Cardiac Energy/control Flashcards
External cardiac work
- moving blood
- only about 10%
- stroke work
SW = SV x MAP
Energy Production
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)
Internal cardiac work
- external work is used an estimator
- roughly 5 x external
- mostly done during isovolumetric contraction
Pressure vs volume work
- pressure is primary determinant
- volume has little effect
- determined by delta in O2 consumption
Heart rate and work
- more costly because the heart spends more time in isovolumetric contraction which is where internal work takes place
Contractility
- 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
Energy req estimate (and limitation)
- Double product = HR x MAP (KNOW)
- not a valid method when ventricles are dilated
CO and SV Eq
CO=SVxHR
SV=EDV-ESV
Autonomic control
- sympathetic (increase HR) NO beat to beat
- parasympathetic (decrease HR) SA node beats naturally at around 100 BPM
Parasympathetic control of heart
- slows HR
- ACh opens Special K channels (increasing phase 4) and decreases Ca conductance
- predominantly the right vagus
Sympathetic control of heart
- 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
Epi vs norepi
- 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
Neural reg of cardiac function location
- frontal lobe
- orbital cortex
- motor/premotor
- solitary and rostral/caudal tract
Baroreflex
- 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
Bainbridge reflex and atrial receptors
- 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
Resp cardiac arrhythmias
- cycle increases on expiration (and visa versa)
- vagus vs. phrenic activity
Venous return during respiration
- increased intrathroacic pressure decreases venous return (passing out during vigorous valsalva)
Chemoreceptors reflex
- respond to low O2 or high CO2 (much stronger drive)
- compensation is rapid
- can see this effect in quadriplegics
Treppe phenomena
- Increase in contraction frequency -> increase in force
- produced by rise in intracellular Ca
Molecular control
- 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
Hormonal control
- thyroid hormones and insulin both are positive inotropes (oddly so is glucagon)
- CO2 reduces contractit
Premature ventricular contraction
Beat generated by PVC is early and sub maximal force due to inadequate filling
Following beat is greater than normal
Ejection fraction formula
EF = SV/EDV = EDV - ESV/EDV
Delta Pressure formula
( essentially V= IR)
Delta P = Q (flow)R
