Principle #12 In order to maintain the harmony of the stakeholders, the leveraging and deleveraging of stakeholders of human life

requires an agreed upon system of fairness and forgiveness that honors all stakeholders. The heart is at the core of that system Principle #16 Every stakeholder of human life has primary sources of energy and matter which ultimately were derived from another stakeholder. Heart is the source of energy and matter for all the cells of the body, which came from other stakeholders. Overview & Ventricle Development Heart Embryolog - mesoderm EMBRYONIC STRUCTURE Truncus arteriosus (TA) Bulbus cordis Primitive ventricle Primitive atria Left horn of sinus venosus ( SV) Right horn of SV R common & anterior cardinal vein GIVES RISE TO Ascending aorta and pulmonary trunk Smooth outflow tracts of both ventricles Trabeculated left and right ventricles TrabecuIated left and right atria Coronary sinus Smooth part of the right atria SVC

Truncus Arteriosus - aka spiral septum/aorticopulmonary septum came from Neural crest cell 6 Truncoconical Spiral Septum Defects Fenestrae Ventral Septal Defect Tetralogy of Fallot * Persistent Truncus Arteriosus * Transposition of great vessels * (RV aorta LV PA) Dextrocardia Embryologic Development of the heart

Heart tube Atria of 4-chambered heart - Tube grows, elongates and folds into S Shape - Atrial chamber lays posteriorly in S and ventricular chamber lays anterior in S - Atrial chamber grows and incorporates superior vena cava and pulmonary vein - septum primum forms - septum secundum forms incompletely (leaving foramen ovale) - cell death in septum primum forms osmium secundum

What divides the R & L atria? Septum Primum & Septum Secundum How is blood shunted from R atrium to the L atrium in an embryo? Through the foramen oval and osmium secundum Ventricles & Outflow Tract Separation - Ventricle chamber lays anteriorly in S shaped heart tube - Muscular ventricular septum forms which begins to divide the ventricles - Truncoconial swellings (ridges) of truncus arterioles meet, fuse, and zip (both superiorly and inferiorly) in a 180 turn to form spiral septum - Inferior portion of spiral septum meets with muscular ventricular septum to divide the ventricles and form aorta and pulmonary arteries

Ventricular remodeling to for AV valves Myocardium erodes - Ventricles enlarge as a result - Residual mesodermal tissue becomes fibrous and forms chord tendinae - Forms papillary muscles & AV valves Fetal Circulation - Umbilical vein brings O2 blood from the placenta to the Liver - Blood mixes O2 blood from umbilical vein with deO2 blood from LE in the Ductus Venosus - Then it enters the Inferior Vena Cava and enters into the R atrium - The blood can go to the L atrium through the Foramen Ovale or to the R ventricle and into the Pulmonary Artery - In pulmonary artery can go to the lungs or the ductus arterioles into the left sided circulation into the aorta - If it enters the lungs it will return to the left atrium and meet with some of the DeO2 blood from the R atrium via Foramen Ovale - Then it goes into the Left ventricle and aorta it will meet with with the other blood from the ductus arterioles and will circulate to the rest of the body - The blood will then recirculate to the umbilical arteries back to the placenta to get more nutrients

Transition into adult circulation - infant takes it first breath closes fetal circulation & opens adult circulation - with breath in intrathoracic pressure and resistance in pulmonary vasculature - sucks blood from R side of heart into lungs and pulling blood from inferior and superior vena cava L atrial pressure > R atrial pressure - Foramen Ovale closes. L sided circulation pressure gets high and pushes out through aorta - Left sided pressure is higher than the R side pressure, the ductus arteriosus will close - if you want to keep ductus arteriosus open, you would give PGE - if it remains opens tin machine like systolic and diastolic murmur with a patent ductus arterioles then

administer anti-PGE like NSAID (endomethacin). Murmurs within first 24 hours of life are not usually pathological Aortic Arch Derivatives 1st arch - maxillary artery 2nd arch - Stapedial artery and hyoid artery 3rd arch - Common Carotid artery & proximal internal carotid artery 4th arch - on L aortic arch on R proximal part of R subclavian 6th arch - Proximal part of pulmonary arteries and on L, ductus arteriosus 1st arch is Maximal Second = Stapedial C is the 3rd letter of the alphabet 4th arch (4 limbs) = systemic 6th = pulm & pulm-to-systemic shunt (ductus arteriosus)

ADS Causes - Ostium secundum gets too big and overlaps the foramen oval - Absence of the sputum secundum - Neither the septum secundum nor the septum primum develop Structures that grow close to the opening/canal btwn the atrial chamber & ventricular chamber into 2 small openings? - Superior and Inferior Endocardial Cushions Genetic Abnormality commonly associated with endocardial cushion defects*** Down Syndrome (trisomy 21) Ductus Arteriosus Closure - Increase in O2, Decreased Prostaglandins - Indomethacin

Foramen Ovale Closure - Decrease in pulmonary vascular resistance, Increase in left atrial pressure Right to Left Shunts Congenital Heart Disease "Blue Babies" - early cyanosis - bypassing pulmonary circulation and not oxygenating enough blood 5 T's RL Shunts - Tetralogy of Fallot (MCC of early cyanosis) - Transposition of great vessels - Trancus Arteriosus - Failure of TA to divide into pulmonary trunk and aorta; + VSD - Tricuspid Atresia - characterized by absence if Tricuspid valve and hypoplastic RV; requires ASD + VSD - Total anomalous pulmonary venous return (TAPVR) - pulmonary veins drain into R heart circulation; associated with ASD and PDA to allow for LR shunting to maintain CO Tetralogy of Fallot - defect in infundibular septum 1. Pulmonary Stenosis 2. RVH 3. Overriding Aorta 4. VSD - infants have cyanotic spells and learn how to squat to after load and prevent excessive RL shunting - Cyanosis & Boot Shaped Heart

Transposition of great Vessels - The spiral did not take place of the spiral septum - Aorta leaves RV and Pulmonary artery leaves LV - separate of systemic and pulmonic circulations - need VSD, PDA or Patent FO to allow mixing of blood (give PGE)

Offspring of Diabetic moms - Transposition of great vessels - Hypoglycemia - Large gestational age - Clavicle Fractures, shoulder dystocia, Erb-Duchenne palsy, failure to progress Eisenmenger Syndrome - Uncorrected LR Shunt overloading pulmonary vasculature - hypertrophy of right ventricle change to RL shunt - less oxygenation

Left to Right Shunts and other anomalies D-Defects: pDa, vsD, asD, avsD VSD - MC congenital cardiac anomaly - 40% close in first 6 months - Loud holosystolic murmur = small defect ASD - loud S1 + wide fixed split S2

- aortic valve closes first before pulmonic due to ASD - due to overload of pulmonary valve Patent Ductus Arteriosus - usually close within first 24 hours - presents with hypoxemia - treat with endomethacin - continuous machinery murmur

Coarctation of Aorta - infantile type - aortic stenosis proximal to insertion of DA (pre ductal); associated with Turner's syndrome (XO) - adult type - stenosis is distal to ligamentum arteriosum (post ductal); associated with rib notching (collateral circulation), UE hypertension, and weak LE pulses - associated with aortic regurgitation due to after load Ebstein's anomaly - associated with maternal lithium use - tricuspid leaflets are displaced into right ventricle, hypo plastic right ventricle, tricuspid regurg or stenosis - 80% have patent foramen ovale with RL shunt - Dilated R atrium causing increased risk of SVT and WPW (Wolf-Parkingson White) - Physical exam: widely split S2, tricuspid regurgitation Congenital Cardiac Defect Associations DISORDER 22q11 (Di'George) syndrome Down syndrome Congenital rubella Turner syndrome Marfan's syndrome Infant of diabetic mother Cardiac Output Variables Cardiac Output DEFECT Truncus Arteriosus, Tetralogy of Fallot ASD, VSD, AV septal defect (endocardial cushion defect) Septal defect, PDA, pulmonary artery stenosis Coarctation of aorta (pre ductal) Aortic insufficiency and dissection (late complication) Transposition of great vessels

CO = SV X HR Fick's Principle : CO = rate of O2 consumption art O2 - venous O2 Mean arterial pressure (MAP) = CO x TPR = Q*R MAP = diastolic pressure + systolic pressure - MAP is important for dosing esp cardiovascular drugs Pulse pressure = systolic pressure - diastolic pressure - pressure involved in the pulse and proportional to SV Pulse pressure : stroke volume SV = CO/HR = EDV - ESV - Early stages of exercise CO is due to SV and then during sustained exercise due to HR - If HR is too high then incomplete diastolic filling CO Cardiac Output Variables**** - More contractility more pushing out blood SV - Afterload - lots of back pressure from aorta harder to push out blood SV - Preload - pushing more blood into your heart push more blood out SV Cardiac Drugs: Sites of Action Contractility: Cathecolamines (1 rc) Ca pump in sarcoplasmic reticulum IC Ca EC Na Digitalis Contracility: 1 blockade Heart failure - less muscle Acidosis, hypoxia, hypercapnea Non-dihydropyridine Calcium Channel Blockers (Verapamil) - SV with Anxiety due to catecholamines or exercise or pregnancy ( preload) - Myocardial Oxygen demand by afterload then heart needs to pump harder and needs more O2 heart size, hypertrophic myopathy - MI - must dec the amount of O2 the heart needs, e.g. ACE inhibitors, decrease contractility, e.g. metropolol, Preload & Afterload - Preload = EDV - comes from Atrial volume, pressure in atrium or central venous pressure - preload: exercise blood volume - prEload: vEnodilators (nitroglycerin) - pool blood into the veins - Afterload = MAP - proportional to peripheral resistance - Afterload: vasodilators (hydrAlAzine) - expand arteries and dec pressure on aorta - Preload & Afterload: ACE Inhibitors & ARBs

Cardiac Drugs & Sites of Action

- Na-CA counter-transporter - if you block Na and Ca will stay in cell more Contractility - IC Na or EC Na Na gradient will affect Ca concentration - Na-K ATPase pump - if you block this pump, you will have less EC Na and then less activity on the ion exchange Ca Digitalis - inhibits Na-K ATPase pump ultimately IC Ca levels contractility

Charting Cardiac Output Starling Curve

- Exercise the curve goes up to the left - for each preload you push more blood out due to contractility - Heart failure shifts the curve to the right - for any preload there is low CO - Fix contractility by giving digoxin/digitalis

Ejection Fraction EF = SV/EDV = (EDV-ESV)/EDV EV = what your heart pumps out / what your heart can hold = the amount of blood your heart ejects EF = Contractility Normal 55% < 55% = Heart failure

Resistance Pressure Flow P = Qx R R = P /Q Viscosity R Polycythemia, Hyperproteinemic States, Herditary spherocytosis Viscosity in anemia Cardiac & Vascular Function Curves Ohm's law V = IR = 8nL / r^4 n = viscosity

-Inotropy = Contractililty - Inotropy = Heart failure, narcotic overdose - Inotropy = Exercise - Add TPR = Afterload - for a given preload you will have less CO as you increase afterload - Shift curve to right - Inotropy or afterload - Shift curve to left - Inotropy or afterload Heart Failure Pathophysiology Normal Pressures - PCWP = measures the pressure in the LA 12 - measured by the Swan-Ganz catheter - placed in the internal jugular vein or subclavian vein into the superior vena cava into right atrium to the right ventricle; inflate the balloon and it enters the heart into the R pulmonary artery until it can't go any father at the branching point (wedge) - measures approximation of the left ventricle diastolic pressure 10

- Mitral stenosis - PCWP > LV Mitral valve is stenosed while the RA is contracting and pressure rises which PCWP

CHF -pump failure - pressure forward will drop and pressure rises in the fluid entering the heart - syndrome due to acquired or inherited abnormality of cardiac structure or function

- contractility pump failure due to MI or Chronic HTN - LV Contractility CO BP body wants to compensate for CO Sympathetic ACT & RAA - Carotid sinus detects CO sympathetic LV contractility CO + Peripheral edema - RAA - retain Na & H2O preload CO + peripheral edema - LV contractility also pulmonary venous congestion RV output pulmonary edema + peripheral edema - Dyspnea on Exertion - fluid backs up on the pulmonary vasculature - Cardiac Dilation - greater Ventricular EDV Left Heart Failure (pulm symptoms) - Pulmonary Edema - Paroxysmal Nocturnal Dyspnea - Orthopnea - SOB lying down and better sitting up Right Heart Failure (peripheral symptoms) - Peripheral pitting edema - JVD - central venous pressure

- Hepatic congestion - hepatomegaly (nutmeg) liver Renin-Angiotensin-Aldosterone System

- Renin is produced in the kidneys, stimulated by 1 Receptors of the sympathetic nervous system or by the macula dense cells can sense reduced Na in filtrate or JG apparatus which senses the bp drop - Renin cleaves Angiotensinogen AGI in liver - AG Converting enzyme in lungs and kidneys turn AGI AGII - Angiotensin II tenses angios (vasoconstrictor) acts on AGII Rc on vascular SM BP - AGII stimulates Aldo release from the Adrenal Cortex (zone glomerulosa) - Aldo creates a favorable Na gradient for Na & Water to be reabsorbed in the kidney Heart Failure Medications CHF Medications Improve Survival: ACE Inhibitors, ARBs, Aldosterone Antagonist, blockers Symptomatic: Loop Diuretics, Thiazides, Nitrates, Digoxin - Chronic Treatment - Contractility CO Digoxin Contractility (Inotroph) CO - RAA ACE Inhibitors/ARBS Angiotensin - Aldosterone Aldosterone Antagonist (Spironolactone or Apleranone) - Na & Water Retention Loop Diuretics (heavy duty) or Thiazide - Sympathetic Activity blockers metoprolol or carvedilol - blocker will help chronically help the effects of the excess sympathetic activity cardiac remodeling - Contraindicated in acute CHF because they depress myocardial contractility **Which 2 beta blockers are indicated for the treatment of chronic heart failure? Carvedilol and Metoprolol (long acting) - Acute Treatment - ER pt with heart failure 4+ pitting edema foaming at the mouth, acute exacerbation + long standing vhf

- LMNOP - Lasix (loop diuretic) - Morphine (for air hunger/relaxation) - Nitrates (dilate peripheral vasculature) - Oxygen (as needed) - Positioning and Pressors (pool blood into legs & inotropic drugs) - stop blocker - start adrenergic agonists - dobutamine or phosphodiesterase inhibitor **Which beta blocker is indicated for acute decompedsated CHF? Contraindicated in acute CHF because they depress myocardial contractility -Nesiritide (BNP) - Recombinant B(brain)-type natriuetic peptide causes in cGMP & vasodilation - Na & water excretion (diuretic) - BNPs are secreted by myocytes when left ventricle is failure and the EDV and heart is stretching, used as a diagnostic test for CHF 100 (vs COPD exacerbation) - Used for acute decompensated heart failure - can cause hypotension, does not improve mortality Cardiac Glycosides (Digoxin) - Myocardial contractility - aka Digitalis, foxglove plant - treat chronic CHF, reduces symptoms - helps control heart rate in Afib, by conduction at the AV node (only resting heart rate) - Lots of side effects and low therapeutic index - cholinergic effects - Blurry yellow vision - ECG - ST scooping, bradycardia** - Antidote is Atropine - will raise the heart rate and reverse the bradycardia, correct hypokalemia (give Mg+), temporary pacemaker, tachycardia (treat with lidocaine), anti -digoxin Fab fragments - Worsened by renal failure, hypokalemia, quinidine

- Ca necessary to stimulate the actin and myosin to contract - more CA more contractility - If you block ion exchange, less Ca leaves the cell, and more contraction - Na-K ATPase maintains the Na gradient by EC Ca - Digoxin blocks the Na-K ATPase Capillaries & Edema Capillary Fluid Exchange - Blood goes into capillaries out to interstitium back to capillaries + lymphatics - Excess fluid in interstitium = edema PC = capillary pressure - hydrostatic pressure - pushes fluid out of capillary Pi = interstitial fluid pressure - hydrostatic pressure - pushes fluid into capillary Arterial end - capillary pressure exceeds the interstitial pressure Venous end - pressures evens out c = plasma colloid osmotic pressure - pulls fluid into capillary i = interstitial fluid colloid osmotic pressure - pulls fluid out of capillary net filtration process = Pnet = [(Pc - Pi) - (c - i)] Kf = filtration constant Jv = net fluid flow = Kf Pnet capillary failure - Pc (heart failure), venous pressure plasma proteins - c (nephrotic syndrome), liver failure, malnutrition capillary permeability - Kf (toxins, infections, burns), histamine, bradykinin interstitial fluid colloid osmotic pressure - i (lymphatic blockage)

Pitting Edema - excess fluid in absence of additional colloid, watery edema, gravity dependent phenomenon, like water balloon Non-pitting edema - no indentation, colloid in interstitial fluid like jello Transudate - capillary pressure plasma proteins water, protein poor Exudate - protein capillary permeability protein rich Na & Water retention - renal disease or RAA Capillaries & Shock Shock - cardiac failure or vascular failure - Hypovolemic - Blood loss (trauma), Burns (insensible fluid loss) - Cardiogenic Shock - MI, PE, CHF, Arrhythmia, Cardiac Tamponade, Tension PTX, Cardiac Contusion

Hypovolemic/cardiogenic Low-output failure TPR CO Cold, clammy pt (vasoconstriction) SVR Hypervolemia Heart Failure Sepsis/Anaphylaxsis Neurogenic Central Lines

Septic High-output failure TPR Dilated Arteriorles, venous return Hot pt (vasodilation) CO IV fluid, blood LMNOP Antibiotics, IV Fluids, NE IV Fluids, steroids

- Femoral - easiest site with least risk; most uncomfortable, max 5-7 days - Subclavian - easy to find, 3-4 weeks, more comfortable, risk of pneumothorax, CI COPD or lung tumors - Internal Jugular - good landmarks, 3-4 weeks, uncomfortable, risk of carotid puncture or pneumothorax or perforating the L SC vein (where IF and L SC meet) - Swan-Ganz Catheter - right IJ > left SC > right SC > left IJ Femoral Region Lateral Medial NAVEL Nerve, Artery, Vein, Empty Space, Lymphaticsx "dirty" STDs lymphatics closest to genitalia Palpate for artery then insert need 1-2 cm medially next to pulse

Atria & Ventricles Cardiac Cycle Pressure & Volume Loop

- Mitral Valve opens - LV Filling at the end the Atrium closes - Systole begins - Isovolumetric contraction - both valves are closed - Aortic valves opens - V pressure < Aortic Pressure - in pressure with cont ventricle contraction - Aortic pressure < Ventricular pressure - Aortic valve closes - Isovolumetric Relaxation ventricular pressure is going down - Left Ventricular pressure < Left atrium Mitral valve opens

- after load pressure before the Aortic valve opens SV

- contractility pressures SV - preload vol in atria vol in ventricle Pressure/Time: Aorta, LV, LA

Dicrotic Notch - pressure goes back up into aorta after aortic valve closes due to elasticity which aortic pressure Coronary pressure takes place after aortic valve closes during diastole which allows perfusion of the arteries of the heart Diseases that affect elasticity of aorta: Marfan syndrome and Syphillis "tree barking of the aorta" Heart Sounds & Jugular Waves Cardiac Cycle Heart sounds - turbulence after valve closes S1 - after Mitral Valve closes S2 - after Aortic Valve closes S3 - early diastole, rapid ventricular filling, associated with filling pressures (preload) in dilated ventricles, children, pregnant women Dilated ventricles - dilated CM, CHF, Mitral Regurge, LR shunts S4 - right before S1, atrial kick, late diastole, atrial pressure associated with ventricular hypertrophy, pushes against a stiff ventricular wall Stiff LV - Hypertrophic CM, aortic stenosis, chronic HTN, after MI Jugular Pulse - Different waves of JVP At Carter's X, Vehicle's Yield - a wave - atrial contraction, before mitral valve closure, maximizing filling of ventricles before systole - c wave - right ventricular contraction with tricuspid bulging from ventricle into atrium - x descent - ventricles are empty, the bulging relaxes into ventricles - v wave - atrial pressure, filling against a closed tricuspid valve - y descent - blood flows from atria to ventricles, during diastole ECG - QRS - mitral valve closure, ventricular contraction, into systole Splitting - Splitting of S2 can be normal esp in younger individuals esp in athletically trained ppl - Normal splitting happens with inspiration - Aortic valve is closing before pulmonic valve - intrathoracic pressure and blood goes more into R atrium - more preload in R ventricle and takes a bit longer to close the pulmonic valve during systole - .interventricular septum gets pushed to the left slightly due to volume vol of L ventricle - Wide splitting of S2 - associated with pulmonic stenosis or RBBB not only with inspiration

- Split S2 on expiration always pathological - Fixed splitting associated with ASD - high pressure on L side of heart, and L atrium is filling the R side of heart - preload from L atrium and more goes into R ventricle - Pulmonic valve takes longer - Paradoxical splitting - aortic stenosis or LBBB - more volume in L ventricle and delaying the Aortic valve in comparison to pulmonic valve

Systolic Murmurs - read clinical scenario, systolic vs diastolic, where is it best heart - listen to diff parts of chest - watch if its louder on inspiration/expiration or splitting Auscultation of the Heart

- A - right 2nd IC space - P - left 2nd IC space - T - left 4th IC space - M - left 5th IC space @ midclavicular line (apex of heart) Benign heart sounds Split S1 Split S2 on inspiration S3 in pt < 40 y/o Early quiet systolic murmur

Heart murmurs - Diastole - filling ventricles, mitral valve & tricuspid are open, aortic and pulmonic are closed murmurs - M or T stenosis, A or P regurgitation - Systole - ventricles are contracting, A & P are open, M & T are closed murmurs - A or P stenosis, M or T regurgitation - Isovolumetric contraction and isovolumetric relaxation Contrxn - M & T valves are closed, S1 is complete, contract ventricles, A & P closed, no systolic murmur or aortic stenosis Relaxation - ventricles relaxed, all valves closed Bedside Maneuvers Inspiration - neg IT pressure, preload, tricuspid mumur Expiration - mitral murmur due to L atrium filling Hand grip - afterload (SVR), mitral regurg Valsalva maneuver - IT pressure, opposite of inspiration, preload & after load, most murmurs, mitral prolapse, hypertrophic cardiomyopathy murmur Squatting - compresses the veins, and lowers the heart venous return, compresses arteries PVR after load, mitral prolapse Hypertrophic CM murmur Systolic Murmurs - Aortic stenosis - no murmur during first part of systole, heart is contracting and the V pr not > aortic pressure so aortic valve is still closed (isometric contrxn) - ejection click , stiff valves opening due to calcifications - systolic murmur, radiates up to carotids, weak pulses (pulsus parvus et tardus), syncope - 5 causes of aortic stenosis: Bicuspid aortic valve (> 40), Senile/degenerative calcs (> 60), chronic rheumatic valve disease, congenital unicuspid valve, syphilis (tree barking of aorta)

- Mitral regurgitation - murmur begins immediately following S1 - holosystolic murmur -- high pitched blowing murmur - radiate to axilla, lying in L lateral decubitis position - enhanced with after load TPR, hand grip or squatting - causes: ischemic heart disease, LV dilation, endocarditis, rheumatic fever - can be associated mitral valve prolapse

Left Lateral Decubitis Murmurs - Mitral regurgitation - Mitral Stenosis - Left sided S3 or S4 heart sounds - Mitral Prolapse - very common usually not problematic - floppy mitral valve, opens back into the atrium mid systolic click - enhanced by valsalva venous return - mitral valve prolapse can predispose to endocarditis only if you have mitral regurgitation - does not cause turbulent blood flow or valve damage

- Tricuspid regurgitation - holosystolic murmur loudest at tricuspid - enhanced by maneuvers that atrial return like inspiration - cause: endocarditis and rheumatic fever, IV Drug Users - VSD murmur - defect in interventricular septum - looks like mitral or tricuspid regurgitation - holosystolic murmur best heard at tricuspid - louder during inspiration, clinical scenario very impt to diff btwn T regurge murmur

Diastolic Murmurs Heart murmurs - Aortic regurgitation - Diastole - Mitral & tricuspid valves are open, A & P are closed - Regurgitation will produce a diastolic murmur begins after S2 - Ventricles are relaxed,you can't hear the mitral valve stenosis until mitral valve opens - heart is contracted and emptied into the aorta and starts to relax - blood is flowing back normal systolic blood pressure, systemic diastolic will be low wide pulse pressure - causes: aortic root dilation, syphilis, marfan syndrome, bicuspid valve, rheumatic fever

- Murmurs associated with Rheumatic Fever

- Mitral regurge or mitral stenosis, aortic regurge or aortic stenosis, tricuspid regurge - Mitral stenosis - not present immediately after S2 because of isometric relaxation - mitral valve opens and is stenotic and snaps open - expiration will enhance the murmur - diff between split S2 sound: diastolic murmur not just snap - S2 split will be more prominent in inspiration - can result in L atrial dilation, rheumatic disease

- Patent Ductus Arteriosus - continuous machine like murmur - always blood flowing through PDA - keep it open with PGE - close it with endomethacin (NSAIDs)

Action Potentials Cardiac Myocyte Physiology - EC Ca enters the muscle during the plateau state of the AP Ca stimulates more release from SR - Cardiac muscle APs have a plateau due to a Ca influx. - Cardiac nodal cells spontaneously depolarize during diastole automaticity due to If channel (constant influx of Na)

- Cardiac myocytes are electrically coupled to each other by gap junctions Ventricular Action Potential - 4 phases - resting membrane potential is determined by what it is freely permeable to - normal resting potential -75 (K) +55 (Na) +20 (Ca) - Phase 0 - starts at -75 then voltage gated Na channels open drives up towards +55 - Phase 1 - Initial repolarization, some Na closes, Voltage gated K channels open up too - Phase 2 - Plateau, voltage gated Ca channels open and drives potential up towards +20 triggers more CA to be released myocyte contraction - Phase 3 - Rapid repolarization, more permeability to K, lose Ca channels - Phase 4 - resting potential, high K permeability steady state around -75 Effective refractory period - phase 0 - phase 3 - can't elicit a phase 0 depolarization; - if you ERP then you will have to wait longer to depolarize again, slow heart rate How to change slope of phase 0 - Na permeability - if you prolong phase 1 by using Na channel blockers How to prolong phase 3 - K permeability - if you prolong it by using K channel blockers

Pacemaker Action Potential

- SA & AV nodal cells - No phase 1 or phase 2 - Phase 4 - resting membrane potential around -60 (freely permeable to K) - gradual increase, Na channels are spontaneously opened till it reaches the threshold - Phase 0 - voltage gated Ca channels opens at threshold - No plateau at all What will inhibit phase 0 - CCB What will affect the slope of phase 4 - blockers, will decrease the slope prolonging phase 4

Antiarrhythmics No Bad Boy Keeps Clean Na+ channel blockers - Phase 0 Na channels open up - Na channels blockers work on phase 0 and elongating ERP Class IA (slows phase 0, prolongs phase 3) - Quinidine, Procainamide, Disopyramide - Procainamide - Wolfs Parkinson White, cause reversible SLE syndrome (SHIPP) - Quinidine - cinchonism, thrombocytopenia, torsades de points ( QT) Double Quarter Pounder Class IB (shortens phase 3) - Lidocaine, Mexiletine, Tocainide, Phenytoin Lettuce Tomato Mayo Pickles - Lidocaine - acute ventricular tachyarrhythmias and slow HR down, digitalis or MI Class IC (markedly slows phase 0) - Flecainide, Propafenone Fries Please -blockers - cAMP and CA currents slope of phase 4 in nodal cells Class II (suppresses phase 4 depolarization rate) - Esomolol - Supraventricuar Tachycardia, afib and atrial flutter - can mask hypoglycemia * : Glucagon

K+ channel blockers - slows release of K and elongates the ERP Class III (prolongs phase 3) - Sotalol, Amiodarone - Afib - Amiodarone - WPW, pulmonary fibrosis, hepatotoxicity and hypo/hyperthyroidism check PFTs, LFTs, and TFTs - 40% Iodine by weight has class I, II, III, IV effects Calcium Channel Blockers - dihydropyridine (nifedapine works on blood vessels) and non-dihydropyridine (work at the heart) - slope of phase 0 in nodal cells, and elongating ERP since Ca causes depolarizations Class IV (slows the action potential) - Verapamil, Diltiazem - constipation, flushing, edema and heart block - do not combine with blockers

Other antiarrhythmics - Adenosine - K leaving the cell hyperpolarizing cell - permeability to Ca cannot depolarize (flatline stop heart) - used to diagnose SVT - blocked by theophylline (COPD) & caffeine - K+ - depresses ectopic pacemakers in hypokalemia and digoxin toxicity; should be above 4 - Mg2+ - effective in torsades and digoxin toxicity; should be above 2

**pt who codes for > 5 minutes - acidosis is associated with hyperkalemia (H+-K+ pump) give Ca and bicarb Atria to AV conduction Electrocardiogram Axis - 12 lead EKG: I, II, III, aVL, aVR, aVF, v1, v2, v3, v4, v5, v6 - Axis of deviation of the electrical conductance of the heart.

- Measures the signal of your heart in a certain direction - Net signal of heart is down and to the left - aVR - measures from center to right, it will have a negative deflection of QRS complex (below the line) - aVL - positive deflection of EKG since vector is in line with axis - Bipolar leads I - R to L II - R arm to L foot III - L arm to L foot

- The net electrical signal (cardiac axis) will fall within the shaded region in normal cardiac pathology

Left axis deviation: inferior wall MI L anterior fascicular block L ventricular hypertrophy LBBB High Diaphragm

Right axis deviation: RV hypertrophy Acute R heart strain (PE) L posterior fascicular block RBBB Dextrocardia

- Look at Limb lead I and II; If they're positive then it's usually normal

- Look at aVR; if positive, there is pathology, completely opposite direction ECG tracings - tiny box - 0.04 seconds - big box 0.2 seconds

- PR interval - through AV node normal < 0.2 sec (1 big box)(1st degree HB) - QRS - ventricular depolarization, equal on both sides < 0.12 sec (3 small boxes) (V arrhythmia) - T wave - ventricular repolarization, inversion (recent MI), peaked T wave ( K), flat T wave ( K) - U wave - associated with K and hypokalemia, another bump after T wave - SA > AV > Bundle of His - Afib irregularly irregular, no discrete P waves SA node not in sync (Atrial enlargement) No coordinated Atrial contraction no P Pooling of blood in atria clot predispose to SVT : time is critical < 48 synchronized cardiovert, > 48 anticoagulation (heparin) then coumadin rate control - just fix rate, stay on anticoagulation therapy Digoxin, blockers, CCB rhythm control - back to sinus rhythm K+ channel blockers: Sodolol and Amiodalone

- A flutter - sd

Problems with the AV conduction - AV block 1 heart block prolonged PR interval > 0.2 secs usually benign, asymptomatic Lyme disease can cause AV nodal block

- Mobitz type I (wenckebach) 2 heart block progressive lengthening of PR until beat is dropped mostly benign (W=warning)

- Mobitz type II 2 heart block no lengthening of the PR interval, just a dropped beat greater tendency to turn into a 3 heart block : pacemaker

- Third Degree atria and ventricles beat independently of each other P & QRS are present but are not coordinated P > QRS, Narrowing of the QRS (from AV node) Lyme disease : pacemaker

Wolf-Parkinson White Syndrome Ventricular pre-excitation syndrome accessory conduction pathway that bypasses the AV node Bundle of Kent blurred ventricular contraction that is called wave can result in a reentry circuit SVT ( : Adenosine) : Procainamide (Na channel blocker), Amniodarone (K channel blocker)

Ventricular Arrhythmias Ventricular premature contractions beats ka PVCs early occurring widened QRS complexes microrentry of the purkinje fibers usually benign

Ventricular Bigeminy PVC follows each sinus beat Normal, big one, normal big one Trigeminy - 2 normal 1 PVC Ventricular Escape Complex (rhythm) failure of the sinus & AV node to generate an impulse widened QRS usually after a pause (larger than a normal RR interval) rate is slow Ventricular Tachycardia 3 or more successive ventricular complexes non-sustained Vtach - during < 30 seconds sustained > 30 sec leads to hemodynamic collapse usually ~100 bpm rhythm is usually regular wider QRS interval

Torsades de pointes Type of Ventricular Tachycardia shifting sinusoidal waveforms on the EKG Ventricular Fibrillation uncontrolled rhythm, on identifiable waves can lead to hemodynamic collapse emergency defibrillation needed

Physiology of BP regulation Maintenance of MAP Body must keep BP in order to perfuse and O2 the organs If BP drops, the body uses the SNS and the RAA (chronic) Renin Angiotensin Aldosterone System Kidney sense low BP at JG apparatus and secretes renin Renin converts Ag AGI ACE in the lungs converts AG I AG II Aldosterone has kidney reabsorb Na & water Baroreceptors & chemoreceptors Medullary vasomotor center (solitary nucleus) sends a vasoconstricting signal to HR Baroreceptors Baroreceptor on aortic arch via vagus ( BP) Baroreceptor on carotid sinus via glossalpharyngeal nerve (/ BP) Sense stretch signal efferent sympathetic firing + Vagus inhibition of heart Adrenergic 1 receptors responsible for vasoconstriction Sense stretch vagus signal to heart to slow heart and BP Use for SVT carotid massage heart rate or Adenosine Chemoreceptors peripheral chemoreceptors in carotid and aortic bodies - respond to low PaO2, PaCO2, pH central chemoreceptors - pH and PCO2 in the brain, do not directly respond to O2 Cushing rxn - cranial pressure constrict arterioles in brain cerebral ischemia CO2 Hypertension Bradycardia + Respiratory Depression Intracranial lesion with Intracranial pressure (e.g. hemorrhage) Physiology of vasoconstriction Smooth Muscle Contraction

- Contraction - Myosin-PO4 + Actin kinases phosphorylate things - CCBs (nifedapine) - inhibit Ca-calmodulin complex no act myosin light chain no phosphorylation muscle relaxation and vasodilation - Epi 2 and PGE - cAMP inhibits myosin light chain kinases relaxation - Myosin phosphatase dephosphorylates Myosin relaxation - ACT by cGMP (act Guanylyl cyclase) - cGMP phosphodiesterase inhibits cGMP contraction Sildenafil inhibits cGMP phosphodiesterase relaxation - L-arginine NO activates Guanylyl cyclase relaxation iNOS - converts L-arginine to NO GNB stimulate iNOS vasodilation and sepsis cNOS - converts L-arginine to NO in endothelial cells IC Ca stimulates cNOS Atrial Natriuretic Peptide - similar to BMP - produced in atria in responses to atrial volume atrial pressure - vasodilator + causes diuresis of water & sodium - works on afferent & efferent arterioles of the renal glomeruli Review of organs involved in BP regulation - Atria - ANP - Aorta - Aortic baroreceptor/chemoreceptor - Carotid Sinus - baroreceptor/chemoreceptor - Medulla - Control of SNS

- Adrenal gland - z. glomerulosa - aldosterone - adrenal gland - z. fasciculata - cortisol - adrenal gland - medullary chromatin cells - Epi & NE - Liver - Angiotensinogen - JGA of kidneys - Renin - Lungs - ACE - Glomerulus - GFR - Tubules - AG II, ADH, Aldosterone - Local tissue effectors - NO, PG, 5HT, Histamine, Bradykinin, Adenosine, Acidosis, Lactate, O2, CO2, K+ Hypertension Circulation through organs Liver - largest part of the systemic output, lots of metabolic functions Kidneys - eliminate harmful waste & maintain fluid & electrolyte balance & pH; receives highest blood flow per gram of tissue Heart - big btwn arterial O2 and venous O2 since heart can extract about 100% of O2 it receives; O2 demands are met by coronary blood flow Autoregulation Organ Heart demand) Brain Kidneys Lungs Skin Local metabolites-C02 (pH) Myogenic and tubuloglomerular feedback Hypoxia causes vasoconstriction Sympathetic stimulation most important mechanism-temperature control Factors determining autoregulation Local metabolites-O2, adenosine, NO Nitrates**** - (Create NO causes decrease in preload, systemic venous dilation O2

Skeletal muscle Local metabolites-lactate, adenosine, K+

Note: the pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only well-ventilated areas are perfused. In other organs, hypoxia causes vasodilation. Hypertension High blood pressure 140/90, 90% is essential CO or TPR afterload Kidney disease - renal failure or renal artery stenosis Other causes: Drugs (cocaine, amphetamines), Medications (OCPs, steroids, NSAIDs, antidepressants), Obstructive sleep apnea, coarctation of the aorta, endocrine (hyperthyroidism, pheochromocytoma, hyperaldosteronism, cushing syndrome) Prehypertension - 120-139/80-8

Left-sided hypertrophy early form of end organ damage due to HTN myocytes get bigger and the wall gets concentrically bigger thickening of the LV wall myocardial O2 demand, LV - stiff and less compliant S4 No in heart diameter, less filling, Precursor left-sided heart failure RF for MI Aortic Dissection tear in the intima of the aorta which allows blood to dissect into the walls of the aorta forming a false lumen heart will pump into both lumens 2 main causes: hypertension and certain diseases (cystic medial necrosis or mar fans) MC in ascending aorta Tearing chest pain that radiates through to the back Widening of mediastinum on Xray High mortality 2 types: Type A - acending aorta, aortic arch; surgical management Type B - descending aorta; medical management : blocker to lower BP in aortic dissection, reduce arterial pressure and slope of rise of BP Antihypertensive Agents ACE inhibitors Captopril, Enalopril, Lisinopril -pril ACE prevents AGI AGII, also inhibits breakdown of bradykinin (vasodilator) Reduces after load & preload Rise of Renin levels due to loss of inhibition Help prevent remodeling of the heart and also mortality Used also in diabetic kidney disease to reduce the rate of proteinuria and diabetic nephropathy SE: C - cough (elevated levels of bradykinin) A - angioedema P - proteinuria (prevent) T - taste changes (dysgeusia) O - hypOtension P - pregnancy problems (teratogenic) R - rash I - Inc Renin L - lowering AGII, Hyperkalemia, reduce GFR and creatinine ARBs Losartan - sartan block AG II receptors, stop stimulation and aldosterone secretion SE: similar SE like angioedema, except no cough

Aliskiren Renin inhibitor only for HTN can still caused hyperkalemia and renal insufficiency contraindicated in pregnancy Hydralazine Vasodilator - cGMP act myosin phosphatase dilates arterioles > veins, reduces afterload Hypertensive crisis, HTN, HTN in pregnancy SE: reflex tachycardia (often given with blocker), fluid retention, drug-induced lupus Drug Induced Lupus "SHIP" Sulfasalazine Hydralazine Isoniazid Procainamide Safe HTN Meds in Pregnancy Hydralazine Methyldopa Labetalol Nifedipine Minoxidil Opens K channels & hyper polarizes SM (Ca channels stay closed) contraction relaxation used for severe HTN or for hair loss (hypertrichosis) SE: hypertrichosis, hypotension, reflex tachy, fluid retention/edema

CCBs Dihydropyridine CCB: nifedipine, amlodipine, felodipine, incardipine, nisoldipine act on vascular SM to cause vasodilation (mostly arteries) HTN, angina, vasospasm, esophageal spasm, migraine prophylaxis SE: peripheral edema, flushing, dizziness, constipation, reflex tachy Non-dihydropyridine CCB: verapamil, diltiazem @ block Ca channels at pacemaker cells HTN, angina, arrhythmias SE: cardiac depression, AV-block, flushing, dizziness, constipation Nitroglycerin, Isosorbide dinitrate cause vasodilation by releasing NO in SM cGMP relaxation work on veins > arteries preload can be in combo with Nitrate and hydrazine to reduce both after load & preload pools blood peripherally (use for pulmonary edema) SE: reflex tachy, hypotension, flushing, headache Antihypertensive Therapy Essential HTN, no comorbidities - Thiazide Diuretic ALLHAT - showed thiazide reduced risk of stroke can add ACE/ARB -blocker, CCB HTN + CHF - Loop Diuretic (Furosemide) blocker, ACE inhibitors, ARBs, and K sparring diuretics (aldo antagonist - spironolactone) can combo no blockers with cardiogenic shock , no CCB HTN + Diabetes - ACE/ARB kidney protective; reduce proteinuria Thiazides are ok blockers can mask hypoglycemia Post-MI/CAD - Thiazide, blocker, ACE/ARB dec mortality use CCB and Nitrates for angina Afib - Diltiazem/verapamil (rate control) Bradycardia - avoid diltiazem/verapamil, blockers slow heart down Renal insufficiency - ACE/ARB dec proteinuria, but can also worsen creatinine hyperkalemia avoid K sparring diuretics Renal artery stenosis avoid ACE/ARB renal insufficiency -pine

BPH - blocker (lower BP and help urinary retention) Hyperthyroidism - Propranolol (manage hyperthyroid symptoms) Hyperparathyroidism - Loop Diuretic (facilitate urinary excretion of Ca) avoid thiazide (retain Ca) Osteoporosis - Thiazide (retain Ca) Gout - avoid Thiazide can cause hyperuricemia Pregnancy - Hydralazine, Methyldopa, Labetalol, Dihydropyridine CCB avoid ACE/ARB Migraines - CCB, blocker Essential Tremor - Propranolol Malignant Hypertension treatment Severe hypertension that is rapidly progressive end-organ damage Nitroprusside - cGMP via direct release of NO, can dilate both arteries and veins short acting, but can cause cyanide toxicity Diaxozide - opens K in cells in pancreas and shuts insulin secretion also opens K channels in vascular SM vasodilation (like Minoxidil)

Atherosclerosis & Coronary Artery Disease Arteriosclerosis - Sclerosis/scarring/hardening of the arteries - Monckeberg's arteriosclerosis - calc in the media of the arteries benign pipestem arteries, does not obstruct blood flow, does not involve intima - Arteriolosclerosis - hyaline thickening of small arteries and arterioles, e.g. diabetes or HTN - Atherosclerosis - fibrous plaques and atheromas that form in the intima of the arteries Atherosclerosis - disease of elastic arteries, involving the intima, in medium sized or muscular arteries - Summary: Start with endothelial cell dysfunction accumulation of M and LDL foam cell formation fatty streaks smooth cell migration (platelet derived growth factor) TGF fibrous plaques atheroma - Location of plaques are important: Abdominal Aorta, Coronary Arteries, Popliteal Artery, Carotid Artery Pathogenesis of Atherosclerosis - Endothelial injury leads to vascular permeability, leukocyte adhesion, and thrombosis - Accumulation of lipoproteins: occurs in the vessel wall and is mostly LDL - Monocyte adhesion to the endothelium: subsequent migration of monocytes into intima and transformation into M and foam cels - Platelet adhesion - Factors release: ACT platelets, M, vascular wall cells, induce SM recruitment - SM cell proliferation and ECM production - Lipid accumulation: occurs extracellularly and within M and SM cells

Complications of Atherosclerosis based on location - smaller vessels can become occluded and then compromise distal tissue perfusion - ruptured plaque can embolize atherosclerotic debris and cause distal vessel obstruction or can lead to acute vascular thrombosis (stroke) - destruction of the underlying vessel wall can lead to aneurysm formation with secondary rupture & thrombosis Abdominal Aortic Aneurysm - atherosclerotic plaque compressing the underlying media - Nutrient and waste diffusion is compromised - Media degenerates and necroses, leading to arterial wall weakness - MC in men over 50 and in smokers - Presents as a pulsating mass in the abdomen - consequences include: rupture leading to fatal hemorrhage, embolism from atheroma, obstruction of a branch vessel and impingement on an adjacent structure (ureter) - monitor by US but if > 5 cm must treat with surgery Coronary Arteries

- RCA Marginal Artery Posterior Descending (Interventricular) artery (80%) -LCA Circumflex LAD PD (20%) - SA and AV nodes - supplied by RCA Arrhythmia - RCA (80)% supplies inferior portion of left ventricle via PDA (right dominant heart) - Coronary Artery occlusion MC occurs: in left anterior descending (supplies anterior interventricular septum) Anterior Wall MI - Coronary arteries fill during diastole - Posterior part of the heart is the left atrium which can cause dysphagia (esophagus) or hoarseness (recurrent laryngeal nerve) Ischemic Heart Disease Angina - narrowing of 75% of the CAD - Stable - predictable, 2 atherosclerosis; ST segment depression on EKG, retrosternal chest pain - Unstable - unpredictable, worsening, ST Depression - Prinzmetal's angina - 2 coronary artery spasm, ST elevation (more ischemia) then reversal dihydropyradine CCB - nifedapine - Coronary steal syndrome - vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to high perfusion - MI - Most often due to acute thrombosis results in myocyte necrosis or sudden cardiac death - Sudden cardiac death - death within one hour usually due to ventricular arrhythmia - Chronic ischemic heart disease - progressive CHF over many years due to chronic ischemic myocardial damage

5 Deathly Causes of Chest Pain - Aortic Dissection (or dissecting aortic aneurysm)- tearing pain, radiating to back - Unstable angina - MI - Tension Pneumothorax - collapsed lung and one way valvular disruption of lung, air gets into pleural cavity - PE Most likely causes of chest pain Prinzmetal's angina - ST segment elevation only during brief episodes of chest pain MSK chest pain - pt is able to point to localize the chest pain with one finger Costochondritis/MSK - chest wall tenderness on palpation Aortic Dissection - rapid onset sharp chest pain that radiates to the scapula Spontaneous Pneumothorax - rapid onset sharp pain in a 20 year old associated with dyspnea GERD, esophageal spasm - occurs after heavy meals and improved by antacids Pericarditis - sharp pain lasting hours-days and is relieved by sitting forward MSK pain - pain made worse by deep breathing and/or motion, pleuritic chest pain Shingles/Herpes Zoster - chest pain in a dermatomal distribution, pain precede rash GERD, MSK pain - MCC of non-cardiac chest pain Costochondritis - inflammation of cartilage where the ribs connect to the sternum - painful when moving chest wall and pressing on it - - NSAIDs Antianginal Therapy MVO2 by decreasing EDV BP Nitrates blockers Combo Contractility HR (reflex) Ejection Time (reflex)

Combo therapy lowers the MVO2 more than Nitrates & blockers alone ACE Inhibitor ( afterload) also used Lipid Lowering Agents HMG CoA reductase inhibitors (-statins) - LDL HDL TG - prevents conversion of HMG-CoA to cholesterol precursor - Hepatotoxicity (LFTs), Rhabdomyolysis Niacin B3 - LDL HDL TG - inhibits lipolysis in adipose tissue and reduced hepatic VLDL secretion - Red flushing, hyperglycemia (acanthosis nigricans) hyperuricemia (gout)

Bile Acid Resins (cholestyramine, colestipol, colesevelam) - LDL - Prevents intestinal reabsorption of bile acids

slightly HDL

slightly TG

- tastes bad, go discomfort, absorption of Fat soluble vitamin, cholesterol gallstones Cholesterol Absorption Blockers (ezetimibe) - LDL - Prevents cholesterol reabsorption at SI brush border - LFTs, diarrhea Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) LDL HDL TG - Upregulates LDL TG clearance - Myositis, hepatotoxcity ( LFTs) cholesterol gallstones Omega 3 FA - fish oil & flaxseed oil - TG - reduce severity of RA and arrhythmias Elevtaed TGs - can lead to pancreatitis, must be 600-700's can get as high as up to 2000 - Fibrates are first line + Omega 3 FA

MI Pathophysiology LAD - MC artery occluded in MI; anterior wall RCA - 2nd most common Circumflex - 3rd most common Adrenergic Sx: Diaphoresis, Tachycardia, Retrosternal pain, Left Arm and Jaw, Dyspnea, Fatigue blockers mask the symptoms, but reduce mortality Older women or diabetics- do not have classic presentation Reversible injury - 30-40 minutes Evolution of an MI 0-4 hours gross: None

micro: None risks: Arrhythmias 4-24 hours gross: Dark mottling micro: Contraction bands (early coag necrosis), Neutrophil emigration, CKMB, Troponin I, CPK risks: Arrhythmia 1-3 days gross: Dark mottling micro: Coag necrosis, loss of nuclei, Striations, Neutrophils risks: Arrhythmias 3-4 days gross: Hyperemia micro: Neutrophils risks: Arrhythmias 5-10 days gross: Hyperemic border, yellow tan softening micro: Margin Granulation tissue risks: Wall rupture tamponade, Papillary muscle rupture, interventricular muscle rupture 10 days - 8 weeks gross: Gray, white scar micro: collagen cellularity risks: Dressler syndrome - fibrous pericarditis > 2 months gross: complete scar micro: dense collagen scar risks: ventricular aneurysm Diagnosis & Treatment of MI ECG diagnosis of MI****

Gold Standard ST elevation of at least 1mm in 2 contiguous leads T wave inversion New LBBB New Q waves (at least 1 block wide or height of total QRS complex) Left anterior Descending Left circumflex Right Coronary Right Coronary Serum diagnosis of an MI CPK - elevated with any type of muscle damage Cardiac troponin I - most specific, rise after 4 hours, elevated 7-10 days, used of Diagnosis CK-MB - elevated to heart muscle, but other muscle can show, used to diagnosis re-infarction Myoglobin - rises quickly before 4 hours for damaged heart muscle ECG - ST elevation (transmural MI), ST depression (subendocardial infarct/ischemia), pathologic Q wave (transmural/old infarct) Types of infarcts Endocardium - superficial layer that lines the chambers, can get infected (endocarditis); most vulnerable since the heart is perfused from the coronary arteries from the outside in Myocardium - muscular layer Pericardium - outside layer of heart that can get inflamed (pericarditis) Transmural Infarcts necrosis Affects entire wall Subendocardial Infarcts due to ischemic necrosis of < 50% of ventricular wall subendocardium esp vulnerable to ischemia Anterior Wall V1-V3 (V4-V5) ST elevation

Lateral Wall aVL V5 V6 Inferior Wall II, III, aVF Posterior Wall R precordial EKG: V4

ST elevation on ECG, Q waves MI complications

ST depression on ECG

1. Cardiac Arrhythmias - MCC of death and first few days during healing Ventricular fibrillation - MC lethal arrhythmia 2. Left Ventricular Failure & Pulmonary Edema - S4 heart sound 3. Cardiogenic Shock 4. Ventricular free wall rupture cardiac tamponade papillary muscle rupture severe mitral regurge interventricular septum rupture VSD + murmur 5. Ventricular aneurysm formation - scar tissue embolism from mural thrombus (anticoagulate) 6. Fibrinous Pericarditis - postinfartion, friction rub, lean forward for relief 7. Dressler's Syndrome - AI phenomenon resulting in fibrinous pericarditis 5-7 weeks post mi MI Treatment "MONA" Morphine - pain/stress Oxygen - get more O2 to heart and body Nitrates - preload, sublingual or topical paste or iv Aspirin - acutely or colpitagril (if allergic to aspirin) blockers - O2 demand, infarct size, mortality, risk risk of acute cardiogenic shock if LV dysfunction ACE - after load, O2 demand, cardiac remodeling, risk of HF and death Statins - stabilize atherosclerotic plaques, inflammation and LDL Mg & K - PRN - MG > 2 and K > 4 prevent arrhythmias Cardiomyopathies & Endocarditis Cardiomyopathies Muscle pathology of the myocardium Dilated CM - most common heart gets bigger and adds sarcomeres in series systolic dysfunction, abnormal contraction S3 sound, laterally displaced PMI causes: Alcohol abuse, wet Ber1Ber1, Coxsackie b virus myocarditis, Cocaine use, Chagas' disease (+megacolon/esophagus), Doxorubicin/Donorubicin toxicity, hematochromatosis, peripartum cardiomyopathy, myocardial ischemia Hypertrophic Obstructive CM - HY aka idiopathic hypertrophic subaortic stenosis concentric hypertrophy - sarcomeres in parallel (disorderly) mostly a hereditary disease (AD) vs LVH is mostly due to HTN lots of hypertrophy of the IV septa, and too close to mitral valve leaflets outflow obstruction

normal sized heart + S4 (stiffen ventricle) apical impulse is enlarged/diffuse systolic murmur (similar to aortic stenosis) valsalva will make it larger (diff vs aortic stenosis) MCC of sudden death in healthy young athletes blocker or non-dihydropyridine CCB (verapamil) slow down the heart and diastolic filling Restrictive obliterative CM depositing stuff onto the myocardium disrupting diastolic function muscle becomes thickened and becomes restrictive sarcoidosis (granulomas), amlyoidosis, post radiation fibrosis, endocardio fibroelastosis (congenital), Loffler's syndrome (eosinophils will endomyocardial fibrosis) hemochromatosis Myocarditis can cause dilated CM Generalized inflammation of the myocardium (not from ischemia) MCC in US: Coxsackievirus (echovirus & influenza virus) Histo diffuse interstitial infiltrate of lymphocytes with myocyte necrosis Bacterial Endocarditis characterized by lesions or vegetation (mass of platelets, fibrin, mass of organisms and inflammatory cells) that sit on valve leaflets subacute bacterial endocarditis - can have vegetations with granulomatous tissue in the center Dx: multiple blood cultures, echocardiogram (TEE) to look for vegetations S&S of endocarditis fever, chills weakness, anorexia, anemia new regurge heart murmur* or heart failure mitral valve is mc; tricuspid mc in IVDU septic pulmonary infarcts splinter hemorrhages in fingernails Osler's nodes (painful red nodules on finger and toe pads) Janeway lesions (erythematous macules on palms and soles) roth spots (retinal hemorrhage with clear central areas) - rare signs of embolism: brain infarct focal neuro defects, renal infarct hematuria, splenic infarct abdo or shoulder pain systemic immune reaction: glomerulonephritis, arthritis Organisms 75% are from: s. aureus (high virulence acute endocarditis) - large vegetations on previously normal valves, rapid viridans streptococci - subacute (low virulence) smaller vegetations on already abnormal valve dental procedures or previous rheumatic fever enterococci (fecalis) - vancomycin resistant endocarditis coagulase (-) staph - staph epidermitis IVDU: Pseudomonas or Candida or Staph epidermitis s. bovis - might also have colon cancer

negative cultures: HACEK organisms: Haemophilus, Actinobacilus, Cardiobacterium, Eikenella, Kingella Complications: Rupture to the chord ten, glomerulonephritis, suppurative pericarditis, embolism, valvular damage Libman-Sacks endocarditis non-infective endocarditis sterile wart-like vegetations on both sides of the valve associated w SLE Other Cardiac Pathology Rheumatic Heart Disease Autoimmune phenomenon 2 to a bacterial infection - Type II HSR Pharyngitis Group A hemolytic Strep Pyogenes (Scarlet fever) Autoantibodies from the disease that attack the heart MC MItral valve but also can be the aortic valve Mitral valve relapse as an early lesion mitral stenosis Aschoff bodies, areas of fibrinoid necrosis + mononuclear multinucleate giant cells (granulomas) Anitchkow's cells and elevated ASO titers

Diagnostic criteria (Jones) for rheumatic fever Evidence of group A strep (ASO titer) 2 Major + 1 Minor Major: JONES joints (migratory polyarthritis) (pancarditis) Nodules (subcutaneous Erythema Marginatum (serpiginous skin rash/annular lesion) Sydenham chorea (chorea of the face, tongue, upper-limb)/St. Vitus dance Minor: arthralgia, fever, ESR or CRP, prolonged PR Pericarditis Pleuritic chest pain, sharp with inspiration, better sitting up and leaning forward distant heart sounds + friction rub diffuse ST segment elevation in most leads or PR depression Fibrinous: Dressler's syndrome, uremia, radiation

Serous: noninfectious inflammatory diseases (lupus), viral pericarditis Suppurative/purulent - usually bacterial infection (pneumococcus, streptococcus) Hemorrhagic - TB or melanoma Can resolve completely or become a restrictive pericarditis Kussmaul's Sign - JVD with inspiration - (pathological) Cardiac Tamponade

Compression of the heart by fluid, blood or pericardial effusion leads to CO and equilibration of diastolic pressures in all 4 chambers hypotension JV, distant heart sound, pulses paradoxes, HR Pulsus Paradoxus Exaggerated response in amplitude of systolic blood pressure during inspiration 10 mmHg take a deep breath and inspire IT pressure blood will rush into R heart pushes on IV septum to the left smaller in inspiration than expiration if left ventricle vol is smaller CO systolic BP is lower in inspiration (normal) sign of cardiac tamponade Causes with exaggerated inspiration: cardiac tamponade, asthma, chronic sleep apnea, pericarditis EKG: Electrical Alternans*** - specific, but sensitive - alternating electrical impulses Alternating QRS amplitude

Kussmaul's Sign vs Pulsus Paradoxus Kussmaul's sign Pulsus Paradoxus

JVD w inspiration capacity of RV Constrictive pericarditis >> tamponade Syphilitic Heart disease

SBP 10 mmHg w inspiration capacity of LV Cardiac Tamponade >> Pericarditis

Tertiary Syphilus disrupts the vasa vasora, BV that supply aorta Dilation of Aorta and valvular ring aorta regurge or stenosis Aortic aneurysms or stenosis tree bark appearance Cardiac tumors Myxomas - MC primary cardiac tumors in adults occur in LA, LA myxoma look like a ball of tissue in the atrium obstruct mitral valve syncope can go into the LV tumor plop Rhabdomyomas - MC in children Associated with tuber sclerosis, astrocytoma and angiomyolipoma (renal) Metastasis - MC cardiac tumor melanoma, lymphoma kussmal's sign - R side of heart can't fill properly JVD with inspiration

Varicose Veins tortuous dilation of the superficial veins due to venous pressure one way valves in veins are worn out - venous insufficiency leads to poor wound healing and ulcers on skin Raynaud Phenomenon Arterial vasospasm poor blood flow to skin and fingers/toes brought on by cold temperatures or emotional stress causes pallor or cyanosis reperfused becomes red can be part of mixed CT disease or Beurger's disease or lupus or crest scleroderma dihydropyradine CCB - vasodilator or low dose aspirin Vascular tumors Sturge-Weber disease congenital d/o that affects capillaries causing intracranial AV malformation leptomeningial hemeangioma affect brain & eye port-wine stain in the opthalmic region of the trigeminal nerve vascular malformation seizures, early onset glaucoma seizures, hemiplegia

Strawberry Hemangioma benign capillary hemangioma of infancy that resolve spontaneously Cherry Hemangioma benign capillary HA of the elderly, looks like mole Pyogenic Granuloma Polypoid capillary hemangioma, ulcerate and bleed trauma and pregnancy Cystic Hygroma cavernous lymphangioma of neck, turner syndrome Glomus tumor benign painful, red-blue tumor under fingernails Bacillary angiomatosis due to Bartonella Henselae infections, benign papules in AIDS pts Kaposi's Sarcoma indolent variant - associated with older men of mediterranean descent endemic variant - in Subsuherent africa Infectious - with HIV or HHV-8 causes proliferation of vessels & lymphatics of the skin and also sometimes internal organs Angiosarcoma liver lesion associated with vinyl chloride, arsenic, and ThO2 Lymphangiosarcoma lymphatic malignancy with persistent lymphedema Small-vessel vasculitis Microscopic polyangiitis affects kidneys pauci-immune glomerulonephritis pANCA + myeloperoxidase (MPO) ANCA Wegener's granulomatosis (Granulomatosis with polyangiitis)**** focal necrotizing vasculitis, necrotizing granulomas in the lung & upper airway, and cANCA necrotizing glomerulonephritis

(Wegener's and Good pastures - only dz that affect both lung and kidneys, diff Wegener's also affect UA and lungs + granulomas) S&S: UA disease, dyspnea, hemoptysis, hematuria : cyclophosphamide and corticosteroids Churg-Strauss syndrome Granulomatous vasculitis with eosinophilia with asthma, sinusitis, peripheral neuropathy Differential Diagnosis for Eosinophilia: NAACP Neoplasm Allergy/Atopy Asthma Addison's disease Collagen vascular diseases Parasites Henoch-Scholein Purpura cause a rash on the buttocks and legs in children, palpable purport arthralgia in knees + abdo pain (intestinal hemorrhage/melena) esp after an URI + IgA immune complexes/nephropathy self-limiting temporary disease Medium Vessel Vasculitis Polyarteritis Nodosa Kawasaki Disease

Buerger Disease Large-Vessel Vasculitis Temporal Arteritis Takayasu Arteritis