GORDON COLLEGE

College of Allied Health Studies

Tapinac Oval Sports Complex, Donor St., East Tapinac, Olongapo City

DETAILED LEARNING MODULE

Title: Shock Course Code: NCM 118

Module No. 7.2 Week: 8

I. Introduction
Welcome to Module 7.2. This module focuses on the nursing care of patients with a shock which
requires ongoing systematic assessment. The module will help the students to differentiate the main
types of shock, recognize clinical signs of shock, and formulate initial nursing care intervention and
management. You will be given preparatory work to read about the overview of shock. You should
be encouraged to record information on the accompanying student learning resources and brainstorm
to answer the questions and other learning tasks.
II. Learning Outcomes
After studying this module, you should be able to:
-describe the concept of shock and its underlying pathophysiology.
-compare clinical findings of the compensatory and progressive stages of shock.
-describe organ damage that may occur with shock.
-compare hypovolemic, cardiogenic, and circulatory shock in terms of causes, pathophysiologic
effects, and medical and nursing management.
-describe indications for varying types of fluid replacement. identify vasoactive medications used in
treating shock, and describe nursing implications associated with their use.
-discuss the importance of nutritional support in all forms of shock.
-identify the role of the nurse in psychosocial support of both the patient experiencing shock and the
family.

III. Topics and Key Concepts/Ideas

Topic
4.1 Shock
3.1.1 Classification of Shock
3.1.2 Stages of Shock
3.1.3 Diagnostic Studies
3.1.4 Collaborative Care
3.1.5 Nursing Management
3.1.6 Evaluation

Key Concepts/Ideas:
Anaphylactic shock, biochemical mediators, blood pressure regulation, cardiogenic shock,
circulatory shock, hypovolemic shock, neurogenic shock, septic shock, vascular responses,

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 IV. Teaching and Learning Materials and Resources
-Medical-Surgical Nursing Books/E-books -Available Open Educational Resources Portal
-Video Clips (e.g. YouTube, Khan Academy, etc.) -Study Notebook
-Slides (attached/provided by Instructor)
-Handouts/Notes (attached/provided by Instructor)

V. Learning Tasks/Activities
1. Read and review your Care of Patients with Shock. (see slides attached/provided by your
instructor)
2. For Synchronous activity:
 The instructor will discuss and present the topic in the selected online platform.
For Offline/Non-Digital activity:
 The instructor will provide the slides/handout notes/video recordings of the topic via
USB flash drive, CD, or any preferred media.
3. Watch lecture related videos if needed.
 YouTube-Shock Overview for Nursing Students
https://www.youtube.com/watch?v=Lx00aCO4GZs
 YouTube-What is Shock? (Shock Pathophysiology)
https://www.youtube.com/watch?v=aT3xsRSKq7Y
 YouTube-"Definition and Pathophysiology of Shock"
https://www.youtube.com/watch?v=J8zW4JT_KDg
 YouTube-Shock, Pathology of Different Types, Animation
https://www.youtube.com/watch?v=WueGqL58tlo
4. Read supplementary references for the topic.
5. Do a quick check of your knowledge of the overview of shock. In your own words, describe
the term given. Write your description down in your Study Notebook. When you’re done,
check the Reading Activity to see how well you did.

READING ACTIVITY:
Overview of Shock
All organs, tissues, and cells need a continuous supply of oxygen to function properly. The lungs first
bring oxygen into the body through ventilation and gas exchange, and the cardiovascular system
(heart, blood, and blood vessels) delivers oxygen by perfusion to all tissues and removes cellular
wastes. Shock is widespread abnormal cellular metabolism that occurs when gas exchange with
oxygenation and tissue perfusion needs are not met sufficiently to maintain cell function. It is a
condition rather than a disease and is the “whole-body” response that occurs when too little oxygen
is delivered to the tissues. All body organs are affected by shock and either work harder to adapt and
compensate for reduced gas exchange or perfusion or fail to function because of hypoxia. Shock is a
“syndrome” because the problems resulting from it occur in a predictable sequence.

Shock
Any problem that impairs oxygen perfusion to tissues and organs can start the syndrome of shock
and lead to a life-threatening emergency. Shock can best be defined as a condition in which systemic
blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular
function (Mikhail, 1999).

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Shock is often a result of cardiovascular problems. Patients in acute care settings are at higher risk,
but shock can occur in any setting. For example, older patients in long-term care settings are at risk
for sepsis and shock related to urinary tract infections. When the body's adaptive adjustments
(compensation) or health care interventions are not effective and shock progresses, severe hypoxia
can lead to cell loss, multiple organ dysfunction syndrome (MODS), and death. Shock is classified
by the type of impairment causing it into the categories of hypovolemic shock, cardiogenic shock,
distributive shock (which includes septic shock, neurogenic shock, and anaphylactic shock), and
obstructive shock. Most manifestations of shock are similar regardless of what starts the process or
which tissues are affected first. These manifestations result from physiologic adjustments
(compensatory mechanisms) that the body makes in the attempt to ensure continued perfusion of vital
organs. These adjustment actions are triggered by the sympathetic nervous system's stress response
activating the endocrine and cardiovascular systems. Manifestations unique to any one type of shock
result from specific tissue dysfunction.

Review of Oxygenation and Tissue Perfusion

Oxygenation with gas exchange and perfusion depend on how much oxygen from arterial blood
perfuses the tissue. Perfusion is related to mean arterial pressure (MAP). The factors that influence
MAP include:
• Total blood volume
• Cardiac output
• Size and integrity of the vascular bed, especially capillaries
Total blood volume and cardiac output are directly related to MAP, so increases in either total blood
volume or cardiac output raise MAP. Decreases in either total blood volume or cardiac output lower
MAP. The size of the vascular bed is inversely (negatively) related to MAP. This means that increases
in the size of the vascular bed lower MAP and decreases raise MAP. The small arteries and veins
connected to capillaries can increase in diameter by relaxing the smooth muscle in vessel walls
(dilation) or decrease in diameter by contracting the muscle (vasoconstriction). When blood vessels
dilate and total blood volume remains the same, blood pressure decreases and blood flow is slower.
When blood vessels constrict and total blood volume remains the same, blood pressure increases and
blood flow is faster. Blood vessels are innervated by the sympathetic nervous system. Some nerves
continuously stimulate vascular smooth muscle so that the blood vessels are normally partially
constricted, a condition called sympathetic tone. Increases in sympathetic stimulation constrict
smooth muscle even more, raising MAP. Decreases in sympathetic tone relax smooth muscle, dilating
blood vessels and lowering MAP. Perfusion (blood flow) to organs varies and adjusts to changes in
tissue oxygen needs. The body can selectively increase blood flow to some areas while reducing flow
to others. The skin and skeletal muscles can tolerate low levels of oxygen for hours without dying or
being damaged. Other organs (e.g., heart, brain, liver, pancreas) do not tolerate hypoxia (low levels
of tissue oxygenation), and a few minutes without oxygen results in serious damage and cell death.

Classification of Shock
Shock can be classified by etiology and may be described as (1) hypovolemic shock, (2) cardiogenic
shock, or (3) circulatory or distributive shock. Some authors identify a fourth category, obstructive
shock, that results from disorders that cause mechanical obstruction to blood flow through the central
circulatory system despite normal myocardial function and intravascular volume.
Examples include pulmonary embolism, cardiac tamponade, dissecting aortic aneurysm, and tension
pneumothorax. In this discussion, obstructive disorders are discussed as examples of noncoronary
cardiogenic shock. Hypovolemic shock occurs when there is a decrease in the intravascular volume.
Cardiogenic shock occurs when the heart has an impaired pumping ability; it may be of coronary or
noncoronary origin. Circulatory shock results from a maldistribution or mismatch of blood flow to
the cells.

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Pathogenesis of shock
◆ Initial stage
◗ Decrease in cardiac output leads to decrease in mean arterial pressure
◗ Sympathetic nervous system is stimulated, leading to initiation of stress response
◗ Signs and symptoms include normal to slightly increased heart rate, normal to slightly decreased
blood pressure, thirst, and pale, cool, moist skin over the face
◆ Compensatory stage
◗ Decrease in mean arterial pressure stimulates the sympathetic nervous system to release
epinephrine and norepinephrine to try to achieve homeostasis
◗ Stimulation of alpha1-adrenergic fibers causes vasoconstriction of vessels in the skin, GI organs,
kidneys, muscles, and lungs, shunting blood to the heart and brain
◗ Stimulation of beta-adrenergic fibers causes vasodilation of coronary and cerebral arteries,
increases heart rate, and increases force of myocardial contractions, resulting in increased cardiac
output
◗ Reduced renal blood fl ow leads to release of renin and production of angiotensin, resulting in
vasoconstriction and stimulation of the adrenal cortex to release aldosterone, increasing renal sodium
reabsorption
◗ Increased serum osmolarity stimulates the release of antidiuretic hormone, resulting in increased
water reabsorption by the kidneys and increased venous blood return to the heart and, ultimately,
increased cardiac output
◗ Signs and symptoms include restlessness, normal or decreasing blood pressure, bounding or
thready pulse, tachycardia, tachypnea, normal or hypoactive bowel sounds, slightly decreased urine
output, and pale, cool skin (flushed and warm in septic shock)
◆ Progressive stage
◗ Compensatory mechanisms become ineffective and possibly even counterproductive
◗ Falling cardiac output and vasoconstriction cause cellular hypoxia and anaerobic metabolism;
metabolic acidosis occurs as lactic acid levels rise
◗ Renal ischemia stimulates the renin-angiotensin-aldosterone system, causing further
vasoconstriction ◗ Fluid shifts from intravascular to interstitial space
◗ Signs and symptoms include falling blood pressure; narrowed pulse pressure; cold, clammy skin;
rapid, shallow respirations; tachycardia; weak, thready, or absent pulses; arrhythmias; absent bowel
sounds; anuria; and subnormal body temperature (subnormal or elevated in septic shock)
◆ Irreversible stage
◗ Compensatory mechanisms are ineffective
◗ Lactic acid continues to accumulate, and capillary permeability dilation increases, resulting in loss
of intravascular volume and tachycardia; this further aggravates falling blood pressure and cardiac
output
◗ Coronary and cerebral perfusion decline, and organ systems fail
◗ Signs and symptoms include unresponsiveness; areflexia; severe hypotension; slow, irregular heart
rate; absent pulses; slow, shallow, irregular respirations; Cheyne-Stokes respirations; and respiratory
and cardiac arrest

Types of Shock
Types of shock vary because shock is a manifestation of a pathologic condition rather than a disease
state. More than one type of shock can be present at the same time. For example, trauma caused by a
car crash may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction
(leading to cardiogenic shock).
Hypovolemic shock occurs when too little circulating blood volume decreases MAP, resulting
in inadequate total body perfusion and oxygenation. Common problems leading to hypovolemic
shock are poor clotting with hemorrhage and dehydration.

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 Cardiogenic shock occurs when the heart muscle is unhealthy and pumping is impaired.
Myocardial infarction is the most common cause of direct pump failure. Any type of pump failure
decreases cardiac output and MAP.
Distributive shock occurs when blood volume is not lost from the body but is distributed to
the interstitial tissues where it cannot perfuse organs. It can be caused by blood vessel dilation,
pooling of blood in venous and capillary beds, and increased capillary leak. All these factors decrease
mean arterial pressure (MAP) and may be started either by nerve changes (neural-induced) or by the
presence of some chemicals (chemical-induced). Neural-induced distributive shock is a loss of MAP
that occurs when sympathetic nerve impulses are decreased and blood vessel smooth muscles relax,
causing vasodilation and poor perfusion. Shock results when vasodilation is widespread. Chemical-
induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak
syndrome. It occurs when certain body chemicals or foreign substances in the blood and vessels start
widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside
the body), but this type of shock also can be induced by substances normally found in the body, such
as excessive amounts of histamine.
Anaphylaxis is an extreme type I allergic reaction. It begins within seconds to minutes after exposure
to a specific allergen in a susceptible person. The result is widespread loss of blood vessel tone, with
decreased blood pressure and decreased cardiac output. Sepsis is a widespread infection that triggers
whole-body inflammation. It leads to distributive shock when infectious microorganisms are present
in the blood and is most commonly called septic shock. Capillary leak syndrome is the response of
capillaries to the presence of body chemicals that enlarge capillary pores and allow fluid to shift from
the capillaries into the interstitial tissues. Once in the interstitial tissue, these fluids are stagnant and
cannot deliver oxygen or remove tissue waste products. Problems causing fluid shifts include severe
burns, liver disorders, ascites, peritonitis, large wounds, kidney disease, hypoproteinemia, and
trauma. Obstructive shock is caused by problems that impair the ability of the normal heart to pump
effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate
filling of the heart or adequate contraction of the healthy heart muscle. The most common cause of
obstructive shock is cardiac tamponade. Although the causes and initial manifestations associated
with the different types of shock vary, eventually the effects of hypotension and anaerobic cellular
metabolism (metabolism without oxygen).
Obstructive shock results from a physical obstruction that reduces cardiac output despite
normal contractility and intravascular volume; it’s caused by pulmonary embolism, dissecting aortic
aneurysm, atrial myxoma, cardiac tamponade, and tension pneumothorax.

Assessment and Diagnostic Findings

Chances of survival depend on the patient’s general health before the shock state as well as the
amount of time it takes to restore tissue perfusion. As shock progresses, organ systems decompensate.
Respiratory Effects The lungs, which become compromised early in shock, are affected at this stage.
Subsequent decompensation of the lungs increases the likelihood that mechanical ventilation will be
needed if shock progresses. Respirations are rapid and shallow. Crackles are heard over the lung
fields. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and carbon dioxide
levels to increase. Hypoxemia and biochemical mediators cause an intense inflammatory response
and pulmonary vasoconstriction, perpetuating the pulmonary capillary hypoperfusion and
hypoxemia. The hypoperfused alveoli stop producing surfactant and subsequently collapse.
Pulmonary capillaries begin to leak their contents, causing pulmonary edema, diffusion abnormalities
(shunting), and additional alveolar collapse. Interstitial inflammation and fibrosis are common as the
pulmonary damage progresses (Fein & Calalang-Colucci, 2000). This condition is sometimes
referred to as acute respiratory distress syndrome (ARDS), acute lung injury (ALI), shock lung, or
noncardiogenic pulmonary edema.
Cardiovascular Effects A lack of adequate blood supply leads to dysrhythmias and ischemia. The
patient has a rapid heart rate, sometimes exceeding 150 bpm.

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The patient may complain of chest pain and even suffer a myocardial infarction. Cardiac enzyme
levels (eg, lactate dehydrogenase, CPK-MB, and cTn-I) rise. In addition, myocardial depression and
ventricular dilation may further impair the heart’s ability to pump enough blood to the tissues to meet
oxygen requirements.
Neurologic Effects As blood flow to the brain becomes impaired, the patient’s mental status
deteriorates. Changes in mental status occur as a result of decreased cerebral perfusion and hypoxia;
the patient may initially exhibit confusion or a subtle change in behavior. Subsequently, lethargy
increases and the patient begins to lose consciousness. The pupils dilate and are only sluggishly
reactive to light.
Renal Effects When the MAP falls below 80 mm Hg (Guyton & Hall, 2000), the glomerular filtration
rate of the kidneys cannot be maintained, and drastic changes in renal function occur. Acute renal
failure (ARF) can develop. ARF is characterized by an increase in blood urea nitrogen (BUN) and
serum creatinine levels, fluid and electrolyte shifts, acid–base imbalances, and a loss of the renal
hormonal regulation of blood pressure. Urinary output usually decreases to below 0.5/mL/kg per hour
(or below 30 mL per hour) but can be variable depending on the phase of ARF. For further
information about ARF, see Chapter 45.
Hepatic Effects Decreased blood flow to the liver impairs the liver cells’ ability to perform metabolic
and phagocytic functions. Consequently, the patient is less able to metabolize medications and
metabolic waste products, such as ammonia and lactic acid. The patient becomes more susceptible to
infection as the liver fails to filter bacteria from the blood. Liver enzymes (aspartate aminotransferase
[AST], formerly serum glutamic-oxaloacetic transaminase [SGOT]; alanine aminotransferase [ALT],
formerly serum glutamate pyruvate transaminase [SGPT]; lactate dehydrogenase) and bilirubin levels
are elevated, and the patient appears jaundiced.
Gastrointestinal Effects Gastrointestinal ischemia can cause stress ulcers in the stomach, placing the
patient at risk for gastrointestinal bleeding. In the small intestine, the mucosa can become necrotic
and slough off, causing bloody diarrhea. Beyond the local effects of impaired perfusion,
gastrointestinal ischemia leads to bacterial toxin translocation, in which bacterial toxins enter the
bloodstream through the lymph system. In addition to causing infection, bacterial toxins can cause
cardiac depression, vasodilation, increased capillary permeability, and an intense inflammatory
response with activetion of additional biochemical mediators. The net result is interference with
healthy cells and their ability to metabolize nutrients (Balk, 2000b; Jindal et al., 2000).
Hematologic Effects The combination of hypotension, sluggish blood flow, metabolic acidosis, and
generalized hypoxemia can interfere with normal hemostatic mechanisms. Disseminated
intravascular coagulation (DIC) can occur either as a cause or as a complication of shock. In this
condition, widespread clotting and bleeding occur simultaneously. Bruises (ecchymoses) and
bleeding (petechiae) may appear in the skin. Coagulation times (prothrombin time, partial
thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require
replacement therapy to achieve hemostasis.

Complications of shock
◆ Myocardial depression may be caused by decreased coronary blood flow and acidosis and can
lead to arrhythmias, MI, and cardiac failure
◆ Acute respiratory distress syndrome, also known as shock lung, may result from decreased
perfusion to pulmonary capillaries
◆ Renal failure may occur when prolonged renal hypoperfusion causes acute tubular necrosis
◆ Hepatic insufficiency may stem from poor perfusion to the liver and can lead to recirculation of
bacteria and cellular debris
◆ Disseminated intravascular coagulation may occur because shock causes excessive consumption
of clotting factors
◆ GI ulcerations may occur when reduced blood fl ow increases acid production

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Nursing interventions
◆ Ensure an adequate airway
◗ Encourage coughing and deep breathing; administer medications for pain as needed to ensure
deep breathing; suction as needed; and position the patient to maintain a patent airway and
maximum ventilation
◗ Turn the patient frequently, and elevate the head of the bed, unless contraindicated
◗ Administer oxygen as prescribed
◗ Perform postural drainage and chest physiotherapy to mobilize secretions
◗ Evaluate breath sounds for crackles and wheezes
◆ Maintain hemodynamic stability
◗ Assess pulse rate and rhythm
◗ Assess blood pressure for changes, using a Doppler ultrasound transducer if a
sphygmomanometer doesn’t provide an audible blood pressure
◆ Maintain a normal temperature
◗ Prevent hypothermia (core temperature less than 95° F [35° C]) by setting the room thermostat
higher, warming the room with infrared lights, covering the patient with warmed blankets, using a
warming mat as prescribed, warming lavage solutions, and using a fluid warmer when infusing I.V.
solutions or blood
◗ Prevent hyperthermia (increase in body temperature and metabolic rate) by removing excess
blankets, administering medications as prescribed to decrease temperature, giving a tepid sponge
bath, and using a cooling mat as prescribed
◆ Maintain normal volume status to prevent fluid imbalance
◗ Assess skin turgor for signs and symptoms of dehydration
◗ Note signs of extreme thirst
◗ Monitor urine output (amount, color, and specific gravity)
◗ Monitor drainage (wound, gastric, and chest tube drainage)
◗ Check for abnormal breath sounds
◗ Assess the patient for weight gain or loss
◗ Infuse fluids as prescribed
◗ Assess blood loss, if possible
◆ Prevent complications of shock
◗ Assess nutritional status to ensure adequate caloric intake to meet metabolic demands
◗ Watch for signs of decreased tissue perfusion, such as changes in skin color and temperature,
level of consciousness (LOC), peripheral pulses, and urine output
◗ Prepare for transfer to the critical care unit if the patient’s status deteriorates
◆ Reduce patient and family anxiety
◗ Explain all procedures in understandable terms
◗ Medicate the patient for pain to ensure patient comfort
◗ Teach the patient relaxation techniques used to reduce anxiety
◗ Give family members time to ask questions and express concerns
◆ Follow infection control policies

Overall Management Strategies in Shock

Management in all types and all phases of shock includes the following:
• Fluid replacement to restore intravascular volume
• Vasoactive medications to restore vasomotor tone and improve cardiac function
• Nutritional support to address the metabolic requirements that are often dramatically increased in
shock.

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 6. Now, read, analyze, and answer the learning tasks below.

TASK 1. CRITICAL THINKING EXERCISE

Instructions: Briefly answer the exercise. (see rubrics for scoring)

Several people are admitted to the critical care unit, including (1) a 79-year-old man with a small
anterior myocardial infarction and no prior cardiac history, (2) a 47-year-old man being given contrast
media during a diagnostic procedure, (3) a 17-year-old adolescent with a cervical spine injury after a
diving accident, and (4) a 72-year-old woman who was admitted with a bowel perforation caused by
intestinal malignancy. Discuss what additional assessment information is needed to determine which
of these patients has the potential to develop shock and the rationale for your decision.

TASK 2. ASSESSING YOUR UNDERSTANDING

Instructions: List down at least three (3) common key features of shock based on specific tissue
dysfunction/manifestations. (1 point each item)

Tissue/Organ Key Features/Manifestations

Cardiovascular
Respiratory
Gastrointestinal
Neuromuscular
Kidney
Integumentary

TASK 3. APPLYING YOUR KNOWLEDGE

Instructions: Briefly answer the following. (see rubrics for scoring)
1. Name three medical management goals for cardiogenic shock.
2. Discuss the four stages of hypovolemic shock.

TASK 4. CASE STUDY

Instructions: Consider the scenarios and answer the questions. Write down your answers in a separate
sheet of paper. At a minimum, you must cite the journal, textbook, article, and other reading materials.
Make sure to cite any references you use. Use APA style (7th edition) for proper citation format for
your references. (see rubrics for scoring)
1. A new nurse on your medical unit tells you that she believes a patient with myocardial
infarction is going into shock. She does not know if the patient is experiencing anaphylactic
shock related to a medication he received or cardiogenic shock due to his cardiac disorder.
How would you differentiate between anaphylactic and cardiogenic shock, and what medical
treatments would you anticipate?
2. An elderly man is admitted from a nursing home with a recent onset of confusion and
combative behavior. You know that sudden changes in mental status may be an early sign of
sepsis in the elderly. How would you assess this patient for the possibility of septic shock,
and how would the management of the elderly patient differ from that of a younger patient?

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Rubrics
Features 5 4 3 2 1
Focus/Analysis All key aspects Only modest Some potential Adequate in Weak
The single identified and abstraction connections parts; gaps in progression of
controlling point is related beyond facts; missed the logical ideas
made with an overly development
awareness of the derivative
task about a specific
topic.
Task achievement Fully addresses Sufficiently Presents a Presents Arranges
Fulfillment of the all parts of the addresses all clear position relevant ideas information and
task being task parts of the task but there may but some may ideas but an
presented by the be a tendency be inadequately unclear
activity. that the developed progression
supporting
ideas may lack
position
Relevance/ The task makes The task makes The task makes The task makes The task makes
Connections appropriate some unclear or undistinguishab no connections
Relation of the task connections appropriate inappropriate le connections between the
to the between the connections connections between the purpose and
concepts/ideas purposes and between the between the purposes and features of the
features of the purposes and purposes and features of the ideas/concepts
ideas/concepts features of the features of the ideas/concepts
ideas/concepts ideas/concepts

Guidelines:
The following instructions shall apply:
1.Free medium to use. You can convert your answer sheet in the following format:
a. Picture/Image b. PDF file c. Microsoft Word
2. Submit your answer to our Google Classroom/GC LAMP and use your GC domain google account.
3. You may also use the GC Academic Assistance Desk for the submission of accomplished modules.
4. At a minimum, you must cite the journal, textbook, article, and other reading materials. Make sure
to cite any references you use. Use APA style (7th edition) for proper citation format for your
references.
VI. References (Online Sources/E-books)
Brunner, L. S. (2014). Study guide for Brunner & Suddarth's textbook of medical-surgical
nursing, 13th edition (Philippine). Lippincott Williams & Wilkins.
Ignatavicius, D. D., & Workman, M. L. (2016). Medical-surgical nursing: patient-centered
collaborative care (8th ed.). Elsevier Saunders.
Smeltzer, S. C., Brunner, L. S., & Suddarth, D. S. (2010). Brunner and Suddarth's textbook of
medical-surgical nursing (12th). Wolters Kluwer. https://www.pdfdrive.com/brunner-and-
suddarths-textbook-of-medical-surgical-nursing-two-volume-set-twelfth-edition-
e162158494.html.
Smeltzer, S. C. E. (2003). Brunner and Suddarth's textbook of medical-surgical nursing. 10th ed.
Lippincott Williams & Wilkins.

NURSING CARE MANAGEMENT 118-1ST SEM 2021-2022. NOT FOR SALE. EXCLUSIVE FOR GORDON COLLEGE ONLY.
 Timby, B. K., & Smith, N. E. (2010). Introductory medical-surgical nursing. Wolters Kluwer
Health/Lippincott Williams & Wilkins.

Wolters Kluwer Health/Lippincott Williams & Wilkins. (2012). Lippincott's review for medical-
surgical nursing certification.

YOU HAVE COMPLETED MODULE 7.2. WELL DONE!

It’s now time for you to discuss your insights and reflections with
your classmates in the Online Discussion. Coordinate with your
Lecturer for the final details and clarifications of the topic. Before
Online Session, make sure you have organized your ideas in your
Study Notebook at hand.
Once you have completed, you may proceed to Module 8.

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