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218  P R I N C I P L E S   A N D   P R A C T I C E   O F   C R I T I C A L   C A R E

         sound due to decreased contractility. A fourth heart sound   electrodes, V7–V9, may be placed over the posterior of
         is common, whereas a third heart sound is uncommon.   the left chest to view the posterior wall. Other indicative
         Many patients develop a pericardial rub after about 48–72   signs of posterior wall damage are a small r wave in V1
         hours due to an inflammatory response to the damaged   and/or ST depression in V3 and V4 as these may be recip-
         myocardium.  Additional  findings  occur  with  complica-  rocal  changes.  The  endocardial  surface  of  the  posterior
         tions,  and  these  are  discussed  in  that  specific  section   wall faces the praecordial leads of the ECG so the signs
         below.                                               of  ischaemia  and  infarction  are  reversed  or  reciprocal
                                                              such as ST depraession or a small r wave. If these signs
         Electrocardiographic examination                     are present a left-sided ECG, V7–V9, should be done to
         Patients with chest discomfort should be assessed by an   confirm or rule out a posterior infarction.
         appropriately qualified person and have an ECG recorded   Continuous ECG monitoring is essential to detect arrhyth-
         within  5  minutes  of  arrival  at  a  healthcare  facility  to   mias, which often accompany AMI and are a common
         determine  the  presence  and  extent  of  myocardial  isch-  cause of death. The arrhythmia may be due to poor perfu-
         aemia, the risk of adverse events and to provide a baseline   sion  of  the  conduction  tissue.  More  often,  arrhythmias
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         for  subsequent  changes.   Most  importantly,  the  ECG  is   occur  because  ischaemic  tissue  has  a  lower  fibrillatory
         essential to determine whether emergency reperfusion is   threshold and ischaemia is not being managed. Arrhyth-
         required, and is recommended as the sole test for select-  mias also result from left ventricular failure.
         ing patients for PCI or thrombolysis. Where ST segment
         monitoring is available, this should be continuous. Alter-  Typical ECG evolution pattern
         natively,  if  chest  discomfort  persists,  ECGs  should  be
         repeated every 15 minutes. Even when chest pain resolves   The initial ECG features of myocardial infarction are ST
         it is important to record a series of 12-lead ECGs during   segment  elevation  with  tall  T-waves  recorded  in  leads
         admission to determine changes over time. (The normal   overlying the area of damaged myocardium. These changes
         ECG  is  covered  in  Chapter  9,  whereas  this  section   gradually change, or evolve, over time, with ST segments
         addresses ischaemic changes in the ECG.)             returning  to  baseline  (within  hours),  while  Q  waves
                                                              develop  (hours  to  days)  and  T  waves  become  inverted
         Myocardial ischaemia, injury or infarction cause cellular   (days  to  weeks).  The  time  course  for  the  evolutionary
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         alterations and affect depolarisation and repolarisation.    changes  is  accelerated  by  reperfusion,  e.g.  PCI,  throm-
         Myocardial ischaemia may be a transient finding on the   bolysis or surgery. Thus an almost fully-evolved pattern
         ECG. Ischaemia results in T wave inversion or ST segment   may be seen within hours if successful reperfusion has
                                                     11
         depression in the leads facing the ischaemic area.  Isch-  been undertaken (see Figures 10.2–10.4 for an example).
         aemic  T  waves  are  usually  symmetrical,  narrower  and   Given the expected time course for evolution, it is possi-
         more pointed. ST segment depression of 1 mm for 0.08   ble to approximate how recently infarction has occurred,
         seconds  is  indicative  of  ischaemia,  especially  when   which is essential in determining management:
                                                    12
         forming  a  sharp  angle  with  an  upright  T  wave.   These
         changes are reversible with reduction in demand (e.g. by   ●  acute  (or  hyperacute):  there  is  ST  elevation  but  Q
         rest, nitrates).                                        waves  or  T  inversion  have  not  yet  developed  (see
                                                                 Figure 10.5).
         On acute presentation, myocardial injury (infarction) is
         most commonly associated with ST segment elevation on   ●  recent: Q waves have developed. ST segment elevation
         the  ECG,  although  this  is  not  universal.  In  addition,  a   may still be present. Evolution is underway. The infarc-
         typical pattern of ECG changes over time (evolution of   tion is more than 24 hours old.
         the ST segments, Q wave development and T wave inver-  ●  old  (fully  evolved):  Q  waves  and  T  inversion  are
         sion) are often seen (described below), but these changes   present. ST segments are no longer elevated. Infarction
         too are not universal. The distinction between the various   occurred anything from a few days to years ago.
         acute coronary syndromes, including ST elevation acute
         coronary  syndrome  (STEACS),  ST  elevation  myocardial   Biochemical markers
         infarction  (STEMI)  and  non-ST  elevation  myocardial   Intracellular cardiac enzymes enter the blood as ischaemic
         infarction (non-STEMI), is important for ensuring appro-  cells die, and elevated levels are used to confirm myocar-
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         priate assessment and protocol-based treatment  for the   dial infarction and estimate the extent of cell death. The
         various presentations.                               cardiac  troponins  T  and  I  (cTnT  and  cTnI)  have  been
         The location and extent of ischaemia or infarction may   found to be both sensitive and specific measures of cardiac
                                                                            14
         be evident on the ECG leads overlying the affected area,   muscle damage.  Troponin I is rapidly released into the
         as follows:                                          bloodstream, so it is especially useful for the diagnosis
                                                              and subsequent risk stratification of patients presenting
         ●  anteroseptal wall of left ventricle, V1–V4;       with chest pain in the early stages. Troponin I is also a
         ●  anterior wall of the left ventricle, V1-V6, I and aVL;  more  appropriate  marker  to  use  in  postoperative  and
         ●  lateral wall of left ventricle, I, aVL,V5 and V6;  trauma  patients  than  creatine  kinase–MB  (CK-MB),  as
         ●  inferior wall of left ventricle, II, III and aVF.
                                                              CK-MB levels will be affected by muscle damage. However,
         Additional  leads  are  needed  to  view  the  right  ventricle   CK-MB is less costly and more readily available, and so
         and posterior wall. Chest electrodes can be placed on the   is still often used, particularly in the presence of a non-
         right chest wall using the same landmarks as the left chest   diagnostic ECG. C-reactive protein assays may prove to
         to  view  the  right  ventricle  (see  Chapter  9).  Further   be useful, as baseline and discharge levels are predictive
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