Final Deck 2 Flashcards
what does first degree AV block look like on ECG
PR segment elongated (>5 little boxes)
Where would we find large clefts in capillary wall
Liver and gut (so water soluble substances can cross)
What is a major. Contributor to osmotic pressure in the blood
Albumin
Whats the largest starling force that influences movement of fluid out of the capillary
Capillary hydrostatic pressure
where in the circulatory system do we usually see starling forces at work allowing fluid passage from a vessel
capillary at arteriolar end
when fluid leads from capillaries into interstitial, how do we get it back into the bloodstream
lymphatics
whats the equation to determine net movement of starling forces
forces out - forces in
Pc+Osmi) - (Pi+Osmc
what condition alters the starling forces
edema
heart failure elevates venous pressure and this greatly affects which of the starling forces
hydrostatic pressure of the capillary (Pc)
capillary osmotic pressure would be greatly affected by a decrease of ___ in the blood which could be due to starvation or liver failure
albumin
how much lymph fluid re-enters the subclavian vein per day
2-3 liters
what happens to vessels (via local metabolic control) when metabolites are high and O2 is low in tissue because of increased metabolic rate
ACTIVE HYPEREMIA: arteriole SM and precapillary sphincter relaxation to allow more blood flow
what is reactive hyperemia
vascular obstruction leads to metabolite build up –> vasodilation
when capillaries dilate for metabolic reasons, what are the upstream effects of the change in blood flow ?
flow in arterioles increases (shear force) causing NO release which leads to vasodilation
sympathetics have what effect on vasculature
vasoconstriction
what does serotonin do to vasculature
vasoconstriction (after damage)
what do histamine and bradykinin do to vasculature
arteriolar vasodilation (and edema)
whats the main mechanism of control for both cerebral and coronary circulation
metabolic
pulmonary arteries have much more ___ than systemic arteries. thus small pressure change significantly dilates these to reduce resistance and maintain low pressure.
compliant
how does sympathetic stimulation effect blood flow to skin
decreases
how does sympathetic stimulation effect blood flow to skeletal muscle
increase
what type of shunt is present if blood is passing from systemic veins to systemic arteries without passing lung tissue
right to left
what type of shunt is present if blood is passing from systemic arteries to systemic veins without passing through a capillary bed
left to right
when vascular SM is stretched, it contracts according to ____. this means when BP increases, there is vasoconstriction in order to keep ___ constant.
myogenic hypothesis, flow
what are the metabolites which can produce vasodilation via metabolic hypothesis of autoregulation
CO2, lactate, H+, K+, adenosine
what is an arterial pressure control mechanism thats rapid, neurally mediated, influences both heart and vasculature
baroreceptor (pressure sensor) reflex
what is an arterial pressure control mechanism thats slow and controlled mainly by the kidneys
hormonal control
where do we find baroreceptors for arterial pressure
carotid sinus, aortic arch
when do carotid and aortic baroreceptors increase their firing rate
in response to increase vascular wall stretch
whats the difference between carotid sinus and carotid body
body- senses blood gas
sinus- senses blood pressure
where do baroreceptors send their messages
vasomotor center in medulla
increased firing rate of baroreceptors (in response to pressure increase) causes an increase in what kind of response
parasympathetic (vagus)
how do we calculate CO
CO = BP/TPR CO = SV*HR
how do we find the ejection fraction of the heart
EF = SV/EDV
what does the amount of total peripheral resistance depend on
sympathetic stimulation of arterioles
what effect does sympathetic stimulation have on the kidney
fluid retention (afferent arteriolar constrict, renin secreted)
how does parasympathetic system slow the heart rate
inhibitory signal to SA node
what enzyme is secreted by the juxtomerular cells in the kidney in response to drop in BP
renin
what does renin do?
angiotensinogen –> angiotensin I (in blood)
where does ACE convert angiotensin I to angiotensin II
lungs
what does angiotensin II do
causes adrenal cortex to secrete aldosterone, increase thirst, ADH secretion… all to raise BP
what does aldosterone do?
Na and water retention by kidney (inc TPR)
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
what are the two triggers for ADH release
angiotenin II
receptors in atria detect low preload
what happens when we have excessive preload of atria and ventricles
natriuretic peptide is released
atrial, brain, c type
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
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
why does our HR, CO, and contractility change when we stand
blood pools in veins, decreases arterial pressure, initiates baroreceptor reflex, increases sympathetic outflow
term for a significant decrease in BP just after a patient stands up
orthostatic hypotension
the baroreceptor reflex would be ___ in a patient who has recently lost a lot of fluid and has a BP of 100/72
decreased
HR 82, EDV 90, ESV 30. what is the ejection fraction?
(EDV-ESV)/EDV = (90-30)/90 = 67%
in an EKG, during which wave is ventricular K+ conductance increasing in ventricular myocytes
t wave
during the period of heart cycle when S2 sound is heard, which stage of AP is occurring in atrial muscle
stage 4 (resting potential)
during which part of an EKG reading would cardiac AP reach the AV node
during P wave
what shows up on an EKG if coronary flow is fully occluded
STEMI
what shows up on an EKG if coronary flow is partially occluded
UA (unstable angina) or NSTEMI
what causes nausea and vomiting in patients experiencing an MI
heightened vagal tone
what is Lavine’s sign
when you ask patient where chest pain is occurring and they point to retrosternal area
whats the EKG evidence of a NSTEMI
St depression, T wave inversion, elevated enzymes
infarction (dead tissue, lack of depolarization) is seen where on EKG
q waves
injury (deficient blood supply, inability to fully polarize) is seen where on EKG
ST segment
ischemia (deficient blood supply, impaired repolarization) is seen where on EKG
T waves
V1-V7 are used to detect MI in what area?
anterior wall (LAD)
leads II, III, and AVF as well as V3R-V6R are used to detect MI in what area?
inferior wall, RV (RCA)
Leas I, AvL, V5, and V6 are used to detect MI in what area?
lateral wall (circumflex a)
V1-V3 are used to detect MI in what area?
posterior wall (posterior descending artery)
what causes T wave inversion
ischemia (can’t repolarize)
what is occurring if ST segment elevation persists weeks or months after an MI
aneurysm
EKG shows inverted t waves and no q waves. patient’s enzymes are up. whats going on?
NSTEMI
EKG shows inverted t waves and no q waves. patient’s enzymes are normal. whats going on?
unstable angina
what lab values are increased in a patient who is having an MI
WBC, CRP, BNP
what are cardiac biomarkers for necrosis
troponin I
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
what binds thrombin to prevent it from working
fibrin
what is made at the time of injury by endothelial cells to cause vasodilation and limit platelet aggregation
PGI2
what works like an anticoagulant when bound to thrombin
antithrombin III
what substance is derived from mast cells and increases antithrombin efficacy
heparin
what is responsible for inhibiting the tPA inhibitor
protein C
what does protein C do
inh tPA inh
inactivates VIII, V
inh fibrin creation
what does tPA do
converts plasminogen to plasmin
what does plasmin do
fibrin lysis
what platelet derived factor serves both to promote vascular spasm and cause platelet to become sticky
TxA2
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
the mutation affects factor V - part of the clotting cascade
leiden
prolonged bleeding time due to longtime before coagulation factors bind exposed collagen is most likely due to what
absence of von willebrand factor
what is stored in platelet granules and released upon activation to make the platelet sticky
ADP, TxA2
during what week of development does the heart beat and circulation begins
4
at the cranial end of the embryo heart fields develop. these are made of what kind of tissue
splanchnic mesoderm
primary heart field becomes what
atria and L ventricle
primary heart field becomes what
R ventricle and outflow tract
the endocardium, myocardium, and epicardium are all derived from what embryonic tissue
splanchnic mesoderm
what embryonic structure obliterates to become the transverse sinus
dorsal mesocardium
what embryonic tissue starts in myelencephalon, migrates through pharyngeal arches, and helps form truncus arterioles and aorticopulmonary septa
neural crest cells
neural crest cell migration and differentiation is controlled by what
RA, Hox, Nf-1, and Pax3
bulbus cordisand ventricles of developing heart grow quickly causing heart to fold in on itself (bulboventricular loop) in what direction
to the right
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)
formation and remodeling of AV cushions is dependent on what signaling method
RA
what holes/ foramen/ osmium do we find in the septum primum of the atria
primum and secundum
what holes/ foramen/ osmium do we find in the septum secundum of the atria
foramen ovale
during fetal circulation blood in the heart is shunted right to left via what pathway between atria
through foramen oval and osmium secundum
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
whats the name for the gap between muscular ventricular septum and endocardial cushions
interventricular foramen
what eventually closes the inter ventricular foramen
formation of membranous portion of inter ventricular septum
membranous part of inter ventricular septum is made of what embryonic tissue
neural crest cells
___ 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
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
valve swellings that will become the semilunar valves and AV valves are made of what embryonic tissue
splanchnic mesoderm (endocardium) AND neural crest cells
how do valve swellings become valve cusps in the heart
blood back flow erodes at the swellings
why would ductus arteriosus remain patent in a newborn
low O2 content (low bradykinin means no closure) OR PGE2 circulating
how do we treat patent ductus arteriosus
cox 2 inh (ibuprofen or indomethacin)
how can patent ductus arteriosus cause pulmonary edema
L to R shunt causes high pressure in R heart and high pressure in lungs —> edema
what kind of atrial septal defect is commonly associated with mitral valve cleft
osmium primum (septum primum does not fuse with endoardial cushion)
what kind of atrial septal defect is caused by failure of septum primum and secundum to fuse
probe patent foramen ovale
what kind of atrial septal defect occurs most often when foramen ovale overlaps with patency of the septum primum
ostium secundum
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
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
is critical pulmonary stenosis a cyanotic or acyanotic defect
cyanotic (blood can’t get past pulmonary valve to lungs so it gets no O2)
a decrease in preload will have what kind of ionotropic effect on the heart
negative (less preload means less efficient actin/myosin overlap)
