Cadiac Output Regulation

cardiac output

• total flow or blood out of the left ventricle'

• total flow that is available to perfuse all the tissues of the body

why is cardiac output not measured in the aorta?

portion of the total output flows to heart itself for coronary circulation

in order to meet the metabolic demands of the body and maintain arterial pressure, cardiac output must?

be able to increase substantially

What happens to cardiac output with exercise?

• can increase 4-5 fold

  • increase HR (3 fold)

  • increase SV (1.5 fold)

with exercise, increase in cardiac output enables an increase in overall O2 consumption of?

12 times

why is CO essential to pressure during exercise

• total peripheral resistance during exercise decreases (1/3 resting value)

• increase in co is essential to maintain mean arterial pressure

• MAP = CO x TPR

systolic and diastolic changes during exercise

• systolic BP increase with linear fashion to workload

• diastolic BP stays same

How would systolic BP drop during exercise? What does this indicate?

• MAP = CO x TPR

• if CO does not increase and TPR decreases = BP down → indication to stop exercise

  • either CO dropped (HR or SV not increasing)

  • or peripheral resistance increased to a greater degree

factors controlling cardiac output

• cardiac factors: characteristics of the cardiac tissues

  • heart rate

  • myocardial contractility

• coupling factors: constitute a functional coupling between heart and blood vessels

  • preload

  • afterload

Graphic techniques have been developed to analyze the interactions between the cardiac and vascular components of the circulatory system. The graphic analysis involves two simultaneous functional relationships between?

• cardiac out put and central venous pressure

• (the pressure in the right atrium and thoracic venae cavae)

2 indicants of preload

• central venous pressure

• EDV

central venous pressure

• pressure in the right atrium and thoracic venae cavea

• central volume mobilization

• blood returning to the right side of the heart and ability to mobilize that blood

• better indicant of preload because more blood returning to right side of heart = increased right atrial pressure

EDV as preload indicant

• coming from left side of the heart

• however, more blood returning to right side of heart = increased right atrial pressure

MSNA effects on right atrial pressure

• increased MSNA = increased right atrial pressure

• MSNA helps to facilitate preload

cardiac function curve

• expression of Frank-Starling relationship

• dependence of cardiac output on preload

  • (ie on central venous, or right atrial pressure)

• *hearts are isolated from rest of circulatory system

• characteristic of the heart itself

vascular function curve

• defines the dependence of the central venous pressure on CO

• depends only on certain vascular system characteristics - peripheral resistance, arterial and venous compliance, and blood volume

• entirely independent of the characteristics of the heart

• can be evaluated even if heart was replaced by mechanical pump

cardiac output is the output of the? What actually determines cardiac output?

• output of the left ventricle

• preload of the right ventricle determines cardiac output

  • left ventricle pumps whatever volume comes to it

  • so filling pressure on right side determines output of left

  • filling pressure = central venous pressure (right atrial pressure)

in the intact circulation, the preload is considered to be?

• the central venous pressure

• = mean arterial pressure

• = right ventricular pressure when tricuspid valve is open

Describe the cardiac function curve

• at a given preload/right atrial pressure, there will be a given stroke volume

• straight line indicates maximum pressure the ventricle can produce at a given volume

  • represents ESVPR - end systolic volume pressure relationship = contractility = dp/dt

draw the corresponding graph

draw the corresponding graph

When contractility is held constant, describe the relationship between preload and stroke volume

• higher preload = higher SV = higher EDV

• lower preload = lower SV = lower EDV

• contractility no change = ESPVR no change

  • ESV does not change when preload changes

draw the corresponding graph

draw the corresponding graph

Describe the relationships happening on graph

• linear line is different = different contractility = raise peak pressure that can be developed at a given left ventricular volume

• increased contractility

  • upward ESPVR and left (increased slope)

  • increased SV

  • decreased ESV

• decreased contractility

• = downward ESPVR and right (decreased slope)

• decrease SV

• EDV is the same because preload is constant

How will a change in contractility affect the cardiac function curve

• completely new cardiac function curve

• still reflects Frank-Starling relationship

relationship between pressure and contractility

• cannot be separated

• increased contractility = increased pressure

• cannot have increased contractility without increased pressure and vice versa

draw the corresponding graph

draw the corresponding graph

afterload

• load experienced by the left ventricle after the aortic valve opens (ending the isovolumic contraction phase)

how do increases in afterload affect the left ventricular PV loop

• higher pressure throughout the ejection phase

why does increasing afterload increase pressure?

when diastolic arterial blood pressure is elevated, the isovolumic contraction must then develop a higher pressure in the left ventricle before the aortic valve can be forced open

how does increased afterload affect ESVPR, SV when contractility is constant

• ESVPR same

• SV decreased

  • because heart is not able to achieve a lower ESV

  • it does not have an increase ability to squeeze down against the elevated pressure

How does a decrease in afterload affect SV and ESV

• increased SV

• lower ESV because heart is able to squeeze down more

how does the change in afterload affect the function curve

• completely new function curve

• still displays the length-dependence of cardiac contraction

If preload held constant, but SV differs from conditions

SV gets its own cardiac function curve

• systolic failure

• HFrEF - heart failure with reduced ejection fraction

• diastolic failure

• HEpEF - heart failure with preserved ejection fraction

systolic failure

• decreased ESPVR slope = decreased contractility

• stroke volume maintained by increased preload

• increased EDV and ESV

• heart gets thick = concentric hypertrophy

diastolic failure

• same ESVPR = same contractility

• passive diastolic pressure volume curve is shifted upward and to the left = increased chamber stiffness = reduced compliance

• SV same

• EDP increased

• heart gets thin = eccentric hypertrophy

aortic stenosis

• Aortic valve not opening all the way

• Have to generate more pressure

• LVSP is higher