Advanced Nursing Application One-Final Review

A-Airway(with cervical spine stabilization &/or immobilization)
B-Breathing
C-Circulation
D-Disability

A triage system identifies and categorizes patients so that the most critical are treated first.

Emergent-Red Priority One (life, Limb, Eye threatening, needs immediate attention)- Continuous evaluation needed.

Urgent-Yellow Prioity Two (Fever greater than 104, diastolic blood pressure greater than 130, kidney stone, simple fracture, abdominal pain, asthma, no respiratory distress, needs treatment in 20 minutes to two hours)-Reevaluation every 30-60 minutes

Nonurgent-Green Priority three (sprain, minor laceration, cold symptoms, rash, simple headache. Can wait hours to days) Reevaluation every 1-2 hours

pH: 7.35-7.45
PCO2: 35-45 mmHg
Bicarbonate (HCO3): 20-30
PO2 80-100 mmHg
Oxygen Saturation 96-100%
Base Excess +/- 2.0 mEq/L

Is defined as a pH less than 7.35 and a PCO2 greater than 45.

A increased pH above 7.45 and a decrease in PaCo2 of below 35

a decreased pH of less than 7.35 and a increased bicarbonate (HCO3) of greater than 30

an increased pH of greater than 7.45 and an increased bicarbonate (HCO3) greater than 30

The frail elderly especially if sick are at increased risk for free-water loss and subsequent development of hypernatremia secondary to the impairment of the thirst mechanism and barriers to accessible fluids.

Syndrome of Inappropriate anti diuretic hormone

SIADH occurs when ADH is released despite normal or low plasma osmolarity. SIADH results from an abnormal production or sustained secretion of ADH and is characterized by fluid retension, serumhypoosmolaity, dilutional hyponatremia, hypochloremia, concentrated urine in the presence of normal or increased intravascular volume, and normal renal function. This syndrome occurs more commonly in older adults. SIADH is thought to be the most common cause of of hyponatremia in older adults. SIADH has many causes, the most common cause is malignancy, especially small cell lung cancer. These cancerous cells are capable of producing, storing, and releasing ADH.
Specific diagnostic criteria that define SIADH include the following:
•Hyponatremia (serum sodium <135 mEq/L)
•Hypotonicity (plasma osmolality <280 mOsm/kg)
•Inappropriately concentrated urine (>100 mOsm/kg water)
•Elevated urine sodium concentration (>20 mEq/L), except during sodium restriction
•Clinical euvolemia
•Normal renal, adrenal, and thyroid function

Bicarbonate HCO3 and the normal range is between 20-30

Carbon dioxide CO2 and the normal range is between 35-45

In regrads to respiratory acidosis and alkalosis the CO2 will be opposite to the pH level. (RO)
In regards to metabolic acidosis or alkalosis the HCO3 will be aiming in the same direction as the pH; Both will either be elevated or both will be decreased. The pH and the normal ranges of each are pH 7.35-7.45 and the HCO3 is 20-30.(AM)
**unless of course it is compensating. But we will not be tested on that.

Risk for injury R/T altered sensorium and decreased level of consciousness secondary to abnormal CNS function.
Potassium elevations due to potassium containing salt-substitutes, GI losses such as dirrhea, vomiting, fistulas and suctioning, diuretics, etc.

4ml lactacted ringer's solution per kg body weight per %TBSA=total fluid requirements for the first 24 hours after burn.

Application:
1/2 of total in first 8 hours
1/4 of total in second 8 hours
1/4 of total in third eight hours

Head and neck 9%
Arms 9%
Anterior trunk 18%
Posterior trunk 18%
legs 18%
Perineum 1%
Total 100%

Remove person from the source of burn abd stop the burning process. Caregiver must protect from burning process.

Electrical burns: Remove patient from contact source.

Chemical burn: Brush solid particles off the skin and water lavage.

Small thermal burns: cover with clean cool tap-water dampened towel.

Large thermal burns: ABCs (airway, breathing & circulation. Do not immerse in cool water, or pack with ice. Wrap in clean dry sheet or blanket. Remove burned clothing.

Colloidal osmotic pressure decreases, resulting in more fluid shifting out of the vascular space into the interstitial spaces.

Red blood cells are hemolyzed by circulating factors released at the time of the burn. Thrombosis occurs. Elevated hematocrit is expected.
Sodium shifts into the interstitial spaces and remains until edema formation ceases. Potassium shift occurs because of injured cells and hemolyzed red bloos cells release potassium into extracellular spaces.

Carbon monoxide poisoning is produced by the incomplete combustion of burning materials. Inhaled CO2 displaces oxygen. This causes: Hypoxia, Carboxyhemoglobinemia and death. Treat with 100% of humidified oxygen. CO2 poisoning may occur with the absence in a burn to the skin. Skin color described as "cherry red" in appearence.
*Mechanical obstruction can occur quickly.
*Presence of facial burns
*Singed nasal hair
*Hoarseness painful swallowing
*Darkened oral and nassal membranes.
* Pulmonary edema may or may not occur for 12-24 hours after the burn.

Escharotomy – removal of the eschar formed on the skin and underlying tissue of severely burned areas; procedure is particularly helpful in restoring circulation to the extremities of patients in which the eschar forms a tight swollen band around the circumference of the limb
Debridement – removal of loose, necrotic skin.
Two types of wound treatment used to control infection are the open method and the use of multiple dressing changes.
Open method – burn is covered with a topical antibiotic and has no dressing over the wound
Multiple dressing changes – sterile gauze dressings are impregnated with or laid over a topic antibiotic; may be changed two to three times every 24 hours to once every three days.

Analgesic Drug Therapy for Burn Patients
Morphine (the drug of choice for pain control)
Meperidine (Demerol)
Fentanyl (Sublimaze)
Buprenorphine (Buprenex)

A hypermetabolic state proportional to the size of the wound is noted.
Resting metabolic expenditure may be increased by 50% to 100% above normal in patients with major burns.
Core temperature is elevated.
Plasma catecholamines, which stimulate heat production, are increased.
Massive catabolism can occur and is characterized by protein breakdown and increased gluconeogenesis.
Caloric needs are often in the 5000 kcal per day range.

Acute renal failure (ARF) is a clinical syndrome characterized by a rapid loss of renal function with progressive azotemia (an accumulation of nitrogenous waste products such as blood urea nitrogen [BUN]) and increasing levels of serum creatinine.

Acute Renal Failure
Description
The sudden loss of kidney function; caused by renal cell damage from ischemia or toxic substances
ARF occurs abruptly and can be reversible
AFR leads to hypoperfusion, cell death, and decompensation in renal function
The prognosis is dependent on the cause and the condition of the client
Near-normal or normal kidney function may resume gradually

Causes
Infection
Renal artery obstruction
Acute kidney disease
Dehydration
Diuretic therapy
Ischemia from hypovolemia, heart failure, septic shock, or blood loss
Toxic substances such as medications, particularly antibiotics.

The three major types of acute renal failure are:
Prerenal (caused include intravascular volume depletion, decreased cardiac output, and vascular failure secondary to vasodilation or obstruction)
Intrarenal (causes include tubular necrosis, nephrotoxicity, and alterations in renal blood flow)
Postrenal (causes include obstruction of urine flow between the kidney and urethral meatus and bladder neck obstruction)

Chronic kidney disease involves progressive, irreversible destruction of nephrons in both kidneys. End-stage renal disease (ESRD) occurs when the glomerular filtration rate (GFR) is less than 15 mL/minute (normal = 125 mL/minute); requiring renal replacement (dialysis/transplantation).

Stages of Chronic Renal Failure
Stage I: Diminished Renal Reserve
Renal function is reduced
No accumulation of metabolic wastes
The healthier kidney compensates
Nocturia and polyuria occur as a result of decreased ability to concentrate urine

Stage II: Renal insufficiency
Metabolic wastes begin to accumulate
Oliguria and edema occur as a result of decreased responsiveness to diuretics

Stage III: End Stage Renal Disease (ESRD)
Excessive accumulation of metabolic wastes
Kidneys are unable to maintain homeostasis
Dialysis or other renal replacement therapy is required

Chronic Kidney Disease (CKD)Chronic Renal Failure
Causes
May follow acute renal failure (ARF)
Renal artery occlusion
Chronic urinary obstruction
Recurrent infections
Hypertension
Metabolic disorders
Diabetes mellitus
Autoimmune disorders

Acute renal failure: Electrolytes are profoundly affected by kidney problems. There must be a balance between extracellular fluid and intracellular fluid to maintain homeostasis. A change in the number of ions or in the amount of fluid will cause a shift in one direction or another. Sodium and chloride are the primary extracellular ions and potassium and phosphate are the primary intracellular ions.

Monitor lab values for both serum and urine to assess electrolyte status, especially hyperkalemia indicated by serum potassium levels over 7 mEq/L and ECG changes; hyperkalemia signs/symptoms include dizziness, weakness, cardiac irregularities, muscle cramps, diarrhea, and nausea; limit high potassium foods (bananas, avocados, spinach, fish) and salt substitutes which are high in potassium
Kayexalate may be prescribed if K+ is too high
Chronic renal failure: Potassium retention
Monitor vital signs and apical pulse
Monitor potassium level
Monitor for dysrhythmias (peaked T waves and widened QRS complex) indicating hyperkalemia
Provide a low-potassium diet
Administer medications as prescribed to lower the potassium level
Prepare the client for dialysis
Phosphorus retention
Phosphorus rises and calcium drops, which leads to stimulation of parathyroid hormone, causing bone demineralization
Treatment is aimed at lowering serum phosphorus levels
Administer aluminum hydroxide preparations or other phosphate binders, as prescribed, that bind phosphorus in the intestine and all the phosphorus to be eliminated. Administer aluminum hydroxide preparations at meals and not with other medications, because they bind medications in the intestinal tract
Administer stool softeners and laxatives as prescribed to prevent constipation, because aluminum hydroxide preparations are constipating
Enforce phosphorus restriction in the diet
Low calcium
Occurs because of the high phosphorus level and because of the inability of the diseased kidney to activate vitamin D
The absence of vitamin D causes a poor absorption of calcium from the intestinal tract
Monitor calcium level
Administer calcium supplements as prescribed
Administer activated vitamin D as prescribed. Metabolic acidosis
The kidneys are unable to excrete hydrogen ions or manufacture bicarbonate, resulting in acidosis
Administer alkalyzers such as sodium bicarbonate as prescribed
Note that client with chronic renal failure adjust to low bicarbonate levels and do not become acutely ill.

Normally, kidneys excrete approximately 1 mL of urine per kg of body weight per hour, which is about 1 – 2 liters per 24-hour period for adults.
Fluid volume overload (symptoms include dyspnea, tachycardia, jugular venous distention [JVD], peripheral edema, and pulmonary edema)
Fluid volume deficit (symptoms include decreased urine output, reduction in body weight, decreased skin turgor, dry mucous membranes, hypotension, and tachycardia)
Monitor I & O accurately; administer only enough fluids during oliguric phase to replace losses, typically 400 – 500 mL/day
Weigh daily on the same scale at the same time; during oliguric phase a weight gain of 1 pound/day may occur.
Monitor vital signs
Monitor I & O (strict)
Monitor weight, noting that an increase of 0.5 to 1 pound daily indicates fluid retention
Monitor BUN, creatinine, and electrolyte values
Monitor for acidosis and treat with sodium bicarbonate as prescribed
Assess urinalysis for protein, hematuria, casts, and specific gravity
Monitor level of consciousness (LOC)
Alternate periods of rest with periods of activity

***Monitor vital signs
Monitor I & O and daily weight
Monitor electrolytes
Monitor for hypertension
Monitor for congestive heart failure (CHF) and pulmonary edema. Potassium retention
Monitor vital signs and apical pulse
Monitor potassium level
Monitor for dysrhythmias (peaked T waves and widened QRS complex) indicating hyperkalemia
Provide a low-potassium diet
Administer medications as prescribed to lower the potassium level
Prepare the client for dialysis. Phosphorus retention
Phosphorus rises and calcium drops, which leads to stimulation of parathyroid hormone, causing bone demineralization
Treatment is aimed at lowering serum phosphorus levels
Administer aluminum hydroxide preparations or other phosphate binders, as prescribed, that bind phosphorus in the intestine and all the phosphorus to be eliminated. Administer aluminum hydroxide preparations at meals and not with other medications, because they bind medications in the intestinal tract
Administer stool softeners and laxatives as prescribed to prevent constipation, because aluminum hydroxide preparations are constipating
Enforce phosphorus restriction in the diet. Low calcium
Occurs because of the high phosphorus level and because of the inability of the diseased kidney to activate vitamin D
The absence of vitamin D causes a poor absorption of calcium from the intestinal tract
Monitor calcium level
Administer calcium supplements as prescribed
Administer activated vitamin D as prescribed.

Special problems in renal failure
Pruritus
Urate crystals are excreted through the skin to rid of excess wastes
This deposit of crystals is called uremic frost and it is seen in advanced stages of renal failure
Monitor for skin breakdown, rash, and uremic frost
Provide good skin care and oral hygiene
Avoid the use of soaps
Administer antipruritics as prescribed.

Anemia
A decreased rate of production of red blood cells (RBCs) occurs as a result of the diseased kidney and the decreased secretion of erythropoeitin
Monitor hemoglobin and hematocrit
Administer epoetin alfa (Epogen) as prescribed to stimulate the production of RBCs
Administer folic acid (vitamin B9) as prescribed, instead of oral iron, because oral iron is not well absorbed by the GI tract in chronic renal failure. Administer blood transfusions if prescribed, but blood transfusions are prescribed only when necessary because they decrease the stimulus to produce RBCs
Monitor bleeding
Instruct the client to use a soft toothbrush
Administer stool softeners as prescribed
Avoid the administration of acetylsalicylic acid (aspirin) because the medication is excreted by the kidneys; and if administered, high toxic levels will occur and prolong bleeding time.

GI bleeding
Urea is broken down to ammonia by the intestinal bacteria, and ammonia is a mucosal irritant that causes ulceration and bleeding
Monitor hemoglobin and hematocrit levels
Monitor stools for occult blood

Muscle cramps
Occurs in the extremities and hands and can be due to electrolyte imbalances
Monitor electrolytes
Administer electrolyte replacements as prescribed
Administer heat and massage as prescribed

Neurological changes
The buildup of active particles and fluids causes changes in the brain cells and leads to confusion and impairment in decision-making ability
Monitor for confusion and monitor level of consciousness (LOC)
Protect the client from injury
Provide a safe and hazard-free environment
Use side rails as needed
Provide a calm and restful environment
Provide comfort measures and backrubs

Psychological problems
Monitor the client for psychological problems such as depression, anxiety, suicidal behavior, denial, dependence/independence conflict, and changes in body image.

Hypertension
Failure of the kidneys to maintain homeostasis of the blood pressure
Monitor vital signs
Maintain fluid and sodium restriction as prescribed
Administer diuretics and antihypertensives as prescribed
Administer propranolol (Inderal), a beta-adrenergic antagonist, as prescribed, which decreases renin release (renin causes vasoconstriction)

Hypervolemia
Monitor vital signs
Monitor I & O and daily weight
Monitor electrolytes
Monitor for hypertension
Monitor for congestive heart failure (CHF) and pulmonary edema. Enforce fluid restriction
Avoid the administration of intravenous fluids
Administer diuretics as prescribed
Instruct the client to avoid foods with sodium
Instruct the client to avoid antacids or cold remedies containing sodium bicarbonate. Monitor vital signs
Monitor I & O and daily weight
Monitor electrolytes
Monitor for hypotension
Monitor for dehydration
Provide replacement therapy based on the electrolyte results
Provide sodium supplements as prescribed, depending on the electrolyte value.

Potassium retention
Monitor vital signs and apical pulse
Monitor potassium level
Monitor for dysrhythmias (peaked T waves and widened QRS complex) indicating hyperkalemia
Provide a low-potassium diet
Administer medications as prescribed to lower the potassium level
Prepare the client for dialysis.
Phosphorus retention
Phosphorus rises and calcium drops, which leads to stimulation of parathyroid hormone, causing bone demineralization
Treatment is aimed at lowering serum phosphorus levels
Administer aluminum hydroxide preparations or other phosphate binders, as prescribed, that bind phosphorus in the intestine and all the phosphorus to be eliminated. Administer aluminum hydroxide preparations at meals and not with other medications, because they bind medications in the intestinal tract
Administer stool softeners and laxatives as prescribed to prevent constipation, because aluminum hydroxide preparations are constipating
Enforce phosphorus restriction in the diet.

Low calcium
Occurs because of the high phosphorus level and because of the inability of the diseased kidney to activate vitamin D
The absence of vitamin D causes a poor absorption of calcium from the intestinal tract
Monitor calcium level
Administer calcium supplements as prescribed
Administer activated vitamin D as prescribed.
Metabolic acidosis
The kidneys are unable to excrete hydrogen ions or manufacture bicarbonate, resulting in acidosis
Administer alkalyzers such as sodium bicarbonate as prescribed
Note that client with chronic renal failure adjust to low bicarbonate levels and do not become acutely ill