cardiac physiology Flashcards
what happens during ventricular systole
the pressure in the ventricules begins increasing. Blood backup closes the AV valves. When the pressure exceeds the pressure of diastole in the pulmonary (~10)and aortic(~80) valves they will open
describe the anatomy of the AV valves
it has a annular ring which the valves are physically attached to. This ring is known as the annula. The valves have chordae tendenae attached to them. Papillary muscles attach the chordae tendenae to the walls of the heart.
Components of S1 why is it significant
M1+T1
you may hear M1 before T1 if you’re listening at the tricuspid because the left ventricular pressure builds quicker then the right therefore the mitral closes first.
what is a click vs a snap
sound made by the opening of a semi lunar valve. A snap is the opening of a AV valve. Clicks are systolic sounds and snaps are diastolic
what is ventricular systole
the time between s1 and s2
when do the atria contract
the end of diastole.
why dont the semilunar valves have cordae tendonae
they are small and thick therefore in a healthy heart they wont reguritate. but the AV valves are long and thin and will reguritate without the help of chordae tendonae
pitch of s1 and s2
s1 is low pitch b/c the ventricle is less elastic. S2 is high pitch b/c the aorta is very elastic . The first sound is longer then the second. (will you marry me? yes)
sounds at the 5 hotspots
5th hotspot (PMI) usually you can only hear M1 here. (this is the apex of the heart) T1 is best heard at 4th. this is the best place to hear splitting of M1 and T1. A slight spilt during inspiration is normal because during inspiration the velocity of blood from the venous circulation coming into the heart is elevated. It takes longer to contract b/c its overloaded.
tilt of the heart
the right ventricle is more anterior then the left.
explain what makes the S1 sound louder
- So at the beginning of Diastole the cusps are wide open. As the blood fills the ventricles the cusps get a little closer together. If there is a condition where the cusps do not get closer together as the ventricles fill then the S1 sound will be louder. Think about a clap from short distance vs long distance. The longer the distance the louder the clap
- positive inotropic effects
- exercise,fever, - valvular pathologies
what are some variables that can keep the leafets wide open before systole
- short PR interval (includes the P wave goes to the beginning of Q)(Norm: .12-.2)
- atria arent done emptying and ventricles contract.
what can cause short PR interval
left ventricular premature excitation such as
- wolf parkinson white syndrome
- normally only AV node is the only connection between atria and ventricles. These people have abnormal connections called bundle of kent. It doesnt hold current like the AV node.
- you can see it as a delta wave on the ECG. which looks like a slow upward slope leading into the QRS complex (no Q is seen).
- this connection is located on the lateral edges - lown ganong levine syndrome
- the abnormal connection is around the AV node and it is connected to the bundle of HIS. it is called the bundle of james. - tachycardia (ventricular filling time (diastole) is more affected during tachycardia vs systole)
mitral stenosis (thickened but not yet heavily calcified)
initally makes s1 louder but then later makes it soft. blood is moving through the mitral valve at a higher pressure causing atrial hypertrophy.This also causes less filling in the ventricle therefore the leafets do not drift toward each other.
advanced mitral stenosis
chordae tendonae are also effected, they are thickened and shortened. The valves are no longer mobile. There will be no M1 sound. but there is still a T1
tricuspid stenosis
same concept
mithral regurgitation
common if the chordae tendonae get thickened and shortened. (they dont close valves but they prevent regugitation) In these regurgitation cases the valves dont close so they dont make a sound.
aortic regurgitation
S1 becomes soft b/c the ventricle becomes over filled.
how can you increase automaticity
drugs such as epi bind to beta 1 adrenergic receptors and cause cation loading.
explain circus movement (re-entry)
when electrical activity has to travel around dead tissue and there is a blockage the electircal activity keeps moving around the dead tissue rather then being propagated forward. which each circle it makes it releases electrical stimulation to surrounding cells causing tachycardia.
sinus arrhythmia
a normal arrhythmia caused by the vagus nerve being stimulated during expirations and then becoming inactive during inspiration. The vagus releases acetylcholine into the SA node to slow it down. It also controls AV node.
sick sinus syndrome
SA node is partially infaracted leading to episodes of tachycardia followed by periods of bradycardia
types of atrials tachyarrthymias
1.artrial tachycardia
-atria is now the pacemaker (120-250)
-multiple p waves, (not good enough to conduct a QRS)
2.atrial flutter
(250-350)
-no p waves, there are F waves (sawtooth like)
3.afib
(350+)-bunch of focci firing in all directions, weak, leading to slight flucuations instead of p waves.(f waves)
Our goal is to stop it but if we cannot we want to slow down the AV node to prevent ventricaluar arrhythmia (calcium channel blockers, bblocker, digoxin, amio)
why does the current in the AV node move slow
- the cells are small so the current has alot of membranes to jump. They also have small diameter so they provide more resistance to current flow.
- few gap junctions
- cells are perpendicular to the direction of current flow
- voltage gated sodium channels are perm closed.b/c the resting membrane potential is -60mV. Furthermore the -60mv causes to cations move in slowly as compared to other cardiac cells which have -90 mV.
ventricular depolarizations
- ventricular septum (right and up)
- major ventricular (left and down)
- basal (right and up)
what does adenosine do to AV node
shuts it down
2:1 second degree heart block
2 p waves per QRS
irritable cardiac cells
normally after a repolarization a normal cardiac cell will not fire again until the adjacent cell supplys it with cations. Even if sodium comes into the cell normally the ATPase channels will just remove them. But in instances when you have reduced ATP such as hypoxia the ATPase pumps do not work and sodium becomes trapped within the cell causing it to fire at random. Also you can have physical injury to the membrane of the cell causing leakage of cations into the cells.
why do you tell patients with irritable cardiac cells to not get to emotional
b/c it releases adrenaline which binds to a G protein receptor(beta1adrenergic receptors) activating the g protein which then activates adenlyl cyclase which converts ATP to cAMP. cAMP creates protein kinase A. Protein kinase A phosphorlates calcium channels causing the cell to become loaded with calcium.
ventricular premature beat
when one of the irriated cells fires. it will make a weird and wide QRS b/c it is not on the normal purkinjee pathway.
T-tubules
during depolarizations only the membrane of the cardiac cell would become depolarized if it wasnt for the invagination of the membrane. These invaginations are called T-tubules and they share the same characteristics as the membrane that theyre attached to. Therefore when the membrane depolarizes the t-tubule also depolarizes. allowing calcium to reach deep into the cell.
sarcoplasmic reticulum
very rich in the active transporter of calcium (only active transport is calcium going in. Calcium going out is passive) Taking it from inside the cell into the sarcoplasmic reticulum. Once calcium from the t-tubules interacts with the SR it causes a massive release of calcium from the SR. This is the trigger calcium. This calcium is now going to participate in a contraction.
actin and myocin
Actin (thin)
-have myosin binding sites but they are protected. it is covered by tropomyosin preventing myosin head from binding.
-Troponin C binds to calcium. The troponin rotates and pulls the tropomyosin, uncovering the binding site.
Myosin(thick)
-have heads that interact with actin
-in between the actin
-the head has enzymes capable of breaking down ATP
The binding of the myosin head to the actin receptors is known as forming cross bridges. The myosin pulls the actin inward.
Once the calcium channels close. intracellular calcium levels start to drop as calcium is moved into SR. This drop in calcium causes troponin to release calcium and it goes back to blocking myosin receptors.
steps to contractions
- depolarization stimulus
- threshold
- sodium dependent depolarization
- plateu
- trigger calcium
- massive release of calcium from SR
- calcium binds to troponin C
- troponin pulls tropomyosin exposing myosin binding site
- myosin heads bind to myosin binding sites on actin and pull inward causing contraction
- repolarization
- trigger calcium thrown back to extracellular
- calcium released from SR is taken back into SR
- calcium on troponin detaches
- troponin goes back to normal
- diastole
how does the calcium that came in during plateu leave.
1.calcium ATPases
