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203.e2 PART IV Noncoronary Diseases: Diagnosis and Management
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differences in complication rate and diagnostic performance.
Circulation. 2010;122:900–909.
38. Rogers TR, Karmarkar K, Campbell-Washburn P, et al. Magnetic
Resonance Imaging Guidance Improves the Diagnostic Yield of
Endomyocardial Biopsy. JACC Basic Transl Sci. 2016;1.
39. Friedrich MG, Sechtem U, Schulz-Menger J, et al. Cardiovascular
magnetic resonance in myocarditis: A JACC White Paper. J Am
Coll Cardiol. 2009;53:1475–1487.
40. Monney PA, Sekhri N, Burchell T, et al. Acute myocarditis
presenting as acute coronary syndrome: role of early cardiac
magnetic resonance in its diagnosis. Heart. 2011;97:1312–1318.
41. Lurz P, Luecke C, Eitel I, et al. Comprehensive Cardiac Magnetic
Resonance Imaging in Patients With Suspected Myocarditis: The
MyoRacer-Trial. J Am Coll Cardiol. 2016;67:1800–1811.
41a. Grani C, et al. Prognostic value of cardiac magnetic resonance
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42. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA
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43. Sharma JR, Sathanandam S, Rao SP, Acharya S, Flood V.
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45. Frustaci A, Chimenti C, Calabrese F, et al. Immunosuppressive
therapy for active lymphocytic myocarditis: virological and
immunologic profile of responders versus nonresponders.
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46. Cooper LT Jr, Hare JM, Tazelaar HD, et al. Usefulness of
immunosuppression for giant cell myocarditis. Am J Cardiol.
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20
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Stress (Takotsubo) Cardiomyopathy
Abhiram Prasad
OUTLINE
Epidemiology, 204
Pathophysiology, 204
Diagnosis, 205
Electrocardiogram, 205
Cardiac Biomarkers, 206
Left Ventricular Imaging and Coronary Angiography, 206
Management, 207
Stress cardiomyopathy (SCM) is a generally reversible acute
cardiac syndrome that was originally described in the Japanese
population over 30 years ago.1 Hence, the Japanese term takotsubo
(an octopus trap with a narrow neck and round bottom, Fig.
20.1) cardiomyopathy/syndrome has gained favor, as it describes
the appearance of the left ventricle during systole. SCM is also
known as apical ballooning syndrome (ABS), broken heart
syndrome, and ampulla cardiomyopathy.
mimic an acute myocardial infarction (MI); therefore, patients
with this syndrome frequently present to the cardiac intensive
care unit (CICU). SCM should be considered in the differential
diagnosis of patients presenting with an acute coronary syndrome.4
The typical patient is a postmenopausal woman presenting with
symptoms of myocardial ischemia that is temporally related to
a physical or emotional stressful event, with positive cardiac
biomarkers and/or an electrocardiogram (ECG) that has evidence
of ischemia or injury.
2,3
The clinical features
EPIDEMIOLOGY
SCM is the final diagnosis in approximately 1% to 2% of all
patients initially suspected of either an acute coronary syndrome
5,6
or MI.
ST elevation myocardial infarction.7 The incidence of SCM among
patients in intensive care units has been estimated at 1.5% and
8% among those with cardiogenic shock.8 However, an accurate
incidence is difficult to ascertain because of underdiagnosis. Over
time, there has been increasing recognition of this entity, as
highlighted by data from the Nationwide Inpatient Sample in
which the mean number of patients with a discharge diagnosis
of SCM from a group of community hospitals increased from
315 per year in 2006 to 6,230 per year in 2012.9 Approximately
90% of all reported cases are in postmenopausal women10 and
5% of the patients are younger than 50 years.
The proportion may be as high as 12% in women with
11
PATHOPHYSIOLOGY
The pathophysiology of SCM remains to be established; however,
several observations suggest that the sympathetic nervous system
plays an important role.12 These include the temporal relationship
with preceding emotional or physical stressful triggers, hyperadrenergic states, such as pheochromocytoma and subarachnoid
hemorrhage causing a transient cardiomyopathy that is similar
to SCM, documentation of high levels of circulating catecholamines,13 SCM being precipitated by inadvertent administration
of supratherapeutic doses of catecholamines,14 animal models
of stress immobilization and exogenous catecholamine administration inducing left ventricular apical hypokinesis,15 and the presence
of contraction band necrosis on endomyocardial biopsies,16 a
feature of catecholamine toxicity. However, elevation in circulating
catecholamines and contraction band necrosis are not always
present.
Early reports of cases with SCM were associated with multivessel epicardial coronary spasm, which was initially proposed as
a potential mechanism for the myocardial stunning. However,
this has not been supported in large case series and is unlikely
to be the underlying cause of SCM in the vast majority of patients.
Aborted MI due to left anterior descending artery plaque rupture
and thrombosis with spontaneous thrombolysis has also been
proposed but seems unlikely to be the underlying mechanism.
Conversely, microvascular dysfunction can be detected in at least
two-thirds of the patients at the time of presentation and its
severity correlates with the magnitude of troponin elevation and
ECG abnormalities.18 The microvascular dysfunction may be a
primary mechanistic feature or an epiphenomenon. Abnormal
glucose and fatty acid metabolism is frequently present, colocalizing with the wall motion abnormality.
A preceding stressful trigger is present in over two-thirds of
patients. The list of potential emotional triggers is extensive, but
19,20
17
204
CHAPTER 20 Stress (Takotsubo) Cardiomyopathy 204.e1
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Keywords
stress cardiomyopathy
apical ballooning syndrome
takotsubo cardiomyopathy
CHAPTER 20 Stress (Takotsubo) Cardiomyopathy 205
AB
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A
Fig. 20.1 (A) Ventriculogram. (B) An octopus pot (“tako-tsubo”). (Courtesy #FOAMed Medical
Education Resources, LITFL.)
most often relates to experiences of significant grief or personal
loss, fear or anxiety, anger and frustration, and interpersonal
conflicts. Common physical triggers include acute medical conditions (e.g., severe exacerbation of obstructive airways disease,
sepsis), neurologic conditions (e.g., subarachnoid hemorrhage,
seizures), falls and other trauma, noncardiac surgery (e.g.,
orthopedic, major abdominal), malignancy, and experiencing
severe pain.21 The absence of such triggers does not exclude the
diagnosis.
Patients who are conscious typically have symptoms that are
similar to that associated with MI,
10,22,23
the most common being
angina-like chest pain, present in approximately 50% of cases.
Other presenting symptoms include dyspnea and, less frequently,
syncope or out-of-hospital cardiac arrest. Among patients presenting primarily with SCM, it is those with ST segment elevation
and severe left ventricular dysfunction who most often are
admitted to the CICU. Typically, the ejection fraction is reduced
to 30% to 40%,10 which may be accompanied by significant
diastolic dysfunction with elevation in left ventricular filling
pressure.24 Myocardial relaxation is impaired due to the ischemia
related to microvascular dysfunction and myocardial edema.
Acute heart failure is a frequent complication, but major hemodynamic decompensation is uncommon, with cardiogenic shock
developing in approximately 10% to 15% of patients.10 These
patients should be particularly assessed for the presence of
transient left ventricular outflow obstruction and clinically
significant mitral regurgitation, which can be exacerbating
factors,25 each being present in approximately 10% to 20% of
cases. The mechanisms for regurgitation appear to be papillary
muscle displacement leading to tethering and impaired coaptation
of the leaflets, and/or systolic anterior motion.
25,26
Outflow tract
obstruction likely occurs owing to a combination of factors,
including hyperdynamic basal function, systolic anterior motion
of the mitral valve, and a sigmoid-shaped ventricle.
Additional complications that may lead to admission to the
CICU include arrhythmias. Atrial fibrillation occurs in approximately 5% of cases,27 whereas ventricular tachycardia, torsade
de pointes, and ventricular fibrillation have been reported in
3% to 4% of patients and asystole in 0.5%.28 Other rare
complications of SCM include left ventricular thrombus, thromboembolism, and cardiac rupture.
29
Patients who develop SCM secondary to a noncardiac illness
or other physical trigger may not have the typical symptoms
described earlier but instead present with ischemic changes on
the ECG, elevated cardiac biomarkers of myonecrosis, pulmonary
edema, and hypotension. Hypotension may due to the reduction
in stroke volume and, in some cases, dynamic left ventricular
outflow tract obstruction.
30
The ventricular dysfunction resolves over days to weeks, with
complete recovery of global systolic function by 4 to 8 weeks. The
prognosis of SCM is good in the absence of significant underlying
comorbid conditions. In-hospital mortality is approximately 3% to
5%. Among those who are discharged, long-term survival appears
to be similar to that of the general age-matched population. The
subgroup of patients in whom there is a physical trigger—such
as major surgery, malignancy, and fractures—appear to have a
worse prognosis, likely related to the underlying condition. The
recurrence rate of SCM is approximately 1% to 2% per year.
31
DIAGNOSIS
There are no diagnostic ECG or biomarker findings that can
differentiate SCM from an acute coronary syndrome or myocarditis; hence, it is a diagnosis of exclusion. The characteristic
features of the syndrome have been incorporated into several
proposed diagnostic criteria.
Clinic criteria that can be applied at the time of presentation.
All four criteria must be present.
Electrocardiogram
Between 30% to 50% of patients have ST segment elevation at
presentation. The precordial leads are most commonly involved,
but ST segment elevation may also occur in the limb leads. The
electrocardiographic findings do not reliably distinguish SCM
from an acute MI.35 Pathologic Q waves may be present transiently.
Some patients present with deep T-wave inversion, nonspecific
T wave abnormality, and the ECG may be normal in some cases.
ST segment depression is infrequently present. Characteristic
32,33
Box 20.1 provides the Mayo
34
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evolutionary changes during hospitalization include resolution
of ST segment elevation and diffuse and often deep T-wave
inversion associated with prolongation of the corrected QT
interval (Fig. 20.2). The electrocardiographic abnormalities usually
resolve gradually over weeks to months but may persist even
after systolic function has recovered.
BOX 20.1 Proposed Mayo Clinic Criteria
for Apical Ballooning Syndrome
1. Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid-
segments with or without apical involvement. The regional wall motion
abnormalities extend beyond a single epicardial vascular distribution. A
stressful trigger is often present, but not always.
2. Absence of obstructive coronary disease or angiographic evidence of acute
plaque rupture.
3. New electrocardiographic abnormalities (either ST segment elevation and/
or T-wave inversion) or modest elevation in cardiac troponin.
4.
Absence of pheochromocytoma, myocarditis.
From Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome
(tako-tsubo or stress cardiomyopathy): a mimic of acute myocardial
infarction. Am Heart J. 2008;155:408–417.
a
There are rare exceptions to these criteria, such as those patients in
whom the regional wall motion abnormality is limited to a single
coronary territory.
b
It is possible that a patient with obstructive coronary atherosclerosis
may also develop apical ballooning syndrome (ABS). However, this is
very rare in our experience and in the published literature, perhaps
because such cases are misdiagnosed as an acute coronary
syndrome.
In both of the above circumstances, the diagnosis of ABS should be
made with caution and a clear stressful precipitating trigger must be
sought.
b
a
Cardiac Biomarkers
Cardiac troponin levels, using contemporary assays, are invariably
elevated on admission and generally peak within 24 to 48 hours.
Creatine kinase MB fraction is elevated in the great majority of
cases. The levels are lower compared to patients with ST segment
elevation MI, but similar to that of patients with non ST elevation
MI and relatively low for the extent of acute left ventricular
systolic dysfunction. Blood level of brain natriuretic peptide
(BNP) or N-terminal pro-BNP, markers of ventricular dysfunction,
are elevated in the majority of patients and may correlate with
left ventricular end-diastolic pressure.
Left Ventricular Imaging and Coronary Angiography
Transthoracic echocardiography can be readily performed in the
intensive care setting and hence is the preferred mode of imaging
to detect systolic dysfunction and potential complications that
accompany SCM. In the classical form of the cardiomyopathy,
basal left ventricular function is preserved and may even be
hyperdynamic, but there is hypokinesis or akinesis of the midand apical segments leading to the “ballooning” appearance
(Fig. 20.3, Video 20.1). The wall motion abnormality virtually
always extends beyond the distribution of a single coronary
artery. In a significant proportion of patients, apical contraction
is preserved and the wall motion abnormality is restricted to
the mid-segments (apical-sparing variant; Video 20.2).40 The
least common variant is known as inverted or reverse takotsubo
in which there is hypokinesis of the basal segment of the left
ventricle with preserved apical function. The variant forms of
SCM have similar clinical characteristics and prognosis as the
typical form. The right ventricle also develops a similar pattern
36–39
I aVR
II
III
II
VI
V5
Fig. 20.2 Twelve-lead electrocardiogram with T-wave inversion in the precordial and limb leads
associated with prolongation of the QT interval.
aVL
aVF
VI
V2
V3
V4
V5
V6
CHAPTER 20 Stress (Takotsubo) Cardiomyopathy 207
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Diastole
Fig. 20.3 Left ventriculogram in diastole and systole of a patient with stress cardiomyopathy
with hyperdynamic basal contraction and akinesis of the mid- and apical segments.
of regional wall motion abnormality in approximately one-third
of cases.41 Biventricular dysfunction SCM is associated with a
worse hemodynamic profile and the patients are often sicker
and more likely to develop acute heart failure.
Cardiac magnetic resonance may be a useful imaging modality
for documenting the extent of regional wall motion abnormality
and differentiating SCM (virtually always characterized by the
absence of delayed gadolinium hyperenhancement) from myocarditis and MI in which delayed hyperenhancement is present.
42
Patients with SCM either have angiographically normal
coronary arteries or mild atherosclerosis. Obstructive coronary
artery disease is infrequent despite most patients being in their
seventh and eighth decade of life.43 When present, the extent
and distribution of obstructive plaque is generally insufficient
to account for the widespread regional wall motion abnormality.
Coronary angiography, either invasive or noninvasive, should
be performed in patients suspected of SCM in order to exclude
an acute coronary syndrome. In contemporary treatment
pathways, the presence of ST segment elevation typically leads
to emergency angiography to exclude coronary thrombotic
occlusion that requires revascularization prior to admission to
the CICU.
MANAGEMENT
The recommendations for SCM management are based on expert
opinion as clinical trials have not been conducted owing, in part,
to the low incidence and the fact that supportive therapy leads
to spontaneous recovery in the great majority of patients. The
initial therapy is frequently directed toward treating myocardial
ischemia with aspirin, anticoagulants, statins, and β-blockers
since an acute coronary syndrome is the presumed diagnosis in
the majority of cases. Aspirin, anticoagulants, and statins can
be discontinued once the diagnosis of SCM has been made unless
there is coexisting coronary atherosclerosis. In the absence of
contraindications, a β-blocker or a combined α- and β-blocker
may be initiated because excess catecholamines have been
implicated in the pathogenesis. Long-term therapy should be
Systole
considered with the aim of reducing recurrence even though
observational data has not supported this recommendation.10
Initiation of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker therapy for acute ventricular dysfunction
is recommended, especially as the diagnosis may not be certain
at the time of discharge. Inhibitors of the renin angiotensin
system may be discontinued once there is complete recovery of
systolic function, though there are observational data that suggest
that they may have long-term benefits.
10
Mild to moderate acute heart failure responds to diuretic
therapy. Severe cases with pulmonary edema may require intubation and mechanical ventilation. If present, left ventricular outflow
tract obstruction may be treated with phenylephrine with the
goal of increasing afterload and left ventricular cavity size.
Phenylephrine use requires close monitoring due to the presence
of systolic dysfunction. In the absence of heart failure, β-blockers
and/or intravenous fluids may be effective.
Inotropes are often used with good effect in cardiogenic shock,
although there are theoretical reasons for avoiding them because
of the potential role of catecholamine toxicity in precipitating
the syndrome. Intraaortic balloon pump counterpulsation or
other mechanical support devices may be preferable. The former
has the potential to exacerbate outflow tract obstruction and
should therefore be used cautiously.
The acute treatment of atrial and ventricular arrhythmias is
similar to other clinical situations. Although torsade de pointes
is rare, patients should be on continuous ECG monitoring until
the QTc is less than or equal to 500 msec. If pause-dependent
torsade occurs, β-blocker therapy should be withheld and
temporary pacing considered. Implantable cardioverterdefibrillator therapy is not routinely indicated for ventricular
tachycardia or fibrillation as the cardiomyopathy is reversible.
In cases of recurrent aborted sudden cardiac death or lifethreatening ventricular arrhythmia, the role of implantable
cardioverter-defibrillator therapy is unclear.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 20 Stress (Takotsubo) Cardiomyopathy 207.e1
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39. Nguyen TH, Neil CJ, Sverdlov AL, et al. N-terminal pro-brain
natriuretic protein levels in takotsubo cardiomyopathy. Am J
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40. Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular
ballooning syndrome: a new variant. J Am Coll Cardiol.
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41. Elesber A, Prasad A, Bybee KA, et al. Transient Cardiac Apical
Ballooning Syndrome: Prevalence and Clinical Implications of
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42. Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible
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43. Hoyt J, Lerman A, Lennon RJ, Rihal CS, Prasad A. Left anterior
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cardiomyopathy). Int J Cardiol. 2010;145:112–115.
21
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Distributive Shock
Joyce Ji, David L. Brown
OUTLINE
Epidemiology, 208
Definition, 208
Etiology, 208
Incidence, 208
Pathogenesis, 209
Pathophysiology, 209
Clinical Presentation, 209
History and Physical Examination, 209
Laboratory Testing, 211
Invasive Hemodynamic Monitoring, 211
Assessment of Microcirculation, 212
Management, 212
Fluid Resuscitation, 212
Pharmacologic Support, 212
Targeted Therapies, 213
Septic Shock, 213
Anaphylactic Shock, 214
Neurogenic Shock, 214
Modulation of Microcirculation, 214
Prognosis, 215
Conclusion, 215
The range of care covered by cardiac intensive care units (CICUs)
has expanded drastically since they were originally developed
as coronary care units (CCUs) for the management of acute
myocardial infarction (MI) in the early 1960s.1 In addition to the
rising complexity of cardiovascular diseases seen in the CICUs,
other critical conditions such as respiratory failure, renal failure,
and sepsis have become increasingly more prevalent as well.2
The overlap in populations between the CICU and other ICUs
continues to grow (Fig. 21.1). Given the expansive breadth of
diseases now seen in contemporary CICUs, it is important to
broaden the knowledge base and training for cardiac intensivists. This chapter explores the epidemiology, pathogenesis,
clinical presentation, and current management of distributive
shock.
EPIDEMIOLOGY
Definition
Shock can be classified into four states: hypovolemic, cardiogenic,
obstructive, and distributive. Of the four, distributive shock is
the most common condition encountered in the critical care
setting. Distributive, or vasodilatory, shock is characterized by
the shunting of oxygen transport to the tissues, resulting in
abnormal distribution of tissue perfusion and impaired regional
oxygen extraction. In contrast to the other categories of shock,
this classically occurs in the presence of normal or increased
cardiac output.
The diagnosis of distributive shock should include the
following:
1. Systolic blood pressure less than 90 mm Hg or mean arterial
pressure (MAP) less than 65 mm Hg for at least 30 minutes.
2. Normal or high cardiac index (≥2.0 L/min per m2). It is
important to note that although distributive shock is typically
characterized by high cardiac output, it is a state that may
result in transient myocardial depression or may occur in a
patient with underlying left ventricular dysfunction.
3. Tissue hypoperfusion manifested by oliguria (<0.5 mL/kg per
hour), altered mental status, elevated lactate (>2 mmol/L).
Etiology
Distributive shock can be further categorized into its different
causes. Septic shock is the classic form of distributive shock, as
it is the most prevalent type of shock encountered in the ICU.
Septic shock occurs as a result of an infection that induces circulatory dysfunction in the host. Neurogenic shock is a form of
distributive shock that occurs in patients with severe traumatic
brain injury and spinal cord injury that result in autonomic
dysfunction. Anaphylactic shock results from a serious immunoglobulin E (IgE)-mediated reaction to an allergen. Distributive
shock may also occur as a component of the systemic inflammatory state encountered in patients with a large acute MI.
Other less common causes of distributive shock include postcardiac arrest, pancreatitis, drug or toxin reactions, burns, air
or fat embolism, adrenal crisis, and thyrotoxicosis.
3,4
Incidence
Of the different types of shock, septic shock is most commonly
encountered in the ICU. In an analysis of 1600 patients who
208
CHAPTER 21 Distributive Shock 209
NOVEL THERAPIES
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to the microcirculatory derangements (Fig. 21.2). Endothelial
Structural Heart Interventions
Durable LVAD
Temporary
MCS
MOST COMMON DIAGNOSES
Sepsis
GI bleeding
Neurologic injury
PATIENT CHARACTERISTICS AND RESOURCES
Blood transfusions
Fig. 21.1 Overlap between contemporary medicine intensive
care units (MICU) and cardiac intensive care units (CICU). GI,
Gastrointestinal; LVAD, left ventricular assist device; MCS,
mechanical circulatory support. (From Katz JN, Minder M,
Olenchock B, et al. The genesis, maturation, and future of critical
care cardiology. J Am Coll Cardiol. 2016;68:69.)
Ischemic heart disease
Respiratory failure
Renal failure
Heart failure
Age, sex
Disease severity
Mechanical ventilation
Dialysis
Vasoactive meds
MICU CICU
Arrhythmia
Shock
Valvular disease
Anti-arrhythmic meds
Swan-Ganz catheters
Transvenous pacing
presented with shock, septic shock occurred in 62%, cardiogenic
shock in 16%, hypovolemic shock in 16%, other types of distributive shock in 4%, and obstructive shock in 2%.5 Rates of sepsis
and septic shock have continued to increase over the years, likely
due to the advancing age of the population, multidrug-resistant
organisms, and the increased use of immunosuppressive agents.
An emphasis on the earlier detection of sepsis may contribute
to this increase as well. While four discrete classifications of
shock are described, it is important to recognize that a substantial
number of patients may present with “mixed” or multifactorial
states of shock. The overlapping features of these presentations
make it challenging to determine the definitive diagnosis and
subsequent management.
PATHOGENESIS
Pathophysiology
Circulatory shock is characterized by a severe deficiency in oxygen
delivery and failure of tissue perfusion. Depending on the etiology
of the shock state, this can occur through a variety of mechanisms.
The end result is the critical impairment of oxidative metabolism,
ultimately leading to organ failure and death. It is important to
identify the etiology of the shock and its underlying pathophysiology in order to manage it rapidly and effectively.
The microcirculation may be considered its own organ system,
consisting of a complex network of vessels involved in the delivery
of oxygen to cells. A variety of factors influence the microcirculatory system. In distributive shock, abnormalities in the microcirculation lead to significant peripheral vasodilatation and
impairment of autoregulatory mechanisms required to maintain
adequate tissue perfusion.
9–12
Multiple mechanisms contribute
cells become more leaky and less responsive to vasoactive agents.
Inflammatory activation leads to upregulation of the nitric oxygen
(NO) system, resulting in shunting of blood flow within the
microcirculation. An imbalance of vasoactive substances also
contributes to alterations in blood flow and, thus, a regional
mismatch in oxygen supply and demand. Additionally, both the
activation of the coagulation cascade and the reduced deformability of erythrocytes and leukocytes lead to microvascular
plugging, further compromising capillary flow. Blood flow is
shunted away from the vital organs, resulting in tissue hypoxia.
The uneven distribution of microcirculatory blood flow can
result in impaired oxygen delivery even when patients are
normotensive.
The prototype of distributive shock is septic shock. In septic
shock, the interaction between the microorganism and the host
immune system creates an exaggerated inflammatory response.
The systemic overexpression of inflammatory mediators, such
as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β),
lead to microcirculatory dysfunction and ineffective distribution
of blood flow away from vital organs.13 Aside from deficient
oxygen delivery, mitochondrial dysfunction within the cells—that
is, cytopathic hypoxia—contributes to inadequate oxygen utilization as well.14 In addition, inflammatory cytokines activate the
coagulation cascade, inducing a procoagulable state that may
subsequently lead to disseminated intravascular coagulation
(DIC). While septic shock typically manifests as a hyperdynamic
state with high cardiac output, the cytokines and endotoxins
activated in sepsis cause myocardial depression.
15,16
induced cardiomyopathy is characterized by ventricular dilatation,
reduction in contractility, and depressed ejection fraction. The
6–8
cardiomyopathy is typically reversible and resolves within 7 to
10 days.
16
Anaphylactic shock is mediated by a systemic IgE-mediated
allergic reaction.13 This occurs when the patient is sensitized to
a particular antigen, resulting in the production of IgE specific
to that antigen. Upon reexposure to the allergen, IgE on mast
cells and basophils recognizes the antigen and activates a cascade
of inflammatory mediators. These mediators cause endothelial
injury, cellular edema, and smooth muscle contraction. This is
manifested by excessive peripheral vasodilatation and capillary
leakage. Properties of other types of shock may contribute as well,
such as cardiogenic shock from decreased myocardial contractility
and obstructive shock from pulmonary vasospasm.
In neurogenic shock, injury to the spinal cord or brain that
affects the sympathetic nervous system leads to severe autonomic
dysregulation.
13
Peripheral vasodilatation results, manifesting as
hypotension. This is classically accompanied by bradycardia, as
there is unopposed parasympathetic activation in the setting of
sympathetic denervation.
CLINICAL PRESENTATION
History and Physical Examination
The clinical presentation depends on the etiology of the distributive shock. Features common to patients presenting with shock
include hypotension (i.e., systolic blood pressure <90 mm Hg;
This sepsis-
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