OXYGENATION & FLUID/ELECTROLYTES

1.Recognize the assessment findings that would indicate oxygenation problems in a client in
all age groups
Nursing assessment, patient health history assessment, vitals, and labs

Physical assessment findings: Assess the patient nostrils, ask about deviated septum,
inspect the membranes of the nostrils, palpate the frontal and maxillary sinuses for
tenderness, then inspect the mouth and throat, asses for Clubbing of the fingers, and
cyanosis,

2.Identify the diagnostic tests and related nursing implications used to evaluate respiratory
function
ABG( arterial blood gas): arterial blood to determine the pressure exerted by oxygen and
carbon dioxide in the blood and blood pH. This test measures the adequacy of oxygenation,
ventilation, and perfusion. Normal results are:
● pH: 7.35–7.45
● PCO2: 35–45 mm Hg
● PO2: 80–100 mm Hg
● HCO3: 22–26 mEq/L
Pulmonary function test: Measures the gas exchange , flow rates, and airway resistance,
along with distribution of ventilation

Pulse oximetry, or SpO2, is a noninvasive method of continuously monitoring the oxygen

saturation of hemoglobin (SaO2). Although pulse oximetry does not replace blood gas
analysis, it is an effective tool to monitor for changes in SaO2 and can easily be used in the
home and various health care settings.

3. Describe the nursing management of clients receiving different modalities of oxygen

therapy, incentive spirometry, nebulizer treatments, and other forms of treatments to
improve oxygenation

Incentive spirometry is a method of deep breathing that provides visual feedback to encourage
the patient to inhale slowly and deeply to maximize lung inflation and prevent or reduce
atelectasis. The purpose of an incentive spirometer is to ensure that the volume of air inhaled is
increased gradually as the patient takes deeper and deeper breaths.
Incentive spirometers are available in two types: volume or flow. In the volume type, the tidal
volume is set using the manufacturer’s instructions. The patient takes a deep breath through the
mouthpiece, pauses at peak lung inflation, and then relaxes and exhales.
OXYGENATION & FLUID/ELECTROLYTES

4.Identify clients who are at risk for atelectasis and the nursing interventions related to its
prevention and management.
atelectasis: collapse or airless condition of the alveoli caused by hypoventilation,
obstruction to the airways, or compression
Incomplete lung expansion or the collapse of alveoli, known as atelectasis, prevents
pressure changes and the exchange of gas by diffusion in the lungs. Areas of the lung with
atelectasis cannot fulfill the function of respiration.

Patients at risk: Post operative, COPD, obstructions of the airway by foreign bodies,
mucus, airway constriction, external compression by tumors or enlarged blood vessels, and
immobility

S/S: increasing dyspnea (shortness of breath), cough, and sputum production.

Diagnostic test to find:A chest x-ray may suggest a diagnosis of atelectasis before clinical
symptoms appear; the x-ray may reveal patchy infiltrates or consolidated areas.

Nursing Prevention: frequent turning, early mobilization, and strategies to expand the
lungs and to manage secretions. Voluntary deep-breathing maneuvers (at least every 2
hours)

5.Describe the pathophysiology of the following disorders which affect oxygenation:

pneumonia, asthma, COPD

Pneumonia: Pneumonia affects both ventilation and diffusion. An inflammatory reaction

can occur in the alveoli, producing an exudate that interferes with the diffusion of oxygen
and carbon dioxide.

Asthma:This chronic inflammatory disease of the airways causes airway

hyperresponsiveness, mucosal edema, and mucus production. This inflammation ultimately
leads to recurrent episodes of asthma symptoms: cough, chest tightness, wheezing, and
dyspnea.The underlying pathology in asthma is reversible diffuse airway inflammation that
leads to long-term airway narrowing. This narrowing, which is exacerbated by various
changes in the airway, includes bronchoconstriction, airway edema, airway
hyperresponsiveness, and airway remodeling

COPD: Progressive pulmonary disease that causes chronic airflow obstruction. COPD
causes the aveoli sacs to lose their elasticity leading to air trapping
OXYGENATION & FLUID/ELECTROLYTES
6. Apply the nursing process in the care of clients with the following disorders which affect
oxygenation: pneumonia, asthma, COPD.
Pneumonia:
Nursing assessment is critical in detecting pneumonia. Fever, chills, or night sweats

NURSING DIAGNOSIS:Impaired airway clearance associated with copious tracheobronchial

secretions

The major goals:improved airway patency, increased activity, maintenance of proper fluid volume,
maintenance of adequate nutrition

Nursing interventions: Removing secretions is important because retained secretions interfere with
gas exchange and may slow recovery. The nurse encourages hydration (2 to 3 L/day), because
adequate hydration thins and loosens pulmonary secretions. Humidification may be used to loosen
secretions and improve ventilation.Maintaining adequate nutrition.

7.Discuss the medications used in the management of clients with oxygenation disorders
including albuterol, fluticasone, montelukast, salmeterol, prednisone, guaifenesin,
loratadine, and dextromethorphan.

Anatomic and Physiologic Overview

The respiratory system is composed of the upper and lower respiratory tracts. Together, the two
tracts are responsible for ventilation (movement of air in and out of the airways). The upper
respiratory tract, known as the upper airway, warms and filters inspired air so that the lower
respiratory tract (the lungs) can accomplish gas exchange or diffusion. Gas exchange involves
delivering oxygen to the tissues through the bloodstream and expelling waste gasses, such as
carbon dioxide, during expiration.

Upper airway structures consist of the nose; paranasal sinuses; pharynx, tonsils, and
adenoids; larynx; and trachea.

The larynx, or voice box, is a cartilaginous epithelium-lined organ that connects the pharynx and
the trachea

The pharynx functions as a passageway for the respiratory and digestive tracts.
OXYGENATION & FLUID/ELECTROLYTES
The trachea, or windpipe, is composed of smooth muscle with C-shaped rings of cartilage at
regular intervals.The trachea serves as the passage between the larynx and the right and left
main stem bronchi, which enter the lungs through an opening called the hilus.

The lower respiratory tract consists of the lungs, which contain the bronchial and
alveolar structures needed for gas exchange.

The lungs are paired elastic structures enclosed in the thoracic cage, which is an airtight
chamber with distensible walls. Each lung is divided into lobes. The right lung has upper,
middle, and lower lobes, whereas the left lung consists of upper and lower lobes.

Respiration is the gas exchange between air and blood between the blood and cells of the body

Ventilation is air in & out the airways; upper respiratory tract is for ventilation and the lower tract
is for diffusion

Perfusion carries oxygenated blood to all body tissues

LUNG VOLUMES:Lung function, which reflects the mechanics of ventilation, is viewed in terms
of lung volumes and lung capacities.
● Tidal volume: VT or TV :The volume of air inhaled and exhaled with each breath
● Inspiratory reserve volume :IRV :The maximum volume of air that can be inhaled after a normal inhalation
● Expiratory reserve volume: ERV :The maximum volume of air that can be exhaled forcibly after a normal exhalatio
● Residual volume:RV:The volume of air remaining in the lungs after a maximum exhalation
Lung Capacities
● Vital capacity:VC: The maximum volume of air exhaled from the point of maximum inspiration: VC = TV + IRV +
● Inspiratory capacity:IC:The maximum volume of air inhaled after normal expiration: IC = TV + IRV
● Functional residual capacity:FRC:The volume of air remaining in the lungs after a normal expiration: FRC = ERV
● Total lung capacity:TLC:The volume of air in the lungs after a maximum inspiration TLC = TV + IRV +ERV + RV
Ventilation and Perfusion Balance and Imbalance
● Adequate gas exchange depends on adequate ventilation–perfusion (V./Q.) ratio.
● Imbalanced V/Q ratio causes shunting of blood and results in hypoxia
● Severe hypoxia results when the amount of shunting exceeds 20%. Supplemental oxygen may eliminate hypoxia, d

Normal Ratio (A):In the healthy lung, a given amount of blood passes an alveolus and is
matched with an equal amount of gas (A). The ratio is 1:1 (ventilation matches perfusion).

Low Ventilation–Perfusion Ratio: Shunts (B)Low ventilation–perfusion states may be called

shunt-producing disorders. When perfusion exceeds ventilation, a shunt exists (B). Blood
bypasses the alveoli without gas exchange occurring. This is seen with obstruction of the distal
airways, such as with pneumonia, atelectasis, tumor, or a mucus plug.

Normal Breath sounds:

● Vesicular: Soft low pitched breezy/ rushing sound; heard on both inspiration and
expiration
OXYGENATION & FLUID/ELECTROLYTES
● Bronchovesicular: Medium pitched hollow; heard more on expiration
● Bronchial(Tracheal): High, loud & hollow tubular
Abnormal( Adventitious) Breath sounds:
● Fine Crackles( Rales): High pitched , crackling sounds (sounds like fire crackling)
Due to: Pulmonary edema, asthma, obstructive disease
● Coarse Crackles (Rales): Low pitched, wet bubbling sound
Due to: Pulmonary edema, Pneumonia, depressed cough reflex
● Wheezes: High pitched musical instrument wit more than one type of sound
quality
Due to: Asthma, bronchitis, chronic emphysema
● Pleural Friction Rub: Low pitched, harsh/ grating sounds
Due to: Pleuritis

Health Assessment:
Ask about past medical history( Previous problems and current symptoms)
Ask about cough, dyspnea , cough, sputum production, chest pain, wheezing, and hemoptysis

FLUIDS & ELECTROLYTES

1.Discuss the role of the kidneys, lungs and endocrine system in regulating the body’s fluids
Kidneys:
● Regulate extracellular fluid (ECF) volume and osmolality by selective retention and
excretion of body fluids
● Regulate electrolyte levels in the ECF by selective retention of needed substances and
excretion of unneeded substances
● Regulate pH of ECF by excretion or retention of hydrogen ions
● Excrete metabolic wastes and toxic substances

Lungs:
● Remove approximately 300 mL of water daily through exhalation (insensible water loss)
in the normal adult
● Eliminate about 13,000 mEq of hydrogen ions (H+) daily, as opposed to only 40–80 mEq
excreted daily by the kidneys
● Act promptly to correct metabolic acid–base disturbances; regulate H+ concentration
(pH) by controlling the level of carbon dioxide (CO2) in the extracellular fluid
Endocrine system:
● Hypothalamus the “ thirst center” secretes ADH
● Pituitary gland stores and releases antidiuretic hormone
● Adrenal glands secretes aldosterone
OXYGENATION & FLUID/ELECTROLYTES
Adrenal glands:
Regulate blood volume and sodium and potassium balance by secreting aldosterone, a
mineralocorticoid secreted by the adrenal cortex, causing sodium retention (and thus water
retention) and potassium loss.
Decreased secretion of aldosterone causes sodium and water loss and potassium retention.
Cortisol, another adrenocortical hormone, has only a fraction of the potency of aldosterone.
However, secretion of cortisol in large quantities can produce sodium and water retention and
potassium deficit.

Pituitary gland: Stores and releases the antidiuretic hormone (ADH) (manufactured in the
hypothalamus), which acts to allow the body to retain water. It acts chiefly to regulate sodium
and water intake and excretion
When blood volume is decreased, an increased secretion of ADH results in water conservation.
When blood volume is increased, a decreased secretion of ADH results in water loss.

Thyroid gland: Increases blood flow in the body by releasing thyroxine, leading to increased
renal circulation and resulting in increased glomerular filtration and urinary output.

2.Identify the effects of aging on fluid and electrolyte regulation

4.Describe complications of intravenous therapy and the measures used for preventing and
treating these complications.

5.Discuss the four regulatory mechanisms for pH control and how the regulatory
mechanisms can maintain acid base balance

Metabolic acidosis or non respiratory acidosis is a proportionate deficit of bicarbonate in

ECF. The deficit can occur as the result of an increase in acid components or an excessive
loss of bicarbonate. It can be produced by a gain of hydrogen ion or loss of bicarbonate.

Metabolic alkalosis or non respiratory alkalosis is associated with an excess of HCO3, a

decrease in H+ ions, or both, in the ECF. This may be the result of excessive acid losses or
increased base ingestion or retention.

Respiratory acidosis is a primary excess of carbonic acid in the ECF. It is produced by

inadequate excretion of CO2 with inadequate ventilation, resulting in elevated plasma CO2
and increased levels of carbonic acid. Any decrease in alveolar ventilation that results in
retention of carbon dioxide can cause respiratory acidosis
OXYGENATION & FLUID/ELECTROLYTES
Respiratory alkalosis is a primary deficit of carbonic acid in the ECF. It is the result of
alveolar hyperventilation, breathing that is faster and deeper, and the consequent increase
in the elimination of CO2. This loss of CO2 leads to a decrease in the carbonic acid level in
the plasma and an increase in the pH.

8.Apply the nursing process in the care of clients with acid base imbalance

NURSING INTERVENTIONS TO MEASURE A PATIENT FLUID INTAKE AND OUTPUT:

Daily weight
Physical assessment
Record intake & output

Sodium (Na+): chief electrolyte of ECF; normal serum concentration of sodium: 135–145
mEq/L
Regulates extracellular fluid volume; Na+ loss or gain accompanied by a loss or gain of water
Affects serum osmolality
Role in muscle contraction and transmission of nerve impulses
Regulation of acid–base balance as sodium bicarbonate

Potassium (K+): major cation of Controls intracellular osmolality

ICF; normal serum concentration
Regulator of cellular enzyme activity
of potassium: 3.5–5.0 mEq/L
Role in the transmission of electrical impulses in nerve,
heart, skeletal, intestinal, and lung tissue; Regulation of
acid–base balance by cellular exchange with H+

Calcium (Ca2+): most abundant electrolyte in the body; normal total serum calcium level:
8.6–10.2 mg/dL; normal ionized serum calcium level: 4.5–5.1 mg/dL:
Role in blood coagulation and in transmission of nerve impulses
Helps regulate muscle contraction and relaxation
Major component of bones and teeth

Magnesium (Mg2+): second most abundant ICF cation after potassium; normal serum
concentration of magnesium: 1.8-3.0 mEq/L:
Metabolism of carbohydrates and proteins
Role in neuromuscular function
Acts on cardiovascular system, producing vasodilation

Chloride (Cl–): major ECF anion; normal serum level of chloride: 97–107 mEq/L
Major component of interstitial and lymph fluid; gastric and pancreatic juices, sweat, bile, and
saliva
OXYGENATION & FLUID/ELECTROLYTES
Acts with sodium to maintain the osmotic pressure
Combines with hydrogen ions to produce hydrochloric acid

Bicarbonate (HCO3–): an anion that is the major chemical base buffer within the body;
found in both ECF and ICF; normal serum bicarbonate level: 25–29 mEq/L
Regulates acid–base balance

Phosphate (PO4–): major ICF anion; a buffer anion in both ICF and ECF; normal serum
phosphate level: 2.5–4.5 mg/dL
Role in acid–base balance as a hydrogen buffer
Promotes energy storage; carbohydrate, protein, and fat metabolism
Bone and teeth formation
Role in muscle and red blood cell function
Hypovolemia – Fluid Volume Deficit
Isotonic fluid loss – loss of both water and solutes in the same proportion from the ECF space
Occurs more rapidly when there is also decreased fluid intake

What clients become hypovolemic?

● Vomiting/Diarrhea, excessive GI suction, excessive sweating
● Decreased fluid intake
● Third space fluid shifts
● Diabetes insipidus
● Adrenal insufficiency
● Osmotic diuresis
● Hemorrhage
● Coma
Assessment and Clinical Manifestations of Hypovolemia
Table 10-4 in Hinkle
Acute weight loss
5% - pronounced
8% - severe
15% - life-threatening
Vital signs
Skin and mucous membranes will be dry
Eyes will be sunken in
Urine will concentrated
Capillary filling time be slow
Muscle cramps be prominent
Weakness and dizziness will occur when changing positions
Diagnostics and Lab Findings
BUN and creatinine
CBC
Hgb/Hct
Serum electrolyte changes
Urine specific gravity
OXYGENATION & FLUID/ELECTROLYTES
Colloids & Crystalloids
Colloids refers to IV fluids that have large molecules that don’t pass through semipermeable
membranes.
● Remain in the intravascular compartments and expand intravascular volume
● Volume/plasma expanders.
● Examples: albumin, dextrans, hydroxyethylstarches

Crystalloid solutions contain small molecules that flow easily across semipermeable membranes
● Allows for transfer from the bloodstream into the cells and body tissues
● Crystalloids are distinguished by their relative tonicity in comparison to plasma
Hypervolemia- Fluid Volume Excess
● Isotonic expansion of the ECF caused by the abnormal retention of water and sodium in
approximately the same proportions in which they normally exist in the ECF
● Secondary to an increase in the total body sodium content
What clients are hypervolemic?
Fluid overload or diminished homeostatic mechanisms
● Heart failure,
● kidney injury,
● cirrhosis of liver
Contributing factors: Consumption of excessive amounts of table salt or other sodium salts
Excessive administration of sodium-containing fluids
Assessment and Clinical Manifestations of Hypervolemia
● Acute weight gain
● VS
● Peripheral edema & ascites
Edema occurs when there is a change in the capillary membrane, increasing the formation of
interstitial fluid or decreasing the removal of interstitial fluid
● Na retention is a frequent cause
Some medications may cause edema
– NSAIDs, estrogens, corticosteroids, and antihypertensive agents
● Distended neck veins
● Crackles
● Urine output
Diagnostic and Lab Findings
● BUN and creatinine
● CBC
● Hgb/Hct
● Serum and urine osmolality
● Urine specific gravity
● Chest X-ray
Nursing Management of Hypervolemia
● I&O and daily weights; assess lung sounds, edema, other symptoms
● Monitor responses to medications—diuretics and parenteral fluids
1) Thiazide diuretics – hydrochlorothiazide (Microzide)
2) Loop diuretics – furosemide (Lasix)
3) Potassium-sparing diuretics – spironolactone (Aldactone)

● Monitor lung sounds and edema

Additional interventions to manage edema include: elevating the extremity, antiembolism
OXYGENATION & FLUID/ELECTROLYTES
stockings, or paracentesis

● Promote adherence to fluid restrictions, patient teaching related to sodium and fluid
restrictions
● Monitor, avoid sources of excessive sodium, including medications and water
● Nutrition counseling
● Promote rest
● Positioning and repositioning
● If renal function is severely impaired, dialysis may be required
Hyponatremia – Na+ <135 mEq/L
Hypo: “under”- Na: Sodium - Emia: Blood
● Acute
Result of fluid overload of a surgical patient
● Chronic: Seen outside of hospital setting, longer duration, less serious neurologic
sequelae
● Exercise associated
More common in women of small stature, extreme temperatures, excessive
fluid intake, prolonged exercise
Causes: Imbalance of water, losses by vomiting, diarrhea,
sweating, diuretics, adrenal insufficiency, certain medications,
syndrome of inappropriate secretion of antidiuretic hormone
(SIADH)
Assessment and Clinical Manifestations
● Poor skin turgor
● Dry mucosa
● Headache
● Decreased salivation
● Blood pressure
● Nausea
● Abdominal cramping
● Neurologic changes
● Altered mental status (lethargy,confusion)
● Muscle twitching
● Focal weakness
● Hemiparesis
● Seizures - Status epilepticus
● Coma
Nursing Management of Hyponatremia
Administer sodium replacement
● 0.9% NaCl or LR (isotonic solutions) if mild
● 3% saline (hypertonic solution) if hyponatremia is severe
Ensure water restriction
Preferred to administering saline if the primary problem is fluid retention
Medications
Assessment
OXYGENATION & FLUID/ELECTROLYTES
● -I&O, daily weight, lab values, CNS changes
● Encourage dietary sodium (broth, tomato juice, processed foods)
● Effects of medications (diuretics, lithium)
Hypernatremia - Na+ >145 mEq/L
Hyper: “excess”- Na: Sodium -Emia: Blood
● Occurs in patients with normal fluid volume, FVD, FVE
● Most affected are very old, very young, and cognitively impaired
● Causes: fluid deprivation (poor thirst response), excess sodium administration,
hypertonic enteral feeds without appropriate free water, diabetes insipidus, heat
stroke,hypertonic IV solutions
Assessment and Clinical Manifestations of Hypernatremia
F: Fever(low grade), flushed skin
R:Restlessness(irritable)
I: Increased fluid retention
E: Edema
D: Decrease urine output, dry mouth
Nursing Management of Hypernatremia
● Gradual lowering of serum sodium level via infusion of hypotonic or isotonic non-saline
electrolyte solution
0.3%NaCl
D5W
● Diuretics
● Assessment for abnormal loss of water and low water intake

● Assess for over-the-counter sources of sodium

○ Alka-Seltzer
● Monitor for CNS changes
Hypokalemia – K+<3.5 mEq/L
Hypo: “under”- Kal: Potassium - Emia: Blood
Causes: GI losses – diarrhea, vomiting, GI suctioning, recent ileostomy
Medications – corticosteroids, amphotericin B,digoxin,Diuretics,carbenicillin
● Tumor of the intestine
● Alkalosis
● Poor dietary intake – starvation, anorexia, bulimia
● Hyperaldosteronism (primary and secondary)
● Insulin hypersecretion
Assessment and Clinical Manifestations of Hypokalemia
ECG changes (ischemia):Flat T wave, inverted T wave,depressed ST segment, elevated Uwave
● Dysrhythmias
● Dilute urine
● Excessive thirst
● Fatigue
● Anorexia
● Muscle weakness
● Decreased bowel motility or ileus
● Paresthesias
● Hypoactive reflexes
OXYGENATION & FLUID/ELECTROLYTES
● Hypotension
● Severe hypokalemia can
● cause death through cardiac or respiratory arrest
Nursing Management of Hypokalemia
Potassium replacement: Increased dietary potassium or IV for severe deficit (<2 mEq/L)
Hypokalemia is LIFE THREATENING and assessment is KEY!
● Monitor I/O
● Monitor ECG for changes
● Monitor ABGs
● Monitor patients receiving digitalis for toxicity
● Monitor for early signs and symptoms
● Monitor Mg level as well
● Treat the underlying cause
● Administer IV potassium only after adequate urine output has been established
● Monitor BUN and creatinine
NEVER push K+
or give it IM/SQ
Use a pump
Hyperkalemia - K+ >5.5 mEq/L
● Seldom occurs in patients with normal renal function
● Increased risk in older adults
● Cardiac arrest is frequently associated
Causes
● Impaired renal function
● Rapid administration of potassium
● Hypoaldosteronism (Addison’sDisease)
● Medications – heparin, B-blockers, potassium sparing diuretics, ACE-inhibitors, NSAIDs,
cyclosporine,tacrolimus
● Tissue trauma, tumor lysis syndrome,Acidosis
Assessment and Clinical Manifestations of Hyperkalemia
● Cardiac changes and dysrhythmias
○ Peaked, narrow T-waves; ST-segment depression, shortened QT interval
○ PR interval becomes prolonged, followed by disappearance of P wave,
decomposition and widening of theQRS complex = ventricular dysrhythmias and
cardiac arrest
● Muscle weakness
● Paresthesias
● Anxiety
● GI manifestations
Nursing Management of Hyperkalemia
● Monitor ECG, assess labs, monitor I&O, obtain apical pulse
● Limitation of dietary potassium and dietary teaching
● Administration of cation exchange resins(Kayexalate)
● Emergent care: IV calcium gluconate, IV sodium bicarbonate, IV regular insulin and
hypertonic dextrose IV, beta-2 agonists, dialysis
● Administer IV slowly and with an infusion pump
Hypocalcemia – Ca2+< 8.6 mEq/L
Causes:
OXYGENATION & FLUID/ELECTROLYTES
● Hypoparathyroidism
Most often surgical
● Malabsorption
● Osteoporosis
● Pancreatitis
● Alkalosis
● Transfusion of citrated blood
● Kidney injury
● Medications
● Aluminum-containing antacids, aminoglycosides, steroids,diuretics, PPIs
● Hyperphosphatemia
● Magnesium deficiency
Assessment and Clinical Manifestations of Hypocalcemia
● Tetany
● Circumoral numbness
● Paresthesias
● Hyperactive DTRs
● Trousseau sign
● Chvostek sign
● Seizures
● Respiratory symptoms of dyspnea and laryngospasm
● Abnormal clotting
● Anxiety
● Cardiac changes
○ Prolonged QT interval
○ (prolonged ST segment),
○ torsades de pointe
● Alkalosis
Nursing Management of Hypocalcemia
IV of calcium gluconate for emergency situations
Ensure dilution in D5W and give slowly using a pump
● Seizure precautions
● Monitor airway
● Oral calcium and vitamin D supplements
● Exercises to decrease bone calcium loss
● Patient teaching related to diet and medications
○ Alcohol, caffeine
○ Phosphorus containing antacids

Hypercalcemia - Ca2+> 10.2 mEq/L

Hypercalcemia crisis has high mortality
50% mortality when not treated properly
Causes
● Malignancy and hyperparathyroidism
OXYGENATION & FLUID/ELECTROLYTES
● Bone loss related to immobility
● Mostly after severe or multiple fractures or spinal cord injury
● Medications – thiazide diuretics, vitamin A and D, lithium
Assessment and Clinical Manifestations of Hypercalcemia
● Polyuria
● Thirst
● Muscle weakness
● Intractable nausea
● Abdominal cramps
● Severe constipation
● Diarrhea
● Peptic ulcer
● Bone pain
● ECG changes
● Short QT and ST segment
● Dysrhythmias – heart block
Nursing Management of Hypercalcemia
● Treat underlying cause
● Administer IV fluids, furosemide, phosphates,
● calcitonin, bisphosphonates
● Increase mobility
● Encourage fluids containing sodium
● Dietary teaching, fiber for constipation
● Ensure safety
● Monitor cardiac rate and rhythm
Hypomagnesemia – Mg2+ < 1.3 mg/dL
● Associated with hypokalemia and hypocalcemia
● Like Ca2+, take into account albumin levels
● Causes
○ Alcoholism
○ GI losses – NG suction, diarrhea, fistulas
○ Enteral or parenteral feeding deficient in magnesium
○ Medications – aminoglycosides, cyclosporine, diuretics,
digoxin, cisplatin, amphotericin
○ Rapid administration of citrated blood
○ Diabetic ketoacidosis
Assessment and Clinical Manifestations of Hypomagnesemia
● Chvostek and Trousseau signs
○ Remember accompanying hypocalcemia
● Marked changes in psych status
○ Apathy, depressed mood, hallucinations, psychosis, ataxia, dizziness,confusion
○ Neuromuscular irritability
● Muscle weakness
○ Dysphagia
● Tremors
OXYGENATION & FLUID/ELECTROLYTES
● ECG changes and dysrhythmias
○ Prolonged the QRS , depressed, ST
○ PVC’s, SVT, Torsades, V-fib
Nursing Management of Hypomagnesemia
Magnesium sulfate IV is administered with an infusion pump, monitor vital signs and urine output
● Given too rapidly can cause heart block and asystole
● Oral magnesium
● Monitor for dysphagia
● Seizure precautions
● Dietary teaching
Hypermagnesemia - Mg2+> 3 mg/dL
Rare electrolyte abnormality, because the kidneys efficiently excrete magnesium
● Causes
● Kidney injury (most common)
● Diabetic ketoacidosis
● Excessive administration of magnesium
○ Used to treat HTN in pregnancy
○ Magnesium based antacids (Maalox, Milk of Magnesia)
● Extensive soft tissue injury
● Can appear falsely elevated if sample hemolyzed
Assessment and Clinical Manifestations of Hypermagnesemia
● Hypoactive reflexes
● Drowsiness
● Muscle weakness
● Hypotension
● Bradycardia
● Depressed respirations
● ECG changes
○ Prolonged PR interval, tall T-waves, wide QRS, prolonged QT
● Dysrhythmias
○ AV blocks
● Cardiac arrest
Nursing Management of Hypermagnesemia
● IV calcium gluconate
● Hemodialysis
● Administration of loop diuretics, sodium chloride, and LR
● Avoid medications containing magnesium
● Patient teaching regarding magnesium-containing over-the-counter medications
● Observe for DTRs and changes in LOC

Hypochloremia – Cl -< 97 mEq/L

● Causes: Addison disease, reduced chloride intake, GI loss, diabetic
ketoacidosis, excessive sweating, fever, burns, medications, metabolic alkalosis
OXYGENATION & FLUID/ELECTROLYTES
● Loss of chloride occurs with loss of other electrolytes, potassium, sodium
● Manifestations: agitation, irritability, weakness, hyperexcitability of muscles, dysrhythmias, seizures, com
● Medical management: replace chloride-IV NS or 0.45% NS
Nursing management
Assessment
● Avoid free water
● Encourage high-chloride foods – tomato juice, bananas, dates, eggs, cheese, milk, salty broth,
canned vegetables, and processed meats
● Patient teaching related to high-chloride foods
Hyperchloremia - Cl--> 107 mEq/L
Causes: excess sodium chloride infusions with water loss,head injury, hypernatremia, dehydration, severe diarrhe

Clinical manifestations are the same as metabolic acidosis:

● Tachypnea; lethargy; weakness; rapid, deep respirations;hypertension; cognitive changes
● Accompanied by high Na+ and fluid retention
Medical management: restore electrolyte and fluid balance, LR, sodium bicarbonate, diuretics
Nursing management: assessment, patient teaching related to diet and hydration
Maintaining Acid–Base Balance
● Normal plasma pH 7.35 to 7.45
Measures hydrogen ion concentration and acidity or alkalinity of the blood
● Major extracellular fluid buffer system; bicarbonate–carbonic acid buffer system
● Kidneys regulate bicarbonate in ECF
Renal compensation is relatively slow(hours and days)
● Lungs, under control of medulla,regulate CO2, and thus the carbonic acid in ECF
Acid-Base Imbalances
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis

Metabolic Acidosis
● Low pH <7.35
● Low bicarbonate <22 mEq/L
● Most commonly due to kidney injury
● Correct underlying problem, correct imbalance
○ Bicarbonate may be administered
Anion gap
Looks at the difference between cations and anions and is used to determine what causes the metabolic
acidosis
Normal anion gap acidosis:
direct losses of bicarbonate like diarrhea, diuretics, lower intestinal fistulas
● Normal anion gap acidosis:direct losses of bicarbonate like diarrhea, diuretics, lower
intestinal fistulas
OXYGENATION & FLUID/ELECTROLYTES
● High anion gap acidosis:excessive accumulation of fixed acid–DKA, lactic acidosis, late
phase salicylate poisoning, uremia,methanol or ethylene glycol toxicity
Assessment and Clinical Manifestations of Metabolic Acidosis
● Headache
● Confusion
● Drowsiness
● Increased respiratory
● rate and depth
● Decreased blood pressure
● Decreased cardiac output
● R/t hyperkalemia
● Dysrhythmias
● Shock
● If decrease is slow, patient may be asymptomatic until bicarbonate is 15 mEq/L or less
Managing Metabolic Acidosis
● Frequent respiratory assessments
● Monitor potassium levels
With acidosis, hyperkalemia may occur as potassium shifts out of cell
● As acidosis is corrected, potassium shifts back into cell, potassium levels
decrease
● Serum calcium levels may be low with chronic metabolic acidosis
■ Must be corrected before treating acidosis
If the cause is renal failure:
● Strict I/O
● Monitor electrolytes
● Dialysis
Metabolic Alkalosis
● High pH >7.45
● High bicarbonate >26 mEq/L
● Most commonly due to vomiting or gastric suction
○ May also be due to medications, especially long-term diuretic use
● Hypokalemia will produce alkalosis
○ Kidneys conserve K+ and therefore excrete more H+
○ Cellular K+ moves into the ECF to try and maintain near- normal serum levels (as
K+moves out of the cell, H+moves in)
Assessment and Clinical Manifestations of Metabolic Alkalosis
● Symptoms related to decreased calcium
● Respiratory depression
● Tachycardia
● Symptoms of hypokalemia
Managing Metabolic Alkalosis
● Correct underlying disorder
● Supply chloride to allow excretion of excess bicarbonate
● Restore fluid volume with sodium chloride solutions
OXYGENATION & FLUID/ELECTROLYTES
● Administer carbonic anhydrase inhibitor (Diamox) in patients who can’t tolerate rapid
fluid volume expansion
○ Reduces the reabsorption of bicarbonate
Respiratory Acidosis
Low pH <7.35
PaCO2 >42 mm Hg
Always due to respiratory problem with inadequate excretion of CO2
With chronic respiratory acidosis, body may compensate, may be asymptomatic
Respiratory center becomes insensitive to CO2 as a respiratory stimulant and starts to depend
on hypoxemia as the major drive for breathing
Assessment and Clinical Manifestations of Respiratory Acidosis
● Rapid shallow respiration
● Hypoventilation -> hypoxia
● Headache
● Hyperkalemia
● Dysrhythmias
● Drowsiness, dizziness, disorientation
● Muscle weakness, hyperreflexia
Managing Respiratory Acidosis
● Potential increased intracranial pressure
● Treatment aimed at improving ventilation
● Place the patient in semi-Fowler’s
● Use extreme caution with O2 administration in chronic respiratory acidosis
● Carbon dioxide narcosis
Respiratory Alkalosis
● High pH >7.45 PaCO2 <35 mm Hg
● Always due to hyperventilation
● Manifestations: lightheadedness, inability to concentrate, numbness and tingling,
sometimes loss of consciousness
● Correct cause of hyperventilation
Assessment and Clinical Manifestations of Respiratory Alkalosis
● Seizures
● Deep, rapid breathing
● Hyperventilation
● Tachycardia
● Low or normal BP
● Hypokalemia
● Numbness & Tingling of extremities
● Lethargy & confusion
● Lightheadedness
● Nausea & Vomiting
Arterial Blood Gasses
OXYGENATION & FLUID/ELECTROLYTES
pH:7.35– (7.4)–7.45
PaCo2:(carbon dioxide)35– (40)–45 mm Hg
HCO3(Bicarbonate):-22– (24)–26 mEq/L
Assumed average values for ABG interpretation
PaO280–100 mm Hg
Oxygen saturation >94%
Base excess/deficit ±2 mEq/L

Partial pressure of carbon