Untitled

Scribd
* Explore
* Community
Upload a Document
Search Books, Presentations, Business, Academics...
* LoginSpinner_mac_gray
* musicath_07
o My Home
o View Public Profile
o My Documents
o My Collections
o Messages
o Settings
o Help
o Log Out
1
First Page
Previous Page
Next Page
/ 71
Zoom Out
Zoom In
Fullscreen
Exit Fullscreen
Select View Mode
View Mode
BookSlideshowScroll
Readcast
Add a Comment
Embed & Share
Readcast
Reading should be social! Post a message on your social networks to let others k
now what you're reading. Select the sites below and start sharing.
Check_27x27Transparent
Check_27x27TransparentLink account
Check_27x27TransparentLink account
Readcast this DocumentTransparent
Readcast Complete!
Click 'send' to Readcast!
edit preferences
Set your preferences for next time... Choose 'auto' to readcast without being pr
ompted.
musicath_07
Link account
Link account
AdvancedCancel
Share & Embed
Link / URL:
Embed Size & Settings:
* Width: Auto
* Height: (proportional to specified width)
* Start on page:
* Preview View:
More share options
Add to Collections
Download
Auto-hide: on
1
ACUTE BIOLOGIC CRISES (24 HOURS)
COURSE OUTLINE
1. High Risk Adult (8 hours)
A. Respiratory Disorders
i. Pulmonary Embolism
ii. Acute Respiratory Distress Syndrome (ARDS)
iii. Respiratory Failure
a. Acute RF
b. Chronic RF
iv. Mechanical Ventilators
B. Endocrine/ Metabolic Disorders
i. Diabetic Ketoacidosis (DKA)
ii. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)
iii. Thyrotoxic Crisis (Thyroid Storm)
iv. Adrenal Crisis (Peochromocytoma)
v. Hepatic Failure (Hepatic Coma)
C. Renal Disorders
i. Renal Failure
a. Acute RF
b. Chronic RF
D. Cardiovascular Disorders
i. Angina Pectoris
ii. Myocardial Infarction
iii. Congestive Heart Failure
a. Right-sided CF
b. Left-sided CF
iv. Cardiogenic Shock
v. Thromboembolism
vi. Pericardial Effusion & Cardiac Tamponade
vii. Cardiac Arrest
viii. Dysrhythmias
a. Sinus Node
1. Sinus Bradycardia
2. Sinus Tachycardia
b. Atrial Dysrhythmias
1. Premature Atrial Complex (PAC)
2. Atrial Flutter
3. Atrial Fibrillation
c. Junctional Dysrhythmias
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
2
d. Ventricular Dsyrhythmias
1. Premature ventricular Complex
2. Ventricular Tachycardia
3. Ventricular Fibrillation
4. Ventricular Asystole
E. Burns
2.High Risk Pregnancy (12 Hours)
Part I.
A. Infections
i. STDsa. Cndidiasis
b. Trichomoniasis
c. Bacterial Vaginosis (Gardnerella)
d. Chlamydia Trachomatis
e. Syphilis
f. Gonorrhea
g. HPV
h. Group B Streptococci
i.
HIV
ii. TORCH infections
B. Hematologic Disorders
i. Anemias
a. Iron Deficiency
b. Folic Acid Deficiency
c. Sickle Cell
ii. Coagulation Disorders
a. Idiopathic Thrombocytopenic Purpura
C. Renal and Urinary Disorders
i. UTI
ii. Chronic Renal Disease
D. Respiratory Disorders
i. Acute Nasopharyngitis
ii. Influenza
iii. Pneumonia
iv. Asthma
v. Tuberculosis
vi. Cystic Fibrosis
NCM 104 1st sem S.Y. 2007-2008
3
E. Rheumatic Disorders
i. Juvenile Rheumatoid Arthritis
ii.Systemic Lupus Erythematosus (SLE)
F. Gastrointestinal Disorders
i. Appendicitis
ii. Hiatal Hernia
iii. Cholecystitis & Cholelithiasis
iv. Viral Hepatitis
v. Inflammatory Bowel Disease
G. Neurologic Disorders
i. Siezure
ii. Myasthenia Gravis
iii. Multiple Sclerosis
H. Musculoskeletal Disorders
i. Scoliosis
I. Cardiovascular Disorders
i. Left Sided Heart Failure
ii. Right Sided heart Failure
iii. Peripartal Heart Disease
iv. Artificial valve Prosthesis
v. Chronic hypertensive Vascular Disease
vi. Venous Thromboembolic Disease
J. Endocrine Disorders
i. Thyroid Dysfunction
a. Hypothyroidism
b. Hyperthyroidism
ii. Diabetes Mellitus
iii. Gestational Diabetes
iv. Hyperglycemia
K. Mental Illness
L. Trauma
i. Trauma Care
ii. Open wounds
iii. Battered woman
PART II. COMPLICATIONS OF PREGNANCY
A. Bleeding During Pregnancy
i.
First Trimester Bleeding
a. Abortion
NCM 104 1st sem S.Y. 2007-2008
4
1. Spontaneous
2. Threatened
3. Imminent
4. Complete
5. Incomplete
6. Missed
7. Recurrent
8. Complications of Abortionb. Ectopic pregnancy
ii.
Second Trimester Bleeding
a. Gestational Trophoblastic Disease (H. Mole)
b. Incompetent Cervix
iii.
Third Trimester Bleeding
a. Placenta Previa
b. Abruptio Placenta
iv.
Preterm labor
v.
Disseminated Intravascular Coagulation (DIC)
vi.
Preterm Rupture of Membrane (PROM)
vii.
Pregnancy Induced Hypertension (PIH)
a. Mild Preeclampsia
b. Severe Preeclampsia
c. Eclampsia
d. HELLP Syndrome
viii.
Multiple Pregnancy
ix.
Polyhydramnios
x.
Post term pregnancy
xi.
Psuedocyesis
xii.
Isoimmunization (RH Incompatibility)
xiii.
Fetal Death
3. High Risk Newborn (4 hours)
A. Part I
i. Small-for-Gestational-Age Infant ii. Large-for-Gestational-Age Infant iii. Pr
eterm Infant
iv. Post Term Infant
B. Part II: Illness of the Newborn
i. Respiratory Distress Syndrome
NCM 104 1st sem S.Y. 2007-2008
5
ii. Transient Tachypnea
iii. Meconium Aspiration Syndrome
iv. Apnea
v. Sudden Infant Death Syndrome (SIDS)
vi. Preventricular Leukomalacia (PVL)
vii. Hyperbilirubinemia
viii. Erythroblastosis Fetalis
a. RH incompatibility
b. ABO incompatibility
ix. Hemorrhagic Disease
x. Twin-to-twin Transfusion
xi. Necrotizing Enterocolitis
C. The Newborn at risk due to:
i. Maternal Infection
a. Group B Hemolytic Streptococcal Infection
b. Congenital Rubella
c. Ophthalmia Neonatorum
d. Hepatitis B
e. Generalized Herpes Virus
ii. Maternal Illness
a. Diabetic Mother
b. Drug Dependent Mother
c. Fetal Alcohol Syndrome (FAS)
NCM 104 1st sem S.Y. 2007-2008
6
ACUTE BIOLOGIC CRISES
HIGH RISK ADULT
RESPIRATORY DISORDERS
PULMONARY EMBOLISM
Occurs when a pulmonary embolus [thrombotic (blood clot) or nonthrombotic (fat)
emboli] lodges in the pulmonary artery system. This
blockage obstructs blood flow to the lung tissue supplied by the affected vessel
. Thrombotic emboli mainly originate from the deep veins of the legs, right vent
ricle of the heart, or pelvis. Nonthrombotic emboli mainly originate from fat re
lease after skeletal injuries, amniotic fluid, air, and foreign bodies.
The Virchow’s Triad
-three conditions and risk factors that can predispose a patient
or that can precipitate the formation of venous thrombi
Venous stasis
eg. atrial fibrillation, heart failure
immobility, polycythemia
pregnancy, varicose veins
Vessel wall injury
Coagulation problems
eg. infection, trauma
Pathophysiologic Changes
embolus
lodge in the pulmonary vasculature
Pulmonary embolism
decreased/nonperfusion of alveoli distal to occlusion
infarction of pulmonary vessel
impaired gas exchange
decreased C02
bronchoconstriction
shunting of blood to ventilated areas of the lungs
increased pulmonary resistance
hypoxia
release of mediators at the injury site
increased right ventricular workload
pulmonary vasoconstriction
right ventricular failure
pulmonary hypertension
left ventricular failure
decreased cardiac output
decreased blood pressure
shock
death
Clinical Manifestations
Shortness of breath and/or tachypnea- a response to the hypoxia that develops fr
om impaired gas exchange
Cough
Hemoptysis – occurs when an infaction at or near the periphery of the lung begin
s to hemorrhage
Chest pain – generally comes from an infarction of the pulmonary vessel near the
area in which the pleural nerves innervate. Usually
worsen when the patient takes a deep breath.
Tachycardia – a response to the decrease in oxygenation and impaired gas exchang
e
Jugular vein distention – a result of pulmonary hypertension and the decreased e
ffectiveness of the right ventricle
NCM 104 1st sem S.Y. 2007-2008
7
Hypotension – observed with large pulmonary embolism and is related to the decre
ase in cardiac output after ventricular dysfunction
Diagnosis
Chest radiograph – excludes other reasons that may cause the same clinical manif
estations. May show pulmonary artery distention, an
elevation of the diaphragm, and small infiltrates or pleural effusions.
ABG analysis – can reveal respiratory alkalosis, low partial pressure of oxygen,
and low partial pressure of carbon dioxide
Electrocardiogram – involve transient nonspecific ST segment and T wave changes
Management
The best treatment for pulmonary embolism is PREVENTION. When patients are at ri
sk for developing pulmonary embolism, prophylactic
measures should be instituted such as intravenous or subcutaneous heparin (Loven
ox) or oral anticoagulants such as warfarin (Coumadin). The
goal of therapy is to prevent thrombi formation, limit thrombi growth, and encou
rage breakdown of existing thrombi.
Management of hypoxia may require supplemental oxygen, intubation and mechanical
ventilation.
Heparin Therapy
-
started with a bolus (usually based on patient’s weight) and a continuous infusi
on adjusted every 4-6 hours, depending on the
institution’s protocol. Activated partial thromboplastin time (apt) should be ma
intained at 1.5-2.0 times the normal value.
-
generally continued for 7-14 days while the patient is on bedrest
-
reversal agent (antidote) is protamine sulfate
The reversal agent for warfarin (Coumadin) is vitamin K or fresh frozen plasma.
Surgical intervention is rarely used and is considered a last resort.Pulmonary e
mbolectomy is the removal of a clot from the larger vessel of the
pulmonary vasculature. This surgery carries a high risk of death and is only use
d in those patients who do not respond or have contraindications to
other interventions.
Nursing Responsibilities
The main nursing goal is to prevent the development of deep venous thrombosis (D
VT) that may lead to a thrombotic pulmonary embolism.
Interventions should include early ambulation, use of pneumatic stockings, suppo
rt hose, and passive range-of-motion exercises. All of these
improve venous blood flow and increase circulation.
Other nursing interventions include the following:
Signs and symptoms of DVT are monitored in the lower extremities (calf pain or t
enderness, redness, swelling, warmth, pain on
dorsiflexion of foot [Homan’s sign]). If Homan’s sign is positive, DO NOT retest
it; doing so may dislodge the clot.
Prescribed oxygen therapy is maintained, and the patient is asked to cough and d
eep breath every 2 hours
Signs and symptoms of respiratory distress or a worsening of pulmonary status (h
eart failure, pulmonary edema) are monitored, and the
physician is notified of any developments.
ABG analysis is monitored and pulse oximetry is continuously taken
Patient is positioned for comfort and maximal oxygenation, as well as to promote
the expulsion of secretions.
Signs and symptoms of bleeding are monitored when anticoagulant or thrombolytic
therapy is in progress. (eg. blood in stool or urine,
pale mucous membranes, petechiae, echymosis, complaints of back or flank pain).
ACUTE RESPIRATORY DISTRESS SYNDROME
A clinical syndrome characterized by a sudden and progressive pulmonary edema,
increasing bilateral infiltrates, hypoxemia refractory to
oxygen supplementation and reduced lung compliance
A syndrome with inflammation and increased permeability of the alveollocapillar
y membrane that occurs as a result of an injury to the lungs.
This inflammation causes noncardiogenic pulmonary edema with severely impaired g
as exchange.
Etiologic Factors Related to ARDS :
1. Aspiration (gastric secretions, drowning, hydrocarbons)
2. Drug ingestion and overdose
3. Hematologic disorders
4. Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive su
bstances
5. Localized infection (bacterial, fungal, viral pneumonia)
6. Metabolic disorders ( pancreatitis, uremia)
7. Shock (any cause)
8. Trauma ( pulmonary contusion, multiple fractures, head injury)
9. Fat or air embolism
10. Systemic sepsis
Pathophysiology
lung injury
immune system initiates an inflammatory response
activation of neutrophils, macrophages, and endotoxins into the lungs
and the release of mediators
increased alveolomembrane permeability
fluid enters into the lung tissue
Acute Respiratory Distress Syndrome
alveolar collapse
narrowing of airways
pulmonary vasoconstriction
hypoxia
pulmonary hypertension
hyperventilation
right ventricular dysfunction
NCM 104 1st sem S.Y. 2007-2008
8
respiratory failure
decreased cardiac output
Clinical Manifestations:
1. Rapid onset of severe dyspnea
2. Anxiety
3. Labored breathing and tachypnea
Assessment: Intercostal retractions and crackles
In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 wil
l decrease as a result of hyperventilation.
Medical Management: The main goals in the treatment of ARDS include improving an
d maintaining oxygenation, maintaining fluid and electrolyte
imbalances, providing adequate nitrition, and preventing respiratory and metabol
ic complications.
1. Primary focus of management includes identification and treatment of the cond
ition.
2. Supportive Therapy: Intubation and mechanical ventilation to maintain adequat
e gas exchange
3. Circulatory support, adequate fluid volume and nutritional support. Fluid res
triction is generally observed to prevent further leakage of fluid into
the alveoli and to decrease pulmonary edema, but fluid restriction can also caus
e a decrease in cardiac output and blood pressure.
4. Supplemental oxygen is used as the patient begins the initial spiral of hypox
emia. Oxygen toxicity may develop if high concentrations of oxygen
are used for longer than 24-48 hours.
5. Positive end-expiratory pressure (PEEP)- generally leads to improved gas exch
ange and allows for lower concentrations of oxygen to be used
6. Hypovolemia must be carefully treated
7. Intravenous crystalloid solutions are administered
8. Pulmonary artery pressure catheters are used to monitor patients fluid status
Nursing Management:
1. Positioning is important. Nurse should turn the patient frequently to improve
ventilation and perfusion in the lungs and enhance secretion
drainage.Prone positioning is an intervention that may improve oxygenation by de
creasing edema and atelectasis, thereby providing an
improved distribution of oxygen throughout the lungs.
2. Nurse must closely monitor rapid changes in oxygenation with changes in posit
ion
3. The nurse should explain all procedures and deliver care in a calm, reassurin
g manner
4. Rest is essential to reduce oxygen consumption
Nursing Diagnosis: Impaired gas exchange r/t inadequate respiratory center activ
ity, chest wall movement, airway obstruction, fluids in the lungs
RESPIRATORY FAILURE
Respiratory failure is a sudden and life-threatening deterioration of the gas e
xchange function of the lung.
Exists when the exchange of oxygen for carbon dioxide in the lungs can not keep
up with the rate of oxygen consumption and carbon dioxide
production by the cells of the body.
ACUTE RESPIRATORY FAILURE (ARF)
Defined as a fall in arterial oxygen tension and a rise in arterial carbon diox
ide tension.
The ventilation and/or perfusion mechanisms in the lung are impaired.
Respiratory system mechanisms leading to ARF include:
1. Alveolar hypoventilation
2. Diffusion abnormalities
3. Ventilation-perfusion mismatching
4. Shunting
Pathophysiology:
Common Causes of Acute Respiratory Failure:
Decreased Respiratory Drive
May occur with severe brain injury, large lesions of the brain stem (multiple s
clerosis), use of sedative medications, and metabolic disorders
such as hyperthyroidism. This disorders impair the normal response of chemorecep
tors in the brain to normal respiratory stimulation
Dysfunction Of The Chest Wall
The impulses arising in the respiratory center travel through nerves that exten
d from the brain stem down the spinal cord to receptors in the
muscles of respiration. Thus, any disease of the nerves, spinal cord, muscles or
neuromuscular junction involved in respiration seriously
affects ventilation and may lead to ARF
Dysfunction Of Lung Parenchyma
Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are co
nditions that interfere with ventilation by preventing
expansion of the lung. These conditions, which may cause respiratory failure, us
ually are produced by an underlying lung disease, pleural
disease, trauma and injury.
Other diseases and conditions of the lung that lead to ARF include pneumonia, s
tatus asthmaticus, lobar atelectasis, pulmonary embolism and
pulmonary edema
Other Factors
In the postoperative period, esp. after major thoracic or abdominal surgery, in
adequate ventilation and respiratory failure may occur. Causes of
ARF during this period include the effects of anesthetic agents, analgesics, and
sedatives; they may depress respiration and lead to
hypoventilation
Early signs are those associated with impaired oxygenation
Restlessness, fatigue, headache, dyspnea, air hunger, tachycardia, tachypnea, c
entral cyanosis, diaphoresis and finally, respiratory arrest
Physical findings: use of accessory muscles, decreased breath sounds
Medical Management:
Objectives of treatment are to correct the underlying cause and to restore adeq
uate gas exchange in the lung
Intubation and mechanical ventilation
Nursing Management:
Assist with intubation
Assess respiratory status by monitoring patient’s level of response, arterial b
lood gases, pulse oximetry and vital signs
Implement strategies to prevent complications: turning schedule, mouth care, sk
in care, ROM
CHRONIC RESPIRATORY FAILURE
Defined as a deterioration in the gas exchange function of the lung that has de
veloped insidiously or has persisted for a long period after an
episode of ARF
NCM 104 1st sem S.Y. 2007-2008
9
Patients develop a tolerance to the worsening hypoxemia and hypercapnia
Patient with chronic respiratory failure may develop Acute respiratory failure
– seen in COPD patients who develops an exacerbation or
infection that causes additional deterioration of the gas exchange mechanism
2 Causes of Chronic Respiratory Failure:
1. COPD
2. Neuromuscular Diseases
What is Mechanical Ventilation?
Mechanical ventilation is a form of artificial ventilation that takes over all o
r part of the work performed by the respiratory muscles and organs. It is initia
ted when the patient’s ability to oxygenate and exchange carbon dioxide is impai
red. Mechanical ventilation may be indicated for the following reasons:•
Hypoxemia
•
Respiratory Distress
•
Atelectasis
•
To reduce intracranial pressure
•
Aspiration
•
Pulmonary Edema
•
Pulmonary Embolism
•
To stabilize the chest wall
•
Respiratory Muscle Fatigue
•
Acute Respiratory Distress
Syndrome
•
Over sedation
The main goal of mechanical ventilation is to support gas exchange until the dis
ease process or condition is resolved.
Positive –pressure ventilation is the most common form of mechanical ventilation
used in the acute care setting. This form of ventilation forces
oxygen into the lungs, either through an endotracheal tube or a tracheostomy tub
e, mimicking respiration.
Modes of Ventilation
There are various modes of ventilation that may be used to ventilate and oxygena
te the patient. Essentially, these modes are ways in which
ventilation is triggered; they allow the patient some or all control over his or
her breathing.
1.Controlled ventilation (CV) delivers a preset volume or pressure at a preset r
ate. This mode takes away all control of breathing from
the patient; it is primarily used for patients who have no respiratory effort at
all.
2.Assist-control ventilation (ACV) delivers a preset volume or pressure whenever
the patient initiates a breath. If the patient does not
initiate a breath by a preset time, the ventilator will give one. This mode is u
sed primarily for the patient with normal breathing but who
has weak respiratory muscles or who cannot achieve an adequate volume on his or
her own.
3.Synchronized intermittent mandatory ventilation (SIMV) delivers a preset volum
e at a preset rate and is synchronized with patient’s
effort. This mode allows for spontaneous breathing between ventilated breaths an
d prevents competition between the patient and the ventilator. When a spontaneou
s breath occurs, it is at the patient’s own rate and tidal volume. SIMV is the m
ost common mode used and allows for weaning from the ventilator.
4.Pressure-controlled ventiation (PCV) delivers a positive pressure breath until
a maximum amount of pressure is reached; then the
breath stops. The maximum pressure limit is preset and helps prevent barotraumas
(damage from the pressure) to the lungs. The
amount of volume that is delivered varies, based on airway resistance and lung c
ompliance. Usually the maximal pressure limit is set to
achieve a goal tidal volume that is designed by the physician.
5.Inverse-ratio ventilation (IRV) is used when the inspiratory time is increased
and the expiratory time is decreased. With IRV the
inspiration-expiration (I/E) ratios used most are 1:1 and 2:1. This mode of vent
ilation allows for a longer period for gas exchange to
improve oxygenation. This mode is generally used in patients with ARDS. This typ
e of ventilatory mode creates an abnormal breathing
pattern for the patient; consequently the patient may become uncomfortable and a
nxious.
6.Constant positive airway pressure (CPAP) provided positive pressure during spo
ntaneous breaths; the ventilator will not initiate any
breaths. This mode increases oxygenation by opening any closed alveoli that may
occur at end-expiration. CPAP generally ranges from 5-10 cm water pressure. Grea
ter than 10 cm water pressure may increase intrathoracic pressure to the point t
hat it affects the patient’s venous return, decreasing cardiac output and blood
pressure. CPAP at this level may also cause a pneumothorax to occur
7.Positive end-expiratory pressure (PEEP) adds positive pressure during expirati
on of each ventilated breath.
Ventilator settings must be individualized to each patient to allow for optimal
gas exchange. Settings are generally based on arterial blood gas
(ABG) measurements and arterial oxygen saturation level.
NCM 104 1st sem S.Y. 2007-2008
10
Ventilator Setting
Description
Ranges
VT (Tidal Volume)
Amount of oxygen delivered to patient
with each preset ventilated breath
5-15 ml/kg (average 10ml/kg)
Respiratory rate
Number of breaths per minute that
ventilator is set to deliver
4-20 breaths/min
FiO2 (Fraction of Inspired Oxygen)
Percentage of oxygen delivered by
ventilator with each breath
21%-100%
I/E Ratio ( inspiratory to expiratory)
Duration of I/E time
1:2 (unless IRV is used)
Sensitivity
Determines amount of effort patient
must generate before ventilator will
give a breath
Too low – patient will have to work
harder to obtain a breath
Too high – patient may fight ventilator
Flow rate
Determines how fast VT will be
delivered during inspiration
High – increase airway pressure
Low – decrease airway pressure
Pressure limits
Regulates maximum amount of
pressure the ventilator will generate to
deliver preset VT
Ventilated breath is stopped when
pressure limit is reached
Barotrauma occurs when high airway pressures cause overdistention of the alveoli
, rupture and leakage of air. Barotrauma can cause
pneumothorax, subcutaneous emphysema, or crepitus. Air can leak under the medias
tinum or into the pericardium or peritoneum, causing
problems with organs located in these areas.
A patient needing long-term ventilatory management will need a tracheostomy plac
ed at some point. Endotracheal tubes (oral or nasal) are not intended for long-t
erm management and may lead to other problems such as mucosal breakdown, skin ul
cerations (lips), sinusitis, and vocal cord paralysis or damage (or both).
The following are practices performed for patients receiving mechanical ventilat
ion.
•
The respiratory status is assessed every 4 hours and more frequently when a chan
ge in condition occurs. Close attention is paid to
breathing sounds and the amount of patient effort.
•
Signs of hypoxia are assessed. These signs include restlessness, anxiety, increa
sed heart rate and blood pressure, increased
respiratory rate, and oxygen saturation via pulse oximetry less than 90%.
•
Endotracheal or tracheostomy tube placement is maintained by properly securing t
he tube and preventing inadvertent extubation by staff
or patient. Placement is maintained until extubation.
•
The endotracheal tube is repositioned per institutional policy to prevent pressu
re sores.
•
Secretions are suctioned to maintain an open airway. Amount, color, and consiste
ncy of the secretions are noted, as well as how the
patient tolerated the procedure.
•
Ventilator settings and alarms are verified once a shift or when any changes occ
ur.
•
Continuous pulse oximetry and ABGs are monitored for assessing the oxygenation s
tatus; the physician is notified of any changes in
parameters.
•
The patient is frequently positioned to allow for optimal ventilation, to preven
t complications, to mobilize secretions, and to promote
comfort.
•
Ventilator circuit is monitored for moisture or water trapping in tubing and emp
tied when necessary. Moisture may impede the flow of
oxygen and may provide a medium for bacterial growth.
•
A functioning manual resuscitation bag is maintained at bedside at all times in
case of malfunctioning equipment.
•
The patient is medicated as needed to decrease anxiety and facilitate oxygenatio
n.
•
Alternative methods of communication are provided for patients to decrease anxie
ty and maintain some control over their environment.
•
Mouth and lip care is provided at least once very shift to keep mucous membranes
moist.
NCM 104 1st sem S.Y. 2007-2008
11
ENDOCRINE/METABOLIC DISORDERS
DIABETIC KETOACIDOSIS
DKA is caused by an absence or markedly inadequate amount of insulin. First, be
cause the beta cells in the pancreas have the inability to
produce insulin, the ensuing hyperglycemia causes a hyperosmolar state. This hyp
erosmolarity results in fluid shifting from inside the cell to the serum; eventu
ally this fluid is lost in the urine, causing electrolyte shifts and total body
dehydration. Other metabolic derangements occur because no insulin exists to all
ow glucose to enter the cells; therefore cells begin to break down fats and prot
eins to use for fuel. This process causes the formation of ketones. Ketones decr
ease the blood pH and the bicarbonate concentration causing a ketosis. DKA is on
e of the more serious metabolic crises that can result from hyperglycemia in pat
ients with uncontrolled diabetes mellitus.
Three Main Clinical Features of DKA:
1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis
Three Main Causes of DKA:
1. Decreased or missed dose of insulin
2. Illness or infection
3. Undiagnosed and untreated diabetes
1. Acetone breath
2. Poor appetite or anorexia
3. Nausea and vomiting
4. Abdominal pain
5. Blurred vision
6. Weakness
7. Headache
8. Dehydration
9. Thirst or polydipsia
10. Orthostatic hypotension
11. Hyperventilation (Kussmaul respirations)
12. Mental status changes in DKA vary from patient to patient
Assessment and Diagnostic Findings :
1. Blood glucose levels may vary from300 to 800 mg/dl
2. The severity of DKA is not necessarily related to the blood glucose level
3. Evidence of DKA is reflected in low serum bicarbonate and low pH values
Prevention :
1. Patients must be taught “sick day “rules for maintaining their diabetes when
ill.
2. The most important issue is not to eliminate insulin doses when nausea and vo
miting occur and then attempt to consume frequent small portions
of carbohydrates
3. Drinking fluids every hour is important to prevent dehydration
4. Patients are taught to have available foods for use on sick days.
5. Supply of urine test strips and blood glucose test strips should be available
. Patients must know how to contact their physician
Medical Management :
1. Rehydration is important for maintaining tissue perfusion and enhancing the e
xcretion of excessive glucose by the kidneys
2. The major electrolyte of concern during treatment of DKA is potassium. Potass
ium replacement is vital to avoid dysrhythmias that may occur with
hypokalemia
3. Insulin is usually infused IV at a slow, continuous rate
4. Dextrose is added to IVF, such as normal saline solution when blood glucose l
evel reach 250 to 300 mg/dl to avoid too rapid drop in the blood
glucose level
Nursing Management :
1. Nursing care focuses on monitoring fluid and electrolyte status, blood glucos
e levels, administering fluids, insulin and other medications and
preventing complications such as fluid overload.
2. Urine output is monitored to ensure adequate renal function
3. ECG is monitored for dysrhythmias
4. VS, arterial blood gases and other clinical findings are recorded on a flow s
heet
HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA
Background: Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic der
angement that occurs principally in patients with adult-
onset diabetes. The condition is characterized by hyperglycemia, hyperosmolarity
, and an absence of significant ketosis.
Despite the name, coma is present in fewer than 10% of cases. Most patients pres
ent with severe dehydration and focal or global neurologic
deficits. In many cases, the clinical features of HHNC and diabetic ketoacidosis
(DKA) overlap and are observed simultaneously.
Pathophysiology: HHNC most commonly develops in patients with diabetes who have
some concomitant illness that leads to a reduced fluid
intake. Infection is the most common cause, but many other conditions can cause
altered mentation and/or dehydration. Frequently, this
concomitant illness is not identifiable.
Hyperglycemia and hyperosmolarity lead to osmotic diuresis and an osmotic shift
of fluid to the intravascular space, resulting in further intracellular
dehydration.
Unlike patients with DKA, patients with HHNC do not develop ketoacidosis, but th
e reason for this is not known. Contributing factors include the limitation on k
etogenesis by hyperosmolarity, the lower levels of free fatty acids available fo
r ketogenesis, the availability of insulin in amounts sufficient to inhibit keto
genesis but not sufficient to prevent hyperglycemia, and the hepatic resistance
to glucagon in these patients.
Management: refer to DKA
THYROTOXIC CRISIS (THYROID STORM)
A severe form of hyperthyroidism marked by sudden release of thyroid hormone in
to the blood stream
Precipitating Factors :
1. Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth ex
traction, insulin reaction, diabetic acidosis, pregnancy, digitalis
NCM 104 1st sem S.Y. 2007-2008
12
intoxication, abrupt withdrawal of anti-thyroid medications, extreme emotional s
tress, or vigorous palpation of the thyroid.
Clinical Manifestations :
1. High fever
2. Diaphoresis
3. Cardiopulmonary symptoms : extreme tachycardia, HPN, arrhythmias, CHF, pulmon
ary edema
4. CNS symptoms : increasing feeling of tremulousness to severe agitation, psych
osis with developing apathy, irritability, coma , heat intolerance
5. GI disturbance : weight loss, diarrhea, abdominal pain
6. Increased T3T4 and elevated BUN
Medical Management:
1. Immediate objectives are to reduced body temperature and heart rate and to pr
event vascular collapse
2. Humidified oxygen is administered to improve tissue oxygenation and meet meta
bolic demands
3. Monitor respiratory status by arterial blood gas or pulse oximetry
4. PTU or methimazole is administered to impede formation of thyroid hormone and
block conversion of T4 to T3, the more active form of thyroid
hormone
5. Hydrocortisone is prescribed to treat shock or adrenal insufficiency.
6. Iodine is administered to decrease output of T4 from the thyroid gland
7. For cardiac problems, Sympatholytic agents may be administered. Propranolol i
n combination with digitalis, has been effective in reducing
severe cardiac problems
ADRENAL CRISIS
Pheochromocytoma
A tumor that originates from the chromaffin cells of the adrenal medulla
Peak incidence is between ages 20 and 50 years old
The cause of high BP in 0.9% to 2.2% of patients with HPN
One form of HPN that is usually cured by surgery
Typical triad of symptoms: Headache, Diaphoresis, Palpitations
HPN may be intermittent or persistent
Tremor, flushing and anxiety
Hyperglycemia may result from conversion of liver and muscle glycogen to glucos
e
Clinical picture is usually characterized by:
1. Acute, unpredictable attacks, lasting seconds or several hours
2. Patient is anxious, tremulous and weak
3. Headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea
4. Polyuria, nausea, vomiting, diarrhea, abdominal pain
5. Feeling of impending doom
6. Palpitations and tachycardia
7. BP as high as 350/200 mm Hg
Assessment/Diagnostic Findings:
Signs of sympathetic nervous system over activity: 5 H’s (HPN, headache, hyperh
idorsis (excessive sweating), hypermetabolism, and
hyperglycemia)
Medical Management:
Pharmacologic Therapy
Close monitoring of ECG changes and careful administration of alpha-adrenergic
blocking agents, muscle relaxants – to lower BP quickly
Long-acting alpha blocker to prepare patient for surgery
Beta-adrenergic blocking agents for patients with cardiac dysrhythmias
Surgical Management:
Adrenalectomy- surgical removal of the tumor
HEPATIC FAILURE (Hepatic Coma)
An end stage of liver disease, usually arises as a complication of conditions t
hat cause liver dysfunction although it can be idiopathic
Also called Hepatic coma because the patient’s neurologic status gradually dete
riorates
Represents the most advanced stage of hepatic encephalopathy
A life threatening crisis may occur if the serum ammonia level rises, causing c
erebral ammonia intoxication
Causes:
1. Cirrhosis
2. Hepatitis
3. Drug or toxin-induced damage
4. Fatty liver
5. Portal HPN
6. Surgically-created portal systemic shunts that bypass the liver and allow tox
ins into the blood
Pathophysiology:
Liver disease alters liver structure and compromises essential functions. This l
eads to impaired protein, fat and carbohydrate metabolism, fluid and
electrolyte imbalance, poor lymphatic drainage, reduced coagulation and impaired
detoxification of ammonia and of the metabolites. Ammonia
accumulation and intoxication is the primary pathogenesis of hepatic failure and
the ensuing encephalopathy. Ammonia accumulates because liver
cells cannot detoxify and convert to urea the ammonia that is in constant supply
in GI tract blood. Remaining liver functions may become impaired
and may be difficult to treat or control. Hepatic failure may progress insidious
ly to a comatose state from which the patient rarely recovers.
Clinical Findings:
Stage 1
Slight personality and mood changes, disorientation, forgetfulness, slurred spe
ech, slight tremors, periods of lethargy and euphoria, mild
confusion, inability to concentrate, hyperactive reflexes, sleep-wake patterns,
handwriting starts to decline and mild asterixis (flapping tremors
of the hand) may appear
Stage 2
The patient grows more disoriented and drowsy. He may display inappropriate beh
avior, mood swings, agitation, apraxia. His hand writing
becomes illegible and asterixes may become pronounced
Stage 3
The patient becomes severely confused and may become combative, incoherent and
hard to arouse. Sleeps most of the time. You may detect
hyperactive deep tendon reflexes and rigid extremities
Stage 4
NCM 104 1st sem S.Y. 2007-2008
13
The pupil is comatose and does not react to stimuli. Pupils are dilated and lac
k corneal and deep tendon reflexes. Extremities are flaccid and
may assume flexion or extension posturing, decebrate rigidity. The EEG is marked
ly abnormal.
Assessment and Diagnostic Findings:
1. Elevated arterial ammonia blood levels
2. The encephalogram shows generalized slowing and an increase in amplitude of b
rain waves and the appearance of characteristic triphasic
waves
3. Occasionally, fetor hepaticus, a characteristic breath odor like freshly mowe
d grass, acetone, or old wine, may be noticed.
4. In a more advanced stage, there are gross disturbances of consciousness and t
he patient is completely disoriented with respect to time and
place
5. With further progression of the disorder, the patient lapses into frank coma
and may have seizures.
Intervention:
1. Anti-infective agents – to decrease bacterial action in the colon.
2. Ammonia detoxicants – to reduce ammonia. Lactulose (Duphulac) is administered
3. Cleansing enemas with diluted acetic acid or neomycin
4. Discontinuation of any precipitating substance: Dietary proteins, sedatives,
diuretic therapy, analgesics
5. IV administration of glucose to minimize protein breakdown
6. Oxygen administration
7. Correction of any electrolyte imbalance
8. Promote rest, comfort and quiet environment
Nursing Diagnosis:
1. Altered thought process
2. Potential impaired skin integrity
3. Impaired skin integrity
RENAL DISORDER
RENAL FAILURE
Renal Failure is a systemic disease and is a final common pathway of many diffe
rent kidney and urinary tract diseases.
Results when the kidneys are unable to remove the body’s metabolic wastes or pe
rform their regulatory functions
The substances normally eliminated in the urine accumulate in the body fluids a
s a result of impaired renal excretion and lead to a disruption
in endocrine and metabolic functions and fluid and electrolyte, an acid-base dis
turbances.
ACUTE RENAL FAILURE
Acute renal failure is a sudden and almost complete loss of kidney function ove
r a period of hours to days.
Categories of Acute Renal Failure:
1. Prerenal Condition (hypoperfusion of kidney). Occurs as a result of impaired
blood flow that leads to hypoperfusion of the kidney and a drop
in the GFR. Common clinical situations are volume-depletion states (hemorrhage o
r gastrointestinal losses), impaired cardiac performance and
vasodilation (sepsis or anaphylaxis)
2. Intrarenal. Intrarenal causes of acute renal failure are the result of actual
parenchymal damage to the glomeruli or kidney tubules. Conditions
such as burns crush injuries, and infections, as well as nephrotoxic agents, may
lead to acute tubular necrosis and cessation of renal function. Severe transfus
ion reaction may also cause intrarenal failure. Medications may also predispose
a patient to intrarenal damage, esp. nonsteroidal anti-inflammatory drugs and AC
E inhibitors
3. Post renal conditions. Postrenal causes of acute renal failure are usually th
e result of an obstruction somewhere distal to the kidney.
PHASES OF ACUTE RENAL FAILURE:
1. Initiation period – begins with the initial insult and ends when oliguria dev
elops.
2. Period of Oliguria – accompanied by a rise in the serum concentration of subs
tances usually excreted by the kidney (urea, creatinine, uric acid,
organic acids and the intracellular cations – potassium and magnesium
3. Period of diuresis – The patient experiences a gradual increase in urinary ou
tput, which signals that glomerular filtration has started to recover.
Laboratory values start rising and eventually begin a downward trend.Uremic symp
toms may still be present. The patient must be closely monitored
for dehydration during this phase; if dehydration occurs, the uremic symptoms ar
e likely to increase.
4. Period of Recovery – signals the improvement of renal function. Laboratory va
lues return to the patient’s normal level.
1. May appear critically ill and lethargic
2. Persistent nausea, vomiting and diarrhea
3. The skin and mucous membranes are dry due to dehydration
4. Uremic fetor – breath have the odor of urine
5. CNS manifestations: drowsiness, headache, muscle twitching, and seizures
1. Changes in urine. The urinary output varies (from scanty to normal volume). H
ematuria may be present and urine has low-specific gravity.
Patients with prerenal azotemia have a decreased amount of sodium. Those patient
s with intrarenal azotemia usually have urinary sodium levels
greater than 40 mEq/L.
2. Increased blood urea nitrogen and creatinine levels (Azotemia)
3. Hyperkalemia
4. Metabolic acidosis
5. Calcium and Phosphorus Abnormalities
6. Anemia – due to reduced erythropoietin production, uremic gastrointestinal le
sions, reduced Rbc lifespan, and blood loss
Prevention:
1. Renal function must be monitored closely if patient has been taking nephrotox
ic antibiotic agents or has been exposed to environmental toxins.
Blood should be drawn for determining baseline and monitoring serum BUN and crea
tinine levels by 24 hours after initiation of medication therapy
Medical Management:
1. Prerenal azotemia is treated by optimizing renal perfusion.
2. Postrenal failure is treated by relieving the obstruction
3. Overall, medical management includes maintaining fluid balance, avoiding flui
d excesses, or performing dialysis
4. The elevated potassium levels may be reduced by administering ion-exchange re
sins (sodium polystyrene sulfonate “kayexalate”)
5. Diuretics are used for management of volume status
6. Low-dose dopamine is often used to dilate the renal arteries
NCM 104 1st sem S.Y. 2007-2008
14
7. Atrial natriuretic peptide – inhibits sodium and water absorption and dilates
the afferent arteriole, thus improving blood flow to the glomerulus
8. Correction of acidosis and elevated phosphate levels. When severe acidosis is
present, the arterial blood gases or serum bicarbonate levels
must be monitored because patient may require sodium bicarbonate therapy or dial
ysis. Patient’s elevated phosphate level may be controlled with
phophate-binding agents (aluminum hydroxide).
9. Nutritional Therapy. Dietary proteins are limited to about 1 g/kg during the
oliguric phase. High-carbohydrate meals to meet caloric requirements.
Foods and fluids containing potassium and phosphorus are restricted.
Nursing Management:
1. Monitoring fluid and electrolyte balance. Hyperkalemia is the most immediate
life-threatening imbalance seen in acute renal failure.
2. Reducing metabolic rate. To reduce catabolism and the subsequent release of p
otassium and accumulation of endogenous waste products. Bed
rest is indicated and fever and infection are prevented or treated promptly.
3. Promoting pulmonary function. Patient is assisted to turn, cough and take dee
p breaths frequently to prevent atelectasis and respiratory
infection.
4. Preventing Infection. Asepsis is essential with invasive lines and catheters
5. Providing skin care. Meticulous skin care is important. Massaging bony promin
ences, turning the patient frequently, and bathing the patient with
cool water are comforting and prevent skin breakdown
6. Providing support. The patient and family will need assistance, explanation a
nd support during this time.
CHRONIC RENAL FAILURE
CRF is a progressive, irreversible deterioration in renal function in which the
body’s ability to maintain metabolic and fluid and electrolyte
balance fails, resulting in uremia or azotemia (retention of urea and other nitr
ogenous wastes in the blood)
Pathophysiology:
As renal function declines, the end products of protein metabolism (which are no
rmally excreted in urine) accumulate in the blood. Uremia develops
and adversely affects every system in the body.
4 Stages of Chronic Renal Disease:
Stage 1
Reduced renal reserve. Characterized by a 40 to 75% loss of nephron function. Th
e patient usually does not have symptoms because the
remaining nephrons are able to carry out the normal functions of the kidney.
Stage 2
Renal Insufficiency. Occurs when 75 to 90% of nephron function is lost. At this
point, the serum creatinine and blood urea nitrogen rise, the kidney
loses its ability to concentrate urine and anemia develops. The patient may repo
rt polyuria and nocturia.
Stage 3
Renal Disease. Edema, metabolic acidosis, and hypocalcemia occur. Patient may ex
hibit overt uremia with cardiovascular, gastrointestinal, and
neurologic complications.
Stage 4
End-stage renal Disease (ESRD). The final stage of CRF occurs when there is less
than 10% nephron function remaining. All of the normal
regulatory, excretory, and hormonal functions of the kidney are severely impaire
d. ESRD is evidenced by elevated creatinine and blood urea
nitrogen levels as well as electrolyte imbalances. Once the patient reaches this
point, dialysis is usually indicated.
Signs And Symptoms Of CRF:
1. Neurologic
Weakness and fatigue; confusion; inability to concentrate; disorientation; trem
ors; seizures; asterixis; restlessness of legs; burning of soles of
feet; behavior changes.
2. Integumentary
Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, b
rittle nails; coarse, thinning hair
3. Cardiovascular
HPN; pitting edema (feet , hands, sacrum), periorbital edema; pericardial frict
ion rub; engorged neck veins; pericarditis; pericardial effusion;
pericardial tamponade; hyperkalemia; hyperlipidemia
4. Pulmonary
Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shor
tness of breath; tachypnea; kussmaul-type respirations; uremic
pneumonitis; “ uremic lung
5. Gastrointestinal
Ammonia odor to breath (uremic fetor); metallic taste; mouth ulcerations and bl
eeding; anorexia; nausea and vomiting; hiccups; constipation
or diarrhea; bleeding from GIT
6. Hematologic
Anemia; thrombocytopenia
7. Reproductive
Amenorrhea; testicular atrophy; infertility; decreased libido
8. Musculoskeletal
Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone f
ractures; foot drop
Assessment And Diagnostic Findings:
•
Glomerular Filtration Rate. Decreased GFR can be detected by obtaining a 24-hour
urine analysis for creatinine clearance. As GFR
decreases, the creatinine clearance value decreases, whereas the serum creatinin
e and BUN levels increase.
•
Sodium and Water Retention. The kidney is unable to concentrate or dilute the ur
ine normally in ESRD. Some patients retain sodium and
water, increasing the risk for edema, CHF, and HPN.
•
Acidosis. With advanced renal disease, metabolic acidosis occurs because the kid
ney is unable to excrete increased loads of acid.
•
Anemia. Anemia develops as a result of inadequate erythoropoietin production, th
e shortened life span of RBC’s, nutritional deficiencies, and
the patient’s tendency to bleed, particularly from GIT
•
Calcium and Phosphorus Imbalance. The body’s serum calcium and phosphate levels
have a reciprocal relationship in the body; as one rises,
the other decreases.
Complications:
1. Hyperkalemia. Due to decreased excretion, metabolic acidosis, catabolism, and
excessive intake (diet, medications, fluids)
2. Pericarditis. Due to retention of uremic waste products and inadequate analys
is
3. Hypertension. Due to sodium and water retention and malfunction of the rennin
-angiotensin-aldosterone system
4. Anemia. Due to decrease erythropoietin, decreased RBC life span, GIT bleeding
and blood loss during dialysis.
5. Bone disease and metastatic calcifications. Due to retention of phosphorus, l
ow serum calcium levels, abnormal vitamin D metabolism, and
elevated aluminum levels
Medical Management:
1. Pharmacologic Therapy
Antacids. Hyperphosphatemia and hypocalcemia are treated with aluminum based ant
acids that bind dietary phophorus in the GIT
NCM 104 1st sem S.Y. 2007-2008
15
Antihypertensive and Cardiovascular agents. HPN is managed by intravascular cont

rol and a variety of hypertensive medications. CHF and pulmonary edema may requi
re treatment with fluid restriction, low sodium diets, diuretics, inotropic agen
ts such as digitalis, or dobutamine, and dialysis.
Anticonvulsants. If seizures occurs. The onset of seizure is recorded along with
the type, duration and general effect on the patient.
Intravenous Diazepam or phenytoin is usually administered to control seizures. T
he side rails must be padded to protect the patient
Erythropoietin. Anemia associated with CRF is treated with recombinant human ery
thropoietin (Epogen)
2. Nutritional Therapy
> Includes careful regulation of protein intake, fluid intake to balance fluid l
osses, sodium intake to balance sodium losses and some restriction of
potassium
3. Dialysis
> Hyperkalemia is usually prevented by ensuring adequate dialysis treatments wit
h potassium removal and careful monitoring of all medications for
their potassium intake
Nursing Management
Nursing Diagnoses:
1. Fluid volume excess r/t decreased urine output, dietary excesses, and retenti
on of sodium and water
2. Altered nutrition; less than body requirements r/t anorexia, nausea and vomit
ing, dietary restrictions, and altered oral mucous membranes
3. Knowledge deficit regarding condition and treatment regimen
4. Activity intolerance r/t fatigue, anemia, retention of waste products, and di
alysis procedure
5. Self-esteem disturbance r/t dependency, role changes, changes in body image,
and sexual dysfunction
Nursing Care:
1. Directed toward assessing fluid status and identifying potential sources of i
mbalance
2. Implementing a dietary program to ensure proper nutritional intake within the
limits of the treatment regimen
3. Promoting positive feelings by encouraging increased self-care and greater in
dependence
CARDIOVASCULAR DISORDERS
ANGINA PECTORIS
-
literally translates as pain in the chest. This symptom occurs as a result of my
ocardial ischemia. Anginal chest
pain is transient, lasting only 3-5 minutes and is usually relieved whenever the
precipitating event is discontinued
or nitroglycerin is administered. The most common cause of angina is preexisting
cardiovascular disease, which
narrows or occludes the arteries that feed the heart muscle. Numerous disorders
occur along the
pathophysiologic continuum of cardiovascular disease; these include atheorsclero
sis, angina, cerebrovascular
accident, myocardial infarction (MI), and heart failure.
The coronary arteries, which arise from the ascending aorta immediately on exiti
ng the heart, normally supplies the myocardium with adequate
oxygen and nutrient-rich blood to meet metabolic demands. In the atherosclerotic
heart, arteries are chronically dilated beyond narrowed or
partially obstructed areas to meet the heart’s metabolic demands at rest. Thus w
hen the myocardium requires more oxygen during times of
increased work, the coronary arteries cannot increase flow because they are alre
ady maximally dilated. An oxygen deficit is created as a result of
the oxygen supply being less than the cellular demands.
The oxygen imbalance created with angina can be quite precarious, and many facto
rs can adversely affect this relationship. The demand for
oxygen is increased whenever anyone of the following is increased: heart rate, a
fterload (hypertension), wall ension (ventricular volume or
pressure), myocardial wall thickness (hypertrophy), or contractility. All of the
se factors make the heart work harder. Conversely, the oxygen supply
is decreased whenever any of the following occur: hypotension, anemia, respirato
ry insufficiency, or tachycardia, which allows minimal time for
diastolic filling.
In the absence of adequate oxygen and glucose, cellular metabolism shifts from t
he efficient oxidative phosphorylation, which yields a large amount of adenosine
triphosphate (ATP) to the inefficient glycolysis; this action not only yields a
very small amount of ATP but it also yields lactic acid as a by-product. This a
cidic environment activates chemical nociceptors, which transmit pain impulses t
o the brain, and the individual experiences chest pain. At this point the damage
is reversible; in other words, if the flow of oxygen and glucose-rich blood is
restored, no permanent damage results. However, if the oxygen deficit continues
and the lactic acid is allowed to build up, cellular metabolism and function can
be altered to the point of irreversible cell death or myocardial infarction (MI
).
Types of Angina
1.Stable angina (classic or exertional angina).
The primary differentiating factor about this type of angina is that it is predi
ctable and occurs intermittently over an extended period. It occurs
with the same pattern of onset, duration, and intensity each time. Further, the
same precipitating activity (most often physical in nature) usually
brings on stable angina. The pain is relieved either when the precipitating even
t is discontinued or when nitroglycerin is administered in the
prescribed fashion. If the pain is unrelieved by either rest or nitroglycerin, t
he patient may then be at risk for an MI. As previously discussed,
stable angina is a result of atherosclerotic plaque that has narrowed the arteri
es. The chronically dilated vessel is unable to dilate further to
meet metabolic demands.
2. Unstable angina (progressive, crescendo, preinfarction angina, acute coronary
insufficiency)
This type is potentially life-threatening because it signifies advanced ischemic
heart disease. This type of angina is most often unpredictable.
Moreover, unstable angina attacks tend to occur with increasing frequency, inten
sity and duration. No precipitating event is necessary. In fact,
these attacks are brought on at times of complete rest. An individual previously
diagnosed with stable angina can progress to unstable angina;
alternatively, unstable angina may be the first clinical manifestation in an ind
ividual with CAD.
3.Prinzmetal’s angina (variant angina)
The least common type of angina. It is unpredictable in onset, duration, and int
ensity and occurs almost exclusively at rest. Vasospasm of
one or more of the coronary arteries is the underlying cause, which can occur wi
th or without associated atherosclerosis.
The cardinal symptom of angina is chest pain or discomfort. However, many patien
ts describe feeling vague sensations of discomfort, tightness, pressure, heavine
ss, aching or squeezing. Others complain of heartburn or indigestion during an a
ttack. The most common location is substernal; however, the pain or discomfort m
ay radiate to the neck, jaw, back, shoulders, left arm, or occasionally the righ
t arm.
When asked to demostrate or point to the location of the pain, typically patient
s will clench one or two fists over the substernal region when
experiencing myocardial ischemia. This display is known as the Levine’s sign. Ot
her associated sighs and symptoms include pallor, diaphoresis,
cold skin, shortness of breath, weakess, dizziness, anxiety, and feelings of imp
ending doom.
When an individual complains of chest pain, the source of pain should be conside
red cardiac until proven otherwise. However, it is prudent
to consider both cardiac and noncardiac causes of chest pain as possible differe
ntials.
Electrocardiogram (ECG) – remains the “gold-standard” for a first-line, noninvas
ive tool for diagnosis.
Percutaneous transluminal coronary angioplasty (PTCA) – involves the passage of
an inflatable balloon catheter into the stenotic coronary
NCM 104 1st sem S.Y. 2007-2008
16
vessel, which is then dilated, resulting in compression of the atherosclerotic p
laque and widening of the vessel
Coronary artery bypass grafting (CABG) – done by harvesting either a saphenous v
ein from the leg or the left internal mammaryartery and then
used to bypass areas of obstruction in the heart
Nursing Responsibilities
In caring for patients with angina, the focus of the nurse’s role is two-fold. T
he first priority is appropriate treatment of the acute attack to alleviate
discomfort and, if possible, to avert untoward sequelae. The second priority is
geared toward extensive education that not only empowers the
patient to become an active participant in his or her well being but also impart
s practical tools with which the patient can effectively manage the
condition at home to achieve the highest level of wellness and independent funct
ioning.
During an acute anginal attack, it is imperative that the nurse performs a rapid
and focused physical assessment and health history. Frequent vital signs and co
ntinuous cardiac monitoring are essential parts of the ongoing assessment. The m
ost crucial part of the assessment focuses on the current attack; emphasis must
be placed on evaluating the pain itself and any precipitating events.
The nurse must ask the following questions:
How severe is the pain? (scale of 1-10)
What does the pain feel like?
Where is the pain? Does it move or radiate? Is it diffused or well localized?
Did the pain start suddenly or gradually?
How long does it last?
How frequently does it occur?
What makes the pain worse? What brings the pain on?
What makes the pain better? What resolves the pain?
Has the pain been increasingly worse with each attack?
Another critical nursing function is prompt institution of prescribed medical an
d pharmacologic therapies such as frequently used acronymMON A,
which stands for:
•
Morphine,
•
Oxygen,
•
Nitroglycerine, and
•
Aspirin.
Although nitrates are unable to dilate severely atherosclerotic vessels that are
already maximally dilated, its administration during an unstable
angina attack can prevent progression to an MI or death in 51% to 72% of patient
s.
Other nursing measures that are beneficial to the patient who is suffering an an
ginal attack include helping the patient into a comfortable position,
promoting rest and relaxation, and encouraging slow, deep breathing.
ACUTE MYOCARDIAL INFARCTION
As with angina, acute myocardial infarction occurs when the heart muscle is depr
ived of oxygen and nutrient-rich blood. However, in the case of MI, this depriva
tion occurs over a sustained period to the point at which irreversible cell deat
h and necrosis take place. This deprivation leads to structural and functional c
hanges within the affected area of myocardial tissue. As with angina, too, under
lying coronary artery disease (CAD) is the most common cause of MI. With these b
asic similarities in mind, many components of the MI disease process and treatme
nt either overlap to some degree or further develop along the continuum of cardi
ovascular diseases.
Infarction results from sustained ischemia and is irreversible causing cellular
death and necrosis.
Circumstances that can cause an imbalance in supply and demand of oxygen and nut
rient-rich blood:
Physical exertion
Emotional stress
Weather extremes
Digestion after a heavy meal
Valsalva maneuver
Hot baths or showers
Sexual excitation
Pathophysiologic chaaracteristics
The hallmark of MI is severe, unrelenting chest pain. As with angina, the pain i
s typically described as crushing, pressure-filled, vise-like, tight,
constricting, or squeezing. The most common location of the pain is substernal,
with radiation to the neck, jaw, or left arm. Leass frequently, pain
is reported in the shoulders, back, or right arm. In addition, a positive Levine
’s sign (one or two fists clenched over the chest area when the
patient is asked to localize the pain) can contribute to the diagnosis.
The major difference in the clinical presentation of MI compared with that of an
gina is the onset, severity, and duration. Chest pain aassociated with MI usuall
y has an abrupt onset and can occur during activity, rest, or even sleep. The pa
in described during MI is typically more severe than anginal pain, lasting at le
ast 20-30 minutes, and it is not relieved with either rest or nitroglycerin.
However, not all patients will experience the same clinical presentation.
During MI, associated clinical manifestations can range from vague sensations of
“just not feeling well” to the loss of consciousness or cardiac
arrest. Often the skin is diaphoretic with a pale or ashen appearance, which occ
urs because of peripheral vasoconstriction as the body shunts
blood to the vital core. The initial surge of catecholamines can contribute to a
variety of signs and symptoms such as tachycardia, hypertension,
anxiety, palpitations, apprehension, and feelings of impending doom. Stimulation
of the medulla is mediated via vasovagal reflexes and can result
in nausea and vomiting. Fever may be present secondary to the activation of the
inflammatory process. As the infarction progresses and the
heart’s pumping ability becomes impaired, cardiac output drops. Associated with
decreased cardiac output is hypotension, restlessness, dyspnea,
jugular vein distention, oliguria, and confusion.
Electrocardiogram – capable of diagnosing MI in 80% of patients, making it an in
dispensable, noninvasive, and cost-effective tool.
Evolving MI will show ST elevation which indicates acute myocardial necrosis. Th
e development of Q wave may be
observed which signifies further electrical abnormalities. It may be an indicati
on of worsening ischemia and necrosis.
Cardiac Enzymes
During the infarction process, cell membranes rupture, allowing intracellular en
zymes to spill out into the blood stream. Blood sample drawn at
certain times during or after MI can be sent to the laboratory where enzymes can
be measured and interpreted to determine the presence of an
NCM 104 1st sem S.Y. 2007-2008
17
infarction.
Cardiac Enzyme Laboratory Findings
Enzyme
Earliest Rise (in hours)
Peak (in hours)
Return to Baseline
Creatinine kinase (CK)
CK-MB
Myoglobin
Troponin 1
2-6
4-8
0.5-1.0
1-6
18-36
15-24
6-9
7-24
3-6 days
3-4 days
12 hours
10-14 days
Troponin 1 is the newest cardiac marker and is a protein found only in myocardia
l cells. It is a quick, rapid test that, if elevated, indicated MI.
First-Line and Initial Treatment for Myocardial Infarction
Provide oxygen
Obtain a 12-lead ECG
Monitor vital signs and pulse oximetry
Monitor continuous cardiac rhythm with ST segment monitoring
Conduct history and physical examinations
Administer medications (thrombolytic therapy and anticoagulant therapy
Nursing Interventions:
1.Bedrest must be enforced.
2. The nurse should assist with all position changes and personal hygiene to avo
id any exertional effort.
3. Monitor I&O particularly urine output because this is a reliable indictor of
cardiac output and systemic perfusion.
4. Administer stool softener as ordered to prevent straining and vasovagal stimu
lation which can cause precipitous bradycardia
CARDIAC FAILURE
CONGESTIVE HEART FAILURE (CHF)
Often referred to as cardiac failure, is the inability of the heart to pump suf
ficient blood to meet the needs of the tissues for oxygenation and
nutrients.
CHF is most commonly used when referring to left-sided and right-sided failure
The incidence of CHF increases with age
Pathophysiology:
Cardiac failure most commonly occurs with disorders of cardiac muscles that resu
lt in decreased contractile properties of the heart. Common underlying condition
s that lead to decreased myocardial contractility include myocardial dysfunction
, arterial hypertension, and valvular dysfunction. Myocardial dysfunction may be
due to coronary artery disease, dilated cardiomyopathy, or inflammatory and deg
enerative diseases of the myocardium. Atherosclerosis of the coronary arteries i
s the primary cause of heart failure. Ischemia causes myocardial dysfunction bec
ause of resulting hypoxia and acidosis (from accumulation of lactic acid). Myoca
rdial infarction causes focal myocellular necrosis, the death of myocardial cell
s, and a loss of contractility; the extent of the infarction is prognostic of th
e severity of CHF.
Dilated cardiomyopathy causes diffuse cellular necrosis, leading to decreased co
ntractility. Inflammatory and degenerative diseases of the
myocardium, such as myocarditis, may also damage myocardial fibers, with a resul
tant decrease in contractility.
Systemic or pulmonary HPN increases afterload which increases the workload of th
e heart and in turn leads to hypertrophy of myocardial muscle
fibers; this can be considered a compensatory mechanism because it increases con
tractility.
Valvular heart disease is also a cause of cardiac failure. The valves ensure tha
t blood flows in one direction. With valvular dysfunction, valve has increasing
difficulty moving forward. This decreases the amount of blood being ejected, inc
reases pressure within the heart, and eventually leads to pulmonary and venous c
ongestion.
Etiologic Factors :
1. Increased metabolic rate (eg. fever, thyrotoxicosis)
2. Hypoxia
3. Anemia
VENTRICULAR FAILURE
LEFT-SIDED CARDIAC FAILURE
Pulmonary congestion occurs when the left ventricle cannot pump the blood out o
f the chamber. This increases pressure in the left ventricle
and decreases the blood flow from the left atrium. The pressure in the left atri
um increases, which decreases the blood flow coming from the pulmonary vessels.
The resultant increase in pressure in the pulmonary circulation forces fluid int
o the pulmonary tissues and alveoli; which impairs gas exchange
Clinical Manifestations :
1. Dyspnea on exertion
2. Cough
3. Adventitious breath sounds
4. Restless and anxious
5. Skin appears pale and ashen and feels cool and clammy
6. Tachycardia and palpitations
7. Weak, thready pulse
8. Easy fatigability and decreased activity tolerance
RIGHT-SIDED CARDIAC FAILURE
NCM 104 1st sem S.Y. 2007-2008
18
When the right ventricle fails, congestion of the viscera and the peripheral ti
ssues predominates. This occurs because the right side of the
heart cannot eject blood and thus cannot accommodate all the blood that normally
returns to it from the venous circulation.
1. Edema of the lower extremities (dependent edema)
2. Weight gain
3. Hepatomegaly (enlargement of the liver)
4. Distended neck veins
5. Ascites (accumulation of fluid in the peritoneal cavity)
6. Anorexia and nausea
7. Nocturia (need to urinate at night)
8. Weakness
Medical Management
The basic objectives in CHF management are the following:
1. Reducing the workload on the heart
2. Increasing the force and efficiency of myocardial contraction
3. Eliminating the excessive accumulation of body water by avoiding excess fluid
, controlling the diet, and monitoring diuretic and angiotensin-
converting enzyme (ACE) inhibitor therapy
Pharmacologic Therapy:
If the patient is in mild failure, usually an ACE inhibitor is prescribed. A diu
retic is added if there is no improvement or if there are signs of fluid
overload. Next, digitalis is added if the symptoms continue. If symptoms are sev
ere, all three medications are usually started immediately.
ACE Inhibitors. Promote vasodilation and diuresis by decreasing afterload and pr
eload eventually decreasing the workload of the heart.
Diuretic Therapy. A diuretic is one of the first medications prescribed to a pat
ient with CHF. Diuretics promote the excretion of sodium and water
through the kidneys.
Digitalis. This medication increases the force of myocardial contraction and slo
ws conduction through the AV node. It improves contractility thus,
increasing left ventricular output.
Dobutamine.(Dobutrex) is an intravenous medication given to patients with signif
icant left ventricular dysfunction. A catecholamine, it stimulates the
beta1-adrenergic receptors. Its major action is to increase cardiac contractilit
y.
Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs the release an
d prevents the uptake of calcium. This in turn, promotes
vasodilation, causing a decrease in preload and afterload and decreasing the wor
kload of the heart.
Other medications. Anticoagulants may be prescribed. Beta-adrenergic blockers ma
ybe indicated in patients with mild or moderate failure.
Nutritional Therapy:
1. A low-sodium diet
2. Avoidance of excessive amount of fluids
Nursing Management:
1. Record intake and output to identify a negative balance (more output than inp
ut)
2. Weigh patient daily at the same time
3. Auscultate lung sounds daily to detect a decrease or an absence of pulmonary
crackles
4. Determine the degree of jugular distention
5. Identify and evaluate severity of dependent edema
6. Monitor pulse rate and BP, and make sure the patient does not become hypotens
ive from dehydration
7. Examine skin turgor and mucous membranes for signs of dehydration
8. Assess for symptoms of fluid overload (orthopnea, paroxysmal nocturnal dyspne
a, and dyspnea on exertion)
Nursing Process: The Patient With Cardiac Failure
Assessment
The focus of the nursing assessment for the patient with cardiac failure is dir
ected toward observing for signs and symptoms of pulmonary and
systemic fluid overload.
Health History
The nurse explores sleep disturbances, particularly sleep suddenly interrupted
by shortness of breath.
The nurse finds out about the number of pillows needed for sleep (indication of
dyspnea)
Find out also the activities of daily living and the activities that causes sho
rtness of breath
Physical Examination
The lungs are auscultated at frequent intervals to detect crackles and wheezes
or their absence. The rate and depth of respiration are also
noted.
The heart is auscultated for an S3 heart sound, a sign that the heart pump is b
eginning to fail and that increased blood volume remains in the
ventricle with each beat. HR and rhythm are also noted.
Jugular vein distention is also assessed. Distention greater than 3 cm above th
e sternal angle is considered abnormal.
Sensorium and level of consciousness must be evaluated
Dependent parts of the patient’s body are assessed for perfusion and edema.
The liver is examined for hepatojugular reflux.
Output is measured carefully to establish a baseline against which to measure t
he effectiveness of diuretic therapy. Intake and output record
are maintained
Nursing Diagnoses:
1. Activity intolerance r/t imbalance between oxygen supply and demand secondary
to decreased CO
2. Excess fluid volume r/t excess fluid/sodium intake or retention secondary to
CHF and its medical therapy
3. Anxiety r/t breathlessness and restlessness secondary to inadequate oxygenati
on
4. Non-compliance r/t to lack of knowledge
5. Powerlessness r/t inability to perform role responsibilities secondary to chr
onic illness and hospitalization.
Potential Complications:
1. Cardiogenic shock
2. Dysrhythmias
3. Thromboembolism
NCM 104 1st sem S.Y. 2007-2008
19
4. Pericardial effusion and pericardial tamponade
Planning And Goals:
1. Promoting activity while maintaining vital signs within identified range
2. Reducing fatigue
3. Relieving fluid overload symptoms
4. Decreasing the incidence of anxiety or increasing patient’s ability to manage
anxiety
5. Teaching the patient about the self-care program.
6. Encouraging the patient to verbalize his ability to make decisions and influe
nce outcomes.
1. Promoting Activity Tolerance
The patient is encouraged to perform an activity more slowly than usual, for a
shorter duration, or with assistance initially.
Barriers that could limit abilities to perform an activity are identified
Pacing and prioritizing activities will maintain the patient’s energy to allow
participation in regular exercise.
Vital signs should be taken before, during and immediately after an activity to
identify whether they are within the predetermined range.
2. Reducing Fatigue
The nurse and patient can collaborate to develop a schedule that promotes pacin
g and prioritization of activities. The schedule should
alternate activities with periods of rest and avoid having two significant energ
y-consuming activities occur on the same day or in immediate
succession.
3. Managing Fluid Volume
The nurse monitors the patient’s fluid status closely. Auscultating the lungs,
comparing daily body weights, monitoring intake and output and
assisting the patient to adhere to a low-sodium diet.
The nurse needs to position the patient or teach the patient how to assume a po
sition that shifts fluid away from the heart.
The nurse needs to assess for skin breakdown and institute preventive measures
4. Controlling Anxiety
The nurse should take steps to promote physical comfort and psychological suppo
rt. A family member’s presence provides reassurance.
Speaking in a slow, calm, and confident manner is helpful. Stating specific, bri
ef directions for an activity is helpful in decreasing anxiety.
5. Minimizing Powerlessness
Patients need to recognize that they are not helpless and that they can influen
ce their direction, their lives, and their outcomes.
The nurse needs to assess for factors contributing to a perception of powerless
ness and intervene accordingly. Contributing factors may
include lack of knowledge, hospital policies, and lack of opportunities to make
decisions.
Taking time to listen to patient encourages them to express their concerns and
questions
Provide the patient with decision-making opportunities
Provide encouragement and praise
Expected Outcomes:
1. Demonstrates tolerance for increased activity
2. Has less fatigue and dyspnea
3. Maintains fluid balance
4. Is less anxious
5. Adheres to self-care regimen
6. Makes decisions regarding care and treatment
7. Absence of complications
CARDIOGENIC SHOCK
Occurs when the heart cannot pump enough blood to supply the amount of oxygen n
eeded by the tissues.
Pathophysiology:
The heart muscle loses its contractile power, resulting in a marked reduction in
SV and CO, sometimes called “forward failure”. The damage to
myocardium results in a decrease in CO, which in turn reduces arterial blood pre
ssure and tissue perfusion in the vital organs (heart, brain,
kidneys). Flow to the coronary artery is reduced, resulting in decreased oxygen
supply to the myocardium, which in turn increases ischemia and
further reduces the heart’s ability to pump. The inadequate emptying of the vent
ricle also leads to increased pulmonary pressures, pulmonary
congestion, and pulmonary edema, exacerbating the hypoxia and resulting ischemia
of vital organs.
1. Tissue hypoperfusion – classic signs of cardiogenic shock manifested as cereb
ral hypoxia (restlessness, confusion, agitation), low blood
pressure, rapid and weak pulse, cold and clammy skin, increased respiratory crac
kles, hypoactive bowel sounds, and decreased urinary output.
2. Initially, arterial blood gas analysis may show respiratory alkalosis.
3. Dysrhythmias are common
1. The use of a Pulmonary Artery catheter to measure left ventricular pressures
and CO is important in assessing the severity of the problem and
planning management. The PA wedge pressure is elevated and the CO is decreased a
s the left ventricle loses its ability to pump.
2. The systemic vascular resistance is elevated due to the sympathetic nervous s
ystem stimulation that occurs as a compensatory response to the
decrease in blood pressure.
3. The decreased blood flow to the kidneys causes a hormonal response that cause
s fluid retention and further vasoconstriction.
4. The increases in HR, circulating volume, and vasoconstriction occur to mainta
in circulation to the brain, heart and lungs, however, the workload
of the heart is increased.
5. Continued cellular hypoperfusion eventually results in organ failure. The pat
ient becomes unresponsive, severe hypotension occurs, and the
patient develops shallow respirations, cold, cyanotic or mottled skin, and absen
t bowel sounds.
6. Arterial blood gas analysis shows metabolic acidosis
7. All laboratory results indicate organ dysfunction.
Medical Management:
1. Reduce any further demand on the heart
2. Improve oxygenation and restore tissue perfusion
3. Diuretics, vasodilators, and mechanical devices (filtration and dialysis)
4. Intravenous volume expanders (normal saline, lactated Ringer’s solution, and
albumin) are given for hypovolemia or low intravascular volume.
5. Strict bed rest to conserve energy
NCM 104 1st sem S.Y. 2007-2008
20
6. Oxygen administration is increased for hypoxemia
7. Intubation and sedation may be necessary to maintain oxygenation balance.
Pharmacologic Therapy:
Most medication are administered IV because of the decreased perfusion to the g
astrointestinal system
1. Pressor agents are medications used to raise BP and increase CO. Many pressor
medications are catecholamines ( norepinephrine and high-
dose dopamine) to promote perfusion to the heart and brain.
2. Diuretics and vasodilators may be administered to reduce the workload of the
heart.
3. Positive inotropic medications are given to increase myocardial contractility
4. Circulatory assist devices: Intra-aortic balloon pump – to augment the pumpin
g action of the heart. The device inflates during diastole, increasing
the pressure in the aorta and therefore increasing perfusion. It deflates just b
efore systole, lessening the pressure within the aorta before
ventricular contraction, decreasing the amount of resistance the heart has to ov
ercome to eject blood and therefore decreasing the amount of work
the heart must complete to eject blood.
Nursing Management:
1. Nurse must carefully assess the patient, observe the cardiac rhythm, measure
hemodynamic parameters, and record fluid intake and urinary
output.
2. The patient must be closely monitored for responses to the medical interventi
ons and for the development of complications
3. The patient is always treated in intensive care environment because of the fr
equency of nursing interventions and the technology required for
effective medical management.
THROMBOEMBOLISM
The decreased mobility of the patient with cardiac diseases and the impaired ci
rculation that accompany these disorders contribute to the
development of intracardiac and intravascular thrombosis.
Intracardiac Thrombus
Detected by an echocardiogram and treated with anticoagulants, such as warfarin
.
A part of the thrombus may become detached and may be carried to the brain, kid
neys, intestines, or lungs
The most common problem is pulmonary embolism. The symptoms of pulmonary emboli
sm include chest pain, cyanosis, and shortness of
breath, rapid respirations and hemoptysis. (see discussion on pulmonary embolism
)
The pulmonary embolus may block the circulation to a part of the lung, producin
g an area of pulmonary infarction
Systemic embolism may present as cerebral, mesenteric, or renal infarction
An embolism can also compromise the blood supply to an extremity
PERICARDIAL EFFUSION AND CARDIAC TAMPONADE
Pathophysiology:
Pericardial effusion refers to the escape of fluid into the pericardial sac. Nor
mally, the pericardial sac contains less than 50 ml of fluid, which the
heart needs to decrease friction for the beating heart. An increase in pericardi
al fluid raises the pressure within the pericardial sac and compresses
the heart. This results in :
Increased right and left ventricular-end diastolic pressures
Decreased venous return
Inability of the ventricles to distend adequately
Pericardial fluid may accumulate slowly without causing noticeable symptoms. A r
apidly developing effusion, however, can stretch the pericardium
to its maximum size and, because of increased pericardial pressure, and reduce v
enous return to the heart, and decrease cardiac output. The
result is cardiac tamponade.
1. The patient may complain of a feeling of fullness within the chest. The feeli
ng of pressure may result from stretching of the pericardial sac
2. Engorged neck veins
3. Shortness of breath
4. A drop and fluctuation in BP
1. Pericardial effusion is detected by percussing the chest and noting an extens
ion of flatness across the anterior aspect of the chest
2. Echocardiogram to confirm diagnosis
Medical Management:
1. Pericardial Fluid Aspiration (pericardiocentesis) – performed to remove fluid
from the pericardial sac
2. Pericardiotomy. A portion of pericardium is sliced to permit the pericardial
fluid to drain into the lymphatic system.
CARDIAC ARREST
Occurs when the heart ceases to produce an effective pulse and blood circulatio
n. It may be due to a cardiac electrical event, as when the HR
is too fast or too slow or when there is no heart rate at all.
1. Loss of consciousness, pulse and BP
2. Ineffective respiratory gasping
3. The pupils of the eyes dilate within 45 seconds.
4. Seizures may or may not occur
Emergency Management:
Cardiopulmonary Resuscitation
1. Airway – maintain open airway
2. Breathing – provide artificial circulation by rescue breathing
3. Circulation – promoting artificial circulation by external cardiac compressio
n
4. Defibrillation – restoring the heart beat
Maintaining Airway and Breathing
The first step in CPR is to obtain an open airway. Any obvious material in the
mouth and throat should be removed. The chin is directed up
and back or the jaw (mandible) is lifted forward. The rescuer “looks, listen. an
d feels” for air movement. An oropharyngeal airway is inserted if available. Two
rescue ventilations over 3 to 4 seconds are provided using a bag or mouth-mask
device. If the first rescue ventilation entered easily, then the patient is vent
ilated with 12 breaths per minute and the open airway is maintained. Endotrachea
l intubation is performed to ensure an adequate airway and ventilation.
Restoring Circulation
After performing ventilation, the carotid pulse is assessed and external cardia
c compressions are provided when no pulse is detected.
1. Compressions are performed with the patient on a firm surface (Cardiac board
, floor)
2. The rescuer (facing the patient’s head) places the heel of one hand on the l
ower half of the sternum, two fingerwidths from the tip of the
NCM 104 1st sem S.Y. 2007-2008
21
xiphoid and positions the other hand on top of the first hand. The fingers shoul
d not touch the chest wall.
3. Using the body weight while keeping the elbows straight, the rescuer presses
quickly downward from the shoulder area to deliver a forceful
compression to the victim’s lower sternum toward the spine.
4. The chest compression rate is 80 to 100 times/minute
Follow-up Monitoring
1. After successful resuscitation, the patient is transferred to an intensive ca
re unit for close monitoring. Continuous electrocardiographic monitoring
and frequent BP assessment are essential until hemodynamic stability is reestabl
ished.
DYSRHYTHMIAS
Disorders of the formation and/or conduction of the electrical impulse within t
he heart. This can cause disturbances of the heart rate, the heart
rhythm, or both.
Normal Electrical Conduction
The electrical impulse that stimulates and paces the cardiac muscle normally ori
ginates in the sinus node, located near the vena cava in the right
atrium. Normally, the impulse occurs at a rate between 60 and 100 times a minute
in the adult. The impulse quickly travels from the sinus node
through the atria to the atrioventricular (AV) node causing the atria to contrac
t. The structure of the AV node slows the impulse, which allows time
for the atria to contract and the ventricles to fill with blood. From the AV nod
e, the impulse travels quickly along the right and left bundle branches
and the Purkinje fibers, located in the ventricular muscle. The electrical stimu
lation of the ventricles, in turn, causes the ventricles to contract
(systole). Then the electromechanical impulse completes the circuit and the cycl
e begins again. In this way, sinus rhythm promotes cardiovascular
circulation. The electrical stimulus causes the mechanical event of the heart.
Depolarization. The electrical stimulation: the mechanicalcontraction is called
systole.
Repolarization. The electrical relaxation and mechanicalrelax ation is called d
iastole.
Influences on Heart Rate and Contractility
Heart rate is influenced by the autonomic nervous system, which consists of sym
pathetic and parasympathetic fibers.
Stimulation of the sympathetic system increases heart rate.
Sympathetic stimulation also causes the constriction of peripheral blood vessel
s and, therefore, an increase in BP
Parasympathetic stimulation slows the heart rate
Manipulation of the autonomic nervous system may increase or decrease the incid
ence of dysrhythmias
Types of Dysrhythmias
1. Sinus Node Dysrhythmias
A. Sinus Bradycardia
Occurs when the sinus node creates an impulse at a slower –than-normal rate.
Etiology:
1. Slower metabolic needs (sleep, athletic training, hypothyroidism)
2. Vagal stimulation (vomiting, suctioning, severe pain, extreme emotions)
3. Medications
4. Increased intracranial pressure and MI
Treatment:
1. Atropine 0.5 to 1.0 mg given quickly and IV as bolus – medication of choice
2. Catecholamines and emergency transcutaneous pacing
B. Sinus Tachycardia
Occurs when the sinus node creates an impulse at a faster-than-normal rate.
It may be caused by acute blood loss, anemia shock, hypovolemia, hypervolemia,
CHF, pain, hypermetabolic state, fever, exercise, anxiety or
sympathomimetic medications.
Treatment:
1. Calcium channel blockers (ex. Diltiazem)
2. Beta-blockers (ex. Propranolol)
C. Sinus Arrhythmia
Occurs when the sinus node creates an impulse at an irregular rhythm; the rate
increases with inspiration and decreases with expiration
2. Atrial Dysrhythmias
A. Premature Atrial Complex (PAC)
This is a single ECG complex that occurs when an electrical impulse starts in t
he atrium before the next normal impulse of the SA node.
The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardi
um
PAC’s are common in normal hearts. The patient may say “My heart skipped a beat
.” A pulse deficit may exist.
If PAC’s are infrequent, no treatment is necessary.
B. Paroxysmal Atrial Tachycardia
A term used to indicate a tachycardia characterized by abrupt onset and abrupt
cessation and a QRS of normal duration.
Now called AV nodal reentry tachycardia
C. Atrial Flutter
Occurs in the atrium and creates impulses at an atrial rate between 250 and 400
times per minute
May cause serious signs and symptoms: chest pain, shortness of breath, and low
blood pressure.
Treatment:
1. If patient is unstable, electrical cardioversion is indicated
2. If patient is stable, diltiazem, verapamil, beta-blockers or digitalis may be
administered IV to slow the ventricular rate.
D. Atrial Fibrillation
Causes a rapid, disorganized, and uncoordinated twitching of atrial musculature
.
The most common dysrhythmias
Usually associated with advanced age, valvular heart disease, cardiomyopathy, h
yperthyroidism, pulmonary disease, moderate to heavy
ingestion of alcohol and the aftermath of open heart surgery
Treatment:
NCM 104 1st sem S.Y. 2007-2008
22
Treatment depends on its cause and duration and the patient’s symptoms and inst
ability
In some cases, AF converts to sinus rhythm within 24 hours without treatment
Both stable and unstable AF of short duration are treated the same as stable an
d unstable atrial flutter
To prevent recurrence and to promote heart rate control over a long period, qui
nidine, procainnamide, flecainide, sotalol, or amiodatone may
be prescribed
Anti-coagulation therapy is indicated if patient is elderly or has hypertension
, heart failure or a history of stroke.
Pacemaker or surgery is sometimes indicated for patients who are unresponsive t
o medications
3. Junctional Dysrhythmias
A. Premature Junctional Complex
An impulse that starts in the AV nodal area before the next normal sinus impuls
e.
Causes include: digitalis toxicity, congestive heart failure, and coronary arte
ry disease
Rarely produce any significant symptoms
Treatment is the same as for frequent PAC’s
B. Junctional Rhythm
Occurs when the AV node, instead of the SA node, becomes the pacemaker of the h
eart.
Junctional rhythm may produce signs and symptoms of reduced cardiac output. If
so, the treatment is the same as for sinus bradycardia.
C. AV Nodal Reentry Tachycardia
Occurs when an impulse is conducted to an area in the AV node that causes the i
mpulse to be rerouted back into the same area over and
over again at a very fast rate.
Factors associated with the development of AV nodal reentry tachycardia include
caffeine, nicotine, hypoxemia, and stress
Signs and symptoms vary with the rate and duration of the tachycardia and the p
atient’s underlying condition. Usually of short duration,
resulting only in palpitations. A fast rate may reduce cardiac output, resulting
in significant signs and symptoms such as restlessness, chest
pain, shortness of breath, pallor, hypotension and loss of consciousness
Treatment:
Treatment is aimed at breaking the reentry of the impulse.
1. Vagal maneuvers, such as carotid sinus massage, gag reflex, breath holding, a
nd immersing the face in ice water – increase parasympathetic
stimulation, causing slower conduction through the AV node and blocking the reen
try of the rerouted impulse.
Because of the risk of a cerebral embolic event, carotid sinus massage is contr
aindicated in patients with carotid bruits.
2. If vagal maneuvers are ineffective, the patient may then receive a bolus of a
denosine, verapamil, or diltiazem.
3. Cardioversion is the treatment of choice if the patient is unstable or does n
ot respond to the medications.
4. Intravenous adenosine may be prescribed to cause a conversion to sinus rhythm
.
4. Ventricular Dysrhythmias
A. Premature Ventricular Complex (PVC)
PVC is an impulse that starts in a ventricle before the next normal sinus impul
se.
PVC’s can occur in healthy people, esp. with the use of caffeine, nicotine, and
alcohol.
Also caused by cardiac ischemia or infarction, increased workload on the heart
(ex. Exercise, fever. Hypervolemia, CHF, and tachycardia),
digitalis toxicity, hypoxia, acidosis, and electrolyte imbalances, esp. hypokale
mia
In the absence of disease, PVC’s are not serious. In the patient with acute MI,
PVC’s may indicate the need for more aggressive therapy.
The following are warning or complex PVC’s (precursors of ventricular tachycard
ia) : (1) more than 6/minute (2) multifocal (having different
shapes), (3) two in a row (pair), and (4) occurring on the T wave (the vulnerabl
e period of ventricular depolarization)
Treatment:
1. Lidocaine is the medication most commonly used for immediate short-term thera
py
B. Ventricular Tachycardia
Defined as three or more PVC’s in a row, occurring at a rate exceeding 100 beat
s/minute.
Ventricular tachycardia is usually associated with coronary artery disease and
may precede ventricular fibrillation.
Ventricular tachycardia is an emergency because the patient is usually unrespon
sive and pulseless.
Treatment:
1. Lidocaine is the initial choice
2. Cardioversion maybe indicated if the medications are ineffective or if the pa
tient becomes unstable
3. Immediate defibrillation
Ventricular tachycardia in a patient who is unconscious and without pulse is tr
eated in the same manner as ventricular fibrillation.
C. Ventricular Fibrillation
A rapid but disorganized ventricular rhythm that causes ineffective quivering o
f the ventricles.
This dysrhythmias is always characterized by the absence of an audible heartbea
t, a palpable pulse, and respirations.
Cardiac arrest and death are imminent if VF is uncorrected
Treatment:
1. Immediate defibrillation and activation of emergency services. Placing a call
for emergency assistance takes precedence over initiating CPR
2. After a successful defibrillation, eradicating causes and administering anti
dysrhythmics medication are treatments to prevent the recurrence of
V F.
D. Idioventricular Rhythm
Also called ventricular rhythm, occurs when the impulse starts in the conductio
n system below the AV node
Commonly causes the patient to lose consciousness and experience other signs an
d symptoms of reduced cardiac output. In such cases,
treatment is the same as for any bradycardia, including identifying the underlyi
ng etiology, administering IV atropine, and initiating emergency
transcutaneous pacing.
Bed rest is prescribed so as not to increase cardiac workload
E. Ventricular Asystole
Commonly called flatline, ventricular asystole is characterized by absent QRS c
omplexes, although P waves may be apparent for a short
duration.
There is no heartbeat, no palpable pulse, and no respiration.
Without treatment, ventricular asystole is fatal.
NCM 104 1st sem S.Y. 2007-2008
23
Treatment:
1. CPR
2. Rapid assessment to identify possible causes
3. Intubation and establishment of IV access are the first recommended actions
4. Bolus of IV epinephrine and to be repeated at 3-5 minutes intervals
5. Sodium bicarbonate maybe administered IV
Nursing Process: The Patient With A Dysrhythmia
Assessment
Major areas of assessment include possible causes of the dysrhythmias and the d
ysrhythmia’s effect on the heart’s ability to pump an
adequate blood volume
When cardiac output is reduced, the amount of oxygen reaching the tissues and v
ital organs is diminished. This diminished oxygen produces
the signs and symptoms associated with dysrhythmias.
A health history is obtained to identify possible causes and past incidences of
syncope (fainting), lightheadedness, dizziness, fatigue, chest
discomfort, and palpitations.
Psychosocial assessment is also performed to identify the possible effects of d
ysrhythmia
Physical assessment is conducted to confirm the data obtained from the history
and to observe for signs of diminished cardiac output during
the dysrhythmic event, esp. changes in level of consciousness. Skin may be pale
and cool. Signs of fluid retention, such as neck vein
distention, crackles and wheezes in the lungs may be detected during auscultatio
n.
The rate and rhythm of apical and peripheral pulses are assessed and any pulse
deficit is noted.
The chest is auscultated for extra heart sounds, esp. S3 and S4, measures BP an
d determines pulse pressures. A declining pulse pressure
indicates reduced cardiac output.
Diagnosis:
1. Potential/actual decrease in cardiac output
2. Anxiety related to fear of the unknown
3. Lack of knowledge about the dysrhythmias and its treatment.
Potential Complications: Ischemic Heart Disease
1. Monitoring and Managing the Dysrhythmias
Controlling the incidence or effect of dysrhythmias is often achieved by the us
e of ant-idysrhythmic medications
A constant serum blood level of the medication is maintained to maximize benefi
cial effects and minimize adverse effects
If the patient is hospitalized, an ECG is initiated and rhythm strips are analy
zed to track dysrhythmias
BP, rate and depth of respirations, pulse rate and rhythm are evaluated regular
ly to determine the hemodynamic effect of the dysrhythmias
2. Minimizing Anxiety
Nurse must maintain a calm and reassuring attitude
Maximize the patient’s control and to make the unknown less threatening
Evaluation
Expected Outcomes:
1. Cardiac output is maintained
2. Anxiety is minimized
3. The patient knows about dysrhythmias and its treatment
Adjunctive Modalities and Management
1. Cardioversion and Defibrillation
Treatment for tachydysrhythmias.
Used to deliver an electrical current to stimulate a critical mass of myocardial
cells. This allows the sinus node to recapture its role as the
heart’s pacemaker.
One major difference between cardioversion and defibrillation has to do with th
e timing of the delivery of electrical current.
Defibrillation is usually performed as an emergency treatment, whereas cardiove
rsion is usually a planned procedure
Cardioversion involves the delivery of a “timed” electrical current to terminat
e a tachydysrhythmia.
Defibrillation is the treatment of choice for ventricular fibrillation and puls
eless ventricular tachycardia.
2. Pacemaker Therapy
An electronic device that provides electrical stimuli to the heart muscle.
Usually used when a patient has a slower-than-normal impulse formation
May also be used to control tachydysrhythmias that do not respond to medication
therapy
Complications of Pacemakers:
1. Local infection at the entry site of the leads or at the subcutaneous site
2. Bleeding and hematoma at the lead-entry sites or at the subcutaneous sites fo
r permanent generator placement
3. Hemothorax from puncture of the subclavian vein or internal mammary artery
4. Ventricular ectopy and tachycardia from irritation of the ventricular wall by
the endocardial electrode
5. Movement or dislocation of the lead placed transvenously (perforation of the
myocardium)
6. Phrenic nerve, diaphragmatic (hiccupping) or skeletal muscle stimulation may
occur if the lead is dislocated or if the delivered energy is set high
7. Rarely, cardiac tamponade occurs after removal of epicardial wires
8. Dislodgement of the pacing electrode – most common complication. Minimizing p
atient activities can help to prevent this complication.
BURNS
There are 4 major goals relating to burns:
1. Prevention
2. Institution of lifesaving measures for the severely burned person
3. Prevention of disability and disfigurement through early, specialized, indivi
dual treatment
4. Rehabilitation through reconstructive surgery and rehabilitative programs
Pathophysiology:
Burns are caused by a transfer of energy from a heat source to the body. Heat ma
ybe transferred through conduction or electromagnetic radiation.
Burns are categorized as thermal (including electrical burns), radiation or chem
ical. Tissue destruction results from coagulation, protein
denaturation, or ionization of cellular contents. The skin and the mucosa of the
upper airways are the sires of tissue destruction. Deep tissues,
including the viscera, can be damaged by electrical burns or through prolonged c
ontact.
The depth of the injury depends on the temperature of the burning agent and the
duration of contact with the agent.
NCM 104 1st sem S.Y. 2007-2008
Reads:
8,645
Uploaded:
08/27/2008
Category:
Uncategorized.
Tags:
Education-Course-Material
Education-Course-Material
(Less)
Rated:
(32 Ratings)
DownloadPrintMobileCollectionsReport Document
Report this document?
Please tell us reason(s) for reporting this document
Spam or junk
Porn adult content
Hateful or offensive
If you are the copyright owner of this document and want to report it, please fo
llow these directions to submit a copyright infringement notice.
Cancel
This is a private document. Question_small
1280440606
Marcus, RN
Ads by Google
HospiMedica International
Daily Critical Care News
Sign Up For Free!
www.HospiMedica.com
Pocket Nurse
Medical Supplies for Education
Nurse Owned & Operated Business
pocketnurse.com
Health and Nutrition
Evaluation of World Bank Support
Download the free report
www.WorldBank.org/IEG/HNP
Share & Embed
Link / URL:
Embed Size & Settings:
* Width: Auto
* Height: (proportional to specified width)
* Start on page:
* Preview View:
More share options
Related
1.
41 p.
TOPICS in Health Care Concept
Reads: 289
953 p.
neonatology_2004
Reads: 102
953 p.
neonatology_2004
Reads: 1507
2.
87 p.
Comp. of Pregnancy
Reads: 636
41 p.
Maternal
Reads: 0
39 p.
15561819 Maternal and Child Health...
Reads: 368
3.
40 p.
Maternal and Child Health Nursing
Reads: 2921
39 p.
15561819 Maternal and Child Health...
Reads: 1083
33 p.
Maternal and Child Health Nursing
Reads: 1150
4.
17 p.
High Risk Pregnancy (Notes)
Reads: 458
30 p.
Acute Biologic Crisis
Reads: 2451
2 p.
Vishant Garg
Reads: 0
5.
4 p.
List of Pronouns
Reads: 0
200 p.
Alternative Cancer Remedies
Reads: 0
2 p.
Notice of Conditional Acceptance
Reads: 0
6.
22 p.
Building Your Theology - Lesson 4 ...
Reads: 0
2 p.
LID:DTW - ILS PRM RWY 03R(CAT II) ...
Reads: 0
6 p.
Land surface water harvesting tech...
Reads: 0
7.
3 p.
Thursday 7.22.10 2 Timothy 3:1
Reads: 0
1 p.
Refer to the Exhibit All Routers A...
Reads: 0
1 p.
Ccna Answers What Do Routers Use t...
Reads: 0
More from this user
1.
4 p.
Ethics and Nursing
From: Marcus, RN
Reads: 14,566
7 p.
Oxygenation
From: Marcus, RN
Reads: 3,263
5 p.
Safety
From: Marcus, RN
Reads: 989
2.
6 p.
Stress and Adaptation
From: Marcus, RN
Reads: 4,405
7 p.
Urinary Elimination
From: Marcus, RN
Reads: 8,265
13 p.
Vital Signs
From: Marcus, RN
Reads: 6,382
3.
5 p.
Care of Patients with IV therapy
From: Marcus, RN
Reads: 11,372
2 p.
Heart Defects
From: Marcus, RN
Reads: 6,793
5 p.
Endocrine Physiology
From: Marcus, RN
Reads: 2,642
4.
11 p.
Diabetes Mellitus
From: Marcus, RN
Reads: 3,785
43 p.
CHN notes
From: Marcus, RN
Reads: 15,458
15 p.
Metabolism Physiology
From: Marcus, RN
Reads: 2,298
5.
11 p.
NURSING CARE OF PATIENTS WITH D...
From: Marcus, RN
Reads: 68,695
57 p.
Perinatal Nursing
From: Marcus, RN
Reads: 10,904
7 p.
Patient s Nutritional Needs
From: Marcus, RN
Reads: 1,713
6.
5 p.
Acid-Base Balance
From: Marcus, RN
Reads: 2,572
6 p.
Asepsis
From: Marcus, RN
Reads: 4,044
2 p.
Nursing Memory Joggers
From: Marcus, RN
Reads: 2,471
7.
13 p.
Fluid and Electrolytes
From: Marcus, RN
Reads: 11,985
12 p.
Perioperative Nursing
From: Marcus, RN
Reads: 13,329
8 p.
Nursing Informatics
From: Marcus, RN
Reads: 13,007
8.
7 p.
Burn Lecture Notes
From: Marcus, RN
Reads: 3,326
25 p.
Skin Integrity and Wound Care
From: Marcus, RN
Reads: 7,889
5 p.
Acute Pain
From: Marcus, RN
Reads: 9,224
9.
12 p.
Metabolism and Elimination
From: Marcus, RN
Reads: 3,601
Add a Comment
Spinner_trans_gray
coninitas readcast this 3 days agoLearn more about Readcast.
Jenard Joniel Olivar
Jenard Joniel Olivar readcast this 07 / 11 / 2010Learn more about Readcast.
mira44 readcast this 06 / 27 / 2010Learn more about Readcast.
aliyah isabel readcast this 06 / 23 / 2010Learn more about Readcast.
aubzone left a comment
sir this is very gud document...sir can i have a copy of this im a nursing s
tudent from baguio..thank you sir...e.cotiwan@yahoo.com
10 / 29 / 2009
ReplySpinner_mac_white
Report
sir this is very gud document...sir can i have a copy of this im a nursing s
tudent from baguio..thank you sir.
10 / 29 / 2009
Report
sir..can i have a copy these is very useful for me thank you sir
10 / 29 / 2009
Report
bebekristine left a comment
hi! can i have a copy of this? This is really useful as a reviewer, it will
help me a lot.. here is my email: valeriesolidum@yahoo.com thanks!
10 / 19 / 2009
Report
halfangle left a comment
hi can you please send me a copy of this? Thanks a lot! e-add is: gaoxiudan1
119@gmail.com
10 / 09 / 2009
Report
pwinzizitah left a comment
hello sir.. can i have a copy of this document coz i really need it for my n
cm 104.. i am very pleased if you will send it to my email.. thanks so much...he
re s my email ad..pwinzizitah214@hotmail.com..
10 / 01 / 2009
Report
Show More
Print this document
High Quality
Open the downloaded document, and select print from the file menu (PDF reader re
quired).
Browser Printing
Coming soon!
Add this document to your Collections
71 p.
1 ACUTE BIOLOGIC CRISES (24 HOURS) COURSE OUTLINE 1. High Risk Adult (8 hours) A
. Respiratory Disorders i. ii. iii. Pulmonary Embolism Acute Respiratory Distres
s Syndrome (ARDS) Respiratory Failure a. b. iv. B. Acute RF Chronic RF Mechanica
l Ventilators Endocrine/...
* From: Marcus, RN
* Uploaded: 08 / 27 / 2008
* Reads: 8648
Transparent
Name:
Description:
Collection Type:
public locked: only you can add to this collection, but others can view it
public moderated: others can add to this collection, but you approve or reject a
dditions
private: only you can add to this collection, and only you will be able to view
it
Cancel
* Loader_black_on_white ncp public - locked
Finished? Back to Document
Add this document to your Collections
Transparent
Name:
Description:
Collection Type:
public locked: only you can add to this collection, but others can view it
public moderated: others can add to this collection, but you approve or reject a
dditions
private: only you can add to this collection, and only you will be able to view
it
Cancel
Finished? Back to Document
Upload a Document
Search Books, Presentations, Business, Academics...
Scribd
* About
* Press
* Jobs
* Contact
* Blog
* Scribd Store
Legal
* Terms - General
* Terms - API
* Terms - Privacy
* Copyright
Help & Tools
* Getting Started
* Community Guidelines
* Support & FAQ
* Web Stuff
Partners
* Partners
* Branded Reader
* Developers / API
Subscribe to Us
* On Scribd
* On Twitter
* On Facebook
Enter your email address:
or Spinner_mac_white
What s New
* We have updated our Terms of Service
* Branded Reader
* Desktop Uploader
scribd. scribd. scribd. scribd. scribd. scribd. scribd. scribd. scribd. scribd.

Untitled

Transféré par

Informations du document

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Untitled

Transféré par

Droits d'auteur :

Formats disponibles

Scribd

Antihypertensive and Cardiovascular agents. HPN is managed by intravascular cont

Vous aimerez peut-être aussi