Shock is defined as a state of cellular and tissue hypoxia that is due to reduced oxygen delivery, increased oxygen consumption by the cells, inadequate utilization of oxygen, or a combination of any of these. There are four main types of shock – hypovolemic, cardiogenic, obstructive, and distributive. This lesson provides an overview of distributive shock. In order to understand shock, it’s important to have some basic knowledge of hemodynamics.

Hemodynamics can be understood in very simple terms with just three key components. 

  • Volume – This is the amount of blood inside the blood vessels.
  • The blood vessels (also called the vasculature) – Think of the vasculature as a bucket that holds all the blood volume in the body. 
  • The heart – This is the pump that forcefully pushes blood through the blood vessels.

Factors that affect blood pressure

Before we can dive into the hemodynamics of distributive shock, we have to understand the factors that affect blood pressure, and ultimately tissue perfusion. There are two key contributors to blood pressure – cardiac output and systemic vascular resistance (SVR).

What is cardiac output?

  • Cardiac output is affected by heart rate and stroke volume (CO = HR X SV).
  • Stroke volume is affected by preload, afterload, and contractility.
    • Preload is the amount of stretch at the end of diastole and is highly dependent on blood volume. The higher the volume, the greater the stretch. With greater stretch we get greater contractility and higher cardiac output.
    • Afterload is the force the ventricles must work against. Tightly constricted vessels increase afterload, causing the heart to have to work harder.
    • Contractility is how effectively the muscle fibers of the heart contract. Stronger contractions create greater stroke volume and increased cardiac output.

What is systemic vascular resistance?

  • SVR is affected by three things – the length of the vascular bed, viscosity of the blood, and vascular tone. Of these, vascular tone is the most variable. When vessels dilate, SVR goes down. When vessels constrict, SVR goes up.

The basics of distributive shock

Distributive shock is a type of shock in which systemic vasodilation leads to hypotension and decreased tissue perfusion. In other words, the bucket is too big for the amount of volume that is present. Remember, when vessels vasoconstrict, blood pressure goes up and oxygen delivery to the tissues is improved. When vessels dilate, blood pressure drops, and oxygen delivery to the tissues is compromised. In distributive shock, the vessels are dilated, blood pressure is low, and tissue perfusion is inadequate. There are three types of distributive shock – anaphylactic shock, neurogenic shock and septic shock. 

Anaphylactic Shock

Anaphylactic shock results from a severe hypersensitivity reaction. Think of a person who has a peanut allergy or who has an anaphylactic reaction to penicillin. When this individual is exposed to the allergen, the body has an overwhelming response which leads to systemic vasodilation and capillary permeability, both of which contribute to the shock state. Let’s talk through the pathophysiology of anaphylactic shock.

  • The individual is exposed to an allergen. 
  • Biochemical mediators are released which cause systemic vasodilation and capillary permeability.
  • Vasodilation increases the size of the “bucket”, so it is now too large for the volume that is present and hypotension results. 
  • Capillary permeability allows fluid to leak into the vascular space, creating an even greater mismatch between volume and vascular tone. In other words, now our bucket is much, much too large for the amount of volume present. 
  • The fluid can also leak into the interstitial space of the airway, causing angioedema and airway compromise. 
  • Up to 35 percent of intravascular volume can leak into the extravascular space within minutes, which means this patient can lose a lot of volume very, very quickly.
  • Decreased volume leads to decreased venous return and preload, which leads to decreased stroke volume and decreased cardiac output.
  • Decreased cardiac output further contributes to hypotension and inadequate tissue perfusion.
  • Inadequate tissue perfusion leads to impaired cellular metabolism and the shock state. 

In addition, anaphylaxis causes other problems as well, including laryngeal edema, excessive mucus production, bronchoconstriction, and coronary vasoconstriction…so now we have airway compromise and cardiac dysfunction, too. Death from anaphylaxis can occur due to cardiovascular collapse, airway obstruction, or both.

What are the signs and symptoms of anaphylaxis?

While we tend to think of anaphylaxis as happening almost immediately when exposed to an allergen, in some cases the symptoms may take up to an hour to appear. They include: 

  • Erythema, urticaria, and pruritus may be present prior to other signs and symptoms.
  • Angioedema may also occur early and can affect the airway as well as the GI tract. Airway involvement causes restlessness, apprehension, coughing, a hoarse voice, inspiratory stridor, wheezing, a sensation of fullness in the throat, dysphagia, dyspnea, and chest tightness.
  • Angioedema in the GI tract can cause abdominal pain, vomiting and diarrhea.
  • Hypotension and tachycardia as the reaction progresses.
  • Flat jugular veins due to decreased right ventricular volumes.
  • Altered level of consciousness as tissue perfusion suffers.
  • Noninvasive hemodynamic assessment shows reduced cardiac index and cardiac output as well as decreased systemic vascular resistance.

How do we treat anaphylaxis? 

Let’s look at each of the problems associated with anaphylaxis and what we can do to address them: 

Exposure to allergen– Stop the exposure immediately if possible.
Disastrous effects of biochemical mediators– Epinephrine stops the further release of mediators.
Airway obstruction– Oxygen and intubation/mechanical ventilation if needed.
– Epinephrine causes bronchodilation, which opens the airways.
Albuterol causes bronchodilation, which opens the airways.
Inadequate tissue perfusion due to vasodilation– Epinephrine causes vasoconstriction, which increases blood pressure.
Deficient fluid volume due to vascular permeability– IV fluids – 0.9% sodium chloride is the preferred solution as lactated ringers can potentially contribute to metabolic alkalosis. 
– If large volumes are needed, normal saline can cause hyperchloremic metabolic acidosis. In some cases a combination of NS and LR may be used.
Myocardial depression due to coronary vasoconstriction– Inotropes such as dopamine.
Patient is taking beta blockers and is not responding adequately to epinephrine– Glucagon may be utilized for its inotropic and chronotropic effects.
– Note that rapid infusion of glucagon can cause vomiting, so protect the patient’s airway!
Itching and hives– Diphenhydramine blocks the histamine response, but can cause sedation. If this is a concern, cetirizine IV may be used.
Risk for biphasic reaction (return of symptoms after treatment)– Glucocorticoids such as methylprednisolone.
  • IM epinephrine – 1:1,000 concentration (more concentrated!)
  • IV epinephrine – 1:10,000 concentration (more dilute!)
  • Epinephrine may also be utilized as a continuous infusion in patients who are not responsive to repeat bolus doses and aggressive fluid resuscitation. 

TL;DR anaphylactic shock

  • Response to an allergen
  • Systemic vasodilation and hypotension
  • Loss of fluids into the interstitial space due to capillary permeability
  • Airway obstruction
  • Key treatments are airway protection, fluids, and epinephrine
Neurogenic Shock

Another type of distributive shock is neurogenic shock. This subtype is most commonly associated with spinal cord injury and involves a loss of sympathetic tone and a disrupted sympathetic nervous system. Let’s break down the pathophysiology:

  • Spinal cord injury causes the transmission of impulses to be interrupted
  • Loss of sympathetic tone causes systemic vasodilation.
    • On the arterial side this leads to decreased systemic vascular resistance, hypotension and poor tissue perfusion. 
    • On the venous side, this leads to pooling of blood and decreased venous return. 
    • Decreased venous return leads to decreased preload, which leads to decreased stroke volume and decreased cardiac output.
    • Decreased cardiac output further contributes to hypotension and inadequate tissue perfusion.
    • Inadequate tissue perfusion leads to impaired cellular metabolism.
  • Loss of sympathetic tone inhibits the baroreceptor response, resulting in bradycardia. This reduces cardiac output even more and tissue perfusion continues to suffer.
  • Loss of sympathetic tone leads to disrupted thermoregulation, and the patient becomes poikilothermic. As a result they are unable to regulate their own body temperature and must rely on the temperature of the environment.
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Signs and symptoms of neurogenic shock

It’s important to understand that neurogenic shock may not happen at the time of injury. In some cases, it can develop hours or even days later due to secondary spinal cord injury related to edema and hemorrhagic necrosis of the gray matter at the site of injury.

The signs of neurogenic shock are:

  • Hypotension
  • Bradycardia
  • Warm and dry skin on the extremities due to the pooling of blood and vasodilation
  • Hypothermia due to heat loss in the periphery
  • Noninvasive hemodynamic monitoring shows reduced cardiac index, reduced cardiac output, and decreased SVR

How is neurogenic shock treated?

Let’s look at each of the problems associated with neurogenic shock and what we can do to address them: 

Prevent further injury– Immobilize the spine
Relative hypovolemia due to vasodilation– IV fluids to “fill the bucket” and improve preload and ultimately cardiac output
Hypotension due to vasodilation– Vasopressors such as norepinephrine cause vasoconstriction, which increases blood pressure
Bradycardia– Atropine or pacing to increase cardiac output
– In some cases, dopamine may be utilized
Hypothermia– Warming devices and maintain a warm environment
Risk for DVT due to venous pooling– SCDs and PROM promote venous return
Anticoagulants prevent the formation of clots 

TL;DR neurogenic shock

  • Usually associated with spinal cord injury
  • Systemic vasodilation and hypotension
  • The only shock state that includes bradycardia
  • Warm, dry skin and poikilothermia
  • Key treatments are fluids, vasopressors, atropine or pacing

The most common type of distributive shock you’ll see in the inpatient setting is septic shock, which results from an overwhelming and dysregulated inflammatory response to infection. Note that the sepsis response ranges in severity and not all patients who have sepsis will go into septic shock. It is, however, a leading cause of death in non-cardiac ICUs, with a mortality rate of 1 in 3.

First, let’s review the levels of severity with sepsis:

  • SIRS (systemic inflammatory response syndrome): Though not all patients with SIRS have sepsis, all patients with sepsis started out with SIRS. SIRS is an exaggerated response to some kind of stressor such as surgery, acute inflammation (ex: pancreatitis), tissue ischemia, and even cancer. To meet SIRS criteria, the patient must have two of the following:
    • Temperature above 38-degrees or below 36-degrees
    • HR above 90 beats per minute
    • RR above 20 breaths per minute or PaCO2 < 32 mmHg (indicating hyperventilation)
    • WBC > 12K or < 4K, or greater than 10% bands
  • Sepsis: SIRS + suspected or confirmed infection.
  • Severe sepsis: Sepsis that has resulted in organ dysfunction. This can include things like increased oxygen requirements, coagulation abnormalities such as PLTs < 100K or an INR > 1.5, elevated bilirubin, decreased urine output or elevated creatinine. Another key indicator of severe sepsis is lactate > 2 mmol/L.
  • Septic shock: Hypotension refractory to fluid resuscitation and/or lactate > 4 mmol/L.

In addition to being the most common type of shock, it is also the most complex. For the purposes of this review, we’ll keep it as simple as possible. The most common triggers for sepsis are pneumonia, urinary tract infections, and infections of the GI tract. Though we tend to look at these as localized infections, they trigger the body’s immune response, and this leads to a systemic reaction that, when left untreated (or only partially treated) can cascade into an overwhelming systemic response.

In a normal inflammatory response there’s a balance between pro-inflammation and anti-inflammation. This means that in most cases, the inflammatory response is mediated, the infection is controlled and the infected tissue heals. In sepsis, the pro-inflammatory mediators are out of balance with the anti-inflammatory mediators, and pro-inflammation wins. The end result is hypoperfusion, tissue ischemia and multiple organ dysfunction syndrome (MODS).

Let’s talk through the pathophysiology of septic shock in its most basic terms:

  • A pathogen invades the body, which activates the body’s immune response. In most cases, this is a bacterial infection of the urinary tract, lungs, soft tissues, or abdominal organs.
  • Mediators, cytokines, and pathogen-related molecules are released which causes coagulation and complement cascades to be activated.
  • Cytokines initiate the overwhelming systemic inflammatory response. 
  • Microvascular thrombosis occurs system wide due to activation of the coagulation cascade. In addition, anti-clotting mechanisms are disrupted, leading to DIC.
  • Endothelial damage and the activation of inflammatory cytokines lead to massive vasodilation. This means the “bucket” is now too large for the amount of fluid inside, a condition referred to as “relative hypovolemia.” When vessels dilate, blood pressure goes down and the result is impaired tissue perfusion.
  • Increased capillary permeability allows fluid to leak into the interstitial space, causing even more hypovolemia. This leads to decreased venous return, decreased preload, decreased cardiac output, hypotension and impaired tissue perfusion.
  • The CNS responds to the invading pathogen by stimulating the SNS, causing a hypermetabolic state. Oxygen demands increase, contributing to cell hypoxia.
  • Without adequate oxygen, cells rely on anaerobic metabolism, resulting in the buildup of lactic acid. 
  • Cellular hypoxia leads to tissue ischemia, multiple organ dysfunction syndrome, organ failure, and death.

Signs and symptoms of septic shock

  • In the hyperdynamic state where shock is initially compensated, the patient may be normotensive, but they could show other signs such as warm extremities, very brisk capillary refill (< 1 second) and bounding pulses. The body cannot maintain this for long and decompensation will follow if aggressive treatment is not initiated.
  • Tachypnea and increased oxygen requirements
  • Tachycardia as the body tries to compensate for hypovolemia and vasodilation
  • Fever or hypothermia
  • Cool extremities
  • Delayed capillary refill
  • Thready pulses
  • Oliguria or anuria
  • Hypotension that is refractory to fluid resuscitation
  • Noninvasive hemodynamic monitoring shows reduced cardiac index, reduced cardiac output, and decreased SVR

How is septic shock treated?

Ideally, we identify sepsis and intervene before it becomes septic shock. In some cases patients progress to septic shock even with early recognition, while other patients may not seek medical care until they are very, very ill. The initial treatment for someone with sepsis or septic shock is to draw a lactate level, obtain blood cultures, initiate antibiotics and give a weight-based fluid bolus. This all must happen very quickly in order for the patient to have their best chance at a good outcome. Every hour that antibiotics are delayed increases mortality by 8%. 

If the patient remains hypotensive after the fluids are administered, newer guidelines recommend a dynamic assessment of fluid responsiveness test. This test helps the MD determine if the patient’s hemodynamics would respond favorably to more fluids or if the patient requires vasopressor support. The reason we don’t just keep giving fluids is because doing so has been shown to increase patient mortality. Instead, we can measure their stroke volume index to determine if more fluids will help or if vasopressors will be more beneficial. 

The treatments for sepsis and septic shock are always going to be based on physician orders, but there are guidelines widely utilized to help guide care. You will usually hear this group of interventions referred to as the “sepsis bundle” or the “SEP-1” bundle. A bundle is simply a group of interventions and assessments that when performed together have been shown to improve patient outcomes. 

Here’s a brief summary of the hemodynamic problems with septic shock and how they are addressed:

Hypotension due to hypovolemia and vasodilation– Weight-based fluid bolus of 30 ml/kg to increase circulating volume, increase preload and improve cardiac output. 
– Lactated Ringer’s is the preferred solution as it decreases the risk of developing hyperchloremic acidosis.
Hypotension refractory to fluid resuscitation– Perform a dynamic assessment to determine fluid responsiveness.
– If fluid responsive, more fluids may be beneficial.
– If not fluid responsive, vasopressors cause vasoconstriction and increase blood pressure.
Overwhelming inflammatory response due to infection– Quick administration of antibiotics.
– Removal of the infection source when possible (for example, Foley catheter removal or I&D of a wound).

TL;DR septic shock

  • Septic shock occurs due to the body’s dysregulated and overwhelming response to infection
  • Patients in septic shock are hypotensive even after fluids are administered
  • Lactate level is elevated in septic shock
  • Key labs include a lactate level and blood cultures
  • Primary treatments are antibiotics, fluids, and vasopressors such as norepinephrine.

To close out, let’s compare each of these subtypes of distributive shock.

CauseAllergic reactionSpinal cord injuryInfection
Key problemsAirway obstruction and hypotensionHypotension, bradycardia, hypothermiaHypotension and MODS
Vasodilation present?YesYesYes
Capillary permeability present?YesNoYes
Meds usedEpinephrine, fluids, dopamine, diphenhydramineFluids, vasopressors, atropineAntibiotics, fluids, vasopressors

Review distributive shock on the go by tuning in to episode 346 of the Straight A Nursing podcast. Listen from any podcast platform, or straight from the website here.


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