Respiratory physiology in awake and anaesthetized patients
Respiratory Physiology in awake
and anaesthetized patients
Moderator: Dr Ramesh Kumar
Presented by: Dr Puneet Verma
• Ventilation refers to movement of gas into and exhaled gas out of lungs.
• Alveolar Ventilation: The portion of the minute ventilation that reaches the alveoli and
respiratory bronchioles each minute and participates in gas exchange is called the
alveolar ventilation , and it is approximately 5 L/min.
• Dead space ventilation: The portion of minute ventilation that can not participate in
gas exchange, it can either be anatomic dead space or physiologic dead space.
• Tidal volume : The volume of gas that moves in and out of the lungs during quiet breathing
and is 6 to 8 mL/kg. Tidal volume falls with decreased lung compliance or when the patient has
reduced ventilatory muscle strength.
• Inspiratory reserve volume: The maximal amount of additional air that can be drawn into
the lungs by determined effort after normal inspiration.
• Expiratory reserve volume: The additional amount of air that can be expired from
the lungs by determined effort after normal expiration.
• Residual volume: The volume of air still remaining in the lungs after the most
forcible expiration possible.
• Inspiratory capacity: It is the largest volume of gas that can be inspired from the resting
expiratory level and is frequently decreased in the presence of signiicant extrathoracic airway
• FUNCTIONAL RESIDUAL CAPACITY: FRC is defined as the volume of gas in the
lung at the end of a normal expiration when there is no airflow. Under these conditions, expansive
chest wall elastic forces are exactly balanced by retractive lung tissue elastic forces.
• Vital capacity: Volume of air that can be forcibly exhaled after a full inspiration.
• Total lung capacity: The volume of air contained in the lungs at the end of a
Transport of Respiratory Gases in
• O2 is carried in blood in two forms:
• 1 :Dissolved Oxygen:
• The amount of O2 dissolved in blood can be derived from Henry's law i.e.
concentration of any gas in solution is proportional to its partial pressure.
• The solubility coefficient for O2 at normal body temperature is 0.003 mL/dL per
• Even with a PaO2 of 100 mm Hg, the maximum amount of O2 dissolved in blood is
very small (0.3 mL/dL) compared with that bound to hemoglobin.
• 2: Associated with hemoglobin
• Each gram of hemoglobin can theoretically carry up to 1.34 mL of O2.
• Each hemoglobin molecule binds up to four O2 molecules
• The complex interaction between the hemoglobin subunits results in nonlinear
binding with O2 represented by Oxygen-Hb dissociation curve.
• Oxygen content of blood can be denoted by equation
– CaO2 =(SaO2 × Hb × O2 combining capacity of Hb) + (O2 solubility × PaO2)
Factors influencing oxygen-Hb
• A rightward shift in the oxygen–hemoglobin dissociation curve lowers O2
affinity, displaces O2 from hemoglobin, and makes more O2 available to
tissues; a leftward shift increases hemoglobin's affinity for O2, reducing its
availability to tissues
• The normal P50 in adults is 26.6 mm Hg (3.4 kPa)
• Left-shifted oxy-Hb curve: Alkalosis (metabolic and respiratory—the Bohr
effect), hypothermia, abnormal fetal Hb, carboxyhemoglobin,
methemoglobin, and decreased RBC 2,3-diphosphoglycerate (2,3-DPG)
• Decreased RBC 2,3-diphosphoglycerate (2,3-DPG) content may occur with
the transfusion of blood stored in acid citrate-dextrose solution, reducing O2
delivery to tissues; storage of blood in citrate-phosphate-dextrose minimizes
changes in 2,3-DPG with time.
• Right-shifted oxy-Hb curve: Acidosis (metabolic and respiratory—the
Bohr effect), hyperthermia, abnormal Hb, increased RBC 2,3-DPG content.
1. Dissolved Carbon Dioxide(7%)
Carbon dioxide is more soluble in blood than O2, with a solubility coefficient
of 0.03 mmol/L/mm Hg at 37°C.
In plasma, although less than 1% of the dissolved CO2 undergoes this
reaction, the presence of the enzyme carbonic anhydrase within
erythrocytes and endothelium greatly accelerates the reaction.
As a result, bicarbonate represents the largest fraction of the CO2 in blood
3. Carbamino Compounds(13%)
At physiological pH, only a small amount of CO2 is carried in this form,
mainly as carbamino-hemoglobin.
Bohr and Haldane Effects
• 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 correspondingly lower) because of local CO2 production.
These circumstances shift the Hb-O2 dissociation curve to the right,
which increases the offloading of O2 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 O2 binding to Hb.
• 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
Distribution of pulmonary perfusion
Zone 1 PA>Ppa>Ppv •Vessels collapsed.
Zone 2 Ppa>PA>Ppv •Blood flow is determined
by mean Ppa-PA
Zone 3 Ppa>Ppv>PA •Vascular pressures
•Blood flow is
Zone 4 Ppa>PISF>Ppv>P
•Fluid can transduate
dependent parts at high
•Blood flow is governed
•Flow is lesser then in
Lung Compliance Distribution of
• Compliance: It expresses how much
distention occurs for a given level of
transpulmonary pressure (PTP).
• Gravity causes differences in vertical Pleural
pressure (Ppl), which in turn causes
differences in regional alveolar volume,
compliance, and ventilation.
• There is relatively more negative pressure
at the top of the pleural space (where the
lung pulls away from the chest wall) and
relatively less negative pressure at the
bottom of the lung (where the lung is
compressed against the chest wall).
• Dependent alveoli are relatively compliant
(steep slope), and nondependent alveoli are
relatively noncompliant (flat slope).
Therefore, most of the tidal volume is
preferentially distributed to dependent
alveoli which expand more per unit pressure
change than the nondependent alveoli.
• Expiration causes the airways to narrow, and deep expiration can cause them to
• The volume remaining above RV where expiration below FRC closes some airways is
termed closing volume (CV), and this volume added to the RV is termed the closing
capacity (CC; i.e., the total capacity of the lung at which closing can occur).
The Ventilation Perfusion 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 (VA/Q)
decreases rapidly at first and then
• VA/Q best expresses the amount of
ventilation relative to perfusion in any
given lung region. It is less then 1 in
overperfused regions and more then
one in overventilated regions.
Nongravitational determinants of
blood flow distribution
• 1. Passive Processes
A: Cardiac output
Pulmonary vascular bed is a high flow- low pressure system.
Pulmonary vascular pressures increase minimally with increase in
Increase in flow distend open vessels and recruit previously closed
vessels, which decreases PVR.
Decrease in flow decrease pressure and radii of pulmonary vessels
and PVR consequently increases.
B: Lung Volume
PVR is minimal at FRC.
At volumes above FRC, PVR increases due to alveolar compression
of small intra alveolar vessels.
At volumes below FRC, PVR increases due to mechanical effect in
large vessels and due to hypoxic pulmonary vasoconstriction.
Hypoxic Pulmonary Vasoconstriction
• It is a compensatory mechanism that diverts blood flow away from hypoxic lung
regions toward better oxygenated regions.The major stimulus for HPV is low alveolar
• The HPV response occurs primarily in pulmonary arterioles of about 200 μm internal
diameter (ID) in humans.
• HPV probably results from a direct action of alveolar hypoxia on pulmonary smooth
muscle cells, sensed by the mitochondrial electron transport chain, with reactive O2
species (probably H2O2 or superoxide) serving as second messengers to increase
calcium and smooth muscle vasoconstriction.
• Elevated PaCO2 has a pulmonary vasoconstrictor effect. Both respiratory acidosis
and metabolic acidosis augment HPV, whereas respiratory and metabolic alkalosis
cause pulmonary vasodilation and serve to reduce HPV.
• Mitral stenosis, volume overload, thromboembolism, hypothermia, vasoactive drugs
can decrease HPV by increasing pulmonary artery pressure.
• Direct vasodilating drugs (e.g., isoproterenol, nitroglycerin, sodium nitroprusside),
inhaled anesthetics and hypocapnia can directly decrease HPV.
• 2. Active Processes and Pulmonary vascular tone
– TISSUE (ENDOTHELIAL- AND SMOOTH MUSCLE–DERIVED) PRODUCTS
• Vasodilatation: Nitric oxide, Prostaglandin PGI2, Endothelin(ETB receptor on
• Vasoconstriction: Prostaglandin PGF2a, Thromboxane A2, Leucotrine, Endothelin(ETA
receptor on smooth muscle).
– ALVEOLAR GASES
• Hypoxia induced vasoconstriction in pulmonary arterioles.
• Elevated Paco2 also has pulmonary vasoconstrictor effect.
– NEURAL INFLUENCES ON PULMONARY VASCULAR TONE
• Sympathetic fibers cause pulmonary vasoconstriction through α1-receptors.
• Parasympathetic (cholinergic) nerve fibers originate from the vagus nerve and cause
pulmonary vasodilation through an NO-dependent process.
• NANC nerves cause pulmonary vasodilation through NO-mediated systems by using
vasoactive intestinal peptide as the neurotransmitter.
– HUMORAL INFLUENCES ON PULMONARY VASCULAR TONE
• Vasodilatation: Histamine, Substance P, Bradykinin, Vasopressin.
• Vasoconstriction: Epinephrine, Norepinephrine, Serotonin, Neurokinin A, Angiotensin.
Nongravitational determinants of
blood flow distribution
Nongravitational determinants of
blood flow distribution
• 3. Alternative (Nonalveolar) Pathways of Blood Flow Through the
Lung (right to left shunt)
– Bronchial and Pleural circulation : 1 to 3% of cardiac output normally
and upto 10% of CO in chronic bronchitis and 5% in pleuritis.
– Intrapulmonary arteriovenous malformations.
– Patent foramen ovale.
Lung volume and respiratory
mechanics during anesthesia
• Resting lung volume or FRC is reduced by 0.6 to 1 L by changing body
position from upright to supine and there is another 0.4 to 0.5 L decrease
when anaesthesia is induced.
• End expiratory lung volume is thus reduced from approx 3.5 to 2 L almost
being close to RV.
ATELECTASIS AND AIRWAY CLOSURE
• Atelectasis is a complete or partial collapse of a lung or lobe of a lung —
develops when the alveoli within the lung become deflated.
• Atelectasis develops in approximately 90% of patients who are
• In addition to shunt, atelectasis may form a focus of infection and can
certainly contribute to pulmonary complications.
PREVENTION OF ATELECTASIS DURING
• Positive End-Expiratory Pressure:
– Application of PEEP (10 cm H2O) has been repeatedly demonstrated to reexpand
– Higher levels of PEEP impairs venous return and reduce cardiac output specially in
presence of hypovolemia.
– It can also cause redistribution of blood flow to less aerated regions.
• Recruitment Maneuvers:
– A sigh maneuver or a large tidal volume is given at an airway pressure 40cm H2O for 7 to 8
– Such inflation is equivalent to a Vital Capacity and can therefore be called a VC maneuver.
• Minimizing Gas Resorption:
– 100% oxygen is avoided as it can be absorbed completely leading to recurrance of
– VC maneuver followed by ventilation with a gas mixture containing 60%N2 (40% O2)
reduced the propensity for reaccumulation of atelectasis with only 20% reappearing 40
minutes after recruitment.
• 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.
– Ketamine does not impair muscle tone and is the only individual anesthetic that does not
– An experimental approach is restoration of respiratory muscle tone by diaphragm pacing.
Decrease in FRC
• Induction of general anesthesia decreases FRC 15 – 20 %
• MAX decrease is within the first few minutes
• FRC decrease in awake patients is very slight, during spontaneous
• FRC decrease continues into the post operative period
• Application of PEEP may restore FRC to normal
Causes of reduced FRC
1. Supine position: FRC is reduced 0.5-1 litres because
diaphragm is displaced 4 cm cephalad and pulmonary
vascular congestion happens. Changing position every hour
2. Induction of GA: Thoracic cage muscle tone change:
loss of inspiratory
tone & increase in end expiratory tone (abdominal) increases
intra abdominal pressure, displaces diaphragm more
cephalad and decreases FRC.
Effect of Surgical position
1. Supine : decrease FRC
2. Trendelenburg: decrease FRC
3. Steep trendelenburg: decrease FRC
4. Lateral decubitus : FRC decrease in dependent lung
and increase FRC in un dependent lung (overall
FRC increases )
5. Lithotomy : FRC decrease more than supine
6. Prone : FRC increases
PREEXISTING LUNG DISEASE
• ANESTHESIA AND OBSTRUCTIVE PULMONARY DISEASE:
– They are at increased risk for reflex bronchoconstriction during
laryngoscopy and intubation – aggressive bronchodilator therapy should
be used preoperatively.
– Increased risk of hypercapnia- Preoperative FEV1 reduction correlates
with the Paco2 increase during anesthesia.
• ANESTHESIA AND RESTRICTIVE PULMONARY DISEASE:
– FRC is reduced, so lower oxygen stores are available during apneic
– Increased risk of barotrauma as higher peak airway pressures are
required to expand lungs.
Anesthetic Depth and
• 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.