Where no recommendation grade is available, the recommendation is that of the present authors etable 1. The effects of the interventions presented on survival and disability-free survival are in some cases not strong.
Source: www. Understand the different pathogenesis and pathophysiology of the four main categories of shock. Hypovolemic shock is a condition of inadequate organ perfusion caused by loss of intravascular volume, usually acute.
The result is a drop in cardiac preload to a critical level and reduced macro- and microcirculation, with negative consequences for tissue metabolism and the triggering of an inflammatory reaction. Hypovolemic shock is divided into four subtypes 2 :. Traumatic hemorrhagic shock, resulting from acute hemorrhage with soft tissue injury and, in addition, release of immune system activators.
Hypovolemic shock in the narrower sense, resulting from a critical reduction in circulating plasma volume without acute hemorrhage. Traumatic hypovolemic shock, resulting from a critical reduction in circulating plasma volume without acute hemorrhage, due to soft tissue injury and the release of immune system mediators. The characteristic feature of both, hemorrhagic and traumatic hemorrhagic shock is bleeding.
However, differences exist between the two subcategories in terms of the extent of soft tissue damage. Clinically the most significant cause of hemorrhagic shock is acute bleeding from an isolated injury to a large blood vessel, gastrointestinal bleeding, nontraumatic vascular rupture e. The shock is triggered by the critical drop in circulating blood volume; massive loss of red blood cells intensifies the tissue hypoxia.
Traumatic hemorrhagic shock is distinguished from hemorrhagic shock by the additional presence of major soft tissue injury which aggravates the shock. A typical example of this type of shock is polytrauma, most usually caused by road traffic accidents and falls from a great height. The soft tissue injury leads to postacute inflammation, further reinforcing this process. At the microcirculatory level, leukocyte—endothelium interactions 5 and destruction of endothelial membrane-bound proteoglycans and glycosaminoglycans cause microvascular dysfunction with capillary leak syndrome.
At the intracellular level a metabolic imbalance arises 6 with possible mitochondrial damage 7 and a negative influence on the vasomotor system 8. Hypovolemic shock in the narrower sense and traumatic hypovolemic shock show significant fluid loss without hemorrhage. Hypovolemic shock in the narrower sense arises from external or internal fluid loss coupled with inadequate fluid intake. It can be caused by hyperthermia, persistent vomiting and diarrhea e. Sequestration of large quantities of fluid in the abdomen, e.
Typical causes of traumatic hypovolemic shock are large surface burns, chemical burns, and deep skin lesions. The trauma also activates the coagulation cascade and the immune system, potentiating the impairment of the macro- and microcirculation.
The inflammatory reaction results in damage to the endothelium, increases capillary leak syndrome, and causes severe coagulopathy 9 , The incidence of gastrointestinal hemorrhage in Germany is around patients per year, of whom roughly 10 suffer hypovolemic shock. These figures, together with those for the remaining subtypes of hypovolemic shock, lead to a total of about 50 patients per year table 1. The preclinical and clinical treatment of hypovolemic shock consists of immediate intravascular volume replacement fluid resuscitation with balanced crystalloids recommendation grade: B using wide-bore peripheral venous access and, in a patient who is hemorrhaging, rapid bleeding control table 2.
To prevent or alleviate hypoxia, endotracheal intubation with normoventilation usually follows recommendation grade: A. Trauma patients with shock should be transferred directly to a trauma center recommendation grade: B. Surgical management should be undertaken as soon as possible using the damage control surgery DCS approach Persisting hypotension, especially in patients with head trauma, should prompt administration of a vasconstrictor e.
Multidisciplinary treatment includes early stabilization of coagulation by means of coagulation factors, either as individual factors or as fresh frozen plasma FFP , together with surgical prevention of further blood loss.
In patients with controllable bleeding up to age-specific and comorbidity-specific hemoglobin threshold values, red cell concentrate RCC transfusions are given. Those with uncontrolled bleeding, irrespective of the current hemoglobin value, should receive transfusions of RCC, fresh frozen plasma FFP , and platelet concentrates PC.
Patients with traumatic or peripartum bleeding should also be given 1 to 2 g tranexamic acid at an early stage recommendation grade: A 14 — Multidisciplinary treatment includes early stabilization of coagulation by means of coagulation factors, either as individual factors or as FFP, together with surgical prevention of further blood loss Distributive shock is a state of relative hypovolemia resulting from pathological redistribution of the absolute intravascular volume and is the most frequent form of shock.
For patients with large burns, the modified Brooke formula can give an indication of the volume replacement required in the first 24 h Distributive shock is a state of relative hypovolemia resulting from pathological redistribution of the absolute intravascular volume and is the most frequent form of shock table 1.
Sepsis is defined according to the current Sepsis-3 criteria as a dysregulated response by the body to an infection resulting in life-threatening organ dysfunctions. Hypovolemia as the sole cause of circulatory failure must be ruled out, for example by echocardiography 19 , Patients over the age of 65 years with immunosuppression or underlying malignant disease are disproportionately affected.
In some patients the inflammatory response is small or nonexistent 19 , 22 , In Germany about patients annually are affected by sepsis; the incidence is rising every year by about 5. The core of the pathophysiology is the endothelial dysfunction, which leads to dysregulation of vascular tone resulting in vasodilation, impaired distribution, and volume shifting in the macro- and microcirculation, and to a rise in vascular permeability capillary leak syndrome 22 — Frequently, biventricular impaired myocardial function is also present in the form of septic cardiomyopathy 26 , which contributes to patient mortality 26 , Septic shock is a mixed form of a variety of pathologies hypovolemia, vasodilation, impaired cardiac function, and mitochondrial dysfunction and is usually associated with complex coagulopathies 22 — In Germany about patients are affected by sepsis every year; the incidence is rising every year by about 5.
Apart from an increased level of alertness and rapid diagnosis, septic shock requires treatment to support the circulation by the infusion of balanced crystalloid solutions recommendation grade: A , administration of vasopressors norepinephrine, vasopressin if needed , in some cases also inotropic drugs e. Advanced invasive monitoring is indicated to allow tailored therapy for the impaired hemodynamics.
Echocardiography has a central part to play here 22 , 24 , In all sepsis patients, as soon as samples have been obtained for microbiological study, calculated broad-spectrum antibiotic therapy and if possible source control causal treatment should be started as soon as possible recommendation grade: A Noninfectious disease involving extensive mediator activation e.
This is due to activation of the same mediator cascade by noninfectious molecular signals of soft tissue damage The pathophysiology and pathogenesis of toxic shock syndrome TSS are related to those of septic shock. TSS is characterized by fever, severe hypotension, and skin rash as the main symptoms. It is usually triggered by toxins from certain staphylococci. The incidence is 0. Treatment is the same as that recommended for septic shock.
Anaphylactic shock is characterized by massive histamine-mediated vasodilation and maldistribution with a shift of fluid from the intravascular to the extravascular space. The clinical presentation varies greatly from one individual to another according to the dose and site of entry of the antigen and the degree of sensitization. Initially, skin manifestations, abdominal symptoms, or respiratory symptoms may be prominent.
Anaphylaxis is an acute systemic reaction usually mediated by IgE-dependent hypersensitivity reactions. The central role is played by mast cells and the histamine they release. Lifetime prevalence is reported at 0. Intensifying factors include physical effort, stress, and acute infection. Anaphylactoid shock is caused by physical, chemical, or osmotic hypersensitivity reactions that are IgE-independent. Mediators are released from mast cells and basophilic granulocytes independently of any antigen—antibody reaction or presensitization.
Typical triggers are X-ray contrast media. Anaphylactic reactions may resolve spontaneously or may progress despite appropriate therapy. In anaphylaxis with fatal outcome, thromboembolic events are seen as often as arrhythmias and ventricular dysfunction Patients with severe anaphylactic reactions require constant monitoring, as late reactions including arrhythmias, myocardial ischemia, and respiratory failure may manifest as late as 12 hours after the initial event.
In terms of drug treatment, for anaphylactic shock especially the administration of epinephrine plus norepinephrine, if necessary and forced fluid replacement are required Histamine antagonists suppress the histaminergic effects table 2. Treatment for anaphylactoid shock is the same as for anaphylactic shock. Neurogenic shock is a state of imbalance between sympathetic and parasympathetic regulation of cardiac action and vascular smooth muscle.
The dominant signs are profound vasodilation with relative hypovolemia while blood volume remains unchanged, at least initially. The pathomechanisms of neurogenic shock can be divided into three groups efigure :. Pathomechanism of neurogenic shock: Connections in the autonomic system for heart rate and blood pressure regulation. Direct injury to the centers for circulatory regulation due to compression brainstem trauma , ischemia e.
Altered afferents to the circulatory center in the medulla oblongata due to fear, stress, or pain or dysregulated vagal reflexes. Interruption of the descending connection from the bulbar regulatory centers to the spinal cord, especially in patients who have sustained trauma above the middle of the thoracic spine paraplegia.
Occasionally, neurogenic shock can be triggered by stress or severe pain, or even after a karate kick. The capacity of the splanchnic venous system and skeletal musculature rises while systemic venous pressure drops markedly. The critical element in treating neurogenic shock is the treatment of the cause. In addition to rapid fluid replacement, norepinephrine is given at increasing dosages until peripheral vascular resistance rises table 1.
To restore vascular tone, direct- or indirect-acting sympathomimetics can also be given Mineralocorticoids to increase plasma volume are also a therapeutic option. According to the German—Austrian S3 guideline, cardiac index determination is not required for a clinical diagnosis of cardiogenic shock In addition to these hemodynamic and clinical criteria, evidence of cardiac dysfunction is required, together with the exclusion of other types of shock differential diagnosis.
The cardiac dysfunction may be due to myocardial, rhythmologic, or mechanical causes figure 1. With the myogenic form, reduction of pump function due to acute coronary syndrome ACS is the preeminent cause. Other causes include various cardiomyopathies, myocarditis, pharmacotoxicity, and blunt trauma to the heart. Mechanical causes include advanced acute and chronic valvular disease and mechanical complications after myocardial infarction or caused by intracavitary structures impeding flow thrombi or tumors.
Tachycardia and bradycardia may also result in the clinical picture of cardiogenic shock. The main symptoms of cardiogenic shock are agitation, disturbed consciousness, cool extremities, and oliguria.
Death in patients in cardiogenic shock is usually caused by hemodynamic instability, multiorgan failure, and systemic inflammation. To maintain adequate cardiac output and hence sufficient organ perfusion, systemic counter-regulation mechanisms such as the sympathetic nervous system and neurohumoral, renal, and local vasoregulation are activated.
Echocardiography and invasive monitoring are the pillars of diagnosis. The primary goal of treatment is removing the cardiac causes of the shock. This includes the earliest possible coronary reperfusion in ACS by means of percutaneous coronary intervention PCI with the insertion of stents bare metal stent, BMS; drug-eluting stent, DES recommendation grade: A , surgical or other interventional treatment of mechanical causes and structural heart disease, and surgical or interventional ablation, and pacemaker therapy 36 , Executive summary of the guidelines on the diagnosis and treatment of acute heart failure.
Eur Heart J. BMJ Best Practice would like to gratefully acknowledge the previous expert contributor, whose work has been retained in parts of the content:.
Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock, ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Glasgow Coma Scale. Needle decompression of tension pneumothorax animated demonstration. Venepuncture and phlebotomy animated demonstration. Heart attack: what is it? What you can do to prevent another heart attack.
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Hypoxic vascular endothelial cells activate white blood cells, which bind to the endothelium and release directly damaging substances eg, reactive oxygen species, proteolytic enzymes and inflammatory mediators eg, cytokines, leukotrienes, tumor necrosis factor.
Septic shock Sepsis and Septic Shock Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. Localized vasodilation may shunt blood past the capillary exchange beds, causing focal hypoperfusion despite normal cardiac output and blood pressure.
Additionally, excess nitric oxide is converted to peroxynitrite, a free radical that damages mitochondria and decreases ATP adenosine triphosphate production. Blood flow to microvessels, including capillaries, is reduced even though large-vessel blood flow is preserved in settings of septic shock. Mechanical microvascular obstruction may, at least in part, account for such limiting of substrate delivery.
Leukocytes and platelets adhere to the endothelium, and the clotting system is activated with fibrin deposition. Multiple mediators, along with endothelial cell dysfunction, markedly increase microvascular permeability, allowing fluid and sometimes plasma proteins to escape into the interstitial space 1 Pathophysiology references Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death.
Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes In the gastrointestinal tract, increased permeability possibly allows translocation of the enteric bacteria from the lumen, potentially leading to sepsis or metastatic infection. Neutrophil apoptosis may be inhibited, enhancing the release of inflammatory mediators. In other cells, apoptosis may be augmented, increasing cell death and thus worsening organ function.
Blood pressure is not always low in the early stages of shock although hypotension eventually occurs if shock is not reversed. Thus, a modest degree of hypotension that is well tolerated by a young, relatively healthy person might result in severe cerebral, cardiac, or renal dysfunction in an older person with significant arteriosclerosis. Initially, when oxygen delivery DO2 is decreased, tissues compensate by extracting a greater percentage of delivered oxygen.
Low arterial pressure triggers an adrenergic response with sympathetic-mediated vasoconstriction and often increased heart rate. Initially, vasoconstriction is selective, shunting blood to the heart and brain and away from the splanchnic circulation. Circulating beta-adrenergic amines epinephrine , norepinephrine also increase cardiac contractility and trigger release of corticosteroids from the adrenal gland, renin from the kidneys, and glucose from the liver.
Increased glucose may overwhelm ailing mitochondria, causing further lactate production. Reperfusion of ischemic cells can cause further injury. As substrate is reintroduced, neutrophil activity may increase, increasing production of damaging superoxide and hydroxyl radicals.
After blood flow is restored, inflammatory mediators may be circulated to other organs. MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock Sepsis and Septic Shock Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection.
Any organ system can be affected, but the most frequent target organ is the lung, in which increased membrane permeability leads to flooding of alveoli and further inflammation. Progressive hypoxia may be increasingly resistant to supplemental oxygen therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome Acute Hypoxemic Respiratory Failure AHRF, ARDS Acute hypoxemic respiratory failure is severe arterial hypoxemia that is refractory to supplemental oxygen.
It is caused by intrapulmonary shunting of blood resulting from airspace filling or The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis Acute Tubular Necrosis ATN Acute tubular necrosis ATN is kidney injury characterized by acute tubular cell injury and dysfunction.
Common causes are hypotension or sepsis that causes renal hypoperfusion and nephrotoxic In the heart, reduced coronary perfusion and increased mediators including tumor necrosis factor and interleukin-1 may depress contractility, worsen myocardial compliance, and down-regulate beta-receptors. These factors decrease cardiac output, further worsening both myocardial and systemic perfusion and causing a vicious circle often culminating in death.
Arrhythmias may occur. In the gastrointestinal tract, ileus and submucosal hemorrhage can develop. Liver hypoperfusion can cause focal or extensive hepatocellular necrosis, transaminase and bilirubin elevation, and decreased production of clotting factors.
Coagulation can be impaired, including the most severe manifestation, disseminated intravascular coagulopathy Disseminated Intravascular Coagulation DIC Disseminated intravascular coagulation DIC involves abnormal, excessive generation of thrombin and fibrin in the circulating blood.
During the process, increased platelet aggregation and coagulation J Pathol —74, Crit Care 19 1 , Biomed Res Int , Hypovolemic shock is caused by a critical decrease in intravascular volume.
Diminished venous return preload results in decreased ventricular filling and reduced stroke volume. Unless compensated for by increased heart rate, cardiac output decreases. A common cause is bleeding hemorrhagic shock , typically due to trauma, surgical interventions, peptic ulcer, esophageal varices, or ruptured aortic aneurysm. Bleeding may be overt eg, hematemesis, melena or concealed eg, ruptured ectopic pregnancy.
Hypovolemic shock may also follow increased losses of body fluids other than blood see table Hypovolemic Shock Caused by Body Fluid Loss Hypovolemic Shock Caused by Body Fluid Loss Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death.
Hypovolemic shock may be due to inadequate fluid intake with or without increased fluid loss. Water may be unavailable, neurologic disability may impair the thirst mechanism, or physical disability may impair access. In hospitalized patients, hypovolemia can be compounded if early signs of circulatory insufficiency are incorrectly ascribed to heart failure and fluids are withheld or diuretics are given.
Distributive shock results from a relative inadequacy of intravascular volume caused by arterial or venous vasodilation; circulating blood volume is normal. In some cases, cardiac output and DO2 is high, but increased blood flow through arteriovenous shunts bypasses capillary beds; this bypass plus uncoupled cellular oxygen transport cause cellular hypoperfusion shown by decreased oxygen consumption. In other situations, blood pools in venous capacitance beds and cardiac output falls.
Distributive shock may be caused by anaphylaxis Anaphylaxis Anaphylaxis is an acute, potentially life-threatening, IgE-mediated allergic reaction that occurs in previously sensitized people when they are reexposed to the sensitizing antigen.
Anaphylactic shock and septic shock often have a component of hypovolemia as well. Cardiogenic shock Hypotension and Cardiogenic Shock Numerous complications can occur as a result of an acute coronary syndrome and increase morbidity and mortality. Complications can be roughly categorized as Electrical dysfunction conduction Obstructive shock is caused by mechanical factors that interfere with filling or emptying of the heart or great vessels.
Causes are listed in the table Mechanisms of Cardiogenic and Obstructive Shock Mechanisms of Cardiogenic and Obstructive Shock Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Altered mental status eg, lethargy, confusion, somnolence is a common sign of shock. The hands and feet are pale, cool, clammy, and often cyanotic, as are the earlobes, nose, and nail beds.
Capillary filling time is prolonged, and, except in distributive shock, the skin appears grayish or dusky and moist. Overt diaphoresis may occur. Peripheral pulses are weak and typically rapid; often, only femoral or carotid pulses are palpable. Tachypnea and hyperventilation may be present.
Blood pressure tends to be low 90 mm Hg systolic or unobtainable; direct measurement by intra-arterial catheter Arterial Catheterization A number of procedures are used to gain vascular access. If blind percutaneous placement Urine output is low. Distributive shock causes similar symptoms, except the skin may appear warm or flushed, especially during sepsis. The pulse may be bounding rather than weak. In septic shock, fever, possibly preceded by chills, is typically present.
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