Review CV Physiology 1

Why doe we weight diastolic more than systolic in MAP calculation?

Because at rest we spend 2/3 of the time in the diastolic phase so this should be more heavily weighted than the systolic pressure.

How come we can chronically elevated blood pressure in someone with HTN?

Because the set-point changes and readjusts to the new norm.

What is the MVO2 give a CBF or 100, arterial O2 of .2 and a venous O2 of .1?

CBF= MVO2/a-v MVO2=CBF (A-V) MVO2= 100(.1) MVO2= 10ml O2/min

What effect does venous pooling have on cardiac output and MAP? Why?

CO and MAP go down. This is because venous return decreases, this decreases CVP which decreases EDV. EDV decreases stroke volume. CO is equal to the SV x the HR so if SV decreases than the CO also decreases. MAP is then equal to CO x TPR so the MAP decreases.

What is CO?

CO is stroke volume x heart rate. During the early stages of exercise CO is maintained by increase in HR and SV. During the late stages of exercise the CO is maintained by an increase in HR only as the SV plateaus.

How can we calculate CO from arterial and venous content?

CO= Rate of O2 consumption/ Arterial02-Venous 02.

The patient's resting BP is 160/95 and HR is 85 BPM. If his cardiac output is 5L/min what is the TPR?

CO=MAP x TPR. 1. Find MAP: DBP+ 1/3 PP 95+22= 117 2. CO=MAP x TPR. TPR= MAP/CO. TPR= 117/5= 23.4 mmHg x min/L

What is CVP?

CVP is central venous pressure or how much blood is coming back to the central point. It is a function of VR so when VR decreases so does CVP. This effects filling pressure and thus EDV.

What are the exchange vessels?

Capillaries

What happens to CVP during exercise?

Central venous pressure increases because of venous constriction from sympathetic activity, muscle pump activity and abdominothoracic pump.

What is compliance? Who do we calculate it?

Compliance is the ability of a vessel to distend and increase volume with increasing transmural pressure. It is calculated via the change in volume/change in pressure. C=DeltaV/DeltaP

Discuss coronary reserve. When is this implicated? How is this implicated in a stenotic lesion and exercise?

Coronary reserve is the difference between the maximal coronary flow and the resting coronary flow. Coronary flow reserve (CFR) is the maximum increase in blood flow through the coronary arteries above the normal resting volume. We have the ability to auto regulate and to cause vasodilation which can increases the coronary blood flow. When there is a stenotic lesion, downstream from the stenosis even at rest there is vasodilation occurring to preserve the profusion of the myocardium. Upon exertion autoregulation also usually causes vasodilation of the coronary arteries (using the coronary reserve). If there is already vasodilation from a stenotic lesions there is no more compensation that can occur and this leads to a problem with O2 delivery during exercise and results in angina. The problem is it is near maximally dilated just so you can have adequate profusion at rest. Already using much of that coronary reserve at rest.

What happens to TPR during exercise?

It decreases overall. This is because there is a balance of sympathetically mediated vasoconstriction of non-active tissue beds and autoregulation resulting in vasodilation of exercising skeletal m.

What happens to CO during exercise?

It increases. During exercise CO increases because both SV and HR increase. The HR increases because there is increased sympathetic output. The SV increases because there is increased contractility due to sympathetic outflow and increased EDV due to muscle pump, cardio-thoracic pump, and venoconstriction.

In which quadrant would we expect the mean QRS vector to be following an LV infarction? What is the general rule for this?

It would be right axis deviation. Shift towards the hypertrophy and away from infarction. The left side is infarcted and there is decreased depolarization due to loss of electrical activity from the infarcted cells. This results in shift towards the right.

What would happen if a patient with a LAD stenosis were prescribed a vasodilator? Would blood flow to the ischemic tissue of the stenosis likely increase or decrease? Why?

It would likely decrease. If arterioles downstream of the stenosis are already maximally dilated in effort to compensate for ischemia, vasodilator action is likely to only impact other vessels in non-ischemic vascular beds. This may result in the additional reduction in perfusion pressure, which can further compromise the blood flow to the ischemic tissue downstream of the stenosis. This is called coronary steal. Coronary steal (with its symptoms termed coronary steal syndrome or cardiac steal syndrome) is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood directed to the coronary circulation.

What is MAP?

MAP is CO x TPR

If the patients blood pressure was 95/65 what is her MAP?

MAP= DBP +1/3 PP 65+ 1/3(30) 65+ 10 75mmHg

How can we calculate the MAP from the blood pressure?

MAP= diastolic pressure plus 1/3 the systolic pressure.

What is in-parallel?

Most of the blood supply to the major organs because it leaves the aorta and then distributed to major organs through larges veins which originated form the aorta. Here major distributing arteries are nin-paralle with eat other.

What does nitroglycerin do to arterioles and veins? How does this interact with the normal baroreceptor reflex.

Nitroglycerin promotes vascular smooth muscle relaxation. It acts on both arteries and veins however Veins>arterioles. This leads to dilation of venous and arterial beds. This opposes the normal reflex response which promotes vasoconstriction of arterioles and veins when you stand up which further promotes pooling within the L.E. veins and decreases VR. Normally the baroreceptor response would fix when standing but when there is nitroglycerin on board this blocks the reflex.

Does the baroreceptor reflex just respond to MAP? When is this important? What is the result?

No it also responds to pulse pressure. This is important because if both the pulse pressure and the MAP drop such as in hemorrhagic shock the response will be amplified.

What can pulse pressure tell us about the state of the aorta?

Normal the aorta is high in elastin and low in collagen so it is very distensible. As the blood is pumped out during systole it gives way and this lowers the pulse pressure. When changes occur (some with age) such that the aorta is now more collagen and stiffer the pulse pressure will increase. The rise in aortic pressure from its diastolic to systolic value is determined by the compliance of the aorta as well as the ventricular stroke volume. In the arterial system, the aorta has the highest compliance, due in part to a relatively greater proportion of elastin fibers versus smooth muscle and collagen. This serves the important function of dampening the pulsatile output of the left ventricle, thereby reducing the pulse pressure (systolic minus diastolic arterial pressure). If the aorta were a rigid tube, the pulse pressure would be very high. Because the aorta is compliant, as blood is ejected into the aorta, the walls of the aorta expand to accommodate the increase in blood volume. As the aorta expands, the increase in pressure is determined by the compliance of the aorta at that particular range of volumes. The more compliant the aorta, the smaller the pressure change during ventricular ejection (i.e., smaller pulse pressure) (see figure). Therefore, aortic compliance is a major determinant, along with stroke volume, of the pulse pressure.

What is Ohm's Law? How does relate to the patent in the standing up case?

Ohm's low can be applied to the local blood flow and it says that flow= pressure gradient/resistance. Such that the pressure gradient is directly proportional and the resistance to flow is indirectly proportional. If we have a decrease in the pressure gradient and a decrease in resistance to flow the overall effect is decreased flow. There is a net reduction of flow and inadequate 02 supply which lead to loss of consciousness. Note this is local effect. The total would be MAP= CO x TPR.

Which cardiac layer is generally first to be compromised during ischemic conditions?

Subendocardium. The vascular supply has to come through the myocardium to get to the endocardium so this is the last in the chain and thus the first to undergo ischemia.

What is the Fick Calculation? When can we use it?

The Fick calculation is used to calculate the myocardial O2 consumption. 1. The myocardial O2 consumption can be calculated by the fick principle if CBF is known and arterial/venous O2 is known. 2. Cardiac output can be calculated if the whole body oxygen consumption and and arterial/venous O2 content is known. q= VO2/a-v02. Q can indicate CO or CBF

What happens to the components of the MAP during exercise?

The SBP rises more than the DBP leading to an increase in pulse pressure. The increased stroke volume increases PP. The MAP increases is due to increases CO but is somewhat offset by a decrease in TPR. As a result it is a mild-moderate change and not directly reflective of the change seen in CO. Vasoconstriction in the inactive vascular beds contributes to maintain MAP to allow for adequate perfusion of active tissues.

Other than cardiac muscle what are some other examples of shifts in blood flow distribution that normally occur with increased physical exertion?

1. Blood flow goes down in the kidneys and GI tract because it is shunted towards the muscles. 2. The majority of the blood supply goes to skeletal muscle. 3. There is also increased profusion to the skin to dissipate the heat generated.

What changes TPR?

1. Changes in blood vessel diameters 2. Viscosity. It is very important to note that SVR can be calculated from MAP and CO, but it is not determined by either of these variables. A more accurate way to view this relationship is that at a given CO, if the MAP is very high, it is because SVR is high. Mathematically, SVR is the dependent variable in the above equations; however, physiologically, SVR and CO are normally the independent variables and MAP is the dependent variable

What increases pulse pressure?

A highly compliant aorta (i.e., less stiff, normal aorta) has a smaller pulse pressure for a given stroke volume into the aorta than a stiff, low compliant aorta. A larger stroke volume produces a larger pulse pressure at any given compliance.

What does afterload and dilated ventricular chambers do to wall-stress? What does this do to Myocardial O2 demand?

Afterload and dilated ventricular chambers will increase the wall stress which increases the myocardial O2 demand. Note aortic stenosis and systemic HTN both increase systemic pressure. Aortic regurgitation increases ventricular radius.

What effects the compliance changes in the aorta?

Aortic compliance decreases with age due to structural changes, thereby producing age-dependent increases in pulse pressure.

Why can we use veins in arterial by-pass grafts?

At higher pressures and volumes the venous compliance is similar to arterial compliance/

What is the normal mechanism by which O2 supply is increased in order to meet the demand of the exercising heart? What is the mechanism?

Autoregulation. When the O2 demand exceeds the O2 supply vasodilation is promoted. This is via active hyperemia: adenosine, increased PCO2, NO, H+, and prostaglandins. Increased tissue metabolism, increases the release of metabolic vasodilators into the ECF. This results in dilation of the arteries. Decreased resistance increases the blood flow. O2 and nutrient supply to the tissues is increased as long as metabolism is increased.

What effects of vasodilators would be beneficial to a patient with exertional angina?

Decreased peripheral resistance, lead to decreased afterload, lead to decreased wall tension, lead to decreased myocardial oxygen demand. If you are dilating systemically then you are decreasing the work the heart has to do just in general.

How come you in the patient case he only experienced angina which physical exercise?

During exercise the HR is increasing which means we will have less O2 delivery to the tissues. When we have a higher HR we spend less time in diastole and thus decrease the flow to the coronary arteries. In someone who has HTN there is increased afterload already so the heart is having to work harder to eject into that high power system. This there is insufficient O2 supply to meet the increased demand during exertion. If there is already a stenotic LAD this leads to ischemia.

Walk through the baroreceptor in the context of normal reflexive response to hypotension?

During hypotension such as standing, the blood pools in the veins which decreases arterial pressure detected by the baroreceptors. This decreases the baroreceptor firing rate. The response to this from the medullary cardiovascular center is to increase the sympathetic outflow and decrease the parasympathetic outflow. This increase in sympathetics effects the heart, the arterioles, and the veins. In the heart it increases HR, Contractility, and cardiac output. In the arterioles it causes constriction increasing TPR, in the veins it causes constriction increasing venous return. All of this contributes to an increase in the arterial pressure toward normal. Slide 18

What is the EDV?

EDV is the preload. It is the volume of blood in the ventricle after diastole and before systole occurs. This also helps determine SV as it is the EDV-ESV

What is a low ejection fraction associated with?

EF is often used as a clinical index to evaluate the the inotropic status of the heart. However, it is important to note that there are circumstances in which EF can be normal, yet the ventricle is in failure. One example is diastolic dysfunction caused by hypertrophy in which filling is impaired because of low ventricular compliance (i.e., "stiff" ventricle) and stroke volume is therefore reduced. In this case, both SV and EDV can be reduced such that EF does not change appreciably. For this reason, low ejection fractions are generally associated with systolic dysfunction rather than diastolic dysfunction.

What is ejection fraction?

Ejection Fraction (EF) is the fraction of blood ejected by the ventricle relative to its end-diastolic volume. This is SV/EDV times 100. Normal is anything above 60%

How come the patient in the case who stood up lost consciousness even though the cerebral circulation is capable of autoregulation in order to maintain consciousness?

Even though resistance to flow can be decreased via autoregulation a sufficient driving force must still be maintained for adequate flow. A sudden and serve drop in MAP is likely below the auto regulatory limit of her cerebral circulation and thus blood flow and 02 was compromised.

What happens to MAP during exercise?

It Increases. MAP=CO x TPR. The CO tends to increase more than the TPR decreases the end result is an increase in MAP. The increases is moderate.

Walk through the factors that increase myocardial O2 supply and the factors that increase O2 demand?

Increase O2 oxygen supply: 1. Diastolic perfusion pressure 2. Coronary vascular resistance: including external compression or intrinsic regulation. 3. O2 carrying-capacity. Increased myocardial oxygen demand: 1. Increased Wall tension 2. Increased HR 3. Increased contractility.

What condition causes a increased afterload? What does this do to O2 demand?

Increased afterload is seen in hypertension. Increased afterload increases wall stress which increases O2 demand.

What is seen in transmural ischemia?

ST elevation.

What EKG findings is seen in subendocardial ischemia?

ST segment depression.

What is SV?

SV is EDV-ESV

What is in series?

Sometimes once in an organ . Once in an organ the vessels are arranged in parallel and in series. A small arteries is series with its two daughter arteries and each of these branches is in parallel to each other.

Walk through the baroreceptor reflex. What is the integration center? What are the firing rates like in HTN versus in decreased VR?

The baroreceptor reflex is located in the aortic and the carotid arteries (baroreceptors are located in the arctic and carotid vessels). The most important arterial baroreceptors are located in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch. It reacts to distention and fires greater when there is more distention and less when there isn't any distention. When volume or filling is low the baroreceptor firing rate is decreased. When volume or pressure is high such as in HTN the firing rate is increased. So after standing the firing rate is decreased. The medullary cardiovascular center is the integration center. Note there is no cerebral input as this is a reflex. These receptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which increases the firing frequency of action potentials generated by the receptors. If arterial blood pressure suddenly falls, decreased stretch of the arterial walls leads to a decrease in receptor firing.

How do the two sites for baroreceptors compare?

The carotid sinus is more sensitive as it detects ranges from 60-120. The arctic arch baroreceptors high a higher threshold. The maximum sensitivity is near the MAP. This makes it so small changes have drastic responses and is the reason why the MAP is relatively well controlled with his reflex.

What is oxygen extraction?

The difference between the arterial O2 content and the venous O2 content.

What is the Laplace's relationship?

The laplace relationship is a determination of wall stress. It says that wall stress is related to transmural pressure, radius, and wall thickness. Wall stress= P x r/2n (where n is wall thickness). Thus systolic ventricular pressure and the radius of the ventricular chamber are proportional to the wall stress. If they increase the wall stress increases. If they decrease the wall stress decreases. The ventricular wall thickness is inversely proportional to the wall stress. So If it increases the wall stress decreases.

What are the capacitance vessels?

The large veins. Venules form larger veins that serve as the primary capacitance vessels of the body - i.e., the site where most of the blood volume is found and where regional blood volume is regulated.

Walk through the distribution of pressures throughout the a-v system.

The mean aortic pressure (solid red line) is about 95 mmHg in a normal individual. The mean blood pressure does not fall very much as the blood flows down the aorta and through large distributing arteries. It is not until the small arteries and arterioles that there is a large fall in mean blood pressure. Approximately 50-70% of the pressure drop along the vasculature occurs within the small arteries and arterioles. By the time blood reaches the capillaries the mean pressure may be 25-30 mmHg, depending upon the organ. The pressure falls further as blood travels into the veins and back to the heart. Pressure within the thoracic vena cava near the right atrium is very close to zero, and fluctuates from a few mmHg negative to positive with respiration.

What is the normal cardiac output? How does this change?

The normal cardiac output is 5L/min. In exercise states this can go up to 25L/min In well trained athletes this can increase tup to 45L/min.

What is the resistance for a series network?

The resistance for a series network is the sum of the individual resistance.

What are the effects of gravity on BP?

There are changes in normal blood volume distribution that occur when moving from supine to standing. The blood volume transfers from the central reservoirs and pools in the highly compliant large veins of the lower extremity. This is because gravity effects a hydrostatic pressure difference, delta H from the heart. This is because the body acts as a fluid column. When the person is lying down (supine position), gravitational forces are similar on the thorax, abdomen and legs because these compartments lie in the same horizontal plane. In this position, venous blood volumes and pressures are distributed evenly throughout the body.When the person suddenly stands upright, gravity acts on the vascular volume causing blood to accumulate in the lower extremities.

What is the effect of nitroglycerin on cardiac tissue? How does this interact with the normal baroreceptor reflex?

There is no effect of nitroglycerin on cardiac tissues. This leads to a normal reflex (baroreceptor) response of increased HR, contractility, and CO when the venous return is decreased such as in orthostatic hypotension. The results is a tachycardia experienced by the patient upon standing.

During what phase of the cardiac cycle doe the left ventricular myocardium revise the majority of the blood flow? What are the factors that affect this?

This occurs during diastole. During systole there are two mechanisms which decrease the flow in or to the coronary arteries thus decreasing the profusion to the ventricular myocardium. 1. The high flow out the left ventricle and into the aorta during systole blocks the openings to the coronary arteries. 2. When the ventricle contracts during systole to lead to ejection, it can obstruct the coronary arteries decreasing the flow.

What types of vessels are responsible for the control of blood pressure in the arterial system?

Together, the small arteries and arterioles represent the primary vessels that are involved in the regulation of arterial blood pressure as well as blood flow within the organ. The larger vessels play virtually no role.

What can veins do in response to pressure?

Veins can accommodate large changes in blood volume with only a small change in pressure.

What does ventricular hypertrophy do to wall stress? What does this do to myocardial O2 demand?

Ventricular hypertrophy decreases the wall stress which leads to a decrease in myocardial O2 demand.

Walk through the baroreceptor reflex for regulation of increased BP.

When there is HTN or increased BP there is increased baroreceptor firing in the carotid arteries and the aorta. This leads to the increase in parasympathetics and decreases in sympathetics from the medullary CV center. The decrease in sympathetic causes vasodilation leading to decreased TPR, decreased force of contraction and decreased HR which decreases CR. The parasympathetic system also works on the SA node to decrease the HR thus decreasing CO. This decrease in CO and decrease in TPR decreases the MAP. Increase in MAP leads to baroreceptor firing rate. Result is a decrease in CO and TPR decreasing MAP.

Walk through why the changes in BP happen as they do when standing up?

When we are supine the arterial pressures at the head, heart, and feet are all very similar. The venous pressure is much lower than that of the arterial pressure but it is also similar between the three locations. When we stand up the difference between the arterial and venous pressure stays the same but it gets redistributed. The head is lower than it was lying down, the heart is about the same, but the pressure in the legs is much higher in both the arteries and the veins. Since the veins are highly compliant as the pressure increases this leads to venous pooling in the lower extremities and decreased venous return. Because venous compliance is high and the veins readily expand with blood, most of the blood volume shift occurs in the veins

Why does walking decrease the venous pressure in the feet?

When we walk or do toe raises versus just standing this decreases the venous pressure for two reasons: the muscle pump and the one-way valves which both facilitate venous return. When we use our muscles this helps the vein pump and move the blood back to the heart. The one way valves that present in the veins prevent back-flow and help increase the venous return.