Cardiovascular Critical Care II
| (2) | Recommended for all non-shockable rhythms to administer epinephrine as soon as |
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feasible (Circulation 2015;132(suppl 2):S315-S367). Data analyses suggest that prompt
(less than 5 minutes from non-shockable rhythms administration of epinephrine was
associated with greater 1-year survival (Circulation 2018;137:2041-51). These results
have been found at both the patient level and the hospital system level (Circulation
2016;134:2105-14). Recent guideline update supports the early usage of epinephrine as
soon as feasible in the nonshockable rhythm context (Circulation 2019;140:e881-e894).
| (b) | Atropine has been removed from the algorithm because of its lack of therapeutic benefit. |
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Role in treating reversible causes
Echocardiography may be helpful, if available, in the management of PEA to help differentiate
| (a) | Intravascular volume status (ventricular volume). |
|---|---|
| (b) | Cardiac tamponade. |
| (c) | Massive pulmonary embolism (right ventricular size, function). |
| (d) | Mass lesions (tumor, clot). |
| (e) | Coronary thrombosis (right and left ventricular function, regional wall motion |
abnormalities).
ii.
Because hypoxia is often a cause of PEA arrest, more focused attention may be given to
placement of airway and oxygen delivery.
iii.
See the specific chapters for pulmonary disorders (massive pulmonary embolism and tension
pneumothorax), cardiology (acute myocardial infarction and cardiac tamponade), shock
(hypovolemic shock), acid-base disorders (acidemia), endocrinologic disorders (hypoglycemia),
and electrolytes (hypo/hyperkalemia).
Controversial interventions in cardiac arrest
Sodium bicarbonate
| (a) | Tissue acidosis and acidemia result during cardiac arrest for several reasons, including |
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inadequate or absent blood flow, arterial hypoxia, or underlying pathophysiology.
| (b) | Mainstays of restoring acid-base status include high-quality chest compressions and |
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appropriate ventilation/oxygenation.
| (c) | Conflicting evidence exists for the use of sodium bicarbonate, with most data showing |
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1989;17(suppl):S161-172; discussion S199-206; J Emerg Med 2020;59:856-64).
| (d) | Data in patients with prolonged CPR efforts (> 20 mins) primarily from VF (~80%) |
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9) after complex retrospective analysis. Caution should be used extrapolating results
because significant limitations exist in the study design and all patients included likely
A prospective, observational, propensity-matched data suggest that OHCA use of
prehospital sodium bicarbonate was associated with a decreased probability of favorable
neurologic outcomes and survival (Resuscitation 2017;119;63-9).
| (e) | Detrimental effects may be associated with sodium bicarbonate in cardiac arrest, including: |
|---|---|
| (1) | Compromised coronary perfusion pressure by reducing systemic vascular resistance |
| (2) | Shifting the oxyhemoglobin dissociation curve to the left by creating an extracellular |
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alkalosis and decreased release of oxygen.
| (3) | Causing hypernatremia and subsequent hyperosmolarity leading to hyperviscosity, |
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potentially impairing blood flow.