Importance of ECGs in management of CV diseases

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Evolving Guidelines for Reducing Time-toTreatment of Patients With AMI

ACC/AHA Guidelines (1999)
Door-to-treatment time: < 30 minutes

NHAAP Recommendations (1997)

Door-to-treatment time: 30 minutes

ACLS Recommendations (1992)

Door-to-treatment time: 30 to 60 minutes

 Myocardial ischemia detected by ambulatory ECG monitoring is common early after acute myocardial infarction and provides prognostic information beyond that available from standard clinical information

Source: John B. Gill, M.D et al, NEJM; 334:65-71 Pre hospital ECG significantly shortens door to needle times without prolonging the overall call to needle time in patients with acute myocardial infarction.
Source: Margaret Maloba ; Manchester Royal Infirmary -26th May 2004

Impulse generation and propagation

Normal ECG

Standard leads

Augmented leads

Precordial leads

QRS Axis ( Frontal Plane )

 The QRS mean electrical axis can be calculated by plotting

the vectors of two on a grid . The grid is simply a rearrangement of Einthoven's triangle as shown in the diagram below.

ECG Description
Rhythm Analysis : State basic rhythm ("normal sinus rhythm", "atrial fibrillation", etc.) ,Identify additional rhythm events if present ("PVC's", "PAC's", etc) Heart rate Conduction Analysis : "Normal" conduction implies normal sino-atrial (SA), atrio-ventricular (AV), and intraventricular (IV) QRS axis : in frontal plane Waveform Description : P, PR , QRS , QT , ST , T , U

ECG Interpretation : (Inferior MI, probably acute , LVH ETC. )

The electrical axis at a glance ... 2 glances actually.

Using leads I and aVF the axis can be calculated to within one of the four quadrants at a glance.

If the axis is in the "left" quadrant take your second glance at lead II.

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

P WAVE

P duration < 0.12 sec P amplitude < 2.5 mm Frontal plane P wave axis: 0o to +75o May see notched P waves in frontal plane

PR

O.12 sec -0.20 sec QRS duration < 0.10 sec Normal q-waves reflect normal septal activation (beginning on the LV septum): narrow (<0.04s duration) small (<25% the amplitude of the R wave)

QRS complex

ST segment

Normal ST segment elevation: this occurs in leads with large S waves (e.g., V1-3) Normal configuration is concave upward ST segment depression is always an abnormal finding, although often nonspecific

T WAVE
The normal T wave is usually in the same direction as the QRS except in the right precordial leads

In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR.

U WAVE
U wave amplitude is usually < 1/3 T wave amplitude in same lead
U wave direction is the same as T wave direction in that lead U waves are more prominent at slow heart rates and usually best seen in the right precordial leads. Origin of the U wave is thought to be related to after depolarizations which interrupt or follow repolarization.

QT interval

Normal ECG Tracing

Sinus Arrhythmia

Wandering Pacemaker

Premature Atrial Contractions

Deviation from NSR

These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.

PVCs

Deviation from NSR

Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes. When there are more than 1 premature beats and look alike, they are called uniform. When they look different, they are called multiform.

RBBB
"Complete" RBBB has a QRS duration >0.12s The frontal plane QRS axis is in the normal range The "normal" ST-T waves in RBBB should be oriented opposite to the direction of the terminal QRS forces rSR' complex : lead V1 S waves : I, aVL, V6

CRBBB

LBBB
Complete" LBBB" has a QRS duration >0.12s
Terminal S waves in lead V1 ( QS ) R waves in lead I, aVL, V6 ( no q wave ) poor R progression from V1 to V3 is common The "normal" ST-T waves in LBBB should be oriented opposite to the direction of the terminal QRS forces

CLBBB

Right Atrial Enlargement (RAE)

Right atrial enlargement

Take a look at this ECG. What do you notice about the P waves?

The P waves are tall, especially in leads II, III and avF.

Right atrial enlargement

To diagnose RAE you can use the following criteria:
II V1 or V2 P > 2.5 mm, or P > 1.5 mm
> 1 boxes (in height)

> 2 boxes (in height)

Remember 1 small box in height = 1 mm

A cause of RAE is RVH from pulmonary hypertension.

Left Atrial Enlargement (LAE)

Left atrial enlargement

Take a look at this ECG. What do you notice about the P waves?

Notched

Negative deflection

The P waves in lead II are notched and in lead V1 they have a deep and wide negative component.

Left atrial enlargement

To diagnose LAE you can use the following criteria:
II V1 > 0.04 s (1 box) between notched peaks, or Neg. deflection > 1 box wide x 1 box deep

Normal

LAE

A common cause of LAE is LVH from hypertension.

Right ventricular hypertrophy

Compare the R waves in V1, V2 from a normal ECG and one from a person with RVH. Notice the R wave is normally small in V1, V2 because the right ventricle does not have a lot of muscle mass. But in the hypertrophied right ventricle the R wave is tall in V1, V2.

Normal

RVH

Left ventricular hypertrophy

Take a look at this ECG. What do you notice about the axis and QRS complexes over the left ventricle (V5, V6) and right ventricle (V1, V2)?
The deep S waves seen in the leads over the right ventricle are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2).

There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2.

Ischemic Disease
A 55 year old man with 4 hours of "crushing" chest pain Acute inferior myocardial infarction ST elevation in the inferior leads II, III and aVF Reciprocal ST depression in the anterior leads

Evolution of AMI

ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:

Before injury

Normal ECG ST depression, peaked T-waves, then T-wave inversion

Ischemia

Infarction

ST elevation & appearance of Q-waves

Fibrosis

ST segments and T-waves return to normal, but Qwaves persist

Non-ST Elevation Infarction

The ECG changes seen with a non-ST elevation infarction are:

Before injury

Normal ECG ST depression & T-wave inversion

Ischemia

Infarction

ST depression & T-wave inversion

Fibrosis

ST returns to baseline, but T-wave inversion persists

ST Elevation

ST Depression

Anterior MI
Acute anterior myocardial infarction ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression in the inferior leads

Anterior MI

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

Posterior MI

Inferior Wall MI
This is an inferior MI. Note the ST elevation in leads II, III and aVF.

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Atrial Fibrillation

Metoprolol in AF
Beta blockers reduces heart rate effectively.

What about rhythm in AF?

VF

Role of Metoprolol in VF

Effect of Metoprolol XL in AMI in reducing VF

Reduces Myocardial Ischemia & thus preserves conduction through damaged tissue

Direct Anti-arrhythmic Effect

Metoprolol XL

Counter acts the sympathetic over activity

Nina Rehnquist et al., Inter J of Cardiology., 15 (1987):301-308

Mortality Benefits with Metoprolol Results from 5 pooled PM I trials

Pooled Result s f rom t he Amst erdam, Belf ast , G, S ockholm, Gt eborg and LIT post -M I S udies (n=5474) t t

Five pooled met-analysis of Post MI patients 42% M showed 42% reduction in the hs involving 5474 arked reduct ion in sudden deatrisk Olsson G, et al. Eur of Sudden cardiac Death. Heart J 1992;13:28-32

References
Chulay M. and Burns, S. M., AACN Essentials of Critical Care Nursing. New York: McGraw-Hill, 2006 Drew, B. J., and Califf, R. M., et al., Practice Standards for Electrocardiographic Monitoring in Hospital Settings An American Heart Association Scientific Statement from the Councils on Cardiovascular Nursing, Clinical Cardiology Disease in the Young. Circulation 2722-2746 (October 26, 2004). George-Gay B. and Chernicky, C. C., Clinical Medical-Surgical Nursing: A Decision-Making Reference (1st ed.): Elsevier Science (2002). Huff, J., ECG Workout; Exercises in Arrhythmia Interpretation (5th ed.). Philadelphia: Lippincott, Williams & Wilkins (2006) Huszar, R. J., Basic Dysrhytmias: Interpretation & Management (3rd ed.): Elsevier Science (2006). Mitchell, T. M., High-Tech/High Care: ECG interpretation: Know the Basics. Men in Nursing, 6-10 (2008, October). Plummer, B., ECG Challenge; How strip savvy are you? American Journal of Nursing, 107(6), 72A-72C (2007, June). Porth, C. M. and Matfin, G., Pathophysiology; Concepts of Altered Health States (8th ed.). Philadelphia: Lippincott, Williams, & Wilkin (2009) Urden, L. D. and Laugh, M. E. et al., Critical Care Nursing; Diagnosis and Management (6th ed.):Elsevier Health Services (2009). BRAUNWALD TEXT BOOK OF THE HEART http://www.med-edu.com/patient http://www.medstat.med.utah.edu/kw/ecg/ACC_AHA.html.

Thank you