Cp Physiology Gu Som

Front 1

Phisiologically, where are some good areas of the body that can act as reservoirs of blood that we can mobilizes PRN? How much is there?

Back 1

The SYSTEMIC VEINS. systemic veins normally contain more than 60% of the BV and can act as a reservoir for blood. Blood can be mobilized from veins during hemorrhage or dehydration as a compensatory measure to help maintain blood pressure until blood volume can be restored.

2/3 of the total blood supply is located in the VEINS
1/3 of the blood supply is located in the systemic arteries, heart and lungs
The 10% of the total blood supply found in the lungs can act as a blood reservoir

Front 2

Contraction of which chamber of the heart is best described as a constriction of the chamber resulting in shortening from base to apex?

Back 2

Contraction of the LEFT VENTRICLE consists of a powerful of the chamber with shortening of the heart from base to apex, resulting in the high pressure required to pump blood through the high resistance systemic circulation.

Front 3

Which part of the circulation receives the smallest blood flow (as a % of CO) at rest?

Back 3

The CORONARY CIRCULATION receives approximately 4% of the cardiac output at rest, while the other listed parts of circulation each receive approximately 15% (brain) to 24% (liver and GI tract) of the circulation.

Front 4

Rapid phase 3 repolarization of cardiac myocytes during the action potential is mainly associated with:
[opening of Na+ channels]
[reduced conductance of inwardly rectified K+ current]
[opening of voltage sensitive slow L-type Ca++ channels]
[inactivation of Na+ channels]
[activation of K+ channels]

Back 4

Following the plateau of the action potential, gradual inacctivation of L-type Ca++ channels leads to activation of K+ channels and rapid repolarization. Opening of Na+ channels is responsible for the phase 0 upstroke; this is accompanied by reduced conductance of the inwardly rectified K+ current. Opening of L-type Ca++ is mainly responsible for the plateau (phase 2); inactivation of Na+ channels and opening of voltage sensitive K+ channels cause the rapid repolarization to the plateau (phase 1)

Front 5

At which (brief) stages of the cardiac cycle are all the valves closed?

Back 5

ISOVOLUMATRIC PEROIDS refer to short intervals when all the heart valves are closed.
The Cardiac Cycle (or Wiggers diagram) is a simultaneous depiction of several parameters related to blood flow and volume, the electrocardiogram, and the echocardiogram through a cycle of cardiac systole and diastole.

Ventricular systole begins with a short period of isovolumetric contraction, (during which all of the heart valves are closed).

This is followed by the ejection phase of systole,

then isovolumetric relaxation (when the heart valves are again all closed.)

after isovolumetric relaxation, cardiac filling occurs

The temporal relationships between features of these various curves or tracings are predictable, based on functional relationships within the cycle.

The a, c, and v waves are identified on both the venous pulse and atrial pressure curves.

Front 6

Pericarditis and myocardial infraction are very similar in their symptoms (continuous central chest pain radiating in one or both arms). BUT it is VERY important to make a proper diagnosis. How can you do this? Why?

Back 6

Unlike MI, pericarditis can be relieved by sitting forward.
An EKG can help differentiate between conditions.

Front 7

Name the flow of the blood through the valves? What surface anatomy do you use to locate the heart valves and WHERE would you LISTEN for heart sounds?

Back 7

To listen to valve sounds, point stethoscope DOWNSTREAM FROM THE FLOW OF BLOOD!

RIGHT HEART: (venae cavae, coronary sinus) → right ATRIUM (atrial appendage, fossa ovalis, limbus of fossa ovalis, crista terminalis, valve of inferior vena cava, valve of coronary sinus) → TRICUSPID valve → right VENTRICLE (conus arteriosus, moderator band/septomarginal trabecula) → PULMONARY valve → (pulmonary artery and pulmonary circulation)
LEFT HEART: (pulmonary veins) → left ATRIUM (atrial appendage) → MITRAL valve (bicuspid) → left ventricle → aortic valve (aortic sinus) → (aorta and systemic circulation)

Front 8

When comparing fetal circulation vs. adult circulation, there are several significant differences between the prenatal and postnatal circulations. WHAT ARE THEY (6)? Why are they needed?

Back 8

The fetus, enveloped in the amniotic sac and floating in the amniotic fluid, is dependent on the placental circulation for exchange of gases and nutrients. To adapt the circulation to prenatal life, there are six structures in the fetus not normally seen in adults (Fig. 12.11):
1.) Two large UMBILICAL ARTERIES, which branch from the systemic arterial circulation and supply the placental circulation, where gas exchange and nutrient and waste exchange occur.
2. The UMBILICAL VEIN, which returns placental blood to the systemic venous circulation, supplying O2 and nutrients to the fetus.
3. DUCTUS VENOSUS a shunt between the umbilical vein and the inferior vena cava. Although most of the placental blood passes through the liver, a fraction of the placental circulation passes directly into the vena cava through the ductus venosus.
4. FORAMEN OVALE: a "right-to-left" shunt through which most of the blood from the inferior vena cava flows into the left atrium, bypassing the right heart and the pulmonary circulation.
5. DUCTUS ARTERIOSUS: another right-to-left shunt between the pulmonary artery and the aorta. Pulmonary vascular resistance is high in the fetus, due to the collapsed state of the lungs and low oxygen tension in the lungs; 90% of pulmonary arterial blood flows through the ductus arteriosus to the aorta.

Front 9

Again, comparing fetal circulation vs. adult circulation, they are both designed/ adapted for efficient exchange of gases/ nutrients/ and wastes either through placental circulation or pulmonary circulation. Which circuit (fetal/embryo or neonate/infant/adult) would you consider a PARALLEL circuit? Which one would be more of a SERIES circuit? What structures develop to cause this switch to happen?

Back 9

The FETAL circulation can be considered a PARALLEL circulation. Much of the right ventricular output is shunted past the lungs to the aorta through the ductus arteriosus, mixing with blood ejected by the left ventricle.

Flow through the pulmonary circulation is not critical, since oxygenation of blood does not take place in the lungs in utero.

CLOSURE of the FORAMEN OVALE and DUCTUS ARTERIOSUS shortly after birth--> transformed to series circulation.

Front 10

In general what do all the residual structures of fetal circulation become (umbilical vein/ artery, ductus venosum/arteriosum, foramen ovale) ?

Back 10

dutus arteriosm/ vein & umbilical artery/ veins--> LIGAMENTS

Foramen Ovale--> FOSSA

Front 11

Describe how the nerve, arteries and veins are arranged in the intercostal rib space? What are the different layers??? If you had to puncture the lung, how many different layers would you poke through? What about in between lung and diaphram?
*think suarez level**

Back 11

Take a look!
• Intercostals are not completely continuous anteriorly and posteriorly; membranous layers help to complete the spaces left unfilled by the muscles.
• Blood vessels and nerves serving the thoracic cage travel in layers that run between internal and innermost intercostals (create highways for nerves to travel anteriorly from spinal cord to sternum).
• The intercostal nerve enters the “highway” between internal and innermost intercostal muscles as part of a neurovascular bundle (vein, artery, nerve). They travel on the underside of the rib in a groove.
•In a PLEURAL TAP, a large bore needle is introduced into the pleural cavity to drain fluid/blood. To avoid damaging nerves and vessels that help to innervate intercostal muscles, the needle is inserted on the upper border of the rib so as to minimize potential damage to the nerves.

Front 12

There are 4 different surface regions to listen to the 4 different valves of the heart... If you listened to the Apex beat
(located @ 5th intercostal space, 3.5” from mid-line) on the left side)
which valve would you be listening to??? (Remember, where you listen to the valve is DOWNSTREAM of where the valve actually is...

Back 12

Mitral valve (tricuspid) is here!

Front 13

Where are the most frequent sites of coronary occlusion? What characteristics might cause this to occur?

Back 13

Left Coronary artery!

Bigger side of heart... need more blood... larger vessel= more opportunity for plaque formation

Front 14

When everything is moving and migrating around during the primitive streak formation etc... how do cells figure which part is going to become what? What mechanisms does it use to do this, cause it doesn't have a whole lot of tools to work with.....

Back 14

It is thought that as cells ingress at different locations along the primitive streak, they migrate through areas of different concentrations of signal molecules (i.e. RETANOIC ACID) which primes them to receive inductive signals.

Hint 14

The source of the inductive signals appears to be a specialized area of hypoblast near the caudal end of the prechordal plate, the anterior visceral endoderm. The cells of the anterior heart field assemble in the presumptive
cephalic region of the embryo.

Front 15

How is the mouth made? Why the hell were we even talking about this in class when we are learning about cardiology?

Back 15

Remember his whole point about how if diffusion is not enough to penetrate+ exchange nutrients ... then that area will die... that's basically what is happening here. The prochordal plate / oopharyngal membrane is an area that is tightly fused, and has almost no mesenchyme at all... so it disintegrates...
A horseshoe-shaped mass of MESODERM coalesces (fuses) above the anterior visceral endoderm at the cranial end of the OROPHARENGYAL MEMBRANE (aka the PROchordal plate), a structure found at the cranial end of the notochord that eventually breaks down to provide access to the developing digestive tube. This horseshoe-shaped mass is known as the CARDIOGENIC PLATE. It is located subjacent and anterior to the neural plate at the cephalic end of the embryo. It will eventually develop a lumen, and will contribute to much of the heart.

Front 16

Which area organizes heart?

Which area(s) organize symmetry, (left/ right + cranial/ caudal)?

When does heart induction occur?

Back 16

Anterior visceral endoderm organizes the heart

Primative node and primative streaks (located on mesoderm + endoderm) organize the symmetry/ left/ right.

Hint 16

Not that important... just curious what FGf8 was.... Fibroblast growth factor 8 is a protein that in humans is encoded by the FGF8 gene.
The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. Temporal and spatial pattern of this gene expression suggests its function as an embryonic epithelial factor. Studies of the mouse and chick homologs revealed roles in midbrain and limb development, organogenesis, embryo gastrulation and left-right axis determination.

Front 17

Common theme in embryology: At which stage is diffusion no longer sufficient?

Back 17

The zygote, morula (~64 cell), and blastocyst (inner cell mass+ trophoblast) obtain their nutrition from diffusion. But as the embryo gets larger, diffusion is not efficient.

In mammals, the manner in which physiologic exchange is improved typically involves the apposition (side by side) of embryo to maternal tissues via placenta.

*note: ICM is usually oriented twards the uterine wall.

Hint 17

During this early phase, transfer of nutrients into the zygote is governed by Fick’s law of diffusion, which maintains that the rate of transfer is proportional to the surface area available between two entities and the efficiency of the exchange mechanism. Fick’s law predicts that diffusion becomes increasingly inefficient when the diameter of the zygote exceeds 0.2 mm. Thus, if a zygote is to grow larger than the maximum diameter of efficiency, a system or a set of mechanisms must develop that will improve the exchange of nutrients and metabolic wastes between zygotes and the maternal organism.

Front 18

Is the first PLACENTAL bloodflow maternal or embryonic? Why? Also, how does this process contribute to the mom's awareness of weather or not she is pregnant?

Back 18

This UTEROPLACENTAL CIRCULATION is ENTIRELY MATERNAL beginning about 14 days after fertilization.

"Spotting" may be possible. This is the KEY stage of structural development & if the mom doesn't even know she is pregnant, she may harm the developing zygote

Hint 18

First Placental Bloodflow is Maternal: Before the vascular system develops, the zygote implants into the endometrium and develops a syncytium from invasive, multinucleated trophoblastic cells. Inside the syncytium, some spaces develop – the lacunae. The embryo burrows into the uterine wall, and the edge of the syncytiotrophoblast erodes into some of the maternal blood vessels. These little lacunar spaces are somewhat interconnected. At 13-14 days post-fertilization, enough erosion will have occurred for maternal blood to flow from the maternal sinusoids into the lacunae, eventually filling them. Differential pressure levels in the lacunae will cause blood to wash through the lacunae and back into maternal veins in the uterine wall. This is uteroplacental circulation – it is entirely maternal, beginning about 14 days after fertilization. It is more efficient than simple diffusion, but it will not be good enough to support the development of the rapidly growing embryo. High resolution ultrasound suggests that the rate of flow may be very low during the first 10 weeks of gestation; this remains a point of controversy.

Front 19

Which layers of the heart (epicardium, myocardium, endocardium) are associated with which embryonic tissue...

don't get tricked... The answer is actually really easy...

Back 19

ALL COME FROM MESODERMAL GERM LAYER!

***technically, it is the SPLANCHNOPLEURIC (visceral) layer of Mesoderm forms the circulatory system and future gut wall (somatic layer forms future body wall)

Hint 19

Again looking at the figure “Organization of the Adult Heart”, notice the thick line representing the epicardium, a stippled area representing the myocardium (the cardiac muscle), and the white area inside representing the endocardium. Don't get confused by the names: all of these tissues arise from the mesodermal germ layer. Endocardium is so called because it is inside the heart; it is continuous with endothelium, which is what lines blood vessels.

Front 20

DRAW a typical ventricular cell action potential, LIST the phases, and DESCRIBE the membrane ionic movements and conductance changes that underlie each phase.

Back 20

FIVE phases (0-4) of AP in ventricular (and atrial) heart cells

PHASE 4 (the resting membrane potential)

PHASE 0 (upstroke of the action potential)

PHASE 1 (rapid repolarization to the plateau)

PHASE 2 (the plateau)

PHASE 3 (repolarization)

** depolarization is largely dependent on Na+ SODIUM INFLUX.

Hint 20

PHASE 4 (the resting membrane potential): The resting membrane potential of these cells is mainly a function of K+ efflux and is close to the Nernst potential for K+. During phase 4, ion concentrations that were altered by the previous action potential are restored to resting levels by the Na+/K+-ATPase and a Na+/Ca2+ exchanger, as well as an ATP-dependent Ca2+ pump.

PHASE 0 (upstroke of the action potential): Rapid depolarization occurs when the cells reach threshold and fast channels for Na+ open. This is accompanied by reduced conductance of the inwardly rectified K+ current (iK1). The rapid upstroke results in rapid spread of depolarization through most of the conducting system of the heart.

PHASE 1 (rapid repolarization to the plateau): This phase is caused by inactivation of Na+ channels and opening of voltage-sensitive K+ channels, producing a transient outward K+ current (iTO).

PHASE 2 (the plateau): The membrane remains depolarized during the plateau due to opening of voltage-sensitive, slow L-type Ca2+ channels and inward current of Ca2+. Simultaneously, an outward K+ current occurs through a voltage-dependent K+ channel (delayed rectifier K+ channel).

PHASE 3 (repolarization): Gradual inactivation of the L-type Ca2+ channels leads eventually to activation of K+ channels, causing rapid repolarization, substantially due to an inwardly rectified K+ current (iK1).

Front 21

What is a *VERY IMPORTANT* distinction between the depolarization of SA + AV nodal cells and the cardiac cells (Atrium and ventricles) and the the His- Purkinje System.

Back 21

depolarization of other cardiac cells is largely dependent on Na+ influx

In contrast to SA and AV nodal cells, are dependent on Ca2+ influx.

Front 22

Action potentials of ventricular and atrial myocytes and cells of the His-Purkinje system are characterized by five distinct phases. LIST the 5 phases?

Back 22

Phase 4 (the resting membrane potential): The resting membrane potential of these cells is mainly a function of K+ efflux and is close to the Nernst potential for K+. During phase 4, ion concentrations that were altered by the previous action potential are restored to resting levels by the Na+/K+-ATPase and a Na+/Ca2+ exchanger, as well as an ATP-dependent Ca2+ pump.
Phase 0 (upstroke of the action potential): Rapid depolarization occurs when the cells reach threshold and fast channels for Na+ open. This is accompanied by reduced conductance of the inwardly rectified K+ current (iK1). The rapid upstroke results in rapid spread of depolarization through most of the conducting system of the heart.
Phase 1 (rapid repolarization to the plateau): This phase is caused by inactivation of Na+ channels and opening of voltage-sensitive K+ channels, producing a transient outward K+ current (iTO).
Phase 2 (the plateau): The membrane remains depolarized during the plateau due to opening of voltage-sensitive, slow L-type Ca2+ channels and inward current of Ca2+. Simultaneously, an outward K+ current occurs through a voltage-dependent K+ channel (delayed rectifier K+ channel).
Phase 3 (repolarization): Gradual inactivation of the L-type Ca2+ channels leads eventually to activation of K+ channels, causing rapid repolarization, substantially due to an inwardly rectified K+ current (iK1).

Front 23

What are some characteristics of an EFFICIENT heart pump as described by VICINI? (Why?)

Back 23

**enough delay between the first and second contraction... (that way the ventricle can have enough time to fill up entirely before it ejects)

** both bottom sides of heart (left and right ventricle) contract pretty close to exact same time.

** no tetanus (all contracting at the same time)

Front 24

What are three factors affecting conduction?

Back 24

Front 25

What are the major parasympathetic outputs to the limbs?*

Back 25

There is NO parasympathetic output to the limbs!!

Front 26

Identify these types of structures, and the structures around it? Where are we looking, and what do they do? What might happen if you cut this?

Back 26

SYMPATHETIC TRUNK GANGLIA

Sympathetic fibers:
*Speed heart rate
*Dilate blood vessels that supply heart wall
*Dilate respiratory air tubes
*Inhibit muscles and glands of esophagus

Hint 26

The pathway is as follows: ventral rootlet -> spinal nerve -> white rami communicans ->
ganglia in the neck.

The postganglionic fiber then travels from the neck ganglia down to the heart and other tissues through the thoracic inlet.

*Resemble a string of beads lying next to the vertebrae
*Attached to ventral rami of spinal nerves by WHITE and GRAY RAMI communicantes

Front 27

Between Autonomic (ANS) vs. SOMATIC nervous system (SNS), which has a faster signal conductance and why?

Back 27

Motor neuron in SNS are HEAVILY MYLELNATED, and signal conduiction is rapid.

In the ANS there will ALWAYS be a pre and post ganglionic neuron. Preganglionic fibers
are slightly myelinated; postganglionic fibers are not myelinated.

signal conduction for neurons in SNS is FASTER than in ANS.

Front 28

What is an important difference between the types of signals between the autonomic neverous system (ANS) and somatic neverous system (SNS)? What can ANS do that SNS can't?

Back 28

ANS has a considerable amount of DIVERGENCE, (which allows few signals to affect a variety of tissues, making signaling more efficient in an all or none flight or fight response)

Front 29

If someone has a scan like this, what might we see on the surface anatomy of the patient? Why is this?

Back 29

Tumor pulls on connective tissue of skin

Peau d'orange- appearance of orange peel texture
Cancer en cuirasse- hardy, wooly texture of skin

Front 30

What makes this REALLY REALLY BAD? What do you need to do immediately? What surface anatomy would you use to drain this?

Back 30

There are two locations that PERICARDIOCENTISIS can be performed (without puncturing the lungs)
*through the 5th or 6th intercostal space at the left sternal border at the cardiac notch of the left lung.
*through the infrasternal angle.

Hint 30

if space in pericardium is comprimised:
less space--> less volume available for heart to expand and pump.

Front 31

In this picture, we see a left coronary arteriogram: How can you tell? Which coronary arteries can you identify? WHY IS IT IMPORTANT TO KNOW WHICH CORONARY ARTERY IS BLOCKED?

Back 31

The left coronary artery supplies the majority of the left side of the heart.

Blockage may lead to left ventricular failure.

Front 32

In this picture, we see a RIGHT coronary arteriogram: How can you tell? Which coronary arteries can you identify? WHY IS IT IMPORTANT TO KNOW WHICH CORONARY ARTERY IS BLOCKED?

Back 32

When the RIGHT CORONARY ARTERY is involved with arterial disease and occludes, associated disorders of cardiac rhythm often result because the sinu-atrial and the atrioventricular nodes derive their blood supplies predominantly from the right coronary artery.

Front 33

Why would we order a coronary artery angiogram for a patient, and how do we achieve visualization of stenosis in the coronary arteries?

Back 33

Coronary angiography-small arterial catheters are maneuvered from a FEMORAL ARTERY puncture site through the femoral artery and AORTA and up to the origins of the CORONARY VESSELS. X-ray contrast medium is then injected to demonstrate the coronary vessels and their important branches. If there is any narrowing (stenosis), angioplasty may be carried out. In angioplasty tiny balloons are passed across the narrowed areas and inflated to refashion the vessel and so PREVENT further CORONARY ISCHEMIA and MYOCARDIAL INFRACTION.

Front 34

Why might a patient with severe chest pain, also feel pain in their arm as well?

Back 34

PERCEIVING HEART PAIN IN THE T1-4 DERMATOMES

Hint 34

When cardiac cells die during a myocardial infarction, pain fibers (visceral afferents) are stimulated. These visceral sensory fibers follow the course of sympathetic fibers that innervate the heart and enter the spinal cord between TI and TIV levels. At this level, somatic afferent nerves from spinal nerves T1 to T4 also enter the spinal cord via the posterior roots. Both types of afferents (visceral and somatic) synapse with interneurons, which then synapse with second neurons whose fibers pass across the cord and then ascend to the somatosensory areas of the brain that represent the T1 to T4 levels. The brain is unable to distinguish clearly between the visceral sensory distribution and the somatic sensory distribution and therefore the pain is interpreted as arising from the somatic regions rather than the visceral organ (i.e., the heart.)

Front 35

What makes the "dub" sound (S2)?

Back 35

Closure of aortic & pulmonary valves

SEMILUMAR VALVES

Hint 35

ps. ** do not mix up the AORTIC valve with the ATRIOVENTRICULAR (AV) valves

Front 36

What makes the "lub" sound (S1)?

Back 36

Closure of the tricuspid & mitral valves

ATRIOVENTRICULAR VALVES

Hint 36

Also correlates with QRS phase of EKG

Front 37

What might happen if you get stabbed in the heart? (or if you have a whole in your heart in general? What would happen to the venous RETURN? What would happen to the venous PRESSURE?

Back 37

Front 38

So... When a patient comes in with a cardiovascular problem, it is your job to figure out , “Where in the cardiovascular system is the
problem?"

What are the four components of the cardiovasular system?

Back 38

1. HEART (pump)
2. VASCULAR SYSTEM (tubes)
3. VOLEMIA (circulating BV)
4. PULMONARY MICROCIRCULATION (a gas-exchange)

** problems in any of these four can throw the whole system out of whack!

Hint 38

A problem in any of these parts of the CV can throw your whole cardiovascular system out of whack

1. HEART
2. VASCULAR SYSTEM: a closed system of living tubes that transport and distribute blood to the periphery, and then collects it and returns it to the right side of the heart.
3. VOLEMIA: the circulating blood volume that fills up the vascular system at a given pressure.
4. PULMONARY MICROCIRCULATION: a gas-exchange system between the blood and the surrounding environment.

Front 39

What happens if you perform a pleaural tap incorrectly? Why?
In which layers do the blood vessels and nerves of the thoracic cage travel in?

Back 39

You DAMAGE the intercostal nerve.

Front 40

What are the significant surface anatomy features for the heart and lungs? What clues do they give to what is on the inside?

1. SUPRASRTERNAL NOTCH:
2. STERNAL ANGLE
3. STERNUM
4. XIPHISTERNAL JOINT
5. NIPPLE (in male):
6. APEX BEAT OF HEART

Back 40

1. SUPRASRTERNAL NOTCH: Suprasternal notch. Suprasternal notch projects posteriorly onto T2 and T3.

2. STERNAL ANGLE: (a.k.a. Angle of Louis) where the manubrium and body of sternum join, projects posteriorly to T4 and T5

3. STERNUM: directly anterior to the heart. Clinical correlate: in CPR you don’t pump on left side (that would crack ribs) you pump over the sternum to compress the heart and pump blood.

4. XIPHISTERNAL JOINT projects to T9 posteriorly.

5. NIPPLE (in male): in the 4th intercostal space (varies in females)

6. APEX BEAT OF HEART. in the 5th intercostal space, 3 ½ ” from midline on the left side
(From the nipple, an inch or two below, you get the apex beat of the heart, where you listen for heartbeat during a physical).

Front 41

The lungs are the only tissue that receive 100% of cardiac output! WHY?!

Back 41

the aorta does not recieve 100% of cardiac output because of the coronary arteries! (Diffusion is not good enough. these blood vessels do a lot of work, and need their own blood supply.

Front 42

What force is causing the AV valves (tricuspid & mitral) to open?

Back 42

The atrioventricular valves open when the pressures in the ventricles fall below those in the atria.

Front 43

There are many different areas of attatchment in the pericardial sac. Normally, this pericardial cavity does not exist! The fibrous pericardium protects the heart from overfilling, but if that space starts to fill up, youre screwed... What are some possible pathologies of this pericardial sac? He mentioned 5. list them.

Back 43

1. PERICARDITIS- inflammation of the pericardium
2. PERICARDIAL EFFUSION– the potential space becomes a real space with build up of fluid
3. CARDIAC TAMPONADE– pericardial effusion -> heart compressed because fibrous pericardium cannot stretch!
4. CARDIOMEGALY – heart becomes larger
5. HEMOPERICARDIUM– blood in the pericardial cavity (acute condition), must be drained -> pericardiocentesis (draining procedures)

Front 44

What two effects are produced when the left ventricle fails?

Back 44

1. CONTRACTILE FORCE IS REDUCED--> reduces the pressure of the ejected blood --> lowers the blood pressure.-->
2. LEFT ATRIUM HAS TO WORK EXTRA HARD TO FILL THE FAILING LEFT VENTRICLE-->
increases left atrial pressure-->
increased pressure in the pulmonary veins-->
higher pulmonary venular pressure--> FLUID LEAKS IN CAPILLARIES (then into the pulmonary interstitium and then into the alveoli) --> PULMONARY EDEMA--> restricts gas exchange---> SHORTNESS OF BREATH

Front 45

There is a potential space in between the 2 serous layers. It’s generally filled with a tiny amount of fluid to lubricate the 2 surfaces, but it’s doesn’t become a true space unless pathological conditions ensue. (analogous to the pleural space), however, there are two CARDIAC SINUSES which are posterior spaces created by the reflections of the serous pericardium... Which cardiac sinus could you exploit for coronary by-pass surgery? How?

Back 45

The TRANSVERSE PERICARDIAL SINUS seperates the arteries from the veins

Surgical clamp is introduced into the space and blood flow of aorta and pulmonary trunk stopped momentarily before great vessels are connected to bypass machine.

Hint 45

The borders of the two cardiac sinuses are where the visceral pericardium extends off the surface of the heart to become continuous with the parietal pericardium.

Front 46

In which direction would the blood flow through in this primitive heart? Which parts here are flipped from what you would normally expect? When during development does this happen?

Back 46

Initially, the future atrium and future ventricle are reversed from where you think they would be....

The bends that arose from the dorsal aorta being pulled down ventrally will become the AORTIC ARCHES.

The segment that connects between the heart and those arches is the TRUNCUS ARTERIOSUS.
The part right below that is really a swelling, the BULBUS CORDIS (bulb of the heart). Below that is the primitive ventricle. Adjacent to the ventricle is another small chamber, the atrium. From either side, there are tributaries called the SINUS VENOSUS which bring blood in from a number of veins. Blood would travel (if it were going in one direction, however, in the early embryo it probably goes in both directions) from the body, to the sinus venosus, through the atrium, through the ventricle, to the bulbus cordis, through truncus arteriosus, to the aortic arches, into the dorsal aorta and around the body.

Front 47

During emryonic folding, how do we twist the hose into a pump? How come the apex of our hear always point to the left side? WHERE DOES IT FOLD IN?

Back 47

This cardiovascular tube, which is now in the midline and located ventrally, is anchored at two points but most of it is free-floating in an open area called the COELOM. It is also growing a little faster than the coelom expands. Consequently, as the tube gets longer, it is forced to bend. It always occurs such that its tip bends to the left of the embryo. The sinus venosus (the inflow tract involved with the atrium) shifts cephalically behind the ventricle. As it does so, it moves up and to the right, coming up behind the heart. It always does that in normal people.

Hint 47

The way it bends, the sinus venosus always goes up and to the right, the atrium always goes behind, and that is how the inflow tract and outflow tract get in the same position, although the inflow tract is posteriorly located. This pushes the bend in the cardiac tube to the left, which puts the apex of the heart on the left side.

Front 48

Which formula would you use with thin walled capillaries? What physiological pathology might this be helpful for?

Hint* T= Pr

Back 48

LaPlace's Law.

Aneurysms!!!

Front 49

Which two septum are required to separate the atria? What may happen if this does not develop properly?

Back 49

Problems from development here could lead to a "blue baby" (too much unoxygenated blood from RA--> LA)

Front 50

What do all six of these have in common? When do the occur during cardiovascular developement?
1. Cellular migration
2. Extracellular Matrix
3. Hemodynamics
4. Targeted growth
5. Cell death
6. Visceral Situs

Back 50

MECHANISMS DRIVING CARDIOVASULAR DEVELOPMENT:
1) Cellular Migration: neural crest cells forming part of the spiral septum; adherons released by epimyocardium acting on some endocardial cells to migrate into cardiac jelly of the endocardial cushions
2) Extracellular Matrix: cardiac jelly: cushioning for cells during folding and contraction; a matrix that allows cellular migration
3) Hemodynamics: important in formation of septa by creating areas of differing pressure
4) Targeted Growth: septa grow in certain directions
5) Cell Death: in septum primum to form ostium secundum; areas beneath valves allowing them to thin
6) Visceral Situs: bending of the heart in the appropriate direction

Front 51

Veins are super complicated: High yield questions: How many parts contribute to the Vena Cava?

Back 51

there are 7 parts contributing to the vena cava (they arise from a ‘swamp’ of tissues that are not as defined as depicted in the text)

you can get alterations in flow that result in gross anatomical anomalies.

Front 52

What do these three veins drain in to? What does it eventually become? Cardinal veins + vitelline veins + umbilical veins =

Back 52

Cardinal veins + vitelline veins + umbilical veins = SINUS VENOSUS--> wall of RA in definitive heart

Front 53

Normally, ribs heal up pretty well by themselves.... What particular kind of rib fx is really, really, really, bad? (aka LIFE-THREATENING)

Back 53

Flail chest/ multiple rib fractures..., paradoxical movement of ribs during breathing--> can cause pulmonary contusion!!--> RESPITORY FAILURE!! Almost half of people that have it DIE

Front 54

Why should you wear a seatbelt? Which types of fractures/ chest trauma are associated with a high mortality rate (in adults)? Why?

Back 54

Flail chest/ multiple rib fractures--- Often, it is the pulmonary contusion, not the flail segment, that is the main cause of respiratory failure/ death

STERNUM- rarely cracked, but mortality = 25-45% because of likelyhood of heart injury!

Front 55

When looking @ x-rays, which ribs of thorax are usually the easiest to fracture? Most difficult?

Back 55

• Ribs 2-7: Most likely to be broken (usually fractured), just anterior to angle of the rib
• 1st Rib: Least likely to be damaged; broad and flat, protected by clavicle

Front 56

How does the composition of the costal cartilage change as you get older? Why do you need to watch out for this as a physician?

Back 56

** in kids, chest trauma may not fx ribs, but compression can still cause injury to organs (cartilage= very elastic)
***in old people, costal cartilage may ossify

Front 57

DO NOT MIX UP these diseases!!! What is the difference between Persistent DUCTUS Arteriosis (PDA) and Persistent TRUNCUS Arteriosis? What causes them?

Back 57

Persistent TRUNCUS Arteriosus MALFORMATION RELATED TO NEURAL CREST CELL MIGRATION
* Neural crest cells do not migrate to form the spiral septum
* Oxygenated and deoxygenated blood mix and systemically recirculate
* Not lethal but decreased physical activity and life span shortened
* Can be surgically repaired

Patent ductus arteriosus (PDA) can be idiopathic (i.e. without an identifiable cause), or secondary to another condition

Front 58

How do we get the rapid expansion of the left and right atria? How come we have all these extra orfices in the L and R artia? EXPLAIN WHY THE WALLS OF THE ATRIA ARE SMOOTHER THAN THE VENTRICLES. HOW DO THEY DO IT?!

Back 58

Intussusception

Front 59

Malformation of what "spiral staircase forming" mechanism can causes these diseases to happen?

Back 59

Malformations Related to Aberrant Neural Crest Cell Migration
1) Persistent TRUNCUS Arteriosus
-Neural crest cells do not migrate to form the spiral septum
-Oxygenated and deoxygenated blood mix and systemically recirculate
-Not lethal but decreased physical activity and life span shortened
-Can be surgically repaired

2)Transposition of Great Vessels
- Septal spiraling in a counter-clockwise direction
-Pulmonary and systemic circulations are not connected
- FATAL

3)Tetralogy of Fallot

Front 60

What is the relationship between cardiac output (CO), heart rate (HR) and stroke volume (SV)?

Back 60

CO = HR x SV
The heart pumps blood in increments (SV)
Valves allow for filling and ejection
Normal resting values are approx. 5 L/min (CO), 70/min (HR), and 70 ml (SV)

Front 61

What proceeds the mechanical events of the heart pumping? Which area of the heart is the NORMAL pacemaker of the cell? Where is there a pause?

Back 61

ELECTRICAL EVENTS precede and initiate mechanical events
SA node (SINUS NODE) is the normal pacemaker
Conduction proceeds from SA node--> internodal pathways--> AV node--(pause)--> HIS-Purkinje system--> ventricular myocardium

Front 62

Where is the largest pulse pressure in the body found?! WHY is that? What about the lowest?

Back 62

Largest pulse pressure is in LEFT VENTRICLE (120/0)
Mean pressure falls as blood flows from aorta to arteries, capillaries, veins, RA
Same pattern is repeated at lower pressures in the pulmonary circulation
Arterial pressures often measured indirectly, by sphygmomanometry
Arterial P can be recorded directly through catheterization; catheters can be guided back (retrograde) to record LV pressures
Venous pressures are recorded directly by catheterization; catheters can be advanced (antegrade) to record RA, RV, PA pressures

Front 63

Which pathology makes the most noise/ is weirdest looking on a phonocardiogram? Why? What does a normal phonocardiogram look like? What causes the two sounds?

Back 63

Front 64

As physicians, how the F*uck are we supposed to measure cardiac output?

Back 64

THE FICK PRINCIPLE!
Organ blood flow can be calculated on the basis of uptake or removal rate of a marker substance and the arterial and venous concentrations of that substance across the organ
Thus, cardiac output can be calculated based on OXYGEN CONSUMPTION and arterial and venous oxygen concentrations
Systemic arterial oxygen concentration and pulmonary artery oxygen concentration are used in this calculation

Front 65

What are the four clinical birth defects contributing to the Tetralogy of Fallot ?

Back 65

i) OVERRIDING AORTA– spiral septum divides incorrectly leaving small pulmonary artery and large aorta
ii) PULMONARY STENOSIS– small pulmonary trunk
iii) INTERVENTRICULAR SEPTAL DEFECT–causing ox/de-ox mixing
iv) RIGHT VENTRICULAR HYPERTROPHY– due to increased resistance of narrow pulmonary artery

Front 66

What is that? How come we see this more in younger people?

Back 66

The Reflected Wave
The heart beat generates a pressure wave that travels along the walls of the aorta.

At about the level of the kidneys it is reflected back to the heart.

In a young person, the reflected
wave arrives back at the heart as
the contraction phase (Systole)
ends and the relaxation phase
(Diastole) begins. The reflected
wave maintains diastolic pressure
and promotes coronary blood flow.

Front 67

What are two ways we increase stroke volume (SV)?

Back 67

Fill the ventricle more, and empty it more!

Front 68

When we excercise, we go from a normal cardiac output (CO) of 5L/ min --> 25 L/min! DAYYYYUM!!

How can we increase cardiac output needed for the increased oxygen demands when we are exercising?

Back 68

CO= SVx HR

increase HR (ejecting blood QUICKER--by itself, not very effective because it reduces diastasis period)
increase SV (fill the heart MORE and empty is MORE)

Front 69

What is DIASTASIS? What is it, why is it important, and where could i find it on the cardiac cycle?

Back 69

PASSIVE refilling of ventricles

Front 70

What is the difference between arterial pressure and MEAN ARTERIAL PRESSURE?

Back 70

ARTERIAL BLOOD PRESSURE is expressed as Systolic P/Diastolic P

MEAN ARTERIAL PRESSURE= Diastolic Pressure + 1/3 Pulse Pressure

Front 71

What are the NORMAL values for cardiac output?

Back 71

CO=HRx SV
5000ml/min= 70 BPM x 70ml

Front 72

Why would memorizing the triplets [300, 150, 100] [75, 60, 50] be helpful in reading EKGs? Where should we look for a start line for measuring rate?

Back 72

An R wave peaks on a heavy black start line

Where the next R wave falls gives the rate!

Each distance b/w the heavy black lines = 1/300 min (.2sec)

Front 73

Sinus bradycardia is present if the SA node produces a heart rate less than one beat per ______
What is another way we can measure this on an EKG?

Back 73

Second (careful!)

<60 BPM (cycles per minute)
rates = cycles/ 6 sec. strip x10

Front 74

What significant fxn do the AV valves have besides preventing backflow of blood? (a UNIQUE fxn you might not see in the semilunar valves. Why?)

Back 74

ELECTRIC INSULATOR!! (only place where electrical impulse can pass is through the AV node--> helps slow electrical impulse down [pause] so atria mechanical contraction )

Front 75

Which electrical activity causes the largest complex to be formed on the EKG

Back 75

QRS complex

Front 76

On an EKG, up is positive, and down is negative.

1. What do you call any initial negative deflection on an EKG? 2. 2. What are all positive deflections on an EKG called?
3. In the EKG, what do we call any negative (-) deflection that follows an R wave?

Back 76

Q wave
R waves
S waves

Front 77

How FAST is the QRS complex?

Back 77

QRS usually lasts <120ms (anything more is very unusual

Front 78

How long does the PR interval last? How long does the QRS complex usually last?

Back 78

.16 s .08 s

Front 79

If the great vessel valves do not form properly, (atresia) or become greatly narrowed (stenosis) it is often very fatal. How do the valves of the heart develop?

Back 79

cells in epi-myocardium secret ADHERONS (TGF-beta, Fibronectins, proteoglycans, inductive signals). -->diffuse through cardiac jelly-->
[*endocardium*]--> migrate into jelly-> MESENCHYMAL CELLS OF ENDOCARDIAL CUSHIONS--> make tissues that seperate atria from ventricles AND supports A/V valves!

Front 80

Both the COELOM and CARDIAC JELLY have very important roles in embryonic development and proper folding. Do not mix up the locations of these two areas!!

Where can we find the cardiac jelly? Where is the coelm?

Back 80

Cardiac jelly = between endomyocardium and epimyocardium in early embryos- protect from kinking

Coelom= free open area where cardiac tube expands faster than coelom--> folding occurs [ the sinous venosus (inflow tract of ATRIUM) normally shifts cephalically behind ventricle.


***The way it bends, the sinus venosus always goes up and to the right, the atrium always goes behind, and that is how the inflow tract and outflow tract get in the same position, although the inflow tract is posteriorly located. This pushes the bend in the cardiac tube to the left, which puts the apex of the heart on the left side. **

Front 81

When all of these respective areas are folding in the pericardial sac, what helps prevent the heart tube from KINKING during development?

Back 81

Cardiac jelly!

In early embryos, the heart tube is composed of an inner area, the endocardium, and an outer area, the epimyocardium. A gelatinous material, called cardiac jelly, occupies the space between these two layers. Cardiac jelly has the consistency of jello. It is a space holder that bends but does not break and likely plays a role in the looping of the heart.

Front 82

What are some vascular structures that are unique and very functional for fetal circulation, but may be pathological in adult circulation?

Back 82

Ductus venosus--> ligamentum venosus

Ductus arteriosis--> Ligamentum arteriosum
[PDA]

Foramen Ovale--> Fossa Ovalis
[probe- patent foramen ovale*]
*about 25% of people have this. doesn't seal off. for some people with congestive heart failure, reopening this valve may save their life.

Front 83

During development, the separation of the ATRIUM begins as the bulbus cordis/ truncus arteriosis cause a bending in the roof of the atria and the first septum grows from the superior posterior wall across and down. What is the NAME of the ever-shrinking HOLE being CLOSED by the SEPTUM PRIMUM? What is the name of the hole that begins to OPEN on the same septum?

Back 83

1st Evershrinking hole= osteum primum

2nd opening in 1st septum= ostium secondum

Front 84

What are some difference between how atrial septum are made, and how the ventricular septum are made? What about atrioventricular septum?

Back 84

Atria- Two septums must be formed in to divide the atria (Septum primum- thin sheet of paper & Septum secundum- stiff & imcomplete allowing unidirectional (R->L) flow of blood in fetus) as foramen--> fossa ovalis = shunt closes b/w atria


The Muscular Interventricular Septum is Formed by Apposition of Adjacent Walls + rapid expansion

A/V septums (and VALVES) formed by release of adherons from epimyocardium.

Front 85

How does this motherf*cuker flip around to form the ventricles?

Back 85

Ventricle bifurcation: Bulbus cordis and truncus arteriosus are connected. As this combined structure folds back on the atria, you can envision the beginnings of left and right atria. The bulbus cordis looks like it is going to give us a ventricle on each side, but it does not do this. The heart continues to grow and, as it does so, the ventricle gets broad laterally and the bulbus cordis leans back on the ventricle. Where the bulbus cordis is attached to the ventricle, there is a little ripple in the floor of the ventricle. That ripple is slightly medial to where the blood is traveling to get out of the heart. So it is a little to the left of the base of the bulbus cordis. This is the site of the early interventricular septum. The septum then "grows" as the walls of the presumptive ventricles expand leaving the tissue of the septum behind and adding to the bottom of the septum. The bulbus cordis is the beginning of an outflow tract for the aorta and the pulmonary trunk.

Blood flows from the sinus venosus to the atrium, through the opening (which is shaped like a dumbbell or an "H") into the ventricle. This is pinched off to form two orifices, one to go into each ventricle.

Front 86

What is the significance of aortic arch 4 and aortic arch 6? Which arches are seen on the left side that are not on the right side?

Back 86

Note that in the embryo, the distal left AA #6 is the ductus arteriosus (which constricts at birth to become the ligamentum arteriosum)

AA 4 & 6 undergo asymmetrical development

Front 87

What are the important things to know about the aortic arches?

Back 87

While all of the aortic arches are important, the two caudalmost arches (aortic arches 4 and 6) are the only ones to undergo asymmetric development – play integral roles in the development of the heart.

The five definitive pairs of aortic arches in mammals are numbered I–VI (aortic arch V is very transient and is not depicted).
develop in a cephalocaudal direction such that arch 1 develops first, followed by arch 2.
As arch 3 appears, arch 1 disappears and is gone when arch 4 appears
The changes are partly driven by development of the neck, which appears as the embryonic face lifts off the chest and the head assumes an erect position.
The aortic arches contribute to the vasculature of the upper chest, neck, and head.

Front 88

The electical conduction of the heart is derived from the neural crest cells, right?

Back 88

WRONG

Front 89

Why do we need to study atrieal developement an aortic arch development? When does it begin?

Back 89

Front 90

What might coarctation of the aorta (a birth defect) present itself in a patient? What might you see if someone had it?

Back 90

*HIGH BP in braches BEFORE NARROWING & HEART
*This results in LOW BP in distal branches of aorta AFTER NARROWING

*High BP in upper body, low BP in lower body.
*intercostal arteries can become enlarged, since the anastomoses of the anterior intercostals (from the internal thoracic artery) with the posterior intercostals can circumvent the narrowing
* more common in some genetic conditions (Turner syndrome) but also can be associated with congenital abnormalities of the aortic valve such as a bicuspid aortic valve

Front 91

A horse voice might result after surgery, diease or or injury to the superior mediastinum. Physiologically, why might these two symptoms be related?

Back 91

*The left recurrent laryngeal nerve passes beneath the arch of the aorta and ascends to the neck between the trachea and the esophagus. Bronchogenic or esophageal carcinoma or an aneurysm of the arch of the aorta can thus affect this nerve
*Surgery, injury, or disease affecting the contents of superior mediastinum can damage either or both recurrent laryngeal nerves, reducing the voice to a hoarse whisper
*The recurrent laryngeal nerve supplies all of the intrinsic muscles of the larynx but one

Front 92

Which congenital defect is the most common?

Back 92

Ventricular Septal Defects (VSDs)
The membranous part of the interventricular septum is the most common site of ventricular septal defects (VSDs)
VSDs account for 25% of all cardiac abnormalities
It can be a result of any one of several developmental anomalies, such as failure of the embryonic endocardial cushions, which form part of the septum, to fuse
A left to right flow of blood occurs with this defect because of the strength of contraction of the left ventricle
This increases the blood flow through the pulmonary trunk to the lungs and results in pulmonary hypertension (increased blood pressure) and an enlarged heart
This condition is potentially fatal if not corrected

Front 93

Which valvular defect is most common? What would it sound like? What are possible causes of it?

Back 93

The mitral valve is the heart valve most frequently affected by disease
It can be caused by endocarditis, myocarditis, rheumatic heart disease, or lupus erythematosus, or can result from a developmental abnormality
The diseased mitral valve allows reversal of blood flow from the left ventricle to the left atrium (mitral regurgitation)
It is characterized by a HIGH PITCHED MURMUR, loudest over the apex of the heart

Front 94

Narrowing of the pulmonary valve (stenosis) is caused by fusion of the valve cusps. How does this happen? If not corrected surgically, what else could it lead to?

Back 94

It can result from a developmental abnormality or diseases such as rheumatic fever or endocarditis
Stenosis of the pulmonary valve leads to right ventricular hypertrophy and heart failure, if not corrected surgically

Front 95

What are clinically significant thoracic VERTEBRAL landmarks? What clues do they give to?

Back 95

Spine of the scapula T2:

Sternal angle (of Louis); level of the bifurcation of trachea, arch T4/T5: of aorta

Level of the heart T5-T8:

Aortic hiatus of the diaphragm; also transmits the thoracic duct T12:

Esophageal hiatus of the diaphragm; also transmits the right and left T10: vagal trunks, esophageal branches of left gastric vessels and lymphatics

Caval opening of the diaphragm;
also terminal branches of the right T8: phrenic nerve

Front 96

Patient comes in to the ER with chest wound in 5th intercostal cavity. They have distention of their neck veins and a collapsing pulse. What is a collapsing pulse?! What might be one possibility for this happening** think bout it!

Back 96

diastolic & systolic pressures become the same (pulse pressure is collapsing)

cardiac tamponadae--> stroke volume becomes compromised with swelling

Front 97

What is the difference between angiogensisi and vasculogensis? Which one would you see in a tumor?

Back 97

Front 98

What kind of placenta do humans have? Why?

Back 98

Front 99

the cardiac system. First to function, but not first to _____. What is the significance of F8FG?

Back 99

Front 100

When does the blood system develop?

Back 100

Front 101

How do the cells know how to fold during embryonic development?

Back 101

Front 102

Heart formation involves 2 different axises. What are the two differen types of folding called?

Back 102

Front 103

What regions of the cardiac tube turn in to what? (in fetus vs. adult)!!

Back 103

Front 104

What two transcription factors cause the heart's apex to always form on the left side? Why is this?

Back 104

Front 105

What is pushing back and up to force ventricles to the anterior + left?

Back 105

Front 106

Veins on which side during development eventually become the vena cava?

Back 106

Front 107

Which opening in the heart is considered a "Flutter valve"?

Back 107

Front 108

How is the coronary sinus made?

Back 108

Front 109

What makes mesenchymal cells different from myocardial cells?

Back 109

Front 110

How is the SPIRAL septum made?

Back 110

Front 111

Where do the AV valves come from?

Back 111

Front 112

Where is the cardiac skeleton located?

Back 112

Front 113

When does the conduction system develope in the heart? How?

Back 113

Front 114

Once again--> fetal structures... what is their purpose and what do they become in adults (hopefully)...

Back 114

Front 115

Decribe the path of fetal circulation, starting from the mom

Back 115

Front 116

Why is it important to wait until the placenta stops pulsing before we tie off the umbilical cord after birth?

Back 116

Front 117

What changes occur immidiately after birth? After first breath? After first year?

Back 117

Front 118

What are the different types of birth defects associated with the mechanisims driving developement?

Back 118

Front 119

What is the most frequently encountered birth defect in humans?

Back 119

Front 120

Which type of defect (most common) spontaneously close within 1st year of life?

Back 120

Front 121

Think about the evolution of the cardiovascular system in mammals. Why is this such an efficent structure? An how freaking lucky are we to have it? What does it do? how does it regulate? How come we dont have to go and lay out on a warm rock before we are ready to go to school everyday?

Back 121

Cardiovascular development is elegantly controlled and implemented. In mammals, the progression of developmental events follows a nearly identical course regardless of species, although the timing of events differs on the basis of the total duration of the gestational period. The rudiments of the cardiovascular system appear early in gestation, and the heart is the first organ system to begin functioning.
During its earliest phase of development, blood islands appear within the embryo in the anterior heart field; these coalesce to form a horseshoe-shaped cardiogenic plate that cavitates to produce the cardiac tube. As the embryo assumes a three-dimensional shape by undergoing cephalocaudal and lateral folding, the cardiac tube assumes a ventral midline position. The developing heart is contained within the nascent pericardial cavity and, with continued growth, it lengthens and undergoes cardiac looping. Cardiac looping results in an anatomic arrangement that prefigures the four chambers of the adult heart.
Thereafter, septa appear that (i) divide the atria and ventricles from each other and, in conjunction with the development of the neural crest-enhanced spiral septum, partitions the outflow tract and (ii) separate the vascular system into a systemic and a pulmonary circulation. Because the lungs do not function until birth, a system of right-to-left shunts allows the circulatory system to function with the placenta serving as the major organ for provision of gases and nutrients to the fetus (and removes carbon dioxide and wastes from the fetal blood) until birth. The final anatomic changes occur shortly after birth as the foramen ovale and ductus arteriosus close.
A variety of morphogenetic processes are involved in the development of the heart, and perturbations of any of them can result in cardiac malformations. The incidence and description of the most common malformations were previously described.

Front 122

Which reflex helps you survive when you are drowning? How does it work? How does it turn on? How does it turn off?

Back 122

Front 123

Which reflex can cause your heartrate to go up when you are in shock? What is the difference between the BAINBRIDGE reflex and the BARORECEPTOR reflex?

Back 123

The Bainbridge reflex and the arterial baroreceptor reflex produce opposite responses to an intravenous infusion. The Bainbridge reflex is usually observed when a rapid intravenous infusion is administered to a subject with a slow heart rate. Stretch of atrial receptors produces a reflexive increase in heart rate under these circumstances. On the other hand, when heart rate is high to begin with, for example, after hemorrhage, intravenous infusion usually decreases heart rate. In this circumstance, the increased ventricular filling associated with the infusion produces an increase in cardiac output and therefore an increase in arterial pressure. The rise in arterial pressure causes stretch of arterial baroreceptors, resulting in diminished sympathetic nervous system activity and enhanced parasympathetic activity, and a slowing of heart rate.

Front 124

Why are you still stressed out long after exam is over?

Back 124

Front 125

What is the difference between the myocardium and the purkinje fibers?

Back 125

Front 126

What are the different ways to measure blood pressure?

Back 126

Front 127

What is the significance of arterioles in overalll peripheral vascular resistance?

Back 127

Front 128

What is significant to remember about pre-ganglionic lengths and post ganglia lengths in the sympathetic nervous systems? How does their structure contribute to their fxn?

Back 128

Front 129

Why the hell does everyone keep talking about the white ramus and grey ramus?? WTF do they do? Where are they?

Back 129

Front 130

How do viseral nerves sene pain?

Back 130

Stretch!

Front 131

Which nrevous system (sympathetic or parasympathetic) is considered more "discrete"? Why is this? how does its structure contribute to fxn?

Back 131

Front 132

What are common pathologies related to the autonomic nervous system? How can you fix them?

Back 132

Front 133

Which part(s) of the conduction system of the heart has a LONGER PLATEAU PHASE (phase 2) during its action potential?

Back 133

Front 134

What is this line measuring? (volume, pressure, blood flow, sounds)? What useful markers are here? What can you calculate from it? Which parts would Synchronize with the EKG wave of this

Back 134

VENTRICULAR VOLUME!
*top is End Diastolic Volume (EDV)
* bottom is End Systolic volume (ESV)

Can use to help calculate EJECTION FRACTION! (proportion of the ventricular EDV that is ejected during SYSTOLE

Front 135

For this VENTRICULAR VOLUME CURVE:
1. second hear sound?
2. Rapid passive ventricular filling?
3. Diastasis?
4. EDV?
5. ESV?

Back 135

Front 136

Which types of cells have this kind of action potential? How can you tell? What ions might cause this?

Back 136

Action potential of SA nodes!

Front 137

Which great vessel (not in the heart) (with 40-60 layers of of elastic fibers throughout tunica media) has the greatest arterial pulse pressure?
What is the area WITH the greatest pulse pressure of the human circulation (SP-DP)?
Why can you see A,C,V waves on a pulsating neck vein for someone with cardiac tamponadae?

Back 137

1. Aorta
2. Left Ventricle
3. Atrial Pressue

Front 138

Think about how the STRUCTURE of a heart can change as a result of disease... what would happen for someone with:
1. Pulmonary Hypertension?
2. Aortic Stenosis (narrowing of the aortic valve)?
3. Mitral Imcompotence (regurgitation)?

How would this change the sounds you hear?

Back 138

PULMONARY HYPERTENSION: Right ventricular hypertrophy may occur in response to the chronically increased work of the right ventricle.
AORTIC STENOSIS: Left ventricular hypertrophy occurs in response to the greater work performed by the ventricle.

MITRAL IMCOMPETANCE: Mitral incompetence: Left atrial dilation may develop as a result of the elevation of left atrial pressure and volume caused by mitral regurgitation (leakage of blood back into the atrium from the left ventricle).

Front 139

So if blood moves based on the difference in pressure gradients.... How the heck can blood still move to a lower branch when the systolic pressure is higher?!

Back 139

As long as the mean pressure is going down, flow goes in the proper direction!

Front 140

What is the dicrotic notch? What is occurring there? What EVENT/ valve(s) are associated with it?

Back 140

AORTIC VALVE CLOSING

Front 141

How might narrowing (STENOSIS) of the AORTA change what you may see on a wigger's diagram? Why? What is happening in the ventricles?

Back 141

*As aorta ages, it gradually becomes more calcified... and may lead to aortic stenosis.

*This sounds like the HARSHEST sounding murmur you may hear. (like waves crashing almost)

*Aortic stenosis (narrowing of the aortic valve): Left ventricular hypertrophy occurs in response to the greater work performed by the ventricle.

Front 142

How might MITRAL VALVE STENOSIS change what you would normally see on a wigger's diagram? Why? What is happening in the ventricles?

Back 142

Once very common b/c of infection [Rhumetic heart diesease]

*late diastolic murmur
*opening snap with diastolic rumble murmur

Front 143

How might AORTIC INSUFFICIENCY or REGURGITATION change what you would normally see on a wigger's diagram? Why? What is happening in these ventricles?

Back 143

*Pansystolic murmur

*Mitral incompetence: Left atrial dilation may develop as a result of the elevation of left atrial pressure and volume caused by mitral regurgitation (leakage of blood back into the atrium from the left ventricle).

Front 144

There are two types of PATHOLOGICAL murmurs that can occur in both systole and diastole that involve either STENOSIS OF VALVES, or INSUFFICIENCY of valves? Which murmurs involve which valves, and how can you tell?

Back 144

Front 145

Compare the two divisions of the ANS [sympathetic & parasympathetic] Where does each system originate from? Name something they have in common. Something that is different?

Back 145

Front 146

Which color is sympathetic? Which color is PARAsympathetic? Which one represents preganglion? Which one represents post ganglion?

Back 146

Front 147

Why do we sometimes see sinus bradycardia (< 60BPM) in serious olympics athletes?

Back 147

parasympatheitc excess--> super slow rate may lead to syncope.

Front 148

When you see an EKG, DON'T GET FREAKED OUT by trying to analyze it all at once... Take it one piece at a time... How?

Back 148

1. Rate
2. Rythym
3. Axis
4. Hypertrophy
5. Infarction

Front 149

Why is the both the QRS phase (ventricular depolarization) an the T phase (ventricular repolarization) both on the positive side of the EKG? How is that possible?

Back 149

Positive charge in T phase is going in opposite direction.

Front 150

Why is it so important to document the strength (1-6) of the murmur you hear? How might you save a patient's life by properly documenting?

Back 150

With an artificial valve, you should hear a very loud, PROMINENT S1
a Muffled sound might indicate thromobosis--> could lead to stroke

Front 151

As Dr. Myers stressed, "Why is pre-loading (EDV) important before contraction? Why is CONTRACTIBILITY of hear not the same as FORCE OF CONTRACTION?

Back 151

? GOOD QUESTION

Front 152

What are mechanisms of local control of blood flow?

There are 3!

Back 152

1. Metabolic regulation

2. Autoregulation (myogenic regulation)

3.Shear stress induced vasodilation

(Neural and humoral mechanisms are mainly aimed at regulation of blood pressure and volume, but also affect flow in regional circulations in a non-uniform manner)

Front 153

How does myogenic regulation relate to the endothelium in the local control of circulation

Back 153

Myogenic Regulation is Endothelium-Independent! (stimulated by stretch/increase in transmural pressure)

Front 154

How does cardiac output relate to blood volume? What would happen during hypervolemia? Hypovolemia?

Back 154

CVP (Central Venous Pressure) and CO are indirectly related to each other!

In frank starling curve:
In Hypervolemia--> shift to right
In Hypovolemia--> shift to the left

*CO and CVP are inversely related when looking at vasular function, and DIRECTLY related when looking at CARDIAC function.

Front 155

What do the A waves, C waves and V waves on an atrial pressure curve represent? Which one might change if a patient had... a murmur? sudden venous return increase?

Back 155

A wave- rise in atrial pressure due to contraction

C wave- rise in atrial pressure due to bulging back of the mitral valve during ventricular contraction

V wave- rise in atrial pressure do to venous return

Front 156

When would the MYOGENIC reflex kick in?

Back 156

Auto regulation (endothelium independent)

Front 157

What are different receptor types we see at neuromuscular junctions in the sympathetic nervous system, and what do they do?

Back 157

The effect of different neurotransmitters at the neuro-effector junction depends on the type of receptor and subsequent transduction pathway of the cell or tissue type. Beta 1 Receptors are the main cardiac receptors for the sympathetic nervous system and they regulate inotropism (contractility) and chronotropism (HR). Beta 2 Receptors cause vasodilation, and Alpha 1 Receptors cause vasoconstriction. Don’t worry about memorizing other receptor types but understand that different tissues have different receptors and as a result, have different responses to the same neurotransmitters.

Also note that with strong sympathetic activity, the adrenal gland will release EPINEPHERINE, WHICH IS A BETTER AGONIST FOR BETA 2 RECEPTORS THAN NOR-epi

Front 158

What type of receptor do we see at the terminal end of a PARAsympatheic neuron?

Back 158

*remember* Ach is only relevant where parasympathetic nerve endings exist in the vasculature!!

Front 159

HOW DOES THE BODY RESPOND TO REDUCED BLOOD VOLUME?

Back 159

Front 160

VERY IMPORTANT! How do the different STRUCTURE of the vessel types relate to their FUNCTION in the body?

Back 160

The histological differences between various types of vessels reflect their functional roles. The thin wall of the capillaries, consisting of only an intimal layer, allows the efficient exchange of nutrients, waste, and dissolved gases between blood and tissues. On a relative basis, the muscular tunica media is more prominent in small arteries and arterioles than in large arteries or veins, reflecting their role in regulation of blood flow. Larger arteries have thick adventitia with significant elastic tissue, consistent with their role as "distributing vessels," whereas veins have more compliant adventitia. The tunica media of veins contains smooth muscle arranged both circularly and longitudinally, reflecting the function of veins as "capacitance vessels." Similarly, elastic tissue in the adventitia of veins is less prominent than in arteries.

Front 161

We used to think the endothelium didn't do anything, and now we come to find that there is a LOT THAT IS DOES. For example, it has a significant relationship with smooth muscle cells in the CV system. What functions does the smooth muscle have?

Back 161

Contractile function: relaxation and contraction of smooth muscle cells underlie changes in resistance and capacitance of vessels

Plasticity: Smooth muscle cells can undergo hypertrophy (increase in size), proliferate and undergo phenotypic changes in vascular disease and development

Secretory function: smooth muscle cells can assume a secretory phenotype in vascular disease, forming and releasing matrix, growth factors, and proteases

Front 162

What is the difference between vascular TONE and VASOMOTION?

Back 162

Vascular tone: Tone or state of contraction due to intrinsic factors (myogenic tone) and extrinsic factors (local, neurogenic and humoral factors)

Vasomotion: A change in caliber of a blood vessel

Front 163

Physiologically, what sorts of things occur in endothelium during a vascular injury? Why? How?

Back 163

VSMC contraction requires calcium elevation, from intracellular sources and from
extracellular Ca through voltage and ligand gated channels
When a constrictor such as NE binds to alpha 1 adrenoreceptors, activates PLC, IP3 raises intracellular Ca. Angiotensin, vasoopressin, etc. etc. ALSO ACH - take note.
ENDOTHELIN: in vascular injury.
Things that raise intracellular cAMP lower Ca - this is the opposite of cardiac - and
relax the vessel. Example is Prostacyclin, or beta adrenergic agents.
Things that act through Gs proteins and lower cAMP raise Ca and constrict: NE
through alpha 2, or NPY
Things that raise cGMP also lower Ca and relax

Front 164

How might increased heart rate affect the frank starling curve?

Back 164

A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis) (because the line curves upwards).
This can be seen most dramatically in the case of premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Because of the Frank–Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.
For example, during vasoconstriction the end diastolic volume (EDV) will decrease due to an increase in TPR (total peripheral resistance) (increased TPR causes a decrease in the stroke volume[citation needed] which means that more blood will be left in the ventricle upon contraction – an increased end systolic volume (ESV). ESV + normal venous return will increase the end diastolic volume). Increased EDV causes the stretching of the ventricular myocardial cells which in turn use more force when contracting. Cardiac output will then increase according to the Frank–Starling graph. (The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.) The S3, or third heart sound can be heard due to this increase in volume which can be pathognomic for heart failure.
By contrast, pericardial effusion would result in a shift along the line to the left, decreasing stroke volume.

Front 165

Why the hell are we learning about pre-loading/ pre stetching all over again?! Didn't we just learn this in MCP? Why is this important for CP? How would this affect the heart?

Back 165

As the heart fills with more blood than usual, the force of cardiac muscular contractions increases.This is a result of an increase in the load experienced by each muscle fiber due to the extra blood load entering the heart. The stretching of the muscle fibers augments cardiac muscle contraction by increasing the affinity of troponin C for calcium[citation needed], causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the End Diastolic Volume of the left and right ventricles.

Front 166

We have heard about Baroreceptors in every friggin class!! Why the fcuk are they so important for us to learn about?

Back 166

The arterial baroreceptor reflex is a key mechanism involved in autonomic regulation of cardiovascular function (see Fig. 11.2). The baroreceptors consist of specialized cells in the vascular wall of the carotid sinuses and aortic arch. Baroreceptors respond to the stretch associated with elevation of arterial pressure by increasing afferent impulses to the medullary cardiovascular center, where autonomic nervous system activity is regulated. In response to increased afferent input, sympathetic nerve activity is reduced, and parasympathetic outflow is increased. The effects of these autonomic responses on the heart and vessels result in a return of arterial blood pressure toward its original level

regulating heart rate is the Bainbridge reflex. When right atrial volume is increased, low-pressure stretch receptors (that is, receptors responding to stretch at the low pressures typical in the atria) initiate a neural reflex that increases heart rate through sympathetic nerves. Note that arterial baroreceptors respond to stretch by decreasing heart rate, whereas atrial baroreceptors respond to stretch by increasing heart rate. In the former case, the response is part of a mechanism to regulate arterial pressure, and in the latter case, the response is to increased blood volume. When atrial stretch results in increased HR, blood volume will be redistributed.

Front 167

What mechanisms in the body contribute to REGULATION OF HEART RATE in the body? How do they work?

Back 167

1. The autonomic nervous system and baroreceptors.
2. The Bainbridge reflex response to atrial stretch.
3. Effects of thoracic pressure changes during respiration on venous return.

Front 168

What does angiotensin II do and how can it help save your life when you are experiencing hemorrhagic shock?

Back 168

Angiotensin II is essential for recovery from hemorrhagic shock

Front 169

What do you predict would be the effects of circulating epinephrine on Arterial Blood Pressure and Cardiac Output (CO)? Which receptors/ nervous system would they affect?

Back 169

Front 170

WTF are vasoactive humoral regulators?

Back 170

Front 171

What are some of the BIG ASS DIFFERENCES between sympathetic nervous system and parasympathetic nervous system in their control of the hearts and vessels?

Back 171

The autonomic nervous system has efferent projections from the Medullary Cardiovascular Center to
both the heart and the blood vessels. The sympathetic nervous system stimulates the SA node to increase
heart rate (HR) and increases both the contractility and conduction velocity of the heart. This increases
the stroke volume (SV) leading to an increase in cardiac output (CO). It also causes vasoconstriction of
the small arteries and arterioles systemically (which is where most of the resistance (R) of the vasculature system is located) to maintain BP when necessary via a sympathetic vascular network.
Additionally, it causes vasoconstriction of the veins, which serves to mobilize blood resulting in greater preload to the heart and subsequently greater CO. THE SYMPATHETIC NERVOUS SYSTEM DOES NOT INNERVATE THE CAPILLARIES, THORACIC AORTA, OR THE ARTERIAL SYSTEM IN THE BRAIN. This system acts to maintain arterial
BP.

The PARASYMPATHETIC SYSTEM DOES NOT INNERVATE THE VENTRICULAR MUSCLES, BUT INSTEAD WORKS TO SLOW DOWN THE HEART AT THE SA NODE! *I repeat* parasympathetic system does NOT innervate the ventricular muscles--> it SLOWS the HR at the SA node!!! It has some limited innervation of the genital and lower GI tract vessels via the sacral parasympathetic nerves where it causes vasodilation. Acetylcholine works through the muscarinic receptor at the neuro-effector junction (vs. nicotinic receptors in the ganglia although Dr. Meyers said he wouldn’t test on this). Note that these two parts of the autonomic nervous system work reciprocally to maintain a normal BP. If the parasympathetic system has increased activity then the
sympathetic system will decrease its activity and vice versa.

Front 172

Stimulation of WHICH sub-division of the nervous system would cause penile TUMESCENCE?

Back 172

PARAsympathetic division gives you an erection. Tumesence = swelling. (PNS-> "points", but SNS--> "shoots")

Front 173

VERY IMPORTANT: Name some differences in the physiological pathways between the BARORECEPTORS and BAINBRIDGE RECEPTORS. Where do you find these kinds of receptors? What do they react to?

Back 173

Arterial Baroreceptors are found in the internal carotid sinus and the aortic arch. These are
specialized cells that respond to changes in arterial BP moment to moment. They function to maintain
homeostasis or constant BP. They send signals to the medullary cardiovascular center where
information is integrated. Efferents are then sent to the body to regulate HR, vascular tone, and BP.
These cells are sensitive to mean arterial pressure as well as changes in pressure, or pulse pressure.
They increase their firing rate as the pressure in the aorta rises. With a constant pressure (no pulse
pressure) they fire less. They are active over the range of 60 - 160 mm Hg. Above 160 mm Hg they are
maximally stimulated to increase parasympathetic output and decrease sympathetic output. Below 60
mm Hg they are not stimulated at all which causes a maximal sympathetic output and low
parasympathetic output. Note that in a pathological state of chronically high BP, this curve will shift to
the right in an effort maintain the new BP setpoint.
There are also baroreceptors that respond to lower pressures. These are called the cardiopulmonary
receptors or low pressure baroreceptors. They respond more to volume than pressure and are found
in the atria and the pulmonary system. As volume increases (or pressure), they send a signal to the
medullary cardiovascular system to enhance sympathetic outflow. The Bainbridge reflex is a subset of
this. As the right atrium is stretched the HR will increase in an effort to pump away the blood.
Increased sympathetic outflow from this baroreceptor reflex will increase the HR, increases urine output
from the kidney (to decrease blood volume), and inhibit the pituitary gland from secreting ADH again
increasing urine production. This is all coordinated by the medullary cardiovascular center.

Front 174

Which type of sensors would be involved when you can't breathe? How do they work? which branch of nervous system do they evoke?

Back 174

The diving reflex is a specialized mechanism for regulation of blood pressure and heart rate. This reflex is an adaptation for conservation of oxygen in diving mammals, allowing protracted stays underwater without breathing. During diving, the heart rate is slowed by increased vagal activity, while pressure is maintained by arterial vasoconstriction. Thus, blood flow to vital organs is maintained, while blood flow to much of the body besides the coronary and cerebral circulations is reduced; the work of the heart is also reduced. Although the diving reflex is weaker in humans, its effects can still be observed when the face is submerged in cold water and breath is held. Receptors in the face and nasal cavities are stimulated, and reflexive bradycardia and peripheral vasoconstriction occur. The diving reflex is thought to be responsible for the survival of some children after long periods of accidental submersion in cold water.

Front 175

Gradual tachycardia (during sinus arrythmia) is actually a pretty normal physiological process (ie. excercise), but sudden tachycardia may be pathological! For the three different types of tachyarrythmias [Paroxysmal, Flutter, and Fibrillation] what are their relative BPM ranges?

*mega Bonus* How can you tell the difference between the atrial and ventricular types on the EKG? WHICH TYPE HAS NO PATTERN AT ALL, and amplitude (voltage) goes down as people die....? What is the pretty looking 'TOURES DE POINTES'?

Back 175

150-250 BPM: Paroxysmal
250-350 BPM: Flutter
+350 : Fibrillation

Ventricular fib = NO PATTERN/ FUBAR


PVT= wide QRS (*fusion)

Atrial Flutter= "saw tooth"
Ventricular flutter= sine waves "toures de pointes"


Atrial fib= only irregular QRS
Ventricular fib= "bag of worms" TOTAL CHAOS/

Front 176

What does parasystole mean? How does parasytole contibute to pacemaker foci that are unable to be "overdrive suppressed?"

Back 176

?

Front 177

What is the definition of cardiac arrest?

Back 177

NO EFFECTIVE CARDIAC OUTPUT

Examples:
Ventricular fibrillation- no pumping action of the heart! (TOTAL CHAOS of multiple foci)

Pulseless Electrical Activity (PEA)- [weak ekg activity, but no mechanical activity]

Asystole (cardiac standstill)- flatlining on EKG

Front 178

Most patients experiencing ventricular tachycardia (VT) are usually elderly. WHY? What would cause the ventricular foci to become irritable?

What are the clinically distinguishable signs of this on an EKG?

Back 178

The patient with ventricular tachycardia is most likely ELDERLY and suffering from diminished coronary blood flow, reducing oxygen supply to ventricular foci.

* Signs of AV dissociation (eg. presence of fusion, or captures or extreme RAD (-90 to -180) are charateristics of VT

Front 179

What type of pathology might you see in a person that has:

1. a mid-systolic click with a late systolic (decrescendo) murmur

1. A wide QRS signal on an EKG= aka PREMATURE VENTRICULAR Contraction (PVC)

What might happening inside the heart that could explain both of these findings? (irritable ventricular foci and

Back 179

MITRAL VALVE PROLAPSE causes PVCs (including runs of VT and multifocal PVC), yet it is actually considered a benign condition. The valve is floppy and "billows" in to left atrium when

During ventricular systole, billowing valves pull on the chorade that tether them to the papillary muscle (in left ventricle). Might cause localized stretch and ischemia--> irriatating local foci

Front 180

Which part of the heart, when irritated, are usually related to wide QRS signals? What might cause this irritable focus signal to occur?

Back 180

An irritability Ventricular focus --> induced by:
1. low O2 [hypoxia]
2. low K+
3. Pathophysiology: Mitral Valve Prolapse, stretch, myocarditis

*lots of things can cause low O2 (airway obstruction, drowning/suffication, poor O2 in air, pulmonary embolisim or pneomothorax [reduced SA for O2], hypovolemia or shock [reduced CO], or poor coronary blood supply [MI]

Front 181

Why is the EKG totally out of order?

Back 181

3rd degree heart block.

heart blocks retard or prevent the conduction of depolarization; can happen in SA node, AV node, the His bundle, bundle branches, or in L / R subdivions of the bundle branches (hemiblock)

Front 182

While scanning an EKG, if you begin to suspect an infarction (necrosis, injury, ischemia). What three sorts of structures would you look for in the EKG?

Back 182

Front 183

Aneurisims (tears in vessel wall) are a serious emergency.

Capillaries have extremely thin walls (required to exchange nutrients). So how come capillaries don't explode all the time explode?

Back 183

Pressure is uniform through a capillary (intramural pressure- like in a ballon), but capillarity are able to keep their wall tension low by MAKING THEIR RADIUS as SMALL as possible. (T= Pr)

Aorta on the other hand, the aorta has a much larger radius, and instead use the thick elastic TUNICA MEDIA to help protect from rupturing--> but doesn't always work.. :(

CC: An aneurysm is a saclike enlargement in the wall of an artery, caused by weakening of the vessel wall. With bulging, wall stress is further increased, through increased radius of the vessel and decreased wall thickness, according to Laplace's equation (T = Ptr). Risk factors for aortic aneurysm include hypertension, smoking, obesity, atherosclerosis, and hypercholesterolemia. Rupture of an aortic aneurysm is a medical emergency involving profuse internal hemorrhage and is often fatal. Dissection of an aneurysm is defined as bleeding into the vascular wall through a tear in the inner layer of the vessel (media intima), a common complication in thoracic aortic aneurysms. Aneurysms are treated by replacement of the affected aortic segment by a synthetic graft, or by endovascular implantation of a graft in the area of the aneurysm.

Front 184

What are some of the ways MYOCARIAL ISCHEMIA (MI) is presented can present itself in a patient? How might you treat a patient that has this?

Back 184

Myocardial Ischemia
Myocardial ischemia is reduced blood flow to heart muscle, resulting in poor oxygenation. Angina, arrhythmias, myocardial infarction, and sudden death may result. In patients with coronary heart disease, buildup of atherosclerotic plaque in epicardial coronary arteries results in reduced perfusion of the affected vessels. Functionally, ischemia and infarction may result in reduced contractility of the heart, arrhythmias, electrocardiogram (EKG) changes, wall motion abnormalities, and even ventricular aneurysm. Myocardial infarction is one of the major causes of congestive heart failure. Severe cases of coronary occlusion are treated by angioplasty or coronary artery bypass graft surgery. In bypass surgery, a section of vessel, typically a piece of saphenous vein, is grafted to bypass the blockage. In angioplasty, a balloon catheter is employed to open the occluded artery. To reduce the occurrence of restenosis (reocclusion), a stent is often deployed.

Front 185

What is the order of normal conduction in the pathway of the heart? What happens when this gets fcuked up? What is it called?

Back 185

SA-> (atrial muscle) -> AV node-> His bundle-> bundle branches-> purkinje fibers-> (ventricular muscle)

When conduction is disrupted in this pathway, ARRYTHMIAS result. Atrioventricular block (heart block) is a group of cardiac arrhythmias associated with altered conduction through the AV node:

1--First-degree AV block is abnormally delayed conduction through the AV node (PR interval on the ECG exceeding 200 msec). Each P wave results in a QRS complex and thus ventricular contraction, as in normal sinus rhythm, but AV conduction is delayed. By itself, first-degree block does not produce bradycardia and is usually benign if not caused by underlying heart disease.
2--Second-degree AV block is characterized by intermittent conduction through the AV node. As a result, some P waves on the ECG are followed by a QRS complex, whereas others are not. Thus, the ventricles contract less frequently than the atria. Myocardial ischemia or infarction may produce second-degree block.
3-Third-degree AV block (complete block) occurs when the wave of depolarization is not conducted through the AV node (from atria to ventricles). On the ECG, both P-P intervals and R-R intervals are regular, but P waves are dissociated from the QRS complexes. When atrial pacemaker activity fails to be conducted to the ventricle, an escape pacemaker may arise in the AV node below the site of block or in the bundle of His, producing a ventricular rate of 40 to 55 beats per minute (as determined by the R-R interval) that is only partially responsive to sympathetic stimulation. When the conduction block occurs in the bundle of His, the ventricular escape rhythm will produce an inadequate heart rate of 20 to 40 beats per minute; cardiac output (flow rate from one ventricle) may be insufficient even at rest, and activity will be greatly restricted due to inability to adequately adjust output. The usual therapy is implantation of a cardiac pacemaker.

Front 186

What is the *MOST* important factors for controlling blood flow to the following speshul regions, and which areas DONT have influence of ANS. Why? :
1. Brain
2. Lungs
3. Heart
4. Skeletal muscle
5. Skin

Bonus* where is blood flow interrupted during systole? Which three areas have ANS influence? Which Definitely DO NOT? Which two are affected by hormones?

Back 186

Brain: local metabolic factors Blood flow must remain CONSTANT (critical organ in a hard shell= little space for large fluxes) Little ANS involvement
Lungs: Changes in O2 tension (increase O2, increased bf)
Coronary ARTERIES: local metabolic factors (little influence of ANS *for arteries, not HEART)
Skeletal Muscle: Major role of TPR, basal flow set by SNS. hormones and metabolites (excercise) increase bf

Front 187

What two special things need to occur in order for the left coronary artery to get proper blood flow? Why does this blood flow get interrupted during systole?

Back 187

1. Compression of the coronary circulation caused by contraction of myocardium.
2. Powerful METABOLIC VASODIALATION during diastole.

Front 188

Both the lungs (pulmonary) and systemic circulation have the same cardiac output, but the lungs have a BP of 25/10 and the systemic capillaries are 120/80. How the heck is this possible for them to still have the same CO/ blood flow?

Back 188

Pulmonary is low pressure, low resistance (very rich with big short vessels)

Systemic is high pressure, high resistance

Front 189

VERY IMPORTANT* why is the left side of the heart so much more affected by intramyocardial pressure than the right side of the heart? Which coronary artery (left or right) has highest blood flow during systole? Diastole? When does this change and why?

Back 189

Intramyocardial pressure greater on left side:
1. release of all wall pressures
2. build of metabolities like adenosine... (REACTIVE HYPEREMIA) causing greater VASODIALATION

Intramyocardial pressure in the L ventricle reaches nearly 150mg during contraction!! (HOLY MUTHERFCUKING SIHT!!)--> because blood is expected to go from low pressure (120) to high pressure (150) the subendocardium will not be perfused during contraction of the heart.!!!!!

Netters: The pumping action of the left ventricle generates the normal resting ARTERIAL pressure of 120/80 mm Hg to supply blood to the systemic circulation. In doing so, the myocardium of the left ventricle (particularly, the subendocardium) must generate an EXTRAVASCULAR TISSUE PRESSURE higher than left ventricles and arterial pressure. extravascular tissue pressure that is higher than left ventricular and arterial pressures. This intramyocardial pressure impedes left coronary flow during systole, when the net coronary perfusion pressure is arterial pressure minus the intramyocardial pressure. Thus, left coronary artery flow is low during systole (see Fig. 12.9). During isovolumetric contraction, there is a rapid decrease in flow because tissue pressure has exceeded arterial pressure. During the remainder of systole, the shape of the left coronary flow curve is similar to the aortic pressure curve, but remains low due to high intramyocardial pressure.
With the onset of isovolumetric relaxation, left coronary artery flow increases markedly due to two factors. During systole, when flow is low, metabolites (H+, CO2, K+, prostaglandins, lactic acid, adenosine, and others) accumulate, and O2 tension falls. These changes produce coronary vasodilation; adenosine is believed to be the major factor involved. The vasodilation, combined with the fall in intramyocardial pressure, results in the large increase in left coronary flow during diastole.
Flow through the right coronary artery is less affected by intramyocardial pressure, because tissue pressure in the right ventricle does not nearly reach that of the left ventricle, and does not exceed arterial pressure. Thus, the shape of the right coronary artery blood flow curve (see Fig. 12.9) resembles the aortic pressure curve, with the highest flow occurring during systole.

Front 190

How are we not completely and totally screwed when a Left anterior decending coronary artery is completely blocked?

Back 190

Front 191

**ARTERIAL blood flow in cerebrum REMAINS THE SAME OVER A WIDE RANGE OF MEAN ARTERIAL PRESSURES (MAP: 50-150) WHY IS STABLE/ CONSTANT blood flow so critical for the brain? How does it do this?

Back 191

brain space had hard shell, but is also a vital organ. too little blood- > pass out
too much blood can cause cerebral hemmoraging

MYOGENIC MECHANISIMS (autoregulation) are the most important reflex in maintaing constant bloodflow. (smooth muscle cells constricting in response to stretch-- epithelium INDEPENDENT!!)

Front 192

During reactive hyperemia of the heart, What is the most powerful metabolite in the heart?

Back 192

ADENOSINE

*overrides the vasocontrictors of the sympathetic nervous system! (autoregulation)

Front 193

Why is it important to keep diastolic pressure as high as possible in people with heart failure? Ionotropic drugs (increase preload/ contractibility) are a bad choice for heart failure patients since a delicate balance needs to be maintained between ____ and _____

Back 193

Diastolic pressure is the pressure that perfuses the left coronary artery!

issue*we want to keep the BLOOD FLOW (CO) HIGH, while keeping the WORK DONE BY HEART DOWN. aka we want heart pumping, but not compromising O2 balance.

Front 194

VERY VERY IMPORTANT!! When talking about the different things that affect stroke volume of the heart, why is CONTRACTILITY not synonymous with FORCE OF CONTRACTION?!?! Why aren't they the same thing?!

Back 194

contractility is not synonymous with force of contraction, because force of contraction is dependent on degree of initial stretch of the muscle fibers (preload).

Stroke volume depends on
1. preload
2. afterload
3. contractibility (inotropism)

Front 195

What is a fancy biophysics term for stretching of vessels??

Back 195

stretch= "sensing an elevation in transmural pressure"

Front 196

In cerebral circulation, blood flow is kept constant by epithelium-independent AUTOREGULATION! But, cerebral blood flow also can be under control of PCO2 concentrations. When two cases where this may happen?

Back 196

*if you are a nervous dork, and you are hyperventalating a lot (give him a paper bag)
* extreme exercise
--> pass out--> fall down--> more blood flow to head

Front 197

VERY VERY HIGH YIELD DO NOT F*CK THIS UP!!!: Even though myogenic (AUTO) regulation is most important for global cerebral blood circulation, ARTERIAL PCO2 levels, and metabolic regulation may participate in distribution of blood flow LOCALLY. THERE ARE TWO OTHER SIGNIFICANT REFLEXES HE MENTIONED that affected flow INDIRECTLY; What reflex is responsible for when people with recent head trauma also have high arterial blood pressure AND decreased HR at the same time (WTF!)? What about the reflex for "last ditch effort" to reverse ischemia?

Back 197

CUSHINGS REFLEX: recent head trauma patient--> increase in intracrandial pressure--> impede blood flow--> strong sympathetic outflow in response--> raise cerebral perfusion (also poss bradycardia as a result of baroreceptor response to BP increase)

CNS ISCHEMIA REFLEX: When [O2] dips below 50mmHg (ischemia) in vasomotor center in the medulla, strong sympathetic outflow acts on the heart and peripheral circulation to increase arterial blood pressure above the autoregulatory range for cerebral blood flow, thus increasing blood flow to the brain in a "last-ditch" effort to reverse the ischemia. tremendous sympathetic discharge--> peripheral vasoconstriction--> forces blood up to brain **REMEMBER NO SYMPATHETIC OUTFLOW TO BRAIN. Arteries unaffected, so peripheral blood rushes in.

Front 198

How many heartbeats can the lungs act as a blood resevoir for?

Back 198

two heartbeats *BONUS* it can also protect from small embolsisms

Good small blood filter. (dual circulation)

Front 199

In systemic circulation, as pressure increases, so will resistance (makes sense cause we don't want blood pooling)

but in pulmonary circulation, as pressure increases, resistance goes down. Why is that?

Back 199

*As pressure increases in the systemic circulation so will the resistance
*Reflexive vasoconstriction in systemic circulation maintains the flow rate by increasing R
*Pulmonary circulation will decrease R with increased P causing an increase in the flow rate
*Recruitment and Distension of pre-existing vessels under high P drops the R
*Critical Closing Pressure is P that must be overcome for recruitment and distension

Hint 199

In the systemic circulation as pressure increases so will resistance. This is due to myogenic
regulation, which will cause reflexive vasoconstriction with increased pressure to raise resistance. It is important to raise the resistance with increased pressure so that the flow rate does not skyrocket!

In the pulmonary circulation, increased pressure leads to decreased vascular resistance and
increased flow. This is due to recruitment and distension of pre-existing vessels in the pulmonary
circulation that did not previously have blood flowing through them. Therefore, there is a critical
opening pressure for the microvasculature in the lung that will allow for this recruitment and distension.
The critical closing pressure is the inverse of the critical opening pressure, and occurs when the
pressure from the pulmonary artery/ arteriole is not high enough to cause recruitment and distension of
additional vessels.

Front 200

The afferent nerve activity in the arterial barorecptors are greatest when MAP and pulse pressure are both high. WHY? How do baroreceptors work?

How might chronic hypertension affect the baroreceptors

Back 200

The high-pressure arterial baroreceptors of the aortic arch and carotid sinus and the associated baroreceptor reflexes are most important for moment-to-moment regulation of arterial pressure. During normal, quiet daily activities, an inverse relationship is usually observed between changes in blood pressure and heart rate, reflecting this role of the baroreceptor reflex in maintaining pressure: when pressure falls, heart rate rises; when pressures rises, heart rate falls. These fluctuations in heart rate reflect changes in sympathetic and parasympathetic outflow from the medullary cardiovascular centers, in response to the degree of baroreceptor stretch.
Efferent sympathetic nerve activity is inversely related to MAP between the range of 60 to 160 mm Hg in a normal individual (see Fig. 11.2). At pressures below 60 mm Hg, sympathetic nerve activity is maximal. In addition to MAP, baroreceptors are also sensitive to pulse pressure. If pulse pressure is dampened while MAP is held constant, afferent nerve impulses from the baroreceptors to the cardiovascular center will be less frequent, and sympathetic efferent activity and thus arterial blood pressure will be elevated.

Netters: "Resetting" of arterial baroreceptor sensitivity occurs when blood pressure is chronically elevated. In a healthy person with normal blood pressure, baroreceptors function to return arterial pressure to the normal level when pressure falls or rises. With chronic hypertension, a new set-point is established, whereby baroreceptor activity is aimed at maintaining the higher resting blood pressure. Although this change appears, on the surface, to be maladaptive, it allows adequate short-term regulation of blood pressure despite higher basal blood pressure.

Front 201

Would you see high or low resistance in a collapsed lung? Why?

Back 201

Collapse of the lung raises R by collapsing the extra-alveolar vessels
Over-inflation of the lung will raise R because alveoli will impinge on alveolar vessels

Front 202

How does gravity indirectly control pulmonary circulation? Would the top lung or bottom lung have HIGH hydrostatic pressure, and HIGH profusion?


hint: Why does zone 1 (the apex) have a higher alveolar pressure?

Back 202

it is best to think of the top of the lung as having low hydrostatic pressure with low perfusion and the bottom of the lung as having high hydrostatic pressure with high perfusion.

*Higher hydrostatic pressures below pulmonary artery entry point
*Reduced hydrostatic pressure above the pulmonary artery entry point
*More ventilation at the base of the lung than at the apex
*******Remember in the lung that increased P leads to increased V and increased Q
*******Apex of lung has lower V and lower Q than the base, but a higher V/Q ratio

Front 203

Unlike the systemic circulation, the pulmonary vessels constrict when they encounter
hypoxia. When would a little vasoconstriction of a pulmonary artery be a good thing for high altitudes? When does it become pathological? How does this help to maintain the proper ventilation/ perfusion (V/Q) ratio?

Back 203

When PAO2 is low, we get HYPOXIC VASOCONSTRICTION in that region of the lung. This is good because you won’t want to perfuse the lung in an area where there is poor ventilation.

With high altitude sickness, one
gets pulmonary edema due to the heightened pulmonary artery pressures. WOMP WOMP

Front 204

Fetal lungs have HIGH resistance and HIGH pressure, so we have the
Ductus venosus( shunts oxygenated blood directly to the IVC and heart)
Foramen ovale shunts oxygenated blood from the right atrium to the left atrium
Fetal lungs are high R and high P
Ductus arteriosus shunts blood from pulmonary artery to aorta
Oxygenated blood preferentially shunts through foramen ovale, deoxygenated goes to RV
Coronary and cerebral arteries get maximally oxygenated blood in fetus

Now... my question is... How do all these shitheads close?

Back 204

1. The arteries will constrict before the umbilical vein causing autotransfusion
of blood from the placenta to the baby’s central circulation.
2. Ductus venosus closes (not sure how)
3. Within seconds after the neonate is born, sympathetic stimulation will exert tremendous
pressure resulting in inspiration of the first breath.
4. reduced pulmonary resistance will reverse flow through the ductus arteriosus and as the oxygenated blood hits this, it will constrict.
5. foramen ovale closes because pressure changes occur in the heart. (With a shut
off of flow from the placenta and lower pulmonary artery pressures, the pressures in the right atrium and
right ventricle will substantially reduce (but will NOT be eliminated). Further, the pressure in the left
atrium rises because blood now returns to it from the lungs via the pulmonary veins.)
6. The closure of the foramen
ovale is a mechanical closure due to pressure differences between the atria. A true anatomical
closure takes a longer time and would explain why some people have a patent foramen ovale
(PFO) rather than a fossa ovalis.

Front 205

Which has more pulsitality , the aorta or pulmonary artery? Why?How could you look at a wigger's diagram and find this out?

Helpful hint:
Pulse Pressure = Systolic Pressure – Diastolic Pressure
Pulsatility = Pulse Pressure/ Systolic = (Systolic-Diastolic)/Systolic = 1 – Diastolic/ Systolic

Back 205

Pulsatility is lower in the aorta than in the pulmonary trunk/ arteries

The waveforms between the aorta and the pulmonary artery for the cardiac cycle diagram are
very similar but the pulmonary artery and right ventricle function at 1/6 less pressure. The pulmonary
artery functions at 25/10 whereas the aorta is 120/80. This translates to a lower pulsatility in the
aorta than in the pulmonary trunk. Pulsatility is pulse pressure divided by systolic pressure.
Therefore the aorta has a pulsatility of 33% whereas the pulmonary artery’s is 66%.

Front 206

What is the difference between the aveolar and extraaveolar vessels?

Back 206

Alveolar capillaries are thin vessels that surround the alveoli. Extra-alveolar vessels run
through the stromal tissue rather than around the alveoli. The alveolar vessels carry red blood cells
in close proximity to the alveoli and thus allow for diffusion of gases between the ventilated alveoli and
the capillary. Oxygenated red blood cells can then perfuse the body. Due to the thin walled nature of
the alveolar vessels, hyperinflation of the alveoli causes them to expand and cut off the vessels, therefore
the alveoli typically fill to an ideal volume (under physiologic conditions) to ensure ideal conditions for
ventilation, diffusion and perfusion.
As previously stated, alveolar vessels are affected by the pressure and volume of the alveoli. An
increase in pressure and volume expansion of the alveoli will impinge on the radius of the vessel.
Further, the most important factor for extra-alveolar vessels is the lung volume. As the lung overinflates
the extra-alveolar vessels can be pulled apart. Further, if the lung collapses, the extra-alveolar vessels will collapse with it.

Front 207

What medical condition can involve clotting that occurs in all the blood
vessels of the body in response
to major trauma, most often
infection? (The entire clotting
cascade in the body is activated,
after which tiny thrombi form
all over the body and exhaust
the body’s supply of clotting
factors. The patient is then
susceptible to bleeding. The consumption of platelets, fibrin, and clotting factors is referred to as
CONSUMPTIVE COAGULOTHERAPY.

Back 207

Front 208

What are the 4 major systems involved with hemostasis?

Back 208

1. the vascular system (blood vessels are the sites of injury),
2. platelets (they help prevent excessive bleeding by forming clots)
3. the coagulation cascade, and
4. the fibrinolytic system (the mechanism that stops clot formation and leads to clot degradation). The process
of hemostasis begins with vascular injury. The injured vessel then constricts to slow down the bleeding.

A weak clot forms during primary hemostasis, followed by a hard clot that completely stops the
bleeding during secondary hemostasis.

CC: There’s a rare condition in which an infant is deficient in Factor XIII and can’t clot
the umbilicus after the umbilical cord is cut. A clot forms, but it is weak and falls off easily because
there isn’t any Factor XIII to cross link it.

Front 209

What role do the blood vessels play in blood clotting interactions? Which part (tunica intima, media or adventitia plays the most important role? Why?)

Back 209

Media and adventitia:
-provide mechanical strength
-Enable blood vessels to constrict or dilate

Sub-endothelial basement membrane(intima):
-Adhesive proteins – collagen, elastin, von Willebrand factor
-These proteins provide binding sites for platelets and leucocytes

Front 210

What are the three groups of coagulation protiens (super simplified version)

Back 210

Contact proteins are activated immediately and
involved in the initial phase of the intrinsic pathway
Prothrombin proteins (factor 2) are very important in activating the coagulation cascade. They are Vitamin K dependent and can be lost after prolonged use of antibiotics – the antibiotics clear the normal bacteria in the gut that are needed for Vitamin K production.
The Fibrinogen group (factor 1) is activated by thrombin and plays a role in secondary
hemostasis.

Both pathways require initiation – subsequent activation of coagulation factors in a ‘domino effect’
Deficiency of any one factor-->
Coagulation CANNOT proceed at a normal rate

Front 211

Briefly describe Extrinsic, Intrinsic, and Common clotting pathway, and what the KEY PROTIEN INTERCONNECTIONS ARE THAT YOU SHOULD DEFINITELY KNOW!!!

Back 211

Activation of Factor X (10) by both intrinsic & extrinsic mechanisms:

Activated Factor X: prothrombin -> thrombin
Thrombin: fibrinogen-> fibrin monomers (weak clot)
XIIIa (13a): fibrin clot-> Cross-linked of fibrin clot (strong clot)

Front 212

Which key protiens help regulate clot formation?

Back 212

Front 213

How does the Firbrinolytic system work?

Back 213

Front 214

What are the three parts of VIRCHOW'S TRIAD: (major influences that predispose to thrombosis)?

Back 214

Virchow’s Triad: There are three major influences that predispose an individual to thrombosis:
1. injury to the endothelium
2. alterations in normal blood flow
3. alterations in blood coagulability. Endothelial injury is the major and most frequent influence. It’s the only influence that can
cause thrombosis on its own.

Abnormal blood flow can cause thrombosis through stasis
(more common in veins) or turbulence (more common in arteries) because they both disrupt normal laminar blood flow.

Hypercoagulability can be primary, in which the patient has a specific defect in a major anti-coagulant or fibrinolytic factor, or secondary, which is acquired. Secondary conditions include pregnancy, which slows venous flow, stasis, or lupus, in which the bloodstream is full of antiphospholipid
antibodies.
Clinical thrombosis occurs due to the interaction of several risk factors. Cancer is the #1 risk for
developing clots. Cancer patients often first present with strange clots because cancer cells activate the
coagulation system. Other risk factors include inactivity due to surgery or obesity and the hormonal
effects of pregnancy or oral contraceptives.

Front 215

What are some of the risk factors for thrombosis?

Back 215

Clinical thrombosis is produced by the interaction of several prothrombotic risk factors:
hereditary e.g. Protein S and C deficiency
acquired e.g. anti phospholipid antibodies
disease states e.g. malignancy
physical factors e.g. surgery, inactivity
hormonal effects e.g. pregnancy, oral contraceptives

Most patients (with DVT or a PE) usually have MORE THAN ONE risk factor