Every critically ill patient we encounter in the field will have an acid-base derangement; therefore, an understanding of acid-base balance is critical to properly treat patients.
First, it’s important you appreciate that every chemical reaction that occurs in the human body is regulated or substantially influenced by the hydrogen ion (H+) concentration in the surrounding tissue, from the way hemoglobin picks up and delivers oxygen to the tissues to the way that sugar, protein and fat are metabolized by the body. The regulation of hydrogen ions, which we measure as “pH,” is what acid-base balance refers to.
The body’s concentration of hydrogen ions must be maintained within a strict range for optimal cellular function, and even a small deviation can significantly affect a patient.1 It’s a complex balancing act that you can affect based upon your assessment of the patient’s vital signs.
An acid has a pH below 7.0 and an increased concentration of hydrogen ions, while an alkaline has a pH above 7.0 and a decreased concentration of hydrogen ions. The body maintains a slightly alkaline pH range of 7.35 to 7.45. Therefore, a pH higher than this range is in a state of alkalosis and a pH below this range is considered to be acidosis. A pH of 6.9 on the acid side and 7.8 on the alkaline side are considered non-compatible with life.1 (See Table 1, above)
An excess of acid is usually produced during the normal process of metabolism, so the body must rid itself of this excess acid to maintain the acid-base balance and keep a normal hydrogen ion concentration. Three defense mechanisms accomplish this:1
- The buffer system;
- The respiratory system; and
- The renal system.
Described by EMS pioneer Nancy Caroline, MD, as being a “chemical sponge,” the buffer system soaks up excessive hydrogen ions and releases them when there’s a deficient concentration. This process occurs in a fraction of a second and is where prehospital assessment and interaction is most beneficial. EMS providers must be aware of the chemical changes that occur via the carbonate system, which consists of a mixture of carbonic acid and bicarbonate in a normal ratio of 1:20. (See Figure 1, top of page.)1
The respiratory system also plays a key role in acid-base regulation. While slower than the buffer system, respiratory centers in the brain become stimulated to increase the rate and depth of respiration when carbon dioxide (CO2) or hydrogen ions levels increase significantly, which increases the rate at which CO2 is exhaled from the lungs. This results in less CO2 available to form carbonic acid.1 As CO2 and hydrogen ion concentrations return toward the normal range, the respiratory center returns the rate and depth of respiration back to normal levels.
The renal system is a much slower process for dealing with hydrogen ion concentration change, taking hours to days. Therefore, it’s more important in the long-term maintenance of acid-base balance and most impacted in the hospital and critical care arena.1
Acid-base derangements are frequently encountered in emergencies, and prehospital patient assessment skills often make the difference in patient outcomes. Understanding acid-base derangements will help prehospital providers select the right strategy for airway management and ventilatory support and use bicarbonate effectively.
What follows are very different patient presentations with commonly encountered acid-base disturbances that complicate underlying illnesses and have a high risk of mortality if poorly managed. By analyzing the root causes of their problems and the pathophysiology behind them, you can select the most appropriate tool from your EMS toolbox.
A 34-year-old female with a history of diabetes is found unresponsive by a family member in bed after she missed work. The patient presents unconscious and tachypneic, with dried vomit on her face and bed linens. Further examination of her primary survey shows an open, clear airway; spontaneous respirations at 40–50 breaths per minute; and palpable radial pulses. Her neurological exam appears to be non-focal, her eyes open to pain. She’s nonverbal and withdrawals from painful stimuli. Her Glasgow coma scale (GCS) is 7. Her skin is hot and dry, with dry mucus membranes. Initial vital signs include a blood pressure (BP) of 132/78, ECG sinus tachycardia at 122 bpm, a respiration rate (RR) of 48 with SpO2 98% on room air. Blood glucose level (BGL) is “HI” on glucometer. Secondary assessment is unremarkable with no signs of trauma or injury.
An 80-year-old male with a history of dementia, coronary artery disease and osteoarthritis is found actively seizing on the floor by his wife. He mistakenly used some oil of wintergreen as a mouthwash. The oil of wintergreen was being used as topical treatment for his arthritis and placed in the bathroom next to his regular mouthwash. His seizure activity was brief and now he presents unconscious, hot to the touch, tachypneic and tachycardic, with a BGL of 47 mg/dL. His neurological exam is flaccid and he has no clonus or tetany and no eye opening to pain. He’s nonverbal and withdraws from painful stimuli. His GCS is 6 and he has no signs of trauma or injury.
A 54-year-old male with a history of diabetes, hypertension, obesity, hypercholesterolemia and recent upper respiratory infection lives alone and is non-compliant with medications. He’s prescribed unknown antibiotics but didn’t complete them. The patient presents lethargic, tachypneic, hypotensive, hypoxic and febrile, with coarse rhonchi throughout his lung fields. On physical exam, he has increased work of breathing, tripod posture and a nonproductive cough. ECG is atrial fibrillation at 110 to 130 bpm, RR is 40, BP is 73/45, SpO2 is 82% on room air. His end-tidal carbon dioxide (EtCO2) is 20 mmHg and BGL is 290 mg/ dL. His skin is hot and dry with no signs of trauma or injury.
A 21-year-old female with a history of IV drug abuse is found unconscious by her parents in her room, hypopneic and cyanotic with constricted pupils. Hypodermic syringes with heroin are found on her bedside table. Her vital signs are: RR of 4, BP of 100/70, ECG sinus tachycardia at 132 bpm. Here SpO2 is 88% on room air with a BGL of 98 mg/dL. She’s tolerating a nasopharyngeal airway (NPA) and an oral airway with noninvasive EtCO2 at 98 mmHg. There are no signs of trauma or injury.
A 17-year-old male with no past medical history and who doesn’t take any medications presents as anxious, emotionally labile and hyperventilating. His fingers and toes are contracted and painful to move. His vital signs are: BP of 118/78, RR of 60, ECG sinus tachycardia at 110 bpm. His SpO2 is 100% on room air and EtCO2 is 17 mmHg. His exam is grossly unremarkable and he has difficulty walking to the EMS stretcher due to the carpal pedal spasms. He denies drug or alcohol abuse or any attempt to harm himself. There are no signs of traumatic injury.
DETERMINING ACID-BASE STATUS
Originally proposed by Peter Stewart, PhD, in the early 1980s and continuing to be a topic in recent critical care literature, the Stewart method uses three independent factors (i.e., things we can vary and change) in the determination of acid-base status of a patient: strong ion difference (SID), weak acid concentration and partial CO2 pressure (pCO2). The calculations are understandably impossible to work out without a patient’s lab values, but a general understanding of the concepts are important.
The strong ions in our bodies are sodium, potassium, calcium, magnesium, chloride, lactate, ketones and sulfate. When added to a solution or IV fluids, they separate and affect our acid-base status.
The SID is normally 42 mEq/L, which has to be electrically balanced with other elements in the system such as weak acids: albumin, globulins and phosphate. When changed, these factors manipulate the patient’s pH. More importantly, if we can figure out why a patient’s pH is off, or what the underlying cause is, our treatment plan will be more successful.2
With the Stewart method, the hydrogen ion concentration, or pH, is caused by changes in a patient’s independent variables: electrolytes, albumin, lactate and ketone levels.
To understand the relationship within the body, we have to consider that an endless supply of hydrogen ions (a dependent variable) is available and how many hydrogen ions are released affects the systematic pH.
With this in mind, we can consider that the pH is based on the charge balance or SID, the amount of weak acids present and the independent variables within the body.2
The key concept is that the pH isn’t affected by the external addition or subtraction of hydrogen ion concentration or bicarbonate. It’s the natural release of hydrogen ions and bicarbonate ions caused by the status of the independent variables. This is due to an unlimited amount of hydrogen and bicarbonate within the body.2
The Stewart method can be summarized with three rules of thumb.2
First, as the SID narrows, metabolic acidosis develops.
Conversely, as the SID widens, metabolic alkalosis prevails.
Lastly, the patient’s albumin level directly affects the acid-base balance; if the albumin is low, as it is in malnutrition or a hypermetabolic state, alkalosis is observed because albumin is an important weak acid within the body. Another metabolic factor that affects the acid-base balance is the production of ketones and lactic acid.2
The patient’s respiratory status can be evaluated with a blood gas pCO2. If a patient’s pCO2 is outside the normal range of 35–45 mmHg, the patient is in a state of respiratory acidosis or alkalosis.
This can be difficult to measure accurately in the prehospital setting, but a close approximation is possible with reliable EtCO2 measurements. EtCO2 values will be < pCO2 values, but are still relevant, and if the EtCO2 is 35 mmHg, the pCO2 is at least 35 due to a leak and unmeasured expired CO2. This can determine hypercapnia and respiratory acidosis well and may be able to identify respiratory alkalosis with a reliable sampling.
The traditional Henderson-Hasselbach equation leads to the overall equilibrium equation:3
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- (carbon dioxide + water ↔ carbonic acid ↔ hydrogen + bicarbonate)
The way we conceptually use this relationship is by eliminating CO2 or adding bicarbonate to drive the equilibrium to the left or right to change the pH. The problem with this equation is that the hydrogen ion concentration is more than a million times that of bicarbonate level, so considering this fact, it’s reasonable to assume other factors, as in the Stewart method, influence the acid-base status of a patient.3
CHOOSING THE RIGHT TOOLS
Let’s examine the acid-base pathophysiology of the five cases presented earlier by applying the Stewart method and identifying cardinal diagnostic signs to select the most appropriate prehosptial intervention. (See Table 2, above, and Table 3, below.)
Should we take control of a tachypneic, unconscious patient’s airway with RSI?
In Case 1, our unconscious patient is tachypneic with a high minute volume (50 breaths per minute and tidal volume of 300 mL has a minute volume of 15 L of gas exchange).
Her rapid breathing is required to compensate for the metabolic acidosis, so, if we sedate and paralyze her, the intrinsic compensation mechanism will be lost and her acidosis can worsen rapidly.
EMS systems have the ability to gain rapid airway control with rapid sequence intubation (RSI). When given a paralytic in the RSI process, gas exchange ceases and apneic oxygenation maintains the oxygen saturation but causes a hypercapnic state. Patients usually tolerate this well, with the exception of those who are profoundly acidotic. If post-RSI ventilations are 10 breaths per minute and tidal volume is 500 mL, the patient has a minute volume of 5 L—a stark difference to the 15 Lpm needed to help compensate for the metabolic acidosis.
Caution must be used with the tachypneic, acidotic patients and consideration of the RSI and ventilation strategy based on a risk/benefit assessment.
If the airway is maintained open and clear without affecting the accelerated respiratory rate, the level of consciousness should improve when we start to fix her underlying problem.
These patients don’t appear to have a gas exchange problem and their clinical course is expected to improve once we address any condition such as diabetic ketoacidosis (DKA) or toxic poisoning.
These patients typically have a reversible cause of altered mental status and, with strict attention to airway preservation, will recover as the metabolic derangement is fixed.
If we’re relatively certain a patient is acidotic, when do we give the bicarbonate?
In Case 1, the patient is acidotic, so, should we give her bicarbonate? The answer is probably not. DKA is a reversible clinical state; once the patient starts receiving insulin and fluid resuscitation, the ketoacid production will slow down and bicarbonate ions will be produced as the ketones are eliminated.4
Case 2 is a different situation, with an unconscious, tachypneic patient with salicylate toxicity. The aspirin poisons the central nervous system (CNS)—particularly the brain stem stimulating the respiratory center—causing a respiratory alkalosis with hyperventilation.
Another clinical feature of aspirin toxicity is the uncoupling of the oxidative phosphorylation system, causing a massive increase in oxygen consumption, metabolic rate and disrupts normal glucose utilization. This dramatically increases lactic acid and ketone production, causing an overwhelming metabolic acidosis.5
This is a patient who needs the bicarbonate IV bolus and infusion. Allow them to maintain their hyperventilations, intervening only in respiratory failure. Rapid correction of the systemic acidosis is necessary to stop the transfer of aspirin into the CNS. Normally, 20% of the salicylates are metabolized in the tissue and 70% are excreted by the kidneys. The bicarbonate administration decreases CNS absorption, decreases serum half-life of the aspirin and enhances urinary excretion of the salicylates. If the kidneys are unable to keep up with the excretion of the aspirin, emergency dialysis should be considered.
Bicarbonate bolus dosing in cases of sepsis, lactic acidosis, respiratory acidosis (e.g., opiate overdose) or cardiac arrest isn’t effective and may be harmful. Supporting or restoring hemodynamics and using a proper ventilation strategy is more effective in the management of hypoxic, shocked acidotic patients.6
When should we consider intervening on a patient’s low blood pressure?
In Case 3, hypotension and acidosis are part of a downward spiral in a septic patient; as the tissue hypoxia worsens, anaerobic metabolism predominates, creating more lactic acid, more acidosis and increases the morbidity and risk of mortality. IV fluid resuscitation, broad spectrum antibiotic therapy and appropriate vasoactive agents would be the treatment of choice.
In Case 4, we see a respiratory acidosis secondary to acute opioid intoxication and respiratory rate (i.e., minute ventilation, depression. If we antagonize the opioid with narcan (Naloxone), we’ll see an immediate increase in respiratory rate and minute ventilation. This will reverse the respiratory acidosis very quickly.
In Case 5, we have the traditional presentation of respiratory alkalosis caused by hyperventilation (i.e., hyperventilation syndrome). Remember, this isn’t that common and should be treated as a diagnosis of exclusion. However, once identified, working with the patient to slow his ventilations and tidal volume to increase his pCO2 (EtCO2) will reverse his respiratory alkalosis.
A recent article shows push dose pressors (PDP) are now entering into our prehospital toolbox as an immediate intervention to temporize non-traumatic hypotension.7 This is a quick, inexpensive and readily available method to raise a hypotensive patient’s blood pressure as you address the root problem. Out of the five cases, the septic shock patient would benefit most from PDP. The best PDPs are direct alpha acting stimulants, such as Neo-Synephrine (phenylephrine) and not indirect-acting sympathomimetics.
What’s a balanced IV fluid and if my only choices are normal saline and lactated Ringer’s (or Hartman’s), which is best?
The difference is in the SID. A strong ion or electrolyte solution is defined by their ability to completely disassociate or separate in biological systems (i.e., in the patient). The crystalloid solutions don’t contain acids— it’s the difference in charge and the dilution effects of the infusion that changes the acidbase balance.
If the patient’s SID is increased by the IV fluid, a metabolic alkalosis will increase and if the patient’s SID is decreased the metabolic acidosis will be exacerbated. Large volume saline infusions can cause a metabolic acidosis by dilution of the plasma/extracellular SID.
Saline is SID zero solution, as explained by the following equation:
154 mEq of Na+ – 154 mEq of Cl– = 0
SID = [strong cation+] – [strong anions–]
Balanced crystalloid solutions can reduce infusion-related metabolic acidosis. Lactated Ringer’s or Hartman’s solutions are considered balanced salt solutions with a SID of approximately 28.8
Things we can do right by our prehospital patients are to aggressively protect the airway of our obtunded patients with reversible causes of depressed mental status and avoid the use of medications to slow or block tachypneic compensations of metabolic acidosis.
Additionally we can start early aggressive fluid resuscitation in shock and dehydration and remember that there are many other factors to a patient’s acid-base status then just pH and bicarbonate measurements.
This brief review article can’t explain all the nuances of acid-base balance, so we encourage you to read more on this important area so you can be an exceptional clinical detective and clinician in the field.
1. Caroline NL: Emergency care in the streets, 2nd ed. Little, Brown and Company: Boston, 1979
2. Kishen R, Honoré PM, Jacobs R, et al. Facing acid–base disorders in the third millennium— The Stewart approach revisited. Int J Nephrol Renovasc Dis. 2014;7:209–217.
3. Seifter JL. Integration of acid–base and electrolyte disorders. N Engl J Med. 2014;371(19):1821–1831.
4. Kamel KS, Halperin ML. Acid-base problems in diabetic ketoacidosis. N Engl J Med. 2015;372(20):546–554.
5. Chin RL, Olson KR. Salicylate toxicity from ingestion and continued dermal absorption. Cal J Emerg Med. 2007;8(1):23–25.
6. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014;371(24):2309–2319.
7. Selde W. Push dose epinephrine: A temporizing measure for drugs that have the side-effect of hypotension. JEMS. 2014;39(9):62–63.
8. Gunnerson KJ. Clinical review: The meaning of acid–base abnormalities in the intensive care unit—Effects of fluid administration. Crit Care. 2005;9(5):508–516.
- Kaplan LJ, Frangos S. Clinical review: Acid-base abnormalities in the intensive care unit—part 2. Crit Care. 2005;9(2):198–203.
- Kellum JA, Elbers PG: Stewart’s textbook of acid-base. Acid-Base.org: Amsterdam, Netherlands, 2009.
- Muniandy RK, Sinnathamby V. Salicylate toxicity from ingestion of traditional massage oil. BMJ Case Rep. 2012;bcr2012006562.
- Story DA, Morimatsu H, Bellomo R. Strong ions, weak acids and base excess: A simplified Fencl-Stewart approach to clinical acid-base disorders. Br J Anesth. 2004;92(1):54–60.