volume of inspired air ends up at the base of the lung compared to the apex.

50
Q

does surfactant reduce the work of breathing

A

yes, By reducing the surface tension, and hence the tendency of the alveoli to collapse, the pressure required to overcome surface tension to inflate the alveoli during inspiration is less than it would be without surfactant.

51
Q

what does a pneumothorax do to vital capacity

A

Vital capacity will be reduced in pneumothorax as the affected lung becomes dysfunctional so the volume of air available for expiration is can be as little as half of normal

52
Q

what does the term shunt describe

A

Shunt describes the situation where blood is effectively “shunted” from one side of the heart to the other without participating in gas exchange in between. It can happen where part of the lung is not being fully ventilated for some reason e.g. tumour, airway obstruction