Cardiac Energy/control Flashcards

0
Q

External cardiac work

A
  • moving blood
  • only about 10%
  • stroke work
    SW = SV x MAP
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1
Q

Energy Production

A

Ox-phos

  • susceptible to injury if low O2 levels
  • brief compensation via glycolysis (lactic acid screws with conduction and low pH screws with calcium release…so this is probably not optimum)
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2
Q

Internal cardiac work

A
  • external work is used an estimator
  • roughly 5 x external
  • mostly done during isovolumetric contraction
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3
Q

Pressure vs volume work

A
  • pressure is primary determinant
  • volume has little effect
  • determined by delta in O2 consumption
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4
Q

Heart rate and work

A
  • more costly because the heart spends more time in isovolumetric contraction which is where internal work takes place
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5
Q

Contractility

A
  • describes the relative ability of the heart to eject a stroke volume (SV) at a given prevailing afterload
  • increases pressure work, but maintains CO at lower heart rate
  • these effects tend to balance each other out
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6
Q

Energy req estimate (and limitation)

A
  • Double product = HR x MAP (KNOW)

- not a valid method when ventricles are dilated

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7
Q

CO and SV Eq

A

CO=SVxHR

SV=EDV-ESV

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8
Q

Autonomic control

A
  • sympathetic (increase HR) NO beat to beat

- parasympathetic (decrease HR) SA node beats naturally at around 100 BPM

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9
Q

Parasympathetic control of heart

A
  • slows HR
  • ACh opens Special K channels (increasing phase 4) and decreases Ca conductance
  • predominantly the right vagus
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10
Q

Sympathetic control of heart

A
  • Right rate;left contractility
  • stimulated by isoproterenol; inhibited by propranolol
  • stimulates increase in K leak -> decreasing length (increasing steepness) of phase 4 and increases Ca conductance
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11
Q

Epi vs norepi

A
  • epi results in decreased resistance -> decreased afterload -> increased CO systolic pressure is increased while diastolic drops -> MAP remains the same
  • Norepi increases contractility -> directly increasing CO. Increases both systolic and diastolic pressure
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12
Q

Neural reg of cardiac function location

A
  • frontal lobe
  • orbital cortex
  • motor/premotor
  • solitary and rostral/caudal tract
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13
Q

Baroreflex

A
  • senses arterial pressure and responds by modulating HR
  • decreased in chronic HTN
  • can produce beat-beat variation (deficit-compensation) as seen in PVCs or in a block
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14
Q

Bainbridge reflex and atrial receptors

A
  • If HR is slow, the Bainbridge will jack up HR in response to infusion
  • if HR is fast, the baroreceptor will slow down the rate upon infusion
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15
Q

Resp cardiac arrhythmias

A
  • cycle increases on expiration (and visa versa)

- vagus vs. phrenic activity

16
Q

Venous return during respiration

A
  • increased intrathroacic pressure decreases venous return (passing out during vigorous valsalva)
17
Q

Chemoreceptors reflex

A
  • respond to low O2 or high CO2 (much stronger drive)
  • compensation is rapid
  • can see this effect in quadriplegics
18
Q

Treppe phenomena

A
  • Increase in contraction frequency -> increase in force

- produced by rise in intracellular Ca

19
Q

Molecular control

A
  • Sympathetics: left greater control over vents
    > Gs stimulates cAMP production -> phosph of Ca channels shift ventricular function to left
  • parasymps: inhibit SA node function. Muscarin ACh (M2) inhibit adenylate cyclase
    > vent shift to right function
20
Q

Hormonal control

A
  • thyroid hormones and insulin both are positive inotropes (oddly so is glucagon)
  • CO2 reduces contractit
21
Q

Premature ventricular contraction

A

Beat generated by PVC is early and sub maximal force due to inadequate filling
Following beat is greater than normal

22
Q

Ejection fraction formula

A

EF = SV/EDV = EDV - ESV/EDV

23
Q

Delta Pressure formula

A

( essentially V= IR)

Delta P = Q (flow)R

24
Q

MAP formula

A

MAP-RAP=(CO)(TPR)

MAP= Pdys + .33(Psys-Pdys) or diastolic + 1/3 pulse pressure

25
Q

Coronary arteries

A
  • RPM: right; posterior IV, marginal

- Left coronary; LAD, circumflex (LLC)

26
Q

Starling curve

A
  • force of contraction is proportional to EDV length of cardiac muscle fibers
27
Q

TPR calculation

A

TPR = MAP-RAP (80)*/CO

  • 80 is the conversion factor for dyn*sys/cm^5
28
Q

A/P conduction velocity

A
  • slowest: AV (as seen in PR interval)

- fastest: purkinje fibers

29
Q

CO, CO (based on O2), SW, DD, MAP, MAP looking at TPR

A
  • CO=(HR)(SV)
  • CO=q/(Pvo2-Pao2)
  • SW=(SV)(MAP)
  • DD=(HR)(MAP)
  • MAP= Pdys + .33(Psys-Pdys)
  • MAP-RAP=(CO)(TRP)