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MEDSURG 2 HESI RATIONALES
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MEDSURG 2 HESI 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.
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