Ch 17. Shock & Hypotension
The detection and management of shock in the prehospital environment has been historically limited. While technical advances and new research have led to significant changes in recent years regarding the prehospital phase of care of these critically ill patients, there remain significant limitations on the ability to manage shock in the field. This creates a difficult balance be- tween stabilization in the field and rapid transport to the hospital for definitive care.
What is shock?
Shock is the widespread failure of the circulatory system to supply adequate oxygen and nourishment to the tissues and organs of the body.
What is perfusion?
Perfusion is the supply of oxygen to cells and tissue with subsequent removal of wastes as a result of blood flow through the capillaries.
What is hypoperfusion?
Hypoperfusion is the inability to supply oxygen and remove wastes from the cells and tissues due to poor circulation of blood.
What is SIRS?
Systemic Inflammatory Response Syndrome (SIRS) may be due to infection, but other causes, such as burns and pancreati- tis, may exist. It requires 2 of the following:
- Temperature < 36oC or > 38oC
- Pulse > 90 beats per minute
- Respiratory rate > 20 breaths per minute or PaCO2 < 32 mmHg
- WBC > 12000 or < 4000 or differential with > 10% bands
Stages of shock
Compensated or Non-progressive
Low perfusion activates multiple systems to maintain and re- store perfusion, resulting in:
- Renal system retaining fluid and volume
- Maximization of blood flow to the brain, lungs, and heart
- Few symptoms
- Aggressive management slows progression
Decompensated or Progressive
Failure to compensate; unable to improve and maintain perfu- sion.
- Symptoms reflect poor perfusion.
- Oxygen deprivation to the brain causes confusion.
Prolonged lack of perfusion results in permanent damage to organs and tissues, resulting in:
- Cardiac failure
- Renal failure
- Cell death
Endpoint is death of the patient.
What are the different types of shock?
Hypovolemic shock is the rapid reduction of blood volume, typically due to hemorrhage, that results in activation of baroreceptors. This has a positive inotropic and positive chronotropic effect. As hypovolemia progresses, catecholamines and hormones are released, resulting in vasoconstriction and tachycardia. Hemorrhage first increases pulse and cardiac contraction and then increases vasoconstriction to maintain tissue perfusion. This narrows pulse pressure.
As blood loss continues, ventricular filling decreases, cardiac output falls, and there is a reduction in systolic BP. As CO2 de- creases, blood flow to noncritical organs and tissues decreases, leading to the production of lactic acid. After 1/3 of total blood volume is lost, cardiovascular reflexes no longer sustain adequate filling of the arterial circuit and frank hypotension occurs. Urine output decreases and thirst is stimulated to maintain circulating volume.
How is hypovolemic shock managed?
Resuscitation strategies are to optimize tissue perfusion while avoiding complications of overaggressive volume replacement. The goal of a trauma assessment is early recognition of circulatory dysfunction prior to development of hypotension and end-organ damage.
If there is a bleeding wound, apply direct pressure. If the wound is on an extremity and bleeding does not cease, elevate the extremity above the level of the heart. Apply additional dressings as needed. If bleeding continues on the arm, apply direct pressure to the brachial artery. If the wound is on a leg, apply direct pressure to the femoral artery. Application of cold packs will cause vasoconstriction.
Additional management techniques include:
- If there as a penetrating injury, stabilize the object if it is still impaled.
- Maintain airway.
- Apply high flow oxygen and be prepared to intubate at any point.
- Do not give an anticoagulant, such as aspirin.
- If there is no concern for a spinal cord injury, place the patient in Trendelenburg position.
- Keep the patient warm.
- Administer bolus of normal saline.
What is permissive hypotension?
A combination of the patient’s natural coagulation cascade, hypotension, and vessel spasm will temporarily arrest traumatic hemorrhage. Often the patient will have no apparent bleeding, but once resuscitation occurs and hypotension reverses, rapid arterial bleeding occurs. Permissive hypotension is the minimization of fluid resuscitation in the prehospital setting in patients with palpable radial pulses and normal mental status. Goal SBP is around 90. Aggressive fluid resuscitation could maintain sufficient blood flow to prolong survival until definitive hemorrhage control occurs. Contraindications to permissive hypotension include traumatic brain injury, spinal cord injury, patients who are hypertensive, patients with angina pectoris and cardiovascular disease, carotid artery stenosis, impaired renal function, and in- termittent claudication stage III/IV.
Distributive shock is peripheral vasodilation and blood flow maldistribution, commonly caused by sepsis or anaphylaxis.
Septic shock is caused by infection with any microbe, although frequently no specific organism is identified. Three major issues must be addressed during resuscitation: hypovolemia, cardiovascular depress, and induction of system inflammation.
Patients have relative hypovolemia as a result of increased ve- nous capacitance, which reduces right ventricular filling. GI loss, tachypnea, sweating, decreased oral intake, and third spacing also contribute to relative hypovolemia.
Cardiovascular depression and induction of systemic inflam- mation are the other two issues addressed during resuscitation. Severe sepsis is SIRS with suspected or confirmed infection and associated organ dysfunction or hypotension. Septic shock is SIRS with suspected or confirmed infection with hypotension despite adequate fluid resuscitation. In the presence of an infec- tion, inadequate tissue perfusion defines septic shock. Hypoxemia is more severe in septic shock.
Anaphylaxis is an antigen mediated immune reaction to a pre- sensitized antigen. This causes increased bronchial muscle tone, increased mucous membrane secretion, decreased vascular tone, capillary leakage, and urticaria. Hypotensive patients should remain supine due to complications from massive fluid shifts during volume depletion. Airway obstruction and cardiovascular collapse are the most common causes of death.
How is septic shock managed?
Airway management is always priority in resuscitation of any patient. Two large bore IVs with aggressive normal saline infusion and vasoactive agents in patients refractory to fluid resuscita- tion should be initiated. Norepinephrine, while not commonly used by ground EMS, is the preferred agent as the patient is typ- ically tachycardic. Blood sugars should be monitored as patients are commonly profoundly hyperglycemic. For those prehospital agencies with established protocols, early antibiotic administration should occur, with the preferred agents being vancomycin and piperacillin/tazobactam due to the broad spectrum nature. (Note: Antibiotics are not common on ground ambulances.)
How is anaphylactic shock managed?
Immediate administration of epinephrine (1:1000) 0.3 mg IM in the lateral thigh should be performed. This may be repeated in severe reactions. Diphenhydramine 50 mg IV/IM, methylprednisolone 125 mg IV, and fluid resuscitation are the mainstays of treatment. Consider albuterol 2.5 mg/3 mL nebulizer if bronchospasm persists following epinephrine. If refractory hypotension persists, dopamine 5 to 20 mcg/kg/min should be initiated if available.
Cardiogenic shock results when more than 40% of the myo- cardium undergoes necrosis from ischemia, inflammation, toxins, or immune destruction. Similar to hemorrhagic shock, alter- ations in circulation and metabolism occur. There is interference with blood flow from the heart, resulting in dyspnea, tachycar- dia, pulmonary or peripheral edema, and cyanosis.
How is cardiogenic shock managed?
The goal of management is adequate oxygenation of the myocardium. Oxygen and continuous positive airway pressure (CPAP) therapy are used to relieve dyspnea. Furosemide may be administered if pulmonary edema is noted upon exam. How- ever, note the furosemide may be detrimental in patients who are dehydrated secondary to infection. Preferred vasopressors for refractory hypotension include dopamine, dobutamine, and norephinephrine if available.
Obstructive shock is an extracardiac obstruction to blood flow. This is commonly caused by a pneumothorax, pulmonary embolism, or pericardial tamponade.
How is obstructive shock managed?
The most important management is to maintain adequate ox- ygenation.
- Tension pneumothorax ↦ Needle decompression on affected side in second intercostal space along mid-clavicular line.
- Pulmonary embolism ↦ High flow oxygen and intubation.
- Pericardial tamponade ↦ Pericardiocentesis.
Neurogenic shock affects autonomic responses. Sympathetic outflow is disrupted, causing unopposed vagal tone. This results in hypotension and bradycardia with warm, dry skin. This is the ONLY type of shock where the skin remains warm and dry. The higher the injury, the more likely severe symptoms will occur. Neurogenic shock, though, is a diagnosis of exclusion.
How is neurogenic shock managed?
Airway management is of utmost importance. For hypotension, fluid resuscitation with normal saline and vasopressors for refractory hypotension should be administered. If symptomatic bradycardia occurs, administer atropine 0.5 mg IV. If atropine does not reverse bradycardia, a transcutaneous pacemaker should be placed. EMS should transfer the patient to a facility with neurological and neurosurgical services.
What is spinal shock?
Spinal shock stems from acute spinal cord injury and results in the loss of all voluntary neurologic activity and reflexes below the level of the injury. Flaccid paralysis and loss of sensation occur. Spinal shock can last months. Some sources group spinal shock and neurogenic shock together. Although spinal and neurogenic shock can occur in the same patient, they are not the same disorder. The management, though, is the same.
Marx J, Hockberger R, Walls R, Adams J, Rosen P. Rosen’s Emergency Medicine: Concepts & Clinical Practice. 7th ed. Maryland Heights, MO: Mosby; 2010.