You are on page 1of 9

CARDIOVASCULAR 17:

SHOCK PORTAL
Introduction

Shock is a state of inadequate oxygen delivery and inadequate tissue perfusion. If


prolonged, shock may lead to general impairment of cellular function.

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

Cardiac output and systemic vascular resistance combine to produce arterial


pressure. A significant decrease in either will affect arterial pressure unless there
is a compensatory elevation of the other.

Cardiac output may be affected by hypovolemia (hemorrhage), myocardial


failure (cardiogenic shock), or circulatory obstruction (pulmonary embolus).

Reduction in systemic vascular resistance by decreased peripheral vasomotor


tone (neurogenic shock) or redistribution of blood into the venous capacitance
bed (septic shock) causes decreased preload and can reduce cardiac output.

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.

VOLUME III—691
SHOCK
CV17
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

Hypotension and hypoperfusion are the 2 main clinical manifestations of shock.


Hypotension is best defined as a decrease of 30 mm Hg or greater below baseline
of the mean arterial blood pressure.

Manifestations of hypoperfusion are altered mental status, agitation, restlessness,


obtundation, cool and clammy skin, and reduced or absent urinary output.
Tachycardia is one of the earliest sign of hypoperfusion. Diaphoresis, nausea,
vomiting, and diarrhea may also occur. Symptoms vary based on the stage of
shock, the extent of hypoperfusion, and the underlying cause.

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.

Estimating Blood Loss Using Vital Signs

Blood volume is about 7% of body weight. A 70 kg male has a blood volume of


about 5 L (70 kg x 0.07 = 4.9 kg). In obese adults, use ideal body weight to make
this calculation.

PEDS: In children, blood volume is 80 to 90 mL/kg.

VOLUME III—692
SHOCK
CV17

Class I hemorrhage: A loss of 15% of blood volume (about 750 mL in a healthy


adult) can be tolerated with few hemodynamic signs. Mild tachycardia may be
seen.
Class II hemorrhage: A loss of 15% to 30% of blood volume (about 1000 mL in an
adult) results in tachycardia and decreased pulse pressure. Systolic BP may not
change, and urinary output is only mildly affected.

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.

Exceptions: When the Clinical Picture Differs from What’s Expected

Geriatric patients decompensate earlier and insidiously with fewer warning


signs. PEDS: Children decompensate relatively later because of their resilient
vascular trees.

Preexisting conditions may lessen the patient's ability to compensate. These


include pacemakers, alcohol and other drug ingestions, pregnancy, seizure
activity, hypothermia and hyperthermia, and anemia.

Some injuries—such as pelvic fractures, femur fractures, and liver ruptures—are


associated with a wide range (from minor to major) of possible hidden blood
loss.

Obligatory edema formation during and following resuscitation may require the
infusion of electrolyte solution beyond the replacement of lost blood volume
alone.

VOLUME III—693
SHOCK
CV17
Treatment

Regardless of the cause, tailor initial treatment toward prompt restoration of


tissue perfusion and cardiac output. Initial management of the airway and
respiratory system is paramount. Adequate oxygenation may improve an
already compromised cardiac output. Consider early ET intubation. Appropriate
venous access is important. Invasive hemodynamic monitoring is usually
necessary. Advanced treatment requires an intensive care unit. CVPs and
pulmonary capillary wedge pressures may need to be monitored to adjust the
therapy regimen.

How to Restore Blood Volume

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.

Avoid hemodilution with resulting coagulopathy, hypothermia, and loss of


blood viscosity. Obtain compatible blood (type O or type specific) early. (You do
not need to use it if the patient stabilizes with the initial bolus, but have it ready.)

Administer fluids through a high-volume fluid warmer. Be careful to avoid air


embolism. In adults, if using NS for fluids, switch to Ringer’s lactate solution
after 2 liters of NS to avoid hyperchloremic acidosis. Add NS to bags of packed
RBCs to speed delivery to the patient.

When hemothorax is present, be prepared to collect shed blood for possible


autotransfusion.

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.

VOLUME III—694
SHOCK
CV17

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

1. Cardiac Arrhythmias: A heart rate between 50 and 150 in a healthy adult is


unlikely to be the cause for a patient developing shock. Parameters must be
adjusted for children and preexisting conditions. The following table
indicates parameters outside of which heart rate may be pathological and
require correction.

Age Lower Upper


Infant < 70 > 200
Child < 60 > 160
Adult < 50 > 150

Rapid correction of any dysrhythmia often leads to prompt improvement of a


patient’s hemodynamic status. Follow ACLS guidelines to treat bradyarrythmias
(Vol III—CV10 BRADYCARDIA) and tachyarrythmias (Vol III—CV8
TACHYCARDIA) quickly and effectively. Pay close attention to hypoxemia or
metabolic abnormalities that may precipitate tachyarrhythmias.

2. Decreased Preload or Vascular Obstruction: Most common in this group is


right ventricular infarction, pulmonary embolus, tension pneumothorax, and
cardiac tamponade. Right ventricular infarction occurs in as many as 30% of
patients with acute inferior infarction. Half of these patients may develop
hemodynamic complications due to the infarction. Direct treatment toward fluid
therapy to improve the left ventricular filling pressure. Dobutamine may also be
helpful by its inotropic effect on the right ventricle. Avoid vasodilatory drugs
such as nitroglycerine and morphine.

Cardiac tamponade and tension pneumothorax result in inadequate cardiac


filling. Volume infusion improves cardiac function.

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.

VOLUME III—695
SHOCK
CV17
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.

As many as 20% of patients in cardiogenic shock have a relative hypovolemia


(left ventricular filling pressure < 15 mm Hg) and benefit from fluid support. If
acute pulmonary edema is not present, give a fluid challenge of 250 to 500 mL
crystalloid (NS or LR). If the hypotension doesn't respond to fluid support,
initiate pressor support. A combination treatment regimen may be necessary to
improve the pumping function. The American College of Cardiology and the
American Heart Association have created guidelines for the early management
of patients with hypotension, shock, and acute pulmonary edema.

Inotropic support from dopamine, dobutamine, or norepinephrine is usually


first-line therapy. In addition, vasodilator therapy to reduce afterload, diuretic or
vasodilator therapy to reduce preload, mechanical assistance such as an intra-
aortic balloon pump, or even surgery may be necessary. The best chance for
survival for patients suffering from cardiogenic shock after an acute MI is with
the use of angioplasty and intra-aortic balloon counterpulsation.

Consider early transfer to a facility capable of cardiac catheterization,


angioplasty, and cardiovascular surgery if patients are seen within the first 12 to
24 hours of symptom onset. Most studies indicate marked improvement of
mortality if revascularization occurs within 16 hours of symptom onset in this
patient subset.

4. Excessive Afterload: Conditions fitting into this category include aortic


stenosis, certain types of cardiomyopathies, and coarctation of the aorta.

VOLUME III—696
SHOCK
CV17

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.

Treatment begins with establishment of an adequate airway and administration


of oxygen. Apply direct pressure to any external wounds to help control
bleeding. If necessary, properly place a nasogastric tube. Promptly obtain
vascular access (usually with 2 large-bore IV catheters). Maintain the patient's
body temperature; monitor frequently.

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.

Close observation to the response of this initial bolus determines further


therapeutic and diagnostic decisions. Monitor urinary output for determination
of adequate replacement.

If blood transfusion is necessary, fully crossmatched blood is preferable. If time


does not allow the use of crossmatched blood, type-specific blood can usually be
provided in 10 minutes. If the patient is exsanguinating and type-specific blood
is not available, use type O Rh-negative packed cells. (If O-negative blood is
unavailable, un-crossmatched O-positive blood may be used in extreme
emergencies for males and for females past reproductive age.)

For patients en route to the operating room or being transferred to another


facility, consider using a pelvic stabilizer (1) for pelvic fractures causing
continuing hemorrhage and hypotension and (2) for intra-abdominal trauma
with severe hypovolemia.

Obtain surgical consultation and evaluation early.

VOLUME III—697
SHOCK
CV17
2. Decreased Vascular Resistance: Three common types of shock in this category
are septic, anaphylactic, and neurogenic.

Neurogenic shock results from a severe midbrain or spinal cord injury.


Neurogenic shock is not caused by an isolated head injury. Shock occurs when
there is a loss of vasomotor tone because of relaxation of the vascular smooth
muscle. Typically, hypotension is present without tachycardia or cutaneous
vasoconstriction. Treat patients initially for hypovolemia. If necessary,
administer vasoactive drugs after volume has been restored.

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.

Large volumes of IV fluids are frequently required to achieve a normal BP. If


necessary, give vasopressor drugs. Ensure ventilation and correct electrolyte and
acid-base disorders.

Specific therapy for septic shock involves antibiotic administration, surgical


intervention (drainage of an abscess or removal of an obstruction), and correction
of nutritional deficits. The choice of antibiotics involves using those with
sensitivities that are most effective against the pathogens likely to invade a
specific site. If a likely pathogen is unknown, begin broad-spectrum

VOLUME III—698
SHOCK
CV17

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.

As in adults, clinical features in infants and children are caused by insufficient


oxygen delivery to tissues and reduced clearance of metabolites. Clinical signs
are caused by end-organ dysfunction due to tissue hypoxia and acidosis.

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.

VOLUME III—699