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Physiology 1 > Cardiac Muscle and Valve Disorders > Flashcards

Cardiac Muscle and Valve Disorders Flashcards

1
Q

how does cardiac muscle work

A
  • muscle fibers are interwoven, not linear like skeletal muscle
  • intercalated discs separate each cell and the intercalated discs of adjacent cells fuse to form a gap junction that transmits ions
  • when one muscle cell contracts, the ionic changes are shared via the gap junctions
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2
Q

resting membrane potential of cardiac muscle cells

A

-85- -95mv

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3
Q

resting membrane potential of conducting cells

A

-90- -100mv

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4
Q

how is the AP in cardiac muscle extended

A

by the action of calcium

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5
Q

refractory periods

A

periods during which the cell cannot contract

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6
Q

AP of cardiac cell vs neuron

A

higher amplitude AP (doesn’t travel as far, so it doesn’t depolarize as much)

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7
Q

Phase 0

A

Na enters the cell and causes depolarization

-fast acting sodium channels

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8
Q

phase 2

A

Ca enters the cell, initiation of the contraction

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9
Q

phase 3

A

K exits the cell and reestablishes balance of normal electrolytes in the cell
-this is the repolarization of the membrane potential

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10
Q

EC Coupling

A
  • T tubule is an invagination of muscle membrane
  • T-tubule creates calcium rich environment
  • voltage gated calcium channels open as a result of change in membrane voltage
  • calcium enters cardiac cell and causes sarcoplasmic reticulum to release calcium
  • the calcium binds to sliding filament and causes contractions
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11
Q

what percent of the cardiac cycle is contraction vs rest

A

40% contraction, 60% rest

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12
Q

Ejection fraction

A

ESV/EDV - normal is 65%

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13
Q

valve most likely to be damaged

A
  • semilunar valve

- tends to be more damaged by pressure and tends to wear out more

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14
Q

What causes the propulsion of blood from the aorta?

A

-elastic recoil of the aorta

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15
Q

what causes the incisura on the aortic pressure curve

A

-closure of the SLV

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16
Q

why will the aortic pressure never reach 0?

A

elastic recoil of the aorta

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17
Q

stroke work output

A

energy per beat

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18
Q

minute work output

A

energy per beat over 60 seconds

19
Q

external work

A

work to overcome pressure

20
Q

kinetic energy

A

the acceleration of blood
ex) kinetic energy increases at aortic root if there is aortic stenosis because the diameter is decreased so the flow must increase - faster

21
Q

why do systolic pressures rise

A

as volume increases, sarcomeres are extended

-increased volume has a bigger effect on systolic than diastolic until you get to 150 and then diastolic is affected

22
Q

diuretics affect systolic or diastolic pressure the most?

A

systolic!

23
Q

preload

A

end diastolic pressure

24
Q

afterload

A

opposition to ejection, comes from the blood in the systemic circuit and the pressure that must be overcome in order to eject blood

25
Q

where is the energy for the heart pumping coming from?

A

OXIDATIVE METABOLISM OF FATTY ACIDS

26
Q

how is output altered

A

intrinsic: response to flow into the heart - filling = stretch
- output increases with ventricular stretch, therefore increased return increases cardiac output

extrinsic: ANS - parasympathetic and sympathetic innervation to the SA and AV nodes

27
Q

how to determine CO

A

CO = SV x HR
HR has a direct effect on CO up until the point where the reduction of the resting phase starts to reduce the filling of the ventricle and thus the CO

28
Q

effect of excess potassium ions

A
  • results in flaccid, dilated heart, slowing its rate or blocking conduction
  • calcium has the opposite effect
29
Q

incompetent valve

A

doesnt close fully and allows blood to leak forward

30
Q

regurgitant valve

A

doesnt close fully and allows blood to leak backward

31
Q

valvular stenosis

A

imparts pressure overload

32
Q

valvular regurgitation

A

imparts volume overload

33
Q

mitral stenosis etiology and stats

A
  • MCC = rheumatic dz
  • increased LA pressure causes pulmonary vasoconstriction and restricted inflow to LV limiting CO
  • 60% reduction in opening area required for sxs
  • W>M, 4th and 5th decade
34
Q

mitral stenosis physical exam and heart sounds

A
  • opening snap and then diastolic murmur
  • low pitched and rumbling, heard at axilla
  • quiet apical impulse
  • parasternal lift
  • loud S1, split S2, no S3 or S4
  • isometric hand-grips increase intensity
  • elevated JVP with edema and ascites
  • accompanied by pulmonic insufficiency (graham steele) diastolic blowing murmur
35
Q

mitral regurgitation etiology and pathophys of Acute, chronic, and decompensated MR

A
  • causes: prolapse, rupture CT, endocarditis, drug effects - phenfen
  • acute MR - blood back flows into LA wastes LV SV causing overload of the LV - stretches LV and LVED volume maximizes
  • chronic MR - regurg unloads LV in systole reducing LVES volume - forward SV is subnormal due to regurg into LA
  • decompensated MR - regurg volume increases LA pressure so get CHF with low CO and pulm congestion despite normal LV contractility
36
Q

mitral regurg signs and sxs

A
  • enlarged ventricle and hyperdynamic impulse
  • pansystolic murmur to neck
  • sxs are similar to L sided HF (dyspnea, orthopnea, PND, fatigue)
  • apical impulse displace down and to the left
  • decreased S1, split S2 and S3 (rapid filling of LV)
37
Q

sxs and PE of mitral valve prolapse

A
  • most people are asymptomatic
  • palpitations, syncope, chest pain
  • sxs are usually due to autonomic dysfunction
  • mid systolic click and late systolic murmur
  • valsalva or standing make click earlier, murmur holosystolic and louder
  • release valsalva or squatting delays click, murmur shortens, becomes fainter
  • EKG normal
  • CXR normal
  • ECHO shows prolapse
  • 10% pts have sequalae (endocarditis, stroke, MR, or sudden death)
  • males progress in severity more frequently than females
38
Q

aortic stenosis

A
  • bicuspid and congenital abnormalities
  • 1% population w/ men affected more than women
  • thickening and calcification develops in 4th, 5th, 6th decade of life
  • can be caused by rheumatic fever, can be diseased in conjunction with ASCAD
  • USUALLY CALCIUM DEPOSITION
  • bimodal distribution
  • increased resistance and reduced output
39
Q

symptoms of aortic stenosis

A

Classic sxs = angina, syncope, HF

  • angina due to myocardial ischemia when LV oxygen demands exceeds supply
  • syncope due to inadequate cerebral perfusion
  • HF due to systolic and diastolic HF (not getting enough out and also hypertrophy of ventricle to compensate and therefore decreased ventricular space for filling)
  • reserve is limited due to decreased capillary ingrowth
  • reduced trans-coronary gradient due to elevated left ventricular end diastolic pressure
  • usually have normal epicardial coronary artery anatomy
40
Q

aortic stenosis heart sounds

A
  • systolic ejection murmur over aortic area radiating to neck
  • pulsus parvis et tardus - you can feel the carotid filling, not a sharp tap that it should be
  • mid systolic crescendo decrescendo murmur
41
Q

aortic regurgitation

A
  • volume overload of left ventricle, leads to LAE, systolic hypertension
  • pulmonary symptoms as disease progresses
42
Q

aortic regurgitation sxs

A
  • sxs of L sided HF (DOE, orthopnea, fatigue)
  • in acute AR, cardiac failure and shock develop rapidly (angina, flushing, carotid artery pain, and awareness of the heart beat)
  • hyperactive apical impulse displaced down and left
  • normal S1 and S2
  • diastolic blowing murmur at LLSB
  • severe AR = Austin FLint murmur or mitral valve rumble
  • wide pulse pressure due to increased SV and decreased systemic arterial resistance
43
Q

Tricuspid regurgitation

A
  • usually due to hemodynamic load of R ventricle and not structural abnormalities
  • COPD and shunts in which there is pulm HTN leads to RV dilation and TR
  • infective endocarditis, IV drug use, carcinoid syndrome, rheumatic heart dz, myxomatous degeneration, RV infarction
  • JVD, hepatic enlargement, liver pulsation, parasternal lift
  • EKG: RV hypertrophy
  • CXR: cardiomegaly
  • ECHO: TR, pulm HTN, RV dilation
44
Q

pulmonic stenosis

A
  • congenital heart disease (usually detected and corrected in childhood)
  • fusion of pulmonic cusps
  • angina, syncope, RHF (ascites, edema, RUQ pain)
  • early systolic ejection click or opening snap
  • systolic ejection murmur radiating to base
  • inspiration makes it softer
  • parasternal lift

Physiology 1 (6 decks)

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