CONTENTS

• Introduction
• Diagnosis
• Causes of shock
• Evaluating the cause of shock
• Stabilization
• Podcast
• Questions & discussion
• Pitfalls

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introduction

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Shock is a state of systemic hypoperfusion, with inadequate blood supply to the tissues. Unfortunately, this may occur in different ways. The most simple physiology of shock is cardiogenic shock, with low cardiac output to the entire body. However, septic shock can occur with an elevated cardiac output due to microvascular dysfunction at the tissue level (blood shunts through some vessels, while ignoring others). Because shock has varying physiologies, it defies any simple operational definition at the clinical level. Shock is a bit like obscenity – after a while, you know it when you see it.

Shock is extraordinarily important because it is generally a final common pathway before death. Most serious diseases are capable of causing shock. Left untreated, shock will progress to multi-organ failure and death. However, shock is often reversible, thereby avoiding death.

The importance of promptly diagnosing shock and discerning its cause cannot be overstated. Unfortunately, shock may present in a variety of ways, so diagnosis isn't always so simple. For example, shock is typically associated with hypotension and reduced cardiac output, but it can also occur with normal blood pressure and an increased cardiac output.

Different types of shock present differently. For example, the stereotypical patient with early sepsis and distributive shock will appear quite different from the patient with cardiogenic shock (table below). Unfortunately, reality isn't quite this simple. Advanced cardiogenic shock often causes bacterial translocation from the intestines, leading to systemic inflammation and vasodilation. Alternatively, advanced septic shock frequently causes a septic cardiomyopathy. Thus, advanced cardiogenic shock and advanced septic shock may be very difficult to sort out.

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diagnosis

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There is no single diagnostic test for shock. Patients with various forms of shock will present differently. Nonetheless, there is a constellation of findings which often occurs in the context of shock. As patients accrue many of these features, the possibility of shock should be seriously considered. 

hemodynamics (trends > absolute values)

• Hypotension (e.g., MAP below ~65 mm, or significant drop from baseline).
• Elevated shock index:
  • Shock index = HR / SBP.
  • Shock index above ~0.8 suggests significant instability.
• Bradycardia: cardiac output is directly proportional to heart rate. Severe bradycardia (e.g. heart rate below ~45) should always raise concern for shock. Even if the blood pressure is maintained by compensatory systemic vasoconstriction, cardiac output and perfusion may still be poor (more on bradycardia here).

oliguria (or dark urine)

• Urine output below ~0.5 cc/kg/hour is worrisome for renal malperfusion.
• Dark urine also suggests renal hypoperfusion (e.g., immediately after Foley catheter insertion, before the urine output is known).
• (More on the approach to oliguria: 📖).

skin perfusion

• Cool hands and knees are an early sign of vasoconstriction with reduced cardiac output. Normal people may have cool hands, but if all extremities are cool that's more specific for hypoperfusion.
• Mottling is less sensitive, but more specific for hypoperfusion and elevated mortality (figure below). Mottling suggests active endogenous vasoconstriction, implying that the patient would benefit from an increase in cardiac output (e.g. an inotrope) – not additional exogenous vasoconstrictors.
• Capillary refill time: The ideal technique may be to compress the fingertip using a slide with enough pressure to cause blanching for ten seconds. Any clear surface can also be used, such as a plastic urine specimen container.(27908340) Normal capillary refill time is <3-4 seconds, whereas >5 seconds suggests impaired perfusion.

delirium

• New-onset delirium can be a sign of shock (especially septic shock). However, this is neither very sensitive nor specific.
  • Most new-onset delirium isn't due to shock.
  • ⚠️ Patients with acute-on-chronic cardiogenic shock can maintain normal mentation despite profoundly low cardiac output.

hyperlactatemia (or jumping anion gap) 

• Lactate >4 mM suggests shock, but this has a broad differential diagnosis. Lactate usually doesn't reflect oxygen deficiency, but rather endogenous epinephrine in response to physiologic stress.🌊 This explains why lactate can be normal in shocked patients who have inadequate sympathetic nervous function.
  • High lactate level is worrisome. This should be interpreted to represent shock or some other impending disaster until proven otherwise.
  • Normal lactate isn't necessarily reassuring (it can occur in shock).
  • (Further discussion of the evaluation of hyperlactatemia: 📖)
• 💡 A sudden jump in the patient's anion gap suggests hyperlactatemia if there is no obvious alternative explanation (e.g., absence of starvation or diabetes that could cause ketoacidosis). In a hospitalized patient, a jumping anion gap represents shock until proven otherwise.
  • (Further discussion of the evaluation of anion gap elevation: 📖)

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causes of shock

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arrhythmic shock

• Tachyarrhythmia (usually >>150 b/m).
• Bradyarrhythmia (usually <45 b/m).

hypovolemic shock

• Hemorrhage:
  • External bleeding (penetrating trauma, postpartum).
  • GI bleed.
  • Retroperitoneal bleed.
  • Intraperitoneal bleed.
  • Hemothorax.
• Hypovolemia:
  • Vomiting and/or diarrhea.
  • Over-diuresis.
  • Post-ATN or postobstructive polyuria.

LV failure (“cardiogenic” shock)

• LV systolic failure:
  • Myocardial infarction.
  • Myocarditis.
  • Overdose (e.g., beta-blocker).
• Acute aortic or mitral valve regurgitation:
  • Endocarditis.
  • Papillary muscle rupture.
  • Aortic dissection.
• Prosthetic valve thrombosis.
• Dynamic LV outflow tract obstruction (LVOTO).

RV failure

• Pulmonary embolism.
• Decompensated chronic pulmonary hypertension.
• Right ventricular myocardial infarction.

obstructive

• Tamponade.
• Tension pneumothorax.
• Elevated intrathoracic pressure:
  • Abdominal compartment syndrome.
  • AutoPEEP.

vasodilatory shock (“distributive” shock)

• Severe systemic inflammation:
  • Septic shock.
  • Pancreatitis.
  • Post-cardiac arrest SIRS.
  • Post-MI SIRS. 
• Anaphylaxis.
• Endocrine:
  • Adrenal crisis.
  • Thyroid storm.
• Neurogenic shock:
  • Trauma.
  • Spinal anesthesia. 
• Liver failure.
• Excess vasodilatory drugs.

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evaluating the cause of shock

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history and data review

• ? Cardiac history (Especially any prior information about cardiac structure/function such as EKG, echo, or even chest CT showing chamber size).
• ? Adrenal disease (Noting: Patients chronically on oral steroid may be assumed to be insufficient).
• ? History of venous thromboembolic disease.
• ? Immunosuppression, ? Invasive devices (e.g. hemodialysis catheters).
• ? Recent procedures or trauma.
• ? Current medications & changes in medication list.

examination

labs

• Electrolytes (including Ca/Mg/Phos).
• Complete blood count with differential.
• Coagulation studies.
• CRP (C-reactive protein).
• Lactate.
• If septic shock is suspected:
  • Blood cultures x2.
  • Urinalysis with reflex culture.
  • Sputum culture if clinically indicated.
  • Procalcitonin (if initiating antibiotics).
• Endocrine evaluation:
  • Random cortisol level (if adrenal insufficiency is possible).
  • TSH (if thyroid storm suspected).
• Troponin (if EKG/history suggest acute MI).

radiologic studies

• EKG is occasionally helpful (e.g., may reveal occlusive MI, or RV strain).
• CXR (e.g., may reveal pneumonia, or cardiogenic edema implying LV failure).
• CT may be considered depending on the clinical scenario:
  • CTA to evaluate for pulmonary embolism.
  • CT abdomen/pelvis to evaluate for septic focus.

differential & categorization

Findings on ultrasonography and physical examination may be integrated as shown below. This tends to work best in previously-healthy patients with a single mechanism of shock. Patients with multiple chronic problems or multifactorial shock may defy categorization.

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stabilization

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Stabilization must start immediately, often before the cause of shock is known. The following are common interventions to consider.

volume resuscitation

• Fluid administration should be tailed to the individual patient's hemodynamic assessment.
• Fluid is often provided in boluses (e.g., 500 ml) with attention to patient response. The total amount of fluid administered should generally be limited to <1-2 liters in the absence of a history suggesting substantial total-body volume depletion (e.g., severe gastroenteritis with a colostomy).
• Fluid administration can be diagnostic and therapeutic in confusing situations where hypovolemia is suspected:
  • If fluid resuscitation alone resolves shock, this supports a diagnosis of hypovolemia.
  • If fluid resuscitation fails, this suggests an alternative diagnosis. This is especially true if fluid resuscitation results in adequate filling pressures (e.g., full IVC) without resolving the shock.

vasopressor administration

• Vasopressor administration should be started immediately if the blood pressure is inadequate (e.g., MAP<60 mm).
• Vasopressors may be administered via peripheral vein.
  • Norepinephrine may be given peripherally with careful monitoring of the IV site for limited periods of time.
  • Phenylephrine or epinephrine have a lower risk of extravasation and may be safer to use in situations with less rigorous monitoring.🌊

antibiotics

• If sepsis is possible, cultures should be performed and empiric antibiotics should be started without delay.
• In patients with possible sepsis, you don't necessarily need to go extremely broad with the antibiotics. A single broad-spectrum agent may be reasonable (e.g., piperacillin-tazobactam).

steroids

• Indicated for patients whom you suspect have adrenal crisis, for example:
  • Patients with known adrenal insufficiency.
  • Patients taking chronic steroids who recently missed doses.
• When in doubt about adrenal insufficiency, a reasonable approach is to give 6 mg dexamethasone and check a cortisol level simultaneously. Dexamethasone doesn't interfere with the cortisol level, allowing you to perform an ACTH-stim test later on if indicated. (More on adrenal crisis 📖)

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podcast

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• Patients who have suffered cardiac arrest or MI will often develop a post-arrest or post-MI distributive shock due to cytokine release and systemic inflammation. This may lead to a confusing multifactorial picture, where distributive shock may obscure the primary problem.
• There is no sign, symptom, or lab which is entirely sensitive for shock. Therefore, no single investigation can exclude shock (e.g. “the patient is mentating well so she cannot be in shock” or “the lactate is normal so that excludes shock” are both incorrect statements).
• Patients in distributive shock may have a normal blood pressure, particularly if they have chronic hypertension.
• Diagnostic algorithms for shock (like any diagnostic algorithms) work best among patients with a single disease process who were previously normal. Unfortunately, many patients have multifactorial shock on an abnormal baseline (e.g. chronically reduced ejection fraction) – so simple algorithms will fail these patients.
• The most common cause of shock of unclear etiology is septic shock. However, other causes should be carefully excluded prior to reaching an empiric diagnosis of septic shock (e.g. echocardiography to evaluate for massive pulmonary embolism or pericardial tamponade).
• Don't forget to evaluate archival data (e.g. old EKGs and CT scans). These may help sort out chronic pathology versus acute pathology.