1. Part V Chest and Pleural Trauma

2. Chapter 21 Flail Chest
Figure Flail chest. Double fractures of three or more adjacent ribs produce instability of the chest wall and paradoxical motion of the thorax. Inset, Atelectasis, a common secondary anatomic alteration of the lungs.

3. Anatomic Alterations of the Lungs
Double fracture of numerous adjacent ribs
Rib instability
Lung restriction
Atelectasis
Lung collapse
Lung contusion
Secondary pneumonia

4. Etiology Direct compression by a heavy object Automobile accident
Industrial accident

5. Overview of the Cardiopulmonary Clinical Manifestations Associated with FLAIL CHEST
The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by Atelectasis (see Figure 9-7) and Pneumonic Consolidation (see Figure 9-8)—the major anatomic alterations of the lungs associated with flail chest (see Figure 21-1).

6. Figure 9-7. Atelectasis clinical scenario.
Figure 9-7. Atelectasis clinical scenario.

7. Figure 9-8. Alveolar consolidation clinical scenario.

8. Clinical Data Obtained at the Patient’s Bedside
Vital signs
Increased respiratory rate
Stimulation of peripheral chemoreceptors
Other possible mechanisms
Decreased lung compliance
Activation of the deflation receptors
Activation of the irritant receptors
Stimulation of the J receptors
Pain/anxiety
Increased heart rate, cardiac output, blood pressure

9. Figure 21-2. Lateral flail chest with accompanying pendelluft.

10. Figure 21-3. Venous admixture in flail chest.

11. Clinical Data Obtained at the Patient’s Bedside
Paradoxic movement of the chest wall
Cyanosis
Chest assessment findings
Diminished breath sounds
On the affected as well as the unaffected side

12. Clinical Data Obtained from Laboratory Tests and Special Procedures

13. Pulmonary Function Study: Lung Volume and Capacity Findings
VT RV FRC TLC
N or    
VC IC ERV RV/TLC%    N

14. Arterial Blood Gases Mild to Moderate Flail Chest
Acute alveolar hyperventilation with hypoxemia
pH PaCO HCO PaO2
   (Slightly) 

15. Alveolar Hyperventilation
Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
100 90
Point at which PaO2 declines enough to stimulate peripheral oxygen receptors 80 70 60
PaO2
PaO2 or PaCO2 50 40 30
PaCO2 20 10
Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.

16. Arterial Blood Gases Severe Flail Chest
Acute ventilatory failure with hypoxemia
pH PaCO HCO PaO2
   (Slightly) 

17. Alveolar Hyperventilation Acute Ventilatory Failure
Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
Acute Ventilatory Failure
100
Point at which disease becomes severe and patient begins to become fatigued 90
Point at which PaO2 declines enough to stimulate peripheral oxygen receptors 80 70
PaCO2
Pa02 or PaC02 60 50 40 30
PaO2 20 10
Figure PaO2 and PaCO2 trends during acute ventilatory failure.

18. Oxygenation Indices QS/QT DO2 VO2 C(a-v)O2   Normal (severe)
O2ER SvO  

19. Hemodynamic Indices (Severe Flail Chest)
CVP RAP PA PCWP
   
CO SV SVI CI
   
RVSWI LVSWI PVR SVR
   

20. Radiologic Findings
Chest radiograph
Increased density
Rib fractures

21. Figure A, Chest X-ray film of a 20-year-old female with a severe right-sided flail chest. B, Close-up of the same X-ray film, demonstrating rib fractures (arrows).

22. General Management of Flail Chest
Mild cases
Medication for pain and routine bronchial hygiene
Severe cases
Volume-controlled ventilation with PEEP
5 to 10 days usually adequate for sufficient bone healing

23. General Management of Flail Chest
Respiratory care treatment protocols
Oxygen therapy protocol
Hyperinflation therapy protocol
Mechanical ventilation protocol

24. Classroom Discussion Case Study: Flail Chest