Study guide

Nursing - NR 507 Pathophysiology Midterm Study Guide Completed

Asthma is a chronic inflammatory disease characterized by sensitization to allergens, bronchial hyperreactivity, and reversible airway obstruction. Asthma is initiated by a type I hypersensitivity reaction primarily mediated by IgE. Airway epithelial exposure to antigen initiates both an innate and an adaptive immune response in sensitized individuals. Many cells and cellular elements contribute to the persistent inflammation of the bronchial mucosa and hyperresponsiveness of the airways, including macrophages (dendritic cells), T helper 2 (Th2) lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils. There is both an immediate (early asthmatic response) and a late (delayed) response. In young children, airway obstruction can be more severe because of the smaller diameter of their airways. Asthma is caused by complex interaction of genetic and environmental factors. Asthma results in excess mucus production and accumulation hypertrophy of bronchial smooth muscle airflow obstruction decreased alveolar ventilation. Asthma can take two forms: extrinsic and intrinsic. The most common symptoms of both extrinsic and intrinsic asthma are: coughing, wheezing shortness of breath rapid breathing chest tightness Extrinsic: The plugs of mucus and pus from this inflammatory process can block alveolar passageways, leading to air-trapping and hyperinflation more signs and symptoms consistent with the diagnosis of asthma This process is illustrated in this image which shows the airway pathology in its entirety mast cell degranulation triggered by the excessive amounts of IGE that have airingly formed this individual that will bind that allergen as it enters the airway that mast cell degranulation releases chemicals that releases mucus production and accumulation as well as chemicals that contribute to smooth muscle constriction that smooth muscle constriction along with mucus plugs that form result in hyperinflation of the alveoli and eventual erosion of airway tissue Intrinsic: can be triggered by a variety of non-allergic factors, each causing a slightly different variation on the inflammatory process. Regardless of the underlying cause of asthma, the disease process has both a bronchoconstriction component and an inflammation component. Pharmacotherapy focuses on one or both of these components to provide fast relief for acute bronchospasms, as well as long-term control to reduce the frequency of asthma attacks. Chronic Bronchitis: pathogenesis of chronic bronchitis which begins with some sort of exposure to airborne irritants which activates bronchial smooth muscle constriction, mucus secretion, and release of inflammatory mediators (histamine, prostaglandins, leukotrienes, interleukins) from immune cells located in the lamina propria These airborne irritants can include air pollution or industrial chemicals & fumes. But the most common irritant is smoke from cigarettes and other tobacco products. Keep in mind that all of these bronchial responses are, in fact, normal responses to occasional inhalation of airborne irritants. Smooth muscle constriction is important to limit passage of the irritant deeper into the respiratory tract. Secretion of mucus and release of inflammatory chemicals are also important to help trap and defend against a potentially harmful substance. The transition from a normal, protective respiratory response to a detrimental effect occurs with …. long-term exposure to airborne irritants which promotes • smooth muscle hypertrophy à increased bronchoconstriction • hypertrophy and hyperplasia of goblet cells à mucus hypersecretion • epithelial cell metaplasia à non-ciliated squamous cells • migration of more WBCs to site à inflammation & fibrosis in bronchial wall • thickening and rigidity of bronchial basement membrane à narrowing of bronchial passageways the smooth muscle constriction, bronchial wall inflammation, and mucus plugs lead to another issue: alveolar hyperinflation. Because of the anatomical changes in the bronchioles associated with chronic irritation ventilation, especially exhalation, is compromised. Pressure differences during inhalation are high enough to force air into the alveoli. However, during exhalation the narrowing and collapse of the air passageways causes air to be trapped in the alveoli resulting in. • alveolar hyperinflation à expanded thorax • hypercapnia, (CO2 retention) and, respiratory acidosis The high concentration of CO2 creates unfavorable conditions for gas exchange, so there is • decreased O2 exchange à ventilation/perfusion (V/Q) mismatch Decreased perfusion of the pulmonary capillaries with oxygenated blood results in • chronic pulmonary hypoxia à cyanosis Poor ventilation, leading to decreased perfusion, causes Right to Left “shunting” to occur. This is the phenomenon where deoxygenated blood passes from the RV to lungs to the LV without adequate perfusion (gas exchange) Similar to other obstructive pulmonary disorders, chronic bronchitis has both a bronchoconstriction component and an inflammation component. Pharmacotherapy includes: • antitussives and expectorants – can be useful to help thin the secretions for easier expulsion and to help control coughing episodes • bronchodilators – fast- and long-acting agents are mainstays of chronic bronchitis treatment • systemic corticosteroids – particularly useful during an acute flareup/exacerbation. • antibiotics – as needed for treatment of bacterial infections; critical to prevent any excessive immune stimulation Prophylactic immunizations (especially the pneumococcus vaccine and annual flu vaccines) are important to reduce likelihood of exacerbations triggered by respiratory infections. Clients also benefit from working with respiratory and physiotherapists to learn relatively simple physical measures that can help optimize quality of life for clients with chronic bronchitis. These physical measures include: • chest physiotherapy using postural drainage (changes in body position) and gravity to facilitate movement of mucus from the congested lower bronchial airways to the trachea for easier expulsion AND • relaxation and breathing techniques, including pursed lip breathing, similar to how you would blow a bubble, to prolong the exhalation period An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. These agents inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, and many other parts of the body. Anticholinergics are divided into three categories in accordance with their specific targets in the central and peripheral nervous system: antimuscarinic agents, ganglionic blockers, and neuromuscular blockers. Cardiovascular: GRANT FRIBERG, ERICA LUDWIG, Sheila Cardoniga review concepts related to cardiac output, cardiac contractility, preload/afterload, systole/diastole, heart valves (when they are open and closed; the production of S1 & S2), stenosis of the heart valves and effects; stroke volume, Cor Pulmonale, heart failure and physiologic processes that lead to heart failure symptoms, hypertension, calcium binding and troponin Review concepts related to cardiac output (cardiac contractility, preload, afterload): cardiac output: how much blood the heart pumps through the circulatory system in 1 minute. cardiac contractility: determined by Ca 2 availability and its interaction with actin-myosin. increased by sympathetic stimulation (e.g. fever, anxiety, ↑ thyroxine). decreased by low ATP levels (e.g. ischemia, hypoxia or acidosis). preload: volume of blood received by the heart, also the pressure of the blood on the muscle fibers in the ventricles of the heart at the end of diastole. degree of myocardial fiber length stretch before contraction. Degree of stretch is influenced by end-diastolic ventricular volume (EDV) which equals the amount of blood entering ventricle during diastole. Increased by CHF and hypervolemia. Decreased by cardiac tamponade or hypovolemia (hemorrhage, dehydration). afterload: pressure or resistance the heart has to overcome to eject blood. amount of tension each ventricle must develop during systole to open SL valves & eject blood. Influenced by ventricle wall thickness (muscle strength), Increased thickness=decreased tension. Influenced by arterial pressure (resistance to ejection), increased pressure=increased tension. Influenced by ventricle chamber size (blood volume capacity), increased chamber size=increased tension. Afterload is increased by systemic hypertension, valve disease or COPD (ex. pulmonary hypertension). Afterload is decreased by hypotension or vasodilation. Systole: diastole: heart valves (when they are open and closed; the production of S1 & S2): stroke volume: volume of blood ejected by each ventricle/systole (70 mL) and is determined by preload, contractility, and afterload. Cor Pulmonale: right heart failure. Inability of the RV to provide adequate blood flow into pulmonary circulation. Caused by pulmonary disease, RV MI, RV hypertrophy, pulmonary SLV or tricuspid valve damage, or secondary to left heart failure. High pulmonary vascular pressure increases RV contraction force (afterload). RV is unable to empty completely which results in increased RV preload. RA is unable to empty completely which results in an increased RA preload. Increased vena cava and systemic venous volume and pressure occurs. The fluid is forced out into peripheral tissues. This causes jugular distention, hepatosplenomegaly, peripheral edema and left heart failure. heart failure: cardiac dysfunction caused by inability of the heart to provide adequate cardiac output, resulting in inadequate tissue perfusion. Types of HF, left heart failure (CHF), right heart failure (cor pulmonale), and high-output failure. Left heart failure: inability of LV to provide adequate blood flow into systemic circulation. Caused by systemic hypertension, LV MI, LV hypertrophy, aortic SLV or bicuspid valve damage secondary to right heart failure. High systemic vascular pressure increases the LV contraction force which causes increased afterload. The LV is unable to eject normal amount of blood which causes an increase in LV preload. The LA is unable to eject normal amount of blood which causes an increased LA preload. This increases the blood volume and pressure in pulmonary veins and fluid is forced out into the pulmonary tissues. This all causes pulmonary edema, dyspnea, and right heart failure. Right heart failure: see Cor Pulmonale High-Output failure: inability of heart to pump sufficient amounts of blood to meet the circulatory needs of the body, despite normal blood volume and cardiac contractility. Caused by severe anemia, nutritional deficiencies, hyperthyroidism, sepsis, extreme febrile state. Cardiac output (CO): the amount of blood the heart pumps throughout the body per minute CO is calculated by multiplying HR (beats per minute) by stroke volume (liter of blood per beat) à(HR X SV=CO), Normal adult CO is approx. 5L/min Stroke volume: the volume of blood ejected per beat during systole The pumping action of the heart consists of contraction and relaxation. Each ventricular contraction and the relaxation that follows makes up the cardiac cycle. Diastole: the period of cardiac relaxation. During diastole, the blood (from the atrium) fills the ventricles. DIASTOLE=RELAXATION Systole: the period of ventricular contraction. The contraction of the ventricles forces blood out of the of the ventricles and into the pulmonary system. SYSTOLE=CONTRACTIONàThink contrACTIONàThe action in contraction is the pushing of the blood out of the heart 4 FACTORS AFFECT CARDIAC OUTPUT: Preload, afterload, contractility, and heart rate Preload: the VOLUME of blood inside the ventricle and the end of diastole (relaxation) . It is determined by the amount of venous blood returning to the ventricle during diastole (relaxation) and the amount of blood remaining in the ventricle after systole (contraction) Afterload: afterload is the RESISTANCE to ejection of blood from the left ventricle. It is the load that the heart muscle needs to move during contraction Contractility: represents the ability of the myocardial muscle to contract. It is the FORCE of heart contraction. It can’t be measured directly. Heart rate: HR is controlled by the SA node in the electrical conduction system of the heart. Many things affect HR including medications, hormones (epinephrine and norepinephrine), and neuropsychological factors (stressors, depression). cardiac output: how much blood the heart pumps through the circulatory system in 1 minute. cardiac contractility: determined by Ca 2 availability and its interaction with actin-myosin. increased by sympathetic stimulation (e.g. fever, anxiety, ↑ thyroxine). decreased by low ATP levels (e.g. ischemia, hypoxia or acidosis). preload: volume of blood received by the heart, also the pressure of the blood on the muscle fibers in the ventricles of the heart at the end of diastole. degree of myocardial fiber length stretch before contraction. Degree of stretch is influenced by end-diastolic ventricular volume (EDV) which equals the amount of blood entering ventricle during diastole. Increased by CHF and hypervolemia. Decreased by cardiac tamponade or hypovolemia (hemorrhage, dehydration). afterload: pressure or resistance the heart has to overcome to eject blood. amount of tension each ventricle must develop during systole to open SL valves & eject blood. Influenced by ventricle wall thickness (muscle strength), Increased thickness=decreased tension. Influenced by arterial pressure (resistance to ejection), increased pressure=increased tension. Influenced by ventricle chamber size (blood volume capacity), increased chamber size=increased tension. Afterload is increased by systemic hypertension, valve disease or COPD (ex. pulmonary hypertension). Afterload is decreased by hypotension or vasodilation. Systole: diastole: heart valves (when they are open and closed; the production of S1 & S2): the production of S1 and S2 Unidirectional blood flow through the heart is maintained by four valves located within the chambers of the heart: two atrioventricular (AV) valves: tricuspid & bicuspid (mitral) two semilunar valves: pulmonary & aortic The superior & inferior vena cava carry systemic DEOXYgenated blood to the right atrium. The tricuspid valve opens to allow blood flow into the right ventricle. The pulmonary semilunar valve opens to allow blood flow into the pulmonary trunk, a large blood vessel which divides to form the left and right pulmonary arteries that carry blood to the lungs and eventually into the alveolar capillaries where gas exchange will occur. The pulmonary veins return the 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 to form the brachiocephalic, left common carotid, and subclavian arteries that will further branch to carry blood to the rest of the body. The system of four valves just described, open and close in response to myocardial contraction and pressure changes within the heart. The cardiac cycle begins with ventricular diastole when the muscle cells in the ventricles are relaxed, allowing for passive movement of 70% of blood from the atria to the ventricles, driven primarily by gravitational flow. The remaining 30% of blood is “pumped” into the ventricles during atrial systole, the contraction of muscle cells located in the left and right atria. This prompts closure of the AV valves to prevent backflow of blood into the atria. The closure of the valves can be auscultated and corresponds to the first heart sound (S1). As pressure builds in the ventricles from the blood volume, this pushes the semilunar valves open. Meanwhile, the muscle cells of the ventricles contract (ventricular systole) and 55-70% of the blood is “pumped” from the ventricles into pulmonary and systemic circulation. This volume of blood is referred to as the cardiac ejection fraction. As the ventricles empty, pressure drops in the ventricles, forcing closure of the semilunar valves to prevent backflow of blood into the ventricles. The closure of these valves can also be auscultated and corresponds to the second heart sound (S2). Stenosis of the heart valves and effects: In valvular stenosis, the 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. Intraventricular or atrial pressure increases in the chamber to overcome resistance to flow through the valve. Increased pressure causes the myocardium to work harder, causing myocardium hypertrophy. In valvular regurgitation (also called insufficiency or incompetence) the valve leaflets, or cusps, fail to shut completely, permitting blood flow to continue even when the valve is supposed to be closed. During systole or diastole some blood leaks back into the chamber proximal to the incompetent valve, producing a murmur on auscultation. Valvular regurgitation increases the volume of the blood the heart must pump and increases the workload of the affected chamber. Increased volume leads to chamber dilation, and increased workload leads to hypertrophy. Aortic stenosis: is the most common valvular abnormality. The three common causes are 1.) calcific degeneration related to aging (aortic sclerosis), 2.) congenital bicuspid valve, 3.) inflammatory damage caused by rheumatic heart disease (RHD). Untreated aortic stenosis can lead to dysrhythmias, MI, and heart failure. The classic manifestation of aortic stenosis are angina, syncope, and heart failure Mitral Stenosis: impairs the flow of blood from the left atrium to the left ventricle. Mitral stenosis is the most common form of RHD. Continued increases in left atrial volume and pressure cause chamber dilation and hypertrophy and eventually result in pulmonary HTN. The outcomes of untreated chronic mitral stenosis are pulmonary HTN and right ventricular failure. The risk of developing atrial dysrhythmias (especially fibrillation) and dysrhythmia-induced thrombi is high. Signs and symptoms such as jugular venous distention and peripheral edema, result from pulmonary congestion and right heart failure. stroke volume: volume of blood ejected by each ventricle/systole (70 mL) and is determined by preload, contractility, and afterload. Cor Pulmonale: right heart failure. Inability of the RV to provide adequate blood flow into pulmonary circulation. Caused by pulmonary disease, RV MI, RV hypertrophy, pulmonary SLV or tricuspid valve damage, or secondary to left heart failure. High pulmonary vascular pressure increases RV contraction force (afterload). RV is unable to empty completely which results in increased RV preload. RA is unable to empty completely which results in an increased RA preload. Increased vena cava and systemic venous volume and pressure occurs. The fluid is forced out into peripheral tissues. This causes jugular distention, hepatosplenomegaly, peripheral edema and left heart failure. heart failure: cardiac dysfunction caused by inability of the heart to provide adequate cardiac output, resulting in inadequate tissue perfusion. Types of HF, left heart failure (CHF), right heart failure (cor pulmonale), and high-output failure. Left heart failure: inability of LV to provide adequate blood flow into systemic circulation. Caused by systemic hypertension, LV MI, LV hypertrophy, aortic SLV or bicuspid valve damage secondary to right heart failure. High systemic vascular pressure increases the LV contraction force which causes increased afterload. The LV is unable to eject normal amount of blood which causes an increase in LV preload. The LA is unable to eject normal amount of blood which causes an increased LA preload. This increases the blood volume and pressure in pulmonary veins and fluid is forced out into the pulmonary tissues. This all causes pulmonary edema, dyspnea, and right heart failure. Right heart failure: see Cor Pulmonale High-Output failure: inability of heart to pump sufficient amounts of blood to meet the circulatory needs of the body, despite normal blood volume and cardiac contractility. Caused by severe anemia, nutritional deficiencies, hyperthyroidism, sepsis, extreme febrile state. Heart Failure and Physiologic processes that lead to heart failure and symptoms, hypertension, calcium binding and troponin