(See also Shock Review Part 2: Goals of Therapy)
Jean-Louis Vincent, editor in chief of Critical Care, has a new review article on circulatory shock in the New England Journal of Medicine, where he’s also the editor of their new critical care section. Daniel De Backer co-authors. (See also the PulmCCM topic, “Vasopressors for septic shock.“)
What’s “circulatory shock”? Just shock, with its four pathophysiologic mechanisms:
Assessment of the cause(s) of shock can be challenging in individual patients, but one study of 1,600 patients in shock concluded that 62% had septic shock, 16% had cardiogenic shock, 16% hypovolemic shock, anaphylaxis or other non-septic distributive shock in 4%, and only 2% had obstructive shock.
Importantly, these mechanisms of shock can coexist, such as in someone with septic shock (distributive) resulting in myocardial depression (cardiogenic), or who has concomitant severe dehydration and also bleeding (hypovolemic) or a PE (obstructive). Failing to recognize and treat co-existing problems and contributors to shock could lead to worse outcomes — for example, under-resuscitating an elderly patient in septic shock who is severely hypovolemic.
In addition to the physical examination, authors advise performing a bedside echocardiogram in all patients with shock whenever possible. Echocardiography may reveal unsuspected reasons for shock (a large pericardial effusion with tamponade), and a skilled echocardiographer can identify clues that might help refine management of shock (measurement of heart chamber sizes and function; predicting volume responsiveness through respiratory variation in vena cava dimensions or the more esoteric “aortic velocity-time integral,” a surrogate for stroke volume).
Need a mnemonic? Authors propose “VIP”: Ventilation (oxygen, intubation etc), Infusion (volume resuscitation), Pump (vasoactive drugs) to manage people in shock. To wit:
Careful with the BiPAP; authors advise intubation and mechanical ventilation for those with severe dyspnea, hypoxemia, or acidemia (pH <7.30) not rapidly resolving. This will include most patients in shock. Mechanical ventilation also reduces work of breathing and oxygen demand, and left ventricular afterload through an increase in intrathoracic pressure. Reduce sedative use to the minimum required, since most reduce blood pressure and cardiac output.
Authors argue all patients in shock deserve some initial fluid resuscitation, even if volume overloaded (e.g., end stage CHF), but “too much fluid carries the risk of edema with its unwanted consequences,” and the amount of fluid should be “closely monitored.”
That reasonable approach is nevertheless consistently challenging, because “[p]ragmatic end points for fluid resuscitation are difficult to define.” See, even Jean-Louis Vincent has a hard time deciding how to fluid-resuscitate his shock patients. The question that remains usually unanswerable is, “Is my patient’s shock fluid-responsive?”
Bedside cardiac output monitors are the current vogue, as a minimally invasive alternative to pulmonary artery catheters. These use various proprietary technologies to calculate beat-to-beat stroke volume variation as a derivation of the arterial pressure waveform. High stroke volume variation with respiration suggests intravascular volume depletion, and therefore fluid responsiveness. The data these monitors produce correlates impressively with PA catheter-obtained values in tightly controlled, small clinical studies. However, their optimal performance is in a mechanically ventilated patient receiving high tidal volumes with no spontaneous respiratory effort (ideally paralyzed) and with no arrhythmia or right ventricular dysfunction. Test performance degrades in patients lacking any of these features.
Passive leg raise test with a bedside cardiac output monitor can identify fluid responsive patients more reliably than guessing. Patients with a 10-15% increase in stroke volume within 30 seconds after passive leg raise are more likely to be fluid responsive.
Absent a bedside cardiac output monitor, very experienced clinicians may claim to accurately detect beat to beat respiratory variation in realtime arterial pressure waveforms, using the naked eye. But identifying under-the-waveform-area changes of 10% this way is probably not achievable by most physicians, in most patients.
Since fluids are being given, a the patient’s actual response to fluids should be used as a test. A fluid challenge should include 4 elements:
Don’t stimulate the patient or titrate other medicines during the fluid challenge. Repeat if needed (especially with good response), but stop after nonresponse to prevent volume overload.
Vasopressors should be started promptly for severe hypotension, or if does not promptly improve with fluid resuscitation. Starting vasopressors during fluid resuscitation is appropriate for severe hypotension; vasopressors can be weaned off quickly if hypovolemia is the only cause for shock.
α-Adrenergic stimulation increases vascular tone and blood pressure. However, this effect can also reduce cardiac output and limit blood flow to tissues; the liver and gut circulation are most vulnerable to this effect. Because of this, authors advise against the general use of the pure α-adrenergic agonist phenylephrine (Neo-Synephrine), calling it “rarely indicated.”
β-Adrenergic stimulation increases blood pressure through increased heart rate, contractility and cardiac output. This may come at a price of myocardial ischemia. The pure β-agonist isoproterenol is limited to treatment of severe bradycardia for this reason.
Most widely used vasopressors have mixed α- and β-adrenergic properties. Authors recommend norepinephrine (Levophed) — an α-agonist with modest β-adrenergic stimulation – as the first-line vasopressor for most people in shock of any cause. Norepinephrine’s α-stimulation supports vascular tone while its β-agonist properties help maintain cardiac output. Guidelines advise the preferential use of norepinephrine for septic shock, in particular.
Dopamine is mostly β-adrenergic at low doses, and α-stimulatory at high doses. Dopamine’s selective dilatation of the gut and renal circulations at lower doses has not been shown to have a meaningful organ-protective effect in controlled trials in the critically ill. Dopamine has been associated with worsened mortality compared to norepinephrine in randomized trials including patients in cardiogenic shock and septic shock. Authors advise against the use of dopamine for shock generally.
Epinephrine is a powerful vasopressor with β-adrenergic effects at low doses, and increasing α-stimulation at higher doses (like dopamine). Epinephrine has not been shown superior to norepinephrine for septic shock in multiple randomized trials, but it may increase risk for arrhythmias, reduce gut blood flow and increase serum lactate (usually without worsening ischemia, but complicating use of that measure of perfusion). Authors consider epinephrine second line for refractory shock.
Vasopressin is only considered useful for patients with distributive shock with high cardiac output (e.g., septic shock) and only in low doses (0.04 U / minute); added to norepinephrine, vasopressin can substantially improve arterial pressure in these patients.
Dobutamine is a first-line β-adrenergic inotrope for use in patients with low cardiac output. Unfortunately, cardiac output is usually hard to quantify. One senses these authors are dobutamine fans; Dr. De Backer has shown that dobutamine can improve organ capillary perfusion at low doses (even without increasing cardiac output), and his current research focuses on perfusion of the sublingual microcirculation as a goal of sepsis and shock treatment. They advise using as low a dose as possible to “achieve adequate tissue perfusion.”
Milrinone and enoximone may have a role as adjuncts to dobutamine in low cardiac output states (cardiogenic shock); intermittent dosing is advised over continuous infusions. Levosimendan (a calcium sensitizer) also improves cardiac output, but has a long half life and may be impractical in shock treatment.
In rare patients, vasodilators like nitrates may actually improve shock by reducing afterload and increasing cardiac output and perfusion. This therapy carries a high risk for worsening shock when used improperly.
(See also Shock Review Part 2: Goals of Therapy)
With gratitude to: Jean-Louis Vincent and Daniel De Backer. Circulatory shock. N Engl J Med 2013; 369:1726-1734
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