cardiac Flashcards
properties of cardiac muscle
-have properties of both skeletal and neural tissue
-when presented with electrial stimulus, cardiac myocytes contract in a coordinated way contributing to pumping mechanism of the heart
automaticity
ability to generate an AP spontaneously. cardiac conduction cells (SA node) display this when they set the HR
excitability
ability to respond to an electrical stimulus by depoloraizing and firing AP
cardiac cells are excitable b/c they can respond (depolarize) when presented with an electrical stimulus
conductance
the ability to transmit electrical current
can ions pass through cell membrane
no- they are charged
ion needs an open channel to cross from one side of the membrane to the other
what does open channel vs closed channel do
open channel- increases conductance of the ion
closed channel- reduces conductance of the ion
chronotropy is in reference to
HR
dromotropy
describes conduction velocity through the heart
(velocity= distance/ time)
lusitropy
describes rate of myocardial relaxation during diastole
RMP
electrical potential across a cell membrane at rest
what determine RMP (3 things)
chemical force (chemical gradient), electrostatic counterforce, na/k atpase
at rest nerve cell continious leaks __
k (loses pos charges)
what is primary determinant of RMP
K
decreased vs increased K
decreased K = rmp becomes more neg- cells more resistance to depolarization
increased K= rmp becomes more pos- cells depolarize more easily
threshold potential
voltage change that must occur to iniate depolorarization
what is the prime determinent of threshold potential
serum ca
decreased vs increased ca
decreased ca= tp becomes more neg
increased ca= tp becomes more pos
depolarization
movement of a cells membrane potential to a more pos value (less of a charge difference between inside and outside of the cell)
a cell depolorizes when na or ca enters the cell
can depolorization be stopped
no depolorization is all or none- once it begins it cannot be stopped
ability of a cell to depolarize is determined by the difference of
rmp and TP
when RMP is closer to TP..
earier to depolarize
when RMP is further from TP
harder to depolarize
repolarization
return of cells membrane potential to more neg value after depolarization
cell repolarizes when ___ or ___
k leaves cell or cl enters cell
during the refractory period can the cell depolarize
cell is resistance to depolarization- this is b/c RMP is further from TP
hyperpolarization
movement of cells membrane potential to a more neg value beyond baseline RMP
when does hyperpolarization happen
after repolarization cell typically hyperpolarizes for short time
in excitable tissue what restores the ionic balance towards RMP
na- k atpase restores ionic balance
what is the purpose of na- k atpase
- removes na that entered the cell during depolarization
-returns k that has left the cell during repolarization
for every 3 na ions it removes, it brings __ k ions into the cell
2
does na- k atpase turn on and off
always on!!
is na- k atpase active
active! - needs atp- duh
how is na- k atpase inhibited
inhibited by digoxin
what happens with severe hyperkalemia
serum k very high- inactives na channels (they arrest in their closed inactive state)
ex: K+ in cardioplegia solution arrests the heart in diastole during CPB, K concentration does not allow the cells to repolarize)
decreased serum ca
TP becomes more neg
cells depolarize more easily
hypercalcemia
tp increases
cells more resistant to depolarization
ex: IV calcium is given to reduce risk of dysrthyhmias in pt with hyperkalemia (increase gap between RMP and TP)
unlike neurons, cardiac myocytes AP have
a plateua phase where depolarization is prolonged. this gives cardiac myocytes time to contract, so the heart has enough time to eject stroke volume
what nodes do not have a plateau phase
SA and AV node
5 phases of cardiac AP
phase 0= depolarization: Na in
phase 1= inital repolarization: Cl in and K out
phase 2= plateau: ca in and k out
phase 3= repolarization: K out
phase 4= maintence of transmembrane potential: k out and na/k atpase function
how does conduction move
sa- intenodal tracts- av- bundle of his- L and R bundle branches- purkinje fibers
sa node action potential characteristics
3 phases (phase 1 or phase 2)
rmp is higher
na/ k atpase re-establishes na and k gradients after repolarization
what cells in myocardium are capable of automaticity
all cells! but they all have a diff rate of spontaneous depolraization
at rest which autonomic tone takes over
pns>sns
pns tone uses what nerves
vagus nerve (CN 10)
what nodes to the R and L vagus nerve innervate
R innervates SA
L innervates AV
sns tone comes from what nerves
cardiac accelerator fibers (t1-t4)
what is the intrinsic firing rate of SA
70-80 (faster in denervated heart)
what is the intrinsic firing rate of AV node
40-60
what is the inrinsic firing rate of purkine fibers
15-40
what 3 ways can you alter the HR
- rate of spontaneous phase 4 depolarization
- threshold potential
- resting membrane potential
what situations (slope changes) increase HR
- slope of phase 4 depol increases
- slope of phase 4 depol remains constant but TP becomes more neg
- slope of phase 4 deol remains constant but RMP becomes less neg- shortens distance between RMP and TP so cells reach threshold faster
what catecholamine and receptor increases HR by sns tone
NE stimulates B1 - increases HR by increasing na and ca conductance - increasing slope of phase 4 (steeper slope)
what receptor slows HR (pns activation)
acetacholine stimulates m2 receptor- increases k conductance and hyperpolarizes SA node
decrease RMP and reduces slope of spontaneous phase 4 depolariazation (less steep slope)
look into oxygen delivery equation
dont know
what does cao2 tell us
oxygen content in the blood- how many grams of o2 is in decileter of arterial blood
most o2 is bound to hgb- small amount is dissolved
what law does the amount of gas dissolved in a solution follow
henrys law- at a constant temp the amount of gas that dissolves in a solution is directly proportional to partial pressure of that gas
whats ohms law
forms the basis for understanding hemodynamics
map=( co x svr)/ 80 + cvp
poiseullies law
an adaptation of ohms law- incorporates vessel diameter, viscosity and tube length
look up formula
flow describes
movement of liquid, electrict or air per unit time
what is the greatest impact on flow
altering radius of tube- raises radius to 4th power
vascular resistance is primarily determined by
radius of arterioles- small changes in vessel diameter can yield big impacts on tissue blood flow
what is reyonlds number used for
can be used to predict if the flow will be laminar or turbulent
what are the numbers to determine reynolds number
re < 2,000 predicts that flow will be mostly laminar
re >4000 predicts that flow will be mostly turbulent
re= 2,000- 4,000 suggests transitional flow
whats the issue with turbulent flow
a lot of energy is lost to heat and vibration
vibrations occuring with turbulent flow can produce
a murmur (valvular ht disease) or bruit (carotid stenosis)`
viscosity
result of friction from intermolecular forces as fluid passes through a tube. blood viscosity is determined by hct and body temp
viscosity is inversely proportional to
temp. a cooler temp increases viscosity and resistance
how does viscosity relate to administering rbcs
can improve flow- can dilute the unit with normal saline (decreased hct) by running it through fluid warmer (inc temp)
CO
hr x sv
5-6 L/min
CI
co/ bsa
2.8-4.2 L/min
sv
edv- esv
50-110 ml/beat
sv index
sv/ bsa
30-65 ml/beats per min2
ejection fraction
edv- esv / edv x 100
60-70%
normal map
70-110
pulse pressure
sbp-dbp
40
svr
map- cvp/ co x 80
800-1500 dynes x sec x cm5
to do svr index just replace co with ci
pvr
mpap - paop / co x 80
150-250 dynes x sec x cm5
sarcomere
the functional unit of contractile tissue in the heart. the amount of tension that each sarcomere can generate is directly r/t the number of cross brides that can be formed before contraction
the greater the tension the ___ the force of contraction
greater- up to a point!
preload
ventricular wall tension at end of diastole (just before contraction
often interchangable with ventricular end diastolic volume
what curve tells reltionship between ventricular volume and ventricular output
frank starling
is contractility dependent on PL and AL
no
inc PL= inc force of contraction (starlings law) not the same as increased contractility!
contractility is the ability of myocardial sarcomeres to perform work (shorten and produce force)
atrial kick contributes to __ % of CO
20-30
when would you be reliant on atrial kick
a non compliant stiff ventricle
conditions associated with reduced myocardial compliance
myocardial hypertrophy, HF with pEF, fibrosis, aging
more likely to see lower CO, cardiac rhythm disturbances, afib, junctional rhythm
