Blood Composition and Functions

Blood

• Blood is a vital fluid circulating in the cardiovascular system, with a volume of 5600ml.

Blood Functions

• Transport function: carries glucose, oxygen, and carbon dioxide.
• Defensive function: includes white blood cells (WBCs) and antibodies.
• Hemostatic function: stops bleeding.
• Homeostatic function: maintains constant tissue fluid composition.

Blood Composition

• 45% cells:
• Red blood cells (RBCs).
• White blood cells (WBCs).
• Platelets.
• 55% plasma:
• 90% water.
• Inorganic substances (Na, Cl).
• Organic substances (protein, lipid, glucose).
• Gases (CO2, O2).

Plasma Proteins

• Concentration: 7.2 gm /dl.
• Composition:
• Albumin: 3.5 – 5 g/dl.
• Globulin: 2.5 g/dl.
• Fibrinogen: 0.4 g/dl.
• Prothrombin: 0.01 g/dl.
• Site of Formation:
• All plasma proteins form in the liver.
• 50% of globulin forms in plasma cells.

Functions of Plasma Proteins

• Specific Functions:
• Osmotic Function: Albumin maintains water balance via osmotic pressure (28 mmHg).
• Defensive Function: Gamma globulin provides defense, while alpha and beta globulins transport.
• Viscosity: Fibrinogen maintains arterial blood pressure.
• Clotting: Fibrinogen and Prothrombin involved.
• Nonspecific Functions:
• Carrier proteins transport vitamins and hormones.
• Buffer function: Plasma proteins adjust blood pH at 7.4. 15% of blood’s buffering capacity is from plasma proteins.
• Diet reserve: rapid tissue protein replacement.
• Capillary permeability: regulates substance movement across capillaries.

Red Blood Corpuscles (RBCs)

• The highest concentration of cells in the body.
• Male: 5.5 million/mm³.
• Female: 4.8 million/mm³.
• Non-nucleated, biconcave shape increases surface area for transport and enhances cell flexibility.
• Life span: 120 days.

Erythropoiesis

• Formation of RBC takes place in:
• Fetus: Liver and spleen.
• Children: Bone marrow of all bones.
• Adults: Bone marrow of long bones.
• Above 20 years: Bone marrow of membranous bones.

Factors Affecting Erythropoiesis

• Healthy bone marrow is essential for RBC formation; its destruction leads to aplastic anemia.
• Liver and kidneys are essential as erythropoietin hormone sites (15% liver, 85% kidney). The liver stores iron and B12.
• Oxygen is important and decreased O2 stimulate erythropoietin, can occur in heart/lung issues, high altitude, haemorrhage.
• Erythropoietin, androgen, cortisone, and thyroid hormone are all hormones that are essential.
• The diet must contain vitamins as folic acid and B12 and metals as iron, copper, and cobalt, and protein.

Erythropoietin Hormone

• Site of Formation:
• Fetus: Liver.
• Adult: 15% liver, 85% kidney.
• Stimulated by:
• Hypoxia.
• Alkalosis.
• Androgen.
• Adenosine.
• Cobalt salt.
• Catecholamine.
• Accelerates erythropoiesis stages in renal failure, developing anemia.

Iron Absorption

• It is ferrous state is absorbed. Dietary iron is ferric.
• Gastric Hcl and ascorbic acid (vitamin C) reduce ferric to ferrous.
• Absorption mainly occurs in the upper part of the small intestine (duodenum).
• Iron is delivered to mitochondria.
• Remaining iron combines with apoferritin (in intestine) or is carried in plasma on transferrin.
• Iron combined with apoferritin becomes ferritin, the main storage form.
• Iron transported in blood is bound mainly to transferrin to all body parts and stored as ferritin in the liver.
• Deficiency results from decreased intake/absorption or chronic blood loss, leading to microcytic anemia.
• Apoferritin is in the intestine and liver.

B12 Absorption

• Intrinsic factor secreted by gastric glands (parietal cells) combines with vitamin B12 for protection/transport.
• Vitamin B12 absorbs from the lower small intestine (ileum).
• Through pinocytosis, vitamin B12 enters mucosal cells with the intrinsic factor.
• To be absorbed by blood and stored in the liver, vitamin B12 is set free and bound to transcobalamineII.
• Deficiency in vitamin B12 leads to macrocytic anemia.

Iron vs. B12 Functions

• Iron: Formation of hemoglobin and myoglobin.
• B12: DNA formation, cell division, cell maturation, and myelin sheath formation.

Storage

• Iron stores in the liver.
• B12 stores in the liver.

Requirement

• Iron: 0.6 mg/day.
• B12: 5 µg/day.

Site Absorption

• Iron: Upper part of the small intestine.
• B12: Lower part of the small intestine.

Need

• Iron: Hcl and vitamin C for ferric-to-ferrous reduction.
• B12: Intrinsic factor for protection from Hcl.

Deficiency

• Iron: Microcytic anemia.
• B12: Macrocytic anemia.

Anemia

• There is a decrease in the number of RBCs, hemoglobin content, or both.
• Anemia is considered when:
• RBC count:
• Males: < 4.5 million.
• Females: < 3.9 million.
• Hemoglobin content:
• Males: < 13.5 gm %.
• Females: < 11.5 gm %.

Blood Indices

• Mean Corpuscular Hb (MCH): = amount of Hb in a single RBC
• Hb content X 10/RBC count in million
• The Normal range is 25-32 picogram.
• Values < 25 picogram are hypochromic.
• Mean Corpuscular Volume (MCV): = volume of a single RBC
• Hematocrit value X 10/RBC count in million
• The Normal range is 80 -95 μ³.
• Values < 80 are microcytes and > 95 are macrocytes.

Anemia Classification

• Normocytic normochromic anemia: Normal blood indices.
• Microcytic hypochromic anemia: Lower blood indices.
• Macrocytic anemia: Higher blood indices.

Types of Anemia

• Normocytic Normochromic Anemia:
• Causes:
• Aplastic anemia: Decreased RBC synthesis due to bone marrow inhibition by antibiotics, malignant tumor, or irradiation.
• Hemolytic anemia: Excessive hemolysis of RBCs.
• Acute blood loss: Acute haemorrhage.
• Microcytic Hypochromic Anemia:
• Small RBC with low Hb content due to iron deficiency.
• Causes of iron deficiency anemia:
• Decreased dietary intake: Starvation in children and pregnancy increases needs.
• Decreased iron absorption: Gastrectomy (absent HCl), small intestine diseases, vitamin C deficiency, increased phosphate & phytate.
• Chronic blood loss: Piles, peptic ulcer & ankylostoma. Note: Tea can decrease iron absorption due to tannic acid & theophylline.
• Macrocytic Anemia:
• Decreased vit B12 or folic acid → decreased DNA → decreased erythroblast proliferation → megalocytes are macorcytes.
  • Causes:
  • Folic acid deficiency.
  • Vit B12 deficiency.
  • Pernicious anemia:
  • Familial disease of the elderly, more common in women.
  • Autoimmune, reacts against gastric parietal cells, causing achlorhydria and absent intrinsic factor.
  • Degeneration of posterior and lateral spinal cord columns leads to neurological issues.

Treatment of Anemia

• Treat The cause:
• Iron deficiency: Give ferrous salts orally and in severe cases give iron by injection.
• Pernicious anemia: Give B12 injections for life.
• Macrocytic anemia due to folic acid deficiency: treated by folic acid.
• In severe cases needs blood transfusions.

Blood Groups (ABO System)

• RBC cell membranes contain mucopolysaccharide antigens (A and B).
• People are classified into four groups by antigens on the RBC membrane (agglutinogen):
• Plasma contains antibodies (agglutinins) versus the absent antigen.
• Group A: - 40% of people, A antigen, anti-B antibody.
• Group B: - 10% of people, B antigen, anti-A antibody.
• Group AB: - 5% of people, A & B antigens, - antibody.
• Group O: - 45% of people, - antigen, anti-A & anti-B antibody.
• Blood Group Characteristics.
• If the antigen is present in RBCs and the plasma contains its corresponding antibodies → agglutination → hemolysis.
• Antigens are called agglutinogens and antibodies are called agglutinins.

Blood Group Importance

• Medicolegal Importance (Disputed Parenthood):
• Inheritance of blood groups occurs with 2 antigens from both parents.
• A and B antigens are dominant, O is recessive.
• Blood groups are a negative test in disputed parenthood.
• Blood Transfusion:
• In incompatible transfusions, donor RBCs are recipient plasma agglutinated, where donor plasma dilutes in the recipient blood.
• Group O is a universal donor because there's no agglutinogen.
• Group AB is a universal recipient because there's no agglutinin.
• Cross-matching tests are before blood transfusions, where recipient plasma mixes with donor RBCs and recipient RBCs mix with donor plasma to see if there is agglutination.

Rh Factor (D Factor)

• A system has C, D, and E antigens.
• Discovered in the Rhesus monkey.
• D is the most antigenic.
• 85% of people are Rh-positive with D antigen.
• 15% of people are Rh-negative and lack D antigen.
• Negative Rh people form anti-D if antigen D is transformed.
• Positive Rh never form anti-D.

Erythroblastosis Foetalis

• (Rhesus hemolytic disease of the newborn) can occur if:
• Rh-negative female married to Rh-positive male carries Rh-positive fetus.
• At first delivery the fetal blood leaks into maternal circulation.
• Mother produces anti-D agglutinins (IgG).
• During next pregnancy, maternal agglutinins (IgG) cross the placenta, causing fetal hemolysis:
• Anemia of the fetus.
• Jaundice increases bile pigments, which cross the undeveloped blood-brain barrier and deposit in basal ganglia (Kernicterus).
• The first baby gets affected by maternal sensitization, previous Rh + Ve blood transfusion, or fetal maternal hemorrhage during pregnancy.
• Can be prevented by avoiding Rh + Ve blood transfusion to Rh - Ve females or injecting Anti-D antibodies to neutralize Rh +Ve fetal cells. No fetal complication occurs during the ABO system because ABO antibodies cannot cross the placenta (IgM). Repeated blood transfusions can cause if Rh - Ve persons get Rh +Ve blood, this will produce agglutinins against the Rh factor. Following transfusion results in agglutination.

Blood Transfusion

• Indications:
• Restore whole blood after haemorrhage.
• To restore elements as RBCs, WBCs & platelets.
• Erythroblastosis foetalis.
• Precautions:
• Compatible.
• Free from contamination.
• High Hb content.
• Free from disease.
• Storage for less than 2 weeks.
• Complications:
• Mechanical: air or fat embolism.
• Physiological: excess transfusion can cause overloading, heart failure, pyrogenic reaction, and fever.
• Infective: infective hepatitis, malaria, or AIDS.
• Incompatibility: Incompatible transfusion clumps and induces hemolysis of RBCs.
• Blockage of blood capillaries is caused from clumping RBCs, which leads to backache and joint pain, and can also trigger angina.
• Intravascular hemolysis can bring on shock due to histamine/vasodilators release, which lowers blood pressure. Liberation of K+ (hyperkalemia) Cardiac arrhythmias. Finally, Hemoglobin can form bilirubin, leading to jaundice, and lead to renal tube blockage and renal failure.

Hemostasis

• Prevents blood loss after injury.
• It contains vascular spasm i.e. vasoconstriction.
• Platelet reactions and temporary hemostatic plug formation.
• Formation of blood clots.

Vascular Spasm

• Results:
• Nervous reflexes upon pain from vessels.
• Myogenic spasm of vessels from trauma.
• Local factors as serotonin, thromboxane A2 (released from platelets).

Platelets

• Platelet count = 150,000 – 300,000 / mm³.
• Non-nucleated, oval shape.
• They form in bone marrow.

Role of Platelets in Hemostasis

• Platelet adhesion:
• Platelets attach to subendothelial collagen with glycoprotein and von-Willebrand factor.
• Platelet activation:
• Platelet swell, shape change, and pseudopodia.
• Stimulated by: ADP, thrombin
• Platelet release:
• Release of contents, including Serotonin, and ADP.
• Platelet aggregation:
• Platelets stick together.
• Stimulated by: Thromboxane A2 and ADP.
• Platelet procoagulant (Help):
• PF3 exposes for ideal clotting.
• Platelet fusion:
• Platelets fuse with ADP.

Clotting Mechanisms

• Clotting factors are inactive in plasma.
• Clotting mechanisms use activation of factors for fibrin clot.
• Fibrin forms through two pathways.

Extrinsic Pathway

• Releases thromboplastin where tissue is injured.
• Thromboplastin then activates Factor VII.
• Active Factor VII activates Factor X.
• Factor X converts prothrombin to thrombin with Ca, platelets, and Factor V.
• Thrombin converts fibrinogen to fibrin monomer.
• Active factor XIII and Ca then converts fibrin monomer to fibrin clot.

Intrinsic Pathway

• Collagen fibers activate Factor XII, triggered via kininogen and kallikrein.
• Active Factor XII triggers Active Factor XI
• Active Factor XI triggers Active Factor IX.
• Active IX, Factor VIII, Ca and platelets turn on the active Factor X complex.
• Factor X turns prothrombin to thrombin with Ca, platelet, and Factor V present.
• Thrombin transforms fibrinogen into fibrin monomer.
• Fibrin monomer becomes a fibrin clot because of active Factor XIII and Ca.

Important Clotting notes

• When a blood vessel ruptures, both systems simultaneously start blood clotting.
• Extrinsic is more rapid (15 sec) and extensive, intrinsic system is slower (1-6 min).
• Ca++ is needed for nearly all steps, Ca++ levels rarely prevents clotting.
• There's a link relating activated factor VII(extrinsic) and factor IX (intrinsic).
• Vitamin K helps with factors II, VII, IX and X.

Anti-Coagulants

• These are substances that prevent blood clotting.
• In vitro: Oxalate salt, Citrate salt, Silicon, and Heparin.
• In vivo: Heparin and Dicumarol.

Dicumarol

• Plant source.
• By mouth.
• Slow onset and duration.
• Similar chemistry to Vitamin K.
• Only in vivo.
• Competes with vitamin K by inhabiting use causing decreased synth of factors II, VII, IX, X, protein C and S.
• Antidote is Vitamin K

Heparin

• From basophils, mast cells, and liver.
• By intravenous/intramuscular injetion (i.v. & i.m).
• Rapid onset & short duration.
• Sulphated mucopolysaccharide chemistry.
• Antidote
• By injection.
• It increases antithrombin III activity, preventing activation of factor IX. Has a clearing action and raises lipase, cleaning lipids.
• Protamine Sulphate (1% basic protein)

Abnormalities of Hemostasis

• Vitamin K Deficiency:
• Vitamin K is important for the synthesis of factors II, VII, IX, and X by the liver.
• It is synthesized by bacterial flora in the intestine (advisable to delay circumcision one month after birth).
• Its deficiency leads to a deficiency of factors II, VII, IX, and X.
• Causes of its deficiency: - Intestinal sterility: Such as in newborn infants or long antibiotic treatments. - Decreased absorption: As in obstructive jaundice or fat malabsorption as vitamin K is fat-soluble. - Liver diseases. - Anticoagulants: which act by competitive inhibition with vitamin K.

Hemophilia

• Hereditary, sex-linked recessive disease carried by females, transmitted always to the males (carried on the X chromosome).
• 3 types:
• Hemophilia A: Deficiency in Factor VIII (85% of cases).
• Hemophilia B: Deficiency in Factor IX (10% of cases).
• Hemophilia C: Deficiency of Factor XI (5% of cases).
• Characterized by severe prolonged bleeding after mild trauma.
• Clotting time is prolonged.

Leukocytes, White Blood Cells (WBCs) and Immunity

• Total Leukocytic Count: Ranges are 4000 - 10,000/mm3 of blood.
• Types (Differential Leukocytic Count): Leukocytes are granular and agranular by cytoplasmic granules.

Types of WBCS

• Granular leukocytes (Granulocytes):
• Neutrophils are 50% - 70% of leukocytic count & phagocytosis of microbes.
• As well, Eosinophils are 1 -5% & function is detoxification of foreign proteins & other substances.
• Basophils are 0-1% & cytoplasmic granules contain mainly heparin (anticoagulant) and histamine (allergy responsible).
• Agranular leukocytes (Agranulocytes): They do not contain cytoplasmic granules.
• Monocytes are 1-6% of the count and form macrophages, large phagocytic cells.
• Also, Lymphocytes represent 20–40% T and B-lymphocytes and are responsible for specific immunity.

Body Defense Mechanisms (Immunity)

Definition:

• Ability to defend pathogenic agents & immunity could be non-specific or specific. Non-Specific: don't depend on the nature of the harmful substance.
• Skin and mucous membranes defend.
• As well as Acid secretion of stomach.
• Certain substances in the blood can attach and destroy toxins.
• Non-specific cellular mechanism happens.
• Microphages deal with neutrophils & Eosinophils.
• Macrophages react through monocyte & tissue macrophages: act by phagocytosis & & produce cytokines.
• Large and Non T non B lymphocytes make up Natural killer cells (NK cells).

Acquired (Specific) Immunity:

• This immunity type specified to an agent & doesn't develop until after 1st attack of a pathogen/toxin.
• 2 types of acquired immunity.

Humoral (B-cell/antibody-mediated immunity):

• The B-lymphocytes become activated by plasma, which secretes specialized antibodies to attack the invading agents.
• Mechanism of Humoral Immune response is where plasma cells form and cause secretion:
• Once the B-lymphocytes bind the specific antigen, they become activated, enlarge, and differentiate into plasma cells.
• Plasma cells are active cells with expanded reticulum, producing antibodies at a rapid rate.

- Formation of memory cells:

• Some activated B-lymphocytes do not differentiate into plasma cells but forms memory cells.
• This makes them memory cells with vigorous response in case its a 2nd attack on immune response.

Structure of immunoglobulins (antibodies):

• Immunoglobulins (Ig) are circulating antibodies of B-cell activation by an antigen.
• A Y-shape makes up the Igs that hold 2 chains by disulphide bonds so that motion of molecule happens.

Types of Antibodies

Immunoglobulin G (IgG):

• Constitutes 75%, causes major antiviral, antibacterial and antitoxic activity.
• Has low molecular weight, thus crosses the placenta till the fetal blood and gives the immune response.
• Antibodies that respond the Rh are IgG.

Immunoglobulin M (IgM):

• A primary response and is in large amounts .
• Does not cross placenta.
• ABO blood groups antibodies are of the IgM type.

Immunoglobulin A (IgA) (secretory immunoglobulin):

The antibody in secretions, breast milk, and saliva has localized protection in external secretions. It plays an important role in first-line defense at mucosal level that protects viral infection.

Immunoglobulin D (IgD):

• Present as an antigen receptor in B lymphocytes.
• Is in charge of antigen recognition in those B cells.

Immunoglobulin E (IgE):

• Key when comes to parasite infestations.
• Helps with allergic responses and has a role in the release & degranulation of Leukotriens and Mast cells.

Cellular Immunity

Acquired (Specific) Immunity

• Formation of T-lymphocytes especially to destroy all agents.
• Can attack antigen exposure.
• Memory T- lymphocytes produce rapid response for the second infection ( Ag in the cell)
• Functions of the activated T- lymphocytes:
• Surface landmarks are markers or help with cell activity.

Helper T-lymphocytes (Th)-CD4:

• Most cell numerous- They will respond in a reaction with MHC-II cells

Cytoxic T-lymphocytes (TC)-CD8:

Will recognize the agitation from MHC-I so all pathological agitation is going to be provided

Functions:

They attack producing holes in all cells infected

• The cells act for important defense to viral infection and fight cancer cells, rejection to transport

Suppressor T-lymphocytes (Ts)-CD8:

• The reaction of activities of B and T lyphocytes produce an action activity to promote negative feedback

Respiration

• 2 part division includes external & internal respiration.

External Respiration

• Pulmonary ventilation.
• Exchange of carbon dioxide and oxygen.
• Transport of carbon dioxide & oxygen between lungs and the body using blood.
• Via diffusion, the carbon dioxide and oxygen exchanges with blood & tissues.

Internal Respiration

• The cellular use of oxygen within mitochondria generates ATP through oxidative phosphorylation. Making carbon dioxide as its waste.

Respiratory Functions of the Lungs

• Regulation of the balance of acid.
• Defends against pathogens.
• Heat & Water loss. Increase in venous return.
• Speech Enhancement.
• Air passes as it comes through pharynx into the trachea so it can branch the bronchi.
• That then divides the lungs.
• The alveoli grows in the total capillaires with the surface area around 100m2.
• The airways use cartilage so it supports the shape .
• Also are surrounded by tissues to change the diameter of tubes ( smooth contraction) Sympathetic -leads to bronchodilation via the receptors in B2.
• Stimulation by vagus causes histamine that affects the brochoconstriction in the walls.

The inner walls contain the inner walls and that has those

Type I- cells overlies the membrane

Type II-cells-Surfactant creation

Alveolar macrophage- helps so it removes the foreign objects to help

Pulmonary Ventilation

• A gradient helps so Air comes in an goes as for pressure the alveoli and the atmosphere
• On a rest the normal Rate is 12-16

tidal volume - the air inspired or expired at normal the value is near 500 cc

• Pulmonary ventilation - = respiratory rate x tidal volume = 12 x 500 = 6000 c

Mechanics of Respiration

Contraction and expansion of the thoracic cage during expiration and inspiration, demonstrating diaphragmatic contraction, func- tion of the intercostal muscles, and elevation and depression of the rib cage.

• Each Cycle:
• Inspiration
• Expiration

Inspiration

• A process that helps
• Volume of thorax happens in increase
• Increase follows the walls of thorax
• Pressure with the intrapleural from -4 up to -6
• Air runs inside as inner alveolar pressure gets to -1
• Inspiratory wall muscle

Inspiratory Muscles

Those are :

diaphragm:- the key and important.

• The part that cervical segments supply(3rd-5th ).when it go's it enlarges the vertical part ( that is for helping) where we help to change (volume to 75%)

The external intercostal muscle is key

• These run near and pull so there is a pull that help contract with increase, by that we are going to elevate the sides (the diameter) by inversion

The muscle group is inspiration

Help when deep is for forced inspiration

Expiration

Passive, that's to help elastic cord as that has chest wall to promote as we inspire

3 stage as we decrease the air and that has chest walls ( relax wall as we are)

That is in decrease and that has force during, where we have asthma, but the air comes as we make

muscles

• Run along and they will push and pull during

Respiratory Pressures

Volume change ( liters).

Intra-alvelor

Inside when air passes

The part is inspiration

• With those measures the pressure is lower ( atmosphere).
• That is around ( with amount (-1)mm Hg. With lungs, air rushes to the inside

While is Normal

• The inta alveolar does is high. Then to make it normal the MM amount is +1 For air forced with that

The end with the measure

• The measure is 0 MMhg

The Intrapleaural Pressure

• Is pressure through the area 1. e- between. Pleural from lubrication in move

Normal there's no atmosphere as with respiration

• Negative to the wall which helps pull and hold inwards is key

Cause of pressure within The Negative Intrepleaural

• This is what gives the volume

The Recoill

This is Lungs by What we have:

That is elasticity, because we make lining of the alveol

Pressure or the chest

• To start there is volume to 25, then so that with volume to liter=5 the wall has to expand.
• Balloon with these things

Measurement of The Wall

The Intra with help through pressure Normal values with IPP:

Volume

• We end with near the reading -4
• Next near we almost read 6
• Inspiration - we reach -12 we have max recoil and volume increases

* Forcful against all

Forcul Against.

against closed

Functions by:

• helps prevent lung crash

Trans-pressure

That helps keep everything and press Ie. The negativity is more

Surfactant

Its area which it reduce surface pressure

Chem Name:

Complex

• Composition are*
• 1 . Phospholipids-dipalmitoyt-tecithin
• 2/ Surfactants
• 3/calcium Ions

Orgins:

Secrete with Alveoli as Type 1

• Key with reducing surface for long expansion
• Aids we prevent crash during the phase as all can get smaller and higher.
• It stops lung failure
• Not enough of the key for what's needed
• Stress syndrome

*Hyaine membrane

• Occurs with only infants, to not enough space/time for expansion*

Long term is to much the 100

• Oxygen as the card gets surge, is cause that effect
• Heavy smoking, this also has this cause

Static

1.V Tidal

Pulmonary

• (5) Inspiratory capacity (8)volume (3) Expiration reserve volume (4)Residual Volume

TidalVolume

Lungs -Volume

Volume air or expires equal with =500oc Air Maximum The Max-air with normal 3000c

• The highest maximum air for forced 110cc
• Volume for ( that has pressure by is as we have maximum =1200
• (B)*

A Lung

One volum

• *air Volume

• -35,00CC*.

• -is volume as has normal expire 23110c*

• -is for capacity, to increase/decrease when air with normal = 320** Is as much when happens lung maximal by all air for 4500cc

Volume by equal

• (8)8- 104,less . in females

Air with spirometer .by

• Volume Tidal

• Air can to volume tidal capacity Volume

• • Air can be measure, principle

Resistance Volume:

• Is when we have volume maximal
• The Normal =1210ml

significan

• Main has blood and that and also
• The concentration helps
• Clinical-*

Ratio-Total The Balance between normal range as low

• By 3 with what makes, the hard with that helps emphysema, increases

3-Medal:

• RV BY volume chest
• After wall can reduce as some

Volume vital capacity

• The amount of what we are max with air
• Measurement*

air volume, the standards 4%60,

, the volume and is for the work and for what gets measured as and is helps measure fitness, air gets, more air to fitness air for that

Volume

Air * air with chest fitness

• Decreases are for older for what may hold a volume. chest*

Lung

• With What happens*:
• The Muscles: May Be With Paratysis*
• The Bones - Kyph, Scoliosis*
• The lung diseases*:
• Bronch air*. The chest

Chest:

• Some as for what happens And that give to a high decrease.
• Wall problems*

A-passage

• (what holds to air or exchange)**

Air exchange:

• From Wall from the Air from chest, to that

Air space.

air 140 cc

• Sigh-: What decrease for dead wall *

Symphy-increase, that what decrease the area

*Importance by

• The Wall air that happens is by gas or blood, that happen from area*. Is chest air where from the remains
• *Protect to Damage.**. By with what gets by,air Key
• The Air gets moisture*,
• The Walls - Is to what happens as mucus that may get with diameter through 18.*
• *There with air will get cough or there where the cilia are *
• (2): Measure :**

(A) method.Air

The walls those for the air (That all that gets) air (what also is there by also With this ( all from with (All the air) 3/ 8 / 11

lung

• All those. what all

The functions where can we find

• Chest wall , that follows wall . with key, those we are. and that for the help all what help for also There those those

The volume