Sepsis , also known as blood poisoning, is a condition caused by infections that lead to bacteria entering your bloodstream. Septic shock occurs when bacteria and their toxins cause serious damage to tissues or organs in your body.
Neurogenic shock is caused by damage to the central nervous system, usually a spinal cord injury. This causes blood vessels to dilate, and the skin may feel warm and flushed.
The heart rate slows, and blood pressure drops very low. This can be caused by severe blood loss, for example, from injuries. Your blood delivers oxygen and vital nutrients to your organs. Serious dehydration can also cause this type of shock. First responders and doctors often recognize shock by its external symptoms. They may also check for:. This can be done by giving fluid, drugs, blood products, and supportive care. To do so, they may order one or more tests, such as imaging or blood tests.
Your doctor may order imaging tests to check for injuries or damage to your internal tissues and organs, such as:. Apply first aid to any visible wounds.
If you suspect the person is experiencing an allergic reaction, ask them if they have an epinephrine auto-injector EpiPen. People with severe allergies often carry this device. It contains an easy-to-inject needle with a dose of hormone called epinephrine.
You can use it to treat anaphylaxis. If they begin to vomit, turn their head sideways. This helps prevent choking. Instead, stabilize their neck and roll their entire body to the side to clear the vomit out. Different types of shock are treated differently. For example, your doctor may use:. Some forms and cases of shock are preventable. Take steps to lead a safe and healthy lifestyle.
For example:. Stay hydrated by drinking plenty of fluids. When you experience a severe allergic reaction, you may experience anaphylaxis. When this happens, your body is flooded with chemicals which can lead…. In a patient with new-onset shock, it is usually possible to categorize the type of shock within minutes based on a concise history and targeted examination.
In a patient with shock, a wide pulse pressure accompanied by warm extremities and brisk capillary refill is evidence of high cardiac output CO; distributive shock. Alternatively, a narrow pulse pressure, cool extremities, and delayed capillary refill suggest low CO.
Low CO shock is comprised of hypovolemia and pump failure. In the subset of low output shock, an assessment of intravascular volume can further differentiate hypovolemia from cardiogenic causes of shock. Bedside goal-directed echocardiography 1 GDE should be performed to clarify or confirm the etiology of shock Table 21—2 ; identify readily treatable contributors such as tension pneumothorax or cardiac tamponade ; and seek clues to fluid-responsiveness. Certainly, there may be overlapping causes, as in the patient with septic shock who has both hypovolemic before resuscitation and distributive components; or following calcium channel blocker overdose when there may be both cardiogenic and distributive contributors.
These more complex cases can generally be recognized by a systematic approach of performing GDE; identifying fluid responsiveness; estimating global perfusion through venous oximetry, lactate clearance, or measures of stroke volume; and repeating these measures until shock remits or a diagnosis is established. For patients already critically ill who progress to new shock, discerning the type may rely on more invasive measurements or diagnostic steps.
Shock often produces significantly elevated blood levels of lactic acid; sometimes this precedes hypotension and serves as an early indicator. The lactic acidosis of sepsis and perhaps some other forms of distributive shock is more complex. In some patients, tissues may be deprived of oxygen , especially before resuscitation or perhaps in the mesenteric circulation, and produce lactic acid anaerobically.
Yet many resuscitated septic patients have high CO, total body oxygen delivery, venous saturations, and tissue oxygen saturations, 5 along with oxidation-reduction ratios that do not support a theory of anaerobic metabolism. These findings cannot exclude oxygen lack, since microvascular dysfunction 6 and maldistribution of blood flow 7 may create hidden zones of hypoxia. Venous oximetry entails measuring the oxyhemoglobin saturation of central or mixed venous blood.
Although central and mixed venous values are not identical, they are closely related and usually change in the same direction. Venous oximetry relies on the Fick Principle for oxygen , stating that the difference between arterial and venous oxygen contents is related inversely to the CO as long as oxygen consumption is constant. Because clinicians defend the arterial content value by maintaining minimum values for arterial saturation, low CO tends to be matched by a low venous saturation value.
Some support for the importance of venous oximetry derives from the trial of Early Goal-Directed Therapy in which resuscitation based on central venous oximetry during the first 6 hours of septic shock led to improved survival.
The pulmonary artery catheter PAC has been widely used to assess CO; mixed venous oxygen saturation; and intrapulmonary and intra-cardiac pressures, and provides a wealth of derived information on the systemic and pulmonary circulation. However its use in the ICU, once considered the standard of care for hemodynamic monitoring, has declined in the last decade due to lack of mortality benefit in critically ill patients, 14 and even in congestive heart failure.
The continuous measurement of oxyhemoglobin saturation in thenar capillaries by near-infrared spectroscopy NIRS has the promise of directly monitoring the microvasculature. This technique has provided an early warning of shock progression during acute hemorrhage following trauma. Stroke volume can be estimated through a variety of techniques, such as arterial pulse contour analysis, bioreactance, bioimpedance, CO 2 rebreathing, and pulse-wave Doppler analysis of the left ventricular outflow tract.
These methods all demonstrate reasonable correlations with invasive measures of stroke volume, with the advantage of minimally or noninvasive technology. None has been shown to improve outcomes in patients with shock so their potential value remains inconclusive.
Further, since large studies of hemodynamic optimization using the PAC failed to demonstrate improved outcomes, it seems unlikely that gathering similar information noninvasively will produce major advances in care.
Bedside GDE is now commonplace for the assessment of shock in the ICU, emergency department, and on rapid-response teams. Typically, an intensivist acquires four standard chest views to evaluate ventricular size and function, along with a subcostal view of the inferior vena cava.
It allows for rapid assessment, often serially in a patient with rapidly changing conditions, and can prove to be crucial in cases of unsuspected ventricular dysfunction, hypovolemia, cardiac tamponade, or severe acute valve failure. The subcostal view is especially helpful in assessing the inferior vena cava, showing significant cyclic variation with respiration in hypovolemic states, as discussed as follows.
Shock is managed 1 at an urgent tempo; and by 2 identifying and treating acute, reversible causes; 3 restoring intravascular volume; 4 infusing vasoactive drugs; 5 using mechanical adjuncts, when applicable; and 6 supporting vital functions until recovery.
Minutes matter when recognizing and resuscitating shock. This golden hour is a time-honored tenet in trauma, and more recently recognized to be also pertinent in septic shock.
The initial Early Goal Directed Therapy EGDT trial demonstrated that rapid resuscitation to endpoints of central venous pressure, mean arterial pressure, and central venous oxyhemoglobin saturation within 6 hours of presentation improved outcomes compared to a less-aggressive resuscitation. One interpretation of these results is that, while the appropriate endpoints of resuscitation remain unclear, an environment that favors early, aggressive resuscitation improves outcomes in septic shock.
The appropriate endpoints of shock resuscitation remain elusive. Importantly, resuscitation to an arbitrarily set MAP of at least 65 mm Hg is not sufficient and possibly not necessary. As an example, treatment with a nitric oxide synthase inhibitor leads to increased blood pressures and lower catecholamine use, but also increased mortality.
Several studies have compared specific blood pressure targets finding that achieving a MAP of higher than 65 mm Hg such as 75 or 85 mm Hg does not improve outcomes.
Targeting microvascular resuscitation is attractive in theory, but real-time assessments of microvascular function are not readily available for clinical use, and effective methods to safely and reliably increase microvascular function have not been found.
We advocate a comprehensive assessment of the adequacy of perfusion to guide resuscitation, rather than merely aiming for an arbitrary mean arterial pressure. Serial assessments are likely to be valuable since shock and its resuscitation can produce dramatic changes within hours.
Several causes of shock require specific identification and treatment because general supportive measures will surely fail. Good examples include tension pneumothorax, cardiac tamponade, and ruptured abdominal aortic aneurysm Table 21—3. These can be subtle at times, requiring a careful, systematic approach to shock.
Intensivist-conducted ultrasound has changed fundamentally the initial examination of the shock patient. Its ability to quickly signal cardiac dysfunction, pericardial effusion, hypovolemia, deep vein thrombosis, pulmonary embolism-in-transit, pneumothorax, aortic rupture, free peritoneal blood, traumatic injuries, sources of sepsis, and other crucial findings makes ultrasound an essential skill for early diagnosis.
Distributive high cardiac output shock. The timing of antibiotics in confirmed or suspected septic shock deserves specific mention in relation to the tempo of shock resuscitation. Appropriate antibiotics must be given within the first hour following the recognition of septic shock. Antibiotic therapy is frequently delayed and often ineffective for the final microbiologic diagnosis. Orders may be delayed due to diagnostic confusion and caregiver attention toward invasive procedures and hemodynamic resuscitation.
Systems issues between ordering and administering antibiotics also contribute to these delays. Antibiotics should then be tailored to microbial susceptibilities, as these data are available, or discontinued promptly if an alternative etiology of shock is identified. Rapid restoration of intravascular volume is an essential principle of shock resuscitation since fluids may promptly restore perfusion and prevent organ failures.
Fluids should be infused at a rapid pace usually much faster than typical ICU infusion pumps will allow , and in sufficient volume which can be many liters. This practice allows for periodic reevaluation for clinical response: slower infusions of small volumes may confound the perception of response.
Although colloid-containing fluids have some theoretical advantages over crystalloids, clinical trials generally show equivalence. Some colloids, especially synthetic starches, are clearly detrimental and should not be used.
Although vasomotor function and vasopressors are both less active in acidemic environments, attempts to correct a metabolic acidosis with bicarbonate infusions do not speed resuscitation nor reduce vasopressor requirements, and may lead to worsening intracellular acidosis. Accordingly, bicarbonate infusions should be avoided. In the setting of acute traumatic shock, questions have been raised about the targets of early fluid resuscitation. Potential downsides of restoring blood pressure to normal before surgical exploration include dilution of clotting factors, hypothermia, and an increased rate of hemorrhage as arterial pressure rises.
Once perfusion declines and oxygen delivery to cells is inadequate for aerobic metabolism, cells shift to anaerobic metabolism with increased production of carbon dioxide and elevated blood lactate levels. Cellular function declines, and if shock persists, irreversible cell damage and death occur. During shock, both the inflammatory and clotting cascades may be triggered in areas of hypoperfusion.
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.
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