anatomy cardiovascular system

cardiovascular system

heart, blood vessels, blood

heart

pumps blood, maintains blood pressure

arteries

carry blood away from the heart

Capillaries

permit the exchange of blood and interstitial fluids

veins

carry blood back to the heart

functions of blood

-transports dissolved gases, nutrients, hormones, and metabolic wastes
-regulates pH and ion composition of interstitial fluids
-restricts fluid loss at injury sites
-defends against toxins and pathogens
-stabilizes body temp

blood

fluid connective tissue

whole blood

blood with all components

plasma

liquid matrix, 55% of the volume of whole blood

formed elements

cells and cell fragments-mainly RBCs, 45% volume of whole blood

hematocrit (packed cell volume (PCV))

% of whole blood from formed elements

plasma proteins

1. albumin - 60% of plasma proteins
2. globulins - 35% of plasma proteins
3. fibrinogen - 4% of plasma proteins

immunoglobulins

(antibodies) attack foreign proteins and pathogens

transport globulins

bind small ions, hormones, lipids, and other compounds

Fibrinogen

plasma protein that is converted to fibrin in the clotting process

plasma solutes

electrolytes, organic nutrients, organic wastes

electrolytes

minerals that help maintain vital cell activities

organic nutrients

lipids, carbohydrates, amino acids

organic waste

carried to sites of breakdown or excretion

Platelets

small membrane-bound cell fragments involved in clotting

white blood cells

fight infection

red blood cells

Blood cells that carry oxygen from the lungs to the body cells.

Hemopoiesis

development of formed elements, occurs in red bone marrow

Hemocytoblast

developed from hematopoietic stem cells, produce lymphoid and myeloid stem cells

lymphoid stem cells

give rise to lymphocytes

myeloid stem cells

give rise to red and white blood cells

lymphoid order

lymphoid stem cells --\> lymphoblasts --\> prolymphocytes --\> lymphocytes

colony stimulating factors

hormones released by activated lymphocytes and other cells during an immune response to stimulate blood cell formation

Erythropoietin (EPO)

released into plasma in response to low tissue oxygen levels (hypoxia)

hematology

study of blood and blood-forming tissues

dyscrasias

blood disorders

complete blood count (CBC)

Determination of numbers of blood cells, hemoglobin concentration, hematocrit, and red cell values

white blood cell differential count

tests to see what percentage of the total white blood cell count is composed of each of the five types of leukocytes

red blood cell count

number of erythrocytes per microliter of blood

rouleax

Stacking of RBCs

red blood cell characteristics

-No nucleus
-No organelles
-large surface area to volume ratio
-packed with hemoglobin
-flexible, can move through diameters smaller than it

Hemoglobin

An iron-containing protein in red blood cells that reversibly binds oxygen.

deoxyhemoglobin

hemoglobin without oxygen

Eythropoeisis

red blood cell formation

hemoysis

destruction of red blood cells

erythroblast

immature red blood cell

hematuria

presence of blood in the urine

blood types

determined by the presence or absence of an antigen on the surface of a red blood cell

anitgens

substances that elicit immune response
-A
-B
-Rh

ABO blood groups

based on the presence of A and B surface antigens

Aggulation

clumping of red blood cells caused by a cross-reaction

cross-reaction

surface antigens on RBCs of one blood type exposed to antibodies from another blood type

Rh blood group

based on presence or absence of Rh antigen
-O negative
-AB positive

blood typing tests

Drops of patient's blood mixed with solutions containing antibodies to surface antigens A, B, and D (Rh)
- Clumping (agglutination) occurs where sample contains the corresponding antigen
*Type A blood will clump with
anti-A antibodies

genetics of blood type

Presence of anti-A and/or anti-B antibodies is genetically determined
- Remains constant throughout life
- No need to be exposed to foreign RBCs to develop those antibodies
- Anti-Rh antibodies are not automatically present
- Rh-negative person will not have any anti-Rh antibodies until exposed to Rh-positive RBCs
- Then, they will develop anti-Rh antibodies

hemolytic disease of the newborn (HDN)

an RBC related disorder caused by a cross reaction between fetal and maternal blood types

WBC types (never let monkeys eat bananas)

neutrophils, eosinophils, basophils, monocytes, lymphocytes

white blood cell properties

-spend a short time in circulation
-can migrate out of bloodstream
-are attracted to chemical stimuli (positive chemotaxis)
-N, E, M are capable of phagocytosis

granular leukocytes

have abundant cytoplasmic granules that absorb histological stains
-Neutrophils
-Eosinophils
-Basophils

agranular leukocytes

contain very small granules that do not appear when stained
-Monocytes
-Lymphocytes

Hemostasis

process responsible for stopping blood loss through walls of damaged blood vessels

hemostasis stage 1: vascular phase

endothelial cells release chemicals and hormones that:
1. cause smooth muscles to contract and promote vascular spasms
2. stimulate division of endothelial cells, smooth muscle cells, and fibroblasts for repair

hemostasis stage 2: platelet phase

platelets stick to endothelial surfaces and each other

Hemostatis Stage 3: Coagulation phase

complex sequence of steps leading to conversion of fibrinogen to insoluble fibrin

Coagulation extrinsic pathway

-Initiated by release of tissue thromboplastin from damaged tissue
-tissue factor combines with Ca2+ and others to activate factor X

Coagulation intrinsic pathway

-begins with activation of proenzyme exposed to collagen fibers at injury site
-pathway proceeds w/ assistance to PF-3
-sequence of enzyme attractions lead to factor X

Coagulation common pathway

-Thrombin converts fibrinogen into insoluble fibrin polymers
-Fibrin fibers become part of the clot

blood flow: changes in pressure

-highest pressure in aorta
-pressure drops at each branch in arterial system

blood flow: changes in diameter from aorta to capillaries

-Blood vessels diverge and branch
-Decreasing diameter increases resistance \= decreased pressure \= decreased flow

blood flow: changes in diameter from capillaries to venae cavae

-Blood vessels converge to form larger vessels
-Increasing diameter decreases resistance \= increased fl

changes in blood flow

-Highest flow in the aorta
-Slowest in the capillaries
-Flow accelerates in venous system

systolic pressure

peak pressure measured during systole

diastolic pressure

peak pressure measured during diastole

pulse pressure

difference between systolic and diastolic pressure

Mean Arterial Pressure (MAP)

Adding one-third of pulse pressure to diastolic pressure
-ex: 90 + (120 - 90)/3 \= 100 mm Hg

capillary exchange

Involves a combination of diffusion, osmosis, and filtration

Capillary hydrostatic pressure (CHP)

pressure within the capillary beds; pushes water and small molecules out of the bloodstream into interstitial fluid

Capillary Exchange: Diffusion

Net movement of substances from an area of higher concentration to lower concentration

1. Distances are short
2. Concentration gradient is large
3. Ions or molecules involved are small.

capillary exchange: filtration

-arterial end of capillary
-blood colloid osmostic pressure increases
-fluid moves out of capillary

Net Filtration Pressure (NFP)

the difference between net hydrostatic pressure and blood colloid osmotic pressure

homeostatic mechanisms

Ensure adequate tissue perfusion (blood flow through tissues)

Autoregulation

-Involves local changes in blood flow within capillary beds
-Regulated by precapillary sphincters in response to chemical
changes in interstitial fluid

central regulation

-neural and endocrine control
-Activated if autoregulation is ineffective

Vasodialators

Local chemicals that increase blood flow

central regulation: neural

-Activation of cardioacceleratory center
-Activation of vasomotor center (controls peripheral
vasoconstriction)
-Can increase cardiac output and reduce blood flow
to nonessential or inactive tissues

central regulation: endocrine

Release of vasoconstrictor (primarily NE), producing long-term increases in blood pressure

baroreceptor reflex

Respond to changes in blood pressure
-Receptors are located in walls of:
1. Carotid sinuses
2. Aortic sinuses
3. Right atrium

chemoreceptor reflexes

respond to blood and cerebrospinal fluid changes in oxygen, carbon dioxide, and pH
-receptors located in:
1. Carotid bodies
2. Aortic bodies
3. ventrolateral surface of medulla oblongata

cardiovascular adjustments at rest

Cardiac output \= 5800 mL/min

cardiovascular adjustments during light excercise

Cardiac output increases to 9500 mL/min

1. Vasodilation occurs, peripheral resistance drops,
and capillary blood flow increases
2. Venous return increases with skeletal muscle
contraction; increased respiration creates
negative pressure in thoracic cavity, drawing
blood back (respiratory pump)

cardiovascular adjustments during heavy excercise

Cardiac output approaches maximal levels (~17,500 mL/min)
1.Major changes in peripheral blood distribution allow large increase in flow to skeletal muscles without overall decrease in systemic blood pressure
2. Increased flow to skeletal muscles
3. Increased flow to skin (promotes heat
loss)
4. Reduced flow to digestive viscera and
kidneys
5. Brain blood flow remains unchanged

shock

Acute cardiovascular crisis marked by:
1. Low blood pressure (hypotension)
2. Inadequate peripheral blood flow

circulatory shock

positive feedback loops beginning when blood loss \>35 percent

Progressive shock stage 1

1. Blood volume drops by more than 35 percent
-Despite sustained vasoconstriction and mobilized venous reserves:
-Blood pressure remains low
-Venous return reduced
-Cardiac output inadequate

Progressive shock stage 2

Low cardiac output reduces blood flow to heart
-Damages myocardium
-Leads to further reduction to cardiac output

Progressive shock stage 3

Reduced cardiac output accelerates oxygen starvation in tissues
-Local chemical changes promote intravascular clotting
-Further restricts peripheral blood flow

Progressive shock stage 4

Local pH changes increase capillary permeability
- Further reducing blood volume

irreversible shock 1

Carotid baroreceptors trigger
vasomotor centers
-Sympathetic output causes widespread vasoconstriction
-Reduces peripheral circulation but increases brain blood flow temporarily

irreversible shock 2

Without treatment, blood pressure will again decline
- Heart is now seriously damaged, and cardiac output declines

irreversible shock: circulatory collapse

Occurs when arteriolar smooth muscles and
precapillary sphincters cannot contract
Leads to:
1. Widespread vasodilation
2. Immediate and fatal decrease in blood pressure
3. Cessation of blood flow

Vasculogenesis

Formation of the first blood vessels by precursor endothelial cells called hemangioblasts

cardinal veins

Series of venous channels that will form the superior and inferior venae cavae

aortic arches

Series of arterial channels that will form the carotid arteries, aortic arch, and part of pulmonary arteries

dorsal aorta

Becomes the descending aorta

Angiogenesis

Growth of new blood vessels from preexisting vessels