You have a new patient!
A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.
What do you need to know?
Importance
Shock is a true emergency. Shock has a wide array of clinical causes (e.g., sepsis, hemorrhage, pulmonary embolism), categories, and different hemodynamic physiologies. The mortality rate of untreated shock is high, but it varies depending on the specific cause and type of shock. For example, the mortality rate of septic shock is 26% and is almost 50% for cardiogenic shock [1]. This means that rapid identification and treatment of shock matters in order to improve outcomes.
Epidemiology
Because shock has many different causes and no single accepted test for diagnosis, it is difficult to measure its prevalence accurately. The different causes of shock may also vary across different country contexts. A systematic review defining shock as a systolic blood pressure under 90 mmHg estimated 0.4-1.3% of patients arrive at the Emergency Department in shock [2]. Other studies have shown variable rates among the different shock categories, but the obstructive shock is typically the least common type of shock [3,4].
Pathophysiology
Shock is a state of circulatory collapse where the body is unable to adequately perfuse tissues to meet the body’s metabolic demands. Shock is characterized by global hypoperfusion and hypoxia. The four major categories of shock are hypovolemic, distributive, cardiogenic, and obstructive shock. Each category of shock has differences in hemodynamics, causes, and treatments. If left untreated, shock will lead to multiorgan system dysfunction and failure. Shock is often associated with hypotension (systolic blood pressure under 90 mmHg), but shock can occur with a “normal blood pressure”. For example, a systolic blood pressure of 100-120 mmHg in conjunction with other signs and symptoms could be considered a relative hypotensive state and indicate shock in a chronically hypertensive patient. The chart below summarizes the different types of shock.
Type of shock | Hemodynamics | Potential causes | Potential treatments |
Hypovolemic | ↓preload ↑SVR ↓CO | Dehydration, vomiting/diarrhea, burns, hemorrhage (GI bleed, traumatic wound, etc.) | IV fluids Blood products (if due to hemorrhage) |
Distributive | ↓preload ↓SVR ↓/↑CO | Sepsis, anaphylaxis, adrenal insufficiency, neurogenic shock | IV fluids +/- antibiotics and vasopressors. Treat underlying cause. Epinephrine (anaphylaxis) Norepinephrine (sepsis or neurogenic) Phenylephrine (neurogenic) |
Cardiogenic | ↑preload ↑SVR ↓CO | Heart failure, tachy/bradyarrythmias, myocardial infarction, valve failure, myocarditis, cardiomyopathy, beta-blocker overdose | Dobutamine or Epinephrine Treat underlying cause |
Obstructive | ↓preload ↑SVR ↓CO | Tension pneumothorax, cardiac tamponade, pulmonary embolism | IV fluids Treat underlying cause. Tension Pneumothorax– Needle decompression then tube thoracostomy Cardiac tamponade-Pericardiocentesis then pericardial window Pulmonary embolism-Anticoagulation, consider thrombolytics or surgical embolectomy |
(CO= Cardiac Output; SVR= Systemic Vascular Resistance)
Medical History
Key questions to ask on history-taking
Since shock has a multitude of causes, the patient’s history helps us identify shock and guides us in determining the underlying cause. Certain nonspecific presenting symptoms, such as generalized weakness, syncope, or altered mental status, can be seen in all types of shock as these symptoms indicate hypoperfusion. History-taking should be symptom based and also include review of the past medical history, past surgical history, medications, allergies, and drug or alcohol use. The mnemonic “OPQRST” (Onset of symptoms, Provoking/Palliating factors, Quality, Radiation, Severity, Timing) can be used to assist in gathering symptom-based information from the patient.
Being able to narrow down the potential causes will help decide which laboratory and imaging investigations to order and what initial treatments are indicated. Suggestions for key questions to ask are illustrated in the table below.
Type of shock | Presenting symptoms that may indicate shock | Key questions to ask based on cause of shock |
Hypovolemic | Weakness Syncope Altered mental status Vomiting/diarrhea Hematemesis Hematochezia/Melena Burn injury Trauma/fall | Dehydration
Vomiting/diarrhea
Hemorrhage (GI bleed, traumatic wound, etc.)
|
Distributive | Weakness Syncope Altered mental status Fever, chills Cough Difficulty breathing Dysuria Lip/tongue swelling Rash | Sepsis
Anaphylaxis
Adrenal insufficiency
Neurogenic shock
|
Cardiogenic | Weakness Syncope Altered mental status Chest pain Back or shoulder pain Palpitations Difficulty breathing Orthopnea Peripheral edema | Heart failure, Cardiomyopathy, Valve failure
Tachy/bradyarrythmias
Myocardial infarction
|
Obstructive | Weakness Syncope Altered mental status Difficulty breathing Chest pain Penetrating chest trauma Unilateral leg pain/edema | Tension pneumothorax
Cardiac tamponade
Pulmonary embolism
|
Identifying “red flags”
Shock can sometimes be subtle without marked hypotension or tachycardia, so it is important to be vigilant for red flags detected on history-taking to aid in early identification. Some red flags include altered mental status or confusion, syncope, or chest pain. These symptoms may indicate hypoperfusion of the brain or heart and can point towards shock. Belonging to a special patient group, such as an elderly or neonatal patient, an immunosuppressed patient, or a pregnant patient, may be associated with a more atypical presentation of shock or less favorable patient outcomes.
Physical Examination
Key physical exam features
Shock is a state of global hypoperfusion, so many physical exam features will reflect this (e.g., delirium, comatose state, tachypnea, etc.). However, shock exists along a continuum of severity and is impacted by patient age, medications, comorbidities, the cause of shock, and other factors. Hypotension and tachycardia are often regarded as key findings of shock, but these vital sign changes may not be present on initial examination depending on where the patient is in the timeline of their shock, as well as other factors described above. For this reason, it is important to look at the combination of the patient’s physical exam findings, rather than a single finding to assist in the diagnosis of shock [1]. Refer to the chart below for physical exam findings seen in shock.
Identifying “red flags”
Similar to patient history-taking, it is important to identify “red flags” during physical examination to aid in the early identification and treatment of shock. Some red flags on physical examination include hypotension with a MAP below 65mmHg, severe bradycardia, low urine output, delirium or altered mental status, and angioedema of lips or tongue [5]. A MAP below 65mmHg indicates severe hypoperfusion that requires prompt aggressive intravenous fluid or vasopressor administration. Bradycardia below 45bpm in shock may indicate poor cardiac output and a lack of physiologic ability to increase cardiac output properly in a shock state. Low urine output and altered mental status are signs of renal and cerebral hypoperfusion, respectively. Angioedema can occur in anaphylactic shock and can pose an acute airway emergency.
Alternative Diagnoses
Shock can have a variety of causes and clinical presentations that can range from the subtle to the severe. Determining the patient’s type of shock and specific diagnosis responsible for the shock state is dependent on details from the patient history, physical exam, and diagnostic testing (discussed more in next section). See the chart below for a list of differential diagnoses for the different categories of shock. Use this table in conjunction with the tables provided in the previous sections to assist in differentiating shock types and causes.
Shock Type | Differential diagnosis 5,6 |
Hypovolemic |
|
Distributive |
|
Cardiogenic |
|
Obstructive |
|
Acing Diagnostic Testing
There is no single diagnostic test to rule in or rule out shock. The diagnosis of shock is based on a constellation of diagnostic test results in combination with the history and physical exam of the patient. Whenever possible, diagnostic testing should be based on the presumed cause of shock (e.g., CT pulmonary angiogram for pulmonary embolism, EKG for myocardial infarction, etc.). The table below summarizes different bedside tests, laboratory tests, and imaging tests to consider ordering in patients with shock. Rational and use behind these tests is discussed in more detail in sections that follow the table.
Bedside tests | Laboratory tests | Imaging tests |
|
|
|
Bedside Tests
The EKG is a basic screening test helpful in all shock patients to assess for cardiac dysrhythmias, myocardial infarction, or EKG interval disturbances from medication overdoses. The EKG is clearly valuable in potential cardiogenic shock patients, but it is also helpful in obstructive shock (e.g., low voltage QRS in cardiac tamponade, EKG changes in pulmonary embolism).
Point of care pregnancy testing can help rule out a ruptured ectopic pregnancy. Glucose testing screens for hypoglycemia which can be seen in septic shock, GI losses with decreased oral intake, and adrenal insufficiency. Point of care blood gas testing can aid in the assessment of the patient’s acid-base and blood gas status which can assist in immediate therapeutic decisions at the bedside.
Laboratory Tests
Lactate is a common test ordered and trended in shock. Lactate is a nonspecific marker for poor perfusion and anaerobic metabolism. An elevated lactate >2mmol/L can occur in all types of shock as it indicates poor perfusion, but it does not necessarily mean the patient has a diagnosis of shock. Increasing lactate levels have been associated with increased mortality in many shock types [1].
CBC and type and screen testing are helpful in hemorrhagic shock to measure hemoglobin and prepare for the need for blood product transfusion. The CBC can assess the white blood count which can be helpful in septic shock, especially when trended overtime. Serum chemistry, a hepatic function panel, and coagulation studies screen for signs of end-organ damage (e.g., acute kidney injury, transaminitis (“shock liver”), coagulopathy, etc.).
Blood gas testing is valuable as a screening test in any type of shock to evaluate acid-base and blood gas balance. Urinalysis testing and cultures, blood cultures, and wound cultures do not change management in the emergency department, but they are helpful in identifying sources of infection in septic shock which can be utilized to make antibiotic therapy more targeted as part of the patient’s larger plan of care. Cortisol testing can be beneficial in making the diagnosis of adrenal insufficiency.
Imaging Tests
The chest X-ray is another basic screening test that can be performed as a portable test in the unstable shock patient. The chest X-ray screens for pneumonia (septic shock), cardiomegaly (cardiogenic and obstructive shock), tension pneumothorax (diagnosis should be made clinically prior to X-ray), pulmonary edema (cardiogenic shock), hemothorax (hemorrhagic shock), amongst other relevant findings.
CT imaging can be used to identify the source of infection or bleeding in septic and hemorrhagic shock, respectively. However, it should be used after reviewing the risks and benefits in an unstable shock patient. For example, CT imaging may involve the patient travelling to a less monitored setting outside of the emergency department with less resources and tools for resuscitation. Contrast-induced nephropathy is another risk to consider when ordering CT imaging with IV contrast in shock patients who likely have hypo-perfused kidneys. Conversely, CT imaging can lead to a definitive diagnosis (e.g., acute appendicitis, retroperitoneal bleed, ruptured spleen, etc.) that can direct management [1].
Ultrasound is an incredibly valuable bedside diagnostic modality in shock. Ultrasound can be used to determine the patient’s type of shock through a physiologic assessment of the heart, lungs, and abdomen. Specific diagnostic information that can be gathered by ultrasound includes the cardiac ejection fraction, presence of a large pericardial effusion with right ventricular compression (cardiac tamponade), right ventricular dilation (may indicate pulmonary embolism), Inferior vena cava (IVC) dilation or collapse, presence of abdominal free fluid in trauma (hemoperitoneum), abdominal aortic aneurysm presence, absence of bilateral lung sliding (pneumothorax), pulmonary edema (cardiogenic shock if diffuse, infectious if localized), and pleural effusions (infectious or hemothorax depending on the historical context). Organized ultrasound protocols exist that aim to assess these body systems in an algorithmic manner. One example is the RUSH protocol (Rapid Ultrasound for Shock and Hypotension) [1,5]. This protocol can be executed using the curvilinear (abdominal) or phase-array (cardiac) probe. Operator competency is needed to obtain meaningful diagnostic data from bedside ultrasound, but with practice and education, proficiency can be achieved. See the images below for a visual representation of the RUSH protocol and a summary of ultrasound findings in the different types of shock [5,7].
Ultrasound findings in shock
Risk Stratification
Since shock has many potential causes and clinical presentations, there is no single risk stratification tool that is broadly applicable to all types of shock. There are some tools available to assist in early diagnosis of sepsis by identifying risk factors, like the SIRS criteria (Systemic inflammatory response syndrome criteria) and qSOFA score (Quick sequential organ failure assessment score) [8]. These scores are not specific and can be “positive” in conditions other than sepsis, like diabetic ketoacidosis or severe anxiety. The shock index measurement is another tool that takes into account heart rate and systolic blood pressure to identify occult shock, especially in trauma or acute hemorrhage. A shock index above 0.5-0.7 may point towards occult shock in the presence of normal vital signs [9].
Shock is ultimately a clinical diagnosis, so clinical assessment of the patient with the history, physical exam, and diagnostic test results are often used in combination with the clinical picture to predict risk. Clinical factors that may be associated with poorer outcomes are high serum lactate levels not responsive to fluid resuscitation, severe acidosis, low MAP, elderly and neonatal patient populations, and immunosuppressed patients [1,5,8].
Management
Initial management in unstable patients
Management of the shock patient starts with the primary survey, or the “ABCs” (Airway, Breathing, Circulation). The primary survey is an algorithmic approach used for ill patients to help organize patient assessment, identify life-threatening conditions quickly, and treat time sensitive conditions.
Airway (“A”)
Establishing a definitive airway may be needed to prevent aspiration or as the precursor to mechanical ventilation for respiratory failure. Listen for any gurgling sounds or poor effort in phonation that may indicate a risk for aspiration. Since shock is a state of hypoperfusion, many patients may have poor cerebral perfusion, somnolence, and require an invasive airway. Positive pressure ventilation and many pre-intubation sedation medications can cause hypotension, so strongly consider initiating volume resuscitation or vasopressors to improve hemodynamics prior to performing intubation [1].
Assess for any obvious external swelling of the face, lips, or tongue, which may occur in anaphylaxic shock. Although this angioedema should improve with prompt epinephrine administration, airway management is sometimes needed. Look for tracheal deviation which can occur in tension pneumothorax. Be sure to consider cervical spinal fracture and provide a rigid cervical collar for spinal immobilization in the presence of trauma.
Breathing (“B”)
Assistance in respiration is sometimes needed in the shock patient due a primary pulmonary cause of shock (e.g., septic shock due to pneumonia), respiratory compensation for lactic acidosis, or respiratory changes due to toxic overdoses causing shock (e.g., distributive shock from salicylate overdose). Noninvasive positive pressure ventilation, such as BIPAP or CPAP, or invasive mechanical ventilation with intubation may be required to manage work of breathing and respiratory failure.
Circulation (“C”)
Shock is a state of systemic hypoperfusion, so a key part of treatment often involves some type of volume resuscitation. Most commonly this involves administration of crystalloid fluids (e.g., normal saline, lactated ringers solution) or blood products. If the specific type or cause of shock is unclear after assessment of the patient, start with administration of small volume boluses of fluids with frequent reassessments. A 250-500mL crystalloid fluid bolus is a reasonable initial intervention in the undifferentiated shock patient. Fluid should be administered rapidly over 5-20minutes to a total of 20-30mL/kg, depending on the cause of shock [1]. Balanced isotonic crystalloid fluids, like lactated ringers solution, may provide a small mortality benefit over normal saline, especially if large volumes of fluid administration are expected [1]. Large volume administration of normal saline can also cause hyperchloremic metabolic acidosis. For this reason, if lactated ringers solution is readily available and a cost-effective alternative to normal saline, it may be a worthwhile alternative. Blood products, rather than crystalloid fluids, should be prioritized if hemorrhagic shock is the assumed cause of shock.
Although volume resuscitation is a crucial component of treatment, caution should be taken in aggressive fluid administration in the presence of cardiogenic shock as this may lead to pulmonary edema. If the patient remains hypotensive after fluid administration with a MAP below 65mmHg, vasopressors should be initiated [1,5].
Medications
Intravenous crystalloid fluids and blood products are common treatments in shock, but depending on the cause of shock, additional medications may be needed. Some examples are broad spectrum antibiotics in septic shock, steroids in adrenal insufficiency, or thrombolytics in massive pulmonary embolism with obstructive shock. See the charts below for a list of adjunctive medications along with their doses and uses.
Common antibiotics used in shock
Drug name (Generic) | Potential use | Dose | Frequency | Maximum Dose | Cautions / Comments |
Piperacillin-Tazobactam | Intra-abdominal, genitourinary, skin/soft tissue, pneumonia infections, febrile neutropenia | 3.375-4.5g (IV) | Q6 hours | 4.5gm IV | Common first line broad spectrum antibiotic in septic shock |
Cefepime | Intra-abdominal, genitourinary, skin/soft tissue, meningitis, pneumonia infections, febrile neutropenia | 1-2g (IV) | Q8-12 hours | 2gm IV | Common first line broad spectrum antibiotic in septic shock.
Similar uses as piperacillin-tazobactam |
Vancomycin | Severe bacterial infections, especially MRSA, pneumonia, endocarditis, systemic anthrax, meningitis | 15-20 mg/kg/ dose (IV) | Q8-12 hours | 3gm IV | Common first line broad spectrum antibiotic in septic shock used in combination with cefepime or piperacillin-tazobactam |
Ceftriaxone | Meningitis, pneumonia, UTI, endocarditis, typhoid fever, gonococcal infections, pelvic inflammatory disease | 1-2g (IV) | Q24 hours | 2gm IV | First line medication for bacterial meningitis in adults, also commonly used for UTIs and community-acquired pneumonia |
Ciprofloxacin | UTI, intra-abdominal infections, prostatitis, pneumonia, bone/joint infections, typhoid fever, salmonella/shigella infections | 200-400mg (IV) | Q8-12 hours | 400mg IV (1000mg PO) | Can prolong QT interval and increase risk for tendon rupture |
Metronidazole | Anaerobic coverage for intra-abdominal infections, Pelvic inflammatory disease, C. difficile | 500mg (IV) | Q8-12 hours | 500mg IV (500mg PO) | Causes disulfiram-like reaction with alcohol (avoid alcohol with this medication) |
Azithromycin | Community-acquired pneumonia, chlamydial infections, COPD exacerbation, MAC treatment, pertussis | 500mg then 250mg (IV) | Q24 hours | 500mg IV (1000mg PO) | Can prolong QT interval Often given IV with ceftriaxone for community acquired pneumonia patients |
Common vasopressors used in shock
Drug name (Generic) | Potential use | Dose | Frequency | Maximum Dose | Cautions / Comments |
Norepinephrine (Noradrenaline) | First line vasopressor for most types of shock, especially if loss of vascular tone is primary problem | 0.02-1 mcg/kg/min (IV) | Titrate as needed to maintain MAP >65 | See dose | May cause tachyarrhythmia |
Epinephrine (Adrenaline) | First line for anaphylactic shock | 0.05-2 mcg/kg/min (IV) 0.3-0.5mg (SubQ or IM) | Titrate as needed to maintain MAP >65 | See dose | In anaphylaxis, start with 0.3mg subQ/IM dose. This can be repeated every 10min as needed versus starting a continuous infusion. May cause tachyarrhythmia |
Dobutamine | Frequently used in cardiogenic shock due to heavy beta-adrenergic receptor preference | 2-20 mcg/kg/min (IV) | Titrate as needed to maintain MAP >65 | See dose | May cause tachyarrhythmia |
Phenylephrine | Pure alpha-adrenergic receptor agonist used as a 2nd or 3rd line vasopressor in shock | 10-200 mcg/min (IV) | Titrate as needed to maintain MAP >65 | See dose | May cause reflex bradycardia and headache Consider use when tachydysrhythmias are present |
Vasopressin | Often used as a 2nd or 3rd line vasopressor after norepinephrine or epinephrine | 0.01-0.04 units/min (IV) | Titrate as needed to maintain MAP >65 | See dose | Primarily causes vasoconstriction, similar to phenylephrine |
Common additional adjunctive medications used in shock
Drug name (Generic) | Potential use | Dose | Frequency | Maximum Dose | Cautions / Comments |
Acetaminophen | Fever or pain | 325-1000mg PO or IV | Q4-6 hours | 4gm daily | Be careful with dosing this common medication to avoid overdose |
Ibuprofen | Fever or pain | 200-800mg PO | Q4-6 hours | 3200mg daily | Can cause GI upset and increase risk for peptic ulcer disease |
Morphine | Moderate-severe Pain | 2.5-10mg (IV) | Q2-6 hours | n/a | Risk of respiratory depression, addiction and abuse, hypotension
Use naloxone for reversal |
Hydrocortisone | Adrenal crisis, vasopressor-refractory hypotension in shock | 100-300mg (IV) | Q6-8 hours | 1200mg daily for septic shock adjunct | Start at 100mg IV for adrenal insufficiency
Taper dose over 5-7 days for septic shock adjunctive treatment |
Dexamethasone | Adrenal crisis, vasopressor-refractory hypotension in shock | 0.03- 0.15 mg/kg/ day | Q6-12 hours | 0.15mg/kg daily for adrenal insufficiency | Alternative to hydrocortisone |
Alteplase | Massive PE with obstructive shock | 100mg (IV) | Single dose over 2 hours | 100mg | Bleeding is main side effect |
Procedures
Some patients in shock may need emergent procedures as part of their treatment plan. The chart below summarizes relevant procedures that may be encountered in the care of the shock patient.
Indication or Problem | Procedure |
Tension pneumothorax | Needle thoracostomy (Followed by tube thoracostomy) |
Cardiac tamponade | Pericardiocentesis (Followed by pericardiotomy) |
Persistent hypotension despite intravenous fluids with need for prolonged vasopressor administration Inability to establish IV access in hemodynamically unstable patient
| Central venous line placement (Triple lumen catheter)
|
Inability to establish IV access in hemodynamically unstable patient
| Intraosseous line placement (or central venous line) |
Respiratory failure or inability to protect airway | Endotracheal tube placement (Intubation) |
Empyema, hemothorax, or after needle decompression of tension pneumothorax | Tube thoracostomy (Chest tube placement) |
Patient reassessment
Reassessment is an important part of management. The primary survey (“ABCs”) is conducted on initial evaluation of the patient to guide management, but it can be repeated after therapies have started as clinical changes can occur. Fluid administration too rapidly in a patient with cardiac or renal comorbidities may result in pulmonary edema, requiring fluid administration to be halted. Patients may develop worsening mental status or hypoxemia overtime due to respiratory muscle fatigue, requiring supplemental oxygen or more aggressive airway management. Complications can develop after procedures, such pneumothorax after internal jugular central venous line placement or re-expansion pulmonary edema after chest tube placement. These changes in clinical course are only identified if the patient is reassessed after treatment is initiated.
Bedside ultrasound can also assist in patient reassessment. A RUSH exam can be repeated or used as a framework to guide sonographic reassessments. Some examples of pertinent findings on reassessment include pulmonary B-lines after IV fluid administration (alveolar fluid present), the absence of lung sliding (may indicate pneumothorax), or changes in the IVC size after IV fluid administration (a flat IVC may indicate fluid responsiveness) [5,7].
Special Patient Groups
Pediatrics
Pediatric patients in shock are often well compensated physiologically and may not have hypotension on initial presentation. For this reason, unexplained tachycardia in the pediatric patient should always raise concern for possible occult or early shock [10]. Hypovolemic shock is the most common type of shock in the pediatric patient population, while obstructive shock is the least common type of shock. Volume status in infants can be assessed through evaluation of the fontanelles (flat or sunken), the presence or absence of tears, and changes in urine output estimated by the number of wet diapers per day (e.g., less than baseline or baseline) [10]. Similar to adults, shock should be managed aggressively with volume resuscitation with the exception of cardiogenic shock where fluids should be used judiciously and vasopressors used early (e.g., epinephrine). Septic shock is the most common type of distributive shock in pediatric patients, and volume resuscitation should be aggressive with up to three 20mL/kg fluid boluses given (60mL/kg total) [10]. This should be contrasted with the recommendation of a 20-30mL/kg fluid bolus in adults for most types of shock [1].
Geriatrics
The diagnosis and treatment of shock in geriatric patients may be more challenging due to unique factors associated with this population. Unlike pediatric patients, elderly patients often do not have a robust physiologic reserve to compensate in a shock state. Elderly patients often have more comorbidities and take more medications than adults and children which may blunt the tachycardia response or lead to an atypical clinical presentation [11,12]. For example, beta blockers and calcium channel blockers may prevent a tachycardic response in a hypoperfusion state. Blood pressure may also be “normal” in elderly patients in shock who are chronically hypertensive [11]. For example, blunt trauma patients over 65 years-old with systolic blood pressures below 110mmHg and heart rates above 90 beats/min have an association with an increase in mortality [12]. Elderly patients with sepsis are also less likely to have a fever or leukocytosis than younger adult patients [13]. Do not rely only on vital signs or abnormal investigations to diagnose shock in the elderly patient.
Management of shock in the elderly patient should involve more gentle volume resuscitation with small fluid boluses (e.g., 250-500mL) and frequent reassessments for response or a change in clinical status (e.g., pulmonary edema). Have a low threshold to start blood products in elderly hemorrhagic shock patients to avoid excess crystalloid fluid administration and volume overload [12]. Consider drug-drug interactions and the impact of baseline comorbidities (e.g., chronic renal insufficiency) when prescribing antibiotics or other therapies for the elderly patient in shock [13].
Pregnant patients
Pregnant patients have physiologic and hormonal changes that make certain causes of shock more likely than others. Some common causes of shock to consider in the pregnant patient include pulmonary embolism, hyperemesis gravidarum, peripartum or postpartum hemorrhage, pyelonephritis, and peripartum cardiomyopathy amongst other causes.
Other pregnancy-related factors include a higher circulating plasma and blood volume in pregnancy, hypercoagulability due to hormonal changes, and risk of vena caval compression by the growing uterus [14]. Volume resuscitation in pregnancy should accommodate for the pregnant patient’s increase in blood and plasma volume. It is recommended that a 50% additional volume of fluids be given to the pregnant patient in shock to account for this [14]. Standard vasopressors administered in shock, like norepinephrine (noradrenaline), dopamine, and vasopressin, may decrease uterine blood flow from vasoconstriction but have limited data on use in pregnancy. However, these medications are typically given in pregnant shock patients as the benefit of restoring normal maternal perfusion and hemodynamics outweighs any potential risk to the fetus [14]. Treatment of the pregnant shock patient should also incorporate positioning the patient in the left lateral decubitus position. This avoids compression of the inferior vena cava by the gravid uterus which could reduce cardiac preload [14].
Other patient groups
Other patient groups that may have more nonspecific or atypical findings in shock are immunosuppressed patients, such as those on chemotherapy for malignancies, post-splenectomy patients, post-transplant patients on immunomodulators, or patients on chronic steroid therapy [5,8]. Diagnosing shock in these special patient groups starts with identifying risk factors and keeping occult shock on the differential diagnosis list. These patient groups should, similar to typical adult patients, receive aggressive and early volume resuscitation, vasopressors when needed, and adjunctive therapies as appropriate (e.g., broad spectrum antibiotics for septic shock).
When to admit shock patients
All patients with a diagnosis of shock should be admitted due to the high morbidity and mortality associated with shock [1]. Many patients may need to go to a hospital ward with a high level of monitoring, such as an intensive care unit, due to risk of hemodynamic decompensation [1]. Although some causes of shock are “reversible”, such as tube thoracostomy for tension pneumothorax, these patients should be admitted for further monitoring and treatment due to high risk for poor outcomes.
Revisiting your patient
A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.
You identify that your patient is hypotensive, tachycardic, tachypneic, and appears to be in a shock state. You quickly perform a primary survey and note that the airway is patent, lungs are clear bilaterally, and distal extremities are cool with bounding pulses. Two large bore peripheral IV lines are placed, comprehensive laboratory investigations are drawn and sent, supplemental oxygen is applied, and 2 liters of normal saline are administered rapidly.
A 12-lead EKG demonstrates sinus tachycardia without acute ischemic abnormalities. A bedside ultrasound exam shows diffuse pulmonary A lines (no alveolar fluid) with good lung sliding bilaterally, no pericardial effusion, and a dilated inferior vena cava. The right ventricle appears dilated and hypokinetic. You diagnose the patient with obstructive shock, likely due to massive pulmonary embolism. You rule out tension pneumothorax and cardiac tamponade as alternative diagnoses with your physical exam and bedside ultrasound findings. Thrombolytics are promptly administered. The patient’s vital signs slowly stabilize, and he is admitted to the medical intensive care unit for continued monitoring and care.
Author
Joseph CIANO
Dr Ciano is an Emergency Medicine Physician from New York, USA. He completed his Emergency Medicine Residency in Brooklyn, NY and a Fellowship in Global Emergency Medicine in the Northwell-LIJ Health System. He is interested in building the educational infrastructure of EM in countries where Emergency Medicine is not yet recognized as a field and in countries that are in the early stages of this process. He has partnered with international NGOs in Emergency Medicine educational projects and works as a visiting Emergency Medicine faculty member in West Bengal, India. He is excited to collaborate with the other authors of the iEM Education Project to contribute to the world of FOAM-ed.
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2018 version of this topic – https://iem-student.org/shock/
References
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Acknowledgement
The patient image was created with the assistance of DALL·E 2 by iEM editorial team.
Reviewed By
Arif Alper Cevik, MD, FEMAT, FIFEM
Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.
