Final Deck 2 Flashcards
1
Q
what does first degree AV block look like on ECG
A
PR segment elongated (>5 little boxes)
2
Q
Where would we find large clefts in capillary wall
A
Liver and gut (so water soluble substances can cross)
3
Q
What is a major. Contributor to osmotic pressure in the blood
A
Albumin
4
Q
Whats the largest starling force that influences movement of fluid out of the capillary
A
Capillary hydrostatic pressure
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
6
Q
when fluid leads from capillaries into interstitial, how do we get it back into the bloodstream
A
lymphatics
7
Q
whats the equation to determine net movement of starling forces
A
forces out - forces in
Pc+Osmi) - (Pi+Osmc
8
Q
what condition alters the starling forces
A
edema
9
Q
heart failure elevates venous pressure and this greatly affects which of the starling forces
A
hydrostatic pressure of the capillary (Pc)
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
11
Q
how much lymph fluid re-enters the subclavian vein per day
A
2-3 liters
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
13
Q
what is reactive hyperemia
A
vascular obstruction leads to metabolite build up –> vasodilation
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
15
Q
sympathetics have what effect on vasculature
A
vasoconstriction
16
Q
what does serotonin do to vasculature
A
vasoconstriction (after damage)
17
Q
what do histamine and bradykinin do to vasculature
A
arteriolar vasodilation (and edema)
18
Q
whats the main mechanism of control for both cerebral and coronary circulation
A
metabolic
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
20
Q
how does sympathetic stimulation effect blood flow to skin
A
decreases
21
Q
how does sympathetic stimulation effect blood flow to skeletal muscle
A
increase
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
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
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
25
what are the metabolites which can produce vasodilation via metabolic hypothesis of autoregulation
CO2, lactate, H+, K+, adenosine
26
what is an arterial pressure control mechanism thats rapid, neurally mediated, influences both heart and vasculature
baroreceptor (pressure sensor) reflex
27
what is an arterial pressure control mechanism thats slow and controlled mainly by the kidneys
hormonal control
28
where do we find baroreceptors for arterial pressure
carotid sinus, aortic arch
29
when do carotid and aortic baroreceptors increase their firing rate
in response to increase vascular wall stretch
30
whats the difference between carotid sinus and carotid body
body- senses blood gas
| sinus- senses blood pressure
31
where do baroreceptors send their messages
vasomotor center in medulla
32
increased firing rate of baroreceptors (in response to pressure increase) causes an increase in what kind of response
parasympathetic (vagus)
33
how do we calculate CO
```
CO = BP/TPR
CO = SV*HR
```
34
how do we find the ejection fraction of the heart
EF = SV/EDV
35
what does the amount of total peripheral resistance depend on
sympathetic stimulation of arterioles
36
what effect does sympathetic stimulation have on the kidney
fluid retention (afferent arteriolar constrict, renin secreted)
37
how does parasympathetic system slow the heart rate
inhibitory signal to SA node
38
what enzyme is secreted by the juxtomerular cells in the kidney in response to drop in BP
renin
39
what does renin do?
angiotensinogen --> angiotensin I (in blood)
40
where does ACE convert angiotensin I to angiotensin II
lungs
41
what does angiotensin II do
causes adrenal cortex to secrete aldosterone, increase thirst, ADH secretion... all to raise BP
42
what does aldosterone do?
Na and water retention by kidney (inc TPR)
43
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?
cushing reaction
44
what are the two triggers for ADH release
angiotenin II
| receptors in atria detect low preload
45
what happens when we have excessive preload of atria and ventricles
natriuretic peptide is released
| atrial, brain, c type
46
whats the response to release of natriuretic peptide after sensing excessive preload
protects from over dilation by:
arteriolar dilation (decrease TPR)
fluid loss (decrease preload)
inhibit renin
47
what are rapid and slow responses to hemmorhage
rapid: sympathetics increase HR, contractility, and vasoconstriction
slow: renin-angiotensin system attempts to conserve fluid to increase BP
48
why does our HR, CO, and contractility change when we stand
blood pools in veins, decreases arterial pressure, initiates baroreceptor reflex, increases sympathetic outflow
49
term for a significant decrease in BP just after a patient stands up
orthostatic hypotension
50
the baroreceptor reflex would be ___ in a patient who has recently lost a lot of fluid and has a BP of 100/72
decreased
51
HR 82, EDV 90, ESV 30. what is the ejection fraction?
(EDV-ESV)/EDV = (90-30)/90 = 67%
52
in an EKG, during which wave is ventricular K+ conductance increasing in ventricular myocytes
t wave
53
during the period of heart cycle when S2 sound is heard, which stage of AP is occurring in atrial muscle
stage 4 (resting potential)
54
during which part of an EKG reading would cardiac AP reach the AV node
during P wave
55
what shows up on an EKG if coronary flow is fully occluded
STEMI
56
what shows up on an EKG if coronary flow is partially occluded
UA (unstable angina) or NSTEMI
57
what causes nausea and vomiting in patients experiencing an MI
heightened vagal tone
58
what is Lavine's sign
when you ask patient where chest pain is occurring and they point to retrosternal area
59
whats the EKG evidence of a NSTEMI
St depression, T wave inversion, elevated enzymes
60
infarction (dead tissue, lack of depolarization) is seen where on EKG
q waves
61
injury (deficient blood supply, inability to fully polarize) is seen where on EKG
ST segment
62
ischemia (deficient blood supply, impaired repolarization) is seen where on EKG
T waves
63
V1-V7 are used to detect MI in what area?
anterior wall (LAD)
64
leads II, III, and AVF as well as V3R-V6R are used to detect MI in what area?
inferior wall, RV (RCA)
65
Leas I, AvL, V5, and V6 are used to detect MI in what area?
lateral wall (circumflex a)
66
V1-V3 are used to detect MI in what area?
posterior wall (posterior descending artery)
67
what causes T wave inversion
ischemia (can't repolarize)
68
what is occurring if ST segment elevation persists weeks or months after an MI
aneurysm
69
EKG shows inverted t waves and no q waves. patient's enzymes are up. whats going on?
NSTEMI
70
EKG shows inverted t waves and no q waves. patient's enzymes are normal. whats going on?
unstable angina
71
what lab values are increased in a patient who is having an MI
WBC, CRP, BNP
72
what are cardiac biomarkers for necrosis
troponin I
73
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
renal failure
74
what binds thrombin to prevent it from working
fibrin
75
what is made at the time of injury by endothelial cells to cause vasodilation and limit platelet aggregation
PGI2
76
what works like an anticoagulant when bound to thrombin
antithrombin III
77
what substance is derived from mast cells and increases antithrombin efficacy
heparin
78
what is responsible for inhibiting the tPA inhibitor
protein C
79
what does protein C do
inh tPA inh
inactivates VIII, V
inh fibrin creation
80
what does tPA do
converts plasminogen to plasmin
81
what does plasmin do
fibrin lysis
82
what platelet derived factor serves both to promote vascular spasm and cause platelet to become sticky
TxA2
83
whats the platelet receptor for TPO ? what would the absence of this receptor cause?
mpl
| without it we would have way too many platelets because there would be lots of TPO floating around
84
the mutation affects factor V - part of the clotting cascade
leiden
85
prolonged bleeding time due to longtime before coagulation factors bind exposed collagen is most likely due to what
absence of von willebrand factor
86
what is stored in platelet granules and released upon activation to make the platelet sticky
ADP, TxA2
87
during what week of development does the heart beat and circulation begins
4
88
at the cranial end of the embryo heart fields develop. these are made of what kind of tissue
splanchnic mesoderm
89
primary heart field becomes what
atria and L ventricle
90
primary heart field becomes what
R ventricle and outflow tract
91
the endocardium, myocardium, and epicardium are all derived from what embryonic tissue
splanchnic mesoderm
92
what embryonic structure obliterates to become the transverse sinus
dorsal mesocardium
93
what embryonic tissue starts in myelencephalon, migrates through pharyngeal arches, and helps form truncus arterioles and aorticopulmonary septa
neural crest cells
94
neural crest cell migration and differentiation is controlled by what
RA, Hox, Nf-1, and Pax3
95
bulbus cordisand ventricles of developing heart grow quickly causing heart to fold in on itself (bulboventricular loop) in what direction
to the right
96
endocardial cushions that grow together are responsible for forming the AV septa. what are the embryonic tissues that make up these cushions
mesoderm, mesenchyme (NC)
97
formation and remodeling of AV cushions is dependent on what signaling method
RA
98
what holes/ foramen/ osmium do we find in the septum primum of the atria
primum and secundum
99
what holes/ foramen/ osmium do we find in the septum secundum of the atria
foramen ovale
100
during fetal circulation blood in the heart is shunted right to left via what pathway between atria
through foramen oval and osmium secundum
101
muscular part of ventricular septum forms from the inferior portion of the heart toward the endocardial cushion and is made of what embryonic tissue?
splanchnic mesoderm
102
whats the name for the gap between muscular ventricular septum and endocardial cushions
interventricular foramen
103
what eventually closes the inter ventricular foramen
formation of membranous portion of inter ventricular septum
104
membranous part of inter ventricular septum is made of what embryonic tissue
neural crest cells
105
___ 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
neural crest cells
106
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
L ventricle from R atrium
107
valve swellings that will become the semilunar valves and AV valves are made of what embryonic tissue
splanchnic mesoderm (endocardium) AND neural crest cells
108
how do valve swellings become valve cusps in the heart
blood back flow erodes at the swellings
109
why would ductus arteriosus remain patent in a newborn
low O2 content (low bradykinin means no closure) OR PGE2 circulating
110
how do we treat patent ductus arteriosus
cox 2 inh (ibuprofen or indomethacin)
111
how can patent ductus arteriosus cause pulmonary edema
L to R shunt causes high pressure in R heart and high pressure in lungs ---> edema
112
what kind of atrial septal defect is commonly associated with mitral valve cleft
osmium primum (septum primum does not fuse with endoardial cushion)
113
what kind of atrial septal defect is caused by failure of septum primum and secundum to fuse
probe patent foramen ovale
114
what kind of atrial septal defect occurs most often when foramen ovale overlaps with patency of the septum primum
ostium secundum
115
transposition of great vessels means that vessels come from the "wrong" ventricles and this is the result of what kind of developmental failure
NC cells do not spiral when forming the aorticopulmonary septum
116
tetralogy of fallot is a failure of neural crest cells and includes what 4 features
overriding aorta
ventricular septal defect
pulmonary stenosis
right ventricular hypertrophy
117
is critical pulmonary stenosis a cyanotic or acyanotic defect
cyanotic (blood can't get past pulmonary valve to lungs so it gets no O2)
118
a decrease in preload will have what kind of ionotropic effect on the heart
negative (less preload means less efficient actin/myosin overlap)
