CHAPTER 

18

Shock Syndromes
Radha S. Gopalan1 and Ewelina Wojtaszek2
1
Banner University Medical Clinics, Scottsdale, AZ, USA
2
Robert Wood Johnson Barnabas Health, New Brunswick, NJ, USA

OV ERALL BOT TOM LI N E

• Development of the syndrome of shock involving multiorgan failure sets off the final downward spiral of
a patient towards death. The cornerstone of pathophysiology is decreased oxygen supply and utilization
by the cells.
• Early diagnosis and intervention is the key to reducing mortality in circulatory shock.
• Shock syndromes carry an unacceptably high mortality rate even with modern treatment for the
multitude of etiologies that can lead to circulatory collapse.
• Clinician’s vigilance is the cornerstone for early identification of shock state and the diagnosis of such a
state is a clinical diagnosis.
• Awareness of the most common pitfalls as well as early identification and institution of appropriate
intervention can prevent the final downward spiral of shock to death.

Background
Definition of disease
• Shock syndrome is a condition that the European Society of Intensive Care Medicine (ESICM) defines as
‘generalized acute circulatory failure which is life threatening and is associated with inadequate oxygen
utilization by cells.’
• It is the final pathway of a state of cellular dysfunction where the circulation is unable to meet the
demands of the tissues, resulting in cellular dysoxia, i.e. mismatch between oxygen delivery and oxygen
consumption, resulting in increased blood lactate levels.

Disease classification
• Shock syndromes are divided into four major groupings (hypovolemic, cardiogenic, distributive, and
obstructive) along with the underlying diseases that cause each particular type of shock (see Differential
diagnosis section).
• It should be emphasized that despite this classification, circulatory collapse resulting in shock generally
has overlapping pathophysiology. For example, hypovolemia can be found in cardiogenic shock or in
septic (distributive) shock.

Incidence/prevalence
• Circulatory shock accounts for one‐third of patients admitted to ICUs in the USA.
• In the SOAP II trial (n = 1679), septic shock accounted for 62.2% (according to the ESICM, reported
incidence of septic shock in patients admitted to the ICU varies between 6.3% and 14.7%). Cardiogenic

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148 
 Shock Syndromes  149

shock accounted for 16.7%, hypovolemia accounted for 15.7%, and the rest were accounted for by
other distributive and obstructive etiologies.
• 4.6% of ACS patients admitted to the hospital developed cardiogenic shock according to an observa-
tional study of 65 119 patients hospitalized.

Etiology
• Circulatory failure or shock is a syndrome that is the final pathway for several etiological conditions that
lead to circulatory collapse.
• While circulatory shock is generally divided into four types (hypovolemic, cardiogenic, distributive, and
obstructive), the conditions that contribute to development of any of these specific type are multitude as
described in the Differential diagnosis section (Figure 18.1).

Pathology/pathogenesis
• The underlying pathologic derangement in shock syndrome is a mismatch between global oxygen deliv-
ery (DO2) and oxygen consumption (VO2).
• DO2 is responsive to changes in any of the three components of DO2 (cardiac output, Hb, and oxygena-
tion) and VO2.
• In the presence of adequate oxygenation and Hb, cardiac output drives DO2 to match VO2.
• The normal DO2:VO2 ratio is 5:1 and is achieved by increasing cardiac output (CO) in response to increased
demand from cellular respiration (consumption drives delivery) and at this ratio cellular respiration is not
supply dependent.
• When the ratio falls below 2:1, cellular respiration becomes supply dependent. This 2:1 ratio corresponds
to maximal oxygen extraction by tissues and is the critical level at which tissue hypoxia (oxygen debt)
results in anaerobic tissue metabolism leading to acidosis and lactic acid formation, hence elevated blood
lactic acid levels.
• Therefore, correction of DO2 by improving CO should improve survival from shock.
• However, this is not the case as other regional and microcirculatory hemodynamic alterations become
active in due course when restoration of DO2 is delayed.
• Compensatory mechanisms that include extrinsic (autonomic nervous system and circulating norepineph-
rine from adrenals) and intrinsic (arteriolar and endothelium mediated) regional and microcirculatory
autoregulation become overwhelmed with delay in treatment, resulting in systemic inflammatory
response syndrome (SIRS). SIRS results in regional flow heterogeneity with shunting of blood supply to
non‐critical areas of the body.
• As shock state progresses, microcirculatory blood flow, microcirculatory oxygen diffusion, and microcircu-
latory oxygen utilization become ineffective resulting in microcirculatory failure. At this stage, even if the
DO2 is re‐established with adequate CO, the downward spiral and the development of multiorgan dys-
function syndrome (MODS) is inevitable. At this point the patient may continue to decline even with
adequate CO.
• If measures to prevent this downward spiral are unsuccessful, death ensues.

Prevention

BOTT OM LINE/ CLI N I CA L PEA RLS

• Shock syndrome is a clinical diagnosis.
• Early recognition of the development of shock by proactive clinical vigilance is the only preventable
measure.
150  Part 2: Cardiovascular Critical Care

Screening
• Critically ill patients are especially at risk for developing shock syndrome. Studies have shown that the
shock syndrome is prevalent in approximately one‐third of patients admitted to ICU.
• Critically ill patients should be routinely screened for the development of shock syndrome.
• Screening involves monitoring and evaluating clinical, hemodynamic, and biochemical parameters.

Diagnosis

B O TTOM L INE/CLIN I CA L PEA RLS

• Diagnosis of inadequate tissue perfusion involves looking at clinical, hemodynamic and biochemical
variables.
• Clinically, inadequate tissue perfusion can be assessed via the skin (evidence of decreased cutaneous
perfusion), kidneys (decreased urine output <0.5 mL/kg/h), and brain (altered mental status).
• Hemodynamically, reliance on hypotension (SBP <90 mmHg or MAP <65 mmHg or a reduction of >40
mmHg from baseline) alone to define shock should be avoided. However, frequent measurement of
blood pressure, heart rate, respiratory rate, temperature, and other variables listed should be carried out.
• Biochemically, blood lactate levels (>2 mEq/L or >2 mmol/L) are useful in detecting mismatch in tissue
oxygen delivery and demand, while keeping in mind that there are other conditions that may result in
increased lactate levels without the presence of such a mismatch.
• Routinely screen patients at risk using this information to detect impending shock so that early
intervention can be instituted.

Differential diagnosis

Differential diagnosiss

Hypovolemic ◼◼ Left or right ventricle

• Hemorrhagic: • Myocardial contusion

• Trauma • Myocarditis
• Gastrointestinal • Cardiomyopathy
• Retroperitoneal • Post ischemic stunning
• Non‐hemorrhagic: • Septic myocardial depression
• External fluid loss • Pharmacologic:
• Dehydration ◼◼ Anthracycline cardiotoxicity

• Vomiting ◼◼ Calcium channel blockers

• Diarrhea • Mechanical:
• Polyuria • Valvular failure (stenotic or regurgitant)
• Interstitial fluid redistribution: • Hypertrophic cardiomyopathy
• Thermal injury • Ventricular septal defect
• Trauma • Arrhythmic:
• Anaphylaxis • Bradycardia
• Increased vascular capacitance: • AV blocks
• Sepsis • Tachycardia:
• Anaphylaxis ◼◼ Supraventricular

• Toxins/drugs ◼◼ Ventricular

Cardiogenic Obstructive
• Myopathy: • Impaired diastolic filling (decreased preload):
• Myocardial infarction: • Vena cava obstruction
 Shock Syndromes  151

• Intrathoracic obstructive tumors • Impaired systolic contraction:

• ↑ intrathoracic pressure • Right ventricle:
• Tension pneumothorax ◼◼ Pulmonary embolus

• Mechanical ventilation ◼◼ Acute pulmonary hypertension

• Decreased cardiac compliance • Left ventricle:

• Constrictive pericarditis ◼◼ Saddle embolus

• Cardiac tamponade: Aortic dissection

◼◼ Acute: Distributive
◼◼ Post‐MI free wall rupture • Septic
◼◼ Traumatic • Toxic shock syndrome
◼◼ Hemorrhagic • Anaphylactic
◼◼ Chronic: • Neurogenic (spinal shock)
◼◼ Malignant • Endocrine:
◼◼ Uremic • Adrenal crisis
◼◼ Idiopathic • Thyroid storm
• Toxins

Typical presentation
• Typically, in adults, the systolic blood pressure is less than 90 mmHg and the mean arterial pressure is less
than 70 mmHg. This is associated with tachycardia.
• This tissue hypoperfusion can be identified early by paying attention to what is referred to as the ‘three
windows’ of the body:
• Cutaneous: skin becomes cold and clammy due to vasoconstriction or due to severely inadequate
cardiac output with vasodilation.
• Kidneys: urine output of <0.5 mL/kg/h.
• Neurologic: altered sensorium (obtundation, disorientation, and/or confusion).
• Hyperlactatemia (>1.5 mmol/L) is typically present.

Clinical diagnosis
History
• The state of circulatory shock is always a life‐threatening condition and is an emergency. It is imperative
that the diagnosis is made as early as possible, preferably at the compensated stage.
• In the compensated state hypotension may not be apparent, therefore reliance on the presence of
­hypotension is not recommended. Additionally, mortality is already increased if hypotension and hypop-
erfusion are present.
• Because survival is dependent on early initiation of therapy for shock, diagnosis of shock is always a clini-
cal diagnosis. Laboratory tests and imaging can be performed to support the diagnosis or to identify the
underlying etiology; however, therapy should not be delayed to accommodate laboratory studies.
• Just as circulatory shock is a common end pathway for a variety of etiologies, treatment of all forms of
shock mainly follows a common pathway.

Physical examination
• Physical exam is extremely important in recognizing shock and can be grouped into two main areas. The
first is recognizing the physical signs of compensatory mechanisms that come into play during the initial
phase (pre‐shock) of shock.
• Examination is accomplished by paying attention to the physical manifestations in the ‘three windows’ of
the body (cutaneous, neurological, renal). Early signs that reflect the body’s effort to compensate include
tachycardia, dyspnea, and oliguria (urine output <0.5 mL/kg/h). Additionally, the extremities are cool and
may get mottled.
152  Part 2: Cardiovascular Critical Care

• Blood pressure may be elevated or even normal initially when the patient is in a compensated state with
maximal sympathetic drive. Clinicians should consider the baseline blood pressure of the patient.
Normotension in a patient who is otherwise hypertensive may indicate hypoperfusion. Frank hypotension
(MAP <60–65 mmHg) will develop if untreated as the shock state progresses.
• Other clinical signs may be sought to identify the type and etiology of the shock:
• Hypovolemic shock – look for decreased JVP.
• Cardiogenic shock – look for elevated JVP and presence of S3 and S4 with or without murmurs.
• Obstructive shock:
◼ Pulmonary embolus – look for signs of RV failure, dyspnea, and hypoxia.

◼ Cardiac tamponade – look for Kussmaul’s sign, distant heart sounds, and pulsus paradoxus.

• Septic shock – look for fever, abnormal WBC, warm extremities, and focus of infection.

Disease severity classification

Circulatory failure resulting in shock and its progression to death, irrespective of etiology, does not show
abrupt changes and is rather a pathophysiologic continuum. However, three stages can be identified.

Stage Explanation of stage

Pre‐shock A stage in the shock continuum where compensatory mechanisms become active and an attempt
to restore tissue perfusion is maintained. During this phase, mild tachycardia, mild to moderate
reduction in blood pressure, and mild elevation of lactate levels may be the only manifestation in a
patient with appropriate setting for development of shock

Shock A stage where the compensatory mechanisms become overwhelmed by the underlying disease
progression with or without therapy. Clinical parameters for the diagnosis of shock such as severe
tachycardia, hypotension, progressive severe lactic acidosis, oliguria, altered mental status, and
other evidence of tissue underperfusion become apparent

End‐organ Irreversible damage to multiple organs results in multiorgan failure. Resistant to therapy with
dysfunction worsening hypotension, severe reduction in cardiac output, acute renal failure, obtundation or
coma, and finally death may ensue in this phase

Laboratory diagnosis
List of diagnostic tests
• Hemoglobin level: check to assess hemorrhage and oxygen‐carrying capacity. Erythrocytosis may be evi-
dent in non‐hemorrhagic hypovolemic shock and in septic shock when extravasation of intravascular fluid
into the interstitium.
• WBC: leucocyte count is usually elevated despite the etiology of shock due to demargination of neutro-
phils but leucopenia can manifest in the case of late shock or sepsis.
• Platelets: platelet count increases acutely due to stress of shock but thrombocytopenia can result with
progression of sepsis or with massive resuscitation efforts to correct hemorrhage.
• Arterial blood gases and electrolytes:
• An anion gap acidosis usually associated with lactic acidosis indicates prolonged periods of tissue
underperfusion.
• Non‐anion gap acidosis in hypovolemia may indicate excessive diarrhea.
• In hypovolemic shock, metabolic alkalosis may indicate vomiting.
• BUN/creatinine: these may be initially normal even if there is underlying renal injury. Isolated increase in
BUN without increase in creatinine may suggest GI bleed.
• Coagulation studies: performed if coagulopathy as a result of shock is suspected.
• ECG: helps detect myocardial ischemia and if pathologic tachycardia is suspected.
 Shock Syndromes  153

List of imaging techniques

• Chest radiograph: to identify pneumonia, pulmonary edema, pneumothorax, and significant pericardial effusion.
• The following are optional:
• Abdominal radiograph is rarely needed unless intra‐abdominal obstructive processes are suspected.
• CT scan of the chest and abdomen are useful in specific situations such as aortic dissection, intra‐
abdominal hemorrhage, and pulmonary embolus.
• Echocardiogram is useful for the diagnosis of multiple etiologies of shock such as pulmonary embolus,
LV or RV failure, pericardial tamponade, and other repairable cardiac lesions such as acute mitral regur-
gitation or aortic regurgitation.
• MRI (if the patient is able to tolerate it) is useful for the diagnosis of acute myocarditis and the presence
of infiltrative cardiomyopathies resulting in restrictive filling and low cardiac output. It is also useful for
accurate RV function assessment.

Diagnostic algorithm (Algorithm 18.1)

Algorithm 18.1  Initial assessment of shock. (Source: Reproduced with permission

from Vincent et al. 2013.)

Arterial hypotension

Absent Signs of tissue hypoperfusion Present

Chronic Brain Circulatory

hypotension? Altered mental shock
Syncope state
(or transient)
Tachycardia Estimate cardiac
output or SvO2
Skin
Mottled
Elevated
Clammy Normal
blood Low
lactate or high
Kidney CVP
Oliguria

Low High

Distributive shock Hypovolemic shock Cardiogenic shock Obstructive shock

Large ventricles and
Normal cardiac Small cardiac In tamponade pericardial
poor contractility
chambers and (usually) chambers and normal effusion: small right and
preserved contractility or high contractility left ventricles, dilated
inferior vena cava; in
pulmonary embolism
or pneumothorax:
dilated right ventricle,
small left ventricle

Echocardiography
154  Part 2: Cardiovascular Critical Care

Potential pitfalls/common errors made regarding diagnosis of disease

• Awaiting development of hypotension to identify development of hypotension is a common error and
results in delay in useful interventions or searching for underlying etiologies in a timely manner.
• Beware of the patient’s baseline systolic pressure. In a hypertensive patient, drop in pressure by 40 mmHg
from baseline can signal development of shock state even if the MAP (<60–65 mmHg) does not meet the
criteria for hypotension.
• Once shock state is clinically identified, awaiting laboratory confirmation to start appropriate therapy is
another common error encountered in the critical care setting.

Treatment
Treatment rationale
• Treatment rationale of shock consists of efforts to maintain adequate perfusion to match oxygen delivery
and oxygen consumption in addition to correcting the underlying etiology of the shock.
• Initial approach is fluid resuscitation along with adequate oxygenation.
• Vasoactive substances are then administered to maintain adequate perfusion.
• Failure of vasoactive medications should lead to consideration for early institution of cardiac assist device
support. Restoration of adequate cardiac output will not result in improvement once microcirculatory
failure ensues.
• If all aggressive measures fail and continuation becomes futile, palliation and comfort care are
considered.
• There are four phases of treatment: salvage, optimization, stabilization, and de‐escalation.

Managing the hospitalized patient

Stage Four phases of treatment

Pre‐shock Salvage
Focuses on achieving adequate blood pressure and cardiac output and immediately correcting the
underlying cause of shock:
• Attempt at maintaining acceptable blood pressure (MAP >60–65 mmHg) is initiated
• Life‐saving interventions are promptly initiated. For example: acute coronary revascularization or
assist devices for cardiogenic shock from acute MI; prompt antibiotic coverage for septic shock;
acute thrombolysis or thrombectomy in the case of massive PE; pericardiocentesis for
tamponade, etc.

Shock Optimization
Focuses on factors that improve cellular oxygen delivery and availability:
• Maintain adequate tissue oxygen availability by optimizing CO, SvO2 and lactate levels

Stabilization
Focuses on preventing organ dysfunction even if hemodynamic stabilization has been established.
Establishing hemodynamic stabilization in shock syndrome does not guarantee end‐organ
function improvement:
• Provide organ support and attempt to minimize complications

De‐escalation
Focuses on weaning from vasoactive agents as the condition of the patient improves:
• Wean from vasoactive agents and achieve negative fluid balance
End‐organ If SIRS and subsequent multiorgan failure/MODS develops, the risk of death increases substantially
dysfunction (>75%). Aggressive treatment may become futile and can perpetuate patient and family
suffering. At this stage it is appropriate to involve the service of palliative care medicine and
initiate goals of care conversation with patient/family
 Shock Syndromes  155

Table of treatment

Treatment Comments

Conservative Fluid administration is a conservative initial measure to improve

Fluid resuscitation cardiac output and microvascular flow. Oxygen is administered
Oxygen delivery (nasal cannula, high flow nasal to improve the oxygen content
cannula, or ventilator)

Medical Once shock state is recognized, vasopressor support is

Norepinephrine (0.1–2.0 μg/kg/min) recommended to maintain arterial perfusion pressure while
Dopamine (2–20 μg/kg/min) inotropic support may be needed to enhance cardiac output
Epinephrine (0.05–2 μg/kg/min and titrated up) of failing ventricles. All patients should be considered for
Vasopressin (0.03 U/min and titrated up) resuscitation with vasoactive medications unless specific
Dobutamine (2–20 μg/kg/min) contraindication exist (e.g. arrhythmia prohibiting the use of
Milrinone (0.125–0.75 μg/kg/min) pro‐arrhythmic drugs such as dobutamine or dopamine)

Surgical Patients who decline despite maximal medical therapy should

Various right and left ventricular devices, usually be considered for early percutaneous short‐term or long‐term
emergent/short-term devices cardiac device support to ensure adequate oxygen delivery. The
Pericardiocentesis choice of device depends on the resources and the experience
Pulmonary thrombectomy of the institution. Surgical pulmonary thrombectomy can be
considered for acute PE resulting in obstructive shock

Radiologic Considered in acute massive PE

Pulmonary thrombectomy

Psychologic All patients and family should receive these interventions when
Spiritual care appropriate
Palliative care

Prevention/management of complications
• Critically ill shock patients frequently have multiple invasive catheters placed for monitoring and ­treatment
purposes.
• One of the most feared complications is the development of line‐related sepsis in addition to an existing
shock from other etiology such as cardiogenic or hypovolemic shock. This can be prevented by vigiliant
monitoring and removing indwelling catheters when not necessary and by limiting the use of indwelling
catheters in general.
• Development of ventilator‐associated pneumonia is another potential complication in patients with
­prolonged ventilator dependence. Application of prophylactic measures and daily assessment for the
liberation from ventilator support should be instituted to prevent this complication.
• Persistent hypotension despite aggressive efforts should raise concern for adrenal suppression/insuffi-
ciency. This can be managed by administering corticosteroids.
• With the use of multiple vasoactive medications, development of arrhythmia is a common complication
that may result in clinical decompensation. Clinicians should consider cardioversion or rhythm control
versus rate control strategies carefully. It is important to carefully select vasoactive medications keeping
the patient’s underlying risk factors in mind.
156  Part 2: Cardiovascular Critical Care

C LI NICAL PEARLS
• Shock syndrome is a condition resulting from a mismatch between oxygen delivery (DO2) and
consumption (VO2). Both oxygen delivery and consumption should be considered when tailoring
interventions.
• Microcirculatory failure of individual organs and specific vascular beds may continue to drive the
downward spiral despite achievement of adequate cardiac output. As a result, continued vigilance and
aggressive clinical support is required despite achieving hemodynamic stability.
• Gut wall integrity as well as perfusion should be optimized to avoid development of septicemia from
translocation of microbes from the gut due to the loss of gut integrity.

Special populations
Pregnancy
• Pregnant women tend to suffer hypovolemic shock from obstetrical hemorrhage.
• Pulmonary embolism (PE) and venous thrombosis are known to occur in the peripartum period. In fact,
PE is the sixth leading cause of maternal mortality.
• Septic shock is not frequent in pregnant women; however, most studies on sepsis have excluded
­pregnant women.
• From a cardiac perspective, peri‐partum cardiomyopathy may result in cardiogenic shock at the time of
delivery due to sudden increase in afterload and could be fatal.
• Principles of treatment are generally extrapolated from the general adult population and applied to the
pregnant population.
• Management of circulatory failure in pregnant women should involve a multidisciplinary team approach
involving maternal–fetal medicine, neonatology, and intensivists as well as cardiac anesthesia if a cesarean
is considered.

Elderly
• Management of shock syndromes in the elderly is very similar to that in other adult patients. However,
more clinical vigilance is recommended as elderly patients are less tolerant of the mismatch of oxygen
delivery and consumption resulting from circulatory shock, and may suffer a rapid decline.
• In very elderly patients, early involvement of geriatric medicine and palliative care medicine may be
beneficial.

Prognosis

B O TTOM L INE/CLIN I CA L PEA RLS

• Circulatory shock from any cause results in very high mortality despite advances in therapy.
• By the time severe shock syndrome and its complications develop, the initial etiology of shock may have
little impact in the prognosis due to the confluence of multiple shock hemodynamics.
• Reversal of the downward spiral in circulatory shock may become irreversible if shock is not detected and
managed at an early stage.
 Shock Syndromes  157

Natural history of untreated disease

• Since circulatory shock is a syndrome that reflects failure of multiple organ systems, the condition will
continue to worsen without early and appropriate interventions.
• The survival of patients with untreated shock remains dismal.

Prognosis for treated patients

• Mortality in cardiogenic shock even when treated remains at an unacceptable rate of more than 40%.
• Fatality of septic shock is estimated at 40–50%, reaching as high as 80%.
• Hypovolemic shock can be successfully treated and survival rates are higher than for septic and cardiogenic
shock. The exception is hypovolemic shock in trauma patients where the mortality is determined by the
severity of trauma that resulted in hypovolemia.
• Mortality of obstructive shock is determined by the underlying etiology.

Follow‐up tests and monitoring

• Early treatment includes hemodynamic stabilization with fluids and vasopressors and treatment of the
underlying etiology. Frequent reassessments are essential.
• It is reasonable to use hemodynamic assessment (pulmonary artery catheterization) in complex patients
who do not respond to initial efforts.
• Insertion of arterial and central venous catheters is also recommended when there is inadequate response
to initial therapy or need for continuous infusion of vasopressors.
• If a central venous catheter is present, measurement of ScvO2 to monitor the underlying pattern and
adequacy of cardiac output to guide therapy is recommended.
• Serial lactate levels have been shown to be useful to assess response to therapy.

Reading list
Cecconi M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task Force of the European Society of
Intensive Care Medicine. Intensive Care Med 2014;40:1795–815.
Kumar A, Unligil U, Parrillo JE. Circulatory shock. In: Unligil U, Parrillo JE (eds), Critical Care Medicine: Principles of
Diagnosis and Management in the Adult, 4th edition. Philadelphia: Elsevier, 2013; pp. 299–324.
Lim HS. Cardiogenic shock: failure of oxygen delivery and oxygen utilization. Clin Cardiol 2016;39(8):477–83.
Reyentovich A, Barghash MH, Hochman JS. Management of refractory cardiogenic shock. Nat Rev Cardiol
2016;13(8):481–92.
Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013;369:1726–34.

Suggested websites
http://www.esicm.org

Guidelines
International society guidelines

Title Source Date and

weblink

Consensus on Circulatory Shock and Hemodynamic European Society of Intensive Care 2014
Monitoring Medicine http://www.esicm.org
158  Part 2: Cardiovascular Critical Care

Image

Distributive shock Hypovolemic shock

(66% of cases) (16% of cases)

Loss of plasma
or blood volume

Vasodilatation

Cardiogenic shock Obstructive shock

(16% of cases) (2% of cases)

Obstruction

VVentricular
en Pericardial
ffailure
ailu
ailu tamponade

Figure 18.1  Frequency of the four main four types of shock

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This includes multiple choice questions.