Topic: Press (Interpreted as Pressors/Vasopressors and Inotropes)

Disclaimer: This information is intended for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Clinicians must always exercise their independent medical judgment and tailor decisions to the individual patient's circumstances, taking into account the full clinical picture and relevant guidelines. Dosages and recommendations are subject to change based on evolving evidence and institutional protocols.

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Pressors (Vasopressors and Inotropes)

Overview

• Definition: Pressors are a class of medications that induce vasoconstriction (vasopressors) and/or increase myocardial contractility (inotropes) to elevate mean arterial pressure (MAP) and improve organ perfusion in critically ill patients, typically those in shock.
• Epidemiology: Pressors are extensively used in critical care settings, particularly in patients with various forms of shock (e.g., septic, cardiogenic, hypovolemic, distributive, neurogenic, anaphylactic). The incidence of pressor use directly correlates with the incidence and severity of shock states, which are leading causes of morbidity and mortality in intensive care units globally.
• Classification:
  • Vasopressors: Primarily increase systemic vascular resistance (SVR) by acting on alpha-adrenergic receptors, leading to vasoconstriction. Examples include norepinephrine, phenylephrine, vasopressin, and angiotensin II. Epinephrine at higher doses also functions as a potent vasopressor.
  • Inotropes: Primarily increase myocardial contractility by acting on beta-1 adrenergic receptors. Examples include dobutamine and milrinone.
  • Inopressors (Mixed Effects): Agents with both significant inotropic and vasopressor properties. Examples include dopamine and epinephrine (at typical clinical doses).

Pathophysiology

• Mechanism: Pressors exert their effects by interacting with specific receptors on vascular smooth muscle cells and cardiomyocytes:
  • Alpha-1 Adrenergic Receptors: Activation leads to arterial and venous vasoconstriction, increasing SVR and venous return, thus raising blood pressure. Key targets for norepinephrine, phenylephrine, dopamine (high dose), epinephrine.
  • Beta-1 Adrenergic Receptors: Activation increases heart rate (chronotropy) and myocardial contractility (inotropy), leading to increased cardiac output. Key targets for dobutamine, dopamine (moderate dose), epinephrine, isoproterenol.
  • Beta-2 Adrenergic Receptors: Activation causes vasodilation (e.g., in skeletal muscle vasculature) and bronchodilation. Can be activated by epinephrine and isoproterenol.
  • V1 Vasopressin Receptors: Activation causes non-adrenergic vasoconstriction, primarily in splanchnic, renal, and cutaneous beds. Target for vasopressin.
  • Angiotensin II Receptors (AT1): Activation causes potent vasoconstriction, aldosterone release, and ADH release. Target for synthetic Angiotensin II.
• Risk Factors (for requiring pressor support):
  • Severe infection (leading to septic shock)
  • Acute myocardial infarction, severe heart failure, valvular heart disease (leading to cardiogenic shock)
  • Severe hemorrhage, extensive burns, severe dehydration (leading to hypovolemic shock refractory to fluids)
  • Spinal cord injury (leading to neurogenic shock)
  • Anaphylaxis
  • Adrenal insufficiency
  • Overdose of vasodilators or sedatives
• Protective Factors (against needing pressor support):
  • Prompt and adequate fluid resuscitation in hypovolemic or distributive shock.
  • Early identification and treatment of the underlying cause of shock (e.g., timely antibiotics for sepsis, revascularization for MI).
  • Maintaining euvolemia and electrolyte balance.
  • Appropriate management of chronic cardiovascular conditions.

Clinical Presentation (of conditions requiring pressors)

Signs and Symptoms

• Cardinal Features:
  • Hypotension: Mean arterial pressure (MAP) persistently <65 mmHg or systolic blood pressure (SBP) <90 mmHg, despite adequate fluid resuscitation (if appropriate).
  • Signs of Organ Hypoperfusion:
    • Central Nervous System: Altered mental status, confusion, decreased level of consciousness.
    • Renal: Oliguria (<0.5 mL/kg/hr) or anuria.
    • Cutaneous: Cool, clammy skin (except in "warm shock" like early septic shock), mottled extremities, prolonged capillary refill time (>2 seconds).
    • Metabolic: Lactic acidosis (elevated serum lactate >2 mmol/L).
• Early Signs: Tachycardia (compensatory), mild tachypnea, subtle changes in mental status, decreased urine output, cool extremities.
• Advanced Signs: Profound hypotension, anuria, coma, severe metabolic acidosis, cardiac arrest, respiratory failure requiring mechanical ventilation.
• Atypical Presentations:
  • "Warm Shock": Seen in early distributive shock (e.g., sepsis), characterized by warm, flushed skin, bounding pulses, and wide pulse pressure due to profound vasodilation, despite severe hypotension and hypoperfusion.
  • Neurogenic Shock: May present with bradycardia (due to loss of sympathetic tone) alongside hypotension, differing from the compensatory tachycardia typically seen in other shock states.

Physical Examination

• Inspection:
  • Mental status (alertness, orientation, GCS).
  • Skin color and temperature (pale/cyanotic vs. flushed/warm), presence of mottling, rash.
  • Respiratory effort (tachypnea, accessory muscle use).
  • Neck veins (distended in cardiogenic shock/fluid overload, flat in hypovolemia).
  • Peripheral edema (fluid overload).
• Palpation:
  • Peripheral pulses (rate, rhythm, quality – weak, thready, bounding).
  • Capillary refill time.
  • Skin turgor (dehydration).
• Special Tests:
  • Passive Leg Raise (PLR) Test: To assess fluid responsiveness in select patients. A positive response (increase in stroke volume or cardiac output by >10-15%) suggests the patient may benefit from further fluid administration.
  • Jugular Venous Pressure (JVP): Can estimate central venous pressure (CVP).
  • Bedside Ultrasound: Focused assessment with sonography for trauma (FAST) for hemorrhage, point-of-care cardiac ultrasound to assess cardiac function and volume status.

Diagnostic Approach (to identify the need for and cause of shock requiring pressors)

History Taking

• Key Questions:
  • Onset and Progression: When did symptoms start? How rapidly did they worsen?
  • Recent Illness/Events: Fever, cough, abdominal pain, diarrhea, recent trauma, surgery, chest pain, syncope, allergic exposures.
  • Medications: Recent changes, new medications, adherence, illicit drug use.
  • Allergies: Especially to medications.
  • Past Medical History: Cardiac disease (MI, CHF), diabetes, renal disease, liver disease, chronic pulmonary disease, immunosuppression, neurological conditions.
  • Fluid Intake/Output: Recent changes in thirst, urination, vomiting, diarrhea.
• Red Flags: Acute onset of severe hypotension, signs of end-organ damage, history of recent severe infection, chest pain, hemorrhage, neurological deficit, or overdose.

Laboratory Tests

• First-Line:
  • Arterial Blood Gas (ABG): pH, PaO2, PaCO2, bicarbonate, base deficit/excess. Crucially, lactate level (elevated lactate >2 mmol/L is a key marker of tissue hypoperfusion).
  • Complete Blood Count (CBC): Hemoglobin, hematocrit (anemia, hemorrhage), WBC count (leukocytosis/leukopenia for infection).
  • Basic Metabolic Panel (BMP) / Comprehensive Metabolic Panel (CMP): Electrolytes (Na, K, Cl), renal function (BUN, creatinine), glucose, liver function tests.
  • Cardiac Enzymes: Troponin I or T (myocardial injury/infarction).
  • Cultures: Blood, urine, sputum, wound cultures if infection suspected.
  • Coagulation Panel: PT, aPTT, INR (coagulopathy, DIC).
• Confirmatory:
  • Procalcitonin, CRP: Markers of inflammation and bacterial infection.
  • BNP/NT-proBNP: Heart failure.
  • Adrenal Function Tests: Cortisol levels (if adrenal insufficiency suspected).
  • Toxicology Screen: If overdose suspected.
  • Thyroid Function Tests: Rarely, severe thyroid dysfunction.
• Monitoring:
  • Lactate Clearance: Serial lactate measurements (e.g., every 2-4 hours) to assess response to resuscitation.
  • Hourly Urine Output: Goal >0.5 mL/kg/hr.
  • Vital Signs: Continuous monitoring (HR, BP, SpO2, temp).
  • Central Venous Oxygen Saturation (ScvO2) / Mixed Venous Oxygen Saturation (SvO2): For goal-directed therapy (if central line is in place).
  • Arterial Blood Gases: To monitor acid-base status and oxygenation.
  • Electrolyte Balance: Frequent checks, especially with continuous infusions or renal dysfunction.

Imaging

• Recommended:
  • Chest X-ray (CXR): To assess for pulmonary edema, pneumonia, effusions, acute respiratory distress syndrome (ARDS), cardiac silhouette.
  • Electrocardiogram (ECG): To evaluate for myocardial ischemia, infarction, arrhythmias, conduction abnormalities.
• Advanced:
  • Echocardiography (Transthoracic or Transesophageal): Essential for assessing cardiac function (ejection fraction, contractility), valvular function, pericardial effusion, and volume status. Can help differentiate types of shock (cardiogenic vs. distributive).
  • CT Scan (Abdomen/Pelvis, Chest, Head): To identify sources of infection (e.g., abscess), hemorrhage, pulmonary embolism, stroke, or other anatomical abnormalities.
  • Abdominal Ultrasound: Can assess for free fluid, organomegaly, or sources of infection.

Management (of Pressor Therapy)

Acute Management

• Immediate:
  1. Airway, Breathing, Circulation (ABC): Secure airway (intubation if needed), ensure adequate ventilation and oxygenation.
  2. Vascular Access: Establish at least two large-bore peripheral IV lines. A central venous catheter (CVC) is highly preferred for continuous pressor infusions to reduce extravasation risk and allow for CVP/ScvO2 monitoring. Arterial line for continuous BP monitoring.
  3. Fluid Resuscitation: Administer intravenous crystalloids (e.g., 0.9% NaCl or Lactated Ringer's) for hypovolemic or distributive shock. Initial target: 30 mL/kg within the first 1-3 hours for sepsis-induced hypoperfusion (Surviving Sepsis Campaign guidelines). Reassess fluid responsiveness frequently.
  4. Identify and Treat Underlying Cause: Broad-spectrum antibiotics for sepsis, reperfusion for MI, control hemorrhage, administer hydrocortisone for adrenal crisis, treat anaphylaxis.
• Stabilization:
  • Initiate Pressors: If hypotension (MAP <65 mmHg) persists despite adequate fluid resuscitation, initiate pressor therapy promptly.
  • Target MAP: Usually ≥65 mmHg. Individualize based on patient's comorbidities (e.g., chronic hypertension might require a higher MAP target, but avoid excessive hypertension).
  • Titrate to Effect: Continuously titrate pressor infusions to achieve and maintain the target MAP while monitoring for signs of improved perfusion (lactate clearance, urine output, mental status).
• Emergency:
  • For profound, life-threatening hypotension or during preparation of continuous infusions, consider push-dose vasopressors (e.g., phenylephrine 50-200 mcg IV bolus q1-5 min or epinephrine 10-20 mcg IV bolus q1-5 min) as a bridge. Use with extreme caution and only via central line if possible, or peripherally for very short durations with close monitoring due to extravasation risk.

Chronic Management (focused on weaning and long-term sequelae)

• Pharmacological:
  • Weaning Pressors: As the underlying condition improves and hemodynamic stability is achieved, pressors should be gradually tapered. This typically involves reducing the dose incrementally, observing for sustained MAP and perfusion. Abrupt cessation can lead to rebound hypotension.
  • Managing Underlying Conditions: Long-term management of chronic heart failure, hypertension, or conditions that predispose to shock.
• Non-pharmacological:
  • Rehabilitation: Physical, occupational, and cognitive therapy for patients recovering from critical illness and prolonged pressor support (Post-Intensive Care Syndrome - PICS).
  • Nutritional Support: Adequate enteral or parenteral nutrition to support recovery.
• Monitoring:
  • Long-term monitoring for organ dysfunction (e.g., chronic kidney disease, heart failure) resulting from prolonged hypoperfusion or pressor complications.
  • Regular follow-up to assess quality of life and functional recovery.

Treatment Algorithms (Specific to Pressors)

First-Line Vasopressors and Inotropes:

• Septic Shock:
  • Norepinephrine: First-line. Dose: Initial 0.01-0.3 mcg/kg/min (or 0.5-30 mcg/min for typical adult), titrate to MAP goal. Maximum usually around 3 mcg/kg/min (or 200-300 mcg/min). Potent alpha-1 and moderate beta-1 effects.
  • Vasopressin: Add to norepinephrine if MAP goal not met or to reduce norepinephrine dose. Dose: Fixed 0.03 units/min (no titration, or 0.01-0.04 units/min range). Non-adrenergic vasoconstrictor (V1 receptor agonist).
• Cardiogenic Shock:
  • Norepinephrine: If hypotension predominates (MAP <65 mmHg) or for mixed shock. Dose: Same as septic shock.
  • Dobutamine: If low cardiac output predominates (signs of hypoperfusion with adequate MAP or normal BP). Dose: 2.5-20 mcg/kg/min, titrate to cardiac index and perfusion. Primarily beta-1 agonist (inotropy).
  • Dopamine: Alternative to norepinephrine in highly selected patients (e.g., bradycardia with hypotension, low risk of tachyarrhythmias). Dose: 5-20 mcg/kg/min (inotropic and vasopressor effects). Lower doses (1-5 mcg/kg/min) for renal/dopaminergic effects are largely discredited.
• Anaphylactic Shock:
  • Epinephrine: First-line. IM (0.3-0.5 mg) for mild-moderate. IV infusion (0.1-0.5 mcg/kg/min or 2-10 mcg/min) for refractory hypotension. Alpha-1, beta-1, beta-2 effects.
• Neurogenic Shock:
  • Norepinephrine: First-line. Dose: Same as septic shock.
  • Phenylephrine: Alternative if patient tolerates bradycardia or has significant tachyarrhythmias with NE. Dose: 0.5-5 mcg/kg/min (or 10-200 mcg/min for typical adult). Pure alpha-1 agonist.

Second-Line and Refractory Cases:

• Septic Shock (refractory):
  • Epinephrine: Can be added as a second or third pressor. Dose: 0.1-0.5 mcg/kg/min (or 1-50 mcg/min). Offers potent vasopressor and inotropic support.
  • Phenylephrine: Consider if tachycardia or arrhythmias are problematic with other catecholamines, but may worsen cardiac output if not careful. Dose: 0.5-5 mcg/kg/min.
  • Angiotensin II: Approved for refractory vasodilatory shock. Dose: Initial 20 ng/kg/min, titrate up to 80 ng/kg/min or until MAP goal is reached.
  • Corticosteroids: Hydrocortisone 200 mg/day IV (e.g., 50 mg IV q6h) if pressor-refractory shock despite adequate fluid resuscitation and suspicion of adrenal insufficiency or profound inflammation.
• Cardiogenic Shock (refractory):
  • Milrinone: Phosphodiesterase-3 inhibitor, provides inotropy and vasodilation. Dose: 0.125-0.75 mcg/kg/min (no bolus in hypotension). Requires normal renal function.
  • Combinations: Often involves combining a vasopressor (e.g., norepinephrine) with an inotrope (e.g., dobutamine) to address both low SVR and low CO.
  • Mechanical Circulatory Support: Intra-aortic balloon pump (IABP), Impella, ECMO (extracorporeal membrane oxygenation) may be required.
• General Refractory Shock:
  • Address uncorrected acidosis (e.g., bicarbonate administration for severe pH <7.1), hypocalcemia, hypomagnesemia.
  • Consider removal of any offending agents (e.g., vasodilators).
  • Re-evaluate underlying diagnosis.

Complications (of Pressor Use)

• Common:
  • Tachyarrhythmias: Especially with agents having significant beta-adrenergic activity (epinephrine, dopamine, dobutamine).
  • Hypertension: If over-titrated, leading to increased afterload and potential cardiac strain.
  • Peripheral Ischemia: Due to excessive vasoconstriction, leading to cold, mottled extremities, digital ischemia, and even necrosis (fingers, toes).
  • Hyperglycemia: Catecholamines can induce insulin resistance and increase glucose production.
  • Anxiety, Tremor: From beta-adrenergic stimulation.
• Serious:
  • Myocardial Ischemia/Infarction: Increased myocardial oxygen demand from increased HR and contractility, or increased afterload, especially in patients with underlying CAD.
  • Severe Arrhythmias: Ventricular tachycardia/fibrillation.
  • Mesenteric Ischemia: Splanchnic vasoconstriction can lead to bowel ischemia and necrosis, particularly with high-dose norepinephrine or vasopressin.
  • Acute Kidney Injury: Renal vasoconstriction can reduce renal blood flow.
  • Extravasation: Leakage of a vasopressor from the vein into surrounding tissue, causing severe local vasoconstriction, tissue ischemia, and necrosis. Treat immediately with phentolamine (5-10 mg diluted in 10 mL saline, injected subcutaneously into the ischemic area).
  • Pulmonary Hypertension: Especially with agents increasing pulmonary vascular resistance.
  • Metabolic Acidosis: Can be worsened by excessive vasoconstriction leading to tissue hypoperfusion.

Prognosis (of conditions requiring pressors)

• Factors:
  • Underlying Cause of Shock: Mortality varies significantly (e.g., cardiogenic shock generally higher mortality than uncomplicated neurogenic shock).
  • Severity and Duration of Hypotension: Prolonged and profound hypotension is associated with worse outcomes.
  • Number of Organ Failures: Greater number of dysfunctional organs, poorer prognosis.
  • Age and Comorbidities: Extremes of age and significant underlying health conditions worsen prognosis.
  • Response to Initial Resuscitation: Timely and effective response to fluids and pressors is crucial.
• Survival: Varies widely. Septic shock mortality can range from 20-50%, cardiogenic shock 40-70%.
• Quality of Life: Survivors of critical illness requiring pressors often experience long-term physical, cognitive, and psychological impairments (Post-Intensive Care Syndrome - PICS), including muscle weakness, fatigue, memory issues, depression, and PTSD.

Prevention

• Primary (Preventing the onset of conditions leading to shock):
  • Vaccination (e.g., influenza, pneumococcal) to reduce infection risk.
  • Strict infection control measures in healthcare settings.
  • Management of chronic diseases (e.g., heart failure, diabetes, hypertension).
  • Prevention of trauma and hemorrhage.
• Secondary (Early detection and intervention to prevent progression to severe shock):
  • Early recognition of sepsis (e.g., using SIRS/qSOFA criteria, NEWS scores).
  • Prompt administration of appropriate antibiotics for suspected infections.
  • Rapid identification and treatment of myocardial infarction.
  • Aggressive fluid resuscitation for hypovolemic and early distributive shock.
  • Early initiation of pressors if fluid resuscitation is insufficient.
• Tertiary (Preventing complications of pressor use and improving long-term outcomes):
  • Careful titration and timely weaning of pressors.
  • Use of central venous access for continuous infusions whenever possible.
  • Close monitoring for signs of peripheral or mesenteric ischemia.
  • Prompt treatment of extravasation.
  • Multidisciplinary rehabilitation post-ICU stay.

Special Populations

• Pediatric:
  • Dosing: All pressor doses are weight-based (mcg/kg/min).
  • First-Line: Dopamine was historically first-line for pediatric septic shock, but norepinephrine is increasingly favored due to better outcomes in some studies and the higher risk of arrhythmias with dopamine.
  • Physiology: Children often compensate longer with tachycardia, and hypotension may be a late and ominous sign.
• Geriatric:
  • Comorbidities: Higher prevalence of underlying cardiovascular disease, renal dysfunction, and polypharmacy.
  • Sensitivity: May be more sensitive to pressor side effects (e.g., arrhythmias, ischemia) and drug interactions.
  • Dosing: Start with lower doses and titrate slowly ("start low, go slow").
  • MAP Targets: May benefit from slightly higher MAP targets if they have chronic hypertension, but this needs individual assessment.
• Pregnancy:
  • Hypotension: Often seen during spinal/epidural anesthesia. Phenylephrine is typically preferred over ephedrine due to less fetal acidosis.
  • Anaphylaxis: Epinephrine is the first-line treatment, maternal stabilization is paramount for fetal well-being.
  • Vasopressin: Caution should be exercised as vasopressin may cause uterine contractions and reduce uterine blood flow.
• Comorbidities:
  • Coronary Artery Disease: Avoid excessive tachycardia and hypertension to prevent myocardial ischemia. Norepinephrine is often preferred over agents with strong beta-1 effects if severe CAD is present.
  • Renal Failure: Some pressors (e.g., dopamine, dobutamine) are metabolized to inactive compounds by the kidney. Adjustments may not be necessary for the pressors themselves, but their effects on hemodynamics and electrolyte balance need close monitoring. Milrinone requires significant dose reduction in renal impairment.
  • Diabetes: Pressors can worsen hyperglycemia. Close glucose monitoring and insulin management are critical.

Clinical Pearls

• Diagnostic: "Hypotension + signs of hypoperfusion = shock until proven otherwise." Always check lactate! A rising lactate despite fluid resuscitation is a strong indicator for pressor initiation.
• Treatment:
  • "Fluids first, then pressors": For hypovolemic and most distributive shock, prioritize initial fluid resuscitation before starting pressors, unless hypotension is profound and life-threatening.
  • Central Line: Strongly prefer central venous access for continuous pressor infusions to minimize the risk of extravasation and allow for CVP/ScvO2 monitoring. Peripheral administration for very short durations or in emergencies only, and with extreme caution.
  • Titrate to MAP: Target MAP is typically ≥65 mmHg, but individualize.
  • Wean Slowly: Gradually decrease pressor doses as the patient stabilizes to avoid rebound hypotension.
  • Address Underlying Causes: Pressors are symptomatic treatment; the definitive management is treating the root cause of shock.
• Pitfalls:
  • Delaying Pressors: Waiting too long to initiate pressors in persistent shock can worsen organ damage and mortality.
  • Inadequate Fluid Resuscitation: Starting pressors without adequate volume expansion (when appropriate) can be detrimental, leading to vasoconstriction on an empty tank.
  • Peripheral Pressor Use: Prolonged or high-dose pressor administration through peripheral IVs significantly increases the risk of extravasation and tissue necrosis.
  • Ignoring Acidosis/Hypocalcemia: Severe acidosis (pH <7.1) and hypocalcemia can impair catecholamine responsiveness.
  • Aggressive Titration: Can lead to overshoot hypertension and increased cardiac workload.

Recent Updates

• Guidelines:
  • Surviving Sepsis Campaign (SSC) 2021 Guidelines: Reaffirm norepinephrine as the first-line vasopressor for septic shock. Recommend adding vasopressin or epinephrine if norepinephrine is insufficient to achieve MAP target. Recommend against dopamine for septic shock except in highly selected patients.
  • Angiotensin II: The ATHOS-3 trial (2017) led to the approval of synthetic Angiotensin II for refractory vasodilatory shock, providing another therapeutic option, particularly in patients maxed out on conventional pressors.
• Evidence:
  • Ongoing research continues to refine optimal MAP targets in different shock states and patient populations.
  • Studies are exploring combination vasopressor strategies and the timing of their initiation.
  • Increased emphasis on personalized medicine approaches, including identifying individual fluid responsiveness and pressor requirements.
• Controversies:
  • Optimal MAP Target: While ≥65 mmHg is standard, some debate exists for higher targets in specific populations (e.g., chronic severe hypertension) versus lower targets in others (e.g., some elderly, specific forms of shock) to minimize pressor-related adverse effects.
  • Role of Vasopressin vs. Epinephrine as Second-Line: The optimal choice between vasopressin and epinephrine after norepinephrine for refractory septic shock remains an area of active debate and depends on clinical context.
  • Utility of Dopamine: While largely discouraged for septic shock, its role in specific scenarios (e.g., profound bradycardia) is still considered by some.

Key References

• Guidelines:
  • Evans L, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Intensive Care Med. 2021 Nov;47(11):1181-1247.
  • American Heart Association (AHA) and American College of Cardiology (ACC) Guidelines for the Management of Patients with Heart Failure and other forms of shock.
• Studies:
  • Russell JA, et al. Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock. N Engl J Med. 2008 Jul 31;358(9):877-87. (VASST trial)
  • Khanna A, et al. Angiotensin II for the Treatment of High-Output Shock. N Engl J Med. 2017 Aug 10;377(5):419-430. (ATHOS-3 trial)
  • De Backer D, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 18;362(9):779-89. (SOAP II trial)
• Reviews:
  • Levy B, et al. Vasopressors and Inotropes in Shock. Intensive Care Med. 2020 Aug;46(8):1579-1594.
  • Cecconi M, et al. Vasopressor and Inotropic Support in Septic Shock: A Systematic Review. Crit Care. 2020 Jan 20;24(1):21.