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is associated with cardiogenic or hemorrhagic shock, and a high ScVO2 is associated with septic shock. One can see how this makes sense in both hemorrhagic and
cardiogenic shock by analyzing the equations in Fig.14.1. Conceptually, in cardiogenic shock, tissues have excess time to extract oxygen as ow is sluggish. In hemorrhagic shock, the amount of oxygen delivered is low due to loss of hemoglobin
and blood volume. Sepsis instead typically presents with vasodilatory shock, minimizing the ability of tissues to extract oxygen, which results in normal to high
ScVO2. However, there are many variables in this equation that limit its accuracy
and can make the interpretation of a single ScVO2 value prone to error. For instance,
in a patient who is mechanically ventilated and has an elevated partial pressure of
oxygen in arterial blood (PaO2), this would result in a higher ScVO2. In this scenario, ruling out cardiogenic shock by that value alone may be a mistake. ScVO2
may provide value when trending, particularly in cardiogenic shock and evaluating
response to therapies. In sepsis, there have been multiple trials that have demonstrated limited utility in determining outcomes and response to therapy as opposed
to utilizing lactic acid and clinical assessment [18–22].
Hematologic derangements are also common in shock. Leukocytosis is commonly seen in both sepsis and other causes of shock [23]. Decreased hemoglobin
and platelets may be seen due to hemorrhagic shock. Increased blood urea nitrogen
(BUN) and creatinine are commonly seen due to impaired renal perfusion. In severe
shock, signicant elevation of AST and ALT may occur. If severe enough, patients
may develop acute liver failure. Elevated troponin is common, especially when utilizing high-sensitivity troponin assays. This occurs even in the absence of acute
coronary occlusion [24]. Metabolic acidosis, most commonly due to lactic acid and/
or renal failure, may be present.
L. R. Goss et al.
14.3.3 Imaging
Imaging is an essential aspect in diagnosing the cause of shock. Bedside ultrasound
assessing for cardiac function, signs of tamponade, pneumothorax, free intraperitoneal uid, and aortic abnormalities may immediately help clinicians narrow down
the primary etiology of shock [25–28]. A chest X-ray may help identify pneumonia,
aortic abnormalities, cardiomegaly, pneumothorax, or other ndings to help determine a cause as well. CT imaging can be highly sensitive for foci of infection, pulmonary embolism, aortic pathology, and more.
14.3.4 Invasive Hemodynamic Monitoring
Although no invasive hemodynamic monitoring device has demonstrated sufcient
evidence that their use improves mortality in shock in randomized controlled trials,
they are commonly used [29, 30]. Arterial lines are helpful to obtain accurate and
14 Sho ck
timely blood pressure measurements, as noninvasive blood pressure cuffs may provide inaccurate measurements in patients with vasoconstriction. Central venous
pressure (CVP) monitoring may be helpful in identifying right heart dysfunction
and signs of venous congestion. Pulmonary arterial catheters (PACs) are used to
determine cardiac output and other hemodynamic variables, which may aid in determining the hemodynamic prole of a patient’s shock state. PACs are now less commonly used, as multiple studies have failed to demonstrate mortality benet for
most cases of shock [31–42]. Point-of-care cardiac ultrasound (POCUS) has now
been used in place of PACs in many cases; however, they remain useful, especially
in cases where echocardiography is limited or in patients with cardiogenic shock.
365
14.4 Classication
Although there are distinct classications and phenotypes of shock, it is clinically
important to recognize that shock is frequently multifactorial, and certain causes of
shock often have phenotypic components of more than one type of shock. Going
forward, we will categorize and describe the phenotypes of the several types of
shock as detailed in Table14.3. In the clinical scenarios, however, at the bedside, it
can be difcult to determine the exact cause or type of shock. By understanding this,
we can improve our ability to diagnose certain types of shock, as well as avoid the
pitfall of not considering more than one etiology of shock.
14.4.1 Distributive
Distributive shock is caused by pathologic peripheral vasodilation. Loss of systemic
vascular resistance (SVR) without adequate uid resuscitation causes a decrease in
left ventricular (LV) lling pressures and cardiac index due to decreased venous
blood volume. However, after uid resuscitation, these parameters may normalize,
and patients commonly have high cardiac output due to decreased systemic vascular
resistance. Despite cardiac output being high, there is ineffective tissue perfusion
due to excessive vasodilation and microcirculatory dysfunction. Clinically, these
patients often have warm, well-perfused extremities, decreased diastolic blood pressure, and increased pulse pressure. Other signs of shock commonly exist, including
tachycardia, tachypnea, and oliguria.
Sepsis is the most common cause of distributive shock and is one of the most
common causes of mortality in the intensive care unit [43]. Sepsis is caused by a
dysregulated host immune response to infection [44]. It is important to point out that
sepsis is not only caused by bacteria, as other forms of infection such as viruses and
fungi can also result in sepsis. This results in inammatory mediators including
cytokines, kinins, complement, coagulation factors, and eicosanoids that cause
vasodilation and multisystem organ dysfunction [45–51]. Sepsis may commonly
present with signs and symptoms of other forms of shock as well. Cardiogenic shock
366
Table 14.3 Classication of the several types of shock and their common causes
Distributive • Sepsis
Cardiogenic
Hypovolemic
Obstructive
• SIRS
• Neurogenic
• Anaph
• Drug or toxin induced
• Adrenal
• Myx
• Th
• Li
• Myopathic
– Myocardial
– Myocarditis
– Nonischemic
– Sepsis-induced
– Drug
– Myocardial
– Hypertrophic
• Arrh
– V
– Supra
– Atrial brillation and utter
– Heart
– T
• Mechanical
– V
– V
• Hemorrhagic
– Gastrointestinal
– T
– Retroperitoneal
• Nonhemorrhagic
– Se
– Deh
– Insensible losses perioperati
• Impaired diastolic lling due to mechanical obstruction
– V
– T
– Mechanical v
– Cardiac
– Constricti
– Restricti
• Impaired right v
– Pulmonary
– Pulmonary
ylactic
crisis
edema coma or decompensated hypothyroidism
yroid storm
ver failure
infarction
cardiomyopathy
cardiomyopathy
toxicity
contusion
obstructive cardiomyopathy
ythmic
entricular tachycardia
ventricular tachycardia
block
oxin-induced arrhythmias
alvular disease
entricular septal defect
bleeding
raumatic hemorrhage
hemorrhage
vere burns
ydration can be secondary to vomiting and diarrhea
vely or during surgery
ena cava obstruction (clot or tumor)
ension pneumothorax
entilation (breath stacking)
tamponade
ve pericarditis
ve cardiomyopathy
entricular systolic contraction
embolism
hypertension
L. R. Goss et al.
may co-occur due to sepsis-induced cardiomyopathy. Hypovolemic shock can occur
secondary to symptoms related to infection and increased insensible losses [52].
Sepsis may also lead to a hypercoagulable state, resulting in pulmonary embolism
and obstructive shock [53].
Systemic inammatory response syndrome (SIRS) can also result in distributive
shock and is characterized by a robust inammatory response to a major insult [54].
14 Sho ck
367
Causes include infection, pancreatitis, burns, major trauma, cardiac arrest, cardiopulmonary bypass, amniotic uid embolism, and fat embolism.
Neurogenic shock is caused by a traumatic brain injury or spinal cord injury that
results in the disruption of autonomic pathways, particularly of the sympathetic
system. This typically results in decreased vascular resistance and increased parasympathetic tone, resulting in vasodilatory shock. Notably, there is often a component of cardiogenic shock from the resultant bradycardia. Severe trauma, however,
often results in multiple injuries, and the diagnosis of neurogenic shock should only
be made after excluding major hemorrhage.
Anaphylaxis is another common form of distributive shock. Anaphylaxis is
caused by an IgE-mediated response to an allergen resulting in mast cell degranulation. In addition to systemic vasodilation, anaphylaxis will commonly cause rash
(urticaria), bronchospasm, gastrointestinal symptoms, and mucosal swelling. Unlike
many other causes of distributive shock, anaphylaxis is often rapidly reversible.
Adrenal crisis and decompensated hypothyroidism (myxedema coma) are two
forms of shock caused by dysfunction of the endocrine system. Adrenal crisis may
be due to primary adrenal insufciency (Addisonian crisis) or secondary adrenal
insufciency.
14.4.2 Cardiogenic
Cardiogenic shock can be classied into three categories, which include cardiomyopathic, arrhythmic, and mechanical. Cardiogenic shock is primarily due to intrinsic
cardiac pump failure, which may be due to many causes. Patients in cardiogenic
shock may present in several ways. Classic cardiogenic shock can present with pulmonary edema, elevated JVP, and cold extremities. Patients, however, may also
present without pulmonary edema, especially in the setting of right ventricular failure. Patients may also present with warm extremities in end-stage decompensated
heart failure. Edema is another common nding in cardiogenic shock; however, it
may not be present, especially in isolated acute left ventricular failure. Bedside
ultrasound is a particularly useful tool available to clinicians to identify cardiac dysfunction at the bedside [55, 56]. Pulmonary ultrasound is useful in evaluating for
pulmonary edema, which may be represented by B lines on lung ultrasound, as seen
in Fig.14.1 [58]. As discussed above, mixed venous or central venous oxygen saturation is classically low. Lactic acid may or may not be elevated, but an elevation in
lactic acid is linked with mortality [14]. More invasive hemodynamic measurements
obtained using devices like the PA catheter may show elevated pulmonary capillary
wedge pressure, elevated central venous pressure, low cardiac output, and low cardiac index.
Cardiogenic shock can be classied into three categories, which include cardiomyopathic, arrhythmic, and mechanical.
Cardiomyopathic causes include acute ischemia, chronic ischemia, dilated cardiomyopathy, post-cardiac arrest myocardial stunning, myocarditis, takotsubo cardiomyopathy, sepsis-induced cardiomyopathy, and post-cardiopulmonary bypass.
368
Fig. 14.1 Characteristics
of B lines on lung
ultrasound. Vertical
echogenic wedge-shaped
lines beginning at the
pleura (bright line) and
extending down the
screen [57]
L. R. Goss et al.
Both tachyarrhythmias and bradyarrhythmias may cause cardiogenic shock and
may be of atrial or ventricular origin. Arrhythmias may be the primary etiology of
shock or contribute to another shock state, such as atrial brillation with rapid ventricular response in a patient with septic shock.
Mechanical causes of cardiogenic shock include acute or acute on chronic valvular pathology, most commonly mitral or aortic. These may be stenotic or regurgitative lesions. Causes include chronic degeneration, masses, endocarditis, papillary
muscle rupture, chordae tendineae rupture, retrograde aortic dissection into the aortic valve ring, and more. Another mechanical cause is cardiac masses such as atrial
myxomas. Cardiac masses may impair outow, cause valve incompetence, cause
impaired contractility, or cause impaired cardiac compliance.
14.4.3 Hypovolemic
Hypovolemic shock is due to intravascular volume depletion. This results in
decreased preload, decreased stroke volume, and decreased cardiac output. As a
result, systemic vascular resistance is high. Lactic acid is often elevated. Mixed
venous oxygen saturation is low, as discussed above. Clinically, patients exhibit
tachycardia, narrow pulse pressure, weak pulses, low JVP, and cool skin.
14 Sho ck
369
Hypovolemic shock can broadly be categorized as hemorrhagic and nonhemorrhagic. The most common causes of hemorrhagic shock are gastrointestinal bleeding, trauma, and bleeding related to surgery. Nonhemorrhagic hypovolemic shock
has many etiologies, which include major burns, vomiting, diarrhea, and insensible
losses during surgery.
14.4.4 Obstructive
Obstructive shock is due to extracardiac causes that impair ow into or out of the
heart. Often, these pathologies are associated with either right ventricular (RV) failure or impaired right ventricular and right atrial lling. Mixed venous oxygen saturation will typically be low. Hemodynamically, this typically manifests with narrow
pulse pressure, elevated CVP, and elevated SVR. Cardiac output and cardiac index
will be low. Lactic acid, as in other causes of shock, is often elevated. Physical exam
ndings are variable and based on the etiology of obstructive shock, which will be
discussed below. Obstructive shock can best be broken down into two categories,
which include pulmonary vascular obstruction and mechanical obstruction.
Pulmonary vascular causes of obstructive shock primarily include pulmonary
embolism and pulmonary hypertension. Pulmonary embolism from venous thromboembolism causes acute right heart failure via several mechanisms. There is an
acute increase in pulmonary vascular resistance from thrombus obstructing pulmonary arterial blood ow. In addition to this, there is the release of vasoactive mediators, which results in pulmonary vascular vasoconstriction. The RV subsequently
cannot pump blood forward effectively. This results in decreased left ventricular
preload and cardiac output. In addition to this, the RV will become dilated, which
has several adverse effects. Signicant right ventricular dilation will result in compression of the LV, further decreasing LV preload and cardiac output. In addition to
this, RV dilation increases RV systolic and end-diastolic pressure, which decreases
coronary perfusion in the RV and results in worsening RV dysfunction. The resultant decrease in LV preload and cardiac output contributes to hypotension, which
further decreases RV coronary perfusion. This can result in rapid hemodynamic
collapse. RV dysfunction may also be further exacerbated by hypoxemia, acidosis,
and positive-pressure ventilation, as these all result in increased pulmonary vascular
resistance [59]. Pulmonary hypertension is a less common cause of pulmonary vascular obstructive shock. Pulmonary hypertension may be due to primary pulmonary
hypertension or a wide variety of other causes. The physiology of shock secondary
to decompensated pulmonary hypertension is similar to that of pulmonary embolism [60]. Lastly, volume overload, sickle cell acute chest syndrome, and hypoxemic respiratory failure can also result in acute right ventricular failure and
obstructive shock.
Mechanical causes of obstructive shock are somewhat broad, but most commonly include pericardial tamponade and tension pneumothorax. Pericardial tamponade can be acute (i.e., traumatic cardiac injury, aortic dissection, LV free wall
370
L. R. Goss et al.
rupture) or chronic (i.e., malignant effusion, uremia, infectious, inammatory).
Cardiac tamponade causes shock by compressing the cardiac chambers, which
impairs their ability to ll as well as provide cardiac output. The rate at which tamponade causes hemodynamic collapse is related to the rate at which uid accumulates. For example, in the case of LV free wall rupture, aortic dissection, and
traumatic cardiac injuries, blood may accumulate rapidly, and the pericardium does
not have time to stretch and accommodate pericardial uid. This results in rapid
compression of the cardiac chambers and hemodynamic collapse. Chronic effusions, however, build slowly over time, allowing the pericardium to stretch and
accommodate more uid. There is a point, however, where the pericardium cannot
accommodate more uid, and tamponade physiology ensues [61]. Pericardial tamponade is primarily a clinical diagnosis, though physical exam and diagnostic testing are essential for aiding in making the diagnosis. On exam, patients will typically
have tachycardia, hypotension, and jugular venous pressure (JVP) elevation.
Echocardiography is essential in diagnosing tamponade. Echocardiography helps
determine the presence, location, and characteristics of an effusion; however, it also
aids in assessing the hemodynamic signicance of an effusion. Supportive ndings
on echocardiography include a dilated inferior vena cava, diastolic collapse of the
right atrium or right ventricle, left-sided chamber collapse, and respiratory variations in volumes or ows [62]. Ultimately, the diagnosis of tamponade can only be
conrmed through hemodynamic improvement after pericardial drainage.
Tension pneumothorax is another common mechanical cause of obstructive
shock. When a large amount of air accumulates between the lung and chest wall,
this may cause compression of the inferior vena cava (IVC), superior vena cava
(SVC), and cardiac chambers. This will result in impaired cardiac lling. This may
be exacerbated by positive-pressure ventilation, as pneumothorax on positive pressure is more likely to increase in size [63]. Large intrathoracic tumors may cause
compression of the great veins, resulting in decreased cardiac lling (Fig. 14.2,
Table14.4).
Fig. 14.2 Echocardiography
demonstrating a large
pericardial effusion in a
patient in tamponade [64].
LV left ventricle, RV right
ventricle, Ao aorta, LA left
atrium
14
Shock
Table 14.4 Chart comparing clinical ndings and hemodynamic variables among the several
types of shock
Distributive Cardiogenic Hypovolemic Obstructive
Extremities
Warm/cold
IVC size/
JVP
Pulse
pressure
Cardiac
output
ScVO
SVR Low High High High
PCWP Normal/low High Low Normal/low
Other Fever POCUS with LV, RV, or
Warm Cold Cold Cold
Normal/
normal
Wide/normal Narrow Narrow Low
High Low Low Low
Normal/high Low Low Low
2
Enlarged/elevated Small/decreased Enlarged/
Positive FAST
biventricular dysfunction
Peripheral edema
exam
Obvious
hemorrhage
Trauma
elevated
RV dilation on
POCUS
Pericardial
effusion
Absent lung
sliding
Pulsus
paradoxus
371
14.5 Management
Any patient presenting with shock needs a detailed history and physical to evaluate
the etiology of shock while simultaneously initiating resuscitation to improve survival. The steps in management are outlined in Flowchart 14.2. Early stabilization
should include management of airway, breathing, and circulation in a critically ill
patient. Adequate oxygenation should be maintained, and oxygen may be administered if oxygen saturation (sO
) is less than 92%. If unable to treat hypoxia, patients
2
may need endotracheal intubation and invasive mechanical ventilation.
Two peripheral wide-bore IV access should be established and uid resuscitation
initiated immediately. In many cases, central venous catheters may be necessary for
infusing vasopressors and inotropes and also obtaining ScV02 values. Crystalloids
are preferred as the uid of choice. Fluid boluses can be given with close monitoring for uid overload with the use of POCUS or invasive monitoring. Early blood
transfusion should be considered in cases of acute blood loss or if severe anemia is
affecting oxygen delivery. The target of resuscitation is to maintain a mean arterial
pressure (MAP) above or equal to 65mmHg.
Studies have shown that longer duration of MAP less than 65mmHg is an independent predictor of mortality in septic shock [65]. Research favors early administration of vasopressors, and it is recommended in septic shock, for improving
perfusion, improving organ blood ow distribution, and decreasing the need for IV
uid and thus avoiding uid overload [66]. Norepinephrine is the vasopressor of
choice and may be started via a peripheral line in an emergency. Initiation of
372
of shock
Treat cause
shock
Obstructive
shock
Cardiogenic
shock
Distributive
shock
Hypovolumic
Drain
effusion
pericardial
ion and
mechanical
revascularizat
Early coronary
control of
Antibiotics
infection in
and source
loss
Control
bleeding/fluid
support.
circulatory
sepsis
embolism
Pulmonary
for massive
Thrombolytics
L. R. Goss et al.
Management of Shock
Airway
Breathing
Circulation
Ensure ABC -
Monitor
circulation
adequacy of
mm Hg
Circulation
MAP goal>= 65
Ensure
adequate
Oxygenation
goal
Urine output
>0.5ml/kg/hr
venous
catheter
2 wide bore IV
access/Central
needed
Invasive
mechanical
ventilation if
FiO2
adequate
Administer
Monitor lactic
acid clearance
Crystalloids
Administer IV
Target
Transfuse
Packed red
cells if acute
70%
Scvo2 >
blood
loss/severe
Capillary refill time
anemia
Vasopressor
less than 5 sec
milrinone if
Dobutamine or
Epinephrine if
and Inotropes
Norepinephrine
contractility
poor cardiac
suspected
anaphylaxis
choice
st
1
Flowchart 14.2 Management of shock
14 Sho ck
373
vasopressors should not be delayed till central venous access is established. Consider
the use of inotropes (dobutamine or milrinone) if there is evidence of poor cardiac
contractility/cardiogenic shock. Epinephrine is used as a drug of choice in anaphylactic shock.
Adequacy of resuscitation should be frequently assessed by the use of surrogate
markers like urine output with a goal of at least 0.5mL/kg/h or capillary rell time
less than 5 s. Restoration of adequacy of tissue perfusion is assessed by lactate
clearance and maintaining of ScVO2 above 70%.
Concomitant treatment of the underlying etiology of shock is of paramount
importance. In patients with hypovolemic shock, early efforts should be directed
towards controlling the source of bleeding and uid loss. If distributive shock is
suspected to be secondary to sepsis, collect cultures, administer broad-spectrum
antibiotics, and control the source of infection to correct septic shock. Coronary
revascularization and mechanical circulatory support like extracorporeal membrane
oxygenation (ECMO) or ventricular assist devices (VADs) should be considered
when treating cardiogenic shock secondary to myocardial ischemia. When obstructive shock is diagnosed, pericardiocentesis should be done if evidence of cardiac
tamponade and thrombolysis/pulmonary thrombectomy should be attempted if
shock is secondary to massive pulmonary embolism. Chest tubes may be necessary
to reverse pneumothorax.
14.6 Conclusion
Shock is a manifestation of poor organ perfusion and thus an imbalance of oxygen
demand and supply to the tissues. Low blood pressure is not equivalent to shock.
Prompt recognition and treatment have been shown to improve survival. Treatment
includes rapid resuscitation to achieve hemodynamic stability and restore organ perfusion, along with treatment of the underlying cause of shock. If untreated, shock
can lead to multiorgan failure and death.
Disclosure Authors report no conict of interest.
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