Heart problems Flashcards
What are Supreventricular tachycardias?
Supraventricular tachycardia (SVT) is an abnormal heart rhythm arising from improper electrical activity of the heart. It is a type of rapid heart rhythm originating at or above the atrioventricular node. It can be contrasted with the potentially more dangerous ventricular tachycardias—rapid rhythms that originate within the ventricular tissue.
What are the different clasifications of SVT?
Sinoatrial origin:1: Sinoatrial nodal reentrant tachycardia (SNRT)Atrial origin:1: Ectopic (unifocal) atrial tachycardia (EAT)2: Multifocal atrial tachycardia (MAT)3: Atrial fibrillation with rapid ventricular response4: Atrial flutter with rapid ventricular response(Without rapid ventricular response, fibrillation and flutter are usually not classified as SVT)Atrioventricular origin (junctional tachycardia):1: AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating tachycardia (JRT). Permanent (or persistent) junctional reciprocating tachycardia (PJRT), a form of JRT that occurs predominantly in infants and children but can occasionally occur in adults2: AV reciprocating tachycardia (AVRT) – visible or concealed (including Wolff-Parkinson-White syndrome)3: Junctional ectopic tachycardia (JET)
What are ventricular tachycardia?
Ventricular tachycardia (V-tach or VT) is a type of regular and fast heart beat that arises from improper electrical activity in the ventricles of the heart. While a few seconds may not result in problems longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillationDiagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 bpm and at least three wide QRS complexs in a row. It is classified as non-sustained versus sustained based on whether or not it lasts less than or more than 30 seconds.
QRS-complex should not be longer that…..
3 small boxes (120ms)
What groups can we use for vtac?
Focal vs. reentrantMonomorphic vs. polymorphicIn monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is myocardial scarring from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. High-dose magnesium is often used as an antidote in cardiac arrest protocols.
What is Torsades de Pointes?
Torsades de pointes or torsade de pointes (TdP), is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). Prolongation of the QT interval can increase a person’s risk of developing this abnormal heart rhythm.
What changes the QT-interval? What is its normal length and what are long QT-interval a risk for?
QT interval is a measure of the time between the start of the Q wave and the end of the T wave in the heart’s electrical cycle. The QT interval represents electrical depolarization and repolarization of the ventricles. A lengthened QT interval is a marker for the potential of ventricular tachyarrhythmias like torsades de pointes and a risk factor for sudden death.Like the R-R interval, the QT interval is dependent on the heart rate. Drugs can also influence QT time.Reference value: Under 440msQT-corrected (QTc) might be necessary to calculate
What are Ventricular fibrillation?
Ventricular fibrillation (V-fib or VF) is when the heart quivers instead of pumps due to disorganized electrical activity in the ventricles. It results in cardiac arrest with loss of consciousness and no pulse. This is followed by irreversible death without treatment. Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, or intracranial hemorrhage. Diagnosis is by an electrocardiogram (ECG) showing unformed QRS complexes without any clear P waves. An important differential diagnosis is torsades de pointes.Treatment is with cardiopulmonary resuscitation (CPR) and defibrillation.
What is ventricular flutter and what is the difference between it and ventricular fibrillation?
Ventricular flutter is an arrhythmia, more specifically a tachycardia affecting the ventricles with a rate over 250-350 beats/min. It is characterized on the ECG by a sinusoidal waveform without clear definition of the QRS and T waves. It has been considered as a possible transition stage between ventricular tachycardia and fibrillation, and is a critically unstable arrhythmia that can result in sudden cardiac death.In ventricular fibrillation, the heart beats at a very fast rate that the body can’t cope with. It ceases to pump efficiently and the heart “fibrillates” or quivers – a cardiac arrest.The difference which differentiates ventricular flutter versus ventricular fibrillation is the nature of the arrhythmia. In the case of ventricular flutter, the electrical stimulation is regular, but very fast, leading to a circular depolarisation of the ventricle and loss of output, although some blood may be ejected from the heart. Often, ventricular flutter will deteriorate into ventricular fibrillation. In this case, depolarisation of the ventricle becomes chaotic and the frequency of beating is much higher. Somebody suffering from ventricular fibrillation (VF) is likely to become unconscious within a few seconds. In VF there is no coronary output. Unless a heart in ventricular fibrillation can be defibrillated (by applying a shock to the heart) and a normal rhythm be restored, death is inevitable.
What is Brugada syndrome?
Genetic disease: One of the most famous channelpathyes. Often in the SCN5A channel.Malignant arrhythmia often orign in right ventricle! The pattern seen on the ECG is persistent ST elevations in the electrocardiographic leads V1-V3 (right precordial leads) with a right bundle branch block (RBBB) appearance, with or without the terminal S waves in the lateral leads that are associated with a typical RBBB. A prolongation of the PR interval (a conduction disturbance in the heart) is also frequently seen. The ECG can fluctuate over time, depending on the autonomic balance and the administration of antiarrhythmic drugs. Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it. (There is a case report of a patient who died while shaving, presumed due to the vagal stimulation of the carotid sinus massage.)
What do bigeminy mean when we talk about PVC?
Regular pattern of PVC: One QRS with sinus rythm to one PVC. 1-1 ratio. Trigeminy refers to two normal sinus beats for every PVC and so on…
Is a PVC occur between to normal QRS complexes we call it?
Interpolated PVC
When do we call ventricular rythm for idioventricular rythm?
Normally, the pacemaker of the heart that is responsible for triggering each heart beat (ventricular contraction) is the SA (Sino Atrial) node. However, if the ventricle does not receive triggering signals at a rate high enough from either the SA node or the AV (Atrioventricular) node, the ventricular myocardium itself becomes the pacemaker (escape rhythm). This is called Idioventricular Rhythm. Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes(> 0.12 sec). The rate is usually 20-40 bpm. If the rate is >40 bpm, it is called accelerated idioventricular rhythm. The rate of 20-40 is the “intrinsic automaticity” of the ventricular myocardium. It can be regarded as a “backup plan” or “redundancy” built into the body.Accelerated vs. “normal”
Which of the bundles (right or left) have a longer refractory period?
The right one have a longer refractory periodWhen a premature atrial inpulse -> aberrancy
what is the criteria for first degree AV-block?
regular P-QRS with PR interval >200 ms