Respirations are RAPID + SHALLOW
Crackles heard over lung fields
< pulmonary blood flow causes arterial oxygen levels to decrease + CO2 levels to increase
Hypoperfused alveoli stop producing surfacant + subsequently collapse. Pulmonary capillaries begin to leak, causing pulmonary edema, diffusion abnormalities (shunting) + additional alveolar collapse called ACUTE LUNG INJURY
Dysrhythmias + ishchemia. HR is rapid, sometimes exceeding 150 bpm. Patient may complain of chest pain + even suffer an MI. Cardiac enzymes + biomarkers increase
Mental status deteriorates, decreased cerebral perfusion + hypoxia. Agitated, confused, lethargery increases + may loose consciousness
When MAP falls < 65 the GFR of kidneys cannot be maintained. ACUTE KIDNEY INJURY causes an increase of BUN + creatinine, fluid + electrolyte shifts, acid-base inbalances + loss of renal-hormonal regulation of BP. Urinary output < 30 mL per hr
Decreased blood flow to liver impairs ability of liver cells to preform metabolic + phagocytic functions. Patient is less able to metabolize meds + metabolic waste products, such as ammonia + lactic acid.
Liver enxymes (AST, ALT) + bilirubin levels increase + patient develops JAUNDICE
GI ischemia causes stress ulcers + mucosa can become necrotic + slough off causing bloody diarrhea
Disseminated intravascualr coagulation can occur
Caused by a severe allergic reaction when patients who have already produced antiboidies to a foreign substance (antigen) develop a systemic antigen-antibody reaction.
This reaction activates inflammatory cytokines, causing widespread vasodilation + capillary permeability
May be present within 5-30 min after exposure, though some can take hours.
Pt may complain of headache, lightheadedness, nausea, vomiting, acute abdominal pain or discomfort, pruritus, feeling of impending doom
Anaphylaxiz has 3 defining characteristics:
1.) Acute onset
2.) Presence of 2 or more symptoms: respiratory compromise, reduced BP, GI distress, skin or mucosal irritation
3.) Cardiovascualr compromise from minutes to hours after exposure
Inhalation injurys are common. Smoke (a colloid) contains airborne solid + liquid particles + gases that result when a substance undergoes combustion
Damage is caused by: smoke, particulates + systemic toxins
Lower airway injuries are uncommon due to the rapid cooling effect of the upper airways
Smoke inhalation injuries cause loss of ciliary action, trigger an inflammatory response causing hypersecretion + produce severe mucosal edema + possibly bronchospasm. Alveolar surfacant production is reduce, resulting in atelectasis.
Expectoriation of carbon particles in sputum is the CARDINAL SIGN
Pulmonary deterioration in severely burned patients can occur without obvious evidence of a smoke inhalation injury + symptoms may be delayed as long as 24-36 hrs after injury
Hypermetabolism + continued catecholamine release lead to increased tissue tissue oxygen consumption, which can lead to hypoxia
Late pulmonary complications: mucosal sloughing of the airway, which can lead to obstruction, increased secretions, inflammation, atelectasis, airway ulceration, pulmonary edema + tissue hypoxia.