Page 400 - Clinical Small Animal Internal Medicine

368 Section 5 Critical Care Medicine

The rationale for the use of vasopressor therapy is conditions that would be likely to increase vagal tone. A
VetBooks.ir grounded in the fact that cardiac output during CPR is a dose of 0.04 mg/kg IV is recommended as higher doses
are more likely to result in severe tachycardia and subse-
fraction of that during spontaneous circulation, making
it imperative that the limited cardiac output is directed
ROSC is achieved. Repeated dosing of atropine is unlikely
to the organs that need it most. Therefore, the provision quently, increased myocardial oxygen consumption if
of vasopressors is intended to increase peripheral vascu- to be of benefit (assuming actions directed at the under-
lar resistance, forcing more blood into the central circu- lying cause have been taken) and should be considered
lation and subsequently improving the perfusion of vital carefully due to the potential for severe tachycardia if
structures (i.e., brain and heart). resuscitation is successful.
Stimulation of the alpha‐1 receptor results in periph- Corticosteroids currently have no place in the CPR
eral vasoconstriction whereas stimulation of the beta‐1 algorithm and their use is not recommended. Given the
receptor increases both inotropy and chronotropy. While lack of documented improvement in outcome and the
epinephrine is a balanced alpha‐ and beta‐adrenergic known deleterious side‐effects, especially in patients
agonist, its utility during CPR comes primarily from its with perfusion impairment, this is unlikely to change.
action at the alpha‐1 receptor. In fact, the effects of The administration of ALS drugs by intravenous or
beta‐1 stimulation may be detrimental as they can lead intraosseous routes (interchangeable in the context of
to increased myocardial oxygen consumption and pre- CPR) is always preferred to the intratracheal route. If IV
dispose to arrhythmias if ROSC is achieved. The best or IO access is not available or not possible then intratra-
dose for epinephrine use during CPR has been a topic of cheal administration of drugs can be considered while
debate for many years, with mixed evidence. High‐dose efforts to attain venous or intraosseous access are con-
epinephrine (0.1 mg/kg IV) has been shown to result in tinued. If this route is utilized, a long catheter should be
slightly higher rates of ROSC but has not been shown to advanced through the endotracheal or tracheostomy
confer a survival benefit. Based on the lack of docu- tube to the level of the carina or beyond. Drugs should be
mented improved survival, the use of low‐dose epineph- diluted with saline or sterile water. The optimal dosing of
rine (0.01 mg/kg) is currently recommended early in drugs for intratracheal administration is not established
CPR efforts, with high‐dose epinephrine being reserved but doses up to 10 times the normal dose have been rec-
for cases of prolonged CPR. Epinephrine should be ommended. Once established, the IV or IO route should
administered following the first cycle of BLS and then be used for all subsequent drug administrations.
following every other cycle. The need for rapid volume expansion with IV crystal-
Adrenergic receptors have been demonstrated to be loid or colloid solutions during CPR is dependent on the
less responsive in acidotic conditions, such as those underlying cause of CPA. Animals suffering CPA from
found during CPA, making an alternative drug that is not severe hemorrhage or hypovolemia should be aggres-
dependent on catecholamine receptors an appealing sively resuscitated with IV fluids to reestablish normal
option. Vasopressin acts on the V1 receptors of vascular circulating volume. Since coronary perfusion pressure is
smooth muscle cells independent of the alpha‐1 recep- determined by the difference between diastolic aortic
tor. In addition, it maintains its efficacy in the face of aci- blood pressure and right atrial pressure, care should be
dosis. Due to the lack of adrenergic effects, vasopressin taken to prevent overresuscitation. IV fluids accumulate
does not cause increases in inotropy or chronotropy, in the venous compartment, increasing the central
minimizing its impact on myocardial oxygen consump- venous and right atrial pressure and consequently reduc-
tion. The human literature regarding the usefulness of ing coronary perfusion pressure. In general, animals that
vasopressin in CPR is mixed, with promising results in were euvolemic or hypervolemic (congestive heart fail-
small trials but failure to demonstrate any clear advan- ure) do not require volume expansion during CPR and
tage over epinephrine in larger metaanalyses. The suc- routine use of IV fluids during CPR on these patients is
cessful use of vasopressin in CPR has been reported in not recommended.
the veterinary literature. Administration of vasopressin Electrolyte and acid–base disturbances are common
(0.8 U/kg IV) in place of or in conjunction with epineph- during CPA. Severe acidemia occurs frequently during
rine may be considered, with subsequent doses adminis- CPA, especially later in the course of resuscitation, and
tered following every other cycle of BLS. can result in vasodilation, predisposition to arrhythmias,
The use of atropine in ALS is somewhat unique in that and impaired neurologic function. The administration of
atropine is a parasympatholytic drug intended to amelio- 1 mEq/kg sodium bicarbonate can be considered in pro-
rate high vagal tone during cardiac arrest rather than longed instances of CPA lasting 10–15 minutes. The
directly stimulating catecholamine receptors. The use of most common electrolyte disturbances during CPA
atropine should be considered in animals that have include hyperkalemia and hypocalcemia. Because of the
asphyxia‐induced cardiac arrest or other co‐morbid lack of documented improvement in outcomes and the