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BMSC 207 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What are the primary and secondary roles of the Circulatory system?

A

Primary: The distribution of dissolved gases and other molecules for nutrition, growth and repair, while simultaneously removing cellular wastes.

Secondary roles:
-chemical signaling to cells by means of circulating hormones or neurohormones
-dissipation of heat by delivering heat from the core to the surface of the body
-mediation of inflammatory and host defense responses against invading microorganisms

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2
Q

What are the three types of transport in the circulatory system?

A
  1. Materials entering the body
  2. Materials moved from cell to cell
  3. Materials leaving the body
    (Table 14.1)
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3
Q

What are the two serial circuits in the cardiac system?

A

Pulmonary and systemic

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4
Q

What carries blood away from the heart?

A

Arteries

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5
Q

What carries blood towards the heart?

A

Veins

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6
Q

Where does transport (transfer) take place?

A

Capillaries

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7
Q

What is the pathway that blood takes through the heart?

A

Vena cava -> right atrium -> right ventricle -> pulmonary arteries -> pulmonary veins -> Left atrium -> left ventricle -> aorta -> system

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8
Q

Which parts of the heart mark the start and end of systemic and pulmonary circuits?

A
  • Right atrium = end of systemic
  • Right ventricle = Start of pulmonary
  • Left atrium = end of pulmonary
  • Left ventricle = start of systemic
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9
Q

How does blood flow according to pressure gradients in the body?

A

-The initial region of high pressure in the cardiovascular system is created by contraction of the heart
-blood then flows out of this high pressure region into the lower pressure vessels

High —————————————————————> Low aorta, arteries, arterioles, capillaries, venues, veins, venaca

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10
Q

How does pressure change in the CV system?

A
  • the walls of the fluid filled ventricles contract, increasing the pressure of the blood within the ventricles. This high pressure created in the ventricles is the driving pressure.
    -when the heart muscles relax and expand the pressure exerted by the blood within the ventricles decreases.
    -aside from pressure changes within the ventricles many vessels have the ability to constrict or dilate also affecting blood pressure.
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11
Q

How does pressure, resistance, radius, length, and viscosity affect flow?

A
  • Flow is directly proportional to pressure gradient
  • Flow is inversely proportional to resistance
  • Flow is directly proportional to the fourth power of radius
  • Flow is inversely proportional to length
  • Flow is inversely proportional to viscosity
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12
Q

How is velocity affected in the CV system?

A

Velocity is dependent on flow rate and cross sectional area.
- When flow rate remains constant, velocity increases as cross sectional area decreases

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13
Q

What is the pericardium?

A

-a double walled sac filled with a thin layer of clear pericardial fluid.
-lubricates the external surface of the heart as it beats within the sac.

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14
Q

What are the different Atrioventricular valves?

A

Atrioventricular valves (AV)- allow flow from the atria into the ventricles
-RA>RV: tricuspid valve (3 flaps). RST; Right Side Triscupid
-LA>LV mitral valve (bicuspid).
-the AV valves are attached to a papillary muscle in each ventricle by chordae tendineae (tendon)
-these muscles only supply stability to the valves and are not able to open them
- Ensure blood flows in one direction

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15
Q

What are the different semilunar valves?

A

Semilunar valves- are one way valves that exist between the ventricle and outflow artery.
-both have 3 cup-like leaflets
-LV>Aorta: aortic valve
-RV>pulmonary artery: pulmonary valve.
-these valves do not need connective tendons due to the shape of them

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16
Q

Which valves are open/closed during ventricular contraction?

A

Open: Semilunar
Closed: AV

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17
Q

Which valves are open/closed during ventricular relaxation?

A

Open: AV
Closed: Semilunar

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18
Q

How does the cardiac conduction system work?

A

Pathway: SA node > Internodal pathways > AV node > AV bundle > bundle branches > Purkinjie fibres

  • The group of autorhythmic cells with the most rapid pacemaker activity set the heart rate.
  • SA has the fastest firing rate so it sets the pace (AV also has firing rate but not as rapid)
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19
Q

What is atrial conduction? How does it work?

A

Atrial muscle has four special conducting bundles:

  • Backman’s bundle- conducts action potentials from the SA pacemaker into the left atrium causing contraction.
  • Anterior, middle and posterior internodal pathways-conduct the action potential from the SA node to the AV node, depolarizing right atrial muscle along the way
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20
Q

What is ventricular conduction? How does it work?

A

-Layer of connective tissue prevents conduction directly from atria to ventricle.
-Conduction slows down through the AV node to allow blood from atria to empty in to ventricles
-depolarization proceeds through the septum to the apex (bundle of His followed by bundle branches)
-then spreads up the walls of the ventricles from apex to base (purkinje fibres)
- Ventricular muscles are spiralled to ensure blood is pushed in the right direction

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21
Q

What is a complete conduction block? How does it affect the heart?

A

Caused by damage in conduction pathway
-Eg. Block at the bundle of His results in a complete dissociation between the atria and ventricles.
-the SA node continues to be pacemaker for the atria, but electrical activity does not make it to the ventricles so the purkinje fibers take over as the pacemaker for the ventricles.
-requires an artificial pacemaker

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22
Q

What is an electrocardiogram? What does it measure?

A
  • Extracellular recording
  • Records the summed electrical activity generated by ALL CELLS of the heart
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23
Q

What is Einthovens triangle?

A
  • hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg.
    -The sides of the triangle are numbered corresponding to the three “leads” (pairs of electrodes) they create.
    -the ECG is recorded one lead at a time, where one electrode acts as a positive electrode and one acts as a negative electrode. (Eg lead 1, left arm is positive electrode, right arm is negative electrode.)
  • Presents a vector reading ~ direction + amplitude
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24
Q

How does different electrical activities affect readings on the ECG?

A
  • If the electrical activity of the heart is moving towards the positive electrode of the lead then an upward deflection is recorded.
    -electrical activity moving away from a positive electrode is recorded as a downward deflection
    -electrical activity moving perpendicular to the axis of the electrodes causes no deflection
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25
Q

What are the different aspects of an ECG (ex. Waves, segments, intervals)?

A

Waves appear as deflections above or below the baseline

Segments are the sections of baseline between two waves

Intervals are the combination of waves and segments

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26
Q

What is the p wave?

A

The P wave is the first little bump on an ECG, it happens when the atria depolarize.
- Connected to the SA node

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27
Q

What is the P-Q or P-R segment?

A

It is the segment immediately following the P wave, it happens when there is conduction through AV node and AV bundle.
- During this the atria contract
- Conduction spreads in all directions

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28
Q

What is the Q,R,S waves individually? And what is the QRS complex?

A

Q wave: small depolarization of interventricular septum
R wave: main mass of ventricles contracting
S wave: Final bit of ventricular depolarizing.
QRS complex: overall represents ventricular depolarization
- Biggest bump on ECG

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29
Q

What is the ST segment?

A

It is the segment immediately following the QRS complex. It happens when all cells plateau.
- During this segment the ventricular contract.

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30
Q

What is the T wave?

A

It is the wave immediately following the ST segment. It represents ventricular repolarization.

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31
Q

What is the heart rate on an ECG?

A

P wave to P wave

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32
Q

How do arrhythmias appear on an ECG?

A
  • Arrhythmias (electrical problems during the generation or conduction of AP’s through the heart) can appear as elongated segments or intervals, altered, missing or additional waves.
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33
Q

What is premature ventricular contractions? How is it perceived on an ECG?

A
  • Happens when the purkinje fibres randomly kick in as pacemaker, can be do to insufficient oxygen to myocardium, excessive Ca2+, hypokalemia, medications, exercise, high levels of adrenaline)
    -perceived as skipped beat or palpitation on ECG
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34
Q

What is Long QT syndrome?

A

An example of an arrhythmia:
- inherited channelopathy (K+, Na+)
-delayed repolarization of the ventricles
-palpitations, fainting, and sudden death due to ventricular fibrillation
-can be drug induced

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35
Q

What is the difference between diastole and systole?

A

Diastole: the time during which cardiac muscle relaxes
Systole: the time during which cardiac muscle contracts
-because the atria and ventricles do not contract and relax at the same time the events are discussed separately.

BOTH refer generally to ventricles but can refer to other things.

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36
Q

What (broadly) are the 5 phases of the cardiac cycle?

A
  1. The heart at rest: (atrial and ventricular diastole, late diastole)
  2. Completion of ventricular filling (atrial systole)
  3. Early ventricular contraction (isovolumetric ventricular contraction)
  4. The heart pumps (ventricular ejection)
  5. Ventricular relaxation (isovolumetric ventricular relaxation, early
    diastole)
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37
Q

What happens during late diastole?

A
  1. The heart at rest: atrial and ventricular diastole (late diastole)
    • Cycle starts with atria relaxed and filling with blood from veins
    • the ventricles begin to relax, when the ventricles are sufficiently relaxed and pressure in atria exceeds ventricles, AV valve opens and ventricles passively fill with blood from atria.
    - Starts at End systolic volume
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38
Q

What happens during Atrial systole?

A
  1. Completion of ventricular filling (atrial systole)
    • Most blood enters ventricles passively but under normal resting conditions the last ~ “20%” enters when the atria contract.
    - Atrial contraction forces a small amount of additional blood into the ventricles.
    - At the end the ventricles are at end diastolic volume
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39
Q

What happens during isovolumetric ventricular contraction?

A
  1. Early ventricular contraction (isovolumetric ventricular contraction)
    • The ventricles begin to contract, this builds up pressure in the ventricles and causes the AV valves to snap shut (first heart sound s1 “lub”)
    • Both valves are now closed and then the ventricle continues to contract building up pressure.
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40
Q

What happens during ventricular ejection?

A
  1. The heart pumps (ventricular ejection)
    • As the ventricles contract pressure in the ventricle exceeds pressure in the outflow arteries (aorta or pulmonary arteries) causing the semi lunar valves to open and blood to flow out.
    - At the end it is at end systolic volume
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41
Q

What happens during isovolumetric ventricular relaxation?

A
  1. Ventricular relaxation (isovolumetric ventricular relaxation)
    • The ventricles then begin to relax, pressure in the outflow arteries begins to exceed the ventricles causing blood to attempt to flow backward into the ventricles causing the semi lunar valves to snap shut (second heart sound s2 “dub”)
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42
Q

Friendly reminder to review all diagrams pertaining to the cardiac cycle <3

A
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43
Q

What is EDV,ESV, and stroke volume?

A

End diastolic volume (EDV)-the maximal volume in the ventricle, after ventricular filling, 70kg man at rest ~135ml

End-systolic volume (ESV)- the minimal amount of blood in the ventricles, blood left after ventricular contraction, ~65ml (decreases during exercise)

Stroke volume (SV) -amount of blood ejected during a single ventricular contraction, ~70ml (L/beat or ml/beat)

SV = EDV-ESV

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44
Q

What is the ejection fraction?

A

Ejection fraction (EF)=(the percentage of EDV that is ejected from the heart (SV)
EF=SV/EDV =70ml/135ml=52%

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45
Q

What is cardiac output?

A

Flow of blood delivered from one ventricle in a given time period (usually 1 minute) is the cardiac output (CO)
- CO’s of the pulmonary and systemic circuit are usually identical.
-if offset, blood tends to pool in the circuit feeding the weaker side of the heart.

Total blood flow (cardiac output) = heart rate x stroke volume
CO=F=HR*SV

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46
Q

How can cardiac output be modified?

A
  • CO can be modified by adjusting Heart rate.(check notes?)
  • CO can be adjusted by modulating stroke volume.
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47
Q

What factors affect the amount of force generated by cardiac muscle?

A
  1. The contractility of the heart
    -the intrinsic ability of a cardiac muscle fibres to contract at any given fibre length and is a function of Ca2+ entering and interacting with the contractile filaments.
  2. The length of the muscle fibres at the beginning of contraction
    -this is determined by the volume of blood in the ventricle at the beginning of contraction (end-diastolic volume)
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48
Q

How is contractility controlled?

A
  • Any chemical that affects contractility is called an inotropic agent and its influence is referred to as an inotropic effect.
    -chemicals increasing contractility have a positive inotropic effect and ones decreasing contractility a negative inotropic effect.
    -Catecholamine’s (Norepinephrine and epinephrine) released from the sympathetic neurons or adrenal medulla cause a positive inotropic effect regardless of EDV.
    -contractility increases as the amount of Ca2+ available for contraction increases.
49
Q

What is sympathetic modulation of contraction?

A
  1. Phosphorylation of Ca2+ channels increases calcium conductance during action potentials.
  2. Phosphorylation of ryanodine receptors enhances sensitivity to Ca2+, increasing release of Ca2+ from the sarcoplasmic reticulum.
  3. Increases rate of myosin ATPase
  4. Phosphorylation of SERCA (PLN) increases the speed of
    Ca2+ re-uptake which increases Ca2+ storage.
50
Q

How does increasing sarcomere length increase force of contraction?

A
  1. Raising sarcomere length increases the Ca2+ sensitivity of the myofilaments.
    -a stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross-bridge cycling.
  2. Raising sarcomere length puts additional tension on stretch- activated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release increasing tension.
51
Q

What is the frank starling law of the heart?

A

-the amount of force developed by the cardiac muscle of a ventricle (as indicated by stroke volume) depends on the initial stretch of the ventricle walls (caused by ventricular filling)

-the degree of myocardial stretch prior to contraction is known as the preload on the heart.

According to frank-starling law, stroke volume increases with increasing end-diastolic volume.

52
Q

What is venous return? What factors affect venous return?

A
  • Increased venous return = increased venous pressure = increased atrial filling = increased ventricular filling

Factors:
1. Skeletal muscle pump: Skeletal muscle activity compresses veins in the extremities pushing blood back to the heart.
-increased muscle activity of the extremities can increase venous return.
2. Respiratory pump: during inspiration the chest expands and diaphragm moves down creating a subatmospheric pressure in the thoracic cavity, this draws blood into the vena cava that exist within this cavity
-also during inspiration veins in the abdomen are compressed also forcing blood back to the heart.
3. Sympathetic constriction of veins: decreases their volume squeezing blood back towards that heart.

53
Q

What is afterload?

A

Afterload is the is the end load against which the heart contracts to eject blood
-primarily determined by the combination of the EDV and the pressure in the outflow artery prior to contraction (aorta or pulmonary artery).
-afterload can be increased in pathological situations (eg. increased arterial blood pressure, decreased aortic compliance)
-clinically arterial blood pressure an indirect indicator of afterload

54
Q

CO flow chart in notes

A
55
Q

What are arteries, arterioles, capillaries, venues, and veins?

A

Arteries: Pressure resivoir that maintains blood flow during ventricular relaxation. Contains: thick smooth muscle layer and elastic fibrous connective tissue.
Arterioles: site of variable resistance (diameter can change)
- Mainly contain vascular smooth muscle
Capillaries: exchange between blood and cells
Veins: serve as an expandable volume resivoir

All contain inner layer of thin endothelial cells and can be wrapped in a combination of elastic tissue, smooth muscle or fibrous tissue.

56
Q

What is vascular smooth muscle?

A

-the amount of smooth muscle in each vessel type varies
-in most vascular smooth muscle there is always a state of partial contraction (tone)
-vascular smooth muscle can be influenced by a variety of substances including neurotransmitters, hormones, paracrines
-these substances bind receptors ultimately resulting in an increase in cytosolic Ca2+ causing contraction

57
Q

How is arterioles diameter controlled by tonic release of Norepinephrine?

A

The main determinant of resistance in the majority of arterioles is the sympathetic nervous system:
-primarily sympathetic neurons innervate arterioles and tonically control arteriolar diameter through activation or deactivation of α1 adrenergic receptors.

-Sympathetic neuron that release norepinephrine act on a receptors to change diameter of vessel
- Moderate = intermediate diameter
- increased norepinephrine = constriction of vessel
- Decreased norepinephrine = dilation of vessel

58
Q

What is micro circulation?

A

-arterioles, capillaries and venules make up the microcirculation
-across the microcirculation you have metarterioles which act as a capillary bypass vessels (also for WBC’s).

59
Q

What are capillaries? What makes up capillaries?

A

-smallest vessels in the cardiovascular system, where the majority of exchange between the blood and interstitial space occur.
-single thin endothelial layer surrounded by a basal lamina (extracellular matrix)
-gases can normally passively diffuse across the endothelial cells
-linked by interendothelial junctions that also aid in the transport of small solutes and water
-Some cells contain fenestrations, membrane lined conduits running through them to allow the transport
-capillaries are often surrounded by pericytes (BBB)

60
Q

What are the types of capillaries?

A

A. Continuous capillary: most common -thicker endothelial cells that do not contain fenestrations. -Only allow passage of water and small ions through intercellular junctions
B. Fenestrated capillary: thin endothelial cells that are perforated with fenestrations. The fenestrations often have a thin diaphragm. -small molecule passage
C. Discontinuous (sinusoidal) capillary: lack a basal membrane, have large open fenestrations as well as gaps between the endothelial cells. (liver and spleen)

61
Q

What are the methods of transport in capillaries?

A

Transcellular transport- diffusion or osmosis across the endothelial cell membrane. -gases, small lipid soluble molecules, water (aquaporin channels).

Paracellular transport: diffusion through interendothelial junctions, pores or fenestrations (water, small water soluble and small polar molecules).

Transcytosis: the combination of endocytosis, vesicular transport, and exocytosis that transports macromolecules across endothelial cells.

62
Q

What is angiogenesis? How does it work?

A

Angiogenesis: the formation of new blood vessels
-Angiogenic growth factors (mitogens-pro mitotic) activate receptors on endothelial cells
-activated endothelial cells produce proteases that degrade the basal lamina so it can move away from the parent vessel
-endothelial cells proliferate into the surrounding matrix and form sprouts towards the angiogenic stimulus in tandem.
-sprouts then form loops to become a full- fledged vessel lumen as cells migrate to the site of angiogenesis

63
Q

What is blood pressure? Where is blood pressure the highest?

A

-pressure highest in the aorta and decreases throughout circuit
-aortic pressure highest during ventricular contraction (systole): systolic pressure (120 mm Hg) and lowest during ventricular relaxation (diastole): diastolic pressure (80 mm Hg).

64
Q

What is pulse pressure?

A

-the difference between the systolic and diastolic pressure is known as the pulse pressure

Pulse pressure= systolic pressure-diastolic pressure

  • Pulse pressure normally only exists on the arterial/arteriole side of circuit
65
Q

What is mean arterial blood pressure?

A

-because the pressure is pulsatile we look at a single value, the mean arterial blood pressure as the driving pressure for blood flow.
-The mean arterial blood pressure is not simply the average of the systolic and diastolic pressures (100 mm Hg) because equal amounts of time are not spent in systole and diastole.

MAP = Diastolic + 1/3 pulse pressure
MAP & CO x peripheral resistance

66
Q

What is the difference between hypotension and hypertension?

A
  • Hypertension represents when the blood pressure is chronically elevated (>140/90)
    • High pressure on the vessel walls can cause them to become weakened or even rupture and leak
  • Hypotension represents when the blood pressure falls too low (<90/60)
    • This can cause the driving force for blood flow to be inadequate to overcome the opposition by gravity
  • Cerebral hem orange: high BP in brain, can cause stroke
67
Q

What is a Sphygmomanometer?

A

A tool to measure blood pressure
Steps:
1. When the cuff is inflated so that it stops arterial blood flow, no sound can be heard through the stethoscope and the pressure measured is your systolic pressure
2. The pressure is slowly released and korotkoff sounds are created by turbulent blood flow.(arterie is still slightly compressed)
3. Blood flow is silent when the artery is no longer compressed the pressure measured is your diastolic

68
Q

What influences Mean arterial blood pressure?

A

Determinants:
1. Blood volume: Fluid intake or fluid loss (may be regulated at kidneys or passive)
2. Effectiveness of the heart as a pump: Heart rate and stroke volume
3. Resistance of the system to blood flow: Diameter of the arterioles
4. Relative distribution of blood between arterial and venous blood vessels: Diameter of the veins

69
Q

What is the relative percentage of volume between veins and arteries?

A
  • Arteries are low-volume vessels that contain ~11% of the total blood volume at any one time
    -veins are high volume vessels and hold ~60% of the circulating blood volume at any one time
70
Q

How does changes in blood volume affect blood pressure?

A
  • Small changes in blood volume occur from ingestion of food and liquids. ~ primarily resolved by kidneys
  • Decreases in blood volume require an integrated response from the kidneys, the cardiovascular system (increase sympathetic output) and ingestion of fluid
    Slide in notes with pathway
71
Q

Which vessel has the highest resistance??

A

Arterioles!
- Vessels with the smallest radius theoretically should have the highest resistance (capillaries).
Not the case
-Aggregate (total) resistance not only depends on the radius of each vessel but also on how vessels are arranged (series vs parallel).
- Because Capillaries are in parallel it lowers their resistance

72
Q

What influences Arteriolar resistance?

A
  1. Local control of arteriolar resistance matches tissue blood flow to the metabolic needs of the tissue:
    -in the heart and skeletal muscle, these local controls often take precedence over reflex control by the CNS
  2. Sympathetic reflexes mediated by the CNS maintain mean arterial pressure and govern blood distribution for certain homeostatic needs such as temperature regulation.
  3. Hormones-particularly those that regulate salt and water excretion by the kidneys, influence blood pressure by acting directly on the arterioles and by altering autonomic reflex control
73
Q

What is myogenic auto regulation?

A
  • An example of local control of the dilation/constriction of arterioles.
    -an increase in blood pressure causes the vascular smooth muscle in the wall of the arteriole to stretch, which then causes the vascular smooth muscle to contract, leading to vasoconstriction.
    -arterioles contain a variety of stretch activated TRP channels, particularly TRPV2, TRPC6, and TRPM4 that are thought to be responsible for the mechano-depolarization leading to a myogenic response
    Good flowchart on slide
74
Q

How do paracrines alter vascular smooth muscle?

A

22

75
Q

How is arterioles diameter controlled by tonic release of epinephrine?

A

The main determinant of resistance in the majority of arterioles is the sympathetic nervous system:
-primarily sympathetic neurons innervate arterioles and tonically control arteriolar diameter through activation or deactivation of α1 adrenergic receptors.

-secondary mechanism involves release of epinephrine from the adrenal medulla in response to sympathetic activation
-epinephrine has a low affinity for alpha receptors that cause vasoconstriction and a high affinity for B2 adrenergic receptors which lead to vasodilation
-depends on relative amount of each receptor (eg. muscles more beta than alpha, GI more alpha than beta)
- Epinephrine = Dilation

76
Q

LOOK AT FIGURE 15.11B SLIDE 34 WEEK 13

A
77
Q

How does the body distribute blood to the tissues? How does this vary based on conditions in the body?

A

total blood flow through all the arterioles equals the CO
-flow for each arteriole depends on the resistance, if an arteriole constricts resistance increases and blood flow through that arteriole decreases. Blood will take the path of least resistance.

-eg skeletal muscle receives ~20% of CO at rest, but that can increase to as high as 85% during strenuous exercise
-at rest regional amount of blood flow depends on the number and size of arteries feeding the organ
-regional variations can occur because arterioles are arranged in parallel (in addition to series branching) meaning they all receive blood at the same time

78
Q

How does the brain regulate CV function?

A

The CNS coordinates reflex control of blood pressure and the distribution of blood to tissues
-main integrating center: medullary cardiovascular control center (CVCC)
-primary function: ensures adequate blood flow to the brain and heart by maintaining sufficient mean arterial pressure.
-CVCC receives input from sensory receptors and other brain regions and has the ability to specifically alter function in a few organs or tissues

79
Q

What is the Baroreceptor reflex?

A
  • The primary reflex pathway for homeostatic control of mean arterial blood pressure is the baroreceptor reflex
    -baroreceptors are tonically active stretch sensitive mechanoreceptors that are situated on the aorta and on the carotid artery
    -when there is an increase in blood pressure the baroreceptors sense the stretch in the artery walls and increase their firing rate
    -decrease blood pressure>decrease firing rate.
  • Reflex is constantly active
80
Q

LOOK AT FIGURE 15.14A AND 15.14B and 15.15 SLIDES 39/40/41

A
81
Q

What do peripheral chemoreceptors do?

A

Peripheral chemoreceptors located on the aortic arch and carotid artery
-sense alterations in blood-gas concentrations [O2], [CO2] as well as changes in blood pH
-send information back to the cardiovascular control center which then results in a change in autonomic output to return blood gas levels to normal values.
-peripheral chemoreceptor activation changes ventilation within the respiratory system

82
Q

How does emotional stress affect the cardiovascular function?

A
  • The hypothalamus is capable of altering cardiovascular function in response to emotional stress
  • Some individuals faint in response to sudden emotional distress, sight of blood, phlebotomy (needle insertion), acute pain: Vasovagal syncope

-results in a large increase in parasympathetic output (decrease CO) and reduction in sympathetic output (large decrease in peripheral resistance) (fall in blood pressure fails to activate normal baroreceptor response)

-the combination of decreased CO and decreased peripheral resistance cause a large fall in mean arterial pressure, primarily parasympathetic decrease in HR

83
Q

What is bulk flow? How is it tied to absorption and filtration?

A
  • bulk flow is the mass movement of fluid as the result of hydrostatic or osmotic pressure gradients.
    -if bulk flow is resulting in fluid moving into the capillaries, absorption is taking place
    -if bulk flow is resulting in the movement of fluid out of the capillaries this is filtration
84
Q

What is hydrostatic pressure? What is oncotic pressure?

A

-the pressure in the blood vessels drives fluid out of the capillaries through pores and cell junctions (filtration) and is known as the hydrostatic pressure (PH)
-the pressure that draws fluid into the capillaries is the pressure created by plasma proteins in the blood and this is known as the colloid osmotic pressure or more simply oncotic pressure (π) (it is the osmotic pressure created by proteins).

85
Q

What factors influence net filtration vs net absorption?

A

-π steady in the capillary and exceeds the interstitial space π (zero)
- PH in vessels decreases as blood travels through the capillaries due to the resistance encountered and exceeds interstitial PH (zero)
-at the arterial end PH exceeds π causing net filtration
-at the venous end π exceeds PH and there is absorption
-overall, there is a net filtration from the entire capillary network resulting in a loss of 3L of fluid/day from the blood

If PH > Pi then there is net filtration
If PH < Pi then there is net absorption

86
Q

What does the lymphatic system do? What does the lymphatic system consist of?

A
  • lymphatic vessels assist the cardiovascular system with returning fluid and proteins lost through the capillaries
    -similar to capillaries, single endothelial cell layer
    -contain large interendothelial junctions that act like one way valves -nodes distributed throughout the lymphatic system contain immune cells
87
Q

How does valve opening/closing work in the lymphatic system?

A
  • In the intital lymphatic segment, the interstitial hydrostatic pressure is higher than inside the lymphatic causing the microvalves to open and fluid to flow in.
  • As it fills up with fluid the lymphatic hydrostatic pressure exceeds interstitial, the microvalves close and the secondary valves open.
  • Collecting lymphatics contain smooth muscle that actively contract to propel fluid and one way valves to prevent backflow, skeletal muscle assists as well
88
Q

What is edema? Why does it occur?

A

Edema: An abnormal accumulation of fluid in the interstitial space
Arises for two different reasons:
1. Inadequate lymph drainage: can occur
from obstructions in the lymphatic system particularly within the lymph nodes.
2. A disruption in normal balance between capillary filtration and absorption(filtration>absorption):
i. Increased capillary hydrostatic pressure (heart failure)
ii. decrease in plasma protein concentration (malnutrition, liver failure)
iii. increase in interstitial proteins (excessive leakage of proteins out of capillaries):injury, inflammation
https://upload.wikimedia.org/wikipedia/commons/8/84/Combinpedal.jpg

89
Q

What is Atherosclerosis? Why does it occur?

A

Inflammatory process leading to hardening or narrowing of arteries
-The role of elevated blood cholesterol is well established -cholesterol is not readily soluble in aqueous solutions, joins with lipoproteins

Clinicians concerned with two types of lipoproteins:
1. High-density lipoprotein-cholesterol complexes (HDL-C)
High levels associated with lower risk of heart attack (H-healthy)
2. Low-density lipoprotein-cholesterol complexes (LDL-C)
“bad” cholesterol, elevated levels associated with coronary heart disease
Necessary for cholesterol transport in to cells, LDL-C’s proteins are digested to amino acids and the freed cholesterol is used to make cell membranes and steroid hormones

90
Q

How does atherosclerotic plaque develop?

A

See 58 wk 13/14

91
Q

What is a myocardial infarction? Why does it occur?

A

• If a clot blocks blood flow to the heart muscle, a myocardial infarction (heart attack) ensues
• Lack of O2 leads to ATP supply declining, the contractile cells become unable to remove Ca2+ from cytosol
•High intracellular[Ca2+] closes gap junctions in the damaged cells, electrically isolating them.
• If the damaged region of myocardium is large, disruption can cause an irregular heart beat (arrhythmia) potentially leading to cardiac arrest or death
• Atherosclerosis in brain vasculature account for 50% of strokes

92
Q

How does hypertension affect cardiovascular health?

A

-doubles the risk for CVD for each 20/10 mmHg increase in blood pressure above the baseline value of 115/75
- 62 wk 13/14

Effects of hypertension
-adaption of the baroreceptors to higher pressure with a down regulation of their activity
- is a risk factor for atherosclerosis, the increased pressure exerted on arterial walls damages the endothelial cell lining and promotes plaque formation
-hypertension increases afterload
-over time the increased force the heart must over come causes myocardial contractile cells to undergo hypertrophy
-eventually the heart cannot meet work load and begins to fail

93
Q

What are some treatments for hypertension?

A

• Ca2+ channel blockers (L-type) to relax the vascular smooth muscle and/or decrease CO (HR and force of contraction)
• Diuretics increase urination removing excess fluid to decrease blood volume
• Beta blockers block B1 adrenergic receptors decreasing CO
• ACE inhibitors and angiotensin receptor blockers prevent vasoconstriction from renin-angiotensin aldosterone axis

94
Q

What is blood (general)? What percentage does each part of blood account for?

A

A connective tissue composed of cellular elements suspended in an extensive fluid matrix that circulates in the CV system.

• Total blood volume:~7-8%of total body weight:
• 70mL/1 kg body weight in an adult female and ~80mL/kg body weight in an adult male.
• Hematocrit(40-45%)is the fraction of the total column occupied by RBC’s
• Buffy coat is WBC’s and platelets (1%<)
• Plasma(55-60%):pale white solution of electrolytes, plasma proteins, carbohydrates and lipids.

95
Q

What are albumins?

A

A type of plasma protien:
- Account for ~60% of plasma proteins
- Come from the liver
- Function as: contributors to colloid osmotic pressure of plasma; carriers for various substances.

96
Q

What are Globulins?

A

A type of plasma protien:
- Come from the liver and lymphoid tissue
- Function as: clotting factors, enzymes, antibodies, carriers for various substances

97
Q

What is FIbrinogen?

A

A type of plasma protien:
- Come from the liver
- Function as: Forming fibrin threads that are essential to blood clotting

98
Q

What is transferrin?

A

A type of plasma protien:
- Come from the liver and other tissues
- Function as: iron transport

99
Q

What is Hematopoiesis? What is its process?

A

Hematopoiesis-production of blood cells
In adult: pelvis, spine, ribs, cranium and proximal ends of long bones.

Hematopoiesis: lineage development guided by cytokines (cell signaling molecules)
Guided by cytokines: Proteins or peptides
released from one cell that affect growth or activity in another cell

Begins with a pluripotent hematopoietic stem cell > uncommitted stem cells > stem cells > circulation

100
Q

What are the three Cytokines involved in hematopoiesis?

A

Erythropoiesis-RBC production (EPO): kidney cells ~ stimulated by low O2

Leukopoiesis- Leukocyte (WBC) production (CSF’s)

Thrombopoiesis-Thrombocyte (platelet) production (TPO): liver

101
Q

What are RBCs? What tasks do they carry out?

A
  • Most abundant cell type in the blood (5 million/ul) (~4
    month lifespan)
  • Non-nucleated biconcave cells with diameter ~7.5um distinctive shape increases surface to volume ratio, decreases diffusion distance
  • Shape: Allows them to squeeze through capillaries, respond to osmotic changes, provide evidence of disease
    RBC’s three major tasks:
    1. Carrying O2 from the lungs to the systemic tissue
    2. Carrying CO2 from the tissues to the lungs
    3. Assisting in the buffering of acids and bases.
102
Q

What is hemoglobin? What does it consist of?

A

RBC’s mainly consist of hemoglobin: the O2 transport protein ~96% of dry weight

Consists of:
- globin proteins: alpha, beta, gamma or delta
-most common two alpha and two beta chains, each contain heme group
-70% of iron in the body found in heme groups of hemoglobin -each heme group can bind one oxygen (O2) molecule

103
Q

What is the process of hemoglobin synthesis?

A
  1. Iron injested from diet
  2. Fe absorbed by active transport
  3. Transferrin protein transports Fe in plasma
  4. Bone marrow uses Fe to make hemoglobin as part of RBC synthesis
  5. RBCs live about 120 days in the blood
  6. Spleen destroys old RBCs and converts Hb to bilirubin
  7. Bilirubin and metabolites are excreted in urine and feces
  8. Liver metabolizes bilirubin and excretes it in bile
  9. Liver stores excess Fe as ferritin
104
Q

What are granulocytes? (WBC subcategory) what are the three types?

A
  1. Granulocytes: contain cytoplasmic granules visualized under microscope
    -brief lifespan in the blood < 12hours, but if activated can migrate into tissues for longer time.

Neutrophil: most abundant leukocyte, contain granules with lysosomal enzymes capable of digesting foreign material (phagocytosis).

Eosinophil: granules contain Major Basic Protein (MBP) which is toxic to parasites and other enzymes. Important in response to virus’ and in allergic reactions

Basophil: least common granulocyte, granules contain histamine, heparin and peroxidase and play a role in
allergic reactions

105
Q

What are non-granule containing lymphocytes and monocytes?

A
  1. Non-granule containing lymphocytes and monocytes
    Lymphocytes: two types T-lymphocytes and B lymphocytes (T-Cell, B-cell); Adaptive immunity.
    -T-cells 70-80% of all lymphocytes and responsible for cell mediated immunity, does not involve antibodies. (TMem, TReg THelp, TNK…)
    -B-cells: responsible for humoral immunity, make antibodies to antigens (Bmem, Breg ….)

Monocytes: spend life in peripheral tissues developing into macrophages, which serve two purposes:
1. Phagocytosis of pathogens or cellular debris
2. Present antigens to lymphocytes

106
Q

What are platelets? What types of granules do they contain? What is their primary role?

A

• Nucleus-free fragment’s of megakaryocytes, 2-3umin diameter in their inactive state ~10 day life span.
• Contain two special types of granules
- Densecoregranules
- α-granules
-contain ATP, ADP, serotonin, Ca2+, von Willebrand factor, platelet activating factor, platelet fibrinogen, and clotting factor V
• Essential for hemostasis, the process which keeps blood within a damaged vessel

107
Q

What is Hemostasis?

A

Hemostasis: the prevention of hemorrhage (bleeding) from a damaged vessel

108
Q

What is vasoconstriction?

A
  1. Vasoconstriction: contributes to hemostasis by closing the vessel and preventing blood flow to the damaged region.
    -can be triggered by direct injury to vascular smooth muscle, the release of paracrine signals from damaged endothelial cells (endothelin) or platelets (serotonin, thromboxane A2)
    -bring down the pressure within the vessel so a secure mechanical seal can be applied in the form of a clot
109
Q

How do platelets become activated when creating platelet plugs?

A
  1. Platelet plug formation:
    -inactivated platelets do not adhere to themselves or to the intact endothelium cells that line the vessel (possibly due to like charges)
    -platelets contain cell surface receptors (integrins)
    - A breach of the endothelium exposes integrins to collagen, fibronectin and laminin, which are all part of the subendothelial layer causing platelets to bind.
110
Q

What are the contents of a platelets granule and how do they help create platelet plug?

A
  • binding of integrins causes the activation of an intracellular signaling pathway in platelets causing them to release the contents of their granules: serotonin (vasoconstrictor), ADP and platelet-activating factor (PAF-activates more platelets)
    -PAF signals platelets to release thromboxane A2 (vasoconstrictor)
    -morphological changes, platelet extends many finger-like filopodia
  • Intact endothelial cells release substances to prevent activated platelets from binding
111
Q

What causes platelets to aggregate? What is the con willer and factor?

A
  • ADP, serotonin and thromboxane A2 released all activate additional platelets causing them to recruit to the site and aggregate
    -von Willebrand factor causes platelets to form molecular bridges between one another.
112
Q

What is the coagulation cascade intrinsic pathway?

A

-Intrinsic pathway:
A plasma protein in the blood known as factor XII is converted to factor XIIa (activated form) when it comes into contact with an activated platelet or damaged vessel wall
-Final product is factor Xa through a series of proteolytic steps.

113
Q

What is the coagulation cascade extrinsic pathway?

A

Extrinsic pathway: another cascade of protease reactions occurring outside the vascular system.
-subendothelial cells express a membrane protein known as tissue factor, which is a receptor for a plasma protein, factor VII
-when factor VII leaves vessel through damaged region and comes into contact with tissue factor its converted (non-proteolytically) to factor VIIa
- Tissue factor, factor VIIa and Ca2+ form a complex that proteolytically cleaves factor X to produce factor Xa
-factor Xa produced from either the intrinsic or extrinsic pathway is important for the common pathway

114
Q

What is the coagulation cascade common pathway?

A

Common pathway:
-factor Xa produced from the intrinsic and extrinsic pathway join together with factor Va and Ca2+ to create prothrombinase.
-Prothrombinase converts prothrombin to thrombin
-thrombin is a central protease of the coagulation cascade
-Fibrinogen (one of the main plasma proteins in blood) is then cleaved by thrombin to fibrin monomers
-the fibrin monomers spontaneously polymerize to form a gel of fibrin polymers that weaves through plug and traps blood cells.
-thrombin also activates factor XIII to XIIIa which assists in forming the fibrin polymers into a stable fibrin mesh.

115
Q

SEE FLOWCHART ON PG 97 WK 13/14

A
116
Q

What is coagulation (simplified)?

A
  1. Coagulation
    – Intrinsic pathway (surface contact pathway)
    • Factor XII is activated when contacting exposed collagen, activated platelets
    • Final product is factor Xa
    – Extrinsic pathway (cell injury pathway)
    • Factor VII leaves vessel and binds to tissue factor receptor and become activated Factor VIIa
    • Final product is factor Xa – Common pathway
    • Factor Xa from intrinsic and extrinsic is used to create thrombin which ultimately converts fibrinogen to a stable fibrin clot
117
Q

What is hemophilia? What are the two types of hemophilia? What are the treatments for hemophilia?

A
  • A name given to several diseases in which one of the factors in the coagulation cascade is defective or lacking.
    -bruise easily, spontaneous bleeding
    -bleeding in the joints and muscles can be painful and disabling and if bleeding occurs in the brain it can be fatal.

Types:
• Hemophilia A: a factor VIII deficiency
– Mostcommon~80%ofcases
• Hemophilia B: factor IX deficiency
• Both X-linked recessive

Treatment:
• Treated with synthetic factors
• Just recently AAV treatment increased factor production in clinical trials

118
Q

What are anticoaguation factors?

A
  • Too much coagulation can be a very bad thing (Thrombus: stroke, heart attack, pulmonary embolism).
  • Endothelial cells also produce a variety of anticoagulant factors that interfere with the clotting cascade.
    • Prostacyclin and NO prevent platelet binding
119
Q

What is Fibrinolysis?

A

The breakdown of blood clots:
-Begins with the conversion of plasminogen (produced in liver) to plasmin through proteolysis.
-endothelial cells produce tissue plasminogen activator (t-PA) that causes this conversion
-Plasmin is capable of breaking down both stable fibrin as well as fibrinogen

Fibrinogen > fibrin polymer > fibrin fragments

BMSC 207 (5 decks)

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