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___ makes up most of the R side of
the heart & the ___makes up most of the L border
RA and LV
In between RA and RV is the ______. The ventricles are separated by
- atrioventricular groove
- anterior interventricular groove
RA receives blood from what four surfaces
- Coronary sinus
- Anterior cardiac vein
TRUE or FALSE. The Fossa ovalis (where foramen ovale is @ birth) stays open in some adults (PFO)
TRUE (about 10%)
The Left atrium receives blood from the ______
pulmonary veins (there are four)
TRUE or FALSE. The LA is thicker and bigger than the RA.
FALSE! The LA is thicker and smaller than the RA.
Just above cusps of AoV are
the aortic sinuses, they are dilations of the ascending aorta and they give
rise to the _________________
right and left coronary arteries
Atrioventricular valves are the ______ & the ______.
- Mitral (only normally bicuspid valve)
The semilunar valves are the
Which valves have soft closure?
The atrioventricular valves (MV and TV)
In the Atrioventricular valves there are papillary muscles attach to valves via chordae tendineae. Why is this important?
The papillary muscles will attach to the veins of the AV valves by chordae tendineae. In systole both ventricle and papillary muscles contract pulls veins of valves of blood in so the backflow of blood doesn’t push the veins into the atrium. (NOT responsible for closure of valve, just to prevent veins from being pushed back) Papillary muscle dysfunction or rupture then veins do go back into atrium causing leak or rupture.
How do the semilunar valves close?
Semilunar, heavier, more backflow needed for a bit longer in order for them to close. They tend to snap close d/t the pressure in PA and Ao being higher.
Why are the semilunar valve (edges) at higher risk for damage?
The valve opening of semilunar are smaller than that of the AV valve. Shen the cross sectional area is smaller than the velocity is faster of blood going through, the ends of semilunar valves are more likely to be damaged from abrasion of mechanical force, they are more subject to injury.
TRUE or FALSE. The semilunar valves do not have chordae tendineae or papillary muscles.
TRUE! No chordae or papillary muscles w/semilunar, need to be strong and still pliable in order to handle the stress.
Normal Aortic Vavle area
is 2.5-3.5 cm2
Normal MV area
is 4-6 cm2
What are the FOUR layers of the heart?
The epicardium is made up of a layer of ________
What is the thin, fibrous sheath or sac that consists of three layers surrounding the heart called?
what is the muscle of the heart called?
Ture or FALSE. The endocardium is made of a
layer of cells similar to endothelium of blood vessels.
What are the 3 layers of the pericardium called?
- Fibrous pericardium
- Parietal pericardium
- Serous (visceral) pericardium
Which layer of the pericardium is the outermost
layer and has physical attachments to the diaphragm & sternum?
The fibrous pericardium
Which layer of the pericardium has endothelial cells that secrete fluid into the space between parietal and serous. (This fluid lubricates the movement of the heart against surrounding structures)
The serous (visceral) pericardium
If a patient has an acute pericardial effusion, would we give anesthesia?
NO! This patient is at risk for tamponade (positive pressure ventilation would be life threatening). Surgeon must to pericardialcentesis with local anesthesia to drain fluid then we can do GA and surgeon can place pericaridal window.
Name some things that could cause pericardial effusions
- Metastatic disease (esp. radiation to mediastinum)
- Infection (viral, bacterial, fungal)
- Trauma (hemopericardium)
The RIGHT coronary artery supplies oxgenated blood to what areas of the heart?
- Most of RV
- Diaphragmatic surface of LV
- Posterior 1/3 of AV septum
- SA node (60% of pts)
- AV node (80% of pts)
Why is RCA occlusion significant for conduction issues?
Because most people receive their SA node and AV node blood supply from the RCA. (SA node is 60% and AV node is 80%)
Where do the right & left coronaries orginate?
coronary sinuses at the base of the aorta behind the cusps of the Aortic valve.
Are the coronary sinuses blocked during systole or do they remain patent during the entire cardiac cycle?
These aren’t blocked by cusps during systole, because have eddy currents, remain patent during entire cardiac cycle.
Describe where the RCA goes in the heart
The RCA passes forward between pulmonary trunk and RA, it descends in the R part of the atrioventricular groove. Then at the inferior border of heart, it continues along the atrioventricular groove and eventually anastomoses with the LCA. Gives off a marginal branch, along the lower border of heart (the right side of the LV) and an interventricular branch that runs forward in the inferior (posterior) interventricular groove.
The LCA supplies what areas of the heart?
- Most of LV
- Part of RV
- Most of interventricular septum
- SA node (40% of pts)
- AV node (20% of pts)
Which coronary artery is bigger, the left or the right?
Describe where the LCA goes in the heart
Passes behind and then to left of pulmonary trunk. Goes to the left part of the atrioventricular groove where it essentially become circumflex artery runs laterally around L border of the heart. The other major branch is the anterior ventircular artery or LAD. (This supplies the anterior part of both ventricles. This is where it passes around the apex of heart to anastomose to branch of RCA)
The coronary sinus gets blood from what four veins?
- Great cardiac vein
- Middle cardiac vein
- Small cardiac vein
- Oblique cardiac vein
Where is the coronary sinus located?
Coronary sinus is in posterior AV groove opens into RA just to the L of the IVC
Where does the anterior cardiac vein drain into?
drains the anterior surface of the heart and opens directly into the RA.
Explain the fetal blood flow from the placenta to the LA
- Blood from placenta goes via umbilical vein → IVC → RA → foramen ovale → LA.
- Most of the blood bypasses the liver via the ductus venosus. Very little mixing of blood in RA.
Where does unoxygenated blood from the SVC in the fetal circulation go?
Blood from SVC goes via tricuspid valve → RV
In the fetal circulation, the blood in the LA (which is mixed with oxygenated blood from RA and unoxygenated blood from the lungs) goes where?
Blood from LA + blood from lungs (small amount) → LV → ascending aorta → brain & heart via vertebral, carotid, and coronary arteries
Fetal lungs are active, what does this mean in regards to fetal blood flow in the pulmonary artery?
Fetal lungs aren’t active. Most of the unoxygenated blood from RV goes from the pulmonary artery through the ductus arteriosus into the descending aorta.
In the fetal circulation, once blood is in the descending aorta, where does it go from there?
This blood goes to abdominal organs, lower limbs then back to placenta to get oxygenated. Gets there through the umbi arteries.
What happens at birth?
The lungs expand and PVR ↓ & an ↑SVR. There is a ↓in RAp & ↑ in LA pressure. These pressure changes cause the septum primum and septum secundum to line up and close (thereby closing the foramen ovale) Because of the ↓ of O2 in blood, the wall of the ductus arteriosus will contract, (muscular) and that causes that functional shunt to close (takes 2-3 months for it to completely close)
True or False. The umbilical vein and arteries can be used to place IVs (central or peripheral) after birth.
TRUE, (depending on how deep it goes and where it ends will decide if it's central vs peripheral)
What are the two types of congenital septal defects?
Atrial septal defect and venticular septal defect
What is an atrial septal defect usually caused by
failure of the forman ovale to close
What are the four major congenital defects in TOF?
- Overriding aorta
- RV hypertrophy
- Pulmonary stenosis or atresia
What is the cardiac myocyte?
the functional unit and pumping mechanism of the heart
What are some similarities of cardiac muscle and skeletal muscle
Cardiac muscle is also striated like skeletal & contains actin/myosin microfilaments. The muscle of the atrium and ventricles contract much like skeletal muscle, but there is a longer duration of the contraction of cardiac muscle compared to skeletal muscle
Cardiac tissue has 3 types of cardiac muscle, what are they?
muscle of the atria, the muscle of the ventricles, and the excitatory/conducting muscle fibers
TRUE or FALSE. Cardiac muscle is different than skeletal muscle because it has automaticity, generates its own rhythm and has it’s own pacemaker.
Cardiac muscle has intercalated discs, which are actually cell membranes that separate individual cardiac muscle cells from one another why are these important?
fuse together, forming permeable “communicating” gap junctions, allowing ions to rapidly diffuse from one cell to another in that unit. This allows the AP to travel easily from one cardiac muscle. Cardiac muscle is referred to as syncytium of many individual cells that are so interconnected when one of these cells becomes excited, the AP spreads to all of the them, from cell to cell throughout the latticework interconnections
How many syncytiums does cardiac muscle have and why is this important?
- Guyton talks about two syncytiums.One for the atrias and one for the ventricles. IT’s the AV
- bundle (conductive tissues) that allows the two to “talk” This allows the atria to contract a little bit ahead of the ventricular contraction. Want sequential contraction not together
Cardiac muscle A. P. differes from skeletal muscle in 3 ways. Name them.
- Self propagating
- Can be conducted from one cell to another (because of the intercalated discs, they work in groups)
- Have a long duration of action.
What are the THREE MOST IMPORTANT ions in the cardiac AP?
Na, K, and Ca (Calcium becomes important to cardiac action potential).
What are the phases of the generic action potential.
- Resting (polarized) -90 mV maintained by
- 1. Na-K-ATPase pump
- 2. K “leak” channels
- 1. Positive potential with overshoot due to
- 2. Voltage-gated Na channel
- 1. Restoration of polarized state
- 2. Voltage-gated K channel
How does Ca+ contribute to a cardiac AP?
- Calcium pump
- Voltage-gatedcalcium channel
- 1. Contributes to depolarization in some cells
- 2. Slower than Na channel activation (10-20 times slower)
- 3. Opening causes more sustained depolarization
- 4. Found extensively in cardiac and smooth muscle
___ responsible for initiating
depolarization and ___ is important for sustaining it.
Na+ and Ca+
In the heart, ____ions are also
important for activating the muscle contraction involved, not just electric but
the physical muscle activity
What happens if Ca+ levels decrease significantly (50% or more)?
The Na channels will become activated from small increase in voltage from small resting levels, results in very excitable tissue, can be repetitive discharge. Tetany can be lethal if it involves muscles of larynx (laryngospasm) from tetanic contraction of larynx muscle.
What are the anions?
- Impermeant intracellular negative ions
- a. Proteins
- b. Phosphates
- c. Sulfates
- Chloride ions
The cardiac A. P has a different appearance, there is a longer depolarization and a plateau of 0.2-0.3 seconds that is characteristic of a cardiac action potential. Why is this?
- the Ca+ slow channels and the K+ channels are slower to open
- (so Ca+ keeps the electrical difference going and K+ takes longer to leave to correct it)
Describe the 4 phases of the cardiac A. P. (including Phase 0)
- Phase 0: upward stroke that’s the start of action potential, intense but brief inward movement of Na into the cell. Changes the peak potential from about -90mV to +20mV.
- Phase 1: the dip after the peak, it s the start of repolarization, Na channels close
- Phase 2: (isoelectric phase of plateau) closure of Na channels but influx of Ca+ ions through the show channels. (what distinguishes it from other A. P.)
- Phase 3: return of normal permeability
- to Na ions and sudden increase to K+ ions (K going out)
- Repolarization is complete at end of phase 3, brings potential to -90mV,
- Phase 4: Na/K ATPase pump is activated.
- *Repolarization is steps 1,2,&3
TRUE or FALSE.. Pacemaker cells, are a little different, they possess automaticity. So they can depolarize spontaneously.
TRUE. This means phase 4 is doesn't wait for stimulation. Always small amount of Na & Ca entering the cell while there is a bit of decrease of the outward flow of K+. Consequently, resting membrane potential is less negative and spontaneous depolarization occurs
Describe the A. P. of cardiac pacemaker cells
The rate of rise of phase 0 is slower & more gradual. (not as steep) The slope of the cells in the SA node and the AV junction is dependent on the rate of Ca entering the cell. (more vertical like phase 0 w/more Ca going in by slow channels). The pacemaker action potential, these cells don’t have phase 1 or phase 2, the upstroke of phase 0 is predominately carried by the Ca (a little by Na) so there is no real plateau, as soon as Ca influx stops and K deflux starts, repolarization begins, no phase 1 or 2 of pacer cells.
Why is the slope of phase 4 in the cardiac pacemaker A. P. important to HR?
Slope of phase 4, it relates to rate, (HR) the steeper the slope the faster the HR. If the slope if more gradual then the rate is lower. Catecholamines will increase slope, thereby increase rate, and enhance automaticity, and vagal stimulation will do the opposite.
How do anti-arrhythmics influence the heart rate?
- Change he rate of depolarization
- Change the threshold level
- Change the resting membrane potential
Catechoalmines (epi) will increase rate of phase 4 (increase HR) Vagal stimulation (release Ach) decreases HR by ______ pacer cells, decreasing slope of phase 4
What is the refractory period and what does relative refractory period mean?
The stimulus will generally not result in stimulation during refractory period. Refractory period is phase 1,2, & 3 (repolarization) the latter part (phase 3) is relative refractory period (stimulus with greater than normal intensity, may result in depolarization).
How do Class I anti-arrhythmic drugs work?
- Inhibit fast sodium channels (phase 0)
- Decrease rate of depolarization & the speed of conduction through the myocardium
There are THREE types of Class I anti-arrhythmic drugs. Explain how each one works.
- Class IA drugs: increase duration of AP & the effective refractory period, cause a moderate slowing of Na influx, moderate Na channel inhibition. Also cause K+ channel blockade, inhibit return of polarized state (repolarization).
- Class IB drugs: less potent, cause a slight slowing of Na influx.
- Class IC drugs: potent Na Channel blockers, they will cause a marked slowing of Na influx
How do Class II anti-arrhythmic drugs work?
Decrease rate of spontaneous phase 4 depolarization (i.e. esmolol, propranolol)--Beta blocker
How do Class III anti-arrhythmic drugs work?
K+ channel blockers, cause prolonged depolarization. Increase duration of the action potential. Increase duration of the effective refractory period.
How do Class IV anti-arrhythmic drugs work?
Ca+ channel blockers, inhibit the slope of the Ca Channel.
What does this picture represent?
A.P. passing over cardiac muscle membrane → A.P. moves to interior of cardiac muscle fiber along the T tubule membrane → T tubule A.P. act on longitudinal sarcoplasmic tubules → Release of calcium ions into sarcoplasm from SR → Calcium ions diffuse into myofibrils & catalyze reactions resulting in myosin and actin sliding and then muscle contraction Calcium ions also diffuse from T tubules at time of A.P. opening voltage-gated Ca channel
What is the complex compartment of membranes within the muscle sarcoplasm cause the release of Ca+ when stimulated by an A. P. of the T tubule on the longtitudinal sarcoplasmic tubule?
The sarcoplasmic retucilum (houses Ca during diastole
TRUE or FALSE. We need the mitochondria need the oxidative phosphorylation to generate ATP that is needed for the high demand of the cardiac muscle cells.
One thing that is different than skeletal muscle, Ca+ ions are released directly from the T tubules. Why is this necessary and important?
Part of that is necessary because the sarcoplasmic reticulum will store Ca but in cardiac muscle it can’t store as much (as in skeletal muscle) so if T tubule couldn’t release Ca there wouldn't be enough Ca to generate a full contraction. Ca is really important for cardiac muscle contraction
TRUE or FALSE. The strength of a contraction of cardiac muscle doesn't depend on the concentration of Ca+.
FALSE. The strength of a contraction of cardiac muscle depends to a great extent on the concentration of Ca+ ions in the ECF.
What happens to Ca+ at the end of the plateau phase?
The influx of Ca+ is abruptly stopped and Ca+ ions in the sarcoplasm are rapidly pumped back out of the muscle fibers into both the sarcoplasmic reticulum and the T tubule ECF. Transport into the SR is done by Ca ATPase pump. Ca is also removed by a Na/Ca exchanger (and the Na put in is then taken out by a Na/K pump)
One of the important thing that’s different of excitation coupling of cardiac vs skeletal. It can be modulated with different intensities of myocardial contractility from a single action potential. The duration of cardiac muscle cell contraction is about the same as the duration of the action potential. Why is that duration piece so important?
Refractory period of the muscle cell, isn’t over until the mechanical response is completed. So what’s important about thatis that tetany isn’t possible, no sustained cardiac contraction like you could for skeletal muscle. Want cyclical contraction, not one sustained cardiac contraction. Refractory period, another impulse won’t cause another muscle contraction, muscle must relax before it retracts again
Explain the concept of the atrial kick
Most of ventricle filling is passive, and when atria contract, 20% of the ventricle filling is from atrial contraction (loose that w/Afib)
What is an Isovolumetric contraction and when does this happen?
- At start of ventricular contraction. After
- closure of AV valves and before opening of aortic & pulmonic valves (muscle itself is tensing but volume remains the same because all the valves are closed)
Contraction of the ventricle but no emptying
What is Isovolumetric Relaxation and when does this happen?
- At end of systole
- After aortic & pulmonic valves close and before AV valves open (volume is the same, but the ventricle is relaxed)
Explain the "a" wave of the atrial pressure tracing.
- Atrial contraction
- RAP ↑s 4-6 mmHg
- LAP ↑s 7-8 mmHg
Explain the "c" wave of the atrial pressure tracing.
- Start of ventricular contraction
- Pressure of ventricular contraction pushes blood back against AV valve into the atria
- (With contraction of ventricle the MV is pushed slightly back into LA and the Lap rises slightly for short period of time, this is immediately followed by the floor of the LA being drawn downward and the small rise and fall of the Lap "c" wave)
Explain the "v" wave of the atrial pressure tracing.
- End of ventricular contraction
- Slow flow of blood into the atria when AV valves are closed during ventricular contraction