Index
Module 12 • Cardiology
Cardiovascular Critical Care II
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Data Tables
Cardiovascular Critical Care II
Patrick M. Wieruszewski ~3 min read Module 12 of 20
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Cardiovascular Critical Care II

(4)Producing excess CO2 through rapid dissociation, which can freely diffuse

intracellularly (e.g., myocardial and cerebral cells) and cause intracellular acidosis

(Science 1985;227:754-6).
(5)Inactivation of concurrently administered catecholamines (e.g., epinephrine) (Hosp

Pharm 1969;4:14-22).

(f)Certain circumstances may warrant sodium bicarbonate use such as tricyclic antidepressant

overdose, bicarbonate (HCO3-)-wasting causes of metabolic acidosis, and hyperkalemia.

In addition, it should be noted that endogenous catecholamines have a blunted response

during acidosis which may improve if the acidosis is corrected. Initial dosage should usually

be 1 mEq/kg intravenous push with monitoring of clinical status, HCO3- concentration,

laboratory values, and blood gas analysis.

(g)Recent meta analysis of RCT’s found that use of sodium bicarbonate was not superior

compared with control in regards to survival and ROSC and may be associated with lower

rates of sustained ROSC and good neurological outcome (Int J Emerg Med 2021;14:21).

(h)A recent RCT in a porcine model of hyperkalemia-induced cardiac arrest discovered that

sodium bicarbonate was associated with increased rates of ROSC and reduced time to

ROSC (Crit Care Med 2024;52:e67-78). Human investigation may be warranted.

ii.

Calcium

(a)No trial has established any impact on survival in either IHCA or OHCA (Ann Emerg Med
1985;14:626-9; Ann Emerg Med 1985;14:630-2). Recent RCT data in OHCA did not confer
benefit of calcium on ROSC (JAMA 2021;326:2268-76).
(b)Consider in patients with preexisting hypocalcemia and signs and symptoms of acute

hypocalcemia (e.g., severe tetany or seizures).

(c)A recent RCT in a porcine model of hyperkalemia-induced cardiac arrest discovered that

calcium chloride was not associated with increased rates of ROSC or time to ROSC (Crit

Care Med 2024;52:e67-78).

iii.

Atropine

(a)No prospective studies have evaluated atropine for bradycardic PEA or asystolic cardiac

arrest.

(b)Conflicting results exist from retrospective analyses and case reports (Acta Anaesthesiol
Scand 2000;44:48-52; Ann Emerg Med 1984;13:815-7; Ann Emerg Med 1981;10:462-7).
(c)Atropine has not been associated with harm in treating bradycardic PEA or asystolic cardiac

arrest, but because of the lack of convincing evidence of benefit, it is no longer recommended

for cardiac arrest but is reserved for symptomatic/life-threatening bradycardia.

iv.

Intravenous fluids

(a)Normothermic, hypertonic, and chilled fluids have been evaluated in animal models and

small human studies, with no survival benefit.

(b)If hypovolemic shock is the suspected cause of the cardiac arrest, fluid resuscitation should

be initiated immediately.

For indications of fibrinolysis for cardiac arrest, see the Pulmonary chapter for treatment of

pulmonary embolism and the Cardiology chapter for treatment of acute myocardial infarction.

vi.

Pacing

(a)Transcutaneous, transvenous, and transmyocardial pacing is not beneficial in cardiac arrest

and does not improve ROSC or survival.

(b)Not recommended for routine use in cardiac arrest.

vii.

Dextrose

(a)Animal data has demonstrated that dextrose administration before, during, or after cardiac
arrest leads to higher rates of mortality and worse neurological outcomes (J Crit Care.

1987;2:4–14; Surgery 1990;72:1005–11; Acta Anaesthesiol 1986;100:505–11).

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