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Cardio > Exam 1, lecture 2 > Flashcards

Exam 1, lecture 2 Flashcards

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0
Q

Cardiac ischemia

A

Insufficient coronary blood flow to meet the needs of the myocardium

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1
Q

Elevated CK-MB suggests what?

A

Recent acute myocardial infarction

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2
Q

Myocardial infarction

A

Death of cardiac muscle cells, from severe cardiac ischemia

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3
Q

AMI stands for

A

Acute myocardial infarction

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4
Q

Pressure volume loop

A

Area enclosed by loop is stroke work

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5
Q

Ees represent what in the pressure volume loop

A

Slope of the end systolic pressure volume relationship= ventricular elastase= ESP/ ESW
STEEPER SLOPE EQUALS GREATER CONTRACTIBILITY

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6
Q

Ea represents what on pressure volume loop

A

Efferent atrial elastance= esp/sv
Pressure developed in the arteries for a given stroke volume
Pressure dependent of elastance and outflow resistance

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7
Q

Laplaces law states

A

Estimates wall stress, wall tension from intraventricular pressure and radius and wall thickness
Wall tension is proportional to pressure inside vessel and to its radius

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8
Q

Wall stress is (eq)

A

Wall stress is wall tension divided by wall thickness

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9
Q

Laplaces law and the failing heart

A

In congested heart failure, dilation of ventricles and increase in EDV coupled with a reduction of EJF

Stroke volume and cardiac output usually maintained

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10
Q

What is maintaining stroke volume at the cost of?

A

Even though EJF is reduced, increase in EDV can maintain stroke volume. This means Elevated wall stress, and this means more oxygen demand and maintains stroke volume is a high metabolic cost
This leads to hypertrophy of the ventricle, compensation for wall thickness to renormalize wall stress

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11
Q

Wall stress

A

Pressure x radius/ ( wall thickness)

Pressure x radius is wall tension.

T/ wall thickness

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12
Q

Things and could increase pressure and volume work in heart ( usually occur together)

A

Increased pressure work (hypertension)
Aortic stenosis (increase pressure)
Increase volume work ( elevated preload)
Increased volume work ( aortic insufficiency from regurgitation)

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13
Q

Myocardial oxygen consumption cardiac work and cardiac efficiency

A

The lower the cardiac work, the higher the cardiac efficiency
So the less oxygen that is consumed for given level of cardiac work, higher the cardiac efficiency

Pressure work demands more oxygen, therefore less efficient work

Increase in pressure work places a higher demand on a coronary blood flow than an increase in volume work

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14
Q

Pain of angina is from

A

Insufficient supply if oxygen to the myocardium via coronary circulation

Common in aortic stenosis

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15
Q

Difference between aortic stenosis and aortic insufficiency

A

Aortic stenosis: pressure required to deliver Norma l cardiac output is higher than normal because of stenotic aortic semilunar valve

Aortic insufficiency: diastolic regurgitation of blood pressure an increase in stroke volume with a smaller change in resistance to ejection

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16
Q

Aortic regurgitation results in what kind of work?

A

Volume. Isovolumic relaxation does not occur. Blood is continuously entering the ventricle from aorta and increasing ventricular volume
EDV is increased
No true isovolumic contraction occurs
When ventricular pressure exceeds aortic diastolic pressure, blood starts being ejected into the aorta, elevating preload, increasing force of contraction and increasing systolic pressure and stroke volume

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17
Q

Aortic stenosis represents.

A

Pressure work
Increase peak of ventricular systolic pressure because large pressure gradient on narrowed aortic valve
After load and ESV increased
SV and EJF decrease
Increased EDV because of incoming venous return
Slow ventricular hypertrophy in response to elevated after load
Force of contraction is increased

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18
Q

Preload is

A

Degree to which ventricle are distended after diastole filling at onset of ventricular systole
EDV, stretching of walls in ventricles

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19
Q

Four major determinants of cardiac output are

A

1 preload
2 cardiac inotropic state
3 heart rate
4 myocardial contractability

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20
Q

After load

A

Ventricular wall tension that must be developed to open the semilunar valves and eject blood into the pulmonary trunk and aorta, or myocardial wall tension during systole

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21
Q

Starlings law ( heterometric autoregulation)

A

Heart behaves as a a self- regulating pump, so insures pumps out what gets from vena cavae into the aorta. The Greater the stretch of ventricular myocardium the greater force generated during systolic and greater is the stroke volume. So consequently stroke volume of each ventricle increases with diastolic filling

Depends on varying lengths of cardiac muscle fibers prior to contraction

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22
Q

Elements of preload

A

Length if ventricular muscle fibers at onset of ventricular systole
End diastolic volume
Central venous pressure, atrial pressure

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23
Q

Elevated preload affects

A

Force in contraction but NOT myocardial contractability

MC is related to force developed by contrasting myocardium for a give muscle fiber length ( homeometric regulation)

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24
Manipulable elements of preload
Blood volume and venous capacity Increased capacity is equivalent in effect to a reduced blood volume and vice versa
25
explains starlings law for a missed beat
heart continues to fill, by the next hear beat the EDV is roughly double its normal value and heart contracts more, expelling extra blood into the aorta and compensating for the missed beat.Second beat is an extra-systole or premature beat, this creates less filling time and EDV is smaller and the beat is weaker, expelling smaller stroke volume. The next beat there is a delay, and extra filling time EDV is larger, beat stronger and expels more. AVERAGE CARDIAC OUTPUT STAYS THE SAME
26
mean filling pressure
pressure within the cardiovascular system
27
what can increase afterload in the left ventricle
1. mean aortic pressure, 2. total systemic resistance (a change in total perpheral resistance doe not affect mean filling pressure but does affect the slope of the vascular function curve 3. aortic or pulmonary valve resistance: resistance increased if valve orifice is narrowed
28
consequence of increased afterload
increases amount of high cost pressure work and therefore myocardial oxygen demand, placing greater demands on coronary circulation
29
heart rate
heart rate and stroke volume determine the cardiac output. Determined by sympathetic and parasympathetic input into the SA node
30
severe drop is stroke volume can cause
impair cardiac output, for example during pathological ventricular tachycardia
31
what does myocardial contractability effect
ESV. increased myocardial contractility the end systolic volume is decreased from ESV to ESV'. If the EDV remains the same, the stroke volume is increased
32
MC depends on what
intracellular calcium ion concentration, which affects the number of available myosin binding sites on actin filament
33
What does extracellular calcium concentration lead to
increased intracellular calcium ion concentration and increased MC
34
Heart rate in relation to MC
increasing heart rate can increase MC due to accumulation of intracellular calcium (force-frequency relationship)
35
what is positive inotropic agents
NE and E: | and cardiotonic drugs like digitalis (dogxin)
36
what does NE and E do to calcium concentration
increase calcium current during cardiac action potential and there increase intracellular calcium ion concentration. Sympathetic origin. Dopamine acts similarly (beta-adenergic receptors) Drug dobutamine binds beta adenergic receptors
37
what does Digitalis do to calcium levels
increases intracellular calcium ion concentration. impairs sodium-potassium exchange pump in sacrolemma, therefore reducing transmembrane sodium gradient and reduces driving to sodium-calcium exchange pump->> internal calcium rises
38
negative inotropic agents
calcium channel blockers: MC is reduced by calcum channel blockers because prevent calcium from entering the myocardial cell
39
myocardial ischemia leads too
heart failure-> depresses MC and starlings law response
40
two major NT of the ANS
acetylcholine and NE
41
which receptors do sympathetic and parasympathetic use?
cholinergic
42
which receptors do postganglionic neurons use
cholinergic
43
which receptors do sympathetic neurons use
adrenergic, except sympathetic in eccrine sweat glands is cholinergic
44
Sympathetic effect on cardiovascular system
vasoconstriction
45
Acetylcholine receptors
Nicotinic and muscarinic receptors
46
Nicotinic receptors
also bind nicotine, which is an agonist of acetylcholine (same effect).
47
Muscarinic receptors
toadstool toxin called muscarine and acts as agonist (pacemarker cells)
48
alpha-adrenergic receptors
bind both NE and E. walls of vessels, alpha 1 adrenegeric receptors mediate vasoconstriction. Alpha 2 inhibit NE release from sympathetic nerve endings
49
beta-adrenergic receptors
bind NE and E. beta 1 group, Pacemarker cells of the myocardium. increasing heart rate and force contraciton. Beta 2 are found in walls of blood vessels and are involved in vasodilation
50
medulla
can increase heart rate or decrease, vasomotor center
51
hypothalamus
controls autonomic motor system, can change heart rate dramatically
52
thalamus
can produce tachycardia
53
What area does the parasympathetic not innervate in the heart
ventricles
54
SA and AV node innervation
left vagus nerve does AV, and right vagus nerve does SA.
55
NE binds beta 1 adrenergic receptors, causes
G coupled receptors-> activate G stimulatory adenylyl cyclase, which converts ATP and cAMP-> activation of protein kinase A-> phosphorylation number or proteins, including L-type voltage-gated calcium channels, ryanodine receptor and phosphorlamban
56
stimulation of beta 1 adrenergic receptors in heart
1. positive inotrpic (increase C) phosphorylation of calcium channel proteins-> open during action potential and permitting larger calcium flux into the cell. Facilitation of calcium release from sacroplasmic reticulum via ryanodine receptors, sensitization of troponin c calcium 2. chronotropic: accelerated firing of pacemaker cells-> accelerated heart rate. 3. dromotropic: increase rate of conduction thru AV) 4. ) lusitropic: phosphorylation of phospholamban
57
beta-blockers
block sympathetic stimulation
58
parasympathetic receptors
cholinergic receptors muscarinic and nictoinic, G inhibitory proteins, decrease cAMP in cell
59
parasympathetic effect on cardiovascular system
release of acetycholine and slow heart rate and reduce rate of the conduction of thru AV node
60
Atropine
blocks acetylcholine, and binds muscarinic receptor, abolishes parasympathetic tone, increases heart rate
61
what keeps the intact innervated heart rate normal?
parasympathetic tone with some degree by a weaker sympathetic tone
62
Propranolol
blocks beta 1 and beta 2 adrenergic receptors, abolishes sympathetic tone and small drop in heart rate
63
sympathetic mainly cause vasoconstricition where?
skin and abdominal viscera NOT coronary or cerebral circulations
64
what governs resistance
arterioles
65
what governs capacitance
veins and muscular venules
66
How does sympathetic nervous system play a role in survival after hemorrhage
drop in mean arterial pressure produces strong sympathetic nervous system via baroreceptor reflex
67
sympathetic role during hemorrhage causes what
1. increased MC->reduces ESV, increases stroke volume-> boosts cardiac output 2. increased heart rate couple with positive lusitropic effect-> boosts cardiac output 3. vasoconstriction
68
increased vasocontriction in arterioles does what?
increases total peripheral resistance and increases mean arterial pressure
69
vasoconstriction in veins and muscular venules?
reduction in capacity of cardiovascular system, which increases mean filling pressure nd causes increase in preload, boost cardiac output according to starlings law

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