Non-pulmonary Critical Care - part 3 ppsx

The Baltimore Longitudinal Study of Aging screened pa-tients aged 60 to 85 years old for cardiovascular disease and followed them for 10 years; nonsustained ventricular tachycardia NSVT

and PR intervals MAT is most often associated with

hypoxia in the setting of pulmonary disease but may

occasionally be due to use of theophylline, metabolic

derangements, and end-stage cardiomyopathy

Treat-ment consists of correcting hypoxia by either or both

treating underlying pulmonary disease and correcting

electrolyte abnormalities.26AV nodal blockers are

some-times useful to control the ventricular response in the

interim

WIDE COMPLEX TACHYCARDIA

The most frequently reported tachyarrhythmia in the

ICU setting is a wide complex tachycardia The first

step in treatment is establishing the diagnosis because VT

is more ominous than SVT with aberrancy VT is defined

by three or more consecutive ventricular beats Sustained

VT is defined as more than 30 seconds of ventricular

beats at a rate of more than 100 bpm.27,28Initial

evalua-tion should include obtaining a 12-lead ECG, and

measurement of serum potassium, calcium, and

magne-sium The ECG should be examined and compared with

prior ECGs with attention to QRS width in sinus

rhythm, prior Q waves that may indicate prior myocardial

infarction (MI), the presence of delta waves, as well as the

QT interval A careful review of medications is

para-mount in excluding iatrogenic causes of VT

VT can be diagnosed using some clinical and

electrocardiographic clues, as outlined following here:

1 Play the odds VT is approximately four times more

common than SVT with aberrancy In one study of

200 consecutive patients with a wide QRS

tachy-cardia, 164 were ventricular, 30 were SVT with

aberrancy, and six were SVT with antegrade

con-duction.29

2 Ask the right questions VT is much more common in

patients who have a history of MI or heart failure

3 Do not rely on hemodynamics alone Circulatory

col-lapse is more common with VT than with SVT, but

patients with VT may maintain a normal blood

pressure

4 Do not count on AV dissociation This is present in less

than 50% of cases of VT and is difficult to identify at

faster heart rates

5 Do not count on irregularity Regularity was identified

in 90% of patients with SVT versus 78% with VT.30

Other clues are useful in distinguishing VT from

SVT A QRS width of more than 0.14 seconds with

right bundle branch block or 0.16 seconds during left

bundle branch block favors VT.31Comparison of QRS

morphology during the tachycardia with the

morphol-ogy of ventricular premature beats in sinus rhythm can be

helpful Other diagnostic clues suggestive of VT are

fusion and capture beats, but these are seen in only 20 to

30% of cases of VT.32 Fusion beats, a hybrid of the supraventricular and ventricular complexes, occur when two impulses, one supraventricular and one ventricular, simultaneously activate the same territory of ventricular myocardium The implication is that the wide complexes are ventricular Capture beats are occasional beats con-ducted with a narrow complex, and such beats rule out fixed bundle branch block

It is better to err on the side of overdiagnosis of

VT The potential consequences of misdiagnosis were demonstrated in a study analyzing adverse events in-curred by patients with VT misdiagnosed as SVT and given calcium channel blockers.33Many of the patients promptly decompensated and some required resuscita-tion Interestingly, all of these patients were hemody-namically stable when first seen in VT

NONSUSTAINED VENTRICULAR TACHYCARDIA

This common clinical problem, occurring equally in women and men, is usually asymptomatic, with an incidence of 0 to 4% in the general population.34,35 A major determinant of prognosis is the presence or absence of underlying structural heart disease The Baltimore Longitudinal Study of Aging screened pa-tients aged 60 to 85 years old for cardiovascular disease and followed them for 10 years; nonsustained ventricular tachycardia (NSVT) did not predict coronary events in this population.36 Therefore, in asymptomatic patients with NSVT, a thorough history and physical examina-tion, echocardiography, and stress testing are usually sufficient to exclude prognostically significant structural heart disease Patients with symptoms of palpitations, syncope, or presyncope should undergo further evalua-tion to exclude episodes of sustained VT or other arrhythmias

Patients who have NSVT with structural heart disease (coronary heart disease, dilated cardiomyopathy,

or valvular heart disease) require more comprehensive evaluation and management As will be discussed here, the prognosis of NSVT following a myocardial MI is dependent upon the timing of onset of VT in relation to the incident MI NSVT occurring in the first 48 hours of

an MI is most likely related to reperfusion or ischemia and has no prognostic significance However, NSVT occurring more than 1 week after MI doubles the risk of sudden cardiac death (SCD) in patients with preserved left ventricular function.37The risk of SCD is increased more than fivefold in patients with left ventricular dysfunction (ejection fraction less than 40%).38 The risk of SCD is greatest in the first 6 months post-MI and persists for up to 2 years

NSVT is present in up to 80% of patients with an idiopathic dilated cardiomyopathy (ejection fraction [EF]< 40%).39 The current American College of Cardiology/American Heart Association guidelines

CARDIAC ARRHYTHMIASIN THEICU/TARDITI, HOLLENBERG 225

recommend implantation of an internal cardiac

defib-rillator (ICD) for nonsustained VT in patients with

coronary disease, prior MI, LV (left ventricular)

dys-function, and inducible VF or sustained VT at

electro-physiological study that is not suppressible by a class I

antiarrhythmic drug.40Initial treatment of NSVT in the

setting of dilated cardiomyopathy should include

cor-rection of electrolyte abnormalities, removal of

exacer-bating factors (hypoxia, dehydration, medications,

vasopressors, etc.), and up titration ofb-blockers

Mitral and aortic valve disease is associated with

NSVT, occurring in up to 20% of patients with mitral

valve prolapse (MVP) and 5% of patients with aortic

stenosis In both severe mitral regurgitation and aortic

stenosis, NSVT does not appear to be associated with

increased risk of SCD.41–43

In patients at high risk as already described,

further evaluation is warranted This may include cardiac

catheterization, electrophysiological testing, and/or

sig-nal-averaged ECG

MONOMORPHIC VENTRICULAR TACHYCARDIA

Monomorphic VT in the setting of a normal QT interval

usually occurs from a fixed substrate (i.e., scar) rather

than acute ischemia The importance of monomorphic

VT depends on the clinical milieu in which it occurs and

on the presence of underlying structural heart disease

Sustained monomorphic VT, either with or without

acute ischemia, portends a worse prognosis even after

hospital discharge.44

The approach to treatment of sustained

mono-morphic VT is based on the presence of hemodynamic

instability and/or other clinical factors (heart failure,

pulmonary congestion, shortness of breath, decreased

level of consciousness, or myocardial ischemia) If any

are present, then synchronized cardioversion is

indi-cated Stable or recurrent monomorphic VT can be

treated with lidocaine, procainamide, or amiodarone

The next step in evaluation and management of the

patient is dependent on left ventricular function If left

ventricular function is normal and the patient is not in

heart failure, treatment with procainamide, amiodarone,

lidocaine, or sotalol is recommended The choices are

limited to amiodarone or lidocaine in those with

im-paired left ventricular function (EF < 40%)

Amiodar-one can be given as a 150 mg IV bolus over 10 minutes

followed by an infusion of 360 mg (1 mg/min) over 6

hours, and then 540 mg (0.5 mg/min) over the

remain-ing 18 hours The maximum total dose is 2.2 g over 24

hours Bradycardia and hypotension can result from IV

amiodarone, in which case the rate of the infusion should

be decreased Lidocaine is administered by IV bolus of

0.5 to 0.75 mg/kg, followed by continuous infusion at 1

to 4 mg/min Procainamide is administered at 20 mg/

min IV for a loading dose of 17 mg/kg, then continued

as an infusion at 1 to 4 mg/min The infusion should be

stopped if the patient becomes hypotensive or the QRS widens by 50% above baseline The most serious side effects of procainamide are hypotension and proarrhyth-mia (most commonly torsades de pointes), both of which increase in frequency in patients with renal insufficiency because of decreased excretion If the QTc is longer than

500 msec the drug should be stopped immediately and the QTc followed closely Cimetidine and amiodarone can increase levels of procainamide and its metabolite N-acetyl procainamide.45Measurement of serum levels may

be useful, especially in patients with renal insufficiency

In patients with transvenous or epicardial pace-makers, overdrive antitachycardia pacing is an option The ventricular pacing rate should be 10 to 20 bpm faster than the VT Absent a reversible cause, an im-plantable cardioverter-defibrillator (ICD) should be considered in patients with recurrent monomorphic

VT and an ejection fraction less than 40% or a history

of syncope

POLYMORPHIC VENTRICULAR TACHYCARDIA

Polymorphic VT with a normal QT interval is consid-ered to be an ischemic rhythm that typically degenerates into VF It is almost never asymptomatic and thus DC synchronized cardioversion is the initial recommended treatment Polymorphic VT with a normal QTc is a more ominous sign than monomorphic VT in patients with myocardial ischemia Medications that might pre-dispose to ischemia, such as inotropes or vasopressors, should be stopped or tapered, if possible, andb-blockers started if blood pressure permits Intraaortic balloon pumping may be useful as a supportive measure, but revascularization is usually required If withdrawal of vasopressors is contraindicated on a clinical basis, IV infusion of lidocaine or amiodarone should be initiated

TORSADES DE POINTES

Torsades de pointes is a French term translated as ‘‘twist-ing of the points.’’ It is a syndrome composed of polymorphic VT and a prolonged QTc interval (by definition  460 millisecondsec) This may be due to various medications, including procainamide, disopyra-mide, sotalol, phenothiazines, quinidine, some antibi-otics (erythromycin, pentamidine, ketoconazole), some antihistamines (terfenadine, astemizole), and tricyclic antidepressants Other etiologies include hypokalemia, hypocalcemia, subarachnoid hemorrhage, congenital prolongation of the QTc interval, and insecticide poisoning.46 A key to treatment is correction of any exacerbating factors and normalization of electrolyte disturbances, particularly hypomagnesemia, hypocalce-mia, and hypokalemia Magnesium should be given 1 to

2 g IV push over 30 to 60 minutes Other potential treatments may include overdrive pacing or isoproterenol

to increase heart rate and thus shorten QTc Admin-istration of sodium bicarbonate IV can be useful to

226 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006

antagonize the proarrhythmic effects of class I

antiar-rhythmics.47

WOLFF-PARKINSON-WHITE SYNDROME

(VENTRICULAR PREEXCITATION)

AVRT using an accessory bypass tract, WPW, occurs in

0.1 to 0.3% of the general population An accessory

pathway bypass tract (bundle of Kent), bypasses the AV

node and can activate the ventricles prematurely in sinus

rhythm, producing the characteristic delta wave The

diagnosis of WPW is reserved for patients with both

preexcitation and tachyarrhythmias In AVRT

conduc-tion can go down the bypass tract and back up the AV

node, producing a wide QRS complex (antidromic) or

down the AV node and back up the bypass tract,

producing a narrow QRS complex (orthodromic)

AVRT should be suspected in any patient whose heart

rate exceeds 200 bpm AF is a potentially

life-threat-ening arrhythmia in patients with WPW syndrome

because it can generate a rapid ventricular response

with subsequent degeneration into VF This is

impor-tant because one third of patients with WPW syndrome

have AF.48

Adenosine should be used with caution in any

young patient suspected of having WPW because it

may precipitate AF with a rapid ventricular response

rate down an antegrade accessory pathway

Procaina-mide, ibutilide, and flecainide are preferred agents

because they slow conduction through the bypass tract

The long-term treatment of choice for symptomatic

patients is radiofrequency catheter ablation of the

accessory pathway

ELECTRICAL STORM

The definition of an electrical storm is more than three

distinct episodes of VT/VF within a 24-hour period.49

In patients with ventricular arrhythmias requiring ICD

implantation, the incidence of ventricular storm ranges

from 10 to 30%.50,51According to one study, the event

occurred at an average of 133 135 days after ICD

implantation Precipitating factors (hypokalemia,

myo-cardial ischemia, and heart failure) were identified in

only 26% of the patients in one study

Evaluation should include measurement of

se-rum electrolytes, obtaining an ECG, and further

eval-uation for ischemic heart disease, which may include

coronary angiography Proarrhythmia secondary to

antiarrhythmic drugs that prominently slow conduction

velocity, such as flecainide, propafenone, and

morici-zine, should be excluded.52,53 Treatment for

proar-rhythmia is hemodynamic support until the drug is

excreted If exacerbating factors (acute heart failure,

electrolyte abnormalities, proarrhythmia, myocardial

ischemia, and hypoxia) are corrected, repeated doses

of IV amiodarone should be given, even if the patient is

already on oral amiodarone.54 Deep sedation can help

reduce sympathetic activation Mechanical ventilatory support and IVb-blockers can be used in conjunction, but IV amiodarone is the pharmacological treatment of choice for this condition If pharmacological therapy and antitachycardia pacing are unsuccessful, electro-physiology mapping–guided catheter ablation can be considered, although this is often difficult in unstable patients.55 The prognosis of patients with electrical storm after ICD implantation is poor, with a 2.4-fold increase in the risk of subsequent death, independent of ejection fraction The risk of SCD is greatest 3 months after an electrical storm

BRADYARRHYTHMIAS AND PACING Asymptomatic bradyarrhythmias do not carry a poor prognosis and in general no therapy is indicated.56 Recommended initial therapy for bradycardia inducing end organ perfusion problems is atropine IV 1.0 mg The presence of syncope, heart failure, or other symptoms accompanying bradycardias is an indication for pace-maker implantation Third degree or advanced heart block with either symptomatic bradycardia, pauses  3 sec, or heart rate < 40 bpm is also an indication for pacemaker insertion Class I indications (general agree-ment that a treatagree-ment is beneficial) for temporary trans-venous pacing after an acute MI are listed here:

1 Asystole

2 Symptomatic bradycardia

3 Bilateral bundle branch block (BBB)

a Alternating BBB or right BBB (RBBB) with alternating left anterior fascicular block (LAFB)/

left posterior fascicular block (LPFB)

4 New or indeterminate age bifascicular block with first-degree AV block

a RBBB with LAFB or LPFB

b Left BBB (LBBB)

5 Mobitz type II second-degree AV block

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CARDIAC ARRHYTHMIASIN THEICU/TARDITI, HOLLENBERG 229

Evaluation and Management of Shock

Olivier Axler, M.D., Ph.D., F.C.C.P.1

ABSTRACT

Shock is one of the most frequent situations encountered in the intensive care unit (ICU) Important new concepts have emerged for shock management in recent years The concept of early goal-directed therapy has evolved from the basic management concepts for septic shock delivered in a structured fashion Numerous cardiovascular techniques, methods, and strategies have been developed as novel alternatives to the use of the pulmonary artery catheter Among these techniques, echocardiography, esophageal Dop-pler, and arterial pulse contour analysis show great promise Prediction of responsiveness to fluid administration is a key component of the management of shock, as is assessing cardiovascular performance The intensivist has several options to evaluate and treat shock Further research should yield additional important advances

KEYWORDS:Shock, cardiovascular protocols, cardiovascular techniques; central venous pressure; pulmonary arterial catheter

Shock is a common cause of admission in any

intensive care unit (ICU) and also occurs frequently

during the course of critical illness Shock is associated

with significant morbidity and mortality and represents a

medical emergency Early, targeted therapy is crucial; the

first hour of care may be key to a successful outcome.1,2

Therefore, it is important that physicians are aware of

updated concepts and management guidelines for

treat-ing patients with shock Although the principles of

shock management are well established, there is

consid-erable heterogeneity of bedside management

This heterogeneity is apparent not only with

accurate clinical identification of a shock state3but also

in regard to evaluation and therapy Critical care

soci-eties and other experts have published evidence-based

guidelines for diagnostic criteria and therapeutic

strat-egies4–8; however, these recommendations generally

fo-cus on severe sepsis and septic shock This article reviews

the traditional criteria and current guidelines for

man-agement of shock, the traditional and newer diagnostic

and monitoring techniques, and therapeutic strategies

OVERVIEW, DEFINITIONS, AND DIAGNOSIS OF SHOCK

Shock is traditionally defined by multisystem organ hypoperfusion, whatever its specific cause, leading to common physical signs It can also be defined as an inability to assure adequate cellular and tissue oxygen supply and removal of waste products of cellular metab-olism, thus overwhelming the compensatory mecha-nisms of the organism

The presentation of shock may be obvious but can also be latent and incomplete, leading to a delayed diagnosis, potentially worsening the prognosis and de-creasing chances of reversal The clinician must be familiar with different clinical patterns of shock and the pathophysiological aspects of shock, including car-diovascular (ventricular pressure–volume curves, cardiac function curves), biochemical (oxygenation cascades), and immunological (mediators and cytokine cascades) features

The clinical signs and symptoms of shock have been known for years9 and have been presented in

1

Cardiology Department, Centre Hospitalier Territorial Gaston

Bourret, Noumea, New Caledonia, France.

Address for correspondence and reprint requests: Olivier Axler,

M.D., Ph.D., F.C.C.P., Cardiology Department, CHT Gaston

Bourret, 98800 Noumea, New Caledonia, France E-mail: olivier.

axler@canl.nc.

Non-pulmonary Critical Care: Managing Multisystem Critical Illness; Guest Editor, Curtis N Sessler, M.D.

Semin Respir Crit Care Med 2006;27:230–240 Copyright # 2006

by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York,

NY 10001, USA Tel: +1(212) 584-4662.

DOI 10.1055/s-2006-945526 ISSN 1069-3424.

230

comprehensive reviews.1,10Several points are worthy of

emphasis First, the diagnosis must be made quickly,

followed by classification of type of shock Second, the

sensitivity and specificity of each sign are highly variable

Third, the quantitative aspects of these signs are useful

but vary depending upon the clinical circumstances The

first step is to begin the correct resuscitation measures,

not only to achieve therapeutic goals but also to confirm

the diagnosis Depending on the response to the

ther-apeutic intervention, the diagnosis can be confirmed or

corrected, allowing adjustment of treatment

In its complete clinical presentation, shock

clas-sically includes: tachypnea; tachycardia; low systolic,

diastolic, and mean blood pressures (BPs); diaphoresis;

poorly perfused skin and extremities; cyanosis; mottling

of cool and moist extremities; altered mental status

(ranging from decreased state of consciousness to

agi-tation); and decreased urine output Joly and Weil

emphasized the role of the ‘‘cold great toe,’’11 whereas

we have noted that cold knees have an excellent

diag-nostic specificity and sensitivity for shock (unpublished

data)

However, these signs are not always present

con-comitantly, and some of these features may be absent or

borderline For instance, in classical shock, BP is

de-creased, and a commonly accepted threshold for a

resuscitation goal in septic shock is 65 mm Hg for

mean arterial pressure (MAP).6However, not all

hypo-tensive states are associated with shock, and not all

shocks present with hypotension In fact, some shock

states present with high BP at the onset because of the

adaptive adrenergic response Early septic shock is

clas-sically ‘‘hyperdynamic,’’ with increased pulse pressure

and warm extremities In addition, low BP is relative

to the baseline BP for a given patient Invasively

meas-ured BP using an intra-arterial catheter is more accurate

than cuff measurements.12Chronotropic medications, or

sinus or atrioventricular dysfunction, can blunt the

tachycardic response Oliguria is often defined as urine

output less than 0.5 mL/kg/hr.6 From a laboratory

standpoint, blood lactate is a robust clue of shock arising

from cellular and tissue hypoxia,3and precedes acidemia

This was recently confirmed,2 with a threshold of

4 mmol/L consistent with shock However, the

specific-ity of blood lactate is imperfect because any condition

exceeding the aerobic threshold leads to increased lactate

levels, and some metabolic conditions increase lactate

levels without shock (i.e., any sympathetic activation).13

Tissue hypercapnia is known to correlate well

with decreased blood flow.14 The first organ to be

studied was the gastric mucosa, but this technique has

largely been abandoned Sublingual PCO2has emerged

as a good predictor of shock (irrespective of cause), and

in some studies was superior to blood lactate levels and

mixed venous oxygen saturation (SVO2) or central

venous oxygen saturation (SCVO ).15,16

TRADITIONAL AND NEWER METHODS AND TECHNIQUES TO ASSESS

MECHANISMS OF SHOCK Several simple tools used in the initial management of shock (e.g., electrocardiogram; chest radiographs; routine hospital chemistries; blood gases) are well known and will not be further discussed here In this section, invasive and noninvasive techniques to assess hemodynamics are dis-cussed Measurement of central venous pressure (CVP)

or pulmonary artery pressure (PAP) may be useful to classify the mechanism of shock Further, measurement

of SCVO2 [via a catheter in the superior vena cava (SVC)] or mixed SVO2(via a pulmonary arterial cathe-ter) may be useful to diagnose and monitor the impact of therapeutic interventions in patients with shock.17 Arterial pulse contour techniques are used to measure cardiac output (CO), and requires arterial access.18,19 This technique is incorporated in more sophisticated devices, measuring other parameters as preload with an estimation of fluid responsiveness for the LiDCO plus System (LiDCO Ltd., Cambridge, UK) via a pulse power analysis.18–20 Another system, PiCCO (Pulsion Medical Systems AG, Munich, Germany) also measures intrathoracic volumes and extravascular lung water from transpulmonary indica-tor dilution.21,22This latter technique mandates fem-oral arterial and central venous access, whereas the former requires only a radial artery and a peripheral vein Analysis of the systemic systolic pressure, pulse pressure and stroke volume (SV), and their respiratory variations, provides an excellent assessment of preload and estimation of fluid responsiveness.19

Ultrasound techniques that are useful to assess fluid status and cardiac function include esophageal Doppler23 and echocardiography (transthoracic and transesophageal).24Methods such as monitoring splanch-nic blood flow or monitoring the microcirculation with videomicroscopy have been utilized in research investiga-tions but have no or limited clinical utility

Traditional Methods

CENTRAL VENOUS PRESSURE MONITORING

Although CVP was recently shown to be somewhat inaccurate to assess preload,25,26 CVP, when integrated into an algorithm, was a useful parameter to guide volume administration in a cohort of septic patients.2However, CVP measurements should be interpreted with caution, even at low or high values, when the value is used in isolation.10,25–28 Some authors emphasize the need to incorporate the cardiac and venous return curves for a correct interpretation of CVP.29,30Indeed, the basic con-cept espoused is to use CVP with simultaneous measure-ment of cardiac output In a study of 33 ICU patients, the right atrial pressure (RAP) decreased at least 1 mm Hg

EVALUATION AND MANAGEMENT OFSHOCK/AXLER 231

with inspiration [with a decreased pulmonary artery

oc-clusion pressure (PAOP) of at least 2 mm Hg with

inspiration] and increases in CO of
250 mL/min.30

This analysis can differentiate ‘‘relative hypovolemia’’ (or

more accurately a fluid responsive state) from euvolemia

This concept was discussed in a recent excellent review.31

Despite the low reliability of CVP to assess preload, this

parameter continued to be widely measured by 93% of a

cohort of European intensivists in 1998.32

CENTRAL VENOUS OXYGEN SATURATION (SCVO 2 )

The O2saturation in a central vein (most often the SVC)

was recently shown to be a key component of early

goal-directed therapy in the emergency department (ED)2;

values < 70% are consistent with incomplete

resuscita-tion This parameter is less useful after several days of

severe critical illness and severe tissue oxygenation

defi-cit.17,33,34A low SVO2generally reflects low CO because

oxygen extraction by the tissues is greater in cardiac

failure.34,35 Low SCVO2 is also associated with a poor

prognosis34 and often appears earlier than any other

clinical sign of shock.2In a cohort of patients with septic

shock, Rivers and colleagues demonstrated mortality

reduction of 15% by maintaining a therapeutic algorithm

that maintained the following parameters: SCVO2

> 70%; CVP > 8 to 12 mm Hg; MAP > 65 mm Hg;

urine output > 0.5 mL/kg/h.2 SCVO2 and SVO2 are

usually similar but can diverge in some cases, particularly

in severe sepsis, due to greater O2 extraction in the

hepatosplanchnic circulation However, SCVO2is

pre-ferred to SVO2because it can be measured more simply

from a central venous catheter rather than a pulmonary

artery catheter (PAC).36–38SCVO2can be continuously

monitored using a special catheter or intermittently by

direct repeated samples SCVO2correlates with outcome

in all kinds of shock, even during cardiopulmonary

resuscitation.17,33,34 The research by Rivers and

col-leagues addressed very early shock,2 and studies have

not demonstrated benefit for patients later in the course

of shock when oxygen extraction may be impaired and

SCVO2exceeds 80%.17,33,34

PULMONARY ARTERY CATHETERS

The PAC has been used to differentiate various

mecha-nisms of shock since the early 1970s, but utilization of data

from PACs has many pitfalls First, hemodynamic values

are frequently misinterpreted, leading to incorrect

treat-ment.37,38Second, recent studies found that the use of

PAC did not confer any benefit compared with no PAC

use36,39,39a,39b; further, some studies suggested deleterious

effects of PACs, particularly in patients presenting

with acute respiratory distress syndrome (ARDS) or

shock.35,36,39However, PAC-directed therapy was shown

to be cost effective in the preoperative period.40–43 In

North America, there continues to be relatively

wide-spread use of PACs,6whereas newer techniques such as

ICU echocardiography24,44 and pulse contour analysis techniques (PiCCO and LiDCO)18,19,21,22 have sup-planted PACs in most European ICUs Despite the limitations of PACs, recent guidelines (e.g., the Survival Sepsis Campaign) continue to recommend PACs for the assessment of severe sepsis and septic shock.6 More-over, a recent paper focusing on ‘‘practice parameters for hemodynamic support of sepsis in adult patients’’ favors the use of PACs, and states that ‘‘echocardiography may also be useful to assess ventricular volumes and cardiac performance.’’7

Several measured and derived values are available from a PAC to determine the mechanism of shock: PAP, PAOP, right ventricular pressure (RVP) and RAP, CO by thermodilution, and its modified deriva-tives: (1) semicontinuous cardiac output (using a thermal coil in the right ventricular portion of the PAC; (2) calculation of right ventricular end-diastolic volume (RVEDV) from measurement of right ventricular ejec-tion fracejec-tion (RVEF); SVO2 and related oygenation variables; oxygen consumption (VO2); oxygen delivery (DO2); and O2extraction ratio (O2ER)

Measurement of PAP is a very important param-eter to diagnose pulmonary arterial hypertension (PAH)

as may be seen in ARDS, pulmonary embolism, right ventricular infarction, obstructive lung disease, left heart diseases, and primary PAH Its measurement is generally easy and its interpretation is the least problematic of all PAC-derived data

Using the PAOP is one of the most controversial issues related to PAC Classically, hypovolemic shock has low right and left heart filling pressures, whereas left ventricular cardiogenic shock is associated with elevated PAOP and RAP Historically, PAOP has been consid-ered to provide information regarding preload and the presence or absence of pulmonary edema However, measurement and interpretation of PAOP may be diffi-cult.37,38,45The utility of PAOP to assess volume status has recently been challenged25,26,46; this is also true for RAP.25,26,46This can be explained by a frequent absence

of linearity between left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic pressure (LVEDP); second, disparity between LVEDP and PAOP may exist The LVEDV/LVEDP relationship can be profoundly modified by LV compliance factors such as left ventricular hypertrophy (LVH), myocardial ischemia, positive end-expiratory pressure (PEEP), and active exhalation Further, PAOP can overestimate LVEDP if mitral stenosis or mitral regurgitation are present, and conversely underestimates LVEDP when diastolic dysfunction or hypervolemia exist These con-ditions are frequent in patients presenting with shock but are often not appreciated Thus PAOP should be inter-preted cautiously.45Notwithstanding these pitfalls, 58%

of European intensivists continued to measure PAOP as part of monitoring critically ill ICU patients in 1998.32

232 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006

Measurement of CO is one of the most important

issues in the management of shock.1,47–49

Thermodilu-tion is the gold standard method for measuring CO for

clinical use because measurement is relatively

straight-forward and does not present the same technical

diffi-culties as PAOP Additionally, the thermodilution

technique was validated against electromagnetic flow,

Fick, and dye dilutions techniques However,

dilution has important limitations Specifically,

thermo-dilution can overestimate CO in low output states,

whereas significant tricuspid regurgitation leads to

underestimation of CO Other confounding issues

in-clude intracardiac shunts and temperature issues.47 In

this context, echocardiography is helpful Recently, the

left ventricular outflow tract (LVOT) pulsed Doppler

method has been employed as an alternative method to

measure CO.49,50Some authors believe that this should

become the new gold standard49,50 unless significant

aortic valve disease exists

Cardiac output can be monitored with a modified

PAC This PAC incorporates a thermal coil in the right

ventricular portion of the catheter, and continuous CO

measurement is based on the delivery of electrically

generated heat to the blood near the right atrium and

ventricle and the resulting temperature change in the

PA This technique avoids performing an intermittent

injection and yields a continuous CO display The

accuracy is good compared with thermodilution,

pro-vided regular calibration is performed.51

Recent refinements of the PAC allow calculation

of RVEF This catheter has a rapid-response thermo

‘‘slur’’ and intracardiac electrocardiogram electrode,

al-lowing the calculation of RVEF Combined with SV,

the RVEF allows the calculation of right ventricular end

diastolic volume (RVEDV) This parameter has been

extensively studied in circulatory shock,52,53 but in the

most important studies comparing RVEDV before and

after a fluid challenge, significant difference was found in

only one of 15 studies.53 Intraindividual changes in

RDEDV with various treatments are more useful than

absolute values.25,52,54 Continuous fiberoptic

measure-ment of SVO2, coupled with traditional PAC

parame-ters, is available with some catheters

Finally, the relationship of oxygen

delivery/con-sumption ratio (DO2/VO2) has been used for both

research and clinical indications among critically ill

patients for more than 3 decades.55However, awareness

and incorporation of these variables into clinical

proto-cols have not been shown to influence outcome.55

Newer Methods

ECHOCARDIOGRAPHY-DOPPLER

Cardiac ultrasound (echocardiography) has increasingly

been utilized in ICUs within the past few years

Trans-thoracic echocardiography (TTE) is noninvasive and relatively easy to perform after an adequate training

Transesophageal echocardiography (TEE) is modestly invasive and requires some degree of sedation for patient comfort but is safe and highly accurate Echocardiog-raphy provides an excellent assessment of cardiac func-tion and estimates left and right heart filling pressures and can be useful to determine the cause of shock.56 Echocardiography provides acceptable estimates of most parameters gleaned from pulmonary artery catheters (PACs) (i.e., CO; right arterial pressure (RAP) from inferior vena cava (IVC) size and ventilatory variations, systolic pulmonary artery pressure (SPAP); left and right ventricular filling pressures; ejection fraction; ventricular interdependence; right heart function; diastolic dysfunc-tion; left ventricular hypertrophy (LVH); ischemic heart disease, valvular diseases, and so on) Recent publications emphasized the value of echocardiography to predict fluid responsiveness using heart–lung interactions ba-sics.57–65Many studies have shown that echocardiogra-phy (either TTE or TEE) may be invaluable to monitor therapeutic interventions or hemodynamic changes in critically ill patients.62–80TEE is more useful than TTE for this purpose.66–79 In most of the studies, TEE provided clinically useful information in 60 to 90% of cases More importantly, TEE had a direct favorable impact on the acute care management.79

Our recent experience with TTE has been favor-able (unpublished data) The value of TTE was recently underscored in a study by Joseph et al, who noted clinically useful and reliable information in 70 to 80%

of critically ill ICU patients who had TTE.80 Recent improvement in imaging, software, and electronic sys-tems have improved the quality and utility of images gleaned from TTE Transthoracic echocardiography is useful as a diagnostic tool for critically ill patients in shock (or impending shock) but in some cases, TEE is necessary for a more accurate assessment.79 Specific indications for TEE include: aortic dissection (when computed tomographic angiography is inconclusive, or

to complete it if necessary); endocarditis (especially when

a valvular prosthesis is present); complicated cardiac surgery; marked obesity; poor echogenicity with TTE;

intracavitary thrombi; and cardiac sources of emboli

TEE is the preferred method to assess the SVC size and its ventilatory variations, a new powerful parameter

to predict fluid volume responsiveness.64

In a patient with shock, echocardiography (usu-ally TTE) can provide prompt (within 15 minutes) assessment of critical variables, including size of cardiac chambers; left and right systolic function; cardiac output (49); wall motion abnormalities; valvular pathology; LV filling pressures from a combination of parameters ob-tained from mitral flow, Doppler tissue imaging (DTI), pulmonary venous flow (PVF), early diastolic mitral flow propagation velocity (Vp), PA pressures; RV filling

EVALUATION AND MANAGEMENT OFSHOCK/AXLER 233

pressures; and pericardial imaging Echocardiography

can estimate fluid volume responsiveness using heart–

lung interactions This concept assumes that the

meas-urement of some parameters before fluid loading can

predict a significant increase of cardiac ouput in

hemo-dynamically unstable patients.54 This estimation uses

inferior vena cava (IVC)62,63 or SVC,64 size and

ven-tilatory variations, as well as the respiratory variations of

the LVOT.57–59These parameters correlated strongly in

these 5 studies with the concept of ‘‘fluid

responsive-ness.’’ The measurement of left heart filling pressures

requires more sophisticated echo devices These two new

steps represent one of the major advances in the

manage-ment of shock

Some echocardiographists prefer to use TTE first,

and then TEE if necessary, and some always use directly

TEE This is an ongoing discussion, and this choice

depends upon the ability of each echocardiographist

Published data regarding the assessment of

pre-load using echocardiography are disappointing Prepre-load

was initially assessed by measuring left ventricular

end-diastolic diameters, areas, or volumes; close correlations

were found with blood loss or expansion in normal

subjects81 or perioperative conditions.82 However, in

ICU settings, recent studies found that the left ventricle

end-diastolic area (LVEDA) failed to accurately predict

fluid requirement or fluid overload status, particularly

when compared with newer methods to assess fluid

responsiveness.57,83–85 Therefore, echocardiographic

measurements of LV and RV size are no longer used

to assess volume status However, diameter of the IVC

and its ventilatory variations are invaluable to predict

fluid responsiveness This measurement is simple to

assess, with a short learning curve (1 hour) The IVC

diameter and its ventilatory variations are measured with

TTE, on a subcostal view, in M mode Measurement

parameters include IVC diameter (D) at end-expiration

(Dmin) and at end-inspiration (Dmax); distensibility

index of the IVC (dIVC) calculated as the ratio of

Dmax-Dmin:Dmin and expressed as a percentage, or

((Dmax-Dmin:Dmaxþ Dmin):2 ).62,63,86Measurement

of IVC size and respiratory variation is useful to predict

response to a fluid challenge.62,63,65The useful threshold

was 12% of variability, with a positive and negative

predictive value of 93% and 92% in one study of septic

patients requiring mechanical ventilation (MV).62

An-other group studied 23 patients in septic shock requiring

MV.63 The size and ventilatory variation of the IVC

(IVCVV) predicted a positive response to a fluid

chal-lenge [
15% increase of the cardiac index (CI)

follow-ing a 7 mL/kg fluid challenge] IVCVV was defined in

this study by Dmax-Dmin:Dmin There was an excellent

correlation (r ¼ 0.9) between an 18% IVCVV at baseline

and
15% increase in CI after a fluid loading, with 90%

specificity and 90% sensitivity.63 Importantly, baseline

CVP did not accurately predict fluid responsiveness

Additionally, in a cohort of septic patients on MV, measurement of the SVC by TEE, and ventilatory collapsibility of the SVC predicted the cardiac response

to fluid challenge.64 The 36% threshold of variability (Dmax-Dmin:Dmax) could define responders and non-responders in CO, with 90% sensitivity and 87% specif-icity.64 Although measurement of IVC diameter ventilatory variations was studied only in septic patients

on MV, we use it in every patient in acute circulatory or acute respiratory failure, even among patients not requir-ing MV However, outcomes data in these other patient populations are lacking

The second important new parameter in assessing shock is the ventilatory variation of left ventricular out-flow tract (LVOT) (called also aortic) Doppler veloc-ities Two studies found that this parameter was a strong predictor of preload responsiveness: one in septic pa-tients on MV (using TEE),57 and one with a rabbit model.58The first study defined the respiratory variation

as the ratio of the difference between maximal velocities

to the mean of these two velocities A ventilatory variation of LVOT blood flow velocity > 12% was associated with a 15% increase of CI with a 91% positive predictive value A ventilatory variation < 12% had a 100% negative predictive value This could imply that no volume expansion was necessary with a high degree of confidence There was a high degree of correlation between baseline ventilatory variation and degree of CI increase after volume expansion.57This important study can be extended to TTE We regularly use this method

in all patients in shock to assess potential fluid respon-siveness Patients must be on MV and well adapted to their ventilator, and must be free of arrhythmias Slama

et al found similar results in a rabbit model, using TTE, with progressive blood withdrawal.58In these two stud-ies, this parameter was more powerful than all other parameters (CVP, PAOP, left ventricular end-diastolic area) that had been used for the past several years The most recent studies showed that ‘‘static’’ echocardio-graphic parameters failed to consistently predict re-sponse to fluid loading.57–59,83–85

The second important advance is the ability of echocardiography to estimate LV and RV filling pres-sures (LVFP and RVFP) These measurements were extensively studied over the past 10 years in the cardio-logical arena86–90but were only recently applied to the critically ill (noncardiac) patients in ICUs.91–93 These measurements do not accurately measure preload, but may predict fluid responsiveness An algorithm is now available to determine if LVFP are predictive of PAOP

as ‘‘high’’ (> 15 mm Hg) or ‘‘not high’’ ( 15 mm Hg) This analysis is usually applied when the LVEF is decreased (< 45%) This algorithm is determined by the analysis of the combination of pulsed Doppler of mitral flow, tissue Doppler imaging, color M-mode of mitral flow, pulmonary venous flow (PVF), left atrial

234 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006