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Cardiology Tunes

Action Potentials
If I heard a click, man
Regional Blood flow
Wake me up before my blood flows
Risk factors for CAD
Oxygen has come too late

Action Potentials
(in the style of "Bare Necessities")

It’s negative 90 millivolts
Before depolarizing cells
You’re resting in phase 4 of an AP!
In phase 0, sodium comes in
When the inside gets less negative
To cross the threshold potential of cells.
And so there’s an upstroke!, and then phase 1
When current goes down ‘cause of Potassium (going out)
In phase 2 the calcium comes rushing in the cell
Its activation is super slow but when it’s open see Ca go
Until it plateaus!
And then the calcium induces SR release . . of Calcium
[Phase three repolarizes.]

If I heard a click, man
(to the tune of “If I were a rich man”)

If I heard a click, man
Early systole with sharp and high-pitched quality, oh yes
I would fear A or P valve stenosis, or dilated aorta!
When my A valve opened,
As it rapidly ascended it’s so hard that it stopped fast!
In dilation the aortic root got tense, just as blood came flowing into it
In the aorta you can hear clicks at the top, and the apex of the heart when you breathe in and you breathe out.
But in the P valve situations change
A click comes only at the base and gets less as you breathe in
Oy how different they sound!
And late clicks signal M/T valve prolapse!

It’s different from a snap, man
Snaps are heard in diastole and OS follows S2
When your mitral or tricuspid is stenosed, a sharp and high pitched snap will come!

Regional blood flow
(to the tune of Yellow Submarine)

When your oxygen goes out , to the body (sales the seas)
The oxygen an organ takes is equal to the O2 delivery
Minus oxygen the veins remove
And the body needs some blood, skeletal muscles have lots of mass,
But they take 20 ercent of the cardiac output you see
If a tissue takes more blood than the oxygen that it needs
Then the exiting O2 content will be so very high
Skin gets lots of blood it doesn’t need.

And when the pressure gets real high, organizes regulate the blood they get.
Intraluminal pressure causes smooth muscle calcium release.
And the vessels can constrict, causing lower diameter
And the vascular resistance increases, constant O2 delivery
We all get constant O2 delivery . . . .

Autoregulation’s good, but sympathetics also affect
The displacement of its curse causing additional vasoconstriction
And the muscle cells can take as much oxygen as they need.
And metabolites like H, K, and phosphate and adenosine
All can relax the vasculature

“Wake me up (before my blood flows)”
(to the tune of George Michael’s “Wake Me Up”)


Interstitial fluid’s got protein, in a higher amount than you’d find in the vessels
But you’ll find in equal amounts – all the other ions that diffuse ‘cross the borders
But proteins cause the only driving force, they cause oncotic pressure that’ll chart the course
25 millimeters mercury, but such a low amount it doesn’t add to osmolarity.

Interstitial oncotic pressure’s 5, Plasma doesn’t obey what Van’t Hoff tells us
As protein levels increase, plasma oncotic rises at an exponential rate,
Blood goes through the capillaries, which transfer 3 liters across the wall daily
Lymphatic vessels return the blood back – so the steady state’ll stay all right!
Contract smooth muscle tight!

Skeletal muscles contract, helping lymph flow up, way up in the body
The hydrostatic pressure controls the rate the interstitial fluid goes to lymphatics
Consider this we’ve got a lot of blood that exerts more force than the interstitial space.
It lets us filter the fluids out but then oncotic pressure comes back into place!

Oncotic pressure in the capillary is higher than oncotic in the interstitia
It tells us, “Reabsorb your fluids, child,” keep all that fluid inside.
The mean hydrostatic pressure is between 20 and 25 mm
As the friction slows blood, at the venous end pressure isn’t so high
It’s 10-15 mm less!

What’s more, in interstitial space, the hydrostatic pressure is subatmospheric
It’s low in lung, muscle, and connective tissue, and it’s over 0 in epithelia that suck water
When pressure rises in the veins, you cause big increase in capillary hydrostatics (Pc)
It’s more than what an increase in arterial pressure makes, cause arteriole resistance is so high!

The radius of the precapillaries will also have a big effect on the Pc
And when you dilate arteriolar vessels, child, Pc gets real high
The big determinants of Pc are venous pressure and arteriole resistance
When all is normal the fluid levels are pretty constant
My foot’s Pc’s so high!

Edema happens when there’s too much fluid in the interstitial or fluid doesn’t leave fast
The lymph keeps the volume constant, and also takes the protein out as it leaks from the plasma
You’ve gotta keep the gradient in check or you’re gonna have trouble with fluid exchange
The filtration coefficient (K) shows how easily the water flows through the capillary!
to the tune of Queen’s “Bicycle”)

Oxygen is consumed, 25 percent –rest
Normally, blood is full with oxygen in arteries, but in the veins it’s pretty low
To find mixed oxygen look in pulm artery
When you exercise lots, you extract 80%, If you’re trained, you’ll get more

All I wanna do is Exercise, Exercise Exercise!
To increase O2 consumption consumption consumption
I’ve got good metabolism and cardiac output
It helps me get more oxygen, and helps me put it where I like!

Skeletals compress veins, Elevate MCP
It’s a pump that helps blood flow from veins to thorax and elevates right atrial pressure
Skeletals sensing change make your symp activate,
You reset baroreceptors, HR up VC down, resistance up

Metabolism goes up, with end products, low resistance
To increase cardiac output (-ac output, -ac output)
When I change my resistance I make changes for O2
This factor is important to increase my cardiac output

I want to fill my atrium with lots and lots of blood
To foster high activity I’m going to fill it
Systolic pressure is getting high fast (but my diastolic stays the same)
Real high pulse pressure is joined by rise
in my MAP moderately

MAP stays same cause BR resets, BR resets, BR resets
Parasymp withdraws, symp starts up, symp starts up, symp starts up
With training HR-QO2 takes on a downward shift
So resting heart rate is reduced and athletes have a low heart rate
(Cause of high parasympathetic tone)

Risk factors (for CAD)
(to the tune of “White Devil, Black Jesus”)
They call ‘em – risk factors, CAD
Hypertension, age, and smoking
Male gender, diabetes
High cholesterol’s a bad one

Family history, type A guys
Couch potatoes, triglycerides
Homocysteine, birth control
But not so likely with alcohol

Other factors, that won’t hurt ye
Are coffee, gout, and obesity
Alcohol might help you
And cutting out risk factors will, too

“Oxygen has come too Late”
(to the tune of “Friday at the Circle K” by the Nields)

Oxygen is consumed in the heart
About five times more than any other body part
The LV takes 20X more
In exercise the venous O2 is just 30%
Arteriovenous difference is huge
O2 capacity will come from Hb
To increase O2 consumption the heart’s got no capacity
Cause at rest, it takes so much

So what can we do now?
We must increase O2 delivered to the heart
We’ve saturated and maxed out Hb
Let’s send more blood into the coronary
Left Perfusion comes in diastole
Myocardium in systole squeezed (on coronary vessels)
Then we encounter vessels with resistance for the heart’s supply

And R1’s big vessels, serves as a capacitor
R3’s wall tension, R2 varies in arterioles!

Normally, in exercise reduce your R2 resistance and shorten up your cycles
But when you’ve some CAD, your R1 increases and so does your R3
Your R2 tries to vasodilate
But then with exercise it just doesn’t rate
Ischemia will hit you up, you stenose and flow’s getting late!