med 18

 

MEDICAL DECISION MAKING

Once shock is recognized, rapidly attempt to identify both

the subtype and inciting factor to determine the appropriate therapy (Table 1 2-1). Time is truly of the essence in

these patients, and any delay will significantly impact

patient outcome. Concurrently address the patient airway,

breathing, and circulation (ABCs) and stabilize all severely

ill patients. Use the ancillary laboratory and imaging studies mentioned previously to guide the diagnosis and treatment (Figure 12-1).

Table 1 2-1. SHOCK: differentia l diagnosis.

Shock Mnemonic

S Septic, spinal (neurogenic)

H Hypovolemic, hemorrhagic

0 Obstructive (pulmonary embol ism, tamponade)

c Cardiogenic

K Kortisol (adrenal crisis), AnaphylaKtic

Continued volume resuscitation,

identify and control ongoing

hemorrhage

CHAPTER 12

Early goal directed therapy

for sepsis

Epineph rine, antih istamines

& steroids and removal of

inciting agent for ana phylaxis

Dopamine and atropine for

neurogenic shock

Pericard iocentesis for

tamponade

Fibrinolysis for

massive PE

Needle thoracostomy

for tension PTX

ACLS care for dysrhythmia

control

Inotropic support with

dobutamine + dopamine

Immediate reperfusion

with PCI

.&. Figure 1 2-1. Shock diagnostic algorithm. ACLS, advanced cardiac life support; PCI, percutaneous coronary

intervention PE, pulmonary embol ism; PTX, pneumothorax.

TREATMENT

The goal of treatment is 2-fold, namely to restore normal

cellular function and reverse the inciting factor. Place all

patients on supplemental 02 and consider early mechanical

ventilation in those with markedly elevated metabolic

demands, as hyperactive respiratory muscles can steal away

up to 50% of normal cerebral blood flow. Place a minimum

of 2 large-bore peripheral N lines in all patients and con ­

sider central line placement in those who will require multiple infusions, vasopressor support, or CVP monitoring.

Administer boluses of normal saline to replenish an absolute

or relative vascular depletion. Transfuse red blood cells as

needed to augment circulating 02 delivery. Initiate vasopressor support in patients who either fail to respond or have a

contraindication ( eg, cardiogenic shock) to repeated fluid

boluses. Place a Foley catheter to accurately measure urine

output. The management of specific types of shock is discussed next.

� Hypovolemic Shock

Restore adequate tissue perfusion by rapidly expanding the

intravascular volume. Infuse several liters of normal saline

followed by several units of packed red blood cells in hemorrhagic patients who fail to respond. Patients with simple

dehydration will improve rapidly. Of note, avoid overly

aggressive volume expansion in trauma patients, as this

may trigger recurrent hemorrhage at previously clotted

sites. Titrate therapy in these patients to a goal mean arte ­

rial pressure (MAP) of 60 mmHg and restoration of nor ­

mal mental status.

� Distributive Shock

Sepsis

Begin early goal-directed therapy in all patients with septic

shock. Monitor the CVP to guide fluid resuscitation in these

patients. Begin treatment by aggressively bolusing several

liters of normal saline to achieve a goal CVP between 8 and

12 mmHg. Initiate vasopressor support with a norepinephrine infusion in patients who remain hypotensive and

titrate to a goal MAP >65 mmHg. Start broad-spectrum

antibiotics targeted at the proposed source and pursue s urgical drainage/debridement when indicated.

Neurogenic Shock

Address all other potential causes of shock first, as neuro ­

genic shock is a diagnosis of exclusion. Aggressively expand

the circulating blood volume by bolusing several liters of

normal saline. Initiate a dopamine infusion for vasopressor

support in all patients who fail to respond. Use small doses

ofN atropine (eg, 0.5 mg) to treat symptomatic bradycardia refractive to the previously mentioned measures.