Physio II Exam 2 Review.docx

Exam 2 Review FUUUUUUUUUUCK THIS EXAM THO Chapter 9 – Cardiovascular system (some shit about part “I”?) Part A–last few topics (slides 23-38) not slide 37 and Part B–all of it Conduction system How the pace of the heart is controlled by the conduction system 3 pacemakers → SA node, AV node...

Exam 2 Review FUUUUUUUUUUCK THIS EXAM THO Chapter 9 – Cardiovascular system (some shit about part “I”?) Part A–last few topics (slides 23-38) not slide 37 and Part B–all of it Conduction system How the pace of the heart is controlled by the conduction system 3 pacemakers → SA node, AV node, Purkinje fibers (see below) What organs/systems can influence heart rate Brain → sympathetic vs parasympathetics Nervous system Endocrine system → hormones How is it controlled otherwise? APs fire down the heart similarly to neurons Fast, electrical, particular direction, etc Ion graph: significance of calcium Na+ leaking into SA node cells → slow rise of SA node AP graph up to threshold of -40 mV → activates slow Ca2+ channels to open → graph shoots up → pacemaker fires → command goes to cardiomyocyte → K+ efflux repolarizes Differences between cardiac AP vs AP in neurons/skeletal muscle Neurons & skeletal muscle use Na (depolarize) and K (repolarize) but NO Ca2+ Cardiac AP plateaus bc it uses Ca2+ too, not just Na+ and K+ Cardiac muscle cells have 2 sources of Ca2+ (outside and inside cell) Skeletal muscle cells only have SR inside as a Ca2+ source Heart cells categories: conduction system (focus on cells being asked about in the questions) Conduction system = cells that SPONTANEOUSLY fire electrical commands to tell the cardiomyocytes that it’s time to contract Cardiomyocytes/Myocardial cells = cardiac muscle cells in the atria and ventricles that actually contract to make the heart beat Name the cells in the structure: SA → purkinje (moderator band) Structure and characteristics of each Moderator band: some electrical signal also continues from the Right Bundle Branch into the Moderator band to ensure the right ventricle gets enough electrical signal Pathway that the electrical signal goes through (the order);Delay at AV node & why its important SA node → Internodal pathways → AV node → AV bundle → LBB (left bundle branch) and RBB (right bundle branch) → Purkinje fibers Delay ensures that the atria have ejected their blood into the ventricles first before the ventricles contract Pacemakers Name the pacemakers of the heart and which takes over when and where they are located and what each pace is → how long/how well it will meet needs of the body What are the 4 pacemakers of the heart? Sinoatrial (SA) node → Located in the right atrium (60-100 bpm) Atrioventricular (AV) node → junction of the atria & ventricles (40-60 bpm) Only takes over if SA node fails! Ventricles: 20-40 bpm → cannot sustain life Atria: 60-80 bpm (not listed as one of the 4 on hers) Purkinje fibers → spread within the ventricular walls (25-35 bpm) Cannot sustain life; Only takes over if SA and AV nodes both fail Ie: you will feel weak, tired, syncopal Functional Syncytium: know what it means basically and importance Function in sync essentially: all atrial cells contract then delay then ventricles get the signal then contract together (all very fast) If they were out of sync → fucks you up Uses intercalated discs & gap junctions Skeletal muscle does not do this, specific to cardiac muscle Chapter 9 Pt B Relationship between excitation and contraction and how they work together Excitation-Contraction Coupling Excitation = fire the AP → move ions in/out of cardiac muscle cell Contraction = Ca2+ that you bring into muscle cell (during plateau) cause actin and myosin to perform contraction of that muscle cell Where calcium is coming from? SR & coming from the outside through L-type channel → activated ryanodine receptor → SR releases Ca into sarcoplasm → stimulates actin/myosin Refractory Periods of Cardiac Muscle Absolute = another AP CANNOT be fired because ion concentrations must be reset Relative = another AP CAN be fired but its harder since ions are fully reset 4 phases (slide 18 on chapter 9 part 2) Phase I: Period of Filling End-systolic volume = 50mL blood remains in ventricle after systole End-diastolic volume = 120mL Phase II: Isovolumetric Contraction Finishes filling → isvolumetric contraction to close valves (S1) before systole Volume of the ventricle does not change; pressure is equal to Aorta (80mmHg) Phase III: Period of Ejection Systolic pressure rises even higher and volume inside ventricle decreases Phase IV: Isovolumetric Relaxation After systole, aortic valve closes (S2) and ventricle pressure = diastolic pressure Compare action potentials in neuron, skeletal muscle, cardiac muscle cell (slide 13-14) Differences between Cardiac AP vs Skeletal AP 1) Skeletal muscle use Na+ to depolarize & K+ to repolarize, but NO Ca2+ 2) Cardiac AP plateaus because it uses Ca2+, too, not just Na+ and K+ Also, cardiac muscle cells have 2 sources of Ca2+ (outside and inside of cell), while skeletal muscle cells only have SR inside as a Ca2+ source Potassium for lethal injection Large quantities of potassium can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle Elevation of K+ can cause severe weakness of the heart, abnormal rhythm, and death Slide 17 – “understand this very very well” “Pressure-Volume-Time” graphs and EKG graph Chapter 10 – Rhythmical Excitation of the Heart LOs on first slide(?) Describe structures and events of conduction system (in previous ppt) Red = AP of Pacemaker cell Na+ leaking in until -40mV → Ca++ rushes to depolarize Peak = action potential triggering cardiomyoctye K+ rushing out = depolarization Green = Cardiomyocyte AP (Phase 4 → 0 → 1 → 2 → 3) Pacemaker AP triggers Na+ to rush in (depolarization) K+ out & Ca++ in create plateau Ca++ closes & K+ rushes out → repolarization Know the structures and events in creating an AV bundle delay (slide 8) Internodal pathways transmit the cardiac impulse throughout the atria How do we accomplish the delay? AV bundle delays cardiac impulse, nodes move through fibrous tissue near the bundle → delay = PR interval SA node as the pacemaker – how does it work? (slide 5/6) Leaking changes the graph AP and helps reach threshold (-40) to fire Ectopic pacemakers What's on the slide → know it, what it is A portion of the heart with a more rapid discharge that surpasses the sinus node Also occurs when transmission from SA node through the A-V node is blocked (A-V block) SA node discharge does not get through, and next fastest area of discharge becomes pacemaker of the heart New pacemaker is in AV node or penetrating part of AV bundle If that region fails, Purkinje fibers take the lead Symp & Para effects on SA node → do they effect the HR or not? SV or not? How? Parasympathetics only decrease HR → decrease CO Nerve fibers (Vagus) are distributed to the SA & AV nodes Sympathetics increase HR and Force of Contraction (SV) → increase CO Nerve fibers are distributed to all parts of the heart; a lot in ventricles Parasympathetics don’t decrease SV, its just LESS sympathetic signal Slide 15 how does the graph shift Idk there’s no fucking info on the slide and nothing is labeled on the graph… Chapter 13 – Cardiac Arrhythmias (same EKG strips as powerpoint) Causes: abnormal rhythm of pacemaker, ectopic pacemaker, blocked impulse, abnormal pathways, spontaneous abnormal impulses from any part of the heart Recognize patterns on EKG strips and what she said about it on the slide SA block → no P waves AV block → ischemia of A bundle, scar tissue, inflammation, vagal stimulation, Dig tox Incomplete Heart Block (1st Degree) → prolonged PR interval (>0.20 sec) Mobitz Type 1 (Wenckebach) → lengthen, lengthen, drop Mobitz Type 2 → fixed PR, random dropped beats Complete (3rd degree) → total block through AV bundle; P waves are random as fuck Incomplete Intraventricular Block (Electric Alternans) – on/off block in Purkinje system Results in abnormal QRS waves (big → small → big → small “alternating”) Causes = ischemia, myocarditis, Digoxin toxicity Name situations when tachy/brady Tachycardia >100 bpm Caused by (1) exercise, (2) increased body temperature, (3) sympathetic stimulation (such as from loss of blood and the reflex stimulation of the heart), and (4) toxic conditions of the heart. Bradycardia < 60 bpm athletes who have a large stroke volume, excessive vagal stimulation (e.g., carotid sinus syndrome) Atrial Paroxysmal Tachycardia – series of rapid heartbeats; suddenly start & then suddenly stop Can be stopped with a vagal reflex or drugs; P wave is inverted if origin is near A-V node Occurs by re-entrant pathways Ventricular Paroxysmal Tachycardia (PVCs) – due to ischemia damage; may lead to VFIB Caused by circus movements – not on the exam A-Flutter → single large impulse wave travels around atria in one direction (200-350 beats/min) Vfib → due to Electrical shock & ischemia Cardiac Arrest → usually due to hypoxic heart prevents muscles & conductive fibers from maintaining electrolyte gradients Unconscious (4-5s), Fatal (1-3mins) if not reversed; Brain damage (5 minutes) A-fib Irregular, fast heart rate occurs because of irregular arrival at the AV node of cardiac impulse from multiple re-entries. Most frequent cause is atrial enlargement. No P wave; QRS frequently of normal duration-voltage-shape. Normal or high ventricular response → Irregular rhythm Efficiency of heart pumping is decreased by 20–30% Defibrillator → all parts of the heart become refractory & stop until new pacemaker is established If used later than 1 minute after fibrillation, heart is too weak to defib → hand-pumped Chapter 14 – Overview of Circulation Blood vessels – physical characteristics and functions Arteries: strong vascular walls, withstand high blood pressure and high velocity Arterioles: control how much blood enters capillary beds Can increase/decrease diameter to direct more/less blood into the capillaries as needed by each tissue at that moment Capillary: thin walls, exchange fluid/nutrient/electrolytes/hormones between blood and interstitium Venules: collect blood from the capillaries → merge w/ larger veins → return the blood to heart Veins: thin walls, but they are muscular enough to contract or expand to serve as a major reservoir of extra blood (during hemorrhage) and have valves to prevent backflow BP in venous system is low pressure bc veins are so far away from the source of pressure (heart) Blood reservoir pressure relationships – how its determined (by distance from the heart) How pressure, flow and resistance relate to each other The closer a blood vessel is to the source (heart) → the higher the pressure Close = arteries (high pressure); Far = veins (low pressure) The larger the cross-sectional area of vessel → the less velocity of blood flow (v) Ex: Aorta = high velocity; Capillaries = very low velocity Laminar vs Turbulent flows and describe relationships Laminar = steady rate (streamline); velocity is fastest in the center of the vessel Turbulent = chaotic as it bounces off vessel walls Increasing resistance (constriction) → decrease in blood flow across the arteriole. At the same time, there’s a larger decrease in pressure across this point because the pressure is lost by overcoming the resistance. Situations that will have turbulent flow 1) if the rate of blood flow (velocity) becomes too great 2) if blood is passing by an obstruction (clot) 3) if the vessel is making a sharp turn (going over ribs) 4) blood passing over a rough surface (atherosclerotic plaque) Reynolds number and how does it relate turbulent flow INCREASES in direct proportion to Velocity, Diameter, Density (P) inverse relationship to Viscosity (N) Re = (V x D x P) / N Low Re = laminar flow; High Re = turbulent flow BP vs mean pressures vs MAP – slide 6 graph (person is supine–why does it matter?) Review slide 8 – know the specific numbers (just copy and paste it here) The mean pressure in the aorta is high = 100 mm Hg Arterial pressure = 120/80 mmHg Mean blood pressure in SVC/IVC = 0 mm Hg Pulmonary arteries = 25/8 mmHg (mean 16 mmHg) The mean pulmonary capillary pressure averages only 7 mm Hg Describe Ohm’s Law (relationships) The relationship between Flow, Pressure, and Resistance Pressure gradient: pressure difference of the blood between the two ends of the vessel Vascular resistance: the impediment to blood flow through the vessel (vasoconstriction) F = ∆P/R Basic principles of circulatory function (slide 9) Remember the effects of sympathetic & parasympathetic nerves on the heart a) increase the force of heart pumping (CO) b) cause contraction of the large venous reservoirs to provide more blood to the heart (increase VR) c) cause generalized constriction of the arterioles in many tissues so that more blood accumulates in the large arteries to increase the arterial pressure (PR) Kidneys increase/decrease BP by regulating blood volume (with water) Total peripheral resistance: know components, units, how it works, what effects it (slide 14) Total Peripheral Resistance (TPR) = the resistance of the entire systemic circulation Pressure difference (from systemic arteries to systemic vein) cardiac output Aorta (100) – SVC/IVC (0) = 100 → then divide by Cardiac Output (100) 100/100 = 1; so normally the TPR should be 1 PRU CO → rate of pumping of blood out of the heart = rate of BF through entire circulatory system 1 PRU = Pressure difference (100 mm Hg) divided by Cardiac Output (100 mL/sec) So if the blood vessel is constricted, the TPR rises (up to 4 PRU) So if the blood vessel is dilated, the TPR decreases (as low as 0.2 PRU) What is Conductance, how does it relate to resistance & diameter Conductance = a measure of blood flow though a vessel for a given pressure difference Conductance is the exact RECIPROCAL of resistance ​​Slight changes in the diameter of a vessel cause tremendous changes in the vessel’s ability to conduct blood when the blood flow is streamlined Conductance increases in proportion to the fourth power of the diameter Poiseuille's law – know slide 16 F (rate of blood flow), ΔP (pressure difference, r (radius of the vessel), l (length of the vessel), and η (viscosity of the blood) Changing radius (vasoconstriction/dilation) how does it change it? Increase radius → massive increase in flow, small radius= slow In the systemic circulation, about two thirds of the total systemic resistance to blood flow is resistance in the small arterioles Arterioles respond with only small changes in diameter to nervous or chemical signals, either to turn off blood flow to the tissue almost completely or cause a vast increase in flow Blood Hematocrit and Viscosity (Know slide 18/21); What is Hct & what effects it & how The greater the viscosity (thicc) → lower the flow in a vessel Large numbers of suspended RBCs in the blood makes the blood viscous Each of RBCs exerts frictional drag against adjacent cells & against the wall of the blood vessel (^ RBC= ^ drag= decrease flow) Hematocrit of 40 = 40% of blood volume is cells, and the remainder is plasma Affected by anemia, degree of bodily activity, and altitude Increased hematocrit = markedly increased viscosity Viscosity @ normal hematocrit = 3-4 Viscocity also affected by plasma protein concentration & types of proteins Effects of BP on resistance & flow and autoregulation What it effects and how (sympathetic effects/vasoconstriction) – not the graph Autoregulation = ability of each tissue to adjust its vascular resistance to maintain normal blood flow during changes in arterial pressure Changes in blood flow are caused by strong sympathetic stimulation (vasoconstriction) and hormonal vasoconstrictors (NE, angiotensin, vasopressin, endthothelin) Each tissue’s local autoregulation eventually overrides effects of vasoconstrictors Slide 23 – blood flow controlled based on the tissues needs and CO is sum of all the flows Total circulation = 5 L/min in adult Chapter 15 – Vascular Distensibility and Functions of A/V Systems What is the advantage of it? → Veins able to be a blood reservoir b/c they are the most stretchy Slide 4 graphs show volume/pressure for A/V How are they different and how do they relate to the distensibility Change artery volume = big change in pressure Change venous volume = small change in pressure How sympathetics will shift the graph Sympathetic stimulation increases the pressure at each volume of the arteries or veins (shifts the graph to left) Sympathetic inhibition decreases the pressure at each volume (graph shifts right) Pressure Pulsations pulsatile flow of arteries (can feel pulse) but none in veins bc flow is continuous not pulsatile Progressively less pulsatile and more continuous as you move from the heart Bc arteries have some compliance/distensibility Normal arterial pressures How it changes over lifetime (20 vs 80 years old) → progressive increase with age Kidneys responsible for long-term regulation of pressure Systolic pressure increase due to decreased distensibility of arteries (atherosclerosis) Final effect is higher systolic pressure & increase in pulse pressure (SBP - DBP) Mean Arterial Pressures Heart spends more time in diastole than systole, so MAP is not equal to avg of sys/dias MAP = DBP + 1/3 (SBP - DBP) Pulse pressure = SBP - DBP Venous Pressures – Central vs Peripheral Central Venous Pressure (CVP) = the pressure in the right atrium (0 mmHg) Regulated by 1) ability of the heart to pump blood out of RA and RV into lungs, and 2) tendency for blood to flow from peripheral veins into RA Heart pumping strongly or hemorrhage = decrease in RA pressure Inside of heart vs systemic – slide 10 What can cause increase and why Factors that can increase the right atrial pressure: (1) increased blood volume; (2) increased large vessel tone and (3) dilation of the arterioles (allows rapid flow of blood from the arteries into the veins) CVP increases (20-30 mmHg) from serious heart failure & massive transfusion of blood What can change Venous Resistance & Pressure (slide 14) Compressed veins going over ribs at sharp angles, squished by organs, supine, etc. The pressure in the neck veins often falls so low that the atmospheric pressure on the outside of the neck causes these veins to collapse The large veins offer some resistance to blood flow, and thus the pressure in the more peripheral small veins in a person lying down is usually +4 to +6 mmHg greater than the right atrial pressure Estimating venous pressure and how its clinically useful Venous pressure can be estimated by observing distention in the neck In the sitting position, the neck veins are never normally distended When the right atrial pressure becomes increased to: +10 mm Hg → lower veins of the neck begin to protrude +15 mm Hg atrial pressure → all the veins in the neck become distended Different Distensibilities – slide 16 The greater the compliance → the slower the velocity Walls of arteries are thicker & stronger than veins Systemic & Pulmonary veins = much more distensible than arteries (low pressure) Systemic arteries = higher pressure, low dist; Pulm arteries = low pressure, high dist Chapter 16 – Microcirculation and Lymphatics What is microcirculation and what is included Small arterioles, metarterioles, capillaries, and venules In small vessels, all the blood is near the walls so the flow is slower (capillaries) How do capillaries work in terms of exchange – how are things getting through endothelial cells? Water, electrolytes, nutrients, & waste products of metabolism diffuse through slit pores between endothelial cells of capillaries Water vs lipid soluble and what can get through pores instead - slide 9 Lipid-soluble diffuse through cell membrane of endothelium (O2 & CO2) Water-soluble diffuse through intracellular pores (H2O, Na+, K+) What determines how you get through (interstitium vs blood) Size, charge, lipid/water solubility, concentration difference (high → low) 4 Starling forces What are they? what are the abbreviations? What do they mean? Which direction is it driving fluid? How is that determined? Four primary forces (Starling forces) determine whether fluid will move out of the blood into the interstitial fluid or in the opposite direction: 1.The capillary hydrostatic pressure (Pc) tends to force fluid outward from the capillary membrane to interstitium 2.The capillary plasma colloid osmotic pressure (Πp) tends to cause osmosis of fluid inward through the capillary membrane 3.The interstitial fluid hydrostatic pressure (Pif) force fluid inward through the capillary membrane when Pif is positive outward towards interstitium when Pif is negative 4.The interstitial fluid colloid osmotic pressure (Πif) tends to cause osmosis of fluid outward through the capillary membrane Equation NFP: net filtration pressures – what does positive vs negative mean? Positive net filtration pressure → a net fluid filtration out of the capillaries Negative net filtration pressure → a net fluid absorption from the interstitial spaces into the capillaries 3 jobs of lymphatic system and how it performs those jobs 1) Fluid Balance → picks up lymph (excess water/protein) and returns to bloodstream 2) Immune Defense → pick up WBC & pathogens and send killing stations (lymph nodes) 3) Transport Lipids & Proteins → Lacteals are lymph vessels that absorb large lipids deliver to larger blood vessels that can absorb them; pick up Proteins in liver & intestines Lymphatic system plays a key role in controlling the interstitial fluids: 1) Protein concentration, 2) Fluid volume, 3) Pressure Long flights – More inclined to develop edema in older pt (flow problems) and why Lymphatic valves aren’t working well + lymphatic pump isn’t working at rest Lymph flow is determined by 1) interstitial fluid pressure and 2) lymphatic pump Pumping by the lymphatic system causes the negative interstitial fluid pressure Negative interstitial fluid pressure holds body tissues together Physical relationship of vessels (slide 6) Metarterial, venule, capillary – how everything is connected to each other Arterioles are highly muscular; Precapillary sphincters connect arterioles to capillaries Precapillary sphincter – if contracted, less blood can get into capillary bed from arteriole Some organs need more or less – helps with blood redirection Metarterioles & precapillary sphincters are in close contact with the tissues → the local conditions of the tissues cause direct effects on the vessels to control local blood flow Plasma proteins Albumin is the most important – 80% of oncotic pressure (too big to cross) Relationship between molecular weight & permeability (↑ size → ↓permeability) Abnormal forces in capillaries Capillary pressure increases too much → edema bc forcing fluids out of it Capillary pressure ↓ (very low) → net reabsorption of fluid into the capillaries ↑ blood volume (increased BP) Chapter 17 – Local and Humoral Control of Tissue Blood Flow Short vs long term factors affecting tissue blood flow (theories) Oxygen Demand Theory Low O2 locally → low O2 to smooth muscle in vessel walls → smooth muscles cannot contract so they relax → vasodilation → increased blood flow Vasodilator Theory Low O2 in, or higher metabolism of O2 → forming vasodilator substances → vasodilation → increased blood flow Short term and long term factors – name them and how long they last Acute (short-term) control is done by rapid changes in local vasodilation or vasoconstriction Nitric oxide, adenosine, oxygen levels, nutrient levels, kidney, brain, skin Long-term control of blood flow is done by changing the size and # of local blood vessels Angiogenesis, oxygen levels, vascular bed remodeling (collateral vessels) Inhibit blood vessel growth = steroid hormones, angiostatin, endostatin Collateral blood vessels (slide 26) – how long will compensation take Blockage → collateral vessels will grow to detour around the blockage Within 1 day 50% of tissue needs are met; within days BF is sufficient Autoregulation and how they do it (2 theories) Metabolic theory: ↑↑ arterial pressure → the excess flow provides too much oxygen → decreases the release of vasodilators → cause the blood vessels to constrict and return flow to nearly normal, despite the increased pressure saying whoaaa we’ve got enough blood & oxygen, we don’t need anymore, so they close up until they use the excess oxygen Myogenic theory: a sudden stretch of small blood vessels causes the smooth muscle of the vessel wall to contract High arterial pressure stretches the vessel→ reactive vascular constriction → ↓ blood flow nearly back to normal Low arterial pressure → less stretch on the vessel wall→ the smooth muscle relaxes → ↓ vascular resistance → ↑ flow toward normal Acute Blood Flow Control in Specific Tissues Kidney Afferent arterioles deliver blood to Glomerular capillares for filtration Macula densa cells & Juxtaglomerular apparatus monitor the blood’s water levels Too much fluid filtered through → macudensa negative feedback to constrict afferent arterioles Reduces renal BF & GFR back to normal Brain Decreased O2 → increased cerebral BF & blood volume → more O2 Increased CO2 → dilate cerebral vessels → increase BF → exchange CO2 & O2 Decrease CO2 → vasoconstriction → decrease BF & blood voume Skin Blood flow linked to body temperature regulation Vasodilate → send blood to extremities close to skin → heat dissipates into air Vasoconstrict → send blood to core & vasoconstrict periphery to avoid heat loss Nutrients and metabolism – how they affect the blood flow Vasodilation occurs in the lack of: Glucose, Amino & Fatty acids, Vitamin deficiencies B vitamin is needed fo ATP production Example: In beriberi (thiamine deficiency), due to alcoholism or poor diet, the peripheral vascular blood flow almost everywhere in the body often increases twofold to threefold What is Active Hyperemia and Reactive? How long do they last? HYPEREMIA: increased amount of blood flow in the vessels of an organ/tissue ACTIVE HYPEREMIA: hyperemia due to a condition or to increased physical activity Higher metabolism → use more nutrients → release vasodilators REACTIVE HYPEREMIA: hyperemia to compensate for lack of blood flow that occurred Taking a BP → blood supply is occluded → relax cuff and it sends extra BF The longer the occlusion lasts, the longer the reactive hyperemia will last to replace the tissue oxygen deficit Vasodilators and Vasoconstrictors – examples of each Vasodilators → low O2, NO, Adenosine, CO2, Histamine, lactic acid, K+, H+ Vasoconstrictors → high O2, Endothelin What cells they affect Which are released by endothelial cells Endothelin Relaxing Factors (Nitric Oxide) Endothelin Constricting Factors (Endothelin-1) Nitric Oxide, Endothelin, Adenosine NO → most important vasodilator; made from arginine, oxygen, and nitrate NO release protects against excessive vasoconstriction Endothelin → most important vasoconstrictor; released from damaged endothelial cells Helps prevent extensive bleeding from arteries Adenosine → local vasodilator in skeletal muscle & cardiac muscle Heart is active → increase metabolism of O2 → decreased conc → degredation of ATP → increased release of Adenosine → coronary vasodilation & BF Long-Term Blood Flow Regulation (Slide 22 – review it) The acute mechanisms for local blood flow regulation are rapid, but regulation is still incomplete (75%) because a 10% to 15% excess blood flow remains in some tissues When the arterial pressure suddenly increases from 100 to 150 mm Hg, the blood flow increases almost instantaneously (about 100%) Then, within 30 seconds to 2 minutes, the flow decreases back to about 10% to 15% above the original control value Vascularity – how it changes with altitude & hyperplasia Oxygen is important both for acute and long- term control of local blood flow Vascularity increases in tissues of animals that live at high altitudes, where the atmospheric oxygen is low Retrolental fibroplasia: in premature babies who are put into oxygen tents, the excess oxygen → cessation of new vascular growth in the retina and degeneration of some of the small vessels when the infant is taken out of the oxygen tent → explosive overgrowth of new vessels → retinal vessels grow out from the retina into the eye’s vitreous humor → blindness Know growth factors also affecting growth of blood vessels & low oxygen levels Factors that increase growth of new blood vessels: VEGF, FGF, PDGF, & angiogenin Oxygen deficiency → expression of hypoxia inducible factors (HIFs) → upregulate gene expression and the formation of vascular growth factors (angiogenic factors) Angiogenesis inhibitors = Steroids, Angiostatin, Endostatin Chapter 18 – Nervous Regulation of Circulation; Use the original LOs minus exercise and respiration How do the parasympathetic and sympathetic nervous systems regulate the functions of heart and vasculature? ALL vessels except capillaries receive messages from sympathetic nerves Vasoconstriction → increased resistance → decrease rate of BF to less critical tissues Veins → vasoconstricton → decrease BV → increase venous return → increase CO What factors affect the differential sympathetic regulation of resistance & capacitance vessels? Sympathetic stimulation of the arteries & arterioles increases resistance to blood flow, which decreases capacitance and thereby decrease the rate of blood flow Baroreceptor vs Chemoreceptor Reflex on arterial pressure Baroreceptors → when BP is low, tell Pituitary to release ADH so Kidneys hold onto H2O Chemoreceptors → Low O2 & High CO2 → increase sympathetic vasoconstriction in muscles, abdominal organs & kidneys to increase BP in their arteries What is CNS ischemic response? As a response to low BP in the brain, we increase HR and constrict the blood vessels Sympathetic impulses from cardiac/vasomotor center of the brain to heart & vessels What is vasovagal syncope? A sudden drop in HR (heart rate) and BP (blood pressure) that leads to fainting due to a stressful trigger, such as: Heat exposure, The sight of blood, Standing for long periods of time, Stress Capacitance/Compliance Veins have a very high capacitance → able to accommodate increased blood volume without drastic changes in blood pressure Affects of Sympathetic/Parasympathetic nerves on muscles and heart Sympathetic vasoconstrictor effect is: powerful in the kidneys, intestines, spleen, and skin less potent (more vasodilation) in skeletal muscle, heart, & brain What are the NTs and where are they binding? Sympathetic = Epi & NE → binds to Alpha-Adrenergic receptors (Beta dilates) Released directly onto the Heart, blood vessles, other organs Organs involved? Are they releasing? Are they receiving? Epi & NE release from sympathetic nerves & from Adrenal Medulla into the blood Brain sends excitatory/inhibitory to Vasomotor center Excitatory = Sympathetic nerves → increase HR & contractility Inhibitory = Vagus nerve → parasymp to decrease HR & contractility Skeletal muscles, heart & brain are essential to surviving the stress → vasodilate Non-essential organs have ALPHA → NE → vasoconstriction Essential organs have BETA → Epi & NE → vasodilation Chapter 20 – Cardiac Output, Venous Return and their regulations Know the definitions on slide 2 and the relationships between them Systole vs Diastole vs EDV/ESV vs all that fucking shit (we know this..) How increase in one will cause decrease/increase in another How sympathetic/parasympathetic will affect each of these Frank Starling Law – using the main terms The greater the EDV or Preload → greater the Force of Contraction or Stroke Volume Why would we want to change our CO, contractility, etc To run from a bear or from this exam… Veins are primary controller of CO? Increased venous return → increase EDV → increase SV → increase CO Direct and indirect mechanisms of hearts ability to pump out whatever it receives Directly affect Cardiac Putput: resting CO avg 5.6 L/m (men) and 4.9 L/min (women) 1) the basic level of body metabolism 2) whether the person is exercising 3) the person’s age 4) the size of the body Direct effect of stretch on HR: Stretch of the SA NODE in the wall of the right atrium has a direct effect on the rhythmicity of the node to increase the heart rate as much as 10–15%. Indirect effect of stretch on HR: Stretch of right atrium initiates a nervous reflex called the Bainbridge reflex, passing first to the vasomotor center of the brain and then back to the heart by way of the sympathetic nerves and vagi, which also indirectly increases the heart rate. How much blood will go where (slide 18) & understand why Not all areas get same amount of CO BF to each organ is dependent on the level of metabolism/need the harder the body is working → the more oxygen they use → the greater the demand for oxygen → increase blood flow to that muscle What causes Hypo vs Hypereffective heart Hypereffective = symp stimulation & parasymp inhibition → increase HR & contracility Hypoeffective = ↑ PVR, symp inhibition, coronary blockage (ischemia), heart disease What increases or decreases CO High CO = result from chronically reduced total peripheral resistance Ex: Beriberi (B1 def), AV fistula, Hyperthyroidism (↑ metabolism = ↑ vasodilators) Low CO Cardiac = Coronary blockages, valvular disease, myocarditis, cardiac tamponade Non-cardiac = ↓ BV, venous obstruction, ↓ metabolic rate, decreased tissue mass Chapter 21 – know the first 18 slides only (lol “only”) 5L blood/min – and lots going to the coronary arteries (5%) because it needs nutrients! Phasic Changes in Coronary BF Coronary blood vessel squished in systole → very full in diastole How we control coronary blood flow and how it relates to metabolism ↑ tissue metabolism → ↑ release of vasodilators → ↓ arteriole resistance → ↑ BF Therefore, the coronary blood flow increases almost in direct proportion to any additional metabolic consumption of oxygen by the heart How ATP is used to meet the needs of the heart Breakdown = ATP → ADP → AMP → Adenosine A little AMP is then degraded (AMP → adenosine) → release adenosine in heart muscle → vasodilation → signals an increase in local coronary blood flow. After the adenosine causes vasodilation, much of it is reabsorbed into the cardiac cells to be reused for production of ATP In severe coronary ischemia, some Adenosine is lost → can’t rebuilt enough ATP After 30+ minutes of ischemia = injury/death or cardiac cells Slide 7 – “recall!” Epi and NE are released during sympathetic states NE → Alpha-adrenergic = vasoconstriction Epi → Alpha or Beta = vasoconstriction/vasodilation Slide 8 – why we get chest pain in stressful situations In some people, the alpha vasoconstrictor effects seem to be disproportionately severe, → vasospastic myocardial ischemia during periods of excess sympathetic drive → anginal pain. Slide 9 – Cardiac Muscle Metabolism Aerobic condition → cardiac muscle consume fatty acids instad of glucose for energy Anaerobic → must use glycolysis for energy → lots of lactic acid in cardiac tissue Lactic acid is probably one of the causes of cardiac pain in ischemia conditions Ischemic Heart Disease Most common cause of death in western culture; ~35% age 65+ Causes = high cholesterol → atherosclerosis → plaques → block blood flow Common site is the first few cenimters of the major coronary arteries Clot = thrombus; breaks away and moves = embolus Lifesaving Collateral Circulation When atherosclerosis constricts the coronary arteries slowly collateral vessels can develop at the same time while the atherosclerosis becomes more and more severe. Therefore, the person may never experience an acute episode of cardiac dysfunction. Causes of Death after Acute Coronary Occlusion 1) decreased cardiac output 2) damming of blood in pulmonary vessels & then death resulting from pulmonary edema 3) fibrillation of the heart 4) rupture of the heart Stages of Recovery Large ischemia → muscle fibers in the center of the area die Dead tissue replaced by furious tissue & scar Immediately around the dead area = nonfunctional area (failure of contraction) Around the nonfunctional area is still contracting but only weakly Normal areas of the heart gradually HYPERTROPHY to compensate for lost muscle Recovers either partially or almost completely within a few months Rest in Treating MI As the heart becomes more active, healthy blood vessels dilate which take most of coronary blood flow, and leaves little blood flow to the ischemia areas → ischemia worsens called “Coronary Steal Syndrome” = rest is important after myocardial infarction!!! Pain in Coronary Heart Disease Angina pectoris is felt beneath the upper sternum → radiate to left arm & shoulder & neck The reason for this distribution of pain is that during embryonic life the heart originates in the neck, as do the arms. Therefore, both the heart and these surface areas of the body receive pain nerve fibers from the same spinal cord segments. Okay last one, accurate as fuck