Το διάστημα QT αντιστοιχεί στην συνολική διάρκεια της κοιλιακής εκπόλωσης και επαναπόλωσης. Μετράτε από την αρχή του QRS μέχρι το τέλος του επάρματος Τ. Η διάρκειά του είναι μεταξύ 0.35 και 0.44 sec και επηρεάζεται από την καρδιακή συχνότητα. Όσο αυξάνει η καρδιακή συχνότητα το QT διάστημα μικραίνει και το αντίστροφο. Γενικά όμως διάστημα QT μεγαλύτερο από το μισό δύο διαδοχικών RR επαρμάτων θεωρείται αυξημένο. Επιμήκυνση ή βράχυνση του QT μπορεί να παρατηρηθεί σε διάφορες καταστάσεις.:
Επιμήκυνση του QT διαστήματος εμφανίζεται σε:
- υποκαλιαιμία
- υποασβεστιαιμία
- λήψη αντιαρρυθμικών (αμιωδαρόνη, κινιδίνη)
- λήψη τρικυκλικών αντικαθλιπτικών
- ισχαιμία και έμφραγμα μυοκαρδίου.
Επιμηκυσμένο είναι το QT διάστημα και ιδιοπαθώς σε κληρονομικά σύνδρομα (Jervell-Lange-Nielsen και Romano-Ward).
Βράχυνση διαστήματος QT εμφανίζεται σε:
- υπερκαλιαιμία
- υπερασβεστιαιμία
- οξέωση
- λήψη δακτυλίτιδας και β-αναστολέων.
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QT DISPERSION
QT dispersion
(maximum QT interval minus minimum QT interval) was originally proposed as an
index of the spatial dispersion of ventricular recovery times. In reality, QT
dispersion is a crude and approximate measure of a general abnormality of
repolarization.
Attempts to
characterize and quantify the inhomogeneity of ventricular repolarization from
the surface electrocardiogram (ECG) using precise mathematical methods, such as
principal component analysis of the T wave, can be traced back to the 1960s. In
clinical practice, however, the ECG assessment of ventricular repolarization
has been limited to the measurement of the QT interval and its heart
rate-corrected value (QTc) and to the description of the ST-T morphology, often
using vague terms such as "non-specific ST-T wave changes."
The QT interval
duration varies between leads on the standard ECG, Frank orthogonal leads, and
body surface potential maps. These interlead differences, called QT interval
dispersion or QT range, were proposed as an index of the spatial dispersion of
the ventricular recovery times. This measurement was an attempt to distinguish
between myocardium that is homogeneous from myocardium that displays
inhomogeneity, which is accompanied by increased dispersion of the ventricular
recovery times and prolongation of repolarization.
However, there
has been much concern about the validity of the concept and the methodology of
the measurement. Despite ongoing controversy, there are a number of reasonable
conclusions about the reliability and applicability of the technique. The
pathophysiology and measurement of QT dispersion will be reviewed here.
PATHOPHYSIOLOGY
OF QT DISPERSION
The initial
concept that QT dispersion is an index of inhomogeneity was supported by the
link between the dispersion of ventricular recovery times and the genesis of
arrhythmias. It was generally believed that the standard 12-lead ECG contained
information about regional ventricular repolarization; thus, when increased QT
dispersion was seen in cardiac diseases in which ventricular recovery times
were known to be heterogeneous, it was assumed that increased QT dispersion was
a direct reflection of the disparity of ventricular recovery times.