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Blood pH
7.35-7.45
- 7.4 is ideal
less than 7.4 is considered acidic, more than 7.4 considered alkaloid
pCO2
35-45 mmHg
PO2
80-100 mmHg
O2 saturation
95-100%
HCO3-
22-26 mEq/L
Metabolic Acidosis:
Identified when the pH and bicarbonate are both low
This can happen for 2 Reasons:
Loss of bicarbonate (which is a base) due to diarrhea / diuretics
“Below the waist, bye base!”
This leaves patient without enough base to balance out the acid, and acidosis occurs
An excessive accumulation of acid from either lactic acidosis, diabetic ketoacidosis, kidney failure, or starvation.
This patient could have a headache, confusion, and increased respiratory rate and depth to compensate
Patient could go into shock if their pH drops below 7
Metabolic Alkalosis:
Occurs when the pH and bicarbonate are both high
This can be caused by:
Loss of potassium or vomiting
“Above the waist, adios acid!”
Clinical Manifestations:
Hypocalcemia symptoms such as Trousseau and Chvostek signs
Slow respiratory rate to compensate
Kidneys trying to excrete more bicarbonate if able
Treatment:
Correct underlying cause
IV fluids
Potassium for hypokalemia
Respiratory Acidosis:
Occurs from LOW pH and HIGH CO2, caused by inadequate excretion of it
The body retains CO2, which can happen due to pulmonary issues, hypoventilation, or an overdose of sedatives.
Manifestations:
Changes in mental status
Hyperkalemia
If more of a chronic process due to lung condition, the patient may be asymptomatic.
Treatment:
Reversal of sedative medications
Intubation
BiPAP (bilevel positive airway pressure)
Hydration
Respiratory Alkalosis:
Occurs with a HIGH pH and a LOW CO2
Caused by:
Hyperventilation from a process such as anxiety
Hypoxemia
Early sepsis
Labor
Hepatic insufficiency
Cerebral tumors
Clinical Manifestations:
Patient may feel lightheaded
Have a change in mental status
Tachycardia
Arrhythmias
Treatment:
Rebreathe exhaled CO2 (people breathe into paper bags)
RAAS:
Initiated by decreased perfusion to the kidneys
The kidneys release renin
Renin combines with angiotensinogen to form angiotensin I
Angiotensin I is converted in the lungs to Angiotensin II
Angiotensin II stimulates the adrenal cortex to release aldosterone
Aldosterone directs the kidney to reabsorb more sodium
Water follows sodium back into ECF
ADH
Secreted by posterior pituitary gland
Released in response to increased osmolality
Increases water retention
Hypovolemia (fluid volume deficit), is diminished blood volume
Conditions that can result in Hypovolemia:
Fluid loss (most common cause)
Hemorrhage
Frequent urination
Vomiting
Diarrhea
Fistulas
Fever
Excessive nasogastric suctioning
Clinical Manifestations & Treatment of Hypovolemia
Clinical Manifestations:
Hypotension / Tachycardia
Thirst / Poor skin turgor
Dry mucous membrane / Decrease urinary output / Flattened neck veins
If severe, there will be a decreased preload to the heart, which causes a decrease in cardiac output, resulting in hypovolemic shock.
Treatment:
Oral or Parenteral fluids
Blood or blood products, if due to hemorrhage
Antidiarrheals if the loss is from diarrhea
Antiemetics if loss is from vomiting
Vasopressors may be orders, if patient is in hypovolemic shock
Hypervolemia: Fluid Volume Excess
Abnormally increased volume of blood
Causes: Increase in sodium and water retention, excessive increase in sodium & water intake or, fluid shifting from intracellular space into extracellular space
Selected Causes of Hypervolemia:
Renal failure
Heart failure
Cirrhosis
Nephrotic syndrome
Clinical Manifestations & Treatment of Hypervolemia
Clinical Manifestations of Hypervolemia:
Dyspnea / Crackles / Tachypnea
Bounding, rapid pulse
Hypertension / Distended neck veins /
Edema / Ventricular gallop / Clammy skin
Treatment:
Identify and treat the underlying cause
Restrict sodium and water fluid intake
If severe, the oxygen therapy, morphine, intravenous diuretics, and mechanical ventilation
Edema:
An accumulation of an excessive amount of watery fluid in cells or intracellular tissues
Excessive accumulation of fluid in the interstitial space
May be: Localized (trauma/inflammation) / Generalized (whole body)
Third Spacing:
Loss of extracellular fluid from the vascular to other body components
Sometimes extracellular fluid becomes trapped in a space where it’s unable to be utilized or excreted, which is called third spacing.
Types
Ascites: Accumulation of serous fluid in the peritoneal cavity
Pleural effusion: Increased fluid in the pleural space, can cause shortness of breath by compression of the lung and/or increased intrathoracic pressure resulting in mediastinal shift and increased work of breathing.
Hyponatremia:
Deficit of sodium (serum sodium level < 135mEq/L)
Causes water to shift out of the extracellular spaces and into the cells
Causes of Hyponatremia:
Loss of sodium due to:
- Excessive diuresis
Diuretic therapy
Sodium-losing nephritis
- Excessive sweating, with nonsodium fluid replacement
- GI fluid loss
Vomiting / Diarrhea / Fistulas
- Adrenocorticoid insufficiency
Excess of water due to:
Excess oral fluids
Excess parenteral administration of dextrose and water solutions such as D5W
Syndrome of inappropriate Antidieuretic Hormone (SIADH)
Excessive IV administration
Other: Psychogenic polydipsia, Excessive administration of 5% dextrose water, frequent tap water enemas, sweating & drinking water
Hyponatremia
Manifestations:
Are due to water shifting into cells, especially brain cells.
Anorexia, nausea, vomiting
Muscle cramps / Depression / Lethargy
Weakness / Disorientation / Seizures
Orthostatic hypotension / agitation
* Apprehension / Headache / Personality Changes / Coma
Treatment:
Identify and treat cause
Restrict fluid intake (until normal sodium levels are reached)
Administer hypertonic 3% sodium chloride solution slowly with caution, and only in clinical areas where close monitoring can be maintained
Hypernatremia:
Excess of sodium (serum sodium level > 145 mEq/L)
Causes water to shift out of the cell into the extracellular fluid
Causes of Hypernatremia:
Intake of excessive sodium due to:
Rapid infusion of hypertonic saline, sodium bicarbonate, or isotonic saline
Drinking salt water
Ingesting large amounts of salt without increasing water intake
Loss of water due to:
Diarrhea / Diabetes insipidus
Increase in insensible loss / Decreased water intake
Unavailability of water / withholding water
Impaired thirst center
Other: Rapid infusion of 3% NaCl, Unconscious state, hypertonic tube feedings, trauma to thirst center
Hypernatremia:
Manifestations:
Are due to intracellular dehydration and intravascular volume depletion.
Thirst / Weak, rapid pulse / Irritability
Dry, sticky mucous membrane
Decreased blood pressure
Oliguria or anuria
Decreased reflexes / disorientation
Hallucinations
Treatment:
Administer hypotonic solution, such as 0.45 NaCl or 3% NaCl
Too rapid a shift can cause cerebral edema
If diabetes insipidus is the cause of hypernatremia, desmopressin or vasopressin may be ordered
Hypokalemia:
Serum potassium level < 3.5 mEq/L
Other causes:
Alcoholism
Alkalosis
Anorexia nervosa
Cushing syndrome
Diuretic agents
Hyperalimentation
Prolonged vomiting/diarrhea
Causes: metabolic alkalosis, loop diuretics, excessive steroid therapy, anorexia nervosa
Manifestations:
Are due to alterations in cardiovascular, skeletal, and gastrointestinal function;
Causes:
Apnea
Hypotonic bowel sounds
Muscle fatigue
Digitalis toxicity
ECG changes with hypokalemia:
Flattened T waves
Prolonged PR interval
Large U wave
Patient Care:
Identify underlying cause and treat it
Replacement therapy, either P.O or IV depending on severity
Foods High in Potassium:
Oranges / Bananas / Canteloupes / Prunes / Squash / Raisins / Dried Beans / Potatoes / Sweet Potatoes
Administer IV potassium with an IV pump
Check policy regarding rate of infusion
Hyperkalemia:
Serum potassium level > 5.0 mEq/L
Other Causes:
Acidosis (H+ into cell so K+ out of cell)
Burns
Crushing injuries
Hypoaldosteronism (primary adrenal insufficiency)
Rapid IV administration
Renal failure
Causes:
Rapid infusion of KCl, third-degree burn, anuria, acidosis
Manifestations of Hyperkalemia:
Are related to potassium’s influence on resting membrane potentials
Causes:
Abdominal pain
Tingling fingers
ECG changes with hyperkalemia:
Tall peaked T waves
Widening QRS complex
Ventricular fibrillation
Cardiac arrest
Patient Care:
Reduce intake of foods high in potassium
Stop potassium-sparing diuretics
Give kayexalate (sodium polystyrene sulfonate)
Administer 50% glucose with insulin IV
Hypochloremia:
Serum chloride level < 95 mEq/L
Causes of Hypochloremia:
Loss of hydrochloric acid from:
Excessive vomiting
GI suctioning
Clinical Manifestations:
Metabolic alkalosis
Hypertonicity of muscles
Depressed respiration
If severe, tetany
Patient Care:
Identify and treat the cause
Replacement therapy
Hyperchloremia:
Serum chloride level > 105 mEq/L
Causes of hyperchloremia:
Excessive ingestion
Decreased excretion by kidney
Clinical Manifestations:
Metabolic acidosis
Stupor
Deep, rapid respirations
Weakness
If severe, coma
Patient Care:
Treat metabolic acidosis
Sodium bicarbonate IV
Lactated Ringer’s solution
Hypophosphatemia:
Serum phosphate levels < 2.5 mg/dL
Causes of Hypophosphatemia
Alkalosis
Diabetic ketoacidosis
Hyperalimentation
Hyperparathyroidism
Phosphate-binding antacids (aluminum & calcium)
Clinical Manifestations:
Hemolysis
Platelet dysfunction
Parasthesia
Seizure
Treatment:
Identify and treat the underlying causes
Replacement therapy either PO or I, depending on severity
Hyperphosphatemia:
Serum phosphate level > 4.5 mg/dL
Causes of Hyperphosphatemia
Renal failure
Hypoparathyroidism
Chemotherapy
Large intake of calcium
Excessive use of phosphate laxatives or enemas
Clinical Manifestations:
Tetany
Hypotension
ECG with shortened QT interval
Treatment:
Identify and treat underlying causes
Restrict intake
Calcium-based phosphate binders
Hypomagnesemia:
Serum magnesium level: < 1.5 mg/dL
Selected Causes of Hypomagnesemia:
Diuretic therapy
SIADH
Small bowel bypass surgery
Hypercalcemia
Malnutrition
Diuretic therapy
Diabetic ketoacidosis
Treatment: replacement therapy
Hypermagnesemia:
Serum magnesium level: > 2.5 mg/dL
Selected Causes of Hypermagnesemia:
Decrease in renal excretion
Increase in intake (antacids, enemas, lax)
Traumatic soft tissue injury
ECG Changes:
Ventricular extrasystole
Prolonged PR interval
Widening of QRS complex
Tall T wave
Complete heart block
Cardiac arrest
Hypovolemic shock / tissue trauma / renal failure
Treatment:
Eliminate ingestion
Calcium
Sodium:
Normal serum rate = 135-145 mEq/L
Potassium:
Normal serum range is 3.5-5.0 mEq/L
Chloride
Normal serum range = 95-105 mEq/L
Calcium
Normal serum range = 8.5 - 10.5 mg/dL
Phosphorus
Normal serum range = 2.5 - 4.5 mg/dL
Magnesium
Normal serum range: 1.5 - 2.5 mg/dL
Hypocalcemia:
Serum calcium level < 8.6 mg/dL
Causes of Hypocalcemia:
Hypoparathyroidism
- surgical removal
- idiopathic
- thyroid cancers
Hyperphosphatemia
Malabsorption
Vitamin D deficiency
Excessive administration of citrated blood
Hypoalbuminemia
Clinical Manifestations:
Numbness, tingling of hands/toes/ around mouth
Weakness/Muscle cramping /Hypotension
Emotional instability
Hyperactive deep tendon reflexes
Chvostek sign (unilateral spasm)
Trousseau sign
Tetany / Seizures / Poor clotting
Decreased myocardial contractility
EKG with shortened GI interval
Treatment:
Oral replacement
- dietary supplement of calcium with vitamin D
IV calcium replacement
- calcium gluconate
- calcium chloride
Hypercalcemia:
Serum calcium level > 10.5 mg/dL
Selected causes for Hypercalcemia:
Hypophosphatemia
Certain cancers
Thyrotoxicosis
Acromegaly
Renal failure
Clinical Manifestations:
Anorexia, nausea, and vomiting
Constipation
Hypertonicity of the muscles
Increase in cardiac contractility
Decrease in heart rate
Renal calculus
EKG with wide T wave
Confusion
Treatment:
Identify and remove the cause, if possible
IV fluids with diuretic