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- 1. ECG BASICS By Dr .Mahipal Reddy
- 2. ECG machine
- 4. Horizontal plane - the six chest leads 6.5 V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 V6 V6 RA LA LV RV
- 5. Colour codes given by AHA
- 7. ECG paper 5 Large squares = 1 second Time 1 Large square = 0.2 second 1 Small square = 0.04 second 2 Large squares = 1 cm 6.1
- 8. STANDARDISATION ECG amplitude scale Normal amplitude 10 mm/mV Half amplitude 5 mm/mV Double amplitude 20 mm/mV
- 9. ECG WAVES
- 10. The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s QTc 0.33-0.43s
- 11. NSR
- 27. Normal Q wave
- 28. Q wave in MI
- 29. Q wave in septal hypertrophy
- 34. V 1 V 2 V 3 V 4 V 5 V 6 The R wave in the precordial leads must grow from V1 to at least V4
- 37. J point Q S ST
- 52. Left Atrial Enlargement Criteria P wave duration in II ≥ 120ms or Negative component of biphasic P wave in V 1 ≥ 1 “small box” in area
- 53. Right Atrial Enlargement Criteria P wave height in II ≥ 2.4mm or Positive component of biphasic P wave in V 1 ≥ 1 “small box” in area
- 68. Stress test ECG – note the ST Depression
- 70. Note the arrows pointing ST depression
- 71. ST depression & Troponin T positive is NON STEMI
- 74. Abnormalities of ST- segment acute MI pericarditis early repolariz. ischemia
- 75. Q waves in myocardial infarction
- 79. QT Interval - Should be < 1/2 preceding R to R interval -
- 80. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
- 81. QT Interval - Should be < 1/2 preceding R to R interval - QT interval
- 82. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
- 83. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
- 84. QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R
- 85. QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm R R
- 86. QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm Normal QT c = 0.46 sec R R
- 87. M
- 88. Atrioventricular (AV) Heart Block
- 89. Classification of AV Heart Blocks Degree AV Conduction Pattern 1 St Degree Block Uniformly prolonged PR interval 2 nd Degree, Mobitz Type I Progressive PR interval prolongation 2 nd Degree, Mobitz Type II Sudden conduction failure 3 rd Degree Block No AV conduction
- 91. 1 st Degree AV Block Prolongation of the PR interval, which is constant All P waves are conducted
- 104. Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted. Constant PR interval with unexpected intermittent failure to conduct Type 2
- 105. Mobitz Type I
- 106. MOBITZ TYPE 1
- 108. Analyze the Rhythm
- 110. Analyze the Rhythm
- 112. Mobitz Type II
- 114. Advanced Second-Degree AV Block Two or more consecutive nonconducted sinus P waves
- 116. 3 rd Degree (Complete) AV Block EKG Characteristics: No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes
- 119. Third-Degree (Complete) AV Block
- 133. Cardiac Pacemakers
- 142. Sinus block
- 143. ARRTHYMIAS AND ECTOPIC BEATS
- 144. normal ("sinus") beats sinus node doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an "atrial" beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Atrial Escape Beat Recognizing and Naming Beats & Rhythms
- 145. there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a "junctional" or a “nodal” beat Junctional Escape Beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Recognizing and Naming Beats & Rhythms
- 146. actually a "retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat Ventricular Escape Beat there is no p wave, indicating that the beat did not originate anywhere in the atria Recognizing and Naming Beats & Rhythms
- 159. Sinus arrest or exit block
- 160. PAC
- 164. Junctional Rhythm
- 173. ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = rate Voltage ~Mass
- 177. Notice a Pattern in the PVC’s?
- 178. Identifying AV Blocks: Name Conduction PR-Int R-R Rhythm Regular (20-40 bpm) Grossly Irregular P > R 3°: Regular Constant P > R 2°:Mobitz II Irregular Progressive P > R 2°:Mobitz I Regular > .20 P = R 1°:
- 184. Regions of the Myocardium: Inferior II, III, aVF Lateral I, AVL, V5-V6 Anterior / Septal V1-V4
- 185. Sinus Arrhythmia
- 186. Sinus Arrest/Pause
- 188. Premature Atrial Complexes (PACs)
- 189. Wandering Atrial Pacemaker (WAP)
- 192. Atrial Flutter
- 194. Premature Junctional Complexes (PJC)
- 195. Junctional Rhythm
- 196. Junctional Rhythm
- 199. Premature Ventricular Complexes (PVC's) Note – Complexes not Contractions
- 201. Uniformed PVC’s
- 202. R on T Phenomena
- 203. Multiformed PVC’s
- 204. PVC Couplets
- 205. PVC Salvos and Runs
- 206. Bigeminy PVC’s
- 207. Trigeminy PVC’s
- 208. Quadrageminy PVC’s
- 213. V Tach
- 215. Torsades de Pointes (TdeP)
- 220. Asystole (Cardiac Standstill)
- 221. Asystole The Mother of all Bradycardias
- 223. Ventricular Pacemaker (Single Chamber) pacemaker
- 224. Dual Paced Rhythm pacemaker
- 227. ventricular bigeminy
- 231. QUESTIONS?
- 232. Thank you all
- 244. NORMAL RULE
- 245. Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 250. Bundle branch block I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Anterior wall MI Left bundle branch block
- 251. Sequence of changes in evolving AMI 1 minute after onset 1 hour or so after onset A few hours after onset A day or so after onset Later changes A few months after AMI Q R P Q T ST R P Q ST P Q T ST R P S T P Q T ST R P Q T
- 252. Anterior infarction Anterior infarction Left coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 253. Inferior infarction Inferior infarction Right coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 254. Lateral infarction Lateral infarction Left circumflex coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
- 262. Lateral Leads V5, V6, I, aVL
- 264. Inferior II, III, AVF Antero-Septal V1,V2, V3,V4 Lateral I, AVL, V5, V6 Posterior V1, V2, V3 RIGHT LEFT
- 266. ST-Segment Elevation
- 268. T wave inversion in an evolving MI
- 269. The ECG in ST Elevation MI
- 276. Reciprocal Changes ie S-T depression in some leads in MI
- 278. Changes in NSTEMI
- 279. Action potentials and electrophysiology + + + + _ _ _ _ 3.2 Ca in(slow) ++ K out + Na in + Resting Depolarised Repolarised Plateau + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + Ca ++ K + K + Na + _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
- 280. LVH and strain pattern Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.
- 281. Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026 Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)
- 282. Examples of T wave abnormalities Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026
- 283. Sick Sinus Syndrome Sinoatrial block (note the pause is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat Severe sinus bradycardia
- 284. Bundle Branch Block
- 286. Right Bundle Branch Block
- 287. Where’s the MI?
- 288. Where’s the MI?
- 289. Where’s the MI?
- 290. Final one…
- 292. Which one is more tachycardic during this exercise test?
- 293. Any Questions?
- 294. Thanks for paying attention. I hope you have found this session useful.
Notes de l'éditeur
- Horizontal plane - the six chest leads Each of the six chest leads has a fixed position. In order to place the precordial leads correctly the fourth intercostal space needs to be identified. The ribs form convenient horizontal landmarks. In order to count them, feel for the ridge with marks the junction of the manubrium and the body of the sternum. When this has been found, run the finger outwards until it reaches the second costal cartilage, which articulates with the sternum at this level. The space immediately above this is the first intercostal space. The spaces should then be counted downwards, well away from the sternum, as they are more easily felt here. V 1 right sternal margin at fourth intercostal space V 2 left sternal margin at fourth intercostal space V 3 midway between V 2 and V 4 V 4 intersection of left midclavicular line and fifth intercostal space V 5 intersection of left anterior axillary line with a horizontal line through V 4 V 6 intersection of mid-axillary line with a horizontal line through V 4 and V 5 . V 1 and V 2 face and lie close to the free wall of the right ventricle, V 3 and V 4 lie near to the interventricular septum with V 4 usually at the cardiac apex, and V 5 and V 6 face the free wall of the left ventricle but are separated from it by a substantial distance. Together the chest leads observe changes in the anterior and lateral aspects of the heart, giving detailed information about the myocardium of the area they lie over.
- ECG paper The electrocardiogram (ECG) is a recording of the electrical activity of the heart. It records the wave of depolarisation that spreads across the heart. The ECG is recorded from two or more simultaneous points of skin contact (electrodes). When cardiac activation proceeds towards the positive contact, an upward deflection is produced on the ECG. As the activation moves away from the electrode, a downward deflection is seen. The neutral position on the ECG is known as the isoelectric line, and is where the tracing rests when there is no electrical activity in the muscle. There are many types of ECG machine, including 3, 6, and 12 channel machines. The ECG trace is printed out on paper composed of a number of 1 and 5 mm squares. The height of each complex represents the amount of electrical potential involved in each complex and an impulse of 1 mV causes a deflection of 10 mm. Horizontally each millimetre represents 0.04 second and each 5 mm represents 0.2 second.
- Rule 6 The normality of QRS complexes recorded from the precordial leads is dependent on both morphological and dimensional criteria.
- Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
- Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated.
- Characteristic changes in AMI The 12-lead ECG is the most useful investigation for confirming the diagnosis of acute myocardial infarction, locating the site of the infarct and monitoring the progress. It is therefore very important to know the changes that occur in this situation. The only diagnostic evidence of a completed myocardial infarction seen on the ECG are those in the QRS complexes. In the early stages changes are also seen in the ST segment and the T wave, and these can be used to assist diagnosis of myocardial infarctions. Shortly after infarction there is an elevation of the ST segment seen over the area of damage, and opposite changes are seen in the opposite leads. Several hours later pathological Q waves begin to form, and tend to persist. Later the R wave becomes reduced in size, or completely lost. Later still, the ST segment returns to normal, and at this point the T wave also decreases, eventually becoming deeply and symmetrically inverted. Although these changes occur sequentially, it is very unlikely they will all be clearly observed by the paramedic or GP. A patient can present at any stage and a progression through the ECG changes will not be seen. It is important to recognise these features as they occur rather than in association with each other. All these changes imply myocardial infarction, and will be discussed in more detail over the next few slides.
- ST elevation ST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change. ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction. ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V 1 and V 2 normally. However, if there is also elevation in V 3 the cause is unlikely to be physiological.
- Deep Q wave The only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation. Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.
- T wave inversion The T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value. Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign. The T wave can be lengthened or heightened by coronary insufficiency. T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts.
- Bundle branch block Bundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block). The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V 1 to V 3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide). Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.
- Sequence of changes in evolving AMI The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction. Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage. The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction. Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist. In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.
- Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V 1–6 ) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V 5 and V 6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V 2–6 , with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V 1–6 , I, and aVL.
- Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.
- Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL.
- Diagnostic criteria for AMI Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis. Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves. Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
- Action potentials and electrophysiology The heart is a hollow organ with walls made of specialised cardiac muscle. When excited, these muscles shorten, thicken and squeeze on the hollow cavities, forcing blood to flow in directions permitted by the valves (as described in the last slide). An action potential refers to the voltage changes occurring inside a cell when it is electrically depolarised, due to ionic movements into and out of the cell. Cardiac muscles can be electrically excited and show action potentials that propagate along the surface membrane, carrying excitation to all parts of the muscle. Cardiac muscle cells (cardiomyocytes) are interconnected by gap junctions, allowing action potentials to pass from one cell to the next. This ensures that the heart as a whole participates in each contraction, making the heartbeat an “all or none” response. The basic ventricular action potential is due to three voltage-dependent currents: sodium, potassium, and calcium. The very rapid rise of the initial spike of an action potential is due to the opening of the sodium channels, allowing sodium ions to rush into the cell from the outside, depolarising the cell further. The sodium channels then inactivate, and calcium channels activate. There is now a small flow of calcium ions flowing into the cell, balancing the small amounts of potassium ions leaking out. This results in the membrane potential being held in a suspended plateau. The potassium channels then open, and the calcium channels close, causing a rush of potassium ions out of the cell and the membrane being rapidly repolarised. The action potential does vary throughout the heart due to the presence of different ion channels. In the cells of the sino-atrial (SA node) and atrioventricular nodes (AV node) calcium channels, rather than sodium channels, are activated by membrane depolarisation, resulting in a different shape of the action potential. A recording of the electrical changes that accompany the cardiac cycle is called an electrocardiogram (ECG). Each cardiac cycle produces three distinct waves, designated P, QRS and T. It should be noted that these waves are not action potentials, they represent any electrical activity within the heart as a whole.