Overall Management Strategies in Shock
As described previously and in the discussion of types of shock to follow, management in all types and all phases of shock includes the following:
• Fluid replacement to restore intravascular volume
• Vasoactive medications to restore vasomotor tone and im-prove cardiac function
• Nutritional support to address the metabolic requirements that are often dramatically increased in shock
Therapies described in this section require collaboration among all members of the health care team to ensure that the manifesta-tions of shock are quickly identified and that adequate and timely treatment is instituted to achieve the best outcome possible.
Fluid replacement is administered in all types of shock. The type of fluids administered and the speed of delivery vary, but fluids are given to improve cardiac and tissue oxygenation, which in part depends on flow. The fluids administered may include crys-talloids (electrolyte solutions that move freely between intravascu-lar and interstitial spaces), colloids (large-molecule intravenous solutions), or blood components.
The best fluid to treat shock remains controversial. In emergen-cies, the “best” fluid is often the fluid that is readily available. Both crystalloids and colloids, as described later, can be given to restore intravascular volume. Blood component therapy is used most frequently in hypovolemic shock.
Crystalloids are electrolyte solutions that move freely between the intravascular compartment and the interstitial spaces. Isotonic crystalloid solutions are often selected because they contain the same concentration of electrolytes as the extracellular fluid and therefore can be given without altering the concentrations of elec-trolytes in the plasma.
Common intravenous fluids used for resuscitation in hypovo-lemic shock include 0.9% sodium chloride solution (normal saline) and lactated Ringer’s solution (Choi et al., 1999). Ringer’s lactate is an electrolyte solution containing the lactate ion, which should not be confused with lactic acid. The lactate ion is con-verted to bicarbonate, which helps to buffer the overall acidosis that occurs in shock.
A disadvantage of using isotonic crystalloid solutions is that three parts of the volume are lost to the interstitial compartment for every one part that remains in the intravascular compartment. This occurs in response to mechanisms that store extracellular body fluid. Diffusion of crystalloids into the interstitial space ne-cessitates that more fluid be administered than the amount lost (Choi et al., 1999).
Care must be taken when rapidly administering isotonic crys-talloids to avoid causing excessive edema, particularly pulmonary edema. For this reason, and depending on the cause of the hypo-volemia, a hypertonic crystalloid solution, such as 3% sodium chloride, is sometimes administered in hypovolemic shock. Hypertonic solutions produce a large osmotic force that pulls fluid from the intracellular space to the extracellular space to achieve a fluid balance (Choi et al., 1999; Fein & Calalang-Colucci, 2000). The osmotic effect of hypertonic solutions re-sults in fewer fluids being administered to restore intravascular volume. Complications associated with use of hypertonic saline solution include excessive serum osmolality, hypernatremia, hy-pokalemia, and altered thermoregulation.
Generally, intravenous colloidal solutions are considered to be plasma proteins, which are molecules that are too large to pass through capillary membranes. Colloids expand intravascular vol-ume by exerting oncotic pressure, thereby pulling fluid into the intravascular space. Colloidal solutions have the same effect as hy-pertonic solutions in increasing intravascular volume, but less volume of fluid is required than with crystalloids. Additionally, col-loids have a longer duration of action than crystalloids because the molecules remain within the intravascular compartment longer.
An albumin solution is commonly used to treat hypovolemic shock. Albumin is a plasma protein; an albumin solution is pre-pared from human plasma and is heated to reduce its potential to transmit disease. The disadvantages of albumin are its high cost and limited availability, which depends on blood donors. Syn-thetic colloid preparations, such as hetastarch and dextran solu-tion, are now widely used. Dextran, however, may interfere with platelet aggregation and therefore is not indicated if hemorrhage is the cause of the hypovolemic shock or if the patient has a co-agulation disorder (coagulopathy).
Close monitoring of the patient during fluid replacement is neces-sary to identify side effects and complications. The most common and serious side effects of fluid replacement are cardiovascular over-load and pulmonary edema.
Patients receiving fluid replacement must be monitored fre-quently for adequate urinary output, changes in mental status, skin perfusion, and changes in vital signs. Lung sounds are aus-cultated frequently to detect signs of fluid accumulation. Adven-titious lung sounds, such as crackles, may indicate pulmonary edema.
Often a right atrial pressure line (also known as a central ve-nous pressure line) is inserted. In addition to physical assessment, the right atrial pressure value helps in monitoring the patient’s re-sponse to fluid replacement. A normal right atrial pressure value is 4 to 12 mm Hg or cm H2O. Several readings are obtained to determine a range, and fluid replacement is continued to achieve a pressure within normal limits. Hemodynamic monitoring with arterial and pulmonary artery lines may be implemented to allow close monitoring of the patient’s perfusion and cardiac status as well as response to therapy.
Vasoactive medications are administered in all forms of shock to improve the patient’s hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Specific medications are selected to correct the particular hemodynamic alteration that is impeding cardiac output. Specific vasoactive medications are pre-scribed for the patient in shock because they can support the pa-tient’s hemodynamic status. These medications help to increase the strength of myocardial contractility, regulate the heart rate, reduce myocardial resistance, and initiate vasoconstriction.
Vasoactive medications are selected for their action on recep-tors of the sympathetic nervous system. These receptors are known as alpha-adrenergic and beta-adrenergic receptors. Beta-adrenergic receptors are further classified as beta1- and beta2-adrenergic recep-tors. When alpha-adrenergic receptors are stimulated, blood vessels constrict in the cardiorespiratory and gastrointestinal systems, skin, and kidneys. When beta1-adrenergic receptors are stimulated, heart rate and myocardial contraction increase. Whenbeta2-adrenergic receptors are stimulated, vasodilation occurs in the heart and skeletal muscles, and the bronchioles relax. The medications used in treating shock consist of various combina-tions of vasoactive medications to maximize tissue perfusion by stimulating or blocking the alpha- and beta-adrenergic receptors.
When vasoactive medications are administered, vital signs must be monitored frequently (at least every 15 minutes until sta-ble, or more often if indicated). Vasoactive medications should be administered through a central venous line because infiltration and extravasation of some vasoactive medications can cause tis-sue necrosis and sloughing. An intravenous pump or controller should be used to ensure that the medications are delivered safely and accurately.
Individual medication dosages are usually titrated by the nurse, who adjusts the intravenous drip rates based on the physi-cian’s prescription and the patient’s response. Dosages are changed to maintain the MAP (usually above 80 mm Hg) at a physiologic level that ensures adequate tissue perfusion.
Dosages of vasoactive medications should be tapered and the patient should be weaned from the medication with frequent monitoring (every 15 minutes) of blood pressure. Table 15-1 presents some of the commonly prescribed vasoactive medica-tions used in treating shock.
Nutritional support is an important aspect of care for the patient with shock. Increased metabolic rates during shock increase en-ergy requirements and therefore caloric requirements. The pa-tient in shock requires more than 3,000 calories daily.
The release of catecholamines early in the shock continuum causes glycogen stores to be depleted in about 8 to 10 hours. Nu-tritional energy requirements are then met by breaking down lean body mass. In this catabolic process, skeletal muscle mass is bro-ken down even when the patient has large stores of fat or adipose tissue.
Loss of skeletal muscle can greatly prolong the recovery time for the patient in shock. Parenteral or enteral nutritional sup-port should be initiated as soon as possible, with some form of en-teral nutrition always being administered. The integrity of the gastrointestinal system depends on direct exposure to nutrients. Additionally, glutamine (an essential amino acid during stress) is important in the immunologic function of the gastrointestinal tract, providing a fuel source for lymphocytes and macrophages. Glutamine can be administered through enteral nutrition (Rauen & Munro, 1998).
Stress ulcers occur frequently in acutely ill patients because of the compromised blood supply to the gastrointestinal tract. There-fore, antacids, histamine-2 blockers (eg, famotidine [Pepcid], ran-itidine [Zantac]), and antipeptic agents (eg, sucralfate [Carafate]) are prescribed to prevent ulcer formation by inhibiting gastric acid secretion or increasing gastric pH.
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