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Cardio > Lecture #2 > Flashcards

Lecture #2 Flashcards

1
Q

Myocardium has ____ ATP content and _____ ATP demand

A

Low, Very High

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2
Q

What supplementary molecule may help the heart maintain ATP levels?

A

Creatine Phosphate going btw mitochondria and contractile units

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3
Q

Name of cardiac creatine phosphokinase

A

CK-MB

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4
Q

What do elevated CK-MB leves imply?

A

Recent Acute Myocardial Infarction

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5
Q

Biggest contributor of energy to the heart? 2nd place?

A

Fatty Acids

Carbohydrates (Primarily Glucose)

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6
Q

Using Pressure-Volume Loop, what is stroke work? stroke volume?

A 
Work = Area Enclosed by loop
Volume = Area between the two isovolumetric volume stages
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7
Q

What are the four points on the pressure-volume loop. Assume A is the first heart sound.

A 
A = Mitral Valve Closure
B = Aortic Semilunar Valve Opens
C = Aortic Semilunar Valve Closes
D = Mitral Valve Opens
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8
Q

Review Loop on P. 68

A

Fuck this class. Fuck this school.

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9
Q

What is laplace’s law used to estimate?

A

Wall Tension and Stress

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10
Q

Wall tension is proportional to….

A

Vessel Pressure and Radius

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11
Q

Ventricular wall tension required to open semilunar vales is a measure of….

A

Afterload

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12
Q

Equation for Wall stress

A

S=Tension/Wall Thickness

(remember Tension = PressureXRadius

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13
Q

Ways to reduce vessel wall stress?

A

Decrease r, decrease P or increase thickness

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14
Q

Effects of congestive heart failure on ventricles, EDV, EJF

A

Dilation of ventricles
Increase in EDV
Decreased EJF

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15
Q

Effect of Increased EDV and Decreased EJF on SV?

A

Initially, nothing.
Eventually, requires hypertrophy and limits are reached
Can’t be maintained

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16
Q

Relationship of Wall Stress, Pressure, and Volume

A

S is proportional to P and proportional to the cube root of volume.

ex. 100% increase in volume increases stress by 26%
100% increase in pressure increases to 100%.

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17
Q

Causes of Increased Pressure Work of the Heart?

A

Elevated MAP (hypertension) or outflow resistance (stenosis)

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18
Q

Causes of Increased Volume Work of the Heart?

A

Elevated Preload (Exercise) or Aortic Insufficiency (regurgitation)

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19
Q

Define Preload.

A

The degree to which the ventricles are distended after diastolic filling

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20
Q

What is Cardiac Efficiency? (concept)

A

Fraction of myocardial metabolic energy used as work

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21
Q

What is Cardiac Efficiancy? (equation)

A

(Cardiac Work) / (Myocardial Oxygen Consumption)

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22
Q

Which is more oxygen demanding, volume or pressure work?

A

Pressure Work

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23
Q

Four Major Determinants of CO?

A

Preload
Afterload
HR
Myocardial Contractility

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24
Q

The greater the stretch of the myocardium……

This is reflected by….

A

the greater the force generated in systole + the SV

Starling’s Law of the Heart

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25
Q

Different ways of expressing preload…

A

Length of ventricular muscle fibers at systole onset
End Diastolic Volume
Central Venous/Atrial Pressure

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26
Q

Preload alters ______, NOT _________

Why not the second blank?

A

Force of Contraction, Myocardial Contractility

MC relates to force at a given muscle fiber length

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27
Q

Two ways of manipulating preload.

A 
Blood Volume (diuretics and fluid infusion)
Venous Capacity (altered by drugs)
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28
Q

How will a missed beat influence preload?

A

Extra Time – Bonus Preload – More pumped out on next beat

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29
Q

What allows average CO to be maintained despite individual HR variances?

A

Starling Law

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30
Q

Relationship between Central Venous Pressure and CO

A

Inverse

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31
Q

What is mean filling pressure?

A

Pressure within the cardiovascular system after the heart is removed and the flow ceases.

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32
Q

If a heart is restarted, why will arterial pressure change faster?

A

Veins are more compliant.

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33
Q

In a cardiac output curve, CO is plotted against…

A

Central Venous Pressure (Preload)

34
Q

Increasing Central Venous Pressure will do what to CO

A

Increase It

35
Q

Increasing CO will do what to Central Venous Pressure

A

Decrease It

36
Q

Why give a shit about cardiac/vascular fxn curves?

A

The point at which they overlap is a state the heart must stay balanced in.

37
Q

Describe what would happen if you dropped CO (in the context of the Cardio/Venous Pressure Curves)

A

Initial Rise in Venous Pressure (Preload)
Rise in CO (Starling)
Drop in Venous Pressure/CO back to operating point

38
Q

Best definition of afterload

A

Myocardial wall tension during systole

39
Q

Three ways to increase ventricular afterload

A

Inc. Mean Aortic Pressure
Inc. Total Peripheral Resistance
Inc. Aortic/Pulmonary Valve Resistance

40
Q

Primary cause of HR variance in an individual?

A

Symp. and PS input at SA node

41
Q

What is myocardial contractility/cardiac inotropic state?

A

The ability of the myocardium to develop contractile force for a given muscle fiber length

42
Q

How to distinguish between myocardial contractility changes and Starling Law Effect?

A

Starling Law is all about increases in fiber length

Myo. cont. is about the ability to generate force at a given length

43
Q

Maximum change in pressure over time can be determined from intraventricular pressure curves at what stage?

A

Isovolumetric Contraction

44
Q

What is strain rate?

A

Shortening Velocity per Fiber Length

45
Q

How are myocardial contractility and end systolic volume related?

A

More MyoCont means that ESV is decreased

If EDV remains the same the increase in stroke volume will reflect the new ESV

46
Q

Ways to influence myocardial contractility via Ca

A 
More extracellular Ca
Increased HR
Pos Inotrophic Agents (Cate. and Digitalis)
Neg Inotropic Agents
Myocardial Ischemia
47
Q

Influence of Heart Failure on SV, Contractility, and Preload

A

Decreased contractility
Elevated Preload
Decreased SV

48
Q

Two major NTs of autonomic system

A

Acetylcholine

Norepinephrine

49
Q

Most sympathetic postganglionic neurons are….

A

Adrenergic

50
Q

Most parasympathetic postganglionic neurons are…

A

Cholinergic

51
Q

Neurosecretory cells of the adrenal medulla? What do they release?

A

Chromaffin cells
80% Epinephrine
20% Norepinephrine

52
Q

Enzyme that breaks down norepinephrine.

A

Monamine Oxidase

53
Q

Acetylcholine binds what two receptor types

A

Nicotinic Receptors

Muscarinic Receptors

54
Q

Where are muscarinic receptors found?

A

Membranes of cells that receive innervation form postganglionic neurons of the PS division

55
Q

Norepinephrine and epinephrine both can bind what two receptors.

A

alpha and beta adrenergic recepters

56
Q

Where are alpha receptors found?

What do they do?

A

BV walls
Alpha-1 –> Vasoconstriction
Alpha-2 –> Inhibition of Norepinephrine Release from Symp.

57
Q

Where are beta adrenergic receptors found?

What do they do?

A

Pacemaker Cells/Myocardium
Beta-1 –> increase HR and Contraction Force
Beta-2 –> In certain blood vessels to help with dilation

58
Q

Which nucleus gets the info from the pressure/chemical sensors?

A

Solitary Nucleus

59
Q

Main control center for autonomics?

A

Hypothalamus

60
Q

Stimulating certain parts of thalamus can produce….

A

Tachycardia

61
Q

Specifically – What part of the heart gets PS input –

A

The SA and AV nodes

62
Q

Stimulation of beta-1 adrenergic receptors in the heart causes…

A

Increased Contractility
Accelerated Pacemaker Firing
Accelerated AV conduction
Increased Myocardial relaxation in diastole

63
Q

What does chronotropic mean?

A

Affecting the rate

64
Q

What does dromotropic mean?

A

Relating to Conductivity of a fiber

65
Q

What does lusitropy relate to?

A

Relaxation of the heart

66
Q

How do you inhibit sympathetic response?

A

beta-blockers (propranolol)

They block Beta-1 and Beta-2 adrenergic receptors

67
Q

Describe molecular process following norepinephrine release

A 
Binding to beta-1 adren. on the heart 
Activate G-stim
Activates Ad Cyc
cAMP generated  --->  PKA
Phos. L-type voltage gated calcium channels, ryanodine, and phospholamban
68
Q

Describe the molecular process following muscarinic receptor activation.

A

Activate G-inhib

Decrease in cAMP

69
Q

Major effect of PS release of acetylcholine?

A

Slow the Heart and Reduce AV conduction rate

70
Q

How do you inhibit parasympathetics on the heart?

A

Atropine

71
Q

Arteries, Arterioles, Muscular Venules, and Veins get main innervation from….

A

Sympathetics

72
Q

Generally speaking…what will symp. stim at vessels do?

A

Activate alpha-adrenergic vasoconstriction

73
Q

T or F. Sympathetic nerves are only active in fight or flight.

A

F. There is continuous vasoconstriction of all innervated blood vessels.

74
Q

Overall sympathetic effect on heart.

A

Increased HR, Contractility, Lusitropy, Dromotropy

beta-adrenergic receptors

75
Q

Sympathetic effects on non-heart CV system.

A

Vasoconstriction (alpha-adrenergics)

Renin Release

76
Q

How does hemorrhage turn on sympathetic support?

A

Baroreceptor Reflex

77
Q

Sympathetic responses to hemorrhage?

A

Inc. myocardial contractility
Inc HR + pos. lusitropic effect
Vasoconstriction

78
Q

benefit of systemic vasoconstriction in hemorrhage?

A

Increased preload, leading to increased CO

79
Q

Three places on heart innervated by vagus

A

SA
AV
Atrial Myocardium

80
Q

Molecular effect of PS stim.

A

Altered properties of K channels

81
Q

Equation for compliance

A

(Change in V) / (Change in P)

82
Q

Equation for Elastance

A

1/Compliance

Cardio (10 decks)

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