Clinical presentation of common pulmonary dieases

idiopathic pulmonary fibrosis pulmonary changes

reduced inspiratory capacity leading to accessory muscle hypertrophy, diminished diffusion from alveolar thickness (most patients on supplemental O2), pulmonary hypertension (scarring in alveoli can scar down capillaries)

clinical manifestations of pulmonary fibrosis

SOB, dry/hacking cough (oversensitization of cough reflex), rapid/shallow breathing, fatigue or malaise, unintended weightloss, clubbing (via chronic hypoxic state)

lab findings for pulmonary fibrosis

normal FEV1/FVC ratio from decreased FEV1 and FVC, low PaO2, low PaCO2, respiratory alkalosis is common (hyperventilating and not fixing the problem)

PT implications of pulmonary fibrosis

early identification improves morbidity, focus on peripheral conditioning to increase efficiency of O2 use

emphysema pulmonary changes

pathological accumulation of air (floppy lung), loss of elastic recoil resulting in airway collapse and air trapping, dynamic hyperinflation and diaphragm flattening, active effort needed for expiration, permanent enlargement/merging of alveoli reducing diffusion due to decreased surface area

emphysema can result in pockets of air such as

blebs or bullae - wasted air space with no gas exchange

bullae large enough can

compress healthy tissue and decrease ability to ventilate, or rupture and cause pneumothorax

clinical manifestations of emphysema

pink puffer - dyspnea (active exhaler and flattened diaphragm), unproductive cough, tachypnea (high rate with shallow volume to comp for poor diffusion), accessory muscles participating with respiration, pulmonary cachexia

pulmonary cachexia

disease driven loss of muscle mass rapidly via metabolic disturbance to fuel accessory muscles to sustain breathing

lab findings for emphysema

FEV1/FVC ratio <70% (takes longer to get air out), ABGs relatively normal via tachypnea

chronic bronchitis pulmonary changes

mucus inflammation and airflow obstruction, poor alveolar ventilation leads to hypoxemia leading to reflex vasoconstriction of pulmonary vessels, pulmonary HTN and R sided HF, RBC production stimulated due to low O2 at kidneys, patients on supplemental oxygen (to limit vasoconstriction and reverse polycythemia)

clinical manifestation of chronic bronchitis

blue bloater - productive cough, wheezing, peripheral edema (right sided HF), diminished respiratory drive (hypoventilation), cyanosis, recurrent infection (bacteria thrives in warm, wet and dark environment)

lab findings for chronic bronchitis

FEV1/FVC <70%, low PaO2, low PaCO2 (accumulated with low RR)

treatment of COPD

smoking cessation, pharmacologic management, oxygen therapy, airways clearance and exercise

PT implications for COPD

often sedentary and deconditioned, exercise can help in all areas and increase total VO2

during exercise with COPD patients, assess

oximetry (88% or above), HR, RR, BP, timing of meds and O2 for max effectiveness

strengthening respiratory muscles

many muscles of upper torso and shoulder girdle have respiratory function and help decrease work of breathing

pursed lip breathing

breathe through nose for 4 seconds and exhale through pursed lips for 6 seconds - increases volume of air going out to make more space for new air

resistance training has been shown to improve

muscle function and physical performance in patients with chronic respiratory diseases