Flashcards in Circulation 7: Special Circulations I Deck (54):
Describe when you hear the 3rd and 4th heart sounds.
not heard in normal person. 3rd is primarily heard under pathological conditions. just understand caused by turbulent flow during rapid filling, not valve problems.
4th-heard frequ. in normal bc of vigorous atrial contraction causing turbulent flow …can be heart under pathological conditions as well.
Describe how the baroreceptor response alters in a patient with hypertension.
relationship moved to right, less sensitive to pressure changes. for given pressure change, you’d get large response in normal person, but in a hypertensive pt. bc shifted to right, get relatively small response to the same change in pressure. pressure ranges shifted to higher pressure. working at higher pressure range. have “normal” for them baroreceptor response. functioning normally bc shift occurs and resets and higher range.
Does arterial pressure effect capillary hydrostatic pressure? Why/why not?
arterial pressure doesn't sig. effect capillary hydrostatic pressure its because of high pre-capillary resistance and regulation of pre capillary resistance and that is auto-regulation. constant flow through capillaries bc of auto-regulation which maintains pre-capillary resistance so not high pressure going into capillaries. pre-capillary resistance IS auto-regulation. this is mechanism that maintains constant flow downstream.
Describe the relationship between myocardial capillaries and myocytes.
What happens in ischemia?
Myocardial capillaries parallel myocytes at a ratio of ~1 (1 capillary per each myocyte, which places each cell in contact with 3-4 capillaries). However, they are not all functional all the time. During ischemia all capillaries are likely to be recruited.
ischemia causes vasodilation and you open up blood vessels. as increase metabolic activity of heart you recruit more capillaries to bring O to heart.
Describe coronary circulation.
large coronaries on the surface of the heart - they dive into myocardium from epicardium surface and get smaller and smaller as they go toward the endocardial surface.
Of what clinical relevance is the fact that in humans, the right coronary artery is dominant in 50% of the individuals, the left coronary is dominant in 20%, and left and right equally dominant in the remaining 30% ?
those % don't need to know- just there is a large variation. imp. pathological implications. if primarily R coronary person then good chunk of heart infarcted if get clot in R coronary. anatomy.. distribution of blood flow. some rare people only have one coronary,
What is the primary determinant of coronary blood flow?
Aortic pressure is the primary determinant of coronary blood flow. (DETERMINANT, NOT REGULATOR)
(if bp goes up or down, changes blood flow into coronaries) but it doesn't regulate… don't change arterial pressure to change blood flow in heart. if you get low bp get low flow in heart
What is the primary regulator of coronary blood flow?
Regulation of coronary blood flow is primarily due to metabolic activity and changes in arteriolar resistance.
LV tissue pressure will influence left or right coronary blood flow more? Why?
Left coronary blood flow is more influenced by LV (tissue) pressure than right coronary blood flow.
(tissue pressure-local regulatory mech. but this not regulating blood flow just effecting blood flow. you cant change tissue pressure, this is just effect of strong LV contraction.)
When does the highest tissue pressure occur? What are the implications for this?
The highest tissue pressure occurs during early systole. Thus, left coronary blood flow may actually reverse in early systole.
early systole- isovlolumic contraction occurring. mitral valve closes and large increase in pressure.
Draw the normal aortic pressure curve over time. Label each peak/opening/closing of valves.
this is normal aortic pressure… opening of aortic valve, not mitral valve (talking about arterial pressure) isotonic ejection, peak. rapid, the declines, closure of aortic valve then diastolic run off as diastolic declines- in arterial system
When aortic valve closes and then there is a diastolic run off as diastolic pressure decreases, what is going on in the LV ventricle in regards to pressure and blood flow? Why?/how?
LV pressure going up… (dont see but increase till meet afterload) during that large increase in pressure, LV blood flow actually goes down bc ventricle squeezing so hard it can actually squeeze blood out of coronaries momentarily. its normal
During systole, when blood flows out of aorta through coronary cusps, describe blood flow in regards to coronaries.
Draw a graph for both R and L coronary arteries over time (corresponding with the aortic pressure graph).
What happens when the aortic valve closes? (What's going on in the LV? arterial pressure? how does this affect coronaries?
not much blood flow into those coronary openings. why? bc such large rush of blood that lateral pressure not that great to push blood in.
tissue pressure compression of LV. squeezing lots of those vessels closed.
when aortic valve closes, high arterial pressure. where is tissue pressure? LV tissue pressure going to 0. blood flow into LV bc of high arterial pressure…LV pressure dropping bc relaxing but still high arterial pressure so its now easy for blood to be squeezed or flow into coronaries. and have secondary pump/recoil of aortic wall pushing blood into those coronaries. not much blood flow into coronaries during systole but lots of blood flow flowing in during diastole.
When does most blood flow into coronaries? Diastole or systole?
When does maximal left coronary blood flow occur?
Maximal left coronary blood flow occurs in early diastole when tissue pressure falls to ~0.
not much blood flow into coronaries during systole but lots of blood flow flowing in during diastole.
tissue pressure compression of LV. squeezing lots of those vessels closed.
when aortic valve closes, high arterial pressure. LV tissue pressure going to 0. blood flow into LV bc of high arterial pressure…LV pressure dropping bc relaxing but still high arterial pressure so its now easy for blood to be squeezed or flow into coronaries (during diastole)
Approximately 60-65% of coronary blood perfusion to the LV myocardium occurs during diastole, while the remainder occurs during systole.
If diastolic arterial pressure started to fall below 50mmHg what would this signify?
What will be affected?
hemorrhage or shock (where have low bp)
anything that drops arterial pressure below 50 you could become ischemic bc most of LV blood flow occurs during diastole.
if diastolic too low then diastolic coronary perfusion is impaired (most of coronary blood perfusion to LV myocardium occurs during diastole) . suffer chances of having heart attack if diastolic pressure drops too low.
Describe how R coronary differs from L coronary artery. Why this difference?
R coronary not that much diff then arterial pressure. equal blood flow during systole and diastole. its bc RV does not generate whole lot of pressure. only about 25 mmHg maximum. doesn't generate enough tissue pressure to impede blood flow and velocity of blood flow from RV is no where near LV. no coronary on pulmonary artery so just tissue pressure mainly on RV that is low that allows perfusion during systole and diastole.
Where is cardiac diastolic pressure greatest? Epicardium or endocardium?
What are the implications for this?
Cardiac diastolic pressure is greater near the endocardium and least near the epicardium due to tissue pressure generated during systole. .
that pressure along inside of endocardial lining of the wall is quite high during diastole. (diastole pressure around 8 or 10 mmHg) pressure on outside of heart is 0. at EDV when heart filled with blood diastolic pressure significant- 8 or 10. so vessels along endocardial surface compressed more than epicardium.
Therefore, endocardial vessels are more compressed than epicardial vessels.
Under normal conditions blood flow to endocardium and epicardium is about equal even though diastolic pressure is greater near the endocardium. Why is blood flow about equal?
because endocardial resistance vessels are more dilated than epicardial resistance vessels.
normally do get equal flow on epicardium and endocardium even tho diastolic pressure on endocardium is greater bc getting dilation of endocardial vessels.
Under abnormal conditions like aortic valve stenosis, regurgitation or congestive heart failure, why is diastolic pressure elevated? What can result?
under abnormal conditions such as aortic valve stenosis, regurgitation or congestive heart failure (where cardiac diastolic pressure is abnormally elevated- bc don't eject all of blood out of LV with stenosis and after load leaves behind more blood… if raise after load you raise ESV. leaving more blood behind. so volume in ventricle greater and so is pressure. end-systolic pressure higher and now when heart fills at even higher end diastolic pressure.)
the greater endocardial tissue pressure can reduce coronary blood flow and produce subendocardial ischemia.
What might happen when diastolic coronary bp falls? When might this happen?
Also, when diastolic coronary blood pressure falls, such as in severe hypotension or partial coronary occlusion, endocardial blood flow will be restricted more than epicardial blood flow.
As a result, the endocardium is more at risk of ischemia than the epicardium. (its more compressed)
What is regurgitation? Congestive heart failure? How does this affect pressure?
regurgitation (through aortic valve back into LV) LV diastolic pressure much elevated.
congestive heart failure-heart congested w blood. end-diastolic pressure elevated. cause compression of endocardial vessels so can produce sub-endocardial ischemia.
Why might you see an ST segment depression on an EKG? What could this signify?
by causing ischemia on endocardial surface, it creates a vector that produces a depression of ST segment. that vector is specific. inferior leads have depression of ST segment
What are some ways you might get ischemia of the endocardial vessels?
increasing pressure in ventricle
coronary diastolic bp falls (shock) partial coronary occlusion, clot, whenever flow is more resistricted
(this is why ischemia or MI caused on endocardial surface first- starts on endocardial surface and then if goes long enough it could become transmural.
What are some neural determinants of coronary blood flow?
don’t influence blood flow too much. v weak vasoconstriction. almost no alpha receptors on coronaries.
Sympathetic adrenergic stimulation activates alpha (α) receptors in the coronaries (inducing weak vasoconstriction).
neural POV-vagus weak vasodilator. sym. vasoconstriction almost nonexistant in coronaries and overriding effect is this metabolic activity which vasodilates.
Describe the role of B-1 adernergic receptors on pacemaker cells and myocardium. What stimulates this response?
(Neural determinants of coronary blood flow)
β-1 adrenergic receptors on pacemaker cells and myocardium cause a strong over-riding coronary vasodilation due to increases in metabolism
Describe the role of B-2 adernergic receptors on coronary smooth muscle?
Coronary smooth muscle also has β-2 adrenergic receptors that mediate vasodilation, but they are less sensitive to NE (sympathetic) stimulation.
Describe the NO-mediated effect on endothelial cells in coronaries. What 2 ways is NO released?
if hold metabolism constant and stimulate vagus can see some vasodilation through NO and can be blocked by atropine. -so muscarinic receptor. vagally induced NO. not major mech. but other mech- blood flow increases through vessel it does release NO from endothelial cells-does play role in vasodilation in coronaries when exercise and increase blood flow through coronaries, does release directly NO from endothelial cells
If the heart is paced at constant rate (to maintain metabolism constant), vagal stimulation results in coronary vasodilation that can be blocked by atropine, suggesting an acetylcholine effect probably mediated via release of nitric oxide (NO) from endothelial cells.
What 3 factors influence metabolic vasodilation of coronaries?
3 factors that influence metabolic vasodilation of coronaries. those are:
HR, beta1 stimulation, contractility (beta1 stimulation) afterload -increase coronary blood flow, cardiac O consumption
beta 1 stimulation acts indirectly through these mech. to increase metabolism to increase blood flow.
What is the major factor in regulation of coronary blood flow?
Describe the relationship between coronary blood flow and myocardial metabolic activity on a graph.
What are the implications for cardiac patients?
The relationship between coronary blood flow and myocardial metabolic activity is LINEAR
increase myocardial metabolism = decrease coronary resistance = increase coronary blood flow
bc most of the therapy that goes into managing cardiac patents is to keep oxygen consumption down. these patients already have reduction in coronary blood flow. don't want to increase myocardial O consumption w a need for O bc they cant get the supply.
What are metabolic substrates for the heart? What are the implications of this?
Metabolic substrates for heart are: 1) fatty acids (60%), 2) carbohydrates (35-40%), and 3) others, like ketones, lactate and proteins. The high fatty acid metabolism makes the heart a particularly large consumer of oxygen (O2).
resting conditions-free fatty acids that it mostly metabolizes. implication is that fatty acids take a lot of O to metabolize. can metabolism more carbs during exercise (glucose) O required to break down fats.
Why is O2 supply to the heart flow limited? How do you increase O2 consumption of the heart?
What are the implications for patients with coronary disease?
O2 supply to the heart is flow limited because most of the O2 (~80%) is removed from blood during its one passage through the heart. Therefore, if O2 consumption of the heart increases, then coronary blood flow must increase (or ischemia results).
O2 to heart is flow limited. CAN’T extract more O like skeletal muscle. extracts about 80 percent w one pass of heart. flow limited means if it needs more O it has to get it from additional flow. coronaries have to dilate and if you have coronary disease you cant dilate. increase demand but cant increase supply thats ischemia and infarction. thats whole basis of pathology. so if O2 consumption increases then coronary flow must increase or ischemia
O2 consumption related to work of heart.
PV loops - area under curve is work of heart.
Define cardiac work. What does cardiac work affect?
How might you increase work?
Cardiac Work = mean arterial pressure (force) x systolic stroke volume (distance).
increase work by MAP (hypertension or any after load really, stenosis) or increase SV or do both
Myocardial oxygen consumption can be approximated by cardiac work.
Pressure work versus Volume work: Which one consumes more oxygen?
Case 1: stroke volume = 60 arterial pressure = 100
Case 2: stroke volume = 100 arterial pressure = 60
Describe how this pertains to hypertension.
Pressure work consumes much more oxygen than volume work.
Hypertension causes a disproportionate increase in oxygen consumption. w hypertension… work goes up. pressure volume loop- after load up here, then you have lot more isovolumic contraction to generate. this is big increase in O consumption. this can be result of hypertension, high diastolic pressure or any sort of after load that prevents heart from shortening (could be aortic stenosis or cardiac myopathy.
hypertension-has to do with interaction of actin/myosin and latching. production of ATP enormous during isometric contraction. not shortening but its making and breaking cross bridges like crazy to try to overcome this force and infinite after load. referred to as internal work of the heart. actual ejection of volume is external work of heart. 2 together make up total work of heart.
danger of hypertension-uses way more O bc generates large isometric force to open aortic valve.
What factors determine the balance of myocardial oxygen supply and demand? Draw a scale.
myocardial oxygen supply= myocardial blood flow x arterial oxygen content
myocardial blood flow:
1) diastolic perfusion pressure (perfusing LV)
2) coronary vascular resistance
(talking about LV… coronaries and their ability to vasodilate. resistance to those coronaries.)
Myocardial oxygen demand:
1) afterload (greater isometric force that you have to generate that resists shortening, lots of O consumption)
2) HR (more beats, more ATP, more O)
3) contractility (more Ca more cross bridges more ATP more O)
What happens if you have arterial sclerosis or a lesion?
then can't vasodilate and get the supply you need to meet the demand
Discuss coronary vascular resistance. External compression and intrinsic regulation.
external compression can influence (strong contraction trying to overcome after load will squeeze those coronaries along endocardial surface) increase resistance
intrinsic factors- normally metabolically dilates heart. NO from endothelial cells. neural innervation is minimal.
Discuss O2 carrying capacity.
factor in myocardial oxygen supply
O carry capacity of blood-how much hemoglobin and O content in atmosphere. if hemoglobin goes down, and lose RBC then supply goes down.
How can you control demand so that a limited supply can meet the demand?
those are controlled. give beta blockers to keep HR down and contractility down and lower bp to keep after load down. to keep O consumption down so limited supply can meet the demand.
Describe ischemia in regards to supply/demand of O.
Myocardial ischemia results from the imbalance between oxygen supply and oxygen demand. This creates a RELATIVE lack of blood flow.
Excessive O2 demand is never a primary cause of ischemia.
normally coronary perfusion then you can never cause ischemia in the heart. wont become ischemic if over-exercise.
if demand is higher you get ischemia..
Describe collateral circulation. Describe how they come into play in sudden infarction vs gradual obstruction of a coronary artery.
The normal human heart has collateral vessels that are insufficient to prevent sudden infarction.
In response to GRADUAL obstruction of a coronary artery, however, collateral vessels can grow enough to restore an adequate blood supply to the myocardium. This process involves a complex sequence of vessel injury, inflammation, and cellular proliferation. The newly formed vessels have considerable vasomotor capability. Thus, they can provide some protection against myocardial ischemia
collateral circulation-overlap, perfusion from L and R coronary perfuse same cells. if block blood flow from one coronary artery, still have flow from other coronary artery… nice to have collateral circulation. angiogenesis-grow additional blood vessels.
if you have heart attack do moderate exercise bc it stimulates angiogenesis to the ischemic area
What is coronary "steal"?
Vascular bed #1 contains atherosclerotic plaques
Vascular bed #2 has no obstruction.
Describe these beds when compensated (no coronary "steal", and when uncompensated "steal")
Under certain conditions, an increase in blood flow in one region of the heart can cause a decrease in blood flow in another region.
Vascular bed #1 contains atherosclerotic plaques which limit blood flow downstream from the lesion, resulting in ischemia. As a result, the arteriolar resistance to this region of tissue is maximally vasodilated to compensate for the low blood flow. Vascular bed #2 has no obstruction and therefore exhibits normal blood flow and vascular tone, i.e. arteriolar resistance is relatively vasocontricted.
Coronary “steal” (uncompensated): During exercise (increased cardiac work) or if a vasodilating agent is administered, the normal (non-ischemic) region (vascular bed #2) vasodilates. Because the ischemic region (vascular bed #1) is maximally vasodilated, it cannot further dilate. As a result of the decrease in arteriole resistance in vascular bed #2, blood flow increases through this region and “steals” blood flow from vascular bed #1, producing more severe ischemia in vascular bed #1.
What are clinical manifestations of coronary "steal"?
Peripheral Arterial Disease (PAD) - claudication (limping) is pain in the calf or thigh muscle that occurs after walking a certain distance, such as a block or two. The pain stops after a short rest period. same mechanism. lesion in artery in lower leg. exercise. normal skeletal muscle vasodilates, metabolically and that shunts blood away from the lesioned area causing it to become ischemic, lactate build up, get pain. stop..then vasodilated-area now constricts bc metabolic activity washed away..blood shunted back to area that has lesion, feel better then start walking again. serious problem bc causes skeletal muscle to become fibrotic over years. can bypass it w vein… doesn't work well. temporary and becomes permanent damage to muscle. not just lack of blood flow bc even when bypass it still doesn't work well. PAD associated with coronary disease bc coronaries are peripheral vessels. they go together in patients often.
(causes changes in bp, EKG. heart ischemic bc of coronary steal to normal tissue
pt who cant run can have stress test w adenosine to vasodilate coronary. inject to heart and see on EKG if heart is becoming stressed, or ischemic as a result of this same mechanism.
Describe skeletal muscle circulation.
How much cardiac output goes to skeletal muscle? Why?
What is the extent of vascular supply related to?
In the resting human, about 20% of cardiac output goes to skeletal muscle. This large cardiac output to muscle occurs not because blood flow is exceptionally high in resting muscle, but because skeletal muscle makes up about 40% of body mass.
Therefore, skeletal muscle constitutes the largest vascular bed in the body, emphasizing its importance in regulation of blood pressure. skeletal muscle blood flow low in resting. can increase up to 20x. largest vascular system in body- why it effects diastolic pressure and maintains that as low bc it vasodilates. large influence on bp.
The extent of vascular supply is related to the type of muscle. Tonic muscle has about 5 times phasic muscle.
When do you see active hyperemia in skeletal muscle? What does this indicate about skeletal muscle flow reserve relative to blood flow at rest? What does this say about vascular tone? What brings about vascular tone?
Describe resting/non-resting state. What influences dominate when resting? What about when contracting? What is the purpose?
Active Hyperemia – increase in blood flow due to metabolic activity. If muscle contraction is occurring during whole body exercise (e.g., running), more than 80% of cardiac output can be directed to the contracting muscles.
Therefore, skeletal muscle has a very large flow reserve (or capacity) relative to its blood flow at rest, indicating that the vasculature in resting muscle has a high degree of vascular tone. This resting tone is brought about by the interplay between vasoconstrictor (e.g., sympathetic adrenergic and myogenic influences) and vasodilator influences (e.g., NO production, and interstitial adenosine, and K+ concentrations).
In the resting state, the vasoconstrictor influences dominate, whereas during muscle contraction, vasodilator influences dominate to increase oxygen delivery to the contracting muscle fibers and to remove metabolic waste products (e.g., lactate, H+, CO2) that accumulate.
Describe arterial circulation in skeletal muscle. What happens to tissue when muscle contracts, what results?
Describe arterial circulation in skeletal muscle during dynamic exercise in regards to compression and free flow. How does this affect resistance?
(What determines resistance?)
When muscle contracts tissue pressure increases, compressing blood vessels.
With dynamic exercise, there is an alternation between extravascular compression and free flow (figure). On average, however, there is a profound reduction in resistance to blood flow to due metabolic vasodilation.
The reduction of vascular resistance (vasodilation) during dynamic exercise results from local metabolic control, in spite of the increase in central sympathetic nerve activity (vasoconstriction).
Discuss what happens in isometric exercise in regards to extravascular compression, blood flow, and vascular resistance. How is CO and arterial pressure affected?
When exercise is isometric, the extravascular compression is similarly sustained.
At isometric tensions of ~70% of maximum or above, blood flow through the contracting muscle approaches zero. Consequently, these isometric tensions cannot be sustained for more than 1-2 min.
During isometric exercise, vascular resistance increases and cardiac output rises, thus, there is often a marked increase in arterial pressure (afterload).
Describe venous circulation in skeletal muscle in regards to muscle contraction.
How does this blood get back to the heart?
Muscle contraction “pumps” blood out the muscle veins. This is assisted by venous valves which maintain unidirectional flow back to the heart. Changes in maintained muscle tone can redistribute considerable amount of blood from legs and abdomen.
What happens in inspiration? Expiration?
decreases in thoracic pressure and increases in abdominal pressure during inspiration distend the thoracic veins and compress the abdominal veins, thereby increasing venous return. Expiration causes the opposite actions.
How does sympathetic activity affect venous return?
Sympathetic venoconstriction increases venous vascular tone; reduces venous capacitance and increases venous return.
venoconstriction- shifts venous function curve up and to the right, increases cardiac function by increasing preload, reduces venous capacitance, making system smaller-reducing fullness by shifting blood back to the heart and arterial system, this increases venous return.
Describe neurohumoral control of skeletal muscle circulation -
What is skeletal muscle vascular primarily innervated by?
What causes vasoconstriction?
What kind of receptors are involved to induce vasodilation? What is released on these receptors and what is the downstream effect?
Skeletal muscle vasculature is primarily innervated by sympathetic adrenergic fibers.
Norepinephrine release binds to alpha-adrenergic receptors to cause vasoconstriction. Under resting conditions, a significant portion of the vascular tone is generated by sympathetic activity.
Skeletal muscle arteries also are innervated by sympathetic cholinergic nerves that release acetylcholine. Acetylcholine causes vasodilation by acting on muscarinic receptors on endothelial cells coupled to nitric oxide (NO) production. Activation of this mechanism in anticipation of exercise and during exercise can contribute to the increase in blood flow associated with exercise.
What does epinephrine released from the adrenal medualla cause? What type of receptors does it act on on high/low concentrations? What is the different effect at high/low concentrations?
Epinephrine released from the adrenal medulla causes vasodilation at low concentrations through activation of beta (β)-2 adrenergic receptors on vessels. At higher concentration, epinephrine causes vasoconstriction through activation of alpha (α) adrenergic receptors.
What would happen if you took an alpha receptor blocking agent? When might you prescribe an alpha receptor blocking agent?
alpha always for vasoconstriction. if took alpha receptor blocking agent, then bp would drop bc alpha receptors cause some amount of peripheral resistance always bc of sympathetic tone and thats why alpha blockers given to patients with hypertension- to passively vasodilate time.
What are the two mechanisms to release NO?
(sympathetic cholinergics) - endothelial release of NO
shear stress across endothelial cells during blood flow causing release of NO