Assessment of Cardiac Filling and Blood Flow

Martin Geisen, Maurizio Cecconi and Andrew Rhodes

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.

Table 3.3

Hemodynamic Parameters—Adult

BP, blood pressure; CO, cardiac output; EF, ejection fraction; HR, heart rate; MAP, mean arterial pressure; MPAP, mean pulmonary artery pressure; PAOP, pulmonary artery occlusion pressure; RAP, right atrial pressure; SV, stroke volume; SVI, stroke volume index.

Table 3.4

Oxygenation Parameters—Adult

CI, cardiac index; CO, cardiac output; Hb, hemoglobin.

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).

Figure 3.1 Graph demonstrating the Frank-Starling principle: The effect of preload on stroke volume in three different myocardial contractility states. LVEDV, left ventricular end diastolic volume; SV, stroke volume.

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

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

Stroke Volume Variation

During mechanical ventilation each positive-pressure breath induces a decrease in venous return. In conditions of decreased volume status, when the right ventricle is responsive to an increase in preload, a reduction in right ventricular outflow will occur and result in a decrease of left ventricular preload after the number of cardiac cycles it takes to pump blood through the lung (pulmonary transit time). If the left ventricle is preload responsive as well, a transient decrease in stroke volume will occur. This cyclic variation in stroke volume (stroke volume variation, SVV) can indicate volume responsiveness if it reaches a certain degree and may describe the response to a volume challenge in relation to changes in cardiac output.17–21

Pulse Pressure Variation

SVV, PPV, and systolic pressure variation (SPV) are automatically calculated by an array of cardiac output monitors.

Plethysmographic Variability Index

The pulse oximeter plethysmographic waveform has been shown to display respiratory variations during mechanical ventilation, which can be predictive of volume responsiveness. Calculation of the plethysmographic variability index (PVI) is performed by measuring changes of the perfusion index (PI = pulsatile infrared signal/nonpulsatile infrared signal × 100) over at least one respiratory cycle.25–27

Indices Derived by Echocardiography

Finally, respiratory variations of the inferior vena cava diameter as measured by transthoracic echocardiography (TTE) or the superior vena cava (SVC) diameter as measured by transesophageal echocardiography (TEE) have been shown to accurately predict volume responsiveness.28,29

It is important to note that these variables are reliable only during controlled mechanical ventilation. Other conditions in which the use of these parameters cannot be advised are as follows:

• Cardiac arrhythmias

• Application of low tidal volumes (i.e., <8 mL/kg)

• Open chest conditions

• Right ventricular failure

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:

• Circulating catecholamines

• Drugs (inotropes, digoxin, calcium solutions)

• Metabolic state (i.e., hyperthermia)

• Sympathetic nervous system activity

• Increased heart rate

The following factors reduce myocardial contractility:

• Hypoxia or hypercapnia

• Metabolic state (acidosis, hypothermia, hyperkalemia, hypocalcemia)

• Drugs (e.g., β-adrenergic receptor antagonists, digoxin)

• Acute and chronic cardiomyopathies

• Parasympathetic nervous system activation

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:

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:

• Anatomic obstruction (e.g., aortic valve stenosis, subvalvular obstruction)

• Raised systemic vascular resistance (SVR)

• Decreased elasticity of the aorta and great vessels

• Increased ventricular volume

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

• Anatomic obstruction (e.g., pulmonary valve stenosis)

• Raised pulmonary vascular resistance (PVR) (e.g., pulmonary hypertension, pulmonary embolism, hypoxia, and hypercarbia)

• Increased ventricular volume

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:

• Flow component—frictional opposition to blood flow through the vessels, with blood viscosity being the major determinant: Vascular resistance increases with an increase in viscosity.

• Frequency-dependent or “reactive” component—related to the compliance of the vessel walls and the inertia of the ejected blood. A low vascular compliance increases vascular resistance.

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

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

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

SVR is calculated as follows:

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:

• Vessel diameter: According to the law of Hagen-Poiseuille resistance is inversely related to the fourth power of the radius. This means that a decrease in vessel diameter during vasoconstriction will result in a significant increase in SVR. Vasodilation decreases SVR.

• Compliance of the systemic circulation

• Blood viscosity and hematocrit

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:

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: