Endocrine/​Hematology/​Gastrointestinal/​Renal/​Integumentary Study Guide for the CCRN

Renal/Genitourinary

The kidneys and genitourinary structures play an important role in waste filtering, nutrient absorption, waste elimination, and electrolyte balance. Damage to these structures can cause serious events, including urinary retention, electrolyte imbalance, and sepsis. Patients with these conditions may be treated acutely or have long-term consequences from the damage done.

Acute Genitourinary Trauma

Acute genitourinary trauma can include any of the organs that compose the genitourinary tract. These include the kidneys, ureters, bladder, urethra, and any reproductive organs. Trauma in this area most commonly occurs via blunt force injury or penetrating trauma. Blunt renal trauma makes up the majority of acute genitourinary trauma cases. Other injuries to the genitourinary system can include bladder injuries from blunt abdominal trauma or pelvic fractures; urethral crush or straddle injuries (most common in men); surgical injury during abdominal procedures, or laceration due to abdominal gunshot or stab wounds.

Symptoms and Diagnosis

Hematuria, pain, and bruising are common symptoms of genitourinary trauma. Diagnosis of trauma can be determined based on patient history, clinical symptoms, and any necessary radiographic imaging.

• In renal and ureteral injuries, microscopic or gross hematuria is the most common symptom. Progressive or prolonged renal injury can lead to renal failure. CT or MRI imaging may identify a perirenal hematoma in the event of blunt trauma. If renal injury is severe, CT imaging with contrast or a diagnostic X-ray procedure called an intravenous pyelography may be performed to assess renal and urinary tract structures.

• Bladder injuries generally present with symptoms of lower abdominal pain, gross hematuria, and difficulty or inability to void. Blood testing may show an increase in serum creatinine as urinary fluids are reabsorbed. Special types of X-ray procedures called retrograde cystography andvoiding cystourethrogram can identify irregularities in the bladder and any areas of perforation.

• Urethral injuries are most common in men. They can occur due to crush injuries of the penis or straddle injuries. Symptoms of urethral injury include initial hematuria, decreased ability or inability to void, scrotal swelling, and changes to the penis (erythema, edema). Diagnosis can be obtained via an X-ray procedure called retrograde urethrogram.

Treatment

Treatment of acute genitourinary trauma can include surgical intervention for ruptured or torn organs (ureters, bladder, or urethra), placement of stents, and prevention of further injury. Patients with bladder injuries should have foley catheters placed to keep the bladder decompressed during healing. If urethral injury is suspected, Foley catheter placement should not be attempted without consultation with genitourinary healthcare specialists to help prevent any additional injury. Patients with urethral injury may require the use of a suprapubic catheter to facilitate urinary drainage and bladder compression instead.

Some patients may just require close observation without surgical intervention. Many patients will be placed on prophylactic antibiotics and bed rest during acute recovery. Nurses should monitor patients closely for any changes in urine output, hematuria, and hemodynamics. Common complications of genitourinary trauma include bleeding, hypertension, infection (pyelonephritis), urinary incontinence, and structural changes to the genitourinary tract.

Acute Kidney Injury

In AKI, sometimes referred to as acute renal injury, a patient has an acute decompensation in renal function. It usually occurs due to decreased perfusion and decreased filtration, which in turn increases the reabsorption of metabolic waste. This increases the patient’s serum creatinine and urea.

Types

AKI can be classified into three types: pre-renal, intrarenal or intrinsic, and post-renal.

• In the pre-renal stage, the kidneys do not receive adequate perfusion.

• In the intrarenal or intrinsic stage, there is direct damage to the kidney itself.

• Post-renal AKI results from the inability to effectively drain urine.

Diagnosis

Elevated serum creatinine is the primary diagnostic, but GFR, BUN, renal ultrasound, kidney biopsy, and urinalysis can be used to support the diagnosis and identify the type and cause. AKI is a common diagnosis for critically ill patients. It is more prevalent in patients with previous renal conditions, elderly individuals, or those with disorders that rely heavily on the functioning of the kidneys (burns, trauma, infection, transfusion reactions), patients taking nephrotoxic medications, and renal obstruction.

Symptoms and Treatment

Symptoms of AKI include malaise, fatigue, weakness, darkening urine, decreased urine volume, flank pain, and confusion. AKIs are usually reversible. Treatment focuses on treating the underlying cause and providing careful fluid and electrolyte replacement. Patients may be prescribed diuretics to increase urine production and if it progresses to acute renal failure, even temporary dialysis (such as continuous renal replacement therapy or CRRT). Patients should be educated on a renal diet and choosing meals and foods with low sodium, low protein, low phosphates, and sometimes fluid restriction.

Acute Tubular Necrosis (ATN)

ATN is classified by a hypoxic injury to the kidneys, causing damage to the glomeruli and ultimately decreased functionality and filtration of the kidneys. ATN may be caused by several systemic complications, including heart attack, hypotension, hyperbilirubinemia, sepsis, surgery, some medications (contrast, chemotherapy, acyclovir, sulfonamides, streptomycin), and complications from birth. ATN is a common intrinsic cause of AKI. Diagnosis is largely clinical, similar to other AKIs, and does not heavily rely on diagnostic imaging. A key pathognomonic finding of ATN on microscopic urinalysis is “muddy brown” granular casts which reflect sloughed tubular epithelial cells.

Symptoms and Treatment

Symptoms of ATN may develop slowly or quickly. Common symptoms of ATN include lethargy, confusion, nausea, vomiting, oliguria, edema, and electrolyte imbalance. ATN, like other types of AKIs, is typically reversible but happens much slower, often from three days to weeks for the renal cells to start to regenerate. Treatment is similar as discussed above and involves treating underlying causes, supportive measures, maintaining appropriate fluid balance, antibiotics if needed, and dialysis.

Diuretics

Diuretics are medications used to help the body produce and eliminate liquid waste products from the body. Different classes of diuretics work on different parts of the renal system to prevent or enhance the absorption of certain electrolytes and fluids. Diuretics remove fluid from the intravascular space and therefore reduce preload. They are commonly administered in conditions such as heart failure, pulmonary edema, renal failure, and any other hypervolemic state.

Loop Diuretics

Loop diuretics are used to prevent reabsorption of sodium and chloride in the ascending loop of Henle. They also work to increase release of calcium, magnesium, and potassium. Patients on loop diuretics must be closely monitored for electrolyte imbalances and dysrhythmias. These medications most commonly cause hypokalemia, and patients may need to take potassium supplements with this medication to help prevent this. Because of this effect, sometimes loop diuretics are given to lower potassium in combination with other medications in the hyperkalemic patient.

Nurses should educate patients that common side effects of these medications include frequent urination, postural hypotension, increased blood glucose, and increased uric acid. They are not often used to control hypertension, as their mechanism is short acting. Because of this quick onset, patients who take these medications typically take them multiple times a day. The most common loop diuretics are bumetanide (Bumex®), ethacrynic acid (Edecrin®), and furosemide (Lasix®).

Thiazide Diuretics

Thiazide diuretics work similarly to loop diuretics; however, they prevent reabsorption in the early distal tubules. This results in an increase in the excretion of sodium and water. Potassium and bicarbonate are also eliminated in this process, and patients taking these diuretics also often require potassium supplementation to prevent hypokalemia. These diuretics last longer than the loop diuretics, with effects lasting between 12 to 72 hours after administration. They can be used more commonly to help control hypertension. Some patients will be prescribed this medication daily while others, due to the extended mechanism of action, may only have it intermittently three to five days a week for edema.

Side effects of thiazide diuretics include dizziness, postural hypotension, headache, blurry vision, itching, and lightheadedness. Patients should be educated that use of these medications can increase photosensitivity and sunscreen should be applied regularly. The most common thiazide diuretics include chlorothiazide (Diuril®), bendroflumethiazide (Naturetin®), chlorthalidone (Hygroton®), and trichlormethiazide (Naqua®).

Potassium-Sparing Diuretics

Potassium-sparing diuretics, just like the loop and thiazide diuretics, prevent the reabsorption of sodium. This, however, is performed in the late distal tubule and collecting duct, rather than prior to the filtration system. These are weaker diuretics but do not have as strong an effect on the patient’s potassium levels. They are often given with loop or thiazide diuretics to counteract the potassium-depleting effects that these diuretics have.

Side effects of potassium-sparing diuretics include blurred vision, dehydration, nausea, insomnia, and potential hormone changes. The most common potassium-sparing diuretics include spironolactone (Aldactone®) and eplerenone. Aldactone® is commonly used either orally or intravenously to treat congestive heart failure. Eplerenone may be substituted for Aldactone if side effects are intolerable, as eplerenone has been shown to have similar outcomes with fewer side effects.

Chronic Kidney Disease (CKD)

CKD develops over time as kidney function declines. In this condition, the kidneys become unable to appropriately filter blood through the kidneys, concentrate urine, and maintain electrolyte balance. When greater than 50% of the renal capacity is damaged or destroyed, kidney function declines significantly. When the damage has progressed to only 15% functioning, it is classified as renal failure, stage 5 kidney disease, or end-stage renal disease (ESRD) and requires dialysis and/or transplant. Like most chronic conditions, patients with CKD can experience acute exacerbations, which in this case are acute kidney injuries. You may see this expressed as “acute on chronic kidney disease”. Unlike AKIs, CKD is not reversible.

Diagnosis

CKD is often difficult to detect early because many patients remain asymptomatic in the initial stages. In fact, diagnosis frequently begins with routine laboratory testing, where an elevated creatinine level may be noted. Because creatinine alone is nonspecific, as it can be seen in both acute and chronic kidney disorders, additional evaluation is needed.

The primary diagnostic is the estimated glomerular filtration rate (eGFR) that reflects overall kidney function. The normal level is around 100 mL/min/1.73m2. CKD is staged based on eGFR:

• Stage 1: eGFR greater than 90 with evidence of kidney damage, such as protein in urine or abnormal imaging
• Stage 2: eGFR 60 to 89
• Stage 3a: eGFR 45 to 59
• Stage 3b: eGFR 30 to 44
• Stage 4: eGFR 15 to 29
• Stage 5: eGFR less than 15 (kidney failure)

While symptoms may be absent early on, progressing CKD can present with fatigue, edema, nausea, back or flank pain, difficulty concentrating, and decreased urine output or other urinary changes.

To clarify the diagnosis and determine any underlying causes, clinicians may use ultrasound, CT imaging, urinalysis, or kidney biopsy.

Treatment

Treatment is often supportive, treating the symptoms caused by CKD. In patients with significantly decreased function and increased/imbalanced electrolytes, dialysis will be initiated.

The two main types of dialysis are hemodialysis (HD) and peritoneal dialysis (PD). In HD, blood is run through an external machine to be filtered to remove toxins and excess fluid. This requires vascular access through a fistula, graft, or central catheter. Treatments are typically performed three times per week and involve rapid shifts in fluid and electrolytes. In PD, the peritoneal membrane is used as the natural filter. A dialysis solution is placed into the abdomen through a catheter and then drained to remove waste products and fluid. PD is done daily and carries a higher infection risk of peritonitis.

In critically ill patients, hemodynamic instability may make them unable to tolerate the rapid fluid and electrolyte shifts of traditional hemodialysis. In these cases, a form of HD called continuous renal replacement therapy (CRRT) provides continuous 24-hour dialysis with much more controlled and gradual removal of fluid and filtration.

Patients may register for a kidney transplant as well. Patients should be instructed on appropriate choices among the renal diet and understand fluid restrictions to prevent fluid overload and other medical managements for comorbidities such as maintaining blood pressure, lowering cholesterol, and controlling diabetes. Calcium and vitamin supplementation and phosphate binders may be used to help manage alterations in electrolytes due to the decreased filtration function.

Infections

Pyelonephritis is a kidney infection that generally stems from bacteria in the urine. It can affect one or both of the kidneys. Patients at high risk for urinary tract infections include catheterized patients and patients with immune deficiency, history of urinary tract infections, kidney stones, and renal/bladder tumors.

Symptoms and Diagnosis

Symptoms of pyelonephritis include fever, flank pain, chills, back pain, abdominal pain, urinary frequency, urgency, dysuria, nausea, and vomiting. Patients may have blood in their urine or pus. Diagnosis may be made with urinalysis testing, urine culture, and a CT scan. Patients with recurrent pyelonephritis should be evaluated for vesicoureteral reflux, which is an abnormal backward flow of urine. This can be assessed with a voiding cystourethrogram.

Treatment

Untreated infection may lead to sepsis, specifically referred to as urosepsis, classified by fever, hypotension, infection, confusion, nausea/vomiting, and difficulty breathing. Often, patients are hospitalized for intravenous antibiotics and supportive therapy. Long-term effects of pyelonephritis may include kidney scarring, hypertension, acute kidney injury, acute tubular necrosis, and kidney failure.

Fluid Imbalances

Fluid imbalances can occur in many situations, including illness, injury, and changes in intake or output. As nurses, it is essential to understand how shifts in fluid volume affect overall stability, organ function, and a patient’s response to treatment. Normal fluid balance, often referred to as euvolemia, means the body has the appropriate amount of fluid to maintain physiologic function. Recognizing the signs of both fluid loss and fluid overload helps guide timely interventions and prevent further complications.

Fluid Deficit

A fluid deficit, also referred to as hypovolemia, occurs when the body loses more fluid than it takes in, leading to decreased volume. Causes may include dehydration, bleeding, vomiting, diarrhea, and medications such as diuretics. Patients may present with hypotension, tachycardia, dry mucous membranes, decreased urine output, and poor skin turgor. When there is less fluid in the blood stream, serum becomes more concentrated leading to lab abnormalities such as hypernatremia. Treatment includes controlling the underlying cause, as well as oral rehydration if appropriate, or IV fluids. If untreated, fluid deficit can progress to hypovolemic shock causing decreased perfusion and organ dysfunction.

Fluid Overload

Fluid overload, also referred to as hypervolemia, occurs when there is excess fluid in the body. It is often associated with heart failure, kidney dysfunction, or excessive fluid administration. Patients may exhibit edema, hypertension, bounding pulses, weight gain, and signs of respiratory distress. Excess fluid can dilute serum concentration making hyponatremia more common. Early recognition can prevent cardiac and respiratory complications.Treatment may include fluid restrictions and diuretics to help remove excess fluid through urination. In severe cases, dialysis may be required.

Electrolyte Imbalances

Electrolyte imbalances may occur under many conditions, including kidney damage or fluid overload. As a nurse, you must understand the appropriate levels of each of the following electrolytes and how patients may react based on elevated or decreased levels.

Sodium

Normal sodium levels range from 135 to 145 mEq/L. Levels above and below this range indicate either hyponatremia or hypernatremia.

Hyponatremia

Sodium levels less than 135 mEq/L indicate hyponatremia. Most cases of hyponatremia are dilutional, meaning there is not necessarily a net loss of sodium but rather a hypervolemic state that causes serum sodium to be diluted. Dilutional hyponatremia may be caused by heart and renal failure, SIADH, and fluid shifts seen in ketoacidosis. Direct sodium loss can be caused by diarrhea, vomiting, NG decompression, and excessive sweating. It is important to understand the cause of hyponatremia as it impacts treatment. If dilutional, removing the excess fluid with diuretics and/or implementing fluid restrictions can restore the sodium levels. If there is sodium depletion, it can be replaced with sodium tablets or isotonic/ hypertonic IV fluids. Sodium must be corrected slowly to prevent brain damage. Patients should be monitored for lethargy and changes in level of consciousness. In severe hyponatremia, cerebral edema, seizures, and coma may occur.

Hypernatremia

If sodium levels are greater than 145 mEq/L, hypernatremia is diagnosed. Just like in hyponatremia, most cases of hypernatremia are due to an imbalance in the body’s fluid levels. It is most commonly seen in dehydration and conditions that cause free-water loss, such as diabetes insipidus or severe hyperglycemia. Less commonly, it may occur from excessive sodium intake or as a result of overcorrection of hyponatremia. Patients may show signs of extreme thirst, irritability, flushing, and lethargy. Patients should also be monitored closely for the same neurological changes that can occur in hyponatremia. Patients should have their sodium levels monitored closely and fluids replaced either orally or intravenously to treat dehydration and thereby correct hypernatremia.

Potassium

Normal potassium levels range from 3.5 to 5 mEq/L, and levels outside of this range indicate either hypokalemia or hyperkalemia.

Hypokalemia

When potassium levels are below 3.5 mEq/L, hypokalemia is indicated. Hypokalemia occurs most commonly due to potassium loss in the GI tract, such as diarrhea, vomiting, and NG decompression, as well as to renal losses due to diuretic use. The hormonal disorder Cushing’s syndrome can also cause hypokalemia. Symptoms of hypokalemia include lethargy, weakness, paresthesia, and tetany. One of the most concerning complications is its effect on the cardiovascular system, as it can lead to fatal cardiac dysrhythmias. For this reason, any patient with a potassium imbalance should be placed on telemetry monitoring.

Treatment focuses on correcting the underlying cause, such as using antiemetics or antidiarrheals for GI losses or adjusting diuretics. Potassium can be replaced orally or intravenously, but because it is a vesicant, it should go through a central line whenever possible. If administered through a peripheral IV, the site must be monitored closely for signs of extravasation. Potassium must never be given IV push or as a bolus, and IV replacement should not exceed 20 mEq/hour.

Hyperkalemia

If potassium levels fall below 2.5 mEq/L, hyperkalemia is diagnosed. Hyperkalemia is most commonly due to impaired renal excretion, such as in acute kidney injury (AKI) or chronic kidney disease (CKD). Other causes include medications (e.g., potassium-sparing diuretics and ACE inhibitors), tissue breakdown (such as in burns or rhabdomyolysis), and endocrine disorders like Addison’s disease. Sometimes, it can be caused by too much potassium in the diet or an overcorrection of hypokalemia.

Patients with diabetes are at increased risk for hyperkalemia because insulin drives potassium into the cells, and when it is absent or insufficient, as in uncontrolled diabetes, potassium remains in the blood stream. This potassium-lowering effect insulin is why it can be used as a treatment for hyperkalemia, usually given with dextrose to prevent hypoglycemia. Other treatments include loop or thiazide diuretics, albuterol, and sodium polystyrene (Kayexalate®), all of which help lower potassium. In severe cases, dialysis may be required to remove the potassium. The symptoms of hyperkalemia can mirror those of hypokalemia and it carries the same risk of fatal cardiac dysrhythmias, especially in levels >6.5 mEq/L. Calcium gluconate may be administered to stabilize the cardiac membrane when dysrhythmias are a concern.

Calcium

Normal calcium levels range between 8.2 to 10.2 mg/dL. Levels outside of this range mean a diagnosis of either hypocalcemia or hypercalcemia.

Hypocalcemia

Calcium levels below 8.2 mg/dL indicate hypocalcemia. Hypocalcemia becomes critical when levels fall lower than 7 mg/dL. Low calcium is typically a result of parathyroid gland dysfunction (hypoparathyroidism) or low vitamin D, which is essential for absorption of calcium. Hypocalcemia shares similar clinical effects with potassium imbalances, especially regarding neuromuscular dysfunction and cardiovascular instability. This includes signs such as muscle cramps, paresthesias, tetany, and cardiac issues. Two pathognomonic indicators of hypocalcemia are Trousseau’s sign and Chvostek’s sign. Trousseau’s sign is a spasm of the hand when inflating a blood pressure cuff, and Chvostek’s sign is a twitching of the facial muscles when stroking the cheek. Correction of calcium levels may be given orally or via IV, depending on the severity. Slow administration of IV calcium is necessary to prevent severe cardiac events. If caused by parathyroid hormone or vitamin D deficiency, those can be supplemented as well.

Hypercalcemia

Hypercalcemia is diagnosed when calcium levels are above 10.2 mg/dL and becomes critical when levels are greater than 14 mg/dL. Most cases of hypercalcemia are caused by hyperparathyroidism or cancer. Temporary causes of hypercalcemia can be excessive intake of vitamin D or calcium carbonate (TUMS®). Patients with hypercalcemia may experience progressive muscle weakness and bone pain, hypotonicity, frequent thirst and urination, anorexia, nausea, vomiting, constipation, and cardiac disturbances. Patients should be addressed for other conditions increasing their calcium levels. Some medications have this as a side effect and may need to be adjusted. If it is determined to be an oversecretion from the parathyroid gland, surgery may be necessary to remove it. Fluids may be used to help dilute and expel the excess calcium.

Phosphorus

Normal phosphorus levels range from 2.5 to 4.5 mEq/L and values outside of this range indicate either hypophosphatemia or hyperphosphatemia.

Hypophosphatemia

Phosphorus levels below 2.5 mEq/L indicate hypophosphatemia. Calcium and phosphate have an inverse relationship, so if someone has hypercalcemia, they will often have hypophosphatemia. Beyond that relationship, phosphate levels can fall in severe malnutrition, long-term alcohol abuse, and acid-base imbalances.

Hypophosphatemia can be asymptomatic. Symptoms of long-term hypophosphatemia include altered mental status, bone pain and fractures, weakness, and loss of appetite. It can lead to respiratory and/or heart failure as well as seizures and coma. Treatment of hypophosphatemia includes correcting other abnormal electrolytes and phosphorus replacement.

Hyperphosphatemia

Phosphorus levels above 4.5 mEq/L indicate hyperphosphatemia. Hyperphosphatemia is often secondary to kidney failure, as impaired renal function prevents the kidneys from excreting phosphate. In CKD, elevated phosphate levels are very common, but outside of kidney disease or injury, hyperphosphatemia is rare and may be attributed to tissue necrosis in malignancies and acid-base imbalances. Remember the inverse relationship between phosphorus and calcium: patients with hyperphosphatemia may exhibit signs of hypocalcemia, such as the positive Trousseau’s and Chvostek’s signs. Chronic phosphate elevations, especially in the setting of CKD, can cause vascular and soft-tissue calcifications and pruritus. In CKD, phosphate levels can be reduced by reducing dietary intake, oral phosphate binders with meals, and dialysis. If the primary problem is hypocalcemia, and hyperphosphatemia is secondary, then correcting the hypocalcemia should help normalize the phosphate level.

Magnesium

Normal magnesium levels range between 1.6 to 2.6 mg/dL and any readings outside of this range indicate either hypermagnesemia or hypomagnesemia.

Hypomagnesemia

If magnesium levels fall below 1.6 mg/dL, a diagnosis of hypomagnesemia is made and with levels less than 1.2 mg/dL, the situation becomes critical. Hypomagnesemia may occur due to chronic alcohol abuse, malnutrition, chronic diarrhea, pancreatitis, diuretics, laxative use, proton pump inhibitors, and endocrine disorders. It primarily affects the neuromuscular and cardiovascular systems. Symptoms of hypomagnesemia include muscular excitability, nystagmus, confusion, headaches, dizziness, seizures, tachycardia, ventricular arrhythmias, respiratory depression, and coma. Treatment focuses on correcting the patient’s magnesium levels via oral or IV magnesium. Administration of magnesium IV should not exceed 2 grams per hour and patients should be monitored closely for hypotension.

Hypermagnesemia

Magnesium levels above 2.6 mg/dL indicate hypermagnesemia and levels greater than 4.9 mg/dL are considered to be critical. Hypermagnesemia may occur in patients with renal failure. It can also be caused by excessive antacid or laxative use. Hypermagnesemia may not cause any symptoms, and one of the first signs can be hypotension not responsive to traditional treatment. Other signs include muscle weakness, nausea and vomiting, and in severe cases, hypoventilation, neuromuscular paralysis, and cardiac dysrhythmias. Patients should be assessed for underlying causes of the hypermagnesemia. IV diuretics may help excrete excess magnesium. In patients with respiratory depression due to elevated magnesium, IV calcium gluconate can help reverse respiratory manifestations. Patients who have persistently elevated levels may need dialysis.

Metabolic Acidosis and Alkalosis

We briefly touched on acid-base balance previously, but now we will focus on metabolic processes. The body strives to maintain homeostasis by balancing acids and bases, with bicarbonate (\(\text{HCO}_3\)) serving as the primary base. When this balance is disrupted, the body uses compensatory mechanisms, often through the lungs, to help correct pH changes. For a more detailed overview, refer back to the respiratory section. Understanding these responses is key to recognizing and managing metabolic acidosis and alkalosis.

Acidosis

Metabolic acidosis occurs when the body is unable to excrete excess acids or maintain base levels. Conditions such as DKA, lactic acidosis, diarrhea, starvation, and renal failure are all potential causes for this condition. Patients with metabolic acidosis can have compensation by driving out \(\text{CO}_2\) levels through tachypnea. Patients with uncompensated metabolic acidosis and arterial blood gas will show decreased pH, decreased \(\text{HCO}_3\), and normal \(\text{PCO}_2\). If the patient experiences compensation, their \(\text{PCO}_2\) will decrease and their pH will begin to normalize.

Alkalosis

Metabolic alkalosis occurs when the body has decreased acid balance or increased base presence. It may occur due to vomiting, gastric suction, diuretics, and excessive antacid intake. Patients can have compensation for this condition if the body is triggered to retain \(\text{CO}_2\) through hypoventilation. In an uncompensated patient, lab results will show an increased pH, increased \(\text{HCO}_3\), and normal \(\text{PCO}_2\). If the patient becomes compensated, their \(\text{PCO}_2\) will increase and the pH will begin to normalize.