Learning Objectives
By the end of this section, you will be able to:
- Describe the principles of acid-base balance
- Identify the principles of acid-base imbalance
- Explain the regulation of balance systems
Understanding principles of acid-base balance is an essential concept in nursing. Many patients are at risk for acid-base imbalance because of chronic diseases such as kidney disease, lung disease, cardiac disease, and endocrine disorders. If acid-base homeostasis is not maintained, the patient can experience severe consequences or even death. Given the severity of potential complications, nurses must be knowledgeable about acid-base disorders, recognize the symptoms of an imbalance, and know how to intervene if acid-base homeostasis is not maintained.
Principles of Acid-Base Balance
Ensuring that the acid-base balance of human blood remains within a normal range is crucial for maintaining health. Many enzymes and cellular processes do not function normally if the blood’s level of acid or base is too high or too low. Having an uncontrolled acid-base imbalance can even lead to death. There are regulatory systems within the body that correct imbalances to bring the acid-base level back into normal range. It is vital for nurses to understand the basic principles of the acid-base balance so that they can intervene early if there is an abnormality (Lewis, 2023).
Acid
An acid is a molecule that can donate a hydrogen ion (H+) in chemical reactions. There are multiple acids in the human body that maintain the acid level at a specific concentration for enzymes to work. For example, pepsin is an enzyme that breaks down protein in the small intestine. To be activated, pepsin must be in an acidic environment. The stomach secretes HCL to activate pepsin when we eat. In this case, HCL is isolated to the gastrointestinal tract and does not affect the acid-base balance of the body as a whole (Patricia & Dhamoon, 2022).
The acid level in the blood is vitally important for homeostasis. The molecule in the human blood that regulates acid levels is PaCO2, or the partial pressure of carbon dioxide. The normal PaCO2 level is 35 to 45 mm Hg. The act of breathing involves the exhalation of carbon dioxide (CO2). Consequently, the respiratory system plays a role in controlling the level of PaCO2 in the bloodstream (Lewis, 2023).
Base
Just as the acid level in the blood is vital to homeostasis, so is the concentration of base. A base is a molecule that donates hydroxide ions (OH–) in chemical reactions. In the human body, base is represented by the bicarbonate ion (HCO3–). The kidneys regulate the bicarbonate level by either excreting bicarbonate in the urine or reabsorbing it back into the bloodstream. The normal serum bicarbonate range is approximately 22 to 29 mmol/L (Hopkins et al., 2022); however, reference ranges may vary slightly by laboratory.
pH
The pH, or potential of hydrogen, serves as the indicator for the acid-base balance in a solution. It is a numerical representation of the concentration of hydrogen ions within that particular solution. The typical pH range for arterial blood falls between 7.35 and 7.45. A pH below 7.35 indicates acidosis, signifying an abundance of hydrogen ions in the blood. Conversely, a pH exceeding 7.45 suggests alkalosis, indicating a shortage of hydrogen ions in the blood (Hopkins et al., 2022). Symptoms of mild alkalemia are related to the underlying cause of the imbalance (Lewis, 2023). Extended or severe alkalemia results in a relative hypocalcemia, as ionized calcium tends to bind more readily to proteins in an alkalotic environment (Hopkins et al., 2022). Symptoms of acidosis are related to the underlying cause. If the acidosis is mild, the patient may be asymptomatic. However, extended or severe acidosis causes potassium ions to shift out of cells to buffer the net influx of positive hydrogen ions, resulting in systemic hyperkalemia (Mount, 2024). The pH of blood and the concentration of available hydrogen ions is determined by the balance of carbon dioxide (CO2) and bicarbonate (HCO3–). The most accurate way to measure the blood pH is through an arterial blood gas sample. Venous blood has considerably less oxygen and more carbon dioxide than arterial blood because venous blood returns cellular waste to the heart and lungs to expel carbon dioxide and pick up oxygen. Although it is also possible to monitor pH via a capillary blood gas or a venous blood gas, both of those tests tend to report more acidotic results. The type of blood gas sample must be considered when interpreting results (Figure 20.4) (Castro & Keenaghan, 2024).
Clinical Safety and Procedures (QSEN)
QSEN Competency: How to Draw a Capillary Blood Gas Sample
Disclaimer: Always follow the facility’s policies.
| Steps | Rationale/Description |
|---|---|
| Choose the puncture site. For infants 0–12 months, puncture the outer aspect of the heel. For adults and children over age 1, puncture the outer aspect of the finger. | A capillary blood gas is a less invasive procedure than an arterial blood gas sample, which makes it a good option for infants and young children whose veins and arteries can be difficult to access. In adults, capillary blood gas sampling can be used when venous or arterial access is difficult, for noncritical assessments, in outpatient settings without ABG equipment, based on patient preference for less invasive procedures, or where ABG equipment is unavailable. However, it is important to use an appropriately sized lancet and to puncture the appropriate body part to avoid patient harm. |
| Attach the cap to one end of the capillary. | Capillary blood gas samples are collected in clear glass tubes. If you do not place a cap on one end of the tube, the blood will leak out while collecting the sample. |
| Clean the puncture site with an alcohol pad and firmly support the site (either the finger or the heel) with your nondominant hand. | Use the nondominant hand to stabilize the puncture site so that the dominant hand is free to puncture and draw the blood. |
| Puncture the site and wipe away the first drop of blood. | The first draw of blood can be contaminated with the alcohol that was used to clean the site, which can lead to inaccurate results. |
| Place the uncapped end of the tube in the center of the drop of blood. Allow the blood to flow freely into the tube without putting excessive pressure on the lanced site. | Applying excessive pressure on the finger or heel can lead to inaccurate results. |
| Once the capillary tube is filled with blood, run the blood gas analysis. Some units have a blood gas analysis machine on the unit. If it needs to be sent to the lab, it must be sent on ice and as a STAT lab. | If a blood gas sample cannot be run immediately, it should be stored on ice. Leaving a blood gas sample at room air temperature leads to inaccurate results. |
Principles of Acid-Base Imbalance
Acid-base imbalances can potentially have a profound impact on patients’ health and well-being (Figure 20.5). Understanding acid-base imbalances is vital to quality nursing care because many patients are at risk for acid-base imbalances. If nurses understand the physiology behind the imbalance, they can recognize the cues early and intervene before the patient suffers severe complications. Acid-bases imbalances fall into two general categories: metabolic imbalances and respiratory imbalances. If an imbalance occurs in one system, the other system will compensate in order to bring the blood pH back into normal range.
Link to Learning
Principles of acid-base balance in the blood is crucial to understanding homeostasis.
Metabolic Acidosis
Acidosis, pH less than 7.35, is any process that increases the concentration of hydrogen ions in a solution. An increase in the hydrogen ion concentration as a result of an abnormally low serum bicarbonate level (HCO3–), or a serum bicarbonate level less than 22 mEq/L is known as metabolic acidosis (Figure 20.6). Metabolic acidosis is never a benign process and signifies an underlying medical problem that needs to be addressed (Burger & Schaller, 2023).
The root cause of metabolic acidosis is divided into four categories: an increase in acid production, a decrease in acid excretion, acid ingestion, and renal or gastrointestinal bicarbonate loss. Another way to separate metabolic acidosis is whether or not an anion gap (the concentration of unmeasured serum anions) exists. Having a large number of unmeasured anions indicates that an acid has been added to the system (Burger & Schaller, 2023).
Bicarbonate and chloride are the most proliferative anions, or negatively charged ions, in the human body. To maintain homeostasis, the human body has regulatory mechanisms to keep the number of anions and cations, or positively charged ions, approximately equal. Sodium, the most common extracellular cation, is equal to bicarbonate and chloride plus the sum of the unmeasured anions. If there are a large number of unmeasured anions in the plasma, the patient has an anion gap metabolic acidosis. The formula for calculating the anion gap is:
A normal anion gap ranges from 4 to 12 mmol/L. Therefore, having a gap greater than 12 mmol/L indicates that the patient has a large number of additional anions in the plasma, indicating an acid has been added to the system. A common cause of an anion gap metabolic acidosis is an elevated lactate level. However, there are many other causes. A useful mnemonic to help a nurse remember the causes of an anion gap is the acronym CAT MUDPILES. Each letter in CAT MUDPILES stands for a specific acid that could be ingested or produced to cause a metabolic acidosis.
- C: cyanide or carbon monoxide poisoning
- A: arsenic
- T: toluene
- M: methanol, metformin
- U: uremia
- D: diabetic ketoacidosis (DKA)
- P: paraldehyde
- I: iron
- L: lactate
- E: ethylene glycol
- S: salicylates (Burger & Schaller, 2023)
Differentiating the type of metabolic acidosis helps determine the underlying problem that needs to be addressed. For example, if a patient presents with anion gap metabolic acidosis, the nurse must consider the possibility that the patient ingested a toxin, poison, or medication. Determining the nature of the anion gap helps guide treatment. Because metabolic acidosis is never a benign clinical state, nurses must understand the causes of metabolic acidosis so that they can make informed decisions about patient care.
The etiology of a nonanion gap metabolic acidosis is bicarbonate loss. Diarrhea and renal tubular acidosis are the two most common causes of nonanion gap metabolic acidosis. Patients with diarrhea lose bicarbonate in their stool. Patients with renal tubular acidosis excrete an excessive amount of bicarbonate in their urine. Once a probable cause of a patient’s metabolic acidosis has been identified, appropriate steps can be taken to correct the underlying problem (Burger & Schaller, 2023).
Metabolic Alkalosis
Alkalosis— when the pH is greater than 7.45—is any process that causes a net increase in bicarbonate ions in the plasma. A net increase in bicarbonate ions due to loss of hydrogen ions or retention of bicarbonate ions by either the renal or gastrointestinal systems is called metabolic alkalosis (Figure 20.7). There are three broad categories that describe how a patient develops metabolic alkalosis: gastrointestinal loss of hydrogen ions, renal loss of hydrogen ions, and retention or addition of bicarbonate (Brinkman & Sharma, 2023).
Gastrointestinal loss of hydrogen ions can occur as a result of vomiting or gastric suctioning. The stomach contents contain a high concentration HCL. When a patient loses a large quantity of these gastric secretions, this correlates to a relative increase in bicarbonate in the blood. Having a relative increase in bicarbonate in the blood is the cardinal feature of metabolic alkalosis (Brinkman & Sharma, 2023).
Renal loss of hydrogen is another common cause of a metabolic alkalosis. Aldosterone triggers the reabsorption of sodium into the bloodstream via a 1:1 exchange for excreting hydrogen ions into the urine. Pathologies that increase the production of aldosterone increase renal loss of hydrogen ions. For example, loop and thiazide diuretics can create a secondary hyperaldosteronism that leads to excess urine excretion of hydrogen. Genetic defects, such as Bartter syndrome or Gitelman syndrome, can also cause excessive hydrogen ion loss in the urine (Brinkman & Sharma, 2023).
The retention or addition of bicarbonate in the blood can be caused by a variety of different processes. One of the most common is overuse of antacids, which contain alkaline substances to neutralize acids. Also, because the renal system buffers for the respiratory system, patients with respiratory acidosis will develop compensatory metabolic alkalosis. As the carbon dioxide level rises in the blood, the kidneys compensate by reabsorbing bicarbonate to keep the total pH within normal limits (Brinkman & Sharma, 2023).
Metabolic alkalosis is a common diagnosis among hospitalized patients. If not corrected, it can lead to decreased myocardial contractility, arrhythmias, decreased cerebral blood flow, confusion, and even death. Given the potentially dire consequences if the condition is left uncorrected, nurses must closely monitor their patients and intervene early. Nursing knowledge of complex physiological problems, such as hospitalization-induced metabolic alkalosis, enables nurses to be better advocates for their patients (Brinkman & Sharma, 2023).
Respiratory Acidosis
Having a blood pH less than 7.35 with a concurrent increase in carbon dioxide (CO2) is called respiratory acidosis. Carbon dioxide levels are normally maintained in a tight window of 35 to 45 mm Hg because chemoreceptors in the medulla sense an increase in CO2 and trigger the patient to breathe more frequently. However, if ventilation is disrupted for some reason, the lungs are not able to exhale excess CO2 and the patient develops respiratory acidosis (Patel & Sharma, 2023).
Respiratory acidosis is subdivided into three subcategories: acute; chronic; and acute and chronic. In acute respiratory acidosis, there is a sudden rise in carbon dioxide levels. This can be caused by an acute respiratory pathology pneumonia. It can also be caused by problems with the central nervous system (CNS), which can include things such as a stroke or the use of CNS depressants such as opioids. Acute respiratory acidosis can also be the result of diaphragm weakness. Patients with myasthenia gravis and Guillain-Barré syndrome can develop acute muscle weakness that affects their ability to breathe or ventilate (Patel & Sharma, 2023).
Chronic respiratory acidosis occurs in patients with long-standing ventilation issues. As a result of consistently elevated carbon dioxide levels, a patient's chemoreceptors become less responsive to carbon dioxide. Patients with chronic ventilation problems, such as patients with chronic obstructive pulmonary disease (COPD), can develop a new baseline range of CO2 that is higher than the CO2 of patients without chronic ventilation issues.
Patients with chronic respiratory acidosis can also have what is called an “acute and chronic” respiratory acidosis. This occurs when a patient has chronic respiratory pathology and develops an acute ventilation problem that makes the acidosis worse. For example, when a patient with COPD develops pneumonia, the result is an acute and chronic respiratory acidosis (Patal & Sharma, 2023).
Respiratory Alkalosis
A systemic acid-base disorder that is caused by a reduction in carbon dioxide, which produces an elevation in pH above 7.45, is called respiratory alkalosis. It may be caused by a hyperventilation disorder in which the patient breathes too quickly and exhales an excess amount of CO2. Respiratory alkalosis may also occur as compensation for an underlying process, such as metabolic acidosis. Finally, respiratory alkalosis may be accidentally induced as part of medical treatment. Patients who are on mechanical ventilation need to have their carbon dioxide levels monitored regularly to ensure that the ventilator settings are appropriate. If the respiratory rate on the ventilator is too high or if the tidal volume is excessive, the patient may develop respiratory alkalosis (Singh Gill, 2019).
Regulation of Balance Systems
Nurses must have a firm understanding of the mechanisms that regulate acid-base homeostasis because many patients have impaired renal, respiratory, and metabolic function that can interfere with the regulation of pH. If the blood pH is not maintained between 7.35 and 7.45, complications can occur. If there are large deviations from this pH range, severe complications are likely. A pH greater than 7.8 or less than 6.8 is often associated with death. To maintain homeostasis, the human body has multiple regulatory systems that bring the pH back into the needed physiological range. The regulatory balance systems that control blood pH are the chemical buffer system, the respiratory regulatory system, and the renal regulatory system (Davies et al., 2019).
Link to Learning
To prevent deviations in the body’s pH, there are several buffer systems that regulate acid-base levels. Review the regulation of acid-base systems with this video.
Chemical Buffer Systems
Excess acids or bases must be neutralized to maintain the blood pH within a normal physiological range and protect cells. One of the primary ways of regulating this balance is through the chemical buffer system. As acids or bases enter the bloodstream, excess amounts are modified or neutralized by the chemical buffer system. Then, either the respiratory regulatory system or the renal regulatory system is activated to complete the process of eliminating the excess acid or base. The chemical buffer system has three pathways: the carbonic acid–sodium bicarbonate system, the phosphate buffer system, and the protein buffer system.
Carbonic Acid–Sodium Bicarbonate System
The carbonic acid–sodium bicarbonate system is the most widely mobilized buffer system in the human body, accounting for more than 50 percent of all chemical buffering (Figure 20.8). This buffering pathway takes place in the extracellular fluid compartment. Carbon dioxide, CO2, is produced as a result of normal cellular metabolism and enters the bloodstream. In the bloodstream, CO2 combines with water and forms carbonic acid. The carbonic acid molecule is a weaker acid than CO2 and does not cause cellular damage. The carbonic acid molecule is transported in the bloodstream to the lungs, where it disassociates back into CO2 and water. The CO2 is then exhaled by the lungs. Any remaining excess CO2 is converted back into carbonic acid and transported via the circulatory system to the kidneys. In the kidneys, the carbonic acid is separated into H+ ions and bicarbonate. At this point, the kidneys sense which molecule is in excess and excrete that substance while retaining the other. For example, if the patient is acidotic, the kidneys excrete hydrogen ions and reabsorb bicarbonate ions to be reused for further buffering.
Phosphate Buffer System
In contrast to the carbonic acid–sodium bicarbonate buffer system, the phosphate buffer system neutralizes excess acid or base in the intracellular fluid, not the extracellular fluid (Figure 20.9). It is one of two buffering systems that work inside of cells to maintain intracellular acid-base homeostasis. In this system, dihydrogen phosphate acts as a hydrogen ion donor to neutralize excess base, and hydrogen phosphate acts as an ion acceptor to neutralize excess acid. With this buffering system, the acids and bases still exist inside the cells, but the phosphates hold onto the ions and prevent them from altering the cell’s pH.
Protein Buffer System
The protein buffer system is the most important buffer system in the intracellular fluid. It accounts for 75 percent of buffering that occurs intracellularly. Almost all proteins can act as buffers. The building blocks of proteins are amino acids, which contain both a positively charged amino group and a negatively charged carboxyl group (Figure 20.10). Because amino acids contain both a positively and negatively charged group, they can buffer both acids and bases. The positively charged amino group acts as a hydrogen ion donor that neutralizes excess base, and the negatively charged carboxyl group acts as a hydrogen ion acceptor that neutralizes excess acid.
Respiratory Regulation System
The respiratory system plays a crucial role in regulating acid-base balance by regulating the exhalation and retention of carbon dioxide, CO2 (Figure 20.11). Carbon dioxide reacts with water in the blood to form carbonic acid, which is the primary acid in the blood. In the lungs, carbonic acid disassociates back into carbon dioxide and water. Increasing the rate and depth of respirations allows the body to exhale more CO2, which lowers the net carbonic acid level in the blood. On the other hand, taking shallow breaths or holding your breath retains CO2, which causes the carbonic acid level in the blood to rise.
The respiratory regulation system acts as a counterbalance to the renal regulation system. If an acid-base imbalance develops as a result of a renal problem, the patient’s respiratory system adjusts the depth and rate of respiration to compensate.
Renal Regulation System
The renal system regulates acid-base balance by controlling serum levels of bicarbonate, HCO3– (Figure 20.12). Bicarbonate is a base, and alterations in excretion or reabsorption of bicarbonate cause acid-base imbalances. If the kidneys excrete an excess of bicarbonate in the urine, the patient develops metabolic acidosis. On the other hand, if the kidneys retain too much bicarbonate, the patient develops metabolic alkalosis. Common causes of metabolic acidosis include chronic diuretic use, chronic renal insufficiency, and elevated blood ketone levels.
The renal system acts as a counterbalance to the respiratory system. If a patient develops respiratory acidosis, their body senses the increase in acid through the use of chemoreceptors, which stimulates the kidneys to reabsorb more bicarbonate. On the other hand, if a patient develops respiratory alkalosis, that stimulates the renal system to excrete more bicarbonate. Having less bicarbonate in the blood offsets the decrease of carbon dioxide, which is bound with water to form carbonic acid in the blood.