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77 Cards in this Set

  • Front
  • Back
6 goals the circulatory system accomplishes
1. Distribute nutrients from digestive tract, liver, and adipose (fat) tissue.
2. Transport O2 from lungs to the entire body and CO2 vice versa.
3. Transport metabolic waste products from tissues to excretory sytem (kidneys).
4. Transport hormones from endocrine glands to targets and provide feedback.
5. Maintain homeostasis of body temp.
6. Hemostasis, blood clotting. (Necessitated by the presence of circulatory system)
1. Perfusion
2. Ischemia
3. Anoxia
1. The flow of blood thru a tissue
2. Inadequate blood flow (results in tissue damage due to O2&nutrients shortage and buildup of metabolic wastes)
3. Adequate circulation but reduced suply of O2. Wastes are still removed
**Ischemia worse than anoxia
Arterioles have smooth muscle and how does it function?
Can acts as a control valve to restrict or increase flow of blood into capillaries
**All exchange of material btw blood & tissues occur in capillaries, not arterioles/venules
1. Pulmonary circulation
2. Systemic circulation
1. flow of blood from heart --> lungs --> heart
2. heart --> rest of the body --> heart
Portal system
Direct transport systems that w/o passing thru the whole body transport
1. nutrients directly from intestine to the liver
2. hormones from hypothalamus to pituitary
1. Atria
2. Ventricles
1. Reservoirs where blood can collect from veins b4 pumped into ventricles
2. Pump blood out of the heart at high pressures into arteries
Pulmo. circ. path
vena cava -> right atrium -> right ventricle -> pulmonary artery -> lungs -> pulmonary vein -> left atrium -> left ventricle -> aorta
**Pumonary artery carried deoxygenated blood
1. Coronary arteries
2. Coronary veins
1. Branch to supply blood to the wall of heart.
2. Where deoxygenated blood from heart collects
Coronary sinus
Formed from coronary veins, located beneath a layer of fat of heart wall. It is an open space, a pool of low-pressure blood. Holds only deoxygenated blood that drains directly into right atrium.
Atrioventricular (AV) valve
Prevents backflow of blood from each ventricle to atrium.
**Ventricular pressure is very ultra high & atrial pressure is lower.
1. Bicuspid (mitral) valve
2. Tricuspid valve
1. AV valve btw left atrium and left ventricle
2. btw right atrium and right ventricle
Semilunar valves
Pulmonary & aortic semilunar valves btw the large arteries and ventricles.
Venous valves
Prevent backflow and have a sucking action. Contraction of skeletal muscles pressurizes venous blood.
**Varicose veins result when the valves fail.
Ventricles are relaxed, and blood is able to flow into them from atria. Atria contract to propel blood flow.
**At the end of diastole, ventricles contract, initiating systole.
Period when ventricles contract('lub' to 'dub'); causes AV valves to shut. Blood pressure in ventricle rises until semilunar valves fly open and blood rushes into aorta/pulmo artery.
**At the end of systole, ventricles are empty and relaxes. Semilunar valves prevents backflow.
"lub-dub" of the heartbeat,
1. lub
2. dub
1. results from the closure of the AV valves at the beginning of systole
2. the sound of semilunar valves closing at the end of systole.
Heart rate (HR) or pulse
# of 'lub-dub' cardiac cycle repeated per minute. 1 beat per sec.
**Stronger heart pumps more blood each time it contracts.
1. Stroke volume (SV)
2. Cardiac output (CO)
1. Amount of blood pumped with each systole.
2. Total amount of blood pumped per minute. =stroke volume(L/beat) * heart rate(beats/min)
Which is larger: the cardiac output of right or left ventricle?
Neither; they are equal.
2 ways to increase cardiac output
1. Increasing heart rate.
2. Larger stroke volume: Frank-starling mechanism - if the heart muscle's stretched by filling it w/ more blood, it will contract more forcefully.
Venous return
Return of blood to the heart by the vena cava. If increased, heart receives more blood, thus muscle stretched and contract more forcefully. Result: more heart pumps blood out to tissues. Larger volume of blood enters heart & heart contracts better.
**Significantly increases stroke volume.
2 ways to increase venous return
1. Increase total volume of blood in circulatory system by retaining water.
2. Contraction of large veins propeling blood toward the heart. Venous valves plays a big role.
Functional syncytium
Happens in cardiac muscles, not neurons.
Cytoplasm of neighboring cells can communicate by depolarization via gap junctions, found in intercalated disks of cardiac muscle cells.
**This is electrical synapse! No chemical synapses btw card. mus. cells**
Effect of functional syncytium
Once an action potential starts, it spreads in a wave of depolarization thruout card. muscle.
**Atria & ventricles are separate syncytia.
What happens if gap junction in the heart was blocked, but voltage-gated ion is functional?
A cell w/ blocked gap junctions would be unable to transmit action potential to neighbor cells.
1. Fast Na+ channels
2. Slow Ca2+ channel (Na-Ca channel)
1. From neurons
2. Involved in card. muscle action potential. When the channels open due to depolarization, they allow passage of both Na & Ca2+ down a gradient. Also stay open LONGER than fast Na+ channels, causing mem. depolarization last longer in card. muscle than in neurons.
A result of long depolarization in card. muscle
Contraction of muscle lasts a long time, strengthening the force w/ which blood is expelled.
3 functions of T tubles in card. muscle.

**Significant portion of Ca2+ that stimulates contraction comes from extracellular pool.
1. Maximize the entry of Ca2+ in the cell.
2. Allow entry of Ca2+ from extracellular envt
3. Induce sarcoplasmic reticulum to release Ca2+
**This combo of intra/extracellular Ca2+ causes contraction of actin-mysin fibers
Heart is not stimulated to contract by
neuronal or hormonal influences, though they can change the rate/strength.
Card. muscle cells will contract on their own free of external influences.
Sinoatrial (SA) node
A special region of right atrium where initiation of action potential that starts each cardiac cycle occurs automatically within heart.
**Has a resting potential about -55mV and special Na+ leak channels responsible for rhythmic automatic excitation
Steps of SA node potential
1. When membrane repolarizes after an action potential, it doesn't remain flat at resting potential.
2. Na+ leaks into the cell, allowing it to reach threshold for opening the voltage-gated ion channels. (At higher resting potential, fast Na+ channels are inactivated, so only slow Na+-Ca2+ channels open)
3. Cells then fire action potential, transmitting it to the rest of the heart, repolarize, then repeats once per heartbeak.
Why don't K+ leak channels cause spontaneous action potentials in neurons or muscle cells?
Depolarization requires Na+ to enter the cell, but K leak channels allow K+ to leave the cell, only polarizing the membrane (opposite effect of Na+ leak channels).
Characteristics of SA node
Has the most Na+ leak channels, thus reaches threshold before any other region of the heat does. AKA pacemaker, where action potential begins and spreads thru atria, causing them to contract and fill ventricles w/ blood.
Atrioventricular (AV) node
Transmits action potentials very rapidly w/o contracting. AKA internodal tract. As impulse travels to AV node almost instantly, it spreads thru atria more slowly b/c the impulse passed more slowly in card. muscle than in conduction fibers.
AV bundle (bundle of His)
Where the impulse passes from AV node to the ventricles after it is delayed slightly at AV node.
Divides into right & left bundle branches.
Purkinji fibers
Allow the impulse to spread rapidly and evenly over both ventricles.
Result: this region of ventricles contracts first, and blood is pushed toward the top of heart.
Track of impulse
SA node AKA pacemaker (Na+ leaks into cell & opens voltage-gated ion channels, thus action potential fired) -> AV node -> AV bundle -> Right/left bundle branch -> Purkinje fibers
1. Driving force for blood flow
2. What is friction and how does it result?
3. Resistance
1. Difference in pressure from arteries to veins.
2. Force opposing flow; results when blood squeezes thru many tiny branching vessels.
3. Opposing force
1. P=QR
2. How is the equation used?
1. Pressure gradient from arterial system to venous system(mmHg) = blood flow (L/min) * resistance
2. It shows that we can only change blood flow by changing either pressure or the resistance.
**P&R are only independent variables.
1. How can pressure be varied?
2. How about resistance?
1. By increasing force or rate of cardiac contraction.
2. By the degree of constriction of arteriolar smooth muscle, aka precapillary sphincters.
** If constricts, blood flow more difficult, thus resistance increases.
1. What controls peripheral resistance (R)?
2. There's pressure in arterial system, and it is provided by:
1. Sympathetic nervous system.
2. A constant level of norepinephrine released by sympathetic postganglionic axons innervating precapillary sphincters.
**This constant nervous input=adrenergic tone (sympathetic)
3 effects of sympathetic system activation
1. Increase the overall peripheral resistance, increasing blood pressure.
2. Divert blood away from one tissue so that another is preferentially perfused.
3. Precapillary sphincters in gut contract & arterioles relax.
**Result: blood flow diverted from gut to skeletal muscle, facilitating fight/flight response.
Systemic arterial pressure
Force per unit area exerted by blood upon walls of arteries.
1. Systolic pressure
2. Diastolic pre.
3. Pulse pressure
1. Highest pressure ever occurs in circulatory system, attained as ventricles contract.
2. Lowest pressure between heartbeats
3. Difference between systolic & diastolic pressure
1. Pressure in vena cava is
2. Highest pressures in circulatory system are achieved in:
1. About 0 mmHg
2. Left ventricle, aorta, & other large arteries.
**Driving pressure in vena cava is negliglble, thus it depends on valves to prevent backflow.
Why does arterial pressure still high in btw heartbeat?
During diastole, elastic/muscular arteries exert pressure on blood, providing a continued driving force for blood.
1. Does nervous system control blood flow?
2. How does local autoregulation work?
**It is the major determinant of blood supply to heart.
1. No; instead tissues of extra blood flow can. (aka local autoregulation)
2. Metabolic wastes have a direct effect on arteriolar smooth muscle, causing it to relax. Thus when wastes build up in tissues, vasodilation occurs automatically.
What increases cardiac output?
Contraction of smooth muscle in walls of large veins.
55% of blood, consists of electrolytes (Na+, K+, Cl-, Ca2+, & Mg2+), buffers (HCO3- keeps to pH 7.4), sugars, blood proteins, lipoproteins, CO, O2, & metabolic waste products dissolved in water.
Bicarbonate (HCO3-) prevents pH changes via
CO2 + H2O <-> H2CO3 <-> HCO3- + H+
1. Sugar in blood
2. Blood proteins
1. Glucose
2. albumin, immunoglobulins (antibodies), fibrinogen, & lipoproteins
1. Albumin
2. Immunoglobulins
3. Fibrinogen
4. Lipoproteins
5. Urea
1. For maintenance of oncotic pressure (osmotic pressure in the capillaries due o plasma proteins).
2. Key parts of immune system
3. For blood clotting
4. Consists of fats, cholesterol, carrier proteins., transporting lipids in bloodstream.
5. Metabolic waste prduct, a breakdown product of a.a, a carrier of excess N.
1. Hematocrit
2. Serum
1. Volume of blood occpied by RBS; 40-45% is normal.
*WBC & platelets about 1%
2. Similar to plasma except it lacks all proteins involved in clotting.
1. Erythropoeitin
2. Erythrocyte
1. made in kidney, stimulates RBC production in bone marrow.
2. Has no nucleus, no mitochondria, lasts 120 days. Requires ATP, thus relies on glycolysis. Has a large surface area for gas exchange.
1. Blood type of "universal acceptors"
2. of "univeral donors"
1. AB. Don't form antibodies to either A or B type surface proteins.
2. O. Have neither type A nor B surface antigens, capable of eliciting an immune response.
1. White blood cells
2. Chemotaxis
Fight infection/dispose debris. Has a normal eukaryotic cell structures. Some moves by amoeboid motility (crawling).
**Able to squeeze out/roam freely in tissues.
2. movement directed by chemical stimuli
6 types of WBC
1. Macrophage
2. B cell
3. T cell
4. Neutrophil
5. Eosinophil
6. Basophil
1. Phagocytose debris & microorganisms, amoeboid motility, & chemotaxis
2. Mature into plasma cell & produce antibodies
3. Kill virus-infected cells and tumor cells; reject tissue grafts; control immune response.
4. Phagocytose bact resulting in pus; amoeboid motility; chemotaxis
5. Destroy parasites; allergic rxns
6. Store and release histamine; allergic rxns
1. Platelets
2. Their function
3. Hemostasis
Have no nuclei and a limited lifespan. Derived from fragmentation of large bone marrow cells (megakaryocytes).
2. Aggregate at the site of damage to a blood vessel, forming a platelet plug.
3. Mechanism of preventing bleeding.
1. Fibrin
2. How is fibrinogen converted to fibrin?
Threadlike protein with hemostatic response; holds platelet plug together. When dried, becomes a scab, sealing/protecting the wound.
2. by thrombin when bleeding occurs.
1. Thrombus
2. Ca2+ necessary for _______
1. A scab circulating in bloodstream.
2. Activation of thrombin and fibrinogen.
Hemoglobin (Hb)
composed of 4 polypeptide subunits, each containing heme, a large ring structure w/ an iron atom bound at its center.
**Each Hb carry 4 O2.
Cooperative binding of O2 on Hb
Tense and low affinity for O2 when no O2 bound to the 4 subunits. The more O2 binds to the subunits, more relaxed Hb becomes and higher the affinity for O2.
Is O2 affinity high or low in tissues?
Low affinity, b/c Hb tends to release O2 it carries, which is used in oxidative phosphorylation.
**Higher affinity due to cooperative binding at lungs.
3 factors that stabilize the tense configuration (low O2 affinity)
1. Decreased pH
2. Increased PCO2
3. Increased temperature
**called Bohr effect.
Percent saturation (%SAT)
# of O2 molecules bound/# of O2 binding sites * 100
3 ways CO2 is transported in blood
1. 73% of CO2 transport accomplished by CO2 + H2O <-> H2CO3 <-> HCO3- + H+ (catalyzed by carbonic anhydrase)
Bicarbonate: water-soluble, easily carried in blood.
2. 20% transported by simply being stuck onto hemoglobin, binding to other sites than O2-binding sites.
3. 7% dissolved in blood & carried from tissues to lungs.
1. 3 substances that pass thru spaces btw endothelial cells that make up capillary wall (intercellular clefts)
2. Is it necessary for O2/CO2 to pass thru the clefts?
1. Nutrients, wastes, & WBC
2. No, they can pass straight thru by simple diffusion
How are wastes taken care of?
Produced during cellular metabolism, they simply diffuse thru capillary walls into bloodstream. Liver removes many wastes by converting them into compounds that are passed to the gut as bile, which are excreted in feces. Other wastes excreted by kidneys.
2 WBC that can squeeze thru clefts
macrophage and neutrophils due to amoeboid motility.
1. 2 reasons water tends to flow out of capillaries thru the clefts.
2. How does circulatory system deal w/ this problem?
3. Would dissolving NaCl in plasma contribute to its high osmolarity?
1. Hydrostatic pressure (fluid pressure) created by heart and high osmolarity of tissues.
2. By giving plasma a high osmolarity
3. No, b/c salts can freely pass out of capillaries
1. Plasma osmolarity provided by__
2. Characteristics of albumin
3. Oncotic pressure
1. High concentrations of large plasma proteins, Albumin.
2. Albumin is too large and rigid to pass thru the clefts, so remains in capillaries and keeps water with it.
3. Osmotic pressure provided by plasma proteins
A cycle of water leaking out (3 steps)
1. Hydrostatic pressure high at the beginning of capillary. Result: water squeezes out.
2. Conc. of plasma proteins increases as water leaves capillary
3. Hydrostatic pressure low at the enf of capillary; blood very conc., thus oncotic pressure very high. Result: water flows back to capillary from tissues.
1. How does inflammation work?
2. What's its result?
1. Capillary endothelial cells retract to make more room for WBC to get into tissues.
2. Plasma protein & water lost into tissues. tissues swell, aka edema.
1. How are fluid, proteins, & WBC returned to bloodstream?
2. What'd occur if capillaries were made more permeable?
3. Albumin is made in liver. Alcoholics w/ diseased livers make less albumin, thus have low oncotic pressure. Result?
1. Via lymphatic system.
2. Large amt of fluid lost from plasma, resulting in decrease of blood volume and cardiac output. Circulatory shock can result.
3. Results in edema of entire body.
Lymphatic system
One-way flow system beginning w/ tiny lymphatic capillaries in all tissues -> larger lymphatic vessels (have valves) -> large lymphatic ducts (walls made of smooth muscle) -> thoracic duct (located in chest; empties into large vein near neck).
How do valves & smooth mus. contribute to lymphatic system?
Lymph. sys. acts like a suction pump to retrieve water, proteins, & WBC from tissues.
1. Lymph
2. Lymph nodes
1. Fluid in lymphatic vessels.
2. Filters lymph; contain millioins of WBC that initiate immune response against foreign matter picked up in lymph.