By Dr. Sabrina Berdouk, peer-reviewed by Dr. Abdolghader Pakniyat
1. What Is Shock? Why Does MAP Fall?
Shock is inadequate tissue perfusion; normal pressure does not exclude it. MAP − right-atrial pressure ≈ cardiac output × systemic vascular resistance; CO = heart rate × stroke volume. Here SVR is in mmHg·min/L and CO in L/min. Oxygen delivery also depends on hemoglobin and arterial oxygenation. Raising resistance can improve pressure while forward flow remains poor. Check skin perfusion, mentation, urine output and lactate trends, then repeat focused echocardiography when the response is unclear. ESICM 2025
Adult bedside guide: vasoactive drugs buy time for diagnosis and definitive treatment. Low preload, vasodilation and pump dysfunction may coexist. Reassess the dominant problem after each intervention.
2. Categories of Shock: The Core Physiology
| Pattern | Immediate question |
|---|---|
| Distributive | Loss of vascular tone; identify infection, anaphylaxis or neurogenic physiology. |
| Cardiogenic | Inadequate pump output; seek ischemia, rhythm or mechanical disease. |
| Obstructive | Blocked filling or ejection; seek PE, tamponade or tension pneumothorax. |
| Hypovolemic | Inadequate circulating volume; control bleeding and replace the relevant loss. |
These patterns overlap. Anaphylaxis needs IM epinephrine; hemorrhage needs bleeding control and blood-product resuscitation. A pressor cannot substitute for either. Obstruction needs urgent relief. Anaphylaxis guidance
3. Septic (Distributive) Shock: “Warm, Empty Pipes”
Physiology
Vasodilation and capillary leak may coexist with myocardial dysfunction. “Warm” skin and a vigorous-looking LV do not establish adequate cardiac output.
Management
SSC 2026: treat infection promptly and obtain source control. Its conditional initial-fluid suggestion is ≥30 mL/kg crystalloid within 3 hours, individualized with repeated reassessment; unstable shock may need concurrent pressors. Start norepinephrine, add vasopressin as requirements escalate, then epinephrine if MAP remains inadequate. With cardiac dysfunction, either norepinephrine or epinephrine is a conditional first-line option. Initial MAP: 65 mmHg; age ≥65 years: a conditional 60–65 range. Cardiac dysfunction with persistent hypoperfusion despite adequate volume and pressure may justify dobutamine plus norepinephrine or epinephrine alone. Guideline
Fluid responsiveness asks whether output will rise; tolerance asks whether more fluid will cause harm. Use a passive-leg-raise response measured by stroke volume/CO when feasible, and separately assess worsening oxygenation, pulmonary or venous congestion. A responsive patient may still poorly tolerate fluid. IVC appearance alone is insufficient. Fluid-tolerance position paper
4. Cardiogenic Shock: “Cold and Wet”
Physiology
Low output can occur with or without pulmonary congestion. Examine both ventricles, valves and pericardium; investigate ischemia and dangerous arrhythmias.
Management
Support severe hypotension with norepinephrine and consider an inotrope for persistent low-output hypoperfusion. Choose both together from pressure, perfusion and echo findings. Treat hypoxemia, arrange cause-specific treatment and involve the shock team early when support is escalating. ESC 2026
In the small, prematurely stopped OptimaCC trial after myocardial infarction, epinephrine produced more refractory shock than norepinephrine despite similar pressure and cardiac-index effects. This is not proof of a universal survival advantage for one pressor.
Check for dynamic LV outflow obstruction (LVOTO) before escalating beta-agonists. A small hyperdynamic LV with systolic anterior mitral motion and a Doppler gradient can require a different approach: reduce provoking inotropy, assess preload carefully, and seek expert echocardiography. Obstructive-HCM guidance recommends phenylephrine or another non-inotropic vasoconstrictor when hypotension persists after fluids; selected beta-blockade requires specialist monitoring. Do not apply that pathway indiscriminately to undifferentiated shock. HCM guideline
5. Right Heart Failure & Pulmonary Hypertension
Physiology
RV pressure overload reduces forward flow and LV filling; excessive volume can worsen septal displacement and systemic congestion.
Management
Correct hypoxemia and significant ventilatory derangements, support systemic pressure, and tailor preload to congestion and response. Selected persistent low output may need an inotrope with pressure support. Inhaled pulmonary vasodilators are specialist rescue/bridging therapies, not established survival treatments. Avoid unnecessary deep sedation and excessive airway pressures; prepare circulatory support when intubation is required. Acute-PE guidance addresses one important RV-failure cause, not every form of pulmonary hypertension.
6. Obstructive Shock (Massive PE)
Physiology
In high-risk PE, acute RV afterload rises and LV filling falls. Echo supports assessment but isolated RV dilation or McConnell’s sign does not diagnose PE.
Management
Use norepinephrine for hypotensive shock while arranging urgent PE-team assessment for reperfusion. Systemic thrombolysis, catheter intervention or surgery depends on severity, bleeding risk and local expertise. Do not delay definitive treatment by repeatedly escalating drugs. Tamponade and tension pneumothorax need their own immediate decompression pathways. 2026 PE guideline
7. Neurogenic Shock (Spinal Cord Injury Above T6)
Physiology
High spinal injury can interrupt sympathetic tone, causing vasodilation and bradycardia. Exclude coexisting hemorrhage; bradycardia may be absent.
Management
Norepinephrine is commonly used, but the 2024 traumatic-SCI guideline does not endorse a specific agent. It weakly suggests MAP augmentation to a lower limit of 75–80 mmHg without actively augmenting above 90–95 mmHg, for 3–7 days; evidence is very low certainty. A spontaneously higher MAP is not an instruction to lower pressure.
A 2025 randomized trial did not detect a neurologic advantage from targeting >85–90 versus >65–70 mmHg, with more respiratory complications in the augmented group. It was underpowered with substantial missing follow-up, and the conventional group’s mean MAP still exceeded 80 mmHg. Individualize with the spinal team; it does not settle the optimal target. Trial
For hemodynamically significant bradycardia, follow the adult bradycardia pathway: atropine when appropriate, then pacing and/or epinephrine or dopamine infusion if ineffective. Dobutamine is not a routine substitute.
8. Peri-Intubation or Sudden Hypotension (Push-Dose Strategy)
Physiology
Induction may remove sympathetic support; positive-pressure ventilation reduces venous return and can worsen RV loading.
Management
Resuscitate the identified physiology before intubation when feasible, while preparing rescue support. Evidence does not establish routine prophylactic norepinephrine for every critically ill intubation. SCCM RSI guideline
Push-dose pressors are a monitored bridge for selected severe hypotension, not a replacement for an infusion. Use pharmacy-standardized preparations, verify drug, concentration, dose in micrograms, line and response, and communicate each dose. Avoid bedside dilution from memory and automatic repeat-dose schedules.
9. Peripheral Vasopressors: Protocolized Safety
In adult septic shock, SSC suggests peripheral initiation rather than waiting for a central line, but provides no universal safe dose, gauge, site or duration.
Use a reliable, visible IV under a drug-specific local protocol, a standardized concentration and pump, frequent patency/site checks, and an escalation plan. Rising requirements, unreliable access or inadequate monitoring should prompt central-access reassessment. A prospective, single-center norepinephrine protocol study reported extravasation in 35/635 patients; none required surgery. It supports protocolized feasibility, not zero risk or generalization to all drugs. Yerke et al.
Suspected extravasation: stop the infusion, do not flush, retain the catheter initially for aspiration, and activate the local drug-specific pathway. Obtain prompt pharmacy/critical-care help. Norepinephrine labeling specifies local phentolamine; have the approved antidote plan available before starting. Prescribing information
10. Dosing Quick Card (for all agents)
These are adult label/trial reference regimens, not interchangeable starting ranges or a mixing chart. Use the local order set and pharmacy concentration. Verify weight convention, mcg versus mg, units/min versus mcg/kg/min, and pump mL/hour independently. Never infer concentration from the drug name. Pediatric regimens differ.
| Agent | Role, adult regimen and main caution |
|---|---|
| Norepinephrine | Predominantly alpha-mediated vasoconstriction, with beta-1 activity. One adult label starts at 8–12 mcg/min, then titrates. This is not a universal weight-based protocol. Label |
| Vasopressin | V1-mediated vasoconstriction. The VASST trial used 0.01–0.03 units/min as an adjunct; its septic-shock label starts at 0.01 units/min and permits titration to 0.07 units/min. Ischemia, reduced cardiac output and hyponatremia matter. Label; VASST |
| Epinephrine | Alpha and beta effects. Adult septic-shock label range: 0.05–2 mcg/kg/min, titrated, using ideal body weight in this product label. Tachyarrhythmia, ischemia and beta-mediated lactate elevation complicate reassessment. Label |
| Phenylephrine | Alpha-1 agonist; may increase afterload and cause reflex bradycardia. Selected vasodilatory-shock label range: 0.5–6 mcg/kg/min. It is not a routine low-output-shock choice; see the LVOTO exception above. Label |
| Dobutamine | Beta-agonist inotrope: may improve output but cause hypotension or tachyarrhythmia. Linked label starts at 0.5–1 mcg/kg/min, then titrates to response. Avoid uncritical escalation in LVOTO. Label |
| Milrinone | PDE-3 inodilator. Label maintenance: 0.375–0.75 mcg/kg/min; renal impairment requires reduction. Loading can worsen hypotension and may be omitted in shock under specialist protocol. Monitor rhythm and pressure. Label |
| Dopamine | Reserve for a defined indication, such as selected bradycardic instability. SOAP II found more arrhythmias than with norepinephrine and no significant overall 28-day mortality difference; the cardiogenic subgroup signal is not a universal mortality claim. SOAP II |
| Hydrocortisone | Adult septic shock: 200 mg/day IV by the selected protocol, often 50 mg every 6 hours or continuous infusion. It is an adjunct, not an automatic consequence of starting a second pressor. ADRENAL; APROCCHSS |
DOREMI randomized 192 patients and found no significant difference in its composite outcome between milrinone and dobutamine. This does not establish equivalence, superiority, or benefit from giving either to every patient with a low ejection fraction. Trial
11. Final Pearls & Bedside Checklist
If pressure improves but perfusion does not, reassess flow, diagnosis and infusion delivery. Seek ongoing bleeding, obstruction or cardiac dysfunction; escalate monitoring and specialist support.
IV corticosteroids are conditionally suggested in septic shock; evidence remains insufficient for routine methylene-blue rescue. SSC 2026
One 91-patient, single-center trial of early methylene blue shortened vasopressor duration, but did not establish a survival benefit or a general rescue regimen. Trial
ADRENAL found faster shock resolution without a significant 90-day mortality benefit from hydrocortisone alone. APROCCHSS found lower 90-day mortality with hydrocortisone plus fludrocortisone in a different population/regimen. These trials do not support a guaranteed steroid survival effect. ADRENAL; APROCCHSS
Angiotensin II improved the short-term pressure endpoint in ATHOS-3, but the trial did not show a statistically significant 28-day survival benefit. Consider specialist rescue only after reassessing the cause and risks, including thrombosis. ATHOS-3; drug safety
How to Use This At Bedside
Ask three questions after every change: Is pressure adequate? Is tissue perfusion improving? Is treatment causing harm? Trend rhythm, ischemia, urine output, capillary refill and respiratory status. State the suspected shock mechanism, current dose and concentration, target, response and next reassessment when handing over.
The interactive guide below navigates to the corresponding sections above. Its categories are teaching prompts; mixed shock and conditions outside the tree still require clinical assessment.
Physiology-Based Shock Flowchart
Choose a teaching pattern to read its section above. Mixed shock is common; these choices are not a diagnostic algorithm.
What is the primary problem?
Pressure, flow and perfusion must be assessed together.
What is the pump problem?
Why are the pipes dilated?
