Chapter Nine - Cardiovascular Structure and Function Flashcards

Question

Draw the ventricular pressure-volume loop. What happens at the moments a, b, c, and d?

Answer 1

From b to c: increase in pressure but no volume change (isovolumetric part of the curve)

Answer 2

Graph A: end-diastolic volume for curve 3 is higher than the one for curve 1. They all reach the same pressure to open the valve, but when they get to the end of their contraction, you can see that the volume ejected in 1 is less then in 3. This is the basic Starling relationship (the more the preload, the more the stroke volume) Graph B (change in afterload): in curve 1, it comes to this end-diastolic volume, contracts, blood is ejected and that is our stroke volume. In curve 3, we fill up to the same end-diastolic volume, but the end-systolic pulmonary resistance (afterload) is higher, so a bigger increase in pressure is needed to eject blood, so very quickly the pressure in the systemic circulation overcomes that, so the valve closes and that is our stroke volume. The afterload is higher, so the stroke volume is lower

Answer 3

Smooth muscle layer: helps arteries contract, endothelial layer: in contact directly with the blood, it is very metabolically active, nerve endings: affect smooth muscles, collagen and various other constituants of the blood vessel wall. She will focus on the endothelial layer

Answer 4

Nitric oxyde is responsible for smooth muscle relaxation and therefore vasodilatation, and its lack is responsible for a lot of the problems we see associated in cardiovascular diseases.

Answer 5

Shear stress = friction that blood makes as it travels through the vessel wall. That is a strong positive stimulus to the production of nitric oxide Important: shear stress created by the friction of blood flowing in the vessels, stimulates nitric oxide production, and nitric oxide is a potent vasodilator

Answer 6

↑ CO (↑ HR, ↑ SV) ↑ BP ↑ (a-v) O2 difference Redistribution of blood flow

Answer 7

Important relationship between increase in heart rate and increase work, represented by VO2max. Stroke volume increases around 40-60 % of the VO2max, and after that we cannot get a much bigger stroke volume. So we can’t use the stroke volume relationship to guide how hard we are working, because you can be working harder but your stroke volume will stop going up. In physiotherapy, we use heart rate.

Answer 8

Linear relationship HR and VO2 Borg Scale: Rate exercise intensity 6-20 Used for: exercise prescription monitoring Normal heart rate: 60 to 200, so he just took out a zero

Answer 9

Blood Pressure  Determines flow through the system  BP = TPR x CO  TPR – total peripheral resistance MAP (mean arterial pressure) - R = 8ln/r^4

Answer 10

Blood Pressure Response During Exercise • ↓TPR (vasodilation) * ↑SBP * ↑CO * little change in DBP \* Large individual variability After exercise or activity, we expect the systolic pressure to go up (for an increase in delivery we need higher pressure), so we can deliver blood to working organs. However, we don’t want to see a change in diastolic pressure of more than 10 mm Hg. If we see a pressure drop with activity, that is not normal and it means that the tissue will not be receiving at the blood flow (people would sometimes faint)

Answer 11

Blood Pressure Control  Balance between demand for blood to active tissues and the need to maintain adequate blood pressure  Control Mechanisms  Neural Control  Hormonal Control  Local regulation Local regulation: at the interface between the blood vessel and the muscle, we have products of metabolism and nitric oxide that cause the blood vessels to dilate or constrict. So when metabolism is going on, you produce carbon dioxide and other things, and we get a vasodilation that says bring more blood hear (take vice products away and bring in O2), This response is local, it is produced right at the site. It is a good thing because it is causing vasodilation RIGHT where we need it. You want the muscles working (ex: in your legs) to get more blood, not the ones that are not working as much

Answer 12

Redirecting blood to active muscle to meet the demand for oxygen & substrate, and for waste removal Affects BP

Answer 13

 The arterio-venous (a-v) O2 difference results from oxygen being delivered and extracted from the blood being delivered to an organ (usually muscle) The unloading creates the difference because the tissue take the oxygen’s blood, so when it leaves on the veinous side, it has less oxygen. Cause-effect (she loooooves this): the gradient is there because the tissue extracts oxygen. The more aerobically active the tissue is, the more this (a-v) difference increases. Exercise is a good demonstration of that: as you work harder, the difference increases

Answer 14

Arterial-Venous Oxygen Difference Fick Equation VO2 = CO x (a-v) O2 \* VO2: how we quantify metabolic work (O2 intake). (a-v)O2 difference is how oxygen the tissue is taking up

Answer 15

Arterial-Venous Oxygen Difference ``` Factors influence (a-v) O2  Ability of mitochondria to use O2  Rate of diffusion of O2 into the cell ```  Perfusion to working muscle  Type of muscle fiber type being used (extraction is 3-5x greater for Type I vs Type II)  O2-Hb dissociation curve  Presence of functional myoglobin

Answer 16

The difference between arms and legs is relevant to us because it makes a difference when we mobilize patients. When the muscles want more blood, we have to take that blood from somewhere else (closed-loop system), so we do some redistribution. We do not need to know these redistribution percentages. Gut and skin: less important, than the muscles and the brain. When we are active, we don’t really need to be digesting our food. Disease: possibly of redistribution being suboptimal. How do we redirect? We change the diameter of the vasculature.

Answer 17

 Control of CO Initial ↑ HR & contractility → CO neural control suppress parasympathetic outflow augment sympathetic outflow Increase Preload → CO ↑ venous return  Ongoing control of blood flow distribution neural (autonomic NS) local metabolic factors  Control of Blood Pressure (BP = TPR x CO) ↑ SBP neural (muscle afferents, baroreceptors, chemoreceptors) hormonal (epi/norepi) local metabolic factors

Answer 18

A way to determine how hard the heart is working. Heart rate and systolic blood pressure multiply, and that determines the rate of the heart. We call that the rate-pressure product ## Footnote How hard is the heart working? RPP = HR x SBP Dimensionless number Reflects myocardial work

Answer 19

Cardiovascular Function During U/E Exercise U/E vs L/E exercise  VO2max is 20-30% lower in response to U/E ex  At a given workload  VO2 & HR are higher less mechanically efficient trunk stabilization (greater input from peripheral receptors)  BP is higher smaller muscle mass greater vascular resistance

Answer 20

VO2max is 20-30% lower Vo2 is higher because my max is higher (or lower?) Higher VO2 in the arms, if we compare the same workload. So given the same workload, the arms are going to work a lot harder.

Answer 21

If you have a weak heart, you don’t want to be doing a lot of arm work, because the blood pressure is going to get higher and the heart is going to work harder to get a similar cardiac output. The same thing happens with heart rate

Answer 22

Cardiovascular Structure & Function Summary Closed-loop distribution system – includes the lungs Flow: pressure gradient and valves Left ventricle is the workhorse Coronary arteries supply the heart muscle CO = HR x SV determinants of each BP = TPR x CO