CONTENTS
- Rapid reference 🚀 Normal values
- When to insert:
- Insertion technique
- Waveforms
- CVP (central venous pressure)
- Wedge pressure
- Cardiac output
- Resistances
- Other indices
- Related
- CVP ⚡️ (central venous pressure): 2-6 mm.
- RV
- RV systolic: 15-30 mm.
- RV diastolic: 0-8 mm.
- PAP (Pulmonary artery pressure):
- PA systolic pressure: 15-30 mm.
- PA diastolic pressure: 4-12 mm.
- Mean PA pressure: 8-20 mm (>20 defines PH).
- PCWP ⚡️ (pulmonary capillary wedge pressure): 4-6 to 12-15 mm (38248013, 30253970)
- CO (cardiac output): 4-8 L/min.
- CI (cardiac index):
- CI = CO/Body Surface Area
- Normal range: 2.5-4 L/min/m2.
- Cardiogenic shock is suggested by CI <1.8 without support or <2.2 with support. (28489331)
- SVR ⚡️ (systemic vascular resistance):
- SVRi (systemic vascular resistance index):
- SVRi = (MAP-CVP)/(CI*80)
- Normal range: 1900-2400 dyne-s/cm5 (although some sources list 1330-3040) (38248013)
- PVR ⚡️ (pulmonary vascular resistance):
- PVR = 80(mPAP-PCWP)/(CO)
- Normal range: 24-160 dyne-sec/cm5
- Normal range: 0.3-2.0 Wood Units (=PVR/80)
- PVRi (pulmonary vascular resistance index):
- PVRi = 80(mPAP-PCWP)/(CI)
- Normal range: 240-280 dyne-s/cm5
- Normal range: 3-3.5 Wood Units (=PVRi/80)
- PAPi ⚡️ (pulmonary artery pulsatility index):
- PAPi = (PA pulse pressure)/CVP
- Normal range: >0.9
- CPO ⚡️ (cardiac power output):
- CPO = (MAP*CO)/451
- Normal CPO: ~0.8-1.1 Watts
- CPOi (cardiac power output index):
- CPOi = (MAP*CI)/451
- Normal CPOi: ~0.5-0.7 Watts/m2
- SV (stroke volume): 60-100 ml
- SVi (stroke volume index): 33-47 ml/m2
- MAP (mean arterial pressure): 65-110 mm (38248013)
- [1] Left bundle branch block, since PA catheterization may cause right bundle branch block. (30947630)
- [2] Arrhythmia risk (e.g., ventricular tachycardia storm).
- [3] Risk of displacing other devices (e.g., a transvenous pacemaker or permanent pacemaker inserted within <1 month). (36017548)
- [4] Mechanical right heart valve, or status post tricuspid valve clip (TriClip).
- [5] Stenosis of the tricuspid or pulmonic valves.
- [6] Thrombus or tumor in the RV or RA.
- [7] Right-sided endocarditis.
- [8] Pending MRI scan: most right heart catheters with thermodilution capabilities are unsafe for MRI. If an MRI is necessary, the catheter may be removed (leaving the introducer in place) and re-floated afterward.
- [9] Large ASD (atrial septal defect). (33646499)
- Other considerations:
- Severe tricuspid regurgitation isn't a contraindication per se, but may make it difficult to float the RHC.
- Other contraindications to central venous access, including severe coagulopathy.
Hemodynamic assessment can generally be made non-invasively. High-quality echocardiographic images with Doppler can provide substantial hemodynamic information (e.g., cardiac output based on the velocity-time integral), making the utility of the RHC debatable. (28595621)
potential indications for RHC include:
- Documentation of hemodynamics to determine candidacy for cardiac transplantation or ventricular assist device.
- Evaluation of pulmonary hypertension.
- Heart failure patients with:
- Failure to respond to therapy (especially worsening renal or respiratory status despite treatment).
- Persistently unclear hemodynamics.
- The potential need for mechanical circulatory support.
- RHC has greater benefits in cardiogenic shock than in decompensated heart failure.
- Right ventricular failure:
- Right heart catheterization may be more valuable in right ventricular failure since RHC directly investigates the affected cardiac chambers.
- RHC may be useful in revealing previously unrecognized right ventricular failure in the context of patients with left ventricular failure.
- Undifferentiated shock with no alternative source of hemodynamic information (e.g., poor transthoracic echocardiographic windows and inability to perform a transesophageal echocardiogram).
- Perioperative management for specific high-risk procedures (e.g., cardiothoracic surgery).
getting started
- Central line access site:
- 1st preference: right internal jugular.
- 2nd preference: left subclavian vein. 🌊
- Set the monitor to display pressures at the end of the RHC (the “VIP port” or “pulmonary artery” port).
- Consider asking an observer to video the monitor during RHC insertion with their phone. This allows for subsequent review of waveforms and pressures in a more leisurely fashion (especially the RV diastolic pressure and waveform, as discussed below).
- Consider recruiting an ultrasonography operator to obtain POCUS images of the right heart during the procedure.
transthoracic echocardiography to help guide RHC insertion
- Real-time POCUS may be used to help guide RHC insertion. (23132951) POCUS may be especially helpful in patients with more deranged physiology that masks typical waveform transitions (e.g., atrial fibrillation; right ventricular failure that produces similar pressures in the RA and RV). (Tan CO et al. 2015)
- Various echocardiographic views may be useful, depending on the patient's anatomy and achievable windows. Some potentially useful views are as follows:
- Subcostal or parasternal short-axis right ventricular inflow-outflow view: This might be the best single view since it allows visualization of the RHC crossing the tricuspid and pulmonic valves.
- Subcostal four-chamber view: This may allow better visualization of the RHC entering the right ventricle. It's often easy to obtain.
- IVC view: if there is concern that the catheter is in the IVC, this misplacement may be easily evaluated by viewing the IVC directly.
zeroing the catheter & verification
- The RHC is generally zeroed in the mid-axillary line (ideally with a level). However, this practice has fallen out of favor, and zeroing is often less precise than it historically was.
- After zeroing the catheter, hold the catheter on the patient's sternal manubrium. The pressure should be roughly +4 mm Hg (since the manubrium of the sternum is ~5 cm above the right atrium in a supine position). (27815151) Record this pressure for future reference. Checking the pressure at the sternal manubrium has the advantage that it is easily performed by the proceduralist without additional materials.
balloon inflation
- Insert the catheter to 15 cm, and then fully inflate the balloon.
- The balloon should be fully inflated (1.5 ml air) whenever the RHC is advanced (to reduce the risk of cardiac perforation). The balloon should be deflated whenever the RHC is being withdrawn (to avoid damaging valves). One exception is that if there is difficulty wedging the catheter, partial inflation of the balloon could be cautiously utilized in the final stage of advancing the RHC within the pulmonary arteries (discussed below).
rough depth benchmarks
- If the catheter needs to be inserted well beyond these benchmarks, it may suggest the possibility of coiling or malposition (e.g., into the inferior vena cava).
- Insertion via the right internal jugular:
- Right ventricle: ~30-35 cm. If the RV waveform isn't obtained by 40 cm, the catheter is likely in the IVC (or, less likely, coiling in the right atrium).
- Pulmonary artery: ~40-45 cm. The PA waveform should be obtained by ~10 cm after entering the right ventricle.
- Wedge tracing: ~50-55 cm. The wedge waveform should be obtained by <~10 cm after entering the right ventricle.
recognizing the PA waveform from the RV waveform
- The primary difference is usually that the RV diastolic pressure is usually close to zero, whereas the PA diastolic pressure is close to the wedge pressure (e.g., ~5-16 mm). However, this diastolic step-up may not be evident in some situations:
- [1] The wedge pressure may be low.
- [2] In RV failure, the RV end-diastolic pressure may be elevated. (33564995)
- The PA pressure slopes downward in diastole, similar to other arterial waveforms. In contrast, the RV diastolic waveform slopes upwards (circles in the figure above).
- Potential abnormalities that may be noted in the RV tracing:
- In RV failure, the RV end-diastolic pressure may be elevated (above the normal range of 0-8 mm), and the RV diastolic waveform may have a progressive oblique upslope. (38248013) In severe RV failure, the waveform may become square-root-shaped (figure below). (33564995)
- RV end-diastolic pressure >1/3 of RV systolic pressure suggests constrictive or restrictive cardiomyopathy. (30253970)
- Very rarely, RV outflow tract obstruction may cause the RV systolic pressure to be substantially higher than the PA systolic pressure (e.g., >25 mm). (33564995)
searching for the wedge waveform
- Once in the pulmonary artery, slow down and observe for a transition to a wedge waveform. The wedge waveform should roughly resemble a CVP waveform (figure above).
- The mean distance from entering the pulmonary artery to a wedge pressure tracing is 7 cm. (16793781)
- Difficulty obtaining a wedge may reflect:
- [1] Mitral regurgitation may generate large V-waves, which can mimic a PA waveform. (33564995)
- [2] This might reflect the pulmonary artery anatomy (e.g., an ovoid artery that doesn't occlude with a circular balloon).
- Troubleshooting difficulty:
- [1] Ensure you're not looking at a wedge tracing with large V-waves that mimic the PA waveform.
- [2] Floating the RHC with the balloon half-inflated may be attempted to form a better seal with the pulmonary artery (but this will result in a distal location of the RHC that could eventually risk pulmonary artery rupture, so the RHC shouldn't be left in such a distal location). (37633442, 20595458)
- [3] In some patients, a wedge waveform cannot be obtained. The PA diastolic pressure may be used as its surrogate in such patients.
- [4] If the wedge waveform is unsuitable (e.g., there are large fluctuations in pressure suggestive of non-Zone-1 location), consider deflating the balloon, withdrawing to the depth of the main pulmonary artery, and re-floating the catheter.
- If a wedge waveform can be found, it should be recorded (ideally with a picture or video), and the wedge pressure should be noted.
consider pulling back to a more proximal position
- For most patients, repeatedly wedging the RHC poses more risk than benefit (discussed below: ⚡️).
- Consider pulling the RHC back ~5 cm to a more proximal position, especially if you plan not to measure wedge pressures repeatedly.
lock the catheter and sheath in place
- The catheter should be locked into place as it enters the sheath to prevent it from being inadvertently withdrawn or advanced. Familiarize yourself with the locking mechanism utilized by your RHC kit and use it correctly.
- The protective sheath should be locked to the distal end of the exposed catheter.
bedside portable radiography as a surrogate for fluoroscopy
- Request a portable radiograph and kindly ask the technician to leave the detector behind the patient until you can look at the radiograph. If the catheter is malpositioned, reposition it immediately and re-shoot a radiograph. This may need to be repeated a few times in challenging patients until an adequate position is obtained.
- Optimal position on chest radiography:
- The ideal position is within the right or left main pulmonary artery or the proximal interlobar pulmonary arteries (within <1-2 cm of the lateral edge of the mediastinum).
- As a general rule of thumb, if the catheter extends beyond the hilum of the lung, it should be retracted. (22013292)
consider ordering daily chest radiographs
- RHC can migrate over time. Especially if the RHC migrates peripherally, this may be dangerous.
- Daily radiographs demonstrate that the RHC is malpositioned in 4% of films. (12022489)
- Daily chest radiographs may be considered to confirm the safe position of the RHC.
normal CVP waveforms
- A wave = Atrial systole
- The A-wave follows the P-wave on the ECG, occurring roughly with the QRS complex.
- C wave = Closure of the tricuspid valve. (33564995)
- This isn't always visible.
- Coincides with the beginning of systole.
- X-descent = pressure drop in the atrial cavity caused by ventricular systole and atrial diastole. (38248013)
- V wave = Right atrial filling against a closed tricuspid valve
- The V-wave follows the T-wave on ECG.
- Large V-waves may reflect valvular regurgitation or impaired chamber compliance. (37633442)
- Y-descent = Tricuspid valve opening, early ventricular filling.
- Y-descent >4 mm implies a right-sided restrictive pattern with preserved systolic function. If seen, this implies that additional fluid will not improve cardiac output. (27815151)
whip artifact in PA waveform
- The whip generates a sharp wave at the beginning of systole.
- Management:
under-damping
- The waveform shows multiple reverberating pressure wavelets (aka ringing artifact, circle above).
- Under-damping causes over-estimation of PA systolic pressure and under-estimation of PA diastolic pressure.
- Management:
- Flush the catheter to eliminate any bubbles.
- Shorten the length of the tubing between the catheter and transducer.
over-damping
- Over-damping causes underestimation of the PA systolic pressure and over-estimation of the PA diastolic pressure.
- Diagnosis: The waveform appears muted with no dichrotic notch.
- Causes:
- Air bubbles or blood clots partially occlude the system.
- The catheter tip is up against the blood vessel wall. (37633442)
- Catheter kinking.
- Loose connections.
- Management:
- Inspect the catheter and tubing (for kinks, loose connections, or air bubbles).
- Flush the catheter. (38960519)
atrial fibrillation
- A-wave is absent (there is no organized atrial contraction).
- C- and V-waves are most prominent. The C-wave may be more prominent than usual due to high end-diastolic atrial volume.
tricuspid regurgitation
- Early, massive holosystolic V-wave.
- X-descent is obliterated.
RV failure (e.g., pericardial constriction, RV infarction, or restrictive cardiomyopathy)
- Tall A- and V-waves.
- Steep X-descent.
- Steep Y-descents: a noncompliant RV leads to a steep Y-descent as blood rushes from a distended and/or noncompliant right atrium to rapidly fill the RV. (37633442) Y-descent >4 mm implies a right-sided restrictive filling pattern with preserved systolic function. (27815151)
tamponade
- Tall A- and V-waves.
- Absent or diminished Y-descent. (33564995)
how to measure the CVP
- Measure the pressure at end-expiration:
- Patient: this will correspond to peak pressures.
- Ventilator with positive pressure ventilation: this will correspond to the lowest pressures.
- Measure at end-diastole.
- This is roughly equal to the mean pressure of the A-wave.
- (Ideally, the CVP might be measured at the base of the C-wave since this reflects the end-diastolic pressure.) (33564995)
interpretation of the CVP
- A normal CVP is often quoted at ~2-6 mm.
- For intubated patients with high PEEP, consider subtracting off part of the PEEP to obtain the transmural filling pressure of the right ventricle.
elevated CVP (≧8 mm)
- [1] Elevated CVP usually implies RV failure, especially if there is also evidence of RV dilation. (35953675) In the absence of RV dilation, elevated CVP might point to other etiologies of RV dysfunction (such as tamponade or constrictive pericarditis) or high airway pressures (including tension pneumothorax).
- [2] If CVP is >>12 mm, this suggests that systemic congestion is present, and diuresis may be beneficial. However, the patient may also require a more nuanced and global optimization of their right ventricular failure.
- ⚠️ Don't assume that an elevated CVP indicates volume overload.
- In the context of known RV failure wherein other variables have been optimized, CVP may be used to guide fluid management (often targeting a mildly elevated CVP of ~8-12 mm 📖).
- [3] Elevated CVP may be an indication to consider targeting a higher MAP goal. For example, a MAP higher than (CVP+60mm) may correlate with improved renal outcomes. (35953675)
- [4] Disproportionate jumps in central venous pressure after PEEP up-titration may indicate that excessive PEEP is causing elevation in the pulmonary vascular resistance by compressing pulmonary capillaries. (36322446)
“reduced” CVP
- Zero or negative CVP readings can be seen in normal people. Consequently, some caution should be employed when assuming that a reduced CVP is pathological (i.e., indicative of either hypovolemia and/or systemic vasodilation).
- Reduced CVP isn't an indication to administer fluid. For example, the treatment of choice for patients with systemic vasodilation causing low CVP may often be a vasopressor (which will increase the CVP indirectly). 🌊
- CVP is a static measurement, so it isn't an indicator of fluid-responsiveness.
respiratory variation in CVP
Kussmaul sign
- Normal physiology during inspiration:
- Downward movement of the diaphragm increases intraabdominal pressure and decreases intrathoracic pressure. This encourages blood flow into the right heart.
- Normally, the right heart is able to accommodate this increase in blood volume. Right-sided pressures normally decrease because the reduction in intrathoracic pressure is a dominant factor.
- Kussmaul sign is an indication of right ventricular failure of any etiology. The right heart cannot accommodate the influx of blood during inspiration, causing a paradoxical increase in CVP during inspiration. This is analogous to hepatojugular reflux (discussed below).
- Some specific causes of the Kussmaul sign include:
- Constrictive pericarditis.
- Tamponade (although the Kussmaul sign is usually absent).
- Right ventricular myocardial infarction.
- Pulmonary hypertension.
hepatojugular reflux test
- Pressure is placed on the abdomen to compress the abdominal venous reservoir and increase venous return. After ten seconds, the pressure is removed.
- Normally, this should only produce a transient increase in jugular venous distension.
- Sustained elevation of the central venous pressure for >10 seconds suggests right ventricular failure with the inability to accept a higher preload. Among other things, it implies a lack of fluid responsiveness. (27815151)
⚠️ avoid unnecessary wedge pressure measurements
reasons to avoid measuring the wedge pressure
- Wedge pressure measurement carries risk:
- When compared to simply inserting a central line, the primary major morbidity associated with a RHC is pulmonary artery rupture. Consequently, avoiding this complication is fundamental to safely utilizing RHCs. Although pulmonary artery perforation is rare, it carries a mortality >50%.
- Over time, the RHC may tend to migrate peripherally. If the balloon is inflated while the RHC is too peripheral, it may rupture the pulmonary artery.
- Wedge pressure measurements are commonly inaccurate:
- Measurement of the wedge pressure may be incorrect if the RHC is either under-wedged, over-wedged or in a non-Zone-3 position. Consequently, serial measurements may be a source of noisy, inaccurate information. This is especially true if the wedge is measured without meticulous attention to the waveform.
- The most common error might be under-wedging of the RHC, which leads to erroneously elevated pressure measurements. This may occur in most patients, especially with less meticulous monitoring ⚡️.
- Compared to the wedge pressure, the PA diastolic pressure is easier to measure in a reliable, repeatable fashion that can be trended precisely.
PA diastolic pressure can usually be used as a surrogate for the wedge pressure
- The PA diastolic pressure is usually ~1-4 mm above the wedge pressure.
- In the absence of pulmonary hypertension (which can be excluded using the RHC), the PA diastolic pressure can be utilized as a surrogate for the wedge pressure.
- One approach is to measure the wedge pressure when the RHC is first inserted. If this correlates with the PA diastolic pressure, then the PA diastolic pressure may be utilized subsequently.
- (Further discussion of the relationship between the wedge and PA diastolic below: ⚡️)
how to measure the wedge pressure
1) obtain a wedge waveform
- Inflate the balloon cautiously.
- If the waveform transitions to a wedge tracing with <1 ml in the balloon, this suggests that the RHC is too distal (obtain a chest radiograph and consider withdrawing the catheter).
- If no wedge tracing is obtainable:
- The RHC may be too proximal.
- The pulmonary arteries may have an eccentric configuration.
- Further discussion on challenges when obtaining a wedge tracing above: ⚡️
2) measure the wedge pressure
- Measure the pressure at end-expiration:
- Patient: this will correspond to peak pressures.
- Ventilator with positive-pressure ventilation: this will correspond to the lowest pressures.
- (Mneumonic: patient=peak; vent=valley).
- Measure at end-diastole. This is roughly equal to the mean pressure of the A-wave. Note that the left-sided A-wave should be relatively delayed compared to right-sided A-waves (so that it occurs somewhat after the QRS complex).
under-wedging
causes of under-wedging:
- If the RHC is too proximal, the balloon may not completely occlude the blood flow through the pulmonary artery, leading to incomplete wedging (aka under-wedging).
- Consequences of under-wedging:
- [1] The wedge pressure will be artificially elevated.
- [2] The pulmonary vascular resistance will be artificially reduced (since PVR = [mPAP-wedge]/CO). (37469534)
- Under-wedging is common. For example, this was observed in half of the patients in one prospective study at a large center. (33016102)
- Severe pulmonary hypertension may make it difficult to wedge the catheter adequately.
signs that the RHC is under-wedged:
- [1] The “wedge” waveform may resemble a blunted PA waveform.
- There should be a shift in the “v” waveform before and after inflating the balloon. In a true PCWP waveform, the V-wave is usually seen after the T-wave on the ECG.
- [2] Blood removed from the wedged catheter should have an oxygen saturation within 5% of systemic oxygen saturation (e.g., >90-95% in the absence of hypoxemia). (38960519) If the oxygen saturation is lower, this indicates that it is under-wedged, causing deoxygenated blood to leak around the balloon.
- [3] The wedge pressure may be unrealistically high. Normally, the wedge pressure should be below the PA diastolic. Additionally, the mean wedge pressure should generally be ~10 mm below the mean pulmonary artery pressure. (Griffin 2022) An aberrantly elevated wedge pressure as compared to the PA pressures suggests under-wedging.
over-wedging
Over-wedging occurs if the RHC is too distal in the pulmonary artery. This is dangerous because it increases the risk of pulmonary artery rupture.
signs of over-wedging
- [1] Inflation of the balloon may cause the catheter tip to press against the pulmonary artery wall, occluding flow through the catheter. This produces a continually rising waveform as pressurized flush solution accumulates within the obstructed catheter system (figure below). (33564995)
- [2] Wedge pressure is higher than PA diastolic pressure.
- [3] Wedge tracing appears with minimal balloon inflation (<1-1.5 ml of air).
management of over-wedging
- Obtain a chest radiograph to evaluate the location of the catheter.
- Withdraw the catheter to the proximal PA, inflate the balloon, and re-advance the catheter.
ensure that the RHC is in Zone 3 of the lung
Zone 3 basics
- Zone 3 of the lung refers to the most dependent lung tissue, where pulmonary capillary pressure exceeds alveolar pressure. It is essential for pulmonary capillary pressure to exceed alveolar pressure to transduce an accurate wedge pressure.
- In a supine position, most of the lung is usually in Zone 3 (although this may not be true among intubated patients with elevated airway pressures). (37469534) Due to blood flow patterns, most catheters will end up in Zone 3 of the lung, but ~30% may not. If the catheter isn't positioned in Zone 3, this may often be corrected by withdrawing it to the main pulmonary artery and re-floating it.
- Note that for a supine patient, lung zones will correspond with the patient's anterior/posterior axis (rather than the cephalad/caudad axis).
features suggesting non-Zone-3 placement
- [1] Marked respiratory variation in the PCWP waveform (e.g., respiratory variation in PCWP is greater than respiratory variation in the pulmonary artery waveform).
- [2] Loss of a normal atrial pressure waveform (lack of a and v-waves).
- [3] PCWP > PA diastolic.
- [4] When PEEP is applied, the wedge pressure increases by >50% of the applied PEEP.
relationship of wedge pressure and PA diastolic
diastolic pulmonary gradient (PA diastolic – wedge)
- Typically, the PA diastolic will be ~1-4 mm higher than the wedge pressure.
- In the absence of pulmonary hypertension, the PA diastolic pressure may be used as a surrogate for the wedge pressure. (Marino 2007)
causes of diastolic pulmonary gradient is >5-7 mm
- Tachycardia (>120-130 b/m) prevents the pulmonary artery diastolic pressure from falling to a normal level during each cardiac cycle.
- Elevated PRV (pulmonary vascular resistance).
wedge > PA diastolic
- This is physiologically implausible (it would cause blood to flow backward).
- Causes include:
- Non-Zone-3 RHC placement.
- Over-wedging.
- Under-wedging.
causes of wedge inaccurately reflecting the LVEDP (LV end-diastolic pressure)
wedge over-estimates LV preload
- Under-wedged PAC causes over-estimation of the wedge pressure.
- Non-zone-3 position.
- PEEP or autoPEEP. Left ventricular transmural pressure may be approximated by subtracting roughly half of the PEEP (noting that PEEP must be multiplied by 0.75 to convert it from cm water to mm Hg). (33564995)
- Corrected wedge = Measured wedge – 0.36(PEEP in cm)
- The effect of PEEP is usually negligible when PEEP is <10 cm. (24350972)
- Mitral valve disease (mitral stenosis or mitral regurgitation).
- Intracardiac shunt (left to right).
- Tachycardia. (33564995)
wedge under-estimates LV preload
- Aortic regurgitation (with regurgitant ventricular filling).
- Pulmonic valve regurgitation.
- Right bundle branch block. (33564995)
clinical utilization of wedge pressure
elevated wedge pressure
- Elevated wedge suggests LV failure (e.g., due to either intrinsic LV failure, valvular dysfunction, or excessive afterload).
- In the presence of cardiogenic pulmonary edema, there is more pressure to take action to reduce the wedge pressure. Alternatively, if the wedge pressure is well tolerated clinically, this is less of a pressing issue.
- Potential interventions to reduce the wedge pressure could include diuresis, the use of an inotropic agent, a systemic vasodilator, and/or mechanical circulatory support.
reduced wedge pressure
- A normal wedge pressure is often quoted at 6-15 mm. Encountering a low wedge pressure (<6 mm) is uncommon, especially in the context of heart failure.
- There might be an assumption that a low wedge pressure should be an indication for fluid administration. However, several additional features should be considered prior to fluid administration:
- [1] Wedge pressure is a static filling pressure, so a low wedge doesn't predict fluid responsiveness. (24286266)
- [2] If the wedge pressure is low but the CVP is normal/elevated, then there is a risk that fluid administration could cause systemic congestion.
- [3] Consider therapies the patient is on that may reduce wedge pressure (e.g., systemic vasodilators, inotropes). A low wedge pressure could be a signal that the left ventricle has improved enough that these supportive treatments might be weaned off.
over-estimation of cardiac output
- Intracardiac shunt (either right-to-left or left-to-right).
- RHC is positioned too distally.
- Injectate is too warm. (33646499)
under-estimation of cardiac output
- Infusion of fluid through the venous port of the RHC or the side port of the sheath. (33646499) Even peripheral fluid infusions might affect cardiac output. (30253970)
inaccurate cardiac output (errors in either direction)
- Atrial fibrillation or other irregular rhythms may cause poor reproducibility.
- Low cardiac output (CO <2.5 L/min may make relative changes in cardiac output difficult to appreciate). (Gaggin 2021)
- Hypothermia or hyperthermia. (33646499)
- (Tricuspid regurgitation is commonly cited as a cause of inaccurate thermodilution cardiac output measurements, but data indicates this is not the case). (10430725, 36607792, 37633442)
direct Fick cardiac output for intubated patients with volumetric capnography
- The Fick Equation allows for calculating the cardiac output based on the metabolic rate (VO2), mixed venous oxygen saturation, and arterial oxygen saturation.
- Direct Fick cardiac output involves calculating the cardiac output based on a direct measurement of the patient's VO2. This is the gold standard for the calculation of cardiac output.
- Unfortunately, for most patients, it is impossible to obtain a direct Fick calculation (because the apparatus isn't available to measure VO2).
- A direct Fick calculation is possible for intubated patients on ventilators that measure volumetric CO2 production. The ventilator displays the VCO2 value. Assuming a respiratory quotient of ~0.8:
- VO2 = 1.25(VCO2)
- Cardiac output can subsequently be calculated as follows:
- CO = VO2 / [13.4(Hemoglobin in mg/dL)(Arterial saturation – venous saturation/100)]
- ⚠️ The use of high FiO2 values may interfere with this calculation (since it doesn't consider dissolved oxygen content in the blood).
indirect Fick cardiac output 🧮
- An indirect Fick calculation is based on equations that estimate VO2 based on the patient's height and weight. This may be considerably inaccurate, especially for patients who are critically ill or have an unusual body habitus.
- The accuracy of an indirect Fick cardiac output as compared to the thermodilution cardiac output is controversial. Articles on right heart catheterization favor the thermodilution cardiac output over indirect Fick cardiac output. (37469534, 34389460) From a practical standpoint, obtaining repeated Fick cardiac outputs is difficult because this involves time delays and phlebotomy.
interpreting the mixed venous oxygen saturation
- Mixed venous oxygen saturation grossly reflects the balance of delivered oxygen (DO2) as compared to the oxygen consumption (VO2).
- A normal mixed venous oxygen saturation might be ~65-80%.
- A mixed venous oxygen saturation <50% may correlate with an increased mortality and increasing risk of tissue malperfusion. (34511212)
- Note that numerous factors affect the mixed venous oxygen saturation. Random flux in these factors may cause the mixed venous oxygen saturation to vary over time. Avoid assuming that changes in the mixed venous oxygen saturation reflect an improvement or decrement in the cardiac output. 🌊
- Causes of artificially high mixed venous oxygen saturation include:
- RHC is occultly wedged (causing blood to reflect pulmonary venous blood, rather than mixed venous blood).
- Left to right shunt.
- Elevated FiO2.
- Reduced systemic oxygen utilization (e.g., hypothermia, severe sepsis, carbon monoxide or cyanide poisoning).
normal SVR
- SVR = 80(MAP – CVP)/(cardiac output)
- Normal range: 800-1200 dyne-s/cm5 (although some sources list 700-1600) (38248013, 24350972)
potential management implications for elevated SVR in cardiogenic shock?
- [1] Do nothing: If the SVR is elevated but the MAP is low or low-normal, the SVR might be compensatory for reduced cardiac output (in which case the patient may not tolerate afterload reduction). Beware of the normalization fallacy (the incorrect belief that any values should be adjusted toward normal)
- [2] Pure vasodilator: Elevated SVR with a MAP that is higher than necessary (e.g., MAP >>60+CVP) suggests a potential benefit from afterload reduction (e.g., nitroprusside, hydralazine).
- [3] Inotrope: Elevated SVR with low cardiac output and poor perfusion may suggest benefit from an inotrope (dobutamine or milrinone).
- [4] Down-titration of vasopressor: If the patient is on a vasopressor, SVR elevation could be a reminder to down-titrate the vasopressor as much as possible (while maintaining an adequate MAP).
normal values
- PVR = (Mean PA pressure – wedge pressure)/(cardiac output)
- Normal range: 24-160 dyne-sec/cm5
- Normal range: 0.3-2.0 Wood Units (=PVR/80)
management implications
- Optimize lung function (e.g., oxygenation, ventilation, pH, avoid excessive PEEP or atelectasis).
- Inotropes (milrinone, dobutamine) or pulmonary vasodilators may be considered, especially if this seems to be a primary driver of instability. 📖
commonly utilized ventricular function indicators
PAPi
- PAPi = (PA systolic – PA diastolic)/CVP
- Normal PAPi is >2. (38960519)
- PAPi <1-2 is used to define RV dysfunction. (37633442)
- PAPi <0.9 is:
- The predictive value of PAPi is superior to traditional indices such as RAP/PCWP and RV stroke work index. (34511212)
LV CPO (left ventricle cardiac power output)
- CPO = [(MAP-CVP)(CO)]/451
- Normal CPO: ~0.8-1.1 Watts
- CPO is one of the strongest predictors of mortality in cardiogenic shock. CPO <0.6 predicts in-hospital mortality and suggests a benefit from mechanical support. (Griffin 2022, 38960519) The combination of CPO <0.6 plus lactate >4 mM following intervention/optimization is especially ominous. (38248013)
- LV CPO is generally regarded as an index of LV function, but it's important to remember that RV failure may also indirectly impair the LV CPO (e.g., due to the underfilling of the left ventricle).
RV CPO (right ventricle cardiac power output)
- RV CPO = [(mean PA pressure-CVP)(CO)]/451
- RV CPO <0.3 watts suggests a poor prognosis.
classification of RV failure vs. LV failure vs. BiV failure in cardiogenic shock
Normally, CVP is roughly half of the PCWP. (37633442) Alterations in this ratio may help diagnose RV-predominant or LV-predominant shock.
RV-predominant shock
- Filling pressures:
- CVP >15 mm.
- PCWP <18 mm.
- CVP/PCWP ratio >0.6-0.8
- Ventricular function indicators:
- PAPi <1-2.
- RV CPO <0.3 Watts.
LV-predominant shock
- Filling pressures:
- CVP <15 mm.
- PCWP >18 mm.
- CVP/PCWP ratio <0.6-0.8
- Ventricular function indicators:
- PAPi >1-2.
- LV CPO <0.6 Watts.
Biventricular shock
- Filling pressures:
- CVP >15 mm.
- PCWP >18 mm.
- Ventricular function indicators:
- PAPi <1-2. (34511212)
- RV CPO <0.3 Watts
- LV CPO <0.6 Watts.
other indices that are utilized less frequently
RV stroke work index
- RVSWI = (13.6)(CI/HR)(mean PAP – CVP)
- The normal range is >8
- RV stroke work index is an estimate of RV workload and contractility.
- Low RVSWI correlates with RV failure after LVAD implantation. (38960519)
LV stroke work index
- LVSWI = (13.6)(CI/HR)(MAP-CVP)
- The normal range may be roughly ~50 – 62 gm-m/m2/beat
- Change in LVSWI may be utilized to evaluate the change in cardiac function due to dobutamine (cardiac reserve). (2393609)
Management needs to be tailored to the clinical context, but the following steps may be considered:
[#1] consider pure afterload reduction
- 🏆 Pure afterload reduction may simultaneously reduce filling pressures and increase cardiac output without increasing cardiac workload.
- Consider pure afterload reduction for patients with elevated SVR plus an unnecessarily high MAP (e.g., MAP >> [60+CVP]). Essentially, the patient has excessive vasoconstriction (beyond a point that appears to be beneficial).
- Options for afterload reduction include:
- Nitroprusside infusion (may be utilized to evaluate the benefit of vasodilation; if successful, may be transitioned to an oral vasodilator). 📖
- Nicardipine infusion (less evidence than nitroprusside, but safer for some patients).
- Oral hydralazine/isosorbide dinitrate (similar to ACE-i without nephrotoxicity). 📖 (3520315)
[#2] consider an inotrope (dobutamine, milrinone)
- Consider an inotrope for patients with low cardiac index and inadequate systemic perfusion markers.
- Dobutamine is generally selected due to its more favorable pharmacokinetics and titratability.
- Milrinone may be superior for patients with right ventricular failure (due to greater pulmonary vasodilation).
[#3] volume optimization
- Volume optimization may be a third step (because afterload reduction and inotrope administration may also reduce filling pressures).
- Consider decongestion with a target of CVP ≦8 mm and PCWP ≦15 mm.
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Guide to emoji hyperlinks
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