NURS 3366: Module 6-9

Specific arterial disease related to atherosclerosis. what is the results of it and what is hypertension related to atherosclerosis

1. PAD - Peripheral arterial dz (aka arterial insufficiency): arterial is very specific to arterial occlusion in the leg. Like all arterial vessel problems, PAD usually manifests as ischemia due to the block and narrowed artery. - S&S of PAD: the 5 P's i. pain = ischemic pain; worsens due to activity and decreases due to rest, known as intermittent claudication. ii. Paresthesia - tingling feelings in the legs iii. pallor - pale, due to less O2 iv. pulselessness - prolong cap refill (more than>2sec) v. Poikilothermia - cool to the touch and no hair growth, skin shinny, ischemic ulcer (no healing) 2. Arterial thromboembolic problem: the thrombi can break free from the arterial wall and become an embolus and travel downward from the bigger arteries into the little ones can causing problems like in the feet and toes. - S&S: the 5 P's 3. Hypertension (HTN) - High blood Pressure: the consistent elevation of the systemic arterial blood pressure. - Normal 110/70 (<120/80) and anything 130/80 is HTN - hypotension - anything below 90/60 = 2 causes of HTN: a. Secondary - uncommon HTN, caused by an underlying problem, most often an adrenal tumor or renal problem. b. Primary - common, also called essential or idiopathic (unknown reasons why an individual had HTN from this problem) - there are certain risk factors why people might develop primary HTN, it has a widespread effect on all the organs in the body. - S&S of HTN is the same as atherosclerosis because HTN occurs when the arteries are stiff and non-stretchy. So individuals who eat a very high-fat diet, who don't excessively, drink a lot of alcohol and high intake of Sodium (when someone eats a lot of salt, you drink water and that would be retained and cause higher pressure in eh circulatory system). Personality traits are linked with HTN (types A and D are known to be at risk for HTN) - Patho of Primary HTN: it's not known why it occurs but there are factors that are linked to why an individual has hypertension. a. Atheroscolsis: non-stretchy, stiff. the over fatty infiltration that will increase pressure on the artery wall as force is exerted. ***(this is already explained, Atheroscolsis can lead to HTN, HTN can lead to Atheroscolsis)*** b. overactivity of the sympathetic nervous system: not sure why this happens but the epinephrine that is in the SNS and if it's overactive and chronically being overpumped can increase BP. This is deemed a genetic predisposition. c. overactivity of RAAS (renin-angiotensin-aldosterone-system): NORMAL - when there is a drop in BP, less blood goes into the kidney triggers the release of renin, and then angiotensin-1, then angiotensin-2; and angiotensin-2 is responsible for vasoconstriction and Increasing blood volume to increase BP. Angiotensin-2 is also responsible to trigger the adrenal gland the secrete aldosterone and it's reasonable to cause sodium and therefore water. - RAAS is only supposed to be triggered when there is a drop in the cardiac output or BP, but for some unknown reason, RAAS is inappropriately triggered when if the CO of the BP is okay. So this trigger causes this chronic vasoconstriction and retention of sodium, which will lead to water retention. That is the reason why it has hypertension = all 3 results ^ in a pathological increase in cardiac output, arterial vasoconstriction, and pathologic increase in BP. - S&S of HTN: none, silent but deadly - there is this deadly pounding pressure on the vasculature of the various tissue in the body. this pending pressure in the blood vessel is responsible for 3 primary system problems. (neuro, renal, heart) a. Neurologic system - that constant pounding in the brain arterial system can lead to stroke. so HTN is the key cause of strokes. - HTN + the consistent pounding, in the tiny arterioles in the eye can cause narrowing with can lead to ischemia and even death to part of the retina. the first S&S when someone has High BP is to seek care bc of vision problems. this is irreversible. b. Renel System: the high pounding pressure on the renal arteries can eventually lead to damaging the nephrons causing hematuria (blood in the Urine) and proteinuria. c. Cardiovascular System: it increases the workload on the heart. (eg. if the sending aorta is super stiff and rigid the left ventricle is trying to pump blood into the aorta it will need to use a lot of force. over time the LV will have problems. Peripheral arterial Disorder: Aneurysms - arterial disorder: localized dilation or outpouching of the arterial vessel wall. - cause of it: chronic atherosclerosis and damage to the arterial vessel can cause this super stiff blood vessel, which weakens the arterial wall then you add atherosclerosis which can lead to hypertension and atherosclerosis can lead to hypertension, and hypertension can lead to Atherosclerosis. it's just that when it's weak it bulges outward and while this out pouches or puff out it can cause the lining of the artery and let blood seep into different layers of the arterial blood vessel which will then cause a problem. The abdominal aortic Aneurysms (AAA) - presented when there is atherosclerosis, plus high pressure of hypertension, there will be an outpouching and abdominal/thoracic aorta. - S&S: often feel pain, pulsatile mass can be palpated (you can feel the outpouching or have abdominal back pain.) = tx of any kind of arterial problems/ dz: manage stress, stop smoking, no drinking, healthy diet, moderate salt intake, keep the LDL (fats) low by having a low-fat diet, taking meds, keep the HDL high by exercise, red wine, and sometimes niacin and omega-3 high (fish, flaxseeds; these are considered the "good fats" bc they fight inflammation.) How it helps is when the LDL gets trapped in the arterial layer of the wall, it triggers inflammation (a bubbly fatty mess) = what medicine is linked to what patho occurs with primary hypertension. 1. Overactivation of the sympathetic nervous system: use beta-blockers 2. Overactivity of RAAS: use an ACEI inhibitor or angiotensin receptor blocker (ARBS) 3. Atheroscolsis: to comeback clots from forming bc of the bubbly brew of fat within the artery liner, use aspirin (help inflammation). - if someone has a venous problem you can elevate their feet but if some have arterial problems evaluating the feet would not help bc blood is supposed to move out of the heart south not have it return to the heart.

Types of Pulmonary low Restrictive disorder - causing less O2 inhalation. (The V = ventilation part of the problem less than V/Q is less than <0.8). What are the 3 main causes of the lung getting less O2? what are the 3 types of Pneumothorax? Define the terms: kyphosis, Stridor, Croup (laryngotracheobronchitis), Pleural effusion, Pleuritic, Pneumothorax, negative intrathoracic pressure, Traumatic Pneumothorax, Spontaneous Pneumothorax, Tension Pneumothorax. Pneumonia, community-acquired Pnueomina (CAP), Nosocominal Pnueomina, Aspiration Pnueomina, Infiltrates, Atelectasis, Consolidation, Pulmonary edema (noncardio), Surfactant. what are the S&S, risk factors, and Tx?

A. Chest wall restriction - kyphosis: they don't have a chest wall that can move up and out to increase space inside causing more negative pressure there is not much are can be sucked in. - Obesity: if there is a large belly then the patient's diaphragm can't drop down. - Neuromuscular disorder: cant bring in air bc of their weak muscle and they cant have the effort to bring in as deep a breath as what is needed to bring in enough 4L of air. B. Airway restriction - Foreign bodies can cause airway restriction - Inflammation: obstruction or restriction on the ability of the patient to bring in enough air. When the upper airway is inflamed as the patient tries to inhale that has something known as Stridor (high pitched, wheezing sound), this is the sound of air entering the air passage through the inflamed airway. = We see Stridor in an individual who has Croup (laryngotracheobronchitis) - inflammation of the larynx, trachea, and bronchi. Occurs more in infants (<1yrs); - S&S: fever, increase RR, barking coughing, stridor; - Tx: cool mist (calm the inflammatory tissue in the upper airway) and sometimes steroids. C. Pleural restriction: - Pleural effusion: the extra fluid in pleural space (between the parietal pleural and visceral pleura) The lung goes up and down and the fluid is lubrication so it doesn't cause friction between the 2 pleura. = with irritation/inflammation from an infectious process where fluid can collect between partial and visceral pleura. Fluid takes up space and the lungs have limited space with there is fluid the lungs can't expand as much will cause less Air. S&S: chills and fever (form microbes or infection), Pleuritic pain (pleurisy - when the plural is inflamed then it hurts when the patient inhales - Pneumothorax: the presence of air between the visceral and parietal pleura. when there is a lot of air in that pleura space it disrupts the normal negative pressure of the lungs, and without that negative intrathoracic pressure, the lung will collapse. - there are 2 problems wherever there is air within the pleural space. (Pneumothorax): 1. Lack of negative intrathoracic pressure, taking no air in and 2. Now making the negative to a positive pressure causes the collapse of various lung tissue. = 3 types of Pneumothorax: 1. Traumatic Pneumothorax: this can be a result from: PENETRATING TRAUMA - (stabbing, knife) that punctures the outside of the chest wall which disrupts the parietal pleura, this allows the air to into the atmosphere into the pleural space collecting air OR a NONPENAETRATING TRAUMA - happening within you (ex: fracture/broken rib) puncturing the lungs causing air to enter. 2. Spontaneous Pneumothorax: can happen in... - Super tall, thin, and smoking people. - alveoli can rupture from within and the air is brought in from the blood space 3. Tension Pneumothorax: can occur in either scenario, often it is from a traumatic pneumothorax but it can occur in a spontaneous, it just depends on the vol. of air that gets into the Intrathoricic cavity, if there is enough air that collects and that cant escape put or around than all the air will take up space on whichever side of the lung is damaged. and when there is so much air it causes a pushing force against the uninjured side as well as the heart. - this can result in a loss of both lungs as well as a reduced cardiac output - Treatment (Tx): usually varies depending on the extent of the disorder, S&S of the patient, etc. but the basis for any pneumothorax: 1. Restore or re-establish negative intrathoracic pressure. and is done by inserting a chest tube between the 2 pleural layers. the air is taken out and trapped within the water when exhaled. ONE-WAY VALVE SYSTEM D. Lung Tissue Restriction - an infection problem, that is Restricting us to bring in air. i. Pnueomina: acute infection of the lower respiratory tract. 6th leading death is the US; Risk factor (more likely to get it if you are...): depending on age (babies or elderly), immunocompromised, underlying lung disease, alcoholism, etc. 3 categories of Pnueomina: they are divided into different types bc of the microbes responsible for the illness. 1. community-acquired Pnueomina (CAP): less-variant of microbes, do not need to be hospitalized 2. Nosocomial Pnueomina: a strong variant of microbes, needs stronger antibiotics 3. Aspiration Pnueomina: this can happen in the community or hospital, this is when they inhaled something that shouldn't be going into the lungs (ex: when drinking you inhaled at the same time it goes down the wrong pipe). - In healthy individuals, they are supposed to bring it back up but in individuals with are unhealthy, stroke individuals, or don't have a mental capacity whos unconscious they lack the ability to bring it up or they have a neurological problem where they have a poor cough reflex and gag reflex. ***Aspiration Pnueomina will not occur in someone with an intact mind, brainstems, or reflexes (gag, cough).*** = Patho of a Pnueomina (seen in any kind ^^^): a microorganism settles into the alveoli and there are alveoli macrophages waiting to eat and destroy things that aren't supposed to be there to attack, while the macrophages attack they will also activate the systemic or local inflammatory response. as they eat away the microbes they will create infectious/inflammatory debris called Infiltrates (not in the lungs but it's called exudate). - once this Infiltrates accumulates it can cause the collapse of the lung bc no air (no gas exchange) is getting into the lungs with so much debris around this is called Atelectasis. - Infiltrates + Atelectases = Consolidation: this is when then the air in the alveoli is replaced with a fluid, such as pus, blood, or water. - S&S: fever, chills, malaise, pleural pain (pain during inhalation), cough, dyspnea. If there is fluid in the alveoli crackles can be heard and diminished breath sounds because no there are no alveoli participating in gas exchange. - more info on Atelectasis: groups of alveoli are collapsed, not available for air exchange, and when lower alveoli cannot get O2. (ex: post-surgery, where the incision cuts right down the chest and abdominal area, It hurt for them to breathe in, they won't have a deep breath) and so not a lot of air is getting down there, those lower alveoli will collapse, these are breeding ground for bacteria causing Pnueomina. *Pnueomina --> Atelectases or Atelectases --> Pnueomina* - tx: moving after surgy is very important, and a respiratory therapist can help, deep breathe E. Pulmonary edema - excess of fluid on the alveoli (there was the cardiogenic Pulmonary edema related to LHF). This is noncardiogenic Pulmonary Edema: Which is an injury to the epithelium. Whenever you inhale smoke. it'll cause irritation and inflammation = leakage, with inflammation there will be increased capillary permeability (vasodilation), and there will be movement of fluids and plasma proteins from the capillary to the alveoli causing edema. - When there is water (fluid) in the alveoli it damages the alveoli cell producing Surfactant (this keeps the alveoli from collapsing) that translates to Atelectasis (groups of alveoli collages no longer alveoli for gas exchange) - S&S: dyspnea, SOB, crackles. pink frothy sputum (blood mixed, bc when water moves in plasma that contains RBC will sneak in too), hypoxemia. F. Lung cancer (bronchogenic carcinoma) - the proliferation of abnormal cells taking over the normal cells.

Peripheral arterial Disorder: Normal arterial system. What are the disorders that are arterial related: Arteriosclerosis and Atherosclerosis

Arteries are much thicker, and muscles vessel, also take oxygenated blood from the heart and circulate it to tissue all over the body. (southbound traveling lane) - the ability of the arteries to work efficiently and maintained the flow of blood from the heart to the tissue are determined by the factors of good arterial sufficiency the muscle tone in the wall of the arteries and the state of their lumen (opening of the arteries) is where the oxygenated blood flow. - muscle tone of the material wall (aka vasomotor tone): the muscle fiber to stay in the normal zone or to have normal vasoconstriction and vasodilate ("just right"). Having good blood pressure depends on the vasomotor tone. - a good arterial blood flow and oxygenation is the state of the lumen, to be smooth and patent (open). free from block. - if both good lumen and vasomotor tone are presented then we know this contributes to good perfusion (=oxygenation). Cardiac Output and the state of the artery = good perfusion. - Even if good CO bc w/o good delivery from the arteries of oxygenated blood to the tissue the individual will not have good perfusion. - S&S of good perfusion: is good blood pressure and pulses. The definition of having a good BP is having an average of ~120/80, it is the measurement of fluid (blood) pressure that is exerting force against the wall of the arteries, bc the arteries is a close pipe system, and it exercises force against that muscular wall and that force is measured of BP. a. systolic pressure: the force of blood that is being ejected out of the heart during systole. this is the top number b. diastolic pressure: is when blood is filing into the ventricle during diastole. this is the bottom number. = the pulses you feel are the results of that arterial blood moving thru the artery. (ex: are the dorsal pedal, radial, cardiac pulse). And we need to know if the artery is barely palpable (is it difficult to feel and is it weak?) or if the bounding of the pulse (is it easy to feel and is it strong?). = normal capillary refill, aka "nail blanching" test, and when you press the nails down and release it, it should only take less than ≤2 sec to refill with blood. = normal organs function: Skin = pink, warm, dry; Heart = good cardiac; Brain = good mentation (be able to Id what they are being asked.); kidney = good urine OP. Pathogenesis of arterial disorder: - the dz sometimes known as arterial insufficiency can lead to ischemia bc there is not enough oxygenated blood being delivered to the needed tissue. a. arterial insufficiency is always due to Atherosclerosis (fats surrounding the arteries). this is caused by an over-consumed of fats, that will get disposed into the layers of the arteries. - What are fats consist of?: fat is needed by every cell in the body and to get to the cell it needs to travel thru the watery parts of our blood but oil and water do not mix. So the oil in our blood must be carried by proteins. i. low-density lipoproteins (LDL) - unhealthy cholesterol ii. high-density lipoproteins (HDL) - healthy cholesterols. = these are floating about in the blood, and at some point, the cell will need fat to do their job, the LDL will go into the cell and they are very picky on how much it can go into and if there is too much fat that crowds into he cell the cell will kick the fat right out and the HLD will escort the LDL out of the cell and move it back into the blood. Unfortunately, if individuals do not have enough HDL the LDL doesn't always go back into the blood. and it gets stuck in the different layers of the muscle arteries. and over time with overconsumption of oily food, the fat will lie down and get bigger and bigger over time making the lumen smaller. = this process is known as Atherosclerosis. - every time LDL gets trapped in the arterial wall when it's not supposed to be there that will trigger inflammation. - the build-up of LDL underneath the fatty layer is known as plaque, with all the fats and bubbling around will cause reduced patency in the blood vessel and whatever tissue is supposed to be getting blood and therefore oxygens will not be delivered and become ischemic. - this can happen in any arteries in the body but it has a tendency to occur in the heart, brain, legs, etc it's system-wide. - although it will reduce the patency but also stiffen the arteries. b. arteriosclerosis: (thickening of the arteries wall) the arteries start being stretchy and good but over time the arteries become damaged. (ex: getting a new car the paint of it is shiny, just like a newborn baby's arterial inside lining). The newborn baby's lining is super smooth and as they get older (is 6-8yrs older), the lifestyle and what they eat, infections, are exposed to toxic fumes from smoking, free radical, all of these substances those toxic substance floats around will damage the inner lining of the artery. It causes these microscope dings to the intima of the arteries, but your body can fix this by laying down collagen fiber, this fiber can cause the muscle layer to become stiff. So aging and damage done to the inner ling of the blood vessel is what causes to lay down within the muscle layer and decrease in elasticity and compliance (stretchiness) = common arterial dz is the alternation of vasomotor tone - the arteries are stiff, brittle, less flexible, less compliant, and the lumen is nonpatent = S&S of arterial insufficiency: compromised perfusion, less oxygenated blood to the tissue therefore ischemia and ischemia pain to any area that artery is blood to. Ischemia pain is exacerbated when there is an extreme increase in extension and diminished with rest. (ex: if we have low o2 and are running we need more o2 so resting will release the pain). The pain is always Distal which means downward stream. (Ex: your patient right femoral arteries have reduced patency from atherosclerosis therefore when they walk they will have pain in that particular calf area. that artery is not able to deliver blood downstream.) (ex: coronary artery is affected there might be a pain in the chest.) - beside ischemic pain and decreased perfusion as S&S there are others such as the: a. periphery (ex: right femoral arteries have reduced patency from atherosclerosis than the pulse down in the right foot going to be diminished or absent, the capillary refill is going to be prolonged (more the >2 sec.), the skin of that right leg can be pale, delayed healing, ischemic skin ulcer. b. if that artery is not patent and full of fat and plaque and that was in the heart, then again if the heart is not getting enough blood, then the function is not going to be as good. c. if it's in the brain - it can alter the level of consciousness that what a stroke is. d. it can happen with the arteries in the kidney, leading to decrease urine output. = Risk factor of arterial dz: divided into 2 different ways 1. non-modifiable risk factor: things that can be changed - family history genetics, advancing age (damaged over time and collagen being laid down over and over making it very stiff) 2. modifiable risk factor - things that can be changed - diet, obesity, sedentary lifestyle, more circulating LDL due to high fat consumption, and heavy alcohol consumption are high in carbs can cause Atherosclerosis, due to the toxic byproduct that comes from breaking down the alcohol that can affect the arterial wall. - Type 2 diabetes, is all about glucose control, and it's modifiable bc individuals can control their glucose. this glucose molec is also very damaging to the arterial wall. and individuals who have diabetes also have high circulating LDL is characterized as Lipostrorphy. - Smoking and all tobacco products all contain toxic byproducts. Nicotine is a powerful vasoconstrictor, so it can lose the efficiency of the vasomotor tone. - all of these are general disorders that are going to cause problems related to Atherosclerosis.

Terms to know for S&S of CKD Kidney malfunction. Urinalysis (UA) and Creatinine clearance urine test

Azotemia: high level of waste in the blood Creatinine, and urea in the blood) - if the patient also tells you they are tired, have nausea, and vomiting, they have Pruritis (itching, bc of the high level of Urea can cause it), and they have Uremic Encephalopathy (neurological problems). All of these S&S are called Uremia - BUN >25 + Sermun >1.2 = Azotemia; Azotemia + S&S above = uremia **** More things to look at besides those listed above... there might be substances missing in the Urine but there might be something that shouldn't be in the Urine this is by... i. Urinalysis (UA): - if there is Blood and Protein in the urine it is glomerulonephritis, meaning there is damage to the glamourous, and inflammation is allowing leaking. - if there is bacteria int eh urine it might be a infection in the kidney or bladder (Cystitis or if it involved all the stature in the pelvic area is UTI) = Normal Urine Specific Gravity: 1.002- 1.028; Oliguria + Urine Specific gravity is less than <1.002 the kidney is not doing the correct job of concentrating urine. = Urine Specific Gravity = Normal Urine Concentration (1.002- 1.028) Causes: - Dehydration: the urine is dark, but it is somewhere around the 1.028 normal urine concentration range, this means the kidney is working to hold on to water bc of dehydration but it is still getting rid of the normal amount of waste. - Lot of water intake: your kidney will increase filtration and get rid of more water, there will be more urine removed, the color is pale yellow and less concentrated (1.002; still normal) but still getting rid of the correct amount of waste. - Kidney nephrons are sick: the amount of water removed is always going to be less, than 30ml/hr. there will be very little waste in the urine. the concentration will be lower than <1.002 maybe (1.000). - With any chronic Kidney disease will be a Low specific gravity and less than 30ml/per urine volume ii. Creatinine Clearance Urine Test: Creatinine is measured in 24 hours from the urine that is excreated out. This is done to know the specific of the Glomerulus Filtration Rate because it's hard to do so. The Kidney removes a very specific amount of Creatinine within a 24hr period. - If the kidney is heavly damaged the serum Creatinine in the blood is HIGH but the Urine Creatinine will be LOW.

Blood Urea Nitrogen (BUN). Where does it come from? Serum Creatinine (what is this?)

Blood urine Nitrogen: scenario: you eat a steak, the liver will break down the substance into protein, and proteins breakdown will create ammonia, which is then breakdown by the liver and then make into Blood Urea Nitrogen (BUN) - people who are on a carnivore diet can cause elevated levels of BUN or just CKD, so when looking at the urine test, MAYBE have a KIDNEY Problem. Creatinine: The liver breakdown this product of muscle creatine kinase into creatinine

Confusing Terms

Cardiovascular - refer to the heart and vessels Peripheral vascular - describe the vessels in the arms and the legs (outside of the heart) Circulatory system - combine peripheral and cardiovascular systems together. Central vs Peripheral:

Peripheral Vascular Disorder - Disorders that can prevent a venous return: Deep veins thrombosis

Deep veins thrombosis (DVT): pathologic clot from the platelet collection that develops in the vein. Once the DVT is formed it will trigger inflammation in the veins known as thrombophlebitis ('phleb' = veins) - S&S: SHEP (swelling (edema), heat (warmth), erythema (redness), pain); seen in one leg; - Ones at risk of developing a DVT: have one or more elements of Virchow's Triad (3) classic: 1. Injury to the endothelium of veins 2. Stasis of blood flow (not moving, sitting still) 3. Hypercoagulability - the tendency to clot easily, can occur when individuals are dehydrated or if these certain illnesses such as cancer more often, birth control pills (more estrogen). Ex of how Virchow's Triad is presented: people who sit long period of time can be at risk of DVT, (airline traveler, desk jockey, couch potatoes), and when sitting you cross your knees and leg which causes microvascular injury; dehydration for long hours, immobilized legs. - Sequal of DVT: can get a compilation of Pulmonary embolus (PE) - when the deep vein breaks free it becomes an embolus and travel move from the back of the knee all the way up to the inferior vena cava, right atrium, right ventral and then into the pulmonary artery. Although the artery is big the clot can travel to the tiny arterioles' blood vessels it can get stuck. - S&S of PE: SOB, chest pain, hemoptysis (blood in sputum), and shock (low BP) = the pulmonary arteries are supposed to go out of the heart and into the alveoli where the blood is oxygenated but with the pulmonary embolus blocking its path the blood doesn't get oxygenated. this is the way some individuals can get SOB, and chest pain bc the oxygen level is down. Also when there is an embolus presented inflammation is triggered in the lining of the pulmonary arterial intima. = when there is inflammation there is leakage, some water and blood vessels will leak out into the alveolar space, which will cause blood-tint water in the alveoli, so the patient will start to cough up bloody sputum. = and if systemic inflammation occurs it will cause massive systemic vasodilation which causes low BP (shock). ex: the reporter flying on a long long flight to the middle east and during that time they became dehydrated, stuck and not moving around the Develop DVT. once he landed he left the pain and went to interview troop that invited him to sit in the tank with him, this plus more dehydrated and hot temp this causes the DVT to become PE, passing away. - tx: encourage mobility, and hydration, and leg and feet elevation help return the venous blood to the heart, and no broken skin preventing ulcers, and blood thinner and anticoagulation to prevent more clotting.

Peripheral Vascular Disorder: Normal Venous system. What are the disorders that are venous related: Chronic venous insufficiency (CVI) and Deep vein thrombosis (DVT)

Normal The veins are supposed to carry the deoxygenated blood from the vessel to the right side of the heart, this is often called venous return. we what good condition that facilitates good venous return and we know that to get the deoxygenated blood from the feet up to the heart that there could be a problem with backflow, due to gravity. Facilitate a good venous return: - Proper functioning Valves in the leg's veins. During systole when the heart is pushing blood, it is using a lot of force on the arterial side of the system will help push blood thru the open valves in the venous system. (ex: if you are in line and people in the back push you forward you will go as well due to the force). and during diastole, the leg valves will close since the heart is filling with blood. the blood drops back down. but the blood is not moving until the next systolic cycle. - well-toned, working muscle tissue around the veins: muscle contract, they squeeze all the nearby veins that can also help move blood up and forward gravity making the blood return to the heart. Disorders that can prevent a venous return: a. Chronic venous insufficiency - venous blood has failed to return in a sufficient amount back to the heart. (usually, the legs, since they are further away from the heart it takes more energy than the arms). If it fails to return to the heart the venous blood will congregate or stasis (static), it is not going up and is hanging down on the venous vessel in the legs. That can push water out of the venous system and get into the feet, known as venous blood congestion over a long period of time. "Gravity winning" - no matter what age as long as you standing for a long period of time gravity will win over and you will have some kind of venous congestion (if it's not server it is not necessary pathophysiologic). i - if severe this venous congestion can cause the formation of varicose veins (not really a pathophysiologic per se). these varicose veins over a long period of time (years), can occur what is known as valve incompetence - that means the valve is not doing its job and this can lead to venous insufficiency - During this chronic stasis of the blood vessel, causes the walls of the veins to stretch and expand, as the wall stretch and expands the valves don't get bigger. This is what leads to venous insufficiency stasis of the veins will cause the veins to be in a consistent overstretch and it won't go back (worn-out elastic). The valves become incompetent. this will allow blood on a chronic base to stay in the venous system. - CVI causes: leg veins that are worn out and become "floppy" the valves are not closing when in diastole, and the blood will flow downward into the feet. this pool of non-moving blood is called venous stasis, which can result in this increase in hydrostatic pressure. this causes water to move put into the tissue space = edema. = when edema occurs this shift the cells further away from the blood vessel and doesn't allow the cells to get the nutrients and the WBC is needed when there is a problem. And just not only edema they can have Venous stasis ulcers "brown sock syndrome". this blood is static in this area and will be edema and brown skin discoloration from the calf down. With stasis and insufficient, if they were to hit their leg on something and if they get a sore there is less healing bc of the edema and inability to get the nutrients needed to heal - Contributing factors to the development of CVI: aging, inherited, obesity, multiple pregnancies, long-term standing jobs. and/or people that don't move their muscles around have low muscle tone, due to inactivity, and immobility. b. Deep veins thrombosis (DVT): pathologic clot from the platelet collection that develops in the vein. Once the DVT is formed it will trigger inflammation in the veins known as thrombophlebitis ('phleb' = veins) - S&S: SHEP (swelling (edema), heat (warmth), erythema (redness), pain); seen in one leg; - Ones at risk of developing a DVT: have one or more elements of Virchow's Triad (3) classic: 1. Injury to the endothelium of veins 2. Stasis of blood flow (not moving, sitting still) 3. Hypercoagulability - the tendency to clot easily, can occur when individuals are dehydrated or if these certain illnesses such as cancer more often, birth control pills (more estrogen). Ex of how Virchow's Triad is presented: people who sit long period of time can be at risk of DVT, (airline traveler, desk jockey, couch potatoes), and when sitting you cross your knees and leg which causes microvascular injury; dehydration for long hours, immobilized legs. - Sequal of DVT: can get a compilation of Pulmonary embolus (PE) - when the deep vein breaks free it becomes an embolus and travel move from the back of the knee all the way up to the inferior vena cava, right atrium, right ventral and then into the pulmonary artery. Although the artery is big, the clot can travel to the tiny arterioles blood vessel it can get stuck. - S&S of PE: SOB, chest pain, hemoptysis (blood in sputum), and shock (low BP) = the pulmonary arteries are supposed to go out of the heart and into the alveoli where the blood is oxygenated but with the pulmonary embolus blocking its path the blood doesn't get oxygenated. this is the way some individuals can get SOB, and chest pain bc the oxygen level is down. Also when there is an embolus presented inflammation is triggered in the lining of the pulmonary arterial intima. = when there is inflammation there is leakage, some water and blood vessels will leak out into the alveolar space, which will cause blood-tint water in the alveoli, so the patient will start to cough up bloody sputum. = and if systemic inflammation occurs it will cause massive systemic vasodilation which causes low BP (shock). ex: the reporter flying on a long long flight to the middle east and during that time they became dehydrated, stuck and not moving around the Develop DVT. once he landed he left the pain and went to interview troop that invited him to sit in the tank with him, this plus more dehydrated and hot temp this causes the DVT to become PE, passing away. - tx: encourage mobility, and hydration, and leg and feet elevation help return the venous blood to the heart, and no broken skin preventing ulcers, and blood thinner and anticoagulation to prevent more clotting.

Now we know that increase in breathing will indicate a pulmonary disease and now we can get into the actual diseases and they are divided into 2 categories: Obstructive Pulmonary Disorder. What is used to test exhalation, what are the 3 disease-related to Obstructive disorder?

Obstructive Pulmonary Disorder (occlusive): diseases that will cause difficulty with exhalation. if a person has difficulty exhaling that, means CO2 retention. and for the body to get rid of CO2 it has an alternate way that it'll force out the CO2 out. - S&S are often "forcing out" exhalation instead of passivity. they use the accessory muscle that should be used when exhaling, and we know that it's going to take much longer since the use of force muscle. - Measure how well they can blow air out. they us a Peak flow test, this meter test how well a certain can blow air out, and the less Peak flow the worse the obstructive pulmonary dz. - Everyone is this obstructive carat goes there breathing pattern of maintenance (maintain their "normal" with dz) and times of exacerbation episode (period of worsening) ex: people who have asthma and during the pollen season that is their exacerbation period. 3 common types of obstructive pulmonary disorder: 1. Asthma - chronic inflammatory disorder, the airway has bronchial hyperresponsiveness, this is a hypersensitivity response to an allergic response and in the bronchial tube (ex: peanuts, pollen, air pollution) - Patho: the individual inhaled something, this will trigger a local inflammatory mediator (histamine, leukotriene, PGs). the histamine and PGs will cause vasodilation in the blood vessel that lies within the bronchial tubes, they will vasodilate and leak bringing in plasma (WBC --> eosinophils: responsible for allergic reaction (bronchial hyperresponsiveness)) and at the same time the bronchial tubes smooth muscle is constricted from the leukotriene, the ends of the bronchial tubes this happens when plasmas is a leak in other gunk and stuff will also come into the bronchial tube obstructing the tube making it swollen and constricted. - S&S: wheezing upon exhale, SO2 dropping, and the patient will start the hyperventilate, so this can create Respiratory Alkalosis (to help get rid of CO2 because they can't have trouble exhaling) and the patient is also Hypoxemia (loss of O2 in the blood) (how!?: if we think of the alveoli as a balloon and you keep it blown up that's how the air goes in and in your body, the alveoli will empty bc that is how O2 gets diffused across the membrane into the blood, then CO2 will jump into the alveoli and the balloon would be filled again. and in an obstructive disorder, if we can't get the air out we cannot get air in. that how over time the O2 decrease overtime) - Tx: monitor peak Flow, medication: Bronchiodilater and anti-inflammatory drugs (bc the allergen will trigger inflammation and the leakage of the blood vessels that line the bronchial tubes that cause a narrowing or obstruction of the bronchial airway. 2. Chronic Obstructive pulmonary disease (COPD): Bronchitis and Emphysema are lumped together bc patients have both bits and pieces of both together - usually caused by individuals that are smokers. - the E-cigs, and regular, smoke pollution are all inhaled causing irritation. and those irritate are what trigger COPD. - Decrease of Peak Flow, acute exacerbation, and worsening, - Tx: smoking cessation (stop smoking), give O2, bronchodilator, steroids a. Emphysema - smoking is the main cause - patho: inspired irritant, will tiger inflammation, this will abnormally increase proteolytic enzymes like elastase. ex: a cluster of alveoli together in one of the bronchioles, the alveoli cells when they go there is the process of life and death (apoptosis) the elastase is there to get rid of the death alveolar cell, and new cells can be formed and do their jobs, with Emphysema the irritate inhaled will cause overactivity of elastase, instead of being an as-needed basis whenever a normal cell has done it the time it goes berserk. The elastase will just eat and eat thru the alveolar walls, so this is why there is a formation of an alveolar bleb. These are the reduced ability of each individual alveoli apartment or the big latter to diffuse and participate in gas exchange. the second thing that is happening this that the Bleb, is stiff, and hyperinflated bc air is trapped there, with no elastic recoil. (think healthy alveoli as trampolines and as air zooms in like jumping off the walls of the alveoli and out it goes and when there is this bleb, the elasticity is gone, so air doesn't zoom in instead it comes in and dumps in and plops, staying there. there is so much trapping of old air because even though it pops in there, the gas exchange can still occur, and then the CO2 is in there and it's stuck) - time decrease of O2 in the blood the brain tells the body to go into chronic hyperventilate to get more air. - S&S: tachypnea, on good days is known as "pink puffers" because they are hyperventilating, huffing and puffing staying pink, getting the O2 they need; they are thin (bc they have hyperventilated all the time, and when er eat we don't breathe while swallowing, but they need to breathe so they each smaller meals); Barrel Chest (air is trapped --> larger chest); Tripod position (this helo maximizes chest expansion to breathe); Pursed lip; Wheezing (the forceful exhalation); might not hear lung sound. - ABGs: they are in a constant respiratory alkalosis because of the rapid RR, blowing off more Co2; pH >7.45; PCO2: <35; HCO3 normal. This is their "normal" iii. Chonchi Bronchities - hypersecretion of mucus and chronic cough (least 3 months of a year for 2 years) - patho: smoke irritants inhaled, they have the inability to expel them due to the irritants causing metaplasia to the cilia, they can no longer sweep away the trash inside the bronchial tube because they are not being made, so the irritant on a day-to-day basis they are supposed to be swept away but it is not. and overtime the irritant in the tube will cause inflammation, and then those leaked plasma carry neutrophils, and macrophages, arrive on sense and go to work, phagocyting will cause the production of a lot of mucus and because of this it can also cause Bronchospams on exhalation, so on the end of inhalation then that Bronchospams occur and between this and the mucus, they close off the air for exhalation. so this air just gets trapped in the alveoli - S&S: "Blue" = hypoxemia, Cyanosis, clubbing of finger; "Bloater" = peripheral edema and Obesity = "Blue Bloater" - because mucus plug in the bronchi causes narrowing and an inability to get exhaled or CO2 out, so that means it's hard to bring O2 in, so over time these individuals will have hypoxemia. = they are called that bc the compensatory mechanism of hyperventilating to get rid of CO2 doesn't work with Chronchi Bronchitis, the Obstruction and constriction in the bronchi wall have collapsed. (they always have mucus clogging up the chinos tube and also coughing), and they develop Cyanosis over time bc not able to get air [last the mucus. = and over a super long period of time with a good O2 capacity, they can also develop clubbing of the finger. = hyperventilating doesn't work so usually if they don't do much work the body should be fine but they are the opposite of pink puffer, they tend to get overweight, (aka bloated) from just sitting and doing nothing. = Cor pulmonale - RHF is caused by lung disease. so Chonchi Bronchitis is what can cause RHF. and in RHF it causes a backup of fluid with results in peripheral edema (bloating) - ABGs: chronic Hypercapnia, they are in a constant respiratory acidiosis, because of CO2 retention; pH <7.35; PCO2: >45; HCO3 normal. PO2 <80, SO2: <97%

Pulmonary disorder: Increased work in breathing. What are the terms: Dyspnea, DOE, Orthopnea, Paroxysmal nocturnal dyspnea, Hypoventilation, bradypnea, Hyperventilation, tachypnea, Hypopnea, Hyperpnea, Apnea, Hemoptysis Respiratory Distress, Respiratory Failure.

S&S indicates increased work in breathing. Step 1: Look for Dyspnea: this is a subjective statement meaning the patient will say "I can't breathe". but as a nurse more questions such as: a. " just by sitting there doing nothing or do you get short of breath on exertion. which is abbrev. as DOE (Dyspnea of Exertion). b. "can you breathe when you're laying down and you have to sit up". this is known as Orthopnea, (inability to breathe easily when lying down). This occurs with an individual with LHF and also respiratory disorders c. "so you wake up at night feeling SOB?" this is known as Paroxysmal nocturnal dyspnea (PND) This occurs when you are sleeping and all of sudden you re-awaken at night feeling SOB. Step 2: observe the breathing pattern, and look at how fast or how slow they are breathing. (The Normal RR is 12-20 breathe/min) a. Hypoventilation (bradypnea): the RR less than <12; the Etiology of a RR problem linked to the central nervous system (CNS), because the brain is in control of the RR and pattern, it defines how deep, how fat, how shallow the breathing is going to be, so anytime there is an intracranial bleeding or high intracranial pressure then that can cause an alteration in the Respiratory Rate (RR) b. Hyperventilation (tachypnea): define as any RR greater than >20. The etiology can be from the CNS issue but it can be also the psychological reason (ex: frightened, Air hunger - pulmonary disorder the need for O2) - Depth-related term: this is the amount of O2 it can bring in and CO2 remove. a. Hypopnea - shallow breathing b. Hyperpnea - increase depth of respiration (more tidal volume) c. Apnea - no respiarion - abnormal muscle use to breathe: when we inhale it required a lot of energy, we use chest muscle, the muscle around the clavicle, and the neck area. and they are supposed to be normal but during exhalation is supposed to be no energy just a rebound of the elasticity of our muscle. if someone is using the muscle to exhale this means it is abnormal. = children often have nasal flaring that causes a whole lot of work on inhalation and exhalation. What are cough and sputum, and how is this related to pulmonary disease? - Look at cough and sputum that are often seen in pulmonary disease. Is it clear, thick, or cloudy? There might be a reason, and irritation in the lung causing the problem or it can just be a protective reflex. = Hemoptysis: bloody sputum, the RBC has snuck into the alveoli and is being brought up with mucus or secretion. the color can be green, yellow, or brown, smelly usually means an infectious process. - When a patient comes and has shown S&S (shown above) of a breathing problem this much is defined as Respiratory Distress, once id the patient's Respatroy rate or depth we would also look at the ABG of the patient, these are tools to look at and ID Respiratory Failure. When the pH, CO2, or O2. either one or two of these are abnormal then the patient has a failure of the pulmonary or respiratory system. When a patient with Respiratory failure they are going to be on ventilation.

Peripheral arterial Disorder: Pathogenesis of arterial disorder: Atherosclerosis and arteriosclerosis, what are the common arterial S&S, risk factors, of both arterial dz.

The dz sometimes known as Arterial Insufficiency can lead to ischemia because there is not enough oxygenated blood being delivered to the needed tissue. - types of Arterial Insufficiency dz. a. arteriosclerosis: (thickening of the arteries wall) the arteries start being stretchy and good but over time the arteries become damaged. (ex: getting a new car the paint of it is shiny, just like a newborn baby's arterial inside lining). The newborn baby's lining is super smooth and as they get older (is 6-8yrs older), the lifestyle and what they eat, infections, are exposed to toxic fumes from smoking, free radical, all of these substances those toxic substance floats around will damage the inner lining of the artery. It causes these microscope dings to the intima of the arteries, but your body can fix this by laying down collagen fiber, this fiber can cause the muscle layer to become stiff. So aging and damage done to the inner ling of the blood vessel is what causes to lay down within the muscle layer and decrease in elasticity and compliance (stretchiness) b. arterial insufficiency is always due to Atherosclerosis (fats surrounding the arteries). This is caused by an over-consumed of fats, that will get disposed into the layers of the arteries. - What are fats consist of?: fat is needed by every cell in the body and to get to the cell it needs to travel thru the watery parts of our blood but oil and water do not mix. So the oil in our blood must be carried by proteins. i. low-density lipoproteins (LDL) - unhealthy cholesterol ii. high-density lipoproteins (HDL) - healthy cholesterols. = these are floating about in the blood, and at some point, the cell will need fat to do their job, the LDL will go into the cell and they are very picky on how much it can go into and if there is too much fat that crowds into he cell the cell will kick the fat right out and the HLD will escort the LDL out of the cell and move it back into the blood. Unfortunately, if individuals do not have enough HDL the LDL doesn't always go back into the blood. and it gets stuck in the different layers of the muscle arteries. and over time with overconsumption of oily food, the fat will lie down and get bigger and bigger over time making the lumen smaller. = this process is known as Atherosclerosis. - every time LDL gets trapped in the arterial wall when it's not supposed to be there that will trigger inflammation. - the build-up of LDL underneath the fatty layer is known as plaque, with all the fats and bubbling around will cause reduced patency in the blood vessel and whatever tissue is supposed to be getting blood and therefore oxygens will not be delivered and become ischemic. - this can happen in any arteries in the body but it has a tendency to occur in the heart, brain, legs, etc it's system-wide. - although it will reduce the patency but also stiffen the arteries. = common arterial dz is the alternation of vasomotor tone - the arteries are stiff, brittle, less flexible, less compliant, and the lumen is nonpatent = S&S of arterial insufficiency: compromised perfusion, less oxygenated blood to the tissue therefore ischemia and ischemia pain to any area that artery is blood to. Ischemia pain is exacerbated when there is an extreme increase in extension and diminished with rest. (ex: if we have low o2 and are running we need more o2 so resting will release the pain). The pain is always Distal which means downward stream. (Ex: your patient right femoral arteries have reduced patency from atherosclerosis therefore when they walk they will have pain in that particular calf area. that artery is not able to deliver blood downstream.) (ex: coronary artery is affected there might be a pain in the chest.) - beside ischemic pain and decreased perfusion as S&S there are others such as the: a. periphery (ex: right femoral arteries have reduced patency from atherosclerosis than the pulse down in the right foot going to be diminished or absent, the capillary refill is going to be prolonged (more the >2 sec.), the skin of that right leg can be pale, delayed healing, ischemic skin ulcer. b. if that artery is not patent and full of fat and plaque and that was in the heart, then again if the heart is not getting enough blood, then the function is not going to be as good. c. if it's in the brain - it can alter the level of consciousness that what a stroke is. d. it can happen with the arteries in the kidney, leading to decrease urine output. = Risk factor of arterial dz: divided into 2 different ways 1. non-modifiable risk factor: things that can be changed - family history genetics, advancing age (damaged over time and collagen being laid down over and over making it very stiff) 2. modifiable risk factor - things that can be changed - diet, obesity, sedentary lifestyle, more circulating LDL due to high fat consumption, and heavy alcohol consumption are high in carbs can cause Atherosclerosis, due to the toxic byproduct that comes from breaking down the alcohol that can affect the arterial wall. - Type 2 diabetes, is all about glucose control, and it's modifiable bc individuals can control their glucose. this glucose molec is also very damaging to the arterial wall. and individuals who have diabetes also have high circulating LDL is characterized as Lipostrorphy. - Smoking and all tobacco products all contain toxic byproducts. Nicotine is a powerful vasoconstrictor, so it can lose the efficiency of the vasomotor tone. - all of these are general disorders that are going to cause problems related to the arthoscolosis

Heart failure (HF) in the cardiovascular system

The failure of the heart to eject or propel blood forward. there can be Left or right Heart failure. The normal flow of blood: when deoxygenated blood comes from the tissue it moves from the IVC or SVC --> RA --> TV --> RV - Pulmonic valve --> PA --> lungs (gas exchange in the alveli) --> oxygenated blood --> Pulomary veins --> LA --> mitral valve --> LV --> aortic valve --> aorta --> body artery. - The problem/patho with HF might be: 1. Pump Problem: the heart contractility is weak, not adequality pumping blood forward. 2. Increase resistance in the vessel (pulmonary artery n vascular system) that the ventricles pump into = Higher workload. 3. Increase Preload: The extra volume increases the heart's workload long-term, causing the heart to be overwhelmed. - Left heart failure: 1. Iit has poor and weak decreased contractility often due to ischemia or Myocardial Infection (MI). When there is a total occlusion in the blood vessel that is supplying oxygenated blood to this part of the heart cell and is cut off and when there is no O2 to these heart cells they die (infarct), then they are not able to pump, bc once MI heart cell dies they don't regenerate. and/or 2. the Left ventricles have to struggle against high resistance from the systemic vascular system, usually, due to systemic hypertension, which means, the left ventricle must pump a lot harder to overcome the resistance to get the blood out of the left ventricle into the aorta. Long-term hypertension and medication destroys the heart cell and induce heart failure and/or 3. The LV is overwhelmed by an increased preload (fluid). = either one of these or all 3 together the outcome is a decrease in CO and an increase in RAAS activation. - S&S: 1. decrease CO leads to Poor perfusion and 2. Fluid backup into lungs - no matter what the reason is but when there is a lot of fluid circulating around the body, all that fluid vol has to move thru the heart. and when it reaches the LV and isn't able to pump blood forward bc of LHF, but blood will keep coming in, therefore there is this increase of backpressure from LV --> LA --> left pulmonary vein --> back into the pulmonary venous system --> eventually lung (causing pressure in the alveoli) water will leak into the blood vessel --> alveoli --> water causes cardiogenic pulmonary edema (S&S: crackles sound in the lungs due to water n, not air; coughing up blood-tinged sputum (Hemoptysis); Orthpnea (SOB when laying down) this happens when they are laying down and they need to get up super suddenly, that bc of the increase the backflow into the lung this worsen the pulmonary edema; Paroxysmal nocturnal dyspnea (PND) - the individual can go to sleep but 2 am in the morning they are woken up get up bc of SOB, it takes some time, bc still worsening the Pulmonary edema; increase RR and decrease SO2. (ex: like in a traffic jam, there is an accident at the LV all blood is stop there, and like a car its stops, and as more car/blood comes in it cant move but like a car in a traffic jam it doesn't go backward so more and more piles up causing this backward pressure) - Right heart failure: 1. It has poor and weak decreased contractility often due to ischemia or Myocardial Infection (MI). there are a lot of different coronary arteries that feed specifically into each aspect of the heart muscle if the muscle is feeding or delivering oxygenated blood to the muscle of the right ventricle was totally occulted then the cell of the RV will die. = no pump = heart failure or/and 2. If the RV must struggle against a high afterload/resistance from the space where the right ventricle pump into that is the pulmonary vascular artery. if there is vasoconstriction on the blood vessel over time the RV gets tired, and this will weaken the RV. - the pulmonary arterial vasoconstriction occurs from lung disease, chronic bronchitis, or Cor Pulmonale. and/or 3. The RV can be overwhelmed if the preload is increased = either one of these or all 3 together the outcome is that the RV cannot send blood downstream to the LV the CO will decrease and an increase in RAAS activation. - S&S: 1. decrease CO, bc the RV is unable to pump blood forward. 2. FLuid backup into periphery: the RV contractility is bad so it causes a backflow from RV --> RA --> SVC or IVC --> jugular veins (right & left) or portal veins, leg and feet veins. this will cause Jugular venous distention (JVD), liver connection, and so enlarged liver and that can lead to ascites (state of extra fluid in eh abdominal cavity) and edema of the legs. - RHF can occur due to MI in the right heart ventricle and increase pulmonary vascular resistance and when an RHF occurs bc of a lung problem from RHF to Cor Pulmonate *RHF is from a heart problem* = Cor Pulmonate: any individual who has chronic bronchitis or lung disease when the lung is not doing its job where it's supposed to oxygenate the blood for the body will compensate by causing pulmonary artery vasoconstriction (with this over a long period of time will increase pulmonary vascular resistance which makes a lot of work on the right ventricle as it ejects blood and over a long time it can cause RHF). - Sequla of HF: 1. diminished CO bc of inability to pump blood forward. 2. with the CO going down there will be fluid overload. - these two happen bc when CO goes down the first organ to complain is the kidney where blood is filtered thru and it needs a lot of it. without enough blood, the kidney is going to release RAAS and angiotensin II is going to release 1. arterial vasoconstriction and 2. stimulate the adrenal to release aldosterone with hold in Na+ leads to water retention. = fluid retention (preload) due to aldosterone and vasoconstriction increase afterload, which causes more work in the heart and what will cause the CO to go down, and if the CO goes more down, the kidney is not gonna be happy. so this is a cycle that is continuous. - Tx: to increase the strength and pump of the heart to increase positive inotropic by giving Digoxin; to help decrease HR, help decrease afterload by giving vasodilator drug such as Nitroglycerin; inhibit the RAAS with ACE inhibitor (ACE is used to stimulate antigen II); decrease preload (fluid) due to RAAS by giving diuretic (pee more) - HF dx: B-type natriuretic peptide (BNP), should be abnormally elevated. when there eid HR (if it's greater than 50pg/ml) = B-type natriuretic peptide (BNP): a substance released whenever there is a stretch in the ventricle.

The general concept of what the normal heart is needed for and the definition of Cardiac output, stroke volume, and heart rate.

The heart is responsible to move the blood continually, throughout the blood vessel, the job is to get oxygenated blood to all the tissues this is called Perfusion. - S&S of good Perfusion: pink skin color, responding you to the environment, if the pulse is strong, cap refill ≤2 secs (fingertip press if it goes back with color its good), good Urine output. - an adequate cardiac output = S&S of good perfusion. i. Cardiac Output (CO) - the average amount of blood the Left ventricle ejects per minute. Normal = 4-6L/min. ii. The amount of blood pumped out by each heartbeat is determined by Stroke Volume. Normal is ~70ml/beat. iii. Heart Rate is to determine the number of times your heart beats per minute. (beat/min) Ex: find CO if SV is 70ml and HR is 80 beat. (80 beats/min x 70ml/beats = 1500ml/min --> 5.6L/min) Good C.O = 1. good HR + heart rhythm 2. Contractility (pump) - strong 3. Preload (volume) - blood vol. return to the heart 4. Afterload (resistance) - to the cardiac blood flow 2-4: deals with SV - all 4 of these = good CO = S&S of good Perfusion.

Pulmonary System: (Arterial blood gas).

To dx a pulmonary alteration and everything, one must undergo a blood gas review from the arterials (Arterial blood gas). When we are talking about acid-base balance there are 2 systems: The respiratory and the metabolic system. The respiratory system rules CO₂ (ACID) and the metabolic system (aka the Kidney) is going to rule the HCO₃ (bicarbonate) and it's all about the BASE - When looking at ABG it determines 5 things: 1. pH levels - indicated the level of acidity in the blood and the normal range is 7.35-7.45, and if anything is less than <7.35 it's an acidosis state, and anytime it's greater than >7.45 is an alkalosis thing. 2. PO₂: the O2 level in the blood; the normal level is 80-100mmHg and anything less than <80mmHg is hypoxemia 3. SO₂: the percentage of modules on the hemoglobin that is carrying the saturated O₂. The normal SO₂ is 97-100%. 4. PCO₂: think of it as CO₂, this is the acid that is ruled by the lung (CO₂). The normal value is 35-45 mmHg. - link CO2 abnormality with Respiratory problems, meaning out of range but the HCO₃ will be okay (metabolic), and vis versa. 5. HCO₃: levels of bicarbonate in the body. The normal is 22-28mEq/l. - if this is out of range it tells that the metabolic systems abnormalities and its respiratory systems stay normal = only one problem at a time = not given on exams remember the numbers.

Review of the genitourinary system for female-specific illness.

Uterine-related problem: flow disturbances 1. Dysmenorrhea - difficult, painful, painful, larger menstruation 2. Amenorrhea - the absence of menus due to cancer diagnosis eating disorder, avid runners. 3. Endometriosis - the endometrium is functioning outside of the uterus. this can bring infertility, - caused by retrograde menstruation, when the uterus sloughs off and, the period starts, and instead of going down and out the blood and slough off endometrial tissue will go up and backward, they will go up the fallopian tube and it can ger out into the pelvic area. Although it's sloughed off endometrial tissue, it is still inside and will respond to the harmonic cycle of women and that can bleed and if you have this bleed tissue on top of the uterus, in the pelvic region, this will trigger c. - every month this will occur then this inflammatory process will have monthly that is going to lead to scarring or adhesion. the scar tissue can warp around the surrounding area like the fallopian tube ovaries and urinary and GI structures - S&S: formation of adhesion (scar tissue), dyspareunia (pain upon sexual intercourse), pelvic pain - Tx: hormonal therapy and surgery 4. Ovarian cancer - malignant neoplasms condition of the ovaries, the cause is unknown. - most related cancer death in women because is often advanced before its diagnosis. - if the ovarian cancer is to spread, it'll go to the colon and up to the liver following the GI tract. - S&S: mild bloating, constipation, pain, ascites (liver involvement), dyspepsia (indigestion problem), vomiting. Infection of female genitourinary: reproductive tract 1. Pelvic inflammatory disease (PID) - often starts from an STI such as chlamydia and gonorrhea, an infection affecting the cervix and causing cervicitis. (inflammation of the cervix) and once it becomes inflamed it can go up and reach all the other reproductive structures causing pelvic inflammatory disease. - S&S: depending on how severe and what structure is involved. There is Vaginal discharge (most tend to ignore it since it is common when going thru the hormonal cycle); very painful on movement so they don't move a lot. - sequela: infertility - Tx: antibiotic, pain killers. 2. urologic infection: can just involve the bladder causing cystitis (inflammation of the bladder) or it can move up to the kidneys causing Pyelonephritis (infection moving from the bladder and traveling up to the kidneys) or just the entire tract with UTI (urinary tract infection) - E. Coli causing UTIs are very common in women, bc of how short the urethra is to the anus. - S&S of UTI (urinary tract infection): dysuria, frequency, and urgency (the feeling of having to go and more frequently but in small amounts.); hematuria (inflammation to the bladder); pyuria (puss in urine); if a kidney is inflamed pain at costovertebral; fever. - Dx: Id by S&S and until the antibiotics fail and the UTI comes back again, then a urinary analysis and urine culture and sensitivity are done.

Cardiovascular system disorder: CAD (coronary artery disease) - what are S&S, risk factors, assessment, and the different classifications? What is the definition of Stable Angina, Acute Coronary Syndrome (ACS), Unstable angina, and Myocardial infarction?

a disorder in which the coronary arteries are narrow, and occluded, and anytime arterial problems = ischemia (the inability to deliver O2 blood to the tissue cell and for CAD it is the heart cell. It's also due to the plaque buildup. - risk factors: hypertension, atrhoscilosisi - how to ID CAD: assessment of BP is going to determine if it's high that is going to be a risk factor. formation of plaque in the arterial walls, draw blood, and look at the LDLs and HDL levels, weight, and pulses (can they be felt) - if you are on a high scale of CAD in addition they are going to do two other blood tests that can bump up to be an immediate risk of having a heart attack (MI) is 1. Homocysteine - if this is elevated in the blood you are at immediate risk of CAD, and 2. an elevated C-reactant protein (CRP) - bc then the LDLs get trapped in the arterial walls, then bubbling and brewing inflammatory goes on it it's bad. - Patho of CAD: is all about the plaque formation in the coronary arteries, and they are very important to provide o2 to the heart cell, also ischemia is a Negative Inotropic (if a paper bag is put over you and you have to climb up a long flight of stairs over and over) this is why O2 is super important and if it's really bad it can lead to cell death and in the heart, it's known as a Myocardial Infarction (MI). - S&S: Angina - Painful constriction in the chest (aka chest pain), the heart muscle is not getting adequate O2. there are different levels of Angina for each person, some might complain of tightness, heaviness in the chest area, or pain radiating to the left arm, jaw, and back. with most ischemia pain, is often exacerbated by exercise and can be lessened by rest. - 2 classifications of CAD are based on the person Conroy occlusion and S&S plus when the S&S occurs: = a person with CAD can be asymptomatic or symptomatic (and with those they are put into the 2 categories): 1. Stable Angina - the pain pattern is very predictable and well-controlled, occurs with activity, and goes away with rest. - patho of stable Angina: the coronary artery blockage occurs slowly and this allows the body to have time to adapt (i.g: start out with a super clean and healthy coronary artery, then you decided to eat a hamburger, and a little plaque is presented then smoking then putting every bad thing possible into your body, more and more plaque is built occurs) whatever the coronary arteries deliver O2 to in the heart muscle is not getting adequate O2, the compensatory mechanism is to stimulate new arteries known as Arteriogenesis, the end results is the established of Collateral Circulation this means going around the block to feed into the heart muscles cells during the slow development of plaque (this is why its stable angina, the better the Collateral circulation the more stable angina will be, the lessen the pain). - tx: maximize Conary patency there fore increase perfusion. (make the arteries that are covered n plaque bigger so there is a bigger diameter, therefore, more blood can be delivered to the heart), decrease the workload of the heart. = for all of that ^ to work give the patients, Nitroglycerin (dilated the coronary artery, so more movent can go thru) and also aspirin (anti-inflammatory, LDL = inflammation, take aspirin to decrease LDL inflammation but spring can cause decrease plate adhesion (clumping) so blood is easier to bleed.) 2. Acute Coronary Syndrome (ACS) - if we go back to the plaque in the arteries and the layer, that plaque will rupture (i.g like a big pimple on the face, it eventually will burst). that bubbling fat in the lining of the arteries will rupture and it'll trigger a clot to form and the clot will partially or totally fill up the lumen of the artery, sometimes its break free becoming an embolus and travel down to smaller branches of the arteries. - S&S (both Unstable angina and MI): key: chest pain, jaw pain, arm pain all at rest, and the pain will not disappear even with nitroglycerin. because they have this seems of doom (I'm going to die) the sympathetic nervous system is going to be activated: sweating (diaphoresis), becoming nauseating, and vomiting. Bc of the activation of SNS there will be tachycardia (from epinephrine) and bradycardia if the right coronary artery, the SA nodes are not getting O2 = ischemia = less bumping), and dysrhythmias (afib, vfib) - there are 2 subcategories: i. Unstable angina (the partially occulted artery) - patho: plaque ruptures --> clot formation --> partially occulted artery - S&S: chest pain suddenly and at rest (woken up at 4 am in the morning, with sudden chest pain), if they have been ID with CAD, will take their Nitroglycerin but the pain doesn't get better. ii. Myocardial infarction (totally occulted artery) Heart Attack = Total Death!!! - The heart cell will die, and present to the hospital with chest pain at rest the EKG will tell the doctor... - when the person comes into the ER with chest pain at rest dx of MI can be shown when the troponin is elevated due to the dying heart cell (specific to the heat cell). Creatine Kinase will also be elevated bc heart cells and muscle cells are also dying. - tx: we must open up the artery asap, compare to unstable angina, bc the longer it takes the more heart cells will die, open the artery within 90 mins. = another problem that occurs with myocardial infarction (heart attack) is Hypertrophy (ex: if there is 10 heart cell working and an MI happened 4 died instantly, and the remaining 6 will have to work harder and pump more to keep up the CO) with this the heat shape will change and become bigger which is called hypertrophy. the change in shape causes the ventricle to be less efficient and ultimately leads to heart failure. In general ACS = worse ischemia = no O2 = no work = low Co = low perfusion: fatuiue, weak, mental changes, hypotension, dyspnea, prolong cap refill, low urine OP. - OUTCOME of CAD: not everyone's going to be experiencing the same level of pain, and not everyone diagnosed with chest pain is stable angina then moves to unstable, some might not have any symptoms at all until all of sudden they have a heart attack. or some have dx of stable angina and they are not going to change their lifestyle choices they can move to unstable angina. but sometimes it can stay at stable angina and some will immediately go into unstable angina. this totally depends on their lifestyles - stable angina depends on the body to produce collateral circulations

Acute Kidney Injury (AKI) (in depth)

a sudden decline of kidney function has occurred within <48 hours or less. - S&S: acute increase in serum creatinine and acute oliguria in the body (due to decreased GFR). - the patient can fix the problem if caught on quickly or they might not recover if it can be fixed. all AKI S&S: are elevated creatinine serum and oliguria in urine. all AKI if not fixed in a timely manner can lead to chronic kidney disease There are 3 subcategories the AKI is placed into: 1. prerenal - Pre "before" the kidney, there is something wrong with the blood flow into the kidney, and that reduces the kidney function. causes: low cardiac output/ Hypotension because of hemorrhages, dehydration, heart failure, massive vasodilation hypotension from infection (sepsis) - tx: fix the original problem since the prerenal injury is based on the other part of the body, (i.e. heart). - if blood flow is not restored then the patient can go into intrarenal acute kidney injury caused by acute tubular necrosis (nephrons death) and also CKD if don't fixed long term wise. 2. intrarenal - somthing has psychically damaged the kidney nephrons, or this can be from the damages by the prerenal or postrenal moving into the intrarenal area, leading to Glomerulonephritis and Acute Tubular Necrosis (ATN) a. Glomerulus damage is caused by autoimmune or post-streptococcal Glomerulonephritis: this often happens in conjunction with recovery from strep throat. either they didn't have adequate healthcare to treat it or they did not complete their rounds of antibiotics and they made the auto-immune complex with the strep bacteria, those autoantibodies for the strep will attach themselves t the Glomerulus irritating it, initiating inflammation. the Glomerulus is a big filter and essentially the holes on the filter get bigger causing the membrane to leak protein and blood into the urine. - S&S: proteinuria and hematuria plus AKI S&S. b. Kidney Tubular damage - caused by direct damage from a certain toxic substance such as renal drugs, antibiotics, and other recreational drugs ex: PCP, spray paint, enviromental agents, and snake venom. - they can lead to acute tubular necrosis, and if the problem from prerenal arent solved it can lead to tubular ischemia and that can lead to ATN or postrenal problems arent solved will backflow on the capillaries tubular and cause Acute Tubular Necrosis. = S&S of intrarenal AKI = elevated creatinine, oliguria, blood, and protein and Cast in urine. 3. postrenal - happens after the kidney and is always an obstructive disorder. - urethral obstruction such as benign prostatic hyperplasia (BPH) in a man and uterine Prolapse in women. - S&S: AKI signs plus obstruction Signs (kidney stones and urine flow) - plus any obstruction will lead to hydronephrosis (backpressure of urine flow) ultimately leading to ATN (acute tubular necrosis) all AKI S&S: are elevated creatinine serum and oliguria all AKI if not fixed in a timely manner can lead to chronic kidney disease Acute Tubular Necrosis Patho: reduce blood flow from whatever it could be, it can cause the death of the tubular cells and they will slough off in a clumps, and under the microscope looking at urine they will be identified as CASTS = ATN

Peripherial Vascular Disease (RRD #6)

https://quizlet.com/_qg5dw?x=1jqt&i=2xa6q8

Overview of the Cardiovascular System

***mirror body image*** Right side of the heart - is deoxygenated (all the blood coming into the heart from the veins) Left side of the heart - is oxygenated, blood that is leaving the heart via the aorta to all arteries and tissue the venous side of the blood is incoming and the arterial side of the blood is outgoing, if one side is affected the other side is not. **All pathologies are caused when there is a backflow of blood.** If we start out on the feet we think about deoxygenated blood coming from the feet moving all the way up into the inferior vena cava, and lands in the right atrium same go for the head the deoxygenated blood goes from the head into the jugular vein all the way to the superior vena cava, landing in the right atrium., then all the blood goes thru the tricuspid valve, into the right ventricle, the blood will then go thru the pulmonary trunk/valve, and it will go into the pulmonary arteries, out into the lungs where it will go thru the alveoli where the blood oxygenated, then it returns to the heart from the pulmonary veins, and lands in the left atrium, the blood will go thru the mitral/bicuspid valve, and will go into the left ventricle. The oxygenated blood will then move out thru the aortic valve into the ascending aorta, aortic arch, thoracic aorta, and then the descending aorta, and all the way down to all the other tissue in the body. Exception: All veins carry deoxygenated blood except in the heart where oxygenated blood comes back thru the pulmonary vein and all arteries carry oxygenated blood except in the heart where deoxygenated leave thru the pulmonary arteries into the lungs.

Non-gender-specific GU problems: STIs (Sexually Transmitted Disease) What are the 4 most common STIs?

1. Chlamydia - lead to Urethritis in males and common cause of PID in women 2. Gonorrhea - common cause of PID usually asymptomatic - both S&S: discomfort, discharge, dysuria 3. Syphilis - transmitted by spirochete treponema pallidum, easily treated with antibiotics early and harder as it goes on. - 1st stage: Primary Syphilis - development of Chancres (lesions) in the genital or oral region. - S&S: it doesn't hang on for long before it moves on to the other stages. 4. Genital Herpes - caused by Herpes Simplex Virus (HSV), subtype (HSV2) i. HSV 1 - invades the lip and surrounding areas and can be transmitted to others by contact (ex. kissing). Not considered an STI because people get it as "Cold Sores" ii. HSV 2 - this is an STI, spread thru the genital region, - S&S: red, rusty painful lesions that break out once in a while, might have Systemic S&S such as fever and malaise. - once the Herpes simplex virus is revolved it hides in the nervous system and during the stressful time it can pop out again. - Tx: antiviral meds to control S&S, but can't cure it. - it's not dangerous unless you are a woman n have it but also preggo, the baby once leaving the vaginal wall can cause illness in newborns bc of the immunity system.

scenario of Acute kidney failure

A patient who comes into the hospital overdoses on drugs, in the hospital, their urine output dropped from 35ml/hr to 15ml/hr within 48 hours of admission. The serum creatinine is elevated. the nurse is going to suspect acute kidney injury bc of acute oliguria and high serum creatinine, the kidneys not putting out waste and urine properly. The nurse is going to suspect intrarenal AKI bc of the initial drug overdoes. the nurse. The sure is also going to suspect acute tubular necrosis bc of the decline of kidney function = nephron not working properly and the in the urine analysis it shows CASTS.

Abnormalities in the Arterial blood gas. All 5. and what is the compensation?

Analyze the ABG to look for abnormalities. 1. Analyze the pH, and determine is it acidosis or alkalosis 2. Analyze the PCO₂, is PCO₂ abnormal. if so is it alkalosis or acidosis in the respiratory origin. 3. Analyze the HCO₃⁻, is it abnormal? the acidosis or alkalosis has a meteablic origin. 4. Analysis of the SaO₂ and PaO₂, Is it low? If so they are hypoxemia. 5. find out what is the cause, is it something that is damaging the lungs and causing breathing problems? or is the kidney being damaged bc of some kind of illness. - ex: pH: 7.30, PaCO₂: 50mmHg, HCO₃⁻: 24mEg/l, PaO₂: 63mmHg, SaO₂: 85% i. the Ph is low - acidosis ii. the PCO2 is ↑ iii. the HCO3 is normal = at this point we can tell its a respiratory acidosis problem since CO2 is abnormal but HCO is normal iv. PO2 is ↓ v. SO2 is ↓ = so we can say this person is respiratory acidosis with hypoxemia - if there is a problem then the compensation is done by the opposite system aka the metabolic system bc the respiratory vi. since CO2 is abnormal then there is some kind of illness damaging the Lungs and causing the breathing problems ex: pH: 7.48, PaCO₂: 40mmHg, HCO₃⁻: 34mEg/l, PaO₂: 88mmHg, SaO₂: 99% i. pH is ↑ - alkalosis ii. PCO2 is normal iii. HCO is ↑ iv. PO2 is normal v. SO2 is normal - this person has metabolic alkalosis w/o hypoxemia (meaning the O2 is normal since the respiratory system is normal) = the compensation is done by the opposite system aka the respiratory systems vi. the causes of metabolic alkalosis are either going to be the addition of bicarbonate or the loss of it.

Peripheral Vascular Disorder: Disorders preventing venous return - Chronic venous insufficiency

Chronic venous insufficiency - venous blood has failed to return in a sufficient amount back to the heart. (usually, the legs, since they are further away from the heart it takes more energy than the arms). If it fails to return to the heart the venous blood will congregate or stasis (static), it is not going up and is hanging down on the venous vessel in the legs. That can push water out of the venous system and get into the feet, known as venous blood congestion over a long period of time. "Gravity winning" - no matter what age as long as you standing for a long period of time gravity will win over and you will have some kind of venous congestion (if it's not server it is not necessary pathophysiologic). i - if severe this venous congestion can cause the formation of varicose veins (not really a pathophysiologic per se). these varicose veins over a long period of time (years), can occur what is known as valve incompetence - that means the valve is not doing its job and this can lead to venous insufficiency - During this chronic stasis of the blood vessel, causes the walls of the veins to stretch and expand, as the wall stretch and expands the valves don't get bigger. This is what leads to venous insufficiency stasis of the veins will cause the veins to be in a consistent overstretch and it won't go back (worn-out elastic). The valves become incompetent. this will allow blood on a chronic base to stay in the venous system. - CVI causes: leg veins that are worn out and become "floppy" the valves are not closing when in diastole, and the blood will flow downward into the feet. this pool of non-moving blood is called venous stasis, which can result in this increase in hydrostatic pressure. this causes water to move put into the tissue space = edema. = when edema occurs this shift the cells further away from the blood vessel and doesn't allow the cells to get the nutrients and the WBC is needed when there is a problem. And just not only edema they can have Venous stasis ulcers "brown sock syndrome". this blood is static in this area and will be edema and brown skin discoloration from the calf down. With stasis and insufficient, if they were to hit their leg on something and if they get a sore there is less healing bc of the edema and inability to get the nutrients needed to heal - Contributing factors to the development of CVI: aging, inherited, obesity, multiple pregnancies, long-term standing jobs. and/or people that don't move their muscles around have low muscle tone, due to inactivity, and immobility.

The pathopsychological failure of the renal system (AKA the kidneys).

It important for the kidney to have enough blood flow and the effective glomerular filtration rate is achvided, and because how the kidney filter is very dependent on how much blood is given to them, and when a person's GFR goes down, then the person has a kidney problem. 2 categories of kidney problem - Acute Kidney Injury (AKI): suddenly onset of kidney injury or failure can get better very quickly as long as it is fixed early. or an individual can come and have an Acute kidney Injury, something happens suddenly, perhaps the problem isn't fixed very carefully, then the indivual will them develop... ↓ - Chronic Kidney Disease: or the idnivual has some kind of dz such as hypertension or diabetes that that slowly over time developed can cause chronic kidney disease. Whether it started from a acute kidney disease, then developed chronic kidney disease or the indivual will just pop in and has chronic kidney disease. They will be staged based on their glourmarlus filtration rate (GFR).

Review of the genitourinary system for Male-specific illness.

Male-specific 1. Benign Prostatic hyperplasia (BPH) aka enlarged prostate - this is a proliferation of cells of the prostate gland, men over 40-45 have some kind of benign prostatic hyperplasia - S&S: enlarged glands can press onto the urethra, and obstruct urinary flow, urgency in peeing, delays in urine flow even though they need to go, decrease in urine flow so go little at a time, this can cause urine retention and over time it can cause an infection - Dx: usually with presenting S&S, enlarged prostate felt of a digital exam (DRE). - Tx: decreasing hyperplasia tissue, surgery. 2. Prostate cancer - malignant neoplasm of the prostate; risk factor: men over 54, family history of diet in saturated fats, and high testosterone level - S&S: similar to BPH or may not be present until its advanced. - Dx: elevated PSA (prostate-specific antigen), yearly PSA testing after 54, digital rectal exam 3. Testicular cancer - neoplastic of the testicles, causes are unknown. Usually in men who have Cryptorchidism undescended testicles, around 15-35 yrs age. - S&S: self-exam to feel for lumps that weren't there, heaviness, dull ache in the lower abdomen - Dx: high cure rate if found early. self-exam 4. infection of male GU tract - 2 most common i. Urethritis - inflammation of the urethra ii. Prostatitis - inflammation of the prostate. - Both are usually caused by sexually transmitted infection (STI) two most common are chlamydia and gonorrhea. - S&S: discomfort, discharge, dysuria.

Pulmonary disorder: ABG: how to determine the acid/base imbalances and compensation - Metabolic Alkalosis (HCO3) (base)

Metabolic Alkalosis: this high pH is caused by the metabolic system, a loss of acid, or an accumulation of alkali guy. = Ex: if your patient is vomiting they are going to lose HCl acid, and the blood acid is decreasing which will cause pH increase. - this shows ABG level as: pH >7.45, PO2 normal, PCO2 normal (lungs), and HCO3 >28. The compensation - is fixed by the Lungs, so CO2 is ruled by the acid, we want to hold on to the acid by increasing CO2 by decreasing RR or depth. Therefore they can retain CO2

Pulmonary system: ABG: how to determine the acid/base imbalances and compensation - Metabolic Acidosis (CO2) (acid)

Metabolic systems rule all acids in the body and acids in the cells of the body outside of the respiratory system. → Metabolic Acidosis: occur because of accumulation of the acids usually form a renal problem or the cell in the body is making too much acid (seem in diabetic ketoacidosis). = any kind of rapid production of acids OVERWHELM the HCO3 system. this causes the acid level to rise and the pH goes down - this shows ABG level as: pH <7.35, PO2 normal, PCO2 normal (lungs), and HCO3 <22. = if we see a low HCO3 (bicarbonate) is either an overproduction of acids or an inability of the kidney to function and produce bicarbonate. The compensation - is fixed by the Lungs, they rule by the CO2 an acid so decreasing the CO2 by increasing hyperventilating (breathing more), while they are doing it the term for rapid and deep breathing is known as Kussmaul. This gets rid of acid and increases the pH.

Pulmonary system: ABG: how to determine the acid/base imbalances and compensation - Respiratory Acidosis (CO2) (acid)

Respiratory Acidosis: occurs bc of inhibition of normal breathing, such as diminished effectiveness of exhaling, the individual can't exhale CO2 making you retain and accumulate it. CO2 is acid so if you hold on to it, it'll increase the acid in the blood. this is known as Hypercapnia - hypoventilation will lead to Hypercapnia because unable to get rid of it. = ex: the patient is unconscious and their breathing is very slow (hypoventilation), therefore retaining CO2, in CO2 in the blood goes up, therefore making the pH low since it's more acidic. - this shows ABG level as: pH <7.35, PO2 <80, PCO2 >45, HCO3 normal (kidney) The compensation - is fixed by the kidneys, since it rules HCO3 it will increase Bicarbonate or decrease its exertion into the urine.

Stroke Volume: Contractility, Preload, and Afterload. (part 2-4 of a good CO)

Preload - "what they just right preload/volume." *not too little nor too much* to blood returning to the heart to work. Contractility - "pump", the heart muscle must have a forceful pump to push out blood from the AV and LV. - inotropic: the effect of different factors on Contractility a. Positive inotropic - a enhances Contractility/pump of the heart b. negative inotropic - a decreased contractility/pump of the heart. Afterload - "resistance", means each chamber of the heart has a resistance to the movement of blood from that chamber. (only talk about the RV and LV) - right ventricle afterload: the RV eject into the pulmonary arteries and all the branches of the pulmonary vascular system and pulmonary arteries and branches can offer resistance, - Left ventricle afterload: is reflexed in the aorta and systemic arterial system. a. if there is a lot of blood in the LV (or RV) blood vessel, and if there is a lot of resistance in the LV that means it has to push really really hard, to get blood into the aorta. ex: now if there is an incident where the aorta will be resistant, that will be when the arteries were vasoconstrictor. This will create a high afterload, leaving more work for the Left ventricle to push the blood. b. Low afterload means less resistance, and the blood vessel can be more vasodilated. Less work for the ventricles, but too floppy. = it's better to have a just right resistance neither too high nor too low.

Types of Pulmonary High Restrictive disorder - causing a decrease of Gas exchange where O2 forms lung into blood and CO2 into the lungs. (the Q = perfusion part of the problem; The V/Q is greater than >0.8),

Pulmonary Embolus (PE) - People who are more at risk of getting this are patients showing S&S of Virchow's Triads (endothelial injury, hypercoagulability, venous stasis) that indicated a DVT. once this is dislodged it becomes an embolus traveling up the venous system making its way into the pulmonary arterial system blocking the pulmonary artery which would then include blood flow from the alveoli that are downstream from it. - the severity of the pulmonary embolus depends on how big the pulmonary embolus is and how big is the artery or what part of the artery is it occluding. - usually, the embolus is stuck in the smaller pulmonary Arterioles, in the lungs, and while it is stuck there the part it's stuck is not getting O2 to pass thru the arteries into the bloodstream and get rid of CO2. That portion of deoxygenated blood is not going to get to the alveoli to get oxygenated blood which causes SOB and Chest pain. - the chest pain is from not enough O2 that's going back into the heart or from the inflammation of the embolus that is irritating the arterial intima. - the Triggering of inflammation is then going to cause leakage of water into the alveoli as well as little RBC, this triggers the cough reflex, and pink and frothy sputum is brought up. - if the pulmonary embolus gets trapped in the larger pulmonary artery and is affecting a rather portion of the lung tissue then it'll not only trigger local but also Systemic Inflammatory Mediators will release the Acute Phase Reactant will cause massive vasodilation which can cause a drop in blood pressure which eventually lead to shock.

Pulmonary system: ABG: how to determine the acid/base imbalances and compensation - Respiratory Alkalosis (CO2) (base)

Respiratory Alkalosis: a state of high pH that is caused by rapid and more intense removal of CO2 = if we exhale a whole lot more then we are going to remove a lot of CO2. Therefore less CO2 in the blood, that means not enough acid in the blood, which makes the pH high. = ex: someone is hyperventilating due to having an anxiety attack - this shows ABG level as: pH >7.45, PO2 normal, PCO2 <35mmHg, and HCO3 normal (kidney). The compensation - is fixed by the kidneys, the kidney is ruled by the HCO3 a base we need to get rid of it so decreasing the HCO3 being made or increasing its excretion into urine.

Now we know that increase in breathing will indicate a pulmonary disease and now we can get into the actual diseases and they are divided into 2 categories Restrictive and Obstructive Pulmonary Disorder.

Restrictive Pulmonary Disorder: dz that will cause difficulty with inhalation, it'll show a low Oxygenation level. the SO2 will be lower than 97% and the PO2 will be less than 80. In Inhalation, there are 2 parts: V = ventilation and Q = perfusion (we need to know the problem either V or Q) i. V = ventilation - the normal amount of air tath should be brought in with each breath ~4Litter ii. Q = perfusion - the normal amount of blood in the lung during gas exchange per min. ~5Litter - Normal V/Q ratio is 0.8. = if there is some kind of inhalation problem it's a restrictive problem causing a low O2, a V/Q scan is done and there will be a V/Q Mismatch. Since it's a ratio the V/Q can either be higher or lower than normal. a. Low V/Q disorder - less O2 coming in. (ex: the patient is unable to bring in air, only 3 litter of air instead of 4L, the perfusion is still 5L the V/Q Ratio is 0.6 b. High V/Q disorder - people with less than normal perfusion. a problem that is causing damage or decrease in the amount of blood that is supposed to be zooming through the lung and getting access to all these alveoli. (ex: normal ventilation for 4 liters but only 4 L of perfusion. The V/Q 4/4 = 1.0. Greater than 0.8.

What happens to the part of the cardiac output is abnormal? The Stroke volume and its 3 factors that makes up the stroke volume. (contractility, preload, afterload)

SV = the amount of vol eject per beat. 1. contractility (pump) - cases of the abnormal pump will be the negative inotropic (less pumping ability), and the what causes this is ischemia, if the coronary artery that feeds the heart muscle is blocked, then those heart muscle certainly not getting oxygen = no work, decrease in the pump. = decrease of CO. 2. Preload (volume) - Increasing volume is a pathological problem, extra volume in the body means extra blood going through the heart and it put a lot of work on the heart, it causes the heart to weaken = and decrease CO; with decrease preload = less volume int he body = decrease of CO. - anytime the CO goes down BP will go down too. 3. Afterload (resistant) - resistant to the ejection of blood from the heart chamber (resistant to forwarding flow). the arteries after the chambers need a "just right" vasomotor tone and their linings have to be smooth and patent, but when they receive blood from the ventricles and the arteries are not smooth and patent and "just right tone" then they create more resistance to the flow of blood into them. - The pulmonary and aorta are the two arteries that cause resistance to the right and left ventricles. a. Right Ventricles pump blood into the pulmonary arteries system therefore the right ventricular afterload (resistant) to the pushing out of blood from the right ventricle is determined by the state of the pulmonary arteries. and if the pulmonary arteries are very tight and vasoconstriction it's going to cause more resistance to the right ventricle. - for there to be a normal Pulmonary artery and its branches that is called Pulmonary vascular resistance. b. Left Ventricles push out blood into the aorta and therefore the left ventricular afterload is determined by the normal status of the aorta (systemic arterial system). - the normal after the left ventricle is called systemic vascular resistance. - For a pathological increase or decrease in the vascular resistance: a. increase of vascular resistance: i. causes of increased afterload to the RV - is from pulmonary vasoconstriction, lung disorder, chronic bronchitis, and emphysema, all of these will cause an increase in pulmonary vascular resistance, which will then cause more work for the right ventricle and over time the RV will weaken. ii. causes of increased afterload to the LV or the systemic vascular resistance: if the aorta had atherosclerosis that will increase the workload = resistance, whenever the LV is pumping out blood and over time the RV will weaken. *** increase afterload = increase workload **** b. decrease of vascular resistance: i. causes of decrease afterload to the LV: this occurs when there is, massive peripheral arterial vasodilation, this is what shock is known as and your BP goes down. - examples: septic shock and anaphylaxis - having floppy blood vessels is not good, and there is no vasomotor tone and which often causes massive vasodilation is the inflammatory mediator - noting the S&S of poor perfusion can determine if the patient has a poor cardiac output. such as delayed cap refill (>2 sec), low BP, poor mental, cool skin, and poor urine OP.

Disorder of the Renal System: Kidney NORMAL Function. What is the flow of blood and flow of urine thru the kidney

The Kidney has a lot about concentration or osmolality (which means the same thing). The path of blood: the renal artery that comes off the descending aorta, and they will branch off till they reach the nephrons, the working units for the kidneys. The artery entreating the nephrons are called the afferent arterioles --> glomerulus --> blood excited the efferent arterioles. Surrounding the nephrons are the peritubular capillaries. The path of urine starts at the: glomerulus --> proximal consulted tubkes and loop of henle --> decsending tubules --> collecting tubules --> renal pelvis Speed pump: Juxtaglomerular apparatus, connects the glomerulus (the beginning part of the filtration) to the Distal tubules. they communicate with the beginning and the end of the flow of blood and urine. - The Function of the Kidney: remove waste and water, and a metabolic function of the kidney a. Maintenance of water and waste: the amount of waste to the amount of water. The kidney decided the "just right" amount of urine Concentration that the body needs at that particular moment. Normal urine is 95% water and only 5% is waste which contains urea, creatinine, Na, K, and PO4. These are the "waste" the kidney has to get rid of. The concentration decision is made in each nephron (the million of nephrons in the kidney do not communicate with each other, they function individually, even if called a working unit of the kidney, they each make their own decision), and the nephrons are made up of two structures, the glomerulus, and the tubules. i. Glomerulus - is what received the blood from the afferent arterioles. Its job is to filter things through their membrane, and it is supposed to keep things in that aren't supposed to go out, keep things out and let things out that should be. - The first decision point is in the Glomerulus where what should be urine begins - the kidney filter blood at ina very consistent rate 24/7, and this filtration of the blood is known as the Glomerular filtration rate (GFR). The entire Glomerulour of the kidney will filter 180L of blood per day (125ml/min). so all the nephrons are filtered this much every min. - Glomerular Filtration Rate (GFR) ensures wastes and water is removed. - if there this something wrong with the kidney then the GRF will go down (filtering less than <125ml/min). And the waste and water are not going out into the urine, and hang out in the blood. the GFR doesn't change unless there is something wrong with the kidney. - Glomerular filtration rate (GFR) decrease is determined by urine decrease (oliguria), less than <30ml/hr ii. Tubules: while the urine is moving through the tubules their job is to reabsorption and secretion - Tubular reabsorption: starts from the blood that is passing the glourmlulrs and is filtered, the substance is now in the kidney tubules, the tubules will then reabsorption the substances thing that is still useful and helpful to the body, back into the blood. Those nearby peritubular capillaries will accept the substances that the tubules kicked out. - Tubular Secretion: if there was a substance in the Glomerulus that zoomed out of the efferent arterioles and landed in the peritubular capillaries, they will move the substance back into the tubules, this need to be removed from the body, this is Tubular Secretion, bc that substance than moved back from the blood space back into the tubular space that will ultimately be removed in the urine. = The waste removed will always have a normal amount of creatininte and urea in the blood and urine if the kidney's working nephrons glomerular and tubules are fine. = Ex: if a person's kidneys arent working properly, their GFR will be LOW/DOWN, and there will be a HIGH of serum creatine and urea nitrogen in the blood since the waste substance that is supposed to be removed from the blood is not going to be removed from the blood the amount in the urine will be LOW. = since the nephrons (glomerulus and tubules) do not communicate with each other, the decisions made to remove certain substances and water are influenced by other factors like: angiotensin II, aldosterone, ADH, natriuretic peptides. - this will take place in one or more nephrons if they don't receive enough blood from the body↓: ex: if your patient has a fluid vol deficit, immediately the speed bump of the kidney aka Juxtaglomerular apparatus, is going to secreted Renin, it'll become angotension II, which vasoconstrictor and will also secrete aldosterone from the adrenal gland. the aldosterone will go to the distal convoluting tubules and tell them to hold on to sodium, so the sodium being reabsorbed from the kidney tubules back into the blood and water will follow along, and that is how water is held on it, as a counterbalance Potassium is removed. (decrease in the blood). - the ADH is secreted from the pituitary gland, it tells the Distal convoluted tubules to more water. = all of these will be cut off once the fluid volume goes up ↑. - if there is the opposite effect with fluid overload, then there is more stretch to the atrium and ventricles in the heart and they will produce BNP and ANP. these will make their way into the kidney to get rid of water. = all of these will be cut off once the fluid volume goes back to normal ↑.

Obstructive disorder in the Urological system: Affects the flow of urine

The flow of urine: kidney makes urine, leaves it goes down into the ureter into the bladder, and out the urethra Anything that blocks the flow of urine out into the toilet. - Harmful Sequela of the Obstruction, if it cants pass the ureter, all the urine gets trapped between the kidney and ureter and it collects, and you have a back pressure, and more and more collects unable to go down this is known as Hydronephrosis (enlargement of and pressure increase in the renal pelvic and calyces), this can cause damage tot he working nephron of the kidneys. Specific obstruction: 1. Tumors: occur anywhere within the urinary or renal apparatus 2. scarring (adhesion): from inflammation, they formed webs that wrap around the structures. 3. Females - Pelvic organ prolapse: when they have a lot of children and with age, the muscle holding on to the uterus falls down and forward onto the bladder 4. Males - Benign Prostatic hyperplasia (BPH): urine can't gets thru the urethra, due to the larger prostate gland causing an obstruction. 5. Neurogenic problems: there is a voluntary muscle in the bladder where it allows to hold urine but there is the involuntary muscle in the bladder where it sends a message up the spinal cord that they need to pee and the voluntary muscle kicks in and hold it in tell there is a toilet. 6. Kidney stones: the stones are called Calculus or Lithiasis. It can occur in any urinary apparatus. - risk factors on who is likely to get it: Male, Having gout (where the uric acid accumulation); dehydration; various diet factors, dz such as Multiple myeloma (cause hypercalcemia--> increase inflammation of kidney stone) - what are the stones: they are certain calcium, uric acid, or other ions that bonds and form crystals, and they attract others and those are how stones are formed. If the stones are greater than>2mm it can obstruct urine flow. and if it formed in the ureter it can cause the retrograde (scar tissue) of urine flow and hydronephrosis and renal damage and failure - S&S: Colicky pain: due to the spasm, that the stone causes as it is stuck in the ureter or urethra tube, its spasm to remove the stones down, the spams pain goes this come and go pain and it is very severe they want to move around all the time; Hematuria (when the stone moves it'll break the lining of the urethra or bladder and will cause blood to be in the urine. - dx: based on clinical presentation; Hematuria blood in urine) -tx: sent home with pain meds and push fluids instruction to help pass the 2mm stone; if the stone is too large surgery is used to remove it.

Electrical properties of heart: HR and rhythm How are the electrical impulses related to the heart rate? What is the mechanical portion of the heat cycle? (part 1 of a good CO)

There is an electrical component to the heart rate. Think of it as a switch, The rate of impulses is generated by the SA nodes that reside in the atrium, sends out the first electrical wave, and that impulse will travel all the way thru the heart in an organized way (PQRST). The SA nodes are responsible to generate it at a consistent heart rate (between 60-100). - if this generates a healthy normal impulse it moves down thru the heart then all the heart cells will depolarize, this is the electrical part and if this is working normally this is A normal sinus rhythm (NSR). Once the electrical impulse has been generated by the SA node and has moved thru the heart cell then that is the signal more the mechanical portion of the heart cycle. This is the actual beating of the heart. and the pushing of the blood is called systole: the RV and LV eject a good amount of blood out of their chamber into the lungs space or the aorta and systemic part. and the second part is the diastole: during this part, this is when the chambers are the filing of blood from the RA and LA. - the goal of the heart is to create an effective cardiac output (CO) = HR (and rhythm) and/or changes in SV (effective by contractility, preload, and afterload.

Chronic Kidney Disease (in depth), what happens if there is a Pathologic accumulation of water and impaired metabolic function.

Varieties of problem that can cause different degrees of kidney failure. - Congenital/Inherited renal problems Polycystic Kidney Disease (PKD): results in cyst being formed in the kidney. - Nephrons Acquired Disease: i. if an individual were to have AKI and over time develop into CKD. ii. A person who has multiple heart attacks, those heart cells die now can cause CKD. iii. Atherosclerosis: the narrowing of the arteries due to stiffing and narrowed can ultimately damage the nephrons, that are supplied by the blood vessel. iv. Hypertension can damage the kidney nephrons and the renal arteries v. Diabetes mellitus: the elevated glucose level will cause CKD in the renal kidney tissue which is the nephrons. Patho and S&S of CKD: the kidney do two things maintain water and waste removal and balanced and Metabolic Function, bc both of these, are chronically happing all the time so if there is CKD there is a problem with it there will be... a. Pathologic accumulation of water: (AKI, PKD, DM, HTN, Arthroscolosis; it doesn't matter which all are gonna lead to nephron damage). Concentration decisions are made by each Nephrons and when those "sick nephrons" are NOT going to make good decisions. They will have decreased glomerulus filtration rate --> decrease urine, in addition, Every ill nephron will start to overproduce RAAS, so a lot of renin --> angiotensin II, ultimately there is fluid retention, this will cause abnormally high volume in the vascular system.--> with a whole lot of renin and fluid in the body it'll cause hypertension --> kidney failure, and when you add water the blood that is going to cause a decreased serum osmolality. when you increase hypertension, which causes the hydrostatic pressure to go up and lower the osmolality that will cause a lot of water shifting from blood to tissue --> Peripheral and Pulmonary edema. b. And when those nephrons are sick... = they make naughty decisions on how much solutes to excrete into the urine. They don't secrete the proper amount of waste, therefore, the waste matter will accumulate in the blood. --> high calculation of phosphate in the blood (hyperphosphataemia), in addition, potassium, is also going also a waste and if the kidney nephrons are not able to get rid of it then it too will accumulate hyperkalemia as well as hypercalcemia will accumulate in the blood. (RAAS). = high serum waste level: high-level serum createine and blood urea nitrogen (BUN) will be present in the blood if the kidney is not working correctly. == Normal BUN is 7-25ml; more than >25 might have a kidney problem == Normal Creatinine level is 0.6-1.2ml/dl; more than >1.2 shows a kidney problem. ***elevated BUN + Creatine = real kidney failure***

Kidney job part 2: Maintenance of metabolic function.

a. They have greatly involved in the acid/base balance since they regulate and remove HCO3. but they also get rid of the acid (H+) too. b. Help promote stable nutrition by holding on to proteins, about everything in the body production of substance is protein-based, so the golmouarus filter needs to hold it on. c. regulating calcium absorption, calcium is hard to absorb from the food we eat, so we need vitenum D in our body to regulate the calcium level. d. Blood Pressure regulating due to the renin-angiotensin system e. help promoted stable hematological status because kidneys make erythropoietin which helps with RBC production and growth and the glamourous make sure no blood enters the urine.

Chronic Kidney Disease (in-depth), What happens if there is a Pathologic accumulation of water and impaired metabolic function.

b. Impaired Metabolic Function: 1. Results in hypocalcemia: the kidney produces a hormone that will activate vitamin D, this helps us absorb the calcium in the food we eat and when the kidney is not working the calcium absorption is low. (RMP = hypocalcemia --> hypopolarization --> shorter pole = hyperactivity of muscle = muscle spasm more sensitive.) they show a positive Chvostek's sign. - Osteoporosis can occur because of low calcium levels in the bodu 2. anima: bc when the kidney is sick it cannot sercte the hormone erythropoietin (make RBC) - S&S: weak, faughe, SOB. 3. acid-base balance: the kidney is responsible to make HCO3, w/o bicarbonate when the kidney re sick then the patient can become metabolic acidosis (acid). 4. Uremic encephalopathy: caused by the accumulation of the body waste, it will cause damage to the brain cells 5. Pruitits: the body will show the waste into the skin cell it'll cause this uremic frost, and they will complain of itchying.

Alterations in the Function of the Heart (RRD #7)

https://quizlet.com/_qgwn4?x=1jqt&i=2xa6q8

Disorders of the Pulmonary System (RRD #8)

https://quizlet.com/_qjbam?x=1jqt&i=2xa6q8

Disorders of the Genitourinary and Renal Systems (RRD #9)

https://quizlet.com/_qpl17?x=1jqt&i=2xa6q8

Pulmonary Disorder: The NORMAL process of the breathing cycle. What are the term Inhalation, Ventalition, perfusion, Exhalation

it consists of 2 phases: 1. Inhalation - during this process the diaphragm will drop down, and the ribcage will up and out, in this process it makes the intrathoracic space bigger causing a further decline of intrathoracic pressure, and when there is a decrease of normal negative intrathoracic pressure then that will cause air from the atmosphere to be sucked in eventually that air will reach the alveoli and that is the process of inhalation. There are two parts to inhalation. a. ventilation: a part of ventilation where the air passes thru the capillaries, within the lungs to make contact with that alveolar space.. b. perfusion: O2 can diffuse from the alveoli into the blood and CO2 can move from the blood into the alveoli tissue and expel out into the air. this is where gas exchange occurs. 2. Exhalation: the elastic respiratory muscles relax. the diaphragm relaxes and becomes small. = if your lungs are healthy and elastic there should be no problem in breathing and it should not take a lot of work to do so.

Part 1: How does the kidney maintain water and waste?

it removes waste and water, and a metabolic function of the kidney. a. Maintenance of water and waste: the amount of waste to the amount of water. The kidney decided the "just right" amount of urine Concentration that the body needs at that particular moment. Normal urine is 95% water and only 5% is waste which contains urea, creatinine, Na, K, and PO4. These are the "waste" the kidney has to get rid of. The concentration decision is made in each nephron (the million of nephrons in the kidney do not communicate with each other, they function individually, even if called a working unit of the kidney, they each make their own decision), and the nephrons are made up of two structures, the glomerulus, and the tubules. i. Glomerulus - is what received the blood from the afferent arterioles. Its job is to filter things through their membrane, and it is supposed to keep things in that aren't supposed to go out, keep things out and let things out that should be. - The first decision point is in the Glomerulus where what should be urine begins - the kidney filter blood at ina very consistent rate 24/7, and this filtration of the blood is known as the Glomerular filtration rate (GFR). The entire Glomerulour of the kidney will filter 180L of blood per day (125ml/min). so all the nephrons are filtered this much every min. - Glomerular Filtration Rate (GFR) ensures wastes and water is removed. - if there this something wrong with the kidney then the GRF will go down (filtering less than <125ml/min). And the waste and water are not going out into the urine, and hang out in the blood. the GFR doesn't change unless there is something wrong with the kidney. - Glomerular filtration rate (GFR) decrease is determined by urine decrease (oliguria), less than <30ml/hr ii. Tubules: while the urine is moving through the tubules ther job is to reabsorption and secretion - Tubular reabsorption: starts form the blood that is passing the glouros and is filtered, the substance is now in the kidney tubules, and the tubules will then reabsorb the substances thing that is still useful and helpful to the body, back into the blood. Those nearby peritubular capillaries will accept the substances that the tubules kicked out. - Tubular Secretion: if there was a substance in the Glomerulus that zoomed out of the efferent arterioles and landed in the peritubular capillaries, they will move the substance back into the tubules, this need to be removed from the body, this is Tubular Secretion because that substance than moved back from the blood space back into the tubular space that will ultimately be removed in the urine. = The waste removed will always have a normal amount of creatine and urea in the blood and urine if the kidney's working nephrons glomerular and tubules are fine. = Ex: if a person's kidneys aren't working properly, their GFR will be LOW/DOWN, and there will be a HIGH of serum creatine and urea nitrogen in the blood since the waste substance that is supposed to be removed from the blood is not going to be removed from the blood the amount in the urine will be LOW. = since the nephrons (glomerulus and tubules) do not communicate with each other, the decisions made to remove certain substances and water are influenced by other factors like: angiotensin II, aldosterone, ADH, natriuretic peptides. - this will take place in one or more nephrons if they don't receive enough blood from the body↓: ex: if your patient has a fluid vol deficit, immediately the speed bump of the kidney aka Juxtaglomerular apparatus, is going to secrete Renin, it'll become angiotensin II, which vasoconstrictor and will also secrete aldosterone from the adrenal gland. the aldosterone will go to the distal convoluting tubules and tell them to hold on to sodium, so the sodium being reabsorbed from the kidney tubules back into the blood and water will follow along, and that is how water is held on it, as a counter balance Potassium is removed. (decrease in the blood). - the ADH is secreted from the pituitary gland, it tells the Distal convoluted tubules to more water. = all of these will be cut off once the fluid volume goes up ↑. - if there is the opposite effect with fluid overload, then there is more stretch to the atrium and ventricles in the heart and they will produce BNP and ANP. these will make their way into the kidney to get rid of water. = all of these will be cut off once the fluid volume goes back to normal ↑.

Treatment of Chronic Kidney Disease (aka any individual whose kidneys are not working). Overview

problem to solve: 1. Oliguria and fluid volume overload: patho: kidney not working (decrease GFR), --> RAAS overreaction --> the kidney doesn't listen to the RAAS system, therefore, there is water is retained but No urine OP. Treatment: Diuretics --> drug that makes kidney get rid of water 2. azotemia and uremia (the acclimation of waste): the kidney stops functioning (decrease GFR) and is unable to remove waste into the urine --> leading to waste ACCUMLATON (BUN (protein breakdown) and SCr) in the blood (azotemia) if the patient is present with more S&S such as nausea, vomiting, Pruritis, confusion (Encephalopathy) is known as Uremia. Treatment: low protein diet, to reduce BUN 3. hyperkalemia - High potassium level in the blood: if the kidney is not functioning --> unable to remove waste and it accumulated --> it K+ that was supposed to leave the body will accumulate --> leading to Hyperkalemia = Hypopolarization --> fast heart rate Treatment: diuretic drug to remove excess water and a very specific diuretic to remove Ka+ 4. hyperphosphatemia - High c level in the blood: if the kidney is not functioning --> unable to remove it and accumulates in the blood. Treatment: oral antacids (ex: tums) it'll bind to phosphate and help it be pooped or pee it out 5. Hypertension (HTN) - High Blood Pressure: the kidney function decrease --> RAAS overload --> renin --> angoiteniosn II --> massive vasoconstriticion --> kidney retaiens water --> volume overload causes angiotension II --> HTN. Treatment: diuretic and anti-HTN medication to counteract the RAAS 6. Anima - if the kidney is not working --> low metabolic function --> erythropoietin is not made --> loss RBC treatment: erythropoietin injection 7. Hypocalcemia and osteoporosis - kidney not working --> low metabolic function --> no production of Vitamin D --> no calcium absorbed from food --> Hypocalcemia --> Hypopolarization --> over actives Parathyroid hormone (PTH) --> ramp up osteoclastic activity = brittle bone treatment: Vitamin D, calcium supplement 8. Metabolic Acidosis: high acid in the body, when the kidney is not working --> metabolic function is down --> low HCO3 production (base) --> will make the body more acid with no HCO3. treatment: administer HCO3 --> antacids 9. Extermine waste and water accumulation: this is when all hem dedication failed and the kidney has stopped working altogether treatment: dialysis and kidney transplant.

What happens to the part of the cardiac output is abnormal? Starting from the heart rate and rhythm. What are Tachycardia and Bradycardia? what can cause it to happen?

the system that gets the heartbeat to occur starts from the SA nodes of the heart, this SA node is located in the Right Atrium, an electoral which, the first thing that initiates, that electoral impulse to change the resting to working, these nodes will send out the simple traveling thru both atrium, and then down through the electrical system bc there is a special electrical current in the heart that will et all the cells in the heart to depolarize. 1. Heart rate a. Tachycardia (fast heart rate; more than >100 bpm): causes can be from: i. The sympathetic nervous system (SNS). the fight or flight system, and when during those times it released Epinephrine will then bind with the beta receptor of the heart, and HR will increase ii. Certain electrolytes changes, HR and Rhtym, and that is Potassium (hyperkalemia --> hypopolarization, (decease in line, more active, and more sensitive). iii. Glitches can occur in the SA nodes and AV nodes. b. Bradycardia (slow heart rate; less than <60 Bpm) - some causes: i. the parasympathetic NS takes over (rest and digest) and some illnesses overtake it, the vegas nurse will decrease acetylcholine the HR will decease ii. the electrolyte such as Potassium can decrease HR, with hypokalemia --> hyperpolarization (longer distinct, slow movement, less sensitive) iii. if there is a blockage in the right coronary artery, where they feed into the SA nodes and if there is a blockage it SA nodes can become ischemic, and won't send out electrical impulses at a normal rate of 60-100 but slower. 2. Rhythm: normal is called normal sinus rhythm then the SA noes is working fine. a. Dysrhythmia or Arrhythmia (Abnormal Rhythm) - is not looking how it's supposed to when looking at an EKG i. any type of ischemia bc all types of heart cells have the ability, to depolarize and as a group to perform a normal sinus wave. and anything that can causes infarction in the part of the heart can interfere with the normal impose conduction therefore an abnormal rhythm ii. Electrolytes imbalances - related the Potassium (K+) either hypo or hyper iii. the age of the wear and tear of the electrical system (ex: buying a house in the 1900s the electrical wiring in that house is not great) - there are 2 types of Arrhythmia a.1 - Atrial fibrillation (Afib): the two atria are like quivering like a bowl of jello. (jiggle, jiggle, wiggle, wiggle) This is what is happening to the atria when there is an abnormal electrical pathway. They are not in an organized contraction. - the Sequal of Afib: 2 of them. i. sometimes there might be a significant decrease in the cardiac output because when the atria are organized there is something called an atrial kick (background normal: when the blood is filing during diastole in the 2 atria (100% filled), and during systole the valves open up to let blood thru into he ventricle (75%) blop thru with no force needed, now the remaining 25% of blood in the atria will be squeezed out when the atria contracts - atrial kick) - with Afib you lose 25% of the blood = CO decrease ii. the leftover 25% of the blood will just sit in the atria and become a static pool and form a blood clot. - since there are 2 atria, the one on the left is arterial blood which is why atrial thrombi can occur, and this goes into the LV out of the atria and up to the brains which is why individuals with Afib are at a much higher risk of a stroke. = S&S of stroke: weakness of one side, confusion, - the right atria contains venous blood therefore venous thrombi can be formed when the blood becomes stasis, this can lead into the pulmonary arteries and lead into the pulmonary arterial system causing a pulmonary embolus (PE). - S&S of PE: SOB, Hemoptisus, chest pain, possibly shock. - tx: they will need medication to slow down the heart, due to the jiggling of the atrium a.2 - ventricular fibrillation: this is when the ventricles are now like a bowl of jello, quivering, and the electrical impulses are chaotic. The ventricles are not contracting and therefore are not ejecting blood, this is a deadly dysrhythmia = bad Cardiac Output. - S&S: no blood flow --> no pulse, no perfusion to the other organs unconsciousness --> death, unless there is medical intervention.

Cardiovascular system disorder part 2: Valvular Disorder.

there are valves that are in between the atrium and ventricles and the exits of the ventricles. Includes Aortic valve (between the LV and the Aorta), mitral valve (between LA and LV), pulmonary valve (between the RV and the pulmonary artery), and tricuspid valve (between the LA and the RV). - like a door, the valves allow entrance and exit. it opens quickly to allow blood to move forward and closes quickly so blood can not goes backward. - 2 valves disorders are: 1. stenosis (narrowing, stiffing), affects the valve opening. - when opened it should allow the flow of blood from one chamber out to the next one (i.e RA into the RV (tricuspid valve or the RV into the pulmonary artery it has to go through the pulmonic valve), But when there is valve stenosis it isn't opened and the RA wants to let the blood go into the RV and the tricuspid valve is stenosis the RA needs to work harder. = if you are listening, there is turbulence called a heart Murmur. (sound *lub, dub wooooosh*) 2. Incompetence (floppiness), is supposed to be when the valves are not closing correctly. - when it closes it should allow blood to flow forward and not backward from the chamber it just left from - For example: every time when the RA is dumping blood into the RV, and the tricuspid valve is incompetent it doesn't fully close it allows blood to sneak back into the RA. the blood is recirculating and creating more work for the chamber. - anytime there is an incompetent or insufficient valve there will be a Heart Murmur. bc the blood is not flowing the same way.