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Anteroseptal Myocardial Infarction Developing in Stages
ELECTROCARDIOGRAM OF THE MONTH Anteroseptal Myocardial Infarction Developing in Stages* HAROLD L I N N , M.D. AND ALFRED PLCKJ M.D. Chicago,
T
HESE
ELECTROCARDIOGRAM S
WERE
obtained from a 67-year-old m a n on the first day of admission for characteristic signs and symptoms of acute myocardial infarction, a n d f o l l o w i n g readmission and surgery on July 3, 1961, for hemorrhagic infarction of the small bowel. In the *From the Cardiovascular Institute, Reese Hospital and Medical Center. 4-So-
éi
Michael
Illinois
record of April 30, the deep symmetrical T wave inversions indicate ischemic changes in the anterior and lateral walls, without evidence of myocardial necrosis. These alterations persisted, with some regression, over six weeks, but were no longer present in the record of July 18. O n July 19, when severe chest pain recurred, development of discordant S-T deviations and of Q S deflec7-fÍ-é/
7-/9-tí
FIGURE 1
7-2/-é/
am.
ifii-JJ
Volume 43, N o . 6 June 1963
A N T E R O S E P T A L MYOCARDIAL
1
tions in the right precordial leads disclosed new injury, this time with necrosis in the anteroseptal area, confirmed by the evolution seen in the record on July 21—A.M. In the afternoon of the same day, after the patient had been resuscitated from sudden syncope by external cardiac massage, the e l e c t r o c a r d i o g r a m revealed that the ischemic process had extended deep into the ventricular septum to cause a right bundle branch block, as well as a variable atrioventricular conduction disturbance; a first degree A-V block (lead I and V ^ - ) changed intermittently to complete A-V dissociation, with an unstable ventricular pacemaker (lead I I ) and protracted periods of ventricular standstill (lead I I I ) . Three such episodes could be controlled by the use of an external pacemaker, but the next one proved fatal. A l t h o u g h n o Q R S alterations were noted in the initial electrocardiogram, the persistence of ischemic T wave alterations for at least six weeks suggested that a small intramural area of infarction, with ' tissue destruction, may have been present
645
INFARCTION
within the ischemic región. While the immediate prognosis of such episodes is usually good and subsequent electrocardiograms may reveal complete restitution, extensive t r a n s m u r a l infarction follows sooner or later in such patients. A-V block of varying degrees occurs in about 8 per cent of recent myocardial infarctions. It is seen more commonly in posterior wall infarction with occlusion of the right coronary artery which supplies, via its ramus septi fibrosi, the A-V node and the common bundle of His. Usually it is transient, and then the A-V block has little effect on immediate prognosis and longterm survival, but when it becomes permanent, the mortality increases with severity of the block. When A-V block complicates an anterior wall infarct, it signifies infarction of the septum and is caused by involvement of the bifurcation of the common bundle and one or both of the bundle branches; the A-V node and the common bundle may be entirely spared. In these cases the immediate mortality is very high.
T R E A T M E N T OF A S P I R A T J O N A N D A T E L E G T A S I S A technique whereby 200 to 400 mi. of saline solution are instilled into the tracheobronchial tree in divided quantities for a five to ten minute period is described. More than 100 patients with atelectasis and aspiration were treated. The effect of this therapy on lung mechanics has been evaluated in dogs by measuring lower airway resistance and lung compliance. Lavage with saline solution produces a small, transient increase in airway resistance, and a more persistent decrease in lung compliance. The effect on lung compliance emphasizes the need for
assisted positive pressure ventilation during and following lavage. Saline lavage is extremely effective in removing thick, tenacious secretions, as well as blood from the tracheobronchial tree with restoration of lung mechanics to normal. The bronchospasm associated with aspiration of gastric juice can be effectively treated by saline lavage. SLMENSTAD, J . O . ,
GALWAY,
C.
F.
AND MACLEAN,
L.
D.:
"The Treatment of Aspiration and Atelectasis by Tracheobronchial Lavege," Surg., Gynec. and Obstet., 115:721, 1962.
M E G H A N I S M OF M Y C O B A G T E R I A L P A T H O G E N I C I T Y There are two separate mechanisms in tuberculous infection which are responsible for production of the characteristic pathologic picture. The first one is local pathogenicity which can be produced by inoculation of dead lyophilized bacilli, and the second is virulence, which depends on multiplication and dissemination of mycobacteria. For suppression of the second mechanism, conventional mycobacteriostatic chemical and antibiotic preparations are
used. For suppression of the local pathogenicity reactions, corticosteroids have some place, but there is a new possibility in reducing pathogenic reactions by the use of proteolytic enzyme inhibitors because it was noticed that local pathogenicity in tuberculous infection starts with an intensive activation of local tissue proteolytic enzymes. MUFTIC, M. H . : "The Mechanism of Mycobacterial Pathogenicity," Brit. }. Dis. Chest, 57:22, 1963.
T
HESE
ELECTROCARDIOGRAM S
WERE
obtained from a 67-year-old m a n on the first day of admission for characteristic signs and symptoms of acute myocardial infarction, a n d f o l l o w i n g readmission and surgery on July 3, 1961, for hemorrhagic infarction of the small bowel. In the *From the Cardiovascular Institute, Reese Hospital and Medical Center. 4-So-
éi
Michael
Illinois
record of April 30, the deep symmetrical T wave inversions indicate ischemic changes in the anterior and lateral walls, without evidence of myocardial necrosis. These alterations persisted, with some regression, over six weeks, but were no longer present in the record of July 18. O n July 19, when severe chest pain recurred, development of discordant S-T deviations and of Q S deflec7-fÍ-é/
7-/9-tí
FIGURE 1
7-2/-é/
am.
ifii-JJ
Volume 43, N o . 6 June 1963
A N T E R O S E P T A L MYOCARDIAL
1
tions in the right precordial leads disclosed new injury, this time with necrosis in the anteroseptal area, confirmed by the evolution seen in the record on July 21—A.M. In the afternoon of the same day, after the patient had been resuscitated from sudden syncope by external cardiac massage, the e l e c t r o c a r d i o g r a m revealed that the ischemic process had extended deep into the ventricular septum to cause a right bundle branch block, as well as a variable atrioventricular conduction disturbance; a first degree A-V block (lead I and V ^ - ) changed intermittently to complete A-V dissociation, with an unstable ventricular pacemaker (lead I I ) and protracted periods of ventricular standstill (lead I I I ) . Three such episodes could be controlled by the use of an external pacemaker, but the next one proved fatal. A l t h o u g h n o Q R S alterations were noted in the initial electrocardiogram, the persistence of ischemic T wave alterations for at least six weeks suggested that a small intramural area of infarction, with ' tissue destruction, may have been present
645
INFARCTION
within the ischemic región. While the immediate prognosis of such episodes is usually good and subsequent electrocardiograms may reveal complete restitution, extensive t r a n s m u r a l infarction follows sooner or later in such patients. A-V block of varying degrees occurs in about 8 per cent of recent myocardial infarctions. It is seen more commonly in posterior wall infarction with occlusion of the right coronary artery which supplies, via its ramus septi fibrosi, the A-V node and the common bundle of His. Usually it is transient, and then the A-V block has little effect on immediate prognosis and longterm survival, but when it becomes permanent, the mortality increases with severity of the block. When A-V block complicates an anterior wall infarct, it signifies infarction of the septum and is caused by involvement of the bifurcation of the common bundle and one or both of the bundle branches; the A-V node and the common bundle may be entirely spared. In these cases the immediate mortality is very high.
T R E A T M E N T OF A S P I R A T J O N A N D A T E L E G T A S I S A technique whereby 200 to 400 mi. of saline solution are instilled into the tracheobronchial tree in divided quantities for a five to ten minute period is described. More than 100 patients with atelectasis and aspiration were treated. The effect of this therapy on lung mechanics has been evaluated in dogs by measuring lower airway resistance and lung compliance. Lavage with saline solution produces a small, transient increase in airway resistance, and a more persistent decrease in lung compliance. The effect on lung compliance emphasizes the need for
assisted positive pressure ventilation during and following lavage. Saline lavage is extremely effective in removing thick, tenacious secretions, as well as blood from the tracheobronchial tree with restoration of lung mechanics to normal. The bronchospasm associated with aspiration of gastric juice can be effectively treated by saline lavage. SLMENSTAD, J . O . ,
GALWAY,
C.
F.
AND MACLEAN,
L.
D.:
"The Treatment of Aspiration and Atelectasis by Tracheobronchial Lavege," Surg., Gynec. and Obstet., 115:721, 1962.
M E G H A N I S M OF M Y C O B A G T E R I A L P A T H O G E N I C I T Y There are two separate mechanisms in tuberculous infection which are responsible for production of the characteristic pathologic picture. The first one is local pathogenicity which can be produced by inoculation of dead lyophilized bacilli, and the second is virulence, which depends on multiplication and dissemination of mycobacteria. For suppression of the second mechanism, conventional mycobacteriostatic chemical and antibiotic preparations are
used. For suppression of the local pathogenicity reactions, corticosteroids have some place, but there is a new possibility in reducing pathogenic reactions by the use of proteolytic enzyme inhibitors because it was noticed that local pathogenicity in tuberculous infection starts with an intensive activation of local tissue proteolytic enzymes. MUFTIC, M. H . : "The Mechanism of Mycobacterial Pathogenicity," Brit. }. Dis. Chest, 57:22, 1963.