Long QT syndrome and Torsade de pointes

28,926views

Long QT syndrome and Torsade de pointes

Cardiothoracic Disease

Cardiothoracic Disease

Respiratory system anatomy and physiology
Lung volumes and capacities
Anatomic and physiologic dead space
Ventilation
Alveolar gas equation
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Alveolar surface tension and surfactant
Airflow, pressure, and resistance
Breathing cycle
Breathing control
Pulmonary chemoreceptors and mechanoreceptors
Ideal (general) gas law
Boyle's law
Dalton's law
Henry's law
Fick's laws of diffusion
Graham's law
Diffusion-limited and perfusion-limited gas exchange
Hypoxia
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Erythropoietin
Carbon dioxide transport in blood
Regulation of pulmonary blood flow
Zones of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Pulmonary changes during exercise
Pulmonary changes at high altitude and altitude sickness
Diffuse parenchymal lung disease: Clinical
Restrictive lung diseases: Pathology review
Restrictive lung diseases
Idiopathic pulmonary fibrosis
Sarcoidosis
Lung cancer: Clinical
Lung cancer and mesothelioma: Pathology review
Mesothelioma
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Cardiac cycle
Normal heart sounds
Abnormal heart sounds
Blood pressure, blood flow, and resistance
Resistance to blood flow
Laminar flow and Reynolds number
Compliance of blood vessels
Pressures in the cardiovascular system
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Measuring cardiac output (Fick principle)
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Stroke volume, ejection fraction, and cardiac output
Frank-Starling relationship
Pressure-volume loops
Changes in pressure-volume loops
Cardiac work
Cardiac preload
Cardiac afterload
Law of Laplace
Baroreceptors
Renin-angiotensin-aldosterone system
Chemoreceptors
Cardiac conduction system
Action potentials in pacemaker cells
Action potentials in myocytes
Cardiac conduction velocity
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac contractility
Cerebral circulation
Coronary circulation
Control of blood flow circulation
Microcirculation and Starling forces
Cardiomyopathies: Clinical
Cardiomyopathies: Pathology review
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Restrictive cardiomyopathy
Sleep apnea
Apnea of prematurity
Aortic aneurysms and dissections: Clinical
Aortic dissections and aneurysms: Pathology review
Aortic dissection
Aneurysms
Marfan syndrome
Peripheral vascular disease: Clinical
Peripheral artery disease: Pathology review
Peripheral artery disease
Arterial disease
Deep vein thrombosis
Leg ulcers: Clinical
Chronic venous insufficiency
Thrombophlebitis
Vasculitis: Pathology review
Vasculitis
Kawasaki disease
Behcet's disease
Nutcracker syndrome
Superior mesenteric artery syndrome
Subclavian steal syndrome
Coronary steal syndrome
Lymphedema
ECG basics
ECG normal sinus rhythm
ECG rate and rhythm
ECG intervals
ECG axis
ECG QRS transition
ECG cardiac hypertrophy and enlargement
ECG cardiac infarction and ischemia
Heart blocks: Pathology review
Premature ventricular contraction
Premature atrial contraction
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Atrioventricular block
Bundle branch block
Long QT syndrome and Torsade de pointes
Ventricular tachycardia
Brugada syndrome
Ventricular fibrillation
Pulseless electrical activity
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Adrenergic antagonists: Presynaptic
cGMP mediated smooth muscle vasodilators
Calcium channel blockers
Heart failure: Clinical
Heart failure: Pathology review
Heart failure
Cor pulmonale
Pulmonary hypertension
Pulmonary edema
Anatomy of the coronary circulation
Asthma: Clinical
Obstructive lung diseases: Pathology review
Asthma
Chronic obstructive pulmonary disease (COPD): Clinical
Chronic bronchitis
Emphysema
Alpha 1-antitrypsin deficiency
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pulmonary corticosteroids and mast cell inhibitors
Non-corticosteroid immunosuppressants and immunotherapies
Cystic fibrosis: Pathology review
Cystic fibrosis
Bronchiectasis
Anatomy of the heart
Anatomy clinical correlates: Heart
Cardiac muscle histology
Marfan syndrome
Ehlers-Danlos syndrome
Arteriole, venule and capillary histology
Cardiac muscle histology
Artery and vein histology
Trachea and bronchi histology
Bronchioles and alveoli histology
Nasal cavity and larynx histology
Coarctation of the aorta
Mitral valve disease
Pulmonary valve disease
Tricuspid valve disease
Aortic valve disease
Ventricular arrhythmias: Pathology review
Supraventricular arrhythmias: Pathology review
Coronary artery disease: Clinical
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Arterial disease
Angina pectoris
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome

Transcript

Watch video only

On a normal ECG, you’ve got the P, Q, R, S, and T waves.

The QT interval spans from the start of the Q to the end of the T wave.

Long QT syndrome, or LQTS, is when somebody’s QT interval is longer than normal, which should typically be less than half of a cardiac cycle.

In fact, for a heart rate of 60 beats per minute, the QT interval’s generally considered to be abnormally long when it’s greater than 440 milliseconds in males or 460 milliseconds in females.

If you measure someone’s QT interval at a different rate though, say 90 beats per minute and it was 400 milliseconds, you can’t really use that to compare that to these value at 60 beats per minute, since the QT interval changes depending on the rate.

As rate increases, the QT interval decreases.

So what we have to do is find the corrected QT interval, or QTc, at the different rate so that you can compare it to the QT interval at 60 beats per minute.

Even though there are several formulas you can use, the Bazett’s formula is probably the simplest, where the corrected QT interval equals the QT interval in milliseconds divided by the square root of the R to R interval in seconds divided by 1 second.

As a bit of a side-note, usually this formula is expressed without the “divide by 1 second” bit, but the astute observer will notice that the units won’t work out if you do that.

Interestingly, the original formula did include dividing by 1 second to get the units to work out, but for some reason in a paper way back when that step wasn’t included, and basically the version without the 1 second, the sort of unit-incorrect version, has been used ever since!

Anyways, let’s do a quick example of a male with a 400 milliseconds QT interval at a rate of 90 beats per minute.

Comparing to the values at 60 beats per minute, 400 milliseconds wouldn’t be considered a long QT, right?

If we use our handy formula, though, we’ll plug in 400 for QT and 90 beats per minute or .66 seconds per beat.

So we have a QT of 400 milliseconds divided by the square root of 0.66 seconds over 1 second, which is 400 milliseconds divided by 0.81, which is unitless, and we get a corrected QT interval of 493 milliseconds, which is greater than 440, so actually, a 400 milliseconds QT interval at 90 beats per minute is considered long.

Alright so the QT interval’s a little long, what’s wrong with that?

Well, the QRS complex corresponds to the ventricles depolarizing and contracting.

After they depolarize, they have to repolarize, and that’s captured by the T wave.

When someone has a long QT interval, it means that they have an abnormally long repolarization of some of their heart cells, but not all of their heart cells - which is an important point to remember.

Specifically some of the heart cells are taking longer than normal to repolarize compared to their neighboring heart cells.

Having some cells with an abnormally prolonged repolarization phase is thought to be caused by abnormalities in the movement of ions through ion channels, which is responsible for both depolarization and repolarization, and each time it depolarizes and repolarizes, it’s called a cardiac action potential, where ions flow in and out of the cell, and this happens in four phases, which we can plot on a graph of membrane potential over time.

During phase 2, potassium channels open and let potassium flow out, which tends to wanna make the membrane potential more negative, but L-type calcium channels open and let calcium flow into the cell, which tends to wanna make the cell more positive and therefore it maintains the “plateau” phase.

During phase 3, the potassium channels stay open, but now the L-type calcium channels close, which let’s the cell repolarize.