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4th Quarter > Pathophysiology Exam #1 > Flashcards

Pathophysiology Exam #1 Flashcards

1
Q

What are the 6 functions of the cardiovascular system?

A
  • Deliver sufficient oxygen to tissues to meet metabolic demand
  • Transport metabolic waste products (carbon dioxide) from tissues and delivery to lungs for elimination
  • Transport of metabolic waste products to the kidneys for elimination
  • Supply of nutrients absorbed from GI tract to the tissues
  • Regulation of body temperature
  • Transport of hormones and other substances that regulate cellular function
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2
Q

How dose the CV system regulate temperature?

A

o vasoconstriction and dilation

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3
Q

In what way does the heart act as an endocrine organ?

A

• Heart is also an endocrine organ; which secretes:
o atrial natriuretic peptide (ANP)
o brain natriuretic peptide (BNP)

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4
Q

The heart is located within the _____;
the mediastinum is located between the _____;
posterior to the _____ and anterior to the _____ _____

A
  • mediastinum
  • lungs
  • sternum
  • vertebral column
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5
Q

From an anterior prospective, you can visual the _____ side of the heart more than the _____ side

A
  • R side

- L side

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6
Q

When the aorta pierces the diaphragm, it changes

from the _____ aorta to the _____ aorta

A
  • thoracic aorta

- abdominal aorta

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7
Q

The heart is enclosed within the _____ cavity.

A

pericardial

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8
Q

The lungs are enclosed with the _____ cavity.

A

pleural

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9
Q

The only thing separating the parietal pericardium with the parietal pleural (these are both the out layer
membranes of the heart and lungs) is this little fibrous band called the?

A

FIBROUS PERICARDIUM; The heart and lungs sit very close together, so you can see why when we make changes to our ventilators (positive pressure ventilation) how that can have CV implications

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10
Q

Where is the right auricle located and what is its function?

A
  • connected to(muscle flap) the right atrium

- It collects deoxygenated blood from the bloodstream and moves it into the heart’s right ventricle

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11
Q

R coronary artery that immediately branches off the _____ and runs thru what is called the _____ _____; which lies between?

A
  • aorta
  • coronary sulcus
  • right and left ventricle

Then that R coronary artery continues on to the posterior aspect of the heart

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12
Q

Which coronary arteries perfuses the majority of the myocardium?

A

Left anterior descending artery(LAD)

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13
Q

Does the superior/inferior vena cava bring oxygenated blood back to the heart or deoxygenated?

A

Superior vena cava bringing deoxygenated blood from the upper part of the body and inferior from the lower

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14
Q

Which brings oxygenated blood from the lungs to the heart, the pulmonary veins or the pulmonary arteries?

A

-Pulmonary arteries bringing deoxygenated blood to the lungs
-Pulmonary veins bringing oxygenated blood
from the lungs
-Away (from the heart) = artery; back to the heart = veins

pulmonary circulation opposite of systemic circulation

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15
Q

In most people, that coronary artery descends down in the sulcus between the L and R ventricles posteriorly;
that is called the _______ _____ _____.

A
  • POSTERIOR DESCENDING ARTERY(PDA)

- R coronary artery: it descends thru the coronary sulcus and then continues around the posterior aspect of the heart

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16
Q

The coronary veins eventually join back together to form the _____ _____ _____. This structure then empties into the _____ _____, which carries _____ blood.

A

-all the veins eventually join back together to form the
GREAT CARDIAC VEIN
-That great cardiac vein will empty into the CORONARY SINUS; the coronary sinus empties all it’s deoxygenated blood

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17
Q

What are two factors that are responsible for a decrease in PaO2 on the left side of the heart as compared tot he pulmonary capillaries?

A

So you have two factors that decrease PaO2: THEBESIAN VEINS and the BRONCHIAL CIRCULATION

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18
Q

How are the Thebesian veins responsible for a decrease of PaO2 on the left heart?

A

-If the thebesian veins are permeating thru the myocardium and emptying deoxygenated blood into the 4 chambers of the heart; that decreases PaO2 on the L side

o That’s one of the reasons why the PaO2 in the L side of the heart is less than the PaO2 at the actual pulmonary capillaries

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19
Q

What are the Thebesian veins?

A

Tiny veins that permeate the walls of the myocardium and

empty their deoxygenated blood to all four chambers of the heart

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20
Q

What are the 2 types of pulmonary circulation?

A

There are two types of pulm circulation:
§ There is the pulm circulation that is picking up freshly
oxygenated from the alveoli
§ There is also the bronchial circulation; we want to think
about the blood being delivered to the conductive airways
v

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21
Q

How is bronchial circulation responsible for a decrease of PaO2 on the left heart?

A

There is also the bronchial circulation; we want to think
about the blood being delivered to the conductive airways
v like the tracheal-bronchial tree
v where gas exchange doesn’t actually occur but those tissues still need to be perfused
v the deoxygenated blood from those tissues is returned back to the L side of the heart; which further decreases the PaO2

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22
Q

What are the three layers of the heart in order from outside to inside?

A
  • epicardium
  • myocardium
  • endocardium

EPI -> MYO ->ENDO; EPI -> MYO ->ENDO;

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23
Q

What are the characteristics of the epicardium?

A

• Outer layer you have the epicardium or the visceral
pericardium (same thing)
o inseparable from the heart
o composed of squamous epithelial cells and
connective tissues and fat

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24
Q

What are the characteristics of the myocardium?

A

• Then you have the myocardium; the muscle cells
o The myocardium or muscle thickness is based
upon which chamber of the heart you look at:
§ L ventricle -> R ventricle -> L atrium -> R atrium (thickest to thinnest)
o When people get cardiomyopathies, this is the
layer that hypertrophies

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25
Q

These finger-like projections are found in all 4 chambers of the heart but especially the left ventricle. They are responsible for creating turbulence of blood flow within the chambers; keeps the blood from clotting. Another theory is they also if the chamber of the heart
was smooth, when it contracted, that smooth
wall would actually collapse in on itself; gives the walls a structure/ function that does not allow them to collapse onto itself during contraction

A

TRABECULAE CARNEAE

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26
Q

The pericardial cavity or the pericardium is made up of two structures what are they?

A
  • fibrous pericardium

- serious pericardium

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27
Q

What is the function of the fibrous pericardium, and what is it attached to?

A

Fibrous pericardium is on the outer portion of the parietal pericardium and that is connective tissues that anchors the heart to adjacent structures

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28
Q

What are the two parts of the serious pericardium?

A

The parietal pericardium and the visceral pericardium

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29
Q

What is the function of the parietal pericardium?

A

It is the outside layer of the serious pericardium that the fibrous pericardium attaches to.

o Both the visceral and parietal pericardium are SEROUS pericardium
§ meaning they secrete a serous fluid into the pericardial cavity
§ normally there is only 15-20 mL of serous fluid in the pericardial cavity

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30
Q

What is the function of the visceral pericardium?

A

that is the pericardial membrane that is directly attached to the heart; inseparable to the heart
o When that visceral pericardium gets up to the great vessels it turns outward on itself and becomes the
parietal pericardium

o Both the visceral and parietal pericardium are SEROUS pericardium
§ meaning they secrete a serous fluid into the pericardial cavity
§ normally there is only 15-20 mL of serous fluid in the pericardial cavity

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31
Q

In between the visceral and parietal pericardium is the?

A

PERICARDIAL CAVTIY or PERICARDIAL SPACE

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32
Q

What is the function of the serous fluid which lies within the pericardial cavity/space?

A

v that very thin layer of serous fluid allows for the pericardial membranes to glide over each other
during systole and diastole

o Both the visceral and parietal pericardium are SEROUS pericardium
§ meaning they secrete a serous fluid into the pericardial cavity

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33
Q

How much serous fluid is located in the pericardial cavity normally?

A

15-20 mls;so if you think about the heart being about the size of a human fist, that is a very thin layer of fluid surrounding the heart

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34
Q

Inflammation of the pericardial membranes, what is the diagnosis?

A

pericarditis

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35
Q

What are the two types of pericarditis?

A

o Infectious: such as microorganisms, bacterial, viral, and fungi
o Non-infectious: idiopathic/ I don’t know why they have it, pericarditis

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36
Q

What is heard via auscultation with pericarditis, and where is the best place to hear it?

A
  • pericardial friction rub(grating sound (two pieces of sand paper rubbing together)
  • Best heard over the 5th intercostal space, L sternal border
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37
Q

How does pericarditis pain differ from MI pain?

A

o MI = constant pain, radiating to the shoulder or arm, pressure pain or elephant on chest
o Pericarditis = very sharp pain, varies with inspiration/ expiration, with no radiating pain to arm

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38
Q

What is a pericardial effusion, and what causes it?

A
  • excessive amount of fluid within the pericardial cavity/ space
  • When you have pericarditis, that increases the capillary permeability in the pericardial membranes, with increase permeability, excess fluid gets within the pericardial cavity/ space; which causes a pericardial effusion
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39
Q

What is a cardiac tamponade?

A

o At some point when the heart cannot compensate anymore and there are CV manifestations, from the pericardial effusions; this is when it becomes a cardiac tamponade
o So if someone has a pericardial effusion that has accumulated over a long period of time; they are able to compensate
o If that fluid accumulates very rapidly, they cannot compensate and develop cardiac tamponade

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40
Q

What is the best anesthesia management of cardiac tamponade(5)?

A
  • “Full, Fast, Forward”
  • Fixed Stroke Volume
  1. Avoid bradycardia
  2. Avoid vasodilators
  3. Optimize volume status to maximize LV filling
  4. Maintain sympathetic tone
  5. Spontaneous ventilation
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41
Q

Why should vasodilators be avoided for the anesthesia management of cardiac tamponade?

A
  • Run the risk of venodilation that will decrease preload

- Preload is everything in these cases

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42
Q

Why should spontaneous ventilation be preferred in the anesthesia management of cardiac tamponade?

A

-Preload is already compromised
-Positive pressure ventilation increases intrathoracic pressure that decreases preload even more and
have profound cardiovascular collapse

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43
Q

Are there any valves between the superior and inferior vena cava and the right atrium?

A

no

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44
Q

Is CVP = R atrial pressure?

A

CVP and R atrial pressure are not equal; there has to be a pressure gradient to move from the vena cava to the R atrium

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45
Q

What is the heart valve located between the right atrium and the right ventricle.

A

The tricuspid valve

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46
Q

What is the sequence of events that causes the tricuspid valve to open?

A

• The coronary sinus empties deoxygenated
blood from the myocardium to the R atrium
• As volume increases in the R atrium, pressure
increase s/t the volume increase; at this point
tricuspid valve is closed
• At a certain point, R atrial pressure is higher
than the R ventricle pressure; at this point the
tricuspid valve leaflets open d/t the pressure
gradient

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47
Q

What causes the closure of the tricuspid valve?

A
  • Blood moves with the pressure gradient from the R atrium to the R ventricle
  • As volume increases, pressure increases, causing the closure of the tricuspid valves
  • THE PRESSURE GRADIENT CLOSES THE TRICUSPID VALVE LEAFLETS
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48
Q

What causes the pulmonic valve to open?

A

• At some point, the R ventricle goes into systole, increasing the pressure even more
• When the R ventricle pressure becomes greater than the pulmonary artery pressure, this opens the pulmonic
valve leaflets and blood is ejected into the pulmonary artery.

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49
Q

What causes the closure of the pulmonic valve?

A

When the pulmonary artery pressure becomes greater than R ventricle pressure, this closes the pulmonic
valve

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50
Q

Oxygenated blood is delivered to the left side of the heart via?

A

Blood is then oxygenated and delivered back to the L side of the heart via the pulmonic veins

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51
Q

Are there valves located between pulmonary views and the left atrium?

A

NOTICE that there are NOT any valves between the pulm veins and the L atrium; blood is continually flowing into the L atrium

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52
Q

What causes the mitral valve to open?

A

-As volume increases in the L atrium, the pressure increases; this opens the mitral valve s/t the pressure
gradient in the L atrium/ L ventricle
-Blood flows into the L ventricle s/t the pressure gradient; as the volume increases in the L ventricle, so does the pressure

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53
Q

What causes the mitral valve to close?

A
  • Pressure in the L ventricle closes the mitral valve, creating even more pressure in the L ventricle
  • The L ventricle eventually goes into systole (which increases the pressure even more)
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54
Q

What causes the aortic valve to open?

A
  • The L ventricle eventually goes into systole (which increases the pressure even more)
  • When L ventricle pressure is greater than aortic pressure, this opens the aortic valve
  • When the pressure in the aorta is greater than the L ventricle, this closes the aortic valve leaflets
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55
Q

So what is responsible for the opening and closing of all the heart valves?

A

pressure gradient

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56
Q

The movement of blood from the R
atrium to the R ventricle (with its pressure gradient) thru the tricuspid valve accounts for _____ of the ventricular preload

A

~75% of preload

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57
Q

At some point, that RA goes into systole which is called _____ _____; that (systole) contributes the final ~25% of ventricular filling

A

atrial kick; 75% WITH THE PRESSURE GRADIENT; THEN THE LAST 25% FROM ATRIAL SYSTOLE

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58
Q

The strings that are attached to the tricuspid valve are called?

A

CHORDAE TENDINEAE

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59
Q

What are the function of the CHORDAE TENDINEAE?

A

-PREVENTS RETROGRADE BLOOD FLOW FROM RV
INTO RA

-The chordae tendineae are attached to papillary muscles; those papillary muscles are continuous with the myocardium of the RV
• Since the papillary muscles are continuous with the
myocardium of the RV; those papillary muscles contract along with the RV
• When they contract, those papillary muscles shorten; and when they shorten that pulls the chordae tendineae downward and tight, which holds the tricuspid valve leaflets closed
• And that prevents retrograde blood flow from RV
into RA

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60
Q

Are there chord tendineae associated with the pulmonic/aortic valves?

A

No chordae tendineae or papillary muscles

associated with pulmonic or aortic valve leaflets

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61
Q

The left side of the heart is like the right in that pressure gradient is responsible for ____ blood flow while atrial kick is responsible for _____?

A

L side same as R side: PRESSURE GRADIENT = 75% and ATRIAL SYSTOLE = 25%

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62
Q

What would be the consequences of having an atrial arrhythmia that caused the atria to contract against a
closed valve?

A

-You would lose that 25% contribution

§ Most people could compensate with a lose of 25% decrease in preload; but if that person were to
exercise, that is when you would see CV manifestations/ complications

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63
Q

What would happen if someone had a MI (transmural infarction) all the way across the myocardium that affected those papillary muscles?

A

REGURGITATION

§ That’s why people that have had a MI have regurgitation; because those papillary muscles do not function properly

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64
Q

When the LV contracts, that causes the mitral valve leaflets to balloon up and into the LA; that causes a transient increase in ___ ____ ____.

A

LA pressure

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65
Q

What causes heart sounds?

A

• Heart sounds are caused when the valve leaflets close
and the blood bounces off the valve leaflets causing
turbulence of the blood flow
• That turbulence of blood flow causes vibrations
which is transmitted to the chest wall

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66
Q

Starting at the left upper as looking at the chest…what is the order of location of heart sounds?

A

Aortic—>Pulmonic
Tricuspid—->Mitral(bicuspid)

All Puppies Take Mild

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67
Q

What is the anatomic location of the auscultation of the aortic valve?

A

2nd intercostal space (ICS), R sternal border

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68
Q

How do you find your 2nd intercostal space?

A

§ Start at the sternal notch til you find the manubrium;
where the manubrium attaches to the sternum is the angle of Louis
§ From the angle of Louis, move your finger over and if your on a rib then move down one;
if you are in an ICS, then that is the 2nd ICS

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69
Q

What is the anatomic location of the auscultation of the pulmonic valve?

A

2nd ICS, L sternal border

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70
Q

What is the anatomic location of the auscultation of the tricuspid valve?

A

5th ICS, L sternal border

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71
Q

What is the anatomic location of the auscultation of the bicuspid(mitral) valve?

A

5th ICS, L midclavicular line

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72
Q

What is the gold standard of diagnosing cardiac valvular disease?

A

Echocardiography

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73
Q

Diastolic murmurs correlate with what type of valvular disease?

A

MS ARD:

  • Mitral valve stenosis
  • Aortic valve regurge
o Tricuspid valve stenosis
o Mitral valve stenosis
o Aortic valve regurgitation (murmur often not heard during auscultation; loudest point may be aortic area
or along lower left sternal border)
o Pulmonic valve regurgitation
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74
Q

Systolic murmurs correlate with what type of valvular disease?

A

MR ASS:

  • Mitral valve regurge
  • Aortic valve stenosis

o Aortic valve stenosis
o Pulmonic valve stenosis
o Tricuspid valve regurgitation
o Mitral valve regurgitation

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75
Q

What is happening if a murmur is heard during diastole?

A

o During ventricular diastole, mitral and tricuspid valves should be open
§ SO if the tricuspid valve should be open and we hear a diastolic murmur at the tricuspid valve auscultatory area during ventricular diastole; that would be indicative of a tricuspid valve stenosis.
§ Cause that valve should be open and blood flow should be easy from the atria to the ventricle
§ Same thing with mitral valve stenosis; if we hear a murmur (over the 5th ICS, midclavicular line)
during vent diastole, that would be indicative of a mitral valve stenosis
§ During ventricular diastole, aortic and pulmonic valves should be closed; so if you hear a murmur at the aortic or pulmonic auscultatory area during diastole, that is indicative of an aortic/ pulmonic valve regurgitation or aortic/ pulmonic valve incompetence (you will hear it both ways)
§ Aortic valve regurg is often not heard during auscultation and the loudest point may actually be at
the aortic area or along the lower L sternal border

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76
Q

What is happening if a murmur is heard during systole?

A

o During systole, the aortic and pulmonic valves should be open.
o If you hear a murmur at the aortic/ pulmonic valve auscultatory area during systole; that would be indicative of aortic/ pulmonic valve stenosis
o Mitral and tricuspid valves should be closed = mitral/ tricuspid regurg

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77
Q

Left main and right coronary arteries branch from the ___ immediately after it exits from the ___ ____.

A
  • aorta

- left ventricle

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78
Q

About ___ of CO circulates through coronary arteries during rest

A

3%

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79
Q

Most perfusion occurs during ventricular ____.

A

-diastole
§ When the ventricle goes into systole, that places pressure and compresses against those arteries,
arterioles and capillaries; which prevent perfusion
§ So most perfusion occurs during ventricular diastole; when those muscles are not contracting

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80
Q

What are the sympathetic effects upon coronary blood flow?

A
  • Epi/Norepi
  • Alpha
  • Beta
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81
Q

Of the sympathetic effects upon coronary blood flow, is alpha or beta usually more dominant and why?

A

BETA;
§ Many more beta-2 receptors than alpha-1 receptors
§ However, in states of advanced shock, when you have an excessive amount of catecholamines (or an
outpouring of catecholamines) that can cause activation and predomination of the alpha-1 receptors; which would cause coronary artery constriction that would eventually lead to coronary ischemia and myocardial infarction

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82
Q

What are the parasympathetic/vagal effects on coronary blood flow?

A

Parasympathetic/vagal stimulation ??
o The coronary arteries may or may not, possibly, maybe, but not necessarily, have parasymp stimulation or innervation
o If they do, it would be thru acetylcholine and muscarinic receptors; which would have a mild dilation of the coronary arteries
o Acetylcholine and muscarinic receptors
o Usually minimal effect; mild dilation

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83
Q

CORONARY ARTERY BLOOD FLOW AND MYOCARDIAL PERFUSION CONTROLLED PRIMARILY BY…………?

A
  • CORONARY ARTERY BLOOD FLOW AND MYOCARDIAL PERFUSION CONTROLLED PRIMARILY BY RATE OF MYOCARDIAL O2 CONSUMPTION !!!
  • Any condition that increases myocardial O2 consumption causes reflex dilation of coronary arteries.
  • Resting state: ~ 75% of O2 extracted from coronary blood flow; A lot greater than other tissue; usually only extract about 25 – 30% of the O2 that passes by those tissues
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84
Q

IF WORK LOAD ON HEART INCREASES, O2 CONSUMPTION ____.

A

increases

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85
Q

FOR O2 SUPPLY TO MEET O2 DEMAND, CORONARY ARTERIES MUST ___ TO INCREASE BLOOD FLOW AND O2 TO THE CARDIAC TISSUES

A

dilate; E.G., Increased strength of contraction, increased afterload, increased preload (more blood coming back to
the heart, more stretch on the cardiac fibers, leading to greater strength of contraction/ EF/ CO), and INCREASED HEART RATE

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86
Q

So if you wanted to do one thing for your patients, that would decrease the workload on the heart; what
would you do?

A

Give them a beta-blocker

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87
Q

What are 4 metabolic processes that cause coronary artery vasodilation?

A
  1. increased CO2
  2. increased H+/decreased pH
  3. lactate
  4. adenosine
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88
Q

Why does increased CO2 cause coronary artery vasodilation?

A

o CO2 is a by-product of metabolism; the more metabolism, more CO2; the more those coronary vessels
need to dilate to deliver O2 to those tissues
o To remove excess CO2 from the tissue spaces

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89
Q

Why does increased H+ ions/decreased pH cause coronary artery vasodilation?

A

o Maybe an outcome of anaerobic metabolism, so we hope more blood, more O2 will convert it to aerobic
metabolism
o as veins dilate, this removes H+ ions and other acid by-products from the tissue spaces

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90
Q

Why does increased lactate cause coronary artery vasodilation?

A

o Lactate accumulation: lactate drops the pH down towards the acid side
o Lactate is a by-product of anaerobic metabolism; with a desired effect of more blood, more O2 to convert back to aerobic metabolism

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91
Q

Why does adenosine cause coronary artery vasodilation?

A

o ATP breaks down to ADP, then to AMP, all the way back down to adenosine
o VERY potent vasodilator of coronary arteries

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92
Q

The right coronary artery (RCA) descends anteriorly in the _____ _____ in between the RA and RV; It continues on around to the posterior side of the heart; toward the middle of the heart and then it descends in the sulcus between the _____ _____ _____.

A
  • coronary sulcus

- L and R ventricle posteriorly

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93
Q

As mentioned earlier, IN MOST PEOPLE, the posterior descending artery (PDA) is a branch of the _____
(~ 85% of people); And about 15% of people, the PDA is a
branch of the _______?

A
  • RCA

- L circumflex

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94
Q

When the PDA is a branch of the RCA, we call that ____ DOMINANT

A

RCA

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95
Q

When the PDA is a branch of the L circumflex, we call that _____?

A

L CORONARY ARTERY DOMINANT

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96
Q

The ___ ___ ___ artery perfuses the largest percentage of the myocardium,regardless of R or L coronary artery dominance

A

Left main coronary (LMC)

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97
Q

The LMC artery branches off the?

A

aorta

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98
Q

The LMC artery branches into the?

A
  • Left anterior descending (LAD) artery

- Left circumflex artery

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99
Q

What is the location of the LAD?

A

toward the apex of the heart; that LAD artery is actually sitting right on top of the interventricular septum, between the RV and LV

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100
Q

What is the location of the left circumflex?

A

Left circumflex artery which goes around the L lateral part of the heart and continues on to the posterior surface of
the heart

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101
Q

Does RCA/LCA dominance have anything to do with amount of blood flow that is delivered to they myocardium?

A

So when I say that someone is RCA dominant, all that means is the PDA is a branch of the RCA; it has nothing to do with the amount of blood flow that the RCA delivers to the myocardium

LEFT MAIN CORONARY ARTERY PERFUSES LARGEST PERCENTAGE OF MYOCARDIUM REGARDLESS OF RIGHT OR LEFT CORONARY ARTERY DOMINANCE*

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102
Q

What coronary artery perfuses the anterior left ventricle?

A

LAD along with the left circumflex

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103
Q

What coronary artery perfuses the anterior inter ventricular septum?

A

LAD

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104
Q

What coronary artery perfuses the right atrium?

A

RCA

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105
Q

What coronary artery perfuses the left atrium?

A

Left circumflex

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106
Q

What coronary artery perfuses the anterior right ventricle?

A

RCA

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107
Q

What coronary artery perfuses the posterior right ventricle?

A

RCA(PDA)

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108
Q

What coronary artery perfuses the Diaphragmatic(inferior) left ventricle?

A

Left circumflex and RCA(PDA)

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109
Q

What coronary artery perfuses the anterior left ventricle?

A

Left anterior descending and left circumflex

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110
Q

What coronary artery perfuses the lateral left ventricle?

A

left circumflex

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111
Q

What coronary artery perfuses the apex of the left ventricle?

A

LAD

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112
Q

What coronary artery perfuses the anterior inter ventricular septum?

A

LAD

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113
Q

What coronary artery perfuses the posterior inter ventricular septum?

A

RCA(PDA)

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114
Q

What coronary artery perfuses the anterior left ventricular papillary muscles?

A

LAD and the Left circumflex

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115
Q

What coronary artery perfuses the posterior left ventricular papillary muscles?

A

Left circumflex and RCA(PDA)

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116
Q

What coronary artery perfuses the SA node?

A

RCA

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117
Q

What coronary artery perfuses the atrial internal pathways?

A

RCA

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118
Q

What coronary artery perfuses the AV node?

A

RCA

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119
Q

What coronary artery perfuses the bundle of His?

A

RCA

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120
Q

What coronary artery perfuses the right bundle branch?

A

LAD

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121
Q

What coronary artery perfuses the anterior left bundle branch?

A

LAD

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122
Q

What coronary artery perfuses the posterior left bundle branch?

A

LAD

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123
Q

Atrial and ventricular muscle fibers are ___ ___ fibers?

A

mechanical contractile

fibers

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124
Q

What are the characteristics of the electrical fibers of the heart?

A

o Form electrical conduction system through heart
o Initiate and conduct action potentials through heart and to mechanical contractile fibers
o Action potentials transferred to contractile fibers and coupled with mechanical contraction
o Electrical impulses (action potential) MUST precede mechanical contraction
§ e.g., PEA

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125
Q

Are the contractile fibers of the heart smooth or striated?

A

striated

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126
Q

What is the ratio of actin to myosin in the contractile fibers of the heart?

A

2:1

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127
Q

What cardiac fibers contain tropomyosin and troponin?

A

Cardiac contractile fibers

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128
Q

In contractile cardiac fibers, what does troponin I attach to?

A

attached to actin myofilaments

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129
Q

In contractile cardiac fibers, what does troponin T attach to?

A

attached to the tropomyosin

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130
Q

In contractile cardiac fibers, what does troponin C attach to?

A

strongly attached to calcium ions

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131
Q

In what way is Intercalated disks and gap junctions in cardiac muscle fibers different that in skeletal muscles?

A

Different from skeletal muscle fibers, cardiac contractile fibers have these intercalated disks between adjacent cardiac contractile fibers that form gap junctions
§ These gap junctions allow for free flow of ions from muscle fiber to adjacent muscle fiber or from sarcolemma to adjacent sarcolemma; which allows for the spread of AP directly from muscle fiber to muscle fiber
v remember with skeletal muscle, each muscle fiber had to be innervated by a collateral of a somatic motor neuron
v cardiac muscle fiber does not because of the intercalated disk and gap junctions that allow for free flow of ions; which allow AP to spread from muscle fiber to muscle fiber, so all those muscle fibers from within a unit will depolarize and contract at about the same time

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132
Q

What are the units within the the heart called that are composed of intercalated disk and gap junctions that allow for the free flow of ions which allow AP to spread from muscle fiber to muscle fiber?

A

v Those units within the heart are called functional syncytium; there are two functional syncytia

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133
Q

What is the name of the two functional syncytia?

A

atrial syncytium (R & L) and ventricular syncytium (R & L)

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134
Q

What are the characteristics of the two functional syncytial?

A

§ Right and left atria
§ Right and left ventricles
§ Separation of atria and ventricles by fibrous tissue with openings for valves and pathway for electrical fibers so impulse can be conducted from atria to ventricles
§ So if they are syncytium, that means that they are a unit and that all of the muscle fibers within that unit become excited and contract at about the exact same time; that allows for more efficient ejection of blood
§ If those muscle fibers were all contracting at different times, that would not be synchronous and would not be conducive to an effective EF, SV, CO.

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135
Q

List the 7 steps of cardiac muscle fiber contraction pathway

A
  1. AP conducted along the muscle fiber
  2. AP goes down the T-Tubule
  3. Sitting adjacent to the T-tubule is the terminal cisterna of the sarcoplasmic reticulum; when that AP gets there, that excites the sarcoplasmic reticulum allowing for opening of voltage-gated Ca++ channels
  4. Then release of Ca++ from the sarcoplasmic reticulum into the sarcoplasm
  5. Ca++ from the EC fluid increases the sarcoplasmic
    Ca++ concentrations
  6. that interacts with troponin C which pulls troponin T and tropomyosin away from the actin binding sites
  7. Myosin heads can then power-stroke, crossbridge,
    and shorten the sarcomere; which shortens the muscle fiber
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136
Q

In the heart, the sarcoplasmic reticulum is not as developed as in the skeletal muscle fibers; so we
have to have an extra source of ____?

Where does this extra source come from?

A
  • Ca++

- extracellular fluid

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137
Q

What are the two sources of Ca++ that is needed for the cardiac contraction cycle?

A
  • sarcoplasm reticulum
  • EC

Changes in the EC fluid would have major implications on cardiac contractility

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138
Q

Why are the cardiac muscle fibers arranged obliquely instead of linear?

A

o That obliqueness allows for more effective EF,
SV, and CO
o Think of it as an old stringed wet mop (more effective to twist and squeeze to wring out)

139
Q

The heart has lots of _____ and requires LOTS of __.

A
  • mitochondria

- O2

140
Q

What are the 3 properties of cardiac electrical fibers?

A
  1. Automaticity
  2. Excitability
  3. Conductivity

All electrical fibers have all 3 properties, BUT some fibers have more of one than the other properties

141
Q

If a cardiac electrical fiber’s role is primarily automaticity, it…………………………..?

A

it automatically generates APs

142
Q

If a cell’s primary role or property is excitability, it…………………………………….?

A

becomes excited in response to APs

143
Q

If a cell’s primary role/ property is conductivity, it………………………..?

A

rapidly conducts APs

144
Q

Where is the SA node located, what size is it, and what is it composed of?

A
  • Located in the upper part of the RA; right were the superior vena cave meets the RA
  • Very small, less than 0.5 cm in diameter
  • composed of P-cells (pacemaker cells)
145
Q

What is the primary electrical fiber property of the pacemaker cells of the SA node?

A

pacemaker cells primary property are

automaticity

146
Q

The thing that the P-cells in the SA node do
better than anything else, is that they will _____ _____ _____
; at a rate of?

A
  • automatically generate APs

- 60– 100 times/ min

147
Q

Once the AP leaves the SA node where does it go?

A

Those APs are then transmitted to the

atrial intermodal pathways

148
Q

What is the atrail internal pathway/tract?

A 
Atrial internodal pathways or tracts
o Run thru the tissue of the RA and the
internodal pathways are hopefully lying
adjacent to mechanical contractile fibers;
so you can have electrical/ mechanical
coupling (RA can contract)
• Interatrial branch of atrial internodal
pathways
o You also have an interatrial branch of
the atrial internodal pathway which is
transmitting APs/ conducting APs from
the SA node to the LA
o THE ATRIAL INTERNODAL PATHWAYS JOIN BACK TOGETHER TO FORM THE AV NODE
149
Q

Where is the AV node located and what is it composed of?

A

Located in the floor of the RA and is
partly composed of T-cells (transition
cells)

150
Q

What are 2 functions of the AV node?

A
  1. One of the functions of the AV node is to
    regulate the amount of APs that can be
    transmitted from the atria to the ventricles
  2. Another function is that it causes a slight, slight slowing of the APs; which allows for the atria to contract right before the ventricles
    contract
151
Q

Why is the AV Node function of regulation of AP important?

A

If you had an atrial arrhythmia like Aflutter/
A-fib, your atria is contracting at
200x a minute; do you want all those APs
to be transmitted to your ventricles, and your ventricles contracting 200x a min? Nope.

152
Q

Why is the AV Node function of slowing of AP important?

A

It slows that AP down just enough so that the atria can contract and contribute that last 25% to ventricular volume before the ventricle contracts

153
Q

The AV node also has these types of cells that are usually not used because the SA node generates AP at a faster rate.

A

o Also has pacemaker cells; those pacemaker cells can automatically
generate APs
o However, it does not usually do that because the SA node generates APs at a faster rate; faster than any of the other pacemaker cells of the heart
o So under normal conditions, the AV node P-cells are overridden because the SA node

154
Q

If the SA node fails to generate APs. The AV node will pick up the slack and generate its own APs at a rate of about ……..?

A

-40 – 60 times/ min.

155
Q

Then the AV node transitions into the …..?

A

bundle of His

156
Q

The bundle of His is located in the ? And that bundle of His divides into the ?

A
  • superior portion of the inter ventricular septum

- R bundle branch and the L anterior/ posterior bundle branch

157
Q

The Right Bundle Branch descends down ___ ___the toward the ___ ___ ___ ; it then terminates into these ___ ___ that run along the walls of the RV

A
  • interventricular septum
  • apex of the heart
  • Purkinje fibers
158
Q

The Left Anterior Bundle Branch descends down ___ ___the toward the apex of the heart ; it then terminates into these Purkinje fibers that run ___ ___ ___ ____?

A
  • interventricular septum

- anterior and lateral aspect of the LV

159
Q

What supplies supplies APs to the posterior aspect of the LV?

A

Left Posterior Bundle Branch

160
Q

Why does the LV have an anterior and a posterior Bundle Branch?

A

The LV has an anterior and a posterior bundle branch because the LV has a lot more muscle that needs to depolarize

161
Q

Where are the 3 locations of Purkinje fibers?

A

o You have to think of this 3-dimensionally:

  1. on the anterior aspect of the RV
  2. on the lateral aspect of the RV
  3. on the posterior aspect of the RV
162
Q

What is the primary electrical fiber property of the Purkinje fibers?

A

The primary property of Purkinje fibers are conductivity; Purkinje fibers are very good at conducting APs

163
Q

We hope that those Purkinje fibers are sitting adjacent to the ___ ___ ___ , so we can have electrical/mechanical coupling and ___ ___ ___.

A
  • mechanical contractile fibers

- effective myocardial contraction

164
Q

In skeletal muscle what is the mV charge of RMP, TP, and what happens once TP is reached? At what mV does repolarization occur?

A
  • Resting membrane potential (RMP) is located at -85mV
  • Threshold potential (TP) is about -60mV; once TP is reached,depolarization occurs
  • Gets up to about +20-30 mV and IMMEDIATELY REPOLARIZATION occurs and brings the AP back down to resting
165
Q

In cardiac(not pace maker cells) what is the mV charge of RMP, TP and at what mV does repolarization occur?

A
  • RMP is at -85 – -90 mV; TP is about -60mV
  • Depolarization occurs with a SLOOOWWWWWW REPOLARIZATION PHASE @ ~ +20mV
  • Then finally it rapidly goes back down to resting
166
Q

Which has the longer repolarization time skeletal muscle or cardiac muscle and why?

A
  • Look at the time difference between the two; total time is about 0.2ms for a skeletal muscle AP and 500ms for cardiac muscle AP
  • Cardiac muscle AP has to be longer than skeletal muscle AP to allow for contraction

-Cardiac muscle has a longer repolarization time because the muscle has to have time to contract
• Mechanical contraction occurs during electrical repolarization
• So if this repolarization phase was very short and then another AP were to occur, that cardiac muscle fiber would not have a long time to contract
• You need a long repolarization phase to allow for mechanical contraction to occur

167
Q

In cardiac muscle cells during the depolarization phase, what is happening to the gated ion channels?

A
  • Voltage gated Na+ channels are open
  • Volted gated K+ channels are closed
  • volted gated Ca+ begin to open
168
Q

In cardiac muscle cells during the early repolarization and plateau phase, what is happening to the gated ion channels?

A
  • Voltage gated Na+ channels close
  • Some voltage gated K+ open, causing early repolarization
  • -Voltage gated Ca+ are open, slowing down repolarization
169
Q

In cardiac muscle cells during the final repolarization phase, what is happening to the gated ion channels?

A
  • Voltage gated Ca+ channels close

- Voltage gated K+ are open

170
Q

What is the RMP of cardiac muscle cells, and what contributes to its negativity?

A
  • RMP is about -90mV (the inside of the cell membrane is -90mV more negative than the outside of the cell membrane)
  • What contributes to the RMP negativity? K-leak channels, Na-leak channels, and Na-K pumps
171
Q

Of the factors contributing to the negativity to the RMP of cardiac muscle cells, which one has the biggest impact upon it, and what is the ion ratio of the Na/K pump?

A

o K-leak channels contribute the most to RMP

o Na-K pump: 3 Na out, 2 K in

172
Q

What happens to causes the initial influx of Na; that brings the RMP upward (less negative) toward threshold(cardiac muscle cells)

A

A stimulus

173
Q

Once enough Na has entered into the cell to bring RMP to TP (about -60mV); you have opening of? (cardiac muscle cells)

A

voltage gated Na+ channels at threshold

174
Q

(cardiac muscle cells)That influx of more Na causes the membrane potential (MP)_____________________________ ; now were at
about _____ mV

A
  • to rise in a less negative fashion

- -40 mV

175
Q

In cardiac muscle cells, from -90 to -40, is called the??

A

EARLY PHASE 0 OF DEPOLARIZATION

176
Q

During EARLY phase 0 of depolarization you also have the K channels that become very ??????

A

impermeable to K; so almost NO outward movement of K

177
Q

What initiated EARLY phase 0 of depolarization?

A

An initial stimulus causes an influx of Na
§ Once that got to TP (about -60mV), we have opening of voltage-gated Na channels; which causes the MP to rise upward in a less negative fashion.
§ Now were at about -40mV;

178
Q

What initiates the LATE PHASE 0 OF DEPOLARIZATION?

A

At -40mV we initiate LATE PHASE 0 OF DEPOLARIZATION; -40mV you have opening of the slow
voltage-gated Ca-Na channels

179
Q

What is happening during Late phase 0 of depolarization?

A

You now have more cations entering into the cell which brings the MP (upward in a less negative fashion) all the way up to about +20mV
§ Now we have the fast voltage-gated Na channels open and the slow Ca-Na channels open
v there called FAST channels because they open and close really fast
v there called SLOW channels because they stay open for an prolonged period of time

180
Q

What initiated LATE phase 0 of depolarization?

A

By opening of the voltage-gated Ca-Na channels at -40mV

181
Q

At what mV does PHASE 1 OF REPOLARIZATION start?

A

Now were at +20mV; we reversed the polarity of the inside of the cell and we are at PHASE 1 OF REPOLARIZATION

182
Q

What happens at Phase 1 of Repolarization?

A

o At this point the fast voltage-gated Na channels have snapped shut at about +20mV
o However, the slow voltage-gated Ca-Na channels remain open; we have less cations moving into the cell
because of the voltage-gated Na channels closing
o So the MP moves from about +20mV, down to zero mV (nether + or –)
o Now at some point between 0mV and here (he never gave me a #) the K channels begin to reopen; so you have influx of Ca thru the slow Ca-Na channels and some outward movement of K at this point

183
Q

What initiated Phase 1 of Repolarization?

A

Closure of the voltage-gated Na channels as well as (at some point) the K channels begin to open up(@ ~ +20 mV)

184
Q

What happens at PHASE 2 OF REPOLARIZATION?

A

PHASE 2 OF REPOLARIZATION: this is called the plateau phase of repolarization; the longest phase of
repolarization.
o Now we have inward movement of Ca from the slow Ca channels; the K channels have completely
opened and we have outward movement of K
o There is an EQUAL movement of cations inward and outward; so the membrane remains at 0mV
throughout phase 2

185
Q

What happens at PHASE 3 OF REPOLARIZATION?

A

PHASE 3 OF REPOLARIZATION: the slow Ca-Na channels finally close while the K channels remain fully open
o That leads to outward movement of cations and minimal inward movement of cations; so the MP
rapidly becomes more negative (back down to RMP)

186
Q

What happens at PHASE 4 OF REPOLARIZATION?

A

PHASE 4 OF REPOLARIZATION: Is just a resting phase between APs; movements of ions are the same as
during the RMP

187
Q

Similar to skeletal muscle fibers, ____ precedes and leads to ___ ___ ___

A
  • AP

- Cardiac Muscle Contraction

188
Q

The heart requires 2 sources of Ca++ to allow for sustained contraction of cardiac muscles to enhance stroke volume and cardiac output. What are these two sources?

A

-Heart requires flow of Ca++ into sarcoplasm from SARCOPLASMIC RETICULUM and from EC FLUID.

189
Q

The inward movement of Ca++ from EC fluid and SR occurs during?????

A

the cardiac AP

190
Q

If your patient is experiencing intra-op hypotension during a Radical Neck Dissection with free-flap, what are two methods for dealing with this?

A

NO VASOCONSTRICTORS

  1. Think fluid status
  2. Thing Ca++ administration
191
Q

If your patient is experiencing intra-op hypotension during a Radical Neck Dissection with free-flap and you are assessing fluid status to choose between fluids and ca++ administration, what things might you look at?

A

o Stroke volume variance (SVV):
§ The more optimized your fluid status is, the less variation you have in your SV from beat-to-beat
§ Normally you want your SVV less than 10%; the more HYPOvolemic your pt is, the more your SV varies
§ And the pt has to be on positive pressure ventilation for this to all work; because that positive
pressure ventilation is what’s causing that SVV
§ So if your HYPOvolemic, think of your vena cava as a garden hose; empty = easier to compress
§ SO we use SVV to assess our patient’s hemodynamic fluid volume status

192
Q

If your patient is experiencing intra-op hypotension during a Radical Neck Dissection with free-flap and you are assessing ca++ administration, what things might you look at?

A

• IF your SVV indicates adequate volume status, look at your labs and think hypocalcemia
• Labs indicate hypocalcemia, the next thing I am thinking is Ca administration
• Benefits of calcium administration
o Increased myocardial contractility
o Calcium dependent exocytosis of neurotransmitter (often forgotten)
§ Think about those sympathetic postganglionic fibers; for NE to be released from the postganglionic symp fibers, you have to have sufficient amounts of CA in the EC fluid
§ If you don’t have enough Ca in the EC fluid, you’re not going to have a large enough gradient to drive the Ca from extracellular to intracellular; you are going to have a decrease release of catecholamines (NE)
§ That is another way that Ca administration can improve their BP when you can’t use vasopressors or if their volume status is already adequate

193
Q

Just like skeletal muscle; ABSOLUTE REFRACTORY

PERIOD (ARP) starts at _____ and last thru?????

A

-threshold
-early and late phase of depolarization, phase 1, 2 and
most of 3 of repolarization

194
Q

When is the end of the absolute refractory period?

A

when the MP gets back to threshold is the end of

the ARP

195
Q

From threshold down to about -85mV (about 5mV from

resting) is the what refractory period and what does that mean?

A

RELATIVE REFRACTORY PERIOD
(RRP)
o During the RRP, you have to have an extra strong
stimulus to initiate another AP

196
Q

Then from about -85 to -90mV is what refractory period _____ _____ _____? What does that mean

A

SUPER NORMAL REFRACTORY PERIOD (SNP)

o Only a mild stimulus will generate another AP

197
Q

Define absolute refractory period, relative refractory period and super normal refractory period.

A
  • ARP: Cell CAN NOT depolarize again regardless of the stimulus.
  • RRP: If an EXTRA STRONG stimulus is applied, depolarization might occur.
  • SNP: Only a MILD STIMULUS applied can cause depolarization.
198
Q

The resting membrane potential of a pace-maker cell is approximately?

A

-55 mV

199
Q

Do pacemaker cells have Na+ gated voltage channels?

A 
• Voltage-gated (fast) Na+ channels
are inactivated in pacemaker cells
• However, pacemaker cells are very
leaky to Na+ ions (causes slow rise in
membrane potential towards
threshold)
200
Q

What is the threshold potential of a pacemaker cell and what happens when the threshold potential is reached??

A
  • approximately -40 mV

- opening of voltage-gated Ca-Na channels (which initiates depolarization).

201
Q

At what point is repolarization initiated in cardiac pacemaker cells?

A
  • When MP reaches +20mV, Ca-Na channels close and K+ channels open (which initiates repolarization).
  • At the end of repolarization, K+ channels close and process starts again
202
Q

What is the inherent rates of the 3 location of cardiac pace maker cells and how surgically are ectopic cell activity treated?

A

• SA node: Normal pacemaker
o Rate of AP generation: 60 – 100/min.
o Overrides lower, slower potential pacemakers
• AV node/junction
o Inherent rate: 40 – 60/min.
• Ventricular Purkinje fibers
o Inherent rate: 15 – 40/min.
• Ectopic pacemakers can occur anywhere in conduction system
o People have to come and get ablations because of the ectopic pacemaker cell activity

203
Q

What is the definition of the cardiac cycle?

A

• Defined as the cardiac events that occur from the beginning of one beat, to the beginning of the
next beat

204
Q

During the cardiac cycle, what does the “p” wave represent?

A
  • The P wave represents ATRIAL DEPOLARIZATION

* It does not represent atrial muscle contraction

205
Q

During the cardiac cycle, what must occur before mechanical contraction can occur?

A

Remember that ELECTRICAL DEPOLARIZATION has to occur before mechanical contraction can occur

206
Q

During the cardiac cycle, what does the “T” wave represent?

A

-T wave represents VENTRICULAR FIBER REPOLARIZATION; there is no visible atrial repolarization because it is lost in the QRS complex

207
Q

During the cardiac cycle, what does the “QRS” represent?

A

QRS complex represents VENTRICULAR DEPOLARIZATION; not ventricular contraction
• Ventricular systole or contraction occurs after electrical depolarization; T wave represents ventricular
repolarization

208
Q

What is happening to the atrial pressure waveform during the cardiac cycle?

A

o Starting with ventricular systole; the ventricle has contracted and has injected blood into the aorta which causes a sharp rise in aortic pressure (seen here in the
waveform)
o Then, when the aortic pressure is greater than the LV pressure, the aortic valve closes
o And when that aortic valve closes, blood falls back onto the aortic valves d/t the arch of the aorta; causing a transient rise in aortic pressure (seen as the dicrotic notch)
o Then the blood moves on into the systemic circulation and the pressure in the aorta will slowly eventually decrease

209
Q

What is happening to the LV pressure waveform during the cardiac cycle?

A

o Starting with atrial systole, that atrial kick will provide the final 25% of LV filling volume
o When the atrial kick occurs it causes a small rise in LV pressure; when LV pressure is greater than LA pressure, the mitral valve will close
o The mitral valve closes, and the aortic valve has not yet opened; but the LV starts going into systole
o The pressure in the LV rises sharply because the size of that chamber gets smaller during systole and because the blood is not moving in or out (because the valves are closed)

210
Q

What is happening to the LA pressure waveform during the cardiac cycle?

A

o LA goes into systole which causes a rise in the LA pressure waveform
o Then the mitral valve closes and the ventricle goes into systole; this causes the mitral valve leaflets to balloon up into the LA, causing the (c) wave in the LA pressure wave form
§ This ballooning up of the mitral valve leaflets helps prevent retrograde blood flow
o There are no valves from the pulm veins and the LA; so blood will continue to flow into the LA and this causes a rise in pressure (which is responsible for the (v) wave)
o When the pressure in the LA is greater than the LV, the mitral valve opens and the blood passively flows into the LV; supplying the LV with 75% of LV filling pressure

211
Q

What is the isovolumetric contraction during the cardiac cycle?

A

§ ISOVOLUMETRIC (isovolumic) CONTRACTION: the sharp rise in ventricular pressure before the aortic
valve opens, with no change in volume

212
Q

What is the isovolumetric relaxation during the cardiac cycle?

A

§ ISOVOLUMETRIC RELAXATION: when the LV size

increases (during diastole) without any increase in volume (from the LA

213
Q

What happens during the LV volume curve during the cardiac cycle?

A

o Starting with atrial systole; provides the final 25% contribution; so the volume in the LV increases
o The LV goes into systole and ejects blood; so the volume in the LV decreases
o The aortic valve closes; then the mitral valve opens
o Then the ventricle volume builds up passively from atria to ventricle (accounting for the 75% LV filling volume); then back to the atrial systole (atrial kick) for the last 25%

214
Q

What is responsible for heart sounds?

A

o Remember that the actual heart sounds are made from the turbulence of the blood when the valves close

215
Q

What is responsible for 1st heard sounds(S1) of the cardiac cycle?

A

o 1st heart sound (S1) is associated with events r/t the closure of the mitral and tricuspid valves (the AV valves)

216
Q

What is responsible for 2nd heard sounds(S2) of the cardiac cycle?

A

o 2nd heart sound (S2) is associated with events r/t the closure of the aortic and pulmonic valves (semilunar valves)

217
Q

What are ways the sympathetic nervous system regulates the cardiac cycle?

A
  1. Norepi and epi

2. Beta 1

218
Q

Where does NE and Epi originate from?

A

§ Norepi and epi from the POSTGANGLIONIC SYMP NERVOUS FIBERS AND THE ADRENAL MEDULLA

219
Q

What are the 3 ways Beta 1 regulates the cardiac cycle?

A
  1. SA node: increased heart rate (positive chronotropic effect) (↑ permeability to Na+)
    2, AV node: increased rate of transmission of those APs (positive dromotropic effect)
  2. Ventricular contractile fibers: increased strength of contraction (positive inotropic effect)
220
Q

In what way does Beta 1 regulation of the cardiac cycle through the SA node occur?

A

Ø When beta−1 receptors are stimulated in the SA node; that increases the HR
Ø Remember those p−cells are very leaky to Na; the way that beta−1 receptor activation works at the SA node is it
actually increases the permeability of those cells to Na even more
Ø So increase permeability to Na, more Na influx; so RMP potential will be reached quicker because that Na will be more permeable and the influx
Ø Faster rate of upstroke means more depolarizations; more depolarizations per unit time = faster HR

221
Q

In what way does Beta 1 regulation of the cardiac cycle through the AV node occur?

A

AV node: increased rate of transmission of those APs (positive dromotropic effect)

222
Q

In what way does Beta 1 regulation of the cardiac cycle through the ventricular contractile fibers occur?

A

v Ventricular contractile fibers: increased strength of contraction (positive inotropic effect)

223
Q

The overall effect of the SNS on the heart is to ________?

A

§ The overall effect of the SNS on the heart is to increase the cardiac output (CO)
§ Strong SNS stimulation can increase CO up to 100%

224
Q

How does the parasympathetic branch of the ANS regulate the cardiac cycle?

A

the Vagus nerve?

225
Q

Which cranial nerve is the vagus, what neurotransmitter is released by the vagus and what receptor does it act upon?

A
  • ten
  • Acetylcholine
  • Acts on Muscarinic receptors of the heart; primarily at the SA node:
226
Q

What is the PNS effect on the SA node?

A

SA node: decreased heart rate (negative chronotropic effect):

227
Q

What is the PNS effect on the AV node?

A

AV node: decreased rate of transmission (negative dromotropic effect)

228
Q

What is the PNS effect on the ventricular contractile fibers?

A

Ventricular contractile fibers: decreased strength of contraction (negative inotropic effect)

229
Q

What is the overall effect on the cardiac cycle of the parasympathetic nervous system?

A

Overall effect of PNS: decreased CO

230
Q

What is the PRIMARY effect of the PNS on the heart?

A

PRIMARY PNS effect on heart (↑ permeability of those cells to K+, hyperpolarization)

231
Q

Describe how the PRIMARY effect of the PNS on the heart takes place.

A

v SA node: decreased heart rate (negative chronotropic effect): PRIMARY PNS effect on heart (↑ permeability of those cells to K+, hyperpolarization)
Ø RMP of the p−cell is about –55 to –60mV
Ø Those cells become more permeable to K; moves K from inside the cell to outside
Ø Hyperpolarizes the cell membrane; so instead of −55mV, RMP is moved further down to about −65mV
Ø Making it harder to reach threshold; slows the rate of upstroke of depolarization
Ø When it takes longer to get there, that means less depolarizations over time; which will decrease the heart rate

232
Q

In regards to the cardiac cycle and the Frank Starling curve, within physiologic limits, all of the blood that returns to the RA is ejected from the___ ___ (on a mL per mL basis) and CO depends on ___ ___.

A
  • left ventricle

- venous return

233
Q

What is the Frank Starling curve?

A

Stretch of LV depends on volume of blood that enters during diastole
o Within physiologic limits, the greater the diastolic filling
volume, the greater the stretch, the stronger the
contraction, the greater the systolic SV, and the greater
the CO

234
Q

What is the “take-home message” from the atrial pressure/ventricle output table in relation to the Starling curve??

A

• On the horizontal axis you have the atrial pressure (mm Hg); primarily determined by VOLUME
• On the vertical axis you have ventricular
output (L/min)
• As you can see on the atrial pressure axis,
up until zero, there is no CO
• From 0 to +8 (on the atrial pressure axis)
there is a more linear relationship
• More pressure = greater ventricular output
• When we get to 8 mm Hg, there is a plateau; so once the ventricles get to a certain point, giving more fluid WILL NOT HELP

235
Q

What actually happens to CO as your volume status(atrial pressure) extends past +8 mmHg on the atrial pressure/ventricle output table?

A
  • If you extend this curve out to about 18–22 mm HG, it starts to curve down
  • The ventricular fibers are over extended, thus decreasing CO
236
Q

R/T the Starling curve, what is the definition of the “optimal” volume status?

A

o Optimal volume = optimal stretch = optimal strength of contraction = optimal EF/ CO
§ Optimal volume status allows for optimal actin–myosin myofilaments interaction

237
Q

What is the result of volume overload in R/T the starling curve?

A

o Increased volume = over stretched
§ Ventricular contractile fibers pulled apart and the sarcomeres are elongated; the actin and myosin
myofilaments are to far apart to interact with each other; causing sub−optimal:
v interaction with one another
v strength of contraction
v length of contraction
v SV, EF, and CO

238
Q

What is the result of volume deficit in R/T the starling curve?

A 
o Decreased volume = under stretched
§ Actin and myosin myofilaments are overlapping each other; causing sub–optimal:
v interaction with one another
v strength of contraction
v length of contraction
v SV, EF, and CO
239
Q

What determines mean arterial pressure?

A
  • MEAN ARTERIAL PRESSURE = CARDIAC OUTPUT x TOTAL PERIPHERAL RESISTANCE
  • MAP = CO x TPR
240
Q

What is the definition of cardiac output, and what determines it?

A

CO = is the amount of blood ejected from the LV each minute
o traditionally expressed in L/min
o CO = HR x SV

241
Q

How does the ANS affect cardiac output?

A

§ HR and SV are affected by theANS
§ SNS increases HR & SV
§ PNS decreases HR
§ However, if your HR is 115−120/min; is that really
going to increase your CO? NO! Not enough time for ventricular filling
§ SV is affected by LVEDV (preload); which is determined
by the atrial volume or pressure in the vascular system
§ Venous return: affected by the overall blood volume and skeletal muscle pump
§ Sympathetic tone of the veins also affects CO

242
Q

What two factors are responsible for total peripheral vascular resistance?

A
  • Arteriolar diameter (most influential determinant of TPR vs. blood viscosity)
  • Blood viscosity is determined by our hematocrit (actual formed cells in the blood)
243
Q

How does arteriolar diameter affect PVR?

A

v Mainly the small and medium sized arteries and arterioles that have the ability to dilate and constrict, based on the amount of sympathetic tone that they have
v i.e., constriction = é TPR… and vice versa

244
Q

How does blood viscosity affect PVR?

A

v Hematocrit
Ø # RBCs (most abundant and biggest contributor to blood viscosity)
Ø WBCs
Ø Platelets
v Pt’s with polycythemia often have LV hypertrophy because chronically elevated TPR because blood viscosity is up
v With decreased RBC/ if your anemic, decreased HCT, decreased blood viscosity, decreased TPR

245
Q

What is Body Surface Area used for and what is the average BSA?

A 
-USED TO CALCULATE CARDIA INDEX
• Surface area of body.
• Based on weight and height.
• Expressed in square meters.
• Data usually obtained from nomograms.
• AVERAGE FOR 70-KG MAN: 1.73 M2
246
Q

What is the definition of PRELOAD/LEFT VENTRICULAR END DIASTOLIC VOLUME/PRESSURE (LVEDV or LVEDP), what determines it and what is normal?

A

• Volume in the left ventricle at the end of diastolic filling and available to be ejected during the next left
ventricular contraction.
• Determined by venous return to the heart and degree of stretch of left ventricular myocardial cells.
o Increased venous return increases LVEDV and compliant myocardium allows for maximal filling.
• LVEDV determines LVEDP, degree of ventricular stretch, and strength of the next systolic contraction, as
stated by the Frank-Starling Law of the Heart.
• NORMAL: 70 ml/m2; average 120 ml.

247
Q

What is the definition of left ventricle stroke volume, what are changes based on, what is the formula for calculating it, and what is the normal value of it?

A

LEFT VENTRICULAR STROKE VOLUME (LVSV)
• Volume ejected from the left ventricle during each left ventricular contraction.
• Changes based on strength of contraction and LVEDV.
• FORMULA: LVSV = CO/HR
• NORMAL: 60 – 100 ml/beat

248
Q

What is the definition of left ventricle ejection fraction(LVEF), what are changes based on, what is the formula for calculating it, and what is the normal value of it?

A
  • Percentage of the LVEDV/preload that is ejected from the left ventricle during each contraction.
  • Changes based on strength of contraction and LVEDV.
  • FORMULA: LVEF = LVSV/LVEDV
  • NORMAL: 55 – 65%
249
Q

What is the definition of left ventricular end systolic volume(LVESV), what are changes based on and what is the formula for calculating it?

A

LEFT VENTRICULAR END SYSTOLIC VOLUME (LVESV)
• Volume remaining in the left ventricle after a left ventricular stroke volume is ejected.
• Changes based on strength of contraction, LVEF, and LVSV.
• FORMULA: LVESV = LVEDV – LVSV

250
Q

What is left ventricular after load and what determines it?

A
  • Resistance to flow of blood from left ventricle during contraction.
  • Determined by blood viscosity and SYSTEMIC VASCULAR RESISTANCE (PRIMARY DETERMINANT).
  • Often used interchangeably with systemic vascular resistance (see below).
251
Q

What is the primary determinant of left ventricular after load?

A

SVR

252
Q

What is the definition of right atrium pressure(RAP), what determines it and what are the normal values?

A
  • Pressure in the right atrium.
  • Determined by venous return and degree of emptying of the right atrium.
  • NORMAL: 2 – 8 mmHg (2 – 6 cm H2O)
253
Q

What is central venous pressure(CVP) and what is the normal value?

A

CENTRAL VENOUS PRESSURE (CVP)
• Pressure in the inferior or superior vena cava just before they join with the right atrium.
• OFTEN USED SYNONYMOUSLY WITH RAP.
• NORMAL: 2 – 8 mmHg (2 – 6 cm H2O)

254
Q

What is the definition of cardiac output(CO), what is the formula to determine it, and what is the normal value of it?

A 
CARDIAC OUTPUT (CO)
• The volume in liters ejected by the left ventricle into the systemic circulation each minute.
• FORMULA: CO = HEART RATE (HR) x LVSV
• NORMAL: 4 – 8 L/MIN
255
Q

What is the definition of cardiac index(CI), what is the formula to determine it, and what is the normal value of it?

A

CARDIAC INDEX (CI)
• Cardiac output correlated with body surface area.
• FORMULA: CI = CO/BSA
• NORMAL: 2.5 – 4 L/min/m2

256
Q

What is the definition of systemic blood pressure(SBP), what is the formula to determine it, and what is the normal value of it?

A 
SYSTEMIC BLOOD PRESSURE
• The pressure exerted on the systemic arteriolar vessels
during systole (SBP) and diastole (DBP).
• FORMULA: BP = CO x AFTERLOAD
• NORMAL: 100 – 140/60 - 90 mmHg
257
Q

What is the definition of pulse pressure, what is the formula to determine it, and what is the normal value of it?

A

PULSE PRESSURE
• The difference between the systolic blood pressure (SBP) and the diastolic blood pressure (DBP)
• FORMULA: PULSE PRESSURE = SBP – DBP
• NORMAL: ~ 40 mmHg

258
Q

What is the definition of mean arterial pressure(MAP), what is the formula to determine it, and what is the normal value of it?

A

MEAN ARTERIAL PRESSURE (MAP)
• The mean or average of the systemic systolic and diastolic blood pressures.
• FORMULA: MAP = SBP – DBP + DBP or 1/3(PP) + DBP
3
• NORMAL: 70 – 105 mmHg

259
Q

What is the definition of systemic vascular resistance(SVR), what is the formula to determine it, and what is the normal value of it?

A

SYSTEMIC VASCULAR RESISTANCE (SVR)
• A major component of afterload or the resistance in the systemic arteriolar vessels that must be overcome
during left ventricular contraction to eject blood into the systemic arteriolar vessels.
• FORMULA: SVR = (MAP – RAP) x 80/ CO
• NORMAL: 800 – 1200 dynes/sec/cm5 or 800 – 1200 dynes x sec-1 x cm-5

260
Q

What is the definition of systemic vascular resistance index(SVRI), what is the formula to determine it, and what is the normal value of it?

A

SYSTEMIC VASCULAR RESISTANCE INDEX (SVRI)
• Systemic vascular resistance correlated with body surface area.
• FORMULA: SVRI = MAP – RAP x 80/CI
• NORMAL: 1970 – 2400 dynes/sec/cm5/m2 or 1970 – 2400 dynes x sec-1 x cm-5/m2

261
Q

What is the definition of pulmonary artery pressure(PAP, what determines what it is, what is the formula to determine it, and what is the normal value of it?

A

PULMONARY ARTERY PRESSURE (PAP)
• Systolic (SPAP) and diastolic (DPAP) pressures in the pulmonary artery.
• Determined by right ventricular output (RVO) and pulmonary vascular resistance (PVR) (see below) and
downstream pressure (e.g., pulmonary hypertension, increased left atrial pressure, mitral valve stenosis).
• FORMULA: PAP = RVO x PVR
• NORMAL: 15 – 30/8 – 15 mmHg

262
Q

What is the definition of mean pulmonary artery pressure(MPAP), what is the formula to determine it, and what is the normal value of it?

A 
MEAN PULMONARY ARTERY PRESSURE (MPAP)
• The mean or average of the pulmonary artery systolic and diastolic pressures.
• FORMULA: MPAP = SPAP – DPAP + DPAP
3
• NORMAL: 10 – 20 mmHg
263
Q

What is the definition of pulmonary artery wedge pressure(PAWP) or pulmonary artery occlusion pressure(PAOP), what does is approximate, and what is the normal value of it?

A

PULMONARY ARTERY WEDGE PRESSURE (PAWP) or
PULMONARY ARTERY OCCLUSION PRESSURE (PAOP)
• The pressure measured with a pulmonary artery catheter (e.g., Swan-Ganz catheter) when the balloon is
inflated in the pulmonary artery, which reflects pressure distal to the point of occlusion.
• Approximates left atrial pressure.
• Also, approximates left ventricular pressure/preload as long as the mitral valve is normal.
• NORMAL: 8 – 15 mmHg (NOTE: This is approximately the same as the pulmonary artery diastolic
pressure. Clinically, the PA diastolic pressure is used to estimate the PAWP rather than inflating the balloon
on the pulmonary artery catheter and actually performing a PAWP measurement.)

264
Q

What is the definition of pulmonary vascular resistance(PVR) , what is the formula to determine it, and what is the normal value of it?

A

PULMONARY VASCULAR RESISTANCE (PVR)
• The resistance in the pulmonary arteriolar vessels that must be overcome by right ventricular contraction to
eject blood into the pulmonary arteriolar vessels.
• FORMULA: PVR = MPAP – PCWP x 80/CO
• NORMAL: 37 – 250 dynes/sec/cm5 or 37 – 250 dynes x sec-1 x cm-5

265
Q

What is the definition of pulmonary vascular resistance index(PVRI) , what is the formula to determine it, and what is the normal value of it?

A

PULMONARY VASCULAR RESISTANCE INDEX (PVRI)
• Pulmonary vascular resistance correlated with body surface area.
• FORMULA: PVRI = MPAP – PCWP x 80/CI
• NORMAL: 180 – 285 dynes/sec/cm5/m2 or 180 – 285 dynes x sec-1 x cm-5/m2

266
Q

What does a left ventricular volume-pressure loop demonstrate, and how many points are represented?

A

-A LV pressure-volume loop describes one
complete cycle of LV contraction, ejection,
relaxation, and filling.
-four

267
Q

In a normal left ventricular volume-pressure loop, what is being represented at point 1?

A

o POINT 1: MITRAL VALVE CLOSES:
§ LV diastolic filling ends.
§ LV end diastolic volume (preload), which is 140 ml in this example, is reached.

268
Q

In a normal left ventricular volume-pressure loop, what is being represented as point 1 changes to point 2?

A

o 1 → 2: isovolumetric contraction.
§ LV begins contraction (systole).
§ Initially mitral and aortic valves are closed, so no blood is entering or leaving the ventricle, that is, the LV is
contracting (becoming smaller) against a closed chamber.
§ Thus, ventricular volume remains constant and ventricular pressure rapidly increases.

269
Q

In a normal left ventricular volume-pressure loop, what is being represented at point 2?

A

o POINT 2: AORTIC VALVE OPENS
BECAUSE:
§ LV pressure exceeds aortic pressure.

270
Q

In a normal left ventricular volume-pressure loop, what is being represented as point 2 changes to point 3?

A

o 2 → 3: LV EJECTION INTO AORTA:
§ LV volume decreases rapidly.
§ Volume of blood remaining in LV at POINT 3 is the LV end systolic volume, which is 70 ml in this example
(140 ml – 70 ml = 70 ml; LVEDV – LVSV = LVESV).
§ Width of pressure-volume loop between points 2 → 3 represents volume of blood ejected (LV stroke volume), which is 70 ml in this example (140 ml – 70 ml = 70 ml;
LVEDV – LVESV = LVSV).

271
Q

In a normal left ventricular volume-pressure loop, what is being represented at point 3?

A

o POINT 3: CLOSURE OF AORTIC VALVE
BECAUSE:
§ Aortic pressure exceeds LV pressure (LV pressure less than aortic pressure).

272
Q

In a normal left ventricular volume-pressure loop, what is being represented as point 3 changes to point 4?

A

o 3 → 4: ISOVOLUMETRIC RELAXATION.
§ LV relaxes (diastole) (chamber becomes larger).
§ Initially mitral and aortic valves are closed, so no blood is entering or leaving ventricle.
§ Thus, LV volume remains constant and ventricular pressure rapidly decreases.

273
Q

In a normal left ventricular volume-pressure loop, what is being represented at point 4?

A

o POINT 4: MITRAL VALVE OPENS BECAUSE:

§ Left atrial pressure exceeds left ventricular pressure.

274
Q

In a normal left ventricular volume-pressure loop, what is being represented as point 4 changes to point 1?

A

o 4 → 1: LEFT VENTRICULAR FILLING:
§ Initially, passive because of pressure gradient, and then active because of LA contraction.
§ Returns to LV end diastolic volume (preload) at point 1.

275
Q

What are the effects of increased LV end diastolic volume (lv preload) on the left ventricular volume-pressure loop?

A

EFFECTS OF INCREASED LV END DIASTOLIC VOLUME (LV PRELOAD)
• Venous return has increased, which increases LV end diastolic volume (preload).
o Note that the distance between points 4 → 1 has increased, which represents the increased LV filling and preload.
• Strength of LV contraction and LV afterload remain constant.
• Based on the frank-starling relationship, increased LVEDV increases LV stretch, strength of contraction, ejection fraction, and stroke volume.
• Note the increased distance between points 2 → 3, which represents increased LV stroke volume.

276
Q

What are the effects of increased after load on the left ventricular volume-pressure loop?

A

EFFECTS OF INCREASED AFTERLOAD
• LV must eject blood against a higher than normal pressure, such as from aortic stenosis or arteriolar vasoconstriction.
• Thus, ventricular pressure must increase higher than normal during isovolumetric contraction and during ejection.
o Note the increased distance between points 1 → 2, which represents the increased pressure during isovolumetric contraction before the aortic valve opens, and the higher than normal pressure between points 2 → 3, which represents LV ejection.
• As a consequence, less blood is ejected from the LV systole.
o Ejection fraction/stroke volume is decreased.
o LV end systolic volume is increased.
o Note the decreased distance between points 2 → 3.

277
Q

What are the effects of increased strength of LV contraction (positive inotropic effect) on the left ventricular volume-pressure loop?

A

• With increased strength of LV contraction, a larger volume of blood than normal will be ejected during systole, that is, the ejection fraction and stroke volume increase.
o Note the increased distance between points 2 → 3, which represents the increased ejection fraction/stroke volume.
• Less blood remains in the LV.
o The LV end systolic volume decreases, as indicated by point 3

278
Q

On an EKG, what does the “p” wave correspond to?

A

atrial muscle depolarization

279
Q

On an EKG, what does the “p-q” interval correspond to?

A

atrial muscle/AV node/Bundle of His depolarization

280
Q

On an EKG, what does the “p-r” interval correspond to?

A

AV node/bundle of His depolarization

281
Q

On an EKG, what does the “QRS” interval correspond to?

A

ventricular muscle fiber depolarization

282
Q

On an EKG, what does the “S-T” interval correspond to?

A

phase 1 and phase 2 of ventricular repolarization

283
Q

On an EKG, what does the “Q-T” interval represent?

A

ventricular depolarization and repolarization

284
Q

ON and EKG, what does the “T” wave represent?

A

phase 3 and phase 4 of ventricular repolarization

285
Q

What is the corresponding ion movement during Early Phase 0 of depolarization? What occurs from resting (−90mV) to threshold (−60mV)?

A

SODIUM; influx of Na caused by an initial

stimulus

286
Q

What happens when threshold is reached(-60 mV) which leads to what?

A

When we reach threshold (−60mV) we have
opening of fast voltage−gated Na channels; which
cause the AP to rise upward (in a less negative
fashion)

287
Q

What is the significance of reaching -40 mV?

A

The start of Late Phase 0 of depolarization; and slow Ca−Na channels open

288
Q

At +20 mV what happens to the AP?

A

That brings us up to about +20mV; this signifies the end of depolarization and initiates the beginning of repolarization
o Fast voltage−gated Na channels close; however the slow Ca−Na channels are still open and K channels open

289
Q

At the ST segment, from the end of the QRS
complex to the beginning of the T wave; the ion
flow is:

A

K out; Ca−Na in; same number of cations moving in as the same going out

290
Q

At the end of phase 2 of repolarization, what is the ion flow?

A
  • slow Ca−Na channels close and the K channels stay open

- starting the rapid repolarization; correlates with the T wave until we get to Phase 4 of repolarization

291
Q

What Phase does the AP correlate with in regards to the absolute refractory periods?

A

§ Early and Late Phase 0 of depolarization
§ Phase 1 of repolarization
§ Phase 2 of repolarization until it gets back to threshold
§ You can see that the ARP correlates with the upstroke of the T wave; so you will never see another depolarization on the upstroke of the T wave

292
Q

What Phase does the AP correlate with in regards to the relative refractory periods?

A

§ Correlates with the down stroke of the T wave

293
Q

What Phase does the AP correlate with in regards to the super normal P(vulnerable period) refractory periods?

A

§ Occurs at about −85mV down to −90mV; which correlates with the final downslope of the T wave
• So you could see another AP on the down stroke of the T wave; which is very dangerous
• Could lead to ventricular dysrhythmias

294
Q 
Blood vessels (BV) are separated into layers, also
called?
A

Tunics

295
Q

What are the three levels of blood vessels called from outside to inside?

A

(3) Layers (from outside in): tunica adventitia, tunica

media, and tunica intima

296
Q

What are the characteristics of the tunica adventitia?

A

• Tunica adventitia:
o Mostly just connective tissue that provides support and structure and anchors those BVs down
o Sympathetic nerve running along the outside of the nerve that innervates the smooth muscle of the BV
§ BVs only have sympathetic nerve fibers; post
ganglionic
§ Predominantly alpha−1 receptors in the smooth muscle; causing vasoconstriction
§ NE released from the presynaptic nerve ending
o BVs running on the outside of the larger BVs are called the VASO VASORUM
§ Large BVs cannot utilize the blood that is flowing thru them to provide O2 and nutrients to the actual BV tissue; only in the very large BVs

297
Q

What are the characteristics of the tunica media?

A

• Tunica media:
o External elastic membrane:
§ Allows the BV to expand and helps the BV recoil to the original size
o Smooth muscle:
§ Wrapped around the BV; the thicker the smooth muscle the more that BV can constrict and dilate
§ Most of the small/ medium arteries and arterioles have the thickest layer of smooth muscle; these BVs constrict and dilate the most

298
Q

What are the characteristics of the tunica intima?

A

• Tunica intima: innermost layer of the BV
o Internal elastic membrane: performs the same functions as the external elastic membrane
o Lamina propria: composed of smooth muscle and connective tissue
o Basement membrane: provides support and structure for the endothelia cells
o Endothelium: lines the walls of the BVs; indirect contact with the blood itself

299
Q

What are the two types of arteries and characteristics of each.

A

• LARGE ELASTIC ARTERIES: as you can see, this large
elastic artery as mostly elastic tissue; which
allows it to recoil when it is stretched
• MUSCULAR ARTERIES: More like the medium and
small size arteries (like mentioned earlier) that
have very thick layers of smooth muscle that
can constrict arteries to control the blood flow

300
Q

What is the characteristics of veins?

A

VEINS
• Veins are typically a lot thinner than arteries; they still have smooth muscle, so they can dilate and constrict
• Veins have valves that allow for one−way blood flow (and make you look like a chump when trying to start an
IV)

301
Q

Why are capillaries known as exchange vessels?

A

• Capillaries are known as exchange vessels;
exchanges O2 and other nutrients from the blood to the interstitium
• CO2 and other waste byproducts from the interstitium into the blood

302
Q

What is the flow of blood from the arteries to the capillaries?

A

Large arteries-> medium arteries -> small
arteries ->arterioles -> metarterioles ->
capillaries

303
Q

What are capillaries made of?

A

• Very thin later of endothelia cells with a basement membrane layer wrapped around it; good for
O2 delivery

304
Q

• Arteriole divides into ___ and the metarterioles divide into the ___ ___.

A
  • metarterioles

- capillary network

305
Q

What are thoroughfare channels?

A

• THOROUGHFARE CHANNELS are vessels that
have an unobstructed flow from the arteriole to the
venous side

306
Q

What are pre capillary sphincters?

A

• PRECAPILLARY SPHINCTERS are bands of
smooth muscles the constrict and dilate to regulate
blood flow through capillaries

307
Q

What determines if a pre capillary sphincter is constricted or dilated?

A

• Whether a pre capillary sphincter is constricted or

dilated mainly depends on the metabolic rate of the tissues that those capillary networks supply;

308
Q

What regulates blood from from met arterioles into capillaries?

A

REGULATION OF BLOOD FLOW FROM METARTERIOLES INTO CAPILLARIES
• O2 demand of tissue supplied by capillary network
• Vasodilators: CO2, lactate, histamine, adenosine, K+, H+, ↓pH, ↓glucose in tissues, nitric oxide, and others

309
Q

Blood moves by a pressure gradient, at what point in the circulation do you see just one single pressure as opposed to two(for example a diastolic/systolic)?

A

• As you travel down the vascular system, from the aorta
down to the arteries, and arterioles; by the time we get to
the capillaries, we have just one single pressure
• From capillaries we have venules, veins and then the vena cava, were the pressure approaches zero
• Again, there is the pressure gradient; moving blood in one single direction

310
Q

What is the objective on the arterial side of the capillary beds?

A
  • On the ARTERIAL side of the capillary, the objective is to filter fluid from the capillary into the interstitium; FILTRATION
  • ARTERIAL = FILTRATION … VENOUS = REABSORPTION
311
Q

What is the objective on the venous side of the capillary beds?

A
  • On the VENOUS side, the objective is REABSORPTION; movement of fluid from the interstitium back into the capillaries
  • ARTERIAL = FILTRATION … VENOUS = REABSORPTION
312
Q

What are the 4 pressures that regulate filtration and reabsorption of the capillary system.

A
  1. • Starting on the arterial end with CAPILLARY
    HYDROSTATIC PRESSURE (CHP)
  2. • The other capillary pressure we need to look at is PLASMA COLLOID OSMOTIC PRESSURE (PCOP); also called ONCOTIC PRESSURE
  3. • NEGATIVE INTERSTITIAL FLUID PRESSURE (NEG. IFP)
  4. INTERSTITIAL FLUID ONCOTIC PRESSURE (IFCOP);
313
Q

What are the characteristics of Capillary Hydrostatic Pressure(CHP)?

A

• Starting on the arterial end with CAPILLARY
HYDROSTATIC PRESSURE (CHP)
o Hydrostatic pressure is the pressure that the fluid exerts against the walls of its container; in this
example the fluid is blood and the walls of the container is the walls of the capillary
o In this example the CHP is ~ 30 mmHg (you do not need to memorize these numbers, just the concepts)
that favors the movement of fluid from the capillary into the interstitium; favors filtration
o CHP favors FILTRATION; from the capillary to the interstitium

314
Q

o CHP favors _____; from the capillary to the interstitium

A

FILTRATION

315
Q

What are the characteristics of plasma colloid osmotic pressure(PCOP); also called oncotic pressure.

A

• The other capillary pressure we need to look at is PLASMA COLLOID OSMOTIC PRESSURE (PCOP);
also called ONCOTIC PRESSURE
o Blood creates the PCOP from the proteins in the blood; primary plasma protein is ALBUMIN
o Albumin levels are going to contribute most to the PCOP; estimated to be 28 mmHg of pressure in this
example
o PCOP favors REABSORPTION; from the interstitium to the capillary

316
Q

o PCOP favors _____; from the interstitium to the capillary

A

REABSORPTION

317
Q

What ar the characteristics of negative interstitial fluid pressure(NIFP)?

A

• NEGATIVE INTERSTITIAL FLUID
PRESSURE (NEG. IFP)
o When I think of a negative pressure, I think of a vacuum; constantly sucking up fluid
o Caused by the LYMPHATIC SYSTEM; terminal lymphatic vessels that lie adjacent to this interstitial fluid are constantly sucking up that interstitial fluid
§ that creates a negative pressure; estimated to be about 3 mmHg, and favors the movement of fluid from the capillary to the interstitium
§ NEG. IFP favors FILTRATION

318
Q

Negative Interstitial Fluid pressure favors _____.

A

Filtration

319
Q

What are the characteristics of Interstitial Fluid Oncotic Pressure?

A

• Normally albumin is to large to get thru capillary
membranes; however, some albumin and some proteins do get thru
o Which is responsible for the INTERSTITIAL FLUID ONCOTIC PRESSURE (IFCOP); estimated to be about 8 mmHg
o IFCOP favors FILTRATION

320
Q

o IFCOP favors?

A

Filtration

321
Q

On the arterial side of the capillary system, what is the overall goal?

A

• Back on the arterial side;
o Overall goal is FILTRATION of fluid from the capillary to the interstitium
o We need to compute the NET ARTERIAL FILTRATION PRESS
§ OUTWARD MINUS INWARD
§ OUT: 30 (CHP) + 3 (IFP) + 8 (IFCOP) = 41
§ IN: 28 (PCOP) − 28
§ NET ARTERIAL FILTRATION PRESSURE = 13 mmHg
o Favors FILTRATION

322
Q

On the venous side of the capillary system, what is the overall goal?

A

• On the venous side:
o Overall goal is REABSORPTION of fluid from the interstitium to the capillary
o We need to compute the NET VENOUS REABSORPTION PRESSURE
§ INWARD MINUS OUTWARD
§ IN: 28 (PCOP) 28
§ OUT: 10 (CHP) + 3 (IFP) + 8 (IFCOP) = (21) − 21
§ NET VENOUS REABSORPTION PRESSURE = 7 mmHg

323
Q

Why has the CHP dropped from 30 mmHg (on the arterial side) to 10 mmHg (on the venous side)?

A

-Less fluid and less pressure in the venous capillary
§ Albumin has stayed in the capillary so the PCOP has stayed the same
§ The lymphatic system is still sucking so the NEG. IFP is still 3 mmHg;
§ PCOP is still the same as well

324
Q

So on the arterial side, what is the outward CHP?

A

30 mmHg

325
Q

On the arterial side, what is the outward -IFP?

A

3 mmHg

326
Q

On the arterial side, what is the outward IFCOP?

A

8 mmHg

327
Q

On the arterial side, what is the inward PCOP?

A

28 mmHg

328
Q

The net arterial filtration pressure is?

A

13 mmHg

329
Q

On the venous side what is the inward PCOP?

A

28 mmHg

330
Q

On the venous side what is the outward CHP?

A

10 mmHg

331
Q

On the venous side what is the outward -IFP?

A

3 mmHg

332
Q

On the venous side what is the outward IFCOP?

A

8 mmHg

333
Q

The net venous filtration pressure is?

A

7 mmHg

334
Q

The fluid that is not reabsorbed from the interstitium into the venous end of the capillary is taken up into the?
and is deposited into the?

A
  • terminal lymphatic vessels and the lymphatic circulation

- into the left and right subclavian veins, so fluid is eventually returned to systemic circulation

335
Q

What causes increased capillary hydrostatic pressure(CHP)?

A 
INCREASED CHP:
• Increased systemic blood pressure
• Increased vascular volume
• Heart failure/increased CVP
• Arterial side of capillary bed
o Favors filtration
• Venous side of capillary bed
o Opposes reabsorption
336
Q

What causes increased interstitial fluid capillary oncotic pressure(IFCOP)?

A 
INCREASED IFCOP:
• Leaky capillaries and loss of albumin into
interstitial fluid
o Sepsis, major trauma, burns, etc
• Arterial side of capillary bed
o Favors filtration (because that albumin has moved into the interstitial fluid and is pulling volume along with it, from the vascular to interstitium)
• Venous side of capillary bed
o Opposes reabsorption
337
Q

What causes decreased capillary hydrostatic pressure(CHP)?

A

• Decreased systemic blood pressure
• Decreased vascular volume
• Arterial side of capillary bed
o Opposes filtration (less CHP to push that fluid from the vascular compartment to the interstitium)
• Venous side of capillary bed
o Favors reabsorption (again CHP to oppose
filtration, favors reabsorption)

338
Q

What causes decreased interstitial fluid capillary oncotic pressure

A 
DECREASED IFCOP:
• Hypoalbuminemia
o Liver dz, burns, etc
• Arterial side of capillary bed
o Favors filtration (because there is not the osmotic gradient pulling fluid back into the compartment)
• Venous side of capillary bed
o Opposes reabsorption
339
Q

What is the net result of an increase in capillary hydrostatic pressure(CHP)?

A

• Net effect
o Interstitial edema
§ this is a compensatory mechanism to decrease the volume in the vascular compartment
§ especially with CHF; way for that person the decrease vasc vol and displace it into the interstitial compartment
§ same with overload a pt with crystalloids; pt gets puffy because the ↑ CHP
o Decreased vascular volume

340
Q

What is the net result of an decrease in capillary hydrostatic pressure(CHP)?

A

• Net effect
o More volume stays in the systemic circulation
o another compensatory mechanism

341
Q

What is the net result of a decrease in interstitial fluid capillary oncotic pressure(IFCOP)?

A

• Net effect
o Interstitial edema
o Decreased vascular volume

342
Q

What is the net result of a increase in interstitial fluid capillary oncotic pressure(IFCOP)?

A

• Net effect
o Interstitial edema
o Decreased vascular volume
• Be careful giving albumin to the septic, trauma or burn pt’s because that cause even greater vascular fluid loss and edema d/t the leaky capillary beds

343
Q

What causes lymphatic obstructions, how and why?

A

LYMPHATIC OBSTRUCTION:
• Obstruction caused by a tumor or lymphadenectomy (from breast CA)
• Because of the proteins in the interstitial fluid; those terminal lymphatic vessels are constantly sucking up that interstitial fluid protein
• And decreasing the protein level as well as the volume in the interstitium that is compensating for that net arterial pressure being greater than the net venous reabsorption pressure
• When you have lymphatic obstruction, that creates edema because those lymphatics can’t compensate
for the net arterial filtration pressure and net venous reabsorption pressure
• Albumin accumulation in interstitial space
• Net effect
o Remember: NET ARTERIAL FILTRATION
PRESSURE = 13 AND NET VENOUS
REABSORPTION PRESSURE = 7 !!!
o Interstitial edema

4th Quarter (11 decks)

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