According to Harrison's, which of the following are key principles of shock treatment: early recognition and assessment of shock type; initiating therapy while evaluating etiology and involving a multidisciplinary team; restoring oxygen delivery and identifying etiologies requiring specific intervention; or all of the above?

Harrison's Key Principles of Shock Treatment

All of the above principles are correct and represent the comprehensive approach to shock management endorsed by major cardiovascular and critical care societies.

Core Principles Validated by Guidelines

Early Recognition and Shock Type Assessment

Early identification of shock is paramount to reducing mortality. 1, 2

• Shock diagnosis requires systolic blood pressure <90 mmHg for >30 minutes (or vasopressor requirement to maintain this threshold) plus evidence of end-organ hypoperfusion including lactate >2 mmol/L, urine output <30 mL/h, altered mental status, or cold extremities 1, 2

• Hemodynamic phenotyping must occur immediately using cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure to differentiate cardiogenic (CI <2.2 L/min/m², elevated PCWP >15 mmHg, elevated SVR), hypovolemic (low CI, low PCWP, elevated SVR), distributive (normal/elevated CI, decreased SVR), and obstructive shock patterns 3, 2

• Point-of-care transthoracic echocardiography should be performed within minutes of presentation to assess ventricular function and identify mechanical complications 2, 1

• The SCAI classification system (Stages A through E) provides standardized staging from "at risk" to "extremis" and guides therapeutic escalation 1, 3

Initiate Therapy Concurrent with Etiologic Evaluation

Treatment must begin immediately while diagnostic workup proceeds—delays in therapy directly correlate with increased mortality. 4

• In a landmark study, implementation of a rapid response system that empowered front-line providers to initiate protocol-driven therapy while mobilizing multidisciplinary teams reduced mortality from 40% to 11.8% over 5 years, with only three patients needing treatment to save one additional life 4

• For AMI-related cardiogenic shock, coronary angiography must occur within 2 hours of hospital admission with intent to revascularize the culprit lesion, as this is the only intervention proven to reduce mortality 1, 2

• Initial stabilization includes high-flow oxygen, establishing large-bore IV access, and administering fluid challenges (10-20 mL/kg boluses up to 60 mL/kg) unless overt pulmonary edema is present 5, 2

• Norepinephrine should be initiated as first-line vasopressor when mean arterial pressure requires pharmacologic support to maintain perfusion pressure >65 mmHg 1, 2

Multidisciplinary Team Involvement

Shock management requires coordinated care from intensivists, cardiologists, interventional specialists, and cardiac surgeons from the moment of recognition. 1

• The American Heart Association explicitly states that "optimization of care requires a multidisciplinary team effort to coordinate early assessment and triage, noninvasive and invasive diagnostics, coronary revascularization, and expert ongoing intensive care management" 1

• Multidisciplinary shock teams using standardized protocols improve outcomes through earlier diagnosis, faster treatment initiation, and appropriate escalation to mechanical circulatory support 2, 1

• Team composition should include cardiology, cardiac surgery, critical care specialists, interventional cardiologists, and palliative care capability 1

• Transfer to Level 1 cardiac intensive care units with 24/7 cardiac catheterization capability and full-spectrum mechanical circulatory support availability should occur early for patients not responding to initial therapy 2

Restore Oxygen Delivery

The fundamental goal is restoring adequate tissue perfusion and oxygen delivery to prevent irreversible end-organ damage. 1, 2

• Target hemodynamic goals include cardiac index >2.0 L/min/m², pulmonary capillary wedge pressure <20 mmHg, mean arterial pressure >65 mmHg, and cardiac power output >0.6 W 2, 1

• Dobutamine serves as first-line inotropic agent when signs of low cardiac output persist despite adequate filling pressures, though duration and dose should be minimized 1, 2

• Lactate clearance and central venous oxygen saturation (target >70%) provide real-time markers of treatment response and tissue perfusion improvement 2, 5

• Invasive hemodynamic monitoring via pulmonary artery catheter should be inserted early in patients not responding to initial therapy to guide precise titration of vasoactive medications and fluid management 2, 6

Identify Etiologies Requiring Specific Intervention

Definitive treatment of the underlying cause is essential—supportive measures alone are insufficient. 1, 2

• Acute myocardial infarction requires urgent revascularization as the paramount intervention, with staged rather than ad hoc multivessel PCI preferred in patients with severe shock 2, 1

• Valvular emergencies (acute severe mitral regurgitation, aortic dissection with acute aortic insufficiency) require cardiac surgery, though percutaneous options may be considered in prohibitive surgical risk 1

• Arrhythmias causing hemodynamic instability mandate immediate restoration of sinus rhythm via cardioversion or antiarrhythmic therapy (amiodarone for atrial fibrillation in shock) 1

• Mechanical complications of AMI (ventricular septal rupture, free wall rupture, papillary muscle rupture) require emergent surgical consultation 2

Critical Implementation Pitfall

The most common error is sequential rather than simultaneous application of these principles. Clinicians must recognize shock early, classify the phenotype, initiate empiric therapy, mobilize the multidisciplinary team, and pursue definitive diagnosis/treatment all within the first 60-120 minutes 4, 2. Delays at any step—waiting for complete diagnostic workup before starting vasopressors, deferring team activation until "sicker," or postponing invasive monitoring—directly increase mortality 4, 6.