Your paramedic crew responds to a cardiac arrest in a large shopping complex. Fortunately, the patient has all the links in the chain of survival in place. Bystander CPR has been initiated, and an automated external defibrillator (AED) was in place in the shopping complex and deployed, the 9-1-1 system was accessed, and your unit arrived rapidly–within six minutes from the time of call. As you approach, you assess the situation, interview bystanders and begin the final link–early advanced care.
For patients in cardiac arrest, the American Heart Association (AHA) has determined this provides the best opportunity for someone to survive cardiac arrest in the prehospital environment. The patient remains in ventricular fibrillation (v fib) despite several AED shocks. You gain IV access and begin pharmacological therapy.
After administering epinephrine and amiodarone, you consider sodium bicarbonate as directed by protocol. You recognize that over the past several years AHA has deemphasized the use of sodium bicarbonate. But what is the controversy? When is it appropriate to give sodium bicarbonate, and are paramedics using it to its fullest advantage? Seasoned paramedics will recall giving multiple ampules of sodium bicarbonate during a cardiac arrest, but today it appears to be an afterthought.
Sodium bicarbonate (NaHCO3) is used primarily to combat acidosis, although it’s the treatment of choice in certain cases of overdose. It works by mixing with lactic acid that forms in low perfusion states and in periods of inadequate oxygenation, such as shock and cardiac arrest. It is then converted to a form of carbonic acid that turns into carbon dioxide, and in turn, is expelled through the lungs during ventilation.
Primarily, NaHCO3 works as a buffer by mixing with acids within the body to reduce the acid—base imbalance. Acidosis can develop when excessive amounts of lactic acid are produced during low perfusion states and in periods of inadequate oxygenation. In the presence of NaHCO3, the excess acid is converted to a form of carbonic acid, and then into carbon dioxide (CO2) and water. The excess CO2 is expelled through the lungs during ventilation. Patients who become hypoxic from hypoventilation or poor perfusion are unable to metabolize the products of anaerobic glycolysis, which causes lactic and metabolic acidosis to develop thereby lowering their pH level.1
A normal pH is 7.35 to 7.45; a pH less than 7.35 places the patient in a state of acidosis. During severe acidosis (pH less than 7.2), the heart is more susceptible to v fib and other arrhythmias. Myocardial contractility is suppressed, hypotension occurs, hepatic blood flow is reduced, and oxygen delivery to tissue is impaired.2 The body uses bicarbonate as a buffer to offset the increase in acid production, attempting to maintain homeostasis.
Several studies have challenged whether treating serum acidosis with bicarbonate actually influences the true acidosis, which occurs at the intracellular level.3
AHA Guidelines: New and Old
The AHA has revised the guidelines for NaHCO3 since the 2000 edition of Standards and Guidelines for CPR and Emergency Cardiac Care (ECC). Bicarbonate is only advised at the discretion of the physician directing the resuscitation.
While the AHA doesn’t recommend the routine use of NaHCO3, the research often times contradicts itself. As early as 1962, researchers reported cases of patients in v fib that were in acidosis and remained refractory until the acidosis was corrected with NaHCO3. This demonstrated that it’s highly unlikely to resuscitate the fibrillating heart if severe acidosis is present.1 This has resulted in a debate over whether acidosis causes the cardiovascular system to be less responsive to medications.
The 2010 AHA Guidelines for CPR and ECC point out that acidosis and resulting acidemia during cardiac arrest and resuscitation are dynamic processes resulting from no blood flow during arrest and CPR.4
The Guidelines further note that these processes are affected by the duration of cardiac arrest, level of blood flow and arterial oxygen content during CPR.
Restoration of oxygen content with appropriate ventilation with oxygen, support of some tissue perfusion and cardiac output with high-quality chest compressions, then rapid return of spontaneous circulation (ROSC) are the mainstays of restoring acid-base balance during cardiac arrest. The problem is, we frequently get to patients with extended down times and no CPR in progress, so they’re already acidic.
Two studies cited in the 2010 Guidelines demonstrated increased ROSC, hospital admission and survival to hospital discharge associated with the use of bicarbonate. The majority of studies showed no benefit or found no relationship with poor outcomes.
The following guidelines state that there are few data to support therapy with buffers during cardiac arrest and note a variety of adverse effects have been linked to administration of bicarbonate during cardiac arrest. 5
1) Bicarbonate may compromise CPR by reducing systemic vascular resistance. 2) It can create extracellular alkalosis that will shift the oxyhemoglobin saturation curve and inhibit oxygen release. 3) It can produce hypernatremia and therefore hypersmolarity. 4) It produces excess CO2, which freely diffuses into myocardial and cerebral cells and may paradoxically contribute to intracellular acidosis. 5) It can exacerbate central venuous acidosis and may inactivate simultaneously administered catecholamines.
It’s generally accepted in emergency medicine that buffer therapy should be based on arterial blood gas (ABG) interpretation, and patients are preferred to be in acidosis rather than alkalosis.
However, the AHA has published data suggesting that ABGs aren’t a true indicator of tissue acidosis and questioning its use in cardiac arrest resuscitation.6 Acidosis begins developing within three minutes with significant acidosis occurring at 18 minutes. In patients who regain normal ventilation and circulation quickly, acidosis generally resolves within 60 minutes although patients who have sustained cardiac arrest develop significant acidosis in 18 minutes.7
NaHCO3 is administered as an IV bolus or by IV infusion. The standard dosage is 1 mg/kg of body weight as the initial dose followed by 0.5 mg/kg every 10 minutes for the duration of the cardiac arrest. A 50-milliliter bolus of NaHCO3 will raise the serum pH approximately 0.1 of a pH unit. If the pH is 7.0, it requires four 50 mEq ampules of HCO3 to correct the pH to 7.40.
The 2010 Guidelines promote high quality CPR and defibrillation to facilitate rapid ROSC as the method of restoring acid-base balance.
Although the 2010 Guidelines do not recommend “routine use” of sodium bicarbonate for patients in cardiac arrest, they note that it can be beneficial in some special resuscitation situations, with a typical initial dose of 1 mEq/kg.5
As in cardiac arrest administration, when bicarbonate is used for special situations, an initial dose of 1 mEq/kg is typical. The 2010 Guidelines further note that, whenever possible, bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement. However, this is a hospital-based determinant that doesn’t apply to prehospital resuscitation.
Other non-CO2 generating buffers such as bicarbonate, Tham Solution or tribonate have shown potential for minimizing some adverse effects of sodium bicarbonate, including CO2 generation, hyperosmolarity, hypernatremia, hypoglycemia, intracellular acidosis, myocardial acidosis and “overshoot” alkalosis. However, clinical experience is greatly limited and outcome studies are lacking.7
Ventilation & Compression
Efficient ventilation and adequate perfusion are the principal determinants of acidosis. Part of the concern is that since NaHCO3 produces CO2 it may actually worsen acidosis.8 CO2, when combined with water, forms carbonic acid, which is a weak acid that diffuses across the cell membrane easily where NaHCO3 cannot. Because NaHCO3 produces CO2, EMS providers can expect a sudden increase in their patient’s CO2 level immediately after administration of NaHCO3.
This is the underlying reason why NaHCO3 isn’t recommended for patients who aren’t being ventilated with definitive airway management.9 For the patient with ongoing end tidal CO2 (EtCO2) monitoring, CO2 levels should return to pre-administration levels after several ventilations. Other medications exist to correct acidosis without the resulting increase in CO2, but they haven’t been embraced in resuscitation due to lack of supporting evidence.10
Although adequacy of ventilation is key, blood flow through the lungs is required for the exchange of oxygen and CO2,, and good cardiac chest compressions will help accomplish this in cardiac arrest. Researchers found that as long as ventilation and pulmonary blood flow were maintained, increases in CO2 could be eliminated without further problems or adverse effects.11
In response to the decreased emphasis on NaHCO3, prior AHA Guidelines encouraged moderate hyperventilation to blow off excess CO2 , thereby assisting in the correction of acidosis. It has since been determined that hyperventilation actually significantly decreases coronary and cerebral perfusion pressures, which subsequently decreases survival rates.
The 2010 Guidelines teach EMS to ventilate at a slower rate of eight to 10 breaths a minute, removing hyperventilation as a means to correct acidosis, yet the correction of acidosis hasn’t been re-addressed in the absence of hyperventilation.9
It has been determined that better neurological outcomes occur with decreased ventilations, but it also has been shown that inadvertent hyperventilation remains a constant problem despite training and the introduction of capnography.12 The prehospital use of waveform capnography can help control ventilation rates in these situations.
Aggressive chest compressions have again become the focus of the 2010 AHA Guidelines, but compressions provide less than 30% of blood flow in cardiac arrest and rescuer fatigue increases with each minute. A concerning 2005 study found that prehospital CPR was really only being accomplished an average of 48% of the time during cardiac arrest, and only 38% when defibrillation and ECG placement is considered.10 EMS providers know the difficulty in maintaining good CPR while moving and transporting patients. Recent studies challenge the benefit of mechanical CPR devices, although they appear to allow for consistent chest compressions in the difficult prehospital transport setting.8
Because bicarbonate crosses the blood-brain barrier, concerns have been raised about creating an inadvertent hypernatremia, which is an elevated sodium level, with the use of NaHCO3. If that were to occur, it would decrease the cerebral perfusion pressures.
However, recent studies have also demonstrated that this only occurs on a limited basis. Animal models have been given as much as 4—6 mEq/kg without adverse sodium shifting. For example, it would take eight ampules of bicarbonate to reach the 4 mEq/kg level in a 220 lb. patient.13
Epinephrine & Bicarbonate
Sodium bicarbonate administration in conjunction with epinephrine was reported to increase survival as early as 1968, with more recent studies demonstrating similar results.14 This was reaffirmed in 2005 when Pittsburgh researchers found that EMS systems administering NaHCO3 with epinephrine within minutes of resuscitation demonstrated a higher ROSC, higher discharge rate and better neurological outcome.15
Seattle continually demonstrates one of the highest survival rates for patients suffering cardiac arrest in the out-of-hospital setting. Resuscitation is reported to be as high as 45% in cardiac arrest secondary to v fib.16 Michael Copass, MD, and his colleagues have studied the effects of NaHCO3 on epinephrine and lidocaine in the outcome of cardiac arrest due to v fib, and they discovered the use of a continuous infusion of NaHCO3 led to an increased ROSC in the prehospital setting even though it doesn’t impact long-term survival.17
Most recently, in a 2006 study in Pittsburgh, researchers evaluated the effects of NaHCO3 administration for documented cases of cardiac arrest. Although they reported no statistical value to the early use of NaHCO3, they found value in using NaHCO3 in prolonged cardiac arrest of greater than 15 minutes.
Their results documented an increase in survival of prehospital cardiac arrest from 15.4% to 32.8%, which led them to question whether the decreased emphasis on NaHCO3 is appropriate.15
Recent interest has focused on neurological outcomes and protective measures in survivors of cardiac arrest. Researchers at John Hopkins University evaluated acidosis and brain pH of dogs during prolonged resuscitation. The group receiving NaHCO3, cerebral pH, cerebral blood flow and oxygen consumption all remained higher at close to pre-cardiac arrest values. The group with uncorrected acidosis had significant reduction in all areas, which led the authors to conclude that cerebral acidosis was correctable by the combination of NaHCO3, adequate ventilation and good compressions.11
In 2002, researchers determined that cerebral acidosis occurs at a much earlier period than arterial acidosis. They concluded buffer administration during CPR promoted cerebral reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during periods of hypotension.18
What Does this Mean for EMS?
Advanced Cardiac Life Support (ACLS) guidelines encourage the consideration of NaHCO3 in cases of prolonged cardiac arrest of more than 10 minutes. It’s important to remember ACLS is taught to multiple medical disciplines, including physicians, pharmacists, nurses, respiratory therapists and paramedics.
Of these, paramedics routinely encounter patients with unwitnessed cardiac arrest or prolonged down times before initiation of advanced care. Although agencies strive for rapid response times, few are calculated the same way, and even fewer take into consideration the time from arrival on scene to patient contact.
One study found that 25% of EMS cardiac arrest calls had an on-scene to patient contact time of more than four minutes.19 Although longer response times are a contributing factor to acidosis, time from onset of event to treatment is a better indicator. Studies show that when NaHCO3 is administered in cardiac arrest, it’s frequently after a prolonged period of time, and significant acidosis has already occurred.
For example, researchers in one Nebraska study evaluated 119 out-of-hospital cardiac arrest patients who arrived to the emergency department with CPR in progress. These researchers found the mean pH of the study group to be 7.18–well below the normal range.9
Paramedics need to recognize that the clock for combating acidosis begins when the patient’s heart stops, not from the time providers arrived at the scene and began care. Other prehospital cases where the consideration of NaHCO3 is warranted include overdoses and patients with increased potassium levels.
Patients who have overdosed from tricyclic antidepressants, diphenhydramine, aspirin, verapamil and cocaine have potentially toxic effects and have benefited from sodium bicarbonate use when symptomatic. It’s been speculated that the increase in the sodium load along with serum alkalization is the mechanism by which bicarbonate assists in reducing QRS prolongation. Patients with symptomatic overdoses that involve cardiac effects have responded favorably with the use of sodium bicarbonate.20
Potassium promotes cardiac relaxation after cardiac contraction. As acidosis increases, potassium levels also increase. Each 0.1% decrease in pH increases potassium 0.7%. Patients with issues related to potassium shifting are at risk for cardiac arrhythmias. Sodium bicarbonate has been a mainstay of treatment for increased potassium years. This includes patients with known or suspected hyperkalemia, such as dialysis patients. It also includes those with crush injuries and positional asphyxia and Taser use.
What Lies Ahead
The use of sodium bicarbonate in the out-of-hospital cardiac arrest that isn’t witnessed by EMS warrants further research and consideration. The literature is sometimes confusing, but it’s likely that the debate on NaHCO3 will continue well into the future.
Most researchers agree that in cases of cardiac arrest where acid-base status was normal prior to a cardiac event, and the patient responds promptly to such standard therapies as defibrillation and ventilation, NaHCO3 use isn’t warranted. However, in cases of prolonged cardiac arrest of greater than 10 minutes from the time of sudden death, it appears that the use of sodium bicarbonate is warranted in the presence of adequate ventilation and good compressions and after reversible causes have been identified and treated.
Frequent and earlier use of NaHCO3 has been associated with higher resuscitation rates and with better long-term outcomes in prehospital cardiac arrest. The impressive improvement in outcome in the prolonged arrest group suggests that abandoning use of bicarbonate would be premature.21,22
Although many argue that cardiac arrest survival to discharge remains low, prehospital protocol development must take into consideration the differences of providing unique challenges to providing care in the out-of-hospital setting. Unless an EMS crew witnesses the cardiac arrest, the patient is already in prolonged cardiac arrest by the time crews make patient contact.
As in all cases, local protocols must take into consideration the differences in providing care in the out-of-hospital setting. The role of EMS is to deliver a patient who has the best chance to survive. The routine use of NaHCO3 may warrant a greater role in the delivery of prehospital care for cardiac arrest patients in the prehospital setting.
Until other options exist for the prehospital assessment and treatment of acidosis, EMS providers need to pay more attention to the length of the patient’s down time and recognize the importance of considering acidosis early on, as well as recognizing that NaHCO3 may be a viable treatment option. JEMS
1. Stephenson HE. Cardiac Arrest and Resuscitation. Mosby. St. Louis. 495, 1974.
2. Kraut JA, Kurtz I. Use of base in the treatment of severe acedemia states. Am J Kidney Dis. 2001;38:703—727.
3. Goldsmith DJ, Forni, LG, Hilton PJ. Bicarbonate therapy and intercellular acidosis. Clin Sci. 1997;93:593—598.
4. 2010 American Heart Association Guidelines for Cardiopulmonary Rescusitation and Emergency Cardiovascular Care, Part 8. Advanced Cardiac Life Support. Circulation. 2010;122:767—777.
5. 2010 AHA Guidelines for CPR and ECC, Part 12: Cardiac Arrest in Special Situations. Circulation. 2010;122:829—861.
6. 2010 AHA Guidelines for CPR and ECC, Part 7.4. Monitoring and Medication. Circulation. 2005;112:78—83.
7. Young GP. Reservations and recommendations regarding sodium bicarbonate administration in Cardiac Arrest. J Emerg Med. 1988;6:321—323.
8. Planta M, Weil MH, Gazmuri RJ, et al. Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation. Circulation. 1989;684—692.
9. Ornato JP, Gonzalez ER. Arterial pH in out-of-hospital cardiac arrest. Response time as a determinant of acidosis. Am J Emerg Med. 1985;3:498—506.
10. Wir L, Kramer J. Quality of CPR in out-of-hospital cardiac arrest. JAMA. 2005;19:299—304.
11. Sanders AB, Kerns KB, Berg RA, et al. Survival and neurological outcome after cardiopulmonary resuscitation with four different chest compression-ventilation ratios. Ann Emerg Med. 2002;40:553—562.
12. Aufderheide TP, Lurie KG. Death by hyperventilation: A common and life-threatening problem during CPR. Crit Care Med. 2004;32:345—351.
13. Vukmir RB, Bircher NG, Radovsky A, et al. Sodium bicarbonate may improve outcome in dogs with brief or prolonged cardiac arrest. Crit Care Med. 1995;23:515—522.
14. Reading J, Pearson J. Resuscitation from v fib, drug therapy. JAMA. 1968;203:255—260.
15. Bar-Joseph G, Abramson NS, Jansen-McWilliams L, et al. Clinical use of sodium bicarbonate during cardiopulmonary resuscitation: Is it used sensibly? Resuscitation. 2002;54:47—55.
16. Wang HE, Yealy DM. How many attempts are required to accomplish out of hospital endotracheal intubation? Soc Acad Emerg Med. 2006.
17. Weaver WD, Fahrenbruch CE, Johnson DD, et al. Effects of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation. 1990;82:2027—2034.
18. Sun S, Weil MH, Tang W, et al. Effects of buffer agents on post resuscitation myocardial dysfunction. Crit Care Med. 1996;24:2035—2041.
19. Cambell JP, Gratton MC, Salamone JA, et al. Ambulance arrival to patient contact: The hidden component of prehospital time intervals. Ann of Emerg Med. 1993;22:1254—1257.
20. Belkman KJ, Parker RB, Harian RJ. Hemodynamic and electrophysiology actions of cocaine effects of sodium bicarbonate as an antidote in dogs. Circulation. 1991;81:1799—1807.
21. Bar-Joseph G, Abramson, NS, Kelsey SF, et al. Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate. Acta Anaesthesiol Scand. 2005;49:6—15.
22. Zartisky AB. Bicarbonate in cardiac arrest: The good, the bad, the puzzling. Crit Care Med. 1995;23:429—431.
This article originally appeared in December 2010 JEMS as “Balanced Equations: Sodium Bicarbonate as Treatment for Cardiac Arrest.”