Week 2 TCU Cardiovascular Students PDF

Cardiovascular Anatomy and Physiology Week 2 NRAN 80413 / Spring 2024 R. Ward, PhD, CRNA, FAANA 1 Cardiac Module Overview/Objectives • Overview of the Circulatory System – Wk 1 • • • • Components of the Circulatory System Pressure, Flow, and Resistance Anatomy of the Heart Coronary Perfusion/My...

Cardiovascular Anatomy and Physiology Week 2 NRAN 80413 / Spring 2024 R. Ward, PhD, CRNA, FAANA 1 Cardiac Module Overview/Objectives • Overview of the Circulatory System – Wk 1 • • • • Components of the Circulatory System Pressure, Flow, and Resistance Anatomy of the Heart Coronary Perfusion/Myocardial Oxygen Balance • Cardiac Blood Supply / EKG Manifestations of CAD • Cardiac Physiology – Wk 2 • Cardiac Performance / Cardiac Output • Cardiac Cycle • Wiggers diagram • Pressure-Volume Loops • Cardiac Pathophysiology – Wk 2 • Valve Disorders • Cardiac Conduction – Wk 1/2 • • • • Conduction System Properties of Cardiac Muscle Excitation-Contraction Coupling Electrophysiology and Action Potentials • Anesthetic Management • EKG Interpretation – Wk 3 2 Electrophysiology and Action Potentials 3 Heartbeat Coordination • Heart is a dual pump • Left and right sides pump separately, but simultaneously into systemic and pulmonary vessels • Atria contract first, followed by ventricles • Contraction of cardiac muscle is triggered by depolarization • Gap junctions interconnect myocardial cells and allow spread of action potentials (AP) • Initial depolarization arises in the SA node • AP then spreads from SA node throughout atria, then into and throughout ventricles 4 Normal Conduction Pathway 5 Path of Spread of Excitation • Right atrium: • SA node: pacemaker of the heart • Depolarization of SA node generates the AP leading to depolarization of all other cardiac muscle cells • Discrete internodal pathways conduct the AP from SA node to AV node • Electrical excitation couples with contraction of cardiac muscle (excitation-contraction coupling) • Conduction occurs rapidly: right and left atria contract essentially at same time 6 Internodal Tracts • Anterior • AKA Bachmann’s bundle • Extends into LA, then down through atrial septum to AV node • Middle • AKA Wenckebach’s tract • Curves behind SVC before descending to AV node • Posterior • AKA Thorel’s tract • Continues along terminal crest to enter atrial septum, then passes to AV node 7 Path of Spread of Excitation • Left atrium: • Bachmann’s bundle • AKA anterior internodal tract • A branch of anterior internodal tract that resides on inner wall of left atrium • During NSR, it is the preferential path for electrical activation of the left atrium • Primary atrial conduction pathway • Plays a role in atrial fibrillation and interatrial block 8 Path of Spread of Excitation • Ventricles: • AV node serves as the link between atrial and ventricular depolarization • Propagation through AV node relatively slow – the delay allows atrial contraction to be complete before ventricular excitation occurs • Bundle of His (AV bundle): fibers that allow conduction from AV node down the interventricular septum • Pass electrical impulse to right and left bundle branches • Right bundle branch > RV • Left bundle branch > LV • Bundle branches separate at apex of heart to pathways composed of Purkinje fibers 9 Path of Spread of Excitation • Purkinje fibers • Large in diameter • Rapidly conduct the action potential to myocytes throughout the ventricles • This causes depolarization of all right and left ventricular cells to occur simultaneously • Ensure a single coordinated contraction 10 Blocked impulse: left ventricle • Dysfunction in left bundle branch results in blocked impulse • LBBB hallmarks: • Excess widths of QRS > 0.12 seconds • Deep, broad S wave in V1/V2 • Broad clumsy R-wave in V5/V6 11 Blocked impulse: right ventricle • Dysfunction in right bundle branch results in blocked impulse • RBBB hallmarks: • QRS duration > 0.12 seconds • QRS is widened and upwardly deflected in lead V1 • Large R’ wave in V1/V2 • Terminal force of QRS is above the baseline (big R wave) • Broad, deep S wave in V5/V6 12 Action Potentials Cardiac (ventricular muscle cell) Neuronal 13 Cardiac Action Potentials • Differences between neuronal and cardiac APs allow specialization for particular roles in the spread of excitation through heart • Different types of heart cells produce different shapes of AP • Must be able to differentiate amongst all of them: • • • • • • • SA node Atrial muscle AV node Common bundle Bundle branches Purkinje fibers Ventricular muscle *note: in Vanders, these are referred to as “nodal cell APs” and “Myocardial cell APs” 14 Ventricular Action Potential 15 Cardiac Action Potential: Ventricle • Ventricular muscle action potential (5 phases): • Phase 0: Upstroke • Fast Na+ channels open (rapid depolarization) • K+ permeability decreased • Phase 1: Initial Repolarization • Na+ channels close; K+ channels open (transient) • Phase 2: Plateau • Ca++ channels open/initiation of contraction • Voltage-gated L-type Ca++ channels (L = long lasting) • Flow of Ca++ into cell just balances flow of K+ out, keeping membrane depolarized at plateau value • Phase 3: Final Repolarization • Ca++ channels close/K+ exits cell • Phase 4: Resting potential • Resting membrane permeability restored • Ca++ inward and K+ out of sarcolemma • Na+ efflux 16 Terms of the Action Potential • Resting membrane potential – 90 mV • The difference in electrical potential between the inside and outside of the cell. • The inside is negative relative to the outside • Threshold potential – 70 mV • The internal voltage at which the cell depolarizes • All or none phenomenon i.e. once it begins, it cannot be stopped • When RMP is closer to TP, the cell is easier to depolarize • When RMP is further from TP, the cell is harder to depolarize • Depolarization • Takes place when there is a reduced polarity across a membrane i.e. when there is less of a charge difference between inside and outside of cell • In excitable tissue, depolarization results in an AP • Repolarization • The restoration of membrane potential towards RMP following depolarization The AP for ventricular muscle is unique: there is a plateau phase where depolarization is prolonged. This gives cardiac myocytes time to contract, so the heart has enough time to eject its stroke volume • Absolute refractory period • Time during which an AP may not be evoked, even if elicited by a stimulus at the cellular level • Lasts from Phase 0 to middle of Phase 3, when membrane potential drops below -60mV • Relative refractory period • Time during which a second AP can be fired, but the stimulus required is greater than normal • Extends from middle of Phase 3 to beginning of Phase 4, when membrane potential ranges from -60mV to -90mV 17 Sodium and Potassium • Potassium • Myocyte permeable to K+, but not other electrolytes or proteins. • Continuously leaks K+ therefore losing + charge – explains why inside of cell negative in relation to outside and why K+ is primary determinant of RMP • When serum K+ ↓, RMP becomes more negative and myocytes become more resistant to depolarization • When serum K+ ↑, RMP becomes more positive and myocytes depolarize more easily • Sodium • When cell is at rest, Na+ permeability is very low compared to K+ • When RMP approaches threshold potential, voltage-gated Na+ channels open and Na+ conductance increases • This depolarizes the cell • Initially, this increases membrane excitability, but w/ prolonged depolarization, the cell membrane becomes more refractory and less likely to fully depolarize 18 Na+/K+ ATPase (pump) • Sodium-Potassium ATPase • Restores ionic balance towards RMP • Serves 2 purposes: • Removes Na+ that enters cell during depolarization • Returns K+ that has left the cell during repolarization • For every 3 Na+ ions it removes, it brings 2 K+ ions into the cell • Na/K-ATPase is always on • Active transport – requires energy 19 Summary of Events: Ventricular AP 20 Antiarrythmic drugs and ventricular AP 21 Nodal Action Potential 22 SA Node’s Unique Characteristics • Higher resting membrane potential: -55 to -60mV • More permeable to Na+ than other myocardial cells • Results in “leakiness” • Rapid depolarization is absent; instead slow depolarization • Known as “pacemaker potential” • This provides the SA node with automaticity • Phase 1 and Phase 2 do not occur * Note the ion responsible for depolarization 23 Cardiac Action Potential: SA Node • SA Node → Internodal tracts → AV Node → Bundle of His → Left & Right bundle branches → Purkinje fibers • Heart rate is a function of: • The intrinsic firing rate of the dominant pacemaker (usually the SA node) • Autonomic tone • SA nodal disease impairs its ability to function as the heart’s dominant pacemaker • Cells with the next highest rate of phase 4 spontaneous depolarization will assume the pacemaker responsibility 0 3 4 RMP • No plateau phase; RMP is higher than ventricular muscle • As a result of higher RMP (-60 mV), SA node is more permeable to Na+ than other atrial myocardial cells • This ‘leakiness’ gradually raises the membrane potential closer to threshold potential (-40 mV) 24 Action Potential of the SA Node – 3 phases 0 3 4 25 Nodal Disorders 26 Ectopic Pacemakers Inherent rates of conduction: SA Node: 60-100 bpm AV Node: 40-60 bpm Purkinjes: 20-40 bpm • SA node disorder: excitable groups of cells cause premature heart beat outside the normally functioning SA node • Normally does not occur due to SA node’s higher intrinsic rate • Ectopic pacemakers: • Atrial pacemakers (SA node): 60-100 bpm • Junctional pacemakers (AV node): 40-60 bpm • Ventricular pacemakers (Purkinjes): 20-40 bpm 27 AV Conduction Disorder • AV node disorder impacts transmission of APs from atria to ventricles • AV blocks: • First-degree AV block • Second-degree AV block • Mobitz type I (Wenckebach) • Mobitz type II • Third-degree AV block • Causes: • Idiopathic fibrosis / sclerosis of the conduction system • Ischemic heart disease • Drugs (beta blockers, Ca++ channel blockers, digoxin, amiodarone) • Increased vagal tone • Congenital heart or genetic diseases • Autorhythmic cells in bundle of His and Purkinje network initiate excitation at their own inherent rate to pace the ventricles • Slow > 25-40 bpm 28 Cardiac Physiology • Cardiac Performance - aka Cardiac Output • Cardiac Cycle – systole and diastole • Wiggers diagram • Pressure-Volume loops 29 Cardiac Performance aka Cardiac Output (CO) CO = HR x SV Cardiac Output Heart Rate Stroke Volume Intrinsic rate Increased sympathetic activity Preload Increased in plasma epinephrine Decreased parasympathetic activity Contractility Afterload 30 Cardiac Output (CO): Definition • Volume of blood each ventricle pumps as a function of time, usually expressed in L/min • In steady state, the CO flowing through systemic and pulmonary circuits is equal • Heart rate (HR) x stroke volume (SV) = CO • HR = number of beats per minute • SV = blood volume ejected by each ventricle with each beat 31 Overview of Control of Cardiac Output • With average total blood volume of approximately 5.5 L in an adult, nearly all blood is pumped around each circuit once/minute! • Factors altering CO → HR and SV • Applies to both right and left sides of heart in steady state conditions • However, they do not always change in the same direction • With increased blood loss, SV decreases, therefore HR increases to maintain CO • Opposing effects on the cardiac output 32 Heart Rate 33 Control of Heart Rate • Inherent autonomous rate of the SA node • 100 beats / minute (bpm) • In absence of nervous or hormonal influences • However, the HR may be higher or lower than this due to constant influence of nerves and hormones • Parasympathetic and sympathetic postganglionic neurons end on the SA node • HR decreases with activity in the parasympathetic neurons (traveling with the vagus nerves) • HR increases with activity in the sympathetic neurons – knowns as chronotropic effects • Resting state results in more parasympathetic activity to the heart • Therefore normal resting heart rate is 70-75 bpm – well below the inherent 100 bpm 34 Control of Heart Rate • Increased: • Stimulation of sympathetic neurons to heart • Increase in plasma epinephrine • Decreased: • Stimulation of parasympathetic neurons to the heart 35 Stroke Volume 36 Control of Stroke Volume • Preload / End-Diastolic Volume (EDV) • The filling pressure of the heart at the end of diastole. • Left atrial pressure (LAP) at end of diastole will determine preload • The greater the preload, the greater will be the volume of blood in the heart at the end of diastole (like blowing up a balloon, the more pressure that is applied, the bigger it will get). • Afterload • The pressure against which the heart must work to eject blood during systole. • If systolic pressure is lower, the heart will be able to contract to a smaller volume at the end of systole resulting in improved SV • Conversely, if the systolic pressure is higher, the heart will be unable to contract to as small a volume at end of systole, and SV will be decreased • Contractility • Inherent strength and vigor or heart’s contraction during systole • This may be increased by sympathetic activity or pharmacologic agents • Sympathetic activity releases epinephrine • Pharmacologic agents: positive inotropic agents increase cardiac contractility i.e. dopamine, epinephrine, digoxin 37 Preload 38 Preload • Preload is the ventricular wall tension at the end of diastole, just before contraction. • Often used interchangeably with ventricular end-diastolic volume (EDV) • Factors that influence preload: • • • • • • Blood volume Atrial kick Venous tone Intra-pericardial pressure Body position Valvular regurgitation 39 Frank-Starling Mechanism • Relationship between ventricular EDV (preload) and SV • States that the heart will eject a greater SV if it is filled to a greater volume at the end of diastole • This relationship is modified by contractility and afterload 40 Ventricular Function Curve • “Frank-Starling Curve” • Plots the relationship between ventricular volume (x axis) and ventricular output (y axis) • Note that the x and y axis terms are all used in terms of ventricular output and ventricular volume – know all of them • Steep upstroke with a plateau at higher filling pressures • Note in the normal and hyperdynamic curves that as pressure increases, LV output increases • SV increases in response to increase in volume of blood filling the heart (EDV) when all other factors remain constant • An increased ventricular volume = larger cardiac output • Plateau at the top where higher filling pressure no longer increases performance, then see decrease ventricular output • At the plateau, add’l volume overstretches ventricular sarcomeres, decreases # of crossbridges that can be formed, and decreases CO 41 Afterload 42 Afterload F = P1 – P2 / R → R = P1 – P2 / F • The force that the ventricle must overcome to eject its stroke volume • Pressure within LV during peak systole • 2 ventricles have drastically different afterloads: SVR and PVR 43 Factors affecting LV afterload • State of the ventricular chamber • Shape, size, and wall thickness of the ventricle • Compliance of arterial vasculature • Systemic vascular resistance (SVR) and mean arterial pressure (MAP) 44 Law of Laplace and Afterload Wall stress = Intraventricular pressure x Radius Ventricular thickness • Wall stress = tension divided by wall thickness • Intraventricular pressure is the force that pushes the heart apart • Wall stress is the force that holds the heart together • Therefore, wall stress is reduced by: • ↓ Intraventricular pressure • ↓ Radius of the ventricle • ↑ Wall thickness Helps us understand how afterload affects myocardial wall stress 45 Afterload and Ventricular Function Curve • Increases in afterload shift the Frank-Starling curve down and to the right, which decreases SV and increases LVEDP • In contrast, a decrease in afterload shifts the FrankStarling curve up and to the left, which increases SV and reduces LVEDP 46 Contractility 47 Contractility • Defined: the intrinsic strength of the heart muscle • Compliance: the ratio of change in volume to change in pressure (stiffness) • Elastance: the ratio of change in pressure to change in volume • Independent of either preload or afterload – intrinsic ability of the myocardium to pump in absence of changes to preload or afterload. • Altered by many pathophysiologic states – neural, humoral, or pharmacological influences 48 Cardiac Cycle 49 What is the cardiac cycle? • Electrical and mechanical events taking place from one heartbeat to the next • Goal is to understand the EKG, pressure, flow, and valve functions as they occur at each phase of the cardiac cycle. • 2 main phases: • Diastole: period of time when ventricles are relaxed and not contracting • Blood passively flowing from LA and RA into LV and RV • Systole : time during which left and right ventricles contract and eject blood into aorta and pulmonary artery 50 Cardiac Cycle: electrical and mechanical events 51 Understanding the Cardiac Cycle • Note that the EKG impulse precedes the mechanical action of the heart • Delay between electric and mechanical events occurs because time is needed for the wave of depolarization to spread across myocardium before contraction can begin • Extends from one ventricular contraction to the next • Divided into 2 main phases: diastole and systole • Both require energy 52 Wigger’s diagram • Atrial pressure waveform • a wave: due to atrial systole • c wave: ventricular contraction • v wave: pressure buildup from venous return before AV valve opens again 53 Wigger’s in 3 minutes! https://www.youtube.com/watch?v=0sogXvxxV0E 54 Cardiac Cycle: Systole and Diastole • Systole • Diastole • Time period when contraction and tension development occur • Occupies about 1/3 of the cycle • Begins immediately prior to MV closure and ends just after AV closure • Phases: • Isovolumetric contraction • Ejection When HR increases, the duration of systole remains constant, but the duration of diastole is shortened → this is why tachycardia is BAD • Time period when blood is entering the ventricle at varying rates preparatory to the next systole • Occupies about 2/3 of the cycle • Relaxation of the ventricular myocardium requires energy in order to reaccumulate Ca++ in the sarcoplasmic reticulum • Phases: • Isovolumetric relaxation • Rapid filling 55 Cardiac Cycle: Isovolumetric Contraction/Relaxation • Isovolumetric Contraction (systole) • Occurs when the LV pressure exceeds LA pressure but is less than aortic pressure • MV closes – 1st heart sound • LV pressure rises rapidly without change in volume • Isovolumetric Relaxation (diastole) • Begins when LV pressure falls below aortic pressure and AV closes • Ends when LV pressure falls below LA pressure and MV opens • Ventricular volume is unchanged • Approximately 50-60 ms 56 Cardiac Cycle: Ejection and Rapid Filling • Ejection (systole) • Occurs when LV pressure exceeds aortic pressure forcing the valve to open – AV opens • A period of rapid ejection occurs in which 1/3 of the SV is ejected followed by a prolonged slow ejection of the remaining 2/3 • Rapid filling (diastole) • Begins when the MV opens which allows a rapid inflow of blood from the LA – initially a passive filling • Atrial systole occurs at the end of diastole, the atrium contracts • This accounts for approx. 15-20% of ventricular filling 57 Cardiac Cycle: Putting it Together 58 Summary of events: systole and diastole 59 Why is understanding of the cardiac cycle so important? https://youtu.be/jLTdgrhpDCg • Mastery of the cardiac cycle will help in understanding pressurevolume loops • A favorite on the NCE!! 60 Pressure Volume Loops 61 Pressure-Volume Loops: Overview • What does the Pressure-Volume Loop Tell Us? • It shows the pressure-volume relationship in the LV during one cardiac cycle • It provides an assessment of systolic and diastolic function as well as the integrity of the cardiac valves • The effects of afterload on ESV and EDV are illustrated by pressure-volume loops • You need to know where on the loop each phase occurs: filling, contraction, ejection, relaxation • You need to know at which point the mitral and aortic valves open and close Aortic valve closes Mitral valve closes 62 What the Pressure-Volume Loops Tell Us 63 Example: • What is stroke volume? • SV = EDV – ESV • Volume blood pumped from LV per beat • Calculate the stroke volume (answer in mL) Pressure • Answer: 120 mL – 50 mL = 70 mL ** if you are given a pressurevolume loop, then the SV is equal to the width of the loop Volume 64 Understanding Pressure-Volume Loops • Period of Ventricular Filling (Diastole) • LV volume is ~ 50 mL (ESV) • LV pressure is 2-3 mmHg • MV opens and ventricular filling begins • AV stays closed • Since LV is compliant, filling doesn’t increase pressure • Atrial kick increases LV pressure to 57 mm Hg • LV fill to ~ 120 mL (EDV) • There is a net gain of 70 mL during ventricular filling 65 Understanding Pressure-Volume Loops • Period of Isovolumic Contraction (Systole) • • • • • • Begins at MV closure LV is stimulated to contract LV pressure exceeds LA pressure MV closes AV is still closed LV builds tension and increased LV pressure • LV volume does not change 66 Understanding Pressure-Volume Loops • Period of Ventricular Ejection (Systole) • • • • • • LV pressure exceeds aortic pressure AV opens MV still closed LV ejects stroke volume Normal SV is 70 mL As SV enters aorta, LV volume decreases • Normal ESV is 50 mL • DBP is measured where the AV opens • SBP is measured at the peak of the ejection curve 67 Understanding Pressure-Volume Loops • Period of Isovolumic Relaxation (Diastole) • • • • • Aortic pressure exceeds LV pressure AV closes MV remains closed LV volume does not change LV returns to starting pressure of 2-3 mm Hg • LV returns to starting volume of 50 mL 68 Understanding Pressure Volume Loops https://www.youtube.com/watch?v=GutMgMKeXzY 69 Sample Question • Calculate the ejection fraction based on the pressure-volume loop to the right (answer in %) • Answer: 58% ** EF = EDV – ESV x 100 EDV ** EF = 120 – 50 x 100 = 58% 120 *** normal EF = 60-70% *** LV dysfunction when EF < 40% 70 Heart Rhythm and Rate • Not depicted in pressure-volume loops • However, must be known prior to utilizing a pressure-volume loop • When SV is constant, cardiac output is directly proportional to heart rate 71 Pathophysiology: Valve Disorders and Anesthetic Management 72 Pressure Volume Loops and Valvular Disease • Pressure (opening) Issue: • Mitral Stenosis • Aortic Stenosis • Volume (closing) Issue : • Mitral Regurgitation • Aortic Regurgitation 73 Valve Disease – open/close problem 74 Pressure Volume Loops and Valvular Disease • Which valvular diseases are associated with eccentric hypertrophy? (Select 2.) a. b. c. d. Mitral stenosis Mitral regurgitation Aortic stenosis Aortic regurgitation 75 Pressure Volume Loops and Valvular Disease • Which valvular diseases are associated with eccentric hypertrophy? (Select 2.) a. b. c. d. Mitral stenosis Mitral regurgitation Aortic stenosis Aortic regurgitation • Eccentric vs. concentric hypertrophy • Eccentric: caused by addition of sarcomeres in series, leading to a large, dilated ventricle w/ relative wall thinning. • Concentric: caused by addition of sarcomeres to myocytes in parallel, resulting in an increase in cardiac wall thickness and reduced chamber volume. 76 Pressure Volume Loops and Valvular Disease • Which valvular diseases are associated with eccentric hypertrophy? (Select 2.) a. b. c. d. Mitral stenosis Mitral regurgitation Aortic stenosis Aortic regurgitation • Correct answers: b and d • Regurgitant lesions tend to produce volume overload; heart compensates w/ eccentric hypertrophy (thin wall + dilated chamber) • Stenotic lesions tend to produce pressure overload; heart compensates w/ concentric hypertrophy (thick wall + smaller chamber) 77 78 Mitral Stenosis: Pathophysiology • Thickening of valve leaflets promotes calcification/rigidity of valve cusps • Restriction of blood flow >> transvalvular pressure gradient dependent on CO, HR (diastolic time), cardiac rhythm • LA is enlarged • Blood flow stasis >> thrombi promotes SVTs/Afib • Treatment: • Onset to incapacitation = 5-10 yrs • Medical management • • • • • • Supportive Limitation of physical activity Na+ restriction Diuretics Beta blockers Anticoagulation if needed • Surgical management • Percutaneous transseptal balloon valvuloplasty (young, pregnant, elderly who are not surgical candidates) • Replacement 79 Mitral Stenosis • • • • Normal mitral valve area = 4–6 cm2 Moderate stenosis = 2 cm2 Severe stenosis = 1 cm2 Critical stenosis = 0.5 cm2 • Causes: • • • • • • Rheumatoid fever Lupus Congenital Left atrial myxoma Carcinoid syndrome Iatrogenic following MV repair • Goals: • Preload: normal to increased LVEDV • Afterload: maintain neutral • Heart Rate: low normal • PVR: avoid increases • Maintain NSR • Avoid afib! • Atrial kick provides up to 40% of CO 80 Mitral Stenosis: Anesthetic Management • Goal: “Full, Slow and Constricted” • Full: normal to increased preload • Slow: avoid tachycardia • Constricted: maintain contractility/large increases in CO • Maintain NSR 81 Mitral Regurgitation/Insufficiency Pathophysiology • Reduction in forward SV due to backward flow of blood into LA during systole • LV compensation: dilating and increasing EDV • Eccentric LV hypertrophy over time • Treatment • Medical management: • Afterload reduction >> increases forward SV and decreases regurgitant volume • Surgical management • Valvuloplasty • Valve repair • Catheter-mediated • MVR 82 Mitral Regurgitation/Insufficiency • Etiology • Disease of the valve leaflets alone • Abnormalities of the papillary muscles • Abnormalities of the chordae tendinae • Causes: • • • • • • • Rheumatic disease Bacterial endocarditis Congenital Connective disorder Direct penetrating trauma Acute MI w/ chordae tendinae rupture Papillary muscle dysfunction • Goals: • Preload: normal to increased • Afterload: decreased • Heart rate: increase / avoid bradycardia • PVR: avoid increases • Avoid myocardial depression ** “fast and forward” -Fast: High HR reduces time spent during diastole and reduces regurgitant fraction -Forward: decreased afterload promotes forward flow 83 Mitral Regurgitation Chronic MR Acute MR 84 Hemodynamic Goals for Mitral Valve Lesions 85 Aortic Regurgitation Pathophysiology • Forward SV reduced due to backward flow into LV during diastole • Chronic aortic regurg = LV dilation and eccentric hypertrophy • Largest EDV of any heart disease • Treatment • Medical management: • Asymptomatic 10-20 years • Once symptoms develop, survival time ~ 5 yrs without valve replacement • Diuretics, afterload reduction, ACE inhibitors • Surgical management: • Surgical AVR 86 Aortic Regurgitation/Insufficiency • Etiology • Congenital • Usually associated w/ other cardiac abnormalities • Acquired • • • • • Rheumatic heart disease Endocarditis Aortic root dissection Cystic medionecrosis Takayasu’s disease • Vasculitis (blood vessels inflamed) • Giant cell arteritis • Goals: • Maintain NSR • Preload: normal to increased • Afterload: decrease • Heart rate: moderate increase • PVR: maintain neutral • Arteries inflamed 87 Aortic Insufficiency/Regurgitation 88 Aortic Insufficiency/Regurgitation • History • Usually occurs in the 4th-5th decade of life • Long (7-10 yr) asymptomatic period during which the LV undergoes progressive eccentric enlargement • Then, CHF, angina, widened pulse pressure, and decreased diastolic pressure • If patient presents with: • Eccentric LV hypertrophy / chamber dilation • Concentric LVH on EKG • Large pulse pressure • Then (if just 2 of these S/S): • 33% chance of CHF, angina, or death in 1 year • 50% chance of CHF, angina, or death in 2 years • 87% chance of CHF, Angina, or death in 6 years • 100% chance of CHF, angina, or death in 10 years 89 Aortic Stenosis Pathophysiology • LV outflow obstruction • Concentric LV hypertrophy allows ventricle to maintain SV • “SAD”: triad of syncope, angina, dyspnea in valve areas < 1cm2 • Treatment • Medical management: • Once symptoms develop, those without surgical treatment die within 2-5 years • Surgical management: • Percutaneous balloon valvuloplasty • Transcatheter aortic valve replacement • Surgical AVR 90 Aortic Stenosis • Concentric hypertrophy (Law of Laplace) Wall stress = Intraventricular pressure x Radius Ventricular thickness • Normal valve orifice = 2.5-3.5 • Severe = < 0.8 cm2 cm2 • Thick LV wall w/ decrease in compliance and narrowed chamber • Reduced myocardial O2 supply and increased heart mass • myocardial ischemia, LV failure, pulm edema • Sudden death < 0.7 cm2 • Goals: • Maintain NSR • Causes: • Congenital • Most common (bicuspid) • Acquired • Calcification of the valve • Rheumatic heart disease • Preload: increase (ensure sufficient) • Afterload : maintain to slight increase • Heart rate: low normal • PVR: maintain 91 Aortic Stenosis 92 Hemodynamic Goals for Aortic Valve Lesions 93