CHAPTER 5

SHOCK

- defined as the failure to meet the metabolic needs of the cell and the consequences that ensue.
- central component of shock is decreased tissue perfusion with consequent decreased delivery of
required metabolic substrates and inadequate removal of cellular waste products.
- the initial cellular injury that occurs is reversible; however, the injury will become irreversible if
tissue perfusion is prolonged or severe enough such that, at the cellular level, compensation is no
longer possible.

CLASSIFICATION OF SHOCK:
1. Hypovolemic shock- most common type; results from loss of circulating blood volume
-may result from loss of whole blood (hemorrhagic shock), plasma, interstitial fluid (bowel
obstruction), or a combination.
2.Vasogenic shock- results from decreased resistance within capacitance vessels, usually seen in sepsis.
3. Neurogenic shock- is a form of vasogenic shock in which spinal cord injury or spinal anesthesia
causes vasodilation due to acute loss of sympathetic vascular tone.
4. Cardiogenic shock- results from failure of the heart as a pump, as in arrhythmias or acute
myocardial infarction (MI).
5. Obstructive shock- is a form of cardiogenic shock that results from mechanical impediment to
circulation leading to depressed cardiac output rather than primary cardiac failure.
-includes etiologies such as pulmonary embolism or tension pneumothorax.
6. Traumatic shock- soft tissue and bony injury leads to the activation of inflammatory cells and the
release of circulating factors, such as cytokines and intracellular molecules that modulate the immune
response.

PATHOPHYSIOLOGY:
-regardless of etiology, the initial physiologic responses in shock are driven by tissue
hypoperfusion and the developing cellular energy deficit.
-the imbalance between cellular supply and demand leads to neuroendocrine and inflammatory
responses, the magnitude of which is usually proportional to the degree and duration of shock.
-specific responses will differ based on the etiology of shock, as certain physiologic responses
may be limited by the inciting pathology.

-organ-specific responses are aimed at maintaining perfusion in the cerebral and coronary
circulation. These are regulated at multiple levels including:
(a) stretch receptors and baroreceptors in the heart and vasculature (carotid sinus and aortic arch)
(b) chemoreceptors
(c) cerebral ischemia responses
(d) release of endogenous vasoconstrictors
(e) shifting of fluid into the intravascular space
(f) renal reabsorption and conservation of salt and water.

PHASES OF SHOCK (HEMORRHAGIC)

1.Compensated Phase- in hemorrhagic shock, the body can compensate for the initial loss of blood
volume primarily through the neuroendocrine response to maintain hemodynamics.
2. Decompensation Phase- with continued hypoperfusion, ongoing cellular death and injury ensues.
-Microcirculatory dysfunction, parenchymal tissue damage, and inflammatory cell activation
can perpetuate hypoperfusion.
-Ischemia/reperfusion injury will often exacerbate the initial insult.
-these effects at the cellular level, if untreated, will lead to compromise of function at the organ
system level, thus leading to the “vicious cycle” of shock.
3. Irreversible Phase- occurs when persistent hypoperfusion results in further hemodynamic
derangements and cardiovascular collapse.
-at this point, there has occurred extensive enough parenchymal and microvascular injury such
that volume resuscitation fails to reverse the process, leading to death of the patient.

RESPONSES TO SHOCK:
Neuroendocrine and Organ-Specific Responses to Hemorrhage:
-goal of the neuroendocrine response to hemorrhage is to maintain perfusion to the heart and the
brain, even at the expense of other organ systems.
-Peripheral vasoconstriction occurs, and fluid excretion is inhibited.
-The mechanisms include autonomic control of peripheral vascular tone and cardiac
contractility, hormonal response to stress and volume depletion, and local microcirculatory
mechanisms that are organ specific and regulate regional blood flow.

Afferent Signals
-transmitted from the periphery and are processed within the CNS and activate the reflexive
effector responses or efferent impulses. These effector responses are designed to expand plasma
volume, maintain peripheral perfusion and tissue O2 delivery, and restore homeostasis.
-initial inciting event usually is loss of circulating blood volume. Other stimuli that can produce
the neuroendocrine response include pain, hypoxemia, hypercarbia, acidosis, infection, change in
temperature, emotional arousal, or hypoglycemia.

Efferent Signals
Cardiovascular Response
-result of the neuroendocrine response and ANS response to shock
-includes the following responses:
● Stimulation of sympathetic fibers innervating the heart leads to activation of β1-adrenergic
receptors that increase heart rate and contractility in this attempt to increase cardiac output.
● Direct sympathetic stimulation of the peripheral circulation via the activation of α1-adrenergic
receptors on arterioles induces vasoconstriction and causes a compensatory increase in systemic
vascular resistance and blood pressure.
 ● Marked redistribution of blood flow with blood shunted away from less essential organ beds
such as the intestine, kidney, and skin. In contrast, the brain and heart have autoregulatory
mechanisms that attempt to preserve their blood flow despite a global decrease in cardiac output.
● Direct sympathetic stimulation also induces constriction of venous vessels, decreasing the
capacitance of the circulatory system and accelerating blood return to the central circulation.
● Increased sympathetic output induces catecholamine release from the adrenal medulla.
Catecholamine effects on peripheral tissues include stimulation of hepatic glycogenolysis and
gluconeogenesis to increase circulating glucose availability to peripheral tissues, an increase in
skeletal muscle glycogenolysis, suppression of insulin release, and increased glucagon release.

Hormonal Response
● activation of the ANS
● activation of the hypothalamic-pituitary-adrenal axis. Shock stimulates the hypothalamus to
release corticotropin releasing hormone, which results in the release of adrenocorticotropic
hormone (ACTH) by the pituitary. ACTH subsequently stimulates the adrenal cortex to release
cortisol. Cortisol acts synergistically with epinephrine and glucagon to induce a catabolic state.
● activation of the renin-angiotensin system
● release of ADH from the pituitary

FORMS OF SHOCK:
1. HYPOVOLEMIC/HEMORRHAGIC
-Shock in a trauma patient or postoperative patient should be presumed to be due to hemorrhage
until proven otherwise.
-The clinical signs of shock may be evidenced by agitation, cool clammy extremities,
tachycardia, weak or absent peripheral pulses, and hypotension. Such apparent clinical shock results
from at least 25% to 30% loss of the blood volume.

Treatment:
-Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in shock.
-Treatment of hemorrhagic shock is instituted concurrently with diagnostic evaluation to identify a
source
-Patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing active
hemorrhage from large vessels and require prompt operative intervention.
-The appropriate priorities in these patients are :
 (a) secure the airway
(b) control the source of blood loss
(c) intravenous (IV) volume resuscitation.
-Control of hemorrhage is achieved in the operating room, and efforts to warm patients and to prevent
coagulopathy using multiple blood products and pharmacologic agents
-Initial resuscitation is limited to keep SBP around 80 to 90 mmHg. This prevents renewed bleeding
from recently clotted vessels.
-Resuscitation and intravascular volume resuscitation are accomplished with blood products and
limited crystalloids.
-Transfusion of packed red blood cells and other blood products is essential in the treatment of patients
in hemorrhagic shock. Current recommendations in stable ICU patients aim for a target hemoglobin of
7 to 9 g/dL
-Platelets should be transfused in the bleeding patient to maintain counts above 50 × 109/L
-Additional resuscitative adjuncts include minimization of heat loss and maintaining normothermia.
The development of hypothermia in the bleeding patient is associated with acidosis, hypotension, and
coagulopathy.
-Hypothermia in bleeding trauma patients is an independent risk factor for bleeding and death.

2. TRAUMATIC SHOCK
-The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that
occurs following the induction of shock. In addition to ischemia or ischemia-reperfusion, accumulating
evidence demonstrates that even simple hemorrhage induces proinflammatory activation that results in
many of the cellular changes typically ascribed only to septic shock.
-At the cellular level, this may be attributable to the release of cellular products termed damage-
associated molecular patterns (DAMPs) that activate the same set of cell surface receptors as bacterial
products, initiating similar cell signaling. These receptors are termed pattern recognition receptors
(PRRs) and include the TLR family of proteins.
Treatment:
● focused on correction of the individual elements to diminish the cascade of proinflammatory
activation
● prompt control of hemorrhage, adequate volume resuscitation to correct O2 debt, débridement
of nonviable tissue, stabilization of bony injuries, and appropriate treatment of soft tissue
injuries

3. SEPTIC/VASODILATORY SHOCK
- is a result of dysfunction of the endothelium and vasculature secondary to circulating inflammatory
mediators and cells or as a response to prolonged and severe hypoperfusion. Thus, in vasodilatory
shock, hypotension results from failure of the vascular smooth muscle to constrict appropriately.
- characterized by peripheral vasodilation with resultant hypotension and resistance to treatment with
vasopressors.
-most frequently encountered form of vasodilatory shock is septic shock
-vasodilatory shock seems to represent the final common pathway for profound and prolonged shock of
any etiology.
-findings include enhanced cardiac output, peripheral vasodilation, fever, leukocytosis, hyperglycemia,
and tachycardia.
4. CARDIOGENIC SHOCK
-defined clinically as circulatory pump failure leading to diminished forward flow and subsequent
tissue hypoxia, in the setting of adequate intravascular volume.
-Hemodynamic criteria include:
● sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes)
● reduced cardiac index(<2.2 L/min per square meter)
● elevated pulmonary artery wedge pressure (>15 mmHg)
-Mortality rates for cardiogenic shock are 50% to 80%.
-Acute, extensive MI is the most common cause of cardiogenic shock
-The pathophysiology of cardiogenic shock involves a vicious cycle of myocardial ischemia that causes
myocardial dysfunction, which results in more myocardial ischemia.
Treatment
-After ensuring that an adequate airway is present and ventilation is sufficient, attention should be
focused on support of the circulation.
-Intubation and mechanical ventilation often are required, if only to decrease work of breathing and
facilitate sedation of the patient.
-maintenance of adequate oxygenation to ensure adequate myocardial O2
delivery and judicious fluid administration to avoid fluid overload and development of cardiogenic
pulmonary edema
-Electrolyte abnormalities, commonly hypokalemia and hypomagnesemia, should be corrected
-When profound cardiac dysfunction exists, inotropic support may be indicated to improve cardiac
contractility and cardiac output.

5. OBSTRUCTIVE SHOCK

-most commonly due to the presence of tension pneumothorax

-The major determinant of the degree of hypotension is the pericardial pressure; reduced filling of the
right side of the heart from either increased intrapleural pressure secondary to air accumulation (tension
pneumothorax) or increased intrapericardial pressure precluding atrial filling secondary to blood
accumulation (cardiac tamponade) results in decreased cardiac output associated with increased central
venous pressure.
-The diagnosis of tension pneumothorax should be made on clinical examination. The classic findings
include respiratory distress (in an awake patient), hypotension, diminished breath sounds over one
hemithorax, hyperresonance to percussion, jugular venous distention, and shift of mediastinal structures
to the unaffected side with tracheal deviation.
-empiric treatment with pleural decompression is indicated; definitive treatment of a tension
pneumothorax is immediate tube thoracostomy.

6.NEUROGENIC SHOCK
- refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds.
Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return,
and decreased cardiac output.
- is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high
thoracic region that disrupt sympathetic regulation of peripheral vascular tone
-The classic description of neurogenic shock consists of:
● decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to
disrupted sympathetic discharge)
● warm extremities (loss of peripheral vasoconstriction)
● motor and sensory deficits indicative of a spinal cord injury
● radiographic evidence of a vertebral column fracture.
Treatment
-After the airway is secured and ventilation is adequate, fluid resuscitation and restoration of
intravascular volume often will improve perfusion in neurogenic shock. Most patients with neurogenic
shock will respond to restoration of intravascular volume alone, with satisfactory improvement in
perfusion and resolution of hypotension.
-Administration of vasoconstrictors will improve peripheral vascular tone, decrease vascular
capacitance, and increase venous return, but should only be considered once hypovolemia is excluded