Unit 5b PDF - Cardiovascular Physiology

Overarching Goal #6 6. Describe the main factors that lead to a myocardial infarction and common drug therapies used to prevent and +eat it. Explain how each of the following are used to treat hypertension: Diuretics: Calcium Channel Blockers: - ↑ urine production...

Overarching Goal #6 6. Describe the main factors that lead to a myocardial infarction and common drug therapies used to prevent and +eat it. Explain how each of the following are used to treat hypertension: Diuretics: Calcium Channel Blockers: - ↑ urine production -inhibit catt entry into cells - sodium and water excretion - vasodilation (Blood vessels widen) - ↓ Blood volume - IHR - ICO - LBP - ↓ BP - ↓ peripheral resistance Beta Blockers: ACE inhibitors: - block beta-adrenergic receptors -inhibit conversion OF ANG 1 → ANG 2 - ↓ HR - lower levels OF ANG 2 = ↓ vasoconstriction - ↓ contractility - ↓ aldosterone secretion - ↓ CO - ↓ Blood volume - vasodilation - ↓BP - ↓ peripheral resistance ANG 2 Receptor Blockers - blocks effects OF ANG 2 - prevents vasoconstriction - ↓ aldosterone secretion - vasodilation - ↓ blood volume - ↓ peripheral resistance Explain how COX inhibitors and tissue plasminogen activators are used to reduce or prevent clotting - aspin and plavix reduce the clumping of platelets -TBA's C'' clot busters") break up clots that have already formed Define inotropic agent and explain how they are used in cardiovascular medicine - inotropic agents are drugs that can increase stroke volume  Consequences of myocardial infarction During heat failure, the heart cannot circulate enough blood at normal cardiac filling pressures to meet the metabolic needs of vital organs The body responds by releasing neurohormones, some can help maintain BP, but over time they cause heart failure to worsen Renin is released by kidneys in response to ↓ diffusion and ↑ sympathetic activity Renin activates the RAAS by splitting angiotensin ogen in the liver to produce ANG 1 which is then converted to ANG 2 by ACE ANG 2 binds to blood vessel walls, causing vasoconstriction ANG 2 also stimulates release of endothelin from endothelial cells ANG 2 and endothelin act on vascular smooth muscle causing constriction of the coronary arteries and systemic arteries and veins vasoconstriction causes the weakened heart to pump harder against ↑ resistance in the arteries constriction of the coronary arteries further compromises the myocardium supply of oxygen ANG 2 stimulates adrenal glands to release aldosterone which causes the kidneys to reabsorb sodium into the bloodstream and water w/ it. This causes a state of fluid overload that is worsened by venous constriction Gaseous exchange in the lungs is inhibited by pulmonary edema Buildup of fluid in and around the lungs ↑ breathing The body also release epinephrine and norepinephrine that ↑ HR and Muasoconstriction over time, chronic volume overload, ANG 2, aldosterone, and endothelin further myocardial injury and escalate heart failure fortunately, additional neuro hormonal response modulate the activity of the RAAS and endothelin and EPI/NOEPI  Overarching Goal #6 6. Describe the main factors that lead to a myocardial infarction and common drug therapies used to prevent and treat it. Describe the process leading up to a myocardial infarction, starting w/ a blocked coronary artery and finishing w/ programmed cell death in myocardial pumping cells. - a blood clot breaking loose in the BV travels to a coronary artery blocks the blood flow to part off the heart muscle is called myocardial infarction. - lipoproteins are used to transport triglycerides and cholesterol in the blood - However, too many low density lipoproteins circulating the blood increase the risk for developing atherosclerosis → which can result in the formation of blood clots -Too much low density lipoproteins end up accumulating underneath the endothelial cells - macrophages (immune system cells) ingest the cholesterol and get converted into a foam cell -The foam cells start secreting a paracrine signal that results in mitosis of smooth muscle cells - the smooth muscle cells take up the cholesterol and then a fatty streak forms - the smooth muscle cells begin to divide even more b/c the bulge in the lumen creates an area of locally higher pressure which becomes a risk for bursting the blood vessel - so to reinforce the blood vessel, the smooth muscle cells multiply and we get calcification inside the lipid core -this is a stable plague, and since the diameter of the lumen is narrower so there's not a lot of room for blood to flow → ↑ BP -if this process continues we end up with an unstable plaque and the plaque can burst open and the blood gets exposed to colloger - then the platelets get exposed to college then a blood clot forms → ↑ MAP - if a clot breaks loose it can travel to a coronary artery and block it - the pumping cells become starved for oxygen and nutrients and b/c they can make ATP by oxidative phosphorylation, they undergo anaerobic glycolysis and acculumate lactic acid → ↓PH - w 10 ATP being made, the CattATP that pump Catt from cytosol back into SR or out of cell, stops functioning and cat levels in cytosol increase - ↑ PH and ↑ cat cause gap junctions to close - AP's can no longer travel b/w myocardial cells - this leads to apoptosis (programmed cell death) - myocardial cells die and the contents of those cells end up being spilled into the blood b/c cells break open - you should never have any cardiac enzymes/proteins in your blood b/c cardiac muscle can't be repaired Describe how death of pumping cells can affer heart rhythm and cardiac output - ↓ contraction - ICO Explain how congestive heart failure occurs Right-sided Heart Failure - backup of blood to body - ↓ amount of blood to lungs - veins bulge - edema Left-sided Heart Failure - ↓ amount of blood to the body - ↓ pulses - backup of blood to the lungs - hard time breathing Treatment ⊕ inotropes - Digoxin → makes heart squeeze stronger → heart slows down  H e m o s t a s is A s p iri n = C O X i n h ib it o r - re d u ce p la te l e t clu m p in g c o a g u l a t ion ,c a d e p la t e le t p lu g T X A , ↳ s t a b le f ib ri n c lo t - 1) T h r o m b in F ib rin o g e n F ib rin T h ro m b i n p l a s m in p la s m in o g e n T B A 's ↳ clo t b u st e r ↑ d is s o lv e s f ib ri n d ru g s w e h a v e a p la te le t p lu g t h a t is a c tiv a t e d w h e n p la te le t s a re e x p o se d to c o lla g en t h e y s e c re t e a p a r a c ri n e s i g n a l , t h r o m b o x a n e s , t h a t a t tra ct m o re p l a t e le t s t o f o rm a p l a t e le t p l u g T h e p l a te le t p lu g b e c o m e s re in f o rc e d a n d s t a b il i z e d b y f i b r i n , w h ic h is p ro d u c e d f ro m f ib r i n o g e n w h e n t h ro m b i n c o n v e r t s i t t o f ib r i n T h r o m b in is p ro d u c e d a t t h e e n d o f t h e c o a g u la t io n c a s c a d e T h ro m b in a ls o co n v e rt s p la s m in o g en t o p la sm in p la sm in is im p o rt a nt f o r d is so lvi n g t h e f i b ri n c lo t s s y n t h e t i c t i s s u e p l a s m i n o g e n a c t i v a t o r s a r e im p o r t a n t b /c t h e y c a n b e g iv en t o v i c t i m s o f a h e a rt a t t a ck t o d is s o l v e t h e c l o t b e f o re it c a u se s t o o m u c h d a m a g e d o w n s tr e a m → T B A 's a re re f e r re d t o a s " c lu t b u s t e r d ru g s " p e o p le c a n t a k e a s p irin w h e n t h e y a re a t ri s k o f d e v e lo p i n g b l o o d c l o t s b /c a s p i r i n is a C O X in h ib ito r w h ic h i n h i b it s T X A , a n d i n h i b it s p l a te le t p lu g s f ro m f o r m in g  O v e r a r c h in g G o a l # 5 5. E x p la in w h y h e m o c rit a n d p l a s m a co m p o s iti o n a r e h o m e o s t a t i c a lly r e g u l a t e d v a ria b le s a n d d e s c rib e h o w clo t s f o rm D e s c r i b e t h e c o m p o s it i o n o f b l o o d w / r e s p e c t t o t h e ce llu l a r e le m e n t s a n d n o r m a l c o m p o s it i o n o f p l a s m a - B l o o d h a s p l a s m a t h a t c o n t a in s d i s s o l v e d n u t rie n t s , h o r m o n e s , i o n s , g a s e s , p ro t e in s , e t c. a n d a c e llu la r p o r t io n D e f in e h e m a t o c r it D e s c rib e h o w a n d w h y t h e co n c e nt ra t i o n of R B C is re g u l a te d b y e r y t h r o p o ie ti n - e r y t h ro p o ie t in ( E P O ) t ra v e l s t o r e c e p t o r s in t h e b o n e m a rro w a n d c a u s e s t h e s y n t h e s is o f m o r e R B C E x p l a i n w h y p l a s m a o s m o l a ri t y i s r e g u l a t e d + p r e d ic t t h e e f f e c t of a b n o r m a l l y h i g h o r l o w o s m o l a rit y o n c e l lu la r e l e m e n t s o f b l o o d - p l a s m a o s m o l a r it y i s r e g u l a t e d t o e n s u r e p r o p e r p r o t e in f u n c t i o n a n d t o m a in t a in t h e p ro p e r s h a p e a n d f u n c t io n o f R B C 's - h y p e r t o n i c p l a s m a = R B C t o s h r in k - h y p o t o n i c p l a s m a = R B C 's t o s w e l l E x p lain co m m o n c a u se s o f j a un d ic e - t h e y a re n o t p ro c e s s in g h e m o g lo b in m e t a b o lit e s e f f ic ie r t y  Overarching Goal #4 4. Describe the factors that can cause local and systemic edema Explain how lymphatic fluid is formed - about 20 L of fluid leak from blood capillaries into surrounding tissue each day due to BP - around 17 L of the fluid is reabsorbed back into the capillaries - the remaining 3 L enter lymphatic capillaries, forming lymphatic fluid - the lymph is then transported through the lymphatic system and eventually returned to the blood stream at the veins. Describe the effect that high MAP, histamine, disturbances to normal protein gradients, liver disease, and parasites have on formation of lymphati fluid - if you have problems w/ your liver that will affect the amount of protein that is made in liver and could disrupt the osmotic balance - if you have abnormally low protein content in your plasma then you won't be able to pull as much fluid back → you will end up losing too much fluid to the interstitial fluid → you can end up looking swollen and puffy -edema -if your hydrostatic pressure is too high you can end up squeezing more fluid out → end up causing edema 1) High Map: increases the pressure in BV leading to more fluid leaking into tissues - will ↑ lymphatic fluid formation - edema 2) Histamine: causes BV to dilate + become more permeable, allowing more fluid to escape into tissues ↑ lymphatic fluid - edema 3) Parasites: can block lymphatic drainage which can lead to fluid buildup and edema.  o t id / K id h e y a p a rt F o rt ic B a ro r e ce p to rs ↑ re n in H V P H T M PP G C C ↑ c o n t ra ct. n + D H ↑ s y m p v a sc u l a r s m o o t h m u s c le ↑ A I p a r a sy m p A R c e lls # H R P u m p in g c e l l s ↑ a l s t e ro n e ↑ f o r ce o f n t ra c t io n w a te r c o n se rv a t io n b y k id n e y  O v e r a r c h i n g G o a l # 3 3. D e f i n e M A P + d e s c ri b e t h e f a c t o r s t h a t in f l u e n c e it u sin g a h o m e o s t a s is lo o p D e fin e M A P : - M A P ( m e a n a r t e ri a l p r e s s u r e ) i s t h e a v e ra g e p r e s s u re in t h e b lo o d v e s se l s c a u se d b y c o n t r a c t io n o f t h e v e n t r ic le s D e s c ri b e t h e p r e s s u r e c h a n g e s t h a t o cc u r in t h e c ir c u l a t o ry s y st e m f r o m t h e a o rt a b a c k t o t h e r ig h t a t ri u m - B P d e c re a s e s p ro g r e s s iv e l y f r o m t h e a o rt a t o t h e R A - p r e s s u re i n t h e a r t e r i a l s i d e o f t h e c ir c u l a t io n c y cl e s b u t t h e p r e s s u r e w a v e s d i m i n i s h i n a p t it u d e w / d i s t a n c e a n d d is a p p e a r a t t h e c a p i ll a ri e s c o m p a re + c o n t r a s t : a r t e ri e s , a r t e rio l e s , c a p il l a r i e s , v e n u l e s a n d v e in s A r t e ri e s : - c a r ry o x y g e n a te d b lo o d A W A Y f ro m h e a rt - t h ic k , m u s c u l a r w a ll s t o w it h s t a n d h ig h p re s s u re → e l a s t ic t o a c c o m m o d a te p u m p i n g A r t e ri o l e s : - s m a lle r b r a n ch e s o f a r t e ri e s t h a t le a d t o c a p illa rie s → h el p r e g u l a te b lo o d flo w a n d p re s su re - t h i n n e r w a ll s t h a n a rt e r i e s → h a v e s m o o t h m u s cle t o c o n t ro l d ia m e t e r C a p il l a ri e s : - s ite of n u t rie n t a n d g a s e x c h a n g e b /w b lo o d a n d t is s u e s - v e ry t h in w a lls t o a llo w e a s y e x ch a n g e V e n u le s : - c o lle c t d e o x y g en a te d b lo o d f r o m c a p i l l a ri e s t o t r a n s p o r t t o v e in s - s m a ll , t h in w a ll e d v e ss e ls t h a t g a th e r b lo o d v e in s : - c a r ry d e o x y g en a te d b loo d B A C K t o t h e h e a rt - t h i n n e r w a l l s t h a n a r t e ri e s → h a v e v a l u e s t o p r e v e n t b a c k f lo w a r t e ri e s c a rr y b lo o d A W A Y fro m h e a rt , w h ile v e in s c a r r y it B A C K a r t e ri e s h a v e H I G H p r e s s u r e , v e in s h a v e L O W p re s su re a rt e rie s h a v e t h in w a lls ; v e in s h a v e t h ic k w a ll s D e s c rib e t h e v a ri a b l e s t h a t i n f l u e n c e t o t a l p e r ip h e r a l r e s i s t a n c e - T P R = r e s is t a n c e b lo o d e n co u n t e rs a s it f lo w s t h ro u g h v e sse ls 1 ) v e s se l d ia m e t e r : → w id e r = le s s r e s is t a n c e → n a rr o w e r = m o r e r e s is t a n ce 2 ) B l o o d v i s c o s it y : → t h ic k e r b l o o d = m o re r e sis t a n ce 3 ) V e sse l le n g t h : → lo n g e r v e s se ls = m o re r e s is t a n c e 4 ) v a s o c o n s t ri c t io n /v a s o d i l a t i o n : → c o n s t ric t io n = ↑ r e s is t a n c e → r e la x a t io n = t r e s is t a n c e E x p l a in r e l a t io n s h ip b /w s t a te o f c o n t r a c t io n of B V a n d C a tt le v e l s in cy t o s o l - C a tt in cy t o s o l t rig g ers c o n t r a c t io n o f s m oot h m u scle c e lls in b lo o d v e s s e ls → le a d in g t o in c r e a se d T P R - w h e n C a tt le v e l s d e c r e a s e , m u s c l e s r e la x c a u s e d v a s o d il a t io n a n d r e d u c e d T P R  Sensors Baroreceptors Heart derror signals" carotid artery Aortic arch afferent Integrating Center(s) Kidney CNS Controlled variable ↓ Trenin ANG ACE CVCC ↓ MAP angio­ (in medulla tensinogen HT/PPG oblegata) +NG 11 ↑thirst vascular circular smooth muscle ↑ AD ↑symp ↑ Peripheral vasoconstriction (vasopressin) output SA Node α-adrenergic (ar cells) MAP ↑HR Myocardial pumping cells Effectors Adjet ↑SV ↑ aldosterone kidney ↑ water conservation  Pr- Net outflow of 32/ day Pr- Pr- Pr- Pr- Pr- Pr- r- Pr protein ↑ Pr- (made in liver) plasma osmolarity is greater than ISF osmolarity Hydrostatic P from heart → fluid leaves Edema = swelling blood -if you have any problems w/ your liver that will affect the amount of colloid (osmotic pressure) protein that is made in the liver and could disrupt the osmotic balance pulls fluid back into blood → - abnormally low protein  Vasodilation 1) EPI/NE binds to B-adrenergic Rs 2) ↓ in agood stuff"CO2, glucose) 3) ↑ ANP 4) ↑ in"bad stuff" (CO2, H+, K+) 5) ↑ in histamine 6) ↑ in nitric oxide Vasoconstriction 1) ↑ ADH/vasopresin 2) ↑ EPI INE → alpha-adrenergic R's 3) ↑ [good stuff] 4) ↓ [bad Stuff] 5) ↑ ANGII