Fundamental Critical Care Support Skill Station
Diagnosis and Management of Shock
Instructor Guide
Estimated completion time: 45-60 minutes
This skill station incorporates the practical application of the concepts presented in the Diagnosis and Management of Shock lecture
and Chapter 7 of the FCCS text. Many institutions have a variety of care management protocols and technologies available. You will
need to be flexible in adapting these scenarios, staffing approaches and criteria for clinical response. The shock station is designed to
provide the Course Director and instructors with flexibility in the presentation of the cases.
Cases presented here are intended to represent common problems encountered with caring for critically ill patients. Recognition of
patients approaching a shock state and the initiation of appropriate initial shock management are key components. Throughout,
please reiterate and reinforce basic physiologic principles and anticipated consequences, both favorable and unfavorable.
At the conclusion of the session, please collect a Participant Evaluation Form from all attendees. Initial in the appropriate space to
prove attendance and return the form to the respective participant.
Station Objectives
The goals of this station are to:
Discuss recognition and management of the patient with shock.
Review approaches to resuscitation and source control in the treatment of shock.
Participant Objectives
After completing this skill station, the student should be able to:
Cite common patient presentations of shock.
List the 4 major classifications of shock.
Discuss resuscitation goals in management of shock.
Summarize general principles of shock management.
Describe the physiologic effects of vasopressor and inotropic agents.
Discuss the diagnosis and management of oliguria.
Q: How is shock commonly classified?
A. Review the classifications of shock.
The scheme presented in Table 7-1of the FCCS text may be
helpful. A summary of the information is presented at the close
of this guide.
Emphasize that many forms of shock may incorporate
characteristics of other types of shock.
Case 1: A 29 year-old female is seen in the emergency
department with fever and lower abdominal pain occurring
one week after delivery. After presenting with normal blood
pressure and mild tachycardia, the patient is sent for an
abdominal computed tomography for further evaluation.
While undergoing the tomogram, the patient’s BP decreases
to 70/30 mm Hg and her heart rate progressively increases
to 130 beats/minute. Imaging is discontinued. Upon return,
her vital signs are: T: 39°C (102.2°F), P: 130 beats/minute; R:
36 breaths/minute, BP 70/30 mm Hg. Her abdomen is
distended and diffusely tender.
Q: What immediate interventions are needed to stabilize
the
patient’s hemodynamic and respiratory status?
Notes of concern
Q: What is the physiology underlying the patient’s
cardiac and
respiratory instability?
A. The patient requires intravenous fluid resuscitation.
While
fluid resuscitation can be done using peripheral venous
catheters, a central venous catheter will ultimately be
valuable to
help measure endpoints of resuscitation and to facilitate
decisions in subsequent management steps.
The patient also must be assessed for the ability to
protect her
airway. If the patient is not alert and/or is unable to
protect her
airway, intubation should be performed.
A. This patient has a classic form of vasodilatory shock with
hypotension and a relatively wide pulse pressure and fever.
These findings are suggestive of septic shock as the etiology of
vasodilatory shock in this patient.
Q: What vasoactive drug therapy should be considered for
this
patient?
Q: How do you titrate drug and fluid therapies?
A. Initial vasoactive drug therapy in the setting of
sepsis is
norepinephrine or dopamine. Norepinephrine may be a better
choice here due to the relative hypotension. Dopamine,
although
an effective vasopressor agent, may worsen the preexisting
tachycardia in this patient. Another drug which may be
considered is vasopressin since depletion of vasopressin
stores
has been noted in the setting of sepsis and hypovolemic
shock.
A. Rivers and coworkers have demonstrated the value of early
aggressive hemodynamic support in patients presenting with
severe sepsis and septic shock. Intravenous fluids should be
given to resuscitate the patient to a CVP of 8-12 mm Hg. In
general, isotonic crystalloids (normal saline or lactated Ringer’s)
are initial fluids of choice.
Mean arterial pressure is then assessed. The patient with a
mean arterial pressure of <65 mm Hg may be considered for
initial administration of dopamine or norepinephrine.
Vasopressin administration may also be considered.
Central venous oxygen saturation is assessed with the patient at
central venous pressure and blood pressure targets. If central
venous oxygen saturation is <70% in the presence of desired
CVP and blood pressure, of measures described above, the
patient may be transfused with packed red blood cells until the
hematocrit is > 30%. Inotropic agents may be considered if the
central venous oxygen saturation remains at <70% in the setting
of appropriate blood pressure, vasoconstrictor drug
administration and packed red cell administration. The ultimate
goal in this patient is optimization of oxygen saturation in
central venous blood (ScvO2).
Optimizing CVP, blood pressures, hematocrit and central venous
oxygen saturation may be done in the emergency department
before the patient is transferred to the intensive care unit.
Q: What are the possible etiologies of shock in this
patient?
Case 1, continued: The radiologist calls to report the
presence of a large amount of gas in the wall of a distended
uterus.
Q: What are your next steps?
Case 1, continued: In the operating room, the blood loss is
2000 mL. Tissue gram stain and multiple blood cultures
grow gram positive organisms and a streptococcal infection
is suspected. The patient continues to be febrile and
intermittently hypotensive. She is now on mechanical
ventilatory support. Norepinephrine is administered to
A. Septic pelvic thrombophlebitis is a complication
sometimes
seen in the postpartum patient. These individuals have
fever and
require treatment with antibiotic therapy and heparin.
Delayed
hemorrhage is also possible but physical exam does note
support this diagnosis. Uterine wall infection is also
possible.
Notes of concern
A. The patient now has vascular access, airway management
and resuscitation is underway. However, management of
severe
sepsis and septic shock will be unsuccessful without
adequate
source control. CT findings describe a complex infection
with
gas-forming organisms involving the uterus and urgent
hysterectomy is indicated.
Notes of concern
maintain a mean arterial blood pressure > 65 mm Hg and a
systolic blood pressure > 90 mm Hg. Urine output has been
15 mL in the past three hours.
Q: What immediate intervention is warranted?
A. The patient is receiving vasoactive drug support to maintain
blood pressure. In the setting of oliguria, review of CVP and a
test dose of fluids may allow weaning of norepinephrine and
evaluation of urine output response.
ScvO2 should again be reviewed. If SvO2 has fallen significantly
below 70%, fluid administration is the initial intervention of
choice. If SvO2 remains <70% with fluid administration,
reassessment of the need for additional packed red blood cells
must also take place. At this time, if central venous pressure is
adequate and hematocrit is ≥ 30%, a second vasoactive agent,
dobutamine, may be considered to enhance cardiac output. The
patient must be followed carefully for hypotension as the betaagonist effect of dobutamine includes mild vasodilation.
Q: What are the possible causes of oliguria in this
patient?
A. Prerenal, renal and postrenal causes are possible.
The patient has just emerged from an operation in which she had
episodes of hypotension and significant blood loss.
Intraoperative resuscitation may be inadequate to maintain
adequate renal perfusion. To eliminate further prerenal insult,
the patient should be resuscitated to at least the goals set in the
early goal-directed therapy protocol.
Due to ischemia with operative blood loss and hypotension, the
patient may have suffered acute tubular necrosis (ATN). In
succeeding hours, evolution of renal function can be assessed.
The chart should be reviewed for exposure to nephrotoxic drugs.
Some antibiotics may cause interstitial renal parenchymal
disease.
In the setting of complex pelvic surgery, this patient is also at risk
for postrenal or obstructive oliguria. Pelvic inflammation could
lead to ureteral stricture. An operative misadventure could lead
to mechanical obstruction of the ureters. Finally, evaluate the
patient for urinary catheter obstruction.
Q: What additional interventions are appropriate?
A. A fluid challenge is almost always an appropriate initial
response. In this case, with the central venous catheter in place,
CVP blood pressure, and ScvO2 can be assessed against target
values given above. A high dose loop diuretic (furosemide 200
mg slow IV push) may also induce urine output. While
stimulation of urine output may not change outcome, fluid
management is easier and dialysis may be avoided. If oliguric
renal failure is confirmed, fluids should be restricted to
replacement of ongoing losses, including insensible losses.
Acid-base, electrolyte, and fluid balances should be evaluated
carefully. Drug dosages may need adjustments for diminished
glomerular filtration and for use with any renal replacement
therapy, which is required.
Q: Should low-dose dopamine be considered to support
kidney
function in this patient?
A. There is no clear role for low-dose dopamine therapy in
the
support of renal function in this patient. Dopamine may be
employed to optimize hemodynamic support of the patient
Case 2: A 60 year-old male is completing radiation therapy
of the mediastinum for lymphoma. He has been followed by
his oncologist for nonspecific chest discomfort and cough.
He is now admitted to the hospital with progressive
dyspnea. There is no history of heart disease. Blood
pressure is 128/70 mm Hg and heart sounds are normal.
Chest x-ray reveals chronic mediastinal fullness consistent
with hematologic malignancy and the lung fields are clear.
The patient is short of breath when lying supine. Pulsus
paradoxus of 15 mm Hg is present. Electrocardiogram has
nonspecific ST- and T-wave changes.
Q: What is the pathophysiology underlying the patient’s
current
distress?
with
severe sepsis or septic shock but there is no role for
dopamine in
support of the septic patient with acute renal
insufficiency.
Notes of concern
A. In the context of mediastinal malignancy and irradiation,
superior vena cava syndrome and cardiac tamponade should be
considered. Echocardiogram will allow the clinician to distinguish
between these two conditions. The echocardiogram, or bedside
ultrasound, should readily demonstrate fluid about the cardiac
chambers. The diagnosis of tamponade is supported by diastolic
collapse of the right atrium or ventricle and distension of the
inferior vena cava.
During inspiration, the right ventricle normally dilates owing to
increase in venous return. When cardiac tamponade occurs,
movement of the free wall of the right ventricle is limited by the
increased pericardial pressure. Consequently, the
interventricular septum protrudes into the left ventricle leading to
a reduction in left ventricular size during inspiration. These
changes in ventricular performance correspond to pulsus
paradoxus, which is a reduction in systolic blood pressure during
inspiration. Up to 10 mm Hg is acceptable pulsus paradoxus. In
this case, a clear elevation in pulsus paradoxus is seen.
Q: What other conditions cause pulsus paradoxus?
A. Obesity, cardiac failure, pulmonary emphysema, asthma,
pulmonary embolism and constrictive pericarditis, along
with
cardiogenic shock may be associated with pulsus paradoxus.
Absence of pulsus paradoxus does not exclude the diagnosis
of
cardiac tamponade, but this clinical sign is one of the
keys to
diagnosis.
Q: What are the options for medical management?
A. As in all etiologies of shock, the “source” must be addressed.
In this case, drainage of pericardial fluid is essential as soon after
the diagnosis is made as possible. However, immediate surgical
drainage may be unavailable. Thus, approaches to temporary
stabilization become important.
In the unstable patient, during preparation for pericardiocentesis
or operative pericardial drainage, measures to stabilize the
patient should be instituted beginning with intravenous fluid
administration. Increasing circulating volume increases filling
pressure to both ventricles and improvement in preload
corresponds to improvement in stroke volume. Even in patients
with high central venous pressure, intravascular volume can be
administered because tamponade is not initially associated with
impaired myocardial contractility and volume challenges are
tolerated.
If tamponade is associated with penetrating cardiac injury, the
response to fluid resuscitation may produce improvement or
deterioration depending on the effect of fluid infusion on
rebleeding. Colloids or isotonic fluid may be used for
resuscitation.
Bradycardia and vagal reflexes are treated with atropine.
Q: What measures for source control are available?
A. Catheter-based therapies for acute or chronic drainage of
pericardial fluid are appropriate. Even in patients with bloody
drainage, removal of the first several milliliters of fluid generally
provides great relief from tamponade, as the progress of
decompensation with tamponade is very rapid as the limit of
pericardial capacity is reached. Removal of even a small amount
of fluid from the tense pericardium rapidly improves cardiac
chamber performance.
Tamponade in the setting of trauma is generally a surgical
problem and an immediate operative approach is warranted.
Q: In addition to mechanical problems, what other
complications
can occur with pericardial fluid drainage?
A. Occasionally pulmonary edema will develop after
pericardial
drainage presumably doe to sudden increase in right
ventricular
output and pulmonary capillary pressure.
Classifications of Shock
Type of Shock
Heart Rate
Cardiac Output
Filling Pressures
Vascular
Resistance
Pulse Pressure
SvO2
Cardiogenic
↑↓
↓
↑
↑
↓
↓
Hypovolemic
↑
↑
↑
↓
↑or N
↓
↓
↓ or N
↑
↑
↓
↑
↓
↑
↓
↓
↑↓or N
↓
Distributive
Obstructive