Trusted medical expertise in seconds.

Access 1,000+ clinical and preclinical articles. Find answers fast with the high-powered search feature and clinical tools.

Try free for 5 days
Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer.

Shock

Last updated: June 1, 2021

Summarytoggle arrow icon

Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation. The numerous causes of shock are classified into hypovolemic shock (e.g., following massive blood/fluid loss), cardiogenic shock (e.g., as a result of acute heart failure), obstructive shock (e.g., due to cardiac tamponade), and distributive shock (due to redistribution of body fluids), which is further classified into septic, anaphylactic, and neurogenic shock. Common clinical findings are hypotension and abnormal heart frequency (most commonly tachycardia; bradycardia in neurogenic shock) accompanied by specific symptoms related to the cause of shock. Diagnosis is mostly clinical but measurement of functional parameters (e.g., PCWP, cardiac output, SVR) can help distinguish between the different types of shock. Management of shock involves circulatory support and treatment of the underlying cause. Shock is associated with a very high mortality rate.

Definitions

  • Shock (circulatory shock): a life-threatening disorder of the circulatory system that results in inadequate organ perfusion and tissue hypoxia, leading to metabolic disturbances and, ultimately, irreversible organ damage [1][2]
  • Shock index = pulse rate/systolic blood pressure
    • Normal range: 0.4–0.7
    • > 1 (positive shock index): consistent with circulatory shock

Types of shock

Overview of the types of shock [3][4][5]
Type Etiology of shock Typical hemodynamic parameters [6] Distinguishing clinical features Treatment options

Hypovolemic shock

(includes hemorrhagic shock)

  • ↓↓ PCWP
  • ↓ CO
  • SVR
  • ↑ HR
Cardiogenic shock
  • PCWP
  • ↓↓ CO
  • SVR
  • Variable HR
Obstructive shock
  • ↑ Or ↓ PCWP
  • ↓↓ CO
  • SVR
  • ↑ HR
Distributive shock

Septic shock

(most common)

  • Normal or PCWP
  • ↑ Or ↓ CO
  • ↓↓ SVR
  • ↑ HR

Anaphylactic shock

  • ↓↓ PCWP
  • ↑ Or ↓ CO
  • ↓↓ SVR
  • ↑ HR
Neurogenic shock
  • ↓↓ PCWP
  • ↓ CO
  • ↓↓ SVR
  • ↓ HR

Key

PCWP: pulmonary capillary wedge pressure (a surrogate marker for preload)

CO: cardiac output (CO = HR × stroke volume)

SVR: systemic vascular resistance (a surrogate marker for afterload)

HR: heart rate

Hemodynamic parameters in shock

Typical hemodynamic parameters of types of shock [3][4][5][6]
Type Estimated cardiac output (CO) Estimated preload (e.g., PCWP) Estimated afterload (e.g., SVR) Likelihood of fluid responsiveness
_Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">Hypovolemic

Cardiogenic

  • ↓↓

Obstructive

  • ↓↓
  • ↓ Or ↑

Distributive

  • Usually ↓
  • ↓↓

Stages of shock

The following stages may not occur in cases of sudden severe cardiovascular collapse , and the progression between stages in septic shock can be indistinct.

Stages of shock
Stage Characteristics
1. Preshock

2. Shock

(progressive phase)

3. End-organ dysfunction

(stage of decompensation)

  • Patients may present at the emergency department with shock or develop shock at any time during hospitalization.
  • Screening for clinical features of shock in patients at risk can allow for early identification and treatment.
  • The clinical picture may vary depending on the stage of shock.
Clinical features of shock [7][8][9]
Feature Classic findings Atypical findings
Vital signs Heart rate
  • Normal or ↓
Blood pressure
  • Normal [7]
Respiratory rate
SpO2
  • Normal
Pulse pressure
Clinical signs of end-organ hypoperfusion [8] Brain
Kidney
Skin

Hypotension may be absent in some patients with shock. [7]

Signs of congestive heart failure alongside shock (e.g., JVP, crackles on lung auscultation) are suggestive of cardiogenic shock.

Approach [4][7][8]

The following should be performed simultaneously:

Act quickly: Provide immediate hemodynamic support and simultaneously try to identify the type of shock and the underlying cause in order to provide appropriate treatment.

Patients in shock are at risk of cardiopulmonary arrest; if the pulse is lost, start CPR!

Management of patients with severe shock can be recalled with the VIP rule: Ventilation as needed, Infuse IV fluids, and Pump vasopressors as needed. [4]

Respiratory support for patients with severe shock [4]

Pulse oximetry measurements are unreliable in patients with shock due to peripheral hypoperfusion and/or vasoconstriction. Consider initial supplementary O2 for potential hypoxemia in all patients, regardless of pulse oximetry results. [4]

Routine investigations can help identify the shock subtype but are not required for diagnosis. Consider further investigations if the subtype remains uncertain.

Shock is a clinical diagnosis.

Routine investigations

Findings allow for evaluation of the following:

In all patients with shock, immediately measure ABGs, lactate levels, capillary glucose, perform an ECG, and order a chest x-ray and general laboratory studies.

Compare any available previous studies to the patient's current test results. Previous studies can help determine if alterations to any laboratory or imaging studies are new and likely the cause of shock, or if they are caused by chronic conditions (e.g., CKD, chronic heart failure).

Further investigations

Further studies should be guided by clinical suspicion of the underlying cause.

Further diagnostic studies for patients in shock
Type of shock Studies to consider
Unclear after initial evaluation
Hypovolemic shock Hemorrhagic shock
Nonhemorrhagic shock
Cardiogenic shock
Obstructive shock
Distributive shock Septic shock
Anaphylactic shock
Neurogenic shock
  • Imaging studies can help identify the underlying injury (e.g., CT or MRI spine, CT or MRI brain).

If hemorrhagic shock is suspected, perform blood type and screen and crossmatch immediately. In emergencies, O-negative blood can be given immediately; however, type-specific and crossmatched blood products are preferred as soon as they are available.

Bedside echocardiography

Simplified cardiac ultrasound can help identify pericardial effusion and indirect signs of right heart failure and cardiomyopathy. [12][13]

Rapid assessment by cardiac echo (RACE) [4][7]
Type of shock Possible findings
Hypovolemic shock
  • Small cardiac chambers
  • Contractility: high or preserved
Cardiogenic shock
  • Large cardiac chambers
  • Poor contractility
Obstructive shock
Distributive shock
  • Normal cardiac chambers
  • Contractility is usually preserved.

IVC ultrasound [14][15][16]

Changes in IVC collapsibility can help predict fluid responsiveness, e.g., after a fluid challenge or passive leg raise test. [17]

Sonographic IVC measurement to estimate volume status and predict fluid responsiveness
IVC diameter measurement [18] IVC collapsibility index [14][19]
Measurement Widest IVC diameter in longitudinal view measured just distal to the IVC-RA junction or 2 cm caudal to the IVC-hepatic vein junction Percentage of change in the IVC diameter over the respiratory cycle in spontaneously breathing patients [20]
Findings suggestive of: [16][21] Volume overload ≥ 2 cm < 50% with inspiration
Volume depletion < 2 cm ≥ 50% with inspiration

Additional point-of-care ultrasound [16][21][22][23]

Monitoring parameters can be used as treatment targets and should be tailored to the patient.

Monitoring parameters for patients with shock [7][24]
Variable Parameters
Clinical features in shock Vital signs
Others
Laboratory Lactate
  • Aim for a lactate level ≤ 2 mEq/L.
  • Monitor for changes over time (i.e., lactate clearance).
Base deficit (BD)
SvO2 and ScvO2 [6][27][28]
Device-based
Central venous pressure (CVP) [6][30]
Cardiac function [6]
Bedside echocardiography/POCUS

Signs of an inadequate response to fluid resuscitation include persistently heart rate, ↓ blood pressure, CVP, and urine output (< 0.5 mL/kg/hour).

Oxygen saturation from peripheral venous blood gases should not be misinterpreted as SvO2 or ScvO2.

IV fluid resuscitation

Start with glucose-free isotonic crystalloids. [32]

Patients with peripheral edema can still be fluid responsive if they have reduced effective arterial blood volume. [4]

Vasopressors [4]

  • Indications: treatment of various shock states in an effort to restore adequate arterial pressure and organ perfusion
  • Available agents
    • Choice is determined based on the underlying shock physiology, the desired pharmacological effects, and potential adverse effects.
    • First-line in undifferentiated shock: norepinephrine
  • Next steps

Additional interventions

Patients with chronic corticosteroid use need steroid stress dosing to prevent adrenal crisis!

General principles [3][35]

Blood pressure does not always correlate with blood flow. Agents that increase blood pressure through vasoconstriction can impair tissue perfusion at high doses.

Although certain vasopressors, inotropes, and inodilators can be combined (e.g., to allow for individual agents to be used in moderate doses), this requires careful titration and specialist consultation.

Inoconstrictor drugs [35][36][37][38]

Agent

Continuous IV infusion dosages

Pharmacology

Clinical applications

Adverse effects

Norepinephrine

(noradrenaline)

  • Initial dosage: 0.01–0.04 mcg/kg/minute
  • Titration increments: 0.02–0.04 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.4 mcg/kg/minute
  • Maximal dosage: 0.5–3.3 mcg/kg/minute [35]
  • α1 > β1
  • ↑↑ SVR , ↑↑ MAP
  • Unchanged/↑ CO, ↑ HR
  • Half-life: ∼ 2 minutes

Epinephrine

(adrenaline)

  • Initial dosage: 0.01–0.05 mcg/kg/minute
  • Titration increments: 0.02–0.05 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.3 mcg/kg/minute
  • Maximal dosage: 2 mcg/kg/minute
  • β12 > α1
  • ↑↑ CO, ↑↑ HR
  • SVR, ↑↑ MAP
  • Half-life: < 5 minutes
Dopamine [37][38][40][41]
  • Initial dosage: 2–10 mcg/kg/minute
  • Titration increments: 2–5 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 2–20 mcg/kg/minute
  • Maximal dosage: 50 mcg/kg/minute [36][42]
Key: α1 = α1-adrenergic receptor; β1 = β1-adrenergic receptor; β2 = β2-adrenergic receptor; AT1 = angiotensin II receptor type 1; SVR = systemic vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure
Pure vasoconstrictor drugs
Agent

Continuous IV infusion dosages

[36][37][38]

Pharmacology

[35][36][37][38]

Clinical applications

[36][37]

Adverse effects

[36]

Phenylephrine
  • Initial dosage: 0.1–0.3 mcg/kg/minute
  • Titration increments: 0.2–0.4 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.1–1.5 mcg/kg/minute
  • Maximal dosage: 6 mcg/kg/minute [43]
Vasopressin
  • Initial dosage: 0.01–0.03 units/minute
  • Titration increments: 0.005 units/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.04 units/minute
  • Maximal dosage: 0.07 units/minute [37]
  • Fixed-dose infusion: 0.03–0.04 units/minute without titration (used as second-line in combination with another vasopressor, e.g., norepinephrine)
  • Refractory shock
Key: α1 = α1-adrenergic receptor; V1 = vasopressin 1a receptor; SVR = systemic vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure

Inodilator drugs

Agent

Continuous IV infusion dosages

[36][37][38]

Pharmacology

[35][36][37][38]

Clinical applications

[36][37]

Adverse effects

[36][46]

Dobutamine
  • Initial dosage: 2.5–5 mcg/kg/minute
  • Titration increments: 2.5–5 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 2.5–20 mcg/kg/minute
  • Maximal dosage: 40 mcg/kg/minute [36][37][42]
  • β1 > β2 >> α1
  • ↑↑ CO, ↑ HR
  • Unchanged/↓ SVR, ↑/↓/unchanged MAP, ↓/unchanged PVR
  • Half-life: 2 minutes
Milrinone
  • Initial dosage: 0.1–0.25 mcg/kg/minute
  • Usual dosage range: 0.25–0.75 mcg/kg/minute
  • Maximal dosage: 0.75 mcg/kg/minute
  • PDE-3 inhibitor (β12-like effect)
  • ↑↑ CO, ↑ HR
  • ↓↓ SVR, ↓/unchanged MAP, PVR
  • Half-life: 2–3 hours
Key: α1 = α1-adrenergic receptor; β1 = β1-adrenergic receptor; β2 = β2-adrenergic receptor; PDE-3 = phosphodiesterase 3; SVR = systemic vascular resistance; PVR = pulmonary vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure

Etiology

Pathophysiology

Loss of intravascular fluid volume → preload and SV ↓ CO → compensatory SVR and HR

Management [4][7][8]

The priority of immediate hemodynamic support is aggressive fluid resuscitation to achieve euvolemia. Further treatment depends on the etiologic category of _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemia (hemorrhagic vs. nonhemorrhagic).

Hemorrhagic shock

Classification of hemorrhagic shock
Class I II III IV
Blood loss (% of total blood volume) < 15% 15–30% 30–40% > 40%
Volume loss (in an average adult) ∼ 750 mL ∼ 750–1500 mL ∼ 1500–2000 mL > 2000 mL
Heart rate (bpm) 70–99 100–120 120–140 > 140
Systolic blood pressure Normal Normal
Pulse pressure Normal or ↑
Respiratory rate (rpm) Normal 20–30 30–40 > 35
Urine output > 30 mL/hour 20–30 mL/hour 5–15 mL/hour Absent
Mental status Normal Mildly anxious Anxious, confused Confused, lethargic

Upon suspecting hemorrhagic shock, perform blood grouping and cross-matching and have packed RBCs at hand for transfusion.

Uncrossmatched RBC type O negative units can be transfused if the hemorrhage is severe.

Nonhemorrhagic hypovolemic shock

Etiology

Pathophysiology

Management approach [50]

Management of cardiogenic shock [43][50][51]
Classification Treatment (see “Vasopressors and inotropes” for dosages)
Dry and cold
Wet and cold

IV fluids can worsen cardiogenic pulmonary edema in most cases of cardiogenic shock. Check fluid responsiveness prior to administration of fluid therapy.

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). [54]

Etiology

Pathophysiology [6]

Despite manifesting with high PCWP, many causes of obstructive shock (e.g., severe pulmonary hypertension, cardiac tamponade) are considered preload-dependent states. [6]

Elevation and equalization of pressures in all the cardiac chambers differentiate cardiac tamponade from other causes of obstructive shock.

Treatment

Etiology

Pathophysiology

Key treatment components

Definition

Management of septic shock

See “Management of sepsis” for details on evaluation and definitive treatment of sepsis. The following recommendations relate to septic shock and are consistent with the 2016 and 2018 Surviving Sepsis Campaign guidelines: [59][60]

6–10 L of IV fluids may be necessary during the first 24 hours. [61]

Protocolized resuscitation target strategies [59][60][62]

There is insufficient evidence to support the use of one target over the others in order to inform decisions about escalating hemodynamic support. [59]

Vasopressors for septic shock [59][60][62][63][64]

Initial management [61][65][66]

Adjunctive treatment (antihistamines and corticosteroids) should only be administered after the initial resuscitation measures (IM epinephrine, fluids and/or vasopressors) have been given.

Refractory anaphylactic shock [61][65][66]

Diagnosis

Neurogenic shock is a clinical diagnosis.

In a patient who develops low blood pressure following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemic and obstructive shock have been ruled out.

Management [67][68][69]

Patients with neurogenic shock can have increased vasovagal responses to common procedures (e.g., suctioning, endotracheal intubation), which can trigger rapid changes in heart rate and blood pressure and increase the risk for complications and refractory shock. [73]

Rescue therapies for shock are for patients who remain in shock despite adequate treatment of the underlying cause. These treatments should be given in consultation with a specialist, and they include: [3]

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

  1. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med.. 2017; 43 (3): p.304-377. doi: 10.1007/s00134-017-4683-6 . | Open in Read by QxMD
  2. Levy MM, Evans LE, Rhodes A. The Surviving Sepsis Campaign Bundle: 2018 update. Intensive Care Med. 2018; 44 (6): p.925-928. doi: 10.1007/s00134-018-5085-0 . | Open in Read by QxMD
  3. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  4. Hernández G, Ospina-Tascón GA, Damiani LP, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock. JAMA. 2019; 321 (7): p.654. doi: 10.1001/jama.2019.0071 . | Open in Read by QxMD
  5. Rhee C, Chiotos K, Cosgrove SE, et al. Infectious Diseases Society of America Position Paper: Recommended Revisions to the National Severe Sepsis and Septic Shock Early Management Bundle (SEP-1) Sepsis Quality Measure. Clinical Infectious Diseases. 2020 . doi: 10.1093/cid/ciaa059 . | Open in Read by QxMD
  6. Kalil AC, Gilbert DN, Winslow DL, Masur H, Klompas M. Infectious Diseases Society of America (IDSA) POSITION STATEMENT: Why IDSA Did Not Endorse the Surviving Sepsis Campaign Guidelines. Clinical Infectious Diseases. 2017; 66 (10): p.1631-1635. doi: 10.1093/cid/cix997 . | Open in Read by QxMD
  7. Summers RL, Baker SD, Sterling SA, Porter JM, Jones AE. Characterization of the spectrum of hemodynamic profiles in trauma patients with acute neurogenic shock. J Crit Care. 2013; 28 (4): p.531.e1-531.e5. doi: 10.1016/j.jcrc.2013.02.002 . | Open in Read by QxMD
  8. Consortium for Spinal Cord Medicine.. Early acute management in adults with spinal cord injury: A clinical practice guideline for health-care professionals.. J Spinal Cord Med. 2008; 31 (4): p.403-79.
  9. Sánchez JAS, Sharif S, Costa F, Rangel JAIR, Anania CD, Zileli M. Early Management of Spinal Cord Injury: WFNS Spine Committee Recommendations. Neurospine. 2020; 17 (4): p.759-784. doi: 10.14245/ns.2040366.183 . | Open in Read by QxMD
  10. Walters BC, Hadley MN, Hurlbert RJ, et al. Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries. Neurosurgery. 2013; 60 (CN_suppl_1): p.82-91. doi: 10.1227/01.neu.0000430319.32247.7f . | Open in Read by QxMD
  11. Popa C, Popa F, Grigorean VT, et al. Vascular dysfunctions following spinal cord injury.. J Med Life. 2010; 3 (3): p.275-85.
  12. Bonner S, Smith C. Initial management of acute spinal cord injury. Continuing Education in Anaesthesia Critical Care & Pain. 2013; 13 (6): p.224-231. doi: 10.1093/bjaceaccp/mkt021 . | Open in Read by QxMD
  13. Squair JW, Bélanger LM, Tsang A, et al. Spinal cord perfusion pressure predicts neurologic recovery in acute spinal cord injury. Neurology. 2017; 89 (16): p.1660-1667. doi: 10.1212/wnl.0000000000004519 . | Open in Read by QxMD
  14. Eldahan KC, Rabchevsky AG. Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management. Auton Neurosci. 2018; 209 : p.59-70. doi: 10.1016/j.autneu.2017.05.002 . | Open in Read by QxMD
  15. Hagen E, Rekand T, Grønning M, Færestrand S. Kardiovaskulære følgetilstander etter ryggmargsskade. Tidsskr Nor Legeforen. 2012; 132 (9): p.1115-1120. doi: 10.4045/tidsskr.11.0551 . | Open in Read by QxMD
  16. Vincent J-L, De Backer D. Circulatory Shock. N Engl J Med. 2013; 369 (18): p.1726-1734. doi: 10.1056/nejmra1208943 . | Open in Read by QxMD
  17. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014; 40 (12): p.1795-1815. doi: 10.1007/s00134-014-3525-z . | Open in Read by QxMD
  18. Vincent J-L, Ince C, Bakker J. Clinical review: Circulatory shock - an update: a tribute to Professor Max Harry Weil. Critical Care. 2012; 16 (6). doi: 10.1186/cc11510 . | Open in Read by QxMD
  19. Thomas D, Wee M, Clyburn P, et al. Blood transfusion and the anaesthetist: management of massive haemorrhage. Anaesthesia. 2010; 65 (11): p.1153-1161. doi: 10.1111/j.1365-2044.2010.06538.x . | Open in Read by QxMD
  20. CRASH-2 trial collaborators., Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial.. Lancet. 2010; 376 (9734): p.23-32. doi: 10.1016/S0140-6736(10)60835-5 . | Open in Read by QxMD
  21. CRASH-2 collaborators., Roberts I, Shakur H, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial.. Lancet. 2011; 377 (9771): p.1096-101, 1101.e1-2. doi: 10.1016/S0140-6736(11)60278-X . | Open in Read by QxMD
  22. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2016; 37 (27): p.2129-2200. doi: 10.1093/eurheartj/ehw128 . | Open in Read by QxMD
  23. Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017; 136 (16). doi: 10.1161/cir.0000000000000525 . | Open in Read by QxMD
  24. Pollard S, Edwin SB, Alaniz C. Vasopressor and Inotropic Management Of Patients With Septic Shock.. P T. 2015; 40 (7): p.438-50.
  25. Long B, Koyfman A, Gottlieb M. Management of Heart Failure in the Emergency Department Setting: An Evidence-Based Review of the Literature. J Emerg Med. 2018; 55 (5): p.635-646. doi: 10.1016/j.jemermed.2018.08.002 . | Open in Read by QxMD
  26. Yealy DM, Callaway C. Emergency Department Critical Care. Oxford University Press ; 2013
  27. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure. J Am Coll Cardiol. 2013; 62 (16): p.e147-e239. doi: 10.1016/j.jacc.2013.05.019 . | Open in Read by QxMD
  28. Hollenberg SM. Vasoactive Drugs in Circulatory Shock. Am J Respir Crit Care Med. 2011; 183 (7): p.847-855. doi: 10.1164/rccm.201006-0972ci . | Open in Read by QxMD
  29. Jentzer JC, Coons JC, Link CB, Schmidhofer M. Pharmacotherapy Update on the Use of Vasopressors and Inotropes in the Intensive Care Unit. J Cardiovasc Pharmacol Ther. 2014; 20 (3): p.249-260. doi: 10.1177/1074248414559838 . | Open in Read by QxMD
  30. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy. Circulation. 2011; 124 (24). doi: 10.1161/cir.0b013e318223e2bd . | Open in Read by QxMD
  31. Töpel I, Zorger N, Steinbauer M. Inflammatory diseases of the aorta. Gefässchirurgie. 2016; 21 (S2): p.87-93. doi: 10.1007/s00772-016-0142-x . | Open in Read by QxMD
  32. Ploumis A, Yadlapalli N, Fehlings MG, Kwon BK, Vaccaro AR. A systematic review of the evidence supporting a role for vasopressor support in acute SCI. Spinal Cord. 2009; 48 (5): p.356-362. doi: 10.1038/sc.2009.150 . | Open in Read by QxMD
  33. Ruiz IA, Squair JW, Phillips AA, et al. Incidence and Natural Progression of Neurogenic Shock after Traumatic Spinal Cord Injury. J Neurotrauma. 2018; 35 (3): p.461-466. doi: 10.1089/neu.2016.4947 . | Open in Read by QxMD
  34. Kounis N, Soufras G, Hahalis G. Anaphylactic shock: Kounis hypersensitivity-associated syndrome seems to be the primary cause. North American Journal of Medical Sciences. 2013; 5 (11): p.631. doi: 10.4103/1947-2714.122304 . | Open in Read by QxMD
  35. Campbell RL, Li JTC, Nicklas RA, Sadosty AT. Emergency department diagnosis and treatment of anaphylaxis: a practice parameter. Ann Allergy Asthma Immunol. 2014; 113 (6): p.599-608. doi: 10.1016/j.anai.2014.10.007 . | Open in Read by QxMD
  36. Lieberman P, Nicklas RA, Randolph C, et al. Anaphylaxis—a practice parameter update 2015. Annals of Allergy, Asthma & Immunology. 2015; 115 (5): p.341-384. doi: 10.1016/j.anai.2015.07.019 . | Open in Read by QxMD
  37. Simmons J, Ventetuolo CE. Cardiopulmonary monitoring of shock. Curr Opin Crit Care. 2017; 23 (3): p.223-231. doi: 10.1097/mcc.0000000000000407 . | Open in Read by QxMD
  38. Hemorrhagic Shock. http://www.cvphysiology.com/Blood%20Pressure/BP031. Updated: April 28, 2014. Accessed: May 31, 2018.
  39. Drucker WR, Chadwick CD, Gann DS. Transcapillary refill in hemorrhage and shock.. Arch Surg. 1981; 116 (10): p.1344-53.
  40. Jentzer JC, Vallabhajosyula S, Khanna AK, Chawla LS, Busse LW, Kashani KB. Management of Refractory Vasodilatory Shock. Chest. 2018; 154 (2): p.416-426. doi: 10.1016/j.chest.2017.12.021 . | Open in Read by QxMD
  41. Overgaard CB, Dzavík V. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease.. Circulation. 2008; 118 (10): p.1047-56. doi: 10.1161/CIRCULATIONAHA.107.728840 . | Open in Read by QxMD
  42. Jentzer JC, Hollenberg SM. Vasopressor and Inotrope Therapy in Cardiac Critical Care. J Intensive Care Med. 2020 : p.088506662091763. doi: 10.1177/0885066620917630 . | Open in Read by QxMD
  43. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced Cardiovascular Life Support. Circulation. 2015; 132 (18 suppl 2): p.S444-S464. doi: 10.1161/cir.0000000000000261 . | Open in Read by QxMD
  44. Gamper G, Havel C, Arrich J, et al. Vasopressors for hypotensive shock. Cochrane Database of Systematic Reviews. 2016 . doi: 10.1002/14651858.cd003709.pub4 . | Open in Read by QxMD
  45. Avni T, Lador A, Lev S, Leibovici L, Paul M, Grossman A. Vasopressors for the Treatment of Septic Shock: Systematic Review and Meta-Analysis. PLoS ONE. 2015; 10 (8): p.e0129305. doi: 10.1371/journal.pone.0129305 . | Open in Read by QxMD
  46. Goertz AW, Lindner KH, Schültz W, Schirmer U, Beyer M, Georgieff M. Influence of Phenylephrine Bolus Administration on Left Ventricular Filling Dynamics in Patients with Coronary Artery Disease and Patients with Valvular Aortic Stenosis. Anesthesiology. 1994; 81 (1): p.49-58. doi: 10.1097/00000542-199407000-00009 . | Open in Read by QxMD
  47. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign. Crit Care Med. 2013; 41 (2): p.580-637. doi: 10.1097/ccm.0b013e31827e83af . | Open in Read by QxMD
  48. Khanna A, English SW, Wang XS, et al. Angiotensin II for the Treatment of Vasodilatory Shock. N Engl J Med. 2017; 377 (5): p.419-430. doi: 10.1056/nejmoa1704154 . | Open in Read by QxMD
  49. Bistola V, Arfaras-Melainis A, Polyzogopoulou E, et al. Inotropes in Acute Heart Failure: From Guidelines to Practical Use: Therapeutic Options and Clinical Practice. Cardiac Failure Review. 2019; 5 (3): p.133-139. doi: 10.15420/cfr.2019.11.2 . | Open in Read by QxMD
  50. Russell FM, Rutz M, Pang PS. Focused Ultrasound in the Emergency Department for Patients with Acute Heart Failure.. Card Fail Rev. 2015; 1 (2): p.83-86. doi: 10.15420/cfr.2015.1.2.83 . | Open in Read by QxMD
  51. Sorensen B, Hunskaar S. Point-of-care ultrasound in primary care: a systematic review of generalist performed point-of-care ultrasound in unselected populations. Ultrasound J. 2019; 11 (1). doi: 10.1186/s13089-019-0145-4 . | Open in Read by QxMD
  52. Pourmand A, Pyle M, Yamane D, Sumon K, Frasure SE. The utility of point-of-care ultrasound in the assessment of volume status in acute and critically ill patients.. World J Emerg Med. 2019; 10 (4): p.232-238. doi: 10.5847/wjem.j.1920-8642.2019.04.007 . | Open in Read by QxMD
  53. Corl KA, George NR, Romanoff J, et al. Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. J Crit Care. 2017; 41 : p.130-137. doi: 10.1016/j.jcrc.2017.05.008 . | Open in Read by QxMD
  54. Gaskamp M, Blubaugh M, McCarthy LH, Scheid DC. Can Bedside Ultrasound Inferior Vena Cava Measurements Accurately Diagnose Congestive Heart Failure in the Emergency Department? A Clin-IQ.. J Patient Cent Res Rev. 2016; 3 (4): p.230-234.
  55. Long E, Oakley E, Duke T, Babl FE. Does Respiratory Variation in Inferior Vena Cava Diameter Predict Fluid Responsiveness. Shock. 2017; 47 (5): p.550-559. doi: 10.1097/shk.0000000000000801 . | Open in Read by QxMD
  56. De Backer D, Fagnoul D. Intensive Care Ultrasound: VI. Fluid Responsiveness and Shock Assessment. Annals of the American Thoracic Society. 2014; 11 (1): p.129-136. doi: 10.1513/annalsats.201309-320ot . | Open in Read by QxMD
  57. Ilyas A, Ishtiaq W, Assad S, et al. Correlation of IVC Diameter and Collapsibility Index With Central Venous Pressure in the Assessment of Intravascular Volume in Critically Ill Patients. Cureus. 2017 . doi: 10.7759/cureus.1025 . | Open in Read by QxMD
  58. Molokoane-Mokgoro K, Goldstein LN, Wells M. Ultrasound evaluation of the respiratory changes of the inferior vena cava and axillary vein diameter at rest and during positive pressure ventilation in spontaneously breathing healthy volunteers. Emergency Medicine Journal. 2018 : p.emermed-2016-205944. doi: 10.1136/emermed-2016-205944 . | Open in Read by QxMD
  59. Russell FM, Ehrman RR, Cosby K, et al. Diagnosing Acute Heart Failure in Patients With Undifferentiated Dyspnea: A Lung and Cardiac Ultrasound (LuCUS) Protocol. Acad Emerg Med. 2015; 22 (2): p.182-191. doi: 10.1111/acem.12570 . | Open in Read by QxMD
  60. Martindale JL, Wakai A, Collins SP, et al. Diagnosing Acute Heart Failure in the Emergency Department: A Systematic Review and Meta-analysis. Acad Emerg Med. 2016; 23 (3): p.223-242. doi: 10.1111/acem.12878 . | Open in Read by QxMD
  61. Hendin A, Koenig S, Millington SJ. Better With Ultrasound. Chest. 2020; 158 (5): p.2082-2089. doi: 10.1016/j.chest.2020.04.052 . | Open in Read by QxMD
  62. Özdemir U, Çimen M, Güney T, Gürsel G. Validity and reliability of pocket-sized ultrasound devices in measurement of optic nerve sheath diameter in ICU patients. J Clin Monit Comput. 2019; 34 (3): p.597-605. doi: 10.1007/s10877-019-00351-7 . | Open in Read by QxMD
  63. Malbrain MLNG, Langer T, Annane D, et al. Intravenous fluid therapy in the perioperative and critical care setting: Executive summary of the International Fluid Academy (IFA). Ann. Intensive Care. 2020; 10 (1). doi: 10.1186/s13613-020-00679-3 . | Open in Read by QxMD
  64. Carsetti A, Cecconi M, Rhodes A. Fluid bolus therapy: monitoring and predicting fluid responsiveness.. Curr Opin Crit Care. 2015; 21 (5): p.388-94. doi: 10.1097/MCC.0000000000000240 . | Open in Read by QxMD
  65. Marik PE, Weinmann M. Optimizing fluid therapy in shock.. Curr Opin Crit Care. 2019; 25 (3): p.246-251. doi: 10.1097/MCC.0000000000000604 . | Open in Read by QxMD
  66. Annane D, Pastores SM, Rochwerg B, et al. Guidelines for the Diagnosis and Management of Critical Illness-Related Corticosteroid Insufficiency (CIRCI) in Critically Ill Patients (Part I). Crit Care Med. 2017; 45 (12): p.2078-2088. doi: 10.1097/ccm.0000000000002737 . | Open in Read by QxMD
  67. Holmes CL, Walley KR. The evaluation and management of shock. Clin Chest Med. 2003; 24 (4): p.775-789. doi: 10.1016/s0272-5231(03)00107-2 . | Open in Read by QxMD
  68. Legrand M, Payen D. Understanding urine output in critically ill patients. Annals of Intensive Care. 2011; 1 (1). doi: 10.1186/2110-5820-1-13 . | Open in Read by QxMD
  69. Privette AR, Dicker RA. Recognition of hypovolemic shock: using base deficit to think outside of the ATLS box. Critical Care. 2013; 17 (2): p.124. doi: 10.1186/cc12513 . | Open in Read by QxMD
  70. Mutschler M, Nienaber U, Brockamp T, et al. Renaissance of base deficit for the initial assessment of trauma patients: a base deficit-based classification for hypovolemic shock developed on data from 16,305 patients derived from the TraumaRegister DGU®. Critical Care. 2013; 17 (2): p.R42. doi: 10.1186/cc12555 . | Open in Read by QxMD
  71. De Backer D. Detailing the cardiovascular profile in shock patients. Critical Care. 2017; 21 (S3). doi: 10.1186/s13054-017-1908-6 . | Open in Read by QxMD
  72. Walley KR. Use of Central Venous Oxygen Saturation to Guide Therapy. Am J Respir Crit Care Med. 2011; 184 (5): p.514-520. doi: 10.1164/rccm.201010-1584ci . | Open in Read by QxMD
  73. Saint Louis Encephalitis. https://www.cdc.gov/sle/technical/symptoms.html. Updated: December 4, 2018. Accessed: December 9, 2020.
  74. De Backer D, Vincent JL. Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions.. Crit Care. 2018; 22 (1): p.43. doi: 10.1186/s13054-018-1959-3 . | Open in Read by QxMD
  75. Hunt SA, Abraham WT, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults. Circulation. 2009; 119 (14). doi: 10.1161/circulationaha.109.192065 . | Open in Read by QxMD
  76. Finfer S, Myburgh J, Bellomo R. Intravenous fluid therapy in critically ill adults. Nat Rev Nephrol. 2018; 14 (9): p.541-557. doi: 10.1038/s41581-018-0044-0 . | Open in Read by QxMD
  77. Cooper MS, Stewart PM. Corticosteroid Insufficiency in Acutely Ill Patients. N Engl J Med. 2003; 348 (8): p.727-734. doi: 10.1056/nejmra020529 . | Open in Read by QxMD
  78. Kurtz I. Acid-Base Case Studies. Trafford Publishing ; 2004
  79. Friesecke S, Stecher S-S, Gross S, Felix SB, Nierhaus A. Extracorporeal cytokine elimination as rescue therapy in refractory septic shock: a prospective single-center study. J Artif Organs. 2017; 20 (3): p.252-259. doi: 10.1007/s10047-017-0967-4 . | Open in Read by QxMD
  80. Nabzdyk CS, Bittner EA. Vitamin C in the critically ill - indications and controversies. World J Crit Care Med. 2018; 7 (5): p.52-61. doi: 10.5492/wjccm.v7.i5.52 . | Open in Read by QxMD
  81. Moskowitz A, Huang DT, Hou PC, et al. Effect of Ascorbic Acid, Corticosteroids, and Thiamine on Organ Injury in Septic Shock. JAMA. 2020; 324 (7): p.642. doi: 10.1001/jama.2020.11946 . | Open in Read by QxMD
  82. Zhang M, Jativa DF. Vitamin C supplementation in the critically ill: A systematic review and meta-analysis.. SAGE Open med. 2018; 6 : p.2050312118807615. doi: 10.1177/2050312118807615 . | Open in Read by QxMD