Cardiac 2 PDF

○​ administers medicine directly into heart WEEK 1: NORMAL VARIANTS (chemo, antibiotics) Within the right atrium ○​ usually stays in patient for days to ​ Crista terminalis: C shaped, fibromuscular...

○​ administers medicine directly into heart WEEK 1: NORMAL VARIANTS (chemo, antibiotics) Within the right atrium ○​ usually stays in patient for days to ​ Crista terminalis: C shaped, fibromuscular weeks ridge -> SVC to IVC ​ Eustachian ridge: run between IVC and Epicardial fat coronary sinus ​ Seen around the RV ​ Eustachian valve: remnant of fetal circulation ​ similar echogenicity to myocardium ○​ From IVC attach IAS ​ Chari network: fenestrated variant of Atrial special aneurysm eustachian valve ​ Out-pouching of the IAS at the level of the fossa ovalis -> often associated with PFO Within the left atrium ​ apical 4CH or subcostal view ​ Pectinate muscles: prominent parallel ridges ​ from parasternal long axis image of RV inflow, of muscle located within LAA -> seen on TEE can be mistaken for patho ​ Coumadin or warfarin ridge: bulbous ​ document on preliminary report partition between LAA and LUPV ​ ASA define as excursion of septal tissue of >10mm f Lipomatous hypertrophy of interatrial septum ○​ total excursion right and left of 15mm ​ Fatty infiltration of interatrial septum with sparing of fossa ovalis WEEK 1: HEMODYNAMICS ​ Asymptomatic and incidental finding Blood flow ​ Dumbbell shaped ​ Measure of movement of blood through a chamber, vessel or organ expressed as a unit Ventricular muscle bands and false tendons of time ​ Moderator band: prominent muscular band ○​ unit: litres/minute found near the RV apex ○​ Q ​ False tendons:fibrous tendons that transverse ​ initiated by heart the LV cavity ​ blood follows pressure gradient from high to ○​ Anywhere in LV and attach to any part low pressure of wall or apparatus ○​ Can be one or multiple ​ Arteries: carry oxygenated blood from heart to body Valve excrescences ○​ thick walled due to high pressures ​ Tiny filamentous strands that form on leaflets ○​ high pulse pressure ○​ Thin, elongated and frequently multiple ○​ flow through arteries aided by pressure ○​ Ventricular side of semilunar valves -> gradient and gravity lambl's excrescences ○​ main function = highway -> no ○​ Atrial side exchange ​ Arterioles: very small artery near the Transverse sinus capillaries ​ Tunnel like structure ○​ most important factor of where blood ​ Posterior to ascending aorta and pulmonary will go trunk, superior to LA ○​ small arteries that branch off from the ​ Aorta and pulmonary artery leave the heart main arteries ○​ contains muscular walls that dilate or Heart catheter restrict to hormones Types: ○​ main function = primary site of vascular ​ Pacing wires - electrical problems resistance ​ PICC lines - peripherally inserted central ​ Capillary beds: smallest vessel, very thin catheter walled  ○​ site of gas exchange -​ increases ability to expand to accept ○​ speed of blood flow slows down in th blood without increased resistance to capillaries to allow time for exchange flow ​ Venules: a very small vein, multiple venules -​ decreased compliance = reduced blood flow = join to for veins atherosclerosis ​ Veins: carry deoxygenated blood back up to -​ more turbulence, higher pressure within the heart vessel ○​ thin walled, large lumens -​ ability of any chamber or vessel to expand to ○​ low pressured and fighting against accommodate incred blood gravity and therefore needs pumps 3.​ volume of blood Blood pressure -​ increased blood volume = increased blood flow ​ Force exerted by blood upon the walls of the because it increased pressure gradient blood vessels or chambers of the heart -​ blood volume is usually constant bu can change in diseased states Venous system -​ Hypovolemia = low blood volume ​ Carries deoxygenated blood back up to the -​ large bleed, dehydration, heart medicines ​ veins and venules -​ hypervolemia = high blood volume -​ retention of water and sodium, ​ Skeletal muscle pump: heart failure ○​ veins have to fight gravity to get blood back to the heart 4.​ viscosity of the blood ○​ skeletal muscle contracts = increase -​ increased blood viscosity = decreased blood pressure in the veins = blood flows flow upwards = opens valves superior to = thickness of blood and cannot realty be changed = contracting muscles constant ​ inferior valves close to prevent -​ can change in diseased state -> plasma blood from back flowing elements and proteins affect blood viscosity -​ eg.anemia, liver disease ​ Venous system respiratory pump: ○​ helps veins in thoracic and abdominal 5.​ blood vessel length and diameter cavities -​ increased vessel length = decreased blood ○​ inhale -> diagram contracts and moves flow downwards = abdominal pressure rises -​ increased vessel radium = increased blood and thoracic pressure drops = flow increased blood enters the RA -​ length: longer = greater resistance -​ increased surface area of blood vessel Variables affecting pressure and blood flow = more friction 1.​ Cardiac output -​ constant except for when we gain or -​ CO = HR x SV -> increased cardiac output = lose weight increased blood flow -​ radius: different vessels have different spices -​ stroke volume = LV volume ED - LV -​ can change throughout the day volume ES -​ increased diameter = less blood -​ measured in litres per minute touching the vessel = less friction = -​ normal CO - 4-8L/min lower resistance = increased blood flow 2.​ compliance Poiseuille’s law -​ increased compliance = increased blood flow ​ Used to explain the idea of resistance to flow ​ the most important and only factor that can easily change is the radius of the vessel  ○​ Decrease vessel size = higher resistance to flow ○​ increase vessel zie = lower resistance to flow Vasoconstriction and vasodilation Arterial system: ​ Vasoconstriction of artery or arterioles = decreased radium = increased resistance and pressure = decreased blood flow ​ site of largest resistance: arterioles ​ arterial vasoconstriction decreases blood flow Right ventricle anatomy into that artery -​ Crescent shaped -​ Tricuspid valve -> apically displaced septal venous system: leaflet ​ The walls of veins are irregular 1)​ Inlet portion ○​ when the vessel contract = more rounded ○​ less surface area = less resistance = increased glow ​ vasoconstriction increased blood flow into the vein Effects of atherosclerosis ​ Normal: patent lumen, normal endothelial function, platelet afforestation inhibited ​ stable angina: lumen narrowed by plaque, a)​ 3 tricuspid leaflets: anterior, posterior inappropriate vasoconstriction and septal ○​ can’t really see in echo but we can see b)​ 3 papillary muscles: anterior, posterior in TEE and septal 2)​ Apical component WEEK 2: VENTRICULAR ANATOMY AND a)​ Highly trabeculated SYSTOLIC FUNCTION -​ Parietal band: muscular band that runs along the free wall of the RV Left ventricular anatomy -​ Septomarginal band (septal band): -​ Bullet shaped muscular band that runs along IVC - 1)​ Inlet potion: forms part of the medial papillary a)​ 2 mitral valve leaflets: anterior and muscles posterior -​ Moderator band: muscular band found b)​ 2 papillary muscles: posteromedial and between base of anterior papillary anterolateral muscle and IVS 2)​ Apical component 3)​ Outlet component a)​ Muscular: thicker walls than RV and a)​ Infundibulum: aka conus arteriosus contains trabeculae carneae -​ Conical pouch/space of RVOT b)​ No muscle bands 3)​ Outlet component b)​ Supraventricular crest: aka crista a)​ Smooth walled supraventricularis b)​ No anatomical features separating inlet -​ Separates the RV inlet and outlet and outlet portions of RV c)​ Transportation centre where blood -​ Made of parietal band (muscular band) leave the LV and infundibular septum Myocardial fibers 1.​ Isovolumetric contraction: hits ventricle and it ​ Muscle is orientated in different layers and begins to contract -> pressure rises but not directions above the aorta ○​ Twisting during systole and untwisting 2.​ Rapid ejection: biggest amount of blood rushes during diastole out and into the ascending ○​ Like wringing out a damp cloth 3.​ Reduced ejection: pressure begins to drop but Layers of myocardial fibers LV pressure still higher than aortic and LV is 1.​ Superficial - subepicardium contracting but there is no blood left ​ Covers both left and right ventricles ​ Roughly 25% of LV wall thickness ​ Spiral pattern ​ Creates longitudinal contraction 2.​ Middle ​ Only present in LV ​ Roughly 55% of LV wall thickness -> pumps to match pressure of ascending aorta = works harder ​ Fibers lay more horizontally than the superficial layer ​ Creates circumferential contraction Isovolumetric contraction 3.​ Deep - subendocardial ​ Period between AV valve closure and ​ Thinnest layer of roughly 20% of LV wall semilunar valve opening thickness ​ Ventricular volume at its maximum volume ​ LV and RV fibers are separated ​ Ventricular muscle fibers are contracting but ​ Creates longitudinal contraction both valves are closed -> pressure rises very rapidly Ventricular interdependence ​ No blood leaves the heart -> volume of ​ Superficial fibers encircle both LV and RV ventricle does not change ​ RV and LV function linked together ​ Shape, size, function and volume of one Rapid ejection phase ventricle will affect other ​ Pressure inside ventricles rises above great ​ 20-40% of RV function depends on contractility arteries -> semilunar valves open of LV ​ Pressure is still rising in ventricles -> due to ventricular muscle fiber contraction Characteristics of ventricles ​ Blood ejects rapidly out of ventricle -> great arteries Right ventricle Left ventricle - Crescent shaped - Bullet shaped Reduced ejection phase - Tricuspid valve (apically - Mitral (bicuspid) valve ​ Ventricular repolarization begins -> walls displaced septal leaflet) - Two discrete pap begins to relax - Coarse apical muscles (no septal ​ As pressure decreases inside the ventricles trabeculations attachment) ​ Pressure gradient drops between ventricles - Multiple small pap - False tendon (ectopic and great artery and rate of blood ejection muscles (septal chordae tendineae) slows down attachment) - Inlet and outlet valves in ​ Once pressure of ventricles drop below that of - Moderator band continuity one great arteries, blood briefly continues to eject due to inertial energy of the blood flow ​ Ejection phase ends when semilunar valve Phases of systole close One cardiac cycle ​ CI = CO/BSA ​ Pressure volume loop represents events in LV ​ Normal = 3-4L/min/m^2 ​ Combining LV pressure and volume -> pressure loop can be created to better Cardiac reserve describe pressure and volume relationship ​ Difference between rate at which the heart pumps blood and its max capacity ​ Tested by dobutamine stress echo ​ Decreases with age and is impaired with heart disease Visual assessment ​ Perform a visual estimation of EF on every patient that you scan ​ Perform visual estimation of RV function on every patient scanned Methods to assess overall heart function ​ Fractional shortening ​ Ejection fraction ​ Stroke volume LV pressure-volume loop ​ Cardiac output 1.​ Diastolic filling: LV volume is increasing and ​ Simpsons biplane EF LV pressure is very slightly increasing Method of assessing LV function 2.​ Mitral valve closure: End of LV filling ​ Cardiac index (diastole) ​ Cardiac reserve a.​ LV end-diastolic pressure (LVEDP) ​ Visual assessment and/or end diastolic volume (LVEDV) ​ E-point septal separation b.​ LV is at maximum volume ​ Aortic root excursion 3.​ Isovolumic contraction: LV pressure is ​ Dp/dt rapidly increasing but the LV volume does not ​ Strain change ​ 3D imaging 4.​ Aortic valve opens: once LV pressure exceeds the pressure in the aorta, the aortic Teichholz method (2D linear) valve opens ​ Not recommended for EF but machine will 5.​ ejection(systole): LV volume is decreasing automatically calculate using the and the LV pressure is increasing measurements 6.​ Aortic valve closes: once the pressure in the ​ Result of geometric assumptions LV falls below the pressure in the aorta, the aortic valve closes E point septal separation a.​ LV end systolic volume ​ Distance between AMVL (E point) and b.​ LV is at minimum volume ventricular septum (early diastole) 7.​ Isovolumetric relaxation: LV pressure is ​ Measurement from M-mode image of MV in rapidly decreasing while LV volume remains early diastole -> AMVL approach septum the same ​ Increased EPSS in patients with decreased EF a.​ All 4 cardiac valves are closed ​ Normal = 6mm or less 8.​ Mitral valve opens: LV pressure falls below ○​ Abnormal = severe dysfunction the LA pressure a.​ LV begins to fill Aortic root excursion ​ Mobility of aortic root between systole and Cardiac index diastole = indicator of LV systolic function ​ Cardiac output indexed to the body surface ​ Normal heart -> moves anteriorly in systole area ​ Decreased EF -> motion is flat  ​ Left main coronary artery - LCC dP/dt ○​ Left anterior descending artery -> ​ Measure of rate of rise of ventricle pressure anterior LV segments during isovolumetric contraction ○​ Circumflex artery -> supplies the lateral ○​ dP = change in LV pressure LV segment ○​ Dt = time for change to develop ​ Right coronary artery - RCC ​ dP/dt is performed by measuring time interval ○​ Right marginal artery + posterior between 1 and 3m/s on the MR velocity descending artery -> RV and inferior spectrum walls ​ Normal LV dP/dt is >1000 mmHg/s ​ Vessels not usually imaged but required for pediatrics Methods to assess RV function ​ Visual assessment ​ Tricuspid annular plane systolic excursion ​ Tissue doppler imaging Tricuspid annular plane systolic excursion (TAPSE) ​ Measure of RV longitudinal fiber shortening during ventricular systole ​ Normal heart during systole -> tricuspid annulus moves inferior toward apex ​ Measured on M-mode ​ Normal ≥16mm Coronary artery dominance Tissue doppler imaging (TDI) ​ ~70% are right dominant -> posterior ​ Allows quantitative assessment of RV systolic descending artery supplied by RCA and diastolic function ​ ~20% are co-dominant -> posterior descending ​ Does not take regional wall motion artery supplied by both RCA and LCA abnormalities into consideration ​ ~10% are left dominant -> posterior ​ Velocity is measured when performing TDI of descending artery supplied by LCA RV ​ Normal ≥ 9.5 cm/sec Collateral circulation ​ Occlusion occurs slowly over a long period of Coronary artery distribution time, collateral vessels will develop ​ Structure of coronary arteries 1.​ Tunica intima - inner lining Electrical system 2.​ Tunica media - middle muscle/elastic ​ SA node and AV node: located in RA and layer supplied by coronary artery 3.​ Tunica adventitia - outer connective tissue layer Papillary muscles ​ Coronary artery branch from sinus of valsalva ​ Anterolateral papillary muscles: supplied by left and supply myocardium with oxygenated blood anterior descending and LCA ​ Coronary veins drain deoxygenated blood to ​ Posteromedial papillary muscle: supplied by the coronary sinus -> RA posterior descending artery -​ Blood flow into coronary arteries is greatest during ventricular diastole -> extravascular WEEK 3: CORONARY ARTERY DISEASE compression by myocardium in systole Causes of LV systolic dysfunction ​ Decreased oxygen supply to the heart -> Coronary arteries coronary artery disease ​ Runs along epicardial surface -> course ​ Increased oxygen demand -> LV hypertrophy, through myocardial and endocardial layer tachycardia  -​ Supply and demand needed to be balance for ​ Reversible ischemia: present at higher decreased and oxygen demand oxygen demands, such as with exercise ​ Decreased contractility -> cardiomyopathy ○​ Oxygen levels cannot rise fast enough (disease of myocardium), excessive preload, ○​ May or may not present regional wall drug use, tachycardia abnormalities ​ 𝑓𝑙𝑜𝑤(𝑄) = 𝑝𝑒𝑟𝑓𝑢𝑠𝑖𝑜𝑛 𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒/𝑟𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 Ischemia ​ Coronary flow occurs in diastole ​ Imbalance between myocardial oxygen supply ​ Depends on: and demand 1.​ Perfusion pressures ​ Leads to decreased oxygen apply = 2.​ Resistance to flow accumulation of waste 3.​ Oxygen carrying content of bloo ​ Symptoms: ○​ None (silent ischemia) Oxygen supply ○​ Chest pain 1.​ Perfusion pressure: because flow occurs in ○​ Jaw pain, arm pain diastole -> reduction of pressure = reductions ○​ Fatigue of perfusion into coronary arteries: ○​ Shortness of breath on exertion a.​ Hypotension (SOBOE) b.​ Aortic insufficiency -> blood leaks out of ​ Fine sitting there but are aorta back into LV = reduces diastolic completely winded going up pressure aortic sinuses of valsalva some stairs 2.​ Resistance to flow: ​ Causes: a.​ Internal factors: atherosclerosis, ○​ Atherosclerosis (#1 cause) -> diet coronary artery spasm lifestyle causes calcifications, wall b.​ External factors: LV hypertrophy; big abnormalities or full blockage heart -> muscle grows bigger and ○​ Coronary artery emboli squeezes the coronary arteries and ○​ Coronary artery dissection -> layers of starts to close them -> pressure grows the artery separate = harder for blood to enter ○​ Coronary artery spasm -> artery 3.​ Oxygen carrying content of the blood: suddenly closes shut (reopens after a a.​ Hemoglobin within blood carries bit of time) but acts like a heart attack oxygen ○​ Decreased myocardial oxygen supply b.​ Issue with oxygenation of blood will ○​ Increased myocardial oxygen demand affect oxygen deliver to heart muscle -> huge heart = demands more oxygen ○​ Coronary artery inflammation Oxygen demand ○​ Congenital coronary artery anomalies ​ Myocardial oxygen demand depends on: 1.​ Oxygen demand of individual cardiomyocyte -> Atherosclerosis determined by LaPlace’s law ​ Often referred to as hardening and narrowing 2.​ Number of cardiomyocytes of arteries 3.​ HR = formation of plaque (fatty material) within -​ Bigger heart = more cardiomyocytes and coronary arteries bigger heart -> needs to word harder -​ Is it distension or big muscles? Oxygen (O2) supply and demand ​ Supply determined by coronary artery blood Oxygen demand of individual cardiomyocytes flow to heart muscles and blood oxygen ​ Determined by ventricular wall stress carrying capacity ​ Increased wall stress = increased tension ​ Demand is determined by wall stress required to pump the heart out of blood ​ Dynamic process - demand changes through 𝑊𝑎𝑙𝑙 𝑠𝑡𝑟𝑒𝑠𝑠 = 𝐿𝑉 𝑠𝑦𝑠𝑡𝑜𝑙𝑖𝑐 𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒*𝑟𝑎𝑑𝑖𝑢𝑠 2*𝑤𝑎𝑙𝑙 𝑡ℎ𝑖𝑐𝑘𝑛𝑒𝑠𝑠 the day -​ LV systolic pressure:  -​ Raised due to increased afterload ​ Last a short amount of time required force ​ Treatment: rest or nitroglycerin inside LV increases = individual cardiomyocyte must contract harder = ○​ Unstable angina, aka acute coronary higher pressure syndrome -​ As LV systolic pressure rises = stress ​ Medical emergency = heart and oxygen demand rises attack -​ LV radius: ​ Unexpected chest pain, at rest -​ Dilated LV - leaky valves, ​ Refers to spectrum of clinical cardiomyopathy presentation associated with -​ As chamber dilates the cardiomyocytes blockage inside of coronary are stretched to non optimal position artery -> lead to myocardium -​ Cardiomyocyctes fights against ​ Most common cause = pressure as they stretch atherosclerotic plaque that -​ As LV dilates - works harder to create ruptures or splits = thrombus tension = increased oxygen demand ​ Imbalance in cardiac oxygen -​ Wall thickness: as LV thickens (concentric supply and demand hypertrophy) there are more muscle cells share the same load -> individual does not ○​ Variant (Prinzmetal’s) angina work as hard ​ Occurs when a person is at rest, -​ Wall thickness increase = oxygen midnight and early morning consumption of individual ​ 2/100 angina cases cardiomyocytes decrease ​ Younger patients ​ Caused by spasm in coronary Myocardial demand - # of muscle cells arteries ​ Oxygen consumption (at given heart rate) = ​ Risk factors: cold weather, number of cardiomyocytes*oxygen stress, medicines, cocaine consumption of individual cardiomyocyte ○​ Atypical angina ​ LaPlace law reduces workload of individual ​ Vague pain cardiomyocyte ​ Typically less severe ​ Heart rate increases = oxygen consumption ​ More common in women increase ​ Causes may or may not be heart related What happens when demand is higher than supply? ​ Systolic dysfunction Myocardial infarction (MI) ​ Regional wall motion abnormality = heart attack ​ Chest pain ​ Complete blockage of coronary artery -> damage to heart muscle Angina pectoris ​ Usually caused by coronary artery disease -> ​ Most common symptom of ischemia heart rupture of atherosclerotic plaque disease ​ Can be caused by coronary artery spasms ​ Squeezing and tightness due to reduced blood supply to myocardium -> myocardial Diagnosis of MI ischemia Types (diagnosed by ECG and blood test for -​ Angina = imbalance in oxygen supply and biomarkers) demain but still have 02 delivery ​ Unstable angina ○​ Stable angina ​ Non-STEMI ​ Only occurs where there is ​ STEMI increased oxygen demand ​ Predictable Electrocardiogram  1.​ Unstable angina (UA): chest pain may occur at ​ Heart attack (myocardial infarction): can be rest -> ECG may be normal (ST flat) sudden or can come on slow over long period 2.​ Non ST segment elevation myocardial of time infarction (NSTEMI): less severe than STEMI ○​ Heart still pumps -> not well a.​ Partial blockage of coronary artery ○​ Symptoms: chest pain, shortness of b.​ Usual ECG finding are ST segment breath, arrhythmias depression or T-wave inversion ○​ Imbalance and there is damage of the 3.​ ST segment elevation myocardial infarction heart- stil beating but part of the heart (STEMI): more severe than NSTEMI is not receiving blood a.​ Complete blockage of coronary artery ​ Cardiac arrest: b.​ Elevation of biomarkers ○​ Heart stops completely ○​ Patient will die within minutes without treatment ○​ Symptoms: loss of conscious, abnormal or absent breathing ○​ Heart is no longer bleeding -​ Causes of cardiac arrest: -​ Coronary artery disease: causes damage to heart muscles and electric system -​ Can cause heart attack - hypoxic cells = pacemakers -​ Other causes of fatal arrhythmias: congenital abnormalities in the electric system -​ Enlarged heart or PEA Pulseless electrical activity - PEA arrest ​ Cardiac electrical activity without a palpable Biomarkers pulse -> heart is contracting but there is no ​ Reveal blood changes in response to oxygen myocardial damage ○​ Electrical system is telling it to contract 1.​ Troponin: but the myocytes do nothing = low a.​ Very sensitive/specific cardiac output; caused by respiratory b.​ Elevated levels indicate cardiac muscle failure cell death -> enzyme released into ​ ECG shows electrical activity but no pulse is blood upon myocardial ischemia found c.​ Rises with 3-4 hrs, peaks 18-36hrs, ​ Heart is unable to contract enough to create a gone in 10-14 days cardiac output compatible with life 2.​ Creatine (phospho) kinase(CK): ​ Usually caused by respiratory failure a.​ Isoenzyme ○​ Hypoxia damages myocardium -> even b.​ Elevation of CK = indication of with electrical activity, the heart is myocardial ischemia unable to contract c.​ Rises in 3-8 hrs, peaks at 24hrs, gone ​ Approx 20% of cardiac arrest that occur in 4 days outside the hospital ​ Prognosis: poor Catheterization lab ​ Treatment: CPR until stable ​ See inside coronary arteries and determines ○​ IV line/intubate/supply O2 cause of MA -> blockage vs spasm ○​ Fix the line ​ We can see which one ​ Often patient falls asleep and never wakes up-painless but process is slow Heart attack vs cardiac arrest Cardiogenic shock Paradoxical septal motion ​ Inadequate tissue perfusion (organ ​ Describe the IVS when motion is away from LV hypoperfusion) due to a damaged heart free wall during systole ​ The most common etiology = acute myocardial ​ Seen in apical 4CH infarction (STEMI) with left ventricular failure ​ Causes: pericardial disease (Effusions and ​ Can be caused by mechanical complications -> inflammation of pericardium-pericarditis) acute mitral regurg or rupture of wither ○​ Disease - CAD and/or myocardial ventricular septal or free wall infarction in IVS ○​ Left bundle branch block ○​ Post heart surgery SUMMARY ​ Angina: chest pain ​ Myocardial infarction: complete or partial Infarcted myocardium blockage of coronary artery leading to ​ Old infarct will cause myocardium to appear ischemia -> damage to cardiomyocytes thin and more echogenic ○​ Heart keeps pumping but is being ○​ Not thicken normally damaged ​ Cardiac arrest: lack of electrical activity and therefore lack of contractions Asses for complications from an acute MI ​ PEA arrest: cardiac electrical activity without ​ LV aneurysm, pseudoaneurysm palpable pulse -> caused by loss of ​ Thrombus formation contractility (often lack of O2) ​ Myocardial rupture ○​ Free wall Role of echo in coronary artery disease ○​ IVS 1.​ Measure EF ○​ Pap muscle 2.​ Assess regional wall motion abnormalities ​ Mitral regurg 3.​ Assess for complications ​ Arrhythmia ​ Pericarditis Assess LV function Ventricular aneurysm ​ Damaged and/or dead myocardium can stretch out = aneurysm ○​ All three layers of the wall are affected ○​ Usually the LV apex ​ Expands in systole -> energy wasted expanding instead of sending blood out to the ​ Visually body ​ Biplane ○​ Heart is not efficient ​ 3D ​ Associated with heart failure, ventricular ​ Strain rate arrhythmias and clots ​ Contrast agents ​ Common non medical emergency and patient ○​ When 2 or more contiguous segments will live with it forever are not visualize ​ Diastole; abnormal myocardium = reduced LV pseudoaneurysm compliance -> changes to diastolic function = contained rupture of the LV free wall - blood is contained within the area Regional wall motion abnormalities (RWMA)’s -​ MEDICAL EMERGENCY ​ Not all walls are moving the same amount ​ May remain the same size or progressively ​ Technologist and physician grades regional enlarge wall motion abnormalities ​ Communicate with body of the left ventricle ​ Lack of regional wall motion abnormalities through a narrow neck does not mean lack of coronary artery disease ​ Spontaneous rupture occurs without warning ​ -⅓  ​ Caused by: LV failure Aneurysm vs pseudoaneurysm -​ Aneurysm: tends to be in apex, entire apex ○​ Myocardial damage = creation of is wider/abnormal shape spontaneous pacemakers -​ Pseudoaneurysms: usually on LV free wall ○​ Ischemic injury to atria (can be in apex) and has a neck ○​ RV infarction ○​ Damage to the conduction system Thrombus formation ​ Increased risk of thrombus formation if there Pericarditis and dressler's syndrome are regional wall motion abnormalities Pericarditis: ​ MEDICAL EMERGENCY ​ Inflammation of pericardial sac 24-96 hours post MI Ruptured myocardium ​ Occurs in 10% of MI ​ Can be in any location: ​ Inflammatory response to the dying tissue ○​ Interventricular septum ○​ LV free wall papillary muscles Dresslers syndrome: ​ Occurs 3-5 days post MI ​ Pericarditis that forms 2-8 weeks post MI ​ Prognosis: depends on many factors including ​ Occurs in 1-3% of MIS portion of myocardium (involved in rupture) ​ Causes: unknown -> possibly autoimmune ​ Very high mortality rate if the free wall rupture reaction to circulating cardiogenic antigens ○​ Damaged cardiomyocytes releases ​ In the IVS = causes VSD hormones and then body reacts = ○​ Occurrence: 0.2% of all MIS inflamed ○​ Document if after heart attack as it can rupture ​ In the free wall: ○​ 0.5% of all MI -> mortality rate is 20% ○​ Usually occurs a bit after IVS rupture ○​ Anywhere 2 weeks post MI ○​ Symptoms: sudden onset of chest pain, nausea, hypotension, pericardial effusion, sudden cardiac death ○​ Treatment = surgery Ruptured papillary muscle ​ Damage to LV walls that contain the pap muscle = damage to pap muscle ○​ Can rupture and tear off the wall ○​ Can be life threatening condition = causes severe mitral regurg Mitral regurgitation Causes: ruptured papillary muscles ​ Dilated LV: valve unable to fully close due to a dilated MV annulus ​ Tethered leaflets: ○​ Damage to the inferolateral wall and WEEK 4: INTRODUCTION TO DIASTOLIC pap muscles = dysfunction FUNCTION ○​ MV annulus doesnt work properly What is diastole? Arrhythmias  ○​ Once LV pressure rises above LA -> MV close and diastole is closed Ventricular relaxation vs ventricular compliance LV relaxation ​ Ability of heart muscle fibers to return to resting length and tension ​ Active process -> energy ​ Occurs in isovolumetric relaxation period and ​ Ability of heart to relax and fill with blood early diastole ​ Defined as: closure of semilunar valves to the ​ Impaired relaxation slows the rate of pressure closure of AV valves decline in LV Phases LV compliance and stiffness 1.​ Isovolumic relaxation: period between AoV ​ Occurs once muscle fibers are relaxed closure and MV openig ​ Ability for heart to expand a.​ All 4 valves close ​ Decreased compliance = LV pressure will rise b.​ LV relax -> pressure in LV should drop more quick quickly ​ LA pressure must increase to overcome higher 2.​ Early rapid filling - E wave LV pressure 3.​ Diastasis - cusps flutter almost closed 4.​ Atrial contraction - A wave Causes of diastolic dysfunction ​ LVH: thicker walls = stiffer walls with decreased Early, rapid filling compliance ​ MV opens, and blood rushes from LA to LV ○​ Eg. hypertension, aortic stenosis ​ Elastic recoid of LV creates suction - blood into ​ Damaged cardiomyocytes: restrictive LV cardiomyopathy and other infiltrative diseases ​ Initial pressure gradient between LV and LA is -> substances infiltrate heart and end up high, blood rushes quickly replacing cardiomyocytes ○​ Blood enters LV -> pressure rises ○​ Heart attack -> scar tissue replace ○​ Blood leaves LA -> pressure drops healthy muscle -> stiffer than healthy ​ After initial E point -> pressure begin to muscle equalize and velocity of blood entering LV ○​ Age: heart becomes less compliant with slows down age ​ In normal heart - phase should contribute to 70-80% of LV filling Consequences of diastolic abnormalities ​ Can go years without symptoms Diastasis ​ Causes increased LA pressure - force blood ​ LV and LA pressure are almost equal -> very into non compliant LV little blood flow into LV ​ High LA pressure is carried into pulmonary ​ Small amount of blood may continue to pass system -> pulmonary hypertension into LV due to inertia ○​ Severe enough = heart failure ​ Duration of diastasis is determined by HR = ​ Symptoms: shortness of breath, trouble tachy causes short diastasis period breathing while laying down, edema, arrhythmias Atrial contraction ​ Patients with diastolic dysfunction have a ​ LA contract = rises pressure higher risk of morbidity and mortality ○​ Rise above LV pressure -> second wave of blood enters the LV Sono assessment of diastolic function ○​ Normal heart, atrial contraction should ​ Ejection fraction contribute around 20% of total filing ​ Left ventricular wall thickness  ​ Left ventricular inflow ​ Influenced by LV compliance and LA ​ Tissue doppler imaging contractile function ​ Left atrial volume ​ Pulmonary vein flow E/A ratio ​ Isovolumetric relaxation time ​ Used to determine filling pattern ​ Right ventricular systolic pressure ​ Normal heart: ○​ E velocity > A velocity -> majority of Ejection fraction flow in early diastole ​ Reduction = some level of diastolic dysfunction ○​ Should be between 0.8 and 2 ○​ DT = 150-200ms LV wall thickness ​ Approx 20% of left ventricular filling occurs ​ LV hypertrophy - leading causes of LV diastolic during the atrial kick phase function ○​ Leads to decreased relaxation -> Tissue doppler diastolic dysfunction ​ Measure myocardial velocities at medial mitral ​ Hypertension = leading cause of hypertrophy annulus and lateral mitral annulus ​ Base of heart moves toward apex in systole LV inflow and toward atria in diastole ​ PW signal of MV inflow- measures velocity of ​ Diastole portion -> tissue doppler mirrors the blood as it enter the LV MV inflow pattern ​ Reflex LV relaxation -> restoring forces and filling pressures ​ PW - 0.5-1cm inferior of MV annulus cursor should be slightly into LV side E,DT,A E= E wave velocity ​ Reflects the LA-LV pressure gradient in early diastole ​ Influenced by the rate of LV relaxation and LA pressures DT = deceleration time ​ Measure slope from peak of E wave to the baseline -> machine calculates time from E wave to baseline ​ Reflects rate of decline by LA/LV pressure gradient ​ Influence by LV relaxation, LV diastolic pressure following MV opening and LV stiffness A=A wave velocity ​ Reflects the LA-LV pressure gradient in late diastole