Obstructive Shock

Although obstructive shock can be caused by a number of different etiologies that result in mechanical obstruction of venous
return (Table 58), in trauma patients this is most commonly due to the presence of tension pneumothorax. Cardiac tamponade occurs when
sufficient fluid
has accumulated in the pericardial sac to obstruct blood flow to the ventricles. The hemodynamic abnormalities in pericardial
tamponade are
due to elevation of intracardiac pressures with limitation of ventricular filling in diastole with resultant decrease in cardiac
output. Acutely, the
pericardium does not distend; thus small volumes of blood may produce cardiac tamponade. If the effusion accumulates slowly
(e.g., in the
setting of uremia, heart failure, or malignant effusion), the quantity of fluid producing cardiac tamponade may reach 2000 mL.
The major
determinant of the degree of hypotension is the pericardial pressure. With either cardiac tamponade or tension pneumothorax,
reduced filling
of the right side of the heart from either increased intrapleural pressure secondary to air accumulation (tension pneumothorax) or
increased
intrapericardial pressure precluding atrial filling secondary to blood accumulation (cardiac tamponade) results in decreased
cardiac output
associated with increased central venous pressure.
Table 5-8 Causes of Obstructive Shock
Pericardial tamponade
Pulmonary embolus
Tension pneumothorax
IVC obstruction
Deep venous thrombosis
Gravid uterus on IVC
Neoplasm
Increased intrathoracic pressure
Excess positive end-expiratory pressure
Neoplasm
IVC = inferior vena cava.

DIAGNOSIS AND TREATMENT

The diagnosis of tension pneumothorax should be made on clinical examination. The classic findings include respiratory distress
(in an awake
patient), hypotension, diminished breath sounds over one hemithorax, hyperresonance to percussion, jugular venous distention,
and shift of
mediastinal structures to the unaffected side with tracheal deviation. In most instances, empiric treatment with pleural
decompression is
indicated rather than delaying to wait for radiographic confirmation. When a chest tube cannot be immediately inserted, such as
in the
prehospital setting, the pleural space can be decompressed with a large caliber needle. Immediate return of air should be
encountered with
rapid resolution of hypotension. Unfortunately, not all of the clinical manifestations of tension pneumothorax may be evident on
physical
examination. Hyperresonance may be difficult to appreciate in a noisy resuscitation area. Jugular venous distention may be
absent in a
hypovolemic patient. Tracheal deviation is a late finding and often is not apparent on clinical examination. Practically, three
findings are
sufficient to make the diagnosis of tension pneumothorax: respiratory distress or hypotension, decreased lung sounds, and
hypertympany to
percussion. Chest x-ray findings that may be visualized include deviation of mediastinal structures, depression of the
hemidiaphragm, and
hypo-opacification with absent lung markings. As discussed above, definitive treatment of a tension pneumothorax is immediate
tube
thoracostomy. The chest tube should be inserted rapidly, but carefully, and should be large enough to evacuate any blood that
may be
present in the pleural space. Most recommend placement in the fourth intercostal space (nipple level) at the anterior axillary line.
Cardiac tamponade results from the accumulation of blood within the pericardial sac, usually from penetrating trauma or chronic
medical
conditions such as heart failure or uremia. Although precordial wounds are most likely to injure the heart and produce
tamponade, any
projectile or wounding agent that passes in proximity to the mediastinum can potentially produce tamponade. Blunt cardiac
rupture, a rare
event in trauma victims who survive long enough to reach the hospital, can produce refractory shock and tamponade in the
multiply-injured
patient. The manifestations of cardiac tamponade, such as total circulatory collapse and cardiac arrest, may be catastrophic, or
they may be
more subtle. A high index of suspicion is warranted to make a rapid diagnosis. Patients who present with circulatory arrest from
cardiac
tamponade require emergency pericardial decompression, usually through a left thoracotomy. The indications for this maneuver
are discussed
in Chap. 7. Cardiac tamponade also may be associated with dyspnea, orthopnea, cough, peripheral edema, chest pain,
tachycardia, muffled

heart tones, jugular venous distention, and elevated central venous pressure. Beck's triad consists of hypotension, muffled heart
tones, and
neck vein distention. Unfortunately, absence of these clinical findings may not be sufficient to exclude cardiac injury and cardiac
tamponade.
Muffled heart tones may be difficult to appreciate in a busy trauma center and jugular venous distention and central venous
pressure may be
diminished by coexistent bleeding. Therefore, patients at risk for cardiac tamponade whose hemodynamic status permits
additional diagnostic
tests frequently require additional diagnostic maneuvers to confirm cardiac injury or tamponade.
Invasive hemodynamic monitoring may support the diagnosis of cardiac tamponade if elevated central venous pressure, pulsus
paradoxus
(i.e., decreased systemic arterial pressure with inspiration), or elevated right atrial and right ventricular pressure by pulmonary
artery
catheter are present. These hemodynamic profiles suffer from lack of specificity, the duration of time required to obtain them in
critically
injured patients, and their inability to exclude cardiac injury in the absence of tamponade. Chest radiographs may provide
information on the
possible trajectory of a projectile, but rarely are diagnostic because the acutely filled pericardium distends poorly.
Echocardiography has
become the preferred test for the diagnosis of cardiac tamponade. Good results in detecting pericardial fluid have been reported,
but the yield
in detecting pericardial fluid depends on the skill and experience of the ultrasonographer, body habitus of the patient, and
absence of wounds
that preclude visualization of the pericardium. Standard two-dimensional or transesophageal echocardiography are sensitive
techniques to
evaluate the pericardium for fluid, and are typically performed by examiners skilled at evaluating ventricular function, valvular
abnormalities,
and integrity of the proximal thoracic aorta. Unfortunately, these skilled examiners are rarely immediately available at all hours
of the night,
when many trauma patients present; therefore, waiting for this test may result in inordinate delays. In addition, although both
ultrasound
techniques may demonstrate the presence of fluid or characteristic findings of tamponade (large volume of fluid, right atrial
collapse, poor
distensibility of the right ventricle), they do not exclude cardiac injury per se. Pericardiocentesis to diagnose pericardial blood
and potentially
relieve tamponade may be used. Performing pericardiocentesis under ultrasound guidance has made the procedure safer and more
reliable.
An indwelling catheter may be placed for several days in patients with chronic pericardial effusions. Needle pericardiocentesis
may not
evacuate clotted blood and has the potential to produce cardiac injury, making it a poor alternative in busy trauma centers.
Diagnostic pericardial window represents the most direct method to determine the presence of blood within the pericardium. The
procedure is
best performed in the operating room under general anesthesia. It can be performed through either the subxiphoid or
transdiaphragmatic
approach. Adequate equipment and personnel to rapidly decompress the pericardium, explore the injury, and repair the heart
should be
present. Once the pericardium is opened and tamponade relieved, hemodynamics usually improve dramatically and formal
pericardial
exploration can ensue. Exposure of the heart can be achieved by extending the incision to a median sternotomy, performing a left
anterior
thoracotomy, or performing bilateral anterior thoracotomies ("clamshell").