SHOCK

Shock is a life-threatening condition of

circulatory failure, causing inadequate
oxygen delivery to meet cellular metabolic
needs and oxygen consumption
requirements, producing cellular and tissue
hypoxia.
The effects of shock are initially reversible,
but rapidly become irreversible, resulting
in multiorgan failure (MOF) and death.
Shock is characterized by decreased
oxygen delivery and/or increased
oxygen consumption or inadequate
oxygen utilization leading to cellular and
tissue hypoxia.
Most commonly manifested as
hypotension (systolic blood pressure less
than 90 mm Hg or MAP less than 65
mmHg).
 The definition of mean arterial pressure (MAP) is
the average arterial pressure throughout one
cardiac cycle (systole and diastole).
 MAP is influenced by cardiac output and systemic
vascular resistance
 CO = STROKE VOLUME X HEART RATE
 Stroke volume affected by
Cardiac contractility
Preload
afterload
MAP = DP + 1/3(PP)
Where DP is the diastolic blood
pressure, and PP is the pulse pressure.
Pulse Pressure = Systolic Blood Pressure
– Diastolic Blood Pressure
 Perfusing vital organs requires the maintenance
of a minimum MAP of 60 – 65 mmHg.
 If MAP drops below this point for an extended
period, ischemia and infarction can occur.
 If the MAP drops significantly, blood will not be
able to perfuse cerebral tissues, there will be a
loss of consciousness, and neuronal death will
quickly ensue
 The fundamental defect in shock is reduced
perfusion of vital tissues.
 Once perfusion declines and oxygen delivery to
cells is inadequate for aerobic metabolism, cells
shift to anaerobic metabolism with increased
production of carbon dioxide and elevated blood
lactate levels.
 Cellular function declines, and if shock persists,
irreversible cell damage and death occur
State of hypoperfusion causes hypoxia
Due to lack of oxygen anerobic metabolism
ensues
The accumulating lactate results in lactic
acidosis
 Low arterial pressure triggers an adrenergic response
with sympathetic-mediated vasoconstriction.
 Vasoconstriction is selective, shunting blood to the
heart and brain and away from the splanchnic
circulation.
 Circulating beta-adrenergic amines (epinephrine,
norepinephrine) also increase cardiac contractility and
trigger release of corticosteroids from the adrenal
gland, renin from the kidneys, and glucose from the
liver.
 The body’s compensatory mechanisms are unable to
maintain adequate perfusion to the brain and vital
organs.
 Cardiac output is dropping resulting in a decrease in
both blood pressure and cardiac function
 The arteriolar smooth muscle and precapillary sphincters
relax such that blood remains in the capillaies.
• Fluid leaks out of capillaries into interstitium and there is
sludging of blood
• There is reduced tissue perfusion leading to hypoxia.
Vital organs have failed and the shock can no
longer be reversed.
Cellular injury and tissue injury is so severe
that condition does not revert back to
normal even after correcting hemodynamic
defects
Brain damage and cell death are occurring,
and death will occur imminently.
Tachycardia
Hypotension
• (low MAP or decrease of 40mmHg from
baseline)
Tachypnea
Reduced pulse pressure
 Brain
 Agitation, confusion, disorientation
 Lethargy, stupor, coma (low GCS)
 Kidney
 Oliguria: urine output < 0.5 mL/kg/hour
 Skin
 Slow capillary refill
 Cold extremities
 Mottled
 Clammy/ diaphoretic
Four types of shock are recognized:
1. Distributive,
2. Cardiogenic,
3. Hypovolemic, and
4. Obstructive.
characterized by severe peripheral vasodilatation
(vasodilatory shock)
Includes
• Septic shock
• Neurogenic shock
• Anaphylactic shock
• Endocrine shock
 Sepsis is defined as life-threatening organ dysfunction
due to dysregulated host response to infection
 Septic shock occurs in a subset of patients with sepsis
 Septic shock is defined by
persisting hypotension requiring vasopressors to
maintain a mean arterial pressure of 65 mm Hg or
higher and
a serum lactate level greater than 2 mmol/L (18
mg/dL) despite adequate volume resuscitation
 Often nonspecific and include the following:
• Fever (usually >101°F [38°C]), chills, or rigors
• Change in mental status eg confusion, anxiety
• Difficulty breathing
• Fatigue, malaise
• Nausea and vomiting
• Tachycardia
• Mottled skin
• Decreased capillary refill
• Start adequate antibiotics (proper spectrum and dose) as
early as possible
• Resuscitate the patient from septic shock by using
supportive measures to correct hypoxia, hypotension, and
impaired tissue oxygenation (hypoperfusion)
• Identify the source of infection and treat with antimicrobial
therapy, surgery, or both (source control)
• Maintain adequate organ system function, guided by
cardiovascular monitoring, and interrupt the progression of
MODS
• Multiple organ dysfunction syndrome (MODS)
• Progressive and potentially reversible failure in the
physiologic function of several organs and/or
systems [6]
• The more organs that are affected, the greater
the mortality risk
• The 3rd international consensus definitions for sepsis
and septic shock recommend the assessment of organ
dysfunction using the SOFA (sequential organ failure
assessment) score
 Associated with cervical and high thoracic spine injury
• Injury to the spinal cord above T6
• The descending sympathetic tracts are disrupted
 Occurs as a result of autonomic dysregulation due to a loss
of sympathetic tone and an unopposed parasympathetic
response.
 Most commonly caused by trauma
 Less common causes: spinal anesthesia, Guillain-Barre
syndrome, autonomic nervous system toxins, transverse
myelitis, and other neuropathies
 • Hypotension with paradoxical bradycardia
• Flushed, dry, and warm peripheral skin, may be
present.
• Other signs of autonomic dysfunction include
ileus, urinary retention, and poikilothermia
The presence of vertebral fracture or dislocation
raises the concern for a neurogenic shock
A focal neurologic deficit is not necessary for the
diagnosis of neurogenic shock.
 Fluid resuscitation – first line therapy
 Vasopressors and inotropes – commonly required
as shock is often refractory to fluids
 Eg norepinephrine and dopamine
 Phenylephrine – not 1st line. Reflex bradycardia
 Treatment for bradycardia is atropine and
glycopyrrolate to oppose vagal tone
 Consult a spine surgeon early to determine need
for spinal decompression
 Clinical syndrome of severe hypersensitivity reaction
mediated by immunoglobulin E (Ig-E), resulting in
cardiovascular collapse and respiratory distress due to
bronchospasm.
 caused by the release of chemical mediators from mast
cells and basophils.
 The immediate hypersensitivity reactions can occur within
seconds to minutes after the presentation of the inciting
antigen.
 Common allergens include drugs (e.g., antibiotics,
NSAIDs), food, insect stings, and latex.
 Initial
• Assess and secure the airway as needed.
• Give supplemental oxygen
• Remove allergen when possible
• Administer epinephrine (1:1000) as soon as possible
and repeat as needed.
• Provide hemodynamic support with fluid
resuscitation.
 Adjunctive treatment with antihistamines and
corticosteroids may be administered after the initial
resuscitation measures.
 Addisonian crisis (adrenal failure due to mineralocorticoid
deficiency)
• In states of mineralocorticoid deficiency, vasodilatation can
occur due to altered vascular tone and aldosterone-
deficiency-mediated hypovolemia.
 Myxedema
• Although thyroid hormone plays a role in blood pressure
homeostasis, the exact mechanism of vasodilation in patients
with myxedema is unclear;
• concurrent myocardial depression or pericardial effusions
likely contribute to hypotension and shock in this population.
 Due to intracardiac causes of cardiac pump failure that result in
reduced cardiac output (CO)
 Causes:
1. Cardiomyopathic: acute myocardial infarction affecting more
than 40% of the left ventricle, severe right ventricular
infarction, cardiac contusion by blunt chest trauma.
2. Arrhythmias: tachyarrhythmias and bradyarrhythmias may
induce hypotension
3. Mechanical: severe aortic insufficiency, severe mitral
insufficiency, rupture of papillary muscles, or chordae
tendinae, rupture of ventricular free wall aneurysm.
 Mostly due to extracardiac causes leading to a decrease in
the ventricular cardiac output
 Causes:
1. Pulmonary vascular - due to impaired blood flow from the
right heart to the left heart. Eg massive pulmonary
embolism, severe pulmonary hypertension.
2. Mechanical - impaired filling of right heart or due to
decreased venous return to the right heart due to
extrinsic compression. Eg tension pneumothorax,
pericardial tamponade, restrictive cardiomyopathy,
constrictive pericarditis.
Results from depletion of intravascular volume,
whether by extracellular fluid loss or blood
loss.
The body compensates with increased
sympathetic tone resulting in increased heart
rate, increased cardiac contractility, and
peripheral vasoconstriction.
Hypovolemic shock can be divided into two
categories: hemorrhagic and nonhemorrhagic
Causes:
 Trauma: both blunt and penetrating
 Gastrointestinal bleeding
 Upper: variceal, PUD
 Lower: diverticular, arteriovenous malformation
 Vascular etiologies (e.g., aortoenteric fistula, ruptured
abdominal aortic aneurysm, tumor eroding into a major
blood vessel)
 Postpartum haemorrhage
 etc
Volume depletion from loss of sodium and water can occur
from a number of anatomic sites
 GI losses - the setting of vomiting, diarrhea, NG suction, or
drains.
 Renal losses - medication-induced diuresis, endocrine
disorders such as hypoaldosteronism.
 Skin losses/insensible losses - burns, Stevens-Johnson
syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.
 Third-space loss - in the setting of pancreatitis, cirrhosis,
intestinal obstruction, trauma.
 Maximize oxygen delivery - completed by ensuring
adequacy of ventilation, increasing oxygen
saturation of the blood, and restoring blood flow
 Control further blood / volume loss
 Fluid resuscitation
Intravenous fluids
In hemorrhagic shock blood transfusion may be
required.
The goal of treatment is to achieve
• a urine output of greater than 0.5 ml/kg/h,
• a central venous pressure of 8–12 mmHg and
• a mean arterial pressure of 65–95 mmHg.
In trauma the goal is to stop the bleeding
which in many cases requires surgical
interventions.