What is the management of shock in the Intensive Care Unit (ICU)?

Management of Shock in the ICU

The management of shock in the ICU requires immediate recognition, aggressive fluid resuscitation targeting specific hemodynamic endpoints, early vasopressor/inotrope therapy tailored to shock phenotype, and consideration of mechanical circulatory support for refractory cases—all guided by invasive hemodynamic monitoring within the first hour. 1

Initial Recognition and Diagnosis

Shock is defined by sustained systolic blood pressure <90 mmHg for ≥30 minutes (or requiring vasopressors to maintain SBP >90 mmHg) with evidence of end-organ hypoperfusion including lactate >2 mmol/L, altered mental status, cold/clammy extremities, or urine output <30 mL/h. 2 The critical first step is identifying the shock phenotype—cardiogenic, distributive (septic), hypovolemic, or obstructive—as this determines the entire treatment pathway. 3

For cardiogenic shock specifically: Hemodynamic criteria include cardiac index <1.8 L/min/m² without support, cardiac power output <0.6 W, and PCWP >15 mmHg for left-dominant phenotypes. 2 Early invasive hemodynamics with pulmonary artery catheter placement should be performed within the first hours for patients not responding to initial therapy, as this was associated with improved outcomes in recent observational data. 4

First Hour Resuscitation Goals

Within the first 60 minutes, you must achieve: capillary refill ≤2 seconds, heart rate normalized for age, and systolic blood pressure ≥90 mmHg in adults. 1 For pediatric patients, restore normal blood pressure thresholds for age within this timeframe. 2

Fluid Resuscitation Protocol

• Adults: Administer 20 mL/kg boluses of isotonic crystalloid (normal saline or lactated Ringer's) up to and exceeding 60 mL/kg until perfusion improves or signs of fluid overload develop (rales, hepatomegaly). 1 More than 4 liters may be required in the first 24 hours for septic shock. 1

• Neonates: Give 10 mL/kg boluses up to 60 mL/kg total, stopping if hepatomegaly develops. 2 Begin prostaglandin infusion (0.05-0.1 mcg/kg/min) immediately until ductal-dependent cardiac lesions are ruled out. 5

• Pediatric patients: Push 20 mL/kg boluses up to and over 60 mL/kg until perfusion improves, unless rales or hepatomegaly develop. 2

Critical pitfall: Do not delay vasopressor initiation while pursuing aggressive fluid resuscitation in distributive shock—begin vasopressors at 15 minutes if fluid-refractory. 2

Subsequent ICU Goals (After First Hour)

Target normal perfusion pressure (MAP - CVP) for age, central venous oxygen saturation (ScvO2) >70%, and cardiac index 3.3-6.0 L/min/m². 1 Urine output should exceed 1 mL/kg/hr in children and be adequate in adults. 1

Vasoactive Agent Selection by Phenotype

Distributive (Septic) Shock

Norepinephrine is the first-line vasopressor after appropriate fluid resuscitation, targeting MAP ≥65 mmHg (though individual patients may require higher targets based on baseline blood pressure). 1 Start at 0.01 units/minute for septic shock if using vasopressin. 6

Vasopressin dosing specifics: Begin at 0.01 units/minute for septic shock, titrate up by 0.005 units/minute at 10-15 minute intervals until target blood pressure is reached, with limited data above 0.07 units/minute. 6 After maintaining target blood pressure for 8 hours without catecholamines, taper by 0.005 units/minute every hour. 6

Cardiogenic Shock

Dobutamine or dopamine (5-10 mcg/kg/min) are first-line inotropes. 1 However, the specific phenotype determines medication selection:

• Left-dominant cardiogenic shock with high afterload: Pure vasodilators like nitroprusside improve cardiac output by reducing afterload; milrinone and dobutamine are also effective for high-afterload LV failure. 2

• Right-dominant cardiogenic shock: The RV has less contractile reserve than the LV, and calcitropic agents have been associated with progressive RV function decline. 2 Concomitant use of agents that increase systemic afterload without increasing pulmonary vascular resistance (vasopressin or norepinephrine) may be needed to maintain RV perfusion during inodilator therapy, particularly with milrinone. 2

• Pulmonary vasodilators (intravenous or inhaled) reduce RV afterload for pulmonary arterial hypertension and RV failure. 2 Minimize intrathoracic positive pressure ventilation, correct acidosis, and improve hypoxic pulmonary vasoconstriction to improve LV filling in RV failure. 2

Pediatric-Specific Protocols

• At 15 minutes (fluid-refractory shock): Begin dopamine up to 10 mcg/kg/min via peripheral/IO access while obtaining central access. 2 Reverse cold shock by titrating central dopamine or epinephrine; reverse warm shock by titrating central norepinephrine. 2

• At 60 minutes (catecholamine-resistant shock): Begin hydrocortisone if at risk for absolute adrenal insufficiency. 2 Monitor CVP and attain normal MAP-CVP and ScvO2. 2

• Neonatal dopamine-resistant shock: Titrate epinephrine 0.05 to 0.3 mcg/kg/min. 2

Adjunctive Therapies

Hydrocortisone should be administered if absolute adrenal insufficiency is suspected or the patient is at risk. 1 This is particularly important in catecholamine-resistant shock. 2

Correct metabolic derangements immediately: hypoglycemia, hypocalcemia, and acidosis must be addressed as they impair cardiovascular function. 2, 5

Advanced Hemodynamic Monitoring

Pulmonary artery catheter placement should be considered early in patients not responding to initial therapy or with unclear shock etiology. 4 Use PAC, transpulmonary thermodilution (PiCCO), or echocardiography to guide therapy in refractory shock. 1

Key hemodynamic parameters to guide therapy:

• PCWP >15 mmHg with PAPI <1.0: Suggests left-dominant cardiogenic shock. 2
• PCWP <15 mmHg with PAPI <1.0: Suggests right-dominant cardiogenic shock. 2
• Cardiac power output <0.6 W with CI <2.2 L/min/m²: Indicates refractory shock requiring consideration of mechanical circulatory support. 2

Critical pitfall: PCWP may not accurately reflect left ventricular end-diastolic pressure in aortic regurgitation, ventricular interdependence, LV hypertrophy, diabetes, obesity, and ischemia. 7 Pressure estimates are generally insensitive indicators of volume status—low values may reflect hypovolemia, but high values don't necessarily indicate volume overload. 7

Mechanical Circulatory Support for Refractory Cardiogenic Shock

Contraindications to MCS must be ruled out first: anoxic brain injury, irreversible end-organ failure, prohibitive vascular access, or DNR status. 2

Device Selection by Phenotype

• Isolated RV failure refractory to medical therapy: Impella RP or Protek Duo platforms bypass the failing RV. 2 The centrifugal pump with Protek Duo allows splicing of an oxygenator for concomitant respiratory insufficiency. 2

• RV failure from progressive pulmonary hypertension: Devices providing only RV support are poorly suited, as the primary lesion is the pulmonary vasculature and forced perfusion may precipitate pulmonary hemorrhage—venoarterial ECMO may be preferred. 2

• Biventricular failure or severe refractory shock: Consider VA-ECMO. 2

Pediatric/neonatal ECMO: Current survival rate for newborn sepsis is 80%. 2 Most centers accept refractory shock or PaO2 <40 mmHg after maximal therapy as sufficient indication. 2 ECMO flows >110 mL/kg should be avoided due to hemolysis risk. 2

Persistent Refractory Shock Management

Rule out and correct reversible causes: pericardial effusion, pneumothorax, intra-abdominal hypertension (>12 mmHg). 2 In neonates, also consider hypoadrenalism, hypothyroidism, inborn errors of metabolism, cyanotic/obstructive heart disease, or critically large patent ductus arteriosus. 2

Continuous renal replacement therapy should be initiated if fluid overload exceeds 10% despite diuretics. 1 In newborns on ECMO with inadequate urine output and 10% fluid overload despite diuretics, CRRT is best performed while on the ECMO circuit. 2

Multidisciplinary Shock Team Approach

A multidisciplinary shock team should be involved early to identify potential candidates for temporary and/or durable MCS. 4 Development of shock networks with regionalized systems of care and dedicated Level 1 shock centers improves clinical outcomes on a large scale. 2 The approach emphasizes early diagnosis, multidisciplinary care, selective MCS use, and invasive hemodynamics to tailor therapies for shock phenotype. 2