CHRONIC OBSTRUCTIVE PULMONARY DISEASE — COPD

- persistent airway limitation - Airflow obstruction due to mucus hypersecretion,edema

& broncospam
- progressive non-reversible
CLASSIFICATION
- loss of elastic recoil
 Chronic Bronchitis - Blue Bloater
 Emphysema- Pink Puffer

PATHO

 Supporting structures of lungs are destroyed  Bronchicles tend to collapse

 Air goes in but remains in lungs  Barrel chest shape

SIGN & SYMPTOMS

 Prolonged expiratory  Dyspnea  Pursed lip breathing

phase  Use of accessory &  Underweight/ anorexia
 Wheezes intercostal  Chronic fatigue
 ↓ breath sound  muscles
 Chronic cough/ sputum  Barrel chest
production  Tripod position

RISK FACTOR

 Cigarettes/Second hand  Severe recurring  Aging

smoker respiratory infections  Asthma
 Chemical/dust  Genetics/ a-antitrypsin
 Air Pollution deficiency

COMPLICATIONS

 Acute respiratory failure  Cor pulmonale: pulmonary hypertension that

 Long term O² causes RSHF

POLYCYTHEMIA

 Overcompensation of hypoxia  Blue/red color of skin

 Increase production of RBC  HQb 2O or more

DIAGNOSIS

 Spirometry: Measures lung function  Imaging: Chest X-ray or CT scan to rule out
(FEV1/FVC ratio). other conditions.
 Symptoms: Chronic cough, wheezing,  Medical history: Assessing risk factors
shortness of breath. (smoking, exposure to pollutants
MEDICATION

 Bronchodilators:  Combination therapy:

Short-acting (SABA): Albuterol, levalbuterol. - LABA + LAMA (e.g.,

indacaterol/glycopyrronium).
Long-acting (LABA): Salmeterol, formoterol.
- LABA + inhaled corticosteroid (ICS) (e.g.,
Long-acting muscarinic antagonists fluticasone/salmeterol).
(LAMA): Tiotropium, umeclidinium.
 Inhaled corticosteroids (ICS): Fluticasone,
budesonide.
 Phosphodiesterase-4 inhibitors:
Roflumilast (for severe COPD).
 Oxygen therapy: Supplemental oxygen for
advanced COPD.

PATIENT CARE

 Pulmonary rehab/exercise ( pursed lip breathing,

huff cough, futter, acapella)
 Only stop up meds not down
 O2 therapy
 High calorie,High protein foods 5-6 small meals
PULMONARY EMBOLISM — PE
— Pulmonary embolism (PE) is a blockage of one or CLASSIFICATION
more pulmonary arteries in the lungs, typically
caused by a blood clot that has traveled from  Fat emboli - Occurs when fat globules enter
another part of the body, such as the deep veins of the bloodstream and lodge in the
the legs. pulmonary arteries, often after a severe
injury or bone fracture.
— Deep Vein Thrombosis (DVT) is a blood
clot/thrombus that forms in the deep veins of the  Air Emboli - when air bubbles enter the
body, typically in the legs. It can cause pain, swelling, bloodstream and block the pulmonary
and warmth in the affected area. If the clot breaks arteries.
loose, it can travel to the lungs and cause a  Amniotic Fluid Emboli - A rare but serious
pulmonary embolism. (Virchrow triad) condition where amniotic fluid enters the
maternal circulation during childbirth.
 VIRCHROW TRIAD  Septic Emboli - Caused by infected material,
 Blood Flow Changes (stasis or
such as bacteria or fungi, that enters the
turbulence)
 Hypercoagulability (increased bloodstream and lodges in the pulmonary
clotting tendency) arteries.
 Endothelial Injury(damage to blood
vessel walls)

PATHO

 Obstruction: Blockage of pulmonary arteries by a blood clot or other material.

 Impairment: Reduced blood flow and gas exchange, leading to hypoxemia.
 Constriction: Vasoconstriction of pulmonary arteries, increasing resistance.
 Consequences: Hypoxemia, right ventricular strain, and potential cardiac dysfunction.
 Failure: Respiratory failure, cardiac failure, and potential multi-organ failure if left untreated or severe.

Signs and Symptoms

 Sudden onset of shortness of breath  Lightheadedness or dizziness

(dyspnea)  Rapid heart rate (tachycardia)
 Chest pain or discomfort  Sweating
 Cough  Leg pain or swelling (if DVT present)

RISK FACTOR

 Heart Disease  Immobility  Pregnancy

 Cancer  Smoking  Family History
 Surgery  Obesity  Age
 Blood clotting disorder  Taking estrogen

MNEMONIC
PE AHEAD

S - Swelling in the leg (DVT symptom) P - Pain (chest pain)

T - Tenderness leg cramps E - Embolus (blood clot)

O - Out of Breath/Oxygen saturation decreased A - Acute onset

P - Pass Out (lightheaded) H - Hypoxemia (low oxygen levels)

E - ECG changes (electrocardiogram abnormalities)

C -Chest pain back pain when breathing A - Anticoagulation (treatment)

L - Leg discoloration D - Dyspnea (shortness of breath)

O - Over drive racing heart

T - Time call for help

COMPLICATION

 Respiratory failure  Pulmonary Hypertension

 Cardiac arrest  Chronic thromboembolic pulmonary
 Pulmonary infraction hypertension (CTEPH)

MEDICATION

 Anticoagulants: Prevent new clots (e.g., heparin, warfarin, DOACs).

 Thrombolytics: Dissolve existing clots (e.g., alteplase).

DIAGNOSIS

 Computed Tomography Pulmonary Angiography (CTPA): Imaging test to visualize clots.

 Ventilation-Perfusion Scan (V/Q scan): Assesses lung function.
 D-dimer test: Blood test to detect clotting.
 Electrocardiogram (ECG): Rules out other condition.
 ABG (hypoxemic hypocapnic respiratory alkalosis)
 Chest X-ray:usually normal unless it have a wedge infract.

 Hampton's Hump: A wedge-  Palla's Sign or Fleischner Sign:

shaped or rounded pleural-based refers to an enlarged pulmonary
consolidation seen on chest X-ray, artery seen on chest X-ray, which
suggestive of pulmonary infarction can be associated with
due to pulmonary embolism (PE).
pulmonary embolism.
 Westermark Sign: A region of
oligemia (decreased vascular
markings) on chest X-ray, indicating
decreased blood flow to the lung
area affected by the pulmonary
embolism.
PATIENT CARE

 Oxygen therapy: Supplemental oxygen.

 Pain management: Analgesics for chest pain.
 Monitoring: Close observation of vital signs.
 Bed rest: Initial management.
 Follow-up care: Regular check-ups to prevent recurrence.
ACUTE RESPIRATORY DISTRESS SYNDROME — ARDS

- cause severe damage to the alveoli due to cause widespread implantation,damage the
implantation and pulmonary edema. alveoli.

- a life-threatening condition characterized by acute

onset of non-cardiogenic pulmonary edema, leading
to hypoxemic respiratory failure CLASSIFICATION

 ARDS is not a primary lung disease it is a  Mild: PaO2/FiO2 ratio 201-300 mmHg
complication from a systemic injury that  Moderate: PaO2/FiO2 ratio 101-200 mmHg
 Severe: PaO2/FiO2 ratio ≤100 mmHg

FiO2 = Fraction Inspired Oxygen

ARDS Stages

Exudative Stage (first 7-10 Proliferative Stage Fibrotic Stage(later

days): (after 7-10 days): stages):

Edema: Accumulation of protein-rich fluid Lung Repair: Proliferation of Fibrosis: Deposition of collagen and
in alveoli type II pneumocytes and scarring
fibroblasts
: Damage to capillary membrane leads to Lung Damage: Permanent damage
pulmonary edema. Collagen Deposition: to lung tissue.
Formation of granulation
Inflammation: Activation of inflammatory tissue. : Alveoli lose liner
cells infrastructure ,which worsen gas
exchange, lung compliance and
Decreased surfactant leads to Atelectasis hypoxia.
(alveoli collapse)

Hyaline membrane start to develop,&

leads to decrease elasticity.

Refractory Hypoxemia: A condition

where severe hypoxemia (low blood Decrease Lung Compliance:
oxygen levels) persists despite high levels Lung continue to become Very Poor Progression : patient is
of supplemental oxygen therapy, often stiffer, worsen hypoxia. ventilator dependent at this point
requiring advanced respiratory support. with the very low chance of
recovery.

PATHO  Increased Permeability: Damage to

alveolar-capillary membrane, leading to
 Inflammation: Activation of inflammatory edema
cells and release of mediators
  Impaired Gas Exchange: Reduced lung  Dyspnea: Sudden onset of shortness of
compliance and hypoxemia breath Earliest Sign
 Hypoxemia: Low oxygen levels in the blood
SIGNS AND SYMPTOMS  Tachypnea: Rapid breathing rate
 Crackles: Bilateral lung crackles on
auscultation

RISK FACTORS COMPLICATIONS

 Direct Lung Injury: Pneumonia, aspiration,  Respiratory Failure: Need for mechanical
inhalation injury ventilation
 Indirect Lung Injury: Sepsis, trauma,  Multi-Organ Dysfunction: Failure of other
pancreatitis, massive transfusion organs, such as kidneys or liver
 Ventilator-Associated Pneumonia:
Secondary lung infection

DIAGNOSIS

 Berlin Definition: Acute onset, bilateral lung infiltrates, and PaO2/FiO2 ratio criteria
 Chest X-ray: Bilateral lung infiltrates
 ABG Analysis: Hypoxemia and respiratory alkalosis

PATIENT CARE

 Mechanical Ventilation: Lung-protective strategy with low tidal volumes

 PEEP: Positive end-expiratory pressure to improve oxygenation
 Fluid Management: Conservative fluid strategy to minimize edema
 Positioning: Prone positioning may be used to improve oxygenation
 Nutritional Support: Adequate nutrition to support recovery
 Monitoring: Close monitoring of vital signs, oxygenation, and organ function