Homework ku( tension pneumothorax)

Tension pneumothorax is the accumulation of air under pressure in the pleural space.
This condition develops when injured tissue forms a 1-way valve, allowing air to enter the pleural space and preventing the air from escaping naturally.
Arising from numerous causes, this condition rapidly progresses to respiratory insufficiency, cardiovascular collapse, and, ultimately, death if unrecognized and untreated. Favorable patient outcomes require urgent diagnosis and immediate management.
Tension pneumothorax is a clinical diagnosis that now is more readily recognized because of improvements in emergency medical services (EMS) and the widespread use of chest x-rays.

This picture shows a chest radiograph with 2 abnormalities: (1) tension pneumothorax and (2) potentially life-saving intervention delayed while waiting for x-ray results. Tension pneumothorax is a clinical diagnosis requiring emergent needle decompression, and therapy should never be delayed for x-ray confirmation.

Etiology

The most common etiologies of tension pneumothorax are either iatrogenic or related to trauma. They include the following:

• Trauma (blunt or penetrating) – Involves disruption of either the visceral or parietal pleura and is often associated with rib fractures (rib fractures not necessary for tension pneumothorax to occur)
  
  

  
  

  Image depicting multiple fractures of the left upper chest wall. The first rib is often fractured posteriorly (black arrows). If multiple rib fractures occur along the midlateral (red arrows) or anterior chest wall (blue arrows), a flail chest (dotted black lines) may result.

  
  
  
  
• Barotrauma secondary to positive-pressure ventilation, especially when using high amounts of positive end-expiratory pressure (PEEP)
  
  

  
  

  
  

  
  

  Pneumomediastinum from barotrauma may result in tension pneumothorax and obstructive shock.

  
  
  
  
  

  
  

  A patient in the intensive care unit (ICU) developed pneumopericardium as a manifestation of barotrauma.

  
  
• Central venous catheter placement, usually subclavian or internal jugular²
• Conversion of idiopathic, spontaneous, simple pneumothorax to tension pneumothorax
• Unsuccessful attempts to convert an open pneumothorax to a simple pneumothorax in which the occlusive dressing functions as a 1-way valve
• Chest compressions during cardiopulmonary resuscitation (CPR)
• Pneumoperitoneum^3,4
• Fiberoptic bronchoscopy with closed-lung biopsy⁵
• Markedly displaced thoracic spine fractures
• In recent years, acupuncture has been reported to result in pneumothorax.^6,7,8
• Preexisting Bochdalek hernia with trauma⁹
• Colonoscopy¹⁰ and gastroscopy have been implicated in case reports.
• Percutaneous tracheostomy¹¹

Pathophysiology

Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal pleura, or the tracheobronchial tree. The disruption occurs when a 1-way valve forms, allowing air inflow into the pleural space and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases with each inspiration because of the 1-way valve effect. As a result, pressure rises within the affected hemithorax. As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure build-up causes the mediastinum to shift toward the contralateral side and impinge on both the contralateral lung and the vasculature entering the right atrium of the heart. This condition leads to worsening hypoxia and compromised venous return. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. It is most evident in trauma patients who may be hypovolemic with reduced venous blood return to the heart.
Researchers still are debating the exact mechanism of cardiovascular collapse, but, generally, they believe the condition develops from a combination of mechanical and hypoxic effects. The mechanical effects manifest as kinking or compression of the superior and inferior vena cava because the mediastinum deviates and the intrathoracic pressure increases. Hypoxia leads to increased pulmonary vascular resistance via vasoconstriction. In either event, decreasing cardiac output and worsening metabolic acidosis secondary to decreased oxygen delivery to the periphery occur, thus inducing anaerobic metabolism. If the underlying problem remains untreated, the hypoxemia, metabolic acidosis, and decreased cardiac output lead to cardiac arrest and death.

Presentation

Clinical interpretation of the presenting signs and symptoms of a tension pneumothorax is crucial for diagnosing and treating the condition.

• Early findings
  
  • Chest pain
  • Dyspnea
  • Anxiety
  • Tachypnea
  • Tachycardia
  • Hyperresonance of the chest wall on the affected side
  • Diminished breath sounds on the affected side
  
  
• Late findings
  
  • Decreased level of consciousness
  • Tracheal deviation toward the contralateral side
  • Hypotension
  • Distention of neck veins (may not be present if hypotension is severe)
  • Cyanosis
  
  

These findings may be affected by the volume status of the patient. In hypovolemic trauma patients with ongoing hemorrhage, the physical findings may lag behind the presentation of shock and cardiopulmonary collapse.
In nonventilated patients, the diagnosis of tension pneumothorax often requires a high level of suspicion and the presence of decreased or absent breath sounds on the affected side.
In ventilated patients, the physician may begin to suspect tension pneumothorax when increased pleural pressures necessitate an increase in peak airway pressure in order to deliver the same tidal volume. Decreased expiratory volumes secondary to air leakage into the pleural space and increased end-expiratory pressure, even after discontinuation of PEEP, are 2 other signs of tension pneumothorax in these patients. Occasionally, the development of tension pneumothorax may be delayed for hours to days after the initial insult, and the diagnosis may become evident only if the patient is receiving positive-pressure ventilation. Tension pneumothorax has been reported during surgery with both single and double lumen tubes.
Increased pulmonary artery pressures and decreased cardiac output or cardiac index are evidence of tension pneumothorax in patients with Swan-Ganz catheters.