Cardiac A&P Flashcards
1
Q
How is cardiac muscle like skeletal muscle?
A
- Actin and myosin filaments
- Capable of contracting
- T-Tubule system and the sarcoplasmic reticulum work to maintain Ca2+ homeostasis
2
Q
How is cardiac muscle like neural tissue?
A
- Generates a RMP
- Can initiate an AP
- Can propagate an AP
3
Q
How is cardiac muscle unlike skeletal muscle?
A
- Tight junctions serve as low resistance pathways to spread AP
- Cardiomyocytes contain more mitochondria than skeletal muscle cells
4
Q
Automaticity
A
Ability to spontaneously generate an AP
5
Q
Conductance
A
Because of their charge, ions do not freely pass through cell membranes; they require an OPEN channel.
An open channel increases conductance; a closed channel reduces conductance.
6
Q
RMP
A
The difference in electrical potential btwn the inside and outside of cell.
The inside is more (-) compared to outside.
7
Q
RMP is established by
A
- Chemicals
- Electrostatic
- Na+/K+ ATP-ase
8
Q
Threshold
A
- The internal voltage at which the cell depolarizes.
- ALL or NONE
9
Q
When RMP is closer to threshold potential . . .
A
it is easier to depolarize the cell
10
Q
When RMP is further from threshold potential . . .
A
it is harder to depolarize the cell
11
Q
Depolarization
A
- Takes place when there is a reduced polarity across the membrane
- There is less charge difference btwn the inside and outside of the cell
12
Q
Hyperpolarization
A
- Takes place when increased polarity across membrane
- There is a large difference between the inside and outside
13
Q
Repolarization
A
Restoration of membrane potential towards RMP
14
Q
Equilibrium potential
A
Equilibrium is achieved when there is no concentration gradient and there no net flow of ions
*NERNST equation can be used to predict an ion’s equilibrium potential
15
Q
Nernst equation
A
E ion = -61.5log ([ion] inside/[ion] outside)
16
Q
K+
-Myocyte
ECF
Equilibrium Potential mV
A
135 mM - myocyte
4 mM - ECF
-94 equilibrium potential
17
Q
Na+
- Myocyte
- ECF
- Equilibrium Potential mV
A
Na+
10 mM -Myocyte
145 mM - ECF
+60 - Equilibrium Potential
18
Q
Cl-
- Myocyte
- ECF
- Equilibrium Potential mV
A
Cl-
4 mM - Myocyte
114 mM - ECF
-97 mV - Equilibrium Potential mV
19
Q
Ca2+
- Myocyte
- ECF
- Equilibrium Potential mV
A
Ca2+
10 mM - Myocyte
2 mM - ECF
+132 - Equilibrium Potential mV
20
Q
Na/K+ - ATPase
A
- Removes Na+ gained during repolarization
- Replaces K+ lost during repolarization
(3 Na+ out/ 2 K+ in)
21
Q
Ventricular AP
Phase 0
A
Na+ In
Threshold potential -70 mV; cell depolarizes
Activation of fast v-gated Na+ channels
Slope (steep) indicates conduction velocity (very fast)
22
Q
Ventricular AP
Phase 1
A
K+ Out
Cl- In
Inactivation of Na+ channels
Cell becomes slightly less (+)
- K+ channels open
- Cl- channels open
23
Q
Ventricular AP
Phase 2
A
Ca+ In
K+ Out
Activation of slow v-gated Ca+ channels counters loss of K+ to maintain depolarization; it delays repolarization
- prolongs refractory period
- sustained contraction necessary for heart pumping
- Absolute refractory period
24
Q
Ventricular AP
Phase 3
A
K+ Out
Ca+ In
K+ channels open K+ leaves faster than Ca+ enters - repolarization Slow Ca+ channels deactivate Restarts RMP = -90 mV *Relative refractory
25
Ventricular AP
| Phase 4
K+ out
Na+/K= ATP-ase
K+ leak channels open
- Maintains RMP - 90mV
Na+/K+ ATPase
26
SA node conduction pathway
```
SA node
Internodal tracts
AV node
Bundle of HIS
LBB/RBB
Purkinje fibers
```
27
The HR is a function of . . .
1. Intrinsic firing rate of dominant PM (usually the SA node)
2. Autonomic tone
28
Intrinsic firing rate of SA node
70-80 bpm
29
Intrinsic firing rate of AV node
40-60 bpm
30
Intrinsic firing rate of Purkinje fibers
15-40 bpm
31
How does the SA node set the HR?
- The rate of spontaneous phase 4 depolarization of SA node determines intrinsic HR
- All cells in the myocardium are capable of automaticity (but with differing rates of depolarization)
- Cells with fastest depolarization determine how often the heart depolarizes
- Each times the SA node fires, it depolarizes the reast of the conduction system
- After the cardiac cycle is complete, the SA is the first to fire again
32
Autonomic influence on HR
PNS tone
CN X - right vagus innervates the SA node and the left vagus innervates the AV node
33
Autonomic influence on HR
SNS tone
Cardiac accelerator fibers T1-T4
34
SA Node AP
| Phase 4
Na+ In (f) - funny
Ca+ In (t-type)
Spontaneous depolarization
35
Describe what is happening in Phase 4 - SA node AP
The membrane is leaky to Na
Na+ enters the cell progressively, making it more (+)
Called "funny current" because activated by hyperpolarization, depolarization
At -50mV, transient Ca- channels open to further depolarize all
36
SA Node AP
| Phase 0
Depolarization
| Ca+ In (L-type)
37
Describe what is happening in Phase 0 - SA node AP
Ca+ enters via v-gated CA+ channels (L-type) - depolarization
Na+ and T-type Ca+ channels close
38
SA Node AP
| Phase 3
Repolarization
| K+ out
39
Describe what is happening in Phase - SA node AP
K+ channels open
K+ exits the cell, making interior more (-)
K+ efflux - repolarization and the return to Phase 4\
Repolarization decreases Ca+ conductance by closing L-type Ca+ channels
40
DO2
How much O2 is carried in the blood and how fast it's being delivered to the tissues
Approximately 1000 mL/min
41
DO2 equation
DO2 = CO [(HgbxSaO2x1.34) + (PaO2x0.003)} x 10
42
CaO2
How much O2 is carried arterial blood
Approximately 20 mL/dL
43
EO2
How much O2 is extracted by tissues
25%
44
VO2
How much oxygen is consumed by the tissues
250 mL/min (at rest)
45
CvO2
How much O2 is carried in venous blood
15 mL/dL
46
Ohm's Law
Current = Voltage difference/Resistance
OR
FLow - Pressure Gradient/Resistance
47
Flow - Term and Symbol
Cardiac output
| Q
48
Pressure Gradient - Term and Symbol
MAP-CVP
| P1-P2
49
Resistance - Term and Symbol
SVR
| R
50
Poiseuille's Law
Adaptation of Ohm's Law that incorporates vessel diameter, viscosity, tube length
Q = pie R^4 (P1-P2)/ 8nL
```
Q = blood flow
R = radius
P1-P2 = arteriovenous pressure gradient
n= viscosity
L = length of tube
```
51
Flow
Describes the movement of liquid, electricity, or air per unit/time
52
Flow is directly proportional to
the tube radius raised to the 4th power
-Vascular resistance is primarily determined by the r of arterioles - small changes in vessel diameter can have profound effects on flow
53
Doubling the radius increases the flow by . . .
16 x
| tripling (r) increase flow 81 x
54
Laminar flow
molecules travel in a parallel path through tube
55
Turbulent flow
non-linear path that will create Eddies
56
Transitional flow
Laminar along vessel walls; turbulent flow in the center
57
Reynold's number
Can be used to predict if flow will be laminar or turbulent
58
Re < 2000
Laminar flow
59
Re > 4000
Turbulent flow - greater amount of energy lost via heat and vibration = murmur
60
Re 2000-4000
Transitional flow
61
Viscosity is the result of
friction of molecules as they pass through a tube
62
What is blood viscosity determined by?
HCT and temp
- inversely proportionate to temp
- proportionate to HCT
63
O2 delivery (picture flow chart)
determined by:
1. tissue blood flow
2. CaO2
64
Tissue blood flow (picture flow chart)
determined by:
1. MAP
2. Local Vascular Resistance
65
MAP (picture flow chart)
determined by:
1. CO
2. SVR
66
CO (picture flow chart)
determined by:
1. SV
2. HR
67
SV (picture flow chart)
determined by:
1. End Diastolic Volume (preload)
2. End Systolic Volume
68
EDV (picture flow chart)
determined by:
1. Filling pressures
2. Compliance
69
ESV (picture flow chart)
determined by:
1. Afterload
2. Contractility
70
CO
Formula
Normal Value
HR x SV
| 5-6 LPM
71
CI
Formula
Normal Value
CO/BSA
| 2.8-4.2 L/min/m^2
72
SV
Formula
Normal Value
EDV-ESV
CO (1000/HR)
50-100 mL/beat
73
SVI
Formula
Normal value
SV/BSA
| 30-65 mL/beat/m^2
74
EF
Formula
Normal value
([EDV-ESV]/EDV) x 100
SV/EDV x 100
60-70%
75
MAP
Formula
Normal Value
(1/3 x SBP) + (2/3 x DBP)
(CO x SVR) + CVP/80
70-105 mmHg
76
Pulse Pressure
Formula
Normal Value
SBP-DBP
SV output/Arterial tree compliance
40 mmHg
77
SVR
Formula
Normal Value
((MAP-CVP)x80)/CO
800-1500 dynes/sec/cm^-5
78
SVRI
Formula
Normal Value
([MAP-CVP]/CI )x 80
1500-2400 dynes/sec/cm^-5/m^2
79
PVR
Formula
Normal value
((MPAP-PAOP)/CO) x 80
| 150-250 dynes/sec/cm^-5
80
PVRI
Formula
Normal value
([MPAP-PAOP] /CI) x 80
| 250-400 dynes/sec/cm^-5^m^2
81
Sarcomere
the functional unit of the contractile tissue in the heart
82
What things affect sarcomere length and why is this important?
```
Preload - ventricular wall tension at the end of diastole. Tension causes stretch/tightness
-Blood volume
-Atrial kick
-Venous tone
-Intrapericardial pressure
- Intrathoracic pressure
Body position
- Skeletal muscle pumping action
```
83
Ventricular Function Curve illustrates what?
rltsp btwn ventricular volume and ventricular output - the Frank Starling Mechanism
- increase in ventricular volume causes increase in CO
- occurs up to plateau; after, add'l volume over stretches ventricular sarcomeres and then causes decrease in sarcomeres
84
contractility
is the ability of sarcomeres to perform work and is independent of preload and afterload. It is affected by chemicals.
Shorten - produce force
85
Things that increase contractility
- SNS stimulation
- Catecholamines
- Ca2+
- Digitalis
- Phosphodiesterase inhibitors
86
Things that decrease contractility
- Myocardial ischemia
- Hypoxia
- Acidosis
- Hypercapnia
- Hyperkalemia
- Hypocalcemia
- Volatile gas
- Propofol
- BB
- Ca+ channel blockers
87
Ventricular Function Curve - Upper most curve
Increased contractility
| "Hyperdynamic"
88
Ventricular Function Curve - Middle curve
Normal
89
Ventricular Function Curve - Bottom most curve
Decreased contractility
"Heart Failure"
Volume overload
90
Ventricular Function Curve - Y axis
CO
SV
LVSW
RVSW
91
Ventricular Function Curve - X axis
1. Filling Pressure
-CVP
PAP
PAOP
LAP
LVEDP
2. End-Diastolic Volume:
- RVEDV
- LVEDV
92
Ventricular Function Curve - Bottom of Y axis
Hypotension
93
Ventricular Function Curve - Right most X axis
Pulmonary congestion
94
Excitation-Contraction coupling
| Step 1
Depolarization of the myocyte opens v-gated L-type Ca+ channels
95
Excitation-Contraction coupling
| Step 2
Influx of CA+ turns on the RyR2 receptor which releases Ca2+ from the sarcoplasmic reticulum
96
Excitation-Contraction coupling
| Step 3
Ca+ binds to troponin C = this is the initiation of contraction
97
Excitation-Contraction coupling
| Step 4
Ca+ unbinds from troponin C = this is the initiation of relaxation
98
Excitation-Contraction coupling
| Step 5
Most Ca+ is returned to SR via SERCA2 pump. The Ca+ binds to storage protein calsequestrin.
99
Excitation-Contraction coupling
| Step 6
Some Ca+ is pumped to cell exterior by Na/Ca+ exchanger
100
Effect of Beta stimulation of excitation-contraction coupling
1. Beta 1 stimulation activates adenylate cyclase which convert ATP to cAMP
2. cAMP increases production of protein kinase A which activates more L-type Ca+ channels and stimulation of ryanodine 2 receptors to release more Ca+ and stimulations SERCA2 pump to increase CA+ uptake faster
3. Therefore more forceful contraction in shorter time.
101
Afterload
(MAP-CVP)/CO x80
| 800-1500 dynes/sec/cm^5
102
Pulmonary vascular resistance
(mPAP-MAOP)/CO x 80
| 150-250 dynes/sec/cm^-5
103
Law of Laplace - wall stress
Wall stress = (Intraventricular pressure x Radius)/ventricular thickness
104
Wall stress is reduced by . . .
decrease in ventricular pressure
decrease in radius
increase in wall thickness
105
Draw Wiggers Diagram and match to ECG
- Isovolumetric Contraction
- Ventricular Ejection
- Isovolumetric Relaxation
- Rapid ventricular filling
- Reduced ventricular filling
- Atrial systole
- AV opens
- AV closes
- MV opens
- MV closes
- Dicrotic notch
- Aortic pressure waveform
- LV pressure waveform
- LV volume
106
Isovolumetric ventricular contraction
- MV Position
- AV Position
SYSTOLE
- Closed
- Closed
107
Isovolumetric ventricular contraction
| key events
LV pressure>LA pressure = MV closes
LV Pressure increase
LV volume is constant
108
Ventricular Ejection
- MV Position
- AV Position
SYSTOLE
- Closed
- Open
109
Ventricular Ejection
| key events
LV pressure>Aortic pressure = AV opens
SV is ejected into aorta
Most SV is ejected during first 1/3 of systole
110
Isovolumetric Ventricular Relaxation
- MV Position
- AV Position
DIASTOLE
- Closed
- Closed
111
Isovolumetric Ventricular Relaxation
| key events
Aortic pressure> LV pressure = AV closes (2nd Heart sound)
LV pressure decreases
LV volume constant
112
Dicrotic notch (incisura)
onset of AV closure causes a short period of retrograde flow from aorta towards AV followed by termination of retrograde flow upon complete AV closure
113
Lusitropy
Relaxation
| Requires ATP to pump Ca+ back into SR
114
Rapid Ventricular Filling
- MV Position
- AV Position
DIASTOLE
- Open
- Closed
115
Rapid Ventricular Filling
| key events
LA pressure> LV pressure = MV opens
LV pressure constant
LV volume increase
80-% LV filling happens here
116
Reduced Ventricular Filling
- MV Position
- AV Position
DIASTOLE
- Open
- Closed
117
Reduced Ventricular Filling
| key events
LV filling continues but at a slower rate
118
Atrial systole
- MV Position
- AV Position
DIASTOLE
- Open
- Closed
119
Atrial systole
| key events
LA contraction = Atrial kick contributes to last 20% of LV filling
End of atrial systole correlates with EDV
120
Ventricular volume loop curve
| 6 stages
1. Rapid filling - diastole
2. Reduced filling - diastole
3. Atrial kick - diastole (end of bottom of loop)
4. Isovolumetric contraction - systole (left side of loop)
5. Ejection - Systole (upward curve to right)
6. Isovolumetric relaxation - Systole - (left side of loop)
121
Height of ventricular volume loop curve measures?
ventricular pressure
122
Width of ventricular volume loop curve measures?
Ventricular volume
123
Corners of ventricular volume loop curve measures?
Where valves open and close
124
Net external work output of ventricular volume loop curve measures?
Myocardial work
125
Phase 1 - Ventricular Filling (diastole)
LV volume is about 50 mL (end systolic volume)
LV pressure is 2-3 mmHg
MV opens and ventricular filling begins
Aortic valve stays closed
Since LV is compliant, filling doesn't increase pressure
Atrial kick increases LV pressure 5-7 mmHg
LV fills to about 120 mL (EDV)
126
Phase 2 - Isovolumetric contraction (systole)
```
LV is stimulated contract
LV pressure exceeds LA pressure
MV closes
Aortic valve is still closed
LV builds tension and increased LV pressure
LV volume does not change (X axis)
```
127
Phase 3: Ventricular Ejection (systole)
```
LV pressure exceeds aortic pressure
AV opens
MV still closed
LV ejects SV = about 70nmL
As SV enters aorta, LV volume decreases
Normal ESV about 50 mL
DBP is measure where aortic valve opens
SBP is measure at peak of ejection curve
```
128
Phase 4: Isovolumetric Relaxation (Diastole)
```
Aortic pressure exceeds LV pressure
Aortic valve closes
MV remains closed
LV volume does not change
LV returns to starting pressure 2-3 mmHg
LV returns to starting value = 50 mL
```
129
Coronary Circulation Pathway
Aorta > RCA and LCA
RCA to Posterior descending artery and Marginal artery
LCA to Circumflex artery and Anterior Interventricular
Small cardiac vein, Middle cardiac vein, Great cardiac Vein > Coronary Sinus
130
What coronary arteries supply blood to the entire heart?
the right and left CA
- first branches off the aorta
- Arise at the sinus of Valsalva at the aortic root
131
What vessel supplies the SA node?
SA nodal artery
- originates in RAC in 50-60%
- originates from circumflex in 40-50%
132
Coronary artery dominance
the coronary vessel that feeds the PDA determines dominance
- RCA supplies PDA = r dominance = 80%
- CxA supplies PDA = left dominance
- RCA and CxA supply PDA = co-dominance
133
Three main coronary veins
1. great cardiac vein (LAD)
2. Middle cardiac vein (PAD)
3. Anterior cardiac vein (RCA)
134
Bipolar leads
I - Lateral, CxA
II - Inferior, RCA
III - Inferior, RCA
135
Limb leads
aVR
aVL - Lateral, CxA
aVF- Inferior, RCA
136
Precordial Leads
```
V1 - Septum, LAD
V2 - Septum, LAD
V3 - Anterior, LAD
V4 - Anterior, LAD
V5 - Lateral, CxA
V6 - Lateral, CxA
```
137
Best TEE view for MI
midpapillary short axis
138
Coronary blood flow
Coronary perfusion pressure/coronary vascular resistance
139
Coronary reserve
Difference between coronary blood flow at rest and at maximal dilation. It is the ability of coronary dilation to increase blood flow in times of stress or exercise
140
Coronary perfusion pressure
Aortic DBP - LVEDP
141
coronary autoregulation
coronary blood flow is autoregulated between a MAP of 60-140 mmHg. This allows a constant coronary blood flow over a wide range of BP. When MAP falls below range of autoregulation, entirely dependent on CPP
142
coronary autoregulation is net effect of . . .
1. local metabolism - adenosine
2. myogenic response
3. ANS
143
Causes of coronary artery constriction
Alpha (epicardial) - Increase in IP3 causes increases in intracellular Ca+
Histamine 1 - INcrease in IP3 causes increase in intracellular Ca+
144
Causes of coronary artery dilation
Beta 2 (endocardial) - increases in cAMP - causes decrease in intracellular Ca+
Histamine 2 - increase in cAMP - causes decrease in intracellular Ca+
Muscarinic - increase in NO
145
Estimate the coronary perfusion pressure:
Aortic DBP - LVEDP
146
Left1. coronary perfusion
LV sub-endocardium is best perfused during diastole
As aortic pressure increases, the LV tissue compresses its own blood supply and decreases blood flow. This is systole. This increases coronary vascular resistance and predisposes to ischemia.
B/c epicardial vessels lay on top of heart, they are not compressed during systole.
147
Right coronary perfusion
The sub-endocardium of RV is well perfused throughout entire cardiac cycle. This is b/c RV has a thinner wall and does not generate pressure high enough to occlude its circulation.
148
Things that decrease O2 delivery
1. Decreased coronary flow
2. Decreased CaO2
3. Decreased O2 extraction
149
Examples of decreased coronary flow
tachycardia
decreased aortic pressure
decreased vessel diameter (hypocapnia)
increased EDP
150
Examples of decreased CaO2
Hypoxemia
| Anemia
151
Examples of decreased oxygen extraction
Left shift of Hgb dissociation curve (decreased P50)
| Decreased capillary density
152
Things that increase O2 demand
```
Tachycardia
HTN
SNS stimulation
increased wall tension
increased EDV
Increased afterload
increased contractility
```
153
What factors affect supply AND demand of oxygen?
heart rate, aortic diastolic pressure, preload
154
Tachycardia - affect on supply and demand
1. decreased supply
- decreased diastolic filling time
- less time to deliver O2 to LV (RV isn't affected)
2. increased demand
- cardiac contraction and relaxation require ATP
- incrase # of cardiac cycles/min which increases ATP and O2 utilization
155
Aortic Diastolic Pressure - affect on supply and demand
1. increased supply
- increased aortic pressure increases pressure that perfuses the coronary arteries (P1-P2_
- increased Aortic DBP-LVEDP = increase in CPP
2. increased demand
- at same time, increase in aortic pressure increases wall tension and afterload. Myocardium requires more O2 as it generates higher pressure to open aortic valve
156
Preload - affect on supply and demand
1. Decreased supply
- an increased EDV causes a decrease in CPP
- Aortic DBP- increase in LVEDP = decrease in CPP
2. Increase in demand
- increased preload causes increased wall stress
157
The importance of CA in vascular smooth muscle
Ca+ has key role in the regulation of peripheral vessel diameter
-increase in Ca= vasoconstriction and v/v
158
Three pathways that affect intracellular Ca+ concentrations:
1. G-protein cAMP pathway - vasodilation
2. Nitric oxide cGMP pathway - vasodilation
3. Phospholipase C pathway - vasoconstriction
159
cAMP pathway
Increase in Protein Kinase A causes decrease in intracellular Ca+ in the vascular muscle cell
PKA manipulates the excitation-coupling pathway by
1. Inhibition v-gated Ca+ channels in sarcolemma
2. Inhibition of Ca+ release from the SR
3. Reduced sensitivity of the myofilaments to Ca+
4. Facilitation of Ca reuptake into SR via the SERCA2 pump
160
Example of cAMP pathway
NE>Beta2>Gs g-protein> Adenylate cyclase> cAMP > Protein Kinase A> decrease in Ca+ > vasodilation
161
what produces NO?
NO is produce by ACh, substance P, bradykinin, serotonin, thrombin, shear stress
162
NO/cGMP pathway
| Step 1
1. NO synthaetase catalyzes conversion of L-arginine to NO
163
NO/cGMP pathway
| Step 2
2. NO diffuses from endothelium to smooth muscle
164
NO/cGMP pathway
| Step 3
3. NOP activates guanylate cyclase
165
NO/cGMP pathway
| Step 4
4. Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
166
NO/cGMP pathway
| Step 5
5. Incrase in cGMP reduces intracellular Ca+, leading to relaxation of smooth muscle
167
NO/cGMP pathway
| Step 6
6. Phosphodiesterase deactivates cGMP to guanosine monophosphate
168
Phospholipase C pathway activators
phenylephrine, NE, angiotensin II, endothelin-1
169
Phospholipase C pathway example
Angiotensin II > ATII receptor > Gq g protein > Phospholipase C > IP3 and DAG > Incarease in Ca+ > Vasoconstriction
170
Phospholipase C pathway
activation of pathway increases production of two second messengers: IP3 and DAG. IP3 augments Ca+ release from SR and DAG activates protein kinase c. This opens v-gated Ca+ channels in the sarcolemma and increases Ca+ influx.
