Hypokalemia produces distinctive changes in the ST-T complex. The most common pattern seen is ST depressions with prominent U waves and prolonged repolarization . With hypokalemia, the U waves typically become enlarged and may even exceed the height of the T waves . Particularly important in Digitalis patients!
Santhiram Medical College NandyalELECTROCARDIOGRAPHY Lecture By Dr.G.Venkata Swamy M.D
HISTORY OF ELECTROCARDIOPHY Agustus – Desire’ Waller was the first person to record cardiac electricity in 1887 But most comprehensive work on human electrocardiography was done by Willem Einthoven in 1903 Willem Einthoven was awarded Nobel prize for his work in electrocardiography in 1924 A few years later Wilson and Goldberger developed the unipolar and augmented unipolar systems respectively
DefinitionsElectrocardiogram (ECG) : It is a graphic recording of electric potentials generated by the heart.Electrocardiography : The process of recording ECG is called electrocardiographyElectrocardiograph : The machine that records the ECG is called electrocardiographLead : Electrode placed on the body is called a lead
Ctn. Electrocardiogram (ECG)• An ECG is a series of waves and deflections recording the heart’s electrical activity from a certain “view.” Many views, each called a lead, monitor voltage changes between electrodes placed in different positions on the body.• Leads I, II, and III are bipolar leads, which consist of two electrodes of opposite polarity (positive and negative). The third (ground) electrode minimizes electrical activity from other sources.• Leads aVR, aVL, and aVF are unipolar leads and consist of a single positive electrode and a reference point (with zero electrical potential) that lies in the center of the heart’s electrical field.• Leads V1–V6 are unipolar leads and consist of a single positive electrode with a negative reference point found at the electrical center of the heart.
Clinical utility of the ECG :1. It is noninvasive inexpensive and highly versatile test2. Useful in detecting a) Arrhythmias b) Conduction disturbances c) myocardial ischemia & infarction and d) metabolic disturbances such as Hyperkalemia and Hypokalemia
Electrocardiogram1. Basics2. Axis determination3. Calculation of Heart Rate4. Arrhythmias5. Bundle Branch Blocks6. Myocardial infarction7. Cardiac enlargement and Hypertrophy8. AV Blocks
Ctn. Structure and Function of the Normal Heart and Blood Vessels
Conduction Systemsinoatrial node located in right atrium inf. to opening of SVC action potential begins here initiates atrial contractionatrioventricular node located in right atrium ant. to opening of coronary sinus main job is to delay the action potential to give atria time to contractbundle of His (AV bundle) only site where atrial impulses can travel to the ventriclesbundle branchesPurkinje fibers (not shown) small branches that travel from endocardium into myocadium
Conduction SystemReview cardiac action potential is initated in the SA node travels quickly through pathways to simultaneously contract the atria the atria and ventricles are insulated from each other so atrial action potentials can only enter ventricles through one pathway action potential enters AV node where the impulses are slowed down and held momentarily this gives the atria time to contract the action potential then travels quickly to the rest of the ventricular myocardium through the AV bundle, bundle branches and purkinje fibers
Electrical Flowresting myocardial cells have a net negativecharge at restwhen an AP reaches a cell it depolarizescausing the internal net charge to becomepositiveelectrically, the action potential travelingthrough the heart can be viewed as a waveof positive chargeVector the average direction of all of the positive charges as they travel through the myocardium the average vector in a normal heart travels to the left and downward
Electrical FlowVector Influencesthings that influence theoverall amount of chargeflowing through themyocardium will change theaverage direction the thecharge is flowingInfarction essentially an area that no longer carries charge what would happen to the vector if the posterior wall of the l. ventricle infarcted?
Electrical FlowVector Influencesthings that influence the overallamount of charge flowing through themyocardium will change the averagedirection the the charge is flowingInfarction essentially an area that no longer carries charge what would happen to the vector if the posterior wall of the l. ventricle infarcted?Hypertrophy essentially an area that carries extra charge how would the vector change with l. ventricular hypertrophy?vector points towards hypertrophy andaway from infarction
ECG PAPER• The horizontal scale represents time, such that, at a standard paper speed of 25 mm/sec, each small box (1 mm) represents 0.04 second and each large box (5 mm) represents 0.20 second.• The vertical scale represents amplitude (10 mm = 1 mV). The heart rate can be estimated by dividing the number of large boxes between complexes (R-R interval) into 300.
In the ECG each wave has a height (positive deflection ) or depth (negative deflection and width) When current flows towards an electrode a tall positive deflection is recorded When current flows away from the electrode a deep negative deflection is recorded When current flows at 900 to the electrode a small ½ positive and
When current flows towards an electrode a tall positive deflection is recorded fig. – E1 electrode
When current flows away from the electrode a deep negative deflection is recorded fig – E2 electrode
When current flows at 900 to the electrode a small ½ positive and ½ negative deflections are recorded fig – E3 electrode
Direction of LEAD – 1 LEAD-2 AXISQRS compels DOMINANTLY DOMINANTY NORMAL POSITIVE POSITIVE
DIRECTION LEAD – 1 LEAD – 2 AXISOF QRS DOMINANTLY DOMINANTLY LADCOMPLEX POSITIVE NEGATIVE1. NORMAL VARANT 2. LVH3. LEFT ANTERIOR FASCICULAR BLOCK4. INFERIOR M I
DIRECTION LEAD1 LEAD2 AXISOF QRS DOMINANTLY DOMINANTLY RADCOMPLEX NEGATIVE POSITIVE1. NORMAL VARIENT 2. DEXTROCARDIA3. SPURIOUS FINDING DUE TO REVERSAL OF RIGHT AND LEFT ARM ELECTRODES
AXIS DETERMINATION TO DETERMINE THE AXIS, LOCATE THE FRONTAL PLANE LEAD WHICH SHOWS SMALL EQUIPHASIC QRS DEFLETION ITS PERPENDICULAR LEAD FORMS THE ELECTRICAL AXIS OF THEHEART WHICH SHOWS MAXIMUM QRS DEFLECTION IF THE DEFLECTION IS POSITIVE THE AXIS IS THE AXIS OF THE POSITIVE POLE OF THAT LEAD IF THE DEFLECTION IS NEGATIVE THE AXIS IS THE AXIS OF THE NEGATIVE POLE OF THAT LEAD
In this figure small equiphasic QRSdeflection is AVR THE LEAD WHICH IS AT 90O IS LIII. IN LIII THEDEFLECTION IS POSTIVE SO THE AXIS IS +1200
IN THIS FIGUER SMALL EQUIPHASIC QRS DEFLECTION IS LII. THE LEAD AT 900 TO LII LEAD IS AVL . IN THIS LEAD THE DEFLECTION IS NEGATIVE SO THE AXIS IS +1500
Ctn. Electrocardiogram (ECG) Methods for Calculating Heart Rate• Method 1: Count Large Boxes: Regular rhythms can be quickly determined by counting the number of large graph boxes between two R waves. That number is divided into 300 to calculate bpm.
Ctn. Electrocardiogram (ECG)• Method 2: Count Small Boxes: Sometimes it is necessary to count the number of small boxes between two R waves for fast heart rates. That number is divided into 1500 to calculate bpm.
Ctn. Electrocardiogram (ECG)• Method 3: Six-Second ECG Rhythm Strip: The best method for measuring irregular rates with varying R-R intervals is to count the• number of R waves in a 6-sec strip and multiply by 10. This gives the average number of bpm.
Sinus BradycardiaRate: Slow (<60 bpm)Rhythm: RegularP Waves: Normal (upright and uniform)PR Interval: Normal (0.12–0.20 sec)QRS: Normal (0.06–0.10 sec)
Sinus TachycardiaRate: Fast (>100 bpm)Rhythm: RegularP Waves: Normal (upright and uniform)PR Interval: Normal (0.12–0.20 sec)QRS: Normal (0.06–0.10 sec)
Sinus ArrhythmiaRate: Usually normal (60–100 bpm);frequently increases with inspirationand decreases with expirationRhythm: Irregular; varies with respirationP Waves: Normal (upright and uniform)PR Interval: Normal (0.12–0.20 sec)QRS: Normal (0.06–0.10 sec)
Sinus Pause (Sinus Arrest)Rate: Normal to slow; determined byduration and frequency of sinus pauseRhythm: Irregular whenever a pause (arrest) occursP Waves: Normal (upright and uniform) except in areas of pause (arrest)PR Interval: Normal (0.12–0.20 sec)QRS: Normal (0.06–0.10 sec)
Sinoatrial (SA) BlockRate: Normal to slow; determined by duration and frequency of SA blockRhythm: Irregular whenever an SA block occursP Waves: Normal (upright and uniform) except in areas of dropped beatsPR Interval: Normal (0.12–0.20 sec)QRS: Normal (0.06–0.10 sec)• The block occurs in some multiple of the P-P interval.• After the dropped beat, cycles continue on time.
Supraventricular Tachycardia (SVT)Rate: 150–250 bpmRhythm: RegularP Waves: Frequently buried in preceding T waves and difficult to seePR Interval: Usually not possible to measureQRS: Normal (0.06–0.10 sec) but may be wide if abnormally conducted through ventricles• This arrhythmia has such a fast rate that the P waves may not be seen.
Atrial Flutter (A-flutter)Rate: Atrial: 250–350 bpm; ventricular: slow or fastRhythm: Usually regular but may be variableP Waves: Flutter waves have a saw-toothed appearancePR Interval: VariableQRS: Usually normal (0.06–0.10 sec), but may appear widened if flutter waves are buried in QRS
Atrial Fibrillation (A-fib)Rate: Atrial: 350 bpm or greater; ventricular: slow or fastRhythm: IrregularP Waves: No true P waves; chaotic atrial activityPR Interval: NoneQRS: Normal (0.06–0.10 sec)• Rapid, erratic electrical discharge comes from multiple atrial ectopic foci.• No organized atrial contractions are detectable.
The 12-Lead ECG The 12-Lead ECG sees the heart from 12 different views. Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart. The rhythm strip is only 1 of these 12 views.
Views of the HeartSome leads get Lateral portiona good view of of the heartthe: Anterior portion of the heart Inferior portion of the heart
ST ElevationOne way todiagnose anacute MI is tolook forelevation ofthe STsegment.
ST Elevation (cont)Elevation of theST segment(greater than 1small box) in 2leads isconsistent witha myocardialinfarction.
Anterior View of the HeartThe anterior portion of the heart isbest viewed using leads V1- V4.
Anterior Myocardial InfarctionIf you see changes in leads V1 - V4that are consistent with amyocardial infarction, you canconclude that it is an anterior wallmyocardial infarction.
Putting it all TogetherDo you think this person is having amyocardial infarction. If so, where?
InterpretationYes, this person is having an acuteanterior wall myocardial infarction.
Other MI LocationsNow that you know where to look foran anterior wall myocardial infarctionlet’s look at how you would determineif the MI involves the lateral wall orthe inferior wall of the heart.
Other MI LocationsFirst, take a Lateral portionlook again at of the heartthis picture ofthe heart. Anterior portion of the heart Inferior portion of the heart
Other MI LocationsNow, using these 3 diagrams let’s figurewhere to look for a lateral wall andinferior wall MI. Limb Leads Augmented Leads Precordial Leads
Anterior MIRemember the anterior portion of theheart is best viewed using leads V1- V4. Limb Leads Augmented Leads Precordial Leads
Lateral MISo what leads do youthink the lateral Leads I, aVL, and V5- V6portion of the heart isbest viewed? Limb Leads Augmented Leads Precordial Leads
Inferior MINow how about theinferior portion of the Leads II, III and aVFheart? Limb Leads Augmented Leads Precordial Leads
Putting it all TogetherNow, where do you think this personis having a myocardial infarction?
Inferior Wall MIThis is an inferior MI. Note the STelevation in leads II, III and aVF.
Anterolateral MIThis person’s MI involves both the anteriorwall (V2-V4) and the lateral wall (V5-V6, I,and aVL)!
Right Ventricular Infarction R.V infarction is associated with inferoposterior infarcation RV infarcation causes signs of sever RV failure ( JVP , Kussmaul’s sign , tender hepatomegaly with or without hypotension ) ST segment elevation is present in V1 V2 and V4 R
Left Atrial Enlargement Criteria P wave duration in II ≥120ms or Negative component ofbiphasic P wave in V1 ≥ 1 “small box” in area
Right Atrial Enlargement CriteriaP wave height in II ≥ 2.4mm or Positive component of biphasic P wave in V1 ≥ 1 “small box” in area
Left Ventricular Hypertrophy Many sets of criteria for diagnosing LVH have been proposed: Sensitivity SpecificityThe sum of the S wave in V1and the R wave in either V5 43% 95%or V6 > 35 mmSum of the largest precordialR wave and the largest 45% 93%precordial S wave > 45 mmRomhilt-Estes Point System 50-54% 95-97%
Left Ventricular Hypertrophy (with frequent PVCs)
A-V BLOCKS Interruption/delay in the conduction of electrical impulses between the atria & ventricles Classified site of block/severity of conduction abnormality 1st degree, 2nd degree Mobitz I (Wenkebach), 2nd degree Mobitz II, 3rd degree (Complete heart block)
1 Degree AV Block st Characterized by PR Interval > 0.20 seconds Delay in conduction AV Node Prolonged PR Interval constant Usually asymptomatic Least concerning of the blocks
2nd Degree Mobitz I (Wenkebach) Successive impulses from SA node delayed slightly longer than the previous impulse Characterized by prolonged PR interval that continues until the P wave is dropped (impulse doesn’t reach ventricle) May have hypotension or lightheadedness
2 Degree Mobitz II nd Less common, more serious Impulses from SA node fail to conduct to ventricles Hallmark PR Interval constant normal or prolonged, doesn’t prolong before dropping, not followed by QRS, can have > 1 dropped in a row Precursor to 3rd Degree Heart Block
3RD DEGREE “COMPLETE HEART BLOCK” Indicates complete absence of impulse between the atria & ventricle Atrial rate > or = ventricular rate Occur @ AV node 40-60 bpm Occur @ bundle branches < 40 bpm wide QRS complex Decreased C.O., P-P & R-R disassociated
Hypokalemia Clinical consequences of hypokalemia usually goes unnoticed. Common findings include weakness, fatigue, constipation, ileus, and respiratory muscle dysfunction. Thus, most of the time K+ gets replaced out of habit or to please the consultants. (e.g. Cardiology likes a K+ of 4.0 or above in MI patients.)
Don’t Forget about EKG ST depressions with prominent U waves and prolonged repolarization
Definition Normal serum potassium 3.5-5.5 mEq/L Hyperkalemia is a serum potassium greater than 5.5 mEq/L