Shock is defined as circulatory failure resulting in hypotension and reduced tissue perfusion. Cardiogenic shock, which can be thought of as “pump failure,” frequently occurs in the setting of acute MI or acute on chronic CHF exacerbation. It is characterized by high preload (congestion/fluid overload), low cardiac output (reduced inotropy), and high afterload (elevated systemic vascular resistence or “clamped down” peripheral vasculature in an effort to preserve perfusion to the most vital organs). These patients often present with evidence of congestion (dyspnea, edema, elevated JVP) and low cardiac output (cool/clammy extremities). The first priority of treatment is to address the underlying cause if possible (for example percutaneous coronary intervention if precipitated by MI). Supportive treatment includes inotropic support and afterload reduction (and ultimately diuresis but this should not be a priority until hemodynamics optimized, unless having trouble oxygenating due to profound pulmonary edema).
Other types of shock include hypovolemic shock such as hemorrhagic shock (low preload, low cardiac output, high afterload), distributive or vasodilatory shock such as septic shock or neurogenic shock (low preload, high cardiac output, low afterload), and obstructive shock such as pulmonary embolism or cardiac tamponade (high right sided but low left sided preload, low cardiac output, high afterload).
Tamponade is a condition in which a pericardial effusion accumulates in response to injury or inflammation and leads to increased intrapericardial pressure. This in turn causes elevation and equilibriation of diastolic pressures in cardiac chambers and ultimately obstructs adequate filling. Consequently, this reduced preload leads to reduced stroke volume and reduced cardiac output, ultimately resulting in obstructive shock. There are many causes of pericardial effusion, including infectous (viral including HIV, bacterial including TB, fungal), post-infarction (Dressler’s syndrome), post-traumatic (including iatrogenic), collagen vascular disease (such as lupus), radiation, metabolic (uremia or myxedema), neoplastic (especially breast, lung, melanoma, lymphoma), and of course idiopathic. Often these patients will have with a history of recent viral syndrome, malignancy, or another potential etiology as above. They generally present with a subacute onset of progressive dyspnea and lightheadedness or pleuritic chest pain relieved by leaning forward. They may have Beck’s triad on exam (hypotension, elevated JVP, muffled hearts sounds) and are frequently tachycardic and tachypneic. Exam should also be notable for pulsus paradoxus (difference of more than 10-12 mmHg between systolic BP in inspiration end expiration) because of ventricular interdependence. With high intrapericardial pressure, the increased right ventricular filling in inspiration results in decreased left ventricular filling and thus a drop in systemic blood pressure. CXR often shows an enlarged cardiac silhouette, and EKG may show low voltage (sensitive) or electrical alternans (specific). Diagnosis is confirmed by echocardiography. Of note, rapidly accumulating effusions (as seen with trauma or injury) can lead to tamponade physiology with as little as 100 mL, whereas slowly accumulating effusions (as seen with malignancy) can exceed 1L before manifesting tamponade physiology. Initial treatment of tamponade consists of administering aggressive IV fluid to increase preload, but this is only a temporizing measure until the fluid can be removed either percutaneously (pericardiocentesis) or surgically (pericardial window).