Physiology Exam 3 Lecture 9A [Cardiac Output and its control: Harata]

Stroke volume (SV) Definition

The amount of blood pumped out by each ventricle with each contraction (systole)

Unit: mL/beat

How is stroke volume measured

SV = (end diastolic volume) - (end systolic volume)

Left ventricle vs right ventricle

SV (left) = SV (right)

on average

Cardiac output definition

Represents the ventricular blood volume pumped per minute

Cardiac output (CO: mL/min)

= heart rate x stroke volume

(Beats/min) x (mL/beat)

CO

HR = 70 (beats/min)

SV = 70 (mL/ beat)

4,900 mL/ min

Total blood volume in the body

5-5.5 L

Cardiac output is calculated for each

ventricle

CO is _________ in real time

flexibly modified

During exercise, CO can increase to

4-5 times the value at rest

What if the cardiac output cannot keep pace with the body's demands for supplies and waste removal

Heart failure and organ failure

SUMMARY: Cardiac Outpute =

Heart rate x Stroke Volume

SUMMARY: CO calculates

how much blood is pumped out every minute

SUMMARY: Co is an important parameter in

determining the hearts function

SUMMARY: CO is adjusted _______ in order to adapt to the constantly changing demands for the blood supply

Real-time

The SA node is innervated by both

sympathetic and parasympathetic nerves, which control heart rate

Ventricular myocardium is innervated by

sympathetic nerves which control ventricular contractility

Ventricles are not innervated by

Parasympathetic nervous system

Just wanted to stress this

Sympathetic activation will

Increase HR (SA node) and contraction (Ventricular myocardium)

Parasympathetic Activation will

Decrease HR (SA node)

Heat rate with nerves

65-70 beats/ min

Heart rate without nerves

100 beats/min

At rest parasympathetic innervation is

dominant and keeps the heart rate within a normal range

I'm a big fan of this image

The Membrane and Ca clocks are both affected by

Autonomic stimulation

Impacting HR

SUMMARY: SA node is affected by both the

sympathetic and parasympathetic nerves

SUMMARY: Ventricular myocardium is affected by

sympathetic nerves only

SUMMARY: Physiological heart rate is determined by

The rate of action potential firing of the SA node cells, which in turn is determined by the diastolic depolarization

SUMMARY: β1 adrenergic stimulation increases and M2 muscarinic stimulation decreases the

cAMP/PKA activity

SUMMARY: β1 facilitates and M2 suppresses the mechanism of

diastolic depolarization (membrane clock and Ca clock)

Key concept when it comes to stroke volume is

contractility

When stimulatory: PKA will phosphorylate

Phospholamban

Un-phosphorylated phospholamban is an

inhibitor of SERCA2

β1 activation will phosphorylate

Phospholamban removing its inhibition increasing the SERCA action

SERCA actioni

increase the Ca storage and lead to more Ca release from the SR and thus more contraction

Frank-Starling law

increased venous return results in increased SV

Sequence of events

Increased venous return --> Increase EDV --> Increase strength of cardiac contraction --> increase SV

Simply put

during systole the heart normally pumps out the volume of blood returned to it during the previous diastole

If more is returned then more has to be pushed out

Extent of filling =

Preload (workload imposed before contraction begins)

Frank-Sterling curve is shifted by sympathetic stimulation

Sympathetic stimulation:

increase in Strength of cardiac contraction --> Increase stroke volume for the same end-diastolic volume

Sympathetic stimulation increase stroke volume and

ejection fraction

Stroke volume =

EDV - ESV

Ejection fraction =

SV/ EDV

Ejection fraction is a good indicator of

contractility

Failing heart experiences

Decreased stroke volume

Sympathetic activation can compensate for

decreased stroke volume (if mildly failing heart)

Sympathetic stimulation:

- Vasoconstriction of veins

- increase venous return

- increase EDV

Contractility regulators in a broad sense

Extrinsic: Sympathetic stimulation

Intrinsic: Frank-starling (increase EDV)

Increase Afterload

Contractility regulators in a narrow sense

Extrinsic control only

- sympathetic stimulation

Preload: EDV

How much volume is in the chamber before it begins to contract

Preload is decreased by

Decreased venous blood pressure, usually resulting form reduced blood volume (hemorrhage)

Increased heart rate (atrial tachycardia); reduces ventricular filling time

Preload is increased by

Increased venous pressure

Increased venous return

Semilunar valve regurgitation or leakage

Reduced heart rate, increases ventricular filling time

Contractility

force of myocardial contraction

Contractility is affected by

Venous return (intrinsic mechanism)

Sympathetic stimulation (extrinsic mechanism

Afterload

Afterload

Primarily aortic pressure:

- The workload imposed on the heart after contraction has begun

- The workload that the heart must eject blood against

Increased afterload ______ stroke volume at the same ventricular pressure/volume

decreases

Afterload increased by

Increased aortic pressure and systemic vascular resistance, such as under hypertension

Decreased aortic compliance (increased stiffness)

Aortic valve stenosis

SUMMARY: Sympathetic stimulation of ventricular muscle increases the contractility by

promoting the intracellular Ca dynamics through B1 receptor mediated activation of cAMP/PKA system. This is an extrinsic mechanism of stroke volume regulation

SUMMARY: Cardiac muscles function in the ascending limb of the length-tension curve. This means that an increase in stretching, in end-diastolic volume, will lead to an increase in

stroke volume

SUMMARY: Frank-starling law is an ________ of stroke volume regulation

intrinsic mechanism

SUMMARY: ____ is a useful indicator of heart function

Ejection fraction

SUMMARY: Increased ____ pressure will decrease stroke voume

aortic