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135 Cards in this Set
- Front
- Back
Dietary modification, exercise program, cessation of smoking, drug therapy |
Four general treatment measures for cardiac disorders |
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Interfere with clotting factor synthesis
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Warfarin |
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Inhibit cardiac workload |
Heparin |
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Percutaneous transluminal coronary angioplasty |
Used in advanced atheromas |
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Coronary artery bypass grafting |
Used in advanced atheromas |
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Laser angioplasty |
Used in advanced atheromas |
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Angina pectoris |
Chest pain |
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Decreased blood supply to heart, increased demand for oxygen by heart, or combination |
Underlying pathology in angina pectoris |
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Most serious complication of angina pectoris |
Myocardial infarction |
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Used to treat acute anginal attack |
Coronary vasodilators |
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B-Adrenergic blockers (Lopressor) |
Blocks B adrenergic receptors, slowing the heart rate, prevents sympathetic nervous system stimulation and increased demand on heart. |
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Calcium channel blockers (Adalat) |
Vasodilator, blocks calcium channel, reducing cardiac contractility and work |
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Nitrates (vasodilators; transdermal or oral form, e.g.: nitroglycerin) |
Reduces cardiac workload, decreases peripheral resistance by vasodilation |
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Digitalis (cardiac glycosides) e.g.: Lanoxin |
Slows conduction through the atrioventricular node, increases the force of contraction (cardiotonic) to increase efficiency |
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Lower blood pressure and cardiac workload |
Antihypertensive |
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Control blood pressure and prevent edema |
Diuretic |
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Lower platelet aggregation and the chance of thrombus formation |
Platelet inhibitor |
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Lower blood cholesterol and LDL levels and slow or arrest progression of atherosclerosis |
Antihyperlipidemic |
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Angioplasty and stent insertion, coronary bypass graft |
Surgical interventions that might be used in treatment of angina |
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Death of cardiac muscle resulting from prolonged ischemia |
Myocardial infarction |
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Thrombus buildup obstructs artery due to atherosclerosis |
Most common cause of myocardial infarction |
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Vasoplasm in presence of partial occlusion |
Cause of myocardial infarction |
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Embolization of thrombus to smaller artery that is totally obstructed |
Cause of myocardial infarction |
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Transmural infarction vs intramural infarction |
Transmural infarction involves all three layers of heart |
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Most common site of myocardial infarction |
Left ventricle |
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Pathophysiology of MI |
Coronary artery is totally occluded, causing prolonged ischemia and cell death or infarction of myocardium |
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MI - area of necrosis is gradually replaced by |
Fibrous (non-functional tissue) |
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ECG changes, and serum enzyme and isoenzyme levels. Serum levels of myosin and cardiac troponin are elevated, serum electrolyte levels may be abnormal, leukocytosis and elevated CRP and ESR are common. Arterial blood gas is altered. Pulmonary artery pressure measurements should be conducted to determine ventricular function |
Diagnosis of myocardial infarction confirmed |
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Intracellular enzymes diffused from necrotic cells into the serum in a typical and predictable pattern that can be measured |
Serum enzymes |
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Subgroups of a specific enzyme, found primarily in one type of tissue |
Isoenzymes |
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Will be altered in areas of severe ischemia or necrosis |
Electrical activity of myocardium |
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Complication of MI responsible for greatest number of deaths |
Arrythmia |
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Cardiogenic shock, congestive heart failure, rupture of necrotic heart tissue, and thromboembolism |
Other complications that may accompany MI |
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Treatment for MI - digoxin |
Generally supports heart function |
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Usually precipitated by something that increases heart rate |
Angina |
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May occur at rest or while asleep |
Myocardial infarction |
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Relieved by nitroglycerin and rest |
Angina |
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Not relieved by nitroglycerin and rest |
Myocardial infarction |
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No tissue death |
Angina |
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Cell death |
Myocardial infarction |
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No changes in cardiac enzymes and isoenzymes |
Angina |
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Cardiac enzymes and isoenzymes elevated |
Myocardial infarction |
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No permanent ECG changes |
Angina |
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Permanent ECG changes |
Myocardial infarction |
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White blood cell count not elevated |
Angina |
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Leukocytosis |
Myocardial infarction |
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CRP and ESR elevated |
With myocardial infarction, not elevated with angina |
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Serum levels of myosin and troponin elevated |
With myocardial infarction, not elevated with angina |
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Atrial depolarization |
P Wave |
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Ventricular repolarization |
QRS complex |
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Ventricular depolarization |
T wave |
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Alteration of cardia rate or rhythm |
Dysrhythmia |
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May occur due to damage to the heart's conduction system or to systemic causes such as electrolyte abnormalities, fever, hypoxia, stress, infection, or drug toxicity |
Cardiac arrythmias |
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Heart rate greater than 350 beats per minute |
Fibrillation |
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Ectopic beat |
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Heart rate less than 60 bpm |
Bradycardia |
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Heart rate between 160 and 350 bpm |
Flutter |
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Heart rate between 100 and 160 bpm |
Tachycardia |
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Slowing or no transmission of impulses between atria and ventricles |
Heart block |
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Additional heartbeat originating in atria |
Premature atrial contraction (PAC) |
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Extra heartbeat arising in ventricles |
Premature ventricular contraction (PVC) |
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Restoration of normal cardiac rhythm by electrical shock |
Cardioversion |
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Cessation of all activity in the heart, no impulse contraction, thus a flat ECG |
Cardiac arrest |
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Causes: a problem in the heart itself (valve defect or MI) or a condition that increases the workload of the heart |
Heart failure |
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Compensatory mechanisms in early heart failure |
Reduced blood flow into systemic circulation to include kidneys, increased rennin and aldosterone secretion, resulting in vasoconstriction and increased blood volume. SNS response increases heart rate and peripheral resistance. Chambers of the heart dilate, and cardiac muscle becomes hypertrophied. |
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The chamber and blood vessels behind or "upstream" from the failing ventricle will not empty properly, resulting in the accumulation or congestion of blood and therefore an increased pressure in these areas |
Backward effects |
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There will be decreased output of blood from the failing ventricle into the vessels "in front" of it, or "downstream". |
Forward effects |
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Cause: Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale) |
Right-sided heart failure |
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Cause: Infarction of left ventricle, aortic valve stenosis, hypertension, hyperthyroidism |
Left-sided heart failure |
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Backward effects: Dependent edema in feet, hepatomegaly and splenomegaly, ascites, distended neck veins, headache, flushed face |
Right-sided heart failure |
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Backward effects: Orthopnea, cough, shortness of breath, paroxysmal nocturnal dyspnea, hemopytsis, rales |
Left-sided heart failure |
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Forward effects: Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance |
Right-sided heart failure |
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Forward effects: atigue, weakness, dyspnea, exercise intolerance, cold intolerance |
Left-sided heart failure |
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Manifestations: See above forward and backward effects. Compensations: tachycardia and pallor, secondary polycythemia, daytime oliguria |
Right-sided heart failure |
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Manifestations: See above forward and backward effects. Compensations: tachycardia and pallor, secondary polycythemia, daytime oliguria |
Left-sided heart failure |
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Septal defect |
A hole or defect in the atrial or ventricular septa |
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Valvular incompetence |
Failure of a valve to close completely |
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Regurgitation |
Backward flow or leaking of blood due to valvular incompetence |
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Prolapse |
Abnormally enlarged and floppy valve leaflets that balloon backward with pressure or posterior displacement of the valve cusp |
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Stenosis |
Narrowing of a valve |
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Heart murmur |
Abnormal heart sounds due to leaky valves |
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Most detected by presence of a heart murmur |
Congenital heart defect |
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Blood from the left side of the heart is recycled to the right side and to the lungs, resulting in increased volume in the pulmonary circulation, decreased cardiac output, and an inefficient system - an acyanotic condition |
Left to right shunt |
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Unoxygenated blood from the right side of the heart bypasses the lung directly and enters the left side of the heart and hence the systemic circulation, producing varying degrees of cyanosis; death may occur in infancy in severe cases |
Right to left shunt |
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Forward effects: Decreased cardiac output |
Mitral stenosis, mitral regurgitation, aortic stenosis |
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Forward effects: Increased stroke volume and cardiac output |
Aortic regurgitation |
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Forward effects: Decreased blood flow through pulmonary circulation, leading to decreased gas exchange and blood to left side of heart |
Pulmonary stenosis |
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Forward effects: Decreased blood flow through pulmonary circulation, leading to decreased gas exchange and blood to left side of heart |
Pulmonary regurgitation |
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Backward effects: Left atrial hypertrophy, atrial arrhythmias, mural thrombi, pulmonary congestion, pulmonary hypertension |
Mitral stenosis, mitral regurgitation |
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Backward effects: Left ventricular hypertrophy, if severe, increased congestion in left atrium and pulmonary congestion |
Aortic stenosis |
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Backward effects: Left ventricular hypertrophy, if severe, heart failure |
Aortic regurgitation |
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Backward effects: Right ventricular hypertrophy, congestion in right atrium and systemic veins, leads to right-sided heart failure |
Pulmonary stenosis, pulmonary regurgitation |
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Manifestations: Dyspnea, orthopnea, cyanosis, fatigue, arrhythmias, heart murmur, increased risk of stroke due to emboli originating in left atrium |
Mitral stenosis |
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Manifestations: Dyspnea, orthopnea, cyanosis, fatigue, dizziness, arrythmias, heart murmur |
Mitral regurgitation |
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Manifestations: Dizziness, fainting, fatigue, heart murmur, if severe, dyspnea, orthopnea, cyanosis, angina |
Aortic stenosis |
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Manifestations: Very strong, bounding pulse, heart murmur, may develop symptoms of heart failure |
Aortic regurgitation |
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Manifestations: Weakness, fatigue, cyanosis, swelling of feet and ankles, symptoms of right-sided heart failure, heart murmur |
Pulmonary stenosis |
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Manifestations: Weakness, fatigue, cyanosis, swelling of feet and ankles, symptoms of right-sided heart failure, heart murmur |
Pulmonary regurgitation |
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Associated with heart murmurs |
Valvular defect, septal defect |
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Pulmonary valve stenosis, ventricular septal defect, dextroposition of the aorta, right ventricular hypertrophy, present in |
Tetralogy of Fallot |
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Microorganism that generally causes rheumatic fever |
Group A B-hemolytic streptococci |
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High risk individuals for rheumatic fever |
Ages 5-15 |
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Pathophysiology of rheumatic fever |
Acute systemic inflammatory condition resulting from abnormal immune reaction of untreated infection. May include inflammation in large joints, migratory polyarthritis, nonpruritic skin rash, nontender subcutaneous nodules of extensor surfaces of wrists, elbows, knees, ankles, and inflammation of basal nuclei, causing involuntary jerky movements. Rheumatic heart disease can develop years later. |
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Aschoff bodies |
Myocarditis as result of rheumatic fever, inflammation develops as localized lesions in the heart muscle |
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Endocarditis from rheumatic fever |
May lead to permanent scarring of heart valves, which leads to rheumatic heart disease. Causes high risk for infective endocarditis |
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Heart valve most commonly affected by rheumatic heart disease |
Mitral valve |
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Defective heart valves infected by organisms with low virulence, i.e. Streptococcus viridans |
Subacute infective carditis |
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Normal valves attacked by highly virulent pathogens, i.e. Staphylococcus aureus |
Acute infective carditis |
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Insidious onset, various new heart murmurs, low grade fever, fatigue, anorexia, splenomegaly, Osler's nodes on fingers, signs of vascular occlusion or infection (abscesses) in remote areas, intermittent high fever |
Subacute infective carditis |
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Sudden onset, sudden, spiked fever, chills, drowsiness. Heart valves badly damaged and may be torn, causing severe impairment of heart function. Septic emboli may cause infarctions and abscesses in remote sites with corresponding signs and symptoms of infection. |
Acute infective carditis |
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High blood pressure (values) |
Systolic above 120 and diastolic above 70 |
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Essential Hypertension (values) |
Consistently above 140/90 mm Hg |
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Idiopathic hypertension |
Essential hypertension |
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Hypertension that results from renal or endocrine disease, or pheochromocytoma |
Secondary hypertension |
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Furosemide, Hydrochlorothiazide |
Diuretics |
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Enalaprilm, Ramipril, Captopril, Fosinopril |
ACE inhibitors |
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Nifedipine, Amlodipine, Diltiazem |
Calcium channel blockers |
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Metoprolol, Atenolol, Propranolol, Nadolol |
B-Adrenergic blockers |
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Localized dilation of an arterial wall |
Aortic aneurysm |
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Causes include atherosclerosis, trauma (particularly car accidents), syphilis, or congenital defects |
Aortic aneuryms |
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Development of a thrombus in a vein in which inflammation is present |
Thrombophlebitis |
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Spontaneous thrombus development in the absence of inflammation |
Phlebothrombosis |
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Blood stasis and sluggish blood flow, endothelial injury, and increased blood coagulability contribute to |
Thrombophlebitis |
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A blood clot or sometimes other material that blocks a pulmonary artery or one of it's branches |
Pulmonary embolus |
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Hypotension resulting from decreased circulating blood volume, resulting in decreased tissue perfusion and general hypoxia. |
Shock |
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Ascites - present in |
Right-sided heart failure |
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Positive Homan's sign - present in |
Thrombophlebitis |
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ECG changes - present in |
Myocardial infarction, arrythmias |
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Positive blood cultures - present in |
Rheumatic fever, endocarditis |
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Claudication - present in |
Thrombophlebitis |
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Hemoptysis - present in |
Heart failure |
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Heart murmur |
Congenital defects, rheumatic fever, rheumatic heart disease, tetralogy of Fallot, septal defects, valvular defects - stenosis and regurgitation |
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Elevated cardiac enzymes - present in |
Myocardial infarction |
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Subcutaneous nodules - present in |
Rheumatic fever |
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Pulmonary edema - present in |
Left sided heart failure, mitral stenosis, mitral regurgitation |