Cardio Physiology Flashcards
What is nernst potential equation?
Ex = RT/zF * ln [Xo]/[Xi]
What is resting membrane voltage?
- 85 mV
- membranes are permeable to K+ but not Na or Ca
What is K equilibrium potential [Ek]?
-89 mV
What is Na equilibrium potential [Ena]?
+70 mV
What is Ca equilibrium potential [Eca]?
+ 133 mV
Which ion sets the resting voltage?
K+
What is phase 0 of ventricular AP? What channels open/closed?
rapid upstroke and depolarization
due to voltage gated Na channels opening [ Na in]
What is phase 1 of ventricular AP? What channels open/closed?
initial repolarization
- inactivation of voltage gated Na channels
- voltage gated K channels begin to open [K out]
What is phase 2 of ventricular AP? What channels open/closed?
plateau phase = voltage decreasing at very slow rate
- Ca in through voltage gated Ca channels [depolarizing]
- balanced by K out [repolarizing]
Ca in triggers Ca release from SR and myocyte contraction
What is phase 3 of ventricular AP? What channels open/closed?
rapid repolarization
lots of K out due to opening voltage-gated slow K channels
- slow voltage gated K open [K out]
- voltage gated Ca close
What is phase 4 of ventricular AP? What channels open/closed?
resting potential
high K permeability through K channels
What is path of action potential propagation in a heartbeat?
- SA node generates AP
- propagated to atrial muscle
- activates AV node between atria and ventricles
- goes down bundles of his to left and right bundle branches
- reaches purkinje fibers of L and R ventricles which excite subendocardium then epicardial surface
How many contractions per AP in cardiac cell? why?
one contraction per AP
because of refractory period after AP –> need time to recover until 2nd AP
What is the absolute refractory period?
time that must elapse before 2nd stimulus can cause an AP
–> impossible to trigger second AP during this time
What is the relative refractory period?
period of time when very large stimulus can produce weak action potential [AP]
stronger signal than normal is required to produce a normal AP
What is phase 0 for SA node?
upstroke
- opening Ca voltage-gated channels
What is phase 2 for SA node?
no phase 2 in SA node
What is phase 3 for SA node?
inactivation of Ca channels and activation of K channels
–> lots of K efflux to repolarize
What is phase 4 for SA node?
slow diastolic depolarization
membrane potentially spontaneously depolarizes as Na conductance increases [If= funny current] , slope of phase 4 determines HR
- If in
- Ca out and Na in [NCX]
What is difference phase 0 ventricular vs SA node cells?
ventricle: Na open/in
SA: Ca channels open/in, no fast voltage-gate Na b/c less negative resting voltage of these cells
phase 0 for ventricular myocyte = much faster [300 V/s]
SA = 20 V/s
What is funny current [If]?
current that depolarizes in phase 4 of SA node contraction
mixed Na/K inward current
not present in ventricle
What is inward rectifier current?
Ik = in ventricle but not SA node
responsible for flat phase 4
How does phase 3 differ ventricle vs SA?
comparable
both have delayed rectifier K channels responsible for repolarization
What is baseline voltage for SA node cells?
-60 mV
[compared to ventricle -85 mV]
What is NCX current?
Na Ca exchanger current
- 3 Na in for 1 Ca out
- net Ca out and Na in
What is single electrode whole cell voltage clamping?
- voltage clamp controls cellular voltage and measure of corresponding ionic current
- record changes in ionic current in response to series of depolarizations
- plot peak current vs voltage to understand underlying characteristics
What is convention inward vs outward currents?
inward = negative outward = positive
What direction does current travel when voltage across membrane is greater than the nernst potential for an ion?
pos current
- ion will move out of cell [assuming + charge ion]
What direction does current travel when voltage across membrane is less than the nernst potential for an ion?
neg current
- ion will move into cell [assuming + charge ion]
What direction will Na/Ca/K go if voltage = 80?
- K out
- Na out
- Ca in
What is mech of activation and speed of activation of Ik/Ach vs If [funny]?
Ik,Ach = activated by gprotein By subunits
If = activated by increased CAMP
- requires intermediate enzyme AC thus much slower
Is parasympathetic or sympathetic effect on HR faster?
parasympathetic = by activation Ik by G protein By subunit
When do voltage gated Na channels [Ina] open? Close?
- open at greater than -60 mV
- close milliseconds later
thus not open at -85 mV resting potential
When do L-type Ca channels [Ica] open? close?
- open at more positive membrane potential than Na
- activates and inactivates 10x slower than Na
What mediates parasympathetic stimulation of heart cells?
via muscarinic ACh receptors
What is effect of parasympathetic stimulation in SA? AV? ventricular?
SA: slower firing by activation of Ik, Ach by G protein By subunits
AV: slower electrical conduction through AV by reduced Ica due to decreased PKA activity
ventricle: no effects
What is the inward rectifying K channel [Ik1]? when is it open/closed?
- open at resting potential
- closes at positive potentials and closed completely at 0 mV
keeps ventricle membrane potential constant at -85 mV
not present in SA node
What are the delayed rectifying K channels [Ikr and Iks]? when are they open/closed?
- closed at resting potential
- open in plateau [phase 2] positive potential
Ikr = rapid delayed rectifier = can be blocked by meds Iks = slow delayed rectifier
What is effect of sympathetic stimulation of heart cells on SA? AV? ventricles?
SA: faster firing by activation If by increase CAMP
AV: faster electrical conduction through AV by increased Ica due to increase PKA activity
ventricle: stronger contraction, faster relaxation
- increased Ica due to increased PKA
- phosphorylation phospholamban, increased SERCA
What receptors mediate sympathetic stimulation of heart cells?
B-adrenergic receptors
What is difference AP vs ECG voltage?
AP = Vin - Voutside of cell
ECG = V2 - V1 = voltages outside of cells at 2 different locations = AP1 - AP2 = subtract APs
What is funny current? another name for the channel?
If = HCN = hyperopolarization-activated cyclic nucleotide gated channel
present in SA and AV node but not ventricle
- closed at more positive potentials, opens when membrane potential less than -50
mixture of Na and K [mostly Na]
depolarizing
Is heart under parasympathetic or sympathetic control? blood vessels?
heart = both; except ventricles just sympathetic
blood vessels = just sympathetic
What is chronotropy?
HR
What does a positive chronotrope do?
increase HR
What is inotropy?
contractile strength
What does a positive inotrope do?
increases force of contraction
What is action of digoxin?
positive inotrope
What is dromotropy?
speed at which electrical impulses propogate through heart
What is lusitropy?
speed of relaxation of ventricle
Upward or downward deflection [wave] in ECG?
- depolarization toward + electrode
- depoarlization away from + electrode
- repolarization toward + electrode
- repolarization away from + electrode
- depolarization toward + electrode
== pos deflection [wave] - depoarlization away from + electrode
== neg deflection [wave] - repolarization toward + electrode
== neg deflection [wave] - repolarization away from + electrode
== pos deflection [wave]
What part of heart is main determinant of dromotropy?
SV node!
What is parasympathetic innervation of SA node?
vagus nerve
Is resting HR in a heart transplant patient higher or lower than normal?
resting HR in heart transplant 90-100 bpm compared to healthy = 60-80
What happens to heart if you give atropine?
atropine = parasympathetic antagonist
–> increase HR
What happens to heart if you give B-blocker?
blocks sympathetics –> HR decrease
Do you get bigger change in HR if you block parasympathetic or sympathetic?
block PNS = much greater rise in HR compared to blocking SNS = not as much decrease HR
What is the cellular basis for T wave?
endocardium activates before and repolarizes after epicardium
if you do Vendo-Vepi you get an upward deflecting t wave
== ventricular repolarization
What is the cellular basis for p wave?
atrial depolarization
What is the cellular basis of QRS complex?
ventricular depolarization
What is equation for aVL from other leads?
aVL = 0.6 * (V1-V3) [L is for left]
What is equation for aVR from other leads?
aVR = 0.6 * (-V1-V2) [R is for Right]
What is equation for aVF from other leads?
aVF = 0.6*(V2 + V3) [F is for food
What angle for aVL?
-30
What angle for aVR?
-150
What angle for II?
+60
What angle for aVF?
+90
What angel for III?
+120
What is Ohm’s equation for BP control?
MAP = CO * TPR
MAP = mean arterial pressure CO = cardiac output TPR = total peripheral resistance
What does increase in MAP do to CO?
nothing!
What are the 3 phases of baroreceptor reflex?
- something happen to change MAP
- reflex response tries to return MAP to level that existed before
- after changes, new steady state reached
What is cellular meaning of PR interval?
propagation through AV node
Why don’t you see a signal from atrial repolarization?
atria are much smaller = the muscle mass is too small
What does baroreceptor reflex do when there is hemorrhage to return MAP to steady state? Effect on myocardium + vessels?
on myocardium:
- increase HR –> increase CO
- increase contractility –> increase CO
on vessels:
- arteriolar smooth muscle contraction –> increase TPR
- venous smooth muscle contraction –> increase preload –> increase CO
What is renin-angiotensin-aldosterone system [RAAS] action to regulate BP?
- detect decreased pressure in kidneys –> release renin from juxtaglomerular cells
- increase renin –> increase angiotensin I –> ACE [angiotensin converting enzyme] –> angiotensin II
- angiotensin II
- -> increase aldosterone –> increase Na reabsorption in kidney –> increase blood volume
- -> vasoconstriction –> increase TPR
What are the 4 phases of cardiac PV Loop?
- isovolumic contraction
- ejection
- isovolumic relaxation
- diastolic filling
What is preload?
amount of pressure/stretch in heart muscle before contraction
What is afterload?
pressure that exists in the aorta/vasculature against which
When does MV close on PV loop?
bottom right = after diastolic filling at start of isovolumic contraction
When does AoV open in PV loop?
top right = after isovolumic contraction at start of ejection
When does AoV close in PV loop?
top left = after ejection at start of isovolumic relaxation
When does MV open in PV loop?
bottom left = after isovolumic relaxation at start of filling
What is EDPVR?
- end diastolic pressure-volume relationship
- bottom right of PV loop [MV closure] occurs along it
What is ESPVR?
- end systolic pressure-volume relationship
- top left of PV loop [AoV closure] occurs along it
What happens to PV loop if increase preload with constant afterload and contractility?
shift up along both ESPVR and EDPVR curves
–> increase stroke volume and arterial BP
What are 2 ways to increase preload?
- increase blood volume
- venoconstriction –> decrease venous compliance
What is starling curve?
relationship preload and stroke volume
increase preload [LVEDP] –> increase stroke volume
What are some things that cause increased preload?
- fluid retention [as in advanced heart failure]
- constriction of veins
What are some things that cause decreased preload?
- blood loss
- dilation of veins
What happens to PV volume if increased TPR with constant preload and contractility?
- stays in same place along EDPVR
- moves up on ESPVR [end systolic volume increases]
- SV decreases [width of loop]
How do you get increased TPR?
arteriolar constriction
What does TPR represent?
afterload
How do you calculate SV from PV loop?
SV = width of loop
= EDV - ESV
What are some things that cause increase afterload?
- temporary constriction of arterioles
- chronic hypertension
- aortic stenosis [valve narrowing or block]
What are some things that cause decrease afterload?
dilation of arterioles
What happens to PV loop if increase contractility with constant preload and afterload?
- increase stroke volume
- increase ejection fraction
- decrease end systolic volume
- shits ESPVR line to the left
What are some ways you can increase contractility?
- B adrenergic stimulation ventricles
- increase plasma Ca
- increase muscle mass [ physiological hypertrophy]
What are some ways you can decrease contractility?
- B adrenergic blockade
- Ca channel blocker
- decrease energy supply [ischemia or hypoxia]
- decrease muscle mass [MI]
How does venous return change with venous/atrial pressure?
as venous return/flow increases, atrial/venous pressure decreases
In steady state was is relationship CO and venous return?
in steady state CO = venous return
What does increased blood volume do to venous return curve?
line shifts up
What does decrease TPR do to venous return curve?
y intercept increases = steeper slope
What does venoconstriction do to venous return curve?
x intercept [mean systemic pressure] increases = shallower slope
