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       (complete atrial excitation) and the ST seg-  myocardium should be depolarizing (first 0.04 s of
       ment (complete ventricular excitation) lie ap-  QRS). The so-called “0.04-sec vector” is therefore
       prox. on the isoelectric line (0 mV). The PQ (or  said to point away from the infarction. Anterior MI is
       PR) interval (! 0.2 s) is measured from the  detected as highly negative Q waves (with smaller R
       beginning of the P wave to the beginning of the  waves) mainly in leads V5, V6, I and aVL. Q wave ab-
                                       normalities can persist for years after MI (! I 2/3), so
       Q wave (or to the R wave if Q wave is absent)  they may not necessarily be indicative of an acute in-
       and corresponds to the time required for atrio-  farction. ST elevation points to ischemic but not (yet)
       ventricular conduction (! B). The QT interval is  necrotic parts of the myocardium. This can be ob-
       measured from the start of the Q wave to the  served: (1) in myocardial ischemia (angina pectoris),
       end of the T wave. It represents the overall  (2) in the initial phase of transmural MI, (3) in non-
       time required for depolarization and repolari-  transmural MI, and (4) along the margins of a trans-
       zation of the ventricles and is dependent on  mural MI that occurred a few hours to a few days
                                       prior (! I 4). The ST segment normalizes within 1 to
       the heart rate (0.35 to 0.40 s at a heart rate of  2 days of MI, but the T wave remains inverted for a
    Cardiovascular System  (Einthoven and Goldberger leads) on the  Excitation in Electrolyte Disturbances
       75 min ).
           –1
                                       couple of weeks (! I 5 and 2).
         Figure E illustrates the six frontal leads
       Cabrera circle. Synchronous measurement of
                                                                causes
       the amplitude of Q, R and S from two or more
                                                      hyperkalemia
                                       Hyperkalemia.
                                                 Mild
       leads can be used to determine any integral
                                       various changes, like elevation of the MDP
       vector in the frontal plane (! G). The direction
                                       (! p. 192) in the SA node. It can sometimes
       axis (! C3 and G, red arrows). If the excitation
                                       B3c). In severe hyperkalemia, the more positive
    8  of the largest mean QRS vector is called the QRS  have positive chronotropic effects (! p. 193
                                                             +
       spreads normally, the QRS axis roughly corre-
                                       MDP leads to the inactivation of Na channels
       sponds to the anatomic longitudinal axis of the  (! p. 46) and to a reduction in the slope and
       heart.                          amplitude of APs in the AV node (negative dro-
         The mean QRS axis (“electrical axis”) of the  motropic effect; ! p. 193 B4). Moreover, the K +
       heart, which normally lies between + 90  conductance (g K) rises, and the PP slope be-
       degrees to –30 degrees in adults (! G, H). Right  comes flatter due to a negative chronotropic
       type (α = + 120" to + 90") is not unusual in  effect (! p. 193 B3a). Faster myocardial re-
       children, but is often a sign of abnormality in  polarization decreases the cytosolic Ca 2+  conc.
       adults. Mean QRS axes ranging from + 90  In extreme cases, the pacemaker is also
       degrees to + 60 degrees are described as the  brought to a standstill (cardiac paralysis). Hy-
       vertical type (! G1), and those ranging from  pokalemia  (moderate)  has  positive
       + 60 degrees to + 30 degrees are classified as  chronotropic and inotropic effects (! p. 193
       the intermediate type (! G2). Left type occurs  B3a), whereas hypercalcemia is thought to
       when α = + 30 degrees to –30 degrees (! G3).  raise the g K and thereby shortens the duration
       Abnormal deviation: Right axis deviation  of the myocardial AP.
                                                        +
       (# + 120") can develop due right ventricular  ECG. Changes in serum K and Ca 2+  induce
       hypertrophy, while left axis deviation (more  characteristic changes in myocardial excita-
       negative than –30") can occur due to left  tion.
       ventricular hypertrophy.        ! Hyperkalemia (# 6.5 mmol/L): tall, peaked T
                                       waves and conduction disturbances associated
       An extensive myocardial infarction (MI) can shift
       the electrical axis of the heart. Marked Q wave abnor-  with an increased PQ interval and a widened
       mality (! I 1) is typical in transmural myocardial in-  QRS. Cardiac arrest can occur in extreme cases.
       farction (involving entire thickness of ventricular  ! Hypokalemia (! 2.5 mmol/L): ST depres-
       wall): Q wave duration # 0.04 s and Q wave ampli-  sion, biphasic T wave (first positive, then nega-
       tude # 25% of total amplitude of the QRS complex.  tive) followed by a positive U wave.
       These changes appear within 24 hours of MI and are  ! Hypercalcemia (# 2.75 mmol/L total cal-
       caused by failure of the dead myocardium to con-  cium): shortened QT interval due to a short-
       duct electrical impulses. Preponderance of the exci-  ened ST segment.
  198  tatory vector in the healthy contralateral side of the
       heart therefore occurs while the affected part of the  ! Hypocalcemia (! 2.25 mmol/L total cal-
                                       cium): prolonged QT interval.
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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