Choice of fluid for volume replacement Medical Assignment Help

BLOOD. This is conventionally given for haemorrhagic shock as soon as it is available. In extreme emergencies, uncross matched group 0 negative blood can be used, but an emergency crossmatch can be performed in about 30 min and is as safe as the standard procedure. Donor blood is often separated into its various components for storage, necessitating the transfusion of packed red cells to maintain haemoglobin and plasma, or a plasma substitute, for volume replacement.
Complications of blood transfusion are discussed. Special problems arise when large volumes of stored blood are transfused rapidly. These include:
TEMPERATURE CHANGES. Bank blood is stored at 4°C and transfusion may result in hypothermia, peripheral venoconstriction (which slows the rate of the infusion) and arrhythmias. Some therefore recommend that if possible blood should be warmed prior to the transfusion.
COAGULOPATHY. Stored blood has essentially no effective platelets and is deficient in clotting factors. Large transfusions can therefore produce a coagulation defect. This may need to be treated by replacing clotting factors with fresh frozen plasma and the administration of platelet concentrates.
METABOLIC ACIDOSIS/ALKALOSIS. Stored blood is now preserved in citrate/phosphate/dextrose (CPD) solution, which is less acidic than the acid/citrate/dextrose (ACD) solution used previously. Metabolic acidosis attributable solely to blood transfusion is rare and in any case rarely requires correction. A metabolic alkalosis often develops 24-48 hours after a large blood transfusion, probably mainly due to metabolism of the citrate; this will be exacerbated if the preceding acidosis has been corrected with intravenous sodium bicarbonate.
HYPOCALCAEMIA. Stored blood is anticoagulated with citrate, which binds calcium ions. This can reduce total body ionized calcium levels and cause myocardial depression. This is uncommon in practice, but if necessary can be corrected by administering 10 ml of 10% calcium chloride intravenously. Routine treatment with calcium is not recommended.
INCREASED OXYGEN AFFINITY. In stored blood, the red cell 2,3-DPG content is reduced, so that the oxyhaemoglobin dissociation curve is shifted to the left. The oxygen affinity of haemoglobin is therefore increased and oxygen delivery is impaired. This effect is less marked with blood stored in CPD. Red cell levels of 2,3-DPG are substantially restored within 12 hours of transfusion.
HYPERKALAEMIA. Plasma potassium levels rise progressively as blood is stored. However, hyperkalaemia is rarely a problem as prewarming of the blood increases red cell metabolism-the sodium pump becomes active and potassium levels fall.
MICROEMBOLISM. Microaggregates in stored blood may be filtered out by the pulmonary capillaries. This process is thought by some to contribute to ARDS.
RED CELL CONCENTRATES. Nutrient additive solutions, i.e. saline, adenine, glucose and mannitol (SAGM), are now available which allow red cell storage in the absence of plasma.
Because of the complications of blood transfusion, in particular the risk of disease transmission, as well as their expense, the use of crystalloid solutions, plasma, plasma substitutes and oxygen-carrying solutions for volume replacement is assuming greater importance.
CRYSTALLOID SOLUTIONS. Although crystalloid solutions, e.g. saline, are cheap, convenient to use and free of side-effects, the administration of large volumes of these fluids to critically ill patients should, in general, be avoided. They are rapidly lost from the circulation into the extravascular spaces and volumes of crystalloid two to four times that of colloid are required to achieve an equivalent haemodynamic response. Although volume replacement with predominantly crystalloid solutions is advocated by some for the uncomplicated, previously healthy patient with traumatic or perioperative hypovolaemia, a more reasonable approach is to use crystalloids initially but to use colloids in addition if there is continued need for volume replacement in excess of about 1 litre.
COLLOIDAL SOLUTIONS. These produce a greater, and more sustained increase in plasma volume, with associated improvements in cardiovascular function and oxygen transport. They also increase colloid osmotic pressure.
Human albumin solution (HAS) is a natural colloid and is not generally used for routine volume replacement, particularly if volume losses are continuing since other cheaper solutions are equally effective in the short term. Some recommend administration of HAS at a later stage in those who are hypoalbuminaemic.
Dextrans are polymolecular polysaccharides in either 5% dextrose or normal saline. They are commercially available as low molecular weight dextran (dextran 40; mol. wt 40000) and dextran 70, and have a powerful osmotic effect. They interfere with cross matching and have a small rate of allergic reactions (0.07-1.1%). Normally a dose of 1.5 g dextran per kilogram of body weight should not be exceeded because of the risk of renal damage. In practice dextrans are rarely used in the UK because of the availability of other agents.
Polygelatin solutions (Haemaccel, Gelofusine) have an average molecular weight of 35 000, which is iso-osmotic with plasma. They are cheap. Large volumes can be administered, since coagulation defects do not occur and renal function is not impaired. However, because theyreadily cross the glomerular basement membrane, their
half-life in the circulation  is approximately 4 hours and they can promote an osmotic diuresis. Allergic reactions occur in up to 10% of cases. These solutions are particularly useful during the acute phase of resuscitation, especially when volume losses are continuing but in many patients colloids with a longer half-life will be required later to achieve haemodynamic stability. Hydroxyethyl starch (HES) has a mean molecular weight of approximately 450000 and a half-life of about 6 hours. Volume expansion is equivalent to, or slightly greater than, the volume infused. The incidence of allergic reactions is approximately 0.1%. Although more expensive than gelatins, HES is a valuable volume expander.
OXYGEN-CARRYING BLOOD SUBSTITUTES are being developed, e.g. fluorocarbon emulsions. Haemoglobin solutions also have potential as oxygendelivering resuscitation fluids, but their use is limited by their short intravascular retention time and their high affinity for oxygen.

Myocardial contractility and inotropic agents

Myocardial contractility can be impaired by hypoxaemia and hypocalcaemia, as well as by some drugs (e.g. (3- blockers, antiarrhythmics and sedatives). Severe lactic acidosis can depress myocardial contractility and may limit the response to inotropes. Attempted correction of acidosis with intravenous sodium bicarbonate, however, generates additional carbon dioxide which diffuses across cell membranes producing or exacerbating intracellular acidosis. Other disadvantages of bicarbonate therapy include sodium overload and a left shift of the oxyhaemoglobin dissociation curve. Also ionized calcium levels may be reduced and, combined with the fall in intracellular pH, may be responsible for impairing myocardial performance. Treatment of lactic acidosis should therefore concentrate on correcting the cause, while acidosis may be most safely controlled by hyperventilation. Bicarbonate should only be administered to correct extreme and persistent metabolic acidosis.
When a patient remains hypotensive despite adequate volume replacement, and perfusion of vital organs is jeopardized, pressor agents may be administered to improve cardiac output and blood pressure. In some cases inotropic agents are given to redistribute blood flow (e.g. dopamine can be used to increase renal perfusionsee below). There is evidence that survival of patients with septic or traumatic shock (as well as following major surgery and in those with ARDS) is associated with supranormal values for cardiac output, oxygen delivery and oxygen consumption. Some now advocate that in the most severely ill patients, and in those who fail to respond to simple measures, treatment should be directed at increasing these variables until they equal or exceed the median values found in survivors.
It must be remembered, however, that all inotropes increase myocardial oxygen consumption, particularly if a tachycardia develops, and that this can lead to an imbalance between myocardial oxygen supply and demand, with the development or extension of ischaemic areas. For this reason such agents should be used with caution, particularly in cardiogenic shock following myocardial infarction and those known to have ischaemic heart disease.
All inotropic agents should be administered via a large central vein, and their effects carefully monitored. Some of the currently available inotropes are considered here.

Adrenaline

Adrenaline stimulates both 0′- and {3-adrenergic receptors, but at low doses {3 effects seem to predominate. This produces a tachycardia, with an increase in cardiac index and a fall in peripheral resistance. At higher doses, 0′- mediated vasoconstriction develops. If this produces a useful increase in perfusion pressure, urine output may increase and renal failure may be avoided. However, as the dose is further increased, cardiac output may actually fall, accompanied by marked vasoconstriction, tachycardia and a metabolic acidosis. A reduction in renal blood flow then occurs, with oliguria and a risk of acute renal failure. Prolonged high-dose administration may eventually cause peripheral gangrene. For these reasons the minimum effective dose should be used for as short a time as possible. The addition of low-dose dopamine to the regimen may help to preserve renal function. Despite its disadvantages, adrenaline remains a useful potent inotrope and is used when other agents have failed. When haemodynamic monitoring is not available adrenaline is probably the agent of choice in septic shock, and should probably be combined with lowdose dopamine.

Noradrenaline

This is predominantly an a-adrenergic agonist. It can be of value in those with severe hypotension associated with a low systemic resistance, for example in septic shock. There is a risk of producing excessive vasoconstriction with impaired organ perfusion and increased after-load. oradrenaline administration must therefore be accompanied by full haemodynamic monitoring, including determination of cardiac output and calculation of the peripheral resistance.

Isoprenaline

This f3-adrenergic stimulant has both inotropic andchronotropic effects. It reduces peripheral resistance by  dilating skin and muscle blood vessels and diverts flow away from vital organs such as the kidneys. The increase in cardiac output produced by isoprenaline is mainly due to the tachycardia, and this, together with the development of arrhythmias, seriously limits its value. There are now few indications for isoprenaline in the criticially ill adult.

Dopamine

This is a natural precursor of noradrenaline which acts on D1 and D2 dopamine receptors, as well as a- and 13- adrenergic receptors. Its main action (at a dose of 3-10 p,g kg:’ min-I) is on f3l-adrenoreceptors on cardiac muscle, increasing cardiac contractility without increasing rate. The dosage, however, is critical.
IN LOW DOSES (1-3 p,g kg” min-‘) dopaminergic vasodilatory receptors in the renal, mesenteric, cerebral and coronary circulations are activated. D1 receptors are located on postsynaptic membranes and mediate vasodilatory effects whilst D2 receptors are presynaptic and potentiate these vasodilatory effects by preventing the release of noradrenaline. This results in an increase in renal plasma flow and glomerular filtration rate with an improved urinary output. It also increases hepatic blood flow.
MEDIUM DOSES (3-10 p,g kg'” min-I) activation of f3l-adrenoreceptors occurs with an increase in heart rate, myocardial contractility and cardiac output. IN HIGH DOSES (>20 p,g kg-I min-‘) dopamine increases noradrenaline and therefore activates aladrenergic receptors leading to vasoconstriction. This causes an increase in after-load and raises the ventricular filling pressures.

Dopexamine

This analogue of dopamine is a vasodilator (f32-agonist) that does not stimulate a-receptors. It is a positive inotrope and increases renal blood flow, but in septic shock may exacerbate hypotension by further reducing systemic vascular resistance. It is likely to be most useful in those with low cardiac output and peripheral vasoconstriction.

Dobutamine

Dobutamine is closely related to dopamine with predominant 131activity and less a constricting activity, but equal positive ‘inotropic’ effect.
• It has no specific effect on the renal vasculature although urine output often increases as cardiac output and blood pressure improve.
• It reduces systemic resistance and improves cardiac performance, thereby decreasing both after-load and ventricular filling pressures.
• It produces a greater improvement in cardiac output than dopamine for a given increase in myocardial oxygen consumption.
For these reasons, dobutamine is probably the agent of choice in patients with cardiogenic shock and cardiac failure.

Enoximone

This agent, active both orally and intravenously, is a phosphodiesterase inhibitor with inotropic and vasodilator properties. Enoximone may, however, cause profound vasodilatation and precipitate or worsen hypotension due to profound vasodilatation. It is sometimes useful in the management of acute cardiac failure.

Summary

Many still consider dopamine to be the inotrope of choice in most critically ill patients, largely because of its effects on splanchnic blood flow, although others favour dopexamine as a means of increasing cardiac output and organ blood flow. Dobutamine is equally popular and is particularly indicated in patients in whom the vasoconstriction caused by dopamine could be dangerous (i.e. patients with cardiac disease and septic patients with fluid overload or myocardial failure). The combination of dobutamine and noradrenaline is currently popular for the management of patients who are shocked with a low systemic resistance. Dobutamine is given to achieve an optimalcardiac output, while noradrenaline is used to restore anadequat e blood pressure by reducing vasodilatation. However this combination can only be used safely when guided by full haemodynamic monitoring. Adrenaline, because of its potency, remains a useful agent in those patients unresponsive to other measures, particularly after cardiac surgery, and is a cheap, effective
agent for the management of septic shock.

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