MEDSURG 2 HESI RATIONALES| VERIFIED SOLUTION

MEDSURG 2 HESI RATIONALES Cardiac The normal level of serum potassium is between 3.5-5.0 mEq/L (3.5 and 5.0 mmol/L). Elevated potassium levels greater than 6 mEq/L (mmol/L) can lead to muscle weakness and cardiac arrhythmias. The normal levels of serum phosphorus are between 2.4-4.4 mg/dL (0.78 and 1.42 mmol/L). The normal levels of serum calcium are usually between 8.6-10.2 mg/dL (2.15 and 2.55 mmol/L). The normal level of serum bicarbonate is between 22 and 26 mEq/L or mmol/L. These findings are not associated with the risk of developing muscle weakness and cardiac arrhythmias. Hypokalemia causes a flattening of the T wave on an electrocardiogram, as observed on the monitor, because of its effect on muscle function. Hypokalemia causes a depression of the ST segment. Hypokalemia causes a widening of the QRS complex. Hypokalemia does not cause a deflection of the Q wave. The consistency of the RR intervals indicates a regular rhythm. A normal P wave before each complex indicates the impulse originated in the sinoatrial (SA) node. Elevation of the ST segment is a sign of cardiac ischemia and unrelated to the rhythm. The number of complexes in a 6-second strip is multiplied by 10 to approximate the heart rate; normal sinus rhythm is 60 to 100 beats/min. Fewer than six complexes per 6 seconds equals a heart rate less than 60 beats/min. The QRS duration should be less than 0.12 seconds; the PR interval should be 0.12 to 0.2 second. Elevated U and flattened T waves reflect low serum potassium levels. U waves are not expected; they signify repolarization of the terminal Purkinje fibers and are seen with hypokalemia. T waves represent ventricular repolarization; T waves flatten with hypokalemia and peak with hyperkalemia. Changes in P waves reflect atrial depolarization and contraction activity; P waves flatten with hyperkalemia, not hypokalemia. Increased P-R intervals are related to a delay in conduction from the sinoatrial (SA) node to the ventricles and are not altered with hypokalemia. Trigeminy and bigeminy reflect ventricular irritability, not the serum potassium level. Cardiac irritability is the cardinal reason for PVCs. Atrial fibrillation is a type of dysrhythmia, not the cause of PVCs; the source of atrial fibrillation is the atrium, not the ventricles. Impending heart block type of dysrhythmia is associated with interference with the conduction system. Ventricular tachycardia is a type of dysrhythmia, not the cause of PVCs. A mild sedative is used because the client must be alert enough during the procedure to follow directions. A cardiac catheterization takes approximately 2 hours, not 15 minutes. The client remains on bed rest with the legs extended for 4 to 6 hours after the femoral method of entry. Blockages can be visualized during the procedure. Angina usually is caused by narrowing of the coronary arteries; the lumen of the arteries can be assessed by cardiac catheterization. Although pressures can be obtained, they are not the priority for this client; this assessment is appropriate for those with valvular disease. Determining the existence of congenital heart disease is appropriate for infants and young adults with cardiac birth defects. Measuring the oxygen content of various heart chambers is appropriate for infants and young children with suspected septal defects. Tingling indicates decreased arterial circulation to the extremity; it may be caused by an embolus distal to the arterial insertion site. Checking all pulses will help locate an embolus. Tingling sensations of an extremity are not related to bleeding, but rather to lack of circulation. Signs of inflammation are associated with thrombophlebitis; tingling is associated with arterial obstruction. Obtaining the temperature, pulse, respirations, and blood pressure will be done if there are systemic responses to compromised heart function; tingling in an extremity is a localized response. Bed rest with immobilization of the leg promotes coagulation and healing at the puncture site of the femoral artery. In the absence of bleeding and the presence of adequate fluid replacement, a cardiac catheterization does not cause orthostatic hypotension. Headache with disorientation is not expected after a cardiac catheterization. A small amount of radiopaque dye is injected (via the catheter) directly into the heart, where the blood dilutes it; it does not create a problem at the puncture site. Bed rest with the leg extended prevents trauma caused by hip flexion and provides time for the insertion site to heal. With the femoral approach, bed rest is maintained for several hours. Mild sedation is used for adult clients; the client is conscious. Postprocedural dietary restrictions are minimal, if any. A cardiac catheterization may cause cardiac irritability; therefore the client’s vital signs should be monitored every 15 minutes for 1 hour and then every 30 minutes for the next 2 hours until stable. The vital signs may then be monitored every 4 hours. When a brachial artery is used for catheter insertion, a low-Fowler, not supine, position usually is recommended because it promotes respirations. Keeping the client’s lower extremities in extension is not necessary. A brachial, not femoral, artery was used for the catheter insertion. Although administering the prescribed oxygen at 4 L/min via nasal cannula may be done, it is not the priority. The client’s response to the procedure is the priority. The purpose of a Holter monitor is to correlate dysrhythmias with the client’s reported activity. A microwave oven will have no effect on the Holter monitor and will not affect the results. The client should take nitroglycerin as needed and note it in the activities diary. It is unnecessary to know the client’s blood pressure and pulse rate every 2 hours during the test to correctly interpret results from a Holter monitor. This pulse rate increase indicates that activity tolerance is exceeded. Rest limits muscle contraction and oxygen demands; these allow the heart to return to its preactivity rate. Activity should be stopped, not continued. Though descending the stairs requires less energy than climbing, rest is essential to permit the heart rate to return to normal. Climbing but at a slower rate still constitutes activity, which increases the cardiac workload. The sternum must be depressed at least 2 inches (5 cm) to compress the heart adequately between the sternum and vertebrae and to simulate cardiac pumping action. Depression of less than this is ineffectual for an adult. Fatigue is caused by a lack of adequate oxygenation of body cells caused by a decreased cardiac output. As the cardiac output decreases, pulmonary congestion increases, resulting in pulmonary edema; coughing, especially when lying down, and blood-tinged sputum occur. Auscultation reveals crackles and rhonchi. Dyspnea is associated with pulmonary edema that occurs as cardiac output decreases and pulmonary congestion increases. Weight gain, not loss, occurs as fluid is retained by the kidneys. Fluid retention, not diuresis, occurs because of decreased circulation to the kidneys, resulting from decreased cardiac output. When ventricular fibrillation is verified, the first intervention is defibrillation; it is the only measure that will terminate this lethal dysrhythmia. Elective cardioversion delivers a shock during the R wave; because there is no R wave in ventricular fibrillation, the dysrhythmia will continue and death will result. Digitalis preparations are not used to treat ventricular dysrhythmias. If not already in place, an IV line should be inserted after the client is defibrillated. COPD causes destruction of capillary beds around the alveoli, interfering with blood flow to the lungs from the right side of the heart. As the heart continues to strain against this resistance, heart failure eventually results. Renal disease causes stress on the left side of the heart. Hypovolemic shock will not cause stress on the right side of the heart. Severe systemic infection probably will produce greater stress on the left side of the heart.