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Flashcards in Cardiac Performance Deck (65)
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1
Q

What is Preload

A

Preload is the muscle length prior to contractility

2
Q

What is the preload of a cardiac muscle dependent on

A

ventricular filling (or end diastolic volume…EDV).

3
Q

What is Contractility

A

the intrinsic force that the muscle can create at the given length

4
Q

What is Afterload

A

the tension which must be developed in the wall of ventricles during systole to open the semilunar valves and eject blood to aorta/pulmonary artery

5
Q

What is Cardiac Output

A

the volume of blood pumped by the heart per minute,

6
Q

Equation for cardiac output

A

CO= SV x HR

7
Q

What is Stroke Volume

A

the volume ejected from the ventricle on a single beat

8
Q

What is End Diastolic Volume

A

the amount of blood collected in a ventricle during diastole

9
Q

What is End Systolic Volume

A

the amount of blood remaining in a ventricle after contraction.

10
Q

What is cardiac performance

A

It demonstrates the capacity of ventricles to pump blood and to maintain blood circulation throughout the body

11
Q

What are the three conditions necessary for optimal cardiac performance

A

Normal structure and functions of the heart (C.O)

  • Normal structure and function of tissue
    surrounding heart
  • Adequate filling of the heart by blood (venous return)
12
Q

Two factors that affect cardiac output

A

Changes in stroke volume or heart rate

13
Q

Two factors that can control heart rate

A

autonomic nervous system

hormonal/humoral control

14
Q

Examples of things that can control stroke volume

A
  • preload, contractility, afterload, number and size of myocytes,
    heart architecture, synchronisation of function of the atrias and
    ventricles
15
Q

Which four factors establish the volume of blood pumped with each heart beat.

A

Heart rate, contractility, preload and afterload

16
Q

Which chamber pressure is preload related to

A

right atrial pressure

17
Q

What are the indices for preload

A

EDV, EDP,
pulmonary capillary wedge pressure (PCWP)
and end diastolic wall stress.

18
Q

What does the Frank Starling principle illustrates

A

This principle illustrates the relationship between cardiac output and left ventricular end diastolic volume

(or the relationship between stroke volume and right atrial pressure.)

19
Q

Which one of the factors that determine the amt of blood pumped out the heart, if increased, incresing tension of the muscle

A

Preload

20
Q

What is the Frank-Starling mechanism (or Starling’s Law of the heart

A

The contraction and therefore stroke volume in response to changes in venous return

21
Q

Stretching of which heart chamber wall directly increases HR by 10 to 20%

A

right atrial wall

22
Q

two things that can increase intracellular calcium concentration and ultimately increase contractility of the heart

A

Catecholamines and inotropic drugs (eg. digitalis)

23
Q

Afterload for the left ventricle is determined by which vessel’s pressure

A

aortic pressure

24
Q

Afterload for the right ventricle is determined by which vessel’s pressure

A

pulmonary artery pressure

25
Q

True or False

If arterial pressure increases, afterload also increases

A

True

26
Q

What does the Law of Laplace state

A

Pressure correlates directly with tension and wall thickness and correlates inversely with radius.

27
Q

Two conditions that can increase left ventricular pressure (which would increase afterload)

A

systemic hypertension and aortic valve stenosis.

28
Q

Two conditions that can increase left ventricular wall thickness

A

chronic hypertension or aortic valve stenosis as a compensatory mechanism to decrease wall stress

29
Q

Two conditions that can increase left ventricular radius

A

valvular heart disease (especially aortic regurgitation) or cardiomyopathies causing systolic heart failure.

30
Q

What are the indices for afterload

A

Aortic pressure, systolic wall tension, LV systolic pressure

31
Q

What regulates the heart rate and what regulates the heart rhythm

A

The rate is controlled by the autonomic nervous system and the rhythm is controlled by the SA node

32
Q

Where are the three baroreceptors

A

carotid sinus reflex
Bainbridge reflex
Aortic sinus reflex

33
Q

Where do each of the baroreceptors maintain blood pressure

A

carotid sinus reflex - maintains BP in brain

Bainbridge reflex – maintains BP in heart

Aortic sinus reflex – maintains BP in aorta

34
Q

What is the function of barorecptors

A

Maintain blood pressure

35
Q

What initiates the Bainbridge reflex

A

increased blood in the atria

36
Q

What does the Bainbridge reflex cause

A

stimulation of the SA node and increased sympathetic nervous system stimulation

37
Q

What is tachycardia

A

Increased heart rate

38
Q

What is bradycardia

A

Decreased heart rate

39
Q

By how much percent can strong vagal stimulation decrease heart muscle contraction

A

20-30%

40
Q

The vagal fibers are distributed mainly to which chambers of the heart

A

the atria and not much to the ventricles

41
Q

Great decrease in heart rate combined with a slight decrease in heart contraction strength can decrease ventricular pumping by about how much percent

A

50%

42
Q

What is the normal cardiac output value

A

~5 L/min

43
Q

What is the normal stroke volume

A

70 ml/beat

44
Q

How do you calculate stroke volume

A

EDV (preload) - ESV (afterload)

45
Q

What is cardiac reserve

A

Cardiac reserve is the difference

between resting and maximal CO

46
Q

How do you calculate ejection fraction

A

Stroke volume / EDV

47
Q

How is the diastolic pressure curve determined

A

filling the heart with progressively greater volumes of blood and then measuring the diastolic pressure immediately before ventricular contraction occurs

48
Q

How is systolic pressure determined

A

by recording the systolic pressure achieved during ventricular contraction at each volume of filling

49
Q

Which volume is usually a little higher EDP or ESP

A

EDP

50
Q

During isovoumetric contraction the pressure inside the ventricle increases to equal the pressure in the aorta, at a pressure value of

A

about 80 mm Hg

51
Q

Which one is preload, EDV or ESV

A

EDV

52
Q

What would change in a Pressure-Volume loop if preload was increased

A

SV- increase

EDV - increases

53
Q

What would change in a Pressure-Volume loop if afterload was increased

A

SV- decreased
ESV- increases
ventricular pressure- increases

54
Q

What would change in a Pressure-Volume loop if contractility was increased

A

SV- increases
ESV- decreases
ventricular pressure -increases

55
Q

Which hormones increase heart rate

A

epinephrine and thyroxine (T4)

56
Q

Which hormones regulate blood pressure

A

Renin
ADH
Aldosterone

57
Q

What happens to the heart when there is Hypocalcemia

A

reduced ionic calcium depresses the heart. Heart stops during systole. (similar to the effect of high potassium)

58
Q

What happens to the heart when there is hypercalcemia

A

dramatically increases heart irritability and leads to spastic contractions.

59
Q

What happens to the heart when there is hypernaturemia

A

blocks heart contraction by inhibiting ionic calcium transport.

60
Q

What happens to the heart when there is hyperkalemia

A

leads to heart block and cardiac arrest.

61
Q

What happens to the heart when there is hyperthermia (fever)

A

increases heart rate, due to increase permeability of cardiac muscle membrane to ions that controls heart rate.

62
Q

What happens to the heart when there is hypothermia

A

decreases heart rate

63
Q

4 ways how hyperkalemia can decrease cardiac performance

A

partially depolarizes the cell membrane, causing the membrane potential to be less negative. which decreases the intensity of the action potential

Decreases the resting membrane potential in the cardiac muscle fibers

block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle.

causes the heart to become dilated and flaccid and slows the heart rate.

64
Q

What are cardiac glycosides

A

Positive inotropic agents (eg. digitalis, quabain)

65
Q

What is the mechanism by which positive inotropic agents act

A

inhibition of Na+-K+ ATPase