Electrolyte Abnormalities and Their Impact on ECG Changes Explained

Good morning, one and all. I am Dr. Vigneshwaran,   Professor of Medicine from Chettinad Academy of  Research and Education. In this uh lecture series   on ECGs, uh we are going to see what  electrolyte abnormalities can do on ECG.  

So, the objectives of my talk will be; first we  will see what are the electrolyte abnormalities   that cause ECG changes. Then we will see  how do these electrolyte abnormalities,   how they how they cause ECG changes.

Then we will see what are the ECG changes that  occur with these electrolyte abnormalities. Then   we will see what are the causes of  these electrolyte abnormalities.   And then, we will see some case scenarios, so that  uh we understand this uh slightly more better.  

So, to start, first is, what are the electrolyte  abnormalities that causes ECG changes?   Normally, there are lot of uh electrolytes we  measure in the serum, like sodium, potassium,   chloride, bicarbonate, calcium,  magnesium and phosphate.

uh As we can see the values, we have a  normal levels for each of these electrolytes.   And as we see, all of them  are in a very narrow range.   Of the electrolytes what I have marked  with, uh we we made it bold and uh italic  

are the 2 electrolytes which are associated  with ECG changes. So, potassium and calcium   are the 2 electrolytes which are associated with  ECG changes. And as you see, the normal potassium   is 3.5 to 5 milliequivalents per litre, and the  normal calcium is 9 to 11 milligram per decilitre.

Now, coming to the next question. Now, how do  these electrolytes cause these ECG changes? Now,   for that, we have to know a bit more in  detail. We have to know what are electrolytes.   And uh is there electro, what is ion and what is  an electrolyte? What are ion channels? And uh are  

ion channels present in the heart muscle? If so,  what channels? And uh then we should understand uh   movement of ions through these channels,  how do they cause action potential changes? And then we should understand how action  potential changes leads on to ECG changes.  

So, we know now, there are 2 electrolytes which  cause ECG changes; one is potassium and calcium.   So, with with that in mind, we will see  what changes it causes in action potential.   So, to the first point there.  What are electrolytes? uh  

Electrolytes are actually minerals and they are  they are all charged minerals. Any charged atom   is called an ion. So, electrolytes are also  ions, and they are actually ions in water. There are 2 types of electrolytes; one is  positively charged electrolyte and another is  

negatively charged electrolyte. uh Positively  charged electrolytes for example are sodium,   potassium, calcium and magnesium. And  negatively charged electrolytes are   chloride, bicarbonate and phosphate. To note,  uh we are concerned about potassium and calcium,  

and both are positively charged electrolytes.  And another point there is calcium,   potassium is mainly an intracellular electrolyte  and calcium is an extracellular electrolyte. Now, second point, uh we have to know what are ion  channels. And what are the ion channels which are  

present in the cardiac muscle? Now, ion channels  are pore forming membrane proteins. As you see,   these are the ion channels, and they are  present in the membrane, and they form,   they actually have a, help us communicate between  extracellular in and intracellular. So, the ions  

move in and out of these ion channels. And this  ion channels are present in all the membranes. And movement of these ions, because of this,  these are all electrically charged, moment   of these ions create membrane potentials. And  there are different types of membrane potential;  

mainly what we are thinking is the resting  membrane potential and the action potential. So,   these are uh altered; these are uh mainly  affected by this movement of these ion channels.   Now, what are the ion channels which  are present in the cardiac muscle?  

There are 3 main ion channels,  sodium, potassium and calcium. Of these, sodium and uh calcium are only  1 type are present in the cardiac muscle,   but there are 5 different types of potassium  channels which are present in the cardiac muscle.  

The first what we call it as tran transient  outward potassium channel or Kto potassium   channels, Kto channels. Then we have  got uh I Kr which is rapid potassium   channel. Then we have got a slow potassium  channel which is I Ks. And then we have got  

inward rectifier potassium channel, I  Ki, inward rectifier potassium channel. And then, there is something called as  ultra-rapid delayed rectifier potassium channels.   So, there are 5 different types of potassium  channels present in the cardiac muscle.  

And as I told you, we are concerned  with potassium and calcium. Okay. Now,   the next question is, how ion movements  create changes in the action potential curve?   Now, this is the figure showing the action  potential curve of a ventricular muscle.  

And if you see, it has got 5 phases. First is what? It it rises up. First it it rises  up. So, that is 1 phase, which is called phase 0.   Then it drops down; so, that is called phase  1. Then it plateaus again; it is called phase  

2. And then it da drops down again, which  is called phase 3. And then you have a a   maintenance at a normal baseline, which is  called as phase 4. So, these 5 phases of   cardiac ventricular muscle action potential is  determined by these 3 channels, which is sodium,  

potassium and calcium. And and as I told you,  we should concentrate on potassium and calcium. uh The phase 0, which is the rapid upstroke,  which is called the depolarisation,   which starts from the resting membrane  potential of around minus 90 and ascends  

up after it reaches a threshold, ascends up, goes  above 0. That is because of the sodium channel.   Now, once that uh you have crossed that, uh  that is the sodium channel. Now, next is,   after it has reached a point, suddenly  what happens, it comes down. That is  

called early repolarisation. First  part of repolarisation is the phase 1. That is because sodium channels close and   the potassium channels open. There are this,  there are 2 potassium channels involved here,  

the transient outward potassium channel and the  ultra-rapid potassium channel. Then there is a   plateau phase, wherein it is maintained at around  0 degree for a long period. this is called phase   2, plateau. So, this phase is because of the  calcium channel, okay, L type calcium channel,  

and also some effect by the slow potassium  channel. Then there is the phase 3, which is what? The late repolarisation; that is, the final  repolarisation. So, this phase 3 is because   of the rapid potassium channel as well as  the inward rectifier potassium channel. So,  

2 channels here play a role. And then, the  fourth uh phase, which is the maintenance of   the resting membrane potential. It is because  of the inward rectifier potassium channel.   So, this, so, what we understand is, a cardiac  act ventricular muscle action potential curve  

has 5 phases; phase 0; phase 1; phase  2, which is the plateau phase; phase 3,   which is the final repolarisation; and phase  4, which is the resting membrane potential. And if you see, calcium plays a very important  role in phase 2, and potassium plays a very  

important role in phase 3; this we have to  keep in mind. To understand the ECG changes,   we have to keep this part in mind. That  is, phase 2 is by calcium predominantly,   and phase 3 by the potassium channel. So, if  you have po uh calcium channel abnormality,  

it is going to affect the phase 2. And if  you have a potassium channel abnormality,   it is going to affect the phase 3. If this point  is clear, then we can easily interpret the ECG. Now, coming to the uh next question, like  how action potential cha change is going to  

affect the ECG. Now, that is what we have been  explaining. As I told you, the calcium channel   is in phase 2. This is the phase 2 or the  plateau phase. And this causes changes in the   ST segment of the ECG. So, ST segment is the,  is a part of the repolarisation phase. That is,  

QRS is the depolarisation; from S to  the T wave full is repolarisation. The   plateau phase is represented in the  ST segment, and that is the phase 2. And phase 3 is represented in the T wave. So,  calcium channel problems are going to affect  

the ST segment, and potassium channels are  going to affect the T waves. So, this is the   important point here. Calcium abnormality is  going to affect ST segment of the ECG. And   potassium abnormality is going to affect the  T wave. Okay. And you know, ST segment denotes  

phase 2 of repolarisation and T wave represents  the phase 3. Now, we understand now that there   will be ECG changes if there is abnormality  with the serum calcium and potassium levels. Now, we will see what are the ECG changes which  happen. Now, first we will see about potassium.  

Now, high potassium is called medically as  hyperkalemia. And now we know the part will   be involved in potassium will be the phase 3.  So, that is, we represent it in the T wave.   And low potassium is represented as hypokalemia,  and that will also, is going to affect the T wave.  

Now, what changes will be there  in the T wave? In hyperkalemia,   you get tall tented T waves; and in  hypokalemia, you get a very sharp T wave. Actually, T wave will actually become lost.  Okay. That is the important point there. Then,  

calcium; we know calcium is going to cause  abnormality with the ST segment. High calcium   is medically called as hypercalcemia and  low calcium is called as hypocalcemia.   And high calcium is going to affect the ST  segment. So, when the ST segment is affected,  

it actually affects the QT interval. What do you  mean by QT interval? QT interval is the time,   is the area which starts from the starting  of the Q to the end of the T wave. So, when the ST segment is prolonged, the QT  interval is prolonged; ST segment is shortened,  

QT interval is shortened. So, hypercalcemia,  what does it do? It shortens the   QT interval. And hypocalcemia shortens  the uh prolongs the QT interval. Now,   what are the ECG changes? We will see in  detail, what are the ECG changes which occur  

in hyperkalaemia. First point is hyperkalemia.  So, we know potassium has to do with T waves. And uh we saw hyperkalemia is high  potassium and it will affect the T wave,   and you get tall tented T waves. So, if you see  this ECG, uh the normal potassium is 3.5 to 5.  

And as the potassium increases to 5.5, you  start to get the T wave; this is the T wave;   and this is starting to uh become,  T wave is starting to become taller;   T wave is starting to become taller and tented.  Then, some changes also occur in the P wave;  

some changes occur in the PR segment; and  then, some changes occur in the QRS complex. And as the potassium increases, we see changes  in the ECG also, very dramatical changes occur.   So, we are going to see this ECG changes in an  order. First what happens is, the pro the problem  

is, will be in the T wave. So, there is narrowing  and peaking of the T wave. So, this is also called   as tenting of the T wave. Next what happens is, if  still potassium is becoming more and more higher,   there is decrease in the amplitude of the P wave;  so, P wave becomes shortened. Then, there is  

prolongation of the PR interval;  so, PR interval gradually prolongs. And if it prolongs, its ca it becomes what  is called as AV block. And it can progress   from first degree to second degree, and then it  can become third degree AV block. Then, as the  

potential further increases, it does some changes  in the QRS complex. It widens the QRS complex.   So, the QRS complex widens. Then what happens,  as uh the potassium still further increases,   total absence of P wave; the P wave amplitude  

decreases very much. So, what happens, you  may not be able to see the P wave at all. And this, so, when P wave is not  there, only QRS complex is there,   it appears as a junctional rhythm, and this  rhythm is called as sinoventricular rhythm.  

Though the rhythm starts from the sinus  node, P wave is not seen. As a result,   you will start to see only a junctional  rhythm, and that is, so, it is called as   sinoventricular rhythm. And the QRS complex  then widens, and it is like a sine wave.  

This is the mathematical sine wave. And  so, this is called as sine wave pattern. And in last, if it is going to become higher and  higher, it is going to even produce asystole,   heart contraction stops, heart stops in  asystole, it does not contract at all. Now,  

so hyperkalemia is now clear. Okay. So,  potassium uh abnormality is going to   cause T waves abnormality. Now, we will  go to hypokalemia. What is hypokalemia?   Low potassium. So, normal potassium is 3.5 to  5; here it will be less than 3.5. And you know,  

it is going to affect the T wave. Now,  what abnormality it is going to cause here? So, what happens is, as the T  wave, as the hypokalemia worsens,   T wave; now, this is the T wave; now, the T  wave now shortens. T wave is no clean seen here.  

It is not, it is becoming less here. So, and  the T wave shortens and it can even invert.   Okay. T wave, this is called flattening  of T waves and it can even invert.   Then what happens? This is called the U wave.  Normally, this U wave is not seen uh well. But  

as the potassium decreases, you can start  to see the U wave becoming prominent. So, there is a prominence of U wave.  And sometimes, what you can see is,   the ST segment is also depressed. So, these  are the ECG changes in hypokalemia. uh  

Now, uh so, uh the point is, potassium  abnormality is going to affect the T waves;   hyperkalemia: tall tented T waves; hypokalemia:  shortening of the T wave and presence of U wave.   So, these are the things with potassium.  Now, we will see uh what ECG changes  

will occur with calcium. Now, first,  we will see about hypercalcemia. So, hypercalcemia, what we saw is, there will  be problems in the ST segment, phase 2 of   the depolarisation curve. So, this is the  normal ECG and this is the ST segment. So,  

this is a small ST segment here. And uh  this interval is called as QT interval. So,   that is from the start of the Q wave to the end  of the T wave; this is called the QT interval.   So, normal QT interval is around 440  milliseconds. uh Now, what happens with  

hypercalcemia? When the calcium is high, what  happens, it tends to, it affects the ST segment. So, what happens here? The ST segment shortens.   As a result, QT interval shortens.  So, this is represented as; normally,  

you have got the normal QT interval of 440  milliseconds, now with hypercalcemia what happens?   The QT interval shortens. So, the thing  is, it affects the ST segment. Now,   in hypocalcemia; what happens in hypocalcemia?  uh And again, normal; this is the QT interval.  

And uh this is, we know is the ST segment.  So, what is going to happen in hypocalcemia? The ST segment is going to be elongated, become  long. And what will happen? So, as a result,   QT will be prolonged. So, QT is prolonged above  440 milliseconds. So, so, now we can uh easily  

remember the uh electrolyte abnormalities uh which  will cause ECG changes. And uh we will see now,   what are the common causes of these electrolyte  abnormalities. Okay. Now, potassium: Potassium   you know, uh the normal level is 3.5 to 5. And  if there is above 5, so, what are the causes?

And if it is below 3.5, what are the possible  causes? uh The first important cause of   hyperkalemia is renal failure. So, kidney is  very important for excretion of potassium.   And uh food contains lot; lot of food contains  potassium, especially fruits and juices,  

tender coconut water, everything contains  lot of potassium. And if kidney does not,   does not function well, potassium is  not excreted. So, renal failure is an   important cause of hyperkalemia. Acidosis: When  body's acid is more, the pH falls below 3.5.

So, what happens is uh, the acidic  environment makes potassium move from,   shift from intracellular to extracellular. So,  the serum potassium will start to increase.   Third important cause is adrenal failure. uh In  adrenal gland, you have got a hormone called as  

aldosterone. And this aldosterone absorbs  sodium, excretes potassium. But if there   is adrenal failure what happens, the potassium  cannot be excreted, so, potassium level increases.   Any lysis of any cell, either it is RBC  or the muscle cells, so, what happens?

The muscles damage. So, muscles release the  intracellular potassium and it that comes out,   and that is another cause for hyperkalemia.  And another common cause of hyperkalemia is   uh usage of potassium sparing diuretics and using  ACE inhibitors and angiotensin receptor blockers  

as antihypertensives. Commonly, ACE inhibitors  and angiotensin receptor blockers are used very   much in diabetic patients, diabetic hypertensive  patients, cardiac failure patients and even in   renal failure patients to prevent progression of  diabetic nephropathy and even other nephropathy.

So, these are commonly used drugs.  So, that can also cause hyperkalemia.   And hypokalemia, what are  the causes? When you vomit,   when there is diarrhoea; when there is diarrhoea,  what happens? uh Potassium is lost in the  

stools. So, you get uh low potassium. Usage  of diuretics: So, all the diuretics cause,   especially the loop diuretics and thiazides, they  cause loss of potassium in the urine. And when the   aldosterone level is very high in the body. So,  there is something called as hyperaldosteronism.

So, what happens? That aldosterone absorbs sodium,  loses potassium. So, that these are the causes of   hypokalemia. Now, coming to calcium; calcium  normal level is 9 to 11 milligram per decilitre.   uh What are the causes where calcium can be above  level? Okay. So, that is hypercalcemia. The more  

important cause there is hyperparathyroidism.  So, parathyroid is the important regulator of   calcium. A parathyroid hormone absorbs calcium  from the kidneys as well as from the intestine. So, when the thyroid parathyroid is in excess,  what happens? The calcium level increases in the  

body. Multiple myeloma is another cause. Multiple  myeloma; see, calcium is stored in the bones.   Multiple Myeloma causes the osteoclast  activity to be more in the bones. So,   what happens? From bone, lot of resorption  occurs and calcium enters into the serum.  

Hypercalcemia of malignancy. So, what happens  in that malignancy, they secrete some,   what is called as para tho  thyroid hormone related peptide. And this, what does it do? It acts like a  parathormone and increases the calcium level.  

Secondaries in the bone: Destruction of the bone;  so, what happens? Calcium starts to increase.   Sarcoidosis:Sarcoido dosis is a condition  where there is lot of granulomas in the body,   uh which are what we call as non-caseating  granulomas. So, these granulomas,  

what does it do? These macrophages  produce lot of 1,25-dihydroxy D3. So,   when D3 levels are high, calcium  absorption is high; so, calcium increases. Thiazide diuretic is another reason for  hypercalcemia. Now, we will see some causes of  

hypocalcemia. Pancreatitis, acute pancreatitis:  What does it do? Pancreatitis means, there is   a lot of lipase enzyme released. So,  what happens? It destroys the pancreas;   saponification occurs; so, which requires  calcium; and calcium gets deposited there.  

Renal failure: Because kidney is a source for  1,25-dihydroxy D3, if it does not produce,   what happens? So, you do not get good  amount of uh 1 2 active form of vitamin D3. So, calcium is not reabsorbed. So, hyperglycemia  occurs. Hyperparathyroidism, one another reason.  

Vitamin D deficiency is another reason. And  hyperventilation is an important reason.   What happens in hyperventilation is that  hyperventilation causes alkalosis; alkalosis   causes a shift in the calcium, calcium. So, what  happens? Ionic calcium decreases and this is the  

reason for hypocalcemia. So, now we have seen  common causes of these electrolyte abnormalities. Now, we will go to some case scenarios, so that  you understand this uh electrolyte abnormalities   better. Okay. uh Now, first case scenario: uh  A 30-year-old female with recent bereavement  

in family; she has lost uh one of her loved ones;  and she comes to the emergency room with dyspnea,   breathing difficulty. And uh when she is  breathing like that, hyperventilating,   what happens is, there is paresthesia; that is,  numbness in the peripheries, uh in the lips,  

in the tongue, in the hand, tip of the  fingers, in the legs, sole of the foot. And she also has got a choking sensation,  difficulty in breathing. And there is   also cramping of the hands. Okay. And when the  examination is done, the respiratory rate is 36,  

and the patient is seemed to ha having a  deep breathing. And if you see the hands, the   photograph of hand, there seems to be, the hand  is going for for some sort of a spasm. The thumb   is coming inside, okay, it comes medially, so, and  it is trying to get pressed here. And uh so, this  

is called as carpal spasm, carpopedal spasm is  both uh hands and legs getting uh spasm like this. So, and now, an ECG was taken. So, what do  you expect now? Okay. That is the question. uh   Now, I will show you the ECG.  

What is seen here uh is, uh if you  see, uhm anything with relation to   what we know; electrolyte abnormalities is going  to cause what? ST segment and T wave problems.   So, is there any problem with the ST segment  and T wave? That is what we are going to see.  

Now, there is 1 lead in  the base. That is what? V5;   now it is given. Now you see, the  ST segment looks a bit long. Okay. All the ST segment looks a bit long. So, then you  know, ST segment means what? It has to do with the  

calcium. Okay. And when ST segment is  long, what happens to the QT interval?   QT interval is, from the start of  the Q wave to the end of the T wave.   So, normal I told you is around 440  milliseconds. Now, if you see this,  

1 large square is 200 milliseconds, second  is 400 milliseconds. This comes around 2;   this comes around 2; so, it is uh more than 480  or 500 milliseconds. So, what is the problem here? ST segment prolonged, QT interval  prolonged; and therefore, the diagnosis  

is hypocalcemia. So, hypocalcemia uh  in addition to these ECG changes causes   what? All the paraesthesias, tingling sensation  and what is called as carpopedal spasm. It usually   occurs with hyperventilation, when ionic  calcium is less. Now, coming to the next  

case scenario. Now, this this should be easy  for you; uh lot of clues here. 55-year-old male   who is a diabetic and hypertensive for 15 years,  uh his glycemic control has not been very good. For the past 2 years; that means what?  His glycemic control is not that good.  

So, uh diabetes, not good control,  some organs can get affected.   For the past 2 years, he has got pedal edema,  facial puffiness. That means what? Facial   puffiness usually comes when there is problem with  the kidney. And there is also dyspnea on exertion;  

that is, breathing difficulty. Retinal  examination; fundus examination shows   that there is evidence for diabetic retinopathy.  So, one organ is affected because of diabetes. So, the eye's fundus is affected. So, then, his  urine shows proteinuria. That means what? The  

kidney is also getting affected, and there is loss  of protein. And in addition, he is taking what?   ACE inhibitors for his ARBs, angiotensin  receptor blockers for his hypertension.   So, some drugs are like that is  telmisartan, valsartan, losartan are  

examples of angiotensin receptor blockers.  And if you see his examination, heart rate   is only 50. So, the rate is become  less. And uh he still is hypertensive. So, now, what are the ECG changes expected? uh  Straightforward, I think, we will see with what  

are the ECG changes. Now, ECG looks very bizarre,  correct? Let us focus on any one point here. Let   us consider this V2. Okay. This is a rhythm strip.  And we will see the ECG here. Is there anything   with the, abnormal with the QRS? QRS seems big  wide. In addition, what is happening is, this is  

the T wave. Okay. Now, there is no gap between the  T wave at all, and ST, the T wave is very tall. So, you are getting what is called as a tall and  tented T wave. Okay. And in addition, P wave is   not at all tall; P wave amplitude is very less.  PR interval is okay, but QRS complex is wide.  

So, what you are ge getting? What are  the points you hear? Tall tented T waves,   shortening of the P wave, QRS complex  widening as if it is like a sine wave.   And all these are classical  features of hyperkalemia. Okay. So,  

this is also a very good example to say about  the electrolyte abnormality of high potassium. Now, we will go to the third scenario. Now, a  35-year-old female had diarrhoea and vomiting   for the past 3 days and she complains of  lot of tiredness and myalgia, muscle pain.  

Examination: She is conscious oriented. Heart rate  is 60. There is diffuse muscle tenderness. If you   press on a muscle, there is all tenderness. And  power, muscle power is also getting less. Okay.   The muscle power is becoming less; she is not able  to use her limbs properly, upper and lower limbs.

The tone is less. That reflexes  are decreased, mildly decreased.   Plantar is flexor. Sensory examination is  normal. So, what is the ECG changes we expect?   So, the electrolyte abnormality  we expect here will be what? Now,  

let us see here. We will focus on one lead. Let  us consider we focus on V5. Okay. Now, what is   happening here? The ST segment looks depressed.  We do not see bit of P wave, T wave at all here,   but what we see is U wave. So, the T wave is  short, U wave is prominent and ST depression.

So, all are very classical to suggest  what? Hypokalemia. So, hope you are getting   the electrolyte abnormalities and the ECG changes  easily now. Now, to summarise the discussion we   had, uh electrolytes are ions and they are all  maintained in a very narrow range in the body.  

There are 3 main ion channels in  the heart muscle, which we know,   sodium, calcium and potassium.  Electrolytes move in and out of   these ion channels and they determine  the cardiac muscle action potential.

So, electrolyte abnormalities cause ECG changes.  The 2 most important electrolytes are potassium   and calcium. And now we know th that these  2 electrolytes produce distinctly changes,   distinct changes in the ECG, and they affect  the action potential curve in distinct areas,  

calcium affecting the ST segment and  potassium affecting the T wave. So,   calcium affecting the ST segment and  potassium affecting the T wave. So,   T wave abnormality in hyperkalemia will be tall  tented T waves; hypokalemia, it will be deeper,  

that is, very low amplitude, low voltage of T  wave and even absent T wave and prominent U wave. So, this is with potassium. With regards to  calcium, it affects ST segment. With low calcium,   you are going to get the ST segment prolonged,  QT interval prolongation. With high calcium,  

what you are getting, is a shortening  of the ST segment and QT interval   shortening. Okay. Thanks a lot.  Thanks a lot for this patient hearing.