Transcript Hemodynamic Principles Cardiac Catheterization Laboratory Simulation Training Curriculum 2-1

Hemodynamic Principles
Cardiac Catheterization Laboratory
Simulation Training Curriculum
2-1
Invasive Cardiovascular Curriculum
Hemodynamic Principles
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-2
Ischemic Heart Disease
Acute Inferior Myocardial Infarction
Adapted from http://www.ecglibrary.com/
2-3
Ischemic Heart Disease
Acute Anterior Myocardial Infarction
Adapted from http://www.ecglibrary.com/
2-4
Ischemic Heart Disease
Acute Posterior Myocardial Infarction
Adapted from http://www.ecglibrary.com/
2-5
Ischemic Heart Disease
Old Inferior Myocardial Infarction
Adapted from http://www.ecglibrary.com/
2-6
Ischemic Heart Disease
Acute Myocardial Infarction in the
Presence of Left Bundle Branch Block
Adapted from http://www.ecglibrary.com/
2-7
Hypertrophy Patterns
Left Ventricular Hypertrophy (LVH)
Adapted from http://www.ecglibrary.com/
2-8
Hypertrophy Patterns
Mitral Stenosis
Adapted from http://www.ecglibrary.com/
2-9
Hypertrophy Patterns
Right Atrial Hypertrophy
Adapted from http://www.ecglibrary.com/
2-10
Hypertrophy Patterns
Left Ventricular Hypertrophy in the
Presence of Left Anterior hemiblock
Adapted from http://www.ecglibrary.com/
2-11
Atrioventricular (AV) Block
First Degree AV block
Adapted from http://www.ecglibrary.com/
2-12
Atrioventricular (AV) Block
2 to 1 AV Block
Adapted from http://www.ecglibrary.com/
2-13
Atrioventricular (AV) Block
Complete Heart Block
Adapted from http://www.ecglibrary.com/
2-14
Atrioventricular (AV) Block
Atrial Fibrillation and Complete Heart Block
Adapted from http://www.ecglibrary.com/
2-15
Bundle Branch Block
Right Bundle Branch Block
Adapted from http://www.ecglibrary.com/
2-16
Bundle Branch Block
Left Anterior Hemiblock
Adapted from http://www.ecglibrary.com/
2-17
Bundle Branch Block
Left Bundle Branch Block
Adapted from http://www.ecglibrary.com/
2-18
Bundle Branch Block
'Trifasicular' Block
Adapted from http://www.ecglibrary.com/
2-19
Supraventricular Rhythms
Sinus Bradycardia
Adapted from http://www.ecglibrary.com/
2-20
Supraventricular Rhythms
Sinus Tachycardia
Adapted from http://www.ecglibrary.com/
2-21
Supraventricular Rhythms
Atrial Bigeminy
Adapted from http://www.ecglibrary.com/
2-22
Supraventricular Rhythms
Atrial Flutter
Adapted from http://www.ecglibrary.com/
2-23
Supraventricular Rhythms
Wolf-Parkinson-White Syndrome With Atrial Fibrillation
Adapted from http://www.ecglibrary.com/
2-24
Ventricular Rhythms
Ventricular Bigeminy
Adapted from http://www.ecglibrary.com/
2-25
Ventricular Rhythms
Polymorphous ventricular tachycardia
(Torsade de pointes)
Adapted from http://www.ecglibrary.com/
2-26
Ventricular Rhythms
Ventricular Fibrillation
Adapted from http://www.ecglibrary.com/
2-27
Invasive Cardiovascular Curriculum
Hemodynamic Principles
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-28
Pressure
Waveforms
Resolution of a normal
ventricular pressure
curve (top) into its first
10 harmonics by
Fourier analysis.
Hϋrthle Manometer
Grossmans “Catheterization” 7th Ed. pg. 135.
2-29
Factors that Influence the Magnitude of
Reflected Waves
Factors that augment pressure wave reflections
Vasoconstriction
Heart Failure
Hypertension
Aortic or ileofemoral obstruction
Valsalva Maneuver- after release
Factors that diminish pressure wave reflections
Vasodilatation
Physiologic (e.g., fever)
Pharmacologic (e.g., nitroglycerin, nitroprusside)
Hypovolemia
Hypotension
Valsalva Maneuver- strain phase
Grossmans “Catheterization” 7th Ed. pg. 135.
2-30
Wave Pressure Generator
Left ventricular pressure measured with a fluid-filled standard catheter and micromanometer
(catheter tip pressure manometer) in a patient undergoing cardiac catheterization
Adapted from Nichols et al. Cardiovasc Res 1978; 12:566
2-31
Practical Evaluation of Dynamic Response
Characteristics of a Catheter-transducer System
2-32
System for Pressure
Measurement with
excellent Frequency
Response
Strain Gauge Pressure
Transducer
Strain Gauge Connection
of the Wheatstone Bridge
2-33
Technique for Measurement
of a Patient’s Anteroposterior
Diameter
2-34
2-35
2-36
2-37
Transformation
of Arterial
Pressure
Waveform with
Transmission to
the Periphery in
a Healthy 30year old man
2-38
Invasive Cardiovascular Curriculum
Physiologic Monitoring
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-39
Invasive Cardiovascular Curriculum
Physiologic Monitoring
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-40
CATHSAP6: Coronary Angiography and Intervention
2-41
Aortic Stenosis
• Most common valve lesion being considered for
surgical replacement in United States
• AVR improves survival of symptomatic patients
(especially in patients over 65)
• Symptomatic state and LV function improve or
normalize in most patients after surgery
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Aortic Stenosis: Etiologies
Age < 70
Passik CS, et al, Mayo Clin Proc 62:119, 1987
Age  70
2-43
Aortic Stenosis: Natural History
Ross J Jr, Braunwald E. Circulation 38[Suppl V]:61, 1968
2-44
CATHSAP6: Coronary Angiography and Intervention
2-45
CATHSAP6: Coronary Angiography and Intervention
2-46
Aortic Stenosis and CHF
• Life expectancy ~ 2 years
• Clinical improvement with AVR is not guaranteed
• With diminishing ejection fraction, both
perioperative and overall mortality increase
2-47
AVR and Preoperative EF
Survival Probability
1
0.8
EF > 60%
EF 46-60%
0.6
EF 30-45%
EF < 30%
0.4
0.2
0
0
1
3
5
7
Postoperative Year
Morris, et al. Ann Thorac Surg 1993: 56:22-30
2-48
AS and LVEF  35%
• Operative Risk of AVR is high
– 30-day mortality 9%
– Worse in setting of concomitant CAD (>= 2
vessel disease associated with RR 4.6)
• However, clinical outcomes are still good, in
general, with surgery
– 76 % show improved EF
– 88% have improvement in symptoms (NYHA
class)
Connolly, H, et al. Circulation. 1997; 95: 2395-2400.
2-49
Pitfalls in Low-Output AS
• Valve Area calculation is flow dependent:
• “Pseudostenosis” is possible if Cardiac
output is less than 4.5 L/min and gradient is
low
• Aortic Valve Resistance may be better
indicator of severity (< 275 dynes/sec/cm-5)
Cannon, et al. JACC 1992; 20:1517-23
2-50
Noninvasive Estimation of AVA
• Doppler Echocardiography utilizes continuity
equation to calculate AVA
– Principle: volumetric flow per unit time in a
flow channel is equal in obstructed and
nonobstructed portions
– FVI1 x CSA1 = FVI2 x CSA2
– Can Measure LVOT diameter, FVI in LVOT
and Aorta by doppler
– AVA = ( ALVOT x FVILVOT ) / FVIAorta
• Also a Flow-Dependent measure
2-51
AVA by ECHO/Doppler (cm2)
AVA: Cath/ECHO Correlation
2.0
1.0
R = 0.87
SEE +/- 0.13
0.0
0.0
1.0
2.0
AVA by Catheterization (cm2)
St. John Sutton, Textbook of ECHO, 1996.
2-52
Clinical Problem: Who Benefits?
• Patients with critical AS and CHF fall into 2 distinct
subgroups
– pure “afterload mismatch”
• Depression of LV function on basis of excessive
wall stress in face of chronic pressure overload
• Reduction in afterload by AVR results in immediate
improvement in ventricular performance
• Excellent prognosis with AVR
– depressed myocardial contractility
• coexisting cardiomyopathy
• Poor prognosis with AVR
2-53
Defining “High-Risk” Patients
• Markers of low wall stress / depressed
contractility*
– Low mean transvalvular gradient (< 30 mm Hg)
– Low LV systolic pressure (< 150 mm Hg)
• Patients with a low transvalvular gradient
have poor prognosis with AVR
– ~ 1/3 die in perioperative period (UT Southwestern
experience)**
– ~ 1/2 (56 %) show symptomatic improvement
*Carabello,
et al. Circulation 1980; 62(1): 42-48.
**Brogan, et al. JACC 1993; 21:1657-1660.
2-54
Dobutamine Stress
• ECHO or simultaneous R/L heart cath to
measure AV hemodynamics with escalating
doses of dobutamine
• Marked improvement in AVA (> 20%) with
dobutamine suggests non-severe AS
• During DSE, demonstration of contractile
reserve or persistence of severe AS (by
calculated AVA) correlates with good surgical
outcomes.
Monin, et al. JACC 2001; 37(8): 2101-7.
Schwammenthal, et al. Chest 2001; 119(6): 1766-77
deFillipi, et al. Am J Card, 1995; 75:191-94.
2-55
Valvular
Hemodynamics
in patients with
AS and LV
dysfunction
N = 24
Schwammenthal, et al. Chest 2001; 119(6): 1766-77
2-56
High-Risk AVR
• Mayo Clinic Experience
• 52 patients : EF  35% , AS with transvalvular
mean gradient  30 mm Hg
– Perioperative (30-day) mortality 21 %
– 62% survival at 3 years
– 74 % with improvement in EF post-op
– 77% of survivors had improvement in
functional status  1 NYHA class
Connolly, et al. Circulation 2000; 101:1940-46
2-57
Survival After AVR
in Patients with LV
Dysfunction
Stratified by AV gradient
Connolly, et al. Circulation 2000; 101:1940-46
2-58
Predicting Outcome with High-Risk AVR
• Predictors of poor operative outcome :
– advanced age at operation
• mean age of survivors 70 +/- 11 years, vs.
77+/- 8 years for those who died
– small aortic valve prosthesis (< 23 mm)
• Predictors of improvement in EF
– female sex
– low preoperative AVA
• Only improvement in functional status predicts
long term survival
Connolly, et al. Circulation 2000; 101:1940-46
2-59
Conclusions
• AVR for severe AS in patients with low EF and
low transvalvular gradient carries high
perioperative risk with diminished long-term
survival
• Surgical outcomes are best in patients with LV
dysfunction due to “afterload mismatch”, which
can be predicted by hemodynamic response to
dobutamine
• Appropriate patient selection may yield
improvement in EF, functional status, and
mortality.
2-60
Mitral Stenosis
CATHSAP6: Coronary Angiography and Intervention
2-61
CATHSAP6: Coronary Angiography and Intervention
2-62
2-63
systolic ejection period
diastolic filling period
2-64
2-65
2-66
LV
200
FA
100
PA
0
2-67
200
FA
100
0
Subvalvular
LV
2-68
LV
FA
Apex
2-69
2-70
PVC
2-71
2-72
Invasive Cardiovascular Curriculum
Physiologic Monitoring
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-73
Constrictive Pericarditis
Etiology
•
•
•
•
•
•
Idiopathic
Irradiation
Post-surgical
Infectious
Neoplastic
Connective tissue
disorder
•
•
•
•
•
Uremia
Trauma
Sarcoid
Methysergide therapy
Epicardial implantable
defibrillator patches
CATHSAP6: Coronary Angiography and Intervention
2-74
CATHSAP6: Coronary Angiography and Intervention
2-75
CATHSAP6: Coronary Angiography and Intervention
2-76
CATHSAP6: Coronary Angiography and Intervention
2-77
CATHSAP6: Coronary Angiography and Intervention
2-78
Kussmaul’s Sign
CATHSAP6: Coronary Angiography and Intervention
2-79
CATHSAP6: Coronary Angiography and Intervention
2-80
CATHSAP6: Coronary Angiography and Intervention
2-81
Cardiac
Tamponade
40
20
0
CATHSAP6: Coronary Angiography and Intervention
2-82
Balloon Pericardiotomy
2-83
Case 1: Constrictive Pericarditis
•
•
•
•
•
64 year old female
1 Year s/p 3-vessel CABG
Presents with 6 months of progressive dyspnea
and atypical chest pain
At angiography, all grafts are patent
Hemodynamics
2-84
40
Right atrium
20
0
2-85
40
20
0
LV vs. RV
2-86
40
20
0
LV vs. RV with Valsalva
2-87
Constrictive Pericarditis
Right Atrial Tracing
X-descent
y-descent
2-88
Constrictive Pericarditis – LV vs. RV.
Tachycardia Obscures Evaluation
PVB
2-89
Kussmaul sign
2-90
CATHSAP6: Coronary Angiography and Intervention
2-92
CATHSAP6: Coronary Angiography and Intervention
2-93
CATHSAP6: Coronary Angiography and Intervention
2-94
Restrictive Cardiomyopathy
2-95
Ventricular Interdependence During Respirations
Differentiates Constrictive Pericarditis from
Restrictive Cardiomyopathy
Constrictive
Pericarditis
(LV and RV discordant)
Hurrell et al, Circulation 1996; 93:2007
Restrictive
Cardiomyopathy
(LV and RV concordant)
2-96
Sensitivities, Specificities, Positive Predictive
Values, and Negative Predictive Values as a
[Return to Article]
Function of Criteria
Table 3. Sensitivities, Specificities, Positive Predictive Values, and Negative Predictive Values as a Function
Criteria
Conventional
LVEDP–RVEDP mm Hg
RVEDP/RVSP >1/3
PASP <55 mm Hg
LV RFW mm Hg
Respiratory change in RAP <3 mm Hg
Dynamic respiratory
PCWP/LV respiratory gradient mm Hg
LV/RV interdependence
5
7
5
Sensitivity,
%
Specificity,
%
PPV,
%
NPV,
%
60
93
93
93
93
38
38
24
57
48
4
52
47
61
58
57
89
25
92
92
93
100
81
95
78
94
94
100
PPV indicates positive predictive value; NPV, negative predictive value; and RAP, right atrial pressure.
[Return
Article]
Hurrellto et
al, Circulation
1996; 93:2007
2-97
Constrictive Pericarditis vs. Restrictive
Cardiomyopathy
• Greater ventricular interdependence in constrictive
pericarditis
• Greater separation of diastolic pressure in restrictive
cardiomyopathy
• LV and RV diastolic filling more rapid in constrictive
pericarditis
• Pulmonary pressures higher in restrictive
cardiomyopathy
• Adjunctive tests: evidence of pericardial thickening
(normal 1-2 mm; thickening ≥ 3 mm); pericardial
calcification, RV biopsy, exploratory thoracotomy
2-98
Case 3: Pericardial Tamponade
• 37 year old female
• 2 day history of dyspnea, fatigue and
dizziness
• Mastectomy for breast cancer 3 years ago
• Echocardiogram suggests pericardial
tamponade
• Hemodynamics
2-99
Cardiac Tamponade
Pulsus Paradoxus
200 Femoral artery
inspiration
expiration
100
0
2-100
40
Right atrium
20
0
2-101
40
Right ventricle
20
0
2-102
40
Pulmonary artery
20
0
2-103
40
Pulmonary capillary wedge
20
0
2-104
40
Before Pericardiocentesis;
Pericardium vs. RA
20
0
2-105
After Pericardiocentesis
40
20
Right atrium
Pericardium
0
2-106
After Pericardiocentesis
40
Right ventricle
20
0
2-107
After Pericardiocentesis
40
Pulmonary capillary wedge
20
0
2-108
Long-Term Effectiveness of
Pericardiocentesis
• 2/3 of patients with malignant pericardial effusions
redevelop tamponade after a median of 7 days
• More than 80% of patients with non-malignant
pericardial effusion require no further intervention
Laham et al, Heart 1996; 75:67
2-109
Variants on Constrictive-Restrictive
Physiology
• Acute enlargement of the heart with constriction
by normal pericardium
– right ventricular infarct, tricuspid regurgitation,
mitral regurgitation
• Low pressure tamponade
• Effusive-constrictive pericarditis
• Single chamber tamponade
• Localized constriction
• Occult constrictive pericarditis
2-110
Severe, Acute
Tricuspid
Regurgitation
Associated With
ConstrictiveRestrictive
Physiology
2-111
Severe, Acute Mitral Regurgitation Associated
With Constrictive-Restrictive Physiology
2-112
Variants on Constrictive-Restrictive
Physiology
• Acute enlargement of the heart with constriction
by normal pericardium
– right ventricular infarct, tricuspid regurgitation,
mitral regurgitation
• Low pressure tamponade
• Effusive-constrictive pericarditis
• Single chamber tamponade
• Localized constriction
• Occult constrictive pericarditis
2-113
Invasive Cardiovascular Curriculum
Physiologic Monitoring
a.
b.
c.
d.
e.
f.
g.
Electrocardiography
Pressure waveforms
Right and left heart catheterization
Valvular heart disease
Pericardial disease
Hypertrophic cardiomyopathy
Dampened and ventricularized waveforms
2-114
2-115
Interpretation of
Electrocardiographic
Abnormalities in Hypertrophic
Cardiomyopathy with Cardiac
Magnetic Resonance
The depth of negative T waves is
related to craniocaudal asymmetry and
apical late-enhancement.
A. EKG in a patient with extensive
hypertrophy involving substantial
portions of the apex, showing giant
negative T waves.
B. CMR image in horizontal long axis
view of the left ventricle demonstrates
A.
apical late-enhancement
B.
Dumont et al. Eur Heart J 2006; 27:1725-31
2-116
Abnormal Q waves reflect the
interrelation between upper
anterior septal thickness and
other regions of the left and
right ventricles.
A.
A. Electrocardiogram in a patient with
extensive hypertrophy involving
substantial portions of both ventricular
septum and apex, showing abnormal Qwaves ≥ 40 ms in leads I and avL.
B. End-diastolic horizontal long axis lateenhancement MR image shows
asymmetrical diffuse thickening of the
septum and concentric hypertrophy of
the apex
Dumont et al. Eur Heart J 2006; 27:1725-31
B.
2-117
Case 1: Hypertrophic Cardiomyopathy
•
•
•
•
•
A.C. is a 37 year old male
Systolic murmur detected 2 years ago
Limited by progressive dyspnea
Occasional chest pressure, no syncope
Physical exam: systolic murmur that becomes
louder during Valsalva maneuver
• Echocardiogram and cardiac catheterization are
performed
2-118
PVB
Valsalva
LV
200
FA
100
PA
0
Spike and Dome2-119
Asymmetric Septal Hypertrophy – Premature
Ventricular Beat Brings out Spike-and Dome
and Brockenbrough-Braunwald Sign
PVB
2-120
Asymmetric Septal Hypertrophy –
Valsalva Increases Gradient and Brings
out Spike-and-Dome
2-121
Provocative Maneuvers for Development of
Systolic Pressure Gradient in Hypertrophic
Cardiomyopathy
1. Valsalva maneuver
2. Amyl nitrite inhalation
3. Postextrasystolic potentiation
4. Isoproterenol
5. Exercise
2-122
200
Spike and Dome –
How come no gradient?
FA
100
0
Subvalvular Location!!
LV
2-123
LV
200
FA
100
0
Catheter Advanced Toward Apex!!
2-124
Asymmetric Septal Hypertrophy - Pullback
2-125
Asymmetric Septal Hypertrophy – Loss of
Atrial Contraction Leads to LV Obstruction
Junctional Rhythm
Sinus Rhythm
2-127
Ethanol Septal Ablation in Asymmetric
Septal Hypertrophy with Obstruction
Before Septal Infarction
After Septal Infarction
LV
FA
Lakkis et al, Circulation 1998; 98:1750
2-128
Subtypes of Hypertrophic Cardiomyopathy
• Asymmetric septal hypertrophy, with or without
obstruction (subaortic gradient may be present;
banana shaped on LVgram in RAO view)
• Apical hypertrophy (apical gradient vs. catheter
entrapment; spade shaped in RAO view)
• Concentric hypertrophy
2-129
Hypertrophic Cardiomyopathy with
Apical Hypertrophy
2-130
Hypertrophic Cardiomyopathy with
Apical Hypertrophy
2-131
Diastolic Dysfunction in Patients with
Hypertrophic Cardiomyopathy
2-132
Invasive Cardiovascular Professionals
ACLS Protocol
Physiologic Monitoring
- Electrocardiography
- Pressure waveforms
- Right and left heart catheterization
- Valvular heart disease
- Pericardial disease
- Hypertrophic cardiomyopathy
- Dampened and ventricularized waveforms
2-133
Arterial Pressure Tracings From
Guiding Catheter
Normal
Ventricularization
CATHSAP6: Coronary Angiography and Intervention
Damped
2-134