Lectures 28-30 Flashcards

1
Q

Cardiac Performance

A

how well the heart pumps blood to organs of the body

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2
Q

Stroke Volume

A

Volume of blood ejected with each contraction

SV = EDV - ESV

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3
Q

SV =

A

EDV - ESV

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4
Q

Cardiac Output

A

blood flow per unit time

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5
Q

CO =

A

SV - HR

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6
Q

Cardiac Index

A

cardiac output divided by the body surface area (to compensate for larger individuals with a greater CO)

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7
Q

Stroke Work

A

amount of work the heart does during a SINGLE contraction

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8
Q

SW =

A

VPP x SV

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9
Q

Left and Right SV and CO is equal physiologically

A

bc its a closed-system, whatever is pumped out of left ventricle must enter the Right atrium

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10
Q

Right SW is not equal to the Left SW

A

bc pressure on the left is much greater than the pressure on the right

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11
Q

Aortic stenosis effect on SW

A

increased SW, but same SV, meaning increased workload but no change in blood perfusion to organs

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12
Q

What 4 factors contribute to cardiac performance

A

preload, afterload, contractility,and heart rate

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13
Q

Preload

A

the forces acting to stretch the cardiac muscle to max length prior to contraction (max EDV); resting tension following diastole

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14
Q

Can’t measure fiber length, but we can measure wall tension of the ventricular wall at end of diastole (rest)

A

Tension = pressure (EDV) x radius

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15
Q

Wall tension determines the

A

resting fiber length

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16
Q

Most easily measured by…

A

EDV is used as an indirect measure of preload; increased EDV > increased fiber length > increased wall tension

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17
Q

What factors effect preload and EDV

A

ventricular filling time, ventricular compliance, filling pressure, atrial contractility, and pericardial restraint

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18
Q

Ventricular filling time

A

time for PASSIVE filling to occur

dependent on HR (if HR increases, time for filling decreases leading to decreased EDV and SV)

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19
Q

Ventricular filling time <0.1sec

A

inadequate amount of time for completion of rapid filling, inability to maintain adequate CO due to reduction in SV at very high HRs (HR150)

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20
Q

INcreased sympathetic stimulation

A

increased HR, INCREASED contractility compensates for reduced filling

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21
Q

Compliance

A

distensibility of the heart for expansion of distension

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22
Q

a compliant structure with a LARGE change in volume

A

would have a small change in pressure

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23
Q

Compliance (C) =

A

dV/dP

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24
Q

Decreased compliance (stiff heart)

A

a change in volume will result in an abnormally large change in pressure

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25
Decreased compliance effects filling
affects pressure gradient needed for ventricular filling, limits filling
26
Conditions that cause decreased compliance
ventricular hypertrophy and ischemia (fibrosis)
27
Ventricular filling pressure
more negative intrathoracic pressure, increased central venous return, increased filling of right ventricle, increased SV, increased Left ventricular filling and SV
28
Atrial contractility
smaller effect than EDV factors, bc it accounts for 15-20% of filling, but during decreased filling times (increased HR, exercise) it accounts for 40% and becomes more important. ineffective atrial contraction (Afib) may impede exercise
29
Pericardial Restraint
accumulation of fluid (tamponade) or fibrosis of the pericardium will restrict ventricular filling and reduce compliance
30
Starling's Law of the Heart/Frank-Starling Mechanism
relationship between EDV and ventricular pressure | increased EDV --> increased SV (contraction)
31
Overfilling of the ventricle can cause the contraction to
contraction to decline (less forceful)
32
Starling curve
Length-tension relationship curve; meaning increased EDV (resting fiber length) causes increased SV
33
How positioning effects EDV
supine vs standing vs exercising
34
lying supine and EDV
supine there is very little End diastolic reserve volume and EDV cannot be increased by increasing venous return (EDV doesn't contribute much to cardiac function while lying)
35
Standing and exercising and EDV
plenty of diastolic reserve volume available for increasing EDV
36
Effects of increased preload on pressure-loop curve
wider; increased EDV
37
Effects of increased afterload on pressure-loop curve
taller, skinnier loop; decreased SV for same EDV (needs to generate more pressure to open valves, increases work)
38
Effects of increased contractility on pressure-loop curve
wider, taller loop; increased SV at same EDV
39
Contractility
increased stroke volume occurs from the same EDV
40
Decreased contractility
same EDV but less SV
41
Increased contractility
same EDV but greater SV
42
Contractility is predominately regulated by
the autonomic nervous system
43
Measuring contractility
maximum rate of pressure change during isovolumetric dP/dt HOWEVER Ejection Fraction is more accurate
44
Ejection fraction (EF) =
SV/EDV
45
Normal EF
50-75%
46
Contractile dysfunction indicated by a EF of
40% or less
47
Heart Rate determines cardiac performance by
directly increasing contractility due to Ca influx and increasing CARDIAC OUTPUT
48
Treppe
Increasing HR causes increasing contractility which causes an increase in SV
49
HR and Cardiac Output
Drastically changes CO
50
CO =
SV x HR
51
Stroke Work SW =
LVPP x SV the area of the pressure-volume rectangle
52
Minute work =
SW x HR
53
External Work
Contractile work, area inside pressure-volume loop, work done by heart to eject blood
54
Internal Work
work done prior to the development of pressure against non-contractile elements (maintains conditions in heart)
55
VPP
SYS BP - DIAS BP
56
Volume Work | equal amount of external work gives less O2 consumption
increasing end diastolic volume causes increased external work, to generate a larger SV
57
Pressure Work | equal amount of external work gives less O2 consumption
increasing afterload pressure that leads to heart having to do more work to overcome pressure, increases internal work on heart and doesn't generate a higher SV
58
Cardiac efficiency
EXTERNAL Work performed/ Oxygen Uptake
59
Cardiac efficiency of healthy heart
12-20%
60
Fick's Principle
Measuring Cardiac Output
61
Cardiac Output
Oxygen taken in / (arterial O2 - venous O2)
62
Left heart failure (systolic)
leads to increased pulmonary venous pressure and increased fluid backup to capillaries, PULMONARY EDEMA (congestive heart failure)
63
Heart failure
decreased contractility, increase in EDV restoring SV but does not make up for decreased contractility (accommodation by Starling effect)
64
Coronary artery disease
disruption of oxygen supply to heart muscle, ishemia, heart attack
65
Hypertension
increase in arterial blood pressure (increase in afterload) increasing work, O2 consumption, energy all for the same cardiac output
66
Cardiomyopathy
damage to heart muscle by infection, diabetes, drugs, etc
67
Abnormal Heart valves
Total SV is increased but effective stroke volume is is significantly less (aortic regurgitation)
68
Arryhthmias
interference of normal filling and pumping resulting in inefficient pumping
69
Congenital heart defect
may result in inefficient pumping
70
Heart failure treatment
exercise, weight loss, low Na, surgery, angioplasty, medications
71
diuretics
Lasix - decrease excess fluid
72
Inotropic drugs
increase contractility, enhancing pumping ability of heart - digitalis
73
Vasodilators
reduce afterload and resistance by lowering blood pressure -hydralazine, ACE inhibitors
74
Beta-blockers
block adrenergic receptors, decreased HR and lower BP (blocks sympathetic)