STARS
Simulation
Training for
Acute
Resuscitation
Skills
Geoffrey K. Lighthall PhD, MD
Assistant Professor, Anesthesia and Critical Care
Stanford University School of Medicine
Palo Alto Veterans Affairs Health Care System
1
STAR Course Syllabus Contents
Welcome to Critical Care
3
Immediate Assessment and Stabilization
4
Respiratory Failure
6
Hypoxemia
8
Production and Elimination of Carbon Dioxide
10
Therapy for Respiratory Problems
12
Physiology and Disruption of Oxygen Transport
14
Circulatory Shock:
16
Therapy for Hemodynamic Instability
20
Acute Blood Loss
23
Acute pain
25
Cognitive Aids and Flow Charts
Hypoxemia
9
Carbon Dioxide
10-11
Shock / Hypotension Diagnostic Tree
19
Shock / Hypotension Treatment Outline
22
2
Welcome to Critical Care
The ICU serves every clinic, specialty, ward or procedure room in the
hospital, and at every hour of the day. Care of a critically ill patient demands
flexibility and the ability to perform under stress, but also a calm, methodical
approach to dynamic situations and the ability to identify priorities. Often, the
need to have expert hands at the bedside leaves the medical student out of the
loop in terms of hands on experience and in the ability to ask questions as they
arise. The purpose of this course is to break down some of this activity into its
component parts and to provide some experiential learning in an environment
that creates no risk to patients. The goals we have set for this experience are
to:
 Alert you to some of the types of patients that have unexpected
admissions to the intensive care unit
 Appropriately equip you with cognitive tools and conditioned responses to
events that arise in medical emergencies.
 Make use of medical simulation to:
- “bring to life” basic knowledge of physiology and pharmacology by
relating such to real medical conditions and lifelike “patients”
- allow you first-hand experience in managing patient emergencies
- reinforce standard methods of patient evaluation
- provide you with expert videotape review of the management of
patient emergencies
The hands-on experience with patient simulation is the most unique and
exciting aspect of the course. In addition to the thrill and responsibility of
caring for a critically ill patient, you should also leave with the following:
 How to recognize a sick patient--an appreciation and ability to detect early
warning signs of deterioration
 The techniques and priorities in stabilizing patients with ABC problems;
what you can do for a patient in the pre-arrest phase
 A sense of urgency (and fear) in evaluating a patient with an abnormal
vital status
 The pathophysiology of problems with the airway, breathing, and
circulation
Components of the course include:


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
An on-screen simulator and worksheet that need to be completed before the
simulation sessions.
This text and a pre-test
A four-hour session in the Human Patient Simulation lab where you will class
manage a variety or critical incidents.
Review and debriefing of simulated critical incidents
3

A post course questionnaire and post test.
4
Immediate Assessment and Stabilization
The overall emphasis of this course and its training exercises is to
understand the physiology of deteriorating patients and think of problems,
therapy, and end points in these terms. While subtle, this represents a
departure from how most branches of medicine operate: “make a diagnosis then
treat the problem.” The lack of a clear diagnosis seems to cause a bit of mental
paralysis during the first 10-15 minutes of a critical patient encounter and this is
exactly when initiating therapy is likely to have the greatest impact. A
physiologic approach to patient care allows one to work with broad categories of
problems and find diagnoses within this framework. More significantly, one gains
the ability to start treatment for that class of problems at an earlier stage.
This chapter will serve provide a general overview of patient resuscitation
as a lead in to more detailed chapters on therapy for airway, breathing and
circulatory disorders.
An example
You are called to evaluate a patient who is
hypotensive. You arrive and find a patient with intact mental function, but with a
BP of 85/49. The patient is warm to the touch and pulses are full. The patient
has a respiratory rate of 24 with clear breath sounds; the chest seems to move
with each heartbeat. From this brief exam, you can be fairly sure that the
patient has no problem with cardiac function or with breathing. The extremities
are warm, so you rule out an increase in vascular tone that one may expect if is
the patient's hypotension was due to bleeding. Instead, you attribute the
hypotension to vasodilation. Now you’re not quite sure whether the problem is
sepsis due to cellulitis (the admitting condition), or due to an anaphylactic
reaction associated with a recent antibiotic. Either way, you know that in a
hypotensive patient with low SVR, administration of fluids and vasopressors is
the mainstay of therapy. Better IV access is obtained, 50 mg of
diphenhydramine and 2L of a crystalloid solution are quickly administered. The
blood pressure improves with several 100mcg boluses of phenylephrine, during
which time more fluids are given. Later, when the patient is more stable, you
look up anaphylaxis and are reminded that a tryptase level would confirm this
diagnosis, and a serum sample is sent. In this case, establishing a definitive
diagnosis (worsening sepsis) lagged a few hours behind supportive therapy, but
at least knowing the nature of the physiologic problem prevented time wasted on
diagnostic studies, and facilitated early stabilization and probably a better
clinical result.
Caring for an unstable patient can be unnerving without some ability to
prioritize problems. In the initial stages of any resuscitation, the focus is on
cardiovascular and respiratory function and the absolute necessity of oxygen
assimilation and delivery to the tissues in order to sustain life. The initial
interventions are therefore:
 address the ABCs,
 collect and assess vital signs,
 assess the components of oxygen delivery.
5
Without a handle on these three basic points, it is unbelievably easy to get
distracted with secondary phenomena and to waste crucial time on
insignificant problems.
While defining an unstable patient's problem in physiologic terms, it is
important to also consider diagnoses that require external personnel or
interventions as early as possible ( ie cardiac cath lab, surgical operation,
special procedure); if in doubt, call for help at a stage when it can be useful.
A more deliberate algorithm describing these priorities is summarized
below, as well as a comparison of the ABCD survey taught in advanced cardiac
life support (ACLS) courses. With cardiac arrest, survival correlates with
conditions (heart rhythms) amenable to rapid correction by cardioversion, and
accordingly, a high priority is assigned to identifying "shockable rhythms."
Likewise, understanding the problem underlying the instability (ventricular
tachycardia, pulseless electrical activity) will help you prevent a second code. In
the absence of an emergency requiring defibrillation, the ACLS ABCD survey
doesn’t provide any insight or guidance into the assessment and management of
unstable patients, rather it suggests you establish a diagnosis for the instability.
A preferable method is one that encompasses the overall issues of tissue oxygen
delivery as it relates to cardiovascular and respiratory status, and one that allows
for diagnosis and stabilization of both “coding” and “non-coding” patients. It is
ABC VDE. As with any patient evaluation, a thorough physical exam should be
performed at the earliest opportunity. Additional help may be needed to examine
the patient, review the chart or computer, and to keep abreast of acute changes.
A
B
C
V
D
E
This scheme
-Airway
-Breathing
-Circulation
-Vital signs--obtain
-DO2—assess with ABG
-Endocrine (check glucose)
ACLS Primary Survey
-Airway
-Breathing
-Circulation
ACLS secondary 20
-Airway
-Breathing
-Circulation
-Defibrillation
-Diagnosis
Why incorporate vital signs into a treatment algorithm? Isn't getting a set of vitals
automatic??? Apparently not. Observations in real emergencies and in
simulated emergencies repeatedly show clinicians standing around and failing to
gather real time data, or relying on vital sign data in an unstable patient without
knowing when it was obtained. The sections below will describe the function,
assessment, and stabilization of abnormal breathing and circulation, and provide
a detailed description of their evaluation.
6
Respiratory Failure: Physiologic and Anatomic Considerations
Respiratory failure is a general term referring to impairment of the body’s
ability to assimilate oxygen and transport it to the pulmonary capillary blood,
eliminate carbon dioxide from the blood, or both. Organ-based derangements
underlying such problems are diverse and include metabolic disturbances,
dysfunction of neural circuitry from the brainstem down to the neuromuscular
junction, abnormalities in the chest wall, alveoli, pulmonary parenchyma, upper
and lower airways, and blood flow to the lung.
In respiratory failure, diagnosis and intervention occur
simultaneously, with support being the higher priority.
Inspection and auscultation of the patient may provide enough information to
initiate therapy, however, knowing whether the problem had a fast or slow onset
will provide diagnostic information (i.e. was there a medicine recently given, was
the patient eating, ambulating, etc). Respiratory failure usual involves an
interplay between a disease process and host factors, all of which need to be
considered as part of a management strategy.
Most patients can tolerate an increased demand on the respiratory system
for a few hours, some less. When a high workload is sustained, many patients
experience respiratory muscle fatigue, and regardless of the inciting event, develop
hypercapnic respiratory failure. When evaluating the patient, consider subjective
complaints of fatigue and distress, and form your own impression of the work
requirements of respiration. A more formal way to think of the patient’s work of
breathing is in terms of the pulmonary compliance curve on the following page.
The normal set point is in the center of the steep slope (FRC); thus little work (P,
upper thin arrow is required for volume exchange. Patients with increased
extravascular lung water, airway obstruction, or increased body girth function at a
lower portion of the pulmonary compliance curve that requires far greater work for
a given tidal volume (thick arrow). Patients with abnormal lung compliance also
tend to breathe in a rapid shallow pattern; the resulting lower tidal volumes provide
less efficient alveolar ventilation.
The need for airway or ventilatory support as well as inquiry into code
status is a prime consideration during the first seconds of an encounter.
Supplemental oxygen should be given. A more detailed guide to the ABC survey
is presented in the table below. Initiation of continuous oximetery and inspection
of patient color provide immediate clues to whether the problem involves
hypoxemia or not. Lastly, a blood gas will provide further assessment of gas
exchange, CO2 elimination, and status of global oxygen delivery.
7
Compliance, C = V/ P
Volume
Inspiratory Pressure
Airway:
Look Can the patient talk, is there misting on mask?
Chest rising?
Abdominal retractions w/o chest rise?
Listen Stethoscope to larynx: is there air movement?
Stridor?
Auscultation of chest
Feel Can you feel breath on your hand?
Chest rise
Breathing:
Look Patient color, speaking with complete sentences?
Muscular movement
Frequency, prolonged expiratory phase
Chest rise, depth of respiration
Does assist bag refill
Listen Adventitious sounds; Diffuse? Focal?
Bilateral air entry
Feel Feel compliance of breathing circuit
Feel chest rise
Circulation
Look Color, capillary refill
Mental function
Listen S1, S2, extra heart sounds
Feel Warmth, pulse character, precordial movement
8
Obviously, the survey does not proceed to breathing and circulation
unless there is a patent airway. When there is time to consider a complete
diagnosis or chain of events, this should be done. Below, is a systematic
framework for evaluating causes of hypercarbia and hypoxemia. The format is
consistent with others used throughout the text: Physiologic roots and their
derivations are printed in black; data obtained from labs, data from examination
and clinical monitors are noted in red, and likely diagnoses or diagnostic
categories are printed in blue. The charts are useful for thinking of problems
physiologically, making diagnoses, and prioritizing diagnostics that may
differentiate different etiologic categories.
Hypoxemia
Hypoxemia can manifest itself in a subtle manner, with secondary signs
such as change in mentation, delirium, and organ dysfucntion. In such cases the
challenge is to correct the hypoxia and figure out why the patient has this
problem. Alternately, hypoxia can be intertwined with a primary complaint as
chest pain in major pulmonary embolus, or cardiogenic shock. In either case,
your job is to provide rapid stabilization, and address the underlying process as
soon as possible. Etiologic categories are listed on the following chart. As with
other charts in this text, broad physiologic categories are noted in black, clinical,
laboratory and monitor findings are noted in red, and possible diagnoses are
written in blue type.
9
Hypoxemia
1. Decreased alveolar pO2
Inadequate FiO2
Machine/ tank /
pipeline malfunction
Altitude
Altered mental status,
Agitation
Oxygen desaturation
CV instability
2
2. Shunt, increased venous admixture
Intracardiac
Intrapulmonary
Anatomic --liver disease
Airway (mainstem intubation)
Alveolar (lung injury, hemorrhage,
PNA, capillary leak 2o allergy, PE, CHF)
3. High Oxygen extraction
exacerbated
by shunt physiology
Decreased SvO2
Decreased CO (see tree)
Hemorrhage
High VO2 from sepsis, fever, etc
4. Inadequate ventilation
Increased CO2
Respiratory rate
Inadequate tidal volume
Obstructed airway
Tongue, soft tissue (angioedema, OSA, allergy)
Airway mass (pharyngeal abscess, epiglottitis, tumor)
Laryngeal (tumor, VC paralyisis 2o to nerve injury or hypocalcemia)
Machine related (valve, power, oxygen supply)
Decrease in compliance of pulmonary system
Static compliance (P plateau)
lung injury, fibrosis, PNA, PTX, pulmonary edema (CHF, large PE)
Dynamic compliance (P peak)
Bronchospasm, mucus plug in airway or in ET, foreign body
hyperinflation
10
Production and Elimination of Carbon Dioxide
Carbon dioxide content is one of the primary determinants of acid / base
status. Obtaining an ABG is essential to understanding CO2 levels, as well as
assessing their contribution to body pH. Abnormally high or low paCO 2 values,
and deviations from baseline values can often provide a valuable window into the
patient’s ventilatory status. Total ventilation (denoted by convention as VE)
consists of ventilation of alveoil (VA) as well as non-perfused parts of the lung
(dead space ventilation, VD), such that VE = VD + VA. Many critically ill patients
have exhaled CO2 sampled and displayed on the bedside monitor; the value
displayed (usually referred to as the end tidal CO2). is a useful adjunct to arterial
CO2 monitoring. The ET CO2 is always going to be less than alveolar CO2 by a
“gradient” that is 5-7 mm Hg in normal subjects, but increases in proportion to
increases in VD/ VE. Patients with emphysema, for example, may have a
gradient of 15. Patients with a shallow respiratory pattern will also have a higher
gradient.
Hypocapnea
Hypocarbia acutely causes a decrease in cerebral blood flow, with
attendant changes in mental status or consciousness. Alkalemia if present, can
cause coronary vasospasm, bronchoconstriction and a left shift in the
hemoglobin dissociation curve. Causes of hypocapnea that you will commonly
see are pain, anxiety, and as compensation for metabolic acidosis.
Hypercapnea
Hypercarbia often manifests as a depressed mental status, tachypnea,
hypertension, tachcardia, and ectopy. Increases in CO2 are attributable to either
decreased elimination of CO2, increased production, or both. The various
etiologies and clinical findings that fall into these general categories are
described below.
Increased Production of CO2
(increased VE –usually, incr. ET CO2 , paCO2)


Non-febrile
Hyperalimentation,
Inadequate anesthesia or sedation,
Excessive shivering
Febrile
Fever, sepsis with poor CO2 elimination
Thyrotoxicosis
Malignant Hyperthermia (MH), neuroleptic malignant syndrome (NMS)
11
Decreased Elimination of CO2 (increase in dead space)
I. Unable to eliminate CO2 from lungs:
( increased VD/VE, decreased VA/VE, RR usually rapid)
 Inadequate tidal volume
 Respiratory muscle fatigue
 Obstructed airway (mechanical, inflamatory)
 Residual paralytic effect
 Hypothermia
 Myxedema coma
II. Unable to get CO2 to the lungs
(Tidal volume usually normal [ > 8mL/ kg ideal body mass], RR usually rapid; ET
CO2 variable, depending on the chronicity of the problem)
a.  Regional Pulmonary blood flow
Pulmonary embolus
ARDS
Emphesema, blebbing
b. Generalized Decrease Cardiac Output
MI
PTX
PE
Exsanguination
12
Therapy for Respiratory Problems
Therapy for Airway problems
I. Foreign body
 Scoop and sweep, forceps removal
 Heimlich maneuver
II. Soft tissue or tongue obstruction, over sedation
 Chin lift, jaw thrust
 Supplemental high flow oxygen (100% non-rebreather bag @ 15 L/ min)
 Nasal and / or oral airway
 Reverse paralytics and sedatives
Benzos--Flumazenil, 0.2 mg IV push, repeat up to 1.0 mg
Non-succinylcholine paralytics--5mg neostigmine + 1.0 mg glycopyrolate
Opiates--40-80 mcg naloxone, repeat as needed
(note: a typical vial contains 400 mcg)
 Bag-assist ventilation via Ambu Bag or Jackson-Reese circuit (need to call
anesthesiologist for help)
III. Stridor, (extrathoracic airway obstruction edema,tumor, infection, VC paralysis)
 Supplemental high flow oxygen (100% non-rebreather bag @ 15 L/ min)
 Immediate call to anesthesiologist; s/he will help you determine need for
surgical airway
 Need to avoid stimulation and stress; this increases turbulence of airflow
 Bag-assist ventilation via a Jackson-Reese circuit or BiPAP machine
(need to call anesthesiologist for help, AMBU bag may not work without
addition of a PEEP valve)
 Call for expert help with airway management: anesthesiology and ENT
 Call RT for Racemic EPI, possible heliox (B2- agonists are not appropriate for
upper airway obstruction)
 ABG
Therapy for Breathing problems
I. Apnea, drive problems
 Bag-assist ventilation via Ambu Bag and O2, use airways as needed
 Consider presence of paralytics and sedatives, reverse
Benzos--Flumazenil, 0.2 mg IV push, repeat up to 1.0 mg
Non-succinylcholine paralytics--5mg neostigmine + 1.0 mg glycopyrolate
Opiates--40-80 mcg naloxone, repeat repeat as needed
(note: a typical vial contains 400 mcg)
 ART line if repeat ABGs are likely
13


Intubate if condition not readily reversible
Consider brainstem infarct or stroke, herniation: CT scan
II.





Airflow problems
Assess severity, assess CO2 changes in response to inspired O2
Unilateral, consider tumor or foreign body, obtain CXR
Diffuse, use bronchodilators, supplemental O2, steroids, IV Epi 10ng/kg/min
ART line if repeat ABGs are likely
May need to intubate or use BiPAP if work of breathing exceeds strength and
reserve
III.






Excessive work of breathing (Rapid-shallow pattern)
BiPAP or mechanical ventilation
ABG
Exam directed to rule out PTX
CXR
Consider ART line if repeat ABGs are likely
Evaluate for metabolic causes of increased respiratory rate
• Remember: patients in extremis have a high catecholamine tone (assume an
invisible Epi drip at 50-75 ng/kg/min). Any type of sedative, anxiolytic, or
induction agent will decrease the catechol drive and cause a rapid circulatory
collapse. Placement of an ART line, and assembly of vasoactive drugs and
fluids should be done whenever possible prior to intubation.
14
Physiology and Disruption of Oxygen Transport
Understanding the physiology of ventilation and oxygen transport is
fundamental to the evaluation and stabilization of any critically ill patient. The
principles of oxygen transport are also used to sort out diagnostic dilemmas, as a
guide to empiric therapy, and to help define end points of therapy.
Oxygen delivery (DO2) is the product of cardiac output and arterial oxygen
content (CaO2) as described in the equation below (see box), and under normal
conditions greatly exceeds the demand for oxygen (VO2: per minute oxygen
uptake or utilization). Under normal conditions we function with a great deal of
physiologic reserve where the oxygen supply–demand relationship is described
by the right portion of the curve below. As oxygen delivery decreases in the
supply-independent region, and while oxygen consumption (VO2) remains
constant, more oxygen is extracted per volume of blood at a given time. In low
cardiac output states and in hemorrhage, this is appreciated by a decrease in
mixed venous O2 saturation from the normal value of 70 percent. When oxygen
delivery decreases into the supply-dependent region, mitochondrial respiration is
limited by oxygen delivery, and a transition to anaerobic metabolism takes place.
The value of DO2 which divides the supply-dependent and supply-independent
regions is termed the critical oxygen delivery threshold.
15
Blood pressure is maintained within a certain range for each individual by
homeostatic mechanisms that include antonomic reflexes, capillary fluid shifts,
and modulation of neurohormones. Blood pressure is important to the body
because the various solid organs have adapted their ability to maintain constant
blood flow to a certain range of blood pressures (autoregulation, see figure
below). For healthy, normotensive people the brain and kidney autoregulate
their blood flow at mean pressures between 50-150 mm Hg (black curve in the
figure below). However, many of our patients have curves shifted to the right-meaning that kidneys, brain and brainstem, etc. may need higher pressures in
order to maintain uniform tissue oxygen delivery (the red curve). The overall
autoregulatory range of your patient needs to be deliberately considered, and
can be inferred in many cases, by a combination of bedside examination and
inspection of historical blood pressure data and its correlation with organ
function. Poorly controlled hypertensives have fairly dramatic right shifts to their
autoregulatiory curves.
Shock results from a mismatch between oxygen supply and demand, the
latter leads to changes in cellular function that may be either short-lived or
permanent.
A normal BP does not assure normal oxygen delivery, and vise versa. For
example, when hemorrhage exceeds 20% of blood volume, will one likely
see a decline in BP. Likewise, the high cardiac output seen in many septic
patients often contributes to an adequate oxygen delivery, but at a blood
pressure that is beneath the renal autoregulatory set point. Both scenarios
can lead to organ failure.
16
Conditions that require evaluation of oxygen delivery status:
Bedside findings
 Hypotension
 Oliguria
 Tachycardia
 Tachypnea
 Fever
 Hypothermia
 Lethargy
 Confusion
Abnormal laboratory findings
 Elevated anion gap
 Anemia
 Acidemia
 Alkalemia
Decreases in oxygen supply cause a short term transition to anaerobic
metabolism; glycolysis without oxidative phosphorylation is unable to sustain
ATP production and cell health for prolonged periods. When cardiac output or
blood pressure is too low for prolonged periods, or when cytokine levels are
elevated, endothelial damage occurs, and microvascular thrombosis further
impairs capillary blood flow. The pathophysiology of single organ failure by either
sepsis or hypoxic damage has a number of key characteristics (cytokine release,
neutrophil and mononuclear cell activation, endothelial cell dysfunction and
microvascular thrombosis) that lead to additional organ failure at other sites.
There are definitions for the various forms of shock that are useful for
research protocols and epidemiologic studies. Attaining diagnostic criteria for
shock is not a prerequisite for aggressive administration of fluids, inotropes,
vasopressors, or admission to an intensive care unit. Overall, organ failure is
further accelerated by prior injury or vulnerability—for example, renal failure or
atherosclerotic disease of any major vascular bed. Known solid organ
vulnerability should push one toward early aggressive therapy.
17
Circulatory Shock: Strategies for Evaluation and Stabilization
Change in mental function, agitation, oliguria, chest pain, and tachypnea
are common clinical findings that are usually seen in the natural history of shock
and organ failure. When called to evaluate patients with such complaints, the
tendency is to hang on to some reassuring sign (such as normal mental status)
and then assume all is well and not seek any additional information. A preferable
approach is one that assumes something is wrong until proven otherwise. Since
the patient is at highest risk for cardiopulmonary arrest if there are problems with
oxygen assimilation and transport, understanding the status of these processes
should quickly follow the initial ABC survey.
Much of what follows is further elaboration on the general ABC-VDE
scheme presented earlier in Immediate assessment and stabilization. A point to
always remember is that problems with oxygen delivery leading to organ
dysfunction are not always accompanied by hypotension. Indeed, the only
hemodynamically-oriented therapy for septic patients that improves survival is
one that incorporates analysis of serum lactate as a trigger point for early
aggressive therapy.19 Lactate is essentially, an convenient measure of the VO2 /
DO2 relationship.
Patient Care Priorities
Stabilize airway and breathing, administer appropriate oxygen
Look for circulatory abnormality—cardiovert if needed; call for help
Obtain vitals and oxygen saturation
Obtain appropriate IV access
Address tissue oxygen delivery with ABG
Consider other studies: stat glucose if pt. is unresponsive, ECG, electrolytes
Use physical exam to evaluate CO, SVR, blood loss, pulmonary function
AB
C
V
D
E
Treatment for stroke, myocardial infarction, hemorrhagic trauma and major
pulmonary embolus are surrounded by the concept of a “golden hour” or similar
time frame within which treatment should be instituted. Treatment of
hypotension, organ dysfunction, sepsis, and most other medical conditions lack
clear time guidelines. Even with this being the case, it’s hard to think of any
physiologic abnormality for which it is acceptable to leave the bedside before
being corrected. Decisions regarding whether a patient belongs in an ICU or
step down unit, the rapidity of resuscitation, how to budget your time, and
whether to call in help depend not only on the current vital status, but also on the
extent of organ dysfunction. A general inventory of end-organ function can be
gained by considering the question on the chart below.
18
Evaluation of Tissue Function and Oxygen Delivery




Question
Is oxygenation and ventilation normal?
Is the body in an anaerobic mode?
Is the problem with bound oxygen?
Is cardiac output adequate
How Addressed
O2 sat, PaO2, PaCO2
pH, base deficit, lactate, anion gap
Hemoglobin, co-oximetery
SvO2 or surrogate, capillary refill,
 pH in presence of normal [Hb], cold patient
Most blood gas analyzers can answer all of these questions with a single sample
Other supporting data can come from exam and laboratory findings that address “organs at risk:”




CNS or brainstem injury?
Metabolic abnormalities?
Renal function?
Liver function?
Orientation, memory, respiratory pattern
Electrolyte analysis, anion gap, lactate
Creatinine and urine output
Tansaminases, bilirubin, PT, PTT
Treating hypotension or a low perfusion state is usually accomplished with
a combination of fluids, blood, inotropes, or direct vasopressors. The most
appropriate choice in a given situation hinges on whether the problem is one of
preload, anemia, contractility, or lack of vascular tone. After quickly establishing
the presence of a blood pressure or organ blood flow problem, it becomes
essential to understand its root cause. The figure on the following page breaks
down decreases in BP and DO2 into their constituent parts. As with similar
figures in this text, physiologic roots are printed in black, findings from monitors,
labs and exam are in red, and common diagnoses for each category are printed
in blue.
While some of the physiologic data is presented as values obtainable by
way of a pulmonary artery (Swan-Ganz) catheter, having such a catheter is not
considered a necessity in caring for the critically ill. What is important is to ask
the right physiologic questions and to assemble them in a coherent picture.
Life Without a Pulmonary Artery Catheter:
Examining Physiology by Physical Exam
 CO
Cold extremities, distant pulses, acidosis, SvO2.
Try to figure out whether a decrease in CO is due to
hypovolemia or due to pump failure.
Pump Failure
Distended neck veins, S3, cold extremities
 Preload (CVP)
Flat or absent neck veins, tachycarida.
 Preload (CVP)
 jugular vein distention, enlarged veins elsewhere
SVR
BP and mental state may be NORMAL.
Findings: Cold extremities, distant pulses
SVR
Hypotension is likely. Patient may be warm with full pulses if CO
is normal or elevated.
Other valuable studies:
 Spot Echo exam of the heart: addresses tamponade, CHF, ischemia, hypovolemia
 O2 saturation from CVP line or PICC line: provides indirect but meaningful estimates of the
adequacy of DO2, cardiac function.
19
Shock / Hypotension Diagnostic Tree
 Oxygen delivery (DO2)
Lactic acidosis
pH, anion gap, BE
Peripheral cyanosis
 end organ function
 Blood Pressure
or
or
 SVR
Sepsis
Spinal shock
Anaphylaxis
Heatstroke
Iatrogenic
 Cardiac Output
or
 Heart Rate
 Arterial Oxygen Content-Hemorrhage, Anemia
Severe hypoxemia
 Stroke Volume
Decreased effective stroke volume--classes of abnormalities
1. Contractility:
MI, Cardio shock, ( CVP,  PaOP,  SVR)
2. Preload / filling
PTX, tamponade, ( CVP,  PaOP,  SVR)
Hypovolemia, hemorrhage ( CVP,  PaOP,  SVR)
Tachycardia, dysrhythmia (loss of “atrial kick”)
3. Obstructive:
Pulm Embolus, ( CVP,  SVR)
High PVR with RV failure, ( CVP,  PAP, SVR)
High SVR, or AS with LV failure ( CVP,  PaOP, SVR)
Goals :
Stabilize BP with empiric fluids and vasopressors
Identify etiology and treat more specifically
Exception: Arterial ruptures: AAA, dissection, intracranial bleed
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Therapy for Hemodynamic Instability
Unstable patients require simultaneous diagnosis and
treatment of underlying physiologic derangements.
In evaluating an unstable patient, it becomes crucial to develop some
sense of how soon you need to normalize a patient’s status (5 minutes, 10
minutes, one hour?). This type of decision can be made quickly, based on
known medical problems, what is know about the acute condition and its natural
history, and the patient’s current status (acidotic, ST changes, chest pain,
oliguria, hypotensive, etc.). For example, you may be able to show a bit more
patience in waiting for fluid infusion to normalize the blood pressure in a young
patient with an infection, than in an elderly patient who also has renal
insufficiency, cerebral vascular disease, or coronary disease. If in doubt, treat
early.
Resuscitation and supportive care of many critically ill patients ends up
using a careful combination of fluids, inotropes, and vasopressors, based on
considerations of the patient’s cardiac status, normal blood pressure, and current
status of oxidative metabolism and solid organ function. The typical manner for
maximizing cardiac performance, oxygen delivery and blood pressure is in order:
titrate in fluids, evaluate cardiac output and use inotropes as indicated, and finally
use alpha agonists to maintain blood pressure in an acceptable range. Because
you’re not going to arrive at this “solution” immediately, you are certainly justified
in treating an abnormally low blood pressure by making crude estimates of filling
pressures, cardiac performance, and SVR and giving fluids or vasoactive drugs
according to your hunches. This will keep your patient alive in the short term,
and buy you some time to get it right later.
In attempting to maximize oxygen delivery, often one forgets the need to
minimize oxygen consumption. The table below gives some examples of how
certain stresses can increase oxygen demand.
Condition
% Increase Over
Resting VO2
Fever
8% (for each 1C increase)
Work of breathing
40%
Severe Infection
60%
Shivering
50% - 100%
Burns
up to 100%
Endotracheal tube suctioning
27%
Sepsis
50% -100%
Head injury, patient sedated
89%
Head injury, patient unsedated
138%
Thus, seemingly insignificant acts such as keeping the patient warm, treating
fever, and planning diagnostic procedures can be as efficacious as increasing
cardiac output with fluids or inotropes. A patient with a severe metabolic acidosis
21
or lung injury can have about 30% of his oxygen consumption dedicated to the
work of breathing. In other conditions where pulmonary compliance is poor, the
amount of work required to maintain a reasonable minute ventilation can be
likewise astronomical.
When blood flow to vital organs is compromised, institution of
mechanical ventilation will “free up” diaphragmatic blood
requirements, and increase the oxygen available to the rest of the
body. Mechanical ventilation should be seriously considered on
these merits alone, independent of lung injury.
On the following pages, a more general scheme for early resuscitation of
hypotension and shock is presented.
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Shock / Hypotension Treatment Outline
The goal of most resuscitative strategies is rapid normalization of blood
pressure and oxygen delivery. The plan for complete resuscitation and
normalization of blood pressure is more negotiable in cases hemorrhagic shock,
cerebral hemorrhage, and arterial bleeding. Rapid identification of such processes
and consultation with an appropriate service is a high priority, and discussions
regarding resuscitation end points should take place quickly. Likewise, suspicion
for cardiogenic shock should lead to immediate consultation with cardiology
regarding early revascularization. Following the ABC-VDE evaluation, use the
guide below as a checklist and a guide to pharmacotherapy. Different centers may
have different methods and protocols for resuscitation. Whichever you end up
using, the most important thing is that you make a constant cycle between: a plan
for action the action an assessment of the action and its impact  and a
reassessment of the situation which leads to the next plan of action, and so on. In
management circles this is known as a PDSA cycle for “plan, do, study, act.”
Priority #1. Normalize Blood Pressure:
 Crystalloid fluid: 1-2L over 10-15 minutes. 2 X 18g, or 16g or percutaneous
introducer. May need pressure bag. Triple lumens are generally inadequate.
 Vasopressor or inotrope to maintain oxygen delivery and BP. Want to normalize BP
in 2-5 minutes after IV access is established. A new stable peripheral IV or PICC
line is OK to use for initiial use of vasopressors.
• Phenylephrine 100mcg IV q 1-5 minutes (may  HR)
• Ephedrine 5-10mg q 3-5 minutes (will HR)
• Epinephrine 10-30mgc IV q 2-5 minutes (will HR)
• Dopamine 3-10 mcg/kg/min. May need bolus of phenylephrine or
ephedrine until target dopamine levels are achieved
 Place Art line. Consider femoral (16g single lumen) if MAP < 55
 Place central line for CVP, vasoactive drips, venous 02 saturation
Priority #2. Define nature and severity of injury:
Labs and Diagnostics:
Exam:
ABG
skin color and warmth
CBC, PT/PTT*, DIC*,
pulse character
Lactate
alertness, memory
Electrolytes including glucose
breath sounds
Mixed venous O2
heart sounds
Type and screen*
pain
CXR*
subjective complaints
EKG,* Echo*
evidence of bleeding
Cultures*
*as indicated by clinical situation
Priority #3. Treat underlying cause as soon as it is known or suspected:
Antibiotics, Gluccocorticoids, Blood and fluid replacement
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Acute Blood Loss
Patients may experience sudden and massive blood loss for a variety of
reasons-the most common being traumatic injury and/or surgical blood loss.
However medical patients can also experience sudden and massive blood loss
(i.e. GI bleed, hemoptysis, leaking AAA) and thus require an expeditious
resuscitation to reduce morbidity and mortality. Traumatic blood loss and
resuscitation is an especially dynamic process involving factor and fibrionogen
consumption, dilutional coagulopathy, and further interaction between the
coagulation system, temperature, and anoxic tissues. A full discussion on the
management of hemorrhagic shock is beyond the scope of this text; instead, the
concentration will be on non-traumatic blood loss.
When faced with massive and sudden blood loss in a patient, one should
immediately call for help to mobilize all available resources. Help includes fellow
residents, a stat surgical consult, anesthesia, crisis/ICU nurses, and the ICU
fellow/team. Initial patient assessment should include ABCs assuring an
adequate airway and placing the patient on 100% oxygen. Circulation should be
assessed with the goal of aggressive treatment of tachycardia and hypotension
with IV fluids.
Stat laboratory tests for CBC, ABG, coags, lactate, and type/cross should
be drawn immediately by bedside personnel and taken directly to the lab for
urgent processing. Care team members should establish adequate IV
access,14-16g peripheral IVs or a “Cordis” introducer for rapid fluid
administration. A triple lumen cath is inadequate. If present and it is difficult to
find additional access consider changing to an introducer over a wire. Nurses
should be alerted that you want blood pumps connected to blood warmers so
that these will be ready at the time you place the IV lines.
If blood is needed immediately, before the blood bank has time to set up
type and crossed units, send a runner to the blood bank and request a “trauma
bucket” which should contain 6 units of O negative blood. Ideally type and
crossed blood should be given. In the event that is not ready, then type specific
uncross-matched blood is preferable followed by O negative. As the initial
resuscitation proceeds, plans for definitive treatment of the bleeding should be
made (i.e. OR/cath lab, etc) as well as transfer to the ICU for further care and
management. Depending on the rate and amount of the blood loss you may
have to replace the circulating blood volume several times until the bleeding is
controlled. As one approaches 1.5 blood volumes transfused (adult range of 7-8
liters), a dilutional thrombocytopenia and coagulopathy may develop. Expect to
give fresh frozen plasma (FFP) and platelets after two blood volumes have been
transfused or earlier if there is laboratory evidence to suggest a more aggressive
transfusion need (platelet count less than 80 or PT/PTT greater than 1.5x
normal). FFP, if given in adequate volume, should replace clotting factors and
fibrinogen. However, if the fibrinogen continues to be less than 1.0 g/L then
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cryoprecipitate should be considered. Throughout the resuscitation heart rate,
blood pressure, SaO2, mental status, and urine output should be monitored
continuously (consider Art line/CVP).
Throughout the resuscitation, heart rate, blood pressure,
SaO2, mental status, and urine output should be monitored
continuously (consider Art-line / CVP / foley).
Rapid Transfusion
Rapid transfusion of large volumes of stored red blood cells can result in several
potential dangerous complications.
When the rate of transfusion exceeds 1 unit every 5 minutes there is a risk of
hypocalcaemia from citrate toxicity. Signs of hypocalcaemia include
hypotension, flat T waves, prolonged QT interval and a widened QRS complex.
This should be treated with 500-1000 mg of IV CaCl2 via a central line or calcium
gluconate via a peripheral IV.
The reduced concentration of 2,3-DPG in the hemoglobin of stored PRBC results
in a left shift in the Hb-oxygen dissociation curve and less availability of oxygen
at the tissue level.
Hyperkalemia can result from increased potassium from lysed red cells in the
stored blood. In blood stored greater than 21 days K can be as high as 35
mEq/L.
Micro aggregate formation occurs in the stored units and can cause pulmonary
insufficiency and ARDS when patients receive massive transfusions (>10
units/24hrs).
PRBC are stored at temperatures between 1-6 degree C. Failure to use a blood
warming device can result in significant hypothermia. This can result in
increased risk for the development of DIC, and less activity of existing clotting
factors. Furthermore, hypothermia is associated with a higher mortality rate in
massively transfused patients.


Failure to warm the blood prior to transfusion can
result in significant hypothermia.
Replacement of red blood cells should take priority
over coagulation factors when resuscitating the
acutely hemorrhaging patient.
Acute pain
25
There is no diagnostic or therapeutic yield in leaving a patient in pain. Major
abdominal pathology, dyspnea and bone pain can still undergo appropriate
evaluation without the added distress of nociception. Some points on the
practical physiology of pain can be summarized:







The perception of pain is highly subjective and cannot be easily quantified across a
heterogeneous population.
Pain is a significant stimulant of the sympathetic nervous system, and can exacerbate
coronary and vascular pathology.
Pain exacerbates psychiatric pathology.
Controlling pain later is generally more difficult than treating at the earliest opportunity.
Poorly controlled pain can lead to other limb-pain syndromes or chronic pain.
Agents such as NSAIDS and acetaminophen are terrible PRN drugs, but great as round-theclock agents in a comprehensive pain control scheme.
Opiate tolerance is not opiate addiction, and may be acceptable in the short term.
Like other abnormalities in the vital status, extreme
pain needs to be controlled acutely at the bedside.
Here is an example of the acute management of incisional pain:





Fentanyl in 25-50 mcg boluses are given to the opiate naïve person with a small
incision; 50-100 mcg with a younger patient, 100-200 if opiate tolerant.
Look at prior dosing histories to get some idea of tolerance and effective doses (cath
lab reports, anesthesia records and ER sheets).
Continue boluses every 2-4 minutes until the pain score becomes 2-3.
Give a few doses of morphine 2-5 mg and monitor for respiratory depression.
A nurse can continue with morphine 2-5 mg q 15 min, until a PCA is ready.
Drug
_______
Morphine
Fentanyl
Dilaudid
Meperedine
Vicodin
Methadone
Equianalgesic
Dose
10 mg
100mcg
2 mg
75 mg
8 tablets
10 mg
Cautions / notes
Venodilation via histamine mechanism, n/v, pruritis
No venodilation
Less pruritis and n/v than morphine
Aviod for pain, use 25-50 mg for shivering & rigors
4g Acetaminophen at this dose--don't exceed
No role for acute control
Some like morphine for acute coronary syndromes because its venodilatory
property also lowers myocardial wall stress.
Reversing opiates
 The ER uses 0.4 mg of Naloxone to reverse possible opiate effects in
comatose patients. For the respiring patient, this is too high a starting dose.
Overdosing naloxone will make your patient absolutely wild, and produce a
dangerous hypertensive crisis.
 1/10 of a vial (40 mcg) in q 1-2 minute escalating doses will reverse
respiratory depression without antagonizing the analgesic properties.
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