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Physiology And Pharmacology Of Systems > Control of Cardiac Output > Flashcards

Control of Cardiac Output Flashcards

1
Q

Definition of preload

A

Filling pressure of right ventricle, related to the CVP

Degree of stretch immediately before contracting

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2
Q

Definition of after load

A

Resistance to outflow from left ventricle, related to the MABP
Force against which the LV pumps to eject blood => aorta

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3
Q

Definition of end diastolic volume

A

Related to the filling pressure fo the heart

CVP=EDP

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4
Q

Definition of heart failure

A

Inability of heart to maintain a CO sufficient to adequately supply the tissues and organs of the body with blood
Can occur acutely and chronically

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5
Q

Definition of ANREP response

A

Autoregulation method where myocardial contractility increases with afterload

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6
Q

Definition of central venous pressure

A

Amount of blood and also capacitance of the veins

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7
Q

Describe the central venous system
What is the venous return equal to?
When is this not the case?

A

CVS is a closed system
CO=venous return
Except in transient events. In orthostasis, CO>VR as some pools in lower extremities. Due to the fact that there is more blood in the venous system than arteriole system

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8
Q

What influences cardiac output

A

Preload and afterload
Contractility
HR

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9
Q

What is the preload

A

Degree of stretch of the heart immediately before it contracts

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10
Q

What is the afterload
What is it due to?
What is it influenced by

A

Force against which the LV pumps to eject blood into the aorta

Mainly due to aortic P

Influenced by TPR and aortic stiffness (particularly with age)

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11
Q

What is the end diastolic volume

A

Related to the filling pressure of the heart

CVP=EDP

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12
Q

Describe the results of the Frank experiment

A

As filling pressure increases, ventricular P increases

The energy released during contraction depends on initial fibre length

  • Filling P increases
  • Fibre length increases
  • Force increases

Hyperbolic relationship

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13
Q

What is the relationship between EDP and EDV

A

EDP is easier to measure but relationship to EDV can change if V stiffens

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14
Q

Why does force increase with increased tension

A

Cross bridge theory

Maximum stretch present when there is max overlap between actin and myosin and the longest sarcomere possible forms

If there is too much overlap between actin filaments and no more cross bridges forming = shorter sarcomere length, results in a smaller % of max tension.

Gives a similar hyperbolic shape (sarcomere length vs % of max tension)

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15
Q

Describe the differences in cardiac and skeletal length tension curves

A

Steeper in cardiac than skeletal

So relatively small changes in preload/stretch => large change in force

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16
Q

How does Ca sensitivity and length dependence affect the amount of stretch and tension

A

As [Ca] increases, tension increases

Probably involves troponin C

17
Q

What are the consequences of Starling’s Law

A

SV of LV = SV of RV
CVP determines CO (assuming constant SNS input)
CO maintained even if afterload increases/contractility decreases

18
Q

How is the RV and LV output made equal

A 
Increase in RV output
Increase in BV in pulmonary veins
Increase in LA P and V
Increased filling of LV and LVEDP
Increased stretch
Increased force of contraction
Increased SV and LV output
LV output = RV output
19
Q

How is the RV and LV output made equal, shown on a ventricular function curve

A

Initially, SV of both LV and RV are the same
However as RV has thinner walls, P and V is higher here

When RV increases, out of sync with LV

LV will match SV of RV by increasing the EDP

20
Q

What is the compliance of a chamber

A

Change in V with a given change in P

21
Q

What is heart failure
When is it acute?
When is it chronic
What is it characterized by?

A

Inability of the heart to maintain a CO sufficient to adequately supply tissues and organs with blood

Can be acute (MI, muscle not working)
Can be chronic (chronic heart failure, microstructure deteriorates)

Characterized by a lower amplitude CO curve

22
Q

Describe the 3 compensatory mechanisms in heart failure

A

Decreased BP => decreased Na and water excretion
This increases BV and CVP => increases SV

Decreased BP and renal F activates SNS and RAAS
This increases water retention, +ve ionotrope and chronotrope, vasoconstriction => increased SV and EDP

Increased venous BV and VC
This increases CVP and EDP

23
Q

Describe the long term effects of the compensatory mechanisms in heart failure

A

Muscles continually weaken so EDP increases to maintain a SV sufficient for survival which continues to fall

24
Q

What is the effects of afterload on cardiac output

A

Increased AL => decreased SV because ejection cannot start until VP> AP
If AP increases, ejection is delayed so there is less time and energy for ejection

25
Q

Describe the mechanism to overcome increased afterload

What happens as a result

A

Ejection fraction falls, more blood remains in the heart at the end of systole so EDV/EDP increases. Restored SV due to Starling mechanism

ANREP effect, release of substances that increase [Ca] in myocytes, increased ionotropy

Depression of CO by baroreceptors, SNS inhibited

CO and SV overall does not change as a result

26
Q

How is the preload regulated, CVP dependent

When does regulation occur?

A

CVP, function of amount of blood in veins and capacitance

Increased SNS => Increased VC => Increased P => Increased CVP
-Occurs in exercise so RV output = Increased LV output for working muscle

Changes in BV can alter CVP
-Occurs in hemorrhage, blood loss decreases CVP => decreased CO

Compensation

  • Increased VC to restore CO
  • Increased renal fluid retention
  • Shift of fluid from interstitium => plasma => increased BV
27
Q

Describe cardiac contractility and what is it regulated by?

A

Amount and rate of cardiac tension developed and ability to eject a SV

Regulated by [Ca] in myocytes via SNS/pH and pO2
NA increases contractility by stimulating B1 and B2

28
Q

How does exercise affect cardiac contractility

A

Increases contractility and venoconstriction => increase EDP and CO

29
Q

How does transfusion and exercise affect cardiac contractility?

A

Increased CVP and CO due to increased BV

30
Q

Describe the SAN and the pacemaker potentials

A

Primary pacemaker with diastolic depolarization (funny current haha)

Has non selective channels for Na, Ca

31
Q

Effects of the ANS agonists on the SNS

A

NA/A

Increased If
Increased rate of diastolic depolarisation (+ lusitrope)
Increased HR (+ chronotrope)

32
Q

Effects of the ANS agonists on the PNS

A

Ach

Decreased If
Opens KAch
Decreased rate of diastolic depolarisation (- lusitrope)
Decreased HR (-ve chronotrope)

Physiology And Pharmacology Of Systems (22 decks)

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