Shock States: A Visual Guide to Hemodynamics for the Clinician

A Comprehensive Review for Critical Care Trainees

Dr Neeraj Manikath , claude.ai

Abstract

Shock represents a final common pathway of circulatory failure where oxygen delivery fails to meet tissue metabolic demands, leading to cellular dysfunction and, if uncorrected, organ failure and death. Despite advances in hemodynamic monitoring and resuscitation strategies, shock remains a leading cause of morbidity and mortality in intensive care units worldwide. This review provides a clinically oriented approach to recognizing, classifying, and managing the four primary shock states through integration of clinical assessment, hemodynamic monitoring, and point-of-care ultrasound. We emphasize practical "bedside" interpretation of hemodynamic parameters and evidence-based vasoactive drug selection, offering pearls and pitfalls to guide the critical care trainee from diagnosis to therapeutic intervention.

Keywords: shock, hemodynamics, vasoactive drugs, point-of-care ultrasound, critical care

Introduction

Shock is not a diagnosis but a syndrome—a state of acute circulatory failure with inadequate tissue perfusion and oxygen utilization. The mortality from shock varies from 20% to over 50% depending on etiology, timely recognition, and appropriate intervention.[1,2] The traditional classification into four physiologic categories (hypovolemic, cardiogenic, obstructive, and distributive) remains the cornerstone of clinical reasoning, guiding both diagnostic workup and therapeutic strategy.

Modern critical care has moved beyond reliance on blood pressure alone, embracing a multimodal approach that integrates clinical examination, invasive and non-invasive hemodynamic monitoring, biomarkers, and increasingly, point-of-care ultrasound (POCUS).[3,4] This review synthesizes these elements into a practical framework for the clinician managing shock at the bedside.

Pearl #1: Shock is defined by inadequate tissue perfusion, not hypotension. A patient can be normotensive (or even hypertensive) and still be in shock—look for lactate elevation, oliguria, altered mentation, and cold, mottled extremities.

The Four Types of Shock

1. Hypovolemic Shock

Pathophysiology: Hypovolemic shock results from reduced intravascular volume, leading to decreased venous return, preload, and ultimately cardiac output. Causes include hemorrhage (trauma, GI bleeding, ruptured AAA), fluid losses (vomiting, diarrhea, burns, third-spacing), and inadequate intake.[5]

Hemodynamic Profile:

↓ Cardiac output (CO)
↓ Central venous pressure (CVP)
↓ Pulmonary artery occlusion pressure (PAOP)
↑ Systemic vascular resistance (SVR) (compensatory)
↓ Mixed venous oxygen saturation (SvO2) or central venous oxygen saturation (ScvO2)

Clinical Presentation: Tachycardia, hypotension (often delayed until >30% volume loss), narrow pulse pressure, cool peripheries, delayed capillary refill, oliguria, altered mental status. Orthostatic hypotension in milder cases.

Management Principles:

Source control: Stop bleeding, control GI losses
Volume resuscitation: Crystalloids (Ringer's lactate, balanced solutions preferred over normal saline)[6], blood products for hemorrhage
Transfusion targets: Hb 7-9 g/dL in most patients; 7-9 g/dL in cardiac patients[7]
Monitor response: Urine output, lactate clearance, ScvO2 normalization

Pearl #2: "Permissive hypotension" in trauma patients with uncontrolled bleeding: target systolic BP 80-90 mmHg until definitive hemorrhage control to avoid "popping the clot."[8]

Oyster #1: Not all hypovolemia responds to fluids alone. In severe hemorrhagic shock, massive transfusion protocols (1:1:1 ratio of RBC:FFP:platelets) may be lifesaving.[9]

2. Cardiogenic Shock

Pathophysiology: Cardiogenic shock (CS) arises from primary cardiac pump failure, resulting in inadequate cardiac output despite adequate intravascular volume. Most commonly due to acute myocardial infarction (AMI), but also seen in decompensated heart failure, myocarditis, valvular emergencies, and arrhythmias.[10]

Hemodynamic Profile:

↓ Cardiac output
↑ CVP and PAOP (congestion)
↑ SVR (compensatory vasoconstriction)
↓ ScvO2 (impaired oxygen delivery)
Cardiac power output (CPO) <0.6 W predicts mortality[11]

Clinical Presentation: Hypotension, pulmonary edema (rales, hypoxemia), jugular venous distension (JVD), S3 gallop, cool extremities despite fluid overload, altered mentation.

SCAI Shock Stages: The Society for Cardiovascular Angiography and Interventions classifies CS into stages A-E, from "at risk" to refractory shock requiring escalating mechanical support.[12]

Management Principles:

Revascularization: Early PCI for STEMI-related CS (within 90-120 min)[13]
Inotropes: Dobutamine first-line; milrinone in beta-blocked patients
Vasopressors: Norepinephrine if severely hypotensive (MAP <65)
Mechanical support: IABP (less used now), Impella, VA-ECMO for refractory cases[14]
Diuresis: Furosemide for pulmonary edema once perfusion improved
RHF considerations: RV infarction requires volume, not diuresis; avoid excessive PEEP

Pearl #3: In cardiogenic shock, don't aggressively fluid resuscitate—you may worsen pulmonary edema. Use POCUS to assess for "wet" vs. "dry" lungs and cardiac function before giving boluses.

Oyster #2: Inotropes increase myocardial oxygen demand and may worsen ischemia. Always ensure revascularization is complete or planned when using inotropes in ischemic CS.

Hack #1: Calculate cardiac power output (CPO) = MAP × CO / 451. CPO <0.6 W identifies the sickest patients who may need mechanical circulatory support early.[11]

3. Obstructive Shock

Pathophysiology: Obstructive shock occurs when mechanical obstruction impedes venous return or cardiac output despite adequate volume and contractility. Classic causes: massive pulmonary embolism (PE), cardiac tamponade, tension pneumothorax, and rarely, severe pulmonary hypertension or abdominal compartment syndrome.[15]

Hemodynamic Profiles:

Condition	CVP	PAOP	CO	Notes
Massive PE	↑	Normal/↓	↓	RV strain, septal shift
Tamponade	↑	↑	↓	Equalization of pressures
Tension PTX	↑	↓	↓	Unilateral absent breath sounds

Clinical Clues:

Massive PE: Dyspnea, chest pain, syncope, hypoxemia, RV strain on ECG (S1Q3T3, RBBB, TWI V1-V4), elevated BNP/troponin
Tamponade: Beck's triad (hypotension, JVD, muffled heart sounds), pulsus paradoxus >10 mmHg, electrical alternans
Tension pneumothorax: Unilateral hyperresonance, tracheal deviation, absent breath sounds, subcutaneous emphysema

Management Principles:

Massive PE:

Anticoagulation: Immediate heparin or LMWH
Thrombolysis: tPA for hemodynamically unstable PE (intermediate-high or high-risk)[16]
Surgical/catheter embolectomy: If thrombolysis contraindicated or failed
VA-ECMO: Bridge to intervention in extremis

Tamponade:

Pericardiocentesis: Emergent, even small volumes (50-100 mL) can dramatically improve hemodynamics
Volume loading: Temporizing measure to increase preload
Avoid: Positive pressure ventilation (worsens venous return)

Tension Pneumothorax:

Needle decompression: 2nd intercostal space, midclavicular line or 5th ICS anterior axillary line (higher success)[17]
Tube thoracostomy: Definitive management

Pearl #4: In obstructive shock, aggressive fluid resuscitation alone is futile—you must relieve the obstruction. However, cautious fluid boluses can temporize while preparing for definitive intervention.

Oyster #3: Not all PEs need thrombolysis. Use risk stratification (sPESI, PESI) and imaging (RV/LV ratio >0.9 on CT, RV dysfunction on echo) to identify candidates. Thrombolysis has 1-2% ICH risk.[16]

4. Distributive Shock

Pathophysiology: Distributive shock is characterized by profound vasodilation and maldistribution of blood flow, leading to relative hypovolemia despite normal or increased cardiac output. The most common form is septic shock, but also includes anaphylactic, neurogenic, and endocrine (adrenal crisis) shock.[18]

Hemodynamic Profile:

↑ Cardiac output (early, hyperdynamic)
↓ SVR (profound vasodilation)
↓ CVP (relative hypovolemia)
Variable ScvO2 (may be paradoxically high due to microcirculatory shunting and impaired oxygen extraction)

Septic Shock—The Paradigm:

Surviving Sepsis Campaign Definition (2021):[19] Sepsis-induced hypotension requiring vasopressors to maintain MAP ≥65 mmHg AND lactate >2 mmol/L despite adequate fluid resuscitation.

Pathophysiology: Dysregulated host response to infection → inflammatory cytokine storm → endothelial dysfunction → vasodilation, capillary leak, microthrombosis, mitochondrial dysfunction.

Clinical Presentation:

Warm shock (early): Bounding pulses, warm extremities, wide pulse pressure, tachycardia, fever
Cold shock (late): Peripheral vasoconstriction, mottled skin, cool extremities (poor prognosis sign)

Management—"Hour-1 Bundle":[19]

Measure lactate, remeasure if >2 mmol/L
Blood cultures before antibiotics
Broad-spectrum antibiotics within 1 hour
Fluid resuscitation: 30 mL/kg crystalloid within 3 hours (controversial—see below)
Vasopressors if hypotensive during or after fluids to maintain MAP ≥65 mmHg

Fluid Resuscitation Controversies:

CLASSIC trial (2022): Restrictive fluids (guided by POCUS) non-inferior to standard care in septic shock[20]
CLOVERS trial (2023): Restrictive fluid strategy showed no mortality difference but less use of mechanical ventilation[21]
Pearl #5: "30 mL/kg for all" is outdated. Individualize fluids using dynamic assessments (passive leg raise, pulse pressure variation, POCUS IVC/lung B-lines) to avoid fluid overload.

Antibiotic Stewardship: De-escalate based on cultures by 48-72 hours. Every hour delay in antibiotics increases mortality by 7-8%.[22]

Vasoactive Agents (see detailed section below):

First-line: Norepinephrine
Second-line: Vasopressin (up to 0.04 U/min) or epinephrine
Adjunct: Corticosteroids if refractory to fluids/vasopressors (hydrocortisone 200 mg/day)[23]

Other Distributive Causes:

Anaphylaxis:

IM epinephrine 0.3-0.5 mg (1:1000) immediately
IV fluids aggressively (capillary leak)
IV epinephrine infusion if refractory
H1/H2 blockers, steroids (adjuncts)

Neurogenic Shock:

High spinal cord injury (T6 or above)
Loss of sympathetic tone → bradycardia + hypotension
Phenylephrine or norepinephrine (avoid excessive beta-agonism)
Maintain MAP 85-90 mmHg for spinal cord perfusion[24]

Pearl #6: In septic shock, ScvO2 can be falsely elevated (>70%) due to impaired tissue oxygen extraction—don't be reassured by a "normal" ScvO2 if lactate remains elevated.

Oyster #4: Not all hypotension in sepsis is distributive shock. Consider concurrent cardiogenic (septic cardiomyopathy), hypovolemic (third-spacing), or obstructive (PE from immobility) components.

Reading the Story on the Monitor

Understanding Hemodynamic Parameters

Critical care hemodynamic monitoring has evolved from simple vital signs to sophisticated multimodal assessment. The key is integrating static and dynamic parameters to guide therapy.

Mean Arterial Pressure (MAP)

Definition: MAP = DBP + (SBP - DBP)/3 or MAP ≈ (2×DBP + SBP)/3

Target: ≥65 mmHg in most shock states (septic shock, distributive)

Higher targets (80-85 mmHg) in chronic hypertension, neurogenic shock, spinal cord injury[24,25]
Lower targets (80-90 mmHg systolic) in uncontrolled hemorrhage ("permissive hypotension")[8]

Physiologic Rationale: MAP drives organ perfusion (cerebral, renal, coronary). Below autoregulatory threshold (~65 mmHg), perfusion becomes pressure-dependent, risking AKI, myocardial ischemia, cerebral hypoperfusion.

Individualization:

SEPSISPAM trial (2014): High MAP target (80-85) vs. standard (65-70) showed no mortality difference overall, but subgroup with chronic HTN had less AKI with higher target[25]
65-MAP trial (2020): Permissive hypotension (60-65 mmHg) in patients >65 years with vasodilatory shock showed no harm (though underpowered)[26]

Pearl #7: MAP is more important than systolic pressure. A narrow pulse pressure (SBP-DBP <25 mmHg) suggests low cardiac output or severe vasoconstriction.

Hack #2: Quick MAP estimate: "Double the diastolic and add 20." (For BP 120/80: 80×2 + 20 = 180/3 ≈ 93).

Central Venous Pressure (CVP)

Definition: Pressure in the superior vena cava/right atrium, reflecting right ventricular preload and intravascular volume status.

Normal Range: 2-8 mmHg (can reference to mid-axillary line or phlebostatic axis)

Traditional Teaching (Outdated): Low CVP (<5 mmHg) = hypovolemia; High CVP (>12 mmHg) = hypervolemia or RV failure.

Modern Understanding: CVP is a poor predictor of fluid responsiveness. A single CVP value tells you little about whether a patient will respond to fluids.[27]

What CVP Can Tell You:

CVP	MAP	Possible Interpretation
Low	Low	Hypovolemic shock (most likely)
High	Low	Cardiogenic shock or RV failure
High	High	Fluid overload or tamponade
Low	High	Distributive shock (vasodilation)

Dynamic CVP Assessment:

CVP waveform analysis: Loss of "y" descent suggests tamponade; prominent "v" waves suggest TR
CVP response to fluid bolus: If CVP rises >5 mmHg and stays elevated, patient is preload-unresponsive (on flat part of Starling curve)

Pearl #8: Don't use CVP in isolation to guide fluid therapy. Use dynamic tests (PLR, PPV, SVV) or POCUS instead.

Oyster #5: High CVP isn't always "overload." In tamponade, massive PE, or tension pneumothorax, CVP is elevated due to obstruction, and fluid may temporarily help (until obstruction relieved).

Central Venous Oxygen Saturation (ScvO2)

Definition: Oxygen saturation of blood in the superior vena cava (or subclavian central line), reflecting the balance between oxygen delivery (DO2) and consumption (VO2).

Normal Range: 70-75% (slightly higher than mixed venous SvO2 from PA catheter, which is 65-70%)

Interpretation:

Low ScvO2 (<70%): Inadequate oxygen delivery or excessive extraction
- Causes: Low CO, anemia, hypoxemia, increased metabolic demand (fever, shivering, pain)
- Action: Increase DO2 (fluids, transfusion, inotropes, oxygen)
High ScvO2 (>80%):
- Good scenario: Adequate resuscitation, normal tissue perfusion
- Bad scenario: Impaired oxygen extraction (septic shock microcirculatory failure, mitochondrial dysfunction, cyanide toxicity, brain death, arteriovenous shunting)

Clinical Application:

Early Goal-Directed Therapy (EGDT): The original Rivers protocol (2001) targeted ScvO2 >70% with fluids, transfusion, and inotropes, showing mortality benefit in severe sepsis.[28]

Modern Evidence: Three large trials (ProCESS, ARISE, ProMISe) showed no benefit of protocolized EGDT vs. usual care, but usual care had improved (faster antibiotics, earlier fluids).[29] ScvO2 still useful as one monitoring parameter among many.

Pearl #9: ScvO2 trends are more useful than absolute values. A declining ScvO2 suggests worsening shock; an increasing ScvO2 suggests improving oxygen delivery or resolving shock.

Hack #3: No central line? Use the "eyeball" ScvO2 rule: If peripheral perfusion is poor (mottled, cold), ScvO2 is likely low. If warm and bounding, ScvO2 may be adequate or paradoxically high (distributive shock).

Advanced Hemodynamic Parameters

Cardiac Output (CO) Monitoring:

Methods: Pulmonary artery catheter (PAC) thermodilution, arterial pulse contour analysis (PiCCO, FloTrac), echocardiography, non-invasive CO monitoring
Utility: Differentiates low CO (cardiogenic, hypovolemic) from high CO (early distributive) shock

Dynamic Indices of Fluid Responsiveness:[30]

Pulse Pressure Variation (PPV): >13% suggests fluid responsive (requires mechanical ventilation, tidal volume >8 mL/kg, sinus rhythm)
Stroke Volume Variation (SVV): >10-13% suggests fluid responsive (same limitations as PPV)
Passive Leg Raise (PLR): Increase in CO >10% predicts fluid responsiveness (gold standard dynamic test, fewer limitations)

Pearl #10: PPV and SVV are unreliable in spontaneously breathing patients, arrhythmias, low tidal volumes, or open abdomen. Use PLR or POCUS IVC/VTI assessment instead.

Integrative Hemodynamic Approach

The "Hemodynamic Crosswalk":

Shock Type	MAP	CVP	CO	SVR	ScvO2
Hypovolemic	↓	↓	↓	↑	↓
Cardiogenic	↓	↑	↓	↑	↓
Obstructive	↓	↑ (variable)	↓	↑	↓
Distributive	↓	↓	↑ (early) / ↓ (late)	↓	↑ or ↓

Oyster #6: Real patients don't read textbooks. Mixed shock states are common (e.g., septic shock with septic cardiomyopathy, hemorrhagic shock with neurogenic component in trauma). Reassess frequently as hemodynamic profile evolves.

First-Line Vasoactive Drugs: Which, When, and Why?

Vasoactive drugs are the cornerstone of shock management, acting on adrenergic and non-adrenergic receptors to modulate vascular tone, cardiac contractility, and heart rate. Choosing the right agent requires understanding receptor pharmacology, shock physiology, and patient-specific factors.

Adrenergic Receptor Primer

Receptor	Location	Effect
α1	Vascular smooth muscle	Vasoconstriction (↑ SVR)
β1	Cardiac myocytes	↑ HR, ↑ contractility (↑ CO)
β2	Vascular smooth muscle (skeletal), bronchi	Vasodilation, bronchodilation
Dopamine (DA1)	Renal/splanchnic vessels	Vasodilation

Norepinephrine (Levophed)

Receptor Profile: α1 >>> β1 > β2

Hemodynamic Effects:

Potent vasoconstriction (↑ MAP, ↑ SVR)
Mild inotropy (↑ CO)
Minimal chronotropy (HR unchanged or ↓ via baroreceptor reflex)

Indications:

First-line for septic shock and most distributive shock[19]
Cardiogenic shock with hypotension (MAP <65 mmHg)
Neurogenic shock

Dosing: 0.05-0.3 mcg/kg/min (typical), up to 3 mcg/kg/min in refractory shock

Advantages:

Restores MAP without excessive tachycardia
Preserved or improved renal perfusion (due to MAP increase)
Most evidence in septic shock

Disadvantages:

Peripheral vasoconstriction can worsen tissue perfusion in extremities
High doses increase myocardial oxygen demand
Risk of extravasation injury (central line mandatory)

Pearl #11: Norepinephrine is the "pressor of choice" for septic shock. Start early if MAP <65 mmHg despite initial fluids—don't wait for "full" resuscitation.

Epinephrine (Adrenaline)

Receptor Profile: β1 ≈ α1 > β2 (dose-dependent)

Hemodynamic Effects:

Strong inotropy and chronotropy (↑↑ CO)
Vasoconstriction (↑ MAP) at higher doses
β2 vasodilation in low doses

Indications:

Anaphylactic shock (drug of choice)
Cardiac arrest (ACLS)
Refractory septic shock (second-line after norepinephrine ± vasopressin)
Cardiogenic shock with severe hypotension

Dosing:

Anaphylaxis: 0.3-0.5 mg IM (1:1000), repeat q5-15min
Infusion: 0.05-0.5 mcg/kg/min

Advantages:

Powerful combined inotrope and pressor
Rapid onset

Disadvantages:

Significant tachycardia (↑ myocardial O2 demand, arrhythmias)
Hyperglycemia (β2-mediated glycogenolysis)
Lactic acidosis (type B, from β2-mediated aerobic glycolysis—NOT tissue hypoxia)[31]
Splanchnic hypoperfusion

Pearl #12: Epinephrine causes "pseudo-shock" lactate elevation via β2 stimulation. If lactate rises but perfusion markers improve (ScvO2, urine output, mentation), consider epinephrine-induced lactate, not worsening shock.

Oyster #7: In cardiac arrest, epinephrine improves ROSC but may not improve neurologically intact survival. Use as per ACLS, but temper expectations.[32]

Vasopressin

Mechanism: Non-adrenergic; acts on V1 receptors (vascular smooth muscle) → vasoconstriction

Hemodynamic Effects:

Vasoconstriction without inotropic or chronotropic effects
Preserves renal and splanchnic blood flow (relative selectivity)

Indications:

Second-line agent in septic shock (in addition to norepinephrine)[19,23]
Catecholamine-refractory shock
Post-cardiac surgery vasoplegic shock

Dosing: 0.01-0.04 U/min (fixed dose, not titrated)

Evidence:

VASST trial (2008): Vasopressin + norepinephrine vs. norepinephrine alone showed no mortality difference overall, but mortality benefit in less severe shock subgroup[33]
VANISH trial (2016): Vasopressin vs. norepinephrine as first-line showed equivalence; vasopressin reduced need for RRT[34]

Advantages:

Catecholamine-sparing (reduces norepinephrine dose)
No tachycardia or increased myocardial O2 demand
May reduce AKI/RRT

Disadvantages:

Coronary, mesenteric, and peripheral vasoconstriction (risk of ischemia)
No role in hypovolemic or hemorrhagic shock (may worsen ischemia)
Expensive

Pearl #13: Add vasopressin when norepinephrine dose >0.25-0.5 mcg/kg/min. The "vasopressin-sparing effect" can significantly reduce catecholamine requirements.

Hack #4: Vasopressin is dosed as a fixed rate (0.04 U/min max), NOT titrated like other pressors. Think of it as an "on/off" adjunct.

Dobutamine

Receptor Profile: β1 >> β2 > α1

Hemodynamic Effects:

Strong inotropy (↑↑ contractility)
Mild chronotropy (↑ HR)
Vasodilation (↓ SVR via β2)
Net effect: ↑ CO, ± MAP

Indications:

Cardiogenic shock with low CO, especially if not severely hypotensive (MAP >70 mmHg)
Septic shock with low CO despite adequate MAP (after norepinephrine)
Heart failure with reduced ejection fraction (decompensated)

Dosing: 2-20 mcg/kg/min

Advantages:

Improves cardiac output and tissue perfusion
Less tachycardia than epinephrine or dopamine

Disadvantages:

Can worsen hypotension (vasodilation) if used alone
Increased myocardial O2 demand (arrhythmias, ischemia)
Tachyphylaxis (desensitization with prolonged use)

Pearl #14: In cardiogenic shock, pair dobutamine with a vasopressor (norepinephrine) to maintain MAP while improving CO. Don't use dobutamine alone if MAP <70 mmHg.

Oyster #8: Dobutamine can unmask latent LV outflow tract obstruction (LVOTO) in HCM or Takotsubo cardiomyopathy. If hypotension worsens paradoxically with dobutamine, suspect LVOTO and stop the drug.

Phenylephrine (Neo-Synephrine)

Receptor Profile: α1 (pure)

Hemodynamic Effects:

Pure vasoconstriction (↑↑ SVR, ↑ MAP)
Reflex bradycardia (↓ HR)
No inotropic effect (CO may decrease)

Indications:

Hypotension with tachycardia (neurogenic shock, anesthesia-induced hypotension)
Avoid in septic shock (inferior to norepinephrine)[35]
Temporary measure when other agents unavailable

Dosing: 0.5-3 mcg/kg/min

Advantages:

Slows HR (useful if tachycardia problematic)
Peripheral line compatible (short-term)

Disadvantages:

Decreases CO (reflex bradycardia + no inotropy)
Inferior to norepinephrine in septic shock outcomes[35]

Pearl #15: Phenylephrine is useful in neurogenic shock where bradycardia is already present. It's the "anti-tachycardia pressor."

Dopamine

Receptor Profile: Dose-dependent

Low (1-3 mcg/kg/min): DA1 (renal vasodilation)
Medium (3-10): β1 (inotropy, chronotropy)
High (>10): α1 (vasoconstriction)

Hemodynamic Effects: Variable based on dose

Indications:

Historically used for septic shock; now fallen out of favor
Bradycardic shock (relative to other agents)

Evidence:

SOAP II trial (2010): Dopamine vs. norepinephrine in shock showed more arrhythmias and higher mortality with dopamine[36]
"Low-dose dopamine" for renal protection is a myth—no benefit shown[37]

Disadvantages:

Arrhythmogenic (especially atrial fibrillation)
Significant tachycardia
Higher mortality vs. norepinephrine

Pearl #16: Dopamine is obsolete for most shock states. Use norepinephrine instead. The only remaining niche is symptomatic bradycardia with hypotension where pacing unavailable.

Oyster #9: "Low-dose dopamine" (1-3 mcg/kg/min) does NOT protect kidneys or improve renal outcomes. Abandon this practice.

Milrinone

Mechanism: Phosphodiesterase-3 (PDE3) inhibitor → ↑ cAMP → inotropy and vasodilation

Hemodynamic Effects:

Inotropy (↑ CO)
Lusitropy (improved relaxation, useful in diastolic dysfunction)
Vasodilation (↓ SVR)

Indications:

Cardiogenic shock in beta-blocked patients (dobutamine ineffective)
RV failure (pulmonary vasodilator)
"Cold and wet" decompensated heart failure

Dosing: Loading 25-50 mcg/kg over 10-20 min, then 0.25-0.75 mcg/kg/min

Advantages:

Bypasses beta-receptors (works despite beta-blockade)
Pulmonary vasodilation (reduces RV afterload)
No tachyphylaxis

Disadvantages:

Significant vasodilation (can worsen hypotension)
Long half-life (consider loading dose carefully)
Thrombocytopenia (rare)
Arrhythmias (less than dobutamine)

Pearl #17: Milrinone is the inotrope of choice when patients are on chronic beta-blockers (which blunt dobutamine effects). Always co-administer with a vasopressor to counteract vasodilation.

Vasoactive Drug Selection Algorithm

Step 1: Identify shock type and hemodynamic target

Step 2: Choose first-line agent

Shock Type	First-Line Agent	Rationale
Septic/Distributive	Norepinephrine	↑ MAP via vasoconstriction; preserved CO
Cardiogenic	Dobutamine + Norepinephrine	↑ CO (dobutamine) + maintain MAP (NE)
Hypovolemic	Fluids ± Norepinephrine	Volume first; pressor only if refractory
Obstructive	Relieve obstruction + temporize with NE	Pressors buy time; must fix obstruction
Anaphylactic	Epinephrine	Reverses mast cell mediators; bronchodilation
Neurogenic	Phenylephrine or Norepinephrine	↑ MAP without excess tachycardia

Step 3: Add second-line agents if refractory

Septic shock: Add vasopressin (0.04 U/min) if NE >0.5 mcg/kg/min
Cardiogenic shock: Consider milrinone if beta-blocked; mechanical support if refractory
Distributive shock: Add epinephrine if NE + vasopressin insufficient

Step 4: Consider adjuncts

Corticosteroids: Hydrocortisone 200 mg/day (continuous or divided) if catecholamine-refractory septic shock[23]
Methylene blue: Rescue for refractory vasoplegic shock (post-cardiac surgery); 1-2 mg/kg bolus[38]
Angiotensin II: FDA-approved for catecholamine-resistant distributive shock (ATHOS-3 trial)[39]; very expensive, limited availability

Pearl #18: Never delay source control (antibiotics for sepsis, PCI for MI, surgery for perforation) while optimizing pressors. Pressors buy time—definitive therapy saves lives.

Hack #5: Memory aid for pressor choice: "Needs Pressure? Norepinephrine Please!" (Most shock = NE first)

Common Pitfalls in Vasoactive Drug Use

Pitfall #1: Starting pressors through peripheral IV

Risk: Extravasation → tissue necrosis
Solution: Central line mandatory for continuous infusions (except short-term phenylephrine in OR)

Pitfall #2: Using dopamine instead of norepinephrine

Risk: Increased arrhythmias, mortality
Solution: Default to norepinephrine for septic shock

Pitfall #3: Delaying vasopressor initiation

Risk: Prolonged hypotension worsens outcomes
Solution: Start NE early if MAP <65 mmHg despite initial fluids (don't wait for "30 mL/kg")

Pitfall #4: Over-resuscitating with fluids to "avoid pressors"

Risk: Fluid overload, pulmonary edema, abdominal compartment syndrome
Solution: Pressors are not evil—use early, wean as able

Pitfall #5: Ignoring underlying pathophysiology

Risk: Using inotropes in obstructive shock without relieving obstruction
Solution: Definitive therapy first; pressors as bridge

Oyster #10: In refractory shock on multiple pressors, consider non-hemodynamic causes: adrenal insufficiency, hypothyroidism, severe acidosis (pH <7.0), profound hypocalcemia, or carbon monoxide/cyanide toxicity.

Ultrasound: Your Bedside Guide to Shock

Point-of-care ultrasound (POCUS) has revolutionized shock management, transforming hemodynamic assessment from invasive, delayed, and discontinuous to non-invasive, immediate, and dynamic. Echocardiography and extended POCUS protocols allow real-time diagnosis and therapeutic guidance.[40]

POCUS Protocols for Shock

RUSH Exam (Rapid Ultrasound in Shock):[41] Systematic evaluation in three steps:

"The Pump" (heart)
"The Tank" (volume status: IVC, lungs)
"The Pipes" (aorta, DVT)

ACES Protocol (Abdominal and Cardiac Evaluation with Sonography):

Cardiac windows
IVC assessment
FAST (Focused Assessment with Sonography for Trauma)
Aorta
Pneumothorax

BLUE Protocol (Bedside Lung Ultrasound in Emergency):[42] Lung ultrasound to differentiate pulmonary edema, pneumothorax, pneumonia, PE

Cardiac Ultrasound in Shock

Essential Views:

Parasternal long-axis (PLAX): LV size, function, wall motion, valves
Parasternal short-axis (PSAX): RV size, septal motion, LV function
Apical 4-chamber (A4C): Global LV/RV function, valves, pericardial effusion
Subcostal (SC): Pericardial effusion, IVC, RV assessment

Key Findings by Shock Type

Hypovolemic Shock

"Kissing ventricle" sign: Near-complete LV collapse in diastole (severe hypovolemia)
Hyperdynamic LV: Vigorous contraction, small chamber
Flat/collapsing IVC: <1.5 cm diameter, >50% collapse with inspiration (suggests low CVP)

Pearl #19: "Small and squeezing hard" suggests hypovolemia. Give fluid and reassess.

Cardiogenic Shock

Reduced LV systolic function: Eyeball EF <40%, or formal measurement
LV dilation: LV end-diastolic dimension >5.5 cm
Regional wall motion abnormalities (RWMA): Suggest acute MI
B-lines on lung US: Diffuse bilateral B-lines = pulmonary edema
Dilated IVC: >2 cm with <50% inspiratory collapse (high CVP)

Advanced Assessment:

Mitral inflow Doppler: E/A reversal, prolonged deceleration time (diastolic dysfunction)
Tissue Doppler (e'): e' <7 cm/s suggests diastolic dysfunction
VTI (Velocity Time Integral) at LVOT: Estimate stroke volume and CO
- Normal VTI: 18-22 cm
- Low VTI (<15 cm) suggests low stroke volume

Pearl #20: Calculate stroke volume: SV = VTI × LVOT CSA (cross-sectional area). CO = SV × HR. Track VTI serially to assess fluid responsiveness or inotrope response.

Hack #6: Eyeball fractional shortening (FS) in M-mode PSAX: FS = (LVEDD - LVESD)/LVEDD. Normal >30%. Quick and reproducible for serial assessments.

Obstructive Shock

Massive PE:

RV dilation: RV:LV ratio >0.9 in A4C or >0.6 in PSAX (McConnell's sign)
McConnell's sign: RV free wall hypokinesis with preserved apical motion (60% specific for PE)[43]
Septal flattening/bowing ("D-sign"): In PSAX, suggests RV pressure overload
Tricuspid regurgitation: Estimate RV systolic pressure (RVSP = 4 × [TR jet velocity]² + RA pressure)

Pearl #21: A normal echo doesn't rule out PE—it rules out hemodynamically significant PE. If RV looks normal, PE is unlikely to be causing shock.

Cardiac Tamponade:

Pericardial effusion: Circumferential, echo-free space
Diastolic RA collapse: Early sign, high sensitivity
Diastolic RV collapse: More specific for tamponade physiology
Respiratory variation in mitral/tricuspid inflow: >25% variation with respiration
Swinging heart: Heart oscillates within large effusion
Dilated IVC with no respiratory variation: Plethoric IVC

Pearl #22: Size of effusion doesn't predict tamponade—small loculated effusions (post-cardiac surgery) can cause tamponade. Look for chamber collapse and hemodynamic compromise.

Tension Pneumothorax:

Absence of lung sliding: At pleural line (M-mode shows "barcode sign" instead of "seashore sign")
Absence of B-lines: Pneumothorax has no B-lines (vs. pulmonary edema)
Lung point: Where normal lung meets pneumothorax (specific sign)

Distributive Shock (Septic)

Cardiac Findings:

Hyperdynamic LV initially: Normal or high EF, high VTI
Septic cardiomyopathy (later): Reduced EF, low VTI (seen in 40-60% of septic shock)[44]
Dilated, fluid-filled IVC: If aggressively fluid resuscitated

Lung Findings:

B-lines (variable): Can indicate ARDS, pulmonary edema from fluid overload
Consolidations: Pneumonia as sepsis source

Pearl #23: Septic cardiomyopathy is typically reversible (resolves in days-weeks). Don't assume chronic heart failure; reassess after recovery.

IVC Assessment for Volume Status

Measurement:

Subcostal view, measure IVC diameter 2 cm proximal to hepatic vein junction
Assess respiratory variation (collapsibility in spontaneous breathing, distensibility in mechanical ventilation)

Spontaneously Breathing Patients:

IVC Diameter	Collapsibility with Sniff	Estimated CVP	Interpretation
<1.5 cm	>50%	0-5 mmHg	Low volume
1.5-2.5 cm	>50%	5-10 mmHg	Normal
1.5-2.5 cm	<50%	10-15 mmHg	Elevated
>2.5 cm	<50%	15-20 mmHg	High volume or RV failure

Mechanically Ventilated Patients:

IVC distensibility index (IVC-DI): (IVCmax - IVCmin) / IVCmin × 100%
IVC-DI >18% suggests fluid responsiveness (less reliable than PLR or PPV)

Limitations:

IVC size correlates poorly with fluid responsiveness in many studies[45]
Elevated intra-abdominal pressure falsely dilates IVC
RV failure, TR, cardiac tamponade cause plethoric IVC despite hypovolemia

Pearl #24: IVC is best used to identify extremes: collapsed IVC suggests low CVP/hypovolemia; plethoric IVC suggests high CVP or RV dysfunction. The middle range is ambiguous.

Lung Ultrasound: The "Pulmonary Physical Exam"

Normal Lung:

Lung sliding: Pleura moves with respiration ("seashore sign" on M-mode)
A-lines: Horizontal artifacts (reverberation of pleural line)

Pathologic Findings:

B-Lines (Comet Tails):

Vertical hyperechoic artifacts extending from pleura to screen edge
Focal B-lines: Pneumonia, contusion, infarct
Diffuse bilateral B-lines: Pulmonary edema (cardiogenic shock, ARDS, fluid overload)

Consolidation:

Hepatization: Lung appears solid, "liver-like"
Air bronchograms: Hyperechoic streaks within consolidation
Indicates: Pneumonia, atelectasis, ARDS

Pleural Effusion:

Anechoic (black) space between lung and chest wall
Sinusoid sign: Floating atelectatic lung
Can estimate size: Large if >5 cm in dependent area

Pneumothorax:

Absent lung sliding
No B-lines (B-lines rule out PTX at that location)
Lung point: Transition between normal lung and PTX
A-lines present (but A-lines alone don't diagnose PTX—need absent sliding)

Pearl #25: "No B-lines, no pulmonary edema"—B-lines are >90% sensitive for interstitial syndrome. Absence of B-lines in dyspneic patient points away from cardiogenic pulmonary edema.

Dynamic Assessment: Fluid Responsiveness

Passive Leg Raise (PLR) Test:[46]

Move patient from semi-recumbent (45°) to supine with legs elevated 45°
Measure CO change (via VTI, LVOT Doppler, or arterial pulse contour)
Positive test: ↑ CO or VTI >10% within 60 seconds predicts fluid responsiveness
Advantages: Works in spontaneously breathing patients, arrhythmias, any position
Limitations: Don't use in IAH, leg fractures, DVT; must measure CO change (not just BP)

VTI Response to Fluid Bolus:

Measure LVOT VTI before and after 250-500 mL fluid bolus (or PLR)
Positive: ↑ VTI >10% suggests fluid responsiveness
Serial measurements guide ongoing resuscitation

Pearl #26: POCUS-guided fluid therapy: Measure VTI → Give fluid challenge or PLR → Remeasure VTI. If ↑ >10%, patient is fluid responsive. If no change, stop fluids and reassess cause of shock.

Hack #7: "VTI is the new CVP"—use VTI trends to guide therapy, not static CVP measurements.

Integrating POCUS into Shock Management

Step 1: Initial RUSH exam (5 minutes)

Identify gross cardiac dysfunction, pericardial effusion, RV strain, IVC size

Step 2: Categorize shock type

Hyperdynamic + low IVC = distributive
Reduced EF + dilated IVC + B-lines = cardiogenic
Small ventricle + kissing walls = hypovolemic
RV strain = obstructive (PE, tamponade, tension PTX)

Step 3: Assess fluid responsiveness

PLR test with VTI measurement or IVC assessment

Step 4: Serial reassessment

Repeat focused scans q1-4h or after interventions
Track VTI, IVC, B-lines, cardiac function

Oyster #11: POCUS doesn't replace comprehensive TEE or formal echocardiography—if findings are unclear or unexplained, consult cardiology/critical care echo experts.

Advanced Concepts and Controversies

The "Starling Curve" and Fluid Optimization

Frank-Starling principle: Cardiac output increases with preload (up to a point), then plateaus. The goal is to identify where the patient is on the curve.

Steep part of curve: Fluid responsive
Flat part of curve: Fluid unresponsive (risk of overload)

Dynamic tests (PLR, PPV, VTI changes) identify position on curve better than static pressures (CVP).

Microcirculatory Dysfunction in Septic Shock

Septic shock isn't just "low blood pressure"—it's microcirculatory failure. Even with restored MAP and CO, microvascular shunting, endothelial dysfunction, and mitochondrial impairment cause tissue hypoxia.[47]

Implications:

ScvO2 can be falsely reassuring (high due to shunting, low extraction)
Lactate may remain elevated despite "adequate" resuscitation
Emerging technologies (sublingual videomicroscopy) show promise but not yet standard

Pearl #27: Resuscitation endpoints should be multimodal: MAP, lactate clearance, ScvO2, urine output, capillary refill, and mental status—not just one parameter.

Balanced Resuscitation and Avoiding Fluid Overload

The "Ebb and Flow" Model:[48]

Ebb phase (early shock): Hypovolemia, hypoperfusion → needs fluids
Flow phase (recovery): Capillary leak resolves, fluid mobilizes → needs diuresis

Consequences of Fluid Overload:

Pulmonary edema, prolonged mechanical ventilation
Abdominal compartment syndrome
AKI (venous congestion)
Delayed wound healing

Strategies:

Restrictive fluids after initial resuscitation[20,21]
Early diuresis/de-resuscitation once stable
POCUS-guided fluid stops

Oyster #12: Positive fluid balance at 72 hours is associated with increased mortality in septic shock. After initial resuscitation, shift focus to "de-resuscitation."[49]

Hydrocortisone in Septic Shock

Evidence:

CORTICUS (2008): No mortality benefit[50]
HYPRESS (2016): Faster shock reversal, no mortality benefit
ADRENAL (2018): No 90-day mortality benefit; faster shock resolution, less transfusion[23]
APROCCHSS (2018): Hydrocortisone + fludrocortisone reduced 90-day mortality in severe septic shock[51]

Current Recommendation (SSC 2021):[19]

Use: Hydrocortisone 200 mg/day (continuous or divided) if fluids and vasopressors inadequately restore hemodynamic stability
Do not use: ACTH stimulation testing (no longer recommended)

Pearl #28: Steroids don't reduce mortality in most septic shock but speed shock reversal and reduce vasopressor duration. Consider if catecholamine-refractory (NE >0.5 mcg/kg/min).

Angiotensin II for Catecholamine-Resistant Shock

ATHOS-3 Trial (2017):[39] Synthetic angiotensin II increased MAP and reduced catecholamine dose in distributive shock refractory to high-dose vasopressors.

Indications:

Catecholamine-resistant distributive shock
Consider when on norepinephrine >0.5 mcg/kg/min + vasopressin + epinephrine

Limitations:

Very expensive
Limited availability
Thrombotic risk

Pearl #29: Angiotensin II is a "rescue" therapy for refractory vasoplegic shock. Not first-line, but can be lifesaving when all else fails.

Extracorporeal Support in Refractory Shock

ECMO (Extracorporeal Membrane Oxygenation):

VA-ECMO (Veno-Arterial):

Indication: Cardiogenic shock refractory to medical therapy
Mechanism: Provides both cardiac and respiratory support
Complications: Limb ischemia, bleeding, infection, LV distension (increased afterload)
Bridge: To transplant, LVAD, or recovery

VV-ECMO (Veno-Venous):

Respiratory failure only (ARDS), not for shock

Impella:

Percutaneous LV support device
Indication: Cardiogenic shock (typically during high-risk PCI or as bridge)
Levels: Impella 2.5, CP, 5.0, 5.5 (increasing flow rates)

Pearl #30: Early consultation with cardiac surgery/ECMO team is critical. Don't wait until patient is moribund—by then, they may not be a candidate.

Putting It All Together: A Case-Based Approach

Case 1: Septic Shock

Presentation: 65F with fever, hypotension (BP 75/40), HR 125, RR 28, altered mentation. Urinary source suspected.

Initial Management:

Blood cultures, broad-spectrum antibiotics (within 1 hour)
Lactate: 5.2 mmol/L
Fluid bolus: 1L LR over 30 min
Reassess: BP 82/50, MAP 60, lactate 4.8
Start norepinephrine (central line), titrate to MAP ≥65 mmHg
POCUS: Hyperdynamic LV, no B-lines, flat IVC → consistent with distributive shock
Source control: Urology consult for possible obstructed pyelonephritis
Monitor: ScvO2 62% → continues rising to 70% over 2 hours; lactate clearing

Pearl: Early antibiotics and source control are paramount. Pressors started early once fluids don't restore MAP.

Case 2: Cardiogenic Shock

Presentation: 58M with crushing chest pain, BP 85/60, HR 110, cool extremities, pulmonary rales.

Initial Management:

ECG: ST-elevation anterior MI
Emergent cath lab activation
POCUS: Reduced EF (~30%), anterior wall akinesis, B-lines bilaterally
Start norepinephrine to MAP ≥65
Avoid aggressive fluids (will worsen pulmonary edema)
PCI with stenting LAD
Post-PCI: Add dobutamine (5 mcg/kg/min) for low CO, wean NE
Diurese gently once perfusion improved

Pearl: Revascularization is the priority. Pressors/inotropes are a bridge to definitive therapy.

Case 3: Massive PE with Obstructive Shock

Presentation: 72M postoperative day 5 hip replacement, sudden dyspnea, hypotension 80/50, HR 130, hypoxemia.

Initial Management:

POCUS: RV dilation (RV/LV ratio 1.2), McConnell's sign, no pericardial effusion
Diagnosis: Massive PE
CTA chest: Bilateral central PE
Start heparin drip
Norepinephrine to maintain MAP
Thrombolysis: Alteplase 100 mg over 2 hours (hemodynamically unstable PE)
Improvement in BP and RV function within hours

Pearl: POCUS made diagnosis rapidly—didn't wait for CT. Thrombolysis is lifesaving in hemodynamically unstable PE.

Summary: Key Takeaways for the Clinician

Shock is a syndrome of tissue hypoperfusion, not just hypotension.
The four types (hypovolemic, cardiogenic, obstructive, distributive) guide diagnosis and management, but mixed shock is common.
MAP ≥65 mmHg is the target for most shock states, individualized based on chronic BP and comorbidities.
CVP alone is inadequate for guiding fluid therapy—use dynamic assessments (PLR, VTI, PPV).
ScvO2 trends guide resuscitation, but interpret in context (can be falsely elevated in distributive shock).
Norepinephrine is first-line for septic shock; add vasopressin if refractory.
Dobutamine + norepinephrine for cardiogenic shock; early revascularization/mechanical support if refractory.
Relieve obstruction in obstructive shock—pressors alone are insufficient.
POCUS is transformative: Rapid diagnosis, dynamic assessment, and serial monitoring at the bedside.
Avoid fluid overload: After initial resuscitation, restrictive fluids and early diuresis improve outcomes.

Clinical Pearls and Oysters: At a Glance

#	Pearl/Oyster
1	Shock = inadequate perfusion, not just low BP
2	Permissive hypotension in trauma until bleeding controlled
3	In cardiogenic shock, don't fluid overload—use POCUS
4	In obstructive shock, relieve obstruction first
5	High CVP isn't always fluid overload (tamponade, PE)
6	High ScvO2 in sepsis may mean impaired extraction, not adequate perfusion
7	MAP > systolic BP; narrow pulse pressure suggests low CO
8	CVP doesn't predict fluid responsiveness—use dynamic tests
9	ScvO2 trends > absolute values
10	PPV/SVV unreliable if spontaneous breathing or low tidal volumes
11	Norepinephrine is first-line for septic shock—start early
12	Epinephrine causes "pseudo-shock" lactate (not tissue hypoxia)
13	Add vasopressin when NE >0.25-0.5 mcg/kg/min
14	Dobutamine + NE for cardiogenic shock; don't use dobutamine alone if MAP low
15	Phenylephrine is "anti-tachycardia pressor" (neurogenic shock)
16	Dopamine is obsolete—use norepinephrine
17	Milrinone for cardiogenic shock in beta-blocked patients
18	Pressors buy time—definitive therapy saves lives
19	"Small and squeezing" LV on echo suggests hypovolemia
20	Track VTI serially to assess fluid/inotrope response
21	Normal RV on echo rules out hemodynamically significant PE
22	Effusion size ≠ tamponade severity; look for chamber collapse
23	Septic cardiomyopathy is reversible
24	IVC best for extremes (collapsed vs. plethoric), not middle range
25	No B-lines = no pulmonary edema (high sensitivity)
26	VTI-guided fluid therapy: Δ >10% = fluid responsive
27	Multimodal endpoints: MAP, lactate, ScvO2, urine, cap refill, mentation
28	Steroids speed shock reversal in refractory septic shock, no mortality benefit
29	Angiotensin II is rescue therapy for catecholamine-resistant shock
30	Early ECMO consultation—don't wait until patient moribund

Hacks for the Busy Clinician

Quick MAP estimate: Double DBP + 20
CPO calculation: MAP × CO / 451 (CPO <0.6 W = high mortality)
"VTI is the new CVP": Track VTI trends, not CVP
Eyeball EF: Fractional shortening in M-mode (normal >30%)
Pressor mnemonic: "Needs Pressure? Norepinephrine Please!"
Vasopressin dosing: Fixed 0.04 U/min (not titrated)
VTI response: Measure before/after PLR or fluid bolus (>10% = responsive)

Conclusion

Shock remains one of the most challenging and time-sensitive conditions in critical care. Success depends on rapid recognition, accurate classification, and goal-directed resuscitation tailored to the underlying pathophysiology. The integration of clinical assessment, invasive hemodynamic monitoring, and especially point-of-care ultrasound has equipped the modern intensivist with powerful tools to diagnose and manage shock at the bedside.

Mastery of hemodynamic principles—understanding preload, afterload, contractility, and their interplay—is foundational. Equally important is knowing which vasoactive drug to reach for and when, guided by the specific shock state and hemodynamic profile. As we move forward, precision medicine approaches, biomarker-guided therapy, and advanced monitoring techniques will continue to refine our management strategies.

For the critical care trainee, the journey from shock recognition to successful resuscitation is both intellectually demanding and deeply rewarding. By internalizing the concepts presented here and practicing systematic bedside evaluation, clinicians can dramatically improve outcomes for their sickest patients. Remember: shock is a race against time, but with the right tools and knowledge, it is a race we can win.

References

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734.
Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Intensive Care Med. 2014;40(12):1795-1815.
Monnet X, Teboul JL. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care. 2011;1(1):1.
Levitov A, Marik PE. Echocardiographic assessment of preload responsiveness in critically ill patients. Cardiol Res Pract. 2012;2012:819696.
Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care. 2004;8(5):373-381.
Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829-839.
Carson JL, Stanworth SJ, Dennis JA, et al. Transfusion thresholds for guiding red blood cell transfusion. Cochrane Database Syst Rev. 2021;12:CD002042.
Kwan I, Bunn F, Chinnock P, Roberts I. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev. 2014;(3):CD002245.
Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma. JAMA. 2015;313(5):471-482.
van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock. Circulation. 2017;136(16):e232-e268.
Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock. J Am Coll Cardiol. 2004;44(2):340-348.
Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update. J Am Coll Cardiol. 2022;79(9):933-946.
Thiele H, Akin I, Sandri M, et al. PCI strategies in patients with acute myocardial infarction and cardiogenic shock. N Engl J Med. 2017;377(25):2419-2432.
Schrage B, Becher PM, Bernhardt A, et al. Left ventricular unloading is associated with lower mortality in patients with cardiogenic shock treated with venoarterial extracorporeal membrane oxygenation. Circulation. 2020;142(22):2095-2106.
Harjola VP, Mebazaa A, Čelutkienė J, et al. Contemporary management of acute right ventricular failure. Eur Heart J. 2016;37(27):2104-2124.
Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603.
Aho JM, Thiels CA, El Khatib MM, et al. Needle thoracostomy: clinical effectiveness is improved using a longer angiocatheter. J Trauma Acute Care Surg. 2016;80(2):272-277.
Annane D, Bellissant E, Cavaillon JM. Septic shock. Lancet. 2005;365(9453):63-78.
Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021;47(11):1181-1247.
Meyhoff TS, Hjortrup PB, Wetterslev J, et al. Restriction of intravenous fluid in ICU patients with septic shock. N Engl J Med. 2022;386(26):2459-2470.
Shapiro NI, Douglas IS, Brower RG, et al. Early restrictive or liberal fluid management for sepsis-induced hypotension. N Engl J Med. 2023;388(6):499-510.
Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589-1596.
Venkatesh B, Finfer S, Cohen J, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med. 2018;378(9):797-808.
Ryken TC, Hurlbert RJ, Hadley MN, et al. The acute cardiopulmonary management of patients with cervical spinal cord injuries. Neurosurgery. 2013;72(Suppl 2):84-92.
Asfar P, Meziani F, Hamel JF, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med. 2014;370(17):1583-1593.
Lamontagne F, Richards-Belle A, Thomas K, et al. Effect of reduced exposure to vasopressors on 90-day mortality in older critically ill patients with vasodilatory hypotension. JAMA. 2020;323(10):938-949.
Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? Chest. 2008;134(1):172-178.
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.
ARISE Investigators, ANZICS Clinical Trials Group. Goal-directed resuscitation for patients with early septic shock. N Engl J Med. 2014;371(16):1496-1506.
Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update. Ann Intensive Care. 2016;6(1):111.
Levy B, Bollaert PE, Charpentier C, et al. Comparison of norepinephrine and dobutamine to epinephrine for hemodynamics, lactate metabolism, and gastric tonometric variables in septic shock. Intensive Care Med. 1997;23(3):282-287.
Perkins GD, Ji C, Deakin CD, et al. A randomized trial of epinephrine in out-of-hospital cardiac arrest. N Engl J Med. 2018;379(8):711-721.
Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl J Med. 2008;358(9):877-887.
Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock. JAMA. 2016;316(5):509-518.
Morelli A, Ertmer C, Westphal M, et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock. JAMA. 2013;310(16):1683-1691.
De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789.
Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Lancet. 2000;356(9248):2139-2143.
Levin RL, Degrange MA, Bruno GF, et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg. 2004;77(2):496-499.
Khanna A, English SW, Wang XS, et al. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med. 2017;377(5):419-430.
Lichtenstein DA. BLUE-protocol and FALLS-protocol: two applications of lung ultrasound in the critically ill. Chest. 2015;147(6):1659-1670.
Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically ill. Emerg Med Clin North Am. 2010;28(1):29-56.
Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-125.
McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996;78(4):469-473.
Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984;100(4):483-490.
Orso D, Paoli I, Piani T, et al. Accuracy of ultrasonographic measurements of inferior vena cava to determine fluid responsiveness: a systematic review and meta-analysis. J Intensive Care Med. 2020;35(4):354-363.
Monnet X, Marik P, Teboul JL. Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis. Intensive Care Med. 2016;42(12):1935-1947.
De Backer D, Donadello K, Sakr Y, et al. Microcirculatory alterations in patients with severe sepsis: impact of time of assessment and relationship with outcome. Crit Care Med. 2013;41(3):791-799.
Malbrain MLNG, Marik PE, Witters I, et al. Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic review with suggestions for clinical practice. Anaesthesiol Intensive Ther. 2014;46(5):361-380.
Boyd JH, Forbes J, Nakada TA, et al. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011;39(2):259-265.
Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358(2):111-124.
Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018;378(9):809-818.

Acknowledgments

The authors thank the critical care community for their ongoing dedication to improving shock management and outcomes. This review synthesizes decades of research and clinical experience from intensivists, emergency physicians, cardiologists, and researchers worldwide who have advanced our understanding of circulatory failure.

Author Contributions

This manuscript represents a comprehensive synthesis of current evidence and clinical practice in shock management, designed specifically for postgraduate critical care trainees.

Disclosure Statement

The authors have no conflicts of interest to declare.

Final Clinical Wisdom

"In shock, time is tissue. Recognize early, classify accurately, resuscitate aggressively but judiciously, and reassess continuously. The hemodynamic puzzle requires all the pieces—clinical exam, monitoring, ultrasound, and above all, sound physiologic reasoning. Master these principles, and you'll save lives."

For correspondence and questions: Critical Care Medicine Review Board [Journal of Intensive Care Medicine]

Word Count: ~12,500 words Figures/Tables: 8 tables embedded References: 51 citations

Appendix: Quick Reference Cards

QR Card 1: Shock Type Differentiation

Finding	Hypovolemic	Cardiogenic	Obstructive	Distributive
Skin	Cold, clammy	Cold, clammy	Cold, clammy	Warm (early)
JVP	↓	↑	↑	↓
Heart sounds	Normal	S3, murmurs	Muffled (tamponade)	Normal
Lung exam	Clear	Rales	Unilateral ↓ (PTX)	Variable
Urine output	↓	↓	↓	↓
Lactate	↑	↑	↑	↑

QR Card 2: First-Line Vasoactive Drug Selection

Septic Shock → Norepinephrine Cardiogenic Shock → Dobutamine + Norepinephrine Hypovolemic Shock → Fluids ± Norepinephrine Obstructive Shock → Fix obstruction + temporize with Norepinephrine Anaphylaxis → Epinephrine IM Neurogenic Shock → Phenylephrine or Norepinephrine

QR Card 3: POCUS in 5 Minutes

Step 1: Parasternal long → EF, pericardial effusion Step 2: Apical 4-chamber → RV size, global function Step 3: Subcostal → IVC diameter and collapsibility Step 4: Lung anterior bilateral → B-lines (pulmonary edema) Step 5: LVOT pulsed-wave Doppler → VTI (track serially)

Interpretation:

Small LV, ↑ contractility, flat IVC → Hypovolemic
↓ EF, ↑ IVC, B-lines → Cardiogenic
↑ RV/LV ratio, ↑ RVSP → Obstructive (PE)
Hyperdynamic LV, flat IVC, no B-lines → Distributive

QR Card 4: Surviving Sepsis "Hour-1 Bundle"

✓ Measure lactate
✓ Obtain blood cultures before antibiotics
✓ Administer broad-spectrum antibiotics
✓ Begin rapid fluid resuscitation (30 mL/kg)
✓ Apply vasopressors if hypotensive during or after fluids (MAP ≥65 mmHg)

Source: Surviving Sepsis Campaign Guidelines 2021

QR Card 5: Hemodynamic Goals in Shock

Parameter	Target	Notes
MAP	≥65 mmHg	Higher (80-85) if chronic HTN
Lactate	<2 mmol/L or ↓ 20% q2h	Clearance more important than absolute
ScvO2	≥70%	Trend more useful than single value
Urine output	≥0.5 mL/kg/h	Early marker of adequate perfusion
CVP	Not a target	Use dynamic tests instead
Capillary refill	<3 seconds	Peripheral perfusion marker

Epilogue: The Art and Science of Shock Management

Critical care is both science and art. While this review has emphasized the scientific foundations—hemodynamic principles, drug pharmacology, evidence-based protocols—the art lies in bedside integration. No two patients are identical; shock states evolve; and clinical judgment remains paramount.

The skilled intensivist synthesizes disparate data points—the patient's story, physical examination findings, laboratory values, hemodynamic parameters, and ultrasound images—into a coherent picture that guides therapy. They recognize when to push fluids and when to pull back, when to escalate vasopressors and when to wean, when to pursue aggressive interventions and when to focus on comfort.

As you develop your expertise, remember these final principles:

Physiology first: Understand the "why" behind interventions, not just the "what."
Individualize therapy: Protocols guide, but patients vary.
Reassess continuously: Shock is dynamic; your management must be too.
Communicate clearly: Multidisciplinary care saves lives; speak the same language.
Know your limits: Early consultation prevents late disasters.
Stay humble: Even the best clinicians face cases that defy expectations.

The journey from trainee to expert intensivist is marked not by the accumulation of facts, but by the development of clinical wisdom—the ability to see patterns, anticipate complications, and act decisively under pressure. May this review serve as a foundation upon which you build a career of excellence in critical care.

Go forth and resuscitate with confidence, compassion, and competence.

Monday, September 29, 2025