Chamber Abnormalities and Intraventricular Conduction Defects




Day 2: Chamber Abnormalities and Intraventricular Conduction Defects



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  1. General statements




    1. Echocardiography and other newer imaging techniques, not the electrocardiogram (ECG), are the gold standards for assessing chamber size and wall thickness.



    2. In general, the sensitivities of the following criteria are moderate (in the range of 50%), and the specificities are very high (> 90%).



  2. Right atrial abnormality (Day 2-1)




    1. The P wave is pointed in II, III, or aVF, and the amplitude is >2.5 mm (historically referred to as P pulmonale).



    2. P wave axis is frequently >70°.



  3. Left atrial (LA) abnormality




    1. In most forms of acquired LA abnormality, the commonest manifestation is a wide (>40 msec) and deep (>1 mm) terminal portion of the P wave in V1. (Day 2-2)



    2. An appearance typical in mitral valvular disease is a “double-humped” P wave, at least 130 msec in duration, in II, III, or aVF (so-called P mitrale). (Day 2-3)



  4. Biatrial abnormality—suggested by a combination of tall P waves in II, III, or aVF, and the terminal negativity in V1. (Day 2-4)


     


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    DAY 2-02



     


    DAY 2-03



     


    DAY 2-04



     



  5. Right ventricular hypertrophy (RVH) (Day 2-5)




    1. RVH is suggested by all the following:




      1. Right axis deviation



      2. A tall R wave in V1 (≥7 mm)



      3. R wave in V1 + S wave in V6 ≥10 mm



      4. R/S ratio in V1 ≥ 1



      5. Incomplete RBBB pattern



      6. Right atrial abnormality



      7. S > R in V6



    2. The diagnosis of RVH requires exclusion of the other causes of a tall R wave in V1 (see Day 9).



    3. RVH in patients with acquired pulmonary disease tends to present in a different form: (Day 2-6)




      1. Deep S waves are present across the precordium.



      2. The R wave transition across the precordium is delayed.



      3. Right axis deviation and right atrial abnormality are frequently present.



      4. Low voltage may be present.



  6. Left ventricular hypertrophy (LVH)




    1. Precordial leads (any of the following) (Day 2-7)




      1. S wave in V1 + R wave in V5 or V6 > 35 mm in adults (> 30 years)



      2. R wave in V5 or V6 > 26 mm



    2. Limb leads (any of the following) (Day 2-8)




      1. R wave in I > 14 mm



      2. R wave in aVL > 11 mm



    3. LVH is frequently accompanied by ST segment and T wave abnormalities, sometimes referred to as a “strain” pattern, but more appropriately as “repolarization” abnormalities.



  7. Low voltage (Day 2-9)




    1. Definition




      1. No QRS complex with an absolute value ≥ 0.1 mv (10 mm)



      2. Or, no limb lead QRS ≥ 0.05 mv (5 mm) (so-called low voltage in the limb leads)


       


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    2. Causes




      1. Decreased voltage production by the myocardium




        1. Restrictive cardiomyopathies (amyloidosis, sarcoidosis, etc.)



        2. Hypothyroidism



      2. Increased impedance between the voltage producing source (the myocardium) and the ECG leads




        1. Fat (obesity)



        2. Air [chronic obstructive pulmonary disease (COPD), tension pneumothorax]



        3. Water (pericardial or pleural effusion, ascites)



  8. Intraventricular conduction defects (IVCDs)




    1. The concept of the intrinsicoid deflection time (IDT) delay


       



       



    2. The genesis of the normal QRS complex in V1 and I or V6




      1. Depolarization begins in the left side of the septum and proceeds initially rightward, resulting in a positive deflection in V1 and a small Q wave in I and V6.



      2. The bulk of the left ventricle is depolarized next to the left, producing a negative deflection in V1 and a tall R wave in I and V6.



      3. Depolarization of the right ventricle (RV) via the right bundle occurs slightly after the onset of left ventricle (LV) depolarization, and any contribution of the RV to the QRS vector is swamped by the electrical forces of the much more massive LV.


       



       



    3. The genesis of the QRS complex in LBBB (Day 2-10) (Day 2-11)




      1. In LBBB, the septum is depolarized initially by the right bundle from right to left, producing an initial small Q wave in V1 and an R wave in I and V6.



      2. The remainder of the depolarization of the LV also occurs from right to left, producing a large negative deflection in V1 and a broad, monophasic R wave in 1 and V6.



      3. Since virtually the entire LV has to be depolarized by movement of current through the myocardium instead of the left bundle, LV activation is delayed in the left chest leads resulting in a delay in the intrinsicoid deflection time in I and V6.


       



       


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      DAY 2-11



       



    4. The genesis of the QRS complex in RBBB (Day 2-12) (Day 2-13) (Day 2-14)




      1. In RBBB, depolarization of the septum (contributed by the left bundle) occurs normally from left to right, producing a small R wave in V1.



      2. Depolarization of the LV proceeds normally, producing a negative deflection in V1 and an R wave in I and V6.



      3. Finally the RV depolarizes from left to right by movement of current through the myocardium, producing a tall R’ wave in V1 and a wide S wave in I and V6.



      4. The very late depolarization of the RV produces a delay in the intrinsicoid deflection time in V1.


       



       



    5. Infarcts in IVCDs




      1. Because the left bundle is responsible for the first 20–30 msec of the QRS complex, the diagnostic implications of Q waves in the presence of RBBB are still valid.



      2. A common combination is RBBB and an old septal myocardial infarction (MI), which produces a QR configuration in V1 as opposed to the expected RSR’. (Day 2-15)



      3. The diagnosis of an old MI cannot be made in the presence of LBBB.


       


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    6. Summary of the rules for naming IVCDs (Day 2-16) (Day 2-17)


       



       



    7. Left anterior fascicular block (LAFB) (Day 2-18) (Day 2-19)




      1. Left axis deviation >45°



      2. Tiny Q waves in I or aVL



      3. Usually slightly prolonged QRS duration (>90 msec)



      4. No other causes for LAD (e.g., LVH, inferior MI, chronic lung disease)



    8. Left posterior fascicular block (LPFB) (Day 2-20) (Day 2-21)




      1. Right axis deviation >100°



      2. Deep S wave in I and a small Q wave in III



      3. Usually slightly prolonged QRS duration (>90 msec)



      4. No other causes for reactive attachment disorder (RAD) (e.g., RVH, chronic lung disease, lateral MI)?


       


      DAY 2-16



       


      DAY 2-17



       


      DAY 2-18



       


      DAY 2-19



       


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      DAY 2-21





Sample Tracings



ECG 1



ECG 2



ECG 3



ECG 4



ECG 5



ECG 6



ECG 7



ECG 8



ECG 9



ECG 10



ECG 11



ECG 12



ECG 13



ECG 14



ECG 15



ECG 16



ECG 17



ECG 18



ECG 19



ECG 20



Chamber Abnormalities and Intraventricular Conduction Defects




Interpretations of Sample Tracings



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ECG 1



Atrial rate: 63



Ventricular rate: 63



Rhythm: Sinus rhythm



P wave: Normal



PR interval: 160 msec



QRS complex:



 Axis: 130°



 Duration: 140 msec, RBBB, LPFB



 Voltage: Normal



 Morphology: Normal



ST segment:



T wave:



QT interval: 480 msec



U wave:



Diagnosis: Sinus rhythm with an occasional premature atrial complex (PAC), right axis deviation, RBBB, and left posterior fascicular block, (right axis deviation >100°, deep S wave in I and small Q wave in III, and an IVCD)



ECG 2



Atrial rate: 64



Ventricular rate: 64



Rhythm: Sinus rhythm with first degree AV block



P wave: Probable left atrial abnormality



PR interval: 210 msec



QRS complex:



 Axis: -60°



 Duration: 150 msec, RBBB, LAFB



 Voltage: Increased in aVL



 Morphology: Normal



ST segment:



T wave:

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Jan 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Chamber Abnormalities and Intraventricular Conduction Defects

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