12 Lead ECG axis and vectors

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The Non Intimidating 12 Lead ECG: Barbara McLean , MN, RN, CCRN, CCNS-NP, FCCM

Arial:

Waveforms

Calibri:

Cardiac Conduction

Times New Roman:

Electrical and Mechanica

Symbol:

Definition The electrocardiogram is a graphic representation of the heart ’ s electrical activity. It does not represent the mechanical events of the heart.

Wingdings:

Interpretation of the ECG requires: Reading ECG ’ s (Descriptive Analysis) Patient ’ s Age (Clinical Analysis) Presenting Complaint Available Prior Tracings Important to use a systematic approach when evaluating and ECG and know the facts of the patient.

Arial Narrow:

Physiological Fundamentals The electrical events precede the mechanical events originating at the cellular level. With stimulation the cells begin to depolaraize - (+) ions rush in as the (-) ions are displaced to the outside. Repolarization begins returning the cell to its resting state and normal polarity. Depolarization begins in the endocardium (innermost) and proceeds to the epicardium (outermost), repolarization is the opposite.

Mistral:

3 Types of Cardiac Cells Pacemaker Cells - Collection of cells that are able to depolarize spontaneously over and over at a particular rater. These cells have automaticity. Electrical Conduction Cells - Long thin cells that make up the conduction system. Myocardial Cells - Constitute major part of cardiac tissue.

Signboard:

Anatomy of the ECG Waveform P wave - Atrial depolarization - The first half of the wave is right atrial depolarization and the second half is predominantly left atrial depolarization.

san diego visuals:

Anatomy of the ECG Waveform PR interval - represents the delay in the conduction from the AV node as the atria finish contracting and ventricles begin allowing the ventricles to fill completely.

The Non Intimidating 12 Lead ECG::

Anatomy of the ECG Waveform QRS complex/interval - Ventricular depolarization - The complex is described b its appearance and can be variable, dependent on the direction of depolarization detected by an electrode.

Waveforms:

QRS If the first deflection is negative labeled as Q wave First upward deflection is positive labeled as R wave If second upward deflection is positive label as R ’ (R-prime)

Cardiac Conduction:

QRS The first downward deflection following an upward deflection is labeled as S wave If the amplitude of the deflection is small (< 3mm) use a lower case letter; If the amplitude is large use a capital letter If there is only a negative deflection this is a QS complex because you cannot differentiate between a Q or an s wave.

Electrical and Mechanica:

Waves of the ECG ST segment - Beginning of ventricular repolarization - Normally isoelectric T wave - ventricular repolarization QT interval - return of the stimulated ventricles to their resting state. Measured from beginning of QRS to end of the T wave U wave - Terminal phase of ventricular repolarization

Definition:

Axis and Vectors

Physiological Fundamentals:

Both I and a VF + ve = normal axis Both I and a VF - ve = axis in the Northwest Territory Lead I + ve and a VF - ve Lead II + ve = normal axis Lead II - ve = left axis deviation Lead I - ve and a VF + ve = right axis deviation

3 Types of Cardiac Cells:

Axis

Anatomy of the ECG Waveform:

Axis

Anatomy of the ECG Waveform:

Axis

Anatomy of the ECG Waveform:

Axis

QRS:

Axis

QRS:

Axis

Waves of the ECG:

Axis

Axis and Vectors:

Axis

PowerPoint Presentation:

Axis

PowerPoint Presentation:

Axis

Axis:

Axis

Axis:

Axis Deviation

Axis:

Axis

Axis:

Axis

Axis:

AXIS Normal axis -30 0 to 120 0 Left axis deviation -30 0 to -90 0 Right axis deviation 120 0 to 180 0 Ind eterminate (extreme) axis deviation -90 0 to 180 0 AXIS

Axis:

NORMAL AXIS

Axis:

LEFT AXIS DEVIATION

Axis:

Normal QRS width with an axis of >100 0 Predominantly positive in leads II and III, and negative in aVL RIGHT AXIS DEVIATION

Axis:

Causes of right axis deviation Normal finding in children and tall thin adults Right ventricular hypertrophy Chronic lung disease even without pulmonary hypertension Anterolateral myocardial infarction Left posterior hemiblock Pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway Atrial septal defect Ventricular septal defect

Axis:

Causes of Left Axis Deviation Left anterior hemiblock Q waves of inferior myocardial infarction Artificial cardiac pacing Emphysema Hyperkalemia Wolf-Parkinson-White syndrome - right sided accessory pathway Tricuspid atresia Ostium primum ASD Injection of contrast into left coronary artery

Axis:

Hypertrophy Atrial Hypertrophy: P wave more than 3 small squares wide [> ,12 sec, wide]. Right Atrial Hypertrophy - large, disphasic P wave with tall initial component. Left Atrial Hypertrophy - large, disphasic P wave with wide terminal component

Axis Deviation:

Ventricular Hypertrophy Right Ventricular Hypertrophy R wave greater than S wave in V1. R wave gets progressively smaller from V1 to V6. S wave persists in V5 and V6. Wide QRS. Left Ventricular Hypertrophy S wave in V1 + R wave in V5 add up to more than 35 mm. Left axis deviation. Wide QRS. T wave slants down slowly and returns up rapidly (inverted).

Axis:

Miscellaneous Pulmonary Effects Emphysema: low voltage in all leads. Pulmonary infarction. “ S1Q3 ” - wide S in I, large Q in III. Inverted T wave V1  V4. ST depressed in II. Often transient Right B.B.B.

Axis:

Electrolytes Increased K+ Decreased K+ Increased Ca++ Decreased Ca++ Patterns Strain Artificial Pacemaker

AXIS:

Miscellaneous (Continued) Drug Effects Digitalis (may cause ST depression) Digitalis Excess: PAT with block, SA block, AV block, Nodal Tachycardia with A-V dissociation. Digitalis Toxicity P.V.C ’ s. Bigeminy, Ventricular Tachycardia, Atrial or Ventricular Fibrillation. Quinidine

NORMAL AXIS:

Understanding Electrical Flow Positive if headed toward electrode Negative if headed away from electrode Initial vector Terminal vector Alternative depolarization

LEFT AXIS DEVIATION:

Left Bundle Branch Block Criteria QRS duration ≥ 120ms Broad R wave in I and V 6 Prominent QS wave in V 1 Absence of q waves (including physiologic q waves) in I and V 6

RIGHT AXIS DEVIATION:

Left Bundle Branch Block

Causes of right axis deviation:

Right Bundle Branch Block Criteria QRS duration ≥ 110ms rSR ’ pattern or notched R wave in V 1 Wide S wave in I and V 6

Causes of Left Axis Deviation:

Right Bundle Branch Block

Hypertrophy:

Conduction Blocks and Secondary Repolarization Abnormalities LBBB RBBB

Ventricular Hypertrophy:

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

Miscellaneous:

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

Electrolytes:

Left Ventricular Hypertrophy Many sets of criteria for diagnosing LVH have been proposed: Sensitivity Specificity The sum of the S wave in V 1 and the R wave in either V 5 or V 6 > 35 mm 43% 95% Sum of the largest precordial R wave and the largest precordial S wave > 45 mm 45% 93% Romhilt-Estes Point System 50-54% 95-97%

Miscellaneous (Continued):

Romhilt-Estes Point System for LVH Criterion Points Amplitude (any of the following: Largest R or S wave in any limb lead ≥ 20mm S in V 1 or V 2 ≥ 30mm R in V 5 or V 6 ≥ 30mm 3 ST depressions or T wave inversions in lateral precordial leads, I, and/or aVL 3 Left atrial enlargement 3 Left axis deviation 2 QRS duration ≥ 90 ms 1 Intrinsicoid deflection in V 5 or V 6 ≥ 50 ms 1 4 points  Probable LVH 5 points  Definite LVH

Understanding Electrical Flow:

Left Ventricular Hypertrophy

Left Bundle Branch Block Criteria:

Right Ventricular Hypertrophy Right axis deviation Right atrial enlargement Downsloping ST depressions in V 1 -V 3 (a.k.a. RV strain pattern) Tall R wave in V 1 Although there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence:

Left Bundle Branch Block:

Right Ventricular Hypertrophy

Right Bundle Branch Block Criteria:

Bundle Branch Block

Right Bundle Branch Block:

Bundle Branch Block

Conduction Blocks and Secondary Repolarization Abnormalities:

Bundle Branch Block

Left Atrial Enlargement:

Bundle Branch Block

Right Atrial Enlargement:

Bundle Branch Block

Left Ventricular Hypertrophy:

Bundle Branch Block

Romhilt-Estes Point System for LVH:

Bundle Branch Block

Left Ventricular Hypertrophy:

Bundle Branch Block

Right Ventricular Hypertrophy:

Bundle Branch Block

Right Ventricular Hypertrophy:

Bundle Branch Block

Bundle Branch Block:

Bundle Branch Block

PowerPoint Presentation:

Review of Basic Lead Groups Inferior heart -II, III, aVF Septal portion - V1, V2 Anterior heart - V2-V4 Lateral heart - V4-V6, I, aVL

PowerPoint Presentation:

Lead Measures Indicative: Face area Inferior : 11, 111, avF Lateral: 1, avL, V5, V6 Ant-Septal : V1, V2 Anterior: V3, V4 Posterior: none Reciprocal: opposite Lateral, Anterior Inferior Posterior Inferior Ant-septal

PowerPoint Presentation:

Acute Myocardial Infarction ST ELEVATIONS Anterior Wall MI Leads V1-V4 Reciprocal changes in leads II, III, and aVF Area supplied by the LAD Inferior Wall MI Leads II, III and aVF Reciprocal changes in leads I, and aVL Area usually supplied by the RCA

PowerPoint Presentation:

Acute Myocardial Infarction ST ELEVATIONS Lateral Wall MI I, aVL, V5 and V6 Area supplied by the Circumflex artery Posterior Wall MI Reflected on the opposite walls Opposite deflections

PowerPoint Presentation:

Lead Measures Indicative: Face area Two leads of group ST up at least 2 mm T wave hyperacute, flat, inverted Q wave in any leads Wider than .04 sec Deeper than 2mm Normal Q in Lead 1, avL, V5, V^6 Reciprocal: opposite Only in STE MI St depressed Upright R Upright T

PowerPoint Presentation:

Anterior ST Elevation MI

PowerPoint Presentation:

Limb Leads

PowerPoint Presentation:

Chest Leads

Review of Basic Lead Groups:

Myocardial Infarction

Acute Myocardial Infarction:

Acute MI

Acute Myocardial Infarction :

Posterior Lateral MI

Lead Measures:

Old MI

Anterior ST Elevation MI:

IPMI and RBB

PowerPoint Presentation:

IMI and RBB

PowerPoint Presentation:

Coronary Arteries blood supply capillaries collaterals

Limb Leads:

Right Coronary Artery: 85% Dominant right atrium sa node av junction right ventricle variable amount of left ventricle posterior portion intraventricular septum

Chest Leads:

Left Coronary Artery Left Anterior Descending anterior intraventricular groove apex and distal surface anterior 2/3 anterior septum right bundle anterior fascicle of left bundle anterior papillary muscle anterior surface

Myocardial Infarction:

Left Coronary Artery Circumflex: 8% Dominant posterior surface base of left heart inferiorly left atrium

PowerPoint Presentation:

Stable Angina

Acute MI:

Unstable Angina or NSTE-MI

Posterior Lateral MI:

STE-MI

Old MI:

Membrane Activity:

IPMI and RBB:

Excitation- Contraction translation of energy from electrical to mechanical troponin tropomyosin actin myosin

IMI and RBB:

Cellular requirements oxygen Na + Ca ++ K + ATP

Coronary Arteries:

Determinants of Myocardial Oxygen : Matching supply oxygen carrying capacity coronary blood flow demand wall tension filling pressure development thickness heart rate contractility

Right Coronary Artery: 85% Dominant:

Pathophysiology of Ischemia impedance of CBF 60-70% stenosis inability to vasodilate

Left Coronary Artery:

Indices of Ischemia stable angina variant angina unstable angina

Left Coronary Artery:

Consequences of Ischemia inadequate myocardial oxygenation local accumulation of metabolic waste products anerobic lactate kinins serotonin adenosine free Ca ++ stimulation of peripheral pain receptors generalized sympathetic and parasympathetic stimulation left ventricular stiffening

Stable Angina:

Membrane Activity

Unstable Angina or NSTE-MI:

Recognizing ECG Changes STABLE ANGINA UNSTABLE ANGINA STE-MI NSTE-MI

STE-MI:

Lead Placement

Membrane Activity: :

Standard Limb Leads

Excitation- Contraction:

Lead placement

Cellular requirements:

Right Sided Leads

Determinants of Myocardial Oxygen : Matching:

Ist Few Hours First 24 Hours First 72 Hours Stages of Acute Q-Wave MI

Pathophysiology of Ischemia:

Tomb stoning is less prominent with the onset of T wave inversions in the anterior precordium. Reciprocal changes are resolving. Evolution of acute anterolateral myocardial infarction at 3 hours

Indices of Ischemia:

Prominent Q waves have developed across the anterior precordium and leads I, aVL. However, ST segment elevation persists. Evolution of acute anterolateral myocardial infarction at 24 hours

Consequences of Ischemia:

Q wave pattern in the anterolateral leads is well established. Persistent ST segment elevation suggests complication by aneurysm or pericarditis Evolution of acute anterolateral myocardial infarction at 72 Hours

Membrane Activity:

ST segment elevation in leads V4R and V5R reveals right ventricular involvement complicating the inferior infarct. Right ventricular infarction (Rt.sided leads)

Recognizing ECG Changes:

Note inferior ST segment elevation as well as atrioventricular dissociation secondary to complete heart block. AV dissociation Complicated Acute inferior myocardial infarction

Lead Placement:

Note inferior ST segment elevation and Q waves as well as progressive prolongation of the PR interval followed by a dropped beat with grouped beating. wenckebach Acute inferior myocardial infarction complicated by Wenkebach

Standard Limb Leads:

Q waves in leads II, III & aVF Tall R wave in lead V 2 with a duration of > 0.04 secs and R/S ratio equal to or >1 (in patients over 30 years of age without RVH) Tall R in V2,R/S >1 Inferoposterior MI

Lead placement:

Causes of ST Elevation "ELEVATION ” E - Electrolytes L - LBBB E - Early Repolarization V - Ventricular hypertrophy A - Aneurysm T - Treatment - Pericardiocentesis I - Injury (AMI, contusion) O - Osborne waves (hypothermia) N - Non-occlusive vasospasm

Right Sided Leads:

Normal ECG

Stages of Acute Q-Wave MI:

Looking for Changes

Evolution of acute anterolateral myocardial infarction at 3 hours:

Big Changes, Big Difference

Evolution of acute anterolateral myocardial infarction at 24 hours:

Practice ECG

Acute inferior myocardial infarction complicated by Wenkebach:

Hyperkalaemia The following changes may be seen in hyperkalaemia Small or absent P waves Atrial fibrillation Wide QRS Shortened or absent ST segment Wide, tall and tented T waves Ventricular fibrillation This man ’ s serum potassium was 9.6 nonol/L

Looking for Changes:

Acute Inferior Myocardial Infarction ST elevation in the inferior leads II, III and a VF Reciprocal ST depression in the anterior leads

Practice ECG:

Acute Anterior Myocardial infarction ST elevation in the anterior leads V1-6, I and VL Reciprocal ST depression in the inferior leads

PowerPoint Presentation:

Acute Posterior Myocardial Infarction Hyperacute - the mirror image of acute injury in leads V1-3 Fully evolved - tall R wave, tall upright T wave in leads V1-3 Usually associated with inferior and/or lateral wall MI

Hyperkalaemia:

Old Inferior Myocardial Infarction A Q wave in lead III wider than 1 mm (1 small square) and A Q wave in lead a VF wider than 0.5 mm and A Q wave of any size in lead II

PowerPoint Presentation:

Acute Myocardial Infaction in the Presence of Left Bundle Branch Block Feature suggesting acute MI ST changes in the same direction as the QRS (as shown here) ST elevation more than you ’ d expect from LBBB alone (e.g. > 5 mm in leads V1-3) Q waves in two consecutive lateral leads (indicating anteroseptal MI)

PowerPoint Presentation:

Myocardial Infarction

PowerPoint Presentation:

Acute MI

PowerPoint Presentation:

Posterior Lateral MI

PowerPoint Presentation:

Old MI

PowerPoint Presentation:

IPMI and RBB

PowerPoint Presentation:

IMI and RBB

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