Fluid responsiveness

Question 1

Fluid Responsiveness

Definition

Answer 1

=>An ↑ in stroke volume (or CO / CI, etc.) by 10–15% following a fluid bolus of ~500 mL crystalloid. (Although volumes may vary.)
->Idea is to induce a change in preload and then to observe a change in CO & BP.
->⚠️** Fluid responsiveness is NOT synonymous with hypovolemia.
**

Question 2

Predicting Flluid responsiveness

Answer 2

Question 3

Interpretation
&
Key points

Answer 3

Interpretation
* Dynamic methods outperform static measures in predicting benefit from fluid challenge.
* Combine multiple indicators (clinical + dynamic) for decision-making rather than relying on a single parameter.

⸻

Key Points
* Always interpret results in clinical context (ventilation mode, rhythm, sedation).
* Non-responders may worsen with fluids → consider vasopressors / inotropes instead.
* Reassess after each bolus — avoid cumulative overload.

Different cut-off values can be used for different pts
* e.g.
 P.S. = Respiratory failure → need higher specificity (since acceptable lower sensitivity)
 P.H.S. = Pre-renal failure → will need tests with higher sensitivity.

Question 4

Passive Leg Raise
* Q. Method
* Q. Physiologic basis
* Q. Limitations

Answer 4

**=>Physiological basis
* Legs are raised passively to 45° in a supine position (from semi-recumbent or sitting).
* This leads to autotransfusion of ~300 mL blood from the lower limbs into the central circulation (IVC → RA → RV).
* ↑ venous return → ↑ LV preload.
* **An increase in CO/CI > 10% **with this manoeuvre would mean fluid responsiveness.
* Reported sensitivity ≈ 97 %, specificity ≈ 95 %.
  (CO/CI measured by pulse contour analysis, Doppler, or echocardiographic LVOT VTI methods.)
Bedside surrogates of SV- ⬆️ in Pulse pressure; ⬆️ in BP; ⬆️ in EtCO2 but all of them are less reliable.

⸻

=>Limitations
->Leg-raising movement contraindicated in:
 * Pelvic trauma
 * Presence of IABP / ECMO
 * Recent angiography
* C-spine or head-injury patients (raised ICP risk)
->Unreliable in:
 * Patients with intra-abdominal hypertension
 * Severely hypovolemic patients (blood pooled in IVC → may be insufficient to augment SV)
 

Question 5

End-expiratory occlusion test:

Answer 5

=>A 15-second pause at end expiration during mechanical ventilation removes the cyclic reduction in venous return caused by positive pressure ventilation. If cardiac output increases ≥5%, the patient is fluid responsive.

=>Physiological principle

During positive-pressure ventilation:
* Inspiration → ↑ intrathoracic pressure
* → ↓ venous return
* → ↓ right ventricular preload

If we pause the ventilator at end-expiration, we temporarily eliminate the inspiratory increase in intrathoracic pressure.

This leads to:
* ↑ venous return
* ↑ right ventricular preload
* ↑ stroke volume / cardiac output if the patient is preload responsive

Thus the test acts as a “reversible mini fluid challenge” without giving fluid.

=>Advantages
* Reversible
* No fluid administration required
* Works even with low tidal volumes (e.g., ARDS)

=>Limitations

Requires:
* Controlled mechanical ventilation
* No spontaneous breathing
* Reliable continuous CO monitoring

Question 6

Pulse Pressure Variation

Definition
Factors that it depends upon

Answer 6

->Defined as
* The Δ (change) in Pulse Pressure that occurs over a single respiratory cycle.

=>Derived / measured from Arterial Pressure waveform
->Depends upon:
1️⃣ Arterial elastance
2️⃣ Stroke volume (i.e., factors influencing preload, afterload & contractility)

Question 7

Physiological basis
of
PPV

Answer 7

->With positive pressure ventilation:
↓ in preload → ↓ in RV stroke volume
↑ in afterload
* RV stroke volume = minimum at end of inspiratory period
*↓LV filling observed after 2–3 heartbeats (d/t pulmonary transit time) →
↓ LV stroke volume = minimum at end of expiratory period

=>Cyclic changes in pulse pressure are greatest when the ventricles operate on the steep rather than flat portion of the Frank–Starling curve.

• Magnitude of changes in pulse pressure across the respiratory cycle is indicative of ventricular preload dependence.
  
  • The higher the PPV, the more the likelihood of fluid responsiveness.

Question 8

PPV Limitations

Answer 8

Limitations
* Unable to interpret in the use of arrhythmias.
* Limited utility in ventilated pts if:
 * Small T.V. (< 8 mL/kg)
 * Spontaneously breathing patients.
* Cannot be used in pts with open chest.

Question 9

Causes of ⬆️ed S.V.V.

Answer 9

• Hypovolemia
• Massive PE
• Arrhythmias
• Tamponade
• LV dysfunction
• ↑ intrathoracic pressure
• Pneumothorax
• Dynamic hyperinflation
• Bronchospasm
• ↑ intracranial pressure

Question 10

CVP Physiological basis

Answer 10

Physiological basis:
* CVP is an approximation of RAP → a major determinant of RV filling.
* Assumption → CVP is a good indicator of preload.
* LV stroke volume is determined by RV stroke volume.
* CVP is considered / assumed to be an indirect measure of LV preload.
* ΔCVP within fluid challenge is thought to be useful in determining fluid responsiveness.

Question 11

Limitations of CVP

Answer 11

CVP determined by factors other than intravascular volume, e.g.
* Venous tone → mean systemic filling pressure
* RA & RV compliance
* LV compliance
* Valvular integrity
* Intrathoracic & pleural pressure
* Intra-abdominal pressure
(from LITFL)
* In critically ill, there is a poor correlation between CVP & RVEDV.