Pulmonary emergencies

By
Roderick T. Vito, MD, FPCEM
 Acute Respiratory Failure
• Acute impairment of oxygen and carbon
dioxide exchange
• Impaired gas exchange or impaired ventilation
• Arterial blood gas : pO2 <60mmHg or pCO2 >
50 mmHg with blood pH < 7.35
 Causes of ARF
• Airway obstruction
• Asthma
• COPD
• Congestive heart failure
• Non cardiogenic pulmonary edema
• Pulmonary embolism
• Massive pulmonary effusion
• Pneumonia
• Pneumothorax
• Advance lung CA
• Toxic inhalation
 Signs and symptoms
• Dyspnea
• Altered level of sensorium
• Generalized seizure
• Cyanosis, diaphoresis, labored breathing
• Nasal flaring, grunting, retractions
 Physical examination
• Tachycardia
• Tachypnea
• Wheezing
• Rales
• Decrease breathsounds
• Chest lagging
 Diagnostics
• Chest x-ray
• Arterial blood gas
• Pulse oximetry
• 12 lead EKG
• V/Q scan or pulmonary angiogram
• toxicology
 Treatment
• High flow oxygen with non re-breathing mask
until pulse oximerty reading >90mmHg.
• Endotracheal intubation with FiO2 100%
• Ventilator
• Rule : oxygenation is more important than
ventilation
• Treat underlying pathology
 Asthma

• Bronchial reactivity, mucus plugging,

inflammatory changes in the bronchial wall
• Airway abnormality: airflow obstruction 
impaired expiratory phase elevated tidal
volume and residual capacity  air trapping
• Treatment : beta agonist inhalational agents,
steroids,
 Chronic Airway obstruction
• Medical challenge due constant battle against
asphyxiation.
• Smokers predisposed
• Non smokers : environmental exposures, genetic
abberations or sustained bronchospatic airflow
obstruction
• 2 types
– Pulmonary emphysema: abnormal permanent
enlargement of air spaces distally  wall destruction
– Chronic bronchitis: mucus secretion in bronchial tree
• Evolution of COPD are clinically impercebtible
• Insidous , slow appearance of dyspnea ( several
decades)

• Pathophysiology : impedence to expiratory airflow:

secretions and mucosal edema, bronchospasm,
bronchoconstriction due to impaired elasticity 
increase resistance, decrease caliber of small bronchi
and bronchioles bronchoconstriction  alveolar
hypoventilation , hypoxemia, hypercarbia
 Pulmonary embolism
• Arise from pelvic vein thrombosis secondary
to pelvic trauma or surgery or during
postpartum period
• Deep vein thrombosis of the lower extremities
• Consider among high risk patients
experiencing and acute cardiopulmonary
complaint
• Chest pain is common
• Thromboembolism migrates to the lungs  platelet
degranulate and release biologically active
substances smooth muscle constriction of the
bronchi and pulmonary arteries
• Airway resistance and decrease lung volume with
uneven ventilation  dyspnea and tachypnea
• Hemodynamic reaction depends on the extent of the
vascular occlusion and patients prior cardiovascular
status
• If 40- 50 % vascular obstruction develop significant
clinical signs
Treatment of pulmonary embolism
• Administration of 4 to 10 L O2 via nasal
cannula  hypoxia sec ventilation- perfusion
imbalance, cardiac arryhthmias
• monitoring vital signs
• Aggressive crystalloid administration
–hypotension due to right ventricular outflow
obstruction and myocardial dysfunction