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First Aid > Cardiovascular - Physiology > Flashcards

Cardiovascular - Physiology Flashcards

1
Q

What is the equation for cardiac output?

A

Stroke Volume(SV) * Heart Rate(HR)

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2
Q

What is Fick’s Law(Equation)

A

CO = rate of O2 consumption/(arterial O2 content - venous O2 content)

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3
Q

What is the equation for mean arterial pressure?

A

MAP = 2/3rd diastolic pressure + 1/3rd systolic pressure

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4
Q

What is the equation for pulse pressure?

A

systolic pressure - diastolic pressure

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5
Q

What is the relationship between pulse pressure and stroke volume?

A

directly proportional

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6
Q

What is the relationship between pulse pressure and arterial compliance?

A

inversely proportional

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7
Q

What is the equation for stroke volume (SV)?

A

EDV - ESV

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8
Q

During the early stages of exercise, CO is maintained by what physiological factors?(2 points)

A

stroke volume and heart rate

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9
Q

During the late stages of exercise, CO is maintained by what physiological factors?(2 points)

A

Increased HR

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10
Q

Why doesn’t stroke volume maintain the CO during late stage of exercise?

A

The SV plateaus

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11
Q

How is the time for diastole affected with increased heart rate?

A

diastole is shortened

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12
Q

How does increased heart rate affect the filling time during diastole?

A

It decreases the filling time

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13
Q

Diastole is preferentially shortened with increase HR; which leads to less filling time. How does this affect CO? What type of phenomena could cause this?

A

There is a decrease in Cardiac Output. Ventricular tachycardia

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14
Q

How is pulse pressure affected in hyperthyroidism?

A

increased pulse pressure

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15
Q

How is pulse pressure affected with aortic regurgitation?

A

increased pulse pressure

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16
Q

How does arteriosclerosis affect pulse pressure?

A

it increases

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17
Q

How does obstructive sleep apnea affect pulse pressure?

A

increase pulse pressure

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18
Q

How does exercise affect pulse pressure?

A

increase pulse pressure but transiently

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19
Q

How does aortic stenosis affect pulse pressure?

A

decreases pulse pressure

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20
Q

How does cardiogenic shock affect pulse pressure?

A

decreases pulse pressure

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21
Q

How does cardiac tamponade affect pulse pressure?

A

decreases pulse pressure

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22
Q

How dose advanced heart failure affect pulse pressure?

A

decreases pulse pressure

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23
Q

What does the nemonic SV CAP tell you?

A

There is increased stroke volume with increase contracility, decreased afterload and increased preload

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24
Q

How do catecholamines affect contractility?

A

Catecholamines increase contractility and stroke volume

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25
Q

How do catecholamines increse stroke volume and contractility?(general mechanism)

A

increased activty of Ca2+ pump in sacroplasmic reticulum)

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26
Q

How does an increase in intracellular Ca2+ affect contractility?

A

it increases contractility

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27
Q

How does increased activity of the Na+/Ca2+ affected contractility?

A

The sodium calcium antiport removes calcium from the cell, therefore, decreasesing contractility. Decrease activty of this antiport is going to increase the intracellular calcium levels promoting more calcium and troponin interactions leading to increase contractility

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28
Q

Why does decreased extracellular sodium increase contractility?

A

It decreases the activy of the sodium/calcium exchange. which results in an increase of intracellular calcium

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29
Q

What is the main mechanism of action of digitalis?(4 points)

A

it blocks the sodium potassium pump leading to an increase in intracellular sodium leading to a decrease in the sodium/calclium exchange leading to a intrease in the intracellular calcium leading to an increase in contractility and SV

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30
Q

How does digitalis affect contractility?

A

it increases contractility

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31
Q

How is contratility affected with β-blockers?

A

decreased

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32
Q

Why do β-blockers result in a decrease in contractility and stroke volume?

A

β-adrenergic receptors are coupled to Gs proteins which activate adenylate cycle to form cAMP from ATP. Increase in cAMP activates PKA that phosphorylates L-type calcium channels, which causes incrase calcium enry into the cell. Therefore increase contractility. Inhibiting this process is going to decease contractility.

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33
Q

How do catecholamines affect stoke volume

A

increase

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34
Q

How does an increase in intracellular Ca2+ affect stoke volume?

A

increase

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35
Q

How does increased activity of the Na+/Ca2+ affected contractility?

A

It’s going to decrase contractility. The sodium calcium antiport removes calcium from the cell, therefore, decreasesing contractility. Decrease activty of this antiport is going to increase the intracellular calcium levels promoting more calcium and troponin interactions leading to increase SV

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36
Q

How does decrease extracellular sodium affect SV?

A

increases stroke volume

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37
Q

Why does increase intracellular sodium increase contractility and SV?

A

it decreases the activity of the sodium/calcium exchange which increases the intracellular calcium

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38
Q

Why does decrease extracellular sodium increase contractility?

A

Decrease extracellular sodium decreases the activity of the sodium calcium exchange which increases the activity of the intracelular calcium ion which induces calcium induced calmodulin release which increases muscle contractility

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39
Q

How does decreased extracellular sodium affect contractility?

A

increases contractility

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40
Q

How does digitalis affect SV?

A

increases it

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41
Q

How is stroke volume affected with β-blockers?

A

It decreases stroke volume

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42
Q

How do β-blockers affect contractility?

A

decreases it

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43
Q

Why do β-blockers decrease contractility?

A

The βlockers decrease the synthesis of cAMP. cAMP activate protein kinase A. PKA phospharlyates the L-type cacium channels, which casues increase calcium entry into the cell.

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44
Q

Why do β-blockers decrease contractility?

A

The βlockers decrease the synthesis of cAMP. cAMP activate protein kinase A. PKA phospharlyates the L-type cacium channels, which casues increase calcium entry into the cell.

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45
Q

How does heart failure with systolic dysfunction affect contractility?

A

decreases it

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46
Q

How does heart failure with systolic dysfunction affect SV?

A

decrease

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47
Q

How does acidosis affect SV?

A

decrease

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48
Q

How does acidosis affect contractility?

A

decrease

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49
Q

How does hypoxia/hypercapnea affect contractility?

A

decrease

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50
Q

How does hypoxia/hypercapnea affect SV?

A

decrease

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51
Q

How does nonhydropyridine calcium channel blockers affect contractility?

A

decrease

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52
Q

How does nonhydropyridine calcium channel blockers affect SV?

A

decrease

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53
Q

Preload is approximated by what type of volume?

A

EDV

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54
Q

Preload depends on what?(2 points)

A

Preload depends on venous tone and circuating blood volume

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55
Q

How do VEnodilators affect preload?

A

they decraese preload

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56
Q

What is an example of a venodilator?

A

nitroglycerin

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57
Q

The afterload is approximated by what?

A

MAP

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58
Q

What does Laplace’s law relate?( 2 points)

A

Left Ventricular Size and afterload

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59
Q

What is Laplace’s Law?

A

Pressure * Radius/(2* Wall Thickness)

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60
Q

How does the left ventricular wall compensate for increase afterload?(2 points)

A

increased thickening of the left ventricular wall in an effort to decrease the wall tension

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61
Q

What type of drug is hydralazine?

A

vasodilator

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62
Q

How does ACE inhibitos and ARBS affect preload and afterload?

A

They decrease preload and afterload

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63
Q

How does chronic hypertension lead to increase Left Ventricular hypertrophy?

A

it increases MAP

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64
Q

How does chronic hypertension affect MAP?

A

It increases it

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65
Q

What is the equation(s) for Ejection Fraction?(2 points)

A

SV/EDV = (EDV - ESV)/EDV

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66
Q

Left ventricular EF is an index of what?

A

ventricular contractility

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67
Q

What is the normal value for the EF?

A

It is much greater than 55%

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68
Q

How is the ejection fraction affected in systolic heart failure?

A

there is a decrease in the ejection fraction

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69
Q

Is the EF normal or abnormla in systolic heart failure?

A

abnormal

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70
Q

Is the EF normal or abnormal in diastolic heart failure?

A

normal

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71
Q

How is SV affected during anxiety?

A

It is increasd during anxiety

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72
Q

How is SV affected during exercise?

A

increased

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73
Q

How is SV affected during pregnancy?

A

increased

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74
Q

A failing heart has what affect on SV?

A

decrease

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75
Q

What type of dysfucntion of the heart do you see in heat faiulre?

A

systolic and diastolic dysfunction

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76
Q

The myocardal O2 demands is increased with what?(4 points)

A

increased afterload, increased heart rate, increase contractility, increae in ventricular diamter(increase in wall tension)

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77
Q

How does an increase in the afterload affect the myocardial oxygen demand?

A

increase

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78
Q

How does an increase in the ventricular wall diameter affect the myocardial oxygen demand?

A

increase

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79
Q

How does an increase in contactility affect the myocardial oxygen demand?

A

increase

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80
Q

What is the relationship between force of contraction and end diastolic length of cardiac muscle fiber?

A

proportional

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81
Q

How does digoxin affect contractility?

A

it increases contarctility

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82
Q

A loss of myocardium affect contractility in what manner? What is an example of a phenomena that causes this?

A

decreases contractility. An example is a myocardial infarction

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83
Q

What is Ohm’s Law?

A

ΔV = IR

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84
Q

What is Ohm’s law in the cardiovascular system?

A

ΔP = Q*R

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85
Q

What is the equation for Resistance in the cardiovascular system?

A

(ΔP)/Q = 8ηL/πr4

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86
Q

What is the total resistance of vessels in series?

A

TR = R1 + R2 + R3+…

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87
Q

What is the total resistance of vessesls in parallel?

A

1/TR = 1/R1 + 1/R2 + 1/R3…

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88
Q

The viscosity of blood mainly depends on what?

A

the hematocrit

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89
Q

How does blood viscosity change with polycythemia?

A

increases

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90
Q

How does blood viscosity change with hyperproteinemic states? What is an example of a disease state that is hyperproteinemic?

A

The blood viscoity incresaes. Multiple Myeloma is one example

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91
Q

How does aHereditary spherocytosis affect blood viscosity?

A

It increases blood viscosity

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92
Q

How does anemia affect blood viscosity?

A

It decreses blood viscosity

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93
Q
A
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94
Q
A
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95
Q

An increase in RA pressure has what affect on CO?

A

increase

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96
Q

What is the relationship between RA pressure and preload?

A

they’re synonomous

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97
Q

An increase in EDV has what affect on venous return?

A

It decreases venous return

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98
Q

What is a example of something that cause negative inotropy?(2 points)

A

drug overdose or uncompensated heart failure

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99
Q

When consider the venous function curve, the mean systemic pressure is what value on the cruve?

A

x-intercept

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100
Q

When considering the venous function curve, the mean systemic pressure changes with what?

A

it changes with the circulating volume/venous tone

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101
Q

What are examples of things that can cause an increase in venous tone or circulating volume?(2 points)

A

fluid infusion or sympathetic activity

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102
Q

What are examples of things that can cause a decrease in circulating volume/venous tone?(2 points)

A

Acute hemorrhage or spinal anesthesia

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103
Q

How does a change in the total peripheral resistance affect the mean systemic pressure?

A

no change

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104
Q

How does a change in the inotropy affect the venous function curve?

A

no change

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105
Q

What are vasopressors?

A

they’re anti-hypotensive agents that act to raise reduced blood pressure

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106
Q

What is an example of something that could increase the total peripheral resistance?(drug group)

A

vasopressors

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107
Q

What can cause a decrease in the total peripheral resistance?

A

exercise or an AV shunt

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108
Q

During exercise, how does inotropy and TPR change to maximize CO?

A

There is an increase in inotropy and a decrease in TPR

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109
Q

During compensatory heart failure, what does the body genreally due when considering the vasculature and circulating blood volume?(2 points)

A

there is an increase in preload and an increae in fluid rention to retain the CO

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110
Q
A

1: isovolumetric contraction; 2: systolic ejection; 3: isovolumetric relaxation; 4: rapid filling; 5: reduced filling

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111
Q

period between aortic valve opening and closing

A

systolic ejection

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112
Q

period just before mitral valve close

A

reduced filling

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113
Q

period between mitral valve closing and aortic valve opening; period of highest O2 consumption

A

isovolumetric contraction

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114
Q

period between aortic valve clsoing and mitral valve opening

A

isovolumetetric relaxation

115
Q

period just before mitral valve opening

A

rapid filling

116
Q
A
117
Q

How does an increase in contractility affect the SV, EF and ESV?

A

SV increases, increase in EF, decrease in ESV

118
Q

How does an increase in afterload affect the aortic pressure, SV and ESV?

A

increase in aortic pressure, decrease in SV, increase in ESV

119
Q

How does increase preload affect SV?

A

increase SV

120
Q

What type of sound is the S1 and where is the sound the loudest?

A

mitral valve/tricuspid valve closure. loudest at mitral area

121
Q

What is the S2 heart sound and where is it the loudest?

A

S2 heart sound is the closure of the aortic/pulmonic valve and it is the loudest in the left sternal border

122
Q

When do you hear S3?(2 points)

A

early diastole during rapid ventricular phase

123
Q

S3 is normal in what groups?(2 points)

A

pregnant women and children

124
Q

S3 is associated with what?

A

increased filling pressure

125
Q

S3 is more common in what heart condition?

A

dilated ventricles

126
Q

When does S4 occur?

A

late diastole

127
Q

S4 is associated with what heart condition?

A

left ventricular hypertrophy

128
Q

What is the reason for the S4 sound?

A

The atrium must push against a stiff LV wall

129
Q

What event takes place during the dicrotic notch?

A

the aortic valve closes

130
Q
A
131
Q

JVP: atrial contraction

A

a wave

132
Q

JVP: blood flow from RA to RV

A

y descent

133
Q

JVP: increase right atrial pressure due to filling against closed tricuspid valve

A

v-wave

134
Q

JVP: RV contraction, closed tricuspid valve bulging into atrium

A
135
Q

x descent is absent in what type of murmur?

A

tricuspid regurgitation

136
Q

When does the Q wave appear in relations to the heart sounds?

A

before the S1 sound

137
Q

JVP: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

A

x-descent

138
Q

Seen in conditions that delay RV emptying (e.g., pulmonic stenosis, right bundle branch block). Delay in RV emptying causes delayed pulmonic sound (regardless of breath). An exaggeration of normal splitting.

A

Wide Splitting

139
Q

Seen in ASD. ASD

A

fixed splitting

140
Q

Inspiration

A

physiological splitting or normal splitting

141
Q

Seen in conditions that delay aortic valve closure (e.g., aortic stenosis, left bundle branch block). Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split.

A

pardoxical splitting

142
Q

What type of splitting is seen in conditions with delay RV emptying?

A

wide splitting

143
Q

Right Bundle branch blocks causes what type of spltting?

A

wide splitting

144
Q

What type of splitting is seen in conditions with delay aortic valve closure?

A

pardoxical splitting

145
Q

What type of splitting is associated with ASD?

A

fixed splitting

146
Q

What are the ausculation areas for the heart?(5 points)

A

aortic area, pulmonic area, tricuspid area, left sternal border and mitral area

147
Q

What type of sounds do you hear at the aortic area(physiologic and pathologic)(4 points)

A

aortic sclerosis, aortic stenosis and flow murmur

148
Q

What pathologic/physiologic murmurs can you auscultate at the left sternal border?(6 points)

A

The systolic murmurs at that region are going to be hypertrophic cardiomyopathy and the diastolic murmurs are going to be aortic regurgitation and pulmonic regurgitation

149
Q

What physiologic/pathologic mururs can you auscultate at the pulmonic area?(3 points)

A

systolic ejection murmurs like pulmonic stenosis and flow murmurs

150
Q

What murmurs can you auscultate in the tricuspid area(6 points)

A

pansystolic murmmurs like ventricular septal defect and tricuspid regurgitation and diastolic murmurs like tricuspid stenosis and atrial septal defect

151
Q

What is a pansystolic murmur?

A

a murmur that is heard thorughout the entire systolic interval, from the first heart sound to the second heart sound

152
Q

What type of physiologic/pathologic murmurs can you auscultate at the mitral area?(4 points)

A

the systolic murmur is a mitral regurgitation and a diastolic murmur is mitral stenosis

153
Q

The atrial septal defect commonly presents with what type of mumrurs**(2 points). **Please take not of the areas where you can auscultate.

A

a diastolic rumble(at the tricuspid area during diastole ofcourse) and a pulmonary flow murmur(a systolic ejection murmur in the pulmonic area)

154
Q

The systolic ejection murmur you auscultate in the pulmonary, specifically referred to a pulmoary flow murmur, that you can auscultate with a patient who has an atrial septal defect is due to what pathologic condition?

A

an increase in flow thorugh the pulmonary valve

155
Q

The diastolic murmur, specifically referred to as a diastolic rumble, that you can auscultate in the tricuspid area with a patient who has an atrieal septal defect is due to what pathologic condition?

A

there is an increase in blood flow through the tricuspid valve

156
Q

Later, the murmur from the atrial septal defect progreses into what? Where can you ausculatate this murmur? What is the pathologic condition?

A

The murmur progresses into a louder diastolic murmur, specfically referred to a pulmonic regurgitation, that you can auscultate at the left sternal border during diastole. This is due to dilitation of the pulmonic artery.

157
Q

A bedside maneuver that instructs the patient to inspire will have effect of the intensity of the right heart sound?

A

increase intensity

158
Q

A bedside maneuver which instructs the patient to perform the valsalva maneuver while they were standing would result in what effect to most murmurs(including AS)? What affects would it have on the intesnity of hypertrophic cardiomyopathy murmur? What affect would it have on the mitral valve prolapse murmur?

A

There would be a decrease intensity in most murmurs. There would be a decrease intensity of the murmur associated with a hypertrophic cardiomyopathy. There would be a decrease intensity of the mitral valve prolapse murmur but their would be an earlier onset for the clicking sound.

159
Q

A bedside maneuver instructing the patient grip their hand will have what affect on the intensity of MR, AR and VSD murmurs? What affects would it have on the intensity of the AS, hypertrophic cardiomyopathy murmurs? What effect would it have on the mitral valve prolapse murmurs?(mention the click sound)

A

There would be an increase in intensity of the MR, AR and the VSD murmurs. There would be a decrease intensity of the AS and the hypertrophic cardiomyopathy murmurs. There would be an increase in intensity of the mitral valve prolapse murmurs and a later click sound.

160
Q

What type of effect does rapid squatting have on the intensity of the hypertrophic cardiomyopathy murmurs? What affect does it have on the intensity of the AS murmur? What affect does it have on the mitral valve prolapse murmur?

A

There is an increase intensity of the hypertrophic cardiomyopathy murmur. There is an increase in the intensity of the AS murmr. There is an increase intensity in the mitral valve prolapse murmur but there is a later onset of click/murmur

161
Q

How does val salva standing affect venous return? How does hand gripping affect systemic vascular resistance?

A

Val salva standing decreases venous return. Hand gripping increases systemic vascular resistance.

162
Q

What general type of murmur is mitral regurgitation? What is a common description of this murmur?Where can you auscultate this murmur the best? Where does this murmur radiate? What type of maneuvers would change the total peripheral resistance to increase the intensity of this mumrmur? What are three disease that usually cause this murmur?

A

Mitral regurgitation is a holosystolic murmur. It is commonly described as a high pitched blowing murmur. This murmur is loudest at the apex. It radiates to the axilla. Any maneuver that increases the total peripheral resistance would increase the intesity of the maneuver, i.e., squatting or hand gripping. Three disease that usually cause it are mitarl valve prolapse, ischemic heart disease and left ventricular dilitation.

163
Q

What general type of murmur is tricuspid regurgitation? What is a common description of this murmur?Where can you auscultate this murmur the best? Where does this murmur radiate? What type of maneuvers at the bedside could increase the intensity of this mumrmur? What heart condtion causes this murmur?

A

Tricuspid regurgitation is a holosystolic murmur. Commonly described as a high-pitched blowing murmur. This murmur is loudest at the tricuspid are and it radiats to the right sternal border. Any maneuver that could increase the venous return tot he Right Atrium, like inspiration, is going to increase the intensity of this murmur. Right ventricular dilitation is known to cause this heart condition.

164
Q

Rheumatic Fever and infective endocarditis are known to cause what murmurs?(2 points)

A

mitral valve regurgitation and tricuspid valve regurgitation

165
Q

What general type of murmur is a aortic stenosis murmur?(4 points) What physiological changes happen in the heart?(2 points) Where is the murmur the loudest? Where does it radiate? What type of pulses?(latin name) What can AS lead to on exertion?(3 points, use nemonic) What congenital or valuve conditions cause this?(2 points)

A

It is a crescend-decresendo systolic ejection murmur. The LV pressure is much high than the aoritc pressure. The murmur is auscultated the base at the heart base. The murmur radiates to the carotid. Pulsus parvus et tardus, which menas weak and delayed pulse. AS can lead to SAD, syncope, angina and dyspnear with exertion. It is often causes by age related dystrophic calcification of the mitral valve or bicuspid aoritc valve.

166
Q

What general type of murmur is caused by a VSD(3 points). Where is the murmur the loudest? How can you attenuate the murmur?(2 points)

A

The murmur caused by a VSD is generally described as a harsh-sounding holosystolic murmur. The murmur is heart the best at the tricuspid area. You can attenuate the murmur by increasing the afterload which increases the total peripheral resistance by instructing the patient to grip their hands.

167
Q

The mid-systolic click you auscultate during a mitral valva prolpase murmur is due to what changesin the musculature of the heart?

A

sudden tensing of the chorae tendinae

168
Q

What general type of murmur is caused by a mitral valve prolapse?(3 points) It is best heard over what area? It is loudest before what heart sound? Most of the time is this disorder benign or severe? This pateint can be predisposed to what pathological condition? What can cause this condition?(3 points) The clicking sound occurs earlier after what maneuver?(2 points)

A

MVP causes a late-systolic crescendo murmur. it is heard best at the apex of the heart. It is loudest just before S2. Most of the time it is benign. The patient can be predisposed to infective endocarditis. This condition can be caused by rhuematic fever, myxomatous degeneration or rupture of the chorae tendinae. The clicking sound occurs earlier if the patient performs a maneuver that decreases the venous return, i.e., val salva maneuver standing.

169
Q

What general type of murmur is caused by an AR?(5 points) What type of pulse pressure when chronic? When can this present?(2 points) AR is often due to what pathological conditions?(4 points) What drugs are known to decrease the intensity of the murmur? What maneuvers increase the intensity of the murmur?(2 points)

A

AR murmurs are generally described as High pitched, blowing, early diastolic decresecendo murmur. The patient may present with a wide pulse pressure when chronic. AR can present itself during head bobbing and bouding pulses. AR if often causes by aortic root dilitation, bicuspid aortic valve, rheumatic fever or endocariditis. Vasodilators decreases the intensity of the murmur. The murmur increase when the patient grips their hand because this increse the systemic resistance.

170
Q

The murmur caused by the mitral stenosis usually follows what particular sound? What is the general description of the murmur?(4 points) What change in what sound interval correlates with increase severity? What pressure changes are physiologically significant during what phase of the heart cycle?(2 points) Mitral stenosis often occurs as a secondary condition due to what? Chronic MS can lead to what type of pathological changes to a chamber? The MS murmur is enhanced in conditions which instructs the patient to do what?

A

MS murmur usually follows an opening snap. The MS murmur is generally described as a delayed, rumbling, late diastolic murmur. A decrease in interval between S2 and the OS correlates to increase severity of the condition. The LA pressure is much greater than than LV pressure. MS is often secondary condition of rheumatic fever. Chronic MS can lead to LA dilitation. The murmur is enhanced during expiration due to the fact that it incrases LA return.

171
Q

What is the most common valvular lesion?

A

mitral valve prolapse

172
Q

The opening snap auscultated in a patient with mitral stenosis is due to what valvular abnormality?

A

abrupt halt in leaflet motion in diastole, after rapid oepning due to fusion at leaflet tips.

173
Q

Patent Ductus Arteriosus cause what general type of murmur? This murmur is loudest during what heart sound? it is often due to what pathological conditions?(2 points) This murmur could be auscultates the best in what area?(2 points)

A

PDA causes a machine like murmur. It is loudest at S2. It is often due to congenital rubella infection or prematurity. The murmur is loudest at the left infraclavicular area.

174
Q

What are the phases of the ventricular action potential?

A
175
Q

Where are two other tissues where ventricular action potential occurs in the heart?(2 points)

A

Bundle of HIS and Purkinje Fibers

176
Q

What generally happens during Phase 0-4 of ventricular action potential?

A
177
Q

What phase of the ventricular muscle action potential: calcium influx through calcium channels balance potassium efflux. Calcium triggers calcium release from sacroplasmic reticulum and myocyte contraction.

A

Phase 2

178
Q

high potassium permeability through potassium channels

A

phase 4

179
Q

massive potassium efflux due to opening of volage gated slow potassium channels and lcose of voltage gated calcium channels

A

phase 3

180
Q

voltage gated sodium channels open

A

phase 1

181
Q

inactivation of voltage gated sodium channels. Voltage gated potassium channels begin to open.

A
182
Q

Ca2+ often triggers what biochemical activity in the cardiac myocte?(2 points)

A

release of calcium from sacroplasmic reticulum and myocyte contraction

183
Q

What are the differences when you compare ventricular acton potentials to skeletal muscle actions potential?(3 points)

A

The plateu during phase 2 is due to influx of calcium from voltage gated calcium channels balance the efflux of potassim from voltage gated potassium channels, myocyte contraction is due to induced calcium release from sacrolasmic reticulum. Cardiac nodal cells spontaneously depolarize during diastole, resulting in automaticity due to If(funny currenet channels resulting in a slow infulx of inward sodium and potassium currents). Cardiac myocyts are electrically coupled to eachother by gap junctions.

184
Q

What happens during phase 3 of ventircular action potential?(2 points)

A

Rapid reploarization due to opening of slow voltage gated potassium channels and close of the voltage gated calcium channel.

185
Q

What causes the leak currents during phase 4 of ventricular action potential?(3 points)

A

Sodium inward current, potassium outward current and calcium inward current

186
Q

The pacemarker action potential occurs in what tissue of the heart?(2 points)

A

SA node and AV node

187
Q

What phase of the ventricular action potential doesn’t occur in the pacemaker action potential?

A

Phase 2, there is no plateau phase

188
Q

How does the AV node prolong transmission from the atrai to the ventricles?

A

Due to the higher voltage gated activation of the calcium channel resulting in the inward current, the activation of the fas inward sodium current doesn’t take place. This allows the AV node to prolong the transmission due to the slow conduction velocity seen in the absence of the fast inward sodium current

189
Q

What feature of the SA nodel and AV nodal action potential deterines heart rate?

A

the slope of phase 4 in SA node

190
Q

What generally happens during all of the phases of the pacemaker action potential?

A
191
Q

What is the membrane potential for ventricular cardiac myocytes and SA nodal myocytes?

A

-85, -40 respectively speaking

192
Q

How do AcH/adenosine affect heart rate? Why?

A

they decreased the heart rate because the decrease the rate of diastolic depolarization.

193
Q

How do catecholamines affect HR? Why?

A

They increase heart rate because they increase the rate of the diastolic depolarization seen during phase 3

194
Q

What phase of the SA nodel AV nodal action potential: membrane potential spontaneously depolarizes as sodium coductance increases?

A

phase 4

195
Q

What physiological activity in the heart causes the P wave?

A

atrial depolarization

196
Q

What wave is the atrial repoloarization? What wave is the atrial depolarization?

A

Atrial repolarization is masked by the QRS complex. Atrial depolarization is the P wave.

197
Q

What physiological activity occurs during the PR Interval?

A

It is the conduction velocity delay through the the AV node (normally less than 200 msec).

198
Q

What physiological activity occurs during the QRS complex?

A

ventricular depolarization

199
Q

What physiological activity occurs during the QT interval?

A

mechanical contraction of the ventricles

200
Q

What physiological activity causes the T wave?

A
201
Q

An inverted T wave is indicative of what cardiovascular problem?

A

recent myocardial problem

202
Q

What physiologic activity occurs during the ST segment?

A

the ventricles are depolarized at this point. It is isoelectric.

203
Q

What causes the U-wave?(2 points)

A

hypokalemia or bradycardia

204
Q

What is the normal time limit for the PR interval? What about the QRS complex? What is the normal time limit for the atrioventricular delay in the AV node? What is the physological purpose for the atrioventricular delay?

A

PR interval is normally 200 msec. The QRS compex is always less than 120 msec. The atrioventricular delay in the AV node is 100msec. The atrioventricular delay allows time for the ventricles to fill.

205
Q

What structurs make up the conduction system of the heart? Please list them in order.(9 points)

A

SA node, AV node, AV internodal pathways, bundle of HIS, right bundle branch, left bundle branch, purkinje system, left anterior fascicle and left posterior fascicle

206
Q

What is the conduction pathway?(7)

A

SA node, atria, AV node, common bundle, bundle branches, Purkinje fibers and ventricles

207
Q

What is the speed of the conduction for the atria, AV node, ventricles and the purkinje system?(4 points)

A

Purkinje System > atria > ventricles > AV node

208
Q

What are the pacemakers in greatest to least?(4 points)

A

SA node, AV node, bundle of His and purkinje/ventricles

209
Q

What structure has an inherant dominance with slow phase of upstroke?

A

Pacemaker

210
Q

What structure of the heart is commonly referred to as the pacemaker?

A

SA node

211
Q
A
212
Q
A
213
Q
A

Torsades de pointes

214
Q
A

Wolf-Parkinson-White Syndrome

215
Q

What is an inherited disorder of myocardial repolarization typically due to ion channel defects? It increases your risk for what? Thisis precipitated by what?

A

Congenital long QT syndrome. It increases your risk for sudden cardiac death and it is precipitated by Torades de pointes.

216
Q

What syndromes are congenital long QT syndromes?(2 points)

A

Romano-Ward syndrome and Jervell and Lange-Nielsen Syndrome

217
Q

What congenital long-QT syndrome is autosomal dominant, pure cardiac phenotype (no deafness)?

A

Romao-Ward Syndrome

218
Q

Waht is the most common type of ventricular pre-exitation syndrome?

A

Wolk-Parkinson White syndrome

219
Q

What is a polymorphic ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG? It can progress to what?

A

Torsades de pointes. It can progress to ventricular fibrillation

220
Q

What is a congenital long QT syndrome that is autosomal recessive and has sensorneural deafness?

A

Jervell and Lange-Nielsen syndrome

221
Q

What sydrome description: an abnormal fast accessory conduction pathway from atria to ventricle by passes the rate-slowing AV node. As a result, ventricles being to partially depolarize earlier, giving rise to characteris delta wave with shortened PR interval on ECG. May result in reentry circuit causing ventricular tachycardia.

A

Wolf-Parkinson White Syndrome

222
Q

What is a nemonic used to help you what can prolong QT intervals?

A

Some Risky Meds Can Prolong QT: Sotalol, Risperidone, Macrolides, chloroquine, Protease inhibitors, Quinidine and Thiazides.

223
Q

Long QT Interval predisposes a person to what electrical/pathological activity of the heart? What electrolyte imbalance is known to cause this? How do you treat?

A

Torsades de pointes. hypokalemia and hypomagnesemia. You can treat with magnesium sulfate.

224
Q

A reenetry circuit seen in Wolf Parkin White syndrome may cause what pathological condition of the heart?

A

ventricular tachycardia

225
Q

What type of ECG tracing description: choatic and erratic baseline (irregularly irregular) with no discrete P waves in between irreguarly spaced QRS complexes. It can result in what? This leads to what? How do you treat?(4 points)

A

atrial fibrillation. It can result in atrial stasis. This leads to thromboembolic stroke. You can treat by controlling the heart rate, anticoagulation, pharmacologic or elecrical cardioversion

226
Q

What is a rapid sucession of identical, back-to back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves. How do you treat?** (5 points)** What is a definitive treatment?

A

atrial flutter. You treat with class IA, IC and III antiarrhytmics. Rate control could be conducted with beta-blockers or calcium channel blockers. Definitive treatment is catheter ablation.

227
Q

A completely erratic rhythm with no idetnfiable waves. What is a result?

A

Ventricular fibrillation. This can result in fatal arrhytmia with no CPR or defibrillation.

228
Q

What is the pathological condition in which there is a QR interval greater than 200 msec? How do you treat?

A

This is a first degree AV Block. It is benign and asymptomatic. There is no treatment.

229
Q

What is an electrical condition of the heart in which there is a progressive lengthening of the PR interval until a beat is “dropped”? What are the symptoms? How do you treat?

A

This is a second degree AV block. Specifically a Mobitz Type I, Wencjkebach. There are no symptoms. No treatment.

230
Q

What is an electrical condition that have dropped beats that are not preceded by a change in the length of the PR inteval. It is often found as 2:1 block, wher there are 2 or more P waves to 1 QRS response. This electrical condition of the heart may progress to what? How is it treated?

A

2nd Degree Block, mobitz type II. It can progress to a third degree block. It is usually treated with a pacemaker.

231
Q

What electrical condition of the heart is being described: The atria and ventricles beat indepedent of each other. Both P waves and QRS complexes are present. What is the usual relationship between the P waves and the QRS complexes? What is the relative rate of the chambers of the muscle?(2 points) How is this condition treated? What disease can cause this electrical condition of the heart?

A

3rd degree heart block. There is no relationship between the P waves and the QRS complexes. This condition is usually treated with a pacemaker. Lyme disease can cause a 3rd degree heart block.

232
Q

This substance is relase from atrial myocytes in response to incrase blood volume and atrial pressure, what is it? What is it’s main effects?**(2 points) **How does it affect the efferent renal arterioles and the afferent renal arterioles? Via what second messenger? This substance promotoes what type of water movement altogether? This is contributed to what common term?

A

The substance is atrial natriuretic peptide. It’s main effect is decrease reabsorption of sodium at the renal tubules and vasodilation. It constricts the efferent arterioles and it dilates the afferant arterioles via cGMP. This substance promotes diuresis and contributing to the aldosterone escape mechanism.

233
Q

What substance is relase from ventricular myocytes in response to increase tension? What is its main affect?(2 points) How does it affect the afferent and effert renal arterioles? The blood test for this is used to diagnose what heart condition? Is it a very good negative or positive predictive value for this condition? What is it used to treat? What is the name of the recombinant form?

A

Brain derived natriuretic peptide. The main effect is decrease reabsorption of sodium in the renal proximal tubules and vasodilation.It constricts the efferent arterioles and it vasodilates the afferent arterioles. It is a very good negative predictive value for heart failure. It is used to treat heart failure. The recombinant form is referred toa s nesitiride.

234
Q
A

Atrial fibrillation

235
Q
A

atrial fibrillation

236
Q
A

atrial flutter

237
Q
A

atrial flutter

238
Q
A

ventricular fibrillation

239
Q
A

ventricular fibrillation

240
Q

The carotid sinus receptor responses to changes in what?

A

pressure

241
Q

The carotid body receptor resposnd to changes in what?

A

it is a chemoreceptor

242
Q

The baroreceptor and the chemoreceptor on the aortic arch transmit via what nerve? To what nuclei? It reponds only to what?

A

It transmits via the vagus nerve to the solitary nucleus of the medulla. It responds only to increase blood pressure

243
Q

Where can you find the carotid sinus? The signnals from the carotid sinus transmits via what nerve to what nucleus? This responds mainly to what?

A

The carotid sinus is a dilated region at the bifurcation of the carotid artery. The signals are transmitted via the glossopharyngeal nerve to the solitary nucleus of the medulla. It responds to a decrease or an increase of bood pressure.

244
Q

How does hypotension affect arterial pressure? This leads to what change in stretch? This leads to what change in afferent barroceptor firing? What changei n efferent sympathetic firing and effferent parasympathetic stimulation? Does this lead to vasoconstriction or vasodilation? How does this affect HR, contratility and BP? This is improtant in response to what pathological condition?

A

Hypotension decrease artrerial pressure which leads to decrease stretch which leads to a decrease in the afferent barroreceptor firing which leads to an incrase in the efferent sympathetic firing and a decrfease in the efferent parasympathetic stimulation. This increase HR, contractility and BP. This is important in response to hemorrhage.

245
Q

How does a carotid massage affect pressure on the carotid sinus, which leads to what change in the stretch, which leads to what change in the afferent barroceptor firing,, which leads to what change in the AV node refractory period, which leads to what change in HR?

A

The carotid message increases the pressure at the carotid sinus, which leads to an increase in strech, which leads to increase in the afferent receptor firing, which leads to an increase in the AV node refractory period, which leads to a decrease in HR.

246
Q

What is the Cushing reaction?(3 points) How does this affect the inracranial pressure, which leads to what circumferential change in the arterioles, which leas to what pathological change in the brain? What does bradycardia occur after this?(5 points)

A

The Cushing reaction is a triad of hypertension, bradycardia and respiratory depression. There is an increase in intracranial pressure which vasoconstricts the arterioles which leads to cerebral ischemia and reflex sympathetic increase in perfusion pressure which leads to hypertension, which increases stretch, increase barroreceptor indcued bradycardia.

247
Q

What are the peripheral chemoreceptors?(2 points) They’re stimulated by change in what?(3 points)

A

carotid body and the chemoreceptor on the aoritc arch. They’re stimualted by a drop of Patial pressure of oxygen below 60 mmHg, changes in partial pressure of carbon dioxide and changes in pH

248
Q

What are the central chemoreceptors?** They’re mainly stimulated by changes in what?(2 points)** Where?(2 points) Which in turn are influenced by what?(2 points) The central chemoreceptors don’t directly respond to change in what value?

A

Chemoreceptors in the brain. They’re mainly stimualted by changes in carbon dioxide and pH in the interstitial fluid of the brain, which in turn are directly influenced by arterial carbon dioxide. They don’t directly respond to changes in partial pressure of oxygen.

249
Q

What organs receives the largest blood flow? What percentage of CO?

A

The lung. They get 100% of CO.

250
Q

What organ has the largest share of systemic CO?

A

liver

251
Q

What organ has the highest blood flow per gram of tissue?

A

kidneys

252
Q

What organ has the largest arteriovenous O2 differnce because O2 extraction is approximately 80%

A

heart

253
Q

The increase O2 demand in the heart is met by by an increase in what type of blood flow? Not by an increase of what?

A

It is met by an increase in coronary blood flow not by an increase in oxygen contraction

254
Q

What is PCWP? It is a good approximation of what type of pressure? In mitral stenosis, what pressure difference do you see? How do you measure?

A

Pulmonary Capillary Wdge Presure. It is a good approximation of left atrial pressure. In MS, PCWP is greater than LV diastolic pressure. It is measure with pulmonary artery catheter.

255
Q

What is the pressure found in the right atrium?

A
256
Q

What is the pressure found in the right ventricle?

A
257
Q

What is the pressure found in the left atrium?

A
258
Q

What is the pressure found in the left ventricle?

A
259
Q

What is the pressure found in the aortic arch?

A
260
Q
A

1st degree AV block

261
Q
A

1st Degree AV Block

262
Q
A

2nd Degree AV Block

263
Q
A

2nd Degree AV Block or Mobitz Type I

264
Q
A

2nd Degree AV Block Mobitz Type II

265
Q
A

2nd Degree AV Block Mobitz Type II

266
Q
A

3rd Degree AV Block

267
Q
A

3rd Degree AV Block

268
Q

What factors determine autoregulation in the heart?**(3 points) **What is their action?

A

CO2, NO and adenosine. Their vasodilatory

269
Q

What are the local metabolities that allows constant blood flow to remain despit wide range of perfusion pressurs? What is their action?

A

CO2 affect on pH. The action of this local metabolitie is vasodilatory.

270
Q

What mechanisms maintain the blood flow to the kidneys despite wide range of perfusion pressures?(2 points)

A

tubuloglomerular feedback and myogenic control

271
Q

What mechanism allow the lungs to maintain constant blood flow despite a wide range of perfusion pressures?

A

hypoxia causing vasoconstriction of the vessels

272
Q

How does the muscle maintain constant blood flow despite a wide range of perfusion pressures?**(5 points) **What type of action?

A

K+, H+, CO2, lactate and adenosine. They’re all vasodilatory.

273
Q

How is blood flow to the skin maintained despite wide ranges of perfusion pressures?** **What is the action?

A

sympathetic stimulation, most important mechanism, temperature control. The action is vasodilation when warm and vasoconstriction when exposed to cold.

274
Q

Why does hypoxia causing vasoconstriction of the pulmonary vessels?

A

it causes vasoconstriction so that only well-ventilated areas are perfused

275
Q

What type of forces determine fluid movement through capillary membranes? What are the 4 types? What is the action of each?

A

Starling Force. The four types of Pc(capillary pressure, pushes fluid out of the capillary), Pi(interstitial fluid pressure, pushes fluid into the capillary), πc(capillary onctic pressure, pushes fluid into the capillary) and πi(pushes fluid out of the capillary)

276
Q

What is the equation for the net filtration pressure?

A

Pnet = [(Pc - Pi)] - [(πc - πi)]

277
Q

What is Κf? What does it tell you?

A

It is the filtration coefficient. It tells you the capillary permeability

278
Q

How is the capillary presure affected with heart failure patients?

A

There is an increase in capillary pressure, Pc

279
Q

How does nephrotic syncrome or liver failure affect plasma proteins level? What statling force does this affect and how?

A

There is a decrease in plasma protein levels. This leads to a decrease in the oncotic pressure, πc

280
Q

How do infection, toxins and burns affect the capillary? What startling force does this affect?

A

It increase the capillary permeability. It doesn’t affect a Starling Force but it does increase Kf, which is the filtration constant which is a reflection of the capillary permeability

281
Q

What is the equation for Jv?

A

Jv(net fluid flow) = (Pnet)*(Kf)

282
Q

How does lymphatic blockage affect the capillary fluid exchange?

A

It increase the interstitial fluid colloid osmotic pressure, πi

283
Q

What are the four common causes of edema?(4 points)

A

An increase in the intersitital osmotic colloid pressure, a decrease in plasma proteins, an increase in capillary pressure or an increase in the capillary permeability

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