Respiratory Disorders PDF

Slide 1 Disorders of the Respiratory System: Respiratory Failure and Restrictive Disorders AHSC 228 Slide 2 The Atmosphere The air around us is composed of mostly nitrogen...

Slide 1 Disorders of the Respiratory System: Respiratory Failure and Restrictive Disorders AHSC 228 Slide 2 The Atmosphere The air around us is composed of mostly nitrogen (78%), oxygen (21%) and trace amounts of other gases, including CO2 – This is consistent no matter where we are – Can be affected by asphyxiation, toxins, supplemental O2 The atmosphere has a total pressure of 760 mmHg at sea level at 15 C; O2 has a partial pressure of 160 mmHg – This changes depending on altitude, temperature and other factors Slide 3 How do we get O2 to our tissues? 1. Ventilation – the flow of gases into and out the lungs: exchange of 02 and C02 2. Perfusion – flow of blood in the pulmonary and system capillaries 3. Respiration – gas exchange (diffusion) between the alveoli and the pulmonary capillaries 4. Transport/distribution – movement of O2 throughout the body, diffusion of gases between the cells and blood vessels, and return of CO2 to the lungs 5. Cellular respiration – aerobic metabolism in cells to created ATP Slide 4 Mechanical exchange of gases between the atmosphere and the 1) Ventilation lungs Mechanical exchange of gases between the Inspiration brings oxygenated air in (21%/160 mmHg) → active atmosphere and the lungs process Inspiration brings oxygenated air in (21%/160 mmHg) Expiration moves carbon dioxide air out → USUALLY a passive Expiration moves carbon dioxide air out process Impairment of ventilation MOSTLY impacts CO2 We need ventilation for oxygenation, BUT when you think of ventilation, think of CO2 Factors affecting ventilation: - Ventilatory drive (neurological) - Body position - Bronchiolar constriction (obstructive) - Lung volume - Lung compliance: - Lung tissue elasticity (recoil), chest wall movement - Surface tensions (H20 in alveoli creates a ‘surface tension’ that helps to deflate alveoli with expiration) Slide 5 Blood flow to the lungs 2) Perfusion Blood flow to the lungs - Pulmonary vessels are thinner and more compliant Pulmonary circulation: – Deoxygenated blood flow in the pulmonary artery to the gas exchange portion of the lung - Offer less resistance to blood flow than those in systemic – Gas exchange in the pulmonary capillary bed to pick up O2 and drop off CO2 circulation because all the arterioles are open at once = – Oxygenated blood returns to the left side of the heart Affected by: decreased resistance – Cardiovascular hemodynamics – – Vascular obstructions (pulmonary embolus) Sensitivity to alveolar hypoxia causes vasoconstriction - Pressure in the pulmonary system is much lower: 22/8 vs 120/80 – Other factors Impairment causes hypoxemia and hypercarbia - But it also makes the vessel walls more susceptible to damage if the pressure does rise as the vessel walls are much thinner. Pulmonary circulation: Deoxygenated blood flow in the pulmonary artery to the gas exchange portion of the lung Gas exchange in the pulmonary capillary bed to pick up O2 and drop off CO2 Oxygenated blood returns to the left side of the heart Affected by: Cardiovascular hemodynamics Vascular obstructions (pulmonary embolus) Sensitivity to alveolar hypoxia causes vasoconstriction What is the purpose of vasoconstriction with hypoxia? - To redistribute blood flow to functioning parts of the lung(s) where gas exchange is occurring. - The goal is to redirect the blood flow from poorly ventilated regions to better ventilated regions to try and increase overall efficiency of gas exchange between air and blood. - This can be beneficial if it only occur regionally in the lungs. - But, generalized hypoxia due to lung disease causes vasoconstriction throughout the lung. - This can lead to pulmonary hypertension and increased workload on the right side of the heart and right sided heart failure (Cor Pulmonale) Other factors Impairment causes hypoxemia and hypercarbia Slide 6 Most gas exchange occurs in lung bases as we have larger alveoli in 3) Respiration Diffusion of O2 from alveoli less numbers than in bases (more surface area) into the pulmonary capillaries and CO2 in reverse Larger alveoli in upper portions are more difficult to inflate (less Diffusion affected by pressure compliant) (partial pressure), concentration (fiO2) and surface area (alveoli) During ventilation, most of the tidal volume is distributed to lung CO2 diffuses 20x more readily bases where compliance is greater (alveolar surface area) than O2 so impairment MOSTLY affects O2 - Tidal volume: the volume of air moved with 1 breath, normal is approximately 500mL but dependent on height (ideal body weight) - Pneumonia and fluid overload affect the bases more = increased impairment of gas exchange; larger impact on ventilation and oxygenation - This is why position impacts both ventilation and respiration - In critical care, we can prone patients to make better use of posterior, basal alveoli CO2 diffuses 20x more readily than O2 Hypoxemia is more common Slide 7 4) Transport/Distribution The movement of oxygenated blood through the body, gas exchange with cells and return of CO2 to the lungs Dependent on: Circulating blood volume Oxygen carrying capacity Vascular tone Cardiac output (stroke volume x heart rate) Slide 8 How gases are transported in the blood 1. Hemoglobin: o SaO2: Arterial oxygen saturation Percentage measurement of how much Hg is saturated with oxygen Normal >94% o SpO2: Arterial oxygen saturation This is the Sa02 measured by the pulse oximeter measured by pulse oximetry 2. Dissociated in serum: o PaO2: Partial pressure of oxygen in arterial blood The pressure exerted on the vessel walls by a gas (in this case oxygen). The measure of actual oxygen content in the blood – dissolved in the blood. Reflects how well oxygen is able to move from lungs to the blood Normal: 75-100mmHg Slide 9 Oxyhemeglobin dissociation curve reflects the relationship between Oxyhemoglobin-Dissociation Oxygen is kept in a dynamic Pa02 and Sa02 balance between bound to hemoglobin for transport through the body and Important for understanding how blood carries and release oxygen: dissociated in the serum for use by the tissues The relationship between Sa02 how readily Hg acquires and releases oxygen molecules and Pa02 is oxyhemoglobin dissociation curve Important for understanding why tissue oxygenation may be Different factors can shift this curve to have more affinity for hemoglobin (shift to the left) or be more dissociated (shift to affected and how to treat this to prevent/treat shock states. the right) An Sp02 of 90% = Pa02 of about 60mmHg Douglas College Human Anatomy & Physiology I. Douglas College, New Westminster BC. Aug 31, 2017. https://pressbooks.bccampus.ca/dcbiol11031109 Factors that can cause a shift in the curve: CADET: C02, Acid, 2-3DPG, Exercise, Temperature Right shift: decreased Hg affinity for oxygen = increased Pa02 as more oxygen released from Hg into blood for transfer to tissues - Increased C02, Increased Acid (low pH), increased 2-3 DPG (liberates O2 from Hg), Exercise, increased temp - States where oxygen demand goes up - A shift too far right can result in ineffective transport throughout the body Left shift: increased Hg affinity for oxygen = decreased Pa02 as oxygen is more tightly held by Hg - Decreased C02, decreased acid (high pH), decreased 2-3 DPG, carbon monoxide (more affinity to Hg than 02, so less oxygen available to the tissues), decreased temperature - A shift too far left can result in less O2 readily available to tissues Slide 10 Blood Components Associated with Causes of reduced Hg: Oxygenation - Anemia: i.e. bleeding, decreased iron, disease states Hemoglobin: iron-rich protein in RBC’s carries oxygen to tissues - Malnutrition, fluid overload – male: 140-165 g/L* female: 120-150 g/L* High Hg: Hematocrit (packed cell volume): percentage of RBC’s in a volume of whole blood - polycythemia, blood transfusion – male: 0.40-0.50* – female: 0.37-0.47* Low Hct: * [Hannon, Pooler, & Porth, 2010, p. 1533] - bleeding, RBC destruction (sickle cell, big spleen), malnutrition High Hct: - Dehydration (blood is more concentrated), decreased oxygen availability (more RBC’s produced to try and increase 02 carrying capacity, i.e. altitude), genetics, erythrocytosis (overproduction of RBC’s by red marrow – thick blood). - A correlated low hemoglobin and hematocrit results in a deficiency in the capability to transport O2 to the distal tissues, leading to hypoxia which leads to anerobic metabolism and eventually cell death. Slide 11 5) Cellular Respiration The cellular use of oxygen in aerobic metabolism to create ATP with CO2 byproducts Different factors can increase cellular demand o Exercise, stress, infection, drugs…. When the cardiopulmonary system is unable to keep up with the metabolic demands of the tissues, we switch from aerobic to anaerobic metabolism (inefficient with lactic acid byproducts) Slide 12 Objective measures of breathlessness: Dyspnea - How long can the patient speak without pausing: A subjective sensation of breathlessness or discomfort breathing, at rest or with exertion. Precipitated by a combination of respiratory muscle - Mild = sentences involvement, chemoreceptors, mechanical receptors and innervation - Moderate = phrases Centered around a decrease in pO2, decrease in pCO2, and/or perceived effort - Severe = words Orthopnea: Dyspnea when lying down Paroxysmal nocturnal dyspnea: Awakening at night with a sense of suffocation Slide 13 Respiratory failure is not a disease – it is condition that is the result Respiratory Failure one or more diseases. Occurs when both gas exchanging functions are inadequate – Failure to oxygenate (O2) vs. failure to ventilate (C02) vs. both – Deficiency in one leads to deficiency in the other = Disease states will produce either: failure Insufficient oxygen supplied to blood - Failure to oxygenate: can’t get enough oxygen (i.e. high altitude, – Oxygen failure = HYPOXEMIC = lack of oxygen pulmonary emboli) Inadequate carbon dioxide is removed from lungs – Ventilatory failure = HYPERCAPNIC = too much C02 - Cardiac issues (failure to pump blood) - Chest wall issues (trauma – inability to move chest wall) - Neuro: Mysathenia gravis, MS, ALS, muscular dystrophy - Failure to ventilate: can’t remove C02 (i.e. oversedation, obesity, COPD) - Asthma, cystic fibrosis, head injury, spinal injury. Respiratory failure occurs when both of these are present: one may lead to the other if not managed. Slide 14 Room air Fi02 = 21% (0.21) Hypoxemic Respiratory Failure Defined as: Pa02 60% Hypoxemia will lead to hypoxia Hypoxemia - Deficient arterial blood oxygen inadequate 02 transfer between alveoli and pulmonary Multiple causes dependent the system involved, see table 70-4 in capillaries Hypoxia - Decrease in tissue oxygenation Lewis. – may also be caused by alterations in other systems – Hypoxia can occur anywhere in body – See Lewis, Table 70-4, pp.1995 3rd ed, 1787 4th ed Slide 15 Causes of Hypoxemic Respiratory Failure 1. Ventilation-perfusion (V/Q) ratio: normal is 0.8:1 - normal conditions: 4L of air in respiratory tract, 5L of blood in capillaries every minute = 0.8:1 - a number higher or lower = V:Q mismatch - Ratio of blood flow to fresh air reaching alveoli 2. Diffusion limitation – Alveolar-capillary membrane thickened or destroyed 3. Alveolar hypoventilation – Also decreased inspired oxygen Slide 16 1. Ventilation-perfusion abnormalities Impaired ventilation = fluid buildup in the aveoli, secretions blocking (McCance & Heuther, 2006) airflow, thickening of airway walls Impaired perfusion = emboli, hypotension V/Q exists at an optimal ratio. V/Q mismatch occurs when factors create either: 1. not enough ventilation 2. not enough perfusion Slide 17 Anatomic dead space: conduction airways (nose, trachea) that do Dead Air Space (High V/Q) Refers to areas of not come into contact with alveoli the lung that are ventilated but in - can also have equipment dead space, i.e. an endotracheal which no gas exchange occurs tube Anatomic dead space – mostly Alveolar dead space: alveoli that are ventilated but not perfused; no normal gas exchange occurs. Alveolar Dead space – caused by lung disease - seen in patients with lung disease, i.e. emphysema (alveoli empty slowly, C02 retained longer, preventing gas exchange) Slide 18 Anatomical shunt = blood supply to the lungs via the bronchial Shunt (Low V/Q) arteries is returned via the pulmonary veins without passing through Blood that moves from the right to left side of the circulation without being oxygenated. the pulmonary capillaries; bypasses gas exchange: Anatomical Shunt Blood passes through anatomical channel in heart - causes: pneumonia, pulmonary edema, ARDS, atelectasis, and bypasses the lungs Intrapulmonary Shunt pulmonary arteriovenous communication (abnormal connection of When blood flows through pulmonary capillaries the pulmonary arteries and veins without gas exchange Slide 19 A: fluid in alveoli Ventilation-Perfusion Abnormalities Secretions Mucous Plug B: mucous plug (affecting airway walls) C: normal D: emboli (decreased blood flow) E: shunt: ventilation to the alveoli, but no perfusion; could also be a collapsed alveoli with perfusion Slide 20 Thickened capillary membrane: 2. Diffusion Limitation - Gas exchange across the alveolar/capillary membrane is compromised (pulmonary hypertension (causes wall thickening), ABNORMAL inflammation: infection, asthma,... ) - Hypoxemia is worse or more likely with exercise: oxygen NORMAL demands go up, but it takes longer for gas exchange to occur. - Blood ‘transit time’ increased: RBC in lungs for shorter time meaning less time for diffusion (tachycardia) Slide 21 Restrictive lung disease: pulmonary fibrosis 3. Alveolar Hypoventilation CNS disease: strokes, trauma, cancer A decrease in ventilation – increased PaCO2 and then decreased PaO2 Chest wall dysfunction: muscle injury (splinting), fractures, nerve – Oxygen has less ‘room’ to diffuse Due to: entrapment, trauma, costochondritis,... – restrictive lung disease – CNS disease – chest wall dysfunction Is a primary mechanism of hypercapneic respiratory failure – mentioned here because hypoxemia is induced. Slide 22 Manifestations of Hypoxemia→Hypoxia Respiratory system Non-specific Tachypnea (rate >20/min) Neurological changes, Dyspnea agitation→coma (late) Prolonged expiration Tachycardia, Intercostal muscle retraction; hypertension→ use of accessory muscles; dysrhythmias , ↓ BP orthopnea Skin cool, clammy, ↓ SpO2 (45mmHg + pH