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Textbook Evidence Based Critical Care A Case Study Approach 1St Edition Robert C Hyzy Eds Ebook All Chapter PDF
Textbook Evidence Based Critical Care A Case Study Approach 1St Edition Robert C Hyzy Eds Ebook All Chapter PDF
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Robert C. Hyzy
Editor
Evidence-Based
Critical Care
123
Evidence-Based Critical Care
Robert C. Hyzy
Editor
Evidence-Based
Critical Care
A Case Study Approach
Editor
Robert C. Hyzy
Division of Pulmonary and Critical Care
University of Michigan
Ann Arbor
MI
USA
Along with Springer International, I am pleased to offer you our new text-
book entitled Hyzy’s Evidence-Based Critical Care Medicine: A Case Study
Approach. In medicine, “teachable moments” usually occur in clinical con-
text, where the engagement in a real case exemplifies principles of diagnosis
or therapy. We have created our new textbook with the teaching moment in
mind: each chapter begins with a real case gleaned from the authors’ clinical
experience. In order to replicate the teaching dyad, each case poses a question
which offers the reader to process and reflect on the components of the case
before offering and answer.
While medical practice attempts to be evidence-based, common approaches
to diagnosis and management incorporate not only evidence but heuristics
and biases which await either validation or repudiation. Hence, we have
divided the discussion section of each chapter into two segments: the
“Principles of Management” section and the “Evidence Contour” section. In
the “Principles of Management” section, the common approach to the care of
patients having a given condition is presented. Here you will find the nuts and
bolts of what you need to know about the condition and the usual approach to
diagnosis and treatment. Evidence-based approaches are emphasized, where
appropriate. However, medical knowledge is ever evolving. The approach to
many aspects of the diagnosis and treatment of a condition remains the sub-
ject of controversy. In the “Evidence Contour” section, each author discusses
the aspects of diagnosis and management which are the subject of ongoing
debate in the medical literature. In the way, the reader will appreciate not only
what appears to be known but also what is becoming known about a given
topic.
We believe the approach we have taken with this textbook successfully
bridges the gulf between the traditional encyclopedic sit-on-your-shelf text-
book and the single-hit online reference, each of which lacks the contextual
elements of effective learning. This is a new way to present knowledge in a
medical textbook and should help critical care practitioners, fellows, resi-
dents, allied health professionals, and students expand their critical care
knowledge in an efficient and effective manner. This approach should also
benefit those preparing for board examinations.
I would like to thank the many friends, colleagues, and former fellows
whose labors went to create this book. In particular, I would like to thank my
section editors, Drs. Robert Neumar, David Morrow, Ben Olenchock, Romer
Geocadin, John Kellum, Jonathan Fine, Robyn Scatena, Lena Napolitano,
vii
viii Preface
and Marie Baldisseri. Without their thoughtful and insightful efforts, this
book would not have been possible. I would also like to thank my editors at
Springer, Connie Walsh and Grant Weston for their vision and for seeing this
work through to fruition.
ix
x Contents
59 Chikungunya���������������������������������������������������������������������������������� 513
Pedro Arriaga and Jorge Hidalgo
60 Leptospirosis���������������������������������������������������������������������������������� 517
Jorge Hidalgo, Gloria M. Rodriguez-Vega, and Pedro Arriaga
Part X Surgical
Lena M. Napolitano
xvii
xviii Contributors
Robert W. Neumar
Cardiac Arrest Management
1
Ronny M. Otero
paused and solicited ideas from the team about end-tidal CO2 with chest compression to close to
possible etiologies for persistent pulseless elec- 35 mm Hg may signal return of spontaneous cir-
trical activity (PEA). culation (ROSC) [15–17].
Achieving a higher blood pressure during
Question What are methods to assess the qual- CPR makes intuitive sense, as thoracic compres-
ity of chest compressions during CPR? sion and thus, cardiac output will be the driving
force behind improving cerebral and systemic
Answer Capnography, arterial blood pressure perfusion. However, the hemodynamics of car-
and coronary perfusion pressure diac arrest is complex and patient-specific factors
may be responsible for the variable responses to
Components of high quality CPR include chest compressions, vasopressors and ventila-
minimizing interruptions of chest compressions tion. One of the main determinants of successful
with a chest compression fraction of >60 %, cor- resuscitation is the coronary perfusion pressure
rect chest compression rate and depth. (CPP), which is the difference between the right
Recommended chest compression rates are atrial pressure (or CVP) and aortic pressure dur-
greater than 100 and a depth of 50 mm with ing diastole (relaxation phase of chest compres-
allowance for chest recoil between compression sion). In the arrested patient there is a delay until
and minimizing ventilations to no more than there is a complete cessation of flow through the
10–12 breaths/minute [9–12]. The emphasis of cardiac chambers and by 1 min there is no flow to
chest compressions over positive pressure venti- the coronary arteries. In a human study a
lation has been supported by studies, which have CPP < 15 mm Hg was associated with not achiev-
shown a mortality benefit of compression only ing ROSC [18]. In animal studies it has been
CPR in witnessed arrest compared with tradi- shown that higher levels of CPP are required to
tional CPR with compressions and ventilation provide cerebral blood flow when CPR is delayed
[13]. How well chest compressions are meeting [19]. Moreover, in studies where ROSC was
the goal of providing circulatory flow to the brain achieved in humans, it was closely tied to CPP
and vital systems is often difficult to ascertain. and aortic diastolic pressure [20]. CPR guided by
Of the readily available parameters capnogra- blood pressure has also shown improved out-
phy and arterial blood pressure monitoring are comes [21]. In the observational human study
the most easily applied measurements to provide evaluating coronary perfusion pressure as the
feedback of the quality of chest compressions. correlate to ROSC a mean maximal aortic relax-
Close attention to the physiologic response to ation pressure (aka diastole) was 35.2 ± 11.5, thus
chest compressions is desirable, as studies indi- the diastolic pressure target should be approxi-
cate that even healthcare professionals have poor mately 40 mm Hg [18]. In settings where a
recall and variable quality when performing chest patient is instrumented with an arterial and a cen-
compressions [14]. tral venous line, aortic diastolic pressure and
Capnography has long-been seen as a poten- right atrial pressure can be substituted by arterial
tial surrogate for blood flow through heart and diastolic pressure and central venous pressure.
the pulmonary circulation [15]. As the technol- The difference between arterial diastolic pressure
ogy has improved so has the portability. and central venous pressure may provide a rough
Capnography can now be measured by side- estimate of CPP [22]. When the ability to monitor
stream technology in non-intubated patients and CPP is unavailable a strategy to assess the effi-
or mainstream capnography in intubated patients. cacy of chest compressions may depend upon
During cardiopulmonary resuscitation the goal of capnography and diastolic pressure.
high quality chest compressions is to achieve an Lastly, emerging technology, which provides
end-tidal CO2 of 20 mm Hg or higher and to instantaneous feedback about the quality of chest
maintain an end-tidal CO2 greater than 10 mm compressions is now available. This CPR-sensing
Hg at all times with compressions. A rapid rise in feedback (FB) system often utilizes accelerome-
1 Cardiac Arrest Management 5
ters to detect rate and depth of compressions (79 ± 18) compared to patients with ROSC
while delivering audio cues to the rescuer. (90 ± 17) [3].
Currently available CPR-FB systems include the Specific goals of high quality CPR include
Phillips Q-CPR ®, Zoll Real CPR Help ® and achieving a compression rate of at least 100–120
Physio-Control compression metronome and compression/minute and a compression depth of
Code Stat ® [23]. It is not known at this time at least 50 mm (2 inches) with an upper limit of
whether utilizing these CPR-FB systems 60 mm (2.4 inches) [9]. Additionally, high quality
improves outcomes. chest compressions should include a chest com-
pression fraction >60 %, meaning when CPR is
performed chest compressions should occupy at
Principles of Management least 60 % of the resuscitation [9]. Patient position-
ing, vascular or intraosseous access, medication
Standard Approach to Resuscitation administration, airway establishment, rhythm
analysis and defibrillation should occupy the
Introduction remaining fraction of time. Maintaining a chest
Achieving optimal outcomes from cardiac arrest compression rate of 100–120 compressions/min-
requires collaboration between several disci- ute can lead to rescuer fatigue. Switching com-
plines including pre-hospital providers, emer- pressors every 2 min may minimize rescuer fatigue
gency physicians, cardiologists, cardiac but lead to frequent interruptions and may nega-
interventionalist as well as several other medical tively impact chest compression fraction. One sug-
professionals and specialists. All providers in this gestion to decrease this “hands-off” time is to have
paradigm should understand each other’s role as rescuers switch from opposite sides of the victim
well as what measures can be expected to be [25]. Between compressions there should be time
offered to a victim of sudden cardiac arrest. allowed for full chest recoil in order for heart to
refill with blood and maximizing CPP.
ecognition of Sudden Cardiac Arrest
R
The ability of laypersons as well as health profes- djuncts to CPR: Oxygen
A
sionals to detect a pulse has been reported to be and Ventilation
extremely poor [14, 24]. Additionally, agonal During the initial rounds of chest compressions
breaths may be seen for several minutes after car- rescuers should focus on the quality of the com-
diac arrest confounding the confirmation that a pressions and use passive oxygenation with the
patient has arrested. Despite these limitations it is highest concentration of oxygen available at the
best to activate emergency response system as time. The delivery of this oxygen is dependent
soon as a patient is unresponsive with a faint or upon the systemic perfusion that may be estab-
absent pulse. lished by chest compressions.
Attempts to establish a definitive airway
Chest Compressions should be postponed unless there is difficulty
After a pulse check of no more than 10 s chest ventilating a patient with a bag valve mask.
compressions should be initiated at once. Health Furthermore, hyperventilation should be avoided
care providers should re-double their efforts to as this has been tied to reducing cardiac output
improve their knowledge and maintain technical [26, 27]. When two providers are resuscitating a
skills relevant to chest compressions. Evidence patient ventilations are delivered in a 30:2
for maintaining these skills may be gleaned from compression-to-ventilation ratio until a definitive
a multi-center study whereby healthcare provid- airway has been established [28]. Using a 1 L bag
ers often performed suboptimal chest compres- mask device a second provider should provide
sion rates. Specifically, the mean chest approximately 600 cc of tidal volume over 1 s.
compression rate was below the recommended This should be performed a total of two times
rate and lowest for patients without ROSC after every 30 compressions. With an advanced
6 R.M. Otero
airway in place rescuers may provide a breath an electrolyte abnormality. If medication toxicity
every 6 s while chest compressions are performed and electrolyte abnormalities are ruled out persis-
continuously. tence of these dysrhythmias should prompt
search for myocardial ischemia.
Defibrillation Different forms of ventricular tachycardia
Defibrillation is indicated for ventricular fibrilla- exist including: monomorphic VT, polymorphic
tion or pulseless ventricular tachycardia. VT, torsade de pointes, right ventricular outflow
Although traditionally monophasic defibrillators tachycardia (idiopathic and arrhythmogenic right
have been used to administer a counter shock, ventricular dysplasia), fascicular tachycardia,
biphasic defibrillators are preferred due to the bidirectional VT and ventricular flutter.
greater first shock success. Newer waveforms Monomorphic VT accounts for the majority of
have been studied which provide patient-specific VT encountered. Most cases of monomorphic
impedance current delivery using biphasic trun- VT are associated with myocardial ischemia.
cated exponential, rectilinear biphasic or pulsed Torsade de pointe is a specific form of polymor-
biphasic wave. At this time there is no specific phic VT where there is progressive widening of
recommendation regarding which waveform is the QT interval. Although most forms of VT are
superior. Current recommendations are to admin- associated with myocardial ischemia there are
ister a single counter shock at an optimal energy forms of idiopathic VT. Of the idiopathic forms
level (between 120 and 360 J for biphasic defi- of VT, most cases are due to abnormalities in the
brillators) with minimal interruptions in CPR outflow tract of the right ventricle. A small num-
before and after the shock [28]. In situations ber of these have an anatomically identified focus
requiring repeated defibrillations use manufac- termed “arrhythmogenic right ventricular dyspla-
turers’ guidelines or consider escalating energy. sia”. Ventricular flutter is an extreme form of VT
For refractory VF and pulseless VT, administra- that has a sinusoidal appearance and may degrade
tion of epinephrine and an anti-dysrhythmic into ventricular fibrillation. Ventricular flutter
agent should be instituted. usually has a rate >200 beats/min. Thus when
confronted with a patient with refractory ventric-
ular dysrhythmias providers should strongly con-
earch for Precipitating Cause
S sider consulting a cardiology specialist to
of Cardiac Arrest evaluate patient for the possibility of a diagnostic
and percutaneous intervention.
Ventricular Dysrhythmias
Survival to discharge for patients with an initial ulseless Electrical Activity (PEA)
P
rhythm of VT or VF is between 15 and 23 % for Patients with PEA have a survival to discharge of
out-of-hospital cardiac arrest and up to 37 % for 2.77 % for patients with out-of-hospital cardiac
patients with an in-hospital cardiac arrest [29, arrest as compared to patient in an in-hospital car-
30]. Resuscitation team leaders must simultane- diac arrest of only 12 % [30, 31]. PEA is defined
ously look for reversible etiologies while admin- as the absence of a pulse when electrical cardiac
istering time-sensitive interventions. Ventricular activity is present. This is further classified as
fibrillation is usually found in patients with “true” PEA, which is when there is no pulse, the
abnormal myocardial perfusion from a prior presence of an electrical signal but no evidence of
infarct or ongoing ischemia. Similarly ventricular cardiac activity usually detected by echocardiog-
tachycardia usually results from foci below the raphy. “Pseudo-PEA” is defined as the absence of
AV node which progresses into a wide and regu- a pulse, presence of an electrical signal and car-
lar tachycardia. When confronted with these diac activity observed by echocardiography.
malignant ventricular dysrhythmias diagnostic It is important to make these distinctions, as
considerations include medication toxicity, pre- there is pathophysiologic and prognostic signifi-
existing channelopathy (Brugada syndrome) or cance. True PEA is when electromechanical uncou-
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