EXAM 3 Chapter 12: Cardiovascular Disorders Circulatory System - Vessels - Fluid - Pump Blood flows from systemic to pulmonary to systemic circulation. Heart - Anatomy - Located in the mediastinum - Located in the pericardial sac - Parietal pericardium - Epicardium (visceral pericardium) - Pericardial cavity - Myocardium - Endocardium - Heart valves - Atrioventricular valves - Semilunar valves - Septum Control of the Heart Cardiac control center in medulla oblongata - Controls rate and force of contraction - Located in the medulla Baroreceptors - Detect changes in blood pressure - Located in the aorta and internal carotid arteries Sympathetic stimulation (cardiac accelerator nerve) - Increases heart rate (tachycardia) Parasympathetic stimulation (CN X vagus nerve) - Decreases heart rate (bradycardia) Factors that Increase Heart Rate - Increased thyroid hormones or epinephrine Elevated body temperature, infection - i.e., Fever Increased environmental temperature - Especially in high humidity Exertion or exercise Smoking Stress response Pregnancy - Pain Coronary Circulation - - - - Right and left coronary arteries - Branch of the aorta immediately distal to aortic valve - Part of the systemic circulation Left coronary artery divides into - Left anterior descending or interventricular artery - Left circumflex artery Right coronary artery branches - Right marginal artery - Posterior interventricular artery Many small branches extend from these arteries to supply the myocardium and endocardium. Collateral circulation is extremely limited. Coronary Arteries Cardiac Cycle Diastole = REST - Relaxation of myocardium required for filling chambers - “Lubb-Dubb” sound is when valves close (during REST) Systole = CONTRACTION - Contraction of myocardium provides increase in pressure to eject blood Cycle begins with - Atria relaxed, filling with blood – AV valves open – blood flows into ventricles – atria contract, remaining blood forced into ventricles – atria relax – ventricles contract – AV valves close – semilunar valves open – blood into aorta and pulmonary artery – ventricles relax Heart Sounds - - “Lubb-dubb” - “Lubb” – closure of AV valves - “Dubb” – closure of semilunar valves Murmurs - Caused by incompetent valves Pulse - Indicates heart rate Pulse deficit - Difference in rate between apical and radial pulse Cardiac Function - - Cardiac output (CO) - Blood ejected by a ventricle in one minute - CO = SV × HR (heart rate) Stroke volume (SV) - Volume of blood pumped out of ventricle/contraction Preload - Amount of blood delivered to heart by venous return Afterload - Force required to eject blood from ventricles - Determined by peripheral resistance in arteries Blood Vessels - Arteries – arterioles - Transport blood away from heart Veins – venules - Bring blood back to the heart Capillaries - Microcirculation within tissues Systemic circulation - Exchange of gasses, nutrients, and wastes in tissues Pulmonary circulation - Gas exchange in lungs Blood Pressure Systolic pressure - Exerted when blood is ejected from ventricles (high) Diastolic pressure - Sustained pressure when ventricles relax (lower) - Blood pressure (BP) is altered by cardiac output, blood volume, and peripheral resistance to blood flow. Changes in blood pressure - Sympathetic branch of ANS - Increased output → vasoconstriction and increased BP - Decreased output → vasodilation and decreased BP - BP is directly proportional to blood volume. - Hormones - Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); renin-angiotensin-aldosterone (vasoconstriction ↑ BP) Heart Disorders Diagnostic Tests for Cardiovascular Function - - - ECG - Useful in the initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, pericarditis Auscultation - Detection of valvular abnormalities or abnormal shunts of blood that cause murmurs Echocardiography - Used to record the heart valve movements, blood flow, and cardiac output Exercise stress tests - To assess general cardiovascular function - - - Chest x-ray films - Used to show shape and size of the heart - Nuclear imaging - Tomographic studies Cardiac catheterization - Measure pressure and assess valve and heart function - Determination of central venous pressure and pulmonary capillary wedge pressure Angiography - Visualization of blood flow in the coronary arteries ← Coronary Angiography - - - Doppler studies - Assess blood flow in peripheral vessels - Records sounds of blood flow or obstruction Blood tests - Assess serum triglycerides, cholesterol levels, levels of sodium, potassium, calcium, other electrolytes Arterial blood gas determination - Check the current oxygen level and acid-base balance Coronary Artery Disease (CAD) or Ischemic Heart Disease (IHD) or Acute Coronary Syndrome Arteriosclerosis + Atherosclerosis Arteriosclerosis - General term for all types of arterial changes - Degenerative changes in small arteries and arterioles - Loss of elasticity - Lumen gradually narrows and may become obstructed - Cause of increased BP Atherosclerosis - Presence of atheromas in large arteries - Plaques consisting of lipids, calcium, and possible clots - Related to diet, exercise, and stress - Thrombus travels throughout the body and becomes an embolus. - Ex. Deep Vein Thrombosis causes - Pulmonary Emblem (Normal) (Atherosclerotic Aorta) Lipid Transport - - Lipids are transported in combination with proteins. Low-density lipoprotein (LDL) - Transport of cholesterol from liver to cells - Major factor contributing to atheroma formation High-density lipoprotein (HDL) - Transport of cholesterol away from the peripheral cells to liver – “good” lipoprotein - Catabolism in liver and excretion Lipoproteins Composition and Transport Risk Factors for Atherosclerosis Non-modifiable - Genetics - Age - Hormones (male vs female sex hormones) - Diabetes (cholesterol) Modifiable - Diet - Exercise - Smoking - Sleep (major cause of HF) - Cholesterol Intake - Weight loss Development of an Atheroma → Diagnostic tests - Serum lipid levels Treatment - Weight loss - Increase exercise - Lower total serum cholesterol and LDL levels by dietary modification - Reduce sodium intake - Control hypertension - Cessation of smoking - Anti-lipidemic drugs - Surgical intervention – i.e., coronary artery bypass graft Consequences of Atherosclerosis Coronary Artery Bypass Graft Angina Pectoris - Occurs when there is a deficit of oxygen to meet myocardial needs - Chest pain may occur in different patterns. - Classic or exertional angina - Variant angina - Vasospasm occurs at rest. - Unstable angina - Prolonged pain at rest – may precede myocardial infarction Angina – Imbalance of Oxygen Supply and Demand - Recurrent, intermittent brief episodes of substernal chest pain Triggered by physical or emotional stress Attacks vary in severity and duration but become more frequent and longer as disease progresses. Relieved by rest and administration of coronary vasodilators - e.g., Nitroglycerin - Primarily acts on reduction of systemic resistance, decreasing the demand for oxygen Emergency Treatment for Angina - Rest, stop activity Seat in an upright position Administration of nitroglycerin – sublingual Checking pulse and respiration Administration of oxygen if necessary Patient known to have angina - - Second dose of nitroglycerin (VASODILATOR) Patient without history of angina - Emergency medical aid Myocardial Infarction - Occurs when coronary artery is totally obstructed Atherosclerosis is most common cause. Thrombus from atheroma may obstruct artery. Vasospasm is cause in a small percentage. Size and location of the infarct determine the damage Warning Signs of a Heart Attack - Feeling of pressure, heaviness, or burning in chest – especially with increased activity - Sudden shortness of breath, weakness, fatigue - Nausea, indigestion - Anxiety and fear - Pain may occur and if present is usually - Substernal - Crushing - Radiating Diagnostic tests - ECG changes ***T WAVE WILL BE HIGH IN EKG*** → indicator of lack of O2 - Serum enzymes and isoenzymes (+ troponin in bloodstream = tissue damage) - Serum levels of myosin and cardiac troponin are elevated. - Leukocytosis, elevated CRP and ESR common - Arterial blood gas measurements may be altered in severe cases. - Pulmonary artery pressure measurements helpful Myocardial Infarction - Complications - Sudden death Cardiogenic shock Congestive heart failure Rupture of necrotic heart tissue/cardiac tamponade Thromboembolism causing CVA (with left ventricular MI) Myocardial Infarction - Treatment - Reduce cardiac demand Oxygen therapy Analgesics Anticoagulants (prevent blood clot from getting bigger) Thrombolytic agents may be used (takes a long time) Tissue plasminogen activator Medication to treat - Dysrhythmias, hypertension, congestive heart failure - Cardiac rehabilitation begins immediately. Cardiac Dysrhythmias (Arrhythmias) Deviations from normal cardiac rate or rhythm - Cause by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity - ECG – method of monitoring the conduction system - Detecting abnormalities Reduction of the efficiency of the heart’s pumping cycle - Many types of abnormal conduction patterns exist. Cardiac Arrest Cessation of all heart activity - No conduction of impulses - Flat ECG Many reasons - Excessive vagal nerve stimulation - Potassium imbalance - Cardiogenic shock - Drug toxicity - Insufficient oxygen - Respiratory arrest - Blow to heart Congestive Heart Failure (CHF) - Heart is unable to pump out sufficient blood to meet metabolic demands of the body. Usually a complication of another cardiopulmonary condition May involve a combination of factors Various compensation mechanisms maintain cardiac output. Some of these often aggravate the condition. When heart cannot maintain pumping capability - Cardiac output or stroke volume decreases - Less blood reaches the various organs - Decreased cell function - Fatigue and lethargy - Mild acidosis develops - Backup and congestion develop as coronary demands for oxygen and glucose are not met. - Output from ventricle is less than the inflow of blood. - Congestion in venous circulation draining into the affected side of the heart Effects of Congestive Heart Failure - Left-sided congestive heart failure - Right-sided congestive heart failure Signs and Symptoms - - - Forward effects (similar with failure on either side) - Decreased blood supply to tissues, general hypoxia - Fatigue and weakness - Dyspnea and shortness of breath Compensation mechanisms - Tachycardia - Cutaneous and visceral vasoconstriction - Daytime oliguria Backup effects of left-sided failure - Are related to pulmonary congestion - Dyspnea and orthopnea - Develops as fluid accumulates in the lungs - - - - Cough - Associated with fluid irritating the respiratory passages Paroxysmal nocturnal dyspnea - Indicates the presence of acute pulmonary edema - Usually develops during sleep - Excess fluid in lungs frequently leads to infections such as pneumonia Signs of right-sided failure and systemic backup - Dependent edema in feet, legs, or buttocks - Increased pressure in jugular veins > distention - Hepatomegaly and splenomegaly - Digestive disturbances Ascites - Complication when fluid accumulates in peritoneal cavity - Marked abdominal distention Acute right-sided failure - Flushed face, distended neck veins, headache, visual disturbances Valvular Defects - - Most commonly affect aortic and pulmonary valves May be classified as stenosis or valvular incompetence - Failure of valve to close completely - Blood regurgitates or leaks backward Mitral valve prolapse - Abnormally enlarged and floppy valve leaflets Surgical replacement - Mechanical or animal (porcine) tissue Rheumatic Fever and Rheumatic Heart Disease - - - - - - Acute systemic inflammatory condition - May result from an abnormal immune reaction - Few weeks after an untreated infection (usually group A beta-hemolytic Streptococcus) Involves heart as well as joints Usually occurs in children age 5 to 15 Long-term effects - Rheumatic heart disease - May be complicated by infective endocarditis and heart failure in older adults Acute stage – inflammation of the heart - Pericarditis - Myocarditis - Endocarditis and incompetent heart valves Other sites of inflammation - Large joints - Erythema marginatum - Non-tender subcutaneous nodules - Involuntary jerky movement of the face, arms, legs Signs and symptoms - Low-grade fever, leukocytosis, malaise, anorexia, fatigue, tachycardia Diagnostic tests - Heart function test - ECG - ASO titer Treatment - Prophylactic antibacterial agents - Anti-inflammatory agents Development of Rheumatic Fever and Rheumatic Heart Disease Infective Endocarditis → Common in people with artificial heart valves Subacute - Streptococcus viridans Acute - Staphylococcus aureus Basic effects - Same regardless of organism Factors that predispose infection - Presence of abnormal valves in heart - Bacteremia - Reduced host defenses Symptoms: - Low-grade fever or fatigue - Anorexia, splenomegaly, congestive heart failure in severe cases - Acute endocarditis - Sudden, marked onset – spiking fever, chills, drowsiness - Subacute endocarditis - Insidious onset – increasing fatigue, anorexia, cough, and dyspnea - Blood culture to identify causative agent - Antimicrobial drugs for several weeks, often IV Pericarditis → Often after open heart surgery → Fluid surrounding heart so v heart sounds - Usually secondary to another condition - Classified by cause or type of exudate - Acute pericarditis - May involve simple inflammation of the pericardium - May be secondary to - Open heart surgery, myocardial infarction, rheumatic fever, systemic lupus erythematosus, cancer, renal failure, trauma, viral infection - Effusion may develop. - Large volume of fluid accumulating in pericardial sac - Leads to distended neck veins, faint heart sounds, pulsus paradoxus - Potential for atelectasis (collapsed part of lung) - Chronic pericarditis - Results in formation of adhesions between the pericardial membranes - Fibrous tissue often results from tuberculosis or radiation to the mediastinum - Limiting movement of the heart during diastole and systole → reduced cardiac output - Inflammation or infection may develop from adjacent structures - Causes fatigue, weakness, abdominal discomfort - Due to systemic venous congestion Vascular Disorders Arterial Diseases – Hypertension High blood pressure - Common - May occur in any age group - More common in individuals of African ancestry Sometimes classified as systolic or diastolic Primary - Essential hypertension - Blood pressure consistently above 140/90 - May be adjusted for age - Increase in arteriolar vasoconstriction - Over long period of time – damage to arterial walls - Blood supply to involved area is reduced. - Ischemia and necrosis of tissues with loss of function Secondary hypertension - Results from renal or endocrine disease, pheochromocytoma (benign tumor of the adrenal medulla) - Underlying problem must be treated to reduce blood pressure. Malignant or resistant hypertension - Uncontrollable, severe, and rapidly progressive form with many complications - Diastolic pressure is extremely high. Development: - - Areas most frequently damaged by hypertension - Kidneys - Heart - Brain - Retina Predisposing factors - Incidence increases with age. - Men affected more frequently and more severely - Incidence in women increases after middle age. - Genetic factors - Sodium intake, excessive alcohol intake, obesity, smoking, prolonged or recurrent stress Effects: - - Frequently asymptomatic in early stages - Initial signs vague and non-specific - Fatigue, malaise, sometimes morning occipital headache Essential hypertension treated in steps - Lifestyle changes - Reduction of sodium intake - Weight reduction - Reduction of stress - Drugs - Diuretics, ACE inhibitors, drug combinations Peripheral Vascular Disease – Atherosclerosis - - Disease in arteries outside the heart Increased incidence with diabetes Most common sites - Abdominal aorta - Carotid arteries - Femoral and iliac arteries Diagnostic tests - Blood flow assessed by Doppler studies and arteriography - Plethysmography measures the size of limbs and blood volume in organs or tissues. Signs and symptoms - Increasing fatigue and weakness in the legs - Intermittent claudication (leg pain) - Associated with exercise due to muscle ischemia - Sensory impairment - Tingling, burning, numbness - Peripheral pulses distal to occlusion become weak. - Appearance of the skin of the feet and legs changes. - Marked pallor or cyanosis - Skin dry and hairless - Toenails thick and hard Treatment - Maintain control of blood glucose - Reduce body mass index - Reduce serum cholesterol - Platelet inhibitors or anticoagulant medication - Cessation of smoking - Increase activity and exercise - Maintain dependent position for legs – improves arterial perfusion - Peripheral vasodilators - Observe skin for breakdown and treat promptly - If gangrene develops, amputation is required. Aortic Aneurysm - Localized dilation and weakening of arterial wall Develops from a defect in the medial layer Different shapes - Saccular - Bulging wall on the side - Thrombus - Fusiform - Circumferential dilation along a section of artery - Dissecting aneurysms - Develops when there is a tear in the intima of the wall and blood continues to dissect or separate tissues Cause - Atherosclerosis - Trauma - Syphilis and other infections - Congenital defects Signs and symptoms - Bruit may be heard on auscultation. - Pulse may be felt by palpation of abdomen. - Frequently asymptomatic until they become large or rupture - Rupture may lead to moderate bleeding but most often causes severe hemorrhage and death. Diagnostic tests - Radiography - Ultrasound - CT scans - MRI Treatment - Maintain blood pressure at normal level - Prevent sudden elevations due to exertion - Prevent stress, coughing, constipation - Surgical repair Venous Disorders Varicose Veins → Irregular, dilated, and tortuous areas of the superficial veins - Familial tendency - Increased body mass index, parity and weight lifting are risks - In the legs - May develop from defect or weakness in vein walls or valves - Appear as irregular, purplish, bulging structures - Treatment - Keep legs elevated, support stockings - Restricted clothing and crossing legs should be avoided. Thrombophlebitis → Thrombus development in inflamed vein, e.g., IV site Phlebothrombosis → Thrombus forms spontaneously without prior inflammation; attached loosely Factors for thrombus development - Stasis of blood or sluggish blood flow - Endothelial injury - Increased blood coagulability Signs and symptoms - Often unnoticed - Aching, burning, tenderness in affected legs - Systemic signs: fever, malaise, leukocytosis Complication: pulmonary embolism Treatment - Preventive measures - Exercise, elevating legs - Anticoagulant therapy - Surgical intervention Shock - Hypovolemic shock (bleeding out) - Loss of circulating blood volume Cardiogenic shock (MI) - Inability of heart to maintain cardiac output to circulation Distributive, vasogenic, neurogenic, septic, anaphylactic shock (blood) - Changes in peripheral resistance leading to pooling of blood in the periphery Early Manifestations Anxiety Tachycardia Pallor Light-headedness Syncope Sweating Oliguria Compensation mechanisms - SNS and adrenal medulla stimulated to increase heart rate, force of contraction, systemic vasoconstriction - Renin secretion increases - Increased ADH secretion - Secretion of glucocorticoids - Acidosis stimulates increased respiration. - With prolonged shock cell metabolism is diminished, waste not removed – leading to lower pH Complications of shock - Acute renal failure - Shock lung, or adult respiratory distress syndrome - Hepatic failure - Paralytic ileus, stress or hemorrhagic ulcers - Infection or septicemia - Disseminated intravascular coagulation - Depression of cardiac function Manifestations Respiratory Disorders Obstructive Lung Diseases Aspiration - - Passage of food, fluid, emesis, other foreign material into trachea and lungs Common problem in young children or individuals laying down when eating/drinking Result may be - Obstruction - Aspirate is a solid object. - Inflammation and swelling - Aspirate is an irritating liquid. Predisposition to pneumonia Potential complications - Aspiration pneumonia - Inflammation – gas diffusion is impaired - Respiratory distress syndrome - May develop if inflammation is widespread - Pulmonary abscess - May develop if microbes are in aspirate - Systemic effects - When aspirated materials (solvents) are absorbed into blood Signs and symptoms - Coughing and choking with dyspnea - Loss of voice if total obstruction - Stridor and hoarseness - Characteristic of upper airway obstruction - Wheezing - Aspiration of liquids - Tachycardia and tachypnea - Nasal flaring, chest retractions, hypoxia - In individuals with severe respiratory distress - Cardiac or respiratory arrest Asthma → Bronchial obstruction - In persons with hypersensitive or hyperresponsive airways - May occur in childhood or have an adult onset - Often family history of allergic conditions Extrinsic asthma - Acute episodes triggered by type I hypersensitivity reactions Intrinsic asthma - Onset during adulthood - Hyperresponsive tissue in airway initiates attack. - Stimuli include - Respiratory infections; stress - Exposure to cold, inhalation of irritants - Exercise - Drugs - - Pathophysiologic changes of bronchi and bronchioles - Inflammation of the mucosa with edema - Bronchoconstriction - Due to contraction of smooth muscle - Increased secretion of thick mucus - In airways Changes create obstructed airways, partially or totally. Signs and Symptoms - Cough, marked dyspnea, tight feeling in chest - Wheezing - Rapid and labored breathing - Expulsion of thick or sticky mucus - Tachycardia - Might include pulsus paradoxus - Pulse differs on inspiration and expiration - Hypoxia Respiratory alkalosis - Initially due to hyperventilation Respiratory acidosis - Due to air trapping Severe respiratory distress - Hypoventilation leads to hypoxemia and respiratory acidosis Respiratory failure - Indicated by decreasing responsiveness, cyanosis Acute Episode Status asthmaticus - Persistent severe attack of asthma - Does not respond to usual therapy - Medical emergency! - May be fatal due to severe hypoxia and acidosis Treatment General measures - Skin tests for allergic reactions - Avoidance of triggering factors - Good ventilation of environment - Swimming and walking - Use of maintenance inhalers or drugs Measures for acute attacks - Controlled breathing techniques - Inhalers - Bronchodilators - Glucocorticoids (v inflammation) - Measures for status asthmaticus - Hospital care if no response to bronchodilator - Prophylaxis and treatment for chronic asthma - Leukotriene receptor antagonists - Block inflammatory responses in presence of stimulus - Not effective in treatment of acute attacks - Cromolyn sodium - Prophylactic medication - Inhalation of a daily basis Useful for athletes and sports enthusiasts No value during an acute attack Chronic Obstructive Pulmonary Disease (COPD) - Group of chronic respiratory disorders Causes irreversible and progressive damage to lungs Debilitating conditions that may affect individual’s ability to work May lead to the development of cor pulmonale Respiratory failure may occur. Chronic Obstructive Pulmonary Disease (COPD) – Emphysema → Destruction of alveolar walls and septae - Leads to large, permanently inflated alveolar air spaces - Classified by specific location of changes - Contributing factors - Genetic deficiency - Genetic tendency - Cigarette smoking - Pathogenic bacteria - - Breakdown of alveolar wall results in - Loss of surface area for gas exchange - Loss of pulmonary capillaries - Loss of elastic fibers - Altered ventilation-perfusion ratio - Decreased support for other structures Fibrosis - Narrowed airways - Weakened walls - Interference with passive expiratory airflow - Progressive difficulty with expiration - Air trapping and increased residual volume - Overinflation of the lungs - Fixation of ribs in an respiratory position, increased anterior-posterior diameter of thorax (barrel chest) - Flattened diaphragm (on radiographs) - Advanced emphysema and loss of tissue - Adjacent damaged alveoli coalesce forming large air spaces - Pneumothorax - When pleural membrane surrounding large blebs ruptures - Hypercapnia becomes marked - Hypoxia becomes driving force of respiration - Frequent infections - Pulmonary hypertension and cor pulmonale may develop in late stage. Signs and Symptoms - Dyspnea - Occurs first on exertion - Hyperventilation with prolonged expiratory phase - Development of “barrel chest” - Anorexia and fatigue (patient is so tired from breathing that they just lose their appetite) - Weight loss - Clubbed fingers - Diagnostic tests - Chest radiograph and pulmonary function tests Treatment - Avoidance of respiratory irritants - Immunization against influenza and pneumonia - Pulmonary rehabilitation - Appropriate breathing techniques - Adequate nutrition and hydration - Improves energy levels, resistance to infection - Bronchodilators, antibiotics, oxygen therapy as condition advances - Lung reduction surgery Chronic Bronchitis → Inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years - History of cigarette smoking or of living in urban or industrial areas - Mucosa inflamed and swollen - Hypertrophy and hyperplasia of mucous glands - Fibrosis and thickening of bronchial wall - Low oxygen levels - Severe dyspnea and fatigue - Pulmonary hypertension and cor pulmonale Signs and Symptoms - Constant productive cough - Tachypnea and shortness of breath - Frequent thick and purulent secretions - Cough and rhonchi more severe in the morning - Hypoxia, cyanosis, hypercapnia - Due to airway obstruction - Polycythemia, weight loss, and signs of cor pulmonale possible - As vascular damage and pulmonary hypertension progress Treatment - Cessation of smoking and reduction of exposure to irritants - Treatment of infection - Vaccination for prophylaxis - Expectorants - Bronchodilators - Appropriate chest therapy - Including postural drainage and percussion - Low-flow oxygen - Nutritional supplements Vascular Disorders Pulmonary Edema → Fluid collecting in alveoli and interstitial area - Can result from many primary conditions - Reduces amount of oxygen diffusing into blood - Interferes with lung expansion May develop when - Inflammation in lungs is present. - Increases permeability of capillaries - Plasma protein levels are low. - Decreases osmotic pressure of plasma - Pulmonary hypertension develops. Signs and Symptoms - Cough, orthopnea, rales – in mild cases - Hemoptysis - Frothy, blood-tinged sputum Treatment - Treat causative factors - Supportive care - Possibility of positive-pressure mechanical ventilation Vascular Disorders – Pulmonary Embolus → Blood clot or mass that obstructs pulmonary artery or a branch thereof - Effect of embolus depends on material, size, and location - Small pulmonary emboli might be “silent” unless they involve a large area of lung. - Large emboli may cause sudden death. - 90% of pulmonary emboli originate from deep vein thromboses in legs and are preventable. Signs and Symptoms - Transient chest pain, cough, dyspnea – small emboli - - - Larger emboli – increased chest pain with coughing or deep breathing; tachypnea and dyspnea develop suddenly - Later: hemoptysis and fever - Hypoxia: causes anxiety, restlessness, pallor, tachycardia Massive emboli - Severe crushing chest pain, low blood pressure, rapid weak pulse, loss of consciousness V Capillary refill Hemoptysis Prevention - Health teaching prior to surgery - Anti-embolic stockings - Exercise to prevent thrombosis - Use of anticoagulant drugs Diagnosis - Radiograph, lung scan, MRI, pulmonary angiography Treatment - Assessment of risk factors - Prolonged bed rest and compression stockings - Surgically inserted filter into vena cava (some cases) - Heparin or streptokinase - Potentially given clot busting med - Mechanical ventilation - Embolectomy - removal of clot Expansion Disorders Atelectasis → Nonaeration or partial or full collapse of a lung or part of a lung - Leads to decreased gas exchange and hypoxia - Alveoli become airless. - Collapse and inflammation or atrophy occurs. - Process interferes with blood flow through the lung. - Both ventilation and perfusion are altered. - Affects oxygen diffusion Mechanisms that can result in atelectasis - Obstructive or resorption atelectasis - Due to total obstruction of airway - Compression atelectasis - Mass/tumor exerts pressure on a part of the lung. - Increased surface tension in alveoli - Prevents expansion of lung - Fibrotic tissue in lungs or pleura (COPD patients have a lot of this) - May restrict expansion and lead to collapse - Postoperative atelectasis - Can occur after surgery Signs and symptoms - Small areas are asymptomatic. - Large areas - Dyspnea - Increased heat and respiratory rates - Chest pain Pleural Effusion → Presence of excessive fluid in the pleural cavity - Causes increased pressure in pleural cavity - Separation of pleural membranes - Exudative effusions - Response to inflammation - Transudate effusions - Watery effusions (hydrothorax) - Result of increased hydrostatic pressure or decreased osmotic pressure in blood vessels Signs and symptoms - Dyspnea - Cyclic chest pain - Increased respiratory and heart rates Treatment - Remove underlying cause to treat respiratory impairment. - Analyze fluid to confirm cause. - Chest drainage, thoracocentesis to remove fluid and relieve pressure Pneumothorax → Air in pleural cavity Closed pneumothorax - Air can enter pleural cavity from internal airways – no opening in chest wall - Simple or spontaneous pneumothorax - Tear on the surface of the lung - Secondary pneumothorax - Associated with underlying respiratory disease - Rupture of an emphysematous bleb on lung surface or erosion by a tumor or tubercular cavitation Open pneumothorax - Atmospheric air enters the pleural cavity through an opening in the chest wall. - “Sucking wound” - Large opening in chest wall (Ex. Stab/gunshot wound) - Tension pneumothorax - Most serious form - Result of an opening through chest wall and parietal pleura or from a tear in the lung tissue and visceral pleura - Air entry into pleural cavity on inspiration but hole closes on expiration, trapping air > increase pleural pressure and atelectasis Acute Respiratory Distress Syndrome → Ex. COVID-19 → Result from injury to the alveolar wall and capillary membrane - Resulting in the release of chemical mediators - Increases permeability of alveolar capillary membranes - Increased fluid and protein in interstitial area and alveoli - Damage to surfactant-producing cells - Diffuse necrosis and fibrosis if patient survives - Multitude of predisposing conditions - Often associated with multiple organ dysfunction or failure Signs and symptoms - Dyspnea - Restlessness - Rapid, shallow respiration - Increased heart rate - Combination of respiratory and metabolic acidosis Treatment - Treatment of underlying cause - Supportive respiratory therapy Acute Respiratory Failure → May result from acute or chronic disorders - Emphysema - Combination of chronic and acute disorders - Acute respiratory disorders - Many neuromuscular diseases - Signs may be masked or altered by primary problem. Treatment - Primary problem must be resolved. - Supportive treatment to maintain respiratory function Chapter 17: Digestive System Disorders Common Manifestations of Digestive System Disorders Anorexia, Nausea, Vomiting May be signs of digestive disorders or other conditions elsewhere in the body - Systemic infection - Uremia - Emotional responses - Motion sickness - Pressure in the brain - Overindulgence of food, drugs - Pain Anorexia and vomiting - Can cause serious complications - Dehydration, acidosis, malnutrition Anorexia - Often precedes nausea and vomiting Nausea - Unpleasant subjective feeling - Simulated by distention, irritation, inflammation of digestive tract - Also stimulated by smells, visual images, pain, and chemical toxins and/or drugs Vomiting (emesis) - Vomiting center located in the medulla - Coordinates activities involved in vomiting - Protects airway during vomiting - Forceful expulsion of chyme from stomach - Sometimes includes bile from intestine Vomiting Center Activation - Distention or irritation in digestive tract Stimuli from various parts of the brain - Response to unpleasant sights or smells, ischemia Pain or stress Vestibular apparatus of inner ear (motion) Increased intracranial pressure - Sudden projectile vomiting without previous nausea Stimulation of chemoreceptor trigger zone - By drugs, toxins, chemicals Vomiting Reflex Activities - Deep inspiration Closing glottis, raising the soft palate Ceasing respiration - Minimizes risk of aspiration of vomitus into lungs Relaxing the gastroesophageal sphincter Contracting the abdominal muscles - Forces gastric contents upward Reverse peristaltic waves - Promotes expulsion of stomach contents Characteristics of Vomitus - Presence of blood – hematemesis “Coffee grounds” – brown granular material indicates action of HCl on hemoglobin Hemorrhage – red blood may be in vomitus Yellow or green-stained vomitus - presence of bile Bile from the duodenum Deeper brown color May indicate content from lower intestine Recurrent vomiting of undigested food Problem with gastric emptying or infection Diarrhea - Excessive frequency of stools - Usually of loose or watery consistency May be acute or chronic Frequently with nausea and vomiting when infection or inflammation develops May be accompanied by cramping pain Prolonged diarrhea may lead to dehydration, electrolyte imbalance, acidosis, malnutrition Common Types of Diarrhea Large-volume diarrhea (secretory or osmotic) - Watery stool resulting from increased secretions into intestine from the plasma - Often related to infection - Limited reabsorption due to reversal of normal carriers for sodium and or glucose Small-volume diarrhea - Often due to inflammatory bowel disease - Stool may contain blood, mucus, pus - May be accompanied by abdominal cramps and tenesmus Steatorrhea – “fatty diarrhea” - Frequent bulky, greasy, loose stools - Foul odor - Characteristic of malabsorption syndromes - i.e., celiac disease or cystic fibrosis - Fat usually the first dietary component affected - Presence interferes with digestion of other nutrients. - Abdomen often distended Blood in Stool Blood may occur in normal stools, with diarrhea, constipation, tumors, or inflammatory conditions. - Frank blood - Red blood – usually from lesions in rectum or anal canal - Occult blood - Small hidden amounts, detectable with stool test - May be caused by small bleeding ulcers - Melena - Dark-colored, tarry stool - May result from significant bleeding in upper digestive tract Gas - From swallowed air, e.g., drinking from a straw Bacterial action on food Foods or alterations in motility Excessive gas causes - Eructation - Borborygmus - Abdominal distention and pain - Flatus Constipation - Less frequent bowel movements than normal Small hard stools Acute or chronic problem May be due to decreased peristalsis - Increased time for reabsorption of fluid Periods of constipation may alter with periods of diarrhea. Chronic constipation may cause hemorrhoids, anal fissures, or diverticulitis. Causes: - Weakness of smooth muscle due to age or illness - Inadequate dietary fiber - Inadequate fluid intake - Failure to respond to defecation reflex - Immobility - Neurologic disorders - Drugs (i.e., opiates) - Some antacids, iron medications - Obstructions caused by tumors or strictures Fluid and Electrolyte Imbalances - Dehydration and hypovolemia are common complications of digestive tract disorders. Electrolytes - Lost in vomiting and diarrhea Acid-base imbalances Metabolic alkalosis - Results from loss of hydrochloric acid with vomiting Metabolic acidosis - Severe vomiting causes a change to metabolic acidosis because of the loss of bicarbonate of duodenal secretions. Diarrhea causes loss of bicarbonate. Basic Diagnostic Tests - Radiographs - Contrast medium may be used - Ultrasound - May show unusual masses - Computed tomographic (CT) scans - Magnetic resonance imaging (MRI) - CT and MRI may use radioactive tracers. - Can be used for liver and pancreatic abnormalities - Fiberoptic endoscopy used in upper GI tract - Biopsy may be done during procedures. - Sigmoidoscopy and colonoscopy - Biopsy and removal of polyps may be done - Laboratory analysis of stool specimens - Check for infection, parasites and ova, bleeding, tumors, malabsorption - Blood tests - Liver function, pancreatic function, cancer markers ***You are looking for if there some type of narrowing in GI tract or blockage (like tumor) that is causing blockage.*** Disorders of the Liver and Pancreas Gallbladder Disorders Cholelithiasis - Formation of gallstones - Solid material (calculi) that form in bile Cholecystitis - Inflammation of gallbladder and cystic duct Cholangitis - Inflammation usually related to infection of bile ducts Choledocholithiasis - Obstruction of the biliary tract by gallstones Biliary Ducts and Pancreas with Possible Locations of Gallstones - - Gallstones vary in size and shape. Form in bile ducts, gallbladder, or cystic duct May consist of - Cholesterol or bile pigment - Mixed content with calcium salts Small stones - May be silent and excreted in bile Larger stones - Obstruct flow of bile in cystic or common bile ducts – causing severe pain, which is often referred to subscapular area Risk factors for gallstones - Women twice as likely to develop stones - High cholesterol in bile - High cholesterol intake - Obesity - Multiparity - Use of oral contraceptives or estrogen supplements - Hemolytic anemia - Alcoholic cirrhosis - Biliary tract infection - Obstruction of a duct by a large calculi - Sudden severe waves of pain - Radiating pain - Nausea and vomiting usually present → pain is so severe causes nausea - - Pain continues and jaundice develops. - Bile backs up into the liver and blood → light colored stool bc no bile - Risk of ruptured gallbladder if obstruction persists - Pain decreases if stone moves into duodenum Surgical intervention may be necessary. - May be removed using laparoscopic surgery - Low-fat diet necessary following surgery (as body adjusts to new normal) Why is the liver important? - Stores vitamins (K, C, D, B12, Iron) Breaks down toxins Helps with clotting Production of RBCs Converts bilirubin (made by broken down RBCs) to bile Breaks down fat Production of albumin (protein) ADH + Aldosterone stored in liver Production of glucagon (maintain normal blood glucose level) Synthesize ammonia (released into bloodstream through breakdown of food products) Some sex hormones Jaundice → Excess buildup of bilirubin in bloodstream Prehepatic jaundice - Result of excessive destruction of red blood cells (incorrect blood transfusion reaction) - Characteristic of hemolytic anemias or transfusion reactions - Unconjugated bilirubin elevated Intrahepatic jaundice - Occurs with disease or damage to hepatocytes - Hepatitis or cirrhosis - Both unconjugated and conjugated bilirubin may be elevated. Posthepatic jaundice - Caused by obstruction of bile flow into gallbladder or duodenum - Tumor, cholelithiasis - Increased conjugated bilirubin - Light-colored stool due to absence of bile Bilirubin Measurement in Jaundice - Direct or conjugated bilirubin can be measured in the blood Total bilirubin is measured in blood Total bilirubin minus direct bilirubin = indirect or unconjugated bilirubin Course of Hepatitis B Infection Viral Hepatitis - Only body defense is formation of antibodies via vaccination. Supportive measures - Rest, diet high in protein, carbohydrate, and vitamins Chronic hepatitis can be treated with interferon. - Decreases viral replication - Effective in only 30% to 40% of individuals - Drug combination (slow-acting interferon plus antiviral drug) more effective Toxic or Nonviral Hepatitis - Variety of hepatotoxins can cause inflammation and necrosis of the liver. - Drugs include: - - Acetaminophen, halothane, phenothiazines, tetracycline - Chemicals include: - Carbon tetrachloride (not used currently), toluene, ethanol Direct effect of toxins May result from sudden exposure to large amounts or from lower dose and long-term exposure Signs and Symptoms - - - Preicteric stage - onset - Fatigue and malaise - Anorexia and nausea - General muscle aching Icteric stage - first signs/symptoms - Onset of jaundice - Stools light in color, urine becomes darker - Liver tender and enlarged, mild aching pain Posticteric stage - recovery stage - Reductions in signs - Weakness persists for weeks Cirrhosis → Progressive destruction of the liver Causes - Alcoholic liver disease - Biliary cirrhosis - Associated with immune disorders - Postnecrotic cirrhosis - Linked with chronic hepatitis or long-term exposure to toxic materials - Metabolic - Usually caused by genetic metabolic storage disorders - Extensive diffuse fibrosis - Interferes with blood supply - Bile may back up. - Loss of lobular organization - Degenerative changes may be asymptomatic until disease is well advanced. - Liver biopsy and serologic test to determine cause and extent of damage Alcoholic Liver Damage - Initial stage – fatty liver - Enlargement of the liver - - - Asymptomatic and reversible with reduced alcohol intake Second stage – alcoholic hepatitis - Inflammation and cell necrosis - Fibrous tissue formation – irreversible change Third stage – end-stage cirrhosis - Fibrotic tissue replaces normal tissue - Little normal function remains → end of life Functional Losses with Cirrhosis - - - - Decreased removal and conjugation of bilirubin Decreased production of bile Impaired digestion and absorption of nutrients Decreased production of blood-clotting factors Impaired glucose/glycogen metabolism Impaired conversion of ammonia to urea Decreased inactivation of hormones and drugs - Drug dosages must be carefully monitored to avoid toxicity. Decreased removal of toxic substances Reduction of bile entering the intestine - Impairing digestion and absorption Backup of bile in the liver - Leading to obstructive jaundice Blockage of blood flow through the liver - Hepatic portal vein backs up - Leading to portal hypertension Congestion in the spleen - splenomegaly - Increasing hemolysis (coughing up blood) Inadequate storage of iron and vitamin B12 Congestion in intestinal walls and stomach - Impairing digestion and absorption Development of esophageal varices - Backup of blood on vasculature of portal vein + vasculature of esophagus. - Pressure on esophagus causes it to BURST → Hemorrhage - life threatening Development of ascites, an accumulation of fluid in the peritoneal cavity - Causing abdominal distention and pressure Development of Ascites w/ Cirrhosis Cirrhosis (cont.) - - Initial manifestations often mild and vague - Fatigue, anorexia, weight loss, anemia, diarrhea - Dull aching pain may be present in upper right abdominal quadrant Advanced cirrhosis - Ascites and peripheral edema - Increased bruising - Esophageal varices - May rupture, leading to hemorrhage, circulatory shock Jaundice, encephalopathy Effects: Treatment: - Avoidance of alcohol or specific cause - Supportive or symptomatic treatment - Dietary restrictions - Balancing serum electrolytes - Paracentesis - Antibiotics to reduce intestinal flora - Emergency treatment if esophageal varices rupture - Liver transplant (really the only thing that can help the person) Common Manifestations of Liver Disease Upper GI Tract Disorders Dysphagia → Difficulty swallowing (CN X - Vagus)
