In general, shock is a circulatory failure that results in inadequate cellular oxygen utilization [1]. According to the mechanism causing the shock, four different types have been defined, including cardiogenic, hypovolemic, distributive and obstructive shock based on a classification by Cox and Hinshaw [2] from 1972. The classification of shock has hardly changed over the past few decades [3, 4]. Common to all types of shock is a mismatch of oxygen supply and consumption, which ultimately leads to poor perfusion and multiple organ failure [5]. Three components affect cardiac output: the blood volume, the cardiac output and vascular resistance [6]. A significant disturbance in any of these three factors may result in a critical undersupply of the whole body, a state which is defined as shock [1]. While cardiogenic and obstructive shock both result in shock due to undersupply with blood [7], it is important to distinguish between those two entities since cardiogenic shock is caused by primary cardiac dysfunction [7] while in obstructive shock is caused by extra cardiac diseases (like cardiac tamponade). The etiology of shock is of immense importance since treatment and underlying diseases differ. The most frequent causes of obstructive shock are given in Table 1 and include pulmonary embolism, pneumothorax and cardiac tamponade.

There are no reliable data on the frequency of obstructive shock. The incidences of the most common causes of obstructive shock are given below and can serve as a surrogate for obstructive shock incidence. A population-based incidence for aortic dissection suggests an incidence of 2.3–16.3/100,000 inhabitants per year [8]. Venous thromboembolism, which includes thrombosis of deep leg and pelvic veins and pulmonary embolism is much more frequent and varies between 100–200/100,000 inhabitants per year. Of these, about one third present with pulmonary embolism [9]. The overall person consulting rate for pneumothorax (primary and secondary combined) in the Great Britain was 24.0/100,000 per year for men and 9.8/100,000 for women [10]. A pericardial effusion is a frequent finding in patients with pulmonary hypertension, AIDS or malignoma. In a study of patients presenting in the emergency department with unexplained dyspnea, 13.6% had a pericardial effusion [11]. However, the frequency of obstructive shock cannot be derived from the incidence of these underlying diseases alone. Therefore, more data is required on this matter in order to understand the incidence of obstructive shock.

Etiologically, obstructive shock is caused by an impaired diastolic filling and thus a reduced cardiac RV- or LV-preload (venous return). A reduced preload is caused by tension pneumothorax, V. cava compression syndrome, mediastinal tumors, pericardial effusion or ventilation with a very high PEEP level. On the other hand, diseases which lead to an increased afterload and thus cardiac output may lead to obstructive shock. Causes associated with an increase in afterload are, for example, an aortic dissection, pulmonary embolism or Leriche syndrome. A pulmonary embolism or mediastinal space-occupying mass increases right-ventricular afterload, while decreasing left ventricular preload. The same mechanisms may occur in case of obstructive intracardial mass as displayed in Fig. 1, (Ref. [12]). Obstruction of the aortic blood flow however increases left ventricular afterload (e.g., Leriche syndrome [aortoiliac occlusive disease], aortic dissection) [13].

Fig. 1.

Transversal (A,B) and coronal (C) reconstructions of a computed tomography (CT) angiography shwoeing a rare cause for obstructive shock. (A) Tumor mass (TU) infiltrating the right ventricular wall and left ventricular ouitflow tract. (B) The tumor (TU) mass compresses the right artrium (RA) and right ventricle (RV). The tumor has no direct contact to the left ventricle (LV). (C) Demonstrates tumor grophs along the right heart in coronal reconstruction. Adapted from [12].

Prognosis depends on the extend of the tension component (valve mechanism) and how quickly therapy is initiated. Without treatment, a fulminant tension pneumothorax is fatal due to a cardiac arrest. If a tension pneumothorax is treated appropriately however, prognosis of the pneumothorax itself is very good. Based on the cause-of-death statistics, disease-specific mortality for spontaneous pneumothorax is 0.094/100,000 population annually, with a lethality of 0.7% [14], and might be even higher in secondary pneumothorax. Mortality rates in Great Britain between 1950–1997 were 1.26/million per year for men and 0.62/million per year for women [10]. It is important however to consider that most of these patients were not in obstructive shock.

According to an epidemiological study from 6 European countries, more than 317,000 deaths were associated with pulmonary embolism in 2004 [15]. Of these, 34% presented with fatal pulmonary embolism; 59% of the deaths were caused by pulmonary embolism that had not been diagnosed during lifetime. The average mortality rate from pulmonary embolism is given as 11% (40,000 deaths/year in Germany), but is significantly higher in patients in shock (40–50%) or in patients requiring resuscitation (70–80%) [15].

Due to the high preclinical mortality and missing forensic and clinical autopsy data, the number of unreported cases can safely be assumed to be very high [8]. 26% of the patients who receive surgical treatment due to a type A dissection die within the clinic. The mortality of the conservatively treated patients was reported 58% [9].

The diagnostic algorithm in case of shock is guided by patient history [16] and is a crucial part of the diagnostic workup. Typical patient histories for pulmonary embolism include previous arterial embolisms, thrombosis, malignant disease, immobilization or surgery in the preceding four weeks [17]. Cardiac tamponade is suspected primarily in trauma patients as possible sequel of rupture of the heart [18] and those who have a history of previous, slowly accumulating cardiac effusion related to preconditions such as viral infections, tuberculosis, uremia or neoplasia [19] or in patients after heart surgery [20]. Tension pneumothorax (and hemothorax) must be suspected especially in trauma patients [21] while spontaneous pneumothorax rarely causes relevant intrathoracic tension [22]. In aortic dissection, sudden onset of chest, back or abdominal pain is the most common symptom and often combined with a neurological deficit as a consequence of reduced cerebral perfusion [9]. Ventilation with high PEEP should also be considered as possible reason for vascular obstruction [23]. An obstructive shock by mediastinal mass can only be suspected in patients with known intrathoracic tumor such as lymphomas. Collapse of large vessels or airways by a mediastinal mass is a known problem under general anesthesia and should be prepared for accordingly [24].

Shock is a life threatening disease and requires immediate treatment. Since the hallmark of shock is undersupply of the whole body, treatment has to support multiple organ systems to different degrees. When shock is presumed, resuscitation should be started while investigating the cause [1]. In obstructive shock, a causal therapy (e.g., paracentesis or lysis) often is the only lifesaving intervention and must not be delayed.

It is important to note that fluid therapy by itself will not be able to reverse an obstructive shock. In tension pneumothorax, venous return (preload) is limited by an increase in intrapleural and secondarily intrathoracic pressure. When intrathoracic pressure exceeds intraventricular pressure, cardiac output runs dry [67, 68] and cannot be restored by fluid therapy. Especially in obstructive shock with right heart dysfunction, volume expansion can aggravate right ventricular failure [69].

Even though obstructive shock is developed in euvolemic patients with normal myocardial function, most patients are to a certain degree volume responsive [67]. Opposing the fluid resuscitation strategies in septic shock, fluid therapy in obstructive shock therefore can only buy time for a causal therapy. Choosing the right clinical surrogate for evaluating volume responsiveness however is hard and the gold standard of measuring cardiac output is dependent on the availability of advanced hemodynamic monitoring or experience in cardiac ultrasound. Passive leg raise maneuver should be used in order to test fluid responsiveness in obstructive shock. This intervention can be performed rather safely even in patients in shock [70]. Performing a passive leg raise maneuver correctly however might be challenging in unstable patients since effects on hemodynamics are transient [71]. In case passive leg raise maneuver is not feasible, a mini-fluid challenge of 100–200 mL crystalloid fluid over 10 minutes can be used in order to test volume responsiveness. Larger volumes should be avoided since fluid overload negatively impacts the outcome [72].

Like in most critically ill patients, vasopressors are frequently used in patients with shock. While vasoplegia is a key feature in septic and anaphylactic shock, it is not in obstructive shock [73], which is more similar to cardiogenic shock presenting with centralization and elevated total vascular resistance. Here, elevated afterload can decrease cardiac output and aggravate the shock [67]. Still, maintaining a mean arterial pressure of 65 mmHg seems reasonable in shock [73] which might necessitate some vasopressor therapy. There are concerns with increased pulmonary resistance in obstructive shock like pneumothorax which might aggravate shock [67]. Some data suggests that vasopressin might not affect pulmonary resistance [74, 75] therefore offering a superior vasopressor in obstructive shock. There are however also studies suggesting a similar inert effect of norepinephrine on pulmonal vascular resistance [69] and the Guideline of the European Society of Cardiology suggests norepinephrine as first line vasopressor in obstructive shock caused by pulmonary embolism [42].

In obstructive shock, low cardiac output is not caused by myocardial dysfunction. Therefore, inotropes are often not required for stabilizing patients in obstructive shock and can be detrimental since inotropes can cause vasodilatation [76] and arrhythmias [77]. Inotropes like dobutamine or levosimendan might be however reasonable in case of chronically reduced cardiac function or in patients with increased pulmonary afterload as seen in pulmonary embolism [78, 79] or pulmonary hypertension [79, 80]. Also, inotropes in conjunction with fluid therapy might be able to increase cardiac output in obstructive shock [67].

Patients in severe shock are frequently intubated [81]. Mechanical ventilation by itself increases afterload of the right ventricle [82], similar in nature to tension pneumothorax [67]. This fact highlights the potential detrimental effects of high pressure ventilation in obstructive shock. In case of mechanical ventilation, a low-volume (following recommendations for ARDS) and low PEEP (positive end expiratory pressure) ventilation should be aimed for in patients with shock due to high right ventricular afterload [83]. Since hypercapnia can further increase pulmonary resistance, it should be avoided [84].

Venoarterial extracorporeal membrane oxygenation can be a lifesaving therapy in obstructive shock caused by pericardial tamponade [85, 86]. It is important to remember that ECMO might also cause pericardial effusion [87]. There are several reports on decreased venoarterial ECMO flow in case of development of obstructive shock in neonates [88] as well as in adults [89]. On the other hand, it has been suggested that RV dysfunction can be improved by venovenous ECMO in case of pulmonary embolism by reduction on hypoxia and hypercapnia induced pulmonary vasoconstriction [90]. Similarly, venovenous ECMO unloads the right ventricle in patients with pneumonia by reducing mean pulmonary artery pressure [91]. On the other hand, venovenous ECMO is contraindicated in severe right heart failure since oxygenated blood will not be pumped into the systemic circulation [92]. Therefore, ECMO configuration and cannula placement has to be carefully evaluated in obstructive shock.

In pulmonary embolism, treatment is guided by short term (in-hospital or 30 day) mortality as proposed by the European Society of Cardiology [42]. Importantly, all patients with hemodynamic instability are considered high risk and need urgent reperfusion therapy either by medical thrombolysis (systemic or catheter guided) or surgical embolectomy [93, 94, 95, 96]. Since best reperfusion strategy depends on patient specific factors including severity of disease and bleeding risk an interdisciplinary team approach is advocated in order to optimize outcomes and might be best organized as a pulmonary embolism response team (PERT) [97]. Independent of the reperfusion strategy, the underlying disease causing PE (carcinoma, blood diseases, etc.) should be investigated and long term anticoagulation should be evaluated.

In patients with acute pericardial tamponade, cardiac index improves and right atrial pressure decreases after pericardiocentesis [98]. The European Society of Cardiology suggests percutaneous pericardiocentesis in acute tamponade [40] can be safely performed using echocardiographic or fluoroscopic guidance. In post-cardiotomy patients (or those with recurrent effusion), surgical pericardiocentesis is frequently indicated. Caution might be reasonable in patients with very high bleeding risk or in those with severe pulmonary hypertension, since pericardiocentesis might lead to dilatation of the right ventricle with poor prognosis [99]. A recent review however found the pericardial decompression syndrome (PDS) to be a rare complication in pericardiocentesis [100].

Unstable patients with tension pneumothorax require immediate intervention. A needle decompression is a fast and feasible treatment, provided the operator is trained and uses the right equipment [101, 102]. Chest tube thoracostomy is the treatment of choice in the hospital [103, 104]. Noteworthy, spontaneous pneumothorax rarely leads to a tension pneumothorax due to the lack of a precipitating cause (mechanical ventilation, lung disease or trauma) [22]. Further diagnostics are frequently indicated in patients with tension pneumothorax in order to identify the underlying disease.