CV a&p Flashcards
do skeletal myocytes or ventricular myocytes contain more mitochondria?
ventricular myocytes contain more mitochondria
normal ventricular RMP and what regulates it
-90mV, regulated by potassium
what does hypocalcemia and hypercalcemia do to threshold potential respectively?
hypocalcemia decreases TP (cells depol more easily bc its closer to RMP)
hypercalcemia increases TP
the wave of depolarization throughout the heart is regulated by gap junctions or t tubules?
gap junctions
equilibrium potential
no net movement across cell membrane. inside potential equals outside potential
which equation relates to equilibrium potential
nernst equation
automaticity
ability to generate AP spontaneously ex) SA node and HR
excitability
ability to respond to electrical stimulus by depolarizing and firing an AP. ex) conduction and contractile CV cells
conductance
ability to transmit electrical current. ions are charged and therefore require an open channel.
open ion channel increases conductance of that ion (duh)
lusitropy
rate of myocardial relaxation
dromotropy
conduction velocity through heart
RMP is determined by 3 things
chemical force (concentration gradient)
electrostatic counter force
Na/K/ATPase
what is the primary determinant for RMP
K. the nerve cell continually leaks this at rest
decreased serum K makes RMP more
negative, cells become more resistant to depol
increased serum K makes RMP more
positive, cells depol more easily
what is the primary determinant of threshold potential
calcium
a cell depolarizes when what enters the cell
Na or Ca2+
what happens during repolarization
K leaves the cell or Cl- enters the cell
resistant to subsequent depol during refractory period
hyperpolarization
movement of cells membrane potential to a more negative value beyond baseline RMP.
purpose of Na/K/ATPase
restores ionic balance towards RMP
1. removes Na that enters the cell during depol
2. returns K that has left the cell during repot
for every _______ ions the Na/K/ATPase pump removes, ___________ ions go back into the cell
for every 3 Na ions it removes, 2 K ions go back into cell
what happens during cardioplegia with high K
Na channels get locked in their closed inactive state
5 phases of myocyte AP
0: depol (Na in)
1: initial repol (K in, Cl- out)
2: plateau (K in, Ca2+ out)
3: repol (K out)
4: maintenance of trans membrane potential (K+ out and Na/K/ATPase fx
what’s the point of the plateau phase in a cardiac myocyte (that neurons dont have)
gives myocytes time to contract and eject SV
relation of myocyte AP to EKG
myocyte events during phase 0: depolarization
TP of -70 is met
activation of fast VgNa channels
slope indicates conduction velocity
myocyte events during phase 1: initial repolarization
inactivation of Na channels
K and Cl- channels open
myocyte events during phase 2: plateau
activation of slow VgCa channels counters loss of K to maintain depolarized state
delays repolarization
maintains fast Na channels in inactivated state
prolongs absolute refractory period
myocyte events during phase 3: final repol
k channels open, delayed rectifier
K leaves cell faster than Ca2+ enters- repol
slow Ca2+ channels deactivate
restores transmembrane potential to -90mV RMP
myocyte events during phase 4: resting phase
K leak channels open (to maintain RMP)
Na/K/ATPase (removes 3 Na gained during depol and replaces 2 K lost during repol)
channel that is the primary determinant of the pace makers intrinsic HR (SA node)
I-f (funny channels). sets rate of spontaneous phase 4 depol. funny channels are activated from hyper polarization
conduction of AP from SA node
SA–> internal tracts –> AV –> bundle of his –> left and right bundle branches –> purkinje fibers
RMP of SA node
-60mV (higher than cardiac myocytes)
SA node AP in relation to EKG
order of SA node AP
phase 4
phase 0
phase 3
SA node events during phase 4: spontaneous depolarization
Na in (via I-f channels) and Ca2+ out via T type channels
at -50mV, t type Ca2+ channels open to further depol the cell.
SA node events during phase 0: depolarization
Ca2+ in via L type channels
Na and T type Ca2+ channels close
SA node events during phase 3: repolarization
K channels open and K exits the cell making it more negative
K efflux repolarizes cell to return it to phase 4
repol decreases calcium conductance by closing L type calcium channels
intrinsic firing rate of SA node
70-80 (faster in denervated heart)
intrinsic firing rate of AV node
40-60
intrinsic firing rate of purkinje fibers
15-40
what 3 variables can we manipulate to alter HR?
rate of spontaneous phase 4 depolarization (slope increases like with NE admin)
threshold potential (TP becomes more negative, closer to RMP)
RMP (RMP becomes more positive, closer to TP)
how does Ach slow HR
stimulates M2 receptor, increases K conductance and hyper polarizes SA node. decreases slope of phase 4 conduction.
baseline CaO2
20 mL/O2/dL
baseline DO2
1000mL/min
baseline VO2
250mL/min or 3.5mL/kg/min
baseline CvO2
15mL/dL
DO2 equation
CO x [(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10
=CO x CaO2 x 10
CaO2 equation
(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)
MAP equation
(CO x SVR)/ 80 + CVP
poiseuilles law
Q= BF
R= radius
Pa-Pv is change in arterial pressure gradient
viscosity
l= length of tube
when radius to the fourth power is tripled, what is the increase in flow
81 x increase
when radius to the 4th power is quadrupled, what is the increase in flow
256 x increase
SV equation and normal value
CO x (1000/HR)
50-110mL/beat
EF equation
[(EDV-ESV)/EDV)] x 100 aka
SV/EDV x 100
SVR equation
[(MAP-CVP)/CO] x 80
CI formula and normal value
CO/BSA
normal: 2.8-4.2L/min^2
SVI and normal value
SV/BSA
normal: 30-65mL/beat/m^2
SVRi and normal value
(MAP-CVP)/CI x 80
normal 1500-2400 dynes/sec/cm-5 per m^2
PVR equation and normal value
(MAP-PAOP)/CO x 80
normal: 150-250 dynes/sec/cm^-5
PVRi and normal value
(MPAP-PAOP) x CI / 80
normal: 250-400dynes/sec/cm-5 per m^2
surrogate measures of LVEDV
LVEDP, LAP, PAOP, CVP
surrogate measures for ventricular output
CO, SV, LVSW, RVSW
surrogate measures for EDV include
RVEDV
LVEDV
describe how B2 increases contractility
- activation of more L type ca channels (more ca enters the cell)
- stimulation of ryanodine 2 receptor to release more Ca
- stimulation of SERCA 2 pump to to increase Ca uptake with subsequent Ca2+ release
net effect is more forceful contraction over shorter time with enhanced relaxation between beats
SV is decreased by (3)
decreased preload
decreased contractility
increased afterload
law of laplace equation in relation to wall stress
wall stress = intraventricular pressure x radius / ventricular thickness
review the wiggers diagram (EKG, aortic pressure, LAP, LVP)
review the left ventricular volume as it relates to left atrium, left ventricle, and mechanical events in the heart (wiggers diagram format)
key events in isometric ventricular contraction
LVP>LAP
MV closes (first heart sound)
key events in isometric ventricular relaxation
aortic pressure > LVP –> AV closes (2nd heart sound)
dichromic notch occurs here because AV closure initiates small retrograde flow that terminates when valve is all the way closed which is where the dichrotic notch happens
lusitropy: where Ca2+ is pumped back into SR
two events that happen during systole include
isometric ventricular contraction and ventricular ejection
name the 6 stages of the cardiac cycle and whether they belong to diastole or systole
- rapid filling (diastole)
- reduced filling (diastole)
- atrial kick (diastole)
- isovolumic contraction (systole)
- ejection (systole)
- isovolumic relaxation (diastole)
when the LV is compliant, does LV filling increase pressure?
no, the LV should stay around 2-3mmHg during filling (until atrial kick that increases LVP to 5-7mmHg)
what is the typical stroke volume
LVEDV-LVESV=
120-50=
70 is typical SV
normal EF
mild dysfunction
moderate dysfunction
severe dysfunction
normal >50%
mild: 41-49%
moderate 26-40%
severe < or = 25%
this pressure volume loop represents
increased preload (ex fluid bolus)
loop gets wider but returns to original ESV. SV increased
this pressure volume loop represents
decreased preload (ex furosemide)
loop gets narrower but returns to original ESV. SV decreased.
this pressure volume loop represents
increased contractility (ex B1)
loop gets wider, taller, and shifts to the left.
this pressure volume loop represents
decreased contractility (ex HFrEF)
decreased SV, decreased chamber emptying, increased ESV. loop gets narrower, shorter, shifts to the right.
this pressure volume loop represents
increased after load (ex acute HTN or phenylephrine)
decreased SV, decreased chamber emptying, increased ESV. loop gets narrower, taller, and shifts ESV to the right.
this pressure volume loop represents
decreased after load (ex vasodilators such as Na nitroprusside)
increased SV, increased chamber emptying, decreased ESV. loop gets wider, shorter, shifts ESV to the right.
which arteries arise from aortic root
LCA and RCA
what does LCA divide into
LAD and circumflex
what does LAD perfuse
anterolateral and apical walls of left ventricle as well as anterior 2/3 of intraventricular septum
what does CXA perfuse
left atrium as well as lateral and posterior walls of LV
what does RCA perfuse
RA, RV, inter arterial septum, posterior third of interventricular septum
what does the posterior descending artery perfuse
inferior wall. origin of this vessel defines coronary dominance
define right dominance
in 70-80% of patients, RCA gives rise to posterior descending artery
define left dominance
circumflex or RCA and circumflex supply PDA which can also be defined as co dominance
where do these conduction points receive blood supply from
SA and AV node usually get perfused by RCA
bundle of his and left bundle branches usually get perfused by LCA
which artery runs alongside these veins
great cardiac vein
middle cardiac vein
anterior cardiac vein
great cardiac vein LAD
middle cardiac vein PDA
anterior cardiac vein RCA
describe the thesbian veins
blood returning to left side of the heart by way of thesbian circulation contributes to small amount of anatomic shunt. volume of deoxygenated blood dilutes PaO2 of oxygenated blood that passes through lungs.
go through coronary artery relation and EKG table
best view (and second best view) for diagnosing LV ischemia for TEE
mid papillary muscle in short axis is first best
second best view is apical segment also in short axis
ID these arteries
coronary BF equation and normal value
coronary perfusion pressure / coronary vascular resistance
OR
aortic DBP - LVEDP
normal value: 225-250mL/min or 4-7% of CO
at rest, myocardium consumes O2 at a rate of
8-10mL/min/100g with an extraction ratio of ~70%
most important determinant of coronary vessel diameter
local metabolism
MOA of adenosine at coronaries
potent coronary vasodilator and byproduct of ATP metabolism
as MVO2 increases, adenosine is released
effect of histamine 1 at coronary arteries
increases Ca2+ and causes constriction
effect of histamine 2 at coronary arteries
increased cAMP, decreased MLCK sensitivity to Ca2+
which waveforms correlate with coronary perfusion for aortic pressure, LCA flow, and RCA flow
in LCA, flow is greatly diminished during systole
in RCA, blood flow is a little more constant because RV doesn’t generate a blood pressure high enough to occlude during systole
how does decreased P50 influence O2 supply to myocardium
shifts curve to the left and decreases supply.
factors that decrease coronary flow
decreased aortic pressure (less P1-P2 gradient) and vessel diameter
increased LVEDP
how does increased aortic diastolic pressure affect supply and demand for coronaries/myocardium
increases supply and demand
increased aortic DPB increases LVEDP and coronary perfusion pressure
increased aortic pressure increases demand via wall tension and afterload
how does increased preload influence supply and demand for coronaires/myocardium
decreased supply and increased demand
increased EDV decreases CPP
increased demand because increased preload increases wall stress
general overview of 3 important pathways that influence calcium concentration in vascular smooth muscle
- G protein cAMP pathway –> vasodilation
- NO cGMP pathway–> vasodilation
- PLC pathway –> vasoconstriction
effect of cAMP and PKA in VSMC’s versus cardiac myocyte
cardiac myocyte: PKA and cAMP increase intracellular calcium
VSMC: increased PKA decreases intracellular calcium
steps in the NO cGMP pathway
- NOS (nitric oxide synthase) catalyzes conversion of L arginine to nitric oxide
- NO diffuses from endothelium to smooth muscle
- NO activates guanylate cyclase
- guanylate cyclase converts GTP to GMP
- increased cGMP increases intracellular Ca2+ leading to smooth muscle relaxation
- PDE5 activates cGMP to guanosine monophosphate
activators of the PLC pathway include (4)
neo, NE, AT2, and endothelin 1
NO production is increased by (7)
Ach, substance P, bradykinin, serotonin, vasoactive peptide (VAP), thrombin, shear stress
list the following arteries in the correct order as they arise from the aorta (first being most proximal to aortic valve):
innominate
left SCA
L coronary artery
L common carotid
- left coronary artery
- innominate artery (brachycephalic)
- left common carotid
- left subclavian artery
list the following vessels that arise from the transverse aortic arch from most proximal to most distal:
left common carotid
innominate (sometimes called brachycephalic)
left subclavian
most proximal: 1. innominate (sometimes called brachycephalic)
2. left common carotid
3. left subclavian
Define frank starling curve and what influences it
relationship between ventricular volume and ventricular output
a reduction of which factor would most likely augment SV
afterload
best TEE view for diagnosing LV ischemia
and second best
mid papillary muscle level in short axis
apical segment also in short axis
what does this graph represent
LCA flow through cardiac cycle (RCA flow is more constant)
what does this graph represent
LCA flow through cardiac cycle (RCA flow is more constant)
right vagus nerve and left vagus nerve innervate which nodes respectively
right: SA
left: AV
