M2 Pulmonary Week 1 - Key Facts Flashcards
3 Major Medullary Controls of Inspiration
Dorsal Resp. Group (DRG) - Inspiration
Ventral Resp. Group (VRG) - Inspiration + Expiration
Pre-Botzinger Complex - Rhythm
Muscles of Inspiration (3) + Expiration (2)
Inspiration - Diaphragm + SCM + External Intercostals
Expiration (Normally Passive) - Internal Intercostals + Rectus Abdominis
Major Respiratory Chemoreceptors (3) - Location + Detection
Carotid Chemoreceptors - CN IX
Aortic Body Chemoreceptors - CN X
Central Chemoreceptors - Medulla
Central only respond to CO2/pH
Peripheral - CO2 still biggest player
Small + Large Vessel Response to Inspiration
Small - Alveoli open - compresses the vessels resulting in “holding” of blood to allow better gas exchange
Large - Inspiration causes dilation and an overall increase in total flow to/from the lungs
Receptors for Bronchodilation and Constriction
Dilation - B2
Constriction - M3
Physiologic Hypoxic Vasoconstriction - Key Pathway
Alveolar hypoxia –> Impedes K+ smooth muscle K+ channels resulting in more intracellular Ca2+ and vasoconstriction - Reduces flow to under-ventilated regions
Perfusion Limitation vs. Diffusion Limitation
Perfusion Limitation = Flow to the lungs all blood leaves fully oxygenated (in capillaries for 75ms but only needs 25ms)
Diffusion Limitation = Blood is not oxygenated due to increased time for diffusion (takes 60ms instead of 25ms) - Increased flow rate with exercise = hypoxemia + dyspnea
Diffusion Limitation Causes - Fibrosis = Inflammation + Mucus + Edema
Oxyhemoglobin Dissociation Curve - Causes of Right Shift (6) + Left Shift (6)
Right Shift - BAT Ace - BPG (2,3) + Altitude (High) + Temp (High) + Acidosis (Low pH) + CO2 (High) + Exercise
Left Shift - Main = Fetal Hb
Also - Low BPG, Temp, and CO2 (High pH)
Compliance vs. Elasticity + Associated Disease
Compliance - Change in Volume/Change in Pressure
Distensibility/Ability to Inflate/Opposite of Stiff
Lost in Restrictive Lung Disease
Elasticity - Opposite of compliance = ability to recoil/snap back
Lost in Obstructive Lung Disease
Anatomical vs. Physiological Dead Space
Anatomical - Volume in conducting airway that does not reach respiratory broncioles - No Gas Exchange - Approx 150ml of 500 ml tidal volume
Physiological - Total volume that does not participate in in gas exchange - Includes functional dead space (ventilated alveoli that do not participate in gas exchange)
Physiological Dead Space Calculation + Normal Value
Dead Space = Tidal Volume * [(PaCO2 - PECO2) / PaCO2]
PaCO2 = Arterial
PECO2 = Expired CO2
Normal Person (with V/Q Matching) - Expired CO2 = 40 mmHg just like PaCO2 = Limited/No Dead Space CO2 used due to rapid diffusion - If the blood gets to the ventilated area it should diffuse
Alveolar Minute Ventilation Calculation
Minute Ventilation = RR * (VT - VD)
RR = Resp. Rate
VT = Tidal Volume
VD = Dead Space
Minute Ventilation = RR * VT
Perfusion Matching in Ventilation - Dehydrated Patient - 2 Keys
Dehydrated Patient = Low volume = decreased apex perfusion
Mechanical Ventilation supplies high ventilation to apex - no flow to balance = high arterial CO2 from increased dead space
Alveolar Gas Equation
PAO2 = FIO2 * ( PATM - 47) - PaCO2 / 0.8
Simplified = PAO2 = 0.21 * (760 - 47) - PaCO2 * 1.25
A-a Gradient - Equation + Normal Range + Indication
A-a = PAO2 - PaO2 - Normal = 100 - 95
Normal Range = 5-15 —– 30 = Definitely Pathology
Hypoxemia with normal A-a = Issue with getting air to the ventilation zone = Not primary lung disease
Hypoxemia with abnormal A-a = Issue with diffusion = Primary Lung Disease
Pathologies Causing Abnormal A-a (3) vs. Pathologies with Normal A-a (3)
Abnormal A-a
1) V/Q Mismatch (Responds to supplemental O2) - Either ventilation without perfusion (PE) or vice-versa (Asthma, Lobar Pneumonia)
2) Pathological Shunting (Does not respond to O2)
3) Diffusion Block - E.g. Exercise (speed up flow) + Pulmonary Fibrosis (to thick)
Normal A-a
1) Low PO2 of Inspired Air - High Altitude
2) Alveolar Hypoventilation - High PaCO2 - Not moving out enough CO2 so it stays in the lungs and prevents O2 from entering
3) Sedation/Muscle Issues
Major Lung Volumes (4) and Capacities (4)
Volumes IRV = Inspiratory Reserve Volume TV = Tidal Volume ERV = Expiratory Reserve Volume RV = Residual Volume
Capacities
IC = Inspiratory Capacity = IRV + TV
FRC = Functional Residual Capacity = ERV + RV
TLC = Total Lung Capacity = IRV + TV + ERV + RV = IC + FRC
VC = Vital Capacity = IRV + TV + ERV = TLC - RV
FVC vs. FEV1 + Ratio - Description + Pathological Changes (2)
FVC = Maximal Exertional VC FEV1 = Maximal Expiration in 1 Second - Normal 80%
FEV1/FVC Ratio - How much of your maximal capacity can you blow out in 1 second?
Normal = 4L of 5L = 80%
Obstructive Disease = Air Trapped in + Can’t Exhale - Low Ratio + High RV + TLC
Restrictive Disease = Everything Decreased Proportional = Normal Ratio
3 Major Classes of Disease with Reduced Diffusion Capacity
1) Obstructive - CF + Emphysema
2) Interstitial Lung Disease (Restrictive)
3) Pulmonary Vascular Disease (Endothelial Damage)
Hypoxemia vs. Hypoxia
Hypoxemia = Low Arterial Oxygen = Free Oxygen - Can't tell how much is in blood (Hb) Hypoxia = Low Oxygen Delivery = More broad (e.g. low cardiac output)
Central vs. Peripheral Cyanosis - Causes
Central
Bluish discolaration of the lips + tongue - Can be warm and well perfused
Causes - Diseaes of Heart/Lung/Hb
Peripheral
Decreased circulation + increased O2 extraction
Causes - CHF + Shock + Raynaud’s + Cold
Example of Tachypnea with no Dyspnea
Acidosis - Breathing hard to get rid of CO2
Four Classes of Diseases Causing Dyspnea + Examples
Structural/Mechanical - Asthma, Chronic Bronchitis etc.
Restriction of Lung Wall - Can’t expand
Intrinsic - Parenchyma (CHF/ARDS)
Extrinsic - Obesity, Ascities, Pregnancy etc.
Increased Dead Space - PE + Emphysema
Increased Respiratory Drive - Hypoxemia = Acidosis + Exercise + Reduced CO/Hb
Cough Pathway + Sensitization + Stimulants (5)
Cough receptors stimulated –> Vagus Nerve –> Nucleus Tractussolitariusof the Medulla –> Effect Response
Causes
1) Cigarette Smoke2
2) Pulmonary Congestion
3) Atelectasis
4) Low Compliance
5) GERD (Stomach Cough Receptors)
Sensitization - Bradykinin/Substance P from inflmmation - Reduces threshold of cough receptors
Timing of Cough (Acute/Sub-Acute/Chronic) + Causes
Acute - Usually Self Limiting (URI)
Sub-Acute - Often-Post Infectious (Resolves with Treatment)
Chronic - Upper Airway Cough Syndrome
Chronic Causes - Post-Nasal Drip + Asthma + GERD + ACE Inhibitors
Asthma Pathology Results (5)
1) Mucous Plugging
2) Basement Membrane Thickening
3) Infiltrate/Eosinophil Invasion
4) Smooth Muscle Hypertrophy - Irreversible Aspect
5) Increased Goblet Cells
Tracheobronchial Sources of Hemoptysis (3)
1) Neoplasma (Carcinmoa + Kaposi’s Sarcoma = Bronchial Carcinoid)
2) Bronchitis
3) Bronchiectasis
Common Hemoptysis Associations (4)
1) Repeated small amounts with blood streaking of sputum - Cancer
2) Fever + Night Sweats + Weight Loss - TB
3) Rusty Colored Sputum - Bacterial Pneumonia - Strep = #1
4) Massive Hemorrhage - Bronchiectasis
Pleuritic Chest Pain + Causes (6)
Sharp/Stabbing pain on inspiration with positional changes
Causes
1) PE
2) Pleural Disease
3) Pneumothroax
4) Lung Cancer
5) Pleural Effusion
6) Musculoskeletal
Asthma Key Feature + Epidemiology
Variable Airway Obstruction (vs. Fixed in Emphysema)
More common in adult female + male youth
Asthma Pathogenesis
Th2 Helper Cell –> IgE Mediated Type 1 Hypersensitivity Reaction
Th2 (Triggered by IL-4) - Produced IL-4/5/9/10/13 - Act on Mast Cells - IL-5 Increases IgE Cross-linking on Eosinophils
Eosinophilic Infiltration vs. Neurtrophils in Chronic Bronchitis
Asthma Pathology Results (5)
1) Mucous Plugging
2) Basement Membrane Thickening
3) Infiltrate/Eosinophil Invasion
4) Smooth Muscle Hypertrophy - Irreversible Aspect
5) Increased Goblet Cells
Asthma Histology Findings
Eosinphil-derived crystals (carcot-leyden) + Major basic protein aggregates + Curshman Spirals
Overview Case 1 - Alcoholic with Pneumonia - Key Points (2)
1) Lobar Consolidation in Alcoholic - Gram (-) Klebsiella
2) Major Histology - Alveoli filled with neutrophil infiltrates
Overview Case 3 Sarcoidosis - Key Points (2)
1) CXR - Bilateral Interstitial Markers + Hilar Lymphadenopathy
2) African American Women - Diagnosis of Exclusion
3) High ACE and Ca2+ - Non-caseating granulomas
Overview Case 4 - Hypersensitivity Pneumonitis - Key Points (4)
1) Allergic Alvoelitis - Restrictive Disease
2) Carpenter - Prolonged Dust Exposure
3) Histology = Thick alveolar walls + Granulomas
4) Common Causes - Farmer’s Lung (Hay) + Air-Conditioning + Pigeon Breeder
Overview Case 12 - Bronchioalveolar Adenocarcinoma - Key Points (3)
1) Adenoacarcinoma Subtype - Terminal bronchioles + produces consolidation like a pneumonia
2) Tumor growth along existing structures without alveolar damage
3) Tombstone cells on histology
Overview Case 7 - Pulmonary Edema - Key Points (4)
1) Hemodynamic Pulmonary Edema –> Increased Hydrostatic Pressure/Decreased Oncotic Pressure
2) Build build up is in the interstitial space
3) Micro-vascular Pulmonary Edema –> LIver like lung (leak and filling)
4) Infectious + Injury = Big Causes - Coxsackie virus in the summer
Overview Case 8 - Nocardia Pneumonia - Key Points (4)
1) Slow progressing aerobic Gram + pneumonia - Filamentous branched chains like fungal hyaphae
2) Most common in immuncompromised
3) Bilateral infiltrates with small nodules of central cavitation
4) Major Causes of Cavitation - TB + Fungi + PE + Wegner’s + Squamous Cell Carcinoma
Overview Case 15 - Mesothelioma - Key Points (3)
1) Old!
2) Pleuritic Check Pain + Smoker + Asbestos = 55x more likely
3) Serpentines (Curved) vs. Amphiboles (Straight) - Amphiboles = More pathogenic
Overview Case 10 - Small Bronchogenic Carcinoma - Key Points (2)
1) Smoker + Hilar Lung Mass with Mets
2) Hyponatremia is common (SIADH) - Paraneoplastic (Also Cushing + Eaton-Lambert)
3) Histology - Salt and Pepper Tumor Cells - Slightly smaller than lymphocytes + without cytoplasm
Overview Case 17 - Aspergilliosis - Key Points (3)
1) HIV - CD4 Count Drops Below 200 -
2) Patchy Lung Infiltrates - Miliary Pattern
3) Branched Hyphae on histology
Overview Case 1 - Key Points (2)
Overview Case 1 - Key Points (2)
Overview Case 13 - Squamous Cell - Key Points (3)
1) Central Mass + Smoker + Bifurcation of main stem bronchos
2) Hypercalcemia due to increased Ca2+ via paraneoplastic syndrome
3) EGFR overexpressed in 80%
Asthma vs. Chronic Bronchitis (2)
COPD = Hyperplasia without eosinophils (asthma has)
COPD = CD8 vs. Asthma = CD4
Overview Case 15 - Mesothelioma - Key Points (3)
1) Old!
2) Pleuritic Check Pain + Smoker + Asbestos = 55x more likely
3) Serpentines (Curved) vs. Amphiboles (Straight) - Amphiboles = More pathogenic
Signs and Symptoms of Chronic Bronchitis
1) Blue Bloaters - Cyanosis - Mucous plug traps CO2 and causes PaO2 to drop and PaCO2 to go up (vs. emphysema where PaO2 stays more normal)
2) Productive Cough
3) Less Dyspnea
4) Risk of Cor Pulmonale - Inappropriate closing of low ventilation zones causes V/Q mismatch (high Q) with low PaO2 and physiological shunting - Pulm. HTN occurs to try and increase PaO2
Chronic Bronchitis - Classic Early Presentation Signs (7)
1) Productive Cough
2) Cyanosis
3) Moderate Hyperinflation on CXR (vs. tons in emphysema)
4) Large Heart + Vessels
5) Hypoxia
6) Respiratory Acidosis
7) Little to no Dyspnea (comes later)
Chronic Bronchitis - Clinical Definition + Pathophysiology
Definition - 3 months of productive cough over 2 years
Pathophysiology - Increased thickness of the mucous glands + submucosal hyperplasia - CD8 Based
Reid Index - Definition
Used for Chronic Bronchitis - % of respiratory epithelium that is submucosal - Normal = 40%
Pathologic = > 50%
A1AT Deficiency - Key Features (3)
1) Autosomal Dominant - Codominant
2) Causes Panacinar (Lower Lobe) Emphysema
3) Mutated Protein Accumulates in Liver - Causes Pink PAS Positive Globules in the hepatocytes
Pathophysiology of Chronic Bronchitis vs. Emphysema
COPD = Low V/Q Ratio with physiologic shunt
More Productive Cough
Emphysema = High V/Q Ratio with increased physiological dead space
More Dyspnea
Signs and Symptoms of Chronic Bronchitis
1) Blue Bloaters - Cyanosis - Mucous plug traps CO2 and causes PaO2 to drop and PaCO2 to go up (vs. emphysema where PaO2 stays more normal)
2) Productive Cough
3) Less Dyspnea
4) Risk of Cor Pulmonale - Inappropriate closing of low ventilation zones causes V/Q mismatch (high Q) with low PaO2 and physiological shunting - Pulm. HTN occurs to try and increase PaO2
Chronic Bronchitis - Classic Early Presentation Signs (7)
1) Productive Cough
2) Cyanosis
3) Moderate Hyperinflation on CXR (vs. tons in emphysema)
4) Large Heart + Vessels
5) Hypoxia
6) Respiratory Acidosis
7) Little to no Dyspnea (comes later)
Bronciectasis - Signs/Symptoms (4)
1) Foul Purulent Smelling Sputum
2) Secondary AA Amyloidosis
3) Clubbing of Fingers
4) Brain Metastasis
Types of Emphysema (2) + Key Feature
Centriacinar - Smoke induced (further “up” the respiratory bronchiole - Upper Lobe
Panacinar - A1AT Deficiency - Whole acinus - Lower Lobe
Classes of Restrictive Lung Disease (2) + Diseases (5 Each)
Granulomatous
1) Sarcoidsis
2) Hypersensitivity Pneumonia/Pneumonitiis
3) Silicosis
4) Beryilliosis
5) Granlomatous Vasculitis - Wegener’s + Churg-Strauss
Non-Granlomatous (Inflammation)
1) Idiopathic
2) Radiation
3) Drugs - Belomycin + Amiodarone
4) Eosinophilic
5) Asbestosis
Emphysema Signs/Symptoms (6)
1) Pink Puffers - Wasting Away
2) Severe Dyspnea
3) Minimal Cough/Sputum
4) Limited Acidosis + Normal to Low PaCO2
5) Increased Physiological Dead Space
6) Barrel Chest (Increased A-P Diameter
Pneumocomiosis - Pathophysiology + Types (4) + Exposures
Path - Interstitial fibrosis due to chronic occupation exposure to small fibrogenic molecules
1) Coal Workers
2) Silicosis - Sandblaster + Potter + Glass
3) Berylliosis - Miner/Aerospace
4) Asbestosis - Construction Worker + Shipyard Worker + Roofer
Bronciectasis - Causes (5)
1) Cystic Fibrosis
2) Kartagenic Syndrome - Mutation in the dyenin arm of the cilia - Also with transposed organs + loss of fertility
3) Tumor
4) Foreign Body
5) Allergic Broncho-pulmonary Aspergilliosis Hypersensitivity Reaction
Coal Worker Pneumocomiosis - Key Points (3)
1) Carbon dust with diffuse fibrosis
2) Caplan Syndrome - Co-Exist With Rheumatoid Arthritis = Nodules in the Lungs
3) Anthracosis - Mild Carbon Exposure in everyone from pollution - not clinically significant
General Restrictive Lung Disease Principles (4)
1) Normal FEV/FVC Ratio - All Volumes Drop but at a normal ratio
2) More dyspnea/less cough vs. Obstructive
3) End Stage for All Disease - Honeycomb Lung
4) Granulomatous = Upper Lobe Non-Granulomatous = Lower Lobe
Classes of Restrictive Lung Disease (2) + Diseases (5 Each)
Granulomatous
1) Sarcoidsis
2) Hypersensitivity Pneumonia/Pneumonitiis
3) Silicosis
4) Beryilliosis
5) Granlomatous Vasculitis - Wegener’s + Churg-Strauss
Non-Granlomatous (Inflammation)
1) Idiopathic
2) Radiation
3) Drugs - Belomycin + Amiodarone
4) Eosinophilic
5) Asbestosis
Asbestosis - Key Points (4)
1) Fibrotic Plaques of Pleaura = Most Common Sqeulla
2) Primary Lung Cancer Second + Mesothelioma Third (Mesothelioma takes an extra 10 years to develop, most people dead from lung cancer)
3) Lesions contain long oglden fibers called asbestos bodies
4) Serpentines (Curved) vs. Amphiboles (Straight) - Amphiboles = More pathogenic
Pneumocomiosis - Pathophysiology + Types (4) + Exposures
Path - Interstitial fibrosis due to chronic occupation exposure to small fibrogenic molecules
1) Coal Workers
2) Silicosis - Sandblaster + Potter + Glass
3) Berylliosis - Miner/Aerospace
4) Asbestosis - Construction Worker + Shipyard Worker + Roofer
Sarcoidosis - Histology (2) + CXR + Exam Findings (3)
1) Histo - Asteroid Bodies within the giant cells of granulomas + epithelial histocytes
2) CXR - Bilateral large nodules especially in the hilar region
3) Dyspnea/Cough with Elevated ACE Enzyme + high calcium from increased Vitamin D
Hypersensitivity Pneumonitis - Pathophysiology + Examples (3)
Granulomatous reaction to inhaled organic antigens - Type III Hypersensitivity Reaction (IgG) - Recovery after stimulus removal
Pigeon Breeder’s Lung
Miller’s lung
Farmers Lung
Hypersensitivity Pneumonitis - Exam Findings (5) + Differences with Asthma (2)
Exam - Fever + Cough + Dyspnea + Leukocytosis
Chronic Exposure - Interstitial Fibrosis (Irreversible)
Differences with Asthma - Type III vs. Type I
Disease of the alveoli vs. asthma = disease of the bronchi
Berylliosis - Key Points (3)
1) Non-caseating granuloma of the lung - looks just like sarcoidosis
2) Hilar Lymph Node Involvement
3) Increases Risk of Primary Lung Cancer
Asbestosis - Key Points (4)
1) Fibrotic Plaques of Pleaura = Most Common Sqeulla
2) Primary Lung Cancer Second + Mesothelioma Third (Mesothelioma takes an extra 10 years to develop, most people dead from lung cancer)
3) Lesions contain long oglden fibers called asbestos bodies
4) Serpentines (Curved) vs. Amphiboles (Straight) - Amphiboles = More pathogenic
Sarcoidosis - Pathophysiogly + Target Population
Non-caseating granulomas of the hilar lymph nodes (likely a CD4 Response)
Middle Aged African American Women
Textile Worker Disease - Exposure + Pathway
Exposure - Byssinosis
Pathway - Bacterial Endotoxin (Gram Negative) IgG Type III - Monday Morning Blues
Hypersensitivity Pneumonitis - Pathophysiology + Examples (3)
Granulomatous reaction to inhaled organic antigens - Type III Hypersensitivity Reaction - Recovery after stimulus removal
Pigeon Breeder’s Lung
Miller’s lung
Farmers Lung
Hypersensitivity Pneumonitis - Exam Findings (4) + Differences with Asthma (2)
Exam - Fever + Cough + Dyspnea
Chronic Exposure - Interstitial Fibrosis (Irreversible)
Differences with Asthma - Type III vs. Type I
Disease of the alveoli vs. asthma = disease of the bronchi
Farmer’s Lung - Exposure + Pathway
Exposure - Thermophilic Actinomycetes (Moldy Hay)
Pathway - IgG Type III and Chronic Leads to Type IV
Silo-Filler’s Disease - Exposure + Pathway
Exposure - NO from Fermentation of Plants
Pathway - IgG Type III
Pigeon Breeder’s Disease - Exposure + Pathway
Exposure - Proteins in Bird Droppigns
Pathway - IgG Type III
Textile Worker Disease - Exposure + Pathway
Exposure - Byssinosis
Pathway - Bacterial Endotoxin (Gram Negative) IgG Type III - Monday Morning Blues
Pathogens Associated with Bronchiectasis (5)
1) TB
2) Mycobacterium Avium
3) Adneovirus
4) Staph. Aureus
5) H. Influenzae
Initial Response to High Altitude
Massive increase in ventialtion - Can’t control the low inspired O2 so the body blows of CO2 to try and compensate in the gas equation - Increases the PAO2
Two Mechanisms to Reduce PaCO2 In High Altitude
1) Hypoxic Ventilator Response (Low PaO2 = Increased cerebral blood flow - Medulla CO2 is removed = high pH - Medulla tries to cause hypoventilaiton
2) Response overridden by peripheral chemoreceptor stimulation (hypoxemia detection) - Decrease in CSF Bicarb = Acidic pH despite low CO2
Result = Hyperventilation even at low PaCO2 - If you expose this person to sea level PCO2 after acclimatization if will cause massive hyperventilation (super sensitive and use to low resting PaCO2)
Hypoxemia Venilatory Response
Delayed - won’t start until PaO2 drops to around 55 mmHg - Eventually superceeds the central response (due to high pH)
Results of Ventilatory Changes in High Altitude (3)
1) Hyperventilation - Low PACO2 and PaCO2
2) Low PACO2 increases the % of PAO2 in the alveoli helping balance the low pressure
3) Low PaCO2 causes respiratory alkalosis
Bohr Changes in High Altitude (2)
1) Respiratory Alkalosis - Results in higher O2 Loading (Left Shift at Top)
2) Increased 2,3 BPG Production - Results in higher O2 Unload (Right shift at bottom)
Hemoglobin Changes in High Altitude (2)
1) Decreased Blood Volume - Increases the % of hemoglobin = increased carrying
2) Increased EPO (from Hypoxia Inductible Factor) = Increased RBC Production = increased carrying
Cardiac Changes in High Altitude (2)
Initial increase in HR that increases CO and delivery
Eventually SV drops and CO returns to normal
Major Changes in High Altitude to Reduce Hypoxia (4) + Timing
Days
1) Hyperventilation = Increased PAO2 %
2) Hyperventilation = Resp. Alkalosis = Increased O2 Loading in Lungs
Weeks
3) Increased 2,3 BPG = Better O2 unloading in tissues
Months
4) Increased EPO + Reduced Volume = Increased Hb concentration (Increased Blood O2 content)
Variables that Decrease During High Altitude Acclimatization (6)
1) PaO2
2) PAO2
3) PaCO2
4) PACO2
5) % Hb Saturation
6) Peripheral O2 Affinity (Better Unloading)
A-a Gradient - Stays the same
Variables that Increase During High Altitude Acclimatization (5)
1) pH
2) 2,3 BPG
3) EPO/RBCs
4) Total Hb
5) Lung O2 Affinity (Better Loading)
High Altitude Pulmonary Edema - Pathophysiology
Accumulation of fluid in the lung at a rate that cannot be cleared by the ENaC Channel
Hypoxia induced pulmonary hypertension resulting in higher hydrostatic pressure - more crosses than you can clear
High Altitude Pulmonary Edema - Signs (4) + Exam Findings (4)
36-72 Hours After Arrival
Signs
1) SOB
2) Dry Cough
3) Fever
4) Weakness
Exam Findings
1) Tachypnea
2) Tachycardia
3) Cyanosis
4) +/- Rales
Potential Causes of High Altitude Pulmonary Edema (3)
1) Reduced NO
2) Increased Endothelian-1
3) Increaed Symp. Activity
All trigger pulmonary hypertension
Exercise Impacts on CV Functions (5)
1) Increased CO from 5L/min - 25/30
2) First 45% via SV then HR Takes Over
3) Linear rise for everyone but trained can rise higher
4) HR is more important for untrained individuals (SV works longer in trained athletes)
5) Oxygen Pulse Calculation = SV = VO2/HR = Oxygen Consumption/HR
Exercise Impacts on Respiratory Function (3)
1) Ventilation Rises with O2
2) Increased Pulm. Blood Flow Reduces the amount of physiological dead space (from about 35% to 15%)
3) Never Reach Maximal Volume (Minute) Ventilation - More training = come closer
Minute Ventilation (VE) Changes in COPD Exercise (20
1) Maximum VE = Lower
2) Can reach the maximum (vs. normal can’t)
Anaerobic Threshold - Definition + Key Points (4)
Anaerobic Threshold = Point where lactic acid production exceeds liver metabolism = point where lactic acid accumlation begins
1) At this point LA begins to drive ventilation
2) Increased LA = Decrease HCO3 to buffer = Increased CO2 to buffer - Result = Increased ventilation to avoid respiratory acidosis
3) CO2 involvement in ventilation means ventilation no longer matches VO2 (demand) - You are now breathing “more” than needed
Anaerobic Threshold in Heart Failure
Heart Failure = Low O2 Delivery to tissues - reach lactic acid threshold much earlier
Exercise Test Parameters/Possible Problem Areas (and associated causes)
Cardiac Markers
1) Limited O2 Pulse (SV)
2) Limited/Early Anaerobic Threshold (AT)
Possible Disease = Coronary Artery Disease + Heart Failure + Cardiomyopathy
Pulmonary Markers
1) Inability to Reach Aneorobic Threshold (means you’re not limited by perfusion to tissue)
2) Using Entire VE Reserve
3) Dead Space Rises on Exercise
Possible Diseases - Obstructive/Restrictive/Chest Wall - Look at other tests like FEV1 etc.
Pulmonary and Cardiac Markers
E.g. Low AT + Low O2 Pulse (Cardiac) with Increased Dead Space (Should Rise) = Both
Possible Disease = Pulmonary HTN + PE
