Ebook Practical cardiovascular hemodynamics: Part 1

(BQ) Part 1 book Practical cardiovascular hemodynamics has contents: Pressure tracings, measurement of cardiac output and vascular resistances, overview of the steps performed during a standard right and left heart catheterization, overview of the steps performed during a standard right and left heart catheterization,.... and other contents.

Medicine is an ever-changing science Research and clinical experience arecontinually expanding our knowledge, in particular our understanding of propertreatment and drug therapy The authors, editors, and publisher have made everyeffort to ensure that all information in this book is in accordance with the state ofknowledge at the time of production of the book Nevertheless, the authors,editors, and publisher are not responsible for errors or omissions or for anyconsequences from application of the information in this book and make nowarranty, express or implied, with respect to the contents of the publication.Every reader should examine carefully the package inserts accompanying eachdrug and should carefully check whether the dosage schedules mentioned therein

or the contraindications stated by the manufacturer differ from the statementsmade in this book Such examination is particularly important with drugs that areeither rarely used or have been newly released on the market

I.8 Establish the zero reference

I.9 Effect of respiration on intracardiac pressures and concept of transmural pressure

II Measurement of cardiac output and vascular resistances

XVI.2 Transvalvular left ventricular assist device (Impella) and TandemHeart XVI.3 Left ventricular pressure-volume loops and effect of left ventricular support devices on cardiac hemodynamics

Despite the advances of imaging techniques, the understanding of invasivecardiovascular hemodynamics continues to be of critical importance in patientswith conflicting or inconclusive noninvasive data Furthermore, invasivehemodynamics remain the backbone for in-depth understanding ofcardiovascular physiology, physical examination, and echocardiographichemodynamics Yet few manuals address cardiovascular hemodynamics in apractical and illustrated format or provide hemodynamic self-assessmentproblems to allow question-guided learning, hence the reason why the topicremains confusing to cardiologists and to our cardiology fellows

The purpose of this book is to provide an in-depth understanding ofwaveforms and tracings seen in various disease states and the pathophysiologybehind those findings This is highlighted throughout Section A of the bookwhere a thorough yet concise dynamic pathophysiology is used to explainhemodynamic findings One example is the book’s illustrated explanation of thesequence of events taking place in constrictive pericarditis in contradiction to theseries of events occurring in restrictive cardiomyopathy, ventricular failure, andobstructive lung disease Practical issues that are rarely discussed or focusedupon in textbooks are highlighted in every part of Section A with detailedwaveform analysis Pitfalls in the hemodynamic assessment of valvular diseases,constrictive pericarditis, tamponade, pulmonary hypertension, shunt pathology,coronary disease, and right and left ventricular failure are provided Goingthrough the illustrations and their detailed legends may provide the reader withmost of the required information

Section B of the book provides case-based and tracing-based assessment problems The reader will learn to identify disease states andwaveform subtleties from single tracings or from case studies The reader willtake the initiative to interpret tracings, understand notches, artifacts, and

Despite its depth, the book is concise and relies on practical explanationsand real-life illustrations to successfully bring about the hemodynamic concepts.Over 300 illustrations and 25 tables with detailed legends are used to allowillustrated learning I believe this book has a great educational value forcardiology fellows, cardiologists, intensive care physicians, anesthesiologists,and catheterization laboratory personnel and nurses

Elias B Hanna

Dr Eliot Schechter, Dr Thomas Hennebry with his commanding personality andcatheterization style, and Dr Mazen Abu-fadel I am also appreciative of theLSU and Oklahoma University catheterization laboratory’s nurses andtechnicians, who allowed the recording of quality tracings fundamental to thisendeavor.

Elias B Hanna

A

BASIC AND ADVANCED HEMODYNAMICS

Correlations between the RA pressure tracing and Doppler tracings of the inferior vena cava, hepatic veins, and trans-tricuspid flow

Description of some abnormalities I.2 Right ventricular pressure tracing—Characteristics of RV failure I.3 Pulmonary artery pressure tracing

I.4 Pulmonary capillary wedge pressure

Description of PCWP waves—Correlation of PCWP with LA pressure Pitfalls in interpreting PCWP

Key points in differentiating PA pressure from PCWP Abnormalities of PCWP tracing

I.5. Left ventricular pressure tracing and interpretation of LVED-left

ventricular failure

LV systolic pressure

LV diastolic pressure and evaluation of LV failure Correlation between LVEDP and a properly done PCWP How to accurately measure LVEDP?

Pitfalls in LVEDP determination

I.6.

Aortic pressure, peripheral arterial pressure, and description of damping and ventricularization of aortic pressure upon coronary engagement

Aortic pressure

Peripheral arterial pressure: Reflected waves and systolic amplification

Damping and ventricularization of the aortic waveform upon coronary engagement

I.7 Pressure damping and Other sources of pressure artifact

I.8 Establish the zero reference

I.9. Effect of respiration on intracardiac pressures and concept of

transmural pressure References

VII.5 Case of low-gradient AS with AVA ≤1 cm 2 and low EF <40%

VII.6. Case of low-gradient AS with AVA ≤1 cm 2 but normal EF

VII.7 Pressure recovery phenomenon

VII.8. LVOT obstruction and LV flow acceleration in aortic stenosis

XI HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

XI.1. Overview of hypertropic obstructive cardiomyopathy (HOCM) and

the hemodynamic findings in HOCM XI.2 Provocative maneuvers

XII.6 Effect of respiration on RV and LV filling in normalindividuals

XII.7 Differentiation between COPD and constriction

XII.8 Transient CP

XII.9 Practical performance of a hemodynamic studywhen CP is suspected References

XIII TAMPONADE

XIII.1 Overview of the hemodynamics of tamponade

XIII.3 Low-pressure tamponade

XIII.4. Cases of underlying RV or LV failure and causes of absent pulsus

paradoxus XIII.5 Regional tamponade

XIII.6 Effusive-constrictive pericarditis

XIII.7. COPD and other causes of pulsus paradoxus and RV-LV respiratory

discordance References

CARDIAC CONDITIONS

XVI.1 Intra-aortic balloon pump

Overview of IABP Triggering and timing Contraindications

XVI.2. Transvalvular left ventricular assist device (Impella) and

TandemHeart Transvalvular assist device Impella contraindications TandemHeart

XVI.3. Left ventricular pressure-volume loops and effect of left ventricular

support devices on cardiac hemodynamics Definition of afterload

Coronary blood flow and myocardial O2 demands Pressure-volume loop

Acute coronary syndrome Microcirculatory dysfunction and LV hypertrophy Artery supplying an old infarcted myocardium—Value of FFR in assessing ischemia and viability

FFR vs nuclear perfusion imaging in multivessel disease

XVII.4 Tricks and pitfalls in FFR performance XVII.5 Evidence supporting the use of FFR

I

Pressure tracings

Pressure contour

Right atrial pressure tracing is characterized by A and V waves and X and Ydescents (A-X-V-Y sequence) (Figure I.1) The A wave represents atrialcontraction and follows the electrocardiographic P wave The X descent is apressure dip that occurs during early ventricular systole and corresponds to theatrial relaxation and to the descent of the tricuspid annulus in early systole The

V wave represents atrial filling during ventricular systole while the tricuspidvalve is closed The Y descent occurs in early diastole as the tricuspid valveopens and the RA rapidly empties Thus, the X descent and the upslope of Vwave are systolic events (coincide with the pulse), whereas the peak of V wave,the Y descent, and the A wave are diastolic events

FIGURE I.1

Atrial pressure tracing with A-X-V-Y Note the timing of the peak

of V wave with respect to the end of the electrocardiographic T wave, and A wave with respect to P wave The C wave is a small positive deflection on the atrial tracing that sometimes interrupts the

X descent and corresponds to the brief protrusion of the tricuspid valve into the RA in early systole during isovolumic ventricular

contraction C wave splits X into a segment that corresponds to atrial relaxation (X) and another segment that corresponds to annular descent (X').

The mean atrial pressure is the average of the instantaneous pressuresunder all these waveforms and is lower than both A and V pressures The normalmean RA pressure is 7 mmHg or less

Normally, in the RA, the A wave is larger than the V wave, whereas in the

LA, the V wave is larger than the A wave This is because the V wave correlateswith the atrial compliance and the atrial ability to distend; the LA, beingconstrained by the pulmonary veins and having thicker musculature, cannotnormally distend as much as the RA

Timing in relation to the ECG and the ventricular tracing

When RA pressure is recorded simultaneously with the ECG and with theventricular tracing, the peak of A wave follows the peak of P wave byapproximately 80 milliseconds, whereas the V wave peaks at or after the end of

T wave and almost intersects with the ventricular pressure descent (Figure I.2)

pressures that peak during the ST/T segment.

Concerning the ventricular pressure:

1 The steepness of increase of the ventricular diastolic pressure relates inversely to ventricular compliance.

2 In decompensated HF, the diastolic pressure increases steeply, sometimes with a sharp increase in early diastole leading to a square root or dip-plateau pattern.

3 There is normally a small gradient between Y of the atrial

This gradient is less prominent in the case of impaired ventricular relaxation with a reduced early ventricular dip and is more

prominent in the case of decompensated HF with an increased atrial V wave (see Section I.5 ).

4 Ventricular EDP corresponds to the peak of the R wave on ECG

(black dot).

Concerning the arterial pressure, the semilunar valve opens at the

end of the QRS complex, beyond EDP, and closes at the end of T wave As opposed to the atrial V wave, arterial pressure peaks during ST/T segments.

Respiratory variations

Normally, RA and LA pressures are affected by respiratory changes inintrathoracic pressure and, therefore, decrease in inspiration The X and Ydescents in particular become deeper with inspiration Pressures are bestmeasured at end expiration, at which time, unless the patient performs activeexpiration, the thoracic pressure is nil In patients breathing spontaneously, end-expiratory pressures are the highest pressures on the tracing

Correlations between the RA pressure tracing and the Doppler tracings of the inferior vena cava, hepatic veins, and trans-tricuspid flow

The X and Y descents “suck” flow from the venous system and thus lead toforward venous flow, whereas the A and V ascents attenuate forward venousflow and may reverse it Thus, the X descent leads to the forward systolic Swave, whereas the Y descent leads to the forward diastolic D wave on theIVC/hepatic venous Doppler The A wave leads to atrial A reversal on thehepatic vein/IVC Doppler tracing The V wave corresponds to the late part of the

S wave wherein the systolic flow is slowed down, and to the systolic flowreversal of the late part of the S wave in case of a large V wave (Figure I.3)

Correlations between A, X, V, and Y waves

on the RA pressure tracing and S, D, and A flow velocities on IVC/hepatic vein Doppler (the ECG and the tracings are aligned in a way that the timing of all waves coincides).

S flow corresponds to the X descent, D flow corresponds to the Y descent, while the A wave corresponds to A flow reversal S and

D flows are antegrade, while A flow is

retrograde The S wave may be notched and divided into S1 and S2 as a result of the C wave Similar correlations apply to LA

pressure and pulmonary venous Doppler flow.

In case of RV failure with elevated atrial pressure, the V wave is large, the Y descent

is deep, and the X descent is usually blunted

because the elevated atrial pressure remains after the small atrial relaxation The blunted

X descent leads to forward S flow blunting with terminal S reversal, and the deep Y descent leads to a large D flow S flow is fully reversed in the case of TR Thus, TR or

RV failure may blunt or reverse X descent/S flow and increase Y descent/D flow.

On the other hand, the gradient between the V wave and the earlyventricular diastolic pressure corresponds to the E flow between RA and RV onthe trans-tricuspid Doppler, whereas the late RA-RV diastolic gradient duringatrial contraction (A wave) corresponds to the A flow (Figure I.4)

FIGURE I.4

Correlation between RA/RV pressures (upper figure), trans-tricuspid Doppler flow (middle figure), and IVC/hepatic venous flow (bottom figure) E flow corresponds to the gradient between

the V wave and Y descent on the one hand and the early RV diastolic dip on the other hand, whereas A flow correlates with the

late RA-RV gradient during A wave (areas marked in gray on the

pressure tracing explain the Doppler flow) Similar correlations apply to LA/LV pressure and transmitral flow.

Description of some abnormalities

1 Deep X and deep Y descents are seen in constrictive pericarditis and inrestrictive cardiomyopathy (see Section XII) However, deep Y may also beseen in any acute or subacute RV failure or severe TR, cases where right heartdilatation “pushes” against a noncompliant pericardium that has not had time

to accommodate the acute change in right heart volume and thus functionallyacts as “constrictive”; in these cases, a deep Y descent may occur along with alarge V wave Deep X and deep Y descents reflect loss of atrial andventricular compliances, wherein atrial pressure goes sharply down and then

of decompensated RV failure with RA volume overload that surpasses RA

3 Deep X (systole) but shallow Y (diastole) is seen in tamponade Intamponade, the pericardial pressure is elevated (usually 15–30 mmHg) andcompresses all cardiac chambers in diastole until the diastolic pressure ofthese chambers equalizes with the pericardial pressure Thus, the flow to the

in all but the very early part of diastole, explaining the deep Y descent As theannulus moves down in early systole, the pressure that built up in the RAsuddenly drops, leading to a deep X descent

4 A prominent A wave reflects reduced ventricular compliance as in RV

7 Sinus tachycardia and atrial fibrillation (Figure I.6)

FIGURE I.5.A

Deep X and deep Y descents giving the RA pressure tracing a characteristic M or W shape A deep Y descent is often

characterized by being ≥5 to 10 mmHg lower than the V wave This could be seen with constrictive pericarditis; in this patient, however,

severe RV dilatation with moderate TR explains this finding Right atrial pressure and V wave are higher, and Y descent is deeper in inspiration (early part of the Figure) Although the negative

intrathoracic inspiratory pressure has a direct effect of reducing RA pressure, the increased venous return into a noncompliant RA

manages to increase RA pressure and V wave during inspiration, which is opposite to the normal RA pressure behavior in inspiration.

FIGURE I.5.B

Note that the V wave is large and wide and peaks during the ST-T segment in a plateau

fashion (top bar) This simulates an RV tracing and is called ventricularization of RA

pressure This large wave starts during isovolumic contraction, which corresponds to

C wave, and is actually a fused C-V wave It

is characteristic of severe TR The shallow X descent and the deep Y descent seen on this

tracing are frequent accompaniments of the large V wave in severe TR or RV failure.

Right atrial pressure and V wave are higher, and Y descent is deeper in inspiration (early part of the tracing).

FIGURE I.6

Sinus tachycardia shortens diastole and thus attenuates Y descent and may make A and V waves appear to merge; only one positive and one negative waves may be identified A similar phenomenon may be seen with a long PR interval, where, in addition, C wave becomes prominent In atrial fibrillation, the A wave is absent and

V wave becomes prominent; the tracing mostly consists of one wave (V) and one descent (Y), but C and X' may be seen.

In summary:

-Deep X and deep Y: constrictive pericarditis

-Deep X and flat Y (diastolic flow blunting): tamponade, but also sinustachycardia (mnemonic: Flat Y Tamponade=FYT)

-Flat X (systolic flow blunting) and deep Y: severe TR and/or RV failure-Large V wave: severe TR and/or RV failure

-Ventricularized RA pressure: severe TR

-Large A wave: impaired RV compliance

-Equally large A and V waves: ASD

CHARACTERISTICS OF RV FAILURE

There are key differences between arterial and ventricular tracings that should benoted while advancing the right heart catheter (Figures I.2 and I.7): (1) theventricular pressure increases in diastole, whereas arterial pressure decreases indiastole; (2) the ventricular pressure tracing in systole has a “rectangular” shape,

as opposed to the “triangular” shape of arterial tracings; (3) ventricular pressurehas an A wave in diastole; and (4) arterial pressure has a dicrotic notch

FIGURE I.7

Right atrial, RV, PA, and PCWP tracings obtained while advancing the catheter from

RA to PA (50 mmHg scale) Mean RA pressure is equal to RV diastolic pressure, and mean PCWP is equal to PA diastolic pressure Right atrial pressure and RV EDP are lower than PCWP and PA diastolic pressure, except in cases of “equalization of

diastolic pressure” (tamponade, constriction, and severe RV failure).

Concerning RA and PCWP pressures: note the A, X, V, and Y waves and the

timing of the A and V waves (V peaks after T wave on ECG) Concerning RV: note

the rapidly upsloping RV diastolic pressure, particularly after the ventricular A wave, with a mildly increased RVEDP (10 mmHg), indicative of impaired RV diastolic

Normally, RV diastolic pressure is equal to RA diastolic pressure duringmost of diastole Only in early diastole is there a gradient between RA and RVpressure that drives the rapid filling in early diastole (E wave on echo) In fact,there is normally an RV pressure dip in early diastole that sucks blood from the

RA A high early RA-RV pressure gradient may be normally seen in youngindividuals who have a potent RV relaxation (“suckers”) It may also be seen inpatients with decompensated right HF who characteristically have elevated RApressure that pushes blood in the RV (“pushers”) Furthermore, because the loss

of RV compliance makes the RV diastolic pressure rise rapidly to a high-levelplateau, RV failure is characterized by an early RV diastolic dip followed by a

“plateaued” high diastolic pressure (dip and plateau pattern) (Figure I.8) Thisdip is a poor compliance dip, not a “sucking” dip, and these patients usually have

a large V wave and sometimes deep X and Y descents on the RA tracing (TableI.1) Notably, the high RV diastolic pressure and the dip-plateau pattern mayalso be seen in constrictive pericarditis and restrictive cardiomyopathy (see

Section XII, Figure XII.1) As a result of prolonged diastasis, a pattern similar todip-plateau pattern may be seen with bradycardia

†Related to RV failure or to secondary TR.

Right ventricular pressure tracing Deep early diastolic dip (lower arrows) followed

by a plateaued elevated diastolic pressure (~20 mmHg) This patient has severe

biventricular failure, with RV dilatation and severe TR that explains this dip-plateau pattern In addition, the alternation in systolic peaks in the absence of arrhythmia

suggests pulsus alternans of RV failure (both findings, dip-plateau pattern and pulsus alternans, also may be seen on LV pressure tracing in LV failure).

Normally, RV systolic pressure is equal to PA systolic pressure Thenormal RV systolic pressure is 35 mmHg or less, and the RV EDP is 8 mmHg orless As opposed to the normal LV and similar to the failing LV, the RV is verysensitive to afterload changes and is more likely to fail from pressure overload(such as pulmonary hypertension, pulmonary embolism) than from volumeoverload (such as ASD, primary TR, or pulmonic regurgitation) This is becausethe RV wall is thinner than the LV wall, with afterload inversely correlating withmyocardial thickness (Section XVI.3) Only a newborn’s RV tolerates pressureoverload because it is thick and accustomed to high pressures during fetal life

Thus, patients with congenital pulmonic stenosis usually do not develop RV

failure, and their RA tracing is characterized by a large A wave but a normal Vwave