Cardiovascular 17, 18, 19 Flashcards

Question

events of hemostasis

Answer 1

1. vascular spasm- smooth muscle contracts, causing vasoconstriction 2. platelet plug formation- injury to lining of vessel exposes collagen fibers; platelets adhere platelets release chemicals that make nearby platelets sticky; platelet plug forms 3. coagulation- fibrin forms a mesh that traps red blood cells and platelets, forming the clot

Answer 2

1. blood returning to the heart fills atria, pressing against the AV valves. the increased pressure forces AV valves open 2. as ventricle fills, AV valve flaps hang limply into ventricles 3. atria contract, forcing additional blood into ventricles

Answer 3

1. ventricles contract, forcing blood against AV valve cusps 2. AV valves close 3. papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria

Answer 4

as ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves, forcing them open

Answer 5

as ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close

Answer 6

This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line

Answer 7

The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels.

Answer 8

is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage.

Answer 9

1. The sinoatrial (SA) node (pacemaker) generates impulses 2. The impulses pause (0.1 s) at the atrioventricular (AV) node. 3. The atrioventricular (AV) bundle connects the atria to the ventricles 4. The bundle branches conduct the impulses through the interventricular septum 5. The subendocardial conducting network depolarizes the contractile cells of both ventricles

Answer 10

1. Atrial depolarization, initiated by the SA node, causes the P wave 2. With atrial depolarization complete, the impulse is delayed at the AV node 3. Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs 4. Ventricular depolarization is complete 5. Ventricular repolarization begins at apex, causing the T wave 6. Ventricular repolarization is complete.

Answer 11

sounds heard in 2nd intercostal space at right sternal margin

Answer 12

sounds heard in 2nd intercostal space at left sternal margin

Answer 13

sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle

Answer 14

sounds typically heard in right sternal margin of 5th intercostal space

Answer 15

* Endothelium * Internal elastic membrane * Subendothelial layer

Answer 16

* External elastic membrane

Answer 17

* Vasa vasorum

Answer 18

Continuous capillaries are the least permeable and most common. * Abundant in skin, muscles, lungs, and CNS. * Often have associated pericytes. * Pinocytotic vesicles ferry fluid across the endothelial cell. * Brain capillary endothelial cells lack intercellular clefts and have tight junctions around their entire perimeter. (This is the structural basis of the blood brain barrier described in Chapter 12.

Answer 19

Fenestrated capillaries have large fenestrations (pores) that increase permeability. * Occur in areas of active filtration (e.g., kidney) or absorption (e.g., small intestine), and areas of endocrine hormone secretion. * Fenestrations are Swiss cheese–like holes that tunnel through endothelial cells. * Fenestrations are usually covered by a very thin diaphragm made of extracellular glycoproteins. This diaphragm has little effect on solute and fluid movement. * In some digestive tract organs, the number of fenestrations in capillaries increases during active absorption of nutrients.

Answer 20

Sinusoid capillaries are the most permeable and occur in limited locations. * Occur in liver, bone marrow, spleen, and adrenal medulla. * Have large intercellular clefts as well as fenestrations; few tight junctions. * Have incomplete basement membranes. * Are irregularly shaped and have larger lumens than other capillaries. * Allow large molecules and even cells to pass across their walls. * Blood flows slowly through their tortuous channels. * Macrophages may extend processes through the clefts to catch “prey” or, in liver, form part of the sinusoid wall.

Answer 21

- systemic veins and venules 60% - systemic arteries and arterioles 15% - pulmonary blood vessels 12% - heart 8% - capillaries 5%

Answer 22

1. Stimulus: Blood pressure (arterial blood pressure rises above normal range). 2. Baroreceptors in carotid sinuses and aortic arch are stimulated. 3. Increase Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center LOOK AT POWER POINT pg 25 ch.19

Answer 23

1. Diffusion through membrane (lipid-soluble substances) 2. Movement through intercellular clefts (water-soluble substances) 3. Movement through fenestrations (water-soluble substances) 4. Transport via vesicles or caveolae (large substances)

Answer 24

input = pulmonary artery coming off of right heart output = pulmonary veins (there are 4) going into the left heart

Answer 25

- right heart chamber is low pressure deoxygenated blood coming from systemic circulation - left heart chamber is high pressure oxygenated blood coming from pulmonary circulation

Answer 26

- going to be the output for the pulmonary circulation and it is going to be delivered to the systemic circulation from the heart itself - going from the right low-pressure heart delivering deoxygenated blood through the pulmonary artery to the pulmonary circulation - going up the pulmonary artery bifurcating delivering a pulmonary trunk to the right and left lung - enter the lung through the hilum - eventually break down into smaller vessels until it becomes capillaries - those capillaries are going to be very intimately associated with the squamous epithelium of the alveoli - the blood will be delivered there and there will be a left shift in the hemoglobin dissociation curve where there is an increased affinity for oxygen hemoglobin allows for oxygenation - for tissue metabolites like carbon dioxide, lactic acid, decrease in pH, acidic environment, low concentration of oxygen, these are factors that are going to right shift the oxygen dissociation curve of hemoglobin allow for a decreased affinity at hemoglobin for oxygen - tissues will have a relative increase affinity for oxygen where they need it

Answer 27

- at the hemoglobin level at the pulmonary circulation you can see how in the lungs in an environment that is very rich in oxygen we have a left shift and an increased affinity for oxygen because we are trying to oxygenate hemoglobin - when we get to the tissue metabolics are going to affect the tertiary structures and the configuration of hemoglobin itself in such a way that oxygen will dissociate from hemoglobin and go to the tissues because we will right shift the dissociation curve and we will favor oxygen leaving hemoglobin and going to the tissues and we call that a decreased affinity of hemoglobin for oxygen

Answer 28

binding of oxygen itself will allosterically modify the hemoglobin - that means that whenever an oxygen molecule binds one of the sites on hemoglobin (there are four oxygen binding sites) the other three become allosterically modified to increase their affinity for oxygen - so when one oxygen binds the next oxygen site will actually increase its affinity and will be more likely to bind another oxygen molecule - and when a second oxygen molecule binds there the third hemoglobin will be modified in such a way allosterically that allows it have an increased affinity and more chance of binding an oxygen - the last one will have the absolute easiest chance of binding to hemoglobin

Answer 29

- carbon monoxide has sixteen hundred times the affinity for hemoglobin that oxygen has - hemoglobin will prefer to bind to carbon monoxide relative to oxygen because carbon monoxide has such a high affinity for oxygen that will outcompete it whenever it is present in the alveoli and thats because we are breathing it in - the same allosteric modification is happening - one carbon monoxide molecule binds and it will increase hemoglobin affinity for binding "oxygen" but in reality it is actually binding more carbon monoxide that is present in the alveoli because that carbon monoxide is outcompeting the oxygen - what is basically happening is that you are consuming all of your hemoglobin stores by binding them to carbon monoxide that has increased affinity for hemoglobin and it is also increasing its affinity more every time it binds - telltale sign of carbon monoxide poisoning is cherry bright red coloration of the skin, color of the hemoglobin itself in the circulatory system and all occupied by carbon monoxide giving off the color because it is very well bound a lot of binding - intervene medically by introducing the patient to hyperbaric oxygen chamber in order to favor oxygen binding to hemoglobin and kick carbon monoxide out

Answer 30

- pulmonary artery coming off the right heart and supplying the lungs capillary beds with deoxygenated blood - so we have pulmonary artery coming from the right heart, deoxygenated blood to the pulmonary capillaries that are intimate with the alveoli - oxygenate the blood at the lung - those capillaries become the output, which is going to be the pulmonary veins - pulmonary veins will eventually condense into four pulmonary veins and become bound to the left atrium of the heart - left atrium will be the left heart chamber

Answer 31

- start with pulmonary veins - oxygenated blood coming from the lungs into four pulmonary veins - pulmonary veins are going to feed into the left atrium - left atrium is going to hold oxygenated blood, opening there with the mitral valve - mitral valve is going to separate the left atrium from the left ventricle - so then oxygenated blood will pass from the atrium to the left ventricle through the mitral valve - on the other side of the heart we have the tricuspid valve - those are both going to be the atrioventricular valves, the AV valves - they are going to seperate the respective chambers, the respective atria from the respective ventricles - and so on the left heart, we pass from left atrium to the left ventricle through the AV valve, that is the mitral valve on the left - when the mitral valve closes, that is going to be S1 (first heart sound) - that is the first heart sound in the lub-dub sounds of the heart, closure of the valves that give the heart sounds, not the opening - so the first, lub in the lub-dub is going to be the closures of the AV valves, the atrioventricular valves, which are tricuspid and mitral - on the left we have the mitral valve - isovolumetric contraction at the heart - then systole, open the aortic valve - pump blood into the aorta - going to go to the systemic circulation, thats systole - then go up the aorta - aortic valve close right before diastole, when the aortic and pulmonic valve close - those are semilunar valves (three cusps while AV=two) - second heart sound (S2) is going to be the closure of the semi-lunar valves (aortic and pulmonic) - through the aortic valve, from the left ventricle, through the aortic valve into the aorta and out to the systemic circulation - aorta is going to break off into elastic arteries and muscular arteries, arterioles - down to capillaries, it's going to oxygenate at the capillaries various organs - venules to valve veins to larger veins - upper extremity, upper appendicular areas, feed into subclavians, then merge into the superior vena cava, coming up from lower extremity there are femoral veins etc - end up becoming the inferior vena cava and feeding up to the heart - deoxygenated blood is going to travel in the systemic veins - systemic veins feed deoxygenated blood through the inferior vena cava for the lower extremity and the superior vena cava from the upper extremity - those are both going to feed in both vena cavae going to feed into the right atrium - which is going to be in the right heart chamber, the low pressure deoxygenated chamber - the right atrium will accept blood from superior and inferior vena cavae and pool into the right atrium - right atrium accepts the oxygenated blood - blood is going to pass through the tricuspid into the right atrium - tricuspid valve closes again, S1 (mitral and tricuspid valve close at the same time) - pass through the tricuspid and to the right ventricle, low pressure ventricle - then during systole, we are going to have isovolumetric contraction and during systole pulmonic valve open - pump blood through the pulmonic valve, which is the semi-lunar valve, into the pulmonary artery - going to do that through the pulmonic valve and then the pulmonary artery and the aorta are both going to close - its going to be S2, closure of those of the semi-lunar valves, which is the dub in the lub-dub cycle - lub closing of the atrioventricular valves and those are the AV valves - they close thats lun and the semi-lunar valves close after systole ends and thats going to be the dub and they are S1 and S2 respectively - aorta is delivering oxygenated blood to the systemic circulation and the pulmonic artery, which is the site of the pulmonic valve, is going to deliver deoxygenated blood to the lungs to be oxygenated and returned to the heart through the pulmonary veins at the left atrium to repeat the cycle

Answer 32

- site where atrial-natriuretic peptide is going to be synthesized by the myocytes, those are detecting stretch in the heart - so as the heart is filling through the two vena cavae, the inferior and superior, as it fills the heart, they are going to detect stretch and synthesize that - site where we have the SA node, sinoatrial node (natural pacemaker of the heart) - nearby is the AV node, atrial ventricular node - the site that regulates the impulse from the SA node, natural pacemaker of the heart - tachycardia, bradycardia, vagus nerve relevant in this region

Answer 33

- right ventricle, low pressure ventricle, faces thoracic wall (sternum), - note a penetrating injury to the chest is going to go through the right ventricle, which is a low pressure chamber; we would rather stab through that than a high pressure chamber like the left ventricle - left atrium faces the esophagus

Answer 34

- heart is turned on its side and faces to the left - left heart chambers face inward into the inferior mediastinum toward the left side - left atrium is going to point towards the esophagus - left ventricle is going to be kinda hidden inward, pointed to the left - facing the outside, facing the sternum, is the right ventricle and the right atrium - heart is kind of twisted off to the left and turned so that the left side of the heart is facing deeper - right ventricle and the right side of the heart is more superficial

Answer 35

- we feel apical pulse at the left fifth intercostal at the midclavicular line - and that's where we hear the mitral valve is because the heart tends to face its left - better access to the left ventricle because of that twist

Answer 36

- pulmonary artery carries deoxygenated blood - pulmonary veins carry oxygenated blood

Answer 37

- bronchial arteries that supply the lung carry oxygenated blood to the lungs - bronchial veins carry deoxygenated blood from the lungs

Answer 38

- bronchial arteries and veins have the traditional systemic sort of pattern of carrying certain types of blood

Answer 39

- heart is superior to the diaphragm and turned left - apex will be the pointed end of the heart, more superficial and to the left - base of the heart will be basically where the vessels are attached, the pulmonary artery and the aorta - apex beat can be measured or palpated at the fifth intercostal at the midclavicular line

Answer 40

- fibrous pericardium (most superficial/surface), parietal layer of the serous pericardium, the pericardial cavity (a potential space), true heart layers - epicardium (the visceral layer of the serous pericardium), myocardium, endocardium, then inside of the heart chamber - fibrous pericardium, the pericardial cavity, and the parietal layer of the serous pericardium all sort of mimic the tunica adventitia in the blood vessels - epicardium mimics the tunica externa - myocardium is like the tunica media of the heart - endocardium is like the tunica intima for the blood vessels - heart does have an abundance of elastic fibers

Answer 41

- pulmonary trunk leaves the right ventricle and twists left - aorta leaves the left ventricle and twist right and then go superior to the pulmonary trunk and then dive downward and become the descending aorta - right ventricle is giving off the pulmonary artery carrying deoxygenated blood and the left ventricle is giving off the aorta - the second right intercostal that we actually hear the aortic valve best at when we auscultate it - we can auscultate the pulmonic valve best at the second left intercostal - auscultate the pulmonary artery at the left second intercostal - auscultate the aorta at the right second intercostal

Answer 42

- right ventricle gives off the pulmonary artery and the pulmonary artery twists to the left - left ventricle gives off the aorta which twists to the right becomes the ascending aorta - its going to give off three branches there and then its going to become the descending aorta and then dive down to supply the rest of the body - its going to be up to those three branches that it gives off, the brachiocephalic trunk, the left common carotid artery, and the left subclavian artery to supply the upper extremity while the descending aorta supplies the lower extremity

Answer 43

- first branches off the aorta are the left and right coronary arteries, specially at the coronary ostia, which are basically the vestibules or the entry points into the coronary arteries - so what are the first branches off the aorta? ans: they are the coronary arteries and then the third, fourth, and fifth branches off the aorta are the brachiocephalic trunk, the left common carotid artery and the left subclavian artery - brachiocephalic trunk will become the right subclavian artery and the right common carotid - left common carotid artery is coming exactly right off the aorta as the fourth branch - left subclavian artery is coming right off the aorta as the fifth branch - remaining aorta will be descending aorta, which twists, which return back to the left, then becomes descending aorta

Answer 44

- emerges from the left ventricle , then it goes and twists to the right, goes superior to the pulmonary artery, where at the bifurcation point of the pulmonary artery goes superior to that, gives off three branches and then goes to the left and descends and becomes the descending aorta - ascending aorta is oriented to the right - descending aorta is oriented to the left - branches of the aorta, two coronary arteries, the main stem coronary arteries, so they start as the left and right main stem coronary arteries - then become the ascending aorta on the right side - go superior to the pulmonary artery at the pulmonary arteries bifurcation point - give off the brachiocephalic trunk and that will become the right subclavian artery and the right common carotid and the right common carotid and then the left common carotid and the left subclavian come directly off the aorta - left common carotid and the left subclavian are coming directly off the ascending aorta - on the right side, we have to go through thus intermediate step where we start off as the brachiocephalic trunk and then bifurcates into the right subclavian and the right common carotid

Answer 45

- ligamentum arteriosum connects the aorta to the pulmonary artery - that was originally the ductus arteriosus in fetal circulation - ductus arteriosus is a vessel, providing communication between the aorta and the pulmonary artery because in fetal circulation it is irrelevant to oxygenate the blood in the lungs - the mother actually oxygenates the blood for the fetus - fetal hemoglobin steals oxygen away from the mother's hemoglobin A, adult hemoglobin - so the fetal hemoglobin has an increased affinity for oxygen, an affinity that can outcompete the mother's hemoglobin's affinity for oxygen - it has a higher affinity, stealing the oxygen from the mother's hemoglobin F

Answer 46

- hydroxyurea and sickle cell disease basically allows adults to resynthesize the hemoglobin F from their heterochromatin - so it reactivates the heterochromatin for the hemoglobin F and it makes it U-chromatin and allow them to resytheize hemoglobin F - which in a way is a way of keeping sickle cell disease at bay by synthesizing a new hemoglobin that has a high affinity for oxygen and is not prone to sickling the way hemoglobin S, the sickle cell anemia will, sickle cell anemia hemoglobin will

Answer 47

- fetuses have hemoglobin F and they have a patent or an open ductus arteriosus, which is the connection between the aorta and the pulmonary artery - in fetal circulation, that connection is basically allowing the aorta to shunt blood away from the pulmonary artery because its senseless to supply the lungs with any blood at all - because the lungs are not, the fetal lungs are not going to be responsible for oxygenating it - the fetus is not breathing inside the uterus or mother's womb - it is relying on the umbilical cord and the umbilical vessels ti supply the maternal blood that is oxygenated from the mother to the fetus in order for the fetus to survive

Answer 48

- basically shunting blood in the fetal circulation away from the pulmonary artery and favoring the aorta in that situation - we don't wanna to waste the blood in fetal circulation on the pulmonary artery because it going to the lungs that are not being used - so while we have the fetus and while we have the neonate as soon as its born, that ligamentum arteriosum is actually a ductus arteriosum (patent or open ductus arteriosum) - once baby born, patent arteriosus becomes ligamentum arteriosum - the pressure inside aorta and the pressures inside the pulmonary artery are going to overwhelm it and going to involute and degrade and eventually become a collagen connection between the aorta and the pulmonary artery - its basically a ligament of collagen there thats a remnant of the ductus arteriosus

Answer 49

- transportation of the great vessels in which you give prostaglandins to keep the patent ductus arteriosus open - prostaglandins for PDA and that's for transportation of the great vessels - a pathology un which diabetic mothers are prone to their diabetic state, hindering the heart's ability to rotate its vessels on a proper axis and that malrotation of the heart vasculature at the base of the heart will lead to transportation of the great vessels - it has the ductus arteriosus left over from its time as a fetus - if we give prostaglandins we are able to encourage the patency of the ductus arteriosus and that will allow the shunting of blood to continue so that we can overcome the fact that you are not oxygenating the body

Answer 50

- they are the first branches off the aorta so it is relevant to note that there is a left and right common main stem coronary - right main stem coronary gives off several branches - theres an oracle for the left atrium and an oracle for the right atrium and how the way that they guard those coronaries from trauma - right coronary going down and give off the right marginal artery, supply the lateral wall of the right ventricle - thats the right coronary artery and then its giving off the right marginal artery and then going to the backside of the heart - its going to supply the heart posteriorly and supply part of the septum of the heart and most importantly the AV node, the atrium ventricular node - majority of population is right coronary circulation dominant - left main stem coronary is hidden by oracle but coming off the aorta - its goin basically between the pulmonary artery and the oracle and then its emerging

Answer 51

- first branch off the left main stem coronary is going to the left anterior descending artery which is the widowmaker - it supplies the largest surface area of the heart, two thirds of the surface area of the anterior that is very relevant - it also supplies the interventricular septum, this houses the purkinje fiber network that is going to be conducting the electrical activity of the heart from the SA and AV nodes respectively - that purkinje system is very relevant to the heart depolarizing in a synchronous fashion and we know that the interventricular septum separates the high pressure left ventricle from the low pressure right ventricle - having those myocytes disrupted and weakened and replaced by scar tissue and a myocardial infarction there is very common at the left anterior descending artery - part of the septum is supplied by the right coronary artery

Answer 52

- at the left coronary twists and it becomes traveling in this left coronary sulcus of course near the oracle, it twists and becomes the circumflex artery - it supplies the lateral wall of the left ventricle so it can be considered when it infarcts there to be a lateral wall infarction - left coronary does twist after giving off the LAD branch, it twist into circumflex and dives and goes posterior supplying the posterior heart - see anastomose and form this compensatory or alternate circulation where there isn't an anastomosis with the right coronary artery - depending on whether theres a blockage in one or the other, we can salvage as much myocardium as possible and save as much of it from ischemia as possible through the anastomosis

Answer 53

- right coronary artery is giving off a branch on the posterior heart called the posterior interventricular artery - that is the artery that supplies one third of the interventricular septum - the anterior two thirds of the interventricular septum were supplied by the left LAD, left anterior descending artery - posterior interventricular artery coming off the right coronary artery on the posterior heart supplying the posterior on third - included in the one third will be the atrioventricular node, the AV node

Answer 54

- left coronary artery, after it became the circumflex, continued on its way and eventually it will anastomose - the coronary sinus and the middle cardiac veins and the great cardiac vein - the great cardiac vein becomes the coronary sinus and the middle cardiac vein feeds into that coronary sinus

Answer 55

- inferior and superior vena cava and the way that the four pulmonary veins are feeding into the left atrium and that the vena cava are feeding into the right atrium - how intimate those vessels are at the base of the heart - bifurcation point superior to the pulmonary veins as they insert into the left atrium - we can see the bifurcation point of the pulmonary artery and superior to that the ascending aorta itself, which is now beginning to become the descending aorta after giving off its third, fourth, and fifth branches - its becoming the descending aorta and twisting back to the left again before it descends into the abdominal cavity - the third branch off of it is the brachiocephalic trunk which bifurcates - left common carotid is the fourth and the fifth is left subclavian artery

Answer 56

- right main stem coronary giving off the right marginal artery, twisting, going posterior to the heart - giving off the posterior interventricular artery, which will supply the one third of the interventricular septum and the AV node - left coronary artery, which is the left main stem - its giving off the left anterior descending artery, the LAD, the widowmaker - then its becoming the left circumflex artery supplying that left lateral wall of the left ventricle, which is a more relevant lateral wall because the left ventricle is a high pressure chamber - after becoming a circumflex artery, its twisting, going posterior and anastomosis with the right coronary artery after the right coronary artery has been extended - that has given off the posterior interventricular artery branch

Answer 57

- left pulmonary veins feeding into right atrium - mitral valve = bicuspid valve - mitral/bicuspid is one of the AV valves - enter that the left atrium through the pulmonary veins, four of them - cross the mitral valve into the left ventricle - chordae tendineae are tethered to papillary muscles that are maintaining that mitral valve - then exit the left atrium through the aorta, through the aortic valve into the aorta - aortic valve is a semilunar valve

Answer 58

- aorta and the pulmonic valves are semi lunar valves - enter the aorta through them - right atrium with the superior and inferior vena cava entering there - right atrium fill up with deoxygenated blood, which will follow into the right ventricle through the tricuspid valve, which is also maintained by the chordae tendineae that are tethered to papillary muscles - exit the right ventricle through the pulmonic valve, the other semilunar valve into the pulmonary and bifurcate to each lung

Answer 59

- lub dub cycle that corresponds to S1 and S2 - S1 is the closer of the AV valves, the atrioventricular valves, the bicuspid and the tricuspid or the mitral and the tricuspid - S2 or dub sound is going to be the closure of the semilunar valves, the aortic and pulmonic - all sets close at the same time, which is what we hear

Answer 60

- situation of afterload in the heart and that is felt at the aorta, the collective resistance that the heart must overcome in order to pump blood to the systemic circulation - afterload is the collective peripheral resistance, the amount of pressure required - hypertension will contribute to the afterload and that extra pressure that the heart must pump against that will lead to malignant transformation of the heart through a positive feedback mechanism of hypertrophy that will end up causing compromise of the heart's ability to fill, which will be diastolic failure - it will not compromise the heart's ejection fraction, it will not compromise the heart's ability to pump until there ischemia - it will compromise the heart's ability to fill and that will be diastolic failure and eventually the heart will hypertrophy to a point where it may become ischemic because the coronary arteries are unable to diffuse enough blood through the thickened hypertrophic myocardium to supply that much muscle that is hypertrophy and lead to ischemia and myocardial infarction - myocardial infarction compromise the heart's systolic function - first have the diastolic dysfunction because the hypertrophy, the first thing it will hinder is the heart's ability to fill

Answer 61

- problem is the preload - heart must overcome afterload in order to pump so if the afterload gets too high the heart can hypertrophy and overcome the afterload and the other parameter is preload - preload is how much blood volume the heart is filling during diastole - if we increase venous return to the heart, we increase the preload - if we decrease the amount of venous return to the heart (decrease the amount of blood that the veins give back to heart), we effectively decrease preload - exercise increase preload by mobilizing all muscles and squeezing on veins more because the muscles are contracting and relaxing, that's pumping more venous blood, increasing venous return to heart though inferior and superior vena cava - decrease venous return to the heart by giving nitrates, those are vasodilators that dilate the veins which are the capacitance vessels allow the veins to retain more venous return and decrease preload - decrease the amount of work that the heart has to do because that's less blood volume that the heart has to pump out - ischemia blood flow (oxygen) is restricted

Answer 62

- diastole allows the heart to fill and distend, - as the heart distends sarcomeres of the heart, allow all Z-discs to align properly - Z-discs are held by desmosomes at the heart so it is zig-zaggy - its zig-zaggy because the heart doesn't want to begin its maximum contraction until its filled during diastole with enough blood volume - adding preload (adding blood volume) during diastole when the heart is filling, it distends sarcomeres gradually going from wavy to straight - at the end of diastole, all sarcomeres will be aligned - then we are going to get the isovolumetric contraction which the traditional way that muscles contract (myosin, actin, calcium) - isometric contraction build up wall tension then get systole - heart pumps, going to blow that stroke volume out through the aorta and blow the amount of blood volume and preload that it loaded into the right ventricle at a lower pressure rate into the pulmonary artery or the pulmonary trunk - pressures in aorta are 120 millimeters of mercury while pressure in pulmonary artery are 8-20 millimeters of mercury - pulmonary artery deliver deoxygenated blood only to the lungs, small relative to the body, small surface area of the pulmonary circulation - aorta supply the entire systemic circulation with blood in a large surface area of blood vessels so much greater pressure gradient - if hypertrophy in left chamber hypertension happens - if pressure in the pulmonary artery rises above 20 millimeters or mercury pulmonary hypertension happens - pulmonary hypertension builds up and transfers into the pulmonary artery - once raising the pulmonary artery pressures above 30 mm, pressure will arrive downstream at the right ventricle - increased pressure in the pulmonary artery leads to heart failure and right heart hypertrophy of the right ventricle is called core pulmonol

Answer 63

- coronary arteries supply the myocardium with its required oxygen demand - the heart has a very high oxygen demand, only muscle that never rests, has the highest concentration of mitochondria per unit of volume - left anterior descending the circumflex and the anastomosis at the back - right main stem coronary giving off the right marginal artery then going to the back giving off the posterior interventricular artery - then anastomosing with the left coronary artery and the posterior heart - heart filling with the left atrium of the heart filling with the four pulmonary veins carrying oxygenated blood from the lung - the left atrium fills the blood goes from the left atrium through the mitral valve into the left ventricle - the mitral valve closes there is isovolumetric contraction then we blow stroke volume through the aortic valve, the semi lunar valve, the aortic valve into the aorta at 120 mm of mercury - the aorta's elastic fibers allow the aorta to balloon out and adapt to this rapid increase in pressure gradient and the pulse pressure propagates forward - aortic valve close, with cusps like leaflets so what left the blood volume from the stroke volume that has been resisted by the afterload washes into the ascending aorta - volume that has been resisted by the afterload back washes into the aorta down the ascending aorta and fills that area - aortic valve has cusps, these cusps make semilunar valve, those cusps allow blood to pool in around the aortic valve and retain it there - gentle lake will slowly fill into coronary ostia, the vestibules of the coronary arteries, their openings all occurring during diastole

Answer 64

- blood is leaving the left atrium through the mitral valve and slowly filling into the left ventricle - left ventricle is filling with oxygenated blood from the mitral valve - right ventricle is also filling with deoxygenated blood through the tricuspid valve from the right atrium - both sides fill and also filling the coronary arteries at the aorta

Answer 65

- inferior and superior vena cava - the vena cava those are filling into the right atrium and going from the right atrium through the tricuspid valve the other AV valve and fill into right ventricle - theres going to be isovolumetric contraction - then during systole, blow stroke volume (output through the pulmonic valve) into the pulmonary artery or the pulmonary trunk

Answer 66

- right atrium is filling with deoxygenated blood from the superior and inferior vena cava - at the same time the left atrium is filling with oxygenated blood from the four pulmonary veins, so both atria are filling - atria contract the AV valves, open the tricuspid and the bicuspid mitral valve both open - during diastole they contract - on right side, the deoxygenated blood is going to leave the right atrium and enter the right ventricle - on left side oxygenated blood is going to leave the left atrium and enter the left ventricle - during diastole, both ventricles are filling, the heart is filling with preload - that heart is descending and all of the sarcomeres as the heart descends are becoming aligned - sarcomeres are fully aligned and the heart has filled with the maximum preload - at that point the AV valves are going to close - there's going to be isovolumetric contraction that going to push and begin to build wall tension and begin to build pressure in those chambers - once the pressures inside the right ventricle become greater than the pressures of the pulmonary artery and once the pressures of the left ventricle become greater than the pressures inside the aorta or afterload - systole and that massive contraction of the heart and the entire cardiac output that will be pushed out of the heart and on the left side, its a high pressure chamber that is where we get stroke volume that is deliver during systole out through the aortic valve - then through the pulmonic valve push at a lower pressure relative to the left, push out output that going to lungs to be oxygenated and returned - returned to the heart through the pulmonary veins as oxygenated blood

Answer 67

- diastole is filling the right atrium with the superior and inferior vena cava - we fill the left atrium with the pulmonary veins - also fill the coronary arteries with backwash of blood returned to the ascending aorta by the afterload - filling those because during systole aortic valve opens up and closes over the coronary osteos and protects them from high pressure - then once it closes back up the backwash of blood returns during diastole and both the right and left atrium are filling up with their vessels respectively - coronary arteries fill with blood from the backwash in the aorta - its ideal for the coronary arteries of the heart to be filled with oxygenated blood during diastole because during diastole the heart is relaxing, the myocardium is relaxing, and the sarcomeres are being aligned - whole consumption of ATP and work that the myocardium undergo only occurs during isovolumetric contraction and during systole - so during diastole, myocardium is descending and the sarcomeres are aligning and myocardium is relaxed; which is perfect time to load up the myocardium with nutrients like oxygen and glucose - during diastole the heart is beginning to gather up resources and when it has them isovolumetric contraction begins - systole begins, we pump the stroke volume out through vessels and myocardium relaxes the aortic valve closes again - afterload delivers backwash of blood down through the aorta and begins to fill the coronary arteries - during diastole, heart is beginning to fill at a low pressure because they are small vessels that only fill during diastole from the backwash not systole

Answer 68

- there are gap junctions - cardiac myocytes must communicate very rapidly with each other, especially in purkinje fiber system which must conduct electrical discharges and action potential very rapidly through the ventricle in order to polarize the ventricular system - function as a syncytium so it functions basically synchronously, gap junctions allow for that so it can function as an entire unit - differences in the sarcoplasmic reticulum: source for calcium for contraction comes only from the sarcoplasmic reticulum in skeletal muscle but it comes from the sarcoplasmic reticulum and extracellular fluid in cardiac muscle - because cardiac muscle had automaticity; cardiac muscle always ready to depolarize voltage gated channel and always allowing an influx of calcium - always approaching action potential resting gradient, positive 30, because myocytes are more permeable to calcium and the extracellular fluid - automaticity is the heart is constantly permeable to ions and always ready to depolarize - heart has a natural pacemaker, sinoatrial node, SA node, constantly depolarizing for the heart to beat - SA node and AV node slows conduction down for the purkinje system - skeletal muscle rely on neurons from the brain to depolarize - tetanus is possible in skeletal but not in cardiac - cardiac is resistant to tetanus and cannot be tetanized - tetanus = fatigue - in skeletal we had to depolarize skeletal muscle to open voltage gated sodium channels however in voltage channels in heart are constantly permeable or leaky

Answer 69

- phase 0, phase 3, phase 4 - during phase 4 there is a constant permeability to sodium through the voltage gated channels; constantly permeable or leaky allowing sodium to leak in; myocytes allow sodium to leak in through channels - that is allowing the heart muscle to have the automaticity, the heart muscle is always slowly beginning to depolarize and always approaching - slope of phase 4 is approaching the positive membrane charge for depolarization, its always in a state of gradual depolarization and thats its automaticity - then phase 0 begins, that discharge from the sinoatrial node and then its conducted to the AV node and then the AV node brings it down to the purkinje fiber system - then conducts through the ventricles down the septum and then up through the ventricles through the lateral walls of the ventricles - SA node and the right atrium, down to the AV node and then down to the purkinje fibers which go down the interventricular septum and then up through both ventricles, the right and left ventricles through their lateral walls - when that discharge from the sinoatrial node occurs, that initiates phase 0, so voltage gated calcium channels open up calcium influxes into the cell and not a lot is needed because there is a bunch of sodium influx into the cell during phase 4 and now phase 0 begin - giant massive influx of calcium on top of that, sodium (NA+) and calcium (CA2+) so we have more positive ion piling in and a quick depolarization during phase 0 and then just in the muscle - phase 3 is the depolarization step with potassium - myocytes is with potassium relevant for lethal injection, hypo/hyper kalemia

Answer 70

- automaticity during phase 4 is because of leaky voltage gated sodium channels, the heart is constantly approaching depolarization through its automaticity, through its voltage gated sodium channels, then we get that discharge from the sinoatrial node, we have the opening of voltage gated calcium channels during phase 0, we get the depolarization of the myocytes which is the isovolumetric contraction and then the stroke volume, the heart beats, thats where the beat happens, is the influx of calcium during phase 0, we depolarize and then we have to get the heart to repolarize, then we have the permeability to the potassium channels during phase 3 - phase 4, automaticity, leaky sodium channels, sinoatrial node depolarizes, we get that discharge from SA node, phase 0 begins, the voltage gated calcium channels open up, calcium influxes, we get action potential, heart beat, depolarize with potassium - phase 4, phase 0, phase 3 - sodium, calcium, potassium, automaticity, sodium, depolarization, calcium, repolarization, potassium

Answer 71

- P wave = atrial depolarization - QRS = heart beat, ventricular depolarization, phase 0 in heart, which is the calcium channels opening up and the depolarization - T wave = ventricular repolarization, which is when the potassium channels are open, phase 3 - phase 4 cant be seen on EKG but its the automaticity of the heart, sodium channels, allowing the heart to approach depolarization but not actually depolarization - P wave atrial depolarization, QRS ventricular depolarization, phase 0 calcium voltage gated calcium channels, T wave ventricular repolarization voltage gated potassium

Answer 72

- overwhelm the heart with potassium, repolarize the heart, making the T wave so big that it becomes a sine wave, entire EKG becomes a sine wave - when we flood with potassium remember they shoot intravenously so it goes right to the heart and hyper repolarizes the heart - it repolarizes it to the point that the heart cannot depolarize; its flooded with positive ions - it goes into cardiac arrest, EKG looks like a sine wave, patient dead - hypokalemia on an EKG will have flattened T waves - T wave is related to potassium - so if you are hypokalemic, you have low potassium, you are going to flatten the T wave - flat T wave = hypokalemia - peaked T wave = hyperkalemia

Answer 73

- first degree heart block = extended PR interval - second degree heart block MOBITZ type one = progressive lengthening of the PR interval until a QRS is dropped - QRS = a beat - one of the P waves is not going to be followed by a QRS complex - second degree heart block MOBITZ type two = dropped beats that are not preceded by a change in the length of the PR interval, there is no pattern when we drop a QRS or a beat, just chaotic - third degree or complete heart block = absolute worst, atria and ventricles beat independently of each other, P waves are not neatly associated with QRS complexes, can occur before or after QRS complexes - treat third degree heart block with a pacemaker - atrial fibrillation = atria are depolarizing and beating chaotically (rapid, ineffective, inefficient), has risk factor for stroke and thrombus formation, ventricular fibrillation (shock them) - congenital long QT syndrome = if interval lengthened they are at a higher susceptibility to developing torsades de pointes, increased QT interval (interval between QRS and T wave) - drugs can prolong QT - it predisposes them to torsades de pointes which may progress to ventricular fibrillation - antidote to torsades de pointes is magnesium; prevent them from going into ventricular fibrillation and can be precipitated by certain agents and those with congenital long QT syndrome - Wolf Parkinson white syndrome = ventricular pre excitation syndrome, they have an abnormal fast accessory conduction pathway through the bundle of Kent (acts as its own aberrant circuit) - it basically conducts it leads to a supraventricular tachycardia because it leads to a reentry circuit - Wolf Parkinson white syndrome = bundle of kent, reentry circuit, supraventricular tachycardia delta wave on EKG

Answer 74

- auscultate the aortic valve in the right second intercostal space - auscultate the pulmonic valve in the left second intercostal space - aorta is the right second intercostal space - pulmonic valve is left second intercostal space - tricuspid is going to be the left fifth parasternal intercostal space - mitral valve, apical beat, apex beat are going to be in the left fifth intercostal space midclavicular - third intercostal parasternal (under pulmonic valve area) called herbs point, best place to hear aortic regurgitation - aortic stenosis = right second intercostal - pulmonic stenosis = left second intercostal - tricuspid endocarditis = flow murmurs, ventricular septal defect

Answer 75

- aortic stenosis = narrow, systole - mitral stenosis = diastole, opening snap - aortic regurgitation = backwash, diastole, rumble - mitral regurgitation = systole, pan or holo

Answer 76

- anterior septum = V1-V4, brickyard left anterior descending - lateral = aVL, left circumflex - inferior = aVF, posterior interventricular artery

Answer 77

atrial fibrillation = irregularly regular atrial flutter = sawtooth stable angina = action, emotion at rest ST prinzmetal angina = coronary artery spasms

Cardiovascular 17, 18, 19 Flashcards

(104 cards)