Acute Myocardial Infarction Respiratory Failure* The Effects of Mechanical Jukka Juhani R#{228}s#{228}nen, M.D.; Perttl Complicated Ventilation Nikki, M.D.; and HeikkiL#{228},M.D. The cardiopulmonary effects of ventilatory support were studied in 12 patients with an acute myocardial infarction complicated by respiratory failure. At constant end-expiratory pressure, controlled mechanical ventilation, intermittent mandatory ventilation with 50 percent mechanical support, and spontaneous breathing all resulted in acceptable blood gas values. Intermittent mandatory ventilation offered hemodynamic advantages over controlled mechanical ventilation, as evidenced by a higher cardiac index and a lower arteriovenous oxygen content difference. Electrocar- S everal events in the infarction requiring functional (AMI) course may support. Since unit, therapy namics and various For Mechanical unfavorably. of AMI, deranged positive see sis. During reduced, weaned tory recovery, 1 final and culatory chanical However, changes ventilation controversial chanical in They changes in myocardial tor therapy. This study examines mandatory support, the use patients left ischemia the the with spontaneous 50 breathing is study the Department Manuscript Reprint Helsinki University of mestudies patients The clinical relevant who an failure data acute requiring at the of the was time of the had monitoring transducers were the patient when recordings were Espoo, Finland) (Fentanyl, needed. continuous were of the not 2.5-5.0 mg Espoo, vasoactive and monitor the position study, IV was monitoring vascular 0.05 medication mg IV The level all the pressure (Diapam, far and Orion, and fentanyl far sedation cardiac a the pressures. at which Finland) and far mid-thoracic diazepam given 90 All patients positioned to the SE) of at least study. pressure the (Bird 2 percent, ± ± 0.8 cmH,O, properly the of 12 volume chest pain if the fluid balance altered. ventilator rate mechanical was of 15 minutes, sures, pulmonary sure, and randomly ventilation with continuous period flat, tidal (44 (7.6 pulmonary During volume The saturation and balanced was lying Orion, The breathing tion systemic to a Corporation, a respiration catheter calibrated made. a tidal throughout intra-arterial thermodihution continuous to deliver oxygen unchanged connected (Bird pressure blood weaning of spontaneous were concentration end-expiratory an arterial and remained continuous oxygen of cardiac and a trial hypercapnia. with monitored onset stable, ventilator was adjusted inspired to secure Swan-Ganz of 72 hours circulation to prevent and The set percent mechanical received April 25; revision accepted August 8. requests: Dr Rasonen, Anesthesiology/IntensIve Care, University Central Haspital, 00290 HelsInki 29, Finland capillary a single-lead either positive airway and wedge pressure, were to to allow pressure. systemic ECG increased or decreased pulmonary central graphically CHEST/85/1/JANUARY,1984 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 had respiratory IMV-Bird which and the positive SE) of within sucient measured were Department Finland. CA), Corporation). me- perlbrmed the patient’s at a rate was support in paand respiratory intermittent of Anesthesia and the First Central Hospital, Helsinki, 12 by time-cycled Springs, controlled Medicine, was when mi/kg The From of complicated from mechanical ventilation at a stage at which breathing was feasible. At this time, the patients Palm conse- with treatment. flow-generated, to ventila- percent consists METHODS study are detailed in ilible 1. The diagnosis ofAMI was confirmed by serial electrocardiograms and an unequivocal rise of serum enzymes. The primary cause of respiratory failure was pulmonary edema in six patients, cardiac arrest requiring resuscitation in five, and cardiogenic shock In one patient. None of the patients had a history of chronic pulmonary disease, and neither was there evidence of lung infection or pulmonary embolism. One of the patients was unconscious ibilowing resuscitation; the others were awake and responsive The be magnitude cardiopulmonary group infarction symptoms ventricular related study AND to speech. cardiocir- of controlled with levels of ventilatory myocardial infarction mechanical ventilation, ventilation and can what also fail to assess any to beibre the patient and positive end-expira- it is not known regarding quences of three tients with acute failure: controlled support result from the withdrawal in AMI patients. Previous ventilation dysfunction. in order work in severe pulmohypercapnia and acido- even discontinued, from oxygen therapy pressure. necessary The ventilator mark- page ventilatory pressure. PATIENTS myocardial Particularly hemody- segments is often respiratory and to correct afrway failure interventions myocardial ventilation diographic evidence of myocardial ischemia was observed in one patient during controlled mechanical ventilation, in one during partial ventilatory support, and in five patients during spontaneous breathing. Myocardial ischemia should be one of the major determinants of mechanical ventilation when a patient with ischemic heart disease is subjected to ventilator treatment. The total withdrawal of ventilatory support carries a risk of marked ischemia and is not recommended until the patient can be extubated. and the heart farm a at one frequently af- comment ischemic myocardial respiratory size.’ unload increased nary congestion are to therapeutic editorial influence infarct of an acute lead the lungs directed facts the other, sometimes during the initial hours edly by produce spontaneous Afier a stabiliza- arterial pres- venous pres- recorded on a 21 1-Clinical Table Data at Tsme Study of CardioPatient CK/CK-MB Location No. Age Sex 1 69 M 2 62 F Etiology thoracic Vasoactive (U/L) Ratio anterior 1,6411158 0.53 NP posteroseptal; 1,068/181 0.53 DB, of Injury 54 M anterior 4 70 M posterolateral; 5 63 M Low ST+ Output Sub- Failure Subgroup group Medication Outcome arrest no yes died pulmonary no yes died arrest no yes survived pulmonary yes yes died no yes survived arrest no no survived pulmonary edema yes no survived pulmonary no no survived yes no survived NTG old anterior 3 of Respiratory edema 3,005/221 0.57 none 0.58 DA, 0.52 NP - NP old anterior edema anterior LD 557 pulmonary edema 6 52 M anterior 1,641/158 0.57 NP 7 52 M inferior; 2,593/365 0.54 DB, 1,042/165 0.52 none NTG old anterior 8 67 M anterior edema 9 57 M anterior 0.58 3,525/682 DB, NTG pulmonary edema 10 65 F inlbroposterior 1,479/136 0.65 none arrest yes no died 11 39 M anterior 8,179/636 0.49 NP shock yes no died 12 51 M anterior 8,620/558 0.58 NTG arrest no no survived (C serum = creatinine <0.04CK; range dopamine; DB multichannel villiers, = = normal lactate (ES-bOo, range F<150 U/L, dehydrogenase, Gould M<250 normal range and 12-lead ECG provide far 50 percent mixed venous recorded. blood samples Thereafter, of the output the patient’s was drawn, rate was ventilation. reset end-exhalation one to three A restabil- A final and the thermodilution respiratory vascular resistance, calculated from The arterial analyzed curve obtained Mean pressures, cycles. and the pulmonary standard and vascular over the resistance the next systemic were farmulas.7 To detect changes pressure-time viability ratio mixed venous in circulatory the index, were creatinine sodium = kinase myocardial nitroprusside; blood samples were the pressure-time to myocardial patient promptly tension-time determined. index, The diastolic which the diastolic relationships ischemia, and the endocardial pressure-time 22 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 subendocardial index two, NTG the with endocardial fraction, normal nitroglycerine, = DA = be circulatory the used reflected in tip the tected have by other of the and pulmonary expiratory, pressure product consumption. pressure Instruments, Equipment Ltd, was used as another study, the but de- for the calthe arterial of three beats Austin, does ischemia tracings Galway, not end- using a TX) and a computer Ireland) measure (Fig 1). The of myocardial rate oxygen “ Directional changes assessed 12-lead were by factors balance, with non-postextrasystolic Houston Digital (PDP-11, were indices wedge caused circulatory necessary made from area measurements capillary this In to which relationship pressure-time (Hipad, ratio. direction supply-demand The a change be by several blood sinus-conducted, digitizer the In of the ratio Moreover, may a cause-effect means. culation the viability shows myocardial necessarily imbalance.91’ ischemia.’2 can be produced endocardial ratio tension-time value relationships in turn, viability changes myocardial pressure-time the endocardial the consumption.’#{176} The ratio ratio, has been used as an viability to predict itself which, ischemia whereas oxygen blood supply-demand artery disease, the absolute coronary in supply,9 to myocardial of subendocardial cannot not blood is proportional patients in the injury by measuring ECG.’”6 the QRS deflection absolute values 12 leads The measurement using of the were currents of myocardial the ST-segment was made the PR-segment ST-segment summed. ischemia deviations in a 60 ms after as the isoelectric elevations Recordings and with standard the end line. from depressions a bundle of The branch block were excluded. with predispose serum NP indicator the a blood gas analyzer (ABL-2, Radiometer, Copenhagen, Denmark) and with an oximeter (IL-282, Instrumentation Laboratories, Lexington, MA). The blood oxygen content, the intrapulmonary shunt, the oxygen transport, and the oxygen consumption were calculated from standard equations.8 A mean total hemoglobin concentration was calculated from the oximeter determinations far each patient, and used when a hemoglobin value was required. could U/L; of the to of 15 minutes repeated. CK-MB <450 index a standard and ventilator minute determined, was allowed beibre the measurements set of measurements was made after 15 minutes of controlled mechanical ventilation or spontaneous breathing, depending on the initial ventilatory mode. The vascular pressures were measured from the graphic recordings at end-expiration. The artifact introduced into the intrathoracic pressure measurements by positive end-expiratory pressure was ignored since the measurements were made at a fixed point in the respiratory cycle, the expiratory airway pressure was not altered, and the comparisons were made with the patients serving as their own controls. Cardiac output was determined by thermodilution in triplicate using 10 ml of 5 percent dextrose at room temperature. During mechanical ventilation, the dextrose was injected at endexpiration of the ventilator breath. At least one spontaneous respiratory cyde usually occurred during the generation of the thermodilution curve when the mechanical support was partial. During unsupported spontaneous breathing, the injection was started at were U/L; reflects Ballain- Instruments, cardiac Subsequently, arterial period serum dobutamine). recorder France). ization klnase, LD The different levels ofventilatory support were compared with patients serving as their own controls. Two-way repeated-measures analysis of variance was employed to test whether the different of ventilatory support had significant effects on the measured ables, and syndrome wedge the whether the (cardiac index pressure >18 ventilator were values of t critical mean ± mm setting. modes to account presence reported pairwise using the comparisons. varioutput capillary to the changes between significance levels cardiac pulmonary the response differences isolated for each of low and Llmurm’ Hg) affected The subsequently for multiple <2.5 or absence the the Bonferroni level t-test. were All values in ventilatory The corrected are given SE. Acute Mvcard Infarction and Reipiratory Failure (Rasan.n, NIkkI, HeikIdia) as . ST (mm) spontaneous hypocapnic, breathing three and hypercapnia controlled mechanical usually ishing required #{149}12 patients was not ventilation the were seen. slightly During patients were asleep. Their alertness increased with diminventilatory support. Additional sedation was in four cases during partial or absent ventila- tory support to prevent the patient’s movements interfering with the measurements. One patient plained of chest pain and dyspnea during ventilatory support, and .4 during intermittent (16.6 0#{149} during 0.7 ± mandatory ml/dl; breathing, controlled and intermediate mechanical 11.8-19.8 ml/dl). ventilation, <0.05) p during (16.8 ventilation The spontaneous oxygen saturation exThe oxygen content of (16.9 ± 0.6 ml/dl) ± lowest spontaneous 0.6 mlldl) (total intrapulmonary during range shunt was equally low during total and partial mechanical ventilation, but increased during spontaneous breathing (p <0,05). The pulmonary vascular resistance did not -4 50 100 change 0 VENTILATORY SUPPORT (%) The ment study was approved of Anesthesia, by the Helsinki ethics committee University of the Central significantly. Circulatory 1. Changes in the sum of the ST-segment deviations (ST) during three levels of ventilatory support in 12 patients with AM!. Controlled mechanical ventilation is used as a reference level. Significant changes are shown by heavy line. FICTJRE The Depart- The in the changes in resulted Table 2. in slight elevation (7.44 rate ranged from mechanical ± Table and from breathing. normocapnia 2-Comparison Ventilatory Support are 0.01). The spontaneous 6 to 20 breaths/mm during spontaneous produced variables mechanical (33 ±1 mm hypocapnia support during port respiratory Controlled 10 Partial in all of Pulmonary to 24 sup- Three all highest spontaneous breathing mechanical when again content delivery ventilation slightly depressed. difference was cardiac was discontin- The higher arterioand the content lower during controlled than during the other ventilaOxygen consumption and oxy- remained of Mechanical The were insignificantly partial ventilatory unchanged. Ventilation in 12 Patients with AMI (%) oxygen mm Hg 50 110± 13 123±12 % 8.3± 1.7 7.8± mechanical breaths/mm 8.5±0.4 spontaneous Arterial carbon breaths/mm mm Hg 0±0 partial pressure Intrapulmonary shunt 0 95±9 1.4 12.5±1.8 1.3 19.3± rate partial Arterial the spontaneous (p <0.001). support; 100 Respiratory during volume indices total than during Levels are summa- variables arterial pressures, and the rate-pressure and the stroke lower during gen During during 3) were mixed venous oxygen mechanical ventilation tory modes (p <0.05). breaths/mm Parameters in the circulatory The pulmonary capillary wedge pressure during total ventilatory support and highest ued, they were venous oxygen respiratory 50 percent ventilatory Mean±SE Arterial summa- ventilation Hg) and pH patients. (Fig breathing. was lowest during rized changes product Hospital. Function Pulmonary Function rized in Table 3. The systemic systemic vascular resistance, RESULTS dioxide 33 ± 1 4.0±0.1 13.8± 0±0 38 ± it 1.2 38 ± it pressure blood *=p<O.05 t two breathing. The arterial blood ceeded 90 percent at all times. the arterial blood was highest from compartial pH 7.44±0.01 compared - ‘p<O.Oi 7.39±0.O1 7.39±0.Oit to 100% :- p<O.0Ol § p<O.05 compared to 50% CHEST Downloaded From: http://publications.chestnet.org/ on 06/09/2014 I 85 / 1 / JANUARY, 1984 23 Table 3-Comparison Ventilatory Mean±SE Support Systolic of Circulatory Parameters during Three of Levels Support Ventilatory in 12 Patients with AM1 (%) arterial 100 50 121 ± 7 0 130 mm Hg 113 ± 7 ± 9t mm Hg 65±4 67±4 71±5t mm Hg 15±2 18±2* 20±2j mm Hg 24 ± 2 25±1 27 ± 2 mm Hg 11±1 11±1 11±1 92±5 90±4 92±4 2.8±0.3 3.0±0.4 2.8±1.3 pressure arterial Diastolic pressure Pulmonary Capillary wedge Mean pressure pultoonary artery pressure Central venous pressure Heart bpm rate Cardiac L/minm2 index Systemic vascular dyn#{149}s/cm5 1,121 ± 141 1,209 ± 139 1,375 ± 157*11 resistance Arteriovenous content Mixed oxygen mI/di 5.8±0.5 5.4±0.4* ml/dl 11.0±0.5 11.5±0.6* 5.4±0.5* difference venous oxygen 11.2±0.7 content * =p<0.05 1=p<O.Ol =p<O.OOl § =p<O.05 II =p<O.Ol compared to 100% compared to 50% - : - ST-segment :- Changes All electrocardiograms EVR VENTILATORY SUPPORT 1%) ment analysis. the ST-segment significant. were A change deviations A difference two ventilator five patients acceptable for ST-seg- of at least 3 mm was arbitrarily of this in the sum considered magnitude between of any settings was recorded on 11 occasions (Fig 1). A 13 mm ST-segment shift iii was measured in one patient who developed chest pain when ventilatory support was reduced to 50 percetit. Fentanyl 0.05 mg IV abolished the pain; the STsegment deviations measured during spontaneous breathing were reduced by 6.5 mm. In another patient, the ST-segment deviations de#{235}reased by 4.5 mm when ventilatory support was reduced to 50 percent and increased latter shift remaining reflected 2. Changes in the endocardial viability ratio (AEVR) during three levels of ventilatory support in ten patients with AM!. Controlled mechanical ventilation is used as a reference level. A decrease in the EVR during spontaneous breathing separates the four patients who developed increased electrocardiographic ischemia from the six others. The method fbr the calculation of the EVR is shown in the inset (DPTI = diastolic pressure-time index, TI’! = tension-time index, PCWP = pulmonary capillary wedge pressure). 24 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 only. segment diographic (Fig Those who In the the ST-segment changes during spontaneous developed marked shifts during the study had more ischemia than the other patients ST- electrocarat all times 3). Viability Endocardial The to it was, discontinued; by chest pain. three patients, the increased ischemia breathing Ficuna by 10 mm when was accompanied quality calculate Acute Myocardlal of the the Infarction pressure endocardial and Respiratory tracings made viability Failure it ratio (Rassnen, possible in ten NIkJci, Heikkila) R PP LIXST (mmHg/min.100) EVR mm) 140 20- 1.21- 120 16 1.0 100 12 80 8 0.6 I. ___________1 I 100 100 0 50 50 VENTILATORY s: ST I 0.81- . 0 SUPPORT 100 50 0 (%) + meanSE O:ST#{149}: mean FIGURE 3. Changes in three parameters reflecting myocardial oxygen and demand supply with in 12 patients AM!. Three levels of ventilatory support are compared. The patients are grouped according to the presence (ST +, n = 5) or absence (ST -, n =7) of increased electrocardiographic ischemia during the study. (RPP = rate pressure product, AIST= sum of the ST-segment deviations, EVR = endocardial viability ratio). The EVR is calculated in ten patients (ST+, n’4; ST-, n’6). patients, four ST-segments. ference viability and the increased mechanical ventilation occasions, a fall in the cided taneous with a minor breathing, ischemia decrease were in the were the during exceptions. endocardial viability ST-segment the patients shift. prone controlled On ratio increased two coin- During sponto experience of Cardiopulmonary Parameters to the Presence (ST +, Grouped Support According n = arterial pressure mm pressure mm capillary mm wedge pressure Heart rate Hg Hg Hg bpm index Uminm2 Arterialbloodoxygen ml/dl content !ntrapulmonary shunt % compared *p<o.o5 *‘=p<O.OS elevated systolic product, increased 0.01 developed when following work and arterial increasing deprived changes deranged pressure lung and intrapulmonary was not seen in these resistance was equally Levels of Ventilatory (ST -, n = compared and ST-segment 50 com- (Table 4). spontaneous with AM1 Shifts . 0 ST+ 119± ST- 108±5 120±7* 123±6* ST+ 65±8 63±9 70±10 ST- 65±3 70±5 73+4* ST+ ST- 14±3 16±2 16±3 19±5* 20±3t1 20±2t ST+ 91±7 88±5 93±3 ST- 93±7 92±7 93±6 ST+ 2.5±0.4 2.7±0.5 2.8±0.4 16 121± 15 140±21 ST- 3.0±0.5 3.2±0.5 2.8±0.4* ST+ 16.2±1.3 16.3±1.2 i5.7±i.3*t ST- 17.2±0.6 ST+ 7.2± ST- 9.1±2.6 17.3±0.6 1.7 7.0± A The systemic in all patients. in 12 Patients Support 7) of Marked function: rate-pressure shunt, patients. elevated elec- of ventilasuggesting arterial blood oxygenation of cardiac output during breathing vascular during Three 5) or Absence who ischemia had the (%) arterial Pulmonary t=p< also cardiac 100 Diastolic Cardiac patients promised depression a Mean±SE Systolic five trocardiographic tory support clearly separated from the rest by endocardial viability ratio (Fig 2). 4-Comparison Ventilatory ischemia of Subgroups The was associated with a change in the endocardial ratio of at least 0.10. The effect of the fentanyl injection Table Analysis of whom had marked differences in their On seven of nine occasions, such a dif- 17.1±0.6 1.0 8.3±2.4 15.6±3.2t 10.3±1.9 to 100% to 50% CHEST/85/1/JANUARV,1984 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 25 The patients shifts ing who had the only did not develop minor changes myocardial (Fig 3). The level similar oxygen with worsening reflect- perfusion balance The end-expiratory groups; the respiratory in the patients breaths/mm to ischemia in the was others. None hypocapnic breathing. The presence drome, defined less than 2.5 with following of the during modes by the different levels of ventilatory Six of the 12 patients, to ischemia, six hours and ischemia ± 1 connection and ± 2 It 18 patients prone spontaneous were of the were end of the discharged study. The the from the of the 12 respiratory output.’7 chanical hospital. because the pressure but represents cycle cardiac authors have perfbrmance reported an following the institution chanical ventilation in patients with lar reserve.2 A depression of the curred in a series of postsurgical controlled mechanical ventilation and intermittent preoperative left ventricular mandatory ejection fraction end-diastolic improvement in of me- poor left ventricucardiac index ocpatients2 when was discontinued ventilation started if the had been low and the pressure high. The de- crease cmH2O in the cardiac index was of positive end-expiratory earlier patients when studies,6 however, the cardiac performance of with acute myocardial infarction improved some spontaneous breathing was allowed whether or not positive used. In the present study, tion slightly depressed compared adjusted small with to give reduction end-expiratory the absence decrease content were seen of low-output in pulmonary gests impaired left ventricle. pressure during the deterioration would indicate a reduction was index, a significant oxygen content in the mixed regardless syndrome. capillary A spontaneous breathing of the ST-segments, or in myocardial 26 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 of the capillary paralwhich compliance The decreased support remained unchanged a more reduced when it The with pressure by direct systemic dent that and The during was depending be discussed served during depressed content value percent cardiac This lead to changes artificial as- ventilation performance. left ventricular They are interac- and by changes state of the clinical improvement in greater controlled when and consumpincrease and volume and mandatory unlikely considering study and our earlier Acute Myocardial oxygen venous return.’ of these and other findings,6 but are unknown yen- discontinued. on the circulatory intermittent in The differsupport in oxygen should on the heart, the composition slight circulatory our earlier this setting have pressure and pulmonary the priorities results partial normal to 50 and spontaneous of the breathing. content content ventilatory support oxygen extraction. intrathoracic sociated whole of the study between artenovenous to was output one in cardiac index support and in an be explained by changes because oxygen consumption with diminishing enhanced tissue differ, simultaneous pressure sug- compliance pulmonary assumption. cannot tion, difference A patient timing in this and spontaneous arteriovenous oxygen mixed venous oxygen difference ventilatory tion, differvenous of the presence The wedge of the tilatory support changes in the ence and in the the generation the it. during cardiac of the difference partial ventilatory have complex effects on cardiac mediated at least by right and ventilaflow when ventilation support. filling or increased An elevation of the wedge leled pressure mandatory mechanical cardiac increase in the arteriovenous ence, and a significant decrease oxygen with 5 In our controlled mechanical the systemic blood intermittent 50 percent in reversible pressure. overestimation the in if at least Therefore, determinations during expected the is output, reflected be value me- breaths When during curve. output this is not mean cardiac cardiac a timed occurs an underestimation between total and mean return ventilation. the relapoint controlled mean is to spontaneously the ventilator venous error mandatory breathing the inspiration smaller intermittent value in actual during of the reduction thermodilution at a certain the between an overestimate similar and mechanical changing obtained obtained probably cardiac Several cycle ventilation positive into by this ventilation. of error value value thermodilution Performance an in the although discontinuation the The an elevation mechanical determinations in the spontaneous difference, during introduces between pressure. during with content the output respiratory DIscussIoN Cardiac that tionship is extubated Seven is likely index associated was evident cardiac were applied. four of the five successfully not subendocardial intracavitary cardiac oxygen ventilation not affect varia- of ventilation. order in which support including was or impaired increased in the arteriovenous was 21 than 18 mm Hg, did in the cardiopulmonary the different also unaffected susceptible rate was or absence of low cardiac output synas the coexistence of a cardiac index L/minm2 and a pulmonary capillary wedge pressure greater the changes observed bles between results were pressure ischemia reduction breathing of positive in both survived ST-segment variables supply-demand breaths/mm within marked in the in It is evimechanisms of the patient material studied. noted in this study ventilation supports as cardiac volume changes in so far, its mechanisms cannot detail. The mechanical function. 2I22 hypocapnia ventilation This is, however, the degree of hypocapnia results in similar patients.6 Infarction and Respiratory Failure (Rasanen, obmay in this NikkI, HeIkkIIa) Myocardial The sympathoadrenergic intracavitary pressure Ischemia protection of ischemic, jeopardized segments during evolving acute is nowadays a major therapeutic recting serious arrhythmias and No report previously rangements. myocardial ischemia to ventilator had marked new of our patients when deprived intermittent controlled taneous ischemia in increase in the the circulatory an and one during one during mechanical ventilation. During sponbreathing, increased electrocardiographic and often chest pain were associated with a reduction the Almost half deviations support, ventilation, derelates unfavorable endocardial viability ratio rate-pressure product, pressure-time relationships direction. The fall an that had in the by an increase viability ratio was caused time index in one patient, and indicating taken pressure-time index in one, and by both in two patients. The reduction in the diastolic pressure-time index was due to elevated pulmonary capillary wedge pressure. Our results do not offer an explanation for the changes in arterial blood oxygenation and mntrapulmonary shunting during spontaneous breathing. Collapse of unstable alveoli in the absence of positive pressure and breaths22 fbllowing tant. The slightly increased were increased pulmonary an elevation arterial blood more in the ischemia, areas threatened by even artery blood oxygen of hypoxia this small reductions content. Thus, to increased ischemia explanation for the ischemia is the the awakeness and the resistance flow breathing tor through circuit. This circulatory changes the patients prone bated within six some are inherent designed. venting systemic blood advise against a total study ACKNOWLEDCMENTS: Blomqvist, R.S.N. RE, increased Muller M, of myocar- associated an endotracheal is suggested response to and spontaneous ex- with by and by the fact that all but to ischemia were successfully hours. All breathing circuits flow resistance The ventilator no matter used study easily during spontaneous breathing and him or her from developing anxiety wish authors Kaulio, one of of in patients to R.S.N., El-Etr E. Effirts Med 1981; AA, Pifarre ventricular to limit the size of 95:736-61 R. patterns in ventilatory left in man. CM. J Anaesth Acta reserve. Hemodynamic in with patients Care Crit of positive Med Scand (Suppl effects of pulmonary Hemodynaxnic 1975; 5 Massumi RA, pulsus paradoxus. Med 1982; in breathing on the 193), 1947; 128:65-72 pressure ventilation. Br 47:761-66 Mason DT, Vera Z, Zelis J Med N Engl respiratory R, OtemJ, 1973; J, P, R#{228}s#{228}nen J, Thhvanainen 6 Nikld failure et al. Reversed 289:1272-75 Makelainen A. Ventilatory from arising acute myocardial and hemodynamic effects of !MV4 vs IPPV,, and PEEP vs PEEP,O. Crit Care Med 1982; 10:75-78 7 Kaplan JA. Hemodynamic monitoring. In: Kaplan JA, ed. Cas’. diac anesthesia. New York: Crane & Stratton, 1979; 71-117 I. Respiratory JR Oxygen. 10 JIE, to have 11 the 13 time J Thorac Hoffman index. perfusion. Cobel product FL, AR, with angina fur by- 69:30-9 of transmural myo- 58:381-91 Nelson of myocardial method cardiopulmonary prediction 1978; reference 192:148-56 A clinical after 1975; and Circulation 1958; AM. Surg determi- with special Physiol ischemia Nordstrom as an index in patients J Am Hemodynamic heart AT, Miyamoto Determinants cardial CH. of the Cardiovasc J!E. of subendocardial Pathophysiology Welch subendocardial exercise pre- E, Marty PA, physiology. 1:76-9 consumption tension Philips pass. 12 1975; respiratory 375-444 CD. J SJ, Braunwald detecting is no Buckberg of oxygen JR Applied 1977; Br Med Sarnoff nants In: Nunn Butterwarths, ischemia. extu- with UK, influence L. The 9 Hoffman of Intern RB. oxygen The rate pressure consumption pectoris. during Circulation 1978; 57:549-56 14 Muller JE, Maroko PR, Braunwald CHEST Downloaded From: http://publications.chestnet.org/ on 06/09/2014 results 10:423-26 London: how well they in this The discontinuation to extubation Braunwald Ann Eao and poor 8 Nunn tube and a ventilathe accompanying JE, to changes 4 Conway in inspiratory and infarcts. 3 Werko be be excluded appearance The Sinikka flow. Finland. circulation of oxygen sympathoadrenergic patients. thank Lisbeth or their skillful technical assistance, Lauri Valsta, M.Sc. fur his help in the statistical analysis, Mikko Katila, M.D. and Markku Kupari, M.D. for reviewing the manuscript, and Martha Caber Abrahamsen for editing it for style. This study was supported by a grant from the Academy of normal exception, although it does compare favorably with many others in this respect.22 The use of partial ventilatory support may assist the patient sufliciently, enabling him or her to overcome the flow resistance more of the this infarction. Another in these monitoring depression responses study. piratory ST-segment continuous When the exact level of mechanical ventilatory support is being determined, the reversal of myocardial ischemia should probably be given priority over a minor pattern dial of the pressure study, 2 Mathru in the coronary the contribution cannot this myocardial may areas perfusion REFERENCES signs of values myocardium the capillary bed. marked enhancement of ischemia frequently occurred during unsupported spontaneous breathing despite normal arterial blood oxygenation, normocapnia, and an acceptable respiratory rate. 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Evaluation / 85 I 1 I JANUARY, of precordial 1984 27 15 electrocardiographic mapping myocardial injury. ischemic J Ross Electrocardiographic Jr. of myocardial 53 (suppl 1):73-81 J, Nieminen MS. ischemla with characterization tion 16 dial man. 17 1976; HeilddlA Acta Med Snyder JV 18 1982; Layer MB. problems in 20 WeberKlJanickiJS, analysis in and infarction. the Circula- Rapid monitoring of regional and 204 (suppl 21 Breivik by shifts in 22 Integrated right with and coronary artery disease. ogy in clinical respiratory and left ventilation on the Crit ventricular In: Prakash function: failure, 0, ed. care. The Hague: Care mitral Applied the Nijhofl JL insufficiency. Cardiovascular Am J Cardlol disturbances 1981; in chronic 47:941-49 L-J PearlmanES, etal. its functional coupling 1982; 24:375-400 Dis E, Safar P. Normalizing Mullen during C, mechanical ventilation. Kelman CR, Creenbaum and alveolar-arterial P02 JT. Effect tion. Care Crit occlusion. Vuori 25 Med respira- 1981; 26 J Am Appl of positive 1978; low arterial Chest 1973; Kain 1968; ventilation M, J. Bay at varying 25:80-7 on oxygena- 6:119-20 necrosis 1975; three E. Effects after of hypoxemia experimental on coronary 35:795-800 hemodynamics, during R, differences Physiol pressure Braunwald Cardiol A. Central J man. Callagher consumption Bobotham tory ShroffS, the heart and Cardiovasc A, Badvang F, Maroko PR, the extent of myocardial 24 valve physiol- Martinus of in anesthetized PaCO2 23 1982 19 tension Hemodynamics thermodilution. acute respiratory Progr H, Crenvik Prys-Roberts 10:677-82 associated behaviour 63:525-31 623):71-95 of mechanical output myocar. ST-segment HunterWC, The contractile to circulation. CO2 Efibets DJ. changes 52:16-27 ST-segment ischemia 1978; of cardiac of assessing 1975; echocardiography Scand Powner measurement Med as a means Circulation transport and oxygen Acta Anesth Scand oxygen methods fur CPAP. 25:376-80 H#{248}rden M. Editorial. Scand Clin Lab Invest 1981; 41:107-16 A Lung thoIogy Dates: March 20-23, 1984. Location: Fairmont Hotel, New Orleans, Louisiana. Sponsor: College of Chest Physicians. Course Co-Directors: William M. Thurlbeck, M.D., FCCP; Andrew Churg, M.D., FCCP; Charles B. Carrington, M.D.; James C. Hogg, M.D. Course Description: This fuw’.day course will provide a comprehensive review and a thorough update on lung pathology The objective of the course is to expose participants to the equivalent of the content of the most up-to-date and complete textbook of pulmonary pathology. The course will be taught by internationally known experts in the area of the lung who teach in their areas of expertise. The content of the course is structured fur pathologists, practicing chest physicians, chest radiologists, and fellows in chest medicine. It will be particularly suitable fur fellows taking Board Examinations. Emphasis will be placed on clinico-pathologic relationships and on recent advances in lung disease. The course will feature the following: diffuse alveolar damage, infectious lung disease, immunologic lung disease, chronic airflow obstruction, pulmonary tumors, disorders of the pulmonary vasculature, pediatric lung disease, infiltrative lung disease, pulmonary cytology, occupational lung disease, noninfectious pulmonary granulomatous disease, and lung infiltrates in the compromised host. Innovations this year include feur case discussions in which a clinician and a pathologist will relate clinical findings, radiology, pulmonary function abnonnalities, and pathology. The final presentation will be a correlation of radiology, abnormalities of pulmonary function and American morphology. For inlhrmation, contact the Department of Education, American cians, 911 Busse Highway, Park Ridge, illinois 60068(312:698-2200). 28 Downloaded From: http://publications.chestnet.org/ on 06/09/2014 Acute Myocardlal College Infarction of Chest and Reepiratory Physi- Failure (Rasanen, Nikid, HalkkHa)