Compensated, decompensated and irreversible shock: what they are and what they determine

By Cristiano Antonino On May 22, 2022

Sometimes, shock is difficult to identify in its early phases and the patient can transition into decompensated shock before you realize. Sometimes that transition occurs prior to our arrival to the scene

In these instances, we need to intervene and intervene quickly because failing to do so will result in the patient progressing to irreversible shock

The better terms to use when describing shock are perfusion and hypoperfusion.

When we are perfusing adequately not only are we delivering oxygen and nutrients to the organs of the body, but we are also removing the waste products of metabolism at an appropriate rate as well.

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There are eight types of shock that we can encounter:

Hypovolemic – the most commonly encountered
Cardiogenic
Obstructive
Septic
Neurogenic
Anaphylactic
Psychogenic
Respiratory insufficiency

The three phases of shock: Irreversible, compensated, and decompsated shock

Phase 1 – Compensated shock

Compensated shock is the phase of shock in which the body is still able to compensate for absolute or relative fluid loss.

During this phase the patient is still able to maintain an adequate blood pressure as well as brain perfusion because the sympathetic nervous system increases the heart and respiratory rates and shunts blood to the core of the body through vasoconstriction of the blood vessels and microcirculation, the precapillary sphincters constrict and decrease blood flow to areas to areas of the body with a high tolerance for decreases in perfusion, e.g. the skin.

This process actually increases the blood pressure initially because there is less room within the circulatory system.

The signs and symptoms of compensated shock include:

Restlessness, agitation and anxiety – the earliest signs of hypoxia
Pallor and clammy skin – this occurs because of microcirculation
Nausea and vomiting – decrease in blood flow to the GI system
Thirst
Delayed capillary refill
Narrowing pulse pressure

Phase 2 – Decompensated shock

Decompensated shock is defined as “the late phase of shock in which the body’s compensatory mechanisms (such as increased heart rate, vasoconstriction, increased respiratory rate) are unable to maintain adequate perfusion to the brain and vital organs.”

It occurs when the blood volume decreases by more than 30%.

The patient’s compensatory mechanisms are actively failing and cardiac output is dropping resulting in a decrease in both blood pressure and cardiac function.

The body will continue to shunt blood to the core of the body, the brain, heart and kidneys.

The signs and symptoms of decompensated shock are becoming more obvious and the increase in vasoconstriction results in hypoxia to the other organs of the body.

Because of the decrease in oxygen to the brain the patient will become confused and disoriented.

The signs and symptoms of decompensated shock include:

Alterations in mental status
Tachycardia
Tachypnea
Labored and irregular breathing
Weak to absent peripheral pulses
A decrease in body temperature
Cyanosis

While the body is trying to increase blood flow to the core of the body the sympathetic nervous system loses control of the precapillary sphincters that assist in the microcirculation mentioned earlier.

The postcapillary sphincters remain closed and this allows for blood pooling, which will progress to disseminated intravascular coagulation (DIC).

In the early stages this issue is still correctable with aggressive treatment.

The blood that is now pooling begins to coagulate, the cells in the area are no longer receiving nutrients and anaerobic metabolism is responsible for the production of adenosine triphosphate (ATP).

DIC starts during this phase and continues to progress during irreversible shock.

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Phase 3 – Irreversible Shock

Irreversible shock is the terminal phase of shock and once the patient progresses into this phase it is the point of no return because there is a rapid deterioration of the cardiovascular system and the patient’s compensatory mechanisms have failed.

The patient will present with severe decreases in cardiac output, blood pressure and tissue perfusion.

In a last-ditch effort to save the core of the body blood is shunted away from the kidneys, liver and lungs to maintain perfusion of the brain and heart.

Treatment

The most important part of treatment is recognition of the event and proactively working to prevent the progression of shock.

As I said earlier, hypovolemic shock is the most commonly encountered form of shock in the prehospital setting.

This makes sense, as the most common cause of death for people ages 1-44 is unintentional injuries.

If the patient is bleeding externally, we know we need to intervene immediately so that we can keep as much blood in the container as possible.

If the patient presents with signs of internal bleeding, we need to transport to a trauma center for surgical interventions.

High-flow oxygen is indicated, even if the patient is still mentating and has a pulse oximetry of 94% or higher.

We know that in these instances if there is a suspicion of underlying hypoxia that oxygen can be administered regardless of what the pulse oximetry displays.

Keep your patient warm, decreases in body temperature impair the body’s ability control bleeding secondary to impaired platelet function and results in an inappropriate breakdown of the clots that have formed.

And lastly, intravenous therapy to maintain a state of permissive hypotension. This means that the systolic blood pressure should be between 80- and 90-mmHG.

We commonly default to 90-mmHg as we are taught that that is the transition from compensated to decompensated shock.

Writted by: Richard Main, MEd, NRP

Richard Main, MEd, NRP, is an EMS instructor. He has worked in EMS since 1993 after obtaining his EMT from Johnson County Community College. He has lived in Kansas, Arizona and Nevada. While in Arizona, Main worked for Avra Valley Fire District in for 10 years and worked in private EMS in Southern Nevada. He currently works as a professor of emergency medical services at the College of Southern Nevada and is lead instructor for Distance CME.

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