This presentation is solely for the students of Medical Electronics and is a brief description of the Physiology of Blood.

1. PHYSIOLOGY OF BLOOD
for MEDICAL ELECTRONICS
DR ELIZABETH J
PROFESSOR OF PHYSIOLOGY

2. BLOOD
COMPOSITION
FUNCTIONS
RED BLOOD CELL - MORPHOLOGY
- COUNT

3. PHYSICAL PROPERTIES OF BLOOD
Blood is a liquid connective tissue
Thick, Viscous, Red, Opaque fluid.
Normal pH ranging 7.35-7.45 (7.4 Avg)
Specific Gravity
Men - 1055 to 1060
Women - 1050 to 1055
Viscosity –3 to 4 times thicker than water.
Plasma is 1.8 times thicker.
Osmotic Pressure – 25 mm Hg

4. COMPOSITION
Blood is a fluid connective tissue containing
Plasma 55%
Formed Elements 45%
PLASMA
- 90% water
- 10% solutes
Ions, e.g., Na+, Cl-, Ca++
Nutrients, e.g., simple sugars, amino acids, lipids
Wastes, e.g., urea, ammonia, CO2
Miscellaneous: O2, hormones, vitamins, plasma
proteins (Albumin, Globulin & Fibrinogen)

5. COMPOSITION (Contd)
Formed Elements
• RBC’s / Red Blood Cells (erythrocytes)
• WBC’s / White Blood Cells (leukocytes)
• PLATELETS /(Thrombocytes)

6. BLOOD CELLS

7. Composition (contd)

8. FUNCTIONS OF BLOOD
 TRANSPORT OF RESPIRATORY GASES.
 TRANSPORT OF FOOD.
 TRANSPORT OF WASTE PRODUCTS.
 TRANSPORT OF HORMONES.
 REGULATION OF BODY TEMPERATURE.

9. FUNCTIONS OF BLOOD (CONTD)
 DEFENCE MECHANISM.
 ACID - BASE BALANCE.
 WATER BALANCE.
 OSMOTIC PRESSURE.
 IRON BALANCE

10. RED BLOOD CELLS - MORPHOLOGY
• 7.2 m diameter.
• 2.2 m thickness in
the periphery.
• 1.0 m in the centre.
• Volume- 78-94 m2
• Biconcave disc
shape
–  surface area
–  efficiency for
diffusion of O2 & CO2

11. RBC’S MORPHOLOGY ( CONTD)
• Double layer of lipids with
membrane proteins in between.
• 50% proteins, 40% lipids & 10%
carbohydrates.
• Structural proteins:
Spectrin and Actin are attached to
the lipid layer by the protein
Ankyrin.

12. RED BLOOD CELLS - MORPHOLOGY

13. VARIATIONS IN SIZE & SHAPE
MICROCYTOSIS
MACROCYTOSIS
ANISOCYTOSIS
POIKILOCYTOSIS
TARGET CELLS
SPUR CELLS – ACANTHOCYTES

14. RBC COUNT’S
Men
5 to 6 million cells/ cu mm of blood.
Women
4.5 to 5.5 million cells/ cu mm of blood.
At birth
6 -7 million cells/ cu mm of blood.
Increase – Polycythaemia.
Decrease – Anaemia.

15. LIFE SPAN & FATE OF THE RBC
• 120 DAY IS THE AVERAGE LIFE SPAN OF THE
RBC. (90-140 DAYS)
• LIFE SPAN IS REDUCED IN HEMOLYTIC
DISEASES.
 Destroyed by the RES (Reticulo- endothelial
system) in the red pulp of the spleen
mainly.
 1% circulating RBC’s are destroyed / day.
 Hemoglobin is degraded into globin and
heme.

16. Blood Groups
Chief blood groups
Classical ‘ABO’ blood groups(1901,Land Steiner)
Rhesus blood groups (Land Steiner & Weiner,1940)
M and N blood groups (Land Steiner & Lewis 1921)

17. A & B- group specific polysaccharide
substances called Agglutinogens
present on RBC membrane
Agglutinins of Ig M type in plasma:
Anti-A or alpha, Anti-B or beta
Reaction b/w agglutinogen and
corresponding agglutinin leads to
clumping of RBCs

18. ABO blood groups-distribution in India
Agglutinogen Agglutinin Blood
group
Distribution
in India
A Beta A 21%
B Alpha B 39%
Both A and B Neither AB 9%
Neither A nor
B
Both O 31%

19. Landsteiner’s law
• If an agglutinogen is present in the RBCs of an
individual, the corresponding agglutinin must be
absent from the plasma;
• If the agglutinogen is absent in the individual
RBCs, the corresponding agglutinin must be
present in plasma.
• Exception( to 2nd part) abs of Rh agtngn on RBC>
not with pres of anti-Rh

20. Determination of Classical Blood Groups
• Mix a drop of isotonic saline
suspension of subject’s
RBCs with a drop of serum
A and serum B separately
on a glass slide; watch for
agglutination.
Anti-B Anti-A Blood
Group
- + A
+ - B
+ + AB
- - O

21. RHESUS (Rh) BLOOD GROUPS
• Landsteiner & Weiner (1940)
• RBCs of Rhesus monkeys injected to rabbits
produces agglutinins
• When immunized rabbit serum tested with human
RBCs-> in 85% agglutination-Rh+ve
• In 15%-> no agglutination- Rh-ve
• Rh system only on RBCs

22. Rh SYSTEM
• Rh antigen called D & antibody Anti-D
• ABYs of IgG type, Reaxn at body temp (warm
antibodies), cross placenta
• Gene is ‘D’; when absent- allelomorph ‘d’
• DD & Dd-> Rh+ve
• Dd-> Rh-ve
• C & E are other Rh antigens less prevalent

23. Uses of Blood Grouping Tests
• 1) In blood transfusion
• 2) In pregnancy (Rh incompatibility)
• 3) Investigating cases of paternity dispute
• 4) Medico legal value
• 5) Cell recognition

24. Indications for Blood Transfusion
• 1) Blood Loss: accidents, surgery.
• 2) Bleeding & clotting disorders: hemophilia,
purpura.
• 3) Hematological diseases: anaemias, leukaemia,
dyscracias.
• 4) Acute infections or fever, when
immunoglobulins are required.
• 5) Shocks, Carbon monoxide poisoning.
• 6) Pre & post op build up.

25. Complications of Blood Transfusion
• 1) Hemolytic reaction due to incompatibility
• 2) Non-hemolytic reactions due to WBC, platelets
& plasma proteins
• 3) Transmission of diseases: Malaria,
Syphilis, AIDS, Viral Hepatitis.
• 4) Hyperkalemia (cardiac effects)

26. Complications (contd)
• 5) Hypocalcaemia due to citrates-tetany
• 6) Volume overload-heart failure
• 7) Bacterial contamination & Pyrogenic reactions
• 8) Allergic reactions: Rash, Anaphylactic
shock, Angioneurotic Oedema, Urticaria, Serum
Sickness

27. Effects of mismatched transfusion
• Mild reaction: Agglutination->hemolysis->jaundice
(clears in 2 wks)
• Severe reaction:
• A) Immediate eff: chills, fever, dyspnoea, joint
pains, chest & abd pains, vomiting & shock
• B) Delayed eff: Hemoglobinuria, Jaundice, Anemia,
Renal failure, Hyperkalemia, Uremia, Shock.

28. Treatment
• Stop transfusion immediately
• Corticosteroid injection
• Anti-histamines
• Dialysis (if anuria present)
• Osmotic diuresis
• Treatment of anemia

29. Blood Storage:
Features
1) Anti-coagulants & preservatives:
a) Acid-Citrate-Dextrose solution (pH=5.4, 1.5:10 volumes of
blood
b) Citrate-Phosphate-Dextrose-Adenine soln:
(pH=5.7, 1:7 volumes of blood)
At 4ْ C, in these solns 14 days storage possible, 80% cell
survival after 1 day, thereafter cell destruction @ 1%/day.
2) Stored blood has no viable WBCs & Platelets>1 day

30. 3) Cold storage es cell metabolism, so
i) Plasma hyperkalemia (20-30 mEq/L)
ii) Intracellular hypernatremia(30-40 mEq/L)
iii) Spontaneous hemolysis
4) On transfusion ‘reconditioning’ with reference
to above changes occurs< 48 hours

31. Coagulation

32. NORMAL COAGULATION
• There are 3 stages in normal coagulation: primary
hemostasis, secondary hemostasis and tertiary
hemostasis.
• Primary hemostasis is provided by platelets.
• Secondary hemostasis is provided by the plasma protein
clotting factors, ie, fibrin clot formation.
• Tertiary hemostasis is the formation of fibrin polymers
and their subsequent resolution through fibrinolysis.

33. Hemostasis
• One of the major components needed to provide hemostasis is the
coagulation system which involves the clotting proteins or Clotting
factors.
• The coagulation factors, except for calcium and thromboplastin, are
proteins and are involved in a sequential reaction or coagulation
cascade.
• The last step of the cascade leads to insoluble fibrin as the end
product.
• The reactions leading to fibrin formation can be divided into the
EXTRINSIC, INTRINSIC AND COMMON PATHWAYS.

34. Coagulation system
The process involves a cascade of enzyme-substrate reactions
Enzyme and substrate are localised in close proximity on the
activated platelet surface

35.  Factor I (Fibrinogen)
 Factor II (Prothrombin)
 Factor III (Tissue Factor)
 Factor IV (Ca++)
 Factor V (Labile Factor)
 Factor VI ABSENT
 Factor VII (Proconvertin)
 Factor VIII ( Antihemophilic Factor A)
 Factor IX ( Christmas Factor or Anti hemophilic Factor B)
 Factor X ( Stuart Prower factor)
 Factor XI ( Antihemophilic factor C)
 Factor XII ( Hageman’s Factor or Glass factor)
 Factor XIII ( Fibrin Stabilising Factor)
Coagulation factors

36. Coagulation cascade

37. XII
Blood comes in Contact (Eg: with
glass or collagen)
XIIa
XI XIa
IX IXa
X Xa
VIIIa
PL
Ca++
Intrinsic Pathway
Hagemans Factor
Hemophilic factor
C
Christmas Factor
Stuart Prower

38. Tissue factor (TF)
VII VIIa- TF
IX IXa
X Xa
XIa
VIIIa
Extrinsic Pathway
Proconvertin
Christmas
Factor
Stuart Prower

39. Intrinsic Pathway
(Contact Activation pathway )
• All procoagulants circulate as inactive
precursors.
• Activated in vivo by endothelial injury, in vitro by
glass or other contact
• A foreign surface such as collagen activates
factor XII.
• Acting as catalysts are HK and kallikrein in the
contact phase.
• Calcium is involved in three steps: the activation
of FIX, X and prothrombin.
• The platelet phospholipid surface acts as
template in the activation of FX and
prothrombin.

40. Intrinsic Pathway
• XII is activated (XIIa activates PK which loops
back and activates more XII)
• XIIa and HMWK convert XI to XIa
• XIa and Ca++ ions activate IX
• IXa forms a complex with PF3, Ca++ and VIII to activate X
• Xa complexes with V, PF3 and Ca++ to form active plasma
thromboplastin
• II Prothrombin plasma thromboplastin → thrombin IIa
• I Fibrinogen thrombin IIa → fibrin Ia
• Factor XIII activated by Ca++ and thrombin IIa
• XIIIa and Ca++ stabilize fibrin clot

41. XII XIIa
XI XIa
IX IXa
X Xa
II IIa
Fibrinogen Fibrin
VIIIa+Ca+Pl
Va+Ca+Pl
Intrinsic Pathway
Tests
PTT
Partial Thromboplastin Time

42. Extrinsic Pathway
(Tissue Factor pathway)
• The extrinsic pathway is initiated by the release of tissue
thromboplastin (Factor III) which is exposed to the blood
when there is damage to the blood vessel.
• Factor VII which is a circulation coagulation factor, forms
a complex with tissue thromboplastin and calcium.
• This complex rapidly converts Factor X to the enzyme
form Factor Xa.
• Factor Xa catalyzes the prothrombin (Factor II) to
thrombin (Factor IIa) reaction which is needed to convert
fibrinogen (Factor I) to fibrin.

43. Extrinsic Pathway
• Cell injury activates tissue thromboplastin (Factor III)
• III complexes with Ca++ and VII to activate X
• Xa complexes with V, PF3 and Ca++ to form active tissue
thromboplastin
• II Prothrombin tissue thromboplastin → thrombin IIa
• I Fibrinogen thrombin IIa → fibrin Ia
• Factor XIII activated by Ca++ and thrombin IIa
• XIIIa and Ca++ stabilize fibrin clot

44. Coagulation cascade
XII
XI
IX
X
VIII
Prothrombin
(II)
thrombin
fibrinogen fibrin
STABILISED FIBRIN
V, Ca, P/L
VII
Intrinsic pathway
Extrinsic pathway
XIII
APTT
PT

45. FINAL COMMON PATHWAY
• THE FINAL COMMON PATHWAY STARTS AFTER FACTOR x IS CONVERTED TO Xa
• THIS LEADS TO CONVERSION OF PROTHROMBIN TO THROMBIN
•
• THROMBIN THEN CONVERTS FIBRINOGEN TO FIBRIN
• FIBRIN POLYMERIZES TO FORM INSOLUBLE FIBRIN THREADS
• THE RBCS ENTANGLE IN THE FIBRIN AND FORM THE CLOT
• THE FACTOR XIII STABILISES THIS CLOT