ࡱ> mojkl5@ ڈbjbj22 3XXϕ0VVVVVVVj2C2C2C8jCLEjfz^F^F(FFFFFFacccccc$R2VLFFLLVVFF L(VFVFaLaDVV1FRF " 2Cu -,a60fYF>X1jjVVVVV10FhHXIJFFFjjd>@d"jj@EKG & Interpretation Coronary circulation L coronary art.: branch off !aorta, into L ant, ! Circ.flex, supplies blood to ant. + lat. wall of LV. supply e& c O2 R coronary art. ( post. ! (LV) + marginal branches (RV). Supplies blood to RV, AVN + inf/post walls of LV. Action potential Resting no elect activity, Na > outside, K > inside -depole - when inside becomes + -repole rtn of memb potential to resting state Phase 0 rapid depole Na moves in rapidly, Ca moves in slowly; K+ moves slowly out -90v ( +20 Phase 1 early repole Na partly close, K+ cont to lv cell (inside +), Na Ch. close; represented as neg deflection on EKG Phase 2 plateau; Ca in, K out; keeps e& contracted so that all blood is able to lv& due to Ca. ST segment on EKG Phase 3  rapid repole  Ca close, K out ; T wave Phase 4  resting  cell memb closed to Na, K moves in  diastol Fast response  not SA, AVN, no pacemaker. Don t initiate, stim by other cells. T-hold leads to Na ch. open( Phase 1. Slow  SA, AV  automaticity; slow leak during Phase 4 until threshold ( depole. Leads to stim of all other e& cells Absolute Refractory - 1, 2, some 3; can t depole. Relative Refractory  strong stim can cauz resp(starts midpt 3-4) Automaticity  specialized cells initiate impulse spontaneously Conductivity  ability to Tx impulse fr 1 e& cell to another Excitability  ability to respond to a stim Contractility  ability to contract p receiving impulse If anything wrong here, e& will malfunction Conduxn pathway  contraxn SA( Interatrial path (AV ( AV junc ( BOH (R/L BB ( Purkinje fibers. SA initiates, stim both atria (p wave is atria depol), leads I, II, avf, V2-6 should be round + upright; aVr inverted. PR Interval  fr begin of atrial depol ( vent depol; amt of time impulse travels fr SA ! BB; .12-.2 sec ; p wave is atrial rate QRS  Q wave 1st neg deflecxn p wave. 1st + deflecxn is R wave. S waves is 1st neg deflecxn p r wave, represents vent depolarization and atrial repolarization ST marks begin of vent repole + the ventric begin to refill. Absolute refractory - lasts fr begin of QRS to mid Tno impulse lead to depole. J Point - end of QRS + begin of T, ! or ! of ST. Depression = ischemia; elevation = injury. 1mm is nml. T waves  ventric repole, last part of ventric systole. R on T phenomenon  leads to vfib; e& not pumping properly. Something other than p-maker is acting, leading to depole. During relative refractory. Peaked Ts - hyperk QT interval prolonged v repole ie: cocaine, organophosphate poisoning, torsades lead to vfib. Ea big box .20s, 1 little box is .04s Q wave > .04 (~1 little square) pathologic (width + depth 1/3 of R wave) MI signature (old or current) ST !: I, aVl, V5 +V6 = lateral wall MI Reciprocal "s  lat, ST !(look in 2, 3, f) Anterolateral  reciprocal "s in 2, 3, avF shows ST ! Inferior  ST !in leads I + avL Posterior  reciprocal "s in V1-V4 avR is always reciprocal BBB  infarct induced can ! mortality 40-60% L ant ! supplied bundles; ant. septal MIs develop BBB Eti: usually ischemic e& dz; leads V1, V6 + lead 1. If impulse is blocked thru BB, ventricle depol slower = wide QRS > .12s  Bunny ears  BBB, caused by ischemic e&dz. turn signal  signal ! = right, ! = L. Always c V1 LVH *Rule of 35: Age > 35, if sum >35 = LVH Age < 35, sum needs to be 53 = LVH * Measure deepest S wave in V1 or V2, tallest R wave in V5 or V6 = >35 is LVH RVH pulm htn, pulm stenosis, V1,V2, V3 r closer to RV; look to c if R is lrgr compared to S. Atrial hypertrophy p pulmonale- tall P wave in II, III, AVF (> 2.5 mm) Left Atrial hypertrophy wide P waves in any lead, >.11 sec, notched or double hump in any p wave, negative deflection in the terminal portion of the p wave Non-e& Surgery in the e& Pt Consider pt s e& status when planning elective surgery Anesthesia, meds, part of tx plan. Be prepared for complications Detection of comorbid Dz  elective surgical procedures H&P: find out if previous surgical intervention or prev complications including post-op MI or just rxn to anesthesia or meds Compliance: clubbing of nails, pale nails, anemia; can have ramifications on plan. Detect unk illness Baseline studies: PT, PTT, coagulation, RBCs, EKGs UA is important; specialized testing ie: echos, stress tests, PFTs Monitoring of e&/comorbid dz: copies of chart, lab reports sent to office; resp. dept to discuss post-op intervention Dripps chart  quantify surgical risk, separates pt into 5 classes; higher the class, the more risk u r. Used for any surgical pt e& risk scale, gives pt. value for ea parameter; add up all pts then use Dripps chart If pts are too high, delay procedure or pt not a candidate for surgery Potentially fatal cardiac complications Post-op MI, pulm edema, v-arrhythmia. Score of < 25, c all factors considered minimal surgical risk. Risk > 5 implies there is some surgical risk. Class II + III benefit fr baseline studies, etc; >26 suggests risk of fatal coronary event Risk/benefit ratio - estimate pts ability to respond to peri-op + post-op stress. There r myocardial risk factors if preexisting cardiac dz; metabolic RFs if enzymes/e-lytes r unstable; hematological RFs ie: intraop blood loss, unanticipated blood loss. - Pulm MCC of post-op morbidity; general anesthesia + regional reduces resp; some alveoli r collapsed at base of lung. In addition, paralyzed so they remain cooperative (neuromusc blocking agents). Postitional "s cause VQ mismatch, pt can t absorb all O2 + have the collapsed alveoli again at the base. [!O2]in relation to Nitrogen. - Factors c endoctracheal assoc  pts c aspiration, self aspiration sets up microtrauma if done incorrectly. - Pt factors: smoking (no smoking 24h b4 surgery, b/c inhaling nicotine depresses nml function of mucocilia), resp dz, obesity, nutritional depletions, resp dz fr occupation. Extended pre-op state higher risk to nosocomial infxtns. e& considerations - noncardiac surgery all req. comprehensive preo-op w/u; evaluate e& function (tolerate stress of surgery, ie: EKGs + compare, CXR, enzymes, echo, pulm art cath. (pt nearing that 26 #; class II or III.) Post MI < 6mo  lose of these Pts; if elective will postpone procedure, including 30% postop 3mo Post MI > 6mo  mortality rate 5%; dramatic improve No e& Hx  mortality rate is 0.5% Unstable angina- unstable at any time ( avoid surgery unless optimizing them for bypass Stable not assoc c an assoc risk. Preop consider all #s + consults Pt c previous CABG( pts have been cured, there is no significantly appreciative danger Rheumatic e& Dz- require prophylactic ABx, b/c !risk. Murmurs- individualized + if assoc CHF; these r diff fr innocent murmurs. Most benign r apical. Never assoc c palpable thrill. Valsalva maneuvers don t " charact. of murmurs c innocent murmur. Aortic stenosis c harsh holosystolic murmur; displaced PMI. Mitral valve insufficiency is assoc c ! risk of post-op problems. Goal  make sure FEV1 of at least 800 ml to 1 L post-op; if not dont remove fr respirator! AMPLE Allergies, Medications, Pmhx, Last meal/last bowel mvmt, Events preceding the emergency Pericarditis, Endocarditis, Tamponade and Myocarditis Pericardium 2 layers, fibrous tissue. Inner visceral attached to e& s epicardium + outer parietal  stabilizes/protect e& Pericardial space  potential space; serous fluid, protects e& Problems: Dz, Ca, pus, infxn, cont spread of bact; trauma to e&  vessel might rupture causing effusion or tamponade Flexible, permit "s in e& size, can t stretch rapidly enough to accommodate rapid dilation. BP drops ( tamponade situation. Can t stretch acutely. Tamponade  compression of e&, accum of blood/fluid in pericardial sac. Prevents e&fr expand properly Life-threat. Pericardialcentesis- allow e& to expand again (QRS !). Recurrent effusions - req surgery, pericardial window, remove piece of it so fluid build! will leak into thoracic cavity. Causes: pericarditis fr bact/viral infxn, e& surgery, dissecting aortic aneurysm, wounds to e&, end-stage lung Ca, + acute MI, rupture of wall p MI, kidney failure (fluid overload, 3rd spacing) Sx: anxiety, restlessness, SOB, fainting, CP, swelling of abd, skin pale, gray/blue, palp; weak pulse, !BP EKG - ! voltage b/c electrodes have ! impedence due to  fluid . Enlarged e& on CXR. Dx: echoCG 1st choice, muffled e& sounds, periph pulses weak or absent; neck veins may b distended, BP may be !. Pulsus paradoxical, deep inhalation and BP drops, light-headed. Fluid in pericard sac may show on: CXR, echoCG, Cx CT, MRI, angiography Tx: fluids (maintain nml BP), meds to ! BP (dopamine, or a1 constrictors), O2 (reduce workload), treat cause Pericarditis swelling/irritation of pericardium sac. Acute/chronic, sharp CP rubs against e& s outer layer. Acute: infxn process, malignancy, radiation, drug tox, hemopericardium, other inflam processes in myocardium or lung. Syndromes c pleuritic CP, dyspnea, friction rub (sandpaper), F + leukocytosis Dx: CXR, ECG (st !, rtn to baseline, t wave inversion), echoCG nml in inflammatory pericarditis, may show pericardial effusion; CXR nml; CBC, BUN, Cr, bact serology, autoimmune serology, thyroid function r/o myxedema; sed rate creatinine kinase Causes: viral (coxsackie, echovirus)/bact (staph, strep, mycobacterium, lyme); fungal, drugs (procainamide, hydralazine minoxidil), radiation, CT dz, uremia, myxedema Sx: sudden/gradual onset sharp/stabbing. CP radiates to bk, neck, L shoulder, arm. Aggravated by mvmt or inspiration + by lying supine; sitting ! + leaning fwd ! pain Tx: viral  symptomatic, NSAIDs, indomethacin best choice for inflam; may b recurrences in 1st few months Bacterial pericarditis - usually very sick; critically ill. Pulm infxn that spreads to e&. Uremic pericarditis  complication of RF; occurs in Tx uremia + stable dialysis Pt; c or s Sx, typically afebrile. Usually resolves c institution or aggressive dialysis. Indomethacin + glucocorticoids r ineffective in uremic pericarditis. Neoplastic pericarditis usually pericardial window b/c recurring, or pericardiectomy; assoc c Ca (breast + renal). Sclerose area, inject tetracycline into potential space, irritate pericardium so visceral + pericardial = one Radiation pericarditis usually c in 1st yr but can recur. Post MI or postcardiotomy pericarditis inflam rxn to transmural myocardial necrosis, usually occurs 2-5d p infarction. Pain recurrence, audible rub, repole "s. Spontaneous resolution usually occurs p a few days Dressler s syndrome  wks!mo p MI or open e& surgery - presents c typical pain, F, malaise, leukocytes, ! sed rate. Lg pericardial, pleural effusion Tx: NSAIDs, corticosteroids, recurrences r common Constriction pericarditis  occurs when fibrous thickening + loss of elasticity of the pericardium results in interference of diastolic filling, usually follows inflame causes: trauma, open e& surgery, intrapericardial hemorrhage, fungal/bacteria, uremic. Sx: develop gradually + mimic restrictive PE: pedal edema, kussmauls, ascites, JVD, no friction rub. Dx: ECG low voltage QRS, echoCG Tx: supportive, symp. pts: pericardiectomy, diuresis, ABx Endocarditis infxn of endocardial surf of e&, include 1 >valves, the mural endocardium or septal defect. Infxn may bactere., common during dental, URI, urologic, !GI dx surgical procedures. Growths may form clots, break off + travel. Infectious  strep viridans responsible for of all bacterial endocarditis Sx: subacute or acute, FUO; fatigue, malaise, HA + night sweats. Anorexia, wt loss, myalgias, SOB, dyspnea. Illness progresses ( sm dk lines, called splinter hemorrhages, under fingernails. "ing murmurs in e&, enlgd spleen + mild anemia. Petechiae, osler nodes (subq nodules on distal fingertips), Janeway lesions (palms + soles) Roth spots (retinal hemorrhages). Murmurs result fr " in blood flow across valves when clumps of bact, fibrin + cellular debris, called vegetations collect on the e& valves. MITRAL VALVE MOST OFTENLY AFFECTED. Native valve acute endocarditis usually aggressive course. Staph + group B strep r typical agents. Subacute more indolent than acute, usually in setting of underlying valvular dz ( causative agent. Drug users: tricuspid + staph aureus. ! mortality rates c elderly, develop of CHF, B& > @&, all age grps. Dx: CBC, e-lytes, Cr, BUN, glucose + >90% sensitivity bacteremia present  3 sets of cultures to narrow !which organism. TEE  look at valves, e&, fr bk (esophageal) Tx: empiric PCN + AMG (gentamycin) IVDA - worried about staph, 1st gen CPS, like nafcillin + gentamycin for MRSA Prosthetic valve MRSA staph aureus vanco + gentamicin. Myocarditis Drug induced; bact cauz include DPT, neisseria, mycoplasma, b-hemolytic strep. Viral : coxsackie, echovirus, influ, parainflu, EBV, HIV Sx: F, tachy, myalgias, HA, rigors, CP due to coexisting pericarditis, severe cases cauz problems like CHF, rales, pedal edema Dx: nonspecific ECG "s, AV block, prolonged QRS, ST ! Nml CXR, enzymes may b !, Tx: supportive, bact ( ABX, spontaneously resolve, others (to dilated e&myopathy. Rarely musc Bx show inflame pattern. Valvular e& Dz e& valves prevent retrograde flow, efficient ejection c contraction of cardiac chambers. Held in place by chordae tendinae; MI affect papillary musc, rupture chordae tendinae, leaflet flap free. Mitral valve: 2 cusps, others have 3. Papillary musc promote effective closure of tricusp + mitral valves. Mitral stenosis common, rheumatic e& dz; specifically targets mitral valve. Dilatation of atria, mitrostenotic valve ( high pressures in atria, dilation of atria& .goes on to develop Afib. Pressure difference b/t LA + LV. May b asymptomatic + CO + atrial pressure may b nml. Severe m. stenosis ( pulm congestion + !CO leading to dyspnea, fatigue, + e& failure. Sx: dyspnea, hemoptysis, orthopnea, precipitated by onset of prego or AFib. Murmur: duration varies, mid-diastolic, crescendos into S2. e& sounds: long snapping S1; apical impulse is sm + tapping due to underfilled LV. Systolic closing of MV. Diastole closing of tricuspid. Dx: echoCG thickened valve,opens poorly, closes slowly; ant. + post. leaflets r fixed, moving together. R/O atrial myxoma (tumor growing in atrium); LA can b measured -ECG notched or biphasic ps, axis, depending on severity -Xray- early finding- straightening of Le&B; pulm congestion, Kerley B lines (CHF, overload of fluid, drains into lymphatics), along c ! in vascular markings. Tx: emboli; warfarin anticoag, p AFib. Surgery for unctrld pulm. edema, pulm HTN, ltd activity . Open mitral commissurotomy, Valve replacement; never will repair LA& dilated for life. Anticoag will relieve. Sx n !pulm edema. Balloon valvuloplasty  effective in pts s m. regurg Mitral regurgitation systolic murmur, begins c S1, may end before S2 Leaflets (-) close nmly during LV systole; blood ejected into LA + AV. Results in ! vol. load on LA. Acute: LA pressure ! abruptly. Sx: SOB, tachy, pulm edema, ECG evidence of acute inf. MI (MC > ant.), no stenosis, little LV dilation; Xray minimally enlgd LA, pulm edema. Chronic: LA dilates, LA pressure rises slowly progressive. Intermittent acute episodes; valvular vegetation or growth, gives valve incontinence Causes: rheumatic, myxomatous degeneration (MVP), CT dz (Marfans) Nonrheumatic may develop suddenly p MI, Inf. MI due to coronary occlusion MCCischemic mitral valve incompetence -Appetite suppressive drugs (fen-phen, dexfenfluramine) assoc c cardiac valve incompetence Dx: echoCG, TEE, nuclear medicine, MRI, cardiac cath MVP mid-systolic click; standing position - poss assoc c nonspecific CP, dyspnea, fatigue, palpitations - MC in @&; most cases no sequelae but if related to chordae tendinae rupture ( turn into something serious - Prophylaxis b4 any procedures to prevent endocarditis Dx: clinical; confirmed c echoCG -Secondary Mitral Regurgitation papillary musc dysfunction or dilation of the mitral annulus in pts c dilated cardiomyopathy of any origin. Surgery wont help unless good EF >30% Aortic Stenosis- usually elderly, becomes !ingly sclerotic + stenotic; MC smokers + HTN MCC  congenital; 2nd rheumatic e&dz + degen. e& dz- Ca2+ e& dz. Tx; surgery, prosthetic valves, anticoag med + replacemt q10yr Ross procedure  switch pt s pulm valve to aortic side; work best, but much more diff. Doesnt require anticoag Percutaneous balloon valvuloplasty catheter thru fem art. ( aorta, inflate balloon in valve. Used often, problem is restenosis will occur in most Pt. Careful not to dislodge Triad: dyspnea, chest pain, syncope Dyspnea usually 1st sx, sudden death usually fr fatal arrhythmia, nml xray early on, eventually LVH, CHF, etc. ECG demonstrates criteria for LVH. Murmur: holosystolic, harsh, paradoxic splitting of S2,S3, and S4 may be present; pulse of sm amp.; slow ! + sustained peak. Aortic Regurgitation Infective endocarditis- majority, remainder fr aortic dissection, bkwds toward valve. Caused by rheumatic e& dz. Many cases have acute pulm edema c pink frothy sputum; F, + chills if endocarditis. Dissection  tearing feeling. EKG "s if dissect. Chronic regurgitation  1/3 have palp; noticed in bed Water hammer pulse- quick ! in upstroke followed by periph collapse. Diastolic, high-pitched, blowing, after S2 Assoc c the appetite suppressives Tricuspid stenosis rheumatic in origin; diastolic rumble along LSB; presystolic liver pulsation, EchoCG + Doppler + e& cath. RV overload- no valve to prevent; IVDA- tricusp valve endocarditis + regurg common. Tricuspid regurgitation inspiratory S3 present; surgical repair prefer over replacement. What is syncope? Sudden, transient LOC c loss of postural tone. Spontaneous recovery. Assoc. sx: lightheadedness, visual blurring, postural sway, N, V, pallor, ashen gray face, sense of feeling bad. Distinguish syncope from Sz: LOC, pain, exercise, micturition, defecation, stressful events. Aura typical of Sz also: myoclonic jerks, rhythmic mvmts, disorientation, HA, slow to rtn to consciousness, tongue biting 1 in ED, exclude life-threat causes of syncope 1st 2  admit to hospital? (family Hx of sudden death) Neurally-mediated  MC young adults, @&. MOA poorly understood; emotional upset may trigger CNS Fainting. Activation of receptors in wall of bladder, esophagus, e&, resp tract + carotid sinus (vagal effect. Cardiac syncope  1 of lrgst causes, c ! CO, ! bp (passout. Orthostatic hypotension  ! in systolic BP or at least 20 + diastolic of 10 Common causes  in young: vasovagal, neurally-mediatedS Elderly- SSS, AV block, VTach, drugs Arrhthmias, obstrux to flow, ischemia. Syncopal episodes admitted to telemetry. LV, think aortic stenosis RV, think pulm congestion, PE Syncope assoc c acute MI, ischemia, c-effort angina; conversion rxn (situational); situational syncope (cough, micturition, defecation), hypoglycemia Sz disorder- abrupt onset, disorient p event, slow rtn to nml; prodrome, incl sweats or N Vasovagal syncope-ETOH, hot surroundings freq triggers; consciousness rtn quick p when pt supine Carotid sinus hypersensitivity  Pt supine; monitor BP while massaging carotids; have atropine available to get HR back. Cardiac cauz assoc c ! mortality. Arrhythmia  exclude c EKG during syncopal episode. Dx: ECG, holter, echo/Doppler, EPS, tilt table test, event recorder, loop recorder, neuro eval, psych eval Hx: meds, assess for hypervent, somatic complaints CHF - #1 cauz 4 hospitalization Iatrogenic vol overload, !intravasc vol, e& wrk harder prego + hyperthyroidism  higher demand for O2. MI cause for acute mitral or aortic regurge In CHF, pt doesn t have high cardiac reserve preload- load ventricles experience during diastole; where Frank Starling : the ! the load, ! stretching, !contractility. preload ! as a result of poor renal perfusion. !CO, kidneys not being perfused, need to ! H2O + salt reabsorption. Will ! amt of blood entering RA. p-load  pressure vent. have to experience when blood ejected fr vents. ! by aortic stenosis, ! BP (! PVR). CHF usually begins in ! in contractility due to prolonged ischemia. Low CO, prod. more catecholalmines (! HR, ! PVR, ! systemic pressure making injured e& work harder). -If more vol enters RA, more vol has to exit LV. ACE inhibitors, ! preload + pload. - < sx at rest than exercising. -diuretics  ! blood vol, ! preload + therefore !pload. Sometimes vasodilatory affectg to ! diuresis. -HR ! c ! in SV; to make up for lack of vol. in ventricles. - ANP  and B type of natiuretic peptide = proteins produced by atria---very specific c stretching of e& musc. Common to get these levels to distinguish this from SOB. Peptides can tell whether or not pulmonary or cardiac. Hypertrophy + remodeling  e& cells begin to reshape, become fibrotic + stiff. Attempt to ! contractile filaments Diastolic dysfunction  ventricles r < compliant, not expanding. 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Decompensated CHF  pulm edema, venous congestion. Compensated CHF - c nml CO (prego, RF, PCV, obesity) Higher HR = better conditioning Low output  impair pumping ability, ischemic + e&myopathies. Low output is worse than high output (anemia, thyrotoxicosis) Nml EF = 50-65%; CHF has EF <40%; ! end-diastolic pressure + ventricular dilatation ! CO. ! end-diastolic pressure Diastolic failure  sm ventric size, very hypertrophied. Ea cell gets bigger, hypertrophied cells r taking ! too much space, < vol to fill c blood. Pressure in capillary bed  leak into interstitium, pulmonary edema, eventually ! pressure in art. pressure in pulm. vasculature. RV trying to eject blood, experience !pressure due to pulm congestion. ! pload for RV  MIP cauz for hypertrophy !e& failure. Ascites liver engorged c blood- liver cells die. Jaundice  metabolic and obstructive causes. More than 2lb gain in 24h; 25lb in week = R/O CHF. Congested IVC, hepatomegaly, hepatocyte death, splenomegaly + ascites; JVD sitting ! + standing = CHF. L e& failure Lead to pulm congestion. Resp. failure !Drown in fluid! Causes: AMI, e& myopathy, c AMI pulm edema happen quickly. Ventricular aneurysm Pt don t survive. Careful c IV rates  don t overload pt. Oncotic pressure goes !, more protein, suck up interstitial fluid, ( cardiac failure. Blood tinged sputum ! fluid pushed out of capillary bed Periph + central cyanosis, ascites, cachexia (severe malnutrition  scaphoid abdomen, not protruding unless there is ascites). Exercise intolerance Fatigue worse at night, b/c e& tires as day goes on. PMI displaced lat. since ventricles r lrgr; faint pulse due to fluid. If ventricles not relaxed, extra heart sound, S3,S4. Accentuation of P2 e& sound  ! pulm congestion, ! pulm pressure, valves have to close harder b/c something trying to keep open. Behind is the pulm pressure. If ventricles r dilated, like a balloon  ? will happen to mitral/aortic valves? Open  holosystolic murmur; valves can t close completely; e& dilated that the leaflets r nt able. CXR  cardiomegaly, interstitial edema, pleural effusion Class 1  asymptomatic 2  mild CHF Sx c vigorous activity 3  moderate to severe sx c routine activity 4  decompensated pts c sx at rest. Confined to bed/chair. Dx: CBC, e-lytes make sure not !K, Ca; TSH (!!thyroid) -BNP (may not be specific for elderly and women) -echoCG  Dx modality of choice assesses LV contractility + EF; fraction of the blood contained in the ventricle at the end of diastole expelled during contraction. CHF, EF ! to <10%, pt can t get out of bed  too strenuous. Estimates pulmonary arterial pressure; -exercise treadmill test  disting b/t e& n pulmonary eti. -EKG- r/o arrhythmias -L + R e& catheterization  r/o valve dz; presence of CAD -MUGA  cannot assess valve + pericardium -Pulse Ox impending resp failure; may want to intubate. < 92% DDx: Pe, valvular dz, RA tumor! myxoma, tamponade, constrictive pericarditis, aortic + mitral valve dz. Tx: systolic dysfunct c ACE; titrate !, start low + go up PRN; same c diuretics. BB for Pt co decompensated CHF -digoxin DOC = + inotropic; contractility. Vs dobutamine (high SEs, not for nml CHF pt) -anticoags b/c of arrhythmias ( emboli; prevent c heparin then coumadin -NTG ! pre/pload. -hydrolazine: direct vasodilator, ! HR; < ! in O2 demand than ACE; safe to give to pregnant women. -nitroprusside  affects sm musc ,relax. Not for AMI b/c BP !. Start very low dose, stabilize BP + switch to something else. Only use if absolutely must or in a HTN crisis. Must be very diligent. Heart/BP monitors and be ready to intubate. Tx diastolic- diuretics; antiHTN. very diff to Dx; -coronary revascu.  take graft fr internal mammary vessels or saphenous veins; e& transplant -implantable D-Fib to prevent sudden death Complications  APE, ischemia, sudden death + unexplained syncope; cardiogenic shock post transplant  1 yr survival 80% and 5 year >70% Cardiomyopathy and Myositis Most cases of myositis are viral. Coxsackie B virus  children; affect any age. Myocarditis - infxtious process; can follow a viral URI. Viral 80%; coxsackie MC; replicates in myocardium, destroying cells. Sx: URI, pharyngitis/tonsillitis/sinusitis HIV  may act directly on e&, Very diff to dx; PCR of pericardial fluid; dilated cardiomyopathy; floppy heart, Immunosuppression susceptible to opportunistic infxn - toxoplasmosis, TB, cryptococcal, HSV, AZT CMV  self-limit; children; can b fatal p e& transplant. Bact  strep pneumoniae; b hemolytic strep = rheumatic F. Rickettsial  fleas; typhus F, Rocky Mtn spotted F, rash + ! URI sx/malaise. C. Perfringes  toxins; cauz gangrene, gas bubble in myocardium DPT  URI charact. thick membrane ( cardiotoxins meningococcal  fatal CHF, pericardial effusion, tamponade mycoplasma  atypical pneumo, ST-T wave ", pericarditis, audible friction rub spirochete infxn - syphilis + lyme Lyme  B. burdorferi  rash, CNS, joints, e&  AVB ! syncope. Rheumatic e& dz  group a beta hemolytic strep -entire e&; valves, peri/myo/endo inflamed. Mitral, Aortic valves, fibrous scar tissue ( murmurs Sx: DOE,murmur, CHF, polyarthralgias, subq nodules over bony prominences (tibia), 10yr > appear; Aschoff bodies pathopneumonic  granulomatous inflammation Protozoans trypanosoma cruzi  aka Chagas dz, travel in the last 5yrs or longer? 1 yr  self-limiting carditis Allergic rxns PCN, HCTZ, methyldopa, sulfa. !Eosin., itchy, maculopap rash Radiation  dmgs DNA + cell integrity meds: doxorubicin, Li, catecholamines, cocaine, AZT systemic dz  vasculitis + CT dz (sarcoidosis, SLE, pheochrom) Pathophysiology  myocarditis organisms invade cells ( necrosis; autoABs cauz dmg, endotoxins fr pathogens, cellular immunity further dmg b/c promote inflam Sx: e& failure, or sudden death. Precordium chest probs, ! SED rate, R + L sided e& failure signs (JVD, ascites, edema), thromboembolism (inflam of the e&, more turbulence or arrhythmia = clots.) pericardial friction rub (S1 + S2 not related to breathing), pleural rub (c breath sounds). Dx: dyspnea n CP p viral illness -enteroviral: IgG  4x !; PCR for viral ID (very specific, quick) -cardiac cath (to exclude other inflammatory causes) -CPK + troponins; ESR ! in 60%; leukocytosis in 25%; endomyocardial Bx is standard Tx: Exercise can exacerbate  rest. e& monitoring  due to e& blocks, if block develop pt experience palp, syncope, ABx, ACE for e& failure, diuretics + DIG. AVOID NSAIDs. Intraaortic balloon pump assistance  inflatable balloon placed into the ! aorta, ! BP + organ perfusion by its pulsatile thrust, deflation ! cardiac work c systole. Cardiomyopathies  don t know why these happen Dilated  MC, B& + AA > 50yo. Diff fr CHF b/c due to infection. Enlgmt of all chambers, ! pulm venous pressure, final stage of CHF; ? eventually kills these Pt. Usually a consequence of myocarditis. Eti: diff. fr CHF. -Persistent dilation  mitral + tricusp regurge; no CO. If no CO, end-systolic vol r very !. More dilation + dysfunction. Sx: sudden e& death, EKG  ST-T ", like myositis Dx: echoCG shows valular dz. Stress test to r/o CAD Tx: avoid RFs, correct if pheoc., thyroid; treat as CHF, ACE, diuretics + anticoag Hypertrophic cardiomyopathy (HCM) Vent. septum is disproportionately enlgd; block outflow. Familial, MC in children + athletes. Genetic mutation that hypertrophies the myocytes. Sx: asymptomatic ( sudden death; strong apical impulse. loud systolic ejection murmur ! c valsalva. Preload !, murmur !  less blood inside the e&; pushes the contraxn. Squat  murmur !; compressing middle of body and not allowing blood to go anywhere. ! c more blood in heart b/c blood is cushioning it. Dx: EKG: LVH, huge QRS echoCG: LV > RV; displaces MV ant. Tx: BB  to ! contractility CCB improve diastolic funct; malignant v-arrhythmias Afib MCC death in young athletes) Restrictive Cardiomyopathy Contract but can t fill. Vent. not expanding. Eti: amyloidosis, radiation, sarcoidosis, CT dz Sx: dyspnea, PND, orthopnea Dx: disting fr constrictive pericarditis. ! LV function (pericarditis has nml LV function + thickened pericardium) Bx- show endomyocardial fibrosis, not in pericariditis Tx: steroids helpful MI MC presenting problem RF: smoking, HTN, !fat, !LDL, DM, stress, inactivity, B&, age/heredity, ! homocysteine + CRP. Key: 10 prevent.  cntrl RF& prevent MI. 20  prevent dz process Hypoxia/ischemia  angina ! CP. Stent open blocked art ANGINA stable  exercise/stress prod. CP. Resolves c rest. Unstable  occurs at rest ACS!ACI!MI Pathophy acute event: plaque build!, ruptures off exposing endothelium, body sends over platelets, fibrin, build a clot on ruptured plaque ( blockage Framingham Study  lrgst long term study of CV dz. 213/708 presented atypically Classic presentation: retrosternal, epigastric cp, tightness, SOB, diaphoresis, N, V, Levine s sign Atypical: MC, Cx discomfort + (-) pain; sweating @ 1st, now gone; previous indigestion, now ok, +/- SOB, vague, EKG nonspecific " s present. Sx: not relieved by rest/NTG, bk/abd pain, radiating to shoulders/arms/Cx, neck/teeth/jaw, pain > 20 min. NTG - dilate BVs, ! preload. PE: rapid pulse, abnl Cx sounds on ausc. (blood can bk ! into lung, (-) pump blood out of LV) make pulm edema/CHF worse. Tests: ECG, echoCG, coronary angiography, stress test (EST, nuclear (more specific, no exercise), troponin I/T (!specificity & sensitivity), CK, CK-MB, myoglobin-serum, LDH may be elevated in time. CBC  status of platelets, if anemic  bleeding? Pt/Ptt  coag profiles , if pt on heparin, want to know. Nml = 40; want to get pt at 60  80; the therapeutic range Start Pt on Warfarin  2-3d b4 effectively anticoag. PO, check PT time. Nml = 12; want 18-24 b4 send Pt home. INR  standardize the measuremt of PT/PTT. Nml 1; INR 2-3. >--< wbc, Hb, Hct, Ptt Na, K+, Cl, HCO3, BUN, Glu, Cr 1st in W/U  12 lead EKG Q-wave, transmural MI Subendocardial MI (non Q-wave MI), or angina Tx: ECG, BP, IV fluids/meds, O2, pulse ox, blood work, urinary catheter (monitor fluid status) ASA  162mg inhibits platelet aggregation. CI: ASA allergy (triad w/ asthma, nasal polyps), GI bleed, bleeding disorder. Nitrates: given in CP, ischemic CAD, r/o MI. Dilates e& arts. Monitor BP, titrate up to as much as pt can tolerate. Tachyphlaxis- p a period of time, body builds up resistance. cauz HA, flushing. IV  NTG 50mg in 250cc to be given at 10 mcg/min; keep SBP >100. CI: R wall infarct, anything affect preload; b/c decr blood flow even more. If press ! stop NTG, add fluids. Morphine MSO4: Reduces pain, NTG 1st, see if that removes physiologic cause of pain . Narcan (direct antagonist, 2g IV). Glycoprotein IIB/IIIA inhibitors Integrillin, Aggrestat, Repro-abciximab. Decouples platelets, competitive inhibition to platelet aggregation. Heparin  anticoag, DVT, PE, monitor levels LMW Heparin Enoxaparin- DOC, no PTT monitoring necessary, no IV. 1mg/kg SQ, q12hr. trials; better than heparin in ! morbidity & mortality. BB- ! mortality & morbidity. B1 selective  atenolol, metoprolol. 5mg/ IV. impotence ACEI - benefit c myocardium remodeling (strngr). ! CHF, !EF cough, !BUN/CR beware in renal stenosis, angioedema, !K+, Use in DM. Cholesterol-lowering meds  statins, SEs: myalgias (try diff statin), monitor LFTs, Thrombolysis EKG 1mm > ST! in 2 or > limbs TPA, Retavase (10cc, inj, wait hr, inj) Streptokinase (antigenic p 1 time use) 2mm or > ST ! in 2 or + precordial leads CI: Hx of CVA/TIA, head trauma, brain tumor, surgeries, MVC, ulcers, bleeding, unctrl HTN, aneurysm, pericarditits (diffuse ST ! V1-V6, great imitator of MI). Aortic Aneurysm lrgst artery, 10 artery carries blood fr e& ! body develop anywhere along aorta. More than occur in abd below RAs (periumbililcal pain) Eti: pressure on wknd section of art. wall (bubble). Dissection: a split in the 3 layers ( blood b/t, !risk of rupture. RF: MCC  ath-sclerosis, CT dz, arteritis, congenital malform, Marfan, FHx, B&>@&, Post. trauma to aorta Sx: (pain! as enlg & press on nerves, organs, vessels), most r symptomless. MC  throbbing, pulsation in abd ! back. Dx Abd palp abnly wide pulsation of abd aorta widening of the mediastinum. R pulses = in arms +legs? CXR- Ca2+ in aortic knob CT w/ IV contrast, MRI US  (98% accuracy in size measuremt) Abd aortography Tx; replace part w/ synthetic graft; BB DOC b/c reduce shearing forces. MC > 6cm wide Types of Aneurysms: Thoracic: pain in shoulders, ! bk, neck, abd, dry cough, tearing feeling, hoarseness fr press on vocal cords Saccular- musc middle layer Fusiform- MC, spindle shaped Dissecting- longitudinal, blood filled split, usu aortic arch Cardiac Dx Testing How good- impedence, fluid in lungs, tamponade  anything that can ! the voltage/ht, electrical activity Ambulatory monitors Loop  pt feels Sx, press button to record Transtelephonic transmitter- use only during phone- monitoring period. Pacemakers can be adjusted by phone. EST  exercises, get ! HR, see how e& responds to stress. HUT  determine cause of fainting; IV access b4, give meds & fluids during procedure Metabolic Exercise Test  more advanced, measure performance of e& & lung Labs: CBC (CP & Hb of 3, no O2 2ndary to anemia), lipids, e-lytes, BNP, enzymes n proteins BNP - !CHF, Natrecor (cGMP ! urination) Troponin I  4-6h, duration 4-7d, specific & sensitive (has replaced LDH) Troponin T  earliest !3-4 hrs, less specific (80%), sensitive >98% CK-MB - !3-4 hrs, duration 24-36h, specific n sensitive LD-1/LD 2  rare cases if think you missed it, look day or 2 later Nuclear imaging  see where radioactive material enters MUGA, PET, Sestamibi EST, Thallium EST. MUGA  eval pumping of ventricles; calculates amt of blood pumped out of e& c each beat PET  blood flow to e&, radioactive tracers, 3D images Dipyridamole- injected, medication causes e& to react as if pt were exercising (bedridden pt) Sestamibi  inject Thallium dye, shows images of e& musc at rest. Then stress lab, IV started ,exercise; give Sestamibi dye. ~ 30 mins p exercise, more pictures taken. Thallium  SAA Dobutamine stress  inj of dobutamine, adrenergic agonist, blockage would become ischemic, pts unable to exercise (bedridden, think there s a problem) TEE  pics of e& valves & chambers, no impedence of Cx wall/ribs. Combine w/ Doppler to assess blood flow. Exercise stress echo  how e& tolerates activity; funct. e&& valves CXR- !Ca2+ = more Ca2+ deposition, !atherosclerosis. Invasive testing  angiograms; cath, EPS, intravascular US Carotid angiography  fluoroscope, dye c if any blockages Carotid endartarectomy  lead to emboli Catherterization  dye lights up chambers, art. Problems  dislodge embolus, dissect coronary ostea & cause MI. IVUS  performed w/ cath & get into e&, get clear pics, risky Myocardial Bx  rare cases, need to know what s going on; sm cath c grasping device, grab piece of e&musc) Use: myocarditis EPS  ? causing arrhythmias, can b reproduced & various meds given to see which controls best. 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