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stenosis; ventriculography or echocardiography for dynamic mitral
regurgitation).
5. A final set of recovery measurements are recorded and the feet are
removed from the cycle.
an arm ergometer or by lifting weights. Increases in heart rate and
CO are less marked with arm exercise because smaller muscles
are recruited, but increases in filling pressures can still be detected.
During arm exercise, patients often perform a Valsalva maneuver
that can spuriously increase all intracardiac pressures owing to
the increase in intrapleural pressure. Therefore, to obtain diagnostic quality data, patients must be coached to avoid engaging this
maneuver.
tion of absolute pressure levels and their proportionality to determine
origin of elevation (e.g., left sided or pulmonary) and changes in stroke
volume and CO. Pulmonary resistance and transvalvular gradients
should be calculated. Patients with heart failure display abnormal
increases in LV filling pressure and pulmonary artery pressure, with
inadequate vasodilation and a depressed CO and heart rate response.
Patients with pulmonary vascular disease have pulmonar y hypertension (mean pulmonary artery pressure >
change in LV filling pressure, and thus an elevated pulmonary resistance (i.e., >2.5 Wood units × m
Research Techniques
If leg ergometry is not possible, exercise may be performed using
Interpretation of hemodynamic findings encompasses examina-
30 mm Hg), no significant
2
).
Isometric Exercise
Isometric exercise (skeletal muscle contraction without shortening)
also may be performed using a handgrip with a graded hand dynamometer. Measurements of hemodynamic data and ventricular function are obtained during sustained handgrip at a predetermined range
(30% to 50% of the maximal handgrip contraction) for 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 does
not involve body motion that may interfere with hemodynamic measurements and is feasible in a larger number of laboratories. Isometric
exercise increases heart rate and CO without significant effects on
vascular resistance. As with arm weights, an involuntary Valsalva
maneuver during straining may occur during unsupervised isometric
exercise; and thus, respiratory patterns should be observed. Careful
monitoring, patient cooperation, and practice in use of the handgrip
dynamometer minimize false hemodynamic information.
Other Physiologic Maneuvers
Valsalva Maneuver
The Valsalva maneuver is performed by having the patient forcibly
expire against a closed glottis and strain as if having a bowel movement. This increases intrathoracic pressure, which initially reduces
afterload (transmural wall stress) in the strain phase, and then subsequently reduces venous return and stroke volume in ensuing phases
(Fig. 9-24). Shortly after Valsalva release, venous return increases,
causing an increase in stroke volume and blood pressure with reflex
bradycardia (overshoot phase). The magnitude of the Valsalva maneuver can be quantified by measuring the pressure against which the
patient expires. An adequate maneuver requires maintenance of
approximately 20- to 30-mm Hg positive intrathoracic pressure for 10
to 15 seconds. The Valsalva maneuver can be performed safely and
without complications by almost any patient. The blood pressure
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1 sec
ECG
200 mm Hg
100 cm/sec
Figure 9-24 Valsalva maneuver showing the effects on aor tic (Ao) pres-
sure, mean coronary velocity (MV), phasic coronar y velocit y (PV), and right
atrial (RA) pressure. The four phases of the Valsalva maneuver (see text)
are enumerated I, II, III, and IV. ECG, Electrocardiogram.
MV
PV
Ao
RA
I
0
II
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Research Techniques 413
III
IV
response to the Valsalva maneuver can be used to assess LV filling
pressures, because the normal drop in systolic arterial pressure is lost
in patients with elevated pulmonary wedge pressure; pulmonary
venous congestion is so extreme that they cannot drop EDV (Figs. 9-24
and 9-25). In addition, hemodynamic findings of hypertrophic cardiomyopathy and different types of valvular lesions may be more pronounced during the Valsalva maneuver because of changes in
ventricular load and ejection (see Chapter 3).
Muller Maneuver
The patient performs the Muller maneuver by inspiring against a
closed glottis; thus, this maneuver is essentially the opposite of the
Valsalva. The subject inhales, reducing intrathoracic pressure to −30
to −
60 mm Hg for 30 seconds. This enhances venous return to the right
side of the heart while also increasing LV afterload (increased transmural wall stress). Increases in LV EDVs and ESVs are noted with
diminished stroke volume, reduced CO, and reduced EF. This maneuver is used to augment right-sided heart murmurs and to decrease the
physical findings of obstructive cardiomyopathy by a reduction in LV
outflow gradient. Right-to-left shunting is enhanced during the Muller
maneuver and also acutely during strain release in the Valsalva
maneuver.
Cold Pressor Testing
Cold pressor testing stimulates the sympathetic nervous system, mediated by cold-induced pain receptor activation in the forearm, hand, or
forehead. Hemodynamic findings occurring with cold pressor testing
include increases in heart rate (5% to 15%), systolic and mean arterial
pressure (15% to 20%), and CO. These responses usually occur within
2 minutes of application of the cold stimulus. In normal subjects, cold
pressor testing increases coronary blood flow and reduces coronary
vascular resistance, possibly through enhanced flow-mediated vasodilation. Cold pressor testing in some patients with coronar y artery
disease causes coronary vasoconstriction, which may be potentiated
by a β-adrenergic blockade. Angina is rarely precipitated, although
changes in regional LV function may occur.
Hyperventilation
Hyperventilation has been used to induce coronary spasm. Deep
breathing (30 breaths/min for 5 minutes) is a commonly used method.
Ischemia is rarely precipitated during hyperventilation but may
commonly occur at the termination of rapid breathing. Heart rate,
oxygen consumption, arteriovenous oxygen difference, and arterial
pH increase during hyper ventilation, whereas arterial pressure,
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Research Techniques
4
200
150
100
(mm Hg)
50
Arterial pressure
A
B
0
150
100
50
(mm Hg)
Arterial pressure
0
200
150
100
(mm Hg)
50
Arterial pressure
0
C
Figure 9-25 Changes in ar terial blood pressure in response to the Val-
salva maneuver. The initial strain phase of the Valsalva (1) produces an
increase in pressure related to the increase in intrathoracic pressure. During
ongoing forced expiration against a closed glottis (2), preload declines in
the normal heart (A), reducing blood pressure. Valsalva release (3) causes
an immediate decrease in pressure due to loss of increased intrathoracic
pressure. Release is then followed by an overshoot phase (4) related to
enhanced venous return and increased stroke volume. C, In patients with
heart failure and markedly elevated left-heart filling pressures, Valsalva
does not result in a sufficient drop in preload to reduce stroke volume
(because of marked congestion), so pressure remains elevated until release.
This is termed the “square wave” response and is indicative of pulmonar y
capillar y wedge pressure (PCWP) of >25 mm Hg. Response B, (termed
“absent overshoot”) is intermediate between normal and the square wave
and is reflective of modestly elevated filling pressures. (From Zema MJ,
Restivo B, Sos T, et al: Lef t ventricular dysfunction— bedside Valsalva
manoeuvre. Br Heart J 44:562, 1980.)
1
2
3
1
2
3
2
1
Start Stop
3
pulmonary artery pressure, and arterial PCO2 fall. Peripheral vascular
resistance, CO, and LV stroke volume are unchanged with the increase
in LVEF seen in normal patients. These abnormalities may not be
observed in patients with stable or variant angina.
Pharmacologic Stress
Pharmacologic stresses are used to assess alterations of ventricular
function.
Nitrates
Nitrates decrease systolic and mean arterial pressure and produce a
reflex increase in heart rate in patients who do not have congestion
at rest. Nitroglycerin is a predominant venodilator and thus serves to
preferentially reduce preload, although afterload reduction may also
be seen, particularly in patients with elevated arterial impedance at
rest. Nitrates do not have direct effects on LV performance, except
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indirectly through reflex autonomic stimulation. Nitroglycerin relieves
coronary vasospasm and ischemia, which may indirectly lead to
improved LV function in some patients.
Amyl nitrite, usually given as an inhalation, acts in a fashion
similar to that of nitroglycerin but is much more rapid in action. This
acute preload reduction makes amyl nitrate useful for detecting
dynamic obstruction in hypertrophic cardiomyopathy.
Nitroprusside is a balanced arterial and venous dilator and can
potently reduce LV preload and afterload. Because of enhanced afterload sensitivity, patients with systolic heart failure may derive marked
benefit from nitroprusside, with improvements in CO, reduction in
filling pressure, and mild or no drop in blood pressure. In contrast,
elderly patients and especially those with heart failure and preserved
EF display much more dramatic reductions in blood pressure with
nitroprusside. Nitroglycerin and nitroprusside are commonly used to
reduce left-heart pressures and determine reversibility of pulmonary
hypertension in heart failure patients. Nitroprusside may also be used
in low-gradient, low-output aortic stenosis to discern whether true
severe valvular stenosis is present.
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Research Techniques 415
β-Adrenergic Stimulation
Dobutamine and isoproterenol are synthetic catecholamines that
increase contractility and heart rate and reduce vascular resistance.
IV infusions and 2D echocardiographic examination of LV wall motion
are used to screen for ischemia. These agents are also given in patients
with low-gradient, low-output aortic stenosis to determine true severity
and evaluate for provocable LV outflow gradients in patients with
hypertrophic cardiomyopathy. Isoproterenol is generally preferred for
the latter type of patient because dobutamine can induce significant
gradients even in nondiseased hearts.
Pacing
Temporary transvenous pacing may be used in the catheterization
laboratory to increase myocardial oxygen demand and blood flow or
examine relationships between heart rate and contractility (forcefrequency response) or relaxation (rate-relaxation response). Pacing
may also be used to regularize heart rate in patients with atrial fibrillation (e.g., for studies examining ventricular interdependence in pericardial constriction, which require a normalized rate). In contrast to
exercise and β-adrenergic agonists, pacing does not increase CO or
enhance venous return, and it cannot be considered as a physiologic
stressor to recapitulate physical exertion.
Rapid Volume Loading
Bolus infusion of saline is often performed to unmask diastolic dysfunction or pericardial constriction in patients with normal right atrial
pressures at baseline. Under normal circumstances, the heart can
accommodate this increase in filling volume and enhance output by
the Frank-Starling mechanism. With diastolic dysfunction and/or pericardial restraint, this ability is compromised, and pressures or signs of
constriction may become more evident. A simpler alternative involves
performing measurements during a straight leg raise, which also
enhances venous return. Approximately 20% of healthy volunteers will
develop a pulmonary wedge pressure of >
infusion, but values >18 mm Hg are strong evidence for abnormal LV
diastolic compliance properties. Like pacing, volume loading cannot
be considered to be an adequate substitute for exercise because the
changes in heart rate, preload, afterload, wall stress, contractility,
and myocardial oxygen demand are quite different between the two
stressors.
15 mm Hg with rapid saline
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Research Techniques
Nurse and Technician Viewpoint
The nursing and technical staff should be presented with a clear,
concise project protocol, which should include the following:
1. Overview of the project with clearly delineated objectives
2. Patient safety
3. Special equipment if necessary
4. Additional staffing if required
5. Data sheets (prepared to facilitate study periods)
If additional sterile equipment is necessary, a “protocol pack”
with all additional equipment aids should be included with setup.
Many research techniques require the use of special catheters that
must be interfaced with various flow meters, computers, and other
equipment. Personnel must be careful not to contaminate the sterile
field when connecting the catheter to the interface cable. There are
two ways to approach this situation. One is to sterilize all interface
cables. The other is to wrap the nonsterile cable in a sterile drape. If
the latter technique is used, the physician must be careful not to pull
the nonsterile cable into the sterile field. If medications are involved,
dose calculation worksheets aid the staff in drug preparation.
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10
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Interventional Cardiology
Procedures
MORTON J. KERN • MICHAEL LEE
Percutaneous coronary and structural heart disease interventional
techniques are commonly performed after diagnostic angiography for
patients with ischemic and structural (e.g., valvular or atrial septal
defects [ASDs]) heart disease. The Interventional Cardiac Catheteriza-
tion Handbook, a companion book to this volume, expands on the
concepts presented in this chapter and provides a more detailed foundation for indications, contraindications, and complications of interventional cardiology techniques. Tables 10-1 and 10-2 list diagnostic
and therapeutic interventional procedures performed in the catheterization laboratory.
Percutaneous Coronary
Interventions
Coronary balloon angioplasty was first performed in 1977. Up to that
time, coronary artery bypass graft (CABG) surgery was the only alternative to medical treatment of coronary artery disease. During CABG,
a segment of leg vein, arm artery, and/or chest wall artery is attached
to the heart to detour blood around the narrowed portion (i.e., stenosis) of a coronary artery. Percutaneous transluminal coronary angioplasty (PTCA) (with the introduction of stents, PTCA is now called
percutaneous coronar y intervention [PCI]) provided an alternative to
CABG. Without surgery, PCI selectively enlarges the narrowed portion
of the artery by the insertion of a long thin balloon to open the blocked
artery. Rarely used by themselves today, coronary balloons are now
used to predilate the lesion and facilitate the delivery of coronary
stents (metal meshlike stainless steel or metal alloy implants) and with
other devices (such as, cutters, grinders, lasers, and aspiration catheters) to treat a wide variety of artery problems. These methods are
collectively referred to as PCI. The nomenclature is informative:
•
Percutaneous refers to the nonsurgical insertion of a catheter into
the body through a small puncture site in the skin, usually into an
artery.
•
Coronary identifies the specific artery to be dilated.
•
Intervention denotes the technique for remodeling a blood vessel
through the introduction of an expandable stent, balloon catheter,
or other specialized tools for treating a diseased arter y.
Figure 10-1 shows the process of performing PCI. A guiding cath-
eter is seated in the coronary ostium. A thin, steerable guidewire is
introduced into the coronary artery to traverse the stenosis into the
distal aspect of the artery. A balloon angioplasty catheter, which is
considerably smaller than the guiding catheter, is inserted through the
guiding catheter and positioned (in the artery) across the stenotic area
by tracking it over the guidewire. The balloon or stent is on the PCI
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Interventional Cardiology Procedures
Table 10 -1
Diagnostic and Therapeutic Procedures in the Cardiac
Catheterization Laboratory
Diagnostic Procedures Therapeutic Procedures
Coronary angiography PCIs (balloon, stents, rotablator,
Ventriculography Valvuloplasty, TAVR, mitral clip
Hemodynamics ASD, PF O, PDA, VSD shunt closure
Shunt detection Thrombolysis, thromboaspiration
Aortic and peripheral angiography Coil embolization
Pulmonary angiogr aphy Pericardiocentesis, window
Coronary hemody namics
Endomyocardial biopsy
ASD, Atrial septal defect; P CI, p ercutaneous coronary inter vention; PDA, patent
ductus arteriosus; PFO, patent foram en ovale; TAVR, t ranscatheter aortic valve
replac ement; VSD, ventricular septal defec t.
cutting balloon, and so on)
Table 10 -2
Applications of Percutaneous Coronary Intervention
Devices
Special Lesion Type Stent
Type A
Complex
Ostial
Diffuse
Total occlusion
Calcified bifurcation
SVG focal
SVG diffuse
SVG thrombotic
Complication
Acute occlusion
Thrombosis
Perforation @ – – –
+++, Highly applicable; + +, somewhat helpful; +, applicable; ±, marginally applicable
depending on status; –, not applicable; @, covered stent; SVG, saphenous vein
graf t.
+++ + ±
++ ++ +
++ ++ +
+ + ++
++ +
± ++ +++
+++ ± ±
+ ±
±
+++
++
+
Cutting
Balloon Rotablator
– –
– –
–
– –
– –
– –
± ±
Thrombus
Aspiration
–
–
–
–
–
–
++
±
+++
catheter. After correct positioning within the area to be treated, the
balloon on the PCI catheter is inflated several times at 10 to 16 atmospheres (atm) for periods ranging from 10 to 30 seconds. The inflation
and deflation of the balloon stent in the blocked artery restores blood
flow to an area of the heart previously deprived by the stenosed artery.
After successful stent implantation, patients usually stay overnight in
the hospital and are discharged the following morning. Patients can
usually resume their normal routine within several days.
How Do Balloon Angioplasty and
Stents Work?
Several theories regarding the mechanisms of angioplasty have been
proposed.
Disruption of Plaque and Arterial Wall
The major effective mechanism of balloon angioplasty involves a
balloon that inflates and exerts pressure against the plaque and
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Interventional Cardiology Procedures 421
PTCA
Treatment
External
elastic
lamina
Restenosis
Internal
elastic
lamina
Intimal
area
A
Stenosed Vessel
External
elastic
Tunica
lamina
media
Lumen
Treatment Restenosis
Internal
elastic
lamina
Intimal
area
Coronary Stenting
External
elastic
lamina
Internal
elastic
lamina
Intimal
area
B
Stent
C
Figure 10-1 Possible mechanisms of restenosis after percutaneous trans-
luminal coronary angioplasty (PTCA) and coronary stenting. A, Atherosclerosis. B, PTCA to left and restenosis following PTCA on right. C, Coronar y
stenting to left and restenosis of stent to right. (With permission from
Monahan FD, et al: Coronary artery disease and dysrhythmias. In PHIPPS’
medical-surgical nursing: health and illness perspective, ed 8, St. Louis,
2007, Mosby, Fig. 29-11.)
arterial wall, fracturing and splitting the plaque. The concentric lesion
fractures and splits at its thinnest and weakest point, whereas an
eccentric lesion splits at the junction of the plaque and the arterial
wall. Dissection, or separation of the plaque from the medial wall,
releases the “splinting” effect that is caused by the lesion and results
in a larger lumen. This is the major effective mechanism of balloon
angioplasty.
Loss of Elastic Recoil
Balloon dilation thins and stretches the medial wall, causing the
medial wall to lose its elastic properties. The degree of elastic recoil
loss is affected by the balloon-to-artery size ratio. Over time (1 to 6
weeks), the artery may re-narrow due to elastic recoil, which is prevented by placement of a stent in the artery.
Redistribution and Compression of
Plaque Components
Shear pressures cause denudation or stripping of endothelial cells and
the extrusion or pushing out of plaque components. Molding of the
softer lipid material may occur, but this effect accounts for a small part
of the overall effect of angioplasty.
Mechanism of Stents
Stents scaffold the lumen and plaque open, holding back dissection
flaps and stopping vessel recoil and re-narrowing of the lumen.
Restenosis is the re-narrowing of the vessel after treatment by
balloon and stent, leading to recurrence of myocardial ischemia and
potentially a return of anginal symptoms. Significant restenosis is not
considered a true complication but is an adverse event that may
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