Alterations in Oxygenation and Blood Flow

Flashcards covering key vocabulary and concepts related to alterations in oxygenation and blood flow.

pH (Normal Arterial Blood Gas Values)

7.35-7.45

PCO2 (Normal Arterial Blood Gas Values)

35-45 mm Hg

PO2 (Normal Arterial Blood Gas Values)

80-100 mm Hg

HCO3 (Normal Arterial Blood Gas Values)

22-28 mEq/L

SaO2 (Normal Arterial Blood Gas Values)

95-100%

Hypoventilation

Insufficient air delivered to alveoli, leading to increased PaCO2 (>45 mm Hg) and hypoxemia.

Etiology of Hypoventilation

Drugs (morphine, barbiturates), obesity, myasthenia gravis, obstructive sleep apnea, chest wall damage, paralysis of respiratory mm, pain R/T SX of thorax or abd.

Hyperventilation

Increased air entering alveoli, leading to hypocapnia (PaCO2 <35 mmHg).

Etiology of Hyperventilation

Pain, fever, anxiety, obstructive and restrictive lung disease, sepsis, brainstem injury, high altitude.

Hypoxemia

Deficient levels of blood O2, measured by low arterial O2 concentration/HGB saturation.

Hypoxia

Decrease in tissue oxygenation due to low blood flow or PaO2.

Hypoxic Hypoxia

Low PaO2 despite normal O2-carrying capacity; causes include high altitude, hypoventilation, airway obstruction.

Anemic Hypoxia

Decrease in O2-carrying capacity.

Circulatory Hypoxia

Normal O2-carrying capacity, but reduced blood flow (e.g., shock, cardiac arrest, severe blood loss, congestive HF).

Histotoxic Hypoxia

Decreased O2 carrying capacity from a toxic substance (e.g., cyanide poisoning).

Vital Capacity

Total volume of gas exhaled during maximal expiration (~4.8 L), includes respiratory reserve volume, tidal volume, and expiratory volume.

Total Lung Capacity

Amount of gas contained in lungs at maximal inspiration (~6 L).

Forced Expiratory Flow Rate (FEF25, FEF50, FEF75)

Volume of air forcibly exhaled per unit time (L/sec or L/min) at 25%, 50%, and 75% of forced vital capacity (FVC).

Obstructive Pulmonary Disorders

Difficulty exhaling; increased airway resistance, shortness of breath & coughing. PFT shows increased residual volume. FEV1/FVC ratio is impaired (70-80% of normal).

Restrictive Pulmonary Disorders

Difficulty inhaling; hard to expand the lungs. FEV1 and FVC equally impaired, ratio is normal. Decreased inspiratory residual volume and inspiratory capacity.

Acute Bronchitis

Acute inflammation of the trachea + bronchi.

Etiology of Acute Bronchitis

Viral or nonviral (coronavirus), heat, smoke inhalation, inhalation of irritant chemicals, & allergic reactions.

Pathogenesis of Acute Bronchitis

Airway becomes inflamed + narrowed from capillary dilation, swelling from exudation of fluid, infiltration w/ inflammatory cells, ↑ mucus production, loss of ciliary fxn, + loss of portions of the ciliated epithelium.

Hallmark of Acute Bronchitis

Recent onset of cough.

Clinical Manifestations of Acute Bronchitis

Mild self-limiting, productive/nonproductive cough, low-grade fever, substernal chest discomfort, sore throat, postnasal drip, fatigue.

Chronic Bronchitis

Type B COPD, dx by a chronic or recurrent productive cough of >3 months duration + occurring >2+ successive yrs. Airway obstruction is persistent + irreversible when paired w/emphysema, hypersecretion of mucus.

Risk Factors for Chronic Bronchitis

Cigarette smoking, repeated airway infections, overweight, genetic predisposition, inhalation of physical or chemical irritants. GREATEST RISK: those >30-40 years old, more common in women.

Clinical Manifestations of Chronic Bronchitis

Excess body fluids (edema/plethora), chronic cough, shortness of breath on exertion, increased sputum, cyanosis (late sign).

Pathogenesis of Chronic Bronchitis

Chronic inflammation + swelling of the bronchial mucasa resulting in scarring, interleukin-8 levels recruit neutrophil activation, CD8 T-lymphocyte elevated, extend into surrounding alveoli prevents proper oxygenation + potentiates airway obstruction, hyperplasia + hypertrophy of bronchial mucous gland /goblet cells leads to ↑ mucus production w/ farmation of mucus plugs from the combination of mucus + purulent exudate.

Emphysema

Type A COPD; destructive changes of the alveolar walls + abnormal enlargement of the distal air sacs + without fibrosis. Assoc. w/ chronic bronchitis + damage is irreversible.

Risk Factors for Emphysema

Smoking >70 packs/year, air pollution, certain occupations (welding, mining, working with or near asbestos), α₁-antitrypsin deficiency.

Pathogenesis of Emphysema

Loss of surface area, release of proteolytic enzymes from neutrophils + macrophages leading to alveolar damage. α₁-antitrypsin deficiency causes alveolar wall destruction smoking causes alveolar damage.

Clinical Manifestations of Emphysema

Progressive, exertional dyspnea, use of accessory muscles, pursed-lip breathing, cough (minimal or absent), digital clubbing of fingernails, barrel chest, thin, wasted individual hunched forward. Decreased breath sounds, lack of crackles + rhonchi, prolonged expiration, hyperresonance.

Sarcoidosis

Acute or chronic systemic disease of unknown cause commonly affecting lungs + lymph nodes.

Pathogenesis of Sarcoidosis

Development of multiple uniform, nancaeseating epithelioid granulamas, abnormal T-cell function is noted.

Clinical Manifestations of Sarcoidosis

Malaise, fatigue, weight loss, fever, dyspnea of insidious onset, dry, non productive cough, erythema nodosum, hepatosplenomegaly, lymphadenopathy.

Hypersensitive Pneumonitis

Extrinsic allergic alveolitis; restrictive + occupational disease, predominant in nonsmokers.

Pathogenesis of Hypersensitive Pneumonitis

Causitive antigen combines with serum antibody in alveolar walls, leading to a type III hypersensitivity ran.

Clinical Manifestations of Acute Hypersensitive Pneumonitis

S/s start 4-6 hr after exposure, resolve in 18-24hr. Chills, sweating, shivering, myalgias, nausea, malaise, lethargy, headache, dyspnea at rest, dry cough, tachypnea, chest discomfort, cyanosis (late), crackles in lung bases.

Pneumothorax

Air enters into pleural space. Can be spontaneous, primary, secondary, or tension.

Pathogenesis of Primary Spontaneous Pneumothorax

Occurs mainly in tall, thin men btwn 20-40 w/out underlying disease factors. Results from the rupture of small subpleural blebs in the apices-tops of lungs.

Pathogenesis of Secondary Pneumothorax

Occurs as a result of complications from pre-existing pulmonary disease.

Tension Pneumothorax

Traumatic in origin, medical emergency! Air enters pleural space during inspiration but cannot escape during expiration. Lung on the ipsilateral (same) side collapses.

Clinical Manifestations of Pneumothorax

Small pneumothoraces (<20%) are usually not detectable on physical exam. Tachycardia, decreased or absent breath sounds on affected side, hyperresonance, sudden chest pain on affected side, dyspnea.

Pleural Effusion

Pathologic collection of fluid or pus in pleural cavity as a result of another disease process.

Transudative Pleural Effusion

Caused by increased hydrostatic or oncotic pressure; assoc. w/ HF or other edematous states, such as cirrhosis w/ ascites.

Exudative Pleural Effusion

Increased production of fluid as a result of increased permeability of the pleural membrane (inflammation) or impaired lymphatic drainage; assoc. w/ malignancies, infections (esp. pneumonia, PE, sarcoidosis.

Empyema

Results from infection in pleural space.

Clinical Manifestations of Pleural Effusion

May be asymptomatic with <300 mL of fluid in pleural cavity, dyspnea, decreased chest wall movement, pleuritic pain, dry cough, absence of breath sounds, dullness to percussion, decreased tactile fremitus over affected area, contralateral tracheal shift.

Kyphoscoliosis

Bone deformity of the chest wall resulting from kyphosis (hunchback appearance; posterior curvature deformity), scoliosis (lateral curvature deformity).

Clinical Manifestations of Kyphoscoliosis

Dyspnea an exertion, rapid, shallow breathing, chest wall deformity, hypoxemia, CO2 retention (late).

Ankylosing Spondylitis

Characterized by chronic inflammation a) the site of ligamentous insertion into the spine or sacroiliac joints.

Clinical Manifestations of Ankylosing Spondylitis

Low- to mid back pain & stiffness increased w/ prolong rest, restrictive lung dysfunction, rib cage movement reduction, chest wall atrophy, breathing by excursion of the diaphragm w/ rib cage immobilization.

Obesity and Pulmonary Issues

Associated w/ hypoventilation, reduced ventilatory drive & work of breathing, increased abdominal size can force the abdominal contents upward into the chest cavity, thus decrease lung expansion + diaphragmatic shortening, obstructive sleep apnea.

Pneumonia

An inflammatory reaction in the alveoli + interstitium of the lung, usually caused by infectious agent (aspiration of oropharyngeal secretions, inhalation of contaminents, contamination from the systemic circulation).

Clinical Manifestations of Pneumonia

Crackles (rales) and bronchial breath sounds over affected lung tissue, chills, fever, cough, purulent sputum.

Pulmonary Tuberculosis

Infection of the lungs and lymph nodes caused by Mycobacterium tuberculosis.

Pathogenesis of Pulmonary Tuberculosis

Inhalation of small droplets containing bacterial. T-cells & macrophages surround organisms in granulamas.

Clinical Manifestations of Pulmonary Tuberculosis

History of contact with infected person, low-grade fever, chronic cough, night sweats, hemoptysis, fatigue, weight loss, malaise, anorexia, apical crackles.

Thrombus

Blood clots that composed of aggregated platelets, clotting factors, & fibrin that adhere to vessel walls.

Embolus

A collection of material that forms a clot within the bloodstream.

Vasospasm

Sudden constriction of arterial smooth muscle that results in an obstruction to flow.

Valvular Incompetence

Intimal folds of veins that form the valves can be damaged, interfering w/ the effective flow of blood through a portion of the venous system.

Arteriosclerosis

Thickening + hardening of arteries.

Atherosclerosis

Hardening of the arteries in which plaque builds up inside the arteries. Plaque consists of cholesterol, fatty substances, cellular waste products, calcium, & fibrin.

Aneurysms

Localized dilation of an arterial wall.

Arteriovenous Fistulas

Abnormal communication btwn arteries & veins.

Lymphedema

Obstruction of lymphatic flow.

Arteriosclerosis

"Hardening of the arteries", diffuse process whereby the muscle fibers & endothelial lining of the walls of small arteries + arterioles become thickened.

Atherosclerosis

Affects intima of large medium-sized arteries. Changes consist of the accumulation of lipids, calcium, blood components, carbs, & fibrous tissue.

Hypertension

Primary: Does not have an identifiable cause; idiopathic and has modifiable/ non-modifiable risk factors. Secondary: Occurs secondary to another identifiable cause.

Hypotension

An ineffective response to position change may be associated w/ problems within the nervous system

Raynaud's Syndrome

An extreme vasoconstriction producing cessation of flow to the fingers & toes.

Thromboangitis Obliterans (Buerger's Disease)

Rare inflammatory condition affecting both small & medium-size arteries+ veins of the upper & lower extremities, producing varying degrees of destruction.

Varicose Veins

Superficial, darkened, raised, and tortuous veins.

Deep Vein Thrombosis

Thrombus formation, typically in the legs.

Chronic Venous Insufficiency

Results when valvular incompetence involves the deep veins.

Thrombocytopenia

Common cause of generalized bleeding that decreases platelets.

Hemophilia

Genetic disorder - X-linked recessive with factor VIII or IX deficiency or abnormal function.

Von Willebrand Disease

Autosomal dominant disorder of factor VIII carrier protein & platelet disorder.

Lymphedema

Normal flow of lymph is obstructed. Commonly caused by surgical removal of lymph nodes

Coronary Heart Disease

Characterized by insufficient delivery of oxygenated blood to the myocardium (ischemia) because of atherosclerotic coronary arteries

Angina

Chest pain associated with intermittent myocardial ischemia

Classifications of Angina

Stable, Prinzmetal Variant, Unstable

Acute Coronary Syndrome

Unstable angina + myocardial infarction

Diagnosis of Myocardial Infarction

S/S + ECG changes +Elevations in the levels of specific marker proteins in the blood MB band of creatine kinase (CK-MB) +Troponin elevated

Stenosis

Failure of a valve to open completely.

Regurgitation

Inability of a valve to close completely

Mitral Valve Stenosis

The flow of blood from the left atrium into the left ventricle is impaired, leads to potential pulmonary issues

Mitral Valve Regurgitation

Backflow of blood from the left ventricle to the left atrium during ventricular systole

Mitral Valve Prolapse

Mitral valve balloons into the left atrium during ventricular systole

Aortic Stenosis

Results in obstruction to aortic outflow from left ventricle into aorta during systole

Atrial Septal Defect

Results from an incompetent aortic valve that allows blood to leak back from the aorta into the left ventricle during diastole

Rheumatic Heart Disease

Complication of rheumatic fever

Jones Criteria

Used to assist in diagnosing Rheumatic Heart Disease. Divided into major and minor criteria.

Infective Endocarditis

Invasion + colonization of endocardial structures by microorganisms w/ resulting inflammation

Pericardial Effusion

Accumulation of fluid in the pericardial sac

Cardiac Tamponade

External compression of the heart chambers such that filling is impaired

Pericarditis

Inflammation of pericardium

Stages of Pericarditis

Acute vs. Chronic stages