CO2 transport Flashcards
Describe the methods of CO2 transport in blood.
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
Define tidal CO2, mention its normal values
the CO2 given by tissues to 100 cc arterial blood
Value: 3.6 – 4mL/ 100 cc (= ~ 3.7 mL)
CO2 released from tissue metabolism (PCO2 of tissues = …………….)and diffuses to blood (PCO2 of blood = ………………….)
46mmHg , 40mmHg
Describe the changes that occur in blood at tissues - Chloride shift phenomenon
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
HCO3 - CL- passive exchanger:
- HCO3 Moves out by ………………………..
- CL- Moves in by ………………………….
- HCO3 Moves out by concentration gradient
- CL- Moves in by electrical gradient
Mention the Effects of Cl- shift phenomenon in plasma and RBCs
plasma: ↑ HCO3 ↓ Cl- RBCs: ↑ HCO3 ↑ Cl- ↑ osmotic pressure ↑ H2O ↑ Hematocrite value
Most of tidal CO2 is transported as HCO3 because………………………
it is more soluble.
Tidal CO2 doesn’t cause marked pH changes in venous blood (pH: 7.36) than in arterial blood (pH:7.4) because ……………………………………
it is buffered as HCO3 & carbamino compounds
What happens when the carbonic anhydrase inhibitors are used?
↓ Formation of HCO3 inside RBCs
↑ CO2 in plasma
↓ Transport of CO2 from tissues
↑ PCO2 in tissues
Describe the CO2 dissociation curve.
Definition: the relation between PCO2 & CO2 content of blood
Shape: linear
Discuss the importance of Haldane effect at the tissues and at the lung levels
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
what is the Bohr’s effect?
↑ CO2 & H+→ ↑ release of O2 from Hb to tissues [shift to the right]
what is the Haldane effect?
↑O2 → ↓ affinity of Hb to CO2 & H+
What is hypoxia? Describe the types,
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
causes of Hypoxic hypoxia =
↓ Arterial blood PO2
↓ Hb saturation
↓O2 content
1) Extrinsic: ↓ PO2 in inspired air O2 poor air in high altitude Hypoventilation 2) Pulmonary diseases: Hypoventilation Ineffective diffusion 3) Venous to arterial shunt
causes of Anemic hypoxia =
Normal PO2
↓ Blood O2 carrying capacity
↓O2 conten
1) Anemia
2) Abnormal Hb
3) CO poisoning
causes of Stagnant (ischemic) hypoxia =
Normal PO2
Normal O2 content
↓ Tissue blood flow
1) Generalized:
- Shock & Heart failure
2) Localized:
- Vascular spasm or block
causes of Histotoxic (cytotoxic) hypoxia =
Normal PO2
Normal O2 content
↓ Tissue use of O2
1) Cyanide poisoning
2) Beriberi: Vitamin B deficiency
Effects of hypoxia
↓ mental activity drowsiness & coma
↓ work capacity of muscles
Severe hypoxia > Cell death
List the conditions where O2 therapy is of value
hypoxic hypoxia in cases of:
Hypoventilation
Ineffective diffusion
High altitude
List the conditions where O2 therapy has no value
1- Hypoxic hypoxia due to venous-Arterial shunt , 𝑽𝒂\𝑸 mismatching
2- Anemic Hypoxia & abnormal Hb
3- Stagnant hypoxia
Give an account on O2 toxicity and on hyperbaric O2 therapy
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
Complications of O2 toxicity
1) On lung:
- Irritation of airways
- Sore throat
- Congestion of nose
- ↓ surfactant
2) In premature
- Damage of retina & blindness
- lung Cysts
Define Cyanosis.and where it Appears
Definition: bluish discoloration of skin & mucous membrane due to excess reduced Hb in blood
- Appears in: lips, nail beds, air lobes
Mention the threshold of Cyanosis
5 gm reduced Hb /100 mL arterial or capillary blood.
List five conditions that cause cyanosis , Explain
your answers.
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
List four conditions that do not cause cyanosis. Explain your answers.
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)
Give an account on the medullary respiratory center
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)
what is the 1ry center In which the automatic rhythmic
respiration is generated
medullary respiratory center
the mainly Inspiratory neurons and Acts during normal inspiration
Dorsal respiratory group (DRG)
it is Inspiratory & expiratory neurons
Acts during deep inspiration & forced expiration
Ventral respiratory group (VRG)
VRG remain inactive during …………………….
normal breathing
VRG is stimulated by ……………………………
DRG (override) during deep ventilation.
The normal respiratory rhythm is generated in ……………………………………………..
Pre-Botzinger network of neurons in the upper end of VRG
Activity of Pre-Botzinger neurons is modified by …………………………………………………
pontine centers & by vagus from lung & airway receptors.
why Lesion in DRG & VRG doesn’t inhibit the respiratory activity ?
because DRG doesn’t generate the basic breathing rhythm
Give an account on the generation of the respiratory rhythm
Neurons of Pre-Botzinger complex → rhythmic ++ of phrenic nerve → ++ of diaphragm
Give an account on the pontine respiratory center
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
What happens when Vagotomy and damage of pneumotaxic center ?
slow, deep & prolonged inspiration (apneusis)
Give an account on the role of pneumotaxic center in control of normal breathing.
Controls the duration of inspiration, So, it helps in:
- Stop inspiration at the proper time.
- Allowing normal expiration to occur.
What happens when Damage of Pneumotaxic center alone or Vagi alone
partial removal of the inhibition on the apneustic center → continuation of breathing but slower & deeper (great tidal volume)
Role of Vagus: [Hering-Breuer reflex]:-
Over inflation of lungs → ↑ Tidal volume → ++ of stretch receptors in bronchi & lung parenchyma → impulses through vagi nerves → – of medullary respiratory center → cut off inspiration.
Give an account on central chemoreceptors.
Site: medulla
Stimulus:
directly by high PCO2
indirectly by H+
Give an account on peripheral chemoreceptors.
Site: aortic bodies (in aortic arch) & carotid bodies (in carotid artery)
Stimulus: ↓ in PO2 less than 60mmHg.
Also ↑ PCO2 & ↑ H+
the 1ry factor that stimulate respiration
↑ PCO2
Describe the ventilatory responses to O2 changes.
- ↓ 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.
Describe the ventilatory responses to CO2 changes
- 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.
Describe the ventilatory responses to H+ ion changes.
- ↑ H+(acidosis e.g Lactic acidosis)
→stimulation of peripheral chemoreceptors mainly → ↑ ventilation. - ↓ H+(alkalosis e.g vomiting)
→ ↓ ventilation →accumulation of acids
