Rubery: Cardiophysiology 2

Front 1

Muscle length-tension: overview

Back 1

Labels on X and Y axes:
-Length of muscle versus tension in the muscle

There are 2 different lines – red and blue
-They are separate lines, they do not connect

Blue line = Tension before contraction
-So stretching a muscle (adding length) does put tension on it – makes sense…
-This is passive stretch because it says, “before contraction” – the muscle is not making this happen, something else is stretching the muscle

Red line = tension during contraction

My green line:
-When the muscle is under no tension at all prior to contraction, it is able to develop a certain amount of additional tension when it contracts – it has a certain contractile strength at that pre-contraction length
-When the muscle is stretched a bit, (to what’s apparently considered “normal” length here), it is under some tension even at rest
-When it contracts, it adds even more tension than it did in the previous slide
-When it’s stretched a whole lot at rest, it can still generate additional tension when it contracts, and the total tension generated (red line) may even be higher than any other conditions
--But a lot of that total tension isn’t due to contractility (the length of my green line)
--A lot of that total tension is due to the pre-existing tension at rest

Front 2

Muscle length-tension: physiology

Back 2

Actin and myosin have to overlap each other in order to work at contraction
There is a “sweet spot” for actin-myosin overlap

Strength of contraction is affected by calcium availability

Front 3

Preload

Back 3

The passive stretch on the muscle prior to contraction.

Front 4

Length-tension ~ Volume-pressure

Back 4

We don’t usually talk about length-tension in the heart. Instead we talk about Pressure-Volume relationships

Tension on the walls of the ventricle is caused by the pressure within the chamber
During systole (contraction), the pressure is influenced mostly by contraction.
During diastole, the pressure is caused by the volume of blood within the chamber
-Volume during diastole = passive stretch = length of fibers prior to contraction

Front 5

Frank-starling mechanism

Back 5

The greater the heart is stretched during filling, the greater the force of contraction and the greater the amount of blood ejected into the aorta (up to a certain point, as we just discussed)

Front 6

Stroke volume

Back 6

Stroke Volume is the amount of blood ejected from the ventricle with each heartbeat
Blood is ejected when the pressure within the left ventricle exceeds the pressure within the aorta
So the ability of the ventricle to contract and generate pressure is the primary driver of the stroke volume
-So for a lot of these graphs, stroke volume is used instead of pressure
-It’s still basically the same graph – the relationships are the same

Front 7

Venous return curve

Back 7

As atrial pressure (x-axis) gets higher, venous return (y-axis) gets lower

The only reason blood flows anywhere is due to a pressure gradient

Front 8

Mean circulatory filling pressure

Back 8

MCFP

at that level of atrial pressure it’s too much – there is no more venous return at all, the heart has nothing to pump

Front 9

Venous return curve and cardiac output curve

Back 9

An increase in atrial pressure causes two things to happen:
-The venous return decreases
--Simple pressure-gradient effect on flow.
-The cardiac output increases
--Preload. Starling’s law.
--Also, ↑cardiac output means better emptying of the atrium, which will decrease the atrial pressure
And that’s how these two curves “find each other” at their steady-state intersection.

Front 10

Changing steady state intersection of venous return and cardiac output curves

Back 10

Adding or decreasing blood volume moves venous return curve up or down

Altering contractility moves cardiac output curve up or down

Increasing total peripheral resistance moves both graphs down. Decreasing total peripheral resistance moves both graphs up.

Front 11

Hemorrhage and the venous return/cardiac output curve in real life

Back 11

The only direct effect of hemorrhage is a shift in the venous return curve – which also means lower cardiac output, and thus decreased organ perfusion

But the body quickly responds by vasoconstriction, which ↑TPR
-This increases the systemic arterial pressure (to maintain organ perfusion pressure - remember ∆P=Q × R) but also increases afterload and thereby decreases cardiac output and venous return

Front 12

Exercise and the venous return/cardiac output curve in real life

Back 12

Increased catecholamines cause increased contractility
Dilation of muscular arterioles decreases TPR
-This allows an even greater increase in cardiac output and venous return

Front 13

Diastole and lusitropy

Back 13

Decreased lusitropy means heart is less able to relax (curve moves up, higher pressure)
-ischemia
-hypertrophy

Increased lusitropy means heart is more able to relax (curve moves down, lower pressure)
-drugs