a lecture series by SWESEMJR

Transcription

1 Electrolyte disturbances Hypokalaemia Decreased extracellular potassium increases excitability in the myocardial cells and consequently the effect of very severe hypokalaemia is ventricular arrhythmia. This can be in the form of VT, VF or Torsade de Pointes. Supraventricular arrhythmias, such as atrial flutter/fibrillation or SVT may also occur but are clearly less severe. In severe hypokalaemia one can see frequent ectopics of both supraventricular and ventricular origin. In the patient with a milder hyperkalaemia, were more subtle signs may be seen on the ECG, what to look for is increased amplitude and length of the P-wave, as the atrial cells react more strongly to the stimulus of the sinus node. The P-R interval is typically prolonged due to this. The T-wave may be either flattened or inverted and is typically followed by a U-wave. These are best seen in the precordial leads and give the impression of a long QT interval. What you re actually looking at, however, is a QU-time.

2 Electrolyte disturbances Hyperkalaemia Increases in extracellular potassium, logically enough, gives us the opposite effect to decreased potassium levels. This means that the myocardial excitability is generally decreased. Depending on the severity of the Hyperkalaemia different signs will appear on the ECG. Perhaps the earliest sign of hyperkalaemia is peaked T-waves. In hypokalaemia the atria became hyperexcitable, giving us high and wide P-waves. In hyperkalaemia the P-waves instead flatten to, eventually, disappear completely. The interval of the QRS-complexes can thus become prolonged as a result of lowered stimulus from the atria. What naturally follows is an active escape rhythm, which can come either from the AV-node or the ventricles themselves. Because of the general inhibition of the myocardial cells conduction blocks may occur. A sign of very severe hyperkalaemia is the sine wave appearance on ECG. This is also called a pre-terminal rhythm and is typically followed quite soon after by cardiac arrest.

3 Electrolyte disturbances Hypocalcaemia A low serum calcium will cause a prolongation of the QT interval by increasing repolarisation time and thus result in an increase of the ST-segment. Even though there have been reports of Torsade de Pointes, Hypocalcaemia is not very likely to cause a serious arrhythmia. Hypercalcaemia In reverse, and it is nice to know that there are things in the world that are simply logical, a high serum calcium will typically shorten the QT interval. In more severe hypercalcaemia Osbourne waves, or J waves, may be seen as part of the QRS-complex. In contrast to severe hypocalcaemia, very severe hypercalcaemia might actually cause myocardial excitability and thus VF arrests have been reported.

4 Medicine toxicity Beta blockers and Calcium channel blockers Beta blocker and heart selective calcium channel blocker (such as verapamil and diltiazem) toxicity shows up on the ECG as sinus or junctional bradycardia or AV-block I, II or III. Early signs of toxicity can also be seen as a prolongation of PR time. Heart specific Beta blockers act on the B1 receptor, which when inhibited, has a negative chronotropic AND inotropic effect. That is, the heart beats slower and with less strength. The natural effect is thus a slowed sinus rhythm. However in an overdose, the sinus AND AV-nodes are inhibited to the point of creating either an AV-block of varying degree, or a Sinus arrest, where the AV-node takes over rate control. This is seen as a slow junctional rhythm.

5 Medicine toxicity Beta blockers and Calcium channel blockers Heart specific calcium channel blockers work by blocking the flow of calcium across the cell membrane, thus inhibiting cell excitability. During intoxication this also gives us the negative inotropic and chronotropic effects and the same findings as with beta blockers. TCA Tricyclic antidepressants are widely known for their cardiotoxic effects and even though the trend leans towards prescribing SSRI or SNRI rather than TCAs they are still very much in use. TCAs in toxic doses block sodium channels in the brain and heart giving patients with severe intoxication not only ECG changes, but also seizures. Sodium is important for the excitability of the myocardial cells and toxicity will generally cause widened QRS complexes. Because of the secondary inhibition of the Sodium-Potassium pumps in the myocytes, an increased QT-interval is seen. Despite the general inhibition, the sinus node is disinhibited and causes tachycardia.

6 Medicine toxicity Digoxin Digoxin works through increasing intracellular calcium, which slows the heart through prolongation of the AV interval, thus creating a negative chronotropic effect. It also increases the automaticity of the myocytes, which in non toxic doses acts as a positive inotropic effect, but in toxicity creates an unstable, overly excitable membrane. This classically creates a fast supraventricular rhythm with a prolonged AV interval, so an AV-block type I, and premature ventricular complexes. Signs of digoxin on the ECG start showing up way before toxic levels are present, so if you have a patient who you re intending to give more digoxin to, who has a biphasic t-wave or a Salvador Dali moustache sign on ECG, you might want to get a concentration before increasing the dose.

7 Pacemaker basics A pacemaker can work in many different ways depending on where it senses, where it paces and what response it has to the sensed sites. It can also have extra functions such as modulating rate or have its own defibrillator. Step one to understanding your patient s pacemaker is to understand what the letter combination of the pacemaker means. Below you see a chart of what the letters mean. For example a patient who has a pacemaker that senses in the atrium, paces in both ventricles and does not modulate rate will have the letter combination AVT0V (in the american system of pacemaker classifications) Chambers paced Chambers sensed Response to sensing Rate modulation Multisite pacing A = Atrium A = Atrium I = Inhibited R = Rate modulation A = Atrium V = Ventricle V = Ventricle T = Triggered V = Ventricle D = Dual (A+V) D = Dual (A+V) D = Dual (T+I) D = Dual (A+V) Now on an ECG you will see the pacemaker pace as a pacing spike. If the pacemaker paces in the atrium you will see a spike directly before the P-wave and if it paces in the ventricles you will see a spike directly before the QRS-complex. If the pacing is in the right ventricle your ECG will look as though the patient has an LBBB and vice versa. If both atrium and ventricles are being paced, you can see a spike before only P-wave, only QRS-complex or before both. Below you can see pacing spikes just before the QRS-complexes, which have the appearance of an LBBB.

8 Pacemaker basics Above we see an ECG with a pacing spike just before the P-wave, thus an atrial pacing. Below we see a spike before the P-wave AND before the QRS-complexes, thus this is a patient with an A-V sequential pacing pacemaker. *All pictures used are from the Life In The Fast Lane ECG library ( This page is my go-to place for studying ECGs, as well as many other things. Do check it out!