How should I assess and manage a patient presenting with shock?

Assessment and Management of Shock

Shock is a life-threatening state of acute circulatory failure with inadequate tissue perfusion that requires immediate recognition, rapid classification into one of four major categories (hypovolemic, distributive, cardiogenic, or obstructive), and category-specific treatment to prevent irreversible organ damage and death. 1

Immediate Recognition and Initial Assessment

Clinical Definition

• Shock is defined by systolic blood pressure < 90 mmHg for > 30 minutes despite adequate volume status plus signs of end-organ hypoperfusion: oliguria (< 0.5 mL/kg/h), cold extremities, altered mental status, lactate > 2 mmol/L, metabolic acidosis, or SvO₂ < 65%. 2

Immediate Diagnostic Actions

• Insert an invasive arterial line immediately for continuous, accurate blood pressure monitoring in all shock patients. 2
• Obtain a 12-lead ECG and bedside transthoracic echocardiography to determine cardiac etiology, assess ventricular function, identify valvular lesions, and detect mechanical complications. 3
• Measure serum lactate and base deficit to estimate the extent of bleeding and tissue hypoperfusion; lactate > 2 mmol/L indicates significant hypoperfusion. 2
• Perform serial laboratory studies including cardiac biomarkers, renal function (creatinine/urea), hepatic biomarkers, and electrolytes to assess end-organ function and monitor response to therapy. 2

Shock Classification Algorithm

The four major categories of shock relate to specific organ systems and require distinct treatment approaches 1:

1. Hypovolemic shock: Intravascular volume loss (blood and fluids compartment)
2. Distributive shock: Pathological redistribution of intravascular volume (vascular system)
3. Cardiogenic shock: Primary cardiac pump dysfunction
4. Obstructive shock: Blockage of circulation with elevated resistance

Classification-Specific Assessment

Hypovolemic Shock (Hemorrhagic)

• Use the ATLS classification system to estimate blood loss based on heart rate, blood pressure, pulse pressure, and clinical presentation. 2
• Apply the Shock Index (heart rate ÷ systolic blood pressure) to draw attention to abnormal values, though it is too insensitive to rule out major injury. 2
• Assess response to initial fluid resuscitation: transient responders and non-responders are candidates for immediate surgical bleeding control. 2
• Use ultrasound (if feasible without delaying transport) to detect hemothorax, hemopericardium, or free abdominal fluid in thoracoabdominal injuries. 2

Cardiogenic Shock

• Apply the SCAI staging system (Stages A–E) to stratify severity and guide treatment intensity. 2, 3
• Consider early pulmonary artery catheterization when the diagnosis is uncertain or the patient fails to respond to initial therapy; observational data suggest improved outcomes with complete hemodynamic profiling. 2
• Target hemodynamic parameters: cardiac index > 2.0–2.2 L/min/m², pulmonary capillary wedge pressure < 20 mmHg, mean arterial pressure ≥ 65 mmHg. 2, 3

Distributive Shock (Including Septic)

• Assess for pathological redistribution of blood volume with relative hypovolemia despite normal or elevated absolute intravascular volume. 1
• Evaluate for dynamic obstruction, fluid responsiveness, fluid tolerance, and ventriculo-arterial coupling using critical care ultrasound. 4

Neurogenic Shock

• Monitor hemodynamic parameters including blood pressure and heart rate with invasive arterial line monitoring. 5
• Perform serial neurological evaluations to detect return of reflex function; spinal shock typically lasts 3–6 months but can persist up to 1–2 years. 5

Category-Specific Management

Hypovolemic Shock Management

• Treat with immediate fluid replacement using balanced crystalloids to restore intravascular volume. 1
• Apply tourniquets to open extremity injuries as an adjunct in the pre-surgical setting. 2
• Apply local compression to open wounds to limit life-threatening bleeding. 2
• Patients with obvious bleeding source or hemorrhagic shock in extremis should undergo immediate bleeding control procedure unless initial resuscitation is successful. 2
• Minimize time elapsed between injury and bleeding control. 2
• Use restricted volume replacement strategy with permissive hypotension until bleeding is controlled. 2

Cardiogenic Shock Management

Immediate Revascularization (ACS-Related)

• Perform emergent percutaneous coronary intervention of the culprit artery within 2 hours of presentation in all patients with acute MI-related cardiogenic shock; this is the only therapy proven to reduce mortality. 2, 3
• When coronary anatomy is unsuitable for PCI or PCI fails, proceed directly to emergency coronary artery bypass grafting. 3
• Do NOT perform routine multivessel PCI during index primary PCI; treat only the culprit lesion to reduce mortality and renal failure risk. 2, 3

Hemodynamic Support

• Give a cautious fluid challenge (≈ 200 mL isotonic crystalloid over 15–30 min) as first-line therapy in hypotensive patients with normal perfusion and no overt fluid overload, after ruling out mechanical complications. 2, 3
• Avoid volume overload in right-ventricular infarction, as it worsens hemodynamics. 3

Vasopressor Therapy

• Use norepinephrine as the first-line vasopressor to achieve mean arterial pressure ≥ 65 mmHg; it is associated with lower mortality and fewer arrhythmias compared with dopamine. 2, 3
• Do NOT use dopamine as first-line therapy due to higher arrhythmia rates (24% vs 12%) and increased mortality. 2, 3

Inotropic Therapy

• Initiate dobutamine (starting at 2–3 µg/kg/min, titrate up to 20 µg/kg/min) as the first-line inotrope when low cardiac output persists after adequate fluid resuscitation. 2, 3
• If norepinephrine plus dobutamine are insufficient—particularly in patients on chronic β-blockers—consider adding levosimendan or milrinone. 2, 3
• Escalate to mechanical circulatory support rather than layering additional inotropes when pharmacologic therapy fails. 3

Respiratory Support

• Provide supplemental oxygen to maintain SpO₂ > 90%. 2, 3
• Endotracheal intubation with positive end-expiratory pressure is indicated for respiratory failure or pulmonary edema. 2, 3

Mechanical Circulatory Support

• Consider short-term MCS in refractory cardiogenic shock defined by persistent tissue hypoperfusion despite adequate dosing of two vasoactive agents and treatment of the underlying cause. 2, 3
• Impella micro-axial pump is recommended to reduce mortality in patients with STEMI-related cardiogenic shock (SCAI stages C–E). 3
• Do NOT use intra-aortic balloon pump routinely; the IABP-SHOCK II trial showed no mortality benefit (Class III recommendation). 2, 3
• Do NOT use veno-arterial ECMO routinely; the ECLS-SHOCK trial demonstrated no reduction in 30-day mortality with higher bleeding and vascular complications. 3

Distributive Shock Management

• Treat with a combination of vasoconstrictors and fluid replacement to address pathological redistribution of intravascular volume. 1
• Use critical care ultrasound to guide hemodynamic management by assessing fluid responsiveness, fluid tolerance, and ventriculo-arterial coupling. 4

Obstructive Shock Management

• Treat hypoperfusion due to elevated resistance with immediate life-saving intervention to remove the obstruction. 1

Neurogenic Shock Management

• Fluid resuscitation is the first line of treatment, with an initial bolus of > 200 mL in 15–30 minutes. 5
• Norepinephrine is the preferred vasopressor for maintaining blood pressure due to its lower complication rate. 5
• Consider early surgical intervention (< 24 hours) after traumatic spinal cord injury to improve neurological recovery. 5

Systems-Based Approach and Transfer

Facility Requirements

• All cardiogenic shock patients should be transferred urgently to a tertiary center with 24/7 cardiac catheterization capability, dedicated ICU/CCU, and short-term mechanical circulatory support resources; failure to transfer is linked to markedly higher mortality. 2, 3
• Severely injured trauma patients should be transported directly to an appropriate trauma facility. 2

Multidisciplinary Team Activation

• Activate a multidisciplinary shock team (interventional cardiology, cardiac surgery, heart failure specialists, intensivists) for cardiogenic shock; team-based care is associated with reduced 30-day mortality (OR 0.61; 95% CI 0.41–0.93). 2, 3
• Management by a multidisciplinary team experienced in shock is reasonable for all shock patients. 2

Monitoring Targets and Serial Assessment

Perfusion Markers

• Aim for urine output > 0.5 mL/kg/h. 2
• Progressive lactate clearance and normalization of base deficit. 2
• Mixed venous oxygen saturation (SvO₂) ≥ 65%. 2
• Improvement in mental status and warming of extremities. 3

Hemodynamic Targets

• Mean arterial pressure ≥ 65 mmHg. 2, 3
• Cardiac index > 2.0–2.2 L/min/m². 2, 3
• Pulmonary capillary wedge pressure < 20 mmHg. 2, 3

Laboratory Monitoring

• Repeated hemoglobin/hematocrit measurements to detect ongoing bleeding. 2
• Early, repeated hemostasis monitoring including PT/INR, fibrinogen, and platelets in trauma patients. 2
• Serial renal function, electrolytes, and cardiac biomarkers. 2

Critical Pitfalls to Avoid

Cardiogenic Shock

• Do NOT delay emergent revascularization; in-hospital mortality remains 40–50% without prompt coronary reperfusion. 3
• Do NOT use routine IABP or multivessel PCI at primary intervention; they do not improve survival and may increase renal complications. 2, 3
• Do NOT combine multiple inotropes without considering escalation to mechanical support when initial regimen fails. 3
• Do NOT use dopamine or epinephrine as first-line agents due to higher arrhythmia and mortality rates. 2, 3

Hemorrhagic Shock

• Do NOT delay surgical bleeding control in patients with penetrating injuries presenting in shock. 2
• Avoid hyperventilation or hypoxemia; maintain normoventilation. 2

General

• Older adults may demonstrate atypical or delayed presentations, necessitating heightened suspicion for timely identification. 2
• Concomitant renal or hepatic dysfunction may potentiate effects and prolong action of vasoactive drugs, especially in older adults. 2
• Restoration of atrioventricular synchrony may significantly enhance cardiac output; promptly treat arrhythmias in hemodynamically unstable patients. 2