Shock

La u ren M. Smith, MD

Nihja 0. Gordon, MD

Key Points

• Do not wait for hypotension to diagnose shock.

• Early ide ntification and i n itiation of aggressive

therapy can significantly improve patient

survival.

INTRODUCTION

More than 1 million patients present to U.S. emergency

departments annually with shock, and despite continued

advances in critical care, mortality rates remain very high.

Shock occurs when the circulatory system is no longer able

to deliver enough 02 and vital nutrients to adequately meet

the metabolic demands of the patient. Although initially

reversible, prolonged hypoperfusion will eventually result

in cellular hypoxia and the derangement of critical bio ­

chemical processes. From a clinical standpoint, shock can

be divided into the following subtypes: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic

shock results from an inadequate circulating blood volume

owing to either profound dehydration or significant hemorrhage. Traumatic hypovolemia is the most common type

of shock encountered in patients <40 years of age.

Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired

pump function or significant dysrhythmia. Myocardial

infarction is the leading cause of cardiogenic shock and

typically occurs once -40% of the myocardium is dysfunctional. Obstructive shock results from an extracardiac

blockage of adequate venous return of blood to the heart

( eg, pericardia! tamponade, tension pneumothorax, and

massive pulmonary embolism [PE) ). Finally, distributive

shock occurs secondary to an uncontrolled loss of vascular

tone (eg, sepsis, anaphylaxis, neurogenic shock, and adrenal

42

• I n itiate early goa l-directed therapy in patients with

septic shock.

• Early revascu larization is key to improving outcome in

patients with cardiogenic shock.

crisis). Neurogenic shock most commonly occurs in

trauma patients with high cervical cord injuries and a

secondary loss of sympathetic tone and should always be

considered a diagnosis of exclusion. Classically these

patients will present with hypotension and a paradoxical

bradycardia. Suspect septic shock in elderly, irnmunocompromised, and debilitated patients who are toxic appearing

despite only vague symptoms. The prognosis for patients

with cardiogenic and septic shock remains grave, with

mortality rates between 30% and 90%.

The pathophysiology of shock can be divided into

3 basic categories: a systemic autonomic response, endorgan cellular hypoxia, and the secretion of proinflammatory mediators. The autonomic system initially responds

to widespread tissue hypoperfusion by globally increasing

the overall cardiac output. As tissue perfusion continues

to decline, the body shunts circulating blood away from

less vital structures including the skin, muscles, kidneys,

and splanchnic beds. Reflexively, the kidneys activate the

renin-angiotensin axis, prompting the release of various

vasoactive substances, with the net effect to preserve perfusion to the most critical organs, namely the brain and

the heart.

When the preceding response is inadequate despite

maximal tissue 02 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism. By nature,

anaerobic metabolism cannot produce enough adenosine

triphosphate to maintain regular cellular function. Tissue

lactate accumulates, resulting in systemic acidosis, and

eventually this breakdown in cellular metabolism leads to

widespread tissue death. Injured and dying cells prompt

the production and secretion of harmful inflammatory

mediators, resulting in the development of the systemic

inflammatory response syndrome, defined by the presence

of fever, tachycardia, tachypnea, and leukocytosis.

CLINICAL PRESENTATION

� History

Vague complaints such as fatigue and malaise may be the

only presenting symptoms, especially in elderly patients.

Friends, family, and emergency medical service personnel

will be vital in obtaining a history in patients with altered

mental status. The past medical history including a list of

active medications might reveal risk factors such as immunosuppression, underlying cardiac disease, and potential

allergic reactions.

� Physical Examination

Although hypotension and tachycardia are the cardinal

features of shock, many patients will presents with normal

vital signs owing to physiologic compensation. Because of

the unmet metabolic demands of the central nervous sys ­

tern, altered mental status is not uncommon. Jugular

venous distention, cardiac murmurs, and pulmonary rales

often accompany cardiogenic shock. A careful skin examination can be invaluable, as patients in distributive shock

frequently exhibit warm hyperemic extremities, whereas

those in cardiogenic, hypovolemic, and obstructive shock

will present with cool mottled extremities secondary to

profound systemic vasoconstriction. Furthermore, abnormal findings such as diffuse urticaria, pronounced erythema, or widespread purpura may help identify the t ype

and source of shock. The abdominal exam should focus on

careful palpation and looking for signs of peritonitis or a

pulsatile mass. Measure urine output, as low volumes indicate an absolute or relative volume deficiency and may help

guide resuscitation.

DIAGNOSTIC STUDIES

� Laboratory

No single laboratory test is diagnostic of shock. Complete

blood count testing may reveal an elevated, normal, or

low white blood cell (WBC) count. No matter the absolute WBC count, a bandernia >10% suggests an ongoing

infectious process. Comprehensive metabolic panel analysis will assess both kidney and liver function and acidbase status. An elevated anion gap may indicate underlying

lactic acidosis, uremia, or toxic ingestion. Blood gas

analysis is useful to determine the serum pH, lactate

level, and base deficit. Serum lactate is a highly sensitive

marker for tissue hypoperfusion and predictive of overall

SHOCK

mortality in septic shock. Lactate levels >4 rnmol!L are

significant and indicate ongoing cellular hypoxia. Other

tests useful in the appropriate clinical scenario include

cardiac markers, urinalyses, coagulation profiles, toxicologic screens, and pregnancy testing. Obtain blood and

urine cultures (and possibly cerebrospinal fluid) if sepsis

is a concern.

� Imaging

No single radiologic test is diagnostic of shock. Chest

x-ray may reveal evidence of an infiltrate (sepsis),

enlarged cardiac silhouette (cardiac tamponade), subdiaphragmatic free air (sepsis), pulmonary edema (cardiagenic shock) or pneumothorax. Bedside ultrasound can

guide the work-up, treatment, and disposition of patients

in shock in multiple clinical situations including sepsis,

blunt abdominal trauma, pregnancy, abdominal aortic

aneurysm, and pericardia! tamponade. Furthermore,

ultrasonographic inferior vena cava measurement can

help guide appropriate fluid resuscitation. Computed

tomography imaging has become the modality of choice

for diagnosing PE, aortic dissection, and intra-abdominal

pathology.

PROCEDURES

Endotracheal intubation may be required in patients with

profound shock to reduce the work of breathing and systemic metabolic demands. Central venous line placement

can expedite fluid or blood product infusion, vasopressor administration, and central venous pressure (CVP)

analysis.

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.

Anaphylaxis

Anaphylactic shock can be rapidly fatal and requires

immediate treatment. Administer normal saline boluses,

N antihistamines, and N corticosteroids to all patients.

Give intramuscular epinephrine (1:1,000 solution) in 0.3-

to 0.5-mg doses as needed to maintain systemic perfusion.

In patients refractive to the preceding, administer 0.3- to

0.5-mg doses of N epinephrine (1:10,000 solution) over a

2- to 3-minute duration. Actively search for and remove

any ongoing allergen exposure ( eg, retained soft tissue bee

stinger).

SHOCK

� Obstructive Shock

Cardiac Tamponade

Administer 1-2 L of normal saline followed by emergent

bedside pericardiocentesis. Perform an emergency department

thoracotomy in patients with penetrating thoracic trauma

who fail to respond.

Pulmonary Embolism

Administer small boluses of normal saline (250-500 mL)

followed by vasopressor support in unstable patients.

Fibrinolysis is the treatment of choice for massive PE presenting with profound hypotension (MAP <60), severe

refractive hypoxemia (Sp02 <90 despite supplemental 02),

or cardiac arrest.

Tension Pneumothorax

Administer 1-2 L of normal saline while performing

emergent needle thoracostomy followed by chest tube

placement.

� Cardiogenic Shock

The goal of treatment is to improve cardiac output while

at the same time reducing myocardial workload.

Administer IV fluids judiciously to avoid undesired elevations in the left ventricular preload and secondary pulmonary edema. Begin inotropic and vasopressor support in

patients who remain hypotensive despite IV fluids. Firstline therapy is often a combination of dopamine and

dobutamine (as dobutamine monotherapy will exacerbate

hypotension), with norepinephrine reserved for patients

who fail to respond. Of note, all of the aforementioned

modalities are temporizing measures pending definitive

revascularization (ie, percutaneous coronary intervention

or fibrinolysis).

DISPOSITION

Admit all patients in shock to a critical care bed.

SUGGESTED READING

Cherkas D. Traumatic hemorrhagic shock: Advances in fluid

management. Emerg Med Pract. 20 1 1;13:1-20.

Dellinger, RP, Levy, MM, et al. Surviving Sepsis Campaign:

International guidelines for management of severe sepsis and

septic shock: 2008. Grit Care Med. 2008;36:296-327.

Otero RM, Nguyen HB, Rivers EP. Approach to the patient in

shock. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ,

Cydulka RK, Meckler GD, eds. Tintinalli's Emergency

Medicine: A Comprehensive Study Guide. 7th ed. New York,

NY: McGraw-Hill, 201 1.

Reynolds HR, Hochman ]S. Cardiogenic shock: Current concepts

and improving outcomes. Circulation. 2008;1 17: