Слайд 1Right Heart Catheterization:
Swan-Ganz Catheter
Слайд 2Right Heart Catheterization
Swan-Ganz Catheter: History
Jeremy Swan (1922-2005), an Irish cardiologist, worked
in the Mayo Clinic, Rochester, and later moved to Cedars-Sinai Medical Center in Los Angeles.
His invention of the catheter is said to have derived from watching the wind playing with sails in Santa Monica.
Слайд 3Swan-Ganz Catheter: History
Jeremy Swan (1922-2005), an Irish cardiologist, worked in
the Mayo Clinic, Rochester, and later moved to Cedars-Sinai Medical Center in Los Angeles.
His description of the invention of the catheter is said to have derived from watching the wind playing with sails in Santa Monica.
William Ganz (born 1919), an American cardiologist, at Cedars-Sinai Medical Center, Los Angeles, a Professor of Medicine, University of California, Los Angeles, CA.
The work of Ganz on the thermodilution method of measuring cardiac output was incorporated into the catheter's use.
Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter.N Engl J Med 1970;283:447-51.
Слайд 5The Pulmonary Artery Catheter:
Swan-Ganz Catheter
Слайд 6Principal Indications for
Swan-Ganz Catheter
Shock of unclear etiology (cardiogenic, RV infarction,
septic, hemorrhagic)
Acute left ventricular failure of unclear etiology
Acute respiratory failure of unclear etiology
Pulmonary hypertension
Cardiac tamponade
Слайд 80
100
200
300
400
500
600
700
800
0
15
30
Atrial Systole
Ventricular Systole
Ventricular Diastole
EKG
Time (msec)
Pressure (mm Hg)
P
QRS Complex
T
P
PA Pressure
Dicrotic Notch
Right
Ventricular Pressure
a
c
v
x
y
Right Atrial Pressure
Right Sided Pressures
Cardiac Cycle
Слайд 9Right Atrium
Right Ventricle
Pulmonary Artery
PC Wedge
Rt Heart Catheterization
Слайд 10Jugular Venous Pulsations
A wave – backward flow of blood produced after
atrial contraction
C wave – tricuspid valve closing after ventricular systole
X descent – just after the c wave, a drop in jugular pressure as a result of isovolumic ventricular contraction and early atrial filling
V wave – resulting from back-pressure from right atrial filling and ventricular contraction
Y descent – follows the V wave , is a result of the tricuspid valve opening and passive filling of the ventricle during ventricular relaxation
Слайд 160
100
200
300
400
500
600
700
800
0
30
60
90
120
Atrial Systole
Ventricular Systole
Ventricular Diastole
EKG
Time (msec)
Pressure (mm Hg)
P
QRS Complex
T
P
Aorta
Dicrotic Notch
Left Ventricular
Pressure
a
c
v
x
y
Left Atrial Pressure
Cardiac
Cycle
Left Sided Pressures
Слайд 18Normal Cardiac Hemodynamics (Adult)
Слайд 19Normal Cardiac Hemodynamics (Adult)
Fick CO
CO 3.5 – 8.5 L/min
CI 2.5 – 4.5 L/min/m2
Vascular
resistance
SVR 640 - 1200 dyne-sec-cm
PVR 45 -120 dyne-sec-cm
Valve gradients
Aortic <10 mmHg
Mitral Negligible
Valve area
Aortic 2.0 - 3.0 cm2
Mitral 4.0 - 6.0 cm2
Ejection fraction 50 – 60 %
Слайд 21Normal Pressures
LA and PCW: Mean 4-12mmHg
Aorta: Systolic 90-140mmHg
Diastolic 60-90mmHg
Mean 70-105mmHg
Left Ventricle:
Systolic 90-140mmHg
End Diastolic 4-12mmHg
Right Ventricle: Systolic 15-30 mmHg
Diastolic 4-12mmHg
Pulmonary Artery: Systolic 15 – 30 mmHg
End Diastolic 1–7mmHg
RA and CVP: Mean 2 - 6 mmHg
Слайд 22Measured Variables
Mean and phasic arterial blood pressure
Heart rate
Mean right atrial pressure/waves
Systolic
and diastolic pulmonary artery and wedge pressures
Cardiac output- Fick and thermodilution
Слайд 23Calculated Variables
Cardiac index
Stroke index
Systemic vascular resistance
Pulmonary vascular resistance
Shunts
Ventricular function
Valvular stenosis
or regurgitation
Слайд 24Stenotic Orifices
Gradients
Valve orifice cross-sectional areas
Measurements assist in making decisions regarding surgical
intervention
Слайд 26Mitral Stenosis
Diastolic gradient from the left atrium to the left ventricle
Atrial
myxoma may produce similar findings
Слайд 27Cardiac Output
Three main invasive methods of measurement
Flick method
Indicator-dilution method
Angiographic method
Слайд 28Fick Method
The amount of oxygen extracted by the lungs from
air = The amount taken up by blood in its passage through the lungs
rate of lung oxygen extraction (estimated)
oxygen content of the pulmonary arterial and pulmonary venous blood
the rate of pulmonary blood flow can be calculated
pulmonary blood flow=cardiac output (Unless there is a shunt)
CO=O2 consumption/AVO2 difference x 1.36 x Hgb x 10 (L/min)
Слайд 29
The Indicator-dilution Technique and Thermodilution Technique
Dilution of an indicator is
proportional to the volume of fluid to which it is added
If the amount and concentration (Temperature) of an indicator is known the volume of fluid in which it is diluted can be calculated
The most common is the thermodilution method
Слайд 30Cardiac Output (High)
Acute
Acute hypervolemia
ARDS, severe pneumonia
Septic shock
Acute intoxications
Fever, heat stress,
malignant hyperthermia
Anxiety, emotional stress
Delirium tremens
Слайд 31Cardiac Output (High)
Chronic
Severe chronic anemia
Cirrhosis
Chronic renal failure
Pregnancy
Thyrotoxicosis
Polycythemia vera
Labile hypertension
Congenital heart disease
(PDA)
Слайд 32Cardiac Output (Low)
Acute
Acute hypovolemia (absolute or relative)
Acute severe pulmonary hypertension
Acute myocardial
pump failure (cardiogenic shock)
extensive MI
myocardial toxic injury (ethanol, CO poisoning, septic shock)
following cardiopulmonary bypass
Acute impairment of ventricular filling
Increased intrathoracic pressure
Cardiac tamponade
Stunned myocardium
Acute ischemia
Слайд 33Cardiac Output (Low)
Acute
Arrhythmias
Sustained VT
Extreme bradycardia
Acute inotropic changes in a failing myocardium
Beta-blockers
Ischemia
Acidosis
Слайд 34Cardiac Output (Low)
Chronic
Chronic severe pulmonary hypertension
Chronic myocardial pump failure
Ischemia
Hypertensive or dilated
cardiomyopathy
Severe valvular heart disease
Chronic impairment of ventricular filling
Constrictive pericarditis
Restrictive cardiomyopathy
Mitral or tricuspid stenosis
Atrial myxoma
Слайд 35Shunts
Demonstrated by an absence of an expected pressure difference
With a significant
ASD the left and right mean atrial pressures are within 5 mmHg
With VSD’s the ventricular pressures may also equilibrate
Слайд 36Shunts
Evaluation of shunts requires:
Detection
Classification
Localization
Quantitation
Слайд 37Left to Right Shunts
Mixing of saturated (systemic arterial or pulmonary venous)
with desaturated (systemic venous or pulmonary arterial) blood on the right side of the circulation
Increased pulmonary blood-flow relative to the systemic blood-flow
Слайд 38Right to Left Shunts
Mixing of desaturated (systemic venous or pulmonary arterial)
with saturated (systemic arterial or pulmonary venous) blood on the left side of the circulation, thus creating a oxygen step-down
Decreased pulmonary blood flow relative to systemic blood flow
Слайд 39Pulmonary Hypertension: Role of Right Heart Catheterization
For diagnosis
For evaluating acute vasodilator
response
For evaluating progression
For treatment selection
Lung vs. heart-lung transplantation
Слайд 40PAH: Hemodynamic Definition
PA = pulmonary artery; PVR = pulmonary vascular resistance;
TPG = transpulmonary gradient
Слайд 41PAH Hemodynamic Calculations
TPG: Transpulmonary gradient = PAmean – PCWmean
CO: Cardiac Output
(L/min)
- by thermodilution
- by Fick
PVR: Pulmonary vascular resistance = TPG/CO (Wood Units); x 80 yields PVR in dynes/sec/cm-5
Слайд 42Swan-Ganz Catheter Related Complications
Harvey S et al. The Lancet 2005; 366:472-477
Слайд 44Left Heart Catheterization: History
First human catheterization by Werner Forssmann: 1929
His work was not recognized until after World War II, when André Cournand and Dickinson W. Richards, working in the US, demonstrated the importance of catheterization to the diagnosis of heart and lung diseases. Forssmann and the two Americans shared the 1956 Nobel Prize in Physiology or Medicine for their work.
Selective coronary angiography by Mason Sones, working at the Cleveland Clinic: 1958
Melvin P. Judkins introduced the method he developed for transfemoral selective coronary angiography, known as the Judkins technique: 1966
Andreas Gruentzig in Zurich, Switzerland performed the first angioplasty on an awake patient, which was the first case to be entered into a worldwide percutaneous transluminal coronary angioplasty (PTCA) registry: 1977
Jacques Puel and Ulrich Sigwart inserted the first stent in a human coronary artery
Слайд 45Vascular Access: Left Heart Cath
Sones’ technique (brachial approach)
Judkin’s technique (femoral approach)
Radial
approach
Слайд 46Left Heart Catheterization
Coronary angiography
Left ventriculogram
Ascending aortogram
Pressure measurements in LV/aorta
Слайд 47Cardiac Angiography: Ventriculography
A contrast roadmap of the left ventricle allows for
evaluation of:
Ventricular chamber dimensions
Global and segmental systolic function
Presence and severity of mitral regurgitation
Congenital defects (VSD)
LVH
Mitral valve prolapse
Слайд 50Coronary Anatomy
Depending on coronary anatomy: 1 VD, 2 VD and 3
Слайд 51Treatment Strategies of CAD
Medical treatment, PCI or CABG
- for
pts with distal CAD; risk factors modification, ASA, b-blockers, Ca-channel antagonists, nitrates
PCI: for pts with treatable lesions in coronary arteries
CABG: for pts with 3 VD, LMCA- disease and lesions that can not be treated with PCI
Слайд 52Percutaneous Coronary Interventions (PCI)
1977: 1st Coronary angioplasty by Gruntzig
Limitation: restenosis
1939-1985
Слайд 53PCI Procedural refinements: Stents
Expandable metal mesh tubes that buttresses the dilated
segment, limit restenosis.
Drug eluting stents: further reduce cellular proliferation in response to the injury of dilatation.
Слайд 54Treatment Strategies of CAD
Stable angina
Unstable angina/non ST-elevation MI
- Risk
stratification; high-risk patients: elderly, history of CAD/MI, ST-T changes and positive cardiac markers (CK-MB and/or Troponin)
- Early invasive approach including coronary angiography within 72 hours followed by medical management (30%), PCI (60%) or CABG (10%)
Слайд 55Treatment Strategies of CAD
Stable angina
Unstable angina/non ST-elevation MI
- Risk
stratification; high-risk patients: elderly, history of CAD/MI, ST-T changes and positive cardiac markers (CK-MB and/or Troponin)
- Early invasive approach including coronary angiography within 72 hours followed by medical management (30%), PCI (60%) or CABG (10%)
STEMI
- Primary PCI as early as possible at any time
- Thrombolysis (STK, TPA, TNK)
Слайд 56STEMI: PCI vs. Thrombolysis
Advantages of PCI
Knowledge of CA anatomy
Complete opening of
the artery with low rates of reinfarction
Low risk of bleeding
Low risk of stroke
Disadvantages
Needs time
Absence of approach
Advantages of Thrombolysis
Very quick
May be given in ambulance as bolus
Disadvantages
Relatively high incidence of bleeding complications
Stroke up to 2%
Reinfarction
Слайд 57Baseline LAO
Baseline LAO/Cranial
Baseline RAO
Baseline Angiogram of Patient with Prolonged Anginal Pain
and ST-elevation in leads II, III and AVF
Слайд 59Left Heart Catheterization: Complications
Early:
Death: 0.1-0.2%
Acute MI : 0.5%
CVA: 0.05%
Severe arrhythmia: 1%
Severe
allergic reaction
Vaso-vagal reaction
Local (access related) complications: ~ 2.5%
- Bleeding (local or retroperitoneal)
- Pseudoaneurysm
- A-V fistula
- Infection
- Femoral/radial/brachial artery injury/thrombosis/stenosis/occlusion
Late:
Contrast induced nephropathy
Radiation injury
Слайд 60Contrast Induced Nephropathy: Pathogenesis
Hemodynamic changes
Reduction renal blood flow
Deceleration of
red blood cell velocity
Decrease in oxygen tension
Prominent vacuolisation
Appearance of intracytoplasmic granular structure
Occasional cell necrosis
Enhanced production of oxygen free radicals
Apoptosis
DNA fragmentation
Increase in activity of caspases
An increased serum level of endothelin
Decrease in PGE2
Decrease in NO production
Increase in adenosine
Change in concentration of vasoactive substances
Direct toxicity to renal epithelium
Слайд 61Risk Factors for the Development of Contrast-Induced Nephropathy
Слайд 62Treatment Modalities Assessed in Randomized Trials on Prevention of CIN
+
positive effect; – no effect; +/– conflicting data
Слайд 63Intraaortic Balloon
Catheter
Inner Pressure Lumen
Gas Shuttle Lumen
Catheter Tip
Membrane
Sheath
Слайд 64• ¯ Cardiac Work
• ¯ Myocardial O2 Consumption
• Cardiac Output
Principles
of Counterpulsation
Systole: IAB Deflation
Слайд 66SYNERGY
1994
1995
1996
1997
1998
1999
2000
2002
2003
2004
2005
2006
2001
Bleeding risk
Ischemic risk
ACUITY
ISAR-REACT 2
Milestones in ACS Management
Anti-Thrombin Rx
Anti-Platelet Rx
Treatment Strategy
Heparin
Aspirin
Conservative
ICTUS
Слайд 67Dynamics of Antithrombotic Therapy in Patients with ACS and Patients Undergoing
PCI
Aspirin
Aspirin
Aspirin
Aspirin
High Dose Heparin
High Dose Heparin
Low Dose Heparin, LMWH
Low Dose Heparin, LMWH
Bare-metal stents
DES
Thienopyridines
Thienopyridines
Thienopyridines
GP IIb/IIIA
GP IIb/IIIa
Direct Thrombin Inhibitors
Anti-Xa
1970-s
1990-s
2000-s
Слайд 68Mechanical Heart Failure Devices
Mancini D, Burkoff D, Circulation, 2005;112:438-446
Слайд 69PARTNER Study Design
N = 358
Inoperable
Standard
Therapy
n = 179
ASSESSMENT: Transfemoral Access
TF TAVR
n =
179
Primary Endpoint: All-Cause Mortality
Over Length of Trial (Superiority)
1:1 Randomization
VS
Symptomatic Severe Aortic Stenosis
Primary endpoint evaluated when all patients reached one year follow-up.
After primary endpoint analysis reached, patients were allowed to cross-over to TAVR.
Severe Symptomatic AS with AVA< 0.8 cm2 (EOA index
< 0.5 cm2/m2), and mean gradient > 40 mmHg
or jet velocity > 4.0 m/s
Inoperable defined as risk of death or serious irreversible morbidity of AVR as assessed by cardiologist and two surgeons exceeding 50%.
Слайд 70All-Cause Mortality Landmark Analysis
Слайд 71Catheter-Based Mitral Valve Repair: MitraClip® System
Слайд 72Investigational Device only in the US; Not available for sale in
the US
EVEREST II Randomized Clinical Trial
Study Design
279 Patients enrolled at 37 sites
Randomized 2:1
Echocardiography Core Lab and Clinical Follow-Up:
Baseline, 30 days, 6 months, 1 year, 18 months, and
annually through 5 years
Control Group
Surgical Repair or Replacement
N=95
Significant MR (3+-4+)
Specific Anatomical Criteria
Device Group
MitraClip System
N=184
Слайд 73Safety & effectiveness endpoints met
Safety: MAE rate at 30 days
MitraClip device
patients: 9.6%
MV surgery patients: 57%
Effectiveness: Clinical Success Rate at 12 months
MitraClip device patients: 72%
MV Surgery patients: 88%
Clinical benefit demonstrated for MitraClip System and MV surgery patients through 12 months
Improved LV function
Improved NYHA Functional Class
Improved Quality of Life
Surgery remains an option after the MitraClip procedure
EVEREST II RCT: Summary