Mechanics of Breathing and Compliance

Mechanics of Breathing

• Muscles perform no work when breathing out passively
• Accessory muscles are required for expiration if having difficulty breathing
• Normal inspiratory muscles include the diaphragm and external intercostals
• Accessory muscles used for inspiration are the sternocleidomastoid and scalene, and indicate respiratory distress
• Expiratory accessory muscles include the abdominal muscles surrounding the diaphragm, and internal intercostals
• Air typically exits passively during expiration
• Elastic properties of the lung and chest wall are prime for inspiration
• The rib cage extends naturally, while the lungs deflate, collapse, and recoil
• Elastic recoil refers to the lungs' tendency to return to a resting state
• Compliance is the distensibility or stretchability of the lung and chest wall

Compliance

• Lung collapse occurs in atelectasis
• Compliance decreases in atelectasis, pneumonia, ARDS, pulmonary fibrosis and pulmonary edema
• Post-operative patients with collapsed alveoli in a wet, dark space are at risk for pneumonia
• Air entry faces resistance, requiring more pressure to inflate the lungs

Reduced Lung Compliance

• Reduced lung compliance is common in respiratory problems, indicating poor distensibility and stretchability
• Emphysema results from increased compliance and is when lungs are easy to inflate due to the loss of elastic recoil
• Minimal pressure is needed for maximum air intake because of very little resistance of distensibility
• Airways dilate a bit when inhaling and constrict when exhaling
• Airway constriction involves no dilation, only constriction
• Lung obstructions worry more when children get edema due to their decreased lung diameter
• Children's lung diameter reduces by 75%, boosting airway resistance 16 fold, making air intake extremely difficult

Airway Diameter and Work of Breathing

• Asthma, chronic bronchitis, and COPD constrict the airway as smooth muscles tighten bronchial tubes, reducing airway diameter
• Secretions in the lungs increase airway resistance
• Work of Breathing (WOB) mechanisms increase oxygen expenditure and energy needs
• Accessory muscles are used for both breathing in and out
• Respiratory muscles facing fatigue can lead to respiratory arrest and death
• Increased WOB leads to respiratory muscle fatigue
• Etiologies of poor compliance, airway resistance, and abnormal elastic recoil cause phenomenal WOB
• Body's breathing energy needs increase dramatically
• Breathing without distress indicates no problem, and noticeable breathing indicates a rate and depth change

Alveolar Ventilation

• Minute volume measures alveolar air intake per minute
• Tidal volume multiplied by respiratory rate equals minute volume
• Tidal volume measures air breathed in or out in one breath
• Alveolar ventilation is gas exchange that meets metabolic needs
• Hypoventilation involves high PaCO2 (hypercapnia), and breathing in too little air per minute causing CO2 retention
• Extra CO2 in the blood reduces space for oxygen, leading to hypoxemia (acidosis)
• Reduced alveolar ventilation increases PaCO2, causing altered mental status, and secondary hypoxemia
• Hypoventilation, respiratory acidosis raises risk for hypoxemia (low oxygen in blood)
• Hyperventilation involves low PaCO2, less than 40, and normal air amount breathed in faster
• Increased respiratory rate blows off more CO2
• Increased alveolar ventilation reduces PaCO2, causing lightheadedness and respiratory alkalosis
• Smaller breaths and decreased tidal volume cause risk for atelectasis, preventing full alveolar inflation

Oxyhemoglobin Dissociation Curve

• Oxyhemoglobin involves oxygen bound to hemoglobin, and over 90% in the blood isn't free floating
• Dissociation involves oxygen unbinding from the hemoglobin when oxygen dissociates from hemoglobin
• Increased affinity (left shift) is when hemoglobin likes and retains oxygen
• Result is hypoxia for the tissue as hemoglobin does not let go of the oxygen
• Increased affinity allows PAO2 to drop as low as 20
• Results in acute alkalosis, decreased PCO2, hypothermia, low levels of 2-3DPG which means low levels of oxygen from stored blood, abnormal hemoglobin, and methemoglobin

Reduced vs. Decreased Affinity and Hypoxemia

• Reduced/decreased affinity (right shift) involves hemoglobin releasing oxygen to the tissue for tissue perfusion
• Oxygen dissociates from the hemoglobin and reaches the tissue on the steep part of the curve
• Normal PACO2 is 26
• Increased PAO2 in the blood for tissue perfusion (right shift) requires decreased affinity for hemoglobin
• Results in acute acidosis, increased PCO2, hyperthermia, and high 2-3DPG levels for oxygen delivery, as well as abnormal hemoglobin
• The level of oxygen saturation isn't always good, and the dissociation should also be tested
• Understanding the increased ventilation/perfusion defects related to oxygen levels getting to the tissues is important

Ventilation / Perfusion

• Hypoxemia requires a PaO2 of 60 or less
• Normal deoxygenated blood goes to the lungs and becomes oxygenated, and then travels to the heart for distribution
• Low V/Q relates to mucus impairing the airway
• Deoxygenated blood comes to lung, picking up less oxygen than normal
• Impaired ventilation (narrowing of the bronchi) causes a PaO2 drop and hypoxemia
• V/Q drops when ventilation gets impaired in asthma and chronic bronchitis
• Shunt (very low) V/Q involves entirely blocked ventilation due to collapsed Alveoli
• Right to left shunt is when blood from the heart's right side bypasses oxygenation in the lungs
• Blood gets redirected to the heart's left side without picking oxygen up from the lungs

Intractable Hypoxemia and Acute Respiratory Failure

• Intractable hypoxemia occurs when blockage stops lungs from receiving oxygen, rendering oxygen increases ineffective
• When ventilation is impaired, V/Q increases, causing ARDSs, Atelectasis, and Pneumonia
• In High V/Q, the lungs are open but there's a perfusion blockage, impeding blood supply and leading to hypoxemia

Failure

• Acute Respiratory failure (ARF) relates to the lungs not working
• The conditions for ARF are a PaO2 of 50 or less, or a PaO2 of 50 or greater with a pH of 7.25 or less
• ARF typically requires a ventilator
• Patients with chronic bronchitis & asthma retain CO2 due to airway constriction
• May have high PaCO2 levels with low oxygen (hypoxemia)
• Chronic bronchitis patients typically have chronic hypoxemia & hypercapnia
• The PaCO2 level is normally less than 60
• 10 mmHg differentiates hypoxemia & acute respiratory distress

Alveolar Capillary Membrane

• The alveolar capillary membrane is the thin barrier between blood and capillaries
• Thickening or enlarging interstitial space complicates gas exchange
• Pneumocytes yield surfactant lining alveoli and preventing collapse
• Impaired surfactant production from pulmonary embolism/hypoxemia causes alveoli collapse (Atelectasis)

Alveolar Surface Tension and Pulmonary Circulation

• Alveolar surface tension makes molecules stick exposed to air
• Tension impedes alveolar expansion
• Surfactant reduces surface tension and LaPlace's Law explains the smaller radius of alveolus requires more pressure to infiltrate
• Pulmonary system normally has low pressure
• Increased pressure on pulmonary vessels from vasoconstriction affects the heart's right side

Pulmonary Hypertension

• Pulmonary Vascular Resistance (PVR) increases with vessel constriction
• The right heart will eject blood against higher pressure, boosting contractility and causing right ventricular hypertrophy from hypertension
• Elevated PVR only impacts the right ventricle
• Pulmonary vasoconstriction results from low alveolar or venous oxygen and low pH (acidosis)
• Inflammatory mediators (neutrophils) boost capillary permeability and damage due to chemotaxis
• Etiology includes increased PVR, inflammatory mediators, COPD, interstitial fibrosis, and obesity
• These factors lead to chronic hypoxemia & chronic acidosis, causing pulmonary artery vasoconstriction
• This in turn escalates pulmonary artery pressure
• Primary vasoconstriction can be treated effectively and can be reversed with effective treatments
• Fibrosis and hypertrophy won't be reversible if treatments aren't effective

Pulmonary Embolism

• Smooth muscles can't be reversed with pulmonary hypertension
• Pulmonary hypertension will leads to "Cor Pulmonale" (Right Heart Failure) because the right heart works harder under increased vascular pressure
• Venous stasis raises thrombus risk
• Thrombus traveling the pulmonary system from a blockage causes a vessel to occlude
• Venous stasis, hypercoagulability, and venous endothelial damage create Virchow's Triad
• Hypoxic vasoconstriction causes reduced surfactant to impair production
• Inflammatory substances release, causing pulmonary edema, atelectasis, tachypnea, pain, hypotension, and shock
• Clinical manifestations include: rapid, difficulty, chest pain, increased dead space, decreased PaO2, hypertension, hypotension, and shock
• Hypoxemia, respiratory alkalosis from compensatory hyperventilation to increase PaO2 causes acidosis

Pulmonary and Cardio Edema

• Pulmonary capillary hydrostatic increases with pulmonary vascular pressure, pushing water out of the capillary leading to pulmonary edema (collecting blood in the left atrium)
• Water enters the interstitial space increases pressure
• Alveoli collapse/injury to capillary endothelium cause noncardiogenic pulmonary edema
• Movement of fluid from capillary increases capillary permeability
• Damage to capillary endothelium from sepsis, unlike the heart causes Pulmonary Edema and distended heart vessels
• Clinical manifestations include difficulty and shortness of breath
• Compliance decreases with more pressure, and is due to stuff building up in the interstitial and alveoli

ABGs

• Hypoxemia occurs
• Hypercapnia is due to diffusion affecting the ability or CO2
• Respiratory acidosis transitions to mixed acidosis
• ARDS is due to capillary endothelial injury and inflammation, endothelial injury, and surfactant inactivation
• Sepsis is the most common cause of ARDS
• Pathophysiology relies on the release of inflammatory mediators
• Platelet aggregation causes microthrombi

Pulmonary Circulation and Acute Injury

• Vasoconstriction with decreased flow cause hypertension, causing V/Q mismatching
• Phase 1, Inflammatory/exudative: a damaged alveolar membrane causes exudation of protein-rich fluid in to interstitial space, causing edema and hemorrhage involving severe alveolar ventilation
• Decreased surfactant function, Increased surface tension, reduced lung compliance, and atelectasis will occur
• Phase 2, Proliferative: macrophages, fibroblasts & type II pneumocytes heal and hyaline membranes thicken
• Phase 3, Fibrotic: progressive fibrosis & tissue remodeling occurs with new lung tissue and systematic and systemic hypoxia occurs

Lung Injury to Pneumonia

• The lungs are never normal again due to the extent of the damage and high mortality
• There is an inability to let oxygen in out as the patient goes into Acute Respiratory Failure
• There is hypoxemia, hypercapnia, and acidosis
• Lung becomes fulminant
• Lung injury causes inflammation and diffuse alveolocapillary injury
• Also causes pulmonary capillary endothelial injury, inflammation and platelet activation and bilateral patchy diffuse infiltrates

Clinical Manifestations and Treatments

• Clinical manifestations include dyspnea, intractable hypoxemia, increased WOB, hypercapnia, and decreased lung compliance
• Complications include non-cardiogenic pulmonary Edema and Atelectasis
• A metabolic acidosis occurs, reduced oxygen is perfused absence of left atrial hypertension and PaO2/FIO2 200
• Intractractable hypoxemia is treated with oxygen and helps the collapsed alveoli

Consolidation and Atelectasis

• ECMO is an external device used to help lung oxygenation
• Lung tissues collapse in atelectasis
• Impaired ventilation in absorption causes gases to not be absorbed and lungs are not able to do exchange with air
• No new air can get in and is impaired in obstruction

Clinical Manifestations and Pulmonary Pneumoniae

• Clinical manifestations dyspnea, cough, fever, and WBCS
• Pneumococall Pneumonia Pathophysiology: Takes multiple days to resolve and treat and treat
• Aspire S pneumonia: adhere to lower alveolar macrophages

Response to Pneumoniae, Hypoxemia, and Treatment

• inflammatory repsonse from capillaries filling in the cells
• Exudate from red hepatization makes the airways solid
• Fibrin gets made and the lungs are red in gray hepatization
• Exudate gets removed or digested and gotten rid of
• Clinical presentations can vary based on the cause to treatment
• O gets used to reat the virus of pneuomina and bacterial treatment

Pneumoniae Complications

• Pneumococcal Pneumonia is caused by streptoccoi
• Bacteria causes an inflammatory response leading to collapsed Alveoli and lung injury

Types of Pleural Effusions

• Can be categorized by the fluids within as well as the location of the effusion
• pressure will push fluids into plural space and will cause hydrothorax which creates fluid

Pressure and Fluid

• Pressure will push blood into the plural space
• The collection of the plural space can cause bacterial infections
• fat droplets are created and is considered an infection
• When fluids collect in space it willl create plurael effusion

Fluid Collection and Treatment

• Blood vessels and lympthaics can cause a draining absess
• A Membrane is used adn has to be permeabble and can spread from copallaries
• A needle can be used and place into a space and will see what type of fluids are there

Plura Fluid

• Fluid will move because the fluid is dependent and will gravitate
• A film will be placed and can depend on te layers can have a dffusion and pneuomina will move
• Breath will have different manifestations and sounds and can result in Plerua Friction rubbing

Plura

• There is a thin layer that helps with surfaces
• A rupture can caus eair in pleural cavity
• Pneumothorax will cause chst discomfort and can couse people to cause issues w breathing

Air

• air will come in and out of the exhalation side
• Air can buildup in the pleural space and will caus epreassure
• Trauma can causes air in places where air is not allowed
• pressure can reverse lungs and causre them to retract

Pulmonary

• Can caues chest pain because the air pushes the lungs and pressure
• Lung volume = pressure
• It’s an emergency and requires treatment immediately
• A needle needs to be placed for the tubes
• A trachael issue and the diaphragm will flatten
• Low BP,no , and altered breath
• ABGs and can be fixed with more o2

Obstructive

• Exposure cuases irritiation and release mediatiors
• early: mast cells will create inflammation and causes response
• Capiliaries creates permiability and caues vascular congestion
• Epihitial fibrosis can cause airway obstruction

Lungs adn Asthma and ABG

• 4 to 8 hours causes a response
• inflammaty pathogenesis helps a patient
• Overtimes that can lead to ineffective issues and remodelling
• remember the release
• ABG LOW PRESSURE LOW CO2

Asthma (cont.)

• High breaths can causde a bad experience
• can result in respiratory issues Can not hear beathing aor can cause a lung disorder

COPD

• immune system creates the issues
• Air pollution is a cause
• Causes inlfamation and then bronchioli isses
• Causes extra stress with Mucis

More Issues

• The body will react with hypercap and a blockage will occuur
• The lings will try to reciol and causes inabiiity and then emphysema. They have lost abilities to cause elatsiticy
• They may have trouble of breathing
• they use oxygen on thier own so taking the stimulus can lead to issues

COPD Issues

• Can caise a decrease in lungs
• airway can have issues to the cause like coughs to infections
• Can use the puffer style or purse breather