Shock

• Shock is a syndrome in which tissue perfusion fails: oxygen delivery no longer matches metabolic demand, and organs begin to fail.
• Four mechanisms produce it: too little volume (hypovolaemic), pump failure (cardiogenic), obstruction to flow (obstructive), and pathological vasodilatation (distributive).
• The bedside diagnosis comes from the history, examination, bedside ultrasound and a few basic tests; the why decides the treatment.
• Lactate and urine output track whether tissues are perfused; a lactate that falls with resuscitation is a good sign.
• Fluids come first in most shock; vasopressors are added for vasodilatory states, but they do not replace lost volume.

By the end of this page you should be able to:

1. Define shock and explain the basic physiology of oxygen delivery and perfusion.
2. Name the four main types, give examples, and state the expected cardiac output, systemic vascular resistance and wedge pressure for each.
3. Assess a shocked patient at the bedside using history, examination and focused ultrasound.
4. Use lactate and urine output to judge perfusion and response to treatment.
5. Choose fluids, vasopressors and inotropes appropriately, and explain why vasopressors do not help in hypovolaemia.
6. Recognise and treat three special causes: source-controlled sepsis, anaphylaxis, and the obstructive emergencies of tamponade and tension pneumothorax.
7. Walk through a step-by-step algorithm for the undifferentiated shocked patient.

Shock is not a blood pressure number. It is a state of inadequate tissue perfusion: the circulation fails to deliver enough oxygen for cells to make ATP, and waste products accumulate. A patient can be in shock with a normal blood pressure, because compensation (tachycardia, vasoconstriction) hides the problem until late. Conversely, a low blood pressure in a well, asymptomatic person is not shock.

The unifying problem is failure of oxygen delivery (DO2 = cardiac output × arterial oxygen content). Cardiac output itself is stroke volume × heart rate, and stroke volume depends on preload, contractility and afterload. Each type of shock breaks a different link in that chain, which is why the same four vital signs produce different patterns.

Every shocked patient needs the same first actions: airway, breathing, circulation, a large-bore intravenous line (two), oxygen, monitoring and a cause-specific plan. The algorithm at the end of this page links those first actions to a search for the cause.

The clinical picture is the combination of a cause (bleeding, infection, allergy, pump failure, obstruction), compensation (tachycardia, cold and clammy skin, delayed capillary refill, oliguria) and failure (confusion, falling blood pressure, rising lactate, organ dysfunction). Blood pressure can be normal throughout compensation. The Surviving Sepsis Campaign defines septic shock as persistent hypotension requiring vasopressors to keep the mean arterial pressure at least 65 mm Hg plus a lactate above 2 mmol/L despite adequate fluids.^[1]

Oxygen travels from lungs to mitochondria in four steps: ventilation, diffusion, circulation and cellular use. In shock the failure is usually circulatory, but the bedside question is where in the chain.

Cardiac output (CO) = heart rate × stroke volume. Stroke volume depends on:

• Preload (venous return, filling pressure),
• Contractility (pump strength),
• Afterload (systemic vascular resistance, SVR).

Systemic vascular resistance is what the heart pumps against. The wedge pressure (pulmonary capillary wedge pressure, PCWP) is a bedside estimate of left atrial pressure and therefore of preload on the left side. Putting these three together — output, resistance, filling pressure — is what lets you tell the types apart.

• Hypovolaemic and late cardiogenic shock: too little filling. Stroke volume falls; the body compensates with tachycardia and vasoconstriction; tissues switch to anaerobic metabolism and lactate rises; kidneys and brain show the damage first.
• Cardiogenic shock: the pump itself fails. Filling pressures rise while output falls — the opposite of hypovolaemia.
• Obstructive shock: a physical block (tamponade, tension pneumothorax, massive pulmonary embolism) stops the pump from filling or emptying. Preload or afterload changes abruptly.
• Distributive shock: pathological vasodilatation drops SVR; relative hypovolaemia follows; in septic shock there is also capillary leak and myocardial depression.

Each mechanism drives a distinct haemodynamic picture (next section).

Tissue hypoperfusion produces lactate (anaerobic glycolysis), activates inflammation, and reduces organ function. The brain (confusion), kidneys (low urine), gut (ileus, infection translocation), skin (cold, mottled) and clotting (disseminated intravascular coagulation in severe cases) tell the story. The key clinical lesson is to treat the perfusion problem, not the blood pressure alone.

Some causes are catastrophic and minutes matter; others smoulder and declare themselves with organ dysfunction.

The table compares the four groups. CO = cardiac output; SVR = systemic vascular resistance; PCWP = pulmonary capillary wedge pressure. These are trends, not fixed numbers: mixed pictures are common (for example, a septic patient who is also bleeding).

• Source of the problem. Bleeding (trauma, haematemesis/melaena, heavy menses), infection (fever, cough, dysuria, abdominal pain), allergy (new drug, food, sting within minutes of symptoms), chest pain or breathlessness (myocardial infarction, pulmonary embolism, asthma), recent procedures or spinal injury.
• Time course. Minutes for allergy and massive haemorrhage; hours for sepsis; days for occult bleeding or pump failure.
• Risk factors. Anticoagulation, heart disease, immunosuppression, pregnancy, diabetes.
• Medications. Beta-blockers mask tachycardia; ACE inhibitors and beta-blockers can blunt the response to catecholamines.
• What was tried. Fluids, antibiotics, adrenaline already given.

General impression: frightened, air-hungry, grey or mottled. Then move head to toe:

• Airway. Stridor, drooling, angioedema, tongue swelling.
• Breathing. Rate, depth, oxygen saturation, symmetry (absent breath sounds one side = pneumothorax/effusion), wheeze, crepitations (pulmonary oedema suggests cardiogenic shock).
• Circulation. Heart rate and rhythm, blood pressure (including postural if safe), capillary refill time, skin temperature and colour (cold, clammy = vasoconstricted; warm and flushed = vasodilated shock such as septic or anaphylactic), pulse quality, neck veins (flat = hypovolaemia; distended = tamponade, tension pneumothorax, right heart failure), heart sounds and murmurs (new murmur of papillary muscle rupture; muffled sounds of tamponade), peripheral pulses.
• Disability. Glasgow Coma Scale or AVPU, confusion, pupil equality, focal signs (stroke from embolism in endocarditis/myxoma; spinal level in neurogenic shock).
• Exposure. Temperature, rash (urticaria of anaphylaxis, purpura of meningococcal disease or DIC), abdomen (tenderness, masses, peritonism), rectal or vaginal bleeding, pregnancy, limb ischaemia.
• Urine. Place a urinary catheter: volume and colour are continuous monitors of renal perfusion.

Performed in the same pass as resuscitation, without delaying it:

• IVC size and collapsibility: suggest volume status (flat and collapsing in hypovolaemia).
• Heart: contractility, pericardial effusion/tamponade physiology, right ventricular size (right ventricular failure or massive pulmonary embolism).
• Lungs: B-lines (pulmonary oedema), pleural fluid, absent sliding and a lung point (pneumothorax).
• Abdomen/pelvis/long bones: free fluid or bleeding source.

Lactate is a perfusion marker: as tissues become hypoxic, anaerobic glycolysis produces it. An elevated lactate makes sepsis (or any shock) more likely, and the Surviving Sepsis Campaign recommends measuring it in suspected sepsis as an adjunct to judge the pre-test probability of sepsis and septic shock.^[1] A lactate that falls with resuscitation (clearance) signals improving perfusion; one that stays high or rises is a warning. The sepsis definition of septic shock uses a lactate above 2 mmol/L in addition to vasopressor-dependent hypotension.^[1] Numerically high or low cut-offs vary between tools (1.6 to 2.5 mmol/L in various studies), so interpret lactate alongside the blood pressure, urine output and mentation, not as a single number.^[1]

The kidneys are an early and sensitive target of hypoperfusion. Urine output gives a continuous, low-tech measure of renal (and therefore general) perfusion; falling output is often the first sign that resuscitation is failing. A urinary catheter (with a urometer) turns this into a watched number. Urine output should be interpreted with the fluid input, the presence of blood in the urine and the clinical picture.

Match the monitor to the clinical question:

• Non-invasive: repeated blood pressure (manual and automated), heart rate, oxygen saturation, capillary refill, mental state. Enough for many hypovolaemic and septic patients after initial fluids.
• Invasive arterial line: continuous beat-to-beat blood pressure for vasopressor titration and frequent blood gases/lactate. Indicated in any shocked patient needing vasopressors or intubation.
• Central venous catheter: central venous pressure (cautiously), access for vasopressors, and venous oxygen saturation (ScvO2). It is a bridge to echocardiography, not a volume target.
• Bedside echocardiography (POCUS): the single most useful tool for distinguishing hypovolaemic, cardiogenic and obstructive shock within minutes. It replaces reliance on static pressures.
• Echocardiography with advanced measures (VTI, stroke volume): to guide fluid responsiveness (passive leg raise or a fluid challenge, watched as the stroke volume rises). The Surviving Sepsis Campaign suggests dynamic measures over static ones when guiding fluids.^[1]
• Transpulmonary thermodilution / other advanced monitoring (PiCCO etc.): for complex or prolonged shock, where usual tools no longer suffice.

Fluids are the first treatment in hypovolaemic, septic and anaphylactic shock; they are potentially harmful in cardiogenic shock and in obstructive shock until the obstruction is removed.

• Choice. Balanced crystalloids (for example, Ringer's lactate / Hartmann's) are the usual starting point. Use 0.9% saline when hyperkalaemia, brain injury with raised intracranial pressure, or specific clinical reasons make it safer, and avoid large volumes of glucose-containing fluids for resuscitation.
• Amount. For sepsis-induced hypoperfusion or septic shock the recommendation is at least 30 mL/kg of intravenous crystalloid within the first three hours of resuscitation.^[1] For other causes, give repeated small boluses (for example, 250 to 500 mL) and reassess between them, stopping when perfusion improves or filling marks rise.
• Blood. In haemorrhagic shock, stop the bleed and replace lost blood with blood and blood products according to local major haemorrhage protocols; crystalloid is a bridge, not the answer, and excessive crystalloid worsens coagulopathy and hypothermia.
• How to give. Through wide, short cannulae or an intraosseous needle if necessary, warmed, and with continuous reassessment of perfusion, lung signs, and oxygen saturation.
• Safety. Fluid is a drug. Watch for pulmonary oedema, especially in older adults, in cardiogenic shock and when neck veins and lung fields are already loaded.

Vasopressors restore blood pressure by constricting vessels; inotropes improve pump function. They complement fluids, they never replace them.

• Why vasopressors are avoided in hypovolaemia. In pure hypovolaemic shock the problem is empty vessels and low stroke volume, not low vascular tone. Adding a vasopressor squeezes already empty pipes, worsens organ and tissue perfusion, produces the appearance of a normal blood pressure a hollow one, and wastes precious time. Vasoconstrictors may even worsen tissue perfusion while masking hypovolaemia. The correct treatment is to replace the lost volume (and blood) while stopping the leak or bleed. Vasopressors have a role only as a life-saving bridge in extreme hypotension while volume is actually being given, or in shock types with true vasodilatation.
• Septic (vasodilatory) shock. The Surviving Sepsis Campaign gives a strong recommendation to use norepinephrine as the first-line vasopressor rather than dopamine, vasopressin, epinephrine or others.^[1] Norepinephrine raises pressure by alpha-1 vasoconstriction with minimal heart-rate effect. The usual haemodynamic target is a mean arterial pressure of at least 65 mm Hg initially.^[1] If norepinephrine alone is insufficient, add vasopressin rather than only escalating the noradrenaline dose, and add epinephrine as a further option.^[1] Vasopressin is usually given at a fixed 0.03 units per minute, occasionally up to 0.06 units per minute, and is typically started when the norepinephrine dose is about 0.25 to 0.5 micrograms per kilogram per minute.^[1] When a vasopressor is unavailable, epinephrine or dopamine may be used as alternatives, with attention to arrhythmia risk.^[1] Dobutamine (or epinephrine alone) is suggested for persistent hypoperfusion due to cardiac dysfunction despite adequate volume and pressure. Corticosteroids (hydrocortisone 200 mg per day as 50 mg four times daily or an infusion) are suggested for septic shock that remains vasopressor-dependent.^[1]
• Anaphylactic shock. First-line is intramuscular adrenaline (epinephrine) in the mid-anterolateral thigh, 0.01 mg/kg up to a maximum of 0.5 mg, repeated as needed,^[3] together with removal of the trigger if possible, a supine position with leg elevation, oxygen, airway care and intravenous fluids (20 mL/kg crystalloid boluses for persistent hypotension after adrenaline).^[3] Intranasal epinephrine is an emerging needle-free alternative.^[2] Adjunctive antihistamines and corticosteroids may help skin symptoms but do not reverse anaphylaxis and must not delay adrenaline.^[2] Refractory shock after two appropriate intramuscular doses needs intravenous adrenaline infusion, vasopressors and advanced airway support.^[3]
• Cardiogenic shock. Avoid injudicious fluids; use small cautious challenges with echocardiographic guidance. Treat the cause (reperfusion for myocardial infarction, rate or rhythm control, valve surgery), and support the pump with an inotrope (commonly dobutamine, or levosimendan in selected cases) and, when available, mechanical circulatory support. Vasopressors are added if hypotension prevents adequate coronary perfusion pressure.
• Neurogenic shock. Fluids first, then vasopressors to compensate for the loss of vascular tone; bradycardia is common and may need atropine or pacing.
• Practical monitoring. Titrate every vasoactive drug to a target, via an arterial line where possible, in a setting with continuous monitoring, ECG and trained staff.

In sepsis and septic shock, controlling the anatomical source of infection is a core part of treatment, not an afterthought. The Surviving Sepsis Campaign recommends rapidly identifying or excluding a specific source requiring emergent control (drainage, debridement, device removal, definitive control of ongoing contamination) and carrying it out as soon as it is medically and logistically practical.^[1] Source control within 6 to 12 hours appears to be advantageous, and without it many severely infected patients will not stabilise.^[1] Use the least invasive effective option (percutaneous drainage, endoscopy) before open surgery where possible.^[1] Remove an intravascular device suspected to be the source once alternative access is established.^[1]

Antibiotics should be started promptly in septic shock (empirically, broad spectrum, adjusted later), ideally with cultures taken first if this does not delay treatment.^[1]

• Cardiac tamponade. Bleeding or fluid under pressure in the pericardium compresses the heart and stops filling. The classic picture is tachycardia, hypotension, a raised jugular venous pressure and muffled heart sounds (Beck's triad), often with pulsus paradoxus (a fall in systolic pressure greater than 10 mm Hg on inspiration), and a chest radiograph showing a globular enlarged heart. Emergency echocardiography confirms it. Treatment is urgent pericardiocentesis (ultrasound-guided), with a surgical drain (window) if it recurs or the fluid is clot.
• Tension pneumothorax. Air under pressure in a pleural space collapses the lung and pushes the mediastinum, kinking the great veins. The clinical signs are sudden breathlessness, hypotension, a unilateral absent air entry, distended neck veins and tracheal deviation away from the affected side. Do not wait for imaging. Treat immediately with needle decompression at the second intercostal space mid-clavicular line (or the fifth intercostal space anterior axillary line according to local protocol), using a large-bore cannula, followed as soon as possible by a formal chest drain.

• Children. Paediatric sepsis guidelines use weight-based fluid boluses (10 to 20 mL/kg, up to 40 to 60 mL/kg in the first hour) and early antibiotics (within an hour in shock). Neonates and children differ; involve paediatric and intensive care teams early.
• Pregnancy. Bleeding and sepsis remain the common causes; left lateral positioning protects aortocaval flow in late pregnancy; early obstetric involvement.
• Older adults. Hypertension shifts the left ventricular curve; fluid and vasopressor responses are blunted; drug-induced hypotension and occult infection are common.
• People on beta-blockers. Tachycardia may be masked, so the absence of a fast pulse does not exclude shock.

• A urinary catheter, a blood pressure cuff, a stethoscope and a rapid bedside lactate (or blood gas) are enough to start.
• Point-of-care ultrasound, even on a basic machine, separates hypovolaemic from cardiogenic and obstructive shock quickly; train one or two staff members per unit.
• Adrenaline is cheap and life-saving in anaphylaxis; have it in every clinical area.
• When blood is unavailable, prioritise stopping haemorrhage and use crystalloid judiciously while arranging transfusion or referral.
• Vasopressors are unavailable in many places; if norepinephrine is not on the shelf, dopamine or epinephrine (with monitoring) are the fallback, and procuring norepinephrine should be a priority.

• Shock is a syndrome of tissue hypoperfusion, not just low blood pressure; it can exist with normal blood pressure.
• Oxygen delivery = cardiac output × arterial oxygen content; cardiac output = heart rate × stroke volume.
• The four types are hypovolaemic, cardiogenic, obstructive and distributive (septic, anaphylactic, neurogenic).
• Lactate and urine output track perfusion and response; dynamic tests guide fluids better than static pressures.
• Fluids first in most shock; vasopressors added for vasodilatory shock; vasopressors do not replace lost volume.
• Norepinephrine is the first-line vasopressor in septic shock; target mean arterial pressure about 65 mm Hg initially.
• Anaphylaxis: intramuscular adrenaline first, 0.01 mg/kg up to 0.5 mg, repeated as needed.
• Source control in sepsis should be done as soon as practically possible (6 to 12 hours is advantageous).
• Tamponade: treated by urgent pericardiocentesis; tension pneumothorax: immediate needle decompression then chest drain.

Shock crosses every discipline. Related MedGrasp topics include sepsis, anaphylaxis, myocardial infarction and acute coronary syndromes, pulmonary embolism, trauma and haemorrhage control, cardiac tamponade and pericardial disease, tension pneumothorax and pleural disease, acute heart failure, and the paediatric emergency topics on dehydration and fluids.