Shock (SHOCK)
Overview
Shock (쇼크) is an acute state of circulatory failure in which an imbalance between tissue oxygen supply and demand leads to cellular hypoxia and metabolic derangement. Although decreased blood pressure is commonly present, the essence of shock is not hypotension itself but failure of tissue perfusion; in the early stage, blood pressure may remain within the normal range because of compensatory mechanisms. It is an emergency condition that progresses to multiple organ failure and death unless the cause is recognized early and corrected promptly.
Key Content
Definition and Pathophysiology
Shock is broadly explained by reduced oxygen-carrying capacity (anemia, hypoxemia), decreased cardiac output, abnormal blood flow distribution due to changes in vascular resistance, and impaired oxygen utilization at the microcirculatory level. Cells switch to anaerobic metabolism, lactate accumulates, and ATP depletion causes cell membrane ion pumps to fail, leading to cell swelling and death. In this process, inflammatory mediators are released, creating a vicious cycle of systemic inflammatory response, endothelial injury, capillary leakage, and microthrombus formation. Clinically, this is sometimes described as the 'circle of death' of perfusion imbalance.
Classification
- Hypovolemic shock: A state of decreased circulating blood volume due to traumatic hemorrhage, gastrointestinal bleeding, burns, severe vomiting or diarrhea, etc.; it is the most common type.
- Cardiogenic shock: A state of sharply decreased cardiac output due to acute myocardial infarction, myocarditis, arrhythmia, valvular rupture, etc.
- Distributive shock: A type in which vasodilation and increased vascular permeability are the main mechanisms, as in septic shock, anaphylaxis, and neurogenic shock (spinal cord injury).
- Obstructive shock: A state in which cardiac filling or ejection is mechanically obstructed, as in cardiac tamponade, tension pneumothorax, and massive pulmonary embolism; immediate procedural resolution is required.
Clinical Symptoms
Altered mental status (anxiety, confusion, lethargy), pallor and cold, clammy skin, delayed capillary refill (more than 3 seconds), weak peripheral pulses, decreased urine output (less than 0.5 mL/kg/h), tachycardia, and tachypnea are typical. In septic shock, an initial 'warm shock' pattern with warm skin may occur, making it easy to miss until hypotension is confirmed. Even if measured blood pressure is normal, shock cannot be excluded if lactate is elevated and perfusion indicators are worsened.
Diagnosis
History taking and physical examination come first; arterial blood gas analysis, blood lactate, electrolytes, renal function, blood typing and crossmatching, electrocardiography, and chest X-ray are basic tests. Emergency ultrasound (POCUS) has become a key tool for rapidly differentiating shock types through evaluation of pericardial fluid, right ventricular dilation, left ventricular function, lung B-lines, and the aorta. Central venous oxygen saturation, arterial pressure waveform analysis, and cardiac output measurement are used to assess treatment response.
Treatment
The principles of treatment are correction of the cause and restoration of perfusion. According to the airway, breathing, and circulation approach (ABCDE), oxygen is administered and intubation is performed if necessary, and large-bore venous access is secured. In hypovolemic shock, balanced crystalloids and blood products are used along with hemorrhage control; in trauma, excessive fluids are avoided according to the concept of damage control resuscitation, and blood pressure targets are individualized. In septic shock, administration of broad-spectrum antibiotics within 1 hour and 30 mL/kg of crystalloids are recommended, and norepinephrine is used as the first-line vasopressor with a target mean arterial pressure of at least 65 mmHg. Cardiogenic shock is definitively treated with reperfusion (PCI) and ventricular assist devices, and obstructive shock with pericardiocentesis, chest tube insertion, thrombolysis, or embolectomy.
Complications and Prognosis
Acute kidney injury, acute respiratory distress syndrome, hepatic dysfunction, disseminated intravascular coagulation, ischemic bowel disease, and multiple organ failure are major complications. Prognosis depends greatly on the cause and speed of correction, and early improvement in lactate clearance and perfusion indicators is closely associated with survival.
Recent Trends
From 2024 to 2025, there is a clear trend in shock management moving from 'fixed protocols' to 'individualized hemodynamic targets.' In septic shock, unconditional preference for large-volume fluids is decreasing, and the approach of assessing fluid responsiveness with dynamic indicators and ultrasound-based evaluation instead of static preload indicators is spreading. Evidence for the safety of early norepinephrine administration and peripheral intravenous administration has accumulated, and the role of non-catecholamine vasopressors such as vasopressin and angiotensin II is being reevaluated. In traumatic hemorrhage, discussions are active on the use of whole blood, permissive hypotension strategies, and indications for REBOA (resuscitative endovascular balloon occlusion of the aorta). AI-based early warning systems, wearable perfusion monitoring, and machine learning-based septic shock prediction models are in the clinical validation stage, and ahead of the revision of the 2025 edition of the international sepsis guidelines, large-scale clinical results on fluid resuscitation volume and blood pressure targets are being published. In cardiogenic shock, early application of temporary mechanical circulatory support and team-based 'shock center' operation are spreading as standards.
Related Topics
- [[Sepsis]]
- [[Hypovolemic shock]]
- [[Cardiogenic shock]]
- [[Anaphylaxis]]
- [[Emergency medicine]]
- [[Damage control resuscitation]]