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Cardiologyc clinics - clinical assessment by anatomicpathophysiologic correlates, cardiac anatomy, mechanical function, and hemodynamics, hemodynamic evaluation of cardinal clinical syndromes

AnatomicPathophysiologic A p p ro a c h t o Hemodynamics: C o m p l e m e n t a r y Ro l e s of Noninvasive and Invasive Diagnostic Modalities
James A. Goldstein, MD*, Amr Abbas, MD
 Hemodynamics  Invasive diagnostic modalities  Noninvasive diagnostic modalities  Cardiovascular system

Symptoms and physical signs reflect distinct pathophysiologic derangements of anatomic components and mechanics, a construct that serves as the foundation for clinical evaluation of the cardiovascular system.1–10 Evaluation of hemodynamic derangements should be based on interrogation of a cardiac anatomic-physiologic approach to circulatory pathophysiology. This article illustrates a pragmatic problem-solving approach to 3 cardinal hemodynamic symptoms and clinical syndromes: (1) right heart failure (RHF), (2) dyspnea, and (3) low-output hypotension. This treatise focuses primarily on the complementary roles of noninvasive and invasive diagnostic studies in clinical hemodynamic assessment. The anatomicpathophysiologic foundations of this approach based on bedside physical examination have been previously published.1–6

The cardiovascular system can be simplistically viewed as a closed fluid system that obeys the

Division of Cardiovascular Medicine, William Beaumont Hospital, Royal Oak, MI, USA * Corresponding author. E-mail address: Cardiol Clin 29 (2011) 173–190 doi:10.1016/j.ccl.2011.01.004 0733-8651/11/$ – see front matter Ó 2011 Elsevier Inc. All rights reserved.

rules of hydraulics and physics. Cardiovascular hemodynamic syndromes reflect derangements of cardiac anatomy and physiologyand may manifest as either forward or backward syndromes. Forward syndromes may be grouped as hypoperfusion syndromes, manifesting early as fatigue and later as organ failure attributable to inadequate cardiac output (CO); similarly, syncope results from transient profound hypoperfusion. Backward syndromes attributable to right heart dysfunction manifest as systemic venous congestion syndromes, including peripheral edema, gastrointestinal-hepatic congestion, and ascites, whereas left heart dysfunction results in pulmonary venous congestion manifest as shortness of breath (dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea). These symptom groups in isolation are nonspecific. Identical complaints reflecting disparate pathophysiologic processes can occur because of a variety of mechanisms. For example, dyspnea is an expected symptomatic manifestation of pulmonary venous hypertension attributable to a spectrum of left heart derangements, the


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underlying mechanisms of which vary greatly (eg, mitral stenosis, mitral regurgitation [MR], left ventricular [LV] cardiomyopathy). The treatments and prognoses also vary greatly. Dyspnea is also commonly of pulmonary origin, with circumstances in which the heart may be completely normal or affected only as an innocent bystander (eg, cor pulmonale). Similarly, peripheral edema and ascites reflect systemic venous congestion resulting from a spectrum of RHF mechanisms (eg, tricuspid valve [TV] disease, right ventricular [RV] cardiomyopathies, pericardial disorders). However, edema may also develop under conditions with normal systemic venous pressures, as may occur in patients with cirrhotic liver disease, inferior vena cavalcompression, and so forth. Thus, for cardiovascular assessment symptoms and signs must be characterized according to the underlying anatomic-pathophysiologic mechanisms, the next step to delineation of the specific cause. This approach can be applied to individual organ beds, such as the lung: D pulmonary blood pressure 5 CO A pulmonary vascular resistance (PVR). Alternatively, from a perfusion perspective, the equation is transformed, whereby: CO 5 Dpressure/vascular resistance The key components of blood pressure can be further considered. Thus, CO 5 heart rate (HR) A stroke volume (SV). SV is a function of 3 cardiac mechanisms: preload, afterload, and contractility. SVR is determined by total blood volume and vascular tone (a function of intrinsic vessel contraction or relaxation interacting with systemic and local neurohormonal influences, metabolic factors, and other vasomotor mediators, and so forth).

To establish an anatomic-pathophysiologic differential diagnosis, it is essential to first consider the anatomic cardiac components (myocardium, valves, arteries, pericardium, and conduction tissue) that may be involved, and then focus on the fundamental mechanisms that affect each anatomic component, asking how such anatomicpathophysiologic derangements and hemodynamic perturbations are reflected in the symptoms, physical signs, and invasive waveforms. The purpose of the cardiovascular system is to generate CO to perfuse the body. However, although perfusion is the bottom line of the heart, the circulation is also a pressure-based system, with organ perfusion determined by arterial driving pressure modulated by vascular bed resistance. The regulation of thecirculation (pressure and flow) can be understood by the application of Ohm’s law. In classical physics applied to an electrical circuit, Ohm’s law states: DV 5 I A R where DV is the driving voltage potential difference across the circuit, I is the current flow, and R is the circuit resistance. Circuit output or current flow thus is a function of the driving voltage divided by circuit resistance or I 5 DV/R. Ohm’s law principles applied to the circulation are the foundation of hemodynamics, whereby: D pressure 5 CO A systemic vascular resistance (SVR)

The hemodynamic evaluation of the circulation may be considered as 2 sides of a single coin of cardiac function: systolic function, the ability of the heart to pump and perfuse; and diastolic performance, the ability of the chambers to fill at physiologic pressures with the preload necessary to generate SV.

Systolic Performance
Systolic function reflects the ability of the ventricle to contract and generate stroke work, a function determined by its loading conditions (both preload and afterload) and the contractile state. Systolic dysfunction then develops because of primary derangements of volume overload, pressure overload, or cardiomyopathic processes. It is important to distinguish depression of systolic performance caused by pressure/volume overload from primary contractile failure related to cardiomyopathy with damage to the contractile apparatus (eg, ischemic or nonischemic cardiomyopathies). Systolic dysfunction reduces SV, leading to low CO, resulting in fatigue and in most severe stages, organ hypoperfusion and hypotension.

Diastolic Function and Cardiac Compliance
Diastolic function is the ability of achamber to obtain its necessary preload at physiologic filling pressures. Functional preload is the amount of blood distending the cardiac chamber. This volume is reflected in filling pressure according

Anatomic-Pathophysiologic Approach to Hemodynamics
to individual chamber compliance. Compliance is a reflection of the relationship between diastolic pressure (DP) and volume in each individual cardiac chamber. There are 4 phases of diastole: isovolumic relaxation (IVRT), early filling, diastasis, and atrial contraction. In addition, because of the absence of valves between the pulmonary veins and the left atrium, diastolic motion during diastole has been shown to be limited during increased left atrial (LA) pressures and diastolic dysfunction. Under normal conditions, there is a defined IVRT, followed by mitral valve (MV) opening; most of the LV filling occurs in this early filling phase, through ventricular suction (lisotropic function); this is followed by equilibration of LA and ventricular pressures and temporary cessation of flow. Finally, there is atrial contraction, the booster pump function that atrial kick delivers additional ventricular preload; atrial booster pump function also optimizes ventricular filling at a lower mean atrial pressure, for the end-diastolic kick increases ventricular end DP as the atria actively relax (X descent), thereby facilitating ventricular-atrial pressure reversal, which closes the atrioventricular (AV) valves (atriogenic valve closure), minimizing the effects of ventricular DP on the back tributaries of filling (ie, the lungs). Measurement of intracardiac filling pressures (eg, pressure at end diastole) is used for 2 basic purposes: to determine (1) whether thereis increased pressure exerting adverse congestive effects and (2) whether preload is adequate to assist with appropriate forward ejection. With respect to assessing true preload, pressure is a convenient surrogate of chamber volume, which is exquisitely influenced by the compliance of the chamber being interrogated. Therefore, filling pressure reasonably reflects chamber volume and preload only if chamber compliance is normal. However, impaired compliance, attributable either to extrinsic influences such as pericardial disease or ventricular interaction, or intrinsic diastolic dysfunction associated with hypertrophy, infiltration or ischemia, or primary pressure and volume overload, influences compliance. In such cases pressure less accurately reflects true chamber volume. For example, LV preload may be markedly reduced but intracardiac pressures strikingly increased under conditions of cardiac tamponade or severe pulmonary hypertension (PHTN). Conversely, chronic volume overload lesion such as aortic regurgitation (AR) may result in dramatically increased chamber volumes, but when cardiac compensation is present, intracardiac pressures are relatively normal as chamber and pericardium dilate and become more compliant.


PERTINENT ASPECTS OF NORMAL PRESSURE WAVEFORMS Relationship of Cardiac Mechanics to Atrial Waveforms, Venous Flow Patterns, and Respiratory Physiology
An appreciation of atrial waveform hemodynamics, the physiology of the venous circulations, and the dynamic effects of intrathoracic pressure (ITP) and respiratory motion on cardiovascular physiology is critical. Analysis of the atrial waveforms yields insight into cardiac chamber and pericardial compliance. The atrial waveforms areconstituted by 2 positive waves (A and V peaks) and 2 collapsing waves (X and Y descents) (see section on normal pressure waveforms). The atrial A wave is generated by atrial systole after the P wave on electrocardiography (ECG). Atrial mechanics behave similarly to ventricular muscle. The strength of atrial contraction is reflected in the rapidity of the A wave upstroke and peak amplitude. The X descent follows the A wave and is generated by 2 events: the initial decline in pressure reflecting active atrial relaxation, with a latter descent component reflecting pericardial emptying during ventricular systole (also called systolic intrapericardial depressurization, a condition that is exaggerated when pericardial space is compromised). The X descent second component is affected by the pericardial space and changes when the ventricles are maximally emptied and therefore pericardial volume and intrapericardial pressure (IPP) are at their nadir. During ventricular systole, venous return results in atrial filling and pressure, which peaks with the V wave, the height of which reflects the atrial pressure-volume compliance characteristics. The subsequent diastolic Y descent represents atrial emptying and depressurization. The steepness of the Y descent is influenced by the volume and pressure in the atrium just before AV valve opening (height of the V wave) and resistance to atrial emptying (AV valve resistance and ventricularpericardial compliance). Venous return to both atria is inversely proportional to the instantaneous atrial pressure, which is itself dependent on atrial compliance. The lowest return occurs when each pressure is highest. Normal IPP is subatmospheric, nearly equal to intrapleural pressure, anddecreases during inspiration. IPP also tracks right atrial (RA) pressure and shows fluctuations that are associated with cardiac cycle. In general, the IPP increases when cardiac volume is increased and vice versa. Under physiologic conditions, venous return to both atria is biphasic, with a systolic peak determined by atrial relaxation (corresponding to the X descent


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of the atrial and jugular venous pressure [JVP] waveforms) and a diastolic peak determined by TV resistance and RV compliance (corresponding to the Y descent of the atrial and JVP waveforms). IPP both approximates and varies with pleural pressure. The inspiratory decrement in pleural pressure normally reduces pericardial, RA, RV, wedge, and systemic arterial pressures slightly. However, IPP decreases more than RA pressure (RAP), thereby augmenting right heart filling and output. Under physiologic conditions, respiratory oscillations exert profound and complex effects on cardiac filling and dynamics. However, the effects on the right and the left heart are disparate, because of differences in the anatomic relationships of the respective venous return systems to the intrapleural space. The left heart and its tributary pulmonary veins are entirely intrathoracic. In contrast, although both right heart chambers are intrathoracic, the tributary systemic venous system is extrapleural. Normally, inspirationinduced decrements in ITP are transmitted through the pericardium to the cardiac chambers. On the right heart, these decrements in ITP enhance the filling gradient from the extrathoracic systemic veins to the right atrium, thereby enhancing the caval-RA gradient and augmenting venous return flow by 50% to 60%, which increasesright heart filling and output. Because pleural pressure changes are evenly distributed to the left heart and pulmonary veins, the pressure gradient from the pulmonary veins to the left ventricle shows minimal change with respiration. Early diastolic transmitral filling pressure as well as LV filling are essentially unchanged throughout the respiratory cycle. However, left heart filling, SV, and aortic systolic pressure normally decrease with inspiration (up to 10–12 mm Hg), a phenomenon termed (normal) pulsus paradoxus or paradoxic pulse. By echo Doppler, normally during inspiration there is increased flow across the TV, with expiratory reversal of flow into the inferior vena cava (IVC) and hepatic veins. reflect diastolic properties, influenced by myriad factors both intrinsic to the chamber (eg, pressure overload hypertrophy, volume overload, ischemia, infiltration, inflammation), as well as extrinsic effects from the pericardium or contralateral ventricle through diastolic interactions.

The noninvasive approach to hemodynamic evaluation using echocardiography with Doppler is based on the same Ohm’s law principles, but derived from different parameters, because pressure, flow, and resistance are not directly measured. Instead, echocardiography Doppler interrogates velocity of flow, which is used as a reflection of either pressure or flow. Thus, the hemodynamic relationships are derived as follows: Flow 5 area A velocity Volume 5 area A time velocity integral (TVI) DP 5 4 A (velocity Because in the absence of a shunt or significant regurgitation, flow across cardiac valves is constant, it therefore follows that flowacross the aortic valve is the same as that across the LV outflow tract (LVOT). This concept is the basis of the continuity equation, the foundation of noninvasive flow assessment, whereby: Flow1 5 A1 A V1 5 Flow2 5 A2 A V2 Thus, echo Doppler, which directly measures area, velocity, and TVI, thereby provides correlates of pressure, flow, and resistance. For example, in aortic stenosis, an increase in resistance across the aortic valve results in an increase in DP between the LV and aorta by invasive measurement; conversely, by noninvasive continuous-wave Doppler, the decreased valve area is reflected by increased flow velocity across the valve. The echo Doppler correlates of right heart hemodynamics are based on delineation of right heart anatomy and measurement of flow patterns, thereby establishing the anatomic-pathophysiologic correlates underlying clinical RHF. Echo delineates RA size, as well as RV size and contractile function. Echo Doppler hemodynamic correlates include the following: A. RAP assessment, based on: IVC diameter and collapse with respiration: a dilated IVC as well as failure to collapse greater than 50% with inspiration (the sniff test) correlates with increased RAP.

Relationship of Cardiac Mechanics to Ventricular Waveforms
Invasive ventricular pressure waveforms reflect the effects of chamber preload, contractility, and afterload. The upstroke in RV or LV pressure (1dP/dT) is influenced by preload and contractility, but is a poor measure of either. Peak ventricular pressure reflects the ventricular afterload. Ventricular relaxation (ÀdP/dT) is an active energy-requiring process and reflects intrinsic aspects of myocardial contractility as the ventricle actively relaxes. Filling pressuresin the ventricles

Anatomic-Pathophysiologic Approach to Hemodynamics
Regional IVRT: an inverse relationship exists between regional IVRT as measured by tissue Doppler of the tricuspid annulus and RAP.
Ratio of the forward and reversed hepatic venous flow velocities: with increased RAP, there is more diastolic and less systolic forward hepatic venous flow with increased retrograde diastolic flow. B. RV systolic pressure (RVSP) analysis: as mentioned earlier, the pressure gradient between 2 chambers is derived from the peak velocity across these chambers. This measurement is obtained by applying the Bernoulli equation. For estimating the RVSP, the peak tricuspid regurgitation (TR) is used. In the presence of a ventricular septal defect (VSD), the peak velocity across the VSD is used. By adding the RAP, the RVSP may be estimated. RVSP can be estimated by 2 methods: Peak tricuspid regurgitation velocity (TRV) through (4 A V2) 1 estimated RAP Systolic blood pressure À 4 A (velocity across a VSD 1 RAP C. Pulmonary artery (PA) assessment: in the absence of pulmonic stenosis, RVSP is equal to PA systolic pressure (PASP). In addition, by applying the Bernoulli equation to the pulmonary regurgitation velocity (PRV), both peak (PRPRV) and end-diastolic (PREDV), we can derive estimates of the PA mean and DPs, respectively. PASP 5 4 A TRV2 1 RAP PADP 5 4 A PREDV 1 RAP PAMP 5 4 A PRPRV 1 RAP D. PVR: increased pulmonary pressure may result from either increased PVR or increased pulmonary blood flow. With increased PASPs, an increased peak velocity of the TR jet occurs, as mentioned earlier. In addition, with increased PVR, there is decreased blood flow across the pulmonic valve. This situation manifests as truncationof the Doppler wave emanating from the RV outflow tract (RVOT TVI) occurs. Because PVR is the ratio of pressure to flow, a noninvasive measure of PVR may be estimated by the equation described by Abbas and colleagues7–10: PVR 5 TRV/RVOT TVI A 10 techniques such as transesophageal echocardiography, cardiac computed tomography [CT], and magnetic resonance imaging [MRI]) directly delineate cardiac anatomy, mechanics, and pathologic conditions. These imaging tools thereby provide crucial insights regarding atrial and ventricular size, LV and RV contractile performance, and valvular architecture, as well as direct delineation of pathologic conditions afflicting the chambers, valves, and pericardium. These imaging data, combined with the hemodynamic insights derived both by noninvasive and invasive techniques, facilitate comprehensive anatomicpathophysiologic assessment of clinical hemodyamic syndromes.


Clinical hemodynamic assessment should be based on interrogation of cardiac anatomy correlated to pathophysiology. The primary goal is establishment of the pathophysiologic differential diagnosis, based on a synthesis of symptoms, history, physical examination, and integrated noninvasive and invasive assessments. To analyze each patient hemodynamically, it is essential to first consider each cardiac structure, enumerate the disease processes that may affect each structure, and then compile a differential diagnostic list of pathophysiologic syndromes that may manifest in symptoms. From a simple anatomic perspective, the components of the heart from outside in include the pericardium, myocardium, valves, coronary arteries, conduction system, andgreat vessels. Each of these structures may undergo various pathophysiologic alterations that result in a spectrum of specific hemodynamic derangements and subsequent symptoms related to those abnormalities.

Myocardial Abnormalities
There are 3 primary determinants of myocardial performance: preload, contractility, and afterload (in aggregate the determinants of SV). It therefore follows that all abnormalities of cardiac performance must be related to: (1) primary volume overload, attributable to valve regurgitation, shunts, or high-output states; (2) primary pressure overload caused by outflow obstruction or increased vascular (outflow) resistance; or (3) primary derangements of contractility as a result of ischemic or nonischemic causes. A dilated and depressed ventricle must result from either intrinsic cardiomyopathy, or decompensation attributable to primary volume or pressure overload. A dilated ventricle with intact contractility

Noninvasive Imaging of Cardiac Architecture and Mechanics
In addition to providing hemodynamic correlates, echocardiography (as well as other noninvasive


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may result from primary volume overload (valve leaks and shunts) or high-output states. As discussed earlier, diastolic dysfunction may be categorized as a result of intrinsic or extrinsic abnormalities. Intrinsic diastolic dysfunction may result from primary chamber volume overload (dilation and hypertrophy), pressure overload (hypertrophy and later dilation), or cardiomyopathic processes (eg, ischemic, infiltrative, inflammatory, fibrotic). Extrinsic factors leading to diastolic dysfunction include those mediated by pericardial restraint, septal-mediated ventricular interactions, orintrapleural influences. Diastolic dysfunction can occur with either preserved or depressed systolic function. Diastolic function is influenced by myriad factors including the intrinsic physical properties of the chamber (eg, thickness, ischemia, infiltration, fibrosis), as well as extrinsic factors, including septal-mediated ventricular interactions, pericardial pressure, intrapleural pressure. Diastolic dysfunction results in abnormal chamber compliance, the result of which is a stiff chamber that has a higher filling pressure for any given preload. Impaired compliance (ie, a stiff heart) leads to pulmonary and/or systemic venous congestion, depending on which side of the heart is involved. Severe diastolic dysfunction reduces filling and results in chamber preload deprivation, contributing to low CO. It is important to differentiate primary and secondary diastolic dysfunction. Primary diastolic dysfunction is designated as abnormal compliance with intact contractility (eg, with LV hypertrophy with normal ejection fraction). Primary diastolic dysfunction may cause pulmonary venous hypertension, resulting in symptoms and signs of congestive heart failure, and in the most extreme states limits maximal LV preload and impairs SV and CO despite normal contractility. Secondary diastolic dysfunction is that associated with ventricular systolic dysfunction. Impaired diastolic properties resulting from poor pumping performance lead to chamber dilatation, complicated by the primary myocardial insult (pressure overload, volume overload, or cardiomyopathy). downstream chamber and therefore reduce the preload or perfusion volume depending on the position of the valve in the downstream conduit. The effect of excess afterloadon the upstream chamber is hypertrophy and ultimately dilatation and pump failure, resulting in higher filling pressures and less forward flow. Obstructions limit preload and therefore maximal SV and CO (preload deprivation). Regurgitant valvular lesions result in primary volume overload of the chambers affected by the leak. In the case of semilunar valve regurgitation, the ventricle bears the predominant load. However, atrioventricular valve insufficiency affects not only the atria suffering the direct brunt of the regurgitant leak, but the ventricle itself, which must receive both the normal forward venous return as well as the excess recirculated volume. Regurgitant lesions result in chamber volume overload, predisposing to diastolic dysfunction; prolonged severe overload leads to systolic dysfunction. Even when ventricular performance is intact, regurgitant leaks may limit forward CO by compromising maximum effective forward stroke work.

Pericardial Abnormalities
Increased IPP exerts deleterious effects on cardiac compliance and filling. This situation is most commonly attributed to (1) primary pericardial disease (constriction or tamponade); or (2) abrupt chamber dilatation, as may occur with acute RV infarction. Regardless of the cause, increased pericardial resistance impairs chamber compliance, resulting in increased filling pressures. Abnormal cardiac compliance also limits ventricular filling with reduced preload, resulting in limited CO.

RHF results in systemic venous congestion manifest initially as peripheral edema. More advanced stages of RHF lead to bowel congestion, hepatomegaly (and cirrhosis), andascites. There are numerous cardiac conditions with disparate pathophysiologic mechanisms that manifest systemic venous congestion. Furthermore, edema and ascites often result from liver disease or peripheral venous derangements unrelated to the right heart. Accordingly, peripheral edema and ascites can be attributed to RHF only under conditions of increased systemic venous pressure (JVP), usually related to RA hypertension. Fig. 1 summarizes the anatomic-pathophysiologic approach to hemodynamic evaluation of RHF. RHF may also

Valvular Pathophysiology
Valvular heart disease can be simplified into 2 categories: obstructive (pressure overload) lesions or regurgitant (volume overload) lesions. Obstructive lesions exert dual adverse effects, imposing increased afterload on the upstream chamber, delivering flow through the narrowed orifice and limiting preload or blood flow into the downstream chamber; they also limit the outflow into the

Anatomic-Pathophysiologic Approach to Hemodynamics


Fig. 1. Anatomic-pathophysiologic approach to RHF.

lead to reduced CO as a consequence of severe RV systolic dysfunction or increased RV afterload.

Increased JVP Without RV Enlargement
If the JVP is increased, the key to differential diagnosis is the presence of RV enlargement (indicated by physical examination by an RV heave [or lift] along the left sternal border, and easily delineated by echo documentation). Superior vena cava obstruction If the JVP is increased and the RV is not enlarged, then moving along the anatomic route from the distended neck veins toward the heart, the first possibility is superior vena cava (SVC) obstruction, characterized by increased mean pressure but an overall blunted waveform,particularly the Y descent which reflects poor flow from the great veins through the obstructed SVC, which also results in blunted respiratory oscillations. A pressure gradient between the cavae and right atrium confirms obstruction (eg, mass), in which case the preobstructive central venous pressure is increased, whereas pressure distal to the obstruction more closely reflects a normal RAP. Even

a small gradient across the obstructive mass can produce significant clinical problems. Noninvasive imaging studies, chest radiography (CXR), and especially CT and MRI, are typically sufficient and definitive, revealing the obstructive mass, and echo Doppler documents both the mass and impaired SVC venous return patterns. RA hypertension Excluding SVC obstruction, increased JVP directly reflects RA hypertension. Entities resulting in RAP increase without RV enlargement may result from RA space-occupying lesions (tumor masses, thrombi, and vegetations), in which the JVP pressure has a blunted waveform, especially the Y descent, reflecting poor transit of blood through the obstructive mass, and blunted inspiratory augmentation of right heart filling possibly with an associated Kussmaul sign. Noninvasive assessment with echocardiography should be sufficient and definitive in delineation of such atrial masses and their pathophysiologic effects. TV obstruction RAP increase without RV enlargement may be caused by TV obstruction (eg, rheumatic heart


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disease, carcinoid), which results in increased mean RAP with a prominent A wave/X descent reflecting augmented atrial contraction boosting flow through the obstructed orifice. The sharp X descent reflects accelerated atrial relaxation coincidentwith augmented atrial contraction. The blunted Y descent reflects poor inflow, resulting in impaired emptying of the RA. Imaging modalities can delineate the nature of TV stenosis and obstruction. In addition, the gradient across the TV, and hence the velocity, increases by Doppler. Primary RV diastolic dysfunction RAP increase without RV enlargement may result from RV diastolic dysfunction (without RV dilation or systolic dysfunction, which would result in enlarged RV, as discussed later). RV diastolic dysfunction may be related to intrinsic disease (hypertrophy, ischemia, restrictive, or other cardiomyopathies) or extrinsic effects as a result of pericardial disease. Regardless of the cause, RV diastolic dysfunction imposes increased afterload on the RA, resulting in augmented A wave/X descent, reflecting enhanced atrial contraction/ relaxation attributable to increased outflow resistance into the noncompliant RV; the Y descent is blunted as a result of impaired RV filling. The RV pressure trace reveals increased filling pressure often with a steep increase to an increased end DP, which may inscribe a dip-and-plateau configuration (the square root sign), reflecting a stiff chamber. Restrictive cardiomyopathy (RCM) deserves special consideration, because the clinical syndrome is pathophysiologically and hemodynamically similar to and often indistinguishable from pericardial constriction. RCM, attributable to infiltrative diseases (eg, amyloid), radiation, and other inflammatory insults, results in increased RAP with a waveform characterized by an M shape with blunted components as a result of impaired atrial contraction and delayed RV inflow. DPs are increased and equalized throughout the cardiac chambers,there is RV dip and plateau, which indicates increased RV stiffness and mean RAP with inspiration (Kussmaul sign), a manifestation of inspiratory augmentation of venous return into the stiff right heart, which cannot appropriately accommodate enhanced preload. With impaired RV diastolic function, changes in the tricuspid inflow pattern suggestive of and similar to those of the MV occur (ie, impaired relaxation, pseudonormal, and restrictive). Impaired RV diastolic function is also reflected in increased RAP manifested as increased IVC diameter, decreased IVC collapse with inspiration, and increased diastolic reversal into the hepatic venous flow pattern. Pericardial disease RAP increase without RV enlargement may result from pericardial perturbations. In cardiac tamponade, the magnitude of JVP increase directly reflects increased RAP and IPP. The waveform is characterized by a prominent A wave and a sharp X descent reflecting enhanced atrial contraction into the RV made stiff by pericardial fluid. The Y descent is blunted, reflecting pandiastolic resistance to RV filling. In tamponade, inspiratory augmentation of venous return to the compressed right heart is intact. The resulting inspiratory competition between the ventricles for preload within the crowded pericardium is responsible for pulsus paradoxus, the magnitude of which reflects the severity of tamponade. Echo Doppler is the gold standard for diagnosis, documenting anatomic fluid including not only the size of effusion but also its effects on cardiac preload evident as RA and RV diastolic collapse. Hemodynamically significant effusions are indicated by enhanced respiratory variation in atrioventricular vale flows, with inspiration leading to an increasegreater than 25% in TV flow but concomitant decrement in MV flow (the Doppler equivalent of pulsus paradoxus). In constrictive pericarditis (CP), increased pericardial resistance more tightly couples the 2 ventricles and increases their interdependence. Pericardial constraint limits total cardiac volume; consequently an increase in filling on 1 side of the heart impedes contralateral filling through intensified septal-mediated interactions. However, in constriction, the heart is isolated from the lungs, resulting in lack of transmission of ITP changes to the encased cardiac chambers. Therefore, in contrast to cardiac tamponade, in which ITP is transmitted through the pericardium and inspiratory augmentation of venous return and right heart filling are intact, in CP, the inelastic fibrocalcific pericardial shell isolates the heart from the lungs, and therefore respiratory changes in ITPs are not fully transmitted to the cardiac chambers. Thus, constriction results in dissociation of respiratory effects on intrathoracic and intracardiac pressures, thereby inducing dynamic respiratory changes in diastolic ventricular filling and flow patterns and ventricular systolic pressures. However, the effects on right and left heart filling and pressures are disparate, because of differences in the anatomic-physiologic relationships of their respective venous return systems to ITP oscillations. On the right heart, the SVC and IVC are intrathoracic and the right atrium and ventricle completely intrapericardial. The constrictive pericardial shell neither fully facilitates inspiratory augmentation of right heart filling, nor accommodates whatever meager increments in filling occur.

Anatomic-Pathophysiologic Approach toHemodynamics
Instead, the inspiratory gradient created between the extrathoracic systemic veins and intrathoracic but extrapericardial cavae, together with increased intraabdominal pressure associated with deep inspiration, augment venous return to the thoracic cage under conditions in which inspiratory augmentation of right heart filling is impeded by the constricted pericardium. The result is an inspiratory increase in JVP and right heart filling pressure (Kussmaul sign, the hemodynamic obverse of a paradoxic pulse). Anatomic-pathophysiologic relationships in the left heart are different. The pulmonary veins are entirely intrathoracic, the left atrium is not fully encased within the pericardium, because of the pericardial reflection around the pulmonary veins, and the left ventricle is fully within the constricted pericardium. Therefore, in constriction there is an inspiratory decrement in pulmonary venous pressure, which is not transmitted to the LV, resulting in reduced transmitral pressure gradient and flow velocity during inspiration. Because the cardiac volume is relatively fixed in CP, there is a reciprocal relation between left and right heart filling as a result of tight ventricular coupling. Therefore, the inspiratory decrease in LV filling allows a small relative increase in tricuspid inflow and RV filling. These disparate effects on ventricular filling lead to opposite directional changes in ventricular systolic pressures, with inspiration inducing an increase in RV but decrease in LV systolic pressure. This phenomenon, called ventricular discordance, indicates enhanced ventricular interaction and may be the most reliable hemodynamic indicator of constriction. As expected, the opposite changes occurduring expiration, with increased left heart filling and reduced right heart filling, which decreases tricuspid inflow velocity and leads to diastolic hepatic venous flow reversals. In CP, the JVP is increased with augmented atrial contraction and relaxation reflected in prominent A wave and X descent. However, in CP, in contrast to tamponade, the first third of diastole is resistance free and thus the RA waveform manifests an augmented A wave and X descent, but a prominent Y descent, reflecting a pattern of late pericardial resistance. The initial third of diastole is resistance free followed by resistance to filling with a pressure plateau, inscribing an RV waveform dip and plateau, together with increased and equalized diastolic filling pressures. Echo Doppler offers important insights into RCM versus constriction, based on assessment of LV thickness and architecture (eg, cardiac amyloid in which echo anatomic data reveal diffuse thickening and hyperrefractile myocardium), as well as flows, including mitral inflow velocity, mitral annular velocity, and hepatic venous flow. With restriction, there is increased velocity across the MV, reflecting increased LA pressure. Similarly, there is decreased mitral annular velocity. The E/E0 ratio increases. Because the restrictive pathology affects the walls of both ventricles as well as the septum, variations in ventricular filling cannot be accommodated by septal shift. Thus, there is no ventricular interdependence. With inspiration, there is increased venous return, which in the setting of a stiff RV and increased RAP leads to inspiratory reversal of hepatic venous flow. Conversely, in constriction, the free walls are affected with the pericardial pathology, butnot the septum. The variation in ventricular filling with respiratory variation is reflected by septal shift. With expiration and increased filling of the left heart, the septum is shifted to the right, with limited right heart filling and expiratory reversal of flow into the hepatic veins. The E wave is variable (higher with expiration and less with inspiration), but the E0 is low. Because RCM and CP are clinically and hemodynamically similar, imaging of pericardial thickness is critical to the distinction of constriction versus RCM. Because of a narrow field of view, even transesophageal echo is limited in evaluation of pericardial thickness. CT and MRI offer distinct advantages in imaging the pericardium. Although both modalities delineate pericardial thickness, MRI is superior, providing more comprehensive imaging with respect to its ability to characterize both pericardial thickness and the dynamic aspects of constriction and adhesion of the pericardial layers to the cardiac chambers.


Increased JVP with RV Enlargement
If RA-JVP pressure is increased and the RV is enlarged (obvious by physical examination as a palpable RV heave, or by ECG or MRI), the differential diagnosis now includes: (1) primary RV pressure overload, (2) primary volume overload, or (3) intrinsic cardiomyopathy (ischemic or nonischemic). The key to the differentiation of these abnormalities is based on the presence or absence of increased RV afterload, rarely in adults as a result of pulmonary stenosis and most commonly as a result of PHTN. Measurement of pulmonary arterial pressure (PAP) and PVR is easily documented by invasive study, but noninvasive Doppler measures of increased RAP, PAP, and PVR are also available. RHF withenlarged RV but normal PAP This syndrome results from either primary RV volume overload (caused by primary TR, pulmonary regurgitation (PR) or atrial septal defect


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[ASD]), or primary RV cardiomyopathy (acute RV infarction or nonischemic causes). Primary volume overload lesions result in RA and RV dilation. Severe primary TR is characterized invasively by prominent RA V wave, with sharp Y descent reflecting rapid early emptying of the overloaded atrium; wide-open TR results in the RA waveform appearing similar to the RV pressure trace. Echo Doppler delineates TR as right heart dilatation with a prominent regurgitant jet by Doppler. There is increased systolic reversal in the hepatic veins with severe TR. Moreover, echo delineates that primary derangements of the valve may be discernible (eg, vegetation, rheumatic changes). In the setting of PR, color Doppler of the regurgitant jet as well decreases in the deceleration time of the PR Doppler waveform. ASD can be easily delineated by both two-dimensional and color Doppler. RV cardiomyopathy resulting from nonischemic causes (which nearly always occur in association with similar LV abnormalities) is evident as increased RV filling pressures and noninvasively as RV dilation with depressed global RV performance. Echo reveals RV dilation and systolic dysfunction, and is often associated with secondary functional TR; there is typically concomitant LV dysfunction attributable to the underlying cardiomyopathic process. Acute RV infarction results in severely depressed RV contractility indicated by a depressed, sluggish RV systolic waveform with diminished upstroke and amplitude, as well as delayed relaxation and increased RV DP. RAP isincreased with RV dilation, but the acutely noncompliant pericardium results in a marked increase of right heart filling pressures. Abrupt RV dilatation within the noncompliant pericardium increases IPP, the resultant constraint further impairing RV and LV compliance and filling. These effects contribute to the pattern of equalized DPs and RV dip and plateau. RV diastolic dysfunction imposes increased preload and afterload on the RA, resulting in enhanced RA contractility that augments RV filling and performance. This finding is reflected in the RA waveform as a W pattern characterized by a rapid upstroke and increased peak A wave amplitude, sharp X descent reflecting enhanced atrial relaxation and blunted Y descent as a result of pandiastolic RV dysfunction. However, very proximal right coronary artery occlusions compromising atrial as well as RV branches result in ischemic depression of atrial function, which compromises RV performance and CO. RA ischemia manifests hemodynamically as more severely increased mean RAP and inscribes an M pattern in the RA waveform characterized by a depressed A wave and X descent, as well as blunted Y descent. Acute RV infarction is hemodynamically similar to tamponade, but the diagnosis is suspected by its association with acute transmural ST elevation inferior myocardial infarction. The differentiation from tamponade is made obvious by ECG, which documents ST elevation MI and echocardiography, which documents the presence of severe RV dilation and systolic dysfunction, and the absence of pericardial fluid. RHF from PHTN RHF from PHTN is evident by increased JVP, an enlarged hypertrophic RV, evident on echo and associated with reversed septal curvature and a D-shaped septum bowinginto the volumedeprived LV. RHF attributable to RV pressure overload often results in RV systolic pump failure with secondary RV volume overload. Under conditions of RV dilatation, the TV is vulnerable to functional incompetence, because the dilated RV tends to tether the tricuspid mural (septal) leaflet, rendering the valve prone to functional leakage. Secondary TR is common when the RV fails and enlarges as a consequence of PHTN, the increased afterload forcing the RV to preferentially regurgitate backward across the lower resistance TV, thereby perpetuating a vicious cycle of right heart dilation and low output. Increased RV afterload leads to increased RVSP. RV outflow obstruction at the subvalvular and valvular levels is identified by a gradient between RV and PA systolic peak and mean pressures. Invasively, PHTN is indicated by equivalent increases of RV and PASPs.
Differential diagnosis of PHTN RHF caused by

PHTN may be differentiated based on whether increased pulmonary resistance is precapillary, intrapulmonary, or postcapillary. Precapillary PHTN reflects primary abnormalities of the pulmonary arterial bed resulting from thromboembolic disease, primary PHTN, or occasionally extrinsic mass obstruction of the major pulmonary arteries from mediastinal tumors. Primary intrapulmonary processes include the broad range of primary obstructive or restrictive lung diseases. Postcapillary PHTN is attributable to increased pulmonary capillary wedge (PCW) pressure. Therefore, postcapillary PHTN resulting in right heart pressure failure can be determined through the same approach used for the evaluation of dyspnea, an algorithm based on why and how LA pressure is increased, as described earlier. PostcapillaryPHTN caused by LA hypertension is suspected whenever PCW pressure is greater than 20 to 25 mm Hg. Echo Doppler is helpful in establishing the presence or absence of left heart

Anatomic-Pathophysiologic Approach to Hemodynamics
anatomic (LA, MV, LV) derangements and dysfunction. With increased PASPs, an increased peak velocity of the TR jet occurs, as mentioned earlier. In addition, with increased PVR, there is decreased blood flow across the pulmonic valve. This situation manifests as truncation of the Doppler wave emanating from the right ventricle (RVOT TVI). Because PVR is the ratio of pressure to flow, a noninvasive measure of PVR may be estimated. Dyspnea can be ascribed to cardiac origin only if the PCW pressure is increased, typically greater than 15 to 20 mm Hg. If the PCW pressure is normal, then dyspnea must either be of primary pulmonary origin (eg, upper airway, lower airway, alveolar processes, parenchymal disease, pulmonary arterial problems) or related to a metabolic condition such as anemia. Accordingly, the differentiation of cardiac and noncardiac dyspnea is based on evidence of anatomical-pathophysiologic perturbations that could result in increased PCW pressure (Fig. 2). Using both noninvasive and invasive modalities, the diagnostic algorithm is based on interrogation of the anatomic course of the circulation from the pulmonary capillaries through the entire left heart. Accordingly, analogous to the anatomicpathophysiologic approach to RHF, assessment of dyspnea proceeds along the course of blood flow (see Fig. 2): if PCW pressure is increased then cardiac dyspnea must reflect pulmonary venous hypertension. A simple anatomic approach reveals a limited number of anatomic mechanismsresponsible for an increased back pressure, which may be found at the bedside and by invasive evaluation. Excepting the rare instances of pulmonary venoocclusive disease, pulmonary venous hypertension equates to LA hypertension, as a result of 1 of several mechanisms, including (1) space-occupying lesions (eg, myxoma) of the left atrium; (2) pressure overload


Pulmonary Capillary Wedge Pressure
Pulmonary 15-20 mmHg

AV Disease
Aortic stenosis Aortic regurgitation


1s LA Disease 1s Pressure Overload
Aortic stenosis Hypertension Aortic coarctation

Atrial myxoma Atrial thrombus

MV Disease 1s Volume Overload
MItral regurgitation Aortic regurgitation Ventricular septal defect

Mitral stenosis Mitral regurgitation

1s Cardiomyopathy
Hypertrophic cardiomyopathy Restrictive cardiomyopathy Dilated cardiomyopathy

Pericardial Disease
Cardiac tamponade Constrictive pericarditis

LV Diastolic Dysfunction

Primary LVDD
Fig. 2. Anatomic-pathophysiologic evaluation of dyspnea.


Goldstein & Abbas
from MV obstruction or LV compliance abnormalities; (3) volume overload caused by MR or increased pulmonary blood flow from ventricular level shunts or high-output states; (4) intrinsic atrial cardiomyopathies, which may be ischemic or nonischemic.
Dyspnea with normal PCW If the PCW pressure is less than 15 mm Hg, then dyspnea is not attributable to a cardiac condition but more likely of primary pulmonary origin. However, several important caveats must be emphasized: (1) in some patients, chronic resting increases of PCW pressure greater than 25 mm Hg may be tolerated without resting dyspnea, as a result of thickening of the pulmonary capillaries, development ofPHTN, and increased capillary lymphatic drainage of the lung; (2) PCW pressure may be normal at rest but increase dramatically during exercise or stress. Thus, in the dyspneic patient, if the resting PCW pressure is normal, hemodynamics should be measured during leg lifts, volume challenge, or after contrast administration; and (3) dyspnea may be also be an angina equivalent, a condition of myocardial ischemia that should be established by coronary arteriography. Stepwise anatomic-pathophysiologic approach to dyspnea Evaluation of the patient with dysp-

disease or LA hypertension caused by spaceoccupying lesions are best established by noninvasive imaging studies (CT angiography and MRI). Generally, detection of an atrial mass (eg, myxoma) as the cause of dyspnea requires noninvasive imaging studies (echocardiography, CT, or MRI).
Evaluation of the MV In the absence of an atrial mass, the next anatomic site to interrogate is the MV, which if primarily to blame for dyspnea must either be obstructed or regurgitant. In mitral stenosis, invasively there is a pressure gradient across the valve that facilitates calculation of the MV area. The PCW pressure in a patient with mitral stenosis is characterized by a prominent A/X and blunted Y descent. Simultaneous LVPCW pressure measurements show a pandiastolic gradient. In the modern era, this condition is easily diagnosed by echo Doppler, which delineates the anatomic calcification and fusion of the valve apparatus, diminished leaflet separation, and mitral orifice. Doppler assessment obtains the mean gradient by tracing the mitral inflow waveform, facilitating measurement of the pressure half-time derived from the deceleration time: The longer the deceleration time,the longer the pressure half-time, and the smaller the MV area. In MR, invasive hemodynamics document increased PCW with a prominent V wave, the height of which reflects the degree of volume overload and LA compliance; if MR is acute, the V wave may be particularly large because the left atrium has not had the opportunity to stretch and accommodate to the volume overload. A prominent V wave may be reflected in the PAP trace, resulting in rabbit ears morphology. Patients with VSD, particularly acquired after infarction, manifest as increased PCW pressure with prominent V waves, the timing of the V wave peak may be delayed but the overall waveform pattern may be indistinguishable from severe MR. LV cineangiography distinguishes MR and VSD, as does oximetry across the right heart, which establishes the presence or absence of a left-to-right shunt. Noninvasive echo Doppler qualitative assessment of the amount regurgitation is performed by visual assessment of the regurgitant flow pattern. The regurgitant volume and the regurgitant orifice area are both calculated by using the PIZA phenomenon, which uses the convergence of the MR color flow pattern, calculating both the volume of regurgitation as well as the area of the valve through which the regurgitation is occurring, the effective regurgitant orifice area. Doppler also delineates the presence and locale of VSD.

nea requires careful synthesis of data from the history, physical examination, CXR, and serologic testing (eg, brain natriuretic peptide and arterial blood gas levels). However, this article focuses only on the role of noninvasive and invasive imaging cardiac diagnostic studies. Invasive evaluation provides the gold-standard hemodynamic data and in themodern noninvasive era has played a still important but often less critical role. Noninvasive interrogation of patients with dyspnea can be approached by the anatomicpathophysiologic processes described. Echocardiography is the technique that provides the most comprehensive data and is most widely available, which may be further enhanced by other advanced imaging techniques (eg, MRI). These imaging techniques delineate the anatomic-mechanical status of the left atrium, the presence or absence of mitral valvular abnormalities that might explain dyspnea, as well as LV size and systolic function. Together with noninvasive echo Doppler evaluation, echo Doppler facilitates evaluation of dyspnea.
Assessment of the left atrium in patients with dyspnea Invasive interrogation of patients with

dyspnea can be approached by the anatomicpathophysiologic processes described in Fig. 2. The rare conditions of pulmonary venoocclusive

Anatomic-Pathophysiologic Approach to Hemodynamics
Assessment of LV diastolic dysfunction If the MV is normal, then dyspnea caused by LA hypertension can be explained only by LV diastolic dysfunction imposing increased afterload on the left atrium. LV compliance abnormalities may reflect either intrinsic chamber processes (eg, primary LV pressure overload, volume overload, or cardiomyopathic processes) or extrinsic abnormalities related to abnormalities of the pericardium. Primary LV volume overload is induced by aortic insufficiency, MR, or ventricular level shunts (VSD and patent ductus artery). LV pressure overload may result from fixed outflow obstructions (aortic stenosis, coarctation), or dynamic obstructions (hypertrophic cardiomyopathy), or increased SVR caused by hypertension (Æcoarctation). LV diastolic dysfunction must also be viewed as occurring either with preserved LV ejection fraction or as a result of LV systolic dysfunction. Regardless of the cause, LV noncompliance increases LV and LA DPs, because of inability of the ventricle to accommodate preload (venous return) without increasing filling pressures. LV DP may show not only increased mid and end DP with a prominent A wave (atrial kick), reflecting LV noncompliance of hypertrophy, fibrosis, infiltration, or external pericardial restraint. If LV and RV diastolic filling pressures are increased and equalized, differential considerations include increased IPP (tamponade, constriction, or as a result of acute RV infarction), RCM or massive acute pulmonary embolus. LV diastolic dysfunction results in prominent A wave/X descent, but there is no end-diastolic gradient on simultaneous LVPCW tracings. Under normal conditions, diastolic waveforms across the MV appear as follows: an IVRT, a rapid filling wave E wave, diastasis, and late filling A wave. Normally, more filling occurs early rather than late (ie, E wave is > A wave). By echo Doppler, early in diastolic dysfunction, there is an impaired relaxation of the ventricle, causing a delay in MV opening with an increased IVRT. In addition, less blood is delivered to the ventricle from the atrium in the early filling phase of diastole, with more blood available later in diastole (thus the A wave is > the E wave). With time, the increased blood volume in the atrium throughout diastole causes an increase in LA pressure. This increase leads to faster opening of the MV, which by echo Doppler is manifest as shorter IVRT, and an increase in ventricular filling volume and rate early indiastole through a high atrioventricular pressure gradient, with less blood left in the atrium at the end of diastole. This situation mimics the normal condition and is referred to as pseudonormalization. The E wave becomes greater than the A


wave again. In advanced stages of diastolic dysfunction, there is marked increased in LA pressure with earlier MV opening and markedly diminished IVRT, further increased LV filling volume and rate early in diastole with lesser contribution of atrial contraction, resulting in a restrictive pattern of diastolic dysfunction with marked increase in E wave velocity and decreased A wave velocity. By echo Doppler, LV diastolic dysfunction ultimately results in increased LA volume together with altered mitral inflow patterns. Early noncompliance is indicated by decreased mitral E velocity with increased A wave velocity (impaired relaxation). Subsequently, further increased LA pressure leads to increased E wave velocity greater than A level (pseudonormal). Progressive stiffness and increased LA pressure then results in increased E velocity but decreased A wave (restrictive). There is also progressive decline in mitral annular motion and velocity (E0 ). Increased LA pressure exaggerates reversal of flow into the pulmonary veins during atrial contraction with diastolic prominence of the pulmonary venous flow pattern and increased A wave reversal.
Assessment of LV systolic dysfunction Echocardiography provides excellent noninvasive delineation of LV systolic performance, including insights into both regional and global LV contractile performance. LV cineangiography provides similar information, but is less critical than before the noninvasive imaging era. Invasively, the LVsystolic pressure waveform may reflect the severity of depression of contractility as indicated by diminished upstroke, reduced peak, and delayed relaxation. These derangements are similarly reflected in the aortic pressure waveform as diminished aortic upstroke, amplitude, and overall small SV. End-stage LV pump failure may result in pulsus alternans. LV systolic dysfunction results in dilatation and secondary diastolic dysfunction, resulting in increased diastolic filling pressures. Assessment of LV afterload: outflow tract and aortic valve Dynamic outflow obstruction as

a result of hypertrophic obstructive cardiomyopathy results in LV-aortic dynamic gradient, which may be present at rest and is shown by a pressure pullback from the LV apex through the body and LVOT into the aorta. An intraventricular gradient is located by carefully watching the slow catheter pullback under fluoroscopy, showing that the gradient occurs within the ventricle before it is pulled across the aortic valve. The arterial pressure waveform pattern often shows unique morphology, a spike and dome or bisfiriens waveform with intact upstroke, midsystolic delay, or notch, reflecting the


Goldstein & Abbas
obstruction and an overall small SV. In the modern era, echo Doppler is definitive, showing patterns of hypertrophy (eg, asymmetric septal), systolic anterior motion of the MV, and an outflow tract gradient, as well as associated MR. Valvular aortic stenosis is evident invasively by fixed gradient across the aortic valve and a dramatic difference in aortic and LV waveform morphologies. The LV upstroke and amplitude are brisk, whereas in the carotid and aortic waveforms there is a depressed upstroke, and a delayed anddiminished peak often with shudder findings, associated with low CO. The aortic waveforms are characteristic with aortic stenosis, revealing a slow rising and diminished amplitude, pulses parvus et tardus. Calculation of aortic valve area is well established by these techniques; the severity of the obstruction is reflected in the mean and peak gradients and CO. Echo Doppler facilitates precise analysis of aortic stenosis, delineating primary derangements of the valve (eg, bicuspid valve, or dense calcification with diminished leaflet excursion). Doppler allows calculation of the gradient across the aortic valve based on the Bernoulli equation. The mean gradient obtained with Doppler correlates well with that obtained invasively. However, the peak gradient is different. With Doppler, the maximum instantaneous gradient is what is measured. That is the gradient at the same instance between the LV and aorta, which is not necessarily the peak gradient of either cavity. However, invasively, the peak-to-peak gradient is measured. These measurements calculate the difference between the highest aortic and highest LV pressure. The aortic area is then calculated by applying the continuity equation. In AR invasive hemodynamics reveal widened aortic pulse pressure and when decompensated leads to increased LV DP. In acute AR, the aorta-LV pressures are equalized at some point in diastole. The magnitude of AR is assessed invasively by aortography, revealing not only the severity of the leak but its effect manifest as LV dilation and later systolic dysfunction. By noninvasive echo Doppler, the LV is dilated and in later stages its contractile performance depressed. Primary derangements of the valve apparatus (eg, vegetations,prolapse, annular dilation, aortic dissection) may be apparent. The severity of AR is assessed visually as well as the PIZA and continuity equation. Assessment of the severity of AR can be performed by color Doppler by measuring the width of the regurgitation jet. In addition, the slope of the Doppler waveform (ie, the pressure half-time) is shortened in cases of advanced AR.

Evaluation of the Syndrome of Low-CO Hypotension
Investigation of hypotension is based on Ohm’s law as applied to the circulation, whereby BP 5 CO A SVR. Accordingly, low-output hypotension must be explained either by diminished CO, low SVR, or both. Specific contributing mechanisms involve the determinants of CO and SVR. CO is a function of HR and SV, the last determined by ventricular preload, contractility, and afterload. SVR is determined by total blood volume and vascular tone (eg, autonomic influences, drugs, sepsis, neuropathies) (Fig. 3). Low-output hypotension because of arrhythmias The first step is assessment of the physiologic cardiac rhythm. Under conditions of low output because of depressed SV, reflex sinus tachycardia is the expected compensatory rhythm; lack thereof suggests chronotropic incompetence, which contributes to hemodynamic compromise. If the patient has a 1 arrhythmia and/or chronotropic incompetence, restoration of physiologic rhythm is the first therapeutic intervention (eg, cardioversion or bolus antiarrhythmic drugs). Low-output hypotension because of low SVR In patients with low-output hypotension and physiologic rhythm, the next step is to assess SVR. SVR, determined by total blood volume and vascular tone, is gauged clinically by peripheral perfusion. Low SVR is suggested by distal extremities that arewarm and pink with brisk capillary refill. In such cases, hypotension likely reflects factors associated with vasodilatory stimulation such as sepsis, autonomic dysfunction, overdose of vasodilating drugs, or peripheral neuropathies (eg, diabetes) and other neurologic disorders. Invasive hemodynamics documents diminished SVR with high output and low aortic pressure. Low-output hypotension because of diminished SV In patients with low-output hypotension and a physiologic cardiac rhythm, low CO can be explained only by diminished SV. An inadequate SV can be explained only by inadequate preload, poor contractility, or excess afterload. Analysis of SV should be approached according to anatomic-pathophysiologic principles, with a stepwise focus on each cardiac chamber, as well as for the heart as a whole. Invasively, it is essential to consider compliance properties pertinent to preload assessment. Cardiac preload is the amount of blood distending the cardiac chamber. In assessment of preload

Anatomic-Pathophysiologic Approach to Hemodynamics


Fig. 3. Bedside hemodynamic evaluation of RHF.


Goldstein & Abbas
measuring the chamber filling pressure is a convenient surrogate of chamber volume. The compliance characteristics of the chamber being interrogated have a striking effect on the pressure-volume relationship. Therefore, filling pressure reasonably reflects chamber volume and preload only if chamber compliance is normal. Because chamber compliance is influenced by numerous intrinsic (eg, hypertrophy, ischemia, infiltration, inflammation) and extrinsic (eg, pericardial pressure increases or intraventricular or intraarterial interactions) factors, it follows that there are numerousconditions in which filling pressure may be increased but preload limited. For example, LV preload may be markedly reduced but intracardiac pressures strikingly increased under conditions of cardiac tamponade or severe PHTN. Conversely, chronic volume overload lesion such as AR may result in dramatically increased chamber volumes, but intracardiac pressures relatively normal as chamber and pericardium dilate, become compliant, and compensate for the pathophysiology. LV filling is the final common preload pathway that generates effective forward SV and thus CO. However, it is not uncommon for the LV to be preload deprived but other chambers to be overloaded. Thus, preload assessment must consider all cardiac chambers and conduits and be interrogated according to the course of venous blood returning to and ultimately delivered to the LV cardiopulmonary circulation.
Low output with decreased total blood volume Low output as a result of systemic hypovo-

gradient indicates inflow obstruction at the level of the SVC or IVC; central venous waveforms proximal to the obstruction are typically blunted. Noninvasive imaging confirms the site and nature of obstruction. Increased RAP exceeding RV DP with an end-diastolic RA-RV gradient indicates either a space-occupying RA mass lesion or TV obstruction. RA mass lesions manifest an overall blunted RA waveform. TV obstruction results in a prominent A wave with sharp X descent resulting from enhanced atrial contraction/relaxation against the stenotic valve, with blunted Y descent reflecting impaired RV inflow. Matched and increased RA and RV filling pressures may indicate primary RV diastolic dysfunction. The differential diagnosis includes primary RV derangements (pressureoverload, volume overload, or cardiomyopathy) or pericardial disease. Increased equalized DPs throughout the cardiac chambers with RV dip-and-plateau configuration suggest either constriction, restriction, or acute RV infarction. The differentiation of these entities is discussed earlier in the section on RHF. Overall, echo Doppler is a superior technique for elucidating these problems, rendering invasive evaluation often unnecessary to establish the diagnosis.
Decreased RV outflow Increased right heart filling

lemia is detected clinically by low JVP, orthostatic blood pressure changes, sinus tachycardia, and clear lungs. Invasive hemodynamics document diminished RA, PCW, and LV diastolic filling pressures. If LV function is intact, the carotid and aortic waveforms reveal intact upstrokes with a small pulse volume. Volume administration restores filling pressures, increases CO, normalizes blood pressure, and resolves the compensatory sinus tachycardia (lower HR). If volume challenge results in dramatic increases in filling pressures without the expected increase in CO and blood pressure, then preload was not the predominant, but certainly may have been a contributing, factor. Persistent hypotension in such patients suggests intense primary vasodilatation as a result of drugs or sepsis. Echo reveals preload deprived cardiac chambers with preserved RV and LV contractility.
Decreased cardiac preload despite increased total blood volume Right heart inflow obstruction Increased JVP

exceeding RAP with a demonstrable JVP-RA

pressures with normal or low PCW pressure indicates impaired delivery of preload from right heart to left heart, attributable to (1) RV systolic dysfunction (eg, RV infarction), (2) excessRV afterload because of outflow obstruction (at the level of the outflow tract or pulmonary valve), or (3) pulmonary arterial hypertension. Diminished effective RV SV limits LV preload not only because of reduced transpulmonary blood flow but also because of the effects of RV pressure/volume overload. RV overload can induce septal-mediated diastolic ventricular interactions, which adversely influence LV compliance and filling. Severe RV infarction depresses RV stroke work, leading to depressed transpulmonary delivery of LV preload. Thus, RV infarction with decreased LV preload results in a syndrome of hypotension, low output with clear lungs, and increased right heart filling pressures. RV infarction and its evaluation is discussed earlier. Excess RV afterload is delineated by increased RVSP: RV outflow obstructions are evident by increased JVP with RV heave and loud latepeaking ejection murmur along the left sternal border. Invasively, RVSP greater than PASP suggests either subvalvular RV outflow obstruction or pulmonary valve stenosis. Clinical evaluation delineates PHTN, characterized by an RV heave and loud P2. Invasive assessment

Anatomic-Pathophysiologic Approach to Hemodynamics
documents increased RVSP 5 PASPs. The magnitude of PA DP increase is dependent on the mechanism of PHTN. Calculated pulmonary resistance is increased and reflects the magnitude of obstruction in the pulmonary bed. If attributable to left heart cause, PHTN is associated with increased PCW. These entities and their differentiation are discussed in the sections on RHF and dyspnea.
Left heart inflow obstruction Under conditions of left heart inflow obstruction, reduced LV preload results in low-output hypotension despiteexpanded total blood volume, increased right heart preload, and increased PCW pressure. Inflow obstruction may occur at the level of the pulmonary veins, LA, or MV. LV preload is reflected by LV DP, which must be interpreted within the context of LV compliance. Increased PCW pressure with an end-diastolic gradient across the MV suggests either a space-occupying lesion in the left atrium or mitral valvular obstruction. The lack of opening snap and diastolic flow rumble on examination excludes mitral stenosis, and should lead to suspicion of an atrial mass or pulmonary venoocclusive disease. Noninvasive imaging is confirmatory. Increased and equal PCW and LV filling pressure indicates LV diastolic dysfunction, which may be primary (with intact LV contractility) or secondary (associated with depressed LV systolic function). Primary LV diastolic dysfunction reflects intrinsic LV abnormalities (primary pressure overload/ outflow obstruction, volume overload, or cardiomyopathic processes) or extrinsic constraint (pericardial disease or intense ventricular interactions from the RV). Occasionally, acute LV ischemia with global paralysis of LV function may result in abrupt diastolic dysfunction with flash pulmonary edema and low-output hypotension LV contractility may be intact or depressed depending on the duration of ischemia. Severe LV diastolic dysfunction may result from a hypertrophic noncompliant cavity (eg, severe hypertensive LV hypertrophy, aortic stenosis, or hypertrophic cardiomyopathy) with increased filling pressures but reduced LV preload and SV further limiting CO. These entities and their differentiation are also discussed in the section on dyspnea (see Fig. 2). Low output because of diminished LV outflowDepressed LV contractility Reduced LV SV may


differentiate contractile failure resulting from ischemic or nonischemic myocardial depression from pump failure attributable to chronic excess afterload conditions such as severe aortic stenosis. Regardless of the cause, systolic dysfunction reduces SV and CO. Transient acute ischemic LV dysfunction is excluded by coronary angiography. If present, severe left main or multivessel equivalents are noted and occasionally result in episodic low-output hypotension, often with flash pulmonary edema; more commonly LV contractility is depressed because of ischemic cardiomyopathy. These entities and their differentiation are also discussed in the section on dyspnea.
Depressed CO because of increased LV afterload Increased LV afterload impairs SV and

CO, either with intact LV contractility or LV systolic dysfunction. Increased LV afterload can be categorized mechanically and anatomically as (1) dynamic LVOT as a result of hypertrophic obstructive cardiomyopathy, or (2) fixed obstructions as a result of subvalvular (membranes) or valvular stenosis or (3) postvalve level resistance attributable to systemic hypertension or aortic coarctation. These entities and their differentiation are also discussed in the section on dyspnea.

McCullough P, Goldstein JA. Heart pressures and catheterization. Diagnostic cardiac catheterization. Blackwell Scientific Publications; 1997. 2. Goldstein JA. An anatomic-pathophysiologic approach to hemodynamic assessment. In: Kern MJ, Lim MJ, Goldstein JA, editors. Hemodynamic rounds: interpretation of cardiac pathophysiology from pressure waveform analysis. Wileya€‘Liss; 2009. p. 429–36. 3. Goldstein JA. Hemodynamicevaluation of dyspnea. In: Kern MJ, Lim MJ, Goldstein JA, editors. Hemodynamic rounds: interpretation of cardiac pathophysiology from pressure waveform analysis. Wileya€‘Liss; 2009. p. 445–6. 4. Goldstein JA. Bedside evaluation of low output hypotension. In: Kern MJ, Lim MJ, Goldstein JA, editors. Hemodynamic rounds: interpretation of cardiac pathophysiology from pressure waveform analysis. Wileya€‘Liss; 2009. p. 449–54. 5. Goldstein JA. Hemodynamic evaluation of right heart failure. In: Kern MJ, Lim MJ, Goldstein JA, editors. Hemodynamic rounds: interpretation of cardiac pathophysiology from pressure waveform analysis. Wileya€‘Liss; 2009. p. 455–9. 6. Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Curr Probl Cardiol 2004 –67.

be attributable to (1) impaired systolic performance, (2) decompensated primary pressure overload (hypertension or outflow resistance), (3) volume overload (mitral insufficiency, AR or ventricular level shunts) or (4) primary cardiomyopathies (either ischemic or nonischemic). It is important to


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7. Abbas AE, Fortuin Schiller NB, Appleton CP, et al. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003 (6):1021–7. 8. Lee KS, Abbas AE, Khandheria BK, et al. Echocardiographic assessment of right heart hemodynamic parameters. J Am Soc Echocardiogr 2007 (6):773–82. 9. Abbas AE, Fortuin FD, Schiller NB, et al. Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol 2003 (11):1373–6. 10. Abbas A, Lester S, Moreno FC, et al. Noninvasive assessment of right atrial pressure using Doppler tissue imaging. J Am Soc Echocardiogr 2004; 17(11):1155–60.

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