MEDICATIONS THAT AFFECTS YOUR ECG-2

TRYCYCLIC ANTIDEPRESSANTS OVERDOSE

Amitriptylin

Tricyclic antidepressants are prescribed by many doctors to treat depressions. They are classified into secondary amines and tertiary amines. Among this amitriptyline is one of the tertiary amines available in the market by the name of Tryptizol, Tryptomer, and Elavil, etc.
Many people are using this drug under any one of the above trade names for their depressive episodes. The following ECG image can reveal how this drug is affecting your heart.

Fig-1

The main effect of amitriptyline on the heart is QT prolongation and a fast heartbeat. See in Fig 1 above the QRS complex is widened in a manner to embed the T-wave so that the QT-interval is elevated and prolonged.P-Q interval also prolonged.

DOXEPIN:-

Fig-2

Doxepin is another tertiary amine very similar to amitriptyline. In Fig-2 the effect of doxepin is shown with a similar pattern of ECG changes to that of amitriptyline. Generally all tricyclic antidepressants produce similar patterns of ECG changes. They produce ventricular tachycardia with prolonged QT-interval.

MEDICATIONS THAT AFFECTS YOUR ECG-1

DIGOXIN

Brand Name:Lanoxin,Digitek

Digoxin is the drug that is used frequently to patients suffering from Congestive Heart Failure.

Digitalis Lanata or purpura is a foxglove plant that gives many glycosides out of which digoxin is the drug more commonly used for CHF.

Nowadays this drug is replaced by many second and third-generation drugs because of its serious side effects.
Digoxin increases the contractility of the heart muscles by Na+/Ca++ ion exchanges.

Digoxin toxicity can be easily studied through ECG. Its toxicity on the heart would be reflected in ECG.

SEE THE ST-SEGMENT DEPRESSION

See in the above figure the ST-segment depression which is the main effect of digoxin. Digoxin causes calcium to build up in the myocytes which cause a slow down of the heart rate (chronotropic) but increases the strength of the contraction (inotropic). The toxic dose of the digoxin leads to an ischemic effect (angina) and that is reflected in ECG as the ST-segment depression.

Digoxin may give the wrong impression in ECG taken in a person with angina on exercise. It gives a normal ST impression instead of depression.

Digoxin Toxicity:-

1.Fatigue, tiredness, and malaise

2.Visual disturbances              

3.Nausea and Vomiting           

4.Digestive problems

5.Abdominal Pain                 

ECG READING EXERCISES-L-MODEL ECG IN CONGESTIVE HEART FAILURE

ECG IN CHF

Note in the above figure the enlarged right and left ventricles. This is the main cause for CHF
CHF is a condition in which the heart is unable to pump the blood sufficiently to the metabolic demand of the body.

Causes:-                               

1.Heart Attack.

2.High B.P

3.Arrhythmia (tachycardia, bradycardia)

4.Defective heart valves

The above causes may either impair the blood output by weakening the heart muscle  (Arrhythmia and Heart Attack) or impose heavy workload on the heart by increasing arterial resistance (Hypertension)

Symptoms:-

1. Left-sided CHF causes lung enlargement, and dyspnea(difficult breathing)

2. Right-sided CHF causes liver enlargement and peripheral edema.

Complementary Physiologic Mechanism:-

1.Increased heartbeat(Adrenergic domination)

2.Reduced kidney blood supply that causes increased salt retention by aldosterone.

3.Enlarged heart(Myocardial Megaly)

Model ECG in CHF:-

Fig-1

In the Fig-1 two models of ECG, rhythms have been shown. One is normal and the other is recorded in CHF. Both are in lead-II.
Usually heart failure can be diagnosed by X-ray which can clearly picture out the enlarged heart.
In ECG this enlarged ventricles can be identified by the uptrend elongated tall R-wave and a widened QRS complex as shown in above Fig-1 by the green lines and the red circles. The QT-interval is also widened which is marked by blue lines in the above Fig-1.
Correction Options:-
1.Improve heart muscle contracting ability

2. Reduce Preload.
3. Reduce arterial resistance after load.
Medicines:-
1.Cardiac Glycosides (Digoxin)
2.Bipyridines
3.Beta-blockers
4.ACE-Inhibitors
5.Vasodilators
6.Diuretics.Continued...
      

ECG READING EXERCISES-K-MODEL ECG IN HEART ATTACKS

ECG IN ANGINAL ATTACKS

In this article we are to practice the interpretation of ECG reports during various conditions of angina pectoris.

Angina is caused by the imbalance between the supply and demand of oxygen by the arteries of the heart muscles (Coronary Arteries). When the demand exceeds supply the affected area of the heart muscle becomes darkened and weakened to act. This condition is called ischemia. This may result in chest pain.
Some people may suffer from angina but on examination there is no visible ischemia on their heart muscle. This may be due to hidden ischemia in the endothelium of the heart muscle which may be due to the block in micro-arteries of the endothelium.

Angina itself is not life-threatening but if it is left untreated it may precipitate a heart attack.

Anginas are many types but the serious one is the suddenly unstable angina.

Types of Angina:-

1.Unstable Angina-More dangerous and a prediction of an immediate heart attack. It is due to coronary artery blockage by clots, atherosclerosis, or by any other means like an air bubble.

2. Stable Angina-It is less severe than unstable angina. It occurs when a person does some work like running, physical exercise, or any other routine work. A brief rest can relieve anginal pain. But the pain may revert again if the person resumes the work.

3. Microvascular, Variant, or Prinzmetal Angina-These are less severe and less serious but proper food control with doctor's advice is necessary.

RISK FACTORS

1.Diabetes Mellitus

2.Cigarette Smoking

3.High Cholesterol

4.High B.P

5.LifeStyles

6.Family History

7.Kidney Failure

8.Over Stress

9.Obesity.

Model ECG in Unstable Angina:-

Fig-1A

Fig 1B

It is very easy to recognize the presence of Unstable Angina (UA) in ECG. The main recognizable feature is ST-segment depression. Check the model ECG in Fig-1B and inspect the ST-depression marked with a small red circle both in lead II and in lead V3.

Lead V3 shows the depression very clearly as it views the heart more closely from the lateral left side.
The exact appearance of ECG waves is simulated in Fig 1A. Compare the images of Fig-1B with Fig 1A.

ECG in Stable Angina:-

Fig 2A

Fig 2B

In Fig-2A and Fig 2B two ECG models taken in patients with Stable Angina have been presented.
Stable Angina or SA is the condition that occurs when the patient is at work and disappears when the patient is at rest.
In the above two figures the ECG waves are normal at rest and show ST-segment depressions after some physical activities such as routine home or office works or lifting something or running etc.etc.The depressions have been marked by small red circles in Fig-2B.

MICROVASCULAR ANGINA

Fig-3

Microvascular angina occurs when tiny arterial blood flow is blocked by clots, atherosclerosis, or air bubbles.

In a similar manner we can understand variant or Prinzmetal anginas. These three anginas can escape from diagnosis and can be detected by ECG examinations which shows typical ST-segment depressions as shown above.

Commonly all anginas have common symptoms like chest pain or chest pressure radiate from the left arm, followed by sweating headache, nausea, vomiting, and loss of consciousness.

Continued...

ECG READING EXERCISES-J-MODEL ECG IN HEART ATTACKS

MYOCARDIAL INFARCTION-HEART ATTACK

We have already seen how to interpret the ECG reports taken in anterior, inferior, and posterior heart attacks in Article-F in this blog. In this article we are to study how to read the ECG reports in various conditions that may results in heart attacks other than the conditions already described. Heart attack can result from any pathological condition of the myocardium-(heart muscle.)

Fig-1A

Fig-1B

Fig-1C

Check and compare the above ECG report shown in Fig-1C with the images shown in Fig-1A and 1B.
In Fig 1A a normal sinus rhythm has been drawn by hand. In Fig 1B another simulated ECG image has been drawn to demonstrate its deviations from the normal rhythm due to heart attack. It is clear from the Fig-1B that the abnormal rhythm contains an elevated and depressed ST segment.
The ST segment represents the time taken and the work done during ventricular relaxation. But the deviation indicates that the ventricles are not properly relaxed.
The elevation confirms the prediction of the immediate event of a heart attack while the depression indicates the presence of ischemic angina which may or may not result in a heart attack immediately.
Now we can interpret the model ECG report shown in Fig-1C. First check the records of the master lead -II which is the important lead that views the heart from the normal axis.
See the deviations marked in small red circles. The ST segment is elevated.
Now we can Check the unipolar electrodes aVL and aVF which also view the heart from left top and bottom respectively. They are also showing the elevation.
The elevation is more clear in the chest leads such as V4, V5, and V6 which view the heart very closely and from the left.
And hence this ECG is foretelling about the event of a severe heart attack.

1.HEART ATTACK WITH BUNDLE BLOCKS: -A- RIGHT BUNDLE BRANCH BLOCK (RBBB):-

First we must know about what is the bundle and its branches, diagrammatically.

In the above diagram it is clearly seen that the electrical current which is conducted from the AV node to the Bundle of His is blocked in the right branch and passed through the left branch and arrived at the RV indirectly from the left. This is RBBB in which the right ventricle cannot receive electrical current from the HIS bundle branch but receiving it from the left ventricular muscle as shown in the diagram above.

In a similar manner the LBBB can also be understood.

RBBB and LBBB are asymptomatic and may not be serious if they are benign. But they become serious if they are with other problems in the heart such as ischemia, arrhythmias, or drug overdoses like BP medicines or antiarrhythmic medicines like beta-blockers and digoxin, etc.

In aged conditions when the heart muscles are weak these benign conditions may become violent.

Fig-2A

Fig-2B

In Fig-2A there are simulated ECG drawings that have been shown to demonstrate the appearance of the rhythm in lead-II,leads-V1, and V6.
See the M shaped rhythm in lead V1 and N shaped rhythm in lead V6.
In V1 and aVR which view the heart from the right the rhythm contains one r, and one R-waves and an S-wave and no Q-wave. Hence this is an RBBB rhythm.
RBBB is many times may not be a serious problem but if it is associated with a heart attack or with a weak heart muscle it can be fatal. In RBBB as we already described the hearts axis is slightly shifted to the right.

B-LEFT BUNDLE BRANCH BLOCK(LBBB):-

Fig 2C

Compare the above model ECG taken during LBBB in Fig-2C with the simulated hand-drawn LBBB image in Fig 2B and observe the camelback like M appearance. Hence this an LBBB rhythm.

Symptoms:-

The most common symptom is syncope (fainting) or presyncope (feelings to syncope).

Causes for Bundle Blocks

1.Beta-blockers like atenolol, metoprolol
2.Calcium canal blockers like amlodipine, nifedipine
3.antiarrhythmic drugs like digoxin
If the drugs are withdrawn in doctors' supervision bundle blocks can be corrected.

                                                                                Continued.......

SUMMARY-ECG EDUCATION-I-EXERCISES-CONTINUED-Palpitations due to diseases-3

SAMPLE ECG EXERCISES-3

1.Ventricular Tachycardia(VT-VPalpitations-1)

Fig-1

See Fig-1 and check the records by lead II which is the master lead. Check the QRS complex. It is widened more than 120 million secs (>3ss). There are 2 LS in between a consecutive R-R. Hence the heartbeats are 300/2=150 bpm. Hence it is ventricular tachycardia. The ECG records by aVL,aVF, V4, V5, and V6 all show similar trends. If VT is left untreated it leads to more serious V.Fibrillation followed by cardiac arrest.
VT is of two types. Monomorphous and Polymorphous (Torsade de Points, TDP).Fig-1 shows a monomorphous VT in which the rhythms are normal.No P-waves. That means the conductions are not from the atria, and AV nodes.

Fig-2

The Fig-2 shows a sample ECG report taken during polymorphous VT or Torsades de Points.
See the Lead-II stripe which shows the poly phases of the rhythm. The rhythm is irregular. It randomly swinging around the baseline as elevations and depressions. Check the heartbeats. It is undoubtedly above 300 bpm as we cannot count squires between any two consecutive R-R waves. Leads V1 to V6 shows swirling rhythms.No P-waves.ST segments are randomly seen elevated. Hence this is polymorphous and Torsades de Points.
The stripe of lead II shows, in the beginning, weak ventricular rhythms with long QT intervals followed by the swinging of waves around the baseline (Torsades de Points).
Causes For VT:-
1. The condition develops due to low potassium, low calcium, or low magnesium.
2.Antiarrhythmic drugs such as quinidine, procainamide(I-a), sotalol, and amiodarone (III), etc.
3.Anti depressives such as amitriptyline, imipramine
4.Antipsychotics such as haloperidol.
3.Antipsychotics such as haloperidol, droperidol, chlorpromazine
If you are taking the mentioned medicines stop to take and consult your doctor.
Treatments:-(Subjected to doctors consulting)
Magnesium sulfate, Calcium salts, or Potassium salts.
4.Beta-blockers
Torsades de Points if left untreated may lead to cardiac arrest.

VENTRICULAR FIBRILLATION(V.Fib):-

V. Fib is another kind of palpitations and is the most serious one.

Fig-3

A sample ECG taken in a patient suffered by V.Fibrillation is shown in Fig-3.
As a general concept lead-II is the hero lead whose records represent 75% of the heart's condition.
Also records by the chest lead V1 which looks the right ventricle, and  V5 and V6 which looks the left ventricles are also important. Generally all the 6 chest leads are very important because unlike the limb leads they watch ventricles very closely.
In Fig-3 in lead II, V1 and V6 are all showing the swinging waves of QRS complex.No P-waves means the ventricles are fibrillating independently. The heart rate is >300 bpm. Beats are very irregular. The conductions are not in a uniform axis. These are known as ectopic conductions.
Finally if ventricular tachycardias are not early diagnosed for correction it may result in serious consequences such as life-threatening V.Fibrillations and death.

SUMMARY-ECG EDUCATION-H-EXERCISES-CONTINUED

                                                         

SAMPLE ECGS-2

A.PALPITATIONS DUE TO DISEASES-1.ATRIAL FIBRILLATIONS

Normal Rhythm

Fig-1

The above ECG sample shows a kind of arrhythmia known as atrial fibrillation (atrial palpitation)

Atria are the upper chambers of the heart. We know the pacemaker SA node is situated at the right atrium. When SA node starts the conduction which spread over all the atria and the atria contract. We know the normal atrial contractions are represented in the ECG as P wave.

See the above Fig 1. The P-waves are almost absent. Instead of P-waves (check the Normal Rhythm Image above) there are fibrillatory waves seen in the electrodes II, III, and aVF which view the heart from the bottom. The electrode I which view the atria from the top gives no clear waves at all but records fibrillatory waves. Hence we can conclude this is ATRIAL FIBRILLATION.
In atrial fibrillation the atria are fibrillating instead of contracting and hence no proper filling and emptying of the blood takes place. The ventricular contractions are also independent of atrial fibrillation and AV node. The R-R intervals are also randomly irregular. There is no PR interval as P-wave is absent. Waves are deviating randomly up and down from the baseline.
Atrial fibrillation may cause pulmonary embolism or brain damage such as stroke.
2.ATRIAL FLUTTER

Fig-2

See the above Fig-2 and compare this image with the previous one and observe the difference between the two atrial arrhythmias(Palpitations). The former is atrial fibrillation while the later is atrial flutter. Analyze the sample ECG image in Fig-2.
First analyze the lead II (the hero electrode) which views the heart from bottom left(normal axis).P-wave replaced by snaky spiral waves and the Q-wave is absent. The ST segment is raised above the isoelectric line. The R-waves are there with randomly elongated R-R intervals.
See the lead I which views the heart from the top.No P waves at all and R-R intervals are elongated.Lead-III which views the heart from the bottom right also record no P-wave. But all recordings shows there are no deviations from the baseline. Hence because of defective P-waves in all the leads, and elongated R-R intervals the problem is in the atria, which is known as ATRIAL FLUTTER.
The difference between A.fib and A.flut is that the former is characterized by elevated heartbeats (>180 bpm) with tachycardia (shortened R-R intervals)and random deviations from the baseline while the later is characterized by depressed heartbeats (<50 bpm), with randomly elongated R-R intervals (bradycardia) and no deviations from the baseline.
The condition is not as serious as A.fib, but if left untreated it may lead to serious consequences.
                                                 Continued.......