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Cardiac Physiology and Diseases > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

What is the Ligamentum Arteriosum?

A

remnant of ductus arteriosus

closes shortly after birth

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2
Q

Name the 3 vessels that drain into the right atrium.

A
  1. SVC
  2. IVC
  3. Coronary sinus
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3
Q

Fossa ovalis

A

where the foramen ovale used to be

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4
Q

chordae tendineae

A

anchor the AV valves to the ventricular papillary muscles

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5
Q

trabeculae carneae

A

muscular projections of the ventricles

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6
Q

T or F: Cardiac myocytes can regenerate

A

false

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7
Q

Effect of volatile anesthetics on cardiac function?

A

depress cardiac contractility

decreased entry of Ca++ into cells during depolarization

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8
Q

Effect of N20 on cardiac function?

A

dose-dependent decrease in contractility

reduced availability of intracellular Ca++ during contraction

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9
Q

Effect of local anesthetics on cardiac function?

A

depress contractility

reduced Ca++ influx and release in dose-dependent fashion

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10
Q

Effect of acidosis on cardiac function?

A

depress contractility

blocks slow Ca++ channels

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11
Q

Effect of phosphodiesterase inhibitors on cardiac function?

A

increase contractility
prevent the breakdown of intracellular cAMP, allowing for continued recruitment of open Ca++ channels

ex: Milrinone

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12
Q

Effect of Digitalis on cardiac function?

A

increases contractility

increases intracellular concentration

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13
Q

Anesthetic-induced cardiac depression is potentiated by

A

hypocalcemia, BB, and CCB

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14
Q

innervation: primary regulation of HR and BP

A

Medulla

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15
Q

innervation: secondary regulation: what regulates CV response to changes in temp?

A

hypothalamus

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16
Q

innervation: what adjusts cardiac rxn to a variety of emotional states?

A

cerebral cortex

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17
Q

Baroreceptors

A

carotid sinus- hering nerve
aortic arch- vagus nerve

signals are conveyed to afferent receptive regions of the medulla through the Hering and vagus nerves–> activation of baroreceptors leads to drop in BP

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18
Q

where are the chemoreceptors located?

A
  1. ) carotid bodies- sit on carotid sinus ( where CCA bifurcates into ICA and ECA)
  2. ) aortic bodies- sit on aortic arch
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19
Q

Brainbridge Reflex

A

an increase in the the CVP and RA volume is noted by stretch receptors (baroreceptors) in the atria–> HR INCREASES

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20
Q

Innervation: which fibers primarily innervate the atria and conducting tissues?

A

parasympathetic

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21
Q

ACh acts on which receptors to produce negative effects? and what are those effects? (3)

A

muscarinic receptors (M2)

Depressed chronotropy, inotropy, and dromotropy.

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22
Q

dromotropy

A

conduction velocity of AV node

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23
Q

lusitropy

A

relaxation of myocardium

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24
Q

where do sympathetic fibers innervate the heart?

A

all over

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25
Q

where do cardiac sympathetic fibers originate?

A

T1-T4

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26
Q

NorEpi release from SNS fibers act primarily on which receptors?

A

B1 adrenergic

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27
Q

where are B2 receptors located in the heart? what happens when they are activated?

A

primarily the atria

activation increases HR, and to a lesser extent, contractility

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28
Q

Changes in HR with insp/ exp? Why?

A

Lung’s vagal fibers are stretched (activated) during inspiration, thus inhibiting the cardioinhibitory center of the medulla–> allows unopposed sympathetic acceleration of HR

expiration–> decrease HR

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29
Q

Baroreceptor Reflex

A

mediated by baroreceptors in the aortic arch and carotid sinus

increased rate of discharge when stretched (increased BP)

neural impulses travel to the medulla

medulla initiates increase in PNS activity:

 1. vasodilation
 2. HR decreases

if patient is HYPOtensive, the reflex causes inc. HR and vasoconstriction

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30
Q

Baroreceptor Reflex: more effective for hyper- or hypotension?

A

more effective at compensating for hypotension

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31
Q

Most important determinant of myocardial blood flow?

A

myocardial O2 demand

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32
Q

Relative contributions to O2 requirements:

A

basal requirements- 20%
electrical activity- 1%
volume work- 15%

PRESSURE WORK- 65%

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33
Q

what percentage of O2 does the myocardium extract from arterial blood?

A

65%

so, myocardium cannot compensate for reductions in blood flow by extracting more O2 from Hgb!

most other tissues only extract about 25% 02 from arterial blood

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34
Q

How must the myocardium meet increased O2 demand??

A

must increase coronary blood flow

already extracts 65% O2 from arterial blood, cannot just increase extraction percentage

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35
Q

How can the heart increase coronary blood flow?

A

increase time in diastole by decreasing HR

increase aortic diastolic pressure–> increase coronary filling pressure

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36
Q

Coronary perfusion pressure equation

A

CPP= aortic DBP- LVEDP

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37
Q

what effect does HR have on CPP?

A

increases in HR decrease CPP bc of disproportionately greater reductions in diastolic time as HR increases

38
Q

Oxygen content equation

A

CaO2= 1.36 mL O2/ gm Hb x SaO2/ 100 + 0.0031 mL O2/ (mmHg) dL x PaO2 (mmHg)

39
Q

How to AS, MR, and decreased coronary diameter affect CPP and myocardial O2 supply?

A

all decrease supply by worsening blood flow to coronaries

40
Q

what effect does increased preload have on myocardial O2 demand? afterload?

A

both will increase oxygen demand by increasing wall tension

41
Q

Cardiac Output equation

A

CO= HR x SV

42
Q

normal cardiac output

A

5-7 L/ min

43
Q

cardiac index equation

A

CI= CO/ BSA

compensates for variations in body size
BSA (m^2)= square root of (wt (kg) x ht (cm)/ 3600)

44
Q

normal cardiac index

A

2.5- 4.2 L/ min/ m^2

45
Q

normal mixed venous oxygen saturation

A

65-75%

46
Q

where do you measure mixed venous oxygen saturation? and why do you need it?

A

pulmonary artery

helpful in assessing the adequacy of CO- are the tissues being perfused?

a decrease in mixed venous O2 saturation in response to increased demand (exercise, sepsis, etc.) usually reflects inadequate tissue perfusion

47
Q

In the absence of hypoxia or severe anemia, what measurement is the best determination of adequacy of CO?

A

mixed venous oxygen saturation

48
Q

T or F: Lactic acid can be used to indirectly assess CO

A

T

lactic acid is a byproduct of anaerobic metabolism

49
Q

normal intrinsic rate of the SA node

A

60-100 bpm

brady for peds- 100

50
Q

cardiac myocytes are oriented ___________ in the ventricular wall

A

circumferentially

51
Q

Law of LaPlace

A

Tension is proportional to Pressure x radius

T prop. P x r

states the physical relationship between wall tension and internal pressure within a circular structure

52
Q

The Frank-Starling Law

A

increased preload–> increased SV

as the heart fills with more blood, the force of the contractions will increase.. to a certain point

stretching of the muscles fibers increases the affinity of troponin C for Ca++

a greater number of cross bridges form within the muscle fibers, thus increasing contractile force

53
Q

what 3 factors affect stroke volume?

A

Preload
Afterload
Contractility

54
Q

preload

A

muscle length prior to contraction

LVEDP

55
Q

afterload

A

tension against which the muscle must contract

56
Q

T or F: Contractility is independent of preload and afterload

A

T

increased by nervous, humoral, and chemical influences

57
Q

Ventricular filling is influenced by:

A
  1. venous return
  2. HR
  3. heart rhythm
58
Q

with an increase in HR, does systole or diastole show a greater reduction in time?

A

diastole

ventricular filling impaired at HR > 120 in adults

59
Q

how do atrial arrhythmias affect vent. filling?

A

reduce vent. filling by 20-30% due to loss of atrial kick.

absent (a-fib)
ineffective (a-flutter)
simultaneous atrial and vent. contraction (junctional rhythm)

60
Q

normal CVP

A

2-8 mmHg

61
Q

how to use CVP

A

useful to monitor TRENDS in CVP as an indicator of preload and volume status

NOT a definitive measure of volume

62
Q

How can patient positioning affect CVP?

A

reverse T-berg–> lowers CVP due to venous pooling in BLE

T-berg–> increases CVP

no actual change in volume status

63
Q

what cardiac pressure does CVP most closely approximate?

A

RVEDP

64
Q

what 6 factors affect CVP/ Preload?

A
  1. ) blood volume- 2/3 of EBV is in the venous system, so the greater the volume, the greater the pressure
  2. ) gravity- redistributes about 500mL of blood from intrathoracic vessels into BLE
  3. ) peripheral venous tone- controlled by SNS
  4. ) muscle pump- repeated compression of the deep veins of the limbs displaces venous blood centrally to increase CVP
  5. ) spontaneous respiration- produces negative intrathoracic pressure and positive intra-abdominal pressure, which increases the venous pressure gradient and promotes filling of the central veins
  6. ) CO- pumping action- decreases CVP by transferring venous blood to arterial system. If uncorrected, the fall in CVP and rise in afterload can lead to heart failure.
65
Q

what fraction of blood is in the venous system?

A

2/3

66
Q

When is the effect of the venous muscle pump lost?

A

when patient is paralyzed

67
Q

T or F: the left and right hearts have equal output

A

true

68
Q

LVEDP = LVEDV

A

assumes normal LV compliance

69
Q

LAP approaches LVEDP

A

assumes normal mitral valve function

70
Q

PCWP = LAP

A

assumes normal airway pressures and PulmVR

71
Q

How do we estimate LVEDP?

A

use PA catheter to measure PCWP

72
Q

equation for SVR

A

SVR= (80 x (MAP-CVP))/ CO

73
Q

normal SVR (arterial impedence to ejection)

A

900-1500 dyn x sec x cm^-5

74
Q

equation for PVR

A

PVR= (80 x (PAP-LAP))/ CO

75
Q

normal PVR (pulmonary)

A

50-150 dyn x sec x cm^-5

76
Q

what has the most important effect on contractility?

A

SNS activity

77
Q

which cardiac tissues does the SNS innervate?

A

atria
ventricles
nodes

78
Q

SNS release of NE in heart does what?

A

NE release enhances contractility via B1 activation

this also increases HR

79
Q

what other 2 factors other than SNS activity affect cardiac contractility and HR?

A

release of EPI from adrenal glands

sympathomimetic drugs

BOTH increase contractility and HR via B1 activation!

80
Q

which cardiac receptors affect HR and contractility?

A

B1

81
Q

what effect does acidosis have on contractility?

A

decrease

82
Q

how can we assess systolic function?

A

LVEF

83
Q

LVEF equation

A

LVEF= (LVEDV- LVESV)/ LVEDV

84
Q

how can we assess diastolic function?

A

Doppler ECHO

85
Q

hypokinesis

A

decreased contraction

86
Q

akinesis

A

failure to contract

87
Q

dyskinesis

A

paradoxic bulging

88
Q

how does stenosis of either AV valve affect stroke volume?

A

decreases ventricular filling/ preload and thus decreases SV

89
Q

how does stenosis of either semilunar valve (pulmonic or aortic) affect SV?

A

increases afterload and thus decreases SV

90
Q

how does regurge affect SV?

A

AV regurge- part of end diastolic volume flows back toward atria during systole

semilunar regurge- part of EDV flows back into ventricle during systole

Cardiac Physiology and Diseases (2 decks)

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