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Shock: Assess and Manage

Gregory A. Schmidt, MD

Clinical Professor

Pulmonary – Critical Care Medicine

July 2020

As chiefs we highly recommend watching the video for Dr. Schmidt’s lecture as he has numerous dynamic ultrasound images with clinical context. We have highlighted the lecture below and provided various other resources to build your knowledge of shock.


  • Learn to ask physiologic questions

    • Is the cardiac output low?

    • Is the heart empty?

    • Is there pump dysfunction?

  • Recognize the causes of shock

  • Know an approach to vasoactive drug infusion (earlier may be better)

Shock Definition:

  • Circulatory failure causing tissue hypoxia

    • Usually MAP is low (blood pressure is a surrogate for blood flow)

    • Usually global oxygen transport is low

    • Microvascular dysfunction may play a role

  • Leading to dysfunction:

    • AKI, Encephalopathy, lactic acidosis, respiratory failure

Etiology of Shock

Two large trials, notice how the majority of shock is hypovolemic, septic, and cardiogenic. Very rarely is it something else. In an ICU, hypovolemic shock is much lower.

You must identify why you think shock is due to a certain etiology so that you can apply the appropriate management. It’s important when considering shock etiology to recognize which objective data points may be helpful and which are nonspecific to …

Physiologic Approach

If the blood pressure is low. Either the systemic vascular resistance is low, or the cardiac output is low.

  • Is cardiac output low?

    • If no, vasodilatory shock

  • If yes, is the heart empty?

    • If yes, hypovolemic shock

    • If no, there is pump dysfunction

      • LV, RV, valve, pericardium, tension pneumothorax, pulmonary embolism


This question is equivalent to asking if the pulse pressure is low.

Pulse pressure is an indicator for stroke volume as the only other variable is aortic compliance which does not change on a day to day, minute to minute basis.

A rise in pulse pressure is a surrogate marker for rise in stroke volume. See the sharp rise between 0 to 50 pulse pressure. Many of our cardiac dysfunction patients will have a vary narrow pulse pressure.

Venous oximetry may help in determining overall cardiac output. The differential diagnosis may be very different from a 78 venous sat versus a 46 venous sat.

POCUS 5 chamber view can demonstrate VTI in a validated, reproducible manner as a surrogate marker for cardiac output.

Every patient in shock should have a detailed POCUS because it can be extremely helpful in terms of diagnosis.

We have a lot of tools to determine if cardiac output is low, demonstrated above. If cardiac output is not determined to be low, then we are dealing with vasodilatory shock. If it is low, then we need to start working on the differential diagnosis for low cardiac output shock such as hemorrhagic, hypovolemic, cardiogenic (LV, RV, pericardia, Valve, PE)


Most of the time it is septic shock, but there is a differential including liver failure, vasodilatory drugs, adrenal insufficiency, pancreatitis, paost-cardiac arrest, post-op vasoplegia, thiamine deficiency. This is a state of systemic inflammation or systemic injury.

Remember that most commonly vasodilatory shock is septic, and the most important factor in determining outcome is time to antibiotics. You do not want to miss something like thiamine deficiency because the treatment is very benign. Remember to check their medication list or see the anesthesia operative report as many medications can cause systemic vasodilation.



We used to think that anyone is low they need a bolus. Many patients with hypotension and oliguria

Even those that responded, many of these responses were transient. If we choose to give a fluid bolus, we should have objective measurements before and after the intervention to know if the fluid was helpful to the patient.

The single center RIVERS trial showed that early goal directed fluid therapy showed benefit to patients. All of the large subsequent trials following could not see benefit to early goal directed fluid therapy.

The question of fluids versus early vasoactive medications is still yet to be determined. The goal is determine those patients that would benefit from fluid by using pulse pressure variability, passive leg raise, IVC change and avoid giving fluids to those patients that may cause harm.

Bryne et all AJRCCM 2018 demonstrated that in an animal model (septic sheep), fluids versus early vasoactive approach, the fluid arm required more norepinephrine and vasopressin doses over time with higher lactate levels compared to the early vasoactive medication arm.

There is little evidence to support large volume of fluids.

There is no harm that has been demonstrated from an early vasoactive approach

Systematic review of RCTs for Lower fluid versus higher fluid boluses. In this systematic review, they found very low quantity and quality of evidence supporting the decision on the volumes of IV fluid therapy in adults with sepsis.

Shown to be ineffective in predicting fluid response.

Dynamic predictors seem to be better at predicting fluid responsiveness. Variations in the systolic pressure and the pulse pressure seemed to be the most predictive.

Passive leg raise if done well seems to be an accurate physical exam maneuver to predict fluid responsiveness.

IVC can be measured if the patient is passively ventilated with a big enough tidal volume. It should be measured 2-3 cm from the right atrium ideally. Here is a M-mode demonstration that does not show variability of the IVC which means they are less…

If the patient is spontaneously breathing, there are many more factors that affect IVC collapse and this measurement should be used cautiously to determine fluid responsiveness as it has not been validated in studies.

Then There’s Pump Dysfunction

21 year old transferred to ICU for liver transplant evaluation, found to have profound systolic dysfunction on POCUS.

Pump Dysfucntion (complex, but can all be visualized with ECHO)

  • LV dysfunction

    • systolic

    • Diastolic

  • RV dysfunction

  • Tamponade

  • Severe valve

    • facility with color doppler.

Attempt a Specific Diagnosis as it will affect outcomes

Cardiogenic Shock due to MI: early revascularization will save lives.

PE shock: thrombolysis

Tamponade: pericardiostomy

Flail mitral valve: valve surgery

Tenstion ptx: Chest tube

Shoshin beriber: thiamine


Norepnephrine has been shown to be our first line agent in all forms of shock:

Dopamine should be our last choice for vasoRx. Associated with greater mortality compared to norpeinehprine.

Epinephrine compared to norepinephrine

Vasopressin has been shown to reduce doses of norepinephrine but does not have impacts on important clinical markers such as survival.

Vasopressin did not impact kidney failure-free days compared to norepinephrine. It was thought to have some selective vaso-sparing effects in the kidneys that would have been beneficial, not seen in this study.

Vasopressin may have some benefit in reducing arrythmia compared to norepinephrine

MAP Target 60-65 mm Hg

Higher targets have been tested in numerous trials showing no benefit. Higher targets may have some adverse effects such as atrial fibrillation.

Negative trial, outcomes were not improved, but there was no difference between the two arms of 60 and 65 in older patients.

Negative trial, outcomes were not improved, but there was no difference between the two arms of 60 and 65 in older patients.

Key Points

  • Shock is classified into three types: (1) hypovolemic (due to inadequate perfusion in the setting of decreased blood volume), (2) cardiogenic (due to poor perfusion from decreased cardiac function), and (3) distributive (due to loss of vascular tone).

  • The basic goals of management in shock, regardless of its type, are to restore perfusion as quickly as possible and to reverse the disease process leading to the shock state.

  • The mainstays of shock treatment include fluid administration, vasopressors, inotropes, and blood transfusion; however, diagnosing and reversing the underlying cause of shock is as important as restoring perfusion.


Additional Resources:

NEJM 360 – Sepsis/Shock


Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016

Rhodes A et al. Intens Care Med 2017.

The most recent version of the Surviving Sepsis Campaign guidelines for management of sepsis.

Watch this video to see the updates from the 2012 to 2016 guidelines.

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

Singer M et al. JAMA 2016.

Updated definitions and clinical criteria for sepsis and septic shock by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine



Rolando Sanchez, MD

Clinical Assistant Professor

Pulmonary – Critical Care Medicine

July 2018


Rolando Sanchez, MD

Clinical Assistant Professor

Pulmonary – Critical Care Medicine

Post by Roger D. Struble MD MPH

July 14 2020