Cardiac 1.2.pptx

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 an...

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 1 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 2 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 3 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 4 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 5 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 6 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 7 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 8 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” 9 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 10 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 11 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, voltagegated 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 12 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 13 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 14 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) 15 Inherent rates of conduction: SA Node: 60-100 bpm AV Node: 40-60 bpm Purkinjes: 20-40 bpm Ectopic Pacemakers • 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): 40 bpm 2016 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 • Autorhythmic cells in bundle of His and Purkinje network initiate excitation at their own inherent rate to pace the ventricles • 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 • Slow > 25-40 bpm 17 Cardiac Physiology • Cardiac Performance - aka Cardiac Output • Cardiac Cycle – systole and diastole • Wiggers diagram • Pressure-Volume loops 18 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 19 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 20 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 21 Control of Heart Rate • Increased: • Stimulation of sympathetic neurons to heart • Increase in plasma epinephrine • Decreased: • Stimulation of parasympathetic neurons to the heart 22 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 23 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 24 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 25 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 cross-bridges that can be formed, and decreases CO 26 AfterloadF = 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 27 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) 28 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 stres 29 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 30 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 31 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 32 Cardiac Cycle: events electrical and mechanical 33 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 34 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 35 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 When HR increases, the duration of systole remains • Ejection 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 36 Cardiac Cycle: Isovolumetric Contraction/Relaxation • Isovolumetric Contraction• Isovolumetric Relaxation (systole) (diastole) • 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 • 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 37 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. 1520% of ventricular filling 38 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 pressurevolume 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 39 What the Pressure-Volume Loops Tell Us 40 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 41 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 5-7 mm Hg • LV fill to ~ 120 mL (EDV) • There is a net gain of 70 mL during ventricular filling 42 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 43 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 • • • • • • 44 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 45 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% 46 Heart Rhythm and Rate • Not depicted in pressure-volume loops • However, must be known prior to utilizing a pressurevolume loop • When SV is constant, cardiac output is directly proportional to heart rate 47 Pathophysiology: Valve Disorders and Anesthetic Management 48 Pressure Volume Loops and Valvular Disease • Pressure (opening) Issue: • Mitral Stenosis • Aortic Stenosis • Volume (closing) Issue : • Mitral Regurgitation • Aortic Regurgitation 49 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 50 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. 51 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) 52 53 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 54 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 55 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 56 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 57 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 58 Mitral Regurgitation Chronic MR Acute MR 59 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 60 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 • Arteries inflamed • PVR: maintain neutral 61 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 62 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 63 Aortic Stenosis • Concentric hypertrophy (Law of Laplace) Wall stress = Intraventricular pressure x Radius Ventricular thickness • Normal valve orifice = 2.5-3.5 cm2 • Severe = < 0.8 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 64