Right Heart Catheterization: Swan-Ganz Catheter презентация

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Right 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

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 4Swan-Ganz Catheter


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 7Right Heart Catheterization


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 20Oxygen Parameters


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 43Wiggers Diagram


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 48Wall Motion Abnormalities


Слайд 49Aortic Stenosis


Слайд 50Coronary Anatomy
Depending on coronary anatomy: 1 VD, 2 VD and 3

VD; LMCA disease

mm


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 58Post PTCA with stent


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 65Impella Device


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


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