Are you more of a visual learner? Check out our online video lectures and start your Emergency Medicine course now for free!


Image: “emergency” by wolfgangfoto. License: CC BY 2.0

Too Little Oxygen

Generally, shock develops because of a decrease in tissue perfusion, which causes oxygen deficiency in the tissue and, thus, the development of metabolic disturbances. The relationship between oxygen demand and oxygen supply is disturbed.

Note: During episodes of shock, insufficient perfusion of tissue with subsequent tissue hypoxia and anaerobic metabolic situation occur.
Oxygen Delivery

Image: What is oxygen delivery determined by? By Lecturio

There are 3 main types of shock:

  1. Hypovolemic
  2. Cardiogenic
  3. Distributive 

General therapy measures for each form of shock include the administration of oxygen, placement of two large-lumen intravascular accesses, application of a central venous catheter (CVC; determination of central venous pressure (CVP) and main arterial pressure), continuous ECG monitoring and pulse oximetry, and placement of a urinary catheter for balancing measures. For this, the patient should be transported to the intensive care unit as soon as possible.

Initial therapy includes hemodynamic stabilization of the patient with regard to the causes. Blood count, inflammation and coagulation parameters, kidney retention parameters, electrolytes, liver values, lactate and BGA, and—in case of possible cardiac causes—heart enzymes (troponin, CK, CK-MB, LDH) should be determined.

Hypovolemic Shock

In volume deficiency shock, or hypovolemic shock, the circulating blood volume cannot sufficiently supply the tissue with oxygen. Causes include vomiting, diarrhea, internal or external bleeding (over 1 L), burns, and fluid shifts in the context of peritonitis.

The course of hypovolemic shock is divided into 3 stages. Initially, patients have cold, pale, and moist skin; blood pressure is normotensive (stage I). As the condition progresses, systolic blood pressure drops below 100 mm Hg, the jugular veins collapse, and the kidney reacts with oliguria (stage II). In the 3rd and final stage, kidney failure occurs. The pulse is almost not palpable, and systolic blood pressure values can drop under 60 mm Hg.

The shock index can be used to diagnose hypovolemic shock; it is calculated via the relation between heart frequency per min/systolic blood pressure value. Shock is confirmed if the heart frequency exceeds the systolic blood pressure (shock index > 1). However, shock must also be considered in the case of an unchanged shock index, if coexisting symptoms suggest shock.

When hypovolemic shock results from a trauma, the cause of bleeding needs to be immediately uncovered and then the bleeding must be stopped using appropriate measures (e.g., pressure bandage).

If the cause of the shock is unclear, CVP can be used for assessment. It is decreased in hypovolemic and distributive shocks and increased in cardiogenic shock. Also, undulations of the arterial pressure profile, depending on respiration, suggest volume deficiency.

Initial management of hypovolemic shock includes the general measures of shock treatment and placing the patient into the shock position (legs elevated 15 degrees). Simultaneously, volume substitution with plasma expanders (e.g., HAES) and crystalloids should begin. Within the hospital, this should be controlled along with the CVP. If bleeding is present, the application of erythrocyte concentrations is indicated. Due to the initially impaired significance of the hemoglobin (absent dilution effect), patients should be transfused without considering the hemoglobin at objective bleeding sources. For further management, the target hemoglobin value is at least 8 g/dl.

If the effect of volume therapy is insufficient, the application of vasoactive substances (e.g., noradrenalin) can be considered.

Note: Prior to volume therapy, a cardiogenic cause for the shock needs to be excluded.

Cardiogenic Shock

Cardiogenic shock is caused by a pumping failure of the heart. The most frequent cause is acute myocardial infarction. Cardiac dysrhythmia, cardiac tamponade (or pericarditis), cardiac valve failures, cardiomyopathy, or lung embolism can also lead to left heart failure.

Signs of cardiogenic shock include sweaty, cool skin, tachypnea, hypotension, and tachycardia. The consequence of left heart failure can be lung edema with gurgling rhonchi. Right heart decompensation expresses in prominent jugular veins and edemas.

Primary treatment of cardiogenic shock includes the general measures of shock management (see above). For relief of heart pain, the patient should be brought into a sitting position (preload reduction).

Note: Shock positioning is contraindicated in patients with cardiogenic shock.

Anamnestic statements (third-party anamnesis, if necessary) and excessive physical examination of the patient (inspection, auscultation of lung and heart, ECG, ECHO, if available) can help clarify causes. Therapy consists of promptly treating the underlying cause:

      • Myocardial infarction: immediate transport to a cardiac catheterization laboratory for percutaneous coronary intervention
      • Cardiac dysrhythmia: termination with an appropriate antiarrhythmic agent
      • Heart insufficiency/cardiomyopathy: pharmacological relief therapy
      • Lung embolism: lysis therapy, surgical embolectomy, if needed
      • Cardiac tamponade: relief puncture

In most cases, for hemodynamic stabilization, supportive medicamentous therapy is needed. Drugs used include:

      • Loop diuretics and nitrates (preload reduction)
      • Vasodilators (afterload reduction)
      • Catecholamines (positive inotropy), especially dobutamine

Distributive Shock

Distributive shock is caused by failure of the peripheral circulatory regulation with peripheral vasodilation and resulting relative volume deficiency. In septic shock, additional volume loss to the interstitium occurs. Distributive shock can be subdivided into septic shock, anaphylactic shock, and neurogenic shock.

1. Septic Shock

Sepsis is defined as a systemic inflammatory reaction (SIRS) as a consequence of a detectable bacterial infection. Septic shock is a complication of sepsis, accompanied by vessel dysregulation and endothelial lesions (capillary leak). It is caused by bacterial endo- and exotoxins, which lead to a massive release of vasodilating mediators out of the inflammatory cells. Also, complement and coagulation activation occur with consecutive vessel wall damage and interstitial fluid loss. If sepsis is not recognized and treated in time, organ function disorders can occur, especially of the kidney (acute kidney failure), the lung (acute respiratory distress syndrome), and the liver.

The main causes of sepsis are pneumonia, abdominal infections, and urinary infections. In the event of administered foreign material (e.g., CVC), catheter infection should also be considered.

Therapy requires balancing the relative volume deficiency with fluid substitution. According to the guidelines, crystalloids should be used; plasma expanders are not recommended. Further treatment consists of antibiotic and, possibly, surgical sanitation of the infect focus. Prior to this, focus diagnostics (chest X-ray, urine status and culture, abdominal sonography) should be performed.

Blood cultures should be taken from peripheral veins and administered catheters before antibiotic therapy is started. Catheters with obvious signs of infection must be removed, and the tip of the catheter should be sent for microbiological examination. Initial antibiotic therapy should cover as wide a pathogen spectrum as possible. Further treatment is performed according to the microbiological findings. In case of cardiac compromise, the application of inotropic agents (dobutamine) can be necessary.

Even with appropriate therapy, septic shock has a poor prognosis (approximately 50% mortality).

2. Anaphylactic Shock

Anaphylactic shock is caused by an immunologically (allergic reaction) or non-immunologically (pseudo-allergic reaction) mediated mast cell degranulation. The biogenic amine histamine released during this process leads to receptor-mediated (H1 receptor) vasodilation and an increase in permeability of the vessel walls. The resulting peripheral volume shift leads to a relative volume deficiency and the typical shock symptoms of tachycardia and hypotension.

Allergic Reaction

Anaphylaxis is the most severe expression of type I hypersensitivity reaction. After invasion of antigens (allergens) into the body, an antigen-antibody reaction occurs. The participating antibodies are IgE-antibodies, which bind to the receptor of the mast cells via their Fc fragment. If antigens bind to the binding site of the IgE antibody, this triggers receptor activation with subsequent degranulation of the mast cell.

AN anaphylactic reaction has 4 degrees of severity, from a locally limited skin reaction to more general symptoms such as vertigo and headaches, a drop in blood pressure and, finally, tachycardia, bronchospasm, and circulatory arrest.

Pseudo-Allergic Reaction

The pseudo-allergic reaction is a non-immunologically mediated reaction. Mast cell degranulation occurs as a response to a direct physical (e.g., thermic influences) or chemical signal.


Anaphylactic shock therapy consists of termination of the allergen exposition and the intravenous administration of antihistamines (H1 and H2 antagonists) and corticoids (prednisolone). For hemodynamic stabilization, the existing volume deficiency should be balanced with crystalloids. If this is insufficient, adrenaline (0.1 mg intravenous) is indicated.

3. Neurogenic Shock

Neurogenic or spinal shock is a rare condition. It occurs in the context of traumas of the medulla or the brain stem. Circulatory insufficiency occurs due to the failure of neurogenic circulatory reaction. Therapy includes the removal of the cause and the administration of volume.

Shock Inadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function. Initially may be reversible but life-threatening if not treated promptly.
Caused by Diagnosis (Preload) PCWP/CVP CO SVR (afterload) Treatment
Hypovolemic Hemorrhage/dehydration/3rd spacing (burns, pancreatitis) Cold/clammy Decreased Decreased Increased IVF
Cardiogenic CHF/Acute MI/ valvular dysfunction/arrhythmia Cold/clammy S3 gallop (CHF) crackles/+JVP Increased Severely Decreased Increased Positive Inotropic agents, diuretics
Obstructive Cardiac tamponade/pulmonary embolism Tracheal deviation/muffled heart sounds (obstructive) Relieve obstruction
Distributive Sepsis Warm/dry/bounding pulses/wide pulse pressure/altered body temperature Decreased Increased Severely Decreased IVF/Pressors


Agent Signs/clues Antidote/treatment
Acetaminophen Liver failure N-acetylcysteine
Salicylates Respiratory alkalosis, metabolic acidosis Alkalize blood/urine, dialysis
Tricyclic antidepressants Wide complex tachycardia Alkalize blood/urine
Benzodiazepines Somnolence, respiratory depression Flumazenil
Opiates Somnolence, respiratory depression Naloxone
Methanol, ethylene glycol, isopropanol Osmolar gap, +/- anion gap Fomepizole, dialysis
β-blockers Bradycardia, hypotension Glucagon, pacing, inotropes
Calcium channel blockers Bradycardia, hypotension Calcium, pacing, inotropes
Digitalis Arrhythmia, lights with halos Digibind, close cardiac monitoring
Rate this article
1 Star2 Stars3 Stars4 Stars5 Stars (Votes: 12, average: 4.58)