Cardiac Muscle and Valve Disorders

Question 1

how does cardiac muscle work

Answer 1

• 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

Question 2

resting membrane potential of cardiac muscle cells

Answer 2

-85- -95mv

Question 3

resting membrane potential of conducting cells

Answer 3

-90- -100mv

Question 4

how is the AP in cardiac muscle extended

Answer 4

by the action of calcium

Question 5

refractory periods

Answer 5

periods during which the cell cannot contract

Question 6

AP of cardiac cell vs neuron

Answer 6

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

Question 7

Phase 0

Answer 7

Na enters the cell and causes depolarization

-fast acting sodium channels

Question 8

phase 2

Answer 8

Ca enters the cell, initiation of the contraction

Question 9

phase 3

Answer 9

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

Question 10

EC Coupling

Answer 10

• 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

Question 11

what percent of the cardiac cycle is contraction vs rest

Answer 11

40% contraction, 60% rest

Question 12

Ejection fraction

Answer 12

ESV/EDV - normal is 65%

Question 13

valve most likely to be damaged

Answer 13

• semilunar valve

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

Question 14

What causes the propulsion of blood from the aorta?

Answer 14

-elastic recoil of the aorta

Question 15

what causes the incisura on the aortic pressure curve

Answer 15

-closure of the SLV

Question 16

why will the aortic pressure never reach 0?

Answer 16

elastic recoil of the aorta

Question 17

stroke work output

Answer 17

energy per beat

Question 18

minute work output

Answer 18

energy per beat over 60 seconds

Question 19

external work

Answer 19

work to overcome pressure

Question 20

kinetic energy

Answer 20

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

Question 21

why do systolic pressures rise

Answer 21

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

Question 22

diuretics affect systolic or diastolic pressure the most?

Answer 22

systolic!

Question 23

preload

Answer 23

end diastolic pressure

Question 24

afterload

Answer 24

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

Question 25

where is the energy for the heart pumping coming from?

Answer 25

OXIDATIVE METABOLISM OF FATTY ACIDS

Question 26

how is output altered

Answer 26

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

Question 27

how to determine CO

Answer 27

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

Question 28

effect of excess potassium ions

Answer 28

- results in flaccid, dilated heart, slowing its rate or blocking conduction - calcium has the opposite effect

Question 29

incompetent valve

Answer 29

doesnt close fully and allows blood to leak forward

Question 30

regurgitant valve

Answer 30

doesnt close fully and allows blood to leak backward

Question 31

valvular stenosis

Answer 31

imparts pressure overload

Question 32

valvular regurgitation

Answer 32

imparts volume overload

Question 33

mitral stenosis etiology and stats

Answer 33

- 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

Question 34

mitral stenosis physical exam and heart sounds

Answer 34

- 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

Question 35

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

Answer 35

- 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

Question 36

mitral regurg signs and sxs

Answer 36

- 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)

Question 37

sxs and PE of mitral valve prolapse

Answer 37

- 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

Question 38

aortic stenosis

Answer 38

- 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

Question 39

symptoms of aortic stenosis

Answer 39

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

Question 40

aortic stenosis heart sounds

Answer 40

- 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

Question 41

aortic regurgitation

Answer 41

- volume overload of left ventricle, leads to LAE, systolic hypertension - pulmonary symptoms as disease progresses

Question 42

aortic regurgitation sxs

Answer 42

- 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

Question 43

Tricuspid regurgitation

Answer 43

- 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

Question 44

pulmonic stenosis

Answer 44

- 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