Physiology Exam 3

what are the different components of the blood?

plasma, buffy coat (leukocytes & platelets), erythrocytes (red blood cells)

what is hematocrit and what can it demonstrate?

the percent of total blood volume made up of RBC. higher hematocrit can indicate polycythemia, lower hematocrit can indicate anemia

what is plasma? what is it made of?

the liquid portion of the blood used for transport, made of 90% water and 10% proteins, electrolytes, nutrients, hormones, waste products

what are the different plasma proteins, and what are their functions?

albumin: maintains osmotic pressure, regulates blood volume and pressure, acts as a carrier protein

globulins: alpha/beta transport lipids, fat-soluble vitamins, and metal ions. gamma are antibodies that fight infection by recognizing and binding to pathogens

fibrinogen: when bleeding occurs, fibrinogen is converted into fibrin which forms a mesh to stop the bleeding

what is the structure and function of erythrocytes?

structure: bioconcave discs, no nucleus/organelles, very flexible

function: transport oxygen from lungs to tissues, transport CO2 from tissues to lungs, help maintain blood pH

understand the structure and function of hemoglobin

structure: 4 subunits, each with a heme group with an iron at its center. oxygen binds to this iron, so 4 oxygens can bind to one hemoglobin

function: bind oxygen in lungs, release oxygen in tissues

how many oxygen molecules does each hemoglobin molecule bind?

4

hemoglobin can bind to other substances other than oxygen. what is the beneficial and harmful binding that can occur?

beneficial: CO2, H+, nitric oxide

harmful: CO, nitrates

what is erythropoiesis and how does it occur?

erythropoiesis is the production of new red blood cells from stem cells in the bone marrow; occurs because hypoxia (low oxygen levels) triggers the kidneys to release erythropoietin, which stimulates the production of RBC. hyperoxic conditions relieve the negative feedback loop

what are the different blood groups, and how are donors and recipients determined in blood transfusions?

antigens are markers on RBCs, antibodies are proteins in plasma that attack foreign antigens.

Blood Type	RBC Antigens	Plasma Antibodies
A	A antigen	Anti-B antibodies
B	B antigen	Anti-A antibodies
AB	A and B antigens	No anti-A or anti-B antibodies
O	No A or B antigens	Anti-A and Anti-B antibodies

what is the universal donor?

O

has no A or B antigen, no Rh antigen

what is the universal recipient?

AB

has A, B, and Rh antigens; does not have anti A or anti B antibodies

How does Rh factor work, and when can it cause complications in pregnancy?

Rh is another antigen, can be + or -, if mother is negative and fetus is positive, her body will try to fight off the foreign antigen

what are leukocytes? what are the five main types and their functions?

leukocytes: white blood cells formed in bone marrow; mobile units of the body’s immune defense system

1. polymorphonuclear granulocytes: granulated cytoplasm, lobed nucleus

   1. neutrophils: phagocytosis

   2. eosinophils: attack parasitic worms

   3. basophils: release histamine

2. mononuclear agranulocytes: no granules, single round nucleus

   1. monocytes: become tissue macrophages, microglia, or osteoclasts

   2. lymphocytes: B produce antibodies, T cell-mediated immunity

what are platelets and what are their functions?

cell fragments from megakaryocytes, function in hemostasis (blood clotting)

explain the three steps of clot formation or hemostasis. how is clot formation accomplished?

1. vascular spasm (vasoconstriction): after injury, blood vessel constricts to restrict flow to damaged area

2. platelet plug formation: platelets adhere to damaged vessel wall and release chemicals to activate more platelets (aggregation), release PF3

3. coagulation (blood clot formation):

   1. prothrombin —> thrombin (requires PF3)

   2. fibrinogen —> fibrin: thrombin converts soluble protein into insoluble fibers

   3. clot formation: fibrin strands form a mesh to trap RBC and platelets, stable blood clot formed

what is the difference between the intrinsic and extrinsic clotting cascade?

intrinsic: activated by damage inside vessel (which activates factor XII, or Hageman), slower, all factors present in blood

extrinsic: activated by damage to external tissue, fast, 4 steps, uses tissue factors external to blood, tissue thromboplastin can activate factor X, common pathway

what is clot retraction?

once blood clot seals a wound, platelets trapped in the fibrin clot contract and shrink the fibrin mesh, pulling the edges of the damaged vessel together

how is clot dissolution accomplished?

plasmin becomes trapped in the clot and later dissolves it by slowly breaking down the fibrin meshwork (plasminogen → plasmin → fibrin breakdown)

why do researchers think some frogs and lizards have green blood? what causes their blood to be green? How do some glass frogs make themselves even more cryptic when on green vegetation?

accumulation of biliverdin makes their blood green; can be useful for camouflage or toxic to parasites; glass frogs move their RBCs to their liver to make themselves more transparent

what are the three main components of the circulatory system? What are their overall functions?

1. heart - established a pressure gradient to pump blood

2. blood vessels - passageways for pumped blood throughout the body

   1. arteries: carry blood away from ventricles

   2. veins: carry blood to atria

3. blood - transport medium, serves body cells

   1. red vs. blue

how does blood flow from and to the heart?

deoxygenated blood enters right atrium via superior/inferior vena cava → right AV (tricuspid) valve → right ventricle → pulmonary semilunar valve → pulmonary arteries → lungs → Co2 released, O2 picked up → pulmonary veins → left atrium → left AV (bicuspid/mitral) valve → left ventricle → aortic semilunar valve → aorta → arteries throughout body → O2 delivered, CO2 picked up → veins → right atrium :)

how do the valves of the heart work?

one way valves prevent backflow of blood, open and close based on pressure differences

explain the differences between the atrioventricular (AV) and semilunar valves

atrioventricular: between atria and ventricles, open when atrial pressure > ventricular pressure

• right side: tricuspid valve

• left side: bicuspid/mitral valve

semilunar: between ventricles and major arteries, opens when ventricular pressure > arterial pressure

• pulmonary: right ventricle → pulmonary artery

• aortic: left ventricle → aorta

what are the three main layers of the heart wall?

endocardium, myocardium, epicardium

understand the intercalated discs of the myocardium, the cell junctions they contain, and their functions.

intercalated discs: cardiac muscle arranged spirally around ventricle, “wrings” blood when it contracts

• desmosomes: mechanical strength

  • resist mechanical stress

  • hold cardiac cells together

• gap junctions: electrical communication

  • areas of low electrical resistance

  • allows action potentials to spread from one cell to adjacent cells

Functional Syncytium: the heart behaves as one coordinated unit because all excited cardiac cells contract together

what is the pericardial sac? what is its function?

a thin, double-layered membrane that encloses the heart

• fibrous pericardium: tough outer layer that anchors heart in place

• serous pericardium: secretory lining to secrete pericardial fluid and provide lubrication to prevent friction between pericardial layers

how is heart contraction triggered at the cellular level?

autorhythmicity: the heart contracts rhythmically as a result of action potentials that it generates by itself

• an action potential reaches a contractile cardiac muscle cell

• depolarization opens voltage-gated L-type Ca2+ channels in the membrane

• a small amount of Ca2+ enters the cell

• this triggers the sarcoplasmic reticulum to release more Ca2+ (calcium-induced calcium release)

• Ca2+ binds troponin, shifting tropomyosin

• actin-myosin cross-bridges form → contraction occurs

what are the differences between autorhythmic and contractile cells, how are they depolarized, and what are their roles in the electrical activity and contraction of the heart?

• autorhythmic: 1%

  • initiate and conduct action potentials responsible for contraction of working cells

  • electrical impulses, do not contract themselves

  • don’t have resting potential

  • slow, drifting depolarization (pacemaker activity)

• contractile: do mechanical work of pumping

  • produce force

  • depolarization triggered by electrical spread from autorhythmic cells via gap junctions

  • stable resting membrane potential

know figure of action potentials of autorhythmic and contractile cells

what are the important ion channels involves in autorhythmic and contractile action potentials?

autorhythmic:

• Na+ funny channels

• T-type Ca2+ channels

• L-type Ca2+ channels

• K+ channels

contractile:

• voltage-gated Na+ channels

• L-type Ca2+ channels

• Ca2+ channels

which ions are driving the formation of action potentials?

Na+, Ca2+, K+

why are long refractory periods in contractile cells important?

prevent tetanic contraction, ensures heart fully relaxes between beats, allows proper filling of chambers before next contraction, essential for coordinated pumping, not continuous tension

where are the noncontractile cells located in the heart?

• SA node: right atrium wall near superior vena cava

• AV node: base of right atrium near septum

• bundle of his: originate at AV node and enter interventricular septum, divides to form right and left bundle branches

• purkinje fibers: extend from bundle of his and spread through ventricular myocardium

how do the locations of the noncontractile cells drive electrical activity around the heart during a contraction/excitation?

they create a controlled electrical pathway so that contraction occurs in order:

1. atria contract first (fill ventricles)

2. ventricles contract second (pump blood out)

electrical conduction pathway:

SA node → atria → AV node → bundle of his → right + left bundle branches → purkinje fibers → ventricular contraction

key role of each region:

• SA node: starts heartbeat

• AV node: delays signal so ventricles fill

• bundle of his: connects atria → ventricles

• purkinje fibers: rapidly distribute signal for strong ventricular contraction

why is the SA node the pacemaker of the heart?

has the fastest spontaneous depolarization rate, its cells reach threshold before other autorhythmic cells, so it cells the dominant rhythm

what happens if the SA node breaks down or is damaged?

other autorhythmic cells take over at slower rates, will still pump but slower and less coordinated with reduced efficiency

• AV node becomes backup pacemaker (~40-60bpm)

• if AV fails, purkinje fibers take over (~20-40bpm)

what is an electrocardiogram and what is it measuring?

a graph of electrical activity from the heart, measuring activity in fluids that reach the body surface. recording represents spread of activity through the heart during depolarization and repolarization

what are the components of the ECG trace and what do they represent in the cardiac cycle?

• P-wave: atrial depolarization

• PR segment: AV node delay

• QRS complex: ventricular depolarization, atria repolarization

• ST segment: ventricles contract (empty)

• T-wave: ventricular repolarization

• TP interval: ventricles relax and fill

what is the purpose of measuring an ECG? What are the heart rate abnormalities that it can pick up on?

• abnormalities in rhythm (arrhythmia)

  • extra systoles (contractions)

  • atrial flutter

• atrial fibrillation: pulse deficit, no P wave

• ventricular fibrillation: uncoordinated contractions, inefficient pumping

• heart block: atrial rate normal, ventricular rate slower

• cardiac myopathies: damage to heart muscle

• myocardial infarction: heart attack, abnormal QRS complex

what is systole and diastole?

systole - contraction and emptying

diastole - relaxation and filling

Explain one complete cardiac cycle, in terms of the ECG trace, the atrial, ventricular, and aortic pressures, the left ventricular volume, and the heart sounds. What is happening in the heart at each step?

1. mid ventricular diastole (filling)

• TP segment

• atrial pressure slightly > ventricular pressure

• AV valve open and passive filling of ventricle occurs

2. late ventricular diastole (filling)

• P wave

• atrial depolarization and contraction

• AV valve open

3. end of ventricular diastole (filling)

• atrial contraction and ventricular filling are complete

• end-diastolic volume (EDC) = 135 mL

4. onset of ventricular systole (contraction)

• QRS complex - ventricular excitation, induces contraction

• backward pressures closes AV valve

• first heart sound

5. isometric ventricular contraction

• after AV closed, ventricular pressure must increase until it exceeds aortic pressure

• all valves close briefly

  • isovolumetric = constant volume and length

  • ventricular pressure continues to rise

6. ventricular ejection

• ventricular pressure > aortic pressure - aortic valve forced open

• blood ejection from heart begins

• SV = stroke volume, amount of blood pumped out of each ventricle

7. end of ventricular systole

• only about half of blood is pumped out

• end-systolic volume (ESV) = 65 mL

• stroke volume (SV) = EDV - ESV = 70 mL

8. onset of ventricular diastole

• T wave

• ventricular pressure < aortic pressure = aortic semilunar valve closes

• closing results in dicrotic notch = second heart sound

9. isometric ventricular relaxation

• all valves closed again

• no blood leaves or enters the ventricle and pressure falls

10. ventricular filling

• ventricular pressure < atrial pressure = AV valve opens

• blood fills ventricle again

Wiggers diagram

some key terms: isometric ventricular ejection, isovolumetric ventricular relaxation, end-diastolic volume, end-systolic volume

• End-Diastolic Volume (EDV): max blood in ventricle (before contraction)

• End-Systolic Volume (ESV): blood left after contraction

• Stroke Volume = EDV − ESV

• Isovolumetric contraction: pressure ↑, volume same (all valves closed)

• Isovolumetric relaxation: pressure ↓, volume same (all valves closed)

what causes the two heart sounds?

lub (1st): associated with closing of AV valves

dup (2nd): associated with closing at semilunar valves

(caused by vibrations, not the valves snapping shut)

what is stroke volume (SV)? how do you calculate it?

stroke volume: how much blood the ventricle pumps out in one beat

SV = EDV - ESV

SV = 135 - 65 = 70

70 mL pumped out of each ventricle during each contraction

(EDV: amount of blood in the ventricle before contraction, ESV: amount of blood left after contraction)

what is ejection fraction? how do you calculate it?

ejection fraction: percentage of blood that is pumped out of the ventricle each beat, tells you how efficiently the heart is pumping

Ef = SV/EDV

what is the relationship between cardiac output, stroke volume, and heart rate?

cardiac output (CO) = stroke volume (SV) x heart rate (HR)

• if SV or HR increases, CO increases

• if SV or HR decreases, CO decreases

how does cardiac output (CO) vary so much with exercise?

goes from ~5L to 20L or more

varies via control of HR and SV

explain the parasympathetic and sympathetic control of heart rate

• parasympathetic: vagus nerve supplies SA and AV nodes → release of acetylcholine → increased permeability to K+ → hyperpolarizes membrane → even slower drift due to threshold → decreased heart rate

• sympathetic: norepinephrine (from sympathetic nerve endings) → decreased K+ permeability → cell depolarized → faster drift to threshold → increased heart rate

• epinephrine: released from adrenal medulla upon sympathetic stimulation, increased sympathetic activity

explain the intrinsic and extrinsic control of stroke volume. draw a diagram

what is the frank-starling curve, or law of the heart?

depicts relationship between EDV and SV or between muscle fiber length and muscle tension

“the more the heart fills with blood during diastole (increased EDV), the stronger it contracts, and the greater the stroke volume (SV)”

how does the frank-starling curve relate to cardiac muscle tension and cardiac muscle fiber length, and stroke volume and end diastolic volume? diagram

• stroke volume is dependent on venous return

• cardiac muscle fibers stretch - greater tension

• increased EDV = more stretch = increased SV

• increased EDV = increased stretch = increased force = increased EDV

fiber length ←→ tension

EDV ←→ Sv

how can sympathetic stimulation compensate for a failing heart?

• sympathetic stimulation can shift curve to the LEFT, increasing stroke volume towards normal

• compensates by increasing EDV above normal

• failing heart pumping same amount of blood at greater cardiac muscle length

has to boost: HR, force of contraction, or EDV

explain how end-diastolic volume, stroke volume and end-systolic volume relate to cardiac output during resting and during sympathetic stimulation of the heart. What if the end-diastolic volume also increases? what is the most important determinant of end-diastolic volume? draw a flow chart

what are the reconditioning organs and what do they do? which organs can withstand decreases in blood supply for short periods, and which cannot?

reconditioning organs: organs that can withstand a temporary reduction or redirection of blood flow (kidneys, digestive tract, skin)

non-conditioning organs: the brain and the heart

explain how the blood flows through the vascular tree

heart → arteries → arterioles → capillaries (gas exchange) → venules → veins → heart

what is microcirculation?

the blood flow through the smallest vessels where actual exchange happens arterioles → capillaries → venules

how do you calculate flow rate? what are they key determinants of flow rate?

flow rate determines how much exchange of O2, CO2, and nutrients takes place

F = delta P/R

F = flow rate of given volume of blood through a vessel

delta P = pressure gradient (from beginning to end of vessel)

R = resistance

blood flows from area of high to low pressure (pressure gradient)

what is resistance (relating to blood flow)?

opposition to blood flow through a vessel

what is resistance proportional to? what is it inversely proportional to?

directly proportional to viscosity (n - thicker blood = more resistance) and vessel length (L - constant in adults, longer vessel = more resistance)

inversely proportion to vessel radius (r) - doubling or halving the radius will decrease/increase resistance by 16-FOLD

what is the major determinant of resistance to blood flow

radius

(since its to a factor of 4, minor changes will drastically change resistance) doubling radius = decrease resistance 16-FOLD

for the same volume of blood: increase in radius decreases surface area in contact with blood and decreases resistance to flow

how do changes in vessel radius change the distribution of cardiac output around the body?

change in vessel radius changes the distribution of cardiac input (blood flow is matched to tissue needs, vasodilation/constriction accordingly)

which body systems or organs receive increased, decreased, or no change in blood flow during moderate exercise/sympathetic stimulation?

• increase: skeletal muscle (1066%), skin (370%), heart (367%)

• neutral: brain

• decrease: digestive system, liver, kidneys, bones

what are the key differences in vessel anatomy between arteries, arterioles, capillaries, and veins?

• arteries: pressure reservoirs

  • very thick

  • high pressure

  • elastic recoil

• arterioles: resistance vessels

  • thin compared to arteries but still muscular

  • significant pressure drop

  • major site of vasoconstriction/dilation

• capillaries: sites of exchange of nutrients and gases

  • one cell thick

  • low pressure

  • thin walls for diffusion/exchange

• venules (veins): blood reservoirs and return to heart

  • thin

  • very low pressure

  • valves to prevent backflow

why are arteries considered pressure reservoirs? explain elastic recoil

they store energy when the heart pumps and release it when the heart relaxes to keep the blood flow and pressure continuous

elastic recoil: ability of arterial walls to stretch and spring back due to their high content of elastic fibers

1. systole (heart contracts): blood is forced into arteries, stretching the arterial walls and storing energy

2. diastole (heart relaxed): arteries recoil (snap back) and stored energy pushes blood forward

describe how you measure blood pressure with a stethoscope and a blood pressure cuff. what indicates systolic pressure? diastolic pressure? what are korotkoff sounds? how do you calculate pulse pressure?

• systolic pressure: 1st sound, maximum pressure when blood ejected into arteries

• diastolic pressure: last sound, minimum pressure while blood drains

• korotkoff sounds: auscultation of blood flow correlated with blood pressure readings

• pulse pressure = systole - diastole

what is mean arterial pressure, and how do you calculate it?

MAP: average pressure in the arteries over one full cardiac cycle (important because it represents the pressure driving blood flow to tissues)

MAP = diastolic - 1/3 (systolic - diastolic) ← (or pulse pressure - same thing)

how does MAP change throughout the vascular tree?

1. arteries: highest MAP, high pressure

2. arterioles: huge drop in MAP due to high resistance (small radius) - protects capillaries from high pressure

3. low pressure (ideal for exchange)

4. venules and veins: very low pressure, approaches 0 mmHg near heart

why are arterioles considered resistance vessels?

their small, adjustable radius produces the greatest changes in resistance and blood flow, MAP drops significantly and pressure drop drives blood flow

what is vascular tone?

baseline level of constriction in blood vessels, normal diameter, established baseline vascular resistance

what is vasoconstriction?

decreased blood vessel radius via smooth muscle contraction

what is vasodilation?

increased blood vessel radius via smooth muscle relaxation

what are the intrinsic/local and extrinsic controls of arteriolar resistance, and thus the distribution of blood flow throughout the body?

review question 42 im confused

what is the difference between active hyperemia, reactive hyperemia, and myogenic autoregulation? understand negative feedback loops!

• active hyperemia: increased blood flow to a tissue because the tissue is working harder

• reactive hyperemia: increased blood flow that occurs after a temporary blockage of blood flow is removed

• myogenic autoregulation: ability of blood vessels (especially arteries) to maintain constant flow despite changes in blood pressure & MAP

negative feedbacks: change disrupts homeostasis → vascular response → correction of that change

• active hyperemia: corrects metabolic imbalance

• reactive hyperemia: corrects oxygen debt

• myogenic: corrects pressure changes

what is the main purpose of capillaries?

exchange of gases and nutrients

how does capillary structure inform their function?

vessel structure minimizes diffusion distances, narrow diameter makes red blood cells squeeze through single-file, extensive branching (capillaries touch ALL cells, maximizes surface area)

explain the change in flow rate vs flow velocity at each level of the vascular tree. how can capillaries have a decreased velocity of flow while maintaining the same blood flow rate?

explain capillary diffusion. how do different substances pass through capillary walls? what can pass through membranes, the pores, via vesicular transport, and what substances are usually excluded?

how do capillary beds open and close? what is the purpose of this?

what are the two processes that allow the exchange between blood and tissues across capillary walls? explain the difference

what hydrostatic and osmotic pressure differences drive bulk flow? which are the most important contributors?

how do you calculate net exchange pressure, and how does this determine the direction of bulk flow?

what are the functions of the lymphatic system?

why is the lymphatic system important for the functioning of the capillaries/maintaining composition?

how does the structure of the lymphatic vessels inform their function, and what happens when they aren’t working properly?

why are veins blood reserves?

how does veins structure inform their function?

how much of the total blood in circulation is typically found in systemic veins at a given time?

what is venous capacity and how is it determined?

what is the circulating blood volume?

what is venous return?

why is venous return important?

what are the many factors that enhance venous return?

what is the skeletal pump and how does it impact venous return?

how does the skeletal pump counteract the effect of gravity?

how do venous valves counteract gravity?

how do baroreceptors monitor mean arterial blood pressure and where are they located?

what is the series of events that occurs if MAP is above normal?

what is the series of events that occurs if MAP is below normal?