SHOCK

dr Budi Enoch SpPD

ESSENTIALS OF DIAGNOSIS
Hypotension, tachycardia,
oliguria, altered mental status.
Peripheral hypoperfusion and
impaired oxygen delivery.
General Considerations
Shock occurs when the rate of arterial
blood flow is inadequate to meet tissue
metabolic needs.
This results in regional hypoxia and
subsequent lactic acidosis from anaerobic
metabolism in peripheral tissues as well as
eventual end-organ damage and failure.
Classification
A. Hypovolemic Shock
B. Cardiogenic Shock
C. Obstructive Shock
D. Distributive Shock
1. Septic shock
2. Systemic inflammatory response syndrome (SIRS)
3. Neurogenic shock
4. Endocrine (new classification)
 Diagnosis
The first changes seen in shock is an increased cardiac output followed
by a decrease in mixed venous oxygen saturation (SmvO2) as
measured in the pulmonary artery via a pulmonary artery catheter.
Central venous oxygen saturation (ScvO2) as measured via a central
line correlates well with SmvO2 and are easier to acquire. If shock
progresses anaerobic metabolism will begin to occur with an increased
blood lactic acid as the result. While many laboratory tests are typically
performed there is no test that either makes or excludes the diagnosis. A
chest X-ray or emergency department ultrasound may be useful to
determine volume state.[2][6]
The shock index (SI), defined as heart rate divided by systolic blood
pressure, is an accurate diagnostic measure that is more useful than
hypotension and tachycardia in isolation.
Under normal conditions, a number between 0.5 and 0.8 is typically
seen. Should that number increase, so does suspicion of an underlying
state of shock. Blood pressure alone may not be a reliable sign for shock,
as there are times when a person is in circulatory shock but has a stable
blood pressure.[4]
Hypovolemic Shock
Hypovolemic shock results from decreased intravascular
volume secondary to loss of blood or fluids and
electrolytes.
The etiology may be suggested by the clinical setting
(eg, trauma) or by signs and symptoms of blood loss (eg,
gastrointestinal bleeding) or dehydration (eg, vomiting or
diarrhea).
Compensatory vasoconstriction may transiently maintain
the blood pressure but unreplaced losses of over 15% of
the intravascular volume can result in hypotension and
progressive tissue hypoxia.
 common causes
Loss of blood (hemorrhagic shock)
External hemorrhage
Trauma, Gastrointestinal tract bleeding,
Internal hemorrhage
Hematoma, Hemothorax or hemoperitoneum
Loss of plasma
Burns, Exfoliative dermatitis
Loss of fluid and electrolytes
External losses
Vomiting, Diarrhea, Excessive sweating
Hyperosmolar states (diabetic ketoacidosis, hyperosmolar
nonketotic coma)
Internal losses (third spacing)

Pancreatitis, Ascites, Bowel obstruction

Cardiogenic Shock
Cardiogenic shock results from cardiac failure with
the resultant inability of the heart to maintain
adequate tissue perfusion.
The clinical definition of cardiogenic shock is
evidence of tissue hypoxia due to decrease cardiac
output (cardiac index < 2.2 L/min/m2) in the
presence of adequate intravascular volume.
This is most often caused by myocardial infarction
but can also be due to cardiomyopathy, myocardial
contusion, valvular incompetence or stenosis, or
arrhythmias.
common causes
Dysrhythmia (tachyarrhythmia,
bradyarrhythmia)
“Pump failure” (secondary to myocardial
infarction or other cardiomyopathy)
Acute valvular dysfunction (especially
regurgitant lesions)
Rupture of ventricular septum or free ventricular
wall
Obstructive Shock
Cardiac tamponade, tension pneumothorax, and
massive pulmonary embolism can cause an acute
decrease in cardiac output resulting in shock.
These are medical emergencies requiring prompt
diagnosis and treatment.
common causes
Tension pneumothorax
Pericardial disease (tamponade, constriction)
Disease of pulmonary vasculature (massive
pulmonary emboli, pulmonary hypertension)
Cardiac tumor (atrial myxoma)
Left atrial mural thrombus
Obstructive valvular disease (aortic or mitral
stenosis)
Distributive Shock
Distributive or vasodilatory shock has many
causes including sepsis, anaphylaxis, systemic
inflammatory response syndrome (SIRS)
produced by severe pancreatitis or burns,
traumatic spinal cord injury, or acute adrenal
insufficiency.
The reduction in systemic vascular resistance
results in inadequate cardiac output and tissue
hypoperfusion despite normal circulatory
volume.
common causes

Septicshock
Anaphylactic shock
Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency
1. Septic shock
Sepsis is the most common cause of distributive
shock and carries a mortality rate of 20–50%.
Sepsis is defined as the presence of infection
(either documented or suspected) in conjunction
with systemic manifestations of infection.
Septic shock is diagnosed when hypotension
from sepsis persists despite adequate fluid
resuscitation
The most common cause of septic shock in
hospitalized patients is infection with gram-
positive or gram-negative organisms;
polymicrobial infections are almost as likely.
The incidence of sepsis from fungal organisms
is increasing but remains less than that for
bacterial infections. Risk factors for septic shock
include bacteremia, extremes of age, diabetes,
cancer, immunosuppression, and history of a
recent invasive procedure
Septic shock is the most common cause of distributive shock.[1]
Caused by an overwhelming systemic infection resulting in
vasodilation leading to hypotension. Septic shock can be caused
by Gram negative bacteria such as (among others) Escherichia
coli, Proteus species, Klebsiella pneumoniae which release an
endotoxin which produces adverse biochemical, immunological
and occasionally neurological effects which are harmful to the
body, and other Gram-positive cocci, such as pneumococci and
streptococci, and certain fungi as well as Gram-positive bacterial
toxins. Septic shock also includes some elements of cardiogenic
shock. In 1992, the ACCP/SCCM Consensus Conference
Committee defined septic shock: ". . .sepsis-induced hypotension
(systolic blood pressure < 90 mmHg or a reduction of 40 mmHg
from baseline) despite adequate fluid resuscitation along with the
presence of perfusion abnormalities that may include, but are not
limited to, lactic acidosis, oliguria, or an acute alteration in mental
status. Patients who are receiving inotropic or vasopressor agents
may have a normalized blood pressure at the time that perfusion
abnormalities are identified."
2. Systemic inflammatory
response syndrome (SIRS)
Defined as a systemic response to a nonspecific infectious or
noninfectious insult—such as from burns, pancreatitis, an
autoimmune disorder, ischemia, or trauma.
The presence of two or more of the following clinical criteria
help establish the diagnosis of SIRS:
(1) body temperature > 38oC (100.4oF) or < 36oC (96.8oF),
(2) heart rate > 90 beats per minute,
(3) respiratory rate more than 20 breaths per
minute or hyperventilation with an arterial carbon dioxide
tension (Paco2) > 32 mm Hg,
(4) abnormal white blood cell
count (> 12,000/mcL or < 4000/mcL or > 10% immature
(band) forms).
When a source of infection is confirmed, SIRS is categorized as
sepsis.
Systemic inflammatory response syndrome (SIRS) is
an inflammatory state affecting the whole body,
frequently a response of the immune system to
infection, but not necessarily so. It is related to sepsis, a
condition in which individuals meet criteria for SIRS and
have a known infection.
It is the body's response to an infectious or noninfectious
insult. Although the definition of SIRS refers to it as an
"inflammatory" response, it actually has pro- and anti-
inflammatory components.
SIRS was first described by Dr. William R. Nelson, of
the University of Toronto, in a presentation to the Nordic
Micro Circulation meeting in Geilo, Norway in February
1983.
 Adult SIRS Criteria
Manifestations of SIRS include, but are not limited to:
Body temperature less than 36°C(96.8°F) or greater than
38°C(100.4°F)
Heart rate greater than 90 beats per minute
Tachypnea (high respiratory rate), with greater than 20
breaths per minute; or, an arterial partial pressure of
carbon dioxide less than 4.3 kPa (32 mmHg)
White blood cell count less than 4000 cells/mm³ (4 x 109
cells/L) or greater than 12,000 cells/mm³ (12 x 109
cells/L); or the presence of greater than 10% immature
neutrophils (band forms). Band forms greater than 3% is
called bandemia or a "left-shift.“
When two or more of these criteria are met with or
without evidence of infection, patients may be diagnosed
with "SIRS
SIRS is frequently complicated by failure of one or more
organs or organ systems.

The complications of SIRS include:

Acute lung injury
Acute kidney injury
Shock
Multiple organ dysfunction syndrome
3. Neurogenic shock
Neurogenic shock is caused by traumatic spinal
cord injury or effects of an epidural or spinal
anesthetic.
This results in loss of sympathetic tone with a
reduction in systemic vascular resistance and
hypotension without a compensatory
tachycardia.
Reflex vagal parasympathetic stimulation
evoked by pain, gastric dilation, or fright may
simulate neurogenic shock, producing
hypotension, bradycardia, and syncope.
Endocrine
Based on endocrine disturbances such as:
Hypothyroidism (Can be considered a form of Cardiogenic
shock) in critically ill patients, reduces cardiac output and
can lead to hypotension and respiratory insufficiency.
Thyrotoxicosis (Cardiogenic shock)
◦ may induce a reversible cardiomyopathy.
Acute adrenal insufficiency (Distributive shock) is
frequently the result of discontinuing corticosteroid
treatment without tapering the dosage. However, surgery and
intercurrent disease in patients on corticosteroid therapy
without adjusting the dosage to accommodate for increased
requirements may also result in this condition.
Relative adrenal insufficiency (Distributive shock) in
critically ill patients where present hormone levels are
insufficient to meet the higher demands
▶Clinical Findings
A. Symptoms and Signs
Hypotension
Hypotension is traditionally defined as a systolic blood
pressure of ≤ 90 mm Hg or a mean arterial pressure of <
60–65 mm Hg but must be evaluated relative to the
patient’s normal blood pressure.
A drop in systolic pressure of > 10–20 mm Hg or an
increase in pulse of > 15 beats per minute with positional
change suggests depleted intravascular volume.
However, blood pressure is often not the best indicator of
end-organ perfusion because compensatory mechanisms,
such as increased heart rate, increased cardiac
contractility, and vasoconstriction can occur to prevent
hypotension.
Patients with hypotension often have cool or
mottled extremities and weak or thready
peripheral pulses.
Splanchnic vasoconstriction may lead to
oliguria, bowel ischemia, and hepatic
dysfunction, which can ultimately result in multi-
organ failure.
Mentation may be normal or patients may
become restless, agitated, confused, lethargic, or
comatose as a result of inadequate perfusion of
the brain.
Hypovolemic shock
Hypovolemic shock is evident when signs of
hypoperfusion, such as oliguria, altered mental
status, and cool extremities, are present.
Jugular venous pressure is low, and there is a
narrow pulse pressure indicative of reduced
stroke volume.
Rapid replacement of fluids restores tissue
perfusion.
 Hemorrhage classes[7
Class Blood loss Response Treatment

min. fast heart rate,

I <15 %(0.75 l) normal blood minimal
pressure

fast heart rate, min.

II 15-30 %(0.75-1.5 l) intravenous fluids
low blood pressure

very fast heart rate,

fluids and packed
III 30-40 %(1.5-2 l) low blood pressure,
RBCs
confusion

critical blood
aggressive
IV >40 %(>2 l) pressure and heart
interventions
rate
Cardiogenic shock
In cardiogenic shock, there are also signs of
global hypoperfusion with oliguria, altered
mental status, and cool extremities.
Jugular venous pressure is elevated and there
may be evidence of pulmonary edema with
respiratory compromise in the setting of left-
sided heart failure.
A transthoracic echocardiogram (TTE) or a
transesophageal echocardiogram (TEE) is an
effective diagnostic tool to differentiate
hypovolemic from cardiogenic shock.
In hypovolemic shock, the left ventricle will be
small because of decreased filling, but
contractility is often preserved.
Cardiogenic shock results from cardiac failure
with a resultant decrease in left ventricular
contractility.
In some cases, the left ventricle may appear
dilated and full because of the inability of the left
ventricle to eject a sufficient stroke volume.
In obstructive shock, the central venous
pressure may be elevated but the TTE or TEE
may show reduced left ventricular filling, a
pericardial effusion in the case of tamponade, or
thickened pericardium as in the case of
pericarditis.
Pericardiocentesis or pericardial window for
pericardial tamponade, chest tube placement for
tension pneumothorax, or catheter-directed
thrombolytic therapy in the case of massive
pulmonary embolism can be lifesaving in cases
of obstructive shock
In distributive shock, signs include hyperdynamic heart
sounds, warm extremities initially, and a wide pulse
pressure indicative of large stroke volume.
The echocardiogram may show a hyperdynamic left
ventricle.
Fluid resuscitation may have little effect on blood
pressure, urinary output, or mentation.
Septic shock is diagnosed when there is clinical
evidence of infection in the setting of persistent
hypotension and evidence of organ hypoperfusion, such
as lactic acidosis, decreased urinary output, or altered
mental status despite adequate volume resuscitation.
Neurogenic shock is diagnosed when there is evidence
of central nervous system injury and persistent
hypotension despite adequate volume resuscitation.
B. Laboratory Findings and
Imaging
Blood specimens should be evaluated for
complete blood count, electrolytes, glucose,
arterial blood gas determinations, coagulation
parameters, lactate levels, typing and cross-
matching, and bacterial cultures.
An electrocardiogram and chest radiograph
should also be part of the initial assessment.
Treatment
A. General Measures
Treatment depends on prompt diagnosis and an accurate
appraisal of inciting conditions.
Initial management consists of basic life support with an
assessment of the patient’s airway, breathing, and
circulation.
This may entail airway intubation and mechanical
ventilation.
Ventilatory failure should be anticipated in patients with
a severe metabolic acidosis in association with shock.
Mechanical ventilation along with sedation can decrease
the oxygen demand of the respiratory muscles and allow
improved oxygen delivery to other hypoperfused tissues
Intravenous access and fluid resuscitation should be
instituted along with cardiac monitoring and assessment
of hemodynamic parameters such as blood pressure and
heart rate.
Cardiac monitoring can detect myocardial ischemia or
malignant arrhythmias, which can be treated by standard
advanced cardiac life support (ACLS) protocols.
Unresponsive or minimally responsive patients should
have their glucose checked immediately and if their
glucose level is low, 1 ampule of 50% dextrose
intravenously should be given. An arterial line should be
placed for continuous blood pressure measurement, and a
Foley catheter should be inserted to monitor urinary
output.
B. Central Venous Pressure
Early consideration is given to placement of a central
venous catheter (CVC) for infusion of fluids and
medications and for hemodynamic pressure
measurements.
A CVC can provide measurements of the central venous
pressure (CVP) and the central venous oxygen saturation
(ScvO2), both of which can be used to manage sepsis and
septic shock.
Pulmonary artery catheters (PACs) allow measurement
of the pulmonary artery pressure, left-sided filling
pressure or the pulmonary capillary wedge pressure
(PCWP), the mixed venous oxygen saturation (SvO2)
and cardiac output.
Central line equipment, in order of typical usage:
1. Syringe with local anesthetic
2. Scalpel in case venous cutdown is needed
3. Sterile gel for ultrasound guidance
4. Introducer needle (here 18 Ga) on syringe with saline to detect backflow of
blood upon vein penetration
5. Guide wire
6. Tissue dilator
7. Indwelling catheter (here 16 Ga)
8. Additional fasteners, and corresponding surgical thread
9. Dressing
Central venous pressure (CVP), also known as mean venous pressure (MVP) is
the pressure of blood in the thoracic vena cava, near the right atrium of the heart.
CVP reflects the amount of blood returning to the heart and the ability of the heart to
pump the blood into the arterial system. CVP is often a good approximation of right
atrial pressure (RAP),[1] however the two terms are not identical, as right atrial
pressure is the pressure in the right atrium. Normal CVP can be measured from two
points of reference:
Sternum: 0–14 cm H2O
Midaxillary line: 8–15 cm H2O
A CVP < 5 mm Hg suggests hypovolemia, and a CVP
over 18 mm Hg suggests volume overload, cardiac
failure, tamponade, or pulmonary hypertension.
A cardiac index < 2 L/min/m2 indicates a need for
inotropic support.
A high cardiac index > 4 L/min/m2 in a hypotensive
patient is consistent with early septic shock.
The systemic vascular resistance is low (< 800 dynes .
s/cm–5) in sepsis and neurogenic shock and high (> 1500
dynes . s/cm–5) in hypovolemic and cardiogenic shock.
Treatment is directed at maintaining a CVP of 8–12
mm Hg, a mean arterial pressure of 65–90 mm Hg, a
cardiac index of 2–4 L/min/m2, and a ScvO2 < 70%.
C. Volume Replacement
Volume replacement is critical in the initial management
of shock.
Hemorrhagic shock is treated with immediate efforts to
achieve hemostasis and rapid infusions of blood
substitutes, such as type-specific or type O negative
packed red blood cells (PRBCs) or whole blood, which
also provides extra volume and clotting factors.
Each unit of PRBC or whole blood is expected to raise
the hematocrit by 3%.
Hypovolemic shock secondary to dehydration is
managed with rapid boluses of isotonic crystalloid (0.9%
saline or lactated Ringer solution) usually in 1-liter
increments.
Cardiogenic shock in the absence of fluid
overload requires smaller fluid challenges, usually
in increments of 250 mL.
Septic shock usually requires large volumes of
fluid for resuscitation (usually < 2 L) as the
associated capillary leak releases fluid into the
extravascular space.
Caution must be used with large-volume
resuscitation with unwarmed fluids because this can
produce hypothermia, which can lead to
hypothermia-induced coagulopathy.
Warming of fluids before administration can avoid
this complication.
D. Early Goal-Directed Therapy
Patients assigned to early goal-directed
care received fluid resuscitation to achieve
a CVP of 8–12 mm Hg; vasopressors to
maintain a mean arterial blood pressure of
at least 65 mm Hg; PRBCs to reach a
hematocrit of 30% if the ScvO2 was <
70%; and if, after PRBC transfusion, the
ScvO2 remained < 70%, dobutamine to
raise the ScvO2 > 70%.
Traditional endpoints of resuscitation such as
blood pressure, heart rate, urinary output, mental
status, and skin perfusion can therefore be
misleading.
Additional endpoints such as lactate levels and
base deficit can help guide further resuscitative
therapy.
Patients who respond well to initial efforts
demonstrate a survival advantage over
nonresponders.
E. Medications
1. Vasoactive therapy—Vasopressors and inotropic
agents are administered only after adequate fluid
resuscitation.
Choice of vasoactive therapy depends on the presumed
etiology of shock as well as cardiac output.
If there is continued hypotension with evidence of high
cardiac output after adequate volume resuscitation, then
vasopressor support
is needed to improve vasomotor tone.
If there is evidence of low cardiac output with high
filling pressures, inotropic support is needed to improve
contractility.
For vasodilatory shock when increased
vasoconstriction is required to maintain an adequate
perfusion pressure, alpha-adrenergic agonists (such as
norepinephrine and phenylephrine) are generally used.
Although norepinephrine is both an alpha-adrenergic
and beta-adrenergic agonist, it preferentially increases
mean arterial pressure over cardiac output.
The initial dose is 1–2 mcg/min as an intravenous
infusion, titrated to maintain the mean arterial blood
pressure to at least 65 mm Hg.
The usual maintenance dose is 2–4 mcg/min
intravenously (maximum dose is 30 mcg/min).
Patients with refractory shock may require
dosages of 10–30 mcg/min intravenously.
Epinephrine, also with both alpha-adrenergic
and beta-adrenergic effects, may be used in
severe shock and during acute resuscitation.
It is the vasopressor of choice for
anaphylactic shock.
For severe shock, give 1 mcg/min as a
continuous intravenous infusion initially and
titrate to hemodynamic response; the usual
dosage range is 1–10 mcg/min intravenously.
Dopamine has variable effects according to dosage.
At low doses (2–5 mcg/kg/min intravenously),
stimulation of dopaminergic and beta-adrenergic
receptors produces increased glomerular filtration, heart
rate, and contractility.
At doses of 5–10 mcg/kg/min, beta-1-adrenergic effects
predominate, resulting in an increase in heart rate and
cardiac contractility.
At higher doses (> 10 mcg/kg/min), alpha-adrenergic
effects predominate, resulting in peripheral
vasoconstriction.
The maximum dose is typically 50 mcg/kg/min.
The use of dopamine as a first-line
vasopressor in septic shock was shown in
a metaanalysis to increase 28-day
mortality and to have a higher incidence of
arrhythmic events.
Dopamine should only be used as an
alternative to norepinephrine in select
patients with septic shock, including
patients with significant bradycardia or
low potential for tachyarrhythmias.
Vasopressin (antidiuretic hormone or ADH) is often
used as an adjunctive therapy to catecholamine
vasopressors in the treatment of distributive or
vasodilatory shock.
Vasopressin causes peripheral vasoconstriction via V1
receptors located on smooth muscle cells and attenuation
of nitric oxide (NO) synthesis and cGMP, the second
messenger of NO.
The rationale for using low-dose vasopressin in the
management of septic shock includes the relative
deficiency of vasopressin in late shock and the increased
sensitivity of the systemic circulation to the vasopressor
effects of vasopressin.
Intravenous infusion of vasopressin at a low dose
(0.01–0.04 units/min) may be safe and beneficial in
septic patients with hypotension that is refractory to
fluid resuscitation and conventional catecholamine
vasopressors.
Higher doses of vasopressin decrease cardiac output
and may put patients at greater risk for splanchnic
and coronary artery ischemia.
Studies do not favor the use of vasopressin as first-
line therapy, but it may be as a second-line agent in
refractory septic or anaphylactic shock; its role as an
initial vasopressor warrants further study.
There is insufficient evidence to recommend a specific
vasopressor for use in cardiogenic shock, but expert
opinion suggests that either norepinephrine or dopamine
should be used as a first-line agent.
Dobutamine, a predominantly beta-adrenergic agonist,
increases contractility and decreases afterload. It is used
for patients with low cardiac output and high PCWP but
who do not have hypotension.
The initial dose is 0.1–0.5 mcg/kg/ min as a continuous
intravenous infusion, which can be titrated every few
minutes as needed to achieve a hemodynamic effect; the
usual dosage range is 2–20 mcg/kg/min intravenously.
2. Corticosteroids
Corticosteroids are the treatment of choice in patients
with shock secondary to adrenal insufficiency but studies
do not support their use in patients with shock from
sepsis or other etiologies.
The observation that severe sepsis may be associated
with relative adrenal insufficiency or glucocorticoid
receptor resistance has led to several trials to evaluate the
role of treatment with corticosteroids in septic shock
Investigators have studied the use of low-dose
corticosteroids in patients who were in septic shock and
had relative adrenal insufficiency, defined by a cortisol
response of 9 mcg/dL or less after one injection of 250
mcg of corticotropin
Metaanalyses of multiple smaller trials of
corticosteroids in patients with septic
shock demonstrated that when shock was
poorly responsive to fluid resuscitation
and vasopressors, low-dose hydrocortisone
(300 mg/d or less in divided doses)
increased the mean arterial pressure but
did not show a mortality benefit.
3. Antibiotics—Definitive therapy for
septic shock includes an early initiation of
empiric broad-spectrum antibiotics after
appropriate cultures have been obtained.
Imaging studies may prove useful to
attempt localization of sources of
infection.
Surgical management may also be
necessary if necrotic tissue or loculated
infections are present
4. Sodium bicarbonate—For patients
with sepsis of any etiology and lactic
acidosis, clinical studies have failed to
show any hemodynamic benefit from
bicarbonate therapy, either in increasing
cardiac output or in decreasing the
vasopressor requirement even in patients
with severe acidemia.
makasih udah denger