A report by:

Torregosa, Cyrus Dan

I. Pleural Effusion
Pleural effusion is excess fluid that accumulates in the fluid-filled space that surrounds
the lungs. Excessive amounts of such fluid can impair breathing by limiting the expansion of the
lungs during inspiration. It is a rarely a primary disease process but is usually occurs secondary
to other disease. Normally the pleural space contains a small amount of liquid (5-15 ml) which
acts as a lubricant that allows the pleural surfaces to move without friction.

Types of fluids
Four types of fluids can accumulate in the pleural space:
 Serous fluid (hydrothorax)
 Blood (hemothorax)
 Chyle (chylothorax)
 Pus (pyothorax or empyema)

 Diagnosis
Effusion fluid often settles at the lowest space due to gravity.
Pleural effusion is usually diagnosed on the basis of medical history and physical exam,
and confirmed by chest x-ray. Once accumulated fluid is more than 500 ml, there are usually
detectable clinical signs in the patient, such as decreased movement of the chest on the
affected side, dullness to percussion over the fluid, diminished breath sounds on the affected
side, decreased vocal resonance and fremitus (though this is an inconsistent and unreliable
sign), and pleural friction rub. Above the effusion, where the lung is compressed, there may be
bronchial breathing.

 Causes
Because pleural effusion formation is a manifestation of underlying disease as opposed
to being a disease process in itself, many underlying etiologies may exist. Pleural effusions are
generally classified as transudates or exudates, based on the mechanism of fluid formation and
pleural fluid chemistry. Transudates result from an imbalance in oncotic and hydrostatic
pressures, whereas exudates are the result of inflammation of the pleura or decreased
lymphatic drainage. In some cases, the pleural fluid may have some characteristics of both
transudatives and exudatives. The etiologic spectrum of pleural effusion is extensive. However,
most pleural effusions are caused by congestive heart failure, pneumonia, malignancy, or
pulmonary embolism.
Transudates
Systemic factors that govern formation of transudates include increased systemic and/or
pulmonary capillary hydrostatic pressure (elevated pulmonary capillary wedge pressure of 10
cm H2 O or higher), decreased colloid osmotic pressure in the systemic circulation, or both.
Pleural membranes are intact and are not involved in pathogenesis of the fluid formation. The
permeability of pleural capillaries to proteins is normal.
Conditions associated with transudate formation include the following:
o Congestive heart failure
o Cirrhosis
o Nephrotic syndrome
o Urinothorax (usually due to obstructive uropathy)
o Myxedema
o Cerebrospinal fluid leaks to the pleura (generally in the setting of
ventriculopleural shunting, or trauma or surgery to the thoracic spine)
o Peritoneal dialysis
o Duropleural fistula (rare but may be a complication of spinal cord surgery)
o Extravascular migration of central venous catheter
Exudates
Local factors governing formation of exudates include altered permeability of pleural
membranes, increased capillary wall permeability or vascular disruption, and decreased or
complete obstruction of lymphatic drainage of pleural space. Pleural membranes are involved
in pathogenesis of the fluid formation. Permeability of pleural capillaries to proteins is high,
resulting in elevated protein content.
Conditions associated with exudates formation include the following:
Malignancy (most commonly lung or breast cancer, lymphoma, and leukemia; less
commonly ovarian carcinoma, stomach cancer, sarcomas, melanoma)
o Pneumonia (often associated with treatment failure)
o Tuberculosis
o Pulmonary embolism
o Fungal infection
o Pancreatic pseudocyst
o Intra-abdominal abscess
o Status-post coronary artery bypass graft surgery
o Postcardiac injury syndrome
o Pericardial disease
o Rheumatoid pleuritis
o Systemic lupus erythematosus
o Asbestos-related pleural disease
o Uremia
o Trapped lung (localized pleural scarring with the formation of a fibrin peel prevents
incomplete lung expansion, at times leading to pleural effusion)
o Extravascular migration of central venous catheter
o Fistula (pancreaticopleural, ventriculoperitoneal, ventriculopleural, biliopleural,
gastropleural)
  Signs and Symptoms
The clinical manifestations of pleural effusion are variable and often are related to the
underlying disease process. The most commonly associated symptoms are progressive dyspnea,
cough, and pleuritic chest pain.
 Dyspnea
o Dyspnea is the most common symptom at presentation and generally indicates
the presence of a large effusion.
o It is reported to occur in 50% of patients with malignant pleural effusions.
o Other factors (eg, underlying lung disease, cardiac dysfunction, anemia) may also
contribute to the development of dyspnea.
 Chest pain
o Chest pain in this setting results from pleural irritation, which can aid in
determining the etiology of the effusion, since most transudative effusions do
not cause direct pleural irritation. Its presence raises the likelihood of an
exudative etiology such as pleural infection, mesothelioma, or pulmonary
infarction.
o Pain may be mild or severe. It is typically described as sharp or stabbing and is
exacerbated with deep inspiration.
o Pain may be localized to the chest wall or referred to the ipsilateral shoulder or
upper abdomen, usually because of diaphragmatic involvement.
o Pain often diminishes in intensity as the pleural effusion increases in size.
 Other symptoms occurring with pleural effusions are associated with the underlying
disease process.
o Increasing lower extremity edema, orthopnea, and paroxysmal nocturnal
dyspnea may all occur with congestive heart failure.
o Night sweats, fever, hemoptysis, and weight loss should
suggest tuberculosis (TB).
o Hemoptysis also raises the possibility of malignancy, other endotracheal or
endobronchial pathology, or pulmonary infarction.
o An acute febrile episode, purulent sputum production, and pleuritic chest pain
may occur in patients with an effusion associated with pneumonia.

 Pathophysiology
Pleural effusion is an indicator of an underlying disease process that may be pulmonary or
nonpulmonary in origin, acute or chronic.
 Normal pleural fluid has the following characteristics:
o Clear ultrafiltrate of plasma that originates from the parietal pleura
o pH 7.60-7.64
o Protein content less than 2% (1-2 g/dL)
o Fewer than 1000 WBCs per cubic millimeter
o Glucose content similar to that of plasma
o Lactate dehydrogenase (LDH) less than 50% of plasma
 o Sodium, potassium, and calcium concentration similar to that of the interstitial
fluid
 The following mechanisms play a role in the formation of pleural effusion:
o Altered permeability of the pleural membranes (eg, inflammation,
malignancy, pulmonary embolus)
o Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, cirrhosis)
o Increased capillary permeability or vascular disruption (eg, trauma, malignancy,
inflammation, infection, pulmonary infarction, drug hypersensitivity,
uremia, pancreatitis)
o Increased capillary hydrostatic pressure in the systemic and/or pulmonary
circulation (eg, congestive heart failure, superior vena cava syndrome)
o Reduction of pressure in the pleural space, preventing full lung expansion (eg,
extensive atelectasis, mesothelioma)
o Decreased lymphatic drainage or complete blockage, including thoracic duct
obstruction or rupture (eg, malignancy, trauma)
o Increased peritoneal fluid, with migration across the diaphragm via the
lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis)
o Movement of fluid from pulmonary edema across the visceral pleura
o Persistent increase in pleural fluid oncotic pressure from an existing pleural
effusion, causing further fluid accumulation
The net result of effusion formation is a flattening or inversion of the diaphragm,
mechanical dissociation of the visceral and parietal pleura, and a restrictive ventilatory defect.

 Medical Management
The free end of the Chest Drainage Device is usually attached to
an underwater seal, below the level of the chest. This allows the air or fluid to
escape from the pleural space, and prevents anything returning to the chest.
Treatment depends on the underlying cause of the pleural effusion.
Therapeutic aspiration may be sufficient; larger effusions may require
insertion of an intercostal drain (either pigtail or surgical). When managing
these chest tubes it is important to make sure the chest tubes do not become
occluded or clogged. A clogged chest tube in the setting of continued
production of fluid will result in residual fluid left behind when the chest tube
is removed. This fluid can lead to complications such as hypoxia due to lung
collapse from the fluid, or fibrothorax, late, when the space scars down.
Repeated effusions may require chemical
(talc, bleomycin, tetracycline/doxycycline) or surgical pleurodesis, in which
the two pleural surfaces are scarred to each other so that no fluid can
accumulate between them. This is a surgical procedure that involves inserting
a chest tube, then either mechanically abrading the pleura, or inserting the chemicals to induce
a scar. This requires the chest tube to stay in until the fluid drainage stops. This can be days to
weeks and can require prolonged hospitilizations. If the chest tube becomes clogged fluid will
be left behind and the pleurodesis will fail.
 Pleurodesis fails in as many as 30% of cases. Other treatments for malignant pleural
effusions include surgical pleurectomy, insertion of a small catheter attached to the drainage
bottle for outpatient management (Pleurex catheter), or implantation of a pleuroperitoneal
shunt which consists of two catheters connected by a pump chamber containing two-one way
valves. Fluids moves from the pleural space to the pump chamber and then to the peritoneal
cavity. The patient manually pumps on the reservoir daily to move fluid from the pleural space
to the peritoneal space. Once a pleural effusion is diagnosed, the cause must be determined.
Pleural fluid is drawn out of the pleural space in a process called thoracentesis. A needle is
inserted through the back of the chest wall in the sixth, seventh or eighth intercostal space on
the midaxillary line, into the pleural space. The fluid may then be evaluated for the following:
1. Chemical composition including protein, lactate
dehydrogenase (LDH), albumin, amylase, pH and glucose
2. Gram stain and culture to identify possible bacterial infections
3. Cell count and differential
4. Cytopathology to identify cancer cells, but may also identify some infective organisms
5. Other tests as suggested by the clinical situation - lipids, fungal culture, viral culture,
specific immunoglobulins

 Nursing Management
Implementing Medical Regimen:
 Prepares and positions the patient for thoracentesis
 Offers support all throughout the procedure
 Record and send thoracentesis fluid amount to laboratory for testing
 Monitoring the system’s function of chest tube drainage and water seal drainage and
recording the amount drainage at prescribed intervals.
 If the patient is to be managed as an outpatient with a pleural catheter for drainage,
the nurse is responsible for educating the patient and the family regarding management
and care of the catheter and drainage system

II. Cardiac Tamponade

Cardiac tamponade also known as pericardial tamponade, is an emergency condition in

which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid
significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling
properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of
blood, shock, and often death.
Cardiac tamponade occurs when the pericardial space fills up with fluid faster than the
pericardial sac can stretch. If the amount of fluid increases slowly (such as in hypothyroidism)
the pericardial sac can expand to contain a liter or more of fluid prior to tamponade occurring.
If the fluid occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml
can cause tamponade.
  Diagnosis
Initial diagnosis can be challenging, as there are a number of differential diagnoses,
including tension pneumothorax, and acute heart failure. In a trauma patient presenting with
PEA (pulseless electrical activity) in the absence of hypovolemia and tension pneumothorax, the
most likely diagnosis is cardiac tamponade.
Classical cardiac tamponade presents three signs, known as Beck's
triad. Hypotension occurs because of decreased stroke volume, jugular-venous distension due
to impaired venous return to the heart, and muffled heart sounds due to fluid inside the
pericardium.
Other signs of tamponade include pulsus paradoxus (a drop of at least 10mmHg in
arterial blood pressure on inspiration), and ST segment changes on
the electrocardiogram, which may also show low voltage QRS complexes, as well as general
signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of
consciousness).
Tamponade can often be diagnosed radiographically, if time allows. Echocardiography,
which is the diagnostic test of choice**, often demonstrates an enlarged pericardium or
collapsed ventricles, and a chest x-ray of a large cardiac tamponade will show a large, globular
heart.

 Causes
Tamponade can occur as a result of any type of pericarditis.
 HIV infection
 Infection - Viral, bacterial (tuberculosis), fungal
 Drugs - Hydralazine, procainamide, isoniazid, minoxidil
 Postcoronary intervention (ie, coronary dissection and perforation)
 Trauma to the chest
 Cardiovascular surgery (postoperative pericarditis)
 Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome)
 Connective tissue diseases -Systemic lupus erythematosus, rheumatoid
arthritis, dermatomyositis
 Radiation therapy to the chest
 Iatrogenic - After sternal biopsy, transvenous pacemaker lead
implantation, pericardiocentesis, or central line insertion
 Uremia
 Anticoagulation treatment
 Idiopathic pericarditis
 Complication of surgery at the esophagogastric junction such as antireflux surgery
 Pneumopericardium (due to mechanical ventilation or gastropericardial fistula)
 Other causes include hypothyroidism, acupuncture, Still disease, and Duchenne
muscular dystrophy
 Type A aortic dissection
Other Problems to Be Considered
Large pleural effusion: Cases of cardiac tamponade have been reported with large
pleural effusions. The increased intrapleural pressure resulting from large pleural effusions can
be transmitted to the pericardial space and impair ventricular filling, thus simulating the
hemodynamic equivalent of cardiac tamponade.
Tension pneumopericardium: The hemodynamic changes simulate acute cardiac
tamponade. Clinically, distant heart sounds, bradycardia, and shifting tympany occur over the
precordium and a characteristic murmur is heard, termed bruit de la roue de moulin. This is
usually observed in infants with mechanical ventilation but is also observed after sternal bone
marrow aspiration, penetrating chest wall injury, esophageal rupture, and bronchopericardial
fistula.
Rapid and labored breathing: Large decreases in intrathoracic pressure with deep
inspirations, often observed during respiratory failure, can accentuate the pulsus paradoxus,
simulating pericardial tamponade.

 Signs and Symptoms

In a retrospective study, the most common symptoms noted by Roy et al are dyspnea,
tachycardia, and elevated jugular venous pressure. Evidence of chest wall injury may be present
in trauma patients. Tachycardia, tachypnea, and hepatomegaly are observed in more than 50%
of patients with cardiac tamponade, and diminished heart sounds and a pericardial friction rub
are present in approximately one third of patients. Some patients may present with dizziness,
drowsiness, or palpitations. Cold, clammy skin and weak pulse due to hypotension are also
observed in patients with tamponade.
 The Beck triad or acute compression triad
o Described in 1935, this complex of physical findings refers to increased jugular
venous pressure, hypotension, and diminished heart sounds.
o These findings result from a rapid accumulation of pericardial fluid. However,
this classic triad is usually observed in patients with acute cardiac tamponade.
 Pulsus paradoxus or paradoxical pulse
o This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in
systemic blood pressure.
o To measure the pulsus paradoxus, patients are often placed in a semirecumbent
position; respirations should be normal. The blood pressure cuff is inflated to at
least 20 mm Hg above the systolic pressure and slowly deflated until the first
Korotkoff sounds are heard only during expiration. At this pressure reading, if the
cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff
sound is not audible during inspiration. As the cuff is further deflated, the point
at which the first Korotkoff sound is audible during both inspiration and
expiration is recorded. If the difference between the first and second
measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is
present.
 o The paradox is that while listening to the heart sounds during inspiration, the
pulse weakens or may not be palpated with certain heartbeats, while S1 is heard
with all heartbeats.
o A pulsus paradoxus can be observed in patients with other conditions, such as
constrictive pericarditis, severe obstructive pulmonary disease, restrictive
cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right
ventricular infarction with shock.
o A pulsus paradoxus may be absent in patients with markedly elevated LV
diastolic pressures, atrial septal defect, pulmonary hypertension, and aortic
regurgitation.
 Kussmaul sign
o This was described by Adolph Kussmaul as a paradoxical increase in venous
distention and pressure during inspiration.
o This sign is usually observed in patients with constrictive pericarditis but
occasionally is observed in patients with effusive-constrictive pericarditis and
cardiac tamponade.
 Ewart sign
o Also known as the Pins sign, this is observed in patients with large pericardial
effusions.
o It is described as an area of dullness, with bronchial breath sounds and
bronchophony below the angle of the left scapula.
 The y descent
o The y descent is abolished in the jugular venous or right atrial waveform.
o This is due to an increase in intrapericardial pressure, preventing diastolic filling
of the ventricles.
 Dysphoria: Behavioral traits such as restless body movements, unusual facial
expressions, restlessness, sense of impending death were reported by Ikematsu in about
26% patients with cardiac tamponade.5
 Low-pressure tamponade: In severely hypovolemic patients, classical physical findings
such as tachycardia, pulsus paradoxus, and jugular venous distension were infrequent.
Sagrista-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac
tamponade. They also reported low-pressure tamponade in 10% of large pericardial
effusions.

 Pathophysiology
The pericardium, which is the membrane surrounding the heart, is composed of 2 layers.
The thicker parietal pericardium is the outer fibrous layer; the thinner visceral pericardium is
the inner serous layer. The pericardial space normally contains 20-50 mL of fluid. Pericardial
effusions can be serous, serosanguineous, hemorrhagic, or chylous.
Reddy et al describe 3 phases of hemodynamic changes in tamponade.
 Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle,
requiring a higher filling pressure. During this phase, the left and right ventricular filling
pressures are higher than the intrapericardial pressure.
  Phase II: With further fluid accumulation, the pericardial pressure increases above the
ventricular filling pressure, resulting in reduced cardiac output.
 Phase III: A further decrease in cardiac output occurs, which is due to equilibration of
pericardial and left ventricular (LV) filling pressures.
The underlying pathophysiologic process for the development of tamponade is markedly
diminished diastolic filling because transmural distending pressures are insufficient to
overcome the increased intrapericardial pressures. Tachycardia is the initial cardiac response to
these changes to maintain the cardiac output.
Systemic venous return is also altered during tamponade. Because the heart is compressed
throughout the cardiac cycle due to the increased intrapericardial pressure, systemic venous
return is impaired and right atrial and right ventricular collapse occurs. Because the pulmonary
vascular bed is a vast and compliant circuit, blood preferentially accumulates in the venous
circulation, at the expense of LV filling. This results in reduced cardiac output and venous
return.
The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on
the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as
little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely
impede cardiac output2 , whereas 1000 mL of fluid may accumulate over a longer period
without any significant effect on diastolic filling of the heart. This is due to adaptive stretching
of the pericardium over time. A more compliant pericardium can allow considerable fluid
accumulation over a longer period without hemodynamic insult.

 Management
Cardiac tamponade is a medical emergency. Preferably, patients should be monitored in an
intensive care unit.
 All patients should receive the following:
o Oxygen
o Volume expansion with blood, plasma, dextran, or isotonic sodium chloride
solution, as necessary to maintain adequate intravascular volume.
o Bed rest with leg elevation: This may help increase venous return.
o Inotropic drugs (eg, dobutamine): These can be useful because they do not
increase systemic vascular resistance while increasing cardiac output.
 Positive-pressure mechanical ventilation should be avoided because it may decrease
venous return and aggravate signs and symptoms of tamponade.
 Further medical care includes pericardiocentesis. Removal of pericardial fluid is the
definitive therapy for tamponade and can be done by the following 3 methods.
o Emergency subxiphoid percutaneous drainage: This is a life-saving bedside
procedure. The subxiphoid approach is extrapleural; hence, it is the safest for
blind pericardiocentesis. A 16- or 18-gauge needle is inserted at an angle of 30-
45° to the skin, near the left xiphocostal angle, aiming towards the left shoulder.
When performed emergently, this procedure is associated with a reported
mortality rate of approximately 4% and a complication rate of 17%.
 o Echocardiographically guided pericardiocentesis (often performed in the cardiac
catheterization laboratory): This is usually performed from the left intercostal
space. First, mark the site of entry based on the area of maximal fluid
accumulation closest to the transducer. Then, measure the distance from the
skin to the pericardial space. The angle of the transducer should be the
trajectory of the needle during the procedure. Avoid the inferior rib margin while
advancing the needle to prevent neurovascular injury. Leave a 16-gauge catheter
in place for continuous drainage.
o Percutaneous balloon pericardiotomy: This can be performed using an approach
similar to that for echo-guided pericardiocentesis, in which the balloon is used to
create a pericardial window.
 Patients should receive treatment of the underlying cause to prevent recurrence.

Surgical Care
For a hemodynamically unstable patient or one with recurrent tamponade, provide the
following care:
 Surgical creation of a pericardial window: This involves the surgical opening of a
communication between the pericardial space and the intrapleural space. This is usually
a subxiphoidian approach with resection of xiphoid. Recently, a left paraxiphoidian
approach with preservation of xiphoid has been described.Open thoracotomy and/or
pericardiotomy3 may be required in some cases, and these should be performed by an
experienced surgeon.
 Pericardiocentesis or sclerosing the pericardium: This is a therapeutic option for
patients with recurrent pericardial effusion or tamponade. Through the intrapericardial
catheter, corticosteroids, tetracycline, or antineoplastic drugs (eg, anthracyclines,
bleomycin) can be instilled into the pericardial space.
 Pericardio-peritoneal shunt: In some patients with malignant pericardial effusions,
creation of a pericardio-peritoneal shunt helps prevent recurrent tamponade.
 Pericardiectomy: Resection of the pericardium (pericardiectomy) through a median
sternotomy or left thoracotomy is rarely required to prevent recurrent pericardial
effusion and tamponade.
Medication
The role of medication therapy in cardiac tamponade is limited. Occasionally, inotropic agents
that do not increase the peripheral vascular resistance, such as dobutamine, may be used.
Adrenergic agonist agents
By stimulating beta-1 receptors in the heart, stroke volume and cardiac output are increased.

Dobutamine (Dobutrex)
Synthetic catecholamine and a direct inotropic agent that stimulates cardiac beta-
receptors with minimal increase in systemic vascular resistance.
 LICEO DE CAGAYAN UNIVERSITY SCORE: ________
COLLEGE OF NURSING
N103

TEACHING LEARNING GUIDE

Topic : Pleural Effusion and Cardiac Tamponade Date and Time : September 15, 2010
Level of student : N103- Section A, Group C2 Reporter : Torregosa, Cyrus Dan A., SN
Venue : Liceo de Cagayan University Campus, HB Room
C.I. : Mrs. Gina Batasin-in, RN, MN

General Objective: At the end of 35 minutes, I will be able to present and discuss effectively the disease topic about Pleural Effusion and Cardiac
Tamponade assigned to me, as well as, the students will gain and increase knowledge from the discussion.

Specific Objective Content Time Teaching Learning Evaluation Reference

Allotment Activities
Teacher Student Books:
At the end of 35 minutes, the Brief discussion of the
students will be able to: Pleural Effusion and “Textbook of Medical-
Cardiac Tamponade Ask Active Surgical Nursing”, 11th
a.Acquire new knowledge about assigned to me: questions listening Quiz Edition, Volume I,
Pleural Effusion and Cardiac and give and (Post- Test) pp.652-654,
Tamponade and verbalize  Definition 35 min further participa- 680”.Lippincott Wiliams
the understanding about it  Causes/Risk Factors information tion. and Wilkins 2008.
 Signs and Symptoms regarding
b.Know the causes, signs and  Diagnostic Exams the topic. Ask Internet Sources:
symptoms, treatment and  Treatment and questions.
management of the disease. Management  http://en.wikipedia.org/
wiki/pleuraleffusion
 http://en.wikipedia.org/
wiki/Cardiac_tampona
de
 http://emedicine.medsc
ape.com/article/15208
 LICEO DE CAGAYAN UNIVERSITY SCORE: ________
COLLEGE OF NURSING
N103

TEACHING LEARNING GUIDE

Topic : The Surgical Experience Date and Time : September 09, 2010
Level of student : N103- Section A, Group C2 Reporter : Torregosa, Cyrus Dan A., SN
Venue : Liceo de Cagayan University Campus, HB Room
C.I. : Mr. Roberto Alli III, RN, MN

General Objective: At the end of 25 minutes, I will be able to present and discuss effectively the topic about the Intra-operative Nursing
Management specifically the Surgical Experience assigned to me, as well as, the students will gain and increase knowledge from the discussion.

Specific Objective Content Time Teaching Learning Evaluation Reference

Allotment Activities
Teacher Student
At the end of 25 Brief discussion of the
minutes, the expanded Intra-operative Books:
students will be able Nursing Management: Ask Active
to: Surgical Experience questions listening and Quiz “Textbook of Medical-Surgical
assigned to me: and give participation (Post- Test) Nursing”, 11th Edition, Volume
c. Acquire new -Types of Anesthesia and 25 min further . I, pp.508-516 ”.Lippincott
knowledge Sedation information Wiliams and Wilkins 2008.
about the Intra-  General Anesthesia regarding Ask
operative  Regional Anesthesia the topic. questions.
Nursing  Moderate Sedation Internet Sources:
Management:  Monitored
Surgical Anesthesia Care http://en.wikipedia.org/wiki/Ane
Experience and  Local Anesthesia sthetic
verbalize the
understanding
about it