ARDS/Pulm effusion Flashcards
(44 cards)
Acute Respiratory Distress Syndrome (ARDS)
general
Life-threatening diffuse inflammatory form of lung injury
Characterized by bilateral lung infiltrates and progressive hypoxemia without cardiac failure
The underlying mechanism of ARDS is capillary endothelial injury and diffuse alveolar damage (DAD)
Epidemiology:
Most common cause of non-cardiogenic pulmonary edema
~190,000 cases of ARDS in the United States each year
~22% of patients who are mechanically ventilated meet the criteria for ARDS
Mortality rate: 9-20%
(you give supplemental O2 and they stay hypozic and desat) (can;t be related to cardio
ARDS
Etiology
Direct lung injury
Results from clinical disorders that affect the lungs either directly or indirectly
Direct lung injury:
Bacterial and viral pneumonia
Aspiration of gastric contents
Pulmonary contusion
Near-drowning incidents
Toxic inhalation injury
Lung transplant
ARDS
Etiology
Indirect lung injury
Indirect lung injury:
Sepsis (most common cause)
Severe trauma with prolonged hypovolemic shock
Drug overdoses
Bone marrow transplantation
Post-cardiopulmonary bypass
Massive blood transfusion
Pancreatitis
Fat or amniotic fluid embolism
ARDS
Patho - 1
EXUDATIVE
(the worst phase)
Occurs in 3 phases – exudative, proliferative, fibrotic
Exudative: 6-72 hours after the eliciting factor
Initial injury (cytokines) causing damage to pneumocytes and pulmonary endothelium → disrupted barriers between capillaries and airspaces (leaky)
Inflammatory reaction is initiated with endothelial cells secreting pro-inflammatory molecules and expressing adhesion molecules on their surface
Immune cells (neutrophils – 1st to arrive) stick and then migrate into the alveoli → neutrophils will release proteases and reactive oxygen molecules, and more cytokines to perpetuate the cycle
Edema fluid, protein, and cellular debris flood the airspaces
Disruption of surfactant → ↑ surface tension → airspace collapse, ventilation-perfusion mismatch, right-to-left shunting of venous blood leading to pulmonary hypertension
ARDS
what kind of shunting do we see?
Right to left.
deoxygenated blood getting back into circulation leading to hypoxia
ARDS
Patho - 2
Proliferative
Beginning stages of lung repair
Alveolar epithelial cells begin proliferating along the alveolar basement membranes
Macrophages clean up cellular debris and attract and activate fibroblasts
New pulmonary surfactant is produced
ARDS
Patho - 3
Fibrotic
Abnormal deposition of collagen in the alveolar ducts and interstitial membranes by fibroblasts
Lung scarring; “stiff” lungs → restrictive lung disease
Stiff lungs – poor lung compliance, reduced diffuse capacity, microvascular occlusion
ARDS
Expected vitals
Mild dyspnea → respiratory distress/failure
Vitals
Tachypnea
Tachycardia
Fever may/may not be present
Hypoxemia despite supplemental oxygen
ARDS
PE findings
Physical exam
Diffuse crackles (rales)
Worse at the bases
Labored breathing
Retractions
Restlessness and/or anxious
Cyanosis
Altered level of consciousness
Exam findingsNOTconsistent with ARDS: new or changed murmur, S3 or S4 gallop, jugular venous distension (JVD), lower extremity pitting edema
ARDS
Dx (4)
Berlin diagnostic criteria of ARDS:
- Acute onset (within 1 week)
- Diffuse bilateral infiltrates on chest x-ray or CT scan
- No evidence of heart failure or fluid overload
- Partial pressure of O2/fraction of inspired O2(PaO2/FiO2) < 300 mmHg:
Mild ARDS:201–300 mm Hg
Moderate ARDS: 101–200 mm Hg
Severe ARDS: ≤ 100 mm Hg
if you have JVD, pulm edema, cardiomegaly,pedal edema its HF not ARDS
CXR Day 1
70-year-old female admitted with acute respiratory failure, fever (38ºC) and dyspnea. She was tachypneic (30 bpm), with lymphopenia and low oxygen saturation (SpO2 85%, PAFI<250). Covid-19 positive.
she died on day 4
ARDS
CXray
Chest X-ray:
ARDS: bilateral pulmonary infiltrates
Finding more consistent with bacterial pneumonia: consolidation
Findings more consistent with cardiogenic pulmonary edema:
Pulmonary venous congestion
Cardiomegaly
Pleural effusion
ARDS
ARDS
Labs
Labs
BNP levels < 100 pg/mL favors ARDS
Arterial blood gas (ABG):
Hypoxemia
Additional testing to determine the underlying cause (example: lipase for possible pancreatitis)
ARDS
Tx
Patients are managed in the ICU
Correct the underlying cause
Supplemental oxygen:
Most patients require a high FiO2 (> 50%)
Delivered via high-flow nasal cannula, nonrebreather face mask, or by intubation (mechanical ventilation)
Failure of oxygen saturation improvement > 90% - suspect right-to-left shunting of blood
Mechanical ventilation:
If oxygen saturation is < 90% on high-flow oxygen
High PEEP
Low tidal volume (6 mL/mg)– most critical factor in reducing mortality rates
Prone positioning improves oxygenation
Fluid management is difficult
Large volume to maintain blood pressure
Fluid restriction to reduce left atrial filling pressure and improve oxygenation
Diuretics can facilitate fluid restriction/removal
Patients will require high PEEP (positive-end expiratory pressure) to keep the alveoli from collapsing
ARDS
Prognosis and RF
Serious condition that is usually associated with high mortality and morbidity
Risk factors forestimating the prognosis in a patient with ARDS:
Advanced age
Direct lung injuries result in twice the number of mortalities
Preexisting organ dysfunction from chronic diseases:
Chronic liver disease
CKD
Immunosuppression
The majority ofpatientsrecover most of their lung function over several months
PE
Pleural Fluid
Forces (hydrostatic and osmotic pressures) responsible for producing pleural fluid within the capillary bed of theparietal pleura
Pleural fluid is absorbed bylymphvessels in the diaphragmatic and mediastinal surfaces of theparietal pleura; ultimately drains into the right atrium
The normal mean rate of production andabsorptionof the pleural fluid is 0.2 mL/kg/hour
The entire volume of pleural fluid normally turns over within 1 hour
How does pleural effusion form?
Formation of a pleural effusion results from:
Overproduction of pleural fluid OR
Inability of the lymphatic system to remove fluid as it is produced
Pleural Effusion
general
Exudative vs transudative
Excessive accumulation of fluid within the pleural cavity (between the parietal and visceral pleura)
Classified as exudative or transudative based on Light’s criteria
Exudative
Caused by inflammation and ↑ capillary permeability
Fluid rich in protein and LDH in the pleural space
Transudative
Caused by a combination of ↑ hydrostatic pressure in the vasculature and ↓ oncotic pressure in the plasma