What is shock? How does it lead to cellular and tissue hypoxia? What are the different types of shock, and how can they be effectively evaluated and treated? Get the answers to these questions and more in this detailed article.

Understanding Shock: An Overview

Shock is a life-threatening manifestation of circulatory failure, characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization, leading to cellular and tissue hypoxia. This hypoxia can result in cellular death and dysfunction of vital organs, with the effects being reversible in the early stages. However, a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Etiology of Shock

Shock is the final manifestation of a complex list of etiologies, and it can be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive. The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made, but the underlying etiology has not been uncovered.

Distributive Shock

Distributive shock is characterized by peripheral vasodilatation, and it can be further divided into several subtypes:

• Septic Shock: A subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion, manifested as hypotension and elevated lactate levels.
• Systemic Inflammatory Response Syndrome (SIRS): A clinical syndrome of vigorous inflammatory response caused by either infectious or noninfectious causes, such as pancreatitis, burns, and air embolism.
• Anaphylactic Shock: A severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm.
• Neurogenic Shock: Can occur in the setting of trauma to the spinal cord or the brain, resulting in disruption of the autonomic pathway and decreased vascular resistance.
• Endocrine Shock: Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (a compensatory mechanism to maintain perfusion in the early stages of shock). In the later stages, cardiac output also decreases, leading to hypotension. Hypovolemic shock can be further divided into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include:

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed)
• Trauma
• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm)

Non-hemorrhagic causes of hypovolemic shock include dehydration, burns, and fluid loss from the gastrointestinal or urinary tract.

Cardiogenic Shock

Cardiogenic shock is characterized by decreased cardiac output and inadequate tissue perfusion due to primary cardiac dysfunction. This can be caused by various cardiac conditions, such as myocardial infarction, myocarditis, cardiomyopathy, and valvular heart disease.

Obstructive Shock

Obstructive shock is caused by mechanical obstruction to blood flow, leading to decreased venous return and cardiac output. Common causes include pulmonary embolism, tension pneumothorax, cardiac tamponade, and aortic dissection.

Evaluation and Management of Shock

The evaluation of a patient potentially in shock involves a comprehensive history, physical examination, and appropriate diagnostic testing. This may include laboratory studies, imaging, and hemodynamic monitoring. The management of shock aims to address the underlying etiology, restore tissue perfusion, and prevent or mitigate organ dysfunction. This may involve fluid resuscitation, vasopressor therapy, antibiotics, and targeted interventions based on the specific cause of shock.

What are the key steps in evaluating a patient with suspected shock?

The key steps in evaluating a patient with suspected shock include:

1. Obtaining a comprehensive history, focusing on the potential underlying cause of shock (e.g., recent trauma, infection, or cardiac history).
2. Performing a thorough physical examination, assessing vital signs, skin perfusion, and signs of end-organ dysfunction.
3. Ordering appropriate diagnostic tests, such as laboratory studies (e.g., complete blood count, electrolytes, lactate, cardiac enzymes), imaging (e.g., chest X-ray, echocardiography), and hemodynamic monitoring (e.g., central venous pressure, cardiac output).
4. Identifying the specific type of shock based on the clinical presentation and laboratory/imaging findings.

How is shock managed?

The management of shock aims to address the underlying etiology, restore tissue perfusion, and prevent or mitigate organ dysfunction. This may involve:

• Fluid resuscitation to restore intravascular volume and cardiac preload
• Vasopressor therapy to maintain adequate blood pressure and perfusion
• Antibiotics for suspected or confirmed infection (e.g., septic shock)
• Targeted interventions based on the specific cause of shock (e.g., thrombolysis for pulmonary embolism, emergency surgery for abdominal catastrophe)
• Supportive care, including mechanical ventilation, renal replacement therapy, and other organ support measures as needed

What is the importance of the interprofessional team in managing patients with shock?

The interprofessional team plays a crucial role in the evaluation and management of patients with shock. This includes physicians (e.g., emergency medicine, critical care, surgery), nurses, pharmacists, respiratory therapists, and other allied health professionals. Effective coordination and communication within the team are essential to ensure timely diagnosis, initiation of appropriate treatment, and optimization of patient outcomes. The interprofessional approach helps to ensure that all aspects of care are addressed, from initial resuscitation to ongoing management and monitoring of the patient’s condition.

Shock – StatPearls – NCBI Bookshelf

Continuing Education Activity

Shock is a life-threatening manifestation of circulatory failure. Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death. This activity reviews the evaluation and management of shock, and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

• Identify the etiology and epidemiology of shock and describe the types of shock.

• Outline the evaluation of a patient potentially in shock.

• Summarize the treatment and management options available for shock.

• Review the importance of improving care coordination among the interprofessional team to improve outcomes for patients in shock.

Access free multiple choice questions on this topic.

Introduction

Shock is a life-threatening manifestation of circulatory failure.  Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages, and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Etiology

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive. [1] The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

1. Distributive Shock

Characterized by peripheral vasodilatation. 

Types of distributive shock include:

Septic Shock

Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic Shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic Shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine Shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma

• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel)

• Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions)

Common causes of non-hemorrhagic hypovolemic shock include:

• GI losses – the setting of vomiting, diarrhea, NG suction, or drains.

• Renal losses – medication-induced diuresis, endocrine disorders such as hypoaldosteronism.

• Skin losses/insensible losses – burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.

• Third-space loss – in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

• Cardiomyopathies – include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.

• Arrhythmias – both tachy- and bradyarrhythmias

• Mechanical – severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output

• Pulmonary vascular – due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]

• Mechanical – impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Epidemiology

Distributive shock is the most common type of shock, followed by hypovolemic and cardiogenic shock. Obstructive shock is relatively less common. The most common type of distributive shock is septic shock and has a mortality rate between 40 to 50%.

Pathophysiology

Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow, which further worsens the tissue hypoxia. [4] In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally, shock has the following three stages:

1. Pre-shock or compensated shock – As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure

2. Shock – During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient.

3. End-organ dysfunction – This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death

History and Physical

A focused history should be obtained from the patient (if feasible) and/or patient’s relatives. Also, a review of the patient’s outpatient medical records (information regarding risk factors, medications, and trend of baseline vital signs including blood pressure), as well as hospital medical records, could give valuable clues regarding the patient’s risk for shock and potential etiology. Clinical features and symptoms can vary according to the type and stage of shock. The most common clinical features/labs which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia.[5][6] Also, features pertaining to the underlying cause of the shock can be present.

Patients with hypovolemic shock can have general features as mentioned above as well as evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have sequelae of chronic liver disease (in case of variceal bleeding).

Patients with septic shock may present with symptoms suggestive of the source of infection (example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-tissue infections), and cutaneous manifestations of infective endocarditis.

Patients with anaphylactic shock can have hypotension, flushing, urticaria, tachypnea, hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of exposure to common allergens such as medications or food items the patient is allergic to or insect stings.

Tension pneumothorax should be suspected in a patient with undifferentiated shock who has tachypnea, unilateral pleuritic chest pain, absent or diminished breath sounds, tracheal deviation to the normal side, distended neck veins and also has pertinent risk factors for tension pneumothorax such as recent trauma, mechanical ventilation, underlying cystic lung disease).

In a patient with undifferentiated shock, diagnostic clues to pericardial tamponade as the etiology include dyspnea, the Beck triad (elevated jugular venous pressure, muffled heart sounds, hypotension), pulses paradoxus, and known risk factors such as trauma, the recent history of pericardial effusion, and thoracic procedures.  

Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.

Evaluation

Resuscitation should not delay while investigating the etiology of undifferentiated shock. Physicians should have a high clinical suspicion for the presence of shock, and an attempt to stratify the severity of the shock should also take place to assess the need for emergent or early interventions. Evaluation of undifferentiated shock should begin with a thorough history and physical examination.

Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show evidence of acute coronary syndrome, arrhythmias, or provide diagnostic clues suggestive of pericardial effusion or pulmonary embolism.

Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile, type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock), blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients with undifferentiated shock and hypotension include chest x-rays to look for the source of infection such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management

The initial approach to management is the stabilization of the airway and breathing with oxygen and oral mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should be obtained. Central venous access may be required in the setting of shock if there is difficulty securing peripheral venous access, or the patient needs prolonged vasopressor therapy or large-volume resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated, followed by vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of shock, specific therapies might also be needed.

Septic shock – initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3 hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mmHg. The first choice of a vasopressor is norepinephrine, with the addition of vasopressin if refractory.[9]

Anaphylactic shock – aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.

In adrenal crisis – judicious fluid resuscitation, IV dexamethasone.

Hypovolemic shock – obtain two large-bore IVs or central line. Place the patient in the Trendelenburg position. Aggressive IV fluid resuscitation with 2 to 4 L of isotonic crystalloids. PRBC transfusion if ongoing bleed.  Appropriate medical or interventional strategies to treat the underlying etiology. Continue with isotonic crystalloids and use vasopressors if needed

Obstructive shock – the judicious use of IV crystalloids. If shock persists, early initiation of vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids but monitor very closely. 

If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has a paradoxical worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing compromising left ventricle filling. 

If tension pneumothorax – needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).

Cardiogenic shock – if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes (dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory shock, and vasopressor (norepinephrine) with inotropes.

If STEMI – consider thrombolysis or coronary revascularization procedures and or IABP.

Differential Diagnosis

Uncovering the etiology of undifferentiated shock is very important. In a patient presenting with undifferentiated shock, the differential diagnosis includes a wide variety of etiologies that falls under the four major categories of shock, as outlined above. Also, sometimes patients can have a combination of shock syndromes. Another differential is “pharmacological shock,” which results from vasodilatation or myocardial depression from medications (e.g., benzodiazepines, beta-blockers, calcium channel blockers, opiates, anticholinergics, and sildenafil).

Prognosis

Sepsis and septic shock, in general, are associated with long-term morbidity and mortality, with many of the survivors requiring placement into long-term acute care facilities or post-acute care centers. [10][11] Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock has a mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock generally have much lower mortality and respond better to timely treatment. 

Pearls and Other Issues

• Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.

• There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.

• An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.

• Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.

• Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.

• Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.

Enhancing Healthcare Team Outcomes

The management of patients with shock calls for a collaborative, interprofessional approach. Clinicians must react promptly to the emergency and determine the precise cause of shock. Nursing will be on hand to assist at every step of the way, assisting with measures such as intubation and administering medications. Pharmacists must rapidly prepare and deliver the needed drugs and yet still verify that dosing and interactions do not present a problem. Depending on the etiology, various specialists may also be called in on the case. Each area will need to act and react as the situation dictates. WIth interprofessional cooperation, these patients will stand a better chance of recovery from shock with minimal deleterious effects. [Level 5]

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2014 Feb 06;370(6):583. [PubMed: 24499231]

2.

Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013 Aug 29;369(9):840-51. [PubMed: 23984731]

3.

Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000 Oct;48(1):23-33. [PubMed: 11033105]

4.

Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May;4(2):161-7. [PubMed: 8774792]

5.

Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74. [PMC free article: PMC5433435] [PubMed: 26903335]

6.

Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2015 Mar 12;372(11):1078-9. [PubMed: 25760366]

7.

Shokoohi H, Boniface KS, Pourmand A, Liu YT, Davison DL, Hawkins KD, Buhumaid RE, Salimian M, Yadav K. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit Care Med. 2015 Dec;43(12):2562-9. [PubMed: 26575653]

8.

Howell MD, Davis AM. Management of Sepsis and Septic Shock. JAMA. 2017 Feb 28;317(8):847-848. [PubMed: 28114603]

9.

Hylands M, Moller MH, Asfar P, Toma A, Frenette AJ, Beaudoin N, Belley-Côté É, D’Aragon F, Laake JH, Siemieniuk RA, Charbonney E, Lauzier F, Kwong J, Rochwerg B, Vandvik PO, Guyatt G, Lamontagne F. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth. 2017 Jul;64(7):703-715. [PubMed: 28497426]

10.

Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M., Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. [PMC free article: PMC4910392] [PubMed: 26903336]

11.

Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet. 2018 Jul 07;392(10141):75-87. [PubMed: 29937192]

Disclosure: Hayas Haseer Koya declares no relevant financial relationships with ineligible companies.

Disclosure: Manju Paul declares no relevant financial relationships with ineligible companies.

Shock: MedlinePlus Medical Encyclopedia

URL of this page: //medlineplus.gov/ency/article/000039.htm

To use the sharing features on this page, please enable JavaScript.

Shock is a life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly. Many organs can be damaged as a result. Shock requires immediate treatment and can get worse very rapidly. As many 1 in 5 people in shock will die from it.

The main types of shock include:

• Cardiogenic shock (due to heart problems)
• Hypovolemic shock (caused by too little blood volume)
• Anaphylactic shock (caused by allergic reaction)
• Septic shock (due to infections)
• Neurogenic shock (caused by damage to the nervous system)

Shock can be caused by any condition that reduces blood flow, including:

• Heart problems (such as heart attack or heart failure)
• Low blood volume (as with heavy bleeding or dehydration)
• Changes in blood vessels (as with infection or severe allergic reactions)
• Certain medicines that significantly reduce heart function or blood pressure
• Slow heart rates and changes in blood vessel tone from spinal injuries

Shock is often associated with heavy external or internal bleeding from a serious injury.

Toxic shock syndrome is an example of shock that is caused by an infection.

A person in shock has extremely low blood pressure. Depending on the specific cause and type of shock, symptoms will include one or more of the following:

• Anxiety or agitation/restlessness
• Bluish lips and fingernails
• Chest pain
• Confusion
• Dizziness, lightheadedness, or faintness
• Pale, cool, clammy skin
• Low or no urine output
• Profuse sweating, moist skin
• Rapid but weak pulse
• Shallow breathing
• Being
  unconscious (unresponsive)

Take the following steps if you think a person is in shock:

• Call 911 or the local emergency number for immediate medical help.
• Check the person’s airway, breathing, and circulation. If necessary, begin rescue breathing and CPR.
• Even if the person is able to breathe on their own, continue to check rate of breathing at least every 5 minutes until help arrives.
• If the person is conscious and DOES NOT have an injury to the head, leg, neck, or spine, place the person in the shock position. Lay the person on the back and elevate the legs about 12 inches (30 centimeters). DO NOT elevate the head. If raising the legs will cause pain or potential harm, leave the person lying flat.
• Give appropriate first aid for any wounds, injuries, or illnesses.
• Keep the person warm and comfortable. Loosen tight clothing.

IF THE PERSON VOMITS OR DROOLS

• Turn the person or their head to one side to prevent choking if you do not suspect an injury to the spine.
• If a spinal injury is suspected, “log roll” the person instead. To do this, keep the person’s head, neck, and back in line, and roll the body and head as a unit.

In case of shock:

• DO NOT give the person anything by mouth, including anything to eat or drink.
• DO NOT move the person with a known or suspected spinal injury.
• DO NOT wait for milder shock symptoms to worsen before calling for emergency medical help.

Call 911 or the local emergency number any time a person has symptoms of shock. Stay with the person and follow the first aid steps until medical help arrives.

Learn ways to prevent heart disease, falls, injuries, dehydration, and other causes of shock. If you have a known allergy (for example, to insect bites or stings), carry an epinephrine pen. Your health care provider will teach you how and when to use it.

• Shock

Angus DC. Approach to the patient with shock. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. Philadelphia, PA: Elsevier; 2020:chap 98.

Puskarich MA, Jones AE. Shock. In: Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier; 2018:chap 6.

Smith SG, Schreiber MA. Shock, electrolytes, and fluid. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 21st ed. St Louis, MO: Elsevier; 2022:chap 4.

Updated by: Jesse Borke, MD, CPE, FAAEM, FACEP, Attending Physician at Kaiser Permanente, Orange County, CA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

What does it mean to “die of shock”

You may have heard the expression “die of shock.” The cause of death in this case is considered to be emotional surprise, for example, fright. But in reality, everything is much more complicated.

Tags:

Netlenka

Diseases

Unsplash

You can often hear in movies that disaster victims died from shock, but what does that mean?

First, you should understand that if you see something shocking, you will not die. The situation in which a person dies is usually caused by a bodily condition called “medical shock”. In this case, the patient’s blood pressure becomes too low, which means that there is not enough oxygenated blood in the body to support vital functions. Simply put, when the patient’s body does not receive enough blood flow, then he is in shock.

Shock can be caused by a number of conditions at once. Some of the most common causes of shock include heart problems (heart failure or stroke), changes in blood vessels (due to infections or severe allergic reactions), low blood volume (due to extensive bleeding or dehydration), or certain medications that lower blood pressure. or adversely affect heart function.

From this we can understand that shock is not about emotional shock. More precisely, it may not arise at all because you were afraid. In total, there are several different types of shock, each of which occurs in different situations and requires “its own” treatment.

ADVERTISING – CONTINUED BELOW

Hypovolemic shock

This type occurs when the volume of blood is significantly reduced, usually due to blood loss, such as trauma. This leads to low blood pressure, so important parts of the body stop getting enough blood.

Cardiogenic shock

When the heart is unable to pump blood throughout the body, it is called cardiogenic shock. Certain conditions, such as a stroke or certain heart conditions (such as cardiomyopathy), prevent a person’s heart from functioning properly.

Septic shock

This shock occurs when blood vessels dilate, thereby lowering blood pressure. Usually such a shock is caused by infections.

Neurogenic shock

This condition develops when a person has an injury to the spinal cord. Because of this, the conduction of impulses of the sympathetic nervous system is disrupted, an increase in the diameter of blood vessels occurs, which leads to a drop in blood pressure.

Obstructive shock

Occurs when blood flow is blocked or stopped for any reason. Thrombus formation is usually the cause of obstructive shock.

Anaphylactic shock

Most people have heard about this type. It occurs due to a severe allergic reaction that causes the blood vessels to dilate.

Endocrine shock

A severely ill person may develop a serious hormonal disorder (such as hypothyroidism) that can prevent the heart from functioning properly. This can easily lead to a drop in blood pressure.

Because shock has different causes, its symptoms may vary from one person to another. However, some of the most common symptoms of shock include shallow, rapid breathing and palpitations, restlessness, shortness of breath, pale and clammy skin, nausea, dizziness, thirst, or dry mouth for no reason.

Pain shock! Do the wounded die from it?

• January 23, 2023

What is shock and how can we help?

Recently, there have been a lot of discussions on the Internet about pain shock! Is there a pain shock at all and people die from it?

What is pain?

The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with or resembling actual or potential tissue damage. ”

Components and mechanism of traumatic shock

What is shock? How is it developing?

Shock is a condition in which the cardiovascular system is unable to provide adequate blood circulation and oxygen delivery to tissues, or such provision is achieved temporarily, due to the consumption of depleted compensatory mechanisms.

In simple words:

In the event of a sudden release of blood from the vascular bed, the body tries to ensure the functioning of vital organs – the heart, brain, lungs, kidneys.
For this, the narrowing of the peripheral vessels (limbs) occurs, and the blood accumulates in the central vessels.

But the lifebuoy does not work for a long time.

Vessels dilate, blood leaves the vascular bed in the tissues.
Severe hypotension sets in. The heart, brain, kidneys, lungs are no longer supplied with blood in the required volume.
Death is coming.

Shock is not the cause of death, the cause of death is the factor that caused its development.

Acronym for Assistance During Warfare

Causes of shock.
Thus, shock develops either when:
– fluid deficiency
– a sharp increase in the volume of the vessel with the same amount of fluid
– in violation of the heart

Main types:

channels outside.
2. Distribution (anaphylactic, septic) – the release of fluid from the vascular bed into the tissues.
3. Cardiogenic – disconnection of the heart from the vascular system.
4. Neurogenic – disconnection of the nervous system from the control of the heart and blood vessels.

It should be noted that “true” shock develops only with blood deficiency, that is, with blood loss.

Do they die from pain shock?

Pain shock – loss of consciousness, and sometimes circulatory arrest with a strong pain impulse, for example, at the time of injury.

In this case, the incoming pain impulse is so intense that the brain briefly loses control over the activity of the sympathetic nervous system, as a result of which the tone is lost.

Pain syndrome is one of the components of traumatic shock, which is not the most significant.

Components of traumatic shock:
– Powerful pain impulses coming from the site of injury to the central nervous system.
– Large internal or external blood loss.
– Respiratory failure.
– Stress reaction.

Stages of assistance:
Therefore, when providing assistance, we should not spend time on pain relief in the first place, because pain itself is not the main cause of death.

The main components of a lethal outcome – blood loss and acute respiratory failure – will first lead to the death of the wounded!

We therefore recommend using the acronym C.U.L.A.K.B.I.T.A.
According to which: first of all, we stop bleeding, remove suffocation and stop pneumothorax, and only after that we proceed to the introduction of anesthesia and antibiotics (section BITA).

All about shock, a detailed scheme of relief will be explained to you in detail in the ADVANCED course. Prehospital care.

Author

Vasily Koval

Co-author

Yulia Migacheva

We are interested in cooperation with experts operating both on the territory of the Russian Federation and abroad. The Regional Academy of Tactical Medicine and First Aid (RATMED) is always ready to provide support and necessary information on first aid. Leave your contacts and we will contact you!

Name

Telephone

Email

Our address:

Office: St. Petersburg, Prosveshcheniya ave., 15, building/st. A, sq./off. 142-N

Lecture hall: St. Petersburg, st. Beloostrovskaya, 22, BC Chernaya Rechka, 4th floor, office 432

Request a call

Training advice:

+7 812 467-82-69

Leave an “audio review”:

+7 812 467-82-69

Vk

Telegram

Vk

Telegram

Payment methods:
Through the cash desk of any bank, payment by invoice, via the payment link

(Confidentiality of the reported personal information is provided by PJSC SBERBANK).