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Primary SOE/ VIVA > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

What is the BOHR effect?

A

Describes the right shift of the Oxy-Hb curve in response to increased PaCO2 and hydrogen ion concentration.

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2
Q

What causes a left shift of the oxy-Hb curve?

A

Decreased H+ ion conc.
Decreased temperature
Decreased 23 DPG

HbF
Methaemoglobinaemia
CarboxyHb
Stored blood

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3
Q

What causes a right shift of the Oxy Hb curve?

A

Increased H+
Increased temperature
Increased 23 DPG
Increased PaCO2

HbS
Anaemia
Pregnancy
Post acclimatisation to altitude

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4
Q

What gives the oxy-Hb curve its characteristic shape, and what is the name of this shape?

A

SIGMOID

  1. ALLOSTERIC MODULATION - when O2 binds, B chains move closer together and relax, when O2 dissociates the reverse happens.
  2. COOPERATIVE BINDING - When O2 binds, relaxed state is favoured which allows higher affinity for further O2 binding. Affinity for 4th O2 molecule is greatest.
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5
Q

What is the DOUBLE BOHR effect?

A

Describes the situation in the placenta where the Bohr effect occurs in maternal and foetal circulations.

Maternal side - increased PaCO2 allows unloading of oxygen.
Foetal side - decreased PaCO2 foetal side increases affinity for loading oxygen.

In summary this leads to left shift in OHBC, and right shift for the mother simultaneously.

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6
Q

What is the Haldane effect?

A

Describes the increased ability of deoxygenated Hb to carry CO2, and reciprocally for oxy-Hb has reduced capacity for CO2. This occurs because de-oxy Hb is a better proton acceptor.

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7
Q

What is the difference in oxygen partial pressure between venous and arterial blood?

What is the P50 of O2?

A

Arterial PaO2 - 13.3kPa

Venous PaO2 - 5.3 kPa

P02 50 - 3.5

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8
Q

Where does the oxy-Hb curve for myoglobin lie and why?

A

There is only a single polypeptide and it can only bind one molecule of O2, therefore the shape is rectangular hyperbola.
It has a higher affinity for O2 so lies to the left of the OHDC.

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9
Q

What are the types of Hypoxia?

A
  1. Hypoxic hypoxia - PaO2 < 12 kPa
  2. Anaemic hypoxia - normal PaO2, but reduced carrying capacity
  3. Stagnant hypoxia - normal PaO2, normal carrying capacity but reduced end organ perfusion ie cardiogenic shock.
  4. Histotoxic Hypoxia - normal PaO2, O2 carrying, and end organ perfusion, but inability of tissue to utilise O2 ie. cyanide poisoning.
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10
Q

Which type of hypoxia would see a change in P50 and PO2 on Oxy-Hb curve?

A
  1. Hypoxic hypoxia, PaO2 reduced to 7.2 and PvO2 reduced to 3.5
  2. Anaemic hypoxia - reduced PvO2 to 3.5
  3. Histotoxic hypoxia - PO2 remains at 13.3, but venous saturation O2 rises to 8kPa
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11
Q

What is oxygen content?

A

It is calculated by addition of bound oxygen to Hb and dissolved O2 in plasma. Can be used to calculate venous and arterial content.

= (Hb. 1.34. SaO2) + (PaO2 . 0.0225)

1.34 - Huffners constant, Each GRAM of HB carries 1.34mls O2

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12
Q

How can oxygen delivery be calculated?

A

Multiplying the arterial oxygen content x cardiac output.

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13
Q

What are the normal values for oxygen content venous/ arterial for a 70kg man?

A

O2

Arterial - 20.4ml/ dL
Venous - 15.2 ml/dL

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14
Q

In the oxygen cascade what is the change in the value of PaO2 at these stages?

  1. Humification in trachea
  2. Mixing with dead space gas
  3. Mixing with alveolar gas
  4. Alveolar - arterial
  5. Arterial blood - capillary blood
  6. Level of mitochondria
A
  1. Humification in trachea: 21 -> 20
  2. Mixing with dead space gas: 15
  3. Mixing with alveolar gas: 13.8
  4. Alveolar - arterial: 13.8 -> 13.3
  5. Arterial blood - capillary blood: 6
  6. Level of mitochondria: 1-2
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15
Q

What is the SVP of water in the trachea?

A

SVP 6.3 kPa at 37 degrees

Therefore O2 = (101 - 6.3) x 0.21 = 19.95 kPa

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16
Q

What are three factors that may cause PO2 to be less in the pulmonary veins than less than alveolar O2? ie. increased A-a gradient

A
  1. Ventilation perfusion mismatch ie. severe hypotension, COPD, LRTI, Asthma
  2. Shunt
    - Intrapulmonary (LRTI/ atelectasis)
    vs extrapulmonary (right to left cardiac shunt)
  3. Diffusion impairment ie. pulmonary oedema/ fibrosis
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17
Q

What is the normal A-a gradient?

A

Should be < 2 kPa

18
Q

How can you increase the oxygen content in dissolved in plasma?

A

Using a hyperbaric oxygen, you increase partial pressure of O2.

PO2 of three atmospheres is sufficient to meet O2 demands)

19
Q

Carbon dioxide values:

  1. Inspired
  2. Expired
  3. Arterial
  4. Alveolar
  5. Venous
A
  1. Inspired - 0.03 kPa
  2. Expired - 4 kPa
  3. Arterial - 5.3 kPa
  4. Alveolar - 5.3 kPa
  5. Venous - 6.1 kPa
20
Q

How is CO2 transported from cells to the lungs?

A

5% - dissolved

5% - carbamino compounds (combines with NH2 on Hb)

90% - bicarbonate

21
Q

How does CO2 combine with Hb?

A

RBC contains carbonic anhydrase, that allows fast formation of
CO2 + H2O –> H2CO3 –> H+ and HCO3

H+ trapped inside Hb, and Cl- diffuses in to maintain electrical neutrality (Chloride shift), and HCO3 diffuses out.

22
Q

What is the alveolar gas equation?

A

PAO2 = PiO2 - (PACO2/ R)

PiO2 = FiO2 - (Patmosphere - SVP H2O)
= FiO2 - (101 kPa - 6.3)

23
Q

How does altitude at 63,000 ft (Patm - 6.3 kPa) effect alveolar gas?

A

PiO2 = 0.21 (6.3 kPa - 6.3 kPa) = 0

Therefore as barometric pressure is equal to the partial pressure of water, a persons blood would boil.

24
Q

How is the respiratory quotient calculated?

A

CO2 production/ O2 consumption

25
Q

Draw a curve to demonstrate how changes in minute ventilation affect alveolar PAO2 and PACO2.

A

As Mv increases, arterial CO2 and therefore alveolar CO2 decreases. Therefore alveolar O2 increases.

26
Q

How do you calculate V/Q ratio?

A

alveolar ventilation /cardiac output

27
Q

How does ventilation vary within the lung from apex to base of the lung?

A
  1. Lungs are suspended within the thoracic cavity, therefore alveoli are subjected to gravity.
  2. In the upright lung, the intrapleural pressure varies from being the most negative at the apex and least negative at the base. (- 8 cm apex, to - 1.5 cm base)
  3. Consequently alveoli at the apex are relatively larger than at the base. Therefore alveoli at the apex are in the flatter part of the pressure volume-curve and less compliant, basal alveoli are more compliant. Hence ventilation is preferentially distributed to the base alveoli.
28
Q

How does pressure vary from the apex to the base of the lung?

A

Pulmonary circulation is a low pressure, low resistance system.
Lungs divided in Wests Zone 1 - 3.

Zone 1: PA > Pa > Pv (capillary collapse, no blood flow, good ventilation) - Alv dead space. But does not exist in healthy subjects.

Zone 2: Pa > PA > Pv (blood flow gradually increase)

Zone 3: Pa > Pv > PA (vascular pressures greater than alveolar pressure, recruitment of blood vessels)

29
Q

Describe control of respiration.

A

Regulated in the homeostasis of pH, PaO2, PaCO2 in blood.
This is done by the respiratory centre in the
- brainstem
- peripheral and central chemoreceptors
- mechanoreceptors in the chest wall and lungs.
- higher CNS input limbic/ hypothalamus

The brainstem contains three main neuronal centres.

  1. Dorsal respiratory group - controls inspiration, has intrinsic automaticity and is responsible for basic ventilatory rhythm. Works by increasing action potential frequency to the diaphragm.
  2. pneumotaxic area - assists in regulating inspiration, and fine tunes inspiration.
  3. ventral respiratory group - regulates expiration. Normally expiration is passive, but VRG stimulated during exercise to drive the expiratory muscles.
30
Q

Which receptors respond to hypoxia?

A

Peripheral chemoreceptors in the aortic and carotid bodies.
Cranial nerves 9 and 10 link receptors to brain stem.
Respond to PaO2
Each carotid body receive 2L/100g tissue per minute.

31
Q

How do peripheral chemoreceptors contribute to homeostasis?

What drug acts on these receptors?

What drugs inhibit these receptors?

A

Aortic bodies - detect low PaO2, and high PaCO2, increase RR

Carotid bodies - detect low PaO2, high PaCO2, pH changes

Doxapram acts as a respiratory stimulant at these receptors.

Volatiles inhibit peripheral chemoreceptor response to hypoxia.

32
Q

What is the role of the central chemoreceptors?

A

Sensitive to changes in hydrogen ion concentration in the CSF.

PaCO2 can diffuse across BBB and dissociate in H+ ions. Stimulates increased RR. The acute drive can last up to 48 hours.

33
Q

Describe the effects of raised CO2 on the body.

A

Resp - Increased RR due to stimulation central and peripheral chemoreceptors.

CVS - systemic vasodilation, myocardial depression, arrhythmias

Pulmonary circulation - increased PVR, respiratory acidosis

CNS - stimulates respiration but at high levels causes narcosis. Increase CBF and ICP.

Renal - slower compensation via bicarbonate retention and urinary H+ ion excretion.

34
Q

How much does atmospheric pressure change with altitude?

A

Halves every 5500 meters.

35
Q

What equation is used to explain changes in respiration at high altitude?

A

Alveolar gas equation

36
Q

What are the physiological changes to compensate at high altitude?

A

ACUTE vs CHRONIC CHANGES

  1. Hyperventilation
  2. OxyHb Curve shifts to the right at moderate altitudes, due to increased 2,3-DPG that favors O2 unloading. At high altitudes left shift due to favouring of oxygen uptake in capillaries.
  3. CVS - increased HR, stroke volume from sympathetic stimulation due to hypoxia.

CHRONIC CHANGES:

  1. Polycythaemia - increase in erythopoeitin to increase RBC count.
  2. Hypoxic pulmonary vasoconstriction - can lead to RHF
  3. Angiogenesis - increase capillary density with time.
37
Q

How does high altitude affect volatile anaesthesia?

A

Gas and Vapour analysers measure partial pressure and assume sea level atmospheric pressure, therefore at high altitude will under read.

TEC vapourisers function normally at altitude, because their SVP is achieved within the vapourised and added to a less dense gas flow, the concentration of the volatile is higher but the partial pressure remains the same.

38
Q

What is acute mountain sickness?

A

It is symptoms of ascending to high altitude, and depends on elevation, rate of ascent and individual susceptability. Usually start 12-24 hours after arrival at altitude and begin to decrease around the 3rd day.

Symptoms: fatigue, headache, nausea and dizziness, SOB, disturbed sleep

39
Q

What is high-altitude pulmonary oedema?

A

Results from increased pulmonary extravascular lung water, preventing oxygen exchange effectively. Severe hypoxaemia can develop.

Symptoms: SOB at rest, persisten cough with white frothy fluid, fatigue, feeling of suffocation, confusion and irrational behaviour.

40
Q

What is high-altitude cerebral oedema? (HACO)

A

Primary SOE/ VIVA (13 decks)

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