SCARED
Stanford
Course on
Active
Resuscitation,
Evaluation, and
Decision making
2005
Geoff Lighthhall MD, PhD
Assistant Professor, Anesthesia and Critical Care
Stanford University School of Medicine
Course Faculty:
Geoff Lighthall MD, PhD
T. Kyle Harrison MD
Department of Anesthesia
Stanford University School of Medicine and
VA Palo Alto
Patient Safety Center of Inquiry
1
SCARED
Introductory Material:
Epidemiology and physiology of patients that experience cardiopulmonary
arrest
3.
5.
Introduction to the course
Medical illness, the golden hour, and missed opportunities to prevent
cardiopulmonary arrest
Evaluation and Stabilization of Critically Ill Patients
Recognition and resuscitation of unstable patients
12.
14.
20.
22.
25.
28.
31.
33.
34.
38.
Immediate assessment and stabilization
Respiratory failure: Physiology of respiration and gas exchange
Stabilization and therapy for respiratory problems
Physiology of oxygen transport abnormalities
Circulatory Shock & Hypotension
Therapy for hemodynamic instability
Acute blood loss and massive transfusion
Acute pain
Leadership in medical emergencies
References
2
I. Technical skills for early resuscitation
Why bother spending another nice evening in the hospital? In short, we
want to leave you confident and ready to tackle the problems of the hospital's
sickest patients, and to start thinking how you may function better as a member
or leader of a resuscitation team. This is an important area that is generally
neglected in medical training, yet in a perfect system, should be the one that
receives extra attention. The drive to offer this course came from discussions
and questionnaire responses from the VA ICU simulator course where
participants voiced an interest receiving additional training in managing
emergencies and cardiac arrests--and specifically, the technical aspects of such
care.
The types of emergencies you will be called to manage can be crudely
classified as cardiac arrests—the four prototypic ACLS emergencies—and pre
arrests. While good skills in managing code patients is important, we also
recognize that even with the best team and effort, a meaningful survival is rare.
Since most cardiac arrests result from medical problems that if corrected, offer a
much better potential for survival, and since such problems persist for a while
before becoming “arrests,” proper management of the pre-arrests is crucial.
Indeed, improving the care of the latter set of patients has provided a great deal
of motivation worldwide for the development of medical emergency teams, and
personal motivation for offering this course.
The patients you will manage in this course may have conditions that
degenerate to cardiac arrest. So while we will provide experience with some
code situations, also think about how tragedy can be averted before the onset of
cardiopulmonary arrest. By the conclusion of this session, you will hopefully
have some fear for the patients who require emergent help as well as the sense
that you have more to offer.
Goals





Provide mentorship and training in specific critical events using both short
discussions and hands-on experience with human patient simulation.
Take what you already know about the pathophysiology of critical illness,
cardiac instability, and ACLS, and repackage that knowledge in a system that
might be of greater utility.
Focus on your role and responsibilities as a team leader
Provide some check lists and hand cards that can be of use in a real
emergency.
Give you some guidelines and pointers on drug dosing and kinetics that you
can use in your practice
3
Overall Philosophy
The ability to prevent further decompensation and codes depends upon
how clearly you understand the nature of a patient’s problem and the need to
correct it. We focus on the issues of respiration and tissue oxygen delivery as
the common origin of most emergencies that result in “codes.” Our approach is to
analyze the physiologic roots of cardiovascular and respiratory problems, and
use this knowledge as a guide toward earlier early empiric therapy, and hopefully
rapid treatment of unstable patients. This approach is apparent in the cards or
“cognitive aids” that we have made.
Cognitive Aids
There is plenty of scientific evidence that people under stress function at a
small fraction of their overall mental capacity. Somehow, medicine has confused
patient safety and administration of acute care with performance art, and has
been reluctant to accept the idea of its practitioners using cards, cheat sheets,
phone calls, or other reference material when lives are at risk. There is no
weakness in using such materials in managing a stressful situation. Once you
accept this view, you will be far more useful and reliable in emergencies.
For this course, we have made a great effort in assembling information in
a relevant format for your use in emergencies. The cognitive aids you will
receive have been developed by the course instructors who have extensive
experience studying how others manage emergencies, how physicians behave
under such stress, what kinds of information physicians need to manage
emergencies, and what type materials currently in use work and don’t work. The
cognitive aids here come in a few flavors:




Simplified ACLS algorithms
Physiologic roots of key hemodynamic and respiratory problems
Check lists for airway, breathing and circulatory emergencies (A, B & C cards)
A card that describes emergency management in general
Each type of generic problem (hypotension, shock, hypercarbia and
hypoxemia), is pulled apart into its various components with possible causes for
each noted. Using the shock/ hypotension card as an example, the physiologic
roots of low Blood pressure and low oxygen delivery are noted in black; “data”
that one may gather from monitors, lab studies and physical exam, are noted in
red; and likely diagnoses are in blue. By walking down a physiologic tree and
using available data to sort out which branches are more likely, one arrives at a
set of provisional diagnoses as well as the nature of the problem to be corrected
(low SVR, for example). If insufficient data is available, the information on the
card may also point out to you what additional studies or findings may be of
greatest yield or utility. Additionally, there is also a section on what the team
leader should be doing for each emergency.
4
II.
Background. Medical illness, the golden hour, and missed
opportunities to prevent cardiopulmonary arrest
In some disease entities such as major pulmonary embolus, myocardial
infarction, stroke and trauma, the benefits of early stabilization and treatment are
well-known. However, the extent to which survival from other forms of clinical
instability can be enhanced by rapid intervention has not been defined. Even
with reasonable face validity, this concept remains under-appreciated.
The educational mission of a teaching hospital may create some delays in
care that are deleterious. In most residency programs, interns and senior
medical students are given the responsibility as primary caretaker for
hospitalized patients. Despite the presence of more experienced fellows,
residents and attendings on the care team, tradition dictates that the team be
contacted through the intern or resident when a patient’s condition changes.
During night hours, the primary team in charge of a patient is rarely intact, with
some form of cross-coverage system (typically consisting of mid level resident) in
charge of emergency calls. Compliance with resident work hour restrictions
requires even greater reliance on shift care or cross-coverage schemes where
there is greater likelihood that physicians will be called about patients for whom
they have little familiarity. Overall, unless a diagnosis is immediately clear,
valuable time can be spent on an intern’s initial evaluation, subsequent resident
evaluation and further evaluation by other consultants before stabilization and
definitive therapy are initiated.
The overall strength of the current system has not been directly tested.
For example for every 1000 ward admissions, we have no idea how may of
these patients show signs of instability that result in calls to the house staff with a
subsequent evaluation or decision-making that corrects the patient’s course
without resulting in an ICU admission,cardiac arrest, or death. However, by
analyzing the converse--the natural histories of patients whose course does
result in death, cardiac arrest, or ICU admission--we do have a data set that is
quite revealing.
Antecedents to Intensive Care Unit admission
Patents admitted to an ICU from an impatient ward have a higher mortality
than those from other hospital locations (2). Studies evaluating patterns of ward
care prior to ICU admission show a general lack of time urgency in evaluating
and treating patients with abnormal vital signs and other forms of deterioration (35) . With appropriate adjustments for co-morbidities and disease severity,
patients initially admitted to hospital wards (as opposed to ICU) had up to a fourfold increase risk of mortality, suggesting that the nature of the care was a more
significant determinant of ultimate clinical trajectory than the admitting diagnosis
(3). Deterioration in the admitting condition or the development of new problems
were key risks for a worse outcome (3).
In another study, a different group investigators had experts rate the
quality of care provided to patients admitted to the intensive care unit (6). Care
5
was rated as either “well managed,” or “deficient,” or “equivocal” if the raters
could not agree. The group of patients considered to have suboptimal care had
twice the ICU mortality rate of the other groups. Areas considered problematic
were: timing of admission (late), and management of oxygen therapy, airway,
breathing, circulation, and monitoring (6). Reasons for underlying suboptimal
care were “failure or organization, lack of knowledge, failure to appreciate clinical
urgency, lack of experience, supervision, and failure to seek advice.” Our own
experience in examining dynamic decision making of house staff in a fully
simulated ICU revealed similar classes of deficiencies, including non-adherence
to established protocols (7).
In reviewing studies of the pre-ICU phase of patient care, it is attractive to
think that all problems would be solved solely by earlier admission or transfer to a
higher level of care. This is not always practical in situations where ICU beds
may be in short supply. Even when ICU beds are abundant, a number of
personal and professional barriers may prevent clinicians from admitting patients
with real but non-catastrophic abnormalities. These barriers can be summarized
as follows:







A lack of familiarity with the ICU that may prevent some from considering
transfer to this setting (17).
A mentality that tends to block admissions to patients unless they need
mechanical ventilation, invasive lines, or other high-order intervention. The
mentality generally ignores the type of patients that are the most likely to gain
the greatest yield from intensive care resources.
A vague sense of personal failure that comes from admitting a patient to the
ICU, and a sense of pride that comes from preventing an ICU admission.
A related sense of personal duty to try to do everything for the patient before
admitting that there are forces you cannot control.
A general reluctance to ask for help or sense that you shouldn’t.
Competing educational missions that prevent one from wanting to give up a
“good teaching case.”
All of the above PLUS lack of involvement of attending physicians.
Antecedents to cardiac arrest calls
Cardiac arrest is not only the result of cardiac decompensation, but the
final common pathway for all lethal disease processes that go uncorrected. The
potential for survival is largely lost at the time of cardiopulmonary arrest. In one
study covering over 12,000 admissions to intensive care units in the UK, 33% of
all mortality followed cardiopulmonary resuscitation (2). Other large series of
cardiac arrests show an initial resuscitation rate of 25-40%, but subsequent ICU,
and hospital survival rates that drop sharply to the range of 10-15%, with even
fewer making a full neurologic recovery (5, 8, 9).
Patients admitted to the ICU following cardiac arrest have allowed
retrospective analysis of factors presaging their decompensation. Two different
studies of antecedents to cardiac arrest demonstrated that between 75%- 85% of
the affected patients had some form of deterioration in the hours prior to the
6
arrest (4, 10). Nearly a third of such abnormalities persisted for greater than 24
hours prior to arrest, with a population mean of 6.5 hours (4). In Schein’s series,
the vast majority (76%) of the disease processes eventually progressing to
cardiac arrest were not considered to be intrinsically rapidly fatal. In yet another
series over half of the arrests presented ample warning of decompensation: the
majority had uncorrected hypotension, and half of these had systolic blood
pressures less than 80mm Hg for more than 24 hours. Others had severe, but
correctable abnormalities such as hypokalemia, hypoglycemia and hypoxemia
(11). The collective experience suggests that the quality of care, more than the
disease may be responsible for the poor immediate survival of these patients.
Inattention to, or unawareness of a developing serious problem causes the
additional problem of hasty decision making at the time of cardiac arrest. Once a
cardiac arrest has occurred, the clinicians hand is forced and ICU admission
becomes mandatory.
Why does this poor care preceding cardiac arrest occur? Problems with
establishing proper care were found to exist at multiple levels: nurses were not
calling physicians for patients with abnormal vital signs or changes in sensorum;
physicians did not fully evaluate abnormalities when they were contacted; ICU
consultants were not called in routinely, and even senior level or consulting ICU
caregivers did not obtain routine studies such as blood gasses, hematocrits and
electrolyte studies that would have defined the patient’s problem. In cases when
laboratory studies were done, they were not always interpreted correctly, and
when they were, therapy was not always initiated (5). The pattern is shown
graphically to demonstrate that the timely pairing between an abnormality and
therapy--the reason to have someone hospitalized---does not occur.
A continuum exists between common physiologic abnormalities and their
deterioration into a code. Thus while you cannot be a ‘little bit’ pregnant,
you can have a ‘little bit’ of VT, VF, pulseless electrical activity and
asystole.
7
The ideal situation for a patient would be one in which a problem requiring
treatment would manifest itself as some type of abnormality that would be
recognized and acted upon in a tolerable amount of time. Given that this is a
multi-step process in hospitals, the best analogy for a successful intervention
would be a series of dominoes aligned such that triggering one is sure to activate
the whole cascade in a predictable manner. What seems to be the case,
however, is the existence of a series of roadblocks that allow only a certain
percentage of traffic on to the next. The efficiency of throughput is highly
variable, and is dependent on individual behavior and skill, cultural factors and
other constraints.
Common denominators amongst critical events
In this case, critical event consists of either a code or an unplanned ICU
admission--events that have been quantified in the literature that can be traced to
underlying conditions or prior care as was done in the sections above. Looking
at the literature as a whole, what stands out is the precarious nature of patients
with the conditions listed below:
8
Conditions underlying critical events (given as a percentage of patients studied):
Condition
Tachypnea
Hypotension
Tachycardia
GI bleed
Cardiac/ MI
Death 3,20
8-15
19-27
4-10
n/d
Unplanned
ICU admission15
Readmitted
to ICU 15
Cardiac
arrest 10
20-50
10-15
8
15
37
10-25
10-30
15
12
Multiple
30-45
26
The bottom line seems to be that respiratory insufficiency, hypotension, and
tachycardia, along with depressed or altered mentation (not shown) are key
findings that define patient deterioration in the pre-code stage. As far as things
go, this is also fairly easy to catch. The vast majority of such abnormalities were
present for hours prior to the “critical event.” That is not to say that all such
abnormalities warrant ICU admission, but they do warrant a real evaluation and
stabilization at a time when survival is possible (now), rather than later when
survival is poor.
III.
The experience with early response teams
Early response teams, or medical emergency teams (METs) were created
with the goal is of improving the care and outcome of acutely worsening
inpatients. The concept was an outgrowth of the work done in Australia and cited
above, documenting the poor care preceding critical events. The common
theme amongst hospitals instituting response teams is the creation of clear
criteria for calling the team for a patient evaluation (see below). (12, 13, 19).
Teams are mostly composed of senior ICU nurses in the UK, and senior
residents and clinical fellows in Australia.
Criteria for Calling VA Palo Alto Emergency Team (e Team)
Airway
Respiratory distress
Threatened airway
Breathing
Resp rate > 30/ min
Resp rate < 6/ min
SaO2 < 90% on oxygen
Difficulty speaking
Circulation
Systolic BP < 90 mm Hg despite treatment
Pulse > 115/ min
Neurology
Any unexplained decrease in consciousness
New onset of agitation or delerium
Repeated or prolonged seizures
Other
Concern about patient
Uncontrolled pain
Failure to respond to treatments
Unable to obtain prompt help or assistance
9
In non-academic centers, a crisis nurse and respiratory therapist constitute the
team. At the University of Pittsburgh, the “medical emergency team” has the
same members as the cardiac arrest team, but is paged in a slightly different
manner. At the start of the 2005-2006 academic year, a medical emergency
team will begin operation at VA Palo Alto (the “e Team”). Criteria for calling the e
Team are listed above.
Evaluation and efficacy of early response teams
The impact of these teams has been evaluated by retrospective,
concurrent, and multi-institutional models. In one UK hospital, vital status criteria
such as those above were distributed and it became compulsory to contact the
primary caregiver if any were present. A medical response team consisting of
senior registrars (PGY 3-5 equivalents) and ICU nurses was created, but was not
required to become involved in the care unstable patients unless requested by
the primary caregiver. Compared to patients not attended to by the emergency
team, the authors found significant decreases in cardiac arrests and ICU
mortality rate (14). In Australia, the impact of an emergency response team
instituted in one hospital was compared to two other hospitals that had traditional
cardiac arrest teams (13). An increase in rates of new DNR orders and a
decrease in mortality in patients with full code status was attributed to the team’s
operation. In another Australian study, Buist described a program that led to
significant decreases in cardiac arrests, hospital mortality and ICU death (19).
Some believe that the success of the latter study is attributable to an increase in
the diversion of terminally ill patients to a palliative mode of care rather than
allowing the usual course of cardiopulmonary resuscitation, ICU admission and
death. If so, this still constitutes a meaningful intervention that promotes patient
comfort, minimizes distress, and conserves valuable resources.
The other value of an ICU-based care team is the follow up of patients
recently discharged from intensive care. As a population, former ICU patients
have a two-fold higher rate of cardiac arrest than other ward patients (5), and a
four to eleven-fold increase in the risk of in hospital death (15, 8). A primarily
nurse-staffed team that followed post-ICU discharges was associated with an
increased likelihood or survival to hospital discharge, and a significant decrease
in ICU readmission (12). A study by Leary, however, did not find confirm that a
medical response team changed the rate of readmission (16).
10
Summary of Rapid Medical Response Teams Described in the Literature
Study author
Mortality
Cardiac arrest
Buist, 200219
Decreased 2.5%
Decreased 50%
Ball, 200312
Decrease 6.8%
Decrease 6.4%
readmissions
NO decrease in
readmissions
17% decrease
Decreased
incidence
Unchanged
Decr. (RRR 65%)
Leary, 200316
DeVita, 2004
Goldhill, 199914
Bristow, 200013
Bellomo, 2003
Bellomo, 2004**
Ball.
Leary
Bellomo *
Unchanged
Decr. (RRR 26%)
Decr. 37%
ICU admission
Morbidity/ LOS
DNR orders
Increased
Decreased
incidence
Decreased (control OR 1.24-2.16)
80% Decr*
Decr. In organ failures (range 57-88%)
Decr. Mean LOS 4 days
Examination of patients post ICU discharge
Examination of patients post ICU discharge
ICU beds occupied by cardiac arrest survivors ** postoperative patients
Summary; the prognosis of deteriorating patients
Disease processes with a reasonable survival are being converted to low survival processes such as cardiac arrest
and multi-organ failure. Some patients are not appropriate for resuscitation. Survival of cardiac arrest victims is uniformly
poor, yet a fair number end up in intensive care units and don’t do well even after staying there for prolonged periods of
time. With warning signs present, many caregivers feel little pressure to act on abnormalities, yet failing to do so may
result in a higher pressure situation (arrest), where decision making may be flawed, and where errors may occur more
frequently. Establishment of a medical emergency/ early response teams have provided a heterogeneous array of
benefits including improved survival, and prevention of futile resuscitation. Establishing such a team requires a
commitment on an institution and its members to acknowledge shortcomings and weaknesses in the current system, and
to reorganize responsibilities and priorities in a manner that is more likely to improve patient survival and hospital resource
use
11
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.
12
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.
13
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 usually 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,
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.
14
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
15
For purposes of clarity, we are considering airway and breathing issues
separately. Examination of pulses and circulatory status should occur
simultaneously, and will help you better understand the entire clinical picture.
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 such
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.
16
Hypoxemia
1. Decreased inspired/ alveolar
oxygen
Inadequate FiO2
Machine/ tank /
pipeline malfunction
Altitude
Extreme hypercapnea
Altered mental status,
Agitation
Oxygen desaturation
CV instability
2. Shunt, increased venous admixture
Intracardiac
Intrapulmonary
Anatomic --liver disease
Airway (mainstem intubation)
Alveolar (lung injury, hemorrhage,
PNA, capillary leak 2o allergy, PE, CHF)
2
3. High Oxygen extraction
exacerbated
by shunt physiology
Decreased SvO2
Decreased CO (see shock fig.)
Hemorrhage
High VO2 from sepsis, fever, etc
4. Inadequate ventilation
Increased CO2
Depressed ventilatory drive
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
Decrease in Static compliance (Increased P plateau)
lung injury, fibrosis, PNA, PTX, pulmonary edema (CHF, large PE)
Decrease in Dynamic compliance (Increased P peak)
Bronchospasm, mucus plug in airway or in tube, foreign body,
hyperinflation
17
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 paCO2 values,
and deviations from baseline values can often provide a valuable window into the
patient’s ventilatory status. Total ventilation (denoted by convention as V E)
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
Low CO2 tensions 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 oxyhemoglobin 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
(usually increased VE –usually normal to increased 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)
18
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; end
tidal 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
19
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
20


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.
21
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.
22
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 curve on the right). 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.
23
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
 Lactic acid elevation
 Increase in Creatinine or liver enzymes
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 involves the unleashing of biochemical mediators and
other processes (cytokine release, neutrophil and mononuclear cell activation,
endothelial cell dysfunction and microvascular thrombosis) that can lead to organ
failure at distant sites. For example, hemorrhage or abdominal sepsis can lead
to ARDS.
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.
24
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, this point is
consistent with current recommendations that lactate levels be measured in
septic patients and if abnormal, used as a trigger for early aggressive therapy. 19
Lactate is essentially, an convenient measure of the VO2 / DO2 relationship that
can be further corroborated with measurement of mixed venous oxygen
saturation.
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
BC
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.
25
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, and 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.
Often a compensation for low preload and/ or low CO.
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.
26
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, var 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
27
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)
Incr. Work of breathing (COPD)
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
28
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.
29
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.16 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.17 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 the business world, 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
See reference 18 for further review of evidence for treatments for septic shock
30
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
31
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, SaO 2,
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
32
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.
33
Leadership in Medical Emergencies.
The team leader has a difficult role and to make matters worse, medical education
offers nearly zero preparation or training for this role. ACLS training gives the
impression that if you can make the right diagnosis and apply the correct algorithm
with a certain amount of precision, everything else falls into place. Anyone can
walk into a room and say “give epi,” but is that realistic? Who has the epi? Is
someone placing an IV? Is there fluid to hook up to the IV when it’s in? Is the
same person who is doing all of the above the only one who knows how to give
drugs, work the monitors, and hook up pacing pads? Managing the chaos of a
code or resuscitation is always hard to script out, but some key principles of
communication and resource allocation are useful to consider and will serve you
well:








Know your environment. Know your team and their capabilities—don’t assign
tasks to non-experts whenever possible. Get better help if you are unsure.
Distribute the workload evenly, don’t create “bottlenecks” where only one
person is asked to do things or has the knowledge to get things done.
Don’t get involved in procedures, CPR, or other tasks that would distract you
from your leadership role or your ability to take in the “big picture.”
Communicate your general thoughts and priorities to the team. Get help if you
need.
Establish goals, and allow some autonomy in reaching those goals. For
example:
• give the nurse a range of doses to work with to reach a goal, state the goal.
• allow respiratory therapist to do whatever is takes short of intubation to
improve respiratory mechanics or O2 saturation.
Focus on significant actions, do not occupy skilled personnel with insignificant
tasks.
Don’t spout commands into the air. Calmly ask people to do things using their
names and eye contact. If more than one task is assigned, establish priorities.
Monitor who is doing what; follow up with individuals on progress at appropriate
intervals.
You can’t learn this overnight—well, maybe you can, but I can’t! Some of the best
ways to train for emergency leadership are to (1) observe others who are good at it
and spend some time thinking about specific things that seemed unusually good,
(2) practice in a controlled environment with proper mentorship (simulation), and
(3) to understand all of the different roles and tasks required by a resuscitation.
The latter can be achieved by going to codes and performing specific tasks (lines,
ABG, chart review), and seeing how these tasks mesh with other parts of the
operation. Likewise, just watch what specific people are doing and ask yourself
whether they are effective or not, overloaded or under loaded, assigned tasks
commensurate with their level of skill, etc. By knowing everything that goes on in
an urgent situation and the times and struggles associated with each, you will have
34
a more realistic idea of what you are asking others to do and how much time and
attention different tasks take.
The other side of leadership is knowing when to step back and look things
over. You may arrive at a scene where there is already adequate leadership.
Don’t let you job description get in the way of the best patient care. Your job isn’t
running the show as much as putting the patient first and doing what’s best for that
person’s survival. Use your leadership skills to support the existing efforts if they
appear to be on target. As you view a resuscitation effort, think about what gaps in
information or care exist, and make yourself useful by filling in these holes.
V. Treatment--General approach
Treatment decisions depend upon your goals, expectations, and what you think
the patient needs or can tolerate. It is important to have a sense of time: how
long the patient can last as is, and how fast things need to be corrected. Your
choice of agents will be impacted greatly by your time goals.
What abnormalities require treatment? Any
abnormal vital sign deserves your attention. But despite our ability to rapidly
normalize many aspects of our patients’ status, and that generally stabilization
should precede an exact diagnosis, the underlying diagnosis will dictate the
appropriateness of different treatment options and the overall goal of treatment.
Some exceptions to aggressive normalization of vital status are presented below.
Anormality
Hypotension
Tachycardia&
Bradycardia
Circumstances that may modify treatment plan
Arterial rupture; out of hospital trauma. Proceed to surgery before full
resuscitation.
If CHF, consider baseline BP (is this a result of therapeutic afterload reduction?)
Sepsis, hypovolemia, anemia. See notes below&
Hyperthermia
Consider observation over treatement if rhythm is NSR, patients is
hemodynamically stable or hypertensive; w/ aortic stenosis or severe CAD
Always treat in some way. Can get late respiratory depression when adding IV
opiates to epidural or spinal opiates. NSAIDS and renal; Tylenol and liver dz.
Modify treatment with head injury or with increased ICP. Caution; reflex
tachycardia with vasodilators. Beta block first with arterial injury or aneurysm.
Very hot or very sick may require aggressive treatment
Hypothermia
May be best untreated with brain injury or CVA if tolerated by heart. d/w neuro
Acute pain*
Hypertension
Hypopnea
May be necessary side effect of difficult to control pain; assess deep breathing,
airway, and alertness for danger signs; expect some resp. acidosis
SaO2 < 95%
Consider patient's baseline if COPD present.
-------------------* Always perform careful assessment; otherwise normal vital signs do not "rule out" a catastrophic
process.
& Sinus tachycardia in hospitalized patients is rarely a primary abnormality. It likely reflects a
compensatory mechanism. First, find the underlying cause, and treat tachycardia only if it is acutely
appropriate. Rate control of rapid A-fib is usually beneficial.
35
Regardless of abnormality, your response as the leader should be the same:
Assess  Plan Treat 
Re-assess  Plan Treat  Re-assess 
You need to treat a clinically significant vital sign abnormality in a single
encounter. If you are at a computer placing an order and not at the bedside with
a syringe in hand, you have missed this point.
Having an idea of entry-level doses and kinetics is important, as you don't
want to overlap doses of agents when the first hasn't had the opportunity to work.
Also, be extra careful when your patient has a low cardiac output; the usual
heart-to-end organ circulation time can be significantly delayed, creating an
impression that the patient didn't respond to the previos dose.
Drug
Entry-level dose
Onset
Fentanyl
Morphine
Morphine PCA
Nitroprusside (drip)
Nitrglycerin (drip)
Phenylephrine
Phenylephrine (drip)
Dopamine (drip)
Epinephrine (drip)
Epinephrine (with pulse present)
Ephedrine
25-50 mcg
1-4 mg
1-4 mg q 10 min
(0.2-0.3 mcg/kg/min)
(0.2-0.3 mcg/kg/min)
50-100 mcg
10-25 mcg/ min
2-3 mcg/kg/min
10-50 ng/kg/min
20-50 mcg
5-10 mg
3-5 minutes
10 min
2-3 hrs
3 min
3 min
1-2 min
4-10 min
5-10 min
3-10 min
45 sec-1.5 min
1.5-2 min
General template for crisis management and leadership
Different clinical situations require specific configurations of the treatment team.
A generic list of priorities and potential task distributions is presented as a vehicle
to stimulate further thinking on your part.
1.
Know your team and environment—who can provide what kinds of help??
Task or knowledge base
Drugs, doses and routes:
IV and arterial access
Respiratory support
Chart review
Lab data retrieval
Vital signs
Physical exam
Potential help
Pharmacist, anesthesiologist (consider phone
call in urgent situation)
Anesthesiologist, surgeon, ICU nurse, ICU fellow
Resp. therapy, RN, anesthesiologist
Medical student and above
RN, Nurse assistant, medical student or above
Nursing student, med student and above
Med student or above, preferably Intern
36
Distribute the workload as evenly as possible. Pair the most highly trained
personnel to the tasks with the highest pressure or skill requirement. If in doubt,
ask your team if they are totally comfortable doing what they were assigned to
do. Call your attending for additional support.
2.
Assign someone to obtain vital signs at an appropriate interval. Establish
data streams and understand their source (Know how frequently the BP cuff is
cycling. Know what ECG leads you are observing. Know what lines the patient
has and if data is being displayed. Know where the pulse ox is connected to the
patient. Know what labs have been drawn, what recent data shows. Assign
someone to watch monitors, assign parameters to be reported back to you.
3.
Establish relative priority for diagnostic and therapeutic efforts. Consider
compartmentalizing diagnostic and therapeutic efforts. Careful to not
overload team members.
4.
Consider the need for urgent consultation with other services and call
others at a time when their efforts can make a difference. Keep in mind that
interventional radiology, the cath lab, and the operating room are complex
services that require significant “set up time.” Factor these time delays into your
therapeutic plans
5.
If in doubt, start early aggressive stabilization of:
• hypovolemia
• hypotension
• hypoxemia
• hypopnea or tachypnea
• MI and cardiogenic shock
(tachycardia in inpatients is rarely the primary abnormality, do not
treat it unless the BP is normal).
6.
Make best estimate of underlying problem (blood loss?, infection?),
begin empiric therapy
7.
Establish therapeutic goals (how quickly to normalize BP, etc).
8.
Pursue diagnostic information as needed to influence plan.
9.
Communicate priorities and plans, keep team focused. Make sure your
team members are communicating any difficulties they are encountering.
Reassign tasks as needed.
37
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