You may find more information in the article “Shock as Cardinal Symptom and an Overview of Differential Diagnosis”.
Too Little Oxygen
Generally, shock develops at a decrease of tissue perfusion. Due to decreased perfusion, oxygen deficiency occurs in the tissue and, thus, metabolic disturbances develop. The relation of oxygen demand and oxygen supply is disturbed.
One distinguishes between different forms of shock, which generally have three main causes:
- Hypovolemic shock
- Cardiogenic shock
- Distributive shock
General therapy measures at each shock form include administration of oxygen, the placement of two large-lumen intravascular accesses, the application of a CVC (determination of CVP and MAP), continuous ECK-monitoring and pulse oximetry, and the 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, while regarding the causes. Concerning laboratory, the 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.
In the event of volume deficiency shock or hypovolemic shock, the circulating blood volume cannot sufficiently supply the tissue with oxygen. Causes for the lack of volume can be vomiting, diarrhea, internal or external bleedings (over 1l), burns, but also fluid shifts in the context of peritonitis.
The course of the hypovolemic shock is divided into three stages: Initially, the patients have cold, pale, and moist skin, the blood pressure is normotensive (stage I). In the course, the systolic blood pressure undercuts 100 mmHg, the jugular veins collapse, the kidney reacts with oliguria (stage II). In the third and last stage, kidney failure occurs. The pulse is almost not palpable, systolic blood pressure values can drop under 60 mmHg.
For orientating diagnostics of the hypovolemic shock, the shock index can be used, which is calculated with the relation of HF per min/systolic blood pressure value. In this context, a shock is present if the heart frequency exceeds the systolic blood pressure (shock index > 1). However, a shock also has to be considered in the case of an unchanged shock index if the coexisting symptoms suggest shock.
At traumatically caused hypovolemic shock, the causing bleeding has to be discovered immediately and to be stopped with appropriate measures (e.g. pressure bandage).
If the cause for the shock is unclear, the central venous pressure (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 (see above) and putting the patient into the shock position (legs elevated by 15°). Simultaneously, volume substitution with plasma expanders (e.g. HAES) and crystalloids should be begun. Within the hospital, this should be controlled with the CVP. If a bleeding is present, the application of erythrocyte concentrations is indicated. Due to the initially impaired significance of the Hb (absent dilution effect), they should be transfused without considering the Hb at objective bleedings sources. For further management, the target Hb 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.
The cause for the cardiogenic shock is pumping failure of the heart. The most frequent cause is acute myocardial infarction. Also, cardiac dysrhythmia, cardiac tamponade or pericarditis, cardiac valve failures, cardiomyopathy, or lung embolism can lead to left heart failure.
Mostly, the clinic characteristically corresponds to the disease. Shock signs are 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 the cardiogenic shock includes the general measures of shock management (see above). For relief of the heart, the patient should be brought into a sitting position (preload reduction).
Anamnestic statements (third-party anamnesis if necessary) and excessive physical examination of the patient (inspection, auscultation of lung and heart, ECK, ECHO if available) serve for clarification of the causes. Therapy of cardiogenic shock consists of quick treatment of the underlying cause:
- Myocardial infarction: quick transport into a cardiac catheterization laboratory for PCI
- 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
For hemodynamic stabilization, supportive medicamentous therapy is needed in most cases. Used drugs are:
- Loop diuretics and nitrates (preload reduction)
- Vasodilators (afterload reduction and
- Catecholamines (positive inotropy), especially dobutamine
The cause for the distributive shock is failure of the peripheral circulatory regulation with peripheral vasodilation and, thus, resulting relative volume deficiency. In septic shock, additional volume loss to the interstitium occurs. The distributive shock can be divided into the septic shock, the anaphylactic shock, and the rare neurogenic shock.
1. Septic Shock
Sepsis is defined as a systemic inflammatory reaction (SIRS) as a consequence of a detectable bacterial infection. The septic shock represents a complication of sepsis, which is accompanied by vessel dysregulation and endothelial lesions (capillary leak). The causes are bacterial endo- and exotoxins, which lead to massive release of vasodilating mediators out of inflammatory cells. Also, complement and coagulation activation occurs with consecutive vessel wall damages 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 (ARDS), and the liver.
Mostly, the causes of sepsis are pneumonias, abdominal infections and urinary infections. In the event of administered foreign material (e.g. CVC), catheter infection also has to be considered.
Therapy of the septic shock requires the balance of the ‘relative volume deficiency’ with fluid substitution. According to the guidelines, crystalloids should be used in this case, plasma expanders are not recommended. Further treatment consists of antibiotic and possibly surgical sanitation of the infect focus. Prior to this, focus diagnostic (chest x-ray, urine status and culture, abdominal sonography) should be made.
Blood cultures should be taken from peripheral veins and from administered catheters before antibiotic therapy is started. Catheters with obvious signs of infection have to be removed and the tip of the catheter has to be sent in for microbiological examination. Initial antibiotic therapy should be chosen to cover pathogen spectrum as wide as possible. Further treatment is performed according to the microbiological findings. In case of cardiac compromise, the application of inotropics (dobutamine) can be necessary.
Even with appropriate therapy, the septic should have a bad prognosis (ca. 50 % lethality).
2. Anaphylactic Shock
The anaphylactic shock is the consequence of an immunologically (allergic reaction) or non-immunologically (pseudo-allergic reaction) mediated mast cell degranulation. The biogenic amine histamine released in this process leads to receptor-mediated (H1-receptor) vasodilation and an increase in permeability of the vessel walls. The thus resulting peripheral volume shift leads to a relative volume deficiency with the typical shock symptoms tachycardia and hypotension.
Anaphylaxis is the worst expression of the type I hypersensitivity reaction. After invasion of the 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 with 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.
The anaphylactic reaction occurs in four severity degrees – from the locally limited skin reaction to further general symptoms like vertigo and headaches to a drop in blood pressure and tachycardia, bronchospasm, and circulatory arrest.
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.
Therapy of the anaphylactic shock consists of termination of the allergen exposition and the intravenous administration of antihistamines (H1- and H2-antihistaminicum) and corticoids (prednisolone). For hemodynamic stabilization, the existing volume deficiency should be balanced with crystalloids. If the effect is insufficient, adrenalin (0.1 mg intravenous) is indicated.
3. Neurogenic Shock
The neurogenic or spinal shock is not very frequent. It occurs in the context of traumas of the medulla or the brain stem. In this case, circulatory insufficiency occurs due to failure of neurogenic circulatory reaction. Therapy occurs causally with the removal of the cause and the administration of volume.