Surgical Critical Care

Stupeficium

I foresee death by culture shock.

Woody Allen

Hi guys… Today we are going to scratch the surface of the universe of shock.

As usual, we will begin this post with a short clinical scenario to introduce the real problem of shock: it may be the consequence of very different mechanisms…

So then… Let’s begin…

You are on call at night, as always. The ED is quiet, and you decide to go to bed. At about 1 AM the ward nurse calls you because the patient in bed 14 is not doing well.

The patient is Mr. Kenneth McCormick, an 82-year-old man who underwent two days ago a laparoscopic right colectomy for colonic cancer. He spent one night in ICU postoperatively, and he was sent back to the surgical ward the day after. His past medical history includes congestive heart failure with moderate left ventricular dysfunction, atrial fibrillation (he is on oral anticoagulants), mild chronic renal failure, type 2 diabetes, and COPD.

When you arrive, the patient is sweaty, agitated, confused, tachypneic (RR 24 bpm), with tachycardia (HR 121 bpm AR), and hypotensive (BP 82/45 mmHg). The patient’s saturation is 89% in room air. The Foley catheter is already in place, and the urine output has been 125 mL in 5 hours (about 25 mL/h).

This patient is clearly in shock… But the problem here is why?!…

Let’s examine some possible explanations…

  1. The patient is bleeding inside the abdomen and is in a hemorrhagic shock;
  2. The patient has an anastomotic leakage (no drain was placed at the end of the operation) and now has developed a septic shock;
  3. The patient has developed an acute heart failure, determining a cardiogenic shock.

Similar presentation, different mechanisms, distinct treatments…

Introduction

Shock is just a word to describe a state of insufficient blood flow to the tissues of the whole body as a result of problems with the circulatory system. This leads to cellular damage and, with time, it can lead to multiple organ failure.

The blood flow is important to all organ systems because it is the carrier of oxygen… No oxygen, no life…

So then, to ensure an adequate blood flow there should be sufficient blood pressure… But blood pressure is the result of something… Let’s see…

  • Blood Pressure = Resistance to Flow X Cardiac Output (i.e. the blood volume pumped by the heart per minute);
  • According to Poiseuille’s law, Resistance to Flow is related to the diameter and the length of the tube (i.e. vessels);
  • Cardiac Output = Heart Rate (beats per minute) X Stroke Volume (i.e. the blood volume pumped by the heart per beat)
  • Stroke Volume = End Diastolic Volume (i.e. the blood volume inside the heart after filling) – End Systolic Volume (i.e. the blood volume inside the heart after contraction)

Another important parameter to remember is the Mixed Venous Oxygen Saturation (SvO2), which is the amount of oxygen coming back to the right side of the heart. It reflects the oxygen extraction for the whole body. However, it is difficult to record, because it needs a pulmonary artery catheter (i.e. Swan-Ganz catheter) to measure it at the pulmonary artery bifurcation level.

In the following section, we are going to illustrate the different types of shock… Remember that each type is the result of an impairment of one of the parameters mentioned above…

But don’t worry… We are going to explain that as well…

Classification

Previously, we have already encountered two different kinds of shock: hemorrhagic shock (Read the previous post The Five Letters on Which Trauma Stands – Part 4) and septic shock (Refer to The Sepsis Six Samurai – Part 1). Today, we are going to classify the distinct types of shock according to their mechanism of action. Additionally, we will try to give you the elements to distinguish them to give the patient the most appropriate treatment.

So then, shock can be classified as follows:

  • Hypovolemic shock – it is the consequence of low circulatory volume and it may be caused by bleeding (i.e. hemorrhagic shock) or dehydration (e.g. burns, vomiting, diarrhea, excessive urination, etc…);
  • Cardiogenic shock – it happens when the heart pumping function fails (e.g. heart attack, valvular diseases, arrhythmias, etc…);
    • Obstructive shock – it is secondary to an obstruction of blood flow in one of the main circulatory systems (e.g. pulmonary embolism, cardiac tamponade, tensive pneumothorax, etc…), impairing the pumping function of the heart;
  • Distributive shock – it is due to excessive vasodilation, thus decreasing blood pressure. It may be caused by sepsis (i.e. septic shock), anaphylaxis (i.e. anaphylactic shock), and damage to the central nervous system (i.e. neurogenic shock). These three mechanisms work differently one to another:
    • Septic shock – as a result of the ongoing overwhelming infection, the immune system releases cytokines that cause diffuse vasodilation. Moreover, the induced damage to the endothelial cells increases fluid leakage from the capillaries, causing circulatory volume loss. Additionally, septic shock patients develop microvascular clotting, further reducing the blood flow;
    • Anaphylactic shock – the immune system reacts to an allergen, releasing a large amount of histamine, which has similar effects to cytokines;
    • Neurogenic shock – after a spinal cord injury, there is a loss of sympathetic tone; therefore, the parasympathetic nervous system is unopposed, causing uncontrolled vasodilation.

Ok… Now, let’s find out why blood pressure decreases in the different types of shock…

  • Hypovolemic shock – the blood volume is reduced, but the cardiac function is maintained. Therefore, the End Diastolic Volume is low and, consequently, the Stroke Volume is reduced. This will decrease the Cardiac Output and so the Blood Pressure. The body response to decreased Cardiac Output is to release catecholamines (i.e. epinephrine and norepinephrine), ADH, and Angiotensin II, in order to induce vasoconstriction, increasing the Resistance to Flow, and raise the Heart Rate. These adaptations aim to increase the Blood Pressure;
  • Cardiogenic Shock – the injured heart is not able anymore to pump enough blood, thus decreasing the Stroke Volume, and so on…
    • Obstructive Shock – in this case, the heart is healthy, but something prevents it to function adequately;
  • Distributive Shock – the blood volume is normal and so is the cardiac function, but there is diffuse vasodilation. Vasodilation, by definition, increases the diameter of vessels, thus reducing the Resistance to Flow and, consequently, the Blood Pressure. However, in this case, the blood flow is fast, which is in contrast with the two other types of shock described before, in which the blood flow is slow.

If in hypovolemic and cardiogenic shock the oxygen transported by the blood flow is not sufficient to fulfill the body needs, in distributive shock the problem is quite the opposite… In fact, in distributive shock, the oxygen is enough, but the low resistance and the fast blood flow prevent it from being handed over to the cells. Moreover, tissues are damaged and are not able to appropriately extract oxygen from the blood. These concepts translate into different SvO2 levels: low in hypovolemic and cardiogenic shock, normal or high in distributive shock.

Clinical Presentation & Diagnosis

From the clinical point of view, shock can present with multiple signs and symptoms, many of which correlate with organ hypoperfusion.

The mainstream of shock is low blood pressure. Additionally, as already stated, it can be followed by signs of organ damage:

  • Brain – confusion, anxiety, low GCS, unconsciousness, coma;
  • Kidney – reduced urine output;
  • Skin – cold extremities, sweating, mottled or bluish skin (remember that distributive shock may present with warm and/or flushed skin due to increased blood flow, fever, and/or hives; this is the reason why distributive shock is defined as “warm shock”, where hypovolemic and cardiogenic shock are described as “cold shock”);
  • Heart – low cardiac output (in case of distributive shock, there may be normal or high cardiac output), cardiac arrest.

To compensate for the reduced organ perfusion, the body increases the heart rate and the respiratory rate. This would improve the organ blood flow and the quantity of oxygen transported. However, this response is not sufficient to resolve the state of shock because the causing agent is still there. Consequently, the next adaptation of the human body to hypoperfusion is to switch the way of producing cellular energy from aerobic to anaerobic metabolism, thus increasing blood lactate levels. Nevertheless, these are just temporary compensations, but, in the end, they will not save our patient.

The diagnosis of shock is quite easy to make. It is based on clinical presentation and laboratory results.

Lab tests may also help to identify the causative mechanism (e.g. leukocytosis and high CRP and procalcitonin in septic shock, high troponin in cardiogenic shock, etc…). However, they should not be used alone to determine which type of shock is ongoing.

The diagnosis of shock and its underlying mechanism should be promptly identified to start the most appropriate treatment as soon as possible.

The most important elements to consider are:

  • Patient’s medical history
  • Clinical examination
  • Arterial blood gas
  • Laboratory exams (e.g. whole blood count, renal and liver function tests, inflammatory markers)
  • Point of care ultrasound (i.e. the RUSH protocol)
Treatment

As already stated, the treatment should be individualized on the type of shock you are dealing with.

However, the cornerstone of all treatments is to restore and stabilize the blood pressure, ensuring enough perfusion to vital organs (i.e. heart and brain). This can be faced using the ABCDE approach, you won’t miss a thing!

In general, this can be achieved through the administration of fluids and/or medications able to increase heart contractility (e.g. dobutamine), induce vasoconstriction (e.g. norepinephrine) and/or retain fluids (e.g. albumin).

Another important way to increase tissue oxygenation is to give the patient supplemental oxygen, thus raising the amount of oxygen transported by the blood flow and making it easier to release.

Ok guys… We think it’s enough now…

We have just scratched the surface of shock… But as you have seen, each shock is a precise and standalone entity… And this post was not meant to analyze each one of them… We aimed to give you just a general overview of the different types of shock and their underlying mechanisms…

We hope you have enjoyed it!!!

See you next time… and until then… Be good, be brave, be acute care surgeons…

References
  1. Osmosis.org. Shock – Clinical Presentation. Medscape. Published on October 15, 2019. Accessed on March 27, 2021. Available at [https://www.youtube.com/watch?v=sJWR93G4UpI].
  2. Marino PL. The little ICU book. 2nd Ed. Philadelphia, PA: Wolters Kluwer; 2017.
  3. Standl T, et al. The nomenclature, definition and distinction of types of shock. Dtsch Arztebl Int 2018;115:757-68.
  4. Kislitsina ON, et al. Shock – Classification and pathophysiological principles of therapeutics. Curr Cardiol Rev 2019;15:102-13.
  5. Gaieski DF, et al. Definition, classification, etiology, and pathophysiology of shock in adults. UpToDate. Published on January 10, 2020. Accessed on March 27, 2021. Available at [https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults].
  6. Alilamedicalmedia.org. Shock, pathology of different types, animation. Alila Medical Media. Published on October 29, 2018. Accessed on March 26, 2021. Available at [https://www.youtube.com/watch?v=WueGqL58tlo].
  7. Weingart SD, et al. The RUSH exam: rapid ultrasound for shock and hypotension. EMCrit. Published on March 2008. Accessed on March 27, 2021. Available at [https://emcrit.org/rush-exam/].
How to Cite This Post

Bellio G, Marrano E. Stupeficium. Surgical Pizza. Published on May 17, 2021. Accessed on July 31, 2021. Available at [https://surgicalpizza.org/critical-care/stupeficium].

3 Comments

    • SurgicalPizza
      SurgicalPizza

      Thank you Kobe!!! 😀
      It doesn’t matter what the patient had (all our clinical cases are made up ad hoc to better present the main topic or a common problem related with it)… The point is not to draw conclusions too soon and too easily… You have always to ask yourself if there is something else you are not considering at that moment… Do not exclude anything… This patient could have had any of the three possibilities listed above or none… The solution is to consider them all… 🙂

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