1. Coronary flow reserve (the increase in coronary blood flow in response to agents that lead to microvascular dilation) begins to decrease when a coronary artery stenosis is 50% or more luminal diameter. However, basal coronary flow does not begin to decrease until the lesion is 80% to 90% luminal diameter.2. The most commonly used criteria to diagnose left ventricular hypertrophy (LVH) are R wave in V5 or V6 + S wave in V1 or V2 > 35 mm, or R wave in lead I plus S wave in lead III > 25 mm. 3. Causes of ST segment elevation include acute myocardial infarction (MI) as a result of thrombotic occlusion of a coronary artery, Prinzmetal angina, cocaine-induced MI, pericarditis, left ventricular (LV) aneurysm, left bundle branch block (LBBB), LVH with repolarization abnormalities, J point elevation, and severe hyperkalemia.4. The initial electrocardiogram (ECG) manifestation of hyperkalemia is peaked T waves. As the hyperkalemia becomes more profound, there may be loss of visible P waves, QRS widening, and ST segment elevation. The preterminal finding is a sinusoidal pattern on the ECG.
5. The classic carotid arterial pulse in a patient with aortic stenosis is reduced (parvus) and delayed (tardus).6. The most common ECG finding in pulmonary embolus is sinus tachycardia. Other ECG findings that can occur include right atrial (RA) enlargement (P pulmonale), right axis deviation, T-wave inversions in leads V1 to V2, incomplete right bundle branch block (IRBBB), and a S1Q3T3 pattern (an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III).7. The major risk factors for coronary artery disease (CAD) are family history of premature CAD (father, mother, brother, or sister who first developed clinical CAD at age younger than 45 to 55 for males and at age younger than 55 to 60 for females), hypercholesterolemia, hypertension, cigarette smoking, and diabetes mellitus.
8. Important causes of chest pain not related to atherosclerotic CAD include aortic dissection, pneumothorax,
pulmonary embolism (PE), pneumonia, hypertensive crisis, Prinzmetal angina, cardiac syndrome X, anomalous origin of the coronary artery, pericarditis, esophageal spasm or esophageal rupture (Boerhaave syndrome), and shingles.
9. The Kussmaul sign is the paradoxical increase in jugular venous pressure (JVP) that occurs during inspiration. JVP normally decreases during inspiration because the inspiratory fall in intrathoracic pressure creates a sucking effect on venous return. Kussmaul sign is observed when the right side of the heart is unable to accommodate an increased venous return, such as can occur with constrictive pericarditis, severe heart failure, cor pulmonale, restrictive cardiomyopathy, tricuspid stenosis, and right ventricular (RV) infarction. 10. Other causes of elevated cardiac troponin, besides acute coronary syndrome and myocardial infarction, that should be considered in patients with chest pains include PE, aortic dissection, myopericarditis, severe aortic stenosis, and severe chronic kidney disease.
11. Prinzmetal angina, also called variant angina, is an unusual angina caused by coronary vasospasm. Patients with Prinzmetal angina are typically younger and often female. Treatment is based primarily on the use of calcium channel blockers and nitrates. 12. Cardiac syndrome X is an entity in which patients describe typical exertional anginal symptoms, yet are found on cardiac catheterization to have nondiseased, normal coronary arteries. Although there are likely multiple causes and explanations for cardiac syndrome X, it does appear that, at least in some patients, microvascular coronary artery constriction or dysfunction plays a role.13. The three primary antianginal medications used for the treatment of chronic stable angina are β-blockers, nitrates, and calcium channel blockers. Ranolazine, a newer antianginal agent, is generally used only as a third-line agent in patients with continued significant angina despite traditional antianginal therapy who have CAD not amenable to revascularization.
14. Findings that suggest a heart murmur is pathologic and requires further evaluation include the presence of symptoms, extra heart sounds, thrills, abnormal ECG or chest radiography, diminished or absent S2, holosystolic (or late systolic) murmur, any diastolic murmur, and all continuous murmurs.15. The major categories of ischemic stroke are large vessel atherosclerosis (including embolization from carotid to cerebral arteries), small vessel vasculopathy or lacunar type, and cardioembolic.16. Hemorrhagic strokes are classified by their location: subcortical (associated with uncontrolled hypertension in 60% of cases) versus cortical (more concerning for underlying mass, arteriovenous malformation, or amyloidosis).17. Common radiographic signs of congestive heart failure include enlarged cardiac silhouette, left atrial (LA) enlargement, hilar fullness, vascular redistribution, linear interstitial opacities (Kerley lines), bilateral alveolar infiltrates, and pleural effusions (right greater than left).18. Classic ECG criteria for the diagnosis of ST elevation myocardial infarction (STEMI), warranting thrombolytic therapy, are ST segment elevation greater than 0.1 mV in at least two contiguous leads (e.g.leads III and aVF or leads V2 and V3) or new or presumably new LBBB.
19. Primary percutaneous coronary intervention (PCI) refers to the strategy of taking a patient who presents with STEMI directly to the cardiac catheterization laboratory to undergo mechanical revascularization using balloon angioplasty, coronary stents, and other measures. 20. The triad of findings suggestive of RV infarction are hypotension, distended neck veins, and clear lungs.21. Cessation of cerebral blood flow for as short a period as 6 to 8 seconds can precipitate syncope.22. The most common causes of syncope in pediatric and young patients are neurocardiogenic syncope (vasovagal syncope, vasodepressor syncope), conversion reactions (psychiatric causes), and primary arrhythmic causes (e.g., long QT syndrome, Wolff-Parkinson-White syndrome). In contrast, elderly
patients have a higher frequency of syncope caused by obstructions to cardiac output (e.g., aortic stenosis, PE) and by arrhythmias resulting from underlying heart disease.
23. Preexisting renal disease and diabetes are the two major risk factors for the development of contrast nephropathy. Preprocedure and postprocedure hydration is the most established method of reducing the risk of contrast nephropathy.24. During coronary angiography, flow down the coronary artery is graded using the TIMI flow grade (flow grades based on results of the Thrombolysis in Myocardial Infarction trial), in which TIMI grade 3 flow
is normal and TIMI grade 0 flow means there is no blood flow down the artery.25. The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) recommends that all adults age 20 years or older should undergo the fasting lipoprotein profile every 5 years. Testing should include total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides.26. Important secondary causes of hyperlipidemia include diabetes, hypothyroidism, obstructive liver disease, chronic renal failure or nephrotic syndrome, and certain drugs (progestins, anabolic steroids, corticosteroids).
27. The minimum LDL goal for secondary prevention in patients with established CAD, peripheral vascular disease, or diabetes is an LDL less than 100 mg/dL. A goal of LDL less than 70 mg/dL should be considered in patients with CAD at very high risk, including those with multiple major coronary risk factors (especially diabetes), severe and poorly controlled risk factors (especially continued cigarette smoking), and multiple risk factors of the metabolic syndrome and those with acute coronary syndrome. 28. Factors that make up metabolic syndrome include abdominal obesity (waist circumference in men larger than 40 inches/102 cm or in women larger than 35 inches/88 cm); triglycerides 150 mg/dL or higher; low HDL cholesterol (less than 40 mg/dL in men or less than 50 mg/dL in women); blood pressure 135/85 mm Hg or higher; and fasting glucose 110 mg/dL or higher.29. Although optimal blood pressure is less than 120/80 mm Hg, the goal of blood pressure treatment is to achieve blood pressure levels less than 140/90 mm Hg in most patients with uncomplicated hypertension.
30. Up to 5% of all hypertension cases are secondary, meaning that a specific cause can be identified. Causes of secondary hypertension include renal artery stenosis, renal parenchymal disease, primary hyperaldosteronism, pheochromocytoma, Cushing disease, hyperparathyroidism, aortic coarctation, and sleep apnea.31. Clinical syndromes associated with hypertensive emergency include hypertensive encephalopathy, intracerebral hemorrhage, unstable angina or acute myocardial infarction, pulmonary edema, dissecting aortic aneurysm, or eclampsia.32. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) recommends that hypertensive emergencies be treated in an intensive care setting with intravenously administered agents, with an initial goal of reducing mean arterial blood pressure by 10% to 15%, but no more than 25%, in the first hour and then, if stable, to a goal of 160/100 to 160/110 mm Hg within the next 2 to 6 hours. 33. Common causes of depressed LV systolic dysfunction and cardiomyopathy include CAD, hypertension,
valvular heart disease, and alcohol abuse. Other causes include cocaine abuse, collagen vascular disease, viral infection, myocarditis, peripartum cardiomyopathy, acquired immunodeficiency syndrome (AIDS), tachycardia-induced cardiomyopathy, hypothyroidism, anthracycline toxicity, and Chagas disease.
34. The classic signs and symptoms of patients with heart failure are dyspnea on exertion (DOE), orthopnea, paroxysmal nocturnal dyspnea (PND), and lower extremity edema. 35. Heart failure symptoms are most commonly classified using the New York Heart Association (NYHA) classification system, in which class IV denotes symptoms even at rest and class I denotes the ability to perform ordinary physical activity without symptoms.36. Patients with depressed ejection fractions (less than 40%) should be treated with agents that block the rennin-angiotensin-aldosterone system, in order to improve symptoms, decrease hospitalizations, and decrease mortality. Angiotensin-converting enzyme (ACE) inhibitors are first-line therapy; alternate or additional agents include angiotensin II receptor blockers (ARBs) and aldosterone receptor blockers.37. The combination of high-dose hydralazine and high-dose isosorbide dinitrate should be used in patients who cannot be given or cannot tolerate ACE inhibitors or ARBs because of renal function impairment or hyperkalemia.
38. High-risk features in patients hospitalized with acute decompensated heart failure (ADHF) include low systolic blood pressure, elevated blood urea nitrogen (BUN), hyponatremia, history of prior heart failure hospitalization, elevated brain natriuretic peptide (BNP), and elevated troponin I or T.39. Atrioventricular (AV) node reentry tachycardia (AVNRT) accounts for 65% to 70% of paroxysmal supraventricular tachycardias (SVTs).40. Implantable cardioverter defibrillators (ICDs) should be considered for primary prevention of sudden cardiac death in patients whose LV ejection fractions remains less than 30% to 35% despite optimal medical therapy or revascularization and who have good-quality life expectancy of at least 1 year.41. The three primary factors that promote venous thrombosis (known together as Virchow triad ) are (1)venous blood stasis; (2) injury to the intimal layer of the venous vasculature; and (3) abnormalities in coagulation or fibrinolysis.
42. Diastolic heart failure is a clinical syndrome characterized by the signs and symptoms of heart failure,a preserved LV ejection fraction (greater than 45% to 50%), and evidence of diastolic dysfunction.43. The four conditions identified as having the highest risk of adverse outcome from endocarditis, for which prophylaxis with dental procedures is still recommended by the American Heart Association, are prosthetic cardiac valve, previous infective endocarditis, certain cases of congenital heart disease, and cardiac transplantation recipients who develop cardiac valvulopathy.44. Findings that should raise the suspicion for endocarditis include bacteremia and/or sepsis of unknown cause, fever, constitutional symptoms, hematuria and/or glomerulonephritis and/or suspected renal
infarction, embolic event of unknown origin, new heart murmurs, unexplained new AV nodal conduction abnormality, multifocal or rapid changing pulmonic infiltrates, peripheral abscesses, certain cutaneous lesions (Osler nodes, Janeway lesions), and specific ophthalmic manifestations (Roth spots).45. Transthoracic echo (TTE) has a sensitivity of 60% to 75% in the detection of native valve endocarditis. In cases where the suspicion of endocarditis is higher, a negative TTE should be followed by a transesophageal echo (TEE), which has a sensitivity of 88% to 100% and a specificity of 91% to 100% for native valves.
46. The most common cause of culture-negative endocarditis is prior use of antibiotics. Other causes include fastidious organisms (Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and various species of Kingella [HACEK group]; Legionella;Chlamydia; Brucella; and certain fungal infections) and noninfectious causes.47. Indications for surgery in cases of endocarditis include acute aortic insufficiency or mitral regurgitation leading to congestive heart failure, cardiac abscess formation or perivalvular extension, persistence of infection despite adequate antibiotic treatment, recurrent peripheral emboli, cerebral
emboli, infection caused by microorganisms with a poor response to antibiotic treatment (e.g., fungi), prosthetic valve endocarditis (particularly if hemodynamic compromise exists), “mitral kissing infection,”and large (greater than 10 mm) mobile vegetations.
48. The main echocardiographic criteria for severe mitral stenosis are mean transvalvular gradient greater than 10 mm Hg, mitral valve area less than 1 cm2, and pulmonary artery (PA) systolic pressure greater than 50 mm Hg.
49. The classic auscultatory findings in mitral valve prolapse (MVP) is a midsystolic click and late systolic murmur, although the click may actually vary somewhat within systole, depending on changes in LV dimension, and there may actually be multiple clicks. The clicks are believed to result from the sudden tensing of the mitral valve apparatus as the leaflets prolapse into the LA (LA) during systole.50. In patients with pericardial effusions, echocardiography findings that indicate elevated intrapericardial pressure and tamponade physiology include diastolic indentation or collapse of the RV, compression of the RA for more than one third of the cardiac cycle, lack of inferior vena cava (IVC) collapsibility with deep inspiration, 25% or more variation in mitral or aortic Doppler flows, and 50% or greater variation of tricuspid or pulmonic valve flows with inspiration.
51. The causes of pulseless electrical activity (PEA) can be broken down to the H’s and T’s of PEA, which are hypovolemia, hypoxemia, hydrogen ion (acidosis), hyperkalemia or hypokalemia, hypoglycemia, hypothermia, toxins, tamponade (cardiac), tension pneumothorax, thrombosis (coronary and pulmonary), and trauma.52. Hemodynamically significant atrial septal defects (ASDs) have a shunt ratio greater than 1.5, are usually 10 mm or larger in diameter, and are usually associated with RV enlargement. 53. Findings suggestive of a hemodynamically significant coarctation include small diameter (less than 10 mm or less than 50% of reference normal descending aorta at the diaphragm), presence of collateral blood vessels, and a gradient across the coarctation of more than 20 to 30 mm Hg.54. Tetralogy of Fallot (TOF) consists of four features: right ventricular outflow tract (RVOT) obstruction, a large ventricular septal defect (VSD), an overriding ascending aorta, and RV hypertrophy.55. The three Ds of the Ebstein anomaly are an apically displaced tricuspid valve that is dysplastic, with a right ventricle that may be dysfunctional.
56. Systolic wall stress is described by the law of Laplace, which states that systolic wall stress is equal to:
(arterial pressure (p) × radius (r))/2 × thickness (h) , or σ = (p × r)/2h (57). Echocardiographic findings suggestive of severe mitral regurgitation include enlarged LA or LV, the color Doppler mitral regurgitation jet occupying a large proportion (more than 40%) of the LA, a regurgitant volume 60 mL or more, a regurgitant fraction 50% or greater, a regurgitant orifice 0.40 cm2 or greater, and a Doppler vena contracta width 0.7 cm or greater.58. The seven factors that make up the Thrombolysis in Myocardial Infarction (TIMI) Risk Score are: age greater than 65 years; three or more cardiac risk factors; prior catheterization demonstrating CAD; ST-segment deviation; two or more anginal events within 24 hours; aspirin use within 7 days; and elevated cardiac markers.
59. The components of the Global Registry of Acute Coronary Events (GRACE) Acute Cardiac Syndrome (ACS) Risk Model (at the time of admission) are age; heart rate; systolic blood pressure, creatinine; congestive heart failure (CHF) Killip class, ST-segment deviation; elevated cardiac enzymes and/or markers; and presence or absence of cardiac arrest at admission.
60. Myocarditis is most commonly caused by a viral infection. Other causes include nonviral infections (bacterial, fungal, protozoal, parasitic), cardiac toxins, hypersensitivity reactions, and systemic disease (usually autoimmune). Giant cell myocarditis is an uncommon but often fulminant form of myocarditis characterized by multinucleated giant cells and myocyte destruction.
61. Initial therapy for patients with non–ST segment elevation acute coronary syndrome (NSTEACS) should include antiplatelet therapy with aspirin and with either clopidogrel, ticagrelor, or a glycoprotein IIb/IIIa inhibitor, and antithrombin therapy with either unfractionated heparin, enoxaparin, fondaparinux, or bivalirudin (depending on the clinical scenario).62. Important complications in heart transplant recipients include infection, rejection, vasculopathy (diffuse coronary artery narrowing), arrhythmias, hypertension, renal impairment, malignancy (especially skin cancer and lymphoproliferative disorders), and osteoporosis (caused by steroid use).63. The classic symptoms of aortic stenosis are angina, syncope, and those of heart failure (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, etc.). Once any of these symptoms occur, the average survival without surgical intervention is 5, 3, or 2 years, respectively.64. Class I indications for aortic valve replacement (AVR) include (1) development of symptoms in patients with severe aortic stenosis; (2) an LV ejection fraction of less than 50% in the setting of severe aortic stenosis; and (3) the presence of severe aortic stenosis in patients undergoing coronary artery bypass grafting, other heart valve surgery, or thoracic aortic surgery.
65. The major risk factors for venous thromboembolism (VTE) include previous thromboembolism, immobility, cancer and other causes of hypercoagulable state (protein C or S deficiency, factor V Leiden, antithrombin deficiency), advanced age, major surgery, trauma, and acute medical illness.66. The Wells Score in cases of suspected pulmonary embolism (PE) includes deep vein thrombosis (DVT) symptoms and signs (3 points); PE as likely as or more likely than alternative diagnosis (3 points); heart rate greater 100 beats/min (1.5 points); immobilization or surgery in previous 4 weeks (1.5 points); previous DVT or PE (1.5 points); hemoptysis (1.0 point); and cancer (1 point).67. The main symptoms of aortic regurgitation (AR) are dyspnea and fatigue. Occasionally patients experience angina because reduced diastolic aortic pressure reduces coronary perfusion pressure, impairing coronary blood flow. Reduced diastolic systemic pressure may also cause syncope or presyncope.
68. The physical findings of AR include widened pulse pressure, a palpable dynamic LV apical beat that is displaced downward and to the left, a diastolic blowing murmur heard best along the left sternal border with the patient sitting upright and leaning forward, and a low-pitched diastolic rumble heard to the LV apex (Austin Flint murmur). 69. Class I indications for aortic valve replacement in patients with AR include (1) the presence of symptoms in patients with severe AR, irrespective of LV systolic function; (2) chronic severe AR with LV systolic dysfunction (ejection fraction 50% or less), even if asymptomatic; and (3) chronic, severe AR in patients undergoing coronary artery bypass grafting (CABG), other heart valve surgery, or thoracic aortic surgery.70. Cardiogenic shock is a state of end-organ hypoperfusion caused by cardiac failure characterized by persistent hypotension with severe reduction in cardiac index (less than 1.8 L/min/m2) in the presence of adequate or elevated filling pressure (LV end-diastolic pressure 18 mm Hg or higher or RV end-diastolic pressure 10 to 15 mm Hg or higher).
71. The rate of ischemic stroke in patients with nonvalvular atrial fibrillation (AF) is about two to seven times that of persons without AF, and the risk increases dramatically as patients age. Both paroxysmal and chronic AF carry the same risk of thromboembolism.72. In nuclear cardiology stress testing, a perfusion defect is an area of reduced radiotracer uptake in the myocardium. If the perfusion defect occurs during stress and improves or normalizes during rest, it is termed reversible and usually suggests the presence of inducible ischemia, whereas if the perfusion
defect occurs during both stress and rest, it is termed fixed and usually suggests the presence of scar (infarct).
73. The main organ systems that need to be monitored with long-term amiodarone therapy are the lungs, the liver, and the thyroid gland. A chest radiograph should be obtained every 6 to 12 months, and liver function tests (LFTs) and thyroid function tests (thyroid-stimulating hormone [TSH] and free T4) should be checked every 6 months.
74. The target international normalized ratio (INR) for warfarin therapy in most cases of cardiovascular disease is 2.5, with a range of 2.0 to 3.0. In certain patients with mechanical heart valves (e.g., older valves, mitral position), the target is 3.0 with a range of 2.5 to 3.5.75. Lidocaine may cause a variety of central nervous system symptoms including seizures, visual disturbances, tremors, coma, and confusion. Such symptoms are often referred to as lidocaine toxicity.The risks of lidocaine toxicity are increased in elderly patients, those with depressed LV function, and those with liver disease.
76. The most important side effect of the antiarrhythmic drug sotalol is QT-segment prolongation leading to torsades de pointes.77. The major complications of percutaneous coronary intervention (PCI) include periprocedural MI,
acute stent thrombosis, coronary artery perforation, contrast nephropathy, access site complications (e.g., retroperitoneal bleed, pseudoaneurysm, arteriovenous fistula), stroke, and a very rare need for emergency CABG.
78. The widely accepted hemodynamic definition of pulmonary arterial hypertension (PAH) is a mean pulmonary arterial pressure of more than 25 mm Hg at rest or more than 30 mm Hg during exercise, with a pulmonary capillary or LA pressure of less than 15 mm Hg.79. Acute pericarditis is a syndrome of pericardial inflammation characterized by typical chest pain, a pathognomonic pericardial friction rub, and specific electrocardiographic changes (PR depression, diffuse ST-segment elevation).
80. Conditions associated with the highest cardiac risk in noncardiac surgery are unstable coronary syndromes (unstable or severe angina), decompensated heart failure, severe valvular disease (particularly severe aortic stenosis), and severe arrhythmias.81. General criteria for surgical intervention in cases of thoracic aortic aneurysm are, for the ascending thoracic aorta, aneurysmal diameter of 5.5 cm (5.0 cm in patients with Marfan syndrome), and
for the descending thoracic aorta, aneurismal diameter of 6.5 cm (6 cm in patients with Marfan syndrome).82. Cardiac complications of advanced AIDS in untreated patients include myocarditis and/or cardiomyopathy (systolic and diastolic dysfunction), pericardial effusion/tamponade, marantic (thrombotic) or infectious endocarditis, cardiac tumors (Kaposi sarcoma, lymphoma), and RV dysfunction from pulmonary hypertension or opportunistic infections. Complications with modern antiretroviral therapy (ART) include dyslipidemias, insulin resistance, lipodystrophy, atherosclerosis, and arrhythmias.
83. The radiation dose of a standard cardiac computed tomography (CT) angiography depends on a multitude of factors and can range from 1 mSv to as high as 30 mSv. This compares to an average radiation dose from a nuclear perfusion stress test of 6 to 25 mSv (or as high as more than 40 mSv in thallium stress/rest tests) and an average dose from a simple diagnostic coronary angiogram of approximately 5 mSv. 84. The ankle-brachial index (ABI) is the ankle systolic pressure (as determined by Doppler examination) divided by the brachial systolic pressure. An abnormal index is less than 0.90. The sensitivity is approximately 90% for diagnosis of peripheral arterial disease (PAD). An ABI of 0.41 to 0.90 is interpreted as mild to moderate peripheral arterial disease; an ABI of 0.00 to 0.40 is interpreted as severe PAD.
85. Approximately 90% of cases of renal artery stenosis are due to atherosclerosis. Fibromuscular dysplasia (FMD) is the next most common cause.86. In very general terms, in cases of carotid artery stenosis, indications for carotid endarterectomy (CEA) are: (1) symptomatic stenosis 50% to 99% diameter if the risk of perioperative stroke or death
is less than 6%; and (2) asymptomatic stenosis greater than 60% to 80% diameter if the expected perioperative stroke rate is less than 3%.87. The most common cardiac complications of systemic lupus erythematosus (SLE) are pericarditis, myocarditis, premature atherosclerosis, and Libman-Sacks endocarditis.88. Cardiac magnetic resonance imaging (MRI) can be performed in most patients with implanted cardiovascular devices, including most coronary and peripheral stents, prosthetic heart valves, embolization coils, intravenous vena caval filters, cardiac closure devices, and aortic stent grafts. Pacemakers and implantable cardioverter defibrillators are strong relative contraindications to MRI scanning, and scanning of such patients should be done under specific delineated conditions, only at centers with expertise in MRI safety and electrophysiology, and only when MRI imaging in particular is clearly indicated.
89. The clinical manifestations of symptomatic bradycardia include fatigue, lightheadedness, dizziness, presyncope, syncope, manifestations of cerebral ischemia, dyspnea on exertion, decreased exercise tolerance, and congestive heart failure.90. Second-degree heart block is divided into two types: Mobitz type I (Wenckebach) exhibits progressive prolongation of the PR interval before an atrial impulse (P wave) is not conducted, whereas Mobitz type II exhibits no prolongation of the PR interval before an atrial impulse is not conducted.91. Temporary or permanent pacing is indicated in the setting of acute MI, with or without symptoms, for (1) complete third-degree block or advanced second-degree block that is associated with block in the His-Purkinje system (wide complex ventricular rhythm) and (2) transient advanced (second-degree or third-degree) AV block with a new bundle branch block.
92. Cardiac resynchronization therapy (CRT) refers to simultaneous pacing of both ventricles (biventricular, or Bi-V, pacing). CRT is indicated in patients with advanced heart failure (usually NYHA class III or IV), severe systolic dysfunction (LV ejection fraction 35% or less), and intraventricular conduction delay (QRS less than 120 ms) who are in sinus rhythm and have been on optimal medical therapy.93. Whereas the left internal mammary artery (LIMA), when anastomosed to the left anterior descending artery (LAD), has a 90% patency at 10 years, for saphenous vein grafts (SVGs), early graft stenosis or occlusion of up to 15% can occur by 1 year, with 10-year patency traditionally cited at only 50% to 60%.94. Myocardial contusion is a common, reversible injury that is the consequence of a nonpenetrating trauma to the myocardium. It is detected by elevations of specific cardiac enzymes with no evidence
of coronary occlusion and by reversible wall motion abnormalities detected by echocardiography.
95. Causes of restrictive cardiomyopathy include infiltrative diseases (amyloidosis, sarcoidosis, Gaucher disease, Hurler disease), storage diseases (hemochromatosis, glycogen storage disease, Fabry disease), and endomyocardial involvement from endomyocardial fibrosis, radiation, or anthracycline treatment.96. Classical signs for cardiac tamponade include the Beck triad of (1) hypotension caused by decreased stroke volume, (2) jugulovenous distension caused by impaired venous return to the heart, and (3) muffled heart sounds caused by fluid inside the pericardial sac, as well as pulsus paradoxus and general signs of shock, such as tachycardia, tachypnea, and decreasing level of consciousness. 97. The most common tumors that spread to the heart are lung (bronchogenic) cancer, breast cancer,
melanoma, thyroid cancer, esophageal cancer, lymphoma, and leukemia.
98. Primary cardiac tumors are extremely rare, occurring in one autopsy series in less than 0.1% of subjects. Benign primary tumors are more common than malignant primary tumors, occurring approximately three times as often as malignant tumors.99. The Westermark sign is the finding in pulmonary embolism of oligemia of the lung beyond the
occluded vessel. If pulmonary infarction results, a wedge-shaped infiltrate (Hampton’s hump) may be visible. 100. Patients with cocaine-induced chest pain should be treated with intravenous benzodiazepines, which can have beneficial hemodynamic effects and relieve chest pain, and aspirin therapy, as well as nitrate therapy if the patient remains hypertensive. β-blockers (including labetalol) should not be administered in the acute setting of cocaine-induced chest pain.