2. TRANSPORT OF RESPIRATORY GASES IN BLOOD
Oxygen is carried in the blood in two forms:
1)O2 bound to hemoglobin and
2) O2 dissolved in the plasma.
The amount of O2 dissolved in blood can be derived from Henry’s law ( i.e. conc. of any
gas in solution is proportional to its partial pressure.
➢The solubility coefficient for O2 at normal body temp. is 0.0003 ml/dl per mmHg.
➢Even with PaO2 of 100mmHg, the maximum amount of 02 dissolved in blood is very
small (0.3 ml/dl) compared with that bound to Hb.
3. The complex interaction between the Hb subunits results in non linear binding with O2
represented by:
Oxygen-Hb dissociation curve.
O2 content of blood can be denoted by equation -
CaO2 = (SaO2 × Hb × O2 combining capacity of Hb) + (O2 solubility × PaO2)
where CaO2 (O2 content) is the milli liters of O2 per 100 mL of blood,
SaO2 is the fraction of Hb that is saturated with O2,
O2-combining capacity of Hb is 1.34 mL of O2 per gram of Hb,
Hb is grams of Hb per 100 mL of blood,
Pao2 is the O2 tension (i.e., dissolved O2), and
Solubility of O2 in plasma is 0.003 mL of O2 per 100 mL plasma for each mm Hg Pao2
4. OXYGEN HEMOGLOBIN DISSOCIATION CURVE
•Shape : Non linear sigmoid shape.
•Po2 : 100 mmHg ➢Plateau (no more Hb available)
•O2:Hb 50% saturation (P50) ➢ 27 mmHg (3.4 Pa)
•A rightward shift in ODC lowers O2 affinity, displaces O2 from Hb, and makes more O2
available to tissues ;
•A leftward shift increases Hb’s affinity for O2, reducing its availability to tissues.
•Different factors can shift this curve to the left or right
6. TRANSPORT OF CARBON DIOXIDE IN BLOOD
Max.Co2 is produced in mitochondria,where co2 levels are highest.
In the blood, CO2 is transported in three main forms:
1. DISSOLVED CO2 (5%)
➢CO2 is more soluble than O2, with a solubility coefficient of 0.03 mmol/L/mmHg at 37 degree C.
2. BICARBONATE ION (HCO3–; almost 90%)
➢In plasma, the presence of enzyme carbonic anhydrase within erthrocytes and endothelium greatly
accelerate the reaction.
➢As a result, HCO3- represents the largest fraction of co2 in blood.
3. CARBAMINO CO2 (5%)
➢CO2 bound to terminal amino groups in Hb molecules; approximately 5%).
➢The usual quantities of CO2 in the arterial and (mixed) venous blood are approximately 21.5
and 23.3 mmol of CO2 per liter of blood.
7. BOHR AND HALDANE EFFECT
Bohr Effect:
➢It describes the effect of PCO2 and [H+] ions on the oxy-Hb curve.
➢In the systemic capillaries, the Pco2 is higher than in the arterial blood
(and the pH is correspondingly lower) because of local CO2 production.
➢These circumstances shift the Hb-02 dissociation curve to the right,
which increases the offloading of 02 to the tissues.
➢In the pulmonary capillaries; the Paco2 is lower (and the pH correspondingly higher)
because of CO2 elimination, and the dissociation curve is shifted to the left to facilitate
02 binding to Hb.
8. HALDANE EFFECT :
➢Increased Pao2 decreases the ability to form carbamino compounds
reducing the amount of CO2 bound to Hb-thereby raising the amount
of dissolved CO2 (i.e., elevated Pco2).
➢This effect is responsible for occasional hypercapnia induced by
supplemental oxygen.
9. VENTILATION
Ventilation refers to the movement of inspired gas into and exhaled gas out of the lungs.
•ALVEOLAR VENTILATION :
➢The portion of the minute ventilation (Ve) that reaches the alveoli and respiratory
bronchioles each minute and participates in gas exchange is called the alveolar
ventilation (VA), and it is approximately 5 L/min.
•DEAD SPACE VENTILATION :
➢The portion of the minute ventilation (Ve) that can not participate in gas exchange, it
can either be anatomic dead space or physiological dead space.
Normal dead space=150 ml
Infants: 3.3ml/kg =15-30ml
Adults: 2ml/kg = 140-150ml
10. ➢Not all of the inspired gas mixture reaches alveoli; some of it remains in the airways and
is exhaled without being exchanged with alveolar gases.
➢The part of the Vt not participating in alveolar gas exchange is known as dead space (Vd).
➢Alveolar ventilation (Va) is the volume of inspired gases actually taking part in gas
exchange in 1 min.
➢Va =Respiratory rate × Vt −Vd
➢Dead space is actually composed of gases in non respiratory airways (anatomic dead
space) and alveoli that are not perfused (alveolar dead space).
➢The sum of the two components is referred to as physiological dead space.
11.
12. LUNG VOLUMES & CAPACITIES
●PULMONARY VOLUMES:
1)Tidal Volume:Volume of Air Inspired or Expired during a Normal Quiet Respiration.Only
Volume same in Male & Female.(Normal Vt=500ml ; i.e 6-8ml/Kg)
2)Inspiratory Reserved Volume [IRV]: Volume of Air Inspired Forcefully over & above Tidal
Inspiration with maximum effort.( Normal IRV Female=1900ml ; male=3300ml)
3)Expiratory Reserved Volume [ERV]:Volume of Air Expired Forcefully over & above Tidal
Inspiration with maximum effort.( Normal ERV Female=700ml ; male=1000ml)
4)Residual Volume [RV]:Volume of Air which remain in Lung at end of maximum Expiration.
(Normal RV Female=1100ml ; male=1200ml)
13. ●PULMONARY CAPACITY:
1)Inspiratory Capacity: IRV(Inspiratory reserved vol.) +Vt ( Tidal Vol.).
2)Expiratory Capacity: ERV ((expiratory reserved vol.) + Vt (Tidal vol.).
3)Vital Capacity/Forced Vital Capacity: Vol. of Air Expired Forcefully after a Forceful
Inspiration. [ FVC=IRV +Vt + ERV ]
4)Total Lung Capacity: Lung Vol. at end of forceful inspiration.
[TLC=IRV +Vt +ERV +RV ]
14.
15. RESPIRATORY MECHANICS
➢Compliance :is the term that expresses how much distention (volume in liters) occurs
for a given level of Trans pulmonary pressure (PTP) ;(it is usually 0.2 to 0. 3 L/cm H2O).
➢Gravity causes differences in vertical Pleural pressure (PPL), which in turn causes
differences in regional volume, compliance, and ventilation.
➢There is relatively more negative pressure at the top of the pleural space (where lung
pulls away from chest wall) and relatively less negative pressure at the bottom of lung
(where the lung is compressed against the chest wall).
16. •The net distending pressure, which is the difference of the (positive) airway pressure
(PAW) and the (negative) pleural pressure (PPL) is termed the transpulmonary pressure
(PTP). Thus : PTP = PAW − PPL
•Clearly, increasing the PAW increases the PTP. In addition, lowering the PPL (which is
usually negative and making it more negative) also increases the PTP.
•Dependent alveoli are relatively compliant (steep slope), and nondependent
alveoli are relatively non compliant (flat slope).
•Therefore, most of the VT is distributed to dependent alveoli (basal regions)which
expand more per unit pressure change than the nondependent alveoli(apical regions).
17.
18.
19. VENTILATION-PERFUSION RATIO
•V/Q RATIO = Alveolar Ventilation/Pulmonary Circulation .
•V/Q = 1 i.e. NORMAL , seen only in middle region of lung.
•V/Q ratio at Apex – 3.2 (highest) more aerated
at Base – 0.6 (lowest) more perfused
•Distribution of Pulmonary Perfusion divided the lung into 4 distinct zones as -
20.
21. V / Q RATIO
🔘Blood flow and ventilation increase linearly down the normal upright lung.
🔘Blood flow increases from a very low value and more rapidly than ventilation does with
distance down the lung.
🔘The ventilation-perfusion ratio (VAQ) decreases rapidly at first and then more slowly.
🔘VA/Q best expresses the amount of ventilation relative to perfusion in any given lung
region. It is less then 1 in over perfused regions and more then 1 in over ventilated
regions.
22.
23. INTRA-OPERATIVE RESPIRATORY EVENTS
LUNG VOLUME AND RESPIRATORY MECHANICS DURING ANESTHESIA
➢Resting lung volume (i.e., FRC) is reduced by almost 1 L by moving from upright to
supine position.
➢Induction of anesthesia further decreases the FRC by approximately 0.5 L.
➢This reduces the FRC from approximately 3.5 to 2 L, a value close to RV.
➢General anesthesia causes a fall in FRC (approximately 20%), whether breathing is
controlled or spontaneous and whether the anesthetic is inhalational or intravenous.
24. ATELECTASIS AND AIRWAY CLOSURE
DURING ANESTHESIA
•ATELECTASIS is a complete or partial collapse of a lung or lobe of lung – develops
when the alveoli within the lung become deflated.
•Atelectasis develops in approximately 90% of patients who are anesthetized, but it is
unrelated to the choice of anesthesia.
•In addition to Shunt, atelectasis may form a focus of infection and can certainly
contribute to pulmonary complications.
25. PREVENTION OF ATELECTASIS
DURING ANESTHESIA
●Positive End-Expiratory Pressure
➢The application of PEEP (10 cm H2O) has been repeatedly demonstrated to re expand atelectasis
in part.
➢First, the higher levels of PEEP can impair venous return, lowering the cardiac output especially in
the presence of hypovolemia.
➢Second, increased PEEP can cause redistribution of blood flow away from the aerated, expanded
regions.
●Recruitment Maneuvers
➢A sigh maneuver, or a large VT, has been suggested for reversing atelectasis; given at airway
pressure PAW of 40 cm H2O for 7-8 sec.
➢In the presence of normal lungs, such inflation is equivalent to
a VC and can therefore be called a VC maneuver .
26. ●Minimizing Gas Resorption
➢The application of FiO2 1.0 has been used.
➢A VC maneuver followed by ventilation with a gas mixture containing 60% N2 (40%
O2) reduced the propensity for re accumulation of atelectasis, with only 20%
reappearing 40 minutes after recruitment.
➢An alternative approach Application of CPAP 10 cm H2O permitted the use of 100%
inspired O2 without formation of significant degrees of atelectasis.
●Maintenance of Muscle Tone
➢loss of muscle tone in the diaphragm or chest wall appears to increase the risk of
atelectasis, techniques that preserve muscle tone may have advantages.
➢Intravenous ketamine does not impair muscle tone and is the only individual
anesthetic that does not cause atelectasis.
27. Factors affecting HPV(Hypoxic pulmonary vasoconstriction
)
●The HPV response occurs primarily in pulmonary arterioles of about 200 micrometer ID
in humans.
●The major stimulus for HPV is low alveolar oxygen tension (PAO2), whether caused by
hypoventilation or by breathing gas with a low PO2.
●Direct Vasodilator drugs e.g. Nitroglycerin, nitric oxide Inhaled anesthetics and
hypocapnia can directly dec. the HPV.
●Indirect inhibitors:
Mitral stenosis, volume overload, hypothermia, thromboembolism.
28. Factors that Influence Respiratory Function
During Anesthesia
FUNCTIONAL RESIDUAL CAPACITY
➢The amount of air in the lungs after an ordinary expiration is called functional residual
capacity (FRC)
➢It is usually 3 to 4 L and occurs because of the balance of inward (lung) forces and
outward (chest wall) forces. The inward force is the “elastic recoil” of the lung and
emanates from the elastic lung tissue fibers, contractile airway smooth muscle, and
alveolar surface tension.
➢The outward force is developed by passive recoil from the ribs, joints, and muscles of
the chest wall.
➢FRC is greater with increased height and age (loss of elastic lung tissue), and smaller
in women and in obesity.
29. Factors known to Alter The FRC Include
the Following:
Body habitus:
➢FRC is directly proportional to height.
➢Obesity, decrease FRC(as a result of reduced chest compliance).
Sex:
➢FRC is reduced by about 10% in females compared with males.
Posture:
➢FRC decreases as a patient is moved from an upright to a supine or prone position.
➢The greatest change occurs between 0° and 60° of inclination.
➢No further decrease is observed with a head-down position of up to 30°.
30. Lung disease:
➢Decreased compliance of the lung, chest, or both is characteristic of restrictive
pulmonary disorders all of which are associated with a low FRC.
Diaphragmatic tone:
➢This normally contributes to FRC.
Causes of reduced FRC :
➢Supine position : FRC reduced 0.5-1 L because diaphragm displaced cephalad and
pulmonary vascular congestion happens.
➢Induction of G.A : Thoracic cage muscle tone change ➡️ loss of inspiratory tone &
increase in expiratory tone ➡️ increases intra-abdominal pr. ➡️ displaces diaphragm
more cephalad and dec.FRC.
31. CLOSING VOLUME & CLOSING CAPACITY
CLOSING CAPACITY:
▪️Small airway lacking cartilaginous support depend on radial traction caused by
the elastic recoil of surrounding tissue to keep them open.
▪️The volume at which these airways begin to close in dependent areas of the lung
is called the closing capacity
▪️At lower lung volumes ,Alveoli continue to be perfused but no longer ventilated
leads to intrapulmonary shunting of deoxygenated blood promoting Hypoxia.
32.
33.
34. Phase I: 0% nitrogen from anatomic
dead space. Phase II: mixture of gas from anatomic dead space and alveoli.
Phase III: “alveolar plateau” gas from alveoli. A steep slope of phase III
indicates nonuniform distribution of alveolar gas. Phase IV: closing volume.
Take-off point (closing capacity) of phase IV denotes beginning of airway
closure in dependent portions of the lung.
35. ANAESTHESIA DEPTH & RESPIRATORY PATTERN
▪️When the depth of anesthesia is inadequate (less than MAC), the respiratory pattern
may vary from excessive hyperventilation and vocalization to breath-holding.
▪️When anesthetic depth approaches MAC (light anesthesia), irregular respiration
progresses to a more regular pattern that is associated with a larger than normal tidal
volume.
▪️As anesthesia deepens to moderate levels, respiration becomes faster and more
regular but shallower.
▪️The respiratory rate is generally slower and the VT larger with nitrous oxide narcotic
anesthesia than with anesthesia involving halogenated drugs.
▪️In the case of very deep anesthesia with all inhaled drugs, respirations often become
jerky or gasping in character and irregular in pattern.
