Fluid Therapy During Cardiopulmonary Resuscitation

Abstract

Cardiopulmonary arrest (CPA), the acute cessation of blood flow and ventilation, is fatal if left untreated. Cardiopulmonary resuscitation (CPR) is targeted at restoring oxygen delivery to tissues to mitigate ischemic injury and to provide energy substrate to the tissues in order to achieve return of spontaneous circulation (ROSC). In addition to basic life support (BLS), targeted at replacing the mechanical aspects of circulation and ventilation, adjunctive advanced life support (ALS) interventions, such as intravenous fluid therapy, can improve the likelihood of ROSC depending on the specific characteristics of the patient. In hypovolemic patients with CPA, intravenous fluid boluses to improve preload and cardiac output are likely beneficial, and the use of hypertonic saline may confer additional neuroprotective effects. However, in euvolemic patients, isotonic or hypertonic crystalloid boluses may be detrimental due to decreased tissue blood flow caused by compromised tissue perfusion pressures. Synthetic colloids have not been shown to be beneficial in patients in CPA, and given their documented potential for harm, they are not recommended. Patients with documented electrolyte abnormalities such as hypokalemia or hyperkalemia benefit from therapy targeted at those disturbances, and patients with CPA induced by lipid soluble toxins may benefit from intravenous lipid emulsion therapy. Patients with prolonged CPA that have developed significant acidemia may benefit from intravenous buffer therapy, but patients with acute CPA may be harmed by buffers. In general, ALS fluid therapies should be used only if specific indications are present in the individual patient.

Keywords: bicarbonate; calcium gluconate; cardiopulmonary resuscitation; cats; dogs; fluid resusciation; lipid emulsion infusion.

Figure 1

Oxygen delivery to the tissues (DO₂) is the product of cardiac output (CO, the volume of blood ejected from the left ventricle into the aorta per minute) and arterial oxygen content (Ca_O2, the volume of oxygen carried in the arterial blood). CO is the product of heart rate (HR) and stroke volume (SV, the volume of blood ejected from the left ventricle with each contraction). SV is determined by preload (the amount of blood in the left ventricle at the end of diastole), contractility (the force with which the left ventricle contracts), and afterload (the pressure against which the left ventricle has to push to get blood into the aorta). Ca_O2 is determined by the amount of hemoglobin per unit of volume of blood ([Hb]) and the amount of that hemoglobin that is saturated with oxygen in the arterial blood (S_aO₂).

Figure 2

The Frank-Starling curve describes the relationship between preload (on the x-axis) and stroke volume (on the y-axis). At low preload, increases in the preload lead to linear increases in stroke volume due to increasing ventricular stretch. As the myocytes reach their maximum stretch capacity, the rate of stroke volume increase begins to drop with increasing preload, and as the myocytes become over-stretched, stroke volume begins to drop with increasing preload.

Figure 3

Pressure tracings during CPR in an experimental swine ventricular fibrillation model. The green tracing is aortic pressure (AoP) and the purple tracing is right atrial pressure (RAP). The peaks correspond to the compression phase of CPR. Coronary blood flow and oxygen delivery occur during the relaxation phase of chest compressions and is proportional to coronary perfusion pressure (CoPP), the difference between aortic pressure and right atrial pressure at the end of the relaxation phase, as denoted by the double arrowed vertical line. The tracing was obtained during mechanical, sternal chest compressions (100/min) delivered by the LUCAS (Lund University Cardiopulmonary Assist System) device to an anesthetized pig with VF arrest. Solid state pressure transducer catheters (Micro-Tip® Transducer, Millar Instruments, Houston, TX) were introduced through the left femoral artery and vein for continuous measurement of AoP and RAP.