4. Hypotension and Its Management

Arterial BP is determined by cardiac output (CO), which is the product of heart rate (HR) and stroke volume (SV), multiplied by systemic vascular resistance (SVR) (i.e. BP = [HR x SV] x SVR).

Causes 10 Hypoxia: pre-terminal hypoxia leads to bradycardia. • Vagal stimulation: profound bradycardia may follow traction on extraocular muscles, anal or cervical dilatation, visceral traction and, sometimes, instrumentation of the airway • Drugs: • Cardiac disease • Metabolic: • Spinal anaesthesia:

medication with drugs such as β-adrenoceptor blockers and digoxin may be responsible. Anaesthetic drugs may also contribute. Volatile agents in high concentrations (halothane in normal concentrations), suxamethonium, opioids anticholinesterases can all be associated with bradycardia. Low doses of atropine may provoke a paradoxical bradycardia (the Bezold–Jarisch reflex).

Cardiac disease: the commonest cause is ischaemic change affecting the conducting system. —Metabolic: acute hyperkalaemia may hyperpolarize the myocardial cell membrane with a resulting fall in HR. in theory, the block of the cardiac accelerator fibres from T1 to T4 should be associated with bradycardia. In practice, this is not often seen.

— Diagnose the cause, and if it is amenable to treatment then act accordingly. Is it hypoxia? Treat immediately. Is it surgical stimulus? Stop traction on the extraocular muscles or the mesentery. If drug treatment is required, the most effective immediate first-line drug is an anticholinergic agent, usually atropine or glycopyrrolate. Neither is a treatment for hypoxia.

The commonest cause is reduced venous return (VR). Determinants of VR include volaemic status, venous tone and the lower limb muscle pump, posture (VR is increased in the Trendelenberg head-down position), the respiratory cycle and the elastic recoil of the right ventricle. Volaemic status is the most important of these and may be reduced by an actual reduction in circulating volume secondary to blood loss or dehydration or to an effective reduction in circulating volume caused by sympathetic block or peripheral vasodilatation from some other cause (such as sepsis). — Reduced contractility: SV may also be diminished because of a failing left ventricle.

— Diagnose the cause. Is it hypovolaemia? Resuscitate with the appropriate fluid. Is position contributing? Revert to recumbency or the head-down position; ensure lateral uterine displacement in the later stages of pregnancy. Beware aortocaval compression by the intra-abdominal mass that is not a gravid uterus. Is it a failing ventricle? Consider using inotropes to support ventricular function.

The commonest cause of inadvertent profound hypotension is probably that which is induced by the sympathetic block associated with a spinal or epidural. It may also occur during anaesthesia in a patient in whom ACE inhibitors or angiotensin II antagonists have not been discontinued prior to surgery. In the context of critical care, the commonest cause is sepsis.

— The rational management of hypotension that has been induced pharmacologically is to treat it pharmacologically. The reduced SVR associated with sepsis is different, but it is still usually managed with a combination of vasopressor, fluids and inotropes

Ephedrine is a naturally occurring compound It is sympathomimetic and acts directly and indirectly, possessing both α- and β-effects. - also breakdown of noradrenaline (norepinephrine) by monoamine oxidase main influence on BP is via an increase in CO. Its α1-effects mediate peripheral vasoconstriction, the β1-effects are positive inotropy and chronotropy, and the β2-effects are bronchodilatation (and vasodilatation). 3–5 mg titrated against response and repeated as necessary. The drug has a rapid onset of action that is said to last for around 60 minutes, depletion of noradrenaline secondary to ephedrine’s indirect action leads to tachyphylaxis.

Clinical usage: traditionally, it has been favoured in obstetric anaesthesia because it does not cause α1-mediated vasoconstriction in the uteroplacental circulation. It has now been superseded by α1-agonists because it is associated with a greater fetal acidosis (probably by increasing fetal metabolic demand). Ephedrine increases myocardial oxygen demand and so should be used in caution in patients with a pre-existing tachycardia or with cardiac disease. It is also arrhythmogenic. It is an effective bronchodilator.

phenylephrine is an α1-agonist with mainly direct actions but with some weak β-activity. Its primary influence on BP is via α1-vasoconstriction and an increase in peripheral resistance. The dose is 50–100 μg titrated against response and repeated as necessary. Onset is rapid, but its duration of action is frequently less than the 60 minutes that is claimed.

it is an effective vasopressor which is especially popular in some cardiac units. It is also used more widely in obstetric anaesthesia despite traditional avoidance of all pressor drugs apart from ephedrine. Given by infusion after subarachnoid block, it maintains arterial blood pressure effectively. A typical starting rate before titrating against response would be 50 μg min–1 (60 ml hr–1 of a 50 μg ml–1 solution). Phenylephrine maintains maternal BP and neonatal cord pH better than ephedrine. It is not arrhythmogenic, but it can cause a reflex bradycardia which may require treatment with atropine or glycopyrrolate. It is useful in patients in whom a tachycardia should be avoided.

metaraminol is a sympathomimetic with both direct and indirect actions and α- and β-effects (α-effects predominate). Its influence on BP is via α1-vasoconstriction and increase in CO with increased coronary blood flow. The dose is 1–5 mg titrated against response and repeated as necessary. The onset of action is rapid (1–3 minutes), and the duration of action is around 20–25 minutes. Clinical usage: it is a potent and effective vasopressor, which is particularly useful for the treatment of hypotension due to sympathetic blockade.

noradrenaline is an exogenous and endogenous catecholamine. It is a powerful α1-agonist with weaker β-effects. Its vasopressor effect is mediated via α1-vasoconstriction and the increase in peripheral resistance. It is administered by intravenous infusion (0.05–0.2 μg kg−1 min−1) and titrated against the desired level of arterial pressure. Its onset and offset of action are rapid.

intensive care medicine than in anaesthesia, particularly to treat the low systemic vascular resistance associated with sepsis. Sudden discontinuation of an infusion may be accompanied by severe rebound hypotension. This explains the occasional requirement for the drug following removal of a noradrenaline-secreting phaeochromocytoma. Reflex bradycardia is common.

Pharmacology: adrenaline is also an exogenous and endogenous catecholamine, which acts both as an α1-and β-agonist. In low doses, β-mediated vasodilatation predominates, but the BP rises because of the increase in CO. In high doses, adrenaline causes α1-vasoconstriction. It is given either as a bolus (1.0 mg intravenously in the case of circulatory arrest) or as an intravenous infusion in the same dose range as noradrenaline (0.05–0.2 μg kg−1 min−1).
Clinical usage: the use of adrenaline as a vasopressor is effectively limited to catastrophic circulatory collapse and cardiac arrest.

Pharmacology: vasopressin acts on the V1 receptors of vascular smooth muscle in the systemic, splanchnic, coronary and renal circulations, where it is a potent vasoconstrictor. (In the pulmonary circulation there is nitric oxide–mediated vasodilatation). It is used to treat the hypotension associated with sepsis and in asystolic cardiac arrest. The infusion rate in sepsis would start at 0.01 I.U. hr–1 titrated according to response.