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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3597_Библиотеки_им_академика_М_И_Перельмана
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Figure 4-45 Left, Arterial pressure shows pulsus paradoxus (inspiratory
decrease >10 mm Hg of systolic pressure). Center, Atrial, pericardial, and
aortic (Ao) pressures in a patient with pericardial tamponade. Before pericardiocentesis, right atrial (RA) pressure blunted “x” and “y” descents.
Right, Af ter pericardiocentesis, pulsus paradoxus is absent and RA waveform is lower and more phasic.
exaggerated [>20 mm Hg] inspiratory decrease in arterial pressure).
In tamponade, two-dimensional (2D) echocardiography shows the
pericardial fluid and diastolic RA and RV chambers collapse due to
periodic high pericardial pressure acting on the RA/RV filling patterns.
(See Chapter 7 on pericardiocentesis for details of tamponade.)
Hemodynamic Data
Hypertrophic Cardiomyopathy
HCM, an inherited autosomal dominant heart disease with a prevalence of 1 in 500 individuals, is characterized by myocardial hypertrophy and fibrosis in the absence of a secondary cause (i.e., hypertension
or valvular heart disease). HCM has variable effects on the myocardium and includes a broad range of phenotypic varieties, including
global hypertrophy, asymmetric septal hypertrophy, apical hypertrophy, biventricular hypertrophy, and variants involving abnormalities
of the mitral valve. Clinically, HCM patients often present with exertional dyspnea or chest pain despite preserved systolic function and
no obstructive coronary disease or syncope. These symptoms are
primarily due to diastolic dysfunction and obstruction of flow across
the left ventricular outflow tract (LVOT) due to septal hypertrophy and
systolic anterior motion of the mitral valve.
The degree of LVOT gradients in HCM depends both on loading
conditions and LV contractile function. During each cardiac cycle,
myocardial contraction promotes bulging of the interventricular
septum, which narrows the LVOT and creates Venturi forces that drag
the anterior leaflet of the mitral valve into the LVOT, thereby worsening
the magnitude of LVOT obstruction. In addition, HCM patients often
have a displaced anterior mitral valve leaflet that is further pulled into
the LVOT during ventricular systole, leading to poor mitral leaflet
coaptation and subsequent mitral regurgitation. Therefore, increased
cardiac contractility (i.e., exercise, inotropes), reduced afterload (i.e.,
vasodilator therapy), or reduced preload (i.e., diuretics or dehydration) can all increase the LVOT gradient. An LVOT gradient >
is associated with symptom progression and identifies potential candidates for septal reduction therapy by surgical myectomy or alcohol
septal ablation.
30 mm Hg
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In most patients, resting LVOT obstruction can be identified by
2D echocardiography. For patients without LVOT obstruction at rest,
exercise echocardiography is the preferred method for provoking
LVOT gradients. Noninvasive methods to provoke LVOT gradients
include exercise, Valsalva maneuver, or pharmacologic provocation
with amyl nitrate or isoproterenol.
Invasive hemodynamic evaluation of HOCM is reserved for preoperative evaluation along with coronary angiography or in cases
where a discrepancy between symptoms and noninvasive testing
exits. First, RHC establishes CO, severity of pulmonary hypertension,
and biventricular filling pressures. Next, resting intracavitar y gradients
are measured within the LV. Depending on the technique used, precise
determination of the LVOT gradient can be challenging. End-hole catheters may become entrapped in the myocardium and catheters with
side holes may produce erroneous pressure measurements. In most
cases, retrograde LV catheterization using a pigtail catheter across the
Ao valve is used with care to keep the side holes along the distal shaft
under the obstructed region. Pigtail catheters can lead to underestimation of LVOT gradients.
Alternative catheters for intracavitar y gradient measurements
include a multipurpose catheter with side holes or the HALO catheter
with multiple side holes around a perpendicular ring that prevents
catheter entrapment. If a resting LVOT gradient >
fied, further provocative testing is not required. If no resting LVOT
gradient is established, a PVC is provoked by the intracavitary catheter.
Postextrasystolic potentiation enhances contractility associated with
the post-PVC beat, leading to four findings associated with obstructive
HCM: (1) increased LVOT gradient, (2) rapid Ao upstroke, (3) narrowed Ao pulse pressure, and (4) spike-and-dome configuration to the
Ao waveform (the Brockenbrough-Braunwald-Morrow effect). In contrast, post-PVC waveforms associated with AS (fixed LVOT) obstruction will exhibit only an increased LVOT gradient. If no LVOT gradient
is observed after a PVC, perform Valsalva maneuver to reduce LV
preload, thereby narrowing the LVOT and augmenting any LVOT gradient. If an LVOT remains undetected and suspicion for obstructive HCM
is high, perform hemodynamics with exercise to increase contractility
and reduce afterload or introduce pharmacologic challenge with isoproterenol (enhanced inotropy) or amyl nitrate (decreased afterload)
(Figs. 4-46, 4-47, and 4-48).
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Hemodynamic Data 223
50 mm Hg is identi-
Invasive Measures of Ventricular
Performance: Pressure and
Volume Recordings
In 1914, Ernest Starling extended findings from Otto Frank and defined
the Frank-Starling mechanism, which describes the ability of the heart
to increase stroke volume (SV) in response to increases in LV pressure
or volume. Numerous observations have shown that during acute or
chronic heart failure, small changes in LV pressure or volume can lead
to hypotension or pulmonary congestion (Fig. 4-49). At each stage of
heart failure (i.e., acute heart failure, stable chronic heart failure, and
decompensated heart failure/cardiogenic shock), therapy is directed
at improving SV and reducing intracardiac volume and pressure overload, while maintaining an adequate mean arterial pressure to support
end-organ tissue perfusion.
During the past four decades, specialized pigtail catheters, known
as conductance catheters, that simultaneously measure ventricular
pressure and volume have been developed to quantify ventricular
function and the effect of therapeutic interventions. At present, these
catheters are primarily reserved for research purposes but are used
more frequently to provide clinically relevant hemodynamic data. By
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LV S/D/ED
FA S/D/M
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Hemodynamic Data
A
Figure 4-46
Proper left ventricular (LV) catheter placement. A, Pigtail
B
catheter entrapment leads to an erroneous lack of an intracavitary gradient
in a patient with known obstructive hypertrophic cardiomyopathy (HCM).
B, In the same patient with a HALO catheter at the LV apex, a 50-mm Hg,
dynamic intracavitary gradient is revealed.
LV-FA gradient
S
S
S
S
S
S
137/62/85
200
S
S
S
121/2/17
S
SS
S
S
S
*
S
100
D
D
ED
0
D
ED
D
D
D
ED
D
D
ED
D
ED
D
D
D
ED
D
D
ED
D
25 mm/sec
Figure 4- 47 Intracavitar y pull back gradient. Retraction of a HALO catheter
reveals an intracavitary gradient from the left ventricular (LV) apex (*) to just
below the aortic (Ao) valve (†; subvalvular) consistent with hypertrophic
obstructive cardiomyopathy (HOCM).
S
S
S
S
†
D
D
ED
ED
D
D
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400
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Hemodynamic Data 225
S
*
200
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
†
S
S
D
0
ED
D
S
D
S
S
D
ED
D
D
ED
ED
D
D
D
D
ED
S
D
D
D
10 mm/sec
Figure 4-48 Postextrasystolic potentiation (the Brockenbrough effect).
The beat following a premature ventricular contraction (PVC) shows a significant increase in the left ventricular outflow tract (LVOT) gradient (*) and a
narrowing of the pulse pressure on the aortic (Ao) tracing (†).
applying a constant electric current across multiple electrodes, the
catheter converts the electrical conductance of blood within the LV
into volume measurements. A solid-state transducer simultaneously
measures LV pressure, and a real-time measurement of pressurevolume relationships across the cardiac cycle can be obtained (Fig.
4-50). These data points provide an advanced measure of hemody-
namic conditions associated with acute and chronic cardiac injury
(Fig. 4-51) and are now more commonly applied as a method to under-
stand the impact of drug and device therapy on changes in cardiac
structure and function.
S
D
D
ED
ED
DD
D
D
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ED
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D
Invasive Hemodynamics with
Exercise and Pharmacologic
Challenges
Symptoms associated with cardiovascular disease are often absent at
rest and provoked by exertion. For this reason, exercise testing in the
cardiac catheterization laboratory can unmask hemodynamic abnormalities that explain exertional symptoms due to coronar y insufficiency, systolic heart failure, impaired diastolic function, valvular
heart disease, and pericardial disease. During exercise, a normal
physiologic response includes an increase in oxygen consumption by
skeletal muscle along with increased oxygen extraction from arterial
blood. To match this rising oxygen demand, HR and contractile function increase resulting in an augmented delivery of oxygen through
increased cardiac CO. Assuming that lung function is normal, arterial
oxygen saturation remains normal, whereas venous oxygen saturation
decreases (due to increased consumption by skeletal muscle). This
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Hemodynamic Data
Arterial elastance (Ea)
ESP
=
Ea
4
Pressure
Potential
energy
Figure 4-49 Basic pressure-volume loop interpretation. Each pressure-
volume (PV) loop represents one cardiac cycle. Beginning at the end of
isovolumic relaxation (1), left ventricular (LV) volume increases during dias-
tole (1 to 2). At end diastole (2), LV volume is maximal and isovolumic
contraction begins (2 to 3). At the peak of isovolumic contraction, LV pressure exceeds aortic (Ao) pressure and blood begins to eject from the LV into
the aor ta (3). During this systolic ejection phase, LV volume decreases until
Ao pressure exceeds LV pressure and the Ao valve closes, which is known
as the end-systolic pressure-volume (ESPV) point (4). Stroke volume (SV) is
represented by the width of the PV loop as the difference between endsystolic and end -diastolic volumes (1 to 2). Load-independent contractility,
also known as end-systolic elastance (Ees), is defined as the maximal slope
of the ESPV point under various loading conditions, known as the ESPV
relationship (ESPVR). Effective ar terial elastance (Ea) is defined as the ratio
of end-systolic pressure and SV. Under steady-state conditions, optimal LV
pump ef ficiency occurs when Ea : Emax approaches 1. Ea is a component
of afterload, which is defined as the resistance to LV ejection throughout
systole, and can be represented as the product of end-systolic pressure (ESP)
and end-diastolic volume (EDV). (Courtesy of Navin Kapur, MD.)
1
End-systolic elastance (Ees)
SV
Afterload = wall stress = ESP × EDV
3
Stroke
volume
Volume
Stroke work (PV area)
2
net increase in the arteriovenous oxygen (AVO2) difference correlates
with an increase in CO.
Exercise may be categorized as dynamic (bicycle ergometr y;
repeated arm or leg lifts) or static (isometric hand grip). Both dynamic
and static exercise increases HR, CO, and systemic arterial pressure,
with either reduced or preserved peripheral vascular resistance.
Hemodynamic measurements using either type of exercise should be
first made under resting conditions, then during peak exercise. An
adequate response to exercise includes:
1. Normal ventilatory responses (i.e., arterial oxygen extraction)
2. Normal HR increases in response to an increase in CO
3. Normal ventricular volume responses (i.e., decrease in cardiac
filling pressures due to higher CO and increase in diastolic
relaxation)
4. Adequate metabolic substrate use (i.e., appropriate use of glucose
as an energy source without generating lactic acid)
Dynamic Exercise
Dynamic exercise measures the ability of the cardiovascular system
to supply oxygen in keeping with the demands of the heart. Oxygen
consumption and work-load increases should be parallel until the
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Stroke volume
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Hemodynamic Data 227
1
Ees
1
2
3
4
Pressure
2
A
C
Figure 4 -50 Hemodynamic conditions associated with stages of cardiac
injury and treatment profiles. A, Frank-Starling curves represent the relationship (slope) between stroke volume (SV) (or cardiac output [CO]) and left
ventricular end-diastolic pressure (LVEDP) or left ventricular end-diastolic
volume (LVEDV). B to D, Pressure volume (PV ) loops represent the relationship between left ventricular (LV) pressure and LV volume. A to D, Resting
conditions are represented by slope 1 and solid- lined PV loops. Increased
LVEDP or LVEDV is associated with increased SV. B, Acute cardiac injur y
reduces the Frank-Starling curve (slope 2) and end- systolic elastance (Ees;
dashed line) and increases end- diastolic volume and pressure. C, Chronic
systolic heart failure is associated with a reduced Frank-Starling curve (slope
3) and Ees. Patients with compensated systolic heart failure may demonstrate preser ved SV (width of the PV loop), increased LVEDV, and normal or
mildly increased LVEDP. Increased LVEDP or LVEDV are associated with
small increases in SV. D, Decompensated systolic heart failure or cardio genic shock is associated with reduced Ees and a flat Frank-Starling curve
(slope 4). In this condition, increased LVEDP or LVEDV are not associated
with increased SV. (Courtesy of Navin Kapur, MD.)
LVEDP or LVEDV
Volume
B
3
D
Volume
4
Volume
maximum oxygen consumption for the patient’s size is reached.
Dynamic exercise in the catheterization laboratory requires simultaneous right- and left-heart pressure measurements at rest and during
exercise. Most commonly, a supine bicycle that allows for quantification of exercise in watts is attached to the catheterization table. The
patient’s oxygen consumption is also measured and compared to
hemodynamic responses. Supine exercise differs from normal upright
exercise in several ways: (1) Ventricular volumes are larger when the
patient is supine rather than upright, (2) HR and diastolic arterial pressure are higher the patient is upright rather than supine, (3) pulmonary
and intracardiac filling pressures are lower when the patient is upright,
(4) SV increases by 100% with maximal exercise when the patient is
upright and only 20% to 50% when the patient is supine, and (5) both
upright and supine exercise is normally associated with increases in
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Hemodynamic Data
2
1
Ees
↑Wall stress = ↑ESP × ∆EDV
EDV
); dashed lines, modulated
1
Ees
Volume
1
2
Ea
Ea
↑ESP
↑↑ SV
Pressure
C
EDV
Volume
B
ESP
=
2
Ees
↓SV
↑Wall stress = ↑ESP × ∆EDV
↑Ea
SV
ESP
=
1
Ea
Pressure
Ees
↑ESP
=
2
↑Wall stress = ↑ESP × ↑EDV
↑SV
Ea
SV
ESP
=
1
Ea
Pressure
EDV
Volume
A
). (Cour tesy of Navin Kapur, MD.)
2
Figure 4- 51 Impact of altered loading conditions on ventricular pressure and volume. A, Increasing preload augments left ventricular (LV) stroke volume (SV) (horizontal arrows)
and increases both end-systolic pressure (ESP) and end- diastolic volume (EDV) without changing elastance at end-systolic elastance (Ees) or arterial elastance (Ea). The net effect
is increased LV wall stress (i.e., afterload) due to increased ESP and EDV. B, Vasopressors increase ESP and reduce SV without affecting EDV or Ees. Both Ea and LV wall stress
are increased due to elevated ESP. C, Inotropes increase myocardial contractility (Ees), ESP, and SV without affecting EDV. Ea is decreased due to increased SV, but LV wall stress
is increased due to increased ESP. Inotropes also increase hear t rate (HR) and promote myocardial oxygen demand. Solid lines, Baseline conditions (
conditions (
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Hemodynamic Data 229
left ventricular end-diastolic volume (LVEDV) and decreases in endsystolic volume (ESV), with a concomitant increase in LV ejection
fraction. In patients with coronary artery disease (CAD), these findings
may not occur.
Methodology for the performance of a dynamic exercise test in
the catheterization laboratory can be as follows:
1. With the patient in a supine position, obtain resting hemodynamic
data. For supine cycle ergometry, record resting hemodynamics
with passive leg elevation before initiation of exercise.
2. Start exercise using either supine cycle ergometry or outstretched
arm adduction weight (4 to 5 lbs.) lifting. Patients performing leg
exercise can cycle at 60 rpm, starting at a 20-watt workload and
increasing by 10-watt increments in 3-minute stages to maximum
tolerated levels.
3. For patients performing arm exercise, increase repetition frequency
gradually to subjective fatigue. HR and hemodynamic changes
including CO can be recorded after 2 minutes of low-level exercise
(20 watts), after 4 minutes, and at peak exercise, and during 1 and
5 minutes of recovery with legs still elevated if using supine cycle
ergometry (Borlaug et al Circ HF 2010; 3:588–595).
Analyze data with respect to change in hemodynamics (i.e., valve
gradients), CO, and oxygen consumption. Patients may be unable to
exercise due to leg weakness, depressed cardiac function, peripheral
vascular disease, or severe deconditioning. These factors may preclude determination of accurate exercise results in the catheterization
laboratory and should be considered before undertaking the study.
Measurements of Response to Exercise
1. CO, a useful measurement for studying practically all types of heart
disease, predicts a normal response and allows categorization of a
given patient’s response.
a. Dexter index: The predicted cardiac index (CI) with exercise is
equal to 2.99 × 0.0059 × measured O2 consumption index with
exercise. The measured CI is the CO divided by body surface
area (BSA). The normal Dexter index equals the measured CI with
exercise, divided by the predicted CI . The result should be >1.
b. Normal exercise factor: For every 100-mL/min increase in O2
consumption with exercise, the CO should increase by at least
600 mL/min. Thus, normal exercise factor = mL/min CO divided
by mL/min O
Note: Exercise factor is calculated directly from observed changes
in CO and O
2. Note appropriate increases in arterial blood pressure and HR.
3. Compute LV volumes (useful in myopathy, coronary, and valvular
heart disease). With exercise, changes in LVEDV and LVEDP (more
commonly used) may be plotted against observed changes in some
parameter of LV systolic function (SV or SW) to define a modified
LV function curve.
4. Recording changes in filling pressures or valvular gradients are
useful in myopathy, coronary, and valvular heart disease. In particular, patients with symptoms of heart failure and preserved systolic function demonstrate significant perturbation of diastolic
filling pressures and CO with provocative exercise testing.
consumption ≥6.
2
consumption; it is not indexed to BSA.
2
Isometric Exercise
Isometric exercise consists of skeletal muscle contraction without
shortening. In the cardiac catheterization laboratory, isometric exercise commonly is performed using a handgrip with a graded hand
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dynamometer. Measurements of hemodynamics and ventricular function are obtained during sustained hand grip at a pre-determined
range (15% to 50% of the maximal handgrip contraction) for a period
of 3 to 4 minutes. The size of the involved muscle group is unimportant,
provided that maximal voluntary contraction is maintained to increase
oxygen demand during the isometric exercise period. Isometric
exercise is easy to perform and repeat and requires inexpensive
equipment. It does not involve body motion that may interfere with
hemodynamic measurements. An involuntary Valsalva maneuver may
occur during unsupervised isometric exercise. Careful monitoring,
patient cooperation, and practice in the use of the handgrip dynamometer will minimize false hemodynamic information. In patients
with CAD, isometric exercise rarely precipitates ischemia but may
induce new LV wall motion abnormalities, a decrease in LV ejection
fraction, and an increase in ESV with no change in diastolic volume.
SV and CO may decline during isometric exercise. In patients with
CHF, HR and systemic pressure may rise appropriately with a fall in
SV and CO, resulting in an increase in LVEDV and PA pressure.
Hemodynamic Data
Pharmacologic Testing
Treatment with vasoactive drugs is another approach to study cardiovascular function using invasive hemodynamics in the catheterization
laboratory. Changes in preload, afterload, and contractility have a
profound impact on ventricular function (see Fig. 4-51). Altering
loading conditions can be helpful when evaluating patients with valvular heart disease. For example, in patients with stage D2 low-output/
low-gradient AS, low-dose dobutamine stress testing with echocardiography or invasive hemodynamic measurements is recommended
to help distinguish patients with moderate or severe AS in the setting
of primary myocardial dysfunction.
Vasodilator testing with invasive hemodynamics is an important
part of the evaluation for patients with primary or secondary pulmonary hypertension. In primary pulmonary hypertension (PPH), vasodilator testing is used to identify potential responders to therapy with
calcium channel blockers and to establish prognosis. In these cases,
RHC is required for the diagnosis of PPH, which is defined by a mean
pulmonary artery pressure (mPAP) >
<15, and a pressure-volume relationship (PVR) >3 Wood units. Vaso-
dilator testing is performed with increasing exposure to vasodilators,
such as epoprostenol, adenosine, or inhaled nitric oxide. An acute
response to vasodilator testing is defined as a decrease in mPAP by at
least 10 mm Hg to an absolute level less than 40 mm Hg without a
decrease in CO.
Provocative testing is also an important part of the evaluation for
patients with advanced systolic heart failure who are being considered
for OHTx. Relative contraindications to OHTx include a PVR ≥5, a
pulmonary vascular resistance index (PVRI) ≥6, and a transpulmonary gradient (TPG) ≥16. A PA systolic pressure ≥
of the aforementioned elevations in pulmonary pressures are associated with increased mortality after OHTx. For these reasons, RHC is
required in all OHTx candidates and should be repeated annually until
transplantation or every 3 to 6 months if the patient has documented
pulmonary hypertension. Vasodilator testing is performed to evaluate
for potentially reversible secondary pulmonary hypertension due to
pulmonary venous congestion and left-sided heart failure. Vasodilator testing is recommended in potential OHTx candidates with a pulmonary artery systolic pressure (PASP) ≥50, TPG ≥15, or PVR ≥3.
Ideally, patients should have a PCWP <25 before testing to limit contribution from ongoing pulmonary venous congestion. Agents (such
as, nitroglycerine, nipride, inhaled nitric oxide, epoprostenol, or milrinone) are often used to assess pulmonary pressures in patients with
advanced heart failure. If acute vasodilator testing fails, patients are
25 mm Hg, a PCWP or LVEDP
60 mm Hg and any
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Hemodynamic Data 231
often admitted for 48 to 72 hours of continuous infusion therapy with
milrinone and diuretics to optimize pulmonary pressures. In select
cases, acute mechanical support can be used to reduce left-heart
filling pressures and evaluate reversibility of secondary pulmonary
hypertension.
Basic Electrocardiography in the
Cardiac Catheterization Laboratory
Basic electrocardiography may be unfamiliar to the new catheterization laboratory technician or nurse. This section reviews the fundamentals of electrocardiography as used in the cardiac catheterization
laboratory for monitoring of patients.
Cardiac Electrical System
Myocardial contraction is triggered by electrical activity. For every
beat on the ECG, a corresponding pressure pulse usually occurs from
myocardial contraction. The heart’s electrical system has specialized
tissue for the origination and transmission of electrical impulses. The
normal sequence of electrical activation is shown in Figure 4-52
and consists of the following: sinoatrial node, atrial tissue, AV node,
bundle of His, bundle branches, Purkinje fibers, and ventricular
myocardium.
Electrocardiogram
The ECG is a graphic recording of electrical impulses that are generated by depolarization (contraction) and repolarization (relaxation) of
the myocardium. The standard ECG includes six limb leads and six
chest leads. The proper placement of electrodes for recording the
12-lead ECG is shown in Figures 4-53 and 4-54.
The ECG 12 leads reflect different electrical views of the heart
depolarization and repolarization. Typically, certain leads are associated with electrical activity from specific parts of the myocardium.
Leads II, III, and aV
heart; leads I and aV
Figure 4-52 Genesis of electrocardiogram (ECG) and pathways through
the hear t. AV, Atrioventricular; SA, sinoatrial. (Modified from the CIBA Collection of Medical Illustrations, Vol. 5.)
reflect electrical activity in the inferior wall of the
F
and chest leads V5 and V6, reflect electrical
L
SA node
Atrial muscle
AV node
Common
bundle
Bundle
branches
Purkinje fibers
Ventricular muscle
Action potentials
P
QRS
0.2 0.4 0.6
Seconds
T
U
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