Torsades de pointes - twisting of the points

 DEFINITION 
Torsades de pointes is a polymorphic ventricular tachycardia that occurs frequently in cases of QT interval prolongation.

This can be due to congenital or acquired Long QT interval syndrome.

It is characterized by a progressive change of the electrical axis, typically rotating 180 degrees in approximately 10 to 12 cycles and the amplitude, as though the depolarization and repolarization of the ventricle was turning on a point.

This results in the characteristic sinusoidal twisting of the peaks of the QRS complexes around the isoelectric line of the recording.

 EKG 

The tachycardia rate typically is in the range of 150 to 300 beats/min.

It is usually a self-limiting arrhythmia that spontaneously dies out after a few tens of cycles and only in a minority of cases that it degenerates into ventricular fibrillation and can lead to sudden cardiac death.

Drugs that can prolong the QT interval and induce Torsades de pointes are:

It can also be caused by electrolyte imbalances like, hypokalemia, hypomagnesemia and less commonly hypocalcemia.


First published on: 31 March 2017

Atrial septal defect device closure

This procedure is called as Atrial septal defect (ASD) device closure.


Transesophageal echocardiography (TEE) is must before procedure for:
1) actual sizing of the defect
2) defining the rims - to hold device in place
3) ruling out anomalous pulmonary venous drainage
4) ruling out significant mitral regurgitation (MR).
Intraprocedural TEE is not mandatory.

N.B How to distinguish between an ASD device and a patent foramen ovale (PFO) device? Left atrial (LA) disk (green arrow) is larger than Right atrial (RA) disk (yellow arrow), thus it is an ASD device.For a PFO device, RA disk will be larger than LA disk.

Further readings:

Mitral facies

Mitral facies is one of the cutaneous manifestations of systemic diseases. The pathology in question here is mitral stenosis. Mitral facies refers to rosy cheeks (bright circumscribed flush over the malar bones) with a bluish tinge. The rose colour is because of the dilatation of malar capillaries while the bluish tinge is because of the cyanosis.

This facies is usually seen in long standing cases of severe mitral stenosis associated with pulmonary hypertension and low cardiac output. 

The picture above is that of a patient with chronic severe mitral stenosis. Yet, the rosy cheeks are not that prominent. The reason for this is that the patient underwent mitral valve replacement surgery and thus the cutaneous signs are regressing. 

Red cheeks may also be seen in weather-beaten people i.e. those who work a lot outside in the open air. Purple cheeks may be seen in congestive heart failure. Finally, in systemic lupus erythematosus (SLE) the cheeks will have a red raised eruption on the bridge of the nose extending to the cheeks, also called as the 'butterfly' distrubution. 

Digitalis purpurea

It is also known as the Common/Purple Foxglove or the Lady's Glove. The flowers are typically purple in colour but they can be pink or even white in some cultivations.

At the end of the 18th century, William Withering introduced digitalis leaves as a tea into the treatment of “cardiac dropsy” (edema of congestive heart failure) and it helped many people. The active principles in these plants are steroids with one or more sugar molecules attached at C3.


Proven clinically, digoxin continues to be obtained from the plants Digitalis purpurea or D. lanata because its chemical synthesis is too difficult and expensive.

Left ventricular function - normal echocardiography values

	Women				Men
Measure		Reference Range	Abnormal			Reference Range	Abnormal
			Mildly	Moderately	Severely		Mildly	Moderately	Severely
Linear method
	Endocardial fraction shortening, %	27-45	22-26	17-21	≤16	25-43	20-24	15-19	≤14
	Midwall fractional shortening, %	15-23	13-14	11-21	≤10	14-22	12-13	10-11	≤10
2D method
	Ejection fraction, %	≥55	45-54	30-44	<30	≥55	45-54	30-44	<30

Right axis deviation - common causes

Right Axis Deviation

I. Spurious: left-right arm electrode reversal (look for negative P wave and negative QRS complex in lead I) II. Normal variant III. Dextrocardia IV. Right ventricular overload A. Acute (e.g., pulmonary embolus or severe asthmatic attack) B. Chronic 1. Chronic obstructive pulmonary disease 2. Any cause of right ventricular hypertrophy (e.g., pulmonic stenosis or primary pulmonary hypertension) V. Lateral wall myocardial infarction VI. Left posterior fascicular block (exclude all other causes of right axis deviation)

Low voltage QRS complexes

Low-Voltage QRS Complexes

1. Artifactual or spurious (especially unrecognized standardization of the ECG at half the usual gain, i.e., 5 mm/mV). Always check this first! 2. Adrenal insufficiency (Addison's disease) 3. Anasarca (generalized edema) 4. Cardiac infiltration or replacement (e.g., amyloid, tumor) 5. Cardiac transplantation, especially with acute or chronic rejection 6. Cardiomyopathies 7. Chronic obstructive pulmonary disease 8. Constrictive pericarditis 9. Hypothyroidism/myxedema (usually with sinus bradycardia) 10. Left pneumothorax (mid-left chest leads) 11. Myocardial infarction, usually extensive 12. Myocarditis, acute or chronic 13. Normal variant 14. Obesity 15. Pericardial effusion/tamponade (latter usually with sinus tachycardia) 16. Pleural effusions

Atrial premature beats

APBs result from ectopic stimuli i.e. these beats arise from somewhere in either the left or right atrium but not in the SA node. After an atrial depolarization, the stimulus that spread normally through the His-Purkinje system into the ventricles gives a normal QRS complex.

APBs have the following major features:  
1. The atrial depolarization is premature, occurring before the next normal P wave is due.
2. The QRS complex of the APB is often preceded by a visible P wave that usually has a slightly different shape and/or different PR interval from the P wave seen with normal sinus beats. The PR interval of the APB may be either longer or shorter than the PR interval of the normal beats. In some cases, the P wave may be buried in the T wave of the preceding beat.
3. After the APB, a slight pause generally occurs before the normal sinus beat resumes. This usually slight delay is due to “resetting” of the SA node pacemaker by the premature atrial stimulus. This slight delay contrasts with the longer, “compensatory” pause often (but not always) seen after VPBs.
 4. The QRS complex of the APB is usually identical or very similar to the QRS complex of the preceding beats. This finding contrasts with VPBs, in which the QRS complex is usually very wide because of abnormal depolarization of the ventricles.
 5. Rarely, APBs result in aberrant ventricular conduction, so that the QRS complex is wider than normal. E.g. APBs associated with right bundle branch block aberrancy. APBs with left bundle branch block aberrancy may also occur.
6. Sometimes when an APB is very premature, the stimulus reaches the AV junction just after it has been stimulated by the preceding normal beat. Because the AV junction, like all other conductive tissues, requires time to recover its capacity to conduct impulses, this premature atrial stimulus may reach the junction when it is still refractory. In this situation the APB may not be conducted to the ventricles and no QRS complex appears. The result is a blocked APB. The ECG shows a premature P wave not followed by a QRS complex. After the blocked P wave, a brief pause occurs before the next normal beat resumes. The blocked APB therefore produces a slight irregularity of the heartbeat.

Two APBs occurring consecutively are referred to as an atrial couplet. Sometimes, each sinus beat is followed by an APB. This pattern is referred to as atrial bigeminy.

Clinical significance:
APBs are very common. They may occur with a normal heart or virtually any type of organic heart disease. Thus the presence of APBs does not necessarily mean that an individual has cardiac disease. In normal people, these premature beats may be seen with
1) emotional stress,
2) excessive intake of caffeine,
3) the administration of sympathomimetic agents (epinephrine, isoproterenol, theophylline).
4) hyperthyroidism.

APBs may produce palpitations and patients may complain of feeling a skipped beat or an irregular pulse. APBs may also be seen with various types of structural heart disease. Frequent APBs are sometimes the forerunner of atrial fibrillation or flutter or other atrial tachyarrhythmias.

ECG T wave changes and interpretation

Ventricular repolarisation produces the T wave.

The normal T wave is asymmetrical, the first half having a more gradual slope than the second half. This is well shown below with an up-slope of a duration of nearly 3 squares and a down-slope in only around 1 and  1/2 squares. 

T wave orientation usually corresponds with that of the QRS complex, and thus is inverted in lead aVR, and may be inverted in lead III. 

But the T waves are discordant with the QRS complexes in Left Bundle Branch Block (LBBB) i.e. T is inverted while the QRS complex is positive or vice-versa.

T wave is positive in lead II. Left-sided chest leads such as V4-V6 normally always show a positive T wave. In the

T wave can be inverted in the right precordial leads in normal persons. T waves are commonly inverted in all precordial leads at birth but usually become upright as time passes. A persistent juvenile pattern with inverted T waves in the leads to the left of V1 occurs in 1-3% of adults and is more common in women than in men and more common in black people. Below is an ECG of persistent juvenile pattern with T inversion from V1 to V3.

The presence of symmetrical, inverted T waves is highly suggestive of myocardial ischaemia, though asymmetrical inverted T waves are frequently a non-specific finding. T wave inversion associated with QT prolongation can sometimes be seen in cases of CVA particularly in subarachnoid hemorrhage.  Particularly prominent inverted T waves, the so-called giant negative T waves, are characteristic of hypertrophic cardiomyopathy with prominent apical thickening. The 3 conditions are shown below. 

No widely accepted criteria exist regarding T wave amplitude. As a general rule, T wave amplitude corresponds with the amplitude of the preceding R wave, though the tallest T waves are seen in leads V3 and V4. Tall T waves may be seen in acute myocardial ischaemia and are a feature of hyperkalaemia.

The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the corresponding R wave; T wave amplitude rarely exceeds 10 mm.

Sick sinus syndrome

Sick sinus syndrome is a term applied to a syndrome encompassing a number of sinus nodal abnormalities, including the following:

(1) Persistent spontaneous sinus bradycardia not caused by drugs and inappropriate for the physiologic circumstance

(2) Sinus arrest or exit block i.e. no P wave on ECG for > 2 s.

(3) Combinations of SA and AV conduction disturbances and

(4) Alternation of paroxysms of rapid regular or irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome).

More than one of these conditions can be recorded in the same patient on different occasions, and their mechanisms often can be shown to be causally interrelated and combined with an abnormal state of AV conduction or automaticity.

Incidence:

3 in every 10,000 persons are affected. Incidence increases with age, seen more after 65 years of age. Men and women are equally affected.

Patients who have sinus node disease can be categorized as having intrinsic sinus node disease unrelated to autonomic abnormalities or combinations of intrinsic and autonomic abnormalities. Symptomatic patients with sinus pauses or SA exit block frequently show abnormal responses on electrophysiologic testing and can have a relatively high incidence of atrial fibrillation.

In children, sinus node dysfunction most commonly occurs in those with congenital or acquired heart disease, particularly after corrective cardiac surgery. Sick sinus syndrome can occur in the absence of other cardiac abnormalities. The course of the disease is frequently intermittent and unpredictable because it is influenced by the severity of the underlying heart disease. Excessive physical training can heighten vagal tone and produce syncope related to sinus bradycardia or AV conduction abnormalities in otherwise normal individuals.

Pathology:

The anatomic basis of sick sinus syndrome can involve

1)      total or subtotal destruction of the sinus node,

2)      areas of nodal-atrial discontinuity,

3)      inflammatory or degenerative changes in the nerves and ganglia surrounding the node, and

4)      pathologic changes in the atrial wall.

5)      Fibrosis and fatty infiltration occur, and the sclerodegenerative processes generally involve the sinus node and the AV node or the bundle of His and its branches or distal subdivisions.

6)      Occlusion of the sinus node artery may be important.

Symptoms:

1)      Palpitations

2)      Fainting, near fainting, light-headedness

3)      Fatigue and weakness

4)      Chest pain

Management:

Diagnosis can be confirmed by doing a Holter monitoring for at least 24 hours.

For patients with sick sinus syndrome, treatment depends on the basic rhythm problem but generally involves permanent pacemaker implantation when symptoms are manifested. Pacing for the bradycardia, combined with drug therapy to treat the tachycardia, is required in those with bradycardia-tachycardia syndrome. The latter also are at greatest risk to develop stroke.

Beck's triad - pericardial tamponade

The triad is still a useful clue to the presence of severe pericardial tamponade. It was described by Dr Claude S. Beck, a thoracic surgeon, in 1935. It consists of :
1) hypotension,
2) muffled heart sounds,
3) elevated jugular venous pressure.

Third degree atrioventricular block / Complete heart block - ECG

Third degree atrioventricular block is also known as complete heart block because there is complete failure of conduction between the atria and the ventricles. As a result of this there is complete independence between atrial and ventricular contractions. It is thus one type of AV dissociation.

The classic characteristics of a complete heart block ECG are as follows :

1) P waves are present and the atrial rate is faster than the ventricular rate,

2) QRS complexes are present and are usually much slower than normal, 

3) the P waves bear no relation to the QRS complexes and thus the PR intervals are completely variable.

Since there is a block in the conduction, a subsidiary pacemaker will take over the function to make the ventricles contract. Depending at the level of block we can have different QRS complex morphologies. 

Below is an ECG showing a complete heart block with the block occurring proximal to the His bundle, usually in congenital cases. The QRS complexes are narrow and the ventricular rate is around 40/min.

The ECG shown below is in an acquired case of complete heart block. The QRS complexes are wide indicating that the block is distal to the bundle of His. The arrows indicate the P waves. The latter are regularly placed and are either alone or mixed with other waves.

Percutaneous coronary intervention

PCI consists of balloon angioplasty followed by stenting.


Balloon angioplasty expands the coronary lumen by stretching and tearing the atherosclerotic plaque and vessel wall. The atherosclerotic plaque is also redistributed a little along its longitudinal axis. Elastic recoil of the stretched vessel wall generally leaves a 30 to 35 percent residual diameter stenosis. Although stand-alone balloon angioplasty is rarely used other than for very small (<2.25 mm) vessels, balloon angioplasty remains integral to PCI for predilating lesions before stent placement, deploying coronary stents, and further expanding stents after deployment.

Coronary stents are currently used in more than 90 percent of PCI procedures worldwide. Coronary stents lowers the incidence of vessel closure. Restenosis after coronary stent placement occurs in some patients due to excessive intimal hyperplasia within the stent.

While bare metal coronary stents reduce the incidence of angiographic and clinical restenosis compared to balloon angioplasty, angiographic restenosis (follow-up diameter stenosis >50 percent) still occurs in 20 to 30% of patients and clinical restenosis (recurrent angina due to restenosis in the treated segment) develops in 10 to 15 percent of patients in the first year after treatment. Restenosis with bare metal coronary stents occurs more often in patients with small vessels, long lesions, and in patients with diabetes mellitus. Use of drugs has not prevented restenosis after stent placement.

Drug-eluting stents, on the other hand, provide sustained local delivery of an anti-proliferative agent at the site of vessel wall injury. Trials have demonstrated the benefit of drug-eluting stents in patients with long (>20 mm length) and small (<2.5 mm) vessels.  This type of stent placement requires extended (up to 1 year) therapy with the combination of aspirin and clopidogrel to prevent stent thrombosis.

Major tachycardias

Narrow QRS complex   

A.     Sinus tachycardia 

            B.     Paroxysmal supraventricular tachycardias (PSVTs)

                     1.     Atrial tachycardias, including single-focus or multifocal (MAT) variants 

                     2.     AV nodal reentrant tachycardia (AVNRT) 

                     3.     AV reentrant tachycardia (AVRT) involving a bypass tract 

            C.     Atrial flutter 

            D.     Atrial fibrillation 

Wide QRS complex   

A.     Ventricular tachycardia   

            B.     SVT/AF or flutter, with aberrant ventricular conduction usually caused by either of the following:  

1.     Bundle branch block patterns 

                        2.     Atrioventricular bypass tract (Wolff-Parkinson-White preexcitation patterns)  

Abciximab - mechanism of action/ indication/ contraindication/ dose

It is a Fab fragment of a humanized monoclonal antibody directed against the glycoprotein IIb/IIIa. The latter is a platelet surface integrin. It is a receptor for fibrinogen which binds platelets to each other causing aggregation.

By inhibiting the receptor, abciximab acts as a potent antiplatelet agent. 

Indications:

1) myocardial ischemia,

2) percutaneous coronary intervention.

Dose:

1) For M.I - initially an I.V bolus of 0.25 mg/kg over 5 min followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for 12 hours.

2) For P.C.I - initially, 0.25 mg/kg I.V bolus over 5 min 20-60 min prior to angioplasty followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for next 12 hours.

Contraindications:

1) bleeding disorder or use of anticoagulant within 7 days,

2) CVA within 2 years,

3) known allergy to this product,

4) major trauma or surgery within 6 weeks,

5) severe uncontrolled hypertension,

6) active internal bleeding,

7) thrombocytopenia i.e platelet count < 100,000/ µL.

Post MI - wait how much before elective surgery

After a myocardial infarction, the longer we wait, the better it is to decrease the risk of post operative attack. But unfortunately we cannot delay the surgery indefinitely. We have to balance the risk for a post-op heart attack versus the risk of delaying the surgery.

Studies have shown that for:
1) 0-30 days, risk is around 33%,
2) 31-60 days, risk is around 19%,
3) 61-90 days, risk is around 8% and
4) 92-180 days, risk is around 6%.

So waiting for at least 2 months after an M.I decreases the risk for post-op heart attack.

Inferior wall and right ventricular infarct - ECG

ECG shows an inferior wall infarct i.e ST segment elevation in leads II, III and aVF.

The precordial V leads are actually right sided on this ECG. This is evident because the tracing in V6 does not resemble lead I and aVL. Also the P waves in V4 to V6 are flat.

ST depression in I and aVL along with ST elevation in right sided V3-V6 indicates right ventricular infarct.

Second degree atrioventricular block - ECG / Mobitz type I, type II

It consists of two types of blocks:
1) Mobitz type I block,
2) Mobitz type II block.

Mobitz type I

It is also called as Wenckebach pattern. In this condition, each stimulus from the atria appears to have more difficult time to pass through the AV junction. Finally one stimulus is not conducted through the defective AV node.

A characteristic ECG shows progressive lengthening of the PR interval until a beat is dropped. i.e. the P wave is not followed by a QRS complex. It is also important to note that the PR interval after the dropped beat is always shorter than that before the non conducted P wave. Also the R-R interval encompassing the non conducted P wave is less than twice the preceding R-R interval.

This ECG is also shows a Wenckebach pattern and we can clearly see at first glance that the narrow QRS complexes appear to be clustered and separated by a pause. This is called as group beating. If ever you find such a pattern, look out for the progressively increasing PR interval to make your diagnosis.
It is usually associated with inferior wall MI and does not progress to complete heart block.

Mobitz type II
It is a more serious condition and usually seen in cases of anterior wall MI. There is high risk of progression to complete heart block and there is usually indication to insert permanent pacemaker.
The ECG has the following characteristics:
1) the P-P intervals are constant
2) constant P-R intervals prior to a non conducted P wave.
3) intermittent failure of conduction of a P wave.

Above is a case of anterior wall MI complicated by a second degree Mobitz type II block. The P-P and P-R intervals are constant and the second P wave on the ECG is not conducted.

A 2:1 block suggests that for every 2 P waves that are conducted 1 P wave is not. The same holds true for 3:1 that means that we have 3 normally conducted P waves followed by QRS complexes while 1 P wave is not conducted.

First degree atrioventricular block - ECG

In this condition, there is a delay in conduction between the atria and the ventricles. There is a prolongation of the PR interval to more than 200 ms. i.e > 5 small squares on a usual 25 mm/s ECG tracing. The normal duration for PR interval is 120 - 200 ms.
A QRS complex follows each P wave and the PR interval is relatively constant from beat to beat.
The pathology is usually due to a delay within the AV node if we have a normal QRS complex. But if the QRS complex is wide, the problem is more distal.

Grading of murmur

The intensity of a systolic murmur is not always proportional to the hemodynamic disturbance. Yet murmurs are classified according to the loudness.
Freeman and Levine were the first to introduce a numerical scale for grading heart murmur intensity in 1933. This grading is still used but with some modifications.

Grade 1 - so faint that it can be heard only with special effort.
Grade 2 - faint but can be heard easily.
Grade 3 - moderately loud but no thrill.
Grade 4 - very loud and thrill may be there.
Grade 5 - extremely loud and can be heard if only the edge of stethoscope is in contact with skin.
Grade 6 - exceptionally loud and can be heard with stethoscope just removed from skin contact.

Keren, Tereschuk and Luan suggested that we can use heart sounds as an internal reference to differentiate between grades 1-3, the only limitation of the study being a small sample used. The grading is the same as above but. . .

Grade 1 - clearly softer than the heart sounds.
Grade 2 - approximately equal in intensity to the heart sounds.
Grade 3 - clearly louder than the heart sounds.