emergency management of shock

Question 1

Define shock.

Answer 1

Shock is a clinical syndrome characterized by widespread inadequate oxygenation and supply of
nutrients to tissues and organs, resulting in cellular dysfunction.

Question 2

How common is shock?

Answer 2

Although the prevalence is not precisely known, it is thought that shock constitutes approximately
1% of all ED visits.

Question 3

What is the overall mortality rate of patients who develop shock?

Answer 3

The mortality rate exceeds 20% for patients across all categories of shock.

Question 4

List the five categories of shock and provide examples of each.

Answer 4

1. Hypovolemic: Examples include trauma, gastrointestinal bleeding, ruptured ectopic pregnancy,
   ruptured abdominal aortic aneurysm, and diabetic ketoacidosis.
2. Cardiogenic: Examples include acute myocardial infarction, cardiomyopathy, and valvular
   dysfunction.
3. Distributive: Examples include sepsis, anaphylaxis, and spinal cord injury.
4. Obstructive: Examples include pulmonary embolism (PE), cardiac tamponade, and tension
   pneumothorax.
5. Toxic/metabolic: Examples of sources include carbon monoxide, cyanide, β-blocker, calcium
   channel blocker, adrenal insufficiency, and thyroid storm.

Question 5

How do I identify a patient in shock?

Answer 5

The successful treatment of an acutely ill patient with a high risk of death is predicated on early
recognition and treatment. A patient in shock will generally appear ill. Shock is a clinical syndrome
that reflects hypoperfusion. A brief focused history and targeted physical examination will help
determine whether shock is present and its underlying cause. Examples of system-based symptoms
and signs include the following:
• Central nervous system: Altered mentation
• Cardiovascular: Decreased cardiac output (CO), tachycardia, hypotension, and weak rapid pulses
• Pulmonary: Tachypnea and hyperpnea
• Renal: Decreased urine output
• Skin: Delayed capillary refill; skin is cool and mottled in the setting of hypovolemic or cardiogenic
shock, and warm and moist in the setting of distributive shock.

Question 6

How should urine output be used during resuscitation of a patient in shock?

Answer 6

Patients experiencing shock should have a Foley catheter in place to accurately measure urine
output. Urine output is an excellent indicator of organ perfusion, assuming the patient had normal
renal function at baseline. A normal urine output is more than 1 mL/kg/h, a reduced urine output
ranges from 0.5 to 1 mL/kg/h, and a severely reduced urine output is less than 0.5 mL/kg/h. During
resuscitation, targeted therapy should additionally focus on improving or normalizing urine output.

Question 7

Describe compensated and decompensated shock.

Answer 7

Shock initiates a sequence of stress responses intended to preserve perfusion to vital organs.
Compensated shock occurs soon after the onset of shock and is marked by the maintenance of
tissue perfusion pressures. Such patients typically have evidence of a stress response (e.g.,
tachycardia and tachypnea) but also have a normal or high blood pressure and normal or mildly
elevated serum lactate concentrations. If left untreated, compensated shock may progress to decompensated shock, which is characterized by profound global tissue hypoperfusion, elevated
serum lactate concentration, and hypotension.

Question 8

What is the initial management of a patient who is experiencing shock?

Answer 8

Management of patients in shock begins with airway, breathing, and circulation (ABCs). Because of
poor delivery and uptake of oxygen, all patients should receive either 15 L of oxygen by
nonrebreather mask or intubation. Additionally, all patients should have large-bore intravenous
access and a cardiac monitor.

Question 9

How useful are vital signs in assessing and treating someone in shock?

Answer 9

Vital signs are crucial. Heart rate, respiratory rate, blood pressure, and pulse oximetry should be
monitored closely in patients experiencing, or with suspected, shock. Physiologic compensation and
decompensation (see Question 7) are commonly reflected in a patient’s vital signs. Additionally,
normalization of abnormal vital signs is one indicator of a patient’s response to resuscitation.

Question 10

If a patient has normal vital signs, should I be reassured?

Answer 10

No. A patient’s heart rate and blood pressure may be normal in the setting of severe illness. In the
setting of shock, heart rate and blood pressure correlate poorly with CO and often do not reflect the
severity of systemic hypoperfusion.

Question 11

Are orthostatic vital signs a sensitive indicator of hypovolemia? What determines
a positive orthostatic test?

Answer 11

To know what is abnormal, you first must know what is normal. Studies on healthy euvolemic
people showed an average increase in pulse of 13 to 18 beats per minute, with a large standard
deviation. A pulse increase of 20 beats per minute as a determinant for hypovolemia is nonspecific
because many normal individuals fall within this range. However, an increase of 30 beats per
minute in heart rate is more specific. A 20% volume loss is required to produce this change in heart
rate, making this an insensitive test at best. The development of symptoms (e.g., lightheadedness
on standing) does not occur in healthy euvolemic individuals upon standing and should be
considered abnormal. Patients thought to be experiencing shock should not be allowed to stand as a
method of assessing changes in vital signs.

Question 12

Are there other signs that are helpful in assessing an acutely ill patient?

Answer 12

Yes. Besides vital signs and components of the physical examination (e.g., level of consciousness,
capillary refill, and urinary output), you should pay close attention to the patient’s serum lactate
concentration, central venous pressure (CVP), and central venous oxygen saturation (ScvO2) or mixed
venous oxygen saturation (SvO2).

Question 13

How should I use and interpret serum lactate concentration?

Answer 13

Serum lactate is a commonly used marker to assess the extent of systemic hypoperfusion and
the degree to which a patient may be responding to resuscitation. In fact it is an early marker
of systemic hypoperfusion and is often elevated before overt changes in a patient’s vital signs.
Therefore liberal use of this marker may help identify patients earlier in their disease processes. A
serum lactate concentration greater than 4 mEq/L is associated with the highest mortality rates.

Question 14

What is the lactate clearance index, and how can it be used during resuscitation
of a patient in shock?

Answer 14

The lactate clearance index refers to measurements of serum lactate concentrations at two or more
times during the course of the resuscitation. If after 1 hour of the beginning of resuscitation efforts the serum lactate concentration has not decreased by 50%, additional steps should be undertaken
to improve systemic perfusion.

Question 15

What is a normal CVP, and how is it measured?

Answer 15

A normal CVP ranges from 5 to 10 cm H2O. CVP is measured by attaching an electronic pressure
transducer or a water manometer to the end of an intravenous line placed into the central venous
system. The zero reference point for measuring a CVP is at the point that bisects the fourth
intercostal space and the midaxillary line in a supine patient, corresponding to the position of
the right atrium.

Question 16

How is CVP used during resuscitation of a patient experiencing shock?

Answer 16

The guiding principal for using CVP is to normalize or supranormalize its value. The target CVP
should range from 10 to 15 cm H2O to maximize cardiac preload. In many shock states, the heart
becomes stiff and its function is depressed. A supranormal CVP thus allows for improved cardiac
filling.

Question 17

What is venous oxygen saturation, and what is the difference between ScvO2
and SvO2?

Answer 17

Venous oxygen saturation provides a measure of tissue oxygenation (i.e., the balance between
DO2 and oxygen demand [VO2]). SvO2 is measured using a pulmonary artery catheter and includes
deoxygenated blood returning to the heart from the body, as well as deoxygenated blood from the
heart via the coronary sinus. It normally ranges between 65% and 75%. ScvO2, on the other hand,
is measured using a central venous catheter and consistently overestimates (albeit to a small
degree) venous oxygen saturation because it does not include sampling of blood mixed with blood
returning from the heart.

Question 18

What is early goal-directed therapy?

Answer 18

Goal-directed therapy refers to the practice of resuscitating patients to defined physiologic end
points (e.g., mean arterial pressure, CVP, urine output, serum lactate concentration, CO, Hgb level,
and SvO2), indicating that systemic tissue perfusion and vital organ function have been restored. In
the ED, goal-directed therapy has been rigorously studied in patients with sepsis; however, it is
being evaluated in patients with postcardiac arrest and trauma. It is likely that early goal-directed
therapies will be evaluated in other forms of shock in the future, thus guiding emergency physicians’
abilities to improve resuscitation end points and survival.

Question 19

List the primary resuscitation goals in patients suffering from shock.

Answer 19

*Maximize oxygenation.
• Establish adequate ventilation.
• Improve hemodynamic dysfunction.
• Treat the underlying cause.

Question 20

Define systemic inflammatory response syndrome (SIRS).

Answer 20

SIRS is defined by two or more of the following conditions:
• Temperature higher than 38° or 36°C
• Heart rate faster than 90 beats per minute
• Respiratory rate greater than 20 breaths per minute or partial pressure of carbon dioxide (PaCO2)
less than 32 mm Hg.
• Serum white blood cell count greater than 12,000 mm3 or less than 4000 mm3 or 10% band forms.
It is important to note that this definition, although standardized, is not specific for defining serious
illness. Although most commonly related to sepsis, SIRS may result from a variety of noninfectious
insults, including trauma, burns, pancreatitis, or overdose.

Question 21

How do I treat cardiogenic shock?

Answer 21

The treatment of cardiogenic shock should focus on improving myocardial contractility and overall
pump function. Provide oxygen and ventilatory support, including the judicious use of noninvasive
positive-pressure ventilation when pulmonary edema is present. Initiate inotropic support
using dobutamine or dopamine, and identify the cause and administer specific treatment (e.g.,
thrombolysis or percutaneous coronary intervention in the setting of acute coronary syndrome).
Consider intraaortic balloon counterpulsation or cardiopulmonary bypass for patients with refractory
shock.

Question 22

Explain the mechanism of dobutamine

Answer 22

Dobutamine is a synthetic catecholamine with primarily β1-receptor (cardiac stimulation) and mild
β2-receptor (vasodilation) agonism

Question 23

Explain the mechanism of dopamine.

Answer 23

Dopamine is an endogenous catecholamine that, when administered intravenously, produces a
dose-dependent activation of adrenergic and dopaminergic receptors. When given in low doses (e.g.,
5 μg/kg/min), dopamine preferentially activates dopaminergic receptors, producing vasodilatation
in renal, mesenteric, and cerebral circulations. When given in intermediate doses (e.g., 5 to
10 μg/kg/min), dopamine stimulates β-receptors, thus increasing CO. When given in high doses
(e.g., >10 μg/kg/min), dopamine activates α-receptors, producing a dose-dependent increase
in systemic vascular resistance. It is important to note that dopamine has modest inotropic
characteristics when compared with dobutamine and that tachyphylaxis may result from its use if
used for a prolonged period of time.

Question 24

Explain the mechanism of epinephrine.

Answer 24

Similar to dopamine, epinephrine is a primary β-receptor agonist at low doses and an α-receptor
agonist at high doses. However, epinephrine is significantly more potent than dopamine.

Question 25

How do I treat shock caused by PE?

Answer 25

Massive PE causes shock by reducing the cross-sectional area of the pulmonary outflow tract, thus
increasing right-sided heart pressures and reducing blood flow to the left side of the heart, all of
which result in a hemodynamic compromised state. Treatment centers on provision of oxygenation
and ventilation, hemodynamic support using crystalloids and vasopressors as necessary, and use of
thrombolytics or surgical embolectomy in the setting of refractory shock.

Question 26

How do I treat shock resulting from cardiac tamponade?

Answer 26

As always, ensure adequate oxygenation and ventilation. Similar to other forms of obstructive shock
(e.g., PE), administration of intravenous fluids may help overcome increased cardiac filling
pressures. However, the principal therapies for cardiac tamponade are pericardiocentesis or
pericardiotomy.

Question 27

What is neurogenic shock, and how is it treated?

Answer 27

Neurogenic shock is a form of distributive shock resulting from spinal cord injury in which central or
peripheral sympathetic tone is lost. Patients experiencing neurogenic shock are commonly
hypotensive with either a normal or low heart rate. Administer intravenous fluids to normalize
intravascular volume. If hypotension persists, several vasopressor options exist, although intravenous
phenylephrine (0.15 to 0.75 μg/kg/min) is considered the classic first-line agent.

Question 28

Explain the mechanism of phenylephrine.

Answer 28

Phenylephrine is a pure and potent α-agonist. Administration of this agent can induce a reflex
bradycardia, resulting in decreased CO.