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 O2 to 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 <45yrs & women <55yrs o Clinical Presentation Asymptomatic, stable angina, unstable angina, MI, sudden cardiac death o Canadian Cardiovascular Society (CCS) Angina Classification: Class I Angina w/strenuous or rapid activity – no angina from ordinary physical activity Class II Slight limitation of ordinary activity – angina after >2 blocks or >1 flight of stairs Class III Marked limitation of ordinary activity – angina after <2 blocks or <1 flight of stairs Class IV Any physical activity causes discomfort – angina may be present at rest o Diagnosis: Resting ECG: Prior MI Q waves UA ST segment or T-wave abnormalities seen during episode of chest pain Stress ECG: Recording ECG before, during & after exercise on treadmill 75% sensitive only if able to exercise sufficiently to reach 85% of predicted maximum HR o Predicted maximum HR = 220 − Patient’s age Should undergo cardiac catheterization if results from stress test Positive findings for CAD: o ST elevation Transmural infarct o ST depression Subendocardial ischemia o Failure to exercise >2mins due to symptoms o Hypotension o Ventricular arrhythmia Stress Echocardiography: Performed before & immediately after exercise – preferred over stress ECG More sensitive in detecting ischemia, can assess LV size, EF & diagnose valvular disease Ischemia evidenced by wall motion abnormalities not seen at rest – akinesis or dyskinesis Should undergo cardiac catheterization if test results Myocardial Perfusion Imaging (MPI): Stress test preformed after injection w/radioisotope – Thallium-201 or Technetium-99 Nuclear imaging obtained immediately after exercise & again after 4hrs Viable cells extract radioisotope from blood – no uptake means no perfusion to area MPI can assess myocardial viability by detecting perfusion, ventricular volume & EF o Reversible ischemia Impaired perfusion only during stress o Infarction Impaired perfusion at rest & during stress MPI has best sensitivity & specificity of exercise stress tests – but more expensive Pharmacologic Stress: If unable to exercise – administer IV agents to stimulate myocardial function Dobutamine Myocardial O2 demand by HR, BP & contractility Adenosine & Dipyramidole Vasodilation actually causes flow to coronary arteries Holter Monitoring Ambulatory ECG useful in detecting silent ischemia Cardiac Catheterization & Coronary Angiography: Most accurate way of identifying severity of vessel involvement – indicated in following: o After positive results from any stress test o If revascularization or other surgical intervention being considered o Angina – difficulty diagnosing, refractory to medical therapy, occurring after MI o Severely symptomatic requiring urgent diagnosis & management o Evaluation of valvular disease to determine need for surgical intervention 1
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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 (<7% total calories) & cholesterol (<200 mg/day) Pharmacologic Management: Aspirin Morbidity & risk of MI – indicated in all pts. w/CAD o Clopidogrel If ASA contraindicated or in combination w/ASA β-blockers O2 demand via HR, contractility, BP o Mortality risk – shown to reduce frequency of coronary events o Cardioselective agents preferred – Metoprolol, Atenolol, Carvedilol Avoids inhibition of peripheral vasodilation & bronchodilation via 2 Nitrates O2 demand via vasodilation – preload, afterload, coronary perfusion o Symptomatic control of angina only – no impact on survival o Tachyphylaxis – prevent tolerance by maintaining daily nitrate-free intervals CCBs O2 demand via coronary vasodilation – afterload, coronary perfusion o 2nd line when β-blockers or Nitrates not fully effective o Caution: Verapamil/Diltiazem + -blockers may cause bradycardia or AV block ACEIs Not used to treat symptomatic CAD – indicated in CHF, HTN, DM, LV dysfunction Revascularization: Percutaneous Coronary Intervention (PCI): o PTCA indicated in moderate one- or two-vessel disease w/normal EF: Medically refractory angina NSTEMI/UA w/TIMI risk score ≥3 Primary PCI for STEMI o Restenosis rates up to 40% within first 6 months – stents significantly rates Coronary Artery Bypass Grafting (CABG): o Indicated in severe multi-vessel disease w/ EF or comorbid DM: Left main artery disease Triple-vessel disease w/ LV function Two-vessel disease w/proximal LAD stenosis Failed or contraindicated PTCA Thrombolysis t-PA, Streptokinase, Urokinase, Anistreplase, Alteplase, Reteplase o Indications STEMI <12hrs after symptom onset or when PCI not viable option Administer as soon as possible – preferably 3hrs after onset Not indicated for NSTEMI or UA as artery not occluded o Absolute contraindications: Active bleeding - Malignant IC neoplasm Prior intracranial hemorrhage - Prior stroke (≤3 months) Recent head trauma (≤3 months) - Suspected aortic dissection o Relative contraindications: HTN – sBP >180 or dBP >110 - Current anticoagulation use Recent major surgery (≤3wks) - Active peptic ulcer
Chronic Stable Angina o Symptom complex resulting from imbalance between oxygen supply & demand in myocardium o Often due to fixed stenosis caused by atheroma – O2 demand exceeds available blood supply Goal of treatment to myocardial O2 demand & O2 supply o Pathophysiology: Factors influencing supply Luminal diameter (most important), duration of diastole, Hb, SaO2 Myocardial O2 supply – atherosclerosis, vasospasm, hypoxemia, tachycardia, anemia Factors influencing demand HR, contractility, wall stress Myocardial O2 demand – tachycardia, AS, myocardial hypertrophy, hyperthyroidism o Clinical Presentation: Chest pain Retrosternal tightness radiating to left ( right) shoulder, arm, neck or jaw 2
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Precipitated by the “3 E’s” – 1) Exertion, 2) Emotion, 3) Eating Brief duration – pain lasts <15mins w/relief after rest or nitrates Anginal equivalents Dyspnea, diaphoresis, acute LVF, flash pulmonary edema Levine’s sign Clutching fist over sternum when describing chest pain Diagnosis Resting ECG – Normal Treatment See Pharmacologic Management of CAD
Unstable Angina (UA) o Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion Oxygen demand unchanged – but O2 supply 2O to reduced resting coronary flow o UA defined by any of the following: Angina at rest New-onset angina Accelerating pain pattern – frequency, duration, pain intensity o Diagnosis & Treatment See NSTEMI section below
Prinzmetal’s (Variant) Angina o Transient coronary vasospasm – 75% ass. w/fixed atherosclerotic lesion o Clinical Presentation Intermittent angina at rest – pain not provoked by exertion o Diagnosis: ECG Hallmark is transient ST elevation during chest pain – represents transmural ischemia Coronary Angiography Definitive test – shows coronary vasospasm after IV Ergonovine o Treatment Vasodilation via Nitrates & CCBs
Myocardial Infarction (MI) o Due to coronary atherosclerosis w/superimposed thrombus on ruptured plaque o Classification: 1) Non-ST Elevation Myocardial Infarction (NSTEMI): Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion Oxygen demand unchanged – but O2 supply 2O to reduced resting coronary flow Defined by presence of 2/3 criteria: o Symptoms of angina or ischemia o Rise & fall of serum MI markers – absent enzyme markers in UA o Ischemic ECG changes – without ST elevation or new LBBB NSTEMI & UA categorized together due to similar etiology & presentation 2) ST Elevation Myocardial Infarction (STEMI): Acute plaque rupture & thrombosis w/total vessel occlusion causing myocardial necrosis Defined by new ischemic ECG changes + 1 or both of ischemic Sx. & cardiac enzymes o ECG ST elevation in 2 contiguous leads or new BBB – either LBBB or RBBB o Clinical Presentation: Chest pain, dyspnea, diaphoresis, weakness, fatigue, N/V Pain similar to angina but more intense & longer duration Up to 1/3 asymptomatic – painless infarcts o Diagnosis: ECG Markers for ischemia/infarction include: Peaked T-waves – occur very early & may be missed ST elevation – transmural injury of entire wall thickness (can be Dx. of acute infarct) ST depression – subendocardial injury involving inner half of wall Q-waves – seen later as specific evidence of necrosis (not seen w/NSTEMI) T-wave inversion – sensitive but not specific Cardiac Enzymes Diagnostic gold standard for myocardial injury Creatine Kinase-MB (CK-MB): o CK-MB within 4-8hrs w/peak at 24hrs – returns to normal after 48-72hrs o Sensitivity & specificity >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 days o Greater sensitivity & specificity than CK-MB for myocardial injury 3
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 Myoglobin Elevated within 1hr – but nonspecific
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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% 4 points = 19.9% 2 points = 8.3% 5 points = 26.2% 3 points = 13.2 % 6-7 points = 40.9% Treatment: Management of NSTEMI: Initial O2 + NTG + -blockers + ASA Morphine Clopidogrel Initiate w/ASA – 300mg loading dose & 75mg daily o Avoid use if emergency CABG likely – discontinue 5 days before CABG Heparin For all pts. w/MI – does not dissolve clots only prevents future formation o LMWH preferred – except in renal failure or if CABG planned within 24hrs GP IIb/IIIa inhibitors Abciximab, Eptifibatide, Tirofiban o If undergoing PCI or at high-risk – ex. Troponin, TIMI >4, DM Invasive Early coronary angiography & revascularization o Indicated w/following high-risk indicators: Recurrent or persistent pain refractory to medical therapy LV dysfunction – EF <40% TIMI risk score ≥3 Sustained VT or dynamic ECG changes High-risk findings on non-invasive stress testing PCI within previous 6 months o Thrombolysis is NOT indicated for NSTEMI or UA! Management of STEMI: Initial O2 + NTG + -blockers + ASA Morphine Invasive Emergency reperfusion indicated if <12hrs from symptom onset o PCI Preform <90mins (EMS-to-balloon) after first medical encounter Advantages over thrombolysis: Mortality rate & rate of MI reoccurrence Risk of intracranial hemorrhage 90% success rate – vs. 60% w/thrombolytics o Thrombolysis Preform <30mins (EMS-to-needle) after first medical encounter Generally preferred if given <3hrs after symptom onset Indicated if PCI contraindicated or unable to preform PCI within 90mins o CABG Indicated if >12hrs after symptom onset or failed PCI Adjunctive medical therapy: o Clopidogrel 300-600mg loading dose & 75mg daily Avoid use if emergency CABG likely – discontinue 5 days before CABG o Heparin Initial bolus of UF advised while in transit to catheterization lab LMWH preferred – except renal failure or if CABG planned within 24hr o GP IIb/IIIa inhibitors If undergoing primary PCI Avoid use if initiating thrombolytic therapy due to risk of bleeding Outpatient Management: Aspirin 81-162mg QD -blockers Metoprolol 25-50mg BID or Atenolol 50-100mg QD o CCBs If -blockers contraindicated in absence of severe LV dysfunction Use non-dihydropyridine CCBs – Diltiazem or Verapamil Clopidogrel 75mg QD x 1-12 months – at least 12 months if stent placed Nitrates Alleviates pain – caution in right-sided MI pts. who are preload dependent 4
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Warfarin If high risk of systemic thromboembolism – A-Fib, CHF, LV thrombus ACEIs Prevents adverse ventricular remodeling – CHF, LVEF <40%, anterior MI o ARBs – if contraindicated or intolerant to ACEIs Statins Early & intensive therapy
Complications: CHF MCC of in-hospital mortality – if severe may lead to cardiogenic shock Myocardial ruptures: Free wall rupture 90% occur within 2wks – MC after 1-4 days w/90% mortality rate o Often leads to hemopericardium & cardiac tamponade o Treat w/immediate pericardiocentesis & surgical repair Interventricular septum rupture Occurs within 10 days after MI o Emergent surgery indicated – likelihood of survival correlates w/size of defect Papillary muscle rupture Leads to MR – if suspected obtain ECHO immediately o Emergent surgery & mitral valve replacement usually necessary o Reduce afterload via Sodium nitroprusside or intra-aortic balloon pump (IABP) Ventricular pseudoaneurysm Incomplete free wall rupture – contained by pericardium o Surgical emergency – likely to progress to free-wall rupture Ventricular aneurysm Rarely rupture – in contrast to pseudoaneurysms o Associated w/ incidence of ventricular tachyarrhythmias o Medical management may be protective or surgery if aneurysm severe Arrhythmias: VT Within 48hrs of MI – usually due to myocardium reperfusion Bradycardia Usually from inferior wall MI – seen in early stages o May be protective mechanism causing O2 demand – treat w/Atropine AV block Due to ischemia of conduction tracts o Inferior wall MI 1st degree or 2nd degree (type I) block – no treatment o Anterior wall MI 2nd degree (type II) or 3rd degree block – requires pacemaker Recurrent infarction Extension of existing infarction or re-infarction of new area Suspect if repeat ST elevation on ECG within first 24hrs after infarction Acute pericarditis Treat w/Aspirin Dressler's syndrome Autoimmune inflammatory reaction occurring weeks to months after MI Consists of fever, malaise, pericarditis, leukocytosis & pleuritis – treat w/NSAIDs
HEART FAILURE
Congestive Heart Failure (CHF) o Failure of heart to pump blood effectively to tissues – heart can not meet demand of body o Pathophysiology: Systolic dysfunction Impaired ventricular ejection – LVEF + SV = CO Findings – apex beat displaced, S3, cardiomegaly, LVEF, LV dilatation Due to impaired myocardial contractility – MI, HTN, DM, alcohol, myocarditis, DCM Diastolic dysfunction Impaired ventricular filling during diastole w/normal EF – MC in elderly LV filling pressures produce upstream pulmonary & systemic venous congestion Findings – HTN, apex beat sustained, S4, normal-size heart, LVH, normal LVEF Due to decreased compliance: o Transient Ischemia – relaxation of myocardium is active & requires ATP o Permanent Hypertrophy (HTN, AS, HCM), RCM, MI High-Output HF CO demand – thiamine, hyperthyroid, A-V fistula, L-R shunt, Paget’s, CRF o Etiology: Most common CAD, HTN, valvular (AS, AR, MR), EtOH (DCM) Less common: Toxic – anthracyclines, radiation, uremia, catecholamines Infectious – Chagas, Coxsackie, HIV Endocrine – Hyperthyroidism, DM, acromegaly Infiltrative – sarcoidosis, amyloidosis, hemochromatosis Genetic – HCM, Friedreich’s ataxia, muscular dystrophy, congenital heart disease Metabolic – thiamine or selenium deficiency 5
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Clinical Presentation: LHF Pulmonary 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, Kussmaul’s sign Nocturia – due to venous return w/elevation of legs Hepatomegaly hepatojugular reflex – RUQ pain due to hepatic congestion Auscultation S3 (right-sided), right ventricular heave, tricuspid regurgitation RHF can present similar to cirrhosis – but w/cirrhosis no JVD or trouble lying flat New York Heart Association (NYHA) Classification: Class I Nearly 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 Diagnosis: CXR Cardiomegaly, pleural effusion, Kerley B-lines, bronchiolar-alveolar cuffing ECHO Assess LV function via LVEF – helps distinguish systolic from diastolic dysfunction Initial test of choice – preform when CHF suspected based on PE findings or CXR ECG Nonspecific – 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 BNP Secreted 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 portion o HF suggested if NT-proBNP >450pg/mL Treatment: Diet Sodium restriction – initially <4g/day Diuretics No effect on prognosis or mortality – Furosemide is most potent diuretic ACEIs Mortality & prolongs survival – venous & arterial dilation = preload & afterload Diuretics + ACEI is initial treatment in most symptomatic cases ACEIs given to all pts. w/systolic dysfunction – even if asymptomatic Start w/low dose to prevent hypotension – monitor BP, K+, BUN, Cr β-Blockers Mortality in pts. w/post-MI heart failure Slows progression of heart failure by slowing down tissue remodeling Use cautiously & titrate slowly as may initially worsen CHF ARBs 2nd line only if unable to tolerate ACEIs Hydralazine & Isosorbide Dinitrates 2nd line only if unable to tolerate ACEIs Less effective on reducing mortality compared to ACEIs Digitalis No effect on mortality – only symptomatic relief Consider use if EF <30%, severe CHF, or severe A-fib Management Guidelines: Mild (NYHA Class I to II) Na+ restriction + ACEI Loop diuretic Moderate (NYHA Class II to III) Loop diuretic + ACEI -blocker Severe (NYHA Class III to IV) Loop diuretic + ACEI + Digoxin Add Spironolactone – if class IV & still symptomatic despite above treatment 6
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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: Viral Coxsackie B (MCC), Echovirus, HIV, CMV, Influenza, EBV, HBV, Adenovirus Bacterial S. pyogenes, C. diphtheriae, Meningococcus, B. burgdorferi, M. pneumoniae Parasitic T. cruzi (Chagas), Toxoplasma, Trichinella, Echinococcus Systemic Kawasaki’s, SLE, sarcoidosis, acute RF Toxic Catecholamines, chemotherapy, cocaine Hypersensitivity Antibiotics, diuretics, lithium, clozapine, insect/snake bites o Clinical Presentation: 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 ECG ST changes, dysrhythmias, conduction disturbances CXR Often normal cardiomegaly or pulmonary venous congestion ECHO Dilated chambers, hypokinetic wall movements, pericardial effusion Myocardial Biopsy o Treatment: CHF ACEIs necrosis & inflammation – also address any underlying causes Dysrhythmias Digoxin – use cautiously as effects may be exaggerated by inflamed myocardium IVIG May be of benefit Contraindicated Immunosuppressives (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 Infectious Coxsackie B, HIV, chagas, lyme disease, rickettsial, acute RF, toxoplasmosis Toxic Alcohol, cocaine, doxorubicin, chloroquine, clozapine, heavy metals (Pb, Hg, Cb) Endocrine DM, hyper/hypothyroidism, pheochromocytoma, acromegaly Metabolic Uremia, hypocalcemia, hypophosphatemia, thiamine (wet-beriberi), selenium Neuromuscular Duchenne’s, myotonic dystrophy, Friedreich’s ataxia Collagen SLE, PAN, dermatomyositis, progressive systemic sclerosis Other Uncontrolled tachycardia (persistent A-Fib), peripartum cardiomyopathy, FHx in 20% o Clinical Presentation: 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+ ECG ST & T-wave abnormalities, conduction defects (BBB), arrhythmias (VT, A-Fib) 7
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CXR Global cardiomegaly & pleural effusion ECHO Enlarged chambers, global hypokinesis, LVEF, MR, TR, mural thrombi Angiography To exclude ischemic heart disease in certain cases Treatment: Initial Address underlying cause & treat CHF accordingly Warfarin Thromboembolism prophylaxis indications: A-Fib, previous thromboembolism, documented thrombus, LVEF <30% (controversial) ICD Consider if life-threatening dysrhythmias Surgical Consider in severe, refractory cases – ex. LVAD, volume reduction, heart transplant Vaccination Influenza & S. pneumoniae Prognosis 20% mortality in 1st year & 10% per year after – often due to CHF, arrhythmias or emboli
Restrictive Cardiomyopathy (RCM) o Impaired ventricular filling – 2O to myocardial stiffening, fibrosis or compliance Usually intact systolic function w/non-dilated & non-hypertrophied ventricle o Etiology: Cardiac Endomyocardial fibrosis, Loeffler’s endocarditis, radiation heart disease Other Carcinoid syndrome, amyloidosis, sarcoidosis, hemochromatosis, Gaucher’s, Hurler’s o Clinical Presentation: CHF – commonly present w/dyspnea & exercise intolerance (RHF usually predominates) Arrhythmias, JVP, Kussmaul’s sign, thromboembolic events Auscultation – S3, S4, MR, TR o Diagnosis: ECG Low voltage, non-specific ST/T-wave changes, conduction abnormalities (left BBB) CXR Enlarged atria & pulmonary venous congestion ECHO LAE, RAE, normal sized ventricles, thicken myocardium, MR or TR May see speckled appearance if amyloid cause Cardiac Catheterization Reveals end-diastolic ventricular pressures Endomyocardial Biopsy May detect eosinophilic infiltration or myocardial fibrosis Can also help distinguish RCM from constrictive pericarditis o Treatment: Initial Address underlying cause & treat CHF accordingly A-Fib Anticoagulation + HR control Permanent pacemaker If complete heart block Heart transplant Consider in refractory cases
Hypertrophic Cardiomyopathy (HCM) o Unexplained ventricular hypertrophy – not caused by systemic HTN or AS Often involve asymmetric pattern of hypertrophy – MC is septal hypertrophy o Etiology 50% inherited defect in cardiac sarcomeric proteins – auto. dominant w/variable penetrance o Pathophysiology: Hypertrophic Obstructive Cardiomyopathy (HOCM) Dynamic LVOT obstruction Systolic flow draws anterior leaflet of mitral valve into tract via Bernoulli effect o Causes dynamic left ventricular outflow tract obstruction Outflow obstruction can cause – left atrial dilatation, A-Fib, CHF, RHF LVEDV = Obstruction Blood volume, negative inotropes, peripheral resistance Diastolic dysfunction Impaired ventricular filling – 2O to LVH which reduces compliance o Clinical Presentation: Asymptomatic Screening important Angina At rest or during exercise – usually unresponsive to NTG May respond to recumbent position – pathognomonic (but rare) Syncope After exertion or Valsalva maneuver CHF Dyspnea, rales, peripheral edema, JVD Arrhythmias A-Fib or VT – sudden death in HCM usually due to arrhythmia Auscultation: Harsh systolic ejection murmur at LLSB w/S4 2O to LVOT obstruction o Enhanced by LVEDV Standing position or Valsalva maneuver 8
HCM is one of few murmurs that diminishes w/squatting ( LVEDV) Paradoxical splitting of S2 Pulmonic valve closes before aortic valve o Inspiration will delay pulmonic closure & cause paradoxical narrowing of split Pansystolic murmur due to MR Pulses Rapid upstroke & bifid carotid pulse Precordial palpation PMI localized & triple apical impulse Diagnosis: ECG LVH, PVCs, A-Fib, prominent Q-waves, high voltages across precordium ECHO Septal hypertrophy, LVH, systolic anterior motion of mitral valve, MR Cardiac Catheterization Preform if considering invasive therapy Treatment: Preventative Avoid factors that obstruction – esp. volume depletion & strenuous exertion Pharmacologic management: -blockers Disopyramide HR, LV filling time, inotropy CCBs (Verapamil) 2nd line – only in pts. without resting or provocable obstruction Avoid ACEI, Nitrates, Diuretics – preload will worsen obstruction & symptoms Refractory cases Septal myectomy or Septal ethanol ablation or Dual chamber pacing Ventricular arrhythmias Amiodarone or ICD Screening 1st degree relatives of HCM pts. screened via physical, ECG & 2D-ECHO Screen annually during adolescence – then serially every 5yrs 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.
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PERICARDIAL DISEASE
Pericarditis o Etiology: Idiopathic Usually presumed to be viral – MCC is Coxsackie virus Infectious Coxsackie, Echovirus, S. pneumoniae, S. aureus, TB, Histoplasmosis, Blastomycosis Acute post-MI Direct extension of myocardial inflammation seen after 1-7 days Dressler’s syndrome Autoimmune response to infarcted myocardium seen after 2-8wks Trauma Post-cardiac surgery (ex. CABG) Metabolic Uremia (common), hypothyroidism Malignancy Hodgkin’s, breast, lung, renal cell carcinoma, melanoma Collagen SLE, polyarteritis, RA, scleroderma Drugs Hydralazine, Procainamide, Isoniazid Other Radiation, dissecting aneurysm o Clinical Presentation: 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: ECG Diffuse ST elevations, PR depressions (specific), low voltage CXR Normal sized heart & pulmonary infiltrates ECHO To assess for pericardial effusion Diagnostic triad 1) Chest pain, 2) Friction rub, 3) ECG changes o Treatment: Self-limited Most cases resolve in 2-6wks NSAIDs Mainstay of therapy – to relieve pain & inflammation Steroids For intractable cases (ex. Dressler’s) o Complications Recurrence, atrial arrhythmia, pericardial effusion, tamponade, constrictive pericarditis 9
Pericardial Effusion o Etiology: Transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism Exudative (serosanguinous or bloody) Causes similar to acute pericarditis May develop acute effusion 2O to hemopericardium – trauma, post-MI rupture, dissection o Clinical Presentation: 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: ECHO Procedure of choice – shows fluid in pericardial sac ECG Low voltage & flat T-waves CXR Cardiomegaly, rounded cardiac contour (“water bottle” appearance) Pericardiocentesis Identify transudate vs. exudate, infectious agents, neoplastic involvement o Treatment: Mild effusion Frequent observation w/serial ECHOs + Anti-inflammatory agents Severe effusion Pericardiocentesis – may develop cardiac tamponade
Pericardial Tamponade o Due to rapid accumulation of fluid in pericardial sac – impairs cardiac filling leading to CO o Etiology Pericarditis, trauma, post-MI rupture, aortic dissection w/rupture, malignancy, uremia o Clinical Presentation: Beck’s 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: ECG Electrical alternans – pathognomonic variation in R-wave amplitude ECHO Pericardial effusion & compression of cardiac chambers (RA & RV) in diastole o Treatment: Pericardiocentesis Preform immediately if unstable Fluids To expand volume & CO – avoid diuretics & vasodilators Pericardiotomy Pericardial window created to allow drainage
Constrictive Pericarditis o Chronic pericarditis resulting in fibrosed, thickened, adherent or calcified pericardium o Etiology Any cause of acute pericarditis may result in chronic pericarditis Idiopathic, viral, TB, radiation (worst prognosis), post-cardiac surgery, uremia, MI o Clinical Presentation: Dyspnea, tachycardia, palpitations, JVD, normal BP, absent pulsus paradoxus Kussmaul’s 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: ECG Low voltage, T-wave flattening or inversion, notched P-waves CXR Pericardial calcification & effusions ECHO/CT/MRI Pericardial thickening Cardiac Catheterization Equalization of end-diastolic chamber pressures – diagnostic o Treatment Diuretics + Na+ restriction – if unresponsive consider Pericardiectomy
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VALVULAR HEART DISEASE (VHD)
Mitral Stenosis (MS) o Etiology MCC is RHD – MC in females & congenital MS rare cause o 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 Auscultation OS 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: ECG LAE, A-Fib, RVH, RAD ECHO Thickening of MV leaflets CXR LAE w/straight left heart border, kerley B-lines (pulmonary effusion), large PA o Treatment: Diuretics & Na+ restriction Digitalis To control ventricular rate in A-Fib Anticoagulation If atrial thrombus or A-Fib present Balloon valvuloplasty Standard of care – indicated in symptomatic pts. w/orifice ≤1.2cm2 Alternatives – Mitral commissurotomy or Valve replacement
Mitral Regurgitation (MR) o MR CO LV/LA pressure LV/LA dilatation CHF + Pulmonary HTN o Etiology: MCC is mitral valve prolapse (MVP) Endocarditis, rheumatic fever, LV dilatation/aneurysm, Marfan’s, HOCM MV annulus calcification or chordae/papillary muscle rupture o Clinical Presentation: Dyspnea, PND, orthopnea, palpitations, peripheral edema, cough Auscultation – loud holosystolic murmur at apex w/radiation to axilla & S3 Murmur enhanced by expiration or TPR o Diagnosis: ECG LAE, LVH ECHO Shows diseased or prolapsed valve Swan-Ganz Catheterization Prominent ‘V’ wave due to systolic overload on LA o Treatment: Asymptomatic Serial ECHOs Diuretics To preload & improve CO Vasodilators To afterload which favors aortic exit – esp. ACEIs Surgery Indicated 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 replacement If 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 Marfan’s, Ehlers-Danlos, RHD, pectus excavatum o Clinical Presentation: Asymptomatic Stabbing chest pain, dyspnea, palpitations, presyncope, systemic emboli Auscultation Mid-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 11
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Other findings Wide splitting of S2 or S3 Diagnosis: ECG Non-specific ST & T-wave changes, paroxysmal SVT, ventricular ectopy ECHO Systolic displacement of thickened MV leaflets into LA Treatment: Asymptomatic No treatment Symptomatic -blockers & avoidance of stimulants – ex. caffeine Anticoagulation If systemic emboli Endocarditis prophylaxis If murmur audible or if myxomatous leaflet Surgical MV repair favored over replacement if significant MR
Aortic Stenosis (AS) o AS Outflow obstruction EDP Concentric LVH LVF o Normal AV area = 3–4cm2 Severe AS = <1cm2 & critical AS = <0.5cm2 o Etiology: Degenerative calcification – idiopathic & seen in older population Bicuspid AV – MC congenital valve abnormality & ass. w/early calcific AS by age 60-70yrs Rheumatic heart disease o Clinical Presentation: Dyspnea, PND, orthopnea, peripheral edema Exertional angina & syncope – CO cannot maintain BP causing syncope & angina Parvus et Tardus – pulses weak compared to heart sounds Narrow pulse pressure, brachial-radial delay & sustained PMI Auscultation: Crescendo-decrescendo SEM radiating to carotid arteries – best over right 2nd interspace o Gallavardin phenomenon – musical quality at apex S4, late S3 & paradoxical splitting of S2 – delayed AV opening causes closure after PV o Diagnosis: ECG LVH & strain, LBBB, LAE ECHO Reduced valve area, pressure gradient, LVH, LV function CXR Calcified valve & post-stenotic aortic root dilatation o Treatment: Asymptomatic Serial ECHOs – avoid exertion, nitrates, arterial dilators & ACEIs Surgery If severe AS or LV dysfunction Valve replacement – definitive therapy Valvuloplasty – temporary improvement as rate of restenosis very high
Aortic Regurgitation (AR) o AR LV dilatation SV + sBP + dBP Wall tension Pressure overload LVH o Etiology: Aortic root Marfan’s, Ehlers–Danlos, dissecting aneurysm, syphilis, CT disease, HTN Associated w/cystic medial necrosis Valvular Congenital bicuspid AV, Turner’s syndrome, large VSD, RHD, endocarditis Acute AR IE, aortic dissection, trauma, failed prosthetic valve o Clinical Presentation: Asymptomatic Until late LVF develops – dyspnea, orthopnea, PND Angina Low pressure in aortic root causes diastolic coronary blood flow Pulses Wide pulse pressure & bounding/waterhammer pulse Pulsus Bisferiens – dicrotic pulse w/2 palpable waves in systole Duroziez sign – diastolic femoral bruit when femoral artery compressed Hill’s sign – sBP in legs >20 mmHg higher than arms Quincke’s sign – alternating blushing & blanching of fingernails when pressure applied De Musset’s sign – bobbing of head w/heartbeat Precordial Hyperdynamic apex & laterally displaced PMI due to LVE Auscultation Early decrescendo diastolic murmur at LLSB (cusp) or RLSB (aortic root) Best heard sitting, leaning forward & on full expiration Soft S1, absent S2 & late S3 12
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Austin Flint murmur – low-pitched diastolic rumble heard in severe regurgitation o Due to regurgitated blood striking anterior mitral leaflet – similar sound to MR
Diagnosis: ECG LVH & LAE ECHO To identify leaflet or aortic root anomalies CXR LVH, aortic root dilation Stress Test Hypotension w/exercise Treatment: Asymptomatic Afterload w/ACEIs, Nifedipine, Hydralazine – avoid exertion Surgery Indicated in severe cases w/LVEF <50% Valve replacement – only definitive treatment Bentall procedure – aortic root replacement
Tricuspid Stenosis (TS) o Etiology RHD, congenital, carcinoid – rare valvular defect o Clinical Presentation: Peripheral edema, JVD, palpitations, Kussmaul’s sign, abdominojugular reflex (AJR) Auscultation Rumbling diastolic murmur – best heard over LSB between 4th–5th interspace o Diagnosis: ECHO Diagnostic CXR RA dilation without pulmonary artery enlargement o Treatment Diuretics ( preload) or Valve replacement (if severe TS)
Tricuspid Regurgitation (TR) o Right ventricle dilatation TR Further RV dilatation RHF o Etiology RHD, IE (IV drugs), RV dilation, PA pressure (LHF, MS, MR), Ebstein anomaly o Clinical Presentation: Peripheral edema, JVD, palpitations, Kussmaul’s sign, AJR Auscultation Holosystolic murmur heard best at LLSB – accentuated by inspiration o Diagnosis ECHO is diagnostic – ECG shows RAE, RVH, A-Fib o Treatment Diuretics ( preload) + Annuloplasty (repair) + Endocarditis prophylaxis
Pulmonic Stenosis (PS) o Etiology Congenital (MCC) or RHD (rare) o Clinical Presentation: Chest pain, syncope, fatigue, peripheral edema, right-sided S4 Auscultation Systolic murmur w/pulmonary ejection click Best heard at 2nd LICS & accentuated by inspiration o Diagnosis ECHO is diagnostic – ECG shows RVH o Treatment Balloon valvuloplasty – if severe symptoms
Pulmonic Regurgitation (PR) o Etiology Pulmonary HTN, IE, RHD, Tetrology of Fallot (post-repair) o Clinical Presentation: Chest pain, syncope, fatigue, peripheral edema Auscultation Graham Steell diastolic murmur at 2nd–3rd LICS – accentuated by inspiration o Diagnosis ECHO is diagnostic – ECG shows RVH o Treatment Rarely requires treatment – valve replacement if severe
Infective Endocarditis o Infection of cardiac endothelium, characterized by vegetations involving valve leaflets or walls Leaflet vegetation Platelet-fibrin thrombi, WBCs & bacteria Valve involvement MV >> AV > TV > PV o Classification: Acute Bacterial Endocarditis (ABE): Infection of healthy valves – MCC is S. aureus Produces metastatic foci & usually fatal if not treated within 6wks Subacute Bacterial Endocarditis (SBE): 13
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Seeding of previously damaged valves (RHD, CHD) – MCC is S. viridans Does not produce metastatic foci
Etiology: ABE S. aureus, GNs SBE S. viridans, oral flora, GAS, Enterococci, S. epidermidis IVDU S. aureus, Streptococci, Enterococci, Candida Don’t TRI drugs – ABE often affects tricuspid valve in IV drug users Prosthetic valves (<20%) S. aureus, S. epidermidis, GN bacilli, fungi Nosocomial Indwelling venous catheters, hemodialysis, CT surgery Clinical Presentation: Systemic Fever, chills, rigors, night sweats, anorexia, weight loss Cardiac New-onset regurgitant murmur, dyspnea, chest pain Vascular: Petechiae Multiple nonblanching red macules on upper chest & mucous membranes Janeway lesions Multiple hemorrhagic nontender macules on palms & soles Splinter hemorrhages Fine linear hemorrhages in middle of nailbed CNS emboli Focal neurological signs Renal emboli Microscopic hematuria, flank pain Septic pulmonary emboli Immune-complex: Osler’s nodes Tender raised subcutaneous nodules on fingers & toes Roth’s spots Retinal hemorrhages w/pale center – seen on fundoscopy Glomerulonephritis & arthritis SBE specific Splenomegaly & clubbing Diagnosis: Duke’s Criteria 2 major or 1 major + 3 minor or 5 minor criteria Major criteria: o Blood Cx. 2 cultures 12hrs apart, or 3 taken at least 1hr apart o ECHO Vegetations pathognomonic – but absence doesn’t R/O endocarditis Transesophageal ECHO more sensitive Minor criteria: o Predisposing valve lesion or IVDU o Fever >38°C o Vascular Arterial emboli, septic pulmonary infarcts, Janeway lesions o Immunologic Osler’s nodes, Roth’s spots o Blood cultures – but not meeting major criteria o ECHO suspicious for endocarditis – but not meeting major criteria Treatment: Antibiotics 1st line = Cloxacillin + Gentamicin – minimum 4wks Ampicillin – add if native valve & non-IVDU Rifampin – add If prosthetic valve Prophylaxis For high-risk pts. – ex. VHD or previous H/O endocarditis Dental/respiratory procedures Amoxicillin 30-60min prior o Clindamycin – if penicillin-allergic
Rheumatic Fever o Inflammatory disease due to antibody cross-reactivity following GAS infection o Diagnosis 2 major criteria or 1 major + 2 minor criteria w/recent strep infection Major criteria: Arthritis Migratory, multiple joints, very warm, tender Pancarditis Involving pericardium, myocardium, endocardium Erythema marginatum Pink macules w/central blanching & nonpruritic Subcutaneous nodules Pea-sized, firm, non-tender nodules (often extensor surfaces) Sydenham’s chorea Clumsiness, difficulty w/handwriting Minor criteria: H/O RF or RHD ESR or CRP or Leukocytosis Fever Prolonged PR interval 14
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Polyarthralgia Recent streptococcal pharyngitis Treatment: Penicillin or Erythromycin For 10 days to eradicate throat carriage of GAS ASA For arthritis Prednisone If severe carditis 2O Prophylaxis 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) Complications: Acute Myocarditis, A-Fib, acute MR, pericarditis Chronic Rheumatic 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 circuits o 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 <60 bpm w/normal P-waves & PR intervals o Precipitants Vagal tone, anti-arrhythmics, vomiting, inferior MI, ICP, hypothyroidism, hypothermia
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Normal variant Bradycardia may be seen in normal adults – esp. athletes & elderly Asymptomatic May have light-headedness or possible syncope Treatment Atropine 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 Pause Delay 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 Arrest Longer 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 escape P-waves w/abnormal morphology Junctional escape P-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 block o Frequently ass. w/episodes of atrial tachyarrhythmias – “tachy-brady syndrome” o Treatment Electronic pacemaker – indicated if symptomatic bradycardia -blocker, CCB, Digoxin Often initiated after pacemaker insertion for tachycardia
AV Conduction Blocks o Precipitants Inferior wall MI, Digitalis toxicity, vagal tone, conduction system disease o 1st Degree AV Block Prolonged PR interval >0.20s – benign & no treatment required o 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 3rd degree complete heart block rd o 3 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 ECG Early 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/β-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 – it’s hidden within wide QRS complex Couplet 2 successive PVCs Bigeminy Sinus beat followed by PVC Trigeminy Sinus 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) 16
“R on T phenomenon” PVC falling on T-wave of previous beat o May precipitate VT or V-Fib – can potentially cause sudden death β-blockers May 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: Initiation Single circuit re-entry or ectopic foci produce atrial tachycardia – 350-600 bpm Impulses then conduct irregularly across atrial myocardium to give rise to fibrillation Maintenance Tachycardia 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 <200 bpm Tachycardia leads to suboptimal cardiac output o Etiology: CAD, MI, HTN, RHD, pericarditis, pulmonary disease, PE, post-op stress Sepsis, hyper-/hypothyroidism, pheochromocytoma, sick sinus syndrome Excessive alcohol – ex. "holiday heart syndrome" o Clinical Presentation: Fatigue, exertional dyspnea, palpitations, dizziness Irregularly irregular pulse, angina, syncope Stroke or TIA – 2O to embolizing thrombi due to atrial stasis o Diagnosis: ECG: No identifiable P-waves due to tachycardia – chaotic fibrillatory baseline Irregular RR intervals due to irregular impulse conduction to ventricles – 100-180 bpm Narrow QRS complexes – unless aberrancy or previous BBB Ashman phenomenon – wide QRS complexes following long-short RR interval ECHO Can identify presence of clot in left atrium Other Absent S4 on auscultation & absent “a” wave in JVP due to loss of atrial contraction o Treatment: Rate control Nondihydropyridine CCBs or β-blockers – target pulse rate 60-100 bpm Consider using Digoxin or Amiodarone in pts. w/HF Cardioversion Convert back to sinus rhythm – after rate control achieved Electrical cardioversion indications: o Hemodynamically unstable Immediate electrical cardioversion o A-Fib <48hr Usually can cardiovert without anticoagulation o A-Fib >48hr Risk of embolization during cardioversion rises to 2-5% Anticoagulate for 3wks before & 4wks after electrical cardioversion Pharmacologic cardioversion Only used if electrical conversion fails or unfeasible o Agents – Ibutilide, Procainamide, Flecainide, Sotalol, Amiodarone Anticoagulation To prevent embolic CVA – target INR of 2-3 A-Fib >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-Fib CCB or β-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 Etiology COPD, CAD, MV disease, ASD, CHF, cardiac surgery, PE, pericarditis, thyrotoxicosis 17
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Diagnosis: ECG Sawtooth flutter baseline in inferior leads (II, III, aVF) Narrow QRS after every second or third “tooth” P-wave Treatment: Rate control -blocker, CCB, Digoxin Cardioversion Preform immediate electrical cardioversion if unstable Chemical cardioversion – Sotalol, Amiodarone, Type I antiarrhythmics Anticoagulation Same guidelines as A-Fib Long-term Catheter 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 Etiology COPD (MCC), hypokalemia, sepsis, theophylline or digitalis toxicity o Diagnosis ECG – at least 3 distinct P-wave morphologies w/variable PR & RR intervals o Treatment: Normal LV function CCBs, β-blockers, Digoxin, Amiodarone, IV Flecainide, IV Propafenone -blockers may be contraindicated in severe pulmonary disease LV function Digoxin, 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 ECG No discernible P-waves – buried within narrow QRS complexes o 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 AVRT Stimulus 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 AVRT Stimulus 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 stimulation Delays AV conduction & blocks reentry mechanism Valsalva, carotid sinus massage, breath holding, head immersion in cold water/ice IV Adenosine 1st line if no response to vagal maneuvers Works by SA & AV nodal activity w/short duration of action CCB, β-blocker, Digoxin Alternatives if LV function preserved Electrical cardioversion If drugs not effective or if unstable – almost always successful Long-term prevention: 1st line Digoxin (preferred), -blocker, CCB 2nd line Anti-arrhythmics – Flecainide or Propafenone 3rd line Radiofrequency 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 18
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Bundle of Kent – abnormal fast conducting fibers that bypass AV node – found in either LA or RA Etiology Congenital defect seen in 1.5/1000 of general population 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 Diagnosis: ECG Wide QRS complex w/slurred upstroke (delta wave) & PR interval <120 msec Tachyarrhythmias – most often AVRT or AF Treatment: Electrical cardioversion If A-Fib w/rapid ventricular response Surgical Radiofrequency catheter ablation of bypass tract – effective treatment Pharmacologic Amiodarone, Flecanide, Procainamide, Propafenone, Sotalol -blockers, CCBs, Digoxin Contraindicated due to conduction blockage at AV node Allows unopposed conduction down accessory bypass tract
Torsades de Pointes o Variant of polymorphic VT occurring in pts. w/baseline QT prolongation – ventricular rate 150-300 bpm o Etiology: Congenital long QT syndromes Drugs Class IA (Quinidine), Class III (Sotalol), Phenothiazines (TCA), Erythromycin, Quinolones Electrolytes Hypokalemia or hypomagnesemia o Diagnosis ECG – QRS complexes “rotate around baseline” changing their axis & amplitude o Treatment IV Magnesium, temporary pacing, Isoproterenol & correct underlying cause of prolonged QT
Ventricular Tachycardia (VT) o Rapid & repetitive firing of 3 or more consecutive PVCs – originates below the bundle of His o Etiology: CAD w/prior MI (MCC), active ischemia, hypotension, cardiomyopathies Prolonged QT syndrome, drug toxicity, congenital defects o Classification: Sustained VT Lasts >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 VT Brief, self-limited runs of VT – usually asymptomatic Risk for sudden death if CAD & LV dysfunction present o Clinical Presentation: Palpitations, dyspnea, light-headedness, angina, impaired consciousness, syncope o Diagnosis: ECG Wide QRS tachycardia – may be monomorphic or polymorphic Monomorphic VT MC type – identical complexes w/uniform morphology Polymorphic VT Constantly changing morphology, amplitude & polarity Other AV dissociation – sinus P-waves continue their cycle unaffected by tachycardia o Treatment: Sustained VT: Hemodynamically stable IV Amiodarone, IV Procainamide, IV Sotalol Hemodynamic compromise Immediate electrical cardioversion o Follow w/IV Amiodarone to maintain sinus rhythm Nonsustained VT Do 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 19
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Most episodes begin w/VT – except in setting of acute ischemia/infarction Etiology: MCC – Ischemic heart disease Prolonged QT – torsades de pointes, anti-arrhythmic drugs WPW w/A-Fib + rapid ventricular response Clinical Presentation: Loss of consciousness if V-Fib >5-6 secs – if untreated can lead to sudden cardiac death BP immeasurable, absent heart sounds & pulse Diagnosis ECG – QRS & P-waves both unidentifiable Treatment: Medical emergency Immediate 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-Fib IV Amiodarone followed by shock 2nd line – Lidocaine, Bretylium, Magnesium, Procainamide Chronic therapy ICD is mainstay – alternative is long-term Amiodarone 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: HTN Pre-HTN: ≥120/89, Stage 1: ≥140/90, Stage 2: ≥160/100 Isolated Systolic HTN sBP ≥140 & dBP <90 – often develops in 5th decade Associated w/progressive reduction in vascular compliance Hypertensive Urgency sBP >210 or dBP >120 w/absent end-organ damage Hypertensive Emergency sBP >220 or dBP >120 + acute end-organ damage Papilledema, retinal hemorrhages, bulging discs, mental status changes, Cr o Etiology: 1O (Essential) HTN MCC of HTN (>90%) – unknown cause 2O HTN: Renal – renal failure, glomerulonephritis, renal artery stenosis Endocrine – cushing’s syndrome, 1O hyperaldosteronism, 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 gender o Clinical Presentation Asymptomatic light-headed, occipital headache, epistaxis, hematuria, vision o Diagnosis: Fundoscopic Check for AV nicking, hemorrhage or papilledema Auscultation Check for renal artery bruits ECG May show LVH or left ventricular strain o Treatment: Lifestyle modification Na+ restriction, low-fat diet, weight loss, exercise, smoking cessation Pharmacologic Thiazides (preferred), ACEIs, CCBs, -blockers Hypertensive Emergency MAP by 25% in 1-2hrs – gradually reduced BP back to normal Severe HTN IV 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 20
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Chronic dissection >2wks – mortality levels up to 75-80% Etiology: Cardiac HTN (longstanding in 70% of cases), bicuspid AV, coarctation of the aorta, PDA Other Marfan’s, Ehlers–Danlos, syphilis, trauma, 3rd trimester pregnancy, cocaine Classification: DeBakey: Type I Ascending & descending aorta – MC type – 50% Type II Ascending aorta only – stops at innominate artery Type IIIA Descending thoracic aorta only – proximal to diaphragm Type IIIB Type 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 Clinical Presentation: 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 Diagnosis: CXR Widened mediastinum & pleural capping (effusion in lung apices) TEE Can 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/MRI Both highly accurate – MRI not ideal in acute setting due to longer time Angiography Invasive – but best test for determining extent of dissection for surgery Treatment: Immediate BP control: IV -blockers To HR & diminish force of LV ejection IV Sodium Nitroprusside To sBP below 120mmHg Surgical Resection of intimal tear & replacement of affected aorta w/prosthetic graft High morality rate due to operative or post-op complications Type A Requires emergent surgery w/cardiopulmonary bypass Hypothermic circulation for transverse arch dissections Valve replacement & coronary re-implantation for aortic root involvement Type B Managed medically – 10-20% may require urgent surgery for complications Complications: Ischemic syndromes Due to dissection or occlusion of aortic branches Coronary (MI), Carotids (stroke, hemiplegia, horner’s), Splanchnic (ischemic gut) AR Due to dissection through aortic root w/unseating of AV cusps Cardiac Tamponade Due to dissection into pericardium Rupture Pleural (dyspnea, hemoptysis) or Peritoneum (hypotension, shock)
Aortic Aneurysm o Localized dilatation aortic segment w/diameter at least 1.5x that of normal o True aneurysm Involves all vessel wall layers – intima, media, adventitia o 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 Marfan’s, Ehlers–Danlos, infectious (syphilis, fungal), mycotic (Salmonella, Staph) 21
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Risk Factors Smoking, HTN, age >65, FHx, M>W, CAD 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) Diagnosis: U/S Test of choice to evaluate size & location of aneurysm – 100% sensitive CT 100% sensitive – but longer time to preform than U/S AXR May show calcifications of dilated segment allowing measurement of aortic diameter But not used to R/O aneurysm – only for quick assessment Treatment: Conservative management: Risk factors Smoking cessation, HTN/DM/hyperlipidemia control, exercise U/S Every 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 guidance o Newer procedure w/ mortality, procedure time & recovery time o Disadvantages – endoleak rates up to 20-30% & high-cost for device 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 – 2O to sudden hemorrhage Signs suggesting expansion & impending rupture: o Sudden onset of severe pain in back or abdomen & radiating to groin/legs o Grey Turner's sign Ecchymoses on back & flanks o 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, hyperhomocystinemia o Clinical Presentation: Intermittent claudication Leg 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 pain Continuous & 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 Pulses May 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 & 2O to local trauma that does not heal End-stage disease – tissue infarction & gangrene 22
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Diagnosis: ABI Ratio of sBP at ankle to sBP at arm is normally ≥1.0 Claudication = ABI <0.7 & Rest pain = ABI <0.4 False ABI seen w/calcified arteries as vessels not compressible – esp. DM Pulse volume recordings Noninvasive assessment of segmental limb perfusion Pulse wave forms represent volume of blood per heart beat at sequential sites down leg Large wave form indicates good collateral blood flow Arteriography Gold standard for diagnosing & locating site of occlusion Invasive & only needed if considering surgery/revascularization Treatment: Conservative management: Smoking cessation Smoking causes vasoconstriction & progression of atherosclerosis Exercise Develops collateral circulation & improves exercise tolerance Atherosclerotic risk factor reduction Control of hyperlipidemia, HTN, DM, weight Avoid extremes of temperature – esp. extreme cold Foot care – esp. in diabetics Pharmacologic management: Anti-platelets ECASA, Clopidogrel – rarely Ticlopidine Cilostazol cAMP-phosphodiesterase inhibitor w/anti-platelet & vasodilatory effects Pain relief Morphine sulphate – supplemented w/NSAIDs o If opiate analgesia inadequate – consider lumbar sympathectomy Surgical indications Claudication interfering w/lifestyle, rest pain, pre-gangrene, gangrene Surgical procedures: Endovascular stenting/angioplasty Arterial bypass grafts – reversed vein graft or synthetic graft (Gor-Tex, Dacron) o Bypass graft sites – aortofemoral, axillofemoral, femoropopliteal, distal arterial Amputation – if not suitable for revascularization and/or gangrene
Acute Arterial Occlusion o Acute occlusion/rupture of peripheral artery MC in LE – femoropopliteal > aortoiliac o Urgent management required Irreversible ischemia & myonecrosis results >6hrs o Etiology: Cardiac emboli (MCC – 80%) A-Fib, post-MI, VHD, endocarditis, atrial myxoma Arterial emboli Proximal arterial aneurysm, atheroembolism Thrombi Atherosclerotic, trauma, hematological disorders & stasis o Clinical Presentation: “6 P’s” – but all may not be present: Pain in LE – progressing within hrs to feeling of cold, numbness & loss of function o 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: Arteriogram To define site of occlusion ECG Check for A-Fib or MI ECHO For evaluation of valves, clot or MI o Treatment: IV Heparin Immediate bolus w/continuous infusion to maintain PTT >60secs Embolectomy via Fogarty balloon catheter Thrombectomy graft bypass Amputation If 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 23
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Most important complications are PE (50% risk w/proximal DVT) & chronic venous insufficiency Virchow’s Triad: 1) Endothelial damage Leads 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, malignancy 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 Homan’s 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) syndrome Pain, edema, hyperpigmentation & skin ulceration MC complication in up to 2/3 of DVT cases – due to small obstructions still remaining 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 symptoms Rules in proximal DVT vDuplex w/o leg symptoms Does not R/O DVT! Venography Best test for diagnosis of distal calf vein thrombi – but invasive & rarely used Visualize deep & superficial venous systems – assesses patency & valvular competence Impedance Plethysmography Noninvasive alternative to doppler U/S High sensitivity for proximal DVT only – but poor specificity due to false positive rate D-dimer Low specificity – may be elevated in MI, CHF, pneumonia, post-operative state Must be combined w/Doppler to R/O DVT Treatment: Acute anticoagulation Unfractionated Heparin or LMWH IV Heparin Bolus w/continuous infusion for 5-10d – goal is aPTT of 1.5–2.5x control LMWH (Dalteparin, Enoxaparin) No lab monitoring, better bioavailability & as effective Chronic anticoagulation Warfarin – 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 Thrombolytics Streptokinase, 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 Preventative Leg 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 2O to 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 o Clinical Presentation: 24
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Pain Aching or tightness of involved leg – often worse at end of day Edema Lower leg & relieved by elevation – opposite is true in arterial insufficiency Skin Stasis dermatitis, pruritus, hyperpigmentation, venous ulcers Diagnosis: Doppler U/S Most commonly used imaging technique Ambulatory Venous Pressure (AVP) Gold standard – but invasive & rarely done Plethysmography Noninvasive Treatment: Conservative Elastic compression stockings, leg elevation, avoid prolonged sitting/standing Surgery If conservative measures fail or recurrent/large ulcers Ligation of perforators – in region of ulcer Greater saphenous vein stripping Venous bypass – if short segment obstruction Ulcers Wet-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: Infectious Suppurative phlebitis – due to complication of IV cannulation Inflammatory Varicose veins, Buerger’s disease, SLE, trauma Other Polycythemia, thrombocytosis, occult malignancy (esp. pancreatic) o Clinical Presentation: Pain w/cord-like swelling along course of involved vein Induration, erythema & tenderness – corresponds to dilated & often thrombosed veins o Diagnosis R/O associated DVT w/non-invasive tests o Treatment: Conservative Bed rest, limb elevation, heat, compression bandages, ASA Suppurative thrombophlebitis IV Antibiotics + I&D of involved vein o Complications Simultaneous DVT (<20%) or recurrent superficial thrombophlebitis
Varicose Veins o Distention of tortuous superficial veins resulting from incompetent valves in venous system Often due to inherited structural valve weakness – important risk factor o MC in greater saphenous system – dilated, tortuous superficial veins along thigh & leg Also in esophagus, anorectum, scrotum – esophageal varices (GI bleed), hemorrhoids, varicocele o Risk Factors Age, females, OCP, occupations requiring standing, pregnancy, obesity, pelvic tumors o Clinical Presentation: Diffuse aching pain & nocturnal cramping – aggravated by prolonged standing Ulceration, hyperpigmentation & induration Brodie-Trendelenberg test Raise leg, compress saphenous vein at thigh & then have pt. stand If veins fill quickly from top down Test for incompetent valves o Treatment: Conservative management Elevation of leg or elastic stockings Surgical Stripping of long saphenous vein, Sclerotherapy or Endovenous laser therapy (EVLT) o Complications Recurrent superficial thrombophlebitis, hemorrhage, ulceration, eczema
Lymphedema o Obstruction of lymphatic drainage resulting in non-pitting edema w/high protein content Primary Milroy’s syndrome Secondary Filariasis (MCC worldwide), LN removal (MCC in US), malignant infiltration o Clinical Presentation Non-pitting edema, limb mobility, discomfort/pain o Treatment Compression bandages/sleeve, skin hygiene, manual lymph drainage, low-intensity exercise If untreated, may become resistant to treatment due to subcutaneous fibrosis
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CONGENITAL HEART DISEASE
Prenatal Circulation o Circulation before birth: Placenta Umbilical vein Ductus venosus IVC RA FO LA LV Aorta 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 & LA o 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 O2 concentration 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) Obstruction Coarctation, aortic stenosis, pulmonary stenosis Present w/pallor, urine, cool extremities, poor pulses, syncope o Cyanotic CHD: Right-to-Left shunts TOF or Ebstein’s anomaly Other TGA, hypoplastic left heart, TAPV, truncus arteriosus Hyperoxic Test To determine if cyanosis is cardiac in origin Obtain preductal, right radial ABG – repeat ABG after child inspires 100% O2 If PaO2 improves 150mmHg – then cyanosis not cardiac in origin
Atrial Septal Defect (ASD) o Classification: Ostium Primum Presents in early childhood – ass. w/Down’s syndrome Findings include murmur or fatigue w/exertion Ostium Secundum MC type – tends to present in late childhood or early adulthood Sinus Venosus Defect located at entry of SVC into RA o Clinical Presentation: Asymptomatic – easy fatigability, frequent respiratory infections, FTT Systolic ejection murmur (SEM) – grade 3/6 pulmonic outflow murmur Wide & fixed split S2 w/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 ECG Right axis deviation (RAD), RVH, PR prolongation CXR Cardiomegaly & pulmonary vasculature o Treatment: Spontaneous closure rate >80% If ASD diameter <8 mm Surgical closure Indicated in CHF or 2:1 ratio of pulmonary to systemic blood flow o Associations Holt-Oram syndrome, down’s, fetal alcohol syndrome
Ventricular Septal Defect (VSD) o Clinical Presentation: Small defects Asymptomatic at birth & often normal development Harsh, high-pitched holosystolic murmur over LLSB 26
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 Diagnosis: ECHO Diagnostic ECG May show LVH, LAH & RVH CXR May show pulmonary vascular, cardiomegaly & CHF Treatment: Small defects Most close spontaneously in first 1-2yrs – monitor via ECHO Surgical repair indications: Symptomatic w/failed medical management Children <1yr w/signs of pulmonary HTN Older children w/larger VSDs not reducing in size over time Associations Apert’s, down’s, fetal alcohol, TORCH, cri du chat, trisomy 13 or 18
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Patent Ductus Arteriosus (PDA) o Failure of ductus arteriosus to close in first few days of life Leads to left-to-right shunt from descending aorta to left pulmonary artery o Risk Factors 1st trimester rubella infection, prematurity, female gender o Clinical Presentation: Often asymptomatic – may have apneic or bradycardic spells, poor feeding, accessory muscle use Large defects – may present w/FTT, recurrent respiratory infections & CHF Continuous “machinery” murmur at sternal border of 2nd left intercostal space & loud S2 Wide pulse pressure, bounding pulses, hyperactive precordium o Diagnosis: ECHO w/color-flow Doppler Diagnostic ECG May show LAE, LVH or RVH CXR May show cardiomegaly & pulmonary vasculature o Treatment: Indomethacin Induces closure of PDA Contraindicated if PDA needed for survival: o Transposition of the great vessels, tetralogy of fallot, hypoplastic left heart Surgical closure If indomethacin fails or if child >6–8 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. o Clinical Presentation: 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 – O2 saturation 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 life o Diagnosis: ECHO w/color-flow Doppler Diagnostic ECG RVH (infancy) & LVH (late) CXR Cardiomegaly & pulmonary congestion “3” sign due aortic wall indentation at site of coarctation “Rib notching” due to collateral circulation via intercostal arteries o Treatment: PGE1 Keeps ductus arteriosus patent – for severe coarctation in infancy Surgical correction or Balloon angioplasty (controversial) o Associations Turner’s syndrome (35%), berry aneurysms, aortic dissection 27
Transposition of the Great Vessels o 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 DiGeorge’s o Clinical Presentation: Critical illness & early cyanosis occur immediately after birth Unresponsive to O2 as ductus arteriosus closes – can cause severe hypoxemia, acidosis & death Single loud S2 – but 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 Diagnosis CXR – “egg on a string” egg-shaped heart w/narrow mediastinum & ECG – RAD & RVH o Treatment: IV PGE1 To maintain or open PDA Surgical correction Arterial or atrial switch Balloon atrial septostomy To create or enlarge ASD – last resort if above measure fail
Tetralogy of Fallot o PROV Pulmonary stenosis, Overriding aorta, RVH & VSD o Early cyanosis results from right-to-left shunt across VSD due to pulmonary stenosis o Risk Factors Maternal PKU & DiGeorge syndrome o 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 Cyanosis Often not present in infancy but develops over first 2 yrs of life Cyanosis often leads to deep sleep & murmur intensity Murmur Systolic ejection murmur at LSB & single loud S2 – due to RV outflow tract obstruction RVOTO is progressive resulting in right-to-left shunt Hypoxemia May cause FTT or AMS – if severe seizures or loss of consciousness o Diagnosis: ECG RAD & RVH CXR “Boot-shaped” heart due to small PA & RVH & pulmonary vascular markings o Treatment: Severe pulmonary stenosis PGE1 to maintain PDA – along w/urgent surgical consultation Tet-spells O2, Propranolol, Phenylephrine, Morphine – squatting & fluids also help Blalock-Taussig shunt Definitive surgical correction
Ebstein’s Anomaly o 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 Treatment Surgical – tricuspid valve repair or replacement o Associations Lithium or Benzodiazepine use in 1st trimester
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 Treatment Surgical 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 o Treatment Surgical repair within first 6 months of life 28
