CRITICAL CARE (EMERGENCY MEDICINE)

HEMOTHORAX
 Each hemithorax is capable of holding up to 50% of the circulating blood volume. And massive
hemothorax is defined as > 1.5 L.
 A large hemothorax could cause some tracheal deviation and reduced breath sounds and dullness
to percussion over the involved side.
 The most common causes of massive hemothorax are traumatic laceration of the lung parenchyma
or damage to an intercostals or internal mammary artery.
 Hemothorax is indistinguishable from pleural effusion on chest x-ray

TRACHEOBRONCHIAL TEAR
 Such injuries typically present with dyspnea, hemoptysis, subcutaneous emphysema, Hamman
sign (audible crepitus on cardiac auscultation) and sternal tenderness.
 A tracheobronchial disruption may cause pneumothorax that does not resolve with chest tube
placement, mediastinal emphysema and/or subcutaneous emphysema on chest x-ray.

ANAPHYLAXIS
 It is an acute, life-threatening, IgE-mediated type I hypersensitivity reaction characterized by
allergic symptoms affecting more than 1 organ system or sudden hypotension after exposure to
the allergen. The clinical course of anaphylaxis is unpredictable
 Anaphylactic shock can progress rapidly to respiratory failure, circulatory collapse, and death.
 Symptoms can involve the oropharynx (stridor, hoarseness), skin (hives, flushing, pruritus),
gastrointestinal tract (lip/tongue swelling, vomiting), lungs (dyspnea, wheezing, stridor,
hypoxia), and cardiovascular system (hypotension).
 Laryngeal edema: stridor and harsh respiratory sounds from the trachea. Wheezing is generally
absent. Laryngeal edema causesa fixed upper-airway obstruction.
o Obstruction limits airflow during inspiration and expiration, causing flattening of the top
and bottom of the flow-volume curve
 The most common triggers are insect stings, medications (eg, beta-lactam) and food (eg, nuts,
shellfish, egg)
 Food allergies are caused by abnormal immunologic responses to food proteins that swiftly
induce inflammation to an organ system
 Anaphylactoid reactions are non-IgE related, are clinically identical and treated the same way,
and do not need preceding sensitization to the antigen.
Treatment
 Early administration of intramuscular epinephrine into the thigh is the first-line treatment.
o Epinephrine is the only medication proven t prevent and reverse progression of
anaphylaxis to anaphylactic shock and death.
o Higher plasma and tissue levels are more effectively attained by the IM route compared to
the subcutaneous.
o Intravenous infusion of epinephrine carries a greater risk of adverse effects (eg,
arrhythmias) and so is reserved for patients who have not responded to IM epinephrine or
are decompensating rapidly
o The benefits of epinephrine result from beta2 and alfa1 adrenergic receptor agonism
leading to bronchial smooth muscle relaxation (eg, decreased wheezing), vasoconstriction
(eg, decreased upper airway edema, raised blood pressure), respectively
 Antihistamine, bronchodilators and corticosteroids can be helpful supplemental therapies.
o A 3- to 5-day course of steroids is often prescribed to prevent relapse of anaphylaxis.
Anaphylaxis by hymenoptera sting
  Patients should carry epinephrine at all times (epinephrine pen)
 In addition, patients should be referred to an allergist for venom immunotherapy, which can
reduce repeat bee sting anaphylaxis risk from 30% to <5%
Anaphylaxis by latex
 The widespread use of latex in medical products has made it a common cause of allergy.
 The development of hives after sexual intercourse in this patient was likely due to sensitization to
latex condoms. Latex gloves used by surgeons provoked the anaphylactic reaction
 Pre-existing atopic dermatitis increases the risk of latex allergy.
 Health care workers and surgical patients, especially those undergoing abdominal or
genitorurinary surgery, are at higher risk as well.
 Latex allergy rates peaked in the 1990s and have since decreased with the use of pwder-free latex
gloves and latex alternatives.

DIAPHRAGMATIC RUPTURE
 Blunt abdominal trauma can cause a sudden increase in intraabdominal pressure that overcomes
the muscular strength of the diaphragm and leads to large radial tears in the muscle or avulsion
from its attachments. The resultant diaphragmatic rupture allows leakage of intrabdominal
contents into the chest, causing compression of the lungs and mediastinal deviation.
 Diaphragmatic rupture is more common on the left side due to congenital weakness in the
diaphragm´s left posterolateral region and the liver´s protective effects on the right side.
 Patients can acutely present with respiratory distress, but some patients with smaller ruptures can
have a delayed presentation with nausea and vomiting.
 Especially children may initially have no symptoms or signs and can have a delayed presentation
(months to years) with expansion of the diaphragmatic defect and herniation of abdominal organs
Diagnosis
 Elevation of the hemidiaphragm on the chest x-ray might be the only abnormal finding.
o The tip of the nasogastric tube is typically seen in the left hemithorax rather than bellow the
diaphragm
 The small bowel is sometimes present in the thoracic cavity.
 Ultrasonography or CT scan of the chest is sometimes required if the chest x-ray does not visualize
the area well.
 Early recognition of diaphragmatic trauma is extremely important because the mortality rate of
undiagnosed injury and subsequent strangulation of the bowel can be 30%-70% dependieng on the
extent of the associated injuries
Treatment
 Most patients require surgical repair and exploration of the abdomen for other traumatic injuries.

ESOPHAGEAL RUPTURE
 It typically presents with subcutaneous crepitus in the chest and appears on x-ray as a
pneumomediastinum

BURNS
Treatment
 Systemic steroids are contraindicated in severely burned patients because their diabetogenic and
immunosuppressive effects.
 Prophylactic antibiotics are not indicated.
Airway thermal injury
 Burn victims are at high risk for respiratory compromise because the supraglottic airway, which
efficiently exchanges heat with inhaled air, is very susceptible to direct thermal injury and acute
obstruction by edema and blistering (In contrast, the subglotic airway is protected from injury by
reflexive closure of the vocal cords upon exposure to extremely hot air)
  Clinical indicator of thermal and smoke inhalation injury include: burns on the face, singeing of
the eyebrows, oropharyngeal inflammation, blistering or carbon deposits, carbonaceous sputum,
stridor, carboxyhemoglobin level >10% and a history of confinement in a burning building
Treatment
 All burn victims should be treated initially with high-flow oxygen vi a non-rebreather mask,
though caregivers should maintain a low threshold for intubation in any patient with physical
evidence of therma damage to the upper airway
 A key reason for early intubation is that progressive airway edema may preclude intubation later
in the patient´s clinical course, potentially necessitating an emergent surgical airway

SHOCK

Septic shock
 It is a form of distributive shock
 The systemic inflammatory response causes peripheral vasodilation and decreased systemic
vascular resistance (SVR). The decreased blood flow returning to the heart also lowers PCWP.
Cardiac output is often increased to compensate and maintain adequate tissue perfusion
(hyperdynamic phase of septic shock or warm shock)
o As sepsis progresses to the hypodynamic phase (“cold shock”), there may be
vasoconstriction with a rise in SVR and a significant decline in CO.
 MvO2 is high due to hyperdynamic circulation, improper distribution of CO, and inability of the
tissues to adequately extract oxygen
 Elevated lactate levels are common.
Treatment
  IV normal saline is the first-line treatment for maintenance of intravascular pressure while
antibiotics are given to correct the underlying infection.
 Vasopressors are indicated for the treatment of hypotension in states of shock only after IV fluids
have failed to restore normotension.
 The use of bicarbonate in the treatment of lactic acidosis is controversial and is recommended only
in severe acute acidosis (pH <7.2)
 Hypertonic saline is used occasionally to rapidly expand the intravascular volume by drawing
fluid out of the extravascular compartment.
Hypovolemic shock

 In trauma or postsurgical patients, shock is presumed secondary to hemorrhage until proven

otherwise.
 The loss of intravascular volume decreases left ventricular preload, resulting in decreased CO and
systemic BP
 PCWP (a measure of left atrial pressure and left ventricular end-diastolic pressure) is decreased
due to intravascular volume loss.
 SVR increases in an attempt to maintain adequate perfusion to the vital organs.
 MvO2 is low due to reduced tissue perfusion and increased oxygen extraction by hypoperfused
tissue.

 In early stages (pre-shock or compensated shock) the increase in SVR maintain adequate CO and
tissue perfusion and BP may be mildly low, normal or occasionally slightly elevates. However, as
the underlying condition worsens further, the increase in HR cannot maintain adequate CO and
shock ensues.

Cardiogenic shock
 It is due to significant left ventricular dysfunction and reduced pump function.
 It can be caused by myocardial contusion.
 Elevated venous filling pressures and jugular venous distention would be expected.
 Once pump failure occurs in cardiogenic shock, blood backs into the lungs, causing increased
PCWP.
 o PCWP increases significantly after infusion of saline without an appreciable change in
systemic blood pressure
 SVR is typically increased to maintain adequate tissue perfusion pressure.
 The decreased cardiac output decreases tissue perfusion, which signals tissues to extract more
oxygen from the blood and decrease MvO2

HYPOTHERMIA

 Mild hypothermia (32-35 C (90-95 F)) causes an increase in HR with peripheral vasoconstriction.
 Moderate hypothermia (28-32 C (82-90 F)) causes progressive bradycardia and hypotension due to
decreased reactivity of pacemaker cells and salt/water loss from cold-induced dieresis.
 Due to decreased reactivity of the pacemaker cells, the bradycardia associated with hypothermia is
often refractory to treatment with atropine and cardiac pacing. However, it usually will improve
with treatment of the hypothermia

MECHANICAL VENTILATION
 Immediately following intubation, a high FiO2 (eg ≥60%, or 0.6) is usually provided and ventilator
settings can subsequently be adjusted based on the results of the first arterial blood gas analysis.
 The PaO2, an important measure of oxygenation, is influenced mainly by FiO2 and PEEP.
o Prolonged high FiO2 can cause oxygen toxicity as it can lead to the formation of
proinflammatory oxygen free radicals and predispose to atelectasis as alveolar nitrogen is
displaced, resulting in worsened oxygenation.
o Although there is no strict cutoff FiO2 value for oxygen toxicity, FiO2 levels <60% are
considered generally safe.
o Although decreasing PEEP can address a increased PaO2, dropping the FiO2 is preferable
to decrease the likelihood of oxygen toxicity.
 The PaCO2, a measure of pulmonary minute ventilation, is affected mainly by the RR and tidal
volume (TV)
o Respiratory alkalosis secondary to hyperventilation can be address by decrease RR.
  Positive pressure mechanical ventilation acutely increases intrathoracic pressure, increasing RA
pressure and decreasing systemic venous return. This sudden loss of venous return may cause
acute circulatory failure and death
 Additionally, the sedative medications used prior to intubation relax venous capacitance vessels
and may themselves cause circulatory failure by acutely decreasing venous return in the
hypovolemic patient.
 Positive pressure mechanical ventilation causes an acute ventricular preload reduction. This effect
would have been even more pronounced at higher tidal volume settings, as higher pressures are
needed to generate larger tidal volumes.
 The assist control mode of mechanical ventilation delivers a predetermined TV with every breath.
Inspiratory cycles can be initiated by the patients, but if the patient fails to breathe at a set
minimum rate, then the ventilator will deliver the tidal volume on its own
Main bronchus intubation
 The ideal location of the distal tip of the endotracheal tube (ETT) is 2 – 6 cm above the carina.
 Because the right mainstem bronchus diverges from the trachea at a relatively non-acute angle, an
ETT advanced too far will prefentially enter into the right main bronchus
 This results in overinflation of the right lung, underventilation of the left lung, and asymmetric
chest expansion.
 Auscultation will show markedly decreased or absent breath sounds.
 Chest x-ray confirms the diagnosis
 Repositioning the ETT by pulling back slightly will move the tip between the carina and vocal
cords and solve the problem.