Management Of Hypotension

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Hypotension is common in the organ donor and its etiology is multifactorial. Hypotension may result from iatrogenic causes such as inadequate fluid resuscitation or fluid replacement, causes related to brain death such as neurogenic diabetes insipidus and loss of central vasomotor control or ventricular dysfunction secondary to myocardial ischemia or traumatic injury. Endocrine failure as a cause of hypotension has received much attention recently. The mechanism and rationale for hormone replacement as treatment will be discussed elsewhere.

Numerous studies have reported a significant increase in ATN and primary nonfunction in kidneys from donors with systolic pressure below 80-90 mm Hg. Blood pressure should therefore be maintained at systolic pressures of 100-120 mm Hg. Attempts to maintain pressures above this range with excess fluids or vasopressors will have deleterious effects on the donor.


Hypovolemia is the most common cause of hypotension in the abdominal organ donor and there are two principal iatrogenic causes. First, in an attempt to avoid CNS edema, deliberate maintenance of volume depletion is pursued in the brain-injured patient. Second, following declaration of brain death, volume depletion may facilitate lung recovery by avoiding pulmonary edema but also contributes to hypotension and hypoperfusion of abdominal organs. Ischemia related to poor perfusion in the organ donor may not itself result in significant injury but rather "primes" the tissue for damage resulting from reperfusion of oxygenated blood. Organ reperfusion injury may occur during subsequent successful resuscitation of the donor or following revascularization in the recipients. Strategies proposed to ameliorate ischemia-reperfusion injury are discussed below.

Ventricular Dysfunction

Ventricular dysfunction following brain death falls along a spectrum from mild to severe. Failure to achieve hemodynamic stability in the donor despite fluid resuscitation and inotrope support (see below) may well be a marker of the severity of myocardial damage. Timely placement of the organs and rapid transport to the operating room may then be necessary prior to cardiac collapse.

Neurogenic Diabetes Insipidus

Neurogenic diabetes insipidus is characterized by polyuria, hyperosmolality with a serum osmolarity greater than 295, a urine osmolarity less than 300 mOsm/L and a urine specific gravity less than 1.005. Treatment requires aggressive replacement of urinary output for the previous hour together with hourly maintenance infusions. If urine output exceeds 400 mL/h and is not related to diuretic administration, fluid loading, inotropes or hyperglycemia, pharmacologic treatment is required with antidiuretic hormone. If not treated or treated inadequately, diabetes insipidus will result in further metabolic derangements of hypernatremia, hypokalemia, hypomagnesemia and hypocalcemia.

DDAVP (desmopressin acetate) is a synthetic analog of the natural pituitary hormone 8-arginine vasopressin (ADH). DDAVP given IV (0.5-1.0 Mg q 2-4 h) has a rapid onset (within minutes) and its duration of action is prolonged (6-20 hours). It has almost no pressor effects and the dose may be repeated if necessary. Administration by other routes is not recommended due to variation in absorption. Pitressin is bovine or porcine derived arginine vasopressin (AVP) and is an alternative if DDAVP is unavailable. AVP may result in decreased renal and splanchnic blood flow further impairing renal, pancreatic and hepatic perfusion. Recommended starting dose of Pitressin is 50 units in 500 mL D5W at 5 units/h titrated to maintain urine output equal to or greater than 100 mL/h. Exacerbation of hyponatremia may occur if vasopressin is administered together with hypotonic fluids. During treatment of neurogenic diabetes insipidus close monitoring of central venous pressures is required to guide therapy and help avoid volume overload.

Goals of Fluid Resuscitation

The goals of fluid resuscitation should be a CVP of 6-12 cm H2O, urine output greater than 100 mL/h and a systolic BP greater than 100 mm Hg on minimal vasopressors (see below). Despite fluid resuscitation and achievement of targeted blood pressure, if urine output is inadequate, mannitol or furosemide should be given. The choice of fluids is based on two important criteria. The first is coexisting electrolyte and glucose abnormalities and the second is the need to avoid edema. Pulmonary edema precludes lung procurement, but if the lungs have been excluded volume expansion is limited insofar as it affects systemic oxygenation.

However, edematous organs, especially the liver, may not flush as well and, therefore, cool less efficiently during the final stages of procurement. Whether edematous organs tolerate prolonged periods of cold storage poorly is not known.

Choice of Fluids

Fluids should be warmed both to prevent the exacerbation of pre-existing hypothermia or the induction of hypothermia. Administration of excess salt solutions during rapid diuresis (induced by diuretics or diabetes insipidus) may aggravate pre-existing hypernatremia. Frequent monitoring of serum sodium is required. Ringer's lactate is a good choice for volume expansion, as it has a lower sodium content (130 mEq/L) as compared to normal saline (154 mEq/L).

Inadequate fluid resuscitation may transform a planned multiorgan retrieval into a kidney only retrieval as the organ donor becomes further unstable during transport to the operating room. Boluses of colloids such as albumin may also be required to correct hypotension and maintain tissue perfusion. Blood should be transfused if the hematocrit is less than 30% especially if a multiorgan recovery is anticipated with a longer operative time and the greater potential for intraoperative blood loss. It is important to ensure that pretransfusion serology has been drawn before giving blood.


If hypotension persists despite adequate fluid resuscitation inotropic agents are required to maintain adequate blood pressure. Dopamine (Intropin) is the preferred first-line drug. Its effects on blood pressure result from its positive inotropic effect on the myocardium and resultant increase in cardiac output. At low doses (0.5-2.0 mg/kg/min), it also acts to vasodilate renal and splanchnic blood vessels thereby increasing perfusion to the abdominal organs. Its onset of action is rapid (5 min) and it must be given as a continuous infusion titrated to the patient's response. At doses greater than 10 mg/kg any advantages of this drug are lost as vasoconstriction occurs (alpha-adrenergic effect). Dopamine often is available from the hospital pharmacy premixed as 400 mg/250 mL which is equivalent to 1600 mg/mL. If a greater concentration is required due to fluid restriction, this needs to be communicated to the pharmacy.

With dopamine, peripheral vasodilation and the resulting decrease in peripheral resistance may counteract the increases in systolic blood pressure and pulse pressure. In practice, low dose dopamine is infrequently sufficient to adequately treat hypotension in the organ donor. Alpha agonists are commonly required such as Levophed or Neosynephrine.

Norepinephrine (Levophed) is identical to the endogenous catecholamine which is synthesized in the adrenal medulla and in sympathetic nervous tissue. It acts predominately by a direct effect on alpha-adrenergic receptors increasing total peripheral resistance with increases in systolic and diastolic blood pressure. However, constriction of renal blood vessels will reduce renal blood flow. Norepinephrine can increase glycogenolysis and inhibit insulin release from the pancreas, resulting in hyperglycemia. This drug must be administered cautiously in

patients chronically receiving tricyclic antidepressants. Administration of Lasix may decrease responsiveness to norepinephrine. Norepinephrine should be administered in the lowest effective dose for the shortest period of time. Generally 2-4 mg/min titrated to blood pressure is recommended.

Phenylephrine (Neosynephrine) also acts predominately by a direct effect on alpha-adrenergic receptors. Like Levophed, Neosynephrine should be administered in the lowest effective dose for the shortest period of time and only after volume resuscitation is complete. The recommended infusion rate is, 10-50 mg/min titrated to blood pressure.

Not infrequently, despite adequate volume resuscitation and combination therapy with Dopamine and other vasopressors as well as correction of other conditions contributing to donor deterioration e.g., pneumothorax, hypotension persists. This is most often due to significant myocardial dysfunction. When inotrope requirements continue to rise or the expected response does not occur, pulmonary artery catheterization (Swan-Ganz) is recommended if not already in place. To minimize the contribution of catecholamines to posttransplant ATN, some centers routinely administer alpha blockade to donors in the operating room (Regitine, 10 mg).

In the situation where the potential organ donor is responding poorly to massive doses of inotropes, some authors have suggested cardiac support in the form of intra-aortic balloon counterpulsation (IABP) or cardiopulmonary bypass. The ability to institute these measures in a timely fashion is limited in most centers. The outcome in the recipients of these organs would likely be poor with a high incidence of primary nonfunction or persistent graft dysfunction.

Sample Calculation

A 70 kg donor has a serum Na of 170 mEq/1 Elevated Na reflects hypertonicity in all fluid compartments. All compartments need water, so space involved is TBW (total body water) = 0.6 x Body Wt (kg) Present Na x Present TBW = Desired Na x Desired TBW OR: 170 mEq/L x 42 L = 150 mEq/L x ? ? = 47.6 L

So, TBW needs to be expanded from 42 to 47.6 Liters 5.6 liters of WATER are needed A quicker way to the same answer:

? = 0.6 x Body Wt (kg) x {Present Na-Desired Na} { Desired Na }

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