Unit 3 Detailed Learning Objectives

96) Define "the work of breathing". List the two general factors that determine the work of breathing. *follow up question* a) normal cost of breathing is around what percentage of your total metabolism?

"the work of breathing* describes the effort, the metabolic cost to expand lung volume, to move air, and sometimes even to quietly exhale two general factors that determine the work of breathing: 1) lung compliance (stretchability) 2) airway resistance *follow up question* a) 3%

12) Define and distinguish between the endocardium, myocardium, epicardium, and pericardium. Why do we have a pericardial sac and fluid?

*1) endocardium:* the innermost layer that lines the surface of the chambers of the heart *2) the myocardium (cardiac muscle cells):* the wall of the heart; the contractile muscle that pumps the blood *3) epicardium (outer surface of the heart that is epithelial tissue):* epicardium wraps around the myocardium and protects the heart and secretes stuff *4) pericardium:* epicardium folds over and come pericardium which is the outermost layer of connective tissue surrounding the heart - we have pericardial fluid/space (in between pericardium and epicardium) because it lubricates and reduces friction of the heart as it moves when beating

13) What are the three types of cardiac muscle cells? What is the "normal" function of each?

*1. autorhythmic cells (AKA pacemaker cells)*: a small fraction of cardiac muscle cell that determines the heart rate (*can spontaneously develop action potentials*) *2) conducting cells:* a smaller fraction of cardiac muscle cells that are responsible for rapidly spreading electrical stimulus throughout the chamber *3) contractile cells:* bigger fraction that make up 99% of cardiac muscle cells that are responsible for generating contraction and pumping blood *all these cardiac muscle cells plays a unique function in a normal heart beat!*

2) List and comment on the three general components of the CardioVascular system.

*1. heart* - the biological pump that generates force to move blood - the heart has 2 components: a mechanical and electrical *2. blood* - the medium through which O2, CO2, waste, nutrients, and messengers like hormones are transported *3. blood vessels* - the "tubing" through which blood flows in; plays an active role in the movement of blood

3) Draw figure 12.1 and describe the parts that blood separates into when spun in a high-speed centrifuge.

*1. plasma (top layer; lighter weight/smaller size)* - averages around 55-58% - plasma is part of the ECF; its like ISF but has 'plasma proteins' (plasma proteins carry hydrophobic hormones) *2. "buffy coat" (middle layer)* - comprised of leukocyte (white blood cells) and platelets *3. erythrocytes/hematocrit (bottom later; heavier weight/larger size)* - averages around 42-45% - mainly for gas transport - is the red blood cell volume

56) a) What are the two main receptor subtypes involved in sympathetic control of vascular smooth muscle? Compare their locations and effects. b) Explain the receptor- and dose-dependent interactions of norepinephrine and epinephrine on arterioles found in skeletal muscle tissues

*2 receptor involved sympathetic control of vascular smooth muscle (vasoconstriction/vasodilation)* *1) alpha 1- adrenergic receptor: induces constriction* - sympathetic post ganglionic neurons release *norepinephrine* that bind to alpha 1- adrenergic receptor as cause vasoconstriction (decrease radius) that decreases blood flow to that location (arterioles) - located on arterioles *2) beta 2- adrenergic receptor induce dilation* - adrenal medulla secrete *epinephrine* into blood that bind to beta 2-adrenergic receptors that cause vasodilation (increase radius) that increases blood flow to that location (arterioles) - located on arterioles b) when epinephrine is at a physiological dose which is typically a low dose (the physiological actual amount that comes out of the adrenal medulla) will bind to beta 2-adrenergic receptor and cause vasodilation *BUT* when we inject epinephrine that causes high doses of epinephrine beyond the normal physiological dose, it will bind onto alpha-1 adrenergic receptors

24) a) Reproduce figure 12.17 and discuss the alignment of single contractile cell action potentials with ECG waves and intervals. How do the parts of an action potential align with the observed events in an ECG recording? b) Add nodal cell (SA node and AV node) and purkijne cell action potentials to figure 12.17 as well. https://mediaspace.wisc.edu/media/Andrew%20Lokuta-Humanities%203650-11_05_21-08%3A46%3A39/1_b7llap8j DRAW THESE OUT!!! *(IDK IF THIS IS CORRECT)*

*ECG correspondence with contractile cells:* 1) Atrial depolarization/contraction (upstroke; action potential) aligns with the P wave 2) the plateau in atrial action potential is the P-R segment where slow conduction of AV node occurs and L-type Ca2+ channels allowing trigger Ca2+ entry. 3) repolarization of atrial contractile cells aligns with the QRS wave and the ventricular depolarization/contraction (upstroke; action potential) aligns with the QRS wave as well! 4) the ST segment aligns with the plateau of ventricular action potential due to L-type Ca2+ channels and also when ventricles are fully depolarized 5) then the T-wave aligns with ventricle depolarization and relaxation b) in ECG the: *SA node:* 1) SA node reaching threshold of -40 mV due to funny Na+ channels and transient Ca2+ channels aligns with the start of P-wave. 2) action potential from SA node reaches peak and aligns with around some point at the end of P-wave 3) repolarization then occurs due to K+ channels and brings membrane potential back to -60 mV (which is around some point at the end of QRS wave.) 4) then opening of funny Na+ channels and transient calcium channels bring -60 to threshold of -40 mV which aligns with the beginning of the next P-wave (back to step 1!) *AV node:* 1) AV node reaches -40 mV threshold and has an upstroke that causes delay of conduction and slow A.P propagation which aligns with the end of the P-wave or the start of the P-R segment 2) upstroke of A.P in AV node fires in the beginning of PR segment and is less steep than SA node because it's a slow conductor. that is the big difference between SA and AV node action potential is the steepness! 3) repolarization occurs after. AV node naturally takes longer to get to threshold than SA node but can have a premature upstroke at the end of the next P-wave and start of the P-R segment due to current injected into them by neighboring gap junctions. - this is why AV node is the latent pacemaker that is hidden! (it has upstroke prematurely) *conducting cell (Purkinje fibers, etc...)* 1) The bundle of His, the bundle branches, the Purkinje fibers, will have their upstroke at the start of the ventricular depolarization (that aligns around the end of the P-R segment and somewhere around Q and R. This is where we have -40 mV which is threshold valve for conducting cells) 2) a short plataeu occurs around the middle of the QRS complex and then a rapid and steep repolarizaton back to -60 mV occurs around the end of QRS wave. 3) then the conducting cell is slowly depolarizing due to funny Na+ channels and transient Ca2+ channels and then BOOM current from neighboring gap junctions by the AV node causes premature upstroke (somewhere around the end of PR segment and somewhere around Q and R.) - this is why conducting cell is the latent pacemaker that is hidden (it has upstroke prematurely and doesn't get to show us its true rate of upstroke since it prematurely stimulated to fire an upstroke)

69) Using your knowledge of lymph formation and flow, describe and explain elephantiasis.

*Elephantiasis* 1) blockage of lymph flow due to infectious filaria worms from mosquito bite 2) infectious filaria worms grows in the lymph system and as it grows in size and number, it blocks the lymph nodes thus cause little to no flow of lymph fluid. 3) this disease represents *edema* - fluid retention - swelling - accumulating ISF *3-4 liters of lymph is not being returned/recovered*

22) a) Draw figure 12.15 (cardiac contractile cell action potential) and explain the ionic events underlying its shape. b) Draw figure 12.16 (cardiac node cell action potential) and explain the ionic events underlying its shape. How does this action potential compare to the cardiac contractile cell action potential in figure 12.15? *follow up question* a) what is the maximum diastolic hyperpolarization? (lecture 2 page 17-18 for diagrams of both these action potential types)

*a) action potential of contractile cardiac cell (99% of the cell of the heart):* 1. we start at resting membrane potential of -89 mV (because of unique K+ channels) that is flat (*there are no graded potentials OR EPSP or EPP*) 2) we get rapid and steep upstroke of depolarization due to rapid opening of voltage-gated Na+ channels that are caused by depolarizing current from neighboring cells through gap junctions NOT EPSP or EPP 3) at the peak of action potential, Na+ channels inactivate and transient K+ channels briefly open causing a little repolarization 4) then a prolonged plateau of depolarization occurs due to slow opening of L-type (long-lasting) voltage-gated Ca2+ channels (aka the DHP receptor that brings in trigger calcium) 5) then K+ exits and repolarization occuers back to -89 mV (RMP) *b) action potential of nodal (SA node and AV node) cardiac cell* 1) K+ channels causes repolarization which then causes the opening of Funny Na+ channels (aka f-type or h-type) allowing Na+ to enter bringing the membrane potential of -60 mV to -50 mV 2) then transient Ca2+ channel opens and Ca2+ enters causing depolarization and brings membrane potential to threshold from -50 mV to -40 mV 3) action potential upstroke (depolarization phase) occurs due to the opening of L-type Ca2+ channels that allow Ca2+ to come in and brings membrane potential to around 5-10 mV 4) then L-type Ca2+ channels inactivates causing the repolarization phase and K+ channels reopen causing repolarization and then back to step 1! *follow up question* a) maximum diastolic hyperpolarization is the most negative membrane potential which in this case is -60 mV

54) Define and describe the mechanisms of active hyperemia, reactive hyperemia, and myogenic flow autoregulation. Use your lecture slides to help describe the events as they occur in time.

*active hyperemia* this is when we have an increased metabolism that causes vasodilation and thus increased blood flow. 1) we have resting arterioles that have resting blood flow, BUT then... 2) during active hyperemia, you have increased tissue metabolism (high CO2, low O2, low pH, high metabolites) which causes arterioles to increase in radius (vasodilate) so there is an increase blood flow to that tissue that is active. 3) There is increase in blood flow until our metabolism decreases and vasocontriction occurs that bring blood flow back to resting levels *myogenic flow autoregulation: a protective mechanism against pressure-induced damage* 1) we have resting arterioles *(1)* that have resting blood flow, BUT then... 2) there is an increased pressure in the artery that causes increased perfusion pressure (pressure pushing out on arteriole walls) in the arterioles *(2)* which increases blood flow and also increases the radius (vasodilation) by pushing outwards on the walls of the arterioles *(this will cause more flow and pressure into the capillaries. but this is damaging because the capillaries are made up of a single layer of endothelium cells making them not very strong)* 3) HOWEVER, the arterioles have a lot of mechano-gated calcium channels in their smooth muscle layer that stretches due to pressure and thus causing them to contract down against the high pressure to limit the increase in radius. so now we end up with a radius of the arterioles that are bigger than resting level arterioles *(1)* but has a smaller radius than the arteriole *(2)*-- so now we end up with an intermediate radius arteriole! *reactive hyperemia: high local blood flow after period of deprivation due to occlusion (blockage)* 1) we have resting arterioles that have resting blood flow, BUT then... 2) we have a vascular occlusion (blockage) in the artery that prevents blood flow into the arterioles 3) arterioles will begin to dilate to increase blood flow but it doesnt help because the blood flow is being blocked in the artery! 4) when occlusion is removed, the arterioles will have a SUPER wide radius and blood will start rapidly rushing out (high bloood flow)

5) Reproduce figure 12.2, highlighting the cellular differentiation that leads to: 1) red blood cells, 2) platelets, 3) tissue macrophages, neutrophils, eosinophils, and basophils, 4) B & T lymphocytes. What are the functions of these cell types?

*all 4 cellular differentiation start as a stem cell* 1. hematopoietic stem cell → reticulocyte → red blood cell *- function: oxygen transport* 2. hematopoietic stem cell → megakaryocytic → platelets *- function: clotting* 3. four white blood cells *(immunity defense)* a) hematopoietic stem cell → blast cell → monocyte → tissue macrophage *(immunity defense)* b) hematopoietic stem cell → blast cell → promyelocyte → band → neutrophil *(immunity defense)* c) hematopoietic stem cell → blast cell → eosinophil *(immunity defense)* d) hematopoietic stem cell → blast cell → basophil *(immunity defense)* 4. hematopoietic stem cell → bone marrow lymphocyte precursor → a) B lymphocytes b) T lymphocytes *- function: immunity defense*

46) Using figure 12.31 and the lecture notes, compare and contrast the wall histology of arteries, arterioles, capillaries, venules, and veins, listing the layers present and the function of each layer.

*arteries (low resistance, and function for moving blood out to the body)* - they have a layer of smooth-lining endothelium (the inner layer that is in contact with the blood) - they have several elastic layers - they have many layers of smooth muscle (function to change radius by constricting or dilating that changes flow) - connective tissue (function to give arteries support and strength) *arterioles (function to controls/regulates the blood flow and flow distribution)* - very thick layer of smooth muscles (function to change radius that control blood flow) - has a layer of endothelium *capillaries (function for exchange of gases, fluids, nutrients; uptake of waste and secretory products of cells)* - only a single layer of endothelium (helps for better diffusion and gas exchange) - known as the FUNCTIONAL UNIT of cardiovascular system *venule (function: the place where white blood cells are released into tissue during inflammation and infection)* - has a layer of endothelium - has a connective tissue *veins (low resistance, and function for moving blood to the heart that can store a significantly larger volume of blood than arteries)* - they are floppy looking because they dont have reinforcements like arteries have - they have a few elastic layers - they have endothelium - they have few smooth muscle and connective tissue

42) Draw and label figure 12.28b; discuss the three parts of a cardiac twitch that are altered by the sympathetic stimulation. *follow up question* what percentage of troponin are bound with Ca2+, at rest?

*at rest. 30% of troponin are bound with Ca2+. BUT sympathetic stimulation will increase L-type Ca2+ and thus more calcium and more troponin binding and because of this we will have...* 1) quicker rise to peak force 2) a higher peak force 3) fast decline of force (because the next heart beat is coming sooner!) *follow up question* a) at rest, 30% of troponin are bound with Ca2+

7) Draw figure 12.4 and describe how the CV system interacts with the Respiratory, Renal, and Endocrine systems.

*cardiovascular system interacts with a lot of systems, for example figure 12.4 shows:* 1. if O2 delivery to kidneys is decreased 2. the kidneys sense and responses by increasing erythropoietin secretion (an endocrine hormone from renal tissue) 3. plasma erythropoietin increases and is transported via the CV system to appendicular skeleton bone marrow 4. bone marrow from the appendicular skeleton increases production of erythrocytes (red blood cells) 5. increase RBC = increase blood hemoglobin (Hb) (transported via the CV system) 6. increases blood O2-carrying capacity 7. restoration of O2 delivery (in CV and respiratory systems/lungs)

76) Describe in detail the development of Cushing's phenomenon.

*cushings phenomenon* 1) elevated intracranial pressure resulting in large increases in systemic MAP *why does this happen?* 1) head trauma (your can't swell outward due to the skull, so it swells inwards and compresses blood vessels in the brain) 2) intracranial bleeding, edema 3) increased intracranial pressure 4) cerebral artery compression 5) increased brain ISF CO2 levels (due to poor blood flow because of compressed vessels) 6) increased chemoreceptor firing - increased CO2 will be detected by chemoreceptors that sends signals to the vasomotor in the sympathetic nuclei center and activates it. 7) activation of vasomotor in the sympaethic nuclei center then vasoconstrict blood vessels like veins and arteries and thus increase blood flow, TPR, CO, and MAP because the brain isn't getting enough blood flow *in essence, cushings phenomenon is when there is an increased blood pressure (MAP) due to decreased blood flow in the brain (because its being blood vessels constricted by inward pressure either by a tumor or head trauma. pressure goes inward because the skull stops the brain from swelling outwards, so the pressure is directed inwards)*

33) Using figure 12.23, discuss the differences and the similarities between a cardiac cycle diagram for the systemic circulation and that for the pulmonary circulation.

*differences between a cardiac cycle diagram for the systemic circulation and that for the pulmonary circulation* - the right side (pulmonary trunk) has a lower pressure compared to the left side (aorta) which has higher pressure *similarities between a cardiac cycle diagram for the systemic circulation and that for the pulmonary circulation* - the timing of all the events from period 1, 2, 3, and 4 are the same! (the difference is the pressure size is bigger for aorta than for pulmonary trunk) *for comparison of pressure sizes* - in the aorta/aortic artery: systolic pressure: 110 mmHg diastolic pressure: 70 mmHg (110/70) - in pulmonary trunk/artery: systolic pressure: 25 mmHg diastolic pressure: 10 mmHg (25/10)

94) Reproduce the flow charts in figures 13.12 and 13.15. *IDK IF THIS IS CORRECT LMFAO*

*figure 13.12 shows the sequence of events during inspiration* 1) begin: diaphragm and inspiratory intercostal muscles contract 2) thorax expands 3) Pressure in intrapleual space becomes more sub-atmospheric (has a lower value than the atmosphere) because it is expanding 4) this increases transpulmonary pressure 5) causing lung to expand 6) pressure in the alveoli becomes subatmospheric (a lower value than the atmosphere) because it is expanding 7) thus, air flows into alveoli *figure 13.15 shows sequence of events during exhalation* 1) diaphragm and inspiratory intercostals stop contracting 2) chest wall recoils inwards 3) Pip moves back toward preinspiration value (orignal value) 4) transpulmonary pressure moves back towards preinspiration value 5) lungs recoils towards preinspiration size (decompresses?) 6) air in alevoli gets compressed 7) pressure in alevoli is now greater than pressure in atmosphere 8) thus causing air to flow out of lungs

82) Using table 13.2 discuss the four functions of the conducting zone.

*functions of the conducting zone* 1) allows for regulation of airflow (bronchioles have smooth muscles that can constrict and dilate) 2) defend against microbes, toxic chemicals, and harmful particles. (this is where we have the ciliary escalator occurring in the bronchi and trachea that expluse foreign/harmful particles up and out of the body) 3) warms and moistens the air 4) participates in sound production (vocal cords)

66) Using your lecture notes, explain how gravity interacts with venous return in different body postures. Describe in detail the four factors that oppose the effects of gravity (include figures 12.48 and 12.49). *follow up question* a) in lecture they discussed arterioles, what happens when you vasoconstrict an arteriole? (hint: think of sympathetic innervation) b) How much pressure is pushing down due to gravity when the muscles are relaxed and when contracted? (hint: think of skeletal pump)

*gravity opposes venous return, but several factors help:* 1) sympathetic innervation - we will sympathetically vasocontrict the veins and thus increase venous return. as we constrict the veins, you decrease the veins storage (capacitance) and drive more blood back to the heart (aka venous return) - Vasomotor (VM) is the sympathetic nuclei in the medulla oblongata that release NE that binds onto alpha 1-adrenergic receptors on the veins to constrict and thus increases venous return 2) skeletal muscle "pump" - when the muscle contract, they squeeze the veins and that drives the blood towards the heart and it interrupts the column of blood sagging down due to gravity. this is why you should stand and stretch after sitting for a long time, muscles squeeze large veins and force blood towards the heart! 3) increasing blood volume - more blood volume, you increase venous pressure and thus, you will have more venous return of blood to back to the heart 4) inhalation movements (inhalation respiratory pump) *IDK IF THIS IS CORRECT* - inhaling will cause thoracic cavity to get bigger and the pressure in the thoracic cavity will go down. as the throacic cavity gets bigger is helps suck blood into the vena cavas of the heart - exhaling will cause thoracic cavity to get smaller and pressure goes up. this helps drive the blood out of the heart - increasing inhalation movements cause venous pressure to increase, then venous return increases as well *follow up question* a) when you vasoconstrict an arteriole, you will limit the flow to a individual capillary bed b) - with leg muscles relaxed we have higher pressure (80 mmHg) in the veins going down the body due to gravity - when leg muscles contract, this interrupts the veins and now we gave a lower pressure (14 mmHg) in the veins going down the body due to gravity

93) Reproduce figure 9.39 and describe the histology of cardiac muscle cells, defining and explaining: intercalated discs, desmosomes, and gap junctions. *(LO for section 9.10)*

*histology* - has striation = sarcomeres - single nucleus - has branched ends (unique to cardiac muscle) *intercalated discs* - present where one cardiac cell touches another cardiac cell; (adjacent cells joined end to end) *desmosome* - hold cells together (aka a spot weld); a mechanism of attachment/stability *gap junction* - channels that connect cytosol to cytosol that allows ions/small solutes to move from cell to cell. this allows for electrical communication (aka an electrical synapse)

10) How does figure 12.8 help us "to see" the importance of vessel radius?

*increase blood vessel radius* causes less blood to scrap against the blood vessels walls which *means less resistance and increase flow* *decrease blood vessel radius* causes more blood to scrap against the blood vessels walls which *means more resistance and decreased flow*

95) Draw the aligned graphs in figure 13.13. Explain each data trace. Highlight the application of Boyle's law. *follow up question* a) what is the tidal volume (TV) at rest? (hint: basically the breath volume in milliliters mL) *IDK IF THIS IS CORRECT*

*intraplueral pressure (Pip) during breathing* 1) we start at the intrapleural space of 756 or -4 mmHg (4 less than atmospheric pressure) 2) as we inhale, the volume of the intrapleural space increases causing a decrease in intrapleural pressure. this occurs because as we inhale, the chest is going outwards but the lungs want to go inward. Thus causes the intrapleural space to increase in volume and decrease in pressure! (boyles law: in a sealed space, when volume go up, pressure goes down!)) 3) when we exhale, the volume of the intrapleural space decrease and the volume compresses thus causing a increase in intrapleural pressure. this occurs because as we exhale, the chest is going inward and thus decreasing the intrapleural volume and thus increasing the pressure! *alveolus pressure (Palv) during breathing* 1) after the end of exhalation, pressure in the alveoli is equal to the atmospheric pressure 2) as we inhale, you expand the volume of the alveoli and your pressure in lungs decrease and thus pressure goes down from 0 to -1, this results in inward airflow 3) at the end of inspiration and beginning of expiration, the chest wall is not expanding. Since the lung size is not changing the airway is open to atmosphere which is why Pip and Palv is equal and there is no airflow. 4) as respiratory muscles relax the lungs and chest passively collapse due to elastic recoil. 4) at mid-expiration, the lungs is collapsing and thus compressing alevolar gas. Thus causing Palv to be higher (a positive number) than atmospheric pressure and thus drives air out. And then finally once the air has been exhaled, the Palv and the pressure in the atmosphere is equal again! *transpulmonary pressure during breathing* 1) think about the equal of transpulmonary pressure; Palv (inside) - Pip (outside) = 2) when we inhale, the transpulmonary pressure gets increases in value from positive 4 to around positive 7. 3) this increasing of positive number indicates that pressure difference that holds lungs open and expanding due to inhalation 4) then when we exhale, the number goes down and gets less positive (not a negative number, its just decreasing in value) from 7 to back to 4 which is a -3 difference). this negative -3 number indicates that the pressure difference that holds chest wall in and causes shrinking of the lung *follow up question* a) typical tidal volume is 500 mL

92) Using figure 12.12 and your lecture notes, thoroughly discuss the regulation of cardiac muscle via the autonomic nervous system. How does each branch affect heart rate and strength of contraction? *(LO for section 9.10)*

*parasympathetic* - vagus nerve (10th cranial nerve) carries and releases ACH neurotransmitter from varicosities onto muscarine ACH receptors - slows down the heart rate - weakens the strength of contraction on ONLY the atria (bc para only innervates the top part of the heart; the atria) - regulates the top of the heart (atria) *sympathetic* - the thoracic spinal nerve carries and releases norepinephrine from varicosities onto beta 1 adrenergic receptors - adrenal medulla releases neurohormone epinephrine that travels via the bloodstream and onto beta 1 adrenergic receptors - accelerates the heart rate - strengthens the contraction of BOTH atria and ventricles (bc beta 1 adrenergic receptors are on both atria and ventricles) - regulates the top and bottom of the heart (atria and ventricles)

37) a) Using figure 12.12 and the lecture slides, draw the ANS innervation of the heart (both parasympathetic and sympathetic pathways). Discuss the relevant neurotransmitters and neurohormones. b)How does each affect the HR, SV, and CO?

*parasympathetic: regulates ONLY the atrium (top part) of heart* a) - efferent action potential travel through vagus nerve (10th cranial nerve) that has long pre-gang. and short post-gang. - short post post-gang. releases ACH *via varicosities* to muscarinic ACH receptors on SA node, AV node, and atrial cells (on the atrium) b) - decrease SA (heart rate) frequency - decrease AV conduction velocity - decrease atrial kick - decrease CO this cause decrease in heart rate (HR) and thus decrease in cardiac output (CO) *(YOU GET A SLOWER HEART)* *sympathetic: regulate the ENTIRE heart; both atriums and ventricles* a) - the thoracic spinal nerve that sends signals to short preganglionic axon and then long post-ganglionic axons - long post-ganglionic axons releases the NT called norepinephrine *via varicosities* onto beta 1 adrenergic receptors all over the heart - the adrenal medulla also releases the neurohormone called epinephrine that travels through the bloodstream and will bind to beta 1 adrenergic receptors all over the heart b) - increases SA (heart rate) frequency - increases conduction velocity of all cells - increases atrial kick - increase stroke volume - increase CO this causes increases heart rate and stroke volume and cardiac output *(YOU GET A FASTER, STRONGER HEART)*

58) Build Table 12.7 and discuss the regulation of flow to these specific organs: -heart -skeletal muscle -kidneys -brain -lungs

*regulation of flow to the heart* 1) controlled mainly by local metabolic factors, particularly adenosine, and flow autoregulation 2) coronary flow occurs mainly during diastole *regulation of flow to the skeletal muscle* 1) controlled by local metabolic factors during exercise 2) Sympathetic activation causes vasoconstriction (mediated by alpha 1 receptors) in reflex response to decrease arterial pressure 3) -Epi causes vasodilation via beta 2 receptors when present in low concentration, and vasoconstriction via alpha adrenergic receptors when present in high concentration (injectons) *regulation of flow to the kidneys* - flow autoregulation (aka the myogenic flow autoregulation) is a major factor - angiotensin II is also a major vasoconstrictor that help converse sodium and water *regulation of flow to the brain* - excellent flow autoregulation ((aka the myogenic flow autoregulation) - distribution of blood controlled by local metabolic factors - vasodilation occurs in response to increase concentration of CO2 in aterial blood - ANS has little influence in flow regulation in brain *regulation of flow to the lungs* - constriction mediated by local factors in response to low oxygen concentration - just the opposite of what occurs in the systemic circulation

78) Using table 13.1, discuss the seven functions of the respiratory system. *follow up question* compare and contrast systemic and pulmonary circulation in terms of: a) what is the blood flow (cardiac output) between these two circulations (L/min) b) what is the pressures? (is it low MAP or high MAP) c) what is the resistance? (in terms of TPR)

*seven functions of the respiratory system* 1) provides oxygen to the blood 2) eliminating CO2 out of the blood 3) regulates the blood pH, in coordination with the kidney 4) forms speech sounds 5) defends against inhaled microbes 6) influences arterial concentrations of chemical messengers by removing some from pulmonary capillary blood and producing adding others to blood 7) traps and dissolves blood clots arising from systemic veins *follow up question* a) - systemic: 5 L/min (cardiac output) - pulmonary: 5 L/min (cardiac output) b) - systemic: high MAP - pulmonary: low MAP c) - systemic: large TPR - pulmonary: low TPR (6.2 times less than systemic)

45) a) Draw figure 12.11 (page 374). How are the two circulatory systems the same? How are they different? b) Distinguish a portal arrangement from the typical blood vessel sequence.

*similarities* pulmonary circulation and systemic circulation are the same in that they leave the heart to go to arteries, arterioles, capillaries, venules and to vein and back into the heart. *differences* 1) in the pulmonary circulation blood comes out the right ventricle into the pulmonary trunk through the pulmonary semilunar valve. 2) in the systemic circulation, blood comes out the left ventricle into the aorta through the aortic semilunar valve 1) in systemic circulation blood goes through the pulmonary veins and into the heart 2) in the pulmonary circulation blood goes through the superior and inferior vena cava and into the heart 1) in the pulmonary circulation blood goes into the lungs 2) in the systemic circulation blood goes throughout the whole body *follow up question* - the typical blood vessel sequence is: 1) arteries 2) arterioles 3) capillaries 4) venules 5) veins - a situation where portal vessel arrangement is involve (during GI-hepatic, hypothalamus anterior pituitary) the sequence will be: 1) arteries 2) arterioles 3) capillaries 4) PORTAL VESSEL/PORTAL VEIN 5) 2ND CAPILLARIES 6) veins

59) Draw figure 12.40a and describe the structural features that define capillaries; discuss how the features contribute to their function. *follow up question* a) what is the functional unit of the cardiovascular system? b) in a capillary what is the arteriole end of a capillary and what is the hydrostatic pressure of it (in mmHg). what is the hydrostatic pressure of the venous end?

*structural features (the capillary structure maximizes their efficiency:* 1) are typically 8 micrometers in diameter 2) has thin walls (because its a single layer of endothelial cells) with pores. this helps maximize the exchange (diffusion) of red blood cells and the ISF because it is closer which facilitates faster diffusion and exchange *follow up question* a) the capillaries! b) - a capillary has an arteriole end that is closer to the arterioles. they also have a venous end that is close to the venules. - in the arteriole end of the capillary has a hydrostatic pressure of 35 mm Hg that is driving the flow. the venous end of the capillary has a a hydrostatic pressure of 15 mmHg

79) Reproduce figure 13.1 and label/discuss all the major anatomical structures a molecule of oxygen would encounter as it passes from room air into the lungs.

*structures O2 will encounter as it goes from the air and into the lungs* 1) O2 will encounter the nostrils and the nasal cavity. (the nasal hairs and nasal sinuses like mucus is what warms, moistens, and filters air) 2) O2 then passes through the pharynx 3) the epiglottis (the flap) opens and allows air to enter into the glottis (the tube or hole) and encounters the vocal cords in the larynx 4) from there it travels through the trachea (the trachea has cartilaginous "C" rings that holds the airway open) 5) the trachea will then branch into a right and left main bronchus 6) the O2 then goes into the lungs

39) Draw figure 12.25 and discuss how sympathetic and parasympathetic innervation can alter the SA node action potential frequency via regulation of ion channels *follow up question* discuss how sympathetic and parasympathetic innervation can alter the AV node action potential frequency via regulation of ion channels

*sympathetic innervation on SA node* 1) norepinephrine and epinephrine release causes MORE depolarizing Na+ (from funny Na+ channels) and Ca2+ (from transient Ca2+ channels) entry and thus causes us to reach to SA node action potential threshold faster - ex: increasing heart rate = more depolarization *parasympathetic innervation on SA node* 1) acetylcholine release causes LESS depolarizing Na+ (from funny Na+ channels) and Ca2+ (from transient Ca2+ channels) entry and MORE K+ exiting and thus cause us to reach SA node action potential threshold slower - ex: decreasing heart rate = less depolarization (MORE K+) *follow up question* 1) sympathetic innervation on AV node: causes MORE depolarizing L-type Ca2+ to enter (increased/steeper conduction velocity). It will move through gap junctions FASTER 2) parasympathetic innervation on AV node: causes LESS depolarizing L-type Ca2+ enter (slower conduction velocity). It will move through gap junctions SLOWER

80) Use your lecture notes to describe the components and function of the "ciliary escalator". *discussed in LIVE class*

*the ciliary escalator components* 1) in the trachea and left and right main bronchi's we have ciliated cells 2) the ciliated cells have cilium (cilia) that are on top of the ciliated cells that can move in a wavy movement back and forth. they are waving and moving a watery substance 3) on top of the watery substance there is mucus that is secreted by goblet cells. mucus serve to trap harmful particles in the air we breathe. 4) the mucus is floating on top of water that is being moved by the cilia. the cilia will move the mucus with trapped harmful particles up to the glottis where we will have a sensation to cough or clear your throat in which we can spit the mucus out of swallow it *ciliary escalator functions to move the sticky mucus that has trapped particles up and out of the lungs*

17) Draw figure 12.13 and describe the major function of each component in the cardiac conduction system.

*the major function of the each component in the cardiac conduction system* *1) SA node is a "true" pacemaker* - they oscillate and get to threshold first - determines the heart rate *2) AV node delays AP propagation; A.P propagation is slow* - this is because it is a chain of cells and because of ion channel density - the only expected electrical connection between atria and ventricle - AV node allows time for atrial contraction to complete before ventricular depolarization (excitation) and contraction occurs *3) Bundle of His and Purkinje Fibers; A.P. propagation is fast* - Bundle of His: constitute the only electrical connection between the atria and the ventricles - Purkinje fibers: extensions of the Bundle of His that branch out and spread the stimulus to ventricular contractile cells (the propagation is FAST!!!). *ALL OF THESE COMPONENTS IS WHAT HELPS US COORDINATE OUR HEARTBEAT!!!!*

95) Using figure 12.15, draw a ventricular muscle cell action potential, explain the ionic events underlying its shape, and describe how changes in ion channel function can modify both electrical and mechanical function (e.g. L-type calcium channels). *(LO for section 9.10)*

*ventricular action potential (NO EPSP or EPP's* - resting membrane potential is -89 mV - we get a rapid depolarization (upstroke) because of current from neighboring cell through *gap junctions* that allow for Na+ to enter rapidly through voltage-gated Na+ channels - at the peak, Na+ voltage-gated channels are inactivated and transient K+ channels open briefly causing a little repolarization - then there is a prolonged "plateau" of depolarization due to the slow but prolonged opening of voltage-gated *calcium channels* (AKA the L-type (long-lasting) channels also known as the DHP receptor!!!! this is where the trigger calcium is coming in which causes the "plateau" of the action potential) - then K+ channels open and causes repolarization back to -89 mV (resting membrane potential)

28) Using figure 12.21 and the lecture slide, describe what happens and why during ventricular filling (diastole) *follow up question* a) what is the EDV? b) what the typical amount of blood (mL) at EDV at rest?

*ventricular diastole (filling) of LEFT VENTRICLE* - there is more pressure/volume in the atria and due to this, we will have a pressure gradient that opens the AV valves and move into the ventricle while closing the semilunar valve and thus allows blood to flows into ventricle. this is called *rapid passive filling* 80-90% of the ventricles - there will be *active filling* that contracts the atria called "the atrial kick" which actively contracts and squeezes more blood into ventricle. In a typical person at rest, this adds about 10-20% of blood to ventricle *follow up question* a) EDV or End Diastolic Volume is the final volume in the ventricle after filling (active and passive filling) b) the final volume (mL) of blood of EDV at rest is ~135 mL

30) Using figure 12.21 and the lecture slide, describe what happens and why during ventricular ejection. How do you calculate the stroke volume given the end-diastolic volume and end-systolic volume? *follow up question* a) what is the ESV? b) wha is the ESV at rest?

*ventricular ejection of LEFT VENTRICLE* - pressure is greater in the ventricle than in the aorta and pulmonary artery that causes semilunar valves to open and push blood out - we are going to have a stroke volume (SV) which is the volume (mL) of blood ejected from each ventricle. At rest it is typically ~70 mL. The SV is the same from right and left ventricle! *follow up question* a) ESV or the End Systolic Volume is the volume of blood remaining in the ventricle after ejection b) ESV at rest = 65 mL ESV = EDV - SV SV = EDV - ESV

29) Using figure 12.21 and the lecture slide, describe what happens and why during ventricular isovolumetric contraction.

*ventricular isovolumetric contraction of LEFT VENTRICLE* - developing higher pressure in the ventricles that closes the AV valves and semilunar valves - ventricles contract and force develops - the 1st heart sound at start of this phase: "LUB" (AV valves close) - volume is constant at EDV (135 mL) *pressure is higher in the aorta and pulmonary artery than the pressure in the ventricles (which is why semilunar valves are closed)* *pressure is higher in the ventricle than the pressure in atria*

31) Using figure 12.21 and the lecture slide, describe what happens and why during ventricular isovolumetric relaxation.

*ventricular isovolumetric relaxation of LEFT VENTRICLE* - the 2nd heart sound at start of this phase: "DUP" (semilunar valves close) - volume constant at ESV (65 mL) - pressure is higher in the aorta and pulmonary artery than pressure in ventricles causes *semilunar valves to close* - pressure is higher in ventricles than pressure in atria causes *AV valves to close*

89) a) Using your lecture notes list the skeletal muscles utilized during quiet/resting inhalation. b) What additional skeletal muscles are used during active/forced inhalation? c) What skeletal muscles are used during quiet/resting exhalation? d) What skeletal muscles are used during active/forced exhalation?

- *skeletal muscles utilized during quiet/resting inhalation.* 1) diaphragm (inhale = flatten diaphragm, exhale = dome-shaped diaphragm) 2) external intercostal muscles (when contracted they help lift the chest upwards; decompress the chest) - *additional skeletal muscles are used during active/forced inhalation* 1) sternocleidomastoid muscles (accessory muscle) 2) scalenes (accessory muscle) 3) pectoralis minor? - *skeletal muscles are used during quiet/resting exhalation* 1) NO MUSCLES CONTRACT DURING QUIET/RESTING EXHALATION - *What skeletal muscles are used during active/forced exhalation* 1) internal intercostals muscles (pull down/compress the volume of chest) 2) rectus abdominis (your abssss) 3) external abdominal (your abssss)

96) Use figures 12.20 and 9.41 to explain the significance of the cardiac action potential duration. *(LO for section 9.10)*

- cardiac muscle has a prolonged (longer) refractory period/action potential duration as compared to skeletal muscle to prevent tetanus and allow for the full contraction of the cardiac muscle cell. (The cardiac muscles can't summate force so that there's no tetanus) - this allows time for ventricles to fill with blood prior to pumping out blood. it makes no sense to have tetanus because there will be no opportunity for heart to relax and refill ventricles with blood for the next pump. prolonged refractory period allows for heart to pump blood out, fill with blood, pump blood out, fill with blood

1) Draw a figure that explains why all cells of the human body need to be within 100µm (micrometer) of a capillary vessel.

- cells within 100µm of a capillary vessel will take milliseconds (faster) for diffusion equilibrium of plasma, cells, oxygen, and nutrients, which is compatible for life. (Diffusion is efficient in small distances) - as opposed to cell more than 100µm away will take longer (seconds to minutes) which is not compatible with life

15) a) Define cardiac valve "prolapse" b) describe how prolapse is normally prevented

- prolapse is when a valve flips backwards into the atrium (thus causing blood to flow backwards which is BAD) - prolapse is normally prevented by chordae tendineae and the papillary muscles that pull the valves down (into the ventricles) when papillary muscles contract (simultaneously with ventricular contraction)

44) Reproduce figure 12.30; explain how CO may be increased (or decreased) by changes in SV and HR. Include ANS components and all molecular details when possible. *follow up question* a) what happens if we want to decrease cardiac output (CO). how will manipulate the variables to change SV and HR so we can have a decreased CO b) what is the formula to find cardiac output?

1) *increase end-diastolic ventricular volume* - intrinsically increase stroke volume of cardiac muscle via Frank-Starling relationship and thus increase cardiac output 2) *increase of sympathetic nerves to heart:* - leads to the release of NE that bind to the beta-1 adrenergic receptors on cardiac muscle that increase contractility and thus increase cardiac output - leads to the release of NE that binds to the beta-1 adrenergic receptor on the SA node that increase heart rate and thus increase cardiac output 3) *simultaneously increased plasma epinephrine:* - binds to beta 1-adrenergic receptor on cardiac muscle that increase contractility and thus increase stroke volume and therefore increase cardiac output - binds to beta 1-adrenergic receptors on SA node causing increase heart rate and thus increase cardiac output 4) *decrease of parasympathetic activity to heart:* - less ACH release onto muscarinic ACH receptors on SA node and thus will SA node will be released from inhibition from parasympathetic and thus increase heart rate and therefore increase cardiac output *follow up question* *in a scenario where we need to make cardiac output (CO) to decrease, we would just reverse all the arrows above* 1) *DECREASE end-diastolic ventricular volume* - intrinsically decrease stroke volume of cardiac muscle via Frank-Starling relationship and thus decrease cardiac output 2) *decrease of sympathetic nerves to heart:* - leads to the decrease of NE that bind to the beta-1 adrenergic receptors on cardiac muscle that decrease contractility and thus decrease cardiac output - leads to the decrease of NE that binds to the beta-1 adrenergic receptor on the SA node that decrease heart rate and thus decrease cardiac output *simultaneously decreased plasma epinephrine:* - decrease the binding to beta 1-adrenergic receptor on cardiac muscle that decreases contractility and thus decreases stroke volume and therefore decrease cardiac output - decrease the binding to beta 1-adrenergic receptors on SA node causing decrease heart rate and thus decrease cardiac output 3) *INCREASE of parasympathetic activity to heart:* - MORE ACH release onto muscarinic ACH receptors on SA node and thus will SA node will decrease heart rate and therefore decrease cardiac output b) SV x HR = CO

34) Describe what determines the opening and closing of all heart valves, and relate the normal heart sounds "Lub" and "Dup" to valve events. *follow up question* describe the heart sound and valve defect 1) Lub-whistle-dup a) which defect (stenotic or insufficient valves)? b) which valve? (AV or SL) 2) Lub-gurgle-dup a) which defect (stenotic or insufficient valves)? b) which valve? (AV or SL) 3) Lub-dup-whistle a) which defect (stenotic or insufficient valves)? b) which valve? (AV or SL) 4) Lub-dup-gurgle a) which defect (stenotic or insufficient valves)? b) which valve? (AV or SL)

1) LUB (the sound when AV valves closes) - semilunar valves open and causes isovolumetric ventricular contraction and ejection (systole) 2) DUP (the sound makes when SL valves closes) - AV valves open and causes isovolumetric ventricular relaxation and filling (diastole) step 1 and 2 repeat.... *follow up question* 1) lub-whistle-dup a) defect: stenotic valve b) semilunar valve 2) lub-gurgle-dup a) defect: insufficient valve b) AV valve 3) lub-dup-whistle a) defect: stenotic valve b) AV valve 4) lub-dup-gurgle a) defect: insufficient b) semilunar valve hint: whistle = poor opening gurgle = poor closing *lub* (AV valve closes) ---(SL valve open)--> *dub* (SL closes) ----(AV valve open)---> *lub* (AV valve closes)

25) Reproduce the figure that demonstrates the relative timing for one beat of the heart organ: 1) Lead I ECG events 2) SA node action potentials 3) atrial contractile cell action potentials 4)AV node action potentials 5) conducting cells (purkinje fibers) action potentials 6) ventricular contractile cell action potentials *follow up question* a) what is meant by "current injection"? b) why do latent pacemakers exist (lecture 2 page 24) https://mediaspace.wisc.edu/media/Andrew%20Lokuta-Humanities%203650-11_05_21-08%3A46%3A39/1_b7llap8j *(IDK IF THIS IS CORRECT)*

1) The LEAD 1 ECG events: P-wave, QRS-wave, and T-wave SA node starts sequence of heart beat. - funny Na+ channels and transient Ca2+ channels gets SA node to threshold - the L-type Ca2+ channels open causing upstroke of SA node which initiates the P-wave 2) gap junctions allows for L-type calcium *(i thought it was fast Na+ channels that causes atrial contractile cell rapid depolarization?, i don't know...)* from SA node to enter atrial contractile cell that causes rapid upstroke which starts the P-wave (atrial contraction/depolarization) 3) then in AV node action potential there are funny Na+ channel and transient Ca2+ channel that is slowly depolarizing and BOOM we have a current via gap junctions from atrial contractile cells causes AV node to prematurely have its shallow upstroke. (occurs during P-R segment) 4) then current via gap junctions from AV node will be injected into conducting cells (like Purkinje gibers, bundle of his, etc...) causing it to have it steep upstroke (fast conduction) which initiates QRS-wave 5) then current from conducting cells will go through gap junctions and be injected into ventricular contractile cells causing it to have a rapid upstroke and cause the QRS-wave (ventricular contraction/depolarization) *follow up question* a) current injection is *depolarizing ions* like sodium and calcium that move through gap junctions from one side of cell to another that causes depolarization b) latent pacemakers don't have to the opportunity to get to threshold themselves so they need injecting current to reach upstroke prematurely. they are important because they take over initiating excitation of the heart only when SA node is unable to generate electrical signals!!!

20) a) Using the lecture slides, define these terms: automaticity, sinus rhythm, latent pacemaker, ectopic pacemaker. b) List the intrinsic depolarization rates of the SA node, AV node, and Purkinje fibers. *follow up question* a) conducting cells function to spread the signal to the ventricles. could they also be pacemakers?

1) automaticity: capable of spontaneous, rhythmical self excitation 2. sinus rhythm: normal cardiac excitation-contraction sequence beginning at the SA node. (electrical stimuli are initiated in the SA node and starts the normal conduction pathway!) - if SA node is driving the excitation-contraction sequence it is a sinus rhythm! 3. latent pacemakers: lying quiet or hidden, not active potential pacemakers. This includes AV node and conducting cells (Purkinje fibers) - they don't exhibit their pacemaker abilities because they are driven by the SA node (sinus rhythem) 4. ectopic pacemaker: abnormal; any site or thing that is driving the ventricular excitation sequence that is NOT the SA node (for example the AV node) - if the AV node or Purkinje fiber is driving the excitation-contraction sequence then its an ectopic pacemaker! b) 1. SA node intrinsic depolarization rates = 100-120 APs/min 2. AV node intrinsic depolarization rates = 60-80 APs/min 3. Purkinje Fiber intrinsic depolarization rates = 30-50 APs/min *follow up question* a) conducting cells can be pacemakers but thats not what they typically do! but they are so slow of a pacemaker, their rate of spontaneous depolarization is too slow (30-50 APs/min)

63) Draw figure 12.44 and define Filtration, Absorption, and Bulk Flow. What does bulk flow do in regards to homeostasis? State what bulk flow is NOT. *follow up question* a) how is bulk flow calculated?

1) filtration: movement of fluid (water) out of the blood (from the plasma into the ISF) 2) absorption/reabsorption: movement of fluid (water) into the blood (from the ISF into the plasma) 3) bulk flow: distribution and balance of the *movement* of fluid (water) that is driven by filtration and absorption between the plasma and the ISF, *not DIFFUSION!* *follow up question* a) filtration - absorption = bulk flow

55) Use the lecture slide to list and describe the effects of vasoactive metabolites involved with local regulation of arteriole contractile state. (for vasodilation) *follow up question* what are the effects of vasoactive metabolites involved with local regulation of arteriole contractile state if they vasoconstrict?

1) if O2 is decreasing, there will be arteriole vasodilation 2) is CO2 is increasing, we will have arteriole vasodilation 3) if pH (more acid?) is decreasing, we have have arteriole vasodilation 4) if ECF K+ is increasing, we will have arteriole vasodilation 5) if adenosine is increasing, we will have arteriole vasodilation *follow up question* a) well we just do the opposite of everything above 1) if O2 is increasing, there will be arteriole vasoconstriction 2) is CO2 is decreasing, we will have arteriole vasoconstriction and so on....

72) Draw figure 12.58 and explain how a change in arterial pressure leads to a change in ANS activity. How does the change in ANS activity restore MAP? *follow up question* what if the arterial pressure (MAP) decreases? what will happen to the the ANS activity?

1) increase in arterial pressure (MAP) 2) causes arterial baroreceptors to fire more action potentials because they detect the high pressure that stretches the walls 3) *ANS activity occurs:* → baroreceptors will fire more IPSP onto the sympathetic medullary control center to release LESS NE and Epi to causing decrease in heart rate, decrease in SV (due to decrease venous pressure, venous return from vasodilation ALSO decrease in contractility that plays a role in decreased SV) and decrease TPR due to vasodilation, and finally decrease in CO → baroceptosr will fire more EPSP onto parasympathetic medullary control center to release MORE Ach and thus will cause a decrease in heart rate (because more inhibition from increase Ach will decrease heart rate) *follow up question* 1) decrease in arterial pressure (MAP) 2) causes arterial baroreceptors to fire less action potentials because they detect the low pressure that in the arterial walls 3) *ANS activity occurs:* → baroreceptors will fire less IPSP onto the sympathetic medullary control center to release MORE NE and Epi to causing increase in heart rate, increase in SV (due to increase venous pressure, venous return from vasoconstriction ALSO increase in contractility that plays a role in increased SV) and increase TPR from vasoconstriction, and finally increase in CO → baroceptosr will fire less EPSP onto parasympathetic medullary control center to release LESS Ach and thus will cause a increase in heart rate because heart rate is not being inhibited as much anymore by Ach

57) Use figure 12.39 to list and describe the major neural, hormonal, and local controllers of arteriole contractile state. *follow up question* a) does parasympathetic NS play a role in arteriole contractile state?

1) neural controls of arteriole contractile state *vasoconstrictors in neural control* - sympathetic nerves release norepinephrine that bind to alpha-1 adrenergic receptors that vasoconstrict arteriolar smooth muscles *vasodilators in neural control* - neurons that release nitric oxide (a gas!) will vasodilate arteriolar smooth muscles 2) hormonal controls of arteriole contractile state *vasoconstrictors in hormonal control* - high dose (injection) of epinephrine will vasoconstrict arteriolar smooth muscles - angiotensin II will vasoconstrict arteriolar smooth muscles - vasopressin (ADH) will vasoconstrict arteriolar smooth muscles *vasodilators in neural control* - low dose (physiological dose) of epinephrine will vasodilate arteriolar smooth muscles - atrial natriuretic peptide from the right atrium will vasodilate arteriolar smooth muscles *3) local control of arteriole contractile state* *vasoconstrictor in local control* - myogenic flow autoregulation where you can regulate the radius of arterioles based on internal pressure - endothelin-1 that is made by endothelial cells that is THE MOST POTENT constrictor in our bodies *vasodilator in local control* - decrease in oxygen - increase in K+, CO2, H+ - decrease pH - increase in osmolarity - increase adenosine - increase substance release during injury - increase nitric oxide *follow up question* - parasympathetic doesn't do much :// there is no dual innervation of vasculature, only sympathetic plays a role in this

83) Using figure 13.3, describe the anatomical and functional interactions between the circulatory and respiratory systems in the lungs.

1) the terminal bronchiole has smooth muscles that can constrict and dilate to regulate airflow, NO GAS EXCHANGE because there are no alveoli 2) then airflow will go to respiratory bronchiole that have alveoli (and rich capillary beds) and GAS EXCHANGE CAN OCCUR *There is close association of airways and blood vessels (a sheet of blood next to a sheet of air). The large surface area allows for rapid exchange of gas.*

19) Draw figure 12.14 and explain the sequence in which cardiac chambers undergo excitation and relaxation during a single beat of the heart. Describe how these events appear in electrocardiographic measurements.

1. SA node reaches threshold and fires A.P. 2. the A.P. from SA node spreads throughout the atria and depolarizes (and thus contractions) forming the *P wave* on the ECG. - *the P-wave* shows that the SA node got to threshold and depolarized the atrium 3. atrial excitation ends and the end of P-wave and relaxes. ventricular excitation begins with a flat line that represents a) the AV node delaying and slowly conducting signal into the Bundle of His b) atrial muscle cells uniformly depolarized and contracting and squeezing blood into ventricles 4. signal does eventually get out of the AV node and goes down into The Bundle of His and Purkinje fibers that causes depolarization and contraction of the ventricular muscles which is represented by the *R wave* 5. and lastly the ventricular relaxation/repolarization is represented as the *T wave*.

6) Using figure 12.3, discuss the unique features of red blood cells *follow up question* describe sickle-cell disease a) what causes sickle-cell disease? b) sickle cell disease vs. sickle cell trait? c) how does the blood flow change? d) how is the spleen affected in sickle-cell disease?

1. biconcave discs that allows for large surface area and a smaller volume 2. a lot of O-hemoglobin protein for O2 binding and transportation of O2 in our blood 3. organelles are extruded (ejected) enabling more oxygen to be transported - NO DNA, DNA is retrieved from the buffy coat *follow up question* a) caused by a genetic mutation b) sickle cell disease is when people have the mutated gene that is fully manifested that alters one amino acid in the hemoglobin chain (has two copies of mutated gene). Individuals with sickle cell trait have one normal gene inherited from one parent and one gene with a mutation inherited from the other parent c) people will sickle-cell disease have RBC that forms sickle shapes or other unusual forms. this causes blockage of capillaries, tissue damage, and anemia. RBC can clump together and can't move easily thus blocking/slowing blood flow. this also negatively affect the transportation of O2 throughout the body d) the spleen is what removes the sicklelike shape red blood cells, but when there is a lot of sickled cells, the spleen can be overfilled with damaged cells and painfully enlarge. it can also block some of the small blood vessels in the spleen and cause pain/damage to the organ.

11) Draw figure 12.9 and label all of the structures in this frontal section of the heart. Then trace the path of a blood cell through the heart, naming in correct order the major vessels, cardiac chambers and valves that are encountered. *follow up question* a) what is the purpose for the interventricular septum?

1. blood drains into the heart through the superior vena cava and the inferior vena cava 2. blood goes into the right atrium 3. blood then goes through the right AV (tricuspid) valve (which is held by the chordae tendineae attached to the papillary muscle) 4. into the right ventricle 5. then into the pulmonary semilunar valve 6. then into the pulmonary trunk 7. then into the right and left pulmonary arteries into the lungs 8. the blood (oxygenated) comes back to the heart through the left and right pulmonary veins into the left atrium 9. blood then goes through the left (bicuspid) AV valve AKA the mitral valve and into the left ventricle 10. blood then goes through the aortic semilunar valve and into the aorta 11. then blood branches out into the arteries and to the head and body (systemic circulation) *follow up question* a) the interventricular septum separates the right and left ventricles and is important for the electrical component of the heart

94) Draw figure 9.40 and detail the steps/components of cardiac EC-coupling. How is this process similar to that in skeletal muscle? How is it different? *(LO for section 9.10)* *follow up question* a) for every 1 trigger calcium that comes in from the DHP receptor, how much calcium is released from the sarcoplasmic reticulum through the RYR receptor? b) what does calcium induce calcium release mean?

1. depolarization by Na+ entry causes action potentials to propagate to T-tubules (no neuron required to cause AP) 2. action potentials open DHP (L-type Ca2+ channel) receptors allowing calcium to enter 3. a small amount of "trigger" Ca2+ then binds to RYR receptors and opens it, allowing Ca2+ in the sarcoplasmic reticulum to be released 4. Ca2+ binds to troponin allowing tropomyosin to move away from blocking cross-bridge binding site on actin 5. myosin binds to actin and cross-bridge cycle occurs and generates contraction/force 6. Ca2+-ATPase pump transports the Ca2+ back in the sarcoplasmic reticulum 7. the trigger calcium that came in from the DHP receptor is removed from the cytosol (ICF) either by Ca2+-ATPase pump (primary active transporter pump) or by the Na+/Ca2+ exchanger (a secondary active transport) *) membrane is repolarized when K+ exit that ends actional potential *follow up question* a) 10 calcium is released from SR (1 trigger Ca2+ results in 10 calcium released from SR) b) local Ca2+ that comes in for L-type Ca2+ channel can induce Ca2+ release from the sarcoplasmic reticulum

68) Using your lecture notes, reproduce the five talking points regarding lymph fluid in general.

1. lymph is interstitial fluid (part of ECF) and is made of absorbed fats and escaped plasma proteins 2) lymph fluid is returned to large veins near the heart 3) lymph vessels contain smooth muscles and one-way valves like veins. smooth muscles can be influenced by NE from sympathetic innervation 4) lymph vessels will come together into lymph nodes - lymph nodes have immune functions - lymph nodes enlarge when fighting an infection - cancer cells can spread through lymph, which is lymph nodes are removed during treatment 5) 3-4 liters/day of lymph is returned/recovered to the circulation

43) Draw figure 12.29 and describe the second messenger pathway by which cardiac contractility is altered, including all cellular targets of modulation and their consequences. *follow up question* with sympathetic innervation (using norepinephrine and epinephrine) what are the 3 key points discussed in lecture of there affect on Ca2+ release, Ca2+ reuptake, and force and velocity contraction

1. norepinephrine and epinephrine bind on to beta 1 adrenergic receptor 2. activates G-protein 3. G-protein stimulates Adenylyl cyclase 4. Adenylyl cyclase converts ATP into cAMP 4. cAMP activates cAMP-dependent protein kinases 5. *cAMP-dependent protein kinases phosphorylates 5 targets:* a) protein kinase phosphorylates DHP receptor (L-type Ca2+ channel) and opens it to allow Ca2+ entry b) protein kinase phosphorylates RYR receptor on SR to open and allow Ca2+ to come out c) protein kinase phosphorylates thin filament activation (Ca2+ to troponin) d) protein kinase phosphorylates the components in the cross-bridge cycling, thick and thin filament sliding, and force generation (and thus greater force and velocity of contraction) e) protein kinase phosphorylates a protein that is associated with the Ca2+ATPase pump that increases reuptake of Ca2+ into SR. *follow up question* with sympathetic innervation we will have: 1) faster and more calcium release (target a & b) 2) faster calcium removal/reuptake (target e) 3) stronger and briefer contraction (target c & d)

8) a) Draw figure 12.5. Reproduce the 6 bullet points we discussed in lecture. Explain what it means to say that systemic vascular beds are "in parallel" b) discuss the 3 implications of parallel arrangement for systemic system.

1. the whole figure shown is the cardiovascular system - composed of a heart, vessels, arteries, and blood 2. - there are 2 pumps a) right atrium/ventricle b) left atrium/ventricle - there are 2 circulator systems a) pulmonary circulatory system (pumps blood from the right side of heart and sends it to the lungs) b) systemic circulatory system (receives blood from pulmonary circ. and sends out to the body) 3. - there are *arteries* that carries blood away from the heart (either into the lungs or throughout the body) - there are *veins* that carries blood towards the heart 4. - left heart wall is thicker because it does more work (more work to pump out blood throughout the body) - right heart wall is thinner because it doesn't do more work (less work to pump blood to the lungs that is closer) 5. perfusion: the passage of blood or fluid through a vascular bed (there are 3 vascular beds!) 6. - *pulmonary circulation (the lungs) are in series with the right side pump* because there is only one place the blood is going which is the lungs - *systemic circulation are in parallel with the left side pump* because the blood is going to many different places (the head, torso, body, or the 3 vascular beds) b) 1. the same quality/type of blood is delivered equally to the vascular beds or throughout the body at the same time 2. can independently regulate the flow of blood to vascular beds (can send less blood to one capillary bed, and more to another) 3. left side pump of the heart does not need to generate ALOT of pressure/energy for perfusion of the systemic circulation because of the parallel arrangement

71) Write the hemodynamic equation that determines mean arterial pressure (MAP) in the systemic vascular circuit. Define "total peripheral resistance (TPR)".

MAP = CO x TPR *definitions given by LAB 7* TPR = Total Peripheral Resistance which is the combined resistance to flow of all the systemic blood flow, mostly due to arterioles MAP = the average pressure in the arteries (or arterioles?) through the cardiac cycle CO= blood volume pumped by each ventricle per minute

49) a) Write the equation for calculating mean arterial pressure. Why is the mean value NOT the simple (SP+DP)/2? b) Discuss the changes to SP, DP, PP, and MAP as we get older. *follow up question* what does the throbbing movement you feel when taking your pulse (from your neck or wrist) represent?

MAP = DP + 1/3(PP) the mean value NOT the simple (SP+DP)/2 because the wave is curvy its not a square wave! MAP = mean arterial pressure DP = diastolic pressure PP = pulse pressure (we can find PP: systolic pressure(SP) - diastolic pressure(DP) = PP) systolic pressure (SP): maximum arterial pressure reached during peak ventricular ejection diastolic pressure (DP): minimum arterial pressure occurs just before ventricular ejection begins b) with increasing age, arterial compliance (how easy artery can expand) decreases; in other words they become "stiff". This means the systolic pressure (SP) is going up and the diastolic pressure (DP) is going down. Thus, the PP (the difference between SP-DP) is higher. Yet MAP can be the same throughout. example: - when your arteries get stiff (not compliant to expanding) they can't expand during systole like they use to. so what happens now is that MORE blood is being pushed out and not used to expand the walls. (*when arteries get stiff, systolic pressure goes up because more of the blood/pressure is being ejected and is not being stored) - during diastole the elastic recoil is smaller and thus a smaller push of blood and pressure out (*when arteries get stiff, diastolic pressure goes down because less of the blood is being stored) *follow up question* - your pulse pressure!

32) Practice drawing and describing the cardiac cycle diagram (aka Wigger's, Figure 12.22). Use the 28 talking points in the textbook to explain in detail the sequence of cause-and-effect relationships that connect the electrical events, pressure changes, and mechanical events during a single pump cycle of the heart. LECTURE 3 *(THIS WAS BE ON THE TEST FOR SUREEEEE)*

START: draw the ventricular volume first graph *1) DIASTOLE (ventricular filling; period 1):* we get a rise in ventricular volume due to rapid passive filling of blood (80-90%) and then an active filling called the "atrial" kick that pushes more blood into ventricles (10-20%). and now we reach EDV of 135 mL. *2) START SYSTOLE (isovolumetric ventricular contraction; period 2)*: we get ventricular contraction - ALL valves are closed *3) DURING SYSTOLE (ventricular ejection; period 3):* after contraction we get ventricular ejection of blood that rapidly decrease ventricular volume that brings us to the ESV of 65 ml - AV valves are closed, SV valves are opened *4) START DIASTOLE (isovolumetric relaxation; period 4):* after ejection we get ventricular relaxation - ALL valves are closed *1) DIASTOLE AGAIN (ventricular filling; period 1):* we get a rise in ventricular volume due to rapid passive filling of blood (80-90%) and then an active filling called the "atrial" kick that pushes more blood into ventricles (10-20%). and now we reach EDV of 135 mL. NEXT: draw the atrial pressure and ventricular pressure graph *1) DIASTOLE (ventricular filling; period 1):* atrial pressure should be higher than ventricular volume because if atrial pressure is higher than ventricular pressure, then we can move blood from atrium to ventricle and thus FILL THE VENTRICLE WITH BLOOD DURING DIASTOLE. - AV valves are open and SL valves are closed *2) START SYSTOLE (isovolumetric ventricular contraction; period 2)*: during this time we see ventricular pressure rise dramatically because ventricles are CONTRACTING and is above atrial pressure. - ALL valves are closed *3) DURING SYSTOLE (ventricular ejection; period 3):* during this time we get ventricular ejection of blood where blood goes to the peak and then drops down. - AV valves are closed and SL valves are opened *4) START DIASTOLE (isovolumetric relaxation; period 4):* we then go into diastole in isovolumetric relaxation. ventricles are relaxing which is why pressure is continuing to drop. ventricle pressure is going to be lower than atrial pressure and we start the whole cycle again where we fill the ventricles up with blood - ALL valves are closed *1) DIASTOLE AGAIN (ventricular filling; period 1):* atrial pressure should be higher than ventricular volume because if atrial pressure is higher than ventricular pressure, then we can move blood from atrium to ventricle and thus FILL THE VENTRICLE WITH BLOOD DURING DIASTOLE. - AV valves are open and SL valves are closed LASTLY: draw the aortic pressure graph *1) DIASTOLE (ventricular filling; period 1):* aortic pressure is continually declining because the BLOOD IS CONTINUALLY DRAINING AWAY INTO THE BODY (systemic circulation) *2) START SYSTOLE (isovolumetric ventricular contraction; period 2)*: aortic pressure is also declining because the BLOOD IS CONTINUALLY DRAINING AWAY INTO THE BODY (systemic circulation) *3) DURING SYSTOLE (ventricular ejection; period 3):* WHEN EJECTION begins, aortic pressure increases because ventricles are contracting and ejecting blood into the aorta. the pressure will reach the peak of the systolic pressure (highest pressure) and decline as blood is being drained away *4) START DIASTOLE (isovolumetric relaxation; period 4):* we get a dicrotic notch which occurs due to the blood that goes backward to the heart as a result from the aorta elastically recoiling and sending blood back to the closed semilunar valve, this is what causes a small increase in pressure during isovolumetric relaxation *1) DIASTOLE AGAIN (ventricular filling; period 1):* we did go back to step 1 where aortic pressure then is continually declining because the BLOOD IS CONTINUALLY DRAINING AWAY INTO THE BODY (systemic circulation)

53) Using the same drawing of figure 12.36, illustrate how constriction of all the arterioles increases TPR and protects the MAP for brain perfusion. *(IDK IF THIS IS CORRECT)*

TPR is the total peripheral resistance (the total resistance of all arteries/arterioles) arterioles protects the MAP for brain perfusion by constricting blood flow to unimportant organs to protest the heart and the brain. arterioles can do this by dynamically adjusting blood distribution by constricting which decreases blood flow and/or dilating which increases blood flow. for example: In times of stress (fight or flight), arterioles increases or keeps blood flow to the heart and head steady while increasing the constriction on all the other arterioles (preventing blood flow to less important organs)

23) a) As we did in class, draw a Purkinje fibers (and ALL other conducting cells) action potential. Explain the ionic events underlying its shape. b) How does this action potential compare to the previous two?

a) *Purkinje fiber (and all other conducting cells like Bundle of His, etc...) action potential* 1) repolarization due to K+ channels causes funny Na channels to open that bring membrane potential of -60 mV to -40 mV 2) then there is transient Ca2+ channels that depolarizes membrane to threshold (-40 mV) 3) there are fast Na+ channels that fires a very steep A.P. upstroke due to Na+ entry 4) and then small and brief repolarization and plateau due to L-type calcium channels 5) then K+ channels open and causes repolarization back to -60 mV, the cycle then starts again --> repolarization causes the opening of funny Na+ channels!!! (conducting cells can also be pacemakers! but they are slowwww) b) SA and AV node action potential: funny Na+ and transient Ca2+ channel, *NO fast Na+ channel*, L-type Ca2+ channel, and K+ channel conducting cells (Purkinje fiber cell, Bundle of His, bundle branches) action potential: funny Na+ and transient Ca2+ channel, fast Na+ channel, L-type Ca2+ channel, and K+ channel contractile cardiac cell (atrial/ventricular muscles) action potential: *NO funny Na+*, *NO transcient Ca2+ channel*, fast Na+ channel, L-type Ca2+ channel, and K+ channel

40) a) Draw and label figure 12.27; explain the Frank-Starling relationship and how it intrinsically regulates SV. Describe four implications of this relationship to the cardiovascular system

a) *frank-starling graph* x axis: ventricular end-diastolic volume (mL) = length of muscle cells (it could be a lot filled or a little filled which alter the size of volume and thus the length) y axis: stroke volume (mL) = force *key points (more filling --> more tension --> more force):* - as you increase the ventricular end-diastolic volume (EDV or in this case length of muscle cell) you increase the stroke volume (the force developed and thus strength) - increasing EDV (length of muscle cell) will influence a better actin and myosin overlap b) increasing EDV and thus stretching muscle cells, you get more calcium release from SR c) increasing EDV increase troponin sensitivity to calcium *four implications of this relationship to the cardiovascular system* 1) control of end-systolic volume - prevents ESV from increasing to prevent clotting in ventricles. - for instance, if all of a sudden EDV is high, the SV will adjust and increase to maintain the normal ESV. 2) matching of LV and RV output - outflow from right and left sides of heart remain equal - If there's increased venous return to either side, there will be more cardiac output from either side 3) prevention of rise in venous pressure - venous return determines EDV 4) prevents blood from backing up into veins/capillaries

51) a) Using the lecture slides, discuss three functions of an arteriole, and explain how they can be "conflicting". These are best understood by drawing depictions that illustrate what you are trying to explain. *follow up question* a) describe the histology of arterioles b) how do the arterioles increase blood flow to wash away metabolic waste?

a) *functions of aterioles:* 1) match flow to local tissue/cellular demand (metabolism of given tissue) 2) maintain and protect MAP of whole system (if there is an emergency, the arterioles will protect the brain and heart and say f*ck everything else) 3) temperature regulation on the skin - arterioles regulate pressure and flow to downstream capillaries but they sometimes have conflicting roles. these functions can be "conflicting" because sometimes what the arterioles would do to fix one problem is the opposite of what they would do for another role and they have to decide which takes priority. *follow up question* - arterioles are made up of thick smooth muscle layers (that can vasoconstrict and vasodilate) that regulates pressure, volume and flow to downstream capillaries b) arterioles will dilate to increase blood flow and thus wash the waste away!

84) a) Draw figure 13.4. Define and describe type 1 and type 2 alveolar cells. b) List the five components of the gas diffusion barrier. Which component is highly variable in thickness? Which component varies with infection and disease? *follow up question* a) How thick is the diffusion barrier between the air and the blood b) describe alveoli and their function

a) *type 1 alveolar cell* - flat, epithelial cells that line the alveoli (1 cell thick that are the air-facing surfaces on the alveolus) - the majority of the cells on alveolar are type 1 *type 2 alveolar cell* - spherical cells that secrete "pulmonary surfactant" (prevents the collapse of the alveoli) *b) the five components of the gas diffusion barrier* 1) type 1 alveolar cell (barrier 1) 2) basement membrane of type 1 alveolar cell (barrier 2) 3) interstitium (barrier 3) 4) basement membrane of capillary 5) endothelial cell of capillary *follow up question* a) diffusion barrier between air and blood is 0.2 micrometer (um) b) - alveoli are tiny, hollow sacs whose open ends are continuous with the lumens of airways - they have large surface areas (there are ~300 million of them) which cause increases in diffusion rate - alveoli is the main site of gas exchange *- pores between alveoli can allow for communication (idk if you need to know this)*

38) a) State the typical value of a person's resting heart rate and the intrinsic AP rate of SA node cells. b) Explain why a person's resting heart rate is generally slower than the intrinsic firing rate of the SA node. c) Then explain why the AV node remains a latent pacemaker in the body. Finally, explain why the Purkinje fibers remain a latent pacemaker in the body

a) *typical value of the SA node, AV node, and Bundle ofHis/Purkinje* - SA node: 100 A.P./min *with resting parasympathetic it goes down to 70 A.P./min* - AV node: 70 A.P./min *with resting parasympathetic it goes down to 50 A.P./min* - Bundle of His/Purkinje: 40 A.P./min *the AP rate of 40 A.P./min doesn't change, it doesn't change because parasympathetic doesn't affect ventricles!* b) a person's resting heart rate is generally slower than the intrinsic (natural) firing rate of the SA node because parasympathetic slows it down (IDK if this is correct) c) AV node and the Purkinje fibers remain latent pacemakers in the body because all these pacemakers still follow the SA node's rate (70 AP/min) because it's still higher than AV node and Bundle of His/Purkinje AP rate despite parasympathetic innervation

86) a) Using figure 13.6, discuss the five steps of respiration. b) What two steps normally match? *follow up question* a) in the lecture we talked about pressure gradients and how they drive 5 mechanisms in physiology. Using ur past knowledge what are they?

a) 1. ventilation - exchange of air between atmosphere and lungs (alveoli) by *bulk flow* - pressure gradients drive ventilation 2) gas exchange in pulmonary circulation (lungs to pulmonary capillaries) - gas exchange of O2 and CO2 between air in lungs and blood in pulmonary capillaries by *diffusion* - "gas exchange" = diffusion 3) gas transport - transport of O2 and CO2 through pulmonary and the systemic circulation via dissolved hemoglobin and buffers by *bulk flow* 4) gas exchange in systemic circulation (tissue capillaries to cells in tissue) - gas exchange of O2 and CO2 between tissue capillaries and cells in tissues by *diffusion* 5) cellular respiration - cellular usage of O2 and production of CO2 by cells (metabolism) b) step 1 (ventilation) and step 5 (cellular respiration; amount of O2 being consumed) MATCH each other. as the need for O2 goes up, the ventilation will also go up *follow up question* a) 1) pressure gradients open up cardiac valves 2) pressure gradients drove blood flow 3) pressure gradients caused lateral stretch for baroreceptors 4) pressure gradients promote filtration of water in the capillaries 5) pressure gradients drive ventilation

87) a) Using figure 13.7, apply the equation relating pressure gradient, airflow, and airway resistance to lung ventilation. b) What are the stepwise changes in pressures that allow air flow during inhalation and exhalation?

a) F = Palv - Patm / R F = air (gas) Palv = pressure in alveoli Patm = atmospheric pressure R = resistance of airways b) stepwise changes in pressure during inhalation and exhalation ~lets say the atmospheric pressure in the room is 760 mmHg~ - *inhalation* 1) we begin by inhaling, as we inhale we are expanding the volume in the lungs (alveoli) 2) which will decrease the pressure in the lungs and be below atmospheric pressure. 3) this allows for pressure gradient to allow air from the room (atmospheric pressure that is higher) to flow into lungs (pressure in the lungs that is lower) - *exhalation* 1) we begin by inhaling and then exhale, we compressing the volume of the lungs (alveoli) 2) which will increase pressure in the lungs and be above atmospheric pressure 3) this allows for pressure gradient to allow air from the lungs (pressure in the lungs that is higher) to flow out to the atmosphere (pressure in the atmosphere that is lower)

9) Using figure 12.7, write the hemodynamic equations of: a) blood flow and pressure equation b) resistance equation Explain the factors that determine the value of each variable. *follow up question* a) what is the flow at rest of blood from the left side pump to out of the body?

a) F = ∆P / R - F = flow (L/min) - ∆P = pressure difference between two points (mmHg) - R = resistance to flow b) R = 8 L η / π r⁴ *thus* F = ∆Pπr⁴ / 8 L η L = vessel length (longer length = more resistance) η= viscosity of fluid (blood thickness) r = radius of vessel (raised to the 4th power) π = 3.1416... *follow up question* a) 5 L or 5000 mL per minute

93) a) Draw figure 13.11. Define atelectasis and pneumothorax. b) Describe two ways a pneumothorax may develop.

a) pneumothorax: the hole (due to trauma or injury) that causes atmospheric air to come into the intrapleural causing issues with pressure gradients *NOT LUNG COLLAPSING!!* atelectasis: lung collapse b) two ways a pneumothorax may develop 1) an physical injury or trauma (like stabbing) that causes a hole in the chest 2) some people have spontaneous pneumothorax that develop holes INSIDE the lungs that are associated with disease, genetics, infection, and ventilator trauma or malfunctions.

41) a) Draw and label figure 12.28a; define what "increased contractility" implies b) calculate the ejection fraction with and without extrinsic sympathetic stimulation. *follow up question* a) what are two ways we can increase stroke volume?

a) "increased contractility" implies the extrinsic mechanism regulation that occurs in the Frank-Starling curve that increases SV without changing EDV due to sympathetic stimulation. (there is increased contractility without changing EDV. *why?* For any given EDV, adding NE or E due to sympathetic extrinsic regulation increases stroke volume and thus increases contractility (makes muscle stronger)) b) ejection fraction: *SV/EDV = EF* when sympathetic stimulation occur in ejection fraction: (more SV/ same EDV) SV = how much blood comes out of left ventricle EDV = how much blood is put into left ventricle EF = percentage of blood leaving your heart each time it squeezes (contracts) *EXAMPLE* resting value: SV = 70mL EDV = 135mL EF = 70/135 = 52% When epinephrine and norepinephrine is added and increases contractility of 135 EDV: SV = 110mL EDV = 135mL (same) EF = 110/135 = 81% *follow up question* a) 1. increase EDV in the ventricle and thus you increase SV (amount of blood that will go out) 2. add sympathetic NE and epinephrine and increase contractility and thus get an increase in SV

81) a) Draw figure 13.2. Describe in sequence the branching airways. Distinguish between airways making up the "conducting zone" and those of the "respiratory zone". b) What feature allows flow regulation? c) Where does the majority of gas exchange occur? *follow up question* a) how do you know if we've transitioned into in the respiratory zone?

a) *conducting zone (aka anatomical dead space; THERE IS NO GAS EXCHANGE IN THIS ZONE)* 1) trachea (1 tube) 2) bronchi (2 tubes) 3) bronchioles (16 tubes) 4) terminal bronchioles *respiratory zone (you know you're in this zone once you see bulges on bronchioles which represents alveoli! this is where gas exchange occurs)* 5) respiratory bronchioles with alveoli (a-lot of tubes lol) 6) alveolar ducts with alot of alveoli (ALOT OF TUBES) 7) alveolar sac with alot of alveoli (ALOT ALOT OF TUBESSS) b) bronchioles have smooth muscles that allow for constriction or dilation which can allow for airflow regulation c) the majority of gas exchange occur in the alveolar sacs of the respiratory zone! *follow up question* a) we start to see bulges that represent alveoli!

35) Using figure 12.24, define stenosis and insufficiency with regard to heart valves. Describe the sequence of sounds associated with stenosis and insufficiency of each of the four heart valves. a) normal open/closed valve b) stenotic valve c) insufficient valve

a) - *in a normal open valve* (allow for high pressure to go from one side of valve to the other side; aka pressure graident) we get a laminar flow of blood (smooth) that is quiet in sound - in a normal closed valve we get no flow that is quiet in sound as well b) - *in a stenotic valve* there is poor opening of valves that causes a narrowed valve. This causes turbulent flow (flow of blood going in the right direction but messily) that gives a whistle sound - since the valve doesn't open all the way, not all the pressure/volume will move through the valve, some may stay upstream which is bad! c) - *in an insufficient valve* there is poor closing of valves (leaky valve). this causes turbulent backflow (flow of blood is leaking back upstream) that gives out a gurgling sound. - some of the pressure will move back upstream which is bad!!

4) a) Define hematocrit, and state the typical value in healthy adult males and females. b) Given the hematocrit and total blood volume, calculate the volume of plasma and red blood cells.

a) - hematocrit is the percentage of blood volume that is erythrocytes (red blood cell). - hematocrit in males: 45% - hematocrit in females: 42% b) Average total volume of blood in a person = 5.5 L erythrocyte volume = 0.45 (hematocrit) x 5.5 L (blood volume) = 2.5 L of RBC plasma volume = 5.5 L - 2.5 L = 3.0 L of plasma

67) a) Describe how lymph fluid is produced and trace the path of lymph flow through the body (use figure 12.50). Explain the location and general function of lymph nodes. b) what are the 3 mechanisms that drive lymph "flow? *follow up question* a) is lymph interstitial fluid or intercellular fluid? What does lymph contain of?

a) - lymph fluid is produced by the 4 L of mismatch (unbalance) between filtration and absorption in the capillaries. (extra bulk flow filtration out into the interstitial fluid that is then collected by lymph capillaries) for example: the arteriole side of capillary we have at NFP (+) it will favor filtration, we have a NFP (-) on the venous side of capillary it will favor reabsorption. These two are not balanced in terms of bulk flow of water because there is usually more filtration than reabsorption. So this bulk flow of water that moves out (filtered) into the ISF and gets captured by the lymph capillaries that becomes lymph fluid - the path of lymph flow through the body: 1) lymph capillaries captures the extra filtration of water that occurs (the mismatch) in the capillaries 2) the lymph capillaries then direct the flow of lymph fluid to lymph vessels and into lymph nodes (the collection points) 3) the lymph fluid then end up being returned back into the veins (superior/inferior vena cavas) near the heart b) *3 ways that drive lymph flow:* 1) increasing the amount of extra filtration at capillaries (more volume of extra filtration means more pressure which increases pressure that then causes more lymph fluid formation and thus more lymph flow) 2) smooth muscles in the lymph vessels and one-way valves 3) sympathetic influence via NE that promotes constriction of smooth muscles on lymph vessels and thus promote lymph flow *follow up question* a) lymph is interstitial fluid (part of ECF) and contains absorbed fats and escaped plasma proteins

14) a) State the purpose of cardiac valves. Name and describe the details of the four cardiac valves. b) What induces the opening/closing of cardiac valves? Describe the sequence of events that lead to valves opening/closing.

a) - the purpose of cardiac valves is to promote a one-way direction of blood flow! *four cardiac valves (two types)* type 1: atrioventricular valves (AV) 1) right AV valve (aka tricuspid valve) 2. left AV valve (aka bicuspid valve or mitral valve) type 2: semilunar valves 1) pulmonary semilunar valve - allow blood to flow into the arteries during ventricular contraction, but prevent blood from moving in the opposite direction during ventricular relaxation 2) aortic semilunar valve - permit blood flow from the ventricle to the aorta but not backward aorta to the ventricle b) - pressure gradients (change in pressure) induces opening and closing of cardiac valves 1) right AV (tricuspid) valve: opens due to pressure gradients (high pressure in atrium moves into ventricle causing high pressure in ventricles) and influences the flow of blood from right atrium to right ventricle but NOT BACKWARDS 2) left AV valve: opens due to pressure gradients (high pressure in atrium moves into ventricle causing high pressure in ventricles) and influences the flow of blood from the left atrium to the left ventricle NOT BACKWARDS 3) pulmonary semilunar valve: regulates the blood flow from right ventricle into the pulmonary trunk (prevents prolapse of blood back into the right ventricle by closing valve) 4) aortic semilunar valve: regulates blood flow from left ventricle into the aorta (prevents prolapse of blood back into the left ventricle by closing valve) *key things to note* 1) if there is more pressure in the atrium, the AV valves will open down into the ventricle a) if there is more pressure in the ventricles, then the valves will close 2) in order for the semilunar valves to closed, there must be higher pressure in the aorta or the pulmonary trunk

21) a) Using the lecture slides, define these terms: tachycardia, bradycardia, fibrillation. b) Discuss why fibrillation is dangerous and fatal if not corrected.

a) 1) tachycardia (used to describe HR): heart rate (HR) greater than 100 beats/min - not a bad thing! because if you're exercising you are tachycardic because your heart rate is above 100 BPM 2) bradycardia (used to describe HR): heart rate (HR) slower than 60 beats/min - not a bad thing too! 3. fibrillation : totally irregular and chaotic AP propagation - totally dysfunctional pump with no organized sequence or pattern of excitation! (oh no!) b) Ventricular Fibrillation is dangerous and fatal if not corrected because the heart is not pumping blood out to the body due to dysfunctional pump caused by irregular and chaotic AP propagation

27) a) Using the lecture slide, define and describe the two cardiac phases. b) Define and describe the four periods within these two phases. - Which chamber is the default reference for these definitions?

a) 1. systole: ventricular contraction and ventricular pressure (blood ejection/squeezing) - the heart spends 1/3 of time in systole (shorter time) - represented by QRS wave to T-wave 2. diastole: ventricular relaxation and ventricular blood filling - the heart spends 2/3 of time in diastole (longer time) - represented by the start of T-wave to the next R wave b) *four periods and two phases (reference to the left ventricle)* 1) ventricular filling → diastole 2) isovolumetric contraction → systole (first part of systole) 3) ejection → systole 4) isovolumetric relaxation → diastole (first part of diastole) - the left ventricle is the default reference to the 4 periods and diastole and systole

18) a) List the seven components of cardiac conduction in a typical order of excitation. b) What three components comprise the "conducting cells"? c) What are four implications of this conduction system?

a) *components of cardiac conduction in order* 1. *SA node* gets to threshold and forms action potential 2. action potentials spreads throughout the *atrial contractile cells* and are stimulated (because everything is connected by gap junctions!) 3. *AV node* is also stimulated but is has slow A.P. propagation. this allows time for atrial contraction to complete before ventricular depolarization and contraction (or excitation) occurs 4. eventually, action potentials move towards the *Bundle of His (conducting cell)* 5. and then down to the *right and left bundle branches (conducting cells)* 6. and then through the *Purkinje Fibers (conducting cells)* and to the ventricular contractile cells b) the three components that comprises the "conducting cells" are the Bundle of His, right and left bundle branches, and the Purkinje Fibers c) the four implications are: 1. it only takes one cell to have an action potential to start the whole conduction pathway (step 1-7) in the heart because everything is connected by gap junctions 2. it only takes one cell to go bad to ruin the whole conduction pathway because everything is connected by gap junctions! 3. every cell of your heart participates in every single heart beat 4. we can externally start/stimulate the conduction pathway with devices that act as artificial pacemakers

64) a) Draw figure 12.45. List the forces (starling forces) that determine bulk flow *follow up question* b) describe the determinants of each in detail, and explain the implication of NFP being (+) or (-).

a) *there are 4 forces (starling forces) that determine bulk flow:* 1) capillary hydrostatic pressure *(Pc)*: when blood comes into capillary it has hydrostatic pressure (Pc) that drives water out of the capillary by pushing them against the capillary wall, this causes *FILTRATION* of water from capillaries and out into the ISF 2) ISF hydrostatic pressure *(PIF)*: if there was a development of significant fluid accumulation and hydrostatic pressure in the ISF, this could drive *ABSORPTION/REABSORPTION* of water from the ISF into the capillary 3) osmotic force due to plasma protein concentration *(πc)*: the plasma proteins that are too larger and too charged in the capillaries attract water and draw them into the capillary, this causes *ABSORPTION/REABSORPTION* of water from the ISF into the capillary 4) osmotic force due to ISF protein concentration *(πIF)*: there are proteins in the ISF that are osmotic that attract water and draw them out of the capillaries, this causes *FILTRATION* of water from capillaries and out into the ISF *net filtration pressure equation:* Pc + πIF - PIF - πc = net filtration pressure example in the figure: a) arterial end of capillary 35 *(Pc)* + 3 *(πIF)* - 0 *(PIF)* - 28 *(πc)* = +10 mmHg net filtration (the positive 10 represents filtration is dominant or is in favor at this arterial end of the capillary) b) venous end of capillary 15 *(Pc)* + 3 *(πIF)* - 0 *(PIF)* - 28 *(πc)* = -10 mmHg net filtration (the negative 10 represents absorption/reabsorption is dominant or is in favor at this venous end of the capillary) *follow up question* - if filtration is higher than the absorption/reabsorption then the NFP is going to be *positive* - if absorption/reabsorption is higher than the filtration then the NFP is going to be *negative* filtration > absorption/reabsorption (NFP +) --> net filtration occurring filtration < absorption/reabsorption (NFP -) --> net absorption/reabsorption occurring

88) a) Draw figure 13.8 and define Boyle's law. b)Explain how it applies to the mechanics of ventilation.

a) Boyle's law states that the pressure of a fixed number of gas molecules is inversely proportional to the volume of the container *(the lower the volume, the greater the pressure and vice versa)* b) in terms of inhalation and exhalation... *inhalation* - when we inhale, we increase the volume in our lungs which means we will have FEWER collisions of the gas molecules and thus explains why pressure is decreased *exhalation* - when we exhale, we decrease the volume in our lungs which means we will have MORE collisions of the gas molecules and thus explains why pressure is decreased

65) a) Draw figure 12.47 (include the relevant blood pressures, mmHg). b) Using your lecture notes, discuss the three bullet points regarding veins in general. With regard to veins, define "capacitance."

a) Venous pressure near beds is 10-15 mmHg while pressure at top is 0-1 mmHg b) *three bullet points regarding veins* 1. veins return blood to the heart (big radius, low resistance) 2) capacitance (storage of blood; the majority of blood is in the vein which is around 61%) 3) low pressure for venous return - low resistance - high capacitance (storage) - VERY compliant (can expand easily) - less elastic, floppy looking (doesn't snap back)

(lecture question) a) what is chronotropy? - what does a positive chronotropic agent do? b) what is dromotropy? - what does a positive dromotropic agent do? c) what is inotropy? - what does a positive inotropic agent do?

a) chronotropy refers to the heart rate and alterations of heart rate at SA node - a positive chronotropic agent will alter the heart rate b) dromotropy refers to conduction rate/velocity and alterations of conduction rate/velocity at AV node - a positive dromotropic agent will alter conduction rate/velocity c) inotropy refers to contractility and alterations of the strength of contractions in atrial and ventricular muscles - a positive inotropic agent will alter contractility (strength of contractions)

16) Describe the coronary circulation. a) Where is it? b) What does it do? c) Where are the openings to coronary arteries and when does blood flow into them?

a) coronary circulation is located around the myocardium (the heart muscle) b) coronaries supply blood to the myocardium because the myocardium is too thick for supply of O2 via diffusion when blood is in the chamber (it is too far!!! so coronaries bring the blood closer) c) the openings of the coronary arteries are from the first branch off the aorta and then branches around the myocardium.

48) a) Draw figure 12.33 and explain the "pressure reservoir" function of arteries. Include definitions for compliance and elastic recoil. b) Quantitate the movement of blood into and out of the arteries during the cardiac cycle.

a) figure 12.33 explains the pressure reservoir: - arteries represent pressure reservoirs. They have a large radius and low resistance, they are also compliant and elastic. This means that in systole when blood is pumped into the artery, the artery EXPANDS (radius increases) allowing some blood to exit via arterioles, but most of the blood and pressure are stored in the arteries that helps expand the arteries until there is an elastic recoil (snap back) during diastole that pushes the blood out - Compliance: how easy to expand - Elastic recoil: strength of snapback of arteries that pushes blood forward *the volume pumped out with single heart beat stretches out the arteries. AND THEN they will elastically recoil back to push blood out during diastole (ventricular relaxation)* b) - Systole: blood moves into vessel, ⅓ stored on both sides, ⅓ leaves - Diastole: ⅓ blood pressure can push in on both sides, so there is a high pressure reservoir and ⅔ can be pushed out

(lecture question) describe the standard limb leads a) where is the reference (-) electrode and the recording (+) electrode in lead 1? b) where is the reference (-) electrode and the recording (+) electrode in lead 2? c) where is the reference (-) electrode and the recording (+) electrode in lead 3?

a) lead 1 (looks at electrical signal across the chest from right to left): - reference (-) electrode: right arm/right wrist - recording (+) electrode: left arm/left wrist b) lead 2 (looks at electrical signals down to your left leg at an angle) - reference (-) electrode: right arm/right wrist - recording (+) electrode: left leg c) lead 3 (looks at electrical signals down at an angle) - reference (-) electrode: left arm/left wrist - recording (+) electrode: left leg *these leads are called the Einthoven's triangle!*

62) a) Using your lecture slide, answer the question: "As perfusion occurs in a capillary, how is solute exchange achieved?". b) include mechanisms by which substances move across capillary walls, and give examples of substances that move by each method. *follow up question* describe the diffusion gradients of oxygen and CO2 a) where is oxygen highest? in the capillary, the ISF, or the ICF of a muscle cell, for instance? b) a) where is CO2 highest? in the capillary, the ISF, or the ICF of a muscle cell, for instance?

a) solute exchange is achieved through diffusion gradients (primary things that drives solute movement) b) solute exchange can occur in different ways: 1) lipid-soluble or hydrophobic solutes can pass through the endothelial cells 2) water-soluble solutes/hydrophilic (Na+, K+, Ca2+, glucose, amino acids) can go through water-filled pores 3) exchangeable proteins are proteins are moved across by vesicular transport (endocytosis and exocytosis!) *plasma proteins in capillaries cannot go out because they are too large and too negatively charged to get through water filled pores* *follow up question* a) oxygen is highest in the capillaries, lower in ISF, and lowest in the ICF of a muscle cell, for instance, because there is metabolism occurring that burns oxygens which is why there is the lowest amount of oxygen. b) CO2 is the highest in the ICF of muscle cell because its begin produced as a byproduct of metabolism, lower in the ICF, and lowest in the capillaries

61) a) Draw figure 12.42b; discuss the concept "Continuity of Flow" as depicted in this figure. b) What two variables are inversely related? c) Differentiate between blood "flow" and blood "velocity" in different vessels of the systemic circuit.

a) the "continuity of flow" is a concept that explains how blood flow is the same everywhere in the body (5 L/min) but the velocity changes in figure 12.42b it shows how total cross-sectional area as: 1) the aorta has a low total cross-sectional area because there is only ONE. 2) but the total cross-sectional area of all the arteries and all the arterioles is high. as we branch from aorta, arteries, and arterioles we start to get a smaller radius. 3) in the capillaries we have the highest total cross-sectional area because there are HELLA capillaries in the body 4) as capillaries regroup into the venules and veins, radius increases and the total cross-sectional area decreases because there are not as much of those as compared to veins. in figure 12.42b it shows how mean linear velocity as: 1) the aorta having the highest velocity 2) ands we branch to the arteries and arterioles velocity decreases 3) and at the capillaries is where we have the lowest velocity (this is good because slow blood flow will allow for adequate gas exchange) 4) and from the capillaries and into the venules and veins, velocity starts to increase b) the two variables that are inversely related are the total cross-sectional area and the mean linear velocity - the larger the cross-sectional area, the slower the velocity of blood c) flow of blood is the same all cross-sectional areas of the vasculatures (continuity of flow) - the blood "flow" represents the volume per time - the blood "velocity" is the length per time

*lecture question* describe the characteristics of cardiac muscle a) are there thick and thin filaments? b) are there sacromeres? c) are there transverse tubules? d) are there gap junctions between cells? e) what is the source of activating Ca2+? f) what is the site of Ca2+ regulation (hint: where does Ca2+ bind to?) g) what is the speed of contraction? (very slow, slow, fast) h) are there spontaneous production of action potentials by pacemakers? i) are their tone? (yes or no) j) what is the effect of nerve stimulation (excitation or inhibition or both?) k) is there effects of hormones of excitability and contraction (yes or no) l) can stretch of cell produce contraction (yes or no)

a) yes there are thick and thin filaments b) yes there are sarcomeres c) yes there are transverse tubules d) yes there are gap junctions e) the sarcoplasmic reticulum and extracellular f) the sit of Ca2+ regulation or binding is troponin g) the speed of contraction is slow h) yes there are a few cells that can spontaneous production of A.P. i) there is NO tone j) there is both excitation and inhibition stimulation k) yes hormones can have an effect on excitiability and contraction l) NO stretch of cell does not produce contraction

73) Draw figure 12.59 and explain the sequence of events and physiological responses that reflexively act to restore MAP when a Hemorrhage occurs.

answer this as practice *this is basically intervention #2 in LAB 7*

36) a) Define cardiac output (CO). Write the equation for its calculation. b) -What is the typical stroke volume - what is the typical (resting) heart rate - What is a typical CO?

cardiac output (CO): the volume of blood coming out of each ventricle per unit time (liters/min) *equation:* CO (flow) = HR x SV HR: heart rate SV: stroke volume CO: cardiac output (or the flow) b) - the typical stroke volume: 70 mls/beat - typical (resting) heart rate: 70 beats/min - typical cardiac output (CO): 5 liter/min (5000 mL) 70 bpm x 70 mls/beat = ~5 liter/min or ~5000 mL

60) Reproduce figure 12.41. Using your lecture notes, discuss the vascular components of this figure. *follow up question* a) what the percentage of blood in capillaries? b) a capillary is a primary point of exchange between the ________ and the ___________

figure 12.41 shows: 1) blood flow goes from the arteriole (which are regulated by smooth muscles) that go through the precapillary sphincters. precapillary sphincters are smooth muscles that are the most local of the control of flow into the capillary bed 2) flow will then go into the capillaries and the metarterioles into the venules. (metarterioles are blood vessels that have some amount of smooth muscles that acts as a local bypass from the arteriole to the venules; a short cut to the venules) 3) flow will then into the venules and then go out to the veins *follow up question* a) capillaries contain only 5% of blood at any moment b) blood and interstitial fluid

91) a) Define "functional residual capacity (FRC)". Explain the balance of forces that exist in that phase of the ventilation cycle. *(IDK IF THIS IS CORRECT)* b) At FRC what is the atmospheric pressure (atm), the alveolar pressure (alv), and the intrapleural pressure (ip)? *follow up question* a) at rest (between breaths) - for the chest walls, if if not attach to anything, the chest would slightly _______ upwards and outwards by ______________. how is it held inward and downward? b) - for the lungs, if it is not attach to anything, the lungs would __________ inwards by ___________. how is it pulled open to larger volume?

functional residual capactiy (FRC) is the volume of air in the lungs after a quiet exhale when respiratory muscles are relaxed. The balance of forces exist by the difference in pressure between the intrapleural space and both the lungs and chest wall *(IDK IF THIS IS CORRECT)* b) at FRC: - Patm (atmospeheric pressure) is 760 or 0 mmHg - Palv (lung pressure) is 760 or 0 mmHg *these two are equal* - the Pip (intrapleural space) is 756 mmHg or -4 mmHg *follow up question* a) at rest, for the chest walls, if not attach to anything, the chest would slightly expand upwards and outwards. the chest wall is prevented from expanding and held inwards and downwards by attachments, transmural pressure gradients and surface tension b) at rest, for the lungs, if it is not attach to anything, the lungs would collapse inwards by elastic recoil. it is pulled over to larger volumes by attachments, transmural pressure gradients and surface tension *the lungs are always trying to collapse and go inwards, but the chest is always trying to go the opposite way and outwards, they are pulling onto each other. the interpleural space pressure is below atmospheric pressure because the chest is try to go out and the lungs are trying to go in. Having lower pressure in the interpleural space (756 mmHg) will allow for stability and balance since the lungs and chest has higher pressure (both at 760 mmHg)

52) Draw figure 12.36. Describe the hemodynamic effects of constricting or dilating an individual arteriole.

hemodynamic effects on individual arteriole constriction and dilation is that they can dynamically adjust blood flow distribution to the organs by relaxation (dilating) and contraction (constricting) smooth muscle in arterioles. - by constricting the individual arteriole there is less blood flow that is allowed to the organ, and then there is dilation of other arterioles for more blood flow into another organ. this occurs when we need more blood flow in one organ than another so they can dynamically adjust by constricting and dilating based on needs

47) Reproduce figure 12.32 which demonstrates the pressure variations in the arteries, arterioles, capillaries, venules and veins of both the systemic and the pulmonary circuit. Discuss the important features and values at each location. *follow up question* a) in response to the __________ contraction of the heart: waves of ________ move through the vasculature, decreasing in ______________ with distance b) explain the dicrotic notch in the figure

in the systemic circulation: 1) the left ventricle will eject blood into the aorta which will cause the first rise in pressure in aorta and then the left ventricle relaxes because it has to refill. while the ventricle is refilling, that blood that was pushed into the aorta leaves the aorta and to the arteries (then, arterioles, etc...) and thus cause the drop in pressure in the aorta (the first wave) 2) then the oscillating pressure from the arteries and then moves across the arterioles which is where we see the biggest drop in pressure. this is where we have a majority of the blood flow regulation (in the arterioles!) thus, oscillations of pressure through arterolies is where we see a decrease in amplitude and pressure 3) then smaller oscillating pressures moves towards and through the capillaries where we also drop in pressure, however the drop in pressure isn't as large as the arterioles! 4) then the oscillating pressure moves through the venules which is where pressure stops oscillating and is now a smooth and straight flow of pressure 5) then the smooth flow of pressure moves through the veins that continues that smooth and straight flow of pressure (no more pulsating/oscillating pressure) remember oscillations of pressure decrease in amplitude and pressure as it moves further away from the heart!!! in pulmonary circulation: 1) all the steps about oscillation of pressure and how it loses it oscillating form as it moves through different vasculatures above applies to the pulmonary circulation, its just the pressure is much higher in the systemic circulation than in the pulmonary circulation! *follow up question* a) pulsatile or pulsating contraction, pressure, amplitude b) dicrotic notch is present as the result of semilunar valves closing and the elastic recoil of the aorta and blood rebounding against the valve causing slight increase in aortic pressure!

91) Use figure 12.9 to discuss the location and function of cardiac muscle. *(LO for section 9.10)* *follow up question* a) what is the role of the interventricular septum?

location: cardiac muscle (aka myocardium) is located on the heart function: cardiac muscles functions to pump blood throughout the body *follow up question* b) interventricular septum is a cardiac muscle that separates the right and left ventricles

85) Draw figure 13.5. Explain the anatomical and functional relationship between the pleura, the lungs, and the chest cavity. How large is the intrapleural space in reality?

the lungs are surrounded by a visceral pleura (in contact with the lungs) and a parietal pleura (in contact with the chest cavity). These two pleura's make up the *pleural sac* - In between the visceral layer and parietal pleura there are intrapleura fluid (water) that is thin and only contains a few mL's of fluid which helps to reduce friction of lungs from movement

26) Using the information you learned in Chapter 9 and figure 12.20, explain the significance of the prolonged refractory period in cardiac muscle cells. Explain why the refractory period lasts for so long. *(IDK IF THIS IS CORRECT)*

the significance of the prolonged refractory period in cardiac muscle is that it allows time for ventricles to adequately fill with blood prior to pumping out blood. if there are constant contractions (tetanus) there is no time for the ventricles to relax and refill with blood and thus prevent the heart from pumping blood *textbook: "if a prolonged, tetanic contraction were to occur in the heart, it would cease to function as a pump because the ventricles can only adequately fill with blood while they are relaxed* they can't relax if there are short refractory period or have tetanic contractions!!!!

92) Using table 13.3 and figure 13.10, explain and calculate both transpulmonary pressure and chest wall pressure.

transmural pressure: P inside - P outside *transpulmonary presssure (Ptp); the lungs as inside and the intrapleural space as outside* a) P alv - P ip (inside - outside) b) 0 - [-4] = 4 mmHg c) you get a positive +4 difference between the lungs (alveolus) and the intrapleural space. this *positive value* which *holds the lungs open* and not allowing the lungs to collapses inward *chest wall (Pcw); the intrapleural space as inside and the atmospheric pressure as outside* a) P ip (inside) - P atm (outside) b) -4 - 0 = -4 mmHg c) you get a negative -4 difference between the intrapleural space and the lungs. this *negative value* which *holds the chest wall in* and not allowing the chest wall to get bigger

50) Reproduce figure 12.35 and explain how the SP and DP values are typically determined.

you can determine SP and DP: *by using a sphygmomanometer (that wraps around upper arm) and a stethoscope placed over the brachial artery just below the cuff* a) the pressure at which sounds (soft tapping sounds) are first heard as the cuff pressure decreases is identified as the *systolic blood pressure* b) when the cuff pressure reaches the diastolic blood pressure, sound stops because artery is now opened and blood flow is laminar and quiet. therefore, *diastolic pressure* is identified as the cuff pressure at which sound disappear. steps for sphygmomanometer 1) we place the cuff around our arm and increase the cuff pressure. it will increase and then it go above the systolic pressure. at this time the artery is full blocked. 2) we then lower the cuff pressure, as it lowers down and goes below systolic pressure we begin to hear a soft tapping sound (turbulent flow). this soft tapping sound indicates the *systolic pressure* where blood can finally begins to move rapidly out 3) as the cuff pressure decreases, the tapping sound will get louder because blood is starting to flow more rapidly out of the artery as the artery begins to slowly open up 4) as the cuff pressure continue to decrease it will eventually decrease below diastolic pressure in which we hear NO sounds because the blood flow is now smooth and laminar (the typical blood flow sound), this indicates the *diastolic pressure*. we are no longer blocking the artery and thus blood can flow freely and quietly.