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(Physio) Clinical Assessment and Treatment > Cardiovascular Structure and Function > Flashcards

Cardiovascular Structure and Function Flashcards

1
Q

What kind of system is the cardiovascular system? What are its three main roles?

A

Closed Loop Distribution System

Role
• Meet tissue metabolic needs

  • Remove waste
  • Temperature regulation
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2
Q

Name the main anatomical structures of the heart.

A

(two pictures)

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3
Q

What is fossa ovalis and why are we concerned about the foramen ovalis?

A

Fossa = closed off foramen

We are more concerned about the foramen ovalis (potential opening between your atria). If blood moves from the right atrium to the left atrium, it misses the lungs, so it does not get oxygenated, so we say that it is ‘shunt’: so the blood has less O2 and more CO2 than is ideal

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4
Q

Name the four cardiac valves.

A

Right lung = three lobes, right atrioventricular valve: tricuspid

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5
Q

Name the main coronary arteries. What is ischemia? What is an infarction? What is a factor that determines its severity?

A

Ischemia: a tissue has less oxygen than it needs and will be injured because of that (you can recover)
Infarction: tissue death (you can’t recover)

The amount of damage to the heart muscle depends on the location of the disruption of the blood supply

She will create a table of the main cardiac arteries and what they supply, and she wants us to know that!

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6
Q

Which vessel is more prone to have an aneurysm? Why is that dangerous?

A

Abdominal aorta is more prone to have an aneurysm, and your blood volume would be going into your abdomen very quickly

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7
Q

What is the anatomy of the myocardium? What is the pericardium like?

A

Pericardium: it is much like the pleural space. If we had fluid in the pericardial cavity, the blood vessel of the heart would be compressed. So if the volume of the fluid is large, then that can become a medical emergency. Mediastinal tube, or pericardial drain, typical post-op and it comes out centrally

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8
Q

What are the two components that influence cardiac output? What two components influence each of these?

A
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9
Q

What is cardiac output? What is stroke volume? What is the average cardiac output of an adult?

A

Cardiac Output

 The amount of blood that is pumped by the heart per unit time, measured in liters per minute (l/min).

 The amount of blood that is pumped out of the left ventricle in one contraction = stroke volume.

 Average adult CO = 5 l/min

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10
Q

What are the three components of heart rate control?

A

Parasympathetic NS – vagus nerve

Sympathetic NS – cardiac accelerator nerves

Catecholamines

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11
Q

How does the parasympathetic control of the heart work (what nerve and where/what is its action (2))?

A

Parasympathetic NS – vagus nerve

 SA & AV nodes

 Resting level of vagal activity → ↑ or ↓ HR
• Withdrawalatbeginningofexercise(↑HRto100bpm)

Parasympathetic Nerves:

↓ HR

↓ contractility

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12
Q

How does the sympathetic control of the heart work (what nerve and where/what is its actions (4))?

A

Sympathetic NS – cardiac accelerator nerves

 β receptors – SA node & ventricles
 ↑ HR, ↑contractility

Sympathetic Nerves:

stimulate HR

↑ contractility

↑ BP

↑ coronary blood flow

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13
Q

What are bêta blockers?

A

Bêta blockers: one of the biggest categories of drugs, they make the heart rate go down (less contractility of the heart, for a heart that is having a hard time beating a lot)

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14
Q

Describe the neural control of the circulation.

A
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15
Q

What center do the neural control mechanisms affect? From which three components does it get input from? (Basically, describe the neural control mechanisms)

A

Neural Control Mechanisms

 Cardiovascular Control Center (CVC)

 Input from

 Baroreceptors
• heart, carotid sinus, aortic bodies, pulmonary vessels

 Chemoreceptors
• Aortic and carotid bodies

• pO2, pH, pCO2

 Muscle afferents
• Metabolic status of the muscle
• Muscle stretch/mechanical deformation
• ↑ BP, ↑ contractility, ↑HR, vasoconstriction

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16
Q

How does age affect HR max?

A

Max heart rate decreases with increasing age

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17
Q

What controls the stroke volume?

A

Stroke Volume Control

 Preload
 Afterload
 Contractility

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18
Q

What is preload?

A

Volume of the ventricle before it contracts (the more you stretch the ventricle, the bigger the recoil, just like a balloon)

OR

Volume of blood in the ventricle just before systole (End Diastolic Volume – EDV)

Bigger preload, bigger cardiac output, until a certain limit. For most of us, this is not a big deal, but when we have an injured heart, this becomes a big deal

Some people cannot lie flat when they have heart disease, because the veinous return is too important and their heart can’t handle it

Loss of elastic recoil after heart injury, if it becomes too full of blood after that, it will have a hard time returning to its original shape (loss of elasticity)

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19
Q

What are the determinants of preload? What is orthostatic hypotension? How does ventilation affect preload?

A

Venous Return (how much blood is the veinous system is dumping in the right atrium) :

 Muscle pump
 Respiratory pump
 Venous constriction

 Posture

Orthostatic hypotension: when you get up and feel light-headed/dizzy

When we breathe in and the thoracic cavity expands, we create a negative pressure for the air to get in AND for the blood to come back up to the heart. The negative pressure also acts on the vascular system, so it helps the blood to return to the heart. That is why we don’t like the Valsalva maneuver

20
Q

What is afterload? How does it affect cardiac output?

A

Load after the left ventricule, it is the pressure that the left ventricule has to EXCEED to get blood through the aortic valve, out of the heart. It is basically the systemic pressure, to push open the aortic valve

OR

 Pressure that the ventricles have to overcome to produce flow

 Mean Arterial Pressure (MAP)
 SV is inversely proportional to afterload

If afterload goes up, cardiac output goes down. High blood pressure impacts afterload. Bigger pressure to overcome to open the aortic valve

21
Q

What does peripheral vascular resistance mean? Give the flow equation.

A

Peripheral Vascular Resistance

 vessel diameter
 Flow = ∆P

R  R = 8ln/r^4

22
Q

What are some factors that affect afterload?

A

Factors that affect afterload

 Hormones

 Epinephrine/norepinephrine
 Sympathetic NS stimulation -> Vasoconstriction, particularly in the gut
 Hypertension
 Local factors associated with exercise. Ex: Atherosclerosis: hardening of the arteries

23
Q

What is contractility? What is it affected by?

A

Inotrophic capacity

 ↑ CO – 15-20% (Inotropes = drugs that increase contractility of the heart)

 Skeletal muscle - ↑ force via ↑ recruitment

Cardiac muscle - ↑ force via ↑ contractility

 Sympathetic NS (cardiac accelerator nerves)

Catecholamines

* Every time the heart contracts, all the muscle fibers are involved, so instead of recruiting more fibers, we increase the contractility (force) that every one of those fibers generate

* Chronotropic… has to do with the rhythm of the heart

24
Q

Draw the graph that explains the relationship between the cardiac output/stroke volume and preload. What is the key concept to retain from this? What are some factors that enhance contractility?

A

At the same preload, the higher the contractility, the higher the stroke volume will be (different curves in the graph)

As you move to the right on the x axis, your stroke volume is increasing

25
Q

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

A

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

26
Q

Describe what a change in preload does in a volume-pressure graph. What would a change in afterload do?

A

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

27
Q

What are the key characteristics of a blood vessel wall structure?

A

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

28
Q

What is nitric oxide responsible for and what does its lack do?

A

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.

29
Q

What is shear stress? What does it stimulate in the blood vessels?

A

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

30
Q

What is the cardiovascular response to activity?

A

↑ CO (↑ HR, ↑ SV)
↑ BP
↑ (a-v) O2 difference

Redistribution of blood flow

31
Q

What can the % of VO2max tell you?

A

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.

32
Q

What is the heart rate response during exercise? What is the relationship between VO2 and HR? What is the Borg Scale and what is it used for?

A

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

33
Q

What does blood pressure determine? How is it impacted by?

A

Blood Pressure

 Determines flow through the system

 BP = TPR x CO
 TPR – total peripheral resistance

MAP (mean arterial pressure)

  • R = 8ln/r^4
34
Q

What is the blood pressure response during exercise? How does the systolic vs the diastolic pressure change with exercise?

A

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)

35
Q

What controls blood pressure? Describe local regulation in detail.

A

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

36
Q

What does the metabolic regulation do as local control of blood pressure?

A

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

Affects BP

37
Q

What is the Arterial-Venous Oxygen Difference?

A

 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

38
Q

What is the Fick equation? What does it represent?

A

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

39
Q

Give some factors that influence the (a-v) O2 difference.

A

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

40
Q

Why does the redirection of blood flow happen? How does it happen (2 ways)?

A

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.

41
Q

Describe the control of CV function during exercise.

A

 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

42
Q

What does the rate-pressure product give us? What is its equation?

A

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

How hard is the heart working?

RPP = HR x SBP

Dimensionless number

Reflects myocardial work

43
Q

What is the cardiovascular function during U/E exercise? What happens to VO2max? To VO2 and HR? To BP?

A

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

44
Q

Is VO2 higher in the arms or legs, for the same workload?

A

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.

45
Q

What wouldn’t you want to be doing a lot of hard work if you have a weak heart?

A

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

46
Q

Read the summary.

A

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

(Physio) Clinical Assessment and Treatment (15 decks)

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