Exam 1 REVIEW Flashcards
(391 cards)
1
Q
The conductive system consists of the following components
A
The sinoatrial (SA) node, the internodal tracts, the AV node, the AV bundle, and the Purkinje system
2
Q
SA node primary pacemaker, rate
A
60-100
3
Q
AV node only pathway between Atria and ventricles, rate
A
40-60
4
Q
Small mass of specialized cells and collagenous tissue located along the epicardial surface
A
The SA node (the Keith-Flack node)
5
Q
At the junction of the superior vena cava and the RA.
A
SA node
6
Q
Three major internodal tracts exist:
A
the anterior, middle, and posterior internodal tracts.
7
Q
The anterior internodal tract, or
A
Bachmann bundle
8
Q
Sends fibers to the LA and then travels down
through the atrial septum to the AV node.
A
Bachmann Bundle
9
Q
The middle internodal tract, or
A
Wenckebach tract,
10
Q
Curves behind the superior vena cava before descending to the AV node.
A
Wenckebach tract,
11
Q
Finally, the posterior internodal tract, or
A
Thorel tract,
12
Q
continues along the terminal crest to enter the atrial septum and then passes to the AV node.
A
Posterior internodal tract
13
Q
The AV node causes a
A
delay in the transmission of action potentials
14
Q
Is the preferential channel for conduction of the action
potential from the atria to the ventricles
A
AV bundle
15
Q
Where is the site with the greatest resistance to the transmission of action potential?
A
Within the AV node
16
Q
Speed of conduction to adjacent cells within the SA is
A
0.5m/sec
17
Q
Intrinsic PM cells of the AV node depolarizes at what rate
A
40-60
18
Q
Conduction velocity from Bundle of his to left and right BBB is
A
Rapid 2m/sec
19
Q
Purkinje system firing rate is
A
20-40 beats/min
20
Q
Purkinje fibers velocity of impulse conduction
A
4m/sec (rapid velocity of impulse conduction) which allows for rapid depolarization of ventricular myocytes.
21
Q
Necessary to inhibit actin and myosin from interacting and initiating muscle contraction
A
Troponin complex
22
Q
When catecholamines interact with B1 receptors, they stimulate intracellular
A
G protein activation
23
Q
Myocardium oxygen demand is determined by
A
preload, afterload, contractility and HR.
24
Q
Myocardial oxygen supply is determined by
A
Arterial blood content Diastolic BP Diastolic time (as dtermined by HR) Oxygen extraction Coronary Blood flow
25
HR affects both
Supply and demand
26
Increasing HR does what
Increases demand
| decreases diastolic time
27
Diastolic filling time is
80-90 % coronary filling and myocardial perfusion occurs.
28
What is the most important factor that negatively affects ?
MvO2
29
Doubling the HR
Doubles MvO2
30
Primary substance responsible for coronary vasodilation is
Adenosine
31
Determinants of MvO2 include
```
myocardial contractility
Myocardial wall tension (preload)
HR
MAP
Afterload
```
32
Oxygen extraction is determined by measurement of the
Difference between the oxygen tension in the pulmonary arterial blood and that in the coronary sinus.
33
Arterial Oxygen content equation (CaO2) =
(SaO2 x Hgb, 1.34) + 0.003 x PaO2
34
Under normal physiologic conditions, the coronary circulation, like other tissues beds in the body, exhibits
Autoregulation
35
Autoregulation is the
ability to maintain coronary blood flow across a range of MAP by dilating or constricting.
36
Coronary blood flow is maintained at a constant flow rate through a MAP range of
60-140 mmHg.
37
Autoregulation: When arterial pressure is less or exceed these pressure limits what happens?
Coronary blood flow becomes pressure dependent.
38
Autoregulation: During HYPOTENSION, when the coronary arteries are
maximally dilated, coronary blood flow is determined by MAP - RAP
39
Where is the SA node located?
Junction of RA and VC
40
AV node depends on________ for propagation of action potentials
L-type Calcium channels
41
Ions is the major determinant of the resting membrane potential.
Potassium
42
Cardiac muscle fibers resemble skeletal muscle fibers in that they are_______ they differ in that they form_______ a, which means that all fibers are electrically connected via
striated; functional syncytium;gap junctions.
43
Normal Coronary Perfusion Pressure is
60-160 mmHg
44
Normal EF
= 60-70%
45
Normal MAP =
70-105 mmHg
46
Normal SVR =
800-1500 dynes/sec/cm^5
47
Normal PVR =
150-250 dynes/sec/cm^5
48
Normal CI =
2.8 – 4.2 L/min
49
Factors that increases myocardial oxygen demand:
| THS inWACEd
```
Tachycardia
HTN
SNS stimulation
increased :
Wall tension
Afterload
Contractility
EDV
```
50
Factors Decreases myocardial oxygen demands
Decrease coronary blood flow (tachycardia, Decreased aortic pressure, decreased vessel diameter, increase EDP
51
Decreased CaO2 caused by
Hypoxemia, Anemia
52
Decreased Oxygen Extraction caused by
Left shift of Hgb dissociation curve: decreased p50, Decreased capillary density
53
Affect both sides of the supply/demand equation (HAP)
HR
Aortic diastolic pressure
Preload.
54
Which factor most negatively affects myocardial oxygen consumption?
HEART RATE
55
How does Tachycardia affect supply?
A shorter diastolic time means that there is less time to deliver oxygen to the L ventricle.
56
LV subendocardium Best perfused during
Diastole
57
Why is RV subendocardium not affected?
The RV usually isn’t affects, because it is well perfused throughout the cardiac cycle.
58
How does Tachycardia increases demand?
Cardiac contraction and relaxation require ATP, therefore increase the number of cardiac Cycles per minutes increases ATP and oxygen utilization
59
How does INCREASE Aortic diastolic pressure affect supply/demand?
Increase supply and demand
60
How does supply increases with increases aortic diastole pressure?
Increase in aortic pressure increase the pressure head that perfused the coronary artery (P1-P2)
61
Increase aortic DBP – LV EDP =
Increased Coronary Perfusion pressure.
62
How does demand increases with increases aortic diastole pressure?
An increased in aortic pressure also increases wall tension and afterload. The myocardium requires more Oxygen as it generates a higher pressure to open the aortic valve.
63
As a general rule the benefits of a increase coronary perfusion pressure
outweighs the drawback of an increase wall tension
64
How does an increased preload affect supply/demand?
Increase preload decrease supply and increase demand
65
How does an increase in preload decrease supply?
Increase EDV decreases coronary prefussion pressure
Because of the CPP formula
CPP = Aortic DBP - (increased) LVEDP = decrease CPP
66
How does an increase in preload increase demand?
Increase preload increases wall stress.
67
Most determines coronary blood flow is
myocardial metabolism
68
VALLEY: Myocardial Oxygen demand: 4 factors determine
1) Heart rate
2) Diastolic wall tension (preload)
3) Systolic wall tension (afterload)
4) Contractility
69
Myocardial oxygen demand is affected by the following important factors:
(1) HR; (2) ventricular wall tension (as determined by preload, afterload, and wall thickness); and
(3) myocardial contractility
70
The rate of myocardial oxygen consumption (MvO2) increases with
increases in HR, increases in wall tension, and increases in contractility.
71
The rate of MvO2 generally decreases with a
decreasing HR, decreasing wall tension, and decreasing contractility.
72
As stated previously, the rate of myocardial oxygen extraction is quite high; further increases in metabolic demand are met primarily by
an increase in coronary blood flow.
73
Tachycardia increases myocardial
oxygen demand
74
Only site where impulse travels to pass from atria to ventricles is the
AV node
75
Conduction velocities from fastest to slowest:
a) Purkinje fibers (4m/s)
b) Ventricular myocytes (1m/s)
c) Atrial myocytes (1m/s)
d) Bundle of His (1m/s)
e) SA and AV nodes (0.01-0.02 m/s)
76
Phase 4 of SA nodal action potentials is generated in part by
Funny” currents produced by inward movement of positively charged ions
77
The duration of the effective refractory period in cardiac cells can by increased by
inhibiting potassium channels
78
Normal SV
50-110 ml/beat
79
Normal SVI
30-65ml/beat/m^2
80
Normal pulse pressure is
40 mmHg
81
Normal SVR Index (SVRI)
1500 - 2400 dynes/sec/cm^5/m^2
82
Normal PVR Index (PVRI)
250-400 dynes/sec/cm^5/m^2
83
Slopes of the graph indicates
Conduction velocity
84
Absolute refractory period represent what on EKG?
QT interval
85
Relative refractory period represent what on EKG?
End of T wave
86
Current responsible for slow phase 4 depolarization in SA node?
I-f (funny current)
87
Cardiac action potential sequence
SA node -->Internodal tract --> AV node --> Bundle of HIS --> left and Right Bundle Branches --> Purkinje fibers.
88
Conduction velocity in non-nodal cardiac cells is decreased by doing what?
by decreasing the slope of phase 0
89
A patient who has mitral valve stenosis. Which of the following occurs as they exercise?
Increased Pulmonary capillary wedge pressure (PCWP)
90
Valve defects is not associated with an increase in PCWP
– PULMONIC VALVE STENOSIS
91
Stenotic aortic valve and PCWP:
Elevated pulmonary capillary wedge pressure
92
Aortic valve regurgitation and SV
Increase LV stroke volume
93
Responsible to keep the TMP
Na-K+ ATPases PUMP
94
NA-K ATPase ions movement
3 Na+ out
| 2 K+ in
95
Explain receptor activation
Receptor -->G protein--> Effector --> 2nd Messenger -->intracellular action
96
When myocytes reach about −70 mV (“threshold”),
fast sodium channels open and an influx of sodium
| ions increase the membrane potential to +30 mV (phase 0).
97
DO2 Formula
CO x {(HgbxSaO2x1.34) + (PaO2 x0.003)} x10
98
Normal CaO2
20ml/dL
99
Normal DO2
1000 ml/min
100
Normal Oxygen Extraction Ratio
25%
101
Normal VO2
250 ml/min
102
Normal CvO2 (venous oxygen content)
15 ml/dL
103
Blood flow relationship to hematocrit
Inversely proportional
104
Ventricular myocytes Resting Membrane potential is
-90mV
105
Nodal Tissues Resting membrane potential is
-60mV
106
```
5 Phases of FAST ventricular action potential and ionic movement during each phase
Phase 0 =
Phase 1 =
Phase 2 =
Phase 3 =
Phase 4=
```
5 Phases of FAST ventricular action potential and ionic movement during each phase
Phase 0 = Depolarization Na+ influx
Phase 1 = Initial repolarization K+ efflux and Cl- influx
Phase 2 = Plateau Ca2+ influx
Phase 3 = repolarization K+ efflux
Phase 4= Na/K ATPase restore resting membrane potential
107
On the other hand, slow action potentials utilized by cells of the SA or AV node yield a similar result but lack the
phase 1 and 2 components
108
3 phases of the SA node action potential and the ionic movement during each phase
Phase 4=
Phase 0 = Depolarization Ca2+ influx
Phase 3 = Repolarization K+ efflux
Phase 4= Spontaneous depolarization: Leaky to Na+ (Ca2+ influx occurs at the very end of phase 4)
Phase 0 = Depolarization : Ca2+ influx
Phase 3 = Repolarization: K+ efflux
109
Nodal tissues have 2 types of leaky channels
Both sodium and potassium leaky channels
110
Phase 4 depolarization is fastest in the_____less than fastest in the ______SLOWEST in______
SA node, AV node; purkinje fibers
111
What ion controls the RMP →
Potassium ions control RMP
112
SA node: What ion controls the Threshold Potential?
Calcium controls the threshold potential
113
Hypokalemia and excitability?
decreased excitability, RMP becomes more polarized (HYPERPOLARIZED ) like -80mV or -90mV (the difference between the resting and the threshold potential increases making the tissue less excitable.
114
Hypokalemia relationship with excitabilty
Directly proportional
115
Hyperkalemia and excitability?
Hyperkalemia increased excitability, RMP become less polarized (depolarized) like -30 numbers. The difference between the resting potential and the threshold potential decreases, THEREBY MAKING it more excitable
116
Hypocalcemia and excitability ?
increases membrane excitabiliy (Decrease stability) The TP increases becomes more negative. The RMP and the TP approach each other, and nerve and cardiac cells become more excitable.
117
Excitability of nerve and muscle is increased when.
hypocalcemia is present
118
As Calcium levels increases, excitability
Decreases.
119
P-wave represents
atria depolarization
120
T wave represents
ventricular repolarization
121
Most diastolic ventricular filling occurs
- Phases part of systole Phase 2 - Isovolumetric contraction Phase 3 - Rapid Ejection Phase 4 - Reduced Ejection Isovolumetric Relaxation Pasive filling (diastasis)
- During what phase of the cardiac cycle does most of ventricular filling occur? Phase 6 Rapid filling.
- The first heart sound signifies closure of which heart valves? Closure of the AV valves
- The second heart sound signifies closure of which heart valves? Aortic and pulmonic valves.
- Ejection phase is complete with closure of the semilunar valves and the start of the relaxation phase. On the ECG, this represents the ST segment
- A dicrotic notch would be detected on the arterial waveform to indicate the closure of the aortic valve
- Preload is also the same LVEDV.
- Curve shift to the left means decrease EDV
passively before atrial contraction.
122
Contraction of atria contributes
20-30% of the ventricular filling
123
a Wave is
Atrial systole
124
c Wave is
Ventricular systole
125
C wave is displayed due to
Bulging of the tricuspid valve into the right ventricle.
126
V venous return before
AV valves open again VENOUS RETURN
127
Phases part of Diastole (4 phases)
Isovolumetric Relaxation
Rapid ventricular filling
Reduced (Passive filling) (diastasis)
Atrial systole.
128
Phases part of systole
Isovolumetric Ventricular contraction
| Ventricular Ejection
129
During what phase of the cardiac cycle does most of ventricular filling occur?
Phase 6 Rapid Ventricular filling.
130
The first heart sound signifies closure of which heart valves?
Closure of the AV valves
131
The second heart sound signifies closure of which heart valves?
Aortic and pulmonic valves.
132
-Ejection phase is complete with
closure of the semilunar valves and the start of the relaxation phase.
133
EJECTION pHase: On the ECG, this represents the
ST segment
134
A dicrotic notch would be detected on the arterial waveform to indicate the
closure of the aortic valve
135
Preload is also the same
LVEDV.
136
Curve shift to the left means
decrease EDV
137
Curve to the right
Increased preload
138
Curve to the left
Increase contractility
139
Filling phase has 2 phases: rapid phase
rapid phase based on the pressure gradient comprising 75% of blood volume, and (2) the slower active atrial systole phase (“atrial kick”) accounting for the remaining (25%) blood volume.
140
Most vulnerable to ischemia is the subendocardium why?
because it has the greatest metabolic demands and is most compressed (NO BLOOD FLOW) during SYSTOLE
141
The Subendocardium has the
densest network of capillaries.
142
LV subendocardium is best perfused during diastole. As aortic pressure increases, the LV tissue
compresses its own blood supply and reduces blood flow.
143
The high compressive pressure in the LV subendocardium coupled with a decreased coronary artery blood flow during systole increase
coronary vascular resistance and predispose this region to ischemia
144
Aortic Stenosis , goal Heart rate
Slow to normal (SINUS RHYTHM)
145
Aortic Stenosis, goal preload
Increase (you don't want low BP ever) because valve is already stenotic, you need enough volume to pass _)
146
Aortic stenosis where do you want SVR and contractility
Maintain normal
147
Aortic stenosis where do you want PVR?
AVOID Increase
148
Aortic stenosis avoid 2 things
Tachycardia
| Increase PVR
149
Aortic Regurgitation goal HR : avoid
AVOID bradycardia and increase in SVR
150
Aortic regurgitation : SVR: Where do you want it
You want Decrease in SVR
151
Aortic regurgitation :preload
Same to elevated (maintain intravascular volume)
152
Aortic regurgitation :PVR and contractility
Maintain
153
Mitral Stenosis: HR where do you want it?
Slow NSR
154
Mitral stenosis PVR
Avoid increase
155
Mitral stenosis maintain
SVR, preload, contractility
156
Mitral stenosis : THIS condition must be treated aggressively and how?
Atrial fibrillation ; Cardioversion
157
Mitral regurgitation : Mitral insufficiency HR where do you want it
Elevated
158
Mitral regurgitation : avoid this
Increase in PVR
159
2 conditions that benefit from Tachycardia
MR
| AR
160
Holodiastolic descrescendo murmur is
Mitral stenosis
161
AS hypotension should be avoided due to
Decrease in CPP
162
Aortic regurgitation avoid what kind of medications?
Alpha agonists, the increase afterload and reflex bradycardia will make the regurgitant condition worst? because it will increase SVR and slow HR
163
Mitral regurgitation avoid: 3 conditions (HAH)
Hypoxia
Hypercabia
ACidosis
164
Mitral regurgitation treat hypotension with
EPHEDRINE
165
Chronic increase in pressure leads to
PCP (pressure - Concentric Hypertrophy - Parallel saracomeres)
166
Chronic increase in volume leads to
VES (Volume- Eccentric Hypertrophy --Series)
167
A 60-year-old female with mitral stenosis has the following post-induction vital signs: HR 125, BP 70/45
followed by sudden supraventricular tachycardia (SV). What will you do first?
Cardioversion
168
In which valvular disease is the pulmonary capillary wedge pressure (PCWP) an overestimation o the left
ventricular end-diastolic pressure (LVEDP)?
MITRAL STENOSIS
169
Which pathologic state will not cause giant, “cannon” a-waves on the CVP wave form?
TRICUSPID REGURGITATION
170
What is the goal of hemodynamic management for the patient with mitral stenosis?
MAINTENANCE OF NORMAL SINUS RHYTHM
171
Mitral stenosis is associated with left atrial and pulmonary hypertension due to the
stenotic transvalvular pressure gradient.
172
The patient with mitral stenosis has impaired
left ventricular filling
173
An adult patient with moderate aortic regurgitation receives a spinal anesthetic. A blood pressure drop to 68/42 is treated with 100 μg o phenylephrine. How will this dose impact the patient’s underlying disease state?
It will exacerbate the regurgitation.
174
Which valvular disorder leads to the largest ventricular volume?
AORTIC REGURGITATION
175
Which valve disorder most likely predisposes a patient to coronary ischemia with hypotension?
AORTIC STENOSIS
176
Which risk actor contributes to myocardial ischemia in a patient with aortic regurgitation?
Heart rate 110-120 beats/minute
177
What arterial line waveform might you observe in a patient with severe aortic regurgitation?
(C) Pulsus bisferiens
178
What compensatory mechanism is commonly seen with aortic regurgitation?
(A) Eccentric hypertrophy (because of volume overload)
179
In which valvular disorder is the left ventricular volume approximately normal, but left ventricular pressure higher than normal?
Mitral regurgitation
180
What increases stroke volume?
Increased Ventricular EDV
181
Mitral regurgitation, in general, factors such as _____HR AND ______SHOULD BE AVOIDED
slow heart rate and acute increases in afterload should be avoided
182
Which actors will exacerbate mitral regurgitation?
Bradycardia and acute increases in afterload.
183
With which patient would the anesthetist most want to maintain spontaneous ventilation?
AORTIC STENOSIS
184
What is the goal of hemodynamic management of the patient with severe mitral valve regurgitation under general anesthesia?
AFTERLOAD REDUCTION (maintain forward flow)
185
AVOID (HAH) → HYPOXIA, HYPERCARBIA and ACIDOSIS
MITRAL REGURGITATION
186
MITRAL Stenosis how to avoid Pulm. HTN?
minimize pulmonary HTN (avoid hypoxemia, hypercarbia, acidosis, hypothermia)
187
Coronary blood flow is autoregulated between
MAP of 60-140 mmhg .
188
Role of autoregulation ?
This allows a constant coronary blood flow over a wide range of BPs. When MAP falls below the range of autoregulation , coronary perfusion becomes entirely dependent on coronary perfusion pressure.
189
When MAP falls below the range of autoregulation , coronary perfusion becomes entirely dependent on
coronary perfusion pressure.
190
Autoregulation is the NET effect of 3 things:
Local Metabolism
Myogenic Response
ANS
191
Autoregulation? What is the most important determinant of coronary vessel diameter?
Local metabolism
192
Autoregulation: ADENOSINE is a
byproduct of ATP metabolism and is a POTENT CORONARY VASODILATOR.
193
Autoregulation: As MVO2 increases, the coronary endothelium release as
adenosine as well as a variety of other vasodilator substances including NO, prostaglandins, hydrogen, potassium and CO2.
194
Autoregulation: Note the HYPOCARBIA causes.
coronary vasoconstriction
195
Autoregulation: As MVO2 increases, the tissue has a mechanism to
increase its own blood flow.
196
Autoregulation: Vasodilation decreases
vascular resistance, increases coronary perfusion and flushed out products of metabolism
197
Autoregulation: What is the myogenic response?
It’s the vessel’s innate ability to maintain a constant vessel diameter.
198
Autoregulation -->With myogenic response: When the vessel’s diameter is increased, it will have the tendency to and
contract,
199
Autoregulation -->With myogenic response when the diameter decreases, it will have a tendency to
dilate.
200
Autoregulation : ANS =>
Can affect coronary vascular tone, although the effects are overshadowed by the products of local metabolism.
201
There are times when the ANS effects
prevail. For examples in patients with PRINZMETAL angina (Vasospastic myocardial ischemia ) are believed to have overactive coronary alpha receptors that can cause intense vasoconstriction and chest pain.
202
Substance that Causes Coronary Artery Constriction how?
Alpha (epicardial) and HISTAMINE-1
| Increase IP3 increases, Increase intracellular Calcium
203
Causes Coronary Artery Dilation - Beta 2
Beta-2 (endocardial) -> Increases cAMP -> Decrease intracellular Ca2+
204
Causes Coronary Artery Dilation - Histamine 2
Increases cAMP -> Decrease intracellular Ca2+
205
Causes Coronary Artery Dilation
Muscarinic --> Increases NO
206
3 substances causing coronary artery dilation
Beta-2
Histamine-2
Muscarinc
207
Metabolic coronary vasodilation in response to enhanced myocardial oxygen consumption during exercise occurs, at least in part, as a result of
enhanced local release of metabolic substrates (e.g., adenosine, ADP) combined with sympathetic nervous system stimulation of the coronary vasculature.
208
CO definition:
HR is controlled by the spontaneous depolarization of the sinoatrial (SA) node (which is controlled by the autonomic nervous system), SV is a function of the following
four factors: (1) preload; (2) afterload; (3) contractility; and (4) wall motion abnormalities.
defined as the volume of blood pumped systemically by the left ventricle each minute.
209
The SV usually ranges between
70 and 120 mL
210
CO men vs women:
CO of 5.6 L/min in men and 4.9 L/min in women
211
Formula CO=
HR x SV
212
Both HR and SV are (relationship)
directly proportional to CO, such that increases in either the HR or the SV produce an increase in CO
213
HR is controlled by the
spontaneous depolarization of the sinoatrial (SA) node (which is controlled by the autonomic nervous system)
214
Spontaneous depolarization of the sinoatrial node controlled by the
ANS
215
SV is a function of 4 factors
Preload
Afterload
Contractility
Wall motion abnormalities.
216
Preload is described with the
Frank Starling Mechanism
217
Afterload →
Ventricular wall tension during systole approximate ventricular afterload
218
SV and afterload have what kind of relationship
inversely proportional
219
Contractility
The sympathetic nervous system has the most profound effect on myocardial contractility as the sympathetic adrenergic fibers release norepinephrine, which stimulates the myocardial beta-1 adrenergic receptors to enhance contractility and CO
220
Which has the most profound effect on myocardial contractility?
SNS
221
Basic components of the circuit?
1. Venous reservoir
2. Oxygenator
3. Heat exchanger
4. Main pump
5. Arterial filter
6. Tubing -> venous blood to the venous reservoir.
Tubing --> oxygenated blood back to the patient.
222
CPB priming
CBP circuit must be primed with typically 1200-1800 ml free of bubbles
223
Reservoir is placed
Below the level of the patient to allow for gravity drainage.
224
Reservoir serves at the
Large mixing chamber for all blood return.
225
The amount drain to reservoir is a factor of
CVP
Gravity
Resistance found in circuit
226
Arterial pump function:
Pull blood from reservoir
| Driving it through the oxygenator (gas exchanger: artificial lung, a heat exchanger, and arterial line filter)
227
Oxygenated warm blood return to patient's arterial system via an
Arterial line positioned in the ASCENDING AORTA
228
Preferred cannulation method is:
Aorto-atriocaval cannulation
229
CPB is associated with
Severe inflammatory response becauce of contact of blood with nonendothelial extracorporeal surface.
230
CPB response lead to
Platelet, endothelium, leukocyte activation, initiation of the coagulation cascade, decrease levels of coargualtion factors.
231
Aorto-atriocaval cannulation : the blood is drained from
The right atrium and returned to the ascending aorta.
232
Roller pump : Flow and air
continuous pulsatile flow ; MAY ENTRAIN AIR
233
Centrifugal Pumps Advantages:
Less traumatic to blood than roller pumps
| Centrifugal pumps DO NOT ENTRAIN AIR IN PATIENT
234
Centrigugal pumps is between the
Oxygenator and the VENOUS RESERVOIR.
235
Disadvantage of centrifugal pumps:
NO well defined volume
236
Five major functions of CPB:
-
```
Circulation of blood
Oxygenation
Ventilation
Systemic cooling, rewarming
Diversion of blood from the heart to provide a bloodless surgical field.
```
237
The CPB allows the surgeon
to operate on a non-beating heart in the setting of a bloodless field while maintaining adequate whole body tissue oxygenation and perfusion.
238
What is the Role of the LV vent?
LV vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt)
239
Which patient is most at risk or catastrophic bleeding upon midline sternotomy?
Patient with previous coronary artery bypass grafting undergoing mitral valve repair
240
In general, one should wait how long after heparinization before initiating CPB
3-5 minutes (after heparinization)
241
For inintiation of CPB ACT should be >
| Heparin 300-400 units /kg
400 seconds
242
Should be given prior to cannulation? and why?
Heparin; decrease risk of thrombosis in both the patinet and the CPB circuit
243
What cannulation is achieve first?
Arterial cannulation first (ascending aorta)
244
Heparin dose
300-400 units/kg
245
Primary method of myocardial protection during CPB remains
the administration of CARDIOPLEGIA and the institution of hypothermia
246
Anterograde Cardioplegia: is catheter placed in the
Proximal Aorta between aortic clamp and aortic valve
247
Retrograde Cardioplegia: Catheter place in the
Coronary sinus. (used for patient with aortic pathologies)
248
Myocardial temperature monitored, wanted myocardial temperature
directly 10-15C desired
| 8-10 C nagelhout
249
Cardioplegia solutions, 2 types
Potassium-rich crystalloid or blood-crystalloid solutions.
250
Cardioplegia must be
repeated every 30 minutes
251
CARDIOPLEGIA → leads to
High K+ , depolarization and cardiac arrest.
252
Cardioplegia is indicated when the
aortic cross-clamp is in place because there is no coronary blood at the time.
253
Cardioplegia leads to electrical
silence and mechanical silence, reduces Myocardial O2 demand by more than 80%.
254
Bicarbonate is given for buffering
excess acid metabolites on bypass
255
Mannitol to reduce
edema
256
Potassium for
arresting the heart, blood or/and crystalloid as carrier
257
Magnesium is given to
Reduce calcium overload
258
Anterograde is delivered to the ____system
ARterial
259
Retrograde: Must be
monitored, High pressure limit is 40 mmhg in order to avoid hemorrhage from damage to the coronary sinus, and venous systems.
260
Cardioplegia: MOST CASES, A combination of
ANTEROGRADE and RETROGRADE is USED for the most complete coverage and protection of the myocardium
261
Dosing of cardioplegia is every ___minutes OR when
20 ; cardiac activity is observed.
262
Hypothermia to ____reduces______by _______
27C reduces O2 requirements by approximately 60%. Benefits,
263
Hypothermia and SVR
increase in SVR caused by hypothermia may offset the decrease in SVR associated with hemodilution alone.
264
3 main good effects of hypothermia:
a) Hepatic blood flow and enzymatic activity are decreased, reducing clearance of drugs eliminated by this route
b) Myocardial preservation is enhanced
c) CNS protection
265
2 key steps prior to initiating CPB →
Anticoagulation AND Vascular cannulation
266
Onset of Bypass and BP
Transient hypotension (MAPs as low as 30 mm Hg) is common following initiation of CPB, and should not be treated unless prolonged.
267
The predominant cause of hypotension following initiation of CPB is
decreased SVR (secondary to reduced blood viscosity, dilution of endogenous catecholamines in priming solution, and differences in pO2, pH, and electrolyte concentrations between the priming solution and native blood).
268
What should the activated clotting time be prior to initiation of cardiopulmonary bypass (CPB)?
>400 seconds
269
A 100-kg patient is administered 40,000 units of heparin. Five minutes later the AC was measured to be 182 seconds. What is the next step?
Administer two units of fresh frozen plasma( contains antithrombin III)
270
Your patient is undergoing an elective coronary artery bypass graft (CABG). The patient was managed on heparin therapy or five days preoperatively. The patient is now on cardiopulmonary bypass and the perfusionist is having difficulty maintaining total heparinization. What is the most likely cause?
( A) Antithrombin deficiency
271
Termination of CPB temp
Patient should be normothermic to maximize cardiac contractility and decrease chance of arrhythmias’
<38
272
Termination of CPB electrolytes
Acid-base, calcium and potassium abnormalities should be addressed.
273
Termination of CPB and Hgb
Hemoglobin should be at least 7 g/dl
274
Infusion, the patient will require this
inotropic support, SHOULD be started after removal of the aortic cross clamp
275
Termination of CPB: Potassium should be approaching
normal range 4-5
276
Termination of CPB: Lungs should be fully expanded,
ventilated and volatile agent administered if patient can tolerate
277
Termination of CPB:Heart rate should be
paced at 90 bpm
278
Termination of CPB: Anticoagulation is reversed with
protamine sulfate and thoracic incision closed.
279
Rewarming : Nasopharyngeal goal temp
36-37C
280
Rewarming: rectal goal temp
>35 but < 37
281
Separation from CPB Hct should be
20-25%
282
TERMINATION : 1ST STEP CLAMPING
| V -A
VENOUS OUTLFOW LINE IS SLOWLY CLAMBED
| AORTIC INFLOW LINE IS CLAMPED
283
INITIATION CLAMPING; 1ST STEP
| A-V
ARTERIAL CANNULATION FIRST
284
Administration of protamine, a heparin antagonist, may have the following adverse reactions:
(l) systemic hypotension, (2) pulmonary hypertension, MYOCARDIAL DEPRESSION and (3) allergic reactions.
285
Adverse effects of protamine sulfate are due to
Histamine release.
286
Pulmonary artery pressure increases because, with
rapid Infusion of protamine pulmonary systemic vascular resistance increases.
287
As you know, protamine also promotes a
decrease in systemic vascular resistance and hypertension. These pulmonary and systemic consequences of protamine result from histamine release
288
3 adverse reactions with Protamine sulfate.
Severe pulmonary artery vasoconstriction
myocardial depression
Severe systemic hypotension.
289
What is the Most common complication during rewarming as BRAIN normothermia is restored in the setting of_______?
Intraoperative AWARENESS decrease anesthetic concentration.
290
May be needed during rewarming?
Additional anesthetic dosing
291
CBP pump flow at normothermia pump flow should be between
50 and 70 ml/kg/min)
292
During rewarming, increased SVR is usually due to
inadequate anesthesia, volatile anesthetic preferred in that case if the patient has good ventricular function. If patient does not have good ventricular function, inhalational agents are avoided because of the potential for myocardial depression after CPB.
293
Aortic cross clamp placed above the
artery of Adamkiewicz can cause ischemia to the lower portion of the anterior spinal cord can result ANTERIOR SPINAL ARTERY SYNDROME also known as BECK’s syndrome.
294
Signs of Anterior spinal artery syndrome
Flaccid paralysis of the LE
Bowel and bladder dysfunction
Loss of temperature and pain sensation
Preverve touch and proprioception
295
Most sensitive intraoperative monitor for detecting MI is
TEE
296
The single best lead for detecting myocardial ischemia
V5.
297
Where do you place V5?
4th intercostal space midclavicular line
298
Not recommended for monitoring perioperative ischemia?
3-lead ECG
299
SA artery
prominent central artery that is a branch of the RCA
300
3 internodal tracts
Anterior middle posterior
301
Equillibrium potential of K
-94
302
Equillibrium potential of Na
60
303
Severe mitral stenosis atrial kick %
40%
304
Cardiac surgery you need to monitor
Automated ST segment monitoring
305
CO =
VO2 / (Ca-Cv) O2
306
Normal ACT is
80 -120 Seconds
307
During aortic cannulation, systolic BP should be
100 mmHg to minimize the risk of dissection.
308
RMP is a balance of 2 opposing forces
Movement of K+ down its concentration gradient, and the electrical attraction of the negative interior for the positive potassium ions. (opposite attracts)
309
Action potential of myocardial cell raises the membrane potential to
+20 mV
310
How long does the plateau phase lasts
0.2 to 0.3 second
311
Whereas the action potential for skeletal muscle and nerve is caused by ___________in cardiac muscle, it is due to opening of both
Fast Na+ Channels
| fast Na channels and slower calcium channels
312
Depolarization is also accompanied by a
Transient decrease in Potassium permeability
313
SA node has a less negative RMP because (-60mV) why
Slow influx of Na+ lead to
Fast Na+ Channels are inactive
Action potential threshold is -40 mV (caused by ION MOVEMENT OF SLOW CALCIUM CHANNELS)
314
When threshold reach is Nodal tissues?
Calcium channels open
| Potassium permeability decreases --> Action potential
315
For nodal tissues, what return the normal RMP?
normal potassium permeability.
316
Anesthetic effects: VA on SA node and AV node
Depress SA node automaticity
| Modest effects on the AV nodes.
317
Opioids on Sa node
Increases AV node conduction and refractory period
318
Myocardial cells contract because of 2 proteins
Actin and myosin
319
Connect actin to the cell membrane
Dystrophin
320
What normally prevent the interaction of troponin and tropomyosin?
Actin and myosin
321
Troponin has 3 subunits?
Troponin I
Troponin C
Troponin T
322
Mechanisml of contraction of myocardial cells: Increase in Intracellular Ca2+ promotes
contraction as calcium Binding to troponin C --> results in conformational changes of those proteins exposes active site on actin that allow interaction with myosin bridges. (active site on myosin function as magnesium-dependent ATPase whose activity) is enhanced by the increased in intracellular calcium concentration
Relaxation occurs as calcium is pumped back into the Sarcoplasmic recticulum by a Ca2+-Mg 2+ ATPase; the resulting drop in calcium allow the troponin-tropomyosin complex to prevent actin and myosin interaction.
323
The force of contraction is directly dependent on
Magnitude of initial calcium influx
324
Parasympathetic receptors
Muscarinic M2 --> Negative chronotropy, dromotropy and inotropy
325
Sympathetic fibers of heart originate in
Thoracic spinal cord T1-T4 and travel through heart initially through CERVICAL GANGLIA (stellate)
326
v wave is the
Result of the pressure buildup from venous return
327
Decline in pressure between the c and v wave, Pulling down of the atrium by ventricular contraction
x-descent
328
Notch in the aortic pressure tracing is referred to as the
INCISURA : transient backflow of blood into left ventricle just before aortic valve closure.
329
Ventricular preload aka
EDV
330
In the absence of pulmonary or RV dysfunction, venous return is a major determinant of
LV preload.
331
Venous return is affect by PPT
PPV
Posture
Tachycardia.
332
The larger the ventricular RADIUS, the ______wall tension
GREATER
333
An increase in ventricular THICKNESS, Reduces
Ventricular WALL TENSION
334
Contraction depends on the
Intracellular calcium concentration during systole.
335
Most anesthetics and antiarrhythmic agents are (inotropy)
Negative.
336
Ventricular wall abnormalities; Hypokinesis
Decreased contraction
337
Ventricular wall abnormalities; Akinesis
Failure to contract
338
Ventricular wall abnormalities; Dyskinesis
Paradoxic bulging
339
Stenosis of an AV valve reduces SV how?
decreasing ventricular preload
340
Stenosis of a semilunar valve reduces SV how?
increasing ventricular afterload.
341
Most tissue beds regulate
Their own blood flow
342
2 causes of autoregulation can be because of
Intrinsic response of vascular smooth muscle to stretch
| Accumulation of vasodilatory metabolic byproducts
343
Vasodilatory metabolic produces may increase
K+, H+, CO2, Adenosine and lactate.
344
Vascular endothelium secretes and modifies substances that control BP-> Vasodilators
Nitric oxide, prostacyclin, PGI2
345
Vascular endothelium secretes and modifies substances that control BP-> Vasoconstrictors
Thromboxane A2, Endothelins
346
Vascular endothelium secretes and modifies substances that control BP-> anticoagulants
Thrombomodulin, protein C
347
Vascular endothelium secretes and modifies substances that control BP-> Fibrinolytics
TPA
348
Vascular endothelium secretes and modifies substances that control BP-> Inhibit platelet aggregation
NO and PGI2
349
Vascular tone and autonomic influences on the heart are controlled by
Vasomotor centers in the reticular formation of the medulla and LOWER Pons.
350
Vasomotor centrers in the reticular formation are also responsible for
Adrenal secretion of catecholamines as well as enhancement of cardiac automaticity and contractility.
351
Coronary vessel tone can be autoregulated between
CPP 50-120mmHg
352
Most vulnerable to ischemia during decrease in CPP
Subendocardium (Endocardium)
353
Dose dependent abolition of autoregulation may be greatest_____and least with ______
ISOFLURANE
| SEVO
354
Volatile anesthetics reduce ______And are protective against_____
Myocardial O2 requirements,
| Reperfusion injury.
355
Risk for PERIOPERATIVE MI
```
Ischemic heart disease
CHF
CVA
High risk surgery
Preoperative insulin therapy
Preoperative creatinine > 2mg/dl
```
356
Perioperative MI can be caused by
Severe HTN or tachycardia
Hypotension, Anemia
Severe AS or AR
357
Sudden this can cause Perioperative myocardial ischemia
Sudden withdrawal of antiangianal medication preoperatively , such as Beta BLOCKERS, can lead to rebound HTN, tachycardia or both
358
Symptoms hx at risk for perioperative Myocardial ischemia
CP , dyspnea, poor exercise tolerance, syncope
359
Beta blockers should be started at least
1 week before surgery
360
If AF, TEE to rule out
Left atrial or left atrial appendage thrombuses
361
Thermodilution CO measurements are falsely elevated in a patients with
TR
362
Why is slow HR increase regurgitation?
Because of the associated disproportionate increase in diastolic time, but increases in diastolic arterial pressure favor regurgitant volume by increasing the pressure gradient for back flow
363
Phenylephrine and MR
Large amount of phenylephrine can increase SVR and worsen regurgitation
364
Critical aortic stenosis is _____Valve area and _______transvalvular gradients
0.5 to 0.7 cm2 ; 50 mmHg
365
AS wth AF
Immediate cardioversion
366
Aortic stenosis and CO
CO becomes rate dependent, and bradycardia is poortly tolerated
367
Contraindicated with AS
Spinal and epidural anesthesia
368
MVP murmur
Midsystolic click
369
Aortic surgeries done with CBP: ascending Aorta?
Ascending Aorta are done with CPB
370
Ascending aorta surgeries give 2 medications
Nicardipine , nitroprusside
371
Aortic dissection medication that should be used
B-Blockers
372
Patient having Ascending aorta surgeries where should the aline be placed and why?
For Ascending aorta surgeries, place A-line in Left radial artery because clamping of the innominate may be required.
373
Aortic arch surgeries, are done with
CPB and deep HYPOTHERMIC CIRCULATORY ARREST
374
Aortic surgeries that may be done without CPB
Descending Thoracic aorta surgeries, may be done through a left thoracotomy without CPB.
375
Where do you place the A-line for the Descending thoracic aorta surgeries
Right radial. because left subclavian may be clamped.
376
Aorta is cross-clamped where is HTN, and HoTN
HTN in aorta above clamp
| HoTN below the lesion (when not using shunt or bypass)
377
After release of aortic clamp you may get
Severe systemic hypotension
378
CPB limit times to less than
120 minutes
379
The aortic cross clamping required during CPB reduces CBF to
0
380
Target K+ , pH, glucose , hct
5.5; >7.20 ; >72; >22%
381
Target HR post bypass is
80 -100 may need pacing
382
When is HR adequate to wean from CPB
HR should start contracting in an empty state for 5-10 minutes before weaning CBP to ensure adequate cardiac rate and rhythm via ECG
383
Pt coming off CPB low SVR tx
Positive inotrope (epi, dopa, dobutamine) with milrinone can be started. With pump failure , CPB may be needed
384
During CPB keep blood flow rate at _____L/min or _____ml/kg/min and MAP
2 - 2.5 L/min
50-60 ml/kg/min
MAP between 50-80 mmHg
385
CPB glucose check
Hourly if DM
| once if none
386
CPB for on pump arterial cannulation is usualy in the
radial artery in non-dominant hand.
387
When is the ideal time to start beta blockers
1 week prior to ensure adequate B-Blockade and to help identify side effects such as HB.
388
For every _______C change in body temperature, Metabolic oxygen requirements decrease by
10C ; 50%
389
Side effects of hypothermia
Platelet dysfunction
Reversible coagulopathy
Depression of Myocardial contractility
390
Aortic regurgitation treamtne needed?
Diuretics and afterload reduction, particular with ACEIO
391
Post bypass you may need heparin reversal as well as
FFP and platelets
