C920 Laboratory Report

Student Name

Western Governors University

C920 Contemporary Curriculum Design and Development in Nursing Education

Prof. Name:

Date

LABORATORY REPORT

Predictions

In patients experiencing acidosis, arterial blood pH is anticipated to be lower than the normal range.
Conversely, patients with alkalosis are expected to have arterial blood pH values above the normal limits.
For those with respiratory acidosis, arterial blood partial pressure of carbon dioxide (pCO2) is predicted to be elevated.
Patients suffering from metabolic acidosis should exhibit reduced bicarbonate (HCO3⁻) concentrations in arterial blood.
In respiratory alkalosis, arterial pCO2 levels are expected to fall below the normal range.
Those with metabolic alkalosis are predicted to have increased arterial HCO3⁻ levels.

Materials and Methods

Variables:

Dependent variables: Respiratory rate and arterial blood values including pH, pCO2, and HCO3⁻ levels.
Independent variable: The specific acid-base imbalance disorder being studied.
Controlled variables: Factors such as age and gender were kept constant to avoid influencing results.

Explanation of Bicarbonate Calculation:
The concentration of bicarbonate (HCO3⁻) in blood can be calculated indirectly using measured pH and pCO2 values. This is possible due to the chemical equilibrium involving carbon dioxide (CO2), water (H2O), carbonic acid (H2CO3), hydrogen ions (H⁺), and bicarbonate ions, which maintain a dynamic balance:

[
\text{CO}_2 + \text{H}_2\text{O} \leftrightarrow \text{H}_2\text{CO}_3 \leftrightarrow \text{H}^+ + \text{HCO}_3^-
]

When the concentration of any component in this reaction shifts, compensatory changes occur in the others to maintain equilibrium. For example, an increase in CO2 leads to increased formation of H⁺ and HCO3⁻, affecting blood pH and bicarbonate concentration.

Results

Table 1. Acid-Base Imbalance Signs and Compensatory Responses

Parameter	Normal Range	Patient 1 (Respiratory Acidosis)	Patient 2 (Metabolic Alkalosis)	Patient 3 (Respiratory Alkalosis)	Patient 4 (Metabolic Acidosis)
Respiratory Rate (breaths/min)	12-18	24 (High)	8 (Low)	39 (High)	28 (High)
pH	7.35 – 7.45	7.25 (Low, Acidic)	7.50 (High, Alkaline)	7.55 (High, Alkaline)	7.29 (Low, Acidic)
pCO2 (mmHg)	35 – 45	72 (High)	49 (High)	27 (Low)	30 (Low)
HCO3⁻ (mEq/L)	22 – 26	31 (High)	38 (High)	23 (Normal)	14 (Low)
Acid-Base Disorder	–	Respiratory Acidosis	Metabolic Alkalosis	Respiratory Alkalosis	Metabolic Acidosis
Compensation Type	–	Metabolic (Renal)	Respiratory	None	Respiratory

Interpretation of Results

Respiratory Rate Comparison

Patient 1 (Respiratory Acidosis): Respiratory rate of 24 breaths per minute, which is elevated above the normal 12-18 range, likely as a compensatory effort to remove excess CO2.
Patient 3 (Respiratory Alkalosis): Exhibits a respiratory rate of 39 breaths per minute, significantly above normal, indicative of hyperventilation.
Patient 4 (Metabolic Acidosis): Shows an elevated respiratory rate of 28 breaths per minute, possibly due to compensatory hyperventilation.
Patient 2 (Metabolic Alkalosis): Respiratory rate is 8 breaths per minute, below the normal range, reflecting hypoventilation as compensation.

Blood pH Values

Patient 1: Blood pH is 7.25, below normal, confirming acidemia associated with respiratory acidosis.
Patient 3: Blood pH of 7.55, above normal, consistent with alkalemia in respiratory alkalosis.
Patient 4: Blood pH of 7.29, below normal, indicative of acidemia from metabolic acidosis.
Patient 2: Blood pH is 7.50, elevated, consistent with metabolic alkalosis.

pCO2 Levels

Patient 1: pCO2 is elevated at 72 mmHg, reinforcing diagnosis of respiratory acidosis.
Patient 3: pCO2 is 27 mmHg, decreased as expected in respiratory alkalosis.
Patient 4: pCO2 is low at 30 mmHg, consistent with respiratory compensation in metabolic acidosis.
Patient 2: pCO2 slightly elevated at 49 mmHg, likely due to hypoventilation compensation.

Bicarbonate Concentrations

Patient 1: Elevated bicarbonate at 31 mEq/L indicates renal compensation in response to respiratory acidosis.
Patient 3: Normal bicarbonate level of 23 mEq/L suggests no metabolic compensation.
Patient 4: Low bicarbonate level of 14 mEq/L confirms metabolic acidosis.
Patient 2: Elevated bicarbonate at 38 mEq/L consistent with metabolic alkalosis.

Discussion

1. Is compensation present in respiratory acidosis, and how does it function?

Yes, compensation is evident in Patient 1, who suffers from respiratory acidosis. The kidneys respond by conserving bicarbonate ions through increased reabsorption in renal tubules and secretion of hydrogen ions in collecting ducts. This renal (metabolic) compensation generates ammonia buffers that neutralize excess acids, thereby elevating blood pH towards normal (Hamilton et al., 2017).

2. Does respiratory alkalosis show compensatory mechanisms?

Patient 3 shows no metabolic compensation as bicarbonate levels remain within normal limits, despite low pCO2 and elevated pH. This indicates no renal response has yet developed or is insufficient to compensate.

3. How does compensation occur in metabolic acidosis?

In Patient 4, compensation is respiratory. Hyperventilation reduces arterial pCO2 by increasing the breathing rate, thus lowering carbon dioxide levels. This decrease in pCO2 helps to raise blood pH by reducing acid load, while low bicarbonate reflects consumption in buffering excess hydrogen ions (Hamilton et al., 2017).

4. What compensation occurs in metabolic alkalosis?

Patient 2 demonstrates respiratory compensation through hypoventilation, decreasing respiratory rate and thereby increasing arterial pCO2. Elevated CO2 counters alkalosis, pushing pH back towards normal. However, hypoventilation may lead to hypoxemia, triggering feedback mechanisms that limit further CO2 rise.

5. Which initial predictions were supported by the data?

Predictions regarding pH deviations in acidosis and alkalosis, as well as alterations in pCO2 and bicarbonate levels corresponding to respiratory and metabolic disturbances, were confirmed. For example, the increased bicarbonate in respiratory acidosis and the low bicarbonate in metabolic acidosis matched predictions. The absence of compensation in respiratory alkalosis was also as anticipated (Hamilton et al., 2017).

Application

1. Why do COPD patients develop respiratory acidosis, and why is their breathing rate elevated?

COPD patients develop respiratory acidosis due to hypoventilation caused by diminished diaphragm function, increased dead space, and reduced respiratory drive. Elevated pCO2 levels result from inefficient CO2 clearance. To compensate, the respiratory rate increases in an effort to improve oxygen intake and CO2 removal (Pahal et al., 2020).

2. What triggers involuntary breathing after breath-holding?

When breath is held, rising CO2 levels and decreasing oxygen trigger chemoreceptors in the brainstem and periphery. These receptors stimulate the respiratory center, activating the diaphragm and intercostal muscles via the phrenic and vagus nerves, forcing involuntary respiration to restore homeostasis (Parkes, 2005).

3. How does anxiety lead to respiratory alkalosis?

Anxiety induces hyperventilation—rapid, shallow breathing—that lowers arterial CO2. This decreases carbonic acid in the blood, raising pH and causing respiratory alkalosis due to an elevated bicarbonate-to-CO2 ratio.

4. What causes metabolic acidosis in uncontrolled diabetes?

In diabetes without sufficient insulin, cells cannot utilize glucose, leading to fat breakdown and ketone body production. Accumulation of acidic ketones causes metabolic acidosis, a dangerous condition called diabetic ketoacidosis (Chiasson et al., 2003).

References

Chiasson, J. L., Aris-Jilwan, N., Bélanger, R., et al. (2003). Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ, 168(7), 859–866.

Hamilton, R., Gurley, K., & Abraham, S. (2017). Acid-base balance and compensation mechanisms. Journal of Clinical Physiology, 12(4), 215-228.