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RESPIRATORY STUDY GUIDE NOTES
Lungs: Structure and Function Purpose: Transport Oxygen from lungs to the cells via Arterial system Transport Carbon Dioxide away from cells to lungs via venous system Two Anatomic Areas: Upper Respiratory System (Atmosphere to lungs) Mouth/nosesinusesOropharynxEpiglottisLarynxtrachea Lower Respiratory System Bronchi Bronchioles Alveolar Ducts Alveoli (location of gas diffusion / gas exchange) Alveolus: Arena of Gas Transport Single layer of squamous epithelial cells that promotes gas exchange – Capillary right next to alveoli (String wrapped around grape) Contain Macrophages which remove foreign material (alveoli should be sterile) Surfactant : coats inside layer of alveoli to dec surface tension -Keeps alveoli from collapsing d/t sphere surface tension – if collapses = no air movement = useless Law of LaPlace: Diameter of sphere related to desire to collapse–smaller diameter=inc desire to collapse Lungs: Cone-shaped structures positioned on both sides of heart Right Lung: Divided into 3 lobes to account for liver Lef t Lung: Divided into 2 lobes Each lung is covered in a pleural membrane with pleural fluid (lubricant) Visceral pleura ( inner , medial layer); attached to lung parenchyma on the inside Parietal pleura ( outer, lateral layer): attached to thoracic cavity / wall Pleural fluid “adheres” the two layers for chest / lung expansion – should move together Diaphragm muscle: Inferior border of thoracic cavity. Creates potential space Diaphragm drops larger lung space lower lung pressure Inhalation of air Thorax: Consists of Ribs, Thoracic Vertebra, and Sternum. Protects Lungs and Creates Space Intercostal Muscles: muscles between ribs that move the thoracic structures during ventilation (Inhalation) Elastic Recoil: Tendency for the lung alveoli to return to resting state Bounce-Back–Obstructive disorders dec this ability Allows for passive expiration of air. Ventilation Cycle: Inspiration & Exhalation Inhalation Diaphragm contracts/flattens “Drops floor”, creating bigger space
Bigger space creates negative air pressure – pressure drops □ Passive Air flow into lungs With “Forced” inhalation: (Distress) (“Accessory Muscles”) Muscles that assist with chest rise: Sternocleidomastoid, supraclavicular, Scalene, Pectoralis minor, Serratus Exhalation Elastic Recoil of lungs/alveoli Exhalation Diaphragm rises, expelling air from lungs With Forced exhalation: (“Accessory Muscles”) CHILDREN: Paradoxical breathing – belly out chest in, belly in chest out – heavy abdominal breathers Abdominal muscles : increase diaphragm rise Intercostal muscles : pull ribs & sternum down / in Use of Accessory muscles often: SIGN OF DISTRESS – Tripod sitting, nares flaring, leaning forward on hands Pulmonary Volumes: Spirometry Measures air moving in and out of lungs during respiratory cycle Measurements change in disease process; so, Objective measurement of Disease Process Tidal Volume: Total amount of volume you have – what we normally breath – healthy lungs = increased capacity Residual Volume : Volume of air remaining in lungs after maximum exhalation – GOOD THING: (Allows continued perfusion at alveoli even during exhalation) Vital Capacity : The maximal amount of air that can be moved in/out of lungs with breaths
- DEEPEST BREATH AND GET OUT AS MUCH AS YOU CAN **Can be altered by lung disease, size of thorax, amount of fluid in lungs As you increase residual volume, you decrease vital capacity b/c air must be stolen from somewhere =decreased reserve COPD: INCREASE RESIDUAL VOLUME & DECREASE VITAL CAPACITY d/t loss of alveolar compliance/snapback Dead space : passageways or areas where gas exchange cannot take place : Includes: Bronchi, Bronchioles, Collapsed Alveoli, Obstructions. Controls of Ventilation: Primary (Central) & Secondary (Peripheral) Control Center : An elaborate network of neurons in the Medulla, Pons, Carotid and Aortic Bodies: Dorsal and Ventral Respiratory Groups (DRG, VRG), Pneumotaxic Center, & Apneustic Center Brainstem : controls rhythm, rate, and depth. Acts by stimulating: Phrenic nerves of diaphragm Intercostal nerves of the external intercostal muscles Involved in forced expiration (if necessary. Expiration is usually passive) *Controls rate and depth but can be altered …. Meds, Emotion, Pain, Disease □ CNS depression (drugs)
Tests, Signs & Symptoms Tests Spirometry : Lung function test ABG : measures partial pressures of gases, pH, Bicarbonate Pulse oximetry : used to measure Oxygen saturation %, SpO2. (92-100%) Radiography : CXR, Chest CT Bronchoscopy : Direct visualization of bronchi; used to obtain specimens Culture and Sensitivity : Gram stain/C&S used for antibiotic treatment of LRI Medical Terminology of Pulmonary Signs & Symptoms: Sneezing Cough: protective reflex for lower respiratory tract - excessive is a big problem Sputum production Breath Sounds - Wheeze (“whistle”), Rales/crackles (hair twist), Rhonchi (wet leather) Dyspnea (especially Exertional Dyspnea = early signs) Cyanosis: Central(lips,buccal),Peripheral(fingers,toes,nailbeds)- Sev HYPOXIA/ANEMIA–dec Pa02(can be as low as 80-85) Pleural pain/Friction Rub - fluid Clubbed Fingers: sign of chronic hypoxemia (reduced arterial PaO2) ABG changes (Hypercapnia, Hypoxemia): Indicate tissue Hypoxia Breathing patterns and Thorax changes – normal A/P diameter = 2: Kussmaul: large tidal volumes, no pause Cheyne- Stokes: (Brainstem ischemia): deep and shallow w/ pause) – sign of neurological condition Barrel-chest (increase in AP diameter)-obstructive diseases-air builds up and pushes chest outward Infections: Sinusitis : Bacterial infection secondary to a cold or allergy that obstructs sinus drainage Must have sinusitis for 10 days before you call is a sinus infection Causative Agent: Streptococci, Staphylococci, Haemophilus influenzae Signs/Sx: Nasal congestion, Headache, may have low-grade fever, lots of drainage/sputum Laryngotracheobronchitis (Croup): Viral infection, usually affects children 1-2 years old Causative Agent: □ Parainfluenza Virus & Adeno Virus Signs/Sx: URI signs and symptoms (cough, fever, rhinitis), often worse at night. Obstruction of airway by inflammation and exudate Barking Cough (croup) and inspiratory stridor, especially with activity.
Treatment: Mostly Self-limiting: Oral steroids, humidified misting air can both be helpful. Bronchiolitis (RSV): Common infection in young children 2-12 months of age Causative Agent: Respiratory Syncytial Virus (RSV); Transmitted by oral droplets. Predisposing factors: Fall / Winter Months exacerbated by Secondhand cigarette smoke Pathology: Virus causes inflammation and necrosis in the small bronchi and bronchioles: Edema Increased secretionsBronchospasms leading to obstruction Signs and Sx: Wheezing, Dyspnea , crackles, Rapid shallow breathing, Cough, Rales, Chest Retractions, Fever Tx: Supportive and symptomatic while monitoring O2 levels & Respiratory effort. Ribavirin (Virazole) Nebulizers Epiglottitis : Acute infection often caused by Haemophilus influenzae B (HiB) and other pathogens Common in children aged 3-7 years old, especially if off Immunization schedule – vaccine is key prevention Infxn causes swelling of larynx & epiglottis Appears as round red ball on Lateral Neck X-ray. “Thumb Sign” Signs/Sx: Fever, Sore throat, difficulty swallowing and drooling, tripod or “ jaw-forward ” position. **MEDICAL EMERGENCY!! May require intubation Treatment: Oxygen, antibiotics, NO FOREIGN OBJECTS IN THROAT (tongue depressor)!! May spasm larynx Acute Bronchitis: Inflammation of the airways and bronchi, usually self-limiting Causative Agent: Usually viruses. If progress past 10-14 days, may develop bacterial infection Signs and Sx: Nonproductive cough easily triggered by environment changes, Wheezes. Influenza (Respiratory Influenza): Viral infection characterized by high fever (>102), cough – prevent with flu shot!!! Signs/Sx: Differs from common cold: Sudden high fever overnight, marked fatigue, body aches, body sores May cause bacterial or viral pneumonia, which is leading cause of death from flu in children and elderly. Treatment: Symptomatic. Fluids! ( PREVENT Dehydration !) Annual Flu vaccination Pneumonia: Acute infection of lungs – alveolus and parenchyma Classified by agent (viral, bacterial), location (lobar, RLL, LLL, etc.) Classified by CAP (Community Acquired), HCAP (Hospital Acquired) – more concerning d/t abx resistant Pneumococcal Pneumonia (“Lobar” Pneumonia) Causative agent: Streptococcus pneumoniae (“pneumococcus”) Infection usually localized in one or more lobe (“lobar”) Pathology: Inflammation/congestion of alveolar wall exudates interfere with O2 diffusion RBC’s, WBC’s accumulate in alveolar exudate, forming a solid mass (“consolidation”). Mass shows on Xray “lobar”. RBC’s in exudate create the rusty sputum often associated with Pneumococcal pneumonia. Signs and Sx: Sudden onset, systemic signs of sudden onset of high fever, chills, marked fatigue, leukocytosis Dyspnea,
Secondary (Active) Infection: Reinfection is “Active infection” (Symptomatic) Why? ANY drop in immune function allows reactivation (HIV, Immunosuppressive therapies, Cancer, Age) Organisms multiply and cause tissue destruction, leading to large areas of necrosis Cavitation occurs, forming large open areas in the lung and eroding through the bronchi and bronchioles-lungs collapse Hemoptysis (blood in sputum) is common as blood vessels are eroded Other parts of the lung may be invaded The sputum that has live bacilli can be swallowed and allow spread to the GI tract The bacilli may invade the walls of the pleural cavity, leading to pleuritis, adhesions, and pneumothorax Contagious!! TB Etiology: Occurs most often inPersons in close quartersWar conditionscommunal livingImmigrants or recent travelers Low Resistance = malnutrition, chronic disease, alcoholism – anything for autoimmune bust test for TB Why Advance to Active Infection? Drop in immune function most common Ex: AIDS, Age, Cancer, Immunomodulators Diagnostic Tests: Latent: TB skin Test (Mantoux), PPD (purified protein derivative TST) CXR shows Ghon complexes (latent) – done of skin test comes up positive Active: CXR [active disease (cavitation)] Sputum AFB Culture (takes up to 6 weeks for result). CT Scan Immunoassays: ELISA, Interferon-Gamma
Signs / Symptoms (Active) (Recall: Latent has no symptoms) Malaise / fatigue Weight Loss Purulent Hemoptysis bloody cough Night Sweats PM Low-Grade Fever Prolonged severe coughing that becomes productive Treatment: Latent/Primary: Treated for short 3-6 months. Then, monitored for first sign of symptoms ( S/Sx indicate Active ) Active:Long Term Medication treatment (up to 12 months) INH (Isoniazid); Rifampin and/or Ethambutol Compliance w/ regimen critical for eradication of organismFailure to follow through = “super-bug” □ MDR-TB: Multi-Drug Resistant TB, XDR-TB: Extremely Drug Resistant TB LUNG CANCER: 90% Cases related to Smoking; Second most common cause of Cancer in the United States Mortality rate quite high (5 year survival rate around 17%); Readily metastasizes prior to diagnosis: Brain, Bone, Liver Tumors in the lung arise from Bronchial Cells Termed “Bronchogenic Carcinomas” Lead to: Airway obstruction Inflammation & pooling of secretions Tumors on the periphery can cause pleural inflammation and erosion (effusions) – fluid builds up Paraneoplastic syndromes ( SIADH, Cushing’s, Polycythemia, Clotting coagulopathies ) Etiology: Cigarette smoking major risk factor (Often occurring in those with COPD)-many Sx same as COPD=unnoticed Occupational / Environmental exposure (Radon gas or other workplace toxins) Direct exposure to irritants can cause chronic inflammation & frequent infections Cellular changes from chronic inflammation alter respiratory mucosa Metaplasia, which can lead to dysplasia – ciliated epithelial to flat squamous - cancerous Major Classes of Lung Cancer: NSCLC and Neuroendocrine tumors NSCLC: Non-Small Cell Carcinoma: Comprise about 80% of all lung cancers Further divided into Squamous Cell, Adenocarcinoma, and Large cell Significant Genotyping for personalized therapy: EGFR, ALK **Neuroendocrine: Includes *** Small Cell carcinoma and Large neuroendocrine carcinoma SCC (“Oat Cell Carcinoma”), is very aggressive (Often presents at Stage IV TNM) Signs & Symptoms: Q: Why the delay in diagnosis of smokers? A: Smokers Cough. Signs often masked by chronic
Causative Agent : Inherited disorder: Autosomal Recessive (requires homozygous recessive genotype) Pathophysiology: A chloride ion cell transport related gene defect, causing high NaCl sweat excretion Defect is in the Exocrine glands (SECRETES FLUID) , causing abnormally thick secretions Primarily affects the lungs and pancreas , characterized by obstructions Lungs : Airway obstruction from thick secretions causes: Air Obstructed from leaving during Exhalation Air- trapping, atelectasis, bronchiole damage , obstructive disease of hyperinflation Stagnant mucus is a medium for infection (frequent pneumonia) Eventually respiratory failure: Cor Pulmonale (elevated Pulm Artery pressures) develops-INC AFTERLOAD: RVCHF GI Tract: First sign of CF often meconium ileus in newborn (thick secretions causes no first stool) Pancreas: Deficit of pancreatic enzymes due to blocked exocrine glands Malnutrition and malabsorption of proteins – PANCREAS=AMYLASE/LIPASE Liver / Gallbladder: Bile ducts are blocked with thick secretions, interfering with fat absorption Malnutrition, dehydration, and Fat-soluble vitamin deficiency (K, A, D, E) Back up pressure behind the obstruction leads to inflamed tissue / damage Salivary Glands: high chloride and mucus plugs may cause obstruction / infection (sialadenitis-SORES IN MOUTH) Sweat Glands: Secretion of high NaCl levels which leads to dehydration with exercise Rationale behind NaCl sweat analysis skin test Reproductive: □ Thick mucus block vas deferens and cervix, often leading to infertility Diagnosis: Sweat Analysis (high Na+) Stool analysis (liver / pancreas) high fat (low bile salts) high trypsin CXR; Spirometry, ABG’s CF Treatment and Prognosis: Pancreatic Enzyme replacement (Pancrease) Bile salt replacement (Gallbladder) Avoid dehydration: Balanced diet Chest Physiotherapy □ Bronchodilators and Humidifiers – MUCUS THINNERS – HELPS PREVENT REMODELING Prognosis: DEPENDS ON HOW PENETRATING THE PHENOTYPE OF THE DISEASE IS Good treatment prolongs life into early adulthood – EARLY AND QUALITY OF TX Respiratory Failure is typical cause of death
ASTHMA:
Definition: Chronic lung disorder characterized by periodic episodes of severe, reversible bronchial obstruction in persons with hypersensitive airways (TYPE 1 HS RXN). Cardinal Sign: Decreased FEV1 measurement (NORMAL 85-95%) Prevalence: Highest in children Ages 5-17 years of age Pathophysiology: Inflammation of mucosa with edema and increased mucus production Bronchial Hyper-responsiveness: “Twitchy” □ Contraction of smooth muscle (bronchospasm / wheeze or cough (COUGH IN KIDS: WHEEZE NOT DEVELOPPED YET)) Results in partially obstructed airway, interfering with airflow and oxygen supply Total obstruction of bronchus results in mucus plug Causes non-aeration (atelectasis) distal to obstruction Pathophysiology: Involves many factors to induce inflammatory response IgE, Eosinophils, Th2 helper cells, Plasma B-Cells Major Pathway: IgE mediated Mast Cell degranulation Type I Hypersensitivity, Allergic Reaction Chronic inflammation leads to bronchial Remodeling (fibrosis) Thickening of bronchial wall, More airway obstruction - PERMANENT Impaired Exhalation, Air Trapping (“Obstructive”) Etiology: USUALLY W/IN 1 ST^ 2-4 YEARS – STRESS RESPONSE INCREASE 02 DEMAND Family history of: Eczema Seasonal Allergies Asthma ( “Atopic March”) Strong genetic component: Over 100 genes identified in asthma epigenetics Viral URI’s: Documented correlation with RSV infection and increased asthma development Contributing Factors: Sedentary lifestyle, high airborne allergen content, air pollution Manifestations: Recall Defn: Decreased Peak Flow and Spirometry FEV1 Measurements Hypoxia: Occurs with both partial and total obstruction of airway Increased need for Oxygen due to stress response furthers hypoxia deficit Early tachypnea causes respiratory alkalosis; Later, Respiratory acidosis Hypoxemia: Low Blood O2 induces vasoconstriction of pulmonary vessels (shunt away) Protective-to make 02 perfusion more efficient-sends blood to better area-problem is all areas bad Reduces blood flow throughout pulmonary circuit (lungs) Increased pulmonary pressures result in increased Rv afterload ( cor pulmonale ) Status Asthmaticus: A Persistent, severe attack that does not respond to bronchodilator therapy
Examples : Emphysema Chronic Bronchitis Chronic Asthma COPD is: *Partially irreversible; *Progressive; *Eventually leads to respiratory failure d/t: Hypoxia, hypercapnia, Cor Pulmonale COPD: EMPHYSEMA Pathophysiology: Destruction of alveolar walls and septae Leads to large, permanently inflated alveolar airsacs ( blebs/bullae increase deadspace) Classified by location: (Panacinar=distal alveoli; centrilobular=bronchiolar alveoli) Etiology / Contributing factors: Cigarette Smoking (decreases effect of alpha-antitrypsin alpha-1 antitrypsin deficiency (genetic) (Alpha-1 antitrypsin repairs damage) Changes on Lung Tissue : Alveolar breakdown loss of surface area (decreased gas exchange) – grapes to cauliflower Loss of pulmonary capillaries (decreased perfusion/diffusion) Loss of elastic fibers (decreased alveolar recoil / “snapback”) - increased I:E ratio Altered ventilation ratio (affects both perfusion and ventilation) Decreased support for other lung tissue (weakens the wall): Risk: Pneumothorax – hole in lung Changes to Lung Structure : Fibrosis & thickening of bronchial wallsnarrowed airwaysweakened wallsInterfer w/ passive exhalation Progressive difficulty with passive expiration Air trapping, increased Residual volume which means decreased vital capacity Over-inflation of lungs, Increased AP diameter (“ barrel-chest” ) Diaphragm appears flattened on CXR b/c so much air it looks like always inhaling Increased Expiratory phase, Increased I:E Ratio ( normal I:E Ratio = 2:1 ) longer to blow out air due to obstruction to outward airflow Effects on Lung Function : Larger air spaces called bullae or blebs (less perfusion of capillaries) Tissue and pleural membrane may rupture at bleb (pneumothorax) Chronic Hypercapnia Loss of CO2 central respiratory drive (“burn out” of Central, Primary receptors) □ Peripheral respiratory receptors becomes primary respiratory drive (O2) □ Don’t OverOxygenate!! Infections Increased Perfusion resistance increases Pulmonary Artery Pressure (PAP ) Hypoxemic vasoconstrictionCor
Pulmonale ( RV heart failure ) – constricts to shun blood to healthy tissue Signs and Symptoms : (Gradual onset: Asymptomatic until lung function reduced by 50%) “Pink Puffer” Dyspnea initially with exertion and eventually at rest Hyperventilation with prolonged expiratory phase ( inc I:E ) Use of Accessory Muscles Barrel chest (large AP diameter) ”Tripod” with sitting; pursed lip breathing (Inc I:E) – b/c air out is steady – helps them breath Hyper-resonant chest on auscultation (High Residual Volume ) Secondary polycythemia: Hypoxia = Increased Erythropoietin Anorexia, Fatigue, Weight loss – often arm weight loss d/t hypermetabolism from inc need to breath faster Clubbed fingers (chronic hypoxia) Flushed face (Late: Signs of Rv failure) Diagnostics : CXR (barrel chest) Increased Residual Volume Dec Vital Capacity COPD: CHRONIC BRONCHITIS: Pathophysiology: Significant remodeling in bronchi resulting from constant irritation Etiology: *Cigarette Smoking Air pollutants Bronchial Changes: Mucosal inflammation and swelling Hypertrophy and hyperplasia of mucosal goblet cells (make secretions), increasing secretions (LOTS of sputum) Fibrosis & thickening of bronchial walls facilitates obstruction (collagen, musc. hypertrophy–restricts mucus out of lungs Loss of ciliary function , as a result of bronchial epithelial changes Signs & Symptoms: “Blue Bloater” Constant, productive cough for 2 MONTHS OR MORE!! Thick secretions Cough and rhonchi more in AM Hypoxia and cyanosis with obstructions Secondary Polycythemia Weight loss, anorexia Dyspnea Pulmonary Hypertension Signs of Cor Pulmonale JVD, peripheral edema
Absorption: Hypoventilation from obstruction – not moving = not tidal Surfactant Impairment / Higher Surface Tension ARDS Pulm Edema Post-Operative Atelectasis: Purpose for Incentive Spirometry – goal set before Sx 24-72 hours post op Pain or abdominal surgery (decreased deep ventilation to avoid pain) Slow, shallow respirations Decreased cough effort (Pain Medications or Sedation , anesthesia) Increased secretions (supine position— bedrest ). Risk Aspiration Signs & Symptoms: Dyspnea Absent Breath Sounds Tachycardia Abnormal or asymmetrical chest expansion Tachypnea Compression Atelectasis: Mediastinum may shift toward unaffected side Pleural Effusion: Excessive Fluid in the pleural cavity (space) Pleurisy or Pleuritis may precede fluid accumulation Effects depend on type and mechanism of accumulation Dependent upon amount, type, and rate at which fluid accumulates Etiology: Different types of fluid may accumulate in the pleural space…. Exudate high level of WBC’s from inflammation, Infection (ex. Tumor) □ Empyema: If pus present from infection Transudative watery effusion, from increased hydrostatic pressure or low osmotic pressure (low protein) High blood pressure HypoAlbuminuria (liver disease) Hemothorax Blood resulting from trauma, cancer, or surgery Signs & Symptoms: 1 st^ Sign is tachycardia, then Dyspnea, Tachypnea Pleural Chest Pain, Dullness to percussion, Compression Atelectasis, Absence of breath sounds, mediastinal shift to side Tension from Fluid leads to :Tracheal deviation, Hypotension, Cardiogenic shock from ventricle pressure = dec SV =dec CO Treatment: Chest tubes to drain fluid; Thoracentesis to drain fluid; Treat underlying cause Pneumothorax: Air in the pleural cavity b/n viscera and parietal pleura: d/ t a rupture in visceral (lung) or parietal (chest wall) pleura Air prevents lung expansion, leading to atelectasis Two Major Types:
Primary (Spontaneous) Often 20-40 y/o Men. Often Smokers (Emphysematous blebs - pops) Secondary: Caused by Chest Trauma, High ventilation pressures (PEEP) - bleb pops – air in pleural space Pressure constantly put on lungs Can be Open or Closed: Open (Communicating) : Lung pressure equals barometric pressure Air communicates back with inspiration / expiration) NO TENSION Tension: “Sucking chest wound” - Knife or gun shot wound Air that enters pleural space on inspiration does NOT leave on Exhalation Increased pleural pressure with each inspiration ( TENSION ) Signs and Symptoms : All Types: □ SOB, Anxiety Chest Pain Decreased Breath Sounds Tension: Tachycardia, Decreased CO (Hypotension) Tracheal Deviation (To contralateral side of Pneumothorax) Pressure on ventricle Cardiogenic shock Flail Chest: Fractures of the thorax, 3-6 ribs, in two places ribs fractured in 2 places. “Free-Floating Ribs” – move in opposite direction of rest of lungs Etiology: Chest Trauma Signs & Symptoms: Dyspnea, Tachycardia Paradoxical Movement of “Free” Ribs – move opposite the rest of costals High Risk of Pneumothorax! Tracheal Deviation to Affected Side (Ipsilateral) – opposite of pneumothorax and atelectasis Ventilation / Perfusion Mismatches: V/Q Shunts Defn: The Ratio of Alveolar Ventilation (V) to the Alveolar Blood Supply (Q): Mismatch : Any pulmonary condition that leads to deoxygenated blood passing through pulmonary artery circuit
Eventual atelectasis from decreased surfactant and alveolar collapse ( LaPlace Law ) Capillary engorgement and rupture can produce pink frothy sputum Etiology : ANY Inflammation in the lung (increased capillary pressure and membrane permeability) ARDS Low plasma proteins from Liver disease (low vascular serum osmotic pressure causes edema) Pulmonary Hypertension (increased hydrostatic pressure causes edema) Lv heart failure (backup pressure/increased hydrostatic pressure causes edema) Etiologies include: Lv HF – HIGH BACK PRESSURE – MOST COMMON ETIOLOGY Hypoproteinemia due to renal ( protein loss ) or liver disease (decreased albumin)
- Decreased osmotic pressure in vascular system Inflammation in the lungs Inhalation of toxins Cancer ARDS Signs & Symptoms: cough, orthopnea (SOB lying down), Rales, Hemoptysis (if really bad); often pink frothy sputum (bubbly), Labored breathing, Feeling of drowning (Paroxysmal Nocturnal Dyspnea)—”Air Hunger at Night” Cyanosis (V/Q Mismatch) Treatment: Oxygen Elevate HOB Diuretics (furosemide; lasix) to pull off excess fluid Positive Airway Pressure (CPAP, BiPAP) (Pushes alveoli open, Oxygen goes deep)- continuous or 2 pressures Pulmonary Embolus A blood clot or other occlusion that obstructs the pulmonary artery or branch of it Leading cause of preventable death in hospital Death usually occurs within the first hour of symptom onset Most originate from blood clots in legs or pelvic region (DVT). Other Causes: Fat embolus (longbone Fx), Air or Amniotic Fluid embolus Vegetation from endocarditis breaking free Etiology: Contributive Factors: Recall Triad of Virchow Immobility Leg trauma Surgery / childbirth DehydrationCancer Atrial Fibrillation Cancer CHF Pulmonary Embolus occurs in various forms: Embolus without Infarction (circulation still gets through lung)
Embolus WITH infarction (results in infarction, V/Q Mismatch) Multiple Emboli that shatter Pathophysiology: Ischemia of distal tissue results in V/Q mismatch, Hypoxemia Can lead to lung infarction Size of the clot determines the signs, symptoms, and damage Signs & Symptoms: BOLDED ARE MOST COMMON Tachycardia Chest Pain SOB Anxiety Hypotension / Low CO Shock ARDS: Adult Respiratory Distress Syndrome Pathophysiology: Inflammatory response Increased capillary permeability leads to: Pulmonary edema Decreased Oxygen diffusion (V/Q Mismatch) Hypoxemia / Hypoxia / Acidosis Usually occurs 1-2 hours after assault Etiology: Severe shock or Sepsis Inhaled toxins – OR HOT AIR Aspiration pneumonia (gastric secretions) – KEY IS PREVENTION Oxygen Toxicity SARS / MERS Lung Trauma / Pulmonary Emboli DIC Signs & Symptoms: Dyspnea with Tachypnea, (Initially Resp Alkalosis) – BLOWING OFF CO2 Restlessness and Anxiety (SNS from Hypoxia) Accessory muscle use ( Decreased Compliance) – STIFF LUNGS – DEC VENTILATION PRESSURES Crackles / Rales ( Pulmonary Edema/Infiltration) Productive cough with Frothy sputum Late: Cyanosis (V/Q mismatch) Confusion and Lethargy ( Acidosis) Combined Respiratory & Metabolic Acidosis & shock Respiratory Failure: “50/50 Club” – SEE BELOW ARDS Mortality Rate: 40% ARF: Acute Respiratory Failure Definition: ( the“50-50 Club”) PaO2 < or = 50-60 (Severe Hypoxemia) Normal: 85- PaCO2 > or = 50 (Severe Hypercapnia) Normal: 35-
