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19 Cards in this Set
- Front
- Back
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INITIAL DRUG THERAPY FOR HYPERTENSION
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*lifestyle changes
*diuretic (non thiazide)/beta blocker *ACE inhibitor/Ca+ channel blocker/ alpha andrenergic blocker *alpha adrenergic blocker + beta blocker |
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ANGINA
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Chest pain resulting from myocardial ischemia caused by inadequate blood and oxygen supply. It is caused by an imbalance between oxygen supply and demand. Causes include obstruction of coronary blood flow resulting from atherosclerosis, coronary artery spasm, or conditions increasing myocardial oxygen consumption.Clinical Manifestations: severity from mild indigestion, to a choking or heavy sensation in the upper chest that ranges form discomfort to agonizing pain. Usually felt deep in the chest behind the sternum. Often feels like tightness or a heavy, choking, or strangling sensation. (Substernal, crushing, squeezing pain, located in the chest, arm, shoulder, neck and back, should only last 5 minutes, pain should be relieved by nitro or rest), dyspnea, pallor, sweating, palpitations, tachycardia, dizziness, faintness, hypertension, and digestive disturbances.
Interventions: assess pain, provide bed rest, administer oxygen, administer nitroglycerin, obtain a 12 lead EKG and provide continuous cardiac monitoring. |
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MYOCARDIAL INFARCTION
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Occurs when myocardial tissue is abruptly and severely deprived of oxygen. If blood is not restored the ischemia can lead to necrosis of tissue. Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infracted area appears blue and swollen. After 2-3 months the necrotic area develops into a scar, which permanently changes the size and shape of the entire left ventricle. Obstruction of the left anterior descending artery results in anterior wall or septal MI, or both. Obstruction of the circumflex artery results in posterior wall MI or lateral wall MI. Obstruction of the right coronary artery results in inferior wall MI.Clinical Manifestations: pain, nausea and vomiting, diaphoresis, dyspnea, dysrhythmias, feelings of impending doom, fear, and anxiety, pallor, cyanosis, coolness of extremities.
Risk Factors: Atherosclerosis, CAD, elevated cholesterol levels, smoking, hypertension, obesity, physical inactivity, impaired glucose tolerance, and stress. • Diagnostic studies: Troponin Level; levels rise within 3 hours and can remained elevated for up to 7 days. Total creatine kinase level; level rises within four hours after the onset of chest pain, levels peak within 24 hours after the damage/death of cardiac tissue. CK-MB isoenzyme test; peak elevation occurs 18-24 hours after the onset of chest pain. Myoglobin, LDH, WBC, and EKG. |
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CONGESTIVE HEART FAILURE
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Inability of the heart to maintain adequate cardiac output to meet the metabolic needs of the body because impaired pumping ability. Diminished cardiac output results in inadequate peripheral tissue perfusion. Congestion of the lungs and periphery may occur.
♣ Compensatory mechanisms: increased HR, improved stroke volume, arterial vasoconstriction, sodium and water retention, and myocardial hypertrophy. Initially these mechanisms help restore cardiac output, however they eventually have a damaging effect. • Clinical Manifestations: Right sided HF; dependent edema, jugular distension, hepatomegaly, splenomegaly, anorexia, nausea, weight gain, nocturnal diuresis, swelling of the fingers and hands, increased BP (fluid volume excess), decreased BP (from pump failure). Left sided HF; signs of pulmonary congestion, dyspnea, tachypnea, crackles in the lungs, dry, hacking cough, paroxysmal nocturnal dyspnea, increased BP and decreased BP. |
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TROPONIN
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a.Troponin is composed of three proteins; troponin C, cardiac troponin 1, and cardiac troponin T
b. Troponin 1 has an especially high affinity for myocardial injury; it rises within three hours and persists for up to 7 days. troponin is a complex of three regulatory proteins that is integral to muscle contraction in skeletal and cardiac muscle, but not smooth muscle. Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. In a relaxed muscle, tropomyosin blocks the attachment site for the myosin crossbridge, thus preventing contraction. When the muscle cell is stimulated to contract by an action potential, calcium channels open in the sarcoplasmic reticulum and release calcium into the sarcoplasm. Some of this calcium attaches to troponin, causing a conformational change that moves tropomyosin out of the way so that the cross bridges can attach to actin and produce muscle contraction. |
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CALCIUM
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*Hypocalcemia can cause ventricular dysrhythmias, prolonged ST and QT intervals, and cardiac arrest. *Hypercalcemia can cause a shortened ST segment and widened T wave, atrioventricular block, tachycardia, bradycardia, digitalis hypersensitivity, and cardiac arrest.
cardiac muscle requires both extracellular calcium and sodium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in cardiac muscle cells is derived from the entry of sodium ions across the sarcolemma in a positive feedback loop. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur under normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which initiates contraction by allowing the contractile proteins, myosin and actin to associate through cross-bridge formation |
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DIGOXIN ANTIDOTE
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Fragment antigen binding(Fab) fragments that bind to digoxin (trade names Digibind and Digifab) as the antidote.
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HEPARIN ANTIDOTE
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Heparin poisoning is given protamine sulfate as the antidote
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WARFARIN ANTIDOTE
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Warfarin poisoning is given vitamin K phytomenadione and fresh frozen plasma as the antidote
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TREATMENT FOR BRADYCARDIA
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*Administer oxygen as prescribed
*Administer atropine to increase HR if prescribed *Be prepared to apply transcutaneous pacemaker if atropine does not increase HR sufficiently *Avoid additional doses of atropine sulfate because it can induce tachycardia |
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TREATMENT FOR ATRIAL FIBRILLATION
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*Administer oxygen
*Administer anticoagulants as prescribed because of the risk of emboli *Administer cardiac medications (amniodarone, adenosine, digoxin, magnesium) as prescribed to control the ventricular rhythm and assist in the maintenance of cardiac output *Prepare for cardioversion |
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PVC
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occur in normal people especially with intake of caffeine, nicotine, or alcohol. They are also caused by cardiac ischemia or infarction, increased workload, digitalis toxicity, hypoxia, acidosis, or hypokalemia.
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VENTRICULAR TACHYCARDIA
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*Amniodarone is the drug of choice for V tach if the patient is stable
*Cardioversion is the treatment of choice for V tach in an asymptomatic patient |
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VENTRICULAR FIBRILLATION
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*Amniodarone is the drug of choice for V tach if the patient is stable
*Cardioversion is the treatment of choice for V tach in an asymptomatic patient |
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COAGULATION PROCESS
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Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium (lining of the vessel). Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: proteins in the blood plasma, called coagulation factors or clotting factors, respond in a complex cascade to form fibrin strands which strengthen the platelet plug. Antiplatelet agents decrease the formation of the platelet plug by decreasing the responsiveness of the platelets to stimuli that would cause them to stick and aggregate on a vessel wall. Anticoagulants interfere with the normal coagulation process. They can affect the process at any step to slow or prevent clot formation. Low molecular weight heparins inhibit thrombus and clot formation by blocking factors Xa and IIa. They do not greatly affect thrombin, clotting, or the PT; therefore they have fewer adverse effects. Thrombolytics work to activate the natural anticlotting system, conversion of plasminogen to plasmin. The activation of this system breaks down the fibrin threads and dissolves any formed clot. Antihemophilic agents are replacement factors for the specific clotting factors that are genetically missing in the particular type of hemophilia. Hemostatic agents are used to stop bleeding.
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CHOLESTEROL
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Cholesterol is required to build and maintain cell membranes; it regulates membrane fluidity over a wide range of temperatures. The liver produces about 1 gram of cholesterol per day, in bile. Helps digest fats, is important for the absorption of the fat soluble vitamins, vitamins A, D, E, and K. It is the main precursor of vitamin D and of the steroid hormones.
< 200; Desirable level corresponding to lower risk for heart disease 200–240; Borderline high risk > 240 High risk |
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HDL
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With HDL (good) cholesterol, higher levels are better. Low HDL cholesterol (less than 40 mg/dL for men, less than 50 mg/dL for women) puts you at higher risk for heart disease. In the average man, HDL cholesterol levels range from 40 to 50 mg/dL. In the average woman, they range from 50 to 60 mg/dL. An HDL cholesterol of 60 mg/dL or higher gives some protection against heart disease.
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LDL
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The lower your LDL cholesterol, the lower your risk of heart attack and stroke. In fact, it's a better gauge of risk than total blood cholesterol. In general, LDL levels fall into these categories:
*Less than 100 mg/dL=Optimal *100 to 129 mg/dL=Near Optimal/ Above Optimal *130 to 159 mg/dL=Borderline High *160 to 189 mg/dL=High *190 mg/dL and above=Very High |
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STATINS (HMG-CoA REDUCTASE INHIBITORS)
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Statins act by competitively inhibiting HMG-CoA reductase, the first committed enzyme of the HMG-CoA reductase pathway. By reducing intracellular cholesterol levels, they cause liver cells to make more LDL receptors, leading to increased clearance of low-density lipoprotein from the bloodstream.
*Combining any statin with a fibrate, another category of lipid-lowering drugs, increases the risks for rhabdomyolysis *Consumption of grapefruit or grapefruit juice inhibits the metabolism of statins *This increases the levels of the statin, increasing the risk of dose-related adverse effects (including myopathy/rhabdomyolysis). *Administer the drug at bedtime because the highest rates of cholesterol synthesis occur between midnight and 5am |
