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Apex > Cardiovascular Anatomy And Physiology > Flashcards

Cardiovascular Anatomy And Physiology Flashcards

1
Q

What is the primary determinant of resting membrane potential (RMP)?

A

Serum potassium (K+)

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2
Q

What is the primary determinant of threshold potential?

A

Calcium

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3
Q

How does hypokalemia affect RMP?

A

Decreased serum K+ ~ potassium leaves the cell for the serum, RMP becomes more negative

Cells become more resistant to depolarization

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4
Q

How does hyperkalemia affect the RMP?

A

Increased serum K+ ~ less K+ leaves the cell ~ RMP is increased

More likely to depolarize

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5
Q

How does hypocalcemia affect the threshold potential? (TP)

A

Less calcium ~ TP becomes more negative ~ also unable to stabilize sodium channels

The cells depolarize more easily

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6
Q

How does hypercalcemia affect threshold potential?

A

Increased Ca ~ threshold potential becomes more positive ~ Ca stabilizes the sodium channels more ~ the cells become more resistant to depolarization

Increases the gap between RMP and TP

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7
Q

What is the rest membrane potential for a cardiac myocyte?

A

-90

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8
Q

What happens in phase 0 of the cardiac action potential?

A

Threshold of -70 is reached, depolarization ~ activation of fast voltage gated Na+ channels

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9
Q

What happens in phase 1 of the cardiac action potential?

A

Initial Repolarization: Inactivation of Na+ channels ~ cell becomes more negative (less positive)

Cl- into cell
K+ out of cell

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10
Q

What happens in phase 2 of the cardiac action potential?

A

Plateau: activation of slow voltage gated Ca channels counter loss of K+ conductance ~ delays repolarization ~ maintains fast Na+ channels in inactivated state ~ prolongs absolute refractory period

This sustained contraction is necessary for the hearts pump

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11
Q

What is phase 3 of the cardiac action potential?

A

Final Repolarization: K+ channels open ~ K+ leaves the cell faster than Ca enters —> Repolarization

Restores membrane potential = -90 mV

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12
Q

What is phase 4 of the cardiac action potential?

A

Resting phase: K+ leak channel opens ~ maintain RMP

Na/K-ATPase pump removes 3 Na and gets 2 K

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13
Q

What is the path of conduction in cardiac cells?

A

SA node > internodal tracts > AV node > bundle of His > Left and Right bundle branches > Purkinje Fibers

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14
Q

What is phase 4 of the cardiac nodal cell action potential?

A

Funny channel leakage (membrane is leaky towards Na+) ~ cell becomes more positive ~ at -50 mV, calcium channels (T-type) open to further depolarize cell

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15
Q

What is phase 0 of the cardiac nodal action potential?

A

Depolarization: Ca enters via voltage gated Ca channels (now L-type) ~ depolarization ~ Na and Ca (Type t channels) close

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16
Q

What is phase 3 of the cardiac nodal action potential?

A

Repolarization: K+ channels open ~ K+ exits cell ~ more negative ~ Repolarizes to repeat Phase 4

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17
Q

What is the equation to oxygen delivery?

A

DO2 = CO x (CaO2) x 10

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18
Q

What is a normal oxygen extraction ratio?

A

25%

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19
Q

What is the normal oxygen consumption?

A

250 mL/min or 3.5 mL/kg/min

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20
Q

What is the normal venous content?

A

CvO2= (Hgb x SvO2 x 1.34) + (PvO2 x 0.003) = 15 mL/dL

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21
Q

What is the equation for MAP?

A

MAP = CO x SVR / 80 + CVP

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22
Q

What is Poiseuille’s law?

A

Q = pie-r4-(pressuregradient)/8nL

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23
Q

What does Reynolds number < 2000 predict?

A

Laminar flow

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24
Q

What does Reynolds > 4000 predict?

A

Turbulent flow

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25
Q

What does Reynolds number 2000-4000 predict? LMA

A

Transitional flow

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26
Q

What is the equation for CO? What a normal value?

A

CO = HR x SV

N: 5-6 L/min

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27
Q

What is the equation for cardiac index? And what is a normal value?

A

CO/BSA

N: 2.8-4.2 L/min per m2

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28
Q

What is the equation for SV? What is a normal value?

A

SV = EDV-ESV or CO x 1000/HR

N: 50-110 mL/beat

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29
Q

What is the equation for stroke volume index? What is a normal value?

A

SV/BSA

N: 30-65 mL/beat per m2

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30
Q

What is the equation to determine EF? What is a normal value?

A

EDV - ESV / EDV x 100

N: 60-70%

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31
Q

What is a normal MAP?

A

70-105 mmHg

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32
Q

What is the equation for pulse pressure? What is a normal value?

A

SBP - DBP
N: 40 mmHg

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33
Q

What is the equation to determine SVR? What is a normal value?

A

SVR = MAP - CVP / CO x 80

N: 800 - 1500 dynes

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34
Q

What is the Equation to determine SVR index? What is normal?

A

MAP - CVP/ CI x 80

N: 1500-2400 dynes per m2

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35
Q

What is the equation to determine PVR? What is a normal value?

A

MPAP - PAOP / CO x 80

N: 150 - 250 dynes

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36
Q

What is the equation to determine PVR index?

A

MPAP - PAOP/ CI x 80

N: 250 - 400

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37
Q

What is preload?

A

Ventricular wall tension at the end of diastole (just before contraction)

38
Q

What factors increase contractility?

A

Hypercalcemia
SNS stimulation
Catecholamines
Calcium
Digitalis
Phosphodiesterase inhibitors

39
Q

What factors decrease contractility?

A

Myocardial ischemia
Severe acidosis
Hypercapnia
Hypocalcemia
Hypoxia
Hyperkalemia (doesn’t allow Na channels to repolarize)
Volatile anesthetics
Propofol
Beta-blockers
Calcium channel blockers

40
Q

How does Beta 1 stimulation work increase contractility?

A

Beta 1 ~ activates enzyme adenylate cyclase ~ convert ATP to cAMP ~ cAMP activates PKA ~ PKA does 3 things

  1. Activates more L-type ca channels
  2. Stimulates the ryanodine receptor to release more Ca from SR
  3. Increase SERCA2 receptor activity (increase Ca reuptake, thus increase supply for Ca release)
41
Q

What is the equation to myocardial wall stress?

A

Wall stress = intraventricular pressure x Radius / ventricular thickness

42
Q

What factors are proportional to an increase in myocardial walk stress?

A

Radius, intraventricular pressure

43
Q

What factor is inversely proportional to wall stress?

A

Ventricular Wall thickness

44
Q

When considering the wiggers diagram, what are the two factors included in systole?

A

Isometric ventricular contraction
Ventricular ejection

45
Q

What are key events during isometric ventricular contraction?

A

LV pressure > LA pressure —> mitral valve closes (1st heart sound)

LV pressure builds

LV volume constant (usually both valves are closed during isometric contraction)

46
Q

What are the key events during Ventricular systole?

A

LV pressure > Aortic pressure —> aortic valve opens

Stroke volume is ejected into the aorta
(Most is ejected during first 1/3 of systole)

47
Q

When considering the Wiggers diagram, what components make up diastole?

A

Isometric relaxation
Rapid LV filling
Reduced LV filling
Atrial Systole

48
Q

What are the key events during isometric ventricular relaxation?

A

Aortic pressure > LV pressure —> AV valve closes (2nd heart sound)

LV pressure decreases
LV volume remains constant ( both valves are usually closed at this point)

49
Q

What are the key events during rapid ventricular filling?

A

LA pressure > LV pressure —> mitral valve opens

LV pressure remains constant
LV volume changes
80% of filling happens during this period

50
Q

What are the key events in reduced ventricular filling? (Diastasis)

A

LV filling continues but at a slower rate

51
Q

What are the key events during atrial systole?

A

LA contraction —> atrial kick contributes 20% of LV filling

The end of atrial systole correlates with end-diastolic volume

52
Q

Where is DBP measured?

A

Where the aortic valve opens

53
Q

Where is SBP measured?

A

Peak of the ejection curve

54
Q

What is considered a normal EF?

A

> 50%

55
Q

What EF % is considered mild dysfunction?

A

41-49%

56
Q

What EF % is considered moderate dysfunction?

A

26-40%

57
Q

What EF % is considered severe dysfunction?

A

< 25%

58
Q

How can we estimate the LV’s external work (EW)? When considering pressure-volume loops

A

Multiplying SV (width) by the mean aortic pressure (height)

59
Q

What is the key point when considering increased preload in a pressure-volume loop?

A

Loop gets wider, BUT returns to the original end-systolic volume

(Fluid bolus)

60
Q

What is the key point when considering decreased preload in a pressure-volume loop?

A

Loops gets narrow, BUT returns to the original end-systolic volume

(Lasix)

61
Q

What is the key point of increased contractility when considering pressure-volume loops?

A

The loop gets wider, taller, and shifts to the left.

(Increased SV ~ decreased ESV)

Beta 1 stimulation

62
Q

What is the key point of decreased contractility when considering pressure-volume loops?

A

The loop gets narrower, short, and shifts to the right

(Heart failure)

63
Q

What is the key point of increased afterload when considering pressure-volume loops?

A

The loop gets narrower, taller, and shifts the ESV to the right

(Acute hypertension)

64
Q

What is the key point of decreased afterload when considering pressure-volume loops?

A

The loop gets wider, shorter, and shifts the ESV to the left.

(Vasodilators)

65
Q

Where does the SA node receive its blood supply?

A

Usually the RCA

66
Q

Where does the AV node receive its blood supply?

A

Usually the RCA

67
Q

Where does the Bundle of His receive its blood supply?

A

LCA

68
Q

Where do the rt and lt. bundle branches receive their blood supply?

A

LCA

69
Q

What are the three main coronary veins and what artery do they run alongside?

A

Great cardiac vein (LAD)
Middle cardiac vein (PDA)
Anterior cardiac vein (RCA)

70
Q

Which leads related to the lateral aspect of the heart? Aka affect the circumflex artery

A

1, aVL, V5, V6

71
Q

Which leads relate to the inferior side of the heart? Aka affect the RCA?

A

II, III, aVF

72
Q

Which leads related to the septal aspect of the heart? Aka affect a portion of the LAD?

A

V1, V2

73
Q

Which leads relate to the anterior side of the heart? Affect a portion of the LAD?

A

V3, V4

74
Q

In regards to TEE, which view is best for diagnosing LV ischemia?

A

Midpapillary muscle level in short axis

Second best is apical segment…also in short axis

75
Q

At rest, how much oxygen does the myocardium consume?

A

8-10 mL/min/100g

76
Q

What is the extraction ratio of the myocardium when it is at rest?

A

70%

77
Q

What is the equation for coronary blood flow?

A

Coronary blood flow = coronary perfusion pressure / coronary vascular resistance

78
Q

What is the equation for coronary perfusion pressure?

A

Coronary perfusion pressure = Aortic DBP - LVEDP

79
Q

What is the normal range the coronary blood flow autoregulates to?

A

60-140 mmHg

80
Q

What is Adenosine?

A

Byproduct of ATP metabolism and is a potent coronary vasodilator

81
Q

What are some causes of coronary artery dilation?

A

Beta-2 agonist (increase cAMP ~ decrease MLCK sensitivity to Ca)

Histamine 2 ( increase cAMP ~ decrease MLCK sensitivity to ca)

Muscarinic ~ increase nitric oxide

82
Q

What are some causes of coronary constriction?

A

Alpha stimulation (increase intracellular Ca)

Histamine 1 ( increase intracellular Ca)

83
Q

What are some factors that decrease oxygen delivery? Think cardiac

A

Tachycardia (decrease diastole/filling time)
Decrease in aortic pressure
Decrease in vessel diameter (spasm or hypocapnia)
Increase in LV end-diastolic pressure

Decreased CaO2 (hypoxemia, anemia)

Decrease O2 extraction (left shift ~ decrease in P50)
Decreased capillary density

84
Q

What are some factors that increase oxygen demand?

A

Tachycardia
Hypertension
SNS stimulation
Increased wall tension
Increased LV end diastolic volume
Increased afterload
Increased contractility

85
Q

When do most postoperative MIs occur?

A

24-48 hours

86
Q

What is the basic sequence in a G-protein response?

A

First messenger —> g-protein coupled receptor —> effector —> second messenger —> cellular response

87
Q

In terms of vascular smooth muscle, what is the G-protein cAMP pathway lead to?

A

Vasodilation

88
Q

In terms of vascular smooth muscle, what does the Nitric Oxide cGMP pathway produce?

A

Vasodilation

89
Q

In terms of vascular smooth muscle, what does the Phosholipase C pathway produce?

A

Vasoconstriction!!!

90
Q

What is the nitric oxide pathway ~ simplified

A

Nitric oxide synthetase is an enzyme that catalyzes the conversion of L-ravine to nitric oxide —> this diffuses from endothelium to smooth muscle —> activates guanylate cyclase —> guanylate cyclase converts GTP to GMP. Increased GMP reduced intracellular Ca

91
Q

What is the Phospholipase c pathway for vascular smooth muscle vasoconstriction?

A

Angiotensin II —> ATII receptor —> Gq G-protein —> phospholipase C —> IP3 and DAG —> increased Ca —> vasoconstriction

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