Hemodynamic Monitoring


Afterload is determined by impedance, which is a combination of resistance and compliance. Thus, arterial blood flow, which is pulsatile, is not simply a function of contractility and resistance. In fact, compliance may play a significant role in blood flow, so much that some recommend abandoning the use of SVR as a clinical measure of afterload [Clin Chest Med 24: 549, 2003] . Hemodynamic monitoring in the intensive care unit.
Pinsky MR.
Abstract Hemodynamic monitoring is a diagnostic tool. Because hemodynamic monitoring often requires invasive procedures, it can be associated with an increased incidence of untoward events. Like any diagnostic tool, its ability to improve outcome will be primarily related to the survival benefit enjoyed by specific therapies that can only be given without complications based on their use. Presently, few specific treatment plans fit into this category. The diagnostic accuracy of preload responsiveness is markedly improved by the use of arterial pulse pressure or stroke volume variation, neither of which require pulmonary arterial catheterization. The field of hemodynamic monitoring is rapidly evolving and will probably continue to evolve at this rapid pace over the next 5 to 10 years as new technologies, information management systems, and our understanding of the pathophysiology of critical illness progresses.

Arterial Blood Pressure

Blood pressure cuff

The blood pressure cuff is known to be inaccurate, yet still used [Lancet 344: 31, 1994]. The bell should be used for Korotkoff sounds, not the diaphragm [Circulation 111: 697, 2005]. Cuffs that are too small will raise blood pressure measurements – the bladder width should cover half the upper arm. Use the bell to detect Korotkoff sounds as it is better at detecting low frequency sounds. Also note that in low flow states, auscultatory methods may underestimate blood pressure, on average by > 25 mm Hg in patients experiencing shock [JAMA 119: 118, 1967]. The oscillometric method also uses a cuff but relies on plethysmography. This is thought to be more accurate than auscultation but are still rarely within 5 mm Hg of intraarterial measurements [J Clin Monitor 6: 284, 1990]

When vascular impedance (compliance + resistance) is abnormal, arterial pressure is no longer a reliable index of arterial flow. Also, systolic blood pressure actually rises as you approach the periphery (due to reflected pressure waves – this phenomenon is particularly prominent in the elderly who make up much of the ICU population) – because of this, use MAP instead of systolic, as it is more accurate (but still not a good indicator of flow)

In the old systems at least, arterial catheters were underdamped (too much fluid between the artery and the transducer), which could lead to overestimates as high as 25 mm Hg. Minimizing the distance between the artery and the transducer solved this problem. Overdamped systems often have air bubbles in the tubing, thus should be flushed. When flushing these systems, look at the resonant frequency of the resultant waveform – ideally it is at least 5x greater than the major frequency in the arterial system (~ 5 Hz), ie 25 Hz. If flushing does not produce any oscillations, the system is overdamped

MAP vs. Systolic

MAP is superior to systolic pressure because 1) it is the true driving force for flow 2) it does not change distally and 3) it is not altered by recording system distortion [Anesthesiology 54: 227, 1981]. It should be intergrated, not estimated (DBP + 1/3 [SBP-DBP]), because in ICU patients diastole may not make up 2/3 of the cardiac cycle

According to Andrews (data unpublished), a-line and cuff MAPs are predictably correlated but NOT identical – the equivalence point is 70 mm Hg, where they are equal. however, a cuff MAP of 90 mm Hg is equivalent to an a-line MAP of 100 mm Hg. In the critically ill patient where MAPs must be 70, do not trust a cuff below 70 mm Hg because below that value it overestimates BP. In the patient treated with hypervolemic or hyperdynamic therapy, the cuff will underestimate MAP, thus a cuff MAP of 100 signifies an a-line MAP of greater than 100. Conclusion: at MAPs ~ 70 mm Hg, a-line and cuff are equivalent. For higher MAPs, cuff will underestimate actual MAP

Respiratory Variation

Infectious Risk of Arterial Catheters

The infectious risk of arterial catheters is generally under appreciated – in fact, the colonization rate or arterial catheters (15.7 per 1000 catheter days) is the essentially the same as for central venous catheters (16.8 per 1000 catheter days). The risk of catheter-related blood stream is supposedly lower but non-trivial (0.92:1000 versus 2.23:1000 catheter days) [Koh DBC et al. Crit Care Med 36: 397, 2008]. Thus, the 2×2 factorial randomized controlled trial comparing chlorhexidine-impregnated sponges and less frequent dressing changes to traditional management of intravascular catheters included these sponges on the arterial catheters, and showed that chlorhexidine-impregnated sponges on both the arterial and central venous catheters lowers CRBSI from 1.4:1000 to 0.6:1000 catheter days [Timsit JF et al. JAMA 301: 1231, 2009; FREE Full-text at JAMA]

Central Venous Pressure and Wedge Pressure

Point of Reference

The point of reference is the intersection between the 4th intercostal space and the mid-axillary line, but this is only valid when patients are supine (not lateral or elevated). Note that pressure changes in the thorax may or may not reflect important transmural changes, as it is impossible to gage the transmission of such pressures throughout the thorax. Intravascular pressures are valid at the end of expiration (except in the face of grunting or PEEP), when thoracic pressure = 1 ATM. Changes in CVP or wedge pressure < 4 mm Hg are clinically insignificant

Alternatives to CVP

As an alternative to a Swan-Ganz, LVEDV (and to a certain extend RVEDV) has be estimated using TEE or even TTE [Am J Cardiol 41: 726, 1978] – this was recently confirmed by comparing TTE to cardiac MR in 25 patients [J Am Soc Echocardiogr 14: 1001, 2001]. One year later, a comparison of TTE vs. TEE in 46 patients showed that both methods correlate highly for LVEDV [Echocardiography 19: 383, 2002]. A recent review in Chest analyzed 24 studies (total of 803 patients) and found the pooled correlation coefficient between CVP and measured blood volume to be 0.16 and the area under the ROC to be 0.56 [Marik. Chest 134: 172, 2008]

Wedge Pressure

Wedge pressure IS NOT left ventricular preload – preload is a volume (EDV), and the wedge only corresponds to this when ventricular compliance is normal (ie not in hypertrophy, positive pressure ventilation, ischemia, etc.). In a ventricle with normal compliance, wedge may not be accurate if there is aortic insufficiency (premature closure of mitral valve) or respiratory failure (constriction of veins in hypoxic regions). A study of 12 normal subjects showed almost no correlation between PCWP and LVEDV (r = 0.04 [Crit Care Med 32: 691, 2004])

Wedge pressure is not pulmonary capillary hydrostatic pressure because it is measured on a static fluid column, whereas in vivo there is blood flow. Furthermore, the pulmonary veins are responsible for 40% of the pressure drop across that circuit. To convert, Pc – PCWP = 0.4(Ppulm.art. – PCWP) or Pc = PCWP + 0.4(Ppulm.art. – PCWP)

Wedge pressure is not a reliable method of distinguishing cardiogenic from other pulmonary edema. If unattainable, wedge is usually within several mm Hg of pulmonary diastolic pressure (except in pulmonary hypertension, etc.)

Wedge is affected by which lung zone you’re in – in zones 1 and 2, the wedge may reflect alveolar pressure and not capillary pressure, thus the Swan-Ganz tip should always be placed in zone 3 (lung regions below the left atrium). Getting a lateral film is time consuming and is the only way to verify this, so the best surrogate is looking at the readout – if there are marked respiratory variations in the wedge, or if the wedge increases by more than 50% when PEEP is applied, the tip is probably not in zone 3. PEEP can actually eliminate zone 3 conditions, so patients who require PEEP should have their wedge measured with PEEP temporarily discontinued (if possible)

Up to 50% of nonpulsatile pressure variations measured by the Swan-Ganz may be the result of damped PA pressure [Crit Care Med 13: 756, 1985] and thus Marino recommends validating with three criteria: 1) Wedge PO2 – Arterial PO2 > 19 mm Hg; 2) Arterial PCO2 – Wedge PCO2 > 11 mm Hg; 3) Wedge pH – Arterial pH > 0.008

Neurosurgical Issues Regarding CVP

Neurosurgical Concerns Regarding Hemodynamics:

  • According to Andrews, CVP 5-10 mm Hg optimizes EDV in the neurosurgical patient without overloading the heart. He further claims that there is little evidence to suggest CVP > 10 improves CPP
  • A study of 82 SAH patients at Columbia treated with 5% albumin to maintain CVP 5 mm Hg (or PA 7 mm Hg) vs. CVP 8 mm Hg (or PA 14 mm Hg) showed no change in CBF, fluid balance, or outcome [Stroke 31:383, 2000]

Criticism of CVP in Literature

All in all, CVP and PCWP are outmoded variables that are near-impossible to measure in ICU patients and have been supplanted by the highly accurate cardiac output/index as well as tissue oxygenation variables. The use of CVP and PCWP should be disbanded [Crit Care Med 33: 243, 2005]

Pulmonary Artery Catheter

Meticulous attention to insertion technique and interpretation are necessary to maximize the patient care benefits of the PA catheter while minimizing the complications associated with its use. To deflate the balloon, disconnect the syringe and allow it to deflate passively. This minimizes the chance of sucking the balloon wall into the orifice of the inflation lumen and causing a rupture. The balloon should not be inflated with a liquid since fluid through the long thin inflation lumin may be difficult and damage occur when the catheter is withdrawn. Tilting the table to take advantage of the buoyancy of the air-filled balloon may help enter the right ventricle. Arrhythmias occur in almost 50% of placements – they most commonly occur when the catheter is in the right ventricle and one should expedite passage through this chamber. Complete heart block or sustained V-tach need to be treated, but these are rare. In 25% of cases no PCWP can be obtained.

Each model of catheter has a specific balloon size and the syringe included should be used so as to prevent over-inflation. The balloon must be deflated between PCWP readings. Never have a pulmonary artery catheter in place without measuring the pressure in the distal lumin. Changes in ventricular size or patient position can allow the catheter to migrate distally (indicated by a “wedge” like tracing that varies significantly with respiration) and cause a pulmonary artery rupture or infarction.

The balloon should be slowly inflated while watching the tracing, and inflation stopped at the first sign of “wedging”. If significantly less than the maximum volume is required to obtain this tracing, the catheter is in too far and should be withdrawn.

BSA (m2) can be estimated within 99% as [Ht(cm) + Wt (kg) – 60]/100 and is often used in indices. The PA catheter can measure multiple cardiac performance parameters including CVP, PCWP, CI, SVI, RVEF, RVEDV, LV stroke work index, RVSWI, SVR/I, and PVR/I, as well as several oxygen transport parameters including DO2, VO2, SVO2, and O2ER (VO2/DO2)

CI CVP RAP PCWP PVRI SVRI VO2 Right Heart Failure ↓ ↑ ↑ ↑ ↔ Left Heart Failure ↓ ↑ ↑ ↑ ↔ Cardiogenic Shock ↓ ↑ ↑ ↓ Hypovolemic Shock ↓ ↓ ↑ Vasogenic Shock ↑ ↓ ↓

Low CI can be the result of left or right heart failure, so always check RAP vs. PCWP and PVRI vs. SVRI. VO2 is essential to tell the difference between heart failure and cardiogenic shock. Vasogenic shock is the only cause of hypotension with a decreased SVRI


Cardiovascular CVP 1-9 mm Hg (optimally 5-10 in NSGY patient) PCWP 5-15 mm Hg CI 2.4 – 4.0 L/min/m2 SVI 40-70 ml/m2 SVRI 1600-2400 dyne•s•scm5/m2 PVRI 200-400 dynes•s•cm5/m2 RVEF 46-50% RVEDVi 80-150 mL/m2 LVEDVi 55 to 65 mL/m2 [Chest 128: 881, 2005]

Oxygen Transport SvO2 70-75% ER 20-30% VO2 110 – 160 ml/min/m2 DO2 520 – 570 ml/min/m2

Recent literature suggests that PA catheters do not affect mortality rate and add additional complication risks in ICU patients [Lancet 366: 472, 2005] and heart failure patients [JAMA 294: 1625, 2005] when compared to clinical assessment alone (jugular venous distension, edema, orthopnea)

Randomized Data on PA Catheters

According to a recent Cochrane Database Review, there are 12 available randomized studies on PA catheters, some of which are reviewed here. Keep in mind that, as mortality rates are low, most of the studies of PA catheters are underpowered to detect a mortality difference – in fact, the Cochrane database review found that only one of 12 studies was sufficiently powered.

Bender JS et. al. Ann Surg. 226: 229, 1997 (104 patients)

104 consecutive patients randomized to have a PAC placed the morning of surgery (group I) or only if clinically indicated (group II). Group I patients were resuscitated to preestablished endpoints before surgery and kept at these points both intraoperatively and postoperatively. Group II patients received standard care. Results: one death in each group, 13 intraoperative or postoperative complications in group I versus 7 in group II (NS). Group I patients received more fluid than did group II patients (5.1L vs. 3.8L, p < 0.003), no difference in intensive care unit LOS

Rhodes A et. al. Intensive Care Med 28: 256, 2002 (201 patients)

Prospective, controlled, trial of 201 intensive care unit patients randomised either to a PAC group (n=95) or the control group (n=106). Results: no significant difference in mortality between the PAC and control groups (47.9% vs. 47.6%, p>0.99). The PAC group had significantly more fluids in the first 24h and an increased incidence of renal failure (35% versus 20%, p<0.05) and thrombocytopenia (p<0.03)

Bonazzi et. al. Eur J Vasc Endovasc Surg 23: 445, 2002 (100 patients)

A consecutive series of 100 patients randomised to either haemodynamic optimisation through the use of a pulmonary artery catheter (CI > 3.0 l/min/sqm, PWP > 10 and <18 mmHg, SVR <1450 dyne/sec/cm(-5), DO(2)> 600 ml/min/sqm) or conventional treatment. Results: no differences in in-hospital mortality, cardiovascular morbidity, postoperative renal failure or duration of hospital stay between the groups

Sandham et. al. N Engl J Med 348: 5, 2003 (1994 patients)

Randomized trial of high-risk patients 60 years of age or older, ASA class III or IV, who were scheduled for urgent or elective major surgery, followed by a stay in an intensive care unit, PA catheter vs. none. Of 3803 eligible patients, 1994 underwent randomization. Mortality was 7.8% in the PAC group, vs. 7.7% in the non-PAC group. 8 PEs in the PAC group, vs. none in the non-PAC group (p=0.004). Median hospital stay was 10 days in each group. Note that in the PAC group, CI and DO2 goals were met 19 and 21% of the time on entry and in 79 and 63% of patients after surgery. In addition, there were no differences in CVP between the PAC and non-PAC groups

Richard C et. al. JAMA 290: 2713, 2003 (676 patients)

Randomized controlled study of 676 patients who fulfilled the criteria for shock, ARDS, or both conducted in 36 French ICUs. Patients randomly assigned to PCA (n = 335) or not (n = 341). Treatment was left to the discretion of each individual physician and not protocolized. Results: no significant differences in 14 day mortality (49.9% with PAC, 51.3% without, p =0.70), or mortality at 28 (p = 0.67) or 90 days (p = 0.71). This study was underpowered for all outcomes other than mortality

Harvey S et. al. Lancet 366: 472, 2005 (1041 patients)

Randomised controlled trial of 1041 patients from 65 UK ICUs, assigned to management with (n=519) or without (n=522) a PAC. “The timing of insertion and subsequent clinical management were at the discretion of the treating clinician.” Results: no difference in hospital mortality (68% vs 66%, p=0.39). There were 46 complications associated with insertion of a PAC, none of which was fatal

Binanay C et. al. JAMA 294): 1625, 2005 (433 patients)

Randomized controlled trial of 433 patients with CHF at 26 sites randomized to receive therapy guided by clinical assessment and a PAC or clinical assessment alone. The target in both groups was resolution of clinical congestion, with additional PAC targets of a pulmonary capillary wedge pressure of 15 mm Hg and a right atrial pressure of 8 mm Hg. Medications were not specified, but inotrope use was explicitly discouraged. Results: PAC did not significantly affect the primary end point of days alive and out of the hospital during the first 6 months (p = 0.99), mortality (p = 0.35), or number of days hospitalized (p = 0.67). In-hospital adverse events were more common among patients in the PAC group (21.9% vs. 11.5%, p = 0.04), although there were no deaths related to PAC use

Non-Randomized Data on PA Catheters

Harvey S et. al. Cochrane Database of Systematic Reviews, Issue 4, 2006

Identified 12 total studies, two of which were multi-center and only one of which was adequately powered. “Efficacy studies are needed to determine optimal management protocols and patient groups who could benefit from management with a PAC.” The pooled OR for mortality in general ICU patients (8 studies) was 1.05 (CI 0.87-1.26), and the pooled OR for mortality in high-risk surgery patients (4 studies) was 0.99 (CI 0.73-1.24)

NEJM 354: 2213, 2006

Data extrapolated from the FACTT Trial (part of the ARDS Network) showing no differences in survival, ventilator free days, renal outcomes, or vasopressor therapy between patients who received PAC or CVP-guided monitoring

Friese RS et al. CCM 34: 1597, 2006

Retrospective analysis of National Trauma Data Bank data identified 1933 patients managed with a PAC and 51,379 patients managed without a PAC, suggesting that in low-risk patients PAC was associated with worse outcomes, whereas in high risk patients PAC was associated with improved outcomes


Be sure to record CO when patients are in a constant position, as it can be up to 30% higher in supine as compared to semi-erect patients. Higher volume lower temperature injectates give you the best S/N ratio, however room temperature injectates are usually adequate as long as 10 mL is used. Ideal injection time is < 2 seconds, although 4 seconds can usually be tolerated. Try and time injections to the same point in respiration, as this reduces respiratory variability from 10 to 5%. Always do serial measurements, discarding the first and relying on the following measurements – if they differ by < 10%, consider them reliable. When following CO by thermodiluation, changes < 10% are considered clinically insignificant [Chest 22: 225, 1994]

Tricuspid regurgitation refluxes the cold indicator, thus prolonging the thermodiluation curve and underestimating cardiac output. Also, in low output states (CI < 2.5 L/min/m2), the S/N ratio is elevated and both low temperature and high volume (10 mL) injectates should be used. Both LR and RL shunts will overestimate cardiac output

The rapid-response thermister allowed ejection fraction (T1 – T2)/(T1) to be measured. Normal RVEF is 0.45 to 0.60 when measured thermally. This allows EDV to be calculated, as thermodilution catheters can measure stroke volume

The Baxter Edwards catheter can measure cardiac output continuously by using a heated filament, and will likely replace the thermodilution method as it has proven to be more accurate [Crit Care Med 23: 994, 1995]

Tissue Oxygenation

O2 Sat vs. Hgb

Do not rely on O2 saturations to assess oxygenation – hemoglobin is MUCH more important. A 50% reduction in Hgb can reduce oxygen delivery by 50%, whereas a 50% reduction in saturation reduces oxygen delivery by only about 20%

DO2 and VO2

DO2 = rate of oxygen delivery. VO2 = rate of oxygen uptake and is usually derived [VO2 = Q x 13.4 x Hb x (SaO2 – SvO2)], however the calculated (as opposed to measured) VO2 can vary by as much as 18%. Also, this calculation does not take into account the use of oxygen by lungs (normally 5%, but in some patients can be up to 20% in ICU patients with inflammatory changes in the lungs). If VO2 is low, you know the patient is going into oxygen debt. If VO2 is normal, you need a blood lactate to determine if oxygenation is adequate. Since ICU patients are rarely hypometabolic, any VO2 that falls below 100 mL/min/m2 is evidence of impaired oxygenation

Parameter Normal Range ? O2 Deficit Oxygen Uptake (mL/min/m2) 110 – 160 < 100 Oxygen Extraction Ratio 0.2 – 0.3 > 0.5* Blood Lactate < 2 mM 4 mM Gastric Intramucosal pH 7.35 – 7.41 < 7.32

* Applies only to conditions where O2 delivery is impaired

Cardiac index is a poor predictor of oxygen uptake and tissue oxygenation (although it is predictive of delivery) because one can have a falling VO2 in the face of normal or increasing CI. Oxygen debt as measured by VO2 has been shown to predict risk of multi-organ failure [Crit Care Med 19: 231, 1991; Chest 102: 208, 1992]

VO2 is not useful in septic patients because the respiratory burst from phagocytes can significantly contribute to VO2 (“non-metabolic VO2 “). In fact, pO2 in the muscles of septic patients has been shown to be elevated, both in vivo and in experimental animals [Crit Care Med 29: 1343, 2001; Crit Care Med 23: 1217, 1995] – the problem in septic patients is one of oxygen utilization by mitochondria, which is why therapy designed to increase O2 delivery may is still a matter of debate – some data supports it [Crit Care Med 30: 1686, 2002] and other data refutes it [Chest 115: 453, 1999]

Oxygen Debt Correction

Oxygen debt should can be corrected by three major interventions 1)  cardiac output with volume or pharmacology 2) correct anemia 3) correct hypoxemia

Oxygen Debt Correction Algorithm: Step I
(CVP or wedge) infuse volume if low (titrate to CVP 8 – 10 mm Hg or PCWP 18 – 20 mm Hg) Step II
(Hgb) if Hgb < 7.0, consider transfusion Step III
(CO) if CO low and filling pressures not high, give volume until CVP 10 – 12 mm Hg or wedge 18 – 20 mm Hg. If CO low and filling pressures are high, start dobutamine 3 ug/kg/min and titrate to CI of 3.0 L/min/m2. If BP is low, use dopamine at 5 ug/kg/min Step IV
(re-assess VO2/lactate) if VO2 < 100 mL/min/m2, or if lactate > 4 mM with other signs of shock, attempt to decrease metabolic rate first (sedation, stop feeding), and consider attempting supranormal oxygenation only as a last resort (difficult to achieve, can cause cardiac and metabolic stimulation)

Assessing O2 Debt: VO2

In ICU patients, VO2 should change at least 15% to be considered physiologically significant. Also, a calculated VO2 is based on systemic measurements and does not take into account the lungs, which usually only contribute 5% – total VO2 in an ICU patient can be up to 25% higher than calculated VO2 because of pulmonary VO2 rises dramatically during ARDS and other pathologies

Assessing O2 Debt: Extraction Ratio

Oxygen extraction ratio > 0.5 can theoretically be used as an indicator of impending VO2 deficit, because once ER is less than 0.5-0.6, VO2 begins to decrease (prior to 0.6 VO2 is independent of DO2). In reality, this metric is not very useful because the DO2:VO2 curve does not have an abrupt transition point and is highly variable among individuals. The DO2:VO2 ratio is probably much more useful in identifying (and avoiding) the aerobic threshold – a DO2:VO2 ratio of 4:1 or greater is recommended in order to avoid anaerobic threshold in critically ill patients [Little, Brown: Crit Care Physio 1996: 1-23]

Assessing O2 Debt: SvO2

SvO2 may be useful – a decrease below 70% suggests that systemic O2 delivery is impaired, and below 50% indicates a global state of dysoxia or impending dysoxia. In general, a 5% change in SvO2 is considered significant. ScvO2 from the SVC (as opposed to the PA) is within 5% of SvO2 if multiple measurements are made (but only within 10% for a single measurement) [Anesthesiology 103: 249, 2005], thus ScvO2 is gaining popularity as a surrogate marker for in patients without a PA catheter. In fact, Recent sepsis guidelines include ScvO2 > 70% as a therapeutic endpoint [Crit Care Med 32: 858, 2004]

Lactate as an Indicator of Oxygenation

Lactate levels in whole blood and plasma are equivalent. In patients undergoing shock, these values may be more predictive of outcome than cardiac index or oxygen uptake [Chest 99: 956, 1991]. Using 4 mM as a cutoff gives sensitivity of only 62% (specificity 88%), whereas using 2 mM as a cutoff gives a sensitivity of 89% (specificity 42%)

Lactate and Survival in Septic Patients

Parameter Survivors     Non-Survivors     Difference Cardiac Index (L/min/m2) 3.8 3.9 2.6% Oxygen Uptake (mL/min/m2)    173 164 5.2% Arterial Lactate (mM) 2.6 7.7 296%

Data taken from patients in septic shock [Chest 99: 956, 1991]

Problems with Using Lactate

Lactate can also be produced in hepatic insufficiency, thiamine deficiency, and alkalosis, and is produced by some enteric microbes. In sepsis, lactate production is secondary to endotoxin inhibition of pyruvate dehydrogenase and not oxygen insufficiency [Ann Surg 224: 97, 1996] and is highly predictive of mortality

One problem with lactate is that it is a marker of global perfusion, not regional perfusion. Some physicians believe that splanchnic hypoperfusion is a more reliable precursor to organ failure, as measured by gastric tonometry [JAMA 1993; 270:1203–1210]. 1) Saline-filled balloon is placed in contact with gastric mucosa 2) Bicarbonate in blood is used as a surrogate for bicarbonate in gastric mucosa 3) intramucosal pH is derived from the H-H equation pH = 6.1 + log10([HCO3–art.]/[PCO2saline. X 0.03]). The threshold for abnormality is pH < 7.32

Gastric Tonometry

Problems with gastric tonometry include native acid secretion (if H2-blockers are inadequate), systemic acid-base disorders confounding the results (especially metabolic acidosis, which is common in shock patients, and respiratory alkalosis in ventilated patients), and the surrogate use of arterial bicarbonate for mucosal bicarbonate (may not be accurate in low flow states). Lastly, there is no data that gastric tonometry improves outcomes [Crit Care Med 31: S658, 2003]