HESI MED RATIONALES

Hesi MEDSURG 2 RATIONALES   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. Heart block is the primary indication for a pacemaker because there is an interference with the electrical conduction of impulses from the atria to the ventricles of the heart. The primary treatment for angina is medication; angina is not an indication for a pacemaker. The primary treatment for chest pain is medication; chest pain is not an indication for a pacemaker. The primary treatment for tachycardia is medication; tachycardia is not an indication for a pacemaker Cessation of the blood flow that normally carries oxygen to the myocardium results in pain because of ischemia of myocardial tissue. Myocardial infarction does not involve compression of the heart. The release of myocardial isoenzymes is an indication of myocardial damage; this does not cause myocardial pain. Vasodilation will increase perfusion and contribute to pain relief, not cause myocardial pain. The presence of a P wave before each QRS complex indicates a sinus rhythm; a heart rate greater than 100 regular beats per minute is referred to as tachycardia. Atrial fibrillation has no well-defined P waves, there are 350 or more beats per minute, there are random ventricular beats, and the rhythm is irregular. Ventricular fibrillation is irregular and shows no PQRST configurations. A first-degree atrioventricular block pattern has a prolonged PR interval and is regular. Dysrhythmias are abnormal and are associated with acute or chronic pathologic conditions. An equal apical and radial pulse is expected; the radial pulse reflects ventricular contractions. The expected range in adults is 60 to 100 beats per minute. An apical rate obtainable at the fifth intercostal space and midclavicular line are the anatomical landmarks for locating the apex of the heart; they are unaffected by aging. Sinus tachycardia is regular rhythm but at a rate higher than 100 beats per min. The client may experience shortness of breath, palpitation, fatigue, and dizziness. Atrial flutter (saw-tooth waves) arises from a conduction defect in the atrium resulting in a rapid atrial rate, usually between 200 to 350 times/minute. The atrial rate is faster than the atrioventricular (AV) node can conduct so that not all atrial impulses are conducted through to the ventricle. Sinus bradycardia is a regular rhythm but at a rate lower than 60 beats per minute. Atrial fibrillation is an irregular rhythm that is a result of multiple irritable foci firing in the atria and bombarding the AV node with irregular conduction of impulses through the node. Cardioversion involves administration of precordial shock, which is synchronized with the R wave to interrupt the heart rate. It is used for atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia with a pulse when pharmaceutical preparations fail. The heart is stopped by the electrical stimulation, and it is hoped that the sinoatrial (SA) node will take over as pacemaker. Because there are no R waves in a cardiac standstill, defibrillation and not cardioversion should be done. Premature ventricular complexes suggest an irritable myocardium and generally respond to antidysrhythmic agents. Pacemaker impulses are represented by a spike (letter B), which should be followed by a QRS complex. Pulsus paradoxus is present in cardiac tamponade. Blood in the pericardial sac compresses the heart so the ventricles cannot fill; this leads to a rapid, thready pulse and muffled heart sounds. The increased venous pressure associated with cardiac tamponade causes jugular vein distention. Tamponade causes hypotension, not hypertension, and a narrowed pulse pressure. As the heart becomes more inefficient, there is a decrease in kidney perfusion and therefore a decrease in urine output. Ventricular fibrillation reflects a rapid, feeble twitching/quivering of the ventricles; it has an irregular sawtooth configuration with unidentifiable PR intervals and QRS complexes. Atrial flutter is characterized by an atrial rate of 200 to 350 beats per min and a ventricular rate of approximately 150 beats per min; flutter to ventricular responses usually are 2:1, 3:1, or 4:1. Atrial fibrillation is characterized by an atrial rate of 350 to 600 beats per min and a variable ventricular rate; the rhythm is grossly irregular. Ventricular tachycardia has a rate of 140 to 200 or even 250 beats per min; the rhythm is usually regular but may vary. P waves are unidentifiable. PR intervals are unmeasurable. QRS complexes are wide and bizarre. Third degree block often is called complete heart block because no atrial impulses are conducted through the AV node to the ventricles. In complete heart block, the atria and ventricles beat independently of each other because the AV node is completely blocked to the sinus impulse and is not conducted to the ventricles. One hallmark of third degree heart block is that the P waves have no association with the QRS complexes and appear throughout the QRS waveform. In first degree AV block, a P wave precedes every QRS complex, and every P wave is followed by a QRS. Second-degree AV block type I, also called Mobitz I or Wenckebach heart block, is represented on the ECG as a progressive lengthening of the PR interval until there is a P wave without a QRS complex. Second degree AV block type II (Mobitz II) is a more critical type of heart block that requires early recognition and intervention. There is no progressive lengthening of the PR interval, which remains the same throughout with the exception of the dropped beat(s). Also called Mobitz I or Wenckebach heart block, second degree AV block type I is represented on the ECG as a progressive lengthening of the PR interval until there is a P wave without a QRS complex. In first degree AV block, a P wave precedes every QRS complex, and every P wave is followed by a QRS. Second degree AV block type II (Mobitz II) is a more critical type of heart block that requires early recognition and intervention. There is no progressive lengthening of the PR interval, which remains the same throughout with the exception of the dropped beat(s). Third degree block often is called complete heart block because no atrial impulses are conducted through the AV node to the ventricles. In complete heart block, the atria and ventricles beat independently of each other because the AV node is completely blocked to the sinus impulse and is not conducted to the ventricles. One hallmark of third degree heart block is that the P waves have no association with the QRS complexes and appear throughout the QRS waveform. Pulse should be immediately assessed because a lead or electrode coming off may mimic this dysrhythmia. Asystole is characterized by complete cessation of electrical activity. A flat baseline is seen, without any evidence of P, QRS, or T waveforms. A pulse is absent, and there is no cardiac output; cardiac arrest has occurred. Once confirmed, Basic Life Support (BLS) and Advanced Cardiovascular Life Support (ACLS) protocols are initiated for asystole. Defibrillation is part of the ACLS protocol for ventricular fibrillation. The cardiac cycle begins with an impulse that is generated from a small concentrated area of pacemaker cells high in the right atria called the sinus or SA node. The impulse quickly reaches the AV node located in the area called the AV junction, between the atria and the ventricles. Here the impulse is slowed to allow time for ventricular filling during relaxation or ventricular diastole. The electrical impulse then is conducted rapidly through the bundle of His to the ventricles via the left and right bundle branches. The bundle branches divide into smaller and smaller branches, finally terminating in tiny fibers called Purkinje fibers that reach the myocardial muscle cells or myocytes. SA, AV, BUNDLE OF HIS, BUNDLE BRANCHES, PURKINJE FIBERS The treatment of ventricular tachycardia depends on the presence of a pulse. Therefore checking for a pulse is the first priority for the nurse. The nurse must rely on client assessment, not solely on the monitor. Cardiac compressions would not be initiated if there was a pulse. Administering oxygen via an ambu bag would only occur if the client was not breathing. The client is not automatically defibrillated. Cardioversion is recommended for slower ventricular tachycardia. Irreversible brain damage will occur if a client is anoxic for more than four minutes. The age of the client does not affect the response by the arrest team. The earlier heart rate is of minimal importance; the rhythm is more significant. Although a variety of emergency medications must be available, their administration is prescribed by the healthcare provider Troponin is the biomarker of choice for a myocardial infarction. Troponin, specifically subtypes cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI), reflects myocardial muscle protein released into circulation soon after injury. Troponin increases as quickly as CK and remains increased for 2 weeks. Although myoglobin is one of the first cardiac markers to increase after a myocardial infarction (MI), it lacks cardiac specificity. Homocysteine is produced when proteins break down, but it is more indicative of cardiovascular disease than a myocardial infarction. CK isoenzyme levels, especially the creatine phosphokinase (MB) subunit, begin to increase in 3 to 6 hours, peak in 12 to 24 hours, and are increased for 48 hours after the occurrence of the infarct. Although reliable in assisting with an early diagnosis of MI, it is not as sensitive or specific as the troponin test. Cardiac arrest causes decreased tissue perfusion, which results in ischemia and cardiac insufficiency. Cardiac insufficiency causes anaerobic metabolism, which leads to lactic acid production. Fat-forming ketoacids occur in diabetes. An irregular heartbeat does not cause acidosis. Too much sodium bicarbonate causes alkalosis, not acidosis. Tea contains caffeine, which stimulates catecholamine release and acts as a cardiac stimulant; tea should be avoided. Hot cocoa contains chocolate, which contains caffeine; it stimulates catecholamine release and acts as a cardiac stimulant. Cocoa should be avoided. The chocolate in chocolate pudding has a high caffeine content, which may stimulate catecholamine release and act as a cardiac stimulant; chocolate should be avoided. Red meat does not stimulate the myocardium; however, it should be decreased or eliminated if serum cholesterol levels are elevated. Club soda does not contain caffeine and does not stimulate the myocardium; however, most club sodas contain sodium, which promotes fluid retention and should be avoided by a client with a cardiac condition. Small, frequent intake of juices, broth, or milk will provide gradual replacement of both fluid and electrolytes without overloading the intravascular compartment. Water does not supply the necessary electrolytes, and hyponatremia may result. No data are presented to indicate that the client cannot take fluids orally; an NG tube is not necessary when the client can take fluids by mouth. A rapid IV infusion of an electrolyte and glucose solution is unsafe; rapid correction of a fluid and electrolyte imbalance is dangerous. Therapy should promote a gradual correction. These symptoms are associated with compromised arterial perfusion. A thrombus is a complication of a femoral arterial cardiac catheterization and must be suspected in the absence of a pedal pulse in the extremity below the entry site. A circulatory assessment should be conducted first; the primary healthcare provider may or may not need to be notified immediately concerning the results of the assessment. Taking the client’s blood pressure is unnecessary; the symptoms indicate a local peripheral problem, not a systemic or cardiac problem. These symptoms are not expected. A decreased urinary output reflects a decreased cardiac output; immediate action is indicated if urinary output decreases. Although anxiety may occur, the priority is to monitor urinary output, which reflects cardiac effectiveness. Cardiac enzyme results do not reflect effectiveness of cardiac contractions; they reflect tissue damage. Although the presence of crackles (rales) will indicate pulmonary edema, it will not determine the effectiveness of ventricular contractions. The primary healthcare provider must be notified immediately so that anticoagulation therapy can be instituted. Applying a warm, moist compress to the incision site is inappropriate because it may promote bleeding; if phlebitis occurs, then warm, moist compresses may be applied. Increasing the intravenous fluid rate by 20 mL hourly will not resolve an embolus. Although monitoring vital signs is appropriate, it is an insufficient intervention; the healthcare provider must be notified so that anticoagulants can be prescribed. Musculoskeletal Muscle spasms are caused by involuntary muscle contractions after fractures. Thermotherapy reduces muscle spasm. Therefore client C with muscle spasms is instructed to undergo this treatment. Client A with a foot drop is advised to keep the foot in a neutral position. Client B with contractures is advised to change positions frequently. Client D with muscle atrophy is advised to practice an isometric muscle-strengthening exercise regimen. The physiologic changes of the musculoskeletal system related to aging are slowed movements, cartilage degeneration, increased bone prominence, decreased bone density, and decreased range of motion. The Achilles tendon attaches the calf muscle to the heel. An inflammation to the Achilles tendon, Achilles tendonitis, may lead to pain in the posterior leg upon movement that worsens at rest. A frequent, audible crackling sound with palpable grating that accompanies movement is crepitus. Chronic joint inflammation and destruction resulting in stiffness is ankylosis. A contracture is a condition in which the muscles and joints become rigid due to fibrosis of the supporting soft tissues. Loss of height and deformity and shortening of the trunk are common in older adults due to vertebral compression and degeneration. Rigidity in the neck, shoulders, back, hips, and knees increases with age due to loss of elasticity in ligaments, tendons, and cartilage. A decline in fine-motor dexterity occurs in the older adult due to slow impulse conduction along motor units. Range of motion (ROM) is limited in the older adult due to cartilage erosion, increased friction between the bones, and overgrowth of bone around joint margins. Spastic gait is a musculoskeletal abnormality, caused by cerebral palsy, that results in short steps and dragging of the foot. Torticollis is a twisting of the client’s neck to one side. Pes planus, also called flatfoot, is an abnormal flatness of the sole and arch of the foot. Steppage gait is an increase in hip and knee flexion to clear the foot from the floor; footdrop will be evident in the affected client. Scoliosis is a lateral S-shaped curvature of the thoracic and lumbar spine. A client with scoliosis has unequal shoulder and scapular height when observed from the back. Kyphosis is an excessive outward curvature of the spine. Torticollis is the twisting of the neck in an unusual position to one side. Pes planus is an abnormal flatness of the sole and arch of the foot. Crepitation, a cracking and popping sound of the joint, is not a normal assessment finding. Muscular atrophy, wasting of the muscle, is also an abnormal finding. Spine tenderness on palpation of spine, joints, or muscles is not a normal finding on physical assessment of the musculoskeletal system. Muscle strength of 5 indicates active movement of the muscle against full resistance without evident fatigue, or normal muscle strength. Full range of motion in the joints is a normal finding. When rating muscle strength, grade 2 indicates complete range of motion with gravity eliminated. Grade 1 indicates no joint motion and slight evidence of muscle contractility. Grade 3 is indicated by complete range of motion against gravity only. If there is complete range of motion against gravity with some resistance, then the grade would be 4. Client C has pes planus; symptoms of this condition include an abnormal flatness of the sole and arch of the foot. Client A has Achilles tendonitis, which is characterized by pain in the posterior leg. Client B has atrophy, which is characterized by a flabby appearance of the muscle. Client D has myalgia, which is characterized by general pain and tenderness in the muscles. A muscle strength rating of 2 signifies a poor ROM. This rating is given if a client completes ROM with gravity eliminated. A rating of 3 is given if the client has a complete range of motion against gravity. A rating of 1 indicates no joint motion and slight evidence of muscle contractility. A rating of 4 is given to a client who has the ability to complete ROM against gravity with some resistance. Also known as knock knees, genu valgum is a condition in which the knees are poorly aligned. The knee joint should be assessed for any abnormalities or presence of effusion. The hip joint is assessed to determine mobility and to find any hip pain experienced in the groin or pain that radiates to the knees. The temporomandibular joint is palpated to determine any weakness or pain in the face. The metacarpophalangeal joint is palpated to assess hand function based on the range of motion. A muscle strength rating of 3 indicates that the client has a fair ROM and can complete ROM against gravity. No evidence of muscle contractility indicates that there is zero muscle strength. No joint motion and slight evidence of muscle contractility indicates trace muscle strength, which is a rating of 1. An ability to complete ROM against gravity with some resistance indicates good muscle strength, a rating of 4. Chinese Americans have an increased incidence of osteoporosis because they have shorter and smaller bones with lower bone density. Irish Americans have taller and broader bones than other Euro-Americans. African Americans have a decreased incidence of osteoporosis. Egyptian Americans are shorter in stature than Euro-Americans and African Americans. Festinating gait, when the neck, trunk, and knees flex when the body is rigid, in client A indicates Parkinson disease. A leg length discrepancy of more than one inch due to arthritis or fracture may lead to the short-leg gait in client B. Neurogenic disorders such as cerebral palsy and hemiplegia may lead to the spastic gait in client C, which is manifested by jerky, uncoordinated, and cross-knee movement. Neurogenic disorders such as peroneal nerve injury and paralyzed dorsiflexor muscles may lead to the steppage gait in client D; this is manifested by increased hip and knee flexion to clear the foot from the floor and foot-dropping while walking.