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81 Cards in this Set
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(H/P) = asymptomatic for most of disease progression; later sequelae include angina, claudication, progressive HTN, retinal changes, extra heart sounds, myocardial infarction (MI), and stroke
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Atherosclerosis
Gradual narrowing of arteries caused by endothelial dysfunction, progressive formation of plaques (which consist of lipids and smooth muscle), and the associated inflammatory response Plaques can calcify, rupture, and thrombose, which leads to further narrowing of arteries and progressive occlusion of blood flow Risk=SHIFT MAID: Smoking, Hypertension (HTN), Insulin (DM type I and II), Family history, Triglycerides and cholesterol (high), Male, Age (increased), Inactivity, Diet. |
Labs = stress testing, echocardiography, nuclear studies, or angiography can be used to detect coronary ischemia
Treatment = management is primarily intended to minimize risk factors (including tobacco use, HTN, hyperglycemia, hypercholesterolemia); diet low in fats and cholesterol and high in antioxidants (e.g., vitamins E and C and β-carotene) is helpful in preventing disease |
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H/P = usually asymptomatic; extremely high triglycerides and LDL lead to xanthomas (i.e., lipid deposits in tendons), xanthelasmas (i.e., lipid deposits in eyelids), and cholesterol emboli in retina (visible on funduscopic examination); symptoms are more severe and appear earlier in life in primary disorders compared with acquired conditions
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Hypercholesterolemia
Abnormal serum cholesterol levels (high low-density lipoprotein [LDL] and/or low high-density lipoprotein [HDL]) that are associated with increased risk of ischemic heart disease Can result from a congenital disorder (less common) or an acquired condition (most common) |
Labs = increased total cholesterol and LDL; possible decreased HDL; total cholesterol may be >300–600 mg/dL in primary disorders; screening for hyperlipidemia is performed in men >35 years of age and women >45 years of age (younger if patient has other risk factors for CAD)
Treatment = focuses on prevention of cardiovascular disease and includes tobacco cessation, exercise, and dietary restrictions (e.g., low fat and low cholesterol); cholesterol-lowering medications are used in patients with increased cardiac risk (see Figure 1-6) or in patients unlikely to achieve ideal cholesterol levels with nonpharmacologic treatment alone (see Table 1-1); goal LDL should be <160 mg/dL in patients with <2 CAD risk factors, <130 mg/dL in patients with 2 or more risk factors, and <100 mg/dL in patients at high risk for CAD (multiple risk factors, advanced age, very high LDL) |
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H/P = substernal chest pain that may radiate to left shoulder, arm, jaw, or back
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Angina pectoris
Temporary myocardial ischemia during exertion that causes chest pain Most commonly caused by CAD; also occurs secondary to arterial vasospasm (Prinzmetal's angina) and valvular disease Gastroesophageal reflux disease (GERD) and esophageal spasm can mimic symptoms |
Labs = stress testing or nuclear studies used for diagnosis
Treatment = sublingual nitroglycerin and cessation of intense activity until completion of workup; full workup (including stress testing or nuclear studies) for cause is needed to define long-term treatment |
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H/P = angina with worse pain and increased frequency than in prior episodes; symptoms occur at rest; less responsive to prior treatment regimens
ECG = ST depression, T-wave flattening or inversion |
Unstable angina
Worsening angina that occurs at rest Frequently caused by plaque rupture, hemorrhage, or thrombosis in coronary arteries 1/3 of patients have an MI within 3 years Any patient suspected of having an MI must have a workup in a hospital setting with an ECG and serial cardiac enzymes |
Treatment = seeks to relieve cause of ischemia and decrease myocardial O2 demand
Pharmacotherapy = aspirin (ASA) and clopidogrel (if no percutaneous intervention planned) or glycoprotein (GP) IIb/IIIa inhibitor (if intervention planned, such as eptifibatide, tirofiban) should be started as antiplatelet therapy; heparin (or low molecular weight heparin) should be started to help prevent further thrombus formation; O2, nitroglycerin, and β-blockers should be administered to reduce cardiac workload; tight glycemic control is important in diabetic patients to improve outcomes Percutaneous transluminal coronary angioplasty (PTCA) Suggested in cases that are nonresponsive to medications Catheter inserted through femoral or brachial artery and maneuvered through heart to stenotic vessel Balloon on catheter inflated to dilate stenosis Catheters can also be used for arthrectomy (i.e., plaque is shaved by burr on catheter) or stent placement (i.e., intravascular support structure) Coronary artery bypass graft (CABG) Considered for left main stenosis >50%, 3-vessel disease, or history of CAD and DM Donor vessel grafted to coronary artery to bypass obstruction Saphenous vein and internal mammary artery are most commonly used |
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H/P = chest pain (“elephant on chest”) in distribution similar to episodes of angina; possible shortness of breath, diaphoresis, nausea and vomiting; examination findings can include tachycardia, decreased blood pressure, pulmonary rales, new S4, and new systolic murmur
ECG = ST elevation and T-wave changes; possible new arrhythmia, left bundle branch block (LBBB), or Q-wave changes |
Myocardial infarction (MI)
Tissue death resulting from ischemia caused by occlusion of coronary vessels or vasospasm; often secondary to thrombus formation following plaque rupture Risk factors = increased age, HTN, hypercholesterolemia, family history of CAD, DM, and tobacco use; males > females; postmenopausal females > premenopausal females Complications = infarct extension, arrhythmias, myocardial dysfunction, papillary muscle necrosis, wall rupture, aneurysm, mural thrombus, pericarditis, Dressler syndrome (fever, pericarditis, and increased erythrocyte sedimentation rate [ESR] 2–4 weeks post-MI) |
Labs = serial cardiac enzymes
Changes in enzymes in the initial 24 hr after MI are helpful for making a diagnosis of acute infarction, so enzymes are measured every 8 hr in the first 24 hr after presentation (3 sets total) CPK-MB increases 2–12 hr post-MI, peaks in 12–40 hr, and decreases in 24–72 hr LDH increases in 6–24 hr and peaks in 3–6 days (rarely used for diagnosis) Troponin-I increases in 3 hr, peaks in 6 hr, and gradually decreases over 7 days Treatment=BeMOAN: Beta-blocker, Morphine, O2, ASA, Nitroglycerin Acutely, give O2, ASA, clopidogrel or GP IIb/IIIa inhibitor, β-blockers, nitroglycerin, morphine (pain control can decrease cardiac demand); achieve tight glycemic control in diabetics with insulin; administer potassium and magnesium to keep levels >4 mEq/L and >2 mEq/L, respectively; consider thrombolysis (t-PA, urokinase) or angioplasty if patient presents in initial 12 hr after start of MI; heparin should be administered for up to 48 hours to reduce thrombus risk if angioplasty performed, stop after procedure); if patient is hypotensive, stop nitroglycerin and give intravenous (IV) fluids; give antiarrhythmic medications for frequent premature ventricular contractions (PVC) or ventricular tachycardia (Vtach) Perform stress test or nuclear study after 5-days post-MI to assess future risk; if test is suggestive of increased risk for repeat MI, perform cardiac catheterization to measure vessel patency and consider possible PTCA or CABG if significant occlusion is found Long-term treatment = risk reduction medications should include low dose ASA or clopidogrel, β-blockers, angiotensin-converting enzyme inhibitors (ACE-I), K-sparing diuretic, and 3-hydroxy-e-methylglutaryl coenzyme A (HMG-CoA) reductase; exercise, smoking cessation, and dietary modifications are also important for risk reduction |
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H/P = asymptomatic
ECG = PR >0.2 sec |
1st Degree Hrt Block
Caused by increased vagal tone or functional conduction impairment |
Treatment = none necessary
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H/P = asymptomatic
ECG = progressive PR lengthening until skipped QRS; PR progression, then resets and begins again |
2nd degree—Mobitz I (Wenckebach)
Caused by intranodal or His bundle conduction defect, drug effects (β-blockers, digoxin, calcium channel blockers), or increased vagal tone |
Treatment = adjust doses of medications associated with heart block; treatment usually not necessary unless symptomatic bradycardia is present (pacemaker indicated)
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H/P = usually asymptomatic
ECG = randomly skipped QRS without changes in PR interval |
2nd degree—Mobitz II
Caused by an infranodal conduction problem (bundle of His, Purkinje fibers) Complications = can progress to third-degree heart block |
Treatment = ventricular pacemaker
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H/P = syncope, dizziness, hypotension
ECG = no relationship between P waves and QRS |
Complete/3rd degree heart block
Cause is absence of conduction between atria and ventricles |
Treatment = avoid medications affecting atrioventricular (AV) conduction; ventricular pacemaker
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H/P = sudden tachycardia; possible chest pain, shortness of breath, palpitations, syncope
ECG = P waves hidden in T waves; 150–250 bpm HR; normal QRS |
Paroxysmal supraventricular tachycardia (PSVT)
Tachycardia (HR >100 bpm) arising in atria or AV junction Occurs mostly in young patients with healthy hearts Cause frequently is reentry anomaly AV nodal reentry—presence of both slow and fast conduction pathways in AV node; conduction proceeds quickly through fast pathway and progresses up slow pathway in retrograde fashion; conduction loop is created, resulting in reentrant tachycardia (see Figure 1-9) |
Treatment = carotid massage or Valsalva maneuver may halt an acute arrhythmia, but cardioversion or calcium channel blocker is required in cases of hemodynamic instability; pharmacologic therapy (e.g., β-blocker or calcium channel blocker for AV nodal reentrant tachycardia) or catheter ablation of accessory conduction pathways is frequently used for long-term control in symptomatic patients
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H/P = sudden tachycardia; possible chest pain, shortness of breath, palpitations, syncope
ECG = P waves hidden in T waves; 150–250 bpm HR; normal QRS, ECG shows a delta wave (i.e., slurred upstroke of the QRS) and shortened PR |
Wolff-Parkinson-White (WPW) syndrome
similar to AV nodal reentry, but instead of fast and slow pathways existing in the AV node, a separate accessory conduction pathway exists between the atria and ventricles that returns a conduction impulse to the AV node to set up a reentry loop; (see Figure 1-10) Antiarrhythmics, other than class IA or IC, are contraindicated for WPW syndrome because they can speed up conduction through the accessory pathway. |
Treatment = carotid massage or Valsalva maneuver may halt an acute arrhythmia, but cardioversion or calcium channel blocker is required in cases of hemodynamic instability; pharmacologic therapy (type IA or IC antiarrhythmic for WPW syndrome) or catheter ablation of accessory conduction pathways is frequently used for long-term control in symptomatic patients
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H/P = usually asymptomatic
ECG = variable morphology of P waves; HR >100 bpm (see Figure 1-12) |
Multifocal atrial tachycardia (MAT)
Caused by several ectopic foci in the atria that discharge automatic impulses (multiple pacemakers), resulting in tachycardia |
Treatment = calcium channel blockers or β-blockers acutely; catheter ablation or surgery to eliminate abnormal pacemakers
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H/P = frequently asymptomatic; possible weakness, syncope
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Bradycardia
HR <50 bpm Caused by increased vagal tone or nodal disease Risk factors = elderly, history of CAD Predisposition to development of ectopic beats |
Treatment = stop precipitating medications; pacemaker if severe
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H/P = possibly asymptomatic; shortness of breath, chest pain, palpitations, irregularly irregular pulse
ECG = no discernible P waves, irregular QRS rate |
Atrial fibrillation (Afib)
Lack of coordinated atrial contractions with independent sporadic ventricular contractions Caused by rapid, disorderly firing from a second atrial focus Risk factors = PIRATES: Pulmonary disease, Ischemia (CAD), Rheumatic heart disease, Anemia, hyper Thyroid, Ethanol, and Sepsis. also HTN, valvular disease, pericarditis Complications = increased risk of MI, heart failure; poor atrial contraction causes blood stasis, which leads to mural thrombi formation and a risk of embolization |
Treatment =
In a patient with Afib, ECG should be performed before cardioversion to rule out mural thrombus formation. anticoagulation; rate control via calcium channel blockers, β-blockers, or digoxin; electric or chemical (i.e., class IA, IC, or III antiarrhythmics) cardioversion if presenting within initial 2 days; cardioversion can be performed in delayed presentation if absence of thrombi is confirmed by transesophageal echocardiogram; if presenting after 2 days or if thrombus is seen on ECG, then anticoagulate and wait 3–4 weeks before cardioversion; AV nodal ablation can be considered for recurrent cases |
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H/P = possibly asymptomatic; palpitations, syncope
ECG = regular tachycardia >150 bpm with occasionally set ratio of P waves-to-QRS; sawtooth pattern of P waves (see Figure 1-14) |
Atrial flutter (Aflutter)
Caused by rapid firing of an ectopic focus in the atria Risk factors = CAD, congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), valvular disease, pericarditis Complications = may degenerate into Afib |
Treatment = rate control with calcium channel blockers, β-blockers; electrical or chemical (class IA, IC, or III antiarrhythmics) cardioversion if unable to be controlled with medication; catheter ablation to remove ectopic focus may be possible in some cases
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H/P = usually asymptomatic; possible palpitations, syncope
ECG = early and wide QRS without preceding P wave followed by brief pause in conduction |
Premature ventricular contraction (PVC)
Caused by ectopic beats from a ventricular origin Common, frequently benign; can also be caused by hypoxia, abnormal serum electrolyte levels, hyperthyroidism, caffeine use Complications = associated with increased risk of sudden death in patients with CAD PVCs become concerning for the development of other ventricular arrhythmias if there are >3 PVCs/min |
Treatment = none if patient is healthy; β-blockers in patients with CAD
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H/P = possibly asymptomatic if brief; palpitations, syncope, hypotension
ECG = series of regular, wide QRS complexes independent of P waves (see Figure 1-15) |
Ventricular tachycardia (Vtach)
Series of 3+ PVCs with HR 160–240 bpm Risk factors = CAD, history of MI Complications = sustained Vtach can quickly deteriorate into Vfib if not corrected Torsades de pointes is Vtach with a sine wave morphology; it carries a poor prognosis and can rapidly convert to Vfib; Mg may be useful in treatment. |
Treatment = electrical cardioversion followed by antiarrhythmic medications (class IA, IB, II, or III); for recurrent Vtach, internal defibrillator may be necessary (senses ventricular arrhythmia and automatically releases electric pulse to restore normal rhythm)
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H/P = syncope, hypotension, pulselessness
ECG = totally erratic tracing; no P waves or QRS |
Ventricular fibrillation (Vfib)
Lack of ordered ventricular contraction leads to no CO and is rapidly fatal Frequently occurs after severe MI, post-Vtach Risk factors = CAD, MI |
Treatment = CPR, immediate electric (± chemical) cardioversion
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H/P = fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, nocturia, cough; displaced point of maximal impulse, S3, jugular vein distention (JVD) peripheral edema, hepatomegaly; symptoms and signs are more severe during exacerbations
Labs = plasma brain natriuretic peptide (BNP) and N-terminal pro-BNP will be increased with left ventricle dysfunction Radiology = chest x-ray (CXR) shows cardiac enlargement, Kerley B lines (i.e., increased marking of lung interlobular septa caused by pulmonary edema), cephalization of pulmonary vessels (i.e., increased marking of superior pulmonary vessels caused by congestion and stasis); echocardiogram can assess chamber size and function |
Congestive heart failure (CHF)
Risk factors = CAD, HTN, valvular disease, cardiomyopathy, COPD, drug toxicity, alcohol use causes of CHF exacerbations by the mnemonic A SMITH PEAR: Anemia, Salt, MI, Infection, Thyroid (high or low), HTN, Pericarditis, Endocarditis, Arrhythmia, Rx (not taking medications). |
Treatment =
Systolic dysfunction—start pharmacologic therapy with loop diuretics (decrease preload) and ACE-I or angiotensin receptor blockers (ARB) (decrease preload and afterload and increase CO); add β-blocker, if needed, once stable dose of ACE-I prescribed; digoxin (increases contractility) can be added to improve symptoms; spironolactone (as adjunct to ACE-I) or vasodilators can be added for persistent symptoms (see Figure 1-16) Diastolic dysfunction—use calcium channel blocker, ARB, or ACE-I to control blood pressure; β-blockers are useful for controlling HR and decreasing cardiac workload; K-sparing diuretics should be given to reduce cardiac hypertrophy caused by aldosterone Recombinant BNP (i.e., nesiritide) improves outcomes during acute exacerbations Treat underlying conditions that cause dysfunction (e.g., HTN, valvular pathology); salt-restricted diet helps avoid excessive intravascular fluid volume; assistive devices or cardiac transplant may be required in progressive cases |
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H&P=Asymptomatic in early/ mild cases
Palpitations Dyspnea on exertion Orthopnea Paroxysmal nocturnal dyspnea Exam=Harsh blowing holosystolic murmur radiating from apex to axilla, S3, Widely split S2, Midsystolic click |
Mitral regurgitation (mitral valve incompetency causes blood backflow to LA)
Causes=Mitral valve prolapse (floppy valve) RHD Papillary muscle dysfunction Endocarditis LV dilation |
Imaging=LVH, LA enlargement on CXR
Echo helpful for diagnosis Treatment=Vasodilators if symptomatic Prophylactic antibiotics for increased infection risk Prophylactic anticoagulation Surgical repair in severe or acute cases |
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H&P=Initially asymptomatic ([asymptotically equal to]10 y)
Dyspnea on exertion Orthopnea Paroxysmal nocturnal dyspnea Peripheral edema Hepatomegaly Exam=Opening snap after S2 Diastolic rumble Loud S1 |
Mitral stenosis (obstructed blood flow to LV causes increased LA volume)
Causes=RHD |
Imaging=RVH, LA enlargement, mitral valve calcification on CXR
Echo helpful for diagnosis Treatment=Diuretics (reduce preload) Antiarrhythmics for Afib secondary to atrial enlargement Surgical repair prior to symptomatic progression |
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H&P=Initially asymptomatic
Dyspnea on exertion Chest pain Orthopnea Exam=Bounding pulses Widened pulse pressure Diastolic decrescendo murmur at right 2nd intercostal space Late diastolic rumble (Austin-Flint murmur) Capillary pulsations in nail bed, more visible when pressure is applied (Quincke's sign) |
Aortic regurgitation (aortic valve incompetency causes blood backflow to LV)
Causes=Congenital defect Endocarditis RHD Tertiary syphilis Aortic- root dilatation (possibly from aortic dissection) |
Imaging=Dilated aorta, LV enlargement on CXR
Echo helpful for diagnosis Treatment=ACE- I, calcium channel blockers, or nitrates (decrease afterload) Valve replacement |
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H&P=Chest pain
Dyspnea on exertion Syncope Exam=Weak prolonged pulse Crescendo-decrescendo systolic murmur radiating from right upper sternal border to carotids Weak S2 Valsalva decreases murmur |
Aortic stenosis (narrowing of aortic valve causes obstructed blood flow from LV)
Causes=Congenital defect RHD Calcification in elderly patients |
Imaging=Calcified aortic valve, dilated aorta on CXR
Echo and cardiac catheterization helpful for diagnosis Treatment=β-blockers Valvuloplasty Valve replacement |
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H&P=Syncope
Dyspnea Palpitations Chest pain Symptoms worse with exertion Exam=S4 Systolic murmur Sustained apical impulse ECG may show arrhythmia, LVH, abnormal Q waves |
Hypertrophic obstructive Cardiomyopathy (HOCM) (Ventricular hypertrophy; thickened septum causes decreased filling, LV outflow obstruction, both systolic and diastolic dysfunction)
Causes=Congenital (autosomal dominant) |
Imaging=Boot- shaped heart on CXR
Echo helpful for diagnosis Treatment=β-Blockers Calcium channel blockers Pacemaker Partial septal excision |
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H&P=Similar to CHF and bi-valvular regurgitation
Exam=S3 Systolic and diastolic murmurs ECG may show ST and T wave changes, weak QRS, tachycardia, LBBB |
Dilated Cardiomyopathy (Ventricular dilation causes systolic dysfunction)
Causes=Idiopathic Alcohol use Beriberi Coxsackie virus B Cocaine use Doxorubicin HIV Pregnancy |
Imaging=Balloon- like heart on CXR
Echo helpful in diagnosis Treatment=Stop alcohol or cocaine use Diuretics ACE-I β-blockers Anticoagulation |
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H&P=Similar to CHF with right-sided symptoms worse
Exam=Ascites JVD Biopsy is diagnostic |
Restrictive (Decreased heart compliance causes impaired diastolic filling)
Causes=Sarcoidosis Amyloidosis |
Imaging=Often normal
Treatment=Treat underlying cause Palliative treatment for heart failure |
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H/P = anterior chest pain with inspiration (i.e., pleuritic chest pain), dyspnea, cough; pain lessens with Leaning forwarD; fever, Friction Rub (best heard when leaning forward); pulsus paradoxus (i.e., fall in systolic blood pressure >10 mm Hg with inspiration) occurs because increased physiologic right ventricle (RV) filling during inspiration combined with pathologic left ventricle (LV) compression by pericardial effusion causes impaired LV filling, decreased stroke volume, and decreased inspiratory systolic blood pressure
ECG = global ST elevation, PR depression |
Acute pericarditis
Acute inflammation of the pericardial sac accompanied by pericardial effusion Caused by viral infection, tuberculosis, systemic lupus erythematosus (SLE), uremia, neoplasm, drug toxicity (e.g., isoniazid, hydralazine), post-MI inflammation (Dressler syndrome), radiation, recent heart surgery Complications = chronic constrictive pericarditis if untreated |
Radiology = CXR is helpful in ruling out other systemic causes; effusion frequently seen on echocardiogram
Treatment = treat underlying cause; pericardiocentesis for large effusions; non-steroidal anti-inflammatory drugs (NSAIDs) for pain and inflammation; colchicine may be useful for preventing recurrence owing to viral or idiopathic causes |
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H/P = symptoms consistent with right-sided heart failure (JVD, dyspnea on exertion, orthopnea, peripheral edema, increasing JVD with inspiration [Kussmaul's sign]); Afib common
Labs = cardiac catheterization shows equal pressure in all chambers |
Chronic constrictive pericarditis
Sequelae of chronic untreated pericardial irritation Diffuse thickening of pericardium, with possible calcifications, leads to decreased diastolic filling and decreased CO Most commonly caused by radiation or heart surgery |
Radiology = possible pericardial calcifications on CXR; echocardiogram, computed tomography (CT), and magnetic resonance imaging (MRI) show pericardial thickening
Treatment = NSAID, colchicine, corticosteroids; surgical excision of pericardium (high mortality) |
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H/P = dyspnea, tachycardia, tachypnea; JVD, pulsus paradoxus;
Beck's triad: hypotension, distant heart sounds, and distended neck veins Radiology = enlarged heart shadow on CXR; large effusion seen on echocardiogram ECG = low voltage, sinus tachycardia |
Cardiac tamponade
Large pericardial effusion causes compression of heart and greatly decreased CO; can result from progressive, acute pericarditis; chest trauma, LV rupture following MI, or dissecting aortic aneurysm High mortality |
Treatment = immediate pericardiocentesis
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H/P = patient may report history of recent upper respiratory infection; pleuritic chest pain, dyspnea, pleuritic chest pain; S3 or S4 heart sound, possible diastolic murmur, possible friction rub
ECG = ST- and T-wave changes, conduction abnormalities |
Myocarditis
Inflammatory reaction in heart limited to cardiac muscle involvement Most commonly caused by infection (e.g., Coxsackie virus, bacteria, rickettsiae, fungi, parasites) Occasionally caused by drug toxicity (e.g., doxorubicin, chloroquine, penicillins, sulfonamides, cocaine, radiation), toxins, or endocrine abnormalities Myocarditis in South and Central America is commonly caused by Trypanosoma cruzi (Chagas' disease) and, in these cases, may be associated with achalasia. Several of the drugs that cause myocarditis are used in cancer therapy (cyclophosphamide, doxorubicin, daunorubicin). |
Radiology = possible cardiomegaly on CXR; echocardiogram useful in assessing heart function
Treatment = treat infection; stop offending medications; avoid exertional activity; treat heart failure symptoms as for acute exacerbation of heart failure |
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HTN w/ DM
Recommended Contraindicated |
Recommended: ACE-I,
Delays renal damage Contraindicated: Thiazide diuretic β-blocker Impaired glucose tolerance & Can mask signs of hypoglycemia |
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H/P = migratory arthritis, hot and swollen joints, fever, subcutaneous nodules on extensor surfaces, Sydenham's chorea (i.e., purposeless involuntary movement), erythema marginatum (i.e., painless rash)
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Rheumatic heart disease (RHD)
Uncommon sequela of untreated group A streptococcus infection Streptococcus infection can provoke autoantibodies that attack heart valves and joints (mitral valve more commonly affected than aortic valve, which is more commonly involved than right-sided valves) Incidence is low in the United States because of antibiotic treatment Diagnosis of RHD made using JONES criteria (see Figure 1-19) Complications = progressive valve damage if untreated |
Labs = increased ESR, C-reactive protein (CRP), and white cell count (WBC); 90% of patients have antistreptococcal antibodies
ECG = increased PR interval Treatment = NSAIDs for joint inflammation; use corticosteroids, if carditis is severe; β-lactam (penicillin family) antibiotic for infection; if valves have been damaged, patient will need prophylactic antibiotics before surgery or dentistry |
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HTN w/ CHF
Recommended Contraindicated |
Recommended: ACE-I, Diuretic
Improves mortality Contraindicated: Calcium channel blocker, Reduced rate/contractility can exacerbate heart failure |
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H/P = fever (very high in acute form), chills, night sweats, fatigue, arthralgias; possible new murmur; small, tender nodules on finger and toe pads (i.e., Osler's nodes); peripheral petechiae (i.e., Janeway lesions), subungual petechiae (i.e., splinter hemorrhages), retinal hemorrhages (i.e., Roth's spots)
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Endocarditis
Bacterial infection of endocardium (i.e., inner lining of heart) with or without valve involvement More common in patients with congenital heart defects, intravenous drug abuse, or prosthetic valves Patients with SLE may present in a similar manner with noninfective endocarditis (Libman-Sacks endocarditis) Both acute (sudden presentation) and subacute (insidious progression) forms Acute endocarditis is caused by Staphylococcus aureus, Streptococcus pneumoniae, Staphylococcus pyogenes, Neisseria gonorrhoeae Subacute endocarditis caused by Streptococcus viridans, Enterococcus, fungi, and Staphylococcus epidermidis Duke criteria are used as guide for making diagnosis (see Table 1-7) Complications = severe damage to endocardium and valves, septic embolization, or abscess formation, if untreated |
Labs = serial blood cultures will grow same pathogen; increased ESR; increased CRP
Negative-culture endocarditis can result from the HACEK bacteria: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella Radiology = echocardiogram (preferably transesophageal echocardiogram [TEE]) may show vegetations on valves; CXR may reveal congestion consistent with septic emboli and right-sided heart failure Treatment = long-term (4–6 weeks) IV antibiotics (initially broad-spectrum, then bug-specific); β-lactam plus an aminoglycoside is the most commonly used regimen (adjusted for resistance and particular pathogen); antibiotic prophylaxis before surgery or dental work if valves are damaged; valve replacement may be necessary for severely damaged valves |
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HTN w/ Post-MI
Recommended Contraindicated |
Recommended: β-Blocker,
ACE-I Improves mortality |
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H/P = asymptomatic until progression, then headache may be the only symptom until complications develop; blood pressure >140/90 mm Hg; arteriovenous nicking (i.e., apparent retinal-vein narrowing secondary to arterial wall thickening), Cotton-wool spots, or retinal hemorrhages (i.e., flame hemorrhageS) on fundu-scopic examination; loud S2, possible S4
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Primary (essential) HTN
Cause is idiopathic Accounts for >95% all cases of HTN Diagnosed when systolic blood pressure >140 mm Hg and/or diastolic blood pressure >90 mm Hg, as measured in three readings taken at three separate appointments Risk factors = family history of HTN, high-salt diet (especially if salt sensitive), tobacco use, obesity, increased age; blacks > whites Complications = untreated or poorly treated disease increases risk of CAD, stroke, aortic aneurysm, aortic dissection, CHF, kidney disease, and ophthalmologic disease |
Treatment = do not start medications until three consecutive high readings have been recorded
Initially, prescribe weight loss, exercise, salt restriction, and alcohol reduction Thiazide diuretic is typically first drug prescribed unless comorbid condition indicates otherwise (e.g., calcium channel-blocker, β-blocker; see Table 1-8, Table 1-9); ACE-I, ARB, calcium channel blockers can be added to regimen if additional control required |
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HTN w/ Benign prostatic hypertrophy
Recommended Contraindicated |
Recommended: Selective α1-blocker
Reduces symptoms |
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H/P = possibly asymptomatic or mildly symptomatic; signs of renal failure, hematuria, change of mental status, papilledema, retinal vascular changes, unstable angina, MI, pulmonary edema
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Hypertensive emergency
Blood pressure >200/120 mm Hg (nonpregnant patient) Malignant HTN = progressive renal failure, encephalopathy, papilledema |
Treatment = for malignant HTN, rapidly reduce diastolic blood pressure to 100 mm Hg using IV nitroprusside, labetalol, nicardipine, or fenoldopam; once blood pressure is controlled, use oral β-blockers and ACE-I to gradually reduce mean diastolic pressure to 100–105 mm Hg over 2 hours; use diuretics to reduce pulmonary edema
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HTN w/ Migraine headache
Recommended Contraindicated |
Recommended:β-Blocker
May reduce symptoms |
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H/P = history should consider allergies, changes in medications, recent medication use, infection history, or recent cardiac/neurologic events; hypotension, cool/clammy skin, changes in mental status, decreased urine output
CHORD ITEM: Clammy skin, Hypotension, Oliguria, Rapid breathing, Drowsiness or mental status changes, Irritability, Tachycardia, Elevated or reduced central venous pressure, Multiorgan dysfunction. |
Shock
Circulatory collapse in which blood delivery is inadequate for tissue demands |
Labs = complete blood count (CBC), electrolyte panel, arterial blood gases (ABG), cardiac enzymes, liver function tests, prothrombin time or partial thromboplastin time (PT/PTT), toxicology screen; urinalysis should be included in workup
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HTN w/ Osteoporosis
Recommended Contraindicated |
Recommended:Thiazide diuretic,
Maintains normal/high serum calcium |
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Shock
MI, arrhythmias, cardiac tamponade, pulmonary embolism |
Cardiogenic
Failure of myocardial pump |
Treatment=IV fluids, pressor agents, intra-aortic balloon pump, PTCA
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HTN w/ Asthma/COPD
Recommended Contraindicated |
Nonselective β-blocker
Exacerbates bronchoconstriction |
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Shock
Gram-negative bacteria, DIC; possibly endotoxin mediated |
Septic
Decreased total peripheral resistance |
Treatment=Treat underlying infection, pressor agents
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HTN w/ Pregnancy
Recommended Contraindicated |
Contraindicated:Thiazide diuretic, Increased blood volume during pregnancy should be maintained
ACE-I & ARB, Teratogenic |
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Shock
Hemorrhage, severe burns, trauma |
Hypovolemic
Inadequate blood or plasma volume |
Treatment=IV fluids, transfusions, surgery may be required to stop volume loss; specialized dressings, skin grafts may be required with severe burns to prevent ongoing fluid loss
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HTN w/ Gout
Recommended Contraindicated |
Contraindicated: Diuretic, Increase serum uric acid
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Shock
Massive release of mast cells and basophils in response to allergic reaction |
Anaphylactic
Generalized hypersensitivity type I reaction |
Treatment=Maintain airway, epinephrine, diphenhydramine, cimetidine, IV fluids
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HTN w/ Depression
Recommended Contraindicated |
Contraindicated: β-blocker, May worsen symptoms
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Shock
CNS or spinal cord injury |
Neurogenic
Widespread peripheral vasodilation |
Treatment=IV fluids, pressor agents
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HTN w/ Renal Dz
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Diagnosis=depends
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Treatment=ACE-I (delays progression)
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HTN
Renal artery bruit |
Renal artery stenosis
<25 years of age (fibromuscular dysplasia) or >50 years of age (atherosclerosis) |
Diagnosis=Arteriography; renal vein renin ratio
Treatment=Angioplasty; stent placement; ACE-I if one-sided; surgical repair |
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HTN
Women >35 years of age; obese women; long- term OCP use |
OCP (combination pill)
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Treatment=Stop use; change to progestin-only pill or intramuscular medroxy-progesterone
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HTN
Episodic HTN, diaphoresis, headaches; symptoms occur suddenly |
Pheochromocytoma
Young patients; patients with history of endocrine tumors |
Diagnosis=Increased 24-hr urinary catecholamines or vanillylmandelic acid; CT, MRI
Treatment=Surgical removal of tumor with pharmacologic control of HTN up until time of surgery |
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HTN
Central obesity, hirsutism, buffalo hump, striae, and glucose intolerance in Cushing's disease |
Primary hyper- aldosteronism (excess aldosterone = Conn's disease; excess glucocorticoids = Cushing's disease)
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Diagnosis=Decreased serum K, increased urinary K, increased serum/urine aldosterone
Treatment=Surgical removal of tumor |
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HTN in arm but not in legs, weak femoral pulse
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Coarctation of the aorta
Male < female; Turner syndrome, aortic valve pathology, PDA |
Diagnosis=Possible LVH on ECG; echocardiogram can localize defect
Treatment=Surgical repair |
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H/P = AAAs are frequently asymptomatic until later progression; possible lower back pain; pulsating abdominal mass, abdominal bruits; thoracic aneurysms can cause dysphagia, hoarseness, dyspnea, hemoptysis, upper body edema; hypotension and severe pain occur with any rupture
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Aortic aneurysm
Localized dilation of aorta Most occur in the abdomen below renal arteries (i.e., abdominal aortic aneurysm [AAA]) Risk factors = atherosclerosis, HTN, tobacco use, family history, age >55 years Marfan's syndrome, Ehlers-Danlos syndrome, and syphilis are common causes of thoracic aortic aneurysms Complications = if untreated, possible MI, rupture, renal insufficiency, ischemic colitis, stroke, or paraplegia |
Radiology = ultrasound (US) can detect location and size quickly; CT or MRI are used for more accurate localization and size determination
Treatment = monitor with periodic US if <5 cm diameter; surgical repair (open or using endovascular stenting) if symptomatic or >5 cm diameter; thoracic aneurysms are repaired if >6 cm diameter or rapidly enlarging |
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H/P = acute, “Ripping” chest pain, syncope; decreased peripheral pulses, normal or increased blood pressure
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Aortic dissection
Intimal tear leads to blood entering media causing formation of false lumen Stanford classification—Stanford A aortic dissection involves ascending aorta; Stanford B is distal to left subclavian artery Risk factors = HTN, trauma, coarctation of the aorta, syphilis, Ehlers-Danlos syndrome, Marfan's syndrome |
ECG = normal or LVH
Radiology = widening of aorta and superior mediastinum on CXR; CT with contrast, echocardiogram, MRI, magnetic resonance angiography (MRA), or angiography good for definite diagnosis Treatment = stabilize blood pressure (e.g., nitroprusside, β-blockers) if unstable; Stanford A dissections need emergency surgery; Stanford B dissections can be treated medically unless rupture or occlusion develops |
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H/P = leg pain with activity that improves with rest (i.e., intermittent claudication), resting leg pain in severe disease; dry skin, skin ulcers, decreased hair growth in affected area; male impotence with aortoiliac disease
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Arterial condition–peripheral vascular disease (PVD)
Occlusion of peripheral blood supply secondary to atherosclerosis Risk factors = HTN, DM, CAD six Ps to grade PVD severity: Pain, Pallor, Poikilothermia, Pulselessness, Paresthesia, and Paralysis. |
Labs = ankle-brachial index (ABI) is ratio of systolic blood pressure at ankle to that at brachial artery; ABI <1 indicates vascular insufficiency at ankle; ABI <0.4 indicates severe disease (frequently seen with resting pain)
Radiology = US is useful for locating stenosis and variations in blood pressure; arteriography will map narrowing in the arterial distribution of interest Treatment = exercise (increases collateral circulation), instruction in foot examination (early detection of ulcers from vascular insufficiency), treat underlying diseases; ASA, Pentoxifylline, or Cilostazol to help to slow occlusion; percutaneous transluminal angioplasty (PTA) indicated for failed nonoperative treatment, significant disability caused by claudication, or predictable benefit and improvement in prognosis; bypass grafting if incapacitating claudication, resting pain, or necrotic foot lesions develop; prolonged ischemia may require limb amputation |
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H/P = usually asymptomatic; pain and fatigue that lessens with leg elevation; possible visible or palpable veins, increased local pigmentation, edema, or ulceration
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Varicosities
Incompetent venous valves that cause elongation, dilation, and tortuosity of veins |
Treatment = exercise, compression hosiery, leg elevation; surgical removal or injection sclerotherapy for cosmetic improvement or symptomatic varicosities
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H/P = palpable, warm, pulsating masses, if superficial; painful if mass compresses adjacent structures
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Arteriovenous malformations (AVM)
Abnormal communications between arteries and veins Congenital or acquired Large AVM can cause local ischemia and increase the risk of thrombus formation |
Treatment = surgical removal or sclerosis, if symptomatic, or if located in brain or bowel
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H/P = possibly asymptomatic; Unilateral deep leg pain, swelling, warmth
Homan's sign (calf pain with passive foot dorsiflexion) |
Deep vein thrombosis (DVT)
Development of thrombosis in large vein; most common in lower extremity Location, in order of decreasing frequency: calf, femoral, popliteal, and iliac veins Can cause inflammation of affected vein (i.e., thrombophlebitis) Risk factors = prolonged inactivity (travel, immobilization), heart failure, disorders of coagulation, neoplasm, pregnancy, oral contraceptive pills (OCP) use, tobacco use, vascular trauma Complications = clot can embolize to lungs (i.e., pulmonary embolus) with 40% mortality; chronic DVT can cause chronic venous insufficiency Virchow's triad = blood stasis, hypercoagulability, and vascular damage increase patient's risk of DVT |
Labs = D-dimer will be elevated with DVT formation, but test is more useful in using a normal result to rule out DVT
Radiology = compressive venous US and contrast venography are used for detection Treatment = leg elevation; low molecular weight heparin or unfractionated heparin initially, warfarin for long-term management; inferior vena cava (IVC) filter should be placed in a patient with contraindications to anticoagulation |
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H/P = fever, HTN, hematuria, anemia, neuropathy, weight loss, joint pain, palpable purpura or ulcers on skin
Labs = increased WBC, decreased hemoglobin (Hgb) and hematocrit, increased ESR, proteinuria, hematuria; Perinuclear antineutrophil cytoplasmic antibodies (p-ANCA) in 50%–80% patientS; arterial biopsy may help in diagnosis |
Polyarteritis nodosa
Inflammation of small or medium arteries leads to ischemia Affects kidneys, heart, gastrointestinal (GI) tract, muscles, nerves, joints (anything with a vascular supply) Risk factors = Hepatitis B or C; young > elderly; men > women |
Radiology = angiography may show numerous aneurysms
Treatment = corticosteroids, immunosuppressive agents |
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H/P = new onset of headache (unilateral or bilateral) with scalp pain, temporal region tenderness, jaw claudication, transient or permanent monocular blindness, weight loss, myalgias, arthralgias, fever; funduscopic examination should be performed to address vision loss (may show thrombosis of ophthalmic or ciliary arteries)
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Temporal (giant cell) arteritis
Commonly caused by subacute granulomatous inflammation of the external carotid and vertebral arteries Risk factors = women > men, 50 years of age and older Half of patients also have polymyalgia rheumatica |
Labs = increased ESR; temporal artery biopsy shows inflammation in vessel media and lymphocytes, plasma cells, or giant cells in vessel adventitia
Radiology = US may show stenosis or occlusion of temporal or occipital arteries Treatment = prednisone for 1–2 months followed by taper; low-dose ASA to reduce risk of vision loss or stroke from vessel occlusion; vitamin D and calcium supplementation to reduce risk of osteoporosis from prolonged high-dose corticosteroid use; ophthalmology follow-up |
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H/P = malaise, vertigo, syncope; fever, decreased carotid and limb pulses
Labs = biopsy of affected vessel shows plasma cells and lymphocytes in media and adventitia, giant cells, and vascular fibrosis |
Takayasu's arteritis
Inflammation of aorta and its branches Can cause cerebrovascular and myocardial ischemia Risk factors = Asian heritage, women 10–40 years of age |
Radiology = arteriography may detect abnormal vessels and stenoses; CT or MRI is useful for detecting vessel wall abnormalities
Treatment = corticosteroids, immunosuppressive agents; bypass grafting of obstructed vessels |
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H/P = asthmatic symptoms, fatigue, malaise, mononeuropathy (pain, paresthesia, or weakness); erythematous or popular rash
Labs = increased serum eosinophils, increased ESR, p-ANCA; lung biopsy may show eosinophilic granulomas |
Churg-Strauss disease (allergic angiitis)
Inflammation of small or medium arteries |
Treatment = corticosteroids, immunosuppressive agents
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H/P = Recent upper respiratory infectioN; polyarticular arthritis, fever, hemorrhagic urticaria, palpable purpura, abdominal paiN, possible GI bleeding
Labs = biopsy of purpura demonstrates IgA deposition; similar findings in renal biopsy |
Henoch-Schönlein purpura
IgA immune complex-mediated vasculitis affecting arterioles, capillaries, and venules More frequently in children than adults |
Treatment = frequently self-limited; use corticosteroids for severe GI symptoms
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H/P = fever, lymphadenopathy, conjunctival lesions, maculopapular rash, edema, eventual desquamation of hands and feet
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Kawasaki disease
Necrotizing inflammation of large, medium, and small vessels Most commonly seen in young children Coronary vasculitis develops in 25% of patients, leading to possible aneurysm, MI, or sudden death |
Labs = possible autoantibodies to endothelial cells
Radiology = echocardiogram can detect coronary artery aneurysms (particularly useful when performed with dobutamine stress test); angiography can detect coronary vessel irregularities Treatment = ASA, IV gamma globulin; frequently self-limited |
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H/P = asymptomatic if small; frequent respiratory infections, failure to thrive, dyspnea, shortness of breath, heart failure symptoms with larger defects; Pansystolic murmur at Lower left sternal bordeR, loud pulmonic S2, systolic thrill
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Ventricular septal defect (VSD)
Opening in ventricular septum allowing shunting of blood (see Figure 1-21A) Most common congenital heart defect Complications = if untreated, Eisenmenger's syndrome develops (irreversible); increased risk of endocarditis |
ECG = left ventricular hypertrophy, right ventricular hypertrophy; frequently normal
Radiology = echocardiogram shows shunt Treatment = clinically, follow small defects; diuretics or ACE-I are useful for decreasing fluid volume and vascular resistance in patients with large shunts; repair large defects soon (before Eisenmenger's syndrome develops) |
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H/P = possibly asymptomatic; large defects can cause cyanosis, heart failure symptoms, dyspnea, fatigue, or failure to thrive; strong impulse at lower left sternal border, Wide fixed split S2, systolic Ejection murmur at upper left sternal border
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Atrial septal defect (ASD)
Opening in atrial septum allowing movement of blood between atria (see Figure 1-21B) Initially, blood flow is left-to-right across defect Complications = untreated ASD leads to right-to-left shunt (i.e., Eisenmenger's syndrome), RV dysfunction, pulmonary HTN, arrhythmias |
ECG = right axis deviation
Radiology = echocardiogram shows blood flow between atria, dilated RV, and large heart; CXR shows increased pulmonary vascular markings caused by pulmonary HTN Treatment = small defects do not need repair, but require antibiotic prophylaxis before surgery or dental work; surgical closure for symptomatic infants or when pulmonary blood flow is twice that of systemic blood flow |
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H/P = possibly asymptomatic; heart failure symptoms, dyspnea; wide pulse pressure, Continuous “machinery” murmur at 2nd left intercostal space, loud S2, bounding pulses
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Patent ductus arteriosus (PDA)
Failure of ductus arteriosus to close after birth (see Figure 1-21C) Left-to-right shunt (aorta to pulmonary artery) Risk factors = prematurity, high altitude, 1st-trimester maternal rubella, maternal prostaglandin administration; females > males |
ECG = possible LVH
Radiology = possible cardiomegaly on CXR; echocardiogram shows large left atrium (LA) and LV; angiography confirms diagnosis Treatment = indomethacin induces closure; surgical closure if unresponsive |
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H/P = cyanosis after birth; cyanosis worsens as PDA closes; loud S2
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Transposition of the great vessels
Parallel pulmonary and systemic circulations; aorta connected to RV; pulmonary artery connected to LV (see Figure 1-21D) Cause is poorly understood, but is likely linked to cardiac septal development in the truncus arteriosus Incompatible with life (fetus is stillborn) unless comorbid PDA or VSD Risk factors = Apert's syndrome, Down syndrome, cri-du-chat syndrome, trisomy 13 or 18 |
Radiology = narrow heart base, abnormal pulmonary markings on CXR; echocardiogram used for diagnosis
Treatment = keep PDA open with prostaglandin E; balloon atrial septostomy to widen VSD; prompt surgical correction |
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H/P = cyanosis after birth; dyspnea, fatigue, failure to thrive; heart failure symptoms soon develop; harsh systolic murmur at lower left sternal border, loud S1 and S2, bounding pulses
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Persistent truncus arteriosus
Failure of aorta and pulmonary artery to separate during development results in a single vessel that supplies systemic and pulmonary circulation (see Figure 1-21E) |
ECG = likely LVH, RVH
Radiology = angiography or echocardiogram used for diagnosis; CXR may show boot-shaped heart, no pulmonary artery, large aorta arching to right side Treatment = surgical correction |
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H/P = incomplete form resembles presentation for ASD; complete form causes heart failure symptoms, pneumonitis; murmurs consistent with particular defect
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Endocardial cushion defect
Malformation of atrioventricular valves, atrial septum, and/or ventricular septum during fetal development causes a variety of valvular and septal defects (see Figure 1-21F) Complete defect has ASD, VSD, and single atrioventricular canal Incomplete defect has ASD and minor atrioventricular valve abnormalities Found in 20% of children with Down syndrome |
ECG = left axis deviation
Radiology = echocardiogram or cardiac catheterization used for diagnosis Treatment = surgical correction |
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H/P = early cyanosis, dyspnea, fatigue; children squat for relief during hypoxemic episodes; systolic ejection murmur at left sternal border, RV lift, single S2
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Tetralogy of Fallot
VSD, RV outflow obstruction, RVH, and overriding aorta (see Figure 1-21G) Risk factors = Down syndrome, cri-du-chat syndrome, trisomy 13 and 18 mnemonic The Problems Of Small Hearts: Pulmonary stenosis, Overriding aorta, Septal defect (ventricular), Hypertrophy (of right ventricle). |
ECG = right axis deviation
Radiology = echocardiogram or cardiac catheterization used for diagnosis; boot-shaped heart seen on CXR Treatment = prostaglandin E to maintain PDA; O2, propranolol, IV fluids, morphine, knee-to-chest positioning during cyanotic episodes; surgical correction |
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Anterior Left Ventricle
Bld Supply EKG leads |
Left Anterior Descending (LAD) of left Coronary
EKG: V2, V3, V4 (anterior) |
also supply anterior 2/3 of interventricular septum via septal branch
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Anterior 2/3 of interventricular septum
Bld Supply EKG leads |
Septal branch of Left Anterior Descending (LAD) of left Coronary
EKG: V1, V2, V3 (septal) |
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Left Atrium, lateral&posterior Left Ventricle
EKG leads |
Circumflex of left Coronary
EKG: I, aVL, V4, V5, V6 (lateral) |
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inferior of Left Ventricle, posterior 1/3 interventricular septum
Bld Supply EKG leads |
Posterior Descending Branch of right Coronary
EKG: II, III, aVF(inferior), V1, V2(posterior) |
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right atrium, right ventricle
Bld Supply EKG leads |
Marginal Branch of rigth Coronary
EKG: II, III, aVF(inferior) |
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SA and AV nodes
Bld Supply |
SA,AV nodal branches
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