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[ ] Cardiology_Midterm.do .doc

  1. 1. Cardiology Midterm Disease Atherosclerosis Monckeberg’s Arteriolosclerosis (Atheroma) Arteriosclerosis Type of Disease Disease of Bloodvessels (Arteriosclerosis) Cause Risk Factors: advancing Unknown but Proliferative fibromuscular and age, HTN, + FHx, DM frequently seen in endothelial thickening of walls (AGEs), Cigarette advancing age of small Arteries and smoking, arterioles with luminal hypercholesterolemia, ↑ narrowing. LDLs, homocystinuria, Chlamydia pneumoniae Pathology Not completely known Band-like Hyaline: Hyperplastic: :Injury Hypothesis – calcifications Endothelial reduplication Endothelial injury allows develop within the injury and of basement lipids to move into vessel media of medium- leakage of membrane wall and smooth muscle, sized and small plasma and smooth cytokines are released, muscular Arteries. proteins into muscle collagen is deposited, arteriolar proliferation fibrosis occurs → Fibro- walls of arteriolar fatty atheroma wall with lumen Common sites: aorta, narrowing coronary A., Cerebral A., popliteal & internal A. Signs & Symptoms Complicated Very little clinical Hyaline: Hyperplastic: plaques:Calcification, significance since associated Associated ulceration, thrombosis, the intima is not with DM and with fibrinoid intraplaque hemorrhage involved. Benign HTN necrosis and Malignant Results in: MI, CVA, Diffuse HTN aneurysm rupture, hyaline mesenteric occlusion, thickening gangrene of intestines often seen in and/or extremities kidneys Diagnosis Sometimes Calcification can be seen on x-rays TreatmentDisease Ischemic Heart Disease (Coronary Artery Disease, Coronary Heart Acute Myocardial Infarction Disease)Type of Disorder of Oxygen supply and demand Conduction Block
  2. 2. Disease Cause *Artherosclerosis (artheroma) Emboli Vasospasm of coronary artery Bleeding into coronary arteries due to plaque Thrombus rupture Spasm Risk Factors: older age, male, FHx, HTN, cigarette smoking, hyperlipidemia, DM, Risk Factors: HTN, cigarette smoking, hyperhomocystinemia hyperlipidemia, DM, hyperhomocystinemiaPathology Decreased blood supply or increased O2 Ischemia leads to necrosis of mycordial fibers demand due to: resulting in loss of conduction and contraction Endothelial-derived Factors (vasoconstrictors) of muscle Obstruction Usually occurs in LV Vasospasm Anemia Lung disease Increased cardiac demand due to: Tachycardia Hyperthyroidism Hypertension Both cause build-up of toxins like lactic acid thus pain Signs & 75% of CAD pts are asx Sudden attack of severe pain – generally lastsSymptoms Symptomatic pt: angina, MI, intermediate >20 to 30 min. and unrelieved by rest or Nitro. ischemic syndromes, sudden cardiac death, Angina (typical or atypical), nausea, diaphoresis, CHF apprehension, restlessness, tachycardia, cold Unstable angina: pt w/ chronic stable angina and clammy, shock, sometimes SOB experiences changes in pain, pt who Often occurs early in a.m. due to circadian experiences angina for first time, chronic variations stable angina progresses to rest angina Complications: Myomalacia Cordis causing Pure exertional angina (stable angina): pt with solid rupture, Sudden Cardiac Death, CHF (due to VSD or MV rupture), Cardiogenic shock, organic stenosis where increasing activity Ventricular rupture w/ cardiac tamponade, causes pain relieved via Nitro. Papillary muscle infarct causing Mitral Pure resting angina: (Prinzmetal’s angina) pt Regurgitation, Thrombosis, Dressler’s with vasospasm, often is awoken from sleep. Syndrome, Pulmonary emboli, arrhythmias, intractable painDiagnosis Hx: especially description of pain – build-up of ↑ Creatine Kinase (CK) pain, diffuse (clenched fist), deep character. ↑ Cardiac troponin I (TnI) Severe, sudden, pressing and substernal pain ↑ LDH & SGOT that sometimes radiates to left arm. Acute ST elevation, pathological Q waves, loss of Vasospasm: rest angina, nl pulse and bp during R waves on EKG anginal episode, ST elevation and + cold pressor test CXR Lab - ↑ homocystiene and CHO Others: Exercise stress test, Radionucleotide studies w/ Thallium, EchocardiogramTreatment Goal: prevent premature death, enhance quality Modify risk factors of life. Lytic Therapy (w/in 3 hrs if NO collateral Supportive therapy: ↓ risk factors, stress circulation is present) modification, control aggravating conditions, Cardiac Catheterization exercise IntraAortic Balloon Pump Pharmacotherapy: Sedation ASA ASA Nitrates Oxygen Beta Blockers Beta Blockers (w/ parameters) Calcium Channel Blockers ACE Inhibitors (w/ parameters)-start 2nd day Combination Therapy Statin drugs Statin Therapy Revascularization (Angioplasty, bypass)
  3. 3. Disease Infective Endocarditis Type of Disease Microbial Infection Cause Native Valve Endocarditis IV Drug Abuser Endocarditis Prosthetic Valve Endocarditis (PVE): (NVE): (IVDAE): Early (<60d from surgery) Staph epi Strep viridans (40%) Staph aureus/epidermidis (>50% ) Staph aureus (30%) (>50%) Gram – (15%) HACEK Enterococcus & other strep Late (>60d from surgery) Staph epi (15%) (35%) Strep 40% Risk Factors: Damaged heart values: aortic stenosis, aortic regurgitation, mitral regurgitation, ventricular septal defect, coarctation of the aorta, mitral valve prolapse w/ regurgitation, bicuspid aortic valve, calcified aortic stenosis, previous episode of infective endocarditis, cyanotic coronary heart disease and any procedure w/ appreciable probability of associated bacteremia (i.e. dental procedures, prostate, urinary tract or GI surgery, vaginal hysterectomy, etc.) Pathology Endocardial infection with microorganisms in lesions (vegetations) on low pressure sites. Sequence of pathology: 1. Nonbacterial Thrombotic Endocarditis (NBTE) 2. Bacteremia 3. Adherence of bacteria to NBTE, proliferation of bacteria, continuous seeding of bacteria into bloodstream Locations: MV > AV > TV > PV Signs & NVE IVDAE PVE Symptom 60 to 80% have 80% of patients have normal 100% pts have prosthetic valves. PVE s predisposing cardiac heart valves. Predisposing usually produces paravalvular leaks lesions: conditions: and valve dehiscence. Rheumatic Heart Ds Right-sided tricuspid valve Coronary Heart Ds Septic pulmonary emboli Mitral Valve Prolaspse Bicuspid Aortic Valve Aortic sclerosis Fever, fatigue, wasting, night sweats, painful fingers, petechiae in mouth & conjunctiva, Janeway lesions, Osler’s nodes, Roth’s spots, possible heart murmurs Necrosis, ulceration and valve perforation may occur Acute or Subacute Bacterial Endocardial: According Dr. Spalter this classification is no longer used due to advances in early detection and treatment. Nonetheless, Dr. Khin still uses it. Diagnosis Changing cardiac murmurs EKG: could show AV block, RBBB, LBBB if conduction system affected Labs: ↑ WBC and ESR, Anemia, ↑ C3, + blood culture, Immune complexes of RF & IgG, Hypergammaglobulinemia, Hypocomplementemia Echocardiogram shows lesions, Transesophageal Echo (TEE) Complications: cerebral emboli, brain abscess, glomerulonephritis, infarcts in spleen, brain or kidney due to septic emobli Treatment IV bactericidal abx for 4 to 6 weeks (PCN, cephalosporins, aminoglycosides, fluoroquinolones) varies w/ etiology: PCN sensitive Stret (Strep viridans): PCN, Ceftraixone Enterococcus: Ampicillin Staph aureus: Nafcillin MRSA or MRSE: Vancomycin Indications for Surgical Therapy- PVE: Abx resistant organisms, dehicense of suture line & unfunctional valve All IE: infection of AV node w/ AV block or with regurgitation and CHF (medical emergency!), abscess Prophylaxis prior to surgery or procedures: aimed at normal colonization of area affected by procedure (i.e. skin – nafcillin, dental – PCN, GI/GU - ampicillinDisease Heart Failure Rheumatic Heart Disease
  4. 4. Type of Disease Pump Failure/Increased Load Autoimmune Reaction Cause Pump Failure (weakness of contraction) – myocardial ischemia (CAD), Rheumatic Fever from Group A Beta Hemolytic strep cardiomyopathy, myocarditis, impaired infection compliance of myocardium rhythm disorder Increased Load – • Increased pressure: systemic HTN, aortic or mitral stenosis, pulmonary HTN • Increased volume: aortic or mitral regurgitation, shunts, anemia, lung disease, thyrotoxicosis, pregnancy Types that make-up CHF: Acute HF: MI, malignant HTN, valve perforation or rupture, pulmonary emboli, acute arrhythmia Chronic HF: acquired valvular heart disease LV Failure: MI, systemic HTN, disease of AV node RV Failure: PHT, COPD, MS, pulmonary emboliPathology Ventricular myocardium falls to maintain Antistreptococcal Ab formed due to GAS infection cross circulation adequate for the needs of the react w/ cardiac Ag and destroy myocardial valves – body – characterized by ↑ in LA pressure 1.inflammation of valve leaflets and chordae, 2. and a ↓ in CO. verracae on line of closure, 3. thickening and fusing of leaflets. Signs & Dyspnea, orthopnea, sense of suffocation, For RF: Pharyngitis, reversible migratory polyarthritis,Symptoms ascites, pleural effusion, nausea, murmurs, febrile, exudative tonsils, chorea, erythema vomiting, ↓ appetite, fatigue, diaphoretic, marginatum, subcutaneous nodules, arthalgia, EKG abnormalities, abdominal pain, epistaxis, pulmonary poor urine flow wt. Gain, cyanosis, infilrates vertigo, hepatosplenomegaly, S3 and S4 For RHD: pancarditis, grtanulomatous rheumatoid present, pulmonary rales, edema, JVD nodules formed in myocardium, endocardium, and ↑ intravascular pressure and volume, ↑ fluid especially pericardium, murmurs of MR, AR, CHF, in lungs, organs pericardial rub or effusion, Late stage - mitral & aortic Compensatory mechanism: myocardial stenosis hypertrophy & ↓ compliance, ↑ blood volume, ↓ CO & vasocontriction, ↑ RBC, activations of RAADiagnosis H&P Jones Criteria (dx for 1st attack) NYHA Classifications: I, II, III, IV Aschoff bodies CXR: cardiomegaly Echocardiogram dilatation of pulmonary artery, pulmonary CXR: bread & butter appearance of the heart, congestion and edema, pleural effusion cardiomegaly EKG: MI, LVH, RVH, or arrhythmias, no Valvular stenosis: MV>AV>TV (fish-mouth appearance) progression of R waves, pathologic Q Secondary effects: Dilitation of LA, LA mural thrombus, cor wave pulmonale Labs: ↑ BUN, creatinine, cardiac enzymes Dx for RF: (↑ ANF) Labs – elevated ESR & C reactive protein Echocardiogram + strep test Cardiac Catheterization (Gold Standard for dx)Treatment Determine underlying cause and treat it. Strep infection: Benzathine PCN (IM), Sulfa, p.o. PCN V, ↓ salt intake Erythromycin and ASA 100mg/kg qd x 2weeks then Restrict physical activity (rest periods) 60mg/kg qd x 6weeks Carditis: Prednisone 60mg/kg x 2weeks tapered over 3-4 ***Diuretics, ACE inhibitors, Beta-blockers weeks and ASA for 1mo Inotropic agents (digoxin) Prophylaxis against RF: p.o. PCN V qd or Benzathine PCN Diuretics (IM) q 4 weeks for 5 years or to age 18 w/out carditis Vasodilators and 10 years for pts w/ carditis Beta Blockers Prophylaxis for Endocarditis: Amoxicillin taken prior to ACE inhibitors dental work or oral surgery
  5. 5. Disease Cardiomyopathies Type of Disease Dx of exclusion from all known cardiology factors Cause Primary: unknown Secondary: myocardial damage occurs due to: Chemical toxicity Infections Immunological mediation Metabolic diseases Neuromuscular diseases Storage disorders Pregnancy Neoplastic/infiltrative diseases Dialated(DCM) Hypertrophic Restrictive Arrhythmogenic Right Viral Unknown Infiltrative lesions ( Ventricular Dysplasia Toxic amyloidosis, endo Hereditary to some Beriberi Thought to be genetically cardial fibrosis) extent Infiltrative determined Idiopathic Types: HOCM(block) IHSS(thickening under valve) ASH (septum thickening)Pathology Four chamber VH and cardiomegaly w/out Impairment of Fibrofatty infiltration dilation with ventricular dilation ventricular filling due usually in RV systolic and to endocardial or progressing to LV – diastolic dysfn myocardial ds associated w/ life- threatening arrhythmias and SCD Signs & CHF, pulmonary Dyspnea, angina, syncope & Right sided heartSymptoms rales, JVD, CHF, JVD, Afib, palpatations, failure, hepatomegaly, systolic murmur systolic murmur, myocyte edema, ascites, of MR, TR, ↓ EF disarray, pulsus bisferiens, anascara, JVD, pulmonary rales, Death due to: “triple ripple” @ apex, pleural effusion, CHF, embolism, splitting of 2nd heart sound systolic murmur of arrhythmias, MR, LA and RA systolic HF Increased risk of SCD enlargement but normal ventricle size Complications: diastolic heart failure, can progress to dilated CMDiagnosis CXR: CXR: cardiomegaly, CXR: Pulmonary EKG: epsilon wave (in V1 cardiomegaly pulmonary edema congestion, pleural looks like a RBBB) EKG: V EKG: LVH, SV or V effusion, enlarged LA arrhythmias, arrhythmias ECHO: fibrous/fatty heart block, LVH, ECHO: SAM of MV EKG: RVH, low QRS tissue infiltrates of RV ST & T voltage abnormalities ECHO: 4 + standing/squatting maneuver chamber dilationTreatment Digoxin and Beta Blockers Transplant or AICD diuretics Calcium Channel blockers ↓ sodium intake AAD ACE inhibitors AICD, if refractory Beta Blockers Myotomy/myectomy AT-1 Blockers Cath Pace Ventricle Transplant (last resort)
  6. 6. Disease Aortic Aortic Mitral Stenosis Mitral Mitral Valve Stenosis Regurgitation Regurgitatio Prolapse nType ofDisease Valvular Heart Disease Cause Senile Disease of RHD Perforated Unknown degenerativ aortic valve Congenital leaflet (IE) e Calcific AS cusps, or LA myxoma MVP Occasionally Congenital annulus: Mitral annular Hypertrophic familial, common bicuspid Dissecting calcification CM in Marfan’s and valve aortic Carcinoid syndrome Mitral annular connective tissue RHD aneurysm, calification d/os IHSS syphilis, RHD Marfan’s Ruptured syndrome, papillary m. SLE LV dilation RHD Marfan’s Infective Syndrome endocarditisPathology Fibrotic Abnormal leak Narrowing of mitral Abnormal flow Abnormal prolapse calcification or retrograde orifice and of blood of MV leaflet from leading to flow of blood obstruction of blood from LV to LV into LA during outflow from aorta flow from LA to LV in LA during systole obstruction back into LV diastole systole during systole during diastole Signs & Angina, heart Angina, sx of Hx of RF, dyspnea, Sudden Mostly benign andSymptom failure sx: LV failure: fatigue, systemic dyspnea and asx s dyspnea, orthopnea, embolization, orthopnea syncope, PND, palpations, due to Occasionally: weak and collapsing hoarseness, pulmonary angina, dyspnea, delayed pulse, high- hemoptysis, sx of RV edema in fatigue, pulses, pitched failure: acute MR, psychiatric systolic diastolic hepatosplenomegaly systolic problems, systolic murmur and murmur , edema, ascites, murmur and click & late thrill, ↓ EF anascarca, thrill, systolic murmur Complications: cyanosis, weak hypertrophy when MR present. LV volume pulse, JVD, diastolic & dilation of overload, murmur & thrill @ all chambers Complications: MR, Complications: MR, Jet apex and thromboembolism LVH lesions on LV pulmonary A. infective (concentric), wall Complications: Giant endocarditis, low BP, CHF, LA, hypertrophy of Complications: arrhythmias severe LA, RV and RA (not PHT, RV arrhythmia, LV), embolism, PHT, failure, CHF sudden Atrial fib, Right heart death failureDiagnosisTreatment Valve MR requires valve replacement replacement
  7. 7. Disease Myocarditis Pericarditis Sudden Cardiac Death Type of Disease Inflammatory Disease Cessation of heart function Cause Viral infection: Infectious: TB, Cardiac causes: MI, CAD - most Coxsackie bacterial common Arrhythmias Influenza “automaticities” (VT leading to Vfib Noninfectious: Pulmonary emboli Others: microbiologic agents, trauma, connective Aortic Rupture immunologically mediated tissue diseases Intracraniel hemorrhage d/o, metabolic d/o, Cardiac Tamponade Idiopathic Aortic stenosis Myocarditis Types: Hypertrophic or dialated Fibrinous: RF, uremia, SLE cardiomyopathy Purulent: bacterial or MV prolapse fungal Long QT Syndrome, Congenital Caseous necrosis: Complete Heart Block, RV dysplasia, TB Hemorrhagic: Rarely: Asystole, profound bardycardia metastatic tumor invasion or TB Risks: advanced age, inducible VT in high risk patients, reduced LV function, LVH, valvular ds, PVCs, LVEF in chronic ischemic heart ds (most powerful indicator)Pathology Inflammation of the myocardium w/ associated myofiber necrosis Signs & May be asx, but can lead toSymptoms debilitating loss of cardiac Varies w/ etiology function Complications: chronic stage may present later as dilated CM, arrhythmias, CHF, SCDDiagnosis Unexpected collapse & death w/in 1 hour and presumed to be cardiac related Syncope is powerful indicator of SCD Abnormal EKG: ↓ functional capacityTreatment H&P EKG: LVH, QT prolongation Echocardiogram, holter monitor Cardiac Enzymes Others done depending on suspected etiology: Angiography, Stress test, Electrophysiology Stimulation Study, VQ scan, Spiral CT scan, Head CT or MRI, cardiac catheterization **Defibrillation Revascularization Pcing **AICD Drugs: beta blockers and AADs