Invasive Hemodynamic Monitoring/Initial Management Invasive hemodynamic monitoring is used selectively in donors to assist in optimizing cardiovascular management prior to organ procurement. In the unstable donor it is essential to determine the relative need for volume expansion versus inotropes versus vasopressors, since appropriate therapy will maximize the number of suitable organs. An arterial line is used for close monitoring of all donors. Central venous pressure monitoring is also useful in most cases for monitoring of volume status and for reliable delivery of drugs. A pulmonary artery catheter is used selectively in situations of hemodynamic instability or questionable cardiac function. The ability to distinguish hemodynamic instability caused by inadequate preload (relative hypovolemia) versus inappropriate afterload (peripheral vasomotor collapse) versus depressed inotropic state (cardiac contractile dysfunction) is essential to guide effective donor management.76 The use of a pulmonary artery catheter can be most useful under these circumstances.
A urinary drainage catheter is placed in all potential donors to monitor urinary output, assess renal function, and keep pace with the large urine output seen with diabetes insipidus which occurs in 50-70% of all organ donors. Although not always considered from the outset of the patient's hospital course, placement of a nasogastric tube is critical to help prevent aspiration in all potential lung donors. Early placement of a nasogastric tube should be stressed to all hospitals and organ procurement organizations caring for multi-organ donors.
Following most forms of brain injury but prior to declaration of brain death, intravenous fluid is usually restricted in an attempt to limit cerebral edema and salvage any existing CNS function. This management, along with the nearly universal occurrence of diabetes insipidus due to pituitary nonfunction, may result in profound hypovolemia. Moreover, as part of the pathophysiology of brain death, there is usually a secondary loss of vasomotor tone. Therefore, when a potential donor is first identified, they are frequently intravascularly volume depleted, vasodilated, and hypotensive. Once a potential donor is declared brain dead, the first maneuver in donor management is to accurately assess the intravascular volume status and the peripheral vasomotor tone and then appropriately pursue aggressive volume repletion, with an intravenous fluid infusion ratio equal to the hourly urine output plus 100 mL/hr, maintaining the CVP in the 4-12 cm H2O range. Vasopressin or DDAVP (water soluble form of shorter acting vasopressin) is often required to sustain euvolemia. Close observation and correction of electrolyte abnormalities is required to avoid hypo- or hyperosmolar states which can have deleterious consequences such as tissue damage and dysrhythmias.
While aggressive volume resuscitation may benefit most solid organs, it will often have a detrimental effect on donor lung function. One report has demonstrated that merely raising the CVP from 4-6 cm H2O up to 8-10 cm H2O with crystalloid solution causes a significant increase in the alveolar arterial oxygen gradient.77 The careful use of colloid solutions is recommended whenever possible in an attempt to maintain intravascular volume. Hemodynamic problems related to peripheral vasomotor tone are best managed with pressor agents with the goal of maintaining a normal systemic vascular resistance. With careful attention to volume management, the need for inotropic or pressor support is less common. Sustained or excessive inotropic requirements in the presence of ad
equate filling pressures and peripheral resistance should raise questions about the suitability of the heart for organ procurement.
Blood products are used very judiciously in organ donors due to the risks of transmissible infectious diseases and of sensitizing the recipient to multiple additional other donor antigens. The role of donor specific transfusion and nonspecific transfusion is not completely understood. We prefer to avoid transfusion of all blood products in both the donor and the recipient unless absolutely necessary. We would prefer to transfuse only leuko-reduced blood products when the oxygen carrying capacity of the blood falls too low (Hemoglobin < 8.0 gm% or SVO2 < 60).
In the donor population, low dose inotropes or pressor agents are often utilized in order to limit the volume of fluid infused (Table 7.4). Additionally, ino-tropic agents can be used as a test to observe the hemodynamic response in a questionable donor. Antiarrhythmic agents are infrequently used, as the more common dysrhythmia would be sinus tachycardia, typically due to hypovolemia. DDAVP (vasopressin), as described above, is commonly used to manage diabetes insipidus. Thyroxine has been used in situations where conventional pressor support is not effective. Support for this practice is controversial in the literature but has been effective in selected clinical settings.78,79
Table 7.4. Frequently utilized medications for donor management
1. Hormonal Agents
Desmopressin (DDAVP) 0.3 mcg/kg IV over 30 min repeat if urine output not controlled maximum total dose-4 mcg
5-10 U q8h IV, or continuous infusion 0.5 to 1 U/hour titrate to maintain urine output between 100 and 300 ml/hour
20 mcg IV followed by a thyroxine infusion of 200 mcg in 500 mL normal saline at 25 mL/hour titrate to maintain adequate blood pressure
2. Inotropic Agents
Dopamine 3-10 mcg/kg/min
Dobutamine 5-10 mcg/kg/min
Epinephrine 0.01-0.03 mcg/kg/min
3. Pressor Agents
Phenylephrine 0.06-0.18 mg/min
After establishing donor status, ventilator management should be directed at limiting barotrauma. A CMV mode is usually appropriate, with a weight proportional tidal volume (10-15 mL/kg). Fraction of inspired oxygen should be maintained at less than or equal to 40%, or sufficient to keep the arterial saturation above 90%. Airway pressures should be in normal range (less than 25 cm H2O), and low levels of PEEP (5 cm H2O) are used to help limit atelectasis. Any changes in lung compliance should be reported to the transplant teams.
Abnormalities in thermoregulation are relatively common after brain death, reflecting hypothalamic dysfunction. Treatment of both hypo- and hyperthermia are important to avoid complications such as dysrhythmias and tissue damage. Management of these temperature fluctuations are relatively basic. For hypothermia, application of warming blankets, heating lights, warmed intravenous fluids and ventilator circuit gases are means to maintain body temperature between 36.5°C-37.5°C. Conversely, treatment of hyperthermia includes the use of cooling blankets, ice packs, and alcohol compresses after searching for systemic infection by obtaining blood, urine, and sputum cultures.
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