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 – 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]

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References

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

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

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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]

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

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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]

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

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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]

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

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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]

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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]

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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.

Hemorrhagic shock – an article from the Vascular Innovation Center

Hemorrhagic shock (HS) is a critical condition of the body associated with acute blood loss, resulting in a crisis of macro- and microcirculation, a syndrome of multiple organ and polysystemic insufficiency. From a pathophysiological point of view, this is a microcirculation crisis, its inability to provide adequate tissue metabolism, satisfy the tissue need for oxygen, energy products, and remove toxic metabolic products.

The body of a healthy person can restore blood loss up to 20% of BCC (approximately 1000 ml) due to autohemodilution and redistribution of blood in the vascular bed. With blood loss of more than 20-25%, these mechanisms can eliminate the BCC deficiency. With massive blood loss, persistent vasoconstriction remains the leading “protective” reaction of the body, in connection with which normal or close to normal blood pressure is maintained, blood supply to the brain and heart is carried out (centralization of blood circulation), but due to weakening of blood flow in the muscles of internal organs, including kidneys, lungs, liver.

Long-term stable vasoconstriction, as a protective reaction of the body, at first maintains blood pressure within certain limits for some time, later, with the progression of shock and in the absence of adequate therapy, it contributes to the consistent development of severe microcirculation disorders, the formation of “shock” organs and the development of acute renal failure and other pathological conditions.

The severity and speed of disorders in HS depends on the duration of arterial hypotension, the ascending state of organs and systems. With ascending hypovolemia, short-term hypoxia during childbirth leads to shock, as it is a trigger for impaired hemostasis.

Hemorrhagic shock clinic

Hemorrhagic shock is manifested by weakness, dizziness, nausea, dry mouth, darkening of the eyes, with increased blood loss – loss of consciousness. In connection with the compensatory redistribution of blood, its amount decreases in the muscles, the skin is manifested by pallor of the skin with a gray tint; the limbs are cold, wet. A decrease in renal blood flow is manifested by a decrease in diuresis, subsequently with impaired microcirculation in the kidneys, with the development of ischemia, hypoxia, and tubular necrosis. With an increase in blood loss, symptoms of respiratory failure increase: shortness of breath, respiratory rhythm disturbance, agitation, peripheral cyanosis.

Four degrees of severity of hemorrhagic shock are distinguished:

• I degree of severity is noted with a BCC deficit of 15%. The general condition is satisfactory, the skin is pale, slight tachycardia (up to 80-90 beats / min), blood pressure within 100 mm Hg, hemoglobin 90g / l, central venous pressure is normal.
• II degree severity – BCC deficiency up to 30%. General condition of moderate severity, complaints of weakness, dizziness, darkening of the eyes, nausea, skin is pale, cold. Blood pressure 80-90 mm Hg, central venous pressure below 60 mm wg, tachycardia up to 100-120 beats/min, reduced diuresis, hemoglobin 80 g/l and below.
• III degree severity occurs with a BCC deficiency of 30-40%. The general condition is severe. There is a sharp lethargy, dizziness, pale skin, acrocyanosis, blood pressure below 60-70 mm Hg, CVP drops (20-30 mm water column and below). There is hypothermia, frequent pulse (130-140 beats / min), oliguria.
• IV degree severity is observed with a BCC deficiency of more than 40%. The condition is very serious, consciousness is absent. Arterial pressure and central venous pressure are not determined, the pulse is noted only on the carotid arteries. Breathing is superficial, rapid, with an abnormal rhythm, mobile excitation, hyporeflexia, anuria are noted.

Treatment of hemorrhagic shock

• Fast and reliable bleeding control.
• Replenishment of BCC and maintaining macro-, microcirculation and adequate tissue perfusion using controlled hemodilution, blood transfusion, rheocorrectors, glucocorticoids, etc.;
• Artificial ventilation of the lungs in the mode of moderate hyperventilation with positive end-expiratory pressure (prevention of “shock lungs”)
• Treatment of disseminated intravascular coagulation, disorders of the acid-base state, protein and water-electrolyte metabolism, correction of metabolic acidosis;
• Anesthesia, medical anesthesia, antihypoxic protection of the brain;
• Maintain adequate urine output at 50-60 ml/hour;
• Maintaining the activity of the heart, liver;

Elimination of the cause of bleeding is the main point in the treatment of hemorrhagic shock. The choice of method to stop bleeding depends on its cause. In the treatment of great importance is the speed of compensation for blood loss and timely surgical treatment. At the II degree of severity, hemorrhagic shock is an absolute indication for the operational stop of bleeding.

Infusion therapy for hemorrhagic shock should be carried out in 2-3 veins: with blood pressure in the range of 40-50 mm Hg. the volumetric infusion rate should be 300 ml/min at a blood pressure of 70-80 mm Hg. – 150-200 ml / min with stabilization of blood pressure up to 100-110 mm Hg. infusion is carried out drip under the control of blood pressure and hourly diuresis.

The ratio of colloids and crystalloids should be 2:1. Infusion therapy includes: rheopolyglucin, volecam, erythromass, native or fresh frozen plasma (5-6 vials), albumin, Ringer-Locke solution, glucose, panangin, prednisolone, corglicon, for the correction of metabolic acidosis – 4% sodium bicarbonate solution, trisamine . In hypotensive syndrome – the introduction of dopamine or dopamine. The volume of infusion should exceed the estimated blood loss by 60-80%, at the same time, blood transfusion is carried out in the amount of not more than 75% of blood loss with its simultaneous replacement, then delayed blood transfusion in smaller doses.

To eliminate vasospasm after eliminating bleeding and eliminating BCC deficiency, ganglionic blockers are used with drugs that improve the rheological properties of blood (rheopolyglucin, trental, complamin, chimes). It is necessary to use high doses of glucocorticoids (30-50mg/kg of hydrocortisone or 10-30mg/kg of prednisone), diuretics, mechanical ventilation.

For the treatment of DIC in HS, fresh frozen plasma is used, protease inhibitors – contrical (trasilol) 60-80000 OD each, Gordox 500-600000 OD each. Dicynon, etamzilat, androxon reduce capillary fragility, enhance the functional activity of platelets. Cardiac glycosides, immunocorrectors, vitamins are used, according to indications – antibacterial therapy, anabolics (nerobol, retabolil), Essentiale.

Mortality in hemorrhagic shock depends on the time of elimination of bleeding, the volume of blood loss and intensive care measures. It currently accounts for about 15% of all cases.

Rehabilitation therapy and therapeutic exercises are of great importance after intensive therapy.

Hemorrhagic shock – causes, symptoms, diagnosis and treatment

Hemorrhagic shock is a complex of hemodynamic and metabolic disorders that occur due to acute blood loss. The cause of the emergency condition are injuries, internal bleeding in case of damage to the integrity of organs and vascular walls. Pathology is manifested by pallor of the skin and cold sweat, cardiac disorders, progressive depression of consciousness up to coma. Diagnosis is carried out according to clinical and laboratory signs and is combined with emergency therapy, which includes the introduction of blood substitutes, correction of metabolic acidosis, elimination of peripheral vascular spasm.

General information

Hemorrhagic shock belongs to the group of hypovolemic shocks and is an emergency requiring treatment of the patient in the intensive care unit. It is not an independent nosology and is a nonspecific pathological syndrome that occurs against the background of other health disorders. Hemorrhagic shock is of particular importance to specialists in all fields of medicine, since it is characterized by rapid progression, severe course and poor prognosis in the absence of emergency care.

Hemorrhagic shock

Causes

The main etiological factor of shock is trauma: fractures of large bones, multiple fractures of bones with multiplication of soft tissues, injuries of internal organs. Less commonly, the cause is blunt abdominal trauma, which is accompanied by rupture of the spleen of the liver or other organs. Injuries most often occur in everyday life, less often in road accidents, at work as a result of criminal or military actions. In addition to trauma, the causes of hemorrhagic shock can be:

• Gastrointestinal diseases . Massive bleeding is observed as a complication of gastric ulcer and duodenal ulcer, reflux esophagitis, Mallory-Weiss syndrome. Blood loss is possible with cirrhosis of the liver, which is complicated by portal hypertension and varicose veins of the esophagus. Less commonly, pathology occurs during the decay of malignant tumors of the stomach and intestines.
• Respiratory diseases . The leading causes of pulmonary bleeding are tumors of the bronchi and lungs in an advanced stage, untreated pulmonary tuberculosis. Less commonly, pathology develops with a complicated course of pneumonia, pulmonary infarction, gangrene and other purulent-destructive processes in the lung tissue.
• Gynecological diseases . In pregnant women, pathology can occur with placenta previa, premature detachment of a normally located placenta, spontaneous abortion. In the birth and postpartum period, bleeding occurs with atony or uterine rupture. In non-pregnant patients, massive metrorrhagia is observed with submucosal myoma.

Risk factors

The main predisposing factor for hemorrhagic shock are hemostasis disorders associated with thrombocytopenia, thrombocytopathy, coagulopathy. Conditions occur with aplastic anemia, thrombocytopenic purpura, hereditary pathologies (hemophilia, von Willebrand disease). The likelihood of profuse bleeding increases in people who take anticoagulants and antiplatelet agents for a long time without monitoring the parameters of the blood coagulation system.

Pathogenesis

Normally, compensatory mechanisms ensure hemodynamic adaptation and prevent the development of shock. If the deficit of circulating blood volume (BCV) exceeds 20%, which corresponds to 1 liter, decompensation develops and homeostasis is disturbed. The pathological process starts with a narrowing of peripheral vessels and a decrease in blood flow in them. This is accompanied by a redistribution of fluid, the passage of water from the cells and interstitial space into the vessels.

If the BCC is not replenished, blood loss leads to a pronounced spasm of peripheral vessels, a critical deterioration in microcirculation and changes in the rheological properties of the blood. Hypoxia increases in the tissues, accompanied by an expansion of the vascular space and an increase in the discrepancy between the volume of blood and the vascular bed. Under-oxidized products accumulate in the body, energy processes are disrupted, and central blood circulation worsens.

In the late stages of hemorrhagic shock, the mechanisms of disseminated intravascular coagulation are activated. DIC is caused by progressive acidosis, which enhances the work of the internal hemostasis system and contributes to the formation of blood clots. In severe cases, shock ends with irreversible activation of the fibrinolytic system, which corresponds to a critical condition and a poor prognosis for the patient.

Hemorrhagic shock

Classification

According to clinical signs, hemorrhagic shock is divided into reversible, which can be compensated and decompensated, and irreversible, diagnosed with massive blood loss and prolonged hypotension. According to the magnitude of BCC losses, a state of mild, moderate and severe severity is distinguished. In emergency medicine, a classification according to clinical and laboratory indicators is widespread, which includes 4 degrees:

• 1 degree . It is diagnosed with a BCC deficiency of 15-20% and is characterized by a satisfactory condition of the patient. It is characterized by a systolic blood pressure (SBP) of about 100 mm Hg. Art., pulse 80-100 beats. The level of hemoglobin in the blood is more than 90 g/l, which corresponds to a mild degree of anemia.
• 2nd degree . It is determined when the BCC is lost from 20% to 30% and is characterized by a progressive deterioration in the victim’s well-being. The SBP indicator decreases to 80-90 mm Hg. Art., heart rate increases to 100-120 beats, hemoglobin level corresponds to moderate or severe anemia.
• 3rd degree . It is established with blood loss within 30-40% of the BCC and is manifested by a severe general condition of the patient. SBP is no more than 60-70 mm Hg. Art., the frequency of contractions of the heart increases to 140 beats, the body temperature drops sharply.
• 4th degree . It is observed with a critical decrease in BCC – more than 40% of the initial values. With this degree of hemorrhagic shock, the measurement of arterial and central venous pressure is difficult. The patient is in a coma.

Symptoms of hemorrhagic shock

At the initial stage, drowsiness, weakness, dizziness and darkening of the eyes occur. The patient has pale and cool skin, rapid, shallow breathing, and a rapid and weak pulse. A decrease in the volume of urination by 2 times is characteristic. At this stage, the consciousness of patients is preserved, they adequately orient themselves in time and space, meaningfully answer questions, however, thinking and the pace of speech are slowed down.

Progression of the disease is manifested by disturbances of consciousness in the form of lethargy, pathological drowsiness, delayed reaction to external stimuli. The skin becomes sharply pale, a bluish tint of the distal extremities (acrocyanosis) is characteristic. Patients are covered with profuse cold sweat, have rapid and irregular breathing. The pulse becomes weak and frequent – up to 130 beats per minute, blood pressure decreases.

Decompensated course of hemorrhagic shock is characterized by loss of consciousness, marble skin pattern, lack of urination. The patient’s breathing becomes weak and irregular. It is not possible to determine the pulse on the peripheral vessels, the heart rate exceeds 140 beats. Systolic pressure is about 60 mm Hg. Art., while diastolic blood pressure is often impossible to determine.

Complications

In the absence of timely correction of blood loss, hemorrhagic shock causes total disturbances of macrocirculation and microcirculation, which culminate in disorders of all types of metabolism. There is a high probability of death, which is due to deep hypoxia of the brain and other vital organs, cardiac arrest against the background of severe hypovolemia, and multiple organ failure.

Diagnosis

Since patients with hemorrhagic shock require emergency treatment, examination is performed in the intensive care unit at the same time as treatment is started. In the presence of signs of blood loss and clinical symptoms of a state of shock, a preliminary diagnosis is not difficult. An extended examination is prescribed to assess the general condition of the patient, to determine the possible causes of the pathology. The diagnostic complex includes the following methods:

• Definition of the Algover shock index . The indicator is used to quickly assess the severity of bleeding. It is equal to the ratio of heart rate in one minute to the systolic pressure. The normal value of the shock index is about 0.5, an increase in the index is observed with hemodynamic disorders.
• Blood tests . It is possible to determine the presence and severity of the loss of BCC by the level of hematocrit, erythrocytes and hemoglobin. To assess the degree of bleeding disorders, a coagulogram is performed. Data from a biochemical blood test provide valuable information about the work of the liver and kidneys, a possible underlying cause of bleeding.
• Instrumental methods . In the absence of a visible source of blood loss and hemorrhagic shock is suspected, abdominal ultrasound, chest x-ray, and other methods of visualizing internal bleeding are performed. In emergency situations, laparoscopy and / or thoracoscopy is performed for therapeutic and diagnostic purposes.

Differential diagnosis

Pathology must be distinguished from other types of critical hypovolemia: traumatic, toxic-infectious, anaphylactic shock. An important role in the diagnosis is played by the clarification of the conditions under which there was a deterioration in well-being, the identification of concomitant symptoms. If there are no obvious signs of blood loss, differential diagnosis is carried out with acute heart failure and other causes of cardiogenic shock.

Blood transfusion in hemorrhagic shock

Treatment of hemorrhagic shock

Restoring the amount of circulating blood is of paramount importance in the management of hemodynamic disorders. For this purpose, infusion solutions are administered – crystalline and colloidal preparations in a ratio of 2: 1. To normalize the blood composition, fresh frozen plasma, erythrocyte and platelet masses are used. The volume of solutions for transfusion is calculated taking into account the loss of bcc and laboratory parameters.

In addition to blood substitutes, sodium bicarbonate solutions are used to eliminate metabolic acidosis, a key pathogenetic factor in the progression of hypoxia and ischemia. To normalize vital functions, inhalations of humidified oxygen, the introduction of osmotic or loop diuretics in case of inadequate diuresis, the use of cardiac glycosides in case of violations of the heart are shown.

An important problem in hemorrhagic shock is peripheral vasoconstriction associated with inadequate blood supply to tissues and aggravation of metabolic disorders. For its correction, warming the patient is shown, which simultaneously eliminates hypothermia and eliminates vasospasm. Vasopressor drugs are not prescribed, despite the severity of hypotension, because they exacerbate vascular spasm and aggravate the patient’s condition.

Prognosis and prevention

The outcome depends on the amount of blood loss and the timeliness of care. With a loss of up to 30% of BCC and the beginning of treatment in the first 2-3 hours from the action of the causative factor, the survival rate is about 80%. With massive blood loss and the start of treatment after more than 4 hours, the prognosis is unfavorable due to irreversible changes in body tissues.