cardiac a+p Flashcards
cardiac output
CO = SV x HR
SV = volume of blood ejected with each beat
amount of blood the heart pumps out of LV in each min
diminished in HF bc LV is weak and cant adequately pump
stroke volume
difference between end diastolic volume and end systolic volume
EDV = volume of blood at end of relaxation
ESV = residual volume of blood remaining in ventricle after ejection
any factor that alters either EDV or ESV will change stroke volume and thus CO
SV factors
preload = volume of blood in heart
afterload = force opposing ejection of blood from ventricle
contractility = contractile capabilities of heart
preload
stretch of cardiac muscle cells before contraction
chamber volume just prior to contraction
lower leads to lower SV and vice versa
frank starling law
increase in testing muscle fiber length results in greater muscle tension
length tension relationship
heart has ability to change its force of contraction and SV in response to changes in venous return
starling’s capillary forces
at every capillary cell interface, there are 3 fluid compartments:
intracellular = inside cells
interstitial = surrounds cells
extracellular = inside capillary
hydrostatic P
fluid in blood
force that attempts to push fluid out of the capillary pores and into the interstitial and intracellular spaces
water pushing pressure
oncotic pressure
osmotic P
particles in blood (albumin, Na, glu)
force that attempts to pull fluid from interstitial and intracellular spaces into capillary
water pulling P
starlings law of cap forces
oncotic P forces and hydrostatic P forces oppose each other at every cap membrane and attempt to balance each other out
afterload
resistance that must be overcome in order to eject blood from the chamber
LV afterload is primarily determined by aortic BP
an increase in afterload will lead to decrease in SV unless heart compensates
contractility
contractile force of heart muscle cells
primarily determined by amount of free Ca w/n myocardial cell
increased contractility increases stroke volume by causing a greater % of V to be ejected
BF through heart
RA recieves from vena cavae and coronary sinus ->
RV pumps to pulm artery and lungs ->
O2 blood from pulm veins to RA ->
LV ->
ejected into aorta
forward effects in LVF
forward failure effects of weak LV cause decreased perfusion of brain, kidneys, other organs
decreased perfusion of vital tissues activates a neurohormonal response that includes stim of RAAS, ADH, and SNS (baroreceptors sense drop in BP, activate adrenergic receptors)
backward effects in LVF
backward affect of failing LV creates buildup of hydrostatic P in LA, pulm veins, pulm capillaries which causes fluid extravasation into pulm interstitial and intracellular spaces (pulm edema)
opening and closing of alveoli against this fluid is heard as crackles through a stethoscope and is exhibited as cough, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea by pt
