Midterm #1 Flashcards
Organization of the Circulatory System
- 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
- Right has less pressure when contracted/relaxed (24/8 mmHg)
- Left has more pressure (120 mmHg/80)
Flow of Blood in Circulatory System: Figure
Chambers of Heart: Shape and Wall Thickness
- 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
Left and Right: Veins/Arteries
- 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
Heart Valves
- 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
Aortic and Pulmonary Valves: Figure
AV valves (triscuspid and mitral): Figure
Echocardiograms
- 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.
Normal Heart Sounds: S1, S2
- 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
Times of systole and diastole
- Time between S1 and S2 is systole
- Time between S2 and next S1 is diastole
Split Sounds
- 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
S3, S4
- 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)
Laminar and Turbulent Flow
- 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
Stenosis
- Narrowing
- If valve leaflets don’t open fully
- Channel that blood flows through is narrower than normally
Isufficiency (Regurgitation)
- 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”
- Ex: Aortic stenosis.
Senile Aortic Stenosis
- 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
Bicuspid Aortic Valve
- In middle age have to be replaced
- Life expectancy is normal
- Genetic
- More prone to stenosis (fibrosis and calcification)
rheumatic fever (heart disease)
- 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
infective endocarditis
- 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
Artificial Valves
- 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.
Coordination of the Heart Beat
- 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
SA Node
- # 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
AV Node
- # 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
AV Bundle (Bundle of His)
- # 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
Right and Left Bundle Branches
- # 4
- Drive heartbeat at 30 bpm
Purkinje Fibers
- # 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
Ventricle Action Potential
- 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
SA Node Action Potential
- No fast Na+ channels
- Do have slow Ca++ and K+ channel
- Slower action potential
- Pattern of the injured cardiac muscle cell
Pacemaker Potential
- 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
Change heart rate by changing slope of pacemaker potential
- 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
- Ach (acetylcholine)
Adenosine
- Paracrine and drug
- Works through trimeric proteins an opens K+
- Reduces excitability and reduces heart beat
Refractory Period
- 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
Action Potentials: Graphs
Basis of Lead II Waveform in Electrocardiogram
- 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
First Degree AV Block
- 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
Second Degree AV Block
- 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
Third Degree AV Block
- 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)
Premature Atrial Contraction
- 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
Premature Ventricular Contraction
- 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
- If see both, then there are two ectopic focuses going on
Bundle Branch Block
- 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.
Sinus Bradycardia
- 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)
supraventricular tachycardia
- 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
AV Node Reentry
- 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
Accesory Pathway an Supraventricular Tachycardia
- 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