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Midterm #1 Flashcards

1
Q

Organization of the Circulatory System

A
  • Left ventricle is the main one that pumps blood throughout body.
  • Right ventricle goes to lungs
  • Makes it so that oxygenated and non-oxygenated don’t mix
  • Pressure
    • Right has less pressure when contracted/relaxed (24/8 mmHg)
      • Easy to push blood through little cappilaries, not need as much pressure
    • Need low pressure in pulmonary capillaries because thin epithelium separating air and blood. Too much pressure, fluid would leave and you would essentially drown
      • Pulmonary edema
      • Goes along with heart failure and other cardiovascular situations
  • Left has more pressure (120 mmHg/80)
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2
Q

Flow of Blood in Circulatory System: Figure

A
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3
Q

Chambers of Heart: Shape and Wall Thickness

A
  • Atria: thin walled
    • Store up blood preparatory for ventricle filling
    • Stretchy
  • Ventricular filling
    • A lot of the blood is “sucked in” (3/4)
    • When atria contract, top off the filling of the ventricle (1/4)
  • Ventricles
    • Right ventricle thinner than left ventricle
    • Left is thicker and circular
      • Create tension for systemic circulation
      • Circular cross section allows muscle contraction to provide efficient pressure
    • Contracts like squeezing fist
  • Right ventricle
    • Shape to move volumes of blood
    • Outer moves towards the inner septum
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4
Q

Left and Right: Veins/Arteries

A
  • Veins are thin, blue, larger, compliant (stretchy, ability to accommodate blood)
  • Right Atrium
    • Vena cava (superior and inferior)
    • Coronary sinus
  • Left Atrium
    • 4 pulmonary veins
  • Right arteries
    • Pulmonary trunk
  • Left arteries
    • Aorta
    • Lots of elastin, less compliant than veins, important for blood pressure. Expands when put blood into in and then springs back
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5
Q

Heart Valves

A
  • ​Through atrioventricular valve into the ventricles
  • Right is tricuspid, left is mitral valve
  • Passive valves
    • open and close because of pressure
    • Flaps that are called leaflets “cuspid”
      • Blood flowing opens the leaflets
      • Blood flowing backward, closes the leaflets
    • Fibrous connective tissue
      • Supports valves
    • Separate atria and ventricle
  • AV Valves
    • Mitral valve
    • Left atrioventricular valve
    • Leaflets extends down, and when they closed they touch each other
    • When open, create a funnel
    • Larger than aortic and pulmonary valves
    • Have connective tissue strands attached to leaflets to prevent leaflets from being blow back
      • Chordae tendineae
      • Connected to mounds of tissue known as papillary muscles
    • When leaflets bulge backwards; prolapsed valve
  • Pulmonary valve and Aortic Valve
    • Blood balloons them down and pushed them together to prevent backflow
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6
Q

Aortic and Pulmonary Valves: Figure

A
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7
Q

AV valves (triscuspid and mitral): Figure

A
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8
Q

Echocardiograms

A
  • Transducer eliciting ultrasound
  • Beam of ultrasounds sweeps around
  • Goes into heart and reflects off of structures and bounces back to sensor
    • Measures the time it takes to bounce back
    • Makes what looks like triangular slice through heart
  • Can add doppler to measure blood flow
    • Sound toward you, beams compressed, higher pitched
    • Sound away from you, beams less compressed, lower pitched
  • Insufficiency: when blood squirts backwards out of valve.
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9
Q

Normal Heart Sounds: S1, S2

A
  • Valve snaps such and then vibrates tissues to produce sound
  • Known as “lub” and “dup”
  • S1, S2 ….. S1, S2 …… S1, S2
  • S1 at start of ventricular contraction (systole)
    • Ventricle continue contraction
  • At the very moment that ventricle begins relaxation, pulmonary valves close
    • S2, pulmonary and aortic valves close
  • Sounds at start of contraction and start of relaxation
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10
Q

Times of systole and diastole

A
  • Time between S1 and S2 is systole
  • Time between S2 and next S1 is diastole
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11
Q

Split Sounds

A
  • Normally S1 is both close at same time and S2 is where pulmonary and aortic close at same time
  • S2 split, asymmetry and not close at same time
  • A little bit of splitting if inhale very deeply (subtle in health person)
  • Bundle branch block
    • Ventricles contracting out of synchrony
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12
Q

S3, S4

A
  • S3 occurs during diastole
    • Rapidly filling of ventricles
    • Ventricles vibrate
    • Weak S3 in small kids
  • In elderly with expanded ECF volume
    • Occurs in CHF
    • Volume overload, ventricles become too weak, during filling, ventricles vibrate during filling.
    • S3 will be more prevalent “lub dup dup” sound
  • S4 just before S1 (and after S3)
    • Atria contract and complete ventricle filling
    • If stiff ventricles due to heart disease (diastolic HF), when atria contract, get vibrating ventricles
  • Not mutually exclusive “lub dup dup dup” (gallop sound)
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13
Q

Laminar and Turbulent Flow

A
  • Sound hearing from blood pressure and valve abnormalities is from turbulent flow
  • Laminar flow
    • Cell in middle of tube will stay in middle of tube
    • Fluid moves in smooth layers/sheets through tube
    • Most efficient way to move fluid through a tube, silent
    • Normal flow through cardiovascular system
  • Turbulent flow
    • Move fluid through faster and faster, fluid will start bonking around everywhere
    • Laminar flow pattern breakdown
    • Creates noise
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14
Q

Stenosis

A
  • Narrowing
  • If valve leaflets don’t open fully
  • Channel that blood flows through is narrower than normally
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15
Q

Isufficiency (Regurgitation)

A
  • Valve leaflets don’t close fully
  • Blood squirts backwards through the hole
  • Be able to go through and determine if murmur is systolic or diastolic for either stenosis or insufficiency
    • Ex: Aortic stenosis.
      • Valve leaflets don’t open fully
      • Aortic open at the beginning of systole
      • Get murmur right after AV valve close and at start of systole
      • “Lub shhhh dup”
      • Diastolic murmur will be “lub dup shhh”
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16
Q

Senile Aortic Stenosis

A
  • Aortic valve is in a stressful position
  • HTN can put stress on aorta
  • Get fibrosis, prevent leaflets from opening fully
  • Inflammation for long periods can cause calcification
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17
Q

Bicuspid Aortic Valve

A
  • In middle age have to be replaced
  • Life expectancy is normal
  • Genetic
  • More prone to stenosis (fibrosis and calcification)
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18
Q

rheumatic fever (heart disease)

A
  • After a person gets strep throat
  • Only 1-2% who get strep throat
  • Ab against streptococcus will also attack valve system in the heart
  • Especially the mitral valve
  • Mitral stenosis
    • Causes left atrial pressure to rise
  • Pulmonary edema
    • Shortness of breath: dyspnea
  • Can progress to congestive heart failure
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19
Q

infective endocarditis

A
  • Happens when get bacteria in the blood
  • Colonize leaflets of valves as go through circulatory system
  • Usually after invasive medical procedure
    • Hospital IV
    • Dentistry (occasionally)
    • IV drug abuse
  • Clots around the leaflets
  • Vegetations, big floppy thing (goobers) sticky around leaflet
  • Can break down chordae tendineae
  • Can cause aortic or mitral insufficiency
  • Mitral insufficiency: pulmonary edema
  • Exercise intolerance because unable to increase cardiac output
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20
Q

Artificial Valves

A
  • Bileaflet totally artificial valve made from carbon fibers, last longer, more likely to form clots
  • Biological (from animal or cadaver), not last as long, less problems associated with them
  • The endothelium is gone and cross-link all proteins, no live cells, cross linked collagen so that there is not immulogical problem
  • Trans-catheter Aortic Valve replacement (TAUR)
    • Balloon at end of catheter that is threaded into position.
    • Balloon expanded and then opens up to push damaged out of place
    • Less invasive.
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21
Q

Coordination of the Heart Beat

A
  • Some heart muscle is myogenic: able to begin contractions by itself
  • Heart still beat even when nerves to it are severed
  • In early embryonic development, all cardiac fibers are myogenic
  • As develop, only some specialized tissue retain this
  • Any injured tissue can cause beating on its own
  • Intercalated discs that connect cells and there are gap junction ion channels
    • Action potentials are able to jump from cell to cell
  • Atrial and ventricular muscle cells are separated by fibrous tissue
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22
Q

SA Node

A
  • # 1; sinoatrial node
  • Shaped like a dime, can’t see it in dissection of heart without special techniques
  • Have myogenic property
  • The natural pacemaker of the heart
  • 100 bpm without any other hormones, nervous input, etc
  • Parasympathetic nerves lower the heart beat
  • Conducts over the atria
  • Then flows to AV node
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23
Q

AV Node

A
  • # 2; atrioventricular node
  • Looks like the SA node
  • Delayed in AV node
  • AP leave the AV node and enter 3, 4, 5
  • If SA node is out of commission, this one comes into effect
    • Has inherent rhythm of 60 bpm
    • Since SA node makes AP at a higher rate than AV node
    • Muscle has long refractory periods and the AV node is reset so that it won’t do its own heartbeat
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24
Q

AV Bundle (Bundle of His)

A
  • # 3
  • Picks up action potential and muscle fibers goes through the layer separating ventricles
  • Big cells and rapidly conduct action potential quickly
  • Quickly through everything
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25
Q

Right and Left Bundle Branches

A
  • # 4
  • Drive heartbeat at 30 bpm
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26
Q

Purkinje Fibers

A
  • # 5, dropped of on the lower inner surface of ventricle
  • Then outwards and downward through the thick ventricular walls.
  • Then conducts up outer wall of ventricle
  • This is usually when the ventricle contracts
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27
Q

Ventricle Action Potential

A
  • Lots of different ion channels
  • Voltage gated ion channels
  • Up sweep of AP (A) is by the fast Na+
    • Lidocaine will block this
  • Action potential has to act a long time (B), not in neuronal action potentials
    • Ca++ channel that is slower opening and slower closing
    • Really positive equilibrium potential
    • Creates the plateau
  • Also need slow K+ channels, (C) like neuronal action potential
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28
Q

SA Node Action Potential

A
  • No fast Na+ channels
  • Do have slow Ca++ and K+ channel
  • Slower action potential
  • Pattern of the injured cardiac muscle cell
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29
Q

Pacemaker Potential

A
  • Doesn’t stay at resting membrane potential
    • Starts creeping up
  • Closing of slow K+, first part of pacemaker potential
  • Opening of “funny “ Na+ channel, open with repolarization rather than with depolarization.
    • Open slowly
  • Calcium channels that open at the same time as well
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30
Q

Change heart rate by changing slope of pacemaker potential

A
  • Speed heart rate by make pacemaker potential reaching threshold faster
  • Slow heart rate by make pacemaker potential reach threshold slower
  • Things altering slope of pacemaker potential:
    • Ach (acetylcholine)
      • Autonomic neural transmitters cause slow postsynaptic potential
      • 7TMD Receptor binding Ach, Trimeric G protein, gamma and opens K+ channel
    • Norepinephrine
      • 7TMDR, Trimeric G protein, opens Ca++ (Na+)
      • Depolarize faster and increase heart beat
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31
Q

Adenosine

A
  • Paracrine and drug
  • Works through trimeric proteins an opens K+
  • Reduces excitability and reduces heart beat
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32
Q

Refractory Period

A
  • Period of time in which ion channels aren’t back to normal configuration
  • Can’t have action potential during that time
  • Really long in cardiac muscle
  • Max heart rate of 190 bpm
  • Long refractory period, after ventricle contract allows time for ventricle to relax
    • Can’t get a steady contraction (tetanus), one action potential after another
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33
Q

Action Potentials: Graphs

A
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34
Q

Basis of Lead II Waveform in Electrocardiogram

A
  • P wave is action potential moving through the atria
  • QRS wave, the action potential moving through the bulk of the ventricle
  • T wave, repolarization, positive because not occurring in the same direction as the depolarization
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35
Q

First Degree AV Block

A
  • Can’t get through the AV node
  • Rather vulnerable part of heart
  • Prone to not working, small cells/muscle fibers
  • Long time between P and QRS wave
  • Slowed conduction velocity, action potential still goes through though
  • Due to heart disease or benign
  • Transient ischemia
  • Athlete, trained heart pumping a lot of blood, needs less bpm, slowed by vagus nerve, ach opens K channels, slows the conduction of the heart
  • Drugs that can cause this as well; Beta-blockers, Calcium channel blockers, digoxin
    • Reduce excitability of the heart
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36
Q

Second Degree AV Block

A
  • P interval gets longer until QRS wave missing
  • Some of the QRS wave are missing
  • Can’t get through the AV node at times
  • Circumstances like the first degree
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37
Q

Third Degree AV Block

A
  • Don’t see QRS right after P
  • See QRS that is big and weird
  • Action potential never gets through AV node
  • Other specialized tissue will then cause the heart to beat
  • AP starts somewhere other than SA node; ectopic focus
    • Instead of going out through ventricular wall quickly, get a right then left contraction, abnormal flow over heart
    • Causes a prolonged and misshaped QRS
  • 30 bpm, person is barely getting enough blood flow to keep themselves going
  • Has serious heart disease, perhaps from a myocardial infarction (MI)
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38
Q

Premature Atrial Contraction

A
  • Instead of waiting normal interval, get a P-QRST stuck in right away
  • From an ectopic focus somewhere in the atria that all of a sudden makes an action potential
  • Could be from heart disease
  • Could also be benign, actually fairly common
  • Know that it is in the atria because the QRST is normal, ventricular tissue getting activated normally
  • Might not have symptoms
  • May have palpitation:
    • Extra beat causes a refractory period, causes a delay before the next heart beat
    • During pause, ventricle fills more fully, so it pumps stronger and person may feel it
  • May have this in older people during stress test; not a good sign
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39
Q

Premature Ventricular Contraction

A
  • Ectopic focus in a ventricle
  • QRS wave is prolonged and misshaped; action potential not all of a sudden dropped to bottom of both ventricles
  • Get a pause because next SA node contraction falls in the refractory period
  • During a stress test; not a good sign, shows damages ventricular muscle
  • QRS waves can be either positive or negative
    • If see both, then there are two ectopic focuses going on
      • start on different sides of the heart
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40
Q

Bundle Branch Block

A
  • Would see normal rhythm but WRS would be distorted in shape and prolong. However QRS wave is occurring in regular intervals
  • Result that both ventricles are not contracting in synchrony
  • Split heart sounds.
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41
Q

Sinus Bradycardia

A
  • Normal ECG with a really slow heart rate
  • Less and 50 bpm
  • Athlete can wake up at 40 bpm, not the same thing
  • Need a pacemaker in this case
  • Eldery, hypothyroidism, cardiovascular disease, drugs (beta blocker, CCB, digoxin)
  • Fatigue, start fainting (syncope)
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42
Q

supraventricular tachycardia

A
  • P waves begin before T wave done
  • AV node and higher in heart driving the heart beat
  • Really fast heart beat, faster than 100 bpm
  • May have episodes of it, or can be a persistent thing
  • Less caffeine, stress reduction, etc.
  • Paroxysmal; all of a sudden, for a period of time, then goes back to normal
  • Increase pumping of heart and changes in blood vessels (need to go hand in hand)
  • Increase pumping and no changes in blood vessels, ventricles not pump properly, may feel woozy and faint
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43
Q

AV Node Reentry

A
  • Most common circumstance that causes supraventricular tachycardia
  • Parts of AV node not working properly
  • AP goes fast through some pathways and slower through other pathways in AV node
  • AP in slow pathway goes into the fast pathway, out of refractory period and causes another AP
  • Goes around and around and around
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44
Q

Accesory Pathway an Supraventricular Tachycardia

A
  • AP potential hits an accessory pathway
  • Scrap of muscle tissue that connects atria and ventricles
    • Not normally there
    • Causes the action potential to loop AP in circular motion back through atria and ventricles
    • Need to destroy that tissue; ablations that heats up tissue with radiofrequency wave that cooks it.
  • Wolff-Parkinson-White Syndrome
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45
Q

Ventricular Tachycardia

A
  • Bad in any circumstance
  • Ectopic focus in ventricle that is going off constantly
  • ICU ward, having a heart attack
  • Hearts racing because chunk of damage to ventricular damage (MI)
  • Genetic causes with abnormal ion channel that makes ventricular fibrillating (myopathy)
  • Will lapse into ventricle fibrillation; death seconds away
  • ECG looks like villi
  • Pacemaker with a defibrillator
    • Defibrillator shocks the crap out of heart to wipe the slate clean
46
Q

Atrial Fibrillation

A
  • 10% of people over 80 have A-fib
  • Atria get stretched out and get slow pathways
  • AP gets into the left atrium
    • Gets past refractory period
    • AP never goes away
  • Atria sitting there and quiver
  • AP shows up at AV node and then contracts
  • Random arrival of AP at the AV node
  • Random heart rate
  • No distinct P wave
  • Hashed/wiggly line and AP at random times
  • May or may not be symptomatic
    • Fatigue
47
Q

Atrial Fibrillation Treatments

A
  • Rate control
    • Beta Blocker (slower HR down)
  • Rhythm control
    • Block sodium channels to reduce excitability
  • Anticoagulation
    • Clot tends to form in the atria
    • Clot in left atria, up into brain, stroke
    • Aspirin and clopidogrel (lowest level and probably will go further; aspirin blocks TXA2 and clopidogrel blcoks ADP)
    • Warfarin
      • Safety net in the fact that it is easy to reverse the effects
    • Dabigatran, etc.
      • Direct thrombin inhibitor
      • Can’t reverse effects quickly
    • Apixaban, etc.
      • Factor Xa inhibitor
      • Can’t reverse effects quickly
  • Ablation around pulmonary veins to get rid of the slow pathways
  • Pacemaker
48
Q

Ventricular Fibrillation

A
  • Fatal within a minute
  • Ventricles siting there and quivering, blood isn’t being pumped
  • Lethal arrhythmias
    • MI (heart attack, clot clogs coronary artery)
    • Myopathy
    • These cause ventricular tachycardia which can lapse into fibrillation
  • Person needs pacemaker with defibrillator
49
Q

Pharmacology for Arrhythmias

A
  • Sodium Channel Blocker
    • Lidocaine
    • Flacainide
  • Beta Adrenergic Blockers
    • Propranol
    • Metoprolol
  • Prolong Repolarization (increase the refractory period)
    • Amiodarone
  • Block Calcium Channels
    • Verapamil
  • Open Potassium Channels
    • Adenosine
50
Q

Cardiac Cycle: Opening and Closing of Valves

51
Q

Cardiac Output

A
  • CO=HR*SV
  • Normal is 5 L/min, exercise 20 L/min, world class athletes are 35 L/min
52
Q

Heart Rate

A
  • Beats per minute
  • Pacemaker potential: sodium, potassium and calcium channels
53
Q

parasympathetic innervation and heart rate

A
  • Ach
  • Predominate effect on heart
  • 100 bpm left to it’s own devices
  • Normal is around 70 bpm due to Ach release
    • Work through trimeric G protein to open potassium channels
  • Ach makes pacemaker potential go up more slowly to increase the refractory period, slows down the heart.
54
Q

sympathetic innervations and epinephrine and heart rate

A
  • Norepi, Calcium and sodium
  • Beta receptor
  • Also epinephrine
55
Q

Stroke Volume: Sympathetic Inervation and Epinephrine

A
  • More calcium stored and released
  • Ventricles contract more forcefully
  • Ejection fraction goes up (EF)
  • Highest EF is when someone is exercising vigorously
56
Q

Stroke Volume:

Increased blood in central veins and increased atrial pressure

A
  • Causes an increase in EDV
  • More ATP expended
    • This causes an increase in stroke volume
    • Stretch cardiac muscle further so that ventricles contract more forcefully.
    • Greater stretch, more ATP energy expended
    • Ventricles fill more fully
57
Q

Stroke Volume: End Diastolic Volume

A
  • End diastolic volume=100 mL, because that is how much is in ventricle when done filling
  • Stroke volume=70 mL
  • Therefore EF=70/100=0.7
58
Q

Frank-Starling Mechanism

A
  • Heart muscle contract more forcefully when stretch it
  • Increased EDV causes Increase SV
59
Q

What causes changes in stroke volume?

A
  • Posture
  • Muscle Contraction
  • FS important to keeps pumping of ventricles pumping exactly the same
    • Premature Heart beat if not
60
Q

Posture: Changes in stroke volume

A
  • Gravity causes blood to pool in leg veins
  • Right ventricular stroke volume is lower
  • If change to laying volume, stroke volume increases
61
Q

Muscle Contractions: Changes in stroke volume

A
  • Locked knees, cause blood to pool in leg veins
  • Stroke Volume is decreased
  • Veins that go through muscle get contracted with muscle contracts-“muscle pumpin”
    • Increases stroke volume
62
Q

Keep pumping of the two ventricles pumping exactly the same!!!

A
  • If right ventricle pumping 1% more than left ventricle (0.7 ml/beat goes into pulmonary from systemic circulation)
    • Blood accumulates in pulmonary veins
    • Get pulmonary edema, lungs fill up with fluid
  • Increase SV in right side, increase pressure in pulmonary veins, increases stroke volume on left side
63
Q

Premature Heart Beat: Changes in stroke volume

A
  • Ectopic focus makes the premature heart beat
  • Pause before next SA node action potential
  • Delay causes ventricle to fill more fully, heart will have a stronger stroke volume
64
Q

Central Venous Pressure

A
  • “Venous Return”
65
Q

Aortic Pressure

A
  • “After load”
  • Effect of dialation of arterioles
    • Influences the aortic pressure
    • Raise aortic pressure makes it harder to left ventricle to pump blood into aorta (decreases SV)
    • Decrease aortic P, Increase in SV
    • CO and blood vessels have to change together when making changes in cardiovascular system
66
Q

Systolic Failure

A
  • Decrease in the ejection fraction
  • Causes:
    • MI
    • Myopathies
    • Alcoholism, valve problem, etc.
67
Q

Systolic Failure: sequence of events; Law of Laplace

A
  • MI causes decreased EF (gets below 0.5, 0.3 is bad, 0.1 can be shock)→Increased blood in central veins (Except Frank-Starling effect to come to the rescue)
  • Since ventricle is weakened, the Frank Starling effect is weakened
  • Increases the EDV (ventricle fills fine, but the SV will not increase), ventricle starts dilating
  • If know tension in walls can calculate the pressure on the inside
    • Law of Laplace
    • Proportional to tension, inversely proportional to radius
    • P=T/R
    • Dilating ventrical needs more tension, starts failing.
  • Increased wall tension sets in motion an abnormal response
68
Q

Increased Tension Causes Abnormal Response

A
  • Hypertrophy
    • Muscle cells increase in size, but abnormally
    • Get fetal isoforms of contractile proteins
    • Capillary growth doesn’t keep up
  • Collagen Damage
    • Abnormal stretch causes collagen damage
    • Fibrosis
  • Abnormal Regulation
69
Q

Abnormal Regulation from Increased Wall Tension

A
  • This is where drug treatments revolve around
  • Constant sympathetic drive in the heart creates an abnormal situation
  • Kidneys release renin
    • Poor renal perfusion
    • Normally regulates ECV; may see poor renal perfusion as low ECV/plasma volume
    • Renin acts on angiotensinogen→angiotensin I (not very potent)
    • ACE converts angiotensin I→angetension II (very potent)
      • ACE and angiotensiongen are always in the blood
    • Constricts arterioles
    • Increase the ECV
      • Volume overload causes congestive heart failure
70
Q

Treatments for Systolic and Diastolic Failure

A
  • ACE inhibitor
    • Diuretic
    • Vasodilation of arterioles
    • Decreasing the afterload
  • Beta Adrenergic I blockers
    • Decreases the counter-productive constant sympathetic input
  • Aldosterone
    • Saves sodium, expands ECV
    • Treatments: aldosterone antagonist
    • Also helps abnormal hypertrophy
  • Diuretics
    • Furosemide (Lasix)
  • Pacemaker with defibrillator
  • Cardiac transplant
71
Q

Diastolic Heart Failure

A
  • Nothing wrong with EF
  • The problem is in the filling
    • The ventricles become too stiff
    • Decreased compliance
  • Cardiac output goes down
  • HTN (longstanding) can causes this
  • Valve problems can cause this
  • Hypertrophy
    • Wall thickness increases
72
Q

Pressure, Flow, and Resistance

A
  • Hydrostatic Pressure
    • The pressure from weight of water
    • Pressure in ankle 100 mmHg more when standing
  • Wall tension
    • Arterial pressure
    • Elastostatic pressure (“Linder’s Name”)
  • Resistance to Flow
    • Factor that determines how much flow given the pressure
    • Determined by diameter of pipe
      • 1 L/min, halve the pipe and get 1/16 L/min
    • Constriction of smallest arterioles determines the flow
73
Q

Structure of Arteries

A
  • Elastic arteries
    • Aorta and major branches
    • Lots of elastin in the walls
  • Muscular arteries
    • Like radial artery
    • Media tunica has smooth muscle rather than elastin
74
Q

Role of Elastic Arteries

A
  • Expands/stretches when blood is pumped into it
  • Stores energy during systole
  • Give energy during diastole
  • Smooth it so that pressure doesn’t have huge swings
75
Q

Compliance: Effect of Age

A
  • Change the pressure and see change of volume in aorta from autopsy and see what happen with push fluid in
  • Made plot with pressure of X and volume on Y
76
Q

Mean Arterial Pressure

A
  • Average pressure over time
  • Balloon with spout on two sides
  • C.O=How fast pump water in it
  • Spout=diameter of arteriole
  • Lump together all arteriole effects=total peripheral resistance
    • Dilation; TPR decreases
77
Q

Pulse Pressure

A
  • High SV increases pulse pressure
  • Reduced compliance increases pulse pressure
    • High pulse pressure in elderly due to reduced compliance
78
Q

Atherosclerosis

A
  • Places that are more likely to happen (distal aorta, common carotids, coronary arteries)
  • Get cholesterol in blood that gums up artery, not a good analogy
79
Q

Atherosclerosis: Sequence of events

A
  • Something wrong with endothelium and tunica intima
  • Inflammation
  • Accumulation of oxidized LDL
  • Macrophages phagocystoze the cholesterol
80
Q

Something wrong with endothelium and tunica intima in atherosclerosis

A
  • Places where there is a lot of flow stress
  • Structurally intact (nothing you can see histologically)
81
Q

Inflammation in atherosclerosis

A
  • Cells are recruited
  • Macrophages
  • Statin drugs have an anti-inflammatory angle to them (as well as cholesterol reducing)
82
Q

Accumulation of oxidized LDL in atherosclerosis

A
  • Gets into the tunica intima
  • Especially small particles
  • ApoB accumulation (only find on LDL, NOT ON HDL)
83
Q

Macrophage phagocytized the cholesterol in atherosclerosis

A
  • Have a protein that would normally make to HDL
  • In atherosclerosis, macrophage starts to loose motility
  • Bind ApoB (LDL)
  • Don’t effectively transfer to HDL
  • Macrophages start accumulating cholesterol
  • Become “foam cells”
  • “Fatty streak” where starting to get atherosclerosis
84
Q

Why atherosclerosis?

A
  • Increases small LDL
  • Motility problems
  • General inflammation
85
Q

Smooth Muscle and Atherosclerosis

A
  • Move into the tunica intima and start synthesizing fibrous connective tissue
  • Growth factors making them do this
  • Makes a fibrous plaque
    • Initially soft
    • Cells in middle not have capillaries to them
    • Get extracellular lipids
    • Makes cholesterol crystals
    • Thick cap=lots fibrous tissue between blood and necrotic region
    • With time thick cap gets calcification
86
Q

Occludes vessels start to get symptoms

A
  • Claudication (BV to legs)
  • Angina pectoris in coronary arteries
  • Syncope in carotid arteries
  • Weakened wall
    • Aneurysm
  • Stress test
    • ECG changes
    • Look between S and T wave
      • Tends to shift with not enough blood flow
  • Visualize vessels with an angiogram
87
Q

Fibrosis plaque with thin cap

A
  • May rupture
    • Exposes extracellular lipids
    • Promotes clotting
  • Clot forming
  • Can cause MI, stroke
88
Q

Atherosclerosis Risk Factors

A
  • HTN damages all parts of CV system
  • Diabetes
  • Smoking
  • Hyperlipidemia
    • Increased LDL (ApoB)
      • Lower this with statin drugs
    • Low HDL
    • High TAG (VLDL)
  • Saturated, Trans Fats
89
Q

Framingham Risk

A
  • Calculates risk of having heart problems soon
  • Blood pressure
  • Diabetes
  • Smoking
  • LDL, HDL
  • Gender, Age
  • High enough risk and taking statin
90
Q

Drugs for Atherosclerosis

A
  • Statins
    • inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis
  • Ezetimibe
    • inhibit cholesterol absorption in small intestine
  • (PCSKa)
    • Ab that blocks enzyme that degrades LDL receptors
    • Undergoing clinical trial
    • Degrade LDL receptors
  • (Fibrates)
    • bind to the nuclear receptor PPAR-alpha
    • Increase HDL and lower TAG
  • (Niacin)
    • Increase HDL by preventing breakdown
  • (CETP inhibitors)
    • Prevents transfer of HDL to LDL
    • increases reverse cholesterol transport
    • anacetrapib and evacetrapib
91
Q

Arterioles: Structure

A
  • Determine the TPR
  • Control the distribution of blood flow
  • Less than half a millimeter
92
Q

Control of arterioles: autonomic nervous system

A
  • Sympathetic nerves
    • Skin, gut, kidneys
    • Alpha receptors
    • Too much sympathetic action to skin is Raynaud’s
      • Strongly vasoconstrictor the arterioles
      • Then vasodilation that causes pain
      • Drugs: Calcium channel I, alpha blockers
  • NO (nitric oxide) releasing nerves
    • Cause vasodilation
    • Penis arterioles, gut
93
Q

Control of arterioles: paracrines

A
  • Inflammatory paracrine
  • NO
  • vasodilation
94
Q

Control of arterioles: hormones

A
  • Angiotensin II
  • Vasopressin
    • Powerful constriction of blood vessels
    • Important during hemorrhage to keep up blood pressure
95
Q

Control of arterioles: local chemical factors

A
  • Local metabolic
  • Increase in Co2, increase in K, osmolarity
    • Osmolarity because metabolism makes big molecules into little molecules
  • Important in muscle/exercise
    • So brain doesn’t have to think about it.
96
Q

Capilaries: Structure

A

Endothelium

97
Q

Capilaries: Permeability

A
  • Permeability
  • Anything smaller than a blood protein
    • Exception: less permeable in brain
98
Q

Fluid balance across capillary wall osmotic effect of blood proteins

A
  • Blood protein osmotic effect opposes the blood pressure
  • Osmosis when solute is not permeable, water is permeable (diffusion of water)
  • Some leaves capillaries and goes to lymphatic system
  • Proteins that are blood proteins
    • Albumin
99
Q

Edema

A
  • Common medical symptom
  • When fluid leaves the capillaries
  • Causes:
    • Increases capillary permeability (inflammatory paracrine)
    • Diabetic retinopathy
    • Decrease in blood proteins (hemorrhage, protein starvation)
    • Increases in ECF (CHF)
    • Increase in venous pressure
    • Blocked lymphatics
    • Hepatic portal vein damage/blockage
      • Ascites
100
Q

Veins: Structure

A
  • Thinner walled (thin tunica media)
  • High compliance
  • Larger
  • Anastomoses
    • Many pathways for blood to get back to the heart
    • When veins divide but then come back together
  • Valves
    • Important in muscles that squeeze blood back to heart
  • Amount of blood: 75% of blood in systemic circulation
    • Can change amount of blood in veins easily
    • Get away with changes in blood volume because of vein compliancy
101
Q

Veins: sympathetic innervation

A
  • Contract the veins
  • Smooth muscle in the adventitia
  • Angiotension II causes vein constriction
  • Constriction doesn’t change the TPR
  • Changes how much blood available for circulation
102
Q

Regulation of Arterial Pressure

A
  • Cardiac output and total peripheral resistance
  • Carotid baroreceptor reflex
  • Hormones
103
Q

Carotid Baroreceptor Reflex

A
  • Short term regulation
  • Most sensitive
  • Understand what carotid massaging does in ER
    • Increases parasympathetic effects to the heart
104
Q

Regulation of Arterial Pressure: Hormones

A
  • Angiotensin II
  • Vasopressin
  • Increase TPR
  • Important for supporting blood pressure when loose fluid volume
105
Q

Hypertension

A
  • >140/>90; HTN1
  • 120-139/80-89; Prehypertension
  • With drugs trying to get pressure under 150
106
Q

Primary HTN

A
  • essential hypertension
  • Not clear what causes it
  • 95% HTN
  • Increase CO that goes with it at the beginning of HTN case (young)
    • The whole MAP goes up
  • Established HTN (old), CO is normal and increased TPR
    • Usually the systolic is higher
107
Q

Secondary HTN

A
  • Because of some other disease process
  • Kidneys; control ECF, release renin, etc.
  • Hormone: adrenal medulla tumor
  • Only 5% of cases
108
Q

HTN: Treatments

A
  • Lifestyle (1st)
    • Weight, aerobic exercise, fruits and vegetables, sodium (<2 grams, HTN <1.5g)
    • (Less salt causes more renin excretion)
  • Thiazide Diuretic
  • Beta blocker
  • ACE inhibitors
  • Angiotensin receptor blocker
  • Calcium channel blockers
109
Q

Standing, Walking

A
  • Counteract pooling of blood in legs by contracting muscles
  • When start walking SV goes up due to Frank-Staring.
110
Q

Standing, Walking Figure

111
Q

Effects of Training

A
  • Will look at in the respiratory section
  • World class athletes have higher VO2max because they have a higher stroke volume.

Conj 403 (7 decks)

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