Cardiac technology

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BASIM ZWAIN LECTURE NOTES
Respiration
Functional Anatomy
The main function of respiratory system is to
take in O2 & give out CO2. It also regulates acid-
base balance & heat & participates in phonation &
vocalization. Respiratory system is divided into
extrathoracic & intrathoracic parts:
Extrathoracic part: Nose, nasopharynx (& mouth
& oropharynx), larynx and upper part of trachea
Intrathoracic part involves lower part of trachea,
carina, two main bronchi (primary bronchi), other
bronchial tree (about 34 generations): Lobar
bronchi (secondary bronchi), lobular or segmental
bronchi (tertiary bronchi), terminal bronchioles,
respiratory bronchioles, alveolar ducts, atria,
alveolar sacs and alveoli.
Functionally, the respiratory system is divided into
two main zones: Conductive zone: no gas exchange,
transmits air to next zone, anatomical dead space,
from nose to terminal bronchioles & respiratory
zone: gas exchange, involves transitional zone, from
respiratory bronchioles to alveoli.
The alveolar epithelial wall is composed of three
types of cells:
Type I pneumocytes: Squamous epithelial cells
Type II pneumocytes: Secrete surfactant
Third type: Alveolar macrophages
Respiratory membrane: 6 µ in diameter, surface
area 140 m2 , six layers:
1. Alveolar fluid lining alveoli (with surfactant)
2. Single layer of squamous alveolar epithelium
3. Basement membrane of alveolar epithelium
4. Narrow interstitial space
5. Basement membrane of capillary endothelium
6. Single layer of squamous capillary endothelium
Functions of upper respiratory system
Warming up of air (within body temperature)
Humidification of air (about fully saturated with
water vapor, otherwise, lung crusting & infection).
Filtration of large foreign particles: Nostrils' hair
Turbulent precipitation: Particles larger than 6μ in
diameter on mucous coat of nose & nasopharynx.
Gravitational precipitation : Smaller than 6μ dia.
particles within bronchioles, taken up by alveolar
macrophages or exhaled out.
Mucous coat & cilia, move to cough or swallow
Muscles of respiration
Normal quiet breathing: Contraction & relaxation
of diaphragm, changes vertical dimension of chest.
Inspiration (inhalation): Active, negative pressure,
syringe-like manner.
Expiration (exhalation): Passive, relaxation of dia-
phragm & elastic recoil of lung, thoracic & abdom-
inal tissues, raises pressure
Heavy inspiration: Increases anteropost. + vertical
dimensions, (exteral intercostal muscles+ diaph.), +
elevation of thoracic cage: sternomastoids, scalenes,
serratus ant. & pectoralis minor.
Heavy expiration: Internal intercostal & abd. m.
Pulmonary volumes and capacities
Pulmonary volumes are:
1-Tidal volume (VT): Volume inspired & expired
each quiet breath. It is about 500 ml.
2-Inspiratory reserve volume (IRV): Maximum
volume can be inspired above VT. About 3000 ml.
3-Expiratory reserve volume (ERV): Maximum
amount expired after VT. About 1100 ml.
4-Residual volume (RV): Volume remaining after
the most forceful expiration. About 1200 ml.
Pulmonary capacities are:
1-Inspiratory capacity (IC)= VT + IRV ≈ 3500 ml.
2-Functional residual capacity (FRC)
FRC = ERV + RV ≈ 2300 ml.
3-Vital capacity (VC) = VT+ IRV+ERV ≈ 4600 ml.
4-Total lung capacity (TLC) = VC + RV ≈ 5800ml.
All these volumes & capacities are in average sized
healthy young males but, they are about 20%-25%
less in females. They are also lower in older,
shorter, asthenic, black complexion, lowlander and
smoker subjects than in younger, taller, athletic,
white complexion, highlander and non-smoker
subjects respectively
Pulmonary and alveolar ventilation
Normal respiratory rate (or respiratory frequency
“RF”) is 12-15 BPM. Pulmonary ventilation (or
minute respiratory vol.) =VTx RF which is amount
of air moved into respiratory passages each min.
500 ml x 12 to 15 BPM = 6000 to 7500 ml min.
About 150 ml is wasted inside dead space (VD).
Alveolar ventilation (VA) is total amount reaches
respiratory zone each minute: VA=RF x (VT-VD)
VA=(12 to 15)x( 500 - 150 )= 4200 to 5250 mlmin

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BASIM ZWAIN LECTURE NOTES
Respiration
Anatomical and physiological dead space
Conductive zone is anatomical DS: There is pulm.
ventilation but no pulm. Perfusion. When there is
alv. ventilation but perfusion temporarily blocked;
this is called physiological DS (e.g. at apex of lung
during upright position: blood pools into base).
When block is permanent, it is pathological DS.
When there is perfusion, but no ventilation, oxyg-
enated Bd will be mixed with deoxygenated Bd &
condition is called shunt. e.g. of anatomical shunt is
oxygenated Bd returned to left atrium via pulm. vv
which is mixed with deoxygenated Bd from lung
tissues. e.g. of physiological shunt is at base of lung
during upright position.
e.g.s of pathological shunt are congenital anomalies
like patent ductus arteriosus (PDA) & patent
foramen ovale (PFO). Patent=open.
Ductus arteriosus (a bv that allows Bd to bypass
baby's lungs before birth) fails to close after birth.
Foramen ovale (a normal opening between left &
right atria of fetal heart) fails to close after birth
Forces controlling lung
volumes
Pleural pressure (intrapleural pressure)
Space between visceral & parietal pleurae is filled
with pleural fluid: lubrication, sliding & prevents
separation. The pressure inside the pleural space is
pleural or intrapleural pressure: always negative
about -5 to -7.5 cmH2O (1cmH2O = 0.75 mmHg).
The pressure inside alveoli is alveolar pressure =
about -1 to +1 cmH2O. Difference between pleural
and alveolar pressures is transpulmonary
pressure.
Airways resistance
Greatest resistance to air flow is in larger bronchi
near trachea (not in smaller airways due to large
number of these airways “about 65000 parallel
terminal bronchioles” & very small amount of air
passing through each. But under certain disease
conditions, greatest resistance occurs in smaller
airways because they’re occluded by secretory
products & greater % of sm. muscles in their walls
Direct sympathetic control of bronchiolar smooth
muscles is weak but, circulating EPI (& to a lesser
extent NE) hormones cause bronchodilatation.
Vagal (parasym.) stimulation results in secretion of
Ach: causes bronchoconstriction (BC). Atropine
(anticholinergic) blocks action of Ach, relieves BC.
Irritation of resp. epith. with noxious gases (as SO2)
cigarette smoke, fumes, dusts, infection …. results
in reflex nervous & local (non nervous) BC
BC is due to allergic reaction (between antibody
& antigen) e.g., when histamine, slow reactive
substance of anaphylaxis or other substances are
released from mast cells in response to exposure to
allergens like pollen in air, or other sensitizing
agents. This is a type of immune reaction.
Surface tension and surfactant
Surface tension is the ability of fluid molecules on
surface with air for extra strong attraction
resulting in tendency of surface to contract. Surface
tension of alv. fluid results in alv. collapse
(atelectasis) but this is prevented by presence of a
surface active agent secreted by type II alveolar
epithelium which is called surfactant. It reduces
surface tension from 50 dynecm to 5-30 dynecm.
Surfactant is complex mixture of phospholipids,
other lipids, proteins, CHO, Ca++ & some ions.
Activity of surfactant depends on conc. & orient-
ation of phospholipids molecules on surface, while
importance of glycoprotein & Ca++ is to enhance
spread of phospholipids over surface. Thyroid &
glucocorticoids accelerate maturation of surfactant,
cigarette smoking reduces its production.
Pressure that causes alv. collapse is alv. collapse pr.
: about 4 cmH2O in presence of surfactant.
Alveolar collapse pressure = 2T r , where T is
surface tension, r is radius of alv.
In many premature babies radius of alv. is about
14th normal with no secretion of surfactant which
increase alv. collapse pr. to 40 cmH2O or more &
baby dies from alv. collapse (RDS or hyaline
membrane disease).
Lung compliance
It is the extent to which lung volume expands for
each unit increase in transpulmonary pressure.
Lung compliance=ΔV ΔP where ΔV is change in
lung vol. & ΔP is change in transpulmonary pr.
Total compliance is about 200 mlcmH2O, while
compliance of lungs & thorax is 110 mlcmH2O.
Compliance is decreased in restrictive pulmonary
diseases (pulmonary fibrosis, pleurisy, pleural
effusion….) while it is increased in emphysema
Elastic and non-elastic work
Work of breathing is elastic & non-elastic work
Elastic (compliance) work: Is work required to
overcome elastic forces of lungs & chest (65% of
total work).
Two thirds of lung elastic forces are due to surface
tension & one third is due to elasticity of lung
tissues themselves. Compliance work = ΔV . ΔP 2
Non-elastic work: which is subdivided into:
•Airways resistance work: Required to overcome
resistance to air movement through respiratory
passages which is about 28% of total work
•Tissue resistance work: Required to overcome
viscosity of lung & chest tissues which is about 7%
of total work
In restrictive pulmonary diseases (pulmonary
fibrosis, pleurisy, pleural effusion….) compliance &
tissue resistance work are especially increased
while in obstructive airway diseases (emphysema,
chronic bronchitis, chronic bronchial asthma….),
airways resistance work is especially increased &
work of expiration becomes even more than work
of inspiration. At rest, only 3-5% of body energy
for ventilatory process, rising 50 folds in exercise
especially in respiratory diseased subjects.

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BASIM ZWAIN LECTURE NOTES
Respiration
Diffusion of gases
A mixture of gases inside a container exerts a total
pr. against its walls which equals the sum of partial
pr.s of its component gases. Partial pr. of each gas is
proportional to its conc. within mixture. Partial pr.
of oxygen is PO2, of carbon dioxide is PCO2 & of
water vapor is PH2O. Alv. PO2 is PAO2, while arterial
PO2 is PaO2 & same thing for CO2.
Henry's law states that partial pr. of dissolved gas
is directly proportional to conc. of its molecules &
inversely proportional to its solubility coefficient in
solvent. Solubility coefficient of CO2 in water is 20
times more than O2 so as diffusion of CO2 across
respiratory membrane. Diffusion of gases is along
partial pr. gradient (from higher to lower)
Partial pr.s of alv. gases are different from inspired
gases due to humidification, O2 is continuously up
taken to & CO2 is continuously added from pulm.
capillary. PO2 of pulmonary vein (95 mmHg) is
different from that of pulmonary capillary (104
mmHg) due to anatomic shunt
Factors affecting diffusion rate
The diffusion rate of O2 is about 230mlmin &
4600 mlmin during exercise. Diffusion rate of gas
molecules across biological membranes is affected
by several factors summarized in equation:
Another factor, temperature which is directly pro-
portional to D but it is constant in healthy human
Diffusion rate is greatly reduced in:
Pulmonary fibrosis: Increased thickness of RM
Emphysema: Decreased surface area of RM
High altitude: Reduced pr. gradient of O2 (hypoxia)
Diffusing capacity
Diffusing capacity (DL) is vol. of gas diffuses across
RM each min. for ΔP = 1 mmHg.
At rest, DLO2 =21 mlmin. mmHg & during exercise
about 65 mlmin. mmHg (increased Bd flow, ideal
distribution & increased surface area of RM due to
capillary distension). DLCO2 = 20 times DLO2.
Diffusion of O2 & CO2 across RM takes 0.3 s,
while Bd traverses pulm. capillary within 0.75s. at
rest. This is called safety factor for exercise when
Bd velocity in pulm. capillary becomes 0.3s
When Bd is saturated with O2 & CO2 , it must
be replaced by perfusion so; uptake of O2 & output
of CO2 is perfusion limited. Another toxic gas (CO)
has no Bd saturation limits & it is diffusion limited

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BASIM ZWAIN LECTURE NOTES
Respiration
Ventilation/perfusion ratio
Normal alveolar ventilation/perfusion ratio (VA/Q)
is about 0.85 (5100 ml/min/6000 mlmin = 0.85).
In blocked ventilation; VA= zero, VA/Q= zero & in
blocked perfusion; Q = zero, VA/Q = ∞
In either case there is no gas exchange.
In upright position, Bd shifts from top to bottom of
lung, so, at top;VA/Q=2.2 & at bottom, VA/Q=0.5
Normal Obstructed ventilation Obstructed perfusion
VAQ
= 0.85
PO2=104
PCO2=40
PO2=104 PCO2=40 PO2=149 PCO2=0.3
PO2=104 PCO2=40
PO2=40 PCO2=45
PO2=104 PCO2=40
VAQ
= zero
VAQ
= ∞
PO2=40
PCO2=45
PO2=149
PCO2=0.3
Transport of gases to the tissues
Gas exchange in pul. capillaries: external respira-
tion while in tissue capillaries: internal respiration.
About 97% of O2 is transported in combination
with hemoglobin (Hb) in RBC & only 3% in
dissolved state in water of plasma & cells while
CO2 is transported in three forms:
- In the form of bicarbonate (HCO3) …. 70%
- With Hb & other plasma proteins….... 23%
- In dissolved state………………..……... 7%
CO2 is diffused from tissue cells to interstitial space
& then through capillary membrane to be dissolved
in plasma, but major amount diffuses into RBC to
combine with water or Hb to form carbonic acid or
carbaminohemoglobin respectively.
CO2 + Hb = CO2Hb
Carbonic anhydrase (CA) enzyme
CO2 + H2O ===================== H2CO3
Carbonic acid is dissociated into bicarbonate & H+
H2CO3 ↔ HCO3
- + H+
H+ will be buffered with Hb (which is strong acid-
base buffer), while HCO3
- is antiported with Cl-
(chloride shift). This is why venous RBC has Cl-
odour & its plasma is alkaline. In pulm. capillary,
the events are reversed.

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BASIM ZWAIN LECTURE NOTES
Respiration
Oxygen-hemoglobin dissociation curve
When PO2 is high: favours loading of Hb with O2
(increased % of saturation of Hb with O2) & when
PO2 is low: favours unloading of O2 from Hb. The
relation between PO2 & % of saturation of Hb with
O2 is drawn as O2-hemoglobin dissociation curve:
PO2 = 95 mmHg→ 97% saturation
PO2 = 40 mmHg→ 75% saturation
PO2 = 28 mmHg→ 50% saturation (p50)
Decreased p50: shift to left and upward
Increased p50: shift to right and downward
Factors cause right shift (increased p50) are:
1. Decreased pH
2. Increased CO2
3. Increased temperature
4.Increased DPG (Diphosphoglycerate)
This right shifting in tissue capillaries favours
unloading of O2 to the tissues
The opposite factors occur in pulmonary capillaries
& cause right shift (decreased p50) which favours
loading of O2 to Hb. Presence of large amounts of
Hbf (fetal Hb) in Bd is another factor that causes
left shift & favours loading of O2 from the maternal
circulation to fetal circulation. Fetal Hb has more
affinity to combine O2 than adult Hb
Bohr's effect states that reduced CO2 & H+ conc.
increase O2 binding with Hb in pulm. capillaries &
that increased CO2 & H+ conc. increase O2 release
from Hb in tissue capillaries.
Haldane's effect states that increased binding of O2
with Hb displaces CO2 from Bd in pulm. capillaries
to alveoli & that increase release of O2 from Hb will
increase CO2 uptake from cells by Bd in tissue
capillaries.
The volume of O2 carried by each 100ml of Bd is
called vol% which also increases with PO2.
In normal subjects, each 100ml of Bd contains 15 g
of Hb, & each gram of Hb can bind 1.34 ml of O2
1.34 x 15 = 20 vol% (100% saturation=20vol%)
which means when Hb is 100% saturated; 20ml of
O2 can be carried by each 100ml of Bd.
In anemic (or polycythemic) patients; Bd contains
less (or more) grams of Hb so; vol% is lower (or
higher) than 20% at same 100% saturation of Hb.
Partial pressure of oxygen (mmHg)
Percent
of
saturation
of
Hb
with
O
2
Volume
Percent
Polycythemia
Normal
Anemia
At PO2= 95 mmHg (arterial)→ 19.4 vol%
At PO2= 40 mmHg (venous)→ 14.4 vol%
19.4 – 14.4 = 5 vol%: (5 ml O2 consumed by tissue
with each 100 ml of Bd at rest), but during exercise,
venous PO2 falls to 15 mmHg at which vol% is 4.4
19.4 – 4.4 = 15 vol%:(15 ml O2 consumed by tissue
during exercise)
Carbon dioxide volume percent curve
PCO2 (mmHg)
CO
2
vol%
Venous
Arterial
46
40
45
50
55
When PCO2 increases, vol% of CO2 increases.
At PCO2 = 40 mmHg (arterial); vol% = 48
At PCO2 = 45 mmHg (venous); vol% = 52
52% - 48% = 4% (4 ml of CO2 is cleared away
from tissue with each 100 ml of blood perfusing
that tissue at rest)
Respiratory quotient
Person with pulmonary ventilation of 7.5 L/min
breathes 10,800 L of gas each day. From this gas, he
takes in 420 L of O2 (19 moles/day)& gives out 340
L of CO2 (15 moles/day). The ratio of CO2
expired/O2 inspired is respiratory quotient (RQ)
RQ = CO2 out/O2 in = 340/420 = 0.81
In cellular resp. of glucose, CO2 out=O2 in; RQ = 1
RQ for metabolizing fat is only 0.7, the overall RQ
< 1 because diet is mixture of carbohydrates & fat
Control of breathing (regulation of respiration)
*Voluntary neural control: directly from cerebral
cortex via corticospinal tracts to spinal neurons of
resp. muscles. It regulates certain activities like
breath holding, hyper-, hypo-ventilation & forceful
respiratory maneuvers
*Involuntary neural control: Respiratory center
(responsible for autonomic resp.) & Pulmonary
receptors (responsible for pulmonary reflexes)
*Central & peripheral chemical control
Respiratory center in the brain stem
Respiratory neurons either type I (inspiration) or
type E (expiration). Resp. center is composed of
several groups of these neurons:
1.Dorsal respiratory group (DRG)
2.Ventral respiratory group (VRG)
3.Pneumotaxic center
4.Apneustic center
DRG located in nucleus of tractus solitarius & reti-
cular substance of medulla, participates in basic
resp. rhythm (quiet insp.), only type I neurons
VRG located ant. & lateral to DRG in nucleus am-
biguous rostrally& nucleus retroambiguus caudally
It is inactive during quiet breathing, contributes to
resp. control of heavy breathing, receives signals
from DRG, contains both types I and E neurons.
Pneumotaxic center located dorsally in nucleus
parabrachialis of pons (Kölliker-Fuse nucleus) &
operates in association with apneustic center in
lower pons to control depth of insp. They switch off
ramp signal of DRG to block over inhalation.
Pulmonary receptors
1.Stretch receptors: in bronchial & bronchiolar sm,
when lungs overinflate; they overstretch& transmit
signals via vagus to DRG, to switch off insp. This is
called Hering-Breuer reflex
2.Irritant receptors: cough, sneeze & bronchocons-
triction reflexes. Receptors for cough found along
bronchial tree (larynx & carina), send impulses via
vagus nerve to medulla & sneeze receptors found in
nasal airways, impulses via trigeminal to medulla
3.J-receptors: sensory nerve endings in alv. wall in
juxtaposition to pulm. capillaries give the person a
feeling of dyspnea during engorgement of pulm.
capillaries or edema like in congestive heart failure.
Central chemical control: chemosensitive areas of
respiratory center, bilateral aggregation of neurons
beneath ventral surface of medulla, sensitive to
changes in H+ & PCO2, direct stimulus for these
neurons is H+, when increased in Bd;the area signal
resp. center to increase activity (hyperventilation)
Peripheral chemical control: pp chemoreceptors,
sensitive to changes in PO2, PCO2 and H+. They
are: Carotid bodies, aortic bodies & others.
Carotid bodies, largest in number, located at bifur-
cations of common carotid arteries, afferent signals
pass via Hering nerves to IXth cranial nn & then to
DRG. Aortic bodies located along arch of aorta &
afferent signals pass via Xth cranial nn to DRG.
Others are few in number, along large arteries.
Control of breathing during exercise
When motor cerebral cortex orders muscles to
contract; it sends collaterals to respiratory center
to increase activity. This may be more or less than
actual need. Proprioceptive endings in muscles &
joints send impulses to adjust activity but final
precise adjustments are by chemical control aided
by changes in PO2, PCO2 and H+.

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BASIM ZWAIN LECTURE NOTES
Respiration
Hypoxia
Low level of PO2 is hypoxia. In blood it is called
hypoxemia. Four types of hypoxia:
1.Hypoxic hypoxia: most common, decline in PaO2.
2.Anemic hypoxia: HbO2 is declined due to anemia
or CO poisoning.
3.Stagnant hypoxia: blood flow is reduced.
4.Histotoxic hypoxia: tissue can not utilize O2 due
to enzymatic inhibition caused by poisons or drugs
e.g. cyanide poisoning.
Hypoxic hypoxia caused by congenital CV disease
(PDA, PFO…), lung failure, pulm. fibrosis, pulm.
emphysema, VA/Q imbalance, pump failure (fatigue
of resp. muscles, pneumothorax or bronchial obstr-
uction) & depression of resp. center (drugs like
heroine, morphine, pithidine) …
Patterns of breathing
Eupnea: normal rhythmic breathing (12-15 BPM)
Apnea: no breathing, dyspnea: conscious shortness
of breathing (as in asthma). Hypopnea: decrease (&
hyperpnea increase) in rate or depth of breathing
regardless of consciousness. If hypo- & hyper-pnea
are not with metabolic requirements; they hypo- &
hyper-ventilation & lastly tachypnea: rapid shallow
breathing.
2 sec. 3 sec. 2 sec. 3 sec. 2 sec. 3 sec. 2 sec.
Abnormal patterns of breathing are:
1. Chyne-Stoke breathing: usually seen in patients
with brain damage or chronic illness and also in
some infants & in healthy persons during sleep
especially high altitudes.Characterized by repeated
cycles of gradually increasing & decreasing tidal
volume & respiratory frequency.
2. Coupled or grouped breathing: in new comers to
high altitudes where PCO2 is high & characterized
by double, triple or more breaths followed by
apnea for several seconds relieved by deep breath.
3. Periodic breathing: in patients with increased
intracranial pr. or mid brain lesions & characteri-
zed by irregular periods of apnea alternated with
periods of normal breathing.
4. Apneustic breathing: in patients with pontine
lesions due to loss of pneumotaxic andor apneustic
centers characterized by sustained cramp like insp.
efforts relieved irregularly by sudden gasp of deep
expiration.