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CVPR: CV Unit I > Heart as a Pump > Flashcards

Heart as a Pump Flashcards

1
Q

Cardiac output definition

A

volume of blood pumped per minute by left ventricle

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2
Q

Stroke volume definition

A

volume of blood pumped per beat of heart

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3
Q

Cardiac output =

A

=heart rate (HR) x stroke volume (SV)

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4
Q

Pressure changes occurring at end of diastole

A

-atrium is filled with blood and contracts –> increase in pressure in both atrium and ventricle

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5
Q

Phases of cardiac cycle (from L side perspective)

A
  1. atrial systole
  2. isovolumic contraction
  3. ejection into aorta
  4. isovolumic relaxation
  5. rapid inflow
  6. diastasis
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6
Q

Pressure changes during isovolumic contraction

A
  • both mitral and aortic valve are closed

- ventricle begins to contract –> blood has no place to go –> dramatic increase in pressure

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7
Q

Pressure changes during ejection

A
  • ventricular pressure exceeds aortic pressure –> aortic valve opens –> blood into aorta
  • ventricle begins to relax –> decreased pressure in ventricle
  • aortic valve closes when pressure in ventricle drops below aorta
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8
Q

Pressure changes during isovolumic relaxtion

A
  • ventricle continues to relax w/both valves closed –> decreasing pressure
  • mitral valve opens when ventricle pressure drops below atrial pressure
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9
Q

End-diastole Pressure-Volume Relationship

A
  • Pressure-volume relationship during filling of heart BEFORE contraction. Determined by passive elastic properties of ventricle (inverse of compliance).
  • Slope of EDPVR is shallow in normal physiological range – there is not much change in pressure w/ change in volume, normal ventricle is compliant. Some pathologies decrease compliance, making EDPVR steeper, which impairs filling of the ventricle. The slope of the EDPVR steepens at very high volumes.
  • The end-diastolic PVR represents the PRELOAD on the heart.
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10
Q

Systolic Pressure-Volume relationship

A
  • Pressure - volume relationship at the peak of isometric contraction
  • Maximum pressure that can be developed by the ventricle for a given set of circumstances (see below)
  • Much steeper than EDPVR – pressure increases a lot even at low volume (ventricle is contracting).
  • Systolic PVR includes the passive properties of the heart (ie, includes the diastolic pressure-volume relationship
  • related to concept of afterload
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11
Q

Afterload definition and analogy

A
  • Afterload=load against which the muscle contracts (for left ventricle = ~aortic pressure)
  • Analogy = small weight (preload) PLUS large weight lifted off table. Muscle contracts with force equal to both.
  • For the ventricle, the pressure developed during a contraction (at the end systolic volume) depends on the afterload (approximately the aortic pressure, strictly defined as wall stress during contraction).
  • Increased afterload increases the pressure with which the ventricle must contract to eject blood.
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12
Q

Active tension definition

A

-difference in force between peak systolic pressure and end diastolic pressure curves, -tension developed by the contraction itself, independent of the preload.

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13
Q

Starling curve definition

A

-plot of cardiac performance (such as active tension or CO or SV) as a function of preload (such as length or EDV)

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14
Q

Statements of Starling’s Law (3)

A

a) Heart responds to an increase in EDV by increasing the force of contraction. (i.e., ventricular output/active tension increases as the end diastolic volume increases).
b) Healthy heart always functions on the ascending limb of the ventricular function curve
c) What goes in, must come out. Cardiac output MUST equal venous return and cardiac output from left and right ventricles MUST match (on average).

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15
Q

Molecular basis for Starling’s Law (3)

A

a) Cardiac titin isoform is very stiff, resists stretch.
b) Ca2+ sensitivity of myofilaments increases as sarcomeres are stretched. So the same intracellular Ca2+ produces a greater force of contraction.
c) Closer lattice spacing – stretched sarcomeres have altered spacing between actin & myosin which results in more force generated per crossbridge.

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16
Q

“a wave” definition

A

-slight bump in atrial and ventricular pressure that corresponds to atrial contraction

17
Q

Cardiac cycle on PV loop diagram

A
  1. Filling phase (A to C):
    - beginning of diastole, when the mitral valve opens (point A). The volume is the END SYSTOLIC VOLUME (ESV).
    - Note that ESV is NOT ZERO.
    - During diastole, the ventricular volume increases as blood flows into the left ventricle from the left atrium.
  2. Isovolumetric contraction phase (C to D):
    - At point C, the ventricle begins to contract
    - mitral valve is pushed closed & aortic valve is still closed
    - constant volume during this phase is the END DIASTOLIC VOLUME (EDV), which is the maximum reached at the end of filling
  3. Ejection phase (D to F):
    - left ventricular pressure exceeds the aortic diastolic pressure, the aortic valve is pushed open and the ejection phase begins (point D).
    - At first the pressure continues to increase (up to point E), as the blood cannot leave the aorta as fast as it is entering
    - myocytes in the ventricle stop contracting, the ventricular pressure begins to fall (E to F).
  4. Isovolumetric relaxation phase (F to A):
    - ventricular pressure < aortic pressure, the aortic valve closes (point F).
    - both valves are closed, so the ventricular volume is constant
    - ventricular pressure falls below the atrial pressure, the mitral valve opens and filling begins again (point A).
18
Q

Blood pressure measurements on PV loop diagram

A

o End diastolic pressure at point D (~80 mm Hg)
o Peak systolic pressure at point E (~130 mm Hg)
o Difference = pulse pressure (~ 50 mm Hg)

19
Q

Stroke volume measurements on PV loop diagram

A

o SV = EDV - ESV

o e.g. EDV ~ 120 ml, ESV ~ 50 ml, so SV ~ 70 ml

20
Q

Ejection fraction measurements on PV loop diagram

A

o The fraction of the EDV ejected during systole.
o EF = SV/EDV = (EDV – ESV) / EDV
o e.g. EF = 70/120 = 58%
o Normal ejection fraction ~ 50-70%, reduced in systolic heart failure

21
Q

Stroke work measurements on PV loop diagram

A

o Stroke work = energy per beat (in Joules), corresponds to the area inside the PV loop diagram
o NOT the same for left & right sides of heart, as systemic circulation has higher pressure, so left heart does more work

22
Q

Factors that affect preload (EDV)

A

o Blood volume (IV fluid, hemorrhage)
o filling pressure (venous blood pressure)
o filling time (reduced at high heart rates)
o resistance to filling (e.g., right atrial pressure, AV valve stenosis)
o resistance to emptying = afterload (e.g., hypertension, pulmonic or aortic stenosis; see below)
o reduced inotropy

23
Q

Effect of decreased compliance

A
  • Decreased compliance causes lower EDV at any given pressure
  • hypertrophy/stiffness –> decreased compliance
24
Q

Compliance definition

A

=ΔV/ΔP

25
Q

Effect of increased preload (increase EDV)

A

o The immediate effect is an increase in stroke volume via Starling’s law (i.e., the heart contracts with more force because sarcomere length is increased).
o The ventricle matches the stroke volume to compensate for an increase in venous pressure on a beat-to-beat basis. Thus, the same ESV is achieved and ejection fraction is increased.
o Note that stroke work is also increased (area inside curve).
o On subsequent beats, SV returns to normal since ESV and contractility are unchanged

26
Q

Factors that determine afterload

A
  • aortic pressure is the major determinant of afterload for the left ventricle
  • pulmonary artery pressure is the main source of afterload for the right ventricle.
  • Wall thickness and ventricular radius also affect afterload: Law of LaPlace (T=(P*r)/u), which shows that wall stress (T) increases as radius (r) increases and wall thickness (μ) decreases, for example in dilated cardiomyopathy.
27
Q

Inotropy definition/regulation

A
  • intropy=strength of contraction at any given preload and afterload (i.e., independent of fiber length, and therefore independent of the Frank-Starling response).
  • regulated by nervous and humoral agents, esp. sympathetic stimulation
28
Q

Effects of increased intropy

A
  • increase in stroke volume and ejection fraction

- decrease in end systolic volume

CVPR: CV Unit I (28 decks)

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