Shock and Fluid Responsiveness


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Shock and Fluid Responsiveness


1. SHOCK


See Chapter 2, Section 2.I for the specific management of cardiogenic shock. See Chapter 38 for ventricular support devices.


I. Shock definition and mechanisms


Shock is defined as sustained hypotension along with evidence of low tissue perfusion (oliguria <30 ml/h for 1 hour, cold or mottled extremities, altered mental status, or elevated serum lactate level>2 mmol/L). Hypotension is usually defined as a mean systemic pressure <65 mmHg or a systolic pressure <90 mmHg for over 30 minutes, or requirement for catecholamine infusion to maintain systolic pressure ≥90 mmHg.1–6 Systemic pressure may be higher in shock patients with chronic hypertension; a decline in systolic pressure of >40 mmHg is commonly used to define hypotension in the previously hypertensive patient.


There are four mechanisms of shock: (1) hypovolemia; (2) low cardiac output, as in left or right cardiogenic shock; (3) vasodilatory shock, also called distributive shock (septic shock, anaphylactic shock, shock from excessive amount of sedatives and vasodilators); (4) obstructive shock, where LV filling is prevented by a right-sided obstruction, such as pulmonary embolism, tamponade or isolated RV shock.


Right heart catheterization establishes the shock mechanism by assessing the three determinants of shock (Table 22.1):



  1. Right- and left-sided filling pressures (CVP, PCWP). The normal CVP is <8 mmHg. If CVP <8 mmHg, particularly <4 mmHg, and PCWP

    <15 mmHg in a patient with shock, there is likely a hypovolemic component of the shock.


  2. Cardiac output (CO). The normal cardiac index is 2.2–4.0 liters/min/m2. If cardiac index <2.2 → cardiogenic component of the shock
  3. Systemic vascular resistance (SVR). Normal SVR is 700–1500 dyn.s.cm–5. If SVR <1000 in shock → vasodilatory component of the shock

Clinically, left-heart cardiogenic shock is defined as a shock with clinical or radiographic evidence of pulmonary congestion, or with the following combination on right heart catheterization: cardiac index <2.2 liters/min/m2 + PCWP>15 mmHg.1,2


Some shock states may be mixed. In septic shock, one may have a hypovolemic component and a cardiogenic component with reduced myocardial contractility, the so-called septic cardiomyopathy, seen in as many as 30% of cases. Furthermore, in septic shock, cardiac output needs to be high enough to match the increased tissue demands and the vasodilated circulation, and to compensate for the maldistribution of flow (skin, fat, and skeletal muscle flow increases, and venous pooling increases, while splanchnic flow is reduced and heterogeneous because of microvascular congestion). A cardiac output that is “normal” in absolute values may be inappropriate in the context of septic shock; this is suggested when the tissue perfusion and SvO 2 are low (SvO 2 <65%) despite normalization of the systemic pressure. Both an adequate mean arterial pressure and an adequate cardiac output are required for end-organ perfusion; this is represented by the cardiac power output (CO x mean arterial pressure/451).


While cardiogenic shock is classically described in patients with acute large MIs, it is also seen in patients with chronic severe cardio- myopathy and decompensating factors, such as acute infection, tachyarrhythmia, excessive vasodilators or sedation, cases where the limited cardiac output reserve cannot match the dilated circulation. In addition, volume overload, by itself, increases ventricular filling pressures, which reduces myocardial perfusion and contractility; and increases afterload, which reduces cardiac output.


In the SHOCK trial of cardiogenic shock secondary to acute MI, 20% of patients had reduced CO and elevated PCWP but relatively low SVR (<1000). This was related to a concomitant infection or to a systemic inflammatory response associated with nitric oxide release in cardiogenic shock.7 In cardiogenic shock, SVR increases to maintain systemic pressure; SVR that is “normal” in value in the absence of vasodilator therapy is, in fact, relatively low.


Table 22.1 Hemodynamic findings in the four different types of shock.


































CVP PCWP Cardiac index SVR
Hypovolemic ↓ ↓ ↓ ↑
Cardiogenic ↑ ↑ ↓ ↑
Low SVR ↓ ↓ ↓, normal, or ↑ ↓
Obstructive a ↑ ↓ ↓ ↑

a Disproportionately elevated PA pressure and CVP in comparison to PCWP suggest pulmonary embolism or precapillary pulmonary hypertension.


In tamponade or isolated RV shock, equalization of CVP and PCWP is often seen.


A shock state with a wide pulse pressure is characteristic of septic shock, AI, or any vasodilatory condition (cirrhosis, vasodilatory drug excess).


Always remember adrenal shock (Addisonian shock), in which three mechanisms of shock are present (hypovolemia, low SVR, and myocardial depression). Importantly, functional adrenal failure may result from septic shock. Also, think of adrenal shock in patients who are acutely sick and who have been receiving chronic steroid therapy; their chronically suppressed adrenal glands cannot generate stress doses of steroids.


II. Goals of shock treatment


Increase mean arterial pressure (MAP) to >65 mmHg and provide good tissue perfusion, manifested as:6



  • Urine output >0.5 ml/kg/h, with a stable creatinine.
  • Absence of acidosis. Serum lactate or gastric pH may be monitored as a marker of perfusion.
  • Mixed venous O2 saturation (SvO2) ≥65–70%.
  • Heart rate <120 bpm.
  • Warm skin with capillary refill ≤2 seconds.

One study addressed a target MAP of 65–70 mmHg vs. 80–85 mmHg in septic shock and found no difference in mortality and overall adverse events, except for more AF in higher MAP arm (from higher vasopressor doses). Only in patients with underlying chronic hypertension did the higher MAP goal reduce the incidence of severe renal failure and the requirement for acute dialysis.8


III. Immediate management of any shock


The shock and the volume status are quickly classified by history and physical exam, with a focus on:



  • Cardiac history.
  • Pulmonary edema, elevated JVP, and peripheral edema, which are signs of volume overload. Unlike pulmonary edema, peripheral edema does not necessarily preclude fluid resuscitation acutely in cases of septic or hemorrhagic shock.
  • Fever and potential sources of infection. ECG and chest X-ray are quickly performed.

A. Intravenous fluid boluses


In the absence of pulmonary edema, a fluid bolus of 1–2 liters is quickly administered in less than an hour (<20 minutes for the first liter) (PRoCESS trial).3 Fluid administration is the first therapy of hypovolemic and low-SVR shocks; patients who have peripheral edema or elevated JVP are hypervolemic and are generally not fluid responsive, but may occasionally be fluid responsive at the onset of septic or hemorrhagic shock.


Beyond the first 1–2 liters, fluids are administered: (i) until signs of fluid repletion develop, or (ii) until CVP is 8–12 mmHg (or 12–15 mmHg in case of positive end-expiratory pressure) or PCWP is 15–18 mm Hg,9 or (iii) based on dynamic maneuvers of fluid responsiveness.


B. If the patient remains hypotensive despite the quick initial 1–2 L of intravenous fluids or if signs of fluid repletion develop (elevated JVP, pulmonary edema, decreased O2 saturation)



  1. Norepinephrine or, less favorably, dopamine is started (norepinephrine ≥0.05 mcg/kg/min, dopamine ≥3 mcg/kg/min). These two drugs are effective whether the shock is cardiogenic or distributive, until more is figured out. Vasopressors are best started early, simultaneously to fluids, after 1–2 liters have been administered. Fluids are continued unless signs of fluid repletion develop.
  2. In a cardiogenic context, inotropes are administered: dobutamine is started at 3 mcg/kg/min if SBP >80 mmHg, whereas norepinephrine or dopamine is started if SBP <70–80 mmHg. Dopamine may be administered at 3–10 mcg/kg/min (at this level, dopamine has mixed α + and β + effects, β+ > α +).
  3. In a septic context, vasopressors are administered: norepinephrine (mixed α + and β + effects, that is, vasoconstrictive and inotropic effects), followed by vasopressin, then phenylephrine (pure α + effect, without β + or inotropic effect).
  4. At this point, along with these initial measures:

    • A central venous line is mainly used if peripheral access is insufficient. In equivocal cases, it may be placed to monitor CVP and help assess the volume status and SvO2. A pulmonary artery catheter (Swan-Ganz) is not routinely needed and has not improved outcomes in any of the following settings: acute lung injury with or without septic shock (ARDS net trial), septic shock and/or acute lung injury (French PAC trial), all critically ill patients (PAC-MAN trial), and severe HF (ESCAPE trial).10–13
    • An arterial line is not mandatory; it has not been mandated in the modern sepsis trials and it is suggested but not mandated by the sepsis guidelines. It may be used for BP monitoring in any shock requiring inotropes and/or vasopressors (weak recommendation).
    • Echocardiography is performed
    • If the diagnosis remains in doubt and the patient does not improve despite the initial measures, a PA catheter may be placed to diag- nose the mechanism of shock and pulmonary edema, and to guide therapy.

C. In the context of septic shock, if low perfusion signs persist despite achieving the target systemic pressure and despite a presumably normal volume status


Assess fluid responsiveness and give 500 ml fluid challenge, over 30 min, if the patient is fluid responsive (may repeat it). If not fluid responsive, consider that the cardiac output or the systemic pressure is still inadequate even if normal or high in absolute value. At this point, inotropes may be administered to increase cardiac output and O2 delivery, allowing it to match the O2 demands (Figure 22.1).

Schematic illustration of aggressive early therapy of septic shock (the first 3 hours).

Figure 22.1 Aggressive early therapy of septic shock (the first 3 hours). Early goal-directed therapy implies the use of a central venous line with monitoring of CVP and SvO2, but this is not necessary.


^Perfusion may be monitored via:



  • Clinical parameters of hypoperfusion: oliguria, mottled skin, capillary refill time >3 sec, altered sensorium.
  • Lactate clearance: a reduction of lactate levels ≥20% at 2-hour intervals suggests an improvement in tissue perfusion.
  • SvO2: SvO2>70% suggests proper tissue perfusion

*Fluid responsiveness is assessed via:



  • Aortic VTI or pulse pressure variation with positive pressure in patients mechanically ventilated (≥15% or 13%, respectively→ fluid responsive); or IVC collapse >15%
  • Aortic VTI or pulse pressure variation with passive leg raising for 30–60 sec in patients breathing spontaneously or mechanically ventilated (>15 or 10%, respectively→fluid responsive)

This algorithm is inspired by references ProCESS and ANDROMEDA trials.3,6 MAP, mean arterial pressure


D. Provide adequate oxygenation (arterial O2 saturation >90–95%), and adequate hemoglobin level


Intubate and mechanically ventilate in the case of any respiratory distress or obtundation. Respiratory effort can consume up to 30% of the cardiac output. Mechanical ventilation, by relieving the work of breathing, helps improve tissue perfusion.


In the absence of acute hemorrhage, red blood cells should only be transfused when hemoglobin decreases to <7–7.5 g/dl, with a target hemoglobin level of 7–9 g/dl (TRICC and TRISS trials).14,15 The original trial of early goal-directed therapy used a target hemoglobin level of 10 g/dl in the first 6 hours of resuscitation; however, this did not prove necessary in three later early resuscitation trials.3–5


E. Perform a quick workup in parallel to the previous steps


ECG, chest X-ray, BNP, cardiac biomarkers, complete blood count, and blood/urine/sputum cultures are obtained. Line infections are considered, and in case of doubt, lines older than 48 hours are removed and replaced. Infectious foci are sought (e.g., abdomen, joints, skin).


Bedside echocardiography is performed:



  • Echocardiography rules out tamponade, cardiogenic shock from LV failure, acute valvular disorders, and massive PE with acute RV failure.
  • Echocardiography helps determine:

    • RA, LA, and PA pressures, which help guide fluid therapy.
    • Fluid responsiveness. Significant variability of aortic VTI with mechanical ventilation or passive leg raising implies fluid responsiveness.

F. Start empiric broad-spectrum, one or several antibiotics whenever there is any suspicion of sepsis (start the antibiotics within 1 hour of this suspicion)


Treat the potential source of infection (e.g., drain any abscess, remove central lines).


G. Administer stress doses of steroids for a shock that persists several hours despite high doses of at least one vasopressor, or for the patient who uses steroids chronically


IV. Sepsis and septic shock


Sepsis is defined as end-organ dysfunction caused by a dysregulated response to an infection. Sequential organ failure assessment (SOFA) score quantifies this organ dysfunction and consists of 6 organ system variables: renal function, PaO2/FiO2 ≤300, hypotension, mental status, platelet and bilirubin levels. To define sepsis, SOFA score ≥2 is required, i.e., severe abnormality of one variable or moderate abnormality of 2 variables.16 In addition, serum lactate level (≥4 mmol/L) reflects tissue hypoxia and is used in the early management of sepsis. The term “severe sepsis” is no longer used, as all sepsis cases are severe.


Septic shock is a subset of sepsis defined as persistent hypotension (mean BP ≤65 mmHg or SBP<90 mmHg), refractory to 1–2 L of fluid resuscitation and requiring vasopressors, with lactate levels>2 mmol/L.16


The Surviving Sepsis guidelines recommend aggressive early (≤ 1 hour) treatment in septic shock but also in sepsis with lactate ≥4 mmol/L, even without shock. This is the “hour-1 bundle” of sepsis therapy.17,18 As such, 1–2 L of crystalloid fluids are recommended within the first hour, and 30 ml/kg within the first 3 hours. If the patient remains hypotensive despite 1–2 L of fluids within 30–60 min, vasopressors are quickly initiated to target a mean arterial pressure ≥65 mmHg, as in the ProCESS trial.3–6 Vasopressors are initiated early on, in the first hour, during rather than after fluid resuscitation, after 1–2 liters have been administered (CENSER trial). Fluid boluses may later be repeated in the absence of clinical signs of congestion, particularly if fluid responsiveness parameters are positive.6 Hypoperfusion is monitored clinically and via serial 2- or 4-hour lactate levels (“lactate clearance”).6


Pitfalls:


  • Serum lactate is a marker of tissue hypoxia but may also result from increased glycolysis without hypoxia in a high catecholamine state. Serum lactate is not a specific marker for sepsis and should not be used for sepsis diagnosis or to justify aggressive fluid administration. Lactate may increase in HF decompensation.
  • The 30 ml/kg early fluid recommendation is derived from what was used in the 3 modern trials of early, clinically-guided sepsis therapy. However, no controlled data supports this exact number. In those trials, ~5 L were given in the first 6 hours.3–5
  • Patients without a definite diagnosis of sepsis whose symptoms may be explained by HF, or patients with evidence of fluid repletion, such as peripheral edema (e.g., combined HF-sepsis or sepsis decompensating HF) should not receive this aggressive fluid resuscitation and may rather be treated straight away with ino-pressors and diuretics.
  • Beyond the first 24–48 hours, a restrictive rather than liberal fluid strategy, with fluid de-escalation and diuresis, is associated with improved outcomes. This was shown in ARDS net trial (patients were randomized at a mean of 43 hours after ICU admission, and 35% were in shock).19 Conversely, in the first 24 hours of an acute illness, RELIEF trial favored a liberal fluid strategy: RELIEF trial compared liberal vs. restrictive fluid strategy in the first 24 hours after abdominal surgery (6.1 L vs. 3.7 L), in elderly patients with no HF. Mortality was similar in both groups, but restrictive strategy had higher AKI (8.6% vs. 5%).20 The main difference is the randomization in the first 24 hours in RELIEF vs. >24 hours in ARDS net.
  • Regarding fluid administration in sepsis:

    • *Fluid boluses are aggressively administered the first 3–6 hours, to establish perfusion (“rescue” phase).
    • *Fluids are then maintained at a slower, steady rate in the first 6–24 hours, to maintain perfusion (“optimization” phase). Sepsis guidelines recommend aggressive fluid resuscitation in the first 24 hours.
    • *Fluids are de-escalated (“de-resuscitated”) beyond the first 24–48 hours aiming for a negative fluid balance, possibly with the help of diuretic therapy as in the ARDS net trial (except if shock). Even non-cardiogenic pulmonary edema benefits from this restrictive fluid strategy/diuresis. Fluids are aggressively used in the first day to fill the dilated, leaky circulation and establish perfusion but have by now leaked into the extravascular space, more so as the intravascular system constricts and shrinks in volume, which causes pulmonary edema and tissue ischemia (tissue edema impedes O2 transport to cells and causes ischemia).21 In fact, over 85% of the volume of administered crystalloids redistributes to the extravascular space in 2–4 hours.
    • *Diuretics are not always necessary in the late phase of sepsis. At around day 3, as vascular system constricts and capillary leak declines, neurohormonal renal stimulation is reduced, which may lead to spontaneous diuresis (the “flow” phase of sepsis).21 Vascular constriction is a two-edge sword that leads to worsening tissue edema, but also to increased renal flow and diuresis.
    • * Beyond the first 30 ml/kg or first 3–6 hours, fluid administration is best guided using dynamic measures of fluid responsiveness , rather than the static CVP (Section 2).6 Short of that, generally aim for conservative fluid management beyond 24–48 hours.

V. Cardiogenic shock


Look for a specific cause and consider specific therapy (Table 22.2). Figure 22.2 provides a general approach to management.22–24 In addition, consider:



  • Surgical correction of an acute valvular regurgitation or a mechanical complication of MI
  • Cardioversion of a fast tachyarrhythmia (130 bpm is the cardioversion cutoff in the setting of HF+shock)
  • Pacing for an inappropriately low heart rate, e.g., shock with a rate <60–70 bpm
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Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Shock and Fluid Responsiveness

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