Term
| What is the basic pathophysiology of dyspnea and exercise intolerance in all airspace filling diseases (e.g. ARDS, pulmonary edema, hemorrhage and Pneumonia) |
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Definition
Alveolar filling reduces Vt and causes V/Q inequality.
1) Decreased Vt leads to increased Vd/Vt and dyspnea
2) Increased V/Q leads to decreased PaO2 and increased dead space ventilation. |
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Term
| What are the 3 critical features of ARDS? |
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Definition
Hypoxemic respiratory failure with loss of lung compliance due to lack of surfactant.
1) Bilateral airspace pulmonary infiltrates (reflecting alveolar edema)
2) No evidence of elevated pulmonary microvascular hydrostatic pressures (Non-cardiogenic edema, PAOP < 18 mm Hg)
3) Significant Hypoxemia has measured by reduced P/F (partial pressure in blood: inspired) ratio (<200)
** Best if FiO2 > 0.5 and PEEP > 10
- If PF ratio < 300, it is Acute Lung injury (ALI)
- If PF ratio <200, it is ARDS (more severe) |
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Term
| How does hypoxemia in ARDS arise? |
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Definition
Shunt produced by alveolar edema due to abnormal fluid movement at the aveolar-capillary membrane.
1) Injury of lung parenchyma leads in increased permeability (PMN mediated), loss of normal surfactant in airspace and capillary thrombi formation.
2) These changes produce shunt physiology, loss of lung compliance with restrictive physiology and pulmonary HTN. |
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Term
| Describe the inflammatory process that occurs in the exudative stage of ARDS. |
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Definition
| Injury leads to PMN and macrophage recruitment to alveolar space, ultimately leading to loss of Type 1 pneumocyte function. |
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Term
| What are the clinical signs and symptoms of ARDS? |
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Definition
1) Dyspnea with acute hypoxemia (maybe hypercapnia)
2) Tachycardia, high RR and elevation of blood pressure |
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Term
| How can you distinguish ARDS from CHF? |
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Definition
Both have tachypnea, tachycardia and dyspnea, producing pulmonary edema.
1) Changes in Weight, fluid balance and EKG may indicate CHF
**May need to use swan ganz catheterization** |
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Term
| What is the clinical course of ARDS? |
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Definition
Exudative and Proliferative stages over 2 weeks.
1) Exudative
- Epithelial injury with cellular swelling, denudation of type 1 cells, hyaline membranes, fibrin deposition and interstitial PMN infiltration.
- Diffuse bilateral alveolar pulmonary infiltrates and marked decrease in oxygenation from shunt physiology.
2) Proliferative
- Organization/clearing of alveolar and interstitial infiltrates with Fibroblast proliferation and Type II cell hyperplasia, as well as lymphocyte infiltration.
- Extensive collagen deposition (decreased compliance) leads to high ventilatory impedance and elevated dead-space fraction |
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Term
| What are the major predisposing conditions and risk modifiers of ARDS? |
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Definition
If you get ALI/ARDS with these features (small %), it is 5X as bad.
1) Predisposing
- Sepsis
- Aspiration
- Emergency surgery
2) Modifiers
- Alcohol (increases risk for given case of predisposition) |
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Term
| What are the major pathologic and radiological findings found in ARDS? |
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Definition
1) Diffuse alveolar damage DAD (50% of the time)
2) Bilateral pulmonary infiltrates |
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Term
| What is the best clinical and physiologic predictor of ALI/ARDS outcomes? |
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Definition
1) Physiological is Deadspace
2) For clinical, trauma is best outcome and sepsis is
worst |
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Term
True or False:
Pulmonary HTN increases mortality associated with ARDS |
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Definition
True
There is a significant vascular component to ARDS, with increased PVR |
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Term
True or False:
Oxygenation defect as measured by PaO2/FiO2 and PEEP predicts outcomes for ARDS patients. |
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Definition
False!
Dead Space is best physiologic predictor and Oxygenation defect is caused by shunt physiology. |
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Term
| What are the important principles of ARDS management? |
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Definition
1) Reduce intrapulmonary shunting without aggravating lung injury (hypoxemic respiratory failure)
2) Regulate airspace edema with compromising CO (noncardiogenic edema)
3) Minimize complications associated with prolonged ICU time (prolonged critical illness) |
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Term
| How is ventilator support used to manage ARDS? |
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Definition
Low Vt management to avoid a) Barotrauma (Pneumothorax, Pneumomediastinum), b) Volutrauma (overinflation damage) and c) Biotrauma (inflammatory mediators)
**Challenging due to heterogeneity of damage**
** May be aided by paralytic cisatracurium**
- Reduced Vt (12 mg/kg) leads to decreased circulating inflammatory mediators (actually influences progression) |
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Term
| How can you address hypoxemia in ARDS? |
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Definition
FiO2, PEEP and Ventilator
1) Increase inspired oxygen concentration (FiO2), but complicated by heterogeneous lung disease
2) PEEP (expiratory) and/or CPAP (spontaneous breathing) to "recruit" collapsed lung and reverse shunt, but watch out for Barotrauma
High PEEP/low FiO2 has barotrauma risk
Low PEEP/high FIO2 has oxygen toxicity risk |
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Term
| What does the paralytic agent, Cisatracurium, have to due to management of ARDS? |
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Definition
| If you give it during first 48 hours of ventilator support, people survive more. |
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Term
| Why is ventilator management so challenging in ARDS? |
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Definition
1) Heterogeneity of damage means V/Q mismatching and barotrauma risk
2) Increased Vd combined with high respiration inflation impedance places demands on mechanical support
3) Hypoxemia demands increased PEEP to reduce shunt physiology without aggravating lung injury. |
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Term
| What paradox of ARDS makes fluid management especially challenging? |
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Definition
Pressure makes edema, but you need pressure for CO
1) Capillary leakage leads to greater Pulmonary edema for given LVED (wedge) pressure.
2) Heart has undergone shift of starling curve to right, so cardiac function NEEDS higher filing pressure to maintain CO
DRY strategy is better, since it reduces transfusion need and ventilator dependence. |
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Term
True or False:
A liberal "wet" fluid management strategy is indicated in ARDS. |
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Definition
False!
FACCT trial shows this increases ventilator time and transfusion need without improving mortality!
Keep the edema so you can keep the CO, basically. |
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Term
| What is the single indicated management strategy for gas exchange defects in ARDS? |
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Definition
| Mechanical ventilation with PEEP, perhaps with neuromuscular blockage in first 48h. |
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Term
| Why do patients who are recovering/recovered from ARDS have reduced physical function? |
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Definition
| Prolonged periods of immobility in ICU |
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Term
| What is the prognosis of ARDS? |
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Definition
| Most recover lung function by 3 months following lung injury |
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Term
| What is the hallmark pathological findings of ARDS? |
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Definition
Diffuse Alveolar Damage (DAD)
Here, "diffuse" means involvement of all parts of a single alveolus (epithelium, endothelium and interstitial space).
"lung" involvement can be either focal or diffuse |
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Term
| What is the disease associated with the emergence of DAD in a previously healthy individual? |
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Definition
| Acute Interstitial Pneumonia or "Hamman-Rich disease." |
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Term
| What gross and histologic findings are associated with ARDS? |
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Definition
1) Gross
- boggy, firm, red and HEAVY lungs (acutely)
- dark and fibrotic (proliferative)
2) Histological
- Acute/exudative in first week
-Hemorrhage EDEMA 1st
- HYALINE membranes
**Type 2 pnuemocyte hyperplasia precedes Proliferative stage**
- Proliferative or Organizing (FIBROSIS) after 1-2 weeks |
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Term
| What are the two gross patterns of bacterial Pnuemonia? |
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Definition
Both tend to occur in lower lobes and may be overlapping/caused by same organisms!
1) Lobar
- acute infection involving large amount of lobe
- S. pneumo
2) Bronchopneumonia (lobular)
- Patchy consolidation of parenchyma. |
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Term
| What are the 4 major pathological stages of Lobar Pneumonia? |
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Definition
1) Congestion (>24h)
- dilated alveolar capillaries
- air spaces filled with eosinophilic fluid with few PMNs
2) Red hepatization (24h-2d)
- Red, firm and airless
- Numerous pnuemococci in PMNs.
3) Grey hepatization (2-3d)
-Decreased capillary congestion and leukocyte migration to alveoli.
4) Resolution
- Macrophage ingestion of debris or fibroblast organization into permanent adhesions. |
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Term
| What are the gross and histopathalogical signs of bronchopneumonia? |
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Definition
S. aureus, S. pyogenes, H. influenzae, K. pnuemonia, Legionella
1) Gross
- Patchy yellow white tan infiltrates
2) Microscopically
- PMNs in bronchi, broncioles and adjacent airspaces |
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Term
| What are the 4 major complications of Pneumonia? |
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Definition
1) Abscess formation from tissue necrosis
- K. pneumonia or type 3 pneumococci
2) Empyema
3) Organization of excavate leading to scarring
4) Bacterial dissemination. |
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Term
| What are the classic causes of Pneumonia in the immnocompromised host? |
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Definition
1) Bacteria
Gram-negative and Gram-positive including Pseudomonas aeruginosa, Mycobacterium sp, Legionella pneumophilia and Listeria monocytogenes)
2) Viral
- CMV, HSV
3) Fungal
- PJP, Candida sp, Aspergillus sp, the Phycomycetes, Cryptococcus neoformans |
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Term
| What are the classic histopathologic features of Atypical pneumonia due to mycoplasma infection? |
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Definition
1) Airway obstruction/bronchiectasis
2) Micro-abscesses and Ill-defined granulomas (no necrosis and few giant cells) |
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Term
| Which of the following is the most commonly infected cell in CMV Pneumonia? |
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Definition
Macrophages (pneumocytes, endothelial and epithelial cells are also common though)
Remember, you see cellular enlargement with nuclear (purple with halo) and cytoplasmic (basophilic on PAS) inclusions |
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Term
| What infections are commonly associated with CMV pneumonia? |
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Definition
Immunocompromised so think Pnuemocystis
Remember, usually there is interstitial pneumonia without necrosis |
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Term
| What are the classic histopathalogical findings in Pnuemocystis Pneumonia? |
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Definition
Organisms are in hyaline membranes within alveolar spaces (no budding)
1) Frothy, foamy or honeycomb exudate within airspaces associated with interstitial pnuemonia (associated with CMV pneumonia as well).
**most often seen in AIDS patients with pneumocystis**
2) DAD in non-AIDS patients
3) Helmet-shaped cysts on GMS staining |
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Term
| What are the 3 forms of aspergillosis lung infection? |
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Definition
- Hemorrhagic infarction with minimal inflammation.
- Fungal hyphae invades blood vessel walls and alveolar septa
- Arterial lumens can be completely occluded by plugs of fungi
1) Invasive
2) Saprophytic
3) Allergic |
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Term
| What are the 3 typical histopathological signs of Aspergilliosis? |
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Definition
1) Hemorrhagic infarction with minimal inflammation.
2) Fungal hyphae invades blood vessel walls and alveolar septa
3) Arterial lumens can be completely occluded by plugs of fungi |
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Term
| What is the difference between how alcohol and sepsis change the course of ARDS? |
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Definition
Sepsis is a serious "pre-disposing" factor. A small number of people with sepsis actually get ARDS, but when they do, it is 5X as bad.
Alcohol is a "modifying factor" that makes Septic ARDS WORSE, but does not predispose to ARDS itself. |
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