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Clinical Medicine
Cardiology Module
| Question | Answer |
|---|---|
| Etiologies of dilated cardiomyopathies | 1-ischemia; 2-idiopathic (viral, heart muscle disease, familial cardiomyopathy); |
| Pathogenesis of dilated cardiomyopathies | Cardiac remodeling; Toxicity of sympathetic activation |
| Etiologies of Hypertrophic cardiomyopathies | unexplained myocardial hypertrophy |
| Pathogenesis of Hypertrophic cardiomyopathies | Impaired ventricular compliance, inappropriate myocardial hypertrophy (septum is disproportionately thick & blocks outflow) |
| Etiologies of Restrictive cardiomyopathies | o Myocardial fibrosis (Becker’s disease), myocardial infiltration by specific proteins (amyloid, sarcoid), endomyocardial scarring, cardiac muscle hypertrophy, Churg-Strauss syndrome, radiation therapy |
| Pathogenesis of Restrictive cardiomyopathies | o Diastolic dysfunction not in proportion with systolic dysfunction, muscles don’t relax well (difficult to differentiate from constrictive pericarditis) |
| Steps in cardiac remodeling (maladaptive response to contractile dysfunction & increased LV volume) | 1. Hypertrophy (increase in #) of myocytes causing dilatation of ventricle; 2. b. Chamber size increases, wall thickness decreases, progressive cardiomyocyte dysfunction occurs (loses its shape and becomes big & floppy so it is unable to contract as well) |
| Clinical Presentation of dilated cardiomyopathy, including signs & symptoms. | Classic CHF symptoms (Right sided, Left sided or bilateral) |
| Right sided CHF | congestion of systemic capillaries; • Symptoms: peripheral edema, nocturia, ascites, hepatomegaly. • Signs: pitting peripheral edema, ascites, hepatomegaly, JVD, parasternal heave |
| Left sided CHF | congest of pulm vascul; Symptoms: dyspnea (especially upon exertion), orthopnea, PND, exercise intolerance; Signs: tachypnea, rales/crackles in lung bases, dullness of lung fields with percus, cyanosis, laterally displaced PMI, gallop rhythm (S3 or S4) |
| Work-up for dilated cardiomyopathies | EKG, Echo, Ichemic work-up (stress test), bloodwork (BUN/Creatinine, electrolytes, BNP) |
| Work-up for Hypertrophic cardiomyopathies | EKG, Echo, Cardiac Cath |
| Work-up for Restrictive cardiomyopathies | EKG, Cardiac Cath (Gold Standard)-Endomyocardial biopsy for infiltrates (sarcoid, amyloid) |
| Describe the patient education needed for the diagnosis of dilated cardiomyopathy | ways to reduce cardiovascular preload. This would include a salt and water restriction. |
| Describe the appropriate pharmacologic therapy for a dilated cardiomyopathy and why each drug would be prescribed ie – mechanism of action. | B blocker - dec symp stimu to the heard to red hr rate and contractility ACE-I- blocks angiotensin resulting in vasodil and a reduc of CV afterload Aldosterone Inhibitor- reduces Na+ and H20 reten Diuretic Therapy- reduces blood volume Anticoag |
| The Mechanical Mechanisms for a Patient with dilated cardiomyopathy that would be indicated if ejection fraction is < 35% | Implantable Cardiac Defibrillator; Biventricular Pacemaker |
| Implantable Cardiac Defibrillator | Mechanical Mechanisms for PT with Dilated cardiopathy w/ ef<35%; detects Vtach or fib then shocks the heart to restore normal rhythm. prevents student cardiac death in patients with known, sustained ventricular tachycardia or fibrillations. |
| Biventricular Pacemaker | Mechanical Mechanisms for PT with Dilated cardiopathy w/ ef<35%; Leads are placed in the r & l vent and the r atrium also. makes the left ventricles contract at the same time as the right ventricle and help the ventricles pump more efficiently |
| Hypertrophic Cardiomyopathy Clinical Presentation - Younger onset (16-18) | Syncope -50% (most likely arrhythmia produced vs. obstructive), sudden cardiac death (arrhythmias), severe effort related chest discomfort (75%), dyspnesa (90%) |
| Hypertrophic Cardiomyopathy Clinical Presentation - Older onset | dyspnea, a. fib.,HT |
| Left Ventricular Outflow track obstruction DDX | Aortic Valve Stenosis Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Restrictive Cardiomyopathy Aortic Regurgitation |
| Describe the outflow murmur seen with a hypertrophic cardiomyopathy and physical exam maneuvers to increase/decrease it. | heard at the l sternal border; prod by dynamic L. vent outflow tract obstruct by the enlarged vent septum and MR and is a hybrid between ejection and regurgitate. increases with the valsalva, upright posit and dec with aquating and isometric handgrip. |
| Describe the appropriate pharmacologic therapy for a hypertrophic cardiomyopathy and why these particular drugs would be chosen. | Beta blockers: decrease HR and increases filling time and emptying time. Calcium Channel Blockers: decrease contractility so blood flow doesn't get obstructed. Anti-Arrythmics: To decreases A-fib Anti-coagulation: Decrease clots from A-fib. |
| List two surgical approaches for treatment of a hypertrophic cardiomyopathy. | Alcohol ablation of the septum Myectomy: manually take out part of the septum |
| Describe the clinical presentation of a restrictive cardiomyopathy and how it may differ from a dilated cardiomyopathy. | In restrict the pt may pres with R > L sided congested and low output symp. The pt may present with dyspnea, PND, Orthopnea, Periphe edema, ascites, weakness, and heart block. In dilated cardio has classic CHF symptoms which occurs more L than r sided. |
| Describe the pharmacologic approach to management Restrictive Cardiomyopathy and what each category of meds does to prevent symptoms or progression of the disease. | Diuretics, Spirolactone, slow heart rate(inc filling time) B Blockers, antiarrhyths(a fib), improve diastolic relazation(c++ blocker, b block, aceI); avoid digitalis, |
| List the causes of myocarditis | virus, bc, proto, spirochetal, Rickket, parasit, fungal, Chagas -Inflamma Dis- sarcoidosis, giant cell, scleroderma, SLE, hypersensitivity rxn’s, Serum sickness (ab, tetanus toxoid, acetazolamide, phenytoin) -Toxic exposure-cocaine, anthracyclines |
| Describe the possible clinical presentations of myocarditis. | a. Self-limited 40% b. Unexplained fever or viral syndrome c. Asymptomatic and symptomatic LV dysfunction d. Acutely decompensated heart failure e. Acute MI with normal coronaries f. Sudden Cardiac Death g. Arrhythmias |
| Describe the syndrome of congestive heart failure. | CHF is a clinical syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood. |
| Compare and contrast systolic from diastolic dysfunction and how the two may or may not be similar in clinical presentation. | Systolic is the inability of the vent to empty normally. Manifest include reduced EF and usually vent dilatation. -Diastolic is the inability of the ventricle to fill normally without a compensatory increase in left atrial pres. no reduce EF |
| Describe high output congestive heart failure and list two possible causes | Cardiac pump function may be supranormal but inadequate when metabolic demands or requirements are excessive. Causes are thyrotoxicosis, severe anemia, A/V shunting, Paget’s disease of bone and thiamine deficiency. |
| Describe (Define) preload | End-diastolic volume and the resultant fiber length of ventricles prior onset of contraction. (The pressure stretching the ventricle of the heart after atrial contraction) |
| Describe (Define) afterload. | Afterload- Impedance LV ejection. (The tension produced by a chamber of the heart in order to contract). |
| Describe appropriate history/questions to ask a patient with suspected congestive heart failure and how the symptoms correlate with the disease process. | DOE, Orthopnea, PND, cough,Insomnia=lung congestion; chest discomfort, palp= Heart is exhausted; synco,fatigue, confusion, depression, oliguria, nocturia=low perfusion; abd pain and nausea = hepatomegaly |
| Left-side Heart Failure PE Findings | SOB, fatique/weak, pulm edema, hemopty, PND, RHR, heaves/thrills, ab/xtra HS, Lungs-crackles, dec breath sounds in base, peripheral edema |
| Right-sided Heart Failure PE Findings | SOB, fatigue/weakness, polyuria, JVD, hepatomegaly, RHR/irregular, ab HS/murmur, ab LS, weight gain, peripheral edema |
| New York Heart Association Classification | Class I Asymptomatic Class II Symptoms with moderate exertion Class III Symptoms with minimal exertion Class IV Symptoms at rest |
| CHF Risk Factors | 1) Hypertension 2) CAD 3) DM 4) Obesity 5) Cardiotoxic drug therapy at any time 6) Alcohol abuse, cocaine 7) Family history of cardiomyopathy |
| two goals of therapy for congestive heart failure | 1) Treatment of symptoms 2) Halt/Slow progression of the disease |
| Describe the use of ace-inhibitors, beta blockers and diuretics in the treatment of congestive heart failure – mechanisms of action (no need to dosing or names of meds-(consider familiarity with drug names). | ACEI-prev peripheral vasocon by blocking the RAS decreases afterload, stops remodling B blockers blocks symp input, stop remodel, inc. EF w/ ACEI Diuretics dec pre-afterload, edema, Thiazide(inhibs NA+ distal T0, loop(in hib NA-K-2cl (medul thick) |
| Describe endothelial dysfunction and how it contributes to atherosclerotic coronary artery disease. | reduced vasodilation(reactivity to NO and NO produced), a proinflammatory state(inc VCAM1, MCP1, MMP, MCSF) and prothrombic properties(plasminogen activator inhibitor1) •caused by chronic injury, |
| Describe dyslipidemia and how it contributes to atherosclerotic coronary artery disease. | disorder of lipoprotein metabolism, High ldl, low HDL, the more ldls you have in your blood the higher likely hood of them becoming oxidized binding to lectin like oxidized LDL-R getting inglulfed by a MAC and causing more inflamation |
| List the five classic risk factors for coronary artery disease. | • Hypertension • Hyperlipidemia high LDL, low HDL • Diabetes Mellitus • Tobacco Use • Family History mother, father, siblings |
| Framingham Risk Factor Calculator | for >=20 year no HD or DM, based on age, sex, smoke, cholesteral, HDL, systolic BP |
| Be able to risk stratify based on clinical presentation of patients with chest pain | Low Risk • Atypical chest pain • Minimal or no risk factors • Young Intermediate Risk: • >70 • Male • Hx of diabetes • Hx of PVD/CVA • Previous EKG changes High Risk: • Ischemic discomfort • Hx of CAD • Hx of CHF • New EKG changes • Elevate |
| Describe classic angina both stable and unstable and describe the disease process that attributes to each one. | Stable: • Supply and demand mismatch • Precipitated by activity but should go away with rest Unstable: • Accelerating or progressive • New onset • Does not go away with rest |
| Anti-ischemic drug-therapy | nitro-inc BF, dec. Afterload; B blocker, dec. o2 demand and Vent irrit(lopressor); Morphine(analgesia, some dil; |
| Anti-thrombotic therapy | LMWH(lovenox), Unfractionated Hep; integrellin, |
| Anterior wall ekg findings | V1-V4(LAD) |
| Lateral wall | V5 and v6(circumflex) |
| interior wall | II, III, AVF(RCA) |
| Anti-platlet | Aspirin(anti-plt); Plavix,integrellin, high dose statin(plaque stabil, anti in flam |
| Revascularization Options | angiogram; pericutaneous angioplasty, stent; CABG |
| EKG Waveform | • P-Wave: Atrial depolarization • QRS Complex: Ventricular depolarization • ST-T-U Complex: Ventricular repolarization • J Point: junction between end of QRS and beginning of ST segment |
| EKG Rate | • Find the QRS complex that is closest to a dark vertical line • Count forward to the next QRS complex • Count off each dark line passed: 300-150-100-75-60-50 • Stop counting once you’ve reached your next QRS complex |
| Axis on EKG | (Lead I, AVF) Normal(++), Right(-+), Left(+-), NW(--), (NW look at lead II left(-) normal(+) |
| List causes for both left and right axis deviation | • Emphysema* • Hyperkalemia* • Lead transposition • Artificial cardiac pacing* • Ventricular tachycardia |
| Causes of RAD | • Normal in children and tall thin adults • RV hypertrophy • Chronic lung disease even without pulmonary hypertension • Anterolateral mI • Left posterior hemiblock • PE • WPW syndrome – left sided • Atrial septal defect • Ventricular septal defect |
| Causes of LAD | • Left anterior hemiblock • Q waves of inferior myocardial infarction • Artificial cardiac pacing • Emphysema • Hyperkalemia • WPW syndrome – Right sided accessory pathway • Tricuspid atresia • Ostium primim ASD • contrast into left coronary arter |
| RVH EKG criteria | • a right axis deviation(-,+, for leads I and AVF) • a large R wave in V1. |
| LVH EKG criteria | • a large wave in V1 and a Large R wave in V5 • the sum of the amplitudes of the S wave in V1 and the R wave in V5 exceeds 35 mm |
| 1st degree AV heart block ekg | Regular rate and rhythm, P wave normal, QRS normal, OR interval longer .2s and is constant, QT nl |
| 2nd Degree type 1 AV heart block ekg | Ventricular rate slow, normal or fast; atrial rate regular, patterned irregularity P waves - present and normal, not all p waves followed by QRS, QRS - nl, progressively longer until qrs is dropped SLLD, QT - NL |
| 2nd-degree type 2 AV heart block 2 ekg | Ventricular rate slow, normal or fast; atrial rate regular, regular, ireg(depends on whether the conduction ratio remains the same, P waves - present and normal, not all followed by QRS, QRS NL, Qt - nl |
| 3rd degree AV heart block ekg | Ventricular rate slow, normal or fast; atrial rate regular, Rhythm ( a and v rhytms normal not in sync) P - nl, qrs - nl, pr interval - not measurable, QT may or may not |
| AV heart block ekg | is caused by scarring of the AV node causing delay or incomplete impulses (HTN, CAD, aging, drugs). |
| 1st degree AV heart block | 1st degree is slowed conduction time in the AV node (PR greater than 1 large box) |
| 2nd degree AV heart block | 2nd degree has some impulses from the atria intermittently fail to reach and activate the ventricles “dropped beats”. |
| 3rd degree AV heart block | has complete AV block so no impulses from the atria reach the ventricles and the heart must rely on independent junctional or ventricular pacemaker with a HR of 20-45 therefore a permanent pacemaker is required. |
| Right Bundle block | V1 and V2 are the right chest leads,double RR, upright |
| Left Bundle Block | V5 and V6 you should see two RR’. If the last QRS deflection in lead V1 is downward the LBBB. If a LBBB is present, infarct pattern, axis, nor ventricular hypertrophy can be diagnosed therefore no more information can be determined |
| Ischemic EKG | T wave invert- symm, non-spec. Concern with pain. Subendo ischemia- ST seg depress Transmural ischemia- ST seg is raised. Has to be two leads and 2mm. (Make sure not J-Point elevat of the term port of the QRS dips back down rising back up to the ST |
| Infarct EKG | • Anterior wall: Leads V1-V4 • Inferior wall: II, III, AVF • Lateral wall: V5-V6 • Posterior wall: large R wave in V1 and V2 with ST depression. |
| Congenital Etiologies of Aortic Stenosis | Congenital:unicuspid, bicuspid, tricuspid(if one leaflet fused together or not normal) or quadricuspid valve. As the patient ages, these abnormal valves will calcify in the patients 20’s or 30’s but will present with symptoms in their 50’s and 60’s. |
| Acquired Etiologies of Aortic Stenosis | senile, calcified degen of a normal valve. presents at around 70yo. RF-usually involve both stenosis and insuff, Endocarditis-inflam or infect of valves Rad therapy- Sclerotic/fibrosis or valve Systemic diseases-amyloid or other infiltrative diseases |
| Pathogenesis of Aortic Stenosis | Pressure overload in LV=LVH=abn diastolic filling pattern=subendo ischemia |
| List the three classic clinical presentations of severe aortic stenosis. | Angina, syncope, CHF |
| physical exam findings of severe aortic stenosis. | mumor at aortic radiates to neck and apex, (mild-mod)ejection click that precedes the mumor; severe harsh ejection mumur with diminished to absent S2(heave or thrill) crescendo/decrescendo with late peak, low amp of carotid pulse delayed upstroke present |
| Congenital Etiologies of Aortic regurgitation(insufficency) | bicuspid, aortopathy systeic medial necrosis or collagen disorders like marafans |
| Acquired etiologies of Aortic regurgitation | Rheumatic, dilated aorta, RA or Ankylosing spondylitis, syphilis |
| Acute Aortic regurgitation | trauma, aortic discet or infectmedical emergency |
| Quincke’s sign | bounding capillary refill, Sign of AR |
| Austin Flint murmur | AR flow hits diastolic filling |
| Pharmacological and surgical intervention of Aortic regurgitation | Afterload reducers(vassodialators) surgery only after LV dysFx |
| Mitral valve anotomy | Made of two leaflets, pulled open by papillary muscles, close by themselves when heart contracts |
| 2 most common causes of mitral stenosis | Rheumatic Heart disease, congenital disease in which the pap muscles are to close together |
| mitral valve stenosis's effect on the heart | decrease left vent filling(preload), Back up into lungs/pulmonary HTN, RVH, TR, RAH = right sided heart failure |
| Signs and symptons of Mitral stenosis | CHF, R+L HF, Hemoptysis, stroke, palpable S1, distolic rumble at apex |
| Pharmacological and surgical treatment of Mitral Stenosis | diuretics to reduce the pressure/volume through the valve, anticoag, and valve replacement, Percutaneous balloon valvuloplasty is dangerous |
| etiologies of Mitral regurgitation | leaflets: myxomatous, RHD, endocard, congenital leaflets; chordae:trauma, degen, infect, endocard; Annulus: calcify, infect, endocard; Pap: cad, infarct, rupture, hypertrophic cardiomyopathy, infiltrates, LV dilation and traum |
| Symptoms of Mitral regurgitation | DOE 2nd to transient rise of pulmonary pressure, orthopnea, PND, fatigue, pulm HTN, RHF, hemoptysis, A fib(systemic emboli; |
| Signs of Mitral Regurgitation | pulse is brisk, apex is hyperdynamic, laterally displaced, ± thrill, late parastern left 2ndary to LA filling. S1-soft to nl, S2-wide split (early A2) unless LBBB, murmur-fixed MR (pansystolic, murmur-dynamic MR-MVP (mid-systolic ± click, inc when stand) |
Created by:
bmg4