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384 Focus exam 1
Fluid and electrolyte imbalances (Na+, Calcium, K+, Magnesium)
Sodium (Na) 135-145 *BRAIN/ Neurological*
Imbalances typically associated with parallel changes in osmolality. Plays a major role in: Extracellular fluid
(ECF) volume and concentration, generation and transmission of nerve impulses, muscle contractility & acid
base balance
HYPONATREMIA
-Loss of sodium containing fluids or from water excess
Causes: loss of sodium rich blood from draining wounds, diarrhea, vomiting, primary adrenal insufficiency,
inappropriate use of sodium free or hypotonic IV fluids, giving fluids to patient w/ renal failure, SIADH
Manifestations:
Mild: headache, irritability, difficulty concentrating
Severe: confusion, vomiting, seizures, coma
Risk for: Electrolyte imbalance, injury, acute confusion
Potential complication: Severe neurologic changes
Nursing Implementation:
Cause is water excess: Fluid restriction, loop diuretics à
Severe symptom (seizures) give small amount of IV
hypertonic saline solution (3% NaCl)
Cause is abnormal fluid loss: fluid replacement with sodium
containing solution, increase oral intake, withhold diuretics, drugs that block vasopressin (ADH) à Convaptan
(Vaprisol): given for water excess & Tolvaptan (Samsca): given for hyponatremia from heart failure or
SIADH
-Sodium serum should not increase more than 6-12 mEq/L per hour in 24 hours à can cause osmotic
demyelination syndrome w/ permanent damage to nerve cells in the brain
-Accurate urine output is essential
-Initiate seizure precautions
HYPERNATREMIA
-Inadequate water intake, excessive water loss or sodium gain
-Causes hyperosmolality leading to cellular dehydration
-Primary protection is thirst from hypothalamus
Causes: Diabetes insipidus, IV administration of hypertonic
saline or sodium bicarbonate, sodium containing drugs,
excessive sodium intake
Manifestations: Thirst, AMS (agitation, delirium,
restlessness, confusion, lethargy), weakness, tetany, (High
temp, BP, ADH & Aldosterone)
Risk for: Electrolyte imbalance, fluid volume deficit & injury
Potential complication: Seizures and coma
Nursing Implementation: Treat underlying cause à
Cause is water deficit- replace fluid orally or IV with isotonic
or hypotonic fluids.
Cause is excess sodium- dilute with sodium free IV fluids (such as 5% dextrose in water) and promote
excretion with diuretics
-Initiate seizure precautions & restrict sodium
- Sodium serum shouldn’t decrease more than 8-15 mEq/L in an 8 hr period à can cause rapid shift of water
into cells causing cerebral edema and neurological complications
1
Potassium (K) (3.5-5) *Cardiac)
Major intracellular fluid (ICF) cation & regulated by kidneys. Necessary for transmission and conduction of
nerve and muscle impulses, cellular growth, maintenance of cardiac rhythms, acid-base balance
Sources: Fruits & veggies (bananas & oranges), salt substitutes, potassium medications & stored blood
HYPOKALEMIA
Causes: Increased loss of potassium via the kidneys or gastrointestinal tract (laxative misuse, vomiting,
diarrhea, ileostomy drainage), increased shift of K+
from ECF to ICF, dietary K+ deficiency (rare)
Manifestations: Cardiac (weak irregular pulse,
arrythmias, ST depression, flattened T wave, prominent
U wave), skeletal muscle weakness (legs), weakness of
respiratory muscles, decreased GI motility,
hyperglycemia, low tendon reflexes, fatigue & lethargy
Risk For: electrolyte imbalance, activity intolerance,
injury
Potential complication: Dysrhythmias (heart block &
lethal ventricular dysrhythmias)
Nursing Implementation: KCl supplements orally or
IV (always dilute IV KCl, NEVER give KCl via IV
push or as a bolus, should not exceed 10 mEq/hr, use an infusion pump), consume potassium rich foods
(fruits & veggies, bran, chocolate, peanut butter, milk, yogurt nuts and seeds)
-Severe hypokalemia can cause paralysis
HYPERKALEMIA
Causes: impaired renal excretion, massive intake shift from ICF to ECF (includes acidosis, or massive cell
destruction such as burns or severe infection)
-Digoxin like drugs and b adrenergic blockers can impair entry of potassium into cells resulting in high ECF
potassium concentrations
-NSAIDS, potassium sparing diuretics, angiotensin II receptor blockers and ACE inhibitors can cause
hyperkalemia by reducing kidneys ability to excrete
calcium
à Most common cause: Renal failure
Manifestations: Cardiac dysrhythmias (bradycardia,
peaked T wave, widened QRS, prolonged pr
interval, elevated ST segment), cramping leg pain,
weak or paralyzed skeletal muscles, abdominal
cramping, Increased GI motility (diarrhea),
paresthesia (pins & needles)
Risk for: Electrolyte imbalance, activity intolerance,
injury
Potential complication: Dysrhythmias (heart block,
ventricular fibrillation (Vfib), or cardiac standstill
Nursing Implementation: Eliminate oral and parenteral K intake & Increase elimination of K (diuretics,
dialysis, kayexalate). Force potassium from ECF to ICF by IV insulin and a b- adrenergic agonist or sodium
bicarbonate. Stabilize cardiac membranes by administering IV calcium chloride or calcium gluconate.
-Use continuous ECG monitoring (those with dangerous dysrhythmias à give IV calcium immediately &
monitor BP, giving rapid calcium can result in hypotension)
-Monitor for hypoglycemia when giving insulin and give glucose as needed
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Calcium (Ca) 8.5-10.5 *Muscles*
Functions: Formation of teeth and bones, blood clotting, transmission of nerve impulses, myocardial
contractions, muscle contractions. Obtained from ingested foods & need vitamin D to absorb. Present in 3
forms: ionized calcium is biologically active. Changes in pH and serum albumin affect levels.
Balance controlled by: parathyroid & calcitonin
HYPOCALCEMIA
Causes: Low levels caused by decreased production of PTH, multiple
blood transfusions, alkalosis, increased calcium loss
Manifestations: Positive Trousseau’s (carpal spasm from BP cuff
being inflated) or Chvostek’s (facial muscle contraction when tapping
Infront of ear) sign, laryngeal stridor, dysphagia, tingling or numbness
around the mouth or in the extremities, cardiac dysrhythmia, tetany,
hyperactive reflexes
Risk for: Electrolyte imbalance, ineffective breathing pattern, acute
pain, injury
Potential complication: fracture, respiratory arrest
Nursing Implementation: Treat cause à oral or IV
calcium supplements, rebreathe into paper bag, treat
pain and anxiety to prevent hyperventilation-induced
respiratory alkalosis
-Closely assess patient who had thyroid or neck surgery for
manifestations of hypocalcemia due to proximity of surgery to the
parathyroid glands
HYPERCALCEMIA
Causes: Hyperparathyroidism (two thirds of cases) & Cancer malignancy
Manifestations: Fatigue, lethargy, weakness,
confusion, hallucinations, seizures, coma, cardiac
dysrhythmias, bone pain, fractures, nephrolithiasis,
polyuria, dehydration, low muscle tone, low reflexes,
stupor, N/V
Risk for: Electrolyte imbalance, inactivity intolerance,
injury
Potential complication: Dysrhythmias à Heart block
and ventricular tachycardia (Vtach)
Nursing Implementation: Excretion of calcium w/
loop diuretic, hydration with isotonic saline infusion,
low calcium diet, mobilization, bisphosphonates (gold
standard treatment when caused by cancer), IM or SC
calcitonin
-Excess calcium acts like a sedative leading to reduced excitability of muscles and nerves
-Must drink 3000-4000mL fluid daily to prevent kidney stone formation (cranberry and prune juice will also
help prevent stone formation)
-Receive calcitonin injection for immediate effect à can result in tachycardia
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Magnesium (1.3-2.1) *Muscles/ neurological*
Coenzyme in metabolism of carbohydrates. Required for DNA and protein synthesis, blood glucose control,
BP regulation & necessary for ATP production. Acts directly on myoneural junction, important for normal
cardiac function, 50-60% contained in bone, absorbed in GI tract & excreted by kidneys.
HYPOMAGNESEMIA
Causes: Prolonged fasting or starvation, chronic alcoholism, fluid loss from GI tract, prolonged parenteral
nutrition without supplementation, diuretics,
hyperglycemic osmotic diuresis, chronic alcohol
use
Manifestations: Hyperactive deep tendon reflexes,
muscle cramps, tremors, seizures, dysrhythmias,
tachycardia, corresponding hypocalcemia &
hypokalemia, Positive Trousseau’s (carpal spasm
from BP cuff being inflated) or Chvostek’s (facial
muscle contraction when taping Infront of ear)
sign, dysphagia, N/V
Management: Treat underlying cause, oral
supplements, increase dietary intake, parenteral IV
or IM magnesium when severe
-Diuretics, proton-pump inhibitors & certain
antibiotics can lead to magnesium loss
-If deficiency is severe or if hypocalcemia is present IV magnesium (mag sulfate) is given à use infusion
pump and watch monitor since rapid administration can lead to hypotension and cardias or respiratory arrest
HYPERMAGNESEMIA
Causes: Increased intake or ingestion of products containing magnesium when renal insufficiency or failure
is present & Excess IV magnesium
administration
Manifestations: Lethargy, N/V, impaired
reflexes, muscle paralysis, bradycardia, low
BP, respiratory and cardiac arrest
Management: Prevention first à restrict
magnesium intake in high risk patients. IV
CaCl or calcium gluconate if symptomatic.
Fluids and IV furosemide to promote urinary
excretion & dialysis.
-Can develop in a pregnant woman taking
magnesium sulfate for treatment of eclampsia
-Avoid magnesium containing foods (green
veggies, nuts, bananas, oranges, peanut butter,
chocolate)
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What causes edema? Best objective way to assess fluid balance?
•
•
•
Edema occurs if venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic
pressure rises. May also develop if an obstruction of lymphatic outflow causes a decrease in the removal of
interstitial fluid
o Plasma to interstitial fluid shift results in edema
o Interstitial fluid drawn into plasma decreases edema
Fluid spacing: distribution of body water
o First spacing: normal distribution of fluid in ICF & ECF
o Second spacing: abnormal accumulation of fluid (edema)
o Third spacing: fluid collects in nonfunctional area of cells,
(fluid is trapped where it is difficult or impossible for it to
move back into cells or blood vessels)
Assess fluid balance:
o Daily weights
o Intake (Proper fluid balance is intake of 2000-3000mL)
o Output (urine specific gravity: Greater than 1.025 =
concentrated & less than 1.010 = dilute)
o Assess Skin turgor à à à à à à à à à
o Labs
§ Fluid volume deficit = increased BUN, sodium,
hematocrit, plasma & urine osmolality
§ Fluid volume excess= decreased BUN, sodium, hematocrit, plasma & urine osmolality
When to use a hypertonic, hypotonic or isotonic solution
Hypotonic
•
•
More water than electrolytes
Pure water lyses RBCs
o Water moves from ECF to ICF by osmosis
o Usually maintenance fluids
o Monitor for changes in mentation
à Treats hypernatremia & good maintenance fluid
Isotonic
•
•
•
Expands only ECF
No net loss or gain from ICF
Ideal to replace ECF volume deficit
àIdeal fluid replacement for patient with ECF
volume deficits, surgery, burns, or GI fluid losses
Hypertonic
•
•
Initially expands and raises the osmolality of
ECF
Require frequent monitoring of: Blood
pressure, lung sounds & serum sodium levels
à Ideal for hyponatremia and trauma patients with
head injury
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ABG interpretation & assessment findings
Practice:
Respiratory alkalosis-Hyperventilation
-Cause: hypoxemia from acute pulmonary
disorders (pneumonia, pulmonary embolus)
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Respiratory acidosis-Hypoventilation
Metabolic acidosis- Acid other than
carbonic acid accumulates in the body or
when bicarbonate is lost in body fluids
Metabolic alkalosis- Loss of acid or gain in
HCO3 occurs
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Anemia
Decreased RBCs
• Lack of B12, B9, FeSo4
Blood loss
• Ulcer, trauma
RBC destruction
• Sickle cell, incompatible blood
à Can lead to tissue hypoxia
Mild = Hgb 10-12 g/dl (may not have symptoms)
Moderate = Hgb 6-10 g/dl (increase in
cardiopulmonary symptoms)
Severe = Hgb <6 g/dl (many manifestations
involving multiple systems)
à Labs:
HGB- (hemoglobin)Amount of oxygen carrying
molecule in blood
o Male: 14-18
o Female: 12-16
HCT- (hematocrit) Percent of RBC in blood
o Male: 40-50%
o Female: 36-44%
MCV- (mean corpuscular volume): Measures the
relative size of RBCS
o 80-100fl
CBC (complete blood count) to Diagnose
à Check RBC & HGB to evaluate therapy
response
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Normocytic Anemia
à 80-100fl Normal
Usual causes:
-Sudden blood loss
-Prosthetic heart valves
-Tumor
-Long term disease
-Decreased erythropoietin caused
by renal failure
-Blood loss can also be normocytic
-Sickle cell disease
Microcytic Anemia
à < 80fl Decreased
Usual causes:
-Iron deficiency
o Chronic blood loss
-Lead poisoning
-Thalassemia
-Inflammation
Macrocytic Anemia
à > 100fl Increased
Usual causes:
-Chemotherapy
-Folate deficiency
-Cobalamin (Vit B12) deficiency
-Alcoholism
How to take orthostatic vital signs:
1. Have patient lie flat for 5
minutes.
2. Take heartrate and BP
3. Sit them up and wait 1-3 minutes
4. Take heartrate and BP
5. Stand them up and wait 1-3
minutes
6. Take heartrate and BP
If systolic drops by 20/ diastolic drops by 10/ If HR increases by 20 / If patient dizzy when stands
= Orthostatic vital signs
TIBC – Total iron binding
capacity
• Measures proteins (i.e.,
transferrin) that bind or
transport iron between
bone marrow to tissues
• Increased in iron
deficiency, decreased in
chronic dz (how much iron
is in blood stream)
Transferrin Saturation
• Measures amount of iron
ready to use for
erythropoiesis
• Ferritin is a carrier protein
which transports iron in
circulation
• Decreased in iron
deficiency, normal or
decreased in chronic
disease (total iron stores in
body)
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Ferritin
• Correlates with normal
body iron stores (1 mg/ml
of ferritin = 8-10 mg of
stored iron)
• Ferritin is present I liver,
spleen, bone marrow,
brain, kidneys, etc. It is the
storage form of iron.
• Decreased in iron
deficiency, normal in
chronic disease (binds and
transports iron in blood
stream)
Nursing Interventions:
• Assess high risk patients
• Assess for improving or worsening symptoms
• Administer blood products – watch for reactions
• Monitor lab values and vital signs
• Oxygen therapy to stabilize patient
• Keep environment safe - monitor for falls, burns, paresthesia
• Patient education (increase folic acid and iron containing foods, stop drinking, medications)
• Iron therapy
• Medications such as erythropoietin (EPO) & vitamin supplements
• Alternate periods of rest with activity (Especially after meals to decrease competition for supply to vital
functions)
• Aid with regular physical activities
• Treat the cause
Iron Deficiency Anemia
à Most common nutritional disorder in the world (Inadequate diet intake, malabsorption, blood loss, or
hemolysis)
Drug Therapy:
à Oral ferrous sulfate or ferrous gluconate (can stain teeth
use straw & sit upright 30 min after taking)
à IM or IV iron dextran, sodium ferrous gluconate, iron
sucrose
à Transfusion of RBCS
Oral iron is a good option but consider these factors:
• Enteric coated or sustained release tablets are
counterproductive and expensive
• Daily dose should be 150-200mg (can be taken in 3-4
doses)
• Iron best absorbed in an acidic environment (take an
hour before meals)
• Take with vitamin C enhances absorption
Blood Transfusions
1.
2.
3.
4.
Consent signed
Two licensed RNs must identify patient
Vitals signs before for baseline
***Remain with the patient during the first 15
minutes or 50 ml of infusion, then retake vital
signs
5. Give between 2-4 hours in most patients
6. Observe for reactions: hemolytic (due to ABO
incompatibly), febrile, allergic, circulatory
overload, etc.
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How to know patient is having a reaction:
• Free hemoglobin in urine or blood
• Fever
• SOB
• Adventitious lung sounds
• Any change in vital signs (i.e., hypertension,
hypotension, tachycardia, tachypnea)
• Nausea, weakness
• Shivering or shaking
What to do if patient is having a reaction:
•
Stop (if severe) or slow down (if mild) transfusion depending
on agency protocol.
•
•
•
•
•
Infuse NS
Notify provider
Monitor Vital signs
Administer medications and oxygen as prescribed.
Notify the blood bank. DO NOT DISCARD BLOOD. Return blood to lab!!
Polycythemia
à Production and presence of increased numbers of RBCS: increase can be so great that blood circulation is
impaired à bone marrow dysfunction
v Causes hyper-viscosity & hypervolemia
v Clotting is a complication
à 2 types: Primary polycythemia (polycythemia vera) &
Secondary polycythemia
• Primary: referred to as Polycythemia Vera
o a myeloproliferative chromosomal disorder
o Increased RBCs, WBCs, and platelets
o Median age 60 > males
• Secondary: a physiological compensation to
chronic hypoxemia
o High altitudes, pulmonary disease & heart
disease
Medical Interventions:
• Reduce blood volume
o Phlebotomy (500 ml every 3 months)
• Hydration to reduce viscosity
• Medications
o Myelosuppressive agents (Hydrea,
Myleran)
o Low dose ASA (prophylaxis of vascular
events)
o Interferon alpha
o Allopurinol (reduce gouty attacks)
• Nutritional evaluation
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Symptoms:
•
Headache
•
•
•
•
Shortness of breath
Weakness
Double vision
Sweating, particularly at
night
Dizziness
Weight loss
Pain and swelling in the
joint (especially in the big
toe)
•
•
•
Diagnostic tests findings:
•
Elevated Hgb & RBC
count
Elevated WBC count
Elevated Platelet count
EPO levels elevated
•
•
•
Nursing Interventions:
•
•
•
•
•
Monitor lab values
Control hypoxia to prevent
secondary polycythemia
vera
Perform or assist with
phlebotomy
Monitor I & O – this
ensures hydration
Prevent thrombus
formation
o Ambulate patient
o Give ASA
Thrombocytopenia
•
•
•
•
Reduction in platelets below 150,000/ microliter
Under 80,000/microliter indicates high risk for hemorrhage
Platelets live 10 days
Interventions are working when
Produced in bone marrow
patient has no evidence of
bleeding or bruising
Major Types:
1. Hereditary
• Hemophilia & Von Willebrand Disease (clotting factor abnormalities)
2. ITP (AKA: Immune thrombocytopenia)
Prolonged bleeding usually
• Lifespan of platelets decreased due to autoimmune processes
does not occur until 50,000
3. TTP (AKA: Thrombotic thrombocytopenia)
at 20,00 life threatening
• Uncommon – caused by deficiency of plasma enzyme, meds, lupus
bleeding usually occurs
4. DIC (AKA: Disseminated intravascular coagulation)
• Clotting and bleeding occurs at same time
due to causes such as arrest, septicemia,
and hemorrhage
5. HIT (AKA: Heparin induced
thrombocytopenia)
Causes:
• Decreased production (bone marrow
suppression)
• Trapped in the spleen (splenomegaly)
• Medication
o Aspirin, Quinine, Thiazides,
Digoxin
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Labs:
Hereditary
ITP
DIC
HIT
Platelet
Low
Low
Low
Low
Size platelets
Normal
Abnormal
Normal
Normal
PT*
Normal
Normal
***High
Normal
Aptt*
Normal
Normal
***High
Normal
à Most lab values will be similar for different thrombocytopenia’s, except for DIC where there are low
platelets and increased bleeding times.
à PT – Prothrombin: Measure of Vitamin K dependent clotting ability. We are using mainly INR to replace
the PT value now because it is more accurate.
aPTT – Activated partial thromboplastin time: How long blood takes to clot with additives.
Lab Values for DIC:
•
If PT and PTT are elevated – think DIC
Assessment:
• Petechia - tiny red dots under the skin that are a result of very small
bleeds
• Purpura - the purple color of the skin after blood has "leaked" under it.
Diagnostic findings:
• Platelets less than 150,000/ microliter
• Normal PT, PTT
• Bone marrow biopsy
• à Prolonged bleeding usually does not occur until 50,000 at 20,00 life threatening
bleeding usually occurs
• àIf PT and PTT are elevated – think DIC
Treatment:
Medications:
Depends on cause:
-ITP: Corticosteroids and immunosuppressants
• First step: Stop heparin and avoid future heparin (If HIT)
-HIT: Anticoagulants with direct thrombin
• Avoid other anticoagulant/antiplatelet medications
inhibitors:
• Platelet infusion for severely low counts
- Argatroban, lepirudin, bivalirudin
• Splenectomy
-Recall that thrombin initiates hemostasis
by
activating
other clotting factors
• Immune suppression for autoimmune etiology
-DIC: Anticoagulants (heparin) can be used to
• Oprelvekin (Neumega) – a platelet growth factor
decrease microclots from forming and using
• Corticosteroids
up clotting factors
Collaborative Care:
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•
•
•
•
•
Early detection is essential
Treatment of underlying cause
Replacement of missing factors for severe hemorrhage
o Cryoprecipitate, FFP, Platelets
Prevent exsanguination
Drug treatments are controversial and not highly effective (heparin, amicar, lovenox)
Nursing Care:
• Protect from injury
• Transfusion of platelets
• Avoid IM injections/procedures/central lines
• Monitor labs, vital signs, assessments
• Monitor response to and side effects from medications
• Education: Soft toothbrush ok, avoid injury, pressure dressings, watch for signs bleeding (tarry stools,
etc.)
Immune Thrombocytopenia
Causes: acquired immune disorder from impaired platelet production & T cell mediated destruction of platelets.
Infection such as Helicobacter pylori or HIV contribute to this disorder.
Treatment: High dose of IV immunoglobulin (IVIG) may be used for patient who is unresponsive to
corticosteroids or splenectomy. Immunosuppressive therapy may be used in refractory cases & platelet
transfusions may increase platelet counts in cases of life-threatening hemorrhage.
DIC (Disseminated intravascular coagulation)
à A serious disorder in which the proteins that control blood clotting become overactive. DIC begins with
excessive clotting and followed by excessive bleeding.
o Sudden DIC: follows surgery or childbirth, bleeding may be uncontrollable. Bleeding may
occur at the site of an intravenous injection or in the brain, digestive tract, skin, muscles, or
cavities of the body, sepsis.
o Slow DIC: cancer, aneurysms (DVT, PE will develop)
Causes: Inflammation in response to injury, infection, or an illness, severe tissue damage (burns or trauma),
clotting factors by some cancers or pregnancy complications.
Treatment: Treat underlying cause à IV fluids & blood transfusions & heparin
Heparin- induced Thrombocytopenia (HIT)
à A low platelet count caused by a reaction against heparin.
• Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by
antibodies to complexes of platelet factor 4 (PF4) and heparin.
o Develop 5-10 days after starting injection of heparin. Ptl drops by more than 50%
o Tx: discontinue heparin. Monitor/prevent VBTE and PE
o May use alternative antithrombotic (Argatroban)
o HIT once= HIT forever! When receiving heparin
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Test your Knowledge Questions:
A nurse is caring for a client who has idiopathic thrombocytopenic purpura (ITP). The nurse should notify the
provider and report possible small-vessel clotting when which of the following is assessed?
A. Petechiae on the upper chest
B. Hypotension
C. Cyanotic nail beds
D. Severe headache
In a patient with prolonged vomiting, the nurse monitors for fluid volume deficit because vomiting results in
a. Fluid movement from the cells into the interstitial space and the blood vessels
b. Excretion of large amounts of interstitial fluid with depletion of extracellular fluids
c. An overload of extracellular fluid with a significant increase in intracellular fluid volume
d. Fluid movement from the vascular system into the cells, causing cellular swelling and rupture
The nurse is administering 3.0 % saline solution IV to a patient with severe hyponatremia. It is most important
for the nurse to observe for what?
a. Decreased heart rate and blood pressure
b. Prolonged QT interval and facial flushing
c. Shortness of breath and increased respiratory rate
d. Increased urine output and decreased urine specific gravity
A patient is admitted with renal failure and an arterial blood pH level of 7.29. Which lab result would the nurse
expect?
a. Serum sodium 138 mEq/L
b. Serum glucose 145 mg/dL
c. Serum potassium 5.9 mEq/L
d. Serum magnesium 0.4 mg/dL
Pneumothorax
à Open pneumothorax: air enters through an opening in the
chest wall and parietal (outer) lining of the pleura.
à Closed pneumothorax: occurs when the visceral (inner) lining
of the pleura is disrupted, allowing air to enter the pleural space
from the lung. There is no external wound.
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Clinical manifestations:
— If a pneumothorax is small, mild tachycardia and dyspnea may be the only manifestations.
— If the pneumothorax occupies a large area, respiratory distress may be present, including shallow, rapid
respirations; dyspnea; air hunger; and oxygen desaturation.
— On auscultation, there are no breath sounds over the affected area.
— A chest x-ray shows the presence of air or fluid in the pleural space and reduction in lung volume.
Types:
àA spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled sacs) located on the
surface of the lung.
• These blebs can occur in healthy, young individuals or as a result of lung disease such as COPD,
asthma, cystic fibrosis, and pneumonia.
• Smoking increases the risk for bleb formation. Other risk factors include being tall and thin, male
gender, family history, and previous spontaneous pneumothorax.
à Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures.
• Example: transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, and
transbronchial lung biopsy all have the potential to injure the lung.
• Barotrauma from excessive ventilatory pressure during manual or mechanical ventilation can rupture
alveoli or bronchioles.
• Esophageal procedures may also be involved in the development of a pneumothorax.
• Tearing during insertion of a gastric tube can allow air from the esophagus to enter the mediastinum and
pleural space.
Tension Pneumothorax:
à Medical emergency, with both the respiratory and cardiovascular systems affected.
• If the tension in the pleural space is not relieved, the patient is
likely to die from inadequate cardiac output or severe hypoxemia.
• Treat with needle decompression and chest tube insertion
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Treatment: Depends on its severity and the nature of the underlying cause
•
•
•
•
If the patient is stable, and has minimal air and/or fluid accumulated in the intrapleural space, no
treatment may be necessary as the condition may resolve spontaneously.
The most definitive and common form of treatment of pneumothorax and hemothorax is to insert a chest
tube and connect it to water-seal drainage.
Repeated spontaneous pneumothorax may need to be treated surgically by a partial pleurectomy,
stapling, or pleurodesis to promote adherence of the pleurae to one another.
Tension pneumothorax is a medical emergency, requiring urgent needle decompression followed by
chest tube insertion to water-seal drainage.
Chest tube & pleural drainage:
This unit has 3 chambers:
(1) collection chamber;
(2) water-seal chamber; and
(3) suction control chamber.
àSuction control chamber requires a connection to a wall
suction source that is dialed up higher than the prescribed
suction for the suction to work. In the water suction unit, the
suction control chamber controls the wall suction pressure.
àIf enough fluid or air accumulates in the pleural space, the
negative pressure becomes positive and the lungs collapse.
• As a result, chest tubes are inserted to drain the
pleural space, reestablish negative pressure, and allow
for proper lung expansion.
• They may also be inserted in the mediastinal space to
drain air and fluid postoperatively.
• Chest tubes are approximately 20 inches (51 cm) long
and vary in size from 12F to 40F. The size inserted is
determined by the patient’s condition. Large (36F to
40F) tubes are used to drain blood, medium (24F to
36F) tubes are used to drain fluid, and small (12F to
24F) tubes are used to drain air.
• Pigtail tubes are very small (10F to 14F) tubes with a
curly end designed to keep them in place. They are a
safe and effective alternative to larger bore chest tubes
for treatment of pneumothorax.
• Brisk bubbling of air often occurs in this chamber when
a pneumothorax is initially evacuated.
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•
•
•
•
•
•
Intermittent bubbling during exhalation, coughing, or sneezing (when the patient’s intrathoracic
pressure is increased) may be observed as long as air is in the pleural space.
Eventually, as the air leak resolves and the lung becomes more fully expanded, bubbling ceases.
Normal fluctuation of the water within the water-seal chamber is called tidaling.
This up-and-down movement of water in concert with respiration reflects intrapleural pressure changes
during inspiration and expiration.
Investigate any sudden cessation of tidaling, as this may signify an occluded chest tube.
Gradual reduction and eventual cessation of tidaling is expected as the lung reexpands.
Management:
• Never elevate the drainage system to the level of the patient’s chest because this will cause fluid to drain
back into the lungs. Secure the unit to the drainage stand.
• Change the unit if the collection chamber is full. Do not try to empty it.
• Mark the time of measurement and the fluid level on the drainage unit according to the unit standards.
Report any change in the quantity or characteristics of drainage (e.g., clear yellow to bloody) to the
physician and record the change. Notify physician if >100 mL/hr drainage.
• Check the position of the chest drainage container.
If the drainage system is overturned and the waterseal is disrupted, return it to an upright position and
encourage the patient to take a few deep breaths,
followed by forced exhalations and cough
maneuvers.
• Clamping of chest tubes during transport or when
the tube is accidentally disconnected is no longer
advocated. The danger of rapid accumulation of air
in the pleural space, causing tension pneumothorax,
is far greater than that of a small amount of
atmospheric air that enters the pleural space.
• If a chest tube becomes disconnected, the immediate
priority is to reestablish the water-seal system. In
some hospitals, when disconnection occurs, the
chest tube is immersed in sterile water (about 2 cm)
until the system can be reestablished. It is important
to know the unit protocol, individual clinical
situation (whether an air leak exists), and HCP
preference before any chest tube clamping occurs.
• Appearance of a new air leak warrants assessment
of the drainage system to identify if the air leak is coming from the patient or the system.
• Once again, the nurse is encouraged to become familiar with the policies and procedures of their
workplace regarding specific clinical situations and circumstances when chest tubes may be clamped.
à If unit overturned, have patient exhale and cough
à Do NOT clamp
à If break in system, place distal end in sterile water to maintain water seal
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Test Your Knowledge
When should a nurse check for leaks in the chest tube and pleural drainage system?
a. When there is continuous bubbling in the water-seal chamber.
b. There is constant bubbling of water in the suction control chamber.
c. Fluid in the water-seal chamber fluctuates with the patient’s breathing.
d. The water levels in the water-seal and suction control chambers are decreased.
True or False:
— In tension pneumothorax, the trachea is deviated toward the unaffected side?
Pneumonia
à Acute infection of lung parenchyma
Types:
• Community-acquired (CAP)
o Occurs in patients who have not been hospitalized or resided in a long-term care facility within
14 days of the onset of symptoms
o Can be treated at home or hospitalized dependent on patient condition
o Empiric antibiotic therapy started ASAP
• Hospital-acquired (HAP)
o HAP: Occurs 48 hours or longer after hospitalization and not present at time of admission
o Associated with longer hospital stays, increased costs, sicker patients, and increased risk of
morbidity and mortality
• Ventilator-associated (VAP)
o VAP: Occurs more than 48 hours after endotracheal intubation
o Associated with longer hospital stays, increased costs, sicker patients, and increased risk of
morbidity and mortality
à Multidrug-resistant (MDR) organisms are major problem in treatment
o Staphylococcus aureus
o Gram-negative bacilli
• Risk factors
o Advanced age
o Immunosuppression
o History of antibiotic use
o Prolonged mechanical ventilation
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•
•
•
•
•
•
•
•
•
Aspiration Pneumonia
Results from abnormal entry of secretions
into lower airway
Major risk factors:
o Decreased level of consciousness
o Difficulty swallowing
o Insertion of nasogastric tubes with or
without tube feeding
Empiric therapy based on severity of illness,
where infection acquired, and probable
causative organism
Opportunistic Pneumonia
Caused by microorganisms that do not
normally cause disease
Patients at risk
o Severe protein-calorie malnutrition
o Immunodeficiencies
o Chemotherapy/radiation recipients
o Long-term corticosteroid therapy
•
•
•
Necrotizing Pneumonia
Rare complication of bacterial lung infection
Often results from CAP
Signs and symptoms
o Immediate respiratory insufficiency
and/or failure
o Leukopenia
o Bleeding into airways
Pneumocystis jiroveci pneumonia (PJP)
• Onset slow and subtle
• Diffuse bilateral infiltrates to massive
consolidation
• Can be life threatening
• Spread to other organs
• Treat with trimethoprim/sulfamethoxazole IV
or orally
Cytomegalovirus (CMV) pneumonia
Herpes virus
Asymptomatic and mild to severe disease
Life threatening in immunosuppressed person
Treat with antiviral medications and high-dose immunoglobulin
Manifestations:
• Most common
o Cough
o Fever, chills
o Dyspnea, tachypnea
o Pleuritic chest pain
o Green, yellow, or rust-colored sputum
• Change in mentation for older or debilitated
patients
Physical examination findings:
• Fine or coarse crackles
• Bronchial breath sounds
• Egophony
• ↑ Fremitus
• Dullness to percussion if pleural effusion
present
Interventions:
• Pneumococcal vaccine
o To prevent Streptococcus pneumoniae
• Prompt treatment with antibiotics is essential
o Response generally occurs within 48-72 hr
o ↓ Temperature
o Improved breathing
o ↓ Chest discomfort
• Repeat chest x-ray in 6-8 weeks
à Supportive care
• Oxygen for hypoxemia
• Analgesics for chest pain
• Antipyretics
• Individualize rest and activity
à No definitive treatment for majority of viral
pneumonias
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à Antivirals for influenza pneumonia
Drug Therapy:
• Start with empiric therapy
o Based on likely infecting organism and risk factors for MDR organisms
o Varies with local patterns of antibiotic resistance
• Should see improvement in 3-5 days
• Start with IV and then switch to oral therapy as soon as patient stable
Nutritional Therapy:
Be cautious giving oxygen to patient
• Adequate hydration
with COPD à over oxygenating
o Prevent dehydration
patient can lead to altered mental
o Thin and loosen secretions
status and further complications
o Adjust for older adults, patients with heart
failure, those with preexisting respiratory
conditions
• High calorie, small, frequent meals
o Monitor for weight loss
Complications:
• Atelectasis
• Pleurisy
• Pleural effusion
• Bacteremia
• Pneumothorax
• Meningitis
• Acute respiratory failure
• Sepsis/septic shock
• Lung abscess
How to know interventions are working:
• Clear breath sounds
• Normal breathing patterns
• No signs of hypoxia
• Normal chest x-ray
• Normal WBC count
• Absence of complications related to
pneumonia
Response Questions
A 56-year-old normally healthy patient at the clinic is diagnosed with bacterial community-acquired
pneumonia. Before treatment is prescribed, the nurse asks the patient about an allergy to
a. amoxicillin
b. erythromycin
c. sulfonamides
d. cephalosporins
The nurse is caring for a patient with pneumonia. If a pleural effusion is developing, the nurse would expect
which finding?
a. Barrel-shaped chest
b. Paradoxical respirations
c. Hyperresonance on percussion
d. Localized decreased breath sounds
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What lung sounds could a nurse hear when assessing a patient with pneumonia?
A.
B.
C.
D.
Rhonchi
Rales
Wheezes
All of the above
Neutropenia
à Reduction in neutrophils (predisposing patient to infection)
à ANC less than 1000 (normal range 2200 – 7700)
à Severe neutropenia ANC less than 500
à Can be an expected effect of certain drugs, most common cause is chemotherapy and immunosuppressive
therapy
• Patient needs private room to be protected from staff and other patients (high priority) à positive
pressure or high efficiency particular air (HEPA)
• Nadir: lowest point of neutropenia in a patient treated with chemotherapy
*Low grade fever great significance greater than 100.4F (38C) à blood culture drawn STAT and antibiotics
started within 1 hour (usually IV route because of rapid lethal effects of infection)
Diagnosis: primary diagnostic tests peripheral WBC count and bone marrow aspiration and biopsy
Management: Identify and remove cause or site of infection (if possible), antimicrobial therapy, blood culture
STAT before antibiotics, patient hygiene (strict hand washing)
1. Determine cause
2. Antibiotic therapy promptly
3. Identify offending organisms if infection developed
4. Give hematopoietic growth factors prophylactically after chemotherapy
5. Implement protective practices
à Hand washing single most effective way to prevent
à Avoid: Unwashed fruit and veggies, raw undercooked meats and eggs and soft cheese with molds
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Nurse Civility
à Foundation for patient safety, a
healthy work environment, healthy
staff
•
•
Results in increased
productivity
Use clear communication
verbally, on-verbally, and in
writing & treat others with
respect, dignity, and kindness
Labs
Sodium
136-145mEq/L
Potassium
3.5-5.0mEq/L
Calcium
9.0-10.5mg/dL
Magnesium:
1.3-2.1mEq/L
Phosphorus:
3.0-4.5mg/dL
Glucose
74-106mg/dL
HctFemale: 37%-47% (0.37-0.47)
Male: 42%-52% (0.42-0.52)
HgbFemale: 12-16g/dL
Male: 14-18g/dL
MCV80-100fL
Platelets150,000-400,000x 103 /L
WBC5,000-10,000/μl
Banded neutrophils:
0%-8%
Segmented neutrophils:
55%-70%
SpO2
94%-99%
SaO2:
>95%
PT:
11-12.5 seconds
aPTT:
30-40 seconds
(1.5-2.5 times the control value w/
heparin therapy)
INR:
0.8-1.1
(Desired goal of 2 to 3 on warfarin
therapy)
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Medications
Iron (Ferrous sulfate)
Class: Antiemetics
Action: Enters blood stream and is transported to organs where it becomes part of iron stores
Indications: Treatment of iron deficiency anemia.
Interventions: Do not take with acid suppressing agents (antacids, eggs, milk, coffee or tea) - take 2 hours apart.
Orange juice and acid environment help with absorption. Peds patient should drink through a straw to decrease
tooth staining. GI upset, constipation, green/black stools common. Give IM Z-track. Watch for CNS toxicity
symptoms.
Adverse Effects: Nausea, vomiting, dark stools, epigastric pain (constipation), staining of teeth
Aspirin
Class: Antipyretic, antiplatelet, analgesic NSAID
Action: Produce analgesia and reduce inflammation and fever, decreases platelet aggregation
Indications: Block prostaglandin activity which decreases inflammatory response. OD can lead to acidosis.
Interventions: Administer with food, can cause antidiuretic effect
Adverse Effects: Dyspepsia, epigastric distress, nausea, hypersensitivity reactions
Erythropoietin
Class: Antiemetics
Action: Stimulates erythropoiesis (production of RBCs)
Indications: Stimulates RBC production, common with renal failure, AIDS, post-surgical, chemo pts.
Interventions: Caution if giving to patient with normal erythropoietin as could turn off the negative feedback
loop. Watch for chest pain, thrombophlebitis, hypertension, facial flushing in athletes that are abusing this
drug.
Adverse Effects: Hypertension, cough, dizziness
Neupogen
Class: Colony stimulating factors
Action: Binds to and stimulates immature neutrophils to divide and differentiate
Indications: Decreases infection improves recovery of neutrophils in cancer treatment.
Interventions: Prevent exposure to infection, provide mouth care and support.
Adverse Effects: Bone pain, headache, fatigue, alopecia, rash, N/V, diarrhea, stomatitis, bone pain.
Hydroxyurea
Class: Antineoplastics
Action: interferes with DNA synthesis and may alter characteristics of RBCs
Indications: Reduction in frequency of painful crisis in sickle cell anemia
Interventions: Anemia may occur, assess for signs of infection and bleeding
Adverse Effects: leukopenia, chills, fever
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Zithromax
Class: Macrolide
Action: Inhibits protein synthesis
Indications: Used to fight infections
Interventions: Take on empty stomach (best for most antibiotics - many cannot be taken with iron or calcium),
complete full course of prescription even if feeling better, may suppress effectiveness of BCPs, liver enzymes
(AST/ALT).
Adverse Effects: GI, supra infections, c-diff. Can prolong QT interval and cause EKG changes which may
result in chest pain and lethal arrhythmias.
Ciprofloxacin & Levofloxacin
Class: Fluoroquinolones
Action: Inhibits bacterial DNA synthesis by inhibiting DN gyrase enzyme
Indications: Used for more serious infections and patients who may be immunocompromised, such as HIV+.
Interventions: Adding aminoglycosides, theophylline, steroids increase toxicity (note: theophylline does not go
well with most drugs),
Adverse Effects: Adding aminoglycosides, theophylline, steroids increase toxicity (note: theophylline does not
go well with most drugs)
Tazobactam & Ceftriazone
Class: B-Lactams
Action: Binds to bacterial cell wall membrane causing cell death à inhibits beta lactamase an enzyme that
destroys penicillin’s
Indications: Intraabdominal infections, Hospital acquired bacteria pneumonia (HAPB), complicated UTIs
Interventions: Observe for anaphylaxis & monitor bowel function
Adverse Effects: Diarrhea, Cdiff
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