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CardioPulm > Final Deck 2 > Flashcards

Final Deck 2 Flashcards

1
Q

what does first degree AV block look like on ECG

A

PR segment elongated (>5 little boxes)

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2
Q

Where would we find large clefts in capillary wall

A

Liver and gut (so water soluble substances can cross)

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3
Q

What is a major. Contributor to osmotic pressure in the blood

A

Albumin

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4
Q

Whats the largest starling force that influences movement of fluid out of the capillary

A

Capillary hydrostatic pressure

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5
Q

where in the circulatory system do we usually see starling forces at work allowing fluid passage from a vessel

A

capillary at arteriolar end

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6
Q

when fluid leads from capillaries into interstitial, how do we get it back into the bloodstream

A

lymphatics

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7
Q

whats the equation to determine net movement of starling forces

A

forces out - forces in

Pc+Osmi) - (Pi+Osmc

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8
Q

what condition alters the starling forces

A

edema

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9
Q

heart failure elevates venous pressure and this greatly affects which of the starling forces

A

hydrostatic pressure of the capillary (Pc)

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10
Q

capillary osmotic pressure would be greatly affected by a decrease of ___ in the blood which could be due to starvation or liver failure

A

albumin

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11
Q

how much lymph fluid re-enters the subclavian vein per day

A

2-3 liters

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12
Q

what happens to vessels (via local metabolic control) when metabolites are high and O2 is low in tissue because of increased metabolic rate

A

ACTIVE HYPEREMIA: arteriole SM and precapillary sphincter relaxation to allow more blood flow

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13
Q

what is reactive hyperemia

A

vascular obstruction leads to metabolite build up –> vasodilation

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14
Q

when capillaries dilate for metabolic reasons, what are the upstream effects of the change in blood flow ?

A

flow in arterioles increases (shear force) causing NO release which leads to vasodilation

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15
Q

sympathetics have what effect on vasculature

A

vasoconstriction

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16
Q

what does serotonin do to vasculature

A

vasoconstriction (after damage)

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17
Q

what do histamine and bradykinin do to vasculature

A

arteriolar vasodilation (and edema)

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18
Q

whats the main mechanism of control for both cerebral and coronary circulation

A

metabolic

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19
Q

pulmonary arteries have much more ___ than systemic arteries. thus small pressure change significantly dilates these to reduce resistance and maintain low pressure.

A

compliant

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20
Q

how does sympathetic stimulation effect blood flow to skin

A

decreases

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21
Q

how does sympathetic stimulation effect blood flow to skeletal muscle

A

increase

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22
Q

what type of shunt is present if blood is passing from systemic veins to systemic arteries without passing lung tissue

A

right to left

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23
Q

what type of shunt is present if blood is passing from systemic arteries to systemic veins without passing through a capillary bed

A

left to right

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24
Q

when vascular SM is stretched, it contracts according to ____. this means when BP increases, there is vasoconstriction in order to keep ___ constant.

A

myogenic hypothesis, flow

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25
Q

what are the metabolites which can produce vasodilation via metabolic hypothesis of autoregulation

A

CO2, lactate, H+, K+, adenosine

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26
Q

what is an arterial pressure control mechanism thats rapid, neurally mediated, influences both heart and vasculature

A

baroreceptor (pressure sensor) reflex

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27
Q

what is an arterial pressure control mechanism thats slow and controlled mainly by the kidneys

A

hormonal control

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28
Q

where do we find baroreceptors for arterial pressure

A

carotid sinus, aortic arch

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29
Q

when do carotid and aortic baroreceptors increase their firing rate

A

in response to increase vascular wall stretch

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30
Q

whats the difference between carotid sinus and carotid body

A

body- senses blood gas

sinus- senses blood pressure

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31
Q

where do baroreceptors send their messages

A

vasomotor center in medulla

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32
Q

increased firing rate of baroreceptors (in response to pressure increase) causes an increase in what kind of response

A

parasympathetic (vagus)

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33
Q

how do we calculate CO

A 
CO = BP/TPR
CO = SV*HR
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34
Q

how do we find the ejection fraction of the heart

A

EF = SV/EDV

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35
Q

what does the amount of total peripheral resistance depend on

A

sympathetic stimulation of arterioles

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36
Q

what effect does sympathetic stimulation have on the kidney

A

fluid retention (afferent arteriolar constrict, renin secreted)

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37
Q

how does parasympathetic system slow the heart rate

A

inhibitory signal to SA node

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38
Q

what enzyme is secreted by the juxtomerular cells in the kidney in response to drop in BP

A

renin

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39
Q

what does renin do?

A

angiotensinogen –> angiotensin I (in blood)

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40
Q

where does ACE convert angiotensin I to angiotensin II

A

lungs

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41
Q

what does angiotensin II do

A

causes adrenal cortex to secrete aldosterone, increase thirst, ADH secretion… all to raise BP

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42
Q

what does aldosterone do?

A

Na and water retention by kidney (inc TPR)

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43
Q

if BP is dropping to the point where we get cerebral ischemia, then vasomotor center increases sympathetic constriction to body to get blood flow to brain. what do we call this?

A

cushing reaction

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44
Q

what are the two triggers for ADH release

A

angiotenin II

receptors in atria detect low preload

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45
Q

what happens when we have excessive preload of atria and ventricles

A

natriuretic peptide is released

atrial, brain, c type

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46
Q

whats the response to release of natriuretic peptide after sensing excessive preload

A

protects from over dilation by:
arteriolar dilation (decrease TPR)
fluid loss (decrease preload)
inhibit renin

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47
Q

what are rapid and slow responses to hemmorhage

A

rapid: sympathetics increase HR, contractility, and vasoconstriction
slow: renin-angiotensin system attempts to conserve fluid to increase BP

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48
Q

why does our HR, CO, and contractility change when we stand

A

blood pools in veins, decreases arterial pressure, initiates baroreceptor reflex, increases sympathetic outflow

49
Q

term for a significant decrease in BP just after a patient stands up

A

orthostatic hypotension

50
Q

the baroreceptor reflex would be ___ in a patient who has recently lost a lot of fluid and has a BP of 100/72

A

decreased

51
Q

HR 82, EDV 90, ESV 30. what is the ejection fraction?

A

(EDV-ESV)/EDV = (90-30)/90 = 67%

52
Q

in an EKG, during which wave is ventricular K+ conductance increasing in ventricular myocytes

A

t wave

53
Q

during the period of heart cycle when S2 sound is heard, which stage of AP is occurring in atrial muscle

A

stage 4 (resting potential)

54
Q

during which part of an EKG reading would cardiac AP reach the AV node

A

during P wave

55
Q

what shows up on an EKG if coronary flow is fully occluded

A

STEMI

56
Q

what shows up on an EKG if coronary flow is partially occluded

A

UA (unstable angina) or NSTEMI

57
Q

what causes nausea and vomiting in patients experiencing an MI

A

heightened vagal tone

58
Q

what is Lavine’s sign

A

when you ask patient where chest pain is occurring and they point to retrosternal area

59
Q

whats the EKG evidence of a NSTEMI

A

St depression, T wave inversion, elevated enzymes

60
Q

infarction (dead tissue, lack of depolarization) is seen where on EKG

A

q waves

61
Q

injury (deficient blood supply, inability to fully polarize) is seen where on EKG

A

ST segment

62
Q

ischemia (deficient blood supply, impaired repolarization) is seen where on EKG

A

T waves

63
Q

V1-V7 are used to detect MI in what area?

A

anterior wall (LAD)

64
Q

leads II, III, and AVF as well as V3R-V6R are used to detect MI in what area?

A

inferior wall, RV (RCA)

65
Q

Leas I, AvL, V5, and V6 are used to detect MI in what area?

A

lateral wall (circumflex a)

66
Q

V1-V3 are used to detect MI in what area?

A

posterior wall (posterior descending artery)

67
Q

what causes T wave inversion

A

ischemia (can’t repolarize)

68
Q

what is occurring if ST segment elevation persists weeks or months after an MI

A

aneurysm

69
Q

EKG shows inverted t waves and no q waves. patient’s enzymes are up. whats going on?

A

NSTEMI

70
Q

EKG shows inverted t waves and no q waves. patient’s enzymes are normal. whats going on?

A

unstable angina

71
Q

what lab values are increased in a patient who is having an MI

A

WBC, CRP, BNP

72
Q

what are cardiac biomarkers for necrosis

A

troponin I

73
Q

what condition can cause a false positive in cTnT (troponinI) lab values and make it look like patient is having a heart attack when they are not

A

renal failure

74
Q

what binds thrombin to prevent it from working

A

fibrin

75
Q

what is made at the time of injury by endothelial cells to cause vasodilation and limit platelet aggregation

A

PGI2

76
Q

what works like an anticoagulant when bound to thrombin

A

antithrombin III

77
Q

what substance is derived from mast cells and increases antithrombin efficacy

A

heparin

78
Q

what is responsible for inhibiting the tPA inhibitor

A

protein C

79
Q

what does protein C do

A

inh tPA inh
inactivates VIII, V
inh fibrin creation

80
Q

what does tPA do

A

converts plasminogen to plasmin

81
Q

what does plasmin do

A

fibrin lysis

82
Q

what platelet derived factor serves both to promote vascular spasm and cause platelet to become sticky

A

TxA2

83
Q

whats the platelet receptor for TPO ? what would the absence of this receptor cause?

A

mpl

without it we would have way too many platelets because there would be lots of TPO floating around

84
Q

the mutation affects factor V - part of the clotting cascade

A

leiden

85
Q

prolonged bleeding time due to longtime before coagulation factors bind exposed collagen is most likely due to what

A

absence of von willebrand factor

86
Q

what is stored in platelet granules and released upon activation to make the platelet sticky

A

ADP, TxA2

87
Q

during what week of development does the heart beat and circulation begins

A

4

88
Q

at the cranial end of the embryo heart fields develop. these are made of what kind of tissue

A

splanchnic mesoderm

89
Q

primary heart field becomes what

A

atria and L ventricle

90
Q

primary heart field becomes what

A

R ventricle and outflow tract

91
Q

the endocardium, myocardium, and epicardium are all derived from what embryonic tissue

A

splanchnic mesoderm

92
Q

what embryonic structure obliterates to become the transverse sinus

A

dorsal mesocardium

93
Q

what embryonic tissue starts in myelencephalon, migrates through pharyngeal arches, and helps form truncus arterioles and aorticopulmonary septa

A

neural crest cells

94
Q

neural crest cell migration and differentiation is controlled by what

A

RA, Hox, Nf-1, and Pax3

95
Q

bulbus cordisand ventricles of developing heart grow quickly causing heart to fold in on itself (bulboventricular loop) in what direction

A

to the right

96
Q

endocardial cushions that grow together are responsible for forming the AV septa. what are the embryonic tissues that make up these cushions

A

mesoderm, mesenchyme (NC)

97
Q

formation and remodeling of AV cushions is dependent on what signaling method

A

RA

98
Q

what holes/ foramen/ osmium do we find in the septum primum of the atria

A

primum and secundum

99
Q

what holes/ foramen/ osmium do we find in the septum secundum of the atria

A

foramen ovale

100
Q

during fetal circulation blood in the heart is shunted right to left via what pathway between atria

A

through foramen oval and osmium secundum

101
Q

muscular part of ventricular septum forms from the inferior portion of the heart toward the endocardial cushion and is made of what embryonic tissue?

A

splanchnic mesoderm

102
Q

whats the name for the gap between muscular ventricular septum and endocardial cushions

A

interventricular foramen

103
Q

what eventually closes the inter ventricular foramen

A

formation of membranous portion of inter ventricular septum

104
Q

membranous part of inter ventricular septum is made of what embryonic tissue

A

neural crest cells

105
Q

___ form ridges in bulbus cordis and truncus arteriosus. these ridges grow together and then form in a spiral fashion as they grow away from the heart. defects cause difficulty with septation between aorta and pulmonary trunk

A

neural crest cells

106
Q

the membranous portion of the inter ventricular septum is made from neural crest cells and is the portion commonly involved in ventricular septal defects. what other septation does it help form in the herat

A

L ventricle from R atrium

107
Q

valve swellings that will become the semilunar valves and AV valves are made of what embryonic tissue

A

splanchnic mesoderm (endocardium) AND neural crest cells

108
Q

how do valve swellings become valve cusps in the heart

A

blood back flow erodes at the swellings

109
Q

why would ductus arteriosus remain patent in a newborn

A

low O2 content (low bradykinin means no closure) OR PGE2 circulating

110
Q

how do we treat patent ductus arteriosus

A

cox 2 inh (ibuprofen or indomethacin)

111
Q

how can patent ductus arteriosus cause pulmonary edema

A

L to R shunt causes high pressure in R heart and high pressure in lungs —> edema

112
Q

what kind of atrial septal defect is commonly associated with mitral valve cleft

A

osmium primum (septum primum does not fuse with endoardial cushion)

113
Q

what kind of atrial septal defect is caused by failure of septum primum and secundum to fuse

A

probe patent foramen ovale

114
Q

what kind of atrial septal defect occurs most often when foramen ovale overlaps with patency of the septum primum

A

ostium secundum

115
Q

transposition of great vessels means that vessels come from the “wrong” ventricles and this is the result of what kind of developmental failure

A

NC cells do not spiral when forming the aorticopulmonary septum

116
Q

tetralogy of fallot is a failure of neural crest cells and includes what 4 features

A

overriding aorta
ventricular septal defect
pulmonary stenosis
right ventricular hypertrophy

117
Q

is critical pulmonary stenosis a cyanotic or acyanotic defect

A

cyanotic (blood can’t get past pulmonary valve to lungs so it gets no O2)

118
Q

a decrease in preload will have what kind of ionotropic effect on the heart

A

negative (less preload means less efficient actin/myosin overlap)

CardioPulm (6 decks)

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