NURS 5315/ NURS5315 Exam 3 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers | Best study material |100 out of 100

NURS 5315/ NURS5315 Exam 3 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers | Best study material |100 out of 100 2026/2027 | GRADED A+ | 100% VERIFIED Question: How does blood flow through the heart chambers/valves? Answer Superior vena cava to inferior vena cave. Blood then enters the right atrium and passes through the tricuspid valve to the right ventricle. The right ventricle pumps the blood to the lungs through the pulmonary valve to the pulmonary arteries where it becomes oxygenated. The oxygenated blood is brought back to the heart by the pulmonary veins which enter the left atrium. From the left atrium blood flows through the bicuspid (mitral) valve into the left ventricle. Question: Which coronary arteries provide blood to which part of the heart? Answer a. ) Left coronary artery i.) Left anterior descending artery:widow maker LV and RV, intraventricular septum ii. ) Circumflex: LA and left lateral wall of LV. b. ) Right coronary artery RV, intraventricular sulcus and small vessels of the RV and LV Question: What factors contribute to blood flow in a vessel? Answer Pressure difference between two ends of a vessel Resistance: r/t diameter of a vessel Viscosity (n) of the blood Length (l) of the vessel Question: What does QP: QS mean and what factors alter a normal ratio? Answer Q=blood flow QP= blood flow to the lungs (pulmonary) : QS= blood flow to the body (systemic) i ) Vascular resistance =measures in woods units ii) Pulmonary vascular resistance (PVR) 1. ) 8 weeks of age: 8-10 woods units/m2 2. ) 8 weeks of age: 1-3 woods units/m2 iii) Systemic vascular resistance 1. ) Infant 10-15 woods units/m2 2.) 1-2 years old: 15-20 woods units/m2 3.) Child to adult: 15-30 woods units/m2 a) Factors affecting resistance i.) Compliance-ease that blood travels through the arteries 1. Constriction and relaxation of smooth muscle of arteries and arterioles a. ) Sympathetic nervous system b.) Local tissue metabolism c.) Hormone responses d.) Changes in chemical environment Explain the process of cardiac contraction and relaxation. Question: What are the roles of actin, myosin, and troponin in this process? Answer At rest, active sites on actin are blocked by troponin and tropomyosin complexes. During action potential, troponin C binds with calcium and moves the complexes off the actin active site. Actin and myosin interact (contract). Question: "Walk-along" theory: Answer Head of myosin cross-bridge attached to the actin filament at the active site. Intra molecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin filament with it (power stroke) Myosin head breaks away and interacts with the next actin active site. Z disc pulls filaments together at the sarcomeres= muscle contraction. Question: What is the effect of Epinephrine on the cardiovascular system? Answer Stronger Alpha 1 than Alpha 2. Works on both, equally strong on Beta 1 (renin release), and Beta 2. Positive inotrope. Increases heart rate, smooth muscle contraction, myocardial contractility, coronary flow, increase systolic blood pressure, mild increase in diastolic blood pressure. Question: What is the effect of Norepinephrine on the cardiovascular system? Answer Slightly stronger Alpha 2 than Alpha 1. Some effect on Beta 1, none on Beta 2. Strong vasoconstriction (smooth muscle contraction). Increase coronary flow, increase systolic and some diastolic BP. Question: What is the effect of Dopamine on the cardiovascular system? Answer Positive inotrope. Increases HR, increases BP (vasoconstriction) Alpha 1, 2, beta 1 and dopamine receptors) Question: What is the process of generating a cardiac action potential? Answer What electrolytes are involved? 0-Depolarization 1-Early repolarization Rapid sodium entering the cell 2. Plateau (repolarization) Slow sodium and calcium enters the cell 3. Potassium moves out of the cells 4. Return to resting potential Sodium, Calcium, Potassium Question: What is the conduction pathway? Answer SA Node, AV Node, Bundle of His, Right & Left Bundle Branches, Perkinje Fibers Question: How does conduction correlate with the EKG and activity in the heart? Answer P-wave: spread of depolarization through the atria followed by atrial contraction. P-R interval: pause in conduction at the A-V node QRS complex: Depolarization of the ventricle, followed by ventricular contraction T wave: depolarization of the ventricles, happens just before the end of ventricular contraction Question: Define preload. Answer Volume of blood returning to the heart from systemic circulations. RA pressure or CVP Question: Define afterload. Answer Systemic pressure=the pressure the heart must pump against to circulate blood=MAP Question: Define stroke volume. Answer Amount of blood ejected with each contraction of the heart Question: Define end-diastolic volume. Answer Amount of blood in the heart after filling, before systole (end of diastole) Question: Define end-systolic volume. Answer Amount of blood that remains in the heart after systole Question: Define ejection faction. Answer Percentage of blood in the chamber that is ejected with each systole Question: Define cardiac output. Answer Amount of blood pumped into the aorta each minute Question: What are the causes, risk factors, pathophysiology and manifestations of atrial fibrillation? Answer Risk factors/causes: Heart failure, ischemic heart disease, HTN, obesity, obstructive sleep apnea, rheumatic heart disease, thyroid disease Patho: Remodeling of the myocytes of the myocardium-atria does not fully contract to empty contents. Estimated 25% loss of blood from the artia to ventricle. Manifestations: Fatigue, dizziness, dyspnea, irregular pulse, palpitations. Untreated: at risk for thrombus formation and stroke Question: What are the causes, risk factors, pathophysiology and manifestations of premature ventricular contractions (PVCs)? Answer Risk factors/causes: Abnormal electrolytes (hypokalemia, hypercalcemia), hypoxia, aging, induction of anesthesia, central line placement, cardiac cath, caffeine intake, drug use, exercise. Patho: Decreased cardiac output from lack of atrial contribution to ventricular preload Manifestations: fluttering, pound, palpitations Question: What is the role of lipproteins? Answer Lipoproteins include lipids, phospholipids, cholesterol, and triglycerides. Manufacture and repair plasma membranes and cholesterol needed for bile salts and steroid hormones. How do the lipproteins inform your knowledge of a persons cardiovascular risk? Answer Very-low-density lipoproteins (triglycerides) Low-density liporoteins (LDL) High-densitity lipoproteins (HDL) Very-low-density lipoproteins (triglycerides): Elevated number is a strong predictor of risk for future coronary events Low-density lipoproteins (LDL): "lousy", indicator of coronary risk but in context of other factors: age, DM, CKD High-density lipoproteins (HDL): "protective" against atherosclerosis-want high level. Can remove excess cholesterol from arterial walls What are the risk factors for dyslipidemia? Answer Primary 1. Geneteitcs reult in abnormal lipid metabolism and/or abnormal cellular lipd receptors. Secondary 1. Lifestyle: Smoking, obesity, sedentary lifestyle, diet 2. Health status: HTN, DM, hypothyroidism, pancreatitis, renal nephrosis, chronic inflammation 2. Medications: Diuretics, beta-blockers, steroids, anti-retrovirals 4. Environmental (not much known): air pollution, exposure to radiation, gut biome. Describe the pathophysiology of atherosclerosis? Answer 1. ) Injury to the endothelium causes an inflammatory response, monocytes and platelets move to the site of injury. 2. ) LDL enters the intimal layer of vessel, causing inflammation and oxidative stress and macrophage activation. LDL is engulfed =foam cells. Foam cell accumulation = fatty streak. 3. ) Further inflmmatory process in response to fatty streak. Causes the smooth mucle cells to produce collagen, which forms over the fatty streak making a plaque. This may calcify: Monckeburg atheroloclerosis 4.) Complicated lesions (unstable plagues): plaque prone to rupture. (cause ongoing inflammation, apoptosis, plaque hemorrhage). Once ruptured, clotting cascade is activated and local thrombus can cause occlusion, leading to ischemia and infarction. Foam cells: form through dysregulated lipid metabolism in mammalian macrophages. As macrophages eat lipids, results in something like white sea foam. Fatty streak: appear when the presence of foam cells at the site of plaque formation expands What is peripheral artery disease and how does it manifest? Answer Atherosclerosis of arteries that perfuse the limbs. Especially lower extremities. May have intermittent claudication Most are silent until there is an ischemic event-severe pain, cool, pulseless, pale. Manifestations: More common in African American population. Answer Intermittent symptoms: pain with ambulation. Rarely symptomatic until they've had an acute ischemic event. Loss of distal pulses. Color change. Increases risk for coronary artery disease. What factors contribute to determining a blood pressure? a.) Regulated by SNS i.) Promotes cardiac contractility ii.) Controls arteriolar vasoconstriction b.) SNS responds to catecholamines i) Epi/Norepi c.) SNS stimulates RAAS What is hypertension and what are common causes? Abnormal (high) blood pressure. Sustained 130/90 (United States metric) Primary causes: Genetics and environmental factors Secondary causes: Underlying disease. Renal disease (RAAS system and increased fluid volume) Pheochromocytoma-stimulates catecholamines release with stress Pregnancy: ?, placenta, increased fluid volume What is the sympathetic nervous system role in hypertension? Abnormal function of the sympathetic nervous system causes vasoconstriction, increased peripheral resistance, and sustained HTN. a.) Increased activity b.) Increases HR and PVR c.) Increased insulin resistance-endothelial dysfunction-vessels narrow (vasospasm) d.) Vascular remodeling - vessels narrow e. ) Procoagulant effects- vessels narrow Describe acute and chronic complications of hypertension? Chronic: Vascular remodeling: fibrosis of vessels leads to injurt of the organs perfused by the vessels (cardiac muscle, retinas, kidneys, brain) Left ventricular hypertrophy: leads to heart failure. Acute: Hypertensive crisis: Rapid increase in SBP 140 causes cerebral arterioles to be unable to regulate blood flow to the cerebral capillaries which cause cerebral edema and encephalopathy. Associated with pregnancy, cocaine and amphetamine use, adrenal tumors, and alcohol withdrawal. MEDICAL EMERGENCY! Discuss how electrolyte imbalances affect conduction, contraction, or resistance? Potassium: Magnesium: Calcium: Sodium: Potassium: Vasodilator. Increased levels lower blood pressure. Significantly elevated levels decrease conduction. Magnesium: Direct vasodilator. Increasing calcium can lower blood pressure. Slow heart rate. Calcium: Deposited in the tunica media, assists with vasoconstriction. High levels of calcium increase blood pressure. Sodium: High sodium leads to increased water retention and increased blood volume. Causes HTN. Need adequate levels of K, Mg, and Ca to help with excretion of Na. Describe coronary artery disease. Atherosclerosis of coronary arteries. Decreased blood supply. Describe myocardial ischemia. Local, temporary oxygen deprivation. Cells live but do not function normally. Describe acute coronary syndrome. Persistent ischemia or complete occlusion of coronary artery. Commonly MI. Explain the pathological steps of myocardial ischemia and myocardial infarction. The occlusion of a coronary artery reduces blood flow to an area of the myocardium, causing ischemia, dysfunction of the myocardium, and eventually myocyte death due to prolonged vascular compromise. The duration and severity of blood flow reduction are the 2 factors that determine the outcome. Describe the persons most at risk for, the etiology of, and the presentation (clinical manifestations) of stable angina? Etiology: Pain transient. Increased lactic acid; ischemic stretching of myocardium-irritates nerve fibers Clinical manifestations: Pain varies with nerve fibers. C3-T4 Describe the persons most at risk for, the etiology of, and the presentation (clinical manifestations) of unstable (prinzmetal) angina? Etiology: Vasospasm (w or w/o) atherosclerosis. Decreased vagal activity, hyperactive SNS, decreased NO activity, altered CA channel function, benign to significant arrhythmias. Clinical manifestations: Pain: unpredictable but generally at rest. Describe the persons most at risk for, the etiology of, and the presentation (clinical manifestations) of silent ischemia? Etiology/at risk: LV sympathetic innervation, DM, post cardiac surgery, mental status. Clinical manifestations: No pain-usually have to deep dive with HPI on these individuals: fatigue, dyspnea, feel uneasy. Define unstable angina and list the clinical manifestations. Definition: Superficial plaque erosion-transient thrombic occlusion-vasoconstriction at site of damage. Clinical manifestations: New onset angina, rest angina 20 minutes, increased frequency/severity. EKG: flipped (inverted) T wave, ST depression-resolve with pain resolution: no change in biomarkers. Define NSTEMI and list the clinical manifestations. Definition: Plaque disruption-clot formation-ischemia: breaks up before complete transmural necrosis. Clinical manifestations: ST depression: T wave inversion; elevated biomarkers. Define STEMI and list the clinical manifestations. Definition: Complete transmural ischemia-cardiac dysfunction Clinical manifestations: ST elevation, deep Q waves: elevate biomarkers Evaluate the differences in the extent of an infarction of the myocardium secondary to a NSTEMI. Extent/severity of infarct: Plaque disruption-clot formation-ischemia: breaks up before complete transmural necrosis. Evaluate the differences in the extent of an infarction of the myocardium secondary to a STEMI. Extent/severity of infarct: Complete transmural ischemia-cardiac dysfunction How might the structure or function of the heart change after a myocardial infarct? a.) myocardial remodeling b.) decreased ability to meet bodies oxygen demands c.) papillary muscle dysfunction, ventricular rupture d.) Symptoms vary on artery involved. i. Stunning: temporary loss of contractile function ii. Remodeling: myocyte:-scarring-loss of distal function-maybe limited or reversed with flow restoration (medications) iii. Myocardial repair: degradation of injury:-scar tissue-long term-decreased cardiac contractility, altered LV compliance, decreased SV/EF, increased LVEDP and volume, SA node dysfunction. This is the key lab used in diagnosing a myocardial infarct ___________________. Other labs that maybe useful in patients with MI and why? Cardiac troponin: most specific for MI. i. ) Detectable within 2-4 hours, repeat at 6-9 hours, and 12-24 hours. ii.) Can help calculate infarct size and therefore complications. Other labs that may be useful in patients who have an MI include ____________, and why? CK-MB and LDH may be elevated Leukocytes (WBC) and CRP may be elevated r/t inflammatory process. Elevated serum glucose: due to release of catecholamines, specifically norepinephrine. Describe the etiology, risk factors, clinical manifestations, and pathophysiology of reduced EF heart failure. Etiology: Old terminology: systolic dysfunction Risk factors: Atherosclerosis-MI, HTN, medications, sarcoid Clinical manifestations: EF 40%, crackles (pulmonary congestion), S4, LVH on EKG, CXR will show cardiomegaly and pulmonary congestion (Kerley B lines)-may result in pulmonary hypertension Pathophysiology: Inability of the heart to generate adequate cardiac output to perfuse tissues. Increased pre-load: contractility decreases. Decreased CO -increased EDV, increased preload-dilation of heart. Describe the etiology, risk factors, clinical manifestations, and pathophysiology of preserved EF heart failure. Etiology: Old terminology: diastolic dysfunction; can co-occur HFpEF/HFrEF Risk factors: Women (possible because of aging-women live longer), hypertrophy, HTN (controlled or uncontrolled) Clinical manifestations: Crackles (pulmonary congestion), S4, LVH on EKG, CXR will show cardiomegaly and pulmonary congestion (Kerley B lines)-may result in pulmonary hypertension Pathophysiology: Decreased LV compliance; abnormal relaxations-increase in LA pressures-pulmonary congestion (edema). Changes in calcium transport from myocytes, autonomic and endothelial dysfunction. Explain the etiology, risk factors, clinical manifestations, and pathophysiology of left-sided heart failure. Etiology: heart related diseases such as coronary artery disease (CAD) or a heart attack and cardiomyopathy. Risk factors: Atherosclerosis-MI, HTN, medications, sarcoid Clinical manifestations: Crackles (pulmonary congestion), S4, LVH on EKG, CXR will show cardiomegaly and pulmonary congestion (Kerley B lines)-may result in pulmonary hypertension Pathophysiology: Decreased LV compliance; abnormal relaxations-increase in LA pressures-pulmonary congestion (edema). Changes in calcium transport from myocytes, autonomic and endothelial dysfunction. Explain the etiology, risk factors, clinical manifestations, and pathophysiology of right-sided heart failure. Etiology: Inability to provide adequate blood to lungs at normal CVP Risk factors: Pulmonary HTN: if only RV failure Large: infection MI Clinical manifestations: JVD, peripheral edema, hepatosplenomegaly (systemic symptoms) Pathophysiology: RV hypertrophy due to increased pulmonary pressure but diastolic and systolic dysfunction Explain the process of ventricular remodeling. Myocytes hypertrophy and ventricle dilate, this impairs contractility Describe the etiology, clinical manifestations, and pathophysiology of Aortic Stenosis. Etiology: Congenital, acquired-inflammation, ischemia, trauma, degenerative processes, or infection. Clinical manifestations: Dizziness, shortness of breath, fatigue, syncope, peripheral edema. Pathophysiology: Narrow valve, restriction of forward flow-calcification, bicuspid, inflammation r/t rheumatic heart disease-decreased blood flow to LV-body-LV hypertrophy. Describe the etiology, clinical manifestations, and pathophysiology of Mitral stenosis. Etiology: Congenital, acquired-inflammation, ischemia, trauma, degenerative processes, or infection. Clinical manifestations: Atrial dysrhythmia and pulmonary edema. Pathophysiology: Limits blood flow from LA-LV (LA hypertrophy) Describe the etiology, clinical manifestations, and pathophysiology of Aortic Regurgitation. Etiology: Congenital, acquired-inflammation, ischemia, trauma, degenerative processes, or infection. Clinical manifestations: Shortness of breath, arrhythmia, lightheadedness, dizziness, chest pain. Pathophysiology: Incomplete closure of valve-back flow to affected chamber-increased workload-LA dilation hypertrophy. Biscupid, degeneration of valves, HTN, rheumatic heart disease, Marfans syndrome. Describe the etiology, clinical manifestations, and pathophysiology of Mitral Regurgitation. Etiology: Congenital, acquired-inflammation, ischemia, trauma, degenerative processes, or infection. Inherited tissue disorders and hyperthyroidism. Clinical manifestations: Pulmonary congestion, shortness of breath, fatigue, peripheral edema, palpitations Pathophysiology: MVP* (Most common in US): back flow to LV-LA (LA hypertrophy-dilation-PHTN-RV failure) MVP -Mitral valve prolapse Discuss the etiology, clinical manifestations, and pathophysiology of Endocarditis. Etiology: a.) Infection/inflammation of endocardium particularly valves. i.) Staph aureus ii.) Steptococci iii.) Enterococci iv.) Viral b.) Prosthetic valves, IV drug use, acquired heart disease, long term indwelling IV catheters - increase risk. Clinical manifestations: possible embolism, fever, night sweats, malaise, murmur, regurgitation, heart failure. Pathophysiology: Endocardial damage-heart/valve/trauma/ bacteremia-adherence to endocardium-forms vegetation possible embolism, fever, night sweats, malaise, murmur, regurgitation, heart failure. Diagnosis: Blood cultures, CBC, Echocardiogram (TEE), CXR, CT, MRI Treatment: Antibiotics, valvular repair (surgical), prevention with prophylaxis (dental, surgical) Two roles of the cardiovascular system 1. Transport nutrients, O2, and hormones throughout the body. 2. Remove waste products Vascular resistance is measured in ___________ Wood units PVR (Pulmonary vascular resistance) 8 weeks- 8-10 woods units/ m2 8 weeks- 1-3 woods units/m2 SVR (Systemic vascular resistance) Infant =10-15 wood units/m2 1-2 years old = 15-20 woods units/m2 List the structures that comprise the conducting airways. Nose, pharynx, larynx- (extra-thoracic), trachea, bronchi, bronchioles-(intrathoracic) List the structures that comprise the respiratory zone. Terminal bronchi, alveoli, alveolar capillaries What factors affect the muscles in the bronchi and bronchiloes? a.) Transpulmonary pressures -keep smooth muscle areas open b.) Smooth-sympathetic (beta 2 receptors-relax smooth muscle-epi) and parasympathetic innervation-vagus nerve0(acetylcholine-contraction of bronchoilar smooth muscle and bronchoconstriction). c.) Lung cells and endothelium=leukotrienes=constriction d.) Histamine and substance from mast cells (anaphylaxis) = contraction e.) Airway resistance: small changes in diameter increases difficulty breathing Describe the intrathoracic pressure changes that result in air movement into and out of the alveoli. a.) Pleural pressure: (between linings of pleura) negative (-5 cm H20) inspiration (expansion)- 7.5 cm H20) -increased suction pulling lungs with ribs b.) Alveolar pressure: measure of respiratory tree, when glottis is open (atmospheric pressure = 0 mm H20; with chest expansion pressures decrease to -1cm H@) - air moves out; recoil - alveolar pressure increases to +1cm and air moves out. c.) Transpulmonary: difference between pleural and alveolar pressure i. Elastic forces: PEEP, surfactant, and closed and glottis. How does a pneumothorax disrupt intrathoracic pressure and change air movement? Breach of pleural spaces: atmospheric air enters and equalizes pressure to atmospheric at 0 (-4 mm of Hg is lost)- lung cannot expand. Air gets in but cannot get out. Clinical manifestations include dyspnea, tachypnea, deviated trachea, decreased breath sounds on affected side and hyperresonance to percussion. Normal compliance curve What the curve looks like: Normal oval Represents: Pressure necessary to get air into lungs Associated disease process: Normal/homeostasis Increased lung compliance curve What the curve looks like: wide oval curve Represents: Greater pressure necessary for exhalation Associated disease process: Obstructive diseases (destruction of the airway-loss of elastin): CIOD; emphysema (asthma to a lesser degree). Decreased lung compliance curve What the curve looks like: Compliance curve on side and narrow (small curve) Represents: Higher pressure required to get air in and when air is in usually a lesser volume Associated disease process: Restrictive diseases: PNE; pulmonary edema, fibrosis Tidal volume (TV) Volume of inspired and expired air with each "normal" breath. Inspiratory reserve volume (IRV) Max effort of air inspired after "normal" inspiration. Expiratory reserve volume (ERV) Max effort of air expired after "normal" expiration. Residual volume Air left in the long at the end of ERV Inspiratory capacity TV+IRV (75-120%) Functional residual capacity ERV + RV (75%-120%) Vital capacity IRV+TV+ERV (TV+ERV is measurement) Total lung capacity VC+RV-max lung expansion (80-120%) Forced expiratory volume FEV and FEV1 (expired in one second) 80-120% What is minute ventilation and how is it measured? Air moved in and out in one minute. TV x RR Alveolar ventilation: rate new air reaches alveoli for gas exchange. What is dead space and how are the two types of dead space different? Conducting zones: anatomical deadd space: no gas exchange: 30%: alveoli without blood flow increases this dead space-physiologic dead space. Anatomic dead space + alveoli without flow=physiologic dead space (Makes it more difficult to expel CO2) Describe the differences in the pediatric and adult airway, chest wall, and alveoli. a.) Infants no epiglottal flap movement between breathing and eating (increased risk of aspiration) b.) Infants and children: more susceptible to problems with resistance (changes in diameter of lung) c.) Thoracic cage: adult: less expansion and contraction: restrictive, limited recoil. d.) Child thoracic cage: less pressure needed for expansion, recoils and collapses easier. e.) Obesity: scoliosis; kyphosis: chest wall compliance is decreased, restrictive disease f.) Airways obstructed with bronchospasm mucous plugging: asthma, anaphylaxis, CF Describe V/Q matching and why it is important for gas exchange Failure in alveoli oxygen concentration-shunts blood away from that alveoli by constriction: occurs within 10 minutes of hypoventilation (typical 70%). Hypoxic Pulmonary Vasoconstriction Response: maximizes ventilation (V) and Perfusion (Q) matching Asthma, chronic bronchitis, PNE, atelectasis, PR. Mismatches result in differences in a) alveolar O2 concentration and PaO2 b) CO2 in expired air (end tidal CO2) and PaCO2 Physiological shunting: V/Q less than normal=inadequate ventilation to oxygenate blood going to alveolar capillaries (poor shunting) Physiological dead space: V/Q above normal=alveoli well ventilated but some are poorly perfused (consider positional changes related to illness and how this relates to hydrostatic pressures) Describe blood flow zones and describe how they work to support or hinder gas exchange. (Deoxy) RV-PA-cap bed (oxygenated)-PV-LA Bronchial vessels-systemic circulation- trach, bronchi, lungs, esophagus, visceral pleura and PA: not involved in gas exchange per se but in maintaining cellular function. Lymphatics Analyze the etiology, clinical manifestations, and pathophysiology of pulmonary edema Etiology: Differences in pressure gradient: excess fluid in alveoli: increased L heart pressures; pulmonary over circulation; increased pulmonary capillary permeability (can't drain to lymphatics). Heart failure, ARDS, toxic gases. Clinical manifestations: Shortness of breath, increased respiratory ratel crackles; pink frothy sputum; chest pain; orthopnea; PND Pathophysiology: Gas exchange impaired; decreased lung compliance, fluid in pulmonary alveolar sacs Analyze the etiology, clinical manifestations, and pathophysiology of pleural effusion Etiology: Excess fluid in pleural space: blocked lymph nodes; L heart failure; decreased plasma oncotic pressure; increased permeability of pleural membrane. Clinical manifestations: Fatigue, shortness of breath, increased respiratory rate Pathophysiology: Impaired gas exchange. Describe how changes in the oxygen-hemoglobin dissociation curve impact the oxygen carrying capacity of hemoglobin. Gases move from areas of high concentration to lower concentration=concentration gradient. New diffusion: movement of gases n/n air and blood. Normal: Expected SvO2 (60-80%) Right shift: Expected SvO2: Most common: less than 75% Pathophysiology: Increased temperature; increased 2, 3 DPG Left shift: Pathophysiology: A 57-year-old female presents to the ED for a complaint of cough and dyspnea. She reports feeling feverish, having a non-productive cough and progressive shortness of breath. Medical history is negative. On exam she has a temperature of 100.3 F, a blood pressure of 105/70 mmHg, a heart rate of 106 and a respiratory rate of 32 a minute. The O2 sat is 92% on room air. The chest is dull to percussion on the left lower base with decreased air exchange audible in the same area. Which is the most likely diagnosis? a.) Pleural effusion b.) Pneumothorax c.) Tuberculosis d.) Heart Failure a.) Pleural effusion The clinical manifestations are most consistent with a pleural effusion secondary to a left lower lobe pneumonia. A 60-year-old male with a history of smoking, has a barrel chest and a productive cough with copious sputum production. His O2 sat is 88%. Which pathological process best describes this patient's condition? a.) Bronchial irritation/inflammation causes hyperplasia of the mucous secreting glands. b.) Dilation of air spaces with destruction of the alveolar sacs. c.) Diffuse leakage of exudate into the alveolar sacs. d.) Granuloma formation in the left lung apex. a.) Bronchial irritation/inflammation causes hyperplasia of the mucous secreting glands. The clinical scenario is most consistent with chronic bronchitis. Option A is the pathologic description of chronic bronchitis. Option B is the pathologic description of emphysema. Option B is the pathologic description of pneumonia. Option D is the pathologic description of tuberculosis. A 3-year-old girl presents to your office with fever, hoarseness and a "seal bark like" cough. Her mother reports she has had a runny nose, nasal congestion, sore throat and a cough for the last few days. The mother brought her to see you because her cough has become louder and more harsh. Which organism is the most common cause of this girl's symptoms? a.) Respiratory syncytial virus b.) Streptococcus pneumoniae c.) Mycoplasma pneumoniae d.) Parainfluenza virus d.) Parainfluenza virus The clinical scenario is most consistent with croup. The most common cause of croup is the parainfluenza virus. A 70-year-old male patient is admitted with profuse diarrhea for three days. He has a history of systolic heart failure and an ejection fraction of 45%. He is weak and his vitals are 98.0oF, pulse 120, respirations 18, and blood pressure 75/60 mmHg. The clinical scenario is most consistent with which diagnosis? a.) Cardiogenic Shock b.) Hypovolemic Shock c.) Neurogenic Shock d.) Acute Coronary Syndrome e.) Anaphylactic Shock b.) Hypovolemic Shock The patient has a hypovolemic shock secondary to significant fluid loss from diarrhea. While he does have systolic heart failure, cardiogenic shock is unlikely because his EF is 45%. Also cardiogenic shock is characterized by persistent hypotension and tissue hypoperfusion resulting from impaired contractility in the presence of adequate intravascular volume. Neurogenic shock is related to a systemic vasodilation which results from an imbalance between parasympathetic and sympathetic nervous stimulation. Anaphylactic shock results in a systemic vasodilation and inflammatory response secondary to an allergen. Finally, he has no clinical manifestations which suggest acute coronary syndrome. An acute right ventricular failure may be caused by which pulmonary condition? a.) Pulmonary Embolus b.) Asthma Exacerbation c.) Lung Cancer d.) Tuberculosis a.) Pulmonary Embolus A pulmonary embolus is the only condition listed which may cause an acute right ventricular failure. A PE may cause this complication if it significantly occludes pulmonary blood flow from the right ventricle. The nurse practitioner is caring for a patient with pulmonary arterial hypertension. For which complication of this disease should the NP monitor? a.) Right ventricular heart failure b.) Liver failure c.) Renal Failure d.) Lung Cancer a.) Right ventricular heart failure The right side of the heart enlarges because it has to push against high pulmonary pressures and eventually this hypertrophy will lead to right sided heart failure. Which test result below is consistent with COPD? a.) A decreased FEV1 b.) A low Residual Volume c.) A high FVC d.) A low Total Lung Capacity a.) A decreased FEV1 COPD patients typically have a low FEV1 and high lung volumes. FEV1 is low due to air trapping. Also, the air trapping is responsible for the high lung volumes. The FVC is normal or low in COPD. A 45-year-old female presents to your office with fever and chills, productive cough with rusty sputum, pleuritic chest pain and dyspnea for 2 days. A CBC shows a neutrophilia and the chest x-ray shows an infiltrate in the left lower lobe. She has not had any sick contacts and has not been hospitalized since she was a child. Which organism is the most likely cause of this patient's condition? a.) Influenza A b.) Streptococcus pneumoniae c.) Staphylococus aureus d.) Hemophilus influenzae b.) Streptococcus pneumoniae The clinical scenario is consistent with a community acquired pneumonia. The neutrophilia is consistent with a bacterial etiology not a viral etiology. The most common cause of community acquired pneumonia is Streptococcus pneumoniae. Which patient is at risk for a pulmonary embolus? a.) A female patient with a factor V Leiden mutation. b.) A male patient with hemophilia. c.) A female patient with a prolonged INR. d.) A male patient with Hageman factor deficiency. a.) A female patient with a factor V Leiden mutation. The only hematologic alteration which causes a hypercoagulable state is the factor V Leiden mutation. The other alterations cause an increased risk for bleeding A 70-year-old male patient is admitted with profuse diarrhea for three days. He has a history of systolic heart failure and an ejection fraction of 45%. He is weak and his vitals are 98.0oF, pulse 120, respirations 18, and blood pressure 75/60 mmHg. Which lab result is consistent with the clinical scenario? a.) Elevated lactate b.) High platelet count c.) Normal white blood cell count d.) Low sodium a.) Elevated lactate This patient has a hypovolemic shock secondary to significant fluid loss from diarrhea. Shock states result in decreased cellular perfusion. The decreased cellular perfusion triggers anaerobic cellular metabolism. During this time more of the pyruvate is shunted toward the production of lactic acid instead of being shunted into the citric acid cycle. The by product of anaerobic pyruvate cellular metabolism is lactic acid. Lactic acid will accumulate during times of poor tissue perfusion. The other lab results are not a result of the hypovolemic shock this patient is experiencing. Why does an elevated PCO2 result in acidosis? Increase in hydrogen ions (carbonic acid-hydrogen cations+bicarbonate anions)=increase in hydrogen and acidosis What are the regulating mechanisms for breathing? Medulla a.) Dorsal respiratory neurons (DRN): inspiration b.) Ventral respiratory neurons (VRN): expirations Pons a.) Pneumotaxic center-respiratory rate and pattern Chemoreceptors a.) Central b.) Peripheral Lung innervation a.) Irritation receptors (epithelium) b.) stretch receptors c.) Pulmonary C-fiber receptors (J receptors) Other What is the process by which the brain stem impacts respiration? i. DRN: vagal/glossopharyngeal nerves-transmit signs from chemo/baroreceptors-signals diaphragm and intercostal muscles-control rate and inspiration time. ii. VRN: inactive during normal breathing-fire during hypoventilation and signal inspiration-stimulate abdominal muscle contraction for expiration What is the process by which the chemoreceptors impact respiration? Central: sense changes in pH of CSF a.) CO2 crossed the BBB + H20 = bicarb b.) Very sensitive to changes in CO2 i.) Changes rate and depth of respirations Exception is in chronic conditions (COPD), compensated acidosis-renal compensation increased serum bicarb Peripheral: chemoreceptors in carotid and aortic bodies Sense change in O2 concentration Decreased PaO2, increased respiratory rate What is the process by which lung innervation impacts respiration? When lungs are irritated by inhalation of particulate matter-cough is induced-bronchospasm and increased respiratory rate result Smooth muscle stretch: in bronchi, bronchioles, lung parenchyma stretch-signals DRN to switch off inspiration (keeps lungs from over-inflating) What is the process by which other mechanisms impact respiration? Voluntary breathing (breathing techniques) CNS Depression: brain injury/anethesia Explain the etiology, clinical manifestations and pathophysiology of pulmonary embolism. Etiology: Thrombosis/fair/air bubble/amniotic fluid post-partum Clinical manifestations: Tachypnea, dyspnea, chest pain, increased dead space, V/Q abnormal, decreased PaO2, pulmonary infections, PHTN, decreased cardiac output, systemic hypotension, shock Patho: Hypoxic vasocontriction Decreased surfactant Release of neurohormonal and inflammatory substances Pulmonary edema Atelectasis (affected area) Dx: D-dimer, CTA, MRA (EKG changes, elevated troponin) Explain the etiology, clinical manifestations and pathophysiology of pulmonary artery hypertension. Etiology: Increase PA pressure 25 mmHg (normal is 15-18) idiopathic, genetic (BMPR2), connective tissue, chronic hypoxia, LV failure, valvular disease, long standing HTN Clinical manifestations: dyspnea, chest pain, tachypnea, cough, JVD, fatigue, tachypnea, palpitations, right sided heart failure Patho: Vasoconstrictors overwhelm vasodilators - resistance of blood flow to lungs-remodeling of RV- cor pulmonale (right sided heart failure), PAH and PAH crisis Dx: Echo, right heart cath Explain the etiology, clinical manifestations, and pathophysiology of asthma Etiology: Chronic inflammation of bronchial mucosal hyper-responsiveness, constriction, obstruction (familial/environmental) Clinical manifestations: Look worse when exhaling, decreased FEV, wheezing (lower airways), stridor (upper airways), dsypnea Patho: Early-antigen response (IgE) - cytokine response-increased capillary permeability- mucosal edema, mucous production, and bronchospasm Late: Inflammatory mediators - bronchospasm - secretions - obstruction - V/Q mismatch - hypoxemia - CO2 retention - acidosis - respiratory failure Explain the etiology, clinical manifestations, and pathophysiology of chronic bronchitis (COPD) GOLD treatment guidelines do not seperate different COPDs Etiology: Hypersecretion of mucous/chronic persisten cough (3 mo/yr for 2+ years) Usually acquired Genetic - alpha1- antitrypsin deficiency (consider if develops before 40 yo and non-smoker) Clinical manifestations: Look worse when exhaling, decreased FEV, wheezing (lower airways), stridor (upper airways), dyspnea, hypoxia - mild cyanosis, DOE, blue bloater, poor exercise tolerance May lead to compensatory polycythemia Patho: Large airways but will affect all smooth muscle Bronchial inflammation - edema - increased number and size of mucosal glands, Goblet cells - air trapping on expiration V/Q mismatch Chronic hypercarbia Explain the etiology, clinical manifestations, and pathophysiology of Emphysema (COPD) Etiology: Enlargement of respiratory zone and destruction of alveolar walls Clinical manifestations: Dyspnea, barrel chest, forward sitting (tripod), pursed lipped breathing, minimal wheezing, punk puffer, hyper resonance on percussion Patho: Breakdown elastin - loss of recoil - air trapping - dyspnea - hypoventilation - hypercabia Structural changes (loss of alveolar cells) - increased area for gas exchange + bullae and blebs- v/q mismatch- hypoxemia Systemic chronic inflammation and infection risk Explain the etiology, clinical manifestations, and pathophysiology of Croup Etiology: Upper airway - acute viral infection Clinical manifestations: barky cough, inspiratory stridor Patho: Subglottic edema - narrows airway - respiratory distress Explain the etiology, clinical manifestations, and pathophysiology of acute epiglottitis Etiology: Associated with H-flu (vaccination rates have improved occurrence) Clinical manifestations: Inspiratory stridor, tripoding, drooling Patho: Rapid edema of epiglottis - severe and life threatening Explain the etiology, clinical manifestations, and pathophysiology of cystic fibrosis Etiology: Autosomal recessive genetic Chloride ion transport defect (GI and respiratory - thick secretions) Clinical manifestations: Cough, wheezing, excessive sputum, PNE, clubbing, barrel chest, rales, recurrent infections (pseudomonas) Patho: Mucous plugging with increased submucosal gland and Goblet cells. Chronic inflammation with excessive cytokines and neutrophil activation, recurrent infections. Explain the etiology, clinical manifestations, and pathophysiology of structural changes Etiology: Kyphosis, scoliosis, MD, obesity Clinical manifestations: Dyspnea, tachypnea, difficulty with secretion clearance Pathophysiology: Increased effort to expand lungs Explain the etiology, clinical manifestations, and pathophysiology of aspiration Etiology: Fluid or solid in lung, dysphagia Clinical manifestations: Pathophysiology: bronchial inflammation-decreased cilia function- bronchospasm alveolocapillary membrane damage - hemorrhagic pneumonitis - stiff non-compliant alveoli Explain the etiology, clinical manifestations, and pathophysiology of atelectasis Etiology: blockage of airway; pressure outside lung (cannot expand); not enough surfactant; bed-bound. Clinical manifestations: Pathophysiology: Increased pulmonary shunt (increased V/Q mismatch) - hypoxia - decreased compliance Explain the etiology, clinical manifestations, and pathophysiology of bronchiolitis Etiology: Inflammation of the bronchioles; chronic bronchitis; viral respiratory illness; toxic gas. Clinical manifestations: Pathophysiology: atelectasis or emphysematous destruction of alveoli beyond area of inflammation Decreased V/Q matching - hypoxemia Decreased V/Q matching - decreased minute ventilation- hypercarbia -tachypnea Explain the etiology, clinical manifestations, and pathophysiology of pulmonary fibrosis Etiology: Excess fibrosis and connective tissue in lungs Scar tissue after pulmonary disease (ARDS, TB, COVID) Autoimmune (RA, sarcoidosis) Inhalation of toxins Idiopathic Clinical manifestations: Pathophysiology: Chronic inflammation - fibrosis of alveolar epithelium - proliferation of myofibroblast - stiff alveoli - decreased compliance- v/q mismatch - hypoxemia Explain the defining characteristics, clinical manifestations, and pathophysiology of hypoxemia Defining characteristics: Reduced PaO2 with or without hypoxia Respiratory failure /= 50 mmHg Clinical manifestations: Tachycardia, cyanosis, confusion Patho: Hypoventilation V/Q mismatch, increased alveolocapillary membrane thickness Ex. heart failure, PE, pulmonary edema, PNE Explain the defining characteristics, clinical manifestations, and pathophysiology of hypercarbia Defining characteristics: Increased CO2 = PaCO2 over 50 mmHg and decreased serum pH /- 7.25 Clinical manifestations: =/- confusion, lethargy Patho: Hypoventilation, decreased respiratory drive, neuromuscular disease, airway obstruction, physiologic dead space, chest wall deformity How can you measure the severity of respiratory failure? Two tests: Alveolar arterial oxygen gradient and PF ratio Alveolar arterial oxygen gradient Defines oxygenation disorders PF ratio Most helpful: ratio of partial pressure of oxygen in arterial blood (PaO2) to the fraction of inspiratory oxygen concentration (FiO2). This is how ARDs is classified. What is the distinction between acute lung injury and acute respiratory distress syndrome? Inflammatory process in lungs that leads to alveolar epithelial and vascular endothelial injury in the lungs, may be infective or non-infective. Criteria: acute onset (7 days), bilateral infiltrates, respiratory distress not related to cardiac or fluid overload Acute lung injury (ALI): PF ration /= 300 Acute respiratory distress syndrome (ARDS) PF ration /= 200 What are some common causes of ALI and ARDS? Direct: PNE, aspiration, pulmonary contusion, fat emboli, near drowning, inhalation injury, reperfusion, pulmonary edema, post transplant Indirect: Sepsis, trauma, cardiopulmonary bypass, drug overdose, acute pancreatitis, blood transfusion What are the clinical manifestations and pathophysiology of the exudative (inflammatory) phase of ARDS? Occurs in the first 72 hours PF ratio: 201-300 Mild Clinical manifestations: Dyspnea, hypoxemia, poor response to oxygenation, hyperventilation, respiratory alkalosis, organ dysfunction, metabolic acidosis, decreased tidal volume, hypercapnia, decreased CO, hypotension Patho: What are the clinical manifestations and pathophysiology of the proliferative phase of ARDS? One to three weeks PF ration: 101-200 Moderate Clinical manifestations: Dyspnea, hypoxemia, poor response to oxygenation, hyperventilation, respiratory alkalosis, organ dysfunction, metabolic acidosis, decreased tidal volume, hypercapnia, decreased CO, hypotension Patho: Early healing, pulmonary edema drain (increased lymphatic drainage), increased pleural effusions, exudates granulate - recovery of cap/alveolar barrier. Surfactant production restarts. What are the clinical manifestations and pathophysiology of the fibrotic phase of ARDS? 14-21 days (overlaps with proliferative) PF ration: less that 100 Severe Clinical manifestations: Dyspnea, hypoxemia, poor response to oxygenation, hyperventilation, respiratory alkalosis, organ dysfunction, metabolic acidosis, decreased tidal volume, hypercapnia, decreased CO, hypotension Patho: Does not occur with everyone. Fibroblast proliferate in alveoli, risk for pulmonary hypertension. What is shock? Inadequate tissue perfusion Decreased O2 and nutrient delivery Impaired cellular metabolism Increased demand and/or decreased removal of waste. Describe the cellular changes associated with anaerobic metabolism in shock states. Lactate: Increase in serum lactate - metabolic acidosis - increased oxy/hgb dissociation - Hgb releasing more O2 - more consumption, feedback loop. Protein metabolism: increased protein metabolism i. As metabolized, serum protein breakdown and loss. Increased muscle wasting (respiratory and cardiac- respiratory and cardiac failure) ii. Decreased immunoglobulin level = decreased immune response. iii. Increase in cellular edema (fluid shifts-decreased albumin-increased edema) - inflammatory response. This activates the clotting cascade. Lysosome enzyme production increases ( cells can not take on process and take in nutrients and O2) ATP: Decreased ATP, increase in intracellular NA and water, decrease circulating water, triggering the clotting cascade, lysosome enzyme production increases-cycle continues. Describe the metabolic changes associated with shock states 1. Glucose increases: increased protein breakdown - converts to increased pyruvate - converts to increased lactate 2. Catecholamines, cortisol, and growth hormone: all increase. Increase in lipolysis, gluconeogenesis, glycogenolysis a.) increase in lipolysis - increase in triglycerides and free fatty acids (increase inflammation) b.) Increase in gluconeogenesis and glycogenolysis - decrease in energy store and increase in cellular failure (death) c.) Both result in increased insulin resistance Describe the three phases of shock. Compensated: for absolute and relative fluid loss; still able to maintain an adequate blood pressure and cerebral perfusion. Vasoconstriction shunts to brain and vital organs Decompensated: late phase: can no longer maintain perfusion of brain and vital organs. Irreversible: rapid deterioration in CV system, compensatory mechanism failure, patient will die. Evaluate the definition, etiology, defining characteristics, and pathophysiology of cardiogenic shock. Definition: Inability of the heart to pump blood to tissues and organs Etiology: Decreased contractility: MI, cardiomyopathy, sepsis, myocarditis, pericarditis, aneurysm, dysrhythmias, contusion, metabolic abnormalities, papillary muscle rupture Impaired diastolic filling: dysrhythmias (SVT with RVR) Obstruction: PE, tamponade, valvular disorders, tumors, wall defects Defining characteristics: Hypotension and hypoperfusions despite adequate LV filling pressure and intravascular volume (preload OK) Patho: Decreased cardiac output - body tries to compensate with: RAAS to increase volume (even though this is not the problem), results in increased preload, SV and HR - increased systemic and pulmonary edema - dyspnea OR Catecholamine release - increased SVR - increased preload, SV and HR - increase in systemic and pulmonary edema - dyspnea. Increase in preload and SV/HR decreased cardiac output and EF - decreased BP - decreased tissue perfusion (resulting in ischemia) - impairs cellular metabolism - myocardial dysfunction (our goal is to decrease SVR) Unique manifestations: Inadequate perfusion to heart and end organs Chest pain, dyspnea, faintness, impending doom Tachycardia, tachypnea, JVD, low cardiac output symptoms. Cyanosis, mottling, cool, low UOP Extra heart tones (S3, S4), pulmonary edema, hypoxemia, elevated end organ labs (LFTs, BUN, Cr) Treatment: Support heart improve relaxation, remove obstruction. Evaluate the definition, etiology, defining characteristics, and pathophysiology of hypovolemic shock Definition: Loss of whole blood, plasma, or interstitial fluid in large amounts Etiology: Whole blood hemorrhage, plasma burns, interstitial fluids: diaphoresis, DM, DI, emesis, diarrhea, diuresis Defining characteristics: Body compensates until it can no longer Patho: Decreased intravascular volume - decreased cardiac output 1- shift of interstitial fluid -aldosterone and ADH - splenic (sometimes liver) discharge resulting in increased volume 2- catecholamine release - increased HR, contractility or increase in SVR. If CO increased - move volume loss, decrease CO- decreased systemic and pulmonic pressures - decreased tissue perfusion - impaired cellular metabolism IF increased SVR - decrease CO - decreased systemic and pulmonic pressures - decreased tissue perfusion - impaired cellular metabolism Unique manifestations: High SVR: cool, pale extremities, thirst, oliguria, low preload (RA and CVP pressures) and tachycardia Treatment: volume replacement with fluid/blood Evaluate the definition, etiology, defining characteristics, and pathophysiology of neurogenic shock Definition: Stimulation of parasympathetic and inhibition of sympathetic activity Etiology: Trauma: cord or medulla Conditions depriving medulla of O2 and glucose Depressive drugs, anesthetic agents, severe emotional stress, pain. Defining characteristics: Patho: Imbalance between sympathetic and parasympathetic stimulation (body has no way to compensate for this) - massive vasodilatation) - decreased vascular tone - decreased SVR - inadequate cardiac output - decreased tissue perfusion - impaired cellular metabolism Unique manifestations: Massive vasodilatation: imbalance in parasympathetic and sympathetic nervous system (most of blood is peripheral) Hypotension with bounding pulases and flash cap refill Bradycardia Treatment: Supportive Evaluate the definition, etiology, defining characteristics, and pathophysiology of anaphylactic shock Definition: Inflammatory and vasodilatory reaction to an allergic antigen Etiology: Allergic antigen - anaphylactoid type: cold, exercise, medication, contaminants Defining characteristics: Similar to neurogenic shock with vasodilatation, peripheral pooling, and tissue edema Bronchoconstriction (smooth muscle) Patho: Antigen (allergy) [antibody IgE - mast cells; ECF-A] activation of complement cascade, histamine, kinins, prostaglandins - increased capillary permeability/peripheral vasodilatation/constriction of smooth muscle (bronchoconstriction, larygnealspasms, GI cramping)/increase in serotonin and leukokinenes-swelling/wheals. Increase heparin-potential hemorrhagic DIC Complement, histamines, kinins, prostaglandins-increase capillary permeability - increase extravasation of intravascular fluids-edema-relative hypotension, decreased cardiac output-decrease tissue perfusion-impaired cellular metabolism Unique manifestations: Hypotension, diaphoresis, pallor Respiratory: SOB, cough, rhinorrhea, throat tightening, wheezing GI: N/V/D, Abdominal pain Cutaneous erythema, puritis, urticaria, angioedema Ominous: anxiety, confusion, impaired mental status Treatment: Epinephrine-stop degranulation of mast cells Fluid resusciation Antihistamines Steroids Evaluate the definition, etiology, defining characteristics, and pathophysiology of septic shock Definition: Progressive organ dysfunction due to infection Etiology: Gram (+/-) viral, fungal PNA, bloodstream intravascular catheter, intra-abdominal, urosepsis, surgical wound Patho: SIRS - Sepsis - Septic shock - MODS Manifestations: General: hyper/hypothermia, tachycardia, tachypnea, AMS, significant edema/poor fluid balance, hyperglycemia Inflammatory: leukocytosis/leukopenias, elevated CRP and or procalcitonin Hemodynamic: hypotension, SvO@, cardiac index 3.5L Organ dysfunction PF ration 300, oliguria, increased creatine, coagulopathy, ileus, thrombocytopenia, hyperbilirubnemia, lactic acidosis, decreased capillary refill Describe the SIRS phase of the sepsis spectrum Systemic inflammatory response syndrome: reaction to anything that stimulates the inflammatory response (infection or not) Defining characteristics: Temp 38C or 36 HR 90 RR 20 or PaCO2 32 WBC 1200 or 4000 or 10% bands. Seen with ECMO If homeostasis is not restored in infectious SIRS patient with progress to sepsis Describe the sepsis phase of the sepsis spectrum Life threatening organ dysfunction caused by dysregulated host response to infection 1.) Commonly affected are: respiratory, hematologic, cardiac, renal, hepatic, and CNS 2.) Systolic hypotension 90 and organ dysfunction (measured by LODS, SOFA, and qSOFA) Sequential organ failure assessment (SOFA) (ICU) P/F ratio +/- mechanical ventilation Platelet count GCS 15 or baseline Billirubin MAP Creatine + if score increased 2 points = organ dysfunction due to hypoperfusion Quick SOFA (qSOFA) Clinic RR 22 GCS 15 or baseline SBP 100 2/3=organ dysfunction for sepsis Bactermia (+/-) (-) release endotoxin - lipopolysaccharide (LPS) containing toxin Lipid-A moiety, other toxic products (+) releases exotoxin-peptdoglycan, lipteichoic acids, superantigens, other toxic products Release of proinflammatory cytokines i. TNF - alpha ii. Interlukin 1 alpha and beta, IL- 6 iii. Other proinflammatory cytokines 1. Activates a. Complement system b. Coagulation system c. Kinin system d. Humoral immunity: Neutrophil, endothelial, and monocyte-macrophage cellular activity i. Release of anti-inflammatory cytokines (LPS binding protein, IL-1 receptors antagonist, IL-10, nitric oxide, other anti-inflammatory cytokines) ii. Results in endothelial cell dysfunciton iii. Capillary leak, microvascular thrombus, cell adhesion, tissue hypoxia, apoptosis, impaired vascular tone, free radical damage Describe the septic shock phase of the sepsis spectrum Subset of sepsis Profund circulatory, cellular, and metabolic abnormalities - significant increased risk of mortality Defining characteristics: VASOPRESSOR required to maintain MAP 65, low SVR and vasodilatation; lactate 2; without hypovolemia Describe the MODS phase of the sepsis spectrum Multi organ dysfunction syndrome Progressive dysfunction of 2+ organ systems from uncontrolled inflammatory response to severe illness or injurt Usually sepsis or sepsis related but may be burns, trauma, heat stroke Risks: older age, tissue injury (trauma), pre-existing conditions 1. Excessive inflammatory reaction after a latent period following initial injury How can organ failure be evaulted/quantified? End organ failure and death (2 organs) 54% mortality 5 organs nearly 100% mortality Define primary MODS and its pathophysiology Definition: Specific ischemic or hypoperfusion Patho: Decreased perfusion: local tissues (organs), generalized hypoperfusion (typically subclinical) sets them up for secondary MODS Define secondary MODS and its pathophysiology Definition: Organ often distant from site of original injury Patho: Three pathways 1.) Macrophages trigger the proinflammatory cytokines-damage the endothelium-neutrophil adhesion-more tissue damage-further inflammation- ntiric oxide- microvacular thrombi-DIC 2.) Heightened stress response- increase catecholamines- hypermetabolism - increased O2 consumption - catabolic states - decreased SVR 3.) Neutrophil activation- inflammatory response-reactive oxygen species injury - damage endothelium Describe the timeline of symptom manifestation in MODS 24 hours post injury: fever, tachycardia, tachypnea, dysnpea, AMS, hypermetabolic state 24-72 hours: Respiratory failure, ARDS 7-10 days: hypermetabolic and hyperdynamic states i. Bactermia (enteric) hepatic, renal, GI failure 14-21 days: worsening organ failure can evolve to death 21+ days: linger - improve slowly or die slowly; rarely is there a rapid improvement or death at this point. Right atrium pressure (& what is considered high)? No definition anything over 8 mmHg Right ventricle systolic pressure (& what is considered high)? Pressure at the peak of systole anything over 28 mmHg Right ventricle end diastolic pressure (& what is considered high)? Pressure at the end of diastolic, right before systole anything over 9 mmHg Left atrium pressure (& what is considered high)? No definition anything over 12 mmHg Left ventricle systolic pressure (& what is considered high)? Pressure at the peak of systole anything over 140 mmHg Left ventricle end diastolic pressure (& what is considered high)? Pressure at the end of diastole, right before systole anything over 12 mmHg Endocardium Innnermost layer of the heart which comes in contact with the blood Made of simple squamous epithelium and underlying connective tissue Myocardium This is the middle layer of the heart Contains myocytes-which are responsible for heart contraction Pericardium The outermost layer of the heart Made up of two layers Fibrous Pericardium Made of connective tissue and provides the heart with stability by connecting to the sternum anteriorly and the diaphragm inferiorly Serous pericardium This has two layers that consist of the epicardium and the parietal layer Epicardium this is the visceral layer of the heart and it lays directly over the heart and contains the coronary arteries Parietal layer Layer of the heart above the epicardium and underneath the fibrous pericardium Left ventricle -This ventricle is the larger of the two because its workload is greater -This ventricle pumps blood to the entire body and has a much higher afterload to push against -This makes the pressure in this side of the heart greater than the other side Right ventricle -This ventricle only pumps blood into the lungs -The pressure in this side of the heart is lower than the other side Umbilical vein This receives oxygenated blood from the placenta It connects to the hepatic circulation but also connects to the inferior vena cava by the ductus venosus Ductus venosus This allows the oxygen-rich blood to enter the vena cava and some blood does enter the hepatic circulation Foramen Ovale This is an opening between the right and left atria This is where the most oxygenated blood in the right atrium is shunted through here into the left atrium One cardiac cycle This consist of one full contraction and relaxation Atrial kick When left ventricular relaxation and the left atrium contracts to push blood into the left ventricle... it is called... It increases the amount of blood put into the left ventricle and represents about 20% of the cardiac output Cardiac output -The amount of blood pushed from the left ventricle in 1 minute -Calculated by multiplying the heart rate in beats per minute by the stroke volume Normal cardiac output 5L/minute Stroke volume -The amount of blood ejected by the ventricle for each cardiac cycle (heart beat) -Highly dependent on the force of the contraction Contraction This is dependent on the amount of preload which stretches the left ventricle, the stimulation of endogenous positive inotropic agent (epi and norepi), the presence of negative inotropic agents (meds and cytokines), and the adequacy myocardial oxygenation A saturation of less than ______% results in a decrease in myocardial contraction 50 Ejection fraction -The percentage of blood which is ejected from the ventricle with each contraction -It is calculated by dividing the stroke volume by the end diastolic volume -Normal range is 55-65% -This value is used to measure cardiac function Preload -The combination of the end diastolic volume and end diastolic pressure -Dependent on the amount of venous return to the heart and amount of blood left in the left ventricle at the end of systole Heart failure May occur as a result of an increased preload, which causes a decline in the stroke volume and a back-up into the pulmonary circulation Afterload -The resistance that the ventricle pushes against to contract -Includes aortic pressure and systemic vascular resistance -This increases the work of the ventricle and results in hypertrophy Arterial blood pressure This is the cardiac output multiplied by peripheral resistance Mean arterial pressure (MAP) The average pressure in the arteries during the cardiac cycle -Dependent on the elisticity of the arterial wall stiffness and stroke volume -Normal is 70-100 mmHg Pulse pressure The difference between SBP and DBP and is directly related to arterial wall stiffness and stroke volume Contraction The degree of tension (aka preload) of the left ventricle and the amount of intracellular calcium are responsible for ______. Decrease Myocardial relaxation occurs when intracellular calcium levels _________. Diltiazem and Verapamil These two drugs are non-dihydropyridine calcium channel blockers and they inhibit the influx of calcium into the myocardium. They decrease intracellular calcium concentration which in turn decreases myocardial tension and contractility. *Should be avoided in patient's with systolic heart failure *Decrease contractility Catecholamines These increase the activity of the calcium pump in the sarcoplasmic reticulum. Therefore, it increases the release of calcium from sarcoplasmic reticulum. *Increase contraction Digitalis Blocks the Na+/K+ pump which increases intracellular Na+, decreases activity of the Na+/Ca+2 exchanger and increases intracellular Ca+2 *Increase contraction Beta Blockers These meds block the effects of the catecholamines (which increase the activity of the calcium pump in the sarcoplasmic reticulum, which increases release of calcium) *Increase contraction SA node Electrical impulses are usually generated from this which are located in the right atrium -This generates impulses of around 60-100 beats per minute AV node Mediates how fast impulses are transmitted to the ventricles -can generate 40-60 beats per minute -this will pass the impulse down the conduction system to the bundle of His -If this fails, the bundle of His will generate an action potential at less than 40 beats per minute Action potential The purpose of this is to transmit an impulse and in the case of the heart to cause cardiac contraction Ventricular action potentials Generated by the bundle of His or the Purkinje fibers -occur in 5 phases Cardiac cells that start with a resting membrane potential of -85 mV are the... Bundle of His and Purkinje fibers Phase 0 Generated by th