http://surgerybook.net/

Bundles

The process of bundling evidence-based care practices allows ICUs to keep up with regulatory changes

and practice the most up to date critical care practices. Unlike checklists, ICU care bundles are always

evidence based. Bundles are comprised of interrelated processes and have a limited number of elements

(typically three to seven) whose key processes must be carried out in the same space and time. Bundles

exist addressing ventilator-associated pneumonia, central line infection, catheter-associated urinary tract

infection and pressure ulcer prevention, diagnosis and treatment of sepsis, and promotion of palliative

care. Large collaborative groups in the United States, including the Voluntary Hospital Association, The

Institute for Healthcare Improvement and the Michigan Health and Hospital Association-Keystone

Project, have shown improved patient outcomes after implementation of various bundles.23 Continuing

education is required to maintain appropriate use and compliance with these management bundles. The

implementation and use of sepsis resuscitation bundle and management bundle were significantly

improved after 2 month nationwide education effort to improve compliance with the care for patients

with severe sepsis.24 These evidence-based guidelines and bundles have been shown to improve

mortality and decrease morbidity and ICU related complications. Severe sepsis and septic shock bundles

are associated with reduced in-hospital mortality (Table 10-2). Mortality rates in these centers using

severe sepsis and septic shock bundles decreased by 16.7%.25 It has also been shown that the

implementation of central venous catheter care bundles led to decreased central line associated blood

stream infections (Table 10-3).26 Awakening, breathing, coordination, delirium, and early mobility

(ABCDE) bundles show some improvement in ICU average length of stay and average days on

mechanical ventilation.27 Finally, some have “bundled” a variety of these disparate bundles together to

drive global evidence-based care. The Surgical Care Improvement Project (SCIP) guidelines are perhaps

the most relevant and robust example.

Table 10-1B Extended FAST HUG – as Modified by the Authors from above

Table 10-2 Surviving Sepsis Care Bundle

299

http://surgerybook.net/

The application of evidence-based guidelines into clinical practice, even facilitated by use of bundles,

is often difficult. Educational and quality improvement programs, described above, can improve the

implementation of and compliance with these evidence-based guidelines. Further, it is important to

realize that bundles and any evidence-based guidelines must be continuously updated as new

information comes to the fore, particularly if the level of evidence or strength of recommendation was

weak. Examples in the care of the septic patient will be discussed below. Finally, although use of

bundles can promote team-building by providing objective feedback of performance, competent and

individualized clinical decision-making should not be sacrificed.

Table 10-3 Central Line Associated Bloodstream Infection (CLABSI) Bundle

Table 10-4 Comparison of ICU Scoring Systems

CRITICAL CARE PROGNOSTICATION AND SCORING

4 ICU scoring systems have been used to provide a framework to describe patients’ severity of illness

for the routine evaluation of ICU performance, quality improvement initiatives and to prognosticate

outcome.28 The most robust prognostication systems compare observed and risk-adjusted hospital

mortality for critically ill patient groups derived from analysis of large data sets. They operate on the

premise that early physiologic derangements prior to resuscitation and therapy present early in the ICU

admission will influence hospital mortality. Other systems have been developed to quantify organ

dysfunction and therapeutic interventions predicted.

The ideal scoring system should be valid, reliable, calibrated, discriminating, and simple. The

Glasgow coma scale score is an apt example. However, since ICU patients are heterogeneous,

documentation is often incomplete and practices are not standardized, such a system is not available in

300

http://surgerybook.net/

the ICU. The most frequently used severity of illness scores in an adult ICU used to prognosticate

hospital mortality are Acute Physiology and Chronic Health Evaluation (APACHE), the Mortality

Probability Model (MPM), and the Simplified Acute Physiology Score (SAPS) with higher scores

portending increased hospital mortality. APACHE and MPM were developed using data predominantly

from the United States; SAPS was more global (Table 10-4). To stay relevant and useful, these scoring

systems require and have undergone regular updates and regional customizations. These scoring systems

are currently in their third and fourth generations. It is vital to remember that these scoring systems

provide prognostication for the outcome of an ICU population more accurately than for an isolated

patient.

APACHE was developed several decades ago by William Knaus and colleagues at George Washington

University. The inaugural version ranked 34 acute variables from one to four and weighted chronic

health conditions A to D to render a score with higher numbers suggesting more acutely ill patients.

Versions two and three decreased the acute variable to 12 and 17, respectively, and created a simpler

way to weight the chronic health evaluation. The proprietary (and expensive) version, APACHE III,

never had large market penetration and was much more complex than earlier versions. APACHE IV29

which included more variables has many components in the public domain; however, without a

regulatory requirement to provide risk-adjusted ICU metrics and the need to employ personnel to verify

and interpret data, it is also not widely used. Further, since the data is collected at the time of ICU

admission, the possibility of lead-time bias exists. APACHE provides an algorithm for prediction of ICU

length of stay. Several studies have indicated that the current version of APACHE, although labor

intensive, is more accurate in prognosticating outcome due to better calibration and discrimination with

fewer excluded patients. This is particularly true for surgical patients.

SAPS shared many variables and weightings common with APACHE but provided separate

prognostication for medical, scheduled and unscheduled surgical patients; cardiac and burn patients are

excluded.30 Further, it provides customizable equations to predict outcome according to seven distinct

geographic locations.

The MPM uses dichotomous physiologic (not laboratory) variables for the most part (simplifying data

collection), collecting data both upon admission and at 24 hours to measure mortality risk at 24 and 48

hours. However, it excludes more patients than does APACHE. MPM-III has been further modified with

additional variables and different patient exclusions and is known as the ICU Outcomes Model (ICOM)

that has been endorsed by the National Quality Forum of the United States for public reporting of riskadjusted hospital mortality of ICU patients.31

The future of ICU prognostication may well involve interpretation of “big data” that relies less on

traditional data acquisition and storage and more on linear or logistic regression modeling. Much work

must be done in this realm before practical applications are available.32

Several organ failure scores exist as well, designed to link homogeneous patients for the purpose of

clinical trials and quality assessment. They can be used to provide initial as well as serial assessments.

The SOFA and Marshall scores consider variables in six categories (respiratory, cardiovascular,

hematologic, central nervous system, renal, and hepatic). The Denver score excludes the hematologic

and neurologic components. A Marshall or Denver score greater than or equal to 4 implies multiorgan

dysfunction (Table 10-5).33,34

TISS provides a sum of all interventions in physiologic categories to assist with resource utilization.

HEMODYNAMIC MONITORING AND TREATMENT

Oxygen Delivery and Consumption

Oxygen delivery (DO2

), the rate at which oxygen is transported to the microcirculation from the lungs,

is the product of cardiac output and arterial oxygen content (CaO2

) and is normally about 1,000

mL/min. CaO2

, in turn, is the product of hemoglobin and oxygen saturation (SaO2

) multiplied by 1.34

(g oxygen per 100 mL hemoglobin) added to the partial pressure of oxygen (PaO2

) multiplied by 0.003.

Thus, delivery falls in instances of cardiac failure, hypovolemia, anemia, or less so due to poor

oxygenation. Oxygen consumption (VO2

), the rate at which oxygen is removed from the blood by the

microcirculation, is the product of cardiac output and the arteriovenous O2 difference (CaO2 − CvO2

)

and is normally 250 mL/min in an average adult. Thus, oxygen extraction (OE) ratio or the ratio of VO2

to DO2

is normally about 25%. (The myocardium has the body’s highest extraction ratio at

301

http://surgerybook.net/

approximately 75%.) Consumption remains constant over a wide range of DO2 by changes in OE. For

example, in situations of decreased delivery such as hemorrhagic or cardiogenic shock, consumption can

be maintained by increasing the extraction ratio. This mechanism may be altered in critically ill patients

who show marked increases in consumption under the influence of stress hormones and catecholamines.

However, there is little evidence that artificially augmenting DO2

to so-called supranormal levels by

means of inotropes or red cell transfusion results in improvement in morbidity or mortality.

Table 10-5 Marshall Multiple Organ Dysfunction Syndrome (MODS) Versus

Denver Multiple Organ Failure (MOF) Organ Failure Scores

Mixed venous oxygen saturation (SvO2

) is expressed as 1-VO2/DO2, with normal values of 60% to

80% that can be continuously displayed with an oximetric pulmonary artery catheter or measured from

the distal port. Reductions in SvO2 reflect a mismatch between DO2 and VO2

(Table 10-6).

Hemodynamic Monitoring

Assessment of volume status and cardiac function of the critically ill patient is evolving. Traditional

static measures of volume assessment using central and pulmonary artery catheters (PACs) are being

replaced in many settings by dynamic or functional measures afforded by technologies such as pulse

waveform analysis and focused cardiac ultrasound (ECHO). Similarly, indirect measurement of cardiac

function by PACs is being subsumed by pulse waveform analysis and systolic and diastolic evaluation of

left and right global and regional function using ECHO.

Assessment of Fluid Responsiveness

The concept of volume status using static measures has evolved to “volume responsiveness” using

dynamic or functional measures to assess whether a fluid bolus will improve the stroke volume (SV) and

cardiac performance of a critically ill patient, the principal goal of resuscitation. Static measures such as

central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) can give inferential

data of cardiac filling pressures at a single time-point, which then extrapolates to cardiac preload (end

diastolic volume) and volume status of the patient. However, these pressures can be altered depending

on cardiopulmonary physiology, do not always correlate with Frank–Starling principles, and give no

indication of whether the patient will respond to a bolus of infused fluid, which is ultimately what those

tasked with resuscitation want to know.

Static measures of volume status include assay of CVP and PAOP. These measures are made at end

expiration when the pleural pressure is closest to atmospheric pressure. Normal venous waveform

components include the “a” wave (corresponding to atrial contraction), the “c” wave (tricuspid valve

closure and isovolumic right ventricular contraction), and the “v” wave (ventricular ejection driving

venous filling of the atrium) (Fig. 10-1). Clinically, the high point of the “a” wave is the atrial pressure

at maximum contraction, where atrial pressure is greater than ventricular diastolic pressure. Here, the

atrium is contracted and the tricuspid valve is open, which is synonymous with right ventricular end

diastolic pressure, making the ventricle, atrium, and vena cava interconnected. Optimally, this is the

point at which the CVP is measured. Unfortunately, many intracardiac and extracardiac interactions can

302

http://surgerybook.net/

alter these pressure relationships in the vena cava and diseased heart, and, thus, affect the CVP

waveform. For example, atrial fibrillation fails to produce an “a” wave, and AV-dissociation produces

irregular augmented (cannon) “a” waves with absent “c” and “v” waves, making calculation of mean

CVP difficult. Tricuspid regurgitation and tamponade may produce augmentation of the v wave and

falsely imply adequate or increased intravascular volume in a patient who may be hypovolemic. Thus,

the CVP waveform may fail to provide an adequate reflection of volume responsiveness in diseased

states.

Table 10-6 Oxygen Delivery and Consumption Equations

Figure 10-1. Normal venous waveform with ECG.

5 Further, the use of CVP to guide resuscitation has not been demonstrated to be beneficial in many

large clinical series. A large meta-analysis revealed a very poor relationship between CVP and blood

volume.35 Additionally, several large recent trials of sepsis resuscitation demonstrated that resuscitation

targeted to CVP endpoints did not improve outcome.36,37

Pulmonary artery catheter-based volume assessment employs the principle that a single column of

fluid forms from the pulmonary artery to the left ventricle during diastole. For a given left ventricular

end-diastolic pressure (LVEDP) and compliance, left ventricular end-diastolic volume (LVEDV) can be

estimated. Based on the Frank–Starling principle, the force of ventricular contraction is proportional to

muscle stretch and LVEDV, thus as PAOP estimates LVEDV for a given cardiac output, preload may be

determined. Numerous physiologic changes may alter the relationship between PAOP and LVEDV,

including veno-occlusive disease, pulmonary hypertension, ARDS, increased intrathoracic pressure,

valvular disease, and altered cardiac compliance. Finally, large clinical trials have failed to demonstrate

a benefit to outcome for those resuscitated to a PAOP endpoint.38

Dynamic or functional measures of volume responsiveness include those on both the arterial side and

venous side of the heart. Normally, the inspiratory increase in pleural pressure during positive pressure

breathing reduces right ventricular preload and stroke volume, manifested on the arterial side within

two to three beats in most. Left ventricular stroke volume diminution is maximal during expiration.

These normal physiologic changes during the mechanically supported respiratory cycle are augmented

with hypovolemia that is volume responsive. Pulse waveform analysis uses analysis of the arterial

303

http://surgerybook.net/

pressure waveform. The area under the curve corresponding to systole (i.e., before the dicrotic notch) is

used to calculate stroke volume (Fig. 10-2). Computer calculation is made of the maximal and minimal

amplitude of the curve. In general, a variation in stroke volume (SVV) of greater than 13% to 15%

reflects volume responsiveness, whereas values below this threshold imply that the patient is beyond

the upper inflection point of the Frank–Starling curve, and will not benefit from further volume loading.

There are instances where it is possible to misinterpret these values. For example, high vasopressor

burden or lack of arterial compliance (such as in diffuse atherosclerosis) may alter blood flow and

arterial wave morphology, respectively. However, clinical applications of SVV as a volume assessment

tool have been promising.39

Venous assessment of volume responsiveness is performed by ECHO, which can also perform arterial

side estimation. ECHO can provide volume assessment with both static and dynamic values. Further,

many static measures can be rendered functional by performing measurements both before and after a

passive leg raise, a maneuver that replicates volume loading. Passive leg raising measurements may be

the only accurate methodology to approximate fluid responsiveness in spontaneously breathing patients.

In these patients, a breath results in an increase in SV and systolic pressure. Static values include

measurement of the inferior vena cava (IVC) on the long axis view, or in some series by the superior

vena cava (SVC) or internal jugular vein (IJV) on the venous side or calculation of the velocity time

integral (VTI) on the arterial side. Collapsibility of the IVC (or SVC/IJV) of at least 15% and as much as

50% during respiration predicts fluid responsiveness.40 Right-sided heart failure may alter the size

relationships of the central veins, thus providing an underestimate of fluid responsiveness using venous

measurements (lack of respiratory variation due to pressure overload and diminished venous return to

the heart). Arterial assessments are typically done of aortic blood velocity approximated from the VTI.

Assessment of Cardiac Function is best understood by recollection of the cardiac pressure–volume

curve depicting the cardiac cycle (Fig. 10-3). Starting at the top right at “A,” the aortic valve opens and

blood is ejected into the outflow tract. At “B” systole ends as the aortic valve closes. A period of

isovolumic relaxation occurs and ventricular pressure falls until the mitral valve opens at “C,” the start

of diastole. Diastole ends as the mitral valve closes at “D” and then there is a period of isovolumic

contraction with both valves closed until the cycle repeats. Note that the distance across the box

represents SV. SV is the amount of blood ejected per beat and is expressed in mL and determined by

preload, afterload, and contractility. The product of SV and heart rate is CO. Ejection fraction (EF), a

more valid estimate of cardiac function, is the proportion of preload or EDV ejected per beat or

SV/EDV.

Figure 10-2. Arterial pressure waveform. Area under systole curve is used to calculate stroke volume. pSBP, peripheral systolic

blood pressure; pPP, peripheral pulse pressure; pDBP, peripheral diastolic blood pressure.

304

http://surgerybook.net/

Figure 10-3. Left ventricular pressure–volume curve. Ees, LV elastance; Ea, arterial elastance; ESV, end-systolic volume; EDV, enddiastolic volume; ESP, end-systolic pressure; EDP, end-diastolic pressure; LV, left ventricle. A: aortic valve opens; B: aortic valve

closes; C: mitral valve opens; D: mitral valve closes.

PA catheters determine cardiac output by thermodilution. The thermodilution technique measures

temperature changes sensed by a balloon at the distal end of the catheter after a cold saline injection is

performed through the proximal port. Based on the modified Stewart–Hamilton equation, which

constructs a plot of temperature change against time, measurements of cardiac output can be obtained.

Thermodilution technique assumes that complete mixing of the blood occurs, that there is constant

blood flow in the heart, and that there is no loss in concentration of the indicator between the point of

injection and the distal balloon tip. Slow injections, incorrect volumes of injectate, incorrect

temperature of injectate, either isolated or in combination with anatomic and physiologic cardiac

derangements can alter the accuracy of cardiac output determination.

Pulse contour analysis can also be used to measure stroke volume (and hence cardiac output). Using

PAC thermodilution as the gold standard, accuracy is acceptable.

ECHO does not suffer from many of the shortcomings of CVP, PAC, or arterial line assessment with

regard to the assessment of cardiac function. ECHO can determine left ventricular function (systolic and

diastolic), right ventricular function, and assess wall motion abnormalities, valve defects, pericardial

fluid, and provide real-time information on effectiveness of inotropic and vasopressor therapy. ECHO

can provide information about heart function in a qualitative or quantitative fashion – it can be used to

assess left and right heart morphology, dynamics, and size, and can determine the difference in EF and

stroke volume, and perform quantitative estimates of pulmonary artery and right ventricular pressure.

ECHO is unique in that it is the only tool available that can provide EF data in addition to SV (CO).

Shock states may be due to impaired EF or contractility (requiring inotropy) or due to diminished

volume status and stroke volume (requiring fluid), which is not discernable with a PAC. Various ECHO

methodologies are available to determine and measure EF, including a purely qualitative one that is

reasonably accurate compared to quantitative means.

ECHO can also discern right heart dysfunction, very common in surgical ICU patients by examining

size, morphology and function of the right ventricle. Underfilling of the left heart, typically treated by

volume loading, requires attention to inotropic support in the case of right heart failure. Finally, unique

to ECHO is the ability to assess for diastolic dysfunction as occurs with sepsis, tamponade, and increased

pleural pressure (as with pneumothorax, abdominal compartment syndrome, and massive pleural

effusions).

TREATMENT OF CARDIAC ARREST AND DYSRHYTHMIAS

Dysrhythmias are extraordinarily common in both cardiac and noncardiac surgical ICU patients. Those

most life-threatening can be treated by following current American Heart Association Advanced Cardiac

Life Support (ACLS) guidelines.41 For patients who become pulseless in the ICU, rapid restoration of the

circulation employing basic life support strategies (BLS) is vital. The most important features of the

current BLS guidelines include the recognition that cardiopulmonary resuscitation (CPR), when

indicated, be delivered by pushing hard and fast with complete recoil at a rate of at least 100

compressions/min to a depth of 2 in in adults. CPR providers should deliver no more than 2 minutes of

305

http://surgerybook.net/

therapy each (or five cycles of compressions) until a personnel switch is made. In adults, the ratio of 30

compressions to 2 breaths is maintained until ventilation can be controlled by intubation and controlled

ventilation. Cricoid pressure is not recommended in current ACLS guidelines. Further, the rapid use of a

defibrillator is key to improving postarrest survival. Of course, in ICU patients, cardiac arrest is often

witnessed and the underlying rhythm known and may not respond to defibrillation. Sadly, cardiac arrest

from a rhythm other than ventricular fibrillation, such as from bradycardia progressing to asystole or

pulseless electrical activity (PEA), portends a poor prognosis, often as the result of acidosis or profound

hypoxia incidental to sepsis and multiple organ failure. Another important feature of the current BLS

and ACLS guidelines that may impact surgical ICU patients is the recognition of the need for postcardiac

arrest care. This certainly includes fluid resuscitation and administration of pressors and inotropes as

needed. However, there may also be a need to interrogate via coronary angiography and treat for acute

coronary syndrome if anticoagulation can be tolerated and for consideration of postarrest hypothermia

to preserve neurologic function. Although hypothermia protocols were established to address out of

hospital cardiac arrest with coma, there has been increasing use of the modality for hospitalized patients

as well. Current guidelines also address new technology with biphasic electrical sources that deliver

shocks for dysrhythmias with a pulse and defibrillation in those with ventricular fibrillation. Another

important component of the recommendations is the use of end-tidal CO2 monitoring to ensure

adequacy of CPR quality.

Three dysrhythmias produce pulselessness: ventricular fibrillation, asystole, and PEA. Only

ventricular fibrillation is responsive to defibrillation which is with 120 to 200 J using a biphasic device

as per manufacturer’s recommendations. PEA and asystole are treated by administration of epinephrine

(1 mg every 3 to 5 minutes) and/or vasopressin (40 U one-time dose). Pulseless ventricular tachycardia

is treated like ventricular fibrillation with additional shocks given after five cycles of CPR (2 minutes).

In addition, epinephrine and vasopressin are administered as CPR continues. Continued pulseless

ventricular tachycardia and fibrillation can be treated with amiodarone (300 mg with a second dose of

150 mg if refractory) or lidocaine (1.0 to 1.5 mg/kg).

For the remainder of dysrhythmias, several key features should be noted. Is the patient,

hemodynamically stable or unstable? Is the EF normal or altered? Is the dysrhythmia acute or long

standing? Hemodynamic instability in association with a rhythm disturbance often renders electrical

therapy more desirable, if possible. In those with a low EF, antiarrhythmics that are also negative

inotropes should be avoided. Finally, even duration of as little as 48 hours can increase the risk of

thrombotic complications of some dysrhythmias (e.g., atrial fibrillation) and can alter therapeutic

decisions.

PULMONARY GAS EXCHANGE

Consists of the intake of oxygen by pulmonary capillaries from the alveoli and the excretion of carbon

dioxide in expired breaths.

Oxygenation

Normal lung function and gas exchange require patent and dry alveoli with a narrow interface with the

pulmonary capillaries. Once red blood cells become saturated with oxygen, the rest dissolves into the

plasma and the measured partial pressure of oxygen (PO2

) is 100 mm Hg with an oxygen saturation

(SaO2

) of 100%. Since a small portion of blood is diverted away from the pulmonary circulation (via

bronchial vessels), a normal PaO2

is 90 mm Hg with 98% saturation. Insufficient blood oxygenation is

termed hypoxemia. This is to be differentiated from hypoxia, which is abnormally low oxygen content

in a tissue or organ. The alveolar to arterial (A-a) oxygen gradient is a common measure of oxygenation

(“A” denotes alveolar and “a” denotes arterial oxygenation). PaO2

is measured by arterial blood gas,

while PAO2

is calculated using the alveolar gas equation: PAO2 = (FiO2 × [Patm − PH2O]) − (PaCO2

÷ R) where FiO2

is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure

(760 mm Hg at sea level), PH2O is the partial pressure of water (47 mm Hg at 37°C), PaCO2

is the

arterial carbon dioxide tension, and R is the respiratory quotient. The normal gradient is about 10 mm

Hg. Dividing the PaO2 by the FiO2 estimates the A-a gradient, which normally approximates 500.

Perturbations causing hypoxia and hypoxemia may be the result of hypoventilation relative to

perfusion (V/Q mismatch), impaired diffusion, or shunt. Hypoventilation, a result of neuromuscular

dysfunction (or more typically iatrogenic due to medications) and impaired diffusion (occurring with

306