Study Design

Reduced Quality Factors

0 = no serious, - = serious,

- - = very serious

Positive Quality Factors

0 = none, + = one, ++ = multiple

Dichotomous Outcome Summary

Non-Dichotomous Outcome Summary

Brief description

Overall Quality

High, moderate, low,
very low, none

No of studies

Study Type

RoB

Indirectness

Imprecision

Inconsistency

Large Effect

Dose-Response

Confounder

# Intervention with Outcome

# Control with Outcome

RR (95% CI)

Outcome: Favorable neurologic outcome

0

Outcome: Survival to discharge

0

Outcome: ROSC

1

Ex

-

- -

0

0

0

0

0

Very low

Outcome: Surrogate markers of perfusion

5

Ex

-

- -

0

0

0

0

0

Very low

Introduction

Fluid boluses have historically been administered during CPR with the goal of increasing cardiac filling in order to increase cardiac output (CO). However, during CPR in euvolemic patients that do not have cardiac filling deficits, coronary perfusion pressure (CoPP) and cerebral perfusion pressure (CePP) may be decreased by fluid boluses in that they may increase central venous and right atrial pressure more than aortic systolic and diastolic pressure. The RECOVER 2012 Guidelines recommended against routine administration of IV fluid boluses during CPR unless patients had known or strongly suspected hypovolemia 1. This was based on the concept that in hypovolemic patients in CPA, fluid boluses will likely increase ventricular filling, leading to increases in aortic systolic and diastolic pressure that exceed increases in central venous and right atrial pressures, improving CoPP and CePP. This PICO question examines the effect on outcome of fluid boluses during CPR in euvolemic patients.

Consensus on science

Outcomes 1, 2: Favorable neurologic outcome, survival to discharge

For the 2 most critical outcomes of favorable neurologic outcome and survival to discharge, no evidence was available to inform an answer to the PICO question.

Outcome 3: Return of spontaneous circulation

There is 1 experimental study that provides some indirect evidence of a beneficial effect of volume loading in euvolemic dogs undergoing CPR (very low quality of evidence, downgraded for serious risk of bias and very serious indirectness). Sanders et al examined

31 mongrel dogs with prolonged induced ventricular fibrillation in which CPR was done for 30 minutes prior to the first shock.2 Dogs receiving fluid boluses and sodium bicarbonate prior to arrest and during the CPR attempt had higher ROSC rates than those that did not receive fluids or sodium bicarbonate (8/11 vs. 0/10). Two additional groups were evaluated with a similar protocol, but 1 group received only fluids and the other only bicarbonate. Incidence of ROSC was similar between these groups (2/12 vs. 5/14), but ROSC incidence was significantly higher in the group of dogs receiving both bicarbonate and fluids.

Outcome 4: Surrogate markers of perfusion

For the outcome of surrogate markers of perfusion, 4 experimental studies in dogs and 1 experimental study in cats (very low quality of evidence, downgraded for serious risk of bias and very serious indirectness due to confounding interventions) overall showed no improvement or a detrimental effect of fluid boluses on CoPP and/or CePP.2–6 Although the studies generally demonstrated a consistent increase in aortic pressure and blood flow, the concurrent increase in CVP in the animals either yielded no net improvement or a decrease in CoPP and/or CePP.

Gentile et al. compared aortic systolic (SAoP) and diastolic pressures (DAoP), right atrial systolic (SRAP) and diastolic pressures (DRAP), and coronary perfusion pressure (CoPP) in 19 healthy anesthetized dogs undergoing CPR for induced ventricular fibrillation (VF) that either received epinephrine and defibrillation alone (n=6), epinephrine plus a 500 mL bolus (16-23 mL/kg) of 0.9% saline intravenously (n=5), or epinephrine plus a 500ml bolus of 0.9% saline into the aorta (n=8).6 SAoP, DAoP, SRAP and DRAP all increased significantly with fluid boluses, but maximal CoPP did not significantly differ between groups. Ditchey and Lenfield studied 12 dogs using a model of induced VF.4 Measurements of carotid blood flow showed increases with fluid boluses (1L of 0.9% NaCl or 10% HES) but cerebral and coronary blood flow decreased with fluid boluses, presumably due to increased venous pressure. In a study of 31 mongrel dogs, Sanders et al. showed no differences in CoPP in a prolonged VF model (CPR was performed for 30 minutes before the first shock) between dogs receiving an infusion of fluids pre-arrest to achieve a right atrial pressure of 6-8 mmHg and infusions of sodium bicarbonate during the arrest and dogs not receiving fluids or sodium bicarbonate.2 Finally, Fischer and Hossman studied 14 cats using an induced VF model.3 All cats had standard CPR with chest compressions, epinephrine and electrical defibrillation. Six cats were additionally volume loaded with 2ml/kg HES over 10 minutes. Cats that received HES had significantly less evidence of cerebral ischemia on necropsy, though they had decreased CoPP and CePP during CPR. All cats achieved ROSC.3

Treatment recommendation

We recommend against the use of intravenous fluid boluses in euvolemic dogs and cats during CPR (strong recommendation, very low quality of evidence).

We recommend the use of intravenous fluid boluses in dogs (20 ml/kg isotonic crystalloid or equivalent) and cats (10-15 ml.kg isotonic crystalloid or equivalent) with known or suspected hypovolemia during CPR (strong recommendation, expert opinion).

Justification of treatment recommendation

All evidence available to inform this treatment recommendation is experimental, is in ventricular fibrillation models, and much of it is confounded by multiple concurrent treatments including sodium bicarbonate administration. However, there is consistent evidence that fluid boluses administered during CPR to dogs and cats that are euvolemic prior to induced CPA lead to increases in right atrial pressure that exceed increases in aortic pressure, leading to decreased CoPP and CePP, suggesting that fluid boluses are in general detrimental in this population. One study showed significant increases in the incidence of ROSC in dogs treated prior to induction of VF with fluid boluses and sodium bicarbonate compared to dogs receiving either fluid boluses alone, sodium bicarbonate alone, or neither.2 This is confounded by the fact that this treatment started prior to induction of VF and by the fact that these were anesthetized, experimental dogs that underwent prolonged CPR for 30 minutes prior to the first attempt at electrical defibrillation.

Knowledge gaps

Although there is compelling experimental evidence suggesting that fluid boluses decrease CoPP and CePP in induced ventricular fibrillation models of CPA, there are no clinical trials evaluating the effects of fluid boluses in clinical patients during CPR. However, given the experimental evidence, it is difficult to suggest that there is adequate clinical equipoise to warrant a clinical trial.