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physiology exam 3 > phys exam 3 > Flashcards

phys exam 3 Flashcards

1
Q

longitudinal vibrations of gas particles in an external medium

A

sound waves

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2
Q

frequency of a sound wave is determined by

A

difference between two maximal pressure phases

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3
Q

outer ear is composed of

A

ear pinna and ear canal

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4
Q

the outer ear funnels sound toward the

A

tympanic membrane

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5
Q

the middle ear is connected to the nasopharynx by

A

eustachian tube

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6
Q

three ossicles of the middle ear

A

malleus
incus
stapes

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7
Q

which ossicles are attached to skeletal muscle to regulate vibration

A

malleus
stapes

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8
Q

skeletal muscle attached to the malleus

A

tensor tympani muscle

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9
Q

skeletal muscle attached to the stapes

A

stapedius muscle

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10
Q

which cranial nerve communicates with the stapedius muscle

A

motor nucleus VII (facial nerve)

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11
Q

which cranial nerve communicated with the tensor tympani muscle

A

motor nucleus V (trigeminal nerve)

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12
Q

3 semicircular canals

A

scala vestibuli (dorsal)
scala media
scala tympani (ventral)

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13
Q

scala vestibuli and scala tympani contain

A

perilymph; high [Na+]

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14
Q

scala media contains

A

endolymph; high [K+]

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15
Q

functional unit of the ear

A

organ of corti

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16
Q

organ of corti is located

A

on top of basilar membrane

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17
Q

on top of the organ of corti is the ____ which contains mechanosensitive K+ channels

A

tectorial membrane

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18
Q

auditory pathway - 1 - hair cell sends signal to

A

spinal ganglion (PNS)

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19
Q

auditory pathway - 2 - spinal ganglion sends signal to ___ via ___

A

cochlear nuclei (medulla) via
cranial nerve VIII (vestibulocochlear)

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20
Q

auditory pathway - 3 - cochlear nuclei sends signal to ____ via ____

A

superior olivary complex (medulla-pons) via
trapezoid body (some fibers will travel from R to L or L to R)

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21
Q

auditory pathway - 4 - superior olivary complex sends signal to ____ via ____

A

inferior colliculus (mesencephalon) via
lateral lemniscus

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22
Q

auditory pathway - 5 - inferior colliculus sends signal to ____ via ____

A

medial geniculate nucleus (diencephalon) via
brachium of the inferior colliculus

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23
Q

auditory pathway - 6 - medial geniculate nucleus sends signal to ___ via ___

A

auditory cortex (telencephalon) via
auditory radiations

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24
Q

the anterior and posterior chambers of the eye contain ____ which provides ___

A

aqueous humor
nutrients for the cornea and lens

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25
Q

the lens is suspended by ligaments called ____ which are attached to ___

A

zonular fibers
ciliary body (ciliary muscles)

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26
Q

the vitreous humor of the eye is composed of

A

gelatinous fluid and phagocytic cells

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27
Q

what is the function of tear fluid

A

lubricates the eye
prevents frost damage of the cornea
moistens the nasal cavity
combat bacteria

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28
Q

tears are produced by

A

lacrimal gland

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29
Q

reflective patch in the eye for nocturnal seeing

A

tapetum lucidum

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30
Q

changes to eye when looking far away

A

ciliary muscle relaxes
inc tension of suspensory ligaments
lens flattened

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31
Q

changes to eye when looking nearby

A

ciliary muscle contraction
dec tension of suspensory ligaments
lens rounded

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32
Q

a spherical lens increases

A

refractive power - increases focus

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33
Q

cells of the retina (outside to inside)

A

retinal pigmented cells
photoreceptors
horizontal cells
bipolar cells
amacrine cells
ganglion cells

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34
Q

retinal cell for nourishment and protection of photoreceptors

A

retinal pigmented cells

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35
Q

rods and cones

A

photoreceptors

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36
Q

retinal cell for lateral interactions among photoreceptors and bipolar cells

A

horizontal cells

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37
Q

retinal cell for connection photoreceptors with ganglion cells

A

bipolar cells

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38
Q

retinal cell for lateral interactions among bipolar cells and ganglion cells

A

amacrine cells

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39
Q

axons that form the optic nerve

A

ganglion cells

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40
Q

part of eye that contains the optic disc and tepetum

A

fundus

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41
Q

characteristics of the rod system

A

most sensitive to light
night vision/low light
low acuity
achromatic
peripheral retina

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42
Q

characteristics of the cone system

A

less sensitive to light
day vision
high acuity
color vision
central retina (fovea)

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43
Q

the visual photopigments contained in the discs of the outer segments

A

opsin (G protein)
retinal (aldehyde of vit. A; retinol)

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44
Q

in darkness, ___ binds to opsin; together produce cGMP

A

11-cis-retinal

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45
Q

production of cGMP in the disc causes

A

Na channels to open, Na in, cell depolarized, glutamate released

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46
Q

when stimulated by light, Na channels ___

A

hyperpolarize

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47
Q

what configuration change does light cause

A

changes 11-cis-retinal to all-trans-retinal; detaches from opsonin

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48
Q

in the presence of light, opsin binds to the G protein ___ which activates ___ to hydrolyze cGMP

A

transducin
phosphodiesterase (PDE)

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49
Q

in the presence of light, the hydrolyzed cGMP causes a reduction in cGMP which leads to ___, ____ and ___

A

Na channels closed
hyperpolarization
less glutamate release

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50
Q

carnivorous species have frontal positioned eyes - how does this affect their vision

A

restricted monocular lateral field
large central binocular field

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51
Q

herbivorous species have lateral positioned eyes - how does this affect their vision

A

wide monocular lateral field
very narrow central binocular vision

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52
Q

where is the lateral geniculate nucleus located

A

thalamus

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53
Q

where is the primary visual cortex located

A

occipital lobe

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54
Q

the reticulo-geniculo-striate pathway goes to the cerebral cortex and crosses at the

A

optic chiasm

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55
Q

direction of travel for vision at the reticulo-geniculo-striate pathway

A

R visual field projects to the L nasal retina; axons travel to the L lateral geniculate nucleus and to the L primary visual cortex
(vice versa for L visual field)

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56
Q

cranial nerves involved in the pupillary light reflex and consensual response

A

optic nerve
oculomotor nerve

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57
Q

the circular muscular fibers constrict the pupil in strong light; how are they innervated

A

parasympathetically

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58
Q

the radial muscles dilate the pupil in low light; how are they innervated

A

sympathetically

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59
Q

what is the consensual response

A

pupillary light reflex in both eyes, even if one is uncovered

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60
Q

olfactory section of the brain; size is varied in different species

A

rhinencephalon

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61
Q

how does air pass through the nasal cavity when the dog is sniffing

A

air passes above the heat exchanger - reaches the olfactory epithelium directly

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62
Q

olfactory cells are (primary or secondary) receptor cells

A

primary

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63
Q

odor receptors are covered by

A

membrane of the cilia

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64
Q

for signal amplification, several unmyelinated axons of olfactory cells synpase with a ____

A

mitral cell in the glomerulus (olfactory bulb)

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65
Q

odor molecules are dissolved in

A

gas or water

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66
Q

what kind of receptor are odorant receptors

A

GPCR

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67
Q

olfactory epithelium sends signal to

A

olfactory bulb

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68
Q

olfactory bulb sends signal to

A

olfactory cortex

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69
Q

components of olfactory cortex

A

anterior olfactory nucleus
piriform cortex
amygdala
entorhinal cortex

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70
Q

thalamus receives olfactory signals from

A

frontal cortex
piriform cortex
caudate nucleus
anterior olfactory nucleus
amygdala

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71
Q

thalamus sends olfactory signal to

A

frontal cortex

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72
Q

entorhinal cortex sends olfactory signal to

A

hippocampus

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73
Q

create and store olfactory gestalts

A

anterior olfactory nucleus

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74
Q

behavioral, cognitive and contextual information

A

piriform cortex

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75
Q

emotional processing of olfactory information

A

amygdala

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76
Q

working memory

A

entorhinal cortex

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77
Q

conscious olfactory experience

A

frontal cortex

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78
Q

olfactory stimuli action

A

thalamus

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79
Q

reward system

A

caudate nucleus

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80
Q

odor threshold; reception of odor

A

hippocampus

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81
Q

paired, cylindrical organ located ventrally and medially in the anterior portion of the nasal septum; connected to the oral cavity; function to recognize odor molecules dissolved in fluids

A

vomeronasal organ

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82
Q

function of flehmen response

A

direct fluids into the vomeronasal organ

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83
Q

taste receptor cells are (primary or secondary)

A

secondary receptor cells

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84
Q

location of taste buds in ruminants

A

mostly basis of the tongue

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85
Q

location of taste buds in dogs

A

mostly in the tip

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86
Q

what species are taste buds poorly developed

A

birds

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87
Q

receptors for salty and sour are

A

ionotropic

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88
Q

receptors for sweet, bitter and umami are

A

metabotropic

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89
Q

what kind of channels does capsaicin bind to

A

heat sensitive channels

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90
Q

which cranial nerves synapse at the first order neuron for gustation

A

cranial nerve VII (facial)
cranial nerve IX (glossopharyngeal)

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91
Q

afferent fibers in the facial and glossopharyngeal nerves synapse with neurons in which tract

A

solitariothalamic tract

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92
Q

where do neurons in the solitary tract go to

A

thalamus then cerebral cortex

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93
Q

fluid phase of blood that contains non-cellular components; including coagulation factors

A

plasma

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94
Q

what components of plasma produce oncotic pressure

A

proteins incl. albumin, globulins, fibrinogen

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95
Q

amount of RBCs in the blood

A

hematocrit

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96
Q

differences in hematocrit values can be due to

A

differences in the number of size of RBCs
nutrition, physical activity, metabolic rate
altitude

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97
Q

what causes inc hematocrit during physical activity

A

increased sympathetic nervous system activity; erythrocytes are mobilized from the spleen and cardiovascular system

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98
Q

function of RBCs

A

transport O2 from the lungs to the body Hb; remove CO2 from tissues

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99
Q

what is essential to RBC function

A

number, shape and Hb concentration

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100
Q

how does Hb bind oxygen

A

reversibly without changing the valence

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101
Q

each of Hb’s 4 subunits contains

A

globular peptide chain (alpha or beta)
heme group that contains iron

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102
Q

where does erythropoiesis take place

A

liver and spleen - fetal
red marrow long bones - birth to adolescence
red marrow flat bones - after adolescence

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103
Q

in the bone marrow, all blood cells are derived from

A

pluripotent stem cells

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104
Q

what type of cell will be seen in high amounts in systemic blood in a patient with regenerative anemia

A

reticulocytes

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105
Q

erythropoiesis requires

A

iron
vitamin B12 and folic acid
erythropoietin

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106
Q

iron is necessary for

A

Hb synthesis

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107
Q

vitamin B12 and folic acid are needed for

A

DNA synthesis

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108
Q

where is erythropoietin produced; what upregulates its production

A

produced in the kidney
upregulated by low oxygen tension in the tissues

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109
Q

as erythrocytes age their membranes becomes less flexible and they are more easily damaged; these damaged cells are removed by ____; this removal takes place in ____

A

macrophages;
spleen, liver, bone marrow

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110
Q

what happens to peptides released from Hb of damaged erythrocytes

A

recycled for protein synthesis

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111
Q

what happens to the heme groups released from Hb of damaged erythrocytes

A

converted into bilirubin that will go into bile

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112
Q

what happens to iron released from Hb of damaged erythrocytes

A

transported to the bone marrow to form new heme groups

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113
Q

lifespan of erythrocytes

A

90-140 days

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114
Q

three general causes of anemia

A

blood loss - hemorrhage
RBC destruction - hemolysis
dec RBC production

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115
Q

clinical symptoms of anemia are caused by

A

reduced amount of Hb and decreased oxygen transport capacity

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116
Q

type of anemia with an increased number of circulating reticulocytes, indicating inc bone marrow erythropoiesis

A

regenerative anemia

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117
Q

regenerative anemia may be caused by ___ and ___

A

hemorrhage and hemolysis

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118
Q

type of anemia where reticulocytes are low and there is no increased erythropoiesis

A

nonregenerative anemia

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119
Q

nonregenerative anemia may be caused by

A

impaired bone marrow function and extramarrow diseases

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120
Q

some intrinsic defects that lead to hemolysis include

A

Hb defects
sickle cell disease
membrane deformation
enzyme deficiencies

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121
Q

some extrinsic defects that lead to hemolysis include

A

chemicals that cause methimaglobin formation, denaturation of Hb
parasitism
immune mediated - hemolytic anemia of the newborn

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122
Q

some causes of impaired bone marrow function include

A

FeLV
chemotherapeutics
congenital disorders

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123
Q

some causes of extramarrow diseases

A

chronic renal failure
liver disease
B12 deficiency
iron deficiency

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124
Q

iron deficiency can cause ___ in piglets

A

microcytic hypochromic anemia
(small cells, low Hb)

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125
Q

transports fluid, proteins, fat
transports pathogens and Ags from tissues into lymphatic tissues

A

lymphatic system

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126
Q

where does lymph accumulate;
where do lymph vessels carry lymph

A

accumulates in tissues - interstitium
brought to thoracic duct and into blood

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127
Q

soluble components of innate immunity

A

interferon
peptides
complement

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128
Q

cell mediated components of innate immunity

A

macrophages
granulocytes
dendritic cells

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129
Q

soluble components of adaptive immunity

A

immunoglobulins from B cells

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130
Q

3 components of hemostasis after injury

A

constriction of injured blood vessel
formation of platelet plug
coagulation

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131
Q

when platelets adhere to collagen fibers in the wall of an injured vessel, they release ___ and ____ to increase platelet adhesiveness and form the platelet plug

A

ADP
TXA2 (thromboxane A2)

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132
Q

platelet adhesiveness is decreased by

A

prostacyclin
nitric oxide (NO)

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133
Q

how long does it take completely seal off a broken vessel

A

30-60 min

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134
Q

blood coagulation requires

A

Ca

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135
Q

intrinsic activation of the coagulation cascade is activated by

A

collagen fibers or other surfaces

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136
Q

extrinsic activation of the coagulation cascade is activated by

A

tissue thromboplastin factor III that is released from surrounding tissues after tissue damage

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137
Q

what coagulation factor is activated by collagen

A

XII

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138
Q

coagulation factor XII activates

A

factor XI

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139
Q

coagulation factor XI activates

A

factor IX

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140
Q

coagulation factor X is activated by

A

factor IX
factor VII

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141
Q

thrombin activates; thrombin can have a positive feedback effect on these coagulation factors

A

factor XI
factor VIII
factor V

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142
Q

thrombin is converted from

A

prothrombin by factor X

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143
Q

fibrinogen is converted into

A

fibrin

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144
Q

which factor is the limiting step in the coagulation cascade

A

factor X

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145
Q

slow process that begins immediately after clot formation

A

fibrinolysis

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146
Q

an active proteolytic enzyme that slowly dissolves a clot

A

plasmin

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147
Q

coagulation factors are produced in

A

liver

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148
Q

hemophilia

A

congenital deficiency in coagulation factors VIII (hemophilia A) or IX (hemophilia B)

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149
Q

the liver requires ___ for carboxylation and synthesis of coagulation factors

A

vitamin K

150
Q

warfarin in rat poison inhibits the enzyme ____, which is necessary for activating vitamin K

A

vitamin K epoxide reductase

151
Q

acetylsalicylic acid, aspirin, inhibits the formation of platelet plugs by inhibiting the synthesis of ____

A

thromboxane A2

152
Q

many anticoagulants like EDTA or citrate are

A

Ca chelators

153
Q

blood group A antigens have an additonal

A

GalNAc group

154
Q

blood group B antigens have an additional

A

Gal group

155
Q

AB0 blood group antigens are

A

glycosphingolipids

156
Q

what occurs after an incompatible blood transfusion

A

agglutination and hemolysis

157
Q

individuals with Rh- blood generate Ab against Rh+ patients; Rh- mothers can pass Ab against their Rh+ fetus causing

A

hemolytic anemia in the baby

158
Q

cross-matching blood is done using

A

donor blood
recipient serum

159
Q

neonatal isoerthyrolysis (hemolytic disease in the newborn) can develop in Aa+ foals of Aa- mothers after the foal consumes the colostrum which contains

A

IgG antibodies against the foal’s Aa+ RBCs

160
Q

valve from RA to RV

A

tricuspid valve

161
Q

valve from RV to pulmonary artery

A

pulmonary valve

162
Q

valve from LA to LV

A

mitral valve

163
Q

valve from LV to aorta

A

aortic valve

164
Q

LV ventricle contracts and ejects blood into the aorta, distending the aorta and raising aortic BP to its peak value called

A

systolic aortic pressure

165
Q

outflow of blood from aorta between ejections; decreases to minimal value of aortic BP reached just before the next cardiac ejection called

A

diastolic aortic pressure

166
Q

average value of pulsatile BP in the aorta; represents a potential energy for driving blood through circulation

A

mean aortic pressure

167
Q

volume of blood pumped each minute by one ventricle; ___ for LV and RV are about equal

A

cardiac output

168
Q

pressure difference between mean aortic pressure and mean venae cavae pressure

A

systemic perfusion pressure
- typically 95 mm Hg

169
Q

pressure difference between mean pulmonary artery BP and mean pressure in pulmonary veins

A

pulmonary perfusion pressure
- typically 8 mm Hg

170
Q

what type of circulation is high pressure high resistance

A

systemic

171
Q

what type of circulation is low pressure low resistance

A

pulmonary

172
Q

what type of vessels are most of a dog’s blood stored in

A

veins/venules

173
Q

what kind of vessel is most abundant, greatest cross-section are and slowest velocity

A

capillaries

174
Q

arrangement of two systemic capillary beds in a series

A

portal system

175
Q

role of splanchnic portal system

A

detoxification

176
Q

role of renal portal system

A

generation of urine; waste removal

177
Q

role of hypothalamic-hypophyseal portal system

A

regulation of hormone secretion in the anterior pituitary

178
Q

common proteins found in plasma

A

globulin
albumin
fibrinogen

179
Q

main electrolytes in plasma

A

Na+
Cl-
HCO3-

180
Q

gases found in plasma

A

O2
CO2
N2

181
Q

mean quantity of Hb in each RBC

A

mean corpuscular hemoglobin (MCH)

182
Q

mean quantity of Hb in each deciliter of packed RBCs; hemoglobin/hematocrit

A

mean corpuscular hemoglobin concentration (MCHC)

183
Q

only a small portion of CO2 is dissolved in the blood, in what other form is it found in the plasma

A

hydrated to form HCO3-
combines with Hb or plasma proteins to form carbamino compounds

184
Q

main nutrients in plasma

A

glucose
amino acids
lipids
some vitamins

185
Q

waste products found in plasma

A

CO2
urea
creatinine
uric acid
bilirubin

186
Q

common hormones found in plasma

A

insulin
epinephrine
thyroxine

187
Q

normal canine hematocrit range

A

35-57%

188
Q

normal RBC range in dogs

A

5000-7900 x 10^3/uL

189
Q

normal WBC range in dogs

A

5-14 x 10^3/uL

190
Q

normal platelet range in dogs

A

210-620 x 10^3/uL

191
Q

normal blood Hb range in dogs

A

12-19 g/dL

192
Q

normal MCH range in dogs

A

21-26 pg

193
Q

normal MCHC range in dogs

A

32-36 g/dL

194
Q

difference between plasma and serum

A

serum contains no clotting factors; no anti-coagulant prior to spinning down

195
Q

abnormally high hematocrit; increases blood viscosity; makes it difficult for the heart to pump and can lead to heart failure

A

polycythemia

196
Q

anemia can be caused by low hematocrit or low MCH and/or MCHC; how can anemia lead to heart failure

A

cardiac output must be increased above normal to deliver the normal amount of oxygen to the tissues

197
Q

by what transport method does blood move through the heart and blood vessels

A

bulk flow

198
Q

sources of energy for bulk flow include

A

perfusion pressure
transmural pressure

199
Q

pressure difference that causes blood to flow through blood vessels;
Pinlet - Poutlet

A

perfusion pressure

200
Q

pressure difference between the BP inside a blood vessel and the fluid pressure in the tissue immediately outside the vessel;
Pinside-Poutside

A

transmural pressure

201
Q

major mode of transport that occurs at capillaries; movement from high to low concentration

A

diffusion

202
Q

specialized cardiac muscle cells that can spontaneously depolarize toward the threshold for APs; source of electrical activity of the heart

A

pacemaker cells

203
Q

RMP of a polarized cardiac cell

A

-60 to -80mV

204
Q

each normal heartbeat is initiated by a spontaneous AP generated by pacemaker cells in the

A

SA node

205
Q

ventricular rate from SA node cells in a resting dog

A

80-90 beats/min

206
Q

emergency pacemaker for ventricles; usually overridden by SA node; created AV delay so the atria and ventricles do not contract at the same time

A

AV node

207
Q

how does the conduction velocity and refractory period of the AV node compare to the SA node

A

slower velocity; longer refractory period

208
Q

part of heart that contributes to nearly synchronous contraction of all fibers in both ventricles

A

purkinje fibers

209
Q

after the ventricles contract, what occurs

A

entire heart relaxes and fills

210
Q

the pause between atrial contraction and ventricular contraction is caused by

A

slow propagation of AP through the AV node

211
Q

when a region of ischemic cardiac muscle develops the abnormal twin properties of slow conduction of APs and only able to conduct in one direction

A

ectopic pacemakers (also called reentrant APs)

212
Q

passage of an AP around and around a nonconducting center; can cause reentrant arrhytmia

A

circus movement

213
Q

the pacemaker potential is caused by spontaneous changes in what 3 ion channels

A

Na+
Ca2+
K+

214
Q

generation of pacemaker potential sequence from RMP

A

K+ channels close; Na+ channels open
slow influx of Na+ until -40mV
Ca2+ channels open; Ca2+ in; depolarization
K+ channels open; K+ out; repolarization

215
Q

which channel is primarily responsible for AP generation in a pacemaker cell

A

Ca2+

216
Q

RMP is formed by

A

Na+ K+ pump - 3 Na out, 2 K in
leaking K+ channels
closed Ca channels

217
Q

cardiac AP formation phase 0

A

cell depolarized to threshold voltage for opening voltage gated Na channels; causes rapid depolarization

218
Q

cardiac AP formation phase 1

A

Na channels inactivate, Na permeability decreases; membrane begins to repolarize

219
Q

cardiac AP formation phase 2

A

some gated K channels close, K permeability decreases; many gated Ca channels (L-type Ca channels) open; Ca permeability increases; prolonged plateau of depolarization

220
Q

Ca entering a cardiac cell during an AP triggers release of additional Ca from ___, initiating cardiac contraction

A

sarcoplasmic reticulum

221
Q

cardiac AP formation phase 3

A

K channels reopen and Ca channels close; cell repolarizes

222
Q

cardiac AP formation phase 4

A

cell returns to stable negative resting potential

223
Q

cardiac muscle cells form a ____ in which specialized gap junctions allow ionic currents to flow quickly into neighboring cells

A

functional syncytium

224
Q

what is the purpose of a long refractory period between cardiac muscle contractions

A

allows heart to completely relax and refill before the next contraction

225
Q

atrial cells have (shorter or longer) APs and refractory periods than ventricular cells

A

shorter

226
Q

norepinephrine and epinephrine are secreted by

A

sympathetic nerve or adrenal medullar glands

227
Q

where does norepi and epi bind on cardiac pacemaker cells

A

B-adrenergic receptors

228
Q

effect of norepinephrine and epinephrine of pacemaker cells

A

elevate HR

229
Q

acetylcholine is secreted by

A

parasympathetic nerves

230
Q

where does Ach bind on pacemaker cells

A

muscarinic cholinergic receptors

231
Q

effect of acetylcholine on pacemaker cells

A

decrease HR

232
Q

intrinsic HR of a normal large dog

A

140 bpm

233
Q

effect of norepinephrine and epinephrine on all cardiac muscle cells

A

taller more positive plateau APs
shorter duration APs
quicker, stronger, shorter duration contractions

234
Q

how does norepinephrine and epinephrine contribute to a taller and more positive plateau AP

A

increases the number of L type Ca channels that open during the plateau phase

235
Q

how does norepinephrine and epinephrine contribute to shorter duration APs

A

the more positive plateau opens K channels sooner, shortening the AP and speeding up repolarization

236
Q

how does norepinephrine and epinephrine contribute to quicker, stronger and shorter contractions

A

more Ca channels opened increases entry of extracellular Ca - quicker and stronger
speeding up Ca pumped back out of cell - shorter duration

237
Q

how does acetylcholine affect atrial cells

A

exerts strong anti-sympathetic influences

238
Q

how does acetylcholine affect ventricular muscle cells

A

indirect effect
inhibits release of norpeinephrine
weakens effects of sympathetic activation

239
Q

cardiac arrhythmias caused by pacemaker cell problems

A

sick sinus syndrome
tachyarrhythmias

240
Q

extreme form of sick sinus syndrome

A

sinus arrest
SA node fails to form APs - AV node keeps ventricles beating at very slow rate

241
Q

less extreme form of sick sinus syndrome

A

sluggish depolarization of SA node
low intrinsic HR
low HR at rest - bradycardia
insufficient inc in HR during exercise

242
Q

treatments of sick sinus syndrome

A

cholinergic muscarinic antagonist drugs (ex. atropine)
B-adrenergic agonist drugs (ex. isoproterenol)
artificial cardiac pacemaker

243
Q

tachycardia caused by abnormally rapid depolarization of SA node pacemaker cells

A

sinus tachycardia

244
Q

tachycardia originating from an ectopic pacemaker in the atria; common in boxers and wolfhounds

A

atrial tachycardia

245
Q

extremely rapid atrial tachycardia

A

atrial flutter

246
Q

rapid atrial contractions that lose synchrony - no blood gets pumped; SA node is still working;
common in horses and dobermans

A

atrial fibrillation

247
Q

tachycardia originating from ectopic pacemakers within AV node or first part of AV bundle

A

junctional tachycardia

248
Q

collective term encompassing sinus, atrial and junctional tachycardia

A

supraventricular tachycardia

249
Q

tachycardia originating from ectopic pacemakers within the ventricles; ventricles do not relax long enough for adequate filling; exacerbated by inappropriately timed atrial contractions

A

ventricular tachycardia

250
Q

each tiny region of the ventricular wall contracts and relaxes at random in response to random and continuous APs; can cause sudden cardiac death

A

ventricular fibrillation

251
Q

complete block of AV node

A

third degree AV node block

252
Q

AV node transmits some atrial APs but not all of them; can be created or exaggerated by strong parasympathetic activity due to increased refractory period of AV node cells

A

second degree AV node block

253
Q

fading and eventual stoppage of a cardiac AP in a slowly conducting region; often involved in 2nd and 3rd degree AV node block

A

decremental conduction

254
Q

every atrial AP is transmitted to the ventricles; AP propagates more slowly and HR is slower

A

first degree AV node block

255
Q

AV node block can be caused by

A

cardiac trauma
toxins
infections
ischemia
congenital defects
cardiac fibrosis
inadvertent damage of AV node during surgical repair of ventricular septal defect

256
Q

treatment of AV node block

A

muscarinic cholinergic antagonist
B-adrenergic receptor agonists
artificial pacemaker applied to ventricles

257
Q

types of antiarrhythmic drugs

A

local anesthetics
calcium channel blockers
cardiac glycosides
beta-adrenergic antagonists

258
Q

how do local anesthetics work

A

bind to some voltage gated Na channels
counteracts membrane depolarization and AP formation

259
Q

how do calcium channel blockers work

A

bind to some L-type Ca channels and prevent them from opening
lowers plateau
lengthens AP - slower opening of K channels
decreases strength of contractions

260
Q

how do cardiac glycosides work

A

inhibiting Na K pump
allow more Ca than normal to accumulate inside, resulting in stronger but slower contractions
inc in parasympathetic tone

261
Q

how do beta-adrenergic antagonists work

A

bind to some of B-adrenergic receptors
prevent activation by norepinephrine
dec HR
lengthen refractory period
slow conduction of AP
reverse sympathetic induced increases in contractility

262
Q

ex of local anesthetics

A

quinidine
lidocaine
procaine

263
Q

ex of calcium channel blockers

A

verapamil
diltiazem
nifedipine

264
Q

ex of cardiac glycosides

A

digitalis

265
Q

ex of beta-adrenergic antagonists

A

propranolol

266
Q

where is lead I recorded; what is it compared with

A

recorded in LF (+)
compared with RF (-)

267
Q

where is lead II recorded; what is it compared with

A

recorded in LH (+)
compared with RF (-)

268
Q

where is lead III recorded; what is it compared with

A

recorded in LH (+)
compared with LF (-)

269
Q

where does the aVR lead measure the voltage from; what is it compared with

A

voltage from the RF
compared with average voltage from other two limb electrodes

270
Q

where does the aVL lead measure the voltage from; what is it compared with

A

voltage from LF
compared with average voltage from other two limb electrodes

271
Q

where does the aVF measure the voltage from; what is it compared with

A

voltage from LH
compared with average voltage from other two limb electrodes

272
Q

P wave corresponds to

A

atrial depolarization

273
Q

how does the voltage compare between the RF and LF during atrial depolarization; why

A

LF is positive
because RA depolarizes and becomes negative first

274
Q

what cannot be detected by ECG

A

atrial repolarization

275
Q

Q wave corresponds to

A

interventricular septum depolarization that spreads from L to R

276
Q

how does the voltage compare between the LF and RF during interventricular septum depolarization

A

LF slightly negative compared to RF

277
Q

R wave corresponds to

A

ventricular depolarization
outward spreading AP in both ventricles

278
Q

S wave corresponds to

A

depolarization of ventricular base
end of depolarization in both ventricles

279
Q

how does the voltage compare between LF and RF during depolarization of ventricular base

A

LF returns to zero then becomes slightly negative for a few ms

280
Q

T wave corresponds to

A

ventricular repolarization of both ventricles

281
Q

what makes a positive T wave

A

repolarization spreads inward through both ventricles;
outermost portion of ventricular wall repolarizes first

282
Q

what makes a negative T wave

A

ventricular repolarization proceeds from in to out

283
Q

time between the start of atrial depolarization and start of ventricular depolarization

A

PR interval;
ex. 0.13 s in a large resting dog

284
Q

time it takes for the ventricles to depolarize once the AP emerges from the AV node and AV bundle

A

QRS complex;
ex. <0.1 s in a large resting dog

285
Q

time from beginning of ventricular depolarization to end of ventricular repolarization; duration of an AP in ventricular tissue

A

QT interval;
ex. 0.2 s in a large resting dog

286
Q

time between atrial depolarizations; can be used to calculate the atrial rate (# of atrial contractions/min)

A

PP interval

287
Q

time between ventricular depolarization; can be used to calculate the ventricular rate

A

RR interval

288
Q

what is the standard vertical calibration on an ECG

A

10 mm = 1 mV

289
Q

different chart speeds of an ECG

A

25 mm/s: 5 mm = 0.2s per major division
50 mm/s: 5mm = 0.1s per major division

290
Q

ECG vary more among (small or large) animals

A

large

291
Q

ECG abnormality: polarity of QRS from lead I is negative - suggesting mass of RV has increased; high voltages of QRS from lead II and III; pronounced negative components in QRS from leads II and III

A

right ventricular hypertrophy

292
Q

ECG abnormality: abnormally low ECG voltage

A

accumulation of fluid within the pericardium

293
Q

ECG abnormality: ST segment elevation due to TP segment depression - inability of ventricular muscle cells to maintain a normal negative RMP

A

ischemic or infarcted area in the inferior part of the ventricle

294
Q

ECG abnormality: abnormal shape and long duration of QRS; premature depolarization originated from an ectopic site; predominant positive voltage in lead I

A

premature ventricular contractions (PVCs)

295
Q

ECG abnormality: fast resting HR; each QRS is preceded by a positive P wave followed by a positive overlapping T wave; rapid HR initiated by SA node pacemakers

A

sinus tachycardia

296
Q

ECG abnormality: slow resting HR; normal P, QRS and T waves; slow and irregular

A

sinus bradycardia

297
Q

ECG abnormality: PR intervals are abnormally long - indicates abnormally slow conduction of AP through the AV node and AV bundle

A

first degree AV node block

298
Q

ECG abnormality: some P waves are not followed by QRS-T waves - indicates some atrial depolarization is conducted through AV node

A

second degree AV node block

299
Q

ECG abnormality: QRS-T waves present but not preceded by P waves - indicates the QRS-T waves were caused by auxiliary pacemakers

A

third degree AV node block

300
Q

ECG abnormality: abnormally shaped ventricular complexes of faster and higher voltage - indicating an ectopic ventricular pacemaker; frequently will degenerate into ventricular fibrillation

A

ventricular tachycardia

301
Q

ECG abnormality: large, irregular voltage fluctuations with no discernible pattern

A

ventricular fibrillation

302
Q

ECG abnormality: random, high frequency, low amplitude voltage fluctuations (f waves); QRS-T normal in shape but occur irregularly; atria do not contract synchronously or effectively

A

atrial fibrillation

303
Q

atrial systole

A

contraction

304
Q

diastole

A

relaxation

305
Q

when do atria contract

A

at the end of ventricular filling

306
Q

what occurs during ventricular systole

A

AV valves (mitral and tricuspid) close
isovolumetric contraction - aortic and pulmonary valves open
rapid and reduced ejection - aortic and pulmonary valves close

307
Q

during ventricular systole, when do the aortic and pulmonary valves open

A

when ventricular pressures exceed the pressure in aorta and pulmonary artery

308
Q

during ventricular systole, when do the aortic and pulmonary valves close

A

at the end of ejection due to the back flow of blood

309
Q

what occurs during ventricular diastole

A

isovolumetric relaxation - mitral valve and tricuspid valves open
rapid and reduced ventricular filling (diastasis)

310
Q

during ventricular diastole, when do the mitral and tricuspid valves open

A

when ventricular pressures fall below atrial pressures

311
Q

how long does diastasis persist

A

until the SA node cells initiate another atrial AP

312
Q

end diastolic volume

A

blood volume in each ventricle at the end of diastole

313
Q

end systolic volume

A

remaining blood volume at the end of systole

314
Q

stroke volume

A

volume of blood ejected from one ventricle in one beat
(end diastolic volume) - (end systolic volume)

315
Q

ejection fraction

A

(stroke volume)/(end diastolic volume)
50-65% typical in resting dogs

316
Q

cardiac output

A

total volume of blood pumped by one ventricle in one minute
stroke volume x HR

317
Q

what factors affect the heart to eject blood

A

end diastolic ventricular volume
ventricular contractility
arterial BP
HR

318
Q

increased end diastolic ventricular volume will cause

A

an inc in stroke volume

319
Q

what is the result of stretching the ventricular muscle fibers during diastole

A

more calcium is released from the sarcoplasmic reticulum during contraction, increasing the force

320
Q

pre load

A

ventricular pressure at the end of diastole

321
Q

increased ventricular preload will cause

A

an inc in end diastolic ventricular volume and stroke volume

322
Q

there are no valves between

A

veins and atria

323
Q

central venous pressure (CVP)

A

pressure in cranial vena cava; equivalent to right ventricular preload

324
Q

starling’s law of the heart (heterometric autoregulation)

A

changes in preload cause corresponding changes in end diastolic ventricular volume and stroke volume

325
Q

compliance

A

measure of the ease with which the ventricular walls stretch to accommodate incoming blood during diastole
change in volume / change in pressure

326
Q

at what point do the ventricles become stiff and less compliant

A

at preloads higher than 10 mm Hg

327
Q

what can cause ventricular walls to become stiffer

A

myocardial ischemia
certain cardiac diseases
advancing age

328
Q

what could cause edema to develop in tissues upstream from the stiff ventricle

A

elevated preload causing elevated atrial and venous pressure

329
Q

filling time

A

length of time available for ventricular filling during diastole

330
Q

what is the main determinant of diastolic filling time

A

heart rate

331
Q

ventricular contractility is increased by the release of ____, which activate B-adrenergic receptors on ventricular muscle cells

A

epinephrine and norepinephrine

332
Q

what kind of drugs increase ventricular contractility

A

B-adrenergic agonists
cardiac glycosides

333
Q

how do cardiac glycosides increase ventricular contractility

A

increase cytosolic Ca concentration during an AP

334
Q

ventricular contractility is decreased by

A

B-adrenergic antagonists (like Ca channel blocking drugs)
barbiturates, opioids and some general anesthetics

335
Q

hallmark of myocardial failure

A

decreased cardiac contractility

336
Q

why does an increase in arterial BP impair ventricular ejection

A

the LV pressure during systole must exceed aortic pressure before ejection of blood from the ventricle can occur

337
Q

cardiac afterload

A

pressure that a ventricle must generate in order to eject blood

338
Q

increased HR reduces

A

diastolic filling time

339
Q

what are some situations that cause an increase in HR but a decrease in cardiac output

A

artificial cardiac pacemakers
certain cardiac arrhythmias - ex paroxysmal atrial tachycardia

340
Q

what situation causes an increase in HR and cardiac output

A

exercise

341
Q

during vigorous exercise in a large dog, what cardiac changes will increase

A

stroke volume
ejection fraction
HR
cardiac output

342
Q

during vigorous exercise in a large dog, what cardiac changes will decrease

A

ventricular end diastolic volume
ventricular end systolic volume

343
Q

which sound is associated with the closure of the AV valves (mitral and tricuspid)

A

S1

344
Q

which sound is associated with closure of the aortic valve on the left side and pulmonic valve on the right side; stronger sound than S1

A

S2

345
Q

which sound is associated with the AV valve opening and a rush of blood in the ventricles causing the ventricular walls to vibrate; early diastole

A

S3

346
Q

which sound occurs at the very end of diastole, as atrial systole causes a sudden rush of blood into the ventricles

A

S4

347
Q

3 common types of heart murmurs

A

systolic
diastole
continuous

348
Q

systolic heart murmurs can be cause by

A

insufficient or incompetent AV valve
ventricular septal defect (VSD)
aortic and pulmonic stenosis

349
Q

large pressure difference between ventricle and atrium causes a rapid backward flow of blood through the partially closed valve (regurgitation)

A

AV valve insufficiency

350
Q

hole in the interventricular septum

A

ventricular septal defect

351
Q

aortic or pulmonary valve fails to open widely; common congenital defect in dogs

A

aortic and pulmonic stenosis

352
Q

diastolic heart murmurs can be caused by

A

mitral or tricuspid stenosis
aortic or pulmonic insufficiency

353
Q

tricuspid stenosis can be caused by

A

heartworm infestation in the right heart

354
Q

aortic regurgitation is common in

A

horses

355
Q

continuous murmurs can be caused by

A

patent ductus arteriosus (PDA)
arteriovenous fistulae

356
Q

persistence of opening between aorta and pulmonary artery after birth; sometimes called “machinery murmur”

A

PDA

357
Q

abnormal openings between peripheral arteries and veins, carries a turbulent flow during systole and diastole

A

arteriovenous fistulae

358
Q

what are common consequences of cardiac defects

A

abnormally high or low blood flow to a region of the body
abnormally high or low BP in a region of the body
cardiac hypertrophy

359
Q

effects of mitral regurgitation

A

LV hypertrophy
pulmonary edema
consequences more noticeable during exercise

360
Q

effects of mitral stenosis

A

atrial fibrillation
pulmonary edema

361
Q

effects of PDA

A

LV hypertrophy
RV hypertrophy
exercise intolerance

362
Q

effect of aortic stenosis

A

exercise intolerance

363
Q

effects of aortic regurgitation

A

LV hypertrophy
pulmonary edema may develop

364
Q

effects of VSD

A

moderate LV hypertrophy
pronounced RV hypertrophy
possible pulmonary edema
probable exercise intolerance

365
Q

effect of pulmonic stenosis

A

pronounced RV hypertrophy

366
Q

minute work of a ventricle

A

(mean aortic/pulmonic pressure) x stroke volume x HR

367
Q

stroke work

A

external work done by the ventricle in one cardiac cycle;
(mean aortic/pulmonic pressure) x stroke volume

368
Q

cardiac internal work

A

wasted work appearing as heat;
~85% of metabolic energy consumed by the heart

369
Q

which side of the heart has the greater cardiac energy consumption

A

left

370
Q

hypertension causes

A

striking LV hypertrophy

371
Q

why is excessive ventricular hypertrophy deleterious

A
  • restricts opening of aortic or pulmonary valves, leading to stenosis
  • coronary circulation may be unable to provide enough blood flow to meet the inc metabolic demand
  • cellular growth factors that mediate hypertrophy also predispose the cardiac muscle to apoptosis

physiology exam 3 (1 decks)

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