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385
arrest. This list is not exhaustive, and additional adjuncts may be considered based
on patient indication.
Magnesium sulfate is an adjunctive agent for patients experiencing polymorphic
VT with a long QT interval (i.e., torsades de pointes) with or without hypomagnesemia [32]. In the setting of cardiac arrest, magnesium should be administered as an
initial 2g IV/IO bolus over 1–2min [33]. Preparations of magnesium sulfate may
vary. If using concentrated magnesium sulfate vials, doses should be diluted in
10mL of dextrose 5% water [34]. Additional bolus doses should be considered until
the cessation of torsades de pointes. Total dose recommendations vary, but 6g is
widely considered the maximum [34]. Serum magnesium levels are generally not
followed in the cardiac arrest setting, but elevated serum concentrations
(>3.5mmol/L) may place patients at risk for toxicity [33]. After cessation of the
inciting rhythm, magnesium and potassium should be replete appropriately to maintain normal serum levels. A medication administration record review should also be
conducted by a pharmacist to ensure that the rhythm was not incited by a pharmacologic agent.
Hyperkalemia is a common etiology for cardiac arrest. Hyperkalemia can initially result in peaked T waves on an echocardiogram, progressing to loss of P
waves, widening of the QRS complex, and ultimately resulting in asystole [35, 36].
A review of recent serum labs or labs available on an arterial blood gas should take
place when considering the cause of the cardiac arrest. If hyperkalemia is present
(>5.5mEq/L), treatment should be initiated. Calcium should be immediately administered to stabilize the cardiac membrane and reduce the risk of ventricular brillation [35]. Calcium chloride 10% 1g administered as an IV/IO bolus is the preferred
modality. Calcium chloride is preferred as the elemental calcium content is approximately three times higher than calcium gluconate. If calcium chloride is unavailable, calcium gluconate can also be considered. Calcium gluconate 1–2g IV/IO
should be administered over 5–10min [37]. Higher doses may be preferable due to
the lower elemental calcium content. It is important to note that in the absence of a
compelling indication (hyperkalemia or hypocalcemia), administration of calcium
chloride had no benet on ROSC achievement [38]. After administration of calcium, the focus should be on shifting potassium intracellularly. The most effective
treatment modality is IV insulin. Insulin has a rapid onset of action (<15min) and
can reduce serum potassium by 0.6–1.2mmol/L within 1h [39, 40]. Insulin dosing
strategies are variable. Historically, 10 units of regular insulin administered with
25g of dextrose 50% (if serum blood glucose <250mg/dL) was considered standard of care; however, this frequently resulted in hypoglycemic episodes, which
have been correlated with increases in mortality [40]. Lower insulin dosing strategies have been evaluated to reduce the frequency of hypoglycemia. A single-center
retrospective study evaluated 0.1units/kg of insulin (maximum 10units) in addition
to dextrose administration. Rates of potassium reduction were similar (1.24 vs.
1.35mmol/L) within 1h, but hypoglycemic events were reduced (12 vs. 27%) [41].
A meta-analysis evaluated reduced insulin dosing strategies (5units, 0.1 unit/kg,
<10units) in comparison to the standard 10units for efcacy in potassium reduction
and hypoglycemia rates. There was no difference seen in potassium reduction (mean
386
A. M. Esteves
difference −0.02mmol/L, 95% CI, −0.11–0.07), but there was a reduction in hypoglycemia events (OR 0.55, 95% CI 0.43–0.69) and severe hypoglycemia (OR 0.41,
95% CI 0.27–0.64) [42]. A common prescribing/administration error with insulin
for hyperkalemia is administration via the subcutaneous route. Insulin absorption
and distribution are less predictable via this route and will impact the efcacy and
rapid potassium reduction required for hyperkalemia correction. Lastly, potassium
can be impacted by acidosis, causing more extracellular potassium to be present. In
prolonged codes, acidosis is common. Sodium bicarbonate administration may be
considered. It is estimated that potassium decreases by 0.3mEq/L for every 0.1 unit
increase in pH above normal [35]. Despite this knowledge, administration of sodium
bicarbonate in this setting is controversial. Sodium bicarbonate administration
resulting in hyperkalemia reduction has a long onset. The exact onset in the code
setting is unknown. Furthermore, the most benet in potassium reduction has been
seen in patients with a pH <7.35, serum bicarbonate <17mmol/L, serum potassium
>6mmol/L, and sodium bicarbonate doses >120mEq [43]. The AHA only recommends sodium bicarbonate 50 mEq IV administered over 5 min, so the ultimate
efcacy of this intervention remains unclear [35]. From an administration standpoint, pharmacists should avoid administration of sodium bicarbonate and calciumcontaining products in the same line in the absence of signicant ushing, as
precipitation can occur [44].
Beyond hyperkalemia, administration of sodium bicarbonate is frequently considered and was recommended in prior AHA versions of the guidelines. The current
AHA algorithm only recommends sodium bicarbonate in the setting of tricyclic
antidepressant (TCA) overdoses [6]. Sodium bicarbonate provides a number of benets in this overdose setting, which is beyond the scope of this chapter, but should
be administered as an IV bolus of 8.4% 1–2 mEq/kg [45]. Sodium bicarbonate
administration in the absence of hyperkalemia or overdose during cardiac arrest has
not improved survival or neurologic outcomes as noted in numerous publications
[46–48].
Although more prevalent in OHCA, opioid-induced/suspected cardiac arrest
may prompt discussion of naloxone administration. One retrospective cohort study
evaluated the use of naloxone in cardiac arrest patients with suspected opioid overdoses. Overall, the study size was small and lacked a comparator; however, it found
that administration of naloxone had improved cardiac rhythms [49]. It is worth noting that the AHA comments that the cardiac rhythm improvement demonstrated in
this study is not founded in enough data to support naloxone use during CPR [50].
With that being said, the AHA algorithm for opioid-associated emergencies for
healthcare providers has a consideration for naloxone if administration will not
impact other portions of ACLS [6]. Naloxone dosing in this setting is unclear but
generally should be administered as an IV, IM, or subcutaneous bolus of 0.4–2mg
with the consideration for additional doses every 2–3min [51]. Continuous infusions of naloxone are not likely to provide a clinical benet in this setting but may
play a role in post-resuscitative care to ensure that rebound hypoxia and somnolence
do not occur in the setting of an opioid overdose. Pharmacists on the code team can
help rule in or rule out the possibility of opioid-induced cardiac arrest based on
15
Cardiac Arrest
387
patient presentation, urine drug screen evaluation, home medications, and/or inpatient medication administration. These data points can help supplement the discussion as to the value of naloxone in this clinical setting.
Thrombolytics may be used as adjunctive therapy in patients that have a suspected or conrmed pulmonary embolism (PE). The normal inciting rhythm during
codes, secondary to massive pulmonary embolism, is PEA [6]. The AHA currently
has a weak recommendation for the administration of thrombolytics in the setting of
cardiac arrest secondary to a suspected/conrmed PE. Non-medication interventions also carry a weak recommendation [52]. Literature surrounding thrombolytic
administration is limited, and many studies have conicting results. To date, thrombolytics have not been found to favorably impact neurologic recovery or survival to
hospital discharge [53–55]. There was some limited benet seen in 30-day survival,
ROSC achievement, and 24-h survival; however, conicting studies exist for all of
these outcomes [54–58]. Bleeding complications are more common in patients with
thrombolysis; however, they were not found to be statistically signicant, and
administration is often a risk/benet discussion [56]. Alteplase dosing is variable
across literature and clinical practice for this indication. Described IV dosing regimens include 100mg over 15min, 50mg over 2min, divided bolus doses totaling
100mg, or weight-based doses of 0.6–1mg/kg (maximum 100mg) [59]. Repeat
doses up to 100 mg total are usually considered with lower initial bolus dosing
strategies. A retrospective cohort review sought to characterize alteplase dosing and
subsequent outcomes related to various dosing regimens. Alteplase 50mg IV bolus
was the most common dosing strategy. The review found that ROSC was associated
with higher doses of alteplase (90.6 vs. 69.4mg; P=0.03) [59]. Tenecteplase may
also be considered and may offer some advantages due to ease of admixture; however, dosing is more complex and weight based (Table15.1) [60]. At this time, there
are no head-to-head trials supporting the clinical safety and efcacy of one thrombolytic agent over another in this clinical setting.
Utilization of vasopressin, as an adjunctive agent or substitutive agent, has
wavered in the AHA guidelines. Prior iterations of the guidelines recommended
vasopressin 40 unit IV/IO bolus as a substitute for the rst or second dose of epinephrine [61]. ETT administration can also be considered for vasopressin with previously described dosing considerations. Current iterations of the guidelines no
longer recommend vasopressin as an alternative agent [6]. Vasopressin was removed
from the guidelines due to lack of benet in ROSC achievement, survival, or
improvement in neurologic outcome [62]. One area of clinical controversy remains
as to whether there is a benet when vasopressin is combined with steroids and
Table 15.1 Tenecteplase dosing in pulmonary embolism [60]
Patient weight (kg) Tenecteplase dose (mg)
<60 30
≥60 to <70 40
≥70 to <80 45
≥90 50
388
A. M. Esteves
epinephrine. A number of trials have evaluated this combination of agents (vasopressin 20units, methylprednisolone 40mg, and epinephrine 1mg) and have found
benet in ROSC achievement [63–65]. Data remains unclear of the benet across
shockable vs. non-shockable rhythms, survival to hospital discharge, long-term
mortality outcomes, or improvement in neurologic function [63–65]. Due to the
limited data with this combination, the AHA has not included this combination in
the ACLS guideline [6]. It is important to note that no benet has been seen with
steroids alone in cardiac arrest [66, 67].
After ROSC attainment, pharmacists can play an additional role in the care provided. The AHA has an algorithm dedicated to post-resuscitative care, including
airway management and corresponding respiratory goals, hemodynamic goals,
pathways for consultative recommendations for targeted temperature management
(TTM), or more in-depth cardiology workups [6]. The AHA recommends maintaining a systolic blood pressure >90mmHg and a mean arterial pressure >65mmHg,
although exact clinical targets vary across ROSC trials [6]. In general, these hemodynamic parameters, or at minimum avoidance of hypotension, have been linked to
improved neurologic recovery and reduced mortality [6, 68]. Pharmacists can aid in
continuous infusion vasopressor initiation, agent selection, and titration, as appropriate, to meet these clinical targets. Appropriate agent selection should be based on
patient-specic factors, including uid responsiveness, underlying myocardial dysfunction, or need for inotropic support [69]. Agent consideration should include
additional uid support, norepinephrine, epinephrine, phenylephrine, dopamine,
dobutamine, and/or milrinone. Furthermore, post-resuscitative sedation and analgesia should be evaluated. These considerations are also patient specic based on the
timing of administration of paralytics for intubation, neurologic status after ROSC
achievement, TTM and subsequent shivering considerations, presence of myoclonus, sources of pain including rib fractures, ventilator synchrony, and neuroprognostication concerns. According to the AHA, neuroprognostication should be in the
setting of minimal sedation for a 72-h period [6]. Pharmacists can aid in agent selection and consideration of bolus vs. continuous infusion strategies for various agents.
Additionally, pharmacists are poised to offer consultation on pharmacodynamics
and pharmacokinetic considerations with various agents in the setting of subsequent
hepatic failure, renal failure, or TTM initiation after ROSC.
15.4 Expanded Role ofthePharmacist
Critical care pharmacists are essential members of the code team. The role of the
critical care pharmacist has evolved over time, and literature or survey responses
can be found documenting pharmacist participation in virtually all primary code
team roles. The Institute for Safe Medication Practices (ISMP) surveyed pharmacists regarding code response in 2022. At the time of the survey, 94% of respondents’ organizations had pharmacists attending codes. Roles of pharmacists varied
greatly in the survey and included medication preparation, medication consultation,
15 Cardiac Arrest
389
chest compressions/ventilation, scribe, debrillation, and intubation assistance [72].
Most commonly, pharmacists are positioned to run the code cart. Code cart leadership takes advantage of pharmacists’ pharmacotherapy knowledge when considering various medication agents, timing, and determining anticipatory needs
throughout the code. The ISMP survey was supported by a position paper on critical
care pharmacy service offerings. The position paper has various levels of recommendations based on ICU structure (Table 15.2) for pharmacist participation in
resuscitation events, attainment of the American Heart Association (AHA) Advanced
Cardiac Life Support (ACLS) certication, and instructing ACLS courses [70, 71].
The position paper specically emphasizes 24-h code coverage by a pharmacist
[70]. It is important to note that this is an area of improvement for many institutions,
as many survey respondents reported a lack of full-time coverage [72]. The position
paper helps strengthen the role of the pharmacist as a leader in a code setting.
Pharmacists are positioned as leaders in their ability to ll a number of code team
roles, which is further strengthened by the “desirable” status for instructing ACLS
courses [70].
Benets of pharmacist presence at code events have been evaluated in a number
of publications. Pharmacist presence and participation in various roles have been
shown to contribute to ACLS guideline compliance [73–75]. Although guideline
compliance does not have any specic long-term outcomes associated, it can be
inferred that improvements in outcomes are likely made based upon the data supporting the series of proposed interventions. A retrospective review that demonstrated an improvement in guideline compliance also found an improvement in
survival to hospital admission when emergency department (ED) pharmacists were
included in code response. Although this survival trend did not persist to discharge,
the preliminary inuence supports that outcome improvements from pharmacist
presence are likely [73]. Additionally, a Medicare database study found a signicant
reduction in mortality when pharmacists participated in cardiopulmonary resuscitation teams (12,880 reduced deaths, P=0.009) [76]. Although not a correlator to
patient outcomes but rather system improvements, pharmacist participation in code
response has also been shown to reduce costs [73].
It is well established that emergency response scenarios are high-risk events and
have an increased incidence of errors [77, 78]. The ISMP notes that the error incidence rate in code events is variable and has ranged from 1% to 15% in published
literature [79]. A medication error database study highlighted that medication errors
in this setting have a signicantly higher likelihood of harm or death when compared to other medication error events [77]. Error types have been variable across
Table 15.2 Summary of critical care pharmacist roles by ICU level [70]
Role ICU level 1* ICU level 2* ICU level 3*
Attendance at resuscitation events Essential Essential Desirable
ACLS certication Essential Essential Desirable
ACLS certication instructor Desirable Desirable Desirable
* ICU levels are dened by critical care capabilities as outlined in prior publications [71]
390
A. M. Esteves
studies and include incorrect medication selection, incorrect dose, improper preparation, and omissions [79]. The ISMP has recommended inclusion of pharmacists
on code teams as a risk-reduction strategy to mitigate medication errors from occurring [79, 80].
Pharmacist training for code response is inconsistent across literature and survey
results. One survey found that the most common training was basic life support
(BLS) certication; however, comfort with code scenarios was correlated with BLS/
ACLS certication and institution training programs [81]. The critical care position
paper highlights the importance that pharmacists responding to codes should be
ACLS certied [70]. Many of the fundamental pieces of ACLS go beyond traditional pharmacy didactic education, including ECG interpretation and other nonpharmacotherapy management portions of emergency resuscitation. A single-center
review evaluated implementation of a pharmacist-centric code of blue education
and found improvements in knowledge of various medication preparation questions, as well as perceived comfort. The training consisted of a 2-h didactic session,
reference materials, and a hands-on skill portion [82]. Another single-center review
evaluated training in addition to ACLS that focused on rhythm identication, ACLS
pharmacology, and participation in multidisciplinary simulation ACLS scenarios.
The addition of these supplemental experiences increased the condence and comfort of the code responders [83].
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