Heller Ch. 3 Flashcards

1
Q

P wave

A

Atrial depolarization

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2
Q

QRS complex

A

Ventricular depolarization

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3
Q

T wave

A

Ventricular repolarization

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4
Q

Aortic pressure

A

Diastole: 80mmHg
Systole: 120mmHg

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5
Q

Left ventricular volume

A

End-Systole: 60mL

End-Diastole: 120mL

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6
Q

Right atrial pressure

A

A wave: contraction
C wave: tricuspid valve ballooning
V wave: Isovolumetric filling

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7
Q

Pulmonary artery pressure

A

Diastole: 10mmHg
Systole: 25mmHg

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8
Q

Valve changes

A

Valve placement is determined by pressure

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9
Q

Sounds

A

Caused by valve closure (AV valves or aortic/pulmonic)

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10
Q

Incisura (dicrotic notch)

A

Dip in aortic pressure caused by a small volume of blood filling the aortic leaflets as the valve closes

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11
Q

S1 sound

A

Closure of AV valves
Immediately after QRS complex
Heard best at the apex

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12
Q

S2 sound

A

Closure of aortic/pulmonic valves
At the end of T wave
Physiological splitting of the second heart sound–the pulmonic valve will lag behind the aortic (particularly with inspiration)

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13
Q

S3 sound

A

Does NOT usually happen
Happens shortly after S2…called ventricular gallop rhythm
During rapid passive ventricular filling
Can be normal in children…otherwise indicates left ventricle failure

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14
Q

S4 sound

A

Does NOT usually happen
Happens shortly before S1…called atrial gallop rhythm
Associated with atrial contraction and rapid active filling of the ventricle
Indicates an increased ventricular diastolic stiffness…can occur with several cardiac disease states

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15
Q

Left ventricle cycle

A
Mitral valve opens-->
Diastolic filling (passive stretch)-->
Reaches end-diastolic volume (length)-->
Isovolumetric contraction (Isometric tension development)-->
Aortic valve opens-->
Ejection (shortening)-->
Reaches end-systolic volume (length)-->
Isovolumetric relaxation (Isometric relaxation)
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16
Q

Cardiac index

A

Cardiac output corrected for the individual’s size…more by surface area than weight

17
Q

Larger end-diastolic volume

A

Larger stroke volume

Peak isometric tension initially increases slower than resting tension

18
Q

Larger afterload (HTN or aortic valve obstruction)

A

Smaller stroke volume

There is less shortening

19
Q

Myocardial substrate use during basal metabolism

A

25%

20
Q

Myocardial substrate use during isovolumetric contraction

A

50%
Depends on afterload
Related more to isometric wall tension development than to intraventricular pressure development

21
Q

Stroke work

A

Pressure x volume

Pressure work adds up more than volume work

22
Q

Heart Rates effect on substrate consumption

A

One of most important determinants

It is better energetically to have a lower HR and an higher SV than the opposite

23
Q

Lusitropic

A

Relaxation rate

24
Q

5 effects of NE

A

Positive chronotropic effect (increases i[f])
Decreases duration (earlier i[K])
Positive dromotropic effect (alters conductivity of gap-junctions)
Positive inotropic effect (activates i[Ca++])
Positive lusitropic effect (increases SR reuptake of Ca++)