Test 2 Flashcards

Question

What is normal BP? what is considered HTN?

Answer 1

• 120/80=normal o 120: systolic pressure ♣ pressure when the ventricles contract o 80: diastolic pressure ♣ pressure when the ventricles relax o you still have pressure even when the ventricles relax, because you are dealing with a closed system • HTN: o >90: diastolic o >140: systolic

Answer 2

* Difference b/w systolic and diastolic blood pressures | * Influenced by stroke volume and peripheral resistance

Answer 3

• Ie. If patient has a BP that is falling, and their pulse pressure is becoming more narrow, then this is indicative of a loss of stroke volume (possible due to blood loss-->dec cardiac output) o Losing left ventricle function-->BP drops, pulse pressure becomes narrow • Ie. If we suddenly throw a clot in a major vessel, this would inc peripheral resistance-->dec BP and narrow pulse pressure • Ie. If patient has a pulse pressure that is wider, then this is often indicative of inc in total peripheral resistance (often due to a stiffness of the arteries)

Answer 4

• Jugular venous pressure: gives you an indication of what is going on on the right side of the heart o Usually, the JVP decreases with inspiration due to reduced pressure in the expanding thoracic cavity, and the increased volume allows right ventricular expansion during diastole • Kussmaul’s sign suggests impaired filling of the right ventricle due to poorly compliant myocardium or pericardium o This impaired filling causes increase blood flow to back up into the venous system, causing jugular venous distention ♣ Seen clinically in the internal jugular veins becoming more readily visible • Kussmaul’s sign: paradoxical rise in JVP with inspiration or a failure in the appropriate fall of the JVP with inspiration o Seen in some forms of heart dz o Usually indicative of limited right ventricular filling due to right heart dysfunction o May cause an increase in the size of the right side of the heart

Answer 5

• S1: lub o Closure of the AV valves (valves separating the atria and ventricles) o Ventricles begin to contract (get smaller)-->P inc in the ventricles below that of the atria-->AV valves (bicuspid, tricuspid) close o When would you hear abnormal AV valve sounds? S1 • S2: dub o Closure of the semilunar valves o P inc in the ventricles-->causes semilunar valves to open-->ventricles relax-->semilunar valves close ♣ So blood you just squeezed out of ventricles toward the lungs starts backflowing and this causes then the closure of the semilunar valves, so there is a small part of the volume that you squirted out of ventricle that goes back into the chamber • There is a split in the S2 heart sound normally o This is due to the aortic valve closes slightly before the pulmonary valve o If there is a longer split b/w the sounds, this is b/c pulmonic is closing before aortic, this is due to the aortic being harder to close or it being stenotic (or stiff)

Answer 6

* Usually abnormal rhythm of the heart * Contains 3-4 heart sounds, so has S1, 2, and then 3 and/or 4 * Can be normal in children or athletes, but can also be a sign of serious problems like heart failure and pulmonary edema * Associated with ventricular overload or sinus tachycardia

Answer 7

• S3: ventricular gallop: thought to be the result of an increase in ventricular filling o Only normal to hear this in children and athletes • S4: atrial gallop o Usually caused by stiffening of the walls of the ventricles which produces abnormally turbulent flow as the atria contract to force flood into the ventricles

Answer 8

• Result of turbulence in the blood flow from one chamber to the next • Typically the turbulence is caused by velocity (how quickly blood is moving from one chamber to the next) or structural abnormalities (blood is having to go over or around something) • Graded I-VI: o I: quiet, can barely if ever hear o VI: you don’t need a stethoscope to hear

Answer 9

• Friction rub: think of fibropurulent exudate being in the pericardial sac, so heart moving against fibrous tissue as it moves in the sac • Normally when heart valves open, then are silent o But with a stiff valve, you can hear the opening: it is a snap/slapping sound, b/c the valve is bouncing against the wall

Answer 10

• Atrial depolarization o Depolarization means it is losing electrical charge • normal 0.12 seconds

Answer 11

o Enlarged atria, hypertrophied atria: it takes longer for atria to depolarize

Answer 12

• this is indicative of a change in the origination of the stimulus of the cardiac event o Normally SA node-->AV node-->Bundle of His-->purkinje fibers: since the SA node fires the most frequently, it is called the pacemaker o If P wave is inverted, it means that the SA node is not firing most frequently, something else is, so the HR will be decreased (b/c SA node is the thing that makes the HR what it is, so if something else is firing then the highest rate will still be lower for what would be normal for the SA node)

Answer 13

• Beginning of P wave to the beginning of the R wave • Normal: 0.12-0.20 seconds • This is the conduction time thru the atria, then we delay the impulse at the AV node (which is normal) in order to give blood time to fill the ventricles before we have them contract o So the PR interval is how much time we delay the AV node from firing.

Answer 14

o delay conduction thru the AV node to longer than 0.20 seconds, but every impulse generated by the SA node gets thru to the ventricles

Answer 15

o impulses from the SA node occasionally fail to get thru the AV node, so often see 3 P waves for every 2 QRS complexes ♣ hallmark of 2nd degree AV block: not every P eave is followed by a QRS complex

Answer 16

complete heart block o AV node has ceased to conduct the depolarization from the atria to the ventricles ♣ SA node fires normally leading to atrial depolarization, but AV node fails to conduct an action potential at all, so the ventricles are not depolarized and fail to contract ♣ Characterized by: complete dissociation of the P waves and QRS complexes, so there is NO PR interval • Atria and ventricles are functioning independently of each other

Answer 17

* Ventricular depolarization and atrial repolarization | * normal 0.08-0.12 sec

Answer 18

it is taking longer for the ventricles to depolarize due to the ventricles being enlarged

Answer 19

• Beginning of the S wave to the end of the T wave • This is the interval b/w the ventricle depolarizing and repolarizing o Referred to as “isoelectric” • normal 0.08-0.12 seconds

Answer 20

myocardial ischemia

Answer 21

myocardial infarction

Answer 22

ventricular repolarization

Answer 23

myocardial ischemia

Answer 24

• too much potassium o It becomes more and more narrow, so the ventricle is not repolarizing, and if it can’t repolarize, the heart won’t beat

Answer 25

* Complete ventricular event | * Sometimes used to see how dysarrhthmics are working

Answer 26

o Both affect the heart rate o Ppl who have these are more prone to develop cardiac arrhythmias o Both have a strong genetic component: ♣ Gene associated with the 2 is the same one associated with schizophrenia

Answer 27

• Balance needs to exist b/w myocardial oxygen supply and demand o If demand inc, then supply has to inc in order to accommodate that demand • 4 determinants of myocardial O2 demand: o rate: if we inc HR, we have inc the demand for O2 b/c the myocardial tissue is 100% oxygen dependent o force: if ventricle contract more forcibly, we have an inc demand for O2 o muscle mass: if we have more hypertrophied muscle in the ventricles, we need more oxygen to allow that muscle to contract o wall tension: if ventricle wall is stiffer/more tense, then we need more O2 to get the ventricles to contract

Answer 28

• The problem is the heart is unique in that it is a pump pumping blood to rest of body and also supplying O2 to itself o When ventricles contract and blood goes to the rest of the body, this is the time when the heart perfuses itself the least o When the ventricles relax, this is when the heart is perfusing itself the most, but the rest of the body is being perfused the least ♣ Only way the heart can inc its own blood supply is to dilate the coronary blood vessels to carry more blood-->carry more O2

Answer 29

• If heart in situation when the demand is greater than the supply of O2, the heart is operating in somewhat of an anaerobic environment, so this is when we have ischemia o Ischemia means to hold back blood, then we would hope that angina occurs b/c the heart has a lack of oxygen o If the ischemia is prolonged, then we have reached the point of no return, so this myocardial tissue has been in a deficit situation that it is irreversible, so this is when we have tissue that is dead--this tissue is necrotic which means we have had an MI ♣ This is irreversible ♣ The area of the heart that is most susceptible to this is the left ventricle • Most susceptible to ischemia and MI

Answer 30

o Coronary atherosclerosis: hardening of the blood vessels, plaque build up ♣ This is a slow process, takes years ♣ Often starts in 40s/50s ♣ Often happens in a vessel at the point where a vessel turns or where a vessel branches ♣ Rule of thumb: pt probably won't have any problems until the vessel is greater than 75% occluded with plaque • b/c body is very accommodating if things happen slowly which it is accommodating by new vessels being formed around the occluded area

Answer 31

• Age: as we inc in age, susceptibility inc • Race: more common in African americans than white population often due to the problem with vitamin D o Vitamin D is under the skin, but not as much as in African Americans, so they have more cholesterol which predisposes them to coronary atherosclerosis • Family: familial disease o Not usually genetics, more based on lifestyle • Sex: more common in males o After menopause, women have a higher risk than males of any age o If you are female w/ CAD, you are more likely to die, b/c they are often not believed ♣ They present differently: nausea, vomiting, pain in jaw, malaise ♣ Men: arm pain, shortness of breath, angina

Answer 32

• Hyperlipidemia o Concerned about triglycerides and cholesterol • Lipids: fats--fat and water don't mix, so we have to come up with a way to transport fats around the vascular system without them plugging up the vasculature o The way we do this is to connect the fat to the protein to carry it around, and this gives us lipoproteins (4 classes): ♣ The classes are based upon: • The type of bond b/w the fat and the protein • The amount of fat that is present vs. the amount of protein that is present ♣ One category has no correlation with CV dz

Answer 33

• increase triglyceride o Don’t measure this when looking at CV dz, b/c most of the mc is triglycerides o Fats are stored in fat cells, and thru a hormonal rxn, we pull the triglycerides out of the cell, convert it to sugar, and use it for energy o Only correlation with CV dz is in middle aged males ♣ No correlation w/ females of any age or young/old males

Answer 34

• inc cholesterol o Most of this mc is cholesterol, little protein o Inc in LDL=inc risk of CV dz

Answer 35

• protein o Most of the mc is protein o Acts as a protective factor against CV dz ♣ So we want HDL to be high and LDL to be low ♣ If HDL is decreased, you have an inc risk of CV dz

Answer 36

• <160 | With high HDL and low LDL

Answer 37

• HTN is correlated with CV dz o Occurs in 25% of the population ♣ Greater in blacks: affects 40% o The higher the BP, the greater your risk of CV dz • As BP rises, the amount of force you are exerting against the walls of the blood vessels is rising, and the innermost part of the blood vessel is becoming damaged, so you need to start repairing it thru inflammation which lays down calcium and fat o So vessel loses some plasticity, so we will not be able to control our BP as much thru vasodilation or constriction o Blood flow is restricted when plaque in the vessel, so the end organ of the vessels runs the risk of not being perfused with enough blood ♣ Body compensates by inc BP, but this causes more inflammation and lays down more plaque, continues in cycle • Can only prevent by keeping someone from getting HTN, b/c once cycle starts, it is continuous o High BP is very insidious: takes a while for pt to have symptoms, so once they do, BP is already pretty high • Kidneys: nephrons of kidneys like vasculature, so if the BP is too high, will blow out a nephron and this will lead to renal failure eveyr time we cycle the blood thru

Answer 38

o Cigarettes: This seems to be correlated more with the number of cigarettes smoked per day rather than the length of time the person has been smoking • If smoking 3 PPD for 10 years, then you are more at risk than someone smoking 2 packs a week for 40 years • Makes sense b/c: ♣ Cigarettes have nicotine and release CO • Nicotine vasoconstricts blood vessels, so the BP will increase • If smoking a lot of day, you are getting a large amount of CO, so a lot of body tissue may not be getting enough O2, so the body thinks you are not getting enough blood supply to the end organs/body tissue, so the body compensates by inc the BP ♣ Ie. Ppl who smoke a lot per day, will have dark purple color in their nail beds • This is due to the combination of CO and hemoglobin o Diabetes: o Predisposes someone to CV dz (moreso with Type I diabetes) o These pts have a higher blood sugar, some over 300 ♣ This blood sugar level damages the endothelial lining of the blood vessel wall, so you start laying down Ca and proteins due to inflammation, so plaque builds up o Obesity: o If you are obese, you almost always have HTN ♣ We send blood out of heart-->aorta-->As-->capillaries-->venous system-->heart • If you add 20 pounds of weight, you add a mile of blood vessels, so to traverse the extra mile you have to have more force to get blood thru all of those vessels o If we see a pt with HTN, the first thing we do is to tell them to lose weight so they don’t have to have as much force

Answer 39

• Myocardial tissue is totally O2 dependent, so has to operate in an aerobic environment o If put it in an anaerobic environment, then forcing the tissue to try to operate with less than optimal levels of oxygen o The greater the anaerobic environment, the greater the lactic acid productionthis acid is building up in the myocardial tissue, so the pH of that tissue drops, and potassium inc!

Answer 40

* Most common area in the heart for this to occur: left ventricle * If you look at this happening in the left ventricle (the muscle in the ventricle is swirled, so the muscle twists b/c it is more effective at ejecting blood), if the myocardium is ischemic, then the ischemic area is not really participating in the contraction * If you look at the area that is ischemic, when the contraction occurs, this area bulges a little bit b/c it is not really participating in the contraction b/c it has to operate in an anaerobic environment * You hope for these types of pts to have angina (chest pain) associated with the ischemia * If the ischemia occurs for 30-45 min, then you are beyond the point of no return, and no longer dealing with transitory event, you are getting permanent cell death and damage, so you are dealing with necrosis and an MI

Answer 41

T wave inversion | ST segment depression

Answer 42

o this is an infarction that goes all the way thru the myocardial tissue from the endocardium to the epicardium ♣ Ischemia was the entire with of the tissue

Answer 43

dealing with about ½ of the myocardial tissue, not all the way thru the myocardial wall

Answer 44

• w/ an MI: you have a muscle that is dead, the infarction would look like a large bruise on the surface of the heart o w/in 24 hours after the MI, the repair process would have already started ♣ repair includes inflammation ♣ w/in about 2-3 days from MI, you would see the end of inflammation • sometimes the pt will survive MI, but die 2-3 days layer b/c with inflammation, you activate Factor XII and you get a fibrous mesh that develops in area of MI, so that is when the area is the most vulnerable and the weakest, b/c you have no scarring yet o pt needs to stay calm, still relaxed. BP and HR need to be in normal ranges b/c we don’t want anything to cause P to build up and blow the healing process ♣ w/in about 3 weeks, healing is over and scarring has occurred

Answer 45

1. pain: chest pain, sweating, nausea, vomiting - but, 40% of MIs are symptom free or they cause symptoms you ignore 2. increases in cardiac enzymes 3. EKG: Q wave and ST segment increased, inverted T wave - overtime ST segment and T wave will revert to normal, but evidence of an old MI in L ventricle is very pronounced QRS complex

Answer 46

• When tissue is damaged, and the tissue has certain kinds of enzymes, so the enzymes are released out into vasculature when tissue damaged o So an indirect way of gauging tissue damage is to look at the level of enzymes, so the greater the level of enzymes, the more tissue damage o 2 problems: ♣ Identifying enzymes that are totally unique to a certain tissue is difficult ♣ When, in time, you measure the enzymes, being able to detect them will depend on their rate of metabolism which varies among the different types of enzymes • So where in time you assay the levels of enzymes will effect how you know if tissue damage and how severe

Answer 47

• This is an enzyme found in cardiac M, skeletal M, brain tissue, and lung tissue • We measure the isoenzymes of CPK (the isoenzymes make up the family of CPK) o MB is the isoenzyme mostly in cardiac M (also a little in skeletal M) ♣ It begins to inc 4-6 hours after an MI, and it peaks in the neighborhood of 18-24 hours, and then back to normal in 2-3 days

Answer 48

* Correlated with CV dz | * Slower to inc (more like 72 hours) and take longer to go back to normal

Answer 49

* Regulatory protein that controls calcium mediation in actin and myosin filaments * Its in cardiac tissue, so when cardiac tissue is damaged, troponin is released, but it is NOT an enzyme * It inc 4-6 hours after MI then decreases very slowly, takes 10 days to get back to normal

Answer 50

♣ When pt comes in, you would draw a baseline of cardiac enzymes, then draw every 8 hours for 24 hours to get a panoramic view of what enzymes are doing

Answer 51

• Can be a major complication of an MI • If pt has an interventricular septal problem with the MI, then this can be a major complication b/c this goes back to inflammation o When you get the mesh forming with Factor XII, it is in the weakest state, but you also have some developing in the interventricular septum, so b/c we have a normal pressure difference b/w the left (higher P) ventricle and R (lower P) ventricle can blow a hole through the interventricular septum and this will shunt deoxy blood through to the L ventricle from the Right o There is not just one vessel that feeds the interventricular septum, so if have a lot of plaque in multiple vessels problem, can be severe • VSD is the most common cardiac condition that children are born with o Not the result of an MI, but still a hole in the septum b/c the foramen ovale didn't close, so blood shunted from Left to right and we are comprising CO ♣ Also will get pulmonary congestion b/c putting too much volume back into the right side of the heart

Answer 52

• Dysrhythmia: one of most common (90% of time) complications from MI • Normal: 60-100 bpm • Bradycardia = less 60 • Tachycardia = greater 100 o Both of these compromise CO which is determined by HR and SV, so if HR dec, then not contracting enough, so CO will be dec, and if HR inc, then ventricles not able to fill up as much as needed so SV is dec, and CO will dec

Answer 53

• Ventricular premature beats are on a continuum: can be occasional which can be a preliminary sign to vent tachycardia-->vent flutter--> vent fibrillation o Premature activation SA node o Not concerned about ventricular premature beats unless you have 8-10 of them in a row and continues, but most ppl have some of these times when the heart skips a beat o Vent. Tachycardia = greater 120

Answer 54

♣ Fibrillation is when you get major twitching of a muscle, so for a ventricle, you have to use electricity to restore the normal rhythm of the heart • If you defibrillate, then you are shutting down the electrical system of the heart o Normally, we have SA node transmits signal to AV node then to Bundle of His and purkinje fibers, so when defibrillate turn off this circuitry which only comes back on b/c the circuit has autorhythmicity which is self excitability ♣ So most of the cells have the ability to re-excite themselves apart from the circuitry: most of these cells that have this ability are in the SA node (pacemaker), so you hope they start functioning again and then hope they have been converted to a sinoatrial rhythm ♣ When someone is killed by electrocution, their circuitry has been hit with such voltage that their system will not be able to restart itself

Answer 55

♣ Can be occasional or atrial tachy-->atrial flutter-->atrial fibrillation ♣ So if atrial rate is 70, then ventricular rate is also 70 • If atria contracting 300 bpm, then ventricle is contracting about 150-160 bpm, and this is b/c of the circuitry o Normally SA node fires and comes to AV node where the impulse is delayed slightly before it continues on to the rest of the circuitry to give time for the ventricle to fill with blood and we have to do this before the ventricles contract, and the length of the delay is reflected in the PR interval on the EKG ♣ How does this delay occur? The width of the fibers coming into the AV node are wider than those coming out of the AV node, so this is what causes the impulse to slow down • Ie. With an atrial rate of 70, all impulses getting thru • Ie. If atria firing 300 times per min, then a huge amt of traffic trying to get thru AV node, so many of them bump into each other and cancel each other out, so only about 1/2 of the impulses that get through (about 150) actually get through to the contraction of the ventricles o Will not kill you quickly, b/c ventricular rate does not match the atrial rate, so there is still CO (and SV) to keep everything perfused

Answer 56

* Ie. Damage is done to the left bundle branch which means the impulse is going to the two ventricles at different times, so they are not contracting in a synchronized fashion, so you would see this on an EKG by having another ventricular event (so they would have what looks like two QRS waves) "rabbit ears" * Ventricles not synchronized, so impulse not reaching ventricles at same time, therefore, the bundle branches are blocked * Will not kill you, but it lets you know that there is damage done to the bundle branches which is irreversible

Answer 57

• CV dz is a dz of the heart valves as well, so we can see abnormalities in the flow of blood and abnormalities in the filling of the chambers of the heart that the valves are controlling o Usually valves allow only unidirectional blood flow o Valves very sensitive to pressure changes, so they open due to these changes or pressure differences w/in the chambers o 2 problems: ♣ stenosis: valves is stiff, so it takes greater pressure to open and close the valve ♣ regurgitation: valve doesn’t close securely so it permits backflow into a chamber

Answer 58

o bicuspid/mitral valve insufficiency o permits a backflow of blood from left ventricle into left atrium due to incompetent valve closure o can be acute or chronic: we don’t adapt as well if acute o generally atria are not as compliant with change as ventricles can be, b/c atria don’t have a lot of muscle ♣ if asking ventricle to be more compliant with volume, we get hypertrophy of muscle ♣ if asking atria to be more compliant, it will still get bigger but also thinner, b/c not as much muscle o often occurs due to rheumatic heart dz caused by the antibody mistaking the heart protein for the M protein of strep throat

Answer 59

valve falls back in o affects 1% of population and more common with females o about 25% of ppl will present with symptoms of an anxiety disorder (heart is racing) ♣ if valve gets sloppy, one of internal mechanisms we have to inc cardiac output is to release or administer adrenaline which will cause symptoms of anxiety o high incidence in ppl with Marfan’s Syndrome: genetic condition ♣ tend to be tall, lanky, eye problems, CV problems

Answer 60

♣ Valve is b/w the atria and ventricle and the valve closes, b/c as ventricle starts to contract the P in ventricle inc higher than atria, so the valve starts to close and always in exactly the same spot due to the chordae tendinae on the valves which look like little strings • Chordae tendinae are anchored in the papillary M, so normally when the electric current comes down thru the Purkinje fibers (which go up into the ventricles), the current reaches the papillary M just slightly before it reaches the Purkinje fibers, so when it reaches the papillary M, it causes the M to constrict which puts tension on chordae tendinae, so when current reaches the ventricle and causes it to contract, there is already tension on the chordae tendinae ♣ Mitral valve prolapse occurs due to chordae tendinae being too long, so it protrudes when the ventricles contract • Also can be caused due to deposition of a mucopolysaccharide (mucus like sugar) on the valve which makes the valve very flimsy, so it is easy to protrude ♣ Most of the time, you will not do anything to deal with this. Really only need to do something b/c of a change in CO or SV • However, if have the mucopolysaccharide, we used to recommend a round of antibiotics before getting teeth cleaned, b/c often get bacteria in blood during teeth cleaning, so if got bacteria and it stuck to the sticky mucopolysaccharide then it would grow and cause a problem, but now don't do this b/c contributing to resistance

Answer 61

• Stiff aortic valve which will obstruct blood flow from the left ventricle into the aorta during systole b/c this valve is difficult to open, so in order to get blood past the stiff valve, the left ventricle has to generate more pressure by hypertrophy to get the blood past the valve to the rest of the body • Pt will normally be fine until a point when opening is greater than 50% reduced o Also ventricular hypertrophy can cause complications seen on EKG as wider and taller Q wave (which represents ventricle depolarizing) ♣ This hypertrophied ventricle also prolongs the contraction which can be a complication

Answer 62

• Backflow of blood from the aorta to the L ventricle during diastole (when the ventricle is relaxed) • Normally, we do get a small amount of backflow, but this is an excessive amount of backflow, so the L ventricle hypertrophies b/c so much more blood to deal with • About 50% of the time, aortic regurgitation is the result of rheumatic heart dz o The protein that matches the M protein is ALSO on the aortic valve (and the mitral valve) o In the past, most of the cases of aortic regurgitation was caused by syphilis, but not as common today

Answer 63

• Heart failure with reduced ejection fraction (a type of CHF): ejection fraction of <40% and an inability of the heart to generate an adequate cardiac output to perfuse vital tissues o CO depends on HR and SV ♣ SV is influenced by contractility, preload, and afterload • Contractility: reduced by diseases that disrupt myocyte activity o MI is the most common cause of decreased contractility o Secondary causes of dec contractility, such as myocardial ischemia and inc myocardial workload, contribute to inflammatory and immune changes that mediate ventricular remodeling • When contractility is decreased, stroke volume falls, and left ventricular end diastolic volume (LVEDV) increases. o This causes dilation of the heart and an increase in preload. o Inc in LVEDV can actually improve cardiac output up to a certain point, but as preload continues to rise, it causes a stretching of myocardium that eventually can lead to dysfunction of the sarcomeres and decreased contractility • Increased afterload is most commonly seen as a result of inc PVR, like in HTN o With inc PVR, there is resistance to ventricular emptying and more workload for the left ventricle, which responds with hypertrophy of the myocardium o Sustained afterload leads to hypertrophy mediated by Angiotensin II and catecholamines-->inc oxygen and energy demand ♣ As CO falls, renal perfusion diminishes with activation of the RAAS which acts to increase PVR and plasma volume-->inc afterload and preload further • Baroreceptor reflex detects the decrease in perfusion and stimulates the SNS to cause more vasoconstrictioncauses hypothalamus to produce ADH

Answer 64

• Body tries to compensate by either inc SV or inc HR both lead to an increase in CO - inc adrenergics - inc preload - hypertrophy of the heart

Answer 65

• SNS activation initially compensates for a decrease in cardiac output by increasing the heart rate and peripheral vascular resistance o Occurs b/c when the CO goes does, the baroreceptors detect this, and they cause the heart to contract harder (stroke volume) or beat faster (HR) o If you overuse the SNS, the receptors start to die off, so there is a decreased response

Answer 66

• Preload increases in order to compensate o Preload is the pressure in the ventricles after they are filled with blood o The more you fill the ventricles, the more pressure or preload you get o In order to inc preload, the body releases ADH and aldosterone ♣ As you fill ventricles with more bloodstretch out ventriclessnaps back/contracts with more forceinc SV o The muscles though contract with more force, so they need more blood, so if no additional blood coming to the heart, then the heart cells die off

Answer 67

• Hypertrophy: heart gains muscle massheart contracts harder o Heart cells become elongated as they grow so the muscle gets larger ♣ These cells contract harder, eject more blood, and inc CO o But b/c these cells doing more work, they require more blood/O2, so these cells get overworked and start to die off ♣ Also if the muscle gets too big, then the actual chambers get smaller, so they don’t fill with as much blood

Answer 68

• One of the most common is difficulty in breathing o Dyspnea • Cough (nonproductive) • Rales: congestion that you can hear in the lungs with breathing due to fluid in the lungs o You can have fine, medium, or coarse rales--depends on where you hear congestion in the lungs when breathing ♣ If hear at the top of inspiration: fine ♣ If hear just at the beginning of inspiration: medium ♣ If hear all the way thru inspiration: coarse • Liver o Some enzymes elevated, liver enlarged • Edema o Swelling in ankles, feet, and sometimes up in calves • Fever o Low grade

Answer 69

• occurs b/c not enough oxygen is being delivered, so decrease in perfusion, so BP is decreasing • Cardiogenic shock and the relationship with tissue perfusion is conceptualized by Mean arterial P = CO x total peripheral resistance o Most dec in MAP (and therefore cardiogenic shock) is due to a decrease in CO, so MAP dec b/c half of ventricle is gone o Way to inc TPR (and therefore compromise MAP) is the person throws a large clot or PE, so the person has greatly inc TPR, so tissue not being perfused, so MAP with decrease • This is a result of sudden loss of a large amount of myocardial tissue, so generally they go into cardiogenic when lose greater than 40% of the left ventricular tissue • If lose this much of the ventricle, only have a certain amount left to contract, and this is not enough to keep the blood pressure up (if you lose a large enough amount), so 80-90% of ppl die from the shock

Answer 70

o Person is having an MI, so to some degree they are experiencing a decrease in myocardial function, so then MAP is compromised-->hypoTN ♣ With decrease in BP, you are not getting blood back into the lungs to blow off CO2, so if retaining CO2, then your blood becomes acidotic, and potassium will increase, so then contributing even more to myocardial dysfunction ♣ w/ decrease in BP, coronary blood flow is compromised which was already compromised by MI, but dec in BP exacerbates the decreased blood flow • dec coronary blood flow-->myocardial tissue becoming anaerobic, so tissue becomes hypoxic and lets off lactic acid-->dec in pH and inc in K-->heart tissue less excitable-->arrhythmias

Answer 71

o systolic less than 90: so dec blood flow to major organs o urine less than 20 mL/hour: due to dec blood to kidneys ♣ this is compensatory b/c if blood pressure is so low, we don’t want to be urinating out fluids • urine will have less Na in it, so retaining Naretaining waterinc in BV-->inc in BP o vasocongestion: cold, clammy skin b/c shunting blood away from skin to get it to major organs o dec mental fcn: shunting blood and O2 from brain o cardiac index less than 2.1 L/min o left side heart: all problems indicate left side heart damagedegree of left side heart damage will indicate mortality which can be high

Answer 72

• Cardiac output in L/min/square meter of body surface

Answer 73

o An aneurysm is a localized dilation of the blood vessels, and there is 2 typical presentations as these relate to the aorta ♣ Fusiform: bulge involving both sides of the artery ♣ Saccular: bulge involving one side of the artery • arteries typically made up of 3 layers (tunicas)—aneurysms typically involve the middle tunica o most often affect abdominal aorta ♣ first symptom: death—b/c if AAA occurs, then the person will bleed out in about 3 min and can’t stop it o more often, we get a dissecting aortic aneurysm which means we have the small hole in the aorta, and b/c of pressure in the aorta, the hole gets bigger and bigger ♣ can also occur in brain, and if it ruptures, you get a stroke ♣ Marfan’s pts more likely to get aortic aneurysm o Occasionally if they occur up in the chest, they are accidently discovered

Answer 74

• Venous dz: veins more thin walled than arteries, and don’t have same pressure in them o At any moment, 70% of blood volume is in the veins, so always have blood volume than the arteries do o Since veins don’t have the pressure in them, we have ways to get blood back to right side of heart ♣ Breathing: Kussmaul’s—when you are sitting and passively breathing, when you inspire the pressure in your chest drops slightly, and abdominal pressure increases, which helps blood get pushed up toward right side of heart more easily ♣ Veins in legs all have one way valves on them, so when you move legs and walk, your valves push blood up to abdomen, then the breathing mechanism takes over

Answer 75

• CHF can happen w/o having an MI, but it is also a complication of MI o The location of the congestion will depend upon the ventricle that is involved ♣ So if left ventricle involved, then we will have pulmonary venous congestion ♣ So if R ventricle involved, then systemic venous congestion • Heart failure: heart is unable to generate an adequate cardiac output so there is inadequate perfusion of tissues or inc diastolic filling of L ventricle, so that pulmonary capillary pressures are increased (unable to meet the blood/O2 demands of the body

Answer 76

systolic heart failure/systolic ventricular dysfunction | diastolic heart failure/diastolic ventricular dysfunction

Answer 77

more common in male than female  inability of the heart to generate an adequate CO to perfuse vital tissue (CO=HR * SV)  EDV (End Diastolic Volume) = amount of blood at end of diastolic, just before systole  ESV (End systolic volume) = amount of blood in ventricle at end of systole.  SV is influence by 3 factors: - preload - afterload - contractility

Answer 78

degree of stretching experienced by ventricular muscle cells during end ventricular diastole

Answer 79

amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood. -The greater the afterload, the shorter the duration of ventricular ejection and the larger the ESV. ▪ Afterload is increased by any factor that restricts blood flow (ex: peripheral blood vessel constriction). If the afterload is too great, the ventricle cannot eject blood thereby causing congestion. This will then increase the preload.

Answer 80

amount of force produced during a contraction, at a given preload. This can be altered by autonomic innervation and circulating hormones, as well as by drugs.

Answer 81

- More common in female than male. - This is pulmonary congestion. - 50% of CHF is due to diastolic heart failure  Causes include: ◦ hypertension induced hypertrophying myocardial ischemia ◦ Aortic and mitral valve diseases. -With lung disease → reduce O2 supply (and RV hypertrophy increases muscle mass so increased need for O2) → RV hypoxia (because more O2 needed and less O2 supplied due to lung disease) → lowers force of V contraction → increases RV preload → increases RA preload → increases peripheral edema

Answer 82

-this reflects a relationship b/c thrombus (process of blood clotting) and embolization (embolus=any substance, like a blood clot, in a vessel that obstructs the vessel) o Can be fat, blood clot, plaque that has broken off o 3 contributing factors: 1. Stasis blood flow: slow down the blood flow 2. Endothelial: insult or injury to the endothelial (innermost) lining of the blood vessel 3. Hypercoagulation: something is occurring that is enhancing coagulation - Ie. Injury to the vessel thru varicose veins - Ie. Hypercoaguable states can be caused by combination birth control pill, not moving such as on a long plane ride - Most likely a familial component to these, b/c they run in the family

Answer 83

o Can occur in upper veins: like in the arms -Result of some kind of IV solution most often (usually due to acidic IV, like heparin; or hypertonic IV) o Can also occur in lower extremities: legs -Usually due to some type of trauma or varicose veins

Answer 84

- most often involves the lower extremities 1. popliteal V 2. superficial femoral V 3. iliofemoral V

Answer 85

- very insidious: ppl complain about cramping feeling that is slightly worse when walking - calf of leg may feel warm - kind of feels like growing pains - DO NOT massage legs, b/c can move clot up to lungs, brain and cause death - birth control and smoking can predispose you for these - put pt on anticoagulant therapy like heparin - can also happen acutely, such as if a patient is on a long flight-->sitting with legs in dependent position can cause hypercoaguable state - can lead to PE

Answer 86

- very acidic - short lived - anticoagulant

Answer 87

- refers to veins that are dilated or engorged - exact etiology unknown but probably something to do w/ structural weakness in walls of certain veins - tend to run in families - certain professions, like nursing predispose you - can't really tx but can wear compression socks to increase blood flow

Answer 88

- chronic obstructive pulmonary dz - common characteristic of 4-5 pathologies that all cause an increased resistance to air in the lungs, so difficult for air to move - ie. emphysema, asthma, bronchitis

Answer 89

- narrowing of the airways that causes shortness of breath - conduction pathways narrow for 3 reasons: 1. spasm 2. inc in mucosal edema: innermost mucosal lining is swollen 3. inc in mucus secretion

Answer 90

1. allergic: almost exclusively in children - Ag-Ab rxn - spasming occurs b/c histamine being released 2. idiopathic: unknown cause - most diagnosed in adults over 40 yo - not a good sign b/c usually a prelim to emphysema or chronic bronchitis 3. mixed: mixture of allergic and idiopathic - can identify some Ags causing the rxn but doesn't explain the whole presentation

Answer 91

Asthma attacks can kill you if block airways Particularly in asthmas that cause edema and inc in mucus-->secondary infection, so bacteria or viral infections occur in that mucus/edema-->pneumonia-->death sometimes

Answer 92

-can be acute or chronic

Answer 93

- bacterial or viral infection causes it | - can tx if bacterial or just let viral run its course

Answer 94

- inc in and hypertrophy o goblet cells which produce mucus - goblet cells are bigger and there is an increased number of them - this causes an excess amount of mucus, but the problem is that the excess mucus means that the pt is more prone to infection b/c easier for bacteria and virus to grow in thick mucus-->pneumonia-->death - etiological correlations: air pollution - coughing and creating more mucus - more common in urban areas

Answer 95

centrilobular panlobular

Answer 96

- selectively affects the respiratory bronchioles - everything distal to bronchioles (alveoli) are unaffected - more common in males - seldom seen in non smokers

Answer 97

- everything in gas exchange (alveolar ducts, sacs, individual alveoli) are all affected - there alveoli are swollen and rounded, so not as much surface area as a healthy alveoli

Answer 98

The respiratory bronchioles is the transition structure. It is part of the conduction system, but there are a few alveoli there so no gas exchange. Everything distal is totally involved in gas exchange. An emphysemic alveoli is rounded at the bottom. The normal has more bumps which increases surface area for gas exchange. Part of the problem with emphysema is that the alveoli get blown up and they're only 1 cell layer thick. If you rupture you can't replace it.

Answer 99

As we sit there breathing, two things help us breath: ◦ The change in gas pressures. The reason we inhale, the pressure in the gas in the lungs is lower than the gas in the room. (always go from high to low pressure) You inhale. When the pressure of the gas in the lungs is greater than the pressure in the room, you quit inhaling. ◦ Lungs have a stretchiness to them. We stretch the lungs out so the gas pressure is higher in the lungs than the room so there's a recoil effect. This recoil compresses your lungs and helps compress your alveoli so you now blow off the CO2.

Answer 100

Part of the reason you're breathing is CO2. Much more important than O2 for breathing. CO2 receptors in your aortic arch and great vessels of your neck (and also have O2 receptors there). They're monitoring CO2 and O2 levels as the blood goes past. They also have nerve fibers connected to your brain and your diaphragm.  Why can' t you hold your breath and kill yourself? ▪ The CO2 receptors are very sensitive to CO2. When your CO2 levels get high, they start firing in your brain and diaphragm causing your diaphragm to start moving which causes you to start breathing. ▪ Swimmers hyperventilate before swimming (blow off CO2 so they can hold their breath longer). If I blow off too much CO2 causes cerebral vessel dilation which means I'll pass out and drown. There's a fine line.  Found body in water and not sure if they drowned or not. Just look at their lungs. Thrown in water, will hold breathe as long as possible until CO2 gets up too high and then gasp and get water in your lungs. If dead when thrown in water, you've got no water in your lungs because you weren't breathing.

Answer 101

In emphysema patients, they lose the elasticity of their lungs so they can't passively expire. To exhale, they have to incorporate thoracic muscles that they don't normally use in order to expire. So, they forcibly expire. Consequently, the chest muscles hypertrophy. We talk about emphysemic patients has having a barrel chest (big chest because they constantly utilize thoracic muscles) they’re trying to produce enough spring effect on the lungs to compress the alveoli and get rid of CO2. It's not working very well because they don't have enough elasticity and the alveoli are blown up. So, these emphysemic patients will have high CO2 levels. ◦ CO2 Receptors have been firing like crazy trying to get their diaphragm and respiratory system to work, but their elasticity in their lungs don't work anymore so can't get rid of the CO2 very well. The receptors have given up, burned out.

Answer 102

We also have O2 receptors in the same locations and they also have nerve fibers that innervate the diaphragm and respiratory centers of the brain. But, the O2 sensors aren't nearly as sensitive to O2 as are CO2 sensors to CO2. Your O2 levels have to get very low before they start firing. ▪ You have very small amounts of free O2 floating in the bloodstream ▪ 97% of O2 is on RBC's ▪ The sensors are sensing the amount of O2 free floating. If most of your O2 is on RBC's, the O2 sensors don't have to be as sensitive. So the sensors don't start firing until the O2 levels are quite low. ▪ What's getting the emphysema patient's diaphragm to move is the fact that they're hypoxic. Their O2 levels are very low and they're relying on the O2 sensors and the hypoxia that they now have to keep them breathing.  Pt. has high CO2 levels and is hypoxic. ◦ You'd want to give them O2, but don't. They'll pink up, look good, and quit breathing. If you give them O2, the O2 receptors will quit firing. The CO2 receptors have already quit firing. Now you've given them O2 so the O2 receptors quit firing and they will stop breathing. Nothing tells the diaphragm to breath.

Answer 103

- characterized by chronic dilation and chronic inflammation of the bronchi and the bronchioles - usually a secondary infection to flu, bronchitis, etc. - most often seen with children - child comes in w/ a fever and coughing up 200 mL of nasty sputum - child has been coughing like this for 3-4 weeks and this was preceded by some kind of infection, but parents ignored it - the only way the lungs can deal with the infection is to create mucus to cough it up, but the thick mucus makes them more at risk for another infection-->pneumonia-->death

Answer 104

- 1/2000 births in white population - characterized by inc in the viscous like secretions of exocrine glands - saliva, sweat glands also affected but become very salty, so can do a salt test on this to dx - w/ viscous secretions, the kids predisposed to secondary infection-->pneumonia - secretions so thick, they will often be coughed up in shape of tube they came out of, and the mucus is so thick, that antibiotics can't get through them - often have to receive lung transplant - requires enormous sacrifice from parents - RECESSIVE: so if child is born with CF, encourage all siblings to be tested for gene - also would need to check your mate - kids present with failure to thrive, not gaining weight, not meeting milestones

Answer 105

–nothing wrong with lung tissue but have pulmonary problems anyway ◦ A very broad category. Lung tissue is fine, but something else is going on. The actual lung tissue has nothing wrong with it. Restrictive lung diseases restrict the lungs' volume. The lungs are unable to expand normally, diminishing the amount of gas that can be inspired.

Answer 106

- pt dies of respiratory failure but lungs fine - drugs: drug suppressed respiratory center of brain - ALS, Polio, Myasthenia Gravis

Answer 107

- "funneled chest:" - on a continuum - more common in males, especially if have Marfan's - most severe: lower end of sternum fused with thoracic spine - so chest is caved in - can't breathe properly so often die at birth

Answer 108

-see this in ppl who are morbidly obese They can't lay down because they can't breathe. ▪ If they lay down, their chest weighs so much they can't expand and contract their lungs. ▪ They have to let gravity help them. ▪ Even sitting up, it's difficult to move their lungs vertically. ▪ They're not taking in as much O2 and definitely not blowing off as much CO2. ▪ If you retain CO2, it makes you feel sleepy, which means you sleep a lot. ▪ Extremely obese people sleep a little and their CO2 is elevated because they can't blow it off. ▪ They DO always have sleep apnea

Answer 109

- often seen in Pickwickian pts - more common in males - correlated w/: being overweight, having a short/fat neck, in ppl who snore, HTN - tx: CPAP: forcing O2 under pressure into the lungs, so when they stop breathing, O2 levels don't drop and CO2 levels don't rise, so they can sleep - most severe: person is asleep, and then stop breathing for a certain length of time which causes CO2 to go up, and when CO2 goes up, the CO2 sensors fire and make you breath - always wakes you up, so do not sleep well

Answer 110

-have to do with the pleural space--pleural membrane really up against the lungs and pleural fluid that is oily is in that space, so this fluid allows the lungs to operate in a friction free environment o If you put something in that pleural space, you create pressure, so this fluid, air, blood, etc causes opposing pressure, so have to compete with that opposing pressure - So there is an increase in pressure in the pleural space, so when trying to fill alveoli, you have this pressure opposing it in the pleural space - Can't collapse an adult lung b/c they have surfactant in them - But in a premature infant, no surfactant, so when expire, you can completely collapse alveoli, so then need to exert more pressure to refill and expand the lungs □ This takes a lot of effort so this can lead them to stop breathing sometimes □ Now, we have synthetic surfactant, so you can inject this into the lungs, so then you don't have to worry as much about their respirations We would do this, b/c if person on free O2, its hard to control that from creating ROS, so also give vitamin E

Answer 111

fluid in pleural space; the pleural fluid holds the membrane and the lungs together. They resist being torn apart. When lung moves, it moves against pleural fluid. Does NOT cause lung compression/collapse

Answer 112

blood in pleural space

Answer 113

air in pleural space | -causes lung to collapse

Answer 114

–air in thorax that we are trapping in there (gas can get in but cannot get out); typically from some type of trauma so when inhale air comes into space (through injury or hole in membrane/space)…exhale the opening closes (like one way door) ▪ Leads to inability to aerate the lung ▪ Put in chest tube which drains air out and relives pressure -can occur due to trauma or spontaneously (often in tall, teenage males)

Answer 115

o It is an inflammation of the lungs due to anything that accumulates in the lung: bacteria, virus, mold, parasites, fungi But most commonly occurs due to bacteria and viruses

Answer 116

Typically present with a fever, an exudate, and consolidation on a chest film If you have a bacterial infection, a lot of WBCs come into the lungs to phagocytize, so then these accumulate and die there and cause pus, and this is what the radiologist will see on chest films Can occur from any type of bacteria, but most commonly caused by Strep The strep that causes pneumonia have a capsule around them, and the capsule protects the bacteria

Answer 117

□ Pneumonia vaccine for ppl with lung pathology or those over the age of 50 yo is a vaccine against Strep - In the vaccine, we pull the protein out of the capsule, and we administer that protein so the body produces an Ab ◊ So if that strep is produced, we have an Ab against the protein in the capsule, so the Ab interacts with that protein and puts holes in the capsule, so now WBCs have easy access to the bacteria that is in the capsule -So with the immunization, we are creating a condition which allows the body's immune system to deal with bacteria

Answer 118

- No WBCs response b/c they can't phagocytize viruses, so does not cause consolidation - More common than bacterial pneumonias - We are concerned about secondary infections with these - For example, secondary infection with a bacteria

Answer 119

-can be very bad -This is why we don't want the patient to lay on their back and vomit because they will aspirate into their lungs. -Bad for a couple of reasons: 1.  Brought up contents of stomach with a PH of 2. It's filled with microbes. 2.  The acid solution and bacteria are now in the lungs. The acidity is going to kill lung tissue (gangrenous lung tissue) . On top of dead, dying lung tissue we carry bacteria down there to grow. A perfect storm 3.  Extremely life-threatening. - seen with lake water and river water: w/ near drownings b/c aspirate water with bacteria in it - also seen with near drownings in chlorinated pools, b/c they are acidic and it kills lung tissue

Answer 120

-pneumonias that occur at the base of lungs - This is why you need to change positions and can't lay in same position for weeks - If don't deep breathe, cough, change positions, then this will cause this type of pneumonia □ b/c when this person hits the step down unit, we give them a spirometer-->makes them deep breathe to help prevent pneumonias - Often kills nursing home pts and elderly who are confined to the beds, b/c they can't aerate the base of the lungs

Test 2 Flashcards

(144 cards)