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A 60-year-old woman is admitted with septic shock due to pyelonephritis. Currently she has received two liters of crystalloid. Her mean arterial pressure is now 55 mm, her pulse is 120 b/m, and she is producing very little urine. Bedside ultrasound shows that her IVC is completely empty (sometimes referred to as a “virtual IVC,” with both walls nearly touching). Her left ventricle is extremely hyperkinetic, almost with end-systolic obliteration of the left ventricular cavity. How should her hemodynamics be managed?
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The standard approach to this patient would be to continue further aggressive volume resuscitation. Her IVC and heart are empty, right? The “tank” needs to be filled. This is the approach which I have learned from many articles, books, and lectures by leaders in the field of critical care ultrasonography. However, I believe that it is incorrect. This post will explore why.
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Cardiac physiology review
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To make sure that we're on the same page, it will be useful to briefly review some cardiac physiology. If this isn't making sense, there are some fantastic lectures about this at heart-lung.org.
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Normal physiology is shown above. The venous return curve (blue) shows blood flow into the right atrium. The mean systemic filling pressure is the pressure that drives venous return, equal to the stressed volume of blood in the venous system divided by the venous compliance. This doesn't include the “unstressed volume,” which is the volume of blood it takes to fill the veins without any distension of the vein wall (if you can image the venous system drained of all blood, the unstressed volume is the volume that you could add to simply un-collapse the veins, without causing anyincrease in pressure).
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The “vascular waterfall” occurs when central venous pressure falls below zero, at which point venous return is maximized and will not increase further no matter how low the CVP is, due to collapse of the systemic veins. This is called a “waterfall” in reference to the fact that the flow over a waterfall is independent of how high the waterfall is, thus de-coupling flow from pressure. The ultrasonographic appearance of the vascular waterfall is a completely collapsed IVC.
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The cardiac output must equal the venous return. Therefore, the yellow circle shows the patient's cardiac output and central venous pressure at the intersection of the venous response curve and the cardiac output curve.
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Physiologic changes in acute sepsis
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Early septic shock (“hyperdynamic sepsis”) is marked by the following physiologic changes:
- The cardiac output curve shifts up dramatically, due to two factors. First, arterial vasodilation reduces the afterload on the heart, increasing cardiac output. Second, sympathetic nervous system activation stimulates increased heart rate and contractility.
- The venous response curve shifts to the left, due to multiple factors. First, venodilation decreases the stressed volume of blood within the veins. Second, venodilation may increase the venous compliance. The combination of decreased stressed volume and increased venous compliance causes a reduction in the mean systemic filling pressure, which shifts the venous response curve to the left. There may also be some extravasation of fluid out of the vasculature (“third spacing”), further reducing the stressed volume in the venous system.
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A Guyton diagram of this is shown below (1). Note that CVP and cardiac output have now decreased, and the patient is now living on the vascular waterfall (with an empty IVC).
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What happens if we treat with volume resuscitation?
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We can all probably agree that this patient is volume responsive. On the vascular waterfall, cardiac output is limited solely by venous return, so an increase in volume will surely improve her cardiac output. Great! Lets suppose that we treat her with enough volume to stabilize her blood pressure. This will shift the venous response curve to the right and improve the cardiac output:
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If the volume doesn't extravasate too quickly from her vasculature, this strategy may succeed in improving her cardiac output and blood pressure. How is it possible to increase her blood pressure while she remains in a vasodilated state? Blood pressure equals the product of cardiac output and systemic vascular resistance (equation below). Therefore, elevating her cardiac output may allow her to achieve an adequate blood pressure despite reduced systemic vascular resistance:
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However, this is not an ideal solution. Essentially, it amounts to masking a vasodilatory shock state by inducing volume overload. This treatment forces her heart to work hard:
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Her heart was not designed to sustain this power output continuously. Although unknown, it is conceivable that an excessive cardiac power output could eventually cause myocardial fatigue and increase her risk of developing sepsis-associated cardiomyopathy (2). It has been shown that intentionally driving systemic oxygen delivery to supranormal levels by elevating cardiac output may be harmful (Hayes 1994).
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What happens if we treat with norepinpehrine?
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Norepinephrine has the following effects:
- Norepinephrine stimulates venoconstriction, which increases the stressed volume of blood in the venous system and also decreases the venous compliance. Increased stressed volume and reduced venous compliance increases the mean systemic filling pressure, shifting the venous return curve back to the right.
- The cardiac output curve will shift downward. Norepinephrine does have some beta-agonist activity which will tend to increase contractility. However, the dominant effect in this scenario is often the increase in systemic vascular resistance which increases afterload, thereby decreasing the cardiac output.
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This illustrates graphically that by causing arterial and venous vasoconstriction, norepinephrine treats the underlying pathophysiologic problem (vasodilatory shock), thereby moving the system back towards normal. Central venous pressure is increased without using any fluid. The effect on cardiac output is mixed: venoconstriction and beta-agonist activity tend to increase cardiac output whereas arterial vasoconstriction tends to decrease cardiac output. Importantly, although not reflected on this graph, norepinephrine also stabilizes systemic blood pressure and improves renal function.
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Take-home points
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1) An empty IVC and hyperkinetic heart does not equal volume depletion.
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This combination of echocardiographic findings may result from either vasodilatory shock (as illustrated above) or hypovolemic shock. If encountered in the setting of hypovolemia (for example, a patient with GI hemorrhage), then volume repletion is clearly indicated. However, if encountered in the setting of vasodilatory shock, then the best treatment may be vasoconstriction with an agent such as norepinephrine. The treatment should correct the underlying problem. Simply because a shocked patient is volume responsive does not mean that volume is the best treatment.
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2) Bedside ultrasonography must be combined with an understanding of physiology.
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One potential pitfall of bedside ultrasonography is that it may be so visually impressive that it seduces us into forgetting physiology. The empty IVC virtually begs us to administer volume. However, we must remain steadfast to the principles of cardiovascular hemodynamics as we carefully consider the entire picture in determining the best possible treatment.
Notes
(1) These physiologic diagrams below are merely hypothetical examples of how a typical patient might respond. There are a wide range of possible responses, and opposing factors may reach a different balance in different patients.
(2) Please note that there is no evidence that increasing cardiac power output increases risk of subsequent cardiomyopathy in septic shock. The pathophysiology of septic cardiomyopathy remains murky and is likely multifactorial. Given that the heart is a muscle, it seems plausible that excessive cardiac power output could promote fatigue with subsequent cardiomyopathy.
Image credits: https://en.wikipedia.org/wiki/Hepatic_vein#/media/File:Gray1121.png
Image credits: https://en.wikipedia.org/wiki/Hepatic_vein#/media/File:Gray1121.png
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Fantastic post Josh! I'm really glad that you bring up these points and describe them nicely with a common clinical scenario. What I teach is that a collapsing IVC may be physiologically uncoupled from both volume status and volume responsiveness. I sometimes use an extreme clinical example – if you consider a patient in florid heart failure, who is totally overloaded and with an EF of 15% – they will likely have a dilated, unvarying IVC with spontaneous inspiration. But if you do nothing to that patient but insert an intra-aortic balloon pump and start it at 1:3, then increase… Read more »
Hello,
thank you for another crystal clear post. I agree with you that we give too much fluids, too easily…
but I would just do a small observation : norepinephrine (in excess) can also reduce venous return. So I agree that in the first phase, quick norepinephrine is a good strategy, but we must try to wean it the fastest as possible.
I would argue that there's a hypocolemic state in the described scenario but it is a 'relative' and not 'absolute' hypovolemia. I get the concept but instead of trying to save a patient an ICU admission, I would argue to the Emcrit 'fluid tolerance' argument in these patients initially. Give them fluids, follow your marker which is PLR or dynamic aortic velocity, LVOT/VTI and/or carotid width/VTI in addition to lung ultrasound for EVLW. What I will say is I think there is a point where a patient may be fluid responsive but more fluids is not the right choice and… Read more »
thank you very much ,this is very simple and excellent description
Thats an awesome explanation. But, how can the heart makes a negative inchamber preassure? Before this point, maybe the coronary perfusion is less than adequate so, corollary cardiovascular copllapse before…. maybe?