Contact Hours: 5
This educational activity is credited for 5 contact hours at completion of the activity.
Course Purpose
To provide healthcare professionals with an overview of the various shock types, common causes and identifying factors, and potential treatment options.
Overview
Shock is a severe manifestation of circulatory failure that results in cellular and tissue hypoxia.1 All cases of shock require rapid and proper identification to restore oxygen delivery to vital organs, as improper identification and delay in treatment can lead to vital organs being irreversibly damaged, causing multiple organ failure and death. This course provides an overview of the different types of shock and their causes, signs and symptoms, and potential treatment options.
Course Objectives
Upon completion of the independent study, the healthcare professional will be able to:
- Define the three stages of shock
- Review the physiologic changes associated with hypoxia.
- Review fluid administration requirements in the setting of shock
- Recognize the four major subtypes of shock, their causes, and their symptoms
- Understand the pharmacologic treatment options for the various shock types
Policy Statement
This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.
Disclosures
Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.
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If you already have an account, please sign in here.
Shock is a severe manifestation of circulatory failure that results in cellular and tissue hypoxia.1 Simply put, it is a life-threatening condition that affects the body’s ability to perfuse organs.2,3 This causes a decreased oxygen output which is inadequate to meet the cellular metabolic demands or oxygen consumption needs.3 All cases of shock require rapid and proper identification to restore oxygen delivery to multiple organs like the heart, brain, liver, and kidneys.1,4
Shock is a reversible condition, especially in the early stages. Still, improper identification and delay in treatment can lead to vital organs being irreversibly damaged and cause multiple organ failure (MOF) and death.1,2,3,4
This course will overview the different types of shock and their causes, signs and symptoms, and treatment options.
Shock is a medical condition in which the patient suffers from cellular and tissue hypoxia.3 This commonly happens when an individual has extremely low blood pressure, and their oxygen delivery to multiple organs is disrupted or stopped.3 However, it is important to note that not all people with low blood pressure experience shock, and even though low blood pressure is generally the cause of shock, it may not be prevalent in the early stages.1
Hypoxia causes multiple physiologic and biochemical changes.2 These changes vary in the early stage and are often reversible, but may be irreversible with multi-organ failure.2 Shock can be divided into three stages:2
Compensation shock – In this stage, the body undergoes compensatory mechanisms to counter the decrease in tissue perfusion, including peripheral vasoconstriction, tachycardia, and changes in systemic blood pressure.
Shock – When the compensatory mechanisms become insufficient, the early signs of organ dysfunction become apparent.
End-organ dysfunction – At this stage, the patient has progressed to the irreversible stage of organ dysfunction, multi-organ failure, and death.
Shock can be caused by multiple pathophysiological mechanisms and result in 4 major types, including:5
Distributive shock that is caused by loss of vascular tone or mediation of vascular permeability because of inflammatory agents like poisoning, vasodilation effects, or sepsis.
Obstructive shock is caused by the anatomical blockage of the great vessels of the heart, leading to decreased venous return, increased afterload, and decreased cardiac output. Tension pneumothorax or pulmonary embolism can cause obstructive shock.
Cardiogenic shock is caused by low cardiac output from circulatory failure that results in end-organ hypoperfusion and tissue hypoxia. Myopathy, myocardial infarction, or a major arrhythmia can cause cardiogenic shock.
Hypovolemic shock from loss of fluids, internally or externally, due to trauma or gastrointestinal bleeding can cause hypovolemia.
These mechanisms can occur separately or in combination. Proper diagnosis of the etiologies helps in finding appropriate treatment options. Unfortunately, there is limited knowledge about the frequency and associated prognosis across etiologies of undifferentiated shock, especially in the emergency department.5 Most of the current research available is based on post-shock management or the most common types of shock, cardiogenic or septic.5
There are four broad categories of shock, namely, cardiogenic, hypovolemic, distributive, and obstructive. Each has its own mechanism, causes, common signs and symptoms, and treatment options.2 The etiologies mentioned above can result in any of these four types and are manifested by the final outcome of shock.2 It is important to note that all types of shock are caused by an imbalance between oxygen supply and demand, leading to multi-organ failure and death.6 However, they are classified based on their pathogenesis and pathophysiology and the different therapeutic interventions required to prevent them from proceeding to the end stage.6
Also known as vasodilatory shock, distributive shock causes inadequate tissue perfusion.7 It is the most frequent form of shock, and results from the pathological redistribution of the absolute intravascular volume.6 In this shock type, systemic vasodilation results in decreased blood flow to vital organs, like the heart, brain, and kidneys, leading to organ failure if timely treatment is not provided.7 The clinical status becomes more complex due to the fluid leakage from capillaries into the surrounding tissue.7
Distributive shock is divided into three subtypes; septic, anaphylactic, and neurogenic.6,
Septic shock is caused by the dysregulated host response to infection.2 It causes severe metabolic, cellular, and circulatory abnormalities resulting in hypoperfusion.2 Septic shock is the most common type of shock overall.8
Sepsis is extremely prevalent and seen in 10 of 1000 hospitalized patients.9 30% of these patients develop multiple organ dysfunction syndrome (MODS), where mortality is observed in 20% of patients with sepsis and 60–80% of patients with septic shock.9
Sepsis is caused by fungi, viruses, bacteria, and parasites.9 Sepsis and septic shock are commonly associated with gram-positive bacteria, including pneumoniae and enterococcus.2 Sepsis can also develop from non-infectious intraabdominal conditions such as trauma, pancreatitis, or urinary infection.9
Most signs and clinical findings are insidious and can manifest in the form of:9
- Decreased urine output
- Fever
- Mental fog
- Temporary hypotension
- Unexplained thrombocytopenia
Sepsis and septic shock can be divided into different clinical phases:9
- Sepsis
- Clinical symptoms of infection
- Systemic inflammatory response syndrome (SIRS) – Having two or more of the following:
- Body temperature of >38°C or <36°C,
- Tachycardia: heart rate more than >90/min,
- Tachypnea (respiratory frequency of >20/min) or mechanical respiratory requirement
- White blood cell count of >12×109/L or <4×109/L
- Severe sepsis
- Hypotension along with sepsis
- Sepsis-induced organ dysfunction
- Septic shock
- Arterial hypotension (systolic arterial pressure of <90 mmHg or mean arterial blood pressure of <65 mmHg), along with severe sepsis
- Multiple organ dysfunction syndrome (MODS)
- More than 2 vital organs affected
These symptoms can lead to coagulation disorder, respiratory and renal failure, or irremediable hypotension if not treated.9
Sepsis commonly occurs in patients over 65 years of age and in those with underlying malignant diseases.6 For many years, sepsis was diagnosed by the presence of an infection and systemic inflammatory response syndrome (SIRS).10 But SIRS has inadequate sensitivity and specificity. Thus, a new and improved method of diagnosis was developed.10 For instance, the quick sepsis related organ failure assessment (qSOFA) is used for screening. It requires an examination of the patient’s consciousness status, blood pressure, and respiration rate.6 Healthcare professionals identify organ dysfunction as an acute change if the total qSOFA score is more than or equal to 2 points related to the parameters (obtunded consciousness, respiration rate = 22/min, systolic blood pressure = 90 mmHg) and infection is suspected.6,10
The data from qSOFA helps in identifying patients with an increased risk of developing poor outcomes, such as death or a 3-day stay at the ICU, or patients that require targeted interventions, frequent observations, or a higher care level.10 Other diagnostic tools include early warning scores (National Early Warning Score (NEWS) and Modified Early Warning Score.10
Healthcare professionals should be educated about the steps before diagnosis, such as recognizing infection in high-risk patients, signs of early organ dysfunction, and clinical deterioration.10 Moreover, patients with new organ system dysfunction who are at risk should undergo rapid evaluation, and if sepsis is confirmed, early therapeutic interventions should be initiated.10
The two most important measures of initial treatment of sepsis and septic shock are source control and antibiotic therapy.10 To prevent organ dysfunction progression, early and aggressive source control is recommended to halt progression of the infectious agent and to improve patient outcomes.
Several studies have focused on the timing of the source control and its overall impact on patient health. For instance, a meta-analysis reviewed the timing of source control in patients with peritonitis and septic shock.10 It found that patients with abdominal source control within two hours had a 98% 60-day survival. In contrast, there were no survivors when patients waited more than 6 hours for initiation of treatment after symptom onset.10
Source control can be achieved with the correct antibiotic therapy. The timing and appropriateness of the therapy are of critical importance and is based on the type and severity of the disease.10 Antibiotic agents should be started as soon as there is an indication of sepsis.10 A culture should also be obtained from the location of the infection for improved outcomes.10
According to the fourth revision of the Surviving Sepsis Campaign (SSC) guidelines, resuscitation is the initial intervention for the management of sepsis and shock.10 Immediate resuscitation or achieving the targeted endpoint of resuscitation in a sepsis or septic shock patient during the first 6 hours significantly improved outcomes.10 Guidelines recommend that the initial fluid resuscitation should include at least 30 mL/kg of intravenous crystalloid fluid given within the first 3 hours.10 After that, the administration of additional fluids depends on the hemodynamic status and the patient’s response to the treatment.10
Parameters to aid in the decision of additional fluid choices include:10
- Blood pressure
- Cardiothoracic ultrasound
- CVP, Scv02
- Heart rate response
- Lactate clearance
- Pulse pressure variation
- Urine output
Septic shock patients with hypotension often require vasopressor support. For septic shock, norepinephrine is considered the first vasoactive agent choice because it includes alpha-1 and beta-1 stimulation, which helps increase peripheral vasoconstriction without significantly compromising cardiac output.7,10 The dosage varies on the patient’s overall health and response and can range from 2 mcg/min to 20 mcg/min.7,10
According to the SSC guidelines, patients should maintain a target mean arterial pressure of 65 mmHg.10,11 Dopamine, epinephrine, vasopressin, and phenylephrine are also considered suitable agents to treat septic shock.10 Previously, dopamine was considered a first-line agent, but its use has a d greater risk of cardiac arrhythmias.10,11 It is now used in selective patients as an alternative to norepinephrine and in patients with low risk of tachyarrhythmias.10
Corticosteroids are also effective as they use immune modulation and cardiovascular modulation mechanisms to increase tissue perfusion.11. Steroids are recommended for to patients in which adrenal suppression is suspected, and vasopressor support is required.10
Currently, the Surviving Sepsis Campaign guidelines recommend against using low-dose corticosteroids if fluid resuscitation and vasopressor therapy are effective.11 However, in case of persistent hemodynamic instability, intravenous hydrocortisone can be added at a dose of 200 mg per day.11
Acute kidney injury is most commonly caused by septic shock and is associated with the highest mortality.11 Renal replacement therapy is recommended for patients with uremia, hyperkalemia, or fluid overload.11 Early intervention with renal replacement therapy can reduce temperature, vasopressor requirement, fluid overload, and limit organ failure.11
- Nutrition – Caloric intake improves mortality in underweight and overweight populations. The preferred feeding option is via enteral access. The patient should receive enteral feeding within 48 hours, and feeding goals should be met ideally within 72 hours of admission to the hospital.10,11
- Positioning – For mechanically ventilated patients, the bed should be elevated between 30° and 45°.11
- Glucose level – The recent Surviving Sepsis consensus statement recommends insulin therapy to lower glucose levels to less than 150 mg/dL. Glucose measurements should be taken until the values stabilize.11
Also known as allergic shock or anaphylaxis, anaphylactic shock is believed to be caused by a hypersensitive reaction by immunoglobulin E (Ig-E), resulting in respiratory distress and cardiovascular collapse.2 The central role is played by the mast cells and basophilic granulocytes that release mediators without any antigen-antibody reaction.6
Anaphylactic shock is characterized by massive histamine-mediated vasodilation. Histamine is released during an allergic reaction, causing the blood vessels to dilate and the blood pressure to drop to critically low levels.6,12 It causes maldistribution and a shift of fluids from the intravascular to the extravascular space, including leaking into the lungs and causing heart rhythm disturbances.6,12
Anaphylaxis can be caused by multiple agents, including drugs, insects (wasps and bee stings) and food.2,6 The allergic reaction is sudden, severe, and life-threatening.12 Other factors like stress, acute infection, and physical effort can intensify the effects of anaphylaxis.6
The clinical presentation of anaphylactic shock varies from person to person and depends on the site of entry and amount of the antigen, exposure type, and the sensitization degree, but it usually manifests in the form of respiratory symptoms, abdominal symptoms, or skin rashes or hives.6
The following are symptoms associated with an anaphylactic shock that can develop and escalate rapidly:6,12
- Abdominal pain and cramps
- Anxiety
- Bluish skin
- Confusion
- Cough
- Diarrhea
- Difficulty breathing
- Generalized itching or hives
- Nausea and vomiting
- Slurred speech
- Swelling of the lips, tongue, and throat
- Wheezing
The symptoms may resolve as suddenly as they develop or progress and become fatal despite appropriate therapy.6 Arrhythmias and ventricular dysfunction are the most common fatal outcomes of anaphylactic shock.6
Because anaphylactic shock results in a dramatic allergic reaction with severe signs and symptoms, it is often easily identified.12 Immediate assessment of the airway, circulatory, and respiratory functions, with appropriate interventions in crucial to improve survival.12
Immediate management is critical to prevent cardiac arrest.13 The first step in initial management is airway assessment. If the airway is compromised and respiratory distress is noted, emergency intubation should be performed.13 In patients with upper airway edema, early intubation is recommended.13
Moreover, as stated above, massive fluid shifts occur during anaphylaxis; thus, intravenous access should be obtained in all cases.13 If a patient is hypotensive and does not respond to epinephrine, they should receive large-volume fluid resuscitation.13 For adults, 1 to 2 liters of normal saline at the fastest flow rate possible should be administered in the first few minutes of treatment.13 For children, boluses of 20 mL/kg of normal saline.13
Additional precautions should be taken for pregnant women. For instance, during labor or delivery, the following considerations are taken:13
- Conduct fetal monitoring
- Maintain a systolic BP of 90 mmHg
- Position the patient on her left side
- Provide high-flow supplemental oxygen
Anaphylaxis is an extremely variable condition, with symptoms varying from mild to severe within minutes. Because of this, after initial management, the administration of epinephrine is the first treatment option to prevent life-threatening symptoms.13 Epinephrine is effective and should be administered even when confirmed diagnostic results are not available yet, but the clinical presentation of symptoms and risk of anaphylaxis is high.13
Intramuscular (IM) injection is the preferred route of administration due to its rapid increase of plasma and tissue concentrations of epinephrine.13 The recommended dose is 0.01 mg/kg (maximum dose of 0.5 mg) per single dose for patients of all ages.13 however, in healthcare settings, an autoinjector is used, and the dosing can vary; for instance,13
- Infants under 10 kgs should be given an exact weight-based dose.
- Infants and children weighing 10 kg to 25 kg can be given 0.15 mg by autoinjector.
- Patients weighing more than 25 kg or up to 50 kg can be given 0.3 mg by autoinjector.
- Patients weighing over 50 kg can be given 0.5 mg by autoinjector.
Intravenous epinephrine is associated with significantly more dosing errors and cardiovascular complications than intramuscular epinephrine and should be avoided when possible. If a patient does not respond to IM epinephrine, slow continuous infusion of epinephrine is preferred at a rate of 0.1 mcg/kg/min and increased every 2-3 minutes by 0.05 mcg/kg/min until the blood pressure and perfusion improves.
These agents are given in combination with epinephrine to treat associating symptoms of anaphylaxis.13 They are not used as first-line treatment and do not affect the upper and lower respiratory tract obstruction or prevention of life-threatening symptoms.13 These adjunctive agents include:
- Glucocorticoidml
- Have a slower onset action14
- Effective against asthma and protracted or biphasic anaphylactic reactions14
- Produce an unspecific membrane stabilizing effect within 10 to 30 minutes of administration14
- If given, a dose of methylprednisolone of 1 to 2 mg/kg/day for one to two days is sufficient13
- H1 antihistamines
- Used to relieve itch and hives13
- If used, recommended dose – diphenhydramine 25-50 mg IV
- Are given only after epinephrine is administered13
- In some cases, higher doses are given but can lead to side effects like dry mouth, tachycardia, urinary retention, and gastrointestinal atony14
- H2 antihistamines
- When given with H1 antihistamines, provides additional relief of hives and symptoms13
- If used, a dose of famotidine 20 mg in adults and 0.25 mg/kg dose (maximum 20 mg/dose) in children, is administered and may be infused IV over at least two minutes13
- Bronchodilators
- Bronchodilators like albuterol or salbutamol are administered by mouthpiece or nebulizer for treating bronchospams13
Neurogenic shock is a result of spinal cord injury or trauma.15 It is characterized by hypotension, temperature dysregulation, and bradyarrhythmias.15 Neurogenic shock is a state of imbalance between sympathetic and parasympathetic regulation of cardiac action and vascular smooth muscle, which can lead to autonomic instability.6,15
Spinal cord injuries are the most common cause of neurogenic shock. Other causes include: 6,15
- Cerebral ischemia
- Meningitis
- Rare causes include pandysautonomia, during or after epileptic seizures, cerebral herniation, or rapid onset of Guillain–Barré syndrome.
- Subarachnoid hemorrhage
- Surgical intervention in the lumbar region
It can also be triggered by stress, severe pain, or even after a karate kick.6
Diagnosis
Diagnosis is difficult and requires extensive investigation.15 The recommended course of action involves ruling out hemorrhagic shock first and then considering neurogenic shock.15 Healthcare professionals should gather information about the mechanism of injury, the presence of midline spinal tenderness, state of consciousness, and assess for intoxication.15
Common signs like a dislocation or vertebral fracture indicate neurogenic shock.15 Other signs include flushed, warm skin, bradyarrhythmia, and hypotension.15
According to the joint committee of the American Spinal Injury Association (ASIA) and the International Spinal Cord Society (ISCoS), the definition of a neurogenic shock is “general autonomic nervous system dysfunction that also includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation.”15
Diagnosis is done through a combination of radiographic imaging, hemodynamic monitoring, and clinical exam.15
A patient shows the following signs:6
- Heart rate to <60/min with obtunded consciousness
- Sudden drop of SAP to <100 mmHg
- The rising capacity of the splanchnic venous system and skeletal musculature while systemic venous pressure drops
Other signs include:15,16
- Bluish (cyanosis) lips and fingernails
- Bradyarrhythmia
- Lack of consciousness
- Low blood pressure
- Warm, flush skin
Hypotension should be treated to prevent secondary injury.
- First-line treatment involves intravenous fluid resuscitation. This helps compensate for vasogenic dilation.15
- Second-line treatment involves vasopressors and inotropes.15
- Phenylephrine is most used as it is a pure alpha-1 agonist that causes peripheral vasoconstriction to counteract the loss of sympathetic tone.
- Norepinephrine is also preferred as it has alpha and beta activity, aiding hypotension, and bradycardia.
- Epinephrine is rarely used and has been cited for refractory cases of hypotension.
- It is recommended to maintain a mean arterial pressure (MAP) of 85 to 90 mmHg for the first 7 days to improve spinal cord perfusion.
Other treatment options include using a Miami J or Philadelphia collar, c-spine immobilization to prevent spinal cord injury, and considering the use of methylprednisolone and corticosteroids when appropriate to reduce inflammation.15
Cardiogenic shock is a hemodynamically complex syndrome that results in decreased cardiac output, hypoxia, and end-organ hypoperfusion.17,18 It has poor clinical outcomes and a mortality rate of 40%.18 It is caused due to systolic or diastolic dysfunction, resulting in a reduced ejection fraction or impaired ventricular filling.6
Cardiogenic shock is known to complicate around 5 to 12% of acute myocardial infarction (MI) cases and is the leading cause of death after MI.17,18 Moreover, MI‐associated cardiogenic shock survivors have an 18.6% risk of 30‐day readmission after discharge, with a median time of 10 days.17 It is prevalent in people over 75 years of age, women, and Asian/Pacific islanders.17
The main cause of cardiogenic shock is decreased cardiac output, which can lead to ischemia, systemic hypoperfusion, vasoconstriction, and volume overload, culminating in multiple organ failures and even death.18 The initial cardiac damage or insult can occur because of various underlying conditions or factors, such as those suggested in the following table:17,18
Table 1: Causes of cardiogenic shock
| Disorder | Causes |
| Arrhythmia | Bradycardia Atrial fibrillation Ventricular tachycardia |
| Left Ventricular Failure | Acute myocardial infarction Myocarditis Myocardial contusion Post-cardiotomy Septic cardiomyopathy Progressive cardiomyopathy Ventricular outflow obstruction |
| Right Ventricular Failure | Acute myocardial infarction Myocarditis Post-cardiotomy Septic cardiomyopathy Progressive cardiomyopathy Pulmonary embolism Worsening pulmonary hypertension |
| Pericardial Disease | Progressive pericardial constriction Tamponade |
| Valvular Or Mechanical Dysfunction | Thrombosis Aortic regurgitation Progressive aortic stenosis Progressive mitral stenosis Myocardial ischemia Ventricular septal defect or free wall rupture |
| Chemotherapeutic, Toxic, Metabolic | Calcium-channel antagonists Adrenergic receptor antagonists Thyroid disorders |
Cardiogenic shock, also known as cardiac shock, is diagnosed through various tests and physical examination.19 First, a patient’s medical history is collected, such as a personal and family history of cardiac conditions, any symptoms of a heart attack before arriving to the hospital, and any medications the patient is currently taking, including over-the-counter medications.19
Next, a physical examination is conducted, which involves a full cardiac and pulmonary assessment and listening to the heart and lungs for any unusual heart rhythms or breathing sounds, measuring vital signs, and assessing for signs of perfusion abnormalities.
After the physical exam, the following tests may be conducted to diagnose cardiogenic shock:19
- Chest X-ray – Analyzes the structures in and around your chest through imaging.
- Coronary angiography – Uses contrast dye to detect blockages in the coronary arteries.
- Echocardiography – Uses sound waves to analyze the shape and size of the heart and its blood pumping rate.
- Electrocardiogram (ECG or EKG) – Records the heart’s electrical activity, such as heart rhythm, timing, and strength of electrical impulses.
The signs and symptoms of patients with cardiogenic shock can be differentiated into two categories, such as “cold and wet,” which reflects a reduced cardiac index (CI), increased systemic vascular resistance (SVR), and increased pulmonary capillary wedge pressure (PCWP).17 Or “dry and cold,” which indicates a reduced CI, increased systemic vascular resistance, and normal PCWP.17
The physical findings can also vary depending on the area that is affected, for instance:17
Table 2: Physical findings of cardiogenic shock
| Suggestive of Right Heart Failure | Shared Findings | Suggestive of Left Heart Failure |
| Sacral edema | Cyanosis | Displaced cardiac apex |
| Lower limb edema | Cool peripheries | Lung crackles |
| Regurgitant murmur in the tricuspid area | Delayed capillary refill | Respiratory wheeze |
| Increased jugular venous distention | Orthopnea | Left-sided heart murmurs |
The Society for Cardiovascular Angiography and Intervention (SCAI) classified cardiogenic shock into stages from A through E. This was developed by a multidisciplinary team from cardiology, emergency medicine, critical care, and cardiac nursing.
Table 3: SCAI stages of shock
| Stage A At risk for cardiogenic shock | A patient has experienced a large myocardial infarction or heart failure, but is not yet in shock, with normal mentation and systolic blood pressure of 100 mm Hg or more. |
| Stage B Beginning shock | A patient has experienced hypotension or tachycardia without features of hypoperfusion and has normal mentation. Systolic BP < 90, mean arterial pressure (MAP) <60 or 30 mm Hg fall in BP. |
| Stage C Classic cardiogenic shock | A patient has hypotension with features of hypoperfusion, needing inotropes and mechanical circulatory support. |
| Stage D Deteriorating | A patient needs multiple inotropes or mechanical circulatory support to maintain perfusion. Initial interventions have failed. |
| Stage E Extremis | A patient is in cardiac arrest with ongoing CPR or ECMO support, nearly pulseless, hypotension despite maximal support. |
In addition to the SCAI stages of shock, the healthcare professional should consider the following:
- A patient’s oxygenation, end-organ failure and electrolyte status should be collected through complete blood count and metabolic panels every 12 to 24 hours.17
- Patients with SCAI stage C or D cardiogenic shock may first necessitate initial stabilization using vasopressor therapy and mechanical ventilation. However, reperfusion should not be delayed.18
- Patients with SCAI stage E or end-stage cardiogenic shock in which progressive therapies are ineffective, healthcare professionals should discuss treatment goals and consider palliative care consultation.18
- Early invasive hemodynamic monitoring using a pulmonary artery catheter (PAC) provides a guideline for medical and device-based therapies.18
- Common parameters to monitor include temperature, urinary output, respiratory rate, continuous blood pressure, and pulse oximetry.17
- Mixed venous oxygen saturation (SvO2) measurement helps assess patient response and should be drawn every 4 hours during initial hemodynamic monitoring.17
- Temporizing inotropic support in acute cardiogenic shock may be indicated, however, adverse effects like increased myocardial oxygen demand, ischemic burden, and malignant arrhythmias are possible. These agents should be used in the lowest effective doses for a small duration.18
Mechanical Circulatory Support (MSC) Devices
Early use of mechanical circulatory support (MSC) devices significantly improves health outcomes and is associated with substantial cardiovascular support without increased risk of myocardial ischemia.17 Moreover, it might lower the myocardial oxygen demand.17 MSC devices are better than vasopressor support therapy.17 The type of device selected depends on multiple factors, such as intensity of illness, degree of circulatory and ventricular support required, vascular access, or anatomy.18
The following are some MSC device evidence based on clinical trial findings.
Table 4: Mechanical Circulatory Support devices clinical trial findings17
| Mechanical Circulatory Support device | Clinical findings |
| Intra-aortic balloon pump (IABP) Shock II (2012) | IABP vs optimal medical therapy (OMT) No mortality benefit at 30 days, 6 months, and 12 months. |
| Protect II Trial (2012) | IABP vs Impella heart pump Impella provided greater cardiac power output (CPO). No major adverse event difference at 30 days, but Impella associated with decreased major adverse events at 90 days. |
| Catheter-based Ventricular Assist Device Registry analysis (2017) | Survival rates improve if the device is implanted early and before vasopressor support and percutaneous coronary intervention. |
| Detroit Cardiogenic Shock Initiative (2018—ongoing) | Reporting 76% survival rates Improvement on stagnant ≈50% mortality rates over the past 2 decades. |
Hypovolemic shock is a life-threatening condition that requires early diagnosis and management to prevent progressive symptoms.20 Hypovolemic shock is characterized by inadequate blood volume circulation and perfusion, causing rapid fluid or blood loss, and leading to multiple organic failures or death.20,21
Initial management requires ruling out other types of shock and determining appropriate treatment action.20 It is the most common type of shock in children due to diarrheal illness, especially in developing countries.20 Hypovolemic shock is divided into two sub-categories; hemorrhagic shock or traumatic shock and non-hemorrhagic shock.20
Hemorrhagic shock is due to an acute reduction in intravascular volume from bleeding.20 The critical drop in circulating blood volume triggers the shock, and the loss of a large amount of red blood cells intensifies tissue hypoxia.6 The following are common causes of hemorrhagic shock:2,6,20
- Gastrointestinal bleeding from upper and lower trauma, such as diverticulosis, variceal bleeding, portal hypertensive gastropathy bleeding, and peptic ulcer.
- Spontaneous bleeding from anticoagulant use.
- Vascular etiologies include an aortoenteric fistula, a tumor eroding into a major blood vessel, or a ruptured abdominal aortic aneurysm.
Hemorrhagic shock is also known as traumatic shock.6 A traumatic hemorrhagic shock is aggravated by a soft tissue injury, such as polytrauma, which is commonly caused by falls from great heights or traffic accidents.6
Non-hemorrhagic shock occurs from sudden reduced effective intravascular volume from body fluid loss.20 Common etiologies include:2,20
- Gastrointestinal losses – Vomiting, diarrhea, drains, and nasogastric suction.
- Renal losses – Medication-induced diuresis, and endocrine disorders like hypoaldosteronism.
- Skin losses – Heatstroke, burns, Stevens-Johnson syndrome, pyrexia, and toxic epidermal necrolysis.
- Third-space loss – Trauma, pancreatitis, cirrhosis, intestinal obstruction.
Multiple laboratory tests are conducted to diagnose hypovolemic shock, including:20,21
- Amylase, lipase, prothrombin time or international normalized ratio
- Arterial blood gas (ABG)
- Blood urea nitrogen
- Cardiac enzymes
- Complete blood count with differential, basic chemistry tests (sodium, potassium, chloride, and serum bicarbonate)
- Creatinine
- Fibrinogen, fibrin split products, or dimer
- Liver function tests
- Partial thromboplastin time
- Toxicology screen and lactate level
- Urinalysis with a detailed sediment analysis
Healthcare professionals may also conduct a chest and abdominal radiograph, a head CT scan, electrocardiogram, or echocardiogram.21 Moreover, central venous pressure monitoring, although not an accurate means of monitoring volume resuscitation, is only used as a rough analysis, and an initially low CVP (<5 mmHg) may indicate hypovolemia.21
Symptoms can vary based on the organ involved, the level of organ function, the intensity of organ dysfunction, compensatory mechanisms, and the cause.21 The following are common causes associated with hypovolemic shock:21
- Agitation
- Cool and clammy skin
- Cyanosis
- Diaphoresis
- Dyspnea
- Faint heart sounds
- Hypotension
- Lactic acidosis
- Mental status changes
- Pallor
- Pinpoint pupils
- Poor urine output
- Tachycardia
- Tachypnea
Treatment Options
For hypovolemic shock, the first step of management requires differentiating between hemorrhagic and non-hemorrhagic shock.20 However, the primary goal of all treatment methods is to maximize oxygen delivery, control further blood loss, and fluid resuscitation.21
- To improve survival rate and blood products transfusion, early resuscitation is critical for prompt bleeding source control.20
- For resuscitation, using blood products resulted in better outcomes than crystalloid resuscitation.20
- Bleeding source control can be done through surgical, endoscopic, or interventional radiology.20
- Balanced transfusion using 1:1:1 or 1:1:2 of plasma to platelets to packed red blood cells results in better hemostasis.20
- A trial concluded that the administration of anti-fibrinolytic to patients with severe, traumatic injury and bleeding within 3 hours decreases the risk of death.20
- Volume resuscitation should be started immediately to compensate for fluid loss. Since the type of fluid loss is difficult to determine, physicians recommend starting with 30ml/kg body weight of warm isotonic crystalloid solution, infused rapidly to restore tissue perfusion quickly.20
- Resuscitation is monitored through peripheral edema, urine output, mental status, heart rate, and blood pressure.20
- In cases of severe volume depletion, crystalloid fluid resuscitation is preferred. The crystalloid type is selected based on the physicians’ reference, the patient’s overall lab results, acid/base status, and estimated resuscitation volume.20
Obstructive shock is triggered by an inadequate blood supply to vital organs; it closely resembles cardiogenic shock, but differentiation is necessary to provide appropriate treatment options.22 The major difference between the two is that cardiogenic shock is caused by primary cardiac dysfunction, while obstructive shock is caused by extracardiac diseases, such as cardiac tamponade.22
The common pathophysiology of obstructive shock is a reduction in the left ventricular (LV) preload.22,23 It can be due to tension pneumothorax, mediastinal tumors, or underlying diseases that affect cardiac output.22
Frequency and incidence rate of obstructive shock are determined by the frequency of the underlying diseases, such as a population-based incidence for aortic dissection suggests an incidence of 2.3–16.3/100,000 inhabitants per year.22 However, this is not accurate, and more data is required.22
The following are the common causes of obstructive shock:22
- Obstruction in the pulmonary circulation
- Intracardiac mass
- Pulmonary embolism
- Pulmonary compression syndrome by mediastinal mass
- Obstruction in the aortic circulation
- Leriche syndrome
- Aortic dissection
- Disorders of diastolic filling
- Cardiac tamponade
- Tension pneumothorax
- Ventilation with high PEEP
- Caval compression syndrome
The diagnosis of obstructive shock is divided into 3 stages; clinical examination, rapid ultrasound in shock, and radiological imaging.22
A physical examination should be conducted to recognize the signs and symptoms of obstructive shocks, such as auscultation for decreased or missing respiratory sounds, inspection, and palpation for detecting tension pneumothorax’s breathing patterns, or an electrocardiogram (ECG) to detect clinical findings of a pulmonary embolism.22
Rapid Ultrasound in Shock (RUSH)
Perera et. al. developed the RUSH Protocol (Rapid Ultrasound in Shock) and offered a structured ultrasound approach for differentiating between different shock types.22
The following are the ultrasonographic findings of obstructive shock by RUSH:22
Table 5: RUSH evaluation for obstructive shock22
| RUSH evaluation | Ultrasonographic findings |
| Pump | RV strain Cardiac thrombus Hypercontractile heart Cardiac tamponade Pericardial effusion |
| Tank | Absent lung-sliding Distended IVC Distended jugular veins Stratosphere phenomenon |
| Pipes | Aortic dissection Pulmonary embolism Complete or incomplete occlusion of the aorta distal to the renal arteries |
If a patient is stable enough for radiological imaging, a CT scan is conducted for determining the cause of the shock.22
The following are the symptoms associated with obstructive shock:22,23
- Dyspnea
- Shivering
- Skin paleness
- Hypotension
- Tachycardia
- Shivering
- Impaired mental status
- Decreased urine output
Treatment Options
- Not a key feature for obstructive shock and is a part of general management.22 The European Society of Cardiology recommends norepinephrine as a first-line vasopressor for obstructive shocks caused by pulmonary embolism.22 Aside from this, vasopressin also shows satisfactory results.22
- Mechanical ventilation increases afterload of the right ventricle, thus, can have damaging effects for patients with obstructive shock.22 If necessary, a low-volume and low PEEP should be considered.22
Extracorporeal Membrane Oxygenation (ECMO)
- A useful treatment option for obstructive shock caused by pericardial tamponade.22 However, there are reports it can cause pericardial effusion and a decreased venoarterial ECMO flow in neonates and adults.22
- On the other hand, multiple studies show that venovenous ECMO improves RV dysfunction. Thus, careful consideration and evaluation are required when using this treatment method.22
Fluid resuscitation is a common and most important treatment option for septic shock. According to international guidelines, aggressive fluid resuscitation results in improved outcomes.24 This is based on the theory that septic shock is strongly associated with hypovolemic shock and is characterized by tissue hypoperfusion.24
The SSC guidelines suggest that fluid resuscitation should be initiated in all patients without any exceptions.24 The recommended dosage is a minimum of 30 mL/kg crystalloid for hypotension or lactate ≥4 mmol/L.24 The justification of this dosage is as provided by the SSC states that “although little literature includes controlled data to support this volume of fluid, recent interventional studies have described this as usual practice in the early stages of resuscitation, and observational evidence is supportive.”24 Fluid resuscitation may correct hypotension and tachycardia in elderly patients with decreased oral intake who have had the condition for some time, but fluids cannot alone reverse the hemodynamic instability, especially in severe sepsis cases.24 On the contrary, evidence suggests that aggressive fluid resuscitation may worsen vasodilatory shock and myocardial dysfunction in elderly pateints.24
Different Intravenous Fluid Types
There are several types of intravenous fluids available, such as:26
- Crystalloids
- For intravascular volume replenishment, isotonic fluids are used. Generally, 0.9% saline or Ringer’s lactate.
- Ringer’s lactate is referred to in hemorrhagic shock as it reduces acidosis. And 0.9% saline is considered for patients with acute brain injury.
- Colloids
- Offer no major advantage over crystalloid solutions.
- Hydroxyethyl starch, albumin, and dextrans are effective in volume replenishment. However, hydroxyethyl scratch increases the risk of renal injury, and albumin harms patients with traumatic brain injury.
- Blood
- In emergency care, 1 to 2 units of type O Rh-negative blood are accepted.
- When > 1 to 2 units are transfused, blood is warmed to 37°C.
- Patients receiving > 6 units may require the replacement of clotting factors with fresh frozen plasma infusion or cryoprecipitate and platelet transfusion.
- Blood substitutes
- These oxygen-carrying fluids are perfluorocarbons or hemoglobin-based, although none are commercially available.
- Perfluorocarbons are IV carbon-fluorine emulsions and carry a large amount of oxygen.
- Hemoglobin-based fluids contain free hemoglobin that is liposome-encapsulated or modified. They can be banked for over a year and do not require cross-matching.
General recommendations of intravenous fluid use for septic shock
- Normal saline is the most used intravenous fluid because of its low cost and easy availability.25
- In septic shock, crystalloids are recommended for initial resuscitation.25
- Balanced crystalloids like Ringer lactate or PlasmaLyte during resuscitation are associated with a lower risk of hyperchloremic acidosis, acute kidney injury (AKI), and overall mortality compared to normal saline.25
The following is the fluid resuscitation protocol in children:27
- First, evaluate pediatric trauma in children and the cause of hemorrhagic shock.
- Next, hypothermia must be prevented. Administering warm intravenous fluids, covering the patient with a warm blanket, connective air warmers, and warmed, humidified ventilation can help maintain core body temperature.
- Initial resuscitation with intravenous fluids and blood is the primary treatment option.
- Initial fluid resuscitation should begin with the warm isotonic crystalloid solution (Ringer’s lactate or isotonic sodium chloride solution) at a bolus of 20 mL/kg. However, fluid resuscitation can also have adverse effects, and thus, its use should be evaluated on a case-by-case basis.
- In children with a head injury, dextrose-containing fluids should not be given because hypotonic solutions can cause cerebral edema.
- Due to the high rate of early coagulopathy and TBI in children, colloids are unsuitable for volume replacement in trauma patients.
The following is the massive transfusion protocol in adults:27
- Massive transfusion is considered in patients that do not respond well to fluid resuscitation.
- RBC and FFP contain fibrinogen and are excellent volume expanders; thus, they are used as volume therapy to treat hypovolemia causing hypoperfusion.
- Existing adult MT protocols recommend PRBC/FFP/PLT in the ratio of 1:1:1. However, this protocol is unsuitable for children weighing less than 30 kgs.
For massive transfusion in children, the following protocol should be considered:27
- MT protocol should be initiated if patients present with hemorrhagic shock and persistent hemodynamic instability or bleeding after 40 mL/kg of crystalloid infusion.
- For pediatric patients >30 kg, 1:1:1 units of PRBC/FFP/PLT with cryoprecipitate were given for low fibrinogen levels (<1-1.5 g/l) or during bleeding after the administration of 1 round of all 3 blood components.
- For pediatric patients <30 kg, a weight-based protocol at a ratio of 30: 20:20 should be initiated.
- Maintain body temperature, blood pH, and serum calcium.
- Consider using rFVIIa in extreme cases.
Shock is a life-threatening condition with several types, etiologies, and underlying conditions resulting in multiple organ failures and poor health outcomes. Thus, a multidisciplinary team containing physicians, nurses, and specialists should be established to provide an appropriate treatment course according to the patient’s changing clinical status.2 Patient education and immediate evaluation and diagnosis are critical to ensure improved health outcomes.2
Different types of shock can be difficult to diagnose due to overlapping symptoms and underlying conditions.8 Moreover, therapies that are effective for one type of shock can be harmful to the other; thus, a thorough understanding of the physiology of the several types of shock and the appropriate treatment option is necessary.8
Nurses should be well-versed in effective vasopressors for different types and ages, fluid resuscitation protocol, and assist in every step, from intubation to medication administration.2
- Shock – Heart and Blood Vessel Disorders. MSD Manual Consumer Version. https://www.msdmanuals.com/home/heart-and-blood-vessel-disorders/low-blood-pressure-and-shock/shock
- Hayas Haseer Koya, Paul M. Shock. Nih.gov. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK531492/
- UpToDate. www.uptodate.com. Accessed March 17, 2023. https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults#H183084763
- Shock; circulatory failure. Cancer Therapy Advisor. Published January 17, 2019. https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/critical-care-medicine/shock-circulatory-failure/
- Gitz Holler J, Jensen HK, Henriksen DP, et al. Etiology of Shock in the Emergency Department: A 12-Year Population-Based Cohort Study. Shock. 2019;51(1):60-67. doi:https://doi.org/10.1097/SHK.0000000000000816
- Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W. The nomenclature, definition and distinction of types of shock. Deutsches Aerzteblatt Online. 2018;115(45). doi:https://doi.org/10.3238/arztebl.2018.0757
- Smith N, Lopez RA, Silberman M. Distributive Shock. PubMed. Published July 25, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470316/
- Kislitsina ON, Rich JD, Wilcox JE, et al. Shock – Classification and Pathophysiological Principles of Therapeutics. Current Cardiology Reviews. 2019;15(2):102-113. doi:https://doi.org/10.2174/1573403×15666181212125024
- Polat G, Ugan RA, Cadirci E, Halici Z. Sepsis and Septic Shock: Current Treatment Strategies and New Approaches. The Eurasian Journal of Medicine. 2017;49(1):53-58. doi:https://doi.org/10.5152/eurasianjmed.2017.17062
- Armstrong BA, Betzold RD, May AK. Sepsis and Septic Shock Strategies. Surgical Clinics of North America. 2017;97(6):1339-1379. doi:https://doi.org/10.1016/j.suc.2017.07.003
- Thompson K, Venkatesh B, Finfer S. Sepsis and septic shock: current approaches to management. Internal Medicine Journal. 2019;49(2):160-170. doi:https://doi.org/10.1111/imj.14199
- Anaphylaxis. www.hopkinsmedicine.org. Published 2021. https://www.hopkinsmedicine.org/health/conditions-and-diseases/anaphylaxis
- UpToDate. Uptodate.com. Published 2020. https://www.uptodate.com/contents/anaphylaxis-emergency-treatment#H19
- Ring J, Beyer K, Biedermann T, et al. Guideline for acute therapy and management of anaphylaxis. Allergo Journal International. 2014;23(3):96-112. doi:https://doi.org/10.1007/s40629-014-0009-1
- Dave S, Cho JJ. Neurogenic Shock. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK459361/#:~:text=Neurogenic%20shock%20is%20a%20combination
- Cleveland Clinic. Neurogenic Shock: Causes, Symptoms and Treatment. Cleveland Clinic. Published November 30, 2021. https://my.clevelandclinic.org/health/diseases/22175-neurogenic-shock
- Vahdatpour C, Collins D, Goldberg S. Cardiogenic Shock. Journal of the American Heart Association. 2019;8(8). doi:https://doi.org/10.1161/jaha.119.011991
- Tehrani BN, Truesdell AG, Psotka MA, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC: Heart Failure. 2020;8(11):879-891. doi:https://doi.org/10.1016/j.jchf.2020.09.005
- Cardiogenic Shock – Diagnosis | NHLBI, NIH. www.nhlbi.nih.gov. https://www.nhlbi.nih.gov/health/cardiogenic-shock/diagnosis
- Taghavi S, Askari R, Nassar A. Hypovolemic Shock. National Library of Medicine. Published October 4, 2022. https://www.ncbi.nlm.nih.gov/books/NBK513297/
- Shagana JA, Dharnaj M, Jain AshishR, Nirosa T. Hypovolemic shock – A review. Drug Invention Today. 2018;10(7).
- Zotzmann V, Rottmann FA, Bode C, Wengenmayer T, Staudacher DL, Müller-Pelzer K. Obstructive Shock, from Diagnosis to Treatment. IMR Press. 2022;23(7):248.
- Kim, K. S. Obstructive Shock. Essentials of Shock Management. 2018; 45–54. doi:10.1007/978-981-10-5406-8_4
- Marik PE, Byrne L, van Haren F. Fluid resuscitation in sepsis: the great 30 mL per kg hoax. Journal of Thoracic Disease. 2020;12(Suppl 1):S37-S47. doi:https://doi.org/10.21037/jtd.2019.12.84
- Gupta S, Sankar J. Advances in Shock Management and Fluid Resuscitation in Children. Indian Journal of Pediatrics. 2023;90(3):280-288. doi:https://doi.org/10.1007/s12098-022-04434-3
- Intravenous Fluid Resuscitation – Critical Care Medicine. MSD Manual Professional Edition. Accessed March 26, 2023. https://www.msdmanuals.com/professional/critical-care-medicine/shock-and-fluid-resuscitation/intravenous-fluid-resuscitation#:~:text=Both%200.9%25%20saline%20and%20Ringer
- Marjanović V, Budić I. Fluid Resuscitation and Massive Transfusion Protocol in Pediatric Trauma. Acta Facultatis Medicae Naissensis. 2016;33(2):91-99. doi:https://doi.org/10.1515/afmnai-2016-0010
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