Maybe lecture 30 Flashcards
Heart failure is…
results in…
eventually becomes
despite adequate venous return, CO is insufficient to meet tissue demands
- compensation-sympathetic drive inc, inc HR, and vasoconstriction
- decompensation(undesirable effects)
in early compensated heart failure inc vasoconstriction of peripheral veins/venules/arterioles leads to
inc venous return/EDV which leads to inc contractility
inc TPR/afterload
and inc cardiac work
RAAS activation in early compensated heart failure leads to
further vasoconstriction inc preload (blood volume-> venous return) and afterload (arteriolar resistance/BP)
inotropes do what
inc the amount of Ca in the cell through cell membrane of SR
What do beta receptors do(2)
change the sensitivity of the Ca channel
activate adenyl cyclase->inc cAMP, opening of RO Ca channels
Cardiac effects from sympathetic stimulation in early compensated heart failure
inc HR, Inc SV->inc CO->inc work on a failing heart
Sympathetic stimulation and Frank Starling principle in early compensated heart failure
Inc EDV->inc CO
but limited capacity to dilate
-start to get bad amount of preload
Chronic activation of the sympathetic nervous system leads to(2)
reduced baroreceptor sensitivity(maintained sympathetic drive even when MAP is appropriate)
Down regulation of Beta receptors in the heart(dec capacity of heart to respond to sympathetic stimulation
Chronic activation of RAAS(3)
persistent vasoconstriction->inc preload and afterload
Inc blood volume->inc preload
inc angiotensin->dec baroreceptor sensitivity
contractility
the amount of tension that can be developed at any given stretch of the cardiac muscle
What determines cardiac contractility
Ca levels inside the cardiac myocyte
intracellular Ca levels alter when(2)
Ca enters through the cell membrane
Ca is released from SR
Physiological modifiers of contractility: SNS
Transmitter?
Receptors?
transduction pathway?
NA
Beta 1 adrenoreceptors
activation of adenyl cyclase->inc cAMP->opening of RO Ca channels
Positive inotropes
what 4 drugs are there
inc cardiac contractility by inc intracellular Ca levels
could be problematic because->inc workload on heart
pimobendan (calcium sensitizers)
PDE inhibitors
Beta agonists
Cardiac glycosides(digoxin)
Negative inotropes
Which two drugs are there
reduce contractility reduce preload ->reduce workload on heart Beta blockers Ca channel blockers