Electrolyte Abnormalities and Their Impact on ECG Changes Explained

[Music] [Music] good morning one and all

i am dr vigneshwaran professor of medicine from chettinado academy of research and

education in this lecture series on ecgs

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'll see

how do these electrolyte abnormalities how the how they cause these ecg changes then we'll

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'll see some case scenarios so that we understand this

slightly more better so to start first is

what are the electrolyte abnormalities that cause ecg changes

normally there are a lot of electrolytes we measure in the serum

like sodium potassium chloride

bicarbonate calcium magnesium

and phosphate 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 we made it bold and italic are the two electrolytes

which are associated with ecg changes so potassium and calcium are the two electrolytes

which are associated with ecg changes and as you see the normal potassium is 3.5 to 5 milli equivalents per liter

and the normal calcium is 9 to 11 milligram per deciliter 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

is there electro what does ion and what is an electrolyte what are ion channels

and are ion channels present in the heart muscle

if so what uh channels and 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 two electrolytes which cause ecg changes one is potassium and calcium

so we with that in mind we will see

what changes it causes in action potential so to the first point there what are electrolytes

electrolytes are actually minerals and they have 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 two types of electrolytes one

is positively charged electrolyte and another is negatively charged electrolyte

positively charged electrolytes for example are sodium potassium calcium and magnesium

and negatively charged electrolytes are chloride bicarbonate and phosphate to note

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

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 poor 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 and

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 movement 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 altered these are mainly affected by this movement of

these ion channels now what are the ion channels which are present in the cardiac muscle there are

three main ion channels sodium potassium and calcium of these sodium and calcium are only one

type are present in the cardiac muscle but there are five different types of potassium channels which are present in

the cardiac muscle the first what we call it does tran transient

outward potassium channel or kt watch potassium channels kto channels then we have got

ikr which is rapid potassium channel then we have got a slow potassium channel which is iks

and then we have got inward rectifier potassium channel iki inward rectifier potassium channel and

then there is something called as ultra rapid delayed rectifier potassium channels so there are five 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 moments

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 five faces first is what it it rises up first it

rises up so that is one face which is called phase zero

then it drops down so that is called phase one then it plateaus again it is called phase two

and then it drops down again which is called phase three and then you have a

maintenance at a normal baseline which is called as phase four so these five phases of

cardiac ventricular muscle action potential is determined by these three channels

which is sodium potassium and calcium and and as i told you we should concentrate on potassium and calcium

the phase 0 which is the rapid upstroke which is called the depolarization which starts from the resting membrane

potential of around minus 90 and ascends up after it reaches a threshold as in sub goes above zero

that is because of the sodium channel now once that

you have crossed that that is the sodium channel now

next is after it has reached a point suddenly what happens uh it comes down that is

called early report region first part of repolarization is the phase one that is because sodium channels close and

the potassium channels open there are this well there are two potassium channels involved here the transient

outward potassium channel and the ultra rapid potassium channel then there is a flat two phase wherein it is maintained

at around zero degree for a long period this is called phase two plate two 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 three which is what the late uh repolarization that is the

final reporterization so this phase three is because of the rapid potassium channel as well as the inward rectifier

potassium channel so two channels here play a role and then the fourth 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 ax ventricular muscle action potential

curve has five phases phase zero phase one

phase two which is the plateau phase phase three which is the final repolarization and phase four which is

the resting membrane potential and if you see calcium plays a very important role in phase two and

potassium plays a very important role in phase three this we have to keep in mind to understand the ecg changes

we have to keep this part in mind that is phase two is by calcium predominantly and phase 3 by the potassium channel so

if you have 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 next question like how action potential change change is going

to affect the ecg now that's what we've been explaining as i told you the calcium channel is in phase two this

is the phase two or the plant two phase and this causes changes in the st segment of the ecg

so st segment is the is part of the repolarization phase that

is qrs is the depolarization from s to the t wavefull is repolarization the plant two 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 ah

calcium abnormality is going to affect st segment of the ecg

and potassium abnormality is going to affect the t wave okay so and you know

uh st segment denotes phase 2 of repolarization 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 three

so that is be represented in the t wave and uh 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

hypergalemia you get tall tinted t waves and in hypokalemia you get a very short 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 a st segment high calcium is medically called as hypercalcemia and low calcium is called

as hypercalcemia 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 queue to the end of the tv so when the st segment

is prolonged the qt interval is prolonged st segment is short and 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'll see in detail what are the ecg changes which

occur in hyperkalemia first point is hypergamia so we know potassium has to do with t

waves and we saw hyperkalemia is high potassium

and that will affect the t wave and you get tall tinted t waves so if you see this ecg

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 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 problem is will be in the t wave

so there is narrowing and peaking of the t wave so this is also called as tinting 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 call it becomes what is called as a v block and it can progress from first degree to

second degree and then it can become third degree a b block then as the potassium 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 pv 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 sine of

ventricular rhythm though the rhythm starts from the sinus node p wave is not seen as a result you start to see only a

junctional rhythm and that's so it's called as cyanoventricular 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 acestilly heart contraction stops heart

stops in a system it doesn't contract at all now

so hyperkalemia is now clear okay so potassium uh abnormality is going to cause t waves

abnormality now we'll go to hypokalemia what is hyperkalemia 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 versus

t wave now this is the t wave now the t wave now shortens t wave is not clean seen here

it's not it's becoming less here so and t wave shortens and it can even invert okay t wave 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

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 sd segment is also depressed so these are the

ecg changes in hypokalemia now so

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'll see

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 two of

the depolarization curve so this is the normal

ecg and this is the st segment so

this is a small st segment here and 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

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 sd 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 hypercalcemia what happens in hypercalcemia and again normal this is the qt interval

and this is we know is the st segment so what is going to happen in hypercalcemia 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

electrolyte abnormalities which will cause ecg changes and we'll see now what are the common

causes of these electrolyte abnormalities okay now potassium

potassium we know 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

the first important cause of hypergalemia is renal failure so kidney is very important for

excretion of potassium and food contains lot lot of food contains potassium especially fruits and juices tender

coconut water everything contains lot of potassium and if kidney doesn't it doesn't function well potassium is not

excreted so renal failure is an important cause of hyperkalemia acidosis when a body's acid

is more the ph falls below 3.5 so what happens is the acidic environment makes potassium

move from shift from intracellular to extracellular so the serum potassium will start to increase

third important causes adrenal failure uh in adenylyl 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 can 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 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 ac inhibitors and angiotensin receptor blockers as antihypertensives commonly

asymmetrics and angiotensin receptor blockers are used very much in diabetic patients

diabetic hypertensive patients cardiac failure patients and even in renal failure operations 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 diarrhea when there is diarrhea what happens potassium is lost in the

stools so you get for 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's 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 deciliter ah what are the causes where calcium can

be above level okay so that's hypercalcemia the more important cause there is hyper parathyroidism so

parathyroid is the important regulator of calcium parathyroid hormone absorbs calcium from

the kidneys as well as from the intestine so when the thyroid parathyroid is

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 absorption occurs and calcium enters into the serum hyper calcium of malignancy so what happens in

that malignancy they secrete some what is called as para thyroid hormone related peptide and this what does it do

it acts like a parathyroid and increases the calcium level secondary is in the bone destruction of the bone so what

happens calcium starts to increase sarcoidosis so sarcoid doses is a condition where there is a lot of

granulomas in the body ah which are what do you call as non case shading granulomas so these

granulomas what does it do these macrophages produce lot of 125 hydroxide d3 so when

d3 levels are high calcium absorption is high so calcium increases thiazide diuretic is another reason for

hypercalcemia now we'll see some cause of hypercalcemia 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 the

source for 125 dihydroxy d3 if it doesn't produce what happens so you don't get good amount of uh one active

form of vitamin d3 so calcium is not reabsorbed so hypercalcemia occurs hypoparathyroidism 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'll go to some case scenarios so that you understand this electrolyte abnormalities better okay

now first case scenario a 30 year old female with recent bereavement in family she has lost as

one of her loved ones and she comes to the emergency room with disney breathing difficulty and

when she's breathing like that hyperventilating what happens is there is parasthesia there is numbness in the

peripheries 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 seem to have having a deep breathing

and if you see the hands the photograph of a hand that seems to be the hand is going for for some part of a spasm the

thumb is coming inside okay it comes medially so and it is trying to get pressed here

and so this is called as carpal spasm carpal pedal spasm is both hands and legs getting

spasm like this so and now an ecg was taken so what do you expect now

okay that is the question now i'll show you the ecg what is seen here ah is

if you see um 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's what we are

going to see now there is one 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 one large square is 200 milliseconds second is 400 milliseconds this comes

around two this comes around two so it's 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

in addition to these ecg changes causes what all the parasthesia is 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 a

lot of clues here 54 year old male who is a diabetic and hypertensive for 15 years

his glycemic control has not been very good for the past two years that means what his glycemic control is not that

good so diabetes not good control some organs can get affected for the past two years

he has got fidelity facial puffiness that means what facial puffiness usually comes when there is problem with the

kidney and there is also disney on exertion there 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 eyes fundus is affected so then his urine shows protein area that means what the kidney

is also getting affected and there is loss of protein and in addition he is taking what ac in

a bit does for his arbs angiotensin receptor blockers for his hypertension so some drugs are like uh

that is tell me sartan uh all those are uh examples

lozarton or examples of angiotensin receptor blockers and if you see his examination heart rate is only 50. so

the rate has become less and he still is hypertensive so now what are

the ecg changes expected straightforward i think we'll see with what are the ecg changes now ecg looks

very bizarre correct let's focus on any one point here let's consider this b2 okay this is the

rhythm strip and we'll see the ecg here

is there anything with the abnormal with the qrs qra 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 if 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 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'll go to the third scenario

now a 35 year old female had diarrhea and vomiting for the past three days and she

complains of lot of tiredness and muscle pain examination she's conscious oriented

heart rate is 60 there is diffuse muscle tenderness if you press on the muscle that 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 ah the reflexes are decreased mildly

decreased plantar reflexer sensory examination is normal so what is the ecg changes we

expect so the electrolyte abnormality we expect here will be what now let's see here

uh we'll focus on one easy one lead let's consider we focus on v5 okay now what is happening here the st

segment looks depressed we don't see bit of p t wave at all here but what we see is u wave so the t wave

is shot u wave is prominent and st depression so all are very classical to suggest what

hypokalemia so hope uh

you are getting the electrolyte abnormalities and the ecg changes easily now now to summarize

the discussion we had electrolytes are ions and they are all maintained in a very narrow range in the

body there are three 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 two most important electrolytes are potassium and calcium

and now we know that these two 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

uh so for calcium affecting the st segment and potassium affecting the t wave so t wave

abnormality in hyperkalemia will be tall tentatives hypokalemia it will be depre that is very low amplitude low uh

voltage of t wave and even absentee wave and prominent ua so this is with potassium with regards to calcium it

affects the st segment with low calcium you are going to get a st segment prolong qt interval prolongation with

high calcium what you are getting going to get is a shortening of the st segment and qt interval

shortening okay thanks a lot thanks a lot for this patient hearing