ATLS Chapt 3: Shock

• First step: recognize shock's presence in trauma patients; initiate treatment based on probable cause.
• Shock: circulatory system abnormality leading to inadequate organ perfusion and tissue oxygenation.
• Diagnosis requires synthesizing clinical findings and lab tests.
• Recognize inadequate tissue perfusion by identifying common clinical findings.
• Second step: identify shock's probable cause, adjust treatment.
• Most injured shock patients have hypovolemia, but may also have cardiogenic, obstructive, neurogenic, or septic shock.
• Tension pneumothorax can reduce venous return, producing obstructive shock.
• Cardiac tamponade inhibits cardiac contractility/output, causing obstructive shock.
• Trauma team members should consider these diagnoses in patients with injuries above the diaphragm.
• Neurogenic shock: spinal cord injury leads to loss of sympathetic tone and vasodilation.
• Brain injury only induces shock if the brainstem is involved.
• Spinal cord injury patients may initially present in shock from vasodilation and hypovolemia.
• Septic shock is unusual; consider in patients with delayed emergency facility arrival, or elderly patients presenting with unrecognized infection.
• Patient response to initial treatment, combined with primary and secondary survey findings, determines shock cause.
• Hemorrhage is the most common cause of shock in trauma patients.

Shock Pathophysiology

• Basic cardiac physiology and blood loss pathophysiology are essential to understanding shock.

Basic Cardiac Physiology

• Cardiac output: volume of blood pumped by the heart per minute determined by multiplying heart rate by stroke volume. Stroke volume: amount of blood leaving the heart with each contraction.
• Stroke volume is classically determined by preload, myocardial contractility, and afterload.
• Preload is the volume of venous blood returning to the heart, determined by venous capacitance, volume status, and the difference between mean venous systemic pressure and right atrial pressure.
• Venous system can be considered a reservoir where blood volume is split into two components.
• One component maintains volume: the second contributes to mean systemic venous pressure. 70% of body's blood volume is in the venous circuit.
• Compliance links venous volume and pressure; pressure gradient drives venous flow and return to heart, blood loss depletes venous voume and reduces the pressure gardient.
• Blood returned to heart determines myocardial muscle fiber length after ventricular filling.
• Starling's law states that muscle fibre length relates to contractile properties.
• Myocardial contractility is the pump that drives the system.
• Afterload, also known as peripheral vascular resistance, is the resistance to forward blood flow.

Blood Loss Pathophysiology

• Early responses to blood loss include vasoconstriction to preserve blood flow to kidneys, heart, and brain.
• Tachycardia is the earliest circulatory sign of shock, attempting to preserve cardiac output.
• Endogenous catecholamines increase peripheral vascular resistance, increasing diastolic pressure and reducing pulse pressure.
• This pressure increase does little to increase organ perfusion and tissue oxygenation.
• Venous return partially preserved in early hemorrhagic shock, compensatory mechanism: contraction of blood volume in venous system.
• Limited compensatory mechanism; Locate and stop bleeding to allow Volume repletion to allow recovery from the shock state.
• Inadequate tissue perfusion deprives cells of substrates for aerobic metabolism, causing shift to anaerobic metabolism and lactic acid production.
• Prolonged shock leads to organ damage and dysfunction.
• Isotonic electrolyte solutions, blood, and blood products help combat this and treatment should focus on stopping bleeding, increasing oxygenation, ventilation and fluid resuscitation.
• Rapid IV access is crucial.
• Definitive hemorrhage control is the main focus. Vasopressors aren't an effective first line treatment as they can worsen tissue perfusion.
• Monitor perfusion indices to detect deterioration and response to therapy. Reassessment helps find patients with compensated shock.
• Most injured patients in shock require early surgery or angioembolization. Surgeons should be immediatey notified.
• Consider transfer such patients to trauma centres.

Initial Patient Assessment

• Clinicians must recognize and differentiate between hemorrhagic and non-hemorrhagic shock.

Recognition of Shock

• Easy to recognize profound circulatory shock, inadequate perfusion of skin, kidneys, and central nervous system.
• Ensure an open airway is maintained with ventilation. Trauma Team members evaluate circulatory status.

Signs of Shock

• Tachycardia and cutaneous vasoconstriction as early signs.
• Relying on systolic BP can delay shock recognition; compensatory mechanisms can sustain BP until 30% of blood volume is lost.
• Watch pulse rate/character, respiratory rate, skin perfusion and puilse pressure (difference between systolic and diastolic pressure)
• Tachycardia and cutaneous vasoconstriction are typical early responses to volume loss in must adults.
• Any injured, cool and tachycardic patient is in shock until proven otherwise.
• Tachycardia is diagnosed when the heart rate beats per minute is greater than 160 in an infant; beats per minute greater than 140 in children under school age.
• Tachycardia is diagnosed when heart rate beats per minute is greater than 120 in children post puberty or above, and tachycardia is diagnosed where beats per minute exceeds 100 in adults typically.
• Elderly patients might present w/o tachycarida due to medication use or limited cardiac response.
• Narrowed pulse pressure implies blood loss and compensatory mechanisms.
• Massive blood loss only slightly decreases hematocrit or hemoglobin concentration.
• A low hematocrit soon after an injury indicates massive blood loss, while normal cannot exclude significant blood loss; use base deficit/lactate levels to determine severity.
• Above diaphragm injuries may cause inadequate organ perfusion due to cardiac performance from blunt myocardial injury, cardiac tamponade or tension pneumothorax; high level of suspicion is key for all forms..
• Initial cause determination requires careful physical examination.
• Chest/pelvic x-rays, FAST exams can confirm cause, but do not delay treatment.

Overview of Hemorrhagic Shock

• Hemorrhage is the most common shock cause after injury.
• With multiple injuries, patients have some degree of hypovolemia.
• Institute treatment as if patient is hypovolemic with signsof shock.
• Identify any other causes complicating presentation of hemorrhagic shock such as cardiac tamponade/tension pneumothorax/spinal cord injury/blunt cardiac infury.
• Stop hemorrhage as the primary step; assess for potential blood loss from chest, etc; Use physical examination; adjunctivie studies include a chest xray and pelvic xray.

Clinical Differentiation of Cause of Shock

• Shock is classified as hemorrhagic or non-hemorrhagic.

Overview of Non-Hemorrhagic Shock

• Non-hemorrhagic shock includes cardiogenic/septic shock, cardiac tamponade and tension pneumothorax.
• Most of these non-hemorrhagic causes are temporarily improved when volume is resuscitated.

Cardiogenic Shock

• Dysfunction is caused by blunt cardiac injury, cardiac tamponade, air embolus, or, myocardial infarction.
• Suspect blunt cardiac injury when injury mechanism involves rapid deceleration.
• All patients with blunt theracic trauma reqire continuous electrocardiographic ECG monitoring to detect injury.
• Shock can be secondary to myocardial infarction, so enzymes may assist these patients (mainly the elderly).

Cardiac Tomponade

• Most commonly found in patients with penetrating thoracic trauma, or blunt.
• Indications include tachycardia and muffled heart sounds, but are not exlusive in diagnosis.
• These indications, alongside Hypotension and insufficeint response to fluid, suggest cardiac tamponade.

Tension Pneumothorax

• This is a true surgical emergency that requires immediate treatment.
• It can be caused when air enters the pleural space, but a flap valve prevents escape.
• Intrapleural pressur rises, resulting in impaired venous return, total lung collapse, and shift of mediastinum.
• Spontaneously breathing patients exhibit extreme tachypnea and air hunger; mechanically ventilated patients show hemodynamic collapse.
• Acute respiratory distress, subcutaneous emphysema, percussion and tracheal shift support diagnosis.
• Immediate thoracic decompression is warranted without xray confirmation.
• Follow this by placing a chest tube with sterile technique
• Isolated intracranial injuries do not cause shock, unless the brainstem is damaged.

Neurogenic Shock

• Head injury patients present with other causes.
• Cervical/upper spinal cord injuries can produce hypotension from sympathetic tone loss.
• Hypovolemia compounds this physiologic effect.
• This can be identified as hypotension with no tachycardia/cutaneous vasoconstriction where narrow pulse pressure is not seen.
• Torso trauma alongside spinal cord is common.
• treat patients in hospital where these shock cases often need fluid for hypovolemia.
• To restore tissue oxygenation when using fluid for hypovolemia, use techniques to monitor intravascular volume status and cardiac output.

Septic Shock

• Uncommon but does occur in some patients that are in the emergency department after a few hours.
• Can occur in abdominal injuries (intestinal contents contaminating peritoneal contents)
• Difficult to distinguish between hypovolemic shock, this can occur due to hypotension and be afebrile;
• With early septic shock: normal circulating volume, modest tachycardia, norml pressure and warm skin

Hemorrhagic Shock

• This is the most common type in traums patients, patients responses can be made more complex via the fluid shifts. These are among fluid compsrtments.
• Severe hemorrhage can result in fliud shifting to extracellular compartments.
• The above should considered alongside severe prolonged shock and the response to reperfusion.

Definition of Hemorrhage

• Acute oss of circulating blood volume.
• Adults account for 7% of blood via weight (70kg males contains 5L on average), overestimation can occur if the estimate is based on obese adults (based on the ideal body weight, a calculation should be based on calculating current actual weight but the amount of blood volume is accounted as a result)
• Blood volume for children is 9% of body weight for children (roughly 70-80mL/kg)

Physiologic Calssificaiton

• Physiologic effects of the above are divided into four classes. Based on useful signs for estimating acute blood loss where subsequent volume repalcement is determined by patients reposnse.
• Class I: individual donating blood (just one unit)
• Class II: uncomplicated hemorrhage for whcih crystalloid fluid resuscitaiton is adequate
• Class III: complicated, crystalloid infusion is required or perhaps blood replacement.
• Class IV: Preterminal event unless mesures account, blood tranfusion is requried

Class I Hemorrhage: - The former is related to an increase in circulating catecholamines increasing tone in the peripheral vesse, therefore it is important to assess the pulse and blood pressure.

• Other sogns include CNS changes. Urinary output is affected with urine flow at 30mL/hr

Class III Hemorrhage: 31%-40% Blood Volume Loss

• Includes inadequate perfusion (marked tachycardia and tachypnea), and changes in mental status.
• Blood loss should be assessed.
• Most patoents require blood and packed red blood cells to reservse the shock.

Class IV Hemorrhage: >40% Blood Volume Loss

• Immediately threatening with tachypnea, significant decrease in systolic, narrowed pulse blood pressure and low blood pressure (diastolic can sometimes get unmeasurable.
• There cn be negligble output and depressed mentla status.
• These patients often need transusion with sugical measures to manage the bleeding as soons e possible

Confounding Factors

• System serves the following/helps the individuals involved in the initial resusciation to recognize patient age, timr interval betweeninitiation and injury
• Patients must fit within the precision. Initiate hemorrhage and when symptoms fo blood loss appear. Do not wait before BP falls but sop when is suspected

Fluid changes sencondary to soft tissue injury

• Major fracture or injuries can comprise haemodinamic states and injury. For example a fractured tibia can loss 750ml, fracture can lose with retroperitoneal heamatoma.
• They also include risk for loss so evaluate and assess bleeding so stabilize and for elderly and obese.

Physical exammination

• The ABCDEs is used to see the resposne to blood, measuring measurements for baseline to asses, and essential levels of consciousness.
• Breathing priorities include supplementaru ocyuen to 95%

Circulation: Hemmorhage control

• Priorities inclcude contorlling haemorage and tissue perfisuiong,. If possible direct pressure.

Disability : Neuro examination

• Will determine conciousness whichis used to address cerebral perfustion ( alterations DO NTO IMPLY INTRACRANIAL injuries
• Compleye undersressing used

Gastric Dilation : Decompression

• It increases risk for inspiration. Put oral tupre for aspirartion and suction

Vascular Assess

• The aim is to obtain assecss. The measure is in gaufe

Initial Fluid Therpy

• Administer in tonic fluid volusm
• Look at blood volume and base any blood on 3.2. If that requires for what is exceeded re assess and injries
• The patients response in terms of initial resuscitation to assist how blood os going to be maintained.

Patients response

• In any event stop more bleeding as adminisrer excess crystalloids and be sure to include important elements. Balance ocygent and perfsion not accepting a lower blood value.