Haemodynamic resuscitation is one of the most consequential aspects of early ICU management. The goal is to restore and maintain adequate organ perfusion pressure — primarily by optimising cardiac output and systemic vascular resistance — while avoiding the harms of over-resuscitation.

Mean Arterial Pressure Targets

A mean arterial pressure (MAP) of at least 65 mmHg is the standard minimum target in most critically ill patients, based on the Surviving Sepsis Campaign guidelines and supported by multiple large trials. This represents the minimum pressure at which most organ beds can autoregulate their own blood flow. Higher targets (MAP 70–80 mmHg) are used in patients with known chronic hypertension, who may have a rightward shift of their autoregulation curve, and in patients with raised intracranial pressure, where a higher MAP is required to maintain adequate CPP.

MAP is measured most accurately via an arterial line, which also provides beat-to-beat variation as a dynamic indicator of fluid responsiveness. A large pulse pressure variation (>13% with mechanical ventilation) suggests that the patient’s cardiac output is preload-dependent and is likely to respond to a fluid bolus. Static measures like CVP are poor predictors of fluid responsiveness and should not be used in isolation to guide resuscitation.

Fluid Resuscitation

The choice of resuscitation fluid matters. Balanced crystalloids — Hartmann’s solution (Ringer’s lactate) and Plasmalyte — are preferred over large volumes of 0.9% normal saline. The reason is physiological: 0.9% saline contains 154 mmol/L of chloride, significantly above plasma chloride of 100–110 mmol/L. Infusing large volumes causes a hyperchloraemic metabolic acidosis that impairs renal function, reduces splanchnic blood flow, and worsens coagulopathy. Several large randomised trials (including SMART and SALT-ED) have confirmed that balanced crystalloids are associated with better outcomes than normal saline.

Fluid should be given as boluses (250–500 mL) with reassessment after each bolus rather than as a prolonged infusion. The key questions after each bolus are: has MAP improved? Has the lactate fallen? Has urine output improved? If the answer to all three is no after two boluses and the patient remains hypotensive, vasopressors should be started — further fluid administration is unlikely to help and risks harm.

Fluid overload is now recognised as an independent cause of harm in ICU. A positive fluid balance of more than 3–5 litres is associated with increased mortality across multiple ICU populations. The concept of de-resuscitation — actively removing fluid in the later phases of critical illness — is increasingly important in modern ICU practice.

Vasopressors

Noradrenaline (norepinephrine) is the first-line vasopressor for most forms of distributive shock, including septic shock. It acts primarily on alpha-1 adrenoceptors to cause vasoconstriction, increasing SVR and MAP without the tachycardia associated with adrenaline. It should be administered via a central venous catheter, though peripheral administration via a well-sited large-bore cannula is acceptable for short periods while central access is being established.

Vasopressin (0.03–0.04 units/minute) can be added as a second-line agent to allow dose reduction of noradrenaline, or in patients who are not responding adequately. Adrenaline may be used in cardiogenic shock (for its inotropic effect) or as a second-line vasopressor. Dobutamine is the inotrope of choice when cardiac output is reduced and filling pressures are adequate.

Drug	Primary Mechanism	Main Use	Key Side Effects
Noradrenaline	α1 agonist (vasoconstriction)	First-line vasopressor in septic/distributive shock	Peripheral ischaemia at high doses; arrhythmias
Vasopressin	V1 receptor (vasoconstriction)	Second-line vasopressor; allows noradrenaline weaning	Splanchnic ischaemia; hyponatraemia
Adrenaline	α1 + β1 agonist	Anaphylaxis; cardiogenic shock; second-line vasopressor	Tachycardia; hyperglycaemia; lactic acidosis
Dobutamine	β1 agonist (inotropy)	Cardiogenic shock with adequate filling pressures	Tachycardia; hypotension at high doses
Milrinone	PDE-3 inhibitor (inotropy + vasodilation)	Cardiogenic shock; right heart failure	Hypotension; arrhythmias