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Modul Kedaruratan Medik – S1

Shock
Dr. MUSOFA RUSLI, SpPD
Dept. Ilmu Penyakit Dalam - FKUA

2015
Introduction
Clinical syndrome that results from inadequate
tissue perfusion
Imbalance between the delivery of and
requirements for oxygen and substrate  cellular
dysfunction
cellular injury  induces the production and
release of damage-associated molecular patterns
(DAMPs or "danger signals") and inflammatory
mediators  further compromise perfusion 
MOF  death
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Shock-induced vicious cycle

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Classification of Shock
Hypovolemic
Traumatic
Cardiogenic
Intrinsic
Compressive
Septic
Hyperdynamic (early)
Hypodynamic (late)
Neurogenic
Hypoadrenal

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A schematic of the host immunoinflammatory
response to shock

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The hemodynamic, oxygen transport, and oxygen utilization
components of shock management

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Definitions, etiologies, and therapies of various shock states (Cecil)

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Physiologic Characteristics of the
Various Forms of Shock (Harrisson’s)

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TYPES OF SHOCK
Hypovolemic
consequence of decreased preload due to intravascular volume loss
Cardiogenic
consequence of cardiac pump failure
Distributive (vasodilatory)
consequence of severely decreased SVR
Combined
patients with septic shock often have a hypovolemic component (due
to decreased oral intake, insensible losses, vomiting, diarrhea)
cardiogenic component (due to sepsis-related myocardial dysfunction)
distributive component (due to the effects of inflammatory and
antiinflammatory cascades on vascular permeability and vasodilation)

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Characteristics of Shock

Physiologic Tissue
Preload Pump function Afterload
variable perfusion

Pulmonary Systemic Mixed venous


Clinical
capillary wedge Cardiac output vascular oxygen
measurement
pressure resistance saturation

Hypovolemic ↓ ↓ ↑ ↓

Cardiogenic ↑ ↓ ↑ ↓

Distributive ↓ or ↔ ↑ ↓ ↑

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STAGES OF SHOCK
a physiologic continuum
Shock: inciting event, such as a focus of
infection (eg, abscess) or an injury (eg,
gunshot wound)  systemic circulatory
abnormality  preshock, shock, and end-
organ dysfunction  irreversible end-organ
damage and death

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STAGES OF SHOCK: CONTINUUM
Preshock
warm shock or compensated shock
Tachycardia, peripheral vasoconstriction, and either a modest increase
or decrease in systemic blood pressure may be the only clinical signs
Shock
compensatory mechanisms become overwhelmed and signs and
symptoms of organ dysfunction appear
tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis,
oliguria, and cool clammy skin
End-organ dysfunction
Progressive end-organ dysfunction leads to irreversible organ damage
and patient death
urine output decreased, anuria, acute renal failure, acidemia
decreases the cardiac output and alters cellular metabolic processes,
and restlessness evolves into agitation, obtundation, and coma

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Cardinal findings of shock
Hypotension
occurs in the majority of shock patients
absolute hypotension (eg, systolic blood pressure <90 mmHg) or
relative hypotension (eg, a drop in systolic blood pressure >40 mmHg)
Oliguria
Oliguria  anuria  renal failure
Change in mental status
agitation, progresses to confusion or delirium, and ends in
obtundation or coma
Cool, clammy skin
Peripheral vasoconstriction
redirecting blood from the periphery to the vital organs  maintaining
coronary, cerebral, and splanchnic perfusion
Metabolic acidosis
decreased clearance of lactate by the liver, kidneys, and skeletal
muscle

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SUGGESTIVE FINDINGS OF SHOCK
Hypovolemic
hematemesis, hematochezia, melena, vomiting, diarrhea, or abdominal
pain
decreased skin turgor (in younger patients), dry skin, dry axillae, dry
tongue, or dry oral mucosa, postural hypotension, decreased jugular
venous pressure, or diminished central venous pressure
Cardiogenic
Depending on the cause  dyspnea, chest pain, or palpitations
jugular venous pressure and central venous pressure may be increased,
while the distal arterial pulses may be diminished
pulmonary congestion or pulmonary edema on a chest radiograph, as well
as recent or current ischemia on an electrocardiogram
Distributive (vasodilatory)
dyspnea, productive cough, dysuria, hematuria, chills, myalgias, rashes,
fatigue, malaise, headache, photophobia, pain, or a recent ingestion
fever, tachypnea, tachycardia, leukocytosis, an abnormal mental status, or
flushing

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Treatment: Shock
Patients in shock require care in an ICU
Careful and continuous assessment of the
physiologic status is necessary
Arterial pressure through an indwelling line,
pulse, and respiratory rate should be
monitored continuously
a Foley catheter should be inserted to follow
urine flow
mental status should be assessed frequently

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Hypovolemic Shock
Most common form of shock
Causes:
loss of red blood cell mass and plasma from hemorrhage
loss of plasma volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible losses
Diagnosis:
signs of hemodynamic instability and the suspected source
of volume loss
initial normal hematocrit does not disprove the presence
of significant blood loss
Plasma losses cause hemoconcentration
free water loss leads to hypernatremia

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Hypovolemic Shock

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Treatment: Hypovolemic Shock
Initial resuscitation:
rapid reexpansion of the circulating intravascular
blood volume
• isotonic saline
• Ringer's lactate
interventions to control ongoing losses
Needs support of respiratory function
Starling’s Law: stroke volume and cardiac output
rise with the increase in preload

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Septic Shock
The hallmark:
decrease in peripheral vascular resistance that occurs despite
increased levels of vasopressor catecholamines
Hyperventilation is often an early sign of the septic
response
Disorientation, confusion, and other manifestations of
encephalopathy may also develop early on, particularly in
the elderly and in individuals with preexisting neurologic
impairment
Stress ulceration can lead to upper gastrointestinal
bleeding
Prolonged or severe hypotension may induce acute hepatic
injury or ischemic bowel necrosis

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Definitions Used to Describe the Condition of Septic Patients

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Septic Shock: THERAPEUTIC
PRIORITIES
Therapeutic priorities for patients with severe
sepsis or septic shock include:

Early initiation of supportive care to correct


physiologic abnormalities, such as hypoxemia and
hypotension.
Distinguishing sepsis from systemic inflammatory
response syndrome (SIRS) because, if an infection
exists, it must be identified and treated as soon as
possible. This may require a surgical procedure (eg,
drainage), as well as appropriate antibiotics.

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Septic Shock: EARLY MANAGEMENT
EARLY MANAGEMENT — The first priority in any
patient with severe sepsis or septic shock is
stabilization of their airway and breathing. Next,
perfusion to the peripheral tissues should be restored
Goals of initial resuscitation — Once it has been
established that hypoperfusion exists, early restoration
of perfusion is necessary to prevent or limit multiple
organ dysfunction, as well as reduce mortality.
Hypoperfusion results from loss of plasma volume into
the interstitial space, decreased vascular tone, and
myocardial depression. The increase in the cardiac
output that is necessary to compensate for the
diminished vascular tone may be limited by the
myocardial depression.
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Treatment: Severe Sepsis and Septic Shock
Antimicrobial Agents
should be started as soon as samples of blood and other
relevant sites have been obtained for culture
Removal of the Source of Infection
Hemodynamic, Respiratory, and Metabolic Support
The primary goals are to restore adequate oxygen and
substrate delivery to the tissues as quickly as possible and
to improve tissue oxygen utilization and cellular
metabolism
General Support
nutritional supplementation
Prophylactic heparinization ?
prevention of skin breakdown, nosocomial infections, and
stress ulcers
tight control of the blood glucose concentration
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Hypoadrenal Shock
The normal host response to the stress of illness,
operation, or trauma requires that the adrenal
glands hypersecrete cortisol in excess of that
normally required
characterized by loss of homeostasis with
reductions in systemic vascular resistance,
hypovolemia, and reduced cardiac output
Critical illness, including trauma and sepsis, may
also induce a relative hypoadrenal state
Diagnosis: ACTH stimulation  inconsistent
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Treatment: Hypoadrenal Shock
Tx for hemodynamically unstable patient:
dexamethasone sodium phosphate 4 mg IV
Simultaneous volume resuscitation and
pressor support are required
The need for simultaneous mineralocoid is
unclear

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Adjunctive Therapies
Dobutamine:
inotropic with simultaneous afterload reduction  minimizing
cardiac-oxygen consumption increases as cardiac output increases.
Dopamine:
inotropic and chronotropic agent
supports vascular resistance in those whose blood pressure will not
tolerate peripheral vascular dilation
Norepinephrine:
primarily supports blood pressure through vasoconstriction and
increases myocardial oxygen consumption while placing marginally
perfused tissues such as extremities and splanchnic organs
at risk for ischemia or necrosis
inotropic without chronotropy.
Arginine-vasopressin (antidiuretic hormone)
increase afterload
may better protect vital organ blood flow and prevent pathologic
vasodilation
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Vasopressor Agents

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Reference
Harrison’s Principle of Internal Medicine, 18th
ed, 2012
Goldman’s Cecil Medicine, 24th ed, 2012

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