Acid-Base Balance Understanding is

Critical to Treat Patients

Fri, Jan 15, 2016

By JamesTanis,MD,NRP , JosephE.DiCorpo,BSC,MMSc,PA , Daniel

Friedman,DO,EMTP , MarkMerlin,DO,EMTP,FACEP

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, its 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 bodys 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.1Its
a complex balancing act that you can affect based upon your assessment of the patients
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
1. The buffer system;
2. The respiratory system; and
3. The renal system.
Described by EMS pioneer Nancy Caroline, MD, as being a chemical sponge,the buffer
systemsoaks up excessive hydrogen ions and releases them when theres 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
Therespiratory systemalso 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 CO2is exhaled from the lungs. This results
in less CO2available to form carbonic acid.1 As CO2and hydrogen ion concentrations
return toward the normal range, the respiratory center returns the rate and depth of
respiration back to normal levels.
Therenal systemis a much slower process for dealing with hydrogen ion concentration
change, taking hours to days. Therefore, its more important in the long-term maintenance
of acid-base balance and most impacted in the hospital and critical care arena.1
PREHOSPITAL RELEVANCE
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 acidbase 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.

Case 1
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 4050 breaths per minute; and
palpable radial pulses. Her neurological exam appears to be non-focal, her eyes open to
pain. Shes nonverbal and withdrawals from painful stimuli. Her Glasgowcomascale
(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.

Case 2
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

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. Hes nonverbal and withdraws from painful stimuli.
His GCS is 6 and he has no signs of trauma or injury.
Case 3
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.
Hes prescribed unknown antibiotics but didnt 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 endtidalcarbondioxide (EtCO2) is 20 mmHg and BGL is 290
mg/ dL. His skin is hot and dry with no signs of trauma or injury.

Case 4
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. Shes
tolerating a nasopharyngeal airway (NPA) and an oral airway with noninvasive EtCO2at 98
mmHg. There are no signs of trauma or injury.

Case 5
A 17-year-old male with no past medical history and who doesnt 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 EtCO2is 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 CO2pressure (pCO2). The
calculations are understandably impossible to work out without a patients lab values, but
a general understanding of the concepts are important.

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 patients pH. More importantly, if we can figure out why a patients
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 patients 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 isnt affected by the external addition or subtraction of
hydrogen ion concentration or bicarbonate. Its 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 patients 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 patients respiratory status can be evaluated with a blood gas pCO2. If a patients
pCO2is outside the normal range of 3545 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 EtCO2measurements. EtCO2values will be <

approximation is possible with reliable EtCO2measurements. EtCO2values will be <

pCO2values, but are still relevant, and if the EtCO2is 35 mmHg, the pCO2is 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 CO2or 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, its reasonable to assume other factors, as in
the Stewart method, influence the acid-base status of a patient.3

CHOOSING THE RIGHT TOOLS

Lets 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 patients 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).

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 postRSI ventilations are 10 breaths per minute and tidal volume is 500 mL, the patient has a
minute volume of 5 La 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 dont 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

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 were 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 centercausing 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 isnt 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 patients 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), well see an immediate increase in respiratory rate and minute
ventilation. This will reverse the respiratory acidosis very quickly.

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 isnt 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.7This is a
quick, inexpensive and readily available method to raise a hypotensive patients 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.

Whats a balanced IV fluid and if my only choices are normal saline and lactated Ringers
(or Hartmans), 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 dont contain acids its the difference in charge and the dilution
effects of the infusion that changes the acidbase balance.
If the patients SID is increased by the IV fluid, a metabolic alkalosis will increase and if the
patients 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
Ringers or Hartmans solutions are considered balanced salt solutions with a SID of
approximately 28.8
CONCLUSION
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 patients acid-base status then just pH
and bicarbonate measurements.
This brief review article cant 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.
REFERENCES
1. Caroline NL:Emergency care in the streets, 2nd ed. Little, Brown and Company: Boston,
1979
2. Kishen R, Honor PM, Jacobs R, et al. Facing acidbase disorders in the third millennium
The Stewart approach revisited.Int J Nephrol Renovasc Dis. 2014;7:209217.
3. Seifter JL. Integration of acidbase and electrolyte disorders.N Engl J Med.
2014;371(19):18211831.
4. Kamel KS, Halperin ML. Acid-base problems in diabetic ketoacidosis.N Engl J Med.
2015;372(20):546554.
5. Chin RL, Olson KR. Salicylate toxicity from ingestion and continued dermal
absorption.Cal J Emerg Med. 2007;8(1):2325.
6. Kraut JA, Madias NE. Lactic acidosis.N Engl J Med. 2014;371(24):23092319.
7. Selde W. Push dose epinephrine: A temporizing measure for drugs that have the sideeffect of hypotension.JEMS. 2014;39(9):6263.
8. Gunnerson KJ. Clinical review: The meaning of acidbase abnormalities in the intensive
care unitEffects of fluid administration.Crit Care. 2005;9(5):508516.
RESOURCES
Kaplan LJ, Frangos S. Clinical review: Acid-base abnormalities in the intensive care unit
part 2.Crit Care. 2005;9(2):198203.
Kellum JA, Elbers PG:Stewarts textbook of acid-base. AcidBase.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):5460.

2004;92(1):5460.

By
JamesTanis,MD,NRP
James Tanis, MD, NRP, is the program medical director for education at
MONOC EMS. Hes an emergency medicine resident at Newark (N.J.) Beth
Israel Medical Center and a paramedic and paramedic supervisor with 19
years of experience.

JosephE.DiCorpo,BSC,MMSc,PA
Joseph E. DiCorpo, BSC, MMSc, PA, is the chief medical officer of Medway
Air Ambulance. He started as an EMT in 1971 and was an EMS chief and
administrator in Ohio and California. He can be reached
atjoedicorpo@aol.com.

DanielFriedman,DO,EMTP
Daniel Friedman, DO, EMT-P, is an EMS fellow at Newark (N.J.) Beth Israel
Medical Center/Barnabas Health. Hes a former paramedic in Newark
and North Carolina.

MarkMerlin,DO,EMTP,FACEP
Mark Merlin, DO, EMT-P, FACEP, is the system medical director of
MONOC EMS, New Jerseys largest EMS system. Hes an associate
professor at Rutgers School of Public Health/Medical School. Hes vicechairman of emergency medicine and EMS fellowship director at Newark
Beth Israel Medical Center/ Barnabas Health. Hes a former paramedic in
Pennsylvania.

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