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Cardio > Heart Mechanism > Flashcards

Heart Mechanism Flashcards

0
Q

Aorta

A
  • receives blood from left ventricle

- large elastic component allows for distention and continuous flow

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1
Q

Cardiac cellular structure

A
  • large dilated T-tubules arranged in diads containing glycocalyx
  • Ca induced Ca release (contractility)
  • functional syncytium
  • maximal force is developed when sarcomere is 2-2.4 micrometers (big heart isn’t always a strong heart)
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2
Q

Arteries

A
  • higher systolic pressure than aorta but lower diastolic so MAP is essentially the same
  • frictional resistance is low so pressure remains high (spikes in arterioles where pressure drops sharply)
  • significant muscle component
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3
Q

Arterioles

A
  • resistance vessels: large drop in BP and velocity
  • from pulsatile -> steady
  • regulates flow into capillary bed
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4
Q

Capillary beds

A
  • high cross sectional area
  • very slow flow (important for exchange)
  • O2 sat post ex: 50-80%
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5
Q

Venules

A
  • 20 micrometers
  • increased velocity
  • no smooth muscle
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6
Q

Veins

A
  • largest container of blood volume
  • pressure continues to drop as they get near the heart
  • they do contain smooth muscle (unlike venules)
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7
Q

Pulmonary O2 sat

A

94-98% after exchange

- 18 to 20 mls O2/100 mls blood

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8
Q

Phases in myocytes contraction

A

Phase 0: rapid depol; fast - Na influx, slow - Ca influx
Phase 1: partial depol; K efflux (only in fast)
Phase 2: plateau - balance of Ca in, K eff
Phase 3: repol - Keff predominates
Phase 4: resting/pacemaker potential

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9
Q

Fast vs slow ap

A
  • fast response occurs in ventricles (propagating through thicker tissue)
    > resting potential more negative
    > amplitude of wave is determined by Na channels
  • slow occurs in SA/AV nodes
    > higher resting membrane potential
    > Ca channel regulated
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10
Q

Overdrive suppression

A
  • fastest pacemaker takes control
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11
Q

Bidirectional block

A
  • no ap is conducted through particular region

- either intense vagal stimulation or cell damage (ischemia)

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12
Q

Unidirectional block

A
  • Anterograde block, retrograde propagation
  • may result in reentry arrythmias
  • elevated extracellular K, extracellular lactic acid
  • trt by speeding up or slowing down conduction to induce bi directional block (lido slows down by blocking Na channels)
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13
Q

Depolarization and Ca release

A
  • Ca induced Ca release
  • glycocalyx has a charge that holds Ca close
  • ryanodine receptors close to Ca channels so release is significant and local from SER
  • pH effects release significantly (basic pH induces, acidic pH inhibits) maximal at 7.4
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14
Q

Preload

A
  • stretching the elastic element (end diastolic volume)

- increasing preload will increase contraction up to maximal response

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15
Q

Afterload

A
  • the pressure the ventricle must work over come to eject (aortic pressure
  • increased afterload will increase pressure during isovolumetric contraction
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16
Q

Velocity and force of contraction

A
  • inverse: no load = highest velocity
  • in isotonic contraction muscle is preloaded and after loaded
  • elastic first with no shortening of external length
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17
Q

Contractility

A
  • aka ionotropic state
  • performance at given pre and afterload
  • EF is a good index for contractility
18
Q

Frank-Starling mechanism

A
  • In an isolated heart, as preload increases so does contraction
  • maximal contraction reqs optimal stretching (not too full, not too empty)
  • increasing afterload will initially decrease SV, heart will compensate the following beat and increase force of contraction maintaining CO, but at greater energy cost
19
Q

Ficks principle

A
  • CO = O2 consumed /(PVO2-PAO2)
  • computed over several beats
  • can be used to measure O2 consumption in a single organ
20
Q

Dilution measurement of CO

A
  • CO = amt Dye injected/(time when dye [] = 0 - time first injected)
  • recirculation is a problem
  • lare central vein/rt side of heart
21
Q

Thermodilution

A
  • measures CO based on ice cold saline in vein, temp measured in pulmonary artery
22
Q

Echo Doppler

A
  • non-invasive! But expensive…

- CO = x-section of aorta multiplied by velocity

23
Q

Fluid movement (starling equation)

A
  • flow = K [(Pc+PiIF) - (Pic+PiIF)]
24
Q

aortic pressure curve follows decreased trajectory (similar pattern but less extreme and lower over all) ejection also happens with greater velocity

A
  • aortic stenosis
25
Q

Normal pressure curve but reduced overall with increased atrial pressure (but overall increased)

A
  • mitral stenosis
26
Q

Normal ventricular and atrial pressure curve but aortic pressure curve drops sharply after ejection

A
  • aortic regurgitation
27
Q

Decreased overall pressure curve, left atrial pressure spikes in diastole

A

Mitral regurgitation

28
Q

A murmur that increases on inspiration

A

Right side defect

- inspiration increases venous return delaying pulmonic valve closure such that it is more easily discerned

29
Q

Murmurs increasing on expiration

A
  • increases volume of blood ejected from left ventricle increasing mitral and/or pulmonic opening
30
Q

Left 3rd IC space

A

Erbs point

- best to auscultation S2 split

31
Q

Phospholambam

A
  • seriously….?
  • modifies speed of Ca pump in SER sequesting Ca
  • when phosphorylated cAMP protein Kinase it activates speeding up sequestration
32
Q

Reynolds number

A
  • measure of viscosity and velocity
    > low velocity and high viscosity = higher Reynolds number
    > Nr ~ 2500 you start to see turbulence
    > most likely in ascending aorta
  • conditions like anemia and polycythemia affect significantly
33
Q

Fahraeus-Lindquist effect

A
  • fastest Lamina in blood flow pulls blood cells toward it and plasma is pushed peripherally and moves slower allowing for the transfer of nutrient and gas exchange
34
Q

Plat vs. Pdyn

A
  • dynamic pressure is the kinetic force and represents ~ 95%
  • In vessels with atherosclerosis, velocity is increased to the Plat is decreased and the smaller collateral vessels can be compromised
  • in a dilated vessel, velocity drops and P lat increases compromising the already damaged intima
35
Q

Pulse pressure

A

Pp = Psys - Pdyn

- hardened arteries show increases PP, less accommodating of pressure change

36
Q

Effect of Loss of compliance on MAP

A
  • diastole drops (weighted) dropping MAP more than the increase raises it.
  • TPR increases to maintain MAP
  • TPR increase -> increase afterload
37
Q

First heart sound

A

Closure of AV valves (lub)

38
Q

Second heart sound

A

AP valves closing

- split may be heard on inspiration or with right AV block

39
Q

Third heart sound

A

Blood hitting incompliant ventricles in early/mid diastole

  • low frequency
  • only common in young; adult 3rd sound is pathological
40
Q

Fourth heart sound

A

Filling of ventricle which cannot expand by atrial systole

- not normally heard

41
Q

Opening snap

A

Blood hitting residual volume in diastole

42
Q

Increase in blood volume (decrease in TPR) on a starling venous return chart

A
  • clockwise rotation of the venous return curve

* Not actually TPR: arteriodilation without venodilation increases venous return

Cardio (14 decks)

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