Edema, Cardiogenic and Non-Cardiogenic: Fluid in the Lungs - Module 4

**[Edema: cardiogenic and non-cardiogenic: fluid in the lungs ]** - [Cardiogenic:] high pulmonary capillary hydrostatic pressure secondary to high pulmonary venous pressure - Accumulation of fluid in the interstitium and alveoli - Heart failure, fluid overload - [Non-cardioge...

**[Edema: cardiogenic and non-cardiogenic: fluid in the lungs ]** - [Cardiogenic:] high pulmonary capillary hydrostatic pressure secondary to high pulmonary venous pressure - Accumulation of fluid in the interstitium and alveoli - Heart failure, fluid overload - [Non-cardiogenic]: increase in filtration due to increase in capillary permeability. - Injury, inflammation, obstruction, high altitude, cancer, toxins, neurogenic trauma, lung re-expansion - Protein leaves capillaries, increasing interstitial oncotic pressure and bringing water or direct hemorrhage. - Interstitium and alveoli fill with fluid - [Lymph blockage:] prevents reabsorption of net filtration - [S/S of pulmonary edema]: Dyspnea on exertion, orthopnea, wheezing, anxiety, wet cough, chest pain, fatigue, frothy sputum, sweating, feeling clammy - Hallmark symptom: the **feeling of suffocating, drowning** Fluid movement Hemoglobin dissociation - **[Flail chest]** - It occurs when a segment of the rib cage breaks from the chest wall. Three or more ribs broken in 2 or more places - It can be caused by trauma to the chest - Life-threatening emergency - s/s: paradoxical breathing, pain, bruising, dyspnea - the fractured section of the chest wall doesn't resist the lung's tendency to pull inward - During inspiration, the broken section of the lungs collapses. During expiration, the vacuum created by the collapsed portion of the lung causes air to be pulled to itself, and that part of the chest flails - **[Pneumothorax]** - It is a collapsed lung caused by a vacuum created by the pleura is disrupted, and air enters the pleural space. - Outside air enters due to disruption of the chest wall and parietal pleura, and this lung air enters due to disruption of the visceral pleura. - Traumatic pneumothorax - [Spontaneous pneumothorax] - Primary: risk factors include young, thin male smokers, abrupt changes in atmospheric pressure - Secondary: due to disease of the lung tissue - Diseases such as COPD, cancer, asthma, cystic fibrosis, interstitial and inflammatory lung disease - [Tension ] - Trapped air can't escape = building pressure of air thoracic cavity, which compresses the lungs and reduces blood flow to the heart. - Life-threatening condition - Creates mediastinal shift: heart, blood vessels, and trachea shift towards the undamaged side due to increased pressure on the pneumothorax side - Hallmark symptom: heart and blood bc and trachea shift towards the undamaged side due to increased pressure on the pneumothorax side - s/s: dyspnea, chest aches, chest tightness, cyanosis, tachycardia, absent breath sounds on the side with collapse, jvd - risk factors: trauma, medical procedures like central line, gunshot or stabbing - **[Atelectasis:]** - collapse of lung tissue. Reduced alveolar ventilation or air inside a plugged alveolus gets absorbed and causes the alveolus to collapse. - Risk factors: confinement to bed, infections, disease, foreign body - It can lead to hypoxia, pneumonia, respiratory failure - s/s: dyspnea, tachycardia, cough, pain, cyanosis, wheezing - **[pleural effusion]** - **[hallmark symptom: pain on inspiration]** - excess fluid pleural space - risk factors: infection, trauma - s/s: dyspnea, cough, pain, inspiration, fever, difficulty taking deep breaths - thoracentesis helps diagnose - types: transudative and exudative - [Transudative]: clear, low protein, no cells, non-inflammatory, salt and fluid retention increase in venous pressure- RAAS activation - Caused by congestive heart failure, cirrhosis, nephrotic syndrome, peritoneal dialysis - [Exudative:] cloudy, thick high protein cells present, inflammatory, blood, bacteria, WBC may be present - [Empyema]: a collection of pus in pleuritic space d/t infection - Caused by infections, malignancy connective tissue disease, inflammatory disease, movement of fluid from the abdomen to pleural space, coronary artery bypass surgery, pulmonary embolism - **[Pulmonary Embolism]**: - [Thrombus:] blood clot forming that is attached to the original vein where it is growing - [Embolism:] a freed blood clot that lodges in the pulmonary vasculature - Travels from the inferior vena cava to the right side of the heart, from the right atrium to the right ventricle, and then to the pulmonary artery. The emboli can get lodged at any point and cause venous destruction - Risk factors: hypercoagulable state, vascular wall injury, circulatory stasis - **[Pneumonia: infection of the lungs in alveoli]** - Gas exchange is impaired - Viral, bacterial, fungal - Causes purulent fluid buildup in alveoli - Risk factors: older than 65, existing lung disease, smoking, unvaccinated; can be hospital-acquired or community-acquired - s/s: cyanosis, fever, sweating, chills, fatigue, tachypnea, dyspnea, tachycardia, chest pain - hallmark symptom: productive cough - can occur as: - lobar: one or more whole sections of lungs - bronchial: patches throughout both lungs - **[Tuberculosis]** - Transmitted via droplet, caused by mycobacterium tuberculosis bacteria - Tubercle formation: granulomatous inflammation filled with caseous necrosis-isolate bacteria and causes cavities within lung tissue - Resistant to most anti-bacterial medications and required multiple different types of medication and long-course treatment - Risks: recent exposure, living in high-rate areas, immune deficiency, housing insecurity, IV drug use, post-organ transplant, health care workers, diseases that lower immune function - s/s: progressive fatigue, malaise, anorexia, wt. loss, chronic cough, **night sweats**, **\`**, pleuritic chest pain - **[Acute Respiratory Distress]** - Acute inflammation caused by trauma or infection; disruption of the alveoli epithelial lining and the capillary endothelial lining and causing leaking of the fluid - Cells lose membrane integrity - Refractory hypoxemia: v/q mismatch - [Phases] - **Exudative**- within 72 hours, alveolocapillary membrane damage increased capillary membrane permeability, pulmonary edema, surfactant inactivated - **Proliferative**: 4-21 days, resolution of the pulmonary edema and proliferation of type II pneumocytes fibroblasts and myofibroblasts, hyaline membranes, and hypoxemia - **Fibrotic**- 14-21 days remodeling and fibrosis alveolar destruction severe right to left shunting acute respiratory failure - **[Asthma:]** chronic inflammatory airway disease of bronchi mucosa characterized by recurrent episodes of wheezing and or breathlessness - Triggers: indoor allergens, secondhand smoke, dust mites, animals, cockroach, cold weather, stress, stress - Risk factors: family history, low birth weight, respiratory complications in infancy, smoking, obesity, allergies, occupation - Pathophysiology: allergen exposure causes immune activation (IL-4 IL-5 IgE production causes mast cell degranulation, causing vasodilation and increased capillary permeability causing bronchospasm, congestion, thickening of airway walls, impaired mucociliary function, mucus secretion, which causes epithelial desquamation and fibrosis and then bronchial hyperresponsiveness and airway obstruction - s/s: wheezing, dyspnea, anxiety, coughing, chest tightness, decreased FEV1 that can be reversed with bronchodilators - **[chronic Obstructive Pulmonary Disorder]** - umbrella for progressive lung disease -- emphysema and chronic bronchitis - risk factors: smoking, breathing in toxins, exposure to smoke, infection, air pollution, genetic abnormalities, asthma, severe childhood respiratory infection in childhood - [emphysema] - the alveoli are damaged and enlarged, which causes loss of lung elasticity, resulting in loss of lung tissue recoil and air - s/s: hyperinflation of the lungs and barrel chest, increased CO2 in lungs, purse lip breathing, dyspnea, barrel chest, use of accessory muscles to breathe - [chronic bronchitis: ] - chronic productive cough and sputum production for over 3 years with mucus secretion and airway obstruction - s/s- cyanosis from hypoxia, airway flow problem, increased sputum, increased respiratory rate, digital clubbing, increase in hgb - **[pulmonary artery hypertension]** - increased pulmonary vasoconstrictors and decreased pulmonary vasodilators, resulting in an increased pulmonary artery pressure - get worse with: hypoxemia, respiratory and metabolic acidosis [Module 5] - **Anatomy and physiology** - Blood gas relations - Immunity - Edema - Fluid movement - Hemoglobin dissociation - **No fetal heart anatomy circulation** - **Pediatric heart abnormalities** - **How blood flow through the heart** - Where it goes - What if it does not happen - **Cardiac terminology** - Cardiac output - Afterload - Preload - Contractility - Stroke volume - Ejection fraction - The formula for cardiac output - **Presented conditions** - General definition - Risks/causes - Underlying pathos - s/s **[module 6]** - **Anatomy and physiology** - Blood gas relations - Immunity - Edema - Fluid movement - Hemoglobin dissociation - **How urine is concentrated/diluted, focusing specifically on where ADH acts in the nephron and the loop of Henle** - **Kidney contribution to the regulation of blood pressure and acid-base balance** - **Labs for renal system** - **Presented conditions** - General definition - Risks/causes - Underlying pathos - s/s