pathophysiology - pulmonology

what makes up the upper airway

nasal passages to trachea

what is the function of the upper airway

has mucous secreting goblets and cilia to trap/sweep foreign particles

what is the lower airway

trachea to lung

what is the function of the lower airway

epith capable of relaxing and dilating to transport air to alveoli

what do the alveoli do

diffuse oxygen and carbon dioxide

what does depth require for pressure

high to low pressure gradiant, and tissue compliance

what parts does ventilation require

CNS, musculoskeleton system, oropharynx, airways

what parts does diffusion of gases require

alveli and capillaries

what parts does perfusion of vessels/tissues require

capillaries and circulation

what parts of the central nervous system are required for ventilation

respiratory center in medulla (sense CO2), chemoreceptors in medulla/peripheral circulation (sense 02), phrenic nerve (diaphragm)

what is part of musculoskelatal system for ventilation

diaphragm, intercoastal/accessory muscles, rib cage

what is atmospheric pressure

intrapleural pressure

what is hypovenilation cause

increase in CO2, acidosis, hypercapnia

what does hyperventilation cause

decrease in CO2, alkalosis, hypocapnia

what are the parts of alveoli for diffusion

acinus (gas exchange structure), surfactant (reduces surface tension), pores of khan

what is the vetilation of alveoli dependant on

depth of respirations, which is influenced by respiratory rate

what do pulmonary arteries do in response to high CO2

constrict (reduced cardiac output —> reduced perfusion)

what do pulmonary arterioles do in response to low CO2

dilate (increased cardiac output —> increased perfusion)

what is dead space + ex

adequate ventilation with diminished perfusion, ex. pulmonary embolus

what is a shunt + ex

adequate perfusion with diminished ventilation, ex. pnuemonia

what does V/Q mismatch result in

decrease in oxygenation, ex. hypoxemia

what is acute respiratory failure

life threatening changes in arterial blood gases and acid/base

what is chronic respiratory failure

derangements in ABG, compensatory mechanisms evident

what are the two main mechanisms of respriatory failure

lung failure when poor gas exchange makes hypoxemia, pump failure: volume of air moving in/out is inadequate, manifested by hypercapnia

in acute respiratory failure, what is hypoxemia respiratory failure

gas exchange problem, PaO2 lower than 60mmgHg, normal/low PaCO2, most common RF, fluid-filling/collapse of alveoli, due to V/Q mismatch (barrier to diffusion), must oxygenate patient

examples of hypoxemic acute respiratory failure

pulmonary edema, pneumonia, pulmonary hemorrhage

for acute respiratory failure, what is hypercapnia respiratory failure

ventilation problem, PaCO2 higher than 50mmHg, respiratory acidosis, due to alveolar hypoventilation, mostly from drug overdose, neuromuscular disease, chest wall abnormalities, severe obstructive diseases, must treat by ventilating patient

what are physiologic effects of hyoxemia

cerebral ischemia (lack of 02 to brain), tachycardia/arrhythmia, pulmonary HTN, renal dysfunction, organ infarction (lack of 02 to organs)

what are the V/Q mismatches for hypoxemic RF

shunt (pneumonia, atelectasis, asthma), dead space (pulmonry embolus), shunting/dead space (emphysema, chronic bronchitis, pleural effusions, pneumothorax)

what are diffusion abnormalities for hypoxemic RF

intersitital fibrosis (occupational lung Dz, drugs), collagen-vascular dz (scleroderma, SLE, rheumatoid lung), sarcoidosis

what are the physiologic effects of hypercapnia

shunt/secondarily decreased o2, acidosis, electrolyte imbalance, vasoconstriction of pulmonary vessels, vasodilation of cerebral vessels

what are the common symptoms of hypercapnia

fatigue, confusion, coma, anxiety, headaches, SOB, sweating

what are the symptoms of hypoxemia

tachycardia, restlessness, bradycardia, aniety, dyspnea

what is hypercapnic RF commonly from for decreased ventilation

CNS injury, sedative or narcotic overdose

respiratory distress symptoms/clinical presentation

tachypnea, accessory muscle use, adventitious breathing sounds (stridor, wheezing, rales), secretion prod (thick, discolored, hemoptysis), abnormal chest wall movement, cyanosis, tachycardia, confusion

respiratory distress diagnosis tools

physical exam, arterial blood gases, chest x-ray/CT, sputum, hemodynamic monitoring, blood tests (CBC)

in respiratory distress management, what are the five big steps

maintainence of adequate oxygenation, improvement of alveolar ventilation, treatment of underlying cause, nutrion/patient mobilization, continuous monitoring and evalution of treatment

what is part of maintaince of adequate oxygenation

oxygen administration, maintenence of adeuqate hemoglobin concentration, maintaince of adequate cardiac output

what is part of improvement of alveolar ventilation

maintenance of patient airway, assisting in mobilizing secretion, relief of bronchospasm, reduction of pulmonary congestion, mechanical ventilation

what is asthma

disease of inflammation, mediated by IgE response, leads to bronchospasm —> air trapping, can be acute/chronic

what is the pathophysiology of acute asthma exacerbations

airway obstruction, V/Q mismatch, hypoxemia, air trapping —> decreased ventilation, hypercapnia

asthma clinical manifestations

wheezing, chest tightness, dyspnea, accessory muscle, prolonged expiratory phase, cyanosis, cough, fatigue, tachypnea, tachycardia, pulus paradoxus

what is polus paradoxus

drop in systolic BP with inspiration

what is COPD characterized by

inflammation/structural damage to airway, progressive lung tissue degeneration, expiratory airway obstruction that doesnt fluctuate, not reversible

what does COPD progress to

respiratory failure from hypercapnia and hypoxia, cor pulmonale

what is the pathophysiology of chronic bronchitis

mucosal inflammation, mucosal gland hypertrophy + hyperplasia (mucus plugging from sputum), sm hypertrophy (thickening/narrowing of bronchial wall), V/Q mismatch (hypercapnia, pulmonary HTN + cor pulmonale), frequent respiratory infections

what is the main problem of emphysema

destruction of alveolar wall —> permanently inflated alveoli, genetic = protein deficiency, smoking = increased neutrophils

pathophysiology of emphysema

decrease alveolar SA, destruction of pulmonary capillaries —> decreased gas exchange, loss of elasticity, v/q mismtach (hypercapnia), pulmonary HTN + cor pulmonale, air trapping/residual volume, necrotic tissue

difference of chronic bronchitis and emphysema

chronic bronchitis = sputum, smoking, emphysema = old/thin, cluster of lemons, severe dyspnea

COPD management

avoid irritants/infections, vaccine, oxygen, bronchodilators, antibiotics/ventiation support, chest PT, education, lung resection

what is the clinical manifestation of sleep apnea

chronic hypoxia, pulmonary HTN, cor pulmonale

sleep apena treatment

CPAP