Exam 3 Learning Guides (1) PDF

Week 8 Workshop 1 Mini lesson 1 Learning Objectives: Distinguish the timing of action potentials and twitch tension in skeletal versus cardiac muscles and explain why the differences are important in muscle function. Skeletal APs brief, twitch tension (single contraction from one AP) last...

Week 8 Workshop 1 Mini lesson 1 Learning Objectives: Distinguish the timing of action potentials and twitch tension in skeletal versus cardiac muscles and explain why the differences are important in muscle function. Skeletal APs brief, twitch tension (single contraction from one AP) lasts much longer Allows for summation of APs and buildup of tension for sustained contraction Cardiac AP much longer (300 ms) because of prolonged Ca2+ influx from L-type channels Extended AP overlaps with twitch duration, preventing summation and tetanus Ensures heart relaxes between beats Key Terms: intercalated disks: connections between cardiac muscle cells, support synchronized contraction. Contain desmosomes (hold cells together), gap junctions (allow electrical signals to pass quickly between cells) Study Questions: 1. How do desmosomes and gap junctions at intercalated disks between cardiac muscle cells allow for the heart to be a functional syncytium? Intercalated disks provide mechanical and electrical connections between cardiac muscle cells Desmosomes provide structural support at intercalated disks (spot welds) They keep cells together as the heart changes dimension and volume 1. What ion channels are responsible for each phase of a ventricular cardiac muscle cell action potential and what are the main differences between a skeletal and cardiac muscle cell action potential? Ventricular cardiac muscle cell AP K+ leak causes very negative RMP (-89 mV) Gap junctions allow current to enter from neighboring cell (no graded potential) Na+ channels open-rapid depolarization ○ Transient K+ open very briefly-small repolarization L type Ca2+ channels prolonged opening causes plateau of depolarization voltage gated K+ channels slow open-repolarization phase Skeletal cell AP Shorter (1-5 ms) No plateau Can summate contractions for greater force Cardiac Muscle Cell AP Longer (~300 ms) Plateau phase (L-type ca2+) Extended refractory period, prevents premature contractions  1. What are all of the steps involved in EC coupling in cardiac muscle (including the excitation and contraction mechanisms) and why is this process referred to as calcium-induced-calcium release (CICR)? 1. Membrane depolarized by Na+ entry as AP begins (excitation=no neuronal input required) 2. Depolarization opens L-type Ca2+ channels in T-tubules 3. Small amt of trigger Ca2+ enters cytosol, contributing to depolarization. Trigger Ca2+ binds to and opens RyR receptor Ca2+ channels in SR membrane 4. Ca2+ flows into cytosol, increasing [Ca2+] 5. Ca2+ binds to troponin exposing XB binding sites on thin filaments 6. XB cycling causes force generation and sliding of thick and thin filaments 7. Ca2+-ATPase pumps return Ca2+ to SR 8. Ca2+-ATPase pumps and Na+/Ca2+ exchangers remove Ca2+ from cell 9. Membrane repolarized when K+ exits to end AP 1. What are the differences in the timing of action potentials and twitch tension in skeletal and cardiac muscles and why is it important that tetany is not possible in cardiac muscle? Skeletal Can have tetanus or sustained contractions Can summate force Cardiac Prolonged refractory period prevents tetanus ○ Allows time for ventricles to relax and fill with blood prior to next heartbeat Cannot summate force 1. What are similarities and differences between the structure and function of skeletal, smooth, and cardiac muscle cells? Skeletal Smooth Cardiac Has troponin and Small and Has troponin and tropomyosin uni-nucleated tropomyosin Arranged in layers Small and and surrounds hollow uni-nucleated cavities Arranged in layers and surrounds hollow cavities All three Contains myosin thick filaments and actin thin filaments Same 4 steps of XB cycle  Sliding filament mechanism of contraction ATP powers generation of force Elevated cytosolic Ca2+ initiates contraction Mini lesson 2 Learning Objectives: Explore causes and consequences of erythrocyte dysfunction in sickle-cell disease. RBCs become misshapen and less flexible, leading to blockages in small blood vessels, impeding blood flow Causes severe pain, increased risk of infection, chronic hemolytic anemia, potential organ damage Compare and contrast the vascular arrangement between the systemic and pulmonary Circulations. Systemic vs. pulmonary circulations 2 pumps and 2 circulatory systems- heart is a dual pump ○ Pump 1: RA and RV pump blood to lungs ○ Pump 2: LA and LV pump blood to systemic circulation Artery- carries blood away from heart Vein- carries blood towards heart Heart wall thicker on left side than right bc left pumps blood farther to whole body Perfusion: passage of blood through a vascular bed; blood moves by bulk flow from high to low pressures Most vascular beds in parallel, but pulmonary circulation is in series Key Terms: Albumin: major plasma protein, maintains osmotic pressure and transports substances Erythrocytes: RBCs, carry oxygen, contain hemoglobin Hemoglobin: protein in erythrocytes that binds oxygen for transport multipotent hematopoietic stem cells: cells in bone marrow that differentiate into different cell types Platelets: cell fragments, play role in blood clotting pulmonary circulation: moves deoxygenated blood from heart to lungs for oxygenation systemic circulation: distributes oxygenated blood from heart to body tissues white blood cells: cells of immune system, defend body from pathogens Study Questions: 1. How does the cardiovascular (CV) system interact with the gastrointestinal, respiratory, renal, and endocrine systems to participate in the maintenance of homeostasis? Provide a specific example as part of your answer. Nutrients to GI system O2/CO2 to respiratory system Wastes to renal system Temperature to skin and muscles Hormones to endocrine system Example: dehydration– endocrine system releases ADH to conserve water in kidneys, while CV system increases HR to maintain BP → helps prevent drastic changes in BV and BP, maintaining homeostasis 2. Why do all cells of the human body need to be within 100 µm of a capillary? Diffusion of solutes 100 um or more would be too slow and inefficient for a large, multicellular organism to exist 3. What are the three general components of the CV system and what are their basic functions? Heart ○ Biological pump ○ Generates force to move blood ○ Electrical and mechanical Blood ○ Fluid connective tissue ○ O2/CO2/wastes/nutrients and messengers like hormones are transported Blood vessels ○ Tubing through which blood flows ○ Dilate and constrict- move blood 4. What components does blood separate into when spun in a high-speed centrifuge? Total BV averages 5.5 L Plasma: 3 L or 55-58% ○ Part of ECF (like ISF, but has plasma proteins which are synthesized by liver and can carry hydrophobic hormones) Buffy coat: insignificant volume ○ Has leukocytes (WBCs) and platelets  Erythrocyte (RBC): 2.5 L or 42-45% ○ Hematocrit ○ Gas transport 5. What is hematocrit and what is its typical value in a healthy adult male and female? Given the hematocrit and total blood volume, calculate the volume of plasma and red blood cells. Hematocrit: % of BV with RBCs 42-45%, or 2.5 L Example: given hematorcrit 45% and total blood volume 5 L Volume of RBC = (hematocrit/100) x total blood volume ○ 0.45 x 5 = 2.25 L Volume of plasma = total blood volume - volume of RBCs ○ 5 - 2.25 = 2.75 L 6. What are the four cellular commitments and functions of hematopoietic stem cells? 1. Oxygen transport ○ Reticulocyte → red blood cell 2. Clotting ○ Megakaryocyte → platelets 3. Immunity defense ○ Monocyte → tissue macrophage ○ Band → neutrophil ○ Eosinophil ○ Basophil 4. Immunity defense ○ B and T lymphocytes 7. What are some unique features of red blood cells and how and why are these cells altered in individuals who have sickle-cell disease? RBCs Biconcave disks Large SA, smaller volume ○ Important for rapid diffusion of gases) ○ 7 um in diameter ○ Carry lots of hemoglobin ○ Organelles are extruded (no DNA, DNA in buffy coat) 8. What does it mean to say that systemic vascular beds are in parallel? What are the advantages of this arrangement? Each major organ system receives blood directly from aorta 1. Blood “quality” to ALL organs 2. Flow regulation to individual organs a. More flow to some, less to others 3. Amount of initial pressure required Mini Lesson 3 Key Terms: aortic (semilunar) valve: valve between LV and aorta, preventing backflow into heart bicuspid valve: left AV valve (mitral) chordae tendineae: fibrous cords anchoring AV valves to papillary muscles, preventing prolapse conducting system: network of cells (incl SA and AV nodes) coordinating heartbeats coronary arteries: vessels supplying blood to heart muscle coronary blood flow: blood circulation through coronary arteries Hemodynamics: study of blood flow and forces involved hydrostatic pressure: pressure exerted by fluid at rest interventricular septum: wall separating L and R ventricles papillary muscles: anchor chordae tendineae, assisting valve function Poiseuille’s law: describes flow of liquid through a cylindrical pipe pulmonary (semilunar) valve: valve between RV and pulmonary artery, prevents backflow tricuspid valve: right AV valve Stenotic valve: poor opening Whistle: stenotic, turbulent flow=murmur Insufficient valve: poor closing Gurgle: insufficient, turbulent backflow=murmur Study Questions: 1. What is the hemodynamic equation that relates flow, pressure, and resistance and what are the factors that determine each variable? F = △P/R F = flow (L/min) P = pressure gradient (mmHg) R = resistance to flow 1. Why is radius the main determinant of resistance and how does this relationship affect blood flow? Draw a figure to support your answer. Smaller radius → more resistance because more blood is scraping on wall, so more friction Larger radius → less resistance because less blood is scraping on wall, less friction F = (△Pπr^4)/8Lη 1. What are all of the structures of the frontal section of the heart? Right atrium Right AV valve Right ventricle Pulmonary SL valve Left atrium Left AV valve Left ventricle Aortic SL valve Interventricular septum Chordae tendineae Papillary muscles Aorta, pulmonary arteries, veins 1. What are differences between the endothelium, myocardium, epicardium, and pericardium, and why is the heart surrounded by a pericardial sac and fluid? Endothelium Innermost layer, made of endothelial cells Lines heart chambers and blood vessels Facilitates smooth blood flow and prevents clot formation Myocardium Thick, muscular middle layer Responsible for contractile function, enables heart to pump blood Epicardium Outer layer of heart, part of pericardium Provides protective layer and contains BVs that supply heart Pericardium Double-walled sac surrounding heart Composed of outer and inner layer with pericardial fluid between to reduce friction between heartbeats and provide cushioning Pericardial sac and fluid allow for movement of heart during contractions and protect it from external shocks 1. What is the location and function of the coronary circulation? Where are the openings to the coronary arteries and when does blood flow into them? Coronary circulation: network of blood vessels that supply blood to heart muscle (myocardium) Delivers oxygen-rich blood and nutrients, removes waste products from heart tissue Openings to coronary arteries Base of aorta Blood flows in during diastole 1. What anatomical structures are encountered when you trace the path of a blood cell through the circulatory system? Name, in correct order, all of the blood vessel types, cardiac chambers, and valves that are encountered as part of your answer. 1. Vein 2. RA 3. Right AV valve (tricuspid) 4. RV 5. Pulmonary SL valve 6. Pulmonary arteries 7. Pulmonary arterioles 8. Pulmonary capillaries 9. Pulmonary venules 10. Pulmonary veins 11. LA 12. Left AV valve (bicuspid/mitral) 13. LV 14. Aortic SL valve 15. Aorta 16. Arties 17. Arterioles 18. capillaries 1. What are the locations and functions of the four cardiac valves and what causes them to open and close? AV valves  ○ Right AV valve (tricuspid) ○ Left AV valve (bicuspid/mitral) SL valves ○ Pulmonary SL valve ○ Aortic SL valve Pressure gradients induce opening and closing Atrial pressure higher than ventricle pressure: valves open Aortic pressure higher than ventricle pressure: valves closed 1. What is cardiac valve prolapse and what prevents it from happening? Hearts valves do not close properly, allowing blood to leak backward Chordae tendineae and papillary muscles prevent prolapse, ensuring valves close properly 1. What are the three types of cardiac muscle cells and the specific function of each? 1. Pacemaker cells a. Small fraction of cardiac muscle cells that have automaticity b. SA node normally determines heart rate i. SA node → 100-120 APs/min ii. AV node → 60-80 APs/min iii. Conducting cells → 30-50 APs/min 2. Conducting cells a. Technically ALL cardiac muscle cells b. Small fraction are specialized to rapidly spread electrical stimulus throughout chambers i. Bundle of his, L and R bundle branches, purkinje fibers 3. Contractile cells a. 99% of cardiac muscle cells whose activity allows blood to be pumped out of the heart Week 8 Workshop 2 Mini lesson 4 Key Terms: ECG leads: electrodes placed on body to measure electrical activity and create ECG, provide different views of hearts activity internodal pathways: pathways in atria that conduct impulses from SA node to AV node, facilitating rapid transmission of electrical impulses Study Questions:  1. What are the seven components of the cardiac conduction system in the typical order of excitation and what is the major function of each component? 1. SA node: hearts pacemaker, initiates electrical impulses that trigger heartbeats 2. Atrial contractile cells: send blood to ventricles 3. AV node: delay so atria can finish before ventricles contract 4. Bundle of his: transmits impulses from AV node to ventricles through interventricular septum 5. Bundle branches: conduct impulses along interventricular septum to each ventricle 6. Purkinje fibers: ensure coordinated contraction 7. Ventricular contractile cells: send blood out of heart 4,5,6- conducting cells 1. What are four implications of every cell in the heart being connected by gap junctions? 1. One cell starts each AP (heartbeat) 2. One diseased cell can cause a fatal arrhythmia 3. Artificial pacemakers are possible to install 4. No recruitment for stronger heart beats; every cell contracts with every heartbeat 1. In what sequence do cardiac structures undergo depolarization and repolarization during a single beat of the heart and how do these events appear on a typical electrocardiogram (ECG)? 1. P wave: atrial depolarization 2. 2: flat line following P wave- AP through AV node 3. QRS complex: ventricular depolarization 4. T-wave: ventricular repolarization Mini lesson 5 Learning Objectives: Predict consequences of disruptions in the excitation pathway to the ECG and to heart function. Key Terms: artificial pacemaker: medical device that delivers impulses to stimulate heartbeats when heart's natural pacemaker is ineffective Automaticity: ability of cardiac cells to generate APs spontaneously without electrical stimulation AV conduction disorder: condition where electrical signals from atria to ventricles are delayed/blocked, affecting heart rhythm and function dihydropyridine (DHP) channels: L-type Ca2+ channels ectopic pacemakers: abnormal pacemaker cells outside normal pacemaking region (SA node) that can initiate APs and disrupt normal heart rhythm pacemaker potential: gradual depolarization of pacemaker cells in heart, leading to AP generation Study Questions: 1. What ion channels are present in cardiac contractile cells and how do ionic events underlie the shape of the action potential in this cell type? Draw the action potential to support your answer. 1) High resting K+ leak, RMP close to -90 mV 2) Threshold reached when AP from neighboring cell arrives through gap junction 3) Rapid depolarization due to Na+ channels (fast) 4) Prolonged plateau due to L-type Ca2+ channels and K+ exit 5) Repolarization due to voltage gated K+ channels 1. What ion channels are present in cardiac nodal cells and how do ionic events underlie the shape of the action potential in this cell type? Draw the action potential to support your answer. 1) Na+ entry through funny channels, then Ca2+ entry through T-type channels a) Cause pacemaker potential, which brings MP to threshold 2) Voltage gated Ca2+ channels cause depolarization upstroke 3) Repolarization by voltage gated K+ channels 1. What ion channels are present in cardiac fast-conducting cells and how do ionic events underlie the shape of the action potential in this cell type? Draw the action potential to support your answer. Funny Na+ channels T-type Ca2+ channels Fast Na+ channels L-type Ca2+ channels K+ channels  1. How do the parts of single atrial and ventricular contractile cell action potentials align with observed events in an ECG recording? Draw a picture as part of your answer. P wave = atrial AP depolarization QRS complex = atrial repolarization, ventricular AP depolarization T wave = ventricular depolarization 1. What is the significance of the prolonged duration of a cardiac contractile cell action potential? Prevents tetanus, allows time for ventricles to fill with blood during diastole in between periods of systole 1. How does each of the following events align in time during a single heartbeat: ECG, SA nodal action potential, atrial contractile cell action potential, and ventricular contractile cell action potential? How do these electrical events relate to cardiac systole and diastole? 1) SA Node AP 2) ECG P wave 3) Atrial contractile cell AP 4) QRS complex 5) Ventricular contractile cell AP 6) T wave Mini lesson 6 Learning Objectives: Use the Wiggers diagram to explain mechanical events of the cardiac cycle – in other words, explain how electrical events trigger mechanical (contractile) events in the heart. Predict different types of valve defects using the timing of heart sounds. Key Terms: atrial fibrillation: a common arrhythmia- rapid, irregular beating of atria, can lead to ineffective atrial contraction and increased risk of stroke dicrotic notch: small dip in arterial pressure waveform that occurs when the aortic valve closes, indicating the end of systole end-diastolic volume (EDV): volume of blood in ventricles at the end of diastole, before contraction end-systolic volume (ESV): volume of blood remaining in ventricles after contraction (systole) heart murmurs: abnormal sounds caused by turbulent blood flow septal defect: congenital heart defect where there is an abnormal opening in the septum separating the heart’s chambers stroke volume (SV): amt of blood ejected by the heart with each beat Study Questions: 1. What are the four phases of the cardiac cycle, and does each correspond with diastole or systole? Ventricular filling → diastole Isovolumetric contraction → systole Ejection → systole Isovolumetric relaxation → diastole 1. What occurs during the ventricular filling phase of the cardiac cycle? Diastole Atrial kick → active contraction, adds 10-20% more blood to ventricle, at rest EDV is reached ○ EDV- final volume in ventricle after filling (~135 mL) 1. What occurs during the isovolumetric ventricular contraction phase of the cardiac cycle? Systole Ventricles contract- tension and pressure development 1st heart sound at start of phase: “lub” (AV valves close) Volume constant at EDV P in ventricles < P in aorta and PA P in ventricles > P in atria 1. What occurs during the ventricular ejection phase of the cardiac cycle? How can stroke volume be measured given the end-diastolic volume and end-systolic volume? P in ventricles > P in aorta and PA  SV: volume of blood ejected from each ventricle at rest (~70 mL) ○ Same from both ventricles Reach ESV: volume of blood remaining in ventricle after ejection ESV = EDV - SV SV = EDV - ESV 1. What occurs during the isovolumetric ventricular relaxation phase of the cardiac cycle? 2nd heart sound at start of phase: “dup” (SL valves close) Volume constant at ESV (65 mL) P in ventricles < P in aorta and PA P in ventricles > P in atria 1. What is the detailed sequence of cause-and-effect relationships that connect the electrical events, pressure changes, and mechanical events during a single cardiac cycle? Draw the Wiggers diagram to support your answer. 1. What are similarities and differences between the cardiac cycle diagram for the systemic circulation and for the pulmonary circulation? Pulmonary circulation has lower pressure than systemic Systemic circulation supplies body with oxygenated blood while pulmonary involves oxygen exchange in the lungs LV has thicker walls than RV due to higher systemic pressure demands 1. What determines the opening and closing of all heart valves and what valve events relate to the normal “Lub” and “Dup” heart sounds? Lub: closing of AV valves Dup: closing of SL valves 1. How do the terms stenosis and insufficiency relate to heart valve defects? Stenosis: insufficient opening Narrowing of a valve, restricting blood flow through heart Insufficiency: insufficient closing Week 9 workshop 1 Mini lesson 1 Learning Objectives: Compare and contrast the ventricular-function curve with the length-tension relationship observed in skeletal muscle. Key Terms: Frank-Starling mechanism: strength of hearts contraction is directly related to degree of stretch of cardiac muscle fibers Preload: initial stretching of cardiac muscle fibers prior to contraction, primarily influenced by volume of blood returning to heart venous return: flow of blood back to heart from peripheral circulation (preload) ventricular-function curve: relationship between preload (ventricular filling) and stroke volume Study Questions: 1. What is the calculation to determine cardiac output and what is its typical, resting value in L/min? CO = HR x SV At rest, Co = 70 bpm x 70 mL/beat = 5 L/min 1. What are the parasympathetic and sympathetic pathways involved in the autonomic nervous system innervation and neurohormonal activation of the heart? As part of your answer, include the relevant neurotransmitters, neurohormones, receptor type, and receptor location. Autonomic 1) Parasympathetic ACh to muscarinic receptors within atria (SA, AV, and atrial contractile cells) 2) Sympathetic NE to B1 adrenergic receptors within whole heart Neurohormonal 1) Sympathetic Epi to B1 adrenergic receptors within whole heart 1. What is the intrinsic action potential firing rate of the three types of pacemaker cells, why do all pacemakers follow the SA node’s rate in a normal heartbeat, and why is the  resting heart rate generally slower than the intrinsic firing rate of the SA node? SA node → 100 APs/min AV node → 70 APs/min His/purkinje → 30 APs/min Pacemakers follow SA nodes rate because it is the highest At rest, you are parasympathetic dominant, so parasympathetic will slow SA node down SA → >50-70 APs/min AV → >40-50 APs/min his/purkinje → 30 APs/min 1. How does sympathetic and parasympathetic innervation and neurohormones alter the SA node cell action potential frequency via regulation of ion channels and how do these chronotropic effects alter cardiac output? Pacemaker potential in SA node cells is slowed by parasympathetic (ACh) and quickened by sympathetic (NE) stimulation Chronotropic effects: alter heart rate Sympathetic (NE) 1) No change of K+ current 2) Increased funny Na+ current 3) Increased T-type Ca2+ current Parasympathetic (ACh) 1) Increased voltage-gated K+ current 2) Decreased funny Na+ current 3) Decreased T-type Ca2+ current 1. How does sympathetic and parasympathetic innervation and neurohormones alter the AV node cell action potential upstroke via regulation of ion channels and how do these dromotropic effects alter cardiac function? Upstroke of AP in SA node and AV node cells is also slowed by parasympathetic and quickened by sympathetic stimulation Dromotropic effects: changes to conduction velocity One ion channel alteration that affects the conduction velocity in nodal cells: Sympathetic (ACh) ○ Increased L-type Ca2+ current Parasympathetic (NE) ○ Decreased L-type Ca2+ current  1. How does the Frank-Starling mechanism intrinsically regulate stroke volume and cardiac output and what are implications of this relationship to the cardiovascular system? More venous return (EDV) (Preload) = increased length of cells = increased tension = increased SV Intrinsic mechanism of regulating sv: if ventricle fills to a larger EDV, next beat is stronger to eject extra blood Implications Prevents a rise in ESV (which prevents clotting) Matching of LV and RV output ○ if venous return increases on either side, CO increases; no pooling in either circuit Prevention of rise in venous pressure ○ if blood backs up into veins and capillaries it causes fluid to be forced out of capillaries, causing edema 1. How does the Frank-Starling mechanism, or the ventricular-function curve, compare to the length-tension relationship observed in skeletal muscle? How is it different? Resting cardiac muscle with normal EDV (preload) is well below its optimal length Typical cell length is well below optimal in the heart compared to skeletal muscle Mini lesson 2 Learning Objectives: Key Terms: Afterload: the resistance the heart must overcome to eject blood during contraction. Higher afterload reduces stroke volume Contractility: the ability of the heart muscle (myocardium) to contract ejection fraction (EF): the percentage of blood ejected from the ventricles during systole inotropic effects: altering the heart’s contractility Study Questions: 1. What is the second messenger pathway by which cardiac contractility is altered upon sympathetic stimulation? As part of your answer include all cellular targets of modulation and their consequences. NE and Epi bind to B1 adrenergic receptors G proteins phosphorylation Adenylyl cyclase converts ATP→ cAMP  Inactive cAMP dependent protein kinase → active cAMP dependent protein kinase Targets Ca2+ enters through DHPR L-type Ca2+ channel Ca2+ exits SR through RyR receptor Thin filament activation (Ca2+ bind to troponin) Cross bridge cycling, thick and thin filament sliding, force generation Ca2+ back into SR through RyR receptor 1. What is meant by “increased contractility” and what does this look like on a ventricular-function curve? How does this inotropic effect alter cardiac output? Increasing the force of contraction, at any given EDV, there is a stronger contraction (and thus a larger SV) (inotropic effect) Inotropic effect: raises cardiac output by boosting stroke volume 1. How is an ejection fraction calculated, and what values are expected with and without extrinsic sympathetic stimulation and in a weak, failing heart? EF = SV/EDV (x100%) Typical EF= 50-75% Sympathetic EF = 80-90% Weak failing EF= 25% 1. What are three parts of a cardiac twitch (ventricular force development) that are altered by sympathetic stimulation? 1) Quicker rise to peak force 2) Higher peak force 3) Faster decline of force 1. How do changes in afterload alter stroke volume and thus cardiac output? Increased afterload lowers sv and co Decreased afterload increases sv and co 1. What are the major factors involved in increasing or decreasing cardiac output via the  regulation of heart rate and stroke volume? As part of your answer include all autonomic nervous system components and pertinent molecular details. From CI center: ACh binds to NAChR SA node: decreased heart rate (chronotropy) AV node: decreased conduction rate (dromotropy) Atrial muscle: decreased contractility (inotropy) Ventricular muscle: no significant effect From CA center: NE binds to beta-adrenergic receptors on heart SA node: increased heart rate (chronotropy) AV node: increased conduction rate (dromotropy) Atrial muscle: increased contractility (inotropy) Ventricular muscle: increased contractility (inotropy) Mini lesson 3 Learning Objectives: Relate the structure of the various blood vessel types to their main functions. Summarize how to use systolic and diastolic pressure measurements to calculate blood pressure using an equation and by using a sphygmomanometer. Key Terms: Arteriosclerosis: hardening and thickening of artery walls → reduced elasticity and blood flow Compliance: ability of a blood vessel to stretch and expand with pressure diastolic pressure (DP): minimum arterial pressure during relaxation between heartbeats Korotkoff’s sounds: sounds heard with a stethoscope, indicate blood flow as cuff pressure changes mean arterial pressure (MAP): average arterial pressure through one cardiac cycle, calculated to estimate blood flow pulse pressure (PP): difference between systolic and diastolic pressures Sphygmomanometer: device for measuring blood pressure with a cuff, pump, and gauge systolic pressure (SP): peak pressure in arteries during contraction Study Questions: 1. What are similarities and differences of the histological layers in the walls of each of the blood vessels and how does the structure of each blood vessel relate to its general function? Arteries: thick, elastic connective tissue, smooth muscle, endothelium Arterioles: thick smooth muscle (for cross-sectional area), endothelium Capillaries: endothelium Venules: thin connective tissue, endothelium Veins: thin connective tissue, thin smooth muscle, endothelium, wide and floppy  1. How does the pressure vary along the systemic and pulmonary vessels and what are the general values at each location? Systemic circulation: Aorta and arteries: 80-120 mmHg Big drop in pressure in arterioles : 40 mmHg Pressure continues to decrease in capillaries, venules, then veins, reaching almost 0 by atrium Pulmonary circulation Aorta and arteries: 10-30 mmHg Systolic drops throughout arterioles, capillaries, venules, veins Diastolic stays at around 10 mmHg 1. How do compliance and elastic recoil relate to the main function of arteries as pressure reservoirs, and quantitatively, how does blood move into and out of the arteries during the cardiac cycle? Elastic recoil (snap back of walls due to high levels of elastin) maintains pressure, continues to push on the blood, keeping it moving forward during diastole. Compliance: how easy the artery walls stretch. Greater compliance means more stretch, more elastic recoil, higher pressure, etc. 1. What is the equation for calculating mean arterial pressure? MAP = DP + ⅓ (PP) 1. How can a sphygmomanometer and stethoscope be used to determine mean arterial pressure? Sphygmomanometer cuts off blood flow, and when cuff pressure goes just below systolic pressure, the first sounds are heard (systolic pressure), when the last sound is heard before silence (diastolic pressure) 1. How do systolic pressure, diastolic pressure, pulse pressure, and mean arterial pressure change with age? With age, compliance and elasticity decrease (arteries become stiffer), making SP trend higher, DP trend higher, PP trends higher, but MAP stays the same. Week 9 workshop 2 Mini lesson 4 Learning Objectives: Detail how arterioles distribute blood flow to match local tissue/cellular metabolic demand. Summarize why arterioles are the main determinants of total peripheral resistance and how this relates to mean arterial pressure. Compare and contrast local control mechanisms that determine arterial blood flow. Compare and contrast effects of extrinsic sympathetic nerves and neurohormones on arteriolar radius. Summarize the major factors that determine arteriolar radius and predict changes in blood flow when these factors are altered. Key Terms: active hyperemia: increased blood flow in response to heightened tissue activity, providing more oxygen and nutrients angiotensin II: a hormone that causes vasoconstriction and increases blood pressure atrial natriuretic peptide: a hormone that reduces blood pressure by vasodilation endothelin-I: a vasoconstrictor produced by endothelial cells flow autoregulation: process by which blood vessels adjust their diameter to maintain stable flow despite changes in blood pressure Hyperemia: increased blood flow to an organ or tissue intrinsic tone: baseline level of contraction in vascular smooth muscle, influenced by local factors local controls: mechanisms within tissues that adjust blood flow according to needs myogenic responses: contraction of smooth muscle in response to stretching, helping stabilize blood flow nitric oxide: vasodilator released by endothelial cells, relaxes smooth muscle reactive hyperemia: increased blood flow following a period of reduced blood supply Vasoconstriction: narrowing of blood vessels, increases blood pressure Vasodilation: widening of blood vessels, decreases blood pressure Vasopressin: hormone promotes vasoconstriction and water retention, raises blood pressure Study Questions: 1. What does it mean when arterioles are described as “variable resistance flow regulators,” and how does this relate to their structure? Conditioning organs Kidney Intestines Skin ○ Receive blood flow in excess of their personal metabolic needs ○ Very tolerant of blood flow reduction ○ These are constricted to protect blood pressure Flow-dependant organs Brain Heart ○ Critically dependent on blood flow for survival ○ No tolerance for ischemia or low blood flow ○ These do not constrict to regulate blood pressure, they benefit from it 1. What are the two major functions of an arteriole, and how can these roles be conflicting? 1) Match blood flow to local tissue/cellular metabolic demand 2) Collectively, to maintain MAP by determining the TPR; they need to protect MABP by TPR cooperation Conflicts: Conflict of skeletal muscle arterioles when you exercise on a very hot day Recall the heatstroke case from week #1 Which organs “win” and which “lose” when supply cannot keep up with demand 1. What are the hemodynamic effects of constricting or dilating an individual arteriole? Constricting an arteriole increases resistance, which reduces blood flow to downstream tissues and raises upstream blood pressure Dilating an arteriole decreases resistance, allowing more blood flow to downstream tissues 1. How would constriction of all arterioles effect total peripheral resistance and thus mean arterial pressure? What organs would benefit from this and when might this be important? Use a drawing or equation to support your answer. -All blood vessels contribute resistance to blood flow, -Arterioles are main contributors to TPR MAP = CO x TPR -Their thick layer of smooth muscle allows them to change their radius; which alters TPR -Changes in TPR directly cause changes in MAP 1. How do local controls including active hyperemia, myogenic flow autoregulation, and reactive hyperemia allow tissues to alter their own arteriolar resistances in order to self-regulate their blood flow? Active hyperemia Increased metabolic activity of organ Decreased O2, increased metabolites in organ interstitial fluid Arteriolar dilation in organ Increased blood flow to organ Myogenic flow autoregulation Increased MAP Increased arteriolar blood pressure Increased arteriolar wall stretch Increased activation of stretch-sensitive Ca2+ channels (mechanoreceptors) Increased influx of Ca2+ from ECF into smooth muscle cells Increased contraction of smooth muscle cells = vasoconstriction Reactive hyperemia Involves a rebound of high blood flow after a period of deprivation Involves the same local metabolic changes as active hyperemia and flow autoregulation 1. How do vasoactive metabolites/factors effect local regulation of the contractile state of the arteriole? Vasoactive metabolites/factors: VASODILATION Decrease ○ O2 ○ pH Increase  ○ CO2 ○ ECF K+ ○ Adenosine (from ATP) VASOCONSTRICTION Increase ○ O2 ○ pH Decrease ○ CO2 ○ ECF K+ ○ Adenosine (from ATP) Local control factors are main regulators of blood flow to brain and heart 1. What are the two main sympathetic receptor types and the neurotransmitter/neurohormone involved in extrinsic controls of arterioles? What is the effect when each receptor is stimulated? a1-adrenergic receptors NE stimulates VASOCONSTRICTION ○ Decreases blood flow to downstream capillaries B2-adrenergic receptors EPI stimulates VASODILATION ○ Increases blood flow to downstream capillaries 1. What are the receptor- and dose-dependent interactions of norepinephrine and epinephrine on arterioles found in skeletal muscle tissues? 1. What are the major neural, hormonal, and local controllers of arteriolar radius? Neural Vasoconstrictors ○ Sympathetic nerves release NE (to a1 receptors) Vasodilators ○ Neurons release nitric oxide Hormonal Vasoconstrictors ○ Epinephrine (HIGH CONC) ○ Angiotensin II ○ Vasopressin = ADH Vasodilators ○ Epinephrine (LOW CONC) ○ Atrial natriuretic peptide = ANP Local controls Vasoconstrictors ○ Internal blood pressure (myogenic response) ○ Endothelin-1 Vasodilators ○ Decreased oxygen ○ K+, CO2, H+ ○ Osmolarity ○ Adenosine ○ Substances released during injury ○ Nitric oxide ○ Also tissue temp Warm → dilate Cold → constrict 1. What are the main factors effecting arteriolar regulation of blood flow within the heart, skeletal muscle, kidneys, brain, and lungs? Heart Controlled mostly by local metabolic factors, particularly adenosine, and flow autoregulation; direct sympathetic influences are small and usually overridden by local factors Coronary flow occurs mainly during diastole Skeletal muscle Controlled by local metabolic factors during exercise Sympathetic activation causes vasoconstriction (a1-adrenergic receptors) in response to decreased arterial pressure Epi causes vasodilation (B2-adrenergic receptors) in low concentration, and vasoconstriction (a1-adrenergic) in high concentrations Kidneys Flow autoregulation is major factor Angiotensin II major vasoconstrictor, helps conserve Na+ and H2O Brain  Excellent flow autoreg Dist. of blood in brain controlled by local metabolic factors Vasodilation occurs in response to increased conc of CO2 in arterial blood Influenced relatively little by ANS Lungs Constriction mediated by local factors in response to low O2 conc Mini lesson 5 Learning Objectives: Detail the Starling forces that govern fluid exchange between capillaries and the interstitial fluid (ISF) and be able to predict changes in fluid movement in response to hydrostatic and osmotic pressure changes. Key Terms: Absorption: movement of fluid from ISF into capillaries capillary hydrostatic pressure: pressure exerted by blood on capillary walls, promoting fluid filtration into tissues Colloids: large molecules, like proteins, that stay in blood vessels, generating osmotic pressure Crystalloids: small molecules, can move across capillary walls (like electrolytes) Edema: excess fluid accumulation in tissues, often from imbalance of starling forces Filtration: movement of fluid from capillaries to ISF fused-vesicle channels: transport pathways in capillaries formed by fusion of vesicles, allows passage of larger molecules intercellular clefts: small gaps between endothelial cells in capillaries, allow movement of small solutes Metarterioles: vessels that regulate blood flow into capillary beds, connecting arterioles and capillaries net filtration pressure (NFP): net balance of starling forces, determines fluid movement direction across capillary walls osmotic pressure: pressure from solute conc differences, drives water across membranes precapillary sphincter: smooth muscle band regulating blood entry from arterioles into capillary beds Starling forces: 4 forces that determine net movement of fluid across capillary walls Study Questions: 1. How does capillary structure maximize their functional efficiency? 5% of circulating blood is in capillaries 8 um diameter with thin wall and variable size pores (intercellular clefts) Single layer of endothelial cells maximizes exchange with RBCs and ISF compartment (no smooth muscle) Longest length of all vessels (~25,000 miles) 1. What are the relationships between total cross-sectional area, velocity, and flow rate as blood flows through the different blood vessels? What is the difference between blood “flow” and blood “velocity?” Flow (L/min) is the same in each cross section, but Velocity (cm/sec) changes Velocity is inversely related to cross-sectional area (slowest v in capillaries, biggest cross-sectional area) Slowest velocity in capillaries maximizes their ability to exchange substances with ISF 1. What is the main mechanism that allows for exchanges of nutrients and metabolic end products across the capillary wall? What are examples of substances that move by this mechanism? Diffusion (across conc gradients) O2 moves from systemic capillaries to muscle cells Glucose moves from systemic capillaries to muscle cells CO2 moves from muscle cell to systemic capillaries 1. What is bulk flow and how does this mechanism contribute to homeostasis? Filtration: movement of fluid out of the blood Absorption: movement of fluid into the blood Bulk flow: net result of filtration and absorption, relies on pressure gradients to distribute and balance fluid volume between two compartments (NOT diffusion) 1. What are the 4 Starling forces that determine bulk flow and how are they used to determine the net filtration pressure? Filtration 1) Capillary hydrostatic pressure (Pc)  ○ Pressure exerted by blood against capillary walls and through capillaries 2) Osmotic force due to ISF protein concentration (πif) ○ Osmotic pressure from proteins pulls fluid out of capillaries Reabsorption 3) Interstitial fluid hydrostatic pressure (Pif) ○ Pressure in ISF, can oppose filtration 4) Osmotic force due to plasma protein concentration (πc) ○ Osmotic force from proteins pulls fluid into capillaries Net filtration pressure = Pc + πif - Pif - πc If NFP is (+), then net filtration If NFP is (-), then net reabsorption 1. What is the effect of bulk flow normally and during pathophysiological conditions when the Starling forces are not balanced? Forces are not exactly balanced, usually small net filtration; all capillaries combined lose about 4L/day into ISF (excluding kidney capillaries) Lymphatic system absorbs extra filtrate and escaped proteins In person mini lesson 6 Learning Objectives: Describe the structures and explain the main functions of the lymphatic system and summarize the factors that contribute to mechanisms of lymph flow. Key Terms: capacitance vessels: veins and venules, can hold a large volume of blood bc of high compliance, allowing them to store blood and help regulate venous return to heart Lymph: clear fluid containing WBCs that circulates through lymphatic system, helps remove waste, toxins, and pathogens from tissues lymphatic capillaries: small, thin walled vessels in tissues, absorb excess ISF and transport it as lymph, beginning lymphatic circulation lymphatic system: network of tissues, vessels, and organs maintaining fluid balance, and aiding in immune function by transporting lymph and immune cells lymphatic vessels: larger vessels transport lymph from capillaries toward lymph nodes, eventually back into bloodstream Lymphedema: swelling caused by accumulation of lymph due to blockages or dysfunction in lymphatic system peripheral veins: veins outside of chest and abdomen, return deoxygenated blood from limbs and extremities to heart respiratory pump: mechanism where breathing movements help facilitate venous return to heart by creating pressure changes in thoracic and abdominal cavities skeletal muscle pump: muscle contractions in limbs compress veins, propelling blood toward heart and helping prevent pooling in legs, esp during exercise/movement Study Questions: 1. How does the structure of veins contribute to their function and why are veins described as capacitance vessels? Big radius, low resistance- return blood to the heart High Capacitance vessels: “storage” VERY compliant (Stretchy) Less elastic, floppy 1. Why is gravity a problem for venous function? Gravity in upright humans opposes venous return Net deficit of ~70 mmHg bc blood pools in legs when standing 1. What are the four factors that oppose gravity and thus help to promote an increase in venous return to the heart? 1) Sympathetic innervation ○ At rest, 60% of total blood volume is in veins ○ Sympathetically mediated venoconstriction can substantially increase venous return to heart, extra blood can be moved elsewhere in circulation Venoconstriction: different from vasoconstriction (arteries, decreased flow). Refers to constriction/smooth muscle contraction in venous system, increases flow 2) Skeletal muscle pump ○ Contraction of leg muscle can cut pressure by significant amount Squeezes large veins, increasing venous pressure This in combination with one-way valves promotes venous return to heart 3) Inhalation movements  ○Inhaling creates lower pressures in thoracic cavity where heart and lungs are located, blood moves from veins that are outside thorax and have higher pressure to veins that are inside the thorax and have lower pressure 4) Blood volume ○ In CV system, volume equates with pressure More volume, more pressure Less volume, less pressure ○ When bv is low overall, venous pressure and thus venous return against gravity are reduced 1. What structures are involved in and what are the main functions of the lymphatic system? Lymphatic fluid (lymph) is the 4 L/day of mismatch between filtration and reabsorption in the capillaries Also includes escaped plasma proteins and absorbed fats System sucks up ISF and pass through lymph nodes, then back into circulation Fluid is returned to large veins near the heart, and put back into CV system Exercise increases lymph flow Lymph nodes enlarge when fighting infection Cancer cells can speak through lymph, sometimes removed as part of treatment Blockage of lymph occurs when filaria worms invade the body (via mosquitos); causes lymphedema 1. What are the mechanisms that enhance lymph flow? 1) Increased filtration at capillaries 2) Smooth muscle contraction and one-way valves within lymphatic vessels 3) Sympathetic stimulation via NE binding to a1 receptors within lymphatic vessels 4) Skeletal muscle pump and respiratory pump 1. What is a cause and consequence of lymphedema? Lymphedema: swelling due to accumulation of lymph fluid Cause: blockage of lymph flow due to infectious filaria worms (via mosquitoes) living in the lymph nodes Consequence: fluid retention, swelling, elephantiasis Week 10 workshop 1 Mini lesson 1 Learning Objectives: Explain how baroreceptor reflexes affect heart and vascular functions to maintain MAP at its normal homeostatic set point in the short-term. As part of your answer, explain, in detail, the various components of the negative feedback pathway. Predict the direct effects of drug interactions and volume changes on heart rate, stroke volume, cardiac output, total peripheral resistance, and mean arterial pressure and summarize changes to these variables as a result of baroreceptor reflex compensation. Key Terms: aortic arch baroreceptor: nerve endings in aortic arch, detect changes in bp by sensing stretch of arterial wall, relays signals to brain arterial baroreceptors: nerve endings in carotid sinuses and aortic arch, monitor bp changes by sensing stretch Carotid sinus baroreceptor: in carotid sinuses, sense stretch and send signals Hemorrhage: loss of blood from circulatory system, decreases bv, lower bp, activates compensatory mechanisms medullary cardiovascular center: brainstem region that processes baroreceptor input, adjusts HR, SV, and bv constriction to regulate bp systemic vascular resistance: resistance to blood flow within systemic circulation, determined by arteriole diameter total peripheral resistance: overall resistance to blood flow in systemic circulation, influencing bp and work Study Questions: 1. Why is it important to maintain an adequate mean arterial pressure (MAP)? MAP: force that drives flow through vasculature; force that provides life High enough to drive blood through tissues Low enough to ○ Minimize work of the heart ○ Prevent vessel rupture (e.g. stroke or aneurysm) MAP = DP + ⅓ (PP) Males avg = 93 (120/80) Female avg = 83 (110/70)  1. What is the equation relating cardiac output (CO), total peripheral resistance (TPR), and mean arterial pressure (MAP)? MAP = CO x TPR 3. What is the mathematical relationship between the following variables: cardiac output (CO), heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), total peripheral resistance (TPR), end-diastolic volume (EDV) and end-systolic volume (ESV)? F = △P/R (for single blood vessel) CO = (MAP-RA Pressure (~0))/TPR (for system) CO = MAP/TPR CO = HR x SV SV = EDV-ESV MAP = CO x TPR 4. What is the location of the sensory receptors that sense changes in MAP? What is their adequate stimulus? Where do they send their information? Baroreceptors (afferent axons of 9th and 10th cranial nerves) Carotid sinus baroreceptor Aortic arch baroreceptor Adequate stimulus: stretch Send information to brainstem cardiovascular control centers (CA, CI, VM) 5. How do baroreceptor reflexes affect heart and vascular functions to maintain MAP at its normal homeostatic set point in the short-term? As part of your answer, draw a diagram that summarizes the neural pathways controlling cardiac output and total peripheral resistance. Include and label: the medulla oblongata, the heart, a representative arteriole, a representative vein, arterial baroreceptors, sympathetic pathways, CA, CI, VM, the vagus nerve, parasympathetic pathways, acetylcholine, norepinephrine, beta-1 adrenergic  receptors, alpha-1 adrenergic receptors, and muscarinic acetylcholine receptors. 1) Cardioinhibitory center (CI) = parasympathetic 2) Cardioacceleratory center (CA)= sympathetic 3) Vasomotor center (VM) = sympathetic Efferent output from these centers is main determinant of MAP in short term 6. How are heart rate, stroke volume, cardiac output, total peripheral resistance, and mean arterial pressure affected by the firing of parasympathetic neurons, and in what direction? Parasympathetic Decreases HR Decreases CO Does Not affect SV Does Not affect TPR Decreases MAP 7. How are heart rate, stroke volume, cardiac output, total peripheral resistance, and mean arterial pressure affected by the firing of sympathetic neurons, and in what direction? Sympathetic Increases HR Increases SV Increases CO Increases TPR Increases MAP Mini lesson 2 Learning Objectives: Describe how and why central chemoreceptors elevate systemic arterial pressure during Cushing’s phenomenon. Key Terms: Cushing’s phenomenon Study Questions: 1. What is the role of blood volume in the long-term regulation of arterial pressure and how are the cardiovascular and renal systems involved? Long-term regulation of blood pressure depends on blood volume, regulated by the cv and renal systems CV system: maintains MAP by adjusting CO and TPR (heart pumps more blood when bv increases, raising CO and MAP. when bv decreases, CO and pressure drop) Renal system: when bp is high, kidneys excrete more Na+ and H2O, reducing blood volume, and lowering pressure. When bp is low, kidneys conserve Na+ and H2O, increasing blood volume, raising pressure Ex: increase of arterial pressure decreases secretion of angiotensin II, aldosterone, and ADH, increasing urinary output from kidneys, losing Na+ and H2O to urine (less in plasma), decreasing plasma volume, thus decreasing blood volume. Then, neg fb loop (frank starling) decreases MAP and Co, decreasing arterial pressure 2. Where are peripheral chemoreceptors located? What stimuli activate them? How does their activation override input from baroreceptors? In what physiologic circumstance might this be important? Peripheral chemoreceptors Located near, but are separate from arterial baroreceptors Known as “aortic bodies” and “carotid bodies” ○ Sense in artery blood (activated by): Decreased O2 Increased CO2 Decreased Ph ○ Then stimulates VM brainstem nuclei, causing vasoconstriction (inc TPR, thus inc MAP) Activation overrides baroreceptors, helps to prioritize respiratory function over maintaining blood pressure 3. What are some situations or conditions that cause an increase or decrease of mean arterial pressure despite the existence of homeostatic blood pressure reflexes? Things that increase MAP 1) Decreased arterial O2 2) Increased arterial CO2 3) Decreased brain blood flow 4) Pain in skin (superficial pain)  5) Psychological stress 6) Physical activity 7) Consuming nutrients 8) Weight gain Things that decrease MAP 1) Deep, bone, or visceral pain 2) Sleeping 3) Happiness 4. What is “Cushing’s phenomenon,” and how are the central chemoreceptors involved? What is their adequate stimulus? Elevated intracranial pressure resulting in large increases in systemic MAP Initiated by central chemoreceptors ○ Located near CA, CI, and VM centers ○ Adequate stimulus: detect CO2 levels in brain ISF Mini lesson 3 Learning Objectives: Explain the role of the respiratory system in the maintenance of homeostasis and the functional connection between the respiratory system and the cardiovascular system. Explain the anatomical relationship between the lungs, pleura, and thoracic wall. Key Terms: alveolar sacs: clusters of alveoli at end of bronchioles CF transmembrane conductance regulator (CFTR): protein that regulates transport of chloride ions across cell membranes, mutations in CFTR gene cause CF, affecting mucus production and lung function cystic fibrosis (CF): genetic disorder affecting CFTR protein, leading to thick, sticky mucus in lungs and digestive system Diaphragm: large dome shaped muscle under lungs, contracts and flattens to allow air to enter, relaxes to push air out intercostal muscles: muscles located between ribs, help expand and contract chest during breathing intrapleural pressure (Pip): pressure within pleural cavity, usually slightly neg relative to Patm, which helps keep lungs expanded Larynx: voice box, contains vocal cords Pharynx: throat region, connects mouth and nasal passages to larynx and esophagus Pleura: double layered membrane surrounding lungs pleural sac: space formed by pleura, surrounds each lung, contains pleural fluid respiratory bronchioles: small airways leading from terminal bronchioles to alveolar sacs Thorax: chest region of body, contains lungs, heart, and other structures Trachea: windpipe, connects larynx to bronchi, lined w cartilage and ciliated epithelium vocal cords: tissue in larynx vibrate to produce sound Study Questions: 1. What are the functions of the respiratory system? 1) Provides O2 to the blood 2) Eliminates CO2 from blood 3) Regulates blood pH w/ kidneys 4) Phonation (forms speech sounds) 5) Defends against inhaled microbes 6) Influences arterial conc of chemical messengers by removing some from pulmonary capillary blood and producing and adding others to this blood (angiotensin-converting enzyme, ACE) 7) Traps and dissolves blood clots from systemic veins, such as in legs 1. What major anatomical structures of the respiratory system would a molecule of oxygen encounter on its journey from room air into the lungs? Nasal hair & mucus sinuses Nasal cavity Nostril Mouth Pharynx Larynx (contains vocal cords) Epiglottis (flap) Glottis (hole) Trachea Cartilaginous “C” rings with 20 generations of branching L and R main bronchus L and R lung diaphragm 1. What are the components and function of the mucous ciliary escalator? Epithelial surfaces of airways to ends of respiratory bronchioles contain cilia that constantly flow upward toward pharynx Also interspersed, specialized cells that secrete watery sticky mucus Particulate matter, like dust, sticks to the mucus, which is slowly and continuously moved by cilia to the pharynx, where it is then swallowed Helps keep lungs clear of particulate matter and bacteria that enter the body on dust particles *can be severely disrupted by noxious agents, like smoke from tobacco products 1. What are the structures that make up the “conducting zone” and the “respiratory zone” of the respiratory system? Conducting zone: anatomical dead space; air in zone does not participate in gas exchange Trachea Bronchi ○ Cartilaginous rings (trachea and bronchi) hold airway open Bronchioles ○ Bronchioles surrounded by smooth muscle, allows for bronchoconstriction or bronchodilation Terminal bronchioles Respiratory zone: where gas exchange takes place between alveoli and pulmonary capillaries Respiratory bronchioles Alveolar ducts Alveolar sacs ○ Gas exchange occurs within alveoli 1. In what airway structures does regulation of airflow take place? What anatomical feature allows for this regulation? Regulation of airflow happens in bronchi and bronchioles ○ Bronchoconstriction or bronchodilation Anatomical feature allowing for regulation: smooth muscle 1. Where does the majority of gas exchange occur? Alveoli: main site of gas exchange Tiny hollow sacs whose open ends are continuous with lumens of airways  Large surface area (~300 million of them) 1. What are the main functions of the conducting zone of the airways? Provides low-resistance pathway for airflow ○ Resistance regulated by changes in contraction of bronchiolar smooth muscle and physical forces acting on airways Defends against microbes, toxic chemicals, and other foreign matter (cilia, mucus, macrophages) Warms and moistens air Participates in sound production (vocal cords) 1. What is the anatomical and functional interaction between the circulatory and respiratory systems in the lungs? Sheet of blood spread across a sheet of alveoli allows for very large surface area and efficient diffusion of gases 1. What is the location and function of type I and type II alveolar cells? Type I alveolar cells Flat epithelial cells Single layer thick Make up majority of alveolar walls Gas exchange Type II alveolar cells Secrete surfactant (helps prevent collapse of alveoli) 1. What is the anatomical relationship between the pleura, the lungs, and the chest cavity? Pleural sac ○ Visceral pleura- inner layer ○ Parietal pleura- outer layer ○ Intrapleural fluid- between Intrapleural space very thin and only contains a few mL of fluid, helps to reduce friction from movement Allow for smooth movement and protects lungs while enabling them to move freely in chest cavity without friction Week 10 workshop 2 Mini lesson 4 Learning Objectives:  Explain how Boyle’s law relates to ventilation and predict the direction of airflow between the lung and atmosphere when the relative pressures in these two compartments change. Explain the balance of transmural pressure gradients that exist at the functional residual capacity and predict consequences if pressure gradients are disrupted due to illness or injury. Key Terms: elastic recoil: ability of lungs and thoracic cavity to return to resting volume after being stretched during inhalation, helps expel air in exhalation transmural pressure: for lungs, transmural pressure is diff between Palv and Pip transpulmonary pressure (Ptp): difference btween Palv and Pip Study Questions: 1. What is the equation that relates pressure, flow, and resistance to lung ventilation? F = (Palv-Patm)/Rairways 1. What is Boyle’s law and how does it apply to the mechanics of ventilation? P1V1=P2V2 At a constant temp, pressure of a fixed # of gas molecules is inversely proportional to volume of container Exhalation: compression Inhalation: decompression 1. What are the stepwise changes in pressure and volume that allow air to flow during inhalation and exhalation? 1) Change volume of lung 2) Pressure changes inside lung (Boyle’s law) 3) New pressure gradient allows flow of air 1. What skeletal muscles are used during quiet/resting inhalation? What additional skeletal muscles are used during exercise/forced inhalation? What skeletal muscles are used during quiet/resting exhalation? What skeletal muscles are used during exercise/forced exhalation? quiet/resting inhalation  Sternocleidomastoid ○ Elevates sternum Scalenes ○ Fix or elevate ribs 1-2 External intercostals ○ Elevate ribs 2-12, widen thoracic cavity Diaphragm ○ Descends, increases depth of thoracic cavity Quiet, resting exhalation NO muscle contractions Exercise/forced exhalation Internal intercostals, interosseous part ○ Depress ribs 1-11, narrow thoracic cavity Diaphragm ○ Ascends, reduces depth of thoracic cavity Rectus abdominis AND external abdominal oblique ○ Depresses lower ribs, pushes diaphragm up by compressing abdominal organs 1. What is the “functional residual capacity (FRC)?” FRC: volume of air remaining in lungs at the end of a quiet exhale when respiratory muscles are relaxed At FRC, outward recoil of chest wall = inward recoil of lung At FRC, alveolar pressure = atmospheric pressure; thus no movement of air 1. How do you calculate the transmural pressure gradients (both transpulmonary pressure and chest wall pressure) at FRC, and how are these forces balanced during this phase of the ventilation cycle? Chest wall If not attached, would expand up and out by elastic recoil Attached to parietal wall of pleural sac, transmural pressure gradients, and surface tension to hold in and down Lungs If not attached, would collapse inward by elastic recoil Pulled open to larger volume bc attached to visceral wall of pleural sac, transmural pressure gradients, and surface tension Inside minus outside = pressure gradient Transmural pressure = Pin-Pout Transpulmonary (Ptp) = Palv-Pip  ○ At rest: 0 - (-4) = 4 mmHg Chest wall (Pcw) = Pip - Patm ○ At rest: -4 - 0 = -4 mmHg Balanced at FRC, bc Patm=Palv, so no air movement 1. What is atmospheric pressure (Patm), alveolar pressure (Palv), and intrapleural pressure (Pip) at the FRC? At FRC Patm = 0 Palv = 0 Pip= -4 1. What is a pneumothorax and atelectasis? How and why might these pathophysiological circumstances occur? Pneumothorax: air in thorax Atelectasis: collapsed lung Injury #1: Trauma Air flows from H→L All pressures become 0 Injury #2: Disease, genetic predisposition, infection, ventilator trauma/malfunction Air flows from H→L All pressures become 0 Mini lesson 5 Learning Objectives: Summarize the skeletal muscle activity and the pressure and volume changes that occur during inhalation and exhalation during a typical respiratory cycle. Key Term: phrenic nerves: originate from cervical spinal cord, play crucial role in respiration, innervate diaphragm Study Questions: 1. How does skeletal muscle activity during quiet/resting breathing and exercise/forced breathing contribute to the process of inhalation? During quiet/resting breathing  Diaphragm controlled by phrenic nerves ○ Contracts and flattens during inhalation, increasing volume of thoracic cavity, creates neg pressure in lungs, causing air to flow into respiratory tract During forced/exercise Diaphragm enhanced activity External intercostal muscles: contract to elevate ribs and expand ribcage Sternocleidomastoid and scales: help lift upper ribs and sternum 1. How does skeletal muscle activity during quiet/resting breathing and exercise/forced breathing contribute to the process of exhalation? quiet/resting exhale Elastic recoil pushes air out of lungs Diaphragm relaxes, decreasing volume of thoracic cavity exercise/forced exhale Diaphragm more forcefully relaxes to expel air faster Internal intercostal muscles contract to pull ribs down and in, decreasing volume of thoracic cavity Abdominal muscles (rectus abdominis, obliques) ○ Contract, push diaphragm up more forcefully 1. What are the relationships between intrapleural pressure (Pip), transpulmonary pressure (Ptp), alveolar pressure (Palv), atmospheric pressure (Patm), and direction of air flow, and breath volume during a typical respiratory cycle? Draw a diagram and/or flowchart(s) to support your answer and highlight the application of Boyle’s law. Pip -4 mmHg at rest -6 mmHg inhalation Less negative (but still neg rel to Patm) exhalation Ptp Inhalation: increases Exhalation: decreases Palv Inhalation: negative (rel to Patm), causing air to flow into the lungs Exhalation: positive (rel to Patm), causing air to flow out of the lungs Patm Remains constant (760 mmHg at sea level) Flow of air in typical respiratory cycle 1) Diaphragm contracts, intercostal muscles elevate ribs, increasing volume of thoracic  cavity 2) Pip becomes more negative, creating a greater pressure gradient across the lungs 3) Ptp increases, expanding lungs 4) Palv becomes neg relative to Patm, causing air to flow into lungs 5) Increase in lung volume as air fills alveoli Exhalation 1) Diaphragm and intercostal muscles relax, reducing volume of thoracic cavity 2) Pip becomes less negative (closer to 0), Ptp decreases 3) Palv increases rel to Patm, causing air to flow out of lungs 4) Lung volume decreases as air is expelled from alveoli Mini lesson 6 Learning Objectives: Explain how lung compliance and airway resistance are the main determinants of the work of breathing and predict how disease states can affect these two factors. Define the normal lung volumes and capacities, including the forced expiratory volume in one second, explain how they are clinically measured, and predict the impact of disease on lung volume and capacity measurements. Key Terms: anti-inflammatory drugs: medications reduce inflammation in airways, often used for asthma, COPD Asthma: bronchoconstriction, increased mucus production bronchodilator drugs: relax bronchial smooth muscle, dilating airways (include B2 antagonists) chronic bronchitis: form of COPD- chronic inflammation and excessive mucus production, persistent productive cough w/ mucus production chronic obstructive pulmonary disease (COPD): progressive lung disease, includes chronic bronchitis and emphysema, chronic airflow limitation and persistent respiratory symptoms expiratory reserve volume (ERV): max volume of air that can be exhaled forcefully after normal tidal expiration forced expiratory volume in 1 second (FEV1): amount of air that can be exhaled forcefully in first second of forced expiration, measured with spirometry functional residual capacity (FRC): volume of air remaining in lungs after normal expiration inspiratory reserve volume (IRV): max volume of air inhaled after a normal tidal inspiration lateral traction: stretching force on small airways, helps keep airways open during exhalation law of Laplace: relationship between surface tension in sphere and its radius (P=2T/r) lung compliance: ease with which lungs expand obstructive lung disease: difficulty exhaling air from lungs bc of obstruction or airway narrowing (asthma, chronic bronchitis, emphysema) residual volume (RV): volume of air in lungs after a forceful exhalation restrictive lung diseases: reduced lung volume due to stiff, less compliant lungs (pulmonary fibrosis, sarcoidosis, interstitial lung disease) surface tension: occurs at air-liquid interface in alveoli, tends to collapse alveoli, surfactant reduces it tidal volume (Vt): volume of air inhaled or exhaled during normal, quiet breathing (~500 mL) vital capacity (VC, or forced vital capacity, FVC): total volume of air can be exhaled after maximal inhalation Study Questions: 1. What are two general factors that determine the work of breathing? 1) Lung compliance 2) Airway resistance 1. What are the determinants of lung compliance and what is the impact of increasing or decreasing it compared to normal compliance? Compliance = △V/△Ptp Increasing lung compliance → easier to inflate Decreasing lung compliance → increases work it takes to inflate Floppy lung tissue INCREASES compliance ○ Emphysema Fibrous tissue (collagen) DECREASES compliance ○ Pulmonary fibrosis Surfactant in alveoli INCREASES compliance 1. What does surfactant do and what is the relationship between surfactant and surface tension in the lung? Surfactant increases compliance  Makes it easier to expand volume Opposes collapsing surface tension from water ○ Disrupts H-bonds from forming (water), H bonds increase surface tension Secreted by type II alveolar cells ○ Deep breath increases secretion by stretching them Lowers surface tension of water layer at alveolar surface, increases lung compliance Effect is greater in smaller alveoli 1. How does surfactant stabilize alveoli by preventing small alveoli from emptying into large alveoli? Law of laplace: P=2T/r Without surfactant Surface tension equal between alveoli Pa 46 Systemic venous blood PO2 = 40 PCO2 = 46 Pulmonary arterial blood PO2 = 40 PCO2 = 46 1. How do partial pressure gradients promote net movement of gases between the atmospheric air and alveoli, between alveoli and pulmonary capillaries,  and between systemic capillaries and cells in the body? Alveolar pressures determine quality of systemic arterial blood 1. How does high altitude affect the availability of atmospheric oxygen and carbon dioxide and what affect does this have on alveolar PO2 and PCO2? Higher altitude → less availability of atmospheric oxygen bc pressure decreases, lower alveolar PO2 To compensate fro less O2 availability, body increases ventilation, lowering alveolar PCO2 1. How do changes in the rate of alveolar ventilation or the rate in metabolism determine alveolar PO2 and PCO2? Hypoventilation: producing CO2 faster than exhaling it; accumulating in the body Alveolar PO2 decreases Alveolar PCO2 increases Hyperventilation: blowing off CO2 faster than producing it Alveolar PO2 increases Alveolar PCO2 decreases 2. What variable distinguishes normal ventilation from hyperventilation and hypoventilation and what is the numerical value that falls into each category? Partial pressure of CO2, normally between 35-45 mmHg Hyperventilation: PCO2 below 35 mmHg Hypoventilation: PCO2 above 45 mmHg 1. What are the layers an oxygen molecule would penetrate in moving from the alveolar air space into the cytosol of a red blood cell? Alveolar air space → type 1 alveolar cells → interstitial space (ECF) → capillary endothelium → plasma (in capillary) → RBC membrane → cytosol of RBC 1. How does the PO2 of blood normally change as it travels along the pulmonary capillaries? Draw a graph to support your answer. Reaches equilibrium at about ⅓ of capillaries length  1. How can certain diseases affect the equilibration of oxygen between alveolar air and pulmonary capillary blood and why is oxygen typically more affected than carbon dioxide? Mini lesson 3 Learning Objectives: Explain how local factors affect airflow and blood flow in the lung in order to match adequate ventilation with adequate blood flow. Explain the ventilation-perfusion inequality that causes the drop in PO2 from alveoli to pulmonary venous blood. Describe how the systemic venous blood reaches a diffusion equilibrium with tissue interstitial fluid. Key Terms: ventilation-perfusion inequality Study Questions: 1. What are two mechanisms that help to match ventilation of different lung areas with the blood flowing to those areas? 1) Local perfusion decreased to match a local decrease in perfusion 2) Local perfusion decreased to match a local decrease in ventilation 1. Why is there typically a 5 mmHg decrease between the alveoli and the pulmonary venous blood? Some blood does not participate in gas exchange, but bypasses alveoli by moving through shunts that connect pulmonary arteries directly to veins. This blood mixes with oxygenated blood, slightly lowering overall PO2 before it reaches the left atrium. Week 11 workshop 2 Mini lesson 1 Learning Objectives: Describe the forms in which O2 is transported in blood and the sequence of events involved in oxygen uptake in the lungs and delivery to the tissues. Explain the physiologic importance of the oxygen-hemoglobin dissociation curve in promoting oxygen loading at the lungs and oxygen delivery at the tissues. Describe the factors that cause left-shifted and right-shifted changes in the affinity of hemoglobin for oxygen and explain the significance of these shifts. Predict the effects of carbon monoxide and anemia on oxygen transport and delivery to tissues. Key Terms: carbon monoxide (CO): colorless, odorless gas, binds to Hb with higher affinity than O2, reduces Hb’s ability to transport oxygen deoxyhemoglobin (Hb): Hb that is not bound to oxygen. More readily available to pick up oxygen in the lungs Globin: protein component of Hb- made of 4 polypeptide chains, surrounds heme groups Heme: molecule within Hb that contains an iron atom capable of binding 1 O2 molecule. Each Hb has 4 heme groups, allowing it to bind 4 O2 molecules. hemoglobin saturation: % of Hb molecules in blood that are fully bound with O2 oxygen-carrying capacity: max amt of O2 that can be transported in the blood, determined by amt of Hb and its saturation oxygen-hemoglobin dissociation curve: graph showing relationship between PO2 and Hb saturation oxyhemoglobin (HbO2): Hb that has bound oxygen, responsible for transporting O2 from lungs to tissues percent hemoglobin saturation: portion of total Hb that is bound to O2 at a given PO2 Study Questions: 1. What are the two ways that oxygen is transported in the plasma? What percentage of oxygen is carried in each of these ways? Which component gives rise to the PO2 of plasma? 1) Dissolved : PO2 (1.5% carried this way) a) O2 is poorly soluble 2) Bound to hemoglobin (98.5% carried this way) a) Once O2 attaches to Hb, it does NOT contribute to partial pressure b) Diffusion of O2 is due to partial pressure gradient 1. What is the basic structure of hemoglobin and how does it bind oxygen? Hb is made up of 4 subunits, each containing a heme group and globin polypeptide. This allows 1 O2 to bind to each heme group, so 4 O2 per Hb 402 + Hb ⇔Hb-O2 1. What does the oxygen-hemoglobin dissociation curve depict? As part of your answer, draw the graph and appropriately label the axes. Depicts PO2 as the Hb saturation % increases. From 0-60 mmHg, small increases in PO2 leads to significant increase in Hb saturation From 60-120 mmHg, small changes in PO2 do not cause much of a change in Hb saturation 1. What is the percent hemoglobin saturation when blood PO2 is 100 mmHg, 60 mmHg, and 40 mmHg? What is the physiological significance of these three data points? PO2 at 40 mmHg = 75% In systemic veins PO2 at 60 mmHg = 90% PO2 at 100 mmHg = 98% In systemic arteries 1. What is the sequence of events involved in oxygen uptake in the lungs and delivery to the tissues? From alveoli to capillary Dissolved oxygen moves first  Saturation of Hb occurs 2nd From capillary to ISF dissolved oxygen moves first Hb unbinding O2 occurs 2nd 1. How do carbon dioxide levels/acidity and temperature affect the oxygen-hemoglobin dissociation curve? What is the physiological significance of a left-shifted vs. a right-shifted curve? In metabolically active tissues: temp increase, CO2 increase = H+ conc increase (decrease pH) Left shift: higher temps, more affinity, O2 binding promoted Right shift: lower temps, less affinity, O2 release promoted 1. Why is carbon monoxide dangerous to your health? How do arterial chemoreceptors respond to carbon monoxide poisoning? CO binds to the same site on Hb as O2 Reduces the content of O2 in the blood Shifts the O2-Hb curve to the left (harder to unload O2 in tissues) With CO poisoning, you suffocate without knowing. PO2 looks normal to chemoreceptors (dissolved content is normal), so you don’t gasp/feel dyspnea 1. What is the effect of anemia on the oxygen-carrying capacity of the blood? Anemia: significant decrease in Hb concentration of blood, reduces oxygen-carrying capacity In person mini lecture Learning Objectives: Describe the forms in which CO2 is transported in blood and the sequence of events involved in carbon dioxide uptake from the tissues and delivery to the lungs. Describe the form in which hydrogen ions are transported in blood between tissues and the lungs. Write the chemical reaction describing the relationship between CO2 and H+ and predict how changes in ventilation affects the pH of the extracellular fluid leading to respiratory acidosis or alkalosis. Key Terms: Carbaminohemoglobin carbonic anhydrase respiratory acidosis respiratory alkalosis total-blood carbon dioxide Study Questions: 1. What are the three ways that carbon dioxide is transported in the plasma? What percentage of carbon dioxide is carried in each of these ways? Which component gives rise to the PCO2 of plasma? What is the chemical reaction that converts CO2 to bicarbonate? 1. What is the sequence of events involved in carbon dioxide uptake from the tissues and delivery to the lungs? 1. What is the significance of the chloride shift mechanism? 1. What is the mechanism that buffers the acidity caused by CO2 carried in systemic venous blood? 1. How does hypoventilation lead to respiratory acidosis and hyperventilation lead to respiratory alkalosis? Use the chemical reaction that converts CO2 to bicarbonate to explain your answer. Quiz week 8 content review Which of the following statements is NOT correct? Skeletal muscle fibers can summate force with an increased stimulation frequency Cardiac muscle fibers cannot summate force with an increased stimulation frequency  Spontaneous production of action potentials occurs in every individual cardiac muscle fiber Spontaneous production of action potentials is not observed in skeletal muscle fibers The prolonged refractory period of cardiac muscle prevents tetanus from occurring in this organ Which of the following distinguishes cardiac muscle cells from smooth muscle cells? Presence actin thin filaments in cardiac cells and absence in smooth cells Need for primary active pumps to remove calcium from cytosol of cardiac cells but not in smooth cells Presence of Transverse tubules in cardiac cells and absence in smooth Need for extracellular calcium to enter cytosol of cardiac cells but not in smooth cells Presence of Sarcoplasmic reticulum in cardiac cells and absence in smooth cells Which of the following options is NOT found in all three types of muscle? ATP is the fuel that powers force generation Desmosomes and gap junctions Elevated cytosolic Ca2+ initiates contraction Negative RMP Sliding filaments and myosin cross bridge cycles Contraction of the ventricular papillary muscles Occurs simultaneously with atrial contraction Opens the atrioventricular valves Open the semilunar valves Closes the atrioventricular valves Prevents backward flow of blood during ventricular systole In a typical healthy individual, blood can be accurately described as: A fluid that is typically found outside the body’s epithelial barrier Approximately one third hematocrit (by volume), approximately 10% white blood cells and platelets (by volume), and approximately two thirds ISF (by volume) A fluid containing the typical ECF solutes plus cells that function in gas transport, clotting, and defense 60% erythrocytes and 40% plasma A fluid that is virtually identical in composition to ICF plus it has red blood cells, white blood cells, and platelets Which of the following statements regarding sickle-cell disease/trait is CORRECT? People that are heterozygous for this mutation are also more resistant to malaria (a blood infection caused by a protozoan parasite) If a person is identified as having sickle-cell trait, then that person has two copies of the mutated gene, one from each parent, and they are homozygous for the mutated gene  If a person identified as having sickle-cell disease, then their spleen will be healthy and unaffected Low oxygen levels in the environment improve the survival for those afflicted with this condition This condition is caused by a genetic mutation that alters several amino acids in the myoglobin subunits Which of the following options would DECREASE the flow of blood the most? Decreasing the radius to half the original value Decreasing the length of the vessel to half the original value Decreasing the viscosity of the blood to half the original value Increasing the radius by doubling the original value Increasing the pressure difference by doubling the original value The sino-atrial (SA) node is referred to as the “true pacemaker” of the heart because: Its pacemaker potential depolarizes to threshold sooner than that in the AV node cells and conducting cells Its fast neuronal-like sodium channels are more numerous than those in the AV nodal and conducting cells It has transient calcium channels while the AV node cells and conducting cells do not It has funny sodium channels while the AV node cells and conducting cells do not Its potassium-dependent repolarization is slower than that in the AV node cells and conducting cells Listening to someone's heart you detect an abnormal sound. It occurs between the typical valve sounds like this: Lub-Dup-Gurgle-Lub-Dup-Gurgle. What is your diagnosis? A stenotic AV valve An insufficient semilunar valve An insufficient AV valve There is a small stream running through their chest A stenotic semilunar valve Which of the following describes the ventricular ejection period? The mitral valve is open and the aortic semilunar valve is closed The aortic semilunar and mitral valves are both open The aortic semilunar valve is open and the mitral valve is closed The aortic semilunar and mitral valves are both closed Which of the following is CORRECT regarding a Lead I ECG Trace Q wave: evidence of depolarization of atrial cells S wave: evidence of depolarization at the apex of both ventricles R wave: evidence of depolarization of the AV node P wave: evidence of atrial hyperpolarization  T wave: evidence of repolarization of ventricles Use this figure to determine the QRS axis diagnosis for this patient typical/healthy Abnormal right ventricle hypertrophy Left axis deviation Extreme right axis deviation Week 9 content review quiz Which of these pressures is the mean arterial blood pressure in a person whose systolic blood pressure is 135 mmHg and pulse pressure is 54 mmHg? 63 mmHg 41 mmHg 99 mmHg 108 mmHg 81 mmHg Which of the following would decrease cardiac output in a typical healthy individual? An increase of blood volume Increased parasympathetic activity Constriction of the large systemic veins An increased EDV Increased sympathetic activity The frank-starling relationship reveals: The influence of ESV on ventricular stroke volume The influence of heart rate on ESV The load-velocity relationship in cardiac muscle The influence of EDV on ventricular stroke volume The influence of conduction velocity on stroke volume Which of the following does NOT happen when we observe vasodilation of a systemic ARTERIOLE? An increase of blood flow through that arteriole An increase of radius for that arteriole An increase of the resistance to flow for that arteriole A decrease of metabolic wastes in the downstream local environment An increase of O2 in the downstream local environment Which of the following would induce vasoconstriction of an arteriole? Nitric oxide Low physiological dose of epinephrine Atrial natriuretic peptide hormone Angiotensin II peptide hormone Increasing adenosine levels in the downstream local environment Which of the following structures has blood that we expect to be low in oxygen content? Systemic artery Pulmonary veins Right ventricle Aorta Left atrium Which of the following characteristics is NOT applicable to the systemic capillaries? Blood flow is typically 5 liter/min when all capillaries are considered together as a group Each capillary has a small diameter of 7-8 um Each capillary has an inner layer of endothelium and an outer thin layer of smooth muscle Blood velocity is slow in each individual capillary All of the capillaries together have a very large cross-sectional area Which of the following does NOT lead to edema in the body? Starvation Heart failure A decreased Pc due to hemorrhaging A decreased protein concentration in the plasma Blocked lymph vessels Factors that aid venous return in the systemic circulation include: Skeletal muscle pumps in combination with one-way semilunar valves Small radius, large resistance venous vessels Floppy, large radius venous vessels Parasympathetic stimulation of the venous vessels Which of the following is TRUE regarding diffusion across the capillary walls? Concentration and pressure gradients are what drive solute and gas movements. Majority of the exchange for gasses, nutrients, and wastes occurs by bulk flow and not by diffusion. Hydrophobic substances diffuse only through pores between the endothelial cells. Plasma proteins diffuse only through the pores between endothelial cells. Hydrophilic substances diffuse directly through endothelial cell membranes. Sympathetic stimulation of the heart: is delivered by the vagus nerve decreases heart rate increases the contractility of the myocardial cells lowers stroke volume at a fixed end-diastolic volume decreases the permeability of K+ channels in sinoatrial node cells Parasympathetic stimulation of the heart: decreases the current through funny sodium channels increases the current through Transient Ca?+ channels regulates both the atria as well as the ventricles is mediated by the neurotransmitter norepinephrine increases the force of contraction in contractile cells Week 10 Content review quiz Which of the following statements about baroreceptor reflex is TRUE? If a greater MAP occurs, then there will be: more aortic wall stretch, an increase of the action potential frequency from baroreceptors, and less activation of the parasympathetic medullary control nuclei If a greater MAP occurs, then there will be: less aortic wall stretch, an increase of the action potential frequency from baroreceptors, and less inhibition of the sympathetic medullary control nuclei A decrease of the action potential frequency from baroreceptors will cause more activation of the parasympathetic medullary control nuclei A decrease in the action potential frequency from baroreceptors will cause less inhibition of the sympathetic medullary control nuclei Joe speedo has an increased MAP due to your dastardly injections into his body. Which of the following would be a possible direct cause of the increased MAP? You gave him an a-1 receptor agonist drug Your drug reduced his heart rate You gave him a B1 receptor antagonist drug You gave him a sympathetic antagonist drug You increased his parasympathetic influence on the SA node What is responsible for the fact that the resting heart rate can be 60-70 beats per minute even though the intrinsic discharge rate of the SA node is 100 per minute? Action potentials from the baroreceptors inhibit the cardioinhibitory center Action potentials from the baroreceptors inhibit the vasomotor center Action potential from the baroreceptors stimulate the cardioacceleratory center Action potentials from the baroreceptors stimulate the cardioinhibitory center Which of the following is TRUE regarding the chemoreceptors we covered in this course? Central chemoreceptors detect the levels of oxygen in arterial blood Central chemoreceptors are located in lung tissue Peripheral chemoreceptors detect amounts of gas in arterial blood Peripheral chemoreceptors detect the amount of oxygen in brain tissue Central chemoreceptors prevent cushing’s phenomenon from occurring With your Home-Physiology kit you measure the vital functions of a fellow student, and they are: 1. Heart Rate = 78 beats/min 2. Blood Pressure = 125/95 3. Respiration Rate = 12 breaths/min 4. ESV = 40 ml 1. Total blood volume = 4.8 Liters 2. EDV = 120 ml 3. Body weight = 175 Ibs, 4. I.Q. = 141 5. Astrological Sign = Capricorn. What is this student's cardiac output? 37.4 L/min 80 mL/min 6.24 L/min 3.12 L/min Insufficient information is provided Which of the following statements is FALSE? Smooth muscle regulates the radius of bronchioles in both zones. Phonation occurs in the respiratory zone.  Gas exchange does not occur in the conducting zone. The respiratory zone moves oxygen and carbon dioxide into and out of the blood. Trachea and large bronchi are part of the conducting zone. Alveoli are part of the respiratory zone. Which of the following muscle types is correctly matched to its role in respiration? Sternocleidomastoid muscle: forced exhalation Diaphragm muscle: unforced exhalation Abdominal muscles: forced inhalation External intercostal muscles: forced exhalation Internal intercostal muscles: forced exhalation Which of the following is NOT a function performed by the respiratory system? adding and subtracting chemical messengers to or from the blood exchange of blood gases increase ADH secretion from the alveoli defense against pathogens Traps and dissolves blood clots Which of these BEST explains why air flows into the lungs during inhalation? the pressure in the intrapleural space rises above atmospheric pressure. the pressure within the alveoli falls below atmospheric pressure the lungs recoil and reduce their volume the pressure in the intrapleural space increases by 2 mmHg the chest cavity reduces volume Which of these changes would make breathing easier? a decrease in the radius of the bronchioles an increase of resistance to flow in the bronchioles an increase of surfactant secretion a decrease in the elastic recoil of the lung a decrease in the compliance of the lung Which of the following is TRUE during a typical quiet inhalation? Contraction of the diaphragm increases the volume of the thoracic cavity. Atmospheric pressure remains below alveolar pressure during the process. The volume of the lungs becomes less than the FRC volume. Intrapleural pressure remains positive throughout the process. Transpulmonary pressure decreases throughout the process. Which of the following is correct? Type I alveolar cells have cilia that function in the mucus escalator. Type I alveolar cells remove airborne infectious agents.  Type I alveolar cells actively pump 02 into the blood while Type II alveolar cells pump CO2 out of the blood. Type Il alveolar cells secrete surfactant. Type Il alveolar cells form the airways in the conducting zone.