Rabbit Trails because there is no defined endpoint or
goal, but everything is connected and circles back again and again.
Ondansetron
(Zofran) is classified as an antiemetic. It blocks specific receptor sites
(selective 5-HT3 Antagonist), which are associated with nausea and vomiting in
the chemoreceptor trigger zone, centrally and at specific sites peripherally.
Zofran can be given IV, IM, and PO. The onset for PO is
30min, while the onset for IV is immediate. IV Zofran can be diluted in either
0.9 NS or in Dextrose 5%, it should be infused slowly over at least 30 seconds, and preferable 2—5min.
Adverse Effects: headache, diarrhea, and constipation. A
serious complication is EKG changes, specifically prolonged QT interval. (the
32mg dose of Zofran was voluntarily removed from the market for this reason)
EKG monitoring is recommended if the patient is suspected to have electrolyte
abnormality, bradycardia, or taking other drugs that can cause QT prolongation
such as Erythromycin, Methadone, and Haldol (there are many more). Out of
respect for potential cardiac arrhythmias, infuse Zofran slowly and keep an eye
on the EKG monitor watching for rhythm changes. (Karch, 2011;
Medscape, 2013).
Zofran is most effective if given prophylactically, once
the N/V chemoreceptors have been triggered the medication is not nearly as
effective. Consider promethazine (Phenergan) which is more effective at curbing
N/V once triggered.
Prolonged QT
interval
The QT interval represents the time in between ventricular
depolarization, QRS wave (ventricular systole) and ventricular repolarization,
the T wave. This time period should be no longer than 0.43—0.45 seconds, (two
big boxes on the EKG strip).
*Because the QT interval is rate dependent an accurate
value must be calculated through the Bazett formula: QT corrected =
QT/square root of RR interval. It is also possible to get close by considering
the QT interval to be 0.4 seconds at a HR of 70, and then subtracting 0.02
seconds for every 10 beat increase in HR, or adding 0.02 seconds for every 10
beat decrease in HR.
During the QT interval the ventricles are actively
contracting and do not relax until the end of the T wave when enough potassium
(K+) ions have left the myocytes; this means that the QT interval can
be used as a gauge of the length ventricular systole. Because of K+
crucial role in repolarization, a long QT interval is often caused by an
electrolyte imbalance, (hypokalemia, hypomagnesemia), or a genetic abnormality
in the ion pump, or medication that effects the ion pumps or electrolyte
levels. The discovery of an individual with long QT syndrome is almost always
only found upon review of an EKG which usually doesn’t happen until the
individual presents with a cardiac event such as syncope, aborted cardiac
arrest, or sudden death (Medscape, 2013).
A prolonged QT
interval, whether it is congenital, drug induced, or pathologic in nature are
vulnerable to dangerous, perhaps deadly, rapid ventricular rhythms (Dubin,
2000).
(Gupta et al., 2007) |
Torsades de
Pointes (Polymorphic Ventricular Tachycardia due to prolonged QT interval)
Torsades de Pointes (TdP) means the twisting of the
points, it is one of the most common abnormal rhythms that is a result of a QT
prolongation. Treatment for (TdP) that does not spontaneously revert is non
synchronized defibrillation for a hemodynamic unstable patient, IV MgSO4,
and the discontinuation of any QT prolonging agent. If the patient is not
hemodynamically unstable then a 2mg bolus of MgSO4 is recommended
regardless of serum level; K+ levels need to be returned to or remain
in the high end of the normal range 4.5-5mmol/L). Short term management can be
achieved with HR pacing >70 due to the prolonging effect that bradycardia
has on the QT interval, long term management involves avoidance of offending
agents, tight electrolyte control, and possibly a pacemaker. (Gupta et al., 2007)
If someone accidently gives way too much mag sulfate,
what should be done?
Reference:
Dubin, D. (2000). Rapid interpretation of
EKG's: an interactive course. Cover Publishing Company.
Gupta, A., Lawrence, A. T., Krishnan, K.,
Kavinsky, C. J., & Trohman, R. G. (2007). Current concepts in the
mechanisms and management of drug-induced QT prolongation and torsade de
pointes. American heart journal, 153(6), 891-899.
Karch, A. M. (Ed.). (2011). 2011 Lippincott's
nursing drug guide. Lippincott Williams & Wilkins.
Medscape. (2013) Reference section accessed
for Ondansetron and Long QT Syndrome. Retrived 11/04/13 from: http://reference.medscape.com/nurses