Crit Care Nurs Q

Vol. 45, No. 3, pp. 225–232

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Shock
Samir Patel, DO; Kyle Holden, DO;
Bob Calvin, MSN, BA, RN, CCRN, NE-BC; Briana DiSilvio, MD;
Tiffany Dumont, DO, FCCP

Shock is a life-threatening condition of circulatory failure that causes an imbalance between cel-
lular oxygen supply and demand resulting in organ dysfunction. It is important to recognize
promptly as it is reversible in earlier stages but will transition to an irreversible phase if left un-
treated. This will result in multiorgan failure and subsequent death. The clinician should therefore
consider shock in the differential for all patients with new organ failure. This article will review the
pathophysiology, classification, evaluation, and management of shock. Key words: distributive,
hypovolemic, obstructive, shock

S HOCK is a commonly encountered con-

dition affecting approximately one-third
of patients in the intensive care unit and is as-
sociated with high morbidity and mortality.1
Caring for these critically ill patients is
challenging requiring an in-depth understand-
ing of the various heterogeneous disease
processes that cause shock. In addition,
a methodical approach during the clinical
evaluation of these patients is of utmost
importance.2
PATHOPHYSIOLOGY
The oxygen supply and demand mismatch
seen in shock can be caused by inad-
equate oxygen delivery, increased oxygen
consumption, or impaired oxygen utilization.
Author Affiliations: Departments of Nursing
(Mr Calvin) and Pulmonary & Critical Care
Medicine (Drs DiSilvio and Dumont), Allegheny
Health Network, Pittsburgh, Pennsylvania (Drs Patel
and Holden); and Drexel University School of
Medicine, Philadelphia, Pennsylvania (Dr Dumont).
The authors have disclosed that they have no signif-
icant relationships with, or financial interest in, any
commercial companies pertaining to this article.
Correspondence: Tiffany Dumont, DO, FCCP, Drexel
University School of Medicine, 2900 W Queen Lane,
Philadelphia, PA 19129 (Tiffany.dumont@ahn.org).
DOI: 10.1097/CNQ.0000000000000407
Circulatory failure leading to inadequate oxy-
gen delivery is the most common cause of
shock. Oxygen supply and utilization are
vital to the life span of a cell as it sup-
ports aerobic metabolism. Oxygen allows
the cell to metabolize glucose to pyruvate,
which then enters the mitochondria where
adenosine triphosphate (ATP) is generated
via oxidative phosphorylation. Without suf-
ficient amounts of oxygen, the cell enters
anaerobic metabolism where pyruvate is me-
tabolized to lactate resulting in significantly
reduced amount of ATP production per unit
of glucose utilized. Humans are dependent
on adequate ATP production as it maintains
osmotic, ionic, and acid-base homeostasis at
the cellular level. Inadequate ATP supply will
lead to an intracellular influx of calcium
leading to activation of calcium-dependent
phospholipases and proteases and ultimately
cellular swelling and death. In addition, cellu-
lar hypoxia can cause leakage of intracellular
contents into the extracellular space, which
activates inflammatory cascades and causes
end-organ damage.2
Oxygen delivery (DO2 ) is determined by
cardiac output (CO) and arterial oxygen con-
tent (CaO2 ). Cardiac output is driven by heart
rate (HR) and stroke volume (SV) where
stroke volume is determined by preload, af-
terload, and myocardial contractility. CaO2 is
composed of oxygen carried by hemoglobin
225

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226 CRITICAL CARE NURSING QUARTERLY/JULY–SEPTEMBER 2022

(Hb) and to a lesser extent oxygen dis- Table 2. Equation for Systemic Blood
solved in the blood. The equation for oxygen Pressure
delivery is listed in Table 1.
Without adequate perfusion, organs will BP = CO × SVR
lose their supply of oxygen. Tissue perfusion
Abbreviations: BP, blood pressure; CO, cardiac output;
is determined by systemic blood pressure
SVR, systemic vascular resistance.
(BP), which is driven by cardiac output and
systemic vascular resistance (SVR). The equa-
SVR. To maintain tissue perfusion or systemic
tion for systemic blood pressure is listed in
blood pressure, CO increases to compensate.
Table 2.
Central venous pressure and pulmonary cap-
A myriad of diseases can cause shock,
illary wedge pressure will be reduced. There
but what they all share in common is that
are many causes of distributive shock includ-
they affect 1 or more of the aforemen-
ing, but not limited to, sepsis, anaphylaxis,
tioned variables including heart rate preload,
adrenal crisis, severe burn injuries, pancreati-
cardiac contractility, systemic vascular resis-
tis, capillary leak syndrome, and severe brain
tance, SaO2 , or hemoglobin. This reduces
or spinal cord injuries.2
oxygen delivery and causes cellular hypoxia.2
In anaphylaxis, patients usually will have a
history of prior exposure to an antigen re-
CLASSIFICATION OF SHOCK sulting in immunoglobulin E (IgE) formation
to that antigen. These IgE molecules at-
For simplification, shock is separated into 4 tach to mast cells and basophils. Subsequent
major classes: distributive, hypovolemic, ob- exposure to the inciting antigen will result
structive, and cardiogenic. This section will
focus on all of these apart from cardiogenic
shock as this will be discussed separately. Table 3. Classification of Shock
Each class has a distinct hemodynamic profile
that clinicians must be familiar with. It must Type of
be noted many patients will not fit perfectly Shock Clinical Examples
into one of the aforementioned categories Distributive Sepsis
and may present with more than 1 type of Severe burn injuries
shock. This is referred to as mixed shock. Anaphylaxis
Tables 3 and 4 later summarize the classes Adrenal crisis
of shock and their associated hemodynamic Pancreatitis
profiles. Capillary leak syndrome
Severe brain or spinal cord
DISTRIBUTIVE SHOCK injuries
Hypovolemic Hemorrhage (GI bleeding,
trauma, spontaneous)
Distributive shock is primarily caused by se- GI losses (severe
vere peripheral vasodilation or a reduction in diarrhea/vomiting)
Severe burn injuries
Table 1. Equation for Oxygen Delivery Renal losses (polyuria
seen in diabetic
DO2 = CO × CaO2 ketoacidosis or
DO2 = (HR × SV) × CaO2 insipidus)
CaO2 = (Hb × 1.34 × SaO2 ) + (PaO2 × 0.003) Obstructive Tension pneumothorax
Cardiac tamponade
Abbreviations: CaO2 , arterial oxygen content; CO, car- Constrictive pericarditis
diac output; DO2 , oxygen delivery; Hb, hemoglobin; HR, Pulmonary embolism
heart rate; PaO2 , arterial oxygen content; SaO2 , oxygen
saturation of hemoglobin; SV, stroke volume. Abbreviation: GI, gastrointestinal.

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Table 4. Hemodynamic Profiles of Shock
Type of Shock CO
Hypovolemic
Obstructive
Cardiogenic
Distributive
Abbreviations: CO, cardiac output; CVP, central venous pressure; PCWP, pulmonary capillary wedge pressure; SVR,
systemic vascular resistance; , decreased; , increased.
in IgE-mediated release of histamine from
mast cells and basophils. This results in sys-
temic vasodilation and capillary fluid leak,
in turn, reducing oxygen delivery to tissues.
Treatment includes, but is not limited to, re-
moval of the inciting cause, intramuscular or
intravenous (IV) injection of epinephrine, vol-
ume resuscitation with IV fluids, and early
intubation if there are any signs of airway
involvement.
Adrenal insufficiency causes distributive
shock by way of decreased expression of
α-1 receptors on arterioles secondary to cor-
tisol deficiency. This results in vasodilation
and reduced oxygen delivery to tissues. Treat-
ment involves determining the etiology of the
adrenal crisis, IV stress dose steroids, volume
resuscitation with balanced crystalloids, and
close monitoring of glucose as hypoglycemia
is common.
Severe burn injuries can cause systemic
inflammatory response syndrome, similar
to sepsis, which in turn can cause shock.
Patients with severe burn injuries develop
shock and multisystem organ dysfunction
at 2 distinct points. Early on, hypoperfu-
sion is generally secondary to hypovolemic
shock from fluid losses. Later on, hypoperfu-
sion usually occurs secondary to distributive
shock from sepsis. Endotoxins and/or exotox-
ins released because of an infection initiate an
inflammatory cascade that causes peripheral
vasodilation, extravascular fluid loss, and or-
gan damage. Not surprisingly, both conditions
will lead to multisystem organ dysfunction.
The risk of multisystem organ dysfunction in-
creases with burn wounds occupying greater
than 20% total body surface area and with
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Shock 227
CVP PCWP SVR
increasing age. Treatment is focused on fluid
resuscitation, wound care and prevention of
infection, early enteral nutrition, and early
liberation from a ventilator.
Similar to severe burn injuries and sepsis,
pancreatitis can cause systemic inflammatory
response syndrome, which can lead to shock.
Pancreatic inflammation activates a cytokine
cascade like that of sepsis and burns causing
peripheral vasodilation, extravascular fluid
loss, and organ damage. Management is aimed
toward fluid resuscitation, pain control, an-
tibiotics (if there is concern for infection),
enteral nutrition, and at times surgical or
advanced endoscopic management.
Capillary leak syndrome is rare and caused
by hypoalbuminemia. Decreased oncotic
pressures leads to fluid leaking into the in-
terstitium, which may lead to hypotension
and shock. Treatment includes airway man-
agement, conservative IV fluid resuscitation,
and vasopressor support. Other therapies do
exist, but data on their efficacy are limited.
Neurogenic shock classically occurs when
there is trauma to the cervical spinal cord re-
sulting in damage to the sympathetic nervous
system. This causes decreased adrenergic in-
put to the blood vessels and heart causing
vasodilation and paradoxical bradycardia and
again results in decreased oxygen delivery
to tissues. In general, treatment consists of
vasopressor support, careful IV fluid resus-
citation so not to cause volume overload
and further spinal cord edema, atropine,
possibly temporary pacing, and careful moni-
toring for respiratory complications, such as
respiratory failure, pneumonia, pulmonary
edema, and/or pulmonary embolism.
228 CRITICAL CARE NURSING QUARTERLY/JULY–SEPTEMBER 2022
Septic shock is the most common cause
of distributive shock and thus will be dis-
cussed in detail.3 Septic shock occurs in
response to an infection that leads to over-
whelming systemic inflammation. Mortality
rate averages anywhere from 30% to 50%.
Septic shock results in systemic vasodilation
which, in turn, reduces ventricular preload
and ventricular afterload (SVR). These hemo-
dynamic changes are attributed to enhanced
production of nitric oxide in vascular en-
dothelial cells. Oxidant injury to the vascu-
lar endothelium leads to fluid extravasation
and hypovolemia. Proinflammatory cytokines
cause cardiac dysfunction, though cardiac
output is usually increased early on due to
tachycardia and volume resuscitation. In ad-
vanced stages of septic shock, cardiac output
is reduced, which is a poor prognostic indica-
tor. Splanchnic blood flow is often reduced,
which could lead to disruption of the intesti-
nal mucosa. This creates risk of translocation
of enteric bacteria and endotoxins across
the bowel mucosa into the systemic circu-
lation, which could add further insult. Poor
tissue oxygenation is the result of a defect
in oxygen utilization in the mitochondria. In
fact, whole body oxygen consumption is in-
creased in sepsis. Oxidants disrupt proteins
in the electron transport chain resulting in
impaired aerobic metabolism and decreased
ATP production. As a result, serum lactate will
accumulate. The management of sepsis con-
sists of bundles that need to be performed in
a time-sensitive manner, which is elaborated
in Table 5.3
Table 5. Surviving Sepsis Bundle
Obtain appropriate cultures
Start antibiotics immediately. Ideally within
1 h of recognition
Administer IV balanced crystalloid
resuscitation (at least 30 mL/kg within first
3 h of resuscitation)
Obtain serum lactate
Abbreviation: IV, intravenous.
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Septic shock is a medical emergency. At
least 30 mL/kg of crystalloid fluid should be
given within the first 3 hours of resuscitation.
Antibiotics should be given immediately, ide-
ally within 1 hour of recognition. Appropriate
culture data should be obtained.
Management also consists of targeting a
mean arterial pressure (MAP) of 65 mm
Hg. Norepinephrine should be used as the
first-line vasopressor. If MAP remains inad-
equate despite norepinephrine, vasopressin
should be added. If the MAP is still in-
adequate despite norepinephrine and vaso-
pressin, epinephrine should be added. In-
travenous steroids should be used to treat
septic shock with ongoing requirement for
vasopressor therapy. Invasive monitoring of
arterial blood pressure is preferred over non-
invasive methods. Sources of infection should
be sought after and treated accordingly. A
low tidal volume ventilator strategy should be
adhered to.3,4
HYPOVOLEMIC SHOCK
Severe hypovolemia or intravascular fluid
depletion can result in hypovolemic shock. It
is driven by a reduction in preload or cen-
tral venous pressure. This, in turn, causes
a reduction in CO and pulmonary capil-
lary wedge pressure. To compensate, the
SVR will be elevated. The most common
cause is due to severe hemorrhage, which
can be spontaneous or mechanical, such as
a gastrointestinal (GI) bleed or trauma, re-
spectively. Other causes include, but are not
limited to, GI losses via diarrhea and vomit-
ing, burn injuries, and renal losses through
polyuria seen in diabetic ketoacidosis or
insipidus.2 Treatment involves IV fluid or
blood resuscitation, the latter being preferred
over crystalloids in hemorrhagic shock, and
treatment of the underlying cause of hypov-
olemia. Surgical evaluation is recommended
in cases of hemorrhagic shock secondary to
trauma. Early gastroenterology and interven-
tional radiology consultation is required in
cases of hemorrhagic shock secondary to GI
bleeding.

OBSTRUCTIVE SHOCK
Obstructive shock is predominantly char-
acterized by a reduction in CO. Dissimilar
to cardiogenic shock, the etiology is related
to an extracardiac process causing physi-
cal obstruction of circulation into or out of
the heart. Tension pneumothorax, cardiac
tamponade, constrictive pericarditis, and pul-
monary embolism can all cause obstructive
shock.2 Tension pneumothorax and pericar-
dial tamponade prevent blood from entering
the right side of the heart. Pulmonary em-
bolism and severe pulmonary hypertension
prevent ejection of blood from the right
side of the heart. Ventricular interdepen-
dence can also be seen in obstructive shock
causing further circulatory compromise. This
describes the dysfunction of 1 ventricle sec-
ondary to a disorder of the other, mainly
due to involvement of the interventricular
septum. For instance, in a pulmonary em-
bolism, the right ventricle filling pressure
increases, pushing the interventricular sep-
tum toward the left ventricle, which, in
turn, increases the left ventricular filling pres-
sure. This reduces filling of the left ventricle
during diastole, which subsequently reduces
stroke volume and cardiac output. The phys-
iology of constrictive pericarditis is similar.
In these cases, the pericardium does not
expand to accommodate increased venous
return to the right side of the heart dur-
ing inspiration and limits cardiac volume.
Because of increased filling pressures, ven-
tricular interdependence is also seen. These
processes decrease stroke volume and car-
diac output. Treatment is directed toward the
underlying cause. For instance, pulmonary
embolism with shock, termed “a massive pul-
monary embolism,” should be treated with
systemic thrombolytic medication if there
are no contraindications. Needle decompres-
sion and chest tube placement would be
the treatment for a tension pneumothorax.
Emergent cardiothoracic surgery evaluation
and pericardiocentesis would be the treat-
ment for cardiac tamponade. Treatment for
shock secondary to constrictive pericarditis
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Shock 229
consists of cardiothoracic surgery evaluation
for pericardiectomy though this is associated
with significant perioperative morbidity and
mortality.
EVALUATION OF SHOCK
The evaluation of a patient in shock be-
gins with appropriate utilization of a history,
physical examination, and testing, which
will allow for prompt diagnosis. A major-
ity of patients will, however, present with
encephalopathy, so history may have to be
obtained from a reliable source such as a
loved one who is familiar with the patient’s
medical history. This allows for expeditious
initiation of therapy and rapid restoration of
oxygen delivery during the reversible phase
of shock.2
A detailed history and physical examination
can many times reveal the type of shock a pa-
tient is in. For a patient in distributive shock
from sepsis, history and physical may reveal
the patient having had a fever or a focal site
of infection. A patient may admit to GI bleed-
ing, which would help identify hemorrhagic
shock. In anaphylactic shock, history may re-
veal exposure to a known allergen such as a
bee sting.
The physical examination on the same pa-
tient may reveal hives, dyspnea, or facial
edema. Pulsus paradoxus, elevated jugular
venous pressure, and distant heart sounds
may be seen in cardiac tamponade. A ten-
sion pneumothorax may be diagnosed by an
absence of breath sounds over the affected
lung, subcutaneous emphysema, or tracheal
deviation away from the affected side.1,2
Other more subtle clues on physical exam-
ination can help identify a patient in shock.
Early on, patients will compensate by an el-
evation in their HR to increase CO. Patients
may present with tachypnea to compensate
for underlying metabolic acidosis from inad-
equate tissue perfusion. Most patients will
present with low blood pressure. Although
this is defined as a systolic blood pressure
less than 90 mm Hg or MAP less than 65
mm Hg, patients who live with chronically
230 CRITICAL CARE NURSING QUARTERLY/JULY–SEPTEMBER 2022
uncontrolled hypertension may have inade-
quate tissue perfusion at what may be con-
sidered a “normal” blood pressure for most
patients. Patients will have decreased capil-
lary refill and cold and clammy skin. Oliguria,
defined as less than 0.5 mL/kg/h urine output,
will also be present. As mentioned earlier,
a majority of patients will also present with
encephalopathy due to decreased central
nervous system perfusion.1,2
LABORATORY FINDINGS
Laboratory evaluation should be performed
in all patients with shock. This testing in-
cludes, but is not limited to, an arterial or
venous blood gas, renal function tests, liver
function tests, cardiac enzymes, a complete
blood count with differential, lactate, coagu-
lation studies, urinalysis with urine sediment,
blood, sputum, and urine cultures. A blood
gas may reveal metabolic acidosis. Lactate
will commonly be elevated suggesting in-
adequate perfusion and oxygen delivery to
tissues. Normally, lactate is produced from
skeletal muscle, the brain, skin, and intestine.
The white blood cell count may be elevated
suggesting infection; or hemoglobin may be
significantly reduced from baseline suggest-
ing hemorrhage. Renal function tests may
show an elevated creatinine signifying kidney
injury from inadequate perfusion. Liver func-
tion tests may reveal elevated liver enzymes in
an obstructive pattern suggesting biliary ob-
struction and potentially indicating a source
of infection. They may conversely be elevated
in a hepatocellular pattern from ischemia. Uri-
nalysis may reveal pyuria identifying a source
of infection. An electrocardiography should
be performed on all patients to help iden-
tify causes of shock such as arrhythmias or a
myocardial infarction. Echocardiography can
help categorize shock and sometimes even es-
tablish the cause of shock. Finally, imaging
such as radiography or computed tomogra-
phy can be a helpful tool in the evaluation of
shock. For example, it may identify a source
of infection, a pneumothorax, or a pulmonary
embolism.2
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MANAGEMENT OF SHOCK
Treatment should be directed toward the
underlying cause of circulatory shock to
restore perfusion and oxygen delivery to
tissues. Management of different causes of
shock is summarized in Table 6. This requires
a multidisciplinary team to evaluate and treat
the patient. Treatment should begin as early
as possible and in a setting such as an in-
tensive care unit where frequent assessments
and invasive monitoring can be performed.
Early IV access should be obtained with a
large bore IV catheter to allow for aggres-
sive volume resuscitation. Placement of a
central venous catheter may be required for
prolonged vasopressor or inotrope admin-
istration. Vasopressor administration should
not be delayed for the placement of a cen-
tral venous catheter though; many of these
medications can safely be run through a pe-
ripheral IV catheter until other access is
obtained. An arterial line can allow for contin-
uous assessment of blood pressure and MAP.
A urinary catheter should be placed for close
monitoring of urine output.2,3
Volume resuscitation can be a primary ther-
apy in certain categories of shock such as
distributive and hypovolemic shock. Admin-
istration of fluids can, however, be harmful in
other categories of shock such as in certain
cardiac conditions. Therefore, assessment of
intravascular volume status should be per-
formed in all patients with shock. This can
prove to be very challenging, however. Phys-
ical examination can be unreliable and there
is no available technology that can accurately
identify a patient’s volume status. Frequent
reassessment is therefore important to en-
sure that the patient is clinically improving
with volume resuscitation rather than de-
compensating. Examples of tools used at the
bedside to assess for intravascular volume
status include, but are not limited to, pas-
sive leg raise, stroke volume variation, and
point-of-care ultrasonography. These have
their own limitations, however, and should
not be solely relied upon during assessment.
Passive leg raise is a predictor of who will
 Table 6. Management of Causes of Shock

Distributive shock Sepsis Refer to Table 5

Severe burn injuries IV fluid resuscitation, wound care, infection prevention,
vasopressor support
Anaphylaxis IV fluid resuscitation, removal of offending agent,
epinephrine, glucocorticoids, bronchodilators,
vasopressor support
Adrenal crisis IV fluid resuscitation, stress dose glucocorticoids, close
monitoring for hypoglycemia, vasopressor support
Pancreatitis IV fluid resuscitation, pain control, enteral nutrition,
antibiotics if suspecting secondary infection, surgical or
advanced endoscopic management in select cases,
vasopressor support
Capillary leak syndrome Conservative IV fluid resuscitation to avoid hypervolemia,
vasopressor support
Severe brain or spinal cord injuries Conservative IV fluid resuscitation, vasopressor support,
atropine and temporary pacing in select cases, careful
monitoring for respiratory complications, treatment of
underlying cause, neurosurgical evaluation
Hypovolemic Hemorrhage Blood transfusion, reversal of coagulopathy,
shock gastroenterology or surgical consultation depending on
cause, vasopressor support
GI and renal losses IV fluid resuscitation, vasopressor support, treatment of
underlying cause
Obstructive shock Tension pneumothorax Needle decompression, chest tube placement, vasopressor
support, thoracic surgery evaluation
Cardiac tamponade Vasopressor and inotropic support, pericardiocentesis,
cardiothoracic surgery evaluation
Constrictive pericarditis Pericardiectomy, cardiothoracic surgery evaluation
Pulmonary embolism Systemic tissue plasminogen activator (tPA) or surgical
thrombectomy, inotropic and vasopressor support,
multidisciplinary evaluation with pulmonology,
Shock

interventional cardiology, cardiothoracic surgery, and

critical care

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231

Abbreviations: GI, gastrointestinal; IV, intravenous.

232 CRITICAL CARE NURSING QUARTERLY/JULY–SEPTEMBER 2022
Table 7. Stroke Volume Variation
SVV = (SVmax – SVmin)/SVmean
Abbreviations: SVmax, maximum stroke volume; SVmin,
minimum stroke volume; SVV, stroke volume variation.
have an increase in stroke volume in response
to fluid administration. It is performed by
sitting a patient at 45° in head-up semirecum-
bent position. From here, the patient’s upper
body is lowered to horizontal and both legs
are passively raised to 45°. If there is a 10%
increase in stroke volume on a cardiac mon-
itor or 10% increase in pulse pressure if no
monitor is available, this is considered a posi-
tive test and predicts fluid responsiveness. Of
note, 30 to 90 seconds should surpass after
raising the legs prior to assessment of pulse
pressure. Stroke volume variation is useful
only in mechanically ventilated patients. The
equation for stroke volume variation is listed
in Table 7 later. This can be calculated using
the waveform off an arterial line, or there are
devices that calculate this independently. A
stroke volume variation greater than 10% can
be predictive of fluid responsiveness. Certain
maneuvers using point-of-care ultrasonogra-
phy can help assess a patient’s volume status.
These include cardiac ultrasonography, lung
ultrasonography, and even measurements of
the inferior vena cava. Finally, Swan-Ganz pul-
monary artery catheters can be used to help
differentiate which class of shock a patient
is in. This is elaborated in Table 7. It should
be noted, however, that they have fallen out
of favor due to their limitations and impli-
cations. Studies have shown that aggressive
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