Editing Lecture 2 Heart Cycle

*continued here from [[Lecture 1 Overview]] on 01/20/11.


*Prof is worried because he hasn't received an object from students.

==Heart cycle==
*There is lots of stuff to memorize here.

===Objectives===

===Valves===
*AV valves
**Bands of muscles called papillary muscles with chordae tendena
**From ventricles
**When vents contract, the papillary contract just before that too keep valves from popping overs.
**1-3 mmHg pops the values opne
*Semilunar valves
**From ventricles to vessels
**Close passively
**have cusps to keep blood from flowing backward into vent
**fold out of the way when ejecting blood
**the cusp is caught by the backflow after contraction
**Open really easily
***No energy spent on these or AV valves
*50 billion heart cycles in 70 years!
**The heart is beautifully made.

===Seven steps of the heart cycle===
*Start with atrial systole

====Listening to the heart====
*Old school: put ear to chest
*1700s, France:
**Didn't want physicians putting faces on bodies of the people.
**Came up with heart trumpet
**Evolved into stethoscope
*1800s, USA: a few physicians started using stethoscopes

====Atrial systole====
*EKG:
**Sturek talked about this, the p wave
**During atrial systole, the atrial contracts, the AV node gets turned on, and we start to react the septum and the lining of the ventrical.
**P = atria contract
**Q & R = something going on in the ventricle
*Mechanical event:
**Atria has been resting and receiving blood from appropriate vessels
***This is a passive event; the arterial and venous pressure cause the blood to enter the atria.
**Atria contract to push blood into the ventricles
*Valve fxn:
**AV valves are open letting blood flow from atria to ventricles.
**Semilunar valves are closed.
**Papillary muscles are just beginning to contract to shut AV valves and resist the force of the soon-to-happen ventricular systole.
*Heart sounds:
**4th heart sound
**It took a long time to find the 4th sound because equipment wasn't good enough to pick up this sound.
**So it's the fourth sound found.
**quite little sound; often not heard in healthy normal poeople.
**heard in heart disease and athletes with great cardiac fxn.
*Ventricular volume:
**Increased about 20% by atrial contraction
**Pretty closed to size at ventricular contraction
*End diastolic volume:
**EDV
**volume in ventricle at the end of atrial systole
**Plumped ventricle up as much as it will hold
*Arterial pressure:
**has been falling since atrial systole because there is no flow from great veins and what was in the chamber is moving into the ventricle.

====Isovolumetric contraction of the ventricles====
*Here we move the pressure in the ventricle of a few mmHg to high pressure (that which needs to be generated in the arteries, 80-90 mmHg).
**Happens in the sound of a clap: soft and flabby to rigid
**this is '''pressurization of the ventricles'''.
*EKG:
**From peak of the R to the S of the QRS complex.
**Also, just a little bit of the ST segment
*Mechanical event:
**Isovolumetric contraction of the ventricles
**Papillary muscles are high tensed
**Pressure in ventricles ins't high enough to get through pulmonary or aortic valves
**all valves are closed
*Valve fxn:
*Heart sounds:
**first heart sound
**Heart vibrates
**heart doesn't open valves but it tenses them and they bulge
**Heart moves up in the chest because of such fast contraction
**Complex noise
*Ventricular volume:
**hasn't changed
*Arterial pressure:
**Falling, though not much because this is such a short phase
**lowest arterial pressure

====Rapid ventricular ejection====
*The ventricles powerfully contract and overcome the pressure in the aorta and pulmonary artery.
*EKG:
**Continuing depolariation and contraction
**Just a wee bit of the vent starts to repolarize
**ST seg and a little T
*Mechanical event:
**vigorous pumping
**Oxytonic contraction: forces change as it contracts
*Valve fxn:
**Semilunars are open
*Heart sounds:
**More of the first heart sound
**Explosive ejection of blood into arteries causes sound.
**We sometimes call this an "opening snap" of the semilunar valves.
**Pressure is so high, it will move a crossed leg.  Drop 5 lbs 3 feet and you get the same force.
*Ventricular volume:
**70% of the volume's ejection volume is thrown out
**Stroke volume = amount of blood pumped in single cycle
***70% of this is ejected
**We got these names because we new about steam engines in the early 1900s when we were discovering hearts.
**So the ventricular volume goes down 70%
*Arterial pressure:
**Peaks at the end of this cycle
**We use peak as the stopping point of rapid ventricular phase

====Reduced ventricular contraction====
*Heart is calming down
*EKG:
**T wave, heart is calming
**Still contracting but not as much now
*Mechanical event:
**Ca++ is still causing contraction but it is leaving
**Heart is calming
**Ventricles are finishing contraction
*Valve fxn:
**Semilunar valves are open as blood rushes into arteries.
**AV valves are tightly closed (via papillary muscles)
*Heart sounds:
**Too quite to hear with non-amplified stethoscope
*Ventricular volume:
**Goes down another 30% (as the rest of the stroke volume leaves)
*Arterial pressure:
**Falling off as contraction weakens


====Isovolumetric ventricular relaxation====
*Finishing of relaxing of ventricles.
*Almost as fast as isovolumetric contraction
*EKG:
**Nothing because T wave is gone because heart has fully relaxed.
*Mechanical event:
**Ventricles relax because they are now fully repolarized
*Valve fxn:
**For a moment in time, the blood runs backward for a small amount of time and graps the cusps of the semilunar valves and pops them together.
**AV valves are closed but papillary muscles are relaxing
*Heart sounds:
**Second heart sound
**Complicated, again
**Blood going backward in aorta / pulmonary arteries to close valves
**Heart is settling down in the chest cavity
*Ventricular volume:
**Smallest it will be in the whole cycle
*End '''systolic''' volume:
**The lowest volume throughout the cycle; the volume at this point in the cycle.
**Ventricle is fully relaxed.
*'''Stroke volume = EDV - ESV'''
**We can get the EDV ESV from ultrasound, estimated
*Arterial pressure:
**The arterial pressure is falling rapidly as the blood flows from the large arteries into the microvessels.

====Rapid ventricular filling====
*Ventricle is now this nice soft piece of tender meat.
*The atria and the venous pressure fill the ventricle.
**Blood from the systemic and pulmonary systems have been filling the atria during the last cycles.
*EKG:
**Nothing
*Mechanical event:
**AV valves open because of pressure of blood in the atria
**These valves are huge; blood drops into the ventricles, not flows.
*Valve fxn:
**AV valves open
**Semilunar valves closed
*Heart sounds:
**Third heart sound
**Filling of the ventricles and sloshing of blood in the ventricles.
**Not heard in healthy people but can be heard with amplified stethoscope or in athletes.
**Heard in people with AV valve trouble or ventricular muscle problems
*Ventricular volume:
**During rapid phase, 60% of the volume enters the heart.
*End diastolic volume:
*Arterial pressure:
**Dropping but not as fast as before.

====Reduced ventricular filling====
*20% of the ventricular volume filled with blood.
*Slow version of rapid ventricular filling.
*Less time for this when heart rate goes up.
**At 100 bpm, there is no reduced ventricular filling.
**So we'd better have really good rapid filling phase and really good atria
**Imperative for heart rates over 100 bpm.

===Catheterization and the Wiggers diagram===
*After WWII we figured out how to cath living animals and people.
*So we could measure pressure and volume in the ventricles.
*Didn't go over this in great detail

===Venous pressure waves===
*A wave is from atrial contraction (atrial wave)
**Sloshing of blood into vena cava when right atria contracts.
**Most blood goes into right ventricle but a little goes into vena cava.
*C wave is called the "contraction of the ventricle wave"
**This venous wave occurs because of the hearts movement in the thoracic cavity and 
**because of the bulging of the right atrioventricular valve because of the force against it from the right ventricle contracting.
**Left ventricle pressure goes from 5 to 80 in a clap.
**blood is pushed in so fast that the arteries swell (can be seen on ultrasound); the blood won't actually flow much until the semilunar valves have closed and the smooth muscle of the arteries can spring back to force blood to flow thorugh the caps
*V wave is called the "ventricle filling wave"
**Inertia keeps the blood flowing such that the arterial pressure is slightly higher than ventricular pressure during the latter half of the ventricular contraction.
**Occurs because during contraction (see C wave) blood was forced through the systemic arteries, then capillaries, and into the venous system and even into the right atrium yet it could not continue on into the ventricle so pressure built up.
**Upon opening of the tricuspid valve, the pressure drops again as blood dumps into the ventricle.


*Lying down down with feet up on pillow, watch the jugular vein pulse three times for each cycle:
**First before arterial pulse is the A wave.
***gives you a sense of the atrial performance
**Second is the C wave
**Third is the V wave


*Heart sounds:
**Can't hear the fourth when the atria contract
**The first sound is heard when heart jumps in the chest and ventricles force semilunar valves open.
**Second heart sound occurs when ventricle is going through isovolumetric relaxation and the semilunar valves are snapping shut.


*Draw these cycles
**Start with the EKG
**You can figure it all out against the EKG.

===Splitting of the second heart sound===
*During inspiration the second heart sound splits.
*This means you can hear the aortic and pulmonary valves closing at different times.
*Particularly in healthy people and in people with cardiac problems.
*During the first heart sound, the ventricles fire so close in time that humans can't detect the slight difference in closing time.
*But during breathing, we can hear the difference in the closing of the AV nodes.
*Aortic sound 2 is earlier than pulmonary sound 2.
*Why?
**When you inspire, blood is pulled into the respiratory tract; the pressure differential between atria and chest is higher.  That is, the pressure is much less in the lung tissue than in the right atrium.
***We say the heart lives inside of an air pressure pump.
**So we have equations that describe the inspiratory and expiratory ventricular filling pressures:
***Inspiratory ventricular filling pressure = atrial pressure - chest pressure = 3 mmHg - -3 mmHg = 6 mmHg.
****This makes sense because on inspiration the lungs are taking up more of the chest cavity and putting pressure on the heart such that blood is forced into the ventricle more readily.
****Then, upon the next ventricular contraction event (i.e. qrs complex), the right ventricle will be extra filled and will therefore contract a little more slowly (recall the length velocity curves) and then the tricuspid valve will close just after the mitral valve.
****So the pulmonary second heart sound comes after the aortic second heart sound.
***Expiratory ventricular filling pressure = atrial pressure - chest pressure = 3 mmHg - +2 mmHg = 1 mmHg.
****This makes sense because there is less pressure on the heart from the deflated lungs (expiration = breathing out) such that the ventricles don't fill as fast.
**Also, the left ventricle just inherently acts faster than the right ventricle; so this is a small part of the difference.

====Examples of second heart sound splitting====
*Decreased contractility or over distended volume of the right ventricle emphasizes the splitting because the right systole takes even longer to contract.
*If right ventricle has an electrical conduction problem, such as impaired Purkinje system, the right contraction is delayed.
*If the left ventricle takes longer than right ventricle to contract, major splitting possible but the timing is reversed. Something very wrong with left ventricle such as conduction, valve outflow or contractility issue.
*'''Most sedentary people have trivial splitting of the second heart sound, but very deep slow breathing will help split the sounds.'''
**You can split the sound with very deep breathing because it will decrease the chest pressure so much that the filling pressure will be really high and therefore the ventricular contraction will be really slow.
*Persons with slow heart rate due to exercise adaptation or some abnormality of the SA node / AV node, typically have well defined splitting of the second sound.
**Can be heard at about 50 bpm.

===Diagram of heart pictures===
*Fill in with arrows to show movement and valve open / closed.
*Do this will wigger's diagram

===Using Wigger's diagram: A case===
*Stolen off the board website.
*Rheumatic fever: infection that starts in the throat, then blood, then inflames heart and valves forming scars.
*Fatigued, dyspnea
*Hear an early diastolic sound
*Then diastolic murmer, rumbling decrescendo
**Always referencing the ventricular activity (hence diastolic murmur is understood to be ventricular diastole).


*stopped here on 01/20/11 at 9AM.
*started here on 01/20/11 at 11AM.


===Case 2: 65yo m===
*Most cardiovascular diseases are detected by listening to hearts.
*Because of the odd way the heart sits in the chest here is where you hear each valve:
**aortic valve on right side
**pulmonary on left side
**tricuspid at bottom of sternum
**mitral a little lower and left
*"best heard on his lower left chest 8 cm from the sternal border" means "mitral valve"
**When mitral valve is open it is making a noise.
**More noise upon walking; makes sense because heart is working more.
**This murmer is heard at both diastole and systole; the valve doesn't open OR close right.
***This is pretty common.
*A: the valve does let some backflow and that's why we hear some noise
*B: no, wrong location of murmur
*C: this is the answer
*D: could be because he may show some noise loss at this location, but kind of not exactly the correct location of murmur
*E: wrong place


*moved on to [[Lecture 3 Cardiac Mechanics]] on 01/20/11 at 11:05 ish.