N170 Cardiac Study Aid
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| Creatine KinaseCK-MB | Iso-enzyme of CPK. An elevation of CK-MB is used to distinguish whether the CPK originated from damage to heart muscle.Rises with in 3 hours of MI
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| LDH 1 | Isoenzyme of LDH specific to cardiac cellular death.Level of LDH1 accounts for 25-45% of the 5 total LDH isoenzymes = LDH 1 < LDH 2 in the normal clientElevated level
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| LDH 2 | Isoenzyme of LDH specific to cardiac cellular death.Level of LDH2 accounts for 35-46% of the 5 total LDH isoenzymes = LDH 2 >LDH 1 in the normal client
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| Troponin T & 1 | Troponin 1--rises within 4 hours of symptoms; very specific for only myocardial muscle damageAlso a predictor of prognosis(higher elevations associated with a worse outcome) Remain elevated for several weeks after MI
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| Creatine PhosphokinaseCPKCreatine KinaseCK | A enzyme found in high concentrations in the heart and skeletal muscles and in much smaller concentrations in the brain. This enzyme is released when there is injury to these tissues.Elevation starts within 4-6 hr of MI
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| LDH “Flip” | LDH 1 > LDH 2 in the client with an MIUseful in the late diagnosis of MI.
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| LDH | Lactic Acid DehydrogenaseAn intracellular enzyme . Elevated levels = cellular deathElevation begin 12-24 hours post MI and can continue for 6-10 days*LDH remains elevated longer than CK in a MILDH peaks in 2-3 days
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| BNP | Brain natriuretic peptide – a neurohormone that assists in regulating BP and fluid volume.Used for diagnosis of Heart Failure
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| Stroke Volume | Amount of blood ejected from the ventricle with each heart beatNormal value in resting heart = 70 mL
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| Afterload | The amount of resistance/pressure that the chamber of the heart has to generate in order to eject blood out of the chamber
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| Ejection Fraction | % of end diastolic blood volume ejected from the ventricle with each heart beatNormal LVEF = 50-70%
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| Cardiac Output | Measurement of blood pumped by ventricle in L/minStroke volume x heart rate = cardiac output
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| Preload | Degree of stretch of cardiac muscle at the end of diastole = when the volume of blood has filled the ventricles, immediately prior to systole
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| Third Space Syndrome | An isotonic fluid volume deficit caused by fluid shift from the vascular space into areas not readily available to ECF, such as interstitial edema, bowel, pleural or peritoneal cavities
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| Contractility | Inotropic state of the myocardium = strength of the myocardial contraction
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| Myocardial Infarction Signs and symptoms | Chest pain, nausea, shortness of breath, diaphoresis
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| Congestive Heart FailureSigns and symptoms | Pulmonary Congestion, shortness of breath, increased respiratory rateIncreased heart rate, distended neck veins, edema
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| Ischemia | Lack of blood supply due to obstructed circulation
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| Homocysteine | An amino acid linked to the development of atherosclerosis
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| Calcium Channel Blocker – Why? Names? | These drugs are given to dilate the coronary arteries and reduce vasospasm, can also treat HTNCardizem, Verapamil
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| Inotropic agent Why? (or sympathomimetic) Name? | Increases contractility and increases left ventricular functionMilrinone(Primacor)
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| ACE Inhibitor – Why? Names? | Given to reduce afterload and prevent heart failure post MI, also treats HTN by decreasing circulating volumeLisinopril, captopril, capoten
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| Beta Blocker - Why? Names? | Decrease bp and HR resistance thereby decreasing the workload of the heart. Also decreases heart rate to allow adequate filling time of ventricles and coronary arteries.Atenolol(Tenormin),metaprolol (Lopressor, Toprol), propranolol (Inderal), Coreg
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| Nitrates – Why? Names? | To reduce preload and afterload, and dilate the coronary arteriesIV NitroglycerineNitrostatDo not administer if sbp<90 mmHg
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| Antianginal Cardiac MedsIV Morphine sulfate – Why? | Vasodilator, decreases afterload
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| Heparin | AnticoagulantsMonitor PTT
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| Coumadin | AnticoagulantMonitor PT (prothrombin time) and INR (international normalized ratio)
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| Aspirin | Antiplatelet Agent
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| Ticlid | Antiplatelet Agent
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| Plavix | Antiplatelet Agent
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