It refers to mechanical obstruction of cardiac function; the term includes tension pneumothorax, cardiac tamponade, and severe valve obstruction.
An obstructive shock is a surprise associated with physical obstruction of the great vessels or the heart. The pulmonary embolism and cardiac tamponade are considered forms of obstructive shock.
Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped.
Some sources do not recognize obstructive shock as a separate category, classifying pulmonary embolism and cardiac tamponade as cardiogenic shock.
Acute obstruction of blood flow in the central vessels of the systemic or pulmonary circulation causes the clinical symptoms of shock accompanied by altered consciousness, centralization, oliguria, hypotension, and tachycardia.
In the case of an acute pulmonary embolism, an intravascular occlusion results in a sharp increase in the afterload of the right ventricle. In the case of a tension pneumothorax, a blockage of the blood vessels supplying the heart is caused by an increase in extravascular pressure.
From a hemodynamic point of view, circulatory shock caused by obstruction is closely followed by cardiac deterioration; however, etiologic and therapeutic options require demarcation of non-obstructive cardiac causes.
The high dynamics of this life-threatening condition are a hallmark of all types of obstructive shock. This requires prompt and helpful diagnosis and prompt, well-targeted therapy.
Shock obstructivo extracardiaco
This form of shock results from acute obstruction to flow in the circulation. Examples include impaired diastolic filling of the right ventricle, right ventricular outlet obstruction, or air embolism resulting from cardiopulmonary bypass or central line placement.
Systemic arterial hypertension severe enough to impair left ventricular function, acute pericardial tamponade, or constrictive pericarditis can also produce a pattern of obstructive shock.
Coarctation / interrupted arch
Infants with an interrupted aortic arch or juxtaductal coarctation of the aorta may depend on the patency of the ductus arteriosus to provide adequate lower body perfusion.
The ductus arteriosus contracts after birth in many of these babies, resulting in severe heart failure, poor systemic perfusion, and academia. Many of the signs and symptoms of coarctation with shock are indistinguishable from the shock of other etiologies.
A high index of suspicion should be maintained for babies who present in shock in the first month of life.
In severely ill infants whose diagnosis of coarctation or interruption of the aorta is clinically suspected, it is appropriate and often life-saving to initiate a continuous infusion of prostaglandin E1 before diagnostic evaluation.
Etiology and pathophysiology
Obstructive shock is caused by the inability to produce adequate cardiac output despite the average intravascular volume and myocardial function. The causal factors may be located within the pulmonary or systemic circulation or associated with the heart itself.
Examples of obstructive shock include:
- Acute pericardial tamponade.
- Tension pneumothorax.
- Pulmonary or systemic hypertension.
- Congenital or acquired outlet obstructions.
Recognition of the characteristics of these syndromes is essential, as most cases can be treated as long as the diagnosis is made early.
Cardiac tamponade is the hemodynamically significant cardiac compression that results from the accumulation of pericardial content that evokes and defeats compensatory mechanisms. The pericardium may contain effusion fluid, purulent fluid, blood, or gas.
The clinical manifestations of tamponade can be insidious, mainly when they occur in conditions such as malignancy, connective tissue disorders, kidney failure, or pericarditis. In the early stages, the symptoms are nonspecific.
As the cardiac output is restricted, the overall picture resembles chronic heart failure (CHF); however, the lungs are generally straightforward.
Physical examination findings suggestive of cardiac tamponade include paradoxical pulse, narrowed pulse pressure, pericardial friction, and jugular venous distention.
Causes of obstructive shock
As mentioned earlier, obstructive shock occurs when obstruction causes less blood to reach the heart. Various diseases or disorders can cause obstructive shock, such as:
- Aortic dissection (the large blood vessel attached to the heart ruptures and cannot effectively transport blood to and from the heart).
- Tension pneumothorax (loss of air from the lungs due to trauma).
- Vena Cava Syndrome (a central vein in the body becomes blocked and cannot carry blood from the body to the heart).
- High blood pressure (pulmonary or systemic hypertension).
- Pulmonary embolism (blood clot in the lungs).
- Heart injuries (obstructing the flow of blood from the heart).
- Cardiac tamponade (a pressure on the heart that keeps it from filling and lowers blood pressure).
Tension pneumothorax and intrathoracic tumors indirectly affect proper ventricular filling by obstructing venous return.
Symptoms of obstructive shock are considered emergencies because they can lead to organ failure, tissue death, and patient death. Symptoms associated with neurological function include confusion, loss of consciousness, and inability to concentrate.
Symptoms that are related to the heart and its function are chest pain, lightheadedness, and a sudden increase in heart rate, along with a weak pulse.
The characteristic hemodynamic and metabolic patterns are, in many respects, similar to other low-performance shock states. Cardiac indices, stroke volume indices, and stroke are usually reduced.
Respiratory symptoms consist of shortness of breath and rapid but shallow breathing. Other symptoms include sweating, decreased urine output, clammy skin, pale skin, and cold hands and feet.
Because tissue perfusion is decreased, oxygen saturation (SO2) is low, the difference in arteriovenous oxygen content is increased, and serum lactate is frequently elevated. Other hemodynamic parameters depend on the site of the obstruction.
Tension pneumothorax and mediastinal tumors can obstruct the great thoracic veins and result in a hemodynamic pattern (decreased cardiac index and elevated systemic vascular resistance) similar to hypovolemia (although distended jugular and peripheral veins may be seen).
Cardiac tamponade generally causes increased left and right ventricular diastolic pressures, pulmonary artery diastolic pressure, central venous pressure, and pulmonary wedge pressure.
In constrictive pericarditis, the left and right ventricular diastolic pressures are elevated and are within 5 mm Hg of each other. The mean proper and left atrial pressure may or may not be the same.
Massive pulmonary embolus causes right ventricular failure with elevated proper heart pressure and high blood pressure, while pulmonary wedge pressure remains normal.
A systolic embolism or aortic occlusion secondary to dissection causes peripheral hypotension and signs of left ventricular failure, including elevated pulmonary wedge pressure. Clinical signs similarly depend on the site of the obstruction.
Ischemic rupture of the free will of the left ventricle (usually 3 to 7 days after myocardial infarction) leads to immediate cardiac tamponade and shock with 150 ml of blood to the pericardium.
Diagnosis and treatment
Survival requires emergency surgery. Similar situations can develop with bleeding into the pericardium after blunt chest trauma or thrombolytic therapy.
Pericardial tamponade secondary to malignant or inflammatory pericardial effusions generally develops slowly.
Although it can still develop shock, it generally requires substantially more pericardial fluid (1–2 L) to cause critical failure of proper ventricular diastolic filling.
Similarly, in patients without the preexisting cardiopulmonary disease, a massive embolus involving two or more lobar arteries and 50% to 60% of the vascular bed can result in obstructive shock.
However, if recurrent smaller pulmonary emboli result in right ventricular hypertrophy, substantially greater total occlusion of the pulmonary vascular bed may be required to cause right ventricular decompensation.
More recent analyzes have suggested that the presence of shock secondary to a pulmonary embolus (regardless of underlying chronic cardiopulmonary dysfunction) indicates a three- to seven-fold increase in the risk of mortality, with most deaths occurring within one hour after the presentation.
Shock secondary to pulmonary embolism is an indication of urgent thrombolysis.
Echocardiography is of particular value in detecting the presence of pericardial effusion and can provide clues to the presence of tamponade. In rapid tamponade caused by bleeding, as in trauma, shock dominates the image. If left untreated, it leads to electromechanical decoupling.
The definitive treatment for cardiac tamponade is removing pericardial fluid or air by surgical drainage or pericardiocentesis. Removing even a small fluid volume can quickly improve blood pressure and cardiac output.
Surgical drainage by thoracotomy or a limited subxiphoid surgical approach should be considered for traumatic tamponade.
Pericardiocentesis should be performed as soon as possible if the patient is considered in a life-threatening situation.
Pericardiocentesis is a blind procedure; needle insertion should be monitored by echocardiography whenever possible. The subxiphoid approach is generally preferable.
Medical treatment is not a substitute for drainage, but it can prevent catastrophe until pericardiocentesis or surgical drainage can be safely performed.
The principles of medical treatment include expansion of blood volume to maintain venta trial gradients and inotropic agents.
Additionally, any anticoagulant or thrombolytic therapy should be discontinued if anticipated pericardiocentesis.