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🌱 來自: Huppert’s Notes
Assessment of Fluid Responsiveness🚧 施工中
Assessment of Fluid Responsiveness
• Hypotension is a common problem in the ICU
• Various methods exist to determine whether a patient with hypotension is likely to be “fluid responsive,” which is defined as an increase in cardiac stroke volume with a fluid bolus
• Each of the following methods can help inform this decision, but no single measure is perfect: 1) Assessment of pulse pressure variation (PPV); 2) Central venous pressure (CVP); 3) Dynamic measurement of the inferior vena cava (IVC using POCUS); and 4) Passive leg raise
• Please note that these measures were validated in specific settings and may not be valid in alternative clinical scenarios
Arterial Line and Pulse Pressure Variation (PPV)
• Indications for arterial line placement:
- Invasive hemodynamic monitoring
- Frequent laboratory draws, often arterial blood gases (ABGs)
• Interpretation of the arterial line tracing:
- Waveform shows systolic peak pressure, dicrotic notch, and end-diastolic pressure (Figure 3.1)
FIGURE 3.1: Arterial Line waveform. The arterial pulse waveform includes a systolic phase, the dicrotic notch, and a diastolic phase. The systolic phase corresponds to left ventricular ejection, the dicrotic notch represents closure of the aortic valve, and the diastolic phase represents runoff into the peripheral circulation.
- Mean arterial pressure (MAP) is calculated and shown on the monitor
- Position of the transducer will affect the blood pressure readings
• Device should be zeroed at the level of the heart
• When the transducer is ABOVE the patient, then the measured pressure will be LOWER than actual
• When the transducer is BELOW the patient, then the measured pressure will be HIGHER than actual
• Measuring PPV using the arterial line: See Figure 3.2
FIGURE 3.2: Physiologic mechanism of pulse pressure variation. Pulse pressure variation (PPV) allows bedside assessment of fluid responsiveness for patients in shock who are breathing passively on positive pressure ventilation. If preload is robust, the pulse pressure does not vary with respiration. In the example above, a breath is delivered with inspiration increasing intra-thoracic pressure and decreasing venous return. This results in decreased RV preload and output. Blood flows through the pulmonary circulation with a time delay (long arrow) and reaches the left heart with reduced LV preload and output. If preload is reduced (suggesting volume responsiveness), pulse pressure will increase with inspiration and decrease with exhalation. Top: Airway Pressure (purple) Bottom: Arterial Pressure Tracing (green). Abbreviations: LV = Left Ventricle, RV = Right Ventricle, PP = Pulse Pressure
- PPV is a predictor of fluid responsiveness in mechanically ventilated patients
• PPV >13% suggests that the patient is fluid responsive
• PPV 9–13% is indeterminate
• PPV <9% suggests that the patient is not fluid responsive
- Pulse Pressure (PP) = (Systolic Pressure – Diastolic Pressure)
• PP maximum occurs during inspiration; PP minimum occurs during expiration
• PPV is calculated with the following formula:
Central Venous Pressure (CVP)
• Importance of CVP:
- Assists in guiding hemodynamic interventions
• In general, a normal CVP is 0–5 mmHg and it is often a good approximation of right atrial pressure; however, this can vary from patient to patient. Note also that goal CVP (e.g., when volume resuscitating a patient with shock) may differ according to the scenario (e.g., patient on positive pressure ventilation or not)
- CVP is a dynamic and not a static measurement
• Relationship to IVC measurement:
- When CVP < intraabdominal pressure, IVC will collapse
- When CVP > intraabdominal pressure, IVC will remain distended
- IVC compliance also dictates this relationship
• Interpretation of CVP waveform: See Figure 3.3
FIGURE 3.3: CVP waveform and correlation with electrical conduction in the heart. The CVP waveform has five distinct components: a wave (atrial contraction), c wave (right ventricular contraction), x descent (atrial relaxation with downward displacement of tricuspid valve with reduction in right atrial pressure), v wave (passive right atrial filling), and y descent (opening of tricuspid value with emptying of the right atrium into the right ventricle).
- a wave
• Atrial contraction
• Correlates with P wave on ECG
• Disappears with atrial fibrillation
• “Cannon a waves” are large a waves and a hallmark of AV dissociation in complete heart block or ventricular tachycardia
- c wave
• RV contraction against a closed tricuspid valve bulges into the right atrium
• Correlates with the end of the QRS complex on ECG
- x descent
• Atrial relaxation and downward displacement of the closed tricuspid valve during RV contraction, which both reduce RA pressure
• Occurs before the T wave on the ECG
- v wave
• Passive RA filling against a closed tricuspid valve during diastole increases RA pressure
• Occurs after the T wave on the ECG
• Tricuspid pathology such as tricuspid regurgitation leads to large v waves
- y descent
• The tricuspid valve opens and blood empties from the RA into the RV, leading to reduced RA pressure
• Occurs before the P wave on the ECG
• Loss of y descent suggests pathology such as tamponade with restricted RV filling
• CVP is influenced by cardiac function and venous return:
- Determinants of cardiac function:
• Cardiac contractility: Reduced cardiac contractility in states such as HFrEF or ACS can lead to impaired forward flow and therefore elevated cardiac filling pressures leading to a high CVP.
• Heart rate: Both bradycardia and tachycardia can reduce cardiac output causing elevated right-sided pressures, increasing CVP.
• Rhythm: The normal cardiac cycle has coordinated contraction of the atria and ventricles. Dysrhythmias and conduction disease can both lead to reduced cardiac output with consequent right-sided overload, increasing CVP.
• Valve function: Properly functioning heart valves ensure that blood moves unidirectionally through the cardiovascular system. Diseased valves may open or close improperly, leading to reduced cardiac function by allowing blood flow in the opposite direction (regurgitant) or by requiring the heart to work harder to move blood across a valve narrowing (stenosis).
- Determinants of venous return:
• Filling pressure: Hypovolemia leads to reduced venous return and thus reduced CVP.
• Venous compliance: Venodilation (e.g., due to furosemide) causes increased venous capacitance and reduced venous return, whereas venoconstriction (e.g., due to alpha agonists) causes reduced venous capacitance and increased venous return.
• Respiration: Spontaneous negative pressure breathing reduces intrathoracic pressure during inspiration, leading to increased venous return to the right heart. Positive pressure breathing (i.e., mechanical ventilation) inverts the cycle such that positive pressure administration during a breath will increase intrathoracic pressure and reduces venous return to the right heart.
IVC Point-of-Care Ultrasound (POCUS)
• Description:
- Common bedside assessment to aid in determining intravascular volume status
- Like all ultrasound, it is user-dependent and requires proper measurement and interpretation
- Along with CVP, PPV, passive leg raise, and other factors, can guide assessment of volume responsiveness
• How to measure the IVC using POCUS:
- Location: Locate and measure the portion of the IVC just distal to the junction of the hepatic vein and the IVC, about 2 cm from the right atrium. See Figure 1.12 in Cardiology Chapter 1.
- Measure the IVC diameter once at end expiration (largest diameter) and again at end inspiration (smallest diameter) to compare the two measurements
• IVC measurement interpretation:
- IVC <2.1 cm and >50% collapsible estimates a CVP <3 mmHg
- IVC <2.1 cm and <50% collapsible estimates a CVP ~8 mmHg (range 5–10)
- IVC >2.1 cm and >50% collapsible estimates a CVP ~8 mmHg (range 5–10)
- IVC >2.1 cm and <50% collapsible estimates a CVP >15 mmHg
• When IVC measurement may be inaccurate:
- Increased intraabdominal pressure (e.g., ascites, pregnancy)
- Positive pressure ventilation (e.g., ventilator or CPAP/bilevel)
Passive Leg Raise (PLR)
• Description:
- Bedside maneuver and diagnostic test to predict fluid responsiveness
- Used in conjunction with other hemodynamic and volume assessments such as IVC POCUS and PPV
- Transiently increases venous return
- Estimates roughly a 250cc bolus
• Technique:
- Sit the patient up in 45-degree position
- Then lay the patient flat and passively raise both legs at 45-degree angle
- Maximal effect at 30–90 seconds
• Interpretation:
- In the literature, a positive test is a 10% increase in cardiac output or stroke volume
- At the bedside, because cardiac output and stroke volume are not directly measured, a positive test is often defined as a >10% increase in pulse pressure on an arterial line