Cardiac Ischemia During Weaning From Mechanical Ventilation

clinical investigations in critical care Cardiac Ischemia During Weaning From Mechanical Ventilation* Wissarn Chatila, MD; Salim Ani, MD; Denise Guaglianone, BS, RZV, MSN; Badie Jacob, MD; Yaw Arnoateng-Adjepong, MD, PhD; and Constantine A. Manthous, MD

In this prospective study, we measured the ST segments, heart rate-systolic BP product (RPP), respiratory rate to tidal volume ratio (RVR), and pulse oximetry saturations of patients in our medicaV cardiac ICUs before and during weaning from mechanical ventilation. Ninety-three patients were enrolled with a mean age of66.5::±:: 15.0 years (mean::±::SD), mean acute physiology and chronic health evaluation (APACHE) II score of 16.0::±::6.9, and mean duration of mechanical ventilation of 5.2::!:::8.6 days. Forty-nine patients had coronary artery disease (CAD). Six of 93 patients (6.4%) experienced ECG evidence of ischemia during weaning. Five of these six had a precedent history of CAD and four failed initial weaning attempts (22% of patients with CAD who failed weaning). The RPP, for the group as a whole, increased significantly during weaning from 12.0::±::3.1 to 13.4::±::4.0 mm Hg·hpm·l0 3 (p<0.01). The rate to volume ratio did not change significantly during weaning, except in the subgroup of patients who failed to wean, in whom it increased from 98.4::±::45.2 to 124.9::±::54.9 hpm!L (p<0.05). Oxygenation also decreased significantly from 0.98::±::0.02 to 0.96::±::0.03 and was significantly associated with weaning failure (risk ratio [RR]=3.9; 95% confidence interval [CI]=L7 to 9.0). Thirty-seven patients failed the initial weaning attempt. Cardiac ischemia (RR=l.8; 95% Cl=l.O to 3.4) and an increased RVR (RR=l.7; 95% Cl=0.9 to 3.4) tended to increase the risk of weaning failure. Cardiac ischemia, although infrequent (6%) in the general population of weaning medicaVcardiac ICU patients, should he considered in patients with CAD who fail to wean. (CHEST 1996; 109:1577-83) Key words: electrocardiogram; ischemia; mechanical ventilation; m:ygen consumption; ST segment; weaning; work of breathing Abbreviations: APACHE=acute physiology and chronic health evaluation; bpm=beats per minute; CAD=coronary artery disease; CI=confldence interval; CPAP=continuous positive airway pressure; MV =mechanical ventilation; RPP':'heart ratesystolic BP product; RR=risk ratio; RVR=respiratory rate to tidal volume ratio; S=Rothman Synergy Index; Vo 2 =oxygen consumption

weaning trials are performed to assess the readiness of mechanically ventilated patients to sustain spontaneous ventilation. Insofar as spontaneous breathing increases basal metabolism (oxygen con-

For editorial comment see page 1421 sumption [Vo2]) compared to that on full mechanical ventilatory support, 1-3 weaning increases cardiopulmo-

*From the Pulmonary and Critical Care Division, Bridgeport (Conn) Hospital and Yale University School of Medicine; l'ilew Haven, Conn. Manuscrigt received September 13, 199.5; revision accepted November lt. Reprint requests: Attn: Carine, c/o Dr. Manthous, Bridgeport Hospital, Dept of Medical Education, 267 Grant St, Bridgeport, CT . 06610

nary demand. In patients with severe coronary artery disease (CAD), this increment in Vo2 and the increase in cardiac loads imposed by the transition to spontaneous breathing could lead to cardiac ischemia during weaning. Few studies have examined the frequency of cardiac ischemia as patients are weaned from mechanical ventilation (MV) 4-8 and no previous studies (to our knowledge) have described the incidence of ischemia and its impact on weaning in medical and cardiac ICUs. In this prospective study, we determined the frequency of ECG changes suggestive of cardiac ischemia during weaning from MV and examined the relationship between ischemia and weaning outcome. In addition, we examined changes in myocardial work, breathing pattern, and arterial oxygenation as possible predictors of weaning failure and myocardial ischemia. CHEST I 109 I 6 I JUNE, 1996

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B FIGURE 1. Representative ST tracings of patient 6 before and during weaning. Panel A presents the "template" (above) and real-time (be1ow) ST segments for leads II, V2, and I before weaning. Panel B presents tracings obtained during weaning after the monitor detected significant ST changes. MATERIALS AND METHODS

Patient Selection

Our hospital investigational review board waived formal review of this study. Patients admitted to the Bridgeport Hospital medical ICU and cardiac care unit between June 1994 and February 1995, who required MV were eligible for this study. Patients were excluded if they had a pacemaker, were receiving digoxin, or had evidence of bundle branch block on their ECGs. All patients were ventilated on ventilators (Puritan-Berrett 7200; Puritan-Bennet Corporation; Carlsbad, Calif). Patients entered the study at the onset of weaning, which was conducted entirely by their primary physicians. Patients were prospectively stratified for presence or absence of CAD which was considered present if the patient had the following: (1) angiographically proven CAD disease (one or more vessels with >50% stenosis); (2) a positive exercise stress test or myocardial infarction in the year prior to study; or (3) admission to hospital with chest pain/shortness of breath and ECG evidence of cardiac ischemia in the year prior to the study. ST Segment Monitoring

Patients were monitored for cardiac ischemia (using the Tram Critical Care Monitor; software version 6B; Marquette Electronics; Milwaukee),9 which included continuous ST segment analysis of leads I (lateral), II (inferior), and V2 (anterior). The monitor displays baseline tracings (referred to as a template, see Fig 1) and continuous ST segments with 30-min trends for each lead. The ECG isoelectric point is determined 25 ms before the Q wave, and the ST segment is measured, with reference to the isolectric point, 60 ms following the J point. ST segments are measured continuously with reference to a dominant template (defined as that with a normal classification and the highest matched beat count). All templates were recorded at a 0.05-Hz frequency response. After skin preparation with rubbing alcohol, the following fivelead configuration was adopted: (l) right and left arm electrodes were placed below the right and left clavicle; (2) right and left leg electrodes were placed on the right and left lower rib cage; and (3) the chest (V2l electrode was placed in the left fourth intercostal space at the sternal border. Weaning

The choice of weaning modality was determined by the patients' primary physicians, and included T-piece or continuous positive airway pressure (CPAP) (with or without pressure support). Re1578

petitive T-piece trials were conducted until patients were able to breathe comfortably for 1 h or more without development of the criteria listed below. Pressure support weaning trials began at between 5 to 15 em H20 inspiratory support with 5 em H20 positive end-expiratory pressure. Inspiratory pressures were decreased by 2 to 5 em H20 every 2 to 3 has tolerated (see below) until inspiratory pressure reached 0 to 5 em H20, at which point patients underwent aT -piece trial. Reinitiation of MV!failed weaning occurred for the following reasons: ( l) respiratory rate greater than 35 breaths per minute (bpm); (2) PaC02 increment of more than 5 mm Hg; (3) Pa02less than 60 mm Hg or pulse oximetry saturation less than 90% on 50% or less inspired oxygen; (4) subjective distress/ diaphoresis; (5) heart rate increment greater than 20 beats per min; (6) systolic BP decrement greater than 20 mm Hg; and (7) arrhythmia (increased premature ventricular beats >41min or new onset of sustained supraventricular rhythm). Successful weaning! liberation from MV was defined as spontaneous unassisted ventilation for more than 24 h. Measurements

Each patient was observed by his/her nurse and one of the investigators. Patients were placed on the ST segment analyzer in the hour preceding, during, and for up to 24 h after the initial weaning trial. ST segment templates and tracings were obtained just before and after 30 min of weaning. ST segment tracings were also recorded with any ischemic episode, defined as more than 1-mm change from baseline. BP (by arterial line or cum, heart rate, pulse oximetry saturation, respiratory rate, and minute volume (determined by a handheld Wrights spirometer through the endotracheal tube) were also measured at the initiation and after 30 min of weaning. The respiratory rate to tidal volume ratio (RVR=bpm/[Umin+bpm)) and heart rate-systolic BP product (RPP=heart rate times systolic BP) were computed at each interval from the above data. The RVR has been validated as an accurate predictor of weaning outcome. 10 The RPP increases with myocardial work and is an index of myocardial perfusion requirement. 11 .12 Ischemia was defined as greater than 1.0-mm ST segment change from the isoelectric baseline and the ST segment monitor alarmed at this threshold. All ST segment tracings were retrospectively reviewed by a cardiologist who was blinded to clinical outcome. ST segments were categorized by the cardiologist as follows: (l) ischemic (> l mm ST segment elevation or ST depression with shape suggestive of ischemia); (2) equivocal (:51 mm change with T-wave Clinical Investigations in Critical Care

Table !-Characteristics of 93 Medical/Cardiac Patients Weaned From MV

Table 2-Therapies for Cardiac Ischemia in Each Group* Therapy

CAD-, S (n=25)

CAD+, S (n=3l)

CAD-, F (n=19)

CAD+, F (n=18)

Nitrates Calcium blockers Beta-blockers

6 (24) 4 (16) 0

18 (58) 6 (19) 2 (6)

3 (16) 3 (16) 0

10 (56) 4 (22) l (6)

Ko. (%)

Characteristic

66.5::!:1.5.0 6 20 67

Age, yr <40 40-60 >60 Sex Male Female APACHE II Duration of MV, d <5 5-10 >10 Respiratory failure Hypoxemic Hypercapnic CAD Non-CAD COPD Pulmonary edema Sepsis

30 (32) 63 (68) 16.0::!:6.9 .5.2::!:8.6 58 26 9 46 47 49 44 2.5 18 :32

*Note that patient with CAD received nitrates more often than patients without CAD regardless of weaning outcome (S=successful weaning, F=failed weaning, percent in parentheses).

(27)

was calculated to determine the presence of interaction on an additive modeJ.l 5 The synergy index is equal to one (S=l) in the absence of an interaction. In such a case, the joint effect of two variables is equal to the sum of their independent effects. A synergy index greater than one (S> l) suggests the presence of synergistic interaction: the observed joint effect is greater than that expected from the sum of the independent effects of the component variables. Conversely, a synergy index less than one (S
(19) (34)

RESULTS

(49) (51) (.53) (47)

abnormalities); (3) nondiagnostic because of the presence of left ventricular hypertrophy artifacts; and (4) no change compared with baseline tracingsB Changes in ST shape that were considered diagnostic of ischemia included the following: (l) upsloping ST depression of 1..5 mm or more, 80 ms following the J point, or (2) horizontal or downsloping ST depression of 1.0 mm or more, 80 ms after the J point.ll,l:l

Data Analysis Initial and 30-min values f(>r the RVR, RPP, and pulse oximetry saturation were compared by paired Student's t test. Nonpaired Student's t tests were performed for subgroups: patients who failed!did not Jail weaning and patients who did!did not experience cardiac ischemia for each variable at the two intervals. A p value of less than 0.05 signified statistical significance. Risk ratios were computed as the primary· measure of associations between weaning failure vs the presence of CAD, myocardial ischemia, and changes in RVR, RPP, and oxygen saturation. Also, risk ratios were computed between myocardial ischemia and changes in RVR, RPP, and oxygen saturation. Ninety-five percent confidence intervals (Cis) were calculated for each of the risk ratios (RRs) computed. The variances were derived using the Greenland and Robbins 14 method for sparse follow-up data. Stratified analyses were used to determine possible interaction between changes in RVR, changes in RPP, myocardial ischemia, and oxygen desaturation in predicting weaning outcome. In addition, the Rothman Synert,ry Index (S)

Tables 1 and 2 describe characteristics and antiischemic therapies of the 93 patients enrolled in this study. Patients ranged in age from 26 to 100 years with a mean age of66.5:±:15.0 years (mean:±:SD). Patients had been ventilated between 1 and 72 days with a mean of .5.2:±:8.6 days (median value was 3 days) and had a mean acute physiology and chronic health evaluation (APACHE) II score of 16.0:±:6.9. Forty-nine patients (53%) had CAD. Sixty-eight (73%) patients were pressure support weaned; 2.5 (27%) were weaned by repetitive T-piece trials. Fifty-six (60%) of the 93 patients were successfully liberated from MV on the first day of weaning. Eighteen of the 37 patients (49%) who failed their first weaning trial had CAD. Six of 93 patients (6%) experienced ischemia during weaning. Table 3 lists the mode of weaning, the time to onset of ischemia, and associated symptoms for these patients. Five of these had CAD. Four of the six patients (Table 3, patients 1 through 3, 6) were noted to have ischemic changes during their initial weaning trial; the conditions of the remaining two patients were diagnosed by a cardiologist on retrospective review of the ST tracings. In patient 6, who had no history of

Table 3-Characteristics of Six Patients Who Experienced Ischemia During Weaning* Patient No.

History

2 3 4 .5 6

CAD, CHF, lung CA, MI CAD, CHF, HTN, syncope CAD, HTN, DYl, CVD CAD, D.'\1, HTN, PYD, CHF CAD. CVD, PVD, CIIF HTN,CYD

Duration of M\', d 2 3 3 7

12 2

Weaning Mode C:PAP/PS.S T-piece T-piece CPAP/PSl2 CPAPIPS5 CPAP/PS5

Onset to Ischemia, min 10

3 15

40

Weaning Outcome F F F F

s s

Symptoms Chest paint None Distress 1 Distress 1 None None

*CHF=congestive heart fllilure; CA=cancer; Ml=rnyocardial infilrction; HTN=hypertension; DM=cliabetes; CYD=cerebral vascular disease; PVD=penpheral vascular disease; F =failed; S=snccessful. 1Symptoms occurred coincident "~th ST segment changes. CHEST /1 09 I 6 I JUNE, 1996

1579

Table 4-Subgroup Analysis of the Rate-Product Index, Rate to Volume Ratio Index, and Oxygen Saturation During Weaning From MV

Subgroup Successful CAD Non-CAD Unsuccessful CAD Non-CAD Total

Before Weaning

During Weaning

p Value

Before Weaning

During Weaning

p Value

Before Weaning

During Weaning

p Value

10.5::'::2.9 12.5::'::3.3

11.9::'::4.0 13.2::'::3.3

<0.01 0.20

62.1::'::27.0 73.5::'::46.1

64.0::'::17.1 63.3::'::30.2

0.67 0.08

97.8::'::1.7 97.6::'::1.8

97.0::'::1.7 96.8::'::2.6

<0.05 =0.09

13.0::'::3.0 12.7::'::2.5 12.0::'::3.1

15.2::'::4.4 14.3::'::4.0 13.4::'::4.0

0.02 <0.01 <0.01

96.5::'::40.7 100.1::'::50.2 78.5::'::42.7

113.5::'::49.0 134.7::'::15.4 85.4::'::47.7

0.27 0.05 0.15

97.9::'::1.3 97.5::'::2.1 97.7::'::1.7

94.2::'::3.6 94.2::'::3.4 95.9::'::3.0

<0.01 <0.01 <0.01

CAD, transient ischemia lasting 4 min was recorded and did not interfere with weaning or extubation. Figure 1 demonstrates tracings before and during weaning in this patient. Four of six patients who experienced cardiac ischemia failed to wean on the initial attempt and their ST segments returned to baseline with the resumption of MV. These patients were later successfully extubated after adjustment of their cardiac medications with no recurrences of ischemia during their subsequent weaning trials. For the group as a whole, the RPP increased from 12.0:!:3.1 to 13.4:!:4.0 mm Hg·bpm·l03 (p<0.05) and oxygen saturation decreased from 97.7:!: 1.7 to 95.9:!:3.0% during weaning (p0.05). Subgroup analyses (Table 4) revealed that oxygen saturation decreased and RPP increased significantly in all subgroups except in patients without CAD who were successfully liberated. The RVR tended to increase from 100.1±50.2 before to 134.7:!: 15.4 bpm/L during weaning (p=0.05) in patients without CAD who failed weaning. Tables 5 and 6 list the risk ratios of the various variables in relation to weaning failure and ischemia. There was an 80% excess risk of weaning failure in those who experienced myocardial ischemia (RR=l.8; 95% CI=l.O to 3.4). Also, there was a 70% excess risk of weaning failure in patients whose RVR increased compared with those in whom it decreased or did not change (RR=l.7; Cl=0.9 to 3.4). Oxygen desaturation was associated with a 2.9-fold increased risk of weaning failure (RR=3.9; Cl=l.7 to 9.0). The presence of Table 5--Risk Ratios and 95% Cis Between Weaning Failure and Selected Variables Variable

RR

95% CI

Oxygen desaturation Myocardial ischemia RVR increase RPP increase CAD

3.9 1.8 1.7 1.3 0.85

1.7-9.0 1.0-3.4 0.9-3.4 0.7-2.5 0.5-1.4

1580

Oxygen Saturation

RVR

RPP

CADwasnotassociatedwithweaningfailure(RR=0.85; CI=0.5 to 1.4). An increase in the RPP tended to be associated with ischemia during weaning (RR=2.2; CI=0.8 to 6.4); no significant relationship existed between other variables and ischemia. There were no interactions between the RVR and RPP, oxygen desaturation and myocardial ischemia, RPP and oxygen desaturation in predicting weaning failure. An increase in the RVR and myocardial ischemia was synergistically associated with weaning failure. DISCUSSION

The principal finding of this study is the relative infrequency (6%) of ECG evidence of cardiac ischemia during weaning of medically ill patients from MV. However, ischemia was detected more frequently in (10% of) patients with a precedent history of CAD and was associated with weaning failure in 22% of these patients. To our knowledge, no similar study has examined the frequency ofweaning-related ST changes in acutely ill medical patients being weaned from MV (Table 7). Although speculative, myocardial ischemia may have contributed to weaning failure in four of six patients in our study (patients 1 through 4), as further antiischemic therapies resulted in successful liberation of these patients from MV without further ST segment changes. We also noted a significantly increased risk of weaning failure among patients who experienced oxygen desaturation and a trend toward increased failure among those who experienced myocardial ischemia or

Table 6--Risk Ratios and 95% Cis Between Ischemia and Selected Variables. Variable

RR

95% CI

CAD RPP increase Oxygen desaturation RVR increase

4.5 2.2 1.3 0.7

0.5-37.0 0.8-6.4 0.3-6.7 0.1-3.0

Clinical Investigations in Critical Care

Table 1-Previous Studies Examining the Incidence of Cardiac Ischemia During Weaning* Study

n

Design

Rasanen et al4

12

Descriptive

ARF after MI

Hurford et al5

15

Descriptive

ARF

Hurford and Favorito6

17

Descriptive

CRF

Abalos et al 7

62

Descriptive

ARF with CAD

Lemaire et al8

15

Descriptive

ARF, COPD, CAD

Population

Findings 6 of 12 patients with ischemia during weaning 7 of 15 had changes in myocardial thallium uptake during weaning without ECG changes 6 of 17 patients had ECG changes that predicted weaning failure 5 of 62 patients had ECG changes during weaning 3 of 15 patients developed gated blood scan evidence of wall motion abnormalities during weaning with increased filling pressures and catechols

*ARF=acute respiratory failure; Ml=myocardial infarction; CRF=chronic renal failure.

rapid shallow breathing. We emphasize that increased risk does not necessarily imply a cause and effect relationship. For example, oxygen desaturation may occur as a consequence of weaning failure rather than as the cause. In contrast, it is plausible to suggest that myocardial ischemia contributes causally to weaning failure. The data suggest that the joint occurrence of cardiac ischemia and rapid shallow breathing dramatically increases the risk of weaning failure. Insofar as the RVR indexes respiratory dysfunction (muscle strength-load imbalance) and ischemia leads to cardiac dysfunction, concomitant insufficiency of both systems signals an increased likelihood of weaning failure. Cardiac ischemia occurs when myocardial oxygen demand exceeds myocardial oxygen delivery via the coronary arteries. Coronary oxygen delivery is inversely proportional to the degree of stenosis of the coronary arteries. Loading of the heart, ie, mechanical loads and/or increased cardiac output to meet increased total body Vo2, increases oxygen demand of the heart. The resumption of spontaneous breathing after MV imposes several loads on the cardiorespiratory system: (I) venous return increases, thus increasing ventricular freload; 16.1 7 (2) left ventricular afterload increases;1 ·18 and (3) total body oxyfen consumption increases by roughly 15 to 25%. 1- Additionally, anxiety associated with weaning/resistive breathing through the endotracheal tube may increase catechols, 8 thus further increasing myocardial work (afterload, preload, chronotropy, and inotropy). We hypothesize that in patients with fixed severe CAD, increased myocardial oxygen demand during weaning exceeds supply, which may lead to a vicious cycle of ischemia, increased catechols (further increasing demand), and worsening ischemia (Fig 2). Despite the fact that resumption of spontaneous breathing increased myocardial demand, signaled by a 12% increase in the RPP, the frequency of ischemia in our cohort was remarkably low. It is possible that ei-

ther the particular ST monitor or the lead configuration used failed to detect some ischemic episodes. Previous studies suggest that even 12-lead ECG may be insensitive in detecting ischemia. 5 However, it is also possible that the frequency of ischemia was truly low. Previous studies have determined that total body oxygen consumption increases by approximately 15 to 25% in patients who are weaned from MV. 2•3 This increase in oxygen consumption is likely accompanied by an increment in cardiac output/increased myocardial oxygen consumption. For purposes of comparison, walking (3 mph) increases total oxygen consumption twofold and exercise testing frequently increases oxygen consumption 4 to 5-fold.l9 The effect of weaning on oxygen consumption is comparable to increasing body temperature from 37 to 39°C (ie, 20%20 ). However, the increased oxygen delivery (cardiac output) required to meet the increased uptake during weaning may require varying degrees of myocardial oxygen consumption dependent on the mechanical loading of the cardiovascular system. For example a 20% increment in cardiac output will cost more myocardial oxygen consumption in situations of increased mechanical load (eg, catechol excess states) than in reduced load states (eg, sepsis/vasodilation). Although a crude measure of myocardial oxygen consumption, 11.12 the 12% increase in the RPP suggests that myocardial work roughly tracked the projected increase in total body oxygen consumption related to weaning. The relative infrequency of weaning-related ischemia may thus suggest the infrequency of critically limiting CAD (to meet a 15 to 20% increment in demand) in our patients. Oxygenation, which reflects both alveolar recruitment and filling (ie, with edema), decreased during the weaning process in patients who failed their weaning trial. Even in the absence of ischemia, pulmonary edema in the weaning period can be explained by increased ventricular preload and afterload.l 6- 18 Note, CHEST/109/6/JUNE, 1996

1581

tvo2 Wenning---,~

t t t

Preload Allerload

)

Contractility

t Heart Rate

~

• • MV0 2>MQ02

..,.

MY'""'dffil Ischemia

FIGURE 2. A proposed mechanism for the pathogenesis of cardiac ischemia .during weaning. Note that in patients with severe CAD, the fncrement in myocardial oxygen demand (MV02) during weaning exceeds myocardial oxygen supply (MQ02) leading to ischemia. Four of the 18 patients with CAD who failed weaning experienced ischemia.

however, that oxygen desaturaton during weaning could also relate to atelectasis, bronchospasm, retained secretions, and hypoventilation (factors that were not examined in this study). Interestingly, in the two study patients who developed ischemia but who were successfully liberated from MV (patients 5 and 6), neither oxygen saturation nor rate-pressure products changed, suggesting that ischemia does not absolutely predict weaning failure or significant increases in myocardial work/decreases in oxygenation. Few studies have examined the frequency of myocardial ischemia during weaning from MV and the effect of occult ischemia on weaning outcome (Table 7). Rasanen et al4 demonstrated ECG evidence of myocardial ischemia in 5 of 12 patients who were weaned from MV following myocardial infarction. Pulmonary artery occlusion pressures also increased significantly with the resumption of spontaneous breathing in both the ischemic and nonischemic groups. Hurford et al5 demonstrated acute left ventricular dilatation (presumed secondary to increased venous return) in 7 of 15 long-term ventilator-dependent patients who had undergone 10 min of spontaneous breathing. Five of the 15 patients had simultaneously abnormal nuclear perfusion images suggesting cardiac ischemia despite unchanged ECGs. It is not clear from the study whether the perfusion abnormalities were definitely ischemic in origin. A history of CAD was not predictive of an abnormal myocardial perfusion scan. Hurford and Favorito6 later demonstrated that 6 of 17long-term ventilated patients who failed to wean from MV experienced ECG evidence of ischemia. Abalos et al7 demonstrated ischemia by ST monitoring in 9 to 14% 1582

of patients with a history of CAD who were weaning from MV after noncardiac surgery. To our knowledge, the clinical utility of ST monitoring during weaning has not been studied. The ST monitor used in our study failed to detect two cases in which the ECG signs of ischemia were qualitative, ie, changes in ST-T wave contour, ll,l3 which the monitor is not designed to detect. Additionally, electrocardiography, even in the hands of a trained cardiologist, may underestimate the fre~uency of occult cardiac ischemia in similar patients. Thus, one must be aware of the limitations of this technology and the resolution of the apparatus used. The infrequency of ST changes in our study (6% in our ICU population, 2% in those without a history of CAD) suggests that routine ST monitoring is unnecessary in the vast majority of medical patients being weaned from MV. However, in patients with a precedent history of CAD (in whom the rate of weaning ischemia was 10%) and/or in patients who are not easily liberated from MV, occult cardiac ischemia could be contributing to weaning failures. In such populations, ST monitoring may aide in the early diagnosis and treatment of weaning-related ischemia.4'6'8 When bedside monitors have ST measurement capability, there is little/no cost associated with ST monitoring; what to do when ST changes occur is less clear (see patients 5 and 6 in Table 3). In conclusion, cardiac ischemia during weaning was relatively rare (6%) in this population of medical critically ill patients. The frequency was greater (10%) in patients with a history of CAD and greatest (22%) in those with CAD who failed to wean. Occult cardiac ischemia should be considered when patients, espeClinical Investigations in Critical Care

cially those with CAD, repeatedly fail to wean from MV. Continuous ST monitoring may be useful in detecting occult ischemia in selected patients. REFERENCES

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