Biomedical Engineering Reference
In-Depth Information
or coarse. Fine ventricular fibrillation may appear similar to
asystole in some leads. Orthagonal leads (lead I and aVF,
lead II and aVL) should be checked to differentiate asystole
from fine ventricular fibrillation, since treatment of asystole
with electrical defibrillation may be detrimental. Coarse
ventricular fibrillation may be more easily converted than
fine fibrillation ( Ford and Mazzaferro, 2005 ). Conversion of
asystole or PEA to ventricular fibrillation may be consid-
ered an intermediate step in resuscitation and a positive
outcome of basic life support measures in CPCR. Once
ventricular fibrillation is recognized, direct current defi-
brillation is considered the treatment of choice. Chest
compressions should be maintained while the defibrillator is
being prepared. To assure safety of personnel all members
of the CPCR team must be trained in the use of electrical
defibrillation devices prior to use. It is important that
contact electrode paste or water-soluble gel such as KY
Jelly be used rather than ultrasound gel or alcohol. It is
recommended that one shock of 2
vasopressin in humans have not been shown to differ from
those of epinephrine in cardiac arrest, one dose of vaso-
pressin may replace either the first or second dose of
epinephrine in the treatment of cardiac arrest ( Neumar
et al., 2010 ). In veterinary medicine, the most common
arrest arrhythmia is asystole and the use of vasopressin has
increased because it has shown efficacy in treating this
arrhythmia ( Plunkett and McMichael, 2008 ). Another
benefit of the use of vasopressin is that it retains its activity
during acidosis, which is often experienced during CPA.
Epinephrine loses much of its pressor effects in acidotic
and hypoxic environments ( Zhong and Dorian, 2005 ). The
currently recommended dosage of vasopressin in veterinary
medicine is 0.8 U/kg i.v., repeated every 3
5 minutes or
e
until ROSC.
Atropine is an anticholinergic drug that decreases vagal
tone and that may decrease the progression of bradycardia
to asystole in the arresting patient. It increases sinoatrial
node automaticity and atrioventricular conduction, which
increases heart rate. As a vagolytic, it is most effective in
the treatment of vagal-induced asystole. Atropine is indi-
cated in patients with bradycardia and imminent arrest. The
dose of atropine in veterinary medicine is 0.1 mg/kg s.q. or
0.05 mg/kg s.q., i.m., i.v. ( Hawk et al., 2005 ). It can be
administered immediately after epinephrine and can be
continued every 2
e
4 joules/kg (monophasic
defibrillator) or 1
2 joules/kg (biphasic defribrillator) be
given followed immediately by chest compressions. Chest
compressions should be given for 2 minutes immediately
after defibrillation, prior to reassessment of rhythm on the
ECG machine ( Neumar et al., 2010 ).
In CPCR, pharmacological intervention employs the
use of drugs that increase myocardial contractility,
increase peripheral vasoconstriction, increase heart rate,
and treat arrhythmias. This section does not contain an
exhaustive list of these medications, but offers general
information on select treatments that will allow the clini-
cian to develop a plan for CPCR and to stock the phar-
macy and crash cart.
Epinephrine HCl is a mixed adrenergic agonist that
acts on alpha and beta receptors. It is one of the most
effective adrenergic drugs used for CPCR and is indicated
for the treatment of asystole. It has positive inotropic (force
of contraction) and chronotropic (rate of contraction)
effects as well as potent vasoconstrictor effects. Epineph-
rine causes an increase in systemic vascular resistance and
arterial blood pressure, which result in shunting of blood to
the brain, heart, and lungs. The optimum dose of
epinephrine is unknown. The current recommended veter-
inary dose range is less than in previous recommendations
and is 0.01
e
5 minutes with epinephrine during
asystole while basic life support procedures are in progress
( Ford and Mazzaferro, 2005 ). In human medicine, atropine
has recently been removed from cardiac arrest algorithms
by the American Heart Association because available
evidence suggests that routine use of atropine during PEA
or asystole is unlikely to have a therapeutic benefit
( Neumar et al., 2010 ).
Amiodarone and Iidocaine are class III and class Ib
antiarrhythmic agents respectively. Amiodarone prolongs
both action potential duration and refractory period. Lido-
caine stabilizes cell membranes by sodium channel
blockade. Amiodarone and lidocaine are indicated for the
treatment of atrial fibrillation, narrow-complex supraven-
tricular tachycardia, ventricular tachycardia, and refractory
ventricular fibrillation that is unresponsive to compres-
sions, defibrillation, and vasopressor administration
( Plunkett and McMichael, 2008 ). According to the 2010
AHA Guidelines, amiodarone is preferred over lidocaine
since lidocaine has shown no proven efficacy in cardiac
arrest ( Neumar et al., 2010 ). Lidocaine should not be used
to treat ventricular fibrillation when electrical defibrillation
is planned, because it may make electrical defibrillation
more difficult by increasing the defibrillation threshold and
decreasing myocardial automaticity ( Ford and Mazzaferro,
2005 ). Lidocaine has been beneficial in treating cases of
ventricular arrhythmia after resuscitation and can be
considered if amiodarone is not available. The dosage for
lidocaine is 2.0
e
5 minutes or
until ROSC ( Ford and Mazzaferro, 2005; Plunkett and
McMichael, 2008 ). If no response is seen to repeated
epinephrine doses, the dose can be increased to 0.1 mg/kg
i.v. or vasopressin can be alternated (see below).
Vasopressin is a pressor agent used in veterinary
medicine to support CPCR. It induces marked peripheral,
coronary and renal vasoconstriction, and improves cerebral
and coronary perfusion. Vasopressin is a nonadrenergic
endogenous pressor peptide that stimulates specific smooth
muscle receptors of the vasculature. Because the effects of
0.02 mg/kg i.v. repeated every 3
e
e
4.0 mg/kg i.v. or i.o. (California National
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