Garman CV3- Mechanical Flashcards

1
Q

Range of normal systolic pressure PA?

A

15-30

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2
Q

Range of normal diastolic pressure PA?

A

3-12

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3
Q

Mean pressure PA?

A

14 mmHg

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4
Q

Range RA pressure? Mean RA pressure

A

0-8 mmHg, NO variation 4 Mean

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5
Q

Systolic range and mean for RV pressure?

A

Systole 15-28 mmHg, Mean 24 mmHg

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6
Q

End diastolic range of pressure RV?

A

0-8 MMhG Mean 4 mmHg

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7
Q

Aortic systolic range?

A

90-140mmHg

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8
Q

Aortic diastolic range?

A

60-90mmHg

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9
Q

Mean aortic pressure?

A

120

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10
Q

LA range pressure?

A

4-12mmHg (no systolic/diastolic range) Mean 8 mmhg

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11
Q

LV Systolic range? Mean?

A

90-140 Mean 130

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12
Q

LV End diastolic range? Mean?

A

7 mmHg

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13
Q

When does mitral valve close in cardiac cycle?

A

Beginning of isovolumetric contraction (Force of ventricular contraction causes blood to push back on AV valve, causing closure)

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14
Q

What happens when mitral valve closes?

A

S1 sound “lubb”

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15
Q

When does aortic valve open?

A

End of isovolumetric contraction.

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16
Q

What electrical event happens right before mitral valve closes?

A

R-wave. (Ventricular depolarization causing ventricular contraction and mitral valve to close)

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17
Q

When does aortic valve close?

A

Beggining of Isovolumetric relaxation Why? Pressure in ventricle begins to decrease during ventricular repolarization (after T wave). Pressure is less in ventricle than aorta, blood flows backward, closing aortic valve.

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18
Q

What happens when aortic valve closes?

A

S2 “dubb” closure of semilunar valves

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19
Q

How many valves are open in the heart during isovolumetric relaxation?

A

0 valves open. (i.e. isovolumetric)

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20
Q

What other time in cardiac cycle are all vavles close?

A

Isovolumetric contraction (no blood leaving heart= all valves closed)

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21
Q

When does mitral valve open?

A

At end of isovolumetric relaxation. Pressure is now lower in ventricle than atria, mitral valve is allowed to open and blood passively fills ventricle.

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22
Q

What happens after mitral valve opens?

A

Blood “rushes into” ventricle causing rapid ventricular filling (rapid passive filling)

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23
Q

What creates S3 sound?

A

Rapid ventricular filling AKA Diastolic filling (from blood sloshing against walls of heart) Can typically only hear in young children.

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24
Q

What happens at a-wave in left atrial pressure waveform?

A

Atrial contraction (after P wave on EKG)

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25
Q

What happens at c wave on left atrial pressure waveform?

A

Bulging back of mitral valve into atrium from ventricle d/t pressure from ventricular contraction

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26
Q

What happens at V wave on left atrial pressure?

A

Ventricular relaxation. Blood beings to flow into ventricle causing decrease in LA pressure

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27
Q

As the blood rushes back into ventricle during vectricular relaxation, does some blood go into LV from aorta?

A

Yes. Small amount causing slight negative deflection in aortic blood flow waveform

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28
Q

What causes S4 on heart sounds?

A

Atrial contraction. Always pathologic

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29
Q

What represents ventricular systole on ekg?

A

R-T

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30
Q

What causes a, c, v wave on venous pulse waveofrm?

A

a- atrial contraction c- mitral valve bulging back v- ventricular relaxation (filling) after atrial filling

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31
Q

What marks closure of AV valves?

A

S1 “lubb”

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32
Q

What marks closure of semilunar valves?

A

S2 “dubb”

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33
Q

What happens if S3 present?

A

Rapid passive filling of ventricle. Normally not heard in adults May be present in children and endurance athletes

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34
Q

What happens at S4?

A

Atrial systole ALWAYS pathological if heard

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35
Q

What is a murmur?

A

Gugling sound made as blood moves through a damaged valve

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36
Q

What is a buirt?

A

Abnormal sound as blood runs past obstruction in arteries

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37
Q

When is jugular venous pulse useful?

A

Diagnosis of heart disease

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38
Q

Why can you see jugular venous pulse?

A

No valve separating RA from central venous space. Seeing backpressure of blood flow

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39
Q

What does SV equal?

A

LVEDV- LVESV Amount of blood left at end of diastole (when ventricle filled)- amount of blood left at end of systole (when ventricle is emptied)

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40
Q

What is compliance defined to be?

A

change in V/change in P

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41
Q

The more ____ aorta is, the greater compliance

A

elastic

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42
Q

During diastole, the aorta ____

A

recoils

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43
Q

What helps maintain pressure during distole?

A

Diastolic recoil

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44
Q

Where does the stroke volume go during systole?

A

Into distention of the aorta, blood goes forward.

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45
Q

Aging generally results in a decrease in aortic _____ and _____

A

elasticity and compliance

46
Q

Decrease in elasticity and compliance leads to increase in ____ _____

A

pulse pressure

47
Q

What happens to PP with decreased HR?

A

Increase in PP and it is not a sign of stiff arteries. Heart just has more time to fill, so therefore high SV, higher PP

48
Q

What does arterial wave form look like in aortic insufficiency

A

Blood is going back into ventricle during systole, therefore LV is becoming more filled each time. Heart ejecting more blood each time, therefore higher pressure generated. Systolic pressure also drops faster than normal since blood is able to go back into LV Diastolic pressure drops because of incompetent valve

49
Q

What happens to arterial pressure waveofrm in arterosclerosis?

A

D/t hardening of arteries, when you eject, a higher systolic pressure is required. Also causes higher diastolic pressure. Makes heart work harder and harder for heart to oxygenate cardiomyocytes as well.

50
Q

What influences SV?

A

Preload (EDV) Contractility Afterload (SBP)

51
Q

Equation for CO?

A

HR(mL/beat) X (EDV-ESV) (beats/min)

52
Q

What makes up autonomic nervous system?

A

Sympathetic innervation, parasympathetic innervation

53
Q

What plays a role in sympathetic innervation

A

Norepinephrine/epinephrine Receptors- beta 1 response Positive chronotropic effect

54
Q

What happens with parasympathetic innervation?

A

Acetylcholine Receptor: muscarinic ach M2 receptor Negative chronotropic effect

55
Q

What is ejection fraction?

A

SV/EDV or (EDV-ESV)/EDV

56
Q

What is normal EF of normal heart?

A

>0.5 (50%)

57
Q

Force of contraction is a function of what?

A

Number of cross-bridges formed

58
Q

What are 2 different mechanisms the heart can increase cross-bridge formation?

A

1) Frank-starling law of heart 2) Contractility

59
Q

How does frank-starling law of heart influence cross bridge formation?

A
  • Increasing functional overlap of myosin and actin Preload-greater filling stretches myocytes–> stronger contraction (until the myosin/actin is expanded too much)
60
Q

How does hte heart increase contractility?

A

Increasing Ca++ in cardiomyocytes normally through SNS activation. E -Epinephrine increases Ca influx -Parasympathetic does not affect contracility. Either heart increases contractility or it contracts at normal strength.

61
Q

Ventricular pressure above _____ doesn’t increase CO and results in slow decline in CO

A

12 mmHg

62
Q

What is mean circulatory pressure when heart is stopped?

A

7 mmHg

63
Q

What does vascular function curve show?

A

Inverse relationship between CO (independent variable) and CVP (dependent variable)

64
Q

What is cardiac function curve

A

Direct relationship between CVP (independent) and CO (dependent) (frank-starling mechanism)

65
Q

What is found by plotting both vascular function curve and cardiac function curve?

A

Resting equilibrium point

66
Q

What is the x-intercept of volume function curve

A

Mean circulatory pressure

67
Q

Which curve moves when the volume status is changes?

A

Vascular function curve

68
Q

Which curve moves when contractility is changed?

A

Cardiac function curve

69
Q

Why does preload decrease with higher CO?

A

Moving more blood, so less left in heart

70
Q

What does increase resistance cause?

A

Accumulation blood on arterial side

71
Q

What is equation for SVR?

A

MAP/CO

72
Q

What does this cardiac pressure volume loop show a change in?

A

Green is decrease in preload

Grey is normal

Red is increase in preload

73
Q

What does this cardiac pressure volume loop show?

A

Green is decrease inotropy

Red is increase inotropy

Grey is control

74
Q

What does this cardiac pressure volume loop show?

A

Green= decrease afterload

Red= increase afterload

75
Q

What effect does increase HR have on cardiovascular system?

A

Increase CO

Increase BP

76
Q

Increased contractility has what effect on heart?

A

Increase contractility–> increase EF, Increase CO, Increase BP

77
Q

What does increase SVR do to cardiovascular system?

A

Increase SVR (constrict artery)–> Decrease CO but Increase BP

78
Q

What does incrase CVP do to cardiovascular system?

A

Increase CVP (constriction veins)–> Increase LVEDV, Increase SV, Increase CO, Increase BP

79
Q

What factors influence venous return?

A

1) Skeletal muscle activity
2) Blood volume
3) Changes in peripheral circulation

80
Q

What influences preload

A

1) Venous return
2) Filling time (limiting factor for HR)

81
Q

What influences contractility

A
  • Autonomic innervation
  • Hormone
82
Q

What influences End-Diastolic volume

A

Preload

83
Q

What influences end-systolic volume?

A
  • Contractility
  • preload
  • Afterload
84
Q

What influences afterload?

A

Vasoconstriction and vasodilation

85
Q

What influences HR

A
  • Atrial reflex—> autonomic innervation
  • Hormones
86
Q

What are baroreceptors?

A
  • Respond to changes in stretch
  • Increased stretch–> increased firing of sensory nerves
  • Decreased stretch–> decreased firing of sensory nerves
87
Q

Where are baroreceptors located?

A
  • Wall of aortic arch–> sensory nerve: vagus nerve
  • Carotid sinues–> sensory nerve: Glossopharyngeal nerve
88
Q

What is the Nucleus tractus solitarii

A

CV center of the brain in the medulla

89
Q

What does the NTS do?

A
  • Take information from baroreceptors
  • If BP needs to lower, cardioinhibitory center is activator–> activate parasympathetic to decrease HR via SA node
  • If BP needs to increase, vasomotor center is activated, activating sympathetic nervous–> increase HR, contractility, constrict arterioles and veins.
90
Q

What is role of atrial natruretic peptide?

A
  • ANP is released in response to atrial stretch from increased atrial pressure
  • ANP dilates some vessels and has important effects on sodium and water balance, and long term regulation of blood pressure
91
Q

What is the Renin-angiotensin-aldosterone system?

A
  • RAAS
  1. Renal juxtaglomerular cells sense decrase in BP and release renin
  2. Renin activated angiotensinogen to angiotensin I
  3. Angiotensin I converted to angiotensin II via angiotensin-converting enzyme (ACE) in lung
  4. Angiotensin II promotes vasoconstriction and stimulates aldosterone secretion from adrenal cortex resulting in…
  5. Renal sodium and water retention and an increase in BP
92
Q

What is MAP?

A

COx TPR (total peripheral resistance (or SVR))

93
Q

What does renin activate?

A

Activates angiotensinogen from liver to angiotensin I

94
Q

What is angiotensin I’s role in RAAS?

A

Concerted to angiotensin II via angiotensin-converting enzyme (ACE) in lung

95
Q

What is angiotenin II’s role in RAAS?

A

Promotes vasoconstriction and stimulates aldosterone secretion from adrenal cortex.

96
Q

What is aldosterone’s role in RAAS?

A

Promote renal sodium and water retenstion to cause incrase in BP

97
Q

What are effector organs for angiotensin II?

A
  • Blood vessels
  • Heart
  • Adrenal cortex
  • Hypothalamus
98
Q

What is effect of AngII on blood vessels?

A

vasoconstriction causing increase SVR

99
Q

What is effect of Ang II on heart?

A

Increase CO

100
Q

What is effect of Angi II on adrenal cortex

A

Aldosterone release increase Na reabsorption by kidney

101
Q

What is effect of Angio II on hypotehalamus?

A

Minor increase in ADH release: increase water reabsorption by kidney

102
Q

What are stimuli for renin relase?

A
  • Decrease in BP (stretch receptors in kidney tubules “renal baroreceptors”
  • Sympathetic activation (tubules innervated with sympathetic nerves)
  • Decreased flow of sodium through kidney tubules
103
Q

What are effects of ANP?

A
  • Increased sodium excretion
  • water excretion
  • vascular smooth muscle relaxation (vasodilation)
  • blocking ADH, aldosterone, NE

Increased blood in atria–> increased atrial stretch–> increased ANP release–> increased sodium and water excretion–> decrease blood volume

THIS IS ONLY BACKUP. Should not happen day-to-day

104
Q

What are chemoreceptor reflexes?

A
  • Specialized receptors in carotid sinus and aortic arch
    • respond to pH levels in blood
    • Eleveated co2= decrease in pH
  • If high CO2 detected, increase cardioacceleratory centers stimulated, vasomotor centers stimulated and cardioinhibitory centers inhibited
    • this causes increase in CO, BP and vasoconstirciton in order to decrease CO2
105
Q

What is myocardium innervated by?

A

Sympathetic nerves

106
Q

What are SA node and AV nodes innervated by?

A

Both sympathetic and parasympathetic nerves

107
Q

Autonomic efferent activity is regulated by _____ reflux

A

baroreceptor

108
Q

Arterial and venous vessels throughout body are innervated by ________

A

sympathetic nerves

109
Q

Which systems are quicker in regulatin BP (short-term response)

A

Baroreceptors

Chemoreceptors

CNS ischemic response

110
Q

What are all the systems activated in response to low blood volume?

A
  • Increase thirst
  • Increase ADH
  • Increase sympathetic nerve activity–> increase renin–> RAAS system activation
  • Increase aldosterone (Na retnetion)
111
Q

What is response to increased blood volume?

A
  • Decrease ADH
  • Decrease sympathetic activity
  • decrease renin and angiotensin II by kidney
  • adrenals decrease aldosterone
  • ANP release causes increase in NaCl and H2O excretion
112
Q
A