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SHOCK PORTAL
Introduction
The initial step in the management of shock is to recognize its existence. The
second step is to identify the cause of shock. The causes are diverse, and patient
signs and symptoms vary. At times, shock may be obvious (eg, the trauma
patient with significant hemorrhage), but often the reason is more obscure (a
patient with unknown diabetes exhibiting diabetic ketoacidosis (DKA) or a
geriatric patient in early septic shock).
The goal of treatment is to restore adequate cellular and organ perfusion with
sufficiently oxygenated blood.
Etiology of Shock
The causes of shock are divided into cardiac and non-cardiac. The cardiac causes
are further broken down into rate problems, impaired contractility/excessive
preload, decreased preload, and excessive afterload. Non-cardiac causes are
separated into volume loss or decreased vascular resistance. As with all
classification schemes, there is some overlap, and in many patients, multiple
factors may be involved, particularly in the later stages of shock.
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The mnemonic SHRIMPCAN is helpful in creating a differential diagnosis for
evaluation and treatment of a patient in shock.
S—Septic: gram-negative infection or other overwhelming infection
H—Hypovolemic: hemorrhage, vomiting, diarrhea, dehydration, burns,
peritonitis, pancreatitis
R—Respiratory: massive pulmonary embolus, tension pneumothorax
I—Ingestions: drug overdoses
M—Metabolic: diabetes mellitus or diabetes insipidus, myxedema, Addison's
disease
P—Psychiatric: psychological manifestation
C—Cardiogenic: acute MI, cardiomyopathies, cardiac tamponade, arrhythmias,
severe CHF, obstructive outflow lesions, myxomas
A—Anaphylactic: immediate hypersensitivity to a specific antigen
N—Neurogenic: severe CNS injury or spinal cord injury
Patient Assessment
Obtain a SAMPLE history and begin to monitor and assess the patient. Measure
BP, heart rate, respiratory rate, temperature, neck vein distension, mental status
evaluation, and skin characteristics. Monitor the mental status, vital signs,
cardiac status, and urinary output frequently. Clinical conditions may change
rapidly.
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Class III hemorrhage: A loss of 30% to 40% of blood volume (about 2000 mL in
an adult) produces signs of decompensation including marked tachycardia,
mental status changes, and a fall in systolic BP.
Class IV hemorrhage: A loss of more than 40% of blood volume (about 2500 mL
in an adult) results in marked tachycardia, significantly low systolic BP, very
narrow pulse pressure, obtundation, and loss of normal skin color and
temperature. The patient becomes unconscious, and the pulse is not obtainable
when more than 50% of blood volume is lost.
Order an ECG, chest x-ray, ABG/VBG, CBC, electrolytes, BUN, creatinine, and
arterial blood lactate level. Other tests are necessary and important but vary
according to the underlying causes of the shock. Tests to consider include
echocardiogram, CT or MRI, V/Q lung scan, pulmonary angiography,
endoscopy, and possibly others, depending on suspected etiologies and
potentially some test results.
Obligatory edema formation during and following resuscitation may require the
infusion of electrolyte solution beyond the replacement of lost blood volume
alone.
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Treatment
The best method is to select a safe volume, infuse it rapidly through large bore
IVs, then stop and reassess. A bolus of 1 to 1.5 L of crystalloid (NS or LR) is
generally safe in hypovolemic adults. PEDS: In children, 20 mg/kg is generally
safe. If instability persists, a second bolus of 20 mg/kg or 10 mg/kg of blood is
recommended. Be aggressive, but use caution.
In the presence of head injury, contused lung, and advanced age, volume
overload is dangerous. Do not hesitate to obtain central venous access in these
patients so that CVP may be used to gauge the adequacy of fluid replacement.
Presume that the patient has continuing hidden blood loss until proven
otherwise. Obtain surgical consultation for any trauma patient where shock is
present. Continuing blood loss is manifested by instability refractory to fluid and
blood replacement and by the loss of stability once achieved. Surgical
intervention is needed as quickly as possible.
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If cardiac failure with increased central venous and pulmonary vascular pressure
is present, direct treatment toward restoring cardiac function. Rapid volume
infusion in this setting may cause or exacerbate pulmonary edema.
Cardiac Causes
Massive pulmonary embolus may cause right heart failure and subsequent
shock. The accompanying shock from pulmonary embolus may be treated with
correction of hypoxemia, possible intubation, IV fluid support, and pressors (if
necessary) to support BP.
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3. Impaired Contractility/Excessive Preload: Cardiogenic shock following acute
MI is the most common reason for impaired contractility.
Other causes include ventricular septal rupture, free wall rupture, acute mitral
insufficiency, or papillary muscle/chordae dysfunction.
When extensive myocardial necrosis (> 30% to 40% of myocardial surface area)
causes shock, the prognosis is particularly poor. Aggressive treatment such as
cardiac catheterization, PTCA, intra-aortic balloon pump, and coronary artery
bypass grafting may result in better short- and long-term survival.
Prognosis also improves for those patients who receive prompt surgical
treatment of complications such as ventricular septal rupture and papillary
muscle dysfunction. Patients with preserved left ventricular function but severe
coronary artery disease causing cardiogenic shock also benefit from early
surgical intervention.
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Non-Cardiac Causes
1. Volume Loss: Quickly identify the hypovolemic patient and detect any occult
blood loss. Signs include orthostatic vital sign changes and a narrowed pulse
pressure. In shock due to hemorrhage, seek the source carefully and quickly. A
complete history and physical is essential. Important components of the physical
exam include chest percussion for dullness, palpation of the abdomen, thigh
girth measurement, and digital rectal exam. In some patients, nasogastric
aspiration and peritoneal lavage may be needed to locate the source of
hemorrhage.
The first fluid bolus is usually 1 to 2 L crystalloid (NS or LR) for adults or
(PEDS:) 20 mL/kg for pediatric patients. The exact amount depends on the
patient's signs and symptoms. Warm all fluids to body temperature. Determine
the rate by the magnitude of the preexisting loss and how fast blood loss is
continuing.
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2. Decreased Vascular Resistance: Three common types of shock in this category
are septic, anaphylactic, and neurogenic.
Anaphylactic shock often causes severe respiratory distress and profound shock.
Laryngeal edema and/or bronchospasm are often present. The preferred drug
for initial treatment is epinephrine. (See Vol III—AIR8 ANAPHYLAXIS for details
about the use of epinephrine in anaphylactic shock.) An adequate airway is
essential. Due to possibly severe laryngeal edema, more advanced airway
management may be necessary. For bronchospasm, give nebulized albuterol or
give aminophylline at a loading dose of 6 mg/kg and infuse intravenously over
20 to 30 minutes. Volume replacement IV may be needed to restore and maintain
tissue perfusion. Consider a vasopressor (dopamine) if hypotension does not
respond to volume infusion. Antihistamines and corticosteroids may also play a
role in the ongoing treatment of anaphylactic shock.
Septic shock is caused by the action of bacterial toxins on the circulatory system.
Although usually caused by gram-negative organisms, shock may also occur
with gram-positive, anaerobic, fungal, or viral infections. Treatment and
evaluation must address the underlying infection as well as the results of the
circulatory compromise.
Two phases usually occur in septic shock. The first phase (warm) is characterized
by an increase in cardiac output and a decrease in peripheral vascular resistance.
During this phase, the patient is warm and diaphoretic. The second (cold) phase
is manifested by decreased cardiac output, normal or increased peripheral
vascular resistance, and cool, vasoconstricted skin.
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antimicrobial therapy (Vol III—IN3 SEPSIS IN ADULTS). The use and efficacy of
corticosteroids remains controversial.
Special Considerations
PEDS: Evaluate shock in infants and children in much the same way as pediatric
respiratory failure. Progressive deterioration from either condition may result in
cardiopulmonary failure. Even though shock and respiratory failure may begin
as separate entities, they both progress to an indistinguishable state of
cardiopulmonary failure and even possibly cardiac arrest.
Signs include altered LOC, hypotonia, tachycardia, and weak central pulses with
absent peripheral pulses. Late and ominous signs include hypotension,
bradycardia, and irregular respirations.
Evaluate any infant or child with respiratory distress, severe multiple or blunt
trauma, a reduced LOC, cyanosis, or pallor. Treat aggressively to determine the
presence of cardiopulmonary failure and to prevent any progression toward
cardiopulmonary arrest.
Conclusion
The causes of shock at any age are diverse. While the scope of this text does not
allow full discussion of evaluation and treatment decisions for every cause of
shock, hopefully a differential diagnosis can be generated to aid in evaluation
and treatment. Initial treatment, regardless of the cause of shock, is directed
toward prompt restoration of tissue perfusion and cardiac output. Most
important is to initially recognize the existence of shock.
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