APEX... FML > Unit 3 - CV A&P > Flashcards

Unit 3 - CV A&P Flashcards

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1
Q

Ventricular monocytes….

A
  • contain more mitochondria than skeletal monocytes
  • resting membrane potiential si -90 mV
  • Hypokalemia decreases resting membrane potential (hyperkalemia increases resting membrane potential)
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2
Q

how are myocytes similar to neural & skeletal tissue

A

Like neural tissue:
- generate Resting membrane potential
- can propagate an AP

Like skeletal tissue:
- contain contractile elements arranged in sarcomeres (actin and myosin)
- have T-tubules

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3
Q

3 things unique to cardiac muscle (vs. skeletal and neural)

A
  1. joined by intercalated discs
  2. gap junctions
  3. consume a lot of O2 at rest - 8-10 mL O2/100g/min (contain a lot more mitochondria than skeletale m.)
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4
Q

what is the purpose of gap junctions in cardiac muscle

A

facilitate spread of cardiac AP through myocardium

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5
Q

why do myocytes consume a lot more O2 at rest vs. skeletal muscle cells

A

contain more mitochondria

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6
Q

what is equilibrium potential?

A

situation where there’s no net movement of an ion across a cell membrane

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7
Q

equation used to predict an ion’s equilibrium potential

A

Nernst equation

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8
Q

what is automaticity

A

ability to generate AP spontaneously

cardiac conduction cells (SA node) display automaticity when they set the HR

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9
Q

what is excitability

A

ability to respond to an electrical stimulus by depolarizing & firing AP

Cardiac cells are excitable - they are albe to depolarize when presented with an electrical stimulus

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10
Q

what is conductance

A

ability to transmit electrical current

Because ions are charged, they don’t freely pass through cell membranes. The ion requres an open channel to cross the membrane. an open ion channel, increases the conductace of that ion, a closed channel reduces the conductance

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11
Q

lusitropy

A

rate of myocardial relaxation during diastole

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12
Q

what is RMP?

A

an electrical potential across a cell membrane at rest

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13
Q

Resting Memebrane Potential is established by what 3 mechanisms

A
  1. chemical force
  2. electrostatic counterforce
  3. Na/K-ATPase
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14
Q

what eletrolyte is continuously leaked by nerve cells at rest

A

K+ (loses positive charge)

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15
Q

what is the primary determinant of RMP?

A

K+

increased serum K (hyperkalemia): RMP more positive - cell depolarizes easily
decreased serum K (hypokalemia): RMP more negative - cell depolaraizes less easily

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16
Q

what is threshold potential

A

voltage change that must occur to initiate depolarization

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17
Q

What is the primary determinate of threshold potential? and how does it affect threshold potential

A

calcium
decreased serum Ca2+ = TP more negative
increased calcium = TP more positive

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18
Q

what is depolarization

A

movement of a cell’s membrane potential to a more positive value (less charge difference between inside and outside of cell)

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19
Q

what happens to HR as distance between threshold potential & RMP narrows

A

increases bc myocardial cells reach threshold faster

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20
Q

what is the all or none phenomenon

A

once depolarization starts, it cant be stopped

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21
Q

what determines the ability to depolarize

A

difference of RMP & TP
- when RMP is closer to TP = cell easier to depolarize
- When RMP is farther from TP = cell is harder to depolarize

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22
Q

what happens after depolarization in excitable tissue

A

action potential

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23
Q

what is repolarization

A

return of cells RMP to more negative value after depolarization

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24
Q

what causes cell repolarization?

A

when K+ leaves the cell or Cl- enters the cell (inside of cell becomes more negative)

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25
when is the cell resistant to subsequent depolarization
refractory period
26
what is hyperpolarization
movement of a cell's membrane potential to a more negative value beyond baseline RMP
27
can a hyperpolarized cell be depolarized?
it's more difficult bc RMP is further from TP
28
2 purposes of Na-K-ATPase
1. removes Na+from the cell that enters cell during depolarization 2. returns K+ to the cell that left cell during depolarization
29
for every ___ Na+ ions removed by Na-K-ATPase, ____ K+ ions are brought in
3 Na 2 K
30
positive inotropic drug that inhibits Na-K-ATPase
digoxin
31
is Na-K-ATPase active or passive transport?
active transport - requires energy in the form of ATP
32
how does hypokalemia affect RMP/TP
- RMP more negative - cells more resistant to depolarization
33
how does hyperkalemia affect RMP
- more positive - cells depolarize more easily
34
What happens to the RMP with severe hyperkalemia?
- when serum K gets really really high, it **inactivated Na+ channels** - they arrest in their closed-inactive state *clinical correlation: K containing cardioplegia solution used during bypass arrests the heart in diastole. The high K concentration does not allow the cells to repolarize, which locks Na+ channels in their closed-inactive state*
35
how does hypocalcemia affect RMP/TP
- TP becomes more negative - cells depolarize more easily
36
how does hypercalcemia affect RMP/TP
- TP more positive - cells more resistant to depolarization *clinical coorelation: IV calcium is given to reduece the risk of dysthythmias in the pt with hyperkalemia (IV Ca++ will increase the gap b/w RMP and TP)*
37
what happens to Na+ channels in severe hyperkalemia
- inactivated - channels arrest in closed-inactivated state
38
how does cardioplegia solution work
- high levels of K+; cells can't repolarize, Na+ channels locked - arrests heart in diastole
39
why does IV calcium reduce the risk of dysrhythmias in hyperkalemic patients
increases the gap between RMP and TP
40
why is depolarization longer in myocytes vs. neurons
AP has a plateau phase - depolarization prolonged ## Footnote this gives the myocytes time to contract and eject SV
41
do SA and AV nodes have a plateau phase?
nope
42
5 phases of myocyte AP and the number associated
* depolarization phase 0 * initial repolarization phase 1 * plateau phase 2 * final repolarization phase 3 * resting phase phase 4
43
what part of EKG tracing reflects depolarization
Q wave
44
What are all the things that happen in Phase 0 of myocyte
* Na+ in * Threshold potential at -70 is met = depolarization * activation of fast voltage-gated Na+ channels (Ina) * Slope indicates conduction velocity
45
Everything that happens during Phase 1 of monocyte
* Cl- in * K+ out * Inactivation of Na+ channels * cell becomes less postitive * K+ channels open (Ito) * Cl- channels open (Icl)
46
Everything that happens in phase 2
* Ca++ in * K+ out * activation of slow VG Ca++ channels (Ica) - this counters loss of K+ ions to maintain the depolarized state * delays repolarization * maintains fast Na+ channels in **inactive state** * prolongs absolute refractory period * sustained contraction is necessary for the heart's pumping action
47
Everything that happens in phase 3 of myocyte
* K+ out * Ca++ in (briefly) * K+ channels open (delayed rectifier) (Ik) * K+ leavs cell faster than Ca++ enters = repolarization * slow Ca++ channels deactivate * restores transmembrane potential to RMP = -90mV
48
Everything that happens in Phase 4 of myocyte
* K+ out * Na/K-ATPase function * K+ leak channels open: these maintain the transmembrane resting potential (-90mV) * Na/K ATPase: removes Na+ and brings back in K+
49
part of EKG tracing that corresponds with final repolarization phase of myocyte AP
T wave
50
during which phase of myocyte AP is the EKG isoelectric
resting phase
51
part of EKG wave that corresponds with plateau phase of myocyte AP
ST segment
52
threshold potential at myocyte depolarization
-70 mV
53
what counters loss of K+ ions to maintain depolarized state in plateau of myocyte AP
activation of slow voltage-gated Ca2+ channels
54
transmembrane resting potential of myocytes
-90 mV
55
purpose of K+ leak channel open in resting phase of myocyte AP
maintains transmembrane resting potential
56
What current is the primary determinant of the SA node spontaneous phase 4 depolarization? (HR)
I-f The funny current sets the spontaneous phase 4 depolarization in the SA node
57
order of normal cardiac conduction
SA node - internodal tracts - AV node - bundle of His - L/R bundle branches - Purkinje fibers
58
how many phases are involved in SA-node AP
3 (no phase 1 or 2)
59
what is the RMP and TP of nodal cells?
RMP = -60 mV TP = -45 mV
60
Difference of AV vs SA node AP
The AV action potential looks similar to the SA node, but the AV node has a lower slope during phase 4 *this means we have a slower intrinsic firing rate*
61
3 phases of SA node AP
spontaneous depolarization depolarization repolarization
62
Everything that happens in phase 4 of SA node AP
- Na+ in (I-f) - Ca2+ in (T-type) - The membrane is "leaky" to Na+ - Na+ enters cell progressively making it more positive - I-f is called the funny current b/c its activated by hyperpolarization (not depolarization) - at -50 mV, transient Ca++ (t-type) open to further depolarize the cell
63
Everything that happens in phase 0 of SA node AP
* Ca2+ in (L-type) * Ca++ entry via VG-Ca++ channels = depolarization * Na+ channels close * Ca++ T-type channels close
64
Everything that happens in Phase 3 of SA node AP
* K+ out * K+ channels open * K+ exits the cell - cell more negative * K+ efflux = repolarization and return to phase 4 * Repolarization will decrease Ca++ conductance by closeing L-type channels
65
what causes depolarization in SA node myocytes
Ca2+ entry via voltage-gated calcium channels (L-type) (T-type calcium channels close)
66
what happens to calcium channels during repolarization of SA node
L-type Ca2+ channels close, Ca2+ conductance decreased
67
what 2 things determine heart rate
1. intrinsic rate of dominant pacemaker (usually SA node) 2. autonomic tone
68
intrinsic firing rates of SA, AV, and purkinje fibers
SA = 70-80 AV = 40-60 purkinje = 15-40
69
where does the SA node reside
right atrium
70
what determines the intrinsic rate of SA node firing
the rate of spontaneous phase 4 depolarization of SA node ## Footnote All the cells in the myocardium are capable of automaticity - however, each cell type has an intrinsic rate of spontaneous depolarization. **the cells with the fastest phase 4 will determine how frequently the heart depolarizes**
71
how do volatiles affect SA node
depress SA node automaticity - can cause junctional rhythm
72
why is a junctional rhythm slow and without a P wave?
disease or hypoxia impairs SA node's ability to function as dominant pacemaker - cells with next highest rate of spontaneous phase 4 depolarization assumes as pacemaker
73
The ANS modulates HR, at rest, what is the dominant ANS system?
PNS - at rest the PNS tone exceeds the SNS tone * CN X * The right vagus innervates the SA node, and the left vagus innervates the AV node
74
responsible for SNS tone
cardiac accelerator fibers (T1-T4)
75
what 3 variables can be manipulated to change the sinus node rate
1. rate of spontaneous phase 4 depolarization 2. threshold potential 3. RMP
76
3 situations that can increase HR and reach threshold potential faster
1. slope of phase 4 depolarization increases 2. slope of phase 4 remains constant but TP becomes more negative 3. slope of phase 4 remains constatnt but RMP becomes less negative *both number 2 and 3 decrease the gap between RMP and TP*
77
how does SNS affect HR
NE stimulates beta-1 receptor, increases HR by Na+ and Ca2+ conductance increases rate of spontaneous phase 4 depolarization (steeper slope of phase 4)
78
how does PNS affect HR
ACh stimulates M2 receptor - slows HR by increased K+ conductance, hyperpolarizing SA node RMP is decreased and reduces the slope of phase 4
79
how does PNS affect RMP
decreases - reduced slope of spontaneous phase 4 depolarization
80
oxygen delivery calculation and the normal
DO2 = CO x [(hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10 DO2 = 1000 mL/min
81
equation for O2 carrying capacity
(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)
82
what is CaO2 and the normal
O2 carrying capacity tells us how many grams of O2 are contained in a dL of arterial blood 20 mL/O2/dL
83
expected VO2 (oxygen consumption) in 70 kg adult
250 mL/min
84
expected CvO2 (venous oxygen content) in 70 kg adult
15 mL/dL
85
solution coefficient for dissolved oxygen
0.003
86
body extraction ratio
EO2 = 25%
87
How does body temp and Hct change blood flow?
Changes in temp: - increased temp = decreased blood viscosity and increased flow - decreased temp = increased viscosity and decreased flow Changes in Hct: - increased hct = increased viscosity and decreased flow - decreased hct = decreased viscosity and increased flow
88
how to calculate MAP using Ohm's law
89
what are the flow, pressure gradient, and resistance factors of blood pressure?
- flow = CO - pressure gradient = MAP - CVP - resistance = SVR
90
What is the equation for Poiseulle's law?
91
primary determinant of vascular resistance
radius of arterioles
92
What is used to predict if flow will be laminar or turbulent
Reynold's number
93
Reynold's number that will predict if flow will be laminar, turbulent, or transitional
- laminar: Re < 2,000 - turbulent: Re > 4,000 - transitional: Re = 2,000 - 4,000 ## Footnote When flow is turbulens, a lot of energy is lost to heat and vibration
94
2 possible assessment findings when there's turbulent flow
vibrations can cause a murmur (valve disease) or bruit (stenosis)
95
what is viscosity the result of
friction from intermolecular forces as fluid passes through a tube
96
what 2 things determine viscosity
- Hct - body temp
97
relationship between blood viscosity and temperature
inversely related *when giving PRBCs, improve flow by diluting the unit with NS (decreased hct) and running it through a warming device (increased tem)*
98
what 2 factors determine EDV (Preload)
- filling pressures - compliance
99
what 2 factors determine ESV
- afterload - contractility
100
what 2 factors determine stroke volume
- EDV (preload) - ESV
101
determinants of CO
- HR - SV
102
determinants of MAP
- CO - SVR
103
determinants of tissue blood flow
- MAP - local vascular resistance
104
determinants of O2 delivery
- tissue blood flow - CaO2
105
normal CO in adult
5-6 L/min
106
cardiac index calculation & normal values
CO/BSA 2.8-4.2 L/min per m^2
107
stroke volume calculation & normal values
EDV - ESV or CO x 1000/HR 50-110 mL/beat
108
stroke volume index calculation & normal values
SV/BSA 30-65 mL/beat per m^2
109
ejection fraction calculation & normal values
(EDV - ESV / EDV) * 100 or (SV/EDV) * 100 60-70%
110
MAP calculations (2) & normal values
(1/3 x SBP) + (2/3 x DBP) or (COxSVR /80) 70-105 mmHg
111
SVR calculation and normal value
(MAP-CVP/CO) x 80 800-1500 dynes * sec * cm-5
112
Pulmonary vascular resistance calculation and normal value
(MPAP - PAOP/CO) x 80 150 - 250 dynes * sec * cm-5
113
Variables involved in the Frank-Starling mechanism?
- Ventricular volume - Ventricular output *make sure to be familiar with different names or similar things i.e. PAOP will give us ventricular volume*
114
amount of oxygen dissolved in blood (PaO2) follows what law
Henry's
115
flow is directly proportional to what 2 factors
1. vessel radius 2. arteriovenous pressure difference
116
flow is inversely proportional to what 2 factors
1. viscosity 2. length of tube
117
how much more flow occurs when the radius of a tube is quadrupled?
256x
118
pulse pressure calculation & normal values
SBP - DBP (stroke volume output / arterial tree compliance) 40 mmHg
119
functional unit of the contractile tissue in the heart
sacromere
120
amount of tension each sarcomere can generate is directly related to:
number of cross-bridges that can be formed before contraction ## Footnote The greater the tension produced, the greater the force of contraction - to a point
121
what is preload
- ventricular **wall tension** at the end of diastole - AKA: (the volume that returns to the heart during diastole)
122
how does A-fib affect preload
loss of atrial kick = reduced preload
123
how does venous tone affect preload
decreased tone (sympathectomy) = decreased preload
124
how does valvular regurgitation affect preload
aortic or mitral regurg increase preload
125
illustrates the relationship between ventricular volume and output
ventricular function curve ## Footnote AKA frank-starling curve
126
what is the Frank Starling mechanism
increased ventricular volume produces a larger CO up to the plateau, after which additional volume overstretches sarcomeres, decreases # cross-bridges that can be formed, and decreases CO
127
commonly used as a surrogate for ventricular volume (since we can't always measure LV volume with a TEE)
filling pressure ## Footnote However, this is sometimes an inacurate subsitution - anything that alters ventricular compliance (MI or hypertrophy) can change the relationship b/w ventrucular volume and pressure
128
x and y axis of ventricular function curve
X-axis = preload (ventricular volume) Y-axis = Output (ventricular output)
129
terms that can be used on the y axis of Frank Starling curve
- CO - SV - LVSW - RVSW (ventricular output)
130
terms that can be used on x axis of Frank Starling curve
filling pressures: - CVP - PAD - PAOP - LAP - LVEDP EDV: - RVEDV - LVEDV
131
ability of myocardial sarcomeres to perform work (shorten & produce force)
contractility (inotropy) *contractility is independent of preload and afterload*
132
reflects ventricular output for given EDV
contractility
133
An increased preload increases ____. This is not the same as ____
An increased preload increases **the force of contraction**. This is not the same as **change in contractility**
134
atrial contraction = ____% of final LDEDV & CO
20-30%
135
why does CO usually decrease in A fib
loss of atrial kick, which contributes 20-30% of final LDEDV & CO
136
a non-compliant ventricle is stiff - therefore what should we know about atrial kick?
ventricle is stiff = much more dependent on a well-timed atrial kick to fill the ventricle and generate SV - the extra pressure generated by the atrial kick will prime the stiff venticle
137
patients more likely to experience a decreased CO with cardiac rhythm disturbances like A-fib or a junctional rhythm?
patients with decreased ventricular compliance: hypertrophy, diastolic failure (preserved EF), fibrosis, aging
138
What conditions impair inotropy? - hyper-K - hypovolemia - hypoxia - hyper-Ca - hypocapnia - hypercapnia
- Hyper-K - Hypoxia - Hypercapnia
139
how do most meds increase or decrease contractility
alter amount of calcium available to bind to myofilaments or impair sensitivity of myocardium to calcium **C**hemicals affect **C**ontractiilty - particularly **c**alcium
140
5 things that increase contractility
1. SNS stimulation 2. catecholamines 3. calcium 4. digitalis 5. PDE inhibitors
141
how does hypercapnia affect contractility
decreases
142
how do hyperkalemia and hypocalcemia affect contractility
decrease
143
how do volatiles affect contractility
decreases
144
2nd messenger in the myocardium
calcium
145
primary substance that determines contractility
calcium
146
Steps for Ca++ causing contraction in the heart
1. AP propagated 2. T-tubule is depolarized and opens VG-Ca channels. Ca++ enters monocyte (phase 2 of AP) 3. Influx of Ca++ activates RyR2 4. Ca++ is released from SR (calcium-induced caldium-release) 5. Ca++ binds to troponin C to stimulate cross-bridge formation = contraction 6. Ca++ unbinds from trop-C = relaxation 7. Most Ca++ is returned to the SR via **SERCA2** pump (ATP-dependent). Inside, Ca++ binds to calsequestrin 8. Some Ca++ is removed from myocyte by Na/Ca exchanger (NCX) 9. Na/K ATPase restores RMP
147
what determines the duration of myocyte contraction?
action potential duration
148
How does B1 stimulation increase contractility with cAMP increasing PKA?
- More L-type Ca++ channels activated - RYR2 is stimulated to release more Ca++ (more binding to tropC) - SERCA2 pump is stimulated to reuptake more and release more (Phospholamban is phosphorylated which stops it from inhibiting SERCA2) = enhanced Ca++ uptake
149
what happens to the myocyte if RMP increases to a level that exceeds a level of normal repolarization
voltage-gated Na+ channels can't fire and get stuck in closed-inactive state
150
how does beta-1 stimulation in the myocyte affect PKA?
activates AC - converts ATP to cAMP - increases PKA activation
151
What normally inhibits SERCA2 activity
phospholamban (PLN)
152
net effect of beta-1 stimulation in myocyte
more forceful contraction over a shorter time (positive inotropy) with enhanced relaxation (positive lusitropy) between beats
153
what is afterload
force the ventricle must overcome to eject its stroke volume
154
3 factors that decrease stroke volume
- decreased preload - decreased contractility - increased afterload
155
what determines the majority of afterload
SVR (arteriolar tone) ## Footnote after load isn't exactly the same thing as SVR - SVR doesn't take into account blood viscosity, blood density, or ventricular wall tension. SVR is only the measure of arteriolar tone.
156
why is the LV thicker than the right?
has to overcome a much higher afterload
157
Law of LaPlace for the heart equation
158
What is intraventricular pressure?
The force that pushes the heart apart
159
what is wall stress in the heart
force that holds the heart together
160
things that reduce myocardial wall stress
- decreased intraventricular pressure - decreased radius - increased wall thickness | Remember LaPlace for heart
161
what explains why pt with HTN compensates with LVH?
increased wall stress increases myocardial O2 consumption. Wall thickness is inversely related to wall stress, so increased wall thickness will decrease wall stress
162
Which phases of the cardiac cycle have the mitral valve open and the aortic valve closed?
- Rapid ventricular filling - Atrial systole - Diastasis (middle third of diastole)
163
during what part of the cardiac cycle are all 4 valves closed
isovolumetric contraction & relaxation
164
valves open and closed during ventricular ejection
- mitral closed - aortic opened
165
valves open/closed during atrial systole
- open: mitral - closed: aortic
166
3 phases of the cardiac cycle assoc. with open mitral valve and closed aortic valve
1. rapid ventricular filling 2. atrial systole 3. diastasis
167
4 events that occur between Q wave & end of T wave
1. rapid ventricular ejection 2. LV systole 3. aortic valve opens 4. stroke volume
168
valves open/closed during ventricular ejection
- mitral closed - aortic open
169
what causes first heart sound
during isovolumetric contraction, LV pressure > LA pressure and mitral valve closes
170
phases of cardiac cycle that occur during systole
1. isovolumetric contraction 2. ventricular ejection
171
phases of cardiac cycle that occur during diastole
1. isovolumetric ventricular relaxation 2. rapid ventricular filling 3. reduced ventricular filling (diastasis) 4. atrial systole
172
when is most SV ejected from LV
first 1/3 of systole
173
what causes the 2nd heart sound
aortic pressure > LV pressure, aortic valve closes
174
what happens to LV pressure and volume during isometric ventricular relaxation
LV pressure decreases, volume constant
175
what does the dicrotic notch represent
onset of aortic valve closure causes a short period of retrograde flow from aorta towards valve, followed by complete termination of retrograde flow upon complete valve closure
176
what causes the mitral valve to open
LA pressure > LV pressure
177
during what parts of cardiac cycle is mitral valve open
- rapid ventricular filling - reduced ventricular filling - atrial systole
178
when does 80% of LV filling occur
during ventricular filling
179
what contributes to last 20% of LV filling
atrial kick
180
the end of atrial systole correlates with what volume?
EDV
181
what do corners measure in a cardiac pressure volume loop
where valves open & close
182
what does net external work output measure in a cardiac pressure volume loop
myocardial work
183
what 2 events measured by pressure volume loop occur in systole
isovolumetric contraction ejection
184
phases of ventricular pressure volume loop
1. ventricular filling (diastole) 2. isovolumetric contraction (systole) 3. ventricular ejection (systole) 4. isovolumetric relaxation (diastole)
185
normal LV volume and pressure at the beginning of diastole
volume ~50 mL (ESV) pressure 2-3 mmHg
186
Calculations for Ejection Fraction
187
net gain during ventricular filling
70 mL (normal SV)
188
when are DBP and SBP measured via Aortic waveform on a pressure volume loop
DBP when aortic valve opens SBP at peak of ejection curve
189
what is ejection fraction
percentage of how much blood is pumped by the heart during each beat
190
EF values: - normal - mild dysfunction - moderate dysfunction - severe dysfunction
- normal > 50% - mild dysfunction 41-49% - moderate 26-40% - severe < 25%
191
what is external work
amount of work the ventricle must do to eject SV ## Footnote AKA stroke work or cardiac work
192
how is external work estimated
multiply SV x mean aortic pressure (width x height of pressure volume loop)
193
2 factors that increase workload of heart
- ventricle accepts increased volume - widens the area of the flow loop - ventricle has to generate more pressure to open aortic valve - this increases the height of the flow loop
194
what happens to pressure volume loop with increased or decreased preload
- increased preload: loop gets wider but returns to original ESV **increased SV and cardiac muscle shortening** - decreased preload: loop gets narrower but returns to original ESV **decreased SV and cardiac muscle shortening**
195
what happens to ESV with increased contractility
decreases - increased contractility = increased cardiac muscle shortening = increased SV (increased chamber emptying)
196
what happens to pressure volume loop with increased contractility
loop gets wider, taller, & shifts to left
197
What happens with ESV with decreased contractility?
Increases - decreased contractility = decreased cardiac muscle shortening = decreased SV (decrased chambe emptying)
198
what happens to pressure-volume loop with decreased contractility
loop gets narrower, shorter, shifts to right
199
pressure volume loop with increased afterload
loop gets narrower, taller, and shifts ESV to the right
200
pressure volume loop with decreased afterload
loop gets wider, shorter, shifts ESV to the left
201
What coronary artery supplies the heart wall shown in blue?
Circumflex a. ## Footnote When using a TEE, the midpapillary muscle level in short axis provides the best view for diagnosing MI.
202
where do LCA & RCA arise from
aortic root (sinus of Valsalva)
203
where does the left coronary artery emerge from
behind pulmonary trunk, divides into LAD and circumflex arteries
204
LAD perfuses what structures of the heart
LAD perfuses the anterolateral and apical walls of LV also anterior 2/3 of interventricular septum
205
what does the circumflex artery supply
LA and lateral and posterior walls of LV
206
RCA perfuses what heart structures?
RCA perfuses the RA, RV, interaterial septum, and posterior 1/3 of interventricular septum
207
perfuses inferior wall of LV
posterior descending artery
208
the origin of which vessel defines coronary dominance
posterior descending artery
209
What is right sided dominance? What is the percentage of Right sided dominance?
Right sided dominance means the PDA comes off of the RCA 70-80% of people are right sided dominant
210
What vessel does the PDA come off if the pt is Left dominant?
Circumflex *if PDA comes off circ AND RCA this is co-dominance*
211
where does SA node receive blood supply from in ~____% of patients? where is it received from in remaining population?
- where does SA node receive blood supply from in ~**70**% of patients? **RCA** circumflex
212
where does the AV node receive blood supply from in ~____% of patients
where does the AV node receive blood supply from in ~**80**% of patients **RCA**
213
what perfuses the bundle of His in ~75% of patients
LCA
214
what almost exclusively supplies the right and left bundle branches
LCA
215
4 main components of coronary venous circulation which coronary artery do they run parallel to?
1. great cardiac vein (runs parallel to LAD) 2. middle cardiac vein (runs parallel to PDA) 3. anterior cardiac vein (runs parallel to RCA) 4. coronary sinus (most blood returns here)
216
where is the coronary sinus located
posterior aspect of RA just superior to tricuspid
217
where does blood returning to coronary circulation from LV drain?
coronary sinus
218
what is cannulated to admin retrograde cardioplegia during CPB
coronary sinus
219
how does blood returning from RV empty directly into RA
anterior cardiac veins bypass coronary sinus and go directly to RA
220
What are the Thebesian veins?
small amount of blood empties directly into all 4 cardiac chambers via these veins *blood returning to the L side of the heart from the Thebesian circulation contributes to the anatomic shunt*
221
What are epicardial vessels? what happens to them with pathology?
- Epicardial vessles lay on top of the heart's surface (RCA, LAD and CxA) - Vascular stenosis typically affects the epicardial vessles
222
The ____ ____ provide the majority of coronary vascular resistance
The **coronary arterioles** (not the epicardial vessels) provide the majority of coronary vascular resistance
223
What are the two best TEE views for diagnosing of LV ischemia?
Best = midpapillary muscle level in short axis second best = apical segment in short axis
224
- At rest the myocardium consumes O2 at a rate of ____ with an extraction ration of ____% - Coronary blood flow is ____mL/min or ____% of the CO - The coronary vasculature autoregulates between a MAP of ____
- At rest the myocardium consumes O2 at a rate of **8-10 mL/min/100g** with an extraction ration of **70**% - Coronary blood flow is **225**mL/min or **4-5**% of the CO - The coronary vasculature autoregulates between a MAP of **60-140**
225
Equation for coronary blood flow
226
what 2 pressures determine coronary perfusion pressure
aortic DBP - LVEDP
227
Outside of the autoregulation of coronary perfusion, coronary blood flow is dependent on what?
Outside of the MAP range of autoregulation, coronary blood flow is dependent on **coronary perfusion pressure**
228
Pathway for coronary vasodialation using G-protein pathway
NE -> B2 -> Adenyl cyclase -> cAMP -> PKA -> **decreased Ca2+** -> vasodialation ## Footnote PKA inhibits VG-Ca channels in sarcolemma, inhibits Ca release from SR, reduces sensitivity of myofilaments to Ca and facilitates Ca reuptake into SR via SERCA2
229
how does histamine-2 activation affect coronary circulation
causes coronary vasodilation
230
how does histamine-1 activation affect coronary circulation
causes coronary vasoconstriction
231
which myocardial arterial bed is most susceptible to ischemia
endocardial blood vessels of the myocardium
232
what area of the LV does lead I monitor
lateral
233
biploar leads & what they monitor
I - lateral LV (circumflex artery) II - inferior LV (RCA) III - inferior LV (RCA)
234
limb leads and what they monitor
aVR aVL - lateral LV (circumflex artery) aVF - inferior LV (RCA)
235
precordial leads and what they monitor
V1 - septum (LAD) V2 - septum (LAD) V3 - anterior (LAD) V4 - anterior (LAD) V5 - lateral (circumflex) V6 - lateral (circumflex)
236
autoregulation of coronary flow is a net effect of what 3 things
1. local metabolism 2. myogenic response 3. ANS
237
how does adenosine affect coronaries
causes vasodilation *Adenosine is a byproduct of ATP metabolism and is a potent vasodialator. As MVO2 increases, the coronary endothelium releases adenosine as well as NO, prostaglandins, hydrogen, K, and CO2*
238
how does hypocapnia affect coronaries
causes vasoconstriction
239
how do coronary vascular resistance or LVEDP affect coronary blood flow
anything that increases resistance or LVEDP can decrease coronary blood flow
240
most important determinant of coronary vessel diameter
local metabolism
241
byproduct of ATP metabolism & potent coronary vasodilator
adenosine
242
how does the coronary endothelium react to increased MvO2
- releases adenosine and a variety of other vasodilators (NO, PGs, hydrogen, K+, CO2) to increase blood flow
243
how does vasodilation affect coronary perfusion
increases
244
refers to a vessel's innate ability to maintain a constant vessel diameter
myogenic response
245
myogenic response when coronary vessel diameter increases
tendency to contract
246
myogenic response to coronary vessel diameter decrease
tendency to dilate
247
times when ANS effects prevail over products of local metabolism to affect coronary vascular tone
Prinzmetal angina (vasospastic myocardial ischemia) - overactive coronary alpha receptors can cause intense chest pain at rest
248
how does endocardial beta-2 stimulation affect the coronaries
- increases cAMP - decreases MLCK sensitivity to Ca2+ - results in coronary vasodilation
249
what is the difference between coronary blood flow at rest and maximal dilation
coronary reserve
250
allows coronary flow to increase in times of HD stress or exercise
coronary reserve
251
coronary reserve in patients with atherosclerotic vessels and increased O2 demand
vessels may be maximally dilated at rest and unable to dilate further decreased coronary reserve
252
what happens to flow through LCA during ventricular systole
greatly diminished
253
what happens to flow through RCA throughout cardiac cycle
remains relatively constant
254
what happens to endocardial vessels during myocardial contraction
dramatically reduced flow during systole d/t mass of LV - the epicardial vessels give rise to lots of endocardial vessels the penetrate deep into the the myocardium. - The muscle mass of the LV during contraciton will compress the endocardial vessles which dramatically reduce flow during systole
255
why can't the RV occlude it's blood supply during systole
doesn't generate a high enough pressure
256
percentage of myocardial O2 consumption at rest
consumes ~70% of the O2 delivered to it
257
normal coronary sinus O2 sat
~30%
258
what must happen to satisfy increased myocardial O2 demand
- coronary blood flow and/or CaO2 must increase - heart can't meaningfully increase its extraction ratio when O2 demand increases
259
contributes to perception of chest pain during ischemia
lactic acid production (r/t anaerobic metabolism) - Inadequate production of ATP and acidosis impair myocardial performance and lead to hemodynamic instability
260
4 things that decrease coronary blood flow and in turn decrease myocardial O2 supply (decreased O2 delivery)
- tachycardia - decreased aortic pressure - decreased vessel diameter (spasm, hypocapnia) - increased LVEDP
261
2 things that decrease CaO2 and myocardial O2 delivery
1. hypoxemia 2. anemia
262
2 things that cause decreased O2 extraction and myocardial O2 delivery
- L shift of hgb dissociation curve (decreased P50) - decreased capillary density
263
how does increased HR affect myocardial O2 supply and demand
decreases O2 supply while increasing demand
264
how does EDV affect myocardial O2 demand
decreased EDV reduces wall stress and decreases demand
265
how does increased aortic DBP affect myocardial O2 supply and demand
Increased aortic DBP - increased supply - increased pressure that perfuses the coronary arteries (increased perfusion pressure) - Increased demand - but increased DBP also increases wall tension and afterload (the myocardium requires more pressure and therefore more O2 to open aortic valve ## Footnote As a general rule, the benefit of increased coronary perfusion pressure outweights the drawback of increased wall tension
266
How does increased preload affect myocardial O2 supply and demand?
Increased Preload - decreased supply: increased EDV decreases coronary perfusion pressure. Aortic DBP with an increased LVEDP will result in decreased coronary perfusion pressure - Increased demand: increased preload increases wall stress ## Footnote At first - this is counterintuitive bc preload should increase supply right? But we are looking at the effect of an increased preload on the oxygen delivery/supply to the myocardium, not the systemic circulation. Preload decreases the supply of O2 to the myocardium by increasing LVEDV which in turn decreased CPP. Preload also increases wall tension - therefore a higher preload increases O2 demand google: While not typically decreasing oxygen supply directly, the increased demand, if not met by coronary blood flow, causes a decrease in the supply/demand ratio
267
3 circumstances that affect both sides of the myocardial O2 delivery/demand equation
- changes in HR - aortic DBP - preload
268
when is the LV best perfused
during diastolic filling time
269
how does diastolic filling time affect myocardial O2 supply
shorter time = less time to deliver O2 to LV = decreased supply
270
usually unaffected by tachycardia, well-perfused throughout cardiac cycle
RV
271
when do most perioperative MIs occur
24-48 hours following surgery
272
Inhaled NO MOA
- NO increases cGMP systhesis on vascular smooth m. This reduces intracellular Ca++ and contributes to Pulm. vasodialation. Therefore **reduced RV afterload** - NO is inactivated by Hgb
273
what is regulation of vascular smooth muscle tone dependent on?
successful integration of ANS, RAAS, local metabolism, myogenic response
274
which electrolyte plays a critical role in regulation of peripheral vessel diameter
calcium
275
as a general rule, how does calcium affect vascular smooth muscle tone
- increased calcium = vasoconstriction - decreased calcium = vasodilation In vessels - different in other organs
276
3 important pathways that use intracellular calcium
1. G-protein cAMP pathway (vasodilation) 2. NO cGMP pathway (vasodilation) 3. PLC pathway (vasoconstriction)
277
how does the G-protein cAMP pathway affect vascular smooth muscle tone
- in vascular muscle cells, increased PKA = decreased intracellular calcium - results in vasodilation
278
how does PKA affect excitation-contraction coupling in cardiac vasculature (Ca++ binding to tropC)
- inhibits voltage gated calcium channels in sarcolemma - inhibits calcium release from SR - reduces sensitivity of myofilaments to calcium - facilitates calcium reuptake into SR via SERCA2 pump | Literally every part of the Ca++ release mechanism within cell
279
things that increase NO production
- ACh - substance P - bradykinin - serotonin - Vasoactive intestinal peptide - thrombin - shear stress ## Footnote Shower thoughts: bradykinin increases NO production, how does it cause angioedema? too much of a good thing - normal amount of bradykinin = increased Ca2+ and eNOS production etc etc large amount of bradykinin = increased vascular permeability and no enzymes to break it down (ACE)
280
6 steps in NO cGMP pathway leading to vasodilation
1. NOS catalyzes conversion of L-arginine to NO 2. NO diffuses from endothelium to smooth muscle 3. NO activates Guanylate Cyclase 4. GC converts GTP to cGMP 5. increased cGMP reduces intracellular calcium and causes smooth muscle relaxation 6. PDE5 deactivates cGMP to guanosine monophosplate
281
activators of Phospho Lipase C pathway
- phenylephrine - NE - Angiotensin2 - endothelin-1
282
how does angiotensin II receptor activation lead to vasoconstriction
Gq G-protein stimulated = PLC = IP3 & DAG = increased calcium = vasoconstriction
283
PLC activation increases production of what 2 second messengers
IP3 & DAG
284
effects of increased IP3 & DAG production in vascular smooth muscle
- IP3: augments calcium release from SR - DAG: activates PKC which opens voltage-gated calcium channels in sarcolemma - increases calcium influx
285
how does iNO affect vascular smooth muscle
increases cGMP = reduced intracellular calcium = pulmonary vasodilation decreased PVR, decreased RV afterload
286
inactivates iNO
hemoglobin
287
why doesn't iNO cause hypotension
inactivated before entering systemic circulation
288
phenylephrine stimulates what effector to ultimately cause vasoconstriction
Phospholipase C
289
in which phase of ventricular AP is conductance greatest for: - Cl- - K+ - Na+ - Ca2+
- Na+ conductance greatest in phase 0 - Cl- conductance greatest in phase 1 - Ca2+ conductance greatest in phase 2 - K+ conductance greatest in phase 3
290
3 things that cause SA node to increase firing rate
1. increased slope of spontaneous phase 4 depolarization 2. TP more negative 3. RMP more positive
291
what causes SR to release calcium
when calcium stimulates RyR2 receptor
292
what is calcium-induced-calcium release
calcium activates RyR2 receptor, which causes large quantities of calcium to be released from SR
293
variables to describe x axis of frank starling curve
Filling pressures or EDV - filling pressures: CVP, PAD, PAOP, LAP, LVEDP - EDV: RVEDV, LVEDV
294
variables to describe y axis of frank starling curve
ventricular output: - CO - SV - LVSW - RVSW
295
2 conditions that set afterload proximal to systemic circulation
aortic stenosis coarctation of aorta
296
which region of the heart is most susceptible to ischemia? why?
LV subendocardium best perfused during diastole - as aortic pressure inc. LV tissue compresses its own blood supply - compression + decreased coronary flow during systole = increased coronary vascular resistance, predisposed to ischemia
297
how does PNS stimulation affect HR
slows HR via increased K conductance (hyperpolarizes SA node)
298
how much of CO does the myocardium receive at rest? (percentage and mLs)
5% (~225 mL/min)
299
most potent vasodilator released by cardiac myocytes
adenosine
APEX... FML
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