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57 Cards in this Set

  • Front
  • Back

Functions and Components of the


Circulatory System


(quick overview)

Heart
– Dual pump system


Blood vessels


– Passageways


Blood
– Transport mechanisms


– Serves many purposes

Circulatory System Functions

Transportation


– Respiratory gases, nutrients, and wastes


Regulation


– Hormonal and temperature


Protection
– Clotting and immune

Circulatory System Components

1.• Cardiovascular system


– Heart: four-chambered pump


– Blood vessels: arteries, arterioles, capillaries, venules, and veins



2.• Lymphatic system


– Lymphatic vessels, lymphoid tissues, lymphatic organs (spleen, thymus, tonsils, lymph nodes)

Composition of the Blood

• 5 Liters of blood


• Liquid, dissolved proteins, cells


• Viscosity: 5-Ames that of water (thickness)


• pH ~ 7.35



• Composition


– Formed elements: 45% (solids)


– Plasma: 55% (liquid portion of blood)

Two components of blood

1. Plasma: fluid part of blood


– Plasma proteins
– Serum


2. Formed elements

Composition of the Blood: Plasma

Nutrients and metabolites


– Glucose, amino acids, fatty acids, etc


• Hormones


– Insulin, glucagon, sex hormones etc.


• Ions
– Na+ (major ion; maintains osmoAc pressure)


– K+, Ca++, Cl-, Mg++ etc


Bicarbonate; important buffer


• Respiratory gasses


– O2, CO2
• Waste products


– Urea, food additives etc.

Plasma: Three types of plasma proteins

-extracelluar (dissolved in blood)


• Proteins consAtute 7-9% of plasma


• Three types of plasma proteins: albumins, globulins, & fibrinogen


1.


2.


3.

Albumin

accounts for 60-80% (Major protein)


• Creates colloid osmotic pressure that draws H20 from interstital fluid into capillaries to maintain blood volume & pressure

Globulins

• Alpha and beta globulins transport lipid soluble molecules


• Gamma globulins are antibodies (fight infection)

Fibrinogen

• a soluble protein that functions in clotting


• Converted to fibrin; an insoluble protein polymer
Serum is fluid len when blood clots (plasma minus fibrinogen)

Erythrocytes

AKA red blood cells


– 4-6 million mm3


– Biconcave


• Shape is critical to function


– Carry oxygen


– Lack nuclei and mitochondria


– Have a 120-day life span


– Contain hemoglobin(binds oxygen) and transferrin

Composition of the Blood: Formed Elements

Platelets (thrombocytes)


- Smallest formed element


– Lack nuclei
- Very short-lived (5−9days)


- Clot blood


- Need fibrinogen

Hematopoiesis

• Is formation of blood cells from stem cells in bone marrow (myeloid tissue) & lymphoid tissue



Erythropoiesis is formation of RBCs


– Stimulated by erythropoietin (EPO) from kidney



Leukopoiesis is formation of WBCs


– Stimulated by variety of cytokines


= autocrine regulators secreted by immune system

Erythropoiesis

• 2.5 million RBCs are produced/sec


• Lifespan of 120 days


• Old RBCs removed from blood by phagocytic cells in liver, spleen, & bone marrow


– Iron recycled back into hemoglobin production

Antigens:

found on the surface of cells to help immune system recognize self cells

Antibodies

secreted by lymphocytes in response to foreign cells

ABO system:


-possibilities

antigens on erythrocyte cell surfaces



• Type A = Has the A antigen


• Type B = Has the B antigen
• Type AB= Has both the A and B antigens
• Type O = Has neither the A nor the B antigen

Red Blood Cell Antigens and Blood Typing

In a transfusion reaction, a person has antibodies against antigens he/she does not have.

agglutination

fill in

erythroblastosis fetalis in

Fill in

Who are universal donors?

fill in

Blood Clotting:


Hemostasis

Hemostasis: cessation of bleeding when a blood vessel is damaged



• Process turns liquid blood into solid (gel) by converting soluble protein (fibrinogen) into insoluble protein (fibrin)



• Damage exposes collagen fibers to blood,


producing:


1. Vasoconstriction
2. Formation of platelet plug
3. Formation of fibrin protein web

Blood Clotting: Platelets

• Platelets don't stick to intact endothelium because of presence of prostacyclin (PGI2--a prostaglandin) & nitric oxide (NO)


– Keep clots from forming & are vasodilators (dilated)



• Also the removal of ADP by CD39 (taking ADP & converting it to AMP) (which keeps from blood clotting)

Blood Clotting: Platelets continued


what if we have an injury>

• Damage to endothelium allows platelets to bind to exposed collagen


releases von Willebrand factor; increases bond by binding to both collagen & platelets


– Platelets stick to collagen & release ADP, serotonin, & thromboxane A2


• = platelet release reaction

Blood Clotting: Platelet aggregation

• Some chemicals (serotonin & thromboxane A2) stimulate vasoconstriction, reducing blood flow to wound


• Other chemicals (ADP& thromboxane A2) cause other platelets to become sticky & attach & undergo platelet release reaction


– This aggregation continues until platelet plug is formed

Blood Clotting: Fibrin

• Fibrinogen turns to fibrin and forms meshwork around platelets



• Calcium and phospholipids (from the platelets) convert prothrombin to the active enzyme thrombin, which converts fibrinogen to fibrin.



• Conversion of prothrombin(inactive) to thrombin(active) done by Factor X



• How Factor X is controlled depends on the nature of the clotting reaction


– Intrinsic pathway


– Extrinsic pathway

Blood Clotting: Fibrin (Intrinsic pathway)

Fibrinogen is converted to fibrin via one of two pathways:


1. Intrinsic pathway: Activated by exposure to a negatively charges surface


1. collagen (or glass)
2. Activation of cascade reaction of other blood


factors.
3. Ultimately Factor X is activated

Blood Clotting: Fibrin (Extrinsic pathway)

Fibrinogen is converted to fibrin via one of two pathways:


2. Extrinsic pathway: shorter/faster pathway


1. Initiated by thromboplastin, only present in tissue


2. Clomng of blood that enters tissues due to injury


3. Thromboplastin directly activates factor X

Role of Fibrin

• Once fibrin network is established clot now contains platelets, fibrin, trapped RBCs



• Platelet plug undergoes plug contraction to form more compact structure


– Physical restructuring of platlets


– Actin contraction • Analogous to smooth muscle contraction

Anticoagulants

• Clotting can be prevented with certain drugs:


– Calcium chelators (sodium citrate or EDTA)


– Heparin: blocks thrombin
– Coumarin: inhibits vitamin K

Dissolution of Clots

When damage is repaired, activated factor XII(12) causes activation of kallikrein


– Kallikrein converts plasminogen to plasmin


• Plasmin digests fibrin, dissolving clot

HEP

intrinsic and extrinxic pathways of clotting. How are they different, how are they similar?

Structure of the Heart: 4 chambers

1. Right atrium: receives deoxygenated blood from the body


2. Left atrium: receives oxygenated blood from the lungs


3. Right ventricle: pumps deoxygenated blood to the lungs


4. Left ventricle: pumps oxygenated blood to the body


• Chambers separated by fibrous skeleton

Structure of the Heart

• Fibrous skeleton:


– Dense collection of connective tissue



– Separates atria from ventricles. The atria therefore work as one unit, while the ventricles work as a separate unit.



– Forms the annuli fibrosi which hold in heart valves

The heart is responsible for the continuous pumping of blood through 2 independent systems

-Oxygen-rich, CO2-poor blood


-Oxygen-poor, CO2-rich blood

Pulmonary Circulations

Pulmonary: between heart and lungs


– Blood pumps to lungs via pulmonary arteries.


– Blood returns to heart via pulmonary veins.

Systemic Circulations

Systemic: between heart and body tissues


– Blood pumps to body tissues via aorta.


– Blood returns to heart via superior and inferior venae cavae.

Circulatory Sequence

-Arteries run in parallel


-All tissues have access to fully oxygenated blood


-fill in from lecture!

Pulmonary & Systemic Circulations

• Resistance in systemic circuit > pulmonary


– Amount of work done by left ventricle pumping to systemic is 5-7X greater


(Causing left ventricle to be more muscular (3-4X thicker))



-much easier to pump blood to lungs, hard to blood blood to the entire body (which is why the left ventricle works much harder )

Valves of the Heart: Atrioventricular valves (AV):

Atrioventricular valves (AV): located between the atria and the ventricles


Tricuspid: between right atrium and ventricle


Bicuspid (mitral): between left atrium and ventricle



Valves: monitors flow (makes sure only flows in one direction)

Valves of the Heart: Semilunar valves

Semilunar valves: located between the ventricles and arteries leaving the heart


Pulmonary: between right ventricle and pulmonary trunk


Aortic: between left ventricle and aorta

Valves of the Heart

Opening & closing of valves results from pressure differences


– High pressure of ventricular contraction is prevented from inverting AV valves by contraction of papillary muscles which are connected to AVs by chorda tendinea

Three Types of Muscle

• Skeletal Muscle


– Voluntary


– Striated
– Not interconnected
– Long and not branched


• Cardiac Muscle


– Involuntary


– Striated


– Interconnected via intercalated discs (Gap junctions)


– Functional syncytium


• Smooth Muscle


– Involuntary


– Non-striated

Structure of Heart Wall

• 3 cell layers
– Endocardium: epithelial tissue


– Myocardium: cardiac muscle


– Epicardium: thin covering of outer surface



Pericardial Sac:


– Anchors the heart


– Double layer


– Secretes pericardial fluid •-> reduces friction

Dividing the heart

Left & right (Pulmonary & systemic)



Top & bottom (atria & ventricle)


-cant both contract at same time)

Myocardium

-a mass of cardiac muscle cells connected to each other via gap junctions.



-Action potentials that occur at any cell in a myocardium can stimulate all the cells in the myocardium



-behaves as a single functional unit (different from skeletal muscle)



-the atria of the heart compose one myocardium & the ventricles of the heart compose another myocardium

Electrical Activity of the Heart

Autorhythmicity: Rhythmic beat of heart produced by producing its own action potentials



Autorhythmic cells: Special cardiomyocytes that initiate and conduct action potentials



-doesn't need any help from CNS, heart can beet on its own

Electrical Activity of the Heart

Sinoatrial (SA) node: "pacemaker"; located in right atrium


– Pacemaker potential: slow, spontaneous depolarization



-where the typical heartbeat starts, they initiate their own AP, & if will travel through the rest of the myocardium



-No need from external stimulus,


-continuously creating own AP, polarizes & depolarizes

Brain's role in Electrical Activity of the Heart

Pacemaker cells in the sinoatrial node depolarize spontaneously, but the rate at which they do so can be modulated:


-PNS slows heart rate (Vagus nerve)


-SNS (epinephrine & norepinephrine) increase the heart rate


-higher level of regulation in medulla

Myocardial action potentials

– Cardiac muscle cells have a resting potential of −90mV.


– They are depolarized to threshold by action potentials from the SA node.



Ap: cardiac AP is about 100 slower than skeletal AP

Calcium Channels in Cardiac Muscle

fill in

Process of Electrical Activity of the Heart

– Action potentials spread via intercalated discs (gap junctions).


• Within a mycocardium – (Atria, ventricle)


– AV node at base of right atrium and bundle of His conduct stimulation to ventricles.


– In the interventricular septum, the bundle of His divides into bundle branches.


– Branch bundles become Purkinje fibers, which stimulate ventricular contraction.

Timing of Electrical Activity of the Heart

– Action potentials from the SA node spread rapidly.


• 0.8–1.0 meters/second


– At the AV node, APs slow


down.


• 0.03−0.05 m/sec


• This accounts for half of the time delay between atrial and ventricular contraction.


– The speed picks up in the bundle of His, reaching 5 m/ sec in the Purkinje fibers.


– Ventricles contract 0.1–0.2 seconds after atria.

Refractory Periods

• Because the atria and ventricles contract as single units, they cannot sustain a contraction.



• Because the action potential of cardiac cells is long, they also have long refractory periods before they can contract again.



• Avoidance of “typical” muscle issues like tetanus

Electrocardiogram

This instrument records the electrical activity of the heart by picking up the movement of ions in body tissues in response to this activity.

Electrocardiogram waves

• P wave: atrial depolarization


• QRS wave: ventricular depolarization


• S-T segment: plateau phase


• T wave: ventricular repolarization

HEP: understand the correlation between ECG, heart sounds, action potentials, contraction

fill in