DAVID STURGESS, DOUGLAS R. HAMILTON, ASHOT E. SARGSYAN, PHILIP LUMB and DIMITRIOS KARAKITSOS

. . . the blood somehow flowed back again from the arteries into the veins and returned to the right ventricle of the heart. In consequence, I began privately to consider that it had a movement, as it were, in a circle . . . by calculating the amount of blood transmitted [at each heartbeat] and by making a count of the beats, let us convince ourselves that the whole amount of the blood mass goes through the heart from the veins to the arteries and similarly makes the pulmonary transit. . . .

William Harvey: De motu cordis. In The circulation of the blood and other writings (1628), translated by Kenneth J. Franklin (1957), Chapter 8, pp 57-58.

Overview

In critical care, the goals of hemodynamic monitoring include mainly detection of cardiovascular insufficiency and diagnosis of the underlying pathophysiology. At the bedside, clinicians are faced with the challenge of translating concepts such as preload, contractility, and afterload into determinants of stroke volume and hence cardiac output. Ultrasound and echocardiography offer unique insight into ventricular filling and systolic function. In recent years there has been a general trend away from invasive hemodynamic monitoring. This was initially motivated by published data suggesting an association between the pulmonary artery catheter (PAC) and excess mortality in critically ill patients.¹ Despite specific risks, subsequent randomized controlled trials have not sustained the concerns about excess mortality.² The PAC should not be regarded as obsolete.

As already discussed in this text, ultrasound is proving useful in guiding safe and timely placement of many components of hemodynamic monitoring systems, including arterial, peripheral, and central venous access devices. Furthermore, because of its real-time nature, ultrasound, including echocardiography, offers the clinician a range of cardiovascular insights that are difficult or impossible to derive with other technologies. Ultrasound can be applied to a wide range of patients and is a safe, noninvasive, and reliable imaging method.

Hemodynamic monitoring devices

An overview of critical care hemodynamic monitoring would be incomplete without putting ultrasound in the context of the techniques available for estimating cardiac output, including nonultrasonic modalities. This broader topic is covered well in the literature³ and is outlined only briefly here. Demonstrating an association between any monitoring modality and improved outcome is challenging. Monitoring must be coupled with an effective change in therapy for a positive association to be observed. Clinical practice is characterized by the subtleties of interpretation, ongoing review, and titration of therapy to response. This does not translate easily into large-scale, randomized, controlled trial designs.

Clinicians differ in their preferences for particular hemodynamic monitoring techniques. Accuracy and degree of invasiveness are not the only considerations. Familiarity, availability of local expertise, cost (equipment and consumables), and applicability to a particular patient and the patient’s status must also be considered. Monitoring techniques tend to not be mutually exclusive and may be combined or changed to achieve the desired effect. For instance, initial hemodynamic evaluation with echocardiography may proceed to continuous monitoring, such as pulse waveform analysis.

Any form of hemodynamic monitoring (Table 36-1) should be viewed as an adjunct to the clinical examination and must be interpreted as an integration of all available data.^3–5 These may include the patient’s mental state, urine output, and peripheral perfusion (temperature and capillary refill time). Heart rate, arterial blood pressure, jugular venous pressure (or central venous or right atrial pressure [RAP]), and electrocardiography should also be incorporated. Other adjuncts to the interpretation of hemodynamic data might include Svo₂, Scvo₂, lactate, blood gases, capnography, gastric tonometry, or other assessment of the microcirculation.

Ultrasound indicator dilution is a novel application of ultrasound technology. Unlike transpulmonary thermodilution, which bases estimates of cardiac output on changes in blood temperature, ultrasound indicator dilution measures changes in ultrasound velocity. Normothermic isotonic saline is injected into a low-volume arteriovenous loop between arterial and central venous catheters. The change measured in ultrasound velocity (blood, 1560 to 1585; saline, 1533 m/sec) allows the formulation of an indicator dilution curve and calculation of cardiac output.⁶

Invasive hemodynamic monitoring

As mentioned previously, observational studies raised questions about increased morbidity and mortality with the use of PACs¹; however, subsequent randomized trials indicated that PACs are generally safe and may yield important information.² The PAC has a trailblazing role in defining cardiovascular physiology and pathophysiology. The method provides “cardiodynamic insight” that other hemodynamic monitoring technologies still fail to elucidate. A PAC is not a therapy and cannot affect the prognosis, but it can be used to guide therapy. The usual clinical indications for placement of a PAC are shown in Box 36-1.

Echocardiographic hemodynamic monitoring

A comprehensive echocardiographic examination is time-consuming. In the management of potentially unstable, critically ill patients, physicians will often prefer to focus their examination on pertinent variables. Several focused hemodynamic echocardiographic protocols have been developed and applied. Among others, these protocols include FOCUS (focused cardiac ultrasound⁷), ELS (Echo in Life Support⁸) and HART scanning (hemodynamic echocardiographic assessment in real time⁹).

As well as being minimally invasive (transesophageal [TEE]) or noninvasive (transthoracic [TTE]), echocardiography also offers unique diagnostic insight into a patient’s cardiovascular status. The presence of intracardiac shunts renders many hemodynamic monitoring devices invalid. Such shunts may be difficult to diagnose without echocardiographic techniques. Likewise, pericardial effusions, collections, and tamponade can also be difficult to diagnose without echocardiography.

In critical illness, cardiac function is not always globally affected. Echocardiography allows screening for and diagnosis of regional pathology, such as myocardial ischemia; furthermore, it allows evaluation of coronary arterial territories by regional wall motion abnormalities. Echocardiography may also disclose abnormalities such as dynamic left ventricular (LV) outflow obstruction and systolic anterior movement of the mitral valve. This may have particular therapeutic implications in critical care. Valvular dysfunction is also important to the critical care physician, and echocardiography is the clinical “gold standard” for detection and characterization (including grading). As an alternative to the PAC, echocardiography potentially offers important information about the right ventricle and pulmonic circulation.

Echocardiographically, cardiac output is calculated as the product of stroke volume and heart rate. Echocardiographic techniques for estimating stroke volume include linear techniques, volumetric techniques (two-dimensional [2D] and three-dimensional [3D] echocardiography), and Doppler. Guidelines have been developed for echocardiographic chamber quantification and should be applied for linear and volumetric assessments. Similarly, guidelines exist for Doppler measurements.

Noncardiac ultrasound hemodynamic monitoring

Additional hemodynamic data can be derived from noncardiac ultrasound, including the integration of lung ultrasound and superior (SVC) and inferior (IVC) vena cava analysis (respiratory variations) in hemodynamic monitoring. Noncardiac ultrasound methods are analyzed extensively elsewhere (see Chapters 39 to 42).

In brief, characteristic artifacts on lung ultrasound (B-lines) reflect underlying interstitial pulmonary edema and presumably an associated hemodynamic disturbance. The sonographically detected interstitial syndrome (“wet lung”) may appear at a preradiologic and preclinical stage (see Chapters 20 to 25). In contrast, the presence of solely A-lines (artifacts representing reflections of the pleural line) in hemodynamic terms reflects a “dry lung” or normal profile. The latter has been used to underpin cases of redistributive shock (e.g., septic shock) in the FALLS protocol (fluid administration limited by lung sonography).¹¹ However, one of the main diagnostic difficulties is that septic patients in the intensive care unit (ICU), who usually require fluid therapy, may well have a B-line profile because of various factors (e.g., pulmonary infection, acute respiratory distress syndrome, mixed type of pulmonary edema in which a cardiac component is integrated as well). Therefore, suggestions were made to incorporate Doppler and tissue Doppler echocardiographic indices (e.g., mitral flow E/E ratio) as measures of LV filling pressure in an effort to further clarify lung ultrasound-derived hemodynamic profiles.¹¹ Further analysis of this perspective is beyond the scope of this chapter.

Analysis of the sonographically detected respiratory variations in SVC and IVC size and diameter is a dynamic method that can be used for hemodynamic ICU monitoring. The aforementioned variations may at least partially reflect RAP and therefore right ventricular filling pressure. In a spontaneously breathing patient, estimation of RAP is improved by M-mode evaluation of IVC diameter and response to a brief sniff. A small IVC (1.2 cm) with spontaneous collapse suggests hypovolemia. Normally, the IVC is less than 1.7 cm, and normal inspiratory collapse (≥50%) suggests normal RAP (0 to 5 mm Hg). A mildly dilated IVC (>1.7 cm) with normal inspiratory collapse suggests mildly elevated RAP (6 to 10 mm Hg). Inspiratory collapse of less than 50% suggests RAP of 10 to 15 mm Hg. A dilated IVC without inspiratory collapse suggests RAP higher than 15 mm Hg. Notably, more refined vena cava analysis algorithms have been implemented in mechanically ventilated patients (Chapters 39 and 40). In general, dynamic indices of cardiac preload (e.g., respiratory variations in Doppler-derived indices of aortic flow or vena cava analysis) and dynamic tests (e.g., the expiratory pause in mechanical ventilation or passive leg raising) are preferred over static indices for prediction of fluid responsiveness in the ICU.

The hola (holistic approach) ultrasound concept in hemodynamic monitoring

In terms of pathophysiology, two critical parameters may be used to optimize noninvasive hemodynamic monitoring in the ICU. The first refers to the ability to “pinpoint” the hemodynamic status of an individual patient as an exact spot on the Frank-Starling curve (and track the spot’s path on the curve) during various therapeutic interventions (e.g., fluid loading, diuresis, changes in body posture). In this case the interventions represent a dynamic element that can be used to detect changes in various ultrasound-derived parameters (e.g., B-lines on lung ultrasound or respiratory variations in aortic flow VTI). The Starling curve relates stroke volume to end-diastolic ventricular volume (EDV). EDV is determined by transmural pressure, which is the difference between LV intracavitary end-diastolic pressure and pericardial constraint. When determining where a patient is on the Starling curve, these two confounding pressures must always be considered in a critically ill patient. Should the patient move along the Starling curve toward more cardiac output, was it because transmural pressure increased, and if so, did LV end-diastolic intracavitary pressure increase or did pericardial constraint decrease? The major issue when implementing dynamic elements in the equation is timing. For example, it takes time to identify the possible effects of fluid loading or diuresis on various ultrasound-derived parameters. Moreover, dynamic maneuvers that are considered to have a rather more “acute” effect (e.g., passive leg raising or expiratory pause in mechanical ventilation) are subject to various limitations. Our group is testing the recently introduced thigh cuff technology (Braslet-M) as a dynamic maneuver because of the fact that most of its effect on central hemodynamics is almost immediate (Figure 36-4).¹² Ultrasound should be helpful in determining the effect of acute hypovolemia induced by cuffs. In the case of volume overload and poor diastolic filling (reduced LV transmural pressure in the presence of increased RAP and pulmonary edema), reduced RAP and improved pulmonary edema are seen with increased EDV. This effect is identical to what occurs with the administration of nitroglycerin except for the absence of a confounding drop in afterload. Furthermore, release of the cuffs should generate an opposite effect. This same pericardial-ventricular interaction can be seen with high pulmonary vascular resistance such as pulmonary embolism. If thigh cuffs acutely improve the cardiac indices and LV EDV seen on echocardiography and reduce septal shift, volume loading of this patient to improve LV EDV might not be the preferred therapy.¹³ Echocardiography provides real-time insight into the dynamic cardiac changes incurred by thigh cuff–induced fluid sequestration and subsequent release. Furthermore, other relatively load-independent parameters (e.g., Tei index) may be used to evaluate myocardial performance during the aforementioned dynamic bedside interventions.¹⁴ The real-time combination of invasive monitoring, ultrasound, and bedside interventions should be investigated further.

The second parameter obviously reflects pertinent changes in cardiovascular morphology. In this case, four-dimensional monitoring of ventricular volume would represent an ideal solution; however, this technology is not yet readily available. Alternative indices that may be appraised are end-systolic obliteration of the LV cavity or a small cavity (not necessarily with end-systolic obliteration); oscillation of the interatrial septum, which if exaggerated could reflect low atrial pressure; or indices of preload dependence if hypovolemia is not overt, including the effect of a dynamic element on LVOT VTI.

The multimodal (integrating lung ultrasound, vena cava analysis, and echocardiography) HOLA ultrasound concept could well operate on binary logistics such as guiding fluid resuscitation with the intention of avoiding alveolar edema (“wet lung”) and impaired gas exchange or optimizing diuretic therapy in patients with cardiogenic (or mixed-type) pulmonary edema. These and some additional ultrasound-derived static and dynamic components are being considered thoroughly by our team for integration into a theoretic model and a resultant straightforward algorithm that will, we hope, be presented in the second edition of this textbook.

Pearls and highlights

References