Acid Pathways	Cause	Measure
Cells produce acid (acid production increases).	Hypermetabolic states, such as pain, hyperthermia, or inflammation. The respiratory and heart rates increase, and bicarbonate is initially consumed by buffering.	HCO₃ ↓
	Tissues are hypoxic; anaerobic metabolism ensues resulting in lactic acidosis.	Lactate level ↑
	Absolute insulin deficiency results in failure of glucose to be transported into cells.	Blood glucose level ↑ Ketoacids ↑
Cells regulate acids.	When acid production (H⁺) increases, pH decreases, bicarbonate is initially consumed by buffering, and CO₂ is exhaled in larger amounts, and H⁺ exchanges for K⁺ as cells buffer acid.	pH ↓ HCO₃ ↓ K⁺ ↑ Total serum CO₂ ↓
Lungs regulate acid.	When acid increases due to hypermetabolic states such as pain, hyperthermia, or inflammation, carbonic acid (H₂CO₃) increases and rapidly converts to CO₂ and H₂O. The respiratory rate increases to blow off CO₂.	Paco₂ ↓
Kidneys regulate acid.	When acid increases, tubules are affected by low blood pH, and work to neutralize increased carbonic acid (H₂CO₃) by separating it into H⁺ and bicarbonate HCO₃. Kidneys excrete what is necessary to sustain normal pH if renal function is normal. If abnormal, kidneys may not perform this task.	HCO₃ ↑ Kidney function is assessed by serum BUN and creatinine; elevated BUN and creatinine indicate abnormal kidney function.

The most important component identified is the H₂CO₃, or carbonic acid. As carbonic acid increases (“goes up”), the pH decreases (“goes down”), reflecting the presence of acid. If the carbonic acid decreases (“goes down”), the pH increases (“goes up”), reflecting the absence of acid. The equation is constantly shifting from left to right and right to left to maintain a normal H₂CO₃ and therefore a normal pH. Whatever causes the change of carbonic acid concentration (may be related to a regulation failure by either the lungs or kidneys or a metabolic acid production state) is the “primary culprit.” Identifying the origin or cause of the change in pH direction identifies the problem. Therefore, if the problem is too much acid (either increased CO₂ or H⁺ ), the carbonic acid goes up and the pH goes down. The primary problem is acidosis. Further evaluation is needed to determine whether failure to regulate the acid was ineffective regulation by the lungs, the kidneys or an increase in cellular acid production (ketoacidosis or lactic acidosis).

Changes in pH are associated with changes in the potassium level. As the plasma level of nonvolatile or metabolic acid (H⁺) increases, H⁺ moves into the cells in order to buffer the acid effect. In this case H⁺ “exchanges places” with the intracellular potassium (K⁺), resulting in a measured serum hyperkalemia but is actually an intracellular hypokalemia. The positively charged intracellular potassium ions are replaced by positively charged hydrogen ions. During an alkalotic state, K⁺ may shift into cells as H⁺ is released into the serum, creating a transient hypokalemia. As pH changes, it is imperative for the care providers to observe the corresponding changes in the K⁺ level, and manage K⁺ carefully. When the pH normalizes, the K1 will shift back to its original location. If a transient K⁺ change is managed too aggressively, the patient may experience dangerous hypokalemia or hyperkalemia when pH normalizes.

Understanding the arterial blood gas

The ABG is the most commonly used measurement to help assess the origins of problems with acid-base imbalance and to guide treatment designed to restore pH balance and effective oxygenation. “Perfect” values for each reflects chemical neutrality. There are normal variations or a range for each value.

Abg values

Blood gas analysis is usually based on sampling of arterial blood. Mixed venous blood sampling from a pulmonary artery (PA) catheter (SvO₂) and central venous sampling from a central intravenous (IV) line (ScVO₂) may also be performed for very critically ill patients. Venous values are given for reference only.

Normal Arterial Values	Normal Venous Values
pH: 7.35–7.45	pH: 7.32–7.38
PaCO₂: 35–45 mm Hg	PvCO₂: 42–50 mm Hg
PaO₂: 80–100 mm Hg	PvO₂: 40 mm Hg
SaO₂: 95%–100%	SvO₂: 60%–80%
Base excess (BE): −2 to +2	BE: −2 to +2 (only calculated on ABG analyzer)
HCO₃⁻: 22–26 mEq/L	total Serum CO₂⁻: 23–27 mEq/L

pH (perfect 7.40, range of normal 7.35 to 7.45): This reflects the level of respiratory and metabolic acids found in the blood during the continuous “balancing act” that regulates the acid environment. If this balance is altered, derangements in pH occur. Any alteration in pH should be evaluated. If the pH has changed from perfect, it can only be one of two reasons: normal variation, or abnormality with compensation. When pH is less than 7.35 or greater than 7.45, it is considered an acute change that is uncompensated. When full compensation is attained for an acid-base imbalance, the pH normalizes. Failure to bring pH to range of normal means that there is failure to compensate, even if there is an attempt. Traditionally this was known as partial compensation. That term is no longer advocated.

Paco₂ (perfect 40, range of normal 35 to 45 mm Hg): This is a measure of pressure (partial pressure which is designated by the P) that the dissolved CO₂ exerts in the arterial blood. The dissolved gas exerts the pressure of CO₂, enabling it to diffuse across the capillary and alveolar cell wall.

CO₂ is released during aerobic metabolism and is the main contributor to serum acid. CO₂ is controlled through ventilation. In the normal lung, CO₂ is regulated by changes in the rate and depth of alveolar ventilation. CO₂ is carried both bound to hemoglobin and dissolved in the blood. The measured CO₂ is termed PaCO₂. PaCO₂ is directly measured (not calculated) and is a reliable indicator of respiratory acid-base regulation. The correlation between PaCO₂ and respiratory-based pH changes is direct, consistent, and linear. In other words if PaCO₂ is up and pH is down, the cause is respiratory deregulation. If the issue is metabolic, and respiratory compensation has occurred, the PaCO₂ will decrease in order to bring pH back to normal levels. Respiratory compensation typically occurs rapidly in metabolic acid-base disturbances as long as respiratory function is not impaired. When a patient hyperventilates, PaCO₂ decreases as it is “blown off” by rapid exhalations. During hypoventilation (slow and/or shallow breathing), PaCO2 increases. Although the only way to evaluate true lung function is by the gas exchange, the capacity of the lungs (CO₂ regulation response) is measured via the minute ventilation (VE or MV). This measures the amount of volume exhaled per minute (V_E) calculated as respiratory rate (RR) × V_T. Normal MV is about 8 to 10 L/min. B

Pao₂ (perfect 95 to 100 mm Hg, normal range 80 to 100 mm Hg): The partial pressure of oxygen (O₂), or PaO₂, is a measure of the dissolved (usable) gas in the arteries. The dissolved gas exerts the pressure of O₂, enabling it to diffuse across the capillary and cell wall to oxygenate cells. PaO₂ normally declines in the older adult.

• Hypoxemia (PaO₂ less than 80 mm Hg): Low partial pressure of O₂ affects the cellular levels of oxygen available and may result in cellular metabolic dysfunction reflected by lactic acid production and metabolic acidosis.

• Fio₂: Fraction of inspired O₂ or the percentage of the atmospheric pressure which is oxygenated. Room air is 21% or 0.21 O₂. O₂ delivery devices can increase the FIO₂ to 100% or 1.00.

P/F ratio (greater than 300): PaO₂ is evaluated in relationship to FIO₂; that is, the higher the percent O₂ pressure that is delivered to the lungs, the higher the O₂ in the blood should be.

Sao₂ (perfect 100% or 1.0, normal range 95% to 100% or 0.95 to 1.0): O₂ saturation (SaO₂) reflects the loading of O₂ onto hemoglobin (Hgb) in the lungs. When Hgb is loaded with O₂, it is termed oxyhemoglobin. Hgb is the primary transporter of O₂ and supplies a reservoir (reserve) of O₂ for cellular use. Each Hgb molecule carries 1.34 to 1.36 ml of O₂. O₂ must be released from the Hgb, dissolve in blood (PaO₂), and exert pressure to diffuse across the cell wall. The uptake/use of O₂ by the tissues is measured by SvO₂ and/or ScVO₂ (mixed venous and/or central venous saturation of Hgb, respectively). Cellular metabolism and O₂ utilization are affected by changes in stress level, temperature, pH, blood flow, and PaCO₂. When the PaO₂ falls to less than 60 mm Hg, there is a large drop in saturation, reflected in the oxyhemoglobin dissociation curve.

• Pulse oximetry (SpO₂): This can be used to noninvasively trend the arterial O₂ saturation and determine ventilation status using a probe fastened to the patient’s finger, earlobe, or forehead. This monitoring technique is frequently used in critical care areas for patients at high risk of ventilation problems, in operating rooms, and in emergency departments. SpO₂ should be correlated with SaO₂ (or oxyhemoglobin) via blood gas analysis when pulse oximetry is initiated, to assess accuracy of SpO₂ readings. Pulse oximetry is a close correlate to SaO₂ under normal physiologic conditions, but if perfusion decreases, the pulse needed for accurate measurement by the SpO₂ probe is decreased, prompting inaccurate readings. Anemic patients should have consistently high readings, so what is usually considered a normal SpO₂ reading may be too low in an anemic patient. The measure of true oxyhemoglobin (Hgb saturated with O₂) requires an ABG analysis. Many centers do not perform a correlation analysis when oximetry is initiated.

BE (perfect 0, normal range −2 to +2): Base excess or base deficit uses a calculation to reflect the presence (excess) or absence (deficit) of buffers. The calculation reflects the tissue and renal tubular presence (or absence) of acid. As the proportion of acid rises, the relative amount of base decreases (and vice versa). Abnormally high values (greater than +2) reflect alkalosis, or an excess of base; low values (less than −2) reflect acidosis, or a deficit of base (base deficit).

• All buffers: Absorb acids (H⁺), but do so with a varying affinity. Buffers are present in all body fluids and cells and act within 1 second after acid accumulation begins. They combine with excess acid to form substances that may not greatly affect pH. Some buffers have a strong affinity to acid; others are weak. The three primary plasma buffers are bicarbonate (HCO3−), intracellular proteins, and chloride (Cl⁻). All are negatively charged to facilitate attraction to positively charged hydrogen ions (H⁺). Combining positively charged with negatively charged ions yields a neutral substance.

• Proteins: Serum and intracellular proteins offer a significant contribution to buffering acids. Hgb not only transports O₂ but also provides a very strong buffer for hydrogen ions (H⁺). Albumin is also a significant buffer, and hypoalbuminemia must be considered when performing anion gap calculations.

• HCO₃⁻ (perfect 24, normal range 22 to 26 mEq/L): Serum bicarbonate (HCO₃⁻) is one of the major components of acid-base regulation by the kidney. Bicarbonate is generated and/or excreted by normally functioning kidneys in direct proportion to the amount of circulating acid to maintain acid-base balance. Because bicarbonate is affected by both the respiratory and metabolic components of the acid-base system, the relationship between metabolic acidosis and bicarbonate is not particularly linear or predictable. When the bicarbonate level changes, the acid level changes in the opposite direction. To determine the cause of bicarbonate changes (as the source of a pH problem versus compensation), the relationship to pH must be evaluated. The pH changes in the presence or absence of acid, and the directional relationship reflects what caused the pH alteration. The kidney is responsible for the regeneration of bicarbonate ions, as well as excretion of the hydrogen ions. Although serum bicarbonate is a buffer, it is usually reported in the standard electrolyte panel from a venous blood sample as “CO₂ content” or “total CO₂” rather than as bicarbonate (HCO₃⁻). The serum HCO₃⁻ concentration is usually calculated and reported separately with ABG analysis. Either value may be used as part of the assessment of acid-base balance (Table 1-2).

• Chloride (Cl−): The number of positive and negative ions in the plasma must balance at all times. Aside from the plasma proteins, bicarbonate and chloride are the two most abundant negative ions (anions) in the plasma. To maintain electrical neutrality, any change in chloride must be accompanied by the opposite change in bicarbonate concentration. If chloride increases, bicarbonate decreases (hyperchloremic acidosis) and vice versa. However the combination of H⁺ and chloride actually exerts an acid effect (HCl). Chloride concentration may influence acid-base balance (see anion gap). Chloride concentration should be observed closely when large amounts of normal saline are administered to patients.

• Other buffers: Other buffers, including phosphate and ammonium, are present in very limited quantities and have a lesser impact on the regulation of acid.

• Cellular electrolytes: The cells also offer protection in the metabolic acid environment. H⁺ may exchange across the cell wall, attracted by negatively charged intracellular proteins in a cellular buffering process. When this happens, K⁺ is released from the proteins and shifts out of the cell, causing an excess of K⁺ in the blood.

• Anion gap: Anion gap is an estimate of the differences between measured and unmeasured cations (positively charged particles, such as Na and H⁺ respectively) and measured and unmeasured anions (negatively charged particles such as HCO₃⁻ and Cl⁻. Normally, cations and anions are equally balanced in live humans (in vivo), but when measured in the laboratory (in vitro), the difference may be between 10 to 12 mmol/L. This difference is termed a normal gap (between + and – ions). Particles that possess charges tend to have high affinity to bind to other particles that possess charges that are opposite their own (hence the term, “opposites attract”). Anion gap is used to determine if a metabolic acidosis is due to an accumulation of nonvolatile acids such as lactic acid or ketoacids. Both contribute a positive charge due to excess H⁺ or from net loss of bicarbonate (e.g., diarrhea). The gap is not affected when a patient has metabolic acidosis purely from kidney failure. The formula for calculation of anion gap is

Table 1-2 DIAGNOSTIC TESTS FOR ACID-BASE BALANCE

Role of the ABG	Measures	Normals
Evaluation of arterial oxygen (dissolved oxygen and oxygen bound to hemoglobin)	Arterial oxygen saturation (oxygen bound to hemoglobin)	Sao₂: 0.95–1.0 or 95%–100%
	Partial pressure of arterial oxygen (dissolved oxygen)	Pao₂: 80–100 mm Hg (decreased over the age of 70)
Calculation of alveolar-arterial (A-a) oxygen gradient	Alveolar-arterial gradient	A-a Do₂: <20 mm Hg
Calculation of alveolar-arterial (A-a) oxygen gradient	Pao₂/Fio₂ ratio	PF ratio: .300
Evaluation of cellular environment	pH (reflects H₂CO₃) i.e., ↑↑ H₂CO₃ then pH ↓↓	pH Perfect: 7.40 Normal range: 7.35–7.45
Evaluation of ventilation	Paco₂	Paco₂ Normal range: 35–45 mm Hg
Evaluation of tissue metabolism	H⁺ inversely (indirectly) reflected by buffers: Bicarbonate (HCO₃⁻) Base measures (+ or −) Total CO₂ i.e., ↑↑ H⁺ then buffers ↓↓	pH Perfect: 7.40 Normal range: 7.35–7.45
		HCO₃⁻: 22–26 mEq/L
		Total CO₂: 20–26
		Base Normal range: −2 to +2
		Anion gap: 12 + or −2
Additional measures of tissue metabolism	Both contribute H⁺ to blood lactic acid Ketoacids	Lactic acid: 1–2 mmol/L
Additional measures of tissue metabolism	Both contribute H⁺ to blood lactic acid Ketoacids	Ketoacids Blood: 0.27–0.5 mmol/L Urine levels Small: <20 mg/dl Moderate: 30–40 mg/dl Large: >80 mg/dl
Evaluation of renal clearance	Appropriate clearance of excessive components: H⁺ or HCO₃⁻ Appropriate clearance of excessive components: BUN and creatinine	pH Perfect: 7.40 Range: 7.35–7.45 BUN: 0–20 mg/dl Creatinine: <2.0 mEq/L

Unmeasured cations: Calcium, magnesium, gamma globulins, potassium (bind negative charged particles)

Unmeasured anions: Albumin, phosphate, sulfate, lactate, hydrogen ion (bind positive charge particles)

Step-by-step guide to abg analysis

A systematic analysis is critical to the accurate interpretation of ABG values to determine the origin of acid-base imbalance, and level of compensation (see Table 1-2).

Step 1: check the ph: determine if ph is perfect (7.40)

When there is a perfect balance of acid and buffer (base), the pH is termed neutral or perfect. If it is not perfect, determine if the direction of the difference is above or below 7.40. Next, determine if it is in the range of normal (7.35 to 7.45). If it is abnormal, identify whether it is on the acidotic (less than 7.35) or alkalotic (greater than 7.45) side of normal. “Perfect pH” occurs when the system preserves neutrality (pH 6.8) inside the cells, where most chemistry occurs, and maintains the serum pH at 7.40. For the purposes of learning, the perfect pH is where all measurement begins. When the system contains too many acid ions (in the form of ↑CO₂ or ↑H⁺), this causes acidemia. When the system contains too few acid ions (in the form of ↓CO₂ or ↓H⁺), this causes alkalemia, and the pH will reflect the change. Any variation in the pH in relationship to perfect (7.40) must be noted by the provider. If the pH is in the range of 7.35 to 7.45, there are only two possibilities: First, the deviation is a normal variation, wherein no abnormalities exist on either the respiratory side (PaCO₂) or the metabolic side (HCO₃⁻) of the pH equation. The second possibility is there is a problem with ventilation (respiratory), cellular acid production (metabolic), or the ability of the kidneys (metabolic) to balance the pH. Diagnosis of a problem with metabolic acid-base balance is more complex, as many conditions generate metabolic acids and renal failure creates an acid clearance deficit.

Ph less than 7.35, acidosis:

Extra acids are present or base is lost. If pH is 7.35 to 7.39, the pH is normal but not perfect (7.40); the pH is considered “on the acidotic side.”

• Acidosis: Extra acids are present or base is lost, with a pH less than 7.35

1. Cellular acidosis: When cells are hypoxic or processing proteins to yield glucose, there is an increase in lactic acid or ketoacid.

2. Respiratory acidosis: If the function of the lungs is inadequate, such as in COPD disease, the failure to effectively ventilate results in the inability to exhale CO₂, and that failure causes carbonic acid to go up (more acid ) and pH to go down.

3. Renal acidosis: If the kidney function is inadequate, the ability to break carbonic acid from H₂CO₃ into hydrogen ions (H⁺) and HCO₃⁻ is reduced or lost. When this failure occurs, carbonic acid goes up (more acid) and pH goes down.

Ph greater than 7.45, alkalosis:

Extra base is present or there is loss of acid. If pH is 7.41 to 7.45, the pH is normal but not perfect (7.40); the pH is considered “on the alkalotic side.”

• Alkalosis: Extra base is present or there is loss of acid, with a pH greater than 7.45.

1. Respiratory alkalosis: When hyperventilation is the primary problem, there is a very rapid removal of CO₂, causing carbonic acid to go down (less acid ) and pH to go up.

2. Renal alkalosis: If the kidney function is overstimulated (for example, with aggressive diuresis), there may be excessive loss of hydrogen ions (H⁺), causing carbonic acid to go down (less acid ) and pH to go up.

3. Other contributors: Gastric and intestinal removal of acids may occur when patients have diarrhea, vomiting, or when excessive gastric drainage removes acidic secretions and influences the acid-base balance.

Step 2: check the paCO₂

Check PaCO₂ for perfect levels (40 mm Hg). If not perfect, determine if the direction of change is above or below 40 mm Hg. Next, determine if CO₂ is in the range of normal (35 to 45 mm Hg). If abnormal, identify whether it is on the acidotic (greater than 45 mm Hg) or alkalotic (less than 35 mm Hg) side of normal. If PaCO₂ has been retained as a result of hypoventilation or overly removed through hyperventilation, the change in pH will be in the opposite direction of the PaCO₂. Elevated CO₂ lowers pH, while decreased CO₂ increases pH. If the change in pH is in normal range but not perfect, or is out of range, with a PaCO₂ value that has traveled in the opposite direction, respiratory acid retentions caused the imbalance. Using this technique helps determine whether the primary problem is respiratory (involving PaCO₂) or metabolic (reflected by HCO₃⁻). The Paco₂ has to be outside of the normal range for there to be a problem.

Step 3: check for base (deficit or excess)

Check bicarbonate (HCO₃⁻) (24 mEq/L) and base (0) for perfect levels. If not perfect, determine if the direction of change is above or below perfect. Next, determine if HCO₃⁻ (22 to 26 mEq/L) and/or base (+2 to −2) is in the normal range. If the values are abnormal, relate the two values to metabolic acid (H⁺). If bicarbonate and base are decreased (a deficit), metabolic acid is increased. If bicarbonate and base are increased (in excess), metabolic acid is decreased. If the change in pH is in normal range but not perfect, or out of range and the assumed H⁺ is in the opposite direction (meaning that the HCO₃⁻ (and/or base are in the same direction as the pH) metabolic issues caused the imbalance. Using this technique helps determine whether the primary problem is respiratory (involving PaCO₂) or metabolic (reflected by HCO₃⁻) or both.

Step 4: (evaluate both paCO₂ and hco₃⁻)

Correlating the direction of the pH change with the direction of change in PaCO₂ and H⁺ (HCO₃⁻ ) is essential. The value that deviates in the opposite direction from the pH suggests the primary disturbance responsible for the altered pH. Assess pH for acidosis or alkalosis, and then evaluate whether the change in CO₂ or H⁺ ( HCO₃⁻ ) is most reflective of the “direction” of the pH change.

A mixed metabolic-respiratory acid-base imbalance or compensation may be responsible for the values reflected by the ABG.

Step 5: check paO₂ and saO₂

Check PaO₂ and O₂ saturation to determine whether they are decreased, normal, or increased. Decreased PaO₂ and O₂ saturation may signal the need for increased concentrations of O₂ or alveolar recruitment strategies. Conversely, high PaO₂ may indicate the need to decrease delivered concentrations of O₂. Oxygen evaluation is the same for all arterial blood gases, although in the presence of metabolic acidosis, a more in-depth investigation will require evaluation of tissue metabolic functions.

Respiratory acidosis

Pathophysiology

Evaluation of an abnormal arterial blood gas resulting in a decreased ph due to hypoventilation

Example: pH 7.28, PaCO₂ 55, HCO₃⁻ 24, PaO₂ 92 mm Hg, SaO₂ 91%

Step 1: ph is 7.28, not perfect or neutral (7.40) and outside the normal range of 7.35 to 7.45.

Ideally the pH should always be perfect (7.40), but a small variation is acceptable (range of 7.35 to 7.45). One must remember that pH changes are a symptom of a problem. So the first issue is to identify the problem.

pH: The primary problem with pH regulation is identified by the direction of the pH change in respect to perfect: Is it on the acid side (less than 7.40) or the alkaline side (greater than 7.40)?

1. pH 7.28: Acid side, outside of range of normal

2. Question: Is there a problem? YES, acidosis (identified by the pH)

3. Where is the acid being generated? Are the acids respiratory or metabolic?

4. PaCO₂: 55 (elevated outside the normal range) → respiratory acid is accumulating

5. HCO₃⁻: 24 (perfect) → metabolic acid is not present, perfect HCO₃

Step 2: paCO₂ is 55 mm hg, not perfect (40 mm hg) and above the normal range of 35 to 45 mm hg indicating an excess of respiratory acid.

Investigation begins:

1. Hypercapnia/elevated Paco2 (Paco2 greater than 45 mm Hg): Signals alveolar hypoventilation. This problem occurs when alveoli are not recruited, there is poor blood flow, the respiratory rate or tidal volume is inadequate, or there is fluid or an increase in the space between alveoli and blood vessel. These conditions may be chronic or acute.

2. If this is the causative problem, the pH has to be below 7.40, reflecting excess acid (CO2) or an increase in carbonic acid (H2CO3), which is a primary acidosis. So now one must investigate what caused the increase in carbonic acid (H2CO3). For every 10 mm Hg increase in CO2, the pH will acutely decrease 0.08 (on the acid side).

3. Problem: Respiratory acidosis

Respiratory acidosis (hypercapnia, hypoventilation) is always related to a ventilation problem caused by inadequate therapeutic interventions or lung pathophysiology, resulting in retention of PaCO₂. PaCO₂ derangements are direct reflections of the degree of ventilatory function or dysfunction. The degree to which the increased PaCO₂ alters the pH depends on the rapidity of onset and the blood and kidney’s ability to compensate via the blood buffer and renal regulation systems. The pH may be profoundly affected initially because of the time required (hours to days) for kidney compensation to occur. The most common cause of inadequate CO₂ excretion (CO₂ retention) is inadequate alveolar ventilation, or alveolar hypoventilation. Alveolar hypoventilation can occur when there is airway obstruction, loss of alveolar recoil, or inadequate time for exhalation affecting the ability to express carbon gas into the environment. For CO₂ to be removed from the blood, the partial pressure of CO₂ in the alveoli must be less than that in the blood. In air-trapping syndrome (loss of alveolar recoil or elasticity or airway obstructive disease) or profound hypoventilation states, the alveolar concentration of CO₂ increases, which then limits the removal of CO₂ from the blood. If the problem is not properly managed, the patient may deteriorate into acute respiratory failure.

Step 3: the hco₃⁻ in the example is perfect at 24 meq/l. the normal range of bicarbonate is 22 to 26 meq/l.

Investigation begins:

1. Normal HCO₃⁻ indicates that there is not a metabolic problem, although compensation should begin within 4 to 48 hours, as opposed to respiratory compensation for metabolic pH imbalances, which happens in minutes.

2. Problem: No apparent kidney or metabolic problems

Is there compensation for the respiratory acidosis?

In order for compensation to occur, the carbonic acid must be presented to the kidney and separated into H⁺ and HCO₃⁻. In other words, the excess CO₂ will be processed into carbonic acid and ultimately into H⁺ (which will be excreted in a functional kidney state) and HCO₃⁻. Kidney or renal compensation for accumulation of respiratory acids is a slow process, After 48 hours if there continues to be an acidotic pH, one must assume that the kidneys have lost the ability to eliminate H⁺ or retain HCO₃⁻.

Step 4: diagnosis begins:

1. Only the CO₂ is elevated, without a change in the HCO₃⁻.

2. pH is down and outside range reflecting the presence of acid in the blood.

3. Problem: The patient has acute respiratory failure, causing an accumulation of respiratory acid (CO₂). There is no compensation, but no evidence is available at this time.

Diagnosis: Acute Respiratory Acidosis

Step 5: paO₂ 92 mm hg (not perfect 98 to 100 mm hg but within normal range 80 to 100 mm hg), saO₂ 91% (not perfect 100% and below normal range of 95% to 100%).

Investigation begins: slight decrease is apparent in paO₂ and saO₂

1. Use of O₂: If O₂ is not in use on a patient with reduced PaO₂ and SaO₂, applying O₂ often corrects the readings. If O₂ is in use, changing to a device that delivers a higher concentration of O₂, such as changing from a nasal cannula to a face mask, may be sufficient to correct the alveolar levels of O₂. If the PaO₂ and SaO₂ do not respond to the first device change or values further deteriorate, a 100% nonrebreather mask may be applied to provide close to 100% O₂. Note: All ABG readings must be recorded with consideration of the mode of O₂ delivery recorded, as well as the FIO₂ or concentration of O₂. Otherwise, evaluation of the PaO₂ and SaO₂ values is meaningless. If the values are NOT recorded, the assumption is made the readings are done on room air, without O₂ in place.

2. Evaluating risk for poor tissue oxygenation: Thus far, ventilation has been evaluated using the ABG, but both ventilation AND perfusion must be evaluated as part of O₂ delivery to the cell level. To objectively and proactively identify the patient at risk for tissue hypoxia, early signs of the perfusion changes that precede increases in serum lactate and the widening anion gap associated with lactic acidosis may be noted. Changes in heart rate (HR), blood pressure (BP), respiratory rate, urine output, saturation of continuous central or mixed venous Hgb, and serum creatinine are common. In the shock setting, normal or near normal PaO₂ and SaO₂ readings are possible on an ABG while capillary bed dysfunction ensues. Normal readings indicate O₂ is being provided in adequate amounts to saturate Hgb effectively; but the ABG is unable to assess whether all tissue beds are receiving O₂ or whether the cells are able to use the O₂. Until metabolic acidosis ensues due to accumulation of lactic acid byproducts of anaerobic metabolism due to hypoperfusion, the ABG and SpO₂ readings may be misleading.

Collaborative management: acute respiratory acidosis

CARE PLAN: RESPIRATORY ACIDOSIS

Impaired gas exchange

Goals/outcomes

Within 24 hours of initiation of treatment, patient improves and is reevaluated. The ultimate goal of adequate gas exchange is evidenced by PaCO₂, pH, and SaO₂ that are normal or within 10% of patient’s baseline.

Respiratory Status Ventilation, Vital Signs Status, Respiratory Status: Gas Exchange, Symptom Control Behavior, Comfort Level, Endurance, Acid-Base Management: Respiratory Acidosis

Respiratory monitoring

1. Monitor serial ABG results to assess patient’s response to therapy. Consult physician for significant findings: increasing PaCO2 with decreasing pH, PaO2, and SaO2 values.

2. Monitor O₂ saturation via pulse oximetry (SpO₂). Compare SpO₂ with SaO₂ values to assess reliability. Watch SpO₂ closely, especially when changing FIO₂ or to evaluate patient’s response to treatment (e.g., repositioning, chest physiotherapy).

3. Assess and document patient’s respiratory status: respiratory rate and rhythm, exertional effort, and breath sounds. Compare pretreatment findings with posttreatment findings (e.g., O₂ therapy, physiotherapy, medications) for evidence of improvement.

4. Assess and document patient’s level of consciousness (LOC). If PaCO₂ increases, be alert to subtle, progressive changes in mental status. A common progression is agitation → insomnia → somnolence → coma. To avoid a comatose state caused by rising CO₂ levels, always evaluate the arousability of a patient with elevated PaCO₂ who appears to be sleeping. Consult physician if the patient is difficult to arouse.

Oxygen therapy

1. Ensure appropriate delivery of prescribed O₂ therapy. Assess the patient’s respiratory status after every change in FIO₂. Patients with chronic CO₂ retention may be very sensitive to increases in FIO₂, resulting in depressed ventilatory drive. If the patient requires mechanical ventilation, be aware of the importance of maintaining the compensated acid-base status. If the PaCO₂ is rapidly decreased by excessive mechanical ventilation (dropping PaCO₂, but a remaining excess of bicarbonate), a severe metabolic alkalosis (posthypercapnic metabolic alkalosis) could develop. The sudden onset of metabolic alkalosis may lead to hypocalcemia or hypokalemia, which can result in tetany (see Hypocalcemia, 57). Severe alkalosis also can precipitate cardiac dysrhythmias.

Ventilation assistance

1. Assess for presence of bowel sounds, and monitor for gastrointestinal (GI) distention, which can impede movement of the diaphragm and further restrict ventilatory effort.

2. Assess for presence of symmetric lung expansion and normal resonance of lung fields. Hyperresonance and asymmetry indicate pneumothorax; dullness and asymmetry indicate solid tissue or fluid occupation of lung or pleural space (e.g., hemothorax, pleural effusion, hyperplasia).

3. In patients who have obstructive lung disease and are not intubated, encourage use of pursed-lip breathing (inhalation through nose, with slow exhalation through pursed lips), which helps airways to remain open and allows for better air excursion. Optimally, this technique will diminish air entrapment in the lungs and make respiratory effort more efficient.

Cough Enhancement, Acid-Base Management, Respiratory Acidosis, Mechanical Ventilation, Artificial Airway Management, Oral Health Maintenance

Additional nursing diagnoses and interventions:

Nursing diagnoses and interventions are specific to the pathophysiologic process. See Acute Pneumonia, (p. 373), Acute Lung Injury and Acute Respiratory Distress Syndrome, (p. 365) and Acute Respiratory Failure, (p. 383), along with Mechanical Ventilation, (p. 99).

Respiratory alkalosis

Pathophysiology

The problem is alveolar hyperventilation, which results in an increased pH

Example: pH 7.48, PaCO₂ 30, HCO₃ 23

Step 1: the ph is not perfect.

The problem is named by the direction of the pH in respect to perfect: Is the pH on the alkaline side greater than 7.40 or the acid side less than 7.40? The pH of 7.48 is on the alkaline side.

Step 2: the paCO₂ has decreased to 30 mm hg, reflecting hypocapnia (paCO₂ less than 35 mm hg).

This signals alveolar hyperventilation (decreased respiratory acid causing an alkaline pH). When minute ventilation is increased, CO₂ decreases, which causes H₂CO₃ to also decrease (production of carbonic acid decreases) and the pH becomes alkalotic. Question: Is there a problem? The CO₂ has decreased and the pH has gone up. The problem is respiratory alkalosis.

Step 3: the hco₃⁻ is 23, which is less than perfect but still in the normal range.

It must be determined if there is a metabolic contribution to the alkalosis or if there is compensation provided by the kidney retaining acid and excreting bicarbonate. The BE is +1, within the normal range.

Step 4: the pCO₂ is low, the ph is high and the hco₃ is normal.

The patient is exhibiting a rapid respiratory rate, with deep breaths.

Step 5: the spO₂ may be normal, as the patient is breathing very rapidly, but effectively. however, when the respiratory rate is very rapid, there is less time for oxygen diffusion, so it is possible that the patient’s oxygen levels may decrease.

Acute respiratory alkalosis

Respiratory alkalosis occurs as a result of an increase in the minute ventilation (alveolar hyperventilation). Defined as PaCO₂ less than 35 mm Hg, acute alveolar hyperventilation results most frequently from anxiety and is commonly referred to as hyperventilation syndrome. Caution must be applied to evaluate whether hyperventilation is actually a compensatory mechanism for primary metabolic acidosis. Although it may become necessary to control the patient’s minute ventilation, in the presence of metabolic acidosis, loss of the hyperventilation compensation may create a life-threatening acidotic pH and profound refractory hypotension and asystole.

In the alkalotic environment, cells release H⁺ and take up K⁺. The result is frequently serum hypokalemia (with intracellular hyperkalemia). Kidney compensation for the respiratory alkalosis is not clinically apparent for 4 to 48 hours. Acute respiratory alkalosis progresses to chronic respiratory alkalosis if it persists for longer than 6 hours and/or renal compensation occurs.

Compensatory response to respiratory alkalosis:

The kidneys, within 4 to 48 hours, should excrete bicarbonate and retain additional H⁺ in an attempt to compensate for the lack of respiratory acid.

• Acute respiratory alkalosis: First 4 to 48 hours HCO3⁻ (and therefore the increase in H⁺) will decrease 2 mEq/L for every 10 mm Hg decrease in PCO₂.

• Chronic respiratory alkalosis: After about 48 hours, the amount of bicarbonate should decrease 4 mEq/L of HCO₃ for every 10 mm Hg decrease in PCO₂.

1. Original problem: pH 7.48, PaCO₂ 30, HCO₃⁻ 23

2. With compensation: pH 7.44, PaCO₂ 30, HCO₃⁻ 19

If there is only one problem contributing to the pH abnormalities, the pH should behave as expected. In other words, a removal of acid by the problem system should be compensated by acid retention by the opposing system.

1. Original problem: ↓↓CO₂ + H₂O ← ↓↓H2CO₃ HCO₃⁻ + H⁺

2. With compensation: ↓↓CO₂ + H₂O ← ↓H2CO₃ ← ↓↓HCO₃⁻ + ↑↑H⁺

Chronic respiratory alkalosis

Chronic respiratory alkalosis is a state of chronic hypocapnia caused by stimulation of the respiratory center. The decreased PaCO₂ stimulates the renal compensatory response and results in a proportionate decrease in plasma bicarbonate (and retention of H⁺) until a new, steady state is reached. Maximal renal compensatory response requires several days to occur and can result in a normal or near-normal pH. Chronic respiratory alkalosis is not commonly seen in acutely ill patients but, when present, it can signal a poor prognosis.

In alkalotic environments

• Sodium and potassium: May be decreased slightly to profoundly (potassium will shift from the extra cellular space to the intracellular space in exchange for H⁺).

• Serum calcium: May be decreased because of increased calcium and bicarbonate binding. Signs of hypocalcemia include muscle cramps, hyperactive reflexes, carpal spasm, tetany, and convulsions.

• Serum phosphorus: May decrease (less than 2.5 mg/dl), especially with salicylate intoxication and sepsis, because the alkalosis causes increased uptake of phosphorus by the cells. No symptoms occur, and treatment usually is not required unless a preexisting phosphorus deficit is present.

Clinical presentation

Presentation includes lightheadedness, anxiety, paresthesias (especially of the fingers), and circumoral numbness. In extreme alkalosis, confusion, tetany, syncope, and seizures may occur.

Physical assessment

Increased rate and depth of respirations (hyperventilation) are present.

Monitoring parameters

Cardiac dysrhythmias are present.

CARE PLAN: RESPIRATORY ALKALOSIS

Ineffective breathing pattern

Goals/outcomes

If the respiratory alkalosis is primary, within 4 hours of initiating treatment, the patient has improved. Final outcome is that the patient’s breathing pattern is effective as evidenced by a state of eupnea: PaCO₂ ≥ 35 mm Hg and pH 7.45.

Respiratory Status: Ventilation, Vital Signs Status, Respiratory Status: Gas Exchange, Symptom Control Behavior, Comfort Level, Endurance; Electrolyte and Acid-Base Balance.

Ventilation assistance

1. To help alleviate anxiety, reassure the patient that a staff member will remain with him or her.

2. Encourage patient to breathe slowly. Pace the patient’s breathing pattern by having him or her mimic your own breathing pattern.

3. Monitor patient’s cardiac rhythm. Consult physician for new or increased dysrhythmias. With acute respiratory alkalosis, even a modest alkalosis can precipitate dysrhythmias in a patient with a preexisting heart disease who is also taking inotropic drugs (see Appendix 6). In part, this is caused by the hypokalemia that occurs with alkalosis.

4. Administer sedatives or tranquilizers as prescribed. Assess and document effectiveness.

5. Have the patient rebreathe into a paper bag as indicated (if practice is supported by institution).

6. Ensure that the patient rests undisturbed after his or her breathing pattern has stabilized. Hyperventilation can result in fatigue.

Hyperventilation may lead to hypocalcemic tetany despite a normal or near-normal calcium level because of increased binding of calcium. For chronic respiratory alkalosis, nursing diagnoses and interventions are specific to the pathophysiologic process.

Additional nursing diagnoses and interventions

Nursing diagnoses and interventions are specific to the pathophysiologic process.

Metabolic acidosis

Pathophysiology

Accumulation of metabolic acids, reflected by decreased HCO₃⁻ (less than 22 mEq/L) with a pH decreased below 7.40. Metabolic acids are circulating acids that cannot be exhaled. These acids should be neutralized by buffers, excreted by the kidneys, or metabolized.

Example: pH 7.28, PaCO₂ 39, HCO₃⁻ 16, PaO₂ 98 mm Hg, SaO₂ 99%

Step 1: the ph is not perfect.

The problem is named by the direction of the pH in respect to perfect: Is the pH on the alkaline side greater than 7.40 or the acid side less than 7.40? The pH of 7.28 is on the acid side.

• Increased acid production: Excessive lactate and ketones cause acidosis and contribute more unmeasured positives (H⁺) into circulation. When an increase in H⁺ occurs, HCO₃⁻ goes down as the role of bicarbonate is to buffer H⁺. The conjugation of H⁺ and HCO₃⁻ yields an increase in carbonic acid. As carbonic acid (H₂CO₃) goes up, the pH goes down.

• Decreased renal tubular function (acute tubular necrosis [ATN] or chronic failure): If the kidney is unable to excrete H⁺, or if the load is beyond tubular transport capabilities, an increase in H⁺ occurs. HCO₃⁻ decreases as the role of bicarbonate is to buffer H⁺ and the kidney has lost the capability to regulate and create appropriate bicarbonate. The conjugation of H⁺ and available HCO₃⁻ yields an increase in carbonic acid. As carbonic acid (H₂CO₃) increases (goes up), the pH decreases (goes down).

• Ingestion of exogenous acids: Certain medications can cause an increase in circulating acids. Alcohols and other ingested acids can facilitate a wide anion gap.

Step 2: the paCO₂ is slightly decreased to 39 but within the normal range.

The patient does not have respiratory alkalosis or acidosis. The lungs are not retaining CO₂ and are not exhaling excessive amounts of CO₂.

Step 3: the hco₃⁻ is 16, which is less than perfect and below the normal range.

This means the metabolic acid (H⁺) is increased. The BE is −6, below the normal range. It must be determined if the acidosis is the problem or a compensatory mechanism for metabolic alkalosis.

Problem: Metabolic acidosis caused by any/or any combination thereof:

• Kidney failure to regulate and excrete acid appropriately (acute or chronic kidney failure)

• Cellular production of acid increases beyond normal regulatory capacity due to metabolic alterations (lactic acidosis or ketosis)

• Ingestion of acids (aspirin, methanol)

Metabolic acidosis is much more difficult to diagnose than the simple presence or absence of acid. One must first diagnose the cause of the acid-base imbalance.

Step 4: the pco₂ is normal, while the hco₃⁻ is decreased.

The patient is exhibiting a normal respiratory rate, with normal depth. With a decreased HCO₃⁻ and normal PaCO₂, the patient is not compensating for a respiratory alkalosis. The PaCO₂ would be decreased with respiratory alkalosis if the decreased HCO₃⁻ was a compensatory response. The decreased HCO₃⁻ is the primary problem; an acute metabolic acidosis. Question: What is the problem? The HCO₃⁻ has decreased, and no compensation is apparent by the lungs. The respiratory rate and depth have not increased.

Step 5: the pao₂ and sao₂ are normal, as the patient is breathing normally.

The patient has normal oxygenation.

Step 6 : performed only in metabolic acidosis: evaluate glucose, ketones, lactate and tissue oxygenation (if necessary).

Example: pH 7.28, PaCO₂ 39, HCO₃⁻ 16, PaO₂ 98 mm Hg, SaO₂ 99%

One must investigate why H+ is increased and bicarbonate is down.

• Is it a compensatory response? If so the H₂CO₃↓ (H⁺↑) and the patient would have a pH on the alkaline side, indicating compensatory response for respiratory alkalosis.

• Is it a kidney problem? In this case, BUN and/or Creatinine would be elevated.

• Is it a high chloride (inadequate buffer) problem? If so, the chloride would have to be high.

• Did the patient ingest acids?

• Is it a tissue metabolism issue? In this case, the patient will have high ketones and/or lactic acidosis.

If the answer to the first four questions is no, or those problems do not seem significant enough for the pH change, a further investigation must be performed.

Evaluation of glucose and ketones may be reviewed (Diabetic Ketoacidosis [DKA], p. 713).

Evaluation of tissue perfusion and oxygenation requires more testing.

1. Lactic acidosis may be caused by an oxygenation-related, metabolic acidosis, which results from a significant increase in lactate production during anaerobic metabolism. This excess lactate production also yields H⁺.

2. Lactic acidosis IS NOT respiratory acidosis! Respiratory acidosis is primarily a ventilation problem, while lactic acidosis is primarily a perfusion-, metabolic stress–, or cellular O₂ consumption or extraction–related problem. Lactic acidosis will be discussed further as part of the section on metabolic acidosis.

3. Additional measures are sometimes used in critically ill patients for evaluation of tissue hypoxia. Mixed venous and/or central venous saturation of Hgb evaluates the tissue use of O₂. The comparison of arterial (precellular) saturation to central or mixed venous (postcellular) is most commonly used to evaluate the tissue O₂ consumption compared to O₂ delivery.

4. Mixed venous (SVO₂) or central venous oxygen saturation (ScVO₂): This value is measured by an indwelling O₂ probe/sensor on the tip of a catheter placed in the central vein (CVP catheter) or PA (PA catheter). Measurement may provide an early indication of perfusion failure or increased tissue demands for O₂, reflected by a decreased mixed venous saturation of Hgb. If this saturation is normal or high but the patient has an increased lactate level, the cells may be unable to extract or use the O₂, which frequently occurs in the later stages of severe sepsis.

5. Mixed venous saturation values (Svo₂): This value should always be correlated with other tissue indicators of hypoxia, base deficit, widening anion gap, serum bicarbonate, and lactate levels. The difference between arterial and venous blood gases is reflective of global O₂ consumption. The following standard parameters are based on mixed venous blood gas and have not yet been standardized for central venous gases; however, the basic principles are the same.

6. SaO₂ reflects reservoir bound O₂ and very indirectly reflects delivery.

a . Normal SaO₂ is 0.95 to 1.00.

7. SvO₂ or ScVO₂ reflects unused O₂ or remaining reservoir after release of needed O₂ has occurred.

b. Normal SvO₂ is 0.60 to 0.80 OR ScVO₂ of 0.65 to 0.85.

8. SaO₂ minus ScVO₂ reflects O₂ consumption.

c. 1.00 − 0.70 = 0.30, about 30% consumption

9. SaO₂ minus SvO₂ divided by SaO₂ reflects O₂ extraction ratio, valued at around 20% to 30%.

d. 1.00 − 0.70 ÷ 1.00 = 30%

10. Normal oxygen extraction ratio is 20% to 30%: In other words, the patient should use normally between 20% and 30% of their total available O₂. O₂ extraction is a mathematical formula that assists in evaluating the compensatory mechanisms: First line of compensation is to increase the delivery of O₂ (increase the cardiac output [CO], amount of Hgb, and O₂ saturation), and the second line is to release O2 from Hgb to provide more dissolved O₂ at the cell level, resulting in a shift to the right in the dissociation curve (Figure 1-1).

11. Patients presenting with a normal Svo₂ and persistent lactic acidosis are NOT normal. They are not using O₂ appropriately. Patients who are using more than 20% to 30% are signaling inadequate O₂ delivery, dipping into second-line compensation, which is very risky, because the cells may undergo acute hypoxia.

Figure 1-1 The oxyhemoglobin dissociation curve.

(From Stillwell SB: Mosby’s critical care nursing reference, ed. 4. St. Louis, 2006, Mosby.)

Lactic acidosis (lactate level greater than 4 mmol/l)

Assessing perfusion and oxygen consumption at the cellular level

Since the early work of Dr. William Shoemaker, it has been well identified that global tissue hypoxia accompanies all categories of shock, including both O₂ delivery and O₂ utilization shock. The work of the Surviving Sepsis Campaign to establish early goal-directed therapy validated the role of lactate measurement as a guide to therapy. When cells are in a shock state, O₂ delivery shock is present. Shock effects the mechanics of delivery, while systemic inflammatory response or severe sepsis, with the secondary effects of endothelial dysfunction, vasodilation, inflammatory mediation, and unopposed procoagulation, interfere with the utilization of O₂ at a microcirculatory and cellular level. Large areas of the capillary beds may be hypoperfused, resulting in cells resorting to anaerobic metabolism to survive. Anaerobic metabolism results in the production of lactic acid, a metabolic acid that can create acidosis if compensation fails. The ABG reflects a decreased pH but does NOT always reflect a markedly decreased PaO₂ and SaO₂. Persistent tissue-level hypoxia further exacerbates the systemic inflammatory response and may lead to multiple organ dysfunction (MODS) and eventually death.

Arterial lactate concentration is dependent on the balance between its production and consumption. In the critically ill septic population, increased glucose metabolism, increased energy expenditures, and profound catabolism are the norm. The corresponding lactic acidosis signals physiologic stress but may not necessarily be evidence of tissue hypoxia. The concomitant energy expenditures—along with metabolic dysfunction—will increase lactate production, but high levels of clearance may mask this disturbing trend.

These conditions, coupled with an out-of-control inflammatory response and increasing oxygenation dysfunction at the tissue level, combine to produce a profound tissue acidosis. The lactate production is further increased via other abnormal pathways that are specifically related to metabolic dysfunction, even in the absence of tissue hypoxia (type B lactic acidosis). The main cause of the significantly increased lactate is still a puzzle. One factor is the failure of ATP production, which clearly occurs in the presence of a profound O₂ supply/demand imbalance (type A lactic acidosis). This in turn affects the mitochondrial ability to utilize pyruvate, and the increased pyruvate is indicative of a profound metabolic hyperlactatemia, an elevated lactate/pyruvate ratio, increased glucose, and low energy production. Ultimately, as severe sepsis progresses, it evolves into a mediator-induced cardiac failure state, with profound intra-arterial hypovolemia.

Special considerations for patients with lactic acidosis

Nguyen et al. (2004), in their work related to early goal-directed therapy when treating sepsis, validated that the higher the clearance of lactate in the first 6 hours after resuscitation, the lower is the mortality. In those first hours of evaluation and resuscitation, achieving a normal ScVO₂ along with an increasing lactate clearance is the desired therapeutic endpoint, reducing the potential for MODS.

Measuring lactic acids

In any patient whose condition arouses suspicion (e.g., with tachycardia, tachypnea, hyperventilation, and/or hypotension), it is essential to directly measure acid.

1. Lactate level: All patients who run the risk of cellular hypoxia must have a sample drawn for a lactate level to evaluate for lactic acidosis. An arterial lactate sample should be placed on ice and taken as soon as possible to the lab. Any lactate greater than 4 mmol/dL needs to be investigated for severe tissue hypoxia and hypoperfusion. Lactates > 2 mmol/dL should be observed along with the clinical conditions of the patient. Serial lactates should be performed to evaluate therapy effectiveness and follow the clearance level. A lactate clearance greater than 10%/24 hr is considered a successful measure of therapeutic intervention for severe sepsis.

a. Limitations to lactate level: The value of lactate is obviously limited due to lactate concentrations that are affected by both production as well as elimination. Liver dysfunction, ketosis, and many medications administered in the critical care unit may affect the measured lactate levels. Therefore, lactate levels by themselves will not give as much beneficial information as those in the presence of wide anion gap and low or normal Scvo2.

Serum ketone level: If the glucose is elevated, a serum ketone level should also be drawn to evaluate for ketoacidosis.

Acute metabolic acidosis

Example: pH 7.28, PaCO₂ 39, HCO₃⁻ 16, PaO₂ 98 mm Hg, SaO₂ 99%

Bicarbonate is decreased, which always means that H⁺ is elevated. If H⁺ is elevated, resulting in increased carbonic acid, and the pH is down even slightly, the problem is acid accumulation. In this case, it is acute metabolic acidosis, without compensation!

As the nonvolatile acid H⁺ increases, it will displace the intracellular potassium, resulting in a serum hyperkalemia but an intracellular hypokalemia. The lungs should increase the rate and depth of respirations to exhale CO₂, to compensate for the excess metabolic acid, so the pH can return to normal range.

Consideration must be allowed for glucose and ketones. If lactic acid is elevated, it may become necessary to find the culprit utilizing tissue oxygenation measures.

Glucose 120, Ketones -, Lactate 6.8

This then points to acute metabolic (lactic) acidosis!

Compensatory response to acute metabolic acidosis

When H⁺ (acid) increases, pH decreases in the plasma. The central respiratory center in the brain responds by increasing the rate and depth of ventilation to 4 to 5 times the normal level to exhale significant amounts of CO₂ and returning the carbonic acid; therefore, the pH is back to normal (but never perfect if there is a problem). The decrease in pH (high presence of H⁺) stimulates respirations. Attempts to compensate occur rapidly, as manifested by lowering of the PaCO₂, which may be reduced to as little as 10 to 15 mm Hg. The most important mechanism for ridding the body of excess H⁺ is the increase in acid excretion through ventilation. In addition, if the kidney is functional, acid will be excreted and bicarbonate reabsorbed. Nonvolatile acids, however, may accumulate more rapidly than the body’s buffers can neutralize them, compensated for by the respiratory system, or excreted by the kidneys.

1. Original problem: Acute metabolic acidosis: pH 7.28, PaCO₂ 39, HCO₃⁻ 16

2. With compensation: pH 7.36, PaCO₂ 30, HCO₃⁻ 16, SaO₂ 99%, PaO₂ 100%

Original problem:CO₂ + H₂O

↑↑ H2CO₃←↓↓HCO₃⁻ + H⁺↑↑

With compensation: ↓↓CO₂ + H₂O ← H2CO₃ ← ↓↓HCO₃⁻ + H⁺↑↑

Step 1: ph 7.36: acid side but in range of normal.

• Question: Is there a problem? Normal variation in pH from perfect, OR a compensated acid-base imbalance?

• Answer: Yes, there is a problem. The pH decrease is not a normal variation because the PaCO₂ and HCO₃ are out of range.

Step 2: paCO₂ 30 mm hg.

On the alkaline side, which does not coincide with the direction of the pH change.

Step 3: hco₃− 16 meq/l.

Decreased and out of range, which means the metabolic acid (H⁺) is increased! HERE is the CAUSE of the problem that decreased the HCO₃⁻.

Step 4: the paCO₂ is increased in the presence of a decreased hco₃−.

Acid reduced the pH, and the lungs compensated by separating the H₂CO₃ into CO₂ and H₂O and, with the help of the respiratory center, exhaled the CO₂. The problem is COMPENSATED metabolic acidosis.

Step 5: the pao₂ and sao₂ are normal, as the patient is breathing normally.

The patient has normal oxygenation.

Collaborative management: acute metabolic acidosis

Care priorities

1. It is most important to treat the underlying disorder if possible.

• Diabetic ketoacidosis: Insulin and fluids. If acidosis is severe (with a pH of less than 7.15 or HCO₃⁻ 6 to 8 mEq/L), judicious administration of NaHCO₃ may be necessary.

• Alcoholism-related ketoacidosis: Glucose and saline.

• Diarrhea: Usually occurs in association with other fluid and electrolyte disturbances; correction addresses concurrent imbalances.

• Acute renal failure: Hemodialysis or peritoneal dialysis to maintain an adequate level of plasma HCO₃⁻.

• Renal tubular acidosis: May require modest amounts (less than 100 mEq/day) of bicarbonate.

• Poisoning and drug toxicity: Treatment depends on drug ingested or infused. Hemodialysis or peritoneal dialysis may be necessary.

• Lactic acidosis: Correction of underlying disorder related to hypoxia and/or hypoperfusion. Mortality associated with lactic acidosis is high. Unless pH is life-threatening, treatment with NaHCO₃ is generally not indicated and may actually be harmful.

2. Measure anion gap:

Anion gap is an estimate of the differences between measured and unmeasured cations (positively charged particles, such as Na and H⁺ respectively) and measured and unmeasured anions (negatively charged particles such as HCO₃⁻ and Cl⁻). Normally, cations and anions are equally balanced in live humans (in vivo), but when measured in the laboratory (in vitro), the difference may be between 10 to 12 mmol/L. This difference is termed a normal gap (between + and – ions). Particles that possess charges tend to have high affinity to bind to other particles that possess charges that are opposite their own (hence the term, “opposites attract”). Anion gap is used to determine if a metabolic acidosis is due to an accumulation of nonvolatile acids such as lactic acid or ketoacids. Both contribute a positive charge due to excess H⁺ or from net loss of bicarbonate (e.g., diarrhea). The gap is not affected when a patient has metabolic acidosis purely from kidney failure. The formula for calculation of anion gap is:

Unmeasured cations: Calcium, magnesium, gamma globulins, potassium (bind negative charged particles)

Unmeasured anions: Albumin, phosphate, sulfate, lactate, hydrogen ion (bind positive charge particles)

3. Treat the ph:

Only if the patient’s life is threatened by the pH. Sodium bicarbonate (NaHCO₃) may be indicated when arterial pH is ≤7.15. The usual mode of delivery is IV drip: 2 or 3 ampules (44.5 mEq/ampule) in 1000 ml D₅W, although NaHCO₃ may be given by IV push in emergencies. Deficit should be calculated and replaced accordingly. Concentration depends on severity of the acidosis and presence of any serum sodium disorders. NaHCO₃ must be given very cautiously to avoid metabolic alkalosis and pulmonary edema as a result of the sodium load. Total body weight × Base deficit/4 = Amount of sodium bicarbonate that must be replaced.

4. Manage hyperkalemia:

Usually, serum hyperkalemia is present, but an intracellular potassium deficit may be present. If a potassium deficit exists (K⁺ less than 3.5), it must be corrected before NaHCO₃ is administered, because when the acidosis is corrected, the potassium shifts back to intracellular spaces. This shift in K⁺ could result in a profound serum hypokalemia with serious consequences, such as cardiac irritability with fatal dysrhythmias and generalized muscle weakness. See Hypokalemia, p. 52, for more information.

5. Support ventilation:

If mechanical ventilation is required on the basis of ABG results and clinical signs, it is important that the patient’s compensatory hyperventilation be allowed to continue to prevent acidosis from becoming more severe. Therefore the respiratory rate on the ventilator should not be set lower than the rate at which patient has been breathing spontaneously, and the tidal volume should be large enough to maintain compensatory hyperventilation until the underlying disorder can be resolved.

Nursing diagnoses and interventions

Nursing diagnoses and interventions are specific to the pathophysiologic process. See nursing diagnoses and interventions in Mechanical Ventilation (p. 99), Acute Respiratory Failure (p. 383), Emotional and Spiritual Support of the Patient and Significant Others (p. 200), Acute Renal Failure/Acute Kidney Injury (p. 584), and Diabetic Ketoacidosis (p. 713).

Chronic metabolic acidosis

Assessment

History and risk factors

Affected patients generally include those with chronic renal failure, renal tubular acidosis, loss of alkaline fluid (e.g., with diarrhea or pancreatic or biliary drainage) for greater than 3 to 5 days.

Clinical presentation

Usually the process leading to chronic metabolic acidosis is gradual and the patient is symptom free until serum HCO₃⁻ is ≤15 mEq/L. Fatigue, malaise, and anorexia may be present in relation to the underlying disease.

Clinical presentation

Findings vary, depending on underlying disease states and the severity of the acid-base disturbance and the speed with which it developed. There may be changes in LOC that range from fatigue and confusion to stupor and coma.

Physical assessment

Tachycardia (until pH less than 7, then bradycardia), decreased BP, tachypnea leading to alveolar hyperventilation (may be Kussmaul respirations), dysrhythmias, and shock state. Depending on the type of shock and the vascular response, skin temperature and color will be affected. Mild metabolic acidosis (HCO₃⁻ 15 to 18 mEq/L) may result in no symptoms, whereas symptoms will develop with a pH less than 7.2.

Monitoring parameters

A waveform suggestive of hyperkalemia (prolonged PR interval, widened QRS, and peaked T waves) may occur. Persistent tachycardia may indicate tissue hypoperfusion.

Ecg:

Detects dysrhythmias, which may be caused by metabolic acidosis or hyperkalemia. Changes seen with hyperkalemia include peaked T waves, depressed ST segment, decreased size of R waves, decreased or absent P waves, and widened QRS complex. Ventricular fibrillation may occur.

Collaborative management: chronic metabolic acidosis

Care priorities

1. Normalize the ph with alkalizing agents:

• For serum HCO₃⁻ levels less than 15 mEq/L, oral alkalis may be administered (NaHCO₃ tablets or sodium citrate and citric acid oral solution [Shohl solution]). They are used cautiously to prevent fluid overload and tetany caused by hypocalcemia.

• Caution: Be alert to the possibility of pulmonary edema, if bicarbonate is administered parenterally to patients with renal insufficiency or cardiovascular disorders.

2. Manage hypophosphatemia with oral phosphates:

• These are given if hypophosphatemia is present; it is not common with chronic renal failure but may result from overuse of phosphate binders given to treat hyperphosphatemia (very common with chronic renal failure).

3. Provide renal replacement therapies:

• Hemodialysis, citrated blood and renal replacement therapy (CRRT), or peritoneal dialysis may be indicated for chronic renal failure or other disease processes (see Acute Renal Failure/Acute Kidney Injury, p. 584).

Nursing diagnoses and interventions for chronic metabolic acidosis

Nursing diagnoses and interventions are specific to the underlying pathophysiologic process.

Metabolic alkalosis

Pathophysiology

Elevated HCO₃⁻ levels (greater than 26 mEq/L) reflect decreasing circulating metabolic acids (H⁺). Caution must be applied to differentiate compensatory alterations in response to respiratory acidosis versus primary disorder. The diagnosis is made by the presence of elevated serum HCO₃⁻ (up to 45 to 50 mEq/L). Acute metabolic alkalosis most commonly reflects:

• Excessive loss of hydrogen ions: Loss of gastric acid from vomiting or gastric suction, diuretic therapy

• Excessive resorption of bicarbonate: Post hypercapnic alkalosis (which occurs when chronic CO₂ retention is corrected rapidly)

• Ingestion or administration of alkaline: Excessive NaHCO₃ administration (i.e., overcorrection of a metabolic acidosis) or ingestion of over-the-counter antacids

Even when the causative factors have been removed, the alkalosis will be sustained until volume and electrolyte disturbances that are contributing to the alkalosis have been corrected. Severe alkalosis (pH greater than 7.6) is associated with high morbidity and mortality. Acidosis is better tolerated than alkalosis. Spo₂ will be used for Step 5, because a discussion of Pao₂ and Sao₂ does not add to knowledge of metabolic alkalosis.

Example: pH 7.58, Paco₂ 40 mm Hg, HCO₃⁻ 35, Sao₂ 99%, Pao₂ 99 mm Hg

Problem: CO₂ + H₂O H₂CO₃↓↓ ↑↑HCO₃⁻ + H⁺↓↓

Step 1: the ph is not perfect.

The problem is named by the direction of the pH in respect to perfect: on the acid side less than 7.40 or the alkaline side greater than 7.40.

Example: pH 7.58 on alkaline side, outside of range of normal

Question: Is there a problem? YES

Step 2: the paco₂ is 40 mm hg, which is perfect.

This indicates Paco₂ is not driving the increase in pH.

Step 3: hco₃⁻ has increased to 35 meq/l, indicating the kidneys are retaining bicarbonate (h+ is decreased).

HERE is the cause of the problem: ACUTE metabolic alkalosis.

HCO₃⁻ is 35 (up and out of range), which means the metabolic acid, and H⁺ is decreased.

Step 4: the paco₂ has not increased in an attempt to help correct or compensate for the increased hco₃⁻.

The patient is exhibiting a normal respiratory rate, with normal depth. With an increased HCO₃⁻, and normal Paco₂, the patient is not compensating for a metabolic alkalosis.

Step 5: the pao₂ and sao₂ are normal, as the patient is breathing normally. the patient has a normal oxygenation.

Compensatory response to metabolic alkalosis

When H⁺ (acid) decreases, pH increases. The central respiratory center in the brain responds by decreasing the rate and depth of ventilation (in the normal lung) to 50% to 75% of the normal level. This method of compensation is very poorly tolerated, as patients will almost stop breathing.

Original problem: pH 7.58, Paco₂ 40 mm Hg, HCO₃⁻ 35

With compensation: pH 7.45, Paco₂ 59 mm Hg, HCO₃⁻ 35

In this example: pH 7.45, Paco₂ 59 mm Hg, HCO₃⁻ 35, Sao₂ 99%, Pao₂ 99 mm Hg

Step 1: ph 7.45.

Alkaline side, inside the normal range

• Question: Is there a problem, despite the normal pH? YES! Other values are abnormal.

Step 2: paco₂ 59 mm hg.

On the acid side, opposite the pH, which is toward the alkaline side. The Paco₂ is not the problem but rather a COMPENSATION. The increased Paco₂ would not increase the pH to alkaline. This measure is in the wrong direction to be the cause.

Step 3: hco₃− 35 meq/l.

Increased and out of range. HERE is the cause of the problem. Metabolic alkalosis is present because the metabolic acid (H⁺) is decreased.

Step 4: the paco₂ is elevated at 59 mm hg.

The Paco₂ has increased response to an increased HCO₃⁻ level. When HCO₃⁻ increases, the pH goes up, indicating less H⁺ is present in the body. The pH normalized on the alkaline side, so the patient has fully compensated metabolic alkalosis.

Step 5: the sao₂ is normal.

The patient has a normal rate and depth of respirations.

Collaborative management: acute metabolic alkalosis

Management will depend on the underlying disorder. Mild or moderate metabolic alkalosis usually does not require specific therapeutic interventions. Correction of chloride deficits is a priority for treatment with many underlying disorders.

Care priorities

1. Manage chloride deficit:

Normal saline infusion may correct volume (chloride) deficit in patients with gastric alkalosis because of gastric losses. Metabolic alkalosis is difficult to correct if hypovolemia and chloride deficit are not corrected.

2. Correct hypokalemia:

Potassium chloride (KCl) is indicated for patients with low potassium levels. KCl is preferred over other potassium salts because chloride losses can be replaced simultaneously.

3. Sodium and potassium chloride:

Effective for post hypercapnic alkalosis, which occurs when chronic CO₂ retention is corrected rapidly (e.g., via mechanical ventilation). If adequate amounts of chloride and potassium are not available, renal excretion of excess HCO₃² is impaired and metabolic alkalosis continues.

4. Cautious IV administration of isotonic hydrochloride solution, ammonium chloride, or arginine hydrochloride:

May be warranted if severe metabolic alkalosis (pH greater than 7.6 and HCO₃² greater than 40 to 45 mEq/L) exists, especially if chloride or potassium salts are contraindicated. The medication is delivered via continuous IV infusion at a slow rate, with frequent monitoring of IV insertion site for signs of infiltration. Ammonium chloride and arginine hydrochloride may be dangerous to patients with renal or hepatic failure.

Nursing diagnoses and interventions for acute metabolic alkalosis

Nursing diagnoses and interventions are specific to the underlying pathophysiologic process.

Chronic metabolic alkalosis

Pathophysiology

Chronic metabolic alkalosis results in a pH greater than 7.45 and HCO₃⁻ greater than 26 mEq/L. Paco₂ will be elevated (greater than 45 mm Hg) to compensate for the loss of H⁺ or excess serum HCO₃⁻. The three clinical situations in which this can occur are the following:

1. Abnormalities in the kidneys’ excretion of HCO₃⁻ related to a mineralocorticoid effect

2. Loss of H⁺ through the GI tract

3. Long-term diuretic therapy, especially with the thiazides and furosemide. A compensatory increase in Paco₂ (up to 50 to 60 mm Hg) may be seen. Respiratory compensation is very limited because of the hypoxemia, which develops as a result of decreased alveolar ventilation.

Compensatory response to chronic alkalosis

When extracellular fluid is alkalotic, the kidneys conserve H⁺ and eliminate HCO₃⁻, resulting in excretion of alkalotic urine. Renal excretion of acid load and increase in circulating buffer represent the major compensation for respiratory deficits and require a normally functioning kidney. Although the kidneys’ response to an abnormal pH level is slow (4 to 48 hours), they are able to facilitate a nearly normal pH level by excreting or retaining large quantities of HCO₃⁻ or H⁺ from the body. Acid-base balance is regulated by increasing or decreasing H⁺ and bicarbonate (HCO₃⁻) concentration in body fluids. A series of complex reactions with H⁺ secretion, sodium ion (Na⁺) resorption, HCO₃⁻ retention, and ammonia synthesis (excretes H⁺ in the urine) occurs.

Clinical presentation

Muscular weakness, neuromuscular instability, and hyporeflexia because of accompanying hypokalemia are present. Decrease in GI tract motility may result in an ileus. Severe alkalosis can result in apathy, confusion, and stupor. Seizures may occur.

Physical assessment

Decreased respiratory rate and depth, periods of apnea, tachycardia (atrial or ventricular) are present.

Monitoring parameters

Atrioventricular dysrhythmias as a result of cardiac irritability secondary to hypokalemia; prolonged QT intervals are present. See Hypokalemia, p. 52.

• Urinalysis: Urine chloride levels can help identify the cause of the metabolic alkalosis. Urine chloride level will be less than 15 mEq/L if hypovolemia and hypochloremia are present, and greater than 20 mEq/L with excess retained HCO₃⁻. This test is not reliable if diuretics have been used within the previous 12 hours.

• ECG findings: To assess for dysrhythmias, especially if profound hypokalemia or alkalosis is present.

Collaborative management: chronic metabolic alkalosis

The goal is to correct the underlying acid-base disorder via the following interventions.

Care priorities

1. Fluid management:

If volume depletion exists, normal saline infusions are given.

2. Potassium replacement:

If a chloride deficit also is present, KCl is the drug of choice. If a chloride deficit does not exist, other potassium salts are acceptable.

• IV potassium: If the patient is undergoing cardiac monitoring, up to 20 mEq/hr of KCl is given for serious hypokalemia. Concentrated doses of KCl (greater than 40 mEq/L) require administration through a central venous line because of blood vessel irritation.

• Oral potassium: This tastes very unpleasant; 15 mEq/glass is all most patients can tolerate, with a maximum daily dose of 60 to 80 mEq. Slow-release potassium tablets are an acceptable form of KCl. All forms of KCl may be irritating to gastric mucosa.

3. Dietary:

The normal diet contains 3 g or 75 mEq of potassium but not in the form of KCl. Dietary supplementation of potassium is not effective if a concurrent chloride deficit also is present.

4. Potassium-sparing diuretics:

These may be added to treatment if thiazide diuretics are the cause of hypokalemia and metabolic alkalosis.

Clinical presentation

Patient may be free of symptoms. With severe potassium depletion and profound alkalosis, patient may experience weakness, neuromuscular instability, and a decrease in GI tract motility, which can result in ileus.

Physical assessment

Decreased respiratory rate and depth, and tachycardia (atrial or ventricular) are present.

Monitoring parameters

Frequent PVCs or U waves with hypokalemia and alkalosis are present.

Nursing diagnoses and interventions for chronic metabolic alkalosis

Nursing diagnoses and interventions are specific to the underlying pathophysiologic process. For NIC and NOC, see Acute Metabolic Alkalosis.

Consciousness is a state of awareness of the self and environment composed of three aspects: arousal (ability to awaken), ability to perceive internal and external stimuli, and ability to perform goal-directed behavior. Alterations in these aspects of consciousness result in a broad spectrum of syndromes including coma, delirium, and cognitive dysfunction. Factors precipitating various alterations in consciousness are listed in Table 1-3. These precipitating factors arise from intrinsic causes (medical condition and associated problems) and extrinsic causes (environmentally produced). Impaired consciousness, regardless of etiology, results in higher complication rates, puts the patient’s safety at risk, causes longer hospital stays, and is linked to higher morbidity and mortality. Three states of impaired consciousness can be recognized in hospitalized patients—coma, delirium, and cognitive dysfunction. While each of these conditions may arise from distinct medical problems, the clinical features often are similar and may be superimposed on each other, making diagnosis and treatment more complex. Change in mental status is often the early warning sign of a medical emergency. The differential diagnosis is critical to the proper treatment of these mental status changes. The following are descriptions of normal mental status variants that require further evaluation.

Table 1-3 FACTORS PRECIPITATING ALTERATIONS IN CONSCIOUSNESS

Delirium

This is a state of disordered attention that reflects an underlying acute or subacute process. It is usually a transient condition (may be prolonged) that develops along a continuum including a clouding of consciousness, confusion, attention deficit, global cognitive impairment, and psychosis. Symptoms include disorientation to time, place, and person; disorganized thinking; fear; irritability; misinterpretation of sensory stimuli (e.g., pulling at tubes and dressings); appearance of being distracted; altered psychomotor activity; altered sleep-wake cycles; memory impairment; hallucinations; inappropriate communication (e.g., yelling, swearing, nonsensical speech); and dreamlike delusions. Lucid intervals alternate with episodes of delirium. Patients may have difficulty following commands. Daytime drowsiness is contrasted with nighttime agitation. Clinical variants of delirium include the hyperactive-hyperalert form, the quiet form, and a combination form that combines the hyperactive-hyperalert and quiet forms to produce both lethargy and agitation (Figure 1-2).

Figure 1-2 Linking sedation and delirium monitoring; a two-step approach to assess consciousness.

(Copyright E. Wesley Ely, MD, MPH, and Vanderbilt University, 2002.)

Coma

Coma is an alteration in arousal and diminished awareness of self and environment. No understandable response to external stimuli or inner need is elicited. No language is spoken. There are no covert or overt attempts at communication or eye opening. Spontaneous purposeful movement and/or localizing movements are absent. Motor responses to noxious stimuli are reflexive and do not result in recognizable defensive movements. Sleep-wake cycles are absent on the electroencephalogram (EEG). The extent of coma is difficult to quantify because limits of consciousness are difficult to define. Self-awareness can only be inferred from appearance and actions. Coma occurs when normal central nervous system (CNS) function is disrupted by alteration in the cerebral structure (brain injury), cerebrovascular impairment (hemorrhage, ischemia, or edema), or metabolic conditions (hepatic encephalopathy). If coma persists for longer than 4 weeks, it is defined as transitioning to a vegetative state.

Differential diagnosis of coma the characteristics of syndromes or mental states described next are useful in determining the differential diagnosis because many have similar presentations.

• Stupor—Deep sleep with responsiveness only to vigorous and repeated stimuli with return to unresponsiveness when the stimulus is removed. Stupor usually is related to diffuse organic cerebral dysfunction but may be confused with the catatonic behavior of schizophrenia or the behavior associated with a severe depressive reaction.

• Minimally conscious state (MCS)—Describes patients who demonstrate inconsistent but reproducible behavior indicating awareness of self and environment. Generally they cannot reliably follow commands or communicate but show visual fixation and tracking and have emotional and/or behavioral responses to external stimuli. Once the patient consistently follows commands, can reliably communicate, and uses objects in a functional way, the minimal conscious state ends. Although the etiology is uncertain, MCS seems to be related to diffuse, bilateral, subcortical, and hemispheric damage.

• Akinetic mutism (AM)—Subcategory of MCS in which a decrease in spontaneity and initiation of actions, thoughts, speech, or emotion is present. Sensory motor function is normal. Visual tracking and eye movements are intact, and there is occasional speech and movement to commands. However, internally guided behavior is absent because cortical activation is inadequate. AM is associated with orbitomesial frontal cortex, limbic system, and reticular formation lesions.

• Vegetative state (VS)—Vegetative state is a subacute or chronic condition that may follow the coma of brain injury or occur independently of coma (e.g., dementia). Transition from coma to VS occurs if coma without detectable awareness of environment persists for longer than 4 weeks. Onset of VS is signaled by a return of wakefulness (eyes are open and sleep patterns may be observed) with return of spontaneous control of autonomic function but without observable signs of cognitive function. The patient cannot follow commands, offers no comprehensible sounds, and displays no localization to stimuli. There is complete loss of meaningful interaction with the environment. When the VS continues for weeks or months, it is considered persistent vegetative state (PVS). PVS may exist for many years because the autonomic and vegetative functions necessary for life have been preserved. PVS generally resolves more quickly in traumatic brain–injured patients than in nontrauma patients.

• Locked-in syndrome (LIS) —Characterized by paralysis of all four extremities and the lower cranial nerves but with preservation of cognition. Associated with deafferentation (disruption of the pathways of the brainstem motor neurons), this condition prevents the patient from communicating with a full range of language and body movement. Generally, consciousness, vertical eye movement, and eyelid blinking are intact and provide a mechanism for communication. LIS is classified by the degree of voluntary speech and motor function preservation. In complete LIS, there is total immobility and anarthria (inability to speak). In incomplete LIS, there is vertical eye movement and blinking function. LIS can be distinguished from a vegetative state because patients give appropriate signs of being aware of themselves and their environment. Often, sleep patterns are disrupted (see Spinal cord injury)

Cognitive dysfunction

This is an alteration in thought process involving many of the following brain functions: memory, learning, language, attention, judgment, reasoning, reading, and writing. Aphasia, or difficulty understanding language or with responding with the proper words, may also be present. Dysphagia, or difficulty swallowing, occurs because of attention deficits or muscle weakness. These cognitive impairments, whether permanent or transitory, are overlooked and therefore underdiagnosed or incorrectly diagnosed. See Table 1-3 for factors contributing to cognitive dysfunction during critical illness.

Assessment: alterations in consciousness

Goal of assessment

• Evaluate for changes in behavior, including ability to both understand and comply with directions.

• Determine if altered behaviors have occurred in the past or occur regularly; new-onset changes in mental status should be very closely evaluated. Considerations of cause may include withdrawal from abused substances, a reaction to a new medication, hypoxia, and hypoglycemia.

• Determine the severity of the change in behavior from baseline; acute changes require prompt action.

• An acute or unexpected change in mental status that occurs should be investigated immediately and requires an extensive medical evaluation with labs, physical examination, and neuroimaging. These patients may need immediate transfer to a higher level of care. Change in mental status is often the earliest warning sign of a medical emergency!

• Resist the temptation to sedate an agitated patient prior to completing a full assessment, to ensure the patient is not hypoxic or hypoglycemic. Assessment for hypoxia should include both a ventilation and a perfusion assessment. The ABG includes an estimated Hgb level, which can prove to be invaluable to determine if patient may have internal bleeding.

History and risk factors

• Age—Older adults (age 60 years and older) more prone to alterations in consciousness, especially with changes in the environment

• Brain injury—Lesions of the cortex, subcortex, and brainstem caused by global or focal ischemia, stroke, or traumatic brain injury (see Traumatic Brain Injury, p. 331)

• Cerebral disorders—Deteriorating brain conditions, such as expanding lesions, hydrocephalus, Parkinson disease, dementia, or mental health disorders (bipolar, depression, schizophrenia)

• Cardiovascular status—Disorders that lower CO (heart failure, myocardial infarction, shock states), procedures that cause post cardiotomy delirium, intra-aortic balloon pump sequelae, hypoperfusion states (altered cerebral perfusion pressure [CPP] and dysrhythmias)

• Pulmonary disorders—Those causing hypoxia and hypoxemia such as pneumonia, ARDS, pulmonary emboli

• Drug therapy—Sedation, analgesia, drug toxicity, drug interactions, drug withdrawal, or drug sensitivity

• Surgical factors—Nature (hip, cardiac, neurosurgery patients at increased risk) and extent of surgery and anesthesia time

• Infection—Bacteremia, urinary tract infections, pneumonia, or sepsis

• Perceptual/sensory factors—Sleep deprivation, sensory overload, sensory deprivation, impaired sensation (hypesthesia, decreased hearing or vision), impaired perception (inability to identify environmental stimuli), and impaired integration (inability to integrate environmental stimuli)

• Metabolic factors—Changes in glucose level, hypermetabolism, hypometabolism, and endocrine crises (diabetic coma, ketoacidosis, pituitary dysfunction or injury)

• Fluid and electrolyte disturbances—Sodium and potassium imbalances, hypovolemia, or dehydration

Vital signs

All of the following vital sign changes may be associated with an alteration in consciousness:

• Fever may indicate possible sepsis and/or bacteremia.

• Tachycardia may indicate hypovolemia, resulting from dehydration or bleeding. If patient has undergone a recent invasive procedure, evaluation for internal bleeding is warranted. Tachycardia is also present with fever and hypoglycemia.

• Tachypnea, if coinciding with tachycardia, may reflect the same findings but is also a compensatory mechanism to help control acidosis. Tachypnea is also present during a panic attack, as well as hypoxia.

• Bradypnea may be associated with high doses of narcotics used for pain control.

• Head-injured patients may exhibit signs of increased intracranial pressure (ICP), which vary depending on the degree of pressure elevation (see Traumatic Brain Injury, p. 331)

• Hypotension may indicate a later sign of shock or may be associated with higher doses of antihypertensive medications, narcotics, or other medications that can slow the HR or reduce the BP.

Observation and neurologic evaluation

• The patient’s normal baseline neurologic status must be documented and used for comparison.

• Baseline neurologic findings elicited from each component of the examination must be documented.

• Requires a thorough evaluation of mental/emotional status, cranial nerve function, motor function, sensory function, and reflex activity. When alterations in consciousness are manifested, the mental/emotional component of the examination is of particular importance.

• In patients who are unconscious or demonstrate low-level function, assessment techniques are used that do not require patient participation, such as coma and cognitive functioning scales. The purpose of assessment is to determine the extent of wakefulness and cognition through observed responses, such as eye opening, movement of the head and body, verbalization, and ability to follow commands. These observations alone will not fully discriminate the subtle differences in altered states of arousal.

• Assessment should be accompanied by an in-depth history focusing on the possible etiology of the change in mental status. Extensive cognitive testing including attention, concentration, memory, and learning assessments is performed when the patient is arousable and aware.

Screening labwork

• ABGs evaluate ventilation, perfusion, estimated Hgb and acid-base status.

• Point-of-care blood glucose readings evaluate for hypoglycemia or extreme hyperglycemia.

• Biochemical panel evaluates for electrolyte imbalances, such as hyponatremia, which are associated with alterations in behavior.

Neurologic evaluation

• Mental status testing—Subjective assessment requiring patient cooperation for best results (Box 1-1).

• Mini-Mental Status Examination—Objective neuropsychologic tool used to measure orientation, recall, attention, calculation, and language. Scores less than 23 (total 25) indicate cognitive dysfunction. Patient participation is necessary for this examination (Box 1-2).

• Glasgow Coma Scale—Quantitative, three-part scale that assesses the patient’s ability to open his or her eyes, to move, and to speak/communicate. Scores range from 3 to 15, with 3 being unresponsive to all stimuli and 15 being awake, alert, and oriented. Patients who are unable to cooperate can be evaluated using this scale. See Appendix 1.

• Coma Recovery Scale—Quantitative 35-item scale used to assess brain function at four levels (generalized, localized, emergent, cognitively mediated). Seven responses are evaluated: arousal and attention, auditory perception, visual perception, motor function, oromotor ability, communication, and initiative. Patients who are unable to cooperate can be evaluated using this scale.

• Confusion Assessment Method (CAM, CAM-intensive care unit)—Four-part scale used to evaluate confusion. Onset and course, inattention, disorganized thinking, and level of consciousness are assessed (Box 1-3).

• Intensive Care Delirium Screening Checklist (ICDSC)—Eight-item scale that rates behavioral responses exhibited by patients in intensive care; delirium is indicated with scores greater than 4 to 8 (Table 1-4).

• Richmond Agitation-Sedation Scale (RASS)—Scores sedation and agitation with a 10-point scale using verbal and physical stimulation to determine patient’s response; used to titrate medications (Table 1-5).

• Rancho Los Amigos (RLA) Cognitive Functioning Scale—Seven-level scale that describes levels of cognitive functioning. Levels range from unresponsive to sensory stimuli to purposeful/appropriate actions. Patients who cannot cooperate can be evaluated using this scale (Table 1-6).

Box 1-3 CAM-ICU WORKSHEET

Feature 1: acute onset or fluctuating course

Positive if you answer ‘yes’ to either 1A or 1B.

Positive or Negative

1A: Is the patient different than his/her baseline mental status?

1B: Has the patient had any fluctuation in mental status in the past 24 hours as evidenced by fluctuation on a sedation scale (e.g., RASS), GCS, or previous delirium assessment?

Yes or No

Feature 2: inattention

Positive if either score for 2A or 2B is less than 8.

Attempt the ASE letters first. If patient is able to perform this test and the score is clear, record this score and move to Feature 3. If patient is unable to perform this test or the score is unclear, then perform the ASE Pictures. If you perform both tests, use the ASE Pictures’ results to score the feature.

Positive or Negative

2A: ASE Letters: record score (enter NT for not tested)

Directions: Say to the patient, “I am going to read you a series of 10 letters. Whenever you hear the letter ‘A,’ indicate by squeezing my hand.” Read letters from the following letter list in a normal tone.

S A V E A H A A R T

Scoring: Errors are counted when patient fails to squeeze on the letter “A” and when the patient squeezes on any letter other than “A.”

Score (out of 10): ______

2B: ASE Pictures: record score (enter NT for not tested)

Directions are included on the picture packets.

Score (out of 10): ______

Feature 3: disorganized thinking

Positive if the combined score is less than 4

Positive or Negative

3A: Yes/No Questions

(Use either Set A or Set B, alternate on consecutive days if necessary):

Set A	Set B
1. Will a stone float on water?

1. Will a leaf float on water?

2. Are there fish in the sea?

2. Are there elephants in the sea?

3. Does one pound weigh more than two pounds?

3. Do two pounds weigh more than one pound?

4. Can you use a hammer to pound a nail?

4. Can you use a hammer to cut wood?

Score ___ (Patient earns 1 point for each correct answer out of 4)

3B: Command

Say to patient: “Hold up this many fingers” (Examiner holds two fingers in front of patient). “Now do the same thing with the other hand” (Not repeating the number of fingers). (If patient is unable to move both arms, for the second part of the command ask patient “Add one more finger”). Score___ (Patient earns 1 point if able to successfully complete the entire command)

Combined Score (3A+3B):_____ (out of 5)

Feature 4: altered level of consciousness

Positive if the Actual RASS score is anything other than “0” (zero)

Positive Negative

Overall CAM-ICU (Features 1 and 2 and either Feature 3 or 4): Positive Negative

Table 1-4 INTENSIVE CARE DELIRIUM SCREENING CHECKLIST

Symptom Checklist (total 0–8)	Level of Consciousness Scoring
Level of Consciousness	Level of Consciousness
Inattentiveness
Disorientation	A = no response: none
Hallucination, delusion, psychosis	B = response to intense, repeated stimuli (loud voice or pain): none
Agitation	C = response to mild or moderate stimulation: 1
Inappropriate speech or mood	D = normal wakefulness: 0
Sleep/wake cycle disturbance	E = exaggerated response to normal stimulation: 1
Symptom fluctuation	(if A or B above do not complete evaluation for the day)

Adapted from Bergeron N, Dubois M-J, Dumont M, Dial S, Skrobik Y: Intensive care delirium screening checklist: evaluation of a new screening tool. Intens Care Med 27(5):859–864, 2001.

Table 1-5 RICHMOND AGITATION-SEDATION SCALE (RASS)*

+4 Combative	Overtly combative or violent, immediate danger to staff
+3 Very agitated	Pulls on or removes tubes or catheters, aggressive behavior toward staff
+2 Agitated	Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1 Restless	Anxious or apprehensive but movements not aggressive or vigorous
0 Alert and calm
−1 Drowsy	Not fully alert, sustained (>10 seconds) awakening, eye contact to voice
−2 Light sedation	Briefly (<10 seconds) awakens with eye contact to voice
−3 Moderate sedation	Any movement (but no eye contact) to voice
−4 Deep sedation	No response to voice, any movement to physical stimulation
−5 Unarousable	No response to voice or physical stimulation
Procedure
1. Observe patient. Is patient alert and calm (score 0)? Does patient have behavior that is consistent with restlessness or agitation? Assign score +1 to +4 using the criteria listed above.
2. If patient is not alert, in a loud speaking voice state patient’s name and direct patient to open eyes and look at speaker. Repeat once if necessary. Can prompt patient to continue looking at speaker. Patient has eye opening and eye contact, which is sustained for more than 10 seconds (score −1). Patient has eye opening and eye contact, but this is not sustained for 10 seconds (score −2). Patient has any movement in response to voice, excluding eye contact (score −3).
3. If patient does not respond to voice, physically stimulate patient by shaking shoulder and then rubbing sternum if there is no response. Patient has any movement to physical stimulation (score −4). Patient has no response to voice or physical stimulation (score −5).
Score Term Description
+4 Combative	Overtly combative, violent, immediate danger to staff
+3 Very agitated	Pulls or removes tube(s) or catheter(s); aggressive
+2 Agitated	Frequent non purposeful movement, fights ventilator
+1 Restless	Anxious but movements not aggressive or vigorous
0 Alert and calm
−1 Drowsy	Not fully alert, but has sustained awakening (eye-opening/eye contact) to voice (>10 seconds)
−2 Light sedation	Briefly awakens with eye contact to voice (<10 seconds)
−3 Moderate sedation	Movement or eye opening to voice (but no eye contact)
−4 Deep sedation	No response to voice, but movement or eye opening to physical stimulation
−5 Unarousable	No response to voice or physical stimulation
Procedure for RASS Assessment
1. Observe patient a. Patient is alert, restless, or agitated. (score 0 to +4)
2. If not alert, state patient’s name and say to open eyes and look at speaker. b. Patient awakens with sustained eye opening and eye contact. (score −1) c. Patient awakens with eye opening and eye contact, but not sustained. (score −2) d. Patient has any movement in response to voice but no eye contact. (score −3)
3. When no response to verbal stimulation, physically stimulate patient by shaking shoulder and/or rubbing sternum. e. Patient has any movement to physical stimulation. (score −4) f. Patient has no response to any stimulation. (score −5)

^* From Sessler CN, Gosnell M, Grap MJ, et al: The Richmond Agitation-Sedation Scale: validity and reliability in adult intensive care patients. Am J Respir Crit Care Med 2002; 166:1338–1344, 2002; and Ely EW, Truman B, Shintani A, et al: Monitoring sedation status over time in ICU patients: the reliability and validity of the Richmond Agitation-Sedation Scale (RASS). JAMA 2003; 289:2983–2991, 2003.

Reproduced with permission from Sessler CN, Gosnell M, Grap MJ, et al: The Richmond Agitation-Sedation scale: Validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med 166:1338, 2002. Copyright © 2002 American Thoracic Society.

Table 1-6 COGNITIVE REHABILITATION GOALS

Level	Response	Goal/intervention
I	None	Goal: Provide sensory input to elicit responses of increased quality, frequency, duration, and variety.
II	Generalized
III	Localized	Intervention: Give brief but frequent stimulation sessions, and present stimuli in an organized manner, focusing on one sensory channel at a time; for example: Visual: Intermittent television, family pictures, bright objects Auditory: Tape recordings of family or favorite song, talking to patient, intermittent TV or radio Olfactory: Favorite perfume, shaving lotion, coffee, lemon, orange Cutaneous: Touch or rub skin with different textures such as velvet, ice bag, warm cloth Movement: Turn, ROM exercises, up in chair Oral: Oral care, lemon swabs, ice, sugar on tongue, peppermint, chocolate
IV	Confused, agitated	Goal: Decrease agitation, and increase awareness of environment. This stage usually lasts 2–4 weeks. Intervention: Remove offending devices (e.g., NG tube, restraints), if possible. Do not demand patient follow through with task. Provide human contact unless this increases agitation. Provide a quiet, controlled environment. Use a calm, soft voice and manner around patient.
V	Confused, inappropriate	Goal: Decrease confusion and incorporate improved cognitive abilities into functional activity.
VI	Confused, appropriate	Intervention: Begin each interaction with introduction, orientation, and interaction purpose. List and number daily activity in the sequence in which it will be done throughout the day. Maintain a consistent environment. Provide memory aids (e.g., calendar, clock). Use gentle repetition, which aids learning. Provide supervision and structure. Reorient as needed.
VII	Automatic, appropriate	Goal: Integrate increased cognitive function into functional community activities with minimal structuring. Intervention: Enable practicing of activities. Reduce supervision and environmental structure. Help patient plan adaptation of ADLs and home living skills to home environment.

ADLs, activities of daily living; NG, nasogastric; ROM, range of motion.

Modified from Rancho Los Amigos Hospital, Inc. Levels of Cognitive Functioning (scale based on behavioral descriptions or responses to stimuli). From Swift CM: Neurologic disorders. In Swearingen PL, editor: Manual of medical-surgical nursing care, ed 4, St. Louis, 1999, Mosby.

Diagnostic tests

Neurodiagnostic testing

See Traumatic Brain Injury, p. 331.

Neuropsychological testing

Although not a routine part of critical care, neuropsychological testing should be planned and implemented for patients with brain injury or altered consciousness when they enter the recovery phase. This testing provides a comprehensive baseline for rehabilitation by evaluating higher cortical functions, such as memory, learning, and language.

Laboratory studies

If there is an acute or unexpected mental status change, lab studies include CBC, electrolytes, cardiac profile, blood and sputum cultures, urinalysis and culture, chest radiograph, and other tests as determined by signs and symptoms.

Collaborative management

Care priorities

When evaluating an alteration in consciousness or a change in mental status, acute and/or life-threatening problems must be ruled out before proceeding. Although severe agitation is difficult to manage, it is imperative that physiologic causes of agitation are ruled out before sedating the patient. Once acute causes of the problem are ruled out, the following measures may be implemented for other causes of behavioral changes:

1. For delirium

• Determine and correct physiologic imbalances and drug interactions.

• Correct sensory/perceptual deficits (e.g., provide hearing aid, eyeglasses).

• Reorient patient to the self and environment.

• Perform neuropsychologic testing.

• Implement appropriate medications to help control behavior.

• Consider geriatric consult.

• Manage pain and assess effectiveness.

• Minimize sedative medications; benzodiazepines are not recommended.

• Check bowel and bladder function.

• Establish sleep/wake cycle.

• Treat agitation.

• See Sedation and neuromuscular blockade, p. 158).

For mild confusion, good outcomes have been reported with the use of reorientation techniques and observation (use of “sitters”), especially by family members. Prophylactic low-dose haloperidol did not prevent delirium but was noted to reduce the severity of delirium in one study. Newer atypical antipsychotic medications, those with fewer extrapyramidal side effects such as quetiapine, olanzapine, and risperidone, have been shown to have an efficacy similar to haloperidol.

2. For coma

• Assess cognitive function using the RLA score or Coma Recovery Scale.

• Initiate a sensory stimulation program for patients with low-level cognition.

• Minimize stimulation for confused or agitated patients.

• Consult with rehabilitation services including physical, occupational, and speech therapy.

• Plan care to prevent or minimize problems related to the injury (e.g., spasticity, swallowing disorders) and complications of immobility (e.g., disuse syndrome, contractures, pressure ulcers).

3. For locked-in syndrome

• Establish a communication system/pattern.

• Consult a mental health professional to assess the psychological impact of this syndrome.

• Consult with rehabilitation (see preceding section on Coma).

• Provide a normal day/night routine to help minimize sleep-wake cycle disturbances.

4. For vegetative state

• Perform neurodiagnostic and neuropsychological testing to confirm the diagnosis.

• Provide essential supportive care to minimize complications such as pressure ulcers and aspiration.

• Initiate a sensory stimulation program for low-level cognitive function, including visual, auditory, tactile, gustatory, and vestibular stimuli (Figure 1-3).

Figure 1-3 Sensory stimulation (SS) programs as an intervention technique in the critically ill.

(From Kater K: Response of head-injured patients to sensory stimulation. West J Nurs Res 11[1]:20–33, 1989; Lewinn E, Dimancescu M: Environmental deprivation and enrichment in coma. Lancet 2:156–157, 1978; Mackay L, et al: Early intervention in severe head injury: long-term benefits of a formalized program. Arch Phys Med Rehabil 73:635–641, 1992; Mitchell S, et al: Coma arousal procedure: a therapeutic intervention in the treatment of head injury. Brain Inj 4:273–279, 1990; Schinner K, et al: Effects of auditory stimuli on intracranial pressure and cerebral perfusion pressure in traumatic brain injury. J Neurosci Nurs 27[6]:336–341, 1994; and Wilson S, et al: Vegetative state and response to sensory stimulation: an analysis of 24 cases. Brain Inj 10(11):807–818, 1996.)

Research has demonstrated positive outcomes from two interventions designed to reduce delirium in the intensive care unit—one was to reduce delirium in postoperative patients by controlling disturbances in the sleep-wake cycle. The second involved the daily visit of a geriatric consult service, which provided targeted recommendations using a 10-item protocol. The protocol included (1) maintenance of CNS O₂ delivery, (2) fluid and electrolyte corrections, (3) pain management, (4) removal of unnecessary medications, (5) bowel/bladder regulation, (6) establishing adequate nutrition, (7) mobilization and rehabilitation, (8) detection/prevention and treatment of surgical complications, (9) sensory stimulation, and (10) treatment of agitational variant of delirium.

CARE PLANS: ALTERATION IN CONSCIOUSNESS

Disturbed sensory perception

Goals/outcomes

If cause of alteration in consciousness is an extracerebral event, within 72 hours of this diagnosis, the patient’s level of arousal and cognition improve and the patient responds consistently and appropriately to stimuli. If the cause is cerebral, increased arousal and improvements in cognition may take days to weeks.

Cognitive Orientation, Distorted Thought Self-Control, Information Processing, Neurological Status: Consciousness

Cognitive ability:

Ability to execute complex mental processes; Ability to identify person, place, and time; Information Processing: Ability to acquire, organize, and use information

1. Eliminate environmental causes of sensory/perceptual deficit.

• Assess patient for potential causes of sensory/perceptual deficits. For the hearing- or vision-impaired patient, wearing eyeglasses or hearing aids will decrease misinterpretation of visual and auditory stimuli.

• Assess environment for potential causes of disorientation and confusion. Maintain day/night environment as much as possible. Keep clocks and calendars within patient’s field of vision.

2. Develop a plan of care consistent with sensory/perceptual deficit.

3. Assess patient for sensory deprivation and sensory overload. Decrease or increase stimulation based on RLA assessment (see Figure 1-3, above) and patient’s needs. For example, agitated and confused individuals require structure and reorientation interventions, whereas those who are comatose or stuporous require stimulation techniques.

• Orient patient to time, place, and person during all interactions. Explain procedures in terms patient can understand.

• Teach significant others reorientation and sensory stimulation strategies, and provide liberal visitation to facilitate their assistance.

• Assess underlying cause of confusion or delirium before using sedation, anxiolytic, analgesic, or antipsychotic drug therapy (see Sedation and neuromuscular blockade, p. 158).

Cognitive Restructuring; Cognitive Stimulation; Environmental Management; Reality Orientation; Dementia Management; Electrolyte Management; Delirium Management

Impaired verbal communication

related to neurologic deficits

Goals/outcomes

If cause of alteration in consciousness is an extracerebral event, within 72 hours of this diagnosis, patient communicates needs and feelings and exhibits decreased frustration and fear related to communication barriers. If cause is cerebral, improvement in communication may take days to weeks.

Communication: Expressive; Communication; Communication: Receptive

Communication enhancement

1. Determine underlying cause of impaired communication, including physiologic (cortical, brainstem, or cranial nerve injury) or psychological (depression, fear, or anger).

2. When communicating with these patients, use their name, face them, use eye contact if they are awake, speak clearly, and use a normal tone of voice.

3. Be alert to nonverbal messages, especially eye movement, blinking, facial expressions, and head and hand movements. Attempt to validate these signals with the patient.

4. Assure patient that you are attempting to find methods that promote communication if the patient’s needs cannot always be understood.

5. For the patient who does not respond to or acknowledge verbal stimulation, continue communication attempts.

6. Teach significant others methods of communication, and encourage them to continue attempts at communication.

7. Brainstem-evoked potentials and audiometry (hearing test) can provide useful information related to a patient’s ability to receive and process auditory stimuli. Detection and treatment of otitis media in patients who have ET tubes will improve hearing.

8. Obtain a speech therapy consultation to assess nature and severity of communication impairment and assist in developing a communication plan. Special attention is required for individuals with locked-in syndrome.

9. Obtain a mental health consultation to assist with a patient who is angry, frustrated, and fearful because of the communication impairment.

Communication Enhancement: Speech Deficit; Support System Enhancement

Impaired physical mobility

Goals/outcomes

By the time of discharge from the critical care unit, patient demonstrates range of motion (ROM) and muscle strength within 10% of baseline parameters.

Mobility, Ambulation

Exercise therapy: joint mobility

1. Assess muscle strength and tone to determine type of interventions required. Consult physical therapy and occupational therapy for evaluation and treatment plan.

2. Manage decreased muscle tone (flaccidity):

• Maintain body alignment and positioning.

• Perform passive ROM and stretching exercises.

• Avoid prolonged periods of limb flexion.

• Apply splints and other adaptive devices to maintain functional position of the extremities.

• Turn patient every 2 hours.

• Consider chair sitting as the patient stabilizes.

3. Manage increased muscle tone (spasticity):

• Avoid supine position; use side-lying, semiprone, prone, and high Fowler’s positions.

• Position limbs opposite flexion posture.

• Use skeletal muscle relaxant, such as baclofen (Lioresal), as prescribed for decreasing tone.

4. Monitor calcium and alkaline phosphatase levels. Increased levels can lead to the development of heterogeneous ossification, which often is seen with states of impaired mobility, such as spinal cord injury. See Fluid and Electrolyte Disturbances, p. 37.

5. Maintain patient’s skin integrity. See Wound and Skin Care, p. 167.

6. Prevent pulmonary complications in the following ways:

• Encourage deep breathing if patient is able, or suction as needed. Coughing is warranted only if sputum is present.

• Assess swallowing ability before initiating oral feedings. Obtain dysphagia consultation (usually from a speech therapist) if swallowing reflexes are impaired.

• Initiate enteral feeding protocol for patients with feeding tubes to prevent aspiration. See Nutritional Support, p. 117.

Bed Rest Care; Positioning; Exercise Promotion; Self-Care Assistance

Additional nursing diagnoses

Also see nursing diagnoses and interventions under Nutritional Support (p. 117), Sedation and neuromuscular blockade (p. 158), Prolonged Immobility (p. 149), and Risk for Disuse Syndrome, in Traumatic Brain Injury (p. 331), Acute Spinal Cord Injury (p. 264), and SIRS, Sepsis, and MODS (p. 924).

Fluid and electrolyte disturbances

The volume and composition of body fluids and electrolytes are affected by hormonal, renal, vascular, and exogenous factors. An understanding of the complexity of chemical currents, cellular function, and distribution of water between the cells and vessels provides the information used to facilitate the best patient outcome.

Water is the major constituent of the human body, comprising 55% to 72% of body mass. Body water decreases with both age and increasing body fat. The average male adult is approximately 60% water by weight, while the average female adult is 55% water by weight. Two-thirds of body fluid is within the intracellular fluid compartment (ICF). ICF contains a high concentration of potassium (K⁺), magnesium (Mg⁺), phosphates (PO₄⁻), proteins, and sulfates. The extracellular fluid (ECF) compartment is composed of interstitial fluid, which surrounds the cells, and intravascular fluid, contained within blood vessels. ECF contains the remaining third of body fluid and has a high concentration of the plasma ions sodium (Na⁺), chloride (Cl⁻), and bicarbonate (HCO₃⁻).

The composition and concentration of ECF are primarily regulated by the concentration of Na⁺, which defines the relative relationship of sodium and water. Although ECF is altered and then modified as the body reacts with its surrounding environment, ICF remains relatively stable. Intracellular stability is important for maintaining normal cellular function.

In addition to water, body fluids contain two types of dissolved substances: electrolytes and nonelectrolytes. Electrolytes are substances that carry an electrical current and can dissociate into ions, which have either a positive or a negative charge. They are measured by their capacity to combine (milliequivalents/liter [mEq/L]) or by the molecular weight in milligrams (millimoles/liter [mmol/L]). Nonelectrolytes are substances such as glucose and urea that do not dissociate in solution and are measured by weight (milligrams per 100 milliliters, or mg/dl). The body fluid compartments are separated by a semipermeable membrane, which allows movement of dissolved substances/particles between compartments, while maintaining the unique composition of each compartment (Table 1-7).

Table 1-7 PRIMARY CONSTITUENTS OF BODY WATER COMPARTMENTS*

Osmolality

Osmolality is the number of particles in solution. This concentration of particles determines the relationship of fluid between the ICF and ECF. Normal osmolality is regulated by a wide variety of mechanisms, which include arterial BP, sympathetic stimulation, renal regulation, and hormonal outflow.

Hormonal influence

Antidiuretic hormone (ADH), or vasopressin, is a hormone released by the posterior pituitary in response to a reduction in intravascular volume (hypovolemia) or an increase in extracellular osmolality. It acts on the kidney at both the glomerulus and the tubules to conserve water by increasing urine concentration. The hormone regulates the electrolyte and fluid balance to keep serum in “perfect” concentration (osmolality). Thirst is stimulated by hypovolemia and increased osmolality.

Aldosterone is another regulator of fluid volume. It is released by the adrenal cortex in response to an increased plasma renin level, acts on the kidney to conserve sodium (along with water), and increases potassium and hydrogen excretion.

Atrial natriuretic peptide (ANP) is a hormone released by the cardiac atria in response to increased atrial pressure (e.g., acute volume expansion). ANP reduces BP and vascular volume by increasing excretion of sodium and water by the kidneys, decreasing release of aldosterone and ADH, and by direct vasodilation.

Fluid disturbances

Fluid changes affect the volume status, regulation, and the composition of body fluids. Fluid loss or gain changes the concentration of particles in fluid compartments.

Hypovolemia

Pathophysiology

ECF volume depletion or hypovolemia may be caused by abnormal skin losses, GI losses, polyuria/diuresis, bleeding, decreased intake, and movement of fluid into a third space (e.g., pleura, peritoneum, interstitium). Depending on the type of fluid lost or “third-spaced,” hypovolemia may be accompanied by acid-base, osmolar, or electrolyte imbalances. Severe ECF volume depletion can lead to hypovolemic shock and cellular dehydration, which causes alterations in electric potentials (the ability to conduct impulse) throughout the body.

Compensatory mechanisms in hypovolemia include increased sympathetic nervous system stimulation: increased HR, increased force of cardiac contraction (positive inotropic effect), vasoconstriction to maintain perfusion to O₂–dependent organs (i.e., heart, lungs, brain), increased thirst, and increased release of aldosterone and ADH (vasopressin). Reduced perfusion to high-flow, low O₂–consuming organs (i.e., kidney, mesenteric bed, skeletal muscles) may lead to acute renal failure, ischemic bowel, and skeletal muscle cell rupture.

Hypovolemic shock develops when the intravascular volume decreases to the point where compensatory mechanisms can no longer maintain the perfusion needed for normal, aerobic cellular function. Without normal levels of O₂, cellular metabolism becomes anaerobic, resulting in acidosis, cardiac depression, intravascular coagulation, increased capillary permeability, and release of toxins. If shock is not adequately treated, it may become irreversible, leading to death.

Hypovolemia assessment

Goal of assessment

Identify the signs and symptoms of hypovolemia

History and risk factors

The following list of factors may be associated with loss of intravascular fluids or overall blood volume:

• Abnormal GI losses: Vomiting, nasogastric suctioning, diarrhea, intestinal drainage

• Abnormal skin losses: Excessive diaphoresis secondary to fever or exercise, burns

• Abnormal renal losses: Diuretic therapy, polyuria/osmotic diuresis seen with DKA, hyperglycemic hyperosmolar nonketotic syndrome (HHNS), nephrotoxicity, rhabdomyolysis, diabetes insipidus, diuretic phase of acute renal failure/acute kidney injury, adrenal insufficiency

• Third-spacing or plasma to interstitial fluid shift: Peritonitis, intestinal obstruction, burns, ascites, severe sepsis

• Hemorrhage: Major trauma, GI bleeding, obstetric complications, postoperative bleeding, high dosage of anticoagulants or antiplatelet medications

• Altered intake: Coma, fluid deprivation

Vital signs

Evaluate BP, HR, temperature, weight, CVP, PAWP, and urine output to determine the extent of volume depletion.

• Check BP lying, sitting, and standing to determine presence of orthostasis.

• HR will be increased (tachycardia).

• Narrowed pulse pressure

• Low CVP (less than 2 mm Hg)

• Low PAWP (less than 3 mm Hg)

• Urine output decreased and may be less than 0.5 ml/kg/hour

• Increased temperature

• Acute weight loss unless third spacing is occurring (Table 1-8)

Table 1-8 WEIGHT LOSS AS AN INDICATOR OF EXTRACELLULAR FLUID DEFICIT IN THE ADULT

Acute Weight Loss	Severity of Deficit
2%–5%	Mild
5%–10%	Moderate
10%–15%	Severe
15%–20%	Fatal

Observation

Evaluate the skin, mucous membranes, and clinical presentation for signs of dehydration including furrowed tongue, dry mucous membranes, sunken eyeballs, flat neck veins, clinical pallor, dizziness, weakness, fatigue, syncope, anorexia, nausea, vomiting, thirst, confusion, and constipation.

Palpation

Chest and abdominal palpation are performed to elicit pain in the abdomen or chest.

Screening labwork

Blood studies can reveal the extent of hypovolemia, as the blood becomes more concentrated as fluid is lost. If bleeding is present, studies will reveal blood loss.

• Hematocrit levels are elevated with dehydration and decreased with bleeding.

• BUN values may be elevated, with a BUN/creatinine ratio of greater than 20:1 suggesting hypovolemia.

• Electrolyte levels will vary depending on the type of fluid lost.

• ABG values depend on the type of fluid lost.

• Serum and urine osmolality depend on the type of fluid lost, and comparison assists in the diagnosis of renal insufficiency.

Earl hypovolemic y shock is often missed. As the HR increases and arteries constrict, BP may be compensated and remain normal or slightly elevated. Widening of pulse pressure (systolic BP + diastolic BP = pulse pressure) is a more accurate tool in early shock. A pulse pressure of 40 mm Hg may indicate shock. CO and mean arterial pressure (MAP) may be compensated by HR and vasoconstriction consecutively.

As shock progresses, HR decreases, and ventricular compliance and filling time decrease, resulting in decreased CVP and PA pressure (PAP). Volume status may be underestimated.

Diagnostic Tests for Hypovolemia

Test	Purpose	Abnormal Findings
Blood urea nitrogen (BUN)	Evaluates the renal response to decreased perfusion. Renal clearance of urea is reduced when renal blood supply is compromised.	Elevated with dehydration, decreased renal perfusion or decreased renal function. BUN/creatinine ratio greater than 20:1 suggests hypovolemia.
Hematocrit	Evaluates for hemoconcentration resulting from loss of fluid in the blood, or blood itself.	Elevated: with dehydration Decreased: with bleeding If both blood and fluid are lost, blood loss may be underestimated due to hemoconcentration.
Serum electrolytes	Assesses abnormalities that may increase morbidity. Changes are dependent on the type of fluid lost.	Hypokalemia: May occur with abnormal GI or renal loss. Hyperkalemia: Associated with adrenal insufficiency. Hypernatremia: Seen with increased insensible loss, and diabetes insipidus. Hyponatremia: Associated with increased thirst and ADH release; may lead to increased water intake, retention and dilution of serum sodium.
Serum total CO₂ (CO₂ content)	Evaluates for metabolic acidosis or alkalosis	Decreased with metabolic acidosis and increased with metabolic alkalosis.
ABG values	Assesses the body’s chemical environment. Acidosis and alkalosis can have a profound effect on electrolyte balance.	Metabolic acidosis may occur with lower GI loses, shock, or diabetic ketoacidosis. Metabolic alkalosis may occur with upper GI losses and diuretic therapy.
Urine specific gravity	Assesses the ability of the kidneys to concentrate urine. With hypovolemia, urine should be more concentrated.	Increased with kidneys’ attempt to conserve water. May be fixed at approximately 1.010 in the presence of renal disease.
Urine sodium	Assesses the ability of the kidneys to conserve sodium in response to increased aldosterone levels	In the absence of renal disease, osmotic diuresis or diuretic therapy, the value should be less than 20 mEq/L.
Serum osmolality	Assess compensation	Variable, depending on the type of fluid lost and the body’s ability to compensate with thirst and ADH
Urine osmolality	Assess concentrating ability of the kidneys. The role of urine production and concentration is to keep serum osmolality perfect.	Level should be increased greater than 450 mOsm/kg as the kidneys attempt to conserve water. If serum is concentrated, urine should be more concentrated. Comparing urine osmolality to serum osmolality assists in the diagnosis of renal insufficiency.

Collaborative management

Care priorities

Identification of patients at risk for volume loss and prevention of continued losses and fluid replacement guide the care plan for these patients.

The type of fluid replacement depends on the type of fluid lost and the severity of the deficit and on serum electrolytes, serum osmolality, and acid-base status. IV fluids are provided to expand intravascular volume or to correct an underlying imbalance in fluids or electrolytes. Fluids should be infused at a rate resulting in a positive fluid balance (e.g., 50–100 ml in excess of all hourly losses). Replacement fluids

• Isotonic solutions (Normal Saline 0.9%): Expand ECF only; do not enter ICF. Appropriate for rapid volume replacement.

• Hypotonic saline solutions (0.45% saline): Expand the ECF and provide some free water to the cells. Used in the management of the patient who is both volume-depleted and hyperosmolar (e.g., in cases of hypernatremia or hyperglycemia).

• Dextrose and water (5% dextrose in water): Provides free water only and will be distributed evenly through both the ICF and ECF; used to treat water deficit.

• Mixed isotonic saline/electrolyte solutions: Provide additional electrolytes (e.g., potassium and calcium) and a buffer (e.g., lactate or acetate). Example: lactated Ringer’s solution (Ringer’s lactate): isotonic solution containing a small amount of K⁺ and lactate, which metabolizes to bicarbonate in the liver to assist blood buffering.

• Blood and albumin: Expand only the intravascular portion of the ECF. Both packed red blood cells and fresh-frozen plasma expand the intravascular volume.

• Dextran or hetastarch, hypertonic saline, hextend: Synthetic colloidal solutions used to expand the intravascular volume.

2. Restore Tissue Perfusion (Hypovolemic Shock)

• Rapid volume replacement with crystalloids: Fluids may be given rapidly as long as cardiac filling pressures and BP remain low. Overaggressive fluid resuscitation in uncontrolled hemorrhage can increase the risk of secondary hemorrhage as the intravascular hydrostatic pressure increases.

• Volume replacement with colloids: Use of volume replacement with colloids to prevent the development of pulmonary edema secondary to rapid volume replacement remains controversial. Solutions include albumin and synthetics such as hetastarch.

• Blood: Administered only if necessary to maintain oxygen-carrying capacity. Hct should not be raised >35%.

• Vasopressors: Used to reduce the size of blood vessels while volume infusions continue to increase blood pressure. Effective for false hypovolemia induced by vasogenic (septic, anaphylactic, neurogenic) shock to control severe vasodilation.

CARE PLANS FOR HYPOVOLEMIA

Deficient fluid volume

Goals/outcomes

Within 24 hours of starting fluid therapy, patient becomes normovolemic as evidenced by urine output ≥0.5 ml/kg/hr, specific gravity 1.010 to 1.030, stable weight, no clinical evidence of hypovolemia (e.g., furrowed tongue), BP within patient’s normal range, HR and pulse pressure normalized, CVP 2 to 6 mm Hg, PAP 20 to 30/8 to 15 mm Hg, CO 4 to 7 L/min, MAP 70 to 105 mm Hg, HR 60 to 100 beats per minute (bpm), and systemic vascular resistance (SVR) 900 to 1200 dynes•sec•cm⁻⁵.

Fluid Balance, Hydration, Kidney Function

Fluid monitoring

1. Monitor input and output (I&O) hourly. During initial therapy, intake should exceed output. Consult physician for urine output less than 0.5 ml/kg/hr for 2 consecutive hours. Measure urine specific gravity every 4 hours as available. Normal range is 1.010 to 1.030. Expect it to decrease with therapy.

2. Monitor vital signs (VS) and hemodynamic pressures for continued hypovolemia. Be alert to decreased BP, CVP, PAP, CO, and MAP and to increased HR and SVR.

3. Weigh patient daily. Daily weight measurements are the single most important indicator of fluid status, because acute weight changes usually indicate fluid changes. A decrease in daily weight of 1 kg is equal to the loss of 1 L of fluid. The adult who is not eating or receiving enteral or parenteral nutrition (PN) may lose 0.25 kg of nonfluid weight daily as body tissues are used for glucose production. Weigh patient at the same time of day (preferably before breakfast) on a balanced scale, with patient wearing approximately the same clothing. Document type of scale used (i.e., standing, bed, chair).

4. Monitor for signs of fluid overload or too-rapid fluid administration: Crackles (rales), decreased O₂ saturation (pulse oximetry/SpO₂), shortness of breath (SOB), tachypnea, tachycardia, increased CVP, increased PA pressures, neck vein distention, and edema.

5. Monitor patient for hidden fluid losses. Measure/record abdominal girth or limb size if indicated.

6. Monitor for signs of abdominal compartment syndrome: Acute increase in ventilator pressures and a decrease in SpO₂.

7. Monitor for signs of bleeding: Decreased hematocrit (Hct), Hgb, tachycardia. Remember that Hct, serum Na⁺, and BUN may decrease in dehydrated patients as rehydration progresses.

8. Monitor for hypocalcemia: May develop in rapidly transfused patients due to the citrate used in banked blood (citrate binds calcium, making it unavailable for cellular uptake). Sudden symptoms may include refractory hypotension (see hypocalcemia p. 57). Calcium chloride or gluconate may be prescribed.

Fluid management

1. Place hypotensive patients in supine position with the legs elevated to 45 degrees to increase venous return. Avoid Trendelenburg position, which causes abdominal organs to lean on the diaphragm, thereby impairing ventilation.

2. Administer oral (PO) and IV fluids as prescribed. Ensure adequate intake, especially in older adults, a population at higher risk for volume depletion. Give water with enteral feedings and supplements.

3. Ensure a patent IV access and availability of blood products if needed.

Fluid Monitoring; Hypovolemia Management; Fluid Resuscitation; Intravenous (IV) Therapy; Invasive Hemodynamic Monitoring; Shock Management; Volume

Ineffective peripheral tissue perfusion

related to lack of blood volume

Goals/outcomes

Within 12 hours after initiation of volume resuscitation, patient has adequate perfusion as evidenced by alertness; warm and dry skin; BP within patient’s normal range; HR ≤100 bpm; urinary output ≥0.5 ml/kg/hr; and capillary refill less than 2 seconds.

Circulation Status, Tissue Integrity: Skin and Mucous Membranes

Positioning

1. Protect patients who are at high risk for falling: those who are confused, dizzy, or weak. Keep side rails up and bed in lowest position with wheels locked. Assist with ambulation. Raise patient to sitting or standing positions slowly.

2. Monitor for orthostatic hypotension: decreased BP, increased HR, dizziness, and diaphoresis. If symptoms occur, return patient to supine position.

Neurologic Monitoring

Hypervolemia is a state of higher-than-normal intravascular volume that occurs in four situations: (1) excessive retention of sodium and water caused by a chronic renal stimulus to conserve sodium and water, (2) abnormal renal functioning causing reduced excretion of sodium and water, (3) excessive administration of IV fluids, and (4) interstitial-to-plasma fluid shifting. Hypervolemia may lead to heart failure and pulmonary edema, especially in the patient with cardiovascular dysfunction.

• Interstitial-to-plasma fluid shifting: Remobilization of fluid after burn treatment, excessive administration of hypertonic solutions (i.e., mannitol, hypertonic saline), excessive administration of colloid oncotic solutions (i.e., albumin)

Test	Purpose	Abnormal Findings
Hematocrit	Assesses for anemia	Decreased: Due to hemodilution by excess fluids in the vasculature
Blood urea nitrogen	Evaluates for presence of renal dysfunction	Decreased: In pure hypervolemia. Increased: With renal failure
Arterial blood gases	Assesses for hypoxemia and acid-base imbalance (acidosis or alkalosis)	Hypoxemia with alkalosis: May be present due to tachypnea associated with early pulmonary edema. Respiratory acidosis: May be present in severe pulmonary edema. Diffusion of oxygen is difficult across the edematous alveolar-capillary membrane.
Serum sodium and serum osmolality	Assesses for water retention	Decreased: If hypervolemia is from water retention (i.e., chronic renal failure)
Urinary sodium	Evaluates efficacy of renal handling of sodium	Elevated: Results from kidneys excreting excess sodium. Sodium excretion prompts fluid excretion. NOTE: Urinary sodium is not elevated with secondary hyperaldosteronism (e.g., heart failure, cirrhosis, nephrotic syndrome) because hypervolemia occurs secondary to a chronic renal stimulus; the aldosterone increases resorption of Na⁺
Urine specific gravity	Evaluates the solute concentrating ability of the kidney	Decreased: If the kidney is excreting excess volume. May be fixed at 1.010 in acute renal failure
Chest radiograph	Assesses for pulmonary edema	May reveal signs of pulmonary vascular congestion (“whiter” appearance)