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afterload
the tension developed by the heart during contraction; it is an important determinant of myocardial energy consumption, as it represents the resistance against which the ventricle must pump and indicates how much effort the ventricles must put forth to force blood into the systemic circulation. Factors that increase afterload include aortic and pulmonarystenosis, systemic and pulmonary hypertension, and high peripheral resistance
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anasarca
generalized massive edema.
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aneurysm
A localized, blood-filled dilation of a blood vessel caused by disease or weakening of the vessel wall.
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angioplasty
a procedure used to widen vessels narrowed by stenoses or occlusions
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anoxia
a condition characterized by an absence of oxygen supply to an organ or a tissue
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atherectomy
a non-surgical procedure to open blocked coronary arteries or vein grafts by using a device on the end of a catheter to cut or shave away atherosclerotic plaque
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atheroma
A deposit or degenerative accumulation of lipid-containing plaques on the innermost layer of the wall of an artery
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atrial tachycardia
a rapid cardiac rate, usually 160–190 per minute, originating from an atrial locus.
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cardiac decompensation
a condition of congestive heart failure in which the heart is unable to ensure adequate cellular perfusion in all parts of the body without assistance. Causes may include myocardial infarction, increased workload, infection, toxins, or defective heart valves.
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commissurotomy
the surgical division of a fibrous band or ring connecting corresponding parts of a body structure. A commissurotomy is commonly performed to separate the thickened, adherent leaves of a stenosed mitral valve
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diastole
the period between contractions of the atria or the ventricles during which blood enters the relaxed chambers from the systemic circulation and the lungs. Ventricular diastole begins with the onset of the second heart sound and ends with the first heart sound
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endocarditis
infection of endocardium, the inner lining of the heart muscle, which also covers the heart valves
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epicarditis
infection of epicarditis, the outermost of the three layers of tissue that form the heart wall
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hypoxia
reduction of oxygen supply to a tissue below physiological levels despite adequate perfusion of the tissue by blood
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infarction
occurring during the period when circulation to a region of the heart is obstructed and necrosis is occurring.
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ischemia
an insufficient supply of blood to an organ, usually due to a blocked artery.
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mitral insufficiency
defective functioning of the mitral valve, with incomplete closure causing mitral regurgitation.
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orthopnea
dyspnea that is relieved in the upright position
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paroxysmal nocturnal dyspnea
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pericarditis
- –An inflammation of the visceral and/or
- parietal pericardium
- –May result in cardiac compression, ¯ LV
- filling and emptying, and cardiac failure
–Pericardial friction rub
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peripheral vascular resistance
a resistance to the flow of blood determined by the tone of the vascular musculature and the diameter of the blood vessels. It is responsible for blood pressure when coupled with stroke volume.
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preload
a resistance to the flow of blood determined by the tone of the vascular musculature and the diameter of the blood vessels. It is responsible for blood pressure when coupled with stroke volume.
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pulse deficit
the difference between the heart rate and the pulse rate in atrial fibrillation.
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pulse pressure
the difference between systolic and diastolic pressures.
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systole
the contraction, or period of contraction, of the heart, especially of the ventricles
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venous pressure
the pressure of blood in the veins
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ventricular standstill
cessation of ventricular contractions, marked by absence of ventricular complexes in the electrocardiogram.
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ventricular tachycardia
a rapid heart beat that originates in one of the lower chambers (the ventricles) of the heart.
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ventricular aneurysm
- –Results when the infarcted
- myocardial wall becomes thinned and bulges outward during contraction
–Ventricular rupture
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Papillary muscle dysfunction
rupture of heart structures caused by necrosis of tissue
–Causes mitral valve regurgitation
- –This condition aggravates an already
- compromised left ventricle
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Dressler syndrome
–Characterized by pericarditis with pericardial effusion and fever that develops 4 to 6 weeks after MI
–An antigen-antibody reaction to the necrotic myocardium
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CK-MB
found in the _myocardium –most specific to cardiac muscle
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Serum troponin levels
- have a greater sensitivity & specificity in detecting myocardial injury. They show myocardial damage quicker than CK levels
- •Three forms of Troponin (I, T and C) each with several isoforms
•Troponin C is found in some skeletal muscles and is therefore not diagnositic of heart damage.
•Troponin T is most strongly predictive of mortality following MI (the higher the Troponin T, the greater the chance of death within 30 days).
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cardiogenic shock
- Occurs when inadequate O2 & nutrients are supplied to the tissues b/c of severe LV failure
- • If more that 40% of the LV is damaged circulatory collapse progresses rapidly
- • Decreased B/P, pulses, shallow respirations, altered LOC, restless, clammy skin, decreased UO, EKG changes
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