Nursing 3366 Pathologic Processes: Disorders of the Circulatory System PDF

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Circulatory System Objectives /outcomes: DESCRIBE/DISCUSS/IDENTIFY: 1. influences upon and results of appropriate, forward, effective, oxygenated blood flow through...

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Circulatory System Objectives /outcomes: DESCRIBE/DISCUSS/IDENTIFY: 1. influences upon and results of appropriate, forward, effective, oxygenated blood flow through the heart and peripheral system, such as normal cardiac structure, cardiac cycle, cardiac output, preload, afterload, contractility, neuroelectrical status of the heart, status of peripheral vessels, perfusion of tissues. 2. relationship between derangements of the above structural and hemodynamic processes and the etiological factors, clinical manifestations, diagnostics, and basic treatment modalities of disorders such as: arteriosclerosis and atherosclerosis peripheral arterial disease venous disorders hypertension coronary artery disease stable angina and acute coronary syndrome valvular disorders heart failure Download & print the “CONCEPT MAP: FACTORS INFLUENCING HEART FUNCTION” cardiogenic shock and the “PICTURE OF HEART” for the A&P review lecture *************** Outline I. Overview of circulatory system A. Repeating some key overarching concepts B. Basic A&P review of heart 1. Medical Vernacular 2. Potentially confusing terms C. More complex A&P review: factors influencing cardiac function II. Venous disorders A. A&P of veins B. Peripheral venous disorders C. Treatment, nursing implications of venous problems III. Arterial disorders A. A&P of arteries B. Pathogenesis of arterial disorders C. Specific arterial diseases D. Treatment, nursing implications, of arterial problems IV. Alterations in the function of the heart. A. Pathologic changes affecting cardiac function B. Coronary artery disease (CAD) C. Other heart problems / disorders 1. valvular disorders 2. heart failure (HF) 3. cardiogenic shock ************************************* PLEASE NOTE IMPORTANT INFO INFO BELOW  2 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ THE NEXT INFORMATION BETWEEN THE SQUIGGLY LINES (pgs 2- 6) WILL BE LECTURED UPON IN “A&P REVIEW” MATERIAL. THIS CONTENT IS COMPLEX ENOUGH TO NEED EXTRA STUDY & DISCUSSION IN PREPARATION FOR THE PATHO LECTURE. I. Overview of the circulatory system A. Repeating some key overarching concepts: 1. get used to “reversing mirror image” when thinking of right & left sides of body 2. when it comes to concepts re: the heart & blood flow to and from it: a. think of right side of heart as venous side-- DEOXYGENATED flow is coming “in” from all the veins & tissues in the body b. think of left side of heart as arterial side—OXYGENATED flow is going “out” via aorta to all arteries & tissues in body. 3. “forward flow” is normal; various pathologies can cause “back-up” of flow; KNOW THE BASIC PATH OF BLOOD (FORWARDS AND BACKWARDS): Right atrium→tricuspid valve→ right ventricle→pulmonic valve→pulmonary artery →pulmonary arterioles→pulmonary capillaries [gas exchange with alveoli occurs here]→ pulmonary venules→ pulmonary veins→left atrium→mitral valve→left ventricle →aortic valve →aorta part of this freshly oxygenated blood goes into coronary arteries, which branch off the aorta just beyond the aortic valve & feed heart. part goes up to brain tissue via carotids rest goes to tissue beds of remainder of body →arterioles of tissues→capillaries [gas exchange with tissue occurs here] →venules →veins→inferior vena cava (from body) or superior vena cava (from head) →right atrium arteries— oxygenated blood out and away from heart  3 B. Basic A&P review of heart 1. medical vernacular a. in describing heart A&P and/or disease processes & their characteristics, sometimes use terms “right heart” and “left heart” b. “right heart” = right atrium (RA) & right ventricle (RV) & valves; “left heart” = left atrium (LA) & left ventricle (LV) & valves. c. also, “chambers” of the heart = LA, LV, RA, RV. d. “receiving” chambers or arteries = blood is coming in from elsewhere; ex: the systemic arterial system (aorta, etc) receives blood from the LV, whereas the pulmonary arterial system (pulmonary artery, etc) receives blood from the RV; the RV is the receiving chamber of blood from the RA, the LV is the receiving chamber from the LA, etc. 1. Be sure you know the flow through the Video of flow: heart—from right to left, including names of http://www.nlm.nih.gov/ aorta chambers, valves, and vessels, as well as medlineplus/ency/anato when the blood is oxygenated vs myvideos/000012.htm deoxygenated. Then be sure you can also plot the flow going backwards—left to right, such as what happens in heart failure. 2. Quick review of heart cycle (see prep for Lungs more): Pulm 1) just prior to systolic ejection of blood, the tricuspid & mitral valves (AV valves) veins SVC have been open while the ventricles fill with fluid; as systole begins, these valves close while the pulmonic & aortic valves open— video of conduction: PA the closing sound of the AV valves makes http://www.nlm.nih.gov RA L “lub” sound of “lub-dub.” /medlineplus/ency/anat 2) the “dub” sound is made as the A R L omyvideos/000021.htm pulmonic & aortic valves close and is the beginning of diastole—the ventricles are beginning to fill right after the “dub.” V V IVC 3) each time this happens is considered one heartbeat, or one “stroke” of the heart. Remember, blood in veins is almost always deoxygenated & blood in arteries is almost always oxygenated; EXCEPTION: a. the only arterial vessels in the body that carry deoxygenated blood are the pulmonary artery and arterioles (the deoxygenated blood travels via pulmonary artery to pulmonary arterioles to pulmonary capillaries, where CO2 diffuses out of the capillaries & into alveoli & is exhaled.) b. the only venous vessels that carry oxygenated blood are the pulmonary venules and veins (the pulmonary capillaries around the alveoli receive oxygenated blood, which travels to the pulmonary venules, then the pulmonary veins, then the left atrium). 2. Potentially confusing terms a. “cardiovascular” most of the time used to refer to heart & its vessels, especially when used to describe disease processes. b. “peripheral vascular” most of time used to describe vessels outside the heart, especially when used to describe disease processes. c. “circulatory system” often used to describe cardiovascular & peripheral vascular systems together  4 d. “central” vs. “peripheral:” 1. general term “central” —usually used to refer to heart, lungs, brain, kidneys– the most crucial areas of the body 2. general term “peripheral” or “periphery”—usually used to refer to anything outside the heart, lungs, brain, kidneys; example—peripheral vessels of arms & legs. 3. uses of these terms sometimes depend on context C. More complex A&P review: factors influencing cardiac function 1. overview of cardiac output (CO) a. the goal of electrical and mechanical functions of heart is to create effective remember, stroke volume, cardiac output (CO) SV, is amt of b. CO is the average amount of blood the LV ejects (and is therefore in blood ejected per beat) circulation) per minute; normal = 4-6L/min c. it can be determined by the formula HR X SV (ex: 80 beats/min X 70 ml / beat = 5600 ml = 5.6 liters/min.) d. clinically we link good CO with S&S of good perfusion—normal BP, pulses, capillary refill, mentation, and skin color & warmth. e. NOTE: good CO is only one part of good perfusion; remember, the other part is having healthy arteries (good vasomotor tone & patent lumen) f. if HR X SV = cardiac output = cardiac output can improve or deteriorate by: 1) changes in HR (and rhythm) and/or will discuss 2) changes in SV, which itself is affected by 3 conditions: normals only here, a) contractility of the cardiac muscles (pump action) then go over patho in class b) preload (blood return to the heart) c) afterload (arterial resistance to cardiac blood flow) 2. HR A) Electrical properties of heart—heart rate & rhythm 1) by placing specialized patches on the skin that act as negative and See Concept positive poles, the electrical pathway that generates cardiac map: FACTORS INFLUENCING contractions can be captured in the form of an electrocardiogram CARDIAC (EKG, AKA ECG) FUNCTION 2) each configuration represents the depolarization and contraction of each part of the heart a) P wave—atrial depolarization b) QRS complex—ventricular depolarization FYI c) T wave— ventricular repolarization d) ST = time interval between end of ventricular depolarization (S) & repolarization (T) know this range 3) the rate of impulses generated by the SA node & traveling throughout the heart is called heart rate; normal is 60-100 impulses/ minute, but since each impulse generates a contraction or “beat” of the heart, we say “beats/minute.” 4) if all is normal & healthy, these impulses proceed in a consistent, regular pattern of PQRST– this is called having a normal rate and rhythm-- normal sinus rhythm (NSR or just SR).  5 5) the HR is normally about 60-100 beats / minute, though sometimes speeding up or slowing down is considered “normal” when occurring appropriately, such as when running (increases) or sleeping (decreases) 6) we will discuss abnormalities in class. B). Relationship of electrical and mechanical properties of the heart-- heart cycle (see side bars & prep) (NOTE: “SA”-= 1) systole sinoatrial. “Sino” a) this is the part of heart cycle in which RV & LV are contracting & comes from the word ejecting blood from their chambers into the pulmonary artery “sinus;” the SA node is and the aorta, respectively. near a venous sinus near the right atrium.) b) it occurs between the “lub” (closure of AV valves) and the “dub” (closure of pulmonic & aortic valves) c) begins with electrical signal generated by SA node→ spreads synonyms: “heartbeat,” “beat,” “ventricular throughout atria to AV node to ventricles; as each cardiac contraction,” “systole.” muscle cell receives an electrical signal, it depolarizes and contracts IMPORTANT: don’t confuse term d) this results in ventricular contraction & simultaneous ejection “stroke” in “stroke volume” with the of blood from right ventricle into pulmonary vasculature & left term used to describe a brain problem, ie, “having a stroke.” In ventricle into systemic vasculature. heart-related issues, think “heart c) the amount of blood ejected PER CONTRACTION-- ie, during beat” and “ventricular contractions” every systole-- is called stroke volume (SV) & the average in association with “stroke.” amount is ~70ml/beat. (sort of a “constant” number) 2) diastole (the part of heart cycle in which RV & LV are receiving blood from RA & LA = filling with blood) 3. stroke volume: a. SV is the ability of the heart to eject ~70 ml (average normal amt) of bloodper beat is contingent upon the status of 3 factors: preload, contractility, and afterload. b. preload -- what comes to the ventricles before contraction. VOLUME 1) heart muscle is like a rubber band—the more it is stretched (up to a certain point), the better it will contract (Frank-Starling law). 2) this stretch is accomplished in the heart through filling of the ventricles with blood--therefore, preload is related to the volume of blood in the ventricles before contraction. 3) preload is considered normal when there is a normal amount of blood in circulation.  6 c. contractility 1) if all is normal & healthy with the cardiac muscle, it is said to have PUMP good contractility (good contractility = good “pump”) ACTION 2) the property of contractility includes how well the cardiomyocytes respond to electrical signals (PQRST) and contract —ie, how efficiently the cardiac cells are working together to eject blood, how “toned” the heart muscle is. 3) inotropic—an adjective used to describe effect of different factors on contractility a) “positive inotropic effect” = something that enhances contractility of the heart b) “negative inotropic effect = something that decreases contractility of the heart d. afterload -- any form of resistance to ejection of blood from a heart chamber; ie, resistance to forward flow of blood. 1) a certain amount of afterload, or resistance, is normal; normal afterload exists when the receiving arteries have: RESISTANCE a) normal vasomotor tone, that is, the arterial walls have a to forward flow muscle tone which is flexible, compliant, not too constricted, not too dilated—“just right” b) their linings are smooth & patent 2) each chamber of the heart has its own normal afterload (we will just concentrate on afterload for LV & RV): a) normal RV afterload = (1) normal status of pulmonary artery & its branches throughout the lungs. (2) this is called pulmonary vascular resistance (PVR). b) normal LV afterload = (1) normal status of aorta & rest of systemic arterial system. (2) this is called systemic vascular resistance (SVR) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ KNOW THE BASIC PATH OF BLOOD (FORWARDS AND BACKWARDS) a. See A&P review above. b. parts II & III of this lecture mostly focus on issues of flow outside the heart, or peripheral flow: aorta→major arteries in legs (ileac, femoral, popliteal)→ pedal arteries (D.P. & P.T.)→arterioles of tissue beds of legs and feet →capillary beds [gas exchange here: O2 from blood to tissue, CO2 from tissue to blood]→venules→ veins of feet & legs→ inferior vena cava.  7 veins— arteries— deoxygenated oxygenated blood in and blood out and towards the away from heart (north heart (south bound-mostly) bound-mostly) II. Venous disorders A. A&P of veins 1. veins are thin-walled vessels that take deoxygenated blood from tissue beds all over the body back to the right side of the heart. 2. this flow back to the heart is often called “venous return” and also sometimes called “venous drainage of tissues.” a. proper-functioning valves in leg veins: 3. conditions that leg veins have numerous valves which work facilitate good venous return like this: (i.e., good drainage of body’s tissues) 1) during systole, when blood is being and pushed into arteries by the heart, the prevent backflow systolic pressure is also helping to push venous blood back towards the (ie, prevent gravity from pulling blood heart; vein valves in the legs are downwards, away from normal return OPEN during this time. to heart) 2) during diastole, the leg vein valves include: CLOSE so that blood doesn’t back flow & succumb to gravity. (Arm veins & most other veins in the body have b. well-toned, working muscle tissue around the valves as well, but since there is not such a gravity problem to fight against, it is not as common to have veins which “massage” the veins, helping to venous disease in the arms; thus we will be direct flow towards the heart during systole concentrating on LEG vein disease.) and also helping to prevent backflow during diastole. Important note: don’t confuse the valves in the veins with the valves in the heart—two very different entities.  8 B. Peripheral venous disorders: chronic venous insufficiency & DVT 1. overview of venous problems a. most venous disorders occur in the legs and usually have to do with some degree of failure to keep entire amount of venous blood flowing in its proper direction—that is upward, towards the heart b. as a result, some venous blood tends to stay and settle out in the veins of the leg and foot tissues—this is known as venous congestion (think of CONGESTION of peripheral tissues when you think of venous issues). c. factors contributing to venous congestion include: 1) gravity “winning” a) ex-- simply being on one’s feet too long can cause gravity to pull fluid downward into distal leg tissues. b) unless severe, this is a type of venous congestion that is “within normal experience”—ie, not necessarily a pathologic process c) increased hydrostatic pressure can also cause such backflow pressures to surface veins that they can become twisted & distorted– varicose veins; these are not usually a health hazard but can become painful and cosmetically distressing to your patients. 2) valve incompetence-- when this is the problem, a pathology is involved, and the disorder is called venous insufficiency. 2. chronic venous insufficiency (CVI) a. pathogenesis / S&S: 1) CVI is most often caused by leg vein valves wearing out and becoming “floppy”—they don’t close tightly during diastole, allowing backflow into distal review of hydrostatic veins of legs & feet (venous congestion) pressure in blood vessels: force 2) this congestion can be pictured as a pool of non-moving blood in the veins exerted by a fluid this is called venous stasis and results in increased hydrostatic pressure (blood) against the wall of the vessel. inside the affected veins. 3) this increased pressure pushes fluid into tissues of legs and feet, causing edema in the affected area a) the edema causes mild to moderate discomfort, but over time can also Mini summary concept map: cause dry, tight skin, often with brownish discolorations Floppy valves→ increased hydrostatic pressure distal to the bad valves because venous blood b) sometimes the area becomes so engorged with edema that the skin can’t return up to heart properly→ engorged peripheral veins→ pushes cells cannot function properly & the tissue easily breaks down fluid out to tissues→ edema. (especially over bony prominences such as heels, ankles, coccyx), Edema essentially causes the main S&S of CVI: swollen, tight, dry, causing venous stasis ulcers. discolored skin which can easily get traumatized & ulcerated. (FYI: remember in assessing & caring for your patients that there are many causes of edema—it may be caused by venous insufficiency, but not always; other disease processes cause edema too; ex—hypoosmolar problems, HTN, right -sided heart failure, kidney disease, an injury, lymphatic problems, etc…many of these processes have been covered or will be covered in the course.)  9 b. contributing factors to development of CVI: 1) aging, inherited predisposition, obesity, sometimes pregnancy (especially multiple), and job-related issues (such as years of standing). AND/OR 2) lack of assistance from musculature, such as when there is poor muscle tone due to immobility and/or inactivity. 3. DVT_—deep vein thrombosis a. a DVT is a clot that develops on the wall of a vein, most of the time in deep veins (not usually surface veins) of thighs & calves 1) once DVT develops, the vein and entire area around vein can become inflamed & swollen 2) this is called thrombophlebitis (“thrombo”—blood clot; “phleb” means “having something to do with veins”) 3) S&S a) local redness, pain, warmth, edema (ie, inflammatory signs) b) usually seen only unilaterally (in one leg) c) can be extreme or hardly noticeable d) also, may have no S&S at all. b. those at highest risk for DVT: 1) have one or more elements of Virchow’s triad; this is the classic triad of: a) injury to endothelium of vein b) stasis of blood flow (1) this can be from an underlying venous disorder such as CVI and/or (2) inactivity of the muscles surrounding the veins (more on this further on…) c) hypercoagulability states (1) most often hypercoagulability is caused by some degree of dehydration (if there is less water in the blood, blood is more concentrated, so clotting factors & platelets can “find each other” more easily to cause pathologic clotting) (2) but can also be due to individual tendencies to clot more easily -- these tendencies are a type of coagulopathy 2) summary of situations in which one or more elements of Virchow’s triad is present; people who: a) sit a lot or for long periods (“desk jockeys,” airline travelers, couch potatoes) b) have casts or other immobilizing devices on legs c) are bed-ridden or wheelchair-bound d) are pregnant e) are obese f) are on medications such as: (1) diuretics (can cause dehydration) (2) certain hormone therapy like BCPs (estrogen can increase the levels of certain clotting factors) g) have pre-existing problems such as circulation issues (eg, CVI) and/or clotting problems and/or recent surgery  10 c. possible DANGEROUS sequela of DVT: PE—pulmonary embolus 1) if thrombus or part of one break free from an existing DVT, it can then become a venous embolus; understanding circulatory flow, here is the usual pattern of travel: DVT of leg→ IVC→ RA→RV→PA→usually gets stuck in tiny pulmonary arterioles 2) 30% of people with DVT develop PE 3) S&S – chest pain, SOB, hemoptysis (blood in sputum), shock (low blood pressure) Mini concept map linking patho S&S of PE: Embolus enters pulmonary artery→ smaller arterioles→ embolus gets stuck →blocks deoxygenated venous blood from getting to alveoli to get oxygenated→ SOB →irritates arterial intima→ inflammation→ leakage of blood into lung tissue→ hemoptysis →if large enough portion of lung tissue inflamed→ massive release of inflammatory mediators → systemic vasodilation → shock (low blood pressure) FYI; Because of the potential for death from a PE, ALL hospitalized patients must be evaluated for DVT risk within 24 hours of their hospital admission. If considered at risk, anticoagulants will be administered to ensure prevention of DVT formation. CTQ (critical thinking question) - How is “at risk” determined? Virchow’s Triad C. Treatment, nursing implications of venous problems: 1. encourage mobility in ALL patients—get your patients moving! Also, devices used on patient’s legs to keep strong muscle tone around veins. 2. encourage hydration during periods of immobility (DVT prevention). 3. elevate legs / feet… why? Promotes venous return back to the heart. _____ 4. be careful of skin breaks—swelling / edema increases risk of skin integrity compromise 5. sometimes blood thinners like Heparin & / or Coumadin or sometimes just aspirin are used to prevent more clotting III. Arterial disorders A. A&P of arteries 1. arteries are thick-walled, muscled vessels that accept oxygenated blood from the heart and circulate it to tissue beds all over the body. 2. the ability of arteries to work efficiently in maintaining flow of oxygenated blood from heart to tissues is greatly determined by the muscle tone of their walls and the state of their lumens. a. muscle tone of arterial wall —AKA vasomotor tone 1) part of arterial walls are made of muscle cells/fibers which respond to various influences and needs of the body 2) these muscular elements can constrict and dilate the artery as needed, and in general, maintain a certain muscle tone to the vessel 3) arteries with a normal, good muscle tone are flexible, compliant, not too constricted, not too dilated— “just right.” 4) having a good blood pressure (BP) is often dependent on having this “just right” vasomotor of the arteries b. state of lumen—healthy lumen lining is smooth & patent (open) – ie, free of blockage of any sort, so forward blood flow is smooth, uninterrupted.  11 3. the above two components (GOOD VASOMOTOR TONE and PATENT LUMEN) contribute to good perfusion (oxygenation) of distal tissues a. perfusion is process of delivery of oxygen and nutrients via arterial system to tissue beds all over body. think “O2 delivery” when you think of perfusion b. good or bad perfusion results in good or bad tissue oxygenation & is determined by cardiac output (discussed later) & other factors such as state of arterial vessels (ie, do the arteries have good vasomotor tone & patent lumens?). c. S&S that are usually associated with good perfusion (ie, desired findings upon assessment) 1) DESIRED BP range is ~ 110/60 to 115/70 (“normal” is under 120/80) BP facts to understand: Blood pressure (BP) is simply a measurement of fluid pressure in the tubes that are called arteries, or arterial system. Blood “pressure” is the force exerted against the walls of the arteries by the blood passing through them. BP is determined by how much resistance there is in the arteries (a more “elastic/stretchy” artery will offer less resistance). 1) systolic pressure is the pressure in the arteries that is exerted when the heart is contracting and ejecting blood out to the arteries (systole) 2) diastolic pressure is the pressure existing in the arteries when the heart is between systoles, or “filling” (not moving blood around-some call it “resting”) (diastole) BP is measured by using an arm cuff & a sphygmomanometer --a machine that shows pressure in mm of mercury (Hg) as it rises or goes down: 1) when a blood pressure cuff is pumped up around the arm, it occludes the artery in that arm (brachial artery); as the pressure is released, the pressure at which the first sound is heard is the pressure in the arteries during systole in mm of Hg. 2) when the cuff pressure continues to go down and becomes less than the diastolic pressure, no pulse is heard; thus, when the sounds stop, the cuff pressure at that point indicates the pressure in the arteries during diastole The measurement is expressed as systolic pressure over diastolic pressure. Desired range is 110/60 to 115/70 Watch this video: http://www.nlm.nih.gov/medlineplus/ency/anatomyvideos/000013.htm Relationship of BP to arterial tone: The pressure of fluid in a container is higher if the walls of the container are rigid & have no “give.” Conversely, the more “relaxed” the walls of the container, the lower the pressure of the fluid in it. 2) NORMAL pulses. a) “pulses” are the pulsations in the arterial system that occur with every heart contraction b) they can be palpated (“felt”) in several areas; most easily felt are: (1) the carotid pulses in the neck (2) the radial pulses in the wrist (3) the pedal pulses: dorsalis pedis (DP) on top of feet & posterior tibialis (PT) on inner side (medial), next to malleolus (ankle bone) Note: “Normal” is not a very specific word unless there is general understanding of what that means. In our class it is used as meaning “within a certain range or parameter that is desired in a particular context.” c) there is a range of “normality” or abnormality in their strength & quality:  12 ex—are the pulses barely palpable (difficult to feel/weak) or are the pulses bounding (very easy to feel/strong)? 3) NORMAL capillary refill-- AKA “nail blanching” a) how quickly does your arterial system refill the empty capillaries? b) normal: ≤ or equal to 2 seconds (means arterial system efficiently refills the capillaries in ≤2 sec) know this number 4) NORMAL organ function; S&S: a) skin: pink (or “usual” color), warm. b) heart: good cardiac function c) brain: good mentation (normal mental activity). d) kidneys: good urine output. B. Pathogenesis of arterial disorders 1. overview a. arterial diseases sometimes known as arterial insufficiency because commonality of ALL of them is insufficient amount of O2 getting to distal tissue, ie, ischemia. b. arterial insufficiency is almost always due to atherosclerosis, a process in which arteries become stiffer (sclerosis) and collect fat (athero) and other unwanted substances in their walls. 2. more about link between atherosclerosis & arterial diseases a. arteriosclerosis—chronic disease of arterial system usually related to aging, in which artery walls become thick & hardened (sclerose = to harden); etiology: 1) over time, arterial vessels are increasingly damaged by hypertension (HTN), smoking, diabetes, infection, high blood levels of cholesterol, and/or other factors such as genetics, free radicals, and “plain old aging.” 2) as the intima (inner lining) of the arterial walls become microscopically damaged, collagen fibers enter the walls & stiffen them (remember, arteries have thick, usually-elastic muscular walls). 3) this process decreases elasticity and compliance of the arteries (thus pathologically altering vasomotor tone.) b. atherosclerosis 1) almost always, as arteriosclerosis develops, there is also atherous involvement (“athero” – fatty deposit)-- hence the name that is most often used for arterial disease—atherosclerosis. 2) not only do collagen fibers collect in arteriosclerotic walls, but so do LDLs— they become “fatty deposits.” 3) when these fatty deposits enter the arterial wall, the tissue becomes irritated and inflammatory & coagulatory responses are triggered. watch this 30-sec video a) plaque formation for good visualization of (1) the combination of stiff arteries, deposits of fat, and atherosclerosis: inflammatory and clotting responses ultimately leads to http://www.nlm.nih.gov/ formation of a fibrous capsule with a fatty middle section in the medlineplus/ency/anatom wall of the artery— this is called a plaque yvideos/000006.htm  13 (2) eventually as it grows, the plaque protrudes into the arterial lumen, thus reducing its patency, and often the decreased patency is enough to reduce blood flow to distal tissues SIDE TRIP MUST KNOW (see page 8-9 in CV prep): Arteriosclerosis & atherosclerosis are sometimes used interchangeably, since rarely does one happen without the other; in the medical world, the term atherosclerosis is most often used to describe the pathogenesis of arterial disease. Atherosclerosis develops mostly because of unneeded cholesterol in the blood, especially extra LDLs. Our bodies (cells) must have a certain amount of lipids to fulfill certain physiologic functions, but our liver makes & processes almost all that we need, so we need very little in our actual diet (in Western society, we overindulge in high-fat foods!!!). Lipids (triglycerides and cholesterol) cannot travel in watery blood to get to the cells. Lipids must combine with proteins to form water-soluble molecules called lipoproteins. VLDL, LDL, HDL are types of lipoprotein. 1. VLDL - has a large concentration of triglyceride, some cholesterol & phospholipid, and very low concentration of protein. As VLDLs are carried in blood to cells, triglycerides are “dropped off” for storage, and the lipoprotein becomes an LDL. 2. LDL – LDL is composed mostly of cholesterol. LDL lipoprotein deliver cholesterol to cells, but excess cholesterol is refused by cell, so can pile up in walls of the vasculature. 3. HDL – HDL is at least 50% protein, small amt cholesterol & phospholipids. HDL is considered the “good fat” because it can pick up “extra” cholesterol from cells and deliver it to liver for processing-- decreases the availability of cholesterol for use in fatty plaques that clog arteries. b) the above general processes are almost always system-wide-- if arterial pathology is found in one area, almost always means it is going on anywhere in the body that arteries are found--heart, brain, kidneys, retina, intestines, legs, etc. c. so, commonalities of arterial disease in ALL parts of body: a) alteration in vasomotor tone – loss of flexibility & responsiveness—ie, loss of causes “just right” status of muscle wall; instead, there is constant constriction & ischemia to brittleness. distal tissue b) non-patent lumen, due to build-up of blockage material such as fat & clots in and along arterial walls. 3. linking patho to S&S: a. because of narrowed, stiff, atheromatous arteries that often have plaques, the end result of most arterial disorders is compromised perfusion (delivery), which results in ischemia (hypoxia of tissues caused by an arterial circulation problem) b. common S&S of this decreased perfusion & ischemia: 1) some degree of ischemic pain a) this type of pain often has the characteristic of increasing with ARTERIAL exertion and diminishing with rest (exertion causes more O2 demand DISORDERS = ischemic probs; on tissue that is barely getting enough O2 even at rest.) can apply ischemic b) the pain will be in the tissue distal to the plaque and/or arterial pattern to any narrowing; ex: diseased artery, (1) when femoral arteries are affected there might be pain in arteriole or capillary calves, especially when patient walks. in the body & the tissue they serve. (2) when coronary arteries are affected there might be pain in distal muscle tissue of heart, which is then perceived as chest pain.  14 2) besides ischemic pain, there are also other S&S of decreased perfusion & ischemia that are specific to the part of the body affected: a) periphery (mainly arteries in arms, legs) (1) pulses: diminished/ absent Remember the (2) delayed capillary refill: >2 seconds pallor of skin seen (3) skin: pale, cool, sometimes mottled or blue-ish (in people of in anemia? That was due to less color, pallor not as obvious-- manifests as duskiness under their RBCs. This pallor is normal coloring and paleness of mucous membranes.) similar but also different (4) sometimes delayed healing; ex: low perfusion to skin→ --less color seen abrasion to skin doesn’t heal because no O2→worsens into because of arterial narrowing or ulceration (ischemic skin ulcer) blockage instead of b) heart—altered function, usually less cardiac output less RBCs. c) brain—altered level of consciousness; stroke (a stroke is what happens when brain doesn’t get enough O2 & there is brain tissue damage). d) kidneys—diminished urine output. 4. some of risk factors of arterial disease: a. non-modifiable risk factors: 1) family history (ex-- inherited tendency toward atherosclerosis and/or familial hypercholesterolemia.) 2) advancing age = stiffer arteries b. modifiable risk factors: 1) diet / obesity /sedentary lifestyle = more LDLs circulating FYI-- 95% of DM2 cases are CAUSED 2) heavy alcohol consumption = toxic byproducts affecting arterial walls BY obesity. When 3) Type II diabetes mellitus (modifiable to a degree) these patients lose enough weight, a) toxic # of glucose molecules will damage affect arterial walls their DM2 b) lipodystrophy, a characteristic of DM2 in which there is increased sometimes goes into remission or circulating LDLs Everyone knows that cigarette smoking even disappears. 4) cigarette smoking is directly linked to lung-cancer- related deaths each year in our country, but did a) toxic byproducts damage arterial walls you know that cigarette smoking is a b) also, nicotine is a powerful vasoconstrictor, primary cause of ~140,000 cardiovascular-related deaths??!! which pathologically narrows arteries & increases BP & HR. 5. specific arterial diseases related to atherosclerosis (to be discussed in individual sections below): a. peripheral arterial disease (PAD) b. arterial thrombi and emboli c. aneurysms HOME STUDY d. hypertension e. coronary artery disease (next lecture)  15 C. Specific arterial diseases 1. PAD – peripheral arterial disease, AKA peripheral arterial insufficiency a. definition of PAD—literally a disease of any arterial vessels outside the heart, but the term “PAD” is most commonly applied to arterial problems of the legs. b. like all arterial vessel problems, PAD usually manifests as problems of ischemia due to narrowed, peripheral arteries; specifically, the S&S are in the legs. c. S&S of PAD – the 5 “Ps The “p’s” of 1) pain = ischemic pain in muscles of legs which may cause limping. Occurs PAD— and is exacerbated (worsens) with exercise and decreases with rest. This pain, type of pain is known as intermittent claudication (the word “claudication” paresthesia, has its roots in the Latin word claudicare”,which means “to limp”) pallor, 2) numbness and tingling of the feet pulselessness, poikilothermia 3) pale 4) diminished pulses, prolonged cap refill >2 secs 5) feet are cool to the touch PLUS 6) no hair grows on legs, skin shiny 7) ischemic skin ulcers --when skin is not “fed” enough O2, it becomes more fragile & traumatizes easily 2. arterial thromboembolic problems a. like venous thrombi, arterial thrombi form where flow is sluggish, and/or where there is narrowing of vessels and/or injuries in vessel walls b. but there are a couple of major differences having to do with direction of flow Remember: 1) when veins get blocked, flow towards the heart is blocked, leading to a type associate distal of back-flow & tissue congestion distal to the blockage. CONGESTION with VENOUS slow-flow 2) when arteries get blocked, it’s a problem of distal tissue ischemia; examples; and/or blockage; a) if there was narrowing / injury / atherosclerosis at bifurcation of associate distal ISCHEMIA with femoral arteries, a thrombus might form. If part of the thrombus (clot) ARTERIAL slow-flow broke free, where would it travel to? distal peripheral arteries and/or blockage. b) what kinds of changes would you see to the distal tissue (legs & feet)? the 5 Ps. 3. hypertension (HTN) a. definition of hypertension—the consistent elevation of systemic arterial blood pressure, measured with sphygmomanometer as “blood pressure (BP)”, with normal/ optimal being ~110/70 (or at least 2 seconds) other low CO S&S f) low urine output 2. fluid 2) S&S of fluid backup into lungs (lung congestion, ie, lung edema): volume a) patho: when LV contractility pathologically decreases and overload (but preload and afterload pathologically increase, the LV cannot manifested in keep all the blood flowing forward and there is a back pressure: different ways LV→ LA→ pulmonary veins→ pulmonary capillaries→ back according to whether it’s pressure forces fluid out into alveolar tissue→this results in LHF or RHF) cardiogenic pulmonary edema_. b) S&S of pulmonary edema: (1) crackles upon auscultation of lungs (2) cough, often with frothy blood-tinged sputum (hemoptysis): (a) the froth is due to air mixed with fluid (b) the blood-tinged or pink color is due to back pressure pushing fluid and some RBCs into alveoli. (3) orthopnea--SOB upon lying down; why? supine position increases backflow into lungs → more lung edema (4) increased respiratory rate (RR) (5) decreased SO2 (oxygen saturation) e. specific S&S of RHF: 1) S&S of decreased CO (see above list under LHF) because RV is failing remember—right to move blood forward into left side of heart to be ejected to body. heart = venous side; 2) S&S of fluid backup into periphery (i.e, peripheral edema):: associate venous a) patho: when RV contractility pathologically decreases and problems with preload and afterload pathologically increase, the RV cannot congestion of keep all the blood flowing forward and there is a back pressure: VENOUS blood RV→ RA superior vena cava (SVC)→ jugular veins inferior vena cava (IVC)→ portal veins, leg & feet veins b) S&Ss of fluid back-up into peripheral veins (peripheral venous congestion): (1) jugular venous distention (JVD) (2) liver congestion, so enlarged liver (3) ascites --the state of extra fluid in the abdominal cavity due to fluid being pushed out of engorged abdominal veins; think of this as a type of edema of the abdominal cavity (4) edema of legs & feet.  30 3) important additional info about RHF a) remember that some of the causes of RHF include ischemia & MI that directly cause reduced contractility; but also RHF can be caused by a pathologically increased PVR (pulmonary vascular resistance). b) *** if RHF is caused by a pulmonary vascular resistance problem, the situation is called cor pulmonale c) an example of cor pulmonale is when a person has RHF that is caused by their chronic bronchitis: (1) people with chronic bronchitis (a type of COPD) often have lungs filled with mucous and congestion, causing decreased blood oxygen levels (hypoxemia). Low oxygen levels cause the pulmonary artery and the pulmonary vessels to vasoconstrict (become narrow). (2) the constriction of the pulmonary vasculature creates a higher pressure in the pulmonary vasculature →it is more difficult (more work) for the RV to pump blood into the pulmonary artery & the rest of the lungs’ vascular system→ the RV fails →fluid backs up→ RV → RA → SVC & IVC → JVD, liver congestion, ascites, leg edema ******Summary / clarification about concepts above that students often find confusing: Lung congestion (pulmonary edema) is caused by LHF and its retrograde (“back-up”) flow. As opposed to: Lung congestion (such as in chronic bronchitis) causes RHF & retrograde venous flow. Lungs Here is a rough “visual” of the retrograde flow (“back-up”) seen in 1: 4: heart failure. Begin with chronic bronch. (pulm. #1 on each side. EX: if edema) 3 an MI causes the LV to become weak & unable to pump all blood forward, RHF RA 4 3 L there will be back pressure & flow to A 2 where? What S&S will L 2 LHF you then see? RV 1 Apply this to right side, V too, only begin with the precipitating element as chronic bronchitis. f. treatment of HF: 1) to increase strength of “pump” & thus increase forward blood flow: a) positive inotropic drugs such as digoxin b) also, may need to decrease heart rate if too high so that workload of heart is lessened. 2) to help decrease resistance to forward flow (afterload —SVR & PVR) give vasodilator drugs such as NTG. 3) Inhibit RAAS with ACE inhibitors.  31 4) to help decrease preload give diuretics (remember, it is the characteristics of hanging on to fluid & back-up of fluid that give heart failure its often-used label of “congestive”—heart failure almost always has fluid overload as a main component, so diuresis is key part of treatment.) Review this prior to class: physiology of natriuretic peptides (see previous notes & prep): a) the natriuretic system is body’s compensatory mechanism that is triggered when we have fluid overload (this is the exact opposite to the RAAS, which is triggered when we have fluid deficit) b) the natriuretic system causes more sodium to be excreted into the urine→ water follows→ thus natriuretic peptides are “natural diuretics” when we need to get rid of fluid c) there are two substances that are part of the natriuretic system and are secreted by the heart in varying amounts into the blood daily as part of natural regulatory system: (1) one is secreted from the atria --atrial natriuretic peptide (ANP) (2) one is secreted from the ventricles-- b-type natriuretic peptide (BNP) (3) both help to increase secretion of sodium & water from the kidneys when we need to get rid of water, as in heart failure. g. diagnosis and measurement of severity of HF 1) when patients present with S&S of HF, the gold standard for confirmation & quantification of the HF is a blood test that measures HIGH BNP = heart is BNP --b-type natriuretic peptide “frantically” and usually unsuccessfully trying to 2) an abnormally elevated serum BNP level confirms that HF is compensate for the occurring; here is what is happening: fluid overload that is a) the patient is in right or left heart failure (or both), and his always a part of HF circulating blood volume (preload) is increasing. b) the heart “notices” a larger-than-normal volume of blood returning to the right atrium (remember that fluid overload is always a part of heart failure) c) ANP & BNP is then secreted by the right atrium & left ventricle, respectively, and these hormones circulate to the kidneys to get them to diurese some of the volume (1) however, remember that the kidneys are already involved with their “misguided” ratcheting up of the RAAS as a part of the original HF. (2) therefore, they do not respond appropriately to the ANP & BNP. d) as preload continues to be high, the heart “frantically” keeps increasing its hormones, so the serum BNP goes up, helping us with diagnosis, but not really helping the patient; the higher the BNP, the worse the HF. 3) clinical example: a) healthy man BNP level = 50 pg/ml b) example of BNP of man in mild HF = 130. c) example of BNP of man in severe HF = 1000. ***************************************************************************  32 The following info is NOT ON TEST & WON’T BE GONE OVER IN CLASS… this info for your own interest & edification. Please DO look it over, as some of the concepts here will feed into and hopefully add to your general knowledge of info that IS on the test… for example, if you REALLY understand about why peripheral vasodilators are given (to decrease SVR) & positive inotropes (to help with contractility) in this disorder, you will know that you have a pretty good handle on the general picture of heart function. 3. cardiogenic shock a. overview 1) definition of shock-- inadequate perfusion of tissues, usually due to hypotension (