Anatomy Ch 20
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What cavity is the heart located in?
Where is the cavity located?
Where are the base & apex of the heart?
The heart is located in the pericardium, which is in the mediastynum, which is in the thoracic cavity.
- The base of the heart is its posterior surface.
- The apex is the inferior tip.
What layer of the heart is the pericardium?
What type of tissue is fibrous pericardium & serous pericardium?
What are the 2 layers of serous pericardium & thier locations?
What is the serous fluid & what is its purpose?
What is pericarditis? How is it treated?
What is pericardial temponade? How is it treated?
- The pericardium is the outer layer of the heart.
- The fibrous pericardium is made of dense irregular CT - it fuses with the great vessels
- The serous pericardium is made of simple squamous epithelium called "mesothelium" (produces serous fluid)
- The serous membrane has two layers:
- 1. Parietal layer - lines the cavity
- 2. viscerl layer - epicardium - on the hearts surface
- Serous fluid is between the two layers of serous membrane to reduce friction
Pericarditis is inflamaiton of the pericardium that is treated with drugs that reduce inflamation and pain such as ibuprofen or aspirin.
Pericardial temponade is a form of acute pericarditis where pericardial fluid builds up and compresses the heart - this is life threatening and can be treated by draining the excess fluid thorugh a needle passed into the pericardial cavity.
Name the 3 layers of the heart and their respective tissue types.
- 1. Epicardium - outer layer - the visceral pericardium - make of loose CT
- 2. myocardium - middle layer - make of cardiac muscle and is very thick
- 3. Endocardium - inner layer - made of epithelial tissue and merges with the endothelium of the great vessels
Draw a picture of the 4 chambers of the heart:
label the chanbers - include the 4 valves , names & number of cusps
label the great vessels that enter/ leave the chamber
Does the pulmonalry trunk carry oxygenated or deoxygenated blood?
The pulmonary trunk carries deoxygenated blood from the right ventrical to the lungs.
What is an auricle - how many are there? Where are they?
What part of the atria is smooth - anterior or posterior?
What's the difference between a pectinate muscle & trabeculae carnae?
Each atrium (R & L) has an auricle on the anterior surface- an auric is a wrinkled pouchlike structure or "ear" to increase atrial volume.
The posterior wall of the atruim is smooth and the anterior wall is rouch with muscular ridges called pectinate muscles. The penticate muscles increase the power of contraction without increasing the mass too much.
What is the structure on the outside of the heart that holds coronary blood vessels called?
Sulci are grooves that contain coronary blood vessels and a variable amount of fat.
Name the septa of the heart.
What is the framen ovale?
Where is it located? What's it called if it's open?
The interatrial septum divides the RA and LA. It contains the framen ovale which is a hole in the internal septum that is part of fetal circulation. During the fetal period the circulatory system bypasses the lungs. The foramen ovale closes soon after birth and leaves an oval depression called the fossa ovalis.
Where is the ductus arteriosus located? Why does it exist? What does it turn into as an adult?
- The ductus arteriosus is a temporary blood vessel that shunts the blood from the pulmonary trunk into the aorta - keep majority of blood from entering nonfunctional fetal lungs
- As an adult it exists as the ligamentum arteriosum which connects the arch of the aorta and pulmonary trunk.
How many pulmonary arteries are there? Where do they go?
How many pulmonary verins are there? Where do they go?
There are two pulmonary arteries that branch of the pulmonary trunk (which comes from the RV) and carry blood to the R and L lungs.
What is a valve cusp? The chordae tendinae? The papillary muscles?
Are the cordae tendinae located in the atria or ventricels or both? What's their purpose?
A valve cusp is a leaflet that forms part of the closed valve. Heart valves are made of denst CT covered by endocardium.
The chordae tendinae are cords that attach the valve cusps to the papillary muscles.
The papillary muscles contract when the ventricles contract - this tightens the cordae tendinae which keeps the valve cusps from swining back into the atria.
The cordae tendinae are locared in the R and L ventricels and are there to keep the valve cusps from swining back into the atria when the ventricels pump powerfully.
Why is LV myocardium thicker than RV myocardium?
The R and L ventricles pump at the same time but the myocardium of the LV is much thicher than the RV becuase the RV only pumps blood a short distance - the the lungs but the LV has to exert force to pump blood throughout the body.
What deternines the one way flow of blood?
What to valves do? What is valunlar " insuffiency" and "stenosis"?
When the papillary muscles contract what happens? - When in the cardiac cycle does this happen?
Which valves have chordae tendineae? Why?
The one way flow of blood is controlled by the valves - they only allow the blood to flow one direction.
The valves close as the heart pumps and keeps the blood from flowing back the way it came.
Insuffiency - the failure of a valve to close completely
Stenosis - a narrowing of a heart valve that restricts blood flow.
When the papillary muscles contract the chordae tendinae tighten which stops the valve cusps from being pushed open into the atrium. The papillary muscles contract as the ventricels contract to keep the pewerful pumping for the ventricales from pushing the valve cusps from prolapsing.
The tricuspid valve from the RA to RV and the mitral valce (or bicuspid valve) from the LA to LV have chordae temdineae and papillary muscles to keep the powerful pumping of the ventricles from causing the valves to prolapse.
Why are the semilunar valves called "semilunar"?
The semilunar vales are called such because they both have three crescent moon-shaped cusps. These are the pulmonary valve and the aortic valve.
Are there valves between the atria and the great vessels that enter them? Why or why not?
There are not valves between the atria and the great vessels that enter them (the venae cavae on R and pulmonary venins in L) becuase as the atrial muscles contract they complress and nearly collapse the venous entry point.
What is mitral valve prolapse?
What causes rheumatic heart disease? What is it?
What's rheumatic fever? Why is Rx of a strep throat important?
Mitral valve prolapse is a mitral insufficiency (the valve does not close completely). The mitral valse connects the LA and LV and in MVP there is a backflow of blood into the LA.
Rheumatic heart disease occurs after a streptococcal infection of the throat. The bacteria trigger an immune response in which the antibodies make to destroy the bacteria instead attack and damage the mitral and aoritc valves.
Name the beginning and send of the:
1. pulmonary circulation
2. systemic circulation
Do their legnths vary? Does one have greater resistance than the other? Does this have anything to do with which side of the heart works harder & why their myocardial layers very? Explain why.
All things being equal - does the LV have a greater chance of having an MI (myocardial infarction) than the RV? Why or why not?
The pulmonary circulation = right atrium - right ventricle - pulminary trunk - R & L pulminary arteries - R & L lungs - pulmonary veins - left atrium
The systemic circuation = Left atrum - left ventrical - aorta - systemic arteries - arterioles - systemic capillaries - systemic venule - systemic veins - right atrium
The systemic circuation is much longer than the pulmonary circulation and so has greater resistance. As a result the LV must pump much harder than the RV and so the myocaridal layer of the LV is much thicher than the RV. The LV does have a greater chance of having a MI (myocardial infarction - heart attack - death of tissue due to interrupted blood supply) becuase there is more tissue on the left side which has a greater blood demand.
What layer is a venous sinus missing?
What is the coronary sinus? What enters it (structure)?
What structure does it empty into?
Does it contain oxygenated or deoxygenated blood? Why?
The venous sinous has no smooth muscle to alter its diameter.
The coronary sinus carries deoxygenated blood from the myocardium to the coronary sulcus on the posterior surface of the heart. It empties into the right atrium.
Describe the coronary artery circulation - its names and locations.
What is anastomosis & why have humans evolved to have them?
What % of normal perfusion can the heart tolerate if it's at rest?
The coronary circulation is the path by which oxygenated blood gets to the tissue of the heart.
R & L coronary arteries branch off the ascending aorta
- 1. L coronary artery - passes inferior to L auricle and divides:
- a. LAD - left anterior descending artery - in anterieor interventricular sulcus - supples walls of both ventricles
- b. circumflex branch - coronary sulcus - supplies LA & LV
- 2. R coronary artery - supples RA then divides:
- a. posterior interventricular branch - posterior interventricular sulcus - supplies walls of both ventricles
- b. marginal branch - coronary sulcus - RV
Anastomosis are connections between two or more arteries that supply the same region - they provide alternative routes called colateral circuits for blood to reach a particular tissue or organ.
Heart muscle can survive in a resting person with as little as 10-15% of normal blood supply
Describe the coronary venous circulation - its names and locations.
Coronary venous circulation carries deoxygenated blood from the myocardium to the coronary veins to the coronary sinus to the RA
Blood comes into the coronary sinus from:
1. Great cardiac vein - anterieor interventricular sulcus - drains blood from LV, LV, LA
2. Middle cardiac vein - posterior interventricular sulcus - LV & RV
3. Small cardiac vein - coronary sulcus - RA & RV
4. Anterior cardiac veins - RV - open directly into the RA
What is MI?
Coronary artery thrombosis?
What is the disease that most commonly causes the above? Why do diabetics have an increase in the above? What is the treatment for each of the above? What's a stent?
MI = myocardial infaction - heart attach - death of tissue because of interrupted blood supply - treatment = thrombolytic (clot-dissolving) agants and heparin (anticoagulent), coronary angoplasty or coronary artery bypass grafting
Ischemia = inadequate perfusion - reduced blood flow to myocardium
Angina = severe pain that acompanies MI - tighness or squeezing of chest
Coronary artery thrombosis = clotting in the coronary artery.
Many of these problems are caused by atherosclerosis (Thickening of the walls of arteries or loss of elasticity)
A stent is metallic wire tube that is permanently placed in an artery to keep the artery patent (open)
Describe a cardiac muscle cell.
What are the 2 components of an intercalated disc?
What is the purpose of this structure?
Why is the heart aerbic?
How does this cardiac muscle repair itself? Can this lead to dysfunction after an MI?
- Cardiac muscle cell:
- -striated, short, thick, and branched
- -1 nucleus per cell
- - large, numerous mitochondria
- - no mitosis - scar tissue for repair
- - small SR (sarcoplasmic reticulum) -smaller calcium reserves
- -interconnected via intercalated discs
Intercalated discs are transverse thickenings of the sarcolemma that contain desmosomes (hold the fibers together) and gap junctions (allow action potentials to conduct from one muscel fiber to another)
The purpose of this structure is to keep the fibers from tearing apart while allowing communication so that the muscle fibers can contract as a single coordinated unit.
The heart is aerobic becuase cardiac muscle contains many mitochondria which need oxygen for the electron transport chain.
Cardiac muscle does not repair itself. It simply replaces damaged tissue with scar tissue. This can lead to problems after an MI when part of the tissue is no longer functioning.
What is your normal pacemaker? What type of cell is it- nervous or cardiac? or both?
Are all cardiac muscle cells the same?
How does the SA node conduct an action potential?
What does "autorhythmic" mean?
Would a heart removed from someone have an intrinsic rate - if it was alive? What rate?
Name the voltage gated channels and their functions in the SA node.
The normal pacemaker is the SA node - sinoatrial node - RA wall. The SA node is made of cardiac muscle cells - the heart does not need nervous stimulation to beat.
The SA node does not have a stable resting potential - they repeatedly depolarize to threshold spontaneously.
Autorhythmic means that the cells are self-excitable
A heart will continue to beat even after is has been removed from the body due to the autorhythmic cells - without any other simulus the autorhymic cells of the SA node will initiate an action potential every .6 seconds or 100 times per minute.
Action potenetial of cardiac muscle has 3 phases:
1. Depolarization - voltage gated fast Na+ channels open - cells fill with Na+ - rapid depolarization
2. Plateau - voltage-gated slow Ca2+ channles open - Ca2+ slowly enters and triggers sarcoplasmic reticulum to release more calcuim
3. Repolarization - voltage gated K+ channels open - outflow of K+ restores negative resing potential
Describe/ Name the sequence of conduction in the heart.
- 1. Sinoatrial node (in RA)
- 2. both atria contract
- 3. atrioventricular note (AV node in interatrial septum)
- 4. AV Bundle of His (in interventricular septumI
- 5. Right and left bundle branches (LBB/ RBB in interventricular septum)
- 6. Purkinje fibers (inserted in ventricular myocardium - travel upward)
- 7. both ventricles contact - apex to base
SA → atria contract → AV → HIS → LBB/RBB → Purkinje fibers → both ventticle contract
Correllate the electrical activity of the heart with pumping? Are R sided functions occuring at the same exact time as L sided functions? Why? What is the R sided heart failure vs L sised? What does each cause (physical signs)? Does the entire ventricle contract at once or is there a spread of contraction? Describe it.
The electrical activity of pumping is seen in the action potential and contraction of contractile fibers (the pumping cells).
R and L sides of the heart function at the same time and move the same volume of blood with each pump. Frank-Starling law of the heart.
If one side of the heart begins to fail (as in congestive heart failure) then it causes the two sides to push different amounts of blood which causes more problems:
If the L ventricle fails first then it cant pump out all the blood it receives from the lungs. Blood backs up in the lungs and causes pulmonary edema - fluid accumulation in the lungs that can cause suffocation
If the R ventricle fails first then the blood backs up on the systemic side which will cause the kidneys to increase blood volume - peripheral edema - most noticible in the feet and ankles.
Ventricle contraction starts in the apex and travels upward to the base of the heart.
What is an "ectopic" pacemaker? Where do they occur?
An ectopic pacemaker is an abnormal pacemaker location in the heart - an abnormal group of cells may generate actions potentials the override those generated by the SA or AV nodes. Where they are located is called the etopic focus.
What does tachycardia and bradycardia mean?
What is considered a normal HR? Normal PB?
Normal CO? Normal blood volume?
Tachycardia = abnormally fast heart beat > 100 beats/min
Bradycardia = abnormally slow heart beat < 60 beats/min
Normal HR = 75 beats/min
Normal BP =
- Normal CO = 5 L/ Min
- CO = SV (stroke volume) x HR (heart rate)
Normal blood volume = 5 L (adult man)
What is atrial fibrillation?
Why do you die from it?
What's worse - ventricular tachycardia or fibrillation? Why?
What is defibrillation?
Atrial fibrillation = rapid, irregular and uncoordinated atrial contractions
Ventriculary fibrillation = ventrical fibers are asynchronous and the ventricels quiver rather than contract in a coordinated way. Caused by inadequate blood flow to heart (corinary artery disease) or myocardial infarction
V-fib causes circulatory failure and death
VT - Ventricular tachycardia causes the ventricels to beat too fast (caused by heart disease or myocardial infarction) - can develop into V-fib and cause death.
Defibrillation (also called cardiversion) is givng a strong, brief, electrical current to the heart that can often stop the v-fib
What is the junctional rhythm?
What is a heart block?
What's a first, second, and third degreee block?
Junctional rhythem is a condition when the AV node becomes the pacemaker for the heart
Heart block -an arrhythmia that occurs when the electrical pathways between the atria and ventricles are blocked - slows transmission of nerve impulses
1st degree block - conduction through AV node slow causing the P-Q interval to be prolinged
2nd degree block - some of the action potential from the SA node are not conductred through the AV node - causes dropped beats becuase excititation doesnt always reach the ventricles - fewer QRS complexes than P waves
3rd degree block - no SA node action potential get through the AV node - autorhythmic fibers pace the atria and ventricles separately - ventricular contraction rate is < 40 beats/ min
Draw and label the eletrical activity curve of a cardia pumping cell.
Name the 3 phases and tell me what's occuring.
What's a voltage gated ion channel?
What are they in the heart?
- 1. Depolarization - Na+ rapid influx
- 2. Plateau - Ca2+ influx - slow
- 3. Repolarization - K+ influx
Voltage gated ion channel - channels that open in response to a change in membrane potental (voltage). In cardic muscle the voltage gated ion channels are on the contractile fibers (the "working" muscle fibers)
Why do increased intracellular calcium (Ca2+) levels increase contractile strength?
What's a calcium channel blocker? Why are they given?
Ca2+ flows into the cells when slow Ca2+ voltage gated ion channels open. As Ca2+ enters the cell it causes the sarcoplamic reticulum to excrete Ca2+ that it was storing - the increase in Ca2+ causes the muscle to contract - calcium binds to troponin allowing the actin and myocin filaments to slide past one another.
Calcium cannel blockers block the Ca2+ channels and slow down heart rate. They are used to treat high blood pressure, abnormal heart rhythems, angina (pain in the heart).
What class of organic molecules are broken down to synthesize ATP from ADP in the heart?
What is cre-phosphate? How does it work?
Is myoglobin similar to hemoglobin? How? Its purpose?
The heart uses mosty fatty acids (60%) and glucose (35%) to produce its ATP
Creatine phosphate stockpikes P when ATP is less in demand - Creatine phosphokinase - CPK - in the blood indicates MI because it only exists in the cells - if it is in the blood them cells have been damaged.
Myoglobin is a protein that stores oxygen in muscle tissue - it does not normally circulate in the blood and its presence in the blood can indicate muscle tissue damage.
What is an EKG & it's purpose?
What does it represent?
What info does it tell you about the heart?
Name the vaves & segments & intervals found on it.
Draw a picture and corellate the waves with atrial and ventricular contractions.
EKG = electrocardiogram - a recording of the electrical signals produced by the heart. These signals are the action potentials of the contractile fibers. The signals can be recorded at the surface of the body.
EKG records the beating of the heart and can be used to diagnose problems with the heart, such as: abnormal rates and thythms, abnormal heart size, heart muscle damage, and inadequate oxygen perfusion.
- 1. P wave - atrial depolarization (atrial contraction)
- 2. QRS complex - ventricualar depolarization (rapid) & contraction of ventricels occurs shortly after the R wave
- 3. T wave - ventricualar repolarization - slower
What's the cardiac cycle? How many beats does it occur in?
What does systole mean? Diastole?
Is there atrial as well as ventricular systole & diastole?
Why does the R side of the heart pump at the same time as the L side?
Describe what the valves are doing in atrial systole, atrial diastole, ventricular systole, ventricular diastole.
What is arial kick?
How many ccs?
Is it present in Afib?
What are the consequences?
What is end - diastolic volume?
- The cardiac cycle represents the evens during 1 heart beat. It consists of periods of atrial and ventrical systole (contractions) and diastole (relaxation).
- Systole = contraciton
- Diastole = relaxation
- The L and R atria contract at the same time and then the L and R ventricles contract at the same time - blood always flows from high pressure to low pressure
- Atrial systole = atria contract, ventricles relax - atrial contraction forces blood throgh open AV valves into ventricels. Atrial kick = blood pushed into ventricels is about 25 cc - added to the 105 cc already there
Atrial diastole = atria relax, ventricles contract - AV valves forced closed by ventricel systole
Ventrical systole = ventricles contract - atria relax - AV valves forced closed by ventrical contraction - short period where all 4 valves are closed - then SL valves open and the ventricles eject 70 cc of blood
Ventrical diastole = ventricels relax - backflow of blood causes the SL valves to close - after a short period the AV valves open and ventricular filling begins.
Atrial kick is not present in A-fib and as a result stagnant blood in the atria can clot and cause a stroke.
End-diastolic volume - EDV- the volume of blood each ventricle at the end of diastole - about 130 cc (105 in vent + 25 from atrial kick)
End-systolic volume - ESV - volume of blood remaining in ventricel at the end of systole ( about 60 cc)
- Stroke volume - the volume ejected from each ventricle per beat
- EDV- ESV = SV
- 130 - 60 = 70 cc
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