ARDS Flashcards
Causes of ARDS
Alveolar capillary interface becomes damaged and more permeable to intravascular fluid –alveoli fill with fluid
Sepsis Pneumonia Aspiration Trauma Massive transfusions Pancreatitis Shock states
Inflammation!!
How do we define ARDS clinically
Acute onset
Bilateral infiltrates
Severe, refractory hypoxemia PaO2/FiO2 ratio
PaO2/FiO2 ratios and severity of ards
200-300 mild
100-200 moderate
<100 severe
Refractory hypoxemia results from & leads to..
Severe V/Q mismatch & shunting of pulmonary capillary blood
Unresponsive to increasing O2 concentrations
Lungs are less compliant
Increased airway pressures must be generated.
Exudative phase changes
Inflammatory mediators • Disruption of alveolar capillary membrane • Fluid in the alveoli • V/Q mismatch • Loss of surfactant=alveolar collapse
Manifestations of Exudative phase
Tachypnea and tachycardia • Mild hypoxemia and respiratory alkalosis caused by hyperventilation • Dyspnea, tachypnea, cough, restlessness • Chest auscultation may be normal or may reveal fine, scattered crackles
Proliferative phase changes
Inflammatory mediators cross ACM = damaged alveolar and capillary epithelium = diffusion defects • V/Q worsens • Pulmonary HTN due to hypoxemic vasoconstriction=R HF • Fibrotic changes
Proliferative phase manifestations
Decreased lung compliance=increased work of breathing=tachypnea • Hypercarbia and worsening refractory hypoxemia • Diaphoresis, decreased LOC, cyanosis, and pallor • Increased peak inspiratory pressures
Fibrotic phase changes
Changes • Diffuse scarring • Worsening pulmonary HTN • Worsening V/Q mismatch, diffusion defects and shunting
Fibrotic phase manifestations
• R sided HF • Decreased BP, CO • Refractory hypoxemia • Tissue hypoxia/lactic acidosis
Diagnostic labs and testing for ARDS
• CXR – bilateral infiltrates – Ground glass appearance • Laboratory testing – ABGs – CBC with differential – Cultures – CMP
Treatment for ARDS
• Treat the Cause! • Mechanical Ventilation with PEEP • Diuresis • Antibiotics • Steroids - improve oxygenation, not survival – use is controversial • Hydration – maintain circulatory volume, decrease viscosity of secretions • Nutrition
Mechanical ventilation
– Low Tidal Volumes to reduce barotrauma
– High PEEP to aid in recruitment
– No mode proven to improve outcomes
– Requires advanced airway
Positive End Expiratory Pressure
PEEP
• Increase FRC and open up collapsed alveoli
• Higher levels of PEEP are often needed to maintain
Pa
O
2 at 60 mm Hg or greater
• High levels of PEEP can compromise venous return
•
↓ Preload, CO, and BP
Nursing O2 managment
Nursing • Optimize O2 delivery – Frequent assessment – hemodynamic and ventilatory – Keep the airways clear • Minimize O2 demand - Decrease O2 consumption – Comfort – Sedation – Pain relief – Neuromuscular blockade
• Positioning for ards
– Prone positioning
– Elevate HOB
– Frequent changes
Risk factors for PE
DVT:Virchow’s triad • Venous stasis/prolonged immobility • Vessel wall damage • Hypercoagulability Smoking Obesity Fractures (hip/leg) Major surgery/trauma Malignancy
Types of PE
Blood clot • Fat embolus • Air embolus • Amniotic fluid • Tumor particles
Pathophysiology of PE
Obstruction in Pulmonary Artery --> Ventilation‐ Perfusion Mismatch (high V/Q/dead space ventilation)---> Hypoxemia Local Vasoconstriction (pulmonary HTN R heart failure)
Classification (massive PE)
– Profound hypotension
– R & L ventricular dysfunction
– Shock/cardiac arrest
Classification: Submassive PE
– Normotensive
– R ventricular dysfunction
– Elevated cardiac markers
Classification: Low risk PE
– Normotensive/No ventricular dysfunction or elevation in cardiac
markers
Pts can have PE w/o symptoms, may or may not need hospitalization
Initial PE clinical manifestations
- Dyspnea
- Chest pain (most common, pleuretic chest pain)
- Tachypnea
- Tachycardia
Submassive/Massive PE
clinical manifestation
• R heart failure with JVD • Hypotension • Anxious/restless/confused • Hypoxia • Poor peripheral perfusion • Hemoptysis with pulmonary infarction
Diagnosis of PE (imagine/labs)
Primarily to R/o other causes -Imaging – CXR – CT scan (w/con) • Laboratory testing – D-dimer (key test) tells us if there are fibrin degradation products in the blood – ABG (massive/submassive) – Cardiac markers(massive/submassive)
Medical management once PE diagnosed
Anticoagulation
• IVC filters - prevent recurrence
• Cautious fluid management (prevent R heart failure)
• Hemodynamically compromised
– Thrombolytics (break down the clot)
– Embolectomy (instrument will break down clot)
– Vasoactive/inotropic support
Nursing assessments for PE
Oxygenation/Spo2 • Chest pain (better/worse?) • VS • Labs – ABGs – Lactate – Coagulation studies – Cardiac markers (damage in cardiac tissue) • Urine output (CO)
Nursing actions for PE
Provide O2 • Elevate HOB • Medication Management • Fluid management • Bleeding precautions
Nursing actions for PE
Provide O2 • Elevate HOB • Medication Management • Fluid management • Bleeding precautions
Pneumo/hemothroax
Collection of air/blood in the pleural
space
Reduction in the negative thoracic
pressure and poor lung expansion
Reduction of gas exchange at the
alveolar level resulting in hypoxemia
Manifestations (Pneumo/hemothorax)
- Decreased oxygenation
- Tachypnea = Respiratory alkalosis
- Later - respiratory acidosis
- Pain (severe) ECG r/o MI
- SOB
- Agitation, anxiety
- Later – Decreased LOC
Chest tube types
Hooked up to drainage system can be water filled or dry/amount of suction to dial in pressure (common)
Pneumo - chest tube higher bc air rises
hemo- low because of gravity
Assessment of chest tube
- Monitor vital signs, SpO2, pain, SOB
- Secure Connections
- Observe tidaling
- Observe for air leak (bubbling in water-seal chamber)
- Monitor drainage
- If break in system, place distal end in sterile water to maintain water-seal
- Do NOT clamp!
