COPD​→​Chronic Obstructive Pulmonary Disease

Definition: Lung disease characterized by chronic obstruction of lung airflow that interferes
with normal breathing and is not full reversible.
-In COPD, airway obstructed​→​air trapped inside the lung ​→​Max amount of air out is
lower​→​Reduce FEV 1 and FVC.
Conversely, TLC (maximum volume of air into lungs) increase due to air trapping.

Risk factors for COPD

● Smoking​→​95%
● Occupation
● Indoor and outdoor pollutant
● Alpha 1-anti trypsin deficiency​→​Cannot defense against protease

COPD Clinical Presentation:

Chronic Bronchitis Emphysema
-Productive cough -Thin
-Increased dyspnea on exertion -Increased dyspnea at rest
-Rales/Ronchi -Tachypnea
-Cyanosis -Pursed-lip breathing
-Blue bloater -Pink puffer

Blue bloater Pink Puffer

Inflammatory changes ​→​Mucocilliary
dysfunction​→​Increase goblet cell
secretion​→​Excessive mucus production​→​Cillia
shorten and less mobile​→​Harder to move the mucus
from bronchioles​→​Productive cough reflex to
remove mucus plaque
Inflammatory response​→​Elastin
breakdown​→​Loss of alveolar
mechanical function/Integrity​→​Loss
alveolar recoil​→​Air
trapping(expiration)​→​Uses of
accessory respiratory muscles to
breath​→​Dyspnea

Bronchioles​→​bronchoconstriction and mucus Alveolar macrophages secrete

hypersecretion​→​Productive cough​→​Airway proteases and
obstruction​→​Wheezing during expiration​→​Alveolar
hypoxia​→​V/Q
mismatch​→​Hypoxemia​→​Hypercapnea​→​Respirator
y acidosis​→
Alveolar hypoxia​→​Pulmonary vessels
constricts​→​Shunt blood to healthier
alveoli​→​Increase pulmonary vascular
pressure​→​Right side heart failure​→​Cor
Pulmonale​→​Increase in JVP​→​Low ventricle
output​→​Low Circulatory volume​→​Activation of
RAAS​→​Fluid retention
cytokines​→​Chemotaxis​→​ Neutrophil
secrete elastase​→​Loss of elastic fibres
around alveolar and capillary
bed​→​Loss alveolar recoil​→​Decrease
in ventilation and perfusion​→​Air
trapping​→​More amount gas traps in
alveolar after expire​→​(Oxygen and
carbon dioxide after
expiration​→​Increase in end expiratory
volume​→​Barrel chest​→​There still
gaseous left and not emptying after
expiration
Less perfusion and decrease in
ventilation​→​V/Q
mismatch​→​Hypoxemia​→​Hypercapnea

STAGE 1​→​ mild​→​ FEV1/FVC Less than 70%

FEV 1: more or equal to 80%
STAGE 2​→​moderate​→​FEV1/FVC Less than 70%
FEV 1: 50-40%
STAGE 3​→​severe​→​ ​FEV1/FVC Less than 70%
FEV 1: 30-50%
STAGE 4​→​very severe​→​FEV 1/FVC Less than 70%
FEV 1:30%

23) How ABG is performed

Definition: Measure of certain gaseous in arterial blood

Site of puncture: Radial artery / Femoral artery
Tic tac toe ABG

Range normal

pH 7.35-7.45

PaCO2 35-45

HCO3 22-24

Bronchodilation
Ipratropium bromide

Mechanism of action: Act as muscuranic receptor antagonist​→​Inhibit the action of M3

receptor (Gq) in bronchus smooth muscle cells ​→​Inactivation of G-protein​→​Inhibit the
PLC​→​Reduce IP3 and DAG ​→​further closure of Calcium channel​→​Reduce the calcium
concentration within smooth muscle cells​→​Reduce Calcium-Calmodulin complex​→​Lead to
inhibition MLCK​→​Activates Myosin Phosphatases​→​Convert myosin phosphate to
myosin​→​Smooth muscle relaxation.

Salbutamol

Mechanism of action: Act as Beta agonist​→​Stimulate Beta 2 Receptor (Gs) in bronchial

smooth muscles cells ​→​ stimulate Gs​→​Activate Adenyl Cyclase​→​Activate
CAMP​→​Phosphorylation of MLCK​→​Myosin phosphate​→​Myosin​→​Muscle relaxation.

Prednisone

Mechanism of action: