NR 507 Pathophysiology

Oxygen transportation step 1 - answer-Air is inhaled through the process of ventilation (mechanical movement of gas or air into or out of the lungs) Oxygen transportation step 2 - answer-oxygen diffused from the alveoli into pulmonary capillaries, moving oxygen from the pulmonary veins to the left side of the heart to the aorta into systemic arterial circulation Oxygen transportation step 3 - answer-Perfusion (exchange of O2 and CO2 in the blood stream, which occurs via the alveoli and pulm capillaries) of the systemic capillaries with oxygenated blood Oxygen transportation step 4 - answer-oxygen is diffused from the systemic capillaries to each and every cell Gas CO2 transport step 1 - answer-Diffusion of blood (deoxygenated) from cells into systemic capillaries Gas CO2 transport step 2 - answer-Perfusion of the systemic capillaries with deoxygenated blood through the venous circulation, to the vena cava into the right side of the heart, to the pulmonary arteries (ART carry deoxygenated blood) Gas CO2 transport step 3 - answer-Diffusion of the CO2 from pulmonary arteries into alveoli through pulmonary capillaries Gas CO2 transport step 4 - answer-Exhalation of air by ventilation of lungs from removal of CO2 What are bronchioles? - answer-smallest of the conducting airways, branch out from the alveoli and connect to the alveoli What are the three layers of the bronchioles? - answer-Epithelial layer (inner layer) mucous containing goblet cells, and ciliated cells. Connective tissue (middle layer) lamina propia- cartilage and WBC's Smooth muscle layer (outer layer) outer layer to constrict and dilate What are the bronchioles controlled by? - answer-The autonomic nervous system Parasympathetic stimulation- mediated via vagus nerve--- release neurotransmitter acetylcholine binds to cholinergic receptors-- leading to bronchial constriction (decreased air flow). Dominates to limit exposure to external substances Sympathetic stimulation- stimulation of neurotransmitter epinephrine-- binds to beta 2- adrenergic receptors-- leading to bronchial dilation What is asthma? - answer-chronic inflammatory disorder of the bronchial mucosa caused by bronchial hyper-responsiveness, construction of airways, and variable airflow obstruction that is reversible. Asthma signs and symptoms - answer-Those are asymptomatic between attacks. Beginning of attacks--chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachypnea, and tachycardia Severe attacks-- use of accessory muscles of respiration, wheezing during both inspiration/expiration, pulsus paradoxus- decrease in SBP during inspiration Anti-cholingeric drugs for asthma - answer-Tiotropium and Ipratropium- these drugs block acetylcholine binding--- leading to bronchodilation through decrease in the parasympathetic response What causes bronchitis and associated pathogenesis? - answer-acute causes- infection or inflammation chronic causes- usually caused by viruses with a nonproductive cough Chronic bronchitis - answer-Inflammation of the bronchi persisting over a long time. Productive cough that continues for at least three months for a year for 2 years consecutive years. Enhanced chronic inflammatory response in the airways to noxious particles or gases. Inspired irritants-- bronchial inflammation-- bronchial edema increase in mucous glands and goblet ells in airway, smooth muscle hypertrophy with fibrosis, narrowing of airways Hypersecretion of thick muscus and cannot be cleared due to impaired ciliary function-- increasing susceptibility to infection contributing to airway injury and ineffective repair. Initially only affects larger bronchi-- eventually all airways involved Chronic bronchitis and acid/base disturbances - answer-narrowed airway--obstruction-- ventilation-perfusion mismatch with hypoxemia Hypercapnia develops as air trapping worsens and the work of breathing increase Reduced tidal volumes-hypoventilation-- respiratory acidosis Polycythemia vera - answer-chronic neoplastic, nonmalignant condition that is characterized by overproduction of red blood cells (often with an increase levels of WBC and platelets) and splenomegaly chronic bronchitis (marked hypoxemia) leads to ... - answer-polycythemia and cyanosis what is an essential component of polycythemia vera - answer-Erythrocytosis; clonal proliferation of erythoid progenitors occurs in the bone marrow independent of erythropoietin, even though the cells express a normal erythropoietin receptor alveolar hyperinflation with asthma - answer-airway obstruction increases airflow resistance and decreases flow rate--- impaired expiration causes air trapping, hyperinflation distal to obstruction and increased work of breathing-- continued air trapping increase intrapleural pressure and alveolar gas pressures-- decreased alveolar perfusion-- hyperventilation is triggered in response to increased lung volume and obstruction (early hypoxemia without Co2 retention and respiratory alkalosis)-- With progressive obstruction of expiratory airflow, airflow trapping more air leading to lungs and thorax hyperexanded, decrease respiratory muscles resulting in a decrease tidal volume and increase in CO2 retention-- causing respiratory acidosis Blood flow between heart and lungs - answer-The superior and inferior vena cava carry systemic DEoxygenated blood to the right atrium-- the tricuspid valve opens to allow for blood flow into the right ventricle-- the pulmonary semilunar valve opens to allow blood flow into the pulmonary truck; a large blood vessel that divides to form the left and right pulmonary arteries that carry blood to the lungs and eventually into the alveolar capillaries where gas exchange occurs-- The pulmonary veins return oxygenated blood to the left atrium-- the bicuspid valve opens to allow blood flow into the left ventricle-- the aortic semilunar valve opens to allow blood flow into the aorta; a large blood vessel that divides into brachiocephalic, left common carotid and subclavian arteries that will further branch to carry blood to the rest of the body. cardiac cycle - answer-atrial systole, atria contracts-- blood pushes through open tricuspid and mitral valves into ventricles. Semilunar valves are closed-- Beginning of ventricular systole, ventricular contract-- increased pressure in ventricles. Tricuspid and Mitral valves close (1st heart sound). As pressure rises, semilunar valves open when ventricles pressure-- atrial pressure-- blood pushed into aorta and pulmonary arteries. Beginning of ventricular diastole, pressure in relaxing ventricles drop below that in the arteries and semilunar valves close (2nd heart sound) As pressure falls, blood flow from veins into relaxed atria. Tricuspid and mitral valves open when pressure ventricle falls below atrial pressure. atrioventricular (AV) node - answer-mitral (left AV valve) and tricuspid (right AV valve) What happens during ventricular relaxation (systole) - answer-the two AV valves (mitral and tricuspid) blood from the atria to the ventricles. Once pressure is high in the ventricles the valves close to prevent from back flow into the atria as the ventricles contract (S1- 1st heart sound) What are the semilunar valves? - answer-pulmonary (RV-- lung) and aortic (LV-- body) what happens during ventricular contraction (Diastole) - answer-The pulmonary and aortic valves open when there is pressure and blood flows out of the ventricle and into the systemic and pulmonary circulation---after ventricular contraction and ejection the pressure decreases and the semilunar valves close when pressure is in the ventricles-- the closure is to prevent back flow into the right and left ventricles (S2- 2nd heart sound) What is cardiac output? - answer-HR x SV; normal CO in healthy adults is about 5L/min What four factors affect CO? - answer-Preload, afterload, heart rate and myocardial contractility. What is Ejection fraction? - answer-SV/ EDV (end diastolic volume) What increase EF? - answer-factors that increase contractility (sympathetic nervous system activity) What would a decrease in EF indicate? - answer-Ventricular failure What is stroke volume? - answer-volume of blood ejected per beat during systole Average SV is 70 mL SV and HR relationship - answer-Inverse relationship-- high HR= shorter fill time= low SV or low HR= longer fill time= high SV What factors determine force of contraction (Contractility)? - answer-Changes in preload Intropic stimuli changes O2 and CO2 levels the available Ca+ and its interaction with actin-myosin actin- myosin turn towards each-other (inotropic) and together create muscle fiber contraction troponin releases Ca+= muscle relaxation decreased in ischemia, hypoxia and decreased ATP what are inotropic stimuli changes for contractility? - answer-Fever, anxiety and SNS neurotransmitters: epi and norepi (positive agents) result in increased contractility Vagus nerve (Acetycholine- negative agent) results in a decreased contractility How does the O2 and CO2 levels change in contractility? - answer-Severe hypoxemia= contractility is decreased Moderate hypoxemia= catecholamines can increase contractility calcium binding and troponin? - answer-In resting muscles- calcium ions are stored in the sarcoplasmic reticulum Action potential reach the muscle cells-- T tubules carry action potential deep into the sarcoplasm-- causing sarcoplasm reticulum to release store of calcium ions-- in resting muscles, myosin binding sites are covered by troponin and tropomyosin. Calcium ions are released into the sarcoplasm as a result of action potential bind to troponin--- tropomysin and troponin move out of the way of the myosin binding sites leaving myosin heads free to bind to the actin microfilament--- ATP is used as an energy molecule to the myosin cross bridge-- the release of the stored energy provides force needed for each cross-bridge to move back to its org position, pulling actin along-- each cross bridge will bing to an actin molecule until another ATP molecule binds to it and pulls it back into a resting position. What is preload? - answer-degree of myocardial stretching before contraction-- the volume inside the ventricle at the END of diastole ((Ventricular end-diastolic volume (VEDV) and pressure (VEDP)) What two factors affect preload? - answer-1)the amount of venous blood returning to the ventricle during diastole 2) the amount of blood in the ventricle after systole (end- systolic volume) What is starlings law? - answer-The volume of blood in the heart at the end of diastole (the length of the muscle fibers) is directly related to the force of the contraction during the next systole. What causes an increase in preload? - answer-CHF and hypervolemia what causes a decrease in preload? - answer-decrease in external pressure on the heart ( Cardiac tamponade and hypovolemia) What is afterload? - answer-amount of tension each ventricle must develop during systole to open semilunar valves and eject blood What causes a decrease in afterload? - answer-low aortic pressure, enables the heart to contract more rapidly hypotension or vasodilation example- shock what causes a increase in after-load? - answer-high aortic pressure, slow contraction and cause higher workloads against which the heart function to eject blood-- usually the result of systemic vascular resistance. systemic hypertension, valve disease, or COPD resulting in pulmonary hypertension What is diastole? - answer-period of relaxation, blood fills the ventricles What is systole? - answer-period of contraction, follows diastole. propels blood out of the ventricles and into the pulmonary and systemic circulation What is stenosis? - answer-valve orifice is constricted and narrowed. What happens during stenosis? - answer-stenosis impedes forward flow of blood-- increases the workload of the cardiac chamber proximal to the diseased valve intraventricular and atrial pressure increases in the chamber to overcome resist