Exam 2 Study Guide PDF

Respiratory Inflammation & Infection Alveoli- gas exchange takes place Lungs Right – 3 lobes (Upper, Middle, & Lower) o Increased risk for aspiration Left – Upper & lower lobes Inside the Bronchioles Mucociliary Apparatus o Cellular mechanism inside th...

Respiratory Inflammation & Infection Alveoli- gas exchange takes place Lungs Right – 3 lobes (Upper, Middle, & Lower) o Increased risk for aspiration Left – Upper & lower lobes Inside the Bronchioles Mucociliary Apparatus o Cellular mechanism inside the bronchioles o Ciliated pseudostratified epithelial cells o Goblet Cells What can affect this? Respiratory infections & smoking What happens during gas exchange? Air is inhaled, oxygen moves across the membrane into the blood, & carbon dioxide is removed from the blood so that it is exhaled. Oxyhemoglobin- Hemoglobin with oxygen attached SaO2 - % of saturation of hemoglobin with oxygen o Measured with pulse oximeter Erythropoietin – stimulated RBC production Kidneys secrete erythropoietin in response to hypoxia- any condition that causes hypoxia will stimulate secretion of erythropoietin (heart disease, lung disease, changes in atmospheric pressure) Erythropoietin responds by stimulating the bone marrow to produce more RBCs which will carry more oxygen to tissues Diaphragm- separates the thoracic and abdominal cavity Moves up during inspiration Moves down during expiration Phrenic nerve- originates at C4 Spinal cord injuries at or above C4 - cause motor and sensory conduction to diaphragm to be interrupted. o Causes the patient to stop breathing o Patient will not have spontaneous respirations o Patient will require rescue breathing & eventually mechanical ventilation Respiratory muscles o External Intercostals o Internal Intercostals o Sternocleidomastoids o Abdominals o Retractions (Respiratory Distress) o Use of Intercostal muscles to breathe Ventilation = Air (Oxygen & CO2) Perfusion = Blood (movement into & out of lung capillary beds) V-Q Ratio – Ratio of air reaching alveoli compared to the amount of blood reaching the alveoli V-Q Imbalance – Lungs have a compensatory mechanism that will attempt to match blood flow & ventilation. o When there is little ventilation, pulmonary arterial vessels constrict, leading to redistribution of blood flow to better ventilated areas of the lung Shunt- area with no ventilation Dead Space- area with no perfusion V-Q Mismatching- Occurs when air cannot flow into an alveolus or blood flow around an alveolus is altered Pulmonary Embolism (Common cause of V-Q mismatching Embolism/clot – prevents blood flow to the alveoli, & gas exchange cannot take place Hypoxia stimulates pulmonary arterial vasoconstriction Chronic hypoxia > chronic pulmonary vasoconstriction > pulmonary hypertension Controllers Behind Breathing Central Chemoreceptors o Located in the Medulla o Responsible for CO2 & pH  o Ex. Hypercapnia or acidosis stimulate increased ventilation Peripheral Chemoreceptors o Located in the Aorta & Carotids o Primary Signal: Decreased arterial oxygen o Hypoxic Drive Hypercapnia = increased CO2 Hypoxic drive = when decreased level of oxygen in the blood is sensed by peripheral chemoreceptors, which stimulates respirations What Stimulates Breathing? Hypercapnia o Prolonged & Chronic Hypercapnia Hypercapnia stimulates the central respiratory center in the medulla & stimulates breathing. Prolonged or Chronic hypercapnia- central chemoreceptors become less responsive to the high CO2 levels. Peripheral chemoreceptors of low O2 takes over as the stimulus of respirations. Respiratory Terminology Dyspnea – shortness of breath o Can be cardiac or pulmonary related Orthopnea – sensation of dyspnea when lying flat (common indicator of heart failure; patients may describe as “feels like I’m drowning”) Cough- Mechanical or chemical stimulation of bronchial tree o Non-productive or productive o Expectoration Hemoptysis- Sputum containing blood, usually bright red color Atelectasis- collapse of small number of alveoli o Compressive force or obstruction can cause this o Common post-operatively o High risk of developing pneumonia Incentive Spirometry- device used to help people breathe in a way that strengthens & expands their lungs Hypoxia- Insufficient oxygen for needs o Caused by many conditions (Pulmonary, cardiac, & carbon monoxide) Hypoxemia- Insufficient oxygen in blood Respiratory Failure- Failure to oxygenate blood or remove CO2 (carbon dioxide) o Hypoxemic – PaO2 less than 60 mm Hg o Causes: pulmonary edema, PE, pneumonia, or pneumothorax o Hypercapnic – PaO2 greater than 50 mm Hg o Causes: COPD & asthma Restrictive & Obstructive Pulmonary Disorders Takes place in the bronchioles- smooth muscle in bronchi & bronchioles o Controls diameter of airway & air flow Innervated by the autonomic nervous system o Sympathetic- Bronchodilation o Parasympathetic- Bronchoconstriction What stimulates bronchoconstriction? o Inflammatory mediators (leukotrienes & histamine) How do lungs go back to their original shape? o Compliance- flexibility of lungs Compliance is reduced by illness that makes the lungs more stiff, increasing o May also be reduced by inflammatory conditions (pulmonary fibrosis) WOB (work of breathing)- takes more effort to breathe (seen in bronchitis & pneumonia when lungs are congested with fluid) What protects the lungs? o Pleural membrane- lines the chest cavity & envelops lungs Pleural Space- “vacuum” Negative intrathoracic pressure. No air or fluid in the space Pleural Effusion- fluid in the pleural space. Adds pressure to the lung tissues, causing lung collapse. Pneumothorax (RESTRICTIVE RESPIRATORY DISORDER)  o Collapsed lung o Air in the pleural cavity causing a collapse of part or whole lobe of the lung tissue Primary Spontaneous- no preceding trauma or underlying lung disease o Tall skinny white boy Secondary Spontaneous- underlying pathological process in the lungs (emphysema, TB, CF) Traumatic Pneumothorax- Penetrating wound of the thoracic cage & pleural membrane. Opening in the pleural cavity & the outside atmosphere. o Ex. GSW (gun shot wound) & stab wound o Treatment: Chest tube Tension Pneumothorax- Escalating buildup of air within lung compresses the lung, bronchioles, cardiac structure, vena cava. o Closed penetrating wound o EMERGENT o Treatment: Needle decompression Iatrogenic Pneumothorax- Complication of medical/surgical procedures o Most commonly results from transthoracic needle aspiration, thoracentesis, pleural biopsy, central line insertion, PPV Treatment for small pneumothorax: High flow oxygen Asthma (OBSTRUCTIVE RESPIRATORY DISORDER) Asthma- Hyperactive airway disease o Airway- CONSTRICTION o Result of attacks: bronchiole changes With each attack, remodeling & inflammatory changes develop in bronchioles Causes of Asthma o Allergy (most common) o Allergens: Exhaust fumes, perfumes, pollen, grasses, flowers, dust, cigarette smoke, animal dander, molds, & spores o Occupational exposure o Employment settings o Farming, painting, construction, landscaping, & janitorial work o Viral infections (common in children) o Cause bronchospasm & copius mucus production  o Exercise- provokes loss of heat & water from the tracheobronchial tree: particularly exaggerated by cold air Involves a link in genetic & environmental factors Patho behind Asthma What is happening? o Bronchoconstriction, bronchial edema, viscous mucus, thickened bronchial basement membrane o Airway remodeling Key Players o T cells, Immunoglobulin E (IgE), leukotrienes, histamine, & eosinophils S/S: dyspnea, wheezing, cough, chest tightness, chest pain Treatment to prevent exacerbations: avoid triggers Maintenance meds: LABA (long acting adrenergic beta-2 agonist), ICS (inhaled corticosteroid), LAMA (long acting muscarinic agent) Acid- Base Imbalance Acid gives hydrogen ions Base receives hydrogen ions Enzyme for volatile acid: carbonic anhydrase in red blood cells Protein – largest buffering system in the body Ex: Hemoglobin Phosphate – Regulate intracellular pH Carbonic acid-bicarbonate buffering – Involves carbon dioxide, carbonic acid, hydrogen ions, bicarbonate. Lungs & kidneys utilize this system to help maintain blood pH HCO3- = weak base H+ = strong acid Carbonic anhydrase: enzyme in erythrocytes Lungs & kidneys: help regulate blood pH Lungs Respond the FASTEST Response cannot be maintained indefinitely Kidneys Takes longer to compensate Response is maintained for longer Long term regulators of pH pH too Acidic: increase ventilation (FASTER) pH too Basic: decrease ventilation (SLOWER) The kidneys will compensate by regulating the excretion or reabsorption of the carbonic acid, bicarbonate system. If pH is too low (acidic), kidneys will excrete more acid (hydrogen) & reabsorb more base (HCO3) this decreases the acids present If pH is too low (alkalotic), kidneys will reabsorb more hydrogen & excrete more HCO3 which will lower pH PCO2: 35-45 mm Hg Blood pH: 7.35-7.45 PO2: 90 – 100 mm Hg HCO3: 22-26 mEq/L SaO2: 95% - 100% Acidosis: blood pH less than 7.35 Alkalosis: blood pH greater than 7.45 Respiratory Abnormality: Carbon Dioxide (CO2) pH & CO2 levels will be moving in the OPPOSITE direction Metabolic Abnormality: Bicarbonate (HCO3-) pH & HCO3- levels will be moving in the SAME direction Respiratory Acidosis pH less than 7.35 CO2 greater than 45 mm Hg  Lungs unable to remove sufficient CO2 HYPOVENTILATION o Compensation: Kidneys retain bicarbonate & excrete hydrogen ions Respiratory Alkalosis pH greater than 7.45 PCO2 less than 35 mm Hg Lungs blow off too much CO2 HYPERVENTILATION o Compensation: Kidney reabsorbs H+, excretes HCO3- Metabolic Acidosis pH less than 7.35 CO2 is normal to low Due to excess of acid NOT related to CO2 Compensation o Lungs: increase ventilation (Kussmaul’s breathing) o Kidneys: excrete H+, reabsorb HCO3- Metabolic Alkalosis pH greater than 7.45 CO2 is normal to high Due to an excess LOSS of acid NOT related to CO2 Increase in bicarbonate levels Compensation o Lungs: decreases ventilation to increase CO2 o Kidneys: excrete HCO3- & retain H+ Red Blood Cells Mean Corpuscular Volume Size of RBC o Macrocytic, microcytic, normocytic Mean Corpuscular Hemoglobin Average amount of hemoglobin in average RBC Color of RBC o Hyperchromic, normochromic, hypochromic Mean Corpuscular Hemoglobin Concentration Average concentration of hemoglobin in a given volume of RBCs Acute Blood Loss- normal in shape & less red blood cells Sudden drop in the red blood cells caused by hemorrhage  Normocytic normochromic anemia Chronic Blood Loss Slow gradual blood loss Iron deficiency anemia Hemolytic Anemia Destruction is faster than production Acute or chronic, intravascular or extravascular Substances needed Protein, Iron, Vitamin B12, Folic Acid Spleen: removes aged, lysed, dead RBCs A patient with a spleen injury will have bleeding on the inside Most of iron is recycled when old RBCs are broken down in the spleen Kidney response to hypoxia: releases erythropoietin > Erythropoietin stimulates bone marrow to produce RBCs > Increase in number of RBCs > Increase in oxygen reversing hypoxia Hemoglobinopathy- Hgb structure is abnormal because of a genetic mutation Ex: Sickle cell anemia – mutation in one of the genes that directs the synthesis of the beta polypeptide chains. Due to this mutation, individuals with sickle cell have a different Hgb called Hgb S. Sickle cell blood cells have a “C” shape. Hyperbilirubinemia – jaundice Jaundice – yellowing of the skin & eyes Transferrin – transports (transfer) iron Anemia – lack of oxygen to tissues