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SEE/BOARD STUDY > AA APEX CARDIAC A&P CONT. > Flashcards

AA APEX CARDIAC A&P CONT. Flashcards

1
Q

Chronotropy is

A

Heart rate

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2
Q

Inotropy is

A

Strength of contraction (contractility)

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3
Q

Lusitropy is

A

Rate of myocardial relaxation (during diastole)

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4
Q

Dromotropy is

A

Conduction velocity (how fast the action potential travels per time)

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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

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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.

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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.

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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

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9
Q

Phase 1: ion movement

A

Initial repolarization → K+ efflux & Cl- influx

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10
Q

Phase 2 ion movement

A

Plateau → Ca+2 influx

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11
Q

Phase 3 ion movement

A

Repolarization → K+ efflux

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12
Q

Phase 4: ion movement

A

Na+/K+ pump restores resting membrane potential

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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)

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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

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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

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16
Q

List the 3 phases of the SA node action potential,

A

Phase 4
Phase 0
Phase 3

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17
Q

What process determines the intrinsic heart rate, and what physiologic factors alter it?

A

Rate of spontaneous phase 4, TP and RMP

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18
Q

Heart rate is determined by the

A

rate of spontaneous phase 4 depolarization in the SA node.

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19
Q

We can increase HR by manipulating 3 variables:
TP N
RMPN

A
  1. The rate of spontaneous phase 4 depolarization increases (reaches TP faster).
  2. TP becomes more negative (shorter distance between RMP and TP).
  3. RMP becomes less negative (shorter distance between RMP and TP).
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20
Q

When RMP becomes less negative what happens?

A

(shorter distance between RMP and TP).

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21
Q

When TP become more negative

A

(shorter distance between RMP and TP).

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22
Q

2 ways to make distance between RMP and TP short?

A

RMP less negative

TP becomes more negative

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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)

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24
Q

MAP if CO is given formula

A

MAP = [(CO x SVR) / 80] + CVP

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25
Q

Normal MAP is

A

Normal = 70 - 105 mmHg

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26
Q

What is the formula for systemic vascular resistance?

A

[(MAP - CVP) / CO] x 80

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27
Q

Normal SVR is

A

Normal = 800 - 1500 dynes/sec/cm^5

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28
Q

What is the formula for pulmonary vascular resistance?

A

[(MPAP - PAOP) / CO] x 80

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29
Q

Normal PVR

A

150 - 250 dynes/sec/cm^5

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30
Q

The Frank-Starling relationship describes the relationship between

A

ventricular volume (preload) and ventricular output (cardiac output):

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31
Q

↑ preload →

A

↑ myocyte stretch → ↑ ventricular output

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32
Q

↓ preload →

A

↓ myocyte stretch → ↓ ventricular output

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33
Q

Increasing preload increases To the right of the plateau

A

ventricular output, but only up to a point.

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34
Q

Increasing preload too much, additional volume does what? Leading to -______and _______PAOP

A

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.

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35
Q

Filling pressures ( other names for frank starling)

A 
CVP
PAD
PAOP
LAP
LVEDP
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36
Q

EDV determinants 2

A

RVEDV

LVEDV

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37
Q

Ventricular output 4 determinants

A

CO
SV
LVSW
RVSW

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38
Q

What factors affect myocardial contractility?

A

Contractility (inotropy) describes the contractile strength of the heart.

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39
Q

Just remember that Chemicals affect

A

Contractility - particularly Calcium

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40
Q

Contractility factors either

A

alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2.

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41
Q

5 things that increase contractility

A 
SNS stimulation
Catecholamines
Calcium
Digitalis
PDE
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42
Q

Myocardial ischemia and contractility

A

Decreases

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43
Q

Hypoxia and contractility

A

Decreases

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44
Q

Acidosis and contractility

A

Decreases

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45
Q

Hypercapnia and contractility

A

Decreases

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46
Q

Propofol and contractility

A

Decreases

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47
Q

BB and CCBs on contractility

A

Decreases

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48
Q

HYPERkalemia and contractility

A

Decreases

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49
Q

Discuss excitation-contraction coupling in the cardiac myocyte.

A

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.

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50
Q

Most of the Ca+2 is returned to the sarcoplasmic reticulum via the

A

SERCA2 pump.

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51
Q

Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called

A

calsequestrin.

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52
Q

During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through

A

L-type Ca+2 channels in the T-tubules.

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53
Q

Ca+2 binds to troponin

A

C (myocardial contraction).

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54
Q

What is afterload, and how do you measure it in the clinical setting?

A

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.

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55
Q

Normal SVR

A

800-1500 dynes/sec/cm-5

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56
Q

What law can be used to describe ventricular afterload?

A

We can apply the law of Laplace to better understand ventricular afterload.

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57
Q

Wall stress =

A

Intraventricular Pressure x Radius) / Ventricular Thickness

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58
Q

The force that pushes the heart apart

A

Intraventricular pressure is

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59
Q

The force that holds the heart together (it counterbalances intraventricular pressure)

A

Wall stress

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60
Q

Wall stress is reduced by:

A

Decreased intraventricular pressure
Decreased radius
Increased wall thickness

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61
Q

List 3 conditions that set afterload proximal to the systemic circulation. (AHC)

A
  1. Aortic stenosis
  2. Hypertrophic cardiomyopathy
  3. Coarctation of the aorta
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62
Q

Diastole phases are (4)

A

Rapid filling
Reduced filling
Atrial kick
Isovolumetric relaxation

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63
Q

Systolic phases are (2)

A

Isovolumetric contraction

Ejection

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64
Q

The ejection fraction is a. It is Said another way, the

A

measure of systolic function (contractility)

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65
Q

The percentage of blood that is ejected from the heart during systole.

A

EF

66
Q

EF is the stroke volume relative to the

A

end-diastolic volume.

67
Q

Normal EF =

A

60 - 70%

68
Q

LV dysfunction is present when

A

EF < 40%

69
Q

SV is calculated as:

A

EDV - ESV

70
Q

Width of the loop

A

SV =

71
Q

Right side of the loop at the x-axis

A

EDV =

72
Q

What is the best TEE view for diagnosing myocardial ischemia?

A

Midpapillary muscle level in short axis

73
Q

What is the equation for coronary perfusion pressure?

A

Coronary Perfusion Pressure = Aortic DBP - LVED

74
Q

Aortic DBP is the

LVEDP is the

A

pushing force

resistance to the pushing force

75
Q

Therefore, CPP can be improved by

A

increasing AoDBP or decreasing LVEDP (PAOP).

76
Q

Which region of the heart is most susceptible to myocardial ischemia? Why?

A

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
Q

The LV subendocardium is best perfused during

A

diastole

78
Q

Factors that increase oxygen demand

HR, BP , stimulation, Wall tension, EDV, Afterload, contractility

A 
Tachycardia
HTN
SNS stimulation
Increased Wall tension
Increased EDV
Increase afterload
Increased contractility
79
Q

Decrease oxygen delivery are

A

Decrease coronary flow
Decrease CaO2
Decrease oxygen extraction

80
Q

Factors leading to decreaed coronary flow?

A

Tachycardia
Decreased aortic pressure
Decreased vessel diameter
Increase EDP

81
Q

Factors that lead to decrease CaO2

A

Hypoxemia

Anemia

82
Q

Factors leading to Decreased oxygen extraction

A

left shift dissociation curve

Decreased capillary density

83
Q

Discuss the nitric oxide pathway of vasodilation.

A

Nitric oxide is a smooth muscle relaxant that induces vasodilation.

84
Q

teps in the nitric oxide cGMP pathway:

A

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
Q

Nitric oxide activates

A

guanylate cyclase.

86
Q

Catalyzes the conversion of L-arginine to nitric oxide.

A

Nitric oxide synthase

87
Q

Increased cGMP and Calcium

A

reduces intracellular calcium, leading to smooth muscle relaxation

88
Q

S1:

A

Closure of mitral and tricuspid valves

89
Q

Marks onset of systole

A

S1

90
Q

S2

A

Closure of aortic & pulmonic valves

91
Q

Marks onset of diastole)

A

S2

92
Q

May suggest systolic dysfunction (

A

S3

93
Q

Normal in kids and athletes

A

S3

94
Q

May suggest diastolic dysfunction

A

download

95
Q

May suggest diastolic dysfunction

A

S4

96
Q

MV opens and closes where on the loop

A

bottom of the loop,

97
Q

AV opens and closes where on the loop

A

top of the loop.

98
Q

What are the two primary ways a heart valve can fail?

A

Stenosis or regurgitation

99
Q

In Stenosis:

A

There is a fixed obstruction to forward flow during chamber systole

100
Q

The chamber must generate a higher than normal pressure to eject the blood in what kind of valve failure?

A

Stenosis

101
Q

In Regurgitation:

A

The valve is incompetent (it’s leaky).

102
Q

Some blood flows forward and some blood flows backwards during chamber systole, in which type of valve failure.

A

Regurgitation

103
Q

Regurgitation main issue

A

Increase volume

104
Q

Stenosis main issue

A

increase pressure

105
Q

How does the heart compensate for pressure overload?

A

PCP
Pressure Overloads
Concentric Hypertrophy
sarcomeres added in PARALLEL

106
Q

How does the heart compensate for Volume overload?

A

VES
Volume Overload
Eccentric Hypertrophy
sarcomeres added in SERIES

107
Q

List the hemodynamic goals for the 4 common valvular defects.
Aortic Stenosis - HR, preload, SVR, contract. PVR

A

HR - Slow normal
Preload increased
SVR 0 to elevated
contractility and PVR 0

108
Q

List the hemodynamic goals for the 4 common valvular defects. Mitral Stenosis – HR, preload, SVR, contract. PVR

A

HR - Slow normal
Preload, SVR, Contractility 0
PVR AVOID increased

109
Q

Avoid SVR increase in 2 valvular defects

A

Mitral stenosis

Mitral insufficiency or regurg.

110
Q

List the hemodynamic goals for the 4 common valvular defects. Aortic Insufficiency – HR, preload, SVR, contract. PVR

A

Heart rate increased
Preload normal or increased
SVR decreased
Contractility and PVR 0

111
Q

Where do you want preload in aortic regurg?

A

normal or increased

112
Q

Where do you want HR in aortic regurg?

A

INCREASED

113
Q

You want SVR decreased in 2 valvular defects

A

Aortic insufficiency

Mitral insufficiency

114
Q

You want tachycardia in 2 valvular defects

A

Aortic insufficiency

Mitral insufficiency

115
Q

Where do you want preload in mitral regurg

A

0 to increased

116
Q

Mitral issues you want to avoid

A

Increased in PVR

117
Q

What is the most common dysrhythmia associated with mitral stenosis?

A

Atrial fibrillation

118
Q

Atrial fibrillation is associated with

A

mitral stenosis

119
Q

List 6 risk factors for perioperative cardiac morbidity and mortality for non-cardiac surgery.

A 
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
Q

What is the risk of perioperative myocardial infarction in the patient with a previous MI?
General population

A

0.3%

121
Q

What is the risk of perioperative myocardial infarction in the patient with a previous MI?
MI if > 6 months =

A

6%

122
Q

What is the risk of perioperative myocardial infarction in the patient with a previous MI?MI if 3 - 6 months =

A

15%

123
Q

What is the risk of perioperative myocardial infarction in the patient with a previous MI? MI < 3 months =

A

30%

124
Q

The highest risk of reinfarction is greatest within

A

30 days of an acute MI.

125
Q

High (Risk > ___%)

A

5%):

126
Q

High (Risk > 5%): procedures

A

♥Emergency surgery (especially in the elderly)
♥Open aortic surgery
♥Peripheral vascular surgery
♥Long surgical procedures with significant volume shifts and/or blood loss

127
Q

Intermediate risk procedures %

A

(Risk = 1-5%):

128
Q

Intermediate procedures risks

A 
Carotid endarterectomy
Head and neck surgery
Intrathoracic or intraperitoneal surgery
Orthopedic surgery
Prostate surgery
129
Q

Low (Risk :

A

<1%)

130
Q

Low (Risk :

A

<1%)

131
Q

What is the Modified New York Association Functional Classification of Heart Failure?

A

Class I: Asymptomatic
Class II: Symptomatic with moderate activity
Class III: Symptomatic with mild activity
Class IV: Symptomatic at rest

132
Q

Infarcted myocardium releases 3 key biomarkers:

A

creatine kinase-MB, troponin I, and troponin T.

133
Q

Cardiac troponins vs CKMB

A

Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction.

134
Q

Initial elevation of all Cardiac enzymes

A

3-12 hours

135
Q

Peak elevation of CKMB

A

24h

136
Q

Peak elevation of CK-MB

A

24h

137
Q

Peak elevation of Troponin I

A

24h

138
Q

Peak elevation of Troponin T

A

12-48 h

139
Q

CK-MB return to baseline when

A

2-3 days

140
Q

Troponin I return to baseline when

A

5-10 days

141
Q

Troponin T return to baseline when

A

5-14 days

142
Q

How do you treat intraoperative myocardial ischemia?

A

Treatment of myocardial ischemia should focus on interventions that make the heart slower, smaller, and better perfused.

143
Q

Increase O2 demand cause by

Treatment

A

Increase BP
increase HR
Increase PAOP

Beta blocker to a HR < 80bpm
Increased depth of anesthesia, vasodilator
Nitroglycerin

144
Q

Decrease O2 supply causes and Treatment.

A

decrease HR, BP
Increase PAOP

Treatment
Anticholinergic, pacing
Vasoconstrictor, reduce depth of anesthesia
NTG, inotrope

145
Q

The diastolic pressure-volume relationship is affected by:

A

Age > 60 years
Ischemia
Pressure overload hypertrophy (aortic stenosis or HTN)
Hypertrophic obstructive cardiomyopathy
Pericardial pressure (increased external pressure)

146
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic Heart Failure – The Ventricle Doesn’t Empty Well

Diastolic Heart Failure – The Ventricle Doesn’t Fill Properly

147
Q

The hallmark of systolic heart failure is a

A

decreased ejection fraction with an increased end-diastolic volume.

148
Q

Volume overload commonly causes what kind of dysfunction?

A

systolic dysfunction.

149
Q

Diastolic failure occurs when the heart is .

A

unable to relax and accept the incoming volume, because ventricular compliance is reduced

150
Q

The defining characteristic of diastolic dysfunction is

A

symptomatic heart failure with a normal ejection fraction

151
Q

Systolic HF preload is

A

HIGH

152
Q

Diastolic HF volume required to stretch noncompliant ventricle LVEDP does not correlate with

A

LVEDV (TEE is best)

153
Q

Why is a left ventricular vent used during CABG surgery?

A

A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt).

154
Q

Solubility of a gas is a function of y extension, this affects the pH.

A

temperature,

155
Q

As temp decreases, more

A

CO2 is able to dissolve in the blood.

156
Q

Alpha-stat

A

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
Q

pH-stat

A

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
Q

This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in

A

ph -Stat ; peds.

159
Q

An aortic cross clamp placed above the artery of Adamkiewicz may cause.

A

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
Q

Beck’s triad occurs in the patient with

A

acute cardiac tamponade.

161
Q

Signs of Beck’s triad include:

A

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)

SEE/BOARD STUDY (20 decks)

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