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Acute Respiratory Distress Syndrome
acute lung injury
from an acute insult at the level of the alveoli, causing severe hypoxemia and decreased compliance of the lungs
Shock
Aspiration
Sepsis
Precipitating Factors of Acute Respiratory Distress Syndrome
Pneumonia
Aspiration
Direct Etiologic/Risk Factors related to ARDS
Sepsis
Severe Trauma
Severe Burns
Indirect Etiologic/Risk Factors related to ARDS
Major Surgery
Hematologic Disorder
Other Etiologic/Risk Factors related to ARDS
Macrophages
Neutrophils
Cellular mediators that are released in ARDS causing injury to the alveolar capillary membrane
Cytokines
Enzymes
Chemical mediators that are released in ARDS causing injury to the alveolar capillary membrane
stiff lungs
In ARDS, lung compliance becomes markedly decreased
decrease in functional residual capacity
severe hypoxemia
The result of ARDS
severe refractory hypoxemia
In ARDS, . the blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing a shunt to develop. This means that blood is interfacing with nonfunctioning alveoli & gas exchange is markedly impaired, resulting in
Crackles
Is heard in ARDS as fluid begins to leak into the alveolar interstitial space
Fibrosing alveolitis
in ARDS, Acute lung injury then progresses to X with persistent severe hypoxemia
4 to 12 mmHg
(ARDS) Normal reading of pulmonary artery wedge pressure reading:
>15 mmHg
Elevated reading of Pulmonary artery wedge pressure which suggest increased left-sided heart failure/cardiogenic pulmonary edema
hypovolemia
reduced preload
In Pulmonary artery wedge pressure reading the “low“ indicates
Mechanical Ventilation
Medical Management of Acute Respiratory Distress Syndrome
35 cm
In ARDS, Protective ventilation, maximum inspiratory pressure of X should be instituted
Positive End-Expiratory Pressure
In ARDS, this should be used to improve PaO2 to keep the alveoli open, thereby improving gas exchange
bronchodilators
corticosteroids
neutrophil inhibitors
Drugs used in Acute Respiratory Distress Syndrome for Medical Intervention
Antibiotics
What drug to use if is it already in the late course of ARDS?
Impaired gas exchange related to fluid in lungs
Acute Respiratory Distress Syndrome Nursing Diagnosis
O2
Teach slow, pursed lip breathing
CPT
Nursing Management in Acute Respiratory Distress Syndrome
60 mmHg
>90 %
in ARDS, Maintain PaO2 of X mmHg or Sao2 X
intubation & initiation of mech vent
In ARDS, Assist with X if patient becomes increasingly lethargic, cannot cough or expectorate secretions, cannot cooperate with therapy, or if pH falls below 7.30
Pneumococcal vaccine
Flu vaccine
Preventive measure of Acute Respiratory Distress Syndrome
Pulmonary Embolism
Obstruction of one or more pulmonary arteries by a thrombus (or thrombi) which becomes dislodged and is carried to the pulmonary vasculature
deep vein of the legs
right side of the heart
upper extremity
Usual origin of Pulmonary Embolism
Pulmonary Infarction
Refers to necrosis of lung tissue that can result from interference with the blood supply
venous stasis
concurrent phlebitis
heart failure, stroke
Predisposing Factors of Pulmonary Embolism
immobilization
obesity
MI
Risk Factors of Pulmonary Embolism
increase in pulmonary vascular resistance
This reaction compounds the ventilation-perfusion imbalance
syncope
sharp & stabbing chest pain
hypocapnia
hypoxemia
Results in Pulmonary Embolism
impending doom
Chest pain with apprehension and a sense of X occurs when most of the pulmonary artery is obstructed
heart gallop
Clinical manifestation of pulmonary embolism: there is a loud pulmonic component of S2 (Split S2)
palpable cord
In Pulmonary Embolism, signs of suggestive deep ein thrombosis is
Thoracic imaging
Pulmonary angiography
venography
D-dimer assay
ABG/Electrolytes levels
CXR
Diagnostic Evaluation of Pulmonary Embolism
Ventilation/Perfusion Scan
V/Q Scan is a test of choice for suspected PE (possibly using single-photon emission computed tomography) or helical contrast-enhanced CT scan
Pulmonary Angiography
if noninvasive testing is inconclusive or not a candidate for noninvasive testing
Contrast studies
should be avoided in persons who are pregnant or have advanced renal failure
Venography
test results confirm or exclude the diagnosis of PE)
D dimer assay
for low to intermediate probability of pulmonary embolism
ABG/Electrolyte levels
decreased PaO2 is usually found in Pulmonary Embolism, due to perfusion abnormality of the lung
respiratory alkalosis
CXR
normal or possible wedge-shaped infiltrate; usually shows sinus tachycardia, PR interval depression, and nonspecific T-wave change
nasal oxygen
perfusion scan
dobutamine or dopamine
digitalis glycosides
continuous ECG monitoring
IV morphine or sedatives
Massive PE is a life-threatening emergency. The immediate objective is to stabilize the cardiopulmonary system:
dabigatran (Pradaxa)
Non-vitamin K antagonist oral anticoagulants for Pulmonary Embolism
Warfarin (Coumadin)
Anticoagulation therapy for pulmonary embolism
urokinase (Kinlytic)
Thrombolytic Therapy for Pulmonary Embolism
IV Morphine
may be given to relieve anxiety, alleviate chest discomfort (which improves ventilation).
4 to 6 hours
In Pulmonary Embolism, IV loading dose usually followed by continuous pump or drip infusion or given intermittently every
1 1/2 to 2
Dosage adjusted to maintain the partial thromboplastin time (PTT) at X times the pretreatment value (if the value was normal)
Protamine sulfate
IV heparin in PE. this may be given to neutralize heparin in event of severe bleeding
Ligation
Plication
clipping of the inferior vena cava
Surgical Management in PE: Interruption of vena cava-reduces channel size to prevent lower extremity emboli from reaching lungs and it is accomplished by
femoral or jugular
Placement of transvenously inserted Intraluminal Filter in inferior vena cava to prevent migration of emboli; inserted through X vein by way of catheter.
Pulmonary Embolectomy
A surgical management in pulmonary embolism that requires a thoracotomy with cardiopulmonary bypass technique
Transvenous catheter embolectomy
a technique in which a vacuum-cupped catheter is introduced transvenously into the affected pulmonary artery. Suction is applied to the end of the embolus and the embolus is aspirated into the cup
Ineffective Tissue Perfusion (Pulmonary) related to decreased blood circulation
Nursing Diagnosis of Pulmonary Embolism
Correcting Breathing Pattern
Nursing Management of Pulmonary Embolism
IV fluids
Vasopressors
In PE, Monitor patient’s response to
Hypoxemia
In PE, This is due to abnormalities of V/Q mismatch
Respiratory Failure
an alteration in the function of the respiratory gas exchange system in either O, (hypoxic respiratory failure) and/or CO, elimination (hypercapnic respiratory failure)
hypoxic respiratory failure
alteration in the function of the respiratory gas exchange system in Oxygen
hypercapnic respiratory failure
alteration in the function of the respiratory gas exchange system in carbon dioxide
Hypoxemic respiratory failure (type 1)
is characterized by arterial oxygen (PaO2 ) level to fall below 60 mmHg (hypoxemia) with a normal or low arterial CO2 tension (PaCO2)
Hypoxemic respiratory failure (type 1)
it is the most common form of respiratory failure, usually associated with acute diseases of the lung
Hypercapnic respiratory failure (type 2)
is characterized by an arterial CO2 (PaCO2) level of 50 mmHg.
Hypoxemia is common while breathing room air.
pH depends on the bicarbonate level, which, in turn, is dependent on the duration of hypercapnia.
acute
chronic
combined acute and chronic
Respiratory failure is classified as
Acute Respiratory Failure
Characterized by hypoxemia (PaO2 <50 mmHg) and/or hypercapnia (PaCO2 >50 mm Hg) and acidosis (pH less than 7.35).
Occurs rapidly, usually in minutes to hours or days
Chronic Respiratory Failure
Characterized by hypoxemia (decreased PaO2) and/or hypercapnia (increased PaCO2) with a normal pH (7.35 to 7.45).
Occurs over a period of days to months to years, allowing for activation of compensatory mechanisms, including bicarbonate retention with normalization of pH
Hypoxemia
Hypercapnia
Tachypnea then bradypnea
Accessory muscles use
Asynchronous resiprations
Clinical Manifestation of Respiratory Failure
Hypoxemia
restlessness, agitation, dyspnea, disorientation, confusion, delirium, loss of consciousness
hypercapnia
headache, somnolence, dizziness, confusion
ABG levels
Nursing Alert in Respiratory Failure
Obtain X whenever the history or signs and symptoms suggest the patient is at risk for developing respiratory failure
oximeter
The need for ABG analysis can be decreased by using an X to continuously monitor oxygen saturation (SaO2
ABG Analysis
shows changes in PaO2, PaCO2, pH, and possibly HCO3 from the patient's normal
<50 mmHg
PaO2 normal value
35 to 45 mmHg
PaCO2 normal value
7.35
pH normal value
elevated
in Respiratory Failure the end tidal CO2 monitoring is elevated or decreased?
decreasing
in Respiratory Failure the pulse oximetry is increasing or decreasing?
CBC
CXR
ECG
to determine underlying cause and patient’s condition in Respiratory Failure
oxygen therapy
how to correct hypoxemia?
bronchodilators
corticosteroid
to reduce bronchospasm and inflammation in RF
Diuretics
For Pulmonary vascular congestion or pulmonary edema in RF
Noninvasive positive pressure ventilation
X using a face mask may be a successful option for short-term support of ventilation
fraction of inspired oxygen
Nursing Alert in patients with Respiratory Failure:
Avoid administration of X (FiO2) of 100% for COPD Patients
Impaired Gas Exchange related to fluid in the lungs
Nursing Diagnosis of Patients with Respiratory Failure
administer O2
Nursing Management of Respiratory Failure
incentive spirometer
nebulization
HOB 30
In respiratory failure, provide measures to prevent atelectasis and promote chest expansion and secretion clearance, as ordered
SpO2
ABG levels
RR
VC
in Respiratory Failure, Monitor adequacy of alveolar ventilation by frequent measurement of
Chest Physiotherapy
is considered for retained secretions in Respiratory Failure
Pneumococcal vaccine
protects against Streptococcus pneumoniac bacteria in Respiratory Failure
Pneumothorax
air in the pleural space
in patients with chest trauma, it is usually the result of a laceration to the lung parenchyma, tracheobronchial tree, or esophagus
the patient's clinical status depends on the rate of air leakage and size of wound
Spontaneous pneumothorax
sudden onset of air in the pleural space with deflation of the affected lung in the absence of trauma
Tension pneumothorax
buildup of air under pressure in the pleural space resulting in interference with filling of both the heart and lungs
Open pneumothorax
sucking wound of chest which implies an opening in the chest wall large enough to allow air to pass freely in and out of thoracic cavity with each attempted respiration
Hemothorax
presence of blood in the pleural space as a result of penetrating or blunt chest trauma
it accompanies a high percentage of chest injuries.
patient may be asymptomatic, dyspneic, hypoxemic, hypotensive, apprehensive, or in shock.
empyema
in hemothorax, can result in hidden blood loss, increased risk of
empyema
collection of thick, infected pus inside the pleural cavity
absent breath sounds
tracheal deviation
diminished or X of affected side, X to unaffected side
Hyperresonance
There is X and diminished breath sounds on the affected side in pneumothorax