BMS 420 EXAM 1 QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026

BMS 420 EXAM 1 QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026 Purpose of a circulatory system - Answers deliver nutrients and remove by-products of metabolism Single-cell organisms - Answers Do diffusion directly with environment, don't need a circulatory system What happens as diffusion distance increases? - Answers Pressure decreases & cells further away get their nutrients slower, and the supply is reduced by closer cells 60-40-20 rule - Answers 60% of body weight is water 40% is found in cells 20% is found in extracellular part Fluid Movement: Sweating - Answers Water is lost from extracellular compartment (interstitial), remaining interstitial fluid becomes hypertonic (inc [solute]) - water pulled from intravascular (plasma) compartment, inc plasma osmolarity leads to osmotic mvmd of water from in cell to out of cell Homeostasis of cells dependent on - Answers composition of interstitial fluid - adequate blood flow - pressure & resistance - minimal diffusion distances Pulmonary circulation is (in series/parallel) with systemic circulation? - Answers in series so all of O2 rich blood can move out into systemic circulation Organs arranged in (series/parallel)? - Answers parallel so blood to all organs has identical composition, flow thru organs can be controlled independently of other organs What influences the distribution of blood flow? - Answers Local metabolism Constricting diameter of vessel = - Answers decrease blood flow downstream, increasing resistance Veins are (conductance/resistance) vessels taking blood (to/away from) heart - Answers conductance, take blood to heart Arteries are (conductance/resistance) vessels taking blood (to/away from) heart - Answers conductance, away from heart arterioles are (conductance/resistance) vessels - Answers resistance - regulate flow to peripheral organs Capillary bed function - Answers ensure that no cell is more than 10 micrometers form the capillaries Capillaries are the site of - Answers exchange of nutrients and waste Process of blood carrying substances to tissues is - Answers convective transport Bulk flow - Answers all constituents of blood move together Rate of transport of any individual substance in blood is determined by - Answers -concentration of the substance - blood flow Formed elements of blood - Answers -RBCs -WBCs -Platelets Plasma in blood is - Answers a solution of electrolytes and proteins - albumin, fibrinogen Hematocrit - Answers the proportion, by volume, of the blood that consists of RBCs (%) Hydrostatic pressure - Answers the pressure exerted by a fluid - varies throughout the system and w/ body orientation - heart must generate enough pressure/force to move blood throughout the system Mean arterial pressure - Answers Pressure in the aorta - any drop in this negatively impacts the ability to perfuse the tissues and maintain homeostasis Hydrostatic pressure equation - Answers P_hydrostatic = column height * relative density of blood to mercury * acceleration force Blood flow equation - Answers Q = pressure difference / resistance Resistance equation - Answers R= P/Q (flow) = 8 * viscosity * length/( pi * radius^4) Poiseuille equation (describes flow through a cylindrical vessel) - Answers Q = (pressure difference) * (pi) * (r^4) / (8) * (length) * (viscosity) Role of arterioles - Answers Resistance vessels, do changes in vessel diameter Pressure difference (w CV as a single unit) equation - Answers Pressure difference = MAP - CVP - CVP will always be 0 mmHg for this class Location of highest resistance/site of regulation - Answers across the arterioles Why is the highest resistance in layer 0 of a vessel - Answers because friction occurs as blood interacts with the lining of the vessel. Known as shear stress Location of lowest friction? - Answers Middle of vessel, least friction Viscosity increases with - Answers - increase hematocrit - decreased temperature Total Peripheral Resistance (TPR) - Answers The overall resistance to flow through entire systemic circulation - influenced by flow pattern Resistance in series - Answers R(total) = R1 + R2 +R3 Resistance in parallel - Answers 1/R(total) = 1/R1 + 1/R2 + 1/R3 Why does velocity increase from capillaries -- venules -- veins? - Answers This is due to the cross sectional areas. The same volume of blood has to go through fewer tubes, so it must go faster in order to maintain its rate. Route of Cardiac Conduction - Answers Sa node - AV node - Bundle of His - bundle branches - purkinjie fibers Propogation of AP: gap junctions - Answers electrostatic attraction causes a local current (ion movement) through the gap junctions Cardiac skeleton - Answers Electrical insulator between atrial muscles and the ventricles - only electrical pathway between atria and ventricles is the AV node/bundle - forces propagation through the AV node Cardiac skeleton prevents - Answers heart from depolarizing as one single unit, so we have adequate filling time Delay at AV node due to - Answers -small size of AV nodal cells (inc resistance) - slow rate of rise of AP in AV nodal cells AV node delay physiological importance - Answers - allows time for atrial depolarization, contraction and emptying into the ventricles - limits frequency of ventricular activation Dromotropic effect - Answers Conduction velocity - fiber diameter (smaller = slower) - rate of rise of AP (influenced by types & # of channels present resistive properties of" - cell membrane - gap junctions - cytoplasm chronotropic effect - Answers Pacemaker activity, heart rate - change diastolic potential - change threshold - change slope of phase 4 depolarization Inotropic effect - Answers contractility lusitropic effect - Answers relaxation SANS and PANS can both influence - Answers heart rate (chronotropy) and dromotropy SANS additionally influences - Answers -force of contraction (inotropy) - relaxation (lusitropy) PANS branch - Answers Vagus nerve -left = AV node -right = SA node -only atrial innervation Primary controller of heart rate under normal circumstances - Answers PANS Vagal tone - Answers Intrinsic heart rate set by the SA node, but this is lowered by vagal tone - low level PANS suppresses the heart rate by 20-30 bpm PANS neurotransmitter - Answers acetylcholine - cholinergic, binds to muscarinic receptor Result of Ach (PANS input) - Answers -decrease # of positive ions coming into the cell through HCN channel, thus going further away form threshold - inside of cell becomes hyperpolarized - increase potassium permeability, more goes out of the cell Step by step of Ach impact - Answers Ach + M2 receptor - inhibitory G protein activation - decreased cAMP - decreased inward pacemaker current thru HCN channel, slowing heart rate Negative chronotropic effect - Answers - normal - longer to reach threshold, hyperpolarized - decreased slope of pre-potential (even longer to reach threshold) lowered HR SANS branch: sympathetic cardiac nerve - Answers left branch - AV node & ventricles right branch - SA node sympathetic cardiac nerve innervations - Answers -SA node (chronotropic) - AV node (dromotropic) - Atria (inotropic & lusitropic) - ventricles (inotropic & lusitropic) Sympathetic input step by step w norepinephrine - Answers NE + B1 receptor - stimulatory G protein activation - more cAMP - more open-state probability of HCN channel - greater current Effect of NE on SA node (chronotropic effect) - Answers -decrease membrane potential due to Na & Ca influx (faster to reach threshold) - increased slope of pre-potential Increased HR NE-induced decrease in AP duration - Answers ^ intracellular Ca - ^ K permeability - terminates phase 2 (plateau) early - early repolarization - shortens absolute refractory period - ^ AP generation - ^ contraction rate Slow response AP cells - Answers cardiac pacemaker cells (auto-rhythmicity) Fast réponse AP cells - Answers Cardiac muscle fibers (contractile) - conduction system electrical events ALWAYS _____ mechanical events - Answers precede/come before There is a _____ of AP types throughout the heart - Answers gradient Cells have different & unique combinations of currents due to - Answers type & number of ion channels AP slow response steps - Answers 1. Hyperpolarization due to K leaking out of cell 2. From HCN channel, Na and Ca leak in, some K leaks out 3. hit pacemaker potential (pre-potential), hit threshold 4. Depolarization with Ca influx, Ca channels open 5. Repolarization. Ca channels close. K efflux via voltage gated delayed rectifier channels. Na gradients reset. Goes back down to -70 mV AP fast response steps - Answers -Phase 4: voltage gates Na channels open -Phase 0: depolarization due to Na influx -Phase 1: very brief. Na channels inactivated. K efflux via VG channels, Ca influx via VG channels -phase 2: Plateau phase. -Phase 3: delayed outward current/repolarization. Ca channels close. K efflux via VG delayed rectifier channels. Na VG channels close - phase 4: K delayed rectifier channels close When is the fast response absolute refractory period? - Answers from depolarization to the beginning of repolarization. The rest of repolarization is the relative refractory period Where are fast response APs present? - Answers -atrial & ventricular muscle -fibers of conduction system How are fast response APs different from that of nervous & skeletal muscle tissue? - Answers The shape of AP due to the plateau phase, where the fast response cannot be tetanized Define cardiac output & its two determinants - Answers Cardiac output is the amount of blood that the heart pumps through the circulatory system in a minute. It is determined by heart rate and stroke volume (volume of blood ejected from ventricles during contraction) Similarities btwn cardiac muscles and skeletal muscles - Answers - have bundles of myofibrils that contain myofilaments (actin & myosin) - T tubules - tropomyosin - troponin regulatory complex How cardiac myocytes are different from skeletal muscle - Answers - shorter - mononucleic - branching (connect to other cardiac myocytes at intercalated disks via gap junctions), form a functional syncytium - high [mitochondria] What happens if one cardiac myocyte is stimulated (based on the functional syncytium)? - Answers All cells will contract unless there is damage or scar tissue blocking flow of electrical signal through the gap junctions Can damaged cardiac myocytes repair themselves? - Answers Not very well. Dead cells are often replaced by scar tissue Are there cardiac stem cells? - Answers Yes, but they don't work as well as the original cells, so cardiac function is reduced excitation-contraction coupling (ECC) - Answers Contraction is initiated by a membrane action potential that is propagated internally to the contractile mechanism of the cardiac myocyte Contractility is influenced by: - Answers - initial cardiomyocyte length - neural innervation excitation-contraction coupling: contraction - Answers - when VG Ca channels open, Ca rapidly moves down its conc gradient into the cell During ECC when Ca is in the cytoplasm: - Answers 1. Ca is used for muscle contraction 2. Ca binds to ryanodin receptors in SR to open Ca channels in the SR (very high [Ca]) - calcium induced calcium release ECC relaxation - Answers Na/Ca exchanger takes 1 Ca out for 3 Na in. Ca ATPase takes Ca out, and Serca pump (bound to phospholamban) does 80% of Ca removal to reset the membrane potential (T/F) Muscle tension develops as a function of inotropic state - Answers True (T/F) contractility relates to the interaction between actin and myosin independent of changes in sarcomere length - Answers True Resting tension - Answers tension due to the initial stretch on fiber at rest (no contraction present) Preload - Answers - volume of blood in ventricle at end of diastole before contraction (systole) - end-diastolic volume - *influences resting tension* Peak isometric tension - Answers Isometric contraction - muscle is activated (contracting) but held at a constant length (no active shortening) peak/max tension for a given starting length is its peak isometric tension. What is this determined by? - Answers determined by inotropic state (number of actin-myosin cross-bridges formed) Isometric contraction - Answers Muscle contracts but there is no movement, muscle stays the same length. Isovolumetric contraction = no change in ventricular volume Isotonic contraction - Answers Muscle tension/contraction stays same (fixed load) with change in muscle length after loaded isotonic contraction - Answers - isovolumetric contraction until muscle tension is greater than afterload - aortic valve opens - muscle shortens - blood is ejected Starling's law of the heart: length-force relationship - Answers The greater the initial stretch (preload), the greater the force of contraction, and the greater the stroke volume - big preload = big contraction, big stroke volume What does sympathetic input do to length-tension relationship? - Answers - positive inotropic effect, mechanism to increase contractility - more ventricular shortening = smaller end systolic volume = more blood ejection (higher ejection fraction) - higher peak isometric tension SANS Input: positive inotropic effect - Answers - NE acts via a beta-1-adrenergic receptor to open Ca channels on membrane & SR - increases intracellular Ca, Ca induced Ca release from SR - Results in more rapid & forceful contraction of ventricular muscles (inotropic effect), inc ejection fraction of blood from ventricles SANS Input: positive inotropic effect steps - Answers NE + B1 receptor - G protein - increased cAMP - increased PKA - phosphorylation of Ca channel - increased rate & force of contraction Sympathetic input: positive lusitrfpic effect - Answers - NE induced phosphorylation of phospholambanon SERCA pump - uses beta-1 adrenergic receptor - increased rate of re-uptake of Ca bySR after contraction -- decreased cytoplasmic [Ca] - dec Ca binding to troponin - dec cross-bridge formation - results in faster myocardial relaxation Sympathetic input: positive lusitrfpic effect steps - Answers NE + B1 receptor - G protein - inc cAMP - inc PKA - phosphorylation of phospholamban SANS positive chronotropic effect - Answers - NE induced decrease in AP duration - inc intracellular [Ca] - inc K permeability - terminates phase 2 (plateau) early - inc AP generation - inc HR P wave represents what - Answers atrial depolarization A difference in P wave duration means what kind of atrial pathology - Answers ischemic damage to atrial cardiomyocytes PR interval represents - Answers activation of SA node (P wave) to the beginning of the ventricular muscle depolarization (start of Q wave) PR interval pathologies - Answers - 1st degree AV block (prolongation of PR interval) - 2nd degree AV block (conduction of atrial impulse through the AV node and/or His bundle is delayed or blocked QRS wave represents - Answers transfer of impulse throughout ventricular muscle - coordinated contraction of both left & right ventricles due to effectiveness of purkinje system (low resistance, fast velocity) QRS pathologies - Answers - bundle branch blockages (widened QRS complex, waveform complex) ST segment - Answers Interval between ventricular (QRS complex) and depolarization (T wave) - plateau phase of fast response AP ST segment pathology - Answers - displacement of ST segment is of particular importance in acute myocardial ischemia ST elevation - Answers acute myocardial infarction ST depression - Answers acute ischemia T wave represents - Answers ventricular repolarization - relative refractory period QT interval represents - Answers the time it takes for the ventricles of the heart to depolarize and repolarize - not affected by pathological conditions, but varies with heart rate (inc HR = dec QT interval) QT interval during exercise - Answers is faster, happens in shorter period of time - SANS input - inc HR - faster ventricular depolarization ECG gives information on: - Answers - conduction disturbances - presence of ischemic damage - orientation of heart in thorax - mass of cardiac muscle - electrical effects of drugs & electrolytes NOT mechanical or contractile properties bc those aren't electrical R-R interval - Answers The time elapsed between two successive R waves of QRS - represents cardiac cycle length (inverse to HR) Why is left heart "pump" high pressure? - Answers left side is systemic circulation, so the blood it pumps out has to go through whole body Why is the right heart "pump" low pressure? - Answers Right side is pulmonary circulation, has less area to force blood through 5 basics for the heart to pump properly - Answers 1. contraction of individual cardiac muscles cells occurs at regular intervals and are synchronized 2. valves open fully (not stenotic) 3. valves cannot leak 4. muscle contractions must be forceful ventricles must fill adequately during diastole The cardiac cycle has one complete sequence of: - Answers - cardiac filling - cardiac muscle excitation & contraction with blood *ejection* - cardiac muscle relaxation 2/3 of cardiac cycle is spent in diastole or systole? - Answers diastole, left AV valve is open, chambers are filling with blood 1/3 of cardiac cycle is spent in diastole or systole? - Answers systole, left AV valve is closed, chambers are contracting Which node determines the duration of the cardiac cycle? - Answers SA node. starts electrical conduction What factors affect cardiac performance? - Answers Heart rate (SA node activity) Stroke volume (preload, after load/aortic BP & contractility) What is heart rate influenced by? - Answers degree of neural innervation; PANS is primary, and there's SANS too (T/F) changes in heart rate result in proportional changes in cardiac output - Answers False. a change in heart rate can inversely impact stroke volume, so CO would stay the same Preload/EDV is influenced by: - Answers - venous pressure - ventricular compliance (inc compliance = inc filling/EDV pressure) - HR (inc heart rate means less filling time, lower EDV) - atrial contraction (contributes to EDV, SANS input inc atrial contraction to maintain EDV at higher HR) - inflow resistance (e.g. AV valve stenosis, regurgitation during systole) - outflow resistance (after load/MAP) - ventricular inotropy (T/F) stretched fibers generate more force per cross-sectional area - Answers True. Greater stretch would cause greater force like a spring. Pathway for an increased starting stretch (Starling's law) - Answers inc venous return - inc EDV - inc preload - inc starting stretch Increasing length develops more active tension via (Starling's law): - Answers 1. increased cross-bridge formation (compression of lattice spacing - inc actin/myosin interaction. Inc Ca affinity of troponin C, inc Ca sensitivity to myofilaments 2. increased tension on stretch-activates Ca channels (enhances Ca entry into the cell - more Ca induced Ca release) How exactly does preload affect cardiac performance? - Answers larger preload = more shortening/muscle contraction, higher SV - EDV increases but ESV stays the same (SV = EDV - ESV) How does after load affect cardiac performance? - Answers increased after load (the downstream pressure that has to be overcome to eject the blood) = less shortening/contraction, heart has to work harder to generate enough force to eject blood - increased ESV What effect does increased after load have on ejection fraction? - Answers EDV will be the same as normal, but SV is smaller so the ejection fraction is decreased Effect of SANS input on cardiac performance/heart pump - Answers muscle can shorten even more due to shift in peak isometric tension What effect does increased waterloos with SANS input have on ejection fraction? - Answers this depends on the degree of SANS input & after load. Same EDV but increased SV as a result of increases SANS = normal/no change in ejection fraction (???) Can an increased stretch/resting tension generate a higher peak tension for a given sarcomere length? - Answers Yes due to increased contractility - only changes in contractility cause a left shift in ESV Negative inotropy results in - Answers - dec contraction velocity - dec muscle shortening - dec stroke volume Regulation of inotropy steps - Answers 1. phosphorylation of L-type Ca channels (enhancing permeability) 2. enhanced Ca release by SR 3. enhanced Ca binding to Tn-C 4. Myosin phosphorylation via inc cAMP 5. Ca uptake by SR by SERCA pump with phosphorylation of phospholamban 6. regulation of Ca efflux form myocyte via Na/Ca exchanger and ATP-dependent Ca pump preventing Ca overload (if inhibited, inotropy is enhanced) Primary fuel for heart - Answers ATP - without ATP regeneration, would deplete stores in 10 seconds