PHYsIOLOGY : MADE EAsSY

134
S2. Normal ejection fraction is (i) 65% (ii) 80% (ii) 45% (iv) 75%.
33. Normal cardiac reserve is (i) 15-25 L/min (i) 30-40 LJmin (ii) 15-25 ml/min (iv) 30-40 ml/min,i
4. Nomal end systolic volume is () 70 ml (ii) 50 ml (ii) 100 ml (iv) 5 lit.
35. Normal cardiac index is (i) 4.5 L (ii) 8.2 L (ii) 3.2 L (iv) 5.4 L.
36. The dye used to determine cardiac output by dye dilution method is usually (i) radioactive inulin
(i)
(in)
Respiration
(i) radioactive iodine ci) Evan's blue (iv) tritium oxide, (ii)
37. Following hormone do not have any role in regulating cardiac output () insulin (i1) glucagon
(11) thyroxine (iv) oxytocin. (iv)
38. Venous retum does not normally depend on following activity (i) atrial pump (i) skeletal muscle
pump (iii) thoracic pump (iv) abdominal pump.
39. Vagal stimulation decreases cardiac output mainly by (i) decreasing cardiac contractility i.e. Stroke
volume (i) decreasing heart rate (ii) both (iv) none. i)
40. Afterload depends primarily on (i) vessel diameter (ii) viscosity of blood (ii) both (iv) none. (ii)
41. Pulse pressure is high in () arterioles (i) capillaries (ii) veins (iv) aorta. (iv)
42. Normal central venous pressure is (i) 5 mmHg (i) 10 mmHg (ii) -5 mmHg (iv) 50 mmHg. )
43. Preload is determined by (i) stroke volume (i) end diastolic volume (i) cardlac output (iv) all of
them. (i)
A. Long type:
44. Following factors are positively inotropic except (i) sympathetic stimulation (ii) parasympathetic
stimulation (ii) glucagon (iv) caffeine. i) 1. Define mechanics of breathing. Explain the sequence of events take place during nor-
45. Vasomotor center receives inputs from (i) aortic and carotid baroreceptors (ii) carotid and aortic mal inspiration and expiration with special reference to pump handle and bucket han
chemoreceptors (i) both (iv) none. dle movements of thoracic ribs and diaphragm.
46. Sino-aortic refiex basically is (i) baroreceptors reflex (ii) chemoreceptor reflex (ii) both (iv) none The Ist step of respiration is ventilation in which exchange of gases takes place in between
atmos
and lungs by bulk now from a region of high pressure to the region of low pressure. The bulk
) phere
now in case of lung can be detemined by the following formula:
47. The rate of O2 consumption of heart is (i) 5.5 ml/100 gm of tissue (i) 15.8 ml /100 gm of tissue
(ii) 9.7 mi/100 gm oftissue (iv) 0.5 ml/100 gm of tissue. (i)
48. Autoregulation of coronary blood flow occurs in the range of blood pressure which is about F-m
R
i) 50-60 mmHg (Gi) 120-140 mmHg (i) 20-40 mmHg (iv) 70-110 mmHg. (iv) Where F bulk Flow, Paum atmospheric pressure, and Pa= alveolar pressure
49. All are the components of triple response except one (i) white reaction (ii) red reaction (ii) whale
when
(iv) flare. Sois outward
Patmflowbecomes more than Pay then
there is inward flow of air and when Pam <Pa, then there
of air from lungs. This increase decrease of intra alveolar air pressure is controlled
or
50. Following is not the fealure of hemorthagic shock (i) hypotension (ii) bradycardia (ii) rapid and
thready pulse (iv) thirst sensation. i) bythoracic
decreasing and increasing the volume of lungs which inturnm is conirolled by the movements of
This mechanical event is called as
51. High cardiac output failure is seen in following cases except (i)severe anemia (i) Paget's disease
cage. Mechanies of breathing.
(ii) byperthyroidism (iv) myocardial infarction. (iv) Mechanism of quiet (Tidal) breathing (Normal respiration): During tidal respiraion expansion
of
the thoracic cavity during the phase of inspiration is mainly (90%) due to movement of diaphragm
and parly due to movement of thoracie cage. This movement of diaphragm and thoräcic cage during
and expiration which results the gaseous exchange in between atmosphere and alveoli is
inspiraion
as follows:
(a) Inspiration: Inspiration is initiated by:
() Contraction of diaphragm, which draws the central tendinous portion of diaphragm downward
(Fig. 5.1) thereby increasing the vertical diameter of the thoracic cage.
(ii) Contraction of external intercostal muscles of 2nd to6 horacic ribs which causes
Elevation of these ribs and also upward and forward movement of stermum (pump handle
movement) to increase antero-posterior diameter of the thoracic cage (Fig. 5.1).

135
 37
130 PHYSIOLOGY MADEEAsv nPInATION

Upward and outward movements of the central part of these ribs which increases transverse Contraction of external
Contraction of diaphragm Contraction of external intercostal muscles of
diameter of the thoracic cage (bucket handle movement) muscles intercostal muscls of
lower costal series
(cii) Contraction of external intercostal muscle of lower costal series (rth to 10th thoracie ribs), upper costal series

which swings outward and upward to increase transverse diameter (Bucket handle movement)
of the thoracic cage (Fig. 5.1). Upward and outward Upward and outward
Downward movement of Mainly upward and forward movements of thoracic
movements of thoracic
home of diaphragm movement of sternumn
ribs (2nd to 6th) ribs (7th to 10th)
(Pump handle movement) (Bucket handle
(Bucket handle
movement) movement)

At rest
Anterio-Posterior Transverse diameter
Vertical diameter of of thorax
thoracic cage diameterof thoracic cage
During inspiration
Enlargement of thorax .

a
Thoracic wall moves slightly
from lung surface

Intrapleural pressure

Expansion of lungs

Palv < Patm

Vertebral column
Vertebral column
Air flows to alveoli

FC 5A: Mechanism of tidal respiration

2. Is the expiration active process? Briefly discuss the mechanism of forceful breathing
during exercise.
Sternum Normal expiration is passive process as it does not require energy. It requires only relaxation of
Stemum inspiratory muscles. But the forceful expiration is active process as during thisinvolvement of additional
B the
expiratory muscles like intermal intercostal muscles and abdominal muscles are required to
now
bring
chart
thoracic cage downward. The detail mechanism of forceful respiration is illustrated by as

Fig. 5.1: Diagrammatic representation of diaphragm movement during inspiration (A), and ribs movement
(B. Bucket handle movemen! and C. Pump handle movement)
Thus the increases of all three diameters of the thorax is responsible for increase of negative pressure
in the thoracic cavity resulting expansion of the lungs and thus the pressure within the alveoli falls below
the atmospheric pressure thal causes the flow of air into the alveolus. The above mechanism is explained
by the help of block diagram (Fig. FC SA).
(b) Expiration: Expiration during tidal breathing is completely due to relaxation of the inspiratory
muscles (i.e. passive process) because of which thoracic cage goes back to it's original position which
inturn results compression of the lungs and thereby decrease in intra alveolar pressure. Rise of Palv
beyond Pain Causes the air to move out of lungs.
follows:
(a) Forceful inspiration: The detail mechanism is illustrated in low chart (FC SB).
(b) Forceful expiration: It is also the active process which is more powerful than quite expiration.
The mechanism is deseribed in flow chart (FC 5C).
3. In which form O, is transported from lungs to tissues? What is O, dissociation curve?
Enumerate the factors affecting O, dissociation curve. What do you mean by Bohr's
effect?
The forms in which 0, is carried in the blood:
The Og in venous blood is transported from lungs to the tissues via heart in two forms
(a) In dissolved form:
Small amount of O, (0.3%) is carried in simple physical solution in plasma and water of RBC.
140 PHYSIOLOGY: MADE EASY fEsPRATIÓN 141
=

Presence of carbon monoxide shifts the curve to the left because of inhibition of 2-3 DPG rapidly combines with Fe" present in it. This is called as allosteric activation or allosteric modulation.
'S'
fomation. Though the uptake of O, by hemoglobin is not increased but decreased due to fors
mation of more carboxy hemoglobin which has more affinity to bind with hemoglobin - i.e.
Thus of
the shape this curve is due to shifting affinity of hemoglobin for O, The detail mechanism of
allosteric medulation is as follows:
In deoxyhemoglobin, the iron atom is about 0.4 Å out of the porphyrin plane towards the proximal
PCO inhibition of 2-3 DPG More altinity of O, with Hb in tissue level histidine: On oxygenation the iron atom moves into the plane of the porphyryin to form a strong bond
with O, and the heme becomes more planner. Thus the iron atom pulls the proximal histidine withit

More affinity of CO to bind with Hb less O release in tissue

when it moves into the plane of the porphyrin. This movement of histidine will ultimately cause the
conformational change and there is the rupture of interchain salt bridges to switch the protein to the '*
form. Thus a structural changes (oxygenation) within a subunit is translated into structural changes
between other subunits. The binding of O at one heme site is thereby communicated to parts of the
More formation of carboxy-Hb
nmolecule that are far away. This mechanism is called as allosteric modulation which can be further
explained by the help oftwo models:
unavailibility of Hb for O2 cariage (1) Sequential model: In deoxyhemoglobin, Hb is in the T state, The binding of O2 to one of the
subunits changes ir'sconformation from T' to 'R' but leaves the other subunits in the T form. The O2
binding affinity of unoccupied sites in RT3 is higher than in Ta because some salt bridges have been
Less O2 uptake broken on binding the first Og. So 2nd moleculeof O, binds with 2nd subunit in a greater affinity to form
D Presence of fetal hemoglobin (HbF) shifs the curve to the left because of less affinity of HbF RT2 and thereby broke some salt bridges again. So R,T,has greater affinity to O, than RT, and binds
for 2-3 DPG. O, with greater affinity to form RyT and ultimately R4

(11) Factors responsible for shiftüng of 0r-dissociation curve to the right: This model can be explained in terms of postage stamp analogy where two perforated edges must be
torn to remove the Ist stamp and then one perforated edge must be torn to remove the 2nd and 3rd stamp
Increased PC0-Increasedrelease PCO, in venous blood at tissue level shifts the 02- dissociation and ultimately the 4th stamp will be free automatically.
curve to the right
favouring of O, to the tissues. Thus reduced venous PCO, in the lungs
causes the increase uptake of in (i) Concerted or MWC model: According to this model al the subunits of a particular mol-
O lung and increased venous PC0 in the tissue capillary ccule must be in the "T form or 'R form, hybrids e.g. TR are forbidden and ligands bind with low
causes the increase release of O% in the tissue. This phenomenon in which loading of co, to
blood causes affinity to the T form and with high affinity to the R form. The binding of each ligand increases the
unloading of O2 and vice versa is known as Bohr's effect. probability that all subunits in that molecule are in the R form and thereby affinity of R form to O
a Decreased pH of blood
is increased.
Increased temperature Advantage (physiological significance) of the sigmoid shapeof O, dissociation curve
Increased level of 2.3 diphosphoglycerate (2-3-DPG)-I is a product of glycolysis which
(a) O, dissociation curve has the plateau above 60 mmHg. This flat upper part indicates that even if
competes with O, for the binding sites on the hemoglobin and thus at a given PO, the % age
the PO, increases from 60 mmHg to 300 mmHg, the O, content of the blood will not vary significantly.
saturation of the hemoglobin with O, will be reduced in the presence of 2-3-DPG resulting shift
the effect of O, lack
right. Similarly
mmHg.
on the body will not be manifested until the PO2 goes down below 60
Bohr's effect: Increased PCcO, in venousblood at tissue level shifts the O-dissociation curve
to theright favouring release of O, to the tissues. Thus reduced venous PCO, in the lungs 6) The steep slope of the curve.indicates that the slight decrease of PO, will cause greater release of
0, from hemoglobin.
causes the increase uptake of O, in lung and increased venous PCO2 in the tissue capillary
causes the increased release of O, in the tissue. This phenomenon in which loading of CO, to 5. How does CO, is transported in blood? What is CO dissociation curve?
blood causes unloading of O, and vice versa is known as Bohr's efect. Co, formed by the metabolic activity of the cell is taken up by the blood and transported to the
lungs from where it is expelled out in the air. The CO% transport by the blood is described in following
4. What is O dissociation curve? Why it is sigmoid in shape? What are the advantages of
this shape? headings:
A. The uptake of CO% from the tissues:
0, dissociation curve: Upto a limit the progressive increase of PO2 causes the progressive increase
of percentage of hemoglobin that binds with O, (Fig. 5.2).This is known as oxyhemoglobin dissociation In the arterial blood the PCO, is 40 mmHg and volume of CO% is 48% whereas in the venous blood
curve. the PCO, in 46 mmHg and volume is 52 ml%. Thus 4 ml ($2-48) of cO, is transported from tissues to
Nature of the oxyhemoglobin dissociation curve is sigmoid ie. 'S' lungs by 100 ml of blood due the pressure difference of Co.
shaped. B.Variousforims in which CO, is transported: CO, is transported by the blood in mainly 3 forms
Causeofsigmoid shape ofthecurve: Each molecule of globin consisis of 4 polypeptide chain to each
of which is attached a heme with Fes" which can combine with one molecule of O2. Thus one i) Dissolved form (7%):
hemoglobin .CO diffuses into blood and dissolves in the plasma and water of RBC. In this fom only
can bind wih 4 molecules of O, in
with 0, the other molecules in the
stepwise process. As as
of
soon
the molecules of heme combines
one
0.3 ml of C02 is transported per 100 ml of blood from tissues tolungs.
same globin
molecules acquires a great affinity for O, in steps. So O
 PHYSIOLOGY: MADE EASY 139
38 RESPIRATION

It's volume is 0.3 ml/100ml of blood/100 mmHg PO2.

Powerfull contraction Contraction of extemal Contraction of extemal Contraction of It is known
of diaphragm intercostal muscles of intercostal muscles of accessory muscles The amount of Oz dissolved in blood is directly proportional
to
the PO, of blood. as

lower costal series upper costal series of inspiration

Increase in vertical
diameter of thoracic
cage
Henry's law.
is small in quantity it has utmost importance
Though the amount of O2 transported through plasma
which determines the amount of O, transported by hemoglobin.
as partial pressure of O2 in blood,
Lifts the sternum and
thoracic ribs upward is determined by the dissolved Op
(b) In combination with Hemoglobin (Hb):
Increase in transverse Increase in antero-posterior in stepwise manner as follows to form
diameter of thoracic diameter of thoracic O combines with heme portions of hemoglobin
oxyhemoglobin.
cage cage
() Hb+O = Hb,O2

(i) Hb,O+O =
Hb,0
More increase in intrathoracic volume (ii) Hb,04+O, = Hb,Og

(iv) Hb,O, +0, = Hd,0g

More fall in intrathoracic pressure
is
This oxyhemoglobin is loose and reversible form i.e. in pulmonary capillaries as PO, high O2
More expansion of lungs binds with hemoglobin to form oxyhemoglobin whereas in tissue as PO; is low, the 02 is re-
leased from oxyhemoglobin.
Palv Patm One gram of Hb can combine with 1.34 ml of O2 and at this stage Hb is considered
as 100%

saturated. Thus a person having Hb concentration of 15 mg % the 100 ml of his blood can cary
Air flows to lungs
1.34 x 15 =20 mlof O, at fullsaturation which is known as O carying capacity ofblood.
0, dissociation curve: Upto a limit the progressive increase of PO, causes the progressive increase
FC 5B: Mechanism of forceful inspiration of percentage of hemoglobin that binds with
O2 (Fig. 5.2). This is known as oxyhemo- PCO,
Temperature
globin dissociation curve. H+ conc.
2-3-DPG
Normal
Factors affecting the oxyhemoglobin
Diaphragm Abdominal muscles External intercostal Intemal intercostal Other accessory dissociation curve: Different factors in-
relaxes contract muscles relax muscles relax muscles c
crease the affinity of hemoglobin for O2
inspiration relax
(Fig. 5.2) causing less release of O in tis
PCO
sue and more uptake of O, in lungs which is Temperature
Downward and Forced further downward and inward known as Shift to the left. Similarly some H+conc.
Dome moves Forced dome 2-3-DPG
upward into to move inward movements movements ofribs and stermum other factors decrease the affinity of
thoracic cavity further upward of ribs hemoglobin for O, (Fig. 5.2) causing more
release of O% in tissue which is known a Shift
to the right.
More decrease in thoracic volume i) The factors responsible for shifting
of Oz dissociation curve to the lefi:
More increase in intrapleural pressure
o Decreased PCO, of blood:
More lung compression Decrease in PCO2 of blood causes
the increase in affinity of Hb for PO (mm Hg)
Palv > Patm O, resulting more uptake of O, in Fig. 5.2: O, dissociation curve (a = shift to left and b
lungs and less release of Oz in shift to right)
Airflows out of alveoli tissues.
a Decreased H' concentration in blood or increase pH of blood.
FC 5C: Mechanism of forceful expiration Decreased body temperature
 142 PHYSIOLOGY: MADE EASY
HdoPIFATION 143
Any rise of PCO causes the rise of CO, in dissolved form in plasma which is known as
CO dissociation curve:
Henry's Law.
The total quantity of CO, that combines with blood
(i) In bicarbonate form (70%); depends on PCO2. If total CO, in blood
Torms are plotted against the PCO of blood the curve obtained is called as cO, dissociation curve
in all

Maximum amount of CO (3 ml per 100 ml of blood) is transported from tissues to lungs in g . 5.4).
this form.
The CO2enters in the blood
oftissue capillary and reacts with water to form carbonic acid by
the enzyme Carbonic anhydrase which is rap-
Tissue Plasma RBC
idly ionised to form H and HCO, as follows:
CO+H0= H,CO =H* +HCO,
Dissolved
H' formed in this reaction are buffered by plasma
CO2 CO proteins and hemoglobin leading increased of 3
HCO concentration inside the red cell as com
pared to that in plasma. Therefore HCO," dif-
H_cO fuses from RBC to plasma. As HCO," is a nega
tively charged particles and the RBC membrane
is relatively impermeable to cation the negatively
HCO HCOg+H charged Cl diffuses from plasma to RBC to
HHb maintain electrical neutrality. This phenomenon
CI- is called Chloride Shift or Hamberger phenom-
i
enon (Fig. 5.3). The reversal ofthis reaction oc
HbO curs in blood of pulmonary capillaries i.e. When PCO2 (mmHg)
the blood reaches the alveoli dissociation
O2
ofNaHCO, in the plasma to form Nat and Fig. 5.4: CO, dissociation curve for whole blood
HCO > Bicarbonate moves in RBCto be (A = oxygenated blood, B = deoygenated blood)
econverted back into CO, which is expelled
outCmoves out of RBCto maintain elec Factors afecting COz dissociation curve: The rise of O2 content in blood causes the shift of the CO

Fig. 5.3: Chloride shift

trical neutrality. This reversal of the reaction
that takes place in lung capillaries is known as
reverse chloride shift.
Some ofthe H*, liberated due to dissociation of H,C0, are bound to reduced Hb in the red
cell (i.e. H + Hb02 = HHb +O,) as reduced Hb is beter proton acceptor (less acid) than the
Oxy-hemoglobin. Thus the presence of reduced Hb in the peripheral blood helps in the load-
ing of CO and the oxygenation which occurs in pulmonary capillary helps in the unloading
of CO, in the lungs. Thus an increase in CO2 in the peripheral blood will cause 0, to be
released from oxy-hemoglobin in the tissues and similarly binding of O, with Hb in the lung
capillaries tends to release CO% from the blood in the lung alveoli. This is called Haldane
elffect
(ii) As carbamino compounds (23%):
0.7 ml per 100 ml of blood of CO2 is transported from tissues to lungs.
CO, reacts with amino (NH2) group ofthe proteins i.e. hemoglobin to form carbamino com
pounds in which form it is transported to the lungs.
C. The release of CO, from the blood in the lungs and it's expulsion:
In the lungs the PCO, of venous blood is 46 mmHg and PC0, in alveolor air is 40 mmHg. Due to
this difference of partial pressure of CO;, the CO, diffuses out from the blood into the alveolar air
which is ultinmately expelled out of alveolus again due to pressure difference existing in berween
alveolar air (CO,) and atmospheric air (CO;).
dissociaion curve to the right resulting more release of CO, from Carboxy-hemoglobin.
6. Describethecomponents of respiratory regulatory mechanisms. Describe the nervous
regulation of respiration.
3 basic elements of the respiratory controlling mechanisms
There are as follows:
A. Central controller: The respiratory center is composed of several widely dispersed groups of
neurones mainly located bilaterally in the medulla oblangata (Medullary centers) and pons (Pon
tine centers).
(a) Medullary centers: In the medulla2 groups of neurones are there which are as follows:
(i) Dorsal respiratory group (DRG) neurones: Most of these neurones are located in he dorsal sur
face (within the nucleus of tractus solitarious and some are in adjacent to reticular substance) of
medulla (Fig. 5.5). These neurones normally discharge the repetitive bursts of action potentials
which is weak in the beginning and increases steadily for about 2 seconds followed by abrupt
cessation of the impulse generation for next 3 secs. This type of signal is known as Ramp signal
or Inspiratory ramp. Because of this signal inspiration starts slowly and then reaches peak gradu-
ally followed by abrupt turming off of inspiration resulting quiet expiration.
(ii) Ventral espiratory group (VRG) neurones: The other group of neurones are present in ventrola
teral surface (in nucleus ambiguus and nucleus retroambiguus of the medulla and known as VRG
neurons, Fig. 5.5). These neurones remain inacive during quite breathing (thusquiet
expiration
is entirely due to inactivation of DRG neurones) and play a role only when there is increased pulmo-
nary ventilation. This area contains the neurones responsible for both inspiration and expiration.
 PHYSIOLOGY: MADE EASY HESPIRATION 145
144

of VRG neurones which are responsible for inspirations are I t sends signal to DRG neurones to prevent the 'switch off ofthe inspiratory ramp signal i.e.
Thus the DRG neurones and the part centers whereas the remaining neurones of it prolongs the inspiration. This patterm of respiration is known as apneusis (prolonged
collectively known as neurones inspiratory
or inspi
known as "E' neurones or expiratory ration with short expiralory gasp).
VRG groups which are responsible for expiration are

center.
(ii) Pneumotaxic center
pontine centers which do not generate the basic rhythm of im- I t is located bi'aterally in nucleus parabrachialis ofthe upper pons (Fig. 5.5).
b) Pontine center: There are two
control the rate and depth of the respiration. These centers are: Normally it inhibits the apneustic center and thus controls the "switch off' point of inspiratory
pulse for inspiration but
i ) Apneustic center
ramp, thus controlling the duration of inspiration.
I t is located bilaterally in lower part of pons (Fig. 5.5). When pneumotaxic signal is strong he rate of respiration increases to 30-40 breaths/ min
because of rapid 'switching off' of ramp signals which reduces duration of inspiration and
therefore also expiration.
(c) Suprapontine centers:
Pneumotaxic center
Some neurones located in cerebral cortex, limbic lobe, amygdala, hypothalamus etc. also regu-
late the respiration.
These can cause only temporary breath holding or temporary
vth ventricle
higher centers hyperventilation
B. Sensors: These are excited in response to any change of the environment and the sensation is
carried to the respiratory centers which inturn signals the respiratory muscles to control the respiration.
Vagus and
These sensors are of 2 types as follows:
glosso
pharyngea (a) Central chemoreceptors:
nerve Apneustic center These are believed to be present about 200-400 um below the ventral surface of medulla.
These are surrounded by CSF which is separated from the blood by Blood-Brain Barier which
VAG neurons is impermeable to H' though molecular CO% diffuses across it
DAG neurons easily
These are directly stimulated by increase of H* concentration in medullary interstitial fluid.
When blood PCO rises it diffuses to CSF and forms H* by following
mechanism
CO+H,0 = H,CO = H*+HCO,
The main (70-80%) effect of C0, on respiration is due to it's effect on central chemoreceptor.
of respiratory center (b) Peripheral chemoreceptors:
Fig. 5.5: Organisation
These are situated in carotid and aortic bodies.
The nerve fiber which carries the sensation from
peripheral chemoreceptors to respiratory
center is Carotid sinus nerve or Hering nerve which
DRG neurons Inhibited joins
the glossopharyngeal nervc.
The stimuli which stimulates these receptors are
Pneumotaxic center

Ramp signal- Prolongs PO2 (below 60 mmHg)

T PCO (by 10 mmHg)
Inspiratory motor neurones withdrawal of inhibition
pH (by 0.1 unit)
C. Effectors: The respiratory muscles are the effectors which
of apneustic center
ultimately control the respiration.
Neural Regulation of respiration:
Contraction of Inspiratory muscles The basic rhythm
of respiration (periodic inspiration and expiration) during quiet breathing is
maintained by periodic ramp signal from the DRG neurones. When
ramp signal is on, there is
enlargement of thorax as illustrated in
(Fig. 5.6) and when there is no ramp signal from the DRG neurones, there is inspiration
(Fig. 5.7) due to relaxation of inspiratory muscles. However this basic expiration
centers. During inspiration pneumotaxic centre remains
rhythm is modulated by pontine
inflation of lungs inactivated leading withdrawl of it's inhibitory
cffect on apneustic center which results
prolongation of inspiratory ramp
thus inspiration tries to be prolonged whereas activation of generated by DRG neurones and
Inspiration ramp leads to inhibition of apneustic center and thus
pneumotaxic center during the
peak impiratory
apneustic center switch off the
inspiratory ramp
Fig. 5.6: Inspiration during Quiet breathing resulting expiration. The detail of this mechanism is illustrated with the
help of (Fig. 5.6)
and (Fig. 5.7).
P.M.E.-10
 PHYSIOLOGY: MADE EASY RESPIRATION
146
= 147

Increase in partial pressure

No ramp signal of inspiratory CO, (PI CO,) beyond 0.3 to 4% increases slowly and
from DRG neurons up to 10% rise of Pl CO causes steep rise of ventilation
Pneumotaxic causes no further rise of PV and
(Fig. 5.8). Above I0% rise of PlI CO%
Stimulated center during thereby results CO% narcosis.
peak of inspiratory ramp Mode of regulation: Increase in PCO, in blood
of previous cycle
increases both the rate of and depth of respiration
directly by acting on peripheral chemoreceptors and
indirectly by stimulating central chemore
ceptor through H" as demonstrated by the flow chart of next page.
Inhibition of inspiratory motor neurones b. PO2 on respiration:
Switch off ramp signal
Decrease in PO% in arterial blood up to 60 mmHg do not affect ventilation but further fall of
relaxation of inspiratory muscles (< 60 mmHg) increases pulmonary ventilation if the PCO2 of arterial blood remains PO%
Inhibition of apneustic center constant at
40 mmHg (Fig. 5.9).
compression of thorax
PCO2 = 40 mmHg

elastic reeoil of lung alveoli

Expiration
Fig. 5.7: Expiration during Quiet Breathing

7. Describe the chemical regulation of respiration.

Different chemical factors like PCO2, PO2 and H' alter the normal rate and depth of respiration by
or both chemoreceptors.
modulating different respiratory center either through central or peripheral 100

a. PCO on respiration: PO2

increases the pulmonary ventilation imespective of any change of PO2 or pH Fig. 5.9: Effect of PO% on pulmonary ventilation
or
Increase in PCO,
both in a following manner: Mode of regulation: Any fall of PO2 in blood 60 mmHg results increase in rate and depth of
Increase in partial pressure of alveolar CO, beyond 35 mmHg
increases the pulmonary ventila- respiration only by stimulating peripheral chemoreceptors. The detail mechanism is as follows:
tion (PV) even if alveolar PO2 remains constant (Fig. 5.8). Decrease in partial pressure of oxygen Hypoxia to glomus cell Stimulation of periph-
>
eralchemoreceptors Impulse through vagus and glossopharyngeal > Stimulation of
Inspiratory center > T Inspiration
PIO=159 mmHg c. H* Concentration:
Increase in H' concentration or decrease in
pH due to any cause like respiratory, metabolic and
Palv O, = 104 mmHg Palv O= 100 mmHg renal acidosis results very slow rise of ventilation if the
PCO, and PO2 remains at nornal level
(Fig. 5.10).

PO2

PCO2
20 40 60 80 8% 20%
20 30
Palv CO PaC PICO
A B

Effect of PCO2 respiration (A effect of Palv CO, B Effect of Part. CO2

and C =
effect of
Fig. 5.8:
=
on

Pinspiratory air CO on pulmonary ventilation)

PV if normal 74
partial pressure of arterial CO2 beyond 40 mmHg increases the
even
Increase in H 7.3
alveolar PO, is maintained i.e. 100 mmHg (Fig. 5.8). Fig. 5.10: Effect of pH on respiration

148
T PCO, in blood (> 40 mm Hg)
T Diffusion of CO, to brain
Stimulation of glomus cell of
peripheral chemoreceptors
PHYSIOLOGY MADE EASY RESPIRATION
8. Define hypoxia. Describe the types, causes, signs and symptoms and effects of hypoxia.
Add a note on 0, therapy.
Definition: Lack of O at tissue level is called as hypoxia whereas the complete absence of O in
tissue is termed as anoxia.
Types: It is four types as follows:
medullary tissues (a) Hypoxic or arterial
(b) Anaemic

Impulse through vagus and

glossopharyngeal nervee
C.A.
HO (c) Hypokinetic or stagnant
(d) Histotoxic
H,CO (a) Hypoxic hypoxia:
Definition: The hypoxia in which the PO, of aterial blood is reduced but O, camying capacity
lonises to Ht and HCO3 of blood and rate of blood flow is normal, is termed as hypoxic hypoxia.
20-30%
Causes: The causes / conditions are

Stimulation of central chemoreceptor by H* High altitude

Breathing ofartificial gas mixture with low PO;
Hypoventilation due to any cause e.g. damage ofrespiratory centers by drugs. Poliomyelitis
etc.
70-80%
Diffusion limitation due to loss of surface area ofrespiratory membrane
Inspiratory center Imbalance of ventilation perfusion ratio ratio leading to physiological shunt formation.
Characteristic feature: Vide table 5.a.
(b) Anaemic hypoxia:
Inspiration Definition: The hypoxia resulting due to decreased O2 carrying capacity of the blood with
normal PO2 of arterial blood and normal rate of blood flow is known as anaemic hypoxia.
in H in blood causes rise of inspiratory rate and depth through
Mode of regulation: IncreaseHowever in case of excessive rise of H* in
blood or damage of BBB Causes: Decreased hemoglobin content or altered hemoglobin which is incapable of O2 Car-
peripheral chemoreceptors. riage e.g. CO poisoning, methoemoglobin etc.

TH (pH<74) Characteristic features: Vide table 5.a.

()Stagnanthypoxia:
Definition: The hypoxia due to inadequate rate of blood flow to the tissue with normal PO, of
arterial blood and
Stimulation of peripheral leakage of H+ from
CSF to O camrying capacity of blood is known as stagnant hypoxia.
medulla due to damage of BBB Causes: Circulatory failure,congestivecardiac failure, atherosclerosis or thrombosis
chemoreceptor
Characteristic features: Vide table S.a.
(d) Histotoxic hypoxia:
H* stimulates central
Vagus nerve chemoreceptor Defnition: The decreased ability of tissues themselves to utilize O is called as histotoxic
hypoxia
Causes: occurs due to cyanidepoisoning
Stimulation of inspiratory center
Characteristic features-vide table 5.a.
Signs of hypoxia: These are: Cyanosis (not always), Tachycardia, Tacypnoea and hyperapnoca.
0, therapy: This is the important method to treat hypoxic patient. O therapy can be done by two
Inspiration
procedures eg
interstitium and thus stimulate central i) Inhalation of 100% pure 0, but this procedure has side effects like-
there may be leakage of H° from blood to medullary chart Nasal congestion, sore throat, sneezing,
The detail mechanism is explained by flow coughing, bronchoconstriction due to stimulation of
chemoreceptor to affect inspiration directly. irritant receptors in respiratory tract.
above.
 PHYSIOLOGY : MADE EASY
150 RESPIRATION 151
muscular twitching, dizziness, cog wheel (Jerking) respi-
0,toxicity which is characterised by
ration, convulsion, and unconsciousness. It is basically due to inhibition of tissue enzyme
Trachea
activity and cerebral vasoconstriction. (zero generation)
) Inhalation of 100% pure O, at high barometric pressure (hyperbarie O, therapy) the main
aim of which is to increase the amount of dissolved O, in plasma and thereby helps in all forms of Bronchus
(1st generation)
hypoxic conditions except hypoxic hypoxia. However in early stages there may O, toxicity.
be

Table 5.a: Characteristic features of different hypoxia Lobar bronchus

(2nd generation)
Parameters Hypoxie Anemic Histotoxic Stagnant
1. Arterial PO N N N
-Segmental bronchus
2. Alveolar PO N N N (3rd generation)
N N
3. Arterial 0, content
4. Hb content N N N

S. Rate of blood flow N N N

6. Cyanosis present absent present absent Terminal bronchus
(16th generaton)
7. Stim of peripheral
Yes No Yes Yes
chemoreceptors
8.A-V O, difference N
= decrease. T = increase, N = Normal Respiratory bronchiole
(17-22nd generation)

B. Short Notes: Alveolar duc

1. Weibel's lung model: Trachea divides into 2 Bronchi-left and right each of which ultimately Alveolus (23rd generation)
trachea
divides into 6x 10 terminal bronchioles (Fig. 5.11). As per Weibel's lung model, between the
and the alveolar sac, the air passage is divided into 23 times in which the itrachea is numbered 'zero
and alveolar sac is 23rd generation. Fig. 5.11: Weibel's lung model
generation, terminal bronchioles are 16th generation
which diffusion of O2 and
2. Respiratory membrane: The alveolar-capillary membrane through
is known as respiraltory membrane. It is basically formed by
the epithelium of the
CO takes place
The different layers of respira-
respiratory unit and endothelium of pulmonary capillaries (Fig. S.12).
follows:
Lory membrane from inside to outside are as

of fluid lining the alveolus including surfactant. Blood

() A layer
(1i) Alveolar epithelial cell layer.
(i) Basement membrane of alveolar epithelial cell layer.
and capillary basement membrane.
(iv) Interstitial space between alveolar epithelium
(v) Capillary basement membrane
(vi) Capillary endothelial cell layer.
0.6 u and total surface area is 70 M
The overall thickness of respiratory membrane is on an average
is 60-140 ml/cycle. So this small
in normal adult and total quantity of blood in the lung capillaries Alr
surface which increases the rapidity of diffusion.
amount of blood spreads over the entire lung

3. Non respiratory functions of lungs: These are mainly mediated by respiratory tract.

A. Defense mechanism:
in air are eliminated by different parts of the tract
(a) Filtering effect: Different dust particles present
Fig. 5.12: Alveolar capillary membrane ( = capillary endothelium layer. 2 = Basement membrane of capillary
e.g hairs of nostrils endothelum, 3 = Basement membrane of alveolar epithelium an 4 = alveolar epithelium)
Large dust particles by
 153
PHYSIOLOGY: MAoE EASY Rr SPIRATION

Particles up to 6 um diameter by 'turbulent precipitation' due to zigzag passage of nasal cavity Normal values: Intra-alveolar pressure
Parameters Intrapleural pressure(mmHg)
and particles' own momentum.
-5 to - 10 -2 to - 4
in the smaller bronchioles. Normal Inspiration
Particles between 1-5 m diameter by gravitationalprecipitations -2 to -5 6 to+ 10
Normal expiration
diffuse into alveoli and adhere to the wall of alveoli however - 40 to - 50
Particles diameter I um or less
of
-

Forced Inspiration -40

less than 0.5 um (¢.g. cigarette smoke) are usually expired out (2/3 of 10 to + 40
particles having diameter
<
Forced expiration with 50
total volume). closed glottis
(b) Protective function: is negative or subatmospheric
in the subcutaneous coat of tracheal wall. Why the intrapleural pressure is negative? Intrapleural pressure
i) By trachea: There are plenty of sero-mucous glands due to 2 opposing forces:
with goblet cells trap dust in the inspired air. Then the ciliary move
These mucous glands along and surface tension in the alveoli.
and bacteria towards mouth at a i) The lung tries to collapse because of it's elasticity
ment (20 times/min.) drives out the entrapped foreign particles
(i) The chest wall always tries to expand.
velocity of 24 mm/min. them resulting a suction
comes in alveoli are destroyed by the phagocytic Thus the pleural layers becomes subjected to a force that tries to separate
(ii) By alveoli: The dust particles which escape and pressure or negative pressure.
action of the macrophages present in the wall of alveoli.
tract initiates some protective reflex like cough reflex The circumstances in which ip becomes positive?
(ii) By initiating some reflexes: Respiratory (Valsalva maneuvere) e.g. during
and sneeze reflex keep
to the air passage free from foreign materials. (i) When expiratory muscles are working against closed glottis
defaecation, coughing, lifting a heavy object.
B. Air conditioning efect: The inspired air is brought to about body temperature and is humidified
to the exterior i.e. pneumothrox
before it's entrance in lungs by the help of moist linning of serous glands (i1) Injury of the chest causing exposure of pleural cavity
e.g. serous fluid (Hydro thorax)
or
(ii) Collection of fluid in the pleuralcavity (Pleural effusion)
C. Excretory function: It is also responsible for excretion of CO2, water vapor and certain volatile formation collection of fluid stained with blood (haemothorax).
pus (pyothorax) or
substance e.g. acetone.
in maintaining acid Significance of intrapleural pressure: It has 2 important significance:
D. Maintenance of pH of the body fluids: Lungs play an important role, caused by elastic recoil of lung tissues.
in the tissues comes in blood to () As it is normally negative it prevents the collapse of lungs
base balance by regulating the CO^ content of blood. CO, produced and exercise (respiratory
in lungs. These volatile CO^ is blown out by (ii) It is responsible for the increased venous retum during inspiration
form bicarbonate which inturn forms CO; again of Increase in negativity
pumps) as-During inspiration increase of negativity intrapleural pressure
ventilation.
of mediastinal pressure expansion veins and vena cava > Decrease of pressure in them
of larger
E. Metabolic function: These are mainly performed by the lungs - The functions are
extrathoracic region > Increase in venous retum Increase in
Sucking into these veins from
of blood
(a) formation of lung surfactant cardiac output.
(ACE) present
b) conversion of angiotensin I to angiotensin -II by the angiotensin converting enzyme 5. Airways resistance: The resistance caused by friction of gas molecules between moving column
in capillary endothelium of respiratory membrane.
of air and respiratory passages through which air pass to alveoli is known as airways resistance. It is
c) secretion of immuoglobulins gA) due to turbulent flow of air.
(d) synthesis of some homonal substances like prostaglandins, serotonin and bradykinin etc. Factors affecting airways resistance:
F. Anticoagulant function: () Cross sectional area of airways: Airway resistance is inversely related with cross sectional area
prevents the in or diameter of the respiratory passages.
Lung contains the mast cells. which secrete heparin. Heparin, anticoagulant,
an
rises and
travascular clotting. i) Phases of respiration: During inspiration the intrapleural and mediastinal negativity
as a result the bronichial diameter increases. Reverse occurs during expiration. Therefore resistance to
G. Acts as left ventricular reservoir due to high compliance of pulmonary vessels.
airflow is nornmally low in inspiration and high in expiration. This is why in bronchial asthma inspiration
in bronchial
4. Intrapleural or intra thoracie pressure: may not be difficult but expiration becomes difficult. This explains why the "Whezze"
Definition: The lungs are covered by.thin serous membrane calledpleural membrane.of the chest
pleu-
The asthma is heard during expiration but not in inspiration.
the walls (li) Tone of bronchial muscles: Various factors can alter the tone of bronchial muscles and thereby
ral membrane is reflected from the root of each lung on the inner surface of
is called
cavity and upper surface of the diaphragm. The membrane covering lung two visceral
the airway resistance. For example:
pleura and the thoracic wall and diaphragm is called the parietal pleura.These layers thus B adrenergic stimulation decrease in tone in bronchial muscle > increase in diameter of
contains a thin
form a closed membrane sac on each site of the chest called pleural cavity which bronchioles decrease in airways resistance.
film of serous fluid that acts as a lubricant and helps the surface to glide over one another during Histamin, PG, Ca2* Channel blockers etc. bronchospasm decrease in diameter ofairways
respiratory movement. The pressure existing in the pleural cavity
in known as intrapleural pres- increase in airways resistance.
sure ip).
 154 HYSIOLOGY : MaDE EASsv ResPIRATION 155

(iv) Types of airflow: (b) Inspiratory reserve volume (IRV): lt is the maximum volume of air that can be breathed in
High resistance during turbulent flow (during rapid breathing). (over and above the tidal volume (Fig. 5.13) after normal
Low resistance during laminar flow (during quiet breathing). normal adult male.
inspiration. Normal value: 2000-3300 ml in
() Rate of gas fMow: 1t is directly related with resistance i.e. the greater the rate, the greater is the
resistance. Resistance offered by intermediate size bronchioles is highest because of it's velocity. Maximal inspiratory level

(VI) Density of inspired air: Directly related with airways resistance.

6. Pleural effusion:
Itis the collection of fluid in the pleural cavity due to Tuberculosis infection, Blockade of lymphatics,
Heart diseases. Hypoprote inaemia etc.
Resting end inspiratory
Significant pleural effusion limits lung expansion and thus decreases gas exchange. level
7. Pneumonia:
I t is the condition in which there is collection
of fluid and blood cells in the alveoli and consoli-
dation of lungs because of porus alveolar cappillary membrane due to Resting end expiratory
pneumococcal infection. level
l t is a type of obstructive disease of lungs.
8. Emphysema: Maximal expiratory level
l t is thedegenerative dìsease in which there is permanent destruction of air spaces distal to temi-
nal bronchioles due to destruction of alveolar
septa.
I n this disease it is much easy to inflate lung i.e. the static
recoil of lungs is less due to which getting air out of lung is
lung compliance is higher but the elast Not detemined by spirometry
severely impaired. Therefore residual Fig. 5.13: Graphical representation of lung volume and capacities
volume becomes abnormally high.
This is
characterisedby: ()Expiratory reserve volume (ERV): k is the extra amount of air that can be breathed out by
More physiological dead space maximum expiratory effort after normal expiration (Fig. 5.13). Normal value: 1100 ml in normal adult
Inadequate alveolar ventilation male.
Hypercapnoea in late stage (d) Residual volume: It is the amount of air that remains in the lungs even after maximum expiratory
Barrel shaped chest effort. Normal value: 1200 ml in normal adult male.
B. Static lung capacity: Lung capacity is defined as the sum total of two or more lang volumes.
Puimonary oedema
There are 4 static lung capacities:
E
Difficulty in breathing
Enlargement of right side of heart (Cor-pulmonale) (a) Inspiratory capacity (IC): It is the maximum volume of air that can be breathed in from end
expiratory position. It is calculated as IC = TV +IRV. Normal value: 3500 ml.
9. Bronchial asthma:
(b) Expiratory capacity (EC): It is the maximum volume of air that can be breathed out from end
l t is a paroxysmal episodic disorderat times with the attack commencing and ending abruptly and inspiratory position (Fig. 5.13).This is calculated as: EC = TV +ERV. Normal value: 1600 ml.
may become a chronic disorder.
(c) Functional residual capacity (FRC):
characterized by wheezing, feeling
Itis
to brocho-constriction.
oftightess in the chest and difficulty to expire resulted due I t is the volume of air remaining in the lungs after quiet expiration (Fig. 5.14). It is calculated as:
FRC= RV + ERV
It is due to:
inflammation ofair passage releases various chemicals that cause bronchospasm.
Normal value: 2200m
I t cannot be measured directly by spirometry but by another 3 techniqnes: (i) N, wash out
hypersensitive reactions affecting the tracheo-bronchial tree. techninqne. (Gi) Body plethysmograph technique. (ii) Helium dilution technique.
pulmonary oedema in left ventricular failure which is known as cardiac asthma. The significance of FRC isthat it helps the continuous exchange of gases even during expiration
In this case lung function is reduced drastically during the atlack and otherwise remains normal. and thus concentration of O, and CO% in blood are maintained constant.
10. Static lung volume and capacities: Lung volumes are defined as the fraction or subdivision of I t is increased in old age, emphysema, asthma and atelectasis.
Jung capacities. (d) Vital Capacity (VC): It is the volume of air that can be breathed out by maximal expiratory
A. There are 4 static lung volumes: effort after maximal inspiration.
(a) Tidal volume (TV): I is the volume of air that can be breathed in or out during normal quiet I t is calculated as IC+ ERV
breathing (Fig. 5.13). Normal value: 500-800 ml in normal adult. Normal value-4500 ml
 PHYSIOLOGY MaDE EASY RESPIRATION
156
related with VC.
muscles: It is directly
O Strength of the respiratory VC is decreased as growing foetus push the diaphragm
to-

(e) Total lung capacity: During pregnancy

hold after a maximum possible inspiration. O Pregnancy: causing less expansion
of thorax.
I t is the volume
of air that lung
can
wards cavity
thoracic
fibrosis, emphysema, pul-
be calculated as TLC =IC+
FRC.
During different lung diseases like poliomyelitis.
I t can a Pathological: reduction of VC.
Normal value = 5700 ml. ascites etc. there is significant
monary oedema, pneumothorax, the subjects to expire maximally
is directly measured by Spirometry by asking
11. Lung surfactant: Measurement: It after taking maximum inspiration
from air.
a mixture of lipoprotein and phospholipids
The type-lI pneumocytes of lung normally produces through the mouthpiece of the Spirometer
tension of the pleural fluid in lungs to oppose the collapsing tendency of lungs per unit change of pressure.
which reduces the surface 13. Lung compliance: It is the volume of expansion
the which is known as lung surfactant.
of lungs
Chemically it is mainly (62%) dipalmitoyl
lecithin (DPL) along with other phospholipids and Normal values: intra-alveolar pressure changes:
neutral lipids.
(i) Compliance in relation to
34 weeks of pregnancy and completed by about 90% in Lungs along-220 ml/cm of HO
Synthesis of lung surfactant starts at about
between 38-40 weeks. Therefore in case of prematurely borm babies due to inadequate surfactant - Lungs and thorax-130 ml/cm of H,O
synthesis lung collapse is the 'major cause of death. (ii) Compliance in relation to intrapleural pressure changes:
in
I n case of hyalin membrane disease of new born also this surfactant is low resulting difficulty - Lungs alone-200 ml/cm of H,O
the refuse expand due to high surface tension. This is why the baby suffers
inspiration as lung to
Lungs and thorax-100 ml/cm of H,0
of new born.
from respiratory distress which is known as Respiratory distress syndrome (RDS)
Surfactant has following function: Variations:
abscess and
prevents lung collapse. Reduction of lung complianceIn restrictive lung disease e.g. tuberculosis, lung
helps edema in the
in preventing lungs by decreasing the interstitial pressure in lungs. respiratory distress syndrome.
decreases the work of breathing so it becomes easier. Increase of lungs compliance-In chronic obstructive lung disease e.g. emphysema.

IgA and apoproteins of surfactants provide innate immunity. Factorsinfluencingcompliance:

in smaller 1. Elasticity oflungs:It is inversely related with lung compliance i.e. decrease in elasticity of lungs
promotes the
alveoli.
alveolarstability by lowering surface tension proportionately more

causes increase in compliance e.g. emphysema:

Surfactant production is stimulated by vagal stimulation, thyroid hormones, glucocorticoids, in-
sulin. growh hormone whereas it is inhibited by hypoxia, smoking and pure O, breathing.
2. Surface tension within alveoli: Thealveoli con-
tains a very thin film of fluid lining at their in-
12. Vital capacity: ner side. The individual molecules of this thin
Itis the volume of airthat can be breathed out by maximal expiratory effort after maximal inspi- fluid attracts each other because of surface ten- P 2T/R
ration. sion and the resultant effect is collapsing of

I t is calculated as IC + ERV. lungs (Fig. S.14). Thus surface tension is also

Normal value 4500 ml inversely related with lung compliance.
Significance: It gives the information about 3. Interdependence: When a few alveoli start to
the neighbouring alveoli also begin to
the strength of the respiratory muscles collapse
be pulled because of their strong anatomical
the pulmonary functions through FEV1
Factors affecting VC: The important factors that influence the vital capacity are: connection. This results the pulling of the walls
of the collapsing alveoli due to Newton's 3d
Physiological: law of motion and thus their
O Sex: Vital capacity is normally more in male due to: collapse is opposed.
This is called interdependence.
increase in chest size
4. Chest wall factors: Various diseases
increase in muscle power (e.g. ky- Fig. 5.14: Diagrammatic representation
increase in body surface area phoscoliosis, ankylosing spondilitis) can cause showing surface tension of alveoli (P = Pressure
O Body build; It is
higher in tall and thin persons than in short and obese persons.
immobility of chest wall and thereby result re and T Tension)
duction in compliance.
a Posture: It is more in standing position than in lying position because in lying position
abdominal contents push the
diaphragm upward i.e. towards the thoracic cavity, 14. Ventilation perfusion ratio:
causing
lesser expansion of thorax. The ventilation perfusion ratio is defined as the ratio of alveolar
ventilation and the amount of
blood that perfuses the alveoli / min.
158 PHYSIOLOGY MADE EASY RESPIRATION 159

The gaseous exchange is maximum at the normal VA/Q ratio of 0.84. Any increase or decrease in
ratio decreases the diffusion of gases through the membrane due to imbalance between alveolar
ventilation and alveolar blood flow

Notmal Alveolar ventilation4200

value Pulmonary blood flow
ml/mina0.84
5000 ml/ min Y
l t is high in the apes of lungs and low in the baseof the lungs.
Due to regional variations of ventilation perfusion tuberculosis occurs more commonly in the
apex because of favourable environment for mycobacterium tuberculosis.
Decrease in ventilaion perfusion results fall of alveolar PO and rise of alveolar PCO, and vice
vers.

15. Diffusion capacity: Fig. 5.15: Graphical representation of timed vital capacity
l t is the volume of gas that diffuses through the respiratory membrane per min. per mm Hg pres
sure difference. Fractions of FEV:
I t is directly related with diffusion of gases i.e. the greater the diffusion capacity the more is the Normally to expire the total amount ofair that was inspired it takes 3 seconds out of which the
diffusion of gases. amount of air that is expired in Ist second is known as FEV, and in2 sec is known as FEV,
l t depends on three factors as per following formula: and in 3 sec is known as
FEV3
Diffusion Capacity = ATxD The normal values it FEV,, FEV2 and FEV, are:

Where A =totalsurface area, T= thickness, D = Difusion coeffcient O FEV = 75% to 85% of vital capacity
(a) Total surface area of respiratory membrane: Rate of diffusion of gases is directly propor- o FEV2= upto 94% of VC

tional to the surface area i.e. with decrease in surface area as occurs in bacterial infection like O FEV = upto 97% VC.

TB. the rate of diffusion of gases decreases. Significance: The FEV, is useful to differenciate the restrictive type lung disease from the ob-

membrane: Rate of diffusion is inversely related with the thick structive type of lungs disease as follows:
(b) Thickness of the respiratory
ness of the membrane. So any thickening of the respiratory membrane due to pulmonary edema I n obstructive lungs disease: FEV, =< 75% to 85% (normally about 40%) but VC = normal
or lung fibrosis results decrease in rate of diffusion of gases. I n restrictivelung disease: FEV, = almost normal but VC is reduced.

(C) Difrusion coefficient: The rate of diffusion is directly proportional to the diffusion coefficient 17. Physiological shunt:
which intum depends on (D a S/N Molecular weight of gases): In some alveoli ventilation is more and alveolar blood flow is less. Available 0, therefore is not
Solubiliry gases-directly related with diffusion coefficient.
of the
Molecular weight of the gases-inversely related with the root of it's MW
transported due to lack of blood flow. So ventilation is wasted. This means that:
(a) all of the blood coming to the alveolus is net oxygenated. This unoxygenated portion of blood is
Thus the solubility and MW of a gas influences the diffusion capacity of a gas by affecting
called shunted blood.
diffusion coefficient. The solubility of CO% is 25 times higher than that of O, but it's MW is (b) also some additional blood flows through the bronchial vessels which is also unoxygenated. The
is about 20 times greater
slightly greater than that of O2. The net result is-diffusibility of CO, total quantity (a + b) of blood per min is called physiological shunt
how a smaller pressure difference compared to O, the rate
despite
than that ofO2. This explains
of CO, diffusion is enough.
In chronic obstructive lung diseases (COLD) some areas
have serious physiological shunt and
some other are serious physiological dead space. So gas exchange in the lungs is severely effected
The diffusion capacity for O under resting condition in young male adult is 21 ml/min/mm Hg
leading to pulmonary disábility. COLD is the most common cause of puimonary disability.
ml/min/mmHg during exercise due to:
which is increased up to 65
surface area of respiratory membrane 18. Dead space air:
opening ofsome previously dormant capillaries>T The amount of the air present in respiratory system which do not take part in gaseous exchange
better perfusion i.e. increase in ventilation-perfusion rañio (VA/Q).
process and thus becomes a wastage is known as Total Dead space, or Physiological dead space air.
It is
16. Forced expiratory volume or forced expiratory vital capacity (FVC) or timed vital constituted by two types of dead space air.
capacity: (i) Anatomical dead space air:
Definition: The volume of air that can be expired forcibly after a maximum inspiration in a given available
The amount of air which is confined in he respiratory passages and thereby are not
unit of time is called FEV or FVC. tor gaseous exchange process is known as anatomical dead space air.
and is then
Recording and measurement: The person is first asked to take maximum inspiraion Normal value: 150 ml
asked to expire in the Spirometer with maximum expiratory effort as rapidly and as completely
as
I t can be measured by N, Washout technique
fast drum.
possible. The record is obtained (Fig. 5.15) on a moving
160 PHYsIOLOGY MADE EAsY RESPIRATION 161

(ii) Alveolar dead space air: 2. Non myelinated C fibers( receptors described by Prof. AS Paintal-present between the alveolar
In normal subjects all ofthe alveoli are not equally perfused. The apical alveoli are adequatcly wall and the capillaries and are stimulated by accumulationof Nuid betweenthe capillary and alveolus in
ventilated but due to poor blood supply most of the ventilation in these alveoli is wasted. This condition like exercise. pulmonary edema etc and cause hyperapnoea and dyspnoea.
amount of air which is not utilized from the alveoli are called alveolar dead space air. 3. Muscle spindle of inspiratory muscles (chest wall proprioceptors)-adjust respiration against high
I t can be measured as per the basis of Bohr's equation as follows: airway resistance and maintain tidal volume.
in expiratory air) 4. Pain receptors-sudden painful stimulus produces a reflex apnoea but sustained painful stimuli
ADS=EXpiratory air volume(PCO,in alveolar air PCO, cause faster and deeper respiration.
PCO, in alveolar air
5. Thermoreceptors also have role in controlling respiration. Sudden cold stimuli results reflex ap-
Physiological dead space air = Anatomical dead space air + alveolar dead space air.
noea and warm stimuli results increase in breathing and ventilation
19. 0, carring capacity: 6. Baroreceptors-sudden stimulation of baroreceptors inhibit respiration center to cause apnoea.
One gram of Hb can combine with 1.34 ml of O, and at this stage Hb is considered as 100% satu-
rated. Thus a person having Hb concentration of 1Smg % the 100 ml of his blood can carry 1.34 x 15-20 24. J-reflex: J receptors:
ml of O, at full saturation which is known as O, carrying capacity of blood. a It is believed to be present in the alveolar walls close to the capillaries (Juxta position to the
capillaries, hence the name J' receptors) as described by Prof. A S Paintal.
20. Pulmonary ventilation Vs Alveolar ventilation:
stimuli are engorgement of pulmonary capillary andincreasein interstitial fluid volume of pulmo.
As it is known that pulmonary ventilation is the total ventilation per minute i.e. RMV=TVx RR, the
value of which is 6-7 lit. But in reality some amount of air (150 ml) is confined in the respiratory
nary tissue (pulmonary oedema)
passages and thus not available for gas exchange process. So the actual ventilation is less than pulmonary stimulation of these receptors causes hyper ventilation (during exercise) and dyspnoea (during
ventilation. This amount of ventilationis known as alveolar ventilation. It can be calculated as: left heart failure. pneumonia, etc.)
Alveolar Ventilation = (TV-dead space volume) x
RR 25. CO narcosis:
= (500-150) ml x 14/min Increase in alveolar PCO, has almost a linear relationship with increase in ventilation but
4.9 li/min. of atmospheric air is too high (CO, content of inspiratory air is more than
when CO content
21. Pso 7%) then PC0, of alveolar air and arterial blood increase abruptly. This results ineffective
I t is the level ofPO2 at which 50% of the hemoglobin is saturated with O2.
elimination of CO,
CO narcosis.
from body
and thus accumulation of in the blood which is known
CO, as

I t assesses the binding affinity ofhemoglobin for O2. It

I n adults at sea level the normal Pso is at PO2 of 27 mmHg.
results CNS depression.
I t is characterised by headache, mental confusion and ullimately coma.
I f the Pso is high it signifies the decrease in affinity of hemoglobin for Og which is seen during
26. Kussmaul breathing:
shiftüing of 0, dissociation curve to right and vice versa.
22. During some clinical conditions like diabetic ketoacidosis there is rapid and deep breathing
Pulmonary stretch receptors: eliminating CO2 and bicarbonate. This type of rapid and shallow breathing is known as Kussmaul
These are slowly adapting myelinated nerves present in the wall ofsmall airways.
These are responsible for initiation
breathing.
of Hering-Breuerreflex
These receplors are activated only when the tidal volume exceeds 1000 ml and thus have no role 27. Breath holding time:
in initiating Hering-Breuer reflex during quiet breathing, theugh these cause bronchodilatation Breathing can be inhibited for a period of 45-60 secs in normal healthy human beings voluntarily.
and rise in respiration rate during exercise through initiating Hering-Breuer retlex. This duration is known as breath
holding time (BHT). The point at which the breathing can no
These are responsible for maintaining the basic respiratory rhythm and prevent overstretching of longer be stopped voluntarily is known as breaking point.
the lungs in the newbom and infants BHT depends on-

23. Non chemical stimuli stimulating respiratory center: phase of respiration during which breathing is arrested.
Though the chemoreceptors are mainly responsible for regulating respiration, there are some re- composition of air breathed-breathing with pure O prolongs the BHT.
flexes arising from upper airways and lungs initiated by non-chemical stimuli and other receptors from rate
of respiration before breath holding.
the other parts of the body which provide a feedback for fine tunning of breathing and also protect the 28. Periodic breathing:
ungs from environmental hazards. These are:
A. Definition: It is the
Pulmonary stretch receptors which are sensitive to change in lung voiume.When stimulated they repeated sequence of apnoea followed by normal respiration.
inhibit inspiration and prolong expiration which is known as Hering -Breuer reflex.
B. Types: It is of two types:
(a) Cheyne-Stokes breathing:

P.M.E-II
 PHYSIOLOGY MADE EASY RESPIRATION
162 163

I is defined as the repeated sequence of gradual onset of apnoea

followed by gradual restora- Mechanism: It is illustrated by following flow chart:
tion of normal respiration (Fig. 5.16).
Foreign particles larynx bifurcation
at or of trachea -> physical or chemical irritation stimulation
ofvagalafferents > sensation to medulla through vagus- deep inspiration is initiated epiglotis,

laryngeal opening get closed entrapping

and internal intercostal mus
2.5 lit ofair into lungs forcible contraction of abdominal
increased intra alveolar pressure- sudden opening of glottis and
vocal card Iungaircomes out at a velocity of l60 km/hour particles are thrown out ofrespiratory
passages.

30. Mountain sickness: It is generally two types

1. Acute mountain sickness:
Ifa person who resides in sea level ascends to high altitude (>10,000 ft above sea level) he devel-
ops the sign and symptoms due to hypoxic hypoxia which are collectively called as high altitude
sickness or Acute mountain sickness.
I t is characterised by:
(a) starts 8-12 hrs after arrival in high alitude
(b) lasts for about 4-8 days
Fig. 5.16: Breathing pattem during different types of abnormal ventilation
(A = Normal breathing. 8 = Hyperventilation. C= Chyene Stoke's breathing and D = Biot's breathing) (c) sign and symptoms: headache, fatigue, nausea, vomiting, loss of appetite, dyspnoea, palpita-
tion, sleep disturbances, insomnia etc. In some cases there may be even cerebral or pulmonary
Causes oedema.
Physiological: Treatment: (a) The person should immediately brought to low level (b) 0, administration.
Voluntary hyperventilation 2. Chronie mountain sickness (Monge's disease): It is the disease occuring in case of failure of
a High altitude long-term acclimatization process to the residents of high altitude. The signs and symptoms
o Sometimes during sleep in infants are:

Pathological: extreme polycythemia

O Heart failure (Chronic) T viscosity of blood- fall of blood f
o Uremia T BP

Brain damage cyanosis, fatigue, exercise intolerance

(b) Bior's breathing: pulmonary oedema.
followed by abrupt onset of
I t is the sequence of 3-4 cycles of nomal respiration
repeated 31. Acclimatization at high altitude (to low landers):
further followed by abrupt onset of normal respiration (Fig. 5.16). The acclimatization refers to the
apnoea compensatory changes in the body to overcome the effect of hypoxic
I t differs from Chyene-Stokes breathing in that- hypoxia in response to slow ascent in high altitude and/or long term exposure to hypoxia. These
al iregular intervals.
compensatory changes are:
it occurs a. Respiratory adjustments:
there is no waxing and waning of tidal volume during the period of respiratory activity
0 Increase in pulmonary ventilation by 5-6 times primarily due to increase in tidal volume which
i t can neverbe physiological.
mayincreaseto50%of vital capacity due to hypoxic stimulation of peripheral chemoreceptors ie. high
Causes: altitude (low barometric pressure) > hypoxia > stimulation of peripheral
chemoreceptorsTrespir-
Meningitis tion T pulmonary ventilation.

Medullary diseases (Brain) (i) Increase in diffusion capacity of lungs due to:
expansion and dilatation of pulmonary capillaries
29. Cough reflex:
increasein lung volume
materials.
Respiratory uract initiates some protective reflex to keep the air passage free from foreign increasein blood volume
One of these reflexes is Cough reflex. Any physical or chemicaliitation in the respiratory tract spe-
increase in perfusion in apical part of alveoli
cially at the larynx and bifurcation of trachea causes the deep inspiration followed by forceful expiration increase in pulmonary arterial pressure
resulting elimination of that particles at a great velocity. This is known as coughing.
 165
PHYSIOLoGY MADE EASY RESPIRATION
164 = - =

characterised by shortness of breathing

(i) Shifting of O-dissociation curve to right
due to increase 2-3 DPG concentration which favours Bubble formation in lung vessels results into 'chokes
and pulmonary oedema.
unloading of O, in tissue.
(iv) Increase in maximum breathing capacity. Treatment: Immediate recompression in a chamberand gradual decompression.
Prevention of decompression sickness: It can be prevented by:
b. Cardio-vascular adjustments: These include:
() hypertrophy of right heart due to more work. ) Gradualascent from sea.
it
(i) dilatation of blood capillaries to
accommodate extra blood.
i iInhalation of O-helium mixture before the ascent. However at high atmospheric pressure
which is characterised by tremors,
to sympathetic stimulation T cardiac produce high pressure nervous syndrome (NPNS)
(i) Increase in heart rate and force of contraction due
» can
drowsiness and depression of a activity in EEG.
output.
careless
of vasomotor center
by hypoxia Mild N narcosis resembles alcohole intoxication and the person becomes very jovial.
(iv) Rise or fall of B.P.--vasoconstriction occurs duc to stimulation and fails to understand the seriousness of the situation. In severe cases the person develops lethergy.
of these two forces
but is opposed by vasodilatation produced by local effects of hypoxia. The resultant
determines the outcome. The BP is also raised due to polycythemia in high altitude. drowsiness, rapid onset of fatigue and loss of consciousness.
c. Hematological adjustments: These include: 34. N, narcosis: See the answer of Caissons disease.
i) Increase in RBC count.
35. Artificial respiration:
(ii) T Blood volume up to 20-30%.
A. Aim of artificial respiration: These are
(iii) Increase in 2-3 DPG concentration in RBC.
a. avoiding asphyxia to brain
d. Cellular changes:
b. oxygenation of body tissue
(i) Increase in number of mitochondria

(i) Increase in concentration of cellular oxidative enzymes. c. ventilation of lung

d. stimulation of spontaneous breathing
32. Acclimatization to Natives (high lander):
B. The conditions when it is indicated?
The acclimatization that occurs in the residents who are residing in the high altitude permanently for Artificial respiration is given to the subject in case of following conditions e.g.
generations after generations, are as follows:
ratio of ventilatory capacity to body (a) Acute respiratory failure due to
(a) short body stature and large sized chest that results high
mass
-
overdose of anesthetic agent
(b) hypertrophy of right heart -CO poisoning
(c) polycythemia Drowning
(d) shifting of O, dissociation curve to right - Electric shock

(e) increase in size of carotid bodies. Hanging

33. Caissons disease: Intake of narcotic drugs
When the diver is working in the deep sea for a long time he is exposed to high alveolar gas -Resuscitation of new bom
pressure (high barometricpressurei.e. hyperbarism) to prevent the collapse of the lungs. The gas (b) Chronic respiratory failure due to
mixture administered to him contains 02, CO% and N, with high pressure, Because of these a large
- Diphtheria
amount of N, is dissolved in his body fluids and fats. Sudden exposure of that diver to low baro-
- Poliomyelitis
metric pressure at sea levelcausestheformation of N, bubblesinbodyfluids and faty, tissues that
- Ascending paralysis
may block capilaries, heartsandalsoaffectnervoussystem badly. This resultsthe development
of some signs and symptoms which are collectively known as Decampression.SicknessorCais C. Methods of artificial respiration: It is of 2 ypes Manual and Mechanical
son diseaseor Dysbarism orDiverkpalsy. So this disease is basically due to effect ofN with (a) Manual:
high pressure known as N2 narcosis.

Signs and symptoms:

-Mouth to
mouthbreathing
- Holger Neilson's Arm lift back pressure (ALBP) or BPAL method
Pain in joints, måscles of legs and arms. Bends Other methods like Schafer's prone pressure method,
-

Sylvester's method, Drinker's method.

Dizziness, paralysis, collapse, unconsciousness, temporary sensory andmotordisturbances (if (b) Mechanical: use of respiratory pump.
nervous system is affected).
 166 PHYSIOLOGY : MADE EASY RESPIRATION 167

D. How long artificial respiration is to be continued? 1t should be continued untill t is characterised as nausea, diziness, irrilability, disturbed vision. disorientation and convul
(i) The subject's own spontaneous respiration reappears. sions.

(11) The subject is hospitalised and appropriate treatment is started. I t also begins to appear at 10 atm pressure of room air after more than 30 sec.
the
36. Resuscitation of new born: Towhich
prevent ill-effect of O, toxicity gas mixtures of O-helium is inhaled at high pressure in
O concentration is reduced at about 20.
This is done to expand the lungs of newbom in case of premature birth of the child in which lungs
is collapsed due to high surface tension which is not minimised because of lack of lung surfactant. 40. Cyanosis:
Definition: Bluish colouration ofskin and or mucous membrane due to presence of at least 5 gm%
Methods followed: of reduced Hb/100 ml of blood in capillaries is termed as cyanosis.
Cutaneous stimulation e.g. slapping. warm or cold water application
Site: Common site of occurrence are - Mucous membrane of undersurface of tongue, Lips, Nail
-Mouthto mouth breathing bed and Tip of nose.
ETI (endo-racheal tube insertion) and insufnation of lungs with CO-O2 mixture Causes: The causes are:
Artilicial respiration should be continued until the subjectdevelops normal rhythmic respiration. (a) Hypoxic hypoxia-Cyanosis results due to increased formation of reduced hemoglobin as
37. VO2 max: arterial PO2 is decreased.

During resting condition the O, consumption by the whole body is about 250 ml/min which is b) Stagnant hypoxia--During this state there is decrease in rate of blood flow-T rate ofextrac
increased up to 15-20 times during maximal exercise. The maximum amount of O2 that can be tion of O2 by tissuesT formation of reduced Hb which leads to cyanosis.
consumed by an individual is called as maximal O2 consumption or VO, max. (c) In anaemic hypoxia there is reduction of formation of reduced Hb (as total Hb is low and in

The normal VO, in an adult is 3Lmin and in athlet it is about histotoxic hypoxia O, is not used by the tissues. This is why during those hypoxic conditions
SL /min. cyanosis is absent.
I t is an important indicator ofthe individuals capacity to carry out aerobic exercise.
(d) Local factors:
The factors affecting this are -cardiac output mainly, ability of tissue to extract O, and size of total
Exposure to mild cold can fesult cyanosis due to vasoconstriction.
muscle mass.
Exposure to severe cold> no cyanosis because offollowing reason:
I is maxmum during adulthood and then declines with advancement ofage.
decrease in O consumption by tissues
38. 02 therapy:
a Shift of O dissociation curve to left > release of O, from Hb.
I t is indicated in acute and severe hypoxia especially whenhypoxia is associated with dyspnoea.
Meth-hemoglobinemia produced due to toxic dose ofsulphanilamides or of acetanilamide.
O therapy can be done by two procedures e.g.
41. Asphyxia:
(i) Inhalation of 100% pure O, but this procedure has side effects like:
Definition: Improper airation of the blood in which hypoxia is associated with hypercapnoea
Nasal congestion, sore throat, sneezing, coughing. bronchoconstriction due to stimulation
(TCO, level) is called as asphyxia.
of imritant receptors in respiratory ract.
Causes: similar to the causes of hypoxia
O toxicity which is characterised by muscular twitching, dizziness, cog wheel (Jerking)
respiration, convulsion, and unconsciousness. It is basically due to inhibition of tissue en-
Stages: 3 stages:
zyme activity and cerebral vasoconstriction. stage of hyperapnoea
(i) Inhalation of 100% pure O at high barometric pressure (hyperbaric 0, therapy): The stage of convulsions
main aim of which is to increase the amount of dissolved O, in plasma and thereby helps in stage ofcollapse
all forms of hypoxic conditions except hypoxic hypoxia. However in early stages there may
be 0, toxicity.
42. Peak Expiratory now rate (PERR):
O , therapy is very useful in hypoxic hypoxia and anemic hypoxia but not in stagnant hy-
Itis the maximum rate ofair flow that is sustained for the period of 10 ms during forced expiration.
poxia (as blood flow to the issue is decreased in this condition) and histotoxic hypoxia (as Normal value:
tissue is unable to utilize O2). a In male =400-600 LImin
39. O2 poisoning: a In female = 300-400 L/min.
During deep sea diving as O, is breathed at a higher pressure (100% O,) the amount of O2 dis- Signilficance: It helps to asses the respiratory diseases. Generally it is reduced in all types of
respiratory diseases however the reduction in obstruetive diseases is more than
solved in the tissue fluid becomes high. This may result fatal condition specially in CNS which is in restrictive
called as O poisoning. diseases.
 169
PHYSIOLOGY: MADE EASY HESPIRATION
168

be recorded by using peak flow meter. I t is performed by placing the palm of the hand flatly on the chest surface and asking the subjectto
It can

one-two-Ihree. The vibrations transmitted to the chest wall felt by

hand are called as vocal
I t is an index of patency of airways. say
fremitus.
43. Dyspnoea: fremitus is increased in consolidation of lung tissue and decreased in pleural effusion.
for increased respiratory effort' or air Vocal
Definition: It is defined as 'a consciousness of necessity 47. Respiratory minute volume (RMV) or Pulmonary ventilation (PV):
hunger resulted due to difficulty in breathing.
I t is the clinical condition characterised by difficulty in breathing. I t is defined as the volume of air that can be breathed in or breathed out per minute-during normal
occurs when Dyspnoeic index falls below 60%. Therefore dyspnoea occurs when respiration.
Dyspnoea I t is calculated as RMV =TV x respiratory rate
i) MVV becomes less than normal (ii) VC. (ii) T Pulmonary ventilation by 4.5 times.
I t occurs duringrespiratorydisorders affecting ventilation, cardiac disorders affecting lung func Normal value = 6-7 LUmin.
tion and metabolic disorder like diabetic acidosis, uremia and etc.
48. Apnoea:
In the early stage, heart failure. dyspnoea occurs during exercise due to failure ofLV output to
Definition: It is defined as the temporary stoppage of breathing
meet the increased 0, demand during exercise. This is known as dyspnoea on exertion whereas in
the late stage of heart failure dyspnoea occurs even at rest due to increased venous pressure or due Causes: The causes are
to gross inadequate ventricular pumping8 DAfter hyperventilation
During severe exercise also it is seen which is an example of physiological dyspnoea. a During sleep (sleep apnoea)
O During deglutition (deglutition apnoea)
44. MBC and MVV:
During Herring-Breuer deflation reflex
I t is the maximum volume of air that can be taken in or given out in each minute.
O During Bezold Jarish reflex
It is calculated as: MVV = VCx Respiratory rate. Voluntary apnoea: A person can arrest his breathing for sometimes up to a certain period
Normal value beyond which breathing starts automatically due to accumulation of O2. This voluntary
D In male = 150- 170 liter/ min stoppage of breathing is known as voluntary apnoea and the period is called as breath
holding time or BHT and the point beyond which it can no longer be held is known as
a In female =
80 100liter/ min breaking point.
Significance: It is an overall index of ventilatory capacity. It's values may be altered by disease of
the respiratory muscles of thoracic cage or by obstruction in airways like emphysema. 49. Mouth to mouth breathing:
The factors affecting MBC are respiratory muscle power, airway patency, compliance, elasticity I t is one
of the important manual method of artificial respiration preferably in adults.
and viscosity of lung. Procedure adopted is:
45. Breathing reserve and dyspnoeic index: O Subject is placed in the supine position.
O Airways is cleaned and neck is extended
Pulmonaiy reserve (PR) or Breathing reserve (BR) (Fig. 5.17).
The nostrils patient
t is the maximum amount of air above the pulmonary ventilation that can be breathed in or out in of the is closed by pinching with the thumb and index finger of the
per
former.
one minute.
I t is calculated as: BR = MVV - RMV. O Air is exhaled forcefully from the mouth of performer to the subjects mouth after taking a decpP
breath.
Dyspnocic inder (DI) Chest expansion is noted.
When BR is expressed as % ofMVV it is known as DI. O Above steps are repeated at a rate of 10-15 /min.
I t is calculated as DI = MVV - RMVx 100/MVV
Advantages:
BRx 100/MV.
a It
can be
applied immediately and simple technique.
Normal value-60% to 70% OGreater tidal volume (1000 ml) can be obtained.
Significarte: When this value reduces below 60% dyspnoea is present. o CO, in
expired air helps to stimulate the subject's respiratory center.
46. Vocal fremitus: Disadvantages:
l t is a There is chance of infection in either direction.
one
important palpatory device to asses he clinical condition of respiratory system. a

OPerformer may go into exhaustion and thus can not be continued for
long time.
 PHYsiOLOGv : MaDE EASY RESPIRATION
170 17

The basic life support is given by:

a Cleaning of the airways
Mouth to mouth breathing at the rate of 16-18/m
a External cardiac massage by-
pressing lower border of sternum by 4-5 cm at the rate of 80-90 times/min.
after every 15 cardiac massage two mouth to mouth (15:2) breathing (if two subjects are
present,
after every 5 cardiac massage l mouth to mouth (5:1) breathing (if one subject is available).
Advanced life support is given by defibrillation and airway management and
O,therapy.
C. Differentiate between:
Terminal bronchi Respiratory bronchi
A s per Weibel's lung model it is numbered O As per Weibel's lung model it is numbered
as 16" generation. as 17" generation.
a No gaseous exchange tàkes place in this a Gaseous exchange takes place in this
Zone zone.
O It is the conductive zone. Q Itis the respiratory zone.

Conductive zone Respiratory zone

I t is a pipe like structure of tracheobronchial
tube through.which air passes.
I t starts from Trachea (Zero generation as
per weibel's lung model) to 16" generation.
Walls of this zone is thicker.
a Mean diameter is less.
O Velocity of air movement is high.
o l consists of balloon like stuctures in
which gaseous exchange takes place.
a It starts from respiratory bronchiole to
alveolar sac.
Walls of this zone is thin.
Mean diameter is more.
a Velocity of air movement is comparatively
less.

External respiration Internal respiration

O Respiration concerned with exchange of
gases between environment and lungs is
aRespiration concemed with exçhange of
gases between the cells and the internal
known as external respiration. environment and it's use to provide energy
is known as external respiration.
N o energy is liberated in this process. aEnergy isliberated in this process.

Fig. 5.17: Methods of anificial respiration. Mouth to mouth breathing (A = the neck is extended by placing one
the Intrapleural pressure Intrapulmonary pressure
hand under the neck and pressing the forehead with other hand, B = perjormer exhales air into parient's
the
mouth by ightily placing his mouth over the patient's mouth keeping the nostritls ofpatient closed, C= allows the
patient to exhale passively by unsealing nose and nostrils) Oltisthe pressure existing in the pleural
Normally it is negative and positive only
cavity a It is the pressure inside the alveolus.
a Normally it is positive and negative only
50. Cardiopulmonary resuscitation: during forceful expiration. during inspiration.
I f the respiration fails along with stoppage ofheart beat this procedure is followed till the person O It helps tò prevent collapsing of lungs. O It helps to drive air in and out of lungs and
is not hospitalised for proper treatment. also controls the exchange of gases
between alveolar air and blood.
 PHYSIOLOGY : MADE EASY
172 RESPIRATION 173

Valsalva maneuver Muller's mancuver Vesicular breath sound Bronchial breath sound

OIt is the forced expiration against closed a It is the forced inspiration against closed No gap is present in between inspiration Silent gap is present in between inspiration
glottis. and expiration and expiration.
glottis. Duration is
o In this situation intraalveolar pressure
a In this situation intraalveolar pressure Duration of inspiration sound is twice of a same.

decreases below 80 mm Hg. expiratory sound.

increases beyond 100 mm Hg above the
atmospheric pressure. Restrictive lung disease
Obstructive lung disease
Dynamic lung volume
Static lung volume Any abnomal respiratory condition which O Any abnormal respiratory condition which
makes it difficult to push the air outside the makes it difficult to get the air into the
The lung volumes when are expressed in
O The lung volumes when not expressed in lungs (expiration) is called as obstructive Jungs (inspiration) is called as restrictive
time is known as static lung volume. time is known as Dynamic lung volume.
lung disease. lung disease
a Clinically is not very much useful. a Clinically is very much useful. O Examples: asthma, emphysema. Examples: kyphosis, ankylosingspondilitis.
D Occurs duc to abnormality in the o Occurs due to abnormality in the lung.
Alveolar ventilation Pulmonary ventilation thoracic cavity and in the nervous system.
respiratory tract.
The amount of air that can be breathed in aFEVI is reduced in this condition but vital a FEVI remains unaffected in this condition
a The amount of air that exchange through
or out per min is called as pulmonary
capacity is unaffected. but vital capacity is reduced.
alveolus per min is called as alveolar

ventilation. ventilation. O Chestexpansion is not restricted only O Chest expansion is restricted.

expiration is obstructed.
a I t excludes the dead space volume. includes the dead space volume.

oItis thus less than pulmonary ventilation. Olt is thus more than alveolar ventilation. High altitude native Newcomer to high altitude
Nomal value 4.9 L/ min. o Normal value-6-7 L/ min. aIncrease in pulmonary ventilation is more.
aIncrease in pulmonary ventilation is less.
OResponse to hypoxic stimulation is more OResponse to hypoxic stimulation is less
Fresh water drawning Sea water drawning
a Urine is alkaline. Urine is acidic.
a Water in the lungs draws fluid from the O Affinity of hemoglobin for O, is less.
Water enters the lungs and thus quickly vascular space of lung tissue resulting
O Affinity of hemoglobin for O is more.
diffuses to blood due to hypotonicity of a Vascularity is more. aVascularity is less.
hypertonicity of body fluid.
fresh water.
D It results hemodilution and thus hemolysis. O It results hemoconcentration and thus no
a Mitochopdria and myoglobin content is high.
a Diffusion capacity is more.
aa
Mitochondria and myoglobin content is
Diffusion capacity is less.
less.
hemolysis.
D. Brainstorming short answer type:
Hyperventilation
Hyperapnoea 1. Why the combination of O, with hemoglobin is called as oxygenation and not oxidation?
O Abnormal increase in pulmonary ventila
O Increased pulmonary ventilation due to tion due to forced breathing which often
lt is because iron remains in ferrous form
after combination with O.
increase in force of respiration is known as
2. Why the O carrying capacity of blood is 19 ml/ 100 ml of blood instead of 20.1 ml/
leads to dizziness and sometimes chest
hyperapnoea. 100 ml of blood?
pain is known as hyperventilation.
It is because the hemoglobin is only 95% saturated with O
Bronchial breath sound 3. What is the 0, carrying capacity of hemoglobin?
Vesicular breath sound
lt is 1.34 ml i.e. 1 gm
hemoglobin can carry 1.34 ml of Oz
O It is produced by passage of air in
and out
produced by passage of air in and out
o ofItisalveoli 4. Whieh protein is responsible for HCOj" and Cl exchange in RBC
in the normal lung tissue. through the trachea and large bronchi. during Humburger
phenomenon?
Normally it is heard overthe healthy chest a Normally it is heard over the trachea. It is band 3 proteins which act like
but most typically over the axillary and antiport in RBC.
5. Why the amount of CO,
infrascapular region. trausported through hemoglobin is more than that of plasma
Inspiratory sound is more loud. O Expiratory sound is more loud. proteins?
It is because the quantity of plasma protein is only half of the quantity of hemoglobin.
 PHYSIOLOGY: MADE EAsY RESPIRATION
175

6. How long the voluntary control of respiration (Voluntary apnoea) is possible? 16. What will happen to breath
holding time after removal of carotid bodies?
It is for abouts 40 secs. It will be increased.
7. What is polypnoea? 17. How mild to moderate
hypoxia stimulation respiration but severe hypoxia depresses
Rapid shallow breathing resembling panting in dogs is known as polypnoea. Here only rate of respi- it?
ration is increased but not force of respiration. Severe hypoxia depresses the respiration by directly inhibiting the
nild moderate respiratory center whereas the
8. What is the efficacy of O, therapy in diferent types of hypoxia?
or hypoxia stimulates respiration center by stimulating peripheral chemoreceptors.
18. Why respiratory chemoreceptors are not stimulated in anemia or CO
This is as follows: poisoning?
I n hypoxic hypoxia: 100 % useful Respiratory chemoreceptors are not stimulated in anemia and CO poisoning as the O, requirement of
these receptors be fulfilled
can
largely by dissolved 02 alone which used
BIn anaemic hypoxia: 70 % useful to be normal during those
conditions.
I n stagnant hypoxia: 50 % useful
I n histotoxic hypoxia: notat al
19. Give physiological basis of pulmonary edema during rapid ascend?
During rapid ascend to high altitude increase in sympathetic activity due to
work, cold and hypoxic stimulation of VMC - vasoconstriction increase in increase physical
9. Why the airways resistance is high in conduction zone as compaired to the respiratory in
zone? pulmonary capillary
hydrostatic pressure diffusion of fluid to interstitial space of lungs from the pulmonary capillaries
The resistance to the air flow is inversely related to the total cross sectional area of the respiratory pulmonary edema.
passage ie. the greater the cross sectional area, the lesser is the airways resistance. As the total cross
20. Give physiological basis of cerebral edema during slow ascent.
sectional area is far more in respiratory zone the airways resistance is comparatively less than that of

conductive zone.
During slow ascend to high altitude > decrease in arterial PO2+ when autoregulatory mechanism
in cerebral blood flow is reached to it's
10. Why the bronchial asthma is a disease of expiratory obstruction? highest limit there is increase in capillary pressure transduation
offluid in brain tissue cerebral edema.
In bronchial asthma broncho-constriction develops resulting decrease in diameter of the airwaysthat
leads to increased airways resistance producing difficulty in breathing. Moreover during expiration these
21. Give physiological basis of alkaline urine in an acclimatized person.
In acclimatized person the alkalosis due to fall in arterial PCO, is
already constricted bronchioles further constrict resulting marked increase in airways resistance.
This is compensated by actively excreting
more HCO,in urine to maintain normal
pH. This results alkaline urine.
why there is extreme difficulty in breathing during expiration.
22. How one can not ascend
11. Why the patients with defects in respiratory membrane suffer initially only hypoxic high with 100% O, inhalation?
With 100% 0, inhalation one can ascent
symptoms not of hypercapnia? upto 45000 ft only because above this height barometric
pressure falls to 110 mmHg with only 33 mmHg PO2. At this PO, there is
This is because the diffusion capacity of CO, is 20 times more than that of O, which result much CO
function. impairement of mental
to O, diffusion to lungs capillaries inspite of decrease in
diffu-
diffusion to the alveolus in comparison 23. Explain: The dangers of high atmosphorie pressure are never due to high arterial
sion capacity.
This is because body expires this excess CO, by hyperventilation.
PCO
12. Which one is more dangerous situation rapid shallow respiration or slow deep
respiration?
24. Explain: 0, therapy may cause death in an individual with severe respiratory failure.
This is because of the fact that
of
Rapid shallow breathing is more dangerous as during this type breathing
alveolar ventilation whate ver respiration is there, it will be due to hypoxic stimulation of
decreases though the pulmonary ventilation remains normal resulting less
air available for gaseous peripheral chemoreceptors. So O, therapy in this condition will result withdrawal of hypoxic condition
the alveolar and pulmonary ventilation are
ofperipheral chemoreceptors leads direct depression of respiratory center by severe. hypoxia and
exchange whereas in slow and deep respiration both
hypercapnoea> death.
normal.
25. Explain: Neonates should never be given 100% O2 inhalation.
13. Why PCV of venous blood is greater than that of arterial blood?
This is because it may result
In the venous blood the HCO, and Cl content in the RBC is far more because of fast operation of proliferation of retinal vessels with the formation of fibrous tissues
chloride shift > results hyper-osmolarity in RBC > more intake of water> more swelling of RBC leading permanent blindness.
more rate of their setling in the tube > increase in PCV (hematocrit). 26. Explain: Mild cold produces cyanosis but not seen in severe cold.
Mild coldcutaneous vasoconstriction to
14. What will happen to respiration after bilateral vagotomy? preserve heat > decrease rate of blood flow in tissue
There will be regular normal respiration (Eupnoca) after bilateral vagotomy.
0 extraction
by the tissue tends to remain normal due to slow passage of blood > increase in reduced
hemoglobin>Cyanosis.
15. What will happen if peripheral chemoreceptors are removed? Whereas in severe cold there is decrease in O2 consumption by the tissues and also
There will be litle change of respiration during rest but the ventilatory response in response to hy shifting of O2
dissociation curve to left leading less release of O to the tissues n o significant rise
30%. of reduced
poxia, hypercapnoea and acidemia will be lost by approximately hemoglobin> no cyanosis.
 177
RESPIRATION
PHYSIOLOGY: MADE EASY
176
22. The switching off of the inspiratory ramp signal is prevented by (i) Apneustic center (11) Pneumotaxix
27. Explain: Cyanosis is not seen in anemic and histotoxic hypoxia. center (ii) Suprapontine center (iv) DRG neurons. i)
is low formation
of enough reduced Hb no cyanosis. in H" in blood (i) increase in H* con.
chemoreceptors are directly stimulated by (i) increase
> no
In anemia total Hb content
23. Central
In histotoxic hypoxia O, is not taken up by the tissues > no significant formation of reduced Hb- in mudullary interstitial fluid (ii) decrease in H* in
blood (iv) decrease in H concentration in

medullary interstitial fluid. 11)

no cyanosis.
24. Arterial PO% is decreased in (i) hypoxic hypoxia (ii) anemic hypoxia (ii) stagnant hypoxia
E: MCQ: i)
(iv) histotoxic hypoxia.
is (i) diaphragm (ii) external intercostal muscle hypoxia (iv) histotoxic
1. The muscle takes part in normal inspiration 25. Cynosis is present in (i) hypoxic hypoxia (ii) anemic hypoxia (ii) stagnant
(ii) both (iv) none.
(ii) (i and ii)
hypoxia.
forceful expiration is (i) intemal intercostal muscle (ii) exter. I cells (ii) Type lI cells (iv) APUD
2. The muscle which do not take part in 26. Surfactant is produced in the alveoli by (i) Macrophage (ii) Type
internal oblique muscle. (in) (11)
nal intercostal muscle (i) abdominal muscle (iv) cells.
of the thoracic ribs are responsible for increase in (i) vertical diam-
level value (ii) han sea level value
value of Pso is (i) less than
more
3. The Bucket Handre movement 27. At high altitude the sea
diameter (1ii) transverse diameter (iv) all of the above. (11)
eter of thoracic cage (1i) antero-postero (iii) same as that of sea level value.
(ii) 28. The O, therapy is useful in (i) hypoxic hypaxia (ii) anemic hypoxia (i) stagnant hypoxia
ribs are responsible for increase in (i) vertical diameter (i)
4. The Pump Handle movement of the thoracic (iv) histotoxic hypoxia.
of thoracic cage (ii) antero-postero diameter (ii)
transverse diameter (iv) all of the above. (ii) there is (i) level of reduced Hb becomes 5 gm (ii) level of reduced Hb
2-6th 7- .
29. Cyanosis develops when
by intercostal muscles of thoracic ribs of (i) (i) 1 gm (iv) (i)
5. The pump handle movement is contributed becomes 2 gm (iii) level of reduced Hb becomes none.

stimulation (ii) VIP (ii) exercise

10th (ii) both (iv) none. 30. All the factors increase bronchial tone except (i) parasympathetic
muscles of thoracic ribs of (6) 2-6t" (ii)
6. The Bucket handle movement is contributed by intercostal (iv) cold ai.
(ii). surfactant maturation is facilitated by (i) glucocorticoid (ii) PTH (ii) ADH
(i) 7-10h (ii) both (iv) none. muscle
31. At full term fetal lung
of i) extemal intercostal
7. The vertical diameter of thoracic cage is altered by the movement
(iv) aldosterone.
lower costal series (ii) diaphragm (iv) all of ;
of upper costal series (1) external intercostal muscle of 32. Closing volume is (i) less than RV (ü) more than RV (ii) equal of RV (iv) equal of FRC. (ii)
the above.
(ii) be measured by spirometry (i) VC (i) TV (ii) RV (iv) MVV.
33. All except the followings can not
to 5 0 mmHg
intrapleural pressure during inspiration is (i) 2 to 5 mmHg (ii) -40 (i)
- -

8. The normal
(ii)-5 to-10 mmHg (iv) 10 to 15 mmHg (in) 34. Hldane effect facilitates (i) release of CO, in lung (ii) release of O, in tissue (ii) transport of O by
related (ii) inversely related (ii) not related anyway
9. Cross sectional area of airways is (i) directly blood (iv) shift of O, dissociation curve to right.
with airways resistance. 35. 0, therapy is not useful in the following conditions except (i) hypoxia due to respiratory center
5000 ml.
10. Normal residual volume is (i)1200 ml (ii) 2000 ml (ii) 500 ml (iv) depression (ii) hypoxia due to A-V shunts (ii) both (iv) hypoxia at high altitude (iv)
11. The normal value of FRC is (i) 1500 ml (i) 2200 ml (ii) 3000 ml (iv) 5000 ml. (i) 36. Vagal stimulation causes (i) bronchial constriction (i) increase in mucous secretion (ii) both

12. FEV, is reduced in obstructive lung disease (i) restrictive lung

(i)
disease (ii) both (iv) none ofthe (iv) bronchodilatation. (ii)
Pulmonary oedema is caused by () increased in capillary hydrostatic pressure (ii) in
above.
ml. (i)
37. decrease oncotic
13. Nomal RMV is (i) 4-5 lit () 6-7 it (ii) 8-10 lit (iv) 2500 pressure (ii) increase in capillary permeability (iv) decrease in capillary hydrostatic pressure,. (iv)
mmHg (ii) 104 mmHg
14. The partial pressure of oxygen in alveolar air is (i) 100 mmHg (ii)
160 38. Bohr's effect helps in (i) unloading of O and loading of CO% (i) loading of Oz and unloading of
(iv) 154 mmHg.
(iii) CO2 (ii) unloading of O and CO, (iv) loading of O2 and CO (i)
m1% (ii) 48 ml% (iv) 19 ml%. (i) 39. Features of restrictive lung disease are as follows except (i) decrease in TLC (i) decrease in VC
15. The CO, content in arterial blood is 52 ml% (i) 0.04
16. The normal ventilation perfusion is (i) 0.84 (Gi) 1.(ii) 8.4 (iv) 0.1. () (ii) decrease in RV (iv) decrease in FEV. iv)
20 ml (ii) 15 ml (iv) 1.72 ml. 40. Following are the example of obstructive lung disease except (i) COPD (i) Asthma (ii) Pulmonary
17. The O2 carrying capacity ofblood is (i) 1.34 ml (ii)
18. Shift to the left of O, dissociation curve occurs in following
conditions except (i) decrease in H* fibrosis (iv) Cystic fibrosis. (ii)
decrease of blood (iv) increased level of 2-3 DPG. (iv)
() presence of CO (ii) PO2
conditions () increase in
19. Shift to the right of O dissociation curve does not occur in following
decrease in phH of blood. (i)
PCO (i) presence of HBF (ii) increase in temperature (iv)
is carried in (i) dissolved form (ii) bicarbonate form (ii) carbamino
20. The maximum amount of CO,
(ii)
compound form (iv) only ii and ii.
center (ii) Suprapontine center
21. Ramp signal is initiated by (i) Apneustic center (i) Pneumotaxix (iv)
(iv) DRG neurons.
PM.E-12