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Histology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Define cardiovascular physiology

A

study of how the heart & blood vessels function

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2
Q

What is rule #2 of the heart

A

the heart is a muscle

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3
Q

If the heart is over-worked, what happens

A

it gets larger

b/c it is a muscle

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4
Q

Cardiac muscle is called

A

myocardium

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5
Q

What are the unique features of myocardium

A 
rapid depolarization (electrical conduction)
high energy needs (glycogen & mitochondria)
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6
Q

What is rule #4 of the heart

A

the heart has 3 functions

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7
Q

Name the 3 primary functions of the heart

A

electrical conduction
contraction during systole
relaxation during diastole

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8
Q

Through the 3 primary functions of the heart, what other important functions does the CVS have

A

delivery of O2, nutrients, water, hormones, & regulatory chemicals to tissues
removes CO2 & metabolic wastes
thermoregulation
supports blood flow dependent functions

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9
Q

What are some examples of blood flow dependent functions

A 
urine formation in kidneys
gas exchange in the lungs
metabolism in working skeletal muscle
digestive processes & absorption
reproductive system functions
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10
Q

What is another name for the RAVV

A

tricuspid valve

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11
Q

Where is the RAVV/ tricuspid valve located

A

b/w RA & RV

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12
Q

Where is the pulmonic valve located

A

b/w RV & pulmonary trunk

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13
Q

What is another name for the LAVV

A

bicuspid or mitral valve

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14
Q

Where is the LAVV/bicuspid/mitral valve located

A

b/w LA & LV

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15
Q

Where is the aortic valve located

A

b/w LV & aorta

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16
Q

What are the 3 layers of the heart

A

endocardium
myocardium
epicardium

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17
Q

Describe the endocardium

A

inner layer

single cell layer of endothelial cells

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18
Q

Describe the myocardium

A

middle layer

thicker layer of cardiac muscle (myocardial) cells

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19
Q

Describe the epicardium

A

outer layer
thin layer of mesothelial cells
also called the visceral serous pericardium

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20
Q

What is the contractile unit of the heart

A

sarcomere

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21
Q

What controls the sarcomere

A

complex proteins

including actin, myosin, troponin, & tropomyosin

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22
Q

Are arteries high or low pressure

A

high

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23
Q

Are veins high or low pressure

A

low

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24
Q

RBC pulmonary circulation

A

RA -> RV -> pulmonary trunk -> pulmonary arteries -> lungs -> pulmonary veins

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25
Q

RBC systemic circulation

A

LA -> LV -> aorta -> systemic organs -> vena cava

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26
Q

What is rule #1 of the heart

A

there are two circulations arranged in series

pulmonary & systemic

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27
Q

What is rule #5 of the heart

A

blood is lazy

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28
Q

Blood is lazy, which means what

A

it moves down its pressure gradient

from high to low pressure

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29
Q

Name the fetal shunts

A

ductus arteriosus
ductus venosus
foramen ovale

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30
Q

Remnant of ductus venosus

A

ligamentum venosum

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31
Q

Remnant of foramen ovale

A

fossa ovalis

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32
Q

When do the fetal shunts close

A

shortly after birth

in response to bp changes & decreased PGE2

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33
Q

Function of the placenta

A

oxygenates blood & removes metabolic wastes

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34
Q

Placenta takes over the job of what organs

A

lungs & liver

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35
Q

What is the function of ductus venosus in fetal circulation

A

allows blood from umbilical vein to bypass the liver on the way to the caudal vena cava

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36
Q

What is the function of foramen ovale in fetal circulation

A

allows blood from RA to bypass the lungs & go directly into the LA

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37
Q

What is the function of ductus arteriosus in fetal circulation

A

allows blood from pulmonary trunk to bypass the lungs & go directly into the aorta

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38
Q

Gas exchange in fetal vs adult circulation

A

fetal- placenta

adult- lungs

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39
Q

High pressure & low pressure systems in fetal vs adult circulation

A

fetal- pulmonary circulation is high pressure while systemic is low pressure
adult- pulmonary circulation is low pressure while systemic is high pressure

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40
Q

Circuitry in fetal vs adult circulation

A

fetal- parallel

adult- series

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41
Q

Where is the patent ductus arteriosus located

A

b/w pulmonary trunk & aorta

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42
Q

In fetal circulation, how did blood move through the ductus arteriosus & why

A

from pulmonary trunk to aorta since the pulmonary trunk had a higher pressure

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43
Q

In adult circulation, how does blood move through the patent ductus arteriosus & why

A

from aorta to pulmonary trunk since the aorta has higher pressure

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44
Q

Why is it incorrect to describe vessels as a plumbing system

A

blood vessels are not passive tubes

not rigid; able to expand & contract

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45
Q

Name the 3 blood vessel layers

A

tunica intima
tunica media
tunica externa

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46
Q

Describe tunica intima

A

intimate contact w/ lumen

simple squamous epithelium continuous w/ the lining of the heart

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47
Q

Function of tunica intima

A

prevents friction

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48
Q

Describe tunica media

A

middle layer

smooth muscle w/ sheets of elastin

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49
Q

Function of tunica media

A

blood pressure regulator the dilates/constricts in response to the autonomic nervous system

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50
Q

Describe tunica externa

A

overcoat

loosely woven collagen fiber

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51
Q

Function of tunica externa

A

protects & reinforces blood vessels

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52
Q

What are capillary walls made of

A

tunica intima only

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53
Q

Thin walls of capillaries allow for what

A

diffusion of gas, nutrients, & waste

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54
Q

Capillary beds have what other functions besides the exchange of gas, nutrients, & wastes

A

regulate blood pressure & thermoregulation

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55
Q

Function of venous valves

A

prevent backflow of blood

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56
Q

Why are valves necessary for veins

A

no pressure gradient available

must work against gravity

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57
Q

Do veins or arteries have a larger lumen

A

veins

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58
Q

Do veins or arteries have a thicker wall

A

arteries

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59
Q

Do veins and arteries have the same layers

A

yes, tunica intima/media/externa

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60
Q

Do veins or arteries have more muscle & elastic fibers

A

arteries

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61
Q

Do veins or arteries have higher compliance

A

veins

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62
Q

Do veins or arteries have higher capacitance

A

veins

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63
Q

Define compliance

A

ability to stretch

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64
Q

Define capacitance

A

ability to hold a large volume under low pressure

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65
Q

Describe elastic arteries

A

large vessels w/ large lumen

thick walls w/ a lot of elastin tissue, smooth muscle, & CT

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66
Q

Function of elastic arteries

A

deliver blood to organs or lungs

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67
Q

Walls of elastic arteries allow the vessels to do what

A

absorb high pressure blood flow as blood is pumped from the ventricles into the elastic arteries

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68
Q

Describe muscular arteries

A

medium sized vessels w/ medium sized lumen

moderately thick wall w/ moderate amounts of elastin tissue, smooth muscle, & CT

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69
Q

Function of muscular arteries

A

deliver oxygenated blood to the organs

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70
Q

Describe arterioles

A

smallest branches of the arteries w/ small lumen

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71
Q

Function of arterioles

A

site of highest resistance to blood flow

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72
Q

Alterations in resistance of arterioles occur in response to what

A

sympathetic nervous system activity
alpha 1 stimulation -> vasoconstriction
beta 2 stimulation -> vasodilation

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73
Q

Where are continuous capillaries found

A

skin, muscle, & brain

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74
Q

Continuous capillaries allow passage of what

A

lipid soluble molecules (O2/CO2) via diffusion across a lipid membrane
sm molecules through intracellular clefts

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75
Q

Where are fenestrated capillaries found

A

sm intestines & kidneys

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76
Q

Fenestrated capillaries allow passage of what

A

sm molecules through fenestrations & intracellular clefts

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77
Q

Where are sinusoidal capillaries found

A

liver, bone, marrow, & spleen

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78
Q

Sinusoidal capillaries allow passage of what

A

lg molecules through lg fenestrations

lack basement membrane, so leaky

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79
Q

Capillaries are located b/w where

A

blood & tissues (systemic) or alveoli (lungs)

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80
Q

Describe the compliance & resistance of the arterial system

A

high resistance

low compliance

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81
Q

Describe the compliance & resistance of the venous system

A

low resistance

high compliance

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82
Q

Define basal tone

A

partial constriction of a vessel even when all external forces are removed

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83
Q

Put the following in order of cross-sectional area:

arterioles, capillaries, & arteries

A

capillaries > arterioles > arteries

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84
Q

Define laminar flow

A

streamlined

layers of fluid moving in series w/ each layer having a dif velocity

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85
Q

Laminar flow is described as being parabolic, what does this mean

A 
max velocity is at the center
minimum velocity (0) is towards the vessel walls
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86
Q

Define turbulent flow

A

when streamlined flow is disrupted
irregular motion
audible vibrations

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87
Q

Audible vibrations from turbulent flow result from

A

major changes in diameter

such as, arterial bifurcations, stenotic vessels, & near valves

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88
Q

Eq for velocity of blood flow

A

V = Q/A

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89
Q

Relationship b/w cross-sectional area of vessels to the velocity of the blood

A

inversely proportional

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90
Q

Arteries cross-sectional area vs velocity

A

low A

high V

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91
Q

Arterioles cross-sectional area vs velocity

A

gradually higher A

gradually lower V

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92
Q

Capillaries cross-sectional area vs velocity

A

high A

low V

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93
Q

Venules cross-sectional area vs velocity

A

gradually lower A

gradually higher V

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94
Q

Veins cross-sectional area vs velocity

A

low A

high V

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95
Q

Eq for Ohm’s law

A

Q = ΔP/R

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96
Q

Relationship b/w blood flow & pressure gradient

A 
directly proportional
(pressure gradient = driving force)
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97
Q

Relationship b/w blood flow & resistance

A 
inversely proportional
(resistance = impediment to flow)
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98
Q

Eq for Poiseulle’s law

A

R = 8nl/πr^4

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99
Q

Relationship b/w resistance to flow & blood viscocity

A

directly proportional

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100
Q

Relationship b/w resistance to flow & length

A

directly proportional

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101
Q

Relationship b/w resistance to flow & radius

A

inversely proportional

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102
Q

What is the main determinant of resistance to flow

A

radius

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103
Q

Eq for Reynold’s number

A

Nr = pdv/n

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104
Q

High Nr means

A

turbulent blood flow

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105
Q

Low Nr means

A

laminar blood flow

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106
Q

Relationship b/w turbulence & velocity of flow

A

directly proportional

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107
Q

Relationship b/w turbulence & blood viscocity

A

inversely proportional

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108
Q

What are the main determinants of turbulence

A

velocity of blood flow & viscosity of blood

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109
Q

How could blood viscosity be increased

A

increased RBCs

dehydration

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110
Q

How could blood viscosity be decreased

A

decreased RBCs

IV fluids

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111
Q

Systolic definition

A

highest arterial blood pressure

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112
Q

Diastolic definition

A

lowest pressure whether in arteries or vein

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113
Q

Pulse pressure definition

A

dif b/w systolic & diastolic pressure

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114
Q

Units to measure blood pressure

A

millimeters of mercury

mmHg

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115
Q

What is the primary parameter responsible for assuring the tissue O2 requirements are met

A

cardiac output

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116
Q

Compare systemic vs pulmonary circulatory systems in regards to blood pressure

A

systemic is higher
(BPd ~ 80 mmHg & BPs ~ 120 mmHg)
pulmonary is lower
(BPd ~ 5 mmHg & BPs ~ 20-40 mmHg)

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117
Q

Explain the contribution of the elastic properties of arteries to systolic pressure

A

elastic walls of aorta stretch to accommodate for the increase in blood being pumped from the LV to the aorta
thick rubber band- able to accept blood, but the pressure increases

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118
Q

Explain the contribution of the elastic properties of arteries to diastolic pressure

A

allow for continued movement forward of blood even as the amount of blood moving is decreased
due to the recoil properties- moves back to its original state & pushing blood into the circulatory system

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119
Q

Mean arterial pressure definition

A

average pressure in a complete cardiac cycle

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120
Q

Mean arterial pressure is the driving force for what

A

perfusion

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121
Q

Eq for mean arterial pressure

A

MAP = 1/3 BPs + 2/3 BPd

or MAP = (BPs + BPd + BPd)/3

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122
Q

Eq for pulse pressure

A

BPs - BPd

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123
Q

Pulse pressure represents what

A

stroke volume

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124
Q

Define stroke volume

A

volume of blood pumped out of the heart w/ each beat

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125
Q

What is felt during an exam by palpating the arterial vessels

A

pulse pressure

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126
Q

If a pulse is normokinetic, what does this mean

A

syn adequate & strong

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127
Q

If a pulse is hyperkinetic, what does this mean

A

syn bounding or water hammer

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128
Q

A hyperkinetic pulse could be due to what (examples)

A

patent ductus arteriosus

aortic regurgitation

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129
Q

If a pulse is hypokinetic, what does this mean

A

syn weak or thready

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130
Q

A hypokinetic pulse could be due to what (examples)

A

subaortic stenosis

hypovolemia

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131
Q

High resistance of arterioles is instilled by what component of the vessel wall

A

high smooth muscle

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132
Q

When measuring the blood pressure in a patient, you are measuring the pressure in what type of vessel

A

systemic arteries

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133
Q

What valve(s) sound louder in the left base

A

pulmonic & aortic valves

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134
Q

What valve(s) sound louder in the right base

A

none

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135
Q

What valve(s) sound louder in the left apex

A

mitral/ bicuspid valve

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136
Q

What valve(s) sound louder in the right apex

A

tricuspid valve

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137
Q

Would a needle w/ a higher gauge have a smaller or larger diameter than a needle with a lower gauge

A

smaller

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138
Q

Sympathetic NS is associated w/ what response

A

fight or flight

increased HR & BP

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139
Q

Parasympathetic NS is associated w/ what response

A

rest & digest

decreased HR & BP

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140
Q

Alpha receptors have what effect on blood vessels

A

constrict smooth muscle

reduce blood flow

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141
Q

Beta receptors have what effect on blood vessels

A

dilate smooth muscle

increase blood flow

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142
Q

What are baroreceptors

A

specialized cells that monitor BP by detecting changes in the stretch of vessel walls

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143
Q

Where are baroreceptors found

A

aortic arch & carotid sinuses

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144
Q

What cardiovascular centers are associated w/ the sympathetic system

A

vasomotor & cardiac accelerator

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145
Q

What cardiovascular centers are associated w/ the parasympathetic system

A

cardiac decelerator

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146
Q

If BP increases, what are the steps of the arterial baroreceptor reflex

A

1) baroreceptors sense mechanical stretch
2) increased frequency of baroreceptor signals to the brain
3) signal travels via glossopharyngeal (CN IX) & vagus (CN X) nerves to the nucleus tractus solitarius in the medulla oblongata
4) decreases vasomotor & cardiac accelerator
increases cardiac decelerator

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147
Q

Summary of arterial baroreceptor reflex when high BP

A

bradycardia (slower HR), arteriolar vasodilation, & decreased contractility

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148
Q

If BP decreases, what are the steps of the arterial baroreceptor reflex

A

1) baroreceptors do not sense mechanical stretch
2) decreased frequency of baroreceptor signals to the brain
3) fewer signals travel via glossopharyngeal (CN IX) & vagus (CN X) nerves to the nucleus tractus solitarius in the medulla oblongata
4) increases vasomotor & cardiac accelerator
decreases cardiac decelerator

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149
Q

Summary of arterial baroreceptor reflex when low BP

A

tachycardia (faster HR), arteriolar vasoconstriction, & increased contractility

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150
Q

What stimulates the Renin-Angiotensin Aldosterone Systems (RAAS)

A

low blood pressure (juxtaglomerular cells)
increased sympathetic tone (arteriolar baroreceptors)
low renal blood flow/ low Na+ (macula densa)

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151
Q

What does renin do

A

converts angiotensinogen (inactive) -> angiotensin I

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152
Q

What does Angiotensin Converting Enzyme (ACE) do

A

converts angiotensin I -> angiotensin II

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153
Q

What does angiotensin II do

A

recruits ADH, aldosterone, & norepinephrine
constricts efferent > afferent in glomerulus
increases Na+ & H2O reabsorption in proximal convoluted tubule

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154
Q

Angiotensin II, ADH, & norepinephrine act as what

A

vasoconstrictors

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155
Q

ADH does what

A

increases H2O reabsorption in the distal convoluted tubule

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156
Q

Aldosterone does what

A

increases Na+ & H2O reabsorption & K+ secretion at distal convoluted tubule

157
Q

Summary of RAAS

A

if decreased bp, then need to increase CO (by adding more volume) & increase VR (by vasoconstriction)

158
Q

What increases CO in the RAAS

A

increased Na+ & H2O reabsorption throughout the kidney (ADH, aldosterone, & angiotensin II)
increased thirst/ water intake (ADH)

159
Q

What increases VR in the RAAS

A

vasoconstriction (angiotensin II, ADH, & norepinephrine)

160
Q

Which response to BP changes is faster & why

A

arterial baroreceptor reflex

occurs in sec to min b/c signals are passed through the NS

161
Q

Which response to BP changes is slower & why

A

RAAS

occurs in min to hours b/c signals are passed through the CVS via hormones

162
Q

Filtration in capillary beds occurs where

A

arterial end

163
Q

Reabsorption in capillary beds occurs where

A

venous end

164
Q

Define hydrostatic pressure

A

pressure of fluids in an enclosed space
in this case, pressure w/in capillaries
pushes fluid out

165
Q

Define oncotic pressure

A

osmotic pressure generated by proteins

pulls fluid in

166
Q

At the arterial end, why does filtration occur

A

increased hydrostatic pressure
oncotic pressure is static
Pc > πc
net outward flow

167
Q

At the venous end, why does reabsorption occur

A

decreased hydrostatic pressure
oncotic pressure is static
Pc < πc
net inward flow

168
Q

Describe the on/off switches when exchange is allowed in the capillaries

A

precapillary sphincters are vasodilated

allows blood to move through the capillaries

169
Q

Describe the on/off switches when exchange is prevented in the capillaries

A

precapillary sphincters are vasoconstricted

blood cannot move through the capillary beds

170
Q

When blood is prevented from entering the capillary beds, where does it go

A

from arterioles into venule via metarterioles

171
Q

What are some vasodilators

A

decreased O2 or increased CO2 in tissues
histamine
adenosine
bradykinin

172
Q

What are some vasoconstrictors

A

angiotensin II
epinephrine/norepinephrine
endothelin
acute stretch in arterioles after increased bp (myogenic autoregulation)

173
Q

Is there net movement across capillaries in the middle

A

no, because Pc = πc

174
Q

Define effusion

A

fluid accumulation in a cavity/ space

175
Q

Define edema

A

fluid accumulation in a tissue

176
Q

Name the two ways that filtration in the interstitial space would increase, resulting in edema

A

increased capillary hydrostatic pressure (Pc)

increased capillary permeability (Kf)

177
Q

What could cause an increase in Pc

A 
arteriolar dilation
venous constriction
increased venous pressure
heart failure
ECF volume expansion
178
Q

What could cause increased Kf

A

burns
inflammation
toxins

179
Q

Name the two ways that there would be decreased removal from the interstitial space, resulting in edema

A

decreased capillary oncotic pressure (πc)

decreased lymphatic drainage

180
Q

What could cause a decrease in πc

A

loss of plasma proteins (ex: via urinary or GI system)

decreased production of proteins (ex: liver failure or malnutrition)

181
Q

What could cause a decrease in lymphatic drainage

A

standing (decreased skeletal muscle compresses lymph vessels)
lymphatic obstruction

182
Q

Summarize what edema is and what causes it

A

increase in interstitial fluid volume due to an increase in filtration or a decrease in absorption/ lymph drainage

183
Q

Temporal relationship b/w mechanical & electrical events in the heart

A

electrical event occurs before the mechanical event

184
Q

What is the sequence of electrical activation in the heart

A

1) SA node
2) atrial myocardium
3) AV node
4) Bundle of His
5) Left & right bundle branches
6) Purkinje fibers
7) Ventricular myocardium

185
Q

What are the driving forces that dictate the flow of ions across the cardiomyocyte membrane

A

electrical & chemical driving forces

186
Q

What is the electrical driving force

A

difference in membrane potential b/w inside & outside of cell

187
Q

What is the chemical driving force

A

difference in cation conc b/w inside & outside of cell

188
Q

What two factors create the polarized state/ resting membrane potential

A

Na-K ATPase activity

Selective permeability to K+

189
Q

Describe the Na-K ATPase & its effect on RMP

A

3 Na+ out for 2 K+ in

Creates electrochemical gradient

190
Q

Describe the selective permeability to K+ & its effect on RMP

A

membrane is permeable to K+, so it diffuses out of the cell down its conc gradient
large neg charged intracellular proteins attract some K+, which prevents complete equilibrium of K+ across the membrane

191
Q

Extracellular charge & ion conc at RMP

A

pos charge
high Na+
low K+

192
Q

Intracellular charge & ion conc at RMP

A

neg charge
low Na+
high K+

193
Q

Depolarization involves what channels

A

voltage-gated Na+ channels (Na+ influx)

phosphorylation-gated Ca2+ channels (Ca2+ influx)

194
Q

Repolarization involves what channels

A

voltage-gated K+ channels (K+ efflux)

195
Q

Describe resting potential of AP

A

no net movement of ions

196
Q

Describe stimulus & response of AP

A

AP not generated until a certain voltage is reached

197
Q

Describe all or none response of AP

A

action potential either occurs or it doesn’t

198
Q

If threshold is reached, what is the effect on the Na+ & K+ voltage-gated channels

A

1) activation gate of Na+ voltage-gated channel opens quickly
2) inactivation gate of Na+ voltage-gated channel opens slowly
3) voltage-gated K+ channel opens slowly

199
Q

Describe propagation of AP

A

only goes in one direction

200
Q

Describe refractory period of AP

A

cells are unresponsive to re-stimulation

201
Q

Describe relative refractory period of AP

A

stronger than normal stimulus from an adjacent cell can prematurely excite the cells

202
Q

Fast response conduction systems are located where

A

atrial & ventricular myocytes

purkinje cells

203
Q

Slow response conduction systems are located where

A

SA & AV node

204
Q

Phases (#’s) in fast response AP

A

4, 0, 1, 2, 3, & back to 4

205
Q

Phases (#’s) in slow response AP

A

4, 0, 3, & back to 4

206
Q

Summary for what happens in the phases for fast response AP

A 
4- K+ efflux &amp; Na+K+ ATPase
0- Na+ influx
1- transient K+ efflux
2- K+ efflux &amp; Ca2+ influx
3- K+ efflux
207
Q

Summary of what happens in the phases for slow response AP

A

4- funny current
0- Ca2+ influx
3- K+ efflux

208
Q

RMP for fast response AP

A

-90 mV

209
Q

RMP for slow response AP

A

-60/-65 mV

210
Q

What is the difference in phase 0 b/w fast & slow response APs

A

fast- rapid influx of Na+ through fast voltage-gated Na+ channels
slow- leisurely upstroke due to a slow influx of Ca2+

211
Q

What is the difference in phase 4 b/w fast & slow response APs

A

fast- K+ ion partitioning is the primary determinant of RMP; no ion movement
slow- continuously drifting towards threshold of -40 mV (via funny current); allows for spontaneous depolarization of pacemaker cells in SA node

212
Q

What is a surface electrocardiogram (ECG)

A

summation of all APs over time

213
Q

What characteristics of electrical waveforms is captured by ECGs

A

amplitude & direction

214
Q

Define arrhythmia

A

electrical activity that has an irregular rhythm and/or abnormal heart rate

215
Q

What does a waveform correlate w/

A

de/repolarization of a specific area of a heart

216
Q

What do the pos & neg poles of an ECG serve as

A

point of reference to code the wave’s amplitude & direction

217
Q

What is the amplitude of deflection dictated by

A

tissue being depolarized & orientation of the waveform relative to the lead

218
Q

What does Einhoven’s triangle describe

A

orientation of a standard 6-lead ECG

219
Q

P wave is what de/repolarization

A

atrial depolarization

220
Q

QRS complex is what de/repolarization

A

ventricular depolarization

221
Q

T wave is what de/repolarization

A

ventricular repolarization

222
Q

Would a waveform that is parallel to an electrode have a higher or lower amplitude compared to one that is angled

A

higher

223
Q

Would a waveform going through a thicker muscle have a higher or lower amplitude compared to one that is thinner

A

higher

224
Q

What are ECGs great at determining

A

heart rate, arrhythmias, & conduction abnormalities

225
Q

What are ECGs good at determining

A

chamber enlargement (specific but not sensitive)

226
Q

What are ECGs bad at determining

A

mechanical activity of the heart

227
Q

1st + deflection is what

A

P wave

228
Q

1st - deflection is what

A

Q wave

229
Q

2nd +, 1st + after 1st -, or 1st large + deflection is what

A

R wave

230
Q
  • deflection after R is what
A

S wave

231
Q

+ or - deflection after QRS complex

A

T wave

232
Q

Do all (normal) patients have every waveform

A

no, many do not have all of the waveforms in the QRS complex

but must have a P & T wave

233
Q

Effect of hyperkalemia on slow response AP

A

mimics effect of PS tone on nodal cells
leads to a reduced slope of phase 4 spontaneous depolarization
ECG shows bradycardia

234
Q

Effect of hyperkalemia on RMP of fast response AP

A

les neg RMP so more Na+ channels are in an inactivated state
leads to reduced or absent excitability & a slower rate of phase 0 depolarization to the ventricles
ECG shows low amplitude/ absent P wave & a wide QRS complex

235
Q

Order of sensitivity to hyperkalemia

A

atrial > ventricular > nodal

236
Q

Effect of hyperkalemia on de/repolarization of fast response AP

A

faster repolarization
leads to shorted AP duration
ECG shows tented T wave

237
Q

Heart rate calculation on ECG for a 25 mm/sec printer

A 
#QRS in 15 big boxes (3 sec) * 20
#QRS in 1 BIC pen (6 sec) * 10
238
Q

Heart rate calculation on ECG for a 50 mm/sec printer

A 
#QRS in 30 big boxes (3 sec) * 20
#QRS in 1 BIC pen (3 sec) * 20
239
Q

How big is a BIC pen

A

150 mm

240
Q

What is considered a regular rhythm

A

beats evenly spaced

241
Q

What is considered an irregular rhythm

A

beats not evenly spaced

242
Q

Describe a regularly irregular rhythm

A

clear pattern to the irregularity

243
Q

Describe an irregular rhythm

A

no clear pattern or lack of pattern to irregularity

244
Q

Describe an irregularly irregular rhythm

A

no pattern to the irregularity

245
Q

For a paper speed of 50 mm/sec and a calibration of 10 mm/1mV, what are the measurements for a small box

A

.1 mV by .02 sec

246
Q

How does a P wave vary for QRS origin from sinus, supraventricular, & ventricular

A 
sinus= wider P wave
supraventricular= +/- P prime waves; narrower
ventricular= P wave may be absent
247
Q

How does a QRS complex vary for QRS origin from sinus, supraventricular, & ventricular

A

sinus & supraventricular= narrow QRS

ventricular= wide QRS

248
Q

Describe the association b/w P waves & QRS complexes for when a QRS originates from sinus, supraventricular, or ventricular

A 
sinus= associated
supraventricular= may be associated or dissociated
ventricular= dissociated
249
Q

Pos deflection goes towards what pole

A

pos pole

250
Q

Neg deflection goes towards what pole

A

neg pole

251
Q

Isoelectric describes what

A

electrical activity moving perpendicular to a lead

252
Q

What does MEA stand for

A

mean electrical axis

253
Q

What does MEA describe

A

average path of electrical activity during ventricular polarization

254
Q

Normally, what direction do the ventricles depolarize

A

cranial-caudal & right-left

255
Q

An abnormal path of depolarization indicates what

A

a side of the heart is diseased

256
Q

A right axis shift is brought about by

A

RV enlargement or R bundle branch block

257
Q

A left axis shift is brought about by

A

LV enlargement or L bundle branch block

258
Q

Steps for finding MEA using the largest QRS method

A

1) circle QRS in all 6 leads
2) compare QRS’s to find the one w/ the largest deflection
3) determine if the QRS from the lead w/ the largest deflection is going towards the pos or neg pole
4) assign the degree that is associated w/ that lead & electrode

259
Q

Normal MEA

A

Dogs: +40 to +100
Cats: 0 to +150

260
Q

Molecule that links excitation (electrical events) & contraction (mechanical events) of the heart

A

calcium

261
Q

Where is calcium stored

A

longitudinal tubules & terminal cisternae of the sarcoplasmic reticulum

262
Q

Cell membrane of cardiomyocytes

A

sarcolemma

263
Q

Endoplasmic reticulum of cardiomyocytes

A

sarcoplasmic reticulum

264
Q

Cytoplasm of cardiomyocytes

A

sarcoplasm

265
Q

Contractile unit of cardiomyocytes

A

sarcomere

266
Q

During excitation-contraction coupling, how does Ca enter the cell sarcoplasm

A

through voltage-gated long acting Ca channels during phase II of ventricular (fast response) action potential

267
Q

During excitation-contraction coupling, what does the small influx of Ca into the cell sarcoplasm trigger

A

Ca release from the sarcoplasmic reticulum by binding to the calcium release receptor

268
Q

What is the name of the calcium release receptor

A

ryanodine receptor

269
Q

During excitation-contraction coupling, what does calcium bind to & what effect does this have on the contractile proteins

A

Ca binds to troponin C in the sarcoplasm

troponin complex undergoes a morphologic change that pulls tropomyosin away to expose the myosin binding site on actin

270
Q

After the myosin binding site is exposed on actin, what happens

A

myosin binds to actin

myosin releases a phosphate, creating a power stroke that results in myocardial contraction

271
Q

During excitation-contraction coupling, for ventricular relaxation to occur, what has to happen

A

Ca must be removed from the sarcolemma

272
Q

How is Ca removed from the sarcolemma

A

re-sequestration of Ca into the sarcoplasmic reticulum by the sarco(endo)plasmic reticulum Ca ATPase & its gatekeeper phospholamban
elimination of Ca from the cell by a Na-Ca exchanger & Ca-ATPase pump

273
Q

What must happen for phospholamban to open the gate for resequestration

A

must be phosphorylated

274
Q

What are the effects of autonomic tone during systole on contractility of the heart

A

sympathetic stimulation-> increases contractility

parasympathetic stimulation-> decreases contractility

275
Q

Drugs that increase/decrease contractility of the heart are called what

A

increase contractility-> positive isotropes

decrease contractility-> negative isotropes

276
Q

What are the effects of autonomic tone during diastole on relaxation of the heart

A

sympathetic stimulation-> increases relaxation

parasympathetic stimulation-> decreases relaxation

277
Q

Drugs that increase/decrease relaxation of the heart are called what

A

increase relaxation-> positive lusitropes

decrease relaxation-> negative lusitropes

278
Q

What happens during mechanical systole

A

ventricles contract

279
Q

What happens during mechanical diastole

A

ventricles relax

280
Q

What is rule #6 of the heart

A

blood pressure is the product of cardiac output & vascular resistance

281
Q

Two phases of systole

A

isovolumic contraction & ejection

282
Q

Position of valves during isovolumic contraction

A

atrioventricular & semiulnar are closed

283
Q

Chambers contracting/relaxing during isovolumic contraction

A

atria relaxing

ventricles contracting

284
Q

Blood flow during isovolumic contraction

A

no blood flow since valves are closed

285
Q

Position of valves during ejection

A

atrioventricular are closed

semiulnar are open

286
Q

Chambers contracting/relaxing during ejection

A

atria relaxing

ventricles contracting

287
Q

Blood flow during ejection

A

from ventricles to aorta/pulmonary trunk

atria filling from vena cava

288
Q

Describe S1 heart sound

A

lub
occurs at time of mitral valve closure
marks start of systole

289
Q

Describe S2 heart sound

A

dub
occurs at time of aortic valve closure
marks end of systole

290
Q

What occurs between S1 & S2

A

systole

291
Q

Describe coronary circulation

A

provides oxygenated blood to cardiac muscle

292
Q

Describe path of coronary vessels

A

branch from aorta, travel on the epicardial surface, & enter into the myocardium

293
Q

Define isovolumic

A

volume of blood does not change b/c the valves are closed

294
Q

Define diastasis

A

period of slower/ reduced filling

295
Q

Four phases of diastole

A

isovolumic relaxation, early rapid filling, diastasis, & atrial contraction

296
Q

Position of valves during isovolumic relaxation

A

atrioventricular & semiulnar are closed

297
Q

Chambers contracting/relaxing during isovolumic relaxation

A

atria & ventricles relaxing

298
Q

Blood flow during isovolumic relaxation

A

no blood flow b/c valves are closed

but atria are filling w/ blood

299
Q

Position of valves during early rapid filling

A

atrioventricular are open

semiulnar are closed

300
Q

Chambers contracting/relaxing during early rapid filling

A

atria & ventricle relaxed

301
Q

Blood flow during early rapid filling

A

LA -> LV

RA -> RV

302
Q

Why do the ventricles fill quickly during early rapid filling

A

large pressure gradient b/w atria & ventricles

303
Q

Position of valves during diastasis

A

atrioventricular are open

semiulnar are closed

304
Q

Chambers contracting/relaxing during diastasis

A

atria & ventricle relaxed

305
Q

Blood flow during diastasis

A

LA -> LV

RA -> RV

306
Q

Why do the ventricles fill slowly during diastasis

A

pressure b/w atria & ventricles are almost the same

307
Q

Position of valves during atrial contraction

A

atrioventricular are open

semiulnar are closed

308
Q

Chambers contracting/relaxing during atrial contraction

A

atria contracting

ventricles relaxing

309
Q

Blood flow during atrial contraction

A

LA -> LV

RA -> RV

310
Q

P wave corresponds w/ what phase of the cardiac cycle

A

atrial contraction during diastole

311
Q

QRS complex corresponds w/ what phase of the cardiac cycle

A

isovolumic contraction during systole

312
Q

T wave corresponds w/ what phase of the cardiac cycle

A

ejection during systole

313
Q

Describe S3 heart sound

A

ah

occurs at the time of early rapid filling (mid-diastole) in patients w/ dilated hearts

314
Q

S3 sound is caused by what

A

oscillation of hemodynamic structures when a dilated ventricle w/ poor compliance fills

315
Q

In small animals, an S3 gallop indicates what

A

dilated cardiomyopathy (DCM)

316
Q

Describe S4 heart sound

A

bah

occurs at the time of atrial contraction (late diastole) in patients w/ hypertrophied ventricles.

317
Q

S4 sound is caused by what

A

oscillation of hemodynamic structures when the atrium tries to fill a hypertrophied ventricle w/ poor compliancee

318
Q

In small animals, an S4 gallop indicates what

A

hypertrophic cardiomyopathy (HCM)

319
Q

How do S3 & S4 sounds differ in large vs small animals

A

normal in large animals

abnormal in small animals (indicate heart disease)

320
Q

Determinants of stroke volume

A

preload, afterload, & contractility

321
Q

Preload definition

A

volume filling the ventricle (~end diastolic volume)

322
Q

Afterload definition

A

pressure needed to pump blood out of the ventricle (~arterial bp)

323
Q

Contractility definition

A

strength of contraction (modulated by drugs or autonomic tone) for a given preload

324
Q

Volume overload disease affects preload or afterload

A

preload

325
Q

Volume overload disease results in concentric or eccentric hypertrophy

A

eccentric

326
Q

Eccentric hypertrophy means what

A

normal wall thickness w/ a dilated chamber

327
Q

What could increase preload

A

IV fluids & mitral/tricuspid valve regurgitation

328
Q

What could decrease preload

A

dehydration & atrial fibrillation

329
Q

Pressure overload disease affects preload or afterload

A

afterload

330
Q

Pressure overload disease results in concentric or eccentric hypertrophy

A

concentric

331
Q

Concentric hypertrophy means what

A

increased wall thickness w/ a small chamber

332
Q

What would increase afterload

A

arterial hypertension, stenosis of aortic or pulmonary valves, & arterial vasoconstriction

333
Q

What could decrease afterload

A

arterial vasodilator

334
Q

Describe the Frank-Starling mechanism

A

when preload increases, the force of contraction is increased by increasing cTn-C affinity for Ca & increasing actin-myosin interaction when stretched

335
Q

What is rule #3 of the heart

A

the heart’s response to disease is predictable

336
Q

What is the equation for tension of the heart

A

tension = [pressure (P)*radius (R)]/wall thickness (h)

337
Q

Why does ventricular hypertrophy occur

A

to reduce ventricular wall tension (compensatory mechanism)

338
Q

When does the mitral valve open

A

when LA P > LV P

339
Q

When does the mitral valve close

A

when LA P < LV P

340
Q

When does the aortic valve open

A

when LV P > Ao P

341
Q

When does the aortic valve close

A

when LV P < Ao P

342
Q

What wave/complex, electrical event, & mechanical event are associated w/ S4

A

P
atrial depolarization
atrial contraction

343
Q

What wave/complex, electrical event, & mechanical event are associated w/ S1

A

QRS
ventricular depolarization
ventricle contraction

344
Q

What wave/complex, electrical event, & mechanical event are associated w/ S2

A

T
ventricular repolarization
ventricle relaxation

345
Q

What wave/complex, electrical event, & mechanical event are associated w/ S3

A

no associated wave/complex or electrical event

early rapid filling

346
Q

Fluid accumulation on the left side is associated w/ what

A

pulmonary edema

347
Q

Fluid accumulation on the right side is associated w/ what

A

ascites, cavitary effusions (pleural, peritoneal, or pericardial), hepatomegaly (enlarged liver), peripheral edema

348
Q

Synonym to forwards heart failure

A

low output

349
Q

Synonym to backwards heart failure

A

congestive

350
Q

Forwards heart failure results from the failure of the heart to do what

A

pump an adequate volume of blood to meet oxygen demands of tissues

351
Q

Backwards heart failure results from the failure of the heart to do what

A

prevent fluid accumulation in tissues

352
Q

Clinical signs of forwards heart failure

A

exercise intolerance, reduced systolic bp & pumping function, syncope (fainting), azotemia, pallor (pale gumbs), cyanosis (blue gums), hypokinetic pulse, pulmonary edema

353
Q

Clinical signs for backwards heart failure-> specifically, left sided congestive heart failure

A

pulmonary edema

354
Q

Clinical signs for backwards heart failure-> specifically, right sided congestive heart failure

A

subcutaneous brisket edema, moderate fluid accumulation in the abdomen (peritoneal effusion), other cavitary effusions (pleural or pericardial), hepatomegaly, ascites, peripheral edema

355
Q

How does the RAAS system work to alter the BP equation to increase BP

A

Retains Na/H2O -> increases preload
Vasoconstriction -> increases preload & afterload
These factors increase SV, which increases CO, which subsequently increases BP

356
Q

Function of the stethoscope bell

A

listening to low frequency sounds

heart sounds & gallops

357
Q

Function of the stethoscope diaphragm

A

listening to high frequency sounds

murmurs

358
Q

How does a flexible (tunable) diaphragm work

A

w/ gentle pressure, behaves like a bell

w/ firm pressure, behaves like a diaphragm

359
Q

How do you conduct a venous assessment

A

view jugular vein on a standing patient

360
Q

Describe jugular pulsation

A

wave-like motion in the jugular vein that moves up the neck

361
Q

Is a jugular pulsation normal

A

only in large animals at the lower 1/3rd of the neck

362
Q

Describe jugular distension

A

jugular vein remains full

363
Q

What causes jugular pulsation/distension

A

right heart pressure/volume overload
pericardial effusion
obstruction by a mass/thrombus

364
Q

How do you conduct an arterial assessment for small animals

A

palpate femoral artery in femoral triangle where it is the largest

365
Q

How do you conduct an arterial assessment for large animals

A

palpate facial artery on the medial aspect of the ramus of the mandible

366
Q

What are some ex of what causes a hypokinetic pulse

A

subaortic stenosis
hypovolemia (dehydration/blood loss)
arrhythmias that result in less filling of the ventricle

367
Q

What are some ex of what causes a hyperkinetic pulse

A 
patent ductus arteriosus
severe aortic regurgitation
bradycardia
decreased vascular resistance (anemia)
high sympathetic tone
368
Q

Define point of maximal intensity

A

location on the chest where the murmur is the loudest

369
Q

SA node ECG correlate

A

none

370
Q

Atrial myocardium ECG correlate

A

P wave

371
Q

AV node ECG correlate

A

PQ interval

372
Q

Bundle of His, left & right bundle branches, & Purkinje fibers ECG correlate

A

QRS interval

373
Q

Ventricular myocardium ECG correlate

A

still QRS interval, there is not anything with the T wave

374
Q

Why are sinus arrhythmias a normal finding in dogs

A

healthy dogs have a predominance of parasympathetic tone

375
Q

Pathological vagal tone (increased parasympathetic tone) may be in response to what

A

disease in the GI, ocular, CNS, or respiratory system

376
Q

Describe the changes of the heart rate during a sinus arrhythmia

A

cyclic changes vary w/ respiratory phase
inspiration = faster hr
expiration = slower hr

377
Q

Explain why ventricular ectopic depolarization take longer than the sinus node depolarization

A

since ventricular ectopic depolarization starts in the ventricular myocardium, the depolarization events do not depolarize the atria or use the His-Purkinje “superhighway” system. As a result, the ventricular ectopic complexes depolarize the ventricular myocardium slowly by travelling from cell to cell

378
Q

Describe the two different kinds of ventricular ectopic beats

A

ventricular premature beats: occur before the next expected sinus beat
ventricular escape beats: occur after the next expected sinus beat (aptly named because the patient escapes from certain death)

379
Q

Why do the QRS complexes in Sinus rhythm with supraventricular premature complexes have a normal width

A

all supraventricular origin beats travel through the AV node & ventricles using the normal conducting system

380
Q

What might cause a sinus rhythm with supraventricular premature complexes

A

atrial enlargement, inflammation/infection of the atrial myocardium, atrial masses, or pressure from masses in the thorax pressing on the myocardium

381
Q

Name for P wave originating from a supraventricular premature complexes

A

P’ waves (just means they have a different morphology than a normal P wave)

382
Q

What is the main feature of 3rd degree AV block

A

dissociated P wave

383
Q

During 3rd degree AV block, the atrial & ventricular depolarization events are unrelated to one another (termed “dissociated”). How does this appear on an ECG

A

two independent rhythms are superimposed over one another on the ECG
sinus/atrial rhythm is usually faster than the ventricular rhythm

384
Q

What are the causes of AV block

A

disease of the AV node (e.g. fibrosis, neoplasia, inflammation/infection most notably Chagas disease or Lyme disease).

385
Q

How is AV block fixed

A

pacemaker implant

386
Q

What are causes of ventricular arrhythmias (think HEADS)

A

Heart disease (ventricular chamber enlargement, fibrosis, ischemia)
Electrolyte imbalances & Endocrine diseases (hyperthyroidism, pheochromocytoma)
Altered Autonomic tone (high sympathetic tone can worsen ventricular arrhythmias), intra-Abdominal disease
Drugs and toxicities (e.g digoxin toxicity)
S*&% surgeons see (gastric dilation and volvulus, splenic disease, sepsis, etc.)

387
Q

What happens when the enlarged & fibrotic atria are too large to maintain the organized atrial depolarization wave

A

disorganized electrical activity (fibrillation) leads to f waves that reach the atrioventricular node at irregular time intervals. Sometimes the AV node is in the refractory period & cannot conduct the impulse. Sometimes it can conduct the impulses very quickly. Impulse is erratically passed to the ventricles in rapid, irregular fashion with no pattern to the irregularity. Following depolarization of the atrioventricular node, the impulse is propagated along the normal path of conduction to the ventricles.

388
Q

What part of the conduction system goes through the cardiac skeleton

A

Bundle of His

Histology (4 decks)

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