NR 507 Week 4 Midterm Study Guide

Study Guide Mid Term Week 4 Pulmonary Review Concepts Related to Anticholinergic Drugs & Treatment for Asthma: Fast-acting Medications: - Tiotropium & ipratropium - Anticholinergic drugs block acetylcholine binding bronchodilation through decreased parasympathetic response Bronchitis & Associated Pathogenesis: Bronchitis – bronchial inflammation, hypersecretion of mucus, chronic productive cough Exposure to airborne irritants activates bronchial: - Smooth muscle constriction - Mucus secretion - Release of inflammatory mediators Chronic Bronchitis & Related Acid/Base Disturbances: Hypercapnia (CO2 retention) respiratory acidosis Perfusion: Perfusion – the actual exchange of O2 and CO2 in the bloodstream, occurs via the alveoli and pulmonary capillaries Ventilation – air movement in/out of the lung, is critical to ensure sufficient perfusion Blood Flow Between the Heart & Lungs: R heart – receives deoxygenated systemic blood and returns it to the lungs = pulmonary circulation L heart – receives oxygenated blood from the lungs and returns it to systemic circulation Right to Left “shunting” – blood passes from R ventricle to lungs to L ventricle without perfusion (gas exchange) Asthma Signs & Symptoms: Coughing Wheezing Shortness of Breath Rapid Breathing Chest Tightness Bronchioles: Composed of a 3-layer tube surrounded the lumen or air passageway - The innermost layer, closest to the lumen, is composed of ciliated solumnar epithelial cells’ the constant sweeping action of the cilia are important to help clear the bronchial passageways or irritants, including infectious agents. This layer also contains mucus producing goblet cells which traps irritants and microbes to prevent their passage into the alveoli - The middle layer, called the lamina propria, is embedded with connective tissue cells, as well as immune cells. These immune cells include a number of different kinds of WBCs, located here to help protect the airways - The outermost layer is composed of smooth muscle cells, responsible for the ability of the airways to constrict and dilate Alveolar Hyperinflation with Asthma: Plugs of mucus and pus from the inflammatory process can block alveolar passageways which leads to air-trapping and alveolar hyperinflation Cardiovascular Review Concepts Related to Cardiac Output & Cardiac Contractility: Cardiac Output – volume of blood ejected by each ventricle per minute CO = HR x SV (heart rate x stroke volume) Cardiac Contractility – (inotropic state) – determined by Ca+2 availability and its interaction with actin-myosin -Increased by sympathetic stimulation (fever, anxiety) -Decreased by low ATP levels (ischemia, hypoxia, acidosis) Preload/Afterload: Preload – degree of myocardial fiber length stretch before contraction - amount of blood entering ventricle during diastole - increased by CHF, hypervolemia - decreased by cardiac tamponade or hypovolemia (hemorrhage, dehydration) Afterload – amount of tension each ventricle must develop during systole to open SL valves and eject blood - influenced by ventricle wall thickness, atrial pressure, ventricle chamber size - increased by systemic hypertension, valve disease, or COPD - decreased by hypotension or vasodilation (shock) Systole/Diastole: Diastole – the period of relaxation when blood fills the ventricles of the heart Systole – ventricle contraction, propelling blood out of the ventricles into the body Heart Valves (when they are open and closed; production of S1 & S2): 2 atrioventricular (AV) valves = tricuspid & bicuspid (mitral) 2 semilunar (SL) valves = pulmonary & aortic - the valves open and close in response to myocardial contraction and pressure changes within the heart - when the AV valves close = 1st heart sound (S1) - when the SL valves close = 2nd heart sound (S2) Stenosis of the Heart Valves and Effects: Valvular Stenosis – valve orifice is constricted and narrowed, impeding the forward flow of blood and increasing the workload of the cardiac chamber proximal to the diseased valve Aortic Stenosis – diminished blood flow from the L ventricle into the aorta Effects = angina, pulmonary edema, MI, heart failure Mitral Stenosis – impairs blood flow from the L atrium to the L ventricle Effects = pulmonary edema, atypical chest pain, respiratory infections Stoke Volume: Volume of blood ejected per beat during systole Preload, afterload & contractility all interact with one another to determine stroke volume and cardiac output 3 major factors determine force of contraction: - changes in the stretching of ventricular myocardium caused by changes in preload - alteration in the inotropic stimuli of the ventricles