Assessment of Cardiac Filling and Blood Flow

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Assessment of Cardiac Filling and Blood Flow

The accurate assessment and manipulation of the circulation are important parts of the management of critically ill patients. The principal objective of cardiorespiratory manipulation is to ensure optimal oxygen delivery. Adequate cellular respiration, adequate delivery of substrates and pharmaceuticals, and eventual recovery of organs and tissues are possible only when this has been achieved. This chapter deals with the physiologic principles governing the cardiovascular system and discusses interpretation of hemodynamic data in a clinical context. With the increasing number of medical devices available to monitor the circulation, this chapter also outlines the principles underlying the design and function of these devices, as well as their uses and limitations (Tables 3.1 to 3.4).

Table 3.1

Primary Measured Hemodynamic Data

Parameter/Formula Normal Range
Arterial blood pressure (BP)  
 Systolic (SBP) 90-140 mm Hg
 Diastolic (DBP) 60-90 mm Hg
Mean arterial pressure (MAP):
[SBP + (2 × DBP)]/3		 70-105 mm Hg
Right atrial pressure (RAP) 2-6 mm Hg
Right ventricular pressure (RVP)  
 Systolic (RVSP) 15-25 mm Hg
 Diastolic (RVDP) 0-8 mm Hg
Pulmonary artery pressure (PAP)  
 Systolic (PASP) 15-25 mm Hg
 Diastolic (PADP) 8-15 mm Hg
Mean pulmonary artery pressure (MPAP):
[PASP + (2 × PADP)]/3		 10-20 mm Hg
Pulmonary artery occlusion pressure (PAOP) 6-12 mm Hg
Left atrial pressure (LAP) 6-12 mm Hg
Cardiac output (CO):
HR × SV/1000		 4.0-8.0 L/min

HR, heart rate; SV, stroke volume.

Table 3.2

Derived Hemodynamic Data

Derived Parameter/Formula Normal Range
Cardiac index (CI):
CO/BSA		 2.5-4.0 L/min/m2
Stroke volume (SV):
CO/HR × 1000		 60-100 mL/beat
Stroke volume index (SVI):
CI/HR × 1000		 33-47 mL/m2/beat
Systemic vascular resistance (SVR):
80 × (MAP − RAP)/CO		 1000-1500 dyn⋅s/cm5
Systemic vascular resistance index (SVRI):
80 × (MAP − RAP)/CI		 1970-2390 dyn⋅s/cm5/m2
Pulmonary vascular resistance (PVR):
80 × (MPAP − PAOP)/CO		 <250 dyn⋅s/cm5
Pulmonary vascular resistance index (PVRI):
80 × (MPAP − PAOP)/CI		 255-285 dyn⋅s/cm5/m2

BSA, body surface area; CO, cardiac output; HR, heart rate; MAP, mean arterial pressure; MPAP, mean pulmonary artery pressure; RAP, right atrial pressure; PAOP, pulmonary artery occlusion pressure.

Cardiac Filling

One of the fundamental concepts of hemodynamic optimization of the critically ill patient is the manipulation of cardiac output as a main determinant of blood flow and oxygen delivery. Cardiac output is defined as the product of stroke volume (SV) and heart rate (HR). Although options to control heart rate are limited, clinical studies investigating hemodynamic optimization protocols have been largely focused on interventions to increase stroke volume. The stroke volume of the heart is determined by the complex interaction of three components: preload, contractility, and afterload. A thorough understanding of the physiology and pathophysiologic principles that define these components is essential for the clinician to successfully control and improve cardiovascular dynamics.

Our current understanding of the relationship between preload and contractility and their effect on stroke volume is based on the experiments of Dario Maestrini, Otto Frank, and Ernest Starling. Culminating in Starling’s “law of the heart,” which states that the force of myocardial contraction is directly proportional to the end-diastolic myocardial fiber length (or “preload”), as determined by the ventricular end-diastolic volume (EDV).1,2 It is this relationship, commonly known as the Frank-Starling mechanism that matches venous return to cardiac output (Fig. 3.1).

The most common intervention used by clinicians to improve stroke volume—the administration of fluids—is aimed at increasing venous return as a main determinant of EDV. In this regard two factors are important to consider: the position of an individual heart on the Frank-Starling curve and the expected response to fluid administration, as well as giving the right amount of fluid in order to achieve a hemodynamic response. The dynamics of venous return have been extensively described by Arthur Guyton, whose theories contribute to our current understanding of the circulation and may help to optimize venous return.3,4

Preload

Based on Ernest Starling’s observations, preload is defined as the tension developed by the stretch of the myocardial fibers: An increase in venous return leads to an increase in EDV which in turn increases myocardial sarcomere length, resulting in an increase of contractility and a rise in stroke volume and cardiac output. Conversely, a decrease in venous return will reduce EDV, resulting in a decreased stroke volume and cardiac output. This mechanism matches the mechanical activity of both ventricles under changing physiologic conditions and functions independent of nervous supply.

Preload is determined by the following factors:

• Circulating blood volume

• Venous capacitance (i.e., sympathetic stimulation resulting in venoconstriction, mechanical compression)

• Posture: The Trendelenburg position (supine, head down) increases venous return. Clinically, a passive leg raise test may be performed to assess volume responsiveness by autotransfusion of approximately 300 mL of blood from the splanchnic and lower limb compartments to the central circulation, increasing preload.

• Intracavitary pressures: Abdominal hypertension and increased intrathoracic pressures (i.e., during positive-pressure ventilation and application of positive end-expiratory pressure [PEEP]) can oppose venous return.

• Ventricular compliance: Ventricular compliance determines the relationship between EDV and end-diastolic pressure (i.e., diastolic dysfunction or impaired relaxation as in ventricular hypertrophy).

• Heart rate: The filling time influences EDV.

• Atrial contraction: Atrial contraction contributes to EDV and may be impaired (i.e., in atrial fibrillation).

Indicators of Preload

In vivo measurement of sarcomere length is not possible. To assess this variable in the clinical setting, ventricular end-diastolic pressures have been traditionally used as surrogate parameters to estimate EDV. Although EDV can be assessed by echocardiography, continuous monitoring of this parameter is currently not possible. Static indices of preload include traditional parameters assessing filling pressures or volumes as well as parameters derived from recently introduced techniques based on thermodilution (see later), which have been classified as volumetric indices of preload. Recently, parameters based on the cyclic changes in intrathoracic pressure during mechanical ventilation have been introduced as estimates of preload responsiveness under certain circumstances, although they do not measure preload per se. These dynamic indices of preload can play a role in predicting an increase of stroke volume after an increase of preload, or in other words, the “fluid responsiveness” of the ventricle.

Static Indicators of Preload

These parameters give an estimate of preload, but their ability to predict a response to fluid administration is limited. Static preload indices have been defined for both sides of the heart:

Static indices of the left side of the heart:

Static indices of the right side of the heart:

It is generally postulated that EDVs correspond to myocardial sarcomere length just prior to ventricular contraction and that end-diastolic pressures correspond with EDVs.

For the left side of the heart these relationships are as follows:

image

For the right side of the heart these relationships are as follows:

image

It is important to note that these assumptions do not hold true in most clinical conditions and all parameters are influenced by physiologic and technologic factors. Ventricular pressures and volumes both are influenced by ventricular compliance, so there is only a poor relationship between the two, and the traditional assumption that CVP, RAP, PAOP, and LAP estimate LVEDP as an indicator of LVEDV has to be questioned. PAOP reflects left ventricular function only if the vascular system between the catheter tip and the left ventricle is free from any pathologic condition that could influence the pressures detected by the catheter.

PAOP overestimates LVEDP in the following conditions:

PAOP underestimates LVEDP in the following conditions:

PAOP readings are accurate only if the tip of the pulmonary artery catheter (PAC) is appropriately wedged in West lung zone 3, corresponding to the lower third of the lung where continuous blood flow can be assumed.

The PAOP does not predict preload and bears little or no relationship to the subsequent response to a volume challenge. It is important to realize, however, that pressure is one of the driving forces responsible for edema formation in the lungs. In this regard, the PAOP may function as more of a safety limit rather than as a guide to therapy.5–7

The CVP reflects RAP and has been traditionally used as a marker of right ventricular preload and, assuming a relationship between CVP, RVEDP, and RVEDV, of left ventricular preload. However, CVP does not accurately reflect left ventricular preload and has been shown to correlate poorly with blood volume.5–7 The main clinical value of measuring CVP is to provide information about the right side of the heart, as in cases of right ventricular failure or in assessing the right ventricular response to pulmonary hypertension. A low CVP in the setting of clinical signs of tissue hypoperfusion may be predictive of a benefit from fluid administration, and a rapid significant rise of CVP during a fluid challenge may indicate that the heart is not fluid responsive.8–12

Volumetric Indicators of Preload

Based on cardiac output measurements using thermodilution and incorporating indicator passage times, volumetric preload parameters have been introduced as an alternative to conventional “static” parameters and have become available with thermodilution-based monitoring techniques such as the PAC, pulse contour continuous cardiac output (PiCCO), and EV1000 systems. The continuous end-diastolic volume index (CEDVI), derived from a modified PAC is a surrogate of RVEDV. Global end-diastolic volume index (GEDVI), intrathoracic blood volume index (ITBVI), and extravascular lung water index (EVLWI) are parameters provided by devices that require transpulmonary thermodilution for the measurement of cardiac output based on pulse pressure analysis (i.e., PiCCO and EV1000 systems, see later). GEDVI represents the total intracardiac volume, and the volume of the descending aorta has been shown to be a better indicator of preload than CVP.13,14

Dynamic Indicators of Preload (or Preload Responsiveness)

Based on the study of heart-lung-interactions a number of so-called dynamic preload indicators have been introduced. Although these parameters are not measures of preload per se, they play an important role in the prediction of the hemodynamic response (i.e., by an increased cardiac output) to an increase in preload (preload or “volume” responsiveness). Generally, these parameters are based on the observation that transient changes in preload occur during mechanical ventilation.15,16

Contractility

Ventricular contractility, or inotropy, describes the strength of ventricular contraction. It is defined as the tension developed by myocardial fibers at a given preload and afterload and the velocity of the shortening of the myocardial sarcomeres. It represents the intrinsic ability of the myocardium to generate a force independent of filamental stretch or ventricular loading conditions. Contractility is influenced by the following factors:

Factors that increase myocardial contractility:

The following factors reduce myocardial contractility:

Contractility is difficult to assess in the clinical setting. The temporal rate of change of ventricular pressure (dP/dt) and its maximum value (peak dP/dt) can be derived invasively (i.e., in the cardiac catheterization laboratory) or estimated less invasively with varying accuracy by echocardiography and some cardiac output monitoring devices. This parameter has been shown to be related to ventricular function in clinical studies. Echocardiography provides additional functional assessment of ventricular wall motion and blood velocity kinetics. Parameters such as the fractional area change (FAC) and ejection fraction (EF) are no accurate measures of contractility but are related to the contractile state of the myocardium and can be used to guide therapy.

Afterload

The afterload of the heart may be considered as the ventricular wall tension required to eject the stroke volume during systole. According to the law of LaPlace, afterload relates to the stress within the wall of the ventricle developing during systolic ejection:

image

where T = tension, P = intraventricular pressure, and r = intraventricular radius. In this equation afterload is mainly dependent on wall thickness and ventricular radius. At a given pressure, an increase in ventricular radius (i.e., dilatation of the ventricle) will increase afterload. An increase in wall thickness (i.e., ventricular hypertrophy) will reduce afterload.

Afterload for the left ventricle is increased by the following factors:

Afterload for the right ventricle is increased by the following factors:

The Anrep effect describes an intrinsic regulatory mechanism of the heart in response to an acute increase in afterload, which results in an initial reduction in stroke volume followed by an increase in EDV, which restores the stroke volume toward near-normal values.

Indicators of Afterload

SVR and PVR are the most commonly used indicators of afterload in the clinical setting for the left and right ventricle, respectively. Vascular resistance can be described as the mechanical property of the vascular system opposing flow of blood into a vascular bed. There are two main components of vascular resistance:

SVR and PVR cannot be measured directly and thus are calculated from Ohm’s law:

image

where V = voltage, I = current, and R = resistance. Applied to cardiovascular physiology this principle looks as follows:

image

in which ΔP is the pressure gradient, CO (cardiac output) is “flow,” and R is the resistance.

SVR is calculated as follows:

image

where MAP = mean arterial pressure (mm Hg), RAP = right atrial pressure (mm Hg), and CO = cardiac output. To convert from mm Hg to dyne × second/cm5 the multiplication by 80 is necessary. Normal values for SVR range from 800 to 1200 dyne × second/cm5. If standardized to body surface area, SVR is quoted as SVRI (SVR index) with normal values for SVRI ranging from 1900 to 2400 dyne × second/cm5/m2.

The following factors affect SVR:

In the same way as SVR, PVR may be calculated using the pressure differential across the pulmonary vasculature, between the mean pulmonary artery pressure (MPAP) and PAOP:

image

Values for PVR are normally below 250 dyne × second/cm5. Again, PVR is often quoted as the PVR index or PVRI with a normal range between 255 to 285 dyne × second/cm5/m2.

The following factors affect PVR:

Clinical Limitations of Systemic Vascular Resistance and Pulmonary Vascular Resistance

Although the concept of vascular resistance permits an intuitive understanding of the circulation, a number of limitations make it unreasonable to use SVR and PVR to guide therapy. First, because SVR and PVR are derived variables, errors inherent in the measurement of their components (i.e., filling pressures) are multiplied, making the derived number less accurate. Further, these calculations assume a linear relation between pressure and flow, which does not exist in vivo (Fig. 3.2). It is therefore wise to use these parameters with caution and consider their limitations in clinical practice.

Clinical Interpretation of Indicators of Preload

It has already been stressed that accurate assessment of the preload status of the heart is important because it may allow for the application of interventions resulting in an improvement of cardiovascular dynamics. However, without knowing whether the heart will actually respond to an increase of a certain status of volume or preload, this information is only of limited value. This concept—the individual response of cardiac output to a volume challenge—has become known as volume responsiveness.30 Intravascular volume expansion is often the initial intervention in patients with circulatory failure. However, only approximately 50% of patients given a fluid challenge will respond by increasing cardiac output. The ability to distinguish fluid-responsive patients from nonresponders is important to avoid inappropriate and potentially harmful fluid challenges in situations in which other interventions (i.e., inotropes or vasopressors) should be preferentially used. Consequences of inappropriate fluid therapy include pulmonary edema, deterioration in gas exchange, and cardiac failure.

There are currently a number of parameters available with different monitoring modalities that can be used as estimates of preload and may predict volume responsiveness under defined conditions.

Static Indicators of Preload

Conventional static markers of cardiac preload, such as CVP and PAOP, are poor predictors of fluid responsiveness. CVP and PAOP reflect intracavitary pressures that frequently show poor correlation with transmural pressures, which are actually related to EDV through chamber compliance. Therefore, EDV is overestimated (i.e., under the application of PEEP) or underestimated (i.e., in concentric left ventricular hypertrophy) in many clinical situations. Furthermore, static parameters do not determine the position of the heart on the “individual” Frank-Starling curve as contractile function is not taken into the account. A patient may fail to respond to a fluid challenge because of ventricular dysfunction or poor ventricular compliance (see Fig. 3.1

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