Patho Exam 2 PDF

Sodium = 135 -145 mEq/L Chloride = 98 - 106 mEq/L poolweather Bicarbonate = 24- 31 mEq/L ofSodain apack 2 Calcium = 8.5 - 10.5 mg/dL w...

Sodium = 135 -145 mEq/L Chloride = 98 - 106 mEq/L poolweather Bicarbonate = 24- 31 mEq/L ofSodain apack 2 Calcium = 8.5 - 10.5 mg/dL weight ofMilk Potassium = 3.5 - 5 mEq/L ofBananas O O O O Electrolyte - contraction of muscles, send nerve impulse, create bones, balance fluid in cells via osmosis, maintain the blood's Acid & Base. Sodium - Primary determinant of blood osmolarity. Hypo = diarrhea, sweating, vomiting. Hyper = loss of body water, high sodium intake. Potassium:Most abundant intracellular, mostly found in muscle; determined by body mass. Hypo = Excessive diuretic, vomit, diarrhea. Hyper = inappropriate use of drugs, renal failure. Chloride: plays a role in acid- base balance. Hypo= vomit, diarrhea, diuretics hyper = dehydration, kidney failure, hemodialysis, brain injury. Calcium: mostly in bones and teeth. Important for metabolic process: activity of enzyme, action potential, muscle contraction. Hypo = heparin, glucagon, thyroid disorder, severe burn, kidney failure, vitamin D deficiency, sepsis. Hyper = thyroid disorder, supplements, excessive bone breakdown. Where do our bodies hold fluids? How do the fluids move in and out of cells and tissues? How do fluids move in and out of circulation (vessels, nephrons)? 60% of the body weight is fluid that is divided into 2 components: Intracellular components consist of the fluid inside the cell 40% (⅔). Extracellular component is 20% or (⅓) into 3 components: - Interstitial Fluid: This fluid surrounds the cells in tissues and provides them with nutrients and removes waste products. - Blood Plasma: Plasma is the liquid component of blood and contains water, electrolytes, proteins, hormones, and various other substances. - Transcellular Fluid: cerebrospinal fluid in the brain and spinal cord, synovial fluid in joints, pleural fluid in the lungs, peritoneal fluid in the abdominal cavity, and aqueous humor in the eyes. Fluids move in and out : through aquaporins (protein channels that transport water between cells). Process of passive transport such as Osmosis and Diffusion. Active transport which is movement of molecules against gradients and requires ATP. VESSELS : Filtration and Reabsorption moves fluid through capillaries and surrounding tissues. Hydrostatic pressure pushes fluid out into interstitial space through filtration, by the pressure though the holes on the capillary walls. Osmotic pressure pulls fluid back into the blood through reabsorption, it goes towards the higher concentration inside the cell. Lymphatic System collects interstitial fluid (lymph) and returns it to the bloodstreams to prevent accumulation of excess fluid in tissue. ALBUMIN: are inside the vessel to help bring the fluid back in from osmotic pressure. NEPHRONS: - (INTAKES) production of Angiotensin II increases Aldosterone which targets the kidney to retain sodium and excretes potassium, sodium attraction indirectly causes fluid to move in. Osmoreceptors promote thirst (caused by the change in BP) which leads to the production of : ADH is released when there is high osmolarity in blood. Targets kidney to conserve water. (urine retention) EXCRETION) Diuretic drugs increase urine production, decrease sodium absorption. Or blocks RAAS. **KIDNEY- Incharge of fluid excretion and BLOOD PH. * How do our bodies regulate fluid intake and excretion? Thirst Mechanism: When the body needs more fluids, the thirst mechanism is triggered. This is controlled by the hypothalamus in the brain, which senses changes in blood concentration or volume. When dehydration occurs or blood becomes more concentrated, signals are sent to the brain to initiate thirst, prompting the individual to drink fluids. Renin-Angiotensin-Aldosterone System (RAAS): When blood volume or pressure decreases, special cells in the kidneys release an enzyme called renin. Renin triggers a cascade of reactions that eventually lead to the production of angiotensin II. Angiotensin II acts on blood vessels to constrict them, increasing blood pressure. It also stimulates the adrenal glands to release aldosterone. Aldosterone promotes sodium reabsorption in the kidneys, leading to water retention and increased blood volume. Vasopressin (ADH): Produced by the hypothalamus and released by the pituitary gland, vasopressin plays a crucial role in regulating water balance. It acts on the kidneys to increase water reabsorption, reducing the amount of water lost in urine. When blood osmolality increases (due to dehydration or high solute concentration), vasopressin secretion is stimulated, leading to increased water reabsorption and more concentrated urine. Atrial Natriuretic Peptide (ANP): Produced by cells in the atria of the heart, ANP is released in response to increased blood volume and pressure. ANP acts on the kidneys to increase sodium excretion and inhibit the release of renin and aldosterone, thereby promoting water excretion and reducing blood volume and pressure.  Osmoreceptors: These are specialized cells in the hypothalamus that detect changes in blood osmolality (concentration of solutes). When blood becomes too concentrated, osmoreceptors stimulate the release of vasopressin to increase water reabsorption and vice versa. Baroreceptors: These are stretch-sensitive receptors located in blood vessels and the heart that detect changes in blood pressure. When blood pressure drops, baroreceptors send signals to the brain to increase thirst and release vasopressin, aldosterone, and other hormones to restore blood pressure and volume. Tonicity, including isotonic, hypertonic, and hypotonic fluids Tonicity: tension of an extracellular solution, allowing water to move in and out of the cell, determined by solutes that can not cross the plasma membrane. Isotonic Solution: ○ In an isotonic solution, the concentration of solutes is the same inside and outside the cell. ○ As a result, there is no net movement of water across the cell membrane, and cells maintain their normal shape and size. ○ Examples of isotonic solutions include normal saline (0.9% NaCl) and lactated Ringer's solution. These solutions are commonly used for intravenous hydration to replace lost fluids and electrolytes without causing a shift in water balance. Hypertonic Solution: ○ In a hypertonic solution, the concentration of solutes is higher outside the cell compared to inside the cell. ○ Water tends to move out of the cell, leading to cell shrinkage (crenation). ○ Hypertonic solutions are used to draw water out of swollen cells or tissues and can be administered intravenously or orally for therapeutic purposes. Examples include 3% saline solution and 5% dextrose in 0.9% saline. Hypotonic Solution: ○ In a hypotonic solution, the concentration of solutes is lower outside the cell compared to inside the cell. ○ Water tends to move into the cell, causing it to swell and potentially burst (lyse). ○ Hypotonic solutions are used to rehydrate cells and tissues and are commonly administered orally or intravenously to treat dehydration. Examples include 0.45% saline (half-normal saline) and 5% dextrose in water. Altered fluid balance: hypovolemia, hemorrhage, dehydration, water intoxication, hypervolemia, edema HYPOVOLEMIA: inadequate fluid intake/excessive excretion; perfusion is decreased  Hemorrhage: excessive bleeding, water and sodium are lost ○ Hemoglobin, and hematocrit are decreased and BUN may be increased ○ damage to organs may be evident if not corrected Dehydration: decreased extracellular fluid volume/increased sodium content ○ can result in cellular shrinkage -> headaches, decrease reflexes, coma, seizures ○ hypertonic saline solutions can be used to increase water elimination ○ Water Intoxication : results from decreased sodium concentration from water replacement after strenuous activity, loss of sodium inhibiting ADH (disturbance of electrolytes) ○ Shock Can treat with lactated Ringers solution, need IV to restore lost fluid volume to HYPERVOLEMIA: increase of fluid volume; typically occurs when body retains too much fluid volume Edema: swelling in the body's tissues due to an accumulation of fluid caused by an imbalance between the movement of fluid into tissues and its removal, leading to increased fluid retention and tissue swelling. Edema: ○ leaves pitting when pressure is applied, like a divot ○ fluid staying inside the blood vessel into the interstitial space ○ if you have an increase of hydrostatic pressure, more water is pushed out ○ if you have low osmotic pressure, no water is coming back in Models: cirrhosis and dehydration Cirrhosis liver disease caused by interference of blood flow and hepatocyte damage. Manifestation: Ascites: The liver is preventing blood flow, the fluid backs up in the tissue. Caused by high osmolarity. The decreased albumin synthesis by the liver leads to reduced oncotic pressure in the blood vessels, causing fluid to accumulate in the peritoneal cavity. High osmotic pressure within the blood vessels relative to the surrounding tissues drives fluid out of the vessels and into the abdominal cavity, resulting in ascites. Treatment: Paracentesis : needle is used take fluid out , Duresis IV Albumin: Dehydration: altered fluid and electrolyte balance: caused by increase fluid output, decrease fluid intake, fluid shift between components (ascites) Manifestations: check vital signs (BP decrease, HR & RR increase to compensate), consciousness, capillary refill time, mucus membrane, decrease urine output, lack tears, shrunk eyes & fontanels. Diagnosis: Fluid I/O should be about equal, character of output (concentration, color), Nutrients. - Check for electrolyte, bicarbonate, BUN, Creatinine, specific gravity. Treatment : IV and oral rehydration (electrolytes). Ch 15: Altered Ventilation and Diffusion Ventilation - process of moving air in and out of trachea, lungs, bronchi Diffusion - process of moving and changing O2 and CO2 across the alveolar capillary membrane. Perfusion - Supplying oxygenated blood to the organs. Respiration - cells in the body using oxygen aerobically to make energy. How does ventilation work? 1. Control center in the brain ANS 2. Lung receptors 3. Chemoreceptors Ventilation - Inspiration (oxygen) and expiration (carbon dioxide). The Autonomic nervous system acts on the smooth muscles. PNS promotes bronco construction. SNS promotes bronchodilation, remembering beta receptors. Lung Receptors have specific roles for lung function. Receptors near epithelium sense irritants and promote reflexes like coughing, etc. Receptors in smooth muscles control expiration to prevent lung inflation. Receptors in capillary detects pressure and reduces it. Chemoreceptors sensory receptors that detect change in chemical composition in blood pH and Cerebrospinal Fluid. Partial oxygen (PaO2), Partial CO (PaCO2), and pH in the blood. Central chemoreceptors (brainstem) detect when CO2 levels increase and acidic blood, it increases the rate and depth of breathing to remove CO2. Peripheral chemoreceptors (near aorta and carotid) senses change in oxygen. When it increases respiration and depth to restore balance. Works surrounding muscles for max inspiration and chest recoil, expiration. How does diffusion work? At the junction between alveoli and capillaries, oxygen and carbon dioxide exchange occurs. Oxygen moves into the bloodstream while carbon dioxide moves out into the alveoli. Type I alveolar cells provide structure for gas exchange, while type II cells secrete surfactant, a lubricant for integrity and facilitating expansion. Without surfactant, breathing would be difficult. Diffusion efficiency depends on factors such as partial pressure, solubility (carbon dioxide being more soluble), and membrane thickness and surface area. Inspiration, expiration, partial pressures, O2 and CO2 transport Inspiration: Breathing in to get oxygen. Air moves from high pressure (atmosphere) to low pressure (the lungs). The chest changes in size to alter the pressure gradient, this draws air into lungs. Chest expands >> increases chest and volume >> pressure decrease >> air comes in. Expiration: Removing CO out Diaphragm moves back up and muscles relax. Gas moves out from high pressure (lungs) to low pressure (outside). Partial Pressure: (increase density,altitude,temperature, promoting collision >> pressure increase.) Dissolved oxygen in the blood plasma is partial arterial oxygen, PaO2, and dissolved carbon dioxide in blood plasma PaCO2. ( PaO2) decrease : hypothermia or high altitude. Increase: fever (PaCO2) decrease : hyperventilation. Increase: greater tissue metabolism such as fever. O2 and CO2 transport: Oxygen (2 ways)- After inspiration and diffusion across the alveolar capillary junction, gasses are transported and dissolved in plasma forming partial pressure. As PaO2 increases, oxygen dissociates from plasma and connects with hemoglobin on RBC. (oxyhemoglobin Hbo2) IRON attaches oxygen to hemoglobin. Oxygen continues to bind to Hg until completely saturated with oxygen. Oxygen saturation (Sao2) refers to the amount of oxyhemoglobin. (not all of them full, it just % that has oxygen in the Hg) ****When 4 oxygen molecules bind to hemoglobin, it is called fully saturated 100%. Oxygen continues to travel and diffuse into plasma until partial pressure oxygen in the arteries and alveoli are equal. Once it is even, it stops until the body needs more oxygen which is detected by the change in PaO2. The dissolved oxygen in plasma is used for cellular metabolism. Oxygen is less soluble than CO2 , that's why 87% - 99% is still bound to hemoglobin and the rest dissolved. Carbon dioxide (3 ways)- When cells are forced into anaerobic respiration, it produces acid metabolic waste in addition to CO2. Body overcomes this by traveling to alveoli and through lungs of exhalation. Carbon dioxide is more dissolvable and moves through capillaries easier. Once it is released from the cells, 5% dissolves into plasma, 20-30% bound to hemoglobin (Carbaminohemoglobin), 60-70% diffuses into RBC, binds with water, catalyzed by carbonic anhydrase FASTEST INSIDE. The diffuse CO2 in RBC is converted to carbonic acid or bicarbonate ions through the buffering system. They help with regulating blood pH. Any excess CO2 is exhaled out of the body through breathing. lung conditions like fibrosis prevents CO2 from being exhaled efficiently, leading to a buildup in the bloodstream. This buildup can cause a condition called acidosis, where the blood becomes too acidic. What happens when ventilation and diffusion are impaired? Impaired ventilation: Problem with airflow, trouble taking in oxygen and removing carbon dioxide out of the body. This is caused by (1) compression of the airway anywhere from the lung to alveoli. This can be from inflammation, edema,exudate, strangulation, etc. (2) disrupted neural transmission that stipulates breathing. This can be from the brain ignoring chemoreceptors or damaged nerves etc. Impaired diffusion: transfer of O2 and CO2 between the lungs and the bloodstream is hindered or compromised. Normally, during the process of gas exchange in the lungs, oxygen from the air in the alveoli diffuses into the bloodstream, while carbon dioxide from the bloodstream diffuses into the alveoli to be exhaled. This can be affected by (1) thickening alveolar membrane (2) decreased surface area, (3) decreased concentration gradient , (4) ventilation perfusion mismatch. (5) Solubility and partial pressure of gas *further discussed in the respiratory conditions* Impaired ventilation-perfusion mismatch: area of the lungs are either not ventilated or perfused properly. This means it can have impaired ventilation (not enough O2 coming in) even though there is enough blood to carry the oxygen. Vice versa, it can have impaired perfusion (no blood flow to the lungs) even when there is enough oxygen, but it has no blood to carry to other cells. Effects: hypoxemia, hypoxia, hypercapnia (restricted ventilation and diffusion: inadequate O2 take in or unable to release CO2)  emia Bloodstream HypOXemia : specifically refers to low levels of oxygen in the bloodstream. It is measured as a decreased partial pressure of oxygen (PaO2) in arterial blood, typically less than 80 mmHg. Causes: oxygen deprived, HYPOventilation, inadequate diffusion, inadequate uptake of oxygen in blood. This leads to Hypoxia: Inadequate supply of O2 to the cells and tissues. The effect is more widespread, all cells in the body become vulnerable. (espc. Heart lung brain). Oxygen deprived cells lead to reduced cell metabolism and function. This forces anaerobic metabolism >> leads to metabolic acidosis. Acidic cells for too long lead to cell death. (it can happen when there is adequate oxygen, like when there is a blockage in certain area, cell die only in that deprived area) HYPERCapnia: Increased carbon dioxide in the blood. CO2 diffuses much easier, so only presented in severe alveolar hypoventilation and alongside severe hypoxia, and prolonged period of air trapped in alveoli. >> leads to respiratory acidosis caused by CO retention. Leads to electrolyte imbalance>> alter cardiac condition and brain function. General manifestations of impaired ventilation and diffusion Local manifestations: (around the airway and lung tissues) are usually inflammatory processes. Ex. vasodilation, permeability, exudate, etc. 1) Cough : acute(3-8 weeks) = infection, allergies, aspiration, pulmonary embolism. Chronic (over 8 weeks) asthma, gastroesophageal reflux, chronic post nasal drainage, bronchitis, lung cancer. 2) Excessive mucus: Phlegm (large amount of sputum) that was expectorated.(cough/spit out). 3) 3) Hemoptysis - coughing up blood. 4) Dyspnea- Feeling of SOB. Based on presence of hypoxemia and hypercapnia > causing low pH. 5) orthopnea - difficulty breathing lying down, need to sit up. 6) Retraction - using accessory muscles 7) Chest pain 8) Chest size - Barrel chest AP to transverse 1:1 Systemic manifestations: caused by the effects of hypoxia and hypercapnia. > Fever, malaise, leukocytosis, increase circulating plasma protein. 1) dusk/cyanotic mucous membrane color 2) Change in ABG (pH, PaO2, PaCO2)  3) Mental status change 4) Clubbing finger How to measure impaired ventilation and diffusion **PEFR (peak expiratory flow rate = volume of air in one exhalation) How to treat impaired ventilation and diffusion Models: COPD: Emphysema, chronic bronchitis; asthma, cystic fibrosis Chronic Obstructive Pulmonary Disease: Inflammation in both the alveoli and the bronchi/bronchioles. Obstructed airway leads to air trapped in the lungs so less exhaled air. It is progressive and irreversible, only having treatments to slow down its progression. Emphysema: Enlargement of the alveoli causes it to lose elasticity and recoil (difficulty to exhale). Mostly caused by smoking, genetics, vascular damage from drugs, immune deficiency, connective tissue disorders. (3 types) centrilobular- mainly the respiratory bronchioles, paraseptal- the alveolar ducts, panacinar- acinus is uniformly damaged. Patho: In the early stage, the inflammation is distal (closer up) can be reduced. When it's mild-severe, there's inflammation in the alveoli, losing elastic recoil in the alveoli which obstructs airflow, which is irreversible. (smoking triggers inflammation>> neutrophil & macrophages >> release proteolytic enzymes like protease and elastase >> destroys extracellular matrix>> less elasticity for alveoli to recoil and release CO2). Without elasticity the alveoli walls collapse and trap gas inside so decrease O2 intake and CO2 release, blood pH go down. AntiProtease enzymes (AAT) synthesized by cells of the lungs help protect it from destructive proteolytic that digest structural protein (elastin). In emphysema, there is more proteolytic than antiprotease. Manifestation: chronic productive cough, insomnia, Dyspnea, barrel chest, pursed lips, tachypnea from regular activities. Diagnosis: (1)Measure the AAT level for non-smokers. (2) Pulmonary function test for expirationary airflow. (3) Auscultate, especially expiration sounds. ( also increase respiration) (4) Check for cyanosis, edema, hyperinflated chest (5) Spirometry: test for FEV1, forced expiration time (FET greater than 6 sec) (6) Measure the ABG for hypercapnia and hypoxemia Treatment: Irreversible, so maintain optimal lung function or low down the process. Quiz smoking or drugs (danazol or tamoxifen) to increase AAT in liver , or give AAT parentally. Bronchodilators, Steroid anti inflammatory drugs, ANTIBIOTICS, mucolytic agent (break down sputum) Chronic Bronchitis: Persistent and productive cough, lots of mucus. 3 months out of the year for 2 years. LAST DIAGNOSIS (excluding all other potential causes). Caused by smoking, exposed to environmental pollutants,genetics. Patho: Inflammation in the Bronchi/Bronchioles: inflammation and edema in the airway, hyperplasia/hyperplasia in the bronchial and smooth muscle, Bronchial walls thicken and development of fibrosis. (inflammation>increased mucus blocking airway> goblet cells hypertrophy> goblet cells blocks the cilia from moving the irritants and mucus) Chronic inflammation in the airways leads to structural changes that narrow the airways, increase mucus production, and impair the body's ability to defend against respiratory infections. manifestations: similar to emphysema, but upon auscultation there is wheezing and crackles form the mucus. Diagnosis: presented for up to 3 months within 2 yrs consecutively. Smoking leading to lung infection. ABG for hypoxemia and hypercapnia. Polycythemia (overproduction of RBC) to combat hypoxemia. Pulmonary function test showing low FEV1 and long FET. Test sputum for presence of pathogen. Treatment: Quit smoking, pulmonary rehabilitation, bronchodilator therapy, steroid anti inflammatory, mucolytic agent, oxygen supply, antibiotics and immunizations. Asthma: Inflammation and narrowing of the airway from environmental triggers, bronchial hypersensitivity, bronchoconstriction, or excessive mucus. Usually develops in childhood but can get to adulthood. Developed asthma are atopic where the body becomes hypersensitive without coming in contact with allergen. Patho: exact cause is unknown, but triggered by environmental allergens: smoke, dust, mites, mold, animal hair. Or triggers bronchospasm: anxiety, temperature extreme, anxiety, illness, exercise. (Mainly includes inflammation and hypersensitivity.) IgE-mediated hypersensitivity reactions release chemical mediators, which promote increased edema and cause bronchoconstriction. Mast cells also release chemical mediators: histamine & prostaglandin. Hours later (6-24 hrs) , leukotrienes are released, producing more bronchospasm, swelling, and could form mucus plugs. Over time cells of chronic inflammatory infiltrate the airway leading to permanent damage of the airway. Manifestation: As it is exacerbating, there might not be any symptoms. During exacerbation, wheezing, breathlessness, chest tightness, excessive sputum production, and coughing at night and morning. During the episode, anxiety, tachypnea, use accessory muscles. Hyperventilation (less CO2) leads to alkalosis, and ineffective expiration leads to acidosis. Diagnosis: evaluation S/S to see if it is attributed to asthma. Check patient family history for asthma and Atopy. Pulsus Paradoxus : big decrease in systolic during inspiration Wheezing or prolonged expiratory phase Check for Atpoic dermatitis, eczema, other forms of hypersensitivity. Test Eosinophilia (allergy wbc) ABG, spirometer and other lab tests. Treatment: (1) Monitor lung function with peak flow test. (2) Control environmental triggers (3) Drugs to reverse inflammation, bronchoconstriction, mucus secretion. Bronchodilators : (albuterol) anticholinergics & methylxanthine help relax the smooth muscle. Anti inflammation : glucocorticoids, cromolyn, leukotriene modifiers. (4) Patient education and have a care plan. Cystic Fibrosis Autosomal (both parents must carry the gene) recessive disorder that produces thick and sticky mucus, primarily affecting the lungs and digestive system, due to mutations in the CFTR gene. It also affects the pancreas. (Mostly affects caucasians, and are diagnosed at early age) Might need saltyFood LOTS of Water PATHO: mutation of the CFTR (cystic fibrosis transmembrane, conductance regulator) gene on Chromosome 7. Different electrolyte ions (mainly chloride) depend on CFTCR to serve as a channel for transportation. The cell's inability to conduct chloride there is less water (chloride attracts water). This leads to thick secretion and obstruction in respiratory tract, pancreas, GI tract sweat glands, etc. Lungs: This leads to mucus plugging, resulting from great volume of mucus, airway dehydration (caused by impaired chloride secretion, excessive sodium absorbed, and decreased water), and impaired ciliary. This attracts bacteria leading to more infection (staphylococcus aureus & Pseudomonas aeruginosa). Inflammatory responses further damage the lung tissues and mucus production. Over time lung tissues fibrosis and cyst form, hence the name. Pancreas / liver : The restricted chloride and water affects the intestines leading to pancreatic insufficiency. This causes digestion and absorption problems. Liver is also affected by mutation in the CFTCR restricts the transport of chloride and water in the biliary duct, causing increased viscosity of bile. Biliary obstruction leads to cirrhosis. JAUNDICE AND GI PROBLEM Manifestation: Thick mucus causing respiratory and GI impairment Recurring respiratory infections with chronic coughing Forceful coughing leading to vomiting Tachypnea, wheezing, hemoptysis, dyspnea, clubbing fingers, etc. Newborns: meconium ileus- trouble passing first stool bc its sticky. Children: poor absorption of fat (causing frequent greasy stool), trouble gaining weight. SWEAT ABNORMALITIES; EXCESSIVE SALT DEPLETION. Affects sexual development: men become sterile and women infertility. DIAGNOSIS: (1) SWEAT TEST: sweat chloride concentration of 60 mEq/L or greater. This test must be taken multiple times. (2) Genetic testing : at least 2 CFTCR mutations with associated symptoms. (3) chest & sinus radiology, sputum analysis (4) Fluid in the bonciolavioloar signs high neutrophil = inflammation. Treatment: maximize ventilation, nutrient, diffusion. -liquify & clear airway -High calorie diet, mineral supplement, reduce absorption. -manage disease complications: diabetes, bowel obstruction, fat liver, cirrosis. Ch 16: Altered Perfusion Perfusion Forcing blood and fluid to flow through vessels to supply tissue with oxygen and nutrients. (have adequate ventilation/diffusion, pulmonary circulation, blood volume, CO, control center in medulla, receptors, etc) Path from ventilation to perfusion Once oxygen enters lungs, and moves across the alveolar capillary junction, the pulmonary circulation distributes the oxygen. The ventilation and perfusion ratio is 0.8-0.9. There is more V/Q in the lower lobes bc it inflates more and more gravity. Circulatory system: pathway, pulmonary, systemic, cardiac -pulmonary circulation: In Charge of O2 and CO2 exchange between the atmosphere and the body. It involves the right side of the heart to carry deoxygenated blood to the lungs There is much less pressure than the systemic side, the slow movement allows maximum gas exchange. -Systemic circulation: Everything except the pulmonary circulation, it involves pumping blood out to the tissue, the left side of the heart. It has much more pressure as it is working against the peripheral tissues. -Coronary Circulation: Part of the systemic circulation, it is the heart supplying itself with oxygen and nutrients. Consist of the right and left coronary arteries, and its extensive branches, to profuse each side of the myocardium. There is increased circulation when there is increased demand or obstruction in tissue. Function of the heart: heart flows in the chambers and valves etc etc …. Cardiac cycle : One contraction (systole) where it forces blood out, and one relaxation (diastole) where blood fills the ventricles. Systole begins with the closure of the AV Valves, both the Tricuspid and Mitral, S1, the LUB. Then the ventricles contract, the semilunar valves (Aortic & Pulmonary) open and eject blood from ventricles, and it rapidly closes to prevent backflow. Closure of the semilunar produces the S2 sounds, the DUB. S3 sounds mean rapid filling of the ventricles and the ventricles are weak. S4 are heard during atrial contraction. Electrical impulses: Electrical impulses from the myocardial cell. Generated by movement of charge ions (SODIUM, CALCIUM, POTASSIUM) throughout the channels. Slow or fast responses stimulate cardiac contraction or relaxation. Induces: rapid depolarization, early repolarization, Plateau, rapid repolarization, resting phase. In depolarization: sodium goes into the cell. Early repolarization: closes sodium channel. Plateau: sodium channel opens and lets in calcium. Rapid Repolarization: sodium-calcium channel closes and lets Potassium out of the cell. ECG/EKG :  verification P wave = Depolarization of the atria (contraction) by the SA NODE (SA node = pacemaker) P-Q = depolarization of the AV node and bundle fibers in QRS= Depolarization of the ventricles T = Repolarization of the ventricles T U= repolarization of the purkinje fibers. Cardiac output measures the heart's efficiency to pump out blood. CO = Stroke Volume (SV) X Heart Rate (HR). Stroke volume = amount of blood pumped out in one ventricle in one beat. HR= Beats per min. CO varies with age, size, metabolic needs of tissue but the average is 3.5 to 8.0 L/min. Every min 8L of blood moves through the heart. (effected by: preload, cardiac contractility, afterload, heart rate, blood volume) Neural control of heart and blood pressure: Systolic = the pressure exerted during contraction in the LV to eject blood out of the aorta. Diastolic = amount of pressure remaining in the atria as the ventricles at rest. Controlled by the Autonomic Nervous System (SNS & PNS) 1. Baroreceptors: Located in vessels and heart, sense change in the pressure and alerts the cardiac control center. (ex beta 1= increase CO, alpha 1 = vasoconstriction) 2. Chemoreceptors: In aorta and carotid arteries, detect change in O2, CO2, and Blood pH. They alter ventilation/vasoconstriction to maximize oxygenation as needed. 3. Renin & Angiotensin : Angiotensin II is a vasoconstrictor increasing BP. Also stimulates aldosterone promotes water retention increasing BP. 4. ADH (vasopressin) 5. Epinephrine Altered perfusion inability to adequately oxygenate tissues. Resulted from low oxygen or poor utilization of oxygen. 1. Ventilation-perfusion mismatch - inadequate ventilation in well perfused areas of the lungs (asthma, pneumonia, pulmonary edema) - inadequate perfusion in well ventilated areas of the lungs. (pulmonary embolism) 2. Impaired circulation- inadequate or excess blood flow to organs. This can be from physical damage or obstruction in the vessel. Most common form of obstruction is from thrombosis. Main factors of thrombus is known as virchow Triad which are: vessel wall  damage, excessive clot, altered blood flow such as turbulence or sluggish blood movement. This leads to Atherosclerosis which is lipid clotting in arteries. Then Low-density lipoprotein (LDL) accumulates into foam cells, forming a fatty streak, turning to Fibrous plaques. EXAMPLES OF IMPAIRED CIRCULATION: Bifurcation: vessel breaches and it slows down the rest of the blood flow. Aneurysm: Outpouch of the vessel due to weakening of the vessel. Venous stasis: reduced venous return caused by heart failure or immobility for a long time. 3. Altered cardiac output: Heart unable to eject the necessary amount of blood to the pulmonary and systemic circulation. (1) Change in Blood volume, composition, and viscosity. (composition meaning how much RBC that can move oxygen around) (2) Impaired ventricular pumping (3) Structural defects : valves, aorta, septum, etc. (Stenosis- narrowing of the valves, causing turbulence, and more force required from the ventricles. Regurgitation - valve doesn't close properly, causing backflow of blood.) (4) Conduction defects causing unresponsive heart rate and rhythm (cardiac dysrhythmias- problem electrical nodes, especially the purkinje since it's in charge of ventricle contraction. This leads to fibrillation which is when the ventricles are vibrating instead of pumping. Heart Block- obstructed peacemaker, the SA node) (5) Excessive/reduced peripheral vascular resistance The change in the blood pressure Changes in perfusion demands Changes in demand depending on the state and condition of the body. This can be from change in blood pressure, obstructive processes, hemorrhages) Altered perfusion: manifestations, lab and diagnostics, treatments Manifestations: The effects of Hypoxia (cyanosis, pallor, cold, etc). Changes in blood volume and peripheral vascular resistance leads to change in BP. Hemorrhages also lead to altered perfusion. Lab and Diagnostic: 1. Echocardiography: ultrasound pics of the cardiac structure 2. Cardiac Catheterization: insert tube for sample, or inject contrast media to see defects. 3. Chest radiograph : check for fluid in the lungs (left side failure) 4. EKG 5. Sphygmomanometer- BP  6. Stress test - exercise and see how heart act 7. Cardiac nuclear scanning- see how blood flows at rest and exercising 8. Doppler Ultrasonography: measures the sound frequency of the blood to see how they flow. Treatment: Surgery : (Coronary artery bypass, Angioplasty, laser angioplasty vaporizes fat, Repair defect in valves) Drugs : Aspirin - (antiplatelet, prevent thrombus. ) any drugs that treat all the manifestations. IV: administer blood or fluid for severe hemorrhage or dehydration. Mechanical Pacemaker hypertension, Systolic over 140 and diastolic over 90. Associated with many other diseases. Caused by increased CO and peripheral resistance. Caused by SNS overstimulation, Renin-Angiotensin Production, Impaired kidney. Patho: Multifactorial disease complex interaction of genetic and environmental. Caused by increased cardiac output and peripheral resistance, causing structural and functional change to the heart. It damages the blood vessel inner wall (initima). The inflammatory response increased permeability also contributing to vessel damage. The walls hypertrophy and become more narrow. This causes the ventricle to work harder and also hypertrophy. Over time it leads to nephrosclerosis which over-stimulates the kidney to produce aldosterone. Manifestation: Often Asymptomatic and is detected in screening. Long term: headache, blurry vision, nausea, vomit, fatigue, confusion, mental status change. Many heart problems. And renal insufficiency. Diagnosis: Early detection to prevent cardiovascular diseases. Must conduct a series (usually 3) of proper BP measure over 3-6 months to diagnose as hypertension. Check the patient's overall risk of cardiovascular disease. Detects electrolyte levels, urinalysis, and tests for renal impairment. Treatment : control weight and exercise. DRUGS that decrease blood volume (diuretics), decrease cardiac contractility (calcium channel blockers), decrease peripheral vascular resistance (ACE and angiotensin ii blockers) shock, Circulatory failure causing impaired perfusion to the organs. Usually related to hypotension. Tachycardiaas the Body compensates Sudden Drop in Hypotention p Blood Pressure Cardiogenic Shock : (ineffective cardiac pumping = MI) loss of perfusion in the heart, leads to myocardial infarction.* increased TROPONIN protein during heart attack * Manifestations MI= Chest pain, SOB, labored breathing, diaphoresis, nausea, vomiting. Hypovolemic shock : (decreased blood volume) loss of fluid and not enough blood to perfuse the body tissues. Manifestation: blood and plasma loss, to treat it you would give them fluid and blood. Septic Shock : wide spread of infection, over exaggerated vessel dilation, dropping blood pressure, leading to decrease of perfusion. manifestations: infections causing fever and flushed warm skin. You would treat it with antimicrobial drugs. Neurogenic shock: Brain system depresses perfusion (head trauma, hypoxia, spinal cord injury) preventing CNS to send messages to the circulatory system. Treatment: treat the affected area and give inotropic drugs. increase cardiac Drugsthat output Anaphylactic: Releases histamine in the HgE, leading to inflammation, then vasodilation, decreases BP, then decreases perfusion. Give corticosteroids to decrease the systemic inflammatory response. Heart Failure: Inadequate pumping of the blood, secondary to structure differences or damages. Impaired cardiac function and excessive workload demands leads to heart failure like MI, structure defects, or inflammation, infection of the heart tissue. Right side: Affects the rest of the body, causes edema to the rest of the body. Left Side: (congestive heart failure) Affects the lungs (respiratory), fluid goes back into the lungs. Wet cough and and does not perfuse properly) Manifestations of the left side: SOB, dyspnea, coughing, cracking, cyanosis, exercise intolerance, poor urine output, sodium retention, anorexia, fatigue. Manifestation of the right side: ischemia of the right ventricle can cause chest pain, jaundice from fluid congestion in the HI and liver. Myocardial Infarction: Impaired coronary circulation. Caused by blockage from atherosclerosis or blood clot causing restricted blood/oxygen (ISCHEMIA), leading to death of myocardial cells. Atherosclerosis can completely block it or break off anc cause platelet aggregation leading to thrombus. When the right coronary artery is obstructed it affects the electrical nodes (SA & AV) which causes ventricular fibrillation, leading to irregular heart rhythm. - Family history - Hypertension and Smoking - Blood Cholesterol levels - Concurrent Diabete Mellitus - Type 2 diabetes elevates blood lipid levels. - High sensitivity C reactive Protein - protein developed by the liver in response to tissue injury which marks inflammation. Risk of MI because inflammation is linked with pathogenesis of atherosclerosis. - Hyperhomocysteinemia: amino acid that forms thrombus and leads to coagulation. Manifestation: Angina, crushing pressure radiating to the left arm, shoulder, and jaws. SOB, dizzy, sweating, pallor, anxiety, edema Diagnosis: ECG reading: ST segment may be elevated indicating problem with ventricular repolarization, prolonged Q waves. Angiography, echocardiography, chest radiography. Treatment: Treat the ABC, supply oxygen and give ASPIRIN which is an anticoagulant which increases perfusion. Nitroglycerin (vasodilator) and Morphine (analgesia) for chest pain. Surgery for percutaneous coronary intervention: angioplasty, Coronary Artery Bypass. Thrombolytic agents are platelet inhibitors. Medications that lower BP: beta blockers, ACE inhibitors, angiotensin blockers) Stroke: Acute neurological injury that results from pathological events such as shock, cerebral hemorrhage, ischemia, that leads to impairment in the cerebral circulation. (CEREBROVASCULAR ACCIDENT) Major risk factors: Hypertension, smoking, diabetes. Thrombotic stroke : forms and blocks an artery or blood vessel leading to the brain. This blockage reduces or completely cuts off blood flow to a part of the brain, resulting in damage to brain tissue due to lack of oxygen and nutrients (Transient Ischemic Attack TIA) Embolic stroke: obstruction caused from an emboli that occurs in the cerebral arteries. Hemorrhage stroke: Bleeding in the brain, accumulating pressure causes the surrounding cerebral vessels to weaken and erode. ending a Manifestations: characteristics of brain injury. The loss of function is based on the part of the brain that was ischemic or compressed by the accumulation of blood. (ex. If the medulla is effected it effects the cardiac and respiratory, sudden death) Cerebellar impacts are: hemiparesis (weakening of one side of the body) , vision, diplopia, dizziness, ataxia (lack of coordination), aphasia( language impair), decrease consciousness. **Stroke paralyzes the opposite side of the body, if the left side of the brain was affected then right side of the body is paralyzed** Diagnosis: Test for anything that could trigger it, such as MI, hemorrhage, infection, etc. Hypoglycemia can mimic stroke, check their glucose level first. Do a CBC, coagulation study, cardiac enzyme to determine the cause of the stroke. CT & MRI. Treatment: IV thrombolytic or anticoagulants for ischemia, Hemorrhagic stroke requires prevention of further bleeding etc.