Introduction

Patients who sustain major trauma may become hemodynamically unstable at various times during their course.  Immediately following a major traumatic injury, hypotension is common, and its diagnosis must often be made on simple clinical grounds, because time for sophisticated hemodynamic monitoring is not available.  Fortunately, such diagnosis is generally obvious: hemorrhage, pneumothorax, and spinal shock are easily diagnosed by the experienced clinician.  Later in the post-traumatic course, hypotension may result from different reasons, including hypovolemia, depression of myocardial function, and vasodilation from inflammation and sepsis.  At this time, the clinical exam may be insufficient to reach a satisfactory diagnosis and institute the appropriate therapy.  Hence, the clinician must resolve to use further monitoring.  At this point, the trauma patient is like any other hemodynamically unstable, critically ill patient in the intensive care unit (ICU).

The goal of hemodynamic monitoring is to maintain adequate tissue perfusion.  In critically ill trauma victims, hypoperfusion of vital organs may lead to multiple organ systems dysfunction and death.

Classical hemodynamic monitoring is based on the invasive measurement of systemic and pulmonary vascular pressures and of cardiac output.  Although burdened with possible flaws, central pressure monitoring is widely used in the operating room and in the ICU.  Newer monitoring techniques are promising but, for various reasons, have not yet reached widespread acceptance, and they will not be described in this lecture.  The aim of this lecture is to guide clinicians through the interpretation of hemodynamic data based on the application of classic circulatory physiology.

Why measure arterial blood pressure.

Regrettably, tissue perfusion (i.e., organ blood flow) cannot be directly measured in clinical practice:

Organ Blood Flow = (arterial pressure - venous pressure) / resistance

Assuming constant venous pressure and constant resistance, measurement of arterial blood pressure is the closest parameter we have to blood flow.  One can easily see how crude this measurement is: by measuring the blood pressure at the radial artery, we hope to estimate the adequacy of blood flow to the kidneys, brain, and coronary circulation.  However, physiology helps our limited capacity: under normal circumstances, organ blood flow is maintained within normal range through ample changes of blood pressure through autoregulation.  Unfortunately, in pathological conditions such as trauma and sepsis, autoregulation is significantly impaired, and blood flow may become directly dependent on perfusion pressure, which therefore must be known.

Despite the limitations of peripheral blood pressure measurement, maintaining a reasonable value of arterial pressure is associated with signs of adequate organ function in most critically ill patients.  The following suggestions may enhance the effectiveness of arterial blood pressure monitoring.

a.   The mean arterial pressure (MAP) is the best physiological estimate of perfusion pressure and is less subject to measurement variability than the systolic pressure.

b.   A MAP > 60 mm Hg is a reasonable target for most patients.  At times (chronic hypertension, cerebral edema, spinal cord ischemia, etc.), higher values are necessary.  Controversy exists on the accuracy of clinical parameters of vital organ function, such as urine output and acid-base status, as early indicators of tissue hypoperfusion.  However, no other proposed parameter, such as serum lactate and gastric mucosal pH, has yet been shown consistently to be superior.

c.   Optimal blood flow through vital organs is first achieved by maintaining an adequate circulating volume.  An increase in blood pressure achieved using vasoconstrictor agents in hypovolemic patients does not provide adequate organ perfusion and can be deleterious.

How to measure arterial blood pressure.

Non invasive (generally automated) oscillometric blood pressure measurement is no longer accurate in the presence of rapidly changing blood pressure, arrhythmias, hypotension and hypertension.  It should not be used in hemodynamically unstable patients.

Intra-arterial blood pressure measurement via a catheter-transducer system is extremely reliable if the system is properly set up, and should be used whenever possible in hemodynamically unstable patients.

Physiological approach to hypotension.

We will limit our discussion of hemodynamics to the interpretation of hypotension, but the general principles illustrated here apply to hemodynamic monitoring in general.  We suggest a simple approach to the diagnosis of hypotension, summarized in Table 1. 

Table 1.  A physiological approach to hypotension

This schema can be applied to clinical practice using increasing levels of monitoring.  Table 2 shows a suggested stepwise approach to the hemodynamic monitoring of a hypotensive trauma patient.

In many cases, the diagnosis can be suggested on clinical grounds.  For example, hypotension in a young patient bleeding from a lower extremity crash injury should be easily attributed to hypovolemia, without the need of invasive monitoring.

In less obvious cases, it is reasonable to “try” an intervention, and confirm or reject the diagnosis post-hoc (“trial and error”).  For example, if our above patient had also a history of coronary artery disease, one should think of myocardial dysfunction as a contributor to the hypotension.  Volume resuscitation could still be a reasonable initial step.

As patients develop complex problems during a prolonged ICU course, the etiology of hypotension becomes be more and more difficult to sort out, thus requiring invasive monitoring. 

Table 2.  Example of a stepwise approach to the hemodynamic monitoring of hypotensive trauma patients 

Central venous pressure (CVP) monitoring provides a useful estimate of the volume status of the systemic circulation and (see below the discussion of interpretation of CVP).  The main limitations of CVP monitoring are that  a) it does not allow measurement of cardiac output, and  b) it does not provide reliable information on the status of the pulmonary circulation in the presence of left ventricular dysfunction.

Pulmonary artery (PA) pressure monitoring with a PA catheter allows to measure (CO) and stroke volume (SV), PA pressure and PA occlusion pressure (PAOP) and hence to separately assess the performance of the right and the left ventricle (RV and LV).

Central pressure measurements are often used to estimate volumes, i.e., the CVP estimates the volume of the systemic circulation and the PAOP estimates the volume of the pulmonary circulation.  As long as the postulate that central pressures accurately reflect volumes holds true, the characteristic hemodynamic findings of hypotensive patients are straightforward, as summarized in Table 3.

Table 3.  Central pressures and cardiac output changes in hypotension  

1.   Make a working diagnosis based on the relationship between pressures (CVP and PAOP) and cardiac output (CO or SV) as summarized in Table 3.  We assume at this point that the CVP and the PAOP are adequate estimates of the RV and LV end-diastolic volumes respectively and that the right (CVP) and left (PAOP) side of the circulation are equally affected by the cause of hypotension.

2.   Revise our basic assumption that CVP » volume of the right side of the circulation and that PAOP » volume of the left side of the circulation.  Unfortunately, this assumption is often flawed.  Knowledge of the basic physiology underlying the pressure/volume relationship in the central circulation is required to accurately interpret central vascular pressure data.  Our basic assumption can be altered under three main circumstances:

a.   When the volume/pressure relationship (compliance) of the RV or LV is abnormal, as it may happen with concentric LV hypertrophy (LVH) from hypertensive cardiomyopathy and aortic stenosis.  In this case, the measured PAOP overestimates the LV end-diastolic volume.

b.   When the pressure measurement does not estimate the actual transmural pressure across a cardiac chamber.  An increase of intrathoracic pressure gets transmitted to the blood vessel where the tip of our catheter is lodged, and increases the measured vascular pressure without any actual increase in circulating volume.  Common causes of increased intrathoracic pressure that mislead the interpretation of CVP and PAOP include PEEP, autoPEEP and increased intra-abdominal pressure.  The fraction of pressure transmitted through the blood vessel depends on a number of factors, including the compliance of the anatomical structures involved and the tension of the blood vessel wall.  A reasonable idea of the amount of pressure transmitted can be derived by considering the values of compliance of the lung and of the chest wall.  For example, transmission of auto-PEEP in a patient with COPD (compliant lungs) may be substantial, while transmission of applied PEEP in a patient with ARDS (stiff lungs) may be minimal.

c.   Mitral stenosis.  Valvular heart disease may affect the interpretation of hemodynamic monitoring in many ways, and yet invasive monitoring may be crucial in the interpretation of hypotension in patients with valvular defects.  With significant mitral stenosis, the PAOP may not correctly estimate the LV end diastolic pressure because of inadequate LV filling time.  Hence, a high PAOP may be recorded when the LV is still underfilled.

d.   Ventricular interaction.  RV volume overload from pulmonary hypertension and/or RV congestive failure may dilate the RV to a degree sufficient to move the interventricular septum towards the LV and limit its filling.  Thus, the LV pressure- and hence the PAOP- will increase despite a lower volume of blood in the LV.

It is important to note that in all the above situations, the pressures measured are indeed correct, rather than measurement errors.  A high PAOP in the presence of severe concentric LVH or mitral stenosis is an accurate reflection of the high pressure in the left atrium and, as such, can result in acute pulmonary edema.  However, the LV may still be underfilled.  This example underscores both the difficulty and the possible benefit of the correct interpretation of invasive hemodynamic monitoring in complex circumstances such as valvular heart disease.

3.   Look at the history.  The hemodynamic values evaluated at each discrete point in time have to be put in the patient’s context.  Although any properly obtained hemodynamic profile should be interpreted as the reflection of a specific moment in time, looking at previous numbers as well as at all other relevant clinical variables improves the accuracy of our measurements.

4.   Separating RV and LV.  The CVP and PAOP may change independently, because they measure two separate entities.  The CVP measures a pressure in the systemic circulation, and the PAOP in the pulmonary circulation.  To better understand this point, let’s examine the effect of a hypothetical episode of acute, isolated LV dysfunction from, e.g., ischemia.  The decreased LV contractility causes a decreased stroke volume (SV), and a few less mls of blood enter the systemic circulation.  This decrease of SV is so minimal in respect to the size of the venous reservoir that has no discernible effect on the venous return to the RV.  Thus, the RV continues to eject an approximately normal SV, which will be “accommodated” by the dysfunctional LV by increasing the LV end-diastolic pressure (~PAOP).  At steady state, the SV of the two ventricles will be again equal and close to normal.  Figure 1 summarizes graphically these events:

Interpretation of the CVP.

The following discussion is designed to assist in the interpretation of the CVP when the measurement of the CO is not available.

Venous return and CO are described by these two curves:

The diagram. on the left shows two venous return curves: the upper represents a normal circulating volume (CO = 6 L/min) and the lower represents hypovolemia.  The diagram on the right shows two contractility (‘Starling’) curves, the lower one representing a decreased contractility.  At steady state, venous return and CO are equal, and the two curves can be constructed on the same graph.  The point at which the two curves intersect is the CVP.

In this graph., the starting CVP is 4 cmH₂O.  If the CVP increases to 8 cmH₂O, the new value can occur at a variety of CO values, as shown by the dotted vertical line, with different physiological implications.  The two possible extremes are that the CVP has increased only due to an increase in volume (new venous return curve) or that it has increased only due to a decrease in contractility (new Starling curve).  Clearly, a combination of both phenomena is possible.  The same thinking process can be illustrated for a decrease in CVP.  Hence, an isolated CVP value can represent very different hemodynamic conditions, and without a CO measurement, we have to use clinical equivalents to interpret the change in CVP.  In a reasonably stable patient, changes in MAP should parallel changes in CO.  An increase in CVP will be likely due to an increased circulating volume if the MAP also increases.  An increase in CVP will be likely due to a decreased contractility if the MAP decreases.  In an unstable patient, measurement of the CO may be necessary. 

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