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physio-essay-RESP > CO2 transport > Flashcards

CO2 transport Flashcards

1
Q

Describe the methods of CO2 transport in blood.

A

CO2 is carried in blood in 3 forms:

1) In physical solution
2) In chemical combination as bicarbonate
3) In chemical combination as carbamino-compounds

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2
Q

Define tidal CO2, mention its normal values

A

the CO2 given by tissues to 100 cc arterial blood

Value: 3.6 – 4mL/ 100 cc (= ~ 3.7 mL)

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3
Q

CO2 released from tissue metabolism (PCO2 of tissues = …………….)and diffuses to blood (PCO2 of blood = ………………….)

A

46mmHg , 40mmHg

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4
Q

Describe the changes that occur in blood at tissues - Chloride shift phenomenon

A 
CO2 enters RBCs
 Inside RBCs, 
by carbonic anhydrase enzyme (CAE) 
CO2 & H2O  → H2CO3
 H2CO3  → H+ and HCO3
↑ HCO3 → exchange with plasma CL- 
↑ CL- inside RBCS → RBCs osmotic forces → suction 
of H2O to RBCs → increase RBCs volume
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5
Q

HCO3 - CL- passive exchanger:

  • HCO3 Moves out by ………………………..
  • CL- Moves in by ………………………….
A
  • HCO3 Moves out by concentration gradient

- CL- Moves in by electrical gradient

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6
Q

Mention the Effects of Cl- shift phenomenon in plasma and RBCs

A 
plasma:
 ↑ HCO3
 ↓ Cl-
RBCs:
↑ HCO3
 ↑ Cl-
 ↑ osmotic pressure 
 ↑ H2O
↑ Hematocrite value
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7
Q

Most of tidal CO2 is transported as HCO3 because………………………

A

it is more soluble.

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8
Q

Tidal CO2 doesn’t cause marked pH changes in venous blood (pH: 7.36) than in arterial blood (pH:7.4) because ……………………………………

A

it is buffered as HCO3 & carbamino compounds

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9
Q

What happens when the carbonic anhydrase inhibitors are used?

A

↓ Formation of HCO3 inside RBCs
↑ CO2 in plasma
↓ Transport of CO2 from tissues
↑ PCO2 in tissues

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10
Q

Describe the CO2 dissociation curve.

A

Definition: the relation between PCO2 & CO2 content of blood
Shape: linear

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11
Q

Discuss the importance of Haldane effect at the tissues and at the lung levels

A 
Lungs:
↑ O2 → ↓ affinity of Hb to CO2 & H+
↓ CO2 & H+ → ↑ affinity of Hb to O2
tissue:
↓ O2 →↑ affinity of Hb to CO2 & H+
 ↑ CO2 & H+ → ↓ affinity of Hb to O2
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12
Q

what is the Bohr’s effect?

A

↑ CO2 & H+→ ↑ release of O2 from Hb to tissues [shift to the right]

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13
Q

what is the Haldane effect?

A

↑O2 → ↓ affinity of Hb to CO2 & H+

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14
Q

What is hypoxia? Describe the types,

A 
Definition: O2 deficiency at the tissue level
types:
1- Hypoxic hypoxia
decrease O2 in arterial blood.
2- Anemic hypoxia
decrease Hb amount of function in arterial blood
3- Stagnant (ischemic)
decrease blood flow to tissues
4- Histotoxic (cytotoxic)
inability of tissues to use O2
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15
Q

causes of Hypoxic hypoxia =
↓ Arterial blood PO2
↓ Hb saturation
↓O2 content

A 
1) Extrinsic:  
 ↓ PO2 in inspired air
 O2 poor air in high altitude
 Hypoventilation 
2) Pulmonary diseases:
Hypoventilation
Ineffective diffusion
3) Venous to arterial shunt
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16
Q

causes of Anemic hypoxia =
Normal PO2
↓ Blood O2 carrying capacity
↓O2 conten

A

1) Anemia
2) Abnormal Hb
3) CO poisoning

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17
Q

causes of Stagnant (ischemic) hypoxia =
Normal PO2
Normal O2 content
↓ Tissue blood flow

A

1) Generalized:
- Shock & Heart failure
2) Localized:
- Vascular spasm or block

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18
Q

causes of Histotoxic (cytotoxic) hypoxia =
Normal PO2
Normal O2 content
↓ Tissue use of O2

A

1) Cyanide poisoning

2) Beriberi: Vitamin B deficiency

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19
Q

Effects of hypoxia

A

↓ mental activity drowsiness & coma
↓ work capacity of muscles
Severe hypoxia > Cell death

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20
Q

List the conditions where O2 therapy is of value

A

hypoxic hypoxia in cases of:
Hypoventilation
Ineffective diffusion
High altitude

21
Q

List the conditions where O2 therapy has no value

A

1- Hypoxic hypoxia due to venous-Arterial shunt , 𝑽𝒂\𝑸 mismatching
2- Anemic Hypoxia & abnormal Hb
3- Stagnant hypoxia

22
Q

Give an account on O2 toxicity and on hyperbaric O2 therapy

A

O2 toxicity Occur with: 80-100% O2 for 8 hours or more
Hyperbaric O2:
-100% O2 at high pressure
-Its use ↑ the onset of O2 toxicity

23
Q

Complications of O2 toxicity

A

1) On lung:
- Irritation of airways
- Sore throat
- Congestion of nose
- ↓ surfactant
2) In premature
- Damage of retina & blindness
- lung Cysts

24
Q

Define Cyanosis.and where it Appears

A

Definition: bluish discoloration of skin & mucous membrane due to excess reduced Hb in blood
- Appears in: lips, nail beds, air lobes

25
Q

Mention the threshold of Cyanosis

A

5 gm reduced Hb /100 mL arterial or capillary blood.

26
Q

List five conditions that cause cyanosis , Explain

your answers.

A

1) Polycythemia: high Hb content, easy to get more than 5gm reduced.
2) Hypoxic hypoxia: very low PO2 & O2 content
3) Stagnant hypoxia: slow blood flow gives more time for O2 extraction
4) Asphyxia: inability to breath oxygenated air
5) Moderate cold → ↓ blood flow →↑ O2 extraction →↑ % of reduced Hb

27
Q

List four conditions that do not cause cyanosis. Explain your answers.

A

1) CO poisoning (cherry red)
2) Histotoxic hypoxia: no O2 consumption by tissues
3) Anemic hypoxia (↓ Hb, not easy to get more than 5 gm reduced Hb)
4) Very cold temperature → ↓O2 consumption by tissues & ↑ Hb affinity to O2 (shift to left)

28
Q

Give an account on the medullary respiratory center

A

the 1ry center In which the automatic rhythmic
respiration is generated.
- It consists of 2 bilateral groups of neurons:
1- Dorsal respiratory group (DRG)
2- Ventral respiratory group (VRG)

29
Q

what is the 1ry center In which the automatic rhythmic

respiration is generated

A

medullary respiratory center

30
Q

the mainly Inspiratory neurons and Acts during normal inspiration

A

Dorsal respiratory group (DRG)

31
Q

it is Inspiratory & expiratory neurons

Acts during deep inspiration & forced expiration

A

Ventral respiratory group (VRG)

32
Q

VRG remain inactive during …………………….

A

normal breathing

33
Q

VRG is stimulated by ……………………………

A

DRG (override) during deep ventilation.

34
Q

The normal respiratory rhythm is generated in ……………………………………………..

A

Pre-Botzinger network of neurons in the upper end of VRG

35
Q

Activity of Pre-Botzinger neurons is modified by …………………………………………………

A

pontine centers & by vagus from lung & airway receptors.

36
Q

why Lesion in DRG & VRG doesn’t inhibit the respiratory activity ?

A

because DRG doesn’t generate the basic breathing rhythm

37
Q

Give an account on the generation of the respiratory rhythm

A

Neurons of Pre-Botzinger complex → rhythmic ++ of phrenic nerve → ++ of diaphragm

38
Q

Give an account on the pontine respiratory center

A

a) Pneumotaxic center:
- In the upper part of pons
- It inhibits apneustic center → makes respiration more rapid & regular
b) Apneustic Center:
- In the lower part of pons:-
- It stimulates the medullary center → inspiration
- It is inhibited rhythmically by:
1) Vagus
2) Pneumotaxic center

39
Q

What happens when Vagotomy and damage of pneumotaxic center ?

A

slow, deep & prolonged inspiration (apneusis)

40
Q

Give an account on the role of pneumotaxic center in control of normal breathing.

A

Controls the duration of inspiration, So, it helps in:

  1. Stop inspiration at the proper time.
  2. Allowing normal expiration to occur.
41
Q

What happens when Damage of Pneumotaxic center alone or Vagi alone

A

partial removal of the inhibition on the apneustic center → continuation of breathing but slower & deeper (great tidal volume)

42
Q

Role of Vagus: [Hering-Breuer reflex]:-

A

Over inflation of lungs → ↑ Tidal volume → ++ of stretch receptors in bronchi & lung parenchyma → impulses through vagi nerves → – of medullary respiratory center → cut off inspiration.

43
Q

Give an account on central chemoreceptors.

A

Site: medulla
Stimulus:
directly by high PCO2
indirectly by H+

44
Q

Give an account on peripheral chemoreceptors.

A

Site: aortic bodies (in aortic arch) & carotid bodies (in carotid artery)
Stimulus: ↓ in PO2 less than 60mmHg.
Also ↑ PCO2 & ↑ H+

45
Q

the 1ry factor that stimulate respiration

A

↑ PCO2

46
Q

Describe the ventilatory responses to O2 changes.

A
  • ↓ PO2 to less than 60 mmHg → Stimulation of peripheral chemoreceptors →↑ Ventilation.
  • Very low PO2 →
    Depression of respiratory center →↑ Ventilation by ↓ PO2 is a life-saving mechanism used by the body in emergency.
47
Q

Describe the ventilatory responses to CO2 changes

A
  • Slight ↑ in PCO2 → (2-5mmHg) →
    Stimulation of central (70%) & Peripheralchemoreceptor →Marked ↑ in ventilation.
  • Very high PCO2 ( > 80mmHg)
    →Depression of respiratory center.
  • ↓ PCO2→ ↓ activity of respiratory center →↓ventilation → accumulation of CO2 back to normal.
48
Q

Describe the ventilatory responses to H+ ion changes.

A
  • ↑ H+(acidosis e.g Lactic acidosis)
    →stimulation of peripheral chemoreceptors mainly → ↑ ventilation.
  • ↓ H+(alkalosis e.g vomiting)
    → ↓ ventilation →accumulation of acids

physio-essay-RESP (6 decks)

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