Transcript Shock (Cont`d)

Focus on Shock
(Relates to Chapter 67, “Nursing Management: Shock, SIRS,
and Multiple Organ Dysfunction Syndrome,” in the
textbook)
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Shock
 Syndrome characterized by
decreased tissue perfusion and
impaired cellular metabolism
 Imbalance in supply/demand for O2
and nutrients
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Shock (Cont’d)
 Classification of shock (table 67-1)
 Low blood
flow
Cardiogenic
 Hypovolemic

 Maldistribution
of blood flow
Septic
 Anaphylactic
 Neurogenic

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Low Blood Flow
Cardiogenic Shock
 Definition
 Systolic
or diastolic dysfunction leads
to compromised cardiac output
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Low Blood Flow
Cardiogenic Shock (Cont’d)
 Precipitating causes
 Myocardial
infarction
 Cardiomyopathy
 Blunt cardiac injury
 Severe systemic or pulmonary
hypertension
 Cardiac tamponade
 Myocardial depression from metabolic
problems
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Pathophysiology of Cardiogenic Shock
Fig. 67-2
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Low Blood Flow
Cardiogenic Shock
 Early manifestations
 Tachycardia
 Hypotension
 Narrowed pulse pressure
 ↑ Myocardial
O2 consumption
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Low Blood Flow
Cardiogenic Shock (Cont’d)
 Physical examination
 Tachypnea, pulmonary congestion
 Pallor;
cool, clammy skin
 Decreased capillary refill time
 Anxiety, confusion, agitation
 ↑ in pulmonary artery wedge
pressure
 Decreased renal perfusion and UO
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Low Blood Flow
Hypovolemic Shock
 Absolute hypovolemia: Loss of
intravascular fluid volume
 Hemorrhage
 GI loss
(e.g., vomiting, diarrhea)
 Fistula drainage
 Diabetes insipidus
 Hyperglycemia
 Diuresis
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Low Blood Flow
Hypovolemic Shock (Cont’d)
 Relative hypovolemia
 Results when fluid volume moves out
of the vascular space into
extravascular space (e.g., interstitial or
intracavitary space)
 Termed third spacing
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Pathophysiology of Hypovolemic Shock
Fig. 67-3
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Low Blood Flow
Hypovolemic Shock (Cont’d)
 Clinical manifestations
 Anxiety
 Tachypnea
 Increase in CO, heart rate
 Decrease in stroke volume, PAWP, UO
 If loss is >30%, blood volume is
replaced
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Maldistribution of Blood Flow
Neurogenic Shock
 Hemodynamic phenomenon that
can occur within 30 minutes of a
spinal cord injury at the fifth thoracic
(T5) vertebra or above and can last
up to 6 weeks
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Maldistribution of Blood Flow
Neurogenic Shock (Cont’d)
 Can be in response to spinal
anesthesia
 Results in massive vasodilation
leading to pooling of blood in vessels
 Compensation is
lost due to the loss of
SNS vasoconstrictor tone
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Pathophysiology of Neurogenic Shock
Fig. 67-4
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Maldistribution of Blood Flow
Neurogenic Shock (Cont’d)
 Clinical manifestations
 Hypotension
 Bradycardia
 Temperature dysregulation (resulting
in heat loss)
 Dry skin
 Poikilothermia (taking on the
temperature of the environment)
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Maldistribution of Blood Flow
Anaphylactic Shock
 Acute, life-threatening
hypersensitivity reaction
 Massive
vasodilation
 Release of inflammatory mediators
 ↑ Capillary permeability
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Maldistribution of Blood Flow
Anaphylactic Shock (Cont’d)
 Clinical manifestations
 Swelling
of the lips and tongue,
angioedema
 Wheezing, stridor
 Flushing, pruritus, urticaria
 Respiratory distress and circulatory
failure
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Maldistribution of Blood Flow
Anaphylactic Shock (Cont’d)
 Clinical manifestations
 Anxiety, confusion, dizziness
 Sense of impending doom
 Chest pain
 Incontinence
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Maldistribution of Blood Flow
Septic Shock
 Sepsis: Systemic inflammatory
response to documented or
suspected infection
 Severe sepsis = Sepsis + Organ
dysfunction
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Maldistribution of Blood Flow
Septic Shock (Cont’d)
 Septic shock = Presence of sepsis
with hypotension despite fluid
resuscitation + Presence of tissue
perfusion abnormalities
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Maldistribution of Blood Flow
Septic Shock (Cont’d)
 Mortality rates as high as 50%
 Primary causative organisms
 Gram-negative and gram-positive
bacteria
 Endotoxin stimulates inflammatory
response
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Pathophysiology of Septic Shock
Fig. 67-5
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Maldistribution of Blood Flow
Septic Shock
 Clinical manifestations
 ↑ Coagulation
and inflammation
 ↓ Fibrinolysis
Formation of microthrombi
 Obstruction of microvasculature

 Hyperdynamic
state: Increased CO and
decreased SVR
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Maldistribution of Blood Flow
Septic Shock (Cont’d)
 Clinical manifestations
 Tachypnea/hyperventilation
 Temperature dysregulation
 ↓ Urine output
 Altered neurologic status
 GI dysfunction
 Respiratory
failure is common
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Stages of Shock
Initial Stage
 Usually not clinically apparent
 Metabolism changes from aerobic to
anaerobic
 Lactic acid accumulates and must be
removed by blood and broken down by
liver
 Process requires unavailable O2
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Stages of Shock
Compensatory Stage
 Clinically apparent
 Neural
 Hormonal
 Biochemical compensatory
mechanisms
 Attempts are aimed at overcoming
consequences of anaerobic
metabolism and maintaining
homeostasis
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Compensatory Stage of Shock
Fig. 67-6
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Stages of Shock
Compensatory Stage
 Baroreceptors in carotid and aortic
bodies activate SNS in response to ↓
BP
 Vasoconstriction
while blood to vital
organs maintained
 ↓ Blood to kidneys activates renin–
angiotensin system
 ↑ Venous return to heart, CO, BP
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Stages of Shock
Compensatory Stage (Cont’d)
 Impaired GI motility
 Risk for paralytic
ileus
 Cool, clammy skin from blood
 Except septic patient who is
warm and
flushed
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Stages of Shock
Compensatory Stage (Cont’d)
 Shunting blood from lungs increases
physiologic dead space
↓ Arterial O2 levels
 Increase in rate/depth of respirations
 V/Q mismatch

 SNS stimulation increases
myocardium O2 demands
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Stages of Shock
Compensatory Stage (Cont’d)
 If perfusion deficit corrected, patient
recovers with no residual sequelae
 If deficit not corrected, patient
enters progressive stage
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Stages of Shock
Progressive Stage
 Begins when compensatory
mechanisms fail
 Aggressive interventions to prevent
multiple organ dysfunction
syndrome
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Progressive Stage of Shock
Fig. 67-7
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Stages of Shock
Progressive Stage (Cont’d)
 Hallmarks of ↓ cellular perfusion and
altered capillary permeability:
Leakage of protein into interstitial space
 ↑ Systemic interstitial edema

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Stages of Shock
Progressive Stage (Cont’d)
 Movement of fluid from pulmonary
vasculature to interstitium
Pulmonary edema
 Bronchoconstriction
 ↓ Residual capacity

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Stages of Shock
Progressive Stage (Cont’d)
 Fluid moves into alveoli
Edema
 Decreased surfactant
 Worsening V/Q mismatch
 Tachypnea
 Crackles
 Increased work of breathing

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Stages of Shock
Progressive Stage (Cont’d)
 CO begins to fall
Decreased peripheral perfusion
 Hypotension
 Weak peripheral pulses
 Ischemia of distal extremities

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Stages of Shock
Progressive Stage (Cont’d)
 Myocardial dysfunction results in
Dysrhythmias
 Ischemia
 Myocardial infarction
 End result: Complete deterioration of
cardiovascular system

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Stages of Shock
Progressive Stage (Cont’d)
 Mucosal barrier of GI system
becomes ischemic
Ulcers
 Bleeding
 Risk of translocation of bacteria
 Decreased ability to absorb nutrients

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Stages of Shock
Progressive Stage (Cont’d)
 Liver fails to metabolize drugs and
wastes
Jaundice
 Elevated enzymes
 Loss of immune function
 Risk for DIC and significant bleeding

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Stages of Shock
Progressive Stage (Cont’d)
 Acute tubular necrosis/acute renal
failure
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Stages of Shock
Refractory Stage
 Exacerbation of anaerobic
metabolism
 Accumulation of lactic acid
 ↑ Capillary permeability
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Refractory Stage of Shock
Fig. 67-8
Stages of Shock
Refractory Stage
 Profound hypotension and
hypoxemia
 Tachycardia worsens
 Decreased coronary blood flow
 Cerebral ischemia
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Stages of Shock
Refractory Stage (Cont’d)
 Failure of one organ system affects
others
 Recovery unlikely
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Diagnostic Studies
 Thorough history and physical
examination
 No single study to determine shock
 Blood studies
Elevation of lactate
 Base deficit

 12-lead ECG
 Chest x-ray
 Hemodynamic monitoring
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Collaborative Care
 Successful management includes
 Identification of patients at risk for
shock
 Integration of the patient’s history,
physical examination, and clinical
findings to establish a diagnosis
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Collaborative Care (Cont’d)
 Successful management includes
 Interventions to control or eliminate
the cause of the decreased perfusion
 Protection of target and distal organs
from dysfunction
 Provision of multisystem supportive
care
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Collaborative Care (Cont’d)
 General management strategies
 Ensure patent airway
 Maximize oxygen delivery
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Collaborative Care (Cont’d)
 Cornerstone of therapy for septic,
hypovolemic, and anaphylactic
shock = volume expansion
 Isotonic crystalloids
(e.g., normal
saline) for initial resuscitation of shock
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Collaborative Care (Cont’d)
 Volume expansion
 If the patient does not respond to 2 to
3 L of crystalloids, blood
administration and central venous
monitoring may be instituted

Complications of fluid resuscitation
 Hypothermia
 Coagulopathy
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Collaborative Care (Cont’d)
 Primary goal of drug therapy =
correction of decreased tissue
perfusion
 Vasopressor
drugs (e.g., epinephrine,
dopamine)
Achieve/maintain MAP >60 to 65 mm Hg
 Reserved for patients unresponsive to
other therapies

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Collaborative Care (Cont’d)
 Primary goal of drug therapy =
correction of decreased tissue
perfusion
 Vasodilator
therapy (e.g., nitroglycerin
[cardiogenic shock],

Achieve/maintain MAP >60 to 65 mm Hg
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Collaborative Care (Cont’d)
 Nutrition is vital to decreasing
morbidity from shock
 Initiate enteral
nutrition within the
first 24 hours
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Collaborative Care (Cont’d)
 Nutrition is vital to decreasing
morbidity from shock
 Initiate parenteral
nutrition if enteral
feedings contraindicated or fail to
meet at least 80% of the caloric
requirements
 Monitor protein, nitrogen balance,
BUN, glucose, electrolytes
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Collaborative Care
Cardiogenic Shock
 Restore blood flow to the
myocardium by restoring the
balance between O2 supply and
demand
 Thrombolytic therapy
 Angioplasty with stenting
 Emergency revascularization
 Valve replacement
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Collaborative Care
Cardiogenic Shock (Cont’d)
 Hemodynamic monitoring
 Drug therapy (e.g., diuretics to
reduce preload)
 Circulatory assist devices (e.g., intraaortic balloon pump, ventricular
assist device)
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Collaborative Care
Hypovolemic Shock
 Management focuses on stopping
the loss of fluid and restoring the
circulating volume
 Fluid replacement
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Collaborative Care
Septic Shock
 Fluid replacement (e.g., 6 to 10 L of
isotonic crystalloids and 2 to 4 L of
colloids) to restore perfusion

Hemodynamic monitoring
 Vasopressor drug therapy if
unresponsive to fluids
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Collaborative Care
Septic Shock (Cont’d)
 Intravenous corticosteroids for
patients who require vasopressor
therapy, despite fluid resuscitation,
to maintain adequate BP
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Collaborative Care
Septic Shock (Cont’d)
 Antibiotics after obtaining cultures
(e.g., blood, wound exudate, urine,
stool, sputum)
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Collaborative Care
Septic Shock (Cont’d)
 Glucose levels <150 mg/dl
 Stress ulcer prophylaxis with
histamine (H2)-receptor blockers
 Deep vein thrombosis prophylaxis
with low-dose heparin or lowmolecular-weight heparin
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Collaborative Care
Neurogenic Shock
 In spinal cord injury: Spinal stability
 Treatment of the hypotension and
bradycardia with vasopressors and
atropine
 Fluids used cautiously as hypotension
is generally not related to fluid loss
 Monitor for hypothermia
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Collaborative Care
Anaphylactic Shock
 Prevent!





Assess for allergies/adverse reactions
Family education
Epinephrine
Knowledge about signs/symptoms
Be prepared for emergency measures
 Epinephrine, diphenhydramine
 Maintaining a patent airway
Nebulized bronchodilators
 Endotracheal intubation or
cricothyroidotomy may be necessary

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Collaborative Care
Anaphylactic Shock (Cont’d)
 Aggressive fluid replacement
 Intravenous corticosteroids if
significant hypotension persists
after 1 to 2 hours of aggressive
therapy
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Nursing Assessment
 ABCs: Airway, breathing, and
circulation
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Nursing Assessment (Cont’d)
 Focused assessment of tissue
perfusion
 Vital signs
 Peripheral
pulses
 Level of consciousness
 Capillary refill
 Skin (e.g., temperature, color,
moisture)
 Urine output
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Nursing Assessment (Cont’d)
 Brief history
 Events leading
to shock
 Onset and duration of symptoms
 Details of care received before
hospitalization
 Allergies
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Nursing Diagnoses
 Ineffective tissue perfusion: Renal,
cerebral, cardiopulmonary,
gastrointestinal, hepatic, and
peripheral
 Fear
 Potential complication: Organ
ischemia/dysfunction
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Planning
 Goals for patient
 Adequate tissue
perfusion
 Restoration of normal or baseline BP
 Return/recovery of organ function
 Avoidance of complications from
prolonged states of hypoperfusion
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Nursing Implementation
 Health Promotion
 Identify patients at risk
(e.g., elderly
patients, those with debilitating
illnesses or who are
immunocompromised, surgical or
accidental trauma patients)
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Nursing Implementation (Cont’d)
 Health Promotion
 Planning
to prevent shock
(e.g., monitoring fluid balance to
prevent hypovolemic shock,
maintenance of handwashing to
prevent spread of infection)
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Nursing Implementation (Cont’d)
 Acute Interventions
 Monitor the patient’s ongoing physical
and emotional status to detect subtle
changes in the patient’s condition
 Plan and implement nursing
interventions and therapy
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Nursing Implementation (Cont’d)
 Acute Interventions
 Evaluate the patient’s response to
therapy
 Provide emotional support to the
patient and family
 Collaborate with other members of the
health team when warranted
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Nursing Implementation (Cont’d)
 Neurologic status: Orientation and
level of consciousness
 Cardiac status
 Continuous ECG
 VS, capillary
refill
 Hemodynamic parameters: central
venous pressure, PA pressures, CO,
PAWP
 Ongoing assessment of CO
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Nursing Implementation (Cont’d)
 Respiratory status
 Respiratory
rate and rhythm
 Breath sounds
 Continuous pulse oximetry
 Arterial blood gases
 Many patients will be intubated and
mechanically ventilated
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Nursing Implementation (Cont’d)
 Urine output
 Tympanic or pulmonary arterial
temperature
 Skin: Temperature, pallor, flushing,
cyanosis, diaphoresis, piloerection
 Bowel sounds
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Nursing Implementation (Cont’d)
 Nasogastric drainage/stools for
occult blood
 I&O, fluid and electrolyte balance
 Oral care/hygiene based on O2
requirements
 Passive/active range of motion
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Nursing Implementation (Cont’d)
 Assess level of anxiety and fear
 Medication PRN
 Talk to patient
 Visit
from clergy
 Family involvement
 Comfort measures
 Privacy
 Call light within reach
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Evaluation
 Normal or baseline, ECG, BP, CVP,
and PAWP
 Normal temperature
 Warm, dry skin
 Urinary output >0.5 ml/kg/hr
 Normal RR and SaO2 ≥90%
 Verbalization of fears, anxiety
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Case Study
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Case Study
 26 -year-old male arrives via
paramedics to ED with multiple gun
shot wounds to abdomen
 Unresponsive, BP 58/30, HR 146
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Case Study (Cont’d)
 Three units type O packed RBC
given for profuse blood loss prior to
surgery
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Case Study (Cont’d)
 Surgery successful in removing
bullets and repairing blood vessels
 Surgeon estimated he lost at least 2 L
of blood prior to surgery
 He is admitted to ICU
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Discussion Questions
1. What complications will you
anticipate with this amount of
blood loss?
2. What fluids can you expect to
administer?
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Discussion Questions (Cont’d)
3. What medications will likely be
ordered?
4. What should you monitor hourly or
every 2 hr?
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