Exam 2 Review PDF

Pulmonary System Objectives: General: 1. Define the terms used early in Cpt 29 that describe lung function, breathing, the signs and symptoms of pulmonary disease (dyspnea, cough, clubbing, pain, hemoptysis, etc) A. Dyspnea = subjective sensation of uncomfortable...

Pulmonary System Objectives: General: 1. Define the terms used early in Cpt 29 that describe lung function, breathing, the signs and symptoms of pulmonary disease (dyspnea, cough, clubbing, pain, hemoptysis, etc) A. Dyspnea = subjective sensation of uncomfortable breathing, slow breathing a. Describes as breathlessness, air hunger, shortness of breath, labored breathing b. Can be from disease process, anxiety, or pain c. There can be compensation→severity may not match level of distress noticed/not noticed d. Nasal flaring, use of accessory muscles, retraction of intercostal spaces e. Someone with a lung injury or disease is experiencing something similar to someone who just ran sprints and is now sucking air into their lungs, bent over, hands on their knees with audible breaths B. Orthopnea = dyspnea when person is lying down a. Result of heart failure b. Abdominal contents exert pressure on the diaphragm and decrease efficiency of the respiratory muscles C. Paroxysmal nocturnal dyspnea (PND) = dyspnea usually at night, awakens a person from sleep→gasping for air a. Can be from pulmonary or heart disease b. Must stand up to relieve the sensation D. Dyspnea on exertion = when one has trouble breathing while moving around, exercising E. Cough = usually a helpful thing, but can be bad a. Acute cough→resolved in 2-3 weeks b. Chronic cough→more than 3 weeks c. Abnormal sputum (spit)-->normal color is clear/white and thin F. Hemoptysis = blood sputum a. Indicates infection or inflammation that damages the bronchi (pneumonia, TB, bronchitis) G. Abnormal breathing patterns (labored breathing): a. Kussmaul Respirations = hyperpnea; increased rate of breathing, no pause after expiration b. Cheyne-Stoke Respirations = alterations of deep/shallow breathing w/periods of apnea i. Neurological impairment, shock, low oxygen in brain c. Restricted breathing = decreased compliance/stiff lungs; small tidal volume, rapid respiratory rate d. Large airway obstruction = slow ventilatory rate; large tidal volume e. Small airway obstruction = rapid ventilatory rate; small tidal volume; wheezing often present H. Pain = can indicate many things so important to investigate a. Inflammation, trauma, pulmonary emboli, coughing, fracture, pneumothorax, muscle pain b. OLDCART→what are the reasons a person may be hurting? I. Cyanosis = late response to poor oxygen, blue color a. Central: blue around mucous membranes shows low oxygenation (pulmonary/cardiac disease) b. Peripheral: blue extremities (stress, cold) J. Clubbing = changes in fingernails, more rounded and circular shape a. Can be causes by COPD or smoking for many years b. From hypoxemia 2. Recognize ways lungs change as a person naturally ages and understand how this may impact manifestations of disease. (Chapter 28) A. Changes to older adult lungs are dependent on physical activity throughout adult life B. Effects of aging on the lungs: a. Compliance ↓ b. Strength ↓ c. Elastic recoil ↓ d. Capillaries ↓ (takes longer for diffusion to occur) e. Support structure ↓ f. Surface area ↓  g. Early airway closure ↑ 3. Understand concepts of ventilation and perfusion A. Ventilation = movement of air into and out of the lungs a. Not about oxygen, just about getting air in B. Perfusion = movement of blood into and out of the capillary beds of the lungs to body organs and tissues a. Pumping blood through body b. Carried out by cardiovascular system C. Diffusion = movement of gasses between air spaces in the lungs and bloodstream a. Going from oxygenated to deoxygenated b. Occurs across alveolocapillary membrane→diffusion of O2 into red blood cell and diffusion of CO2 out into alveoli 4. Identify the clinical indicators of pulmonary disease. A. Most common signs and symptoms = dyspnea, cough, abnormal sputum, hemoptysis, abnormal breathing, hyper/hypoventilation, cyanosis, clubbing B. Pulmonary embolus = occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or an air bubble a. Something traveling and lands in pulmonary vascular system b. Commonly arise from the deep veins in the lower extremities c. Virchow triad: venous stasis, hypercoagulability and injuries to the endothelial cells that line the vessels d. Tachypnea, dyspnea, chest pain, V/Q imbalances, decreased PaO2, pulmonary infarction/hypertension, decreased cardiac output, systemic hypotension, shock C. Pulmonary hypertension = increased pulmonary arterial pressure, harder for blood to move through lungs a. Risk factors: idiopathic, drugs, connective tissue disease, left heart disease, chronic lung disease, COPD most common b. Endothelial dysfunction with overproduction of vasoconstrictors c. Growth factors cause fibrosis and thickening of vessel walls and abnormal lumen narrowing and vasoconstriction→increases pressure to pulmonary arteries and right ventricle d. Increased workload of RV leads to hypertrophy and right heart failure e. Manifestations: delayed until late stages→fatigue, chest pain, tachypnea, dyspnea, peripheral edema 5. Define and understand concepts of hyperventilation and hypoventilation. A. Hypoventilation = inadequate alveolar ventilation, not enough oxygen to lungs, poorly ventilated a. Caused by alterations in pulmonary mechanics or neurological problems b. Carbon dioxide removal slower→higher levels in the blood (hypercapnia) c. Slower respiration rate since not breathing fast enough to remove CO2 B. Hyperventilation = alveolar ventilation exceeds demands, high amounts of oxygen in the lungs a. Lungs removed carbon dioxide faster than its produced→lower levels in the blood (hypocapnia) b. Faster respiration rate since breathing all the CO2 out 6. Discuss alterations in arterial blood gas values that indicate pulmonary disease. A. Arterial blood gasses = oxygen, carbon dioxide, bicarbonate, pH level of the blood, determines gas exchange across alveolar-capillary membrane B. Normal pH: 7.35-7.45 a. Lower = acidotic b. Higher = alkaline C. Normal PaCO2 (partial pressure of CO2): 35-45 mmHg a. CO2 drives respiration b. High CO2 = not breathing, breathe to blow off CO2, usually more acidic i. Hypercapnia = increased PaCO2 in arterial blood c. Low CO2 = hyperventilation, get rid of too much CO2 D. Normal PaO2 (partial pressure of O2): 80-100 mmHg a. Hypoxemia = reduced oxygenation of arterial blood ( 130 and/or >80 b. Diagnosis after 3 elevated BPs over 3 months c. Possible to have transient elevated BP with stress but not have HTN d. Genetic and environmental factors e. Affects 92-95% of individuals with HTN f. Asymptomatic g. Risk factors: high sodium intake, natriuretic peptide abnormalities, obesity, insulin resistance B. Secondary Hypertension = caused by a systemic disease process that raises peripheral vascular resistance or cardiac output and raises BP a. Represents 5% of HTN population b. Caused by hyperthyroidism, PIH, adrenal tumor, drug use, alcoholism c. Other causative reasons: renal artery stenosis, renal disease, medications d. If cause is fixed = pressure normalizes C. Complications of Hypertension (both types) a. Chronic hypertensive damage to the walls of systemic blood vessels b. Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media c. Elevated BP causes vasoconstriction of vasculature d. Affects heart, kidneys, retina, MI, stroke, blindness, kidney failure e. Can result in transient ischemic attack/stroke, cerebral thrombosis, aneurysm, dementia, blindness (due to retinal vessel rupture) f. S. East U.S. known as Stroke Belt 3. Describe the characteristics of types of emboli, and where pulmonic and systemic emboli originate. A. Embolism = obstruction of a vessel by an embolus—a bolus of matter circulating in the bloodstream. B. Causes ischemia or infarction in tissues distal to the obstruction, producing organ dysfunction and pain a. May consist of a dislodged thrombus; an air bubble; an aggregate of amniotic fluid; an aggregate of fat, bacteria, or cancer cells; or a foreign substance b. Most emboli arise from venous or arterial thrombi and travel in the bloodstream until they reach a vessel through which they cannot pass c. Pulmonary emboli→originate on the venous system (mostly from the deep veins of the legs) or in the right heart d. Arterial emboli→originate in the left heart and are associated with thrombus formation associated with MI, valvular disease, left heart failure, endocarditis, and dysrhythmias. 4. Describe various diseases of the veins and arteries discussed in the slides and know risk factors, pathophysiology and clinical manifestations. A. Arteriosclerosis = chronic disease of the arterial system a. Abnormal thickening and hardening of the vessel walls b. Smooth muscle cells and collagen fibers migrate to the tunica intima B. Atherosclerosis = form of arteriosclerosis a. Thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall b. Plaque development (hardens and changes diameter of blood vessel) c. Leading cause of peripheral artery disease, cerebrovascular disease, coronary artery disease d. Progression: inflammation of endothelium, cellular proliferation, macrophage migration and adherence, LDL oxidation (foam cell formation), fatty streak, fibrous plaque, complicated plaque e. Risk factors: hyperlipidemia/dyslipidemia, diabetes, smoking, hypertension f. Results in: inadequate perfusion, ischemia, necrosis  C. Varicose Veins = a vein in which blood has pooled a. Distended, tortuous, and palpable veins b. Caused by trauma or gradual venous distention c. Risk Factors: age, female gender, family history, obesity, pregnancy, peep vein thrombosis, or prior leg injury D. Chronic Venous Insufficiency = inadequate venous return over a long period due to varicose veins or valvular incompetence a. Damaged valves and finished use of leg muscle pump results in venous insufficiency b. Venous stasis ulcers result from pooling of blood in lower extremities due to poor circulation E. Deep Vein Thrombosis = obstruction of venous flow leading to increased venous pressure a. Resulting from accumulation of platelets and clotting factors b. Symptoms: pain, swelling, redness c. Risk factors: cancer, orthopedic surgery/trauma, heart failure, immobility 5. Characterize coronary artery disease; distinguish between myocardial ischemia and myocardial infarction and list complications and symptoms of each. A. Coronary artery disease (CAD) = caused by atherosclerosis, primary cause of heart disease a. Diminishing myocardial blood supply until so severe it causes myocardial ischemia i. Persistent ischemia causes acute coronary syndromes such as heart attack or myocardial infarction (MI) B. CAD Risk Factors a. Modifiable i. Dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, obesity/sedentary lifestyle, atherogenic diet b. Major i. Increased age, family history, male gender or female gender post menopause c. Nontraditional i. Markers of inflammation and thrombosis = high density C-reactive protein inflammatory marker- synthesized in liver and is a measure of plaque related inflammation ii. Hyperhomocysteinemia = an amino acid produced when proteins are broken down. Means there may be a vitamin B deficiency and as a result there is higher risk for arterial damage and blood clots iii. Adipokines = hormones released from adipose cells. Causes increased inflammation that leads to diabetes, hypertension, CAD C. Myocardial Ischemia = develops when the oxygenation is insufficient to meet the needs of the myocardial cells a. Usually caused by atherosclerotic plaques/CAD b. Plaque size increase can occlude the vessel and cause ischemia during exertion (exercise, tachycardia, valve disease) c. Myocardial cells are ischemic within 10 seconds of occlusion d. Cells are viable for 20 minutes under these conditions e. IF PERFUSION ISN'T RESTORED = MI OCCURS (heart attack) D. Myocardial Ischemia Symptoms/Manifestations a. Stable Angina Pectoris = chronic obstruction that yields recurrent predictable chest pain i. Worsens with activity or stress, better with rest and relaxation ii. Chest discomfort (may feel like indigestion) iii. May report pain that radiates to the arm, jaw, back b. Prinzmetal angina = chest pain that is attributed to transient ischemia but is unpredictable and can be at rest i. Caused by vasospasm and may not be associated with atherosclerosis ii. Occurs often at night, usually benign E. Myocardial Infarction (MI) = aka heart attack→results when there is a PROLONGED ischemia causing IRREVERSIBLE damage to the heart muscle (prolonged coronary blood flow interruption) a. Plaque progression, subsequent clot formation then clot ruptures and travels to block blood flow b. Sudden cardiac death can occur F. MI Complications: a. Cardiac cells can be ischemic for about 20 minutes before they undergo irreversible cell death  b. Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical impulse instability G. MI Symptoms/Manifestations: a. Sudden angina pectoris (8-10 seconds of decreased blood flow uses up all oxygen reserves, creates referred pain) b. Pain may radiate to arm and/or jaw, nausea, vomiting, diaphoresis, dyspnea 6. Characterize the terms associated with pericardial disease. A. Pericardial disease = localized manifestation of another disorder, such as infection (bacterial, viral, fungal, rickettsial, or parasitic); trauma or surgery; neoplasm; or a metabolic, immunologic, or vascular disorder (uremia, rheumatoid arthritis, systemic lupus erythematosus, periarteritis nodosa) B. The pericardial response may consist of acute pericarditis, pericardial effusion, or constrictive pericarditis C. Acute pericarditis = acute inflammation of the pericardium a. Due to viral infection or idiopathic b. Fever, chest pain that may radiate to the back, malaise, difficulty getting comfortable, friction rub on auscultation c. Can lead to effusion D. Pericardial effusion = can be from acute pericarditis a. Effusion needs to be analyzed-serous, exudative, serosanguineous, blood b. Manifestations: dyspnea on exertion, muffled heart sounds, poorly palpable apical pulse, dull chest pain c. Tamponade may occur→serious life threatening condition where pressure from effusion will put pressure on heart, impairing its ability to pump properly 7. Discuss contractility, preload and afterload as mechanisms for both right and left heart failure. A. Contractility = force of contraction of ventricles B. Preload = volume and pressure inside ventricles at end of diastole C. Afterload = resistance to ejection of blood from the ventricle, recorded as systolic BP D. Right heart failure: RV backs up to RA and can get to capillaries or lower extremities a. Normal heart→RV hypertrophy→RV failure b. Decreased RV contractility c. Increased preload in RV and RA→blood backs up to into the veins and edema in lower extremities can result E. Left heart failure: LV backs up to LA and goes to lungs a. Decreased LV contractility→backs up to pulmonary system b. Increased blood volume (preload) in LV→increased volume in LA→increased volume in pulmonary system→pulmonary edema c. Increased resistance to ventricular resistance (afterload) →increased workload for LV 8. Understand and differentiate between the different types of shock, and be able to list the consequences of shock. A. Hypovolemic (most common) = caused by loss of whole blood, plasma, or interstitial fluid in large amounts a. Begins to develop when intravascular volume has decreased by about 15% b. Symptoms: high SVR, poor skin turgor, thirst, oliguria, low systemic and pulmonary preloads, rapid heart rate, threads pulse, and mental status deterioration B. Neurogenic (aka vasogenic shock) = occurs with cervical or upper thoracic cord injury about T6 and may be seen in addition to spinal shock a. Symptoms: vasodilation, hypotension, bradycardia, and failure of body temperature regulation b. May be complicated by hypovolemic or cardiogenic shock if there is concurrent heart failure or blood loss C. Anaphylactic = shock begins with exposure of a sensitized individual to an allergen a. Common allergens known to cause these reactions are insect venoms, shellfish, peanuts, latex, and medications such as penicillin b. Usually sudden, and progression to death can occur within minutes unless emergency treatment is given c. Manifestations: anxiety, dizziness, difficulty breathing, strider, wheezing, pruritus with hives (urticaria), swollen lips and tongue, abdominal cramping D. Septic a. begins with an infection that progresses from bacteremia to sepsis to septic shock, and finally to MODS  b. can be caused by community-acquired or health care associated infections, especially pulmonary, intra-abdominal and UTI’s c. Manifestations: the result of inflammation, decreased perfusion of vital tissues, and an alteration in oxygen extraction by all cells E. Cardiogenic a. least common b. Defined as decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume c. most cases of cardiogenic shock follow MI, but can also follow left heart failure, dysthymias, acute valvular dysfunction, ventricular or septal rupture, myocardial or pericardial infections, massive pulmonary embolism, cardiac tamponade, and drug toxicity d. Manifestations: caused by widespread impairment of cellular metabolism; including impaired mentation, dyspnea and tachypnea, systemic venous and pulmonary edema, dusky skin color, marked hypotension, oliguria, and ileus 9. Describe the role of the renin-angiotensin-aldosterone system (RAAS) in heart failure. FROM ZOOM: Blood pressure goes down, the body activates norepinephrine and epinephrine; they bind, start in the kidney and initiate the RAAS system. RAAS system is activated= renin comes out, finds anotensiogen, and converts it to angiotensinogen 1 (which is inactive); Ang. 1 crosses over the endothelial cells and finds the ACE enzyme, which takes Ang. 1 to Ang 2 (the active metabolite); this will go to the vascular smooth muscle and bind to its receptor and cause the blood pressure to go up; it also goes to the adrenal glands and causes the secretion of aldosterone which retains water and sodium, and gets rid of potassium Someone with heart failure can’t move blood volume as well; 2 segments die and RAAS system is activated (never turns off after MI) A. RAAS is activated early in heart failure as a compensatory mechanism→raises blood volume by retaining sodium and water B. Responsible for increased preload and afterload→by retaining water and raising blood volume C. RAAS system is now decompensatory, and with the extra volume from the heart attack LV heart failure is a concern a. LV can’t handle all the extra blood since not pumping at max. strength 10. Understand and differentiate between the various cardiac infections discussed in the slides to include risk factors, pathophysiology, and symptoms. A. Valvular dysfunctions = mitral and aortic valves more commonly affected than tricuspid and pulmonary→valvular stenosis/regurgitation, MVPS a. Primary and secondary causes, develops slowly b. Mitral valve prolapse = one or both cusps of mitral valve prolapse into left atrium during systole, allows regurgitation into atrium i. Most common valve disorder ii. Can be asymptomatic iii. Symptoms: palpitations, dizziness, dyspnea, chest pain, fatigue, syncope iv. Disorder of endocardium B. Acute rheumatic fever = systemic, inflammatory disease caused by delayed and exaggerated immune response to Group A Strep a. Occurs in those who are genetically predisposed b. Minor manifestations: fever, lymphadenopathy, arthralgia, nausea, vomiting, pain, tachycardia c. Major manifestations: carditis, chorea, subcutaneous nodules, polyarthritis d. Can cause scarring of cardiac structures and lead to rheumatic heart disease e. Disorder of endocardium C. Rheumatic heart disease = progressive fibrosis occurs and valves can lose elasticity over several years a. Atrial fibrillation, cardiomegaly, left heart failure may occur b. Endocarditis→myocarditis→fibrinous pericarditis c. Disorder of endocardium D. Infective endocarditis = inflammation and infection of endocardium  a. Agents: bacteria (most common) b. Pathogenesis: damaged (prepared) endocardium→blood-borne microorganism adherence→proliferation of microorganism (vegetations) c. Manifestations: classic findings are fever, new/changed cardiac murmur, petechial lesions of skin, conjunctiva, oral mucosa d. Characteristic physical findings (late onset): osler nodes (painful erythematous nodules on pads of fingers and toes), janeway lesions (nonpainful hemorrhagic lesions on palms and soles) e. Other: weight loss, back pain, night sweats, heart failure f. Disorder of endocardium E. Dilated (congestive) cardiomyopathy = impaired systolic function leading to ventricular dilation a. Result of many disease states b. Manifestations: dyspnea, fatigue, S3 heart sound, pedal edema, pulmonary congestion c. Disorder of myocardium F. Hypertrophic cardiomyopathy = thickening of myocardium a. Hypertrophy of monocytes in response to increased workload demand, impaired systolic function and heart failure b. Manifestations: angina, dyspnea on exertion, murmurs, extra heart sounds c. Disorder of myocardium G. Restrictive cardiomyopathy = myocardium becomes rigid and non compliant which impedes ventricular filling a. Leads to right heart failure b. Disorder of myocardium 11. Compare and contrast left and right heart failure. A. Left Heart Failure (Congestive heart failure) = can’t get volume out secondary to damage usually from an MI, hypertension, diabetes, excessive ETOH use, genetic heart condition, renal failure, age, obesity, cardiac defects a. Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation b. LV backs up to LA c. Decreased LV contractility d. Backs up to pulmonary septum i. Pulmonary edema ii. PND, SOB, dyspnea e. Manifestations: dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema f. Physical examination often reveals pulmonary edema (cyanosis, crackles, pleural effusions), hypotension or hypertension and evidence of underlying CAD or hypertension B. Right Heart Failure = most commonly caused by a diffuse hypoxia pulmonary disease a. Can result from left heart failure when an increase in left ventricular filling pressure is reflected back into the pulmonary circulation b. Can also result from COPD, CF, and ARDS c. Finally, MI, cardiomyopathies, and pulmonic valvular disease interfere with right ventricular contractility and can lead to right heart failure INCREASE IN PRELOAD, DECREASE IN CONTRACTILITY **LV is responsible for pulse and blood pressure