hypokalemia predisposes to digoxin toxicity and digoxin use causes hyperkalemia.
hyponatremia (and dehydration) predisposes to lithium toxicity and lithium (polyuria) causes hypernatremia.
hypercalcemia predisposes to pancreatitis and pancreatitis causes hypocalcemia.
severe hypokalemia causes rhabdomyolysis and rhabdomyolysis causes hyperkalemia.
Friday 22 April 2011
Sunday 17 April 2011
the heart sings
abnormal heart sounds. the way textbooks describe them, just doesn't help me form a lasting memory of what they are.
S3, rapid ventricular filling.
S4, at atrial systole, blood hits stiff LV.
so you memorise these factoids, but really, without understanding the mechanism of how these sounds come about, you can't say you know your S3s and S4s.
let's start with S4. blood hitting stiff LV. what makes the LV stiff? what makes the LV lose it's normal flexibility?
hypertrophy! increased mass. STIFF. atrial systole, blood goes from LA to LV...it cannot stretch, so the blood SMACKS on its stiff walls =S4.
so someone who has had HT for years and years. the LV has been contracting against an increased systemic pressure. it hypertrophies. it grows stiff. you hear the S4.
what else would mess with the normal structure of the LV and therefor mess with its flexibility?
infarctions. think: new onset S4. infarcted tissue will fibrose. fibrous tissue is inflexible. it cannot stretch as well as cardiac muscles. blood sent from the LA at atrial systole will smack into the fibrous walls that won't stretch to accommodate its arrival.
incidentally, you can apply this theory to real life as well. it's pathological to be stiff/ inflexible.
it's intelligent to be accommodating and flexible.
=)
now S3, is the evil heart sound. with S4, you treat the underlying HT (there's nothing much you can do about the infarcted tissue) and try to decrease systemic resistance, so that the heart doesn't have to pump against high pressures and grow stiffer.
you hear an S3, think splish splash. the patient is having a fluid overload. normally, there shouldn't be splishy splashy sounds of blood filling into the ventricle. when there's too much fluid, it RAPIDLY FILLS THE VENTRICLE. before the ventricles have had a chance to pump out what was already there, more comes in and splashes against the blood already in the ventricle. more. more. more. splish. splash. slosh. too much fluid. it starts to back up? you get where this is going? congestive heart failure? congestion. what are you congested with? excess fluid!
how to you fix this? you decrease the fluid levels. how do you do that? DIURETICS. ACEi. Bb.
ACEi decrease fluid levels (affects renin, therefore inhibits aldosterone) AND is cardioprotective.
Bb...why would you give someone with a failing heart something that would slow his heart rate? aren't Bb a contraindication? NO! Bb lower mortality! they decrease the sympathetic affect on the heart. they increase diastolic time, allowing the coronary arteries time to profuse the heart muscles.
and diuretics, they make you pee out all that excess fluid.
so, S4, have a Bb...relax. don't be so stiff.
S3...time to get rid of fluid before you get congested. pee it out (diuretics), stop holding it in (ACEi blocking aldosterone, whose main function is to retain Na+, which in turn holds onto water), and have Bb. block that sympathetic system from activating the juxtoglomerular apparatus and increasing renin output. don't let angiotensin stress you out (constrict your vessels and increase your BP) and have its friend aldosterone keep sodium around, because we know that where there's sodium, there's water (best of buds) and when there's too much water, there's splishy splashy S3 sound because the heart can only handle so much at a time, dammit.
=)
see, cardio isn't that hard. think of it as a plumbing system: a pump connected to lots of pipes. don't overload the system. don't let the system leak. don't clog the pipes. don't let in bugs that can mess up the pump.
don't just read the text. picture it happening. it helps retain the information and all this information will help you help someone one day.
happy studying folks =)
S3, rapid ventricular filling.
S4, at atrial systole, blood hits stiff LV.
so you memorise these factoids, but really, without understanding the mechanism of how these sounds come about, you can't say you know your S3s and S4s.
let's start with S4. blood hitting stiff LV. what makes the LV stiff? what makes the LV lose it's normal flexibility?
hypertrophy! increased mass. STIFF. atrial systole, blood goes from LA to LV...it cannot stretch, so the blood SMACKS on its stiff walls =S4.
so someone who has had HT for years and years. the LV has been contracting against an increased systemic pressure. it hypertrophies. it grows stiff. you hear the S4.
what else would mess with the normal structure of the LV and therefor mess with its flexibility?
infarctions. think: new onset S4. infarcted tissue will fibrose. fibrous tissue is inflexible. it cannot stretch as well as cardiac muscles. blood sent from the LA at atrial systole will smack into the fibrous walls that won't stretch to accommodate its arrival.
incidentally, you can apply this theory to real life as well. it's pathological to be stiff/ inflexible.
it's intelligent to be accommodating and flexible.
=)
now S3, is the evil heart sound. with S4, you treat the underlying HT (there's nothing much you can do about the infarcted tissue) and try to decrease systemic resistance, so that the heart doesn't have to pump against high pressures and grow stiffer.
you hear an S3, think splish splash. the patient is having a fluid overload. normally, there shouldn't be splishy splashy sounds of blood filling into the ventricle. when there's too much fluid, it RAPIDLY FILLS THE VENTRICLE. before the ventricles have had a chance to pump out what was already there, more comes in and splashes against the blood already in the ventricle. more. more. more. splish. splash. slosh. too much fluid. it starts to back up? you get where this is going? congestive heart failure? congestion. what are you congested with? excess fluid!
how to you fix this? you decrease the fluid levels. how do you do that? DIURETICS. ACEi. Bb.
ACEi decrease fluid levels (affects renin, therefore inhibits aldosterone) AND is cardioprotective.
Bb...why would you give someone with a failing heart something that would slow his heart rate? aren't Bb a contraindication? NO! Bb lower mortality! they decrease the sympathetic affect on the heart. they increase diastolic time, allowing the coronary arteries time to profuse the heart muscles.
and diuretics, they make you pee out all that excess fluid.
so, S4, have a Bb...relax. don't be so stiff.
S3...time to get rid of fluid before you get congested. pee it out (diuretics), stop holding it in (ACEi blocking aldosterone, whose main function is to retain Na+, which in turn holds onto water), and have Bb. block that sympathetic system from activating the juxtoglomerular apparatus and increasing renin output. don't let angiotensin stress you out (constrict your vessels and increase your BP) and have its friend aldosterone keep sodium around, because we know that where there's sodium, there's water (best of buds) and when there's too much water, there's splishy splashy S3 sound because the heart can only handle so much at a time, dammit.
=)
see, cardio isn't that hard. think of it as a plumbing system: a pump connected to lots of pipes. don't overload the system. don't let the system leak. don't clog the pipes. don't let in bugs that can mess up the pump.
don't just read the text. picture it happening. it helps retain the information and all this information will help you help someone one day.
happy studying folks =)
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