AA APEX CARDIAC A&P CONT. Flashcards
1
Q
Chronotropy is
A
Heart rate
2
Q
Inotropy is
A
Strength of contraction (contractility)
3
Q
Lusitropy is
A
Rate of myocardial relaxation (during diastole)
4
Q
Dromotropy is
A
Conduction velocity (how fast the action potential travels per time)
5
Q
What is the function the Na/K ATPAse? .
A
The sodium-potassium pump maintains the cell’s resting potential. Said another way, it separates charge across the cell membrane keeping the inside of the cell relatively negative and the outside of the cell relatively positive
6
Q
How it works: Sodium Potassium ATPase
A
It removes the Na+ that enters the cell during depolarization.It returns K+ that has left the cell during repolarization.
7
Q
Na and K+ how many ions in and out
A
For every 3 Na+ ions it removes, it brings 2 K+ ions into the cell.
8
Q
List the phases 0 of the ventricular action potential, and describe the ionic movement during each phase.
A
Phase 0: Depolarization → Na+ influx
9
Q
Phase 1: ion movement
A
Initial repolarization → K+ efflux & Cl- influx
10
Q
Phase 2 ion movement
A
Plateau → Ca+2 influx
11
Q
Phase 3 ion movement
A
Repolarization → K+ efflux
12
Q
Phase 4: ion movement
A
Na+/K+ pump restores resting membrane potential
13
Q
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase.
Phase 4:
A
Spontaneous depolarization → Leaky to Na+ (Ca+2 influx occurs at the very end of phase 4)
14
Q
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase.
Phase 0:
A
Depolarization → Ca+2 influx
15
Q
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase. Phase 3:
A
Repolarization → K+ efflux
16
Q
List the 3 phases of the SA node action potential,
A
Phase 4
Phase 0
Phase 3
17
Q
What process determines the intrinsic heart rate, and what physiologic factors alter it?
A
Rate of spontaneous phase 4, TP and RMP
18
Q
Heart rate is determined by the
A
rate of spontaneous phase 4 depolarization in the SA node.
19
Q
We can increase HR by manipulating 3 variables:
TP N
RMPN
A
- The rate of spontaneous phase 4 depolarization increases (reaches TP faster).
- TP becomes more negative (shorter distance between RMP and TP).
- RMP becomes less negative (shorter distance between RMP and TP).
20
Q
When RMP becomes less negative what happens?
A
(shorter distance between RMP and TP).
21
Q
When TP become more negative
A
(shorter distance between RMP and TP).
22
Q
2 ways to make distance between RMP and TP short?
A
RMP less negative
TP becomes more negative
23
Q
What is the calculation for mean arterial blood pressure? If given DBP and SBP
A
MAP = (1/3 x SBP) + (2/3 x DBP)
24
Q
MAP if CO is given formula
A
MAP = [(CO x SVR) / 80] + CVP
25
Normal MAP is
Normal = 70 - 105 mmHg
26
What is the formula for systemic vascular resistance?
[(MAP - CVP) / CO] x 80
27
Normal SVR is
Normal = 800 - 1500 dynes/sec/cm^5
28
What is the formula for pulmonary vascular resistance?
[(MPAP - PAOP) / CO] x 80
29
Normal PVR
150 - 250 dynes/sec/cm^5
30
The Frank-Starling relationship describes the relationship between
ventricular volume (preload) and ventricular output (cardiac output):
31
↑ preload →
↑ myocyte stretch → ↑ ventricular output
32
↓ preload →
↓ myocyte stretch → ↓ ventricular output
33
Increasing preload increases To the right of the plateau
ventricular output, but only up to a point.
34
Increasing preload too much, additional volume does what? Leading to -______and _______PAOP
overstretches the ventricular sarcomeres, decreasing the number of cross bridges that can be formed and ultimately reducing cardiac output. This contributes to pulmonary congestion and increases PAOP.
35
Filling pressures ( other names for frank starling)
```
CVP
PAD
PAOP
LAP
LVEDP
```
36
EDV determinants 2
RVEDV
| LVEDV
37
Ventricular output 4 determinants
CO
SV
LVSW
RVSW
38
What factors affect myocardial contractility?
Contractility (inotropy) describes the contractile strength of the heart.
39
Just remember that Chemicals affect
Contractility - particularly Calcium
40
Contractility factors either
alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2.
41
5 things that increase contractility
```
SNS stimulation
Catecholamines
Calcium
Digitalis
PDE
```
42
Myocardial ischemia and contractility
Decreases
43
Hypoxia and contractility
Decreases
44
Acidosis and contractility
Decreases
45
Hypercapnia and contractility
Decreases
46
Propofol and contractility
Decreases
47
BB and CCBs on contractility
Decreases
48
HYPERkalemia and contractility
Decreases
49
Discuss excitation-contraction coupling in the cardiac myocyte.
a) The myocardial cell membrane depolarizes.
b)During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through L-type Ca+2 channels in the T-tubules.
c) Ca+2 influx turns on the ryanodine-2 receptor, which releases Ca+2 from the sarcoplasmic reticulum (this is called calcium-induced calcium-release).
d) Ca+2 binds to troponin C (myocardial contraction).
e)Ca+2 unbinds from troponin C (myocardial relaxation).
Most of the Ca+2 is returned to the sarcoplasmic reticulum via the SERCA2 pump.
f)Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called calsequestrin.
The next time the cardiac myocyte depolarizes, the whole process repeats.
50
Most of the Ca+2 is returned to the sarcoplasmic reticulum via the
SERCA2 pump.
51
Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called
calsequestrin.
52
During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through
L-type Ca+2 channels in the T-tubules.
53
Ca+2 binds to troponin
C (myocardial contraction).
54
What is afterload, and how do you measure it in the clinical setting?
Afterload is the force the ventricle must overcome to eject its stroke volume.
we use the systemic vascular resistance as a surrogate for LV afterload.
55
Normal SVR
800-1500 dynes/sec/cm-5
56
What law can be used to describe ventricular afterload?
We can apply the law of Laplace to better understand ventricular afterload.
57
Wall stress =
Intraventricular Pressure x Radius) / Ventricular Thickness
58
The force that pushes the heart apart
Intraventricular pressure is
59
The force that holds the heart together (it counterbalances intraventricular pressure)
Wall stress
60
Wall stress is reduced by:
Decreased intraventricular pressure
Decreased radius
Increased wall thickness
61
List 3 conditions that set afterload proximal to the systemic circulation. (AHC)
1. Aortic stenosis
2. Hypertrophic cardiomyopathy
3. Coarctation of the aorta
62
Diastole phases are (4)
Rapid filling
Reduced filling
Atrial kick
Isovolumetric relaxation
63
Systolic phases are (2)
Isovolumetric contraction
| Ejection
64
The ejection fraction is a. It is Said another way, the
measure of systolic function (contractility)
65
The percentage of blood that is ejected from the heart during systole.
EF
66
EF is the stroke volume relative to the
end-diastolic volume.
67
Normal EF =
60 - 70%
68
LV dysfunction is present when
EF < 40%
69
SV is calculated as:
EDV - ESV
70
Width of the loop
SV =
71
Right side of the loop at the x-axis
EDV =
72
What is the best TEE view for diagnosing myocardial ischemia?
Midpapillary muscle level in short axis
73
What is the equation for coronary perfusion pressure?
Coronary Perfusion Pressure = Aortic DBP - LVED
74
Aortic DBP is the
| LVEDP is the
pushing force
| resistance to the pushing force
75
Therefore, CPP can be improved by
increasing AoDBP or decreasing LVEDP (PAOP).
76
Which region of the heart is most susceptible to myocardial ischemia? Why?
The LV subendocardium is most susceptible to ischemia. . As aortic pressure increases, the LV tissue compresses its own blood supply and reduces blood flow. The high compressive pressure in the LV subendocardium coupled with a decreased coronary artery blood flow during systole increase coronary vascular resistance and predisposes this region to ischemia.
77
The LV subendocardium is best perfused during
diastole
78
Factors that increase oxygen demand
| HR, BP , stimulation, Wall tension, EDV, Afterload, contractility
```
Tachycardia
HTN
SNS stimulation
Increased Wall tension
Increased EDV
Increase afterload
Increased contractility
```
79
Decrease oxygen delivery are
Decrease coronary flow
Decrease CaO2
Decrease oxygen extraction
80
Factors leading to decreaed coronary flow?
Tachycardia
Decreased aortic pressure
Decreased vessel diameter
Increase EDP
81
Factors that lead to decrease CaO2
Hypoxemia
| Anemia
82
Factors leading to Decreased oxygen extraction
left shift dissociation curve
| Decreased capillary density
83
Discuss the nitric oxide pathway of vasodilation.
Nitric oxide is a smooth muscle relaxant that induces vasodilation.
84
teps in the nitric oxide cGMP pathway:
Nitric oxide synthase catalyzes the conversion of L-arginine to nitric oxide.
Nitric oxide diffuses from the endothelium to the smooth muscle.
Nitric oxide activates guanylate cyclase.
Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate.
Increased cGMP reduces intracellular calcium, leading to smooth muscle relaxation.
Phosphodiesterase deactivates cGMP to guanosine monophosphate (this step turns off the NO mechanism).
85
Nitric oxide activates
guanylate cyclase.
86
Catalyzes the conversion of L-arginine to nitric oxide.
Nitric oxide synthase
87
Increased cGMP and Calcium
reduces intracellular calcium, leading to smooth muscle relaxation
88
S1:
Closure of mitral and tricuspid valves
89
Marks onset of systole
S1
90
S2
Closure of aortic & pulmonic valves
91
Marks onset of diastole)
S2
92
May suggest systolic dysfunction (
S3
93
Normal in kids and athletes
S3
94
May suggest diastolic dysfunction
download
95
May suggest diastolic dysfunction
S4
96
MV opens and closes where on the loop
bottom of the loop,
97
AV opens and closes where on the loop
top of the loop.
98
What are the two primary ways a heart valve can fail?
Stenosis or regurgitation
99
In Stenosis:
There is a fixed obstruction to forward flow during chamber systole
100
The chamber must generate a higher than normal pressure to eject the blood in what kind of valve failure?
Stenosis
101
In Regurgitation:
The valve is incompetent (it's leaky).
102
Some blood flows forward and some blood flows backwards during chamber systole, in which type of valve failure.
Regurgitation
103
Regurgitation main issue
Increase volume
104
Stenosis main issue
increase pressure
105
How does the heart compensate for pressure overload?
PCP
Pressure Overloads
Concentric Hypertrophy
sarcomeres added in PARALLEL
106
How does the heart compensate for Volume overload?
VES
Volume Overload
Eccentric Hypertrophy
sarcomeres added in SERIES
107
List the hemodynamic goals for the 4 common valvular defects.
Aortic Stenosis - HR, preload, SVR, contract. PVR
HR - Slow normal
Preload increased
SVR 0 to elevated
contractility and PVR 0
108
List the hemodynamic goals for the 4 common valvular defects. Mitral Stenosis -- HR, preload, SVR, contract. PVR
HR - Slow normal
Preload, SVR, Contractility 0
PVR AVOID increased
109
Avoid SVR increase in 2 valvular defects
Mitral stenosis
| Mitral insufficiency or regurg.
110
List the hemodynamic goals for the 4 common valvular defects. Aortic Insufficiency -- HR, preload, SVR, contract. PVR
Heart rate increased
Preload normal or increased
SVR decreased
Contractility and PVR 0
111
Where do you want preload in aortic regurg?
normal or increased
112
Where do you want HR in aortic regurg?
INCREASED
113
You want SVR decreased in 2 valvular defects
Aortic insufficiency
| Mitral insufficiency
114
You want tachycardia in 2 valvular defects
Aortic insufficiency
| Mitral insufficiency
115
Where do you want preload in mitral regurg
0 to increased
116
Mitral issues you want to avoid
Increased in PVR
117
What is the most common dysrhythmia associated with mitral stenosis?
Atrial fibrillation
118
Atrial fibrillation is associated with
mitral stenosis
119
List 6 risk factors for perioperative cardiac morbidity and mortality for non-cardiac surgery.
```
High risk surgery
History of ischemic heart disease (unstable angina confers the greatest risk of perioperative MI)
History of CHF
History of cerebrovascular disease
Diabetes mellitus
Serum creatinine > 2 mg/dL
```
120
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
General population
0.3%
121
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
MI if > 6 months =
6%
122
What is the risk of perioperative myocardial infarction in the patient with a previous MI?MI if 3 - 6 months =
15%
123
What is the risk of perioperative myocardial infarction in the patient with a previous MI? MI < 3 months =
30%
124
The highest risk of reinfarction is greatest within
30 days of an acute MI.
125
High (Risk > ___%)
5%):
126
High (Risk > 5%): procedures
♥Emergency surgery (especially in the elderly)
♥Open aortic surgery
♥Peripheral vascular surgery
♥Long surgical procedures with significant volume shifts and/or blood loss
127
Intermediate risk procedures %
(Risk = 1-5%):
128
Intermediate procedures risks
```
Carotid endarterectomy
Head and neck surgery
Intrathoracic or intraperitoneal surgery
Orthopedic surgery
Prostate surgery
```
129
Low (Risk :
<1%)
130
Low (Risk :
<1%)
131
What is the Modified New York Association Functional Classification of Heart Failure?
Class I: Asymptomatic
Class II: Symptomatic with moderate activity
Class III: Symptomatic with mild activity
Class IV: Symptomatic at rest
132
Infarcted myocardium releases 3 key biomarkers:
creatine kinase-MB, troponin I, and troponin T.
133
Cardiac troponins vs CKMB
Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction.
134
Initial elevation of all Cardiac enzymes
3-12 hours
135
Peak elevation of CKMB
24h
136
Peak elevation of CK-MB
24h
137
Peak elevation of Troponin I
24h
138
Peak elevation of Troponin T
12-48 h
139
CK-MB return to baseline when
2-3 days
140
Troponin I return to baseline when
5-10 days
141
Troponin T return to baseline when
5-14 days
142
How do you treat intraoperative myocardial ischemia?
Treatment of myocardial ischemia should focus on interventions that make the heart slower, smaller, and better perfused.
143
Increase O2 demand cause by
Treatment
Increase BP
increase HR
Increase PAOP
Beta blocker to a HR < 80bpm
Increased depth of anesthesia, vasodilator
Nitroglycerin
144
Decrease O2 supply causes and Treatment.
decrease HR, BP
Increase PAOP
Treatment
Anticholinergic, pacing
Vasoconstrictor, reduce depth of anesthesia
NTG, inotrope
145
The diastolic pressure-volume relationship is affected by:
Age > 60 years
Ischemia
Pressure overload hypertrophy (aortic stenosis or HTN)
Hypertrophic obstructive cardiomyopathy
Pericardial pressure (increased external pressure)
146
What is the difference between systolic and diastolic heart failure?
Systolic Heart Failure – The Ventricle Doesn't Empty Well
| Diastolic Heart Failure – The Ventricle Doesn't Fill Properly
147
The hallmark of systolic heart failure is a
decreased ejection fraction with an increased end-diastolic volume.
148
Volume overload commonly causes what kind of dysfunction?
systolic dysfunction.
149
Diastolic failure occurs when the heart is .
unable to relax and accept the incoming volume, because ventricular compliance is reduced
150
The defining characteristic of diastolic dysfunction is
symptomatic heart failure with a normal ejection fraction
151
Systolic HF preload is
HIGH
152
Diastolic HF volume required to stretch noncompliant ventricle LVEDP does not correlate with
LVEDV (TEE is best)
153
Why is a left ventricular vent used during CABG surgery?
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt).
154
Solubility of a gas is a function of y extension, this affects the pH.
temperature,
155
As temp decreases, more
CO2 is able to dissolve in the blood.
156
Alpha-stat
does not correct for the patient's temperature. This technique aims to keep intracellular charge neutrality across all temperatures. It is associated with better outcomes in adults
157
pH-stat
corrects for the patient's temperature. This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in peds.
158
This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in
ph -Stat ; peds.
159
An aortic cross clamp placed above the artery of Adamkiewicz may cause.
ischemia to the lower portion of the anterior spinal cord. This can result in anterior spinal artery syndrome – otherwise known as Beck’s syndrome (different from Beck's triad)
160
Beck's triad occurs in the patient with
acute cardiac tamponade.
161
Signs of Beck's triad include:
Hypotension (decreased stroke volume)
Jugular venous distension (impaired venous return to right heart)
Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
