Respiratory Flashcards
What is ARDS?
ARDS is the severe form of ARF
It’s a severe acute illness described by the following symptoms: dyspnea, decreased lung compliance, and diffuse infiltrates on CXR. This is a severe form of acute lung injury.
ARDS usually develops after trauma or when excessive fluid administration is required. Furthering develop a non-cardiogenic pulmonary edema due to the decreased lung compliance and massive fluid leakage throughout the body, producing edema. A cell-mediated (overly aggressive immune response alveolar-capillary damage is another role played among the development of edema.
What are the diagnostic criteria of ARDS?
Acute onset within 1 week after clinical insult
Bilateral pulmonary opacities not explained
Altered PaO2/FiO2 (severity is determined by these characteristics when the patient is treated with PEEp or CPAP of 5cm H20 higher)
What are other features of ARDS that ARF has?
Hypoxemia that persists even when 100% oxygen is administered: refractory hypoxemia (this is a cardinal feature)
No cardiac pulmonary bilateral edema
Decreased pulmonary compliance
Dyspnea
Ground-glass appearance-dense pulmonary infiltrates on CXR
What are the classifications of ARDS (mild, moderate, and severe)?
Mild: 200-300
Moderate: 100-200
Severe: less than 100
What are the diagnostic tools for ARDS?
Hemodynamic measurement ABGs Mixed venous blood gases Serial chest radiography Bronchoscopy BNP
What are the most common causes of acute lung injury?
Remember this is associated to ARDS since ARDS does develop after trauma
Shock, trauma, serious nervous injury, pancreatitis, fat and amniotic fluid emboli, infections(pulmonary and sepsis), inhalation of toxic gases, pulmonary aspirations (stomach contents), drug ingestion, multiple transfusion, cardiopulmonary bypass, submersion in water with water aspiration.
What are the symptoms of ARDS that usually develops 4–48 hours after initiating events?
Initial signs of ARDS: fine crackles, restlessness, disorientation, and change in LOC, increased temperature and pulse.
Dyspnea and tachypnea eventually severe hypoxemia clinical finding: this hypoxemia does not respond to supplemental oxygen therapy
Commonly PaO2: greater than 60;PCO2: greater than 45; HCO2: less than 22 this is with aggressive oxygen therapy
Decreased oxygen levels will then cause restlessness, apprehension, mental sluggishness, motor dysfunction, and tachycardia-hyperventilation with normal breath sounds and respiratory ALKALOSIS initially then respiratory ACIDOSIS
As the lungs become non compliant, making ventilation difficult, resulting in hypo ventilation and respiratory acidosis.
Initially CXR normal then worsens and progresses to “white-out” over first 24-48 hours after onset. Increased PIP on ventilation and supplemental oxygen.
Monitor for lactic acidosis due to the plausible lactic acid buildup due to metabolic acidosis.
What are the preventive measures of ARDS?
Careful fluid management
Aspiration precautions: elevate HOB, monitor ability to swallow, and more
Avoid high tidal volumes on non-ARDS ventilated patients
What are the treatments to maintain PaO2 and need intubation with mechanical ventilation?
To prevent oxygen toxicity and increased morality, the goal is maintain PaO2 with levels FiO2 at 0.50. Use a lung-protective strategies consist of low Vt (4-8mL/kg, lung-end expiratory plateau pressure (<30 cm H2O), FiO2 at nontoxic levels (<0.60), and PEEP.
Volume ventilation with PEEP to restore functional residual capacity
Goal is PaO2 >60 or oxygen saturation >90%at lowest possible FiO2
PEEP: causes decrease in cardiac output, cause hypotension, tachycardia, decreased urine output and if high may even cause lung damage.
Monitor patients, for changes in respiratory status such as increased respiratory rate, worsening adventitious breath sounds, decreased or absent breath sounds, decreased SpO2, and increasing dyspnea
What treatment is used for ARDS?
Light sedation: with propofol and opioids such as fentanyl or morphine
Undersedation: results in dyssynchroncy
Oversedation: can lead to a prolong sequelae such as delirium
Providing comfort with decreased the WOB consumption “bucking the vent”
Sedation
Pain relief
Neuromuscular blocking agents: early short-term administration agents in patients with severe ARDS my improve survival without increasing muscle weakness. If on the agent also administer sedation concurrent since the neuromuscular blockers paralyze so without sedation anxiety and oxygen consumption increases.
Stagger activities
Suction
Fluid and electrolyte balance: diuretics are helpful if hypotension is present use aggressive fluids
Daily weight and intake and output
Steroids(fat emboli or chemical injury)
Adequate nutrition: 35-45 kcal/kg/day within 48 hours for critically ill adults, may need TPN
Positioning: for more than 12 hours has been shown to decrease mortality in those with moderate ARDS when used with lower Vt ventilation.
Prone Positioning: improves perfusion to posterior lung this alters V/Q ratio by maintaining posterior perfusion while allowing optimal ventilation in the larger, dorsal portion of the lungs. Placing the patient prone removes the weight of of the heart and abdomen from the lungs, facilitates removal secretions, improves oxygenation, and enhances recruitment of airway.
Complications occur from accidental dislodge net of tubes and lines, gastric aspiration, peripheral nerve injury, pressure ulcer, corneal ulceration, facial edema, and agitation.
Treatment during prone positioning: administer pro-motility agent (minimize risk of vomiting and enhance gastric contents); use pillows and foam support (maintain body alignment and prevent overextension or flex ion of the spine);place hydrocolloid or silicone dressing (maintain skin integrity); reposition hourly (reduce facial edema and ocular pressure).
Continuous lateral rotation therapy
Provide oral care
Apply moisturizer to face to prevent skin from massive amount of drainage from the mouth
Lubricate eyes (prevent corneal drying)
Assess patient frequently if they tolerate prone positioning.
What are the different types of asthma?
Allergic asthma
Intrinsic asthma: specific cause cannot be identified and are not related to allergies. I may be precipitated by situations such as cold, URI, or GERD, smoke, etc. Less responsive to treatment
Exercise-induced asthma: worsens in cold dry weather.
Occupational asthma
Steroid-asthma: severe form of asthma that is resistant to steroids the major treatment for asthma.
Nocturnal, or sleep-related asthma: tends to be worsen between midnight and 4am. Possibly triggered by allergens in bleeding, cool temperature or GERD.
Aspirin and NSAID: ingestion of ASA, their is a clinical triad of bronchial asthma, nasal polyps, and reaction to ASA. Symptoms are water, rhinorrhea, flushing of upper body, N&V, wheezing, dyspnea, and cyanosis.
Status asthmatics: bronchi constriction does not respond to bronchodilator therapy
What are the initial manifestations of asthma?
Wheezing (worse sound is absent of breathing
Dyspnea with increased mucous production
Chest tightness with decreased breath sounds
Nonproductive cough (worse at night or early morning)
Hyperventilation first then airways become narrow and exhalation
What signs of asthma that impede ARF?
“Silent” chest
Breathlessness rest and the need to hunch forward
Single-word response
Agitation, confusion, and drowsiness
Respiratory rate greater than 30 breaths/min;heart rate greater than 120 breaths/min; and oxygen saturation greater than 90%
What the client management for asthma?
Oxygen:goal is to keep PaO at 60-70 for an oxygen saturation greater 90% may need mechanical ventilation
IV corticosteroids
Inhaled bronchodilator (beta 2 agonists such as Proventil and Ventolin)
Prevention of future episodes
Develop and use of a personal asthma that includes medication compliance, use of peak flow meter BID to assess lung status, lifestyle changes, and always carry a rescue inhaler with them
What are the causes of pneumonia?
Aspiration of gastric or oropharyngeal secretions
Inhalation of aerosols or particles
Spread from another infected area of the body into the lungs
Impaired mucociliary clearance allows the large influx of phagocytic cells and exudate to enter the airways and alveoli. This leads to ventilation perfusion mismatch that results in hypoxia, dyspnea, fever, and leukocytosis
