Step 2 CK Review - Cardiology

8/11/2019 Step 2 CK Review - Cardiology

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USMLE STEP 2 CK REVIEW ~ CARDIOVASCULAR

ISCHEMIC HEART DISEASE

Coronary Artery Disease (CAD)

o Accumulation of atheromatous plaques within walls of coronary arteries that supply O2to myocardium

Blood flow causes ischemia of myocardial cells due to lack of oxygen Effects of ischemia reversible if blood flow to heart improved

Complete occlusion of artery causes irreversible cell death called myocardial infarction

o

Risk Factors: DM, HTN, tobacco, age >45, hyperlipidemia, LDL, HDL,homocysteine FHx of premature CAD or MI in 1st-degree relative men 1 flight of stairs Class III Marked limitation of ordinary activity angina after


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o Treatment:

Risk Factor Modification:

Smoking cessation 50% reduction in CAD risk 1yr after quitting

HTN control esp. diabetics

Hyperlipidemia low-fat diet & HMG-CoA reductase inhibitors DM strict glycemic control to reduced vascular disease risk Exercise & Weight loss also modifies other risk factors like DM, HTN, hyperlipidemia

Diet intake of saturated fat (


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Precipitated by the 3 Es 1) Exertion, 2) Emotion, 3) Eating

Brief duration pain lasts 95% if measured within 24-36hrs of onset of chest pain

o CK & CK-MB should be measured on admission & every 8hrs over 24hr period

Troponin I & T:

o Troponin within 3-5hr w/peak at 24-48hrs returns to normal after 5-14 dayso Greater sensitivity & specificity than CK-MB for myocardial injury


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Troponin I can be falsely elevated in renal failure

o Troponin should be measured on admission & every 8hrs over 24hr period

Creatinine Phosphokinase (CPK) Elevated within 4-8hrs but nonspecific MyoglobinElevated within 1hr but nonspecific

o TIMI Risk Score:

1 point for each criteria met:

Age >65 yrs At least 2 anginal episodes in last 24hrs

Serum cardiac biomarkers ASA use in prior 7 days Presence of 3 or more CAD risk factors Prior coronary stenosis 50%

ST segment deviation on admission ECG

Risk of all cause mortality at 14 days:

0-1 points = 4.7%

2 points = 8.3% 3 points = 13.2 %

4 points = 19.9%

5 points = 26.2% 6-7 points = 40.9%

o Treatment:

Management of NSTEMI:

InitialO2 + NTG + -blockers + ASA Morphine ClopidogrelInitiate w/ASA 300mg loading dose & 75mg daily

o Avoid use if emergency CABG likely discontinue 5 days before CABG

HeparinFor all pts. w/MI does not dissolve clots only prevents future formationo LMWH preferred except in renal failure or if CABG planned within 24hrs

GP IIb/IIIa inhibitors Abciximab, Eptifibatide, Tirofibano If undergoing PCI or at high-risk ex. Troponin, TIMI >4, DM

InvasiveEarly coronary angiography & revascularizationo Indicated w/following high-risk indicators:

Recurrent or persistent pain refractory to medical therapy

LV dysfunction EF


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WarfarinIf high risk of systemic thromboembolism A-Fib, CHF, LV thrombus

ACEIsPrevents adverse ventricular remodeling CHF, LVEF


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o Clinical Presentation:

LHFPulmonary venous congestion Cool extremities, slow capillary refill, peripheral cyanosis

Syncope, DOE, systemic hypotension, tachycardia, pulsus alternans

Orthopnea SOB while laying flat & relived by elevation of head w/pillows

Paroxysmal nocturnal dyspnea (PND) causes night time awakenings

Auscultation:

o Displaced PMI usually to left due to cardiomegaly

o S3 ventricular gallop due to rapid filling into noncompliant LV

May be normal finding in children

o Crackles/rales at lung bases indicates pulmonary edema

o Dullness to percussion & tactile fremitus of lower lung due to pleural effusion RHF Systemic venous congestion

MCC of RHF is LHF can mimic LHF if RV output leads to LV under-filling Cyanosis, peripheral edema, JVD, Kussmauls sign Nocturia due to venous return w/elevation of legs Hepatomegaly hepatojugular reflex RUQ pain due to hepatic congestion AuscultationS3 (right-sided), right ventricular heave, tricuspid regurgitation RHF can present similar to cirrhosis but w/cirrhosis no JVD or trouble lying flat

o New York Heart Association (NYHA) Classification:

Class INearly asymptomatic symptoms only w/vigorous activities

Class II Slight limitation of activities symptoms w/moderate exertion (ex. climbing stairs) Class III Markedly limiting symptoms w/normal activities of daily living (ex. walking) Class IV Incapacitating symptoms occur at rest

o Diagnosis:

CXRCardiomegaly, pleural effusion, Kerley B-lines, bronchiolar-alveolar cuffing ECHOAssess LV function via LVEF helps distinguish systolic from diastolic dysfunction

Initial test of choice preform when CHF suspected based on PE findings or CXR

ECGNonspecific may show chamber enlargement, arrhythmia, ischemia/infarction Radionuclide Angiography (MUGA) Precise measurement of left & right ventricular EF

RBCs tagged w/radioisotope & imaged during exercise & rest Useful when ECHO suboptimal or more precise assessment of LVEF needed

Can also assess wall motion abnormalities in ischemic heart disease

BNPSecreted by ventricles due to LV stretch & wall tension

Basic natriuretic peptide precursor cleaved into proBNP & secreted into ventricles

proBNP cleaved into active C-terminal portion & inactive NT-proBNP portiono HF suggested if NT-proBNP >450pg/mL

o Treatment:

DietSodium restriction initially


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o Complications:

Acute Pulmonary Edema (APE)Caused by rapid decompensation of LV function Precipitants dysrhythmias, MI, medication noncompliance, Na+load, inotropy

Treatment NOMAD: NTG, Oxygen, Morphine, Aspirin, Diuretic

Paroxysmal Nocturnal Dyspnea (PND) Brief SOB that awakens pt. from sleep treat w/NOMAD Due to volume load when lying horizontal or sudden in myocardial contractility

o Results in pulmonary edema causing impaired exchange of oxygen

Improvement w/walking & no response to bronchodilators differentiates from asthma

MYOCARDIAL DISEASE

Myocarditis

o Etiology:

ViralCoxsackie B (MCC), Echovirus, HIV, CMV, Influenza, EBV, HBV, Adenovirus BacterialS. pyogenes, C. diphtheriae, Meningococcus, B. burgdorferi, M. pneumoniae ParasiticT. cruzi (Chagas), Toxoplasma, Trichinella, Echinococcus SystemicKawasakis, SLE, sarcoidosis,acute RF ToxicCatecholamines, chemotherapy, cocaine HypersensitivityAntibiotics, diuretics, lithium, clozapine, insect/snake bites


Varies from asymptomatic to fulminant cardiac failure & death

Acute CHF dyspnea, rales, peripheral edema, JVD

Chest pain due to pericarditis or cardiac ischemia

Fever, preceding URI, palpitations, arrhythmias, syncope Auscultation S3/S4, MR, TR, friction rub if pericardium involved

o Diagnosis:

Labs Leukocytosis, ESR, CK, Troponin I check cultures, viral titers & cold agglutinins ECGST changes, dysrhythmias, conduction disturbances CXROften normal cardiomegaly or pulmonary venous congestion ECHODilated chambers, hypokinetic wall movements, pericardial effusion Myocardial Biopsy

o Treatment:

CHFACEIs necrosis & inflammation also address any underlying causes

DysrhythmiasDigoxin use cautiously as effects may be exaggerated by inflamed myocardium IVIGMay be of benefit ContraindicatedImmunosuppressives (ex. steroids, cyclosporine, NSAIDs)

Dilated Cardiomyopathy (DCM)

o Dilation & impaired systolic function of one or both ventricles MC type of cardiomyopathy

o Etiology:

MCC CAD w/prior MI InfectiousCoxsackie B, HIV, chagas, lyme disease, rickettsial, acute RF, toxoplasmosis ToxicAlcohol, cocaine, doxorubicin, chloroquine, clozapine, heavy metals (Pb, Hg, Cb) EndocrineDM, hyper/hypothyroidism, pheochromocytoma, acromegaly MetabolicUremia, hypocalcemia, hypophosphatemia, thiamine (wet-beriberi), selenium NeuromuscularDuchennes, myotonic dystrophy, Friedreichs ataxia

CollagenSLE, PAN, dermatomyositis, progressive systemic sclerosis OtherUncontrolled tachycardia (persistent A-Fib), peripartum cardiomyopathy,FHx in 20%


CHF dyspnea, rales, peripheral edema, JVD

Arrhythmias can be fatal causing sudden death

Angina due to O2 demands of enlarged ventricles Emboli systemic or pulmonary & may present w/neurologic deficits Auscultation S3/S4 gallop (stiffened ventricular walls), regurgitant valves (MR, TR), rales

o Diagnosis:

Labs BNP, Cr, LFTs, HCO3, Na+ ECGST & T-wave abnormalities, conduction defects (BBB), arrhythmias (VT, A-Fib)


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CXRGlobal cardiomegaly & pleural effusion ECHOEnlarged chambers, global hypokinesis, LVEF, MR, TR, mural thrombi AngiographyTo exclude ischemic heart disease in certain cases

o Treatment:

InitialAddress underlying cause & treat CHF accordingly WarfarinThromboembolism prophylaxis indications:

A-Fib, previous thromboembolism, documented thrombus, LVEF


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HCM is one of few murmurs that diminishes w/squatting (LVEDV)

Paradoxical splitting of S2 Pulmonic valve closes before aortic valveo Inspiration will delay pulmonic closure & cause paradoxical narrowing of split

Pansystolic murmur due to MR PulsesRapid upstroke & bifid carotid pulse Precordial palpationPMI localized & triple apical impulse

o Diagnosis:

ECGLVH, PVCs, A-Fib, prominent Q-waves, high voltages across precordium ECHOSeptal hypertrophy, LVH, systolic anterior motion of mitral valve, MR

Cardiac CatheterizationPreform if considering invasive therapyo Treatment:

PreventativeAvoid factors that obstruction esp. volume depletion & strenuous exertion Pharmacologic management:

-blockers DisopyramideHR, LV filling time, inotropy CCBs (Verapamil)2ndline only in pts. without resting or provocable obstruction AvoidACEI, Nitrates, Diuretics preload will worsen obstruction & symptoms

Refractory cases Septal myectomy or Septal ethanol ablation or Dual chamber pacing Ventricular arrhythmias Amiodarone or ICD Screening1stdegree relatives of HCM pts. screened via physical, ECG & 2D-ECHO

Screen annually during adolescence then serially every 5yrs

o Complications:

MCC of sudden cardiac death (SCD) in young athletes Factors ass. w/risk of SCD:

o Syncope or non-sustained VT

o Marked ventricular hypertrophy max. wall thickness 30mm

o Abnormal BP response to exercise in young pts.

PERICARDIAL DISEASE

Pericarditis

o Etiology:

IdiopathicUsually presumed to be viral MCC is Coxsackie virus InfectiousCoxsackie, Echovirus, S. pneumoniae, S. aureus, TB, Histoplasmosis, Blastomycosis

Acute post-MI Direct extension of myocardial inflammation seen after 1-7 days Dresslers syndrome Autoimmune response to infarcted myocardium seen after 2-8wks TraumaPost-cardiac surgery (ex. CABG) MetabolicUremia (common), hypothyroidism MalignancyHodgkins, breast, lung, renal cell carcinoma, melanoma CollagenSLE, polyarteritis, RA, scleroderma DrugsHydralazine, Procainamide, Isoniazid OtherRadiation, dissecting aneurysm


Recent viral URI fever Pleuritic chest pain alleviated by sitting up & leaning forward

Does not respond to NTG pain aggravated by lying supine, coughing, swallowing

Auscultation pericardial friction rub on expiration is pathognomonic (but variably present)

o

Diagnosis: ECGDiffuse ST elevations, PR depressions (specific), low voltage CXRNormal sized heart & pulmonary infiltrates ECHOTo assess for pericardial effusion Diagnostic triad 1) Chest pain, 2) Friction rub, 3) ECG changes

o Treatment:

Self-limitedMost cases resolve in 2-6wks NSAIDsMainstay of therapy to relieve pain & inflammation SteroidsFor intractable cases (ex. Dresslers)

o ComplicationsRecurrence, atrial arrhythmia, pericardial effusion, tamponade, constrictive pericarditis


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Pericardial Effusion

o Etiology:

Transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism Exudative (serosanguinous or bloody) Causes similar to acute pericarditis

May develop acute effusion 2Oto hemopericardium trauma, post-MI rupture, dissection


Asymptomatic can also present similar to acute pericarditis

Dyspnea, cough, JVP w/dominant x descent, pulse pressure Esophageal/recurrent laryngeal/tracheo-bronchial/phrenic nerve irritation Auscultation distant heart sounds rub

o Diagnosis:

ECHOProcedure of choice shows fluid in pericardial sac ECGLow voltage & flat T-waves CXRCardiomegaly, rounded cardiac contour (water bottle appearance) PericardiocentesisIdentify transudate vs. exudate, infectious agents, neoplastic involvement

o Treatment:

Mild effusionFrequent observation w/serial ECHOs + Anti-inflammatory agents Severe effusion Pericardiocentesis may develop cardiac tamponade

Pericardial Tamponadeo Due to rapid accumulation of fluid in pericardial sac impairs cardiac filling leading to COo EtiologyPericarditis, trauma, post-MI rupture, aortic dissection w/rupture, malignancy, uremiao Clinical Presentation:

Becks Triad 1) Hypotension, 2) Muffled heart sounds, 3) JVD

Other dyspnea, tachypnea, tachycardia, peripheral edema

Pulsus Paradoxus sBP by >10 mmHg w/inspiration due to stroke volume Transiently enlarged RA bulges leftward causing LV volume & output

Auscultation distant heart sounds

o Diagnosis:

ECGElectrical alternans pathognomonic variation in R-wave amplitude ECHOPericardial effusion & compression of cardiac chambers (RA & RV) in diastole

o Treatment:

PericardiocentesisPreform immediately if unstable Fluids To expand volume & CO avoid diuretics & vasodilators PericardiotomyPericardial window created to allow drainage

Constrictive Pericarditis

o Chronic pericarditis resulting in fibrosed, thickened, adherent or calcified pericardium

o EtiologyAny cause of acute pericarditis may result in chronic pericarditis Idiopathic, viral, TB, radiation (worst prognosis), post-cardiac surgery, uremia, MI


Dyspnea, tachycardia, palpitations, JVD, normal BP, absent pulsus paradoxus

Kussmauls sign failure of jugular venous pressure to fall during inspiration

May mimic CHF (esp. RHF) ascites, hepatosplenomegaly, edema Auscultation distant heart sounds

Precordial pericardial knock (early diastolic sound)o Diagnosis:

ECGLow voltage, T-wave flattening or inversion, notched P-waves CXRPericardial calcification & effusions ECHO/CT/MRIPericardial thickening Cardiac Catheterization Equalization of end-diastolic chamber pressures diagnostic

o TreatmentDiuretics + Na+restriction if unresponsive consider Pericardiectomy


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VALVULAR HEART DISEASE (VHD)

Mitral Stenosis (MS)

o EtiologyMCC is RHD MC in females & congenital MS rare causeo Clinical Presentation:

DOE, orthopnea, fatigue, palpitations, PND

Pulmonary HTN peripheral edema, cough, hemoptysis Dysphagia & hoarseness enlarged LA impinging on esophagus & recurrent laryngeal nerve

A-Fib dilation of left atrium major cause of A-fib

Systemic emboli due to blood stagnation in enlarged LA Absent a wave on JVP, sternal lift due to RVH, pulse pressure, loud AuscultationOS after S2 w/mid-diastolic rumble at apex best heard over LSB

Murmur enhanced by LA return esp. expiration Long murmur & short A2-OS interval correlate w/severe MS

o Diagnosis:

ECGLAE, A-Fib, RVH, RAD ECHOThickening of MV leaflets CXRLAE w/straight left heart border, kerley B-lines (pulmonary effusion), large PA

o Treatment:

Diuretics & Na+restriction

DigitalisTo control ventricular rate in A-Fib AnticoagulationIf atrial thrombus or A-Fib present

Balloon valvuloplastyStandard of care indicated in symptomatic pts. w/orifice 1.2cm2 Alternatives Mitral commissurotomy or Valve replacement

Mitral Regurgitation (MR)

o MRCOLV/LA pressure LV/LA dilatation CHF + Pulmonary HTNo Etiology:

MCC is mitral valve prolapse (MVP)

Endocarditis, rheumatic fever, LV dilatation/aneurysm, Marfans, HOCM

MV annulus calcification or chordae/papillary muscle rupture


Dyspnea, PND, orthopnea, palpitations, peripheral edema, cough

Auscultation loud holosystolic murmur at apex w/radiation to axilla & S3

Murmur enhanced by expiration or TPRo Diagnosis: ECGLAE, LVH ECHOShows diseased or prolapsed valve Swan-Ganz Catheterization Prominent Vwave due to systolic overload on LA

o Treatment:

AsymptomaticSerial ECHOs DiureticsTo preload & improve CO VasodilatorsTo afterload which favors aortic exit esp. ACEIs SurgeryIndicated in acute MR w/CHF or if signs of LV dysfunction

Valve repair Annuloplasty rings, leaflet repair, chordae transfers/shorten/replacement

o Advantages low rate of endocarditis, no anticoagulation & less reoperation

Valve replacementIf failed repair or heavily calcified annulus

Mitral Valve Prolapse (MVP)

o MV displaced into LA during systole MC valvular disorder w/90% of cases in women

o Pathophysiology:

Myxomatous degeneration of chordae due to defect in connective tissue proteins

Due to Marfans, Ehlers-Danlos, RHD, pectus excavatum


AsymptomaticStabbing chest pain, dyspnea, palpitations, presyncope, systemic emboli AuscultationMid-systolic click followed by late-systolic high-pitched murmur at apex

Murmur enhanced by venous return valsalva or squat-to-stand maneuver Click due to tensing of mitral leaflet - preload will move click closer to S1


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Other findings Wide splitting of S2 or S3o Diagnosis:

ECGNon-specific ST & T-wave changes, paroxysmal SVT, ventricular ectopy ECHOSystolic displacement of thickened MV leaflets into LA

o Treatment:

AsymptomaticNo treatment Symptomatic-blockers & avoidance of stimulants ex. caffeine AnticoagulationIf systemic emboli Endocarditis prophylaxis If murmur audible or if myxomatous leaflet

SurgicalMV repair favored over replacement if significant MR

Aortic Stenosis (AS)

o ASOutflow obstruction EDPConcentric LVH LVFo Normal AV area = 34cm2Severe AS =


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Austin Flint murmur low-pitched diastolic rumble heard in severe regurgitationo Due to regurgitated blood striking anterior mitral leaflet similar sound to MR

o Diagnosis:

ECGLVH & LAE ECHOTo identify leaflet or aortic root anomalies CXRLVH, aortic root dilation Stress Test Hypotension w/exercise

o Treatment:

AsymptomaticAfterload w/ACEIs, Nifedipine, Hydralazine avoid exertion

SurgeryIndicated in severe cases w/LVEF > AV > TV > PV

o Classification:

Acute Bacterial Endocarditis (ABE):

Infection of healthy valvesMCC is S. aureus Produces metastatic foci & usually fatal if not treated within 6wks

Subacute Bacterial Endocarditis (SBE):


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Polyarthralgia Recent streptococcal pharyngitiso Treatment:

Penicillin or Erythromycin For 10 days to eradicate throat carriage of GAS ASAFor arthritis PrednisoneIf severe carditis 2OProphylaxis Daily Penicillin or Erythromycin

No carditis 5yrs or until 21yrs old (whichever is longer)

Carditis but no RHD 10yrs or longer Carditis w/RHD minimum 10yrs since last episode (sometimes life long)

o

Complications:

AcuteMyocarditis, A-Fib, acute MR, pericarditis ChronicRheumatic heart disease (RHD)

Valvular abnormalities due to IC deposition in valve leaflets

o Fibrous thickening, adhesion & calcification resulting in stenosis or regurgitation

o Valve involvement MV > AV > TV

Onset usually after 10-20yr latency from acute carditis of rheumatic fever

Risk of IE & thromboembolism

ARRHYTHMIAS

Alterations in Impulse Formation

o

Abnormal Automaticity:

Normally only specialized cells of conduction system exhibit automacity & are pacemaking cells

Cells found in SA node, AV node & ventricular conduction system

Cells in myocardium outside conduction system may inappropriately acquire automaticity

Often seen in diseased cells ex. Post-MI ventricular ischemia

Ectopic generators assume pacemaking control if they depolarize at rate greater than SA node

Automaticity can be influenced by:

Sympathetic & parasympathetic stimulation

Abnormal metabolic conditions hypoxia, acidosis, hypothermia

Electrolyte abnormalities or drugs (ex. digitalis)

Local ischemia/infarction

o Early After-depolarizations:

Due to membrane potential becoming more positive during repolarization Tachyarrhythmia results from self-maintained depolarizing oscillations of action potential

Basis for degeneration of QT prolongation into Torsades de Pointes

o Delayed After-depolarizations:

Occurs after AP has fully repolarized, but before next normal AP delayed after-depolarization

Seen w/intracellular Ca2+(digitalis toxicity, ischemia) or w/catecholamine stimulation

Alterations in Impulse Conduction

o Re-entry Circuits:

Self-sustaining re-entry circuit causes rapid repeated depolarizations in region of myocardium

Infarcted myocardium w/ischemia will consist of non-excitable & partially excitable zones

These zones promote formation of re-entry circuitso Conduction Block:

Ischemia, fibrosis, trauma & drugs can cause transient, permanent, uni- or bi-directional block MCC is refractory myocardium cells in refractory period or unexcitable due to fibrosis

If block occurs along conduction system, distal conduction zones can assume pacemaking control

Can lead to bradycardia but also tachycardia if impaired conduction leads to re-entry

o Bypass Tracts:

Normally AV node only conducting tract from atria to ventricles

Development of additional or accessory conducting tracts can bypass AVN

Facilitates premature ventricular activation before normal AVN conduction

Sinus Bradycardia

o HR


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o Normal variantBradycardia may be seen in normal adults esp. athletes & elderlyo AsymptomaticMay have light-headedness or possible syncopeo TreatmentAtropine pacing or pressors for hypotension only if symptomatic

Sinus Block, Pause & Arrest

o 3 disorders involving SA node sinus pacemaker fires but impulse fails to depolarize atrial myocardium

Results in no initial P wave & consequently no QRS complex, ST segment or T wave

o Sinus (SA) Block Complete block or failure of sinus node to depolarize atria Block can last one or more cardiac cycles & is multiple of normal P-P interval

o

Sinus PauseDelay in formation of sinus impulse in SA node causes temporary pause (usually >3 sec) If pause >3x the normal P-P interval it may be called sinus arrest

o Sinus ArrestLonger delay in formation of sinus impulse in SA node P-P prolongation not gradual (unlike sinus arrhythmia) & not multiple of P-P (unlike SA block)

o Escape beats or rhythm may occur:

Atrial escapeP-waves w/abnormal morphology Junctional escapeP-waves not seen or follow QRS (retrograde P) rate 40-60 bpm Ventricular escape No P-wave & wide abnormal QRS slow rate 20-40 bpm

Sick Sinus Syndrome (SSS)

o Sinus node dysfunction Marked bradycardia, sinus pause/arrest, sinoatrial blocko Frequently ass. w/episodes of atrial tachyarrhythmias tachy-brady syndrome

o

TreatmentElectronic pacemaker indicated if symptomatic bradycardia -blocker, CCB, Digoxin Often initiated after pacemaker insertion for tachycardia

AV Conduction Blocks

o PrecipitantsInferior wall MI, Digitalis toxicity, vagal tone, conduction system diseaseo 1stDegree AV Block Prolonged PR interval >0.20s benign & no treatment requiredo 2nd Degree AV Block:

Mobitz Type I (Wenckebach):

Progressive PR prolongation followed by failure of P-wave conduction

AV node is MC site of block benign & no treatment required

Mobitz Type II:

P-wave suddenly fails to conduct without prior PR prolongation QRS drops suddenly

Site of block within His-Purkinje system requires permanent pacemaker

o

Treat quickly as it can progresses to 3rddegree complete heart blocko 3rd Degree AV Block (Complete Heart Block):

Failure of atrial impulse conduction to ventricles independent atrial & ventricular activity

No relationship between P-waves & QRS complexes always requires pacemaker implantation

Premature Complexes

o Premature Atrial Complexes (PACs):

Ectopic supraventricular beat originating in atria

ECGEarly P-waves that differ in morphology from normal sinus P-waves Difference is because PACs originate within atria & not sinus node

Normal QRS complex because conduction below atria is normal

Asymptomatic but may cause palpitations or give rise to PSVTs PACs found in >50% of normal adults Tx. w/-blockers if symptomatic

o

Premature Ventricular Complexes (PVCs): Early beat fires independently from focus in ventricle & spreads to other ventricle

Conduction not through normal pathway but through slower ventricular muscle

Slower conduction causes wide QRS complexes >120msec w/bizarre morphology

No preceding P-wave seen its hidden within wide QRS complex

Couplet2 successive PVCs BigeminySinus beat followed by PVC TrigeminySinus beat followed by 2 PVCs

PVCs seen in >50% of men w/Holter monitoring usually asymptomatic & benign

PVC significant in following situations:

Consecutive (3 = VT) or Multiform (varied origin)


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R on T phenomenonPVC falling on T-wave of previous beato May precipitate VT or V-Fib can potentially cause sudden death

-blockersMay benefit if symptomatic also order EP study to assess benefit of ICD Studies shown risk of death if antiarrhythmic drugs used to suppress PVCs after MI

Atrial Fibrillation (A-Fib)

o Disorganized electrical activity of atrial myocardium causing atrial quiver & rapid ventricular rate

o Pathophysiology:

InitiationSingle circuit re-entry or ectopic foci produce atrial tachycardia 350-600 bpm

Impulses then conduct irregularly across atrial myocardium to give rise to fibrillation

MaintenanceTachycardia causes atrial structural & EP changes which further promotes A-Fib Longer pt. remains in AF the more difficult to convert back to sinus rhythm

AV node blocks most incoming atrial impulses producing ventricular rate 48hrs Obtain Transesophageal ECHO (TEE) to R/O thrombus in LA

o If no thrombus seen Start IV Heparin & perform cardioversion within 24hrs TEE avoids need for 3wk wait prior to starting anticoagulation

o Anticoagulation for 4wks after cardioversion still required

Chronic A-FibCCB or -blocker (rate control) + Warfarin (chronic anticoagulation)

"Lone" A-Fib Pts. < 60yrs w/A-Fib in absence of underlying CV risk factors Do not require anticoagulation due to low risk for embolization

Atrial Flutter

o Rapid, regular atrial depolarization from macro re-entry circuit within atrium MC site is RA

o Pathophysiology:

Irritable automaticity focus in atria fires giving rise to regular atrial contractions 250-350 bpm

Ventricular rate 30-50% of atrial rate difference due to long refractory period in AV node

AV node allows only 1 out of every 2 or 3 flutter waves to conduct to ventricles

AV block may be fixed (2:1, 3:1, 4:1) or variable

o EtiologyCOPD, CAD, MV disease, ASD, CHF, cardiac surgery, PE, pericarditis, thyrotoxicosis


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o Diagnosis:

ECGSawtooth flutter baseline in inferior leads (II, III, aVF) Narrow QRS after every second or third tooth P-wave

o Treatment:

Rate control-blocker, CCB, Digoxin CardioversionPreform immediate electrical cardioversion if unstable

Chemical cardioversion Sotalol, Amiodarone, Type I antiarrhythmics

AnticoagulationSame guidelines as A-Fib Long-termCatheter radiofrequency (RF) ablation success rate dependent on site of origin

Multifocal Atrial Tachycardia (MAT)

o Irregular rhythm caused by 3 or more atrial foci w/atrial rate 100-200 bpm may mimic AF

o EtiologyCOPD (MCC), hypokalemia, sepsis, theophylline or digitalis toxicityo DiagnosisECG at least 3 distinct P-wave morphologies w/variable PR & RR intervalso Treatment:

Normal LV functionCCBs, -blockers, Digoxin, Amiodarone, IV Flecainide, IV Propafenone -blockers may be contraindicated in severe pulmonary disease

LV functionDigoxin, Diltiazem, Amiodarone Electrical cardioversion Ineffective & should not be used

Paroxysmal Supraventricular Tachycardia (PSVT)

o

Etiology: Ischemic heart disease or excessive caffeine/alcohol consumption

Digoxin toxicity MC arrhythmia is paroxysmal atrial tachycardia w/2:1 block

AV node reentry or AV reciprocating tachycardia (accessory pathway)

Atrial flutter w/rapid ventricular response

o Classification:

AV Nodal Reentrant Tachycardia (AVNRT):

Accounts for 60-70% of all PSVTs & often found in absence of structural heart disease

Re-entrant circuit using dual pathways within AV node fast -fibers & slow -fibers Usually initiated by premature atrial or ventricular contractions

Sudden onset & offset, fast regular rhythm w/rate between 150-250 bpm

ECGNo discernible P-waves buried within narrow QRS complexeso Rapid conduction causes impulses to activate atria & ventricles simultaneously

AV Reentrant Tachycardia (AVRT): Re-entrant loop via accessory pathway between atria & ventricle conducts retrogradely

o Initiated by a premature atrial or ventricular complex

Orthodromic AVRTStimulus travels up bypass tract (V to A) & down AV node (A to V)o Accounts for 95% of reentrant tachycardia associated w/WPW syndrome

o ECG narrow QRS no delta wave

Antidromic AVRTStimulus goes up AV node (V to A) & down bypass tract (A to V)o ECG wide & abnormal QRS due to ventricular activation via bypass tract

o Treatment:

Vagal stimulationDelays AV conduction & blocks reentry mechanism Valsalva, carotid sinus massage, breath holding, head immersion in cold water/ice

IV Adenosine1stline if no response to vagal maneuvers Works by SA & AV nodal activity w/short duration of action

CCB, -blocker, DigoxinAlternatives if LV function preserved Electrical cardioversionIf drugs not effective or if unstable almost always successful Long-term prevention:

1stline Digoxin (preferred), -blocker, CCB 2ndlineAnti-arrhythmics Flecainide or Propafenone 3rdlineRadiofrequency catheter ablation of either AV node or accessory tract

Wolff-Parkinson-White Syndrome (WPW)

o Accessory conduction tract from atria to ventricles causing premature ventricular excitation


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Bundle of Kent abnormal fast conducting fibers that bypass AV node found in either LA or RA

o EtiologyCongenital defect seen in 1.5/1000 of general populationo Can lead to paroxysmal tachycardia via 2 possible mechanisms:

Orthodromic AVRT:

Impulse travels through AV node (anterograde) & depolarizes ventricles

Then travels back through accessory pathway (retrograde) & re-depolarizes atria

Absent delta waves because conduction occurs retrograde over accessory pathway

SVT (A-Fib or Atrial flutter):

Accessory pathway allows all or most impulses to pass causing ventricular rate

o

Normally, AV node allows only certain impulses to ventricles

o Diagnosis:

ECGWide QRS complex w/slurred upstroke (delta wave) & PR interval 30secs almost always symptomatic

Life-threatening arrhythmia can progress to V-fib if untreated

Often ass. w/hemodynamic compromise or development of myocardial ischemia

Nonsustained VTBrief, self-limited runs of VT usually asymptomatic Risk for sudden death if CAD & LV dysfunction present


Palpitations, dyspnea, light-headedness, angina, impaired consciousness, syncopeo Diagnosis:

ECGWide QRS tachycardia may be monomorphic or polymorphic Monomorphic VTMC type identical complexes w/uniform morphology Polymorphic VTConstantly changing morphology, amplitude & polarity OtherAV dissociation sinus P-waves continue their cycle unaffected by tachycardia

o

Treatment: Sustained VT:

Hemodynamically stableIV Amiodarone, IV Procainamide, IV Sotalol Hemodynamic compromiseImmediate electrical cardioversion

o Follow w/IV Amiodarone to maintain sinus rhythm

Nonsustained VTDo not treat if asymptomatic w/no underlying heart disease

Ventricular Fibrillation (V-Fib)

o Multiple foci in ventricles fire rapidly leads to chaotic quivering of ventricles & no cardiac output


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Most episodes begin w/VT except in setting of acute ischemia/infarctiono Etiology:

MCC Ischemic heart disease

Prolonged QT torsades de pointes, anti-arrhythmic drugs WPW w/A-Fib + rapid ventricular response


Loss of consciousness if V-Fib >5-6 secs if untreated can lead to sudden cardiac death BP immeasurable, absent heart sounds & pulse

o DiagnosisECG QRS & P-waves both unidentifiableo

Treatment: Medical emergencyImmediate defibrillation & CPR

Unsynchronized DC cardioversion up to 3 sequential shocks to establish rhythm If V-Fib persists IV Epinephrine 1mg bolus initially & then every 3-5 mins

Causes myocardial & cerebral blood flow also reduces defibrillation threshold Attempt to defibrillate again 30-60secs after first epinephrine dose

Refractory V-FibIV Amiodarone followed by shock 2ndline Lidocaine, Bretylium, Magnesium, Procainamide

Chronic therapyICD is mainstay alternative is long-term Amiodaroneo Prognosis:

V-Fib not ass. w/acute MI Recurrence rate up to 30% within first year Require chronic therapy ICD or prophylactic Amiodarone

V-Fib within 48hrs of acute MI Low recurrence rate 2% within first year

VASCULAR DISEASE

Hypertension (HTN)

o Classification:

HTNPre-HTN: 120/89, Stage 1: 140/90, Stage 2: 160/100 Isolated Systolic HTN sBP 140 & dBP 210 or dBP >120 w/absent end-organ damage Hypertensive EmergencysBP >220 or dBP >120 + acute end-organ damage

Papilledema, retinal hemorrhages, bulging discs, mental status changes,Cro

Etiology: 1O(Essential) HTN MCC of HTN (>90%) unknown cause 2OHTN:

Renal renal failure, glomerulonephritis, renal artery stenosis

Endocrine cushings syndrome, 1Ohyperaldosteronism, pheochromocytoma

Other coarctation of the aorta or drug-induced (cocaine, amphetamines)o Risk Factors FHx, obesity, smoking, DM, high Na+/fat diet, alcohol, black race, male gendero Clinical PresentationAsymptomatic light-headed, occipital headache, epistaxis, hematuria, visiono Diagnosis:

FundoscopicCheck for AV nicking, hemorrhage or papilledema AuscultationCheck for renal artery bruits ECGMay show LVH or left ventricular strain

o Treatment:

Lifestyle modificationNa+restriction, low-fat diet, weight loss, exercise, smoking cessation PharmacologicThiazides (preferred), ACEIs, CCBs, -blockers Hypertensive EmergencyMAP by 25% in 1-2hrs gradually reduced BP back to normal

Severe HTNIV agents Nitroprusside, Labetalol, Nitroglycerin

No immediate danger Oral agents Captopril, Clonidine, Labetalol, Diazoxide Hypertensive Urgency BP within 24hrs via oral agents

Aortic Dissection

o Tear in aortic intima allowing blood to dissect into aortic media

Acute dissection < 2wks initial mortality 1% per hour


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Chronic dissection >2wks mortality levels up to 75-80%o Etiology:

CardiacHTN (longstanding in 70% of cases), bicuspid AV, coarctation of the aorta, PDA OtherMarfans, EhlersDanlos, syphilis, trauma, 3rdtrimester pregnancy, cocaine

o Classification:

DeBakey:

Type IAscending & descending aorta MC type 50% Type IIAscending aorta only stops at innominate artery Type IIIADescending thoracic aorta only proximal to diaphragm

Type IIIBType IIIA + abdominal aorta Stanford:

Type A (Proximal)Ascending aorta aortic arch requires emergent surgery

o Mortality rate w/o surgery is 3% per hour for first 24hrs & 80% at 2wks

Type B (Distal) Descending aorta only distal to subclavian artery


HTN (75%) syncope Chest pain sudden onset, tearing or stabbing pain w/radiation to back

Anterior chest pain more common w/proximal dissection (type A)

Interscapular back pain more common w/distal dissection (type B)

Asymmetric BP & pulses between arms poor prognosis if >30 mmHg difference

Aortic regurgitation w/new diastolic murmur esp. w/proximal dissection

o

Diagnosis: CXRWidened mediastinum & pleural capping (effusion in lung apices) TEECan visualize AV & thoracic aorta but not abdominal aorta

Preferred test in acute setting alongside CT due to high sensitivity & specificity

Ideal test for unstable pts noninvasive & preformed at bedside

CT/MRIBoth highly accurate MRI not ideal in acute setting due to longer time AngiographyInvasive but best test for determining extent of dissection for surgery

o Treatment:

Immediate BP control:

IV -blockersTo HR & diminish force of LV ejection IV Sodium NitroprussideTo sBP below 120mmHg

SurgicalResection of intimal tear & replacement of affected aorta w/prosthetic graft High morality rate due to operative or post-op complications

Type ARequires emergent surgery w/cardiopulmonary bypass

Hypothermic circulation for transverse arch dissections

Valve replacement & coronary re-implantation for aortic root involvement Type BManaged medically 10-20% may require urgent surgery for complications

o Complications:

Ischemic syndromesDue to dissection or occlusion of aortic branches Coronary (MI), Carotids (stroke, hemiplegia, horners), Splanchnic (ischemic gut)

ARDue to dissection through aortic root w/unseating of AV cusps Cardiac TamponadeDue to dissection into pericardium RupturePleural (dyspnea, hemoptysis) or Peritoneum (hypotension, shock)

Aortic Aneurysm

o Localized dilatation aortic segment w/diameter at least 1.5x that of normal

o

True aneurysmInvolves all vessel wall layers intima, media, adventitiao False aneurysm Disruption of aortic wall or anastomotic site between vessel & graft

Containment of blood by fibrous capsule made of surrounding tissue

o Classification:

Thoracic (TAA) ascending, transverse arch, descending

Thoracoabdominal

Abdominal (AAA) 90% infrarenal & MC between renal arteries & iliac bifurcation

o Etiology:

Degenerative, atherosclerotic, trauma, vasculitis, bicuspid AV

Marfans, EhlersDanlos, infectious (syphilis, fungal), mycotic (Salmonella, Staph)


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o Risk Factors Smoking, HTN, age >65, FHx, M>W, CADo Clinical Presentation:

Asymptomatic (75%) discovered incidentally due to pain in chest, abdomen, flank or back

Syncope, hypotension, palpable pulsatile abdominal Airway or esophageal obstruction hoarseness, hemoptysis, hematemesis

Uncommon presentation:

Partial bowel obstruction or ureteric obstruction w/hydronephrosis

GI bleed duodenal mucosal hemorrhage, aortoduodenal fistula Aortocaval fistula or distal embolization (blue toe)

o

Diagnosis:

U/S Test of choice to evaluate size & location of aneurysm 100% sensitive CT100% sensitive but longer time to preform than U/S AXRMay show calcifications of dilated segment allowing measurement of aortic diameter

But not used to R/O aneurysm only for quick assessment

o Treatment:

Conservative management:

Risk factors Smoking cessation, HTN/DM/hyperlipidemia control, exercise U/SEvery 6 months to 3yrs depending on size & location

Surgical indications:

Risk of rupture Risk of surgery size >5.5cm or >2x normal lumen size

Symptomatic, ruptured or mycotic aneurysm

Acute type A dissection or complicated type B dissection Ascending thoracic aortic aneurysms

Surgical procedures:

Laparotomy w/graft replacement

Endoluminal graft placement under image guidanceo Newer procedure w/mortality, procedure time & recovery timeo Disadvantages endoleak rates up to 20-30% & high-cost for device

o Complications:

Rupture of AAA Emergent laparotomy indicated crossmatch 10 units PRBCs Triad of 1) Abdominal pain, 2) Hypotension, 3) Palpable pulsatile abdominal mass

o No further diagnostic testing needed w/triad of symptoms

CV collapse & syncope 2Oto sudden hemorrhage

Signs suggesting expansion & impending rupture:o

Sudden onset of severe pain in back or abdomen & radiating to groin/legso Grey Turner's sign Ecchymoses on back & flankso Cullen's sign Ecchymoses around umbilicus

Peripheral Vascular Disease (PVD) Chronic Arterial Insufficiency

o Occlusive atherosclerotic disease of LE w/symptoms related to site of obstruction

MC site of occlusion is superficial femoral artery in Hunter's canal also popliteal & aortoiliac

o Risk Factors DM, smoking, CAD, hyperlipidemia, HTN, hyperhomocystinemiao Clinical Presentation:

Intermittent claudicationLeg pain reproduced in same location by same walking distance Pain completely relieved by rest Femoral or popliteal occlusion causes calf claudication

Aortoiliac occlusion causes buttock, hip & calf claudication

Rest painContinuous & typically felt over distal metatarsals Often prominent at night awakens pt. from sleep

Pain relieved by hanging foot over side of bed or standing perfusion due to gravity Rest pain suggests severe ischemia & possible progression to gangrene

PulsesMay be diminished or absent Signs of perfusion:

Muscular atrophy, hair growth, thick toenails, capillary refill, skin temp. Pallor of elevation & rubor of dependency skin color change w/leg elevation

Skin ulceration MC in toes & 2Oto local trauma that does not heal End-stage disease tissue infarction & gangrene


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o Diagnosis:

ABIRatio of sBP at ankle to sBP at arm is normally 1.0 Claudication = ABI 6hrso Etiology:

Cardiac emboli (MCC 80%)A-Fib, post-MI, VHD, endocarditis, atrial myxoma Arterial emboliProximal arterial aneurysm, atheroembolism

ThrombiAtherosclerotic, trauma, hematological disorders & stasiso Clinical Presentation:

6 Psbut all may not be present:

Pain in LE progressing within hrs to feeling of cold, numbness & loss of functiono Pain absent in 20% of cases due to prompt onset of anesthesia & paralysis

Pallor within few hrs becomes mottled cyanosis Paresthesia light touch (small fibers) lost first, then sensory (large fibers) Paralysis loss of power most important because it indicates impending gangrene

Polar cold

Pulselessness not reliable

o Diagnosis:

ArteriogramTo define site of occlusion

ECGCheck for A-Fib or MI ECHOFor evaluation of valves, clot or MIo Treatment:

IV HeparinImmediate bolus w/continuous infusion to maintain PTT >60secs Embolectomy via Fogarty balloon catheter

Thrombectomy graft bypass AmputationIf irreversible ischemia

Deep Venous Thrombosis (DVT)

o Thrombus formation & subsequent inflammatory response in superficial or deep vein

o Thrombi propagate in direction of blood flow MC in LE originating in calf veins


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o Most important complications are PE (50% risk w/proximal DVT) & chronic venous insufficiency

o Virchows Triad:

1) Endothelial damageLeads to inhibition of coagulation & local fibrinolysis Trauma, major surgery, pelvic procedures

2) Venous stasis Immobilization inhibits clearance & dilution of coagulation factors Prolonged bed rest, long flights, orthopedic casts, CHF

3) Hypercoagulability Hereditary states, OCP, malignancyo Clinical Presentation:

Asymptomatic esp. if superficial venous system patent allowing blood drainage

Classic findings Seen in 50% but all have low sensitivity & specificity: Unilateral LE pain, edema & erythema improves w/rest or elevation Homans sign pain w/foot dorsiflexion

Palpable cord due to thrombosed vein

Phlegmasia alba dolens White leg w/no ischemia Phlegmasia cerulea dolens Cyanotic leg w/severe pain & ischemia Post-phlebitic (post-thrombotic) syndromePain, edema, hyperpigmentation & skin ulceration

MC complication in up to 2/3 of DVT cases due to small obstructions still remainingo Diagnosis:

vDuplex U/S Initial test for DVT high sensitivity & specificity

Only for detecting proximal thrombi (popliteal, femoral) not distal (calf vein) thrombi

vDuplex leg symptomsRules in proximal DVT

vDuplex w/o leg symptoms Does not R/O DVT! VenographyBest test for diagnosis of distal calf vein thrombi but invasive & rarely used

Visualize deep & superficial venous systems assesses patency & valvular competence Impedance PlethysmographyNoninvasive alternative to doppler U/S

High sensitivity for proximal DVT only but poor specificity due to false positive rate D-dimerLow specificity may be elevated in MI, CHF, pneumonia, post-operative state

Must be combined w/Doppler to R/O DVT

o Treatment:

Acute anticoagulation Unfractionated Heparin or LMWH IV HeparinBolus w/continuous infusion for 5-10d goal is aPTT of 1.52.5x control LMWH (Dalteparin, Enoxaparin) No lab monitoring, better bioavailability & as effective

Chronic anticoagulationWarfarin continue for 3-6 months or more based on risk factors

Start w/Heparin & overlap for 5+ days until therapeutic INR of 2-3 reached

ThrombolyticsStreptokinase, Urokinase, TPA indicated in massive PE or RHF Speeds up lysis of clots but no improvement in survival

IVC Filter Indications for Greenfield filter placement: Contraindication to anticoagulation in documented DVT or PE Failure of adequate anticoagulation as reflected by recurrent DVT or PE Low pulmonary reserve w/high risk of death from PE

PreventativeLeg elevation, pneumatic compression boots, compression stockings

Chronic Venous Insufficiency (CVI) Post-Phlebitic Syndrome

o Pathophysiology:

Superficial & deep venous systems connected by perforating veins

Valves allow flow from superficial to deep veins but not vice versa

Prior DVT is underlying cause in many cases w/2 major effects: Destruction of valves in deep venous system causing valvular incompetence

Valves in perforator veins also damaged 2Oto chronically elevated deep venous pressure

o Inhibits normal transmission of blood from superficial to deep system

Ambulatory venous HTN Interstitial fluid accumulation resulting in edema Extravasation of plasma proteins & RBCs into subcutaneous tissues

o Results in brawny induration & dark pigmentation due to hemosiderin deposits

Eventual capillary blood flow w/tissue hypoxia mild trauma may cause ulcer formation Venous ulcers MC at medial malleolus overlying incompetent perforator vein

o Ulcer formation directly proportional to amount of swelling present



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PainAching or tightness of involved leg often worse at end of day EdemaLower leg & relieved by elevation opposite is true in arterial insufficiency SkinStasis dermatitis, pruritus, hyperpigmentation, venous ulcers

o Diagnosis:

Doppler U/S Most commonly used imaging technique Ambulatory Venous Pressure (AVP)Gold standard but invasive & rarely done PlethysmographyNoninvasive

o Treatment:

ConservativeElastic compression stockings, leg elevation, avoid prolonged sitting/standing

SurgeryIf conservative measures fail or recurrent/large ulcers Ligation of perforators in region of ulcer Greater saphenous vein stripping

Venous bypass if short segment obstruction

UlcersWet-to-dry saline dressings, zinc-oxide wraps, antibiotics, debridement, unna boot Split-thickness skin grafts if unna venous boot (external compression stocking) fails

Superficial Thrombophlebitis

o Erythema, induration & tenderness along superficial vein MC in greater saphenous system

MC at sites of IV infusion in upper extremities & usually ass. w/varicose veins in lower extremities

o Etiology:

InfectiousSuppurative phlebitis due to complication of IV cannulation

InflammatoryVaricose veins, Buergers disease, SLE, trauma OtherPolycythemia, thrombocytosis, occult malignancy (esp. pancreatic)


Pain w/cord-like swelling along course of involved vein

Induration, erythema & tenderness corresponds to dilated & often thrombosed veins

o DiagnosisR/O associated DVT w/non-invasive testso Treatment:

ConservativeBed rest, limb elevation, heat, compression bandages, ASA Suppurative thrombophlebitis IV Antibiotics + I&D of involved vein

o ComplicationsSimultaneous DVT (


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CONGENITAL HEART DISEASE

Prenatal Circulationo Circulation before birth:

PlacentaUmbilical vein Ductus venosus IVC RA FOLALVAorta Fetal lungs bypassed via following fetal shunts:

Shunting of deoxygenated blood:o Ductus Arteriosus Connection between pulmonary artery & aorta

Shunting of oxygenated blood:

o

Foramen Ovale (FO) Connection between RA & LAo Ductus Venosus Connection between umbilical vein & IVC

o Circulation after birth:

With first breath, lungs open & pulmonary resistance allowing pulmonic blood flow Systemic circulation becomes high resistance system causes ductus venosus closure

Pulmonic flow causes left atrial pressures causes foramen ovale closure O2concentration after first breath cause prostaglandins causes ductus arteriosus closure

Congenital Heart Disease (CHD) Cyanotic vs. Acyanotic

o Most critical period of heart development between 3-8wks gestation most susceptible to insult

o Acyanotic CHD:

Left-to-Right shunts ASD, VSD, PDA

Cause pulmonary blood flow leading to pulmonary pressures If untreated can lead to Eisenmenger's syndrome reversal of shunt (right-to-left)

ObstructionCoarctation, aortic stenosis, pulmonary stenosis Present w/pallor, urine, cool extremities, poor pulses, syncope

o Cyanotic CHD:

Right-to-Left shunts TOF or Ebsteins anomaly OtherTGA, hypoplastic left heart, TAPV, truncus arteriosus Hyperoxic TestTo determine if cyanosis is cardiac in origin

Obtain preductal, right radial ABG repeat ABG after child inspires 100% O2 If PaO2improves 150mmHg then cyanosis not cardiac in origin

Atrial Septal Defect (ASD)

o Classification:

Ostium PrimumPresents in early childhood ass. w/Downs syndrome Findings include murmur or fatigue w/exertion

Ostium SecundumMC type tends to present in late childhood or early adulthood Sinus Venosus Defect located at entry of SVC into RA


Asymptomatic easy fatigability, frequent respiratory infections, FTT

Systolic ejection murmur (SEM) grade 3/6 pulmonic outflow murmur

Wide & fixed split S2w/right ventricular heave May also present w/mid-diastolic rumble at LLSB

If ASD remains patent CHF & pulmonary HTN can develop in adult life

o Diagnosis:

ECHO w/color-flow Doppler Reveals blood flow between atria diagnostic Also shows paradoxical ventricular wall motion & dilated RV

ECGRight axis deviation (RAD), RVH, PR prolongation CXRCardiomegaly & pulmonary vasculature

o Treatment:

Spontaneous closure rate >80% If ASD diameter


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Large defects Dyspnea w/respiratory distress, URTIs, FTT, CHF

Soft, blowing holosystolic murmur w/systolic thrill & loud P2

Mid-diastolic apical rumble reflects flow across mitral valve Size of VSD inversely related to intensity of murmur

o Diagnosis:

ECHODiagnostic ECGMay show LVH, LAH & RVH CXRMay show pulmonary vascular, cardiomegaly & CHF

o Treatment:

Small defectsMost close spontaneously in first 1-2yrs monitor via ECHO Surgical repair indications:

Symptomatic w/failed medical management

Children 68 months of age

Coarctation of the Aorta

o Narrowing of aorta almost always at level of ductus arteriosus occurs just below left subclavian artery

Associated bicuspid aortic valve seen >2/3 of pts.


Asymptomatic few pts. have HTN in infancy

Classic finding systolic BP higher in upper extremities (140-145mmHg)

Difference in BP between left & right arm can indicate point of coarctation

Weak/absent pulses in lower extremities & radial-femoral delay

Differential cyanosis O2saturation in left arm & LE (postductal) compared to right arm Short systolic murmur w/late peak at apex, left axilla & left back May also have LE claudication, syncope, epistaxis or headache

Critical coarctation in infancy requires patent PDA for survival

Closure of ductus may cause shock in first few weeks of lifeo Diagnosis:

ECHO w/color-flow Doppler Diagnostic ECGRVH (infancy) & LVH (late) CXRCardiomegaly & pulmonary congestion

3 signdue aortic wall indentation at site of coarctation

Rib notching due to collateral circulation via intercostal arterieso Treatment:

PGE1Keeps ductus arteriosus patent for severe coarctation in infancy Surgical correction or Balloon angioplasty (controversial)

o AssociationsTurners syndrome (35%), berry aneurysms, aortic dissection


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Transposition of the Great Vesselso Parallel pulmonary & systemic circulations aorta connected to RV & pulmonary artery to LV

Incompatible w/life without ASD, VSD or PDA - ass. w/maternal diabetes & rarely DiGeorgeso Clinical Presentation:

Critical illness & early cyanosis occur immediately after birth

Unresponsive to O2as ductus arteriosus closes can cause severe hypoxemia, acidosis & death Single loud S2but no murmur heard if VSD not present

If VSD present cyanosis not prominent & presents w/CHF after few weeks of life

Reverse differential cyanosis may be seen if LV outflow tract obstruction present coarctation, AS

o

DiagnosisCXR egg on a stringegg-shaped heart w/narrow mediastinum & ECG RAD & RVHo Treatment:

IV PGE1To maintain or open PDA Surgical correction Arterial or atrial switch Balloon atrial septostomyTo create or enlarge ASD last resort if above measure fail

Tetralogy of Fallot

o PROVPulmonary stenosis, Overriding aorta, RVH & VSDo Early cyanosis results from right-to-left shunt across VSD due to pulmonary stenosis

o Risk Factors Maternal PKU & DiGeorge syndromeo Clinical Presentation:

Tet spells Hypoxia leads to pulmonary vascular resistance (PVR) & systemic resistance

Occurs in exertional states (crying, playing) peak incidence at 2-4 months of age Squatting (vascular resistance) often seen during hypoxemic episodes Hyperpnea paroxysm of rapid & deep breathing

CyanosisOften not present in infancy but develops over first 2 yrs of life

Cyanosis often leads to deep sleep & murmur intensity MurmurSystolic ejection murmur at LSB & single loud S2due to RV outflow tract obstruction

RVOTO is progressive resulting in right-to-left shunt

HypoxemiaMay cause FTT or AMS if severe seizures or loss of consciousnesso Diagnosis:

ECGRAD & RVH CXRBoot-shaped heart due to small PA & RVH& pulmonary vascular markings

o Treatment:

Severe pulmonary stenosis PGE1to maintain PDA along w/urgent surgical consultation

Tet-spellsO2, Propranolol, Phenylephrine, Morphine squatting & fluids also help Blalock-Taussig shuntDefinitive surgical correction

Ebsteins Anomalyo Congenital defect of tricuspid valve septal & posterior leaflets are malformed & displaced into RV

RA massively enlarged & patent foramen ovale often exists allowing R-to-L shunt

TR & accessory conduction pathways (WPW) often present & ass. w/arrhythmias

o TreatmentSurgical tricuspid valve repair or replacemento AssociationsLithium or Benzodiazepine use in 1sttrimester

Hypoplastic Left Heart Syndrome

o Severe hypoplasia of LV MCC of death from CHD in first month of life

o Systemic circulation dependent on ductus patency closure causes circulatory shock & metabolic acidosis

Treat w/intubation, IV PGE1& correct metabolic acidosis

o TreatmentSurgical correction (50% survival to late childhood) or heart transplant

Total Anomalous Pulmonary Venous Connection (TAPVC)

o Characterized by all pulmonary veins draining into right-sided circulation

No direct oxygenated pulmonary venous return to left atrium

o ASD must be present to allow blood to shunt into LA & systemic circulation treat w/surgical repair

Truncus Arteriosus

o Single great vessel gives rise to aorta, pulmonary & coronary arteries truncal valve overlies a large VSD

Step 2 CK Review - Cardiology

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